FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Ference, J
Curtin, S
AF Ference, Jennifer
Curtin, Suzanne
TI Attention to lexical stress and early vocabulary growth in 5-month-olds
at risk for autism spectrum disorder
SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY
LA English
DT Article
DE Speech perception; Lexical stress; Vocabulary development; Autism
spectrum disorder; Infant siblings; Language
ID INFANT-DIRECTED SPEECH; WORD SEGMENTATION; PATTERN-DISCRIMINATION; YOUNG
INFANTS; LANGUAGE; PERCEPTION; PREFERENCE; PROSODY; CHILDREN; ENGLISH
AB Typically developing infants differentiate strong-weak (trochaic) and weak-strong (iambic) stress patterns by 2 months of age. The ability to discriminate rhythmical patterns, such as lexical stress, has been argued to facilitate language development, suggesting that a difficulty in discriminating stress might affect early word learning as reflected in vocabulary size. Children with autism spectrum disorder (ASD) often have difficulty in correctly producing lexical stress, yet little is known about how they perceive it. The current study tested 5-month-old infants with typically developing older siblings (SIBS-TD) and infants with an older sibling diagnosed with ASD (SIBS-A) on their ability to differentiate the trochaic and iambic stress patterns of the word form gaba. SIBS-TD infants showed an increased interest in attention to the trochaic stress pattern, which was also positively correlated with vocabulary comprehension at 12 months of age. In contrast, SIBS-A infants attended equally to these stress patterns, although this was unrelated to later vocabulary size. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Ference, Jennifer; Curtin, Suzanne] Univ Calgary, Dept Psychol, Calgary, AB T2N 1N4, Canada.
RP Curtin, S (reprint author), Univ Calgary, Dept Psychol, 2500 Univ Dr NW, Calgary, AB T2N 1N4, Canada.
EM scurtin@ucalgary.ca
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NR 59
TC 4
Z9 4
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-0965
EI 1096-0457
J9 J EXP CHILD PSYCHOL
JI J. Exp. Child Psychol.
PD DEC
PY 2013
VL 116
IS 4
BP 891
EP 903
DI 10.1016/j.jecp.2013.08.006
PG 13
WC Psychology, Developmental; Psychology, Experimental
SC Psychology
GA 252GJ
UT WOS:000326992800008
PM 24077464
ER
PT J
AU Thaler, NS
Allen, DN
Sutton, GP
Vertinski, M
Ringdahl, EN
AF Thaler, Nicholas S.
Allen, Daniel N.
Sutton, Griffin P.
Vertinski, Mary
Ringdahl, Erik N.
TI Differential impairment of social cognition factors in bipolar disorder
with and without psychotic features and schizophrenia
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Bipolar disorder; Social cognition; Psychosis; Theory of mind; Emotion
processing; Factor analysis
ID HIGH-FUNCTIONING AUTISM; EMOTION PERCEPTION; MIND DEFICITS; RECOGNITION;
INTELLIGENCE; METAANALYSIS; MARKERS; ADULTS
AB While it is well-established that patients with schizophrenia and bipolar disorder exhibit deficits in social cognition, few studies have separately examined bipolar disorder with and without psychotic features. The current study addressed this gap by comparing patients with bipolar disorder with (BD+) and without (BD-) psychotic features, patients with schizophrenia (SZ), and healthy controls (NC) across social cognitive measures. Principal factor analysis on five social cognition tasks extracted a two-factor structure comprised of social/emotional processing and theory of mind. Factor scores were compared among the four groups. Results identified differential patterns of impairment between the BD+ and BD- group on the social/emotional processing factor while all clinical groups performed poorer than controls on the theory of mind factor. This provides evidence that a history of psychosis should be taken into account while evaluating social cognition in patients with bipolar disorder and also raises hypotheses about the relationship between social cognition and psychosis. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Thaler, Nicholas S.; Allen, Daniel N.; Sutton, Griffin P.; Vertinski, Mary; Ringdahl, Erik N.] Univ Nevada, Las Vegas, NV 89154 USA.
RP Thaler, NS (reprint author), 760 Westwood Plaza,C8-746, Los Angeles, CA 90095 USA.
EM Nthaler@mednet.ucla.edu
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NR 47
TC 4
Z9 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
EI 1879-1379
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD DEC
PY 2013
VL 47
IS 12
BP 2004
EP 2010
DI 10.1016/j.jpsychires.2013.09.010
PG 7
WC Psychiatry
SC Psychiatry
GA 253ST
UT WOS:000327110300023
PM 24112946
ER
PT J
AU Anderson, LC
Bolling, DZ
Schelinski, S
Coffman, MC
Pelphrey, KA
Kaiser, MD
AF Anderson, L. C.
Bolling, D. Z.
Schelinski, S.
Coffman, M. C.
Pelphrey, K. A.
Kaiser, M. D.
TI Sex differences in the development of brain mechanisms for processing
biological motion
SO NEUROIMAGE
LA English
DT Article
DE Sex differences; Brain development; Biological motion; fMRI; Amygdala
ID EMOTIONAL FACIAL EXPRESSIONS; GENDER-DIFFERENCES; AMYGDALA ACTIVATION;
SOCIAL-PERCEPTION; NEURAL MECHANISMS; DE-NOVO; AUTISM; ATTENTION;
CHILDREN; CEREBELLUM
AB Disorders related to social functioning including autism and schizophrenia differ drastically in incidence and severity between males and females. Little is known about the neural systems underlying these sex-linked differences in risk and resiliency. Using functional magnetic resonance imaging and a task involving the visual perception of point-light displays of coherent and scrambled biological motion, we discovered sex differences in the development of neural systems for basic social perception. In adults, we identified enhanced activity during coherent biological motion perception in females relative to males in a network of brain regions previously implicated in social perception including amygdala, medial temporal gyrus, and temporal pole. These sex differences were less pronounced in our sample of school-age youth. We hypothesize that the robust neural circuitry supporting social perception in females, which diverges from males beginning in childhood, may underlie sex differences in disorders related to social processing. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Anderson, L. C.; Bolling, D. Z.; Schelinski, S.; Coffman, M. C.; Pelphrey, K. A.; Kaiser, M. D.] Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06520 USA.
RP Anderson, LC (reprint author), Yale Univ, 230 South Frontage Rd, New Haven, CT 06520 USA.
EM laura.anderson8588@gmail.com
FU Yale Magnetic Research Resonance Imaging Center; Simons Foundation;
National Institute of Mental Health; NIH [T32 NS07224]
FX We thank the children and adults who made this research possible. We
would also like to thank the Yale Magnetic Research Resonance Imaging
Center for their support. This work was funded by grants from the Simons
Foundation and the National Institute of Mental Health (to K.A.P.).
D.Z.B. was supported by an NIH T32 training grant (T32 NS07224).
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NR 79
TC 8
Z9 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
EI 1095-9572
J9 NEUROIMAGE
JI Neuroimage
PD DEC
PY 2013
VL 83
BP 751
EP 760
DI 10.1016/j.neuroimage.2013.07.040
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 251TN
UT WOS:000326953700069
PM 23876243
ER
PT J
AU Carter, CJ
AF Carter, Chris J.
TI Susceptibility genes are enriched in those of the herpes simplex virus
1/host interactome in psychiatric and neurological disorders
SO PATHOGENS AND DISEASE
LA English
DT Article
DE Alzheimer's disease; multiple sclerosis; schizophrenia; mood disorders
ID PROGRAMMED CELL-DEATH; ALZHEIMERS-DISEASE; MULTIPLE-SCLEROSIS; BIPOLAR
DISORDER; HUMAN-EVOLUTION; NEURODEGENERATIVE DISORDERS; CCR5-DELTA-32
POLYMORPHISM; SYSTEMATIC METAANALYSES; HELICOBACTER-PYLORI;
PARKINSONS-DISEASE
AB Herpes simplex virus 1 (HSV-1) can promote beta-amyloid deposition and tau phosphorylation, demyelination or cognitive deficits relevant to Alzheimer's disease or multiple sclerosis and to many neuropsychiatric disorders with which it has been implicated. A seroprevalence much higher than disease incidence has called into question any primary causal role. However, as also the case with risk-promoting polymorphisms (also present in control populations), any causal effects are likely to be conditional. During its life cycle, the virus binds to many proteins and modifies the expression of multiple genes creating a host/pathogen interactome involving 1347 host genes. This data set is heavily enriched in the susceptibility genes for multiple sclerosis (P=1.3E-99)>Alzheimer's disease>schizophrenia>Parkinsonism>depression>bipolar disorder>childhood obesity>chronic fatigue>autism>and anorexia (P=0.047) but not attention deficit hyperactivity disorder, a relationship maintained for genome-wide association study data sets in multiple sclerosis and Alzheimer's disease. Overlapping susceptibility gene/interactome data sets disrupt signalling networks relevant to each disease, suggesting that disease susceptibility genes may filter the attentions of the pathogen towards particular pathways and pathologies. In this way, the same pathogen could contribute to multiple diseases in a gene-dependent manner and condition the risk-promoting effects of the genes whose function it disrupts.
This article reports the analysis of existing information on the susceptibility genes for psychiatric and neurological disorders and find that they, with the exception of ADHD, are enriched in the gene set of the herpes simplex (HSV-1)/host interactome. This could shed light on their pathogenesis, and introduces an intriguing hypothesis of a potential viral etiology of these diseases.
C1 [Carter, Chris J.] PolygenicPathways, Hastings, E Sussex, England.
RP Carter, CJ (reprint author), Flat 2,40 Baldslow Rd, Hastings TN34 2EY, E Sussex, England.
EM chris_car@yahoo.com
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NR 157
TC 3
Z9 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 2049-632X
J9 PATHOG DIS
JI Pathog. Dis.
PD DEC
PY 2013
VL 69
IS 3
BP 240
EP 261
DI 10.1111/2049-632X.12077
PG 22
WC Immunology; Infectious Diseases; Microbiology
SC Immunology; Infectious Diseases; Microbiology
GA 255CJ
UT WOS:000327216600009
PM 23913659
ER
PT J
AU Melchior, L
Bertelsen, B
Debes, NM
Groth, C
Skov, L
Mikkelsen, JD
Brondum-Nielsen, K
Tumer, Z
AF Melchior, Linea
Bertelsen, Birgitte
Debes, Nanette Mol
Groth, Camilla
Skov, Liselotte
Mikkelsen, Jens D.
Brondum-Nielsen, Karen
Tumer, Zeynep
TI Microduplication of 15q13.3 and Xq21.31 in a Family With Tourette
Syndrome and Comorbidities
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE Tourette syndrome; ADHD; PABPC5; PCDH11X; CHRNA7; CHRFAM7A
ID X-CHROMOSOME INACTIVATION; NICOTINIC RECEPTOR GENE; COPY NUMBER
VARIANTS; DELETION POLYMORPHISM; PARTIAL DUPLICATION; SEX-CHROMOSOMES;
CHRNA7 GENE; MICRODELETION; CHRFAM7A; SCHIZOPHRENIA
AB Tourette syndrome (TS) is a childhood onset neurodevelopmental disorder. Although it is widely accepted that genetic factors play a significant role in TS pathogenesis the etiology of this disorder is largely unknown. Identification of rare copy number variations (CNVs) as susceptibility factors in several neuropsychiatric disorders such as attention deficit-hyperactivity disorder (ADHD), autism and schizophrenia, suggests involvement of these rare structural changes also in TS etiology. In a male patient with TS, ADHD, and OCD (obsessive compulsive disorder) we identified two microduplications (at 15q13.3 and Xq21.31) inherited from a mother with subclinical ADHD. The 15q duplication included the CHRNA7 gene; while two genes, PABPC5 and PCDH11X, were within the Xq duplication. The Xq21.31 duplication was present in three brothers with TS including the proband, but not in an unaffected brother, whereas the 15q duplication was present only in the proband and his mother. The structural variations observed in this family may contribute to the observed symptoms, but further studies are necessary to investigate the possible involvement of the described variations in the TS etiology. (c) 2013 Wiley Periodicals, Inc.
C1 [Melchior, Linea; Bertelsen, Birgitte; Brondum-Nielsen, Karen; Tumer, Zeynep] Copenhagen Univ Hosp, Kennedy Ctr, Rigshosp, DK-2600 Glostrup, Denmark.
[Debes, Nanette Mol; Groth, Camilla; Skov, Liselotte] Herlev Univ Hosp, Dept Pediat, Tourette Clin, DK-2730 Herlev, Denmark.
[Mikkelsen, Jens D.] Univ Copenhagen Hosp, Neurobiol Res Unit, Rigshosp, DK-2100 Copenhagen, Denmark.
RP Tumer, Z (reprint author), Copenhagen Univ Hosp, Kennedy Ctr, Rigshosp, Gl Landevej 7, DK-2600 Glostrup, Denmark.
EM zeynep.tumer@regionh.dk
FU Lundbeck Foundation [R24-A2419, R24-2419]; Strategic Research Council
Cognito
FX Grant sponsor: Lundbeck Foundation; Grant numbers: R24-A2419, R24-2419;
Grant sponsor: Strategic Research Council Cognito.
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NR 40
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4841
EI 1552-485X
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD DEC
PY 2013
VL 162
IS 8
BP 825
EP 831
DI 10.1002/ajmg.b.32186
PG 7
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 246AE
UT WOS:000326506700004
PM 23894120
ER
PT J
AU Daviss, WB
O'Donnell, L
Soileau, BT
Heard, P
Carter, E
Pliszka, SR
Gelfond, JAL
Hale, DE
Cody, JD
AF Daviss, William B.
O'Donnell, Louise
Soileau, Bridgette T.
Heard, Patricia
Carter, Erika
Pliszka, Steven R.
Gelfond, Jonathan A. L.
Hale, Daniel E.
Cody, Jannine D.
TI Mood Disorders in Individuals With Distal 18q Deletions
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE depression; bipolar disorder; Chromosome 18; 18q-; hemideletion; mood
disorders; ZADH2; TSHZ1
ID BIPOLAR AFFECTIVE-DISORDER; AUTISM SPECTRUM DISORDERS; CHROMOSOME-18 DNA
MARKERS; GENOME-WIDE ASSOCIATION; EARLY-ONSET; TELEPHONE INTERVIEW;
SUSCEPTIBILITY LOCI; MAJOR DEPRESSION; LINKAGE ANALYSIS; II DISORDER
AB We examined 36 participants at least 4 years old with hemizygous distal deletions of the long arm of Chromosome 18 (18q-) for histories of mood disorders and to characterize these disorders clinically. Since each participant had a different region of 18q hemizygosity, our goal was also to identify their common region of hemizygosity associated with mood disorders; thereby identifying candidate causal genes in that region. Lifetime mood and other psychiatric disorders were determined by semi-structured interviews of patients and parents, supplemented by reviews of medical and psychiatric records, and norm-referenced psychological assessment instruments, for psychiatric symptoms, cognitive problems, and adaptive functioning. Sixteen participants were identified with lifetime mood disorders (ages 12-42 years, 71% female, 14 having had unipolar depression and 2 with bipolar disorders). From the group of 20 who did not meet criteria for a mood disorder; a comparison group of 6 participants were identified who were matched for age range and deletion size. Mood-disordered patients had high rates of anxiety (75%) and externalizing behavior disorders (44%), and significant mean differences from comparison patients (P<0.05), including higher overall and verbal IQs and lower autistic symptoms. A critical region was defined in the mood-disordered group that included a hypothetical gene, C18orf62, and two known genes, ZADH2 and TSHZ1. We conclude that patients having terminal deletions of this critical region of the long arm of Chromosome 18 are highly likely to have mood disorders, which are often comorbid with anxiety and to a lesser extent with externalizing disorders. (c) 2013 Wiley Periodicals, Inc.
C1 [Daviss, William B.; O'Donnell, Louise; Pliszka, Steven R.] Univ Texas Hlth Sci Ctr San Antonio, Dept Psychiat, San Antonio, TX 78229 USA.
[O'Donnell, Louise; Soileau, Bridgette T.; Heard, Patricia; Carter, Erika; Hale, Daniel E.; Cody, Jannine D.] Univ Texas Hlth Sci Ctr San Antonio, Dept Pediat, San Antonio, TX 78229 USA.
[Gelfond, Jonathan A. L.] Univ Texas Hlth Sci Ctr San Antonio, Dept Epidemiol & Biostat, San Antonio, TX 78229 USA.
[Cody, Jannine D.] Chromosome 18 Registry & Res Soc, San Antonio, TX USA.
RP Cody, JD (reprint author), Chromosome 18 Clin Res Ctr, Dept Pediat, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM cody@uthscsa.edu
FU Chromosome 18 Registry and Research Society; MacDonald family; CHRISTUS
Santa Rosa Children's Hospital; Institute for the Integration of
Medicine and Science (CTSA) [8UL1TR000149]
FX Grant sponsor: Chromosome 18 Registry and Research Society; Grant
sponsor: MacDonald family; Grant sponsor: CHRISTUS Santa Rosa Children's
Hospital; Grant sponsor: Institute for the Integration of Medicine and
Science (CTSA); Grant number: 8UL1TR000149.
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NR 61
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4841
EI 1552-485X
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD DEC
PY 2013
VL 162
IS 8
BP 879
EP 888
DI 10.1002/ajmg.b.32197
PG 10
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 246AE
UT WOS:000326506700011
PM 24006251
ER
PT J
AU Sasaki, R
Uchiyama, H
Okamoto, T
Fukada, K
Ogiuchi, H
Ando, T
AF Sasaki, Ryo
Uchiyama, Hiroto
Okamoto, Toshihiro
Fukada, Kenji
Ogiuchi, Hideki
Ando, Tomohiro
TI A toothbrush impalement injury of the floor of mouth in autism child
SO DENTAL TRAUMATOLOGY
LA English
DT Article
DE autism; floor of mouth; impalement; penetrating injury
ID PENETRATING INJURIES; SOFT PALATE; MANAGEMENT; TRAUMA
AB - Penetrating injuries in the oral cavity are common in children. However, penetrating injuries with retained foreign bodies are rare. We report a case of a toothbrush impalement injury of the floor of the mouth in a child with autism. A 5-year-old boy with autism presented with an accidentally impaled toothbrush in the oral cavity. He was taken to the operation room and examined under general anesthesia. The handle of the toothbrush was cut off using rib scissors for mask ventilation, and intra-oral intubation was performed. The toothbrush was located approximately 2.5cm into the floor of the mouth. The toothbrush was removed uneventfully. Intravenous antibiotic therapy was instituted during hospitalization, and discharge from the hospital occurred 4days after the operation.
C1 [Sasaki, Ryo; Uchiyama, Hiroto; Okamoto, Toshihiro; Fukada, Kenji; Ogiuchi, Hideki; Ando, Tomohiro] Tokyo Womens Med Univ, Sch Med, Dept Oral & Maxillofacial Surg, Shinjuku Ku, Tokyo 1628666, Japan.
[Sasaki, Ryo] Tokyo Womens Med Univ, Inst Adv Biomed Engn & Sci, Shinjuku Ku, Tokyo 1628666, Japan.
RP Sasaki, R (reprint author), Tokyo Womens Med Univ, Sch Med, Dept Oral & Maxillofacial Surg, Shinjuku Ku, 8-1 Kawada cho, Tokyo 1628666, Japan.
EM sasaki@oms.twmu.ac.jp
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NR 9
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1600-4469
EI 1600-9657
J9 DENT TRAUMATOL
JI Dent. Traumatol.
PD DEC
PY 2013
VL 29
IS 6
BP 467
EP 468
DI 10.1111/j.1600-9657.2012.01116.x
PG 2
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 248HL
UT WOS:000326688700008
PM 22296118
ER
PT J
AU Al-Amin, MM
Uddin, MMN
Rahman, MM
Reza, HM
Rana, MS
AF Al-Amin, Md. Mamun
Uddin, Mir Muhammad Nasir
Rahman, Md. Mahbubur
Reza, Hasan Mahmud
Rana, Md. Sohel
TI Effect of diclofenac and antidepressants on the inflammatory response in
astrocyte cell culture
SO INFLAMMOPHARMACOLOGY
LA English
DT Article
DE Astrocyte; Serotonin; Tryptophan; Lipopolysaccharide
ID DEPRESSIVE-LIKE BEHAVIOR; INDOLEAMINE 2,3-DIOXYGENASE; INTERFERON-GAMMA;
RAT-BRAIN; T-CELLS; EXPRESSION; ALPHA
AB Central nervous system (CNS) has a completely separate immune system that communicates with the neurons by small molecules called cytokines. Cytokines are involved in many crucial processes in neuron including cell metabolism and neurotransmitter synthesis. It has been reported that cytokine imbalance is involved in the progression of many CNS diseases such as neuropsychiatric disorders (depression, schizophrenia, autism, and bipolar disorder) and neurodegenerative disorders (Parkinson's and Alzheimer's disease). Here, the effects of diclofenac, different antidepressants (sertraline, venlafaxine, and fluvoxamine), and vitamin B-6 (pyridoxine) on IL-10 and tumor necrosis factor-alpha (TNF-alpha) change with and without immune challenges with lipopolysaccharide (LPS) were investigated in in vitro culture of astrocytes from 2-day-old Swiss-Albino mice. Diclofenac and Sertraline significantly (p < 0.05) improves anti-inflammatory cytokine (IL-10) while suppress (p < 0.05) LPS-induced elevated level of pro-inflammatory mediators (TNF-alpha) in astrocyte culture. Pyridoxine was not able to reduce (p > 0.05) TNF-alpha in the astrocyte culture. Antidepressant (sertraline) showed positive effects (increased IL-10 and reduced TNF-alpha level) possibly through the suppression of Th1 lymphocytes and monocytes and stimulation of Th2 lymphocytes and monocytes/macrophages. NSAID (diclofenac) showed positive immune regulation effect possibly through the inhibition of cyclo-oxygenase enzyme. Based on these findings, it may conclude that, diclofenac and antidepressants (sertraline) may positively contribute in the cytokine production in astrocyte cell culture.
C1 [Al-Amin, Md. Mamun; Reza, Hasan Mahmud] North South Univ, Dept Pharm, Dhaka 1229, Bangladesh.
[Uddin, Mir Muhammad Nasir] Chittagong Univ, Dept Pharm, Chittagong, Bangladesh.
[Rahman, Md. Mahbubur] Univ Lubeck, Inst Pharmacol, D-23538 Lubeck, Germany.
[Rana, Md. Sohel] Jahangirnagar Univ, Dept Pharm, Dhaka 1342, Bangladesh.
RP Al-Amin, MM (reprint author), North South Univ, Dept Pharm, Plot 15,Block B, Dhaka 1229, Bangladesh.
EM alamin@northsouth.edu
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NR 15
TC 1
Z9 1
PU SPRINGER BASEL AG
PI BASEL
PA PICASSOPLATZ 4, BASEL, 4052, SWITZERLAND
SN 0925-4692
EI 1568-5608
J9 INFLAMMOPHARMACOLOGY
JI Inflammopharmacology
PD DEC
PY 2013
VL 21
IS 6
BP 421
EP 425
DI 10.1007/s10787-013-0181-9
PG 5
WC Immunology; Pharmacology & Pharmacy; Toxicology
SC Immunology; Pharmacology & Pharmacy; Toxicology
GA 248IX
UT WOS:000326693700005
PM 23896940
ER
PT J
AU Dewinter, J
Vermeiren, R
Vanwesenbeeck, I
van Nieuwenhuizen, C
AF Dewinter, Jeroen
Vermeiren, Robert
Vanwesenbeeck, Ine
van Nieuwenhuizen, Chijs
TI Autism and normative sexual development: a narrative review
SO JOURNAL OF CLINICAL NURSING
LA English
DT Article
DE Asperger's disorder; autism; review; sexual development; sexual health
ID GENDER IDENTITY DISORDER; ASPERGERS-SYNDROME; SPECTRUM DISORDER;
PARENTAL PERSPECTIVE; MENTAL-RETARDATION; CHILDREN; ADULTS; ADOLESCENTS;
BEHAVIOR; INDIVIDUALS
AB Aims and objectivesTo explore the existing knowledge on sexuality and autism spectrum disorders. To this end, the concept of normative sexual development was used as an organising framework.
BackgroundSexual health can be seen as a developmental task for all children, adolescents and adults. Core autism features are related with skills central to sexual development and functioning. More insight in sexual development in people with autism is relevant for education, support and interventions by parents and professionals in somatic and mental health care.
MethodsA comprehensive search of scientific online databases and reference lists was conducted. Publications based on qualitative and quantitative research, including case studies, were selected.
ResultsFifty-five articles and reports were selected and discussed. Information was grouped according to three domains: sexual behaviour, sexual selfhood and sexual socialisation.
ConclusionSexual development is a part of life for people with autism of all developmental levels and is generally understudied in this population. Most information was available on behavioural aspects and experiences of socialising agents, such as parents and professionals. Developmental processes and the relation between sexual behaviour, selfhood and socialisation remained unclear.
Relevance to clinical practiceNurses working in schools, institutions and general health care support children, adolescents and adults with autism and advice their families, teachers, other educators and caregivers on sexuality issues. They can have an important role in daily assessment and support of this developmental domain by actively enquiring about the different aspects of sexual development and by offering information. Our findings offer an overview on the existing knowledge and support the idea that sexual development is normative for people with autism just as for anybody else.
C1 [Dewinter, Jeroen; van Nieuwenhuizen, Chijs] Tilburg Univ, NL-5000 LE Tilburg, Netherlands.
[Dewinter, Jeroen; van Nieuwenhuizen, Chijs] GGzE, Ctr Child & Adolescent Psychiat, NL-5600 AX Eindhoven, Netherlands.
[Vermeiren, Robert] Curium LUMC, Dept Child & Adolescent Psychiat, Oegstgeest, Netherlands.
[Vermeiren, Robert] VU Univ Med Ctr VUMC, Amsterdam, Netherlands.
[Vanwesenbeeck, Ine] Univ Utrecht, Utrecht, Netherlands.
[Vanwesenbeeck, Ine] Res Rutgers WPF, Utrecht, Netherlands.
RP Dewinter, J (reprint author), GGzE, Ctr Child & Adolescent Psychiat, Postbus 909, NL-5600 AX Eindhoven, Netherlands.
EM j.dewinter@ggze.nl
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NR 66
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0962-1067
EI 1365-2702
J9 J CLIN NURS
JI J. Clin. Nurs.
PD DEC
PY 2013
VL 22
IS 23-24
SI SI
BP 3467
EP 3483
DI 10.1111/jocn.12397
PG 17
WC Nursing
SC Nursing
GA 247VK
UT WOS:000326650400025
PM 24112137
ER
PT J
AU Singer, JA
Blagov, P
Berry, M
Oost, KM
AF Singer, Jefferson A.
Blagov, Pavel
Berry, Meredith
Oost, Kathryn M.
TI Self-Defining Memories, Scripts, and the Life Story: Narrative Identity
in Personality and Psychotherapy
SO JOURNAL OF PERSONALITY
LA English
DT Article
ID POSTTRAUMATIC-STRESS-DISORDER; AUTISM SPECTRUM DISORDERS;
AUTOBIOGRAPHICAL MEMORY; REDUCED SPECIFICITY; BIPOLAR DISORDER;
OLDER-ADULTS; DEPRESSION; ADOLESCENCE; INTEGRATION; EXPERIENCE
AB An integrative model of narrative identity builds on a dual memory system that draws on episodic memory and a long-term self to generate autobiographical memories. Autobiographical memories related to critical goals in a lifetime period lead to life-story memories, which in turn become self-defining memories when linked to an individual's enduring concerns. Self-defining memories that share repetitive emotion-outcome sequences yield narrative scripts, abstracted templates that filter cognitive-affective processing. The life story is the individual's overarching narrative that provides unity and purpose over the life course. Healthy narrative identity combines memory specificity with adaptive meaning-making to achieve insight and well-being, as demonstrated through a literature review of personality and clinical research, as well as new findings from our own research program. A clinical case study drawing on this narrative identity model is also presented with implications for treatment and research.
C1 [Singer, Jefferson A.; Berry, Meredith] Connecticut Coll, New London, CT 06320 USA.
[Blagov, Pavel; Oost, Kathryn M.] Whitman Coll, Walla Walla, WA 99362 USA.
RP Singer, JA (reprint author), Connecticut Coll, Dept Psychol, New London, CT 06320 USA.
EM jasin@conncoll.edu
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NR 121
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3506
EI 1467-6494
J9 J PERS
JI J. Pers.
PD DEC
PY 2013
VL 81
IS 6
BP 569
EP 582
DI 10.1111/jopy.12005
PG 14
WC Psychology, Social
SC Psychology
GA 245LY
UT WOS:000326466400006
PM 22925032
ER
PT J
AU Barnard-Brak, L
Rojahn, J
Wei, TL
AF Barnard-Brak, Lucy
Rojahn, Johannes
Wei, Tianlan
TI Psychometric Analysis of the Behavior Problems Inventory Using an
Item-Response Theory Framework: A Sample of Individuals with
Intellectual Disabilities
SO JOURNAL OF PSYCHOPATHOLOGY AND BEHAVIORAL ASSESSMENT
LA English
DT Article
DE IRT; Behavior problems inventory; Self-injury; Stereotypy; Aggression;
Differential item functioning
ID AUTISM SPECTRUM DISORDERS; CHALLENGING BEHAVIORS;
DEVELOPMENTAL-DISABILITIES; AGGRESSIVE-BEHAVIOR; FACTOR VALIDITY;
RATING-SCALE; EM ALGORITHM; SHORT FORM; ADULTS; PREVALENCE
AB The current study used an item response theory (IRT) framework to examine the psychometric properties of the long and short forms of the Behavior Problems Inventory (BPI-01 and BPI-S respectively). The BPI measures self-injurious, aggressive/destructive, and stereotyped behaviors as manifested among individuals with intellectual and developmental disabilities. With a sample of 1,122 individuals with intellectual and developmental disabilities, it is the first IRT examination of either form of the BPI. Results reveal acceptable psychometric properties for each form of the BPI as well as minimal differential item functioning according to sex.
C1 [Barnard-Brak, Lucy; Wei, Tianlan] Texas Tech Univ, Dept Educ Psychol & Leadership, Lubbock, TX 79409 USA.
[Rojahn, Johannes] George Mason Univ, Dept Psychol, Fairfax, VA 22030 USA.
RP Barnard-Brak, L (reprint author), Texas Tech Univ, Dept Educ Psychol & Leadership, POB 41071, Lubbock, TX 79409 USA.
EM lucy.barnard-brak@ttu.edu
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NR 69
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0882-2689
EI 1573-3505
J9 J PSYCHOPATHOL BEHAV
JI J. Psychopathol. Behav. Assess.
PD DEC
PY 2013
VL 35
IS 4
BP 564
EP 577
DI 10.1007/s10862-013-9356-3
PG 14
WC Psychology, Clinical
SC Psychology
GA 248WE
UT WOS:000326735400014
ER
PT J
AU Bessa, C
Maciel, P
Rodrigues, AJ
AF Bessa, Carlos
Maciel, Patricia
Rodrigues, Ana Joao
TI Using C-elegans to Decipher the Cellular and Molecular Mechanisms
Underlying Neurodevelopmental Disorders
SO MOLECULAR NEUROBIOLOGY
LA English
DT Review
DE Neurodevelopment; C. elegans; Autism; Epilepsy; Intellectual disability
ID LINKED MENTAL-RETARDATION; NEMATODE CAENORHABDITIS-ELEGANS;
GLUTAMIC-ACID DECARBOXYLASE; NICOTINIC ACETYLCHOLINE-RECEPTORS;
IDIOPATHIC GENERALIZED EPILEPSY; AUTISM SPECTRUM DISORDER; NEURONAL
MIGRATION DEFECTS; SYNDROME CRITICAL REGION-1; POLYCYSTIC
KIDNEY-DISEASE; TAU-INDUCED NEUROTOXICITY
AB Neurodevelopmental disorders such as epilepsy, intellectual disability (ID), and autism spectrum disorders (ASDs) occur in over 2 % of the population, as the result of genetic mutations, environmental factors, or combination of both. In the last years, use of large-scale genomic techniques allowed important advances in the identification of genes/loci associated with these disorders. Nevertheless, following association of novel genes with a given disease, interpretation of findings is often difficult due to lack of information on gene function and effect of a given mutation in the corresponding protein. This brings the need to validate genetic associations from a functional perspective in model systems in a relatively fast but effective manner. In this context, the small nematode, Caenorhabditis elegans, presents a good compromise between the simplicity of cell models and the complexity of rodent nervous systems. In this article, we review the features that make C. elegans a good model for the study of neurodevelopmental diseases. We discuss its nervous system architecture and function as well as the molecular basis of behaviors that seem important in the context of different neurodevelopmental disorders. We review methodologies used to assess memory, learning, and social behavior as well as susceptibility to seizures in this organism. We will also discuss technological progresses applied in C. elegans neurobiology research, such as use of microfluidics and optogenetic tools. Finally, we will present some interesting examples of the functional analysis of genes associated with human neurodevelopmental disorders and how we can move from genes to therapies using this simple model organism.
C1 [Bessa, Carlos; Maciel, Patricia; Rodrigues, Ana Joao] Univ Minho, Sch Hlth Sci, Life & Hlth Sci Res Inst ICVS, Braga, Portugal.
[Bessa, Carlos; Maciel, Patricia; Rodrigues, Ana Joao] ICVS 3Bs PT Govt Associate Lab, Braga, Portugal.
RP Rodrigues, AJ (reprint author), ICVS 3Bs PT Govt Associate Lab, Braga, Portugal.
EM ajrodrigues@ecsaude.uminho.pt
RI Maciel, Patricia/B-5989-2009
OI Maciel, Patricia/0000-0002-0920-6350
FU Fundacao para a Ciencia e Tecnologia (FCT) [PTDC/SAU-GMG/112577/2009];
FCT [SFRH/BPD/33611/2009, SFRH/BPD/74452/2010]
FX The authors would like to acknowledge Fundacao para a Ciencia e
Tecnologia (FCT) (PTDC/SAU-GMG/112577/2009). AJR and CB are recipients
of FCT fellowships: SFRH/BPD/33611/2009 and SFRH/BPD/74452/2010,
respectively.
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NR 294
TC 2
Z9 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0893-7648
EI 1559-1182
J9 MOL NEUROBIOL
JI Mol. Neurobiol.
PD DEC
PY 2013
VL 48
IS 3
BP 465
EP 489
DI 10.1007/s12035-013-8434-6
PG 25
WC Neurosciences
SC Neurosciences & Neurology
GA 248PX
UT WOS:000326714700007
PM 23494747
ER
PT J
AU Agazzi, H
Tan, R
Tan, SY
AF Agazzi, Heather
Tan, Robin
Tan, Sim Yin
TI A Case Study of Parent-Child Interaction Therapy for the Treatment of
Autism Spectrum Disorder
SO CLINICAL CASE STUDIES
LA English
DT Article
DE parent training; PCIT; ASD
ID PERVASIVE DEVELOPMENTAL DISORDER; RANDOMIZED CONTROLLED-TRIAL; EARLY
INTERVENTION; YOUNG-CHILDREN; PDD-NOS; BEHAVIOR; FAMILIES
AB Comorbid disruptive behavior disorders occur in up to 80% of children with Autism Spectrum Disorder (ASD). Children with ASD often present as inattentive, noncompliant, and aggressive, making it difficult for them to engage in learning and social activities across settings. Parents and school staff report spending excessive time managing disruptive behaviors at the expense of engaging these children in meaningful skill development. Identifying effective interventions to decrease disruptive behaviors and increase positive skill development is of critical importance to improving outcomes for children with ASD. This case study presents the effectiveness of Parent-Child Interaction Therapy, an evidence-based intervention for young children with disruptive behavior, for addressing behavioral problems in a 7-year-old boy with ASD. Results suggested improvements in child compliance and decrease in disruptive behaviors. Further, parents increased their use of positive parenting strategies, including giving effective commands all of which serve to improve the parent-child relationship. Treatment implications for working with young children with ASD are discussed.
C1 [Agazzi, Heather; Tan, Robin; Tan, Sim Yin] Univ S Florida, Tampa, FL 33612 USA.
RP Agazzi, H (reprint author), Univ S Florida, Dept Pediat, 13101 N Bruce B Downs Blvd,CMS 1057, Tampa, FL 33612 USA.
EM hcurtiss@health.usf.edu
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NR 41
TC 1
Z9 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1534-6501
EI 1552-3802
J9 CLIN CASE STUD
JI Clin. Case Stud.
PD DEC
PY 2013
VL 12
IS 6
BP 428
EP 442
DI 10.1177/1534650113500067
PG 15
WC Psychology, Clinical; Psychiatry
SC Psychology; Psychiatry
GA AW9OU
UT WOS:000346587800003
ER
PT J
AU Chiat, S
Roy, P
AF Chiat, Shula
Roy, Penny
TI Early Predictors of Language and Social Communication Impairments at
Ages 9-11 Years: A Follow-Up Study of Early-Referred Children
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE language disorders; social communication; specific language impairment;
syntax; phonology
AB Purpose: In this study, the authors aimed to evaluate hypotheses that early sociocognition will predict later social communication and early phonology will predict later morphosyntax in clinically referred preschoolers. Method: Participants were 108 children ages 9- 11 years who had been referred to clinical services with concerns about language at age 2 - 3 years. Predictors at Time 1 ( T1) were measures of sociocognition, word/ nonword repetition, and receptive language. Outcome measures at Time 3 ( T3) included a social communication questionnaire completed by parents and tests of nonword repetition, morphosyntax, and receptive language. Results: Group- and case- level analyses revealed early sociocognition to be the strongest predictor of social communication problems, which by T3 affected almost one third of the sample. At the group level, early phonology, which was a significant problem for the majority of children at T1, was a weak predictor of morphosyntax at T3. However, at the case level the majority of children with poor morphosyntax and nonword repetition at outcome had had very low repetition scores at T1. Conclusions: In early language referrals, it is important to identify and address sociocognitive problems, a considerable risk for later social communication and autism spectrum disorders. The majority of early- referred children had phonological problems, often severe, but these require further investigation to determine their longer term significance for language.
C1 [Chiat, Shula; Roy, Penny] City Univ London, London, England.
RP Chiat, S (reprint author), City Univ London, London, England.
EM shula.chiat.1@city.ac.uk
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NR 46
TC 1
Z9 1
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
EI 1558-9102
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD DEC
PY 2013
VL 56
IS 6
BP 1824
EP 1836
PG 13
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA V37NY
UT WOS:000209283700010
PM 23926296
ER
PT J
AU Arciuli, J
Stevens, K
Trembath, D
Simpson, IC
AF Arciuli, Joanne
Stevens, Kirsten
Trembath, David
Simpson, Ian Craig
TI The Relationship Between Parent Report of Adaptive Behavior and Direct
Assessment of Reading Ability in Children With Autism Spectrum Disorder
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE autism; autism spectrum disorder (ASD); reading; literacy; Vineland
Adaptive Behavior Scales-II; parent report
AB Purpose: This study was designed to shed light on the profile of reading ability in children with autism spectrum disorder (ASD). A key aim was to examine the relationship between parent report of adaptive behavior and direct assessment of reading ability in these children. Method: The authors investigated children's reading ability using the Wide Range Achievement Test- Fourth Edition ( Wilkinson & Robertson, 2006) and the Neale Analysis of Reading Ability- Third Edition ( Neale, 2007). Parent report data was collected using the Vineland Adaptive Behavior Scales- Second Edition ( Sparrow, Cicchetti, & Balla, 2005). Participants were 21 children with ASD ( 6-11 years) and their primary caregivers. Results: Direct assessment of children's reading ability showed that some children with ASD have difficulty learning to read and exhibit particular weaknesses in comprehension. The results revealed positive relationships between Vineland Adaptive Behavior Scales scores in the Adaptive Communication domain and direct assessment of children's reading ability across 3 measures of reading ( word- level accuracy, passagelevel accuracy, and passage- level comprehension). Conclusions: Although literacy levels vary among children with ASD, some clearly struggle with reading. There is a significant relationship between parent self- report of adaptive behavior and direct assessment of children's reading ability.
C1 [Arciuli, Joanne; Stevens, Kirsten; Trembath, David; Simpson, Ian Craig] Univ Sydney, Sydney, NSW 2006, Australia.
RP Arciuli, J (reprint author), Univ Sydney, Sydney, NSW 2006, Australia.
EM joanne.arciuli@sydney.edu.au
RI Simpson, Ian/A-7492-2013
OI Simpson, Ian/0000-0002-4657-120X
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Sussman F., 1999, MORE WORDS HELPING P
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NR 55
TC 0
Z9 0
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
EI 1558-9102
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD DEC
PY 2013
VL 56
IS 6
BP 1837
EP 1844
PG 8
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA V37NY
UT WOS:000209283700011
PM 23926295
ER
PT J
AU Angoa-Perez, M
Kane, MJ
Briggs, DI
Francescutti, DM
Kuhn, DM
AF Angoa-Perez, Mariana
Kane, Michael J.
Briggs, Denise I.
Francescutti, Dina M.
Kuhn, Donald M.
TI Marble Burying and Nestlet Shredding as Tests of Repetitive,
Compulsive-like Behaviors in Mice
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Behavior; Issue 82; compulsive-like behaviors; obsessive-compulsive
disorder (OCD); autism spectrum disorders (ASD); marble burying; nestlet
shredding; TPH2 KO mice
AB Obsessive-compulsive disorder (OCD) and autism spectrum disorders (ASD) are serious and debilitating psychiatric conditions and each constitutes a significant public health concern, particularly in children. Both of these conditions are highlighted by the repeated expression of meaningless behaviors. Individuals with OCD often show checking, frequent hand washing, and counting. Children with ASDs also engage in repetitive tapping, arm or hand flapping, and rocking. These behaviors can vary widely in intensity and frequency of expression. More intense forms of repetitive behaviors can even result in injury (e.g. excessive grooming, hand washing, and self-stimulation). These behaviors are therefore very disruptive and make normal social discourse difficult. Treatment options for repetitive behaviors in OCD and ASDs are somewhat limited and there is great interest in developing more effective therapies for each condition. Numerous animal models for evaluating compulsive-like behaviors have been developed over the past three decades. Perhaps the animal models with the greatest validity and ease of use are the marble burying test and the nestlet shredding test. Both tests take advantage of the fact that the target behaviors occur spontaneously in mice. In the marble burying test, 20 marbles are arrayed on the surface of clean bedding. The number of marbles buried in a 30 min session is scored by investigators blind to the treatment or status of the subjects. In the nestlet shredding test, a nestlet comprised of pulped cotton fiber is preweighed and placed on top of cage bedding and the amount of the nestlet remaining intact after a 30 min test session is determined. Presently, we describe protocols for and show movie documentation of marble burying and nestlet shredding. Both tests are easily and accurately scored and each is sensitive to small changes in the expression of compulsive-like behaviors that result from genetic manipulations, disease, or head injury.
C1 [Angoa-Perez, Mariana; Kane, Michael J.; Briggs, Denise I.; Francescutti, Dina M.; Kuhn, Donald M.] Wayne State Univ, Sch Med, John D Dingell VA Med Ctr, Res & Dev Serv, Detroit, MI 48202 USA.
[Angoa-Perez, Mariana; Kane, Michael J.; Briggs, Denise I.; Francescutti, Dina M.; Kuhn, Donald M.] Wayne State Univ, Sch Med, Dept Psychiat & Behav Neurosci, Detroit, MI 48202 USA.
RP Kuhn, DM (reprint author), Wayne State Univ, Sch Med, John D Dingell VA Med Ctr, Res & Dev Serv, Detroit, MI 48202 USA.
EM donald.kuhn@wayne.edu
FU Department of Veterans Affairs; National Institutes of Health
FX This work was supported by grants from the Department of Veterans
Affairs and the National Institutes of Health.
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NR 21
TC 0
Z9 0
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD DEC
PY 2013
IS 82
DI 10.3791/50978
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36RR
UT WOS:000209229000052
ER
PT J
AU Ross, AS
Hunter, SK
Groth, MA
Ross, RG
AF Ross, Anne Spencer
Hunter, Sharon Kay
Groth, Mark A.
Ross, Randal Glenn
TI P50 Sensory Gating in Infants
SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS
LA English
DT Article
DE Behavior; Issue 82; Child Development; Psychophysiology; Attention
Deficit and Disruptive Behavior Disorders; Evoked Potentials; Auditory;
auditory evoked potential; sensory gating; infant; attention;
electrophysiology; infants; sensory gating; endophenotype; attention;
P50
AB Attentional deficits are common in a variety of neuropsychiatric disorders including attention deficit-hyperactivity disorder, autism, bipolar mood disorder, and schizophrenia. There has been increasing interest in the neurodevelopmental components of these attentional deficits; neurodevelopmental meaning that while the deficits become clinically prominent in childhood or adulthood, the deficits are the results of problems in brain development that begin in infancy or even prenatally. Despite this interest, there are few methods for assessing attention very early in infancy. This report focuses on one method, infant auditory P50 sensory gating.
Attention has several components. One of the earliest components of attention, termed sensory gating, allows the brain to tune out repetitive, noninformative sensory information. Auditory P50 sensory gating refers to one task designed to measure sensory gating using changes in EEG. When identical auditory stimuli are presented 500 ms apart, the evoked response (change in the EEG associated with the processing of the click) to the second stimulus is generally reduced relative to the response to the first stimulus (i.e. the response is "gated"). When response to the second stimulus is not reduced, this is considered a poor sensory gating, is reflective of impaired cerebral inhibition, and is correlated with attentional deficits.
Because the auditory P50 sensory gating task is passive, it is of potential utility in the study of young infants and may provide a window into the developmental time course of attentional deficits in a variety of neuropsychiatric disorders. The goal of this presentation is to describe the methodology for assessing infant auditory P50 sensory gating, a methodology adapted from those used in studies of adult populations.
C1 [Ross, Anne Spencer; Hunter, Sharon Kay; Groth, Mark A.; Ross, Randal Glenn] Univ Colorado, Sch Med, Dept Psychiat, Boulder, CO 80309 USA.
[Ross, Anne Spencer] Colorado State Univ, Ft Collins, CO 80523 USA.
RP Ross, RG (reprint author), Univ Colorado, Sch Med, Dept Psychiat, Boulder, CO 80309 USA.
EM randy.ross@ucdenver.edu
FU National Institutes of Health (NIH) [MH086383, MH056539, MH015442];
Institute for Children's Mental Disorders
FX This work was funded, at least in part, by the National Institutes of
Health (NIH grant numbers MH086383, MH056539 and MH015442) and by the
Institute for Children's Mental Disorders.
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NR 26
TC 0
Z9 0
PU JOURNAL OF VISUALIZED EXPERIMENTS
PI CAMBRIDGE
PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA
SN 1940-087X
J9 JOVE-J VIS EXP
JI J. Vis. Exp.
PD DEC
PY 2013
IS 82
DI 10.3791/50065
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA V36RR
UT WOS:000209229000001
ER
PT J
AU Cambridge, P
AF Cambridge, Paul
TI A rights approach to supporting the sexual fetish of a man with learning
disability: method, process and applied learning
SO BRITISH JOURNAL OF LEARNING DISABILITIES
LA English
DT Article
DE gender; learning (intellectual) disabilities; male and female sex lives;
sexuality
ID INTELLECTUAL DISABILITIES; MEN; SERVICE; PEOPLE; ABUSE
AB Accessible summary
Some men with learning disabilities have a sexual fetish which may present a support challenge for staff or carers. Sexual fetish in people with learning disabilities is often ignored, seen as pathological or associated with risk. It is possible to support sexual fetish in person-centred ways which respect individual rights and informed choice.
SummaryThis paper reports on a psycho-educational intervention associated with the sexual fetish of a man with mild learning disability and autism which centred on his use of nappies and baby paraphernalia. It outlines the nature and expression of his sexual fetish and the risks perceived to be associated with it and describes the approach developed to support him, including the aims which underpinned the work and the methods and processes employed. It was found that a person-centred psycho-educational approach from a rights based perspective achieved important changes in his life and self-esteem and helped challenge assumptions about his sexual risk. The paper also reflects on the organisational location of this work and identifies the applied learning for supporting the sexual fetish of people with learning disabilities, of value for informing sex education and sexuality support for people with learning disabilities more widely.
C1 Univ Kent, Dept Social Work, Chatham ME4 4AG, Kent, England.
RP Cambridge, P (reprint author), Univ Kent, Dept Social Work, Chatham ME4 4AG, Kent, England.
EM P.Cambridge@kent.ac.uk
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Department of Health, 2000, NO SECR GUID DEV IMP
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NR 39
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1354-4187
EI 1468-3156
J9 BRIT J LEARN DISABIL
JI Brit. J. Learn. Disabil.
PD DEC
PY 2013
VL 41
IS 4
BP 259
EP 265
DI 10.1111/j.1468-3156.2012.00750.x
PG 7
WC Education, Special
SC Education & Educational Research
GA 241QP
UT WOS:000326182600003
ER
PT J
AU James, DM
Hall, A
Phillipson, J
McCrossan, G
Falck, C
AF James, Deborah Michelle
Hall, Alex
Phillipson, John
McCrossan, Geraldine
Falck, Claire
TI Creating a person-centred culture within the North East Autism Society:
preliminary findings
SO BRITISH JOURNAL OF LEARNING DISABILITIES
LA English
DT Article
DE Autism; intervention; person-centred; qualitative methods; video
feedback; workforce
ID DISCRETE-TRIAL INSTRUCTION; TRAINING STAFF; METAANALYSIS
AB Accessible Summary
Staff who care for people with autism were shown video of themselves at work. Only good bits of video were shown to staff. Good bits were chosen because the video showed that the staff and the people with autism were enjoying being with each other. We asked four members of staff how watching the good bits of video made them think and feel. In this paper, we report what the staff said. We grouped their ideas into sets. In this paper, we report exactly what the staff said. We found that all staff felt more confident after watching the videos. They could see more ways that the people with autism were communicating with them. They could imagine being better at making relationships with people with autism. We think that finding positive moments of enjoyment using video is a good way to make things work better for staff and for the people with autism.
SummaryThis paper provides preliminary findings of the impact of a workforce coaching intervention that used video feedback in a service for children and adults with autism. The proposed mechanism for change in the intervention was the way that video footage was highlighted through editing on the part of the practitioner and the positive coaching conversation that was used to review the video edits. Four participants who had received the intervention were interviewed after the intervention. Thematic analysis of the participants' responses during the narrative style interview was conducted. The results suggest that the participants found the intervention a positive experience that raised their confidence in their work role. They reported heightened awareness of the individual needs of the people they worked with and a new appreciation of the potential for relationship between themselves and the services' users.
C1 [James, Deborah Michelle] Northumbria Univ, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England.
[James, Deborah Michelle; Falck, Claire] Univ Nottingham, NIHR Natl Biomed Res Unit Hearing, Nottingham NG7 2RD, England.
[Hall, Alex] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Phillipson, John; McCrossan, Geraldine] North East Autism Soc, Sunderland, Durham, England.
RP James, DM (reprint author), Northumbria Univ, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England.
EM deborah.james@northumbria.ac.uk
RI Hall, Alex/B-7157-2013
OI Hall, Alex/0000-0002-8849-744X
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Department of Health, 2010, VAL PEOPL NOW SUMM R
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NR 23
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1354-4187
EI 1468-3156
J9 BRIT J LEARN DISABIL
JI Brit. J. Learn. Disabil.
PD DEC
PY 2013
VL 41
IS 4
BP 296
EP 303
DI 10.1111/j.1468-3156.2012.00757.x
PG 8
WC Education, Special
SC Education & Educational Research
GA 241QP
UT WOS:000326182600008
ER
PT J
AU Yochim, EC
Silva, VT
AF Yochim, Emily Chivers
Silva, Vesta T.
TI Everyday Expertise, Autism, and "Good" Mothering in the Media Discourse
of Jenny McCarthy
SO COMMUNICATION AND CRITICAL-CULTURAL STUDIES
LA English
DT Article
DE autism; expertise; mothering in the media; ethopolitics; Jenny McCarthy;
postfeminism
AB We examine Jenny McCarthy's mediated crusade to cure and prevent autism to better understand contemporary discourses about mothering, expertise, and gender. McCarthy distrusts traditional scientific and medical expertise and exalts what have long been seen as feminine modes of knowing such as instinct and experience. Her claims dismiss the medical community as wholly corrupt while reifying women's stereotypical identity as mothers. Furthermore, her campaign demonstrates the ways in which our current ethopolitical culture - which values multiple streams of knowledge and democratizes expertise - intersects with a postfeminist culture to limit women's power and create a culture of anxiety around motherhood.
C1 [Yochim, Emily Chivers; Silva, Vesta T.] Allegheny Coll, Dept Commun Arts & Theatre, Meadville, PA 16335 USA.
RP Yochim, EC (reprint author), Allegheny Coll, Dept Commun Arts, 520 N Main St, Meadville, PA 16335 USA.
EM eyochim@allegheny.edu
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NR 31
TC 0
Z9 0
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1479-1420
EI 1479-4233
J9 COMMUN CRIT-CULT STU
JI Commun. Crit.-Cult. Stud.
PD DEC 1
PY 2013
VL 10
IS 4
BP 406
EP 426
DI 10.1080/14791420.2013.841320
PG 21
WC Cultural Studies; Communication
SC Cultural Studies; Communication
GA 241HG
UT WOS:000326156400004
ER
PT J
AU Ennis, RP
Jolivette, K
Fredrick, LD
Alberto, PA
AF Ennis, Robin Parks
Jolivette, Kristine
Fredrick, Laura D.
Alberto, Paul A.
TI Using Comparison Peers as an Objective Measure of Social Validity:
Recommendations for Researchers
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE behavior; special education; research
ID TREATMENT ACCEPTABILITY; CLASSROOM-BEHAVIOR; SCHOOL-STUDENTS;
MANAGEMENT; DISABILITIES; EDUCATION; AUTISM
C1 [Ennis, Robin Parks; Jolivette, Kristine; Fredrick, Laura D.; Alberto, Paul A.] Georgia State Univ, Atlanta, GA 30302 USA.
RP Ennis, RP (reprint author), Georgia State Univ, Dept Educ Psychol & Special Educ, POB 3979, Atlanta, GA 30302 USA.
EM rennis1@gsu.edu
CR Alberto P. A., 2013, APPL BEHAV ANAL TEAC
Boden L., 2012, TEACHING EXCEPTIONAL, V45, P32
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Coyle C, 2004, J INTELLECT DEV DIS, V29, P3, DOI 10.1080/08927020410001662642
Crone D. A., 2010, RESPONDING PROBLEM B
Eber L, 2002, J EMOT BEHAV DISORD, V10, P171, DOI 10.1177/10634266020100030501
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NR 24
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 195
EP 201
DI 10.1177/1088357612475078
PG 7
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200001
ER
PT J
AU Buggey, T
Ogle, L
AF Buggey, Tom
Ogle, Lindsey
TI The Use of Self-Modeling to Promote Social Interactions Among Young
Children
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE autism; video modeling; social interaction; young children
ID AUTISM SPECTRUM DISORDERS; INITIATIONS; PRESCHOOLERS; INTERVENTION;
BEHAVIOR; PLAY
AB Video self-modeling (VSM) has been used to teach social skills to children with autism older than 4 years of age. Attempts to use VSM with younger children with disabilities have produced less than favorable results; however, it is unclear whether VSM could be used to promote social initiations by typically developing children. Thirty minutes of staged filming, in which the four typically developing participants were prompted to interact with a peer with autism on the playground and inside during center time, was edited into 2.5- to 3-min clips. Each clip took less than 2 hr to edit. Data were collected on frequency of solitary play, initiations, parallel play, and engaged play and were then analyzed in a multiple-baseline-across-participants single-case design. Visual analysis led to the conclusion that VSM did not affect the typically developing children's behavior. Limitations of the study and cautions for using VSM with very young children are discussed.
C1 [Buggey, Tom; Ogle, Lindsey] Univ Tennessee, Chattanooga, TN 37402 USA.
RP Buggey, T (reprint author), Univ Tennessee, 205 Hunter Hall, Chattanooga, TN 37402 USA.
EM tom-buggey@utc.edu
CR Akullian J., 2007, EXCEPT CHILDREN, V73, P261
American Psychiatric Association, 2000, DIAGN STAT MAN MENT
Bandura A, 2001, ANNU REV PSYCHOL, V52, P1, DOI 10.1146/annurev.psych.52.1.1
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Buggey T, 2011, FOCUS AUTISM DEV DIS, V26, P25, DOI 10.1177/1088357609344430
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Kennedy C, 2005, SINGLE CASE DESIGNS
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NR 28
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 202
EP 211
DI 10.1177/1088357612464518
PG 10
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200002
ER
PT J
AU Downs, A
Downs, RC
AF Downs, Andrew
Downs, Robyn Conley
TI Training New Instructors to Implement Discrete Trial Teaching Strategies
With Children With Autism in a Community-Based Intervention Program
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE training; discrete trial teaching; supervision; preschools
ID BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; SKILLS; STUDENTS
AB The effects of training and supervision on instructor knowledge and performance of discrete trial teaching (DTT) within three domains (DTT Technical Skills; Work Session Preparation/Conclusion; and Student Engagement/Management) were examined in this study. Eight undergraduate student instructors received an 8-hr training in DTT and support skills accompanied by a pre- and post-test of knowledge. The instructors then taught a variety of skills to six students with autism in a community-based preschool, where instructor competence was tracked and performance feedback provided using the Discrete Trial Teaching Competency Checklist for Instructors. Competence in all three domains improved over time with performance feedback. However, significant variability was observed within and between instructors, and performance in some areas remained below optimal levels even with regular supervision and performance feedback. Implications for training and supervising instructors to implement DTT with children with autism in community-based settings are discussed.
C1 [Downs, Andrew] Univ Portland, Portland, OR 97203 USA.
[Downs, Robyn Conley] Portland State Univ, Portland, OR 97207 USA.
RP Downs, A (reprint author), Univ Portland, Dept Social & Behav Sci, MSC 185,5000 N Willamette Blvd, Portland, OR 97203 USA.
EM downs@up.edu
CR Arnal L., 2007, DEV DISABILITIES B, V35, P131
BABEL DA, 2008, DEV DISABILITIES B, V36, P67
Belfiore PJ, 2008, FOCUS AUTISM DEV DIS, V23, P95, DOI 10.1177/1088357607311445
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LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3
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NR 37
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 212
EP 221
DI 10.1177/1088357612465120
PG 10
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200003
ER
PT J
AU Fletcher-Watson, S
Leekam, SR
Findlay, JM
AF Fletcher-Watson, Sue
Leekam, Susan R.
Findlay, John M.
TI Social Interest in High-Functioning Adults With Autism Spectrum
Disorders
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE high-functioning autism; Asperger syndrome; content analysis; social
interest
ID ASPERGER-SYNDROME; ANIMATED SHAPES; EYE-MOVEMENTS; MENTAL STATES;
ATTENTION; ATTRIBUTION; PERCEPTION; PATTERNS; CHILDREN; INDIVIDUALS
AB Autism spectrum disorders (ASD) are principally characterized by impairments in social functioning. Experimental investigation often is conducted using methods measuring social attention, social cognition, and social communication. In this study, we instead measured interest in social information, making a distinction between basic-level person-centered social information such as physical attributes of people (human information) and high-level social information such as hypotheses about mental states, emotion, and relationships (social information). Based on content analysis of verbal descriptions of color images, 31 young adults (4 women), aged 17 to 25 years with ASD, and 35 typically developing young adults (8 women), aged 17 to 31 years, devoted similar proportions of their descriptions to human and social topics. Results are interpreted in the context of current calls for more ecologically valid methodology and in relation to other assessments of social processing in ASD.
C1 [Fletcher-Watson, Sue] Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland.
[Leekam, Susan R.] Cardiff Univ, Cardiff CF10 3AX, S Glam, Wales.
[Findlay, John M.] Univ Durham, Durham DH1 3HP, England.
RP Fletcher-Watson, S (reprint author), Inst Educ Community & Soc, Moray House Sch Educ, Holyrood Rd, Edinburgh EH8 8AQ, Midlothian, Scotland.
EM sue.fletcher-watson@ed.ac.uk
CR Abell F, 2000, COGNITIVE DEV, V15, P1, DOI 10.1016/S0885-2014(00)00014-9
American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
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Wechsler D, 1999, WECHSLER ABBREVIATED
WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288
NR 26
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 222
EP 229
DI 10.1177/1088357613480829
PG 8
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200004
ER
PT J
AU Strid, K
Heimann, M
Gillberg, C
Smith, L
Tjus, T
AF Strid, Karin
Heimann, Mikael
Gillberg, Christopher
Smith, Lars
Tjus, Tomas
TI Deferred Imitation and Social Communication in Speaking and Nonspeaking
Children With Autism
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE autism; social communication; deferred imitation; joint attention
ID EARLY LANGUAGE-ACQUISITION; JOINT ATTENTION; DIAGNOSTIC INTERVIEW;
SPECTRUM DISORDER; YOUNG-CHILDREN; DEVELOPMENTAL-CHANGES; 24-MONTH-OLD
INFANTS; MEMORY; IMMEDIATE; 14-MONTH-OLD
AB Deferred imitation and early social communication skills were compared among speaking and nonspeaking children with autism and children developing typically. Overall, the children with autism showed a lower frequency on measures of deferred imitation and social communication compared with typically developing children. Deferred imitation was observed at a significantly lower level among the speaking and nonspeaking groups of children with autism. However, when comparing the speaking autism group with the typical group, many differences in observed social communication disappeared. These results underscore the importance of considering children's verbal ability in autism research and clinical practice, and indicate that there are specific difficulties in deferred imitation in autism but that the social communication deficits that are observed are greatly influenced by low level of verbal ability.
C1 [Strid, Karin; Gillberg, Christopher; Tjus, Tomas] Univ Gothenburg, Gothenburg, Sweden.
[Heimann, Mikael] Linkoping Univ, S-58183 Linkoping, Sweden.
[Heimann, Mikael] Swedish Inst Disabil Res, Linkoping, Sweden.
[Smith, Lars] Reg Ctr Child & Adolescent Mental Hlth East & Sou, Oslo, Norway.
RP Strid, K (reprint author), Gothenburg Univ, Dept Psychol, Box 500, SE-40530 Gothenburg, Sweden.
EM karin.strid@psy.gu.se
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NR 61
TC 1
Z9 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 230
EP 240
DI 10.1177/1088357612468030
PG 11
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200005
ER
PT J
AU Hughes, C
Bernstein, RT
Kaplan, LM
Reilly, CM
Brigham, NL
Cosgriff, JC
Boykin, MP
AF Hughes, Carolyn
Bernstein, Rebekah T.
Kaplan, Lauren M.
Reilly, Caitlin M.
Brigham, Nicolette L.
Cosgriff, Joseph C.
Boykin, Michaela P.
TI Increasing Conversational Interactions Between Verbal High School
Students With Autism and Their Peers Without Disabilities
SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE autism; high school; communication books; general education peers;
conversational interactions
ID GENERAL-EDUCATION PEERS; SOCIAL-SKILLS INTERVENTIONS; INTELLECTUAL
DISABILITIES; SPECTRUM DISORDERS; ADOLESCENTS; YOUTH; CHILDREN; IMPROVE
AB Self-prompted communication books were used in combination with conversational peer orientation to increase conversational interactions of verbal high school students with autism or autistic-like behavior with their peers without disabilities. Previous investigators have used communication books only with students with autism or intellectual disability with limited or no verbal or reading skills. The six high school participants in this study could read and were verbal. We sought to determine whether the communication books would be accepted by peers without disabilities in general education classrooms or whether the books would stigmatize the students with disabilities. Finally, we assessed the effects of having a peer with a learning disability as the teacher of conversational interaction skills. We interpreted our results to conclude that the communication book package was associated with increased conversational interactions for all participants with their general education peers and that communication books were viewed positively by conversational partners.
C1 [Hughes, Carolyn; Bernstein, Rebekah T.; Kaplan, Lauren M.; Reilly, Caitlin M.; Brigham, Nicolette L.; Cosgriff, Joseph C.; Boykin, Michaela P.] Vanderbilt Univ, Nashville, TN 37203 USA.
RP Hughes, C (reprint author), Vanderbilt Univ, Dept Special Educ, Box 228 Peabody,230 Appleton Pl, Nashville, TN 37203 USA.
EM carolyn.hughes@vanderbilt.edu
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NR 27
TC 6
Z9 6
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1088-3576
EI 1538-4829
J9 FOCUS AUTISM DEV DIS
JI Focus Autism Dev. Disabil.
PD DEC
PY 2013
VL 28
IS 4
BP 241
EP 254
DI 10.1177/1088357613487019
PG 14
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 245GK
UT WOS:000326450200006
ER
PT J
AU Woolcott, G
AF Woolcott, Geoff
TI Giftedness and cultural accumulation: an information processing
perspective
SO HIGH ABILITY STUDIES
LA English
DT Article
DE expertise; giftedness; cultural accumulation; environmental interaction;
information processing systems
ID EDUCATION; NEUROSCIENCE; MIND; INTELLIGENCE; EVOLUTION; COGNITION;
ABILITY; SCIENCE; AUTISM; BRAINS
AB There appears to be differing approaches, in modern education, to the identification and development of gifted students, but researchers are beginning to find some cohesiveness through approaches that examine giftedness from within broad views of human cognition and behavior. This paper takes such an approach by considering learning and memory as concerned with the processing of environmental information and its accumulation across society, where such cultural accumulation results from environmental interaction. This paper outlines a framework, developed from studies of learning and memory and environmental interaction, which is based in a novel description of information and information processing systems. This framework may be useful in providing a new way of thinking about human cognition and behavior in an evolutionary context as well as in relation to the overall accumulation of culture across human society. This framework may be useful, therefore, in examining giftedness by providing useful insights into the identification and development of gifted students, in particular, those with the high levels of expertise considered valuable as human cultural accumulation.
C1 So Cross Univ, Sch Educ, Lismore, NSW 2480, Australia.
RP Woolcott, G (reprint author), So Cross Univ, Sch Educ, Lismore, NSW 2480, Australia.
EM Geoff.woolcott@scu.edu.au
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NR 80
TC 0
Z9 0
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1359-8139
EI 1469-834X
J9 HIGH ABIL STUD
JI High Abil. Stud.
PD DEC 1
PY 2013
VL 24
IS 2
BP 153
EP 170
DI 10.1080/13598139.2013.838897
PG 18
WC Education, Special
SC Education & Educational Research
GA 248CS
UT WOS:000326671900006
ER
PT J
AU Wang, Y
Zhou, WD
Yuan, Q
Li, XL
Meng, QF
Zhao, XH
Wang, JW
AF Wang, Yu
Zhou, Weidong
Yuan, Qi
Li, Xueli
Meng, Qingfang
Zhao, Xiuhe
Wang, Jiwen
TI COMPARISON OF ICTAL AND INTERICTAL EEG SIGNALS USING FRACTAL FEATURES
SO INTERNATIONAL JOURNAL OF NEURAL SYSTEMS
LA English
DT Article
DE Electroencephalogram (EEG); nonlinear features; blanket dimension;
fractal intercept
ID FUZZY SYNCHRONIZATION LIKELIHOOD; EPILEPTIC SEIZURE DETECTION; NEURAL
NETWORK METHODOLOGY; WAVELET-CHAOS METHODOLOGY; AUTISM SPECTRUM
DISORDER; ALZHEIMERS-DISEASE; CORRELATION DIMENSION; NONLINEAR FEATURES;
FEATURE-EXTRACTION; CLASSIFICATION
AB The feature analysis of epileptic EEG is very significant in diagnosis of epilepsy. This paper introduces two nonlinear features derived from fractal geometry for epileptic EEG analysis. The features of blanket dimension and fractal intercept are extracted to characterize behavior of EEG activities, and then their discriminatory power for ictal and interictal EEGs are compared by means of statistical methods. It is found that there is significant difference of the blanket dimension and fractal intercept between interictal and ictal EEGs, and the difference of the fractal intercept feature between interictal and ictal EEGs is more noticeable than the blanket dimension feature. Furthermore, these two fractal features at multi-scales are combined with support vector machine (SVM) to achieve accuracies of 97.58% for ictal and interictal EEG classification and 97.13% for normal, ictal and interictal EEG classification.
C1 [Wang, Yu; Zhou, Weidong; Yuan, Qi; Li, Xueli; Meng, Qingfang] Shandong Univ, Sch Informat Sci & Engn, Jinan 250100, Peoples R China.
[Zhao, Xiuhe; Wang, Jiwen] Shandong Univ, Qilu Hosp, Jinan 250100, Peoples R China.
RP Zhou, WD (reprint author), Shandong Univ, Sch Informat Sci & Engn, 27 Shanda Rd, Jinan 250100, Peoples R China.
EM wdzhou@sdu.edu.cn
FU Program of Science and Technology of Suzhou [ZXY2013030]; Independent
Innovation Foundation of Shandong University [2012DX008]; National
Natural Science Foundation of China [61201428]
FX The support of the Program of Science and Technology of Suzhou (No.
ZXY2013030), the Independent Innovation Foundation of Shandong
University (No. 2012DX008), and the National Natural Science Foundation
of China (No. 61201428) is gratefully acknowledged.
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NR 60
TC 12
Z9 12
PU WORLD SCIENTIFIC PUBL CO PTE LTD
PI SINGAPORE
PA 5 TOH TUCK LINK, SINGAPORE 596224, SINGAPORE
SN 0129-0657
EI 1793-6462
J9 INT J NEURAL SYST
JI Int. J. Neural Syst.
PD DEC
PY 2013
VL 23
IS 6
AR 1350028
DI 10.1142/S0129065713500287
PG 11
WC Computer Science, Artificial Intelligence
SC Computer Science
GA 245FV
UT WOS:000326448400004
PM 24156671
ER
PT J
AU Guevara-Campos, J
Gonzalez-Guevara, L
Puig-Alcaraz, C
Cauli, O
AF Guevara-Campos, Jose
Gonzalez-Guevara, Lucia
Puig-Alcaraz, Carmen
Cauli, Omar
TI Autism spectrum disorders associated to a deficiency of the enzymes of
the mitochondrial respiratory chain
SO METABOLIC BRAIN DISEASE
LA English
DT Article
DE Mitochondrial alteration; Autism; Lactate; Muscular biopsy
ID CHILDREN; DISEASES; PREVALENCE; DIAGNOSIS; GENETICS; INFANTS
AB Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by a combination of reciprocal social deficits, communication impairment, and rigid ritualistic interest and stereotypies. The etiology is generally multifactorial, including genetic, immunological and/or environmental factors. A group of ASD has been linked to mitochondrial dysfunction with subsequent deficiency in energy production. Patients with ASD and mitochondrial disease often show signs and symptoms uncommon to idiopathic ASD such as cardiac, pancreatic or liver dysfunction, cardiac, growth retardation, fatigability, but in some cases semiology is different. We show two clinical cases of ASD associated to a deficiency of the mitochondrial respiratory chain (complex I+III and IV) with different clinical presentations. In one case, signs and symptoms of mitochondrial disorder were mild and the second diagnosis was attained many years after that of ASD. These findings support the recent growing body of evidence that ASD can be associated with mitochondrial disorder. Children with ASD and abnormal neurologic or systemic findings should be evaluated for mitochondrial disorder.
C1 [Guevara-Campos, Jose; Gonzalez-Guevara, Lucia] Univ Oriente, Serv Pediat, Felipe Guevara Rojas Hosp, El Tigre, Anzoategui, Venezuela.
[Gonzalez-Guevara, Lucia] Epilepsy & Encephalog Unit, El Tigre, Anzoategui, Venezuela.
[Puig-Alcaraz, Carmen] Area 4 Sagunto, Psychiat Unit, Valencia, Spain.
[Cauli, Omar] Univ Valencia, Dept Nursing, Valencia 46010, Spain.
RP Cauli, O (reprint author), Univ Valencia, Dept Nursing, C Jaume Roig S-N, Valencia 46010, Spain.
EM omar.cauli@uv.es
RI Cauli, Omar/L-6063-2014
OI Cauli, Omar/0000-0001-5669-4943
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NR 38
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0885-7490
EI 1573-7365
J9 METAB BRAIN DIS
JI Metab. Brain Dis.
PD DEC
PY 2013
VL 28
IS 4
BP 605
EP 612
DI 10.1007/s11011-013-9419-x
PG 8
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 240OJ
UT WOS:000326106200008
PM 23839164
ER
PT J
AU Crivelli, B
Rocca, P
AF Crivelli, Barbara
Rocca, Paola
TI Differential diagnosis between schizophrenia and autism in adulthood: A
case report
SO NEUROCASE
LA English
DT Article
DE Autism spectrum disorders; Pervasive developmental disorders;
Schizophrenia; Neuropsychology; Cognition
ID PERVASIVE DEVELOPMENTAL DISORDERS; COMORBID PSYCHIATRIC-DISORDERS;
SPECTRUM DISORDERS; ASPERGER-SYNDROME; THOUGHT-DISORDER; COGNITIVE
IMPAIRMENT; FUNCTIONING AUTISM; VERBAL FLUENCY; NORMATIVE DATA; CHILDREN
AB The clinical distinction between autism spectrum disorders (ASD), also called pervasive developmental disorders (PDD), and schizophrenia is often difficult to make. Here we describe a case of an adult patient presenting with a diagnosis of schizophrenia based on a history of functional deterioration and presumed persecutory delusions. A psychiatric and psychological assessment conducted from a developmental perspective, in association with direct observation and neuropsychological evaluation for intellectual disabilities and autism, led to a diagnosis of PDD not otherwise specified, with revision of the initial diagnosis of schizophrenia.
C1 [Crivelli, Barbara; Rocca, Paola] Univ Turin, Dept Neurosci, I-10126 Turin, Italy.
RP Rocca, P (reprint author), Univ Turin, Dept Neurosci, Via Cherasco 11, I-10126 Turin, Italy.
EM paola.rocca@unito.it
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NR 85
TC 1
Z9 1
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1355-4794
EI 1465-3656
J9 NEUROCASE
JI Neurocase
PD DEC 1
PY 2013
VL 19
IS 6
BP 604
EP 612
DI 10.1080/13554794.2012.713492
PG 9
WC Clinical Neurology; Psychiatry; Psychology
SC Neurosciences & Neurology; Psychiatry; Psychology
GA 239HL
UT WOS:000326013100010
PM 22934940
ER
PT J
AU Liu, KPY
Wong, D
Chung, ACY
Kwok, N
Lam, MKY
Yuen, CMC
Arblaster, K
Kwan, ACS
AF Liu, Karen P. Y.
Wong, Denys
Chung, Anthony C. Y.
Kwok, Natalie
Lam, Madeleine K. Y.
Yuen, Cheri M. C.
Arblaster, Karen
Kwan, Aldous C. S.
TI Effectiveness of a Workplace Training Programme in Improving Social,
Communication and Emotional Skills for Adults with Autism and
Intellectual Disability in Hong Kong - A Pilot Study
SO OCCUPATIONAL THERAPY INTERNATIONAL
LA English
DT Article
DE workplace training; social and communication skills; adults with autism
and intellectual disability
ID SPECTRUM DISORDERS; ADOLESCENTS; PEOPLE; OUTCOMES; LIFE
AB This pilot study explored the effectiveness of workplace training programme that aimed to enhance the work-related behaviours in individuals with autism and intellectual disabilities. Fourteen participants with autism and mild to moderate intellectual disability (mean age=24.6years) were recruited. The workplace training programme included practices in work context and group educational sessions. A pre-test-post-test design was used with the Work Personality Profile, the Scale of Independent Behaviour Revised and the Observational Emotional Inventory Revised to evaluate the targeted behaviours. Improvement in social and communication skills specific to the workplace was achieved. For emotional control, participants became less confused and had a better self-concept. However, improvement in other general emotional behaviours, such as impulse control, was limited. The results indicated that a structured workplace training programme aimed at improving social, communication and emotional behaviours can be helpful for people with autism and intellectual disability. Further study with a larger sample size and a control group is recommended. The development of specific programme to cater for the emotional control needs at workplace for people with autism is also suggested. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Liu, Karen P. Y.; Arblaster, Karen] Univ Western Sydney, Penrith, NSW 2751, Australia.
[Wong, Denys; Kwan, Aldous C. S.] Fu Hong Soc, Hong Kong, Hong Kong, Peoples R China.
[Liu, Karen P. Y.; Chung, Anthony C. Y.; Kwok, Natalie; Lam, Madeleine K. Y.; Yuen, Cheri M. C.] Hong Kong Polytech Univ, Dept Rehabil Sci, Hong Kong, Hong Kong, Peoples R China.
RP Liu, KPY (reprint author), Univ Western Sydney, Sch Sci & Hlth, Locked Bag 1797, Penrith, NSW 2751, Australia.
EM Karen.Liu@uws.edu.au
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NR 27
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0966-7903
EI 1557-0703
J9 OCCUP THER INT
JI Occup. Ther. Int.
PD DEC
PY 2013
VL 20
IS 4
BP 198
EP 204
DI 10.1002/oti.1356
PG 7
WC Rehabilitation
SC Rehabilitation
GA 248MO
UT WOS:000326704400004
PM 23861094
ER
PT J
AU Zuo, LJ
Wang, KS
Zhang, XY
Pan, XH
Wang, GL
Krystal, JH
Zhang, HP
Luo, XG
AF Zuo, Lingjun
Wang, Kesheng
Zhang, Xiangyang
Pan, Xinghua
Wang, Guilin
Krystal, John H.
Zhang, Heping
Luo, Xingguang
TI Sex chromosome-wide association analysis suggested male-specific risk
genes for alcohol dependence
SO PSYCHIATRIC GENETICS
LA English
DT Article
DE alcohol dependence; homolog; male specificity; NLGN4X; synaptogenesis; Y
chromosome
ID SYNAPSE FORMATION; NEUROLIGINS; AUTISM; NEUREXINS; NLGN4; EXPRESSION;
EVOLUTION; REGION
AB BackgroundAlcohol dependence is more common among men than among women. Potential explanations for this include the role of genes in sex chromosomes (X and Y). In the present study, we scanned the entire Y chromosome and its homologs on the X chromosome in men to identify male-specific risk genes for alcohol dependence.MethodsTwo thousand nine hundred and twenty-seven individuals in two independent cohorts were analyzed. The European-American male cohort (883 cases with alcohol dependence and 445 controls) served as the discovery cohort and the European-American female cohort (526 cases and 1073 controls) served as a contrast group. All individuals were genotyped on the Illumina Human 1M beadchip. Two thousand two hundred and twenty-four single nucleotide polymorphisms (SNPs) on the Y chromosome or in the homologs on the X chromosome were analyzed. The allele frequencies were compared between cases and controls within each cohort using logistic regression analysis.ResultsWe found that, after experiment-wide correction, two SNPs on the X chromosome were associated significantly with alcohol dependence in European-American men (P=1.0x10(-4) for rs5916144 and P=5.5x10(-5) for rs5961794 at 3 UTR of NLGN4X), but not in the women. A total of 26 SNPs at 3UTR of or within NLGN4X were nominally associated with alcohol dependence in men (5.5x10(-5)P0.05), all of which were not statistically significant in women.ConclusionWe conclude that NLGN4X was a significant male-specific risk gene for alcohol dependence in European-Americans. NLGN4X might harbor a causal variant(s) for alcohol dependence. A defect of synaptogenesis in neuronal circuitry caused by NLGN4X mutations is believed to play a role in alcohol dependence.
C1 [Zuo, Lingjun; Krystal, John H.; Luo, Xingguang] Yale Univ, Sch Med, Dept Psychiat, West Haven, CT 06516 USA.
[Pan, Xinghua] Yale Univ, Sch Med, Dept Genet, West Haven, CT 06516 USA.
[Wang, Guilin] Yale Univ, Sch Med, Yale Ctr Genome Anal, Dept Genet, West Haven, CT 06516 USA.
[Zhang, Heping] Yale Univ, Sch Publ Hlth, Dept Biostat, New Haven, CT USA.
[Wang, Kesheng] E Tennessee State Univ, Coll Publ Hlth, Dept Biostat & Epidemiol, Johnson City, TN 37614 USA.
[Zhang, Xiangyang] Baylor Coll Med, Menninger Dept Psychiat & Behav Sci, Houston, TX 77030 USA.
RP Luo, XG (reprint author), Yale Univ, Sch Med, Dept Psychiat, West Haven, CT 06516 USA.
EM lingjun.zuo@yale.edu; xingguang.luo@yale.edu
FU National Alliance for Research on Schizophrenia and Depression (NARSAD)
Award [17616]; ABMRF/The Foundation for Alcohol Research; National
Institute on Drug Abuse (NIDA) [K01 DA029643, K24 DA017899, R01
DA016750, K02 DA026990, R01 DA013423]; National Institute on Alcohol
Abuse and Alcoholism (NIAAA) [R01 AA016015, R21 AA020319, K24 AA013736,
P50 AA012870, U10 AA008401]; Genes, Environment and Health Initiative
(GEI) [U01HG004422, U01HG004438]; GENEVA Coordinating Center [U01
HG004446]; National Cancer Institute [P01 CA089392]; NIH
[HHSN268200782096C]; Department of Veterans Affairs (the VA Alcohol
Research Center); Department of Veterans Affairs (VA National Center for
PTSD); Department of Veterans Affairs (Depression REAP)
FX The authors thank NIH GWAS Data Repository, the Contributing
Investigator(s) (Drs. Bierut, Edenberg, etc.) who contributed the
phenotype and genotype data (SAGE and COGA) from his/her original study,
and the primary funding organization that supported the contributing
study. Assistance with data cleaning was provided by the National Center
for Biotechnology Information. Genotyping was performed at the Johns
Hopkins University Center for Inherited Disease Research or at deCODE.
Grant sponsor: National Alliance for Research on Schizophrenia and
Depression (NARSAD) Award (L.Z.); Grant number: 17616; Grant sponsor:
ABMRF/The Foundation for Alcohol Research (L.Z.); Grant sponsor:
National Institute on Drug Abuse (NIDA); Grant numbers: K01 DA029643,
K24 DA017899, R01 DA016750, K02 DA026990, R01 DA013423; Grant sponsor:
National Institute on Alcohol Abuse and Alcoholism (NIAAA); Grant
numbers: R01 AA016015, R21 AA020319, K24 AA013736, P50 AA012870, U10
AA008401; Grant sponsor: Genes, Environment and Health Initiative (GEI);
Grant numbers: U01HG004422, U01HG004438; Grant sponsor: GENEVA
Coordinating Center; Grant number: U01 HG004446; Grant sponsor: National
Cancer Institute; Grant number: P01 CA089392; Grant sponsor: NIH
contract 'High throughput genotyping for studying the genetic
contributions to human disease'; Grant number: HHSN268200782096C; Grant
sponsor: Department of Veterans Affairs (the VA Alcohol Research Center,
the VA National Center for PTSD, and the Depression REAP).
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NR 36
TC 0
Z9 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0955-8829
EI 1473-5873
J9 PSYCHIAT GENET
JI Psychiatr. Genet.
PD DEC
PY 2013
VL 23
IS 6
BP 233
EP 238
DI 10.1097/YPG.0b013e328364b8c7
PG 6
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 247AB
UT WOS:000326583200002
PM 23907288
ER
PT J
AU Camacho-Garcia, RJ
Hervas, A
Toma, C
Balmana, N
Cormand, B
Martinez-Mir, A
Scholl, FG
AF Camacho-Garcia, Rafael J.
Hervas, Amaia
Toma, Claudio
Balmana, Noemi
Cormand, Bru
Martinez-Mir, Amalia
Scholl, Francisco G.
TI Rare variants analysis of neurexin-1 beta in autism reveals a novel
start codon mutation affecting protein levels at synapses
SO PSYCHIATRIC GENETICS
LA English
DT Article
DE autism; mutation; neurexin; neuroligin; NRXN; synapse; translation
ID NEUROLIGINS; GENES
AB Neurexins are synaptic plasma membrane proteins encoded by three genes (NRXN1, -2, -3) with alternative promoters. Mutations in neurexin genes have been identified in different neurodevelopmental disorders, including autism. Recently, two point mutations altering the translation initiation site of NRXN1 (c.-3G>T and c.3G>T) have been described in patients with autism and mental retardation. In this study, we analyzed the NRXN1 gene in a sample of 153 patients with autism. We report the identification of a novel mutation, c.3G>A (p.Met1), affecting the translation initiation site. Expression analysis showed that the c.3G>A mutation switches the translation start site of NRXN1 to an in-frame downstream methionine and decreases synaptic levels of the mutant protein in cultured neurons. These data reinforce a role for synaptic defects of NRXN1 in neurodevelopmental disorders.
C1 [Camacho-Garcia, Rafael J.; Martinez-Mir, Amalia; Scholl, Francisco G.] Virgen Rocio Univ Hosp, CSIC, Seville Biomed Res Inst IBiS, Seville, Spain.
[Scholl, Francisco G.] Univ Seville, Dept Physiol & Med Biophys, Seville, Spain.
[Hervas, Amaia; Balmana, Noemi] Mutua Terrassa Univ Hosp, Child & Adolescent Mental Hlth Unit, Terrassa, Spain.
[Toma, Claudio; Cormand, Bru] Univ Barcelona, Fac Biol, Dept Genet, E-08007 Barcelona, Spain.
[Toma, Claudio; Cormand, Bru] Univ Barcelona, Biomed Network Res Ctr Rare Dis CIBERER, E-08007 Barcelona, Spain.
[Cormand, Bru] Univ Barcelona, Inst Biomed IBUB, E-08007 Barcelona, Spain.
RP Scholl, FG (reprint author), Campus Hosp Univ Virgen Rocio, Inst Biomed Sevilla IBiS, Avda,Manuel Siurot S-N, Seville 41013, Spain.
EM fgs@us.es
RI Toma, Claudio/L-7853-2014
OI Toma, Claudio/0000-0003-3901-7507
FU Instituto de Salud Carlos III, Spain (ISCIII-FIS) [PI111058]; Ministerio
de Economia y Competitividad, Spain [PIM2010ERN-0070, SAF2012-33484];
Fundacio La Marato de TV3 [092010]; Fundacion Alicia Koplowitz; Agencia
de Gestio d'Ajuts Universitaris i de Recerca-AGAUR, Generalitat de
Catalunya [2009SGR00971]; Instituto de Salud Carlos III [FI08/00730];
European Union [PIEF-GA-2009-254930]
FX This study was supported by grants from Instituto de Salud Carlos III,
Spain (ISCIII-FIS; PI111058), Ministerio de Economia y Competitividad,
Spain (PIM2010ERN-0070, SAF2012-33484), Fundacio La Marato de TV3
(092010), Fundacion Alicia Koplowitz and Agencia de Gestio d'Ajuts
Universitaris i de Recerca-AGAUR, Generalitat de Catalunya
(2009SGR00971). R.J.C.-G. was a recipient of a fellowship from Instituto
de Salud Carlos III (FI08/00730) and C. T. was supported by the European
Union (Marie Curie, PIEF-GA-2009-254930).
CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
Bucan M, 2009, PLOS GENET, V5
Camacho-Garcia RJ, 2012, NEUROBIOL DIS, V47, P135, DOI 10.1016/j.nbd.2012.03.031
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NR 15
TC 3
Z9 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0955-8829
EI 1473-5873
J9 PSYCHIAT GENET
JI Psychiatr. Genet.
PD DEC
PY 2013
VL 23
IS 6
BP 262
EP 266
DI 10.1097/YPG.0000000000000013
PG 5
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 247AB
UT WOS:000326583200008
PM 24064682
ER
PT J
AU de Bruin, CL
Deppeler, JM
Moore, DW
Diamond, NT
AF de Bruin, Catriona L.
Deppeler, Joanne M.
Moore, Dennis W.
Diamond, Neil T.
TI Public School-Based Interventions for Adolescents and Young Adults With
an Autism Spectrum Disorder: A Meta-Analysis
SO REVIEW OF EDUCATIONAL RESEARCH
LA English
DT Article
DE autism spectrum disorder; meta-analysis; intervention; public schools;
adolescents
ID SOCIAL-SKILLS INTERVENTIONS; PERSONAL DIGITAL ASSISTANT; SINGLE-SUBJECT
RESEARCH; OF-THE-LITERATURE; SPECIAL-EDUCATION; MODELING INTERVENTIONS;
COMMUNITY SETTINGS; ASPERGER-SYNDROME; STUDENTS; VIDEO
AB This article reviews research on the effectiveness of four categories of intervention when implemented in public schools with adolescents and young adults diagnosed with an autism spectrum disorder. The study's inclusionary criteria include a setting of public schools, participants aged between 12 and 22 years, and the investigation of an antecedent-, consequence-, self-management-, or video-based intervention strategy to influence skills or behaviors in students. A total of 34 studies met these criteria. The procedures of the What Works Clearinghouse Standards for Single-Case Designs and Evidence are used to evaluate whether sufficient high-quality research in using antecedent-, consequence-, self-management-, and video-based strategies exists to consider these evidence-based practices. Intervention effectiveness is estimated using PAND scores and phi coefficients. The results suggest that sufficient research exists to consider antecedent-, video-, and consequence-based interventions evidence-based practices for adolescents and young adults in public schools. The need for more applied research with adolescents and young adults is highlighted.
C1 [de Bruin, Catriona L.; Deppeler, Joanne M.] Monash Univ, Fac Educ, Melbourne, Vic 3004, Australia.
[Moore, Dennis W.] Monash Univ, Melbourne, Vic 3004, Australia.
[Diamond, Neil T.] Monash Univ, Dept Econometr & Business Stat, Melbourne, Vic 3004, Australia.
RP de Bruin, CL (reprint author), Monash Univ, Fac Educ, Melbourne, Vic 3004, Australia.
EM catriona.debruin@monash.edu
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NR 84
TC 3
Z9 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0034-6543
EI 1935-1046
J9 REV EDUC RES
JI Rev. Educ. Res.
PD DEC
PY 2013
VL 83
IS 4
BP 521
EP 550
DI 10.3102/0034654313498621
PG 30
WC Education & Educational Research
SC Education & Educational Research
GA 242KM
UT WOS:000326239900002
ER
PT J
AU Sowden, H
Clegg, J
Perkins, M
AF Sowden, Hannah
Clegg, Judy
Perkins, Michael
TI The development of co-speech gesture in the communication of children
with autism spectrum disorders
SO CLINICAL LINGUISTICS & PHONETICS
LA English
DT Article
DE ASD; autism; autism spectrum disorder; children; development; gesture;
speech; audio-visual integration; supplementary gesture
ID EARLY LANGUAGE-DEVELOPMENT; YOUNG-CHILDREN; 2-WORD SPEECH; TRANSITION;
COMPREHENSION; INTEGRATION; PROFILES; WORDS
AB Co-speech gestures have a close semantic relationship to speech in adult conversation. In typically developing children co-speech gestures which give additional information to speech facilitate the emergence of multi-word speech. A difficulty with integrating audio-visual information is known to exist for individuals with Autism Spectrum Disorder (ASD), which may affect development of the speech-gesture system. A longitudinal observational study was conducted with four children with ASD, aged 2;4 to 3;5 years. Participants were video-recorded for 20 min every 2 weeks during their attendance on an intervention programme. Recording continued for up to 8 months, thus affording a rich analysis of gestural practices from pre-verbal to multi-word speech across the group. All participants combined gesture with either speech or vocalisations. Co-speech gestures providing additional information to speech were observed to be either absent or rare. Findings suggest that children with ASD do not make use of the facilitating communicative effects of gesture in the same way as typically developing children.
C1 [Sowden, Hannah] Univ Leeds, Sch Modern Languages & Cultures, Leeds LS2 9JT, W Yorkshire, England.
[Clegg, Judy; Perkins, Michael] Univ Sheffield, Sheffield, S Yorkshire, England.
RP Sowden, H (reprint author), Univ Leeds, Sch Modern Languages & Cultures, Leeds LS2 9JT, W Yorkshire, England.
EM H.Sowden@leeds.ac.uk
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NR 47
TC 1
Z9 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0269-9206
EI 1464-5076
J9 CLIN LINGUIST PHONET
JI Clin. Linguist. Phon.
PD DEC
PY 2013
VL 27
IS 12
BP 922
EP 939
DI 10.3109/02699206.2013.818715
PG 18
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 240TD
UT WOS:000326119000006
PM 23944149
ER
PT J
AU Huang, SF
Oi, M
AF Huang, Su-Fen
Oi, Manabu
TI Responses to Wh-, Yes/No-, A-not-A, and choice questions in Taiwanese
children with high-functioning autism spectrum disorder
SO CLINICAL LINGUISTICS & PHONETICS
LA English
DT Article
DE A-not-A questions; choice questions; high-functioning autism spectrum
disorder; Taiwanese; Wh-questions; Yes/No questions
ID JAPANESE CHILDREN; ASPERGER-SYNDROME; DOWN-SYNDROME; ASKING;
COMPREHENSION; DIFFICULTIES; IMPAIRMENTS; DISABILITY; ADEQUACY; SPEECH
AB The present study investigated the hypothesis that children with high-functioning autism spectrum disorder (HFASD) have a greater difficulty in responding to Wh- than Yes/No questions across languages. Conversations between Taiwanese children and their mothers were investigated and the children's response adequacy to maternal questions in a semi-structured setting were examined. Twelve Taiwanese children with HFASD, ranging in age from 7.1 to 14.9 years old, were compared with 12 typically developing (TD) children matched on age, sex, IQ and mean length of utterance in syllable (MLUs). Compared to TD children, HFASD children produced more inadequate or inappropriate responses to Wh-and Yes/No questions than to A-not-A and Choice questions. Taiwanese HFASD children share a greater difficulty in responding to maternal Wh-questions with their Japanese counterparts and do not show a relative ease in responding to Yes/No questions, while A-not-A and Choice questions were easier to respond to for the Taiwanese children.
C1 [Huang, Su-Fen] Natl Taitung Univ, Dept Early Childhood Educ, Taitung, Taiwan.
[Oi, Manabu] Kanazawa Univ, United Grad Sch Child Dev, Kanazawa, Ishikawa 9208640, Japan.
RP Oi, M (reprint author), Kanazawa Univ, United Grad Sch Child Dev, B-B43,13-1 Takaramachi, Kanazawa, Ishikawa 9208640, Japan.
EM oimanabu@ed.kanazawa-u.ac.jp
FU Japan Society for Promotion of Science [18330202]
FX The authors declare no conflicts of interest. The authors alone are
responsible for the content and writing of this article. This research
was supported by a Grant-in-Aid for Scientific Research (No. 18330202)
from the Japan Society for Promotion of Science.
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NR 35
TC 0
Z9 0
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0269-9206
EI 1464-5076
J9 CLIN LINGUIST PHONET
JI Clin. Linguist. Phon.
PD DEC
PY 2013
VL 27
IS 12
BP 969
EP 985
DI 10.3109/02699206.2013.835446
PG 17
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 240TD
UT WOS:000326119000009
PM 24093161
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PT J
AU Shaughnessy, N
AF Shaughnessy, Nicola
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LA English
DT Article
DE drama; autism; neuroaesthetics; performance
AB Perspectives on the phenomenology of the autistic experience are presented with particular reference to the imagination in autism and what may be conceptualized as 'neurodivergent aesthetics'. Drawing upon a research project that explored the potential of drama as an 'intervention' in autism, an attempt is made to de-mythologize the condition by challenging stereotypes and by suggesting that the multimodalities of performance offer an appropriate space for 'encounters' with autistic states of being while also questioning the dualisms which distinguish between the aesthetic and non-aesthetic.
C1 Univ Kent, Canterbury CT2 7NZ, Kent, England.
RP Shaughnessy, N (reprint author), Univ Kent, Canterbury CT2 7NZ, Kent, England.
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TC 0
Z9 0
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 0308-0188
EI 1743-2790
J9 INTERDISCIPL SCI REV
JI Interdiscip. Sci. Rev.
PD DEC
PY 2013
VL 38
IS 4
BP 321
EP 334
DI 10.1179/0308018813Z.00000000062
PG 14
WC Multidisciplinary Sciences; Social Sciences, Interdisciplinary
SC Science & Technology - Other Topics; Social Sciences - Other Topics
GA 239JK
UT WOS:000326018700005
ER
PT J
AU Baeza-Velasco, C
Michelon, C
Rattaz, C
Pernon, E
Baghdadli, A
AF Baeza-Velasco, Carolina
Michelon, Cecile
Rattaz, Cecile
Pernon, Eric
Baghdadli, Amaria
TI Separation of Parents Raising Children with Autism Spectrum Disorders
SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES
LA English
DT Article
DE Autism; Separation; Timing of separation; Sociodemographic variables;
Cohort
ID FAMILIES; DISABILITIES; ADJUSTMENT; DIVORCE; MOTHERS; HEALTH; RISK
AB We examined the occurrence and timing of separation of parents raising children with Autism Spectrum Disorders followed over a 10-year period (n = 119). We also compared the clinical characteristics of children and sociodemographic variables between parents who remained as a couple versus parents who separated. The results showed that after 10 years of follow-up 74.8 % of the couples remained together (n = 89), representing a separation rate of 25.2 %. This rate remained stable over the study period. There was no significant difference in any of the clinical and sociodemographic variables between comparison groups. Our results suggest that raising a child with autism does not often lead to the dissolution of the parents' relationship, as is commonly believed. The occurrence of parental separation in children with Autism Spectrum Disorders does not appear to vary according to their stage of life (childhood or adolescence). Lastly, the clinical profile of children and sociodemographic variables do not seem to influence the relationship status of parents.
C1 [Baeza-Velasco, Carolina; Michelon, Cecile; Rattaz, Cecile; Pernon, Eric; Baghdadli, Amaria] Univ Montpellier, Autism Resources Ctr, CHRU Montpellier & Lab Epsylon, EA 4556, F-34059 Montpellier, France.
[Baeza-Velasco, Carolina] Autism Resources Ctr, F-34295 Montpellier 05, France.
RP Baeza-Velasco, C (reprint author), Autism Resources Ctr, 39 Ave Charles Flahaut, F-34295 Montpellier 05, France.
EM c-baeza_velasco@chu-montpellier.fr
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TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1056-263X
EI 1573-3580
J9 J DEV PHYS DISABIL
JI J. Dev. Phys. Disabil.
PD DEC
PY 2013
VL 25
IS 6
BP 613
EP 624
DI 10.1007/s10882-013-9338-0
PG 12
WC Rehabilitation
SC Rehabilitation
GA 240NY
UT WOS:000326105000003
ER
PT J
AU Lorah, ER
Tincani, M
Dodge, J
Gilroy, S
Hickey, A
Hantula, D
AF Lorah, Elizabeth R.
Tincani, Matt
Dodge, Jessica
Gilroy, Shawn
Hickey, Anna
Hantula, Donald
TI Evaluating Picture Exchange and the iPad (TM) as a Speech Generating
Device to Teach Communication to Young Children with Autism
SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES
LA English
DT Review
DE Autism; Mand; Picture exchange; Speech generating device; Voice output
communication aid; Augmentative and alternative communication
ID DEVELOPMENTAL-DISABILITIES; FUNCTIONAL COMMUNICATION; GRAPHIC SYMBOLS;
PECS; STUDENTS; VOCA
AB The purpose of the study was to compare picture exchange (PE) and an iPad (TM) -based speech generating device (SGD) in teaching mands to five preschool boys diagnosed with autism. Participants' preferences for each device were assessed following training. Three participants met mastery criterion for mands using the SGD more quickly, while two participants met mastery criterion for mands using PE more readily. However, the overall rate of independent manding across training and maintenance was higher for four participants using the SGD. Four participants demonstrated a clear preference for the SGD device and one for PE. Results are consistent with previous research showing that acquisition of alternative communication modalities varies across children with autism, and supports the use of assessment to determine modality preference.
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RP Lorah, ER (reprint author), Temple Univ, Philadelphia, PA 19122 USA.
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NR 23
TC 10
Z9 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1056-263X
EI 1573-3580
J9 J DEV PHYS DISABIL
JI J. Dev. Phys. Disabil.
PD DEC
PY 2013
VL 25
IS 6
BP 637
EP 649
DI 10.1007/s10882-013-9337-1
PG 13
WC Rehabilitation
SC Rehabilitation
GA 240NY
UT WOS:000326105000005
ER
PT J
AU Gilmore, L
Campbell, M
Shochet, I
Roberts, C
AF Gilmore, Linda
Campbell, Marilyn
Shochet, Ian
Roberts, Clare
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TYPICALLY DEVELOPING PEERS
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID MENTAL-HEALTH; SELF-CONCEPT; ADOLESCENTS; MOTIVATION; PEOPLE;
PARTICIPATION; INTERVENTIONS; CONSTRUCT; DISORDER; AUTISM
AB Intellectual disability (ID) is associated with a range of risk factors that make children more vulnerable to adverse developmental outcomes, including mental health problems. Nevertheless, some children with ID do much better than others, presumably because of the presence of protective factors that increase their resilience. The current study compared resiliency profiles of children with ID (n = 115; mean age, 11.9 years) and their typically developing peers (n = 106; mean age, 11.8 years) using the Resiliency Scales for Children and Adolescents and the Healthy Kids Resilience Assessment. In many respects, children with ID and their typically developing peers reported similar levels of the protective factors that are associated with resilience. However, the children with ID reported higher levels of emotional sensitivity and lower tolerance, as well as fewer future goals. Compared with typically developing children, those with ID reported more support at school and less support within their communities. These findings have important implications for interventions that aim to promote positive developmental outcomes and to prevent the adverse sequelae that have been associated with low intelligence.
C1 [Gilmore, Linda; Campbell, Marilyn; Shochet, Ian] Queensland Univ Technol, Kelvin Grove, Qld 4059, Australia.
[Roberts, Clare] Curtin Univ, Perth, WA, Australia.
RP Gilmore, L (reprint author), Queensland Univ Technol, Sch Learning & Profess Studies, Victoria Pk Rd, Kelvin Grove, Qld 4059, Australia.
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NR 32
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD DEC
PY 2013
VL 50
IS 10
BP 1032
EP 1043
DI 10.1002/pits.21728
PG 12
WC Psychology, Educational
SC Psychology
GA 240BD
UT WOS:000326068800006
ER
PT J
AU Sudarov, A
AF Sudarov, Anamaria
TI Defining the Role of Cerebellar Purkinje Cells in Autism Spectrum
Disorders
SO CEREBELLUM
LA English
DT Article
DE ASD; Tsc1; Purkinje cells; Behavior; Synapses
ID TUBEROUS SCLEROSIS COMPLEX; MOUSE MODEL; TSC1; SURVIVAL
AB Understanding the contribution of cerebellar dysfunction to complex neurological diseases such as autism spectrum disorders (ASD) is an ongoing topic of investigation. In a recent paper, Tsai et al. (Nature 488:647-651, 2012) used a powerful combination of conditional mouse genetics, electrophysiology, behavioral tests, and pharmacological manipulations to address the role of Tuberous sclerosis complex 1 (Tsc1) in Purkinje cells and cerebellar function. The authors make the staggering discovery that morphological and electrophysiological defects in Purkinje cells are linked to system-wide ASD-like behavioral deficits. In this journal club, I discuss the major findings of this paper and critically assess the implications of this seminal work.
C1 Weill Cornell Med Coll, Brain & Mind Res Inst, New York, NY 10065 USA.
RP Sudarov, A (reprint author), Weill Cornell Med Coll, Brain & Mind Res Inst, New York, NY 10065 USA.
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NR 22
TC 3
Z9 3
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1473-4222
EI 1473-4230
J9 CEREBELLUM
JI Cerebellum
PD DEC
PY 2013
VL 12
IS 6
BP 950
EP 955
DI 10.1007/s12311-013-0490-y
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 236VK
UT WOS:000325827300021
PM 23703312
ER
PT J
AU Avcioglu, H
AF Avcioglu, Hasan
TI Effectiveness of Video Modelling in Training Students with Intellectual
Disabilities to Greet People When They Meet
SO KURAM VE UYGULAMADA EGITIM BILIMLERI
LA English
DT Article
DE Video Modelling; Social Skills; Skill of Greeting People and
Intellectual Disabilities
ID AUTISM SPECTRUM DISORDERS; SEVERE MENTAL-RETARDATION; CONVERSATION
SKILLS; MEAL PREPARATION; SELF-MANAGEMENT; YOUNG-CHILDREN; TEACH;
ADULTS; REINFORCEMENT; TECHNOLOGY
AB This practice aims to teach students who have intellectual disabilities how to greet people when they meet them. The purpose of this research is to see the effects of video modelling practice over the mental retarded students, when they meet people. In this research, teaching the social skills to the students with mental retardations were evaluated with the effectiveness of teaching with video modelling, model of multiple probe design between subjects from research models of single subject design. In this research four students, whose ages ranged from ten to eleven attending a special education class at a primary school in Ankara and who had intellectual disabilities were participated. The peers group consisted of 3 girls and 2 boys who studied at the same elementary school with the target students (all of them were 11 years old and continue their studied at 5th grade class). Research findings showed that using the video modelling in teaching students with intellectual disabilities help them to acquire the skill of greeting people and after gaining those skills they continued to use the skills and have shown that they continue to use in different situation and to different people. After the interviews done with the mothers and the teachers of the students about the results of teaching the skill of "greeting when meet people" through video modelling, it was seen that they were satisfied with these skills to have been taught to the students. They also expressed that the students had more interaction with their friends around them in much earlier time.
C1 [Avcioglu, Hasan] Cyprus Int Univ, Nicosia, Northern Cyprus, Cyprus.
RP Avcioglu, H (reprint author), Cyprus Int Univ, Fac Educ, Dept Mentally Handicapped Teaching, Nicosia, Northern Cyprus, Cyprus.
EM hasana@ciu.edu.tr
CR Akmanoglu N, 2008, THESIS ANADOLU U
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NR 57
TC 0
Z9 0
PU EDAM
PI ISTANBUL
PA KISIKLI MH ALEMDAG CD YAN YOL SK, SBK IS MERKEZI NO 5, KAT 1 USKUDAR,
ISTANBUL, 81190, TURKEY
SN 1303-0485
J9 KURAM UYGUL EGIT BIL
JI Kuram Uygulamada Egit. Bilim.
PD WIN
PY 2013
VL 13
IS 1
BP 466
EP 477
PG 12
WC Education & Educational Research
SC Education & Educational Research
GA 094LO
UT WOS:000315264600023
ER
PT J
AU Ergul, C
Baydik, B
Demir, S
AF Ergul, Cevriye
Baydik, Berrin
Demir, Seyda
TI Opinions of In-Service and Pre-Service Special Education Teachers on the
Competencies of the Undergraduate Special Education Programs
SO KURAM VE UYGULAMADA EGITIM BILIMLERI
LA English
DT Article
DE Undergraduate Special Education Programs; Field Competencies; Special
Education Teachers; Pre-Service Teachers; Special Education Teaching
Certificate
AB The purpose of this study was to examine the opinions of in-service and pre-service special education teachers on the undergraduate special education programs, field competencies, and their own professional competence. Participants' suggestions for improving undergraduate special education programs and in-service training programs including topics they need for their own professional development were also obtained. The study designed as a survey model included 107 special education teachers and 160 seniors in the undergraduate special education programs of 4 different universities. The data were gathered using an information form and the Special Education Teacher Program Field Competencies Scale which were developed by the researchers. Results showed that the teachers who graduated from an undergraduate special education program perceived themselves and their teaching education more sufficient than both subject matter teachers and teachers with a special education teaching certificate. Teaching academic skills, classroom management, teaching speech, and language skills and autism were the topics on which the majority of participants found themselves inadequate and requested in-service training. Extending the duration of the practicum, spreading it over the whole duration of the program, and making the courses more field-oriented were the most frequently suggested changes by the participants to be made in the undergraduate special education programs. Based on the results of the study, implications for practice were discussed.
C1 [Ergul, Cevriye] Ankara Univ, TR-06590 Ankara, Turkey.
[Baydik, Berrin; Demir, Seyda] Ankara Univ, Fac Educ Sci, Dept Special Educ, TR-06590 Ankara, Turkey.
RP Ergul, C (reprint author), Ankara Univ, Fac Educ Sci, Dept Special Educ, TR-06590 Ankara, Turkey.
EM cergul@ankara.edu.tr
CR Balci A., 2005, ACIKLAMALI EGITIM YO
Bettencourt L. U., 2004, EXCEPTIONALITY, V12, P225
Brownell MT, 2005, J SPEC EDUC, V38, P242, DOI 10.1177/00224669050380040601
Buyukozturk S., 2006, SOSYAL BILIMLER ICIN
Celikten M., 2005, ERCIYES U SOSYAL BIL, V19, P207
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NR 40
TC 0
Z9 0
PU EDAM
PI ISTANBUL
PA KISIKLI MH ALEMDAG CD YAN YOL SK, SBK IS MERKEZI NO 5, KAT 1 USKUDAR,
ISTANBUL, 81190, TURKEY
SN 1303-0485
J9 KURAM UYGUL EGIT BIL
JI Kuram Uygulamada Egit. Bilim.
PD WIN
PY 2013
VL 13
IS 1
BP 518
EP 522
PG 5
WC Education & Educational Research
SC Education & Educational Research
GA 094LO
UT WOS:000315264600025
ER
PT J
AU Odluyurt, S
AF Odluyurt, Serhat
TI A Comparison of the Effects of Direct Modeling and Video Modeling
Provided by Peers to Students with Autism who are Attending in Rural
Play Teaching in an Inclusive Setting
SO KURAM VE UYGULAMADA EGITIM BILIMLERI
LA English
DT Article
DE Children with Autism; Video Modeling Education; Modeling Education;
Single Subject Designs
ID DEVELOPMENTAL-DISABILITIES; IN-VIVO; CHILDREN; PRESCHOOLERS; BEHAVIOR
AB In the present research, the peers of children with autism at primary school level and in an inclusive environment were taught using direct modeling and video modeling education processes, and it was observed whether or not they could effectively and efficiently teach how to play games to their friends with autism. This study used adapted alternating treatments design from single subject designs. The research included 21 students from the first and second grades of primary education, 18 of whom participated as peer tutors with normal development, and 3 of whom participated as peer tutees with autism. The dependent variable of the research was the game learning skills determined through interviews with teachers for each sample. The independent variables were the implementation of direct modeling education and video modeling education by peers. The effectuality results of the study indicated that the participants played these games at 83-100% accuracy level and generalized it to different environments. In addition, the participants were observed to have the rules of games at 83-100% level one and three weeks after the completion of the implementation. Comparing the efficiency of the two education implementations, no significant difference was observed between direct modeling and video modeling education implementations in terms of the efficiency variable. The social validity findings of the research indicated the positive expressions of peer tutors regarding the study.
C1 [Odluyurt, Serhat] Anadolu Eylul Univ, Eskisehir, Turkey.
RP Odluyurt, S (reprint author), Anadolu Univ, Res Inst Handicapped, Eskisehir, Turkey.
EM syildiri@anadolu.edu.tr
CR Arntzen E, 2003, J APPL BEHAV ANAL, V36, P367, DOI 10.1901/jaba.2003.36-367
Bellini S, 2007, EXCEPT CHILDREN, V73, P264
Buffington DM, 1998, J AUTISM DEV DISORD, V28, P535, DOI 10.1023/A:1026056229214
Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276
Corbett B., 2003, BEHAV ANAL TODAY, V4, P367
D'Ateno P, 2003, J POSIT BEHAV INTERV, V5, P5, DOI 10.1177/10983007030050010801
Gena A, 2005, J AUTISM DEV DISORD, V35, P545, DOI 10.1007/s10803-005-0014-9
Gene D., 2010, THESIS ANADOLU U ESK
Hine JF, 2006, TOP EARLY CHILD SPEC, V26, P83, DOI 10.1177/02711214060260020301
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Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P82, DOI 10.1177/108835769901400203
Nikopoulos C., 2006, VIDEO MODELING BEHAV
Odluyurt S., 2009, KURAM UYGULAMADA EGI, V9, P1819
Reagon K. A., 2006, EDUC TREAT CHILD, V29, P517
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Sevinc M., 2004, OYUN ERKEN COCUKLUK
Sturmey P, 2003, J POSIT BEHAV INTERV, V5, P3, DOI 10.1177/10983007030050010401
Sturmey P., 2007, AUTISM SPECTRUM DISO
Sucuoglu B., 2006, ETKILI KAYNASTIRMA U
Tekin-Iftar E., 2006, OZEL EGITIMDE YANLIS, V2nd
Tekin-Iftar E., 2003, EDUC TRAIN DEV DISAB, V38, P74
TRYON AS, 1986, J ABNORM CHILD PSYCH, V14, P537, DOI 10.1007/BF01260522
Yavuzer H., 1995, ANA BABA OKULU
Yildirim S., 2002, OZEL EGITIM DERGISI, V3, P67
NR 25
TC 0
Z9 0
PU EDAM
PI ISTANBUL
PA KISIKLI MH ALEMDAG CD YAN YOL SK, SBK IS MERKEZI NO 5, KAT 1 USKUDAR,
ISTANBUL, 81190, TURKEY
SN 1303-0485
J9 KURAM UYGUL EGIT BIL
JI Kuram Uygulamada Egit. Bilim.
PD WIN
PY 2013
VL 13
IS 1
BP 536
EP 540
PG 5
WC Education & Educational Research
SC Education & Educational Research
GA 094LO
UT WOS:000315264600026
ER
PT J
AU Wacker, DP
Harding, JW
Morgan, TA
Berg, WK
Schieltz, KM
Lee, JF
Padilla, YC
AF Wacker, David P.
Harding, Jay W.
Morgan, Theresa A.
Berg, Wendy K.
Schieltz, Kelly M.
Lee, John F.
Padilla, Yaniz C.
TI AN EVALUATION OF RESURGENCE DURING FUNCTIONAL COMMUNICATION TRAINING
SO PSYCHOLOGICAL RECORD
LA English
DT Article
DE functional communication training; resurgence; negative reinforcement
ID DIFFERENTIAL REINFORCEMENT; ALTERNATIVE BEHAVIOR; STIMULUS-CONTROL;
EXTINCTION; HISTORY; VARIABILITY; RESISTANCE; AUTISM; MODEL; RATS
AB Three children who displayed destructive behavior maintained by negative reinforcement received functional communication training (FCT). During FCT, the children were required to complete a demand and then to mand (touch a card attached to a microswitch, sign, or vocalize) to receive brief play breaks. Prior to and 1 to 3 times following the initiation of FCT, extinction probes were conducted to evaluate the resurgence of destructive behavior when the microswitch without the mand card was present or the microswitch and the mand card were absent to determine if different patterns,of resurgence occurred when the microswitch was present or absent and, for 2 of the children, if changes in resurgence occurred at different points in treatment. Results showed that FCT led to relatively rapid reductions in destructive behavior. During all extinction sessions, resurgence of destructive behavior occurred with only minimal differences across the switch/no card and no-switch conditions.
C1 [Wacker, David P.; Harding, Jay W.; Morgan, Theresa A.; Berg, Wendy K.; Schieltz, Kelly M.; Lee, John F.; Padilla, Yaniz C.] Univ Iowa, Iowa City, IA 52242 USA.
RP Wacker, DP (reprint author), Ctr Disabil & Dev, 100 Hawkins Dr,Room 251, Iowa City, IA 52242 USA.
EM david-wacker@uiowa.edu
CR Bacha-Mendez G, 2007, J EXP ANAL BEHAV, V87, P5, DOI 10.1901/jeab.2007.55-05
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NR 37
TC 4
Z9 4
PU PSYCHOLOGICAL RECORD
PI CARBONDALE
PA SOUTHERN ILLINOIS UNIV, REHABILITATION INSTITUTE, CARBONDALE, IL
62901-4609 USA
SN 0033-2933
J9 PSYCHOL REC
JI Psychol. Rec.
PD WIN
PY 2013
VL 63
IS 1
BP 3
EP 20
PG 18
WC Psychology, Multidisciplinary
SC Psychology
GA 087BC
UT WOS:000314735200001
ER
PT J
AU Odom, SL
Cox, AW
Brock, ME
AF Odom, Samuel L.
Cox, Ann W.
Brock, Matthew E.
CA Natl Professional Dev Ctr ASD
TI Implementation Science, Professional Development, and Autism Spectrum
Disorders
SO EXCEPTIONAL CHILDREN
LA English
DT Article
AB The increased prevalence of autism spectrum disorders (ASD) has intensified the need for high-quality special education services designed for children and youth with ASD and their families. Implementation science provides guidance for moving innovation, such as utilizing evidence-based practices for students with ASD, into regular practice in schools. The National Professional Development Center on ASD (NPDC) incorporated the principles of implementation science, the scientific knowledge about evidence-based practices, and the measurement of program quality into an intervention approach for students with ASD. This article presents the NPDC model as an example of using implementation science to build systems of professional development that increase the quality of services and promote teachers' use of evidence-based practices.
C1 [Odom, Samuel L.; Cox, Ann W.] Univ N Carolina, FPG Child Dev Inst, Chapel Hill, NC 27514 USA.
[Brock, Matthew E.] Vanderbilt Univ, Nashville, TN USA.
Univ Wisconsin, Waisman Ctr, Madison, WI 53706 USA.
[Natl Professional Dev Ctr ASD] Univ Calif Davis, Sch Med, MIND Inst, Davis, CA USA.
RP Odom, SL (reprint author), Univ N Carolina, FPG Child Dev Inst, CB 8180,105 Smith Level Rd, Chapel Hill, NC 27514 USA.
EM slodom@unc.edu
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NR 11
TC 10
Z9 10
PU COUNCIL EXCEPTIONAL CHILDREN
PI ARLINGTON
PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA
SN 0014-4029
J9 EXCEPT CHILDREN
JI Except. Child.
PD WIN
PY 2013
VL 79
IS 2
SI SI
BP 233
EP 251
PG 19
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 066LB
UT WOS:000313221200008
ER
PT J
AU Ewing, L
Leach, K
Pellicano, E
Jeffery, L
Rhodes, G
AF Ewing, Louise
Leach, Katie
Pellicano, Elizabeth
Jeffery, Linda
Rhodes, Gillian
TI Reduced Face Aftereffects in Autism Are Not Due to Poor Attention
SO PLOS ONE
LA English
DT Article
ID SPECTRUM DISORDERS; FACIAL IDENTITY; VISUAL-ADAPTATION; SOCIAL-STIMULI;
RECOGNITION; CHILDREN; MECHANISMS; INSIGHTS; MIND
AB This study aimed to determine why face identity aftereffects are diminished in children with autism, relative to typical children. To address the possibility that reduced face aftereffects might reflect reduced attention to adapting stimuli, we investigated the consequence of controlling attention to adapting faces during a face identity aftereffect task in children with autism and typical children. We also included a size-change between adaptation and test stimuli to determine whether the reduced aftereffects reflect atypical adaptation to low-or higher-level stimulus properties. Results indicated that when attention was controlled and directed towards adapting stimuli, face identity aftereffects in children with autism were significantly reduced relative to typical children. This finding challenges the notion that atypicalities in the quality and/or quantity of children's attention during adaptation might account for group differences previously observed in this paradigm. Additionally, evidence of diminished face identity aftereffects despite a stimulus size change supports an adaptive processing atypicality in autism that extends beyond low-level, retinotopically coded stimulus properties. These findings support the notion that diminished face aftereffects in autism reflect atypicalities in adaptive norm-based coding, which could also contribute to face processing difficulties in this group.
C1 [Ewing, Louise; Leach, Katie; Pellicano, Elizabeth; Jeffery, Linda; Rhodes, Gillian] Univ Western Australia, Sch Psychol, Australian Res Council, Ctr Excellence Cognit & Its Disorders, Perth, WA 6009, Australia.
[Pellicano, Elizabeth] Univ London, Inst Educ, Ctr Res Autism & Educ, London WC1N 1AZ, England.
RP Ewing, L (reprint author), Univ Western Australia, Sch Psychol, Australian Res Council, Ctr Excellence Cognit & Its Disorders, Perth, WA 6009, Australia.
EM louise.ewing@uwa.edu.au
RI Ewing, Louise/H-9158-2014
FU Australian Research Council Centre of Excellence in Cognition and its
Disorders [CE110001021]; Australian Research Council Professorial
Fellowship [DP0877379]; Australian Research Council [DP0770923];
University of Western Australia; Australian Federation of University
Women; Clothworkers' Foundation; Pears Foundation
FX This work was supported by the Australian Research Council Centre of
Excellence in Cognition and its Disorders (project number CE110001021)
and an Australian Research Council Professorial Fellowship to G. R
(project number DP0877379). It was also supported by an Australian
Research Council Discovery Grant (DP0770923) to LJ and GR, and awards to
L. E. from the University of Western Australia and the Australian
Federation of University Women. Research at the Centre for Research in
Autism and Education (CRAE) is supported by The Clothworkers' Foundation
and Pears Foundation (E.P.). The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 43
TC 3
Z9 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 29
PY 2013
VL 8
IS 11
DI 10.1371/journal.pone.0081353
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261MX
UT WOS:000327670300031
PM 24312293
ER
PT J
AU Haas, BW
Anderson, IW
Smith, JM
AF Haas, Brian W.
Anderson, Ian W.
Smith, Jessica M.
TI Navigating the complex path between the oxytocin receptor gene (OXTR)
and cooperation: an endophenotype approach
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Review
DE OXTR; genetics; oxytocin; social-cognition; cooperation
ID FUSIFORM FACE AREA; INTRANASAL OXYTOCIN; BEHAVIOR; ASSOCIATION; AUTISM;
MIND; VASOPRESSIN; COGNITION; AMYGDALA; HUMANS
AB Although cooperation represents a core facet of human social behavior there exists considerable variability across people in terms of the tendency to cooperate. One factor that may contribute to individual differences in cooperation is a key gene within the oxytocin (OT) system, the OT reception gene (OXTR). In this article, we aim to bridge the gap between the OXTR gene and cooperation by using an endophenotype approach. We present evidence that the association between the OXTR gene and cooperation may in part be due to how the OXTR gene affects brain systems involved in emotion recognition, empathy/theory of mind, social communication and social reward seeking. There is evidence that the OXTR gene is associated with the functional anatomy of the amygdala, visual cortex (VC), anterior cingulate and superior temporal gyrus (STG). However, it is currently unknown how the OXTR gene may be linked to the functional anatomy of other relevant brain regions that include the fusiform gyrus (FG), superior temporal sulcus (STS), ventromedial prefrontal cortex (VMPFC), temporoparietal junction (TPJ) and nucleus accumbens (NAcc). We conclude by highlighting potential future research directions that may elucidate the path between OXTR and complex behaviors such as cooperation.
C1 [Haas, Brian W.; Anderson, Ian W.] Univ Georgia, Dept Psychol, Athens, GA 30602 USA.
[Haas, Brian W.; Smith, Jessica M.] Univ Georgia, Interdisciplinary Neurosci Grad Program, Athens, GA 30602 USA.
RP Haas, BW (reprint author), Univ Georgia, Dept Psychol, 125 Baldwin St, Athens, GA 30602 USA.
EM bhaas@uga.edu
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NR 65
TC 4
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 28
PY 2013
VL 7
AR 801
DI 10.3389/fnhum.2013.00801
PG 6
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 266PW
UT WOS:000328037200001
PM 24348360
ER
PT J
AU Padmanabhan, A
Lynn, A
Foran, W
Luna, B
O'Hearn, K
AF Padmanabhan, Aarthi
Lynn, Andrew
Foran, William
Luna, Beatriz
O'Hearn, Kirsten
TI Age related changes in striatal resting state functional connectivity in
autism
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE autism; fMRI; resting state; functional connectivity; striatum;
development
ID POSITRON-EMISSION-TOMOGRAPHY; SPECTRUM DISORDERS; MAGNETIC-RESONANCE;
EXECUTIVE FUNCTION; SENTENCE COMPREHENSION; CEREBELLAR FUNCTION; SYMPTOM
SEVERITY; WORKING-MEMORY; SOCIAL BRAIN; MOTOR TASK
AB Characterizing the nature of developmental change is critical to understanding the mechanisms that are impaired in complex neurodevelopment disorders such as autism spectrum disorder (ASD) and, pragmatically, may allow us to pinpoint periods of plasticity when interventions are particularly useful. Although aberrant brain development has long been theorized as a characteristic feature of ASD, the neural substrates have been difficult to characterize, in part due to a lack of developmental data and to performance confounds. To address these issues, we examined the development of intrinsic functional connectivity, with resting state fMRI from late childhood to early adulthood (8-36 years), using a seed based functional connectivity method with the striatal regions. Overall, we found that both groups show decreases in cortico-striatal circuits over age. However, when controlling for age, ASD participants showed increased connectivity with parietal cortex and decreased connectivity with prefrontal cortex relative to typically developed (TD) participants. In addition, ASD participants showed aberrant age-related connectivity with anterior aspects of cerebellum, and posterior temporal regions (e. g., fusiform gyrus, inferior and superior temporal gyri). In sum, we found prominent differences in the development of striatal connectivity in ASD, most notably, a typical development of connectivity in striatal networks that may underlie cognitive and social reward processing. Our findings highlight the need to identify the biological mechanisms of perturbations in brain reorganization over development, which may also help clarify discrepant findings in the literature.
C1 [Padmanabhan, Aarthi; Lynn, Andrew; Foran, William; Luna, Beatriz; O'Hearn, Kirsten] Univ Pittsburgh, Dept Psychiat, Lab Neurocognit Dev, Pittsburgh, PA 15206 USA.
RP Padmanabhan, A (reprint author), Univ Pittsburgh, Dept Psychiat, Lab Neurocognit Dev, 121 Meyran Ave,Loeffler Bldg 108, Pittsburgh, PA 15206 USA.
EM padmanabhana@upmc.edu
FU NIMH from the Eunice Kennedy Shriver National Institute of Child Health
& Human Development [5 R01 MH067924]; NIH from the Eunice Kennedy
Shriver National Institute of Child Health & Human Development
[HD055748]; NIMH [K01 MH081191]; NICHD ACE [HD055648]; NICHD CPEA
[HD35469]
FX This work was completed at the University of Pittsburgh and supported by
NIMH 5 R01 MH067924 (PI Luna), NIH HD055748 (PI Minshew) from the Eunice
Kennedy Shriver National Institute of Child Health & Human Development,
and NIMH K01 MH081191 (PI O'Hearn). The content is solely the
responsibility of the authors and does not necessarily represent the
official views of the National Institutes of Health. Recruitment was
supported by NICHD ACE grant HD055648 and CPEA grant HD35469. We thank
the participants, their families, Jennifer Fedor, and the staff at the
Autism Center for Excellence for their generous help.
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NR 114
TC 6
Z9 6
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 28
PY 2013
VL 7
AR 814
DI 10.3389/fnhum.2013.00814
PG 16
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 266RJ
UT WOS:000328041100001
PM 24348363
ER
PT J
AU O'Leary, C
Cole, SJ
Langford, M
Hewage, J
White, A
Cooper, HM
AF O'Leary, Conor
Cole, Stacey J.
Langford, Michael
Hewage, Jayani
White, Amanda
Cooper, Helen M.
TI RGMa Regulates Cortical Interneuron Migration and Differentiation
SO PLOS ONE
LA English
DT Article
ID REPULSIVE GUIDANCE MOLECULE; MEDIAL GANGLIONIC EMINENCE;
CENTRAL-NERVOUS-SYSTEM; NEURAL-TUBE CLOSURE; SPINAL-CORD-INJURY;
GABAERGIC INTERNEURONS; AXON GUIDANCE; RECEPTOR NEOGENIN;
CEREBRAL-CORTEX; CELL-MIGRATION
AB The etiology of neuropsychiatric disorders, including schizophrenia and autism, has been linked to a failure to establish the intricate neural network comprising excitatory pyramidal and inhibitory interneurons during neocortex development. A large proportion of cortical inhibitory interneurons originate in the medial ganglionic eminence (MGE) of the ventral telencephalon and then migrate through the ventral subventricular zone, across the corticostriatal junction, into the embryonic cortex. Successful navigation of newborn interneurons through the complex environment of the ventral telencephalon is governed by spatiotemporally restricted deployment of both chemorepulsive and chemoattractive guidance cues which work in concert to create a migratory corridor. Despite the expanding list of interneuron guidance cues, cues responsible for preventing interneurons from re-entering the ventricular zone of the ganglionic eminences have not been well characterized. Here we provide evidence that the chemorepulsive axon guidance cue, RGMa (Repulsive Guidance Molecule a), may fulfill this function. The ventricular zone restricted expression of RGMa in the ganglionic eminences and the presence of its receptor, Neogenin, in the ventricular zone and on newborn and maturing MGE-derived interneurons implicates RGMa-Neogenin interactions in interneuron differentiation and migration. Using an in vitro approach, we show that RGMa promotes interneuron differentiation by potentiating neurite outgrowth. In addition, using in vitro explant and migration assays, we provide evidence that RGMa is a repulsive guidance cue for newborn interneurons migrating out of the ganglionic eminence ventricular zone. Intriguingly, the alternative Neogenin ligand, Netrin-1, had no effect on migration. However, we observed complete abrogation of RGMa-induced chemorepulsion when newborn interneurons were simultaneously exposed to RGMa and Netrin-1 gradients, suggesting a novel mechanism for the tight regulation of RGMa-guided interneuron migration. We propose that during peak neurogenesis, repulsive RGMa-Neogenin interactions drive interneurons into the migratory corridor and prevent re-entry into the ventricular zone of the ganglionic eminences.
C1 [O'Leary, Conor; Cole, Stacey J.; Langford, Michael; Hewage, Jayani; White, Amanda; Cooper, Helen M.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
RP Cooper, HM (reprint author), Univ Queensland, Queensland Brain Inst, Brisbane, Qld, Australia.
EM h.cooper@uq.edu.au
FU National Health and Medical Research Council of Australia Project Grant
[569638]; Australian Government Australian Postgraduate Award;
Queensland State Government Smart Futures Fellowship
FX i) National Health and Medical Research Council of Australia Project
Grant (569638). ii) Australian Government Australian Postgraduate Award
iii) Queensland State Government Smart Futures Fellowship The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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NR 77
TC 1
Z9 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 27
PY 2013
VL 8
IS 11
AR e81711
DI 10.1371/journal.pone.0081711
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 261GG
UT WOS:000327652100093
PM 24312340
ER
PT J
AU Typlt, M
Mirkowski, M
Azzopardi, E
Ruettiger, L
Ruth, P
Schmid, S
AF Typlt, Marei
Mirkowski, Magdalena
Azzopardi, Erin
Ruettiger, Lukas
Ruth, Peter
Schmid, Susanne
TI Mice with Deficient BK Channel Function Show Impaired Prepulse
Inhibition and Spatial Learning, but Normal Working and Spatial
Reference Memory
SO PLOS ONE
LA English
DT Article
ID ACTIVATED POTASSIUM CHANNELS; ACOUSTIC STARTLE RESPONSE; CA2+-ACTIVATED
K+ CHANNELS; TRANSMITTER RELEASE; SPONTANEOUS-ALTERNATION; PYRAMIDAL
NEURONS; NERVE-TERMINALS; RAT-BRAIN; CALCIUM; SCHIZOPHRENIA
AB Genetic variations in the large-conductance, voltage-and calcium activated potassium channels (BK channels) have been recently implicated in mental retardation, autism and schizophrenia which all come along with severe cognitive impairments. In the present study we investigate the effects of functional BK channel deletion on cognition using a genetic mouse model with a knock-out of the gene for the pore forming a-subunit of the channel. We tested the F1 generation of a hybrid SV129/C57BL6 mouse line in which the slo1 gene was deleted in both parent strains. We first evaluated hearing and motor function to establish the suitability of this model for cognitive testing. Auditory brain stem responses to click stimuli showed no threshold differences between knockout mice and their wild-type littermates. Despite of muscular tremor, reduced grip force, and impaired gait, knockout mice exhibited normal locomotion. These findings allowed for testing of sensorimotor gating using the acoustic startle reflex, as well as of working memory, spatial learning and memory in the Y-maze and the Morris water maze, respectively. Prepulse inhibition on the first day of testing was normal, but the knockout mice did not improve over the days of testing as their wild-type littermates did. Spontaneous alternation in the y-maze was normal as well, suggesting that the BK channel knock-out does not impair working memory. In the Morris water maze knock-out mice showed significantly slower acquisition of the task, but normal memory once the task was learned. Thus, we propose a crucial role of the BK channels in learning, but not in memory storage or recollection.
C1 [Typlt, Marei; Mirkowski, Magdalena; Azzopardi, Erin; Schmid, Susanne] Univ Western Ontario, Schulich Sch Med & Dent, Dept Anat & Cell Biol, London, ON, Canada.
[Ruettiger, Lukas] Univ Tubingen, Hearing Res Ctr, Tubingen, Germany.
[Ruth, Peter] Univ Tubingen, Inst Pharm, Tubingen, Germany.
RP Schmid, S (reprint author), Univ Western Ontario, Schulich Sch Med & Dent, Dept Anat & Cell Biol, London, ON, Canada.
EM Susanne.Schmid@schulich.uwo.ca
RI Schmid, Susanne/J-3201-2012
OI Schmid, Susanne/0000-0001-5366-8061
FU Canadian Institute for Health Research (CIHR) MOP [114870]; Deutsche
Forschungsgemeinschaft (DFG)
FX Canadian Institute for Health Research (CIHR) MOP#114870 to S. Schmid
Deutsche Forschungsgemeinschaft (DFG) scholarship to M.Typlt Ontario
Ministry of Training, Colleges and Universities scholarship to E.
Azzopardi. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript
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NR 50
TC 5
Z9 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 26
PY 2013
VL 8
IS 11
AR e81270
DI 10.1371/journal.pone.0081270
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259SK
UT WOS:000327546400055
PM 24303038
ER
PT J
AU Starck, T
Nikkinen, J
Rahko, J
Remes, J
Hurtig, T
Haapsamo, H
Jussila, K
Kuusikko-Gauffin, S
Mattila, ML
Jansson-Verkasalo, E
Pauls, DL
Ebeling, H
Moilanen, I
Tervonen, O
Kiviniemi, VJ
AF Starck, Tuomo
Nikkinen, Juha
Rahko, Jukka
Remes, Jukka
Hurtig, Tuula
Haapsamo, Helena
Jussila, Katja
Kuusikko-Gauffin, Sanna
Mattila, Marja-Leena
Jansson-Verkasalo, Eira
Pauls, David L.
Ebeling, Hanna
Moilanen, Irma
Tervonen, Osmo
Kiviniemi, Vesa J.
TI Resting state fMRI reveals a default mode dissociation between
retrosplenial and medial prefrontal subnetworks in ASD despite motion
scrubbing
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE autism; resting state; fMRI; ICA; default mode; motion
ID INDEPENDENT COMPONENT ANALYSIS; AUTISM SPECTRUM DISORDERS; FUNCTIONAL
CONNECTIVITY MRI; SCHOOL-AGE-CHILDREN; ASPERGER-SYNDROME; POSTEROMEDIAL
CORTEX; EPISODIC MEMORY; SUBJECT MOTION; BRAIN ACTIVITY; HEAD MOTION
AB In resting state functional magnetic resonance imaging (fMRI) studies of autism spectrum disorders (ASDs) decreased frontal-posterior functional connectivity is a persistent finding. However, the picture of the default mode network (DMN) hypoconnectivity remains incomplete. In addition, the functional connectivity analyses have been shown to be susceptible even to subtle motion. DMN hypoconnectivity in ASD has been specifically called for re-evaluation with stringent motion correction, which we aimed to conduct by so-called scrubbing. A rich set of default mode subnetworks can be obtained with high dimensional group independent component analysis (ICA) which can potentially provide more detailed view of the connectivity alterations. We compared the DMN connectivity in high-functioning adolescents with ASDs to typically developing controls using ICA dual-regression with decompositions from typical to high dimensionality. Dual-regression analysis within DMN subnetworks did not reveal alterations but connectivity between anterior and posterior DMN subnetworks was decreased in ASD. The results were very similar with and without motion scrubbing thus indicating the efficacy of the conventional motion correction methods combined with ICA dual regression. Specific dissociation between DMN subnetworks was revealed on high ICA dimensionality, where networks centered at the medial prefrontal cortex and retrosplenial cortex showed weakened coupling in adolescents with ASDs compared to typically developing control participants. Generally the results speak for disruption in the anterior-posterior DMN interplay on the network level whereas local functional connectivity in DMN seems relatively unaltered.
C1 [Starck, Tuomo; Nikkinen, Juha; Remes, Jukka; Tervonen, Osmo; Kiviniemi, Vesa J.] Oulu Univ Hosp, Dept Diagnost Radiol, Oulu 90029, Oys, Finland.
[Starck, Tuomo; Tervonen, Osmo; Kiviniemi, Vesa J.] Oulu Univ, Dept Diagnost Radiol, Oulu, Finland.
[Rahko, Jukka; Hurtig, Tuula; Haapsamo, Helena; Jussila, Katja; Kuusikko-Gauffin, Sanna; Mattila, Marja-Leena; Ebeling, Hanna; Moilanen, Irma] Oulu Univ Hosp, Inst Clin Med, Dept Child Psychiat, Oulu 90029, Oys, Finland.
[Rahko, Jukka; Hurtig, Tuula; Haapsamo, Helena; Jussila, Katja; Kuusikko-Gauffin, Sanna; Mattila, Marja-Leena; Ebeling, Hanna; Moilanen, Irma] Oulu Univ, Oulu, Finland.
[Remes, Jukka] Oulu Univ, Elect & Informat Engn Dept, Oulu, Finland.
[Jansson-Verkasalo, Eira] Univ Turku, Dept Behav Sci & Philosophy, Turku, Finland.
[Pauls, David L.] Harvard Univ, Sch Med, Psychiat & Neurodev Genet Unit, Boston, MA USA.
RP Starck, T (reprint author), Oulu Univ Hosp, Dept Diagnost Radiol, POB 50, Oulu 90029, Oys, Finland.
EM tuomo.starck@ppshp.fi
RI Remes, Jukka/E-4217-2015
OI Remes, Jukka/0000-0003-1685-8346
FU Alma and K. A. Snellman Foundation, Oulu, Finland; Child Psychiatric
Research Foundation, Finland; Emil Aaltonen Foundation, Finland;
Rinnekoti Research Foundation, Espoo, Finland; Sigrid Juselius
Foundation, Finland; Thule Institute, Oulu, Finland; Finnish Academy
Grant [117111]; Finnish Medical Foundation grants; Graduate School of
Circumpolar Wellbeing Health and Adaptation; National Alliance for
Autism Research
FX We wish to thank the adolescents and their families for participating.
This study received financial support from the Alma and K. A. Snellman
Foundation, Oulu, Finland, the Child Psychiatric Research Foundation,
Finland, the Emil Aaltonen Foundation, Finland, the Rinnekoti Research
Foundation, Espoo, Finland, the Sigrid Juselius Foundation, Finland and
the Thule Institute, Oulu, Finland. This study was funded by Finnish
Academy Grant # 117111 and Finnish Medical Foundation grants. The
Graduate School of Circumpolar Wellbeing Health and Adaptation is
acknowledged for its support. We would also like to thank the National
Alliance for Autism Research for financial support granted to Prof David
Pauls.
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NR 85
TC 3
Z9 3
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 22
PY 2013
VL 7
AR 802
DI 10.3389/fnhum.2013.00802
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 266PZ
UT WOS:000328037500001
PM 24319422
ER
PT J
AU Kruger, S
Sokolov, AN
Enck, P
Krageloh-Mann, I
Pavlova, MA
AF Krueger, Samuel
Sokolov, Alexander N.
Enck, Paul
Kraegeloh-Mann, Ingeborg
Pavlova, Marina A.
TI Emotion through Locomotion: Gender Impact
SO PLOS ONE
LA English
DT Article
ID POINT-LIGHT DISPLAYS; BIOLOGICAL MOTION; SEX-DIFFERENCES; BRAIN;
PERCEPTION; EPIDEMIOLOGY; JUDGMENTS; AUTISM; CUES; RECOGNITION
AB Body language reading is of significance for daily life social cognition and successful social interaction, and constitutes a core component of social competence. Yet it is unclear whether our ability for body language reading is gender specific. In the present work, female and male observers had to visually recognize emotions through point-light human locomotion performed by female and male actors with different emotional expressions. For subtle emotional expressions only, males surpass females in recognition accuracy and readiness to respond to happy walking portrayed by female actors, whereas females exhibit a tendency to be better in recognition of hostile angry locomotion expressed by male actors. In contrast to widespread beliefs about female superiority in social cognition, the findings suggest that gender effects in recognition of emotions from human locomotion are modulated by emotional content of actions and opposite actor gender. In a nutshell, the study makes a further step in elucidation of gender impact on body language reading and on neurodevelopmental and psychiatric deficits in visual social cognition.
C1 [Krueger, Samuel; Kraegeloh-Mann, Ingeborg; Pavlova, Marina A.] Univ Tubingen, Sch Med, Dept Pediat Neurol & Dev Med, Childrens Hosp, Tubingen, Germany.
[Sokolov, Alexander N.; Enck, Paul] Univ Tubingen, Sch Med, Dept Psychosomat Med & Psychotherapy, Tubingen, Germany.
[Sokolov, Alexander N.] Univ Tubingen, Sch Med, Ctr Pediat Clin Studies, Tubingen, Germany.
[Kraegeloh-Mann, Ingeborg] Univ Tubingen, Werner Reichardt Ctr Integrat Neurosci, Tubingen, Germany.
[Pavlova, Marina A.] Univ Tubingen, Inst Womens Hlth Baden Wurttemberg, Tubingen, Germany.
RP Pavlova, MA (reprint author), Univ Tubingen, Sch Med, Dept Pediat Neurol & Dev Med, Childrens Hosp, Tubingen, Germany.
EM marina.pavlova@uni-tuebingen.de
FU Else Kroner Fresenius Foundation [P2010_92, P2013_127]; Werner Reichardt
Center for Integrative Neuroscience, CIN [2009-24]; Deutsche
Forschungsgemeinschaft (DFG); Reinhold Beitlich Foundation; Heidehof
Foundation; Berthold Leibinger Foundation; [EXC 307]
FX This work was supported by the Else Kroner Fresenius Foundation (Grants
P2010_92 and P2013_127), the Werner Reichardt Center for Integrative
Neuroscience, CIN (pool project 2009-24), EXC 307 funded by Deutsche
Forschungsgemeinschaft (DFG), the Reinhold Beitlich Foundation, the
Heidehof Foundation, and the Berthold Leibinger Foundation to MAP. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript. The authors
acknowledge support toward open access publishing by Deutsche
Forschungsgemeinschaft and Open Access Publishing Fund of Eberhard Karls
University of Tubingen.
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NR 61
TC 5
Z9 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 22
PY 2013
VL 8
IS 11
AR e81716
DI 10.1371/journal.pone.0081716
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259QP
UT WOS:000327541700070
PM 24278456
ER
PT J
AU Ondobaka, S
Newman-Norlund, RD
de Lange, FP
Bekkering, H
AF Ondobaka, Sasha
Newman-Norlund, Roger D.
de lange, Floris P.
Bekkering, Harold
TI Action Recognition Depends on Observer's Level of Action Control and
Social Personality Traits
SO PLOS ONE
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; MIRROR NEURON SYSTEM; UNDERSTANDING ACTION;
AUTOMATIC IMITATION; FUNCTIONING AUTISM; JOINT ACTION; TOOL-USE; MIND;
INTENTIONS; BRAIN
AB Humans recognize both the movement (physical) goals and action (conceptual) goals of individuals with whom they are interacting. Here, we assessed whether spontaneous recognition of others' goals depends on whether the observers control their own behavior at the movement or action level. We also examined the relationship between individual differences in empathy and ASD-like traits, and the processing of other individual's movement and action goals that are known to be encoded in the "mirroring" and "mentalizing" brain networks. In order to address these questions, we used a computer-based card paradigm that made it possible to independently manipulate movement and action congruency of observed and executed actions. In separate blocks, participants were instructed to select either the right or left card (movement-control condition) or the higher or lower card (action-control condition), while we manipulated action-and movement-congruency of both actors' goals. An action-congruency effect was present in all conditions and the size of this effect was significantly correlated with self-reported empathy and ASD-like traits. In contrast, movement-congruency effects were only present in the movement-control block and were strongly dependent on action-congruency. These results illustrate that spontaneous recognition of others' behavior depends on the control scheme that is currently adopted by the observer. The findings suggest that deficits in action recognition are related to abnormal synthesis of perceived movements and prior conceptual knowledge that are associated with activations in the "mirroring" and "mentalizing" cortical networks.
C1 [Ondobaka, Sasha; de lange, Floris P.; Bekkering, Harold] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
[Newman-Norlund, Roger D.] Univ S Carolina, Dept Exercise Sci, Columbia, SC 29208 USA.
RP Ondobaka, S (reprint author), Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
EM s.ondobaka@donders.ru.nl
RI de Lange, Floris/D-2860-2009
OI de Lange, Floris/0000-0002-6730-1452
FU NWO Top grant [NWO: 407-11-040]
FX The present study was supported by the NWO Top grant (NWO: 407-11-040).
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 73
TC 0
Z9 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 22
PY 2013
VL 8
IS 11
DI 10.1371/journal.pone.0081392
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259QP
UT WOS:000327541700062
PM 24303046
ER
PT J
AU Sia, GM
Clem, RL
Huganir, RL
AF Sia, G. M.
Clem, R. L.
Huganir, R. L.
TI The Human Language-Associated Gene SRPX2 Regulates Synapse Formation and
Vocalization in Mice
SO SCIENCE
LA English
DT Article
ID ACTIVITY-DEPENDENT REGULATION; ULTRASONIC VOCALIZATION; HIKARU-GENKI;
SPEECH; FOXP2; DISORDERS; PROTEIN; AUTISM; DIFFERENTIATION; DROSOPHILA
AB Synapse formation in the developing brain depends on the coordinated activity of synaptogenic proteins, some of which have been implicated in a number of neurodevelopmental disorders. Here, we show that the sushi repeat-containing protein X-linked 2 (SRPX2) gene encodes a protein that promotes synaptogenesis in the cerebral cortex. In humans, SRPX2 is an epilepsy- and language-associated gene that is a target of the foxhead box protein P2 (FoxP2) transcription factor. We also show that FoxP2 modulates synapse formation through regulating SRPX2 levels and that SRPX2 reduction impairs development of ultrasonic vocalization in mice. Our results suggest FoxP2 modulates the development of neural circuits through regulating synaptogenesis and that SRPX2 is a synaptogenic factor that plays a role in the pathogenesis of language disorders.
C1 [Sia, G. M.; Huganir, R. L.] Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, Baltimore, MD 21205 USA.
[Sia, G. M.; Huganir, R. L.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA.
[Clem, R. L.] Mt Sinai Sch Med, Friedman Brain Inst, New York, NY 10029 USA.
RP Huganir, RL (reprint author), Johns Hopkins Univ, Sch Med, Howard Hughes Med Inst, 725 North Wolfe St, Baltimore, MD 21205 USA.
EM rhuganir@jhmi.edu
FU National Institutes of Health [P50MH084020, NS050274]; Millipore
FX We thank M. Pletnikov and J. Yocum of the Behavioral Core Facility and
M. Pucak of the Multiphoton/Electrophysiology Core Facility. We also
thank H. Vega, S. Yang, N. O'Sullivan, and X. Wang for technical
assistance. This study was supported by National Institutes of Health
grant P50MH084020 to R.L.H. and grant NS050274 to the Multiphoton Core
Facility. Under a licensing agreement between Millipore and the Johns
Hopkins University, R.L.H. is entitled to a share of royalties received
by the University on sales of products described in this article. R.L.H.
is a paid consultant to Millipore. The terms of this arrangement are
being managed by the Johns Hopkins University in accordance with its
conflict-of-interest policies.
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NR 32
TC 13
Z9 17
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD NOV 22
PY 2013
VL 342
IS 6161
BP 987
EP 991
DI 10.1126/science.1245079
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255EZ
UT WOS:000327223500045
PM 24179158
ER
PT J
AU Sultan, KT
Brown, KN
Shi, SH
AF Sultan, Khadeejah T.
Brown, Keith N.
Shi, Song-Hai
TI Production and organization of neocortical interneurons
SO FRONTIERS IN CELLULAR NEUROSCIENCE
LA English
DT Review
DE neocortex; inhibition; interneurons; neurogenesis; migration;
organization
ID MEDIAL GANGLIONIC EMINENCE; CORTICAL GABAERGIC INTERNEURONS; GROWTH
FACTOR/SCATTER FACTOR; PROJECTION NEURON SUBTYPES; DEVELOPING
CEREBRAL-CORTEX; MAMMALIAN BASAL FOREBRAIN; ADHESION MOLECULE TAG-1;
FATE MAPPING REVEALS; INHIBITORY INTERNEURONS; SOMATOSENSORY CORTEX
AB Inhibitory GABA (gamma-aminobutyric acid)-ergic interneurons are a vital component of the neocortex responsible for shaping its output through a variety of inhibitions. Consisting of many flavors, interneuron subtypes are predominantly defined by their morphological, physiological, and neurochemical properties that help to determine their functional role within the neocortex. During development, these cells are born in the subpallium where they then tangentially migrate over long distances before being radially positioned to their final location in the cortical laminae. As development progresses into adolescence, these cells mature and form chemical and electrical connections with both glutamatergic excitatory neurons and other interneurons ultimately establishing the cortical network. The production, migration, and organization of these cells are determined by vast array of extrinsic and intrinsic factors that work in concert in order to assemble a proper functioning cortical inhibitory network. Failure of these cells to undergo these processes results in abnormal positioning and cortical function. In humans, this can bring about several neurological disorders including schizophrenia, epilepsy, and autism spectrum disorders. In this article, we will review previous literature that has revealed the framework for interneuron neurogenesis and migratory behavior as well as discuss recent findings that aim to elucidate the spatial and functional organization of interneurons within the neocortex.
C1 [Sultan, Khadeejah T.; Brown, Keith N.; Shi, Song-Hai] Mem Sloan Kettering Canc Ctr, Dev Biol Program, New York, NY 10075 USA.
[Sultan, Khadeejah T.; Brown, Keith N.; Shi, Song-Hai] Weill Cornell Med Coll, Grad Program Neurosci, New York, NY USA.
RP Shi, SH (reprint author), Mem Sloan Kettering Canc Ctr, Dev Biol Program, 1275 York Ave, New York, NY 10075 USA.
EM shis@mskcc.org
FU National Institute of Health [R01DA024681, P01NS048120]; McKnight
Foundation
FX We apologize to the authors whose work we could not cite owing to space
limitations, and thank the anonymous reviewers whose insightful comments
significantly improved the paper. Our research is supported by grants
from the National Institute of Health (R01DA024681 and P01NS048120) and
the McKnight Foundation.
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NR 175
TC 3
Z9 3
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5102
J9 FRONT CELL NEUROSCI
JI Front. Cell. Neurosci.
PD NOV 21
PY 2013
VL 7
DI 10.3389/fncel.2013.00221
PG 14
WC Neurosciences
SC Neurosciences & Neurology
GA 264BI
UT WOS:000327851500001
PM 24312011
ER
PT J
AU Wondolowski, J
Dickman, D
AF Wondolowski, Joyce
Dickman, Dion
TI Emerging links between homeostatic synaptic plasticity and neurological
disease
SO FRONTIERS IN CELLULAR NEUROSCIENCE
LA English
DT Review
DE synaptic plasticity; homeostasis; neurological disease; retrograde
signaling; presynaptic plasticity
ID FAMILIAL HEMIPLEGIC MIGRAINE; SCHIZOPHRENIA SUSCEPTIBILITY GENE; AUTISM
SPECTRUM DISORDER; FRAGILE-X-SYNDROME; PRESYNAPTIC FUNCTION DRIVEN;
TUBEROUS SCLEROSIS COMPLEX; MENTAL-RETARDATION PROTEIN;
GTPASE-ACTIVATING PROTEIN; TYROSINE KINASE MUSK; RETINOIC ACID
AB Homeostatic signaling systems are ubiquitous forms of biological regulation, having been studied for hundreds of years in the context of diverse physiological processes including body temperature and osmotic balance. However, only recently has this concept been brought to the study of excitatory and inhibitory electrical activity that the nervous system uses to establish and maintain stable communication. Synapses are a primary target of neuronal regulation with a variety of studies over the past 15 years demonstrating that these cellular junctions are under bidirectional homeostatic control. Recent work from an array of diverse systems and approaches has revealed exciting new links between homeostatic synaptic plasticity and a variety of seemingly disparate neurological and psychiatric diseases. These include autism spectrum disorders, intellectual disabilities, schizophrenia, and Fragile X Syndrome. Although the molecular mechanisms through which defective homeostatic signaling may lead to disease pathogenesis remain unclear, rapid progress is likely to be made in the coming years using a powerful combination of genetic, imaging, electrophysiological, and next generation sequencing approaches. Importantly, understanding homeostatic synaptic plasticity at a cellular and molecular level may lead to developments in new therapeutic innovations to treat these diseases. In this review we will examine recent studies that demonstrate homeostatic control of postsynaptic protein translation, retrograde signaling, and presynaptic function that may contribute to the etiology of complex neurological and psychiatric diseases.
C1 [Wondolowski, Joyce; Dickman, Dion] Univ So Calif, Dept Biol, Los Angeles, CA 90089 USA.
RP Dickman, D (reprint author), Univ So Calif, Dept Biol, 3641 Watt Way, Los Angeles, CA 90089 USA.
EM dickman@usc.edu
FU Ellison Medical Foundation; National Institute of Mental Health
[MH092351]
FX This work was supported by an award from the Ellison Medical Foundation
and a grant from the National Institute of Mental Health (MH092351) to
Dion Dickman.
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NR 116
TC 12
Z9 12
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5102
J9 FRONT CELL NEUROSCI
JI Front. Cell. Neurosci.
PD NOV 21
PY 2013
VL 7
AR 223
DI 10.3389/fncel.2013.00223
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 264BI
UT WOS:000327851500003
PM 24312013
ER
PT J
AU Kramvis, I
Mansvelder, HD
Loos, M
Meredith, R
AF Kramvis, Ioannis
Mansvelder, Huibert D.
Loos, Maarten
Meredith, Rhiannon
TI Hyperactivity, perseveration and increased responding during attentional
rule acquisition in the Fragile X mouse model
SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE Fragile X; attention; hyperactivity; 5-choice serial reaction time task;
learning; perseveration; MPEP; prefrontal cortex
ID AUTISM SPECTRUM DISORDERS; MGLUR5 ANTAGONIST MPEP; REACTION-TIME-TASK;
PREFRONTAL CORTEX; MENTAL-RETARDATION; BEHAVIORAL FLEXIBILITY;
REPETITIVE BEHAVIOR; YOUNG MALES; MICE; FMR1
AB Attentional deficits and executive function impairments are common to many neurodevelopmental disorders of intellectual disability and autism, including Fragile X syndrome (FXS). In the knockout mouse model for FXS, significant changes in synaptic plasticity and connectivity are found in the prefrontal cortex (PFC)-a prominent region for attentional processing and executive control. Given these alterations in PFC synaptic function, we tested whether adult Fragile X knockout mice exhibited corresponding impairments in inhibitory control, perseveration, and sustained attention. Furthermore, we investigated individual performance during attentional rule acquisition. Using the 5-choice serial reaction time task, our results show no impairments in inhibitory control and sustained attention. Fragile X knockout mice exhibited enhanced levels of correct and incorrect responding, as well as perseveration of responding during initial phases of rule acquisition, that normalized with training. For both knockout and wild type mice, pharmacological attenuation of metabotropic glutamate receptor 5 signaling did not affect response accuracy but reduced impulsive responses and increased omission errors. Upon rule reversal, Fragile X knockout mice made more correct and incorrect responses, similar to the initial phases of rule acquisition. Analogous to heightened activity upon novel rule acquisition, Fragile X knockout mice were transiently hyperactive in both a novel open field (OF) arena and novel home cage. Hyperactivity ceased with familiarization to the environment. Fragile X knockout mice. We therefore provide evidence for subtle but significant differences in the processing of novel stimuli in the mouse model for the FXS.
C1 [Kramvis, Ioannis; Mansvelder, Huibert D.; Meredith, Rhiannon] Vrije Univ Amsterdam, Ctr Neurogen & Cognit Res, Dept Integrat Neurophysiol, NL-1081 HV Amsterdam, Netherlands.
[Kramvis, Ioannis; Loos, Maarten] Sylics Synaptol BV, Amsterdam, Netherlands.
[Loos, Maarten] Vrije Univ Amsterdam, Ctr Neurogen & Cognit Res, Dept Mol & Cellular Neurobiol, NL-1081 HV Amsterdam, Netherlands.
RP Meredith, R (reprint author), Vrije Univ Amsterdam, Ctr Neurogen & Cognit Res, Dept Integrat Neurophysiol, De Boelelaan 1085, NL-1081 HV Amsterdam, Netherlands.
EM r.m.meredith@vu.nl
RI Loos, Maarten/A-2768-2012; Meredith, Rhiannon/A-4657-2010
OI Loos, Maarten/0000-0003-1629-2928;
FU Nederlandse Organisatie voor Wetenschappelijke Onderzoek (NWO)
[917.10.372]; European Commission [FP7-People_ITN-2008-238055];
Agentschap NL (NeuroBasic PharmaPhenomics Consortium, LSH) [FES0908]
FX These experiments were supported by the Nederlandse Organisatie voor
Wetenschappelijke Onderzoek (NWO #917.10.372 to Rhiannon Meredith) and
by the European Commission Seventh Framework Programme grant agreement
FP7-People_ITN-2008-238055 ("Brain Train" project; Ioannis Kramvis,
Rhiannon Meredith). This work was in part supported by Agentschap NL
(NeuroBasic PharmaPhenomics Consortium, LSH framework FES0908). We thank
Rolinka van der Loo, Ruud Wijnands, Bastijn Koopmans for technical
assistance and Oliver Stiedl for comments on the manuscript.
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NR 48
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5153
J9 FRONT BEHAV NEUROSCI
JI Front. Behav. Neurosci.
PD NOV 21
PY 2013
VL 7
AR 172
DI 10.3389/fnbeh.2013.00172
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 263BY
UT WOS:000327782800001
PM 24312033
ER
PT J
AU Zehendner, CM
Wedler, HE
Luhmann, HJ
AF Zehendner, Christoph M.
Wedler, Hannah E.
Luhmann, Heiko J.
TI A Novel In Vitro Model to Study Pericytes in the Neurovascular Unit of
the Developing Cortex
SO PLOS ONE
LA English
DT Article
ID BLOOD-BRAIN-BARRIER; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; SYSTEMIC
INFLAMMATION; NEURONAL APOPTOSIS; CEREBRAL-CORTEX; WHITE-MATTER; INJURY;
CNS; SCHIZOPHRENIA; EXPRESSION
AB Cortical function is impaired in various disorders of the central nervous system including Alzheimer's disease, autism and schizophrenia. Some of these disorders are speculated to be associated with insults in early brain development. Pericytes have been shown to regulate neurovascular integrity in development, health and disease. Hence, precisely controlled mechanisms must have evolved in evolution to operate pericyte proliferation, repair and cell fate within the neurovascular unit (NVU). It is well established that pericyte deficiency leads to NVU injury resulting in cognitive decline and neuroinflammation in cortical layers. However, little is known about the role of pericytes in pathophysiological processes of the developing cortex. Here we introduce an in vitro model that enables to precisely study pericytes in the immature cortex and show that moderate inflammation and hypoxia result in caspase-3 mediated pericyte loss. Using heterozygous EYFP-NG2 mouse mutants we performed live imaging of pericytes for several days in vitro. In addition we show that pericytes maintain their capacity to proliferate which may allow cell-based therapies like reprogramming of pericytes into induced neuronal cells in the presented approach.
C1 [Zehendner, Christoph M.; Wedler, Hannah E.; Luhmann, Heiko J.] Johannes Gutenberg Univ Mainz, Inst Physiol & Pathophysiol, Univ Med Ctr, Mainz, Germany.
RP Zehendner, CM (reprint author), Johannes Gutenberg Univ Mainz, Inst Physiol & Pathophysiol, Univ Med Ctr, Saarstr 21, Mainz, Germany.
EM Zehendner@uni-mainz.de
FU University Medical Center of the Johannes Gutenberg-University of Mainz;
DFG
FX CMZ was supported by a Stage 1 grant of the University Medical Center of
the Johannes Gutenberg-University of Mainz. This work was supported by
DFG grants to HJL. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 54
TC 3
Z9 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 21
PY 2013
VL 8
IS 11
AR e81637
DI 10.1371/journal.pone.0081637
PG 17
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 259PW
UT WOS:000327539800138
PM 24278454
ER
PT J
AU Willsey, AJ
Sanders, SJ
Li, MF
Dong, S
Tebbenkamp, AT
Muhle, RA
Reilly, SK
Lin, L
Fertuzinhos, S
Miller, JA
Murtha, MT
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Niu, W
Cotney, J
Ercan-Sencicek, AG
Gockley, J
Gupta, AR
Han, WQ
He, X
Hoffman, EJ
Klei, L
Lei, J
Liu, WZ
Liu, L
Lu, C
Xu, XM
Zhu, Y
Mane, SM
Lein, ES
Wei, LP
Noonan, JP
Roeder, K
Devlin, B
Sestan, N
State, MW
AF Willsey, A. Jeremy
Sanders, Stephan J.
Li, Mingfeng
Dong, Shan
Tebbenkamp, Andrew T.
Muhle, Rebecca A.
Reilly, Steven K.
Lin, Leon
Fertuzinhos, Sofia
Miller, Jeremy A.
Murtha, Michael T.
Bichsel, Candace
Niu, Wei
Cotney, Justin
Ercan-Sencicek, A. Gulhan
Gockley, Jake
Gupta, Abha R.
Han, Wenqi
He, Xin
Hoffman, Ellen J.
Klei, Lambertus
Lei, Jing
Liu, Wenzhong
Liu, Li
Lu, Cong
Xu, Xuming
Zhu, Ying
Mane, Shrikant M.
Lein, Ed S.
Wei, Liping
Noonan, James P.
Roeder, Kathryn
Devlin, Bernie
Sestan, Nenad
State, Matthew W.
TI Coexpression Networks Implicate Human Midfetal Deep Cortical Projection
Neurons in the Pathogenesis of Autism
SO CELL
LA English
DT Article
ID SPECTRUM DISORDERS; NOVO MUTATIONS; GENES; RISK; CNVS
AB Autism spectrum disorder (ASD) is a complex developmental syndrome of unknown etiology. Recent studies employing exome- and genome-wide sequencing have identified nine high-confidence ASD (hcASD) genes. Working from the hypothesis that ASD-associated mutations in these biologically pleiotropic genes will disrupt intersecting developmental processes to contribute to a common phenotype, we have attempted to identify time periods, brain regions, and cell types in which these genes converge. We have constructed coexpression networks based on the hcASD "seed'' genes, leveraging a rich expression data set encompassing multiple human brain regions across human development and into adulthood. By assessing enrichment of an independent set of probable ASD (pASD) genes, derived from the same sequencing studies, we demonstrate a key point of convergence in midfetal layer 5/6 cortical projection neurons. This approach informs when, where, and in what cell types mutations in these specific genes may be productively studied to clarify ASD pathophysiology.
C1 [Willsey, A. Jeremy; Sanders, Stephan J.; Dong, Shan; Muhle, Rebecca A.; Reilly, Steven K.; Niu, Wei; Cotney, Justin; Gockley, Jake; Liu, Wenzhong; Noonan, James P.; State, Matthew W.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
[Willsey, A. Jeremy; Sanders, Stephan J.; State, Matthew W.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Li, Mingfeng; Tebbenkamp, Andrew T.; Fertuzinhos, Sofia; Bichsel, Candace; Han, Wenqi; Xu, Xuming; Zhu, Ying; Sestan, Nenad] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06510 USA.
[Li, Mingfeng; Tebbenkamp, Andrew T.; Muhle, Rebecca A.; Fertuzinhos, Sofia; Bichsel, Candace; Niu, Wei; Han, Wenqi; Xu, Xuming; Zhu, Ying; Noonan, James P.; Sestan, Nenad] Yale Univ, Sch Med, Kavli Inst Neurosci, New Haven, CT 06510 USA.
[Dong, Shan; Wei, Liping] Peking Univ, Sch Life Sci, Ctr Bioinformat, State Key Lab Prot & Plant Gene Res, Beijing 100871, Peoples R China.
[Muhle, Rebecca A.; Niu, Wei; Ercan-Sencicek, A. Gulhan; Gupta, Abha R.; Hoffman, Ellen J.; State, Matthew W.] Yale Univ, Sch Med, Child Study Ctr, New Haven, CT 06510 USA.
[Lin, Leon] Yale Univ, Dept Computat Biol & Bioinformat, New Haven, CT 06511 USA.
[Miller, Jeremy A.; Lein, Ed S.] Allen Inst Brain Sci, Seattle, WA 98103 USA.
[Murtha, Michael T.; Ercan-Sencicek, A. Gulhan; Hoffman, Ellen J.; State, Matthew W.] Yale Univ, Sch Med, Program Neurogenet, New Haven, CT 06510 USA.
[Gupta, Abha R.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06510 USA.
[He, Xin; Roeder, Kathryn] Carnegie Mellon Univ, Ray & Stephanie Lane Ctr Computat Biol, Pittsburgh, PA 15213 USA.
[Klei, Lambertus; Devlin, Bernie] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
[Lei, Jing; Liu, Li; Lu, Cong; Roeder, Kathryn] Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA.
[Mane, Shrikant M.] Yale Univ, Sch Med, Yale Ctr Genom Anal, New Haven, CT 06417 USA.
[Wei, Liping] Natl Inst Biol Sci, Beijing 102206, Peoples R China.
[State, Matthew W.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06510 USA.
RP Devlin, B (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
EM devlinbj@upmc.edu; nenad.sestan@yale.edu; matthew.state@ucsf.edu
RI Liu, Li/G-1897-2015
FU Overlook International Foundation; Simons Foundation; Kavli Foundation;
National Institute of Mental Health [RC2 MH089956, U01 MH081896, R37
MH057881]; Foster-Davis Foundation Inc. (NARSAD DI); Howard Hughes
Medical Institute; Canadian Institutes of Health Research
FX We are grateful to the families participating in the Simons Foundation
Autism Research Initiative (SFARI) Simplex Collection (SSC). This work
was supported by a gift from the Overlook International Foundation (to
M. W. S., N. S., B. D., K. R., and J. N.), as well as grants from the
Simons Foundation (to M. W. S., N. S., K. R., and J. N.), the Kavli
Foundation (to N. S.), the National Institute of Mental Health (RC2
MH089956 to M. W. S., U01 MH081896 to N. S., and R37 MH057881 to B. D.
and K. R.), the Foster-Davis Foundation Inc. (NARSAD DI to N. S.), the
Howard Hughes Medical Institute (International Student Research
Fellowship to both S. J. S. and W. H.), and the Canadian Institutes of
Health Research (Doctoral Foreign Study Award to A. J. W.). We would
like to thank the SSC principal investigators (A. L. Beaudet, R.
Bernier, J. Constantino, E. H. Cook, Jr, E. Fombonne, D. Geschwind, D.
E. Grice, A. Klin, D. H. Ledbetter, C. Lord, C. L. Martin, D. M. Martin,
R. Maxim, J. Miles, O. Ousley, B. Peterson, J. Piggot, C. Saulnier, M.
W. State, W. Stone, J. S. Sutcliffe, C. A. Walsh, and E. Wijsman) and
the coordinators and staff at the SSC clinical sites; the SFARI staff,
in particular M. Benedetti; the Rutgers University Cell and DNA
repository for accessing biomaterials; the Yale Center of Genomic
Analysis, in particular J. Overton, S. Umlauf, I. Tikhonova, and A.
Lopez, for generating sequencing data; T. Brooks-Boone, N. Wright-Davis,
and M. Wojciechowski for their help in administering the project at
Yale; and H. Rankin for unwavering support.
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NR 27
TC 63
Z9 66
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 21
PY 2013
VL 155
IS 5
BP 997
EP 1007
DI 10.1016/j.cell.2013.10.020
PG 11
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259AU
UT WOS:000327500600006
PM 24267886
ER
PT J
AU Parikshak, NN
Luo, R
Zhang, A
Won, H
Lowe, JK
Chandran, V
Horvath, S
Geschwind, DH
AF Parikshak, Neelroop N.
Luo, Rui
Zhang, Alice
Won, Hyejung
Lowe, Jennifer K.
Chandran, Vijayendran
Horvath, Steve
Geschwind, Daniel H.
TI Integrative Functional Genomic Analyses Implicate Specific Molecular
Pathways and Circuits in Autism
SO CELL
LA English
DT Article
ID DE-NOVO MUTATIONS; COMMON GENETIC-VARIANTS; SPECTRUM DISORDERS;
INTELLECTUAL DISABILITY; TRANSCRIPTIONAL REGULATION; NEURAL DEVELOPMENT;
BRAIN-DEVELOPMENT; MESSENGER-RNAS; CHROMATIN; NETWORK
AB Genetic studies have identified dozens of autism spectrum disorder (ASD) susceptibility genes, raising two critical questions: (1) do these genetic loci converge on specific biological processes, and (2) where does the phenotypic specificity of ASD arise, given its genetic overlap with intellectual disability (ID)? To address this, we mapped ASD and ID risk genes onto coexpression networks representing developmental trajectories and transcriptional profiles representing fetal and adult cortical laminae. ASD genes tightly coalesce in modules that implicate distinct biological functions during human cortical development, including early transcriptional regulation and synaptic development. Bioinformatic analyses suggest that translational regulation by FMRP and transcriptional coregulation by common transcription factors connect these processes. At a circuit level, ASD genes are enriched in superficial cortical layers and glutamatergic projection neurons. Furthermore, we show that the patterns of ASD and ID risk genes are distinct, providing a biological framework for further investigating the pathophysiology of ASD.
C1 [Parikshak, Neelroop N.; Won, Hyejung; Lowe, Jennifer K.; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Program Neurobehav Genet, Los Angeles, CA 90095 USA.
[Parikshak, Neelroop N.; Zhang, Alice; Geschwind, Daniel H.] Univ Calif Los Angeles, Interdept Program Neurosci, Los Angeles, CA 90095 USA.
[Luo, Rui; Horvath, Steve; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
[Luo, Rui; Lowe, Jennifer K.; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Ctr Autism Treatment & Res, Los Angeles, CA 90095 USA.
[Chandran, Vijayendran; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Program Neurogenet, Los Angeles, CA 90095 USA.
[Horvath, Steve] Univ Calif Los Angeles, Dept Biostat, Los Angeles, CA 90095 USA.
RP Geschwind, DH (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Program Neurobehav Genet, Los Angeles, CA 90095 USA.
EM dhg@ucla.edu
FU Simons Foundation Autism Research Initiative; Autism Genetic Resource
Exchange; Brain Span consortium; Allen Brain Institute; NIMH Training;
NRSA Fellowship [T32MH073526, F30MH099886]; NIMH [5R37MH060233,
5R01MH094714]; Autism Center for Excellence network grant
[9R01MH100027]; Simons Foundation [SFARI 206744]; Medical Scientist
Training Program at UCLA; NINDS Informatics Center for Neurogenetics and
Neurogenomics [P30NS062691]
FX We thank the Simons Foundation Autism Research Initiative
(http://www.sfari.org) and the Autism Genetic Resource Exchange
(http://www.agre.org) and all families involved for making this work
possible. We gratefully acknowledge data resources from the Brain Span
consortium and the Allen Brain Institute http://www.brain-map.org). This
work was supported by a NIMH Training and NRSA Fellowship (T32MH073526
and F30MH099886, N.N.P.), NIMH grants (5R37MH060233 and 5R01MH094714, D.
H. G.), an Autism Center for Excellence network grant (9R01MH100027),
the Simons Foundation (SFARI 206744, D. H. G.), and the Medical
Scientist Training Program at UCLA. We thank the NINDS Informatics
Center for Neurogenetics and Neurogenomics (funded by grant P30NS062691)
at UCLA for computing resources, and we specifically thank Yeongshnn Ong
and Giovanni Coppola for making the interactive network available. We
thank Jason Chen, Michael Gandal, and Jason Stein for critically reading
the manuscript, as well as Willsey et al. (2013) for sharing their
findings prior to publication.
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NR 66
TC 70
Z9 74
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
EI 1097-4172
J9 CELL
JI Cell
PD NOV 21
PY 2013
VL 155
IS 5
BP 1008
EP 1021
DI 10.1016/j.cell.2013.10.031
PG 14
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 259AU
UT WOS:000327500600007
PM 24267887
ER
PT J
AU Magrelli, S
Jermann, P
Noris, B
Ansermet, F
Hentsch, F
Nadel, J
Billard, A
AF Magrelli, Silvia
Jermann, Patrick
Noris, Basilio
Ansermet, Francois
Hentsch, Francois
Nadel, Jacqueline
Billard, Aude
TI Social orienting of children with autism to facial expressions and
speech: a study with a wearable eye-tracker in naturalistic settings
SO FRONTIERS IN PSYCHOLOGY
LA English
DT Article
DE autism spectrum conditions; eye-tracking; social orienting; overt
attention; facial expressions of emotion; speech
ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; ASPERGER-SYNDROME; HOME
VIDEOTAPES; REVISED VERSION; DIAGNOSTIC INTERVIEW; EMOTION-RECOGNITION;
ATTENTION SHIFTS; BASIC EMOTIONS; NORMAL ADULTS
AB This study investigates attention orienting to social stimuli in children with Autism Spectrum Conditions (ASC) during dyadic social interactions taking place in real-life settings. We study the effect of social cues that differ in complexity and distinguish between social cues produced by facial expressions of emotion and those produced during speech. We record the children's gazes using a head-mounted eye-tracking device and report on a detailed and quantitative analysis of the motion of the gaze in response to the social cues. The study encompasses a group of children with ASC from 2 to 11-years old (n = 14) and a group of typically developing (TD) children (n = 17) between 3 and 6-years old. While the two groups orient overtly to facial expressions, children with ASC do so to a lesser extent. Children with ASC differ importantly from TD children in the way they respond to speech cues, displaying little overt shifting of attention to speaking faces. When children with ASC orient to facial expressions, they show reaction times and first fixation lengths similar to those presented by TD children. However, children with ASC orient to speaking faces slower than TD children. These results support the hypothesis that individuals affected by ASC have difficulties processing complex social sounds and detecting intermodal correspondence between facial and vocal information. It also corroborates evidence that people with ASC show reduced overt attention toward social stimuli.
C1 [Magrelli, Silvia; Nadel, Jacqueline; Billard, Aude] Ecole Polytech Fed Lausanne, Learning Algorithms & Syst Lab, CH-1015 Lausanne, Switzerland.
[Jermann, Patrick] Ecole Polytech Fed Lausanne, Ctr Digital Educ, CH-1015 Lausanne, Switzerland.
[Noris, Basilio; Ansermet, Francois] Hop Univ Geneve, Dept Child & Adolescent Med, Serv Child & Adolescent Psychiat, Geneva, Switzerland.
[Hentsch, Francois] CNRS, Emot Ctr, Paris, France.
[Hentsch, Francois] Univ Paris 06, Paris, France.
RP Magrelli, S (reprint author), Ecole Polytech Fed Lausanne, Learning Algorithms & Syst Lab, EPFL STI LASA I2S, Stn 9, CH-1015 Lausanne, Switzerland.
EM silvia.magrelli@epfl.ch
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NR 103
TC 4
Z9 4
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-1078
J9 FRONT PSYCHOL
JI Front. Psychol.
PD NOV 20
PY 2013
VL 4
AR 840
DI 10.3389/fpsyg.2013.00840
PG 16
WC Psychology, Multidisciplinary
SC Psychology
GA AB1VV
UT WOS:000331582900001
PM 24312064
ER
PT J
AU Hopkins, WD
Russell, J
McIntyre, J
Leavens, DA
AF Hopkins, William D.
Russell, Jamie
McIntyre, Joe
Leavens, David A.
TI Are Chimpanzees Really So Poor at Understanding Imperative Pointing?
Some New Data and an Alternative View of Canine and Ape Social Cognition
SO PLOS ONE
LA English
DT Article
ID PAN-TROGLODYTES; INTENTIONAL COMMUNICATION; PONGO-PYGMAEUS; CUES;
COMPREHENSION; INFERENCES; AUTISM; FOLLOW; GAZE
AB There is considerable interest in comparative research on different species' abilities to respond to human communicative cues such as gaze and pointing. It has been reported that some canines perform significantly better than monkeys and apes on tasks requiring the comprehension of either declarative or imperative pointing and these differences have been attributed to domestication in dogs. Here we tested a sample of chimpanzees on a task requiring comprehension of an imperative request and show that, though there are considerable individual differences, the performance by the apes rival those reported in pet dogs. We suggest that small differences in methodology can have a pronounced influence on performance on these types of tasks. We further suggest that basic differences in subject sampling, subject recruitment and rearing experiences have resulted in a skewed representation of canine abilities compared to those of monkeys and apes.
C1 [Hopkins, William D.; Russell, Jamie] Georgia State Univ, Inst Neurosci, Atlanta, GA 30303 USA.
[Hopkins, William D.; Russell, Jamie] Georgia State Univ, Language Res Ctr, Atlanta, GA 30303 USA.
[Hopkins, William D.; Russell, Jamie; McIntyre, Joe] Yerkes Natl Primate Res Ctr, Div Dev & Cognit Neurosci, Atlanta, GA USA.
[Leavens, David A.] Univ Sussex, Dept Psychol, Brighton, E Sussex, England.
RP Hopkins, WD (reprint author), Georgia State Univ, Inst Neurosci, Atlanta, GA 30303 USA.
EM whopkins4@gsu.edu
RI Leavens, David/B-2750-2014
FU NIH [MH-92923, NS-42867, NS-73134, HD-60563]; National Center for
Research Resources [P51RR165]; Office of Research Infrastructure
Programs/OD [P51OD11132]
FX This research was supported by NIH grants MH-92923, NS-42867, NS-73134
and HD-60563 to WDH and National Center for Research Resources P51RR165
to YNPRC, which is currently supported by the Office of Research
Infrastructure Programs/OD P51OD11132). The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 42
TC 1
Z9 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2013
VL 8
IS 11
AR e79338
DI 10.1371/journal.pone.0079338
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256LY
UT WOS:000327313100018
PM 24278128
ER
PT J
AU Yoshimura, Y
Kikuchi, M
Ueno, S
Okumura, E
Hiraishi, H
Hasegawa, C
Remijn, GB
Shitamichi, K
Munesue, T
Tsubokawa, T
Higashida, H
Minabe, Y
AF Yoshimura, Yuko
Kikuchi, Mitsuru
Ueno, Sanae
Okumura, Eiichi
Hiraishi, Hirotoshi
Hasegawa, Chiaki
Remijn, Gerard B.
Shitamichi, Kiyomi
Munesue, Toshio
Tsubokawa, Tsunehisa
Higashida, Haruhiro
Minabe, Yoshio
TI The Brain's Response to the Human Voice Depends on the Incidence of
Autistic Traits in the General Population
SO PLOS ONE
LA English
DT Article
ID LINGUISTIC PITCH PATTERNS; EVENT-RELATED POTENTIALS; ASPERGER-SYNDROME;
MISMATCH NEGATIVITY; SPECTRUM DISORDERS; AUDITORY-CORTEX; STEM RESPONSE;
SPEECH; ATTENTION; CHILDREN
AB Optimal brain sensitivity to the fundamental frequency (F0) contour changes in the human voice is important for understanding a speaker's intonation, and consequently, the speaker's attitude. However, whether sensitivity in the brain's response to a human voice F0 contour change varies with an interaction between an individual's traits (i.e., autistic traits) and a human voice element (i.e., presence or absence of communicative action such as calling) has not been investigated. In the present study, we investigated the neural processes involved in the perception of F0 contour changes in the Japanese monosyllables "ne" and "nu." "Ne" is an interjection that means "hi" or "hey" in English; pronunciation of "ne" with a high falling F0 contour is used when the speaker wants to attract a listener's attention (i.e., social intonation). Meanwhile, the Japanese concrete noun "nu" has no communicative meaning. We applied an adaptive spatial filtering method to the neuromagnetic time course recorded by whole-head magnetoencephalography (MEG) and estimated the spatiotemporal frequency dynamics of event-related cerebral oscillatory changes in beta band during the oddball paradigm. During the perception of the F0 contour change when "ne" was presented, there was event-related de-synchronization (ERD) in the right temporal lobe. In contrast, during the perception of the F0 contour change when "nu" was presented, ERD occurred in the left temporal lobe and in the bilateral occipital lobes. ERD that occurred during the social stimulus "ne" in the right hemisphere was significantly correlated with a greater number of autistic traits measured according to the Autism Spectrum Quotient (AQ), suggesting that the differences in human voice processing are associated with higher autistic traits, even in non-clinical subjects.
C1 [Yoshimura, Yuko; Kikuchi, Mitsuru; Hiraishi, Hirotoshi; Hasegawa, Chiaki; Munesue, Toshio; Higashida, Haruhiro] Kanazawa Univ, Res Ctr Child Mental Dev, Kanazawa, Ishikawa, Japan.
[Ueno, Sanae; Shitamichi, Kiyomi; Minabe, Yoshio] Kanazawa Univ, Grad Sch Med Sci, Dept Psychiat & Neurobiol, Kanazawa, Ishikawa, Japan.
[Okumura, Eiichi] Yokogawa Elect Corp, Dept MEG, Tokyo, Japan.
[Remijn, Gerard B.] Kyushu Univ, Int Educ Ctr, Fukuoka 812, Japan.
[Tsubokawa, Tsunehisa] Kanazawa Univ, Grad Sch Med Sci, Dept Anesthesiol, Kanazawa, Ishikawa, Japan.
RP Kikuchi, M (reprint author), Kanazawa Univ, Res Ctr Child Mental Dev, Kanazawa, Ishikawa, Japan.
EM mitsuru@zc4.so-net.ne.jp
FU Hokuriku Innovation Cluster for Health Science (MEXT Program for
Fostering Regional Innovation); MEXT, Japan; [24000012]
FX This study was supported by Grant-in-Aid for Specially Promoted
(Research Number 24000012), the Hokuriku Innovation Cluster for Health
Science (MEXT Program for Fostering Regional Innovation), and the
Strategic Research Program for Brain Sciences from MEXT, Japan. The
funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 63
TC 3
Z9 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 20
PY 2013
VL 8
IS 11
AR e80126
DI 10.1371/journal.pone.0080126
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256LY
UT WOS:000327313100075
PM 24278247
ER
PT J
AU Kouser, M
Speed, HE
Dewey, CM
Reimers, JM
Widman, AJ
Gupta, N
Liu, SN
Jaramillo, TC
Bangash, M
Xiao, B
Worley, PF
Powell, CM
AF Kouser, Mehreen
Speed, Haley E.
Dewey, Colleen M.
Reimers, Jeremy M.
Widman, Allie J.
Gupta, Natasha
Liu, Shunan
Jaramillo, Thomas C.
Bangash, Muhammad
Xiao, Bo
Worley, Paul F.
Powell, Craig M.
TI Loss of Predominant Shank3 Isoforms Results in Hippocampus-Dependent
Impairments in Behavior and Synaptic Transmission
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; 22Q13.3 DELETION SYNDROME; POSTSYNAPTIC
DENSITY PROTEINS; MICE LACKING; MUTANT MICE; MUTATIONS; GENE; CHILDREN;
RECEPTOR; FAMILY
AB The Shank3 gene encodes a scaffolding protein that anchors multiple elements of the postsynaptic density at the synapse. Previous attempts to delete the Shank3 gene have not resulted in a complete loss of the predominant naturally occurring Shank3 isoforms. We have now characterized a homozygous Shank3 mutation in mice that deletes exon 21, including the Homer binding domain. In the homozygous state, deletion of exon 21 results in loss of the major naturally occurring Shank3 protein bands detected by C-terminal and N-terminal antibodies, allowing us to more definitively examine the role of Shank3 in synaptic function and behavior. This loss of Shank3 leads to an increased localization of mGluR5 to both synaptosome and postsynaptic density-enriched fractions in the hippocampus. These mice exhibit a decrease in NMDA/AMPA excitatory postsynaptic current ratio in area CA1 of the hippocampus, reduced long-term potentiation in area CA1, and deficits in hippocampus-dependent spatial learning and memory. In addition, these mice also exhibit motor-coordination deficits, hypersensitivity to heat, novelty avoidance, altered locomotor response to novelty, and minimal social abnormalities. These data suggest that Shank3 isoforms are required for normal synaptic transmission/plasticity in the hippocampus, as well as hippocampus-dependent spatial learning and memory.
C1 [Kouser, Mehreen; Speed, Haley E.; Dewey, Colleen M.; Reimers, Jeremy M.; Widman, Allie J.; Gupta, Natasha; Liu, Shunan; Jaramillo, Thomas C.; Powell, Craig M.] Univ Texas SW Med Ctr Dallas, Dept Neurol & Neurotherapeut, Dallas, TX 75390 USA.
[Powell, Craig M.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA.
[Bangash, Muhammad; Xiao, Bo; Worley, Paul F.] Johns Hopkins Univ, Dept Neurosci, Sch Med, Baltimore, MD 21205 USA.
RP Powell, CM (reprint author), Univ Texas SW Med Ctr Dallas, Dept Neurol & Neurotherapeut, Dallas, TX 75390 USA.
EM craig.powell@utsouthwestern.edu
FU National Institute of Child Health and Human Development [R01HD069560,
R01HD069560-0251]; National Institute of Mental Health [R01MH093697,
P50MH084020]; National Institute of Neurological Disorders and Stroke
[R01NS070301]; National Institute on Drug Abuse [T32DA007290]; Autism
Speaks; Autism Science Foundation Postdoctoral Fellowship; Autism Speaks
Dennis Weatherstone Predoctoral Fellowship; BRAINS for Autism; Hartwell
Foundation; National 973 Basic Research Program of China [20009CB941400]
FX This work was funded by National Institute of Child Health and Human
Development Grants R01HD069560 (C. M. P.) and R01HD069560-0251 Diversity
Supplement (T.C.J.), National Institute of Mental Health Grants
R01MH093697 (C. M. P.) and P50MH084020 (P. F. W.), National Institute of
Neurological Disorders and Stroke Grant R01NS070301 (P. F. W.), National
Institute on Drug Abuse Grant T32DA007290 (J.M.R.), Autism Speaks (C. M.
P.), Autism Science Foundation Postdoctoral Fellowship (H. E. S.),
Autism Speaks Translational Postdoctoral Fellowship (H. E. S.), Autism
Speaks Dennis Weatherstone Predoctoral Fellowship (M. K., M. A. B.),
BRAINS for Autism (C. M. P.), The Hartwell Foundation (C. M. P.), and
National 973 Basic Research Program of China Grant 20009CB941400 (B.X.).
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NR 51
TC 10
Z9 11
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 20
PY 2013
VL 33
IS 47
BP 18448
EP 18468
DI 10.1523/JNEUROSCI.3017-13.2013
PG 21
WC Neurosciences
SC Neurosciences & Neurology
GA 258HC
UT WOS:000327449000011
PM 24259569
ER
PT J
AU Rutishauser, U
Tudusciuc, O
Wang, S
Mamelak, AN
Ross, IB
Adolphs, R
AF Rutishauser, Ueli
Tudusciuc, Oana
Wang, Shuo
Mamelak, Adam N.
Ross, Ian B.
Adolphs, Ralph
TI Single-Neuron Correlates of Atypical Face Processing in Autism
SO NEURON
LA English
DT Article
ID SPECTRUM DISORDERS; FACIAL EXPRESSION; AMYGDALA DAMAGE; MONKEY AMYGDALA;
GAZE-FIXATION; BRAIN; INFORMATION; RECOGNITION; RESPONSES; ABNORMALITIES
AB People with autism spectrum disorder (ASD) show abnormal processing of faces. A range of morphometric, histological, and neuroimaging studies suggest the hypothesis that this abnormality may be linked to the amygdala. We recorded data from single neurons within the amygdalae of two rare neurosurgical patients with ASD. While basic electrophysiological response parameters were normal, there were specific and striking abnormalities in how. individual facial features drove neuronal response. Compared to control patients, a population of neurons in the two ASD patients responded significantly more to the mouth, but less to the eyes. Moreover, we found a second class of face-responsive neurons for which responses to faces appeared normal. The findings confirm the amygdala's pivotal role in abnormal face processing by people with ASD at the cellular level and suggest that dysfunction may be traced to a specific subpopulation of neurons with altered selectivity for the features of faces.
C1 [Rutishauser, Ueli; Mamelak, Adam N.] Cedars Sinai Med Ctr, Dept Neurosurg, Los Angeles, CA 90048 USA.
[Rutishauser, Ueli] Cedars Sinai Med Ctr, Dept Neurol, Los Angeles, CA 90048 USA.
[Adolphs, Ralph] CALTECH, Div Biol, Pasadena, CA 91125 USA.
[Rutishauser, Ueli; Tudusciuc, Oana; Wang, Shuo; Adolphs, Ralph] CALTECH, Pasadena, CA 91125 USA.
[Ross, Ian B.] Huntington Mem Hosp, Pasadena, CA 91105 USA.
RP Rutishauser, U (reprint author), Cedars Sinai Med Ctr, Dept Neurosurg, Los Angeles, CA 90048 USA.
EM rutishauseru@csmc.edu
RI Rutishauser, Ueli/E-5721-2011
FU Simons Foundation; Gordon and Betty Moore Foundation; Max Planck
Society; Cedars-Sinai Medical Center; Autism Speaks; Conte Center from
the National Institute of Mental Health
FX We thank all patients and their families for their help in conducting
the studies; Lynn Paul, Daniel Kennedy, and Christina Corsello for
performing ADOS; Christopher Heller for neurosurgical implantation in
some of our subjects; Linda Philpott for neuropsychological assessment;
and William Sutherling and the staff of the Huntington Memorial Hospital
for their support with the studies. We also thank Erin Schuman for
advice and providing some of the electrophysiology equipment, and
Frederic Gosselin, Michael Spezio, Julien Dubois, and Jeffrey Wertheimer
for discussion. This research was made possible by funding from the
Simons Foundation (to R.A.), the Gordon and Betty Moore Foundation (to
R.A.), the Max Planck Society (to U.R.), the Cedars-Sinai Medical Center
(to U.R. and A.M.), a fellowship from Autism Speaks (to O.T.), and a
Conte Center from the National Institute of Mental Health (to R.A.).
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NR 51
TC 12
Z9 12
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD NOV 20
PY 2013
VL 80
IS 4
BP 887
EP 899
DI 10.1016/j.neuron.2013.08.029
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 256AD
UT WOS:000327281200007
PM 24267649
ER
PT J
AU Feng, L
AF Feng, Lei
TI Autism in Children Born After In Vitro Fertilization
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
ID MENTAL-RETARDATION; RISK
C1 [Feng, Lei] Natl Univ Singapore, Dept Psychol Med, Singapore 119228, Singapore.
RP Feng, L (reprint author), Natl Univ Singapore, NUHS Tower Block,1 E Kent Ridge Rd, Singapore 119228, Singapore.
EM pcmfl@nus.edu.sg
CR American Psychiatric Association, 2013, DIAGN STAT MAN MENT
Cedars MI, 2013, JAMA-J AM MED ASSOC, V310, P42, DOI 10.1001/jama.2013.7223
Sandin S, 2013, JAMA-J AM MED ASSOC, V310, P75, DOI 10.1001/jama.2013.7222
Suren P, 2013, JAMA-J AM MED ASSOC, V309, P570, DOI 10.1001/jama.2012.155925
NR 4
TC 0
Z9 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 20
PY 2013
VL 310
IS 19
BP 2100
EP 2101
DI 10.1001/jama.2013.278595
PG 2
WC Medicine, General & Internal
SC General & Internal Medicine
GA 253OQ
UT WOS:000327098900030
PM 24240941
ER
PT J
AU Sandin, S
Hultman, C
Reichenberg, A
AF Sandin, Sven
Hultman, Christina
Reichenberg, Abraham
TI Autism in Children Born After In Vitro Fertilization Reply
SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
LA English
DT Letter
C1 [Sandin, Sven; Reichenberg, Abraham] Kings Coll London, Inst Psychiat, London SE5 8AF, England.
[Hultman, Christina] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
RP Sandin, S (reprint author), Kings Coll London, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England.
EM sven.sandin@kl.ac.uk
CR Hultman CM, 2011, MOL PSYCHIATR, V16, P1203, DOI 10.1038/mp.2010.121
McPartland JC, 2012, J AM ACAD CHILD PSY, V51, P368, DOI 10.1016/j.jaac.2012.01.007
NR 2
TC 0
Z9 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA
SN 0098-7484
EI 1538-3598
J9 JAMA-J AM MED ASSOC
JI JAMA-J. Am. Med. Assoc.
PD NOV 20
PY 2013
VL 310
IS 19
BP 2101
EP 2101
DI 10.1001/jama.2013.278610
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 253OQ
UT WOS:000327098900031
PM 24240943
ER
PT J
AU Baron-Cohen, S
Johnson, D
Asher, J
Wheelwright, S
Fisher, SE
Gregersen, PK
Allison, C
AF Baron-Cohen, Simon
Johnson, Donielle
Asher, Julian
Wheelwright, Sally
Fisher, Simon E.
Gregersen, Peter K.
Allison, Carrie
TI Is synaesthesia more common in autism?
SO MOLECULAR AUTISM
LA English
DT Article
ID GRAPHEME-COLOR SYNESTHESIA; FUNCTIONING AUTISM; ASPERGER-SYNDROME;
SAVANT MEMORY; CONNECTIVITY; PREVALENCE; ACTIVATION; EXPERIENCE;
PATTERNS; HEARING
AB Background: Synaesthesia is a neurodevelopmental condition in which a sensation in one modality triggers a perception in a second modality. Autism (shorthand for Autism Spectrum Conditions) is a neurodevelopmental condition involving social-communication disability alongside resistance to change and unusually narrow interests or activities. Whilst on the surface they appear distinct, they have been suggested to share common atypical neural connectivity.
Methods: In the present study, we carried out the first prevalence study of synaesthesia in autism to formally test whether these conditions are independent. After exclusions, 164 adults with autism and 97 controls completed a synaesthesia questionnaire, Autism Spectrum Quotient, and Test of Genuineness-Revised (ToG-R) online.
Results: The rate of synaesthesia in adults with autism was 18.9% (31 out of 164), almost three times greater than in controls (7.22%, 7 out of 97, P <0.05). ToG-R proved unsuitable for synaesthetes with autism.
Conclusions: The significant increase in synaesthesia prevalence in autism suggests that the two conditions may share some common underlying mechanisms. Future research is needed to develop more feasible validation methods of synaesthesia in autism.
C1 [Baron-Cohen, Simon; Johnson, Donielle; Asher, Julian; Wheelwright, Sally; Allison, Carrie] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England.
[Fisher, Simon E.] Max Planck Inst Psycholinguist, NL-6500 AH Nijmegen, Netherlands.
[Fisher, Simon E.] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
[Gregersen, Peter K.] North Shore LIJ, Feinstein Inst Med Res, Robert S Boas Ctr Genom & Human Genet, Manhasset, NY 11030 USA.
RP Johnson, D (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England.
EM doniellenjohnson@gmail.com
RI Fisher, Simon/E-9130-2012
OI Fisher, Simon/0000-0002-3132-1996
FU Gates Foundation; MRC UK; Max Planck Society
FX This work was submitted in part fulfilment of the degree of Master of
Philosophy by DJ. It was conducted in association with the NIHR CLAHRC
for Cambridgeshire and Peterborough. DJ was funded by the Gates
Foundation. SBC and SW were funded by the MRC UK. SEF was funded by the
Max Planck Society.
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NR 44
TC 2
Z9 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 20
PY 2013
VL 4
AR 40
DI 10.1186/2040-2392-4-40
PG 6
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254YY
UT WOS:000327207400001
PM 24252644
ER
PT J
AU Eisinger, BE
Saul, MC
Driessen, TM
Gammie, SC
AF Eisinger, Brian E.
Saul, Michael C.
Driessen, Terri M.
Gammie, Stephen C.
TI Development of a versatile enrichment analysis tool reveals associations
between the maternal brain and mental health disorders, including autism
SO BMC NEUROSCIENCE
LA English
DT Article
DE Autism; Schizphrenia; Bipolar disorder; Depression; ADHD; Mental health;
Enrichment analysis; Maternal brain; Lateral septum
ID GENE SET ENRICHMENT; NEURAL STEM-CELLS; SUSCEPTIBILITY GENE; DEVELOPING
NEOCORTEX; POSTMITOTIC NEURONS; SOCIAL BEHAVIORS; PROGENITOR CELLS;
COMMUNICATION; LANGUAGE; SPECTRUM
AB Background: A recent study of lateral septum (LS) suggested a large number of autism-related genes with altered expression in the postpartum state. However, formally testing the findings for enrichment of autism-associated genes proved to be problematic with existing software. Many gene-disease association databases have been curated which are not currently incorporated in popular, full-featured enrichment tools, and the use of custom gene lists in these programs can be difficult to perform and interpret. As a simple alternative, we have developed the Modular Single-set Enrichment Test (MSET), a minimal tool that enables one to easily evaluate expression data for enrichment of any conceivable gene list of interest.
Results: The MSET approach was validated by testing several publicly available expression data sets for expected enrichment in areas of autism, attention deficit hyperactivity disorder (ADHD), and arthritis. Using nine independent, unique autism gene lists extracted from association databases and two recent publications, a striking consensus of enrichment was detected within gene expression changes in LS of postpartum mice. A network of 160 autism-related genes was identified, representing developmental processes such as synaptic plasticity, neuronal morphogenesis, and differentiation. Additionally, maternal LS displayed enrichment for genes associated with bipolar disorder, schizophrenia, ADHD, and depression.
Conclusions: The transition to motherhood includes the most fundamental social bonding event in mammals and features naturally occurring changes in sociability. Some individuals with autism, schizophrenia, or other mental health disorders exhibit impaired social traits. Genes involved in these deficits may also contribute to elevated sociability in the maternal brain. To date, this is the first study to show a significant, quantitative link between the maternal brain and mental health disorders using large scale gene expression data. Thus, the postpartum brain may provide a novel and promising platform for understanding the complex genetics of improved sociability that may have direct relevance for multiple psychiatric illnesses. This study also provides an important new tool that fills a critical analysis gap and makes evaluation of enrichment using any database of interest possible with an emphasis on ease of use and methodological transparency.
C1 [Eisinger, Brian E.; Saul, Michael C.; Driessen, Terri M.; Gammie, Stephen C.] Univ Wisconsin, Dept Zool, Madison, WI 53706 USA.
[Gammie, Stephen C.] Univ Wisconsin, Neurosci Training Program, Madison, WI 53706 USA.
RP Eisinger, BE (reprint author), Univ Wisconsin, Dept Zool, Madison, WI 53706 USA.
EM beeisinger@wisc.edu
FU United States National Institutes of Health [R01 MH 085642]; National
Science Foundation [IOS-0921706]
FX This work was primarily funded by United States National Institutes of
Health Grant R01 MH 085642 to S. G. Additional support was provided by
the National Science Foundation Grant IOS-0921706 to S. G. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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NR 60
TC 6
Z9 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2202
J9 BMC NEUROSCI
JI BMC Neurosci.
PD NOV 19
PY 2013
VL 14
AR 147
DI 10.1186/1471-2202-14-147
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 285XJ
UT WOS:000329428000001
PM 24245670
ER
PT J
AU Yang, M
Loureiro, D
Kalikhman, D
Crawley, JN
AF Yang, Mu
Loureiro, Darren
Kalikhman, David
Crawley, Jacqueline N.
TI Male mice emit distinct ultrasonic vocalizations when the female leaves
the social interaction arena
SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE
LA English
DT Article
DE ultrasonic vocalizations; USV; mouse models of autism; mouse model of
communication; social interaction; social behaviors
ID PLUS TF/J MICE; MOUSE MODEL; MUS-MUSCULUS; VOCAL COMMUNICATION; UNUSUAL
REPERTOIRE; MUTANT MICE; AUTISM; BEHAVIOR; EXPERIENCE; COURTSHIP
AB Adult male mice emit large number of complex ultrasonic vocalizations (USVs) when interacting with adult females. Call numbers and call categories differ greatly among inbred mouse strains. Little is known about USV emissions when the social partner departs. To investigate whether call repertoires and call rates are different when the male is interacting with a female and after the removal of the female, we designed a novel male-female social interaction test in which vocalizations were recorded across three phases. During phase 1, the male subject freely interacts with an unfamiliar estrus female mouse in a clean cage for 5 min. During phase 2, the female is removed while the male remains in the cage for 3 min. During phase 3, the same female is returned to the cage to rejoin the male subject mouse for 3 min. C57BL/6J (B6), FVB.129P2-Pde6b(+) Tyr(c-ch)/Ant (FVB), and BTBR T+ tf/J (BTBR) male subject mice were tested in this paradigm. All three strains emitted USVs during their initial interaction with the female partner. When the female was reintroduced in phase 3, numbers of USVs were similar to the initial introductory phase 1. Strain comparisons indicated fewer calls in pairs of BTBR males and stimulus females than in pairs of B6 males and stimulus females and pairs of FVB males and stimulus females. In the absence of the female, all FVB males vocalized, while only one third of B6 males and one third of BTBR males vocalized. In all three strains, changes in call category repertoires were detected after the female was removed. Call categories reverted to the phase 1 pattern when the female was returned in phase 3. Present findings indicate that males of commonly used inbred strains emit USVs when a partner female leaves the testing arena, suggesting that removing a salient social stimulus may be a unique approach to elicit USVs from mice. Our three-phase paradigm may also be useful for studying attention to social cues, and qualitative differences in vocalizations when a social partner is present vs. suddenly absent.
C1 [Yang, Mu; Crawley, Jacqueline N.] Univ Calif Davis, Dept Psychiat & Behav Sci, Sch Med, Sacramento, CA 95817 USA.
[Yang, Mu; Loureiro, Darren; Kalikhman, David; Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
RP Yang, M (reprint author), Univ Calif Davis, Dept Psychiat & Behav Sci, Sch Med, Room 1001,Res 2 Bldg 96,4625 2nd Ave, Sacramento, CA 95817 USA.
EM mu.yang@ucdmc.ucdavis.edu
FU National Institute of Mental Health Intramural Research Program; MIND
Institute
FX This work was supported by the National Institute of Mental Health
Intramural Research Program. The experiments were conducted at National
Institutes of Health. A significant portion of data analysis was done in
our current laboratory at University of California, Davis, with support
from the MIND Institute.
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NR 59
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5153
J9 FRONT BEHAV NEUROSCI
JI Front. Behav. Neurosci.
PD NOV 19
PY 2013
VL 7
AR 159
DI 10.3389/fnbeh.2013.00159
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 263AC
UT WOS:000327778000001
PM 24312027
ER
PT J
AU Luck, AN
Bobst, CE
Kaltashov, IA
Mason, AB
AF Luck, Ashley N.
Bobst, Cedric E.
Kaltashov, Igor A.
Mason, Anne B.
TI Human Serum Transferrin: Is There a Link among Autism, High Oxalate
Levels, and Iron Deficiency Anemia?
SO BIOCHEMISTRY
LA English
DT Article
ID PH-SENSITIVE TRIAD; ENDOSOMAL PH; N-LOBE; C-LOBE; SPECTRUM DISORDERS;
BINDING-SITE; RELEASE; RECEPTOR; OVOTRANSFERRIN; LACTOFERRIN
AB It has been previously suggested that large amounts of oxalate in plasma could play a role in autism by binding to the bilobal iron transport protein transferrin (hTF), thereby interfering with iron metabolism by inhibiting the delivery of iron to cells. By examining the effect of the substitution of oxalate for the physiologically utilized synergistic carbonate anion M each lobe of hTF, we sought to provide a molecular basis for or against such a role. Our work clearly shows both qualitatively (6 M urea gels) and quantitatively (kinetic analysis by stopped-flow spectrofluorimetry) that the presence of oxalate in place of carbonate in each binding site of hTF does indeed greatly interfere with the removal of iron from each lobe (in the absence and presence of the specific hTF receptor). However, we also clearly demonstrate that once the iron is bound within each lobe of hTF, neither anion can displace the other. Additionally, as verified by urea gels and electrospray mass spectrometry, formation of completely homogeneous hTF anion complexes requires that all iron must first be removed and hTF then reloaded with iron in the presence of either carbonate or oxalate. Significantly, experiments described here show that carbonate is the preferred binding partner; i.e., even if an equal amount of each anion is available during the iron loading process, the hTF carbonate complex is formed.
C1 [Luck, Ashley N.; Mason, Anne B.] Univ Vermont, Coll Med, Dept Biochem, Burlington, VT 05405 USA.
[Bobst, Cedric E.; Kaltashov, Igor A.] Univ Massachusetts, Dept Chem, Amherst, MA 01003 USA.
RP Mason, AB (reprint author), Univ Vermont, Dept Biochem, Burlington, VT 05405 USA.
EM anne.mason@uvm.edu
FU National Institutes of Health [R01 DK 21739, R01GM061666]; AHA
[10PRE4200010]; National Science Foundation [CHE-0923329]
FX This work was supported by National Institutes of Health Grants R01 DK
21739 (to A.B.M.) and R01GM061666 (to I.A.K.). A.N.L. was funded by an
AHA Predoctoral Fellowship (10PRE4200010). Acquisition of an FT
transform ICR mass spectrometer was supported by National Science
Foundation Grant CHE-0923329 (through the Major Research Instrumentation
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NR 48
TC 1
Z9 1
PU AMER CHEMICAL SOC
PI WASHINGTON
PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA
SN 0006-2960
J9 BIOCHEMISTRY-US
JI Biochemistry
PD NOV 19
PY 2013
VL 52
IS 46
BP 8333
EP 8341
DI 10.1021/bi401190m
PG 9
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 252WY
UT WOS:000327044800017
PM 24152109
ER
PT J
AU Shi, Y
Jiang, H
AF Shi, Yang
Jiang, Hui
TI rSeqDiff: Detecting Differential Isoform Expression from RNA-Seq Data
Using Hierarchical Likelihood Ratio Test
SO PLOS ONE
LA English
DT Article
ID BETA-PEPTIDE PRODUCTION; BIOLOGICAL VARIATION; NRCAM GENE; AUTISM;
DISEASE; PROTEIN; QUANTIFICATION; BRAIN; TRANSCRIPTOME; ASSOCIATION
AB High-throughput sequencing of transcriptomes (RNA-Seq) has recently become a powerful tool for the study of gene expression. We present rSeqDiff, an efficient algorithm for the detection of differential expression and differential splicing of genes from RNA-Seq experiments across multiple conditions. Unlike existing approaches which detect differential expression of transcripts, our approach considers three cases for each gene: 1) no differential expression, 2) differential expression without differential splicing and 3) differential splicing. We specify statistical models characterizing each of these three cases and use hierarchical likelihood ratio test for model selection. Simulation studies show that our approach achieves good power for detecting differentially expressed or differentially spliced genes. Comparisons with competing methods on two real RNA-Seq datasets demonstrate that our approach provides accurate estimates of isoform abundances and biological meaningful rankings of differentially spliced genes. The proposed approach is implemented as an R package named rSeqDiff.
C1 [Shi, Yang; Jiang, Hui] Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
[Jiang, Hui] Univ Michigan, Ctr Computat Med & Bioinformat, Ann Arbor, MI 48109 USA.
RP Jiang, H (reprint author), Univ Michigan, Dept Biostat, Ann Arbor, MI 48109 USA.
EM jianghui@umich.edu
FU Rackham Centennial Summer Research Fellowship; Summer Internship Funds
of Certificate in Public Health Genetics (CPHG) Program at University of
Michigan; NIH [5U54CA163059-02]; GAPPS Grant from the Bill & Melinda
Gates Foundation
FX YS was supported by the Rackham Centennial Summer Research Fellowship
and Summer Internship Funds of Certificate in Public Health Genetics
(CPHG) Program at University of Michigan. HJ's research was supported in
part by an NIH grant 5U54CA163059-02 and a GAPPS Grant from the Bill &
Melinda Gates Foundation. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 42
TC 1
Z9 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 18
PY 2013
VL 8
IS 11
AR e79448
DI 10.1371/journal.pone.0079448
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 256KH
UT WOS:000327308500062
PM 24260225
ER
PT J
AU Homberg, JR
Kolk, SM
Schubert, D
AF Homberg, Judith R.
Kolk, Sharon M.
Schubert, Dirk
TI Editorial perspective of the Research Topic "Deciphering serotonin's
role in neurodevelopment"
SO FRONTIERS IN CELLULAR NEUROSCIENCE
LA English
DT Editorial Material
DE serotonin; neurodevelopment; placental serotonin; sensory system;
prefrontal cortex; raphe nuclei; cortical integrity; autism
C1 [Homberg, Judith R.; Schubert, Dirk] Radboud Univ Nijmegen, Ctr Med, Donders Inst Brain Cognit & Behav, Dept Cognit Neurosci, NL-6525 ED Nijmegen, Netherlands.
[Kolk, Sharon M.] Radboud Univ Nijmegen, Dept Mol Anim Physiol, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
RP Homberg, JR (reprint author), Radboud Univ Nijmegen, Ctr Med, Donders Inst Brain Cognit & Behav, Dept Cognit Neurosci, NL-6525 ED Nijmegen, Netherlands.
EM j.homberg@cns.umcn.nl
RI Homberg, Judith/D-2473-2010; Kolk, Sharon/A-9055-2011; Schubert,
Dirk/B-4339-2011
OI Kolk, Sharon/0000-0003-2116-5456; Schubert, Dirk/0000-0002-1202-4363
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Zhang JL, 2013, FRONT CELL NEUROSCI, V7, DOI 10.3389/fncel.2013.00067
NR 10
TC 2
Z9 2
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5102
J9 FRONT CELL NEUROSCI
JI Front. Cell. Neurosci.
PD NOV 18
PY 2013
VL 7
AR 212
DI 10.3389/fncel.2013.00212
PG 2
WC Neurosciences
SC Neurosciences & Neurology
GA 264AH
UT WOS:000327848800002
PM 24302896
ER
PT J
AU Liyanage, VRB
Zachariah, RM
Rastegar, M
AF Liyanage, Vichithra R. B.
Zachariah, Robby M.
Rastegar, Mojgan
TI Decitabine alters the expression of Mecp2 isoforms via dynamic DNA
methylation at the Mecp2 regulatory elements in neural stem cells
SO MOLECULAR AUTISM
LA English
DT Article
DE Epigenetics; Mecp2e1; Mecp2e2; Decitabine/5-aza-2'-deoxycytidine; DNA
methylation; Autism
ID RETT-SYNDROME; CANCER-CELLS; MILD OVEREXPRESSION; GENE-EXPRESSION; MOUSE
MODEL; IN-VITRO; NEURONS; MICE; PROMOTER; 5-AZA-2'-DEOXYCYTIDINE
AB Background: Aberrant MeCP2 expression in brain is associated with neurodevelopmental disorders including autism. In the brain of stressed mouse and autistic human patients, reduced MeCP2 expression is correlated with Mecp2/MECP2 promoter hypermethylation. Altered expression of MeCP2 isoforms (MeCP2E1 and MeCP2E2) is associated with neurological disorders, highlighting the importance of proper regulation of both isoforms. While known regulatory elements (REs) within the MECP2/Mecp2 promoter and intron 1 are involved in MECP2/Mecp2 regulation, Mecp2 isoform-specific regulatory mechanisms are unknown. We hypothesized that DNA methylation at these REs may impact the expression of Mecp2 isoforms.
Methods: We used a previously characterized in vitro differentiating neural stem cell (NSC) system to investigate the interplay between Mecp2 isoform-specific expression and DNA methylation at the Mecp2 REs. We studied altered expression of Mecp2 isoforms, affected by global DNA demethylation and remethylation, induced by exposure and withdrawal of decitabine (5-Aza-2'-deoxycytidine). Further, we performed correlation analysis between DNA methylation at the Mecp2 REs and the expression of Mecp2 isoforms after decitabine exposure and withdrawal.
Results: At different stages of NSC differentiation, Mecp2 isoforms showed reciprocal expression patterns associated with minor, but significant changes in DNA methylation at the Mecp2 REs. Decitabine treatment induced Mecp2e1/MeCP2E1 (but not Mecp2e2) expression at day (D) 2, associated with DNA demethylation at the Mecp2 REs. In contrast, decitabine withdrawal downregulated both Mecp2 isoforms to different extents at D8, without affecting DNA methylation at the Mecp2 REs. NSC cell fate commitment was minimally affected by decitabine under tested conditions. Expression of both isoforms negatively correlated with methylation at specific regions of the Mecp2 promoter, both at D2 and D8. The correlation between intron 1 methylation and Mecp2e1 (but not Mecp2e2) varied depending on the stage of NSC differentiation (D2: negative; D8: positive).
Conclusions: Our results show the correlation between the expression of Mecp2 isoforms and DNA methylation in differentiating NSC, providing insights on the potential role of DNA methylation at the Mecp2 REs in Mecp2 isoform-specific expression. The ability of decitabine to induce Mecp2e1/MeCP2E1, but not Mecp2e2 suggests differential sensitivity of Mecp2 isoforms to decitabine and is important for future drug therapies for autism.
C1 [Liyanage, Vichithra R. B.; Zachariah, Robby M.; Rastegar, Mojgan] Univ Manitoba, Regenerat Med Program, Dept Biochem & Med Genet, Fac Med, Winnipeg, MB R3E 0J9, Canada.
RP Rastegar, M (reprint author), Univ Manitoba, Regenerat Med Program, Dept Biochem & Med Genet, Fac Med, Rm 627,Basic Med Sci Bldg,745 Bannatyne Ave, Winnipeg, MB R3E 0J9, Canada.
EM rastegar@cc.umanitoba.ca
FU Natural Sciences and Engineering Research Council of Canada (NSERC)
[3724052009]; Scottish Rite Charitable Foundation of Canada (SRCFC)
[10110]
FX We thank Mr Carl Olson in the Rastegar laboratory for neurosphere
sectioning. This work was supported by funds from the Natural Sciences
and Engineering Research Council of Canada (NSERC Discovery Grant
3724052009), and Scottish Rite Charitable Foundation of Canada (SRCFC,
Grant 10110). VRBL and RMZ are recipients of MHRC-MICH studentship
awards. The NESTIN monoclonal antibody developed by Susan Hockfield was
obtained from the Developmental Studies Hybridoma Bank, developed under
the auspices of the NICHD and maintained by The University of Iowa,
Department of Biology, Iowa City, IA 52242.
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NR 74
TC 6
Z9 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 15
PY 2013
VL 4
AR 46
DI 10.1186/2040-2392-4-46
PG 21
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA AC2LP
UT WOS:000332332900001
PM 24238559
ER
PT J
AU Lanz, TA
Guilmette, E
Gosink, MM
Fischer, JE
Fitzgerald, LW
Stephenson, DT
Pletcher, MT
AF Lanz, Thomas A.
Guilmette, Edward
Gosink, Mark M.
Fischer, James E.
Fitzgerald, Lawrence W.
Stephenson, Diane T.
Pletcher, Mathew T.
TI Transcriptomic analysis of genetically defined autism candidate genes
reveals common mechanisms of action
SO MOLECULAR AUTISM
LA English
DT Article
ID DE-NOVO MUTATIONS; MICROTUBULE-ASSOCIATED PROTEIN-2; SPECTRUM DISORDERS;
NUCLEUS-ACCUMBENS; PHOSPHORYLATION; ASSOCIATION; PLASTICITY; BRAIN; ERK;
ABNORMALITIES
AB Background: Austism spectrum disorder (ASD) is a heterogeneous behavioral disorder or condition characterized by severe impairment of social engagement and the presence of repetitive activities. The molecular etiology of ASD is still largely unknown despite a strong genetic component. Part of the difficulty in turning genetics into disease mechanisms and potentially new therapeutics is the sheer number and diversity of the genes that have been associated with ASD and ASD symptoms. The goal of this work is to use shRNA-generated models of genetic defects proposed as causative for ASD to identify the common pathways that might explain how they produce a core clinical disability.
Methods: Transcript levels of Mecp2, Mef2a, Mef2d, Fmr1, Nlgn1, Nlgn3, Pten, and Shank3 were knocked-down in mouse primary neuron cultures using shRNA constructs. Whole genome expression analysis was conducted for each of the knockdown cultures as well as a mock-transduced culture and a culture exposed to a lentivirus expressing an anti-luciferase shRNA. Gene set enrichment and a causal reasoning engine was employed to identify pathway level perturbations generated by the transcript knockdown.
Results: Quantification of the shRNA targets confirmed the successful knockdown at the transcript and protein levels of at least 75% for each of the genes. After subtracting out potential artifacts caused by viral infection, gene set enrichment and causal reasoning engine analysis showed that a significant number of gene expression changes mapped to pathways associated with neurogenesis, long-term potentiation, and synaptic activity.
Conclusions: This work demonstrates that despite the complex genetic nature of ASD, there are common molecular mechanisms that connect many of the best established autism candidate genes. By identifying the key regulatory checkpoints in the interlinking transcriptional networks underlying autism, we are better able to discover the ideal points of intervention that provide the broadest efficacy across the diverse population of autism patients.
C1 [Lanz, Thomas A.; Guilmette, Edward; Fitzgerald, Lawrence W.; Stephenson, Diane T.] Pfizer Inc, Neurosci Res Unit, Cambridge, MA 02140 USA.
[Gosink, Mark M.] Pfizer Inc, Invest Toxicol, Groton, CT 06340 USA.
[Fischer, James E.] Pfizer Inc, Compound Safety Predict, Groton, CT 06340 USA.
[Pletcher, Mathew T.] Pfizer Inc, Rare Dis Res Unit, Cambridge, MA 02140 USA.
RP Pletcher, MT (reprint author), Pfizer Inc, Rare Dis Res Unit, Cambridge Pk Dr, Cambridge, MA 02140 USA.
EM Mathew.Pletcher@pfizer.com
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NR 72
TC 4
Z9 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 15
PY 2013
VL 4
AR 45
DI 10.1186/2040-2392-4-45
PG 17
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 291OC
UT WOS:000329837000001
PM 24238429
ER
PT J
AU Moldrich, RX
Leanage, G
She, D
Dolan-Evans, E
Nelson, M
Reza, N
Reutens, DC
AF Moldrich, Randal X.
Leanage, Gayeshika
She, David
Dolan-Evans, Elliot
Nelson, Michael
Reza, Nargis
Reutens, David C.
TI Inhibition of histone deacetylase in utero causes sociability deficits
in postnatal mice
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Sodium valproate; Autism; Trichostatin A; Histone deacetylase;
Sociability; Histone acetylation
ID VALPROIC ACID; ANTIEPILEPTIC DRUGS; SODIUM VALPROATE; ANIMAL-MODEL;
PRENATAL EXPOSURE; MOOD STABILIZER; RAT PUPS; AUTISM; MOUSE;
ANTICONVULSANT
AB Exposure to sodium valproate (VPA) in utero increases the risk of language impairment and a diagnosis of autism spectrum disorder (ASD). Mice exposed to VPA while in utero have also shown postnatal social deficits. Inhibition of histone deacetylase (HDAC) is one of VPA's many biological effects. The main objective of this study was to test the hypothesis that HDAC inhibition causes these behavioral outcomes following prenatal VPA exposure in mice. We exposed embryonic mice to VPA, the HDAC inhibitor trichostatin A (TSA), or vehicle controls. TSA (1 mg/kg) inhibited HDAC in embryonic tissue at a level comparable to 600 mg/kg VPA, resulting in significant increases in histone H3 and H4 acetylation, and histone H3 lysine 4 tri-methylation. Postnatally, decreases in ultrasonic vocalization, olfactory motivation and sociability were observed in TSA and VPA-exposed pups. Treated mice exhibited elevated digging and grooming suggestive of mild restrictive and repetitive behaviors. Olfactory social preference, social novelty and habituation were normal. Together, these data indicate that embryonic HDAC inhibition alone can cause abnormal social behaviors in mice. This result serves as a molecular understanding of infant outcomes following mild VPA exposure in utero. Crown Copyright (C) 2013 Published by Elsevier B.V. All rights reserved.
C1 [Moldrich, Randal X.; Leanage, Gayeshika; She, David; Dolan-Evans, Elliot; Nelson, Michael; Reza, Nargis; Reutens, David C.] Univ Queensland, Ctr Adv Imaging, Brisbane, Qld 4072, Australia.
RP Moldrich, RX (reprint author), Univ Queensland, Ctr Adv Imaging, Bldg 57,Res Rd, Brisbane, Qld 4072, Australia.
EM r.moldrich@uq.edu.au
FU University of Queensland
FX The study was funded by The University of Queensland. The authors wish
to thank Drs. Tom Burne and Gilyana Borlikova for technical assistance
and advice with the behavior experiments.
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NR 58
TC 3
Z9 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 15
PY 2013
VL 257
BP 253
EP 264
DI 10.1016/j.bbr.2013.09.049
PG 12
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 273EZ
UT WOS:000328519200032
PM 24103642
ER
PT J
AU Fong, BMW
Tam, S
Leung, KSY
AF Fong, Bonnie Mei-Wah
Tam, Sidney
Leung, Kelvin Sze-Yin
TI Determination of plasma cholesterol sulfate by LC-APCI-MS/MS in the
context of pediatric autism
SO TALANTA
LA English
DT Article
DE Plasma cholesterol sulfate; LC-APCI-MS/MS; Chinese pediatric reference
interval; Autism
ID X-LINKED ICHTHYOSIS; SPECTRUM DISORDER; KERATINOCYTES; INHIBITOR;
STANDARD
AB Cholesterol sulfate (CS) has various biological functions. Previously, plasma CS was measured primarily as a means to diagnose X-linked ichthyosis; however, a recent hypothesis suggests that CS deficiency might be related to autism. As such, an assay capable of measuring both very high (in the case of X-linked ichthyosis) and very low (in the case of autism) plasma CS levels is required. Here we describe a novel LC-APCI-MS/MS method for the determination of CS in human plasma, and we propose normal CS ranges for children, based on studies of a local population of normal Chinese children between the ages of 2 and 10. In addition, we have used this method to measure plasma CS in autistic children. CS was isolated by solid-phase extraction, and quantified by isotope-dilution LC-APCI-MS/MS in negative ion mode monitoring 465.3 > 97.1 m/z (CS) and 472.3 >97.1 m/z (CS-d7). Mean recovery of the assay ranged from 88.1 to 112.7%; within- and between-run imprecisions have CVs less than 7.2 and 8.1%, respectively. The assay was linear up to at least 100 mu mol L-1. The reference interval of plasma CS in males (range: 1.16-4.23 mu mol L-1) was found to be higher than in females (range: 0.86-3.20 mu mol L-1). Comparison of normal and autistic children showed no statistically significant difference in the plasma CS level. In conclusion, a robust LC-APCI-MS/MS method for plasma CS was developed, and a pediatric reference interval was derived from applying the method to normal and autistic children. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Fong, Bonnie Mei-Wah; Leung, Kelvin Sze-Yin] Hong Kong Baptist Univ, Dept Chem, Kowloon Tong, Hong Kong, Peoples R China.
[Fong, Bonnie Mei-Wah; Tam, Sidney] Queen Mary Hosp, Dept Clin Biochem, Hong Kong, Hong Kong, Peoples R China.
RP Leung, KSY (reprint author), Hong Kong Baptist Univ, Dept Chem, Kowloon Tong, Hong Kong, Peoples R China.
EM s9362284@hkbu.edu.hk
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NR 27
TC 3
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0039-9140
EI 1873-3573
J9 TALANTA
JI Talanta
PD NOV 15
PY 2013
VL 116
BP 115
EP 121
DI 10.1016/j.talanta.2013.04.075
PG 7
WC Chemistry, Analytical
SC Chemistry
GA 268MW
UT WOS:000328176000018
PM 24148381
ER
PT J
AU Costain, G
Lionel, AC
Merico, D
Forsythe, P
Russell, K
Lowther, C
Yuen, T
Husted, J
Stavropoulos, DJ
Speevak, M
Chow, EWC
Marshall, CR
Scherer, SW
Bassett, AS
AF Costain, Gregory
Lionel, Anath C.
Merico, Daniele
Forsythe, Pamela
Russell, Kathryn
Lowther, Chelsea
Yuen, Tracy
Husted, Janice
Stavropoulos, Dimitri J.
Speevak, Marsha
Chow, Eva W. C.
Marshall, Christian R.
Scherer, Stephen W.
Bassett, Anne S.
TI Pathogenic rare copy number variants in community-based schizophrenia
suggest a potential role for clinical microarrays
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID 22Q11.2 DELETION SYNDROME; AUTISM SPECTRUM DISORDERS; DEVELOPMENTAL
DELAY; GENETIC RESEARCH; RISK-FACTORS; PERSPECTIVES; DISEASE; ADULT;
SUSCEPTIBILITY; DUPLICATIONS
AB Individually rare, large copy number variants (CNVs) contribute to genetic vulnerability for schizophrenia. Unresolved questions remain, however, regarding the anticipated yield of clinical microarray testing in schizophrenia. Using high-resolution genome-wide microarrays and rigorous methods, we investigated rare CNVs in a prospectively recruited community-based cohort of 459 unrelated adults with schizophrenia and estimated the minimum prevalence of clinically significant CNVs that would be detectable on a clinical microarray. A blinded review by two independent clinical cytogenetic laboratory directors of all large (500 kb) rare CNVs in cases and well-matched controls showed that those deemed to be clinically significant were highly enriched in schizophrenia (16.4-fold increase, P 0.0001). In a single community catchment area, the prevalence of individuals with these CNVs was 8.1. Rare 1.7 Mb CNVs at 2q13 were found to be significantly associated with schizophrenia for the first time, compared with the prevalence in 23 838 population-based controls (42.9-fold increase, P 0.0002). Additional novel findings that will facilitate the future clinical interpretation of smaller CNVs in schizophrenia include: (i) a greater proportion of individuals with two or more rare exonic CNVs 10 kb in size (1.5-fold increase, P 0.0109) in schizophrenia; (ii) the systematic discovery of new candidate genes for schizophrenia; and, (iii) functional gene enrichment mapping highlighting a differential impact in schizophrenia of rare exonic deletions involving diverse functions, including neurodevelopmental and synaptic processes (4.7-fold increase, P 0.0060). These findings suggest consideration of a potential role for clinical microarray testing in schizophrenia, as is now the suggested standard of care for related developmental disorders like autism.
C1 [Costain, Gregory; Russell, Kathryn; Lowther, Chelsea; Yuen, Tracy; Chow, Eva W. C.; Bassett, Anne S.] Ctr Addict & Mental Hlth, Clin Genet Res Program, Toronto, ON M5S 2S1, Canada.
[Lionel, Anath C.; Merico, Daniele; Marshall, Christian R.; Scherer, Stephen W.] Hosp Sick Children, Ctr Appl Genom & Program Genet & Genome Biol, Toronto, ON M5G 1L7, Canada.
[Lionel, Anath C.; Marshall, Christian R.; Scherer, Stephen W.] Univ Toronto, Dept Mol Genet, Toronto, ON M5G 1L7, Canada.
[Lionel, Anath C.; Marshall, Christian R.; Scherer, Stephen W.] Univ Toronto, McLaughlin Ctr, Toronto, ON M5G 1L7, Canada.
[Forsythe, Pamela] Horizon Hlth, St John, NB E2L 4L4, Canada.
[Forsythe, Pamela] Dalhousie Univ, St John, NB E2L 4L4, Canada.
[Husted, Janice] Univ Waterloo, Hlth Studies, Waterloo, ON N2L 3G1, Canada.
[Stavropoulos, Dimitri J.] Hosp Sick Children, Dept Pediat Lab Med, Cytogenet Lab, Toronto, ON M5G 1X8, Canada.
[Stavropoulos, Dimitri J.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON M5S 1A1, Canada.
[Speevak, Marsha] Credit Valley Hosp, Dept Genet, Mississauga, ON L5M 2N1, Canada.
[Chow, Eva W. C.; Bassett, Anne S.] Univ Toronto, Dept Psychiat, Toronto, ON M5T 1R8, Canada.
RP Bassett, AS (reprint author), 33 Russell St,Room 1100, Toronto, ON M5S 2S1, Canada.
EM anne.bassett@utoronto.ca
RI Scherer, Stephen /B-3785-2013
OI Scherer, Stephen /0000-0002-8326-1999
FU Canadian Institutes of Health Research (CIHR) [MOP-89066, MOP-111238];
University of Toronto McLaughlin Centre; NeuroDevNet; Genome Canada;
Ontario Genomics Institute; CIHR; Canadian Institute for Advanced
Research; Canada Foundation for Innovation; government of Ontario;
Autism Speaks; Hospital for Sick Children Foundation; CIHR Vanier Canada
Graduate Scholarship; NeuroDevNet doctoral fellowship
FX This work was supported by the Canadian Institutes of Health Research
(CIHR) (MOP-89066 to A. S. B., MOP-111238 to A. S. B.). A. S. B. holds
the Canada Research Chair in Schizophrenia Genetics and Genomic
Disorders and the Dalglish Chair in 22q11.2 Deletion Syndrome. A. C. L.
holds a NeuroDevNet doctoral fellowship. G. C. holds a CIHR Vanier
Canada Graduate Scholarship. S. W. S. is supported by grants from the
University of Toronto McLaughlin Centre, NeuroDevNet, Genome Canada and
the Ontario Genomics Institute, the CIHR, the Canadian Institute for
Advanced Research, the Canada Foundation for Innovation, the government
of Ontario, Autism Speaks, and The Hospital for Sick Children
Foundation. S. W. S. holds the GlaxoSmithKline-CIHR Chair in Genome
Sciences at the University of Toronto and The Hospital for Sick
Children.
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NR 68
TC 15
Z9 15
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 15
PY 2013
VL 22
IS 22
BP 4485
EP 4501
DI 10.1093/hmg/ddt297
PG 17
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 248EA
UT WOS:000326675300004
PM 23813976
ER
PT J
AU Mennes, M
Biswal, BB
Castellanos, FX
Milham, MP
AF Mennes, Maarten
Biswal, Bharat B.
Castellanos, F. Xavier
Milham, Michael P.
TI Making data sharing work: The FCP/INDI experience
SO NEUROIMAGE
LA English
DT Article
DE Open-access; Open science; fMRI; R-fMRI; Database; Informatics;
Neuroinformatics
ID DEMENTED OLDER-ADULTS; OPEN ACCESS SERIES; MRI DATA; FUNCTIONAL
CONNECTIVITY; DISCOVERY SCIENCE; BRAIN-FUNCTION; NEUROSCIENCE; AUTISM;
REPLICATION; CHALLENGES
AB Over a decade ago, the fMRI Data Center (fMRIDC) pioneered open-access data sharing in the task-based functional neuroimaging community. Well ahead of its time, the fMRIDC effort encountered logistical, sociocultural and funding barriers that impeded the field-wise instantiation of open-access data sharing. In 2009, ambitions for open-access data sharing were revived in the resting state functional MRI community in the form of two grassroots initiatives: the 1000 Functional Connectomes Project (FCP) and its successor, the International Neuroimaging Datasharing Initiative (INDI). Beyond providing open access to thousands of clinical and non-clinical imaging datasets, the FCP and INDI have demonstrated the feasibility of large-scale data aggregation for hypothesis generation and testing. Yet, the success of the FCP and INDI should not be confused with widespread embracement of open-access data sharing. Reminiscent of the challenges faced by fMRIDC, key controversies persist and include participant privacy, the role of informatics, and the logistical and cultural challenges of establishing an open science ethos. We discuss the FCP and INDI in the context of these challenges, highlighting the promise of current initiatives and suggesting solutions for possible pitfalls. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Mennes, Maarten] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Dept Cognit Neurosci, Med Ctr, NL-6525 ED Nijmegen, Netherlands.
[Biswal, Bharat B.] Univ Med & Dent New Jersey, Dept Radiol, Newark, NJ 07103 USA.
[Mennes, Maarten; Castellanos, F. Xavier] NYU Child Study Ctr, Phyllis Green & Randolph Cowen Inst Pediat Neuros, New York, NY USA.
[Biswal, Bharat B.; Castellanos, F. Xavier; Milham, Michael P.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA.
[Milham, Michael P.] Child Mind Inst, Ctr Dev Brain, New York, NY 10022 USA.
RP Milham, MP (reprint author), Child Mind Inst, Ctr Dev Brain, 445 Pk Ave, New York, NY 10022 USA.
EM Michael.milham@childmind.org
RI Mennes, Maarten/C-9924-2011; Milham, Michael/K-9501-2014
OI Mennes, Maarten/0000-0002-7279-3439;
FU Joseph P. Healy and the Stavros Niarchos Foundation; NIMH [R03 MH096321,
R01MH094639, R01MH083246]; Leon Levy Foundation; Stavros Niarchos
Foundation; NIH Blueprint for Neurosciences Research
FX Current financial support for the INDI team is provided by gifts from
Joseph P. Healy and the Stavros Niarchos Foundation, and an endowment
provided to the NYU Child Study Center by Phyllis Green and Randolph
Cowen. Additional current support includes NIMH awards to MPM (R03
MH096321, R01MH094639) and FXC (R01MH083246). Past support to MPM was
provided by the Leon Levy Foundation and to FXC by the Stavros Niarchos
Foundation. NITRC is funded by an NIH Blueprint for Neurosciences
Research (neuroscienceblueprintnih.gov) contract to TCG, Inc.
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NR 48
TC 20
Z9 20
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 15
PY 2013
VL 82
BP 683
EP 691
DI 10.1016/j.neuroimage.2012.10.064
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 220FQ
UT WOS:000324568400065
PM 23123682
ER
PT J
AU Doesburg, SM
Vidal, J
Taylor, MJ
AF Doesburg, Sam M.
Vidal, Julie
Taylor, Margot J.
TI Reduced theta connectivity during set-shifting in children with autism
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE ASD; autism; neural synchrony; neural oscillation;
magnetoencephalography; set-shifting; executive function; functional
connectivity
ID SPECTRUM DISORDERS; FUNCTIONAL CONNECTIVITY; EXECUTIVE FUNCTION;
PREFRONTAL CORTEX; NEURAL SYNCHRONY; WORKING-MEMORY; BRAIN NETWORKS;
GAMMA-POWER; TASK; EEG
AB Autism spectrum disorder (ASD) is a characterized by deficits in social cognition and executive function. An area of particular difficulty for children with ASD is cognitive flexibility, such as the ability to shift between attentional or response sets. The biological basis of such deficits remains poorly understood, although atypical development of structural and functional brain connectivity have been reported in ASD, suggesting that disruptions of normal patterns of inter-regional communication may contribute to cognitive problems in this group. The present magnetoencephalography study measured inter-regional phase synchronization while children with ASD and typically developing matched controls (6-14 years of age) performed a set-shifting task. Reduced theta-band phase synchronization was observed in children with ASD during extradimensional set-shifting. This reduction in task-dependent inter-regional connectivity encompassed numerous areas including multiple frontal lobe regions, and indicates that problems with communication among brain areas may contribute to difficulties with executive function in ASD.
C1 [Doesburg, Sam M.; Taylor, Margot J.] Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada.
[Doesburg, Sam M.; Taylor, Margot J.] Hosp Sick Children, Res Inst, Neurosci & Mental Hlth Program, Toronto, ON M5G 1X8, Canada.
[Doesburg, Sam M.; Taylor, Margot J.] Univ Toronto, Dept Med Imaging, Toronto, ON, Canada.
[Doesburg, Sam M.; Taylor, Margot J.] Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada.
[Vidal, Julie] Paris Descartes Univ, Paris, France.
[Vidal, Julie] CNRS, UMR 3521, Paris, France.
RP Doesburg, SM (reprint author), Hosp Sick Children, Dept Diagnost Imaging, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM sam.doesburg@sickkids.ca
FU NSERC [RGPIN-435659]
FX We would like to thank Travis Mills, Annette Ye, and Carmen Schafer for
their help with data analyses. We would also like to thank CIHR
(MOP-81161) for financial support of this project to Margot J. Taylor,
and NSERC (RGPIN-435659) for financial support to Sam M. Doesburg.
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NR 80
TC 8
Z9 8
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 14
PY 2013
VL 7
AR 785
DI 10.3389/fnhum.2013.00785
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 265GI
UT WOS:000327937800001
PM 24294201
ER
PT J
AU Shcheglovitov, A
Shcheglovitova, O
Yazawa, M
Portmann, T
Shu, R
Sebastiano, V
Krawisz, A
Froehlich, W
Bernstein, JA
Hallmayer, JF
Dolmetsch, RE
AF Shcheglovitov, Aleksandr
Shcheglovitova, Olesya
Yazawa, Masayuki
Portmann, Thomas
Shu, Rui
Sebastiano, Vittorio
Krawisz, Anna
Froehlich, Wendy
Bernstein, Jonathan A.
Hallmayer, Joachim F.
Dolmetsch, Ricardo E.
TI SHANK3 and IGF1 restore synaptic deficits in neurons from 22q13 deletion
syndrome patients
SO NATURE
LA English
DT Article
ID SCAFFOLDING PROTEIN SHANK3; AUTISM SPECTRUM DISORDERS; PLURIPOTENT
STEM-CELLS; CORTICAL-NEURONS; HUMAN FIBROBLASTS; MUTANT MICE; MUTATIONS;
DYSFUNCTION; GENERATION; CONVERSION
AB Phelan-McDermid syndrome (PMDS) is a complex neurodevelopmental disorder characterized by global developmental delay, severely impaired speech, intellectual disability, and an increased risk of autism spectrum disorders (ASDs)(1). PMDS is caused by heterozygous deletions of chromosome 22q13.3. Among the genes in the deleted region is SHANK3, which encodes a protein in the postsynaptic density (PSD)(2,3). Rare mutations in SHANK3 have been associated with idiopathic ASDs(4-7), non-syndromic intellectual disability(8), and schizophrenia(9). Although SHANK3 is considered to be the most likely candidate gene for the neurological abnormalities in PMDS patients(10), the cellular and molecular phenotypes associated with this syndrome in human neurons are unknown. We generated induced pluripotent stem (iPS) cells from individuals with PMDS and autism and used them to produce functional neurons. We show that PMDS neurons have reduced SHANK3 expression and major defects in excitatory, but not inhibitory, synaptic transmission. Excitatory synaptic transmission in PMDS neurons can be corrected by restoring SHANK3 expression or by treating neurons with insulin-like growth factor 1 (IGF1). IGF1 treatment promotes formation of mature excitatory synapses that lack SHANK3 but contain PSD95 and N-methyl-D-aspartate (NMDA) receptors with fast deactivation kinetics. Our findings provide direct evidence for a disruption in the ratio of cellular excitation and inhibition in PMDS neurons, and point to a molecular pathway that can be recruited to restore it.
C1 [Shcheglovitov, Aleksandr; Shcheglovitova, Olesya; Yazawa, Masayuki; Portmann, Thomas; Shu, Rui; Krawisz, Anna] Stanford Univ, Dept Neurobiol, Stanford, CA 94305 USA.
[Sebastiano, Vittorio] Stanford Univ, Dept Obstet & Gynecol, Stanford, CA 94305 USA.
[Sebastiano, Vittorio] Stanford Univ, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA.
[Froehlich, Wendy; Bernstein, Jonathan A.] Stanford Univ, Dept Pediat, Stanford, CA 94305 USA.
[Froehlich, Wendy; Hallmayer, Joachim F.] Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
[Dolmetsch, Ricardo E.] Novartis Inst Biomed Res, Cambridge, MA 02139 USA.
RP Dolmetsch, RE (reprint author), Novartis Inst Biomed Res, Cambridge, MA 02139 USA.
EM Ricardo.dolmetsch@novartis.com
FU National Institutes of Health (NIH) [NS069375]; California Institute for
Regenerative Medicine CIRM; Autism Science Foundation; Phelan-McDermid
Syndrome Foundation; Swiss National Science Foundation; Japan Society
for the Promotion of Research Abroad; American Heart Association;
National Institute of Mental Health (NIMH) [R33MH087898]; NIH
[5DP1OD3889]; CIRM [RT2-01906]; Simons Foundation; JDH; Flora foundation
FX We are grateful to participants and their families for their support; M.
Adam for assistance with recruitment; to X. Jia, A. Cherry, C. Bangs, P.
Jones, and J. Williams for assistance with tissue culture; P. Liao for
help with multiplex ligation-dependent probe amplification (MLPA); M.
Fabian for astrocyte preparations; H.N. Nguyen for consultations on the
neural differentiation protocol and spectral karyotyping (SKY); V. Vu
and G. Lin for help with data analysis; T. Sudhof, T. Boeckers, A.
Grabruker, C. Garner and C. Sala for antibodies; R. Xavier for SHANK3
complementary DNA; R. Reijo-Pera and members of the Dolmetsch laboratory
for commenting on the manuscript; E. Nigh for editing the manuscript. We
also thank the Stanford Neuroscience Microscopy Service (supported by
National Institutes of Health (NIH) NS069375). Support for this study
came from the California Institute for Regenerative Medicine CIRM, the
Autism Science Foundation and the Phelan-McDermid Syndrome Foundation
(to A. S.), the Swiss National Science Foundation (to T. P.), the Japan
Society for the Promotion of Research Abroad and American Heart
Association (to M.Y.), the National Institute of Mental Health (NIMH)
grant R33MH087898 (to J. F. H.); NIH Pioneer Award (5DP1OD3889), CIRM
(grant RT2-01906) and Simons Foundation (to R. E. D.). We are also
grateful for funding from the JDH research fund, N. Juaw, B. and F.
Horowitz, M. McCafferey, B. and J. Packard, P. Kwan and K. Wang, and the
Flora foundation.
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NR 32
TC 28
Z9 33
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD NOV 14
PY 2013
VL 503
IS 7475
BP 267
EP +
DI 10.1038/nature12618
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 250YX
UT WOS:000326894200052
PM 24132240
ER
PT J
AU Ewing, L
Pellicano, E
Rhodes, G
AF Ewing, Louise
Pellicano, Elizabeth
Rhodes, Gillian
TI Using Effort to Measure Reward Value of Faces in Children with Autism
SO PLOS ONE
LA English
DT Article
ID SPECTRUM DISORDERS; FACIAL ATTRACTIVENESS; SOCIAL MOTIVATION;
RECOGNITION; DEFICITS; MECHANISMS; BEAUTY; GAZE
AB According to one influential account, face processing atypicalities in autism reflect reduced reward value of faces, which results in limited attention to faces during development and a consequent failure to acquire face expertise. Surprisingly, however, there is a paucity of work directly investigating the reward value of faces for individuals with autism and the evidence for diminished face rewards in this population remains equivocal. In the current study, we measured how hard children with autism would work to view faces, using an effortful key-press sequence, and whether they were sensitive to the differential reward value of attractive and unattractive faces. Contrary to expectations, cognitively able children with autism did not differ from typically developing children of similar age and ability in their willingness to work to view faces. Moreover, the effort expended was strongly positively correlated with facial attractiveness ratings in both groups of children. There was also no evidence of atypical reward values for other, less social categories (cars and inverted faces) in the children with autism. These results speak against the possibility that face recognition difficulties in autism are explained by atypical reward value of faces.
C1 [Ewing, Louise; Pellicano, Elizabeth; Rhodes, Gillian] Univ Western Australia, Sch Psychol, Ctr Excellence Cognit & its Disorders, Australian Res Council, Perth, WA 6009, Australia.
[Pellicano, Elizabeth] Univ London, Inst Educ, Ctr Res Autism & Educ, London WC1N 1AZ, England.
RP Ewing, L (reprint author), Univ Western Australia, Sch Psychol, Ctr Excellence Cognit & its Disorders, Australian Res Council, Perth, WA 6009, Australia.
EM louise.ewing@uwa.edu.au
RI Ewing, Louise/H-9158-2014
FU Australian Research Council Centre of Excellence in Cognition and its
Disorders [CE110001021]; Australian Research Council Professorial
Fellowship [DP0877379]; University of Western Australia; Australian
Federation of University Women; Clothworkers' Foundation; Pears
Foundation
FX This work was supported by the Australian Research Council Centre of
Excellence in Cognition and its Disorders (project number CE110001021)
and an Australian Research Council Professorial Fellowship to G.R
(project number DP0877379). It was also supported by awards to L.E. from
the University of Western Australia and the Australian Federation of
University Women. Research at the Centre for Research in Autism and
Education (CRAE) is supported by The Clothworkers' Foundation and Pears
Foundation (E.P.). The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 42
TC 2
Z9 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 13
PY 2013
VL 8
IS 11
AR e79493
DI 10.1371/journal.pone.0079493
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255QK
UT WOS:000327254700139
PM 24236140
ER
PT J
AU Mejia, LA
Litterman, N
Ikeuchi, Y
de la Torre-Ubieta, L
Bennett, EJ
Zhang, C
Harper, JW
Bonni, A
AF Mejia, Luis A.
Litterman, Nadia
Ikeuchi, Yoshiho
de la Torre-Ubieta, Luis
Bennett, Eric J.
Zhang, Chi
Harper, J. Wade
Bonni, Azad
TI A Novel Hap1-Tsc1 Interaction Regulates Neuronal mTORC1 Signaling and
Morphogenesis in the Brain
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID TUBEROUS SCLEROSIS COMPLEX; TSC1-TSC2 COMPLEX; POLARITY; IDENTIFICATION;
PROTEIN; GENE; TSC1; EXPRESSION; HAMARTIN; PATHWAY
AB Tuberous sclerosis complex (TSC) is a leading genetic cause of autism. The TSC proteins Tsc1 and Tsc2 control the mTORC1 signaling pathway in diverse cells, but how the mTORC1 pathway is specifically regulated in neurons remains to be elucidated. Here, using an interaction proteomics approach in neural cells including neurons, we uncover the brain-enriched protein huntingtin-associated protein 1 (Hap1) as a novel functional partner of Tsc1. Knockdown of Hap1 promotes specification of supernumerary axons in primary hippocampal neurons and profoundly impairs the positioning of pyramidal neurons in the mouse hippocampus in vivo. The Hap1 knockdown-induced phenotypes in primary neurons and in vivo recapitulate the phenotypes induced by Tsc1 knockdown. We also find that Hap1 knockdown in hippocampal neurons induces the downregulation of Tsc1 and stimulates the activity of mTORC1, as reflected by phosphorylation of the ribosomal protein S6. Inhibition of mTORC1 activity suppresses the Hap1 knockdown-induced polarity phenotype in hippocampal neurons. Collectively, these findings define a novel link between Hap1 and Tsc1 that regulates neuronal mTORC1 signaling and neuronal morphogenesis, with implications for our understanding of developmental disorders of cognition.
C1 [Mejia, Luis A.; Litterman, Nadia; Ikeuchi, Yoshiho; de la Torre-Ubieta, Luis; Zhang, Chi; Bonni, Azad] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA.
[Mejia, Luis A.; Litterman, Nadia; de la Torre-Ubieta, Luis; Bonni, Azad] Harvard Univ, Sch Med, Program Neurosci, Boston, MA 02115 USA.
[Ikeuchi, Yoshiho; Bonni, Azad] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
[Bennett, Eric J.; Harper, J. Wade] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA.
RP Bonni, A (reprint author), Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
EM bonni@wustl.edu
RI ikeuchi, yoshiho/C-1713-2014
OI ikeuchi, yoshiho/0000-0002-2829-3840
FU National Institutes of Health [NS041021]; Harvard-Roche; F31 National
Research Service Award fellowship [NS068037]
FX This work was supported by National Institutes of Health Grant NS041021
to A.B., a Harvard-Roche grant to A.B., and F31 National Research
Service Award fellowship NS068037 to L.A.M. We thank Mathew E. Sowa and
John R. Lydeard for expert help with MS and A.B. laboratory members for
helpful discussions.
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TC 1
Z9 2
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD NOV 13
PY 2013
VL 33
IS 46
BP 18015
EP 18021
DI 10.1523/JNEUROSCI.2290-13.2013
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 252PU
UT WOS:000327020600006
PM 24227713
ER
PT J
AU Burrows, EL
Hannan, AJ
AF Burrows, Emma L.
Hannan, Anthony J.
TI Decanalization mediating gene-environment interactions in schizophrenia
and other psychiatric disorders with neurodevelopmental etiology
SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE
LA English
DT Editorial Material
DE schizophrenia; autism; brain disorders; brain development;
decanalization; gene-environment interactions; environmental enrichment;
animal models
ID AUTISM SPECTRUM DISORDERS; PHENOTYPIC PLASTICITY; MISSING HERITABILITY;
PSYCHOSOCIAL STRESS; COMPLEX DISEASE; NURSES HEALTH; RISK;
TRANSCRIPTOME; NEUREGULIN-1; EVOLUTION
C1 [Burrows, Emma L.; Hannan, Anthony J.] Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia.
[Hannan, Anthony J.] Univ Melbourne, Dept Anat & Neurosci, Parkville, Vic 3052, Australia.
RP Burrows, EL (reprint author), Univ Melbourne, Florey Inst Neurosci & Mental Hlth, Parkville, Vic 3052, Australia.
EM emma.burrows@florey.edu.au; anthony.hannan@florey.edu.au
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NR 50
TC 3
Z9 3
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5153
J9 FRONT BEHAV NEUROSCI
JI Front. Behav. Neurosci.
PD NOV 13
PY 2013
VL 7
AR 157
DI 10.3389/fnbeh.2013.00157
PG 5
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 250SW
UT WOS:000326875700001
PM 24312026
ER
PT J
AU Lockwood, PL
Bird, G
Bridge, M
Viding, E
AF Lockwood, Patricia L.
Bird, Geoffrey
Bridge, Madeleine
Viding, Essi
TI Dissecting empathy: high levels of psychopathic and autistic traits are
characterized by difficulties in different social information processing
domains
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE psychopathy; autism spectrum disorder; alexithymia; empathy; affective
resonance; cognitive perspective-taking
ID ASPERGER-SYNDROME; FUNCTIONING AUTISM; GENERAL-POPULATION; ANIMATED
SHAPES; MENTAL STATES; ALEXITHYMIA; BRAIN; MIND; RESPONSIVENESS;
CHILDREN
AB Individuals with psychopathy or autism spectrum disorder (ASD) can behave in ways that suggest lack of empathy towards others. However many different cognitive and affective processes may lead to unempathic behavior and the social processing profiles of individuals with high psychopathic vs. ASD traits are likely different Whilst psychopathy appears characterized by problems with resonating with others' emotions, ASD appears characterized by problems with cognitive perspective-taking. In addition, alexithymia has previously been associated with both disorders, but the contribution of alexithymia needs further exploration. In a community sample (N = 110) we show for the first time that although affective resonance and cognitive perspective-taking are related, high psychopathic traits relate to problems with resonating with others' emotions, but not cognitive perspective taking. Conversely, high ASD traits relate to problems with cognitive perspective-taking but not resonating with others' emotions. Alexithymia was associated with problems with affective resonance independently of psychopathic traits, suggesting that different component processes (reduced tendency to feel what others feel and reduced ability to identify and describe feelings) comprise affective resonance. Alexithymia was not associated with the reduced cognitive perspective-taking in high ASD traits. Our data suggest that (1) elevated psychopathic and ASD traits are characterized by difficulties in different social information processing domains and (2) reduced affective resonance in individuals with elevated psychopathic traits and the reduced cognitive perspective taking in individuals with elevated ASD traits are not explained by co-occurring alexithymia. (3) Alexithymia is independently associated with reduced affective resonance. Consequently, our data point to different component processes within the construct of empathy that are suggestive of partially separable cognitive and neural systems.
C1 [Lockwood, Patricia L.; Bridge, Madeleine; Viding, Essi] UCL, Div Psychol & Language Sci, London WC1H 0AP, England.
[Bird, Geoffrey] Kings Coll London, Inst Psychiat, MRC Social Genet & Dev Psychiat Ctr, London WC1H 0AP, England.
[Bird, Geoffrey] UCL, Inst Cognit Neurosci, London WC1H 0AP, England.
RP Lockwood, PL (reprint author), UCL, Div Psychol & Language Sci, 26 Bedford Way, London WC1H 0AP, England.
EM p.lockwood@ucl.ac.uk
FU Medical Research Council; Baily Thomas Charitable Fund [3089/1]
FX This work was supported by a Doctoral Training Account studentship from
the Medical Research Council awarded to Patricia L Lockwood. Essi Viding
is a Royal Society Wolfson Research Merit Award holder. Geoffrey Bird
was supported by a grant from the Baily Thomas Charitable Fund (3089/1).
Geoffrey Bird completed the paper while a Senior Fellow at the
Netherlands Institute for Advanced. Study in the Humanities and Social
Sciences. We would. like to thank Prof. Craig Neumann for his help and
advice with regard to the Self-Report Psychopathy Scale.
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NR 40
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 13
PY 2013
VL 7
DI 10.3389/fnhum.2013.00760
PG 6
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 250SS
UT WOS:000326875300001
ER
PT J
AU Richard, AE
Lajiness-O'Neill, RR
Bowyer, SM
AF Richard, Annette E.
Lajiness-O'Neill, Renee R.
Bowyer, Susan M.
TI Impaired prefrontal gamma band synchrony in autism spectrum disorders
during gaze cueing
SO NEUROREPORT
LA English
DT Article
DE autism spectrum disorder; eye gaze; gamma band synchrony;
magnetoencephalography
ID EYE GAZE; CHILDREN; BRAIN; PERCEPTION; OSCILLATIONS; INDIVIDUALS;
DEFICITS
AB Orienting to eye gaze is a vital social skill that is absent or developmentally delayed in autism spectrum disorders (ASD). Neural synchrony in the gamma frequency band is believed to be involved in perceptual and cognitive functions such as eye-gaze processing, and has been found to be abnormal in ASD. The current study used magnetoencephalography to measure neural synchrony in the gamma frequency band in neurotypicals (n=8) and individuals with ASD (n=10) while performing a directional eye-gaze processing task. Results support impaired generation of neural synchrony in the gamma frequency band during eye-gaze processing in ASD. Impaired gamma oscillatory activity in the prefrontal cortex may be associated with impairments in social cognitive functions such as eye-gaze processing in ASD.
C1 [Richard, Annette E.; Lajiness-O'Neill, Renee R.; Bowyer, Susan M.] Eastern Michigan Univ, Dept Psychol, Ypsilanti, MI 48197 USA.
RP Richard, AE (reprint author), Eastern Michigan Univ, Dept Psychol, Mark Jefferson Sci Complex, Ypsilanti, MI 48197 USA.
EM annette.e.richard@gmail.com
FU Eastern Michigan University
FX The current manuscript was prepared from the first author's master's
thesis, completed at Eastern Michigan University in partial fulfillment
of the requirements of the Clinical Psychology doctoral degree. This
research was supported in part by grants from a new faculty award (NFA)
and a faculty research fellowship award (FRF) from Eastern Michigan
University awarded to the second author.
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Wilson TW, 2007, BIOL PSYCHIAT, V62, P192, DOI 10.1016/j.biopsych.2007.07.002
NR 24
TC 3
Z9 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0959-4965
J9 NEUROREPORT
JI Neuroreport
PD NOV 13
PY 2013
VL 24
IS 16
BP 894
EP 897
DI 10.1097/WNR.0000000000000015
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 231OQ
UT WOS:000325427000004
PM 24077557
ER
PT J
AU Tchanturia, K
Smith, E
Weineck, F
Fidanboylu, E
Kern, N
Treasure, J
Cohen, SB
AF Tchanturia, Kate
Smith, Emma
Weineck, Felicitas
Fidanboylu, Eliz
Kern, Nikola
Treasure, Janet
Cohen, Simon Baron
TI Exploring autistic traits in anorexia: a clinical study
SO MOLECULAR AUTISM
LA English
DT Article
DE nervosa; Autism spectrum conditions; Set-hifting; Detail focus; Theory
of mind; Intervention
ID SELF-REPORT QUESTIONNAIRE; COGNITIVE REMEDIATION THERAPY;
EATING-DISORDER PATIENTS; HIGH-FUNCTIONING AUTISM; NORMAL
SEX-DIFFERENCES; SPECTRUM DISORDERS; ASPERGER-SYNDROME;
SOCIAL-ADJUSTMENT; CENTRAL COHERENCE; NERVOSA
AB Background: The objectives of this study were to explore associations between autistic traits and self-reported clinical symptoms in a population with anorexia nervosa (AN). Experimental and self-report evidence reveals similarities between AN and autism spectrum condition (ASC) populations in socio-emotional and cognitive domains; this includes difficulties with empathy, set-shifting and global processing. Focusing on these similarities may lead to better tailored interventions for both conditions.
Methods: A cross-sectional independent-groups design was employed. Participants with AN (n = 66) and typical controls (n = 66) completed self-report questionnaires including the Short (10-Item) Version Autism Spectrum Quotient (AQ-10) questionnaire (the first time this has been implemented in this population), the Eating Disorder Examination Questionnaire, the Hospital Anxiety and Depression Scale and the Work and Social Adjustment Scale. Group differences and the relationship between autistic traits and other questionnaire measures were investigated.
Results: The AN group had a significantly higher AQ-10 total score and a greater proportion scored above the clinical cut-off than the control group. Seven out of ten AQ-10 items significantly discriminated between groups. In the AN group, levels of autistic traits correlated with a greater self-reported anxiety and depression and a lower ability to maintain close relationships; however, eating disorder symptoms were not associated with autistic traits.
Conclusions: Women with anorexia possess a greater number of autistic traits than typical women. AQ-10 items that discriminated between groups related to 'bigger picture' (global) thinking, inflexibility of thinking and problems with social interactions, suggesting that autistic traits may exacerbate factors that maintain the eating disorder rather than cause the eating disorder directly. Using screening instruments may improve understanding of patients' problems, leading to better tailoring of intervention. We conclude that further investigation of autistic traits in AN could inform new intervention approaches based on joint working between ASC and eating disorder services.
C1 [Tchanturia, Kate; Smith, Emma] Inst Psychiat, Kings Coll London, London SE5 8AF, England.
[Tchanturia, Kate; Smith, Emma; Kern, Nikola; Treasure, Janet] South London & Maudsley NHS Trust, Psychol Med Clin Acad Grp, London, England.
[Tchanturia, Kate; Weineck, Felicitas; Fidanboylu, Eliz; Treasure, Janet] Inst Psychiat, Kings Coll London, Mental Hlth Studies Programme, London SE5 8AF, England.
[Cohen, Simon Baron] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
[Cohen, Simon Baron] Cambridgeshire & Peterborough NHS Fdn Trust, Cambridge, England.
RP Tchanturia, K (reprint author), Inst Psychiat, Kings Coll London, De Crespigny Pk, London SE5 8AF, England.
EM Kate.Tchanturia@kcl.ac.uk
FU Medical Research Council; NIHR CLAHRC for Cambridgeshire and
Peterborough NHS Foundation Trust; Autism Research Trust; Swiss Anorexia
Foundation; Mental Health Studies Programme of King's College London
FX The authors would like to thank the Swiss Anorexia Foundation and the
Mental Health Studies Programme of King's College London for financial
support of this study. SBC was supported by the Medical Research
Council, the NIHR CLAHRC for Cambridgeshire and Peterborough NHS
Foundation Trust, and the Autism Research Trust during the period of
this work. The authors would also like to thank Dr Daniel Stahl and Nick
Lao-Kaim for their guidance and expertise regarding the statistical
analysis.
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NR 61
TC 17
Z9 17
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 12
PY 2013
VL 4
AR 44
DI 10.1186/2040-2392-4-44
PG 8
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 291NP
UT WOS:000329835700001
PM 24220604
ER
PT J
AU Gheldof, N
Witwicki, RM
Migliavacca, E
Leleu, M
Didelot, G
Harewood, L
Rougemont, J
Reymond, A
AF Gheldof, Nele
Witwicki, Robert M.
Migliavacca, Eugenia
Leleu, Marion
Didelot, Gerard
Harewood, Louise
Rougemont, Jacques
Reymond, Alexandre
TI Structural Variation-Associated Expression Changes Are Paralleled by
Chromatin Architecture Modifications
SO PLOS ONE
LA English
DT Article
ID COPY NUMBER VARIATION; WILLIAMS-BEUREN-SYNDROME; HUMAN GENOME;
GENE-EXPRESSION; HISTONE MODIFICATIONS; MOUSE GENOME; HI-C; CHROMOSOME;
LANDSCAPE; CELLS
AB Copy number variants (CNVs) influence the expression of genes that map not only within the rearrangement, but also to its flanks. To assess the possible mechanism(s) underlying this "neighboring effect", we compared intrachromosomal interactions and histone modifications in cell lines of patients affected by genomic disorders and control individuals. Using chromosome conformation capture (4C-seq), we observed that a set of genes flanking the Williams-Beuren Syndrome critical region (WBSCR) were often looping together. The newly identified interacting genes include AUTS2, mutations of which are associated with autism and intellectual disabilities. Deletion of the WBSCR disrupts the expression of this group of flanking genes, as well as long-range interactions between them and the rearranged interval. We also pinpointed concomitant changes in histone modifications between samples. We conclude that large genomic rearrangements can lead to chromatin conformation changes that extend far away from the structural variant, thereby possibly modulating expression globally and modifying the phenotype. GEO Series accession number: GSE33784, GSE33867.
C1 [Gheldof, Nele; Witwicki, Robert M.; Migliavacca, Eugenia; Didelot, Gerard; Harewood, Louise; Reymond, Alexandre] Univ Lausanne, Ctr Integrat Gen, Lausanne, Switzerland.
[Migliavacca, Eugenia; Leleu, Marion; Rougemont, Jacques] SIB, Lausanne, Switzerland.
[Leleu, Marion; Rougemont, Jacques] Ecole Polytech Fed Lausanne, Sch Life Sci, Lausanne, Switzerland.
RP Gheldof, N (reprint author), Nestle Inst Hlth Sci, Lausanne, Switzerland.
EM nele.gheldof@rd.nestle.com; alexandre.reymond@unil.ch
FU European Commission anEUploidy Integrated Project [037627]; Swiss
National Science Foundation; SNSF Sinergia grant; doctoral school of the
Faculty of Biology and Medicine, University of Lausanne
FX This work was supported by the European Commission anEUploidy Integrated
Project (grant 037627), the Swiss National Science Foundation and a SNSF
Sinergia grant to AR. RMW was supported by a fellowship from the
doctoral school of the Faculty of Biology and Medicine, University of
Lausanne. NG is a grantee of the Marie Heim Vogtlin and the Pro-Women
programs of the SNSF and the Faculty of Biology and Medicine, University
of Lausanne, respectively. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 64
TC 3
Z9 4
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 12
PY 2013
VL 8
IS 11
AR e79973
DI 10.1371/journal.pone.0079973
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 255PK
UT WOS:000327252100124
PM 24265791
ER
PT J
AU Lim, KC
Crino, PB
AF Lim, K-C
Crino, P. B.
TI FOCAL MALFORMATIONS OF CORTICAL DEVELOPMENT: NEW VISTAS FOR MOLECULAR
PATHOGENESIS
SO NEUROSCIENCE
LA English
DT Review
DE malformations of cortical development; mTOR; epilepsy; autism; rapamycin
ID TUBEROUS SCLEROSIS COMPLEX; TEMPORAL-LOBE EPILEPSY; AUTISTIC-LIKE
BEHAVIOR; DYSPLASIA TYPE-IIB; MOUSE MODEL; MAMMALIAN TARGET;
HUMAN-PAPILLOMAVIRUS; SIGNALING PATHWAY; GROWTH-FACTOR; MTOR PATHWAY
AB Focal malformations of cortical development (FMCD) are highly associated with several neurological disorders including intractable epilepsy and neurocognitive disabilities. Over the past decade, several FMCD subtypes have been linked to hyperactivation of the mammalian target of rapamycin (mTOR) signaling cascade. In view of the roles that mTOR plays in cell proliferation, size, motility, and stem cell phenotype, many of the features of FMCD such as cytomegaly, disorganized lamination, and expression of stem cell markers can be explained by enhanced mTOR signaling. FMCD result from several distinct and fascinating molecular mechanisms including biallelic gene inactivation, somatic mutation, and potentially, viral infection. These mechanisms have been directly linked to mTOR activation. Perhaps most compelling, pharmacological inhibition of mTOR has been implemented successfully in clinical trials for select FMCD and provides a new vista for treatment. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Lim, K-C] Univ Penn, Med Ctr, Dept Neurol, Philadelphia, PA 19104 USA.
[Crino, P. B.] Temple Univ, Sch Med, Dept Neurol, Shriners Hosp,Pediat Res Ctr, Philadelphia, PA 19140 USA.
RP Crino, PB (reprint author), Temple Univ, Sch Med, Dept Neurol, Shriners Hosp,Pediat Res Ctr, 6th Floor Med Educ & Res Bldg,3500N Broad St, Philadelphia, PA 19140 USA.
EM peter.crino@temple.edu
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NR 115
TC 13
Z9 13
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
EI 1873-7544
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 12
PY 2013
VL 252
BP 262
EP 276
DI 10.1016/j.neuroscience.2013.07.037
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 236YS
UT WOS:000325836000024
PM 23892008
ER
PT J
AU Wei, H
Alberts, I
Li, X
AF Wei, H.
Alberts, I.
Li, X.
TI BRAIN IL-6 AND AUTISM
SO NEUROSCIENCE
LA English
DT Review
DE autism; brain; Interleukin-6; neuroimmune response; behavior
ID CEREBELLAR GRANULE NEURONS; DENDRITIC SPINE DENSITY; SPECTRUM DISORDERS;
INDUCED NEUROTOXICITY; SYNAPTIC PLASTICITY; INTERLEUKIN-6 IL-6; IMMUNE
ACTIVATION; GENE-EXPRESSION; CHILDREN; SCHIZOPHRENIA
AB Autism is a severe neurodevelopmental disorder characterized by impairments in social interaction, deficits in verbal and non-verbal communication, and repetitive behavior and restricted interests. Emerging evidence suggests that aberrant neuroimmune responses may contribute to phenotypic deficits and could be appropriate targets for pharmacologic intervention. Interleukin (IL)-6, one of the most important neuroimmune factors, has been shown to be involved in physiological brain development and in several neurological disorders. For instance, findings from postmortem and animal studies suggest that brain IL-6 is an important mediator of autism-like behaviors. In this review, a possible pathological mechanism behind autism is proposed, which suggests that IL-6 elevation in the brain, caused by the activated glia and/or maternal immune activation, could be an important inflammatory cytokine response involved in the mediation of autism-like behaviors through impairments of neuroanatomical structures and neuronal plasticity. Further studies to investigate whether IL-6 could be used for therapeutic interventions in autism would be of great significance. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Wei, H.] Shanxi Med Univ, Cent Lab, Shanxi Prov Peoples Hosp, Taiyuan 030012, Peoples R China.
[Alberts, I.] CUNY, Dept Nat Sci, LaGuardia CC, New York, NY 11101 USA.
[Li, X.] New York State Inst Basic Res Dev Disabil, Dept Neurochem, Staten Isl, NY 10314 USA.
RP Wei, H (reprint author), Shanxi Med Univ, Cent Lab, Shanxi Prov Peoples Hosp, 29 Shuangta Rd, Taiyuan 030012, Peoples R China.
EM hongenwei@gmail.com
FU National Natural Science Foundation of China [81201061]
FX This work was supported by grants to H. Wei from the National Natural
Science Foundation of China (No. 81201061).
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NR 81
TC 7
Z9 7
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
EI 1873-7544
J9 NEUROSCIENCE
JI Neuroscience
PD NOV 12
PY 2013
VL 252
BP 320
EP 325
DI 10.1016/j.neuroscience.2013.08.025
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 236YS
UT WOS:000325836000028
PM 23994594
ER
PT J
AU Simon, DM
Corbett, BA
AF Simon, David M.
Corbett, Blythe A.
TI Examining associations between anxiety and cortisol in high functioning
male children with autism
SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Anxiety; Stress; Cortisol; Self-report
ID COMPLEX DEVELOPMENTAL DISORDER; COGNITIVE-BEHAVIORAL THERAPY; SPECTRUM
DISORDERS; SOCIAL STRESS; CONTROLLED-TRIAL; PSYCHIATRIC-SYMPTOMS;
INFORMANT AGREEMENT; PSYCHOSOCIAL STRESS; SALIVARY CORTISOL;
CIRCADIAN-RHYTHMS
AB Background: Autism spectrum disorder (ASD) is characterized by deficits in communication and social ability, as well as restricted interests and repetitive behavior. Anxiety is a persistent anticipation or apprehension about one or more situations to which a person is exposed, and affects many people, including children with ASD. Stress, by contrast, is a response to situations that are threatening, uncontrollable, or unexpected. Indices of anxiety are often measured through informants, with parents and teachers serving as the primary sources of reported anxiety in children. However, self-report measures exist, allowing current (state) and persistent (trait) anxiety to be assessed. The current study was designed to evaluate whether children with autism could identify their own levels of anxiety and the degree to which these levels were associated with symptom profile and physiological arousal.
Methods: Self-reported state and trait anxiety were collected during exposure to different stress paradigms for 40 children (21 typically developing, 19 with autistic disorder) and compared to parent reported social ability (Social Responsiveness Scale) and stress responsivity (cortisol).
Results: Significant differences were found between typically developing and children with autism for both state and trait anxiety across all conditions. Associations were identified between severity of parent-reported social impairment and both types of self-report anxiety. No relationship was found between stress (salivary cortisol) and anxiety in children with autism.
Conclusions: Children with autism are able to consistently report their persistent level of anxiety symptoms in stressful situations of benign character. Therefore, the inclusion of such measures may be useful in identifying and tracking symptoms in children with autism under appropriate circumstances.
C1 [Simon, David M.; Corbett, Blythe A.] Vanderbilt Univ, Dept Psychiat, Nashville, TN 37203 USA.
[Simon, David M.; Corbett, Blythe A.] Vanderbilt Kennedy Ctr, Nashville, TN USA.
RP Corbett, BA (reprint author), Vanderbilt Univ, Dept Psychiat, 230 Appleton Way, Nashville, TN 37203 USA.
EM blythe.corbett@vanderbilt.edu
FU National Institute of Health [R01 MH085717]
FX This work was supported in part by National Institute of Health R01
MH085717 awarded to BAC. We are grateful to all the children and
families who continue to support our research.
CR American Psychiatric Association, 2000, DIAGNOSTIC AND STATI
American Psychiatric Association, 2013, DIAGNOSTIC AND STATI
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NR 76
TC 2
Z9 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1866-1947
EI 1866-1955
J9 J NEURODEV DISORD
JI J. Neurodev. Disord.
PD NOV 11
PY 2013
VL 5
AR 32
DI 10.1186/1866-1955-5-32
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 281SS
UT WOS:000329121900001
PM 24216056
ER
PT J
AU Horwitz, B
Hwang, C
Alstott, J
AF Horwitz, Barry
Hwang, Chuhern
Alstott, Jeff
TI Interpreting the effects of altered brain anatomical connectivity on
fMRI functional connectivity: a role for computational neural modeling
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE neural modeling; fMRI; functional connectivity; brain disorders; huma
nbrain
ID HUMAN CEREBRAL-CORTEX; ALZHEIMERS-DISEASE; WORKING-MEMORY; NEURONAL
DYNAMICS; NETWORK ANALYSIS; VISUAL PATHWAYS; STATE; SCHIZOPHRENIA;
SYSTEMS; AUTISM
AB Recently, there have been a large number of studies using resting state fMRI to characterize abnormal brain connectivity in patients with a variety of neurological, psychiatric, and developmental disorders. However, interpreting what the differences in resting state fMRI functional connectivity (rsfMRI-FC) actually reflect in terms of the underlying neural pathology has proved to be elusive because of the complexity of brain anatomical connectivity. The same is the case for task-based fMRI studies. In the last few years, several groups have used large-scale neural modeling to help provide some insight into the relationship between brain anatomical connectivity and the corresponding patterns of fMRI-FC. In this paper we review several efforts at using large-scale neural modeling to investigate the relationship between structural connectivity and functional/effective connectivity to determine how alterations in structural connectivity are manifested in altered patterns of functional/effective connectivity. Because the alterations made in the anatomical connectivity between specific brain regions in the model are known in detail, one can use the results of these simulations to determine the corresponding alterations in rsfMRI-FC. Many of these simulation studies found that structural connectivity changes do not necessarily result in matching changes in functional/effective connectivity in the areas of structural modification. Often, it was observed that increases in functional/effective connectivity in the altered brain did not necessarily correspond to increases in the strength of the anatomical connection weights. Note that increases in rsfMRI-FC in patients have been interpreted in some cases as resulting from neural plasticity. These results suggest that this interpretation can be mistaken. The relevance of these simulation findings to the use of functional/effective fMRI connectivity as biomarkers for brain disorders is also discussed
C1 [Horwitz, Barry; Hwang, Chuhern] Natl Inst Deafness & Other Commun Disorders, Brain Imaging & Modeling Sect, NIH, Bethesda, MD 20892 USA.
[Hwang, Chuhern] Natl Inst Biomed Imaging & Bioengn, NIH, Bethesda, MD USA.
[Hwang, Chuhern] Univ Virginia, Dept Biomed Engn, Charlottesville, VA USA.
[Alstott, Jeff] NIMH, Sect Crit Brain Dynam, NIH, Bethesda, MD 20892 USA.
[Alstott, Jeff] Univ Cambridge, Brain Mapping Unit, Behav & Clin Neurosci Inst, Cambridge CB2 1TN, England.
RP Horwitz, B (reprint author), Natl Inst Deafness & Other Commun Disorders, Brain Imaging & Modeling Sect, NIH, 10 Ctr Dr,Room 5D39,MSC 1402, Bethesda, MD 20892 USA.
EM horwitzb@nidcd.nih.gov
FU ntramural Research Programs of the National Institute on Deafness; Other
Communication Disorders, the National Institute of Mental Health;
National Institute of Biomedical Imaging and Bioengineering; National
Institutes of Health
FX This work was supported by the Intramural Research Programs of the
National Institute on Deafness and Other Communication Disorders, the
National Institute of Mental Health, and the National Institute of
Biomedical Imaging and Bioengineering, all part of the National
Institutes of Health. The simulations performed for this paper utilized
the high-performance computational capabilities of the Biowulf Linux
cluster at the National Institutes of Health, Bethesda, MD. The authors
wish to thank the two reviewers for a number of useful comments and
suggestions
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NR 81
TC 4
Z9 4
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 11
PY 2013
VL 7
AR 649
DI 10.3389/fnhum.2013.00649
PG 11
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 248TU
UT WOS:000326727600001
PM 24273500
ER
PT J
AU Lehnhardt, FG
Gawronski, A
Pfeiffer, K
Kockler, H
Schilbach, L
Vogeley, K
AF Lehnhardt, Fritz-Georg
Gawronski, Astrid
Pfeiffer, Kathleen
Kockler, Hanna
Schilbach, Leonhard
Vogeley, Kai
TI The Investigation and Differential Diagnosis of Asperger Syndrome in
Adults
SO DEUTSCHES ARZTEBLATT INTERNATIONAL
LA English
DT Review
ID AUTISM SPECTRUM DISORDERS; FUNCTIONING AUTISM; EPIDEMIOLOGY; QUOTIENT;
OVERLAP; AQ
AB Background: As a result of the increased public interest in autism spectrum disorders (ASD), certain core manifestations of ASD-impaired social interaction and communication, bizarre interests-are now commonly recognized as being typical of autism, not only in children, but in adults as well. More often than before, general practitioners, neurologists, and psychiatrists find themselves being asked whether a patient is suffering from previously unrecognized Asperger syndrome (AS). The prevalence of ASD is estimated at 1%, and the ratio of diagnosed to undiagnosed cases at about 3:2. Little is known about the diagnostic evaluation of AS in adulthood.
Methods: We selectively searched the Medline database for pertinent literature, paying special attention to diagnostic manuals and to the guideline of the United Kingdom's National Institute for Health and Care Excellence (NICE).
Results: Centrally important aspects of the diagnosis of AS include an assessment of the patient's ability to assume the emotional perspectives of others, non-verbal modes of expression, repetitive behavior patterns, and childhood social behavioral history. The autism quotient (AQ) is now established as a simple but nonspecific screening test. Up to 70% of all affected adults have comorbid disturbances, most often depression and anxiety disorders. The differential diagnosis includes personality disorders, anxiety disorders, obsessive-compulsive disorder, and attention deficit-hyperactivity disorder. The diagnostic assessment should proceed in stepwise fashion, starting from simple screening in primary care and then moving on to evaluation of the suspected diagnosis by a mental health care specialist, followed by extensive further investigation in an outpatient clinic specifically devoted to patients with autism spectrum disorders.
Conclusion: The diagnostic assessment of autism in adults requires knowledge of the core and accompanying manifestations of autism and of their differential diagnoses. More research is needed for the development of further screening tests and the precise determination of diagnosis rates, differential diagnoses, and comorbidities.
C1 [Lehnhardt, Fritz-Georg; Gawronski, Astrid; Pfeiffer, Kathleen; Kockler, Hanna; Schilbach, Leonhard; Vogeley, Kai] Univ Cologne, Dept Psychiat & Psychotherapy, Cologne, Germany.
[Vogeley, Kai] Forschungszentrum Julich, Inst Cognit Neurosci, Inst Neurosci & Med INM 3, D-52425 Julich, Germany.
RP Lehnhardt, FG (reprint author), Uniklin Koln, Klin & Poliklin Psychiat & Psychotherapie, Kerpener Str 62, D-50937 Cologne, Germany.
EM Fritz-Georg.Lehnhardt@uk-koeln.de
RI Vogeley, K/E-4860-2012
OI Vogeley, K/0000-0002-5891-5831
FU Volkswagen Foundation
FX Dr. Schilbach received financial support from the Volkswagen Foundation
for an interdisciplinary research project on social cognition.
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NR 40
TC 4
Z9 4
PU DEUTSCHER AERZTE-VERLAG GMBH
PI COLOGNE
PA DIESELSTRABE 2, POSTFACH 400265, D-50859 COLOGNE, GERMANY
SN 1866-0452
J9 DTSCH ARZTEBL INT
JI Dtsch. Arztebl. Int.
PD NOV 8
PY 2013
VL 110
IS 45
BP 755
EP 763
DI 10.3238/arztebl.2013.0755
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 258SD
UT WOS:000327478100001
PM 24290364
ER
PT J
AU Stoccoro, A
Karlsson, HL
Coppede, F
Migliore, L
AF Stoccoro, Andrea
Karlsson, Hanna L.
Coppede, Fabio
Migliore, Lucia
TI Epigenetic effects of nano-sized materials
SO TOXICOLOGY
LA English
DT Article
DE Epigenetics; Nano-sized materials; Nanoparticles; DNA methylation;
Histone modifications; MicroRNA
ID DNA METHYLATION PATTERNS; CERIUM OXIDE NANOPARTICLES; MATTER
AIR-POLLUTION; OXIDATIVE STRESS; PARTICULATE MATTER; GENE-EXPRESSION;
HIGH-THROUGHPUT; GOLD NANOPARTICLES; CPG ISLANDS; ENVIRONMENTAL-FACTORS
AB The term epigenetics includes several phenomena such as DNA methylation, histone tail modifications, and microRNA mediated mechanisms, which are able to mold the chromatin structure and/or gene expression levels, without altering the primary DNA sequence. Environmental agents can exert epigenetic properties and there is increasing evidence of epigenetic deregulation of gene expression in several human diseases, including cancer, cardiovascular diseases, autism spectrum disorders, autoimmune diseases, and neurodegeneration, among others. Given the widespread use and dispersion in the environment of nano-sized materials, this article summarizes the studies performed so far to evaluate their potential epigenetic properties. Those studies highlight the ability of certain nano-sized compounds to induce an impaired expression of genes involved in DNA methylation kactions leading to global DNA methylation changes, as well as changes of gene specific methylation of tumor suppressor genes, inflammatory genes, and DNA repair genes, all potentially involved in cancer development. Moreover, some nano-sized compounds are able to induce changes in the acetylation and methylation of histone tails, as well as microRNA deregulated expression. We also provided a detailed description of currently available methodologies to evaluate epigenetic modifications. Standard protocols are currently available to evaluate cytotoxic and genotoxic effects of nano-sized materials. By contrast, there are at present no available standard protocols to evaluate the epigenetic potential of any given compound. The currently available methodologies offer different, but often complementary information to characterize potential epigenetic changes induced by exposure to nano-sized compounds. Given the widespread use and dispersion in the environment of nano-sized materials, at present and foreseeable in the near future, and in light of the indication of potential epigenetic properties here reviewed, more attention should be paid to unravel the consequences of such effects in future studies. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
C1 [Stoccoro, Andrea; Migliore, Lucia] Univ Pisa, Med Genet Lab, Dept Translat Res & New Technol Med & Surg, I-56126 Pisa, Italy.
[Karlsson, Hanna L.] Karolinska Inst, Inst Environm Med, Div Mol Toxicol, S-10401 Stockholm, Sweden.
[Coppede, Fabio] Pisa Univ Hosp AOUP, Dept Lab Med, Pisa, Italy.
RP Migliore, L (reprint author), Univ Pisa, Div Med Genet, Dept Translat Res & New Technol Med & Surg, Via S Giuseppe 22, I-56126 Pisa, Italy.
EM l.migliore@geog.unipi.it
FU FP7 project NanoRetox [CP-FP 214478-2]; FP7 project SANOWORK [280716];
Swedish Council for Working Life and Social Research (FAS)
FX This study was financially supported by the FP7 projects No CP-FP
214478-2, NanoRetox and No 280716, SANOWORK and the Swedish Council for
Working Life and Social Research (FAS).
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NR 117
TC 11
Z9 11
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
IRELAND
SN 0300-483X
J9 TOXICOLOGY
JI Toxicology
PD NOV 8
PY 2013
VL 313
IS 1
SI SI
BP 3
EP 14
DI 10.1016/j.tox.2012.12.002
PG 12
WC Pharmacology & Pharmacy; Toxicology
SC Pharmacology & Pharmacy; Toxicology
GA 251DK
UT WOS:000326907800002
PM 23238276
ER
PT J
AU Buard, I
Rogers, SJ
Hepburn, S
Kronberg, E
Rojas, DC
AF Buard, Isabelle
Rogers, Sally J.
Hepburn, Susan
Kronberg, Eugene
Rojas, Donald C.
TI Altered oscillation patterns and connectivity during picture naming in
autism
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE magnetoencephalography; gamma-band; beta-band; oscillations; functional
connectivity; Granger causality; fusiform gyrus; endophenotype
ID INDEPENDENT COMPONENT ANALYSIS; HIGH-FUNCTIONING AUTISM; WORD FORM AREA;
SPECTRUM DISORDERS; GAMMA-OSCILLATIONS; LANGUAGE LATERALIZATION;
CORTICAL NETWORKS; ASPERGER-SYNDROME; FUSIFORM GYRUS; YOUNG-CHILDREN
AB Similar behavioral deficits are shared between individuals with autism spectrum disorders (ASD) and their first-degree relatives, such as impaired face memory, object recognition, and some language aspects. Functional neuroimaging studies have reported abnormalities in ASD in at least one brain area implicated in those functions, the fusiform gyrus (FG). High frequency oscillations have also been described as abnormal in ASD in a separate line of research. The present study examined whether low- and high-frequency oscillatory power, localized in part to FG and other language-related regions, differs in ASD subjects and first-degree relatives. Twelve individuals with ASD, 16 parents of children with ASD, and 35 healthy controls participated in a picture-naming task using magnetoencephalography (MEG) to assess oscillatory power and connectivity. Relative to controls, we observed reduced evoked high-gamma activity in the right superior temporal gyrus (STG) and reduced high-beta/low-gamma evoked power in the left inferior frontal gyrus (IFG) in the ASD group. Finally, reductions in phase-locked beta-band were also seen in the ASD group relative to controls, especially in the occipital lobes (OCC). First degree relatives, in contrast, exhibited higher high-gamma band power in the left STG compared with controls, as well as increased high-beta/low-gamma evoked power in the left FG. In the left hemisphere, beta- and gamma-band functional connectivity between the IFG and FG and between STG and OCC were higher in the autism group than in controls. This suggests that, contrary to what has been previously described, reduced connectivity is not observed across all scales of observation in autism. The lack of behavioral correlation for the findings warrants some caution in interpreting the relevance of such changes for language function in ASD. Our findings in parents implicates the gamma- and beta-band ranges as potential compensatory phenomena in autism relatives.
C1 [Buard, Isabelle; Kronberg, Eugene; Rojas, Donald C.] Univ Colorado Denver, Dept Psychiat, UCD Magnetoencephalog Lab, Aurora, CO 80045 USA.
[Rogers, Sally J.] UC Davis MIND Inst, Sacramento, CA USA.
[Hepburn, Susan] Univ Colorado JFK Partners, Aurora, CO USA.
RP Rojas, DC (reprint author), Univ Colorado Denver, Dept Psychiat, Magnetoencephalog Lab, Anschutz Med Campus,13001 East 17th Pl F546, Aurora, CO 80045 USA.
EM don.rojas@ucdenver.edu
FU NIH [RO1 MH082820]; Cure Autism
FX This work was funded by NIH RO1 MH082820 and Cure Autism Now (currently
Autism Speaks). The authors of the manuscript declare that they have no
conflict of interest to report regarding this manuscript.
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NR 74
TC 7
Z9 7
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 8
PY 2013
VL 7
AR 742
DI 10.3389/fnhum.2013.00742
PG 11
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 248EJ
UT WOS:000326676200001
PM 24265611
ER
PT J
AU Moseley, RL
Mohr, B
Lombardo, MV
Baron-Cohen, S
Hauk, O
Pulvermuller, F
AF Moseley, Rachel L.
Mohr, Bettina
Lombardo, Michael V.
Baron-Cohen, Simon
Hauk, Olaf
Pulvermueller, Friedemann
TI Brain and behavioral correlates of action semantic deficits in autism
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE Autism; semantics; motor systems; action
ID HIGH-FUNCTIONING AUTISM; MIRROR-NEURON SYSTEM; LONG-TERM-MEMORY; WORD
FORM AREA; MOTOR SYSTEM; SPECTRUM DISORDERS; VISUAL-CORTEX; LANGUAGE;
SELF; CHILDREN
AB Action-perception circuits containing neurons in the motor system have been proposed as the building blocks of higher cognition; accordingly, motor dysfunction should entail cognitive deficits. Autism spectrum conditions (ASC) are marked by motor impairments but the implications of such motor dysfunction for higher cognition remain unclear. We here used word reading and semantic judgment tasks to investigate action-related motor cognition and its corresponding fMRI brain activation in high-functioning adults with ASC. These participants exhibited hypoactivity of motor cortex in language processing relative to typically developing controls. Crucially, we also found a deficit in semantic processing of action-related words, which, intriguingly, significantly correlated with this underactivation of motor cortex to these items. Furthermore, the word-induced hypoactivity in the motor system also predicted the severity of ASC as expressed by the number of autistic symptoms measured by the Autism-Spectrum Quotient (Baron-Cohen et al., 2001). These significant correlations between word-induced activation of the motor system and a newly discovered semantic deficit in a condition known to be characterized by motor impairments, along with the correlation of such activation with general autistic traits, confirm critical predictions of causal theories linking cognitive and semantic deficits in ASC, in part, to dysfunctional action-perception circuits and resultant reduction of motor system activation.
C1 [Moseley, Rachel L.; Hauk, Olaf; Pulvermueller, Friedemann] MRC, Cognit & Brain Sci Unit, Cambridge CB2 7EF, England.
[Mohr, Bettina] Charite, Dept Psychiat, D-13353 Berlin, Germany.
[Lombardo, Michael V.; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
[Pulvermueller, Friedemann] Free Univ Berlin, Dept Philosophy & Humanities, Brain Language Lab, Berlin, Germany.
RP Moseley, RL (reprint author), MRC, Cognit & Brain Sci Unit, 15 Chaucer Rd, Cambridge CB2 7EF, England.
EM rachel.moseley@cantab.net
FU Medical Research Council [MC_US_A060_0034, U1055.04.003.00001.01]; Freie
Universitat Berlin; Deutsche Forschungsgemeinschaft (Excellence Cluster
Languages of Emotion); Engineering and Physical Sciences Research
Council (UK) (BABEL grant)
FX The authors would like to thank the following: Clare Cook, Yury Shtyrov,
and Francesca Carota for help and input at various stages of theoretical
discussion and imaging analysis; Amanda Ludlow for early help with ASC
participant recruitment; and staff at the ARC, particularly Bonnie
Aeyeung and Carrie Allison, who assisted with participant recruitment.
This work was supported by the Medical Research Council
(MC_US_A060_0034, U1055.04.003.00001.01 to Friedemann Pulvermuller), the
Freie Universitat Berlin (startup grant to Friedemann Pulvermuller), the
Deutsche Forschungsgemeinschaft (Excellence Cluster Languages of
Emotion), and the Engineering and Physical Sciences Research Council
(UK) (BABEL grant).
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NR 70
TC 4
Z9 4
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 8
PY 2013
VL 7
AR 725
DI 10.3389/fnhum.2013.00725
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 248EF
UT WOS:000326675800001
PM 24265609
ER
PT J
AU Schaer, M
Ottet, MC
Scariati, E
Dukes, D
Franchini, M
Eliez, S
Glaser, B
AF Schaer, Marie
Ottet, Marie-Christine
Scariati, Elisa
Dukes, Daniel
Franchini, Martina
Eliez, Stephan
Glaser, Bronwyn
TI Decreased frontal gyrification correlates with altered connectivity in
children with autism
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE cortical folding; cerebral morphometry; tractography; neuroimaging;
autism spectrum disorder
ID HUMAN CEREBRAL-CORTEX; LIKELIHOOD ESTIMATION METAANALYSIS; 22Q11.2
DELETION SYNDROME; SUBJECT DIFFUSION DATA; SURFACE-BASED ANALYSIS;
MIRROR-NEURON SYSTEM; SPECTRUM DISORDER; CORTICAL THICKNESS;
CORPUS-CALLOSUM; FUNCTIONAL CONNECTIVITY
AB The structural correlates of functional dysconnectivity in autism spectrum disorders (ASD) have been seldom explored, despite the fact that altered functional connectivity is one of the most frequent neuropathological observations in the disorder. We analyzed cerebral morphometry and structural connectivity using multi-modal imaging for 11 children/adolescents with ASD and 11 matched controls. We estimated regional cortical and white matter volumes, as well as vertex-wise measures of cortical thickness and local Gyrification Index (lGI). Diffusion Tensor Images (DTI) were used to measure Fractional Anisotropy (FA) and tractography estimates of short- and long-range connectivity. We observed four clusters of lGI reduction in patients with ASD, three were located in the right inferior frontal region extending to the inferior parietal lobe, and one was in the right medial parieto-occipital region. Reduced volume was found in the anterior corpus callosum, along with fewer inter-hemispheric frontal streamlines. Despite the spatial correspondence of decreased gyrification and reduced long connectivity, we did not observe any significant relationship between the two. However, a positive correlation between lGI and local connectivity was present in all four clusters in patients with ASD. Reduced gyrification in the inferior fronto-parietal and posterior medial cortical regions lends support for early-disrupted cortical growth in both the mirror neuron system and midline structures responsible for social cognition. Early impaired neurodevelopment in these regions may represent an initial substrate for altered maturation in the cerebral networks that support complex social skills. We also demonstrate that gyrification changes are related to connectivity. This supports the idea that an imbalance between short- and long-range white matter tracts not only impairs the integration of information from multiple neural systems, but also alters the shape of the brain early on in autism.
C1 [Schaer, Marie] Stanford Univ, Sch Med, Stanford Cognit & Syst Neurosci Lab, Palo Alto, CA 94304 USA.
[Schaer, Marie; Ottet, Marie-Christine; Scariati, Elisa; Franchini, Martina; Eliez, Stephan; Glaser, Bronwyn] Univ Geneva, Sch Med, Dept Psychiat, Off Medicopedagog, CH-1211 Geneva, Switzerland.
[Dukes, Daniel] Univ Neuchatel, Ctr Cognit Sci, CH-2000 Neuchatel, Switzerland.
[Dukes, Daniel] Univ Geneva, Swiss Ctr Affect Sci, Geneva, Switzerland.
[Eliez, Stephan] Univ Geneva, Sch Med, Dept Genet Med & Dev, CH-1211 Geneva, Switzerland.
RP Schaer, M (reprint author), Stanford Univ, Sch Med, Stanford Cognit & Syst Neurosci Lab, 1070 Arastradero Rd,Suite 220, Palo Alto, CA 94304 USA.
EM marie.schaer@unige.ch
FU Eagle Foundation; FHMS ("Fondation Handicap Mentaland Societe");
Fondation Dora; Fondation 1796; Center of Biomedical Imaging; National
Center of Competence in Research (NCCR)" SYNAPSY-The Synaptic Bases of
Mental Diseases"; Swiss National Science Foundation; Swiss National
Foundation of Science [145760]
FX We would like to thank the children, adolescents and families who
participated in this study. The families were recruited as a part of a
remediation study supported by the Eagle Foundation, the FHMS
("Fondation Handicap Mentaland Societe"), the Fondation Dora and the
Fondation 1796. Further support for MRI acquisition was provided by the
Center of Biomedical Imaging. 5 MS was supported by a grant from the
National Center of Competence in Research (NCCR)" SYNAPSY-The Synaptic
Bases of Mental Diseases" financed by the Swiss National Science
Foundation, and then by a fellowship from the Swiss National Foundation
of Science (#145760). The authors would like to extend a special thank
you to Hilary Woodde Wilde and Sonia Martinez for their help with
patients' assessment.
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NR 88
TC 8
Z9 8
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 8
PY 2013
VL 7
DI 10.3389/fnhum.2013.00750
PG 13
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 248EL
UT WOS:000326676400001
PM 24265612
ER
PT J
AU Dodell-Feder, D
Lincoln, SH
Coulson, JP
Hooker, CI
AF Dodell-Feder, David
Lincoln, Sarah Hope
Coulson, Joseph P.
Hooker, Christine I.
TI Using Fiction to Assess Mental State Understanding: A New Task for
Assessing Theory of Mind in Adults
SO PLOS ONE
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; VENTROMEDIAL PREFRONTAL CORTEX; COGNITIVE
ENHANCEMENT THERAPY; 1ST EPISODE PSYCHOSIS; SOCIAL-COGNITION;
ASPERGER-SYNDROME; MORAL JUDGMENT; FALSE-BELIEF; INDIVIDUAL-DIFFERENCES;
1ST-EPISODE PSYCHOSIS
AB Social functioning depends on the ability to attribute and reason about the mental states of others - an ability known as theory of mind (ToM). Research in this field is limited by the use of tasks in which ceiling effects are ubiquitous, rendering them insensitive to individual differences in ToM ability and instances of subtle ToM impairment. Here, we present data from a new ToM task - the Short Story Task (SST) - intended to improve upon many aspects of existing ToM measures. More specifically, the SST was designed to: (a) assess the full range of individual differences in ToM ability without suffering from ceiling effects; (b) incorporate a range of mental states of differing complexity, including epistemic states, affective states, and intentions to be inferred from a first-and second-order level; (c) use ToM stimuli representative of real-world social interactions; (d) require participants to utilize social context when making mental state inferences; (e) exhibit adequate psychometric properties; and (f) be quick and easy to administer and score. In the task, participants read a short story and were asked questions that assessed explicit mental state reasoning, spontaneous mental state inference, and comprehension of the non-mental aspects of the story. Responses were scored according to a rubric that assigned greater points for accurate mental state attributions that included multiple characters' mental states. Results demonstrate that the SST is sensitive to variation in ToM ability, can be accurately scored by multiple raters, and exhibits concurrent validity with other social cognitive tasks. The results support the effectiveness of this new measure of ToM in the study of social cognition. The findings are also consistent with studies demonstrating significant relationships among narrative transportation, ToM, and the reading of fiction. Together, the data indicate that reading fiction may be an avenue for improving ToM ability.
C1 [Dodell-Feder, David; Lincoln, Sarah Hope; Hooker, Christine I.] Harvard Univ, Dept Psychol, Cambridge, MA 02138 USA.
RP Dodell-Feder, D (reprint author), Harvard Univ, Dept Psychol, 33 Kirkland St, Cambridge, MA 02138 USA.
EM feder@fas.harvard.edu
FU Harvard University
FX This work was supported by Harvard University research funds to
Christine I. Hooker and David Dodell-Feder. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 134
TC 3
Z9 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 7
PY 2013
VL 8
IS 11
DI 10.1371/journal.pone.0081279
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 254KD
UT WOS:000327162900087
PM 24244736
ER
PT J
AU Steinberg, J
Webber, C
AF Steinberg, Julia
Webber, Caleb
TI The Roles of FMRP-Regulated Genes in Autism Spectrum Disorder: Single-
and Multiple-Hit Genetic Etiologies
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID FRAGILE-X-SYNDROME; DE-NOVO MUTATIONS; COPY-NUMBER VARIATION; RARE;
PROTEIN; MOUSE; ASSOCIATION; VARIANTS; NETWORK; BIOLOGY
AB Autism spectrum disorder (ASD) is a highly heritable complex neurodevelopmental condition characterized by impairments in social interaction and communication and restricted and repetitive behaviors. Although roles for both de novo and familial genetic variation have been documented, the underlying disease mechanisms remain poorly elucidated. In this study, we defined and explored distinct etiologies of genetic variants that affect genes regulated by Fragile-X mental retardation protein (FMRP), thought to play a key role in neuroplasticity and neuronal translation, in ASD-affected individuals. In particular, we developed the Trend test, a pathway-association test that is able to robustly detect multiple-hit etiologies and is more powerful than existing approaches. Exploiting detailed spatiotemporal maps of gene expression within the human brain, we identified four discrete FMRP-target subpopulations that exhibit distinct functional biases and contribute to ASD via different types of genetic variation. We also demonstrated that FMRP target genes are more likely than other genes with similar expression patterns to contribute to disease. We developed the hypothesis that FMRP targets contribute to ASD via two distinct etiologies: (1) ultra-rare and highly penetrant single disruptions of embryonically upregulated FMRP targets ("single-hit etiology") or (2) the combination of multiple less penetrant disruptions of nonembryonic, synaptic FMRP targets ("multiple-hit etiology"). The Trend test provides rigorous support for a multiple-hit genetic etiology in a subset of autism cases and is easily extendible to combining information from multiple types of genetic variation (i.e., copy-number and exome variants), increasing its value to next-generation sequencing approaches.
C1 [Steinberg, Julia; Webber, Caleb] Univ Oxford, MRC, Dept Physiol Anat & Genet, Funct Genom Unit, Oxford OX1 3QX, England.
[Steinberg, Julia] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.
RP Webber, C (reprint author), Univ Oxford, MRC, Dept Physiol Anat & Genet, Funct Genom Unit, Oxford OX1 3QX, England.
EM caleb.webber@dpag.ox.ac.uk
FU Wellcome Trust [093941/Z/10/Z, 090532/Z/09/Z]; Medical Research Council;
European Union [241995]; National Institute of Mental Health
[1U24MH081810]
FX We thank the anonymous reviewers for their comments and suggestions.
This work was supported by the Wellcome Trust (grants 093941/Z/10/Z to
J.S. and 090532/Z/09/Z to the Wellcome Trust Centre for Human Genetics),
Medical Research Council (funding to C.W), and the European Union's
Seventh Framework Programme project GENCODYS (grant 241995 to C.W.). We
gratefully acknowledge the resources provided by the Autism Genetic
Resource Exchange (AGRE) Consortium and the participating AGRE families.
The AGRE is a program of Autism Speaks and is supported, in part, by
grant 1U24MH081810 from the National Institute of Mental Health to Clara
M. Lajonchere (principal investigator). The funders had no role in the
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 56
TC 7
Z9 7
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD NOV 7
PY 2013
VL 93
IS 5
BP 825
EP 839
DI 10.1016/j.ajhg.2013.09.013
PG 15
WC Genetics & Heredity
SC Genetics & Heredity
GA 252HU
UT WOS:000326996600004
PM 24207117
ER
PT J
AU Suls, A
Jaehn, JA
Kecskes, A
Weber, Y
Weckhuysen, S
Craiu, DC
Siekierska, A
Djemie, T
Afrikanova, T
Gormley, P
von Spiczak, S
Kluger, G
Iliescu, CM
Talvik, T
Talvik, I
Meral, C
Caglayan, HS
Giraldez, BG
Serratosa, J
Lemke, JR
Hoffman-Zacharska, D
Szczepanik, E
Barisic, N
Komarek, V
Hjalgrim, H
Moller, RS
Linnankivi, T
Dimova, P
Striano, P
Zara, F
Marini, C
Guerrini, R
Depienne, C
Baulac, S
Kuhlenbaumer, G
Crawford, AD
Lehesjoki, AE
de Witte, PAM
Palotie, A
Lerche, H
Esguerra, CV
De Jonghe, P
Helbig, I
AF Suls, Arvid
Jaehn, Johanna A.
Kecskes, Angela
Weber, Yvonne
Weckhuysen, Sarah
Craiu, Dana C.
Siekierska, Aleksandra
Djemie, Tania
Afrikanova, Tatiana
Gormley, Padhraig
von Spiczak, Sarah
Kluger, Gerhard
Iliescu, Catrinel M.
Talvik, Tiina
Talvik, Inga
Meral, Cihan
Caglayan, Hande S.
Giraldez, Beatriz G.
Serratosa, Jose
Lemke, Johannes R.
Hoffman-Zacharska, Dorota
Szczepanik, Elzbieta
Barisic, Nina
Komarek, Vladimir
Hjalgrim, Helle
Moller, Rikke S.
Linnankivi, Tarja
Dimova, Petia
Striano, Pasquale
Zara, Federico
Marini, Carla
Guerrini, Renzo
Depienne, Christel
Baulac, Stephanie
Kuhlenbaeumer, Gregor
Crawford, Alexander D.
Lehesjoki, Anna-Elina
de Witte, Peter A. M.
Palotie, Aarno
Lerche, Holger
Esguerra, Camila V.
De Jonghe, Peter
Helbig, Ingo
CA EuroEPINOMICS RES Consortium
TI De Novo Loss-of-Function Mutations in CHD2 Cause a Fever-Sensitive
Myoclonic Epileptic Encephalopathy Sharing Features with Dravet Syndrome
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; DNA-BINDING PROTEIN-2; GENE; PHENOTYPE;
DELETION; DISEASE; MEMBER; RATES; SCN1A
AB Dravet syndrome is a severe epilepsy syndrome characterized by infantile onset of therapy-resistant, fever-sensitive seizures followed by cognitive decline. Mutations in SCN1A explain about 75% of cases with Dravet syndrome; 90% of these mutations arise de novo. We studied a cohort of nine Dravet-syndrome-affected individuals without an SCN1A mutation (these included some atypical cases with onset at up to 2 years of age) by using whole-exome sequencing in proband-parent trios. In two individuals, we identified a de novo loss-of-function mutation in CHD2 (encoding chromodomain helicase DNA binding protein 2). A third CHD2 mutation was identified in an epileptic proband of a second (stage 2) cohort. All three individuals with a CHD2 mutation had intellectual disability and fever-sensitive generalized seizures, as well as prominent myoclonic seizures starting in the second year of life or later. To explore the functional relevance of CHD2 haploinsufficiency in an in vivo model system, we knocked down chd2 in zebrafish by using targeted morpholino antisense oligomers. chd2-knockdown larvae exhibited altered locomotor activity, and the epileptic nature of this seizure-like behavior was confirmed by field-potential recordings that revealed epileptiform discharges similar to seizures in affected persons. Both altered locomotor activity and epileptiform discharges were absent in appropriate control larvae. Our study provides evidence that de novo loss-of-function mutations in CHD2 are a cause of epileptic encephalopathy with generalized seizures.
C1 [Suls, Arvid; Weckhuysen, Sarah; Djemie, Tania; De Jonghe, Peter] VIB, Dept Mol Genet, Neurogenet Grp, B-2610 Antwerp, Belgium.
[Suls, Arvid; Weckhuysen, Sarah; Djemie, Tania; De Jonghe, Peter] Univ Antwerp, Inst Born Bunge, Neurogenet Lab, B-2610 Antwerp, Belgium.
[Jaehn, Johanna A.; von Spiczak, Sarah; Helbig, Ingo] Univ Kiel, Univ Med Ctr Schleswig Holstein, D-24105 Kiel, Germany.
[Kecskes, Angela; Siekierska, Aleksandra; Afrikanova, Tatiana; Crawford, Alexander D.; de Witte, Peter A. M.; Esguerra, Camila V.] Univ Louvain, Dept Pharmaceut & Pharmacol Sci, Lab Mol Biodiscovery, B-3000 Louvain, Belgium.
[Weber, Yvonne; Lerche, Holger] Univ Tubingen, Hertie Inst Clin Brain Res, Dept Neurol & Epileptol, D-72076 Tubingen, Germany.
[Craiu, Dana C.; Iliescu, Catrinel M.] Carol Davila Univ Med, Dept Neurol, Pediat Neurol Clin 2, Bucharest 050474, Romania.
[Craiu, Dana C.; Iliescu, Catrinel M.] Carol Davila Univ Med, Dept Pediat Neurol, Bucharest 050474, Romania.
[Craiu, Dana C.; Iliescu, Catrinel M.] Carol Davila Univ Med, Dept Psychiat, Bucharest 050474, Romania.
[Craiu, Dana C.; Iliescu, Catrinel M.] Carol Davila Univ Med, Dept Neurosurg, Bucharest 050474, Romania.
[Craiu, Dana C.; Iliescu, Catrinel M.] Prof Doctor Alexandru Obregia Clin Hosp, Pediat Neurol Clin, Bucharest 041914, Romania.
[Gormley, Padhraig; Palotie, Aarno] Wellcome Trust Sanger Inst, Hinxton CB10 1SA, Cambs, England.
[Kluger, Gerhard] Schon Klin Vogtareuth, Tagesklin Neuropadiatrie, Epilepsiezentrum Kinder & Jugendliche, D-83569 Vogtareuth, Germany.
[Talvik, Tiina; Talvik, Inga] Univ Tartu, Dept Pediat, EE-51014 Tartu, Estonia.
[Talvik, Tiina; Talvik, Inga] Tartu Univ Hosp, Dept Neurol & Neurorehabil, Childrens Clin, EE-50406 Tartu, Estonia.
[Meral, Cihan] GATA Haydarpasa Teaching Hosp, Dept Pediat Neurol, TR-34668 Istanbul, Turkey.
[Caglayan, Hande S.] Bogazici Univ, Dept Mol Biol & Genet, TR-34342 Istanbul, Turkey.
[Giraldez, Beatriz G.; Serratosa, Jose] Hosp Univ Fdn Jimenez Diaz, Epilepsy Unit, Madrid 28040, Spain.
[Giraldez, Beatriz G.; Serratosa, Jose] Ctr Invest Biomed Red Enfermedades Raras, Madrid 28040, Spain.
[Lemke, Johannes R.] Univ Childrens Hosp, Inselspital, Div Human Genet, CH-3010 Bern, Switzerland.
[Hoffman-Zacharska, Dorota] Inst Mother & Child Hlth, Dept Med Genet, PL-01211 Warsaw, Poland.
[Szczepanik, Elzbieta] Inst Mother & Child Hlth, Clin Neurol Child & Adolescents, PL-01211 Warsaw, Poland.
[Barisic, Nina] Univ Zagreb, Sch Med, Univ Hosp Ctr Zagreb, Dept Paediat, Zagreb 10000, Croatia.
[Komarek, Vladimir] Univ Hosp Motol, Child Neurol Dept, Prague 15006, Czech Republic.
[Hjalgrim, Helle; Moller, Rikke S.] Danish Epilepsy Ctr, DK-4293 Dianalund, Denmark.
[Hjalgrim, Helle] Univ Southern Denmark, Inst Reg Hlth Res, DK-5230 Odense, Denmark.
[Linnankivi, Tarja] Univ Helsinki, Childrens Hosp, Helsinki 00029, Finland.
[Linnankivi, Tarja] Univ Helsinki, Cent Hosp, Helsinki 00029, Finland.
[Dimova, Petia] St Naum Univ Hosp Neurol & Psychiat, Clin Child Neurol, Sofia 1113, Bulgaria.
[Striano, Pasquale] Univ Genoa, Dept Neurosci, Pediat Neurol & Muscular Dis Unit, I-16147 Genoa, Italy.
[Striano, Pasquale] Univ Genoa, Dept Rehabil, I-16147 Genoa, Italy.
[Striano, Pasquale] Univ Genoa, Dept Ophthalmol, I-16147 Genoa, Italy.
[Striano, Pasquale] Univ Genoa, Dept Genet, I-16147 Genoa, Italy.
[Striano, Pasquale] Univ Genoa, Dept Maternal & Child Hlth, I-16147 Genoa, Italy.
[Striano, Pasquale] Gaslini Inst, I-16147 Genoa, Italy.
[Zara, Federico] Gaslini Inst, Dept Neurosci, Neurogenet Lab, Pediat Neurol & Muscular Dis Unit, I-16147 Genoa, Italy.
[Marini, Carla; Guerrini, Renzo] Univ Florence, Meyer Childrens Hosp, Pediat Neurol Unit, I-50132 Florence, Italy.
[Marini, Carla; Guerrini, Renzo] Univ Florence, Meyer Childrens Hosp, Pediat Neurol Labs, I-50132 Florence, Italy.
[Depienne, Christel; Baulac, Stephanie] Hop La Pitie Salpetriere, Ctr Rech, INSERM, Inst Cerveau & Moelle Epiniere,U975, F-75013 Paris, France.
[Depienne, Christel; Baulac, Stephanie] Hop La Pitie Salpetriere, Ctr Rech, CNRS 7225, Inst Cerveau & Moelle Epiniere, F-75013 Paris, France.
[Baulac, Stephanie] Univ Paris 06, UMR S 975, F-75013 Paris, France.
[Depienne, Christel] Hop La Pitie Salpetriere, AP HP, Dept Genet & Cytogenet, Unite Fonct Neurogenet Mol & Cellulaire, F-75013 Paris, France.
[Kuhlenbaeumer, Gregor] Univ Kiel, Inst Expt Med, Dept Neurol, D-24105 Kiel, Germany.
[Crawford, Alexander D.] Univ Luxembourg, Luxembourg Ctr Syst Biomed, L-4362 Esch Sur Alzette, Luxembourg.
[Lehesjoki, Anna-Elina] Folkhalsan Inst Genet, Helsinki 00290, Finland.
[Lehesjoki, Anna-Elina] Univ Helsinki, Res Programs Unit, FIN-00290 Helsinki, Finland.
[Lehesjoki, Anna-Elina] Univ Helsinki, Ctr Neurosci, FIN-00290 Helsinki, Finland.
[Palotie, Aarno] Univ Helsinki, Inst Mol Med Finland, FIN-00290 Helsinki, Finland.
[Palotie, Aarno] Broad Inst MIT & Harvard, Program Med & Populat Genet & Genet Anal Platform, Cambridge, MA 02142 USA.
RP De Jonghe, P (reprint author), VIB, Dept Mol Genet, Neurogenet Grp, B-2610 Antwerp, Belgium.
EM peter.dejonghe@molgen.vib-ua.be
RI Esguerra, Camila/D-7657-2014
OI Esguerra, Camila/0000-0001-7891-1427
FU European Science Foundation; state budget of Romania; Scientific and
Technological Research Council of Turkey; National Science Centre Poland
[800/N-ESF-EuroEPINOMICS/10/2011/0]; MH CZ-DRO, University Hospital
Motol, Prague [00064203]; "Investissements d'avenir" [ANR-10-IAIHU-06];
Academy of Finland [141549, 251704]; Folkhalsan Research Foundation;
Wellcome Trust [WT089062, 098051]; Academy of Finland Center of
Excellence in Complex Disease Genetics grants [213506, 129680]; European
Community [HEALTH-F4-2007-201413]; Synaptic Systems grant [242167];
Sigrid Juselius Foundation; European Commission [261123]; Federal
Ministry of Education and Research [NGENplus/EMINet 01GS08123,
IonNeurONet 01GM1105A]; German Research Foundation (DFG) [Le1030/11-1];
German Society for Epileptology; Fund for Scientific Research Flanders
(FWO); Flemish government Methusalem excellence grant; University of
Antwerp
FX We thank the probands and their families for their cooperation. The
research was supported by the EUROCORES program EuroEPINOMICS of the
European Science Foundation; funds from the state budget of Romania,
managed by the Executive Agency for Higher Education, Research,
Development, and Innovation Funding for Project 6-EUROC; the Scientific
and Technological Research Council of Turkey; National Science Centre
Poland funding for project 800/N-ESF-EuroEPINOMICS/10/2011/0; MH CZ-DRO,
University Hospital Motol, Prague (00064203); "Investissements d'avenir"
ANR-10-IAIHU-06; the Academy of Finland (grant 141549) and Folkhalsan
Research Foundation; Wellcome Trust grants WT089062 and 098051; Academy
of Finland grant 251704; Academy of Finland Center of Excellence in
Complex Disease Genetics grants 213506 and 129680; the European
Community's Seventh Framework Programme (FP7/2007-2013) ENGAGE
Consortium (grant HEALTH-F4-2007-201413); Synaptic Systems grant 242167;
the Sigrid Juselius Foundation; European Commission FP7 project 261123
(gEUVADIS); Federal Ministry of Education and Research NGENplus/EMINet
01GS08123; IonNeurONet 01GM1105A; German Research Foundation (DFG)
Le1030/11-1; the German Society for Epileptology; the Fund for
Scientific Research Flanders (FWO); the Flemish government Methusalem
excellence grant; and the University of Antwerp. We thank the VIB
Genetic Service Facility and the institute of Clinical Molecular Biology
in Kiel for providing Sanger sequencing, supported in part by DFG
Cluster of Excellence "Inflammation at Interfaces" and "Future Ocean."
We thank technicians S. Greve, S. Arndt, and T. Henke for technical
support. G.K. is a member of the DFG-funded Cluster of Excellence
"Inflammation at Interfaces." A.S. is a FWO postdoctoral fellow. T.D.
and A.K. are Institute of Science and Technology PhD fellows.
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NR 34
TC 26
Z9 26
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD NOV 7
PY 2013
VL 93
IS 5
BP 967
EP 975
DI 10.1016/j.ajhg.2013.09.017
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 252HU
UT WOS:000326996600017
PM 24207121
ER
PT J
AU Voineagu, I
Eapen, V
AF Voineagu, Irina
Eapen, Valsamma
TI Converging pathways in autism spectrum disorders: interplay between
synaptic dysfunction and immune responses
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Review
DE autism spectrum disorders; immune response; synapses; genomics; gene
expression
ID DE-NOVO MUTATIONS; GENE-EXPRESSION; RETT-SYNDROME; MICROGLIAL
ACTIVATION; BRAIN; PATHOLOGY; CHILDREN; CELLS; NEUROBIOLOGY; ALPHA
AB Autism spectrum disorders (ASD) are highly heritable, yet genetically heterogeneous neurodevelopmental conditions. Recent genome-wide association and gene expression studies have provided evidence supporting the notion that the large number of genetic variants associated with ASD converge toward a core set of dysregulated biological processes. Here we review recent data demonstrating the involvement of synaptic dysfunction and abnormal immune responses in ASD, and discuss the functional interplay between the two phenomena.
C1 [Voineagu, Irina] Univ New S Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW 2052, Australia.
[Eapen, Valsamma] Univ New S Wales, Dept Infant Child & Adolescent Psychiat, Acad Unit Child Psychiat, Sydney, NSW 2052, Australia.
RP Voineagu, I (reprint author), Univ New S Wales, Sch Biotechnol & Biomol Sci, Biol Sci Bldg,Room 217B, Sydney, NSW 2052, Australia.
EM i.voineagu@unsw.edu.au
FU Ramaciotti Establishment Grant; NARSAD
FX This work was supported by a Ramaciotti Establishment Grant and a NARSAD
Young Investigator Award (IV).
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NR 44
TC 4
Z9 4
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 7
PY 2013
VL 7
AR 738
DI 10.3389/fnhum.2013.00738
PG 5
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 247OQ
UT WOS:000326628400001
PM 24223544
ER
PT J
AU Han, K
Holder, JL
Schaaf, CP
Lu, H
Chen, HM
Kang, H
Tang, JR
Wu, ZY
Hao, S
Cheung, SW
Yu, P
Sun, H
Breman, AM
Patel, A
Lu, HC
Zoghbi, HY
AF Han, Kihoon
Holder, J. Lloyd, Jr.
Schaaf, Christian P.
Lu, Hui
Chen, Hongmei
Kang, Hyojin
Tang, Jianrong
Wu, Zhenyu
Hao, Shuang
Cheung, Sau Wai
Yu, Peng
Sun, Hao
Breman, Amy M.
Patel, Ankita
Lu, Hui-Chen
Zoghbi, Huda Y.
TI SHANK3 overexpression causes manic-like behaviour with unique
pharmacogenetic properties
SO NATURE
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; SCAFFOLDING PROTEIN SHANK3; 22Q13.3 DELETION
SYNDROME; BIPOLAR DISORDER; PSYCHIATRIC-DISORDERS; POSTSYNAPTIC DENSITY;
GENE; MUTATIONS; DYSFUNCTION; PROFILIN
AB Mutations in SHANK3 and large duplications of the region spanning SHANK3 both cause a spectrum of neuropsychiatric disorders, indicating that proper SHANK3 dosage is critical for normal brain function. However, SHANK3 overexpression per se has not been established as a cause of human disorders because 22q13 duplications involve several genes. Here we report that Shank3 transgenic mice modelling a human SHANK3 duplication exhibit manic-like behaviour and seizures consistent with synaptic excitatory/inhibitory imbalance. We also identified two patients with hyperkinetic disorders carrying the smallest SHANK3-spanning duplications reported so far. These findings indicate that SHANK3 overexpression causes a hyperkinetic neuropsychiatric disorder. To probe the mechanism underlying the phenotype, we generated a Shank3 in vivo interactome and found that Shank3 directly interacts with the Arp2/3 complex to increase F-actin levels in Shank3 transgenic mice. The mood-stabilizing drug valproate, but not lithium, rescues the manic-like behaviour of Shank3 transgenic mice raising the possibility that this hyperkinetic disorder has a unique pharmacogenetic profile.
C1 [Han, Kihoon; Schaaf, Christian P.; Lu, Hui; Kang, Hyojin; Cheung, Sau Wai; Yu, Peng; Breman, Amy M.; Patel, Ankita; Zoghbi, Huda Y.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Han, Kihoon; Lu, Hui; Zoghbi, Huda Y.] Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA.
[Han, Kihoon; Holder, J. Lloyd, Jr.; Schaaf, Christian P.; Lu, Hui; Chen, Hongmei; Kang, Hyojin; Tang, Jianrong; Wu, Zhenyu; Hao, Shuang; Yu, Peng; Sun, Hao; Lu, Hui-Chen; Zoghbi, Huda Y.] Texas Childrens Hosp, Jan & Dan Duncan Neurol Res Inst, Houston, TX 77030 USA.
[Holder, J. Lloyd, Jr.; Chen, Hongmei; Tang, Jianrong; Wu, Zhenyu; Hao, Shuang; Sun, Hao; Lu, Hui-Chen; Zoghbi, Huda Y.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
[Holder, J. Lloyd, Jr.] Baylor Coll Med, Div Neurol & Dev Neurosci, Houston, TX 77030 USA.
[Chen, Hongmei; Sun, Hao; Lu, Hui-Chen] Texas Childrens Hosp, Cain Fdn Labs, Houston, TX 77030 USA.
[Cheung, Sau Wai; Breman, Amy M.; Patel, Ankita] Baylor Coll Med, Med Genet Labs, Houston, TX 77030 USA.
[Lu, Hui-Chen; Zoghbi, Huda Y.] Baylor Coll Med, Program Dev Biol, Houston, TX 77030 USA.
[Lu, Hui-Chen; Zoghbi, Huda Y.] Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA.
RP Zoghbi, HY (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
EM hzoghbi@bcm.edu
FU Howard Hughes Medical Institute; National Institutes of Health (NIH)
ARRA grant [1R01NS070302]; Baylor Intellectual and Developmental
Disabilities Research Center [P30HD024064]; Cancer Prevention and
Research Institute of Texas (CPRIT) [RP110784]; Thrasher Research Fund;
NIH [2T32NS043124]; Ting Tsung and Wei Fong Chao Foundation; Joan and
Stanford Alexander family; Doris Duke Clinical Scientist Development
Award
FX We are indebted to the patients and families who participated in this
study; to J. W. Belmont and N. Miller for contributing patients to this
study; G. Feng for sharing Shank3B mice; G. Schuster for injection of
Shank3 BAC; and C. Spencer for behavioural assays training. This project
was supported by The Howard Hughes Medical Institute (H.Y.Z.), National
Institutes of Health (NIH) ARRA grant (1R01NS070302) (H.Y.Z.), the
Baylor Intellectual and Developmental Disabilities Research Center
(P30HD024064) confocal, electrophysiology and mouse neurobehavioral
cores, and the Cancer Prevention and Research Institute of Texas (CPRIT)
RP110784. J. L. H. was supported by an Early Career Award from the
Thrasher Research Fund, NIH 2T32NS043124 and the Ting Tsung and Wei Fong
Chao Foundation; C. P. S. was supported by the Joan and Stanford
Alexander family, the Ting Tsung and Wei Fong Chao Foundation and the
Doris Duke Clinical Scientist Development Award.
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NR 55
TC 24
Z9 30
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
EI 1476-4687
J9 NATURE
JI Nature
PD NOV 7
PY 2013
VL 503
IS 7474
BP 72
EP +
DI 10.1038/nature12630
PG 19
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 247AS
UT WOS:000326585600034
PM 24153177
ER
PT J
AU Kratovac, S
Corbin, JG
AF Kratovac, Sebila
Corbin, Joshua G.
TI Developmental changes in expression of inhibitory neuronal proteins in
the Fragile X Syndrome mouse basolateral amygdala
SO BRAIN RESEARCH
LA English
DT Article
DE Fragile X Syndrome; Basolateral amygdala; Development; GABA(A) receptor;
Inhibitory synapse; Autism
ID MENTAL-RETARDATION PROTEIN; FMR1 KNOCKOUT MOUSE; GABA(A) RECEPTOR
SUBTYPES; MESSENGER-RNA; GABAERGIC SYNAPSES; DENDRITIC SPINES; YOUNG
MALES; FEAR MEMORY; OUT MICE; IN-VIVO
AB In humans, Fragile X Syndrome (FXS) is characterized by enhanced fear, hyperactivity, social anxiety, and, in a subset of individuals, autism. Many of the emotional and social deficits point to defects in the amygdala. We have previously shown defects in inhibitory neuron drive onto excitatory projection neurons in the basolateral amygdala (BLA) of juvenile Fmr1(-/y) knockout (KO) mice. Using pharmacological approaches, we have also previously revealed dynamic functional deficits in alpha 1, alpha 2, and alpha 3 subunit-containing GABA(A) receptors (GABA(A)Rs alpha 1, alpha 2, and alpha 3) during early postnatal development. In this study, we sought to determine whether these defects in GABA(A)R function are accompanied by changes in protein expression of GABA(A)Rs alpha 1, alpha 2, and alpha 3 and the post-synaptic GABA(A)R-clustering protein gephyrin. Interestingly, we found that while the expression of these proteins did not significantly differ between wildtype (WT) and KO mice at each time point, the timing of developmental expression of GABA(A)R alpha 1, alpha 2, and gephyrin was altered. Collectively, these data reveal novel defects in inhibitory synapse protein expression during critical periods of early postnatal development that could contribute to observed inhibitory neurotransmission deficits in the KO mouse BLA. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Kratovac, Sebila; Corbin, Joshua G.] Childrens Natl Med Ctr, Ctr Neurosci Res, Washington, DC 20010 USA.
[Kratovac, Sebila] Univ Maryland, Dept Biol, College Pk, MD 20742 USA.
RP Corbin, JG (reprint author), Childrens Natl Med Ctr, Ctr Neurosci Res, 111 Michigan Ave, Washington, DC 20010 USA.
EM jcorbin@cnmcresearch.org
FU FRAXA; Autism Speaks; NSF
FX This research was supported by FRAXA and Autism Speaks grants to J.G.C.,
and an NSF Graduate Research Fellowship to S.K. We also thank Luis
Olmos-Serrano for technical support.
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NR 84
TC 4
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
EI 1872-6240
J9 BRAIN RES
JI Brain Res.
PD NOV 6
PY 2013
VL 1537
BP 69
EP 78
DI 10.1016/j.brainres.2013.08.052
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 264XV
UT WOS:000327915200008
PM 24008143
ER
PT J
AU Roberts, TPL
Lanza, MR
Dell, J
Qasmieh, S
Hines, K
Blaskey, L
Zarnow, DM
Levy, SE
Edgar, JC
Berman, JI
AF Roberts, Timothy P. L.
Lanza, Matthew R.
Dell, John
Qasmieh, Saba
Hines, Katherine
Blaskey, Lisa
Zarnow, Deborah M.
Levy, Susan E.
Edgar, J. Christopher
Berman, Jeffrey I.
TI Maturational differences in thalamocortical white matter microstructure
and auditory evoked response latencies in autism spectrum disorders
SO BRAIN RESEARCH
LA English
DT Article
DE Magnetoencephalography; Autism spectrum disorder; Auditory evoked
response; Fractional anisotropy; White matter; M50
ID LANGUAGE IMPAIRMENT; DIFFUSION; CHILDREN; BRAIN; ADOLESCENCE;
ANISOTROPY; SYSTEM; FIELDS
AB White matter diffusion anisotropy in the acoustic radiations was characterized as a function of development in autistic and typically developing children. Auditory-evoked neuromagnetic fields were also recorded from the same individuals and the latency of the left and right middle latency superior temporal gyrus auditory similar to 50 ms response (M50)(1) was measured. Group differences in structural and functional auditory measures were examined, as were group differences in associations between white matter pathways, M50 latency, and age. Acoustic radiation white matter fractional anisotropy did not differ between groups. Individuals with autism displayed a significant M50 latency delay. Only in typically developing controls, white matter fractional anisotropy increased with age and increased white matter anisotropy was associated with earlier M50 responses. M50 latency, however, decreased with age in both groups. Present findings thus indicate that although there is loss of a relationship between white matter structure and auditory cortex function in autism spectrum disorders, and although there are delayed auditory responses in individuals with autism than compared with age-matched controls, M50 latency nevertheless decreases as a function of age in autism, parallel to the observation in typically developing controls (although with an overall latency delay). To understand auditory latency delays in autism and changes in auditory responses as a function of age in controls and autism, studies examining white matter as well as other factors that influence auditory latency, such as synaptic transmission, are of interest. (C) 2013 Published by Elsevier B.V.
C1 [Roberts, Timothy P. L.; Lanza, Matthew R.; Dell, John; Qasmieh, Saba; Hines, Katherine; Blaskey, Lisa; Zarnow, Deborah M.; Edgar, J. Christopher; Berman, Jeffrey I.] Childrens Hosp Philadelphia, Lurie Family Fdn, MEG Imaging Ctr, Dept Radiol, Philadelphia, PA 19104 USA.
[Blaskey, Lisa; Levy, Susan E.] Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA.
RP Roberts, TPL (reprint author), Childrens Hosp Philadelphia, Lurie Family Fdn, MEG Imaging Ctr, Dept Radiol, Wood Bldg,Suite 2115,34th St & Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM robertstim@email.chop.edu
FU NIH [R01DC008871, P30-HD026979, K01-MH 096091]; Nancy Lurie Marks Family
Foundation; Pennsylvania Department of Health
FX This study was supported in part by the NIH Grants R01DC008871 (T.R.),
P30-HD026979, K01-MH 096091 (J.B.) and a grant from the Nancy Lurie
Marks Family Foundation. This research has been funded, in part, by a
grant from the Pennsylvania Department of Health. The Pennsylvania
Department of Health specifically disclaims responsibility for any
analyses, interpretations, or conclusions. Dr. Roberts gratefully
acknowledges the Oberkircher Family for the Oberkircher Family Chair in
Pediatric Radiology at the Children's Hospital of Philadelphia.
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NR 22
TC 5
Z9 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
EI 1872-6240
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PY 2013
VL 1537
BP 79
EP 85
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PG 7
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SC Neurosciences & Neurology
GA 264XV
UT WOS:000327915200009
PM 24055954
ER
PT J
AU McClure, I
AF McClure, Iain
TI METHYLPHENIDATE FOR MODERATE ADHD Over-prescribing methylphenidate won't
be cured by autism-style assessments Reply
SO BMJ-BRITISH MEDICAL JOURNAL
LA English
DT Letter
C1 Royal Hosp Sick Children, Edinburgh EH9 1LF, Midlothian, Scotland.
RP McClure, I (reprint author), Royal Hosp Sick Children, Edinburgh EH9 1LF, Midlothian, Scotland.
EM iain.mcclure@ed.ac.uk
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NR 5
TC 0
Z9 0
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BMJ-BRIT MED J
JI BMJ-British Medical Journal
PD NOV 6
PY 2013
VL 347
AR f6621
DI 10.1136/bmj.f6621
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 250XO
UT WOS:000326890300009
PM 24196506
ER
PT J
AU Timimi, S
AF Timimi, Sami
TI METHYLPHENIDATE FOR MODERATE ADHD Over-prescribing methylphenidate won't
be cured by autism-style assessments
SO BMJ-BRITISH MEDICAL JOURNAL
LA English
DT Letter
ID DISORDER
C1 Lincolnshire Partnership NHS Fdn Trust, Sleaford NG34 8GG, England.
RP Timimi, S (reprint author), Lincolnshire Partnership NHS Fdn Trust, Sleaford NG34 8GG, England.
EM stimimi@talk21.com
CR Currie J, 19105 NBER
Government of Western Australia Department of Health, 2010, RAINE ADHD STUD LONG
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NR 6
TC 2
Z9 2
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BMJ-BRIT MED J
JI BMJ-British Medical Journal
PD NOV 6
PY 2013
VL 347
AR f6622
DI 10.1136/bmj.f6622
PG 1
WC Medicine, General & Internal
SC General & Internal Medicine
GA 250XO
UT WOS:000326890300010
PM 24196507
ER
PT J
AU Zuko, A
Kleijer, KTE
Oguro-Ando, A
Kas, MJH
van Daalen, E
van der Zwaag, B
Burbach, JPH
AF Zuko, Amila
Kleijer, Kristel T. E.
Oguro-Ando, Asami
Kas, Martien J. H.
van Daalen, Emma
van der Zwaag, Bert
Burbach, J. Peter H.
TI Contactins in the neurobiology of autism
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE Autism spectrum disorder; Contactins Neurobiology Behavior; Cell
adhesion molecules; Dendrites; Synapse
ID RECOGNITION MOLECULE NB-3; FRAGILE-X-SYNDROME; COPY NUMBER VARIATION;
CELL-ADHESION; NEURODEVELOPMENTAL DISORDERS; MYELINATED AXONS;
IMMUNOGLOBULIN SUPERFAMILY; CHROMOSOMAL LOCALIZATION; SPECTRUM
DISORDERS; NEURITE OUTGROWTH
AB Autism is a disease of brain plasticity. Inspiring work of Willem Hendrik Gispen on neuronal plasticity has stimulated us to investigate gene defects in autism and the consequences for brain development. The central process in the pathogenesis of autism is local dendritic mRNA translation which is dependent on axodendritic communication. Hence, most autism related gene products (i) are part of the protein synthesis machinery itself, (ii) are components of the mTOR signal transduction pathway, or (iii) shape synaptic activity and plasticity. Accordingly, prototype drugs have been recognized that interfere with these pathways. The contactin (CNTN) family of Ig cell adhesion molecules (IgCAMs) harbours at least three members that have genetically been implicated in autism: CNTN4, CNTN5, and CNTN6. In this chapter we review the genetic and neurobiological data underpinning their role in normal and abnormal development of brain systems, and the consequences for behavior. Although data on each of these CNTNs are far from complete, we tentatively conclude that these three contactins play roles in brain development in a critical phase of establishing brain systems and their plasticity. They modulate neuronal activities, such as neurite outgrowth, synaptogenesis, survival, guidance of projections and terminal branching of axons in forming neural circuits. Current research on these CNTNs concentrate on the neurobiological mechanism of their developmental functions. A future task will be to establish if proposed pharmacological strategies to counteract ASD-relaLed symptomes can also be applied to reversal of phenotypes caused by genetic defects in these CNTN genes. (C) 2013 Elsevier B.V. All tights reserved.
C1 [Zuko, Amila; Kleijer, Kristel T. E.; Oguro-Ando, Asami; Kas, Martien J. H.; Burbach, J. Peter H.] UMC Med Ctr Utrecht, Brain Ctr Rudolf Magnus, Dept Neurosci & Pharmacol, NL-3584 CG Utrecht, Netherlands.
[van Daalen, Emma] UMC Med Ctr Utrecht, Brain Ctr Rudolf Magnus, Dept Psychiat, NL-3584 CG Utrecht, Netherlands.
[van der Zwaag, Bert] Univ Med Ctr Utrecht, Dept Med Genet, NL-3584 CG Utrecht, Netherlands.
RP Burbach, JPH (reprint author), UMC Med Ctr Utrecht, Brain Ctr Rudolf Magnus, Str 4-205,POB 85060, NL-3508 AB Utrecht, Netherlands.
EM j.p.h.burbach@umcutrecht.nl
FU EU-AIMS (European Autism Interventions); Innovative Medicines Initiative
joint Undertaking [115300]; European Union from the European Federation
of Pharmaceutical Industries [P7/2007-2013]; Canon foundation research
fellowship in Europe; Dutch Brain Foundation [F2008(1)-08, 2011(1)-10]
FX Authors of this review were supported by EU-AIMS (European Autism
Interventions), which receives support from the Innovative Medicines
Initiative joint Undertaking under Grant agreement no. 115300, the
resources of which are composed of financial contributions from the
European Union's Seventh Framework Programme Grant (P7/2007-2013), from
the European Federation of Pharmaceutical Industries and Associations
Companies in-kind contributions, and from Autism Speaks, resulting in a
total of (sic)29.6 million (K.T.E.K., M.J.H.K., and J.P.H.B.), by a
Canon foundation research fellowship in Europe (A.O.A.), by a Fellowship
from the Dutch Brain Foundation no. F2008(1)-08 (B.V.D.Z.), and a
project Grant from the Dutch Brain Foundation no. 2011(1)-10 (E.V.D.).
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TC 11
Z9 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD NOV 5
PY 2013
VL 719
IS 1-3
BP 63
EP 74
DI 10.1016/j.ejphar.2013.07.016
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 258VQ
UT WOS:000327487200009
PM 23872404
ER
PT J
AU Verpelli, C
Montani, C
Vicidomini, C
Heise, C
Sala, C
AF Verpelli, Chiara
Montani, Caterina
Vicidomini, Cinzia
Heise, Christopher
Sala, Carlo
TI Mutations of the synapse genes and intellectual disability syndromes
SO EUROPEAN JOURNAL OF PHARMACOLOGY
LA English
DT Review
DE Intellectual disability; Brain synapses; Dendritic spine; Autism
ID LINKED MENTAL-RETARDATION; AUTISM SPECTRUM DISORDER; ACCESSORY
PROTEIN-LIKE; 22Q13.3 DELETION SYNDROME; DEPENDENT REGULATION; DENDRITIC
SPINES; MESSENGER-RNA; SHANK3; IL1RAPL1; OLIGOPHRENIN-1
AB Intellectual disability syndromes have been found associated to numerous mutated genes that code for proteins functionally involved in synapse formation, the regulation of dendritic spine morphology, the regulation of the synaptic cytoskeleton or the synthesis and degradation of specific synapse proteins. These studies have strongly demonstrated that even mild alterations in synapse morphology and function give rise to mild or severe alteration in intellectual abilities. Interestingly, pharmacological agents that are able to counteract these morphological and functional synaptic anomalies can also improve the symptoms of some of these conditions. This review is summarizing recent discoveries on the functions of some of the genes responsible for intellectual disability syndromes connected with synapse dysfunctions. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Verpelli, Chiara; Montani, Caterina; Vicidomini, Cinzia; Heise, Christopher; Sala, Carlo] Univ Milan, CNR Inst Neurosci, I-20129 Milan, Italy.
[Verpelli, Chiara; Montani, Caterina; Vicidomini, Cinzia; Heise, Christopher; Sala, Carlo] Univ Milan, Dept Med Biotechnol & Translat Med, I-20129 Milan, Italy.
[Sala, Carlo] Neurol Inst Fdn Carlo Besta, I-20133 Milan, Italy.
RP Sala, C (reprint author), Univ Milan, CNR Inst Neurosci, Via Vanvitelli 32, I-20129 Milan, Italy.
EM c.sala@in.cnr.it
RI Sala, Carlo/A-2493-2009
OI Sala, Carlo/0000-0003-0662-9523
FU Telethon - Italy [GGP11095]; Fondazione CARIPLO; Italian Institute of
technology; Seed Grant; Ministry of Health in the frame of ERA-NET
NEURON; Marie Curie Actions 7 Framework Programme: SyMBad Marie Curie
(Synapse: from molecules to brain diseases) International Research and
Training program
FX Funding This work was supported by Grants Telethon - Italy (Grant no.
GGP11095), Fondazione CARIPLO, Italian Institute of technology, Seed
Grant and Ministry of Health in the frame of ERA-NET NEURON. C.H. is
supported by Marie Curie Actions 7 Framework Programme: SyMBad Marie
Curie (Synapse: from molecules to brain diseases) International Research
and Training program 2002-2007.
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NR 62
TC 2
Z9 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0014-2999
EI 1879-0712
J9 EUR J PHARMACOL
JI Eur. J. Pharmacol.
PD NOV 5
PY 2013
VL 719
IS 1-3
BP 112
EP 116
DI 10.1016/j.ejphar.2013.07.023
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 258VQ
UT WOS:000327487200013
PM 23872408
ER
PT J
AU Garcia-Junco-Clemente, P
Chow, DK
Tring, E
Lazaro, MT
Trachtenberg, JT
Golshani, P
AF Garcia-Junco-Clemente, Pablo
Chow, David K.
Tring, Elaine
Lazaro, Maria T.
Trachtenberg, Joshua T.
Golshani, Peyman
TI Overexpression of calcium-activated potassium channels underlies
cortical dysfunction in a model of PTEN-associated autism
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE gain; visual cortex; SK; mTOR; sensory processing
ID PRIMARY VISUAL-CORTEX; TUMOR-SUPPRESSOR GENE; DE-NOVO MUTATIONS;
SPECTRUM DISORDERS; SYNAPTIC-TRANSMISSION; DENDRITIC SPINES; SK
CHANNELS; IN-VIVO; EXCITABILITY; MOUSE
AB De novo phosphatase and tensin homolog on chromosome ten (PTEN) mutations are a cause of sporadic autism. How single-copy loss of PTEN alters neural function is not understood. Here we report that Pten haploinsufficiency increases the expression of small-conductance calcium-activated potassium channels. The resultant augmentation of this conductance increases the amplitude of the afterspike hyperpolarization, causing a decrease in intrinsic excitability. In vivo, this change in intrinsic excitability reduces evoked firing rates of cortical pyramidal neurons but does not alter receptive field tuning. The decreased in vivo firing rate is not associated with deficits in the dendritic integration of synaptic input or with changes in dendritic complexity. These findings identify calcium-activated potassium channelopathy as a cause of cortical dysfunction in the PTEN model of autism and provide potential molecular therapeutic targets.
C1 [Garcia-Junco-Clemente, Pablo; Chow, David K.; Tring, Elaine; Trachtenberg, Joshua T.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurobiol, Los Angeles, CA 90095 USA.
[Lazaro, Maria T.; Golshani, Peyman] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
RP Golshani, P (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
EM pgolshani@mednet.ucla.edu
FU National Institutes of Health [NS-056210, MH-101198, MH082935]; Spanish
Ministry of Education, Culture and Sport [EX2009-0750]
FX We thank Dr. Sandra Kuhlman for her help and advice during the analysis
of the data. We also thank Dr. Mathias Groszer, Dr. Tom Otis, Dr. Dario
Ringach, and Dr. Larry Zipursky for their critical discussions of the
data. This work was supported by National Institutes of Health K08 Grant
NS-056210 and NIH R01 Grant MH-101198 (to P. G.) and NIH R01 Grant
MH082935 (to J.T.T. and P. G.). P.G.-J.-C. was supported by postdoctoral
Fellowship EX2009-0750 from the Spanish Ministry of Education, Culture
and Sport.
CR Alarcon M, 2008, AM J HUM GENET, V82, P150, DOI 10.1016/j.ajhg.2007.09.005
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NR 42
TC 1
Z9 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD NOV 5
PY 2013
VL 110
IS 45
BP 18297
EP 18302
DI 10.1073/pnas.1309207110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 246PG
UT WOS:000326550800065
PM 24145404
ER
PT J
AU El-Ansary, A
Shaker, G
Siddiqi, NJ
Al-Ayadhi, LY
AF El-Ansary, Afaf
Shaker, Ghada
Siddiqi, Nikhat J.
Al-Ayadhi, Laila Y.
TI Possible ameliorative effects of antioxidants on propionic
acid/clindamycin - induced neurotoxicity in Syrian hamsters
SO GUT PATHOGENS
LA English
DT Article
DE Autism; Clindamycin; Propionic acid; Carnosine; Carnitine; Cortex;
Medulla
ID AUTISTIC SPECTRUM DISORDERS; CHAIN FATTY-ACIDS; METABOLISM; MICROFLORA;
CARNOSINE; CARNITINE; CHILDREN; PRODUCT; DAMAGE; MODEL
AB Background: Propionic acid (PA) found in some foods and formed as a metabolic product of gut bacteria has been reported to mimic/mediate the effects of autism. The present study was undertaken to compare the effect of orally administered PA with that of clindamycin-induced PA-microbial producers in inducing persistent biochemical autistic features in hamsters. The neuroprotective potency of carnosine and carnitine supplements against PA toxicity was also investigated.
Methods: The following groups were studied. 1. Control group, which received phosphate buffered saline orally, 2. Propionic acid treated group which were given PA at a dose of 250 mg/kg body weight/day for 3 days orally, 3. Clindamycin treated group which received a single dose of the antibiotic orogastrically at a dose of 30 mg/kg on the day of the experiment, 4. Carnosine-treated group which were given carnosine at a dose of 10 mg/kg body weight/day orally for one week, 5. Carnitine treated group given 50 mg/kg body weight/day carnitine orally daily for one week. Group 6. Carnosine followed by PA, Group 7. Carnitine followed by PA. Dopamine, adrenaline and noradrenaline, serotonin and Gamma amino-butyric acid (GABA) were measured in the cortex and medulla of the nine studied groups.
Results: PA administration caused significant decrease in the neurotransmitters in the brains of treated hamsters while clindamycin caused a significant decrease only in dopamine in hamster brains (cortex and medulla) and GABA in the cerebral cortex of the treated hamsters. Administration of carnosine and carnitine which are known antioxidants caused no significant changes in the levels of neurotransmitters when administered alone to hamsters. However when administered with PA both carnosine and carnitine restored the altered neurotransmitters to near normal levels.
Conclusion: Carnosine and carnitine may be used as supplements to protect against PA neurotoxicity.
C1 [El-Ansary, Afaf; Siddiqi, Nikhat J.] King Saud Univ, Dept Biochem, Coll Sci, Riyadh 11495, Saudi Arabia.
[Shaker, Ghada] Zagazig Univ, Dept Microbiol & Immunol, Coll Pharm, Zagazig, Egypt.
[Al-Ayadhi, Laila Y.] King Saud Univ, Dept Physiol, Fac Med, Riyadh 11495, Saudi Arabia.
[El-Ansary, Afaf; Al-Ayadhi, Laila Y.] Autism Res & Treatment Unit, Riyadh, Saudi Arabia.
[El-Ansary, Afaf; Al-Ayadhi, Laila Y.] King Saud Univ, Shaik AL Amodi Autism Res Chair, Riyadh 11495, Saudi Arabia.
[El-Ansary, Afaf] Natl Res Ctr, Therapuet Chem Dept, Dokki, Guiza, Egypt.
RP El-Ansary, A (reprint author), King Saud Univ, Dept Biochem, Coll Sci, POB 22452, Riyadh 11495, Saudi Arabia.
EM elansary@ksu.edu.sa
FU Research Center of the Center for Female Scientific and Medical Colleges
in King Saud University
FX This research project was supported by a grant from the Research Center
of the Center for Female Scientific and Medical Colleges in King Saud
University.
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NR 35
TC 0
Z9 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1757-4749
J9 GUT PATHOG
JI Gut Pathogens
PD NOV 4
PY 2013
VL 5
DI 10.1186/1757-4749-5-32
PG 6
WC Gastroenterology & Hepatology; Microbiology
SC Gastroenterology & Hepatology; Microbiology
GA 273QC
UT WOS:000328550000002
PM 24188374
ER
PT J
AU Nuytens, K
Tuand, K
Di Michele, M
Boonen, K
Waelkens, E
Freson, K
Creemers, JWM
AF Nuytens, Kim
Tuand, Krizia
Di Michele, Michela
Boonen, Kurt
Waelkens, Etienne
Freson, Kathleen
Creemers, John W. M.
TI Platelets of mice heterozygous for neurobeachin, a candidate gene for
autism spectrum disorder, display protein changes related to aberrant
protein kinase A activity
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism spectrum disorder; AKAP; Calpain; Candidate gene; Neurobeachin;
Platelets; Serotonin; Talin-1
ID COPY NUMBER VARIANTS; WISTAR FURTH RAT; MOLECULAR-MECHANISMS; INTEGRIN
ACTIVATION; BEACH FAMILY; SEROTONIN; CALPAIN; ACTIN; SITE;
PHOSPHORYLATION
AB Background: Neurobeachin (NBEA) has been identified as a candidate gene for autism spectrum disorders (ASD) in several unrelated patients with alterations in the NBEA gene. The exact function of NBEA, a multidomain scaffolding protein, is currently unknown. It contains an A-kinase anchoring protein (AKAP) domain which binds the regulatory subunit of protein kinase A (PKA) thereby confining its activity to specific subcellular regions. NBEA has been implicated in post-Golgi membrane trafficking and in regulated secretion. The mechanism of regulated secretion is largely conserved between neurons and platelets, and the morphology of platelet dense granules was found to be abnormal in several ASD patients, including one with NBEA haploinsufficiency. Platelet dense granules are secreted upon vascular injury when platelets are exposed to for instance collagen. Dense granules contain serotonin, ATP and ADP, which are necessary for platelet plug formation and vascular contraction.
Methods: To further investigate possible roles for NBEA in secretion or dense granule morphology, platelets from Nbea(+/-) mice were analyzed morphometrically, functionally and biochemically. A differential proteomics and peptidomics screen was performed between Nbea(+/-) and Nbea(+/+) mice, in which altered Talin-1 cleavage was further investigated and validated in brain samples. Finally, the phosphorylation pattern of PKA substrates was analyzed.
Results: Platelet dense granules of Nbea(+/-) mice had a reduced surface area and abnormal dense-core halo, but normal serotonin-content. Nbea haploinsufficiency did not affect platelet aggregation and ATP secretion after collagen stimulation, although the platelet shape change was more pronounced. Furthermore, peptidomics revealed that Nbea(+/-) platelets contain significantly reduced levels of several actin-interacting peptides. Decreased levels were detected of the actin-binding head and rod domain of Talin-1, which are cleavage products of Calpain-2. This is most likely due to increased PKA-mediated phosphorylation of Calpain-2, which renders the enzyme less active. Analysis of other PKA substrates revealed both increased and reduced phosphorylation.
Conclusion: Our results show the pleiotropic effects of alterations in PKA activity due to Nbea haploinsufficiency, highlighting the important function of the AKAP domain in Nbea in regulating and confining PKA activity. Furthermore, these results suggest a role for Nbea in remodeling the actin cytoskeleton of platelets.
C1 [Nuytens, Kim; Tuand, Krizia; Boonen, Kurt; Creemers, John W. M.] Katholieke Univ Leuven, Dept Human Genet, Biochem Neuroendocrinol Lab, B-3000 Louvain, Belgium.
[Nuytens, Kim; Tuand, Krizia; Freson, Kathleen; Creemers, John W. M.] Katholieke Univ Leuven, Leuven Autism Res Consortium LAuRes, B-3000 Louvain, Belgium.
[Di Michele, Michela; Freson, Kathleen] Katholieke Univ Leuven, Ctr Mol & Vasc Biol, Dept Cardiovasc Sci, B-3000 Louvain, Belgium.
[Waelkens, Etienne] Katholieke Univ Leuven, Lab Prot Phosphorylat & Prote, Dept Cellular & Mol Med, B-3000 Louvain, Belgium.
RP Creemers, JWM (reprint author), Katholieke Univ Leuven, Dept Human Genet, Biochem Neuroendocrinol Lab, B-3000 Louvain, Belgium.
EM John.Creemers@med.kuleuven.be
RI Tuand, Krizia/E-1657-2015
OI Tuand, Krizia/0000-0003-2670-5415
FU agentschap voor Innovatie door Wetenschap en Technologie Vlaanderen
(IWT-Vlaanderen); Fund for Scientific Research (FWO-Vlaanderen)
[G.0490.10 N, G.0743.09]; steunfonds Marguerite-Marie Delacroix, KU
Leuven [IDO/08/013, GOA/2009/13, GOA/12/24]; Interuniversity Attraction
Poles Programme - Belgian Federal Science Policy [P7/13]
FX We would like to thank Sandra Meulemans and Chantal Thys for the
technical assistance, and the EM-facility of the Center of Human
Genetics, VIB KU Leuven for the use of their appliances. This work was
supported by the agentschap voor Innovatie door Wetenschap en
Technologie Vlaanderen (IWT-Vlaanderen), the Fund for Scientific
Research (FWO-Vlaanderen) (grants G.0490.10 N and G.0743.09) steunfonds
Marguerite-Marie Delacroix, KU Leuven (IDO/08/013; GOA/2009/13;
GOA/12/24), and a grant of the Interuniversity Attraction Poles
Programme (P7/13) - Belgian Federal Science Policy). The funding sources
were not involved in the design, collection, analysis or interpretation
of the data; in writing the manuscript; or in the decision to submit the
manuscript for publication.
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NR 63
TC 2
Z9 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 4
PY 2013
VL 4
AR 43
DI 10.1186/2040-2392-4-43
PG 13
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254ZB
UT WOS:000327207700002
PM 24188528
ER
PT J
AU Wang, L
Christophersen, CT
Sorich, MJ
Gerber, JP
Angley, MT
Conlon, MA
AF Wang, Lv
Christophersen, Claus T.
Sorich, Michael J.
Gerber, Jacobus P.
Angley, Manya T.
Conlon, Michael A.
TI Increased abundance of Sutterella spp. and Ruminococcus torques in feces
of children with autism spectrum disorder
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism spectrum disorder; Gut; Feces; Microbiota; Sutterella
ID SP NOV.; CAMPYLOBACTER; PREVALENCE; MUCIN
AB Background: A recent report indicated that numbers of Sutterella spp. are elevated in gastrointestinal biopsies taken from children with autism spectrum disorder (ASD). We have recently reported changes in the numbers of some bacteria within the stool of ASD children, and now examine whether numbers of Sutterella spp. and some other mucosa-associated bacteria linked with gastrointestinal disease (Ruminococcus gnavus and Ruminococcus torques) are also altered in the stool of these children.
Findings: We show that numbers of Sutterella spp. are elevated in feces of ASD children relative to controls, and that numbers of R. torques are higher in the children with ASD with a reported functional gastrointestinal disorder than those without such a disorder.
Conclusions: We show further evidence of changes in the gut microbiota of children with ASD and confirm that the abundance of Sutterella spp. is altered in stool.
C1 [Wang, Lv; Sorich, Michael J.; Gerber, Jacobus P.; Angley, Manya T.] Univ S Australia, Sansom Inst Hlth Res, Adelaide, SA 5001, Australia.
[Christophersen, Claus T.; Conlon, Michael A.] CSIRO Anim Food & Hlth Sci, Preventat Hlth Natl Res Flagship, Adelaide, SA 5001, Australia.
RP Conlon, MA (reprint author), CSIRO Anim Food & Hlth Sci, Preventat Hlth Natl Res Flagship, Gate 13,Kintore Ave, Adelaide, SA 5001, Australia.
EM michael.conlon@csiro.au
RI Conlon, Michael/H-6769-2013; Gerber, Jacobus/F-4423-2013
FU Australian Rotary Health Research Fund from Australian Rotary Health
FX This research was supported by the Australian Rotary Health Research
Fund from Australian Rotary Health. We wish to express our gratitude to
the participating children and their parents. We would also like to
acknowledge Dr Richard Couper, pediatric gastroenterologist, for medical
advice, and Emma Watson, Michelle Vuaran and Jennifer Giles for
technical assistance. The authors have no conflicts of interest to
declare.
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NR 19
TC 12
Z9 12
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 4
PY 2013
VL 4
AR 42
DI 10.1186/2040-2392-4-42
PG 4
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254ZB
UT WOS:000327207700001
PM 24188502
ER
PT J
AU Ananthaswamy, A
AF Ananthaswamy, Anil
TI Brain stimulation brings social side to autism
SO NEW SCIENTIST
LA English
DT News Item
NR 0
TC 0
Z9 0
PU REED BUSINESS INFORMATION LTD
PI SUTTON
PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND
SN 0262-4079
J9 NEW SCI
JI New Sci.
PD NOV 2
PY 2013
VL 220
IS 2941
BP 15
EP 15
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 249KP
UT WOS:000326776400012
ER
PT J
AU Ke, FF
Im, T
AF Ke, Fengfeng
Im, Tami
TI Virtual-Reality-Based Social Interaction Training for Children with
High-Functioning Autism
SO JOURNAL OF EDUCATIONAL RESEARCH
LA English
DT Article
DE autism; multiple-based across-subjects design; social interaction
training; virtual reality
ID SPECTRUM DISORDERS; ASPERGER-SYNDROME; YOUNG-CHILDREN; SKILLS;
INTERVENTION; ADOLESCENTS; PEOPLE; COMMUNICATION; ENVIRONMENTS;
EDUCATION
AB Employing the multiple-baseline across-subjects design, the authors examined the implementation and potential effect of a virtual-reality-based social interaction program on the interaction and communication performance of children with high functioning autism. The data were collected via behavior observation and analysis, questionnaires, and interviewing. The children participants demonstrated increased performance of responding, initiation, greeting, and positive conversation-ending during the intervention, and improved social competence measures after the intervention. The study also contributed salient themes on the adaptive design of a virtual-reality-based learning environment for learners with special needs. The study findings should extend the discussion on the design and usage of technology-supported informal learning environment for children with diverse characteristics and learning needs.
C1 [Ke, Fengfeng; Im, Tami] Florida State Univ, Tallahassee, FL 32306 USA.
RP Ke, FF (reprint author), Florida State Univ, 3205C Stone Bldg, Tallahassee, FL 32306 USA.
EM fke@fsu.edu
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NR 55
TC 2
Z9 2
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 0022-0671
J9 J EDUC RES
JI J. Educ. Res.
PD NOV 2
PY 2013
VL 106
IS 6
SI SI
BP 441
EP 461
DI 10.1080/00220671.2013.832999
PG 21
WC Education & Educational Research
SC Education & Educational Research
GA 225QK
UT WOS:000324977200004
ER
PT J
AU Hendrickson, JM
Carson, R
Woods-Groves, S
Mendenhall, J
Scheidecker, B
AF Hendrickson, Jo M.
Carson, Rori
Woods-Groves, Suzanne
Mendenhall, Janis
Scheidecker, Bethany
TI UI REACH: A Postsecondary Program Serving Students with Autism and
Intellectual Disabilities
SO EDUCATION AND TREATMENT OF CHILDREN
LA English
DT Article
ID TRANSITION-AGE STUDENTS; DEVELOPMENTAL-DISABILITIES; SPECTRUM DISORDERS;
COLLEGE; EDUCATION; SCHOOL; EXPERIENCES; TEACHERS; OUTCOMES; CHILDREN
AB Across the United States postsecondary education (PSE) options for young adults with autism and intellectual disabilities (ID) are emerging as a result of parent-professional advocacy group actions and legislation such as the Higher Education Opportunity Act of 2008 (HEOA). In this article the University of Iowa Realizing Educational and Career Hopes (UI REACH) Program, a thriving, well-integrated two year certificate program is described. We discuss the UI REACH model-its mission, student-centered and program goals, and strategies employed to ensure quality, sustainability, and continuous improvement. The student population, curriculum, staffing needs, and day-to-day operating issues are described. The experiences and perceptions of 14 students with autism spectrum disorder (ASD) suggest that the program facilitates a positive campus living-learning experience for these students. Challenges and recommendations for institutions of higher education considering developing, or in the early stages of developing, similar programs are presented.
C1 [Hendrickson, Jo M.; Carson, Rori; Woods-Groves, Suzanne; Mendenhall, Janis; Scheidecker, Bethany] Univ Iowa, Iowa City, IA 52242 USA.
RP Hendrickson, JM (reprint author), Univ Iowa, REACH Program, Lindquist Ctr 229, Iowa City, IA 52242 USA.
EM jo-hendrickson@uiowa.edu
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NR 48
TC 0
Z9 0
PU WEST VIRGINIA UNIV PRESS
PI MORGANTOWN
PA COMMUNICATIONS BLDG PATTESON DR, PO BOX 6295, MORGANTOWN, WV 26506-6295
USA
SN 0748-8491
EI 1934-8924
J9 EDUC TREAT CHILD
JI Educ. Treat. Child.
PD NOV
PY 2013
VL 36
IS 4
BP 169
EP 194
PG 26
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA AP0JK
UT WOS:000341747400009
ER
PT J
AU Roesler, CP
Flax, J
MacRoy-Higgins, M
Fermano, Z
Morgan-Byrne, J
Benasich, AA
AF Roesler, Cynthia P.
Flax, Judy
MacRoy-Higgins, Michelle
Fermano, Zena
Morgan-Byrne, Julie
Benasich, April A.
TI Sensory Desensitization Training for Successful Net Application and
EEG/ERP Acquisition in Difficult to Test Children
SO COMMUNICATION DISORDERS QUARTERLY
LA English
DT Article
DE ASD; EEG/ERPs; sensory desensitization; behavior modification; tactile
reactivity; nonverbal
ID AUTISM SPECTRUM DISORDERS; YOUNG-CHILDREN; DEVELOPMENTAL DELAY; TYPICAL
DEVELOPMENT; SENSITIVITY; PATTERNS
AB This study examined the effectiveness of sensory desensitization training for 12 nonverbal children with autism to facilitate participation in an electrophysiological study assessing linguistic processing. Sensory desensitization was achieved for 10 of the 12 children and thus allowed collection of usable data in a passive linguistic paradigm. Application of such desensitization methods may be useful as a precursor to other assessment protocols for individuals who are difficult to test.
C1 [Roesler, Cynthia P.; Flax, Judy; Fermano, Zena; Morgan-Byrne, Julie; Benasich, April A.] Rutgers State Univ, Newark, NJ 07102 USA.
[MacRoy-Higgins, Michelle] CUNY Hunter Coll, New York, NY 10021 USA.
RP Roesler, CP (reprint author), Rutgers State Univ, Ctr Mol & Behav Neurosci, 197 Univ Ave, Newark, NJ 07102 USA.
EM croesler@andromeda.rutgers.edu
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Yu Y. H., 2012, P 36 ANN BOST U C LA, V2, P686
NR 15
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1525-7401
EI 1538-4837
J9 COMMUN DISORD Q
JI Comm. Disord. Q.
PD NOV
PY 2013
VL 35
IS 1
BP 14
EP 20
DI 10.1177/1525740113489167
PG 7
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA AL7SJ
UT WOS:000339335100003
ER
PT J
AU Paloscia, C
Baglioni, V
Alessandrelli, R
Rosa, C
Guerini, R
Aceti, F
Pasini, A
AF Paloscia, Claudio
Baglioni, Valentina
Alessandrelli, Riccardo
Rosa, Caterina
Guerini, Rossella
Aceti, Franca
Pasini, Augusto
TI Executive function deficits in ADHD and Asperger syndrome
SO RIVISTA DI PSICHIATRIA
LA Italian
DT Article
DE Asperger syndrome; ADHA; working memory; inhibition response; cognitive
flexibility; children
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; AUTISM DIAGNOSTIC INTERVIEW;
WORKING-MEMORY; HYPERACTIVITY DISORDER; CHILDREN; PERFORMANCE; SPECTRUM;
PSYCHOPATHOLOGY; RELIABILITY; DYSFUNCTION
AB Background. The aim of this study is to evaluate the executive functioning of children with attention deficit hyperactivity disorder combined subtype (ADHD-C) and Asperger syndrome (AS) compared to a control group. Methods. A sample of 79 children (28 ADHD-C; 24 AS; 27 subjects with typical development) was tested on a wide range of tasks related to major domains of executive functioning: inhibition response (prepotent and interference), visual working memory, planning and cognitive flexibility. Results. Patients with AS showed deficits on visual working memory and cognitive flexibility. ADHD-C children were impaired on inhibition control (prepotent response) but also showed deficits on working memory and cognitive flexibility. The only executive functioning measure that differentiated ADHD from AS was inhibition of prepotent response and a more high deficit in cognitive flexibility and working memory in AS compared to ADHD-C. Conclusions. This study confirms recent evidence about the identification of specific executive profiles in these disorders. Other studies are warranted to evaluate the presence and specifity of a dysexecutive syndrome in ADHD and AS in a larger sample with girls.
C1 [Paloscia, Claudio; Alessandrelli, Riccardo; Rosa, Caterina; Pasini, Augusto] Univ Roma Tor Vergata, Dipartimento Neuropsichiatria Infantile, I-00173 Rome, Italy.
[Baglioni, Valentina] Univ Roma La Sapienza, Dipartimento Pediat & Neuropsichiatria Infantil, Rome, Italy.
[Guerini, Rossella] Univ Trento, Dipartimento Psicol & Sci Cognit, Trento, Italy.
[Aceti, Franca] Univ Roma La Sapienza, Dipartimento Psichiatria & Psicol Clin, Rome, Italy.
RP Paloscia, C (reprint author), Univ Roma Tor Vergata, Dipartimento Neuropsichiatria Infantile, I-00173 Rome, Italy.
EM claudiopaloscia@yahoo.it
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NR 51
TC 1
Z9 2
PU PENSIERO SCIENTIFICO EDITOR
PI ROME
PA VIA BRADANO 3/C, 00199 ROME, ITALY
SN 0035-6484
EI 2038-2502
J9 RIV PSICHIATR
JI Riv. Psichiatr.
PD NOV-DEC
PY 2013
VL 48
IS 6
BP 441
EP 447
PG 7
WC Psychiatry
SC Psychiatry
GA AL4XB
UT WOS:000339137000004
PM 24441520
ER
PT J
AU Erden, MS
AF Erden, Mustafa Suphi
TI Emotional Postures for the Humanoid-Robot Nao
SO INTERNATIONAL JOURNAL OF SOCIAL ROBOTICS
LA English
DT Article
DE Emotion; Posture; Humanoid-robot; Social interaction
ID STATIC BODY POSTURES; ATTRIBUTING EMOTION; MOVEMENT; CHILDREN; AUTISM;
INTERVENTION; EXPRESSION
AB This paper presents the development of emotional postures for the humanoid robot Nao. The approach is based on adaptation of the postures that are developed for a virtual human body model to the case of the physical robot Nao. In the paper the association between the joints of the human body model and the joints of the Nao robot are described and the transformation of postures is explained. The non-correspondence between the joints of the actual physical robot and the joints of the human body model was a major challenge in this work. Moreover, the implementation of the postures into the robot was constrained by the physical structure and the artificial mass distribution. Postures for the three emotions of anger, sadness, and happiness are studied. Thirty two postures are generated for each emotion. Among them the best five postures for each emotion are selected based on the votes of twenty five external observers. The distribution of the votes indicates that many of the implemented postures do not convey the intended emotions. The emotional content of the selected best five postures are tested by the votes of forty observers. The intended emotions received the highest recognition rate for each group of these selected postures. This study can be considered to be the last step of a general process for developing emotional postures for robots. This process starts with qualitative descriptions of human postures, continues with encoding those descriptions in quantitative terms, and ends with adaptation of the quantitative values to a specific robot. The present study demonstrates the last step of this process.
C1 Ecole Polytech Fed Lausanne, Learning Agorithms & Syst Lab, Lausanne, Switzerland.
RP Erden, MS (reprint author), Ecole Polytech Fed Lausanne, Learning Agorithms & Syst Lab, Lausanne, Switzerland.
EM mustafasuphi.erden@gmail.com
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NR 36
TC 2
Z9 2
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1875-4791
EI 1875-4805
J9 INT J SOC ROBOT
JI Int. J. Soc. Robot.
PD NOV
PY 2013
VL 5
IS 4
BP 441
EP 456
DI 10.1007/s12369-013-0200-4
PG 16
WC Robotics
SC Robotics
GA AE1VW
UT WOS:000333760400003
ER
PT J
AU Cabibihan, JJ
Javed, H
Ang, M
Aljunied, SM
AF Cabibihan, John-John
Javed, Hifza
Ang, Marcelo, Jr.
Aljunied, Sharifah Mariam
TI Why Robots? A Survey on the Roles and Benefits of Social Robots in the
Therapy of Children with Autism
SO INTERNATIONAL JOURNAL OF SOCIAL ROBOTICS
LA English
DT Article
DE Social robots; Autism spectrum disorder; Autism therapy; Human-robot
interaction; Robot design
ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; PREVALENCE;
AGENT; GAZE
AB This paper reviews the use of socially interactive robots to assist in the therapy of children with autism. The extent to which the robots were successful in helping the children in their social, emotional and communication deficits was investigated. Child-robot interactions were scrutinized with respect to the different target behaviors that are to be elicited from a child during therapy. These behaviors were thoroughly examined with respect to a child's development needs. Most importantly, experimental data from the surveyed works were extracted and analysed in terms of the target behaviors and of how each robot was used during a therapy session to achieve these behaviors. The study concludes by categorizing the different therapeutic roles that these robots were observed to play, and highlights the important design features that enable them to achieve high levels of effectiveness in autism therapy.
C1 [Cabibihan, John-John; Javed, Hifza] Natl Univ Singapore, Dept Elect & Comp Engn, Singapore 117548, Singapore.
[Ang, Marcelo, Jr.] Natl Univ Singapore, Dept Mech Engn, Singapore 117548, Singapore.
[Aljunied, Sharifah Mariam] Minist Educ, Educ Serv Div, Singapore, Singapore.
RP Cabibihan, JJ (reprint author), Natl Univ Singapore, Dept Elect & Comp Engn, Singapore 117548, Singapore.
EM elecjj@nus.edu.sg
FU National University of Singapore Academic Research Funding Grant
[R-263-000-A21-112]
FX This work was supported by the National University of Singapore Academic
Research Funding Grant No. R-263-000-A21-112.
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NR 88
TC 6
Z9 6
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1875-4791
EI 1875-4805
J9 INT J SOC ROBOT
JI Int. J. Soc. Robot.
PD NOV
PY 2013
VL 5
IS 4
BP 593
EP 618
DI 10.1007/s12369-013-0202-2
PG 26
WC Robotics
SC Robotics
GA AE1VW
UT WOS:000333760400013
ER
PT J
AU Rutter, M
AF Rutter, Michael
TI Developmental psychopathology: A paradigm shift or just a relabeling?
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID INDUCED MOVEMENT THERAPY; LIFE-COURSE-PERSISTENT; DSM-V;
ANTISOCIAL-BEHAVIOR; CANNABIS USE; FOLLOW-UP; SCHIZOPHRENIFORM DISORDER;
ENVIRONMENT INTERACTIONS; ADOLESCENT DEPRESSION; CONDUCT DISTURBANCE
AB Developmental psychopathology is described as a conceptual approach that involves a set of research methods that capitalize on developmental and psychopathological variations to ask questions about mechanisms and processes. Achievements are described in relation to attachment and attachment disorders, autism, schizophrenia, childhood antecedents of adult psychopathology, testing for environmental mediation of risk effects, gene-environment interplay, intellectual and language functioning, effects of mentally ill parents on the children, stress and vulnerability to depression, ethnicity and schizophrenia, and drug response. Continuities and discontinuities over the course of development are discussed in relation to attention-deficit/hyperactivity disorder, antisocial behavior, eating disorders, substance abuse and dependency, pharmacological and behavioral addictions, and a range of other disorders. Research challenges are considered in relation to spectrum concepts, the adolescent development of a female preponderance for depression, the mechanisms involved in age differences in response to drugs and to lateralized brain injury, the processing of experiences, the biological embedding of experiences, individual differences in response to environmental hazards, nature-nurture integration, and brain plasticity.
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RP Rutter, M (reprint author), Kings Coll London, MRC, Inst Psychiat, Social Genet & Dev Psychiat Ctr, POB 080,De Crespigny Pk,Denmark Hill, London SE5 8AF, England.
EM camilla.azis@kcl.ac.uk
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NR 137
TC 3
Z9 3
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1201
EP 1213
DI 10.1017/S0954579413000564
PN 2
PG 13
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500002
PM 24342835
ER
PT J
AU Jaffee, SR
Price, TS
Reyes, TM
AF Jaffee, Sara R.
Price, Thomas S.
Reyes, Teresa M.
TI Behavior genetics: Past, present, future
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; EQUAL ENVIRONMENTS ASSUMPTION; DISCORDANT
MONOZYGOTIC TWINS; CALLOUS-UNEMOTIONAL TRAITS; SEROTONIN TRANSPORTER
GENE; AUTISM SPECTRUM DISORDERS; MESSENGER-RNA EXPRESSION; COMMON SNPS
EXPLAIN; HIGH-FAT DIET; DE-NOVO
AB The disciplines of developmental psychopathology and behavior genetics are concerned with many of the same questions about the etiology and course of normal and abnormal behavior and about the factors that promote typical development despite the presence of risk. The goal of this paper is to summarize how research in behavior genetics has shed light on questions that are central to developmental psychopathology. We briefly review the origins of behavior genetics, summarize the findings that have been gleaned from several decades of quantitative and molecular genetics research, and describe future directions for research that will delineate gene function as well as pathways from genes to brain to behavior. The importance of environmental contributions, at both genetic and epigenetic levels, will be discussed. We conclude that behavior genetics has made significant contributions to developmental psychopathology by documenting the interplay among risk and protective factors at multiple levels of the organism, by clarifying the causal status of risk exposures, and by identifying factors that account for change and stability in psychopathology. As the tools to identify gene function become increasingly sophisticated, and as behavioral geneticists become increasingly interdisciplinary in their scope, the field is poised to make ever greater contributions to our understanding of typical and atypical development.
C1 [Jaffee, Sara R.; Price, Thomas S.; Reyes, Teresa M.] Univ Penn, Philadelphia, PA 19104 USA.
[Jaffee, Sara R.] Kings Coll London, London WC2R 2LS, England.
RP Jaffee, SR (reprint author), Univ Penn, Dept Psychol, 3720 Walnut St, Philadelphia, PA 19104 USA.
EM srjaffee@psych.upenn.edu
RI Price, Thomas/B-7372-2008
OI Price, Thomas/0000-0001-7356-2109
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NR 202
TC 0
Z9 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1225
EP 1242
DI 10.1017/S0954579413000588
PN 2
PG 18
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500004
PM 24342837
ER
PT J
AU Plomin, R
Simpson, MA
AF Plomin, Robert
Simpson, Michael A.
TI The future of genomics for developmentalists
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID COPY-NUMBER VARIANTS; AUTISM SPECTRUM DISORDERS; GENERAL
COGNITIVE-ABILITY; WIDE ASSOCIATION; COMMON DISEASES; STRUCTURAL
VARIATION; DNA METHYLATION; PSYCHIATRIC-DISORDERS; LEARNING-ABILITIES;
CHILD-DEVELOPMENT
AB The momentum of genomic science will carry it far into the future and into the heart of research on typical and atypical behavioral development. The purpose of this paper is to focus on a few implications and applications of these advances for understanding behavioral development. Quantitative genetics is genomic and will chart the course for molecular genomic research now that these two worlds of genetics are merging in the search for many genes of small effect. Although current attempts to identify specific genes have had limited success, known as the missing heritability problem, whole-genome sequencing will improve this situation by identifying all DNA sequence variations, including rare variants. Because the heritability of complex traits is caused by many DNA variants of small effect in the population, polygenic scores that are composites of hundreds or thousands of DNA variants will be used by developmentalists to predict children's genetic risk and resilience. The most far-reaching advance will be the widespread availability of whole-genome sequence for children, which means that developmentalists would no longer need to obtain DNA or to genotype children in order to use genomic information in research or in the clinic.
C1 [Plomin, Robert; Simpson, Michael A.] Kings Coll London, London SE5 8AF, England.
RP Plomin, R (reprint author), Kings Coll London, MRC, Inst Psychiat, Social Genet & Dev Psychiat Ctr, De Crespigny Pk,Denmark Hill, London SE5 8AF, England.
EM robert.plomin@kcl.ac.uk
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NR 115
TC 8
Z9 8
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1263
EP 1278
DI 10.1017/S0954579413000606
PN 2
PG 16
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500006
PM 24342839
ER
PT J
AU Wiggins, JL
Monk, CS
AF Wiggins, Jillian Lee
Monk, Christopher S.
TI A translational neuroscience framework for the development of
socioemotional functioning in health and psychopathology
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; SEROTONIN TRANSPORTER GENE; GENOME-WIDE
ASSOCIATION; GENERALIZED ANXIETY DISORDER; MAJOR DEPRESSIVE DISORDER;
MEDIAL PREFRONTAL CORTEX; EMOTIONAL FACIAL EXPRESSIONS; PROMOTER REGION
POLYMORPHISM; BIAS MODIFICATION TREATMENT; BRAINS DEFAULT NETWORK
AB The development of socioemotional functioning is a complex process that occurs over a protracted time period and requires coordinating affective, cognitive, and social faculties. At many points in development, the trajectory of socioemotional development can be deleteriously altered due to a combination of environmental insults and individual vulnerabilities. The result can be psychopathology. However, researchers are just beginning to understand the neural and genetic mechanisms involved in the development of healthy and disordered socioemotional functioning. We propose a translational developmental neuroscience framework to understand the transactional process that results in socioemotional functioning in both healthy and disordered populations. We then apply this framework to healthy socioemotional development, pediatric anxiety, pediatric depression, and autism spectrum disorder, selectively reviewing current literature in light of the framework. Finally, we examine ways that the framework can help to frame future directions of research on socioemotional development and translational implications for intervention.
C1 [Wiggins, Jillian Lee; Monk, Christopher S.] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Wiggins, JL (reprint author), NIMH, Sect Bipolar Spectrum Disorders, Emot & Dev Branch, Bldg 15K,MSC-2670, Bethesda, MD 20892 USA.
EM jillian.wiggins@nih.gov
RI Monk, Christopher/J-1805-2014
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NR 167
TC 1
Z9 1
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1293
EP 1309
DI 10.1017/S095457941300062X
PN 2
PG 17
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500008
PM 24342841
ER
PT J
AU Dawson, G
Bernier, R
AF Dawson, Geraldine
Bernier, Raphael
TI A quarter century of progress on the early detection and treatment of
autism spectrum disorder
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID INTENSIVE BEHAVIORAL INTERVENTION; PERVASIVE DEVELOPMENTAL DISORDERS;
DE-NOVO MUTATIONS; YOUNG-CHILDREN; JOINT ATTENTION; FOLLOW-UP;
COMMUNICATION DEVELOPMENT; ENVIRONMENTAL ENRICHMENT;
NONVERBAL-COMMUNICATION; LANGUAGE-DEVELOPMENT
AB The last 25 years have witnessed tremendous changes in our ability to detect autism very early in life and provide interventions that can significantly influence children's outcomes. It was once questioned whether autism could be recognized before children had developed language and symbolic play skills; now changes in early behaviors, as well as structural brain changes, have been documented in infants 6-12 months of age who later develop autism. Advances in brain imaging and genetics offer the possibility of detecting autism before the syndrome is fully manifest, thereby reducing or preventing symptoms from developing. Whereas the primary mode of behavioral intervention a few decades ago relied on operant conditioning, recent approaches integrate the methods of applied behavioral analysis within a developmental, relationship-focused intervention model that are implemented by both parents and clinicians. These interventions have been found to have positive effects on children's developmental trajectory, as measured by both behavioral and neurophysiological assessments. Future approaches will likely combine both behavioral and pharmacological treatments for children who have less robust responses to behavioral interventions. There has been a paradigm shift in the way that autism is viewed, evolving from a lifelong condition with a very poor prognosis to one in which significant gains and neuroplasticity is expected, especially when the condition is detected early and appropriate interventions are provided. The grand challenge for the future is to bridge the tremendous gap between research and the implementation of evidence-based practices in the broader community, both in the United States and worldwide. Significant disparities in access to appropriate health care for children with autism exist that urgently require advocacy and more resources.
C1 [Dawson, Geraldine] Duke Univ, Durham, NC 27701 USA.
[Bernier, Raphael] Univ Washington, Seattle, WA 98195 USA.
RP Dawson, G (reprint author), Duke Univ, Sch Med, Dept Psychiat & Behav Sci, Durham, NC 27701 USA.
EM geraldine.dawson@duke.edu
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NR 188
TC 3
Z9 4
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1455
EP 1472
DI 10.1017/S0954579413000710
PN 2
PG 18
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500017
PM 24342850
ER
PT J
AU Beauchaine, TP
McNulty, T
AF Beauchaine, Theodore P.
McNulty, Tiffany
TI Comorbidities and continuities as ontogenic processes: Toward a
developmental spectrum model of externalizing psychopathology
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY
DISORDER; OPPOSITIONAL DEFIANT DISORDER; ONSET CONDUCT PROBLEMS;
CALLOUS-UNEMOTIONAL TRAITS; PRENATAL COCAINE EXPOSURE; STRIATAL DOPAMINE
RELEASE; BRAIN-STIMULATION REWARD; RESEARCH DOMAIN CRITERIA; SUBSTANCE
USE DISORDERS
AB Research on child and adolescent mental health problems has burgeoned since the inaugural issue of Development and Psychopathology was published in 1989. In the quarter century since, static models of psychopathology have been abandoned in favor of transactional models, following the agenda set by editor Dante Cicchetti and other proponents of the discipline. The transactional approach, which has been applied to autism, depression, self-injury, and delinquency, (a) specifies vulnerabilities and risk factors across multiple levels of analysis spanning genes to cultures, (b) identifies multifinal and equifinal pathways to psychopathology, and (c) transcends traditional disciplinary boundaries. However, as noted by Rutter and Sroufe (2000), specific mechanisms of continuity, discontinuity, and comorbidity of psychopathology must be identified if we wish to understand etiology fully. In this article, we present a model of early-onset externalizing behavior in which comorbidities and continuities are viewed as ontogenic processes: products of complex longitudinal transactions between interdependent individual-level vulnerabilities (e.g., genetic, epigenetic, allostatic) and equally interdependent contextual risk factors (e.g., coercive parenting, deviant peer group affiliations, neighborhood criminality). Through interactions across levels of analysis, some individuals traverse along the externalizing spectrum, beginning with heritable trait impulsivity in preschool and ending in antisociality in adulthood. In describing our model, we note that (a) the approach outlined in the DSM to subtyping externalizing disorders continues to obscure developmental pathways to antisociality, (b) molecular genetics studies will likely not identify meaningful subtypes of externalizing disorder, and (c) ontogenic trait approaches to psychopathology are much more likely to advance the discipline in upcoming years.
C1 [Beauchaine, Theodore P.; McNulty, Tiffany] Ohio State Univ, Columbus, OH 43210 USA.
RP Beauchaine, TP (reprint author), Ohio State Univ, Dept Psychol, 225 Psychol Bldg,1835 Neil Ave, Columbus, OH 43210 USA.
EM beauchaine.1@osu.edu
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NR 282
TC 7
Z9 7
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
SI SI
BP 1505
EP 1528
DI 10.1017/S0954579413000746
PN 2
PG 24
WC Psychology, Developmental
SC Psychology
GA AC2YP
UT WOS:000332382500020
PM 24342853
ER
PT J
AU Eisen, A
Heller, I
Plotkin, A
Weissbrod, A
Zachor, D
Sobel, N
AF Eisen, A.
Heller, I
Plotkin, A.
Weissbrod, A.
Zachor, D.
Sobel, N.
TI Olfaction in autism
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 21st Annual Meeting of the Israel-Society-for-Neuroscience / 1st
Binational Australian-Israeli Meeting on Neuroscience
CY DEC 15-15, 2012
CL Eilat, ISRAEL
SP Israel Soc Neuroscience
C1 [Eisen, A.; Heller, I; Plotkin, A.; Weissbrod, A.; Sobel, N.] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel.
[Zachor, D.] Asaf Harofeh Med Ctr, Autism Ctr, Zerifin, Israel.
NR 0
TC 0
Z9 0
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
EI 1559-1166
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2013
VL 51
SU 1
BP S34
EP S34
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA AC9DF
UT WOS:000332833800081
ER
PT J
AU Braddick, O
Atkinson, J
AF Braddick, Oliver
Atkinson, Janette
TI Visual control of manual actions: brain mechanisms in typical
development and developmental disorders
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Review
ID DORSAL-STREAM VULNERABILITY; COORDINATION DISORDER; WILLIAMS-SYNDROME;
MOTION COHERENCE; DEPTH-PERCEPTION; CHILDREN; INFANTS; INFORMATION;
ATTENTION; COGNITION
AB Some key stages in the development of manual actions have been discussed in this supplement based on the idea of the dorsal cortical stream as the pathway for translating visual information into action control. We argue that visual information, transmitted through specialized visuomotor dorsal-stream modules, is required in the control of manual actions for selecting and attending to the target object of the action, translating visual spatial information into motor programmes and planning a coordinated sequence of actions so as to reach an optimal end-state. In typical development, we illustrate dorsal-stream processing through results on the use of stereoscopic information to guide infants' reaches, and changes in target selection and detailed kinematics of reaches depending on age, object size, and reaching in darkness (when dorsal-stream information rapidly decays). We hypothesize 'dorsal-stream vulnerability' as a widespread feature of neurodevelopmental disorders, such as autism, Williams syndrome, and children born very preterm. Such deficits, identified as abnormal visuomanual actions, are seen in bimanual coordination, visual guidance of action in the 'postbox' task, and failures in motor planning for end-state comfort. We discuss the possible application of these approaches to a wider range of disorders including developmental coordination disorder.
C1 [Braddick, Oliver] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England.
[Atkinson, Janette] UCL, Dept Dev Sci, Visual Dev Unit, London, England.
RP Braddick, O (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England.
EM oliver.braddick@psy.ox.ac.uk
FU Medical Research Council [G0601007, G7908507]; Medical Research Council;
Economic and Social Research Council; Oxford University Clarendon Fund
FX We thank members of the Visual Development Unit, University College
London and Oxford, who contributed to work reviewed here, in particular
Shirley Anker, Erin Babinsky, Dee Birtles, Kate Breckinridge, Bruce
Hood, John King, Chris Newman, and John Wattam-Bell. Research reviewed
here was supported by Medical Research Council programme grants G0601007
and G7908507, and by studentship funding from the Medical Research
Council, the Economic and Social Research Council, and Oxford University
Clarendon Fund.
CR Atkinson J, 2003, COGNITIVE NEUROSCIEN, P43
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NR 39
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1622
EI 1469-8749
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD NOV
PY 2013
VL 55
SU 4
SI SI
BP 13
EP 18
DI 10.1111/dmcn.12300
PG 6
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA AA5MW
UT WOS:000331144700005
PM 24237273
ER
PT J
AU Yu, RR
Xu, Y
Wang, YG
Qiu, FY
AF Yu, Rong-Rong
Xu, Yun
Wang, Yong-Gu
Qiu, Fei-Yue
TI Chemical Environment Influence the Incidence of Childhood Autism
SO ASIAN JOURNAL OF CHEMISTRY
LA English
DT Review
DE Chemicals; Autism; Incidence; Prevention
ID SPECTRUM DISORDERS; GENE VARIANTS; RISK
AB This review summarizes the environmental factors in particular chemicals involved in autism with either increasing or reducing effect in disease incidence, which will be helpful for prevention and treatment of the disease.
C1 [Yu, Rong-Rong; Xu, Yun; Wang, Yong-Gu; Qiu, Fei-Yue] Zhejiang Univ Technol, Sch Educ Sci & Technol, Hangzhou 310032, Zhejiang, Peoples R China.
RP Yu, RR (reprint author), Zhejiang Univ Technol, Sch Educ Sci & Technol, Hangzhou 310032, Zhejiang, Peoples R China.
EM libin0571@zju.edu.cn; qfy@zjut.edu.cn
FU Ministry of Education of Humanities and Social Science Project
[10YJCXLX053]; Zhejiang Provincial Natural Science Foundation of China
[LQ12H09005]; Fundamental "Zhijiang Qingnian" Research of Zhejiang
Provincial Philosophy and Social Science Foundation of China
[11ZJQN065YB]; Zhejiang Provincial Ministry of education of Humanities
and Social Science Project [Y201018729]; Major Program of the National
Social Science Foundation of China [12ZD229]; National Science &
Technology Pillar Program [2012BAI34B02, 2012BAI34B03]
FX This work was supported by The Ministry of Education of Humanities and
Social Science Project (10YJCXLX053), Zhejiang Provincial Natural
Science Foundation of China (LQ12H09005), the Fundamental "Zhijiang
Qingnian" Research of Zhejiang Provincial Philosophy and Social Science
Foundation of China (11ZJQN065YB), Zhejiang Provincial Ministry of
education of Humanities and Social Science Project (Y201018729); Project
supported by the Major Program of the National Social Science Foundation
of China (12&ZD229), Projects in the National Science & Technology
Pillar Program d(2012BAI34B02, 2012BAI34B03).
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Zhang J., 2005, MAT CHILD HLTH CARE, V20, P2395
NR 30
TC 0
Z9 0
PU ASIAN JOURNAL OF CHEMISTRY
PI SAHIBABAD
PA 11/100 RAJENDRA NAGAR, SECTOR 3,, SAHIBABAD 201 005, GHAZIABAD, INDIA
SN 0970-7077
EI 0975-427X
J9 ASIAN J CHEM
JI Asian J. Chem.
PD NOV
PY 2013
VL 25
IS 16
BP 8835
EP 8837
PN B
PG 3
WC Chemistry, Multidisciplinary
SC Chemistry
GA 297CX
UT WOS:000330234000001
ER
PT J
AU Jalbrzikowski, M
Krasileva, KE
Marvin, S
Zinberg, J
Andaya, A
Bachman, P
Cannon, TD
Bearden, CE
AF Jalbrzikowski, Maria
Krasileva, Kate E.
Marvin, Sarah
Zinberg, Jamie
Andaya, Angielette
Bachman, Peter
Cannon, Tyrone D.
Bearden, Carrie E.
TI Reciprocal social behavior in youths with psychotic illness and those at
clinical high risk
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; CHILDHOOD-ONSET SCHIZOPHRENIA;
PSYCHIATRIC-DISORDERS; TRAITS; CONNECTIVITY; METAANALYSIS; ADOLESCENCE;
PERFORMANCE; FRIENDSHIPS; POPULATION
AB Youths at clinical high risk (CHR) for psychosis typically exhibit significant social dysfunction. However, the specific social behaviors associated with psychosis risk have not been well characterized. We administer the Social Responsiveness Scale (SRS), a measure of autistic traits that examines reciprocal social behavior, to the parents of 117 adolescents (61 CHR individuals, 20 age-matched adolescents with a psychotic disorder [AOP], and 36 healthy controls) participating in a longitudinal study of psychosis risk. AOP and CHR individuals have significantly elevated SRS scores relative to healthy controls, indicating more severe social deficits. Mean scores for AOP and CHR youths are typical of scores obtained in individuals with high functioning autism (Constantino & Gruber, 2005). SRS scores are significantly associated with concurrent real-world social functioning in both clinical groups. Finally, baseline SRS scores significantly predict social functioning at follow-up (an average of 7.2 months later) in CHR individuals, over and above baseline social functioning measures (p < .009). These findings provide novel information regarding impairments in domains critical for adolescent social development, because CHR individuals and those with overt psychosis show marked deficits in reciprocal social behavior. Further, the SRS predicts subsequent real-world social functioning in CHR youth, suggesting that this measure may be useful for identifying targets of treatment in psychosocial interventions.
C1 [Jalbrzikowski, Maria; Krasileva, Kate E.; Marvin, Sarah; Zinberg, Jamie; Andaya, Angielette; Bachman, Peter; Cannon, Tyrone D.; Bearden, Carrie E.] Univ Calif Los Angeles, Los Angeles, CA 90095 USA.
RP Bearden, CE (reprint author), Univ Calif Los Angeles, Dept Psychiat & Behav Sci, Box 956968,300 Med Plaza,Room 2267, Los Angeles, CA 90095 USA.
EM cbearden@mednet.ucla.edu
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NR 48
TC 1
Z9 1
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
EI 1469-2198
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2013
VL 25
IS 4
BP 1187
EP 1197
DI 10.1017/S095457941300045X
PN 1
PG 11
WC Psychology, Developmental
SC Psychology
GA 298XT
UT WOS:000330358700022
PM 24229557
ER
PT J
AU Yasuda, H
Tsutsui, T
AF Yasuda, Hiroshi
Tsutsui, Toyoharu
TI Assessment of Infantile Mineral Imbalances in Autism Spectrum Disorders
(ASDs)
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Review
DE autism spectrum disorders; etiology of neurodevelopment disorders;
infantile zinc deficiency; toxic metal burdens; metallomics profiles;
epigenetic alterations; infantile window
ID BLOOD LEAD LEVELS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT
HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; PRENATAL
ZINC-DEFICIENCY; DE-NOVO MUTATIONS; TRACE-ELEMENTS; SCALP HAIR;
HEMODIALYSIS-PATIENTS; RANDOMIZED-TRIAL
AB The interactions between genes and the environment are now regarded as the most probable explanation for autism. In this review, we summarize the results of a metallomics study in which scalp hair concentrations of 26 trace elements were examined for 1,967 autistic children (1,553 males and 414 females aged 0-15 years-old), and discuss recent advances in our understanding of epigenetic roles of infantile mineral imbalances in the pathogenesis of autism. In the 1,967 subjects, 584 (29.7%) and 347 (17.6%) were found deficient in zinc and magnesium, respectively, and the incidence rate of zinc deficiency was estimated at 43.5% in male and 52.5% in female infantile subjects aged 0-3 years-old. In contrast, 339 (17.2%), 168 (8.5%) and 94 (4.8%) individuals were found to suffer from high burdens of aluminum, cadmium and lead, respectively, and 2.8% or less from mercury and arsenic. High toxic metal burdens were more frequently observed in the infants aged 0-3 years-old, whose incidence rates were 20.6%, 12.1%, 7.5%, 3.2% and 2.3% for aluminum, cadmium, lead, arsenic and mercury, respectively. These findings suggest that infantile zinc-and magnesium-deficiency and/or toxic metal burdens may be critical and induce epigenetic alterations in the genes and genetic regulation mechanisms of neurodevelopment in the autistic children, and demonstrate that a time factor "infantile window" is also critical for neurodevelopment and probably for therapy. Thus, early metallomics analysis may lead to early screening/estimation and treatment/prevention for the autistic neurodevelopment disorders.
C1 [Yasuda, Hiroshi; Tsutsui, Toyoharu] La Belle Vie Res Lab, Chuo Ku, Tokyo 1030006, Japan.
RP Yasuda, H (reprint author), La Belle Vie Res Lab, Chuo Ku, 8-4 Nihonbashi Tomizawacho, Tokyo 1030006, Japan.
EM yasuda@lbv.co.jp
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NR 89
TC 7
Z9 7
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD NOV
PY 2013
VL 10
IS 11
BP 6027
EP 6043
DI 10.3390/ijerph10116027
PG 17
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA 301GM
UT WOS:000330520800042
PM 24284360
ER
PT J
AU Hartley, SL
Schaidle, EM
Burnson, CF
AF Hartley, Sigan L.
Schaidle, Emily M.
Burnson, Cynthia F.
TI Parental Attributions for the Behavior Problems of Children and
Adolescents With Autism Spectrum Disorders
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE autism; behavior problems; attribution; parents; parenting stress
ID SOCIAL COGNITION; MOTHERS; EMOTION; FATHERS; SAMPLES; STRESS; ADULTS
AB Objective: The authors examined parental attributions for child behavior problems in 63 married couples of children and adolescents (aged 3-20 years) with autism spectrum disorders (ASDs). Both child-referent attributions (i.e., beliefs about causes related to the child or adolescent) and parent-referent attributions (i.e., beliefs about causes related to the parent) were examined along the dimensions of locus, stability, and controllability. Parent and child/adolescent factors related to parental attributions were identified, and the associations between parental attributions and parenting burden were explored. Method: Mothers and fathers independently completed self-reported measures of parental attributions, parenting burden, and child behavior problems. Couples jointly reported on their son or daughter's severity of autism symptoms, intellectual disability status, age, and gender. Results: Parents tended to attribute the behavior problems of their child/adolescent with an ASD to characteristics that were not only internal to and stable in the child/adolescent but also controllable by the child/adolescent. Mothers were more likely to attribute their son or daughter's behavior problems to characteristics that were less internal to and less stable in the child/adolescent with an ASD than were fathers. In addition, parents with a higher level of symptoms of the broader autism phenotype, parents of younger children, and parents of children/adolescents with intellectual disability, a higher severity of autism symptoms, and a higher severity of overall behavior problems were more likely to attribute their son or daughter's behavior problems to characteristics that were more internal to and stable in the child/adolescent and factors that were less controllable by the child/adolescent. Parental attributions were related to parents' level of parenting burden. Implications: Findings have implications for designing appropriate interventions and services for families of children and adolescents with ASDs.
C1 [Hartley, Sigan L.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
[Hartley, Sigan L.] Univ Wisconsin, Dept Human Dev & Family Studies, Madison, WI 53705 USA.
RP Hartley, SL (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave, Madison, WI 53705 USA.
EM hartley@waisman.wisc.edu
FU National Institute of Mental Health [1R01MH099190-01A1]; University of
Wisconsin Graduate School
FX This research was supported by grants from the University of Wisconsin
Graduate School and National Institute of Mental Health
(1R01MH099190-01A1 to S. Hartley).
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NR 30
TC 1
Z9 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
EI 1536-7312
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD NOV-DEC
PY 2013
VL 34
IS 9
BP 651
EP 660
PG 10
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 298YB
UT WOS:000330359500003
PM 24217029
ER
PT J
AU Danial, JT
Wood, JJ
AF Danial, John T.
Wood, Jeffrey J.
TI Cognitive Behavioral Therapy for Children With Autism: Review and
Considerations for Future Research
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Review
DE cognitive behavior therapy; autism treatment; anxiety; disruptive
behavior; social functioning
ID RANDOMIZED CONTROLLED-TRIAL; HIGH-FUNCTIONING CHILDREN; SPECTRUM
DISORDERS; ASPERGER-SYNDROME; ANXIETY DISORDERS; INTELLECTUAL
DISABILITY; PSYCHIATRIC-DISORDERS; CHILDHOOD ANXIETY; SOCIAL-SKILLS;
YOUNG-PEOPLE
AB Objective: Cognitive behavioral therapy (CBT) is now commonly used for high-functioning children with an autism spectrum disorder. The objective of this article was to describe the methods and results of cognitive behavioral interventions for children with autism. Method: This article reviews CBT programs targeting anxiety, disruptive behavior, and core autism symptoms for children with autism. Results: There is emerging evidence suggesting that CBT is possibly efficacious for anxiety and autism symptoms, but methodological weaknesses must be addressed before clear conclusions can be drawn. Conclusion: More research needs to be conducted to examine the effectiveness of CBT for children with autism. Specifically, future research should use more stringent methodology and assess the effectiveness of specific cognitive strategies and autism-related adaptations.
C1 [Danial, John T.; Wood, Jeffrey J.] Univ Calif Los Angeles, Dept Educ, Los Angeles, CA USA.
RP Danial, JT (reprint author), Moore Hall 3132A,405 Hilgard Ave, Los Angeles, CA 90095 USA.
EM jdanial@ucla.edu
FU Graduate Summer Research Mentorship program at University of California,
Los Angeles
FX Some of this project was funded by the Graduate Summer Research
Mentorship program at University of California, Los Angeles.
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NR 64
TC 9
Z9 9
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
EI 1536-7312
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD NOV-DEC
PY 2013
VL 34
IS 9
BP 702
EP 715
PG 14
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 298YB
UT WOS:000330359500009
PM 23917373
ER
PT J
AU Phelps, R
Nickel, R
Eisert, D
Stein, MT
AF Phelps, Randall
Nickel, Robert
Eisert, Debi
Stein, Martin T.
TI Parental Influence on a Child's Autistic Traits
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Editorial Material
DE autistic behaviors; parent behavior; parent assessment
ID FAMILY
AB CASE: Robbie is a 4-year-old boy whose parents are concerned about his speech, social skills, and repetitive behaviors. He has poor articulation; at time, he is difficult to understand. On the other hand, he has a fair vocabulary, and he has good intent to communicate. He is generally able to communicate his needs and wants. He likes to tell his parents about his day.
When he begins the day at preschool, Robbie initially stands by himself and watches. He slowly warms up and eventually participates in activities. He engages in parallel play or follows other children. He knows names of children at preschool, and he is well liked. He is affectionate with his parents. When Robbie is excited, he wiggles his fingers, flaps his arms, and grimaces. He can be quite rigid; for example, he gets very distressed when his mother sets his cup down on his right side instead of his left. However, in general, Robbie has a sunny personality. He likes to watch children's television shows. He pretends plays with action figures. Robbie is an only child who lives with both parents. His mother works full-time, and his father is in home with Robbie during the day.
When examined in the office, Robbie had a bright affect, good eye contact, and social referencing. He demonstrated good communicative intent, but poor articulation and some jargoning. He frequently wiggled his fingers and flapped his hands with excitement. Robbie had a borderline score on the Autism Diagnostic Observation Schedule.
During the visit, the pediatrician noted that Robbie's father was rather quiet and rarely responded to questions. When he did respond, he had a monotone quality to his voice. He maintained either a flat or nervous affect throughout the visit. He made limited eye contact, and occasionally he stared excessively.
C1 [Phelps, Randall; Nickel, Robert; Eisert, Debi] Oregon Hlth & Sci Univ, Dept Pediat, Inst Dev Disabil, Portland, OR 97201 USA.
[Stein, Martin T.] Univ Calif San Diego, Div Gen Acad Pediat Child Dev & Community Hlth, San Diego, CA 92103 USA.
RP Phelps, R (reprint author), Oregon Hlth & Sci Univ, Dept Pediat, Inst Dev Disabil, 3181 Sw Sam Jackson Pk Rd, Portland, OR 97201 USA.
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NR 3
TC 0
Z9 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
EI 1536-7312
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD NOV-DEC
PY 2013
VL 34
IS 9
BP 730
EP 732
PG 3
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 298YB
UT WOS:000330359500011
PM 24217028
ER
PT J
AU Visser, E
Zwiers, MP
Kan, CC
Hoekstra, L
van Opstal, J
Buitelaar, JK
AF Visser, Eelke
Zwiers, Marcel P.
Kan, Cornelis C.
Hoekstra, Liesbeth
van Opstal, John
Buitelaar, Jan K.
TI Atypical vertical sound localization and sound-onset sensitivity in
people with autism spectrum disorders
SO JOURNAL OF PSYCHIATRY & NEUROSCIENCE
LA English
DT Article
ID FUNCTIONAL CONNECTIVITY MRI; DORSAL COCHLEAR NUCLEUS; AUDITORY
BRAIN-STEM; SUPERIOR OLIVE; ACOUSTIC STRIAE; SPATIAL HEARING; HEAD
MOTION; CHILDREN; RESPONSES; ADULTS
AB Background: Autism spectrum disorders (ASDs) are associated with auditory hyper-or hyposensitivity; atypicalities in central auditory processes, such as speech-processing and selective auditory attention; and neural connectivity deficits. We sought to investigate whether the low-level integrative processes underlying sound localization and spatial discrimination are affected in ASDs. Methods: We performed 3 behavioural experiments to probe different connecting neural pathways: 1) horizontal and vertical localization of auditory stimuli in a noisy background, 2) vertical localization of repetitive frequency sweeps and 3) discrimination of horizontally separated sound stimuli with a short onset difference (precedence effect). Results: Ten adult participants with ASDs and 10 healthy control listeners participated in experiments 1 and 3; sample sizes for experiment 2 were 18 adults with ASDs and 19 controls. Horizontal localization was unaffected, but vertical localization performance was significantly worse in participants with ASDs. The temporal window for the precedence effect was shorter in participants with ASDs than in controls. Limitations: The study was performed with adult participants and hence does not provide insight into the developmental aspects of auditory processing in individuals with ASDs. Conclusion: Changes in low-level auditory processing could underlie degraded performance in vertical localization, which would be in agreement with recently reported changes in the neuroanatomy of the auditory brainstem in individuals with ASDs. The results are further discussed in the context of theories about abnormal brain connectivity in individuals with ASDs.
C1 [Visser, Eelke; Zwiers, Marcel P.; Buitelaar, Jan K.] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Ctr Cognit Neuroimaging, NL-6525 EN Nijmegen, Netherlands.
[Visser, Eelke; Zwiers, Marcel P.; Hoekstra, Liesbeth; Buitelaar, Jan K.] Radboud Univ Nijmegen, Med Ctr, Dept Cognit Neurosci, NL-6525 EN Nijmegen, Netherlands.
[Kan, Cornelis C.; Hoekstra, Liesbeth] Radboud Univ Nijmegen, Med Ctr, Dept Psychiat, NL-6525 EN Nijmegen, Netherlands.
[van Opstal, John] Radboud Univ Nijmegen, Dept Biophys, NL-6525 EN Nijmegen, Netherlands.
[van Opstal, John] Ctr Neurosci, Donders Inst Brain Cognit & Behav, Nijmegen, Netherlands.
[Hoekstra, Liesbeth; Buitelaar, Jan K.] Karakter Child & Adolescent Psychiat Univ Ctr, Nijmegen, Netherlands.
RP Visser, E (reprint author), Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Kapittelweg 29, NL-6525 EN Nijmegen, Netherlands.
EM eelke.visser@donders.ru.nl
RI Zwiers, Marcel/D-2968-2009
OI Zwiers, Marcel/0000-0001-5483-2935
FU University Medical Centre, Radboud University
FX C. Kan is on the ADHD Advisory Board at Eli Lilly and has received
royalties for 2 Dutch books on autism. J.K. Buitelaar declares an
internal grant from the University Medical Centre, Radboud University.
No other competing interests declared.
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NR 55
TC 2
Z9 2
PU CMA-CANADIAN MEDICAL ASSOC
PI OTTAWA
PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 5W8, CANADA
SN 1180-4882
EI 1488-2434
J9 J PSYCHIATR NEUROSCI
JI J. Psychiatry Neurosci.
PD NOV
PY 2013
VL 38
IS 6
BP 398
EP 406
DI 10.1503/jpn.120177
PG 9
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 301IM
UT WOS:000330526000007
PM 24148845
ER
PT J
AU Kim, P
Arizpe, J
Rosen, BH
Razdan, V
Haring, CT
Jenkins, SE
Deveney, CM
Brotman, MA
Blair, JR
Pine, DS
Baker, CI
Leibenluft, E
AF Kim, Pilyoung
Arizpe, Joseph
Rosen, Brooke H.
Razdan, Varun
Haring, Catherine T.
Jenkins, Sarah E.
Deveney, Christen M.
Brotman, Melissa A.
Blair, James R.
Pine, Daniel S.
Baker, Chris I.
Leibenluft, Ellen
TI Impaired fixation to eyes during facial emotion labelling in children
with bipolar disorder or severe mood dysregulation
SO JOURNAL OF PSYCHIATRY & NEUROSCIENCE
LA English
DT Article
ID VISUAL SCAN PATHS; AMYGDALA ACTIVATION; NEURAL CIRCUITRY; FACE
RECOGNITION; RATING-SCALE; SCHIZOPHRENIA; EXPRESSIONS; GAZE; PERCEPTION;
AUTISM
AB Background: Children with bipolar disorder (BD) or severe mood dysregulation (SMD) show behavioural and neural deficits during facial emotion processing. In those with other psychiatric disorders, such deficits have been associated with reduced attention to eye regions while looking at faces. Methods: We examined gaze fixation patterns during a facial emotion labelling task among children with pediatric BD and SMD and among healthy controls. Participants viewed facial expressions with varying emotions (anger, fear, sadness, happiness, neutral) and emotional levels (60%, 80%, 100%) and labelled emotional expressions. Results: Our study included 22 children with BD, 28 with SMD and 22 controls. Across all facial emotions, children with BD and SMD made more labelling errors than controls. Compared with controls, children with BD spent less time looking at eyes and made fewer eye fixations across emotional expressions. Gaze patterns in children with SMD tended to fall between those of children with BD and controls, although they did not differ significantly from either of these groups on most measures. Decreased fixations to eyes correlated with lower labelling accuracy in children with BD, but not in those with SMD or in controls. Limitations: Most children with BD were medicated, which precluded our ability to evaluate medication effects on gaze patterns. Conclusion: Facial emotion labelling deficits in children with BD are associated with impaired attention to eyes. Future research should examine whether impaired attention to eyes is associated with neural dysfunction. Eye gaze deficits in children with BD during facial emotion labelling may also have treatment implications. Finally, children with SMD exhibited decreased attention to eyes to a lesser extent than those with BD, and these equivocal findings are worthy of further study.
C1 [Kim, Pilyoung; Rosen, Brooke H.; Razdan, Varun; Haring, Catherine T.; Jenkins, Sarah E.; Deveney, Christen M.; Brotman, Melissa A.; Blair, James R.; Pine, Daniel S.; Leibenluft, Ellen] NIMH, Emot & Dev Branch, NIH, US Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
[Kim, Pilyoung] Univ Denver, Dept Psychol, Denver, CO 80208 USA.
[Arizpe, Joseph; Baker, Chris I.] NIMH, Lab Brain & Cognit, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA.
RP Kim, P (reprint author), Univ Denver, Dept Psychol, 2155 South Race St, Denver, CO 80208 USA.
EM pilyoung.kim@du.edu
RI Brotman, Melissa/H-7409-2013; Arizpe, Joseph/N-1399-2014
OI Arizpe, Joseph/0000-0001-8958-7757
FU Intramural Research Program of the National Institute of Mental Health
(NIMH), National Institutes of Health
FX Funding for this study was provided exclusively by the Intramural
Research Program of the National Institute of Mental Health (NIMH),
National Institutes of Health. We thank the staff of the Emotion and
Development Branch at NIMH and the children and families for their
participation.
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NR 59
TC 2
Z9 2
PU CMA-CANADIAN MEDICAL ASSOC
PI OTTAWA
PA 1867 ALTA VISTA DR, OTTAWA, ONTARIO K1G 5W8, CANADA
SN 1180-4882
EI 1488-2434
J9 J PSYCHIATR NEUROSCI
JI J. Psychiatry Neurosci.
PD NOV
PY 2013
VL 38
IS 6
BP 407
EP 416
DI 10.1503/jpn.120232
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 301IM
UT WOS:000330526000008
PM 23906351
ER
PT J
AU Moskowitz, LJ
Mulder, E
Walsh, CE
McLaughlin, DM
Zarcone, JR
Proudfit, GH
Carr, EG
AF Moskowitz, Lauren J.
Mulder, Emile
Walsh, Caitlin E.
McLaughlin, Darlene Magito
Zarcone, Jennifer R.
Proudfit, Greg Hajcak
Carr, Edward G.
TI A Multimethod Assessment of Anxiety and Problem Behavior in Children
With Autism Spectrum Disorders and Intellectual Disability
SO AJIDD-AMERICAN JOURNAL ON INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE anxiety; problem behavior; autism; multimethod
ID PERVASIVE DEVELOPMENTAL DISORDERS; HEART-RATE-VARIABILITY;
FRAGILE-X-SYNDROME; CHALLENGING BEHAVIORS; YOUNG-CHILDREN; SETTING
EVENT; INTERVENTION; PHOBIAS; INDIVIDUALS; ASSOCIATION
AB Despite the increased risk for anxiety disorders in children with autism spectrum disorders (ASD), there is a lack of research on the assessment and treatment of anxiety in this population, particularly for those with an intellectual disability (ID). The present study evaluated a multimethod strategy for the assessment of anxiety and problem behavior in three children with ASD and ID. Anxiety was operationally defined using: (1) behavioral data from anxious behaviors, (2) affective/contextual data from parent-report and observer ratings of overall anxiety, and (3) physiological data (heart rate [HR] and respiratory sinus arrhythmia [RSA]). A functional assessment of problem behavior during high-and low-anxiety conditions was conducted. Higher levels of problem behavior and HR and lower RSA were found in the high-anxiety than in the low-anxiety conditions.
C1 [Moskowitz, Lauren J.] NYU Langone Med Ctr, NYU Child Study Ctr, New York, NY 10016 USA.
[Mulder, Emile; Walsh, Caitlin E.; Proudfit, Greg Hajcak; Carr, Edward G.] SUNY Stony Brook, Stony Brook, NY USA.
[McLaughlin, Darlene Magito] Posit Behav Support Consulting & Psychol Resource, Centerport, NY USA.
[Zarcone, Jennifer R.] Johns Hopkins Sch Med, Baltimore, MD USA.
RP Moskowitz, LJ (reprint author), NYU Langone Med Ctr, NYU Child Study Ctr, New York, NY 10016 USA.
EM ljmoskowitz@gmail.com
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NR 69
TC 4
Z9 4
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1944-7515
EI 1944-7558
J9 AJIDD-AM J INTELLECT
JI AJIDD-Am. J. Intellect. Dev. Disabil.
PD NOV
PY 2013
VL 118
IS 6
BP 419
EP 434
DI 10.1352/1944.7558.118.6.419
PG 16
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 296LC
UT WOS:000330185500004
PM 24432856
ER
PT J
AU Tonnsen, BL
Shinkareva, SV
Deal, SC
Hatton, DD
Roberts, JE
AF Tonnsen, Bridgette L.
Shinkareva, Svetlana V.
Deal, Sara C.
Hatton, Deborah D.
Roberts, Jane E.
TI Biobehavioral Indicators of Social Fear in Young Children With Fragile X
Syndrome
SO AJIDD-AMERICAN JOURNAL ON INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Fragile X; respiratory sinus arrhythmia; heart activity; anxiety;
autism; attention
ID BEHAVIORAL-INHIBITION; AUTISTIC BEHAVIOR; VISUAL-ATTENTION; ANXIETY;
BOYS; INFANTS; DISORDERS; SYMPTOMS; TODDLERS; MALES
AB Anxiety is among the most impairing conditions associated with Fragile X syndrome (FXS) and is putatively linked to atypical physiological arousal. However, few studies have examined this association in young children with FXS. The authors examined whether patterns of arousal and behavior during an experimental stranger approach paradigm differ between a cross-sectional sample of 21 young children with FXS and 19 controls (1258 months old). Groups did not differ in mean levels of behavioral fear. Unlike the control group, however, the FXS group demonstrated increased facial fear at older ages, as well as age-dependent changes in associations between heart activity and distress vocalizations. These findings may inform theoretical models of anxiety etiology in FXS and early detection efforts.
C1 [Tonnsen, Bridgette L.; Shinkareva, Svetlana V.; Deal, Sara C.; Roberts, Jane E.] Univ S Carolina, Columbia, SC 29201 USA.
[Hatton, Deborah D.] Vanderbilt Univ, Nashville, TN USA.
RP Roberts, JE (reprint author), Univ S Carolina, 1512 Pendleton St, Columbia, SC 29201 USA.
EM jane.roberts@sc.edu
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NR 48
TC 2
Z9 2
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1944-7515
EI 1944-7558
J9 AJIDD-AM J INTELLECT
JI AJIDD-Am. J. Intellect. Dev. Disabil.
PD NOV
PY 2013
VL 118
IS 6
BP 447
EP 459
DI 10.1352/1944-7558-118.6.447
PG 13
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 296LC
UT WOS:000330185500006
PM 24432858
ER
PT J
AU Klusek, J
Martin, GE
Losh, M
AF Klusek, Jessica
Martin, Gary E.
Losh, Molly
TI Physiological Arousal in Autism and Fragile X Syndrome: Group
Comparisons and Links With Pragmatic Language
SO AJIDD-AMERICAN JOURNAL ON INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE autism; ASD; fragile X syndrome; arousal; vagal tone; heart rate;
pragmatic language; social communication; endophenotype
ID DIAGNOSTIC-OBSERVATION-SCHEDULE; CHILD-DIRECTED SPEECH; SPECTRUM
DISORDERS; YOUNG-CHILDREN; DOWN-SYNDROME; VAGAL TONE; CONVERSATIONAL
CHARACTERISTICS; DEVELOPMENTAL DISORDER; POLYVAGAL PERSPECTIVE; REVISED
ALGORITHMS
AB This study tested the hypothesis that pragmatic (i.e., social) language impairment is linked to arousal dysregulation in autism spectrum disorder (ASD) and fragile X syndrome (FXS). Forty boys with ASD, 39 with FXS, and 27 with typical development (TD), aged 4-15 years, participated. Boys with FXS were hyperaroused compared to boys with TD but did not differ from boys with ASD. Dampened vagal tone predicted pragmatic impairment in ASD, and associations emerged between cardiac activity and receptive/expressive vocabulary across groups. Findings support autonomic dysfunction as a mechanism underlying pragmatic impairment in ASD and suggest that biophysiological profiles are shared in ASD and FXS, which has implications for understanding the role of fragile X mental retardation-1 (FMR1, the FXS gene) in the pathophysiology of ASD.
C1 [Klusek, Jessica] Frank Porter Graham Child Dev Inst, Chapel Hill, NC USA.
[Martin, Gary E.] Univ N Carolina, Chapel Hill, NC USA.
[Losh, Molly] Northwestern Univ, Evanston, IL 60208 USA.
RP Losh, M (reprint author), Northwestern Univ, Roxelyn & Richard Pepper Dept Commun Sci & Disord, 2240 Campus Dr, Evanston, IL 60208 USA.
EM m-losh@northwestern.com
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NR 133
TC 3
Z9 4
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1944-7515
EI 1944-7558
J9 AJIDD-AM J INTELLECT
JI AJIDD-Am. J. Intellect. Dev. Disabil.
PD NOV
PY 2013
VL 118
IS 6
BP 475
EP 495
DI 10.1352/1944.7558-118.6.475
PG 21
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 296LC
UT WOS:000330185500008
PM 24432860
ER
PT J
AU Mohammadi, MR
Yadegari, N
Hassanzadeh, E
Farokhnia, M
Yekehtaz, H
Mirshafiee, O
Akhondzadeh, S
AF Mohammadi, Mohammad-Reza
Yadegari, Nourrollah
Hassanzadeh, Elmira
Farokhnia, Mehdi
Yekehtaz, Habibeh
Mirshafiee, Omid
Akhondzadeh, Shahin
TI Double-Blind, Placebo-Controlled Trial of Risperidone Plus Amantadine in
Children With Autism: A 10-Week Randomized Study
SO CLINICAL NEUROPHARMACOLOGY
LA English
DT Review
DE amantadine; autism; glutamate; randomized controlled trial; risperidone
ID SPECTRUM DISORDERS; ABERRANT BEHAVIOR; MEMANTINE; SYMPTOMS; THERAPY;
SCHIZOPHRENIA; DYSFUNCTION; MICROGLIA; MECHANISM; DISEASE
AB Objective: This study aimed to investigate the effect of adding amantadine to risperidone for treatment of autism.
Methods: Forty outpatients aged 4 to 12 years, who were diagnosed with autism spectrum disorders based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision criteria, were assigned to this double-blind clinical trial. The subjects were divided randomly into 2 groups. One group received risperidone plus amantadine, and the other group received risperidone plus placebo. The dose of risperidone was titrated between 1 and 2.0 mg/d, and the dose of amantadine was 100 or 150 mg/d for patients less than 30 kg or more than 30 kg, respectively. The patients were assessed using the Aberrant Behavioral Checklist-Community (ABC-C) and adverse effects checklist as well as clinical global impression-improvement (CGI-I) at 2 checkpoints of 5-week intervals after the baseline. Informed consent was obtained from the parents of each participant.
Results: Among ABC-C subscales, Hyperactivity and Irritability showed significantly greater reduction in the amantadine group than the placebo group. There was no significant difference in adverse effects between the 2 groups. The CGI-I scores show significant improvement in the amantadine group compared to the placebo group.
Conclusions: The present study suggests that amantadine may be a potential adjunctive treatment strategy for autism and it was generally well tolerated.
C1 [Mohammadi, Mohammad-Reza; Yadegari, Nourrollah; Hassanzadeh, Elmira; Farokhnia, Mehdi; Yekehtaz, Habibeh; Mirshafiee, Omid; Akhondzadeh, Shahin] Univ Tehran Med Sci, Roozbeh Hosp, Psychiat Res Ctr, Tehran 13337, Iran.
RP Akhondzadeh, S (reprint author), Univ Tehran Med Sci, Roozbeh Psychiat Hosp, Psychiat Res Ctr, South Kargar St, Tehran 13337, Iran.
EM s.akhond@neda.net
FU Tehran University of Medical Sciences [10797]
FX No conflict of interest exists for any of the authors associated with
the manuscript and there was no source of extra-institutional commercial
funding. This study was supported by a grant from Tehran University of
Medical Sciences to Prof Shahin Akhondzadeh (Grant 10797). The funding
organization had no role in the design and conduct of the study; in the
collection, analysis, and interpretation of the data; or in the
preparation, review, or approval of the manuscript and the decision to
submit the paper for publication.
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NR 32
TC 3
Z9 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0362-5664
EI 1537-162X
J9 CLIN NEUROPHARMACOL
JI Clin. Neuropharmacol.
PD NOV-DEC
PY 2013
VL 36
IS 6
BP 179
EP 184
DI 10.1097/WNF.0b013e3182a9339d
PG 6
WC Clinical Neurology; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 299BK
UT WOS:000330369400001
PM 24201232
ER
PT J
AU Caravagna, C
Soliz, J
Seaborn, T
AF Caravagna, Celine
Soliz, Jorge
Seaborn, Tommy
TI Brain-derived neurotrophic factor interacts with astrocytes and neurons
to control respiration
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Review
DE astrocyte; brain-derived neurotrophic factor; brainstem; rhythmogenesis;
TrkB
ID PRE-BOTZINGER COMPLEX; CENTRAL-NERVOUS-SYSTEM; CENTRAL HYPOVENTILATION
SYNDROME; KOLLIKER-FUSE NUCLEUS; RETT-SYNDROME; MOUSE MODEL;
PREBOTZINGER COMPLEX; GROWTH-FACTOR; IN-VITRO; SYNAPTIC-TRANSMISSION
AB Respiratory rhythm is generated and modulated in the brainstem. Neuronal involvement in respiratory control and rhythmogenesis is now clearly established. However, glial cells have also been shown to modulate the activity of brainstem respiratory groups. Although the potential involvement of other glial cell type(s) cannot be excluded, astrocytes are clearly involved in this modulation. In parallel, brain-derived neurotrophic factor (BDNF) also modulates respiratory rhythm. The currently available data on the respective roles of astrocytes and BDNF in respiratory control and rhythmogenesis lead us to hypothesize that there is BDNF-mediated control of the communication between neurons and astrocytes in the maintenance of a proper neuronal network capable of generating a stable respiratory rhythm. According to this hypothesis, progression of Rett syndrome, an autism spectrum disease with disordered breathing, can be stabilized in mouse models by re-expressing the normal gene pattern in astrocytes or microglia, as well as by stimulating the BDNF signaling pathway. These results illustrate how the signaling mechanisms by which glia exerts its effects in brainstem respiratory groups is of great interest for pathologies associated with neurological respiratory disorders.
C1 [Caravagna, Celine; Soliz, Jorge; Seaborn, Tommy] Univ Laval, Dept Pediat, Ctr Rech, Hop St Francois Assise,Ctr Hosp Univ CHU Quebec, Quebec City, PQ, Canada.
RP Seaborn, T (reprint author), Univ Laval, Dept Pediat, Ctr Rech, Hop St Francois Assise,Ctr Hosp Univ CHU Quebec, 10 Rue Espinay,Room D0-742, Quebec City, PQ, Canada.
EM Tommy.Seaborn@crchuq.ulaval.ca
FU Respiratory Health Network of the Quebec Health Research Funds (FRQS);
Foundation of Stars for Children's Health Research; Molly Towell
Foundation; Faculty of Medicine of Laval University
FX The authors thank Drs Aida Bairam and Vincent Joseph for their helpful
comments, as well as Dr Richard Kinkead for his thoughtful reading of
the manuscript and Miss NagaPraveena Uppari for partial revision of the
English. Celine Caravagna is a PhD student supported by the Faculty of
Medicine of Laval University. This work was supported by the Respiratory
Health Network of the Quebec Health Research Funds (FRQS) (Dr Tommy
Seaborn), and by the Foundation of Stars for Children's Health Research
and the Molly Towell Foundation (Dr Jorge Soliz). The authors have no
actual or potential conflicts of interest to declare.
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NR 102
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
EI 1460-9568
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD NOV
PY 2013
VL 38
IS 9
BP 3261
EP 3269
DI 10.1111/ejn.12320
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 295FF
UT WOS:000330101300001
PM 23930598
ER
PT J
AU Pardoe, HR
Abbott, DF
Jackson, GD
AF Pardoe, Heath R.
Abbott, David F.
Jackson, Graeme D.
CA Alzheimer's Dis Neuroimaging Initi
TI Sample Size Estimates for Well-Powered Cross-Sectional Cortical
Thickness Studies
SO HUMAN BRAIN MAPPING
LA English
DT Article
DE MRI; neuroimaging; study design; power analysis; morphometry; cortical
thickness
ID CEREBRAL-CORTEX; CHILDREN; DISEASE; MRI; AUTISM
AB Introduction: Cortical thickness mapping is a widely used method for the analysis of neuroanatomical differences between subject groups. We applied power analysis methods over a range of image processing parameters to derive a model that allows researchers to calculate the number of subjects required to ensure a well-powered cross-sectional cortical thickness study. Methods: 0.9-mm isotropic T-1-weighted 3D MPRAGE MRI scans from 98 controls (53 females, age 29.1 +/- 9.7 years) were processed using Freesurfer 5.0. Power analyses were carried out using vertex-wise variance estimates from the coregistered cortical thickness maps, systematically varying processing parameters. A genetic programming approach was used to derive a model describing the relationship between sample size and processing parameters. The model was validated on four Alzheimer's Disease Neuroimaging Initiative control datasets (mean 126.5 subjects/site, age 76.6 +/- 5.0 years). Results: Approximately 50 subjects per group are required to detect a 0.25-mm thickness difference; less than 10 subjects per group are required for differences of 1 mm (two-sided test, 10 mm smoothing, = 0.05). Sample size estimates were heterogeneous over the cortical surface. The model yielded sample size predictions within 2-6% of that determined experimentally using independent data from four other datasets. Fitting parameters of the model to data from each site reduced the estimation error to less than 2%. Conclusions: The derived model provides a simple tool for researchers to calculate how many subjects should be included in a well-powered cortical thickness analysis. Hum Brain Mapp 34:3000-3009, 2013. (c) 2012 Wiley Periodicals, Inc.
C1 [Pardoe, Heath R.; Abbott, David F.; Jackson, Graeme D.] Austin Hosp, Melbourne Brain Ctr, Florey Neurosci Inst, Brain Res Inst, Heidelberg, Vic 3084, Australia.
[Pardoe, Heath R.; Abbott, David F.; Jackson, Graeme D.] Univ Melbourne, Dept Med, Melbourne, Vic 3010, Australia.
[Jackson, Graeme D.] Univ Melbourne, Dept Radiol, Melbourne, Vic 3010, Australia.
RP Jackson, GD (reprint author), Austin Hosp, Melbourne Brain Ctr, Florey Neurosci Inst, Brain Res Inst, 245 Burgundy St, Heidelberg, Vic 3084, Australia.
EM BRI@brain.org.au
RI Abbott, David/E-5412-2010; Jackson, Graeme/A-9064-2013
OI Abbott, David/0000-0002-7259-8238;
FU National Institutes of Health [NIH-NINDS R37-31146]; Victorian Life
Sciences Computation Initiative (VLSCI; Peak Computing Facility at the
University of Melbourne, an initiative of the Victorian Government)
[VR0056]; Victorian Government's Operational Infrastructure Support
Program; Scobie nd McKinnon Trust; NHMRC program [628952]; Alzheimer's
Disease Neuroimaging Initiative (ADNI; National Institutes of Health)
[U01 AG024904]
FX Contract grant sponsor: National Institutes of Health; contract grant
number: NIH-NINDS R37-31146; Contract grant sponsor: Victorian Life
Sciences Computation Initiative (VLSCI; Peak Computing Facility at the
University of Melbourne, an initiative of the Victorian Government);
Contract grant number: VR0056; Contract grant sponsor: Victorian
Government's Operational Infrastructure Support Program; Contract grant
sponsor: Scobie nd McKinnon Trust; Contract grant sponsor: NHMRC
program; Contract grant number: 628952; Contract grant sponsor:
Alzheimer's Disease Neuroimaging Initiative (ADNI; National Institutes
of Health); Contract grant number: U01 AG024904.
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NR 23
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1065-9471
EI 1097-0193
J9 HUM BRAIN MAPP
JI Hum. Brain Mapp.
PD NOV
PY 2013
VL 34
IS 11
BP 3000
EP 3009
DI 10.1002/hbm.22120
PG 10
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 295FG
UT WOS:000330101400021
PM 22807270
ER
PT J
AU Oakes, A
Kover, ST
Abbeduto, L
AF Oakes, Ashley
Kover, Sara T.
Abbeduto, Leonard
TI Language Comprehension Profiles of Young Adolescents With Fragile X
Syndrome
SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY
LA English
DT Article
DE adolescents; developmental disorders; language; syntax
ID WITHIN-SYNDROME DIFFERENCES; DOWN-SYNDROME; EXPRESSIVE LANGUAGE;
RECEPTIVE LANGUAGE; WORKING-MEMORY; BOYS; CHILDREN; AUTISM; ADULTS;
SKILLS
AB Purpose: In this study, the authors sought to characterize the language phenotype of fragile X syndrome (FXS), focusing on the extent of impairment in receptive syntax, within-syndrome variability in those impairments in relation to gender, and the syndrome specificity of those impairments.
Method: The Test for Reception of Grammar, Version 2 (Bishop, 2003), was used to examine the overall receptive syntactic skills of adolescents with FXS (n = 35; 30 males, 5 females), adolescents with Down syndrome (DS; n = 28; 18 males, 10 females), and younger typically developing (TD) children (n = 23; 14 males, 9 females) matched on nonverbal cognition. Performance on specific grammatical constructions and error types was examined for a subset of matched participants.
Results: Participants with FXS had overall receptive syntax scores that were lower than those of the TD participants but higher than those of the participants with DS; however, there was no difference in performance between the FXS and DS groups when females were excluded. Grammatical constructions that were especially difficult for participants with FXS and those with DS were identified, especially relative clause constructions and reversible constructions requiring attention to word order encoded by syntactic features.
Conclusion: The current findings have implications for understanding the nature of the language learning difficulties of individuals with FXS and for language interventions.
C1 [Oakes, Ashley; Abbeduto, Leonard] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
[Oakes, Ashley; Abbeduto, Leonard] Univ Calif Davis, Davis, CA 95616 USA.
[Kover, Sara T.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
RP Oakes, A (reprint author), Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
EM ashley.oakes@ucdmc.ucdavis.edu
FU National Institute on Child Health and Human Development [R01 HD024356,
P30 HD003352]; National Institute on Deafness and Other Communication
Disorders [F31 DC010959]
FX This research was supported by National Institute on Child Health and
Human Development Grants R01 HD024356 and P30 HD003352, awarded to the
third author, and by National Institute on Deafness and Other
Communication Disorders Grant F31 DC010959, awarded to the second
author. The study reported in this article was completed to fulfill the
requirements for the first author's master's degree from the University
of Wisconsin-Madison. We offer special thanks to Jan Edwards and Susan
Ellis Weismer, and to the families who participated in the study. A
portion of the results from the current study were presented at the 2011
Symposium on Research in Child Language Disorders.
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NR 41
TC 2
Z9 2
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1058-0360
EI 1558-9110
J9 AM J SPEECH-LANG PAT
JI Am. J. Speech-Lang. Pathol.
PD NOV 1
PY 2013
VL 22
IS 4
BP 615
EP 626
DI 10.1044/1058-0360(2013/12-0109)
PG 12
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 294FG
UT WOS:000330027900004
PM 23813199
ER
PT J
AU Nagele, P
AF Nagele, Peter
TI Exome Sequencing One Small Step for Malignant Hyperthermia, One Giant
Step for Our Specialty-Why Exome Sequencing Matters to All of Us, Not
Just the Experts
SO ANESTHESIOLOGY
LA English
DT Editorial Material
ID AUTISM SPECTRUM DISORDERS; MUTATIONS; PARADIGM
C1 Washington Univ, Sch Med, Dept Anesthesiol & Genet, St Louis, MO 63130 USA.
RP Nagele, P (reprint author), Washington Univ, Sch Med, Dept Anesthesiol & Genet, St Louis, MO 63130 USA.
EM nagelep@wustl.edu
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PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
EI 1528-1175
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2013
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BP 1006
EP 1008
DI 10.1097/ALN.0b013e3182a8a90c
PG 3
WC Anesthesiology
SC Anesthesiology
GA 290ZS
UT WOS:000329797900004
PM 24195944
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LA English
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Z9 1
PU AMER EPILEPSY SOCIETY
PI WEST HARTFORD
PA 342 NORTH MAIN STREET, WEST HARTFORD, CT 06117-2507 USA
SN 1535-7597
EI 1535-7511
J9 EPILEPSY CURR
JI Epilepsy Curr.
PD NOV-DEC
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BP 282
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PG 6
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SC Neurosciences & Neurology
GA 293NO
UT WOS:000329979100008
PM 24348128
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PT J
AU Stafstrom, CE
AF Stafstrom, Carl E.
TI Issues in Clinical Epileptology: A View from the Bench. A Festschrift in
Honor of Philip A. Schwartzkroin, PhD
SO EPILEPSY CURRENTS
LA English
DT Editorial Material
ID TEMPORAL-LOBE EPILEPSY; ANIMAL-MODELS; INFANTILE SPASMS; KNOCKOUT MICE;
MOUSE MODEL; IN-VITRO; SEIZURES; HIPPOCAMPUS; AUTISM; EPILEPTOGENESIS
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NR 52
TC 0
Z9 0
PU AMER EPILEPSY SOCIETY
PI WEST HARTFORD
PA 342 NORTH MAIN STREET, WEST HARTFORD, CT 06117-2507 USA
SN 1535-7597
EI 1535-7511
J9 EPILEPSY CURR
JI Epilepsy Curr.
PD NOV-DEC
PY 2013
VL 13
IS 6
BP 291
EP +
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 293NO
UT WOS:000329979100012
PM 24348132
ER
PT J
AU Arnold, LE
AF Arnold, L. Eugene
TI Placebo Response and the Company It Keeps
SO JAMA PEDIATRICS
LA English
DT Editorial Material
ID CHILDREN; RISPERIDONE; AUTISM
C1 Ohio State Univ, Dept Psychiat, Sunbury, OH 43074 USA.
RP Arnold, LE (reprint author), Ohio State Univ, Dept Psychiat, 479 S Galena Rd, Sunbury, OH 43074 USA.
EM l.arnold@osumc.edu
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NR 5
TC 0
Z9 0
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 1000
EP 1001
DI 10.1001/jamapediatrics.2013.2704
PG 2
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300008
PM 24061596
ER
PT J
AU King, BH
Dukes, K
Donnelly, CL
Sikich, L
McCracken, JT
Scahill, L
Hollander, E
Bregman, JD
Anagnostou, E
Robinson, F
Sullivan, L
Hirtz, D
AF King, Bryan H.
Dukes, Kimberly
Donnelly, Craig L.
Sikich, Linmarie
McCracken, James T.
Scahill, Lawrence
Hollander, Eric
Bregman, Joel D.
Anagnostou, Evdokia
Robinson, Fay
Sullivan, Lisa
Hirtz, Deborah
TI Baseline Factors Predicting Placebo Response to Treatment in Children
and Adolescents With Autism Spectrum Disorders A Multisite Randomized
Clinical Trial
SO JAMA PEDIATRICS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; REPETITIVE BEHAVIOR;
ABERRANT BEHAVIOR; SECRETIN; RISPERIDONE; IRRITABILITY; METAANALYSIS;
HYPERACTIVITY; ARIPIPRAZOLE
AB IMPORTANCE The finding of factors that differentially predict the likelihood of response to placebo over that of an active drug could have a significant impact on study design in this population.
OBJECTIVE To identify possible nonspecific, baseline predictors of response to intervention in a large randomized clinical trial of children and adolescents with autism spectrum disorders.
DESIGN, SETTING, AND PARTICIPANTS Randomized clinical trial of citalopram hydrobromide for children and adolescents with autism spectrum disorders and prominent repetitive behavior. Baseline data at study entry were examined with respect to final outcome to determine if response predictors could be identified. A total of 149 children and adolescents 5 to 17 years of age (mean [SD] age, 9.4 [3.1] years) from 6 academic centers were randomly assigned to citalopram (n = 73) or placebo (n = 76). Participants had autistic disorder, Asperger syndrome, or pervasive developmental disorder, not otherwise specified; had illness severity ratings that were moderate or more than moderate on the Clinical Global Impression-Severity scale; and scored moderate or more than moderate on compulsive behaviors measured with the modified Children's Yale-Brown Obsessive-Compulsive Scale.
INTERVENTIONS Twelveweeks of treatment with citalopram (10 mg/5 mL) or placebo. The mean (SD) maximum dose of citalopramwas 16.5 (6.5) mg by mouth daily (maximum dose, 20 mg/d).
MAIN OUTCOMES AND MEASURES A positive response was defined as having a score of at least much improved on the Clinical Global Impression-Improvement scale at week 12. Baseline measures included demographic (sex, age, weight, and pubertal status), clinical, and family measures. Clinical variables included baseline illness severity ratings (the Aberrant Behavior Checklist, the Child and Adolescent Symptom Inventory, the Vineland Adaptive Behavior Scales, the Repetitive Behavior Scale-Revised, and the Children's Yale-Brown Obsessive-Compulsive Scale). Family measures included the Caregiver Strain Questionnaire.
RESULTS Several baseline predictors of response were identified, and a principal component analysis yielded 3 composite measures (disruptive behavior, autism/mood, and caregiver strain) that significantly predicted response at week 12. Specifically, participants in the placebo group were significantly less likely than participants in the citalopram group to respond at week 12 if they entered the study more symptomatic on each of the 3 composite measures, and they were at least 2 times less likely to be responders.
CONCLUSIONS AND RELEVANCE This analysis suggests strategies that may be useful in anticipating and potentially mitigating the nonspecific response in randomized clinical trials of children and adolescents with autism spectrum disorders.
C1 [King, Bryan H.] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[King, Bryan H.] Seattle Childrens Hosp, Dept Psychiat & Behav Med, Seattle, WA 98105 USA.
[Dukes, Kimberly; Robinson, Fay] DM STAT Inc, Malden, MA USA.
[Donnelly, Craig L.] Dartmouth Hitchcock Med Ctr, Lebanon, NH 03766 USA.
[Sikich, Linmarie] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA.
[McCracken, James T.] Univ Calif Los Angeles, Jane & Terry Semel Inst Neurosci & Human Behav, Los Angeles, CA 90024 USA.
[Scahill, Lawrence] Emory Univ, Dept Pediat, Atlanta, GA 30322 USA.
[Hollander, Eric] Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY USA.
[Bregman, Joel D.] Ctr Autism, Philadelphia, PA USA.
[Anagnostou, Evdokia] Univ Toronto, Dept Pediat, Toronto, ON M5S 1A1, Canada.
[Sullivan, Lisa] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA.
[Hirtz, Deborah] NINDS, Bethesda, MD 20892 USA.
RP King, BH (reprint author), Seattle Childrens Hosp, Dept Psychiat & Behav Med, 4800 Sand Point Way NE, Seattle, WA 98105 USA.
EM bhking@uw.edu
FU National Institute of Mental Health; Eunice Kennedy Shriver National
Institute of Child Health and Human Development; National Institute of
Neurological Disorders and Stroke; National Institute on Deafness and
Other Communication Disorders; National Institute of Environmental
Health Sciences via STAART Center contract Boston University/Dartmouth
[U54-MH066398]; National Institute of Environmental Health Sciences via
STAART Center contract DM-STAT, Inc [U01-HD045023]; National Institute
of Environmental Health Sciences via STAART Center contract Mount Sinai
[U54-MH066673]; National Institute of Environmental Health Sciences via
STAART Center contract UCLA [U54-MH068172]; National Institute of
Environmental Health Sciences via STAART Center contract University of
North Carolina [U54-MH066418]; National Institute of Environmental
Health Sciences via STAART Center contract Yale University
[U54-MH066494]
FX This work was funded by the National Institute of Mental Health, the
Eunice Kennedy Shriver National Institute of Child Health and Human
Development, the National Institute of Neurological Disorders and
Stroke, the National Institute on Deafness and Other Communication
Disorders, and the National Institute of Environmental Health Sciences
via the following STAART Center contracts: Boston University/Dartmouth
(U54-MH066398), Helen Tager-Flusberg, principal investigator (PI);
DM-STAT, Inc (U01-HD045023), Kimberly Dukes, PI; Mount Sinai
(U54-MH066673), Eric Hollander, PI; UCLA (U54-MH068172), Marian Sigman,
PI; University of North Carolina (U54-MH066418), Joseph Piven, PI; and
Yale University (U54-MH066494), Fred Volkmar, PI.
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NR 46
TC 3
Z9 3
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-6203
EI 2168-6211
J9 JAMA PEDIATR
JI JAMA Pediatr.
PD NOV
PY 2013
VL 167
IS 11
BP 1045
EP 1052
DI 10.1001/jamapediatrics.2013.2698
PG 8
WC Pediatrics
SC Pediatrics
GA 291PX
UT WOS:000329842300017
PM 24061784
ER
PT J
AU Millan, MJ
Bales, KL
AF Millan, Mark J.
Bales, Karen L.
TI Towards improved animal models for evaluating social cognition and its
disruption in schizophrenia: The CNTRICS initiative
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE Sociability; Social recognition; Emotion; Negative symptoms; Affective
behaviour; Psychosis; Antipsychotic; Oxytocin; Gaze; Eye-tracking;
Mouse; Rat; Non-human primate
ID AUTISM SPECTRUM DISORDERS; VOLES MICROTUS-OCHROGASTER; DOPAMINE D-3
RECEPTORS; TEMPORAL VISUAL AREA; INTRANASAL OXYTOCIN; NOVELTY
DISCRIMINATION; PARTNER PREFERENCE; RHESUS-MONKEYS; MOUSE MODELS;
EYE-TRACKING
AB Social cognition refers to processes used to monitor and interpret social signals from others, to decipher their state of mind, emotional status and intentions, and select appropriate social behaviour. Social cognition is sophisticated in humans, being embedded with verbal language and enacted in a complex cultural environment. Its disruption characterises the entire course of schizophrenia and is correlated with poor functional outcome. Further, deficits in social cognition are related to impairment in other cognitive domains, positive symptoms (paranoia and delusions) and negative symptoms (social withdrawal and reduced motivation). In light of the significance and inadequate management of social cognition deficits, there is a need for translatable experimental procedures for their study, and identification of effective pharmacotherapy. No single paradigm captures the multi-dimensional nature of social cognition, and procedures for assessing ability to infer mental states are not well-developed for experimental therapeutic settings. Accordingly, a recent CNTRICS meeting prioritised procedures for measuring a specific construct: "acquisition and recognition of affective (emotional) states", coupled to individual recognition. Two complementary paradigms for refinement were identified: social recognition/preference in rodents, and visual tracking of social scenes in non-human primates (NHPs). Social recognition is disrupted in genetic, developmental or pharmacological disease models for schizophrenia, and performance in both procedures is improved by the neuropeptide oxytocin. The present article surveys a broad range of procedures for studying social cognition in rodents and NHPs, discusses advantages and drawbacks, and focuses on development of social recognition/preference and gaze-following paradigms for improved study of social cognition deficits in schizophrenia and their potential treatment. (C) 2013 Elsevier Ltd. All rights reserved.
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[Bales, Karen L.] Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA.
RP Millan, MJ (reprint author), IDR Servier, Unit Res & Discovery Neurosci, 125 Chemin Ronde, F-78290 Croissy Sur Seine, France.
EM mark.millan@fr.netgrs.com; klbales@ucdavis.edu
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NR 214
TC 5
Z9 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
EI 1873-7528
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD NOV
PY 2013
VL 37
IS 9
BP 2166
EP 2180
DI 10.1016/j.neubiorev.2013.09.012
PN B
PG 15
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 292EC
UT WOS:000329884000008
PM 24090822
ER
PT J
AU Rustan, OG
Folsom, TD
Yousefi, MK
Fatemi, SH
AF Rustan, Oyvind G.
Folsom, Timothy D.
Yousefi, Mahtab K.
Fatemi, S. Hossein
TI Phosphorylated fragile X mental retardation protein at serine 499, is
reduced in cerebellar vermis and superior frontal cortex of subjects
with autism: implications for fragile X mental retardation
protein-metabotropic glutamate receptor 5 signaling
SO MOLECULAR AUTISM
LA English
DT Letter
DE mGluR5; FMRP; Cerebellar vermis; Superior frontal cortex;
Phosphorylation of FMRP
ID TRANSLATION; POSTMORTEM; FMRP
AB Lohith et al. (Mol Autism 4: 15, 2013) recently identified increased metabotropic glutamate receptor 5 (mGluR5) expression in the frontal cortex (FC) of subjects with fragile X syndrome. These results are consistent with postmortem findings in cerebellar vermis and FC of subjects with autism (Fatemi and Folsom, Mol Autism 2: 6, 2011; Fatemi et al. Anat Rec 294: 1635-1645, 2011), suggesting that increased mGluR5 signaling is common to multiple autism spectrum disorders. Increased mGluR5 signaling may be associated with reduced phosphorylation of fragile X mental retardation protein (FMRP), which could result in the inactivation of this protein. In the current study, we report on reduced expression of phosphorylated FMRP in cerebellar vermis of adults and children with autism and in FC of adults with autism.
C1 [Rustan, Oyvind G.; Folsom, Timothy D.; Yousefi, Mahtab K.; Fatemi, S. Hossein] Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, Minneapolis, MN 55455 USA.
[Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Pharmacol, Minneapolis, MN 55455 USA.
[Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA.
RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Div Neurosci Res, Dept Psychiat, 420 Delaware St SE,MMC 392, Minneapolis, MN 55455 USA.
EM fatem002@umn.edu
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NR 9
TC 3
Z9 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD NOV 1
PY 2013
VL 4
AR 41
DI 10.1186/2040-2392-4-41
PG 3
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 291NL
UT WOS:000329835300001
PM 24180586
ER
PT J
AU Friedman, SH
Dani, N
Rushton, E
Broadie, K
AF Friedman, Samuel H.
Dani, Neil
Rushton, Emma
Broadie, Kendal
TI Fragile X mental retardation protein regulates trans-synaptic signaling
in Drosophila
SO DISEASE MODELS & MECHANISMS
LA English
DT Article
ID METABOTROPIC GLUTAMATE-RECEPTOR; HEPARAN-SULFATE PROTEOGLYCANS; WINGLESS
MORPHOGEN GRADIENT; ANAPLASTIC LYMPHOMA KINASE; DALLY-LIKE PROTEIN;
NEUROMUSCULAR-JUNCTION; MESSENGER-RNA; NERVOUS-SYSTEM; MATRIX
METALLOPROTEINASES; EXTRACELLULAR-MATRIX
AB Fragile X syndrome (FXS), the most common inherited determinant of intellectual disability and autism spectrum disorders, is caused by loss of the fragile X mental retardation 1 (FMR1) gene product (FMRP), an mRNA-binding translational repressor. A number of conserved FMRP targets have been identified in the well-characterized Drosophila FXS disease model, but FMRP is highly pleiotropic in function and the full spectrum of FMRP targets has yet to be revealed. In this study, screens for upregulated neural proteins in Drosophila fmr1 (dfmr1) null mutants reveal strong elevation of two synaptic heparan sulfate proteoglycans (HSPGs): GPI-anchored glypican Dally-like protein (Dip) and transmembrane Syndecan (Sdc). Our recent work has shown that Dlp and Sdc act as co-receptors regulating extracellular ligands upstream of intracellular signal transduction in multiple trans-synaptic pathways that drive synaptogenesis. Consistently, dfmr1 null synapses exhibit altered WNT signaling, with changes in both Wingless (Wg) ligand abundance and downstream Frizzled-2 (Fz2) receptor C-terminal nuclear import. Similarly, a parallel anterograde signaling ligand, Jelly belly (Jeb), and downstream ERK phosphorylation (dpERK) are depressed at dfmr1 null synapses. In contrast, the retrograde BMP ligand Glass bottom boat (Gbb) and downstream signaling via phosphorylation of the transcription factor MAD (pMAD) seem not to be affected. To determine whether HSPG upregulation is causative for synaptogenic defects, HSPGs were genetically reduced to control levels in the dfmr1 null background. HSPG correction restored both (1) Wg and Jeb trans-synaptic signaling, and (2) synaptic architecture and transmission strength back to wild-type levels. Taken together, these data suggest that FMRP negatively regulates HSPG co-receptors controlling trans-synaptic signaling during synaptogenesis, and that loss of this regulation causes synaptic structure and function defects characterizing the FXS disease state.
C1 [Friedman, Samuel H.; Dani, Neil; Rushton, Emma; Broadie, Kendal] Vanderbilt Univ, Dept Biol Sci, Kennedy Ctr Res Human Dev, Nashville, TN 37212 USA.
RP Broadie, K (reprint author), Vanderbilt Univ, Dept Biol Sci, Kennedy Ctr Res Human Dev, Nashville, TN 37212 USA.
EM kendal.broadie@vanderbilt.edu
FU FRAXA Research Foundation; National Institutes of Health [MH084989,
MH096832]
FX This work was supported by research grants to K.B. from the FRAXA
Research Foundation and National Institutes of Health (MH084989 and
MH096832).
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SN 1754-8403
EI 1754-8411
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD NOV
PY 2013
VL 6
IS 6
BP 1400
EP 1413
DI 10.1242/dmm.012229
PG 14
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 283VL
UT WOS:000329275000011
PM 24046358
ER
PT J
AU Wachtel, LE
Schuldt, S
Ghaziuddin, N
Shorter, E
AF Wachtel, L. E.
Schuldt, S.
Ghaziuddin, N.
Shorter, E.
TI The potential role of electroconvulsive therapy in the 'Iron Triangle'
of pediatric catatonia, autism, and psychosis
SO ACTA PSYCHIATRICA SCANDINAVICA
LA English
DT Letter
ID ECT
C1 [Wachtel, L. E.] Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD USA.
[Wachtel, L. E.] Johns Hopkins Univ, Sch Med, Dept Child & Adolescent Psychiat, Baltimore, MD USA.
[Schuldt, S.; Ghaziuddin, N.] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Shorter, E.] Univ Toronto, Fac Med, Hist Med Program, Toronto, ON, Canada.
RP Wachtel, LE (reprint author), Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD USA.
EM wachtel@kennedykrieger.org
CR Breese GR, 1995, MENT RETARD DEV D R, V1, P111, DOI 10.1002/mrdd.1410010207
Fink M, 2013, ACTA PSYCHIAT SCAND, V127, P1, DOI 10.1111/acps.12038
Shorter E, 2013, ACTA PSYCHIAT SCAND, V128, P21, DOI 10.1111/acps.12082
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NR 6
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0001-690X
EI 1600-0447
J9 ACTA PSYCHIAT SCAND
JI Acta Psychiatr. Scand.
PD NOV
PY 2013
VL 128
IS 5
BP 408
EP 409
DI 10.1111/acps.12158
PG 2
WC Psychiatry
SC Psychiatry
GA 282UE
UT WOS:000329198300011
PM 23773168
ER
PT J
AU Han, JC
Thurm, A
Williams, CG
Joseph, LA
Zein, WM
Brooks, BP
Butman, JA
Brady, SM
Fuhr, SR
Hicks, MD
Huey, AE
Hanish, AE
Danley, KM
Raygada, MJ
Rennert, OM
Martinowich, K
Sharp, SJ
Tsao, JW
Swedo, SE
AF Han, Joan C.
Thurm, Audrey
Williams, Christine Golden
Joseph, Lisa A.
Zein, Wadih M.
Brooks, Brian P.
Butman, John A.
Brady, Sheila M.
Fuhr, Shannon R.
Hicks, Melanie D.
Huey, Amanda E.
Hanish, Alyson E.
Danley, Kristen M.
Raygada, Margarita J.
Rennert, Owen M.
Martinowich, Keri
Sharp, Stephen J.
Tsao, Jack W.
Swedo, Susan E.
TI Association of brain-derived neurotrophic factor (BDNF)
haploinsufficiency with lower adaptive behaviour and reduced cognitive
functioning in WAGR/11p13 deletion syndrome
SO CORTEX
LA English
DT Article
DE Brain-derived neurotrophic factor; WAGR syndrome; 11p Deletion; IQ;
Autism
ID MESSENGER-RNA EXPRESSION; INTELLECTUAL DISABILITY; WAGR SYNDROME;
MENTAL-RETARDATION; VISUAL IMPAIRMENT; CHRONIC DISEASES; AUTISM;
CHILDREN; SPECTRUM; ADOLESCENTS
AB In animal studies, brain-derived neurotrophic factor (BDNF) is an important regulator of central nervous system development and synaptic plasticity. WAGR (Wilms tumour, Aniridia, Genitourinary anomalies, and mental Retardation) syndrome is caused by 11p13 deletions of variable size near the BDNF locus and can serve as a model for studying human BDNF haploinsufficiency (+/-). We hypothesized that BDNF+/- would be associated with more severe cognitive impairment in subjects with WAGR syndrome. Twenty-eight subjects with WAGR syndrome (6-28 years), 12 subjects with isolated aniridia due to PAX6 mutations/microdeletions (7-54 years), and 20 healthy controls (4-32 years) received neurocognitive assessments. Deletion boundaries for the subjects in the WAGR group were determined by high-resolution oligonucleotide array comparative genomic hybridization. Within the WAGR group, BDNF+/- subjects (n = 15), compared with BDNF intact (+/+) subjects (n = 13), had lower adaptive behaviour (p = .02), reduced cognitive functioning (p = .04), higher levels of reported historical (p = .02) and current (p = .02) social impairment, and higher percentage meeting cut-off score for autism (p = .047) on Autism Diagnostic Interview-Revised. These differences remained nominally significant after adjusting for visual acuity. Using diagnostic measures and clinical judgement, 3 subjects (2 BDNF+/- and 1 BDNF+/+) in the WAGR group (10.7%) were classified with autism spectrum disorder. A comparison group of visually impaired subjects with isolated aniridia had cognitive functioning comparable to that of healthy controls. In summary, among subjects with WAGR syndrome, BDNF+/- subjects had a mean Vineland Adaptive Behaviour Compose score that was 14-points lower and a mean intelligence quotient (IQ) that was 20-points lower than BDNF+/+ subjects. Our findings support the hypothesis that BDNF plays an important role in human neurocognitive development. Published by Elsevier Ltd.
C1 [Han, Joan C.; Fuhr, Shannon R.; Hicks, Melanie D.; Huey, Amanda E.; Hanish, Alyson E.; Danley, Kristen M.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, Unit Metab & Neuroendocrinol, NIH, Bethesda, MD USA.
[Han, Joan C.; Brady, Sheila M.] NICHD, Program Dev Endocrinol & Genet, Sect Growth & Obes, NIH, Bethesda, MD 20892 USA.
[Thurm, Audrey; Williams, Christine Golden; Joseph, Lisa A.; Swedo, Susan E.] NIH, Pediat & Dev Neurosci Branch, Bethesda, MD 20892 USA.
[Zein, Wadih M.] NEI, Ophthalm Genet & Visual Funct Branch, NIH, Bethesda, MD 20892 USA.
[Butman, John A.] NIH, Ctr Clin, Bethesda, MD 20892 USA.
[Hanish, Alyson E.] NINR, Div Intramural Res, NIH, Bethesda, MD 20892 USA.
[Raygada, Margarita J.; Rennert, Owen M.] NICHD, Sect Clin & Dev Genom, NIH, Bethesda, MD 20892 USA.
[Martinowich, Keri] Lieber Inst Brain Dev, Baltimore, MD USA.
[Sharp, Stephen J.; Tsao, Jack W.] Uniformed Serv Univ Hlth Sci, Dept Neurol, Bethesda, MD 20814 USA.
RP Han, JC (reprint author), NICHD, Unit Metab & Neuroendocrinol, NIH, 10 Ctr Dr,Bldg 10-CRC,Room 1-3330,MSC 1103, Bethesda, MD 20892 USA.
EM hanjo@mail.nih.gov
FU Intramural Research Programs of the Eunice Kennedy Shriller National
Institute of Child Health and Human Development [ZIAHD008898,
Z1AHD00641]; National Institute of Mental Health of the National
Institutes of Health (NIH) [ZIAMH002868]; NIH Bench-to-Bedside Program
FX This study was funded by the Intramural Research Programs of the Eunice
Kennedy Shriller National Institute of Child Health and Human
Development (ZIAHD008898 and Z1AHD00641) and the National Institute of
Mental Health (ZIAMH002868) of the National Institutes of Health (NIH),
and by the NIH Bench-to-Bedside Program. We thank the members of
International WAGR Syndrome Association for assistance in identifying
families who were willing to participate in this study. We thank Jack
Yanovski and Daniel Weinberger for helpful discussions. We thank
Margaret Pekar, Miriya Tune, Mark Lee, Matthew Tsang, Tanvee Singh,
Emily Yin, Jamila Grossman, and Rachel Kim for assistance with
psychological testing and administrative support. Disclaimer: the
opinions or assertions contained herein are the private views of the
authors and are not to be construed as official or as reflecting the
views of the Department of the Navy or the Department of Defense.
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NR 53
TC 2
Z9 2
PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 0010-9452
EI 1973-8102
J9 CORTEX
JI Cortex
PD NOV-DEC
PY 2013
VL 49
IS 10
BP 2700
EP 2710
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PG 11
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SC Behavioral Sciences; Neurosciences & Neurology
GA 282AM
UT WOS:000329142500011
PM 23517654
ER
PT J
AU Reed, CL
McIntosh, DN
AF Reed, Catherine L.
McIntosh, Daniel N.
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SO CORTEX
LA English
DT Editorial Material
ID EMOTIONAL FACIAL EXPRESSIONS; BODY PERCEPTION; MIMICRY; AUTISM
C1 [Reed, Catherine L.] Claremont Mckenna Coll, Claremont, CA 91711 USA.
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EM clreed@cmc.edu
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NR 15
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PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 0010-9452
EI 1973-8102
J9 CORTEX
JI Cortex
PD NOV-DEC
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VL 49
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BP 2960
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PG 2
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 282AM
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PM 23768764
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PT J
AU Williams, JHG
AF Williams, Justin H. G.
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LA English
DT Editorial Material
ID IMITATION; AUTISM; CORTEX
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TC 1
Z9 2
PU ELSEVIER MASSON
PI MILANO
PA VIA PALEOCAPA 7, 20121 MILANO, ITALY
SN 0010-9452
EI 1973-8102
J9 CORTEX
JI Cortex
PD NOV-DEC
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IS 10
BP 2962
EP 2963
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PG 2
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 282AM
UT WOS:000329142500041
PM 23830007
ER
PT J
AU van Kerkhof, LWM
Damsteegt, R
Trezza, V
Voorn, P
Vanderschuren, LJMJ
AF van Kerkhof, Linda W. M.
Damsteegt, Ruth
Trezza, Viviana
Voorn, Pieter
Vanderschuren, Louk J. M. J.
TI Functional integrity of the habenula is necessary for social play
behaviour in rats
SO EUROPEAN JOURNAL OF NEUROSCIENCE
LA English
DT Article
DE adolescence; c-fos; habenula; social behaviour; social isolation
ID VENTRAL TEGMENTAL AREA; MEDIAL PREFRONTAL CORTEX; IN-SITU HYBRIDIZATION;
LATERAL HABENULA; ADOLESCENT RATS; JUVENILE RATS; MESSENGER-RNA;
ELECTRICAL-STIMULATION; RATTUS-NORVEGICUS; FOS EXPRESSION
AB During post-weaning development, a marked increase in peer-peer interactions is observed in mammals, including humans, which is signified by the abundance of social play behaviour. Social play is highly rewarding, and known to be modulated through monoaminergic neurotransmission. Recently, the habenula has received widespread attention because of its role in the regulation of monoaminergic neurotransmission as well as in a variety of emotional and cognitive functions. Therefore, in the present study, we investigated the involvement of the habenula in social play behaviour. Using the neuronal activity maker c-fos, we showed that the habenula was activated after 24h of social isolation in adolescent rats, and that a subsequent social play interaction reduced c-fos activity in the medial part of the lateral habenula. This suggested that habenula activity modulated the aversive properties of social isolation, which was alleviated by the positive effects of social play. Furthermore, after functional inactivation of the habenula, using a mixture of the GABA receptor agonists baclofen and muscimol, social play behaviour was markedly reduced, whereby responsiveness to play solicitation was more sensitive to habenula inactivation than play solicitation itself. Together, our data indicate an important role for the habenula in the processing of positive (i.e. social play behaviour) and negative (i.e. social isolation) social information in adolescent rats. Altered habenula function might therefore be related to the social impairments in childhood and adolescent psychiatric disorders such as autism, attention deficit/hyperactivity disorder and early-onset schizophrenia.
C1 [van Kerkhof, Linda W. M.; Damsteegt, Ruth; Trezza, Viviana; Vanderschuren, Louk J. M. J.] Univ Med Ctr Utrecht, Dept Neurosci & Pharmacol, Brain Ctr Rudolf Magnus, Utrecht, Netherlands.
[Trezza, Viviana] Univ Roma Tre, Dept Sci, Sect Biomed Sci & Technol, Rome, Italy.
[Voorn, Pieter] Vrije Univ Amsterdam, Dept Anat & Neurosci, Med Ctr, Amsterdam, Netherlands.
[Vanderschuren, Louk J. M. J.] Univ Utrecht, Fac Vet Med, Dept Anim Sci & Soc, Div Behav Neurosci, NL-3584 CM Utrecht, Netherlands.
RP Vanderschuren, LJMJ (reprint author), Univ Med Ctr Utrecht, Dept Neurosci & Pharmacol, Brain Ctr Rudolf Magnus, Utrecht, Netherlands.
EM l.j.m.j.vanderschuren@uu.nl
FU National Institute on Drug Abuse [R01 DA022628]; Netherlands
Organization for Scientific Research (NWO) Veni [91611052]; Marie Curie
Career Reintegration [PCIG09-GA-2011-293589]
FX This work was supported by the National Institute on Drug Abuse (grant
R01 DA022628 to L.J.M.J.V.), Netherlands Organization for Scientific
Research (NWO) Veni (grant 91611052 to V. T.) and Marie Curie Career
Reintegration (grant PCIG09-GA-2011-293589 to V. T.). The authors have
no conflict of interest to disclose.
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NR 88
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-816X
EI 1460-9568
J9 EUR J NEUROSCI
JI Eur. J. Neurosci.
PD NOV
PY 2013
VL 38
IS 10
BP 3465
EP 3475
DI 10.1111/ejn.12353
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 253AM
UT WOS:000327054000008
PM 24103016
ER
PT J
AU Battaglia, A
Doccini, V
Bernardini, L
Novelli, A
Loddo, S
Capalbo, A
Filippi, T
Carey, JC
AF Battaglia, Agatino
Doccini, Viola
Bernardini, Laura
Novelli, Antonio
Loddo, Sara
Capalbo, Anna
Filippi, Tiziana
Carey, John C.
TI Confirmation of chromosomal microarray as a firsttier clinical
diagnostic test for individuals with developmental delay, intellectual
disability, autism spectrum disorders and dysmorphic features.
SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY
LA English
DT Article
DE Chromosomal microarray (CMA); Array-CGH; Developmental delay;
Intellectual disability; Neurodevelopmental disorders; Autism spectrum
disorders; Dysmorphic features
ID IDIOPATHIC MENTAL-RETARDATION; COMPARATIVE GENOMIC HYBRIDIZATION;
CONGENITAL-ANOMALIES; ETIOLOGIC YIELD; SINGLE-GENE; CHILD; STANDARDS;
COMPLEX; RAS; SON
AB Background and objectives: Submicroscopic chromosomal rearrangements are the most common identifiable causes of intellectual disability and autism spectrum disorders associated with dysmorphic features. Chromosomal microarray (CMA) can detect copy number variants <1 Mb and identifies size and presence of known genes. The aim of this study was to demonstrate the usefulness of CMA, as a first-tier tool in detecting the etiology of unexplained intellectual disability/autism spectrum disorders (ID/ASDs) associated with dysmorphic features in a large cohort of pediatric patients.
Patients and methods: We studied 349 individuals; 223 males, 126 females, aged 5 months-19 years. Blood samples were analyzed with CMA at a resolution ranging from 1 Mb to 40 Kb. The imbalance was confirmed by FISH or qPCR. We considered copy number variants (CNVs) causative if the variant was responsible for a known syndrome, encompassed gene/s of known function, occurred de novo or, if inherited, the parent was variably affected, and/or the involved gene/s had been reported in association with ID/ASDs in dedicated databases.
Results: 91 CNVs were detected in 77 (22.06%) patients: 5 (6.49%) of those presenting with borderline cognitive impairment, 54 (70.13%) with a variable degree of DD/ID, and 18/77 (23.38%) with ID of variable degree and ASDs. 16/77 (20.8%) patients had two different rearrangements. Deletions exceeded duplications (58 versus 33); 45.05% (41/91) of the detected CNVs were de novo, 45.05% (41/91) inherited, and 9.9% (9/91) unknown. The CNVs caused the phenotype in 57/77 (74%) patients; 12/57 (21.05%) had ASDs/ID, and 45/57 (78.95%) had DD/ID.
Conclusions: Our study provides further evidence of the high diagnostic yield of CMA for genetic testing in children with unexplained ID/ASDs who had dysmorphic features. We confirm the value of CMA as the first-tier tool in the assessment of those conditions in the pediatric setting. (C) 2013 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.
C1 [Battaglia, Agatino; Doccini, Viola; Filippi, Tiziana] Stella Maris Clin Res Inst Child & Adolescent Neu, I-56128 Pisa, Italy.
[Bernardini, Laura; Novelli, Antonio; Loddo, Sara; Capalbo, Anna] Casa Sollievo Sofferenza Hosp, IRCCS, Mendel Lab, San Giovanni Rotondo, FG, Italy.
[Carey, John C.] Univ Utah, Hlth Sci Ctr, Dept Pediat, Div Med Genet, Salt Lake City, UT USA.
RP Battaglia, A (reprint author), Stella Maris Clin Res Inst Child & Adolescent Neu, Via Giacinti 2, I-56128 Pisa, Italy.
EM agatino.battaglia@inpe.unipi.it
FU Italian Ministry of Health
FX This study was supported by grants from the Italian Ministry of Health
to AB and LB.
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NR 33
TC 13
Z9 13
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1090-3798
EI 1532-2130
J9 EUR J PAEDIATR NEURO
JI Eur. J. Paediatr. Neurol.
PD NOV
PY 2013
VL 17
IS 6
BP 589
EP 599
DI 10.1016/j.ejpn.2013.04.010
PG 11
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 277GM
UT WOS:000328807000010
PM 23711909
ER
PT J
AU Olsson, I
Danielsson, S
Hedstrom, A
Nordborg, C
Viggedal, G
Uvebrant, P
Rydenhag, B
AF Olsson, Ingrid
Danielsson, Susanna
Hedstrom, Anders
Nordborg, Claes
Viggedal, Gerd
Uvebrant, Paul
Rydenhag, Bertil
TI Epilepsy surgery in children with accompanying impairments
SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY
LA English
DT Article
DE Epilepsy surgery; Children; Learning disability; Cerebral palsy
ID DRUG-RESISTANT EPILEPSY; CORTICAL DYSPLASIA; SURGICAL-TREATMENT;
POPULATION; CHILDHOOD; OUTCOMES; PSYCHOPATHOLOGY; DISORDERS; SEIZURES;
AUTISM
AB The aim of this study was to assess seizure outcome 2 years after epilepsy surgery in a consecutive series of paediatric patients, with special focus on children with learning disabilities and other neuroimpairments in addition to the epilepsy.
Outcome 2 years after surgery was assessed in 110 of 125 children operated upon for drug resistant epilepsy in Gothenburg 1987-2006.
More than half of the children had learning disabilities, 43% motor impairments and 30% a neuropsychiatric diagnosis. Fifty-six per cent of those with an IQ < 70 became seizure-free or had a >75% reduction in seizure frequency, and two thirds if the operation was a resection. The corresponding figure in those with more than 100 seizures per month was 15 out of 31, and another seven had a 50-75% reduction in seizure frequency.
The message is that learning disability, motor impairment and psychiatric morbidity should not be contraindications for paediatric epilepsy surgery. More than half of the children with learning disabilities had a worthwhile seizure outcome, with even better results after resective surgery. Children with drug resistant epilepsy and additional severe neurological impairments should have the benefit of referral to a tertiary centre for evaluation for epilepsy surgery. (C) 2013 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.
C1 [Olsson, Ingrid; Viggedal, Gerd; Uvebrant, Paul] Gothenburg Univ, Sahlgrenska Acad, Inst Clin Sci, Dept Paediat, Gothenburg, Sweden.
[Danielsson, Susanna] Cty Hosp Ryhov, Jonkoping, Sweden.
[Hedstrom, Anders; Rydenhag, Bertil] Gothenburg Univ, Sahlgrenska Acad, Inst Neurosci & Physiol, Gothenburg, Sweden.
[Nordborg, Claes] Gothenburg Univ, Sahlgrenska Acad, Dept Pathol, S-41124 Gothenburg, Sweden.
RP Olsson, I (reprint author), Queen Silvia Childrens Hosp, Dept Paediat, S-41685 Gothenburg, Sweden.
EM ingrid.b.olsson@vgregion.se
FU Margarethahem Foundation; Sahlgrenska Academy at Gothenburg University
through the ALF agreement
FX The authors wish to thank epilepsy nurse and coordinator Birgitta
Olovson for the contribution of data. The work was funded by The
Margarethahem Foundation and the Sahlgrenska Academy at Gothenburg
University through the ALF agreement.
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NR 28
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1090-3798
EI 1532-2130
J9 EUR J PAEDIATR NEURO
JI Eur. J. Paediatr. Neurol.
PD NOV
PY 2013
VL 17
IS 6
BP 645
EP 650
DI 10.1016/j.ejpn.2013.06.004
PG 6
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 277GM
UT WOS:000328807000018
PM 23948291
ER
PT J
AU Dinwiddie, DL
Bracken, JM
Bass, JA
Christenson, K
Soden, SE
Saunders, CJ
Miller, NA
Singh, V
Zwick, DL
Roberts, CC
Dalal, J
Kingsmore, SF
AF Dinwiddie, Darrell L.
Bracken, Julia M.
Bass, Julie A.
Christenson, Kathy
Soden, Sarah E.
Saunders, Carol J.
Miller, Neil A.
Singh, Vivekanand
Zwick, David L.
Roberts, Charles C.
Dalal, Jignesh
Kingsmore, Stephen F.
TI Molecular diagnosis of infantile onset inflammatory bowel disease by
exome sequencing
SO GENOMICS
LA English
DT Article
DE Inflammatory bowel disease; Crohn's disease; IL10RA; IL10; Hematopoietic
stem cell transplantation; Colitis; Exome sequencing
ID DE-NOVO MUTATIONS; GENETIC-VARIATION; DISORDERS; RECEPTOR; STANDARDS;
VARIANTS; DATABASE; AUTISM
AB Pediatric-onset inflammatory bowel disease (IBD) is known to be associated with severe disease, poor response to therapy, and increased morbidity and mortality. We conducted exome sequencing of two brothers from a non-consanguineous relationship who presented before the age of one with severe infantile-onset IBD, failure to thrive, skin rash, and perirectal abscesses refractory to medical management. We examined the variants discovered in all known IBD-associated and primary immunodeficiency genes in both siblings. The siblings were identified to harbor compound heterozygous mutations in IL10RA (c.784C>T, p.Arg262Cys; c.349C>T, p.Arg117Cys). Upon molecular diagnosis, the proband underwent successful hematopoietic stem cell transplantation and demonstrated marked clinical improvement of all IBD-associated clinical symptoms. Exome sequencing can be an effective tool to aid in the molecular diagnosis of pediatric-onset IBD. We provide additional evidence of the safety and benefit of HSCT for patients with IBD due to mutations in the IL10RA gene. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Dinwiddie, Darrell L.; Soden, Sarah E.; Saunders, Carol J.; Miller, Neil A.; Kingsmore, Stephen F.] Childrens Mercy Hosp, Ctr Pediat Genom Med, Kansas City, MO 64108 USA.
[Dinwiddie, Darrell L.; Bracken, Julia M.; Bass, Julie A.; Christenson, Kathy; Soden, Sarah E.; Saunders, Carol J.; Miller, Neil A.; Roberts, Charles C.; Dalal, Jignesh; Kingsmore, Stephen F.] Childrens Mercy Hosp, Dept Pediat, Kansas City, MO 64108 USA.
[Dinwiddie, Darrell L.; Saunders, Carol J.; Singh, Vivekanand; Zwick, David L.; Kingsmore, Stephen F.] Childrens Mercy Hosp, Dept Pathol, Kansas City, MO 64108 USA.
[Dinwiddie, Darrell L.; Bracken, Julia M.; Bass, Julie A.; Soden, Sarah E.; Saunders, Carol J.; Singh, Vivekanand; Zwick, David L.; Roberts, Charles C.; Dalal, Jignesh; Kingsmore, Stephen F.] Univ Missouri, Sch Med, Kansas City, MO 64110 USA.
[Dalal, Jignesh] Childrens Mercy Hosp, Div Hematol Oncol, Kansas City, MO 64108 USA.
[Bracken, Julia M.; Bass, Julie A.; Christenson, Kathy; Roberts, Charles C.] Childrens Mercy Hosp, Div Pediat Gastroenterol, Kansas City, MO 64108 USA.
[Dinwiddie, Darrell L.] Univ New Mexico, Hlth Sci Ctr, Dept Pediat, Albuquerque, NM 87131 USA.
[Dinwiddie, Darrell L.] Univ New Mexico, Clin Translat Sci Ctr, Albuquerque, NM 87131 USA.
RP Dinwiddie, DL (reprint author), 1 Univ New Mexico, MSC08 4635, Albuquerque, NM 87131 USA.
EM dldinwiddie@salud.unm.edu; jmbracken@cmh.edu; jabass@cmh.edu;
kchristenson@cmh.edu; ssoden@cmh.edu; csaunders@cmh.edu;
nmiller@cmh.edu; vsingh@cmh.edu; dzwick@cmh.edu; croberts@cmh.edu;
jddalal@cmh.edu; sfkingsmore@cmh.edu
FU Marion Merrell Dow Foundation; Patton Trust; WT Kemper Foundation;
Children's Mercy Hospital
FX This work was funded by the Marion Merrell Dow Foundation, the Patton
Trust, the WT Kemper Foundation and Children's Mercy Hospital.
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NR 35
TC 6
Z9 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0888-7543
EI 1089-8646
J9 GENOMICS
JI Genomics
PD NOV-DEC
PY 2013
VL 102
IS 5-6
BP 442
EP 447
DI 10.1016/j.ygeno.2013.08.008
PG 6
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 278UE
UT WOS:000328914500002
PM 24001973
ER
PT J
AU Hall, SS
Jiang, HD
Reiss, AL
Greicius, MD
AF Hall, Scott S.
Jiang, Heidi
Reiss, Allan L.
Greicius, Michael D.
TI Identifying Large-Scale Brain Networks in Fragile X Syndrome
SO JAMA PSYCHIATRY
LA English
DT Article
ID MENTAL-RETARDATION PROTEIN; DEFAULT-MODE NETWORK; IDIOPATHIC AUTISM;
INSULAR CORTEX; BEHAVIOR; FMRI; IDENTIFICATION; LOCALIZATION;
CONNECTIVITY; MORPHOMETRY
AB IMPORTANCE Fragile X syndrome (FXS) is an X-linked neurogenetic disorder characterized by a cognitive and behavioral phenotype resembling features of autism spectrum disorder. Until now, research has focused largely on identifying regional differences in brain structure and function between individuals with FXS and various control groups. Very little is known about the large-scale brain networks that may underlie the cognitive and behavioral symptoms of FXS.
OBJECTIVE To identify large-scale, resting-state networks in FXS that differ from control individuals matched on age, IQ, and severity of behavioral and cognitive symptoms.
DESIGN, SETTING, AND PARTICIPANTS Cross-sectional, in vivo neuroimaging study conducted in an academic medical center. Participants (aged 10-23 years) included 17 males and females with FXS and 16 males and females serving as controls.
MAIN OUTCOMES AND MEASURES Univariate voxel-based morphometric analyses, fractional amplitude of low-frequency fluctuations (fALFF) analysis, and group-independent component analysis with dual regression.
RESULTS Patients with FXS showed decreased functional connectivity in the salience, precuneus, left executive control, language, and visuospatial networks compared with controls. Decreased fALFF in the bilateral insular, precuneus, and anterior cingulate cortices also was found in patients with FXS compared with control participants. Furthermore, fALFF in the left insular cortex was significantly positively correlated with IQ in patients with FXS. Decreased gray matter density, resting-state connectivity, and fALFF converged in the left insular cortex in patients with FXS.
CONCLUSIONS AND RELEVANCE Fragile X syndrome results in widespread reductions in functional connectivity across multiple cognitive and affective brain networks. Converging structural and functional abnormalities in the left insular cortex, a region also implicated in individuals diagnosed with autism spectrum disorder, suggests that insula integrity and connectivity may be compromised in FXS. This method could prove useful in establishing an imaging biomarker for FXS.
C1 [Hall, Scott S.; Reiss, Allan L.] Stanford Univ, Ctr Interdisciplinary Brain Sci Res, Dept Psychiat & Behav Sci, Sch Med, Stanford, CA 94305 USA.
[Jiang, Heidi; Greicius, Michael D.] Stanford Univ, Funct Imaging Neuropsychiat Disorders Lab, Dept Neurol & Neurol Sci, Sch Med, Stanford, CA 94305 USA.
[Reiss, Allan L.] Stanford Univ, Sch Med, Dept Radiol, Stanford, CA 94305 USA.
[Reiss, Allan L.] Stanford Univ, Sch Med, Dept Pediat, Stanford, CA 94305 USA.
[Reiss, Allan L.] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA.
RP Hall, SS (reprint author), Stanford Univ, Ctr Interdisciplinary Brain Sci Res, Dept Psychiat & Behav Sci, Room 1365,401 Quarry Rd, Stanford, CA 94305 USA.
EM hallss@stanford.edu
FU National Institutes of Health [K08MH081998, MH064708, NS073498]
FX This study was funded by grants K08MH081998 (Dr Hall), MH064708 (Dr
Reiss), and NS073498 (Dr Greicius) from the National Institutes of
Health.
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NR 53
TC 5
Z9 6
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD NOV
PY 2013
VL 70
IS 11
BP 1215
EP 1223
DI 10.1001/jamapsychiatry.2013.247
PG 9
WC Psychiatry
SC Psychiatry
GA 279GP
UT WOS:000328948700014
PM 24068330
ER
PT J
AU D'Onofrio, BM
Class, QA
Rickert, ME
Larsson, H
Langstrom, N
Lichtenstein, P
AF D'Onofrio, Brian M.
Class, Quetzal A.
Rickert, Martin E.
Larsson, Henrik
Langstrom, Niklas
Lichtenstein, Paul
TI Preterm Birth and Mortality and Morbidity A Population-Based
Quasi-experimental Study
SO JAMA PSYCHIATRY
LA English
DT Article
ID SWEDISH NATIONAL COHORT; MATERNAL SMOKING; RISK-FACTORS;
GESTATIONAL-AGE; SOCIOECONOMIC ACHIEVEMENTS; PSYCHIATRIC-DISORDER;
BEHAVIORAL OUTCOMES; BIPOLAR DISORDER; INDIVIDUALS BORN; YOUNG ADULTHOOD
AB IMPORTANCE Preterm birth is associated with increased mortality and morbidity. However, previous studies have been unable to rigorously examine whether confounding factors cause these associations rather than the harmful effects of being born preterm.
OBJECTIVE To estimate the extent to which the associations between early gestational age and offspring mortality and morbidity are the result of confounding factors by using a quasi-experimental design, the sibling-comparison approach, and by controlling for statistical covariates that varied within families.
DESIGN, SETTING, AND PARTICIPANTS A population-based cohort study, combining Swedish registries to identify all individuals born in Sweden from 1973 to 2008 (3 300 708 offspring of 1 736 735 mothers) and link them with multiple outcomes.
MAIN OUTCOMES AND MEASURES Offspring mortality (during infancy and throughout young adulthood) and psychiatric (psychotic or bipolar disorder, autism, attention-deficit/hyperactivity disorder, suicide attempts, substance use, and criminality), academic (failing grades and educational attainment), and social (partnering, parenthood, low income, and social welfare benefits) outcomes through 2009.
RESULTS In the population, there was a dose-response relationship between early gestation and the outcome measures. For example, extreme preterm birth (23-27 weeks of gestation) was associated with infant mortality (odds ratio, 288.1; 95% CI, 271.7-305.5), autism (hazard ratio [HR], 3.2; 95% CI, 2.6-4.0), low educational attainment (HR, 1.7; 1.5-2.0), and social welfare benefits (HR, 1.3; 1.2-1.5) compared with offspring born at term. The associations between early gestation and mortality and psychiatric morbidity generally were robust when comparing differentially exposed siblings and controlling for statistical covariates, whereas the associations with academic and some social problems were greatly or completely attenuated in the fixed-effects models.
CONCLUSIONS AND RELEVANCE The mechanisms responsible for the associations between preterm birth and mortality and morbidity are outcome-specific. Associations between preterm birth and mortality and psychiatric morbidity are largely independent of shared familial confounds and measured covariates, consistent with a causal inference. However, some associations, particularly predicting suicide attempt, educational attainment, and social welfare benefits, are the result of confounding factors. The findings emphasize the importance of both reducing preterm birth and providing wraparound services to all siblings in families with an offspring born preterm.
C1 [D'Onofrio, Brian M.; Class, Quetzal A.; Rickert, Martin E.] Indiana Univ, Dept Psychol & Brain Sci, Bloomington, IN 47405 USA.
[Larsson, Henrik; Langstrom, Niklas; Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
RP D'Onofrio, BM (reprint author), Indiana Univ, Dept Psychol & Brain Sci, 1101 E 10th St, Bloomington, IN 47405 USA.
EM bmdonofr@indiana.edu
FU National Institute of Child Health and Human Development [HD061817];
National Institute of Mental Health [MH094011]; Swedish Research Council
(Medicine); Swedish Prison and Probation Services
FX The study was supported by grant HD061817 from the National Institute of
Child Health and Human Development, grant MH094011 from the National
Institute of Mental Health), the Swedish Research Council (Medicine),
and the Swedish Prison and Probation Services.
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NR 56
TC 14
Z9 14
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 2168-622X
EI 2168-6238
J9 JAMA PSYCHIAT
JI JAMA Psychiatry
PD NOV
PY 2013
VL 70
IS 11
BP 1231
EP 1240
DI 10.1001/jamapsychiatry.2013.2107
PG 10
WC Psychiatry
SC Psychiatry
GA 279GP
UT WOS:000328948700016
PM 24068297
ER
PT J
AU Lind, SE
Williams, DM
Raber, J
Peel, A
Bowler, DM
AF Lind, Sophie E.
Williams, David M.
Raber, Jacob
Peel, Anna
Bowler, Dermot M.
TI Spatial Navigation Impairments Among Intellectually High-Functioning
Adults With Autism Spectrum Disorder: Exploring Relations With Theory of
Mind, Episodic Memory, and Episodic Future Thinking
SO JOURNAL OF ABNORMAL PSYCHOLOGY
LA English
DT Article
DE autism spectrum disorder; episodic memory; episodic future thinking;
spatial navigation; theory of mind
ID ASPERGER-SYNDROME; SEX-DIFFERENCES; ANIMATED SHAPES; COGNITIVE MAPS;
MENTAL STATES; KNOWLEDGE; BRAIN; CHILDREN; ABILITY; HUMANS
AB Research suggests that spatial navigation relies on the same neural network as episodic memory, episodic future thinking, and theory of mind (ToM). Such findings have stimulated theories (e. g., the scene construction and self-projection hypotheses) concerning possible common underlying cognitive capacities. Consistent with such theories, autism spectrum disorder (ASD) is characterized by concurrent impairments in episodic memory, episodic future thinking, and ToM. However, it is currently unclear whether spatial navigation is also impaired. Hence, ASD provides a test case for the scene construction and self-projection theories. The study of spatial navigation in ASD also provides a test of the extreme male brain theory of ASD, which predicts intact or superior navigation (purportedly a systemizing skill) performance among individuals with ASD. Thus, the aim of the current study was to establish whether spatial navigation in ASD is impaired, intact, or superior. Twenty-seven intellectually high-functioning adults with ASD and 28 sex-, age-, and IQ-matched neurotypical comparison adults completed the memory island virtual navigation task. Tests of episodic memory, episodic future thinking, and ToM were also completed. Participants with ASD showed significantly diminished performance on the memory island task, and performance was positively related to ToM and episodic memory, but not episodic future thinking. These results suggest that (contra the extreme male brain theory) individuals with ASD have impaired survey-based navigation skills-that is, difficulties generating cognitive maps of the environment-and adds weight to the idea that scene construction/self-projection are impaired in ASD. The theoretical and clinical implications of these results are discussed.
C1 [Lind, Sophie E.; Williams, David M.; Peel, Anna] Univ Durham, Dept Psychol, Durham DH1 3HP, England.
[Raber, Jacob] Oregon Hlth & Sci Univ, Dept Behav Neurosci, Portland, OR 97201 USA.
[Raber, Jacob] Oregon Hlth & Sci Univ, Dept Neurol, Portland, OR 97201 USA.
[Bowler, Dermot M.] City Univ London, Dept Psychol, London EC1R 0JD, England.
RP Lind, SE (reprint author), City Univ London, Dept Psychol, Whiskin St, London EC1R 0JD, England.
EM Sophie.lind.2@city.ac.uk
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NR 44
TC 4
Z9 4
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0021-843X
EI 1939-1846
J9 J ABNORM PSYCHOL
JI J. Abnorm. Psychol.
PD NOV
PY 2013
VL 122
IS 4
BP 1189
EP 1199
DI 10.1037/a0034819
PG 11
WC Psychology, Clinical; Psychology, Multidisciplinary
SC Psychology
GA 280PU
UT WOS:000329044000025
PM 24364620
ER
PT J
AU Rhodes, G
Jeffery, L
Taylor, L
Ewing, L
AF Rhodes, Gillian
Jeffery, Linda
Taylor, Libby
Ewing, Louise
TI Autistic traits are linked to reduced adaptive coding of face identity
and selectively poorer face recognition in men but not women
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Autistic traits; Broader autism phenotype; Face recognition; Face
identity aftereffects; Individual differences
ID SPECTRUM QUOTIENT AQ; MEMORY TEST; INDIVIDUAL-DIFFERENCES; ENDOPHENOTYPE
CONCEPT; CHILDREN; PHENOTYPE; ABILITY; POPULATION; ADAPTATION;
PERCEPTION
AB Our ability to discriminate and recognize thousands of faces despite their similarity as visual patterns relies on adaptive, norm-based, coding mechanisms that are continuously updated by experience. Reduced adaptive coding of face identity has been proposed as a neurocognitive endophenotype for autism, because it is found in autism and in relatives of individuals with autism. Autistic traits can also extend continuously into the general population, raising the possibility that reduced adaptive coding of face identity may be more generally associated with autistic traits. In the present study, we investigated whether adaptive coding of face identity decreases as autistic traits increase in an undergraduate population. Adaptive coding was measured using face identity aftereffects, and autistic traits were measured using the Autism-Spectrum Quotient (AQ) and its subscales. We also measured face and car recognition ability to determine whether autistic traits are selectively related to face recognition difficulties. We found that men who scored higher on levels of autistic traits related to social interaction had reduced adaptive coding of face identity. This result is consistent with the idea that atypical adaptive face-coding mechanisms are an endophenotype for autism. Autistic traits were also linked with face-selective recognition difficulties in men. However, there were some unexpected sex differences. In women, autistic traits were linked positively, rather than negatively, with adaptive coding of identity, and were unrelated to face-selective recognition difficulties. These sex differences indicate that autistic traits can have different neurocognitive correlates in men and women and raise the intriguing possibility that endophenotypes of autism can differ in males and females. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Rhodes, Gillian; Jeffery, Linda; Taylor, Libby; Ewing, Louise] Univ Western Australia, Sch Psychol, ARC Ctr Excellence Cognit & Its Disorders, Crawley, WA 6009, Australia.
RP Rhodes, G (reprint author), Univ Western Australia, Sch Psychol, ARC Ctr Excellence Cognit & Its Disorders, 35 Stirling Highway, Crawley, WA 6009, Australia.
EM gillian.rhodes@uwa.edu.au
RI Ewing, Louise/H-9158-2014
FU Australian Research Council Centre of Excellence [CE110001021]; ARC
Professorial Fellowship [DP0877379]; ARC Discovery Outstanding
Researcher Award [DP130102300]
FX This research was supported by the Australian Research Council Centre of
Excellence in Cognition and its Disorders (CE110001021), an ARC
Professorial Fellowship to Rhodes (DP0877379) and an ARC Discovery
Outstanding Researcher Award to Rhodes (DP130102300). We thank Mayu
Nishimura and Daphne Maurer for co-creating the Robbers Game used in the
Identity Aftereffects task and Ainsley Read for assistance with testing.
Ethical approval was granted by the Human Research Ethics Committee of
the University of Western Australia.
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NR 50
TC 6
Z9 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
EI 1873-3514
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD NOV
PY 2013
VL 51
IS 13
BP 2702
EP 2708
DI 10.1016/Lneuropsychologia.2013.08.016
PG 7
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 278DN
UT WOS:000328869400023
PM 23994355
ER
PT J
AU Bagni, C
Oostra, BA
AF Bagni, Claudia
Oostra, Ben A.
TI Fragile X Syndrome: From Protein Function to Therapy
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Review
DE fragile X syndrome; FMR1; FMRP; intellectual disability; treatment;
review; Fmr1 KO mouse; protein function
ID MENTAL-RETARDATION PROTEIN; LONG-TERM DEPRESSION; FMR1 KNOCKOUT MICE;
MESSENGER-RNA LOCALIZATION; PRIMARY SOMATOSENSORY CORTEX; MOUSE MODEL;
SYNAPTIC PLASTICITY; GABA(A) RECEPTOR; DENDRITIC SPINES; BINDING PROTEIN
AB Fragile X syndrome (FXS) is the leading monogenic cause of intellectual disability and autism. The FMR1 gene contains a CGG repeat present in the 5-untranslated region which can be unstable upon transmission to the next generation. The repeat is up to 55 CGGs long in the normal population. In patients with fragile X syndrome (FXS), a repeat length exceeding 200 CGGs generally leads to methylation of the repeat and the promoter region, which is accompanied by silencing of the FMR1 gene. The disease is a result of lack of expression of the fragile X mental retardation protein leading to severe symptoms, including intellectual disability, hyperactivity, and autistic-like behavior. The FMR1 protein (FMRP) has a number of functions. The translational dysregulation of a subset of mRNAs targeted by FMRP is probably the major contribution to FXS. FMRP is also involved in mRNA transport to synapses where protein synthesis occurs. For some FMRP-bound mRNAs, FMRP is a direct modulator of mRNA stability either by sustaining or preventing mRNA decay. Increased knowledge about the role of FMRP has led to the identification of potential treatments for fragile X syndrome that were often tested first in the different animal models. This review gives an overview about the present knowledge of the function of FMRP and the therapeutic strategies in mouse and man. (c) 2013 Wiley Periodicals, Inc.
C1 [Bagni, Claudia] Catholic Univ Louvain, VIB Ctr Biol Dis, B-3000 Louvain, Belgium.
[Bagni, Claudia] Univ Rome, Dept Biomed & Prevent, Tor Vergata, Italy.
[Oostra, Ben A.] Erasmus MC, Dept Clin Genet, NL-3000 CA Rotterdam, Netherlands.
RP Oostra, BA (reprint author), Erasmus MC, Dept Clin Genet, POB 2040, NL-3000 CA Rotterdam, Netherlands.
EM b.oostra@erasmusmc.nl
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NR 179
TC 9
Z9 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2013
VL 161
IS 11
SI SI
BP 2809
EP 2821
DI 10.1002/ajmg.a.36241
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 267ZP
UT WOS:000328137500018
PM 24115651
ER
PT J
AU De Wolf, V
Brison, N
Devriendt, K
Peeters, H
AF De Wolf, Veerle
Brison, Nathalie
Devriendt, Koenraad
Peeters, Hilde
TI Genetic Counseling for Susceptibility Loci and Neurodevelopmental
Disorders: The del15q11.2 as an Example
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Review
DE genetic counseling; del15q11; 2; neurodevelopmental disorders;
susceptibility locus
ID HEREDITARY SPASTIC PARAPLEGIA; PRADER-WILLI-SYNDROME; COPY-NUMBER
VARIANTS; DE-NOVO MUTATIONS; VARIABLE EXPRESSIVITY; MENTAL-RETARDATION;
NIPA1 GENE; RECURRENT MICRODELETIONS; INTELLECTUAL DISABILITY;
DEVELOPMENTAL DELAY
AB In recent years, several recurrent copy number variations (CNVs) that confer risk of neurodevelopmental disorders have been identified (e.g., del and dup 16p11.2, del15q13.3, del and dup 1q21.1, del16p13.3, del15q11.2). They are often inherited from an unaffected parent and lack phenotypic specificity. Although there is growing evidence from association studies to consider them as susceptibility CNVs, their clinical utility is debated. Yet the clinician is frequently challenged to deal with these counseling situations without guidelines or consensus. In this report, counseling issues and research opportunities are discussed, with the recurrent 15q11.2 BP1-BP2 (including CYFIP1, NIPA1, NIPA2, TUBGCP5) as an example. Several clinical reports have been published describing patients with del15q11.2 featuring intellectual disability, developmental delay, neurological problems, autism spectrum disorder (ASD), attention problems, speech delay, and dysmorphism. The del15q11.2 was found to be significantly associated with intellectual disability, schizophrenia, epilepsy, and ASD. In this report we discuss how patient-specific and family-specific information may alter the interpretation of del15q11.2 as a contributing factor to the disorder in practical counseling situations. In addition, an association study for ASD in a Belgian Flemish cohort and an overview of reported association studies, clinical reports and genomics data for del15q11.2 are presented. (c) 2013 Wiley Periodicals, Inc.
C1 [De Wolf, Veerle; Brison, Nathalie; Devriendt, Koenraad; Peeters, Hilde] Katholieke Univ Leuven, Ctr Human Genet, Univ Hosp Leuven, Louvain, Belgium.
RP Peeters, H (reprint author), Univ Louvain, Ctr Human Genet, Herestr 49, B-3000 Louvain, Belgium.
EM hilde.peeters@med.kuleuven.be
FU Concerted Research Actions KULeuven [GOA/12/015]; Foundation
"Marguerite-Marie Delacroix"; Scientific Research-Flanders FWO Belgium;
Clinical Research Foundation of UZ Leuven [IWT-O&O-100629-Cartagenia];
Belgian government Interuniversitary Attraction Poles programme;
Foundation Jerome Lejeune
FX Grant sponsors: Concerted Research Actions KULeuven (GOA/12/015);
Foundation "Marguerite-Marie Delacroix"; Foundation Jerome Lejeune;
Scientific Research-Flanders FWO Belgium; Clinical Research Foundation
of UZ Leuven. IWT-O&O-100629-Cartagenia; Belgian government
Interuniversitary Attraction Poles programme.
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NR 46
TC 3
Z9 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2013
VL 161
IS 11
SI SI
BP 2846
EP 2854
DI 10.1002/ajmg.a.36209
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 267ZP
UT WOS:000328137500021
PM 24123946
ER
PT J
AU Roman, GC
Ghassabian, A
Bongers-Schokking, JJ
Jaddoe, VWV
Hofman, A
de Rijke, YB
Verhulst, FC
Tiemeier, H
AF Roman, Gustavo C.
Ghassabian, Akhgar
Bongers-Schokking, Jacoba J.
Jaddoe, Vincent W. V.
Hofman, Albert
de Rijke, Yolanda B.
Verhulst, Frank C.
Tiemeier, Henning
TI Association of Gestational Maternal Hypothyroxinemia and Increased
Autism Risk
SO ANNALS OF NEUROLOGY
LA English
DT Article
ID FETAL-BRAIN DEVELOPMENT; GENERATION-R; THYROID-FUNCTION;
EARLY-PREGNANCY; NEUROPSYCHOLOGICAL DEVELOPMENT; COMPREHENSIVE
METAANALYSIS; BEHAVIORAL-PROBLEMS; SPECTRUM DISORDER; CHILDREN; REELIN
AB ObjectiveTransient gestational hypothyroxinemia in rodents induces cortical neuronal migration brain lesions resembling those of autism. We investigated the association between maternal hypothyroxinemia (gestational weeks 6-18) and autistic symptoms in children.
MethodsThe mother-and-child cohort of the Generation R Study (Rotterdam, the Netherlands) began prenatal enrollment between 2002 and 2006. At a mean gestational age of 13.4 weeks (standard deviation = 1.9, range = 5.9-17.9), maternal thyroid function tests (serum thyrotropin [TSH], free thyroxine [fT(4)], and thyroid peroxidase [TPO] antibodies) were assessed in 5,100 women. We defined severe maternal hypothyroxinemia as fT(4) < 5th percentile with normal TSH. Six years later, parents reported behavioral and emotional symptoms in 4,039 children (79%) using the Pervasive Developmental Problems (PDP) subscale of the Child Behavior Checklist and/or the Social Responsiveness Scale (SRS). We defined a probable autistic child by a PDP score > 98th percentile and SRS score in the top 5% of the sample (n = 81, 2.0%).
ResultsSevere maternal hypothyroxinemia (n = 136) was associated with an almost 4-fold increase in the odds of having a probable autistic child (adjusted odds ratio = 3.89, 95% confidence interval [CI] = 1.83-8.20, p < 0.001). Using PDP scores, children of mothers with severe hypothyroxinemia had higher scores of autistic symptoms by age 6 years (adjusted B = 0.23, 95% CI = 0.03-0.37); SRS results were similar. No risk was found for children of TPO-antibody-positive mothers (n = 308).
InterpretationWe found a consistent association between severe, early gestation maternal hypothyroxinemia and autistic symptoms in offspring. Findings are concordant with epidemiological, biological, and experimental data on autism. Although these findings cannot establish causality, they open the possibility of preventive interventions. Ann Neurol 2013;74:733-742
C1 [Roman, Gustavo C.] Methodist Neurol Inst, Houston, TX 77030 USA.
[Roman, Gustavo C.] Weill Cornell Med Coll, Dept Neurol, New York, NY USA.
[Ghassabian, Akhgar; Jaddoe, Vincent W. V.; Hofman, Albert] Generat R Study Grp, Rotterdam, Netherlands.
[Ghassabian, Akhgar; Verhulst, Frank C.; Tiemeier, Henning] Erasmus Univ, Dept Child & Adolescent Psychiat, Med Ctr, Rotterdam, Netherlands.
[Bongers-Schokking, Jacoba J.; Jaddoe, Vincent W. V.; Hofman, Albert; Tiemeier, Henning] Erasmus Univ, Dept Epidemiol, Med Ctr, Rotterdam, Netherlands.
[Bongers-Schokking, Jacoba J.] Erasmus Univ, Dept Endocrinol, Med Ctr, Rotterdam, Netherlands.
[Jaddoe, Vincent W. V.] Erasmus Univ, Dept Pediat, Med Ctr, Rotterdam, Netherlands.
[de Rijke, Yolanda B.] Erasmus Univ, Dept Internal Med, Med Ctr, Rotterdam, Netherlands.
[de Rijke, Yolanda B.] Erasmus Univ, Dept Clin Chem, Med Ctr, Rotterdam, Netherlands.
[Tiemeier, Henning] Erasmus Univ, Dept Psychiat, Med Ctr, Rotterdam, Netherlands.
RP Roman, GC (reprint author), Methodist Neurol Inst, 6560 Fannin St,Suite 802, Houston, TX 77030 USA.
EM GCRoman@tmhs.org
FU Nancy Lurie Marks Family Foundation, Wellesley, Massachusetts; European
Community [212652]; Erasmus University Trust Fund; Janivo Foundation;
Merck-Serono; Dutch Research Council; Ministry of Family Affairs (the
Netherlands)
FX The work of G.C.R. is supported by a grant from the Nancy Lurie Marks
Family Foundation, Wellesley, Massachusetts. The work of H.T. and A.G.
was supported by a research grant from the European Community's 7th
Framework Program (FP7/2008-2013) under grant agreement 212652
(Nutrimenthe project, "The Effect of Diet on the Mental Performance of
Children"). Measurements of thyroid parameters have been made possible
by Ortho Clinical Diagnostics, Jan Dekker/Ludgardine Bouwman Foundation,
Fa. Merck, and Foundation Zeist. Funding was also received from the
Erasmus University Trust Fund, Janivo Foundation, Merck-Serono, Dutch
Research Council, and Ministry of Family Affairs (the Netherlands).
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PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD NOV
PY 2013
VL 74
IS 5
BP 733
EP 742
DI 10.1002/ana.23976
PG 10
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 273NX
UT WOS:000328543200013
PM 23943579
ER
PT J
AU Johnson, RA
Barrett, MS
Sisti, DA
AF Johnson, Rebecca A.
Barrett, Marna S.
Sisti, Dominic A.
TI The Ethical Boundaries of Patient and Advocate Influence on DSM-5
SO HARVARD REVIEW OF PSYCHIATRY
LA English
DT Article
DE Diagnostic and Statistical Manual of Mental Disorders; ethics; mental
disorders; patient advocacy; social stigma
ID PSYCHOSIS RISK SYNDROME; MENTAL-ILLNESS; DIAGNOSTIC-CRITERIA;
DECISION-MAKING; UNITED-STATES; HEALTH; DISORDER; HEBEPHILIA; POLICY;
CLASSIFICATION
AB This article discusses the relationship between disease-advocacy groups and the revision process for the Diagnostic and Statistical Manual of Mental Disorders. We discuss three examples in which patient-advocacy groups engaged with the DSM-5 revision process: Autism Speaks' worries about the contraction of the autism diagnostic category, the National Alliance on Mental Illness's support for the inclusion of psychosis risk syndrome, and B4U-ACT's critique of the expansion of pedophilia. After a descriptive examination of the cases, we address two prescriptive questions. First, what is the ethical basis for patient and advocate influence on DSM diagnoses? Second, how should the American Psychiatric Association proceed when this influence comes into conflict with other goals of the revision process? We argue that the social effects of, and values embedded in, psychiatric classification, combined with patient and advocates' experiential knowledge about those aspects of diagnosis, ethically justify advocate influence in relation to those particular matters. However, this advocate influence ought to have limits, which we briefly explore. Our discussion has implications for discussions of disease categories as loci for social movements, for analyses of the expanding range of processes and institutions that advocacy groups target, and for broader questions regarding the aims of the DSM revision process.
C1 [Johnson, Rebecca A.] Univ Penn, Perelman Sch Med, Dept Bioeth, NIH, Philadelphia, PA 19104 USA.
[Johnson, Rebecca A.; Sisti, Dominic A.] Univ Penn, Perelman Sch Med, Scattergood Program Appl Eth Behav Healthcare, Dept Med Eth & Hlth Policy, Philadelphia, PA 19104 USA.
[Barrett, Marna S.] Univ Penn, Perelman Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA.
RP Johnson, RA (reprint author), 10 Ctr Dr,Rm 1C118, Bethesda, MD 20892 USA.
EM BJohnson88@gmail.com
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NR 68
TC 2
Z9 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1067-3229
EI 1465-7309
J9 HARVARD REV PSYCHIAT
JI Harv. Rev. Psychiatr.
PD NOV-DEC
PY 2013
VL 21
IS 6
BP 334
EP 344
DI 10.1097/HRP.0000000000000010
PG 11
WC Psychiatry
SC Psychiatry
GA 273BE
UT WOS:000328507000004
PM 24201823
ER
PT J
AU Susser, E
St Clair, D
AF Susser, Ezra
St Clair, David
TI Prenatal famine and adult mental illness: Interpreting concordant and
discordant results from the Dutch and Chinese Famines
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Editorial Material
DE Famine
ID AUTISM SPECTRUM DISORDERS; FOLIC-ACID SUPPLEMENTS; HUNGER WINTER; COHORT
PROFILE; GREAT LEAP; SCHIZOPHRENIA; EXPOSURE; RISK; HEALTH;
UNDERNUTRITION
C1 [Susser, Ezra] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Susser, Ezra] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[St Clair, David] Univ Aberdeen, Sch Med, Inst Med Sci, Aberdeen AB9 2ZD, Scotland.
[St Clair, David] Shandong Jiaotong Univ, Jinan, Peoples R China.
[St Clair, David] Columbia Univ, New York, NY USA.
RP Susser, E (reprint author), Mailman Sch Publ Hlth, Dept Epidemiol, 722 W 168th St,Off 1030, New York, NY 10032 USA.
EM ess8@columbia.edu
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NR 41
TC 10
Z9 10
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD NOV
PY 2013
VL 97
SI SI
BP 325
EP 330
DI 10.1016/j.socscimed.2013.02.049
PG 6
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 264WG
UT WOS:000327911100038
PM 23557675
ER
PT J
AU Mateos-Moreno, D
Atencia-Dona, L
AF Mateos-Moreno, Daniel
Atencia-Dona, Lidia
TI Effect of a combined dance/movement and music therapy on young adults
diagnosed with severe autism
SO ARTS IN PSYCHOTHERAPY
LA English
DT Article
DE Dance; Music; Therapy; Autism; Functions; Disorders; Behavior
ID CHILDHOOD; SCALE
AB Current literature is scarce on the potential effects of combined dance/movement and music therapy on adults diagnosed with severe autism, particularly in distinguishing these effects on different areas of psychopathological disorders. We set two goals: first, to assess the effectiveness based on the score the participants obtained from the Revised Clinical Scale for the Evaluation of Autistic Behavior (ECA-R) after a series of dance/movement and music therapeutic procedures on adults with severe autism; second, to contrast the differences in effectiveness in concrete areas defined by subscales of the ECA-R, especially in its defined 2 factors and 12 functions. An overall of 36 one-hour sessions were carried out during 17 weeks on a sample of 8 participants with severe autism (approximately 2 sessions per week). During the treatment 8 measurements were taken (1 every 3 weeks) from this sample and from a control sample, which was also comprised of 8 subjects who were equally monitored at the same care center by two independent psychologists. Our experimental study seems to suggest that combined dance/movement and music therapy could be effective if used regularly for the improvement of autistic symptoms in adults diagnosed with severe autism. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Mateos-Moreno, Daniel; Atencia-Dona, Lidia] Univ Malaga, E-29071 Malaga, Spain.
RP Mateos-Moreno, D (reprint author), Univ Malaga, Fac Psicol & Ciencias Educ, Campus Teatinos S-N, E-29071 Malaga, Spain.
EM danielmm@uma.es
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NR 29
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0197-4556
EI 1873-5878
J9 ART PSYCHOTHER
JI Arts Psychother.
PD NOV
PY 2013
VL 40
IS 5
BP 465
EP 472
DI 10.1016/j.aip.2013.09.004
PG 8
WC Psychology, Clinical; Rehabilitation
SC Psychology; Rehabilitation
GA 270JO
UT WOS:000328314900003
ER
PT J
AU Mesman, J
Emmen, RAG
AF Mesman, Judi
Emmen, Rosanneke A. G.
TI Mary Ainsworth's legacy: a systematic review of observational
instruments measuring parental sensitivity
SO ATTACHMENT & HUMAN DEVELOPMENT
LA English
DT Review
DE maternal sensitivity; observation; instruments; positive affect; review
ID INFANT-MOTHER ATTACHMENT; RANDOMIZED CONTROLLED-TRIAL; AUTISM SPECTRUM
DISORDER; MATERNAL SENSITIVITY; EMOTIONAL AVAILABILITY; DIFFERENTIAL
SUSCEPTIBILITY; COGNITIVE-DEVELOPMENT; CHILDRENS DEVELOPMENT;
ENVIRONMENTAL-FACTORS; POSTNATAL DEPRESSION
AB Since Mary Ainsworth's formulation of the Sensitivity-Insensitivity to Infant Signals and Communications observational scale, new instruments have been developed to observe parental sensitivity. In this paper, we provide an overview of eight commonly used observational instruments to measure parental sensitivity. Their similarities and differences in comparison to the original Ainsworth sensitivity construct and its applications will be discussed. Consistent with the search criteria, each of the instruments clearly includes the key elements of Ainsworth's definition of sensitivity. Notable deviations from the original scale are the use of composite scales rather than a single global scale and the related inclusion of new elements, and specifically the inclusion of positive affect as an indicator of sensitivity. Further, most of the instruments have a wider scope than Ainsworth's sensitivity scale in terms of target age groups and the assessment of sensitivity in fathers. We discuss the interpretation of the sensitivity construct depending on variations in how the construct is defined in different observational instruments, and advances in the application of the construct.
C1 [Mesman, Judi; Emmen, Rosanneke A. G.] Leiden Univ, Ctr Child & Family Studies, Leiden, Netherlands.
RP Mesman, J (reprint author), Leiden Univ, Ctr Child & Family Studies, Leiden, Netherlands.
EM mesmanj@fsw.leidenuniv.nl
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NR 123
TC 1
Z9 1
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1461-6734
EI 1469-2988
J9 ATTACH HUM DEV
JI Attach. Hum. Dev.
PD NOV 1
PY 2013
VL 15
IS 5-6
SI SI
BP 485
EP 506
DI 10.1080/14616734.2013.820900
PG 22
WC Psychology, Developmental
SC Psychology
GA 268SC
UT WOS:000328189800004
PM 24299131
ER
PT J
AU Edvardson, S
Ashikov, A
Jalas, C
Sturiale, L
Shaag, A
Fedick, A
Treff, NR
Garozzo, D
Gerardy-Schahn, R
Elpeleg, O
AF Edvardson, Simon
Ashikov, Angel
Jalas, Chaim
Sturiale, Luisa
Shaag, Avraham
Fedick, Anastasia
Treff, Nathan R.
Garozzo, Domenico
Gerardy-Schahn, Rita
Elpeleg, Orly
TI Mutations in SLC35A3 cause autism spectrum disorder, epilepsy and
arthrogryposis
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Neurology
ID NUCLEOTIDE-SUGAR TRANSPORTER; UDP-N-ACETYLGLUCOSAMINE; COMPLEX VERTEBRAL
MALFORMATION; MOLECULAR-CLONING; GENE; GOLGI; EXPRESSION;
IDENTIFICATION; SPECIFICITY; DISEASES
AB Background The heritability of autism spectrum disorder is currently estimated at 55%. Identification of the molecular basis of patients with syndromic autism extends our understanding of the pathogenesis of autism in general. The objective of this study was to find the gene mutated in eight patients from a large kindred, who suffered from autism spectrum disorder, arthrogryposis and epilepsy.
Methods and results By linkage analysis and exome sequencing, we identified deleterious mutations in SLC35A3 in these patients. SLC35A3 encodes the major Golgi uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) transporter. In Golgi vesicles isolated from patient fibroblasts the transport of the respective nucleotide sugar was significantly reduced causing a massive decrease in the content of cell surface expressed highly branched N-glycans and a concomitant sharp increase of lower branched glycoforms.
Conclusions Spontaneous mutation in SLC35A3 has been discovered in cattle worldwide, recapitulating the human phenotype with arthrogryposis and additional skeletal defects known as Complex Vertebral Malformation syndrome. The skeletal anomalies in the mutant cattle and in our patients, and perhaps even the neurological symptoms are likely the consequence of the lack of high-branched N-glycans and the concomitant abundance of lower-branched glycoforms at the cell surface. This pattern has previously been associated with growth arrest and induction of differentiation. With this study, we add SLC35A3 to the gene list of autism spectrum disorders, and underscore the crucial importance of UDP-GlcNAc in the regulation of the N-glycan branching pathway in the Golgi apparatus.
C1 [Edvardson, Simon; Shaag, Avraham; Elpeleg, Orly] Hadassah Hebrew Univ, Med Ctr, Dept Genet Res, Jerusalem, Israel.
[Ashikov, Angel; Gerardy-Schahn, Rita] Hannover Med Sch, Inst Cellular Chem, D-30625 Hannover, Germany.
[Jalas, Chaim] Bonei Olam Ctr Rare Jewish Genet Disorders, Brooklyn, NY USA.
[Sturiale, Luisa; Garozzo, Domenico] CNR, Inst Chem & Technol Polymers, Sect Catania, I-00185 Rome, Italy.
[Fedick, Anastasia; Treff, Nathan R.] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Mol Genet, Piscataway, NJ 08854 USA.
[Treff, Nathan R.] Reprod Med Associates New Jersey, Morristown, NJ USA.
RP Elpeleg, O (reprint author), Hebrew Univ Jerusalem, Med Ctr, Monique & Jacques Roboh Dept Genet Res, IL-91120 Jerusalem, Israel.
EM Gerardy-Schahn.Rita@mh-hannover.de; Elpeleg@Hadassah.org.il
RI Garozzo, Domenico/I-8839-2014
OI Garozzo, Domenico/0000-0002-9087-9818
FU Bonei Olam organization
FX We are grateful to Professor Jorgen S Agerholm for the contribution of
figure 2G. This work was supported in part by Rabbi S Bochner of the
Bonei Olam organization and impact oriented funding (LOM) to the
Institute of Cellular Chemistry at Hannover Medical School.
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NR 30
TC 3
Z9 5
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD NOV
PY 2013
VL 50
IS 11
BP 733
EP 739
DI 10.1136/jmedgenet-2013-101753
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 268AY
UT WOS:000328141400003
PM 24031089
ER
PT J
AU Capo-Chichi, JM
Tcherkezian, J
Hamdan, FF
Decarie, JC
Dobrzeniecka, S
Patry, L
Nadon, MA
Mucha, BE
Major, P
Shevell, M
Bencheikh, BOA
Joober, R
Samuels, ME
Rouleau, GA
Roux, PP
Michaud, JL
AF Capo-Chichi, Jose-Mario
Tcherkezian, Joseph
Hamdan, Fadi F.
Decarie, Jean Claude
Dobrzeniecka, Sylvia
Patry, Lysanne
Nadon, Marc-Antoine
Mucha, Bettina E.
Major, Philippe
Shevell, Michael
Bencheikh, Bouchra Ouled Amar
Joober, Ridha
Samuels, Mark E.
Rouleau, Guy A.
Roux, Philippe P.
Michaud, Jacques L.
TI Disruption of TBC1D7, a subunit of the TSC1-TSC2 protein complex, in
intellectual disability and megalencephaly
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE Clinical genetics; Molecular genetics
ID TUBEROUS SCLEROSIS COMPLEX; MUTATIONS; DISORDERS; GERMLINE; RHEB; GENE
AB Background Mutations in TSC1 or TSC2 cause the tuberous sclerosis complex (TSC), a disorder characterised by the development of hamartomas or benign tumours in various organs as well as the variable presence of epilepsy, intellectual disability (ID) and autism. TSC1, TSC2 and the recently described protein TBC1D7 form a complex that inhibits mTORC1 signalling and limits cell growth. Although it has been proposed that mutations in TBC1D7 might also cause TSC, loss of its function has not yet been documented in humans.
Methods and Results We used homozygosity mapping and exome sequencing to study a consanguineous family with ID and megalencephaly but without any specific features of TSC. We identified only one rare coding variant, c.538delT:p.Y180fsX1 in TBC1D7, in the regions of homozygosity shared by the affected siblings. We show that this mutation abolishes TBC1D7 expression and is associated with increased mTORC1 signalling in cells of the affected individuals.
Conclusions Our study suggests that disruption of TBC1D7 causes ID but without the other typical features found in TSC. Although megalencephaly is not commonly observed in TSC, it has been associated with mTORC1 activation. Our observation thus reinforces the relationship between this pathway and the development of megalencephaly.
C1 [Capo-Chichi, Jose-Mario; Hamdan, Fadi F.; Patry, Lysanne; Nadon, Marc-Antoine; Mucha, Bettina E.; Major, Philippe; Samuels, Mark E.; Michaud, Jacques L.] Ctr Hosp Univ CHU St Justine Res Ctr, Montreal, PQ H3T 1C5, Canada.
[Tcherkezian, Joseph; Roux, Philippe P.] Univ Montreal, IRIC, Montreal, PQ, Canada.
[Decarie, Jean Claude] CHU St Justine, Dept Med Imaging, Montreal, PQ, Canada.
[Dobrzeniecka, Sylvia; Bencheikh, Bouchra Ouled Amar] CHUM Res Ctr, Montreal, PQ, Canada.
[Shevell, Michael] McGill Univ, Dept Neurol & Neurosurg, Montreal, PQ, Canada.
[Shevell, Michael] Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada.
[Bencheikh, Bouchra Ouled Amar; Rouleau, Guy A.] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
[Joober, Ridha] McGill Univ, Douglas Mental Hlth Univ Inst, Dept Psychiat, Montreal, PQ, Canada.
[Roux, Philippe P.] Univ Montreal, Dept Pathol & Cell Biol, Montreal, PQ, Canada.
RP Michaud, JL (reprint author), Ctr Hosp Univ CHU St Justine Res Ctr, 3175 Cote St Catherine, Montreal, PQ H3T 1C5, Canada.
EM jacques.michaud@recherche-ste-justine.qc.ca
FU March of Dimes [12-FY10-236]; Canadian Institutes for Health Research
[MOP123408]
FX This work was supported by March of Dimes (grant no. 12-FY10-236 to MS
and JLM) and the Canadian Institutes for Health Research (grant no.
MOP123408 to PPR).
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Z9 8
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
EI 1468-6244
J9 J MED GENET
JI J. Med. Genet.
PD NOV
PY 2013
VL 50
IS 11
BP 740
EP 744
DI 10.1136/jmedgenet-2013-101680
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 268AY
UT WOS:000328141400004
PM 23687350
ER
PT J
AU Zeyer, A
Cetin-Dindar, A
Zain, ANM
Jurisevic, M
Devetak, I
Odermatt, F
AF Zeyer, Albert
Cetin-Dindar, Ayla
Zain, Ahmad Nurulazam Md
Jurisevic, Mojca
Devetak, Iztok
Odermatt, Freia
TI Systemizing: A Cross-Cultural Constant for Motivation to Learn Science
SO JOURNAL OF RESEARCH IN SCIENCE TEACHING
LA English
DT Article
DE motivation; gender; attitudes; cognitive science; international
education
ID SELF-EFFICACY BELIEFS; STRUCTURAL EQUATION MODELS; HIGH-FUNCTIONING
AUTISM; NORMAL SEX-DIFFERENCES; NONSCIENCE MAJORS; ASPERGER-SYNDROME;
MEASUREMENT INVARIANCE; GENDER-DIFFERENCES; EMPATHY QUOTIENT;
SCHOOL-STUDENTS
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C1 [Zeyer, Albert; Odermatt, Freia] Univ Zurich, Inst Educ, CH-8006 Zurich, Switzerland.
[Cetin-Dindar, Ayla] Middle E Tech Univ, Fac Educ, TR-06531 Ankara, Turkey.
[Zain, Ahmad Nurulazam Md] Univ Sains Malaysia, Sch Educ Studies, George Town, Malaysia.
[Jurisevic, Mojca; Devetak, Iztok] Univ Ljubljana, Fac Educ, Ljubljana, Slovenia.
RP Zeyer, A (reprint author), Univ Zurich, Inst Educ, Beckenhofstr 31, CH-8006 Zurich, Switzerland.
EM albert.zeyer@ife.uzh.ch
RI boran, gul hanim/C-5889-2014
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Zhang L.-F., 2006, THE NATURE OF INTELL
NR 94
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-4308
EI 1098-2736
J9 J RES SCI TEACH
JI J. Res. Sci. Teach.
PD NOV
PY 2013
VL 50
IS 9
BP 1047
EP 1067
DI 10.1002/tea.21101
PG 21
WC Education & Educational Research
SC Education & Educational Research
GA 272LX
UT WOS:000328463300002
ER
PT J
AU Pascual-Castroviejo, I
Hernandez-Moneo, JL
Pascual-Pascual, SI
Viano, J
Gutierrez-Molina, M
Velazquez-Fragua, R
Tapia, DQ
Bastos, CM
AF Pascual-Castroviejo, I.
Hernandez-Moneo, J. L.
Pascual-Pascual, S. I.
Viano, J.
Gutierrez-Molina, M.
Velazquez-Fragua, R.
Quinones Tapia, D.
Morales Bastos, C.
TI Significance of tuber size for complications of tuberous sclerosis
complex
SO NEUROLOGIA
LA Spanish
DT Article
DE Tuberous sclerosis complex; Tubers; Seizures in tuberous sclerosis
complex; Autism in tuberous sclerosis complex; Mental retardation in
tuberous sclerosis complex; Magnetic resonance imaging in tuberous
sclerosis complex
ID GIANT-CELL ASTROCYTOMAS; CORTICAL TUBERS; EPILEPSY SURGERY; INFANTILE
SPASMS; CHILDREN; FOCI; MR; POPULATION; IMPAIRMENT; SEVERITY
AB Introduction: Tuberous sclerosis complex (TSC) is one of the most frequent neurocutaneous disorders. Cortical tubers are the most common pathological changes in TSC and they are directly related to the disease's main clinical manifestations: seizures, mental retardation, and autistic behaviour.
Objective: The aim of this study is to establish a correlation between tuber size and the severity of clinical features in TSC.
Material and methods: We performed a retrospective study of the clinical and imaging findings from 45 TSC patients (22 females and 23 males) and compared the clinical features with the location, size, and number of the cortical tubers in each patient.
Results: Four patients had voluminous tubers located in 1 or both cerebral hemispheres. All of these patients had intractable seizures and severe mental retardation; 3 of these cases also presented with autistic behaviour, despite tubers having been resected in all 4 patients. Thirteen patients had tubers of large-to-average size, and all patients in this group showed intractable seizures and mental retardation. Nine patients who had experienced infantile spasms during the first year of life presented autistic behaviour. Multiple tubers of small to average size were found in 28 patients. In general, this group had seizures that responded well to antiepileptic drugs and a low prevalence of autism. In 3 patients who all presented good seizure control and normal intelligence, single cortical/subcortical tubers were located in the frontal or occipital lobes. Of the total of 45 patients, 13 had cerebellar as well as cerebral tubers; these were generally present in cases with more severe clinical features.
Conclusions: Although large tubers are less common than small to medium-sized ones, they are much more likely to be accompanied by severe clinical symptoms (seizures, mental retardation and autistic behaviour), even when the smaller tubers are quite numerous. (C) 2012 Sociedad Espanola de Neurologia. Published by Elsevier Espana, S.L. All rights reserved.
C1 [Pascual-Castroviejo, I.; Pascual-Pascual, S. I.; Velazquez-Fragua, R.] Hosp Univ La Paz, Serv Neurol, Madrid, Spain.
[Hernandez-Moneo, J. L.] Hosp Gen Toledo, Serv Neurocirugia, Toledo, Spain.
[Viano, J.; Quinones Tapia, D.] Hosp Rosario, Unidad Imagen, Madrid, Spain.
[Gutierrez-Molina, M.; Morales Bastos, C.] Hosp Univ La Paz, Secc Neuropatol, Madrid, Spain.
RP Pascual-Castroviejo, I (reprint author), Hosp Univ La Paz, Serv Neurol, Madrid, Spain.
EM i.pcastroviejo@neurologia.e.telefonica.net
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NR 49
TC 1
Z9 1
PU ELSEVIER DOYMA SL
PI BARCELONA
PA TRAVESERA DE GARCIA, 17-21, BARCELONA, 08021, SPAIN
SN 0213-4853
EI 1578-1968
J9 NEUROLOGIA
JI Neurologia
PD NOV-DEC
PY 2013
VL 28
IS 9
BP 550
EP 557
DI 10.1016/j.nr1.2012.11.002
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 272DC
UT WOS:000328439500004
PM 23274119
ER
PT J
AU Walton, JC
Selvakumar, B
Weil, ZM
Snyder, SH
Nelson, RJ
AF Walton, James C.
Selvakumar, Balakrishnan
Weil, Zachary M.
Snyder, Solomon H.
Nelson, Randy J.
TI Neuronal nitric oxide synthase and NADPH oxidase interact to affect
cognitive, affective, and social behaviors in mice
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE nNOS; p47phox; Schizophrenia; Hippocampus; Autism
ID LONG-TERM POTENTIATION; PROTEIN S-NITROSYLATION; HIPPOCAMPAL AREA CA1;
KNOCK-OUT MICE; INBRED STRAINS; PREPULSE INHIBITION; SYNAPTIC
PLASTICITY; AGGRESSIVE-BEHAVIOR; NUCLEUS-ACCUMBENS; OXIDATIVE STRESS
AB Both nitric oxide (NO) and reactive oxygen species (ROS) generated by nNOS and NADPH oxidase (NOX), respectively, in the brain have been implicated in an array of behaviors ranging from learning and memory to social interactions. Although recent work has elucidated how these separate redox pathways regulate neural function and behavior, the interaction of these two pathways in the regulation of neural function and behavior remains unspecified. Toward this end, the p47phox subunit of NOX, and nNOS were deleted to generate double knockout mice that were used to characterize the behavioral outcomes of concurrent impairment of the NO and ROS pathways in the brain. Mice were tested in a battery of behavioral tasks to evaluate learning and memory, as well as social, affective, and cognitive behaviors. p47phox deletion did not affect depressive-like behavior, whereas nNOS deletion abolished it. Both p47phox and nNOS deletion singly reduced anxiety-like behavior, increased general locomotor activity, impaired spatial learning and memory, and impaired preference for social novelty. Deletion of both genes concurrently had synergistic effects to elevate locomotor activity, impair spatial learning and memory, and disrupt prepulse inhibition of acoustic startle. Although preference for social novelty was impaired in single knockouts, double knockout mice displayed elevated levels of preference for social novelty above that of wild type littermates. These data demonstrate that, depending upon modality, deletion of p47phox and nNOS genes have dissimilar, similar, or additive effects. The current findings provide evidence that the NOX and nNOS redox signaling cascades interact in the brain to affect both cognitive function and social behavior. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Walton, James C.; Weil, Zachary M.; Nelson, Randy J.] Ohio State Univ, Wexner Med Ctr, Dept Neurosci, Columbus, OH 43210 USA.
[Selvakumar, Balakrishnan; Snyder, Solomon H.] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD 21205 USA.
RP Walton, JC (reprint author), Dept Neurosci, 636 Biomed Res Tower,460W,12th Ave, Columbus, OH 43210 USA.
EM walton.315@osu.edu
RI Walton, James/F-7435-2010; Weil, Zachary/A-2439-2008; Weil,
Zachary/B-5003-2008
OI Walton, James/0000-0002-3049-1029; Weil, Zachary/0000-0003-3758-1809
FU NIH [MH18501]; NINDS [P30 NS045758]
FX We thank Shan Chen and Erika Sulecki from the Nelson lab for technical
assistance. We also thank Masoumeh Saleh from the Snyder lab for
technical assistance with maintaining mice. This research was supported
by NIH grant MH18501 to SHS, and NINDS grant P30 NS045758 to OSU
Neuroscience Center.
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TC 4
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 1
PY 2013
VL 256
BP 320
EP 327
DI 10.1016/j.bbr.2013.08.003
PG 8
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 267JO
UT WOS:000328094100040
PM 23948215
ER
PT J
AU Sacrey, LAR
Bryson, SE
Zwaigenbaum, L
AF Sacrey, Lori-Ann R.
Bryson, Susan E.
Zwaigenbaum, Lonnie
TI Prospective examination of visual attention during play in infants at
high-risk for autism spectrum disorder: A longitudinal study from 6 to
36 months of age
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Disengage; Engage; Reaching; Infant sibling; Autism spectrum disorder;
Visual attention
ID PERVASIVE DEVELOPMENTAL DISORDERS; EYE-HAND COORDINATION;
YOUNG-CHILDREN; HOME VIDEOTAPES; DEFICITS; DISENGAGEMENT; RECOGNITION;
SACCADES; COMMUNICATION; MOVEMENTS
AB Regulation of visual attention is essential to learning about one's environment. Children with autism spectrum disorder (ASD) exhibit impairments in regulating their visual attention, but little is known about how such impairments develop over time. This prospective longitudinal study is the first to describe the development of components of visual attention, including engaging, sustaining, and disengaging attention, in infants at high-risk of developing ASD (each with an older sibling with ASD). Non-sibling controls and high-risk infant siblings were filmed at 6, 9, 12, 15, 18, 24, and 36 months of age as they engaged in play with small, easily graspable toys. Duration of time spent looking at toy targets before moving the hand toward the target and the duration of time spent looking at the target after grasp were measured. At 36 months of age, an independent, gold standard diagnostic assessment for ASD was conducted for all participants. As predicted, infant siblings subsequently diagnosed with ASD were distinguished by prolonged latency to disengage ('sticky attention') by 12 months of age, and continued to show this characteristic at 15, 18, and 24 months of age. The results are discussed in relation to how the development of visual attention may impact later cognitive outcomes of children diagnosed with ASD. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Sacrey, Lori-Ann R.; Zwaigenbaum, Lonnie] Univ Alberta, Dept Pediat, Edmonton, AB, Canada.
[Bryson, Susan E.] Dalhousie Univ, Dept Pediat, Halifax, NS, Canada.
[Bryson, Susan E.] Dalhousie Univ, Dept Psychol, Halifax, NS, Canada.
[Bryson, Susan E.] IWK Hlth Ctr, Halifax, NS, Canada.
[Zwaigenbaum, Lonnie] Glenrose Rehabil Hosp, Edmonton, AB T5G 0B7, Canada.
RP Sacrey, LAR (reprint author), Glenrose Rehabil Hosp, Autism Res Ctr E209, 10230-111 Ave, Edmonton, AB T5G 0B7, Canada.
EM sacrey@ualberta.ca
FU CIHR; Autism Speaks Canada; Stollery Children's Hospital Foundation
Chair in Autism Research; Alberta Innovates-Health Solutions Scholar
Award; Craig Chair in Autism Research; Dalhousie Medical Research
Foundation; CIHR Autism Research Training Program Postdoctoral
Fellowship award
FX The authors would like to thank Ellen Robertson for her assistance in
the collection and blinding of infant tapes. This research is supported
by CIHR and Autism Speaks Canada. LZ is supported by the Stollery
Children's Hospital Foundation Chair in Autism Research and an Alberta
Innovates-Health Solutions Scholar Award. SEB is supported by the Craig
Chair in Autism Research and the Dalhousie Medical Research Foundation.
LRS is supported by a CIHR Autism Research Training Program Postdoctoral
Fellowship award.
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NR 75
TC 7
Z9 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 1
PY 2013
VL 256
BP 441
EP 450
DI 10.1016/j.bbr.2013.08.028
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 267JO
UT WOS:000328094100054
PM 24004846
ER
PT J
AU Ey, E
Torquet, N
Le Sourd, AM
Leblond, CS
Boeckers, TM
Faure, P
Bourgeron, T
AF Ey, Elodie
Torquet, Nicolas
Le Sourd, Anne-Marie
Leblond, Claire S.
Boeckers, Tobias M.
Faure, Philippe
Bourgeron, Thomas
TI The Autism ProSAP1/Shank2 mouse model displays quantitative and
structural abnormalities in ultrasonic vocalisations
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Autism spectrum disorder; Mouse model; ProSAP1/Shank2; Synaptic protein;
Ultrasonic vocalization; Peak frequency
ID SPECTRUM DISORDER; MUTANT MICE; FEMALE MICE; SHANK3; BEHAVIORS;
MUTATIONS; AGE; DYSFUNCTION; DEFECTS; SONGS
AB Mouse ultrasonic vocalisations have been often used as a paradigm to extrapolate vocal communication defects observed in patients with autism spectrum disorders (ASD). The role of these vocalisations as well as their development, structure and informational content, however, remain largely unknown. In the present study, we characterised in depth the emission of pup and adult ultrasonic vocalisations of wild-type mice and their ProSAP1/Shank2(-/-) littermates lacking a synaptic scaffold protein mutated in ASD. We hypothesised that the vocal behaviour of ProSAP1/Shank2(-/-) mice not only differs from the vocal behaviour of their wild-type littermates in a quantitative way, but also presents more qualitative abnormalities in temporal organisation and acoustic structure. We first quantified the rate of emission of ultrasonic vocalisations, and analysed the organisation of vocalisations sequences using Markov models. We subsequently measured duration and peak frequency characteristics of each ultrasonic vocalisation, to characterise their acoustic structure. In wild-type mice, we found a high level of organisation in sequences of ultrasonic vocalisations, suggesting a communicative function in this complex system. Very limited significant sex-related variations were detected in their usage and acoustic structure, even in adult mice. In adult ProSAP1/Shank2(-/-) mice, we found abnormalities in the call usage and the structure of ultrasonic vocalisations. Both ProSAP1/Shank2(-/-) male and female mice uttered less vocalisations with a different call distribution and at lower peak frequency in comparison with wild-type littermates. This study provides a comprehensive framework to characterise abnormalities of ultrasonic vocalisations in mice and confirms that ProSAP1/Shank2(-/-) mice represent a relevant model to study communication defects. (C) 2013 The Authors. Published by Elsevier B.V. All rights reserved.
C1 [Ey, Elodie; Torquet, Nicolas; Le Sourd, Anne-Marie; Leblond, Claire S.; Bourgeron, Thomas] Inst Pasteur, F-75015 Paris, France.
[Ey, Elodie; Torquet, Nicolas; Le Sourd, Anne-Marie; Leblond, Claire S.; Bourgeron, Thomas] Inst Pasteur, CNRS URA Genes Synapses & Cognit 2182, F-75015 Paris, France.
[Ey, Elodie; Torquet, Nicolas; Le Sourd, Anne-Marie; Leblond, Claire S.; Bourgeron, Thomas] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
[Boeckers, Tobias M.] Univ Ulm, Inst Anat & Cell Biol, D-89069 Ulm, Germany.
[Faure, Philippe] Univ Paris 06, CNRS, UMR 7102, Paris, France.
[Faure, Philippe; Bourgeron, Thomas] Lab Excellence Biol Psychiat Labex BIOPSY, Paris, France.
RP Ey, E (reprint author), Inst Pasteur, 25 Rue Docteur Roux, F-75015 Paris, France.
EM elodie.ey@pasteur.fr
FU Fondation de France; ANR FLEXNEURIM [ANRO9BLANO34003,
ANR08-MNPS-037-01-SynGen]; Neuron-ERANET (EUHF-AUTISM); Fondation
Orange; Fondation FondaMentale; Fondation Bettencourt-Schueller;
Innovative Medicines Initiative Joint Undertaking [115300]; European
Union
FX This work was supported by the Fondation de France; by the ANR
FLEXNEURIM [ANRO9BLANO34003]; by the ANR [ANR08-MNPS-037-01-SynGen]; by
Neuron-ERANET (EUHF-AUTISM); by the Fondation Orange; by the Fondation
FondaMentale; by the Fondation Bettencourt-Schueller. The research
leading to these results has also received support from the Innovative
Medicines Initiative Joint Undertaking under grant agreement no. 115300,
resources of which are composed of financial contribution from the
European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA
companies' in kind contribution.
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NR 56
TC 11
Z9 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 1
PY 2013
VL 256
BP 677
EP 689
DI 10.1016/j.bbr.2013.08.031
PG 13
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 267JO
UT WOS:000328094100083
PM 23994547
ER
PT J
AU Hahn, N
Geurten, B
Gurvich, A
Piepenbrock, D
Kastner, A
Zanini, D
Xing, GL
Xie, W
Gopfert, MC
Ehrenreich, H
Heinrich, R
AF Hahn, Nina
Geurten, Bart
Gurvich, Artem
Piepenbrock, David
Kaestner, Anne
Zanini, Damiano
Xing, Guanglin
Xie, Wei
Goepfert, Martin C.
Ehrenreich, Hannelore
Heinrich, Ralf
TI Monogenic heritable autism gene neuroligin impacts Drosophila social
behaviour (vol 252, pg 450, 2013)
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Correction
C1 [Hahn, Nina; Geurten, Bart; Piepenbrock, David; Zanini, Damiano; Goepfert, Martin C.; Heinrich, Ralf] Univ Gottingen, Inst Zool, Dept Cellular Neurobiol, D-37077 Gottingen, Germany.
[Gurvich, Artem; Kaestner, Anne; Ehrenreich, Hannelore] Max Planck Inst Expt Med, D-37077 Gottingen, Germany.
[Xing, Guanglin; Xie, Wei] Southeast Univ, Inst Life Sci, Key Lab Dev Genes & Human Dis, Nanjing 210096, Jiangsu, Peoples R China.
RP Heinrich, R (reprint author), Univ Gottingen, Inst Zool, Dept Cellular Neurobiol, D-37077 Gottingen, Germany.
EM rheinri1@gwdg.de
CR Hahn N, 2013, BEHAV BRAIN RES, V252, P450, DOI 10.1016/j.bbr.2013.06.020
NR 1
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
EI 1872-7549
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD NOV 1
PY 2013
VL 256
BP 690
EP 690
DI 10.1016/j.bbr.2013.08.019
PG 1
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 267JO
UT WOS:000328094100084
ER
PT J
AU Rudie, JD
Dapretto, M
AF Rudie, Jeffrey David
Dapretto, Mirella
TI Convergent Evidence of Brain Overconnectivity in Children with Autism?
SO CELL REPORTS
LA English
DT Editorial Material
ID HIGH-FUNCTIONING AUTISM; SYNCHRONIZATION; CONNECTIVITY
C1 [Rudie, Jeffrey David; Dapretto, Mirella] Univ Calif Los Angeles, Brain Mapping Ctr, Los Angeles, CA 90095 USA.
[Rudie, Jeffrey David] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Dapretto, Mirella] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
RP Dapretto, M (reprint author), Univ Calif Los Angeles, Brain Mapping Ctr, Los Angeles, CA 90095 USA.
EM mirella@ucla.edu
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NR 11
TC 1
Z9 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2013
VL 5
IS 3
BP 565
EP 566
DI 10.1016/j.celrep.2013.10.043
PG 2
WC Cell Biology
SC Cell Biology
GA 269SY
UT WOS:000328263400001
PM 24238089
ER
PT J
AU Keown, CL
Shih, P
Nair, A
Peterson, N
Mulvey, ME
Muller, RA
AF Keown, Christopher Lee
Shih, Patricia
Nair, Aarti
Peterson, Nick
Mulvey, Mark Edward
Mueller, Ralph-Axel
TI Local Functional Overconnectivity in Posterior Brain Regions Is
Associated with Symptom Severity in Autism Spectrum Disorders
SO CELL REPORTS
LA English
DT Article
ID CONNECTIVITY MRI; MOTION; OPTIMIZATION; IMAGES; CORTEX; CONNECTOMICS;
REGISTRATION; PERCEPTION; REGRESSION; IMPACT
AB Although growing evidence indicates atypical long-distance connectivity in autism spectrum disorder (ASD), much less is known about local connectivity, despite conjectures that local overconnectivity may be causally involved in the disorder. Using functional connectivity MRI and graph theory, we found that local functional connectivity was atypically increased in adolescents with ASD in temporo-occipital regions bilaterally. Posterior overconnectivity was found to be associated with higher ASD symptom severity, whereas an ASD subsample with low severity showed frontal underconnectivity. The findings suggest links between symptomatology and local connectivity, which vary within the autism spectrum.
C1 [Keown, Christopher Lee; Nair, Aarti; Peterson, Nick; Mulvey, Mark Edward; Mueller, Ralph-Axel] San Diego State Univ, Brain Dev Imaging Lab, Dept Psychol, San Diego, CA 92120 USA.
[Keown, Christopher Lee; Mulvey, Mark Edward] San Diego State Univ, Computat Sci Res Ctr, San Diego, CA 92182 USA.
[Shih, Patricia] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Nair, Aarti; Mueller, Ralph-Axel] San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA 92182 USA.
[Nair, Aarti; Mueller, Ralph-Axel] Univ Calif San Diego, San Diego, CA 92182 USA.
[Peterson, Nick] San Diego State Univ, Dept Math & Stat, San Diego, CA 92182 USA.
RP Muller, RA (reprint author), San Diego State Univ, Brain Dev Imaging Lab, Dept Psychol, San Diego, CA 92120 USA.
EM rmueller@mail.sdsu.edu
FU National Institutes of Health [R01-MH081023]; Autism Speaks (Dennis
Weatherstone Predoctoral Fellowship) [7850]; NIH [T32-MH020068]
FX This study was supported by the National Institutes of Health
(R01-MH081023) with additional funding from Autism Speaks (Dennis
Weatherstone Predoctoral Fellowship 7850 to A.N.) and NIH T32-MH020068
(to P.S.). Special thanks to the participants and their families.
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NR 47
TC 16
Z9 16
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2013
VL 5
IS 3
BP 567
EP 572
DI 10.1016/j.celrep.2013.10.003
PG 6
WC Cell Biology
SC Cell Biology
GA 269SY
UT WOS:000328263400002
PM 24210815
ER
PT J
AU Supekar, K
Uddin, LQ
Khouzam, A
Phillips, J
Gaillard, WD
Kenworthy, LE
Yerys, BE
Vaidya, CJ
Menon, V
AF Supekar, Kaustubh
Uddin, Lucina Q.
Khouzam, Amirah
Phillips, Jennifer
Gaillard, William D.
Kenworthy, Lauren E.
Yerys, Benjamin E.
Vaidya, Chandan J.
Menon, Vinod
TI Brain Hyperconnectivity in Children with Autism and its Links to Social
Deficits
SO CELL REPORTS
LA English
DT Article
ID STATE FUNCTIONAL MRI; LOW-FREQUENCY FLUCTUATION; SPECTRUM DISORDERS;
DIAGNOSTIC INTERVIEW; PREFRONTAL CORTEX; NEURAL SYSTEMS; CONNECTIVITY;
NETWORK; ORGANIZATION; UNDERCONNECTIVITY
AB Autism spectrum disorder (ASD), a neurodevelopmental disorder affecting nearly 1 in 88 children, is thought to result from aberrant brain connectivity. Remarkably, there have been no systematic attempts to characterize whole-brain connectivity in children with ASD. Here, we use neuroimaging to show that there are more instances of greater functional connectivity in the brains of children with ASD in comparison to those of typically developing children. Hyperconnectivity in ASD was observed at the whole-brain and subsystems levels, across long- and short-range connections, and was associated with higher levels of fluctuations in regional brain signals. Brain hyperconnectivity predicted symptom severity in ASD, such that children with greater functional connectivity exhibited more severe social deficits. We replicated these findings in two additional independent cohorts, demonstrating again that at earlier ages, the brain of children with ASD is largely functionally hyperconnected in ways that contribute to social dysfunction. Our findings provide unique insights into brain mechanisms underlying childhood autism.
C1 [Supekar, Kaustubh; Uddin, Lucina Q.; Khouzam, Amirah; Phillips, Jennifer; Menon, Vinod] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94304 USA.
[Gaillard, William D.; Kenworthy, Lauren E.; Yerys, Benjamin E.; Vaidya, Chandan J.] Childrens Natl Med Ctr, Ctr Autism Spectrum Disorders, Washington, DC 20010 USA.
[Yerys, Benjamin E.] Grad Hosp Philadelphia, Ctr Autism Res, Philadelphia, PA 19146 USA.
[Vaidya, Chandan J.] Georgetown Univ, Dept Psychol, Washington, DC 20057 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94304 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Program Neurosci, Stanford, CA 94304 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Stanford Inst Neuroinnovat & Translat Neurosci, Stanford, CA 94304 USA.
RP Supekar, K (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94304 USA.
EM ksupekar@stanford.edu; menon@stanford.edu
FU Singer Foundation; Isadore and Bertha Gudelsky Foundation; Stanford
Institute for Neuro-Innovation & Translational Neurosciences; Children's
National Medical Center; National Institutes of Health [HD047520,
HD059205, DC0111095, MH084164, MH084961, K01MH092288, K23MH086111,
P30HD40677]
FX This research was supported by grants from the Singer Foundation, the
Isadore and Bertha Gudelsky Foundation, Stanford Institute for
Neuro-Innovation & Translational Neurosciences, Children's National
Medical Center, and the National Institutes of Health (grants HD047520,
HD059205, DC0111095, MH084164, MH084961, K01MH092288, K23MH086111, and
P30HD40677). We would like to thank Brian Koser and Dan Hall for their
valuable assistance in obtaining data from the National Database of
Autism Research. We greatly appreciate the contributions of the
participants, without whom this work would not be possible.
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NR 71
TC 22
Z9 22
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 2211-1247
J9 CELL REP
JI Cell Reports
PD NOV
PY 2013
VL 5
IS 3
BP 738
EP 747
DI 10.1016/j.celrep.2013.10.001
PG 10
WC Cell Biology
SC Cell Biology
GA 269SY
UT WOS:000328263400019
PM 24210821
ER
PT J
AU Theoharides, TC
AF Theoharides, T. C.
TI Extracellular Mitochondrial ATP, Suramin, and Autism? (vol 35, pg 1454,
2013)
SO CLINICAL THERAPEUTICS
LA English
DT Correction
CR Theoharides TC, 2013, CLIN THER, V35, P1454, DOI 10.1016/j.clinthera.2013.07.419
NR 1
TC 0
Z9 0
PU ELSEVIER
PI BRIDGEWATER
PA 685 ROUTE 202-206, BRIDGEWATER, NJ 08807 USA
SN 0149-2918
EI 1879-114X
J9 CLIN THER
JI Clin. Ther.
PD NOV
PY 2013
VL 35
IS 11
BP 1863
EP 1863
DI 10.1016/j.clinthera.2013.10.003
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 267LF
UT WOS:000328098500022
ER
PT J
AU Gentile, I
Zappulo, E
Coppola, N
Bonavolta, R
Portella, G
Cernia, DS
Riccio, MP
Settimi, A
Pascotto, A
Borgia, G
Bravaccio, C
AF Gentile, Ivan
Zappulo, Emanuela
Coppola, Nicola
Bonavolta, Raffaele
Portella, Giuseppe
Cernia, Daniela Spalletti
Riccio, Maria Pia
Settimi, Alessandro
Pascotto, Antonio
Borgia, Guglielmo
Bravaccio, Carmela
TI Prevalence of HHV-6 and HHV-8 Antibodies in Patients with Autism
Spectrum Disorders
SO IN VIVO
LA English
DT Article
DE Autism spectrum disorder; HHV-6; HHV-8
ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; HERPES-SIMPLEX ENCEPHALITIS;
EPSTEIN-BARR-VIRUS; HUMAN HERPESVIRUS-6; MULTIPLE-SCLEROSIS;
VIRAL-INFECTIONS; DEVELOPMENTAL REGRESSION; ANTIVIRAL DEFENSE;
INFANTILE-AUTISM; EXANTHEM-SUBITUM
AB Background/Aim: The etiology of autism spectrum disorders (ASD) still eludes investigators. Several viral infections have been associated with ASD etiopathogenesis but few studies have ever focused on the role of HHV-6 and HHV-8, two members of the herpesviridae family. The aim of the present study was to evaluate seropositivity rate and levels of antibodies to HHV6 and HHV-8 in children with ASD compared to controls. Patients and Methods: We measured and compared seropositivity rate and levels of antibodies to HHV-6 and HHV-8 in 30 children with ASD (14 with autistic disorder and 16 with non-autistic disorder ASD) and in 28 healthy controls of the same age. Results: Seropositivity rate and levels of the two antibodies were similar in cases and controls. Seropositivity rate and levels of antibodies were not correlated with disease severity in children with ASD. Conclusion: Levels and seropositivity rate of antibodies to HHV-6 and HHV-8 do not differ between children with ASD and controls.
C1 [Gentile, Ivan; Zappulo, Emanuela; Borgia, Guglielmo] Univ Naples Federico II, Dept Clin Med & Surg, Infect Dis Sect, I-80131 Naples, Italy.
[Bonavolta, Raffaele; Portella, Giuseppe; Cernia, Daniela Spalletti; Settimi, Alessandro; Bravaccio, Carmela] Univ Naples Federico II, Dept Med Translat Sci, I-80131 Naples, Italy.
[Coppola, Nicola; Riccio, Maria Pia; Pascotto, Antonio] Univ Naples 2, Dept Mental Hlth & Publ Med, Naples, Italy.
RP Gentile, I (reprint author), Univ Naples Federico II, Dept Clin Med & Surg, Infect Dis Sect, Via S Pansini 5, I-80131 Naples, Italy.
EM ivan.gentile@unina.it
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NR 85
TC 3
Z9 3
PU INT INST ANTICANCER RESEARCH
PI ATHENS
PA EDITORIAL OFFICE 1ST KM KAPANDRITIOU-KALAMOU RD KAPANDRITI, PO BOX 22,
ATHENS 19014, GREECE
SN 0258-851X
EI 1791-7549
J9 IN VIVO
JI In Vivo
PD NOV-DEC
PY 2013
VL 27
IS 6
BP 843
EP 849
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 264WZ
UT WOS:000327913000024
PM 24292591
ER
PT J
AU Dennis, EL
Thompson, PM
AF Dennis, Emily L.
Thompson, Paul M.
TI Mapping connectivity in the developing brain
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Review
DE Development; Brain connectivity; DTI; HARDI; rs-fMRI; Autism; ADHD;
Fragile X; 22q11.2 DS; Turner syndrome; Williams syndrome
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY
DISORDER; STATE FUNCTIONAL CONNECTIVITY; WHITE-MATTER DEVELOPMENT; HUMAN
CEREBRAL-CORTEX; FRAGILE-X-SYNDROME; 22Q11.2 DELETION SYNDROME; DEFAULT
MODE NETWORK; DIFFUSION-TENSOR; SEX-DIFFERENCES
AB Recently, there has been a wealth of research into structural and functional brain connectivity, and how they change over development. While we are far from a complete understanding, these studies have yielded important insights into human brain development. There is an ever growing variety of methods for assessing connectivity, each with its own advantages. Here we review research on the development of structural and/or functional brain connectivity in both typically developing subjects and subjects with neurodevelopmental disorders. Space limitations preclude an exhaustive review of brain connectivity across all developmental disorders, so we review a representative selection of recent findings on brain connectivity in autism, Fragile X, 22q11.2 deletion syndrome. Williams syndrome; Turner syndrome, and ADHD. Major strides have been made in understanding the developmental trajectory of the human connectome, offering insight into characteristic features of brain development and biological processes involved in developmental brain disorders. We also discuss some common themes, including hemispheric specialization - or asymmetry - and sex differences. We conclude by discussing some promising future directions in connectomics, including the merger of imaging and genetics, and a deeper investigation of the relationships between structural and functional connectivity. (C) 2013 ISDN. Published by Elsevier Ltd. All rights reserved.
C1 [Dennis, Emily L.; Thompson, Paul M.] Univ Calif Los Angeles, Imaging Genet Ctr, Lab Neuro Imaging, Sch Med, Los Angeles, CA 90095 USA.
RP Dennis, EL (reprint author), Univ Calif Los Angeles, Imaging Genet Ctr, Lab Neuro Imaging, Sch Med, 635 Charles Young Dr South,Suite 225, Los Angeles, CA 90095 USA.
EM eldennis@ucla.edu
FU NIH Training Grant in Neurobehavioral Genetics [T32MH073526-06];
National Institute of Child Health and Human Development [R01 HD050735];
National Health and Medical Research Council Australia [NHMRC 486682,
1009064]; NIH R01 [EB008432, EB008281, EB007813, P41 RR013642]
FX ED was funded, in part, by an NIH Training Grant in Neurobehavioral
Genetics (T32MH073526-06). Our work on brain connectivity reported here
is supported in part by the National Institute of Child Health and Human
Development (R01 HD050735), and the National Health and Medical Research
Council (NHMRC 486682, 1009064), Australia. Additional support for
algorithm development was provided by NIH R01 grants EB008432, EB008281,
EB007813 and P41 RR013642.
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NR 190
TC 14
Z9 14
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
EI 1873-474X
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD NOV
PY 2013
VL 31
IS 7
SI SI
BP 525
EP 542
DI 10.1016/j.ijdevneu.2013.05.007
PG 18
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 269JG
UT WOS:000328237000009
PM 23722009
ER
PT J
AU Feliciano, DM
Lin, TV
Hartman, NW
Bartley, CM
Kubera, C
Hsieh, L
Lafourcade, C
O'Keefe, RA
Bordey, A
AF Feliciano, David M.
Lin, Tiffany V.
Hartman, Nathaniel W.
Bartley, Christopher M.
Kubera, Cathryn
Hsieh, Lawrence
Lafourcade, Carlos
O'Keefe, Rachel A.
Bordey, Angelique
TI A circuitry and biochemical basis for tuberous sclerosis symptoms: from
epilepsy to neurocognitive deficits
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Review
DE Tuberous sclerosis complex; Tuber; Mental retardation; Neurogenesis;
mTOR; Epilepsy; Autism; SEGA; Seizures; FMRP; Spine; Dendrite;
Migration; Differentiation; Stem cell; Progenitor cell
ID GIANT-CELL ASTROCYTOMA; LONG-TERM DEPRESSION; IMPAIRED SYNAPTIC
PLASTICITY; RAPAMYCIN SIGNALING PATHWAY; FOCAL CORTICAL DYSPLASIA;
GAP-RELATED DOMAIN; MAMMALIAN TARGET; CEREBRAL-LESIONS; MOUSE MODEL;
ADULT NEUROGENESIS
AB Tuberous sclerosis complex (TSC) is an autosomal dominant monogenetic disorder that is characterized by the formation of benign tumors in several organs as well as brain malformations and neuronal defects. TSC is caused by inactivating mutations in one of two genes, TSC1 and TSC2, resulting in increased activity of the mammalian Target of Rapamycin (mTOR). Here, we explore the cytoarchitectural and functional CNS aberrations that may account for the neurological presentations of TSC, notably seizures, hydrocephalus, and cognitive and psychological impairments. In particular, recent mouse models of brain lesions are presented with an emphasis on using electroporation to allow the generation of discrete lesions resulting from loss of heterozygosity during perinatal development. Cortical lesions are thought to contribute to epileptogenesis and worsening of cognitive defects. However, it has recently been suggested that being born with a mutant allele without loss of heterozygosity and associated cortical lesions is sufficient to generate cognitive and neuropsychiatric problems. We will thus discuss the function of mTOR hyperactivity on neuronal circuit formation and the potential consequences of being born heterozygous on neuronal function and the biochemistry of synaptic plasticity, the cellular substrate of learning and memory. Ultimately, a major goal of TSC research is to identify the cellular and molecular mechanisms downstream of mTOR underlying the neurological manifestations observed in TSC patients and identify novel therapeutic targets to prevent the formation of brain lesions and restore neuronal function. (C) 2013 ISDN. Published by Elsevier Ltd. All rights reserved.
C1 [Feliciano, David M.; Lin, Tiffany V.; Hartman, Nathaniel W.; Bartley, Christopher M.; Kubera, Cathryn; Hsieh, Lawrence; Lafourcade, Carlos; O'Keefe, Rachel A.; Bordey, Angelique] Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT 06520 USA.
[Feliciano, David M.; Lin, Tiffany V.; Hartman, Nathaniel W.; Kubera, Cathryn; Hsieh, Lawrence; Lafourcade, Carlos; O'Keefe, Rachel A.; Bordey, Angelique] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06520 USA.
[Bartley, Christopher M.] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA.
RP Bordey, A (reprint author), Yale Univ, Sch Med, 333 Cedar St,FMB 422, New Haven, CT 06520 USA.
EM angelique.bordey@yale.edu
FU Department of Defense grant (Idea development award) [W81XWH-10-1-0041];
McKnight Disorder award, a CT stem Cell grant; National Institute of
Health [NRSA 10668225]; NIH [MSTP TG T32GM07205]
FX This work was supported by a Department of Defense grant (Idea
development award, W81XWH-10-1-0041), a McKnight Disorder award, a CT
stem Cell grant (A.B.), a National Institute of Health NRSA 10668225
(D.M.F) and NIH MSTP TG T32GM07205 (C.M.B.).
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NR 166
TC 8
Z9 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
EI 1873-474X
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD NOV
PY 2013
VL 31
IS 7
SI SI
BP 667
EP 678
DI 10.1016/j.ijdevneu.2013.02.008
PG 12
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 269JG
UT WOS:000328237000025
PM 23485365
ER
PT J
AU Saban, F
Arikan, D
AF Saban, Fatma
Arikan, Duygu
TI The self-esteem and anxiety of children with and without mentally
retarded siblings
SO JOURNAL OF RESEARCH IN MEDICAL SCIENCES
LA English
DT Article
DE Mental retardation; self-esteem; sibling; trait anxiety
ID DEVELOPMENTAL-DISABILITIES; BEHAVIORAL-ADJUSTMENT; ADOLESCENT SIBLINGS;
DISABLED-CHILDREN; AUTISM; RETARDATION; COMPETENCE
AB Background: The study was carried out with the aim of determining the factors affecting and to evaluate anxiety situations and self-esteem of children with and without mentally retarded siblings. Materials and Methods: The sampling included 227 healthy children: 108 of them have mental retarded sibling and 119 of them do not have mental retarded sibling. The context of this study consisted of 15-18 year of age healthy children with mentally retarded siblings and 15-18 year of aged healthy children having at least one sibling between the dates February 15st and June 26st 2010. Personal Information Form, Rosenberg Self-Esteem Scale and Trait Anxiety Scale were used. Results: It was found out that trait anxiety of 17-18 aged of children with mental retarded sibling (47.04 +/- 7.3) was higher than that of the children without mental retarded siblings (44.05 +/- 11.23) (P < 0.05). It was observed that self-esteem of children with mentally retarded sibling was not affected from the handicap of their siblings (P > 0.05). Trait anxiety score averages of children with mentally retarded sibling and experience some difficulties due to his or her siblings's handicap (47.00 +/- 7.76) were found higher than those of those of the children without any problem with the environment (42.61 +/- 7.48) (P < 0.05). Conclusion: Although the average score of trait anxiety and self-esteem in both groups were not significant different, score of trait anxiety for children with mentally disabled siblings was higher in comparison. It was concluded that anxiety of children with and without mentally retarded siblings increased as self-esteem of these children decreased.
C1 [Saban, Fatma; Arikan, Duygu] Ataturk Univ, Dept Child Hlth Nursing, Fac Hlth Sci, TR-25240 Erzurum, Turkey.
RP Arikan, D (reprint author), Ataturk Univ, Dept Child Hlth Nursing, Fac Hlth Sci, TR-25240 Erzurum, Turkey.
EM darikan@atauni.edu.tr
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NR 43
TC 0
Z9 0
PU ISFAHAN UNIV MED SCIENCES
PI ISFAHAN
PA HEZARJERIB AVE, PO BOX 81745-319, ISFAHAN, 00000, IRAN
SN 1735-1995
EI 1735-7136
J9 J RES MED SCI
JI J. Res. Med. Sci.
PD NOV
PY 2013
VL 18
IS 11
BP 961
EP 969
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 267QP
UT WOS:000328112900007
PM 24523782
ER
PT J
AU Trabzuni, D
Ramasamy, A
Imran, S
Walker, R
Smith, C
Weale, ME
Hardy, J
Ryten, M
AF Trabzuni, Daniah
Ramasamy, Adaikalavan
Imran, Sabaena
Walker, Robert
Smith, Colin
Weale, Michael E.
Hardy, John
Ryten, Mina
CA North Amer Brain Expression
TI Widespread sex differences in gene expression and splicing in the adult
human brain
SO NATURE COMMUNICATIONS
LA English
DT Article
ID X-CHROMOSOME; PARKINSONS-DISEASE; GENDER-DIFFERENCES; SEQUENCE; AUTISM;
GENOTYPE; TRANSCRIPTOME; INFLAMMATION; METAANALYSIS; NEUROSCIENCE
AB There is strong evidence to show that men and women differ in terms of neurodevelopment, neurochemistry and susceptibility to neurodegenerative and neuropsychiatric disease. The molecular basis of these differences remains unclear. Progress in this field has been hampered by the lack of genome-wide information on sex differences in gene expression and in particular splicing in the human brain. Here we address this issue by using post-mortem adult human brain and spinal cord samples originating from 137 neuropathologically confirmed control individuals to study whole-genome gene expression and splicing in 12 CNS regions. We show that sex differences in gene expression and splicing are widespread in adult human brain, being detectable in all major brain regions and involving 2.5% of all expressed genes. We give examples of genes where sex-biased expression is both disease-relevant and likely to have functional consequences, and provide evidence suggesting that sex biases in expression may reflect sex-biased gene regulatory structures.
C1 [Trabzuni, Daniah; Imran, Sabaena; Hardy, John; Ryten, Mina] UCL Inst Neurol, Dept Mol Neurosci, Reta Lilla Weston Labs, London WC1N 3BG, England.
[Trabzuni, Daniah] King Faisal Specialist Hosp & Res Ctr, Dept Genet, Riyadh 11211, Saudi Arabia.
[Ramasamy, Adaikalavan; Weale, Michael E.; Ryten, Mina] Kings Coll London, Guys Hosp, Dept Med & Mol Genet, London SE1 9RT, England.
[Walker, Robert; Smith, Colin] Univ Edinburgh, Dept Neuropathol, MRC Sudden Death Brain Bank Project, Edinburgh EH8 9AG, Midlothian, Scotland.
RP Ryten, M (reprint author), UCL Inst Neurol, Dept Mol Neurosci, Reta Lilla Weston Labs, Queen Sq, London WC1N 3BG, England.
EM mina.ryten@ucl.ac.uk
RI Trabzuni, Daniah/C-4034-2012; Hardy, John/C-2451-2009; Weale,
Michael/F-2587-2010; Ramasamy, Adaikalavan/G-2632-2010
OI Trabzuni, Daniah/0000-0003-4826-9570; Weale,
Michael/0000-0003-4593-1186; Ramasamy, Adaikalavan/0000-0002-7598-2892
FU MRC through the MRC Sudden Death Brain Bank [G0802462]; King Faisal
Specialist Hospital and Research Centre, Saudi Arabia; Intramural
Research Program of the National Institute on Aging, National Institutes
of Health, part of the US Department of Health and Human Services [ZIA
AG000932-04]; National Institute of Neurological Disorders and Stroke
[U24 NS072026]; National Institute on Aging [P30 AG19610]; Arizona
Department of Health Services [211002]; Arizona Biomedical Research
Commission [4001, 0011, 05-901, 1001]; Michael J. Fox Foundation for
Parkinson's Research; National Institute for Health Research (NIHR)
Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust;
National Institute for Health Research (NIHR) Biomedical Research Centre
at King's College London
FX This work was supported by the MRC through the MRC Sudden Death Brain
Bank (C.S.), a Project Grant (to J.H. and M.E.W.) and Training
Fellowship (G0802462 to M.R.). D.T. was supported by the King Faisal
Specialist Hospital and Research Centre, Saudi Arabia. The work
performed by the North American Brain Expression Consortium was
supported in part by the Intramural Research Program of the National
Institute on Aging, National Institutes of Health, part of the US
Department of Health and Human Services; project number ZIA AG000932-04.
We are grateful to the Banner Sun Health Research Institute Brain and
Body Donation Program of Sun City, Arizona for the provision of human
biospecimens. The Brain and Body Donation Program is supported by the
National Institute of Neurological Disorders and Stroke (U24 NS072026
National Brain and Tissue Resource for Parkinson's Disease and Related
Disorders), the National Institute on Aging (P30 AG19610 Arizona
Alzheimer's Disease Core Center), the Arizona Department of Health
Services (contract 211002, Arizona Alzheimer's Research Center), the
Arizona Biomedical Research Commission (contracts 4001, 0011, 05-901 and
1001 to the Arizona Parkinson's Disease Consortium) and the Michael J.
Fox Foundation for Parkinson's Research. Computing facilities used at
King's College London were partially supported by National Institute for
Health Research (NIHR) Biomedical Research Centre based at Guy's and St
Thomas' NHS Foundation Trust and King's College London.
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NR 47
TC 14
Z9 14
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2041-1723
J9 NAT COMMUN
JI Nat. Commun.
PD NOV
PY 2013
VL 4
DI 10.1038/ncomms3771
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 266KY
UT WOS:000328023900009
PM 24264146
ER
PT J
AU Ricci, S
Businaro, R
Ippoliti, F
Lo Vasco, VR
Massoni, F
Onofri, E
Troili, GM
Pontecorvi, V
Morelli, M
Ricciardi, MR
Archer, T
AF Ricci, S.
Businaro, R.
Ippoliti, F.
Lo Vasco, V. R.
Massoni, F.
Onofri, E.
Troili, G. M.
Pontecorvi, V.
Morelli, M.
Ricciardi, M. Rapp
Archer, T.
TI Altered Cytokine and BDNF Levels in Autism Spectrum Disorder
SO NEUROTOXICITY RESEARCH
LA English
DT Article
DE Autism; Immune system; Cytokines; Handicap; Immunoexcitotoxicity
ID POSSIBLE CENTRAL MECHANISM; ELEVATED SERUM-LEVELS; NEUROTROPHIC FACTOR;
INCREASED FREQUENCY; BRAIN INFLAMMATION; ALZHEIMERS-DISEASE; NEURON
NUMBER; CHILDREN; STRESS; PROTEIN
AB The contribution of neuroimmune functioning and brain-derived neurotrophic factor (BDNF) to functional dysregulation in autism spectrum disorder was assessed in 29 patients under treatment in two specialized centers of Basilicata (Chiaromonte and Matera), Southern Italy, through analysis of serum levels of cytokines and BDNF. Elevated levels of the pro-inflammatory cytokine, including interleukin-1, interleukin-6, interleukin-12, interleukin-23, tumor necrosis factor-alpha and BDNF were observed, regardless of age and gender. Comparisons were made with age-and gender-related healthy controls. The present findings reinforce current notions regarding immunoexcitotoxic mechanisms contributing to the pathophysiology of autistic disorder.
C1 [Ricci, S.; Massoni, F.; Onofri, E.; Troili, G. M.] Univ Roma La Sapienza, Dept Anat Histol Legal Med & Orthopaed, I-00161 Rome, Italy.
[Businaro, R.; Pontecorvi, V.; Morelli, M.] Sapienza Univ, Dept Medicosurg Sci & Biotechnol, I-04100 Latina, Italy.
[Ippoliti, F.] Univ Roma La Sapienza, Dept Expt Med, I-00161 Rome, Italy.
[Lo Vasco, V. R.] Univ Roma La Sapienza, Dept Organi Senso, I-00161 Rome, Italy.
[Ricciardi, M. Rapp; Archer, T.] Univ Gothenburg, Dept Psychol, S-40530 Gothenburg, Sweden.
[Ricciardi, M. Rapp; Archer, T.] Linnea Univ, Dept Psychol Educ & Sports Sci, Kalmar, Sweden.
RP Ricci, S (reprint author), Univ Roma La Sapienza, Dept Anat Histol Legal Med & Orthopaed, Viale Regina Elena 336, I-00161 Rome, Italy.
EM serafino.ricci@uniroma1.it
RI Lo Vasco, Vincenza Rita/F-9290-2010
FU REGIONE BASILICATA, ASP (Azienda Sanitaria Provinciale) Potenza,
Italy-General Director Dott. Mario Marra; Center for Diet- Related
diseases "G. Gioia", CHIAROMONTE Hospital
FX Research funded by REGIONE BASILICATA, ASP (Azienda Sanitaria
Provinciale) Potenza, Italy-General Director Dott. Mario Marra; Center
for Diet- Related diseases "G. Gioia", CHIAROMONTE Hospital (PZ), ASP
Potenza, Italy-Director Dott.ssa Rosa Trabace-Head of laboratory
Dott.ssa Nicolina La Sala-Psychologist/ Psychotherapist Dott.ssa Maria
Tosti; ASP (Azienda Sanitaria Provinciale) Ospedale
Chiaromonte/Lagonegro, Potenza, Italy-Pediatrician Dott. Rocco Orofino,
MD-Childish Neuropsychiatrist Dott. Vincenzo D'Onofrio,
MD-Administrative Manager Dott. Giacomo Chiarelli; ASP (Azienda
Sanitaria Provinciale) Matera, Italy Hospital "Madonna delle Grazie"
Department of Children and Adolescent Neuropsychiatry-Director U.O.C.
Dott. Carlo Calzone, MD-Neuropsychiatrist Dott. Caterina Lattarulo, MD;
Stella Maris Mediterraneo Foundation, ASP Potenza, Italy; Dr. Lars Goran
Wallgren provided excellent technical assistance.
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NR 57
TC 16
Z9 17
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1029-8428
EI 1476-3524
J9 NEUROTOX RES
JI Neurotox. Res.
PD NOV
PY 2013
VL 24
IS 4
BP 491
EP 501
DI 10.1007/s12640-013-9393-4
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 268CJ
UT WOS:000328145300004
PM 23604965
ER
PT J
AU Zettergren, A
Jonsson, L
Johansson, D
Melke, J
Lundstrom, S
Anckarsater, H
Lichtenstein, P
Westberg, L
AF Zettergren, Anna
Jonsson, Lina
Johansson, Daniel
Melke, Jonas
Lundstrom, Sebastian
Anckarsater, Henrik
Lichtenstein, Paul
Westberg, Lars
TI Associations between polymorphisms in sex steroid related genes and
autistic-like traits
SO PSYCHONEUROENDOCRINOLOGY
LA English
DT Article
DE Autism spectrum disorders; Autistic-like traits; Sex steroids; Gene;
Association; 5-alpha-reductase; Estrogen receptor; Testosterone
ID BREAST-CANCER RISK; RECEPTOR-ALPHA GENE; POLYCYSTIC-OVARY-SYNDROME;
HORMONE-BINDING GLOBULIN; SPECTRUM DISORDERS; PROSTATE-CANCER;
5-ALPHA-REDUCTASE TYPE-1; NEUROPSYCHIATRIC DISORDERS; TELEPHONE
INTERVIEW; ALCOHOL DEPENDENCE
AB Sex differences in psychiatric disorders are common, which is particularly striking in autism spectrum disorders (ASDs) that are four times more prevalent in boys. High levels of testosterone during early development have been hypothesized to be a risk factor for ASDs, supported by several studies showing fetal testosterone levels, as well as indirect measures of prenatal androgenization, to be associated with ASDs and autistic-like traits (ALTs). Further, the importance of sex steroid related genes in ASDs is supported by studies reporting associations between polymorphisms in genes involved in sex steroid synthesis/metabolism and ASDs and ALTs. The aim of the present study was to investigate possible associations between 29 single nucleotide polymorphisms (SNPs) in eight genes related to sex steroids and autistic features. Individuals included in the study belong to a subset (n = 1771) from The Child and Adolescent Twin Study in Sweden (CATSS), which are all assessed for ALTs. For two SNPs, rs2747648 located in the 3'-UTR of ESR1 encoding the estrogen receptor alpha and rs523349 (Leu89Val) located in SRD5A2 encoding 5-alpha-reductase, type 2, highly significant associations with ALTs were found in boys and girls, respectively. The results of the present study suggest that SNPs in sex steroid related genes, known to affect gene expression (rs2747648 in ESR1) and enzymatic activity (Leu89Val in SRD5A2), seem to be associated with ALTs in a general population. In conclusion, the current findings provide further support for a role of sex steroids in the pathophysiology of ASDs. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Zettergren, Anna; Jonsson, Lina; Johansson, Daniel; Melke, Jonas; Westberg, Lars] Univ Gothenburg, Inst Neurosci & Physiol, Dept Pharmacol, SE-40530 Gothenburg, Sweden.
[Lundstrom, Sebastian; Anckarsater, Henrik] Univ Gothenburg, Ctr Eth Law & Mental Hlth CELAM, Inst Neurosci & Physiol, SE-40530 Gothenburg, Sweden.
[Lundstrom, Sebastian] Univ Gothenburg, Gillberg Neuropsychiat Ctr, Inst Neurosci & Physiol, SE-40530 Gothenburg, Sweden.
[Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
RP Zettergren, A (reprint author), Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Pharmacol, POB 431, SE-40530 Gothenburg, Sweden.
EM anna.zettergren@pharm.gu.se
FU Swedish Research Council; Swedish Research Council for Working Life and
Social Research; Swedish Brain Foundation; Svenska Sallskapet for
Medicinsk Forskning (SSMF); Fredrik and Ingrid Thurings stiftelse; Ake
Wibergs stiftelse; Ahlen-stiftelsen; Jeanssons-stiftelsen; Mangus
Bergvalls stiftelse; Soderstrom-Konigska stiftelsen; Marta Lundqvists
stiftelse; Novo Nordisk Foundation
FX Funding for the study was provided by grants from the Swedish Research
Council, Swedish Research Council for Working Life and Social Research,
Swedish Brain Foundation, Svenska Sallskapet for Medicinsk Forskning
(SSMF), Fredrik and Ingrid Thurings stiftelse, Ake Wibergs stiftelse,
Ahlen-stiftelsen, Jeanssons-stiftelsen, Mangus Bergvalls stiftelse,
Soderstrom-Konigska stiftelsen, Marta Lundqvists stiftelse and the Novo
Nordisk Foundation.
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NR 89
TC 2
Z9 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4530
J9 PSYCHONEUROENDOCRINO
JI Psychoneuroendocrinology
PD NOV
PY 2013
VL 38
IS 11
BP 2575
EP 2584
DI 10.1016/j.psyneuen.2013.06.004
PG 10
WC Endocrinology & Metabolism; Neurosciences; Psychiatry
SC Endocrinology & Metabolism; Neurosciences & Neurology; Psychiatry
GA 268MT
UT WOS:000328175700018
PM 23867117
ER
PT J
AU Shaw, JS
Norlin, C
Gillespie, RJ
Weissman, M
McGrath, J
AF Shaw, Judith S.
Norlin, Chuck
Gillespie, R. J.
Weissman, Mark
McGrath, Jane
TI The National Improvement Partnership Network: State-Based Partnerships
That Improve Primary Care Quality
SO ACADEMIC PEDIATRICS
LA English
DT Article
DE maternal and child health; preventive services; quality improvement
ID PREVENTIVE SERVICES; HEALTH-CARE; CHILDREN; CHILDHOOD; OBESITY;
EDUCATION; DELIVERY; CENTERS
AB Improvement partnerships (IPs) are a model for collaboration among public and private organizations that share interests in improving child health and the quality of health care delivered to children. Their partners typically include state public health and Medicaid agencies, the local chapter of the American Academy of Pediatrics, and an academic health care organization or children's hospital. Most IPs also engage other partners, including a variety of public, private, and professional organizations and individuals. IPs lead and support measurement-based, systems-focused quality improvement (QI) efforts that primarily target primary care practices that care for children. Their projects are most often conducted as learning collaboratives that involve a team from each of 8 to 15 participating practices over 9 to 12 months. The improvement teams typically include a clinician, office manager, clinical staff (nurses or medical assistants), and, for some projects, a parent; the IPs provide the staff and local infrastructure. The projects target clinical topics, chosen because of their importance to public health, local clinicians, and funding agencies, including asthma, attention-deficit/hyperactivity disorder, autism, developmental screening, obesity, mental health, medical home implementation, and several others. Over the past 13 years, 19 states have developed (and 5 are exploring developing) IPs. These organizations share similar aims and methods but differ substantially in leadership, structure, funding, and longevity. Their projects generally engage pediatric and family medicine practices ranging from solo private practices to community health centers to large corporate practices. The practices learn about the project topic and about QI, develop specific improvement strategies and aims that align with the project aims, perform iterative measures to evaluate and guide their improvements, and implement systems and processes to support and sustain those improvements. Since 2008, IPs have offered credit toward Part 4 of Maintenance of Certification for participants in some of their projects. To date, IPs have focused on achieving improvements in care delivery through individual projects. Rigorous measurement and evaluation of their efforts and impact will be essential to understanding, spreading, and sustaining state/regional child health care QI programs. We describe the origins, evolution to date, and hopes for the future of these partnerships and the National Improvement Partnership Network (NIPN), which was established to support existing and nurture new IPs.
C1 [Shaw, Judith S.] Univ Vermont, Coll Med, Dept Pediat, Vermont Child Hlth Improvement Program, Burlington, VT 05405 USA.
[Norlin, Chuck] Univ Utah, Hlth Sci Ctr, Dept Pediat, Utah Pediat Partnership Improve Healthcare Qual, Salt Lake City, UT USA.
[Gillespie, R. J.] Oregon Hlth & Sci Univ, Dept Pediat, Oregon Pediat Improvement Partnership, Portland, OR 97201 USA.
[Weissman, Mark] Childrens Natl Med Ctr, Childrens Natl Hlth Network, DC Partnership Improve Childrens Healthcare Qual, Div Gen Pediat & Community Hlth, Washington, DC 20010 USA.
[McGrath, Jane] Univ New Mexico, Dept Pediat, Hlth Sci Ctr, Envis New Mexico, Albuquerque, NM 87131 USA.
RP Shaw, JS (reprint author), Univ Vermont, Coll Med, Dept Pediat, Vermont Child Hlth Improvement Program, N329 Courtyard Given,89 Beaumont Ave, Burlington, VT 05405 USA.
EM judith.shaw@uvm.edu
FU US Department of Health and Human Services, Centers for Medicare &
Medicaid Services [CFDA 93.767]
FX This document was developed, in part, under grant CFDA 93.767 from the
US Department of Health and Human Services, Centers for Medicare &
Medicaid Services. However, these contents do not necessarily represent
the policy of the US Department of Health and Human Services, and you
should not assume endorsement by the Federal Government.
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American Board of Medical Specialties, MAINT CERT
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NR 32
TC 0
Z9 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1876-2859
EI 1876-2867
J9 ACAD PEDIATR
JI Acad. Pediatr.
PD NOV-DEC
PY 2013
VL 13
IS 6
SU S
BP S84
EP S94
PG 11
WC Pediatrics
SC Pediatrics
GA 261TY
UT WOS:000327688700017
PM 24268091
ER
PT J
AU Ajzenman, HF
Standeven, JW
Shurtleff, TL
AF Ajzenman, Heather F.
Standeven, John W.
Shurtleff, Tim L.
TI Effect of Hippotherapy on Motor Control, Adaptive Behaviors, and
Participation in Children With Autism Spectrum Disorder: A Pilot Study
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Article
DE activities of daily living; adaptation, psychological; autistic
disorder; equine-assisted therapy; motor skills; postural balance
ID SENSORY PROCESSING DISORDERS; YOUNG-CHILDREN; IMPAIRMENT
AB OBJECTIVE. The purpose of this investigation was to determine whether hippotherapy increased function and participation in children with autism spectrum disorder (ASD). We hypothesized improvements in motor control, which might increase adaptive behaviors and participation in daily activities.
METHOD. Six children with ASD ages 5-12 participated in 12 weekly 45-min hippotherapy sessions. Measures pre- and post-hippotherapy included the Vineland Adaptive Behavior Scales-II and the Child Activity Card Sort. Motor control was measured preintervention and postintervention using a video motion capture system and force plates.
RESULTS. Postural sway significantly decreased postintervention. Significant increases were observed in overall adaptive behaviors (receptive communication and coping) and in participation in self-care, low-demand leisure, and social interactions.
CONCLUSION. These results suggest that hippotherapy has a positive influence on children with ASD and can be a useful treatment tool for this population.
C1 [Ajzenman, Heather F.] Childrens Therapy Associates, Hillsborough, NC USA.
[Standeven, John W.] Washington Univ, Sch Med, Human Performance Lab, Program Occupat Therapy, St Louis, MO 63108 USA.
[Shurtleff, Tim L.] Washington Univ, Sch Med, Program Occupat Therapy, St Louis, MO 63108 USA.
RP Ajzenman, HF (reprint author), Childrens Therapy Associates, Hillsborough, NC USA.
CR American Hippotherapy Association, 2010, HIPP TREATM STRAT
American Psychiatric Association, 2000, DIAGN STAT MAN MENT
American Psychiatric Association, 2013, DIAGN STAT MAN MENT
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Engel B., 2007, ENHANCING HUMAN OCCU
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Su CT, 2010, AM J OCCUP THER, V64, P443, DOI 10.5014/ajot.2010.09074
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Winter DA, 2005, BIOMECHANICS MOTOR C
NR 27
TC 1
Z9 1
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
EI 1943-7676
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2013
VL 67
IS 6
BP 653
EP 663
DI 10.5014/ajot.2013.008383
PG 11
WC Rehabilitation
SC Rehabilitation
GA 260FB
UT WOS:000327579300005
PM 24195899
ER
PT J
AU Classen, S
Monahan, M
Wang, YN
AF Classen, Sherrilene
Monahan, Miriam
Wang, Yanning
TI Driving Characteristics of Teens With Attention Deficit Hyperactivity
and Autism Spectrum Disorder
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Article
DE attention deficit disorder with hyperactivity; automobile driving; child
development disorders, pervasive; cognition; psychomotor performance
ID SPECIAL-EDUCATION SERVICES; FIELD-OF-VIEW; DEFICIT/HYPERACTIVITY
DISORDER; UNITED-STATES; OLDER-ADULTS; CHILDREN; PERFORMANCE; ADHD;
ADOLESCENTS; PERCEPTION
AB Vehicle crashes are a leading cause of death among teens. Teens with attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), or both (ADHD ASD) may have a greater crash risk. We examined the between-groups demographic, clinical, and predriving performance differences of 22 teens with ADHD ASD (mean age = 15.05, standard deviation [SD] = 0.95) and 22 healthy control (HC) teens (mean age = 14.32, SD = 0.72). Compared with HC teens, the teens with ADHD ASD performed more poorly on right-eye visual acuity, selective attention, visual motor integration, cognition, and motor performance and made more errors on the driving simulator pertaining to visual scanning, speed regulation, lane maintenance, adjustment to stimuli, and total number of driving errors. Teens with ADHD ASD, compared with HC teens, may have more predriving deficits and as such require the skills of a certified driving rehabilitation specialist to assess readiness to drive.
C1 [Classen, Sherrilene] Univ Western Ontario, Elborn Coll, Sch Occupat Therapy, London, ON N6A 5B9, Canada.
[Classen, Sherrilene; Monahan, Miriam] Univ Florida, Coll Publ Hlth & Hlth Profess, Inst Mobil Act & Participat, Gainesville, FL USA.
[Classen, Sherrilene; Monahan, Miriam] Univ Florida, Coll Publ Hlth & Hlth Profess, Dept Occupat Therapy, Gainesville, FL USA.
[Wang, Yanning] Univ Florida, Coll Publ Hlth & Hlth Profess, Dept Epidemiol, Gainesville, FL USA.
RP Classen, S (reprint author), Univ Western Ontario, Elborn Coll, Sch Occupat Therapy, London, ON N6A 5B9, Canada.
EM sclassen@uwo.ca
CR American Psychiatric Association, 2013, DIAGN STAT MAN MENT
Ashwin E, 2009, BIOL PSYCHIAT, V65, P17, DOI 10.1016/j.biopsych.2008.06.012
Ball K, 1993, J Am Optom Assoc, V64, P71
Barkley RA, 1997, PSYCHOL BULL, V121, P65, DOI 10.1037//0033-2909.121.1.65
Beery K. E., 2010, BERRY BUKTENICA DEV, V6th
Bitterman A, 2008, J AUTISM DEV DISORD, V38, P1509, DOI 10.1007/s10803-007-0531-9
Brouwer W H, 1994, Disabil Rehabil, V16, P149
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Centers for Disease Control and Prevention, 2012, AUTISM SPECTRUM DISO
Visser S. N., 2010, Morbidity and Mortality Weekly Report, V59, P1439
Classen S, 2010, AM J OCCUP THER, V64, P211
Classen S, 2011, AM J OCCUP THER, V65, P579, DOI 10.5014/ajot.2011.001073
Classen S, 2013, TRAFFIC INJ PREV, V14, P188, DOI 10.1080/15389588.2012.700747
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Schnoes C, 2006, EXCEPT CHILDREN, V72, P483
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Teen Drivers, 2012, TEEN DRIV FACT SHEET
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Wechsler D., 2004, WECHSLER INTELLIGENC
NR 38
TC 1
Z9 1
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
EI 1943-7676
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2013
VL 67
IS 6
BP 664
EP 673
DI 10.5014/ajot.2013.008821
PG 10
WC Rehabilitation
SC Rehabilitation
GA 260FB
UT WOS:000327579300006
PM 24195900
ER
PT J
AU Yonkman, J
Lawler, B
Laity, J
O'Neil, J
Bull, M
AF Yonkman, Janell
Lawler, Bryanna
Laity, Judith
O'Neil, Joseph
Bull, Marilyn
TI Safely Transporting Children With Autism Spectrum Disorder: Evaluation
and Intervention
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Article
DE child development disorders, pervasive; child restraint systems; motor
vehicles; safety; transportation
AB OBJECTIVE. The purpose of this study was to investigate transportation practices of caregivers who transport children diagnosed with autism spectrum disorders (ASD).
METHOD. We reviewed documented transportation evaluations of children with ASD. The evaluations were conducted by pediatric occupational therapists at an outpatient center of a large children's hospital.
RESULTS. A review of 82 charts of patients diagnosed with ASD revealed that 74% of children with ASD were escaping their child safety restraint. More than 20% of parents reported that their child demonstrated aggressive or self-injurious behavior during travel, affecting not only their own safety but also that of others in the vehicle, including the driver.
CONCLUSION.. Escaping from a child restraint can be a life-threatening problem among children with ASD. Parents, caregivers, and health care professionals should be aware of services available from trained therapists, certified child passenger safety technicians, or both to maximize safety during personal travel in the family vehicle.
C1 [Yonkman, Janell; Lawler, Bryanna; Laity, Judith; O'Neil, Joseph; Bull, Marilyn] Indiana Univ Hlth, Riley Hosp Children, Natl Ctr Safe Transportat Children Special Health, Indianapolis, IN 46202 USA.
RP Yonkman, J (reprint author), Indiana Univ Hlth, Riley Hosp Children, Natl Ctr Safe Transportat Children Special Health, 1120 South Dr,Fesler Hall 207, Indianapolis, IN 46202 USA.
EM jyonkman@iuhealth.org
CR Centers for Disease Control and Prevention, 2012, MMWR-MORBID MORTAL W, V60, P1
Falkmer T., 2004, SCANDINAVIAN J OCCUP, V11, P90, DOI 10.1080/11038120410020575
National Center for Injury Prevention and Control, 2010, WEB BAS INJ STAT QUE
National Center for Injury Prevention and Control, 2011, CHILD PASS SAF FACT
National Highway Traffic Safety Administration, 2004, 809671 DOT HS NAT HI
National Highway Traffic Safety Administration, 2007, 810731 DOT HS NAT HI
Weber K., 2000, UMTRI RES REV, V31, P311
NR 7
TC 1
Z9 1
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
EI 1943-7676
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2013
VL 67
IS 6
BP 711
EP 716
DI 10.5014/ajot.2013.008250
PG 6
WC Rehabilitation
SC Rehabilitation
GA 260FB
UT WOS:000327579300011
PM 24195905
ER
PT J
AU Senechal, C
Larivee, S
Thermidor, G
AF Senechal, Carole
Larivee, Serge
Thermidor, Ghitza
TI Parents as co-therapists: A winning solution for treating autistic
children
SO ANNALES MEDICO-PSYCHOLOGIQUES
LA French
DT Article
DE Autism; Early intervention; Parental involvement
ID EARLY INTERVENTION; YOUNG-CHILDREN; SPECTRUM DISORDER; COMMUNICATION;
KNOWLEDGE; BEHAVIOR; BELIEFS; PROGRAM; MOTHERS; FAMILY
AB Objectives. - This article aims to report on the effects of an intervention program carried out in a clinical context and destined to parents of autistic children. The program was part of a diagnostic evaluation process and sought to provide parents with essential support as soon as their child was diagnosed. It was also designed to increase their knowledge of autism's particular characteristics. Method. - Each of the fourteen families participating in this research had a child aged between two and six years old who had been diagnosed with autism. They were assessed with the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule Generic (ADOS-G) by a team from Riviere-des-Prairies Hospital, in the Montreal area, specialized in Pervasive Developmental Disorder. The specification identified for this study was a quasi-experimental protocol with a pre- and post-test and a non-equivalent control group. The first eight families registered with the clinic were part of the experimental group; the other six formed the control group. The experimental group was composed of six boys and two girls whose average age was 48 months (span: 34-72). The implemented program contained two intervention targets: communication and the child's learning. Five individual sessions of approximately 90 minutes each were provided to each family. A psycho-educator directed activities chosen according to the developmental level of each child. Because one of the objectives of the program was to help parents intervene with their child, they were involved in the intervention each in turn, either by observing or by practising those intervention techniques identified for their child. In order to measure the change in parental practices, the Maternal Behavior Rating Scale was used. This observation table is composed of 12 items assessed with a Likert-type five-point scale, one meaning very low, and five meaning very elevated, evaluating four scales of parental educational practices designed to improve children's development: the parent's response (three items), the parent's animation (five items), the parent's support with the task (two items) and his or her authority (two items). The program's impact with the child was assessed with the Child Behavior Rating Scale, an observation table comprised of two scales recognized as preconditions to children's development: attention (four items) and initiation (two items). These items were assessed by two observers with a Likert-type five-point scale, one meaning very low and five meaning very elevated. Inter-rater coefficients varied between 0.88 and 0.93. Results. Variance analyses undertaken from the results obtained with the Maternal Behavior Rating Scales and the Child Behavior Rating Scales before and after the intervention showed that both groups improved but that this improvement did not vary significantly from one group to the other. Conclusions. Four elements may help explain the absence of significant results. Firstly, all children except one were recipients of other services during the intervention. Secondly, with regards to the objective of helping parents better understand their child's diagnostic, five 90-minute individual sessions appeared to be sufficient, but obviously that was not the case. Thirdly, there were difficulties with the recruitment and the sample's non-homogeneity. Fourthly, over and above their good psychometric qualities, the two instruments used were not sufficiently attuned to more subtle changes.
Finally, we must insist on the importance, especially in human and social sciences, of publishing results considered as negative in as much as those results form an integral part of the scientific process. (C) 2013 Elsevier Masson SAS. All rights reserved.
C1 [Senechal, Carole] Univ Ottawa, Ottawa, ON K1N 6N5, Canada.
[Larivee, Serge; Thermidor, Ghitza] Univ Montreal, Ecole Psychoeduc, Montreal, PQ H3C 3J7, Canada.
RP Senechal, C (reprint author), Univ Ottawa, Pavillon Lamoureux,145 Jean Jacques Lussier, Ottawa, ON K1N 6N5, Canada.
EM carole.senechal@uottawa.ca
CR Aldred C, 2004, J CHILD PSYCHOL PSYC, V45, P1420, DOI 10.1111/j1469-7610.2004.00338.x
American Psychiatric Association, 1996, DSM 4 MAN DIAGN STAT, V4th
[Anonymous], 2012, SUMMARIES SCI RES IN
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NR 39
TC 0
Z9 0
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
SN 0003-4487
EI 1769-6631
J9 ANN MED-PSYCHOL
JI Ann. Med.-Psychol.
PD NOV
PY 2013
VL 171
IS 9
BP 603
EP 609
DI 10.1016/j.amp.2012.11.013
PG 7
WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology,
Multidisciplinary
SC Pharmacology & Pharmacy; Psychiatry; Psychology
GA 260FF
UT WOS:000327579700002
ER
PT J
AU Velloso, RD
Duarte, CP
Schwartzman, JS
AF Velloso, Renata de Lima
Duarte, Cintia Perez
Schwartzman, Jose Salomao
TI Evaluation of the theory of mind in autism spectrum disorders with the
Strange Stories test
SO ARQUIVOS DE NEURO-PSIQUIATRIA
LA English
DT Article
DE child developmental disorders; pervasive; autism; theory of mind
ID ASPERGER-SYNDROME; CHILDREN; ADOLESCENTS; PERFORMANCE; REPLICATION;
ADULTS; TASKS
AB Objective: To evaluate the theory of mind in autism spectrum disorders (ASD) and control individuals by applying the Strange Stories test that was translated and adapted to the Portuguese language. Method: Twenty-eight children with ASD and 56 controls who were all mate and aged between 6 and 12 years participated in the study. Results: There were significant differences between the median scores of the groups for each of the 12 stories of the test and for the sum total of all the median scores. The median scores for all stories were significantly greater in the control group than those in the experimental group (children with ASD). In addition, the protocol had excellent internal consistency. Conclusion: The theory of mind skills assessed with the Strange Stories test indicated alterations in children with ASD compared with children in the control group.
C1 [Velloso, Renata de Lima; Duarte, Cintia Perez] Univ Presbiteriana Mackenzie, Sao Paulo, Brazil.
[Schwartzman, Jose Salomao] Univ Fed Sao Paulo, Sao Paulo, Brazil.
[Schwartzman, Jose Salomao] Univ Presbiteriana Mackenzie, Programs Posgrad Disturbios Desenvolvimento, Sao Paulo, Brazil.
RP Velloso, RD (reprint author), Rua Piaui 181, BR-01241001 Sao Paulo, Brazil.
EM relimavelloso@yahoo.com.br
CR APA American Psychiatric Association, 2002, DIAGN STAT MAN MENT
BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8
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Frith U., 1996, AUTISM ASPERGERS SYN
HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093
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Hermelin B, 1985, COMMUNICATION PROBLE, P283
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Kaland N, 2002, J CHILD PSYCHOL PSYC, V43, P517, DOI 10.1111/1469-7610.00042
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O'Hare AE, 2009, J AUTISM DEV DISORD, V39, P916, DOI 10.1007/s10803-009-0699-2
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Sattler J, 1992, ASSESSMENT CHILDRE S
Sperber D., 1986, RELEVANCE COMMUNICAT
Wechsler D, 2002, WECHSLER INTELLIGENC, V3rd
WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288
World Health Organisation, 2000, INT CLASS DIS ICD 10
NR 22
TC 0
Z9 0
PU ASSOC ARQUIVOS NEURO- PSIQUIATRIA
PI SAO PAULO SP
PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL
SN 0004-282X
EI 1678-4227
J9 ARQ NEURO-PSIQUIAT
JI Arq. Neuro-Psiquiatr.
PD NOV
PY 2013
VL 71
IS 11
BP 871
EP 876
DI 10.1590/0004-282X20130171
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 263SH
UT WOS:000327827800010
ER
PT J
AU Ponde, MP
Rousseau, C
Carlos, MAC
AF Ponde, Milena Pereira
Rousseau, Cecile
Costa Carlos, Marco Antonio
TI Pervasive developmental disorder in the children of immigrant parents:
comparison of different assessment instruments
SO ARQUIVOS DE NEURO-PSIQUIATRIA
LA English
DT Article
DE autism spectrum disorder; diagnosis
ID AUTISM SPECTRUM DISORDERS; OBSERVATION-SCHEDULE ADOS; CHILDHOOD AUTISM;
RATING-SCALE; BEHAVIOR; DIAGNOSIS
AB The objective of this study was to describe how the Childhood Autism Rating Scale (CARS) behaves in relation to the Autism Diagnostic Observation Schedule (ADDS) and to clinical diagnosis based on the criteria defined in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) for children of immigrant parents. Forty-nine children of parents who had immigrated to Canada were evaluated. In this sample, the ADOS and the DSM-IV showed complete agreement. Using the standard cut-off point of 30, the CARS showed high specificity and poor sensitivity. The study proposes a cut-off point for the CARS that would include pervasive developmental disorder not otherwise specified (PDD-NOS). Reducing the cut-off point to 20/21 increased the specificity of the instrument for this group of children without significantly reducing its sensitivity.
C1 [Ponde, Milena Pereira; Costa Carlos, Marco Antonio] Bahiana Sch Med & Publ Hlth, Interdisciplinary Lab Autism Res LABIRINTO, Salvador, BA, Brazil.
[Rousseau, Cecile] McGill Univ, Div Social & Cultural Psychiat, TRIT, Montreal, PQ, Canada.
RP Ponde, MP (reprint author), Av Dom Joao 6 275, BR-40290000 Salvador, BA, Brazil.
EM milenaponde@bahiana.edu.br
FU Bahia State Research Foundation (FAPESB) [0086/2009]
FX This study formed part of a postdoctoral thesis by the first author and
was financially supported by the Bahia State Research Foundation
(FAPESB), Grant No 0086/2009.
CR American Psychiatric Association (APA), 2012, DSM 5 PROP CRIT AUT
APA, 2000, DSM 4 TR DIAGN STAT
Bolte S, 2004, Z KINDER JUG-PSYCH, V32, P45, DOI 10.1024/1422-4917.32.1.45
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Lord C., 2006, AUTISM DIAGNOSTIC OB
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SHAFFER D, 1983, ARCH GEN PSYCHIAT, V40, P1228
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Volkmar F, 2005, ANNU REV PSYCHOL, V56, P315, DOI 10.1146/annurev.psych.56.091103.070159
NR 19
TC 0
Z9 0
PU ASSOC ARQUIVOS NEURO- PSIQUIATRIA
PI SAO PAULO SP
PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL
SN 0004-282X
EI 1678-4227
J9 ARQ NEURO-PSIQUIAT
JI Arq. Neuro-Psiquiatr.
PD NOV
PY 2013
VL 71
IS 11
BP 877
EP 882
DI 10.1590/0004-282X20130091
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 263SH
UT WOS:000327827800011
PM 24394875
ER
PT J
AU Wolstenholme, JT
Goldsby, JA
Rissman, EF
AF Wolstenholme, Jennifer T.
Goldsby, Jessica A.
Rissman, Emilie F.
TI Transgenerational effects of prenatal bisphenol A on social recognition
SO HORMONES AND BEHAVIOR
LA English
DT Article
DE Endocrine disrupting chemicals; Social recognition; Transgenerational
inheritance; Attention deficit hyperactivity disorder; Autism;
Epigenetics
ID ENDOCRINE-DISRUPTING CHEMICALS; ESTROGEN-RECEPTOR-ALPHA; PERINATAL
EXPOSURE; GESTATIONAL EXPOSURE; AGGRESSIVE-BEHAVIOR; MATERNAL-BEHAVIOR;
AUTISTIC TRAITS; GENE-EXPRESSION; SEX-DIFFERENCES; WATER MAZE
AB Bisphenol A (BPA) is a man-made endocrine disrupting compound used to manufacture polycarbonate plastics. It is found in plastic bottles, canned food linings, thermal receipts and other commonly used items. Over 93% of people have detectable BPA levels in their urine. Epidemiological studies report correlations between BPA levels during pregnancy and activity, anxiety, and depression in children. We fed female mice control or BPA-containing diets that produced plasma BPA concentrations similar to concentrations in humans. Females were mated and at birth, pups were fostered to control dams to limit BPA exposure to gestation in the first generation. Sibling pairs were bred to the third generation with no further BPA exposure. First (F1) and third (F3) generation juveniles were tested for social recognition and in the open field. Adult F3 mice were tested for olfactory discrimination. In both generations, BPA exposed juvenile mice displayed higher levels of investigation than controls in a social recognition task. In F3 EPA exposed mice, dishabituation to a novel female was impaired. In the open field, no differences were noted in F1 mice, while in F3, BPA lineage mice were more active than controls. No impairments were detected in F3 mice, all were able to discriminate different male urine pools and urine from water. No sex differences were found in any task. These results demonstrate that BPA exposure during gestation has long lasting, transgenerational effects on social recognition and activity in mice. These findings show that BPA exposure has transgenerational actions on behavior and have implications for human neurodevelopmental behavioral disorders. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Wolstenholme, Jennifer T.; Goldsby, Jessica A.; Rissman, Emilie F.] Univ Virginia, Sch Med, Dept Biochem & Mol Genet, Charlottesville, VA 22908 USA.
RP Rissman, EF (reprint author), Univ Virginia, Sch Med, Dept Biochem & Mol Genet, Charlottesville, VA 22908 USA.
EM Rissman@virginia.edu
FU NIH [R01 MH057759]; [F32 ES019404]
FX This work is supported by NIH R01 MH057759 (EFR). JTW is supported by
F32 ES019404.
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NR 61
TC 14
Z9 14
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0018-506X
EI 1095-6867
J9 HORM BEHAV
JI Horm. Behav.
PD NOV
PY 2013
VL 64
IS 5
BP 833
EP 839
DI 10.1016/j.yhbeh.2013.09.007
PG 7
WC Behavioral Sciences; Endocrinology & Metabolism
SC Behavioral Sciences; Endocrinology & Metabolism
GA 261TO
UT WOS:000327687700010
PM 24100195
ER
PT J
AU Field, T
Ezell, S
Nadel, J
Grace, A
Allender, S
Siddalingappa, V
AF Field, Tiffany
Ezell, Shauna
Nadel, Jacqueline
Grace, Ava
Allender, Susan
Siddalingappa, Vijaya
TI Reciprocal Imitation Following Adult Imitation by Children with Autism
SO INFANT AND CHILD DEVELOPMENT
LA English
DT Article
DE imitation; social attention; children with autism
ID LANGUAGE
AB This study examined the effects of adult imitation and adult playfulness on the imitation, social attention and initiation of new behaviours by non-verbal preschoolers with autism. Videotapes taken from a previous study were recoded for the adult's imitation and playful behaviour and the children's imitation, social attention (looking at the adult's actions) and initiation of new behaviours. In the original study, twenty non-verbal, 4- to 6-year-old children with autism were randomly assigned to an imitation or a contingent responsivity group. Both groups of children engaged in an intervention phase (during which the adult imitated the children or contingently responded to them) and a subsequent spontaneous play phase (during which the adult interacted spontaneously with the children). ANOVA for the current study revealed that the imitation group children versus the contingent responsivity group children spent a greater percent time showing social attention and initiating new behaviours during the intervention phase and showing social attention and imitating the adult's behaviours during the subsequent spontaneous play phase. A correlation analysis yielded significant correlations between the percent time the adult imitated the child during the intervention phase and the percent time the child showed social attention during the same intervention phase and imitating the adult during the subsequent spontaneous play phase. Adult imitation and playfulness during the spontaneous play phase were also correlated with the children's social attention during that phase. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Field, Tiffany] Univ Miami, Sch Med, Dept Pediat, Miami, FL 33152 USA.
[Field, Tiffany; Ezell, Shauna; Grace, Ava; Allender, Susan; Siddalingappa, Vijaya] Univ Miami, Fielding Grad Univ, Sch Med, Miami, FL USA.
[Nadel, Jacqueline] Hop La Pitie Salpetriere, Ctr Emot, CNRS, USR 3246, Paris, France.
RP Field, T (reprint author), Univ Miami, Sch Med, Dept Pediat, Miami, FL 33152 USA.
EM tfield@med.miami.edu
CR Cardon TA, 2011, J AUTISM DEV DISORD, V41, P654, DOI 10.1007/s10803-010-1086-8
Field T., 2008, EARLY CHILD DEV CARE, V178, P1
Field T, 2001, AUTISM, V5, P317, DOI 10.1177/1362361301005003008
Heimann M, 2006, INFANT CHILD DEV, V15, P297, DOI 10.1002/icd.463
Ingersoll B, 2006, J AUTISM DEV DISORD, V36, P487, DOI 10.1007/s10803-006-0089-y
Ingersoll B, 2012, J AUTISM DEV DISORD, V42, P1768, DOI 10.1007/s10803-011-1423-6
Katagiri M, 2010, RES AUTISM SPECT DIS, V4, P474, DOI 10.1016/j.rasd.2009.11.004
Nadel J., 2008, EARLY CHILD DEV CARE, V178, P461, DOI 10.1080/03004430600801699
Nadel J., 2006, IMITATION SOCIAL MIN, P118
Vanvuchelen M, 2011, RES DEV DISABIL, V32, P148, DOI 10.1016/j.ridd.2010.09.010
NR 10
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1522-7219
J9 INFANT CHILD DEV
JI Infant Child Dev.
PD NOV
PY 2013
VL 22
IS 6
BP 642
EP 648
DI 10.1002/icd.1812
PG 7
WC Psychology, Developmental
SC Psychology
GA 264ST
UT WOS:000327901500006
ER
PT J
AU Tajeran, M
Baghbani, F
Hassanzadeh-Nazarabadi, M
AF Tajeran, Massoumeh
Baghbani, Fatemeh
Hassanzadeh-Nazarabadi, Mohammad
TI A Case of Autism with Ring Chromosome 14
SO IRANIAN JOURNAL OF PUBLIC HEALTH
LA English
DT Article
DE Autistic disorder; Ring chromosome 14; Cytogenetic analysis
ID SPECTRUM DISORDERS; MUTATIONS; DELETIONS; GENETICS; LOCUS; ETIOLOGY;
EPILEPSY; SHANK3; GENES
AB Background: Autism is a complex neuropsychiatric disorder that manifests in early childhood. Although the etiology is unknown yet but, new hypothesis focused on identifying the key genes related to autism may elucidate its etiology. The main objective of the present study was to verify the value of karyotyping in autistic children and identifying association between chromosome abnormalities and autism.
Methods: We examined the peripheral blood lymphocytes cell culture for cytogenetic alterations by GTG-banding technique. The investigation was carried out on 50 autistic patients referred by Pediatric neurologist to Cytogenetic Laboratory in Khorasan-e-razavi Province, Iran.
Results: Using GTG-banding technique, the chromosome analysis of patients identified an unbalanced male karyotype with a r (14) in all 50 metaphases were examined.
Conclusion: Since structural abnormalities may have a critical role in the etiology of autism, according to the region where is affected and number of related genes, therefore an outcome with wide spectrum of clinical manifestations could be expected. Furthermore by considering of recent study, the results indicated that there is an association between chromosome 14 with brain development and neurological disorders, but, in conclusion, it could not be suggested that in order to postulate cytogenetic testing in idiopathic autism patients, specifically screening for chromosome 14 which might has diagnostic value.
C1 [Tajeran, Massoumeh; Baghbani, Fatemeh; Hassanzadeh-Nazarabadi, Mohammad] Mashhad Univ Med Sci, Dept Med Genet, Sch Med, Mashhad, Iran.
RP Hassanzadeh-Nazarabadi, M (reprint author), Mashhad Univ Med Sci, Dept Med Genet, Sch Med, Mashhad, Iran.
EM nazarabadim@mums.ac.ir
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NR 33
TC 0
Z9 0
PU IRANIAN SCIENTIFIC SOCIETY MEDICAL ENTOMOLOGY
PI TEHRAN
PA SCHOOL PUBLIC HEALTH & INST HEALTH RESEARCH, TEHRAN UNIV MEDICAL
SCIENCES, P O BOX 6446-14155, TEHRAN, 00000, IRAN
SN 2251-6085
EI 2251-6093
J9 IRAN J PUBLIC HEALTH
JI Iran J. Public Health
PD NOV
PY 2013
VL 42
IS 11
BP 1316
EP 1320
PG 5
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 262NX
UT WOS:000327743500015
ER
PT J
AU Jaarsma, P
Welin, S
AF Jaarsma, Pier
Welin, Stellan
TI Human capabilities, mild autism, deafness and the morality of embryo
selection
SO MEDICINE HEALTH CARE AND PHILOSOPHY
LA English
DT Article
DE Autism; Reproduction; Genetic selection; Ethics; Human capabilities;
Procreative beneficence; Quality of life
ID ASPERGERS; CHICKENS; BLIND
AB A preimplantation genetic test to discriminate between severe and mild autism spectrum disorder might be developed in the foreseeable future. Recently, the philosophers Julian Savulescu and Guy Kahane claimed that there are strong reasons for prospective parents to make use of such a test to prevent the birth of children who are disposed to autism or Asperger's disorder. In this paper we will criticize this claim. We will discuss the morality of selection for mild autism in embryo selection in a hypothetical in vitro fertilization (IVF) situation where preimplantation genetic diagnosis is performed and compare this with a similar selection for congenital deafness. To do this we first discuss relevant human differences. We then introduce the principle of human capabilities (PC) and compare this principle with the principle of procreative beneficence (PB) introduced by Savulescu and Kahane. We apply the two principles to selection for mild autism and selection for congenital deafness. We argue that PC allows for the selection for mild autism but rules out selection for congenital deafness. PB will not give clear answers; the ruling of PB depends to a large extent on expected social, cultural and political developments. We will argue that PC is preferable to PB. We will discuss arguments for the value of mild autism for individuals who have this condition and argue that they are able to lead a life with human dignity provided autism-friendly social circumstances are present. Neither PC nor PB yields strong reasons for prospective parents to seek to prevent the birth of children who are disposed to mild autism spectrum disorder.
C1 [Jaarsma, Pier; Welin, Stellan] Linkoping Univ, IMH, Div Hlth & Soc, SE-58183 Linkoping, Sweden.
RP Jaarsma, P (reprint author), Linkoping Univ, IMH, Div Hlth & Soc, SE-58183 Linkoping, Sweden.
EM pier.jaarsma@liu.se
CR ALI A, 1985, POULTRY SCI, V64, P789
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Grandin Temple, 2006, THINKING PICTURES MY, Vrev
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Nussbaum M., 2004, THINKING FEELING CON
Nussbaum Martha, 2006, FRONTIERS JUSTICE DI
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NR 37
TC 0
Z9 0
PU SPRINGER
PI DORDRECHT
PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS
SN 1386-7423
EI 1572-8633
J9 MED HEALTH CARE PHIL
JI Med. Health Care Philos.
PD NOV
PY 2013
VL 16
IS 4
BP 817
EP 824
DI 10.1007/s11019-013-9464-6
PG 8
WC Ethics; History & Philosophy Of Science
SC Social Sciences - Other Topics; History & Philosophy of Science
GA 253ZE
UT WOS:000327128500021
PM 23334404
ER
PT J
AU Frye, RE
Rose, S
Slattery, J
Wynne, R
Tippett, M
Melynk, S
James, SJ
AF Frye, Richard E.
Rose, Shannon
Slattery, John
Wynne, Rebecca
Tippett, Marie
Melynk, Stephan
James, S. Jill
TI Mitochondrial dysfunction in immune cells derived from children with
autism spectrum disorder (ASD): A unique metabolic endophenotype of
children with ASD
SO MITOCHONDRION
LA English
DT Meeting Abstract
C1 [Frye, Richard E.; Rose, Shannon; Slattery, John; Wynne, Rebecca; Tippett, Marie; Melynk, Stephan; James, S. Jill] Univ Arkansas Med Sci, Dept Pediat, Arkansas Childrens Hosp, Res Inst, Little Rock, AR 72202 USA.
NR 0
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
EI 1872-8278
J9 MITOCHONDRION
JI Mitochondrion
PD NOV
PY 2013
VL 13
IS 6
MA 37
BP 910
EP 910
DI 10.1016/j.mito.2013.07.034
PG 1
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 255ZY
UT WOS:000327280500074
ER
PT J
AU Coskun, PE
Nemantinejad, Z
Schwarts, PH
Brick, DJ
Busciglio, J
AF Coskun, Pinar E.
Nemantinejad, Zahra
Schwarts, Phillip H.
Brick, David J.
Busciglio, Jorge
TI Mitochondrial dysfunction in autism fibroblasts
SO MITOCHONDRION
LA English
DT Meeting Abstract
C1 [Coskun, Pinar E.; Nemantinejad, Zahra; Busciglio, Jorge] Univ Calif Irvine, Dept Neurobiol & Behav, iMIND, Irvine, CA 92697 USA.
[Coskun, Pinar E.; Busciglio, Jorge] Univ Calif Irvine, CNLM, Irvine, CA 92697 USA.
[Schwarts, Phillip H.; Brick, David J.] Childrens Hosp Orange Cty Res Inst CHOC, Neurosci Labs, Ctr Neurosci, Orange, CA 92868 USA.
[Schwarts, Phillip H.; Brick, David J.] Childrens Hosp Orange Cty Res Inst CHOC, Neurosci Labs, Ctr Translat Res, Orange, CA 92868 USA.
NR 0
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
EI 1872-8278
J9 MITOCHONDRION
JI Mitochondrion
PD NOV
PY 2013
VL 13
IS 6
MA 108
BP 937
EP 938
DI 10.1016/j.mito.2013.07.100
PG 2
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 255ZY
UT WOS:000327280500140
ER
PT J
AU Moraes, CT
Anderson, V
Mohan, C
AF Moraes, Carlos T.
Anderson, Vernon
Mohan, Charles
TI Translational research in primary mitochondrial diseases: Challenges and
opportunities
SO MITOCHONDRION
LA English
DT Article
DE Workshop; Mitochondrial diseases; Animal models; NIH
AB On March 8-9, 2012, the NIH intramural and extramural research communities as well as representatives from industries and foundations with a common interest in primary mitochondrial diseases met in Bethesda to identify the major barriers to the development of better treatment for mitochondrial diseases. Besides the importance to the patient population, it has become clear in the last decade that advances in understanding and treating primary mitochondrial diseases will impact research into a large number of degenerative conditions known to have a significant mitochondrial dysfunction component in their pathogenic mechanisms (secondary mitochondrial diseases) that affect millions of people, including Alzheimer's disease, Parkinson's disease, diabetes, ALS, autism spectrum disorders, and many others.
We would like to make this discussion available to the scientific community, as it provides a framework on how patient advocacy groups, individual academic units, pharmaceutical companies, and the NIH can interact to address problems related to mitochondrial diseases.
The main goals of this workshop were as follows: (1) to share information related to primary mitochondrial disease among the NIH Intramural and Extramural Research Program Investigators, (2) to develop and/or enhance systems to facilitate future collaboration and sharing of information, (3) to survey obstacles, needs and priorities of primary mitochondrial diseases research, and (4) to develop mechanisms to enhance translation of basic science discoveries to diagnostics and therapeutics.
C1 [Moraes, Carlos T.] Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
[Anderson, Vernon] NIGMS, Div Pharmacol Physiol & Biol Chem, Bethesda, MD USA.
[Mohan, Charles] United Mitochondrial Dis Fdn, Pittsburgh, PA USA.
RP Moraes, CT (reprint author), Univ Miami, Miller Sch Med, Dept Neurol, Miami, FL 33136 USA.
EM cmoraes@med.miami.edu
FU UMDF/NIH
FX A UMDF/NIH sponsored workshop to identify barriers to treatments to
mitochondrial diseases.
NR 0
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1567-7249
EI 1872-8278
J9 MITOCHONDRION
JI Mitochondrion
PD NOV
PY 2013
VL 13
IS 6
BP 945
EP 952
DI 10.1016/j.mito.2013.08.002
PG 8
WC Cell Biology; Genetics & Heredity
SC Cell Biology; Genetics & Heredity
GA 255ZY
UT WOS:000327280500155
PM 23962609
ER
PT J
AU Ozcaliskan, S
Dimitrova, N
AF Ozcaliskan, Seyda
Dimitrova, Nevena
TI How Gesture Input Provides a Helping Hand to Language Development
SO SEMINARS IN SPEECH AND LANGUAGE
LA English
DT Article
DE Gesture production; gesture input; language development; gesture-speech
combination
ID JOINT ATTENTION; YOUNG-CHILDREN; DOWNS-SYNDROME; MOTHERS SPEECH;
INFANTS; COMMUNICATION; COMPREHENSION; VOCABULARY; WORDS; AUTISM
AB Children use gesture to refer to objects before they produce labels for these objects and gesture-speech combinations to convey semantic relations between objects before conveying sentences in speecha trajectory that remains largely intact across children with different developmental profiles. Can the developmental changes that we observe in children be traced back to the gestural input that children receive from their parents? A review of previous work shows that parents provide models for their children for the types of gestures and gesture-speech combinations to produce, and do so by modifying their gestures to meet the communicative needs of their children. More importantly, the gestures that parents produce, in addition to providing models, help children learn labels for referents and semantic relations between these referents and even predict the extent of children's vocabularies several years later. The existing research thus highlights the important role parental gestures play in shaping children's language learning trajectory.
C1 [Ozcaliskan, Seyda; Dimitrova, Nevena] Georgia State Univ, Dept Psychol, Atlanta, GA 30302 USA.
RP Ozcaliskan, S (reprint author), Georgia State Univ, Dept Psychol, POB 5010, Atlanta, GA 30302 USA.
EM seyda@gsu.edu
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NR 73
TC 0
Z9 0
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0734-0478
EI 1098-9056
J9 SEMIN SPEECH LANG
JI Semin. Speech Lang.
PD NOV
PY 2013
VL 34
IS 4
BP 227
EP 236
DI 10.1055/s-0033-1353447
PG 10
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 260XR
UT WOS:000327628400003
PM 24297615
ER
PT J
AU Naigles, LR
AF Naigles, Letitia R.
TI Input and Language Development in Children with Autism
SO SEMINARS IN SPEECH AND LANGUAGE
LA English
DT Article
DE Language; maternal effects; autism
ID PARENT VERBAL RESPONSIVENESS; TYPICAL DEVELOPMENT; SPECTRUM DISORDERS;
JOINT ATTENTION; YOUNG-CHILDREN; DOWN-SYNDROME; SPEECH; GROWTH;
COMMUNICATION
AB The social deficits associated with autism spectrum disorders (ASD) have been implicated in the language delays and deficits of children with ASD. Consequently, the extent to which children with ASD utilize their language-related interactions and input in the same ways as typically developing children is only just beginning to be investigated. The current article summarizes the role of input for typically developing children learning language, and then reviews in some detail recent studies demonstrating influential effects of maternal responsivity (e.g., following in on children's focus of attention) and aspects of maternal speech (e.g., word frequency, word diversity, structural complexity) on the language production and comprehension of young children with ASD. Maternal responsivity appears to play a particularly influential role with children who are minimally verbal whereas the content and structure of maternal speech facilitate language in children who are already verbal.
C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA.
RP Naigles, LR (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd U-20, Storrs, CT 06269 USA.
EM Letitia.naigles@uconn.edu
FU National Institutes of Health (NIH-DCD) [R01 DC07428]; National Alliance
for Autism Research
FX The research described in this article was supported by the National
Institutes of Health (NIH-DCD, R01 DC07428) and the National Alliance
for Autism Research. I am happy to acknowledge my collaborators Deborah
Fein, Lauren Swensen Meade, and Anthony Goodwin. Gratitude goes to our
parent and child participants, and to Rose Jaffery, Janina Piotroski,
and the many undergraduate students of the UConn Child Language
Laboratory for their assistance in data collection, coding, and
analysis. I would also like to thank James Dixon, Inge-Marie Eigsti,
James Green, Andrea McDuffie, and Manuela Wagner for their helpful
suggestions and commentary on this research. This chapter was written
while the author was on sabbatical leave; she thanks the University of
Connecticut for providing the leave and the MIND Institute at UC Davis
for providing such a stimulating place to spend the sabbatical.
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NR 45
TC 1
Z9 1
PU THIEME MEDICAL PUBL INC
PI NEW YORK
PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA
SN 0734-0478
EI 1098-9056
J9 SEMIN SPEECH LANG
JI Semin. Speech Lang.
PD NOV
PY 2013
VL 34
IS 4
BP 237
EP 248
DI 10.1055/s-0033-1353446
PG 12
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 260XR
UT WOS:000327628400004
PM 24297616
ER
PT J
AU Foxx, RM
AF Foxx, Richard M.
TI The Maintenance of Behavioral Change: The Case for Long-Term Follow-Ups
SO AMERICAN PSYCHOLOGIST
LA English
DT Article
DE maintenance of behavior change; follow-ups
ID SELF-INJURIOUS MAN; CIGARETTE ABSTINENCE; PHYSICAL RESTRAINT; CONTROLLED
SMOKING; RETARDED-ADULTS; SKILLS; OVERCORRECTION; THERAPY; CAFFEINISM;
ECHOLALIA
AB This article discusses response maintenance, the durability of behavior change after therapy, treatment, or training ends. Response maintenance is one of the three forms of generalized behavior change, with the others being setting/situation generalization and response generalization. Long-term maintenance of treatment effects is an important issue after behavior change has taken place and is the goal of most programs. Areas discussed include factors affecting the study of maintenance, techniques for programming it, and analyzing and evaluating strategies for promoting it. This article presents a number of long-term follow-ups of programs designed to treat the addictive behaviors of typical adults (Foxx, 1982; Foxx, Brown, & Katz, 1981) and to teach social skills (Foxx & Faw, 1992) and language (Foxx & Faw, 1990) to individuals with intellectual disabilities and autism as well as to decrease their severe maladaptive behaviors (Foxx, 1990; Foxx & Livesay, 1984). In the process, various factors that appeared to contribute to long-term maintenance are identified. The article concludes with some recommendations regarding the study of maintenance.
C1 [Foxx, Richard M.] Penn State Harrisburg, Middletown, PA 17057 USA.
RP Foxx, RM (reprint author), Penn State Harrisburg, Psychol Program, 777 W Harrisburg Pike, Middletown, PA 17057 USA.
EM rmf4@psu.edu
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NR 55
TC 1
Z9 1
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0003-066X
EI 1935-990X
J9 AM PSYCHOL
JI Am. Psychol.
PD NOV
PY 2013
VL 68
IS 8
BP 728
EP 736
DI 10.1037/a0033713
PG 9
WC Psychology, Multidisciplinary
SC Psychology
GA 257FB
UT WOS:000327367900025
PM 24320663
ER
PT J
AU Schneider, D
Slaughter, VP
Bayliss, AP
Dux, PE
AF Schneider, Dana
Slaughter, Virginia P.
Bayliss, Andrew P.
Dux, Paul E.
TI A temporally sustained implicit theory of mind deficit in autism
spectrum disorders
SO COGNITION
LA English
DT Article
DE Implicit theory of mind; Social cognition; Autism spectrum disorders;
Eye-movements
ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME;
FALSE-BELIEF; MENTAL STATES; ADULTS; ATTENTION; QUOTIENT; INFANTS;
OTHERS
AB Eye movements during false-belief tasks can reveal an individual's capacity to implicitly monitor others' mental states (theory of mind - TOM). It has been suggested, based on the results of a single-trial-experiment, that this ability is impaired in those with a high-functioning autism spectrum disorder (ASD), despite neurotypical-like performance on explicit ToM measures. However, given there are known attention differences and visual hypersensitivities in ASD it is important to establish whether such impairments are evident over time. In addition, investigating implicit ToM using a repeated trial approach allows an assessment of whether learning processes can reduce the ASD impairment in this ability, as is the case with explicit ToM. Here we investigated the temporal profile of implicit ToM in individuals with ASD and a control group. Despite similar performance on explicit ToM measures, ASD-diagnosed individuals showed no evidence of implicit false-belief tracking even over a one-hour period and many trials, whereas control participants did. These findings demonstrate that the systems involved in implicit and explicit ToM are distinct and hint that impaired implicit false-belief tracking may play an important role in ASD. Further, they indicate that learning processes do not alleviate this impairment across the presentation of multiple trials. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Schneider, Dana; Slaughter, Virginia P.; Dux, Paul E.] Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia.
[Bayliss, Andrew P.] Univ E Anglia, Sch Psychol, Norwich NR4 7TJ, Norfolk, England.
RP Schneider, D (reprint author), Univ Queensland, Sch Psychol, McElwain Bldg, St Lucia, Qld 4072, Australia.
EM msdanaschneider@gmail.com; pau-l.e.dux@gmail.com
RI Dux, Paul/I-1098-2014
OI Dux, Paul/0000-0002-4270-2583
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NR 49
TC 10
Z9 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0010-0277
EI 1873-7838
J9 COGNITION
JI Cognition
PD NOV
PY 2013
VL 129
IS 2
BP 410
EP 417
DI 10.1016/j.cognition.2013.08.004
PG 8
WC Psychology, Experimental
SC Psychology
GA 257FH
UT WOS:000327368500019
PM 23994318
ER
PT J
AU Zager, A
Pinheiro, ML
Ferraz-de-Paula, V
Ribeiro, A
Palermo-Neto, J
AF Zager, Adriano
Pinheiro, Milena Lobao
Ferraz-de-Paula, Viviane
Ribeiro, Alison
Palermo-Neto, Joao
TI Increased cell-mediated immunity in male mice offspring exposed to
maternal immune activation during late gestation
SO INTERNATIONAL IMMUNOPHARMACOLOGY
LA English
DT Article
DE Prenatal LPS; Th1/Th2/Th17 cytokines; Th1 immunity; Delayed-type
hypersensitivity; Neutrophils; Dendritic cell
ID PRENATAL EXPOSURE; LIPOPOLYSACCHARIDE; BEHAVIOR; INFLAMMATION;
PREGNANCY; SYSTEM; AUTISM; RATS; LPS
AB Early life experiences, particularly during the gestational period, are homeostatic determinants for an individual's brain development. However, recent data suggest that the immune response of the offspring is also affected by events during the gestational period. Here, we evaluated the impact of prenatal immune activation on the innate and adaptive immune responses of adult offspring. Pregnant Swiss mice received saline or lipopolysaccharide (LPS) on gestational day 17. In adulthood, male offspring were analyzed using 2 experimental techniques: in vitro analysis of cytokine production and immune cell activity and development of the delayed-type hypersensitivity (DTH) responses of ovalbumin-sensitized mice. We analyzed Th1/Th2/Th17 cytokine production in vitro, neutrophil and dendritic cell function, and the DTH response. Offspring from LPS-treated dams displayed increased cell-mediated immunity as indicated by increased IL-12 production by cultured antigen-presenting cells and an enhanced DTH response as well as impaired production of the regulatory cytokine IL-10. This study provides new insights regarding the influence of immune activation during late gestation on the immunological homeostasis of offspring, particularly on Th1 immunity. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Zager, Adriano; Pinheiro, Milena Lobao; Ferraz-de-Paula, Viviane; Ribeiro, Alison; Palermo-Neto, Joao] Univ Sao Paulo, Sch Vet Med, Dept Pathol, Neuroimmunomodulat Res Grp, BR-05508270 Sao Paulo, Brazil.
RP Zager, A (reprint author), Univ Sao Paulo, Sch Vet Med, Dept Pathol, Av Prof Dr Orlando Marques de Paiva 87,Cidade Uni, BR-05508270 Sao Paulo, Brazil.
EM adrianozager@hotmail.com
FU CNPq; FAPESP [09/51886-3, 09/51998-6]
FX This work was supported by grants from the CNPq and FAPESP (Thematic
Awards #09/51886-3 to JPN, #09/51998-6 to AZ).
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NR 25
TC 1
Z9 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1567-5769
EI 1878-1705
J9 INT IMMUNOPHARMACOL
JI Int. Immunopharmacol.
PD NOV
PY 2013
VL 17
IS 3
SI SI
BP 633
EP 637
DI 10.1016/j.intimp.2013.08.007
PG 5
WC Immunology; Pharmacology & Pharmacy
SC Immunology; Pharmacology & Pharmacy
GA 255ZU
UT WOS:000327280100021
PM 23994465
ER
PT J
AU Pilarski, R
Burt, R
Kohlman, W
Pho, L
Shannon, KM
Swisher, E
AF Pilarski, Robert
Burt, Randall
Kohlman, Wendy
Pho, Lana
Shannon, Kristen M.
Swisher, Elizabeth
TI Cowden Syndrome and the PTEN Hamartoma Tumor Syndrome: Systematic Review
and Revised Diagnostic Criteria
SO JNCI-JOURNAL OF THE NATIONAL CANCER INSTITUTE
LA English
DT Article
ID RILEY-RUVALCABA-SYNDROME; AUTISM SPECTRUM DISORDERS;
LHERMITTE-DUCLOS-DISEASE; CORE-NEEDLE-BIOPSY; GENOTYPE-PHENOTYPE
CORRELATIONS; LIFETIME CANCER-RISKS; GERMLINE PTEN; MULTIPLE HAMARTOMA;
BREAST-CANCER; GASTROINTESTINAL POLYPOSIS
AB Background PTEN hamartoma tumor syndrome (PHTS) refers to a spectrum of disorders caused by mutations in the phosphatase and tensin homolog (PTEN) gene. Diagnostic criteria for Cowden syndrome, the principal PTEN-related disorder, were first established in 1996 before the identification of the PTEN gene and the ability to molecularly confirm a clinical diagnosis. These consortium criteria were based on clinical experience and case reports in the existing literature, with their inherent selection biases. Although it was initially reported that approximately 80% of patients with Cowden syndrome had an identifiable germline PTEN mutation, more recent work has shown these diagnostic criteria to be far less specific. In addition, increasing evidence has documented the association of a broader spectrum of clinical features with PTEN mutations. Our goal was to develop revised, evidence-based diagnostic criteria and to include features of the broader spectrum of PTEN-related clinical syndromes.
Methods We performed a systematic search and review of the medical literature related to clinical features reported in individuals with a PTEN mutation and/or a related clinical diagnosis.
Results We found no sufficient evidence to support inclusion of benign breast disease, uterine fibroids, or genitourinary malformations as diagnostic criteria. There was evidence to include autism spectrum disorders, colon cancer, esophageal glycogenic acanthosis, penile macules, renal cell carcinoma, testicular lipomatosis, and vascular anomalies.
Conclusions We propose revised, evidence-based criteria covering the spectrum of PTEN-related clinical disorders. Additional research on clinical features associated with PTEN mutations is warranted.
C1 [Pilarski, Robert] Ohio State Univ, Dept Internal Med, Div Human Genet, Columbus, OH 43240 USA.
[Pilarski, Robert] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43240 USA.
[Burt, Randall; Kohlman, Wendy; Pho, Lana] Huntsman Canc Inst, Salt Lake City, UT USA.
[Burt, Randall; Kohlman, Wendy] Univ Utah, Sch Med, Salt Lake City, UT USA.
[Pho, Lana] Univ Utah, Dept Dermatol, Salt Lake City, UT USA.
[Shannon, Kristen M.] Massachusetts Gen Hosp, Ctr Canc, Ctr Canc Risk Assessment, Boston, MA USA.
[Swisher, Elizabeth] Univ Washington, Med Ctr, Seattle Canc Care Alliance, Seattle, WA 98195 USA.
RP Pilarski, R (reprint author), Ohio State Univ, Clin Canc Genet Program, 2001 Polaris Pkwy, Columbus, OH 43240 USA.
EM robert.pilarski@osumc.edu
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NR 116
TC 31
Z9 31
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0027-8874
EI 1460-2105
J9 JNCI-J NATL CANCER I
JI JNCI-. Natl. Cancer Inst.
PD NOV
PY 2013
VL 105
IS 21
BP 1607
EP 1616
DI 10.1093/jnci/djt277
PG 11
WC Oncology
SC Oncology
GA 251ZL
UT WOS:000326973900007
PM 24136893
ER
PT J
AU Kral, TVE
Eriksen, WT
Souders, MC
Pinto-Martin, JA
AF Kral, Tanja V. E.
Eriksen, Whitney T.
Souders, Margaret C.
Pinto-Martin, Jennifer A.
TI Eating Behaviors, Diet Quality, and Gastrointestinal Symptoms in
Children With Autism Spectrum Disorders: A Brief Review
SO JOURNAL OF PEDIATRIC NURSING-NURSING CARE OF CHILDREN & FAMILIES
LA English
DT Review
DE Children; Autism spectrum disorders; Eating behaviors; Dietary intake;
Gastrointestinal health
ID TYPICALLY DEVELOPING-CHILDREN; INTESTINAL BARRIER; FOOD SELECTIVITY;
YOUNG-CHILDREN; PREVALENCE; ACCEPTANCE; SUPPLEMENT; PATTERNS; GLIADIN
AB Children with autism spectrum disorders (ASD) and their caregivers face unique challenges in the children's daily eating routines and food intake patterns. The aim of this brief review is to describe eating behaviors of children with ASD, including increased food neophobia and food selectivity, and review findings on children's diet quality, and gastrointestinal (GI) symptoms. Advancing knowledge about the interrelationships between these nutrition-related domains in children with ASD is expected to have important implications for clinical nursing practice and caregiver care. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Kral, Tanja V. E.; Eriksen, Whitney T.; Souders, Margaret C.; Pinto-Martin, Jennifer A.] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
[Kral, Tanja V. E.; Pinto-Martin, Jennifer A.] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Kral, TVE (reprint author), Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
EM tkral@nursing.upenn.edu
FU Hillman Scholars Program in Nursing Innovation
FX We acknowledge funding support from the Hillman Scholars Program in
Nursing Innovation.
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NR 54
TC 4
Z9 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0882-5963
J9 J PEDIATR NURS
JI J. Pediatr. Nurs.
PD NOV-DEC
PY 2013
VL 28
IS 6
BP 548
EP 556
DI 10.1016/j.pedn.2013.01.008
PG 9
WC Nursing; Pediatrics
SC Nursing; Pediatrics
GA 251NX
UT WOS:000326937600016
PM 23531467
ER
PT J
AU Giarelli, E
Ruttenberg, J
Segal, A
AF Giarelli, Ellen
Ruttenberg, Jean
Segal, Andrea
TI Bridges and Barriers to Successful Transitioning as Perceived by
Adolescents and Young Adults With Asperger Syndrome
SO JOURNAL OF PEDIATRIC NURSING-NURSING CARE OF CHILDREN & FAMILIES
LA English
DT Article
DE Asperger syndrome; Autism spectrum disorder; Transition to community;
Adolescents
ID AUTISM SPECTRUM DISORDERS; CHILDREN; BEHAVIOR; SCHOOL
AB In this thematic content analysis we examined the expectations, and perceived facilitators of (referred to as bridges) and barriers to transition to community as reported by adolescents and young adults with Asperger syndrome. Participants were adolescents/young adults, ages 18-23 years were from the East Coast of the United States. Seventy percent of adolescents hoped for employment (n = 10). Thirty percent desired to find a partner and raise a family. Perceived barriers were: self-assessed behavioral problems, self-assessed associated features, other personal factors, and institutional factors. Bridges to facilitate transition were: accommodations in the community, cognitive abilities, personal qualities/strengths, and mentor's qualities. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Giarelli, Ellen] Drexel Univ, Coll Nursing & Hlth Profess, Philadelphia, PA 19104 USA.
[Ruttenberg, Jean] Ctr Autism, Philadelphia, PA USA.
[Segal, Andrea] Drexel Univ, Sch Arts & Sci, Philadelphia, PA 19104 USA.
RP Giarelli, E (reprint author), Drexel Univ, Coll Nursing & Hlth Profess, Philadelphia, PA 19104 USA.
EM eg446@drexel.edu
FU Philadelphia Health Care Trust
FX The project was funded by a grant from the Philadelphia Health Care
Trust.
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NR 52
TC 1
Z9 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0882-5963
J9 J PEDIATR NURS
JI J. Pediatr. Nurs.
PD NOV-DEC
PY 2013
VL 28
IS 6
BP 563
EP 574
DI 10.1016/j.pedn.2012.12.010
PG 12
WC Nursing; Pediatrics
SC Nursing; Pediatrics
GA 251NX
UT WOS:000326937600018
PM 23541737
ER
PT J
AU Bohm, HV
Stewart, MG
Healy, AM
AF Bohm, H. V.
Stewart, M. G.
Healy, A. M.
TI On the Autistic Spectrum Disorder concordance rates of twins and
non-twin siblings
SO MEDICAL HYPOTHESES
LA English
DT Article
AB Using the Interactive Autism Network Research Database, the Autistic Spectrum Disorder concordance rates for twins and non-twin siblings were calculated. For males, females and both genders together, the concordance rate for dizygotic twins is approximately twice that of non-twin siblings. We also determined that the concordance rate for non-twin siblings decreases as the interval between pregnancies increases. Our results appear to indicate that the uterine environment may contribute to autism concordance rates. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Bohm, H. V.; Stewart, M. G.] Wayne State Univ, Dept Phys & Astron, Detroit, MI 48202 USA.
[Healy, A. M.] Wayne State Univ, Univ Lib, Detroit, MI 48202 USA.
RP Stewart, MG (reprint author), Wayne State Univ, Dept Phys & Astron, Detroit, MI 48202 USA.
EM stewart@physics.wayne.edu
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NR 10
TC 2
Z9 2
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 0306-9877
EI 1532-2777
J9 MED HYPOTHESES
JI Med. Hypotheses
PD NOV
PY 2013
VL 81
IS 5
BP 789
EP 791
DI 10.1016/j.mehy.2013.08.019
PG 3
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 257DI
UT WOS:000327363400010
PM 24055096
ER
PT J
AU Mehta, SQ
Golshani, P
AF Mehta, Sunil Q.
Golshani, Peyman
TI Clinical Neurogenetics Autism Spectrum Disorders
SO NEUROLOGIC CLINICS
LA English
DT Article
DE Autism; Autism spectrum disorders; Genetic testing; Chromosomal
microarray
ID PERVASIVE DEVELOPMENTAL DISORDERS; COPY-NUMBER VARIATION; DIAGNOSTIC
OBSERVATION SCHEDULE; DORSOLATERAL PREFRONTAL CORTEX; RANDOMIZED
CONTROLLED-TRIAL; TUBEROUS SCLEROSIS COMPLEX; COMMON GENETIC-VARIANTS;
FRAGILE-X-SYNDROME; DE-NOVO MUTATIONS; DELETION SYNDROME
AB Autism spectrum disorders are neurodevelopmental disorders characterized by deficits in social interactions, communication, and repetitive or restricted interests. There is strong evidence that de novo or inherited genetic alterations play a critical role in causing Autism Spectrum Disorders, but non-genetic causes, such as in utero infections, may also play a role. Magnetic resonance imaging based and autopsy studies indicate that early rapid increase in brain size during infancy could underlie the deficits in a large subset of subjects. Clinical studies show benefits for both behavioral and pharmacological treatment strategies. Genotype-specific treatments have the potential for improving outcome in the future.
C1 [Mehta, Sunil Q.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Golshani, Peyman] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA.
RP Mehta, SQ (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
EM SMehta@mednet.ucla.edu
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NR 120
TC 1
Z9 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0733-8619
EI 1557-9875
J9 NEUROL CLIN
JI Neurol. Clin.
PD NOV
PY 2013
VL 31
IS 4
BP 951
EP +
DI 10.1016/j.ncl.2013.04.009
PG 20
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 261QP
UT WOS:000327680000005
PM 24176418
ER
PT J
AU Rodrigues, JL
Goncalves, N
Costa, S
Soares, F
AF Rodrigues, Jose L.
Goncalves, Nuno
Costa, Sandra
Soares, Filomena
TI Stereotyped movement recognition in children with ASD
SO SENSORS AND ACTUATORS A-PHYSICAL
LA English
DT Article; Proceedings Paper
CT 26th European Conference on Solid-State Transducers (Eurosensors)
CY SEP 09-12, 2012
CL Krakow, POLAND
HO Wroclaw Univ Technol, Fac Microsystem Elect & Photon
DE Accelerometer sensor; Stereotyped motor movements; Gesture recognition
AB Autism Spectrum Disorders (ASD) manifest in different behaviors, being one of them body rocking, mouthing, and complex hand and finger movements [1]. The traditional methods for recording the number of occurrences and duration of stereotypes are inadequate and time consuming. Therefore, it was used a commercial system with accelerometers sensors that records the movement of wrist. The collected data is sent through a wireless network to the computer, where an application was developed to distinguish the movement made by the children as a stereotyped gesture, hand flapping movement, from a normal gesture. The system was previously tested in laboratory environment and during the intervention sessions. Statistical methods were used to characterize the signal acquired from a previously expressed stereotype recorded from a child with ASD. The parameters that were analyzed are: Root Mean Square (RMS), Standard Variation, Peaks and Valleys. At the end, the proposed methodology facilitates to identify behavioral patterns special relevant when studying interaction skills in children with ASD. (C) 2013 Published by Elsevier B.V.
C1 [Rodrigues, Jose L.; Goncalves, Nuno; Costa, Sandra; Soares, Filomena] Univ Minho, R&D Ctr Algoritmi, P-4800058 Guimaraes, Portugal.
RP Soares, F (reprint author), Univ Minho, R&D Ctr Algoritmi, Campus Azurem, P-4800058 Guimaraes, Portugal.
EM filomena.soares@algoritmi.uminho.pt
CR Albinali F., RECOGNIZING STEREOTY
Baek J, 2004, LECT NOTES ARTIF INT, V3215, P610
Costa S., 2009, EMBC 2009 ENG MED BI
Costa S., 2011, ROMAN 2011 20 IEEE I
Costa S., 2010, EMBC 2010 ENG MED BI
Goodwin MS, 2011, J AUTISM DEV DISORD, V41, P770, DOI 10.1007/s10803-010-1102-z
Silva S., 2012, 2 PORT M BIOENG PORT
NR 7
TC 0
Z9 0
PU ELSEVIER SCIENCE SA
PI LAUSANNE
PA PO BOX 564, 1001 LAUSANNE, SWITZERLAND
SN 0924-4247
J9 SENSOR ACTUAT A-PHYS
JI Sens. Actuator A-Phys.
PD NOV 1
PY 2013
VL 202
SI SI
BP 162
EP 169
DI 10.1016/j.sna.2013.04.019
PG 8
WC Engineering, Electrical & Electronic; Instruments & Instrumentation
SC Engineering; Instruments & Instrumentation
GA 252KO
UT WOS:000327003800025
ER
PT J
AU Schreck, KA
Russell, M
Vargas, LA
AF Schreck, Kimberly A.
Russell, Melissa
Vargas, Luis A.
TI AUTISM TREATMENTS IN PRINT: MEDIA'S COVERAGE OF SCIENTIFICALLY SUPPORTED
AND ALTERNATIVE TREATMENTS
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID SPECTRUM DISORDERS; CHILDREN; COMPLEMENTARY; PARENTS; MEDICINE
AB Professionals, celebrities, and media frequently suggest to parents the possible treatment options for their children with autism. Some treatment recommendations advocate for scientifically supported treatments whereas others suggest novel, untested interventions, or potentially ineffective or harmful treatments. The current study examined the print media's coverage of applied behavior analysis (ABA) and non-scientifically supported autism treatments. Over the last 10years, print media have increasingly published articles referring to autism treatments with little scientific support and a decreased coverage of ABA. Print media's positive statements about non-scientifically supported treatments also increased over the last decade, whereas positive statements about ABA decreased. ABA received two times as many positive comments as negative; however, non-scientifically supported treatments as a group received four times as many positive comments as negative. These results could contribute to parents' decisions to implement treatments for their children with autism. To contribute to future positive perception of ABA, we provided suggestions for the dissemination of information to increase positive reporting of ABA in print media. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Schreck, Kimberly A.; Russell, Melissa; Vargas, Luis A.] Penn State Harrisburg, Middletown, PA 17057 USA.
RP Schreck, KA (reprint author), Penn State Harrisburg, 777 West Harrisburg Pike, Middletown, PA 17057 USA.
EM kas24@psu.edu
CR [Anonymous], 2011, WALL STREET J
Centers for Disease Control and Prevention (CDC), 2010, AUT SPECTR DIS ASDS
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NR 26
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
EI 1099-078X
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2013
VL 28
IS 4
BP 299
EP 321
DI 10.1002/bin.1370
PG 23
WC Psychology, Clinical
SC Psychology
GA 254ZA
UT WOS:000327207600003
ER
PT J
AU Lequia, J
Machalicek, W
Lyons, G
AF Lequia, Jenna
Machalicek, Wendy
Lyons, Gregory
TI PARENT EDUCATION INTERVENTION RESULTS IN DECREASED CHALLENGING BEHAVIOR
AND IMPROVED TASK ENGAGEMENT FOR STUDENTS WITH DISABILITIES DURING
ACADEMIC TASKS
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; STRUCTURED DESCRIPTIVE ASSESSMENT; SCHOOL
INVOLVEMENT; CONTROLLED-TRIAL; YOUNG-CHILDREN; HOMEWORK; ADHD;
ACHIEVEMENT; TODDLERS; STRESS
AB Children with developmental disabilities and attention deficit hyperactivity disorder often engage in challenging behavior when presented with academic demands. Parents of school-age children with such diagnoses are commonly asked to assist their child with academic tasks but may struggle to do so as a result of challenging behavior. This study evaluated the effects of a parent education intervention on the challenging behaviors and task engagement of three school-age children with disabilities during academic activities. Parent education consisted of (i) weekly didactic instruction; (ii) modeling; (iii) role-play; and (iv) in vivo coaching and performance feedback. Using a non-concurrent multiple baseline across participants with embedded individual multi-element design, this study demonstrates that a parent education intervention results in decreases in challenging behavior and increases in task engagement. These results suggest that parent education focused on addressing challenging behavior during one-to-one instruction may facilitate completion of academic tasks. Implications for practice and suggestions for future research are discussed. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Lequia, Jenna; Lyons, Gregory] Univ Wisconsin, Madison, WI 53706 USA.
[Machalicek, Wendy] Univ Oregon, Eugene, OR 97403 USA.
RP Lequia, J (reprint author), Univ Wisconsin, 1000 Bascom Mall,461 Educ Bldg, Madison, WI 53706 USA.
EM lequia@wisc.edu
CR Anderson CM, 2002, J APPL BEHAV ANAL, V35, P137, DOI 10.1901/jaba.2002.35-137
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NR 36
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
EI 1099-078X
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2013
VL 28
IS 4
BP 322
EP 343
DI 10.1002/bin.1369
PG 22
WC Psychology, Clinical
SC Psychology
GA 254ZA
UT WOS:000327207600004
ER
PT J
AU Gutierrez, A
Fischer, AJ
Hale, MN
Durocher, JS
Alessandri, M
AF Gutierrez, Anibal, Jr.
Fischer, Aaron J.
Hale, Melissa N.
Durocher, Jennifer S.
Alessandri, Michael
TI DIFFERENTIAL RESPONSE PATTERNS TO THE CONTROL CONDITION BETWEEN TWO
PROCEDURES TO ASSESS SOCIAL REINFORCERS FOR CHILDREN WITH AUTISM
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID PREFERENCE; DISABILITIES
AB Historically, reinforcer assessment procedures focus primarily on identifying nonsocial reinforcers (e.g., tangibles and edibles). Far less empirical attention has been allocated to the systematic identification of social consequences that function as reinforcers. This discrepancy is problematic given that social consequences are commonly incorporated into behavioral treatment programs without systematic evaluation of their efficacy. In this study, two methodologies (a single operant and a concurrent choice) were used to assess social reinforcers for children with autism. Results highlighted differences in response allocation to the control condition between procedures. Specifically, responding occurred in the control condition of the single-operant procedure but not in the concurrent-operant procedure. These differences highlight the need for further evaluation of procedures to assess social reinforcers. Copyright (c) 2013 John Wiley & Sons, Ltd.
C1 [Gutierrez, Anibal, Jr.] Florida Int Univ, Miami, FL 33199 USA.
[Fischer, Aaron J.] Louisiana State Univ, Baton Rouge, LA 70803 USA.
[Hale, Melissa N.; Durocher, Jennifer S.; Alessandri, Michael] Univ Miami, Coral Gables, FL 33124 USA.
RP Gutierrez, A (reprint author), Florida Int Univ, 11200 SW 8th St,AHC 1, Miami, FL 33199 USA.
EM anibal.gutierrez@fiu.edu
CR DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519
FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491
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Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947
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NR 12
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
EI 1099-078X
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2013
VL 28
IS 4
BP 353
EP 361
DI 10.1002/bin.1372
PG 9
WC Psychology, Clinical
SC Psychology
GA 254ZA
UT WOS:000327207600006
ER
PT J
AU Lado, FA
Rubboli, G
Capovilla, P
Avanzini, G
Moshe, SL
AF Lado, Fred A.
Rubboli, Guido
Capovilla, Pippo
Avanzini, Giuliano
Moshe, Solomon L.
TI Pathophysiology of epileptic encephalopathies
SO EPILEPSIA
LA English
DT Article
DE Epileptic encephalopathy; Epilepsy; Mental retardation; Cognitive
impairment; Interneuron; Genetics; Subcortical nuclei; Synapse; Synaptic
plasticity; Animal models
ID INFANTILE SPASMS; INTERNEURON DISTRIBUTION; CORTICAL DYSPLASIA; MOUSE
MODEL; SEIZURES; CNTNAP2; AUTISM; SLEEP; CLASSIFICATION; SUSCEPTIBILITY
AB The application of metabolic imaging and genetic analysis, and now the development of appropriate animal models, has generated critical insights into the pathogenesis of epileptic encephalopathies. In this article we present ideas intended to move from the lesions associated with epileptic encephalopathies toward understanding the effects of these lesions on the functioning of the brain, specifically of the cortex. We argue that the effects of focal lesions may be magnified through the interaction between cortical and subcortical structures, and that disruption of subcortical arousal centers that regulate cortex early in life may lead to alterations of intracortical synapses that affect a critical period of cognitive development. Impairment of interneuronal function globally through the action of a genetic lesion similarly causes widespread cortical dysfunction manifesting as increased delta slow waves on electroencephalography (EEG) and as developmental delay or arrest clinically. Finally, prolonged focal epileptic activity during sleep (as occurring in the syndrome of continuous spike-wave in slow sleep, or CSWSS) might interfere with local slow wave activity at the site of the epileptic focus, thereby impairing the neural processes and, possibly, the local plastic changes associated with learning and other cognitive functions. Seizures may certainly add to these pathologic processes, but they are likely not necessary for the development of the cognitive pathology. Nevertheless, although seizures may be either a consequence or symptom of the underlying lesion, their effective treatment can improve outcomes as both clinical and experimental studies may suggest. Understanding their substrates may lead to novel, effective treatments for all aspects of the epileptic encephalopathy phenotype.
C1 [Lado, Fred A.] Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10467 USA.
[Lado, Fred A.; Moshe, Solomon L.] Montefiore Med Ctr, Bronx, NY 10461 USA.
[Rubboli, Guido] Epilepsihosp, Danish Epilepsy Ctr, Dianalund, Denmark.
[Rubboli, Guido] Bellaria Hosp, Dept Neurosci, Neurol Unit, Bologna, Italy.
[Capovilla, Pippo] Carlo Poma Hosp, Epilepsy Ctr, Dept Child Neuropsychiat, Mantua, Italy.
[Avanzini, Giuliano] IRCCS Fdn, Neurol Inst, Dept Neurophysiol, Milan, Italy.
[Moshe, Solomon L.] Albert Einstein Coll Med, Saul R Korey Dept Neurol, Dominick P Purpura Dept Neurosci, Bronx, NY 10467 USA.
[Moshe, Solomon L.] Albert Einstein Coll Med, Montefiore Einstein Epilepsy Management Ctr, Dept Pediat, Lab Dev Epilepsy, Bronx, NY 10467 USA.
RP Lado, FA (reprint author), Montefiore Med Ctr, EEG Lab, 111 E 210 St, Bronx, NY 10461 USA.
EM flado@montefiore.org
FU NINDS, NIH [RO1-NS-20253, UO1-NS045911, RO1-NS043209, R21-NS-78333];
Department of Defense: CURE: The Heffer Family Medical Foundation; Segal
Family Foundation
FX Supported in part by grants RO1-NS-20253, UO1-NS045911, RO1-NS043209,
and R21-NS-78333 from NINDS, NIH; Department of Defense: CURE: The
Heffer Family Medical Foundation; and the Segal Family Foundation.
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NR 49
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0013-9580
EI 1528-1167
J9 EPILEPSIA
JI Epilepsia
PD NOV
PY 2013
VL 54
SU 8
SI SI
BP 6
EP 13
DI 10.1111/epi.12417
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 250JT
UT WOS:000326849800016
PM 24571111
ER
PT J
AU van Steijn, DJ
Oerlemans, AM
de Ruiter, SW
van Aken, MAG
Buitelaar, JK
Rommelse, NNJ
AF van Steijn, Daphne J.
Oerlemans, Anoek M.
de Ruiter, Saskia W.
van Aken, Marcel A. G.
Buitelaar, Jan K.
Rommelse, Nanda N. J.
TI Are parental autism spectrum disorder and/or
attention-deficit/Hyperactivity disorder symptoms related to parenting
styles in families with ASD ( plus ADHD) affected children?
SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorder; Attention-deficit/hyperactivity disorder;
Parental symptoms; Parenting styles
ID DEFICIT HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS;
GENERAL-POPULATION; BEHAVIOR PROBLEMS; QUOTIENT AQ; SELF-REPORT; ADULTS;
PERSONALITY; VALIDITY; TRAITS
AB An understudied and sensitive topic nowadays is that even subthreshold symptoms of autism spectrum disorder (ASD) and attention-deficit/Hyperactivity disorder (ADHD) in parents may relate to their parenting styles. The aim of this study was to explore the influence of (the combined) effect of child diagnosis (ASD or ASD + ADHD affected/unaffected children) and parental ASD and/or ADHD on parenting styles. Ninety-six families were recruited with one child with a clinical ASD (+ADHD) diagnosis, and one unaffected sibling. Parental ASD and ADHD symptoms were assessed using self-report. The Parenting Styles Dimensions Questionnaire (PSDQ) self- and spouse-report were used to measure the authoritative, authoritarian, and permissive parenting styles. Fathers and mothers scored significantly higher than the norm data of the PSDQ on the permissive style regarding affected children, and lower on the authoritative and authoritarian parenting style for affected and unaffected children. Self- and spouse-report correlated modestly too strongly. Higher levels of paternal (not maternal) ADHD symptoms were suboptimally related to the three parenting styles. Further, two parent-child pathology interaction effects were found, indicating that fathers with high ADHD symptoms and mothers with high ASD symptoms reported to use a more permissive parenting style only towards their unaffected child. The results highlight the negative effects of paternal ADHD symptoms on parenting styles within families with ASD (+ADHD) affected offspring and the higher permissiveness towards unaffected offspring specifically when paternal ADHD and/or maternal ASD symptoms are high. Parenting training in these families may be beneficial for the well-being of all family members.
C1 [van Steijn, Daphne J.; Oerlemans, Anoek M.; Buitelaar, Jan K.; Rommelse, Nanda N. J.] Karakter Child & Adolescent Psychiat Univ Ctr, NL-6525 GC Nijmegen, Netherlands.
[Oerlemans, Anoek M.; de Ruiter, Saskia W.; Rommelse, Nanda N. J.] Radboud Univ Nijmegen, Med Ctr, Dept Psychiat, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
[van Aken, Marcel A. G.] Univ Utrecht, Dept Dev Psychol, Utrecht, Netherlands.
[Buitelaar, Jan K.] Radboud Univ Nijmegen, Med Ctr, Dept Cognit Neurosci, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
RP van Steijn, DJ (reprint author), Karakter Child & Adolescent Psychiat Univ Ctr, Reinier Postlaan 12, NL-6525 GC Nijmegen, Netherlands.
EM d.vansteijn@karakter.com
RI Rommelse, Nanda/D-4872-2009
OI Rommelse, Nanda/0000-0002-1711-0359
FU Netherlands Organisation for Scientific Research (NWO) [91610024]
FX We would like to thank parents, teachers, and children for participating
in this project. This study was partly funded by a grant assigned to Dr.
N. Rommelse by the Netherlands Organisation for Scientific Research (NWO
grant # 91610024).
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NR 72
TC 1
Z9 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1018-8827
EI 1435-165X
J9 EUR CHILD ADOLES PSY
JI Eur. Child Adolesc. Psych.
PD NOV
PY 2013
VL 22
IS 11
BP 671
EP 681
DI 10.1007/s00787-013-0408-8
PG 11
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 253GC
UT WOS:000327070800003
PM 23564208
ER
PT J
AU South, ST
Lee, C
Lamb, AN
Higgins, AW
Kearney, HM
AF South, Sarah T.
Lee, Charles
Lamb, Allen N.
Higgins, Anne W.
Kearney, Hutton M.
CA Amer Coll Med Genetics Genomics
TI ACMG Standards and Guidelines for constitutional cytogenomic microarray
analysis, including postnatal and prenatal applications: revision 2013
SO GENETICS IN MEDICINE
LA English
DT Article
DE constitutional; guidelines; microarray; postnatal; prenatal; standards
ID COPY NUMBER VARIANTS; MEDICAL GENETICS; AMERICAN-COLLEGE; RESOURCES;
ABNORMALITIES; PLATFORMS; DATABASE
AB Microarray methodologies, including array comparative genomic hybridization and single-nucleotide polymorphism detecting arrays, are accepted as an appropriate first-tier test for the evaluation of imbalances associated with intellectual disability, autism, and multiple congenital anomalies. This technology also has applicability in prenatal specimens. To assist clinical laboratories in validation of microarray methodologies for constitutional applications, the American College of Medical Genetics and Genomics has produced the following revised professional standards and guidelines.
C1 [South, Sarah T.; Lamb, Allen N.] ARUP Labs, Salt Lake City, UT USA.
[South, Sarah T.; Lamb, Allen N.] Univ Utah, Dept Pathol, Salt Lake City, UT USA.
[Lee, Charles] Harvard Univ, Brigham & Womens Hosp, Sch Med, Boston, MA 02115 USA.
[Higgins, Anne W.] UMass Mem Med Ctr, Dept Pathol, Worcester, MA USA.
[Higgins, Anne W.] Univ Massachusetts, Sch Med, Worcester, MA USA.
[Kearney, Hutton M.] Mission Hlth, Fullerton Genet Ctr, Asheville, NC USA.
RP South, ST (reprint author), ARUP Labs, Salt Lake City, UT USA.
EM Sarah.South@aruplab.com
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NR 14
TC 9
Z9 11
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
EI 1530-0366
J9 GENET MED
JI Genet. Med.
PD NOV
PY 2013
VL 15
IS 11
BP 901
EP 909
DI 10.1038/gim.2013.129
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 250LB
UT WOS:000326853200011
PM 24071793
ER
PT J
AU Shin, NY
Kang, DH
Jang, JH
Park, SY
Hwang, JY
Kim, SN
Byun, MS
Park, HY
Kim, YC
AF Shin, Na Young
Kang, Do-Hyung
Jang, Joon Hwan
Park, Soo Young
Hwang, Jae Yeon
Kim, Sung Nyun
Byun, Min Soo
Park, Hye Youn
Kim, Yong Chul
TI Impaired Recognition of Social Emotion in Patients With Complex Regional
Pain Syndrome
SO JOURNAL OF PAIN
LA English
DT Article
DE Complex regional pain syndrome; chronic pain; emotion; cognitive
function; social cognition; social perception
ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; NEUROPATHIC PAIN; BRAIN;
MIND; SCHIZOPHRENIA; NEUROBIOLOGY; INVENTORY; DYSTONIA; ANXIETY
AB Multiple brain areas involved in nociceptive, autonomic, and social-emotional processing are disproportionally changed in patients with complex regional pain syndrome (CRPS). Little empirical evidence is available involving social cognitive functioning in patients with chronic pain conditions. We investigated the ability of patients with CRPS to recognize the mental/emotional states of other people. Forty-three patients with CRPS and 30 healthy controls performed the Reading Mind in the Eyes Test, which consists of photos in which human eyes express various emotional and mental states. Neuropsychological tests, including the Wisconsin Card Sorting Test, the stop-signal test, and the reaction time test, were administered to evaluate other cognitive functions. Patients with CRPS were significantly less accurate at recognizing emotional states in other persons, but not on other cognitive tests, compared with control subjects. We found a significant association between the deficit in social-emotion recognition and the affective dimension of pain, whereas this deficit was not related to the sensory dimension of pain. Our findings suggest a disrupted ability to recognize others' mental/emotional states in patients with CRPS.
Perspective: This article demonstrated a deficit in inferring mental/emotional states of others in patients with CRPS that was related to pain affect. Our study suggests that additional interventions directed toward reducing distressful affective pain may be helpful to restore social cognitive processing in patients with CRPS. (C) 2013 by the American Pain Society
C1 [Shin, Na Young] Seoul Natl Univ, Interdisciplinary Cognit Sci Program, Seoul 110744, South Korea.
[Kang, Do-Hyung; Jang, Joon Hwan; Kim, Sung Nyun; Byun, Min Soo; Park, Hye Youn] Seoul Natl Univ, Coll Med, Dept Psychiat, Seoul 110744, South Korea.
[Park, Soo Young; Kim, Yong Chul] Seoul Natl Univ Hosp, Dept Anesthesiol & Pain Med, Seoul 110744, South Korea.
[Hwang, Jae Yeon] SMG SNU Boramae Med Ctr, Dept Psychiat, Seoul, South Korea.
RP Kang, DH (reprint author), Seoul Natl Univ, Coll Med, Dept Psychiat, 28 Yeongon Dong, Seoul 110744, South Korea.
EM basuare@paran.com
FU Original Technology Research Program for Brain Science through the
National Research Foundation of Korea; Ministry of Education. Science
and Technology [20120006587]
FX This study was supported by the Original Technology Research Program for
Brain Science through the National Research Foundation of Korea funded
by the Ministry of Education. Science and Technology (20120006587).
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Veldhuijzen DS, 2012, J PAIN, V13, P507, DOI 10.1016/j.jpain.2012.02.011
NR 33
TC 1
Z9 1
PU CHURCHILL LIVINGSTONE
PI EDINBURGH
PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE,
LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND
SN 1526-5900
J9 J PAIN
JI J. Pain
PD NOV
PY 2013
VL 14
IS 11
BP 1304
EP 1309
DI 10.1016/j.jpain.2013.05.008
PG 6
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 252YD
UT WOS:000327047900004
PM 23876283
ER
PT J
AU Zaslav, AL
Marino, MA
Jurgens, CY
Mercado, T
AF Zaslav, Ann-Leslie
Marino, Marie Ann
Jurgens, Corrine Y.
Mercado, Theresa
TI Cytogenetic Evaluation: A Primer for Pediatric Nurse Practitioners
SO JOURNAL OF PEDIATRIC HEALTH CARE
LA English
DT Article
DE Cytogenetics; karyotyping; FISH; CGH; chromosomal microarrays
ID HUMAN CHROMOSOMES; HUMAN GENOME; COPY NUMBER; MICROARRAY; HYBRIDIZATION;
STATEMENT; GENETICS
AB Patients with genetic disorders require specific types of cytogenetic testing for accurate diagnosis and prognosis followed by prompt treatment. This primer will serve as a guide for pediatric nurse practitioners on the use of various cytogenetic testing for the diagnosis of genetic disorders. Knowledge of the latest cytogenetic technologies will facilitate diagnosis and counseling related to genetic abnormalities such as inherited disorders, mental retardation, developmental delay, and autism. This reference will enable pediatric nurse practitioners to help identify patients with various inherited genetic disorders and provide subsequent monitoring and treatment.
C1 [Zaslav, Ann-Leslie; Mercado, Theresa] SUNY Stony Brook, Med Ctr, Dept Pathol, Cytogenet Lab, Stony Brook, NY 11794 USA.
[Marino, Marie Ann; Jurgens, Corrine Y.] SUNY Stony Brook, Sch Nursing, Stony Brook, NY 11794 USA.
RP Jurgens, CY (reprint author), SUNY Stony Brook, Sch Nursing, HSC L2-246, Stony Brook, NY 11794 USA.
EM corrine.jurgens@stonybrook.edu
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NR 27
TC 0
Z9 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0891-5245
EI 1532-656X
J9 J PEDIATR HEALTH CAR
JI J. Pediatr. Health Care
PD NOV-DEC
PY 2013
VL 27
IS 6
BP 426
EP 433
DI 10.1016/j.pedhc.2012.04.006
PG 8
WC Health Policy & Services; Nursing; Pediatrics
SC Health Care Sciences & Services; Nursing; Pediatrics
GA 253PQ
UT WOS:000327102000005
PM 22595375
ER
PT J
AU Zhan, QT
Pan, PP
Xu, XR
Lou, HY
Lou, YY
Jin, F
AF Zhan, Qi-tao
Pan, Pei-pei
Xu, Xiang-rong
Lou, Hang-ying
Lou, Yi-yun
Jin, Fan
TI An overview of studies on psychological well-being in children born
following assisted reproductive technologies
SO JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B
LA English
DT Review
DE Assisted reproductive technologies; Psychological well-being; Behavior
problems; Parent-child relationship
ID IN-VITRO FERTILIZATION; INTRACYTOPLASMIC SPERM INJECTION;
BECKWITH-WIEDEMANN-SYNDROME; QUALITY-OF-LIFE; SPONTANEOUSLY CONCEIVED
CHILDREN; PSYCHOMOTOR DEVELOPMENT; COGNITIVE-DEVELOPMENT; SINGLETON
CHILDREN; MOTOR DEVELOPMENT; PARENT
AB Over the course of the past 35 years, assisted reproductive technologies (ARTs) have been increasingly used worldwide, while debates on their safety have been generated. Birth defects and imprinting disorders were reported in previous research. Thus, the psychological development of children born following ARTs has become a major concern nowadays. This review gives a systematic view of psychological well-being of children conceived by different types of ART, including in vitro fertilization, intracytoplasmic sperm injection (ICSI), preimplantation genetic diagnosis/screening, and in vitro maturation. The previous studies are analyzed in three sections: (1) cognitive, motor, and language developments, (2) behavior problems and socio-emotional development, and (3) parent-child relationship. We conclude that although the majority of the studies on cognitive, motor, and language developments reported comparable achievements in the ART group vs. the naturally conceived group, lower intelligence quotient (IQ) scores, worse visual-motor ability or locomotor development, and delayed receptive language competence were found in the ART group. The results on the socio-emotional development were reassuring. As for the behavior problems, a higher prevalence of behavior problems existed in ART children; moreover, ICSI children were found to be at a higher risk of autism than the general population. Meanwhile, ART parents tended to have positive parental attitudes and be more protective of their children. Some suggestions for further research are also given in this review.
C1 [Zhan, Qi-tao; Pan, Pei-pei; Xu, Xiang-rong; Lou, Hang-ying; Lou, Yi-yun; Jin, Fan] Zhejiang Univ, Sch Med, Womens Hosp, Dept Reprod Endocrinol, Hangzhou 310006, Zhejiang, Peoples R China.
RP Jin, F (reprint author), Zhejiang Univ, Sch Med, Womens Hosp, Dept Reprod Endocrinol, Hangzhou 310006, Zhejiang, Peoples R China.
EM jinfan@zju.edu.cn
FU National Basic Research Program (973) of China [2012CB944901]; National
Natural Science Foundation of China [81070532, 81070541]; Zhejiang
Provincial Natural Science Foundation of China [Y2100822, LZ13H040001]
FX Project supported by the National Basic Research Program (973) of China
(No. 2012CB944901), the National Natural Science Foundation of China
(Nos. 81070532 and 81070541), and the Zhejiang Provincial Natural
Science Foundation of China (Nos. Y2100822 and LZ13H040001)
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NR 118
TC 2
Z9 2
PU ZHEJIANG UNIV
PI HANGZHOU
PA EDITORIAL BOARD, 20 YUGU RD, HANGZHOU, 310027, PEOPLES R CHINA
SN 1673-1581
EI 1862-1783
J9 J ZHEJIANG UNIV-SC B
JI J. Zhejiang Univ.-SCI. B
PD NOV
PY 2013
VL 14
IS 11
BP 947
EP 960
DI 10.1631/jzus.B1300101
PG 14
WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology;
Research & Experimental Medicine
GA 251NK
UT WOS:000326936000001
PM 24190441
ER
PT J
AU Eckstein, M
Hurlemann, R
AF Eckstein, M.
Hurlemann, R.
TI Oxytocin. Evidence for a therapeutic potential of the social
neuromodulator
SO NERVENARZT
LA German
DT Article
DE Mental disorders; Oxytocin; Social cognition; Treatment; Human studies
ID RANDOMIZED-CONTROLLED-TRIAL; AUTISM SPECTRUM DISORDERS; INTRANASAL
OXYTOCIN; ANXIETY DISORDER; HUMANS; STRESS; FACES; SCHIZOPHRENIA;
PERCEPTION; RESPONSES
AB Only few substances have achieved such a great prominence in recent years as the hypothalamic neuropeptide oxytocin, which is also widely known as the love hormone. Oxytocin is a potent neuromodulator which can improve social cognitive functions including empathy, trust, cooperation and social learning. However, oxytocin can also promote negative social behavior and increase poor memory and feelings of fear in social situations. Positive data from initial clinical trials give rise to the hope that oxytocin will prove to be a substance which is suitable for targeted treatment of poor social-cognitive behavior in neuropsychiatric diseases. This review article summarizes the most important recent preclinical and clinical human studies and discusses the findings presented with respect to current concepts of personal and contextual influences.
C1 [Eckstein, M.; Hurlemann, R.] Klin & Poliklin Psychiat & Psychotherapi, Abt Med Psychol & Soziol, D-53105 Bonn, Germany.
RP Hurlemann, R (reprint author), Klin & Poliklin Psychiat & Psychotherapi, Abt Med Psychol & Soziol, Sigmund Freud Str 25, D-53105 Bonn, Germany.
EM renehurlemann@me.com
RI Hurlemann, Rene/G-4164-2012
OI Hurlemann, Rene/0000-0003-2628-565X
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NR 52
TC 4
Z9 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0028-2804
EI 1433-0407
J9 NERVENARZT
JI Nervenarzt
PD NOV
PY 2013
VL 84
IS 11
BP 1321
EP 1328
DI 10.1007/s00115-013-3832-6
PG 8
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 253IX
UT WOS:000327079400007
PM 24190030
ER
PT J
AU Maister, L
Simons, JS
Plaisted-Grant, K
AF Maister, Lara
Simons, Jon S.
Plaisted-Grant, Kate
TI Executive Functions Are Employed to Process Episodic and Relational
Memories in Children With Autism Spectrum Disorders
SO NEUROPSYCHOLOGY
LA English
DT Article
DE autism spectrum disorder; relational memory; hippocampus; posterior
parietal cortex; executive functions
ID FREE-RECALL; AUTOBIOGRAPHICAL MEMORY; ASPERGERS-SYNDROME; TEMPORAL-LOBE;
PARIETAL LOBE; COGNITIVE DEFICIT; RETRIEVAL; ADULTS; ITEM;
DISCRIMINATION
AB Objective: Long-term memory functioning in autism spectrum disorders (ASDs) is marked by a characteristic pattern of impairments and strengths. Individuals with ASD show impairment in memory tasks that require the processing of relational and contextual information, but spared performance on tasks requiring more item-based, acontextual processing. Two experiments investigated the cognitive mechanisms underlying this memory profile. Method: A sample of 14 children with a diagnosis of high-functioning ASD (age: M = 12.2 years), and a matched control group of 14 typically developing (TD) children (age: M = 12.1 years), participated in a range of behavioral memory tasks in which we measured both relational and item-based memory abilities. They also completed a battery of executive function measures. Results: The ASD group showed specific deficits in relational memory, but spared or superior performance in item-based memory, across all tasks. Importantly, for ASD children, executive ability was significantly correlated with relational memory but not with item-based memory. No such relationship was present in the control group. This suggests that children with ASD atypically employed effortful, executive strategies to retrieve relational (but not item-specific) information, whereas TD children appeared to use more automatic processes. Conclusions: The relational memory impairment in ASD may result from a specific impairment in automatic associative retrieval processes with an increased reliance on effortful and strategic retrieval processes. Our findings allow specific neural predictions to be made regarding the interactive functioning of the hippocampus, prefrontal cortex, and posterior parietal cortex in ASD as a neural network supporting relational memory processing.
C1 [Maister, Lara; Plaisted-Grant, Kate] Univ Cambridge, Dept Expt Psychol, Cambridge Lab Res Autism, Cambridge CB2 3EB, England.
[Simons, Jon S.] Univ Cambridge, Dept Expt Psychol, Memory Lab, Cambridge CB2 3EB, England.
RP Maister, L (reprint author), Univ London, Dept Psychol, Royal Holloway, Egham Hill, Egham TW20 0EX, Surrey, England.
EM lara.maister@rhul.ac.uk
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NR 82
TC 1
Z9 1
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0894-4105
EI 1931-1559
J9 NEUROPSYCHOLOGY
JI Neuropsychology
PD NOV
PY 2013
VL 27
IS 6
BP 615
EP 627
DI 10.1037/a0034492
PG 13
WC Psychology, Clinical; Neurosciences; Psychology
SC Psychology; Neurosciences & Neurology
GA 252YX
UT WOS:000327049900001
PM 24245930
ER
PT J
AU Spencer, D
Marshall, J
Post, B
Kulakodlu, M
Newschaffer, C
Dennen, T
Azocar, F
Jain, A
AF Spencer, Donna
Marshall, Jaclyn
Post, Brady
Kulakodlu, Mahesh
Newschaffer, Craig
Dennen, Taylor
Azocar, Francisca
Jain, Anjali
TI Psychotropic Medication Use and Polypharmacy in Children With Autism
Spectrum Disorders
SO PEDIATRICS
LA English
DT Article
DE administrative claims; autism spectrum disorder; commercially insured;
psychotropic polypharmacy
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; YOUNG-CHILDREN; DRUG-USE;
ADOLESCENTS; TRENDS; PREVALENCE; MANAGEMENT
AB OBJECTIVE: The objectives of this study were to examine rates and predictors of psychotropic use and multiclass polypharmacy among commercially insured children with autism spectrum disorders (ASD).
METHODS: This retrospective observational study used administrative medical and pharmacy claims data linked with health plan enrollment and sociodemographic information from 2001 to 2009. Children with ASD were identified by using a validated ASD case algorithm. Psychotropic polypharmacy was defined as concurrent medication fills across >= 2 classes for at least 30 days. Multinomial logistic regression was used to model 5 categories of psychotropic use and multiclass polypharmacy.
RESULTS: Among 33 565 children with ASD, 64% had a filled prescription for at least 1 psychotropic medication, 35% had evidence of psychotropic polypharmacy (>= 2 classes), and 15% used medications from >= 3 classes concurrently. Among children with polypharmacy, the median length of polypharmacy was 346 days. Older children, those who had a psychiatrist visit, and those with evidence of co-occurring conditions (seizures, attention-deficit disorders, anxiety, bipolar disorder, or depression) had higher odds of psychotropic use and/or polypharmacy.
CONCLUSIONS: Despite minimal evidence of the effectiveness or appropriateness of multidrug treatment of ASD, psychotropic medications are commonly used, singly and in combination, for ASD and its co-occurring conditions. Our results indicate the need to develop standards of care around the prescription of psychotropic medications to children with ASD.
C1 [Spencer, Donna; Kulakodlu, Mahesh] OptumInsight, Life Sci, Eden Prairie, MN USA.
[Marshall, Jaclyn; Post, Brady; Dennen, Taylor; Jain, Anjali] Lewin Grp, Falls Church, VA 22042 USA.
[Newschaffer, Craig] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
[Azocar, Francisca] OptumHlth Behav Solut, San Francisco, CA USA.
RP Jain, A (reprint author), Lewin Grp, 3130 Fairview Pk Dr,Suite 600, Falls Church, VA 22042 USA.
EM anjali.jain@lewin.com
FU National Institute of Mental Health (NIMH), National Institutes of
Health, Department of Health and Human Services [HHSN-271-2010-00033-C];
National Institutes of Health (NIH)
FX Sponsored by the National Institute of Mental Health (NIMH), National
Institutes of Health, Department of Health and Human Services
(HHSN-271-2010-00033-C). The NIMH was given a copy of the final draft of
the manuscript, but the content of the manuscript is solely the
responsibility of the authors and does not necessarily represent the
views of the NIMH, the National Institutes of Health, or the federal
government. Funded by the National Institutes of Health (NIH).
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NR 29
TC 5
Z9 5
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2013
VL 132
IS 5
BP 833
EP 840
DI 10.1542/peds.2012-3774
PG 8
WC Pediatrics
SC Pediatrics
GA 245PE
UT WOS:000326475000051
PM 24144704
ER
PT J
AU Bilder, DA
Bakian, AV
Viskochil, J
Clark, EAS
Botts, EL
Smith, KR
Pimentel, R
McMahon, WM
Coon, H
AF Bilder, Deborah A.
Bakian, Amanda V.
Viskochil, Joseph
Clark, Erin A. S.
Botts, Elizabeth L.
Smith, Ken R.
Pimentel, Richard
McMahon, William M.
Coon, Hilary
TI Maternal Prenatal Weight Gain and Autism Spectrum Disorders
SO PEDIATRICS
LA English
DT Article
DE autism; prenatal; weight gain; risk factors; epidemiology
ID BREAST-CANCER; PREGNANCY; BIRTH; RISK; SEX; HEPATOBLASTOMA; INDIVIDUALS;
PREVALENCE; ESTROGENS; STEROIDS
AB BACKGROUND: The rising population of individuals identified with an autism spectrum disorder (ASD) calls for further investigation of its underlying etiology. A disturbance in the fetal steroid hormone environment may be a mechanism in which environmental and genetic risk factors interact. The mother, fetus, and placenta collectively create the fetal steroid environment. Prepregnancy BMI and pregnancy weight gain have served as markers for fetal steroid hormone exposure in other disease states. This study's objective is to determine whether prepregnancy BMI and pregnancy weight gain are associated with increased ASD risk across study designs and cohorts while controlling for important confounding variables.
METHODS: A population-based Utah ASD cohort (n = 128) was ascertained in a 3-county surveillance area and gender-and age-matched to 10 920 control subjects. A second, research-based ASD cohort of Utah children (n = 288) and their unaffected siblings (n = 493) were ascertained through participation in an ASD genetics study. Prenatal variables were obtained from birth certificate records.
RESULTS: ASD risk was significantly associated with pregnancy weight gain (adjusted odds ratio = 1.10, 95% confidence interval: 1.03 to 1.17; adjusted odds ratio = 1.17, 95% confidence interval: 1.01 to 1.35 for each 5 pounds of weight gained), but not prepregnancy BMI, in population and research-based cohorts, respectively. When analyses were restricted to ASD cases with normal IQ, these associations remained significant.
CONCLUSIONS: ASD risk associated with a modest yet consistent increase in pregnancy weight gain suggests that pregnancy weight gain may serve as an important marker for autism's underlying gestational etiology. This justifies an investigation into phenomena that link pregnancy weight gain and ASD independent of prepregnancy BMI.
C1 [Bilder, Deborah A.; Bakian, Amanda V.; Viskochil, Joseph; Botts, Elizabeth L.; McMahon, William M.; Coon, Hilary] Univ Utah, Dept Psychiat, Salt Lake City, UT USA.
[Clark, Erin A. S.] Univ Utah, Dept Obstet & Gynecol, Salt Lake City, UT USA.
[Smith, Ken R.; Pimentel, Richard] Univ Utah, Dept Populat Sci, Salt Lake City, UT USA.
RP Bilder, DA (reprint author), Utah Autism Res Program, 650 Komas Dr,Suite 206, Salt Lake City, UT 84108 USA.
EM deborah.bilder@hsc.utah.edu
FU Centers for Disease Control and Prevention [CCU822365]; National
Institute of Mental Health [R01 MH069359, R01 MH094400]; National
Institute on Aging [R01 AG022095]; National Institutes of Health (NIH)
FX Partially funded by the Centers for Disease Control and Prevention under
Cooperative Agreement CCU822365 to establish Population-Based
Surveillance of Autism Spectrum Disorders, the Utah Registry of Autism
and Developmental Disabilities, the National Institute of Mental Health
grants R01 MH069359 and R01 MH094400, National Institute on Aging grant
R01 AG022095, and Autism Speaks. Funded by the National Institutes of
Health (NIH).
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NR 45
TC 3
Z9 3
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2013
VL 132
IS 5
BP E1276
EP E1283
DI 10.1542/peds.2013-1188
PG 8
WC Pediatrics
SC Pediatrics
GA 245PE
UT WOS:000326475000019
PM 24167172
ER
PT J
AU Sukhodolsky, DG
Bloch, MH
Panza, KE
Reichow, B
AF Sukhodolsky, Denis G.
Bloch, Michael H.
Panza, Kaitlyn E.
Reichow, Brian
TI Cognitive-Behavioral Therapy for Anxiety in Children With
High-Functioning Autism: A Meta-analysis
SO PEDIATRICS
LA English
DT Review
DE autism spectrum disorder; cognitive-behavior therapy; anxiety; children;
adolescents; randomized controlled trial; meta-analysis
ID PERVASIVE DEVELOPMENTAL DISORDERS; RANDOMIZED CONTROLLED-TRIAL; SPECTRUM
DISORDERS; OPEN-LABEL; PSYCHIATRIC-DISORDERS; REPETITIVE BEHAVIOR;
ASPERGER-SYNDROME; CLINICAL-TRIAL; ADOLESCENTS; SYMPTOMS
AB BACKGROUND: Anxiety is a common and impairing problem in children and adolescents with autism spectrum disorder (ASD). There is emerging evidence that cognitive-behavioral therapy (CBT) could reduce anxiety in children with high-functioning ASD.
OBJECTIVE: To systematically review the evidence of using CBT to treat anxiety in children and adolescents with ASD. Methods for this review were registered with PROSPERO (CRD42012002722).
METHODS: We included randomized controlled trials published in English in peer-reviewed journals comparing CBT with another treatment, no treatment control, or waitlist control. Two authors independently screened 396 records obtained from database searches and hand searched relevant journals. Two authors independently extracted and reconciled all data used in analyses from study reports.
RESULTS: Eight studies involving 469 participants (252 treatment, 217 comparison) met our inclusion criteria and were included in meta-analyses. Overall effect sizes for clinician-and parent-rated outcome measures of anxiety across all studies were d = 1.19 and d = 1.21, respectively. Five studies that included child self-report yielded an average d = 0.68 across self-reported anxiety.
CONCLUSIONS: Parent ratings and clinician ratings of anxiety are sensitive to detecting treatment change with CBT for anxiety relative to waitlist and treatment-as-usual control conditions in children with high-functioning ASD. Clinical studies are needed to evaluate CBT for anxiety against attention control conditions in samples of children with ASD that are well characterized with regard to ASD diagnosis and co-occurring anxiety symptoms.
C1 [Sukhodolsky, Denis G.; Bloch, Michael H.; Panza, Kaitlyn E.; Reichow, Brian] Yale Univ, Yale Child Study Ctr, New Haven, CT USA.
RP Sukhodolsky, DG (reprint author), Yale Child Study Ctr, 230 South Frontage Rd, New Haven, CT 06520 USA.
EM denis.sukhodolsky@yale.edu
FU National Institutes of Health (NIH); [K01 MH079130]; [K23MH091240]
FX Supported in part by grants K01 MH079130 (Dr Sukhodolsky) and
K23MH091240 (Dr Bloch). Funded by the National Institutes of Health
(NIH).
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NR 77
TC 4
Z9 4
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
EI 1098-4275
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2013
VL 132
IS 5
BP E1341
EP E1350
DI 10.1542/peds.2013-1193
PG 10
WC Pediatrics
SC Pediatrics
GA 245PE
UT WOS:000326475000027
PM 24167175
ER
PT J
AU Jarmolowska, B
Teodorowicz, M
Fiedorowicz, E
Sienkiewicz-Szlapka, E
Matysiewicz, M
Kostyra, E
AF Jarmolowska, Beata
Teodorowicz, Malgorzata
Fiedorowicz, Ewa
Sienkiewicz-Szlapka, Edyta
Matysiewicz, Michal
Kostyra, Elzbieta
TI Glucose and calcium ions may modulate the efficiency of bovine
beta-casomorphin-7 permeability through a monolayer of Caco-2 cells
SO PEPTIDES
LA English
DT Article
DE beta-Casomorphin-7; Caco-2 cells monolayer; Food allergy; Infant
formula; Permeability coefficient
ID BETA-CASOMORPHIN; OPIOID-PEPTIDES; TIGHT JUNCTIONS; ENDOTHELIAL
PERMEABILITY; INTESTINAL PERMEABILITY; GENE-EXPRESSION; TRANSPORT; MILK;
ABSORPTION; IV
AB Milk and dairy products provide a lot of valuable nutritive elements. They are also sources of biologically active peptides, including beta-casomorphins that manifest the properties of morphine. An activity of DPPIV seems to be most crucial factor decreasing the efficiency of the beta-casomorphin-7 (BCM7) transport. The increase of BCM7 concentration in blood may intensify symptoms of apparent life threatening events (ALTE), autism, schizophrenia, and allergy. This study aimed at identifying the influence of several selected substances on a transport efficiency of bovine BCM7 through an intestinal monolayer in a Caco-2 cell model system. Applying the ELISA method, the permeability coefficient of BCM7 through the Caco-2 monolayer was calculated. TEER values were used to evaluate the integrity of Caco-2 cell monolayers. An increase of glucose and Ca2+ concentrations in the culture medium was accompanied by an increase of the BCM7 transport efficiency. The lowest permeability coefficients of BCM7 were observed for the membranes with high electrical resistances. The transport was enhanced in the presence of milk infant formulas, whereas no changes were observed when using mu-opioid receptor antagonist (casoxin-6). The results may be useful in understanding the pathogenesis of inflammation and food allergy in infants. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Jarmolowska, Beata; Fiedorowicz, Ewa; Sienkiewicz-Szlapka, Edyta; Matysiewicz, Michal; Kostyra, Elzbieta] Univ Warmia & Mazury, Fac Biol & Biotechnol, Dept Biochem, PL-10719 Olsztyn, Poland.
[Teodorowicz, Malgorzata] Univ Wageningen & Res Ctr, Cell Biol & Immunol Grp, NL-6708 WD Wageningen, Netherlands.
RP Kostyra, E (reprint author), Univ Warmia & Mazury, Fac Biol & Biotechnol, Dept Biochem, Ul Oczapowskiego 1A, PL-10719 Olsztyn, Poland.
EM elzbieta.kostyra@uwm.edu.pl
FU [NN 312 3153 37]
FX The authors would like to thank all their collaborators who participated
in the research presented in this study. This scientific research has
been financed from the resources designed for science in 2009-2012 as
Research Project No. NN 312 3153 37.
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NR 58
TC 2
Z9 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0196-9781
EI 1873-5169
J9 PEPTIDES
JI Peptides
PD NOV
PY 2013
VL 49
BP 59
EP 67
DI 10.1016/j.peptides.2013.08.017
PG 9
WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy
GA 251PA
UT WOS:000326941100009
PM 24004919
ER
PT J
AU Medeiros, K
Curby, TW
Bernstein, A
Rojahn, J
Schroeder, SR
AF Medeiros, Kristen
Curby, Timothy W.
Bernstein, Alec
Rojahn, Johannes
Schroeder, Stephen R.
TI The progression of severe behavior disorder in young children with
intellectual and developmental disabilities
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Intellectual disability; Developmental disability; Autism spectrum
disorder; Down syndrome; Challenging behaviors; Behavior disorders;
Self-injury; Stereotypy; Aggression; Structural equation modeling
ID SELF-INJURIOUS-BEHAVIOR; CHALLENGING BEHAVIORS; PROBLEMS-INVENTORY;
ADULTS; SPECTRUM; PEOPLE; TODDLERS; VALIDITY; INFANT
AB Behavior disorders, such as self-injurious, stereotypic, and aggressive behavior are common among individuals with intellectual or developmental disabilities. While we have learned much about those behaviors over the past few decades, longitudinal research that looks at developmental trajectory has been rare. This study was designed to examine the trajectory of these three forms of severe behavior disorders over a one year time period. The behaviors were measured on two dimensions: frequency of occurrence and severity. Participants were 160 infants and toddlers at risk for developmental delays in Lima, Peru. Using structural equation modeling, we found that the frequency of self-injury and stereotypic behavior and the severity of aggressive behavior remained stable over the 12-month period. Uni-directional structural models fit the data best for self-injurious and aggressive behavior (with frequency being a leading indicator of future severity of sel-injury and severity being a leading indicator of future frequency for aggression). For stereotypic behavior, a cross-lagged autoregressive model fit the data best, with both dimensions of frequency and severity involved as leading indicators of each other. These models did not vary significantly across diagnostic groups, suggesting that toddlers exhibiting behavior disorders may be assisted with interventions that target the specific frequencies or severities of behaviors, regardless of diagnostic category. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Medeiros, Kristen; Curby, Timothy W.; Bernstein, Alec; Rojahn, Johannes] George Mason Univ, Fairfax, VA 22030 USA.
[Schroeder, Stephen R.] Univ Kansas, Lawrence, KS 66045 USA.
RP Rojahn, J (reprint author), George Mason Univ, 10340 Democracy Lane,Suite 202,MSN 2C6, Fairfax, VA 22030 USA.
EM kmedeiro@gmu.edu; tcurby@gmu.edu; abernst2@gmu.edu; jrojahn@gmu.edu;
schroeder@ku.edu
CR Achenbach T., 2000, HDB DEV PSYCHOPATHOL, P41
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NR 37
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 3639
EP 3647
DI 10.1016/j.ridd.2013.08.002
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900002
PM 24012587
ER
PT J
AU Mazzone, L
Postorino, V
De Peppo, L
Fatta, L
Lucarelli, V
Reale, L
Giovagnoli, G
Vicari, S
AF Mazzone, Luigi
Postorino, Valentina
De Peppo, Lavinia
Fatta, Laura
Lucarelli, Valeria
Reale, Laura
Giovagnoli, Giulia
Vicari, Stefano
TI Mood symptoms in children and adolescents with autism spectrum disorders
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Autism spectrum disorders; Depressive symptoms; Mood symptoms; Global
functioning; Comorbidity
ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; MANIA
RATING-SCALE; ASPERGER-SYNDROME; DEPRESSIVE SYMPTOMS; ANXIETY SYMPTOMS;
ITALIAN CHILDREN; ADULTS; COMORBIDITY; VERSION
AB Asperger Syndrome (AS) and High Functioning Autism (HFA) are psychiatric conditions belonging to the Autistic Spectrum Disorders (ASDs), characterized by social dysfunction and focused interest, in the absence of mental retardation. Previous reports suggest that AS/HFA may be associated with important psychiatric comorbidities. Among the psychiatric internalizing disorders, depression and anxiety are probably the most common disorders. The aim of this study is to evaluate the prevalence of mood disorders and identifying peculiar clinical features in subjects suffering from AS and HFA. 30 male patients with AS/HFA, 30 male patients affected by Major Depression (MD) and 35 male Typically Developing (TD) comparison were assessed with the CDI and the CDRS-R. Participants' parents were invited to complete the CBCL and the P-YMRS. Moreover, the CGAS was rated by the clinicians. The evaluation of depressive symptoms showed that AS/HFA group reported higher depressive symptoms, as showed by CDI total, CBCL internalizing and CDRS-R total, compared to the TD group. No significant difference of depressive symptoms was found between the AS/HFA and the MD group, with the exception of CDRS-R total score. Moreover, linear regression analysis in the AS/HFA group between CGAS and depressive symptoms revealed that a higher level of depressive symptoms increased the risk of poorer global functioning. These results suggest that the depressive symptoms in AS/HFA patients may be associated with poorer global functioning, with a consequent impairment in their psychological profile and social adjustment, and should alert clinicians to the importance of assessing mood disorders in order to choose the appropriate treatment. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Mazzone, Luigi; Postorino, Valentina; De Peppo, Lavinia; Fatta, Laura; Lucarelli, Valeria; Giovagnoli, Giulia; Vicari, Stefano] IRCCS Childrens Hosp Bambino Gesu, Dept Neurosci, Child Neuropsychiat Unit, I-00165 Rome, Italy.
[Reale, Laura] Univ Catania, Dept Pediat, Div Child Neurol & Psychiat, I-95124 Catania, Italy.
RP Mazzone, L (reprint author), IRCCS Childrens Hosp Bambino Gesu, Dept Neurosci, Child Neuropsychiat Unit, Sq S Onofrio 4, I-00165 Rome, Italy.
EM gigimazzone@yahoo.it
CR Achenbach T. M., 1983, MANUAL CHILD BEHAV C
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NR 72
TC 5
Z9 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 3699
EP 3708
DI 10.1016/j.ridd.2013.07.034
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900010
PM 24029798
ER
PT J
AU Lai, DC
Tseng, YC
Guo, HR
AF Lai, Der-Chung
Tseng, Yen-Cheng
Guo, How-Ran
TI Trends in the prevalence of childhood disability: Analysis of data from
the national disability registry of Taiwan, 2000-2011
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Autism spectrum disorders; Childhood disability; Intellectual
disability; Prevalence; Taiwan
ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM SPECTRUM DISORDERS;
LOW-BIRTH-WEIGHT; INTELLECTUAL DISABILITY; GEOGRAPHIC DIFFERENCES;
CHILDREN ANALYSIS; MENTAL-RETARDATION; INCOME COUNTRIES; EPIDEMIOLOGY;
GENDER
AB Childhood disability is not uncommon, but data at the national level are limited, especially those on the changes in the prevalence over time. On the basis of the Disabled Welfare Act, Taiwan began to certify disabled residents and provide various services in 1980. All the cases receiving services are registered, and the registry provides a rare opportunity for studying childhood disability at the national level. Using the data from 2000 to 2011, we calculated the age-specific prevalence of all disability combined and assessed the changes over time. We also calculated the prevalence rate and the proportion in all disabilities combined for each disability category and assessed the trends. As certification before 3 years old is generally discouraged by the government, we limited analyses to children between 3 and 17 years old. We found that the registered cases ranged from 49,242 to 61,717 from 2000 to 2011 and that intellectual disability (ID), had been the leading category all through the years. The proportion of autism spectrum disorders (ASD) had been increasing rapidly and become the third leading disability in 2011. The prevalence of all disabilities combined increased constantly from 9.98/1000 to 15.41/1000 (p < 0.01), and increases were generally observed every year in all age groups (p < 0.01). The increase could largely be attributable to the increases in ID and ASD, while the increasing trends were also significant in "multiple disabilities," "speech or language impairment," and "other disabilities listed by the Department of Health" (p < 0.01 for all the five categories). An increase with age in the prevalence of all disabilities combined could be observed all through the years (p < 0.01 in all calendar years). We concluded that the prevalence of childhood disability has been increasing in Taiwan, with ID contributing the most cases and ASD as an emerging problem. However, the increase of prevalence cannot be attributed entirely to the increase in the occurrence of cases, and an increase in the proportion of cases registered was an more important factor, which may be in turn attributable to a better service of the related agencies, lower discrimination against the patients, higher awareness of the disorder, and more willingness of the guardians to register. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Lai, Der-Chung] Chia Yi Christian Hosp, Ditmanson Med Fdn, Dept Phys Med & Rehabil, Chiayi, Taiwan.
[Lai, Der-Chung] Chia Nan Univ Pharm & Sci, Dept Senior Citizen Serv Management, Tainan, Taiwan.
[Tseng, Yen-Cheng] Chang Jung Christian Univ, Dept Business Adm, Tainan, Taiwan.
[Tseng, Yen-Cheng] Chang Jung Christian Univ, Language Educ Ctr, Tainan, Taiwan.
[Guo, How-Ran] Natl Cheng Kung Univ, Dept Environm & Occupat Hlth, Tainan 70428, Taiwan.
[Guo, How-Ran] Natl Cheng Kung Univ Hosp, Dept Occupat & Environm Med, Tainan 70428, Taiwan.
RP Guo, HR (reprint author), Natl Cheng Kung Univ, Dept Environm & Occupat Hlth, 138 Sheng Li Rd, Tainan 70428, Taiwan.
EM hrguo@mail.ncku.edu.tw
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NR 38
TC 3
Z9 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 3766
EP 3772
DI 10.1016/j.ridd.2013.08.001
PG 7
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900017
PM 24021391
ER
PT J
AU Somogyi, E
Kiraly, I
Gergely, G
Nadel, J
AF Somogyi, Eszter
Kiraly, Ildiko
Gergely, Gyoergy
Nadel, Jacqueline
TI Understanding goals and intentions in low-functioning autism
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Autism; Understanding goals; Intentionality; Deferred imitation
ID SPECTRUM DISORDERS; YOUNG-CHILDREN; MENTAL STATES; IMITATION; INFANTS;
LANGUAGE; OTHERS; COMMUNICATION; IMPAIRMENT; PREDICTORS
AB We investigated ability to understand goals and attribute intentions in the context of two imitation studies in low-functioning, nonverbal children with autism (L-F CWA), a population that is rarely targeted by research in the domain. Down syndrome children (DSC) and typically developing children (TDC) were recruited to form matched comparison groups. In the two sets of simple action demonstrations only contextual indicators of the model's intentions were manipulated. In the Head touch experiment the model activated a button on a toy by pushing it with the forehead, whereas in the Hidden box experiment the model used a ball with a magnet to lift a box out of its container. Both actions were unusual and non-affordant with regards to the objects involved, none of the children in the baseline condition produced them. L-F CWA imitated the experimenter exactly, regardless of the model's intention. TDC showed appreciation of the model's intention by imitating her actions selectively. DSC reproduced only the intentional action as often as they imitated the experimenter exactly. It is concluded that L-F CWA attributed goals to the observed model, but did not show an appreciation of the model's intentions even in these simplified, nonverbal contexts. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Somogyi, Eszter] Eotvos Lorand Univ, Dept Cognit Psychol, H-1064 Budapest, Hungary.
[Kiraly, Ildiko; Gergely, Gyoergy] Cent European Univ, Dept Cognit Sci, Cognit Dev Ctr, H-1051 Budapest, Hungary.
[Nadel, Jacqueline] Hop La Pitie Salpetriere, Ctr Emot, UMR 7593, F-75013 Paris, France.
RP Somogyi, E (reprint author), Eotvos Lorand Univ, Dept Cognit Psychol, Izabella U 46, H-1064 Budapest, Hungary.
EM somogyi.eszter@ppk.elte.hu
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NR 56
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 3822
EP 3832
DI 10.1016/j.ridd.2013.07.039
PG 11
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900023
PM 24021392
ER
PT J
AU Bicer, AH
Alsaffar, AA
AF Bicer, Ayse Humeyra
Alsaffar, Ayten Aylin
TI Body mass index, dietary intake and feeding problems of Turkish children
with autism spectrum disorder (ASD)
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Autism; BMI-for-age; Dietary intake; Feeding problems; Turkey
ID TYPICALLY DEVELOPING-CHILDREN; FOOD SELECTIVITY; REPETITIVE BEHAVIORS;
DIAGNOSTIC INTERVIEW; EATING BEHAVIORS; YOUNG-CHILDREN; ASSOCIATION;
ACCEPTANCE; CHILDHOOD; PATTERNS
AB The body mass index of 164 children (aged 4-18 years) attending four autism rehabilitation centers in Istanbul, Turkey, was determined and assessed using the BMI-for-age percentile charts by the World Health Organization (WHO). The mean intake of energy and nutrients of 115 children were calculated using three-day food records. The feeding assessment surveys filled in by the parents/caregivers indicated that the major feeding problem among children was food selectivity. The majority of the children were overweight or obese (58.5%). A total of 11% of children were found to be severely thin and thin. The calcium, zinc, vitamin B6 and folate intake of the majority of children were inadequate. The salt consumption in all age groups and cholesterol intake in normal, overweight and obese children were high. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Bicer, Ayse Humeyra] Yeditepe Univ, Dept Nutr & Dietet, Istanbul, Turkey.
[Alsaffar, Ayten Aylin] Ozyegin Univ, Sch Appl Sci, TR-34794 Istanbul, Turkey.
RP Alsaffar, AA (reprint author), Ozyegin Univ, Sch Appl Sci, Nisantepe Mah Orman Sok 13, TR-34794 Istanbul, Turkey.
EM aylin.alsaffar@ozyegin.edu.tr
RI Alsaffar, Ayten/A-6578-2015
OI Alsaffar, Ayten/0000-0001-5642-939X
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NR 79
TC 3
Z9 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 3978
EP 3987
DI 10.1016/j.ridd.2013.08.024
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900037
PM 24029808
ER
PT J
AU Straccia, C
Tasse, MJ
Ghisletta, P
Barisnikov, K
AF Straccia, Claudio
Tasse, Marc J.
Ghisletta, Paolo
Barisnikov, Koviljka
TI The French version of the Reiss Screen for Maladaptive Behavior: Factor
structure, point prevalence and associated factors
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE RSMB; Intellectual disability; Psychopathology; Mental illness; Adults;
Age; Gender; Down syndrome
ID MENTAL ILL-HEALTH; INTELLECTUAL DISABILITIES; DOWN-SYNDROME;
PSYCHIATRIC-DISORDERS; GENDER-DIFFERENCES; ADULTS; EPIDEMIOLOGY;
ILLNESS; PEOPLE; SCALE
AB The main aims of the present study were to examine the factor structure and the internal consistency of the factors in the French version of the Reiss Screen of Maladaptive Behavior in a French-speaking European sample. The prevalence of psychopathology and the influence of associated factors were also examined. The Reiss Screen was administered to 467 adults (age range: 18-73) with intellectual disability living in the French-speaking regions of Switzerland and Belgium. A confirmatory factor analysis was performed to replicate the original factor structure. Internal consistency was examined by using Cronbach's alpha. Analyses of variance were computed to study the influence of gender, age and Down syndrome etiology. The original factor structure of the Reiss Screen was replicated. The overall rate of psychopathology in the sample was 37%. No linear relationship between age and psychopathology was found. However, adults aged less than 26 years had lower scores than older adults on several psychopathological domains. Males had higher scores than females on the Autism and the Avoidant Disorder subscales. Participants with Down syndrome had lower scores on all domains, with the exception of the Autism subscale. The results of this study suggest that the French version of the Reiss Screen can be a useful tool to detect psychopathology in adults with intellectual disability. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Straccia, Claudio; Barisnikov, Koviljka] Univ Geneva, Child Clin Neuropsychol Unit, Dept Psychol, CH-1211 Geneva 4, Switzerland.
[Tasse, Marc J.] Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA.
[Ghisletta, Paolo] Univ Geneva, Methodol & Data Anal Unit, Dept Psychol, CH-1211 Geneva 4, Switzerland.
RP Straccia, C (reprint author), Univ Geneva, Child Clin Neuropsychol Unit, Uni Mail 6164, CH-1211 Geneva 4, Switzerland.
EM Claudio.Straccia@unige.ch
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NR 40
TC 1
Z9 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 4052
EP 4061
DI 10.1016/j.ridd.2013.08.034
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900045
PM 24042171
ER
PT J
AU Werner, S
Shulman, C
AF Werner, Shirli
Shulman, Cory
TI Subjective well-being among family caregivers of individuals with
developmental disabilities: The role of affiliate stigma and
psychosocial moderating variables
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Stigma; Developmental disabilities; Caregiving; Subjective well-being
ID QUALITY-OF-LIFE; MENTAL-ILLNESS; INTELLECTUAL DISABILITY; STUDENTS
ATTITUDES; CONJOINT-ANALYSIS; CHILDREN; PARENTS; AUTISM; EXPERIENCES;
PEOPLE
AB Studies have shown that stigmatization is linked to lower quality of life; however, only scant research has examined the association between family caregivers' internalization of stigma (affiliate stigma) and their subjective quality of life (subjective well-being, SWB). Furthermore, studies have rarely examined this association via comparison between caregivers of individuals with different developmental disabilities in addition to examining the influence of psychosocial protective factors. These were the aims of the current study. Family caregivers (N = 176) of individuals with autism spectrum disorders (ASD), intellectual disabilities (ID), and physical disabilities (PD) completed a self-report structured questionnaire including scales measuring SWB, affiliate stigma, burden, positive meaning in caregiving, social support and self-esteem. Results showed that SWB of family caregivers was below the average normative level and especially low for caregivers of individuals with ASD. The strongest predictors of SWB were caregivers' self-esteem, social support, positive meaning in caregiving, and affiliate stigma. Furthermore, an interaction was found between affiliate stigma and diagnosis, showing that among caregivers of individuals with ASD, greater levels of stigma were associated with lower ratings of SWB, whereas such an association was not found among caregivers of individuals with ID or PD. Findings from this study point to the importance of supporting caregivers across the life-span in order to decrease stigma, improve social support and self-esteem and improve SWB. Further, findings point to the need to respond differentially to the various developmental disabilities. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Werner, Shirli; Shulman, Cory] Hebrew Univ Jerusalem, Paul Baerwald Sch Social Work & Social Welf, IL-91905 Jerusalem, Israel.
RP Werner, S (reprint author), Hebrew Univ Jerusalem, Paul Baerwald Sch Social Work & Social Welf, IL-91905 Jerusalem, Israel.
EM shirlior@mscc.huji.ac.il
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NR 57
TC 2
Z9 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 4103
EP 4114
DI 10.1016/j.ridd.2013.08.029
PG 12
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900049
PM 24055712
ER
PT J
AU Jansen, R
Ceulemans, E
Grauwels, J
Maljaars, J
Zink, I
Steyaert, J
Noens, I
AF Jansen, Rianne
Ceulemans, Eva
Grauwels, Jolien
Maljaars, Jarymke
Zink, Inge
Steyaert, Jean
Noens, Ilse
TI Young children with language difficulties: A dimensional approach to
subgrouping
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Language difficulties; Early diagnosis; Cluster analysis; Intentional
communication; Symbol understanding
ID AUTISM SPECTRUM DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE;
LOW-FUNCTIONING CHILDREN; SYMBOLIC PLAY; JOINT ATTENTION; BEHAVIORAL
DIFFICULTIES; IMPAIRED CHILDREN; ADOS SCORES; FOLLOW-UP; COMMUNICATION
AB A dimensional approach was used to create bottom-up constructed subgroups that captured the behavioral heterogeneity in 36 Dutch-speaking children with language difficulties. Four subgroups were delineated based upon differences in cognitive ability, symbol understanding, joint attention and autism spectrum disorder related characteristics. Children with a different developmental disorder were found within a single cluster. Therefore, the results of this study suggest that bottom-up constructed subgroups might capture the heterogeneous behavioral profiles of young children with developmental difficulties in a more meaningful way. Furthermore, joint attention and symbol understanding seem important skills to assess in young children presenting with language difficulties. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Jansen, Rianne; Maljaars, Jarymke; Noens, Ilse] Katholieke Univ Leuven, Parenting & Special Educ Res Unit, Louvain, Belgium.
[Jansen, Rianne; Maljaars, Jarymke; Steyaert, Jean; Noens, Ilse] Katholieke Univ Leuven, Leuven Autism Res LAuRes, Louvain, Belgium.
[Ceulemans, Eva; Grauwels, Jolien] Katholieke Univ Leuven, Methodol Educ Sci Res Unit, Louvain, Belgium.
[Zink, Inge] Katholieke Univ Leuven, Dept Neurosci, ExpORL, Louvain, Belgium.
[Zink, Inge] UZ Leuven, Dept Otorhinolaryngol Head & Neck Surg, Louvain, Belgium.
[Steyaert, Jean] Katholieke Univ Leuven, Dept Neurosci Child & Adolescent Psychiat, Louvain, Belgium.
[Steyaert, Jean] Univ Maastricht, Dept Clin Genet, Maastricht, Netherlands.
RP Jansen, R (reprint author), Katholieke Univ Leuven, Parenting & Special Educ Res Unit, Louvain, Belgium.
EM rianne.jansen@ppw.kuleuven.be
RI Steyaert, Jean/B-5326-2015
OI Steyaert, Jean/0000-0003-2512-4694
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NR 82
TC 1
Z9 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 4115
EP 4124
DI 10.1016/j.ridd.2013.08.028
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900050
PM 24051364
ER
PT J
AU Turygin, N
Matson, JL
Tureck, K
AF Turygin, Nicole
Matson, Johnny L.
Tureck, Kimberly
TI ADHD symptom prevalence and risk factors in a sample of toddlers with
ASD or who are at risk for developmental delay
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE ADHD; Toddlers; Autism; Early intervention; Child development;
Developmental trajectory; Developmental delay
ID AUTISM SPECTRUM DISORDERS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER;
DEFICIT-HYPERACTIVITY DISORDER; PSYCHIATRIC-DISORDERS; COMORBID
PSYCHOPATHOLOGY; EXECUTIVE FUNCTIONS; YOUNG-CHILDREN; BEHAVIORS;
DIAGNOSIS; BOYS
AB Individuals with attention deficit/hyperactivity disorder (ADHD) experience difficulties with inattention, hyperactivity, and impulsivity which significantly interfere with their daily functioning. Symptoms of the disorder occur in children, but the developmental trajectory of ADHD symptoms is not known. The present study examines the prevalence of ADHD symptomology in a sample of 2956 children who were determined to be at risk for developmental delay. Prevalence rates for ADHD in the overall sample was 4.50%, and prevalence rates by gender, race, and presence of autism spectrum disorder (ASD) were comparable. The prevalence was not significantly different in children with an ASD diagnosis. No significant effects of gender or ASD diagnosis were observed. ADHD should be considered as a diagnosis among young children who present to clinics for children at risk for developmental delay, and future researchers should further study its developmental trajectory, beginning at an early age. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Turygin, Nicole; Matson, Johnny L.; Tureck, Kimberly] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Turygin, N (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM nturyg1@tigers.lsu.edu
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NR 69
TC 1
Z9 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 4203
EP 4209
DI 10.1016/j.ridd.2013.07.020
PG 7
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900060
PM 24077069
ER
PT J
AU Marchal, JP
Maurice-Stam, H
Hatzmann, J
van Trotsenburg, ASP
Grootenhuis, MA
AF Marchal, Jan Pieter
Maurice-Stam, Heleen
Hatzmann, Janneke
van Trotsenburg, A. S. Paul
Grootenhuis, Martha A.
TI Health related quality of life in parents of six to eight year old
children with Down syndrome
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Down syndrome; Parents; Health related quality of life; Predictors;
Cross-sectional study; Social support; Leisure
ID DEVELOPMENTAL-DISABILITIES; INTELLECTUAL DISABILITY;
BEHAVIORAL-PROBLEMS; SWEDISH PARENTS; SOCIAL SUPPORT; MENTAL-HEALTH;
STRESS; MOTHERS; AUTISM; CARE
AB Raising a child with Down syndrome (DS) has been found to be associated with lowered health related quality of life (HRQoL) in the domains cognitive functioning, social functioning, daily activities and vitality. We aimed to explore which socio-demographics, child functioning and psychosocial variables were related to these HRQoL domains in parents of children with DS. Parents of 98 children with DS completed the TNO-AZL adult quality of life questionnaire (TAAQOL) and a questionnaire assessing socio-demographic, child functioning and psychosocial predictors. Using multiple linear regression analyses for each category of predictors, we selected relevant predictors for the final models. The final multiple linear regression models revealed that cognitive functioning was best predicted by the sleep of the child (beta = .29, p < .01) and by the parent having given up a hobby (beta = -.29, p < .01), social functioning by the quality of the partner relation (beta = .34, p < .001), daily activities by the parent having to care for an ill friend or family member (beta = -.31, p < .01), and vitality by the parent having enough personal time (beta. = .32, p < .01). Overall, psychosocial variables rather than socio-demographics or child functioning showed most consistent and powerful relations to the HRQoL domains of cognitive functioning, social functioning, daily activities and vitality. These psychosocial variables mainly related to social support and time pressure. Systematic screening of parents to detect problems timely, and interventions targeting the supportive network and the demands in time are recommended. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Marchal, Jan Pieter; Maurice-Stam, Heleen; Hatzmann, Janneke; Grootenhuis, Martha A.] Emma Childrens Hosp, Acad Med Ctr, Psychosocial Dept, NL-1100 DD Amsterdam, Netherlands.
[van Trotsenburg, A. S. Paul] Emma Childrens Hosp, Acad Med Ctr, Dept Endocrinol, NL-1100 DD Amsterdam, Netherlands.
RP Grootenhuis, MA (reprint author), Emma Childrens Hosp, Acad Med Ctr, Psychosocial Dept, A3-241,Post Box 22660, NL-1100 DD Amsterdam, Netherlands.
EM m.a.grootenhuis@amc.uva.nl
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NR 57
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV
PY 2013
VL 34
IS 11
BP 4239
EP 4247
DI 10.1016/j.ridd.2013.09.011
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 251BD
UT WOS:000326901900064
PM 24083990
ER
PT J
AU Chen, YN
Wang, J
Zhang, J
Li, SJ
He, L
Shao, DD
Du, HY
AF Chen, Yan-Ni
Wang, Jue
Zhang, Jie
Li, Su-Jiao
He, Li
Shao, Dong-Dong
Du, Hui-Ying
TI Effect of thimerosal on the neurodevelopment of premature rats
SO WORLD JOURNAL OF PEDIATRICS
LA English
DT Article
DE dopamine D4 receptor; neurodevelopment; serotonin 2A receptor;
thimerosal
ID EXPOSURE; VACCINES; INFANTS; NEURONS; BRAIN
AB Background: This study was undertaken to determine the effect of thimerosal on the neurodevelopment of premature rats.
Methods: Thimerosal was injected into premature SD rats at a dose of 32.8, 65.6, 98.4 or 131.2 mu g/kg on postnatal day 1. Expression of dopamine D4 receptor (DRD4) and serotonin 2A receptor (5-HT2AR), apoptosis in the prefrontal cortex on post-injection day 49, and learning and memory function were studied and compared with those in a control group injected with saline.
Results: Expression of DRD4 and 5-HT2AR and learning function decreased, and apoptosis increased significantly in the 131.2 mu g/kg group (P<0.001). Memory function was significantly impaired by 65.6 (P<0.05), 98.4 and 131.2 mu g/kg (P<0.001).
Conclusions: The negative adverse consequences on neurodevelopment observed in the present study are consistent with previous studies; this study raised serious concerns about adverse neurodevelopmental disorder such as autism in humans following the ongoing worldwide routine administration of thimerosal-containing vaccines to infants.
C1 [Chen, Yan-Ni; Wang, Jue; Li, Su-Jiao] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Key Lab Biomed Informat Engn, Minist Educ, Xian 710049, Peoples R China.
[Chen, Yan-Ni; Wang, Jue; Li, Su-Jiao] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Inst Biomed Engn, Xian 710049, Peoples R China.
[Chen, Yan-Ni; Zhang, Jie; He, Li; Shao, Dong-Dong; Du, Hui-Ying] Xi An Jiao Tong Univ, Xian Childrens Hosp, Coll Med, Xian 710002, Peoples R China.
RP Wang, J (reprint author), Xi An Jiao Tong Univ, Sch Life Sci & Technol, Key Lab Biomed Informat Engn, Minist Educ, Xian 710049, Peoples R China.
EM Juewang1@126.com
FU Natural Science Foundation of Shannxi Province, China [2009JM4030]
FX Project supported by the Natural Science Foundation of Shannxi Province,
China (Grant No. 2009JM4030).
CR ABDELRAHMAN M, 2013, J APPL PHARM SCI, V3, P48
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NR 19
TC 4
Z9 4
PU ZHEJIANG UNIV SCH MEDICINE
PI HANGZHOU
PA CHILDRENS HOSPITAL, 57 ZHUGAN XIANG, HANGZHOU, 310003, PEOPLES R CHINA
SN 1708-8569
EI 1867-0687
J9 WORLD J PEDIATR
JI World Journal of Pediatrics
PD NOV
PY 2013
VL 9
IS 4
BP 356
EP 360
DI 10.1007/s12519-013-0443-z
PG 5
WC Pediatrics
SC Pediatrics
GA 252YS
UT WOS:000327049400012
PM 24235069
ER
PT J
AU Kerekes, N
Brandstrom, S
Lundstrom, S
Rastam, M
Nilsson, T
Anckarsater, H
AF Kerekes, Nora
Brandstrom, Sven
Lundstrom, Sebastian
Rastam, Maria
Nilsson, Thomas
Anckarsater, Henrik
TI ADHD, autism spectrum disorder, temperament, and character: Phenotypical
associations and etiology in a Swedish childhood twin study
SO COMPREHENSIVE PSYCHIATRY
LA English
DT Article
ID DEFICIT HYPERACTIVITY DISORDER; PERSONALITY-DISORDERS; TELEPHONE
INTERVIEW; JUNIOR TEMPERAMENT; GENETIC INFLUENCES; KOREAN CHILDREN;
7-FACTOR MODEL; A-TAC; INVENTORY; SAMPLE
AB Objective: To explore the links between neurodevelopmental disorders attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) and personality in a population-based, genetically sensitive study of children.
Method: A population-based sample of 1886 twins aged 9 and 12, enriched for childhood mental health problems, was recruited from the Child and Adolescent Twin Study in Sweden (CATSS). Parents were interviewed over the telephone using the Autism-Tics, AD/HD and other Comorbidities (A-TAC) inventory, and in a second step they rated their children according to the Junior Temperament and Character Inventory (JTCI).
Results: ADHD was strongly correlated with novelty seeking, while ASD was correlated positively with harm avoidance and negatively with reward dependence. The strongest associations between personality traits and neurodevelopmental disorders were negative correlations between the character dimensions of self-directedness and cooperativeness and ADHD and ASD alike. Cross-twin cross-trait correlations between ADHD, ASD, and personality dimensions in monozygotic twins were more than double those in dizygotic twins, indicating a strong genetic effect behind the phenotypic covariation between neurodevelopmental disorders and personality.
Conclusions: Neurodevelopmental disorders are linked specifically to particular temperament profiles and generally to hampered development of the self-governing strategies referred to as "character." Poor self-agency and cooperation may be core functional outcomes in the separation of children with handicapping conditions from those with traits only reminiscent of neurodevelopmental disorders. The associations between neurodevelopmental disorders and personality are at least partly due to genetic effects influencing both conditions. As a consequence, personality must be broadly considered in neuropsychiatry, just as neuropsychiatric disorders and their genetic, neurodevelopmental, and cognitive susceptibilities have to be in personality research and clinical treatment. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Kerekes, Nora; Brandstrom, Sven; Lundstrom, Sebastian; Nilsson, Thomas; Anckarsater, Henrik] Univ Gothenburg, Ctr Eth Law & Mental Hlth CELAM, S-43141 Molndal, Sweden.
[Rastam, Maria] Lund Univ, Inst Clin Sci, S-22100 Lund, Sweden.
[Kerekes, Nora; Lundstrom, Sebastian] Swedish Prison & Probat Serv, R&D Unit, Gothenburg, Sweden.
[Lundstrom, Sebastian] Univ Gothenburg, Inst Neurosci & Physiol, Gillberg Neuropsychiat Ctr, S-43141 Molndal, Sweden.
RP Kerekes, N (reprint author), Univ Gothenburg, CELAM, Wallinsgatan 8, S-43141 Molndal, Sweden.
EM nora.kerekes@neuro.gu.se
RI Kerekes, Nora/C-6474-2009
FU Swedish Council for Working Life and Social Research [CATSS-9112];
Swedish Research Council (Medicine)
FX The CATSS-9112-study is supported by the Swedish Council for Working
Life and Social Research and the Swedish Research Council (Medicine).
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NR 40
TC 1
Z9 1
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0010-440X
EI 1532-8384
J9 COMPR PSYCHIAT
JI Compr. Psychiat.
PD NOV
PY 2013
VL 54
IS 8
BP 1140
EP 1147
DI 10.1016/j.comppsych.2013.05.009
PG 8
WC Psychiatry
SC Psychiatry
GA 248OA
UT WOS:000326709600002
PM 23790516
ER
PT J
AU Wu, Z
Pan, JT
Su, YJ
Gros-Louis, J
AF Wu, Zhen
Pan, Jingtong
Su, Yanjie
Gros-Louis, Julie
TI How joint attention relates to cooperation in 1- and 2-year-olds
SO INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT
LA English
DT Article
DE cooperation; ESCS; joint action; joint attention; toddlers
ID PRESCHOOL-CHILDREN; SOCIAL COMPETENCE; INFANT; AUTISM; LANGUAGE; POINT;
COMMUNICATION; TEMPERAMENT; INTENTIONS; SYSTEM
AB Joint attention has been suggested to contribute to children's development of cooperation; however, few empirical studies have directly tested this hypothesis. Children aged 1 and 2 years participated in two joint action activities to assess their cooperation with an adult partner, who stopped participating at a specific moment during the tasks. Children's joint attention skills were measured by the Early Social Communication Scales (ESCS). Results showed that children's responding to joint attention ability contributed to their successful cooperation in an activity that required parallel roles, whereas initiating joint attention ability contributed to their successful cooperation in an activity that required complementary roles. These results suggest a complex relationship between joint attention and cooperative abilities when considering RJA and IJA separately.
C1 [Wu, Zhen; Pan, Jingtong; Su, Yanjie] Peking Univ, Beijing 100871, Peoples R China.
[Wu, Zhen; Gros-Louis, Julie] Univ Iowa, Iowa City, IA 52242 USA.
[Pan, Jingtong] Tufts Univ, Medford, MA 02155 USA.
RP Su, YJ (reprint author), Peking Univ, Dept Psychol, Beijing 100871, Peoples R China.
EM yjsu@pku.edu.cn
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NR 45
TC 0
Z9 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0165-0254
EI 1464-0651
J9 INT J BEHAV DEV
JI Int. J. Behav. Dev.
PD NOV
PY 2013
VL 37
IS 6
BP 542
EP 548
DI 10.1177/0165025413505264
PG 7
WC Psychology, Developmental
SC Psychology
GA 246KS
UT WOS:000326537400008
ER
PT J
AU Giusti-Rodriguez, P
Sullivan, PF
AF Giusti-Rodriguez, Paola
Sullivan, Patrick F.
TI The genomics of schizophrenia: update and implications
SO JOURNAL OF CLINICAL INVESTIGATION
LA English
DT Review
ID RARE CHROMOSOMAL DELETIONS; AUTISM SPECTRUM DISORDERS; GATED
CALCIUM-CHANNELS; COPY NUMBER VARIANT; DE-NOVO MUTATIONS;
PSYCHIATRIC-DISORDERS; WIDE ASSOCIATION; BIPOLAR DISORDER; COMMON
VARIANTS; TRANSCRIPTOMIC ANALYSIS
AB Schizophrenia is strongly familial yet rarely (if ever) exhibits classical Mendelian inheritance patterns. The advent of large-scale genotyping and sequencing projects has yielded large data sets with higher statistical power in an effort to uncover new associations with schizophrenia. Here, we review the challenges in dissecting the genetics of schizophrenia and provide an update of the current understanding of the underlying genomics. We discuss the breadth of susceptibility alleles, including those that may occur with low frequency and high disease risk, such as the 22q11.2 hemideletion, as well as alleles that may occur with greater frequency but convey a lower risk of schizophrenia, such as variants in genes encoding subunits of the voltage-gated L-type calcium channel. Finally, we provide an overview of the clinical implications for the diagnosis and treatment of schizophrenia based on progress in understanding the underlying genetic basis.
C1 [Giusti-Rodriguez, Paola; Sullivan, Patrick F.] Univ N Carolina, Dept Genet, Ctr Psychiat Genom, Chapel Hill, NC 27599 USA.
[Sullivan, Patrick F.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Sullivan, Patrick F.] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
RP Sullivan, PF (reprint author), Univ N Carolina, Dept Genet, CB 7264, Chapel Hill, NC 27599 USA.
EM pfsulliv@med.unc.edu
FU NIH [U01 MH094421, P50 HG006582]
FX We thank our colleagues worldwide (particularly in the Psychiatric
Genomics Consortium), the tens of thousands of people who participated
in the primary studies, and Thomas Lehner of the NIMH for his support.
This work was supported by NIH grants U01 MH094421 and P50 HG006582.
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NR 102
TC 13
Z9 13
PU AMER SOC CLINICAL INVESTIGATION INC
PI ANN ARBOR
PA 35 RESEARCH DR, STE 300, ANN ARBOR, MI 48103 USA
SN 0021-9738
EI 1558-8238
J9 J CLIN INVEST
JI J. Clin. Invest.
PD NOV
PY 2013
VL 123
IS 11
BP 4557
EP 4563
DI 10.1172/JCI66031
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 247IU
UT WOS:000326611900003
PM 24177465
ER
PT J
AU Iacobas, DA
Iacobas, S
Chachua, T
Goletiani, C
Sidyelyeva, G
Veliskova, J
Velisek, L
AF Iacobas, D. A.
Iacobas, S.
Chachua, T.
Goletiani, C.
Sidyelyeva, G.
Veliskova, J.
Velisek, L.
TI Prenatal Corticosteroids Modify Glutamatergic and GABAergic Synapse
Genomic Fabric: Insights from a Novel Animal Model of Infantile Spasms
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Review
DE glucocorticoids; cortisol; corticosterone; ACTH; steroids; neuroactive
steroids; GABA
ID CORTICOTROPIN-RELEASING HORMONE; REPEATED ANTENATAL CORTICOSTEROIDS;
CONGENITAL ADRENAL-HYPERPLASIA; CEREBRAL GLUCOSE-UTILIZATION; AUTISM
SPECTRUM DISORDERS; CRYPTOGENIC WEST SYNDROME; GROWTH-FACTOR-I;
TERM-FOLLOW-UP; GLUCOCORTICOID-RECEPTOR; BRAIN TRANSCRIPTOME
AB Prenatal exposure to corticosteroids has long-term postnatal somatic and neurodevelopmental consequences. Animal studies indicate that corticosteroid exposure-associated alterations in the nervous system include hypothalamic function. Infants with infantile spasms, a devastating epileptic syndrome of infancy with characteristic spastic seizures, chaotic irregular waves on interictal electroencephalogram (hypsarhythmia) and mental deterioration, have decreased concentrations of adrenocorticotrophic hormone (ACTH) and cortisol in cerebrospinal fluid, strongly suggesting hypothalamic dysfunction. We have exploited this feature to develop a model of human infantile spasms by using repeated prenatal exposure to betamethasone and a postnatal trigger of developmentally relevant spasms with NMDA. The spasms triggered in prenatally primed rats are more severe compared to prenatally saline-injected ones and respond to ACTH, a treatment of choice for infantile spasms in humans. Using autoradiography and immunohistochemistry, we have identified a link between the spasms in our model and the hypothalamus, especially the arcuate nucleus. Transcriptomic analysis of the arcuate nucleus after prenatal priming with betamethasone but before trigger of spasms indicates that prenatal betamethasone exposure down-regulates genes encoding several important proteins participating in glutamatergic and GABAergic transmission. Interestingly, there were significant sex-specific alterations after prenatal betamethasone in synapse-related gene expression but no such sex differences were found in prenatally saline-injected controls. A pairwise relevance analysis revealed that, although the synapse gene expression in controls was independent of sex, these genes form topologically distinct gene fabrics in males and females and these fabrics are altered by betamethasone in a sex-specific manner. These findings may explain the sex differences with respect to both normal behaviour and the occurrence and severity of infantile spasms. Changes in transcript expression and their coordination may contribute to a molecular substrate of permanent neurodevelopmental changes (including infantile spasms) found after prenatal exposure to corticosteroids.
C1 [Iacobas, D. A.] New York Med Coll, Dept Pathol, Valhalla, NY 10595 USA.
[Iacobas, S.; Chachua, T.; Goletiani, C.; Sidyelyeva, G.; Veliskova, J.; Velisek, L.] New York Med Coll, Dept Cell Biol & Anat, Valhalla, NY 10595 USA.
[Veliskova, J.] New York Med Coll, Dept Obstet & Gynecol, Valhalla, NY 10595 USA.
[Veliskova, J.; Velisek, L.] New York Med Coll, Dept Neurol, Valhalla, NY 10595 USA.
[Velisek, L.] New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA.
RP Velisek, L (reprint author), New York Med Coll, Dept Cell Biol & Anat, BSB-A20,40 Sunshine Cottage Rd, Valhalla, NY 10595 USA.
EM libor_velisek@nymc.edu
FU NINDS/NIH [NS072966, NS056093]; Citizens United for Research in Epilepsy
(CURE) Infantile Spasms Research Initiative
FX Supported by grants NS072966 and NS056093 from NINDS/NIH, and by the
Citizens United for Research in Epilepsy (CURE) Infantile Spasms
Research Initiative.
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NR 163
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
EI 1365-2826
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD NOV
PY 2013
VL 25
IS 11
BP 964
EP 979
DI 10.1111/jne.12061
PG 16
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 246DJ
UT WOS:000326517100002
PM 23763471
ER
PT J
AU Kigar, SL
Auger, AP
AF Kigar, S. L.
Auger, A. P.
TI Epigenetic Mechanisms may Underlie the Aetiology of Sex Differences in
Mental Health Risk and Resilience
SO JOURNAL OF NEUROENDOCRINOLOGY
LA English
DT Review
DE epigenetics; juvenile; play behaviour; sexual differentiation;
methylation; steroid hormones; amygdala
ID CONGENITAL ADRENAL-HYPERPLASIA; ESTROGEN-RECEPTOR-ALPHA; JUVENILE SOCIAL
PLAY; AUTISM SPECTRUM DISORDERS; DNA METHYLTRANSFERASE 3A;
CENTRAL-NERVOUS-SYSTEM; MATERNAL-BEHAVIOR; ANOREXIA-NERVOSA;
MOUSE-BRAIN; RAT-BRAIN
AB In this review, we propose that experiential and hormonal influences on biological sex during development may produce differences in the epigenome, and that these differences play an important role in gating risk or resilience to a number of neurological and psychiatric disorders. One intriguing hypothesis is that the framework belying sex differences in the brain creates differences in methylation and demethylation patterns, and these in turn confer risk and resilience to mental health disorders. Here, we discuss these concepts with regard to social behaviour in rodent models and briefly discuss their possible relevance to human disease.
C1 [Kigar, S. L.] Univ Wisconsin, Mol & Cellular Pharmacol Training Program, Madison, WI 53706 USA.
[Auger, A. P.] Univ Wisconsin, Neurosci Training Program, Dept Psychol, Madison, WI 53706 USA.
RP Auger, AP (reprint author), Univ Wisconsin, Neurosci Training Program, Dept Psychol, Madison, WI 53706 USA.
EM apauger@wisc.edu
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NR 135
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0953-8194
EI 1365-2826
J9 J NEUROENDOCRINOL
JI J. Neuroendocrinol.
PD NOV
PY 2013
VL 25
IS 11
BP 1141
EP 1150
DI 10.1111/jne.12074
PG 10
WC Endocrinology & Metabolism; Neurosciences
SC Endocrinology & Metabolism; Neurosciences & Neurology
GA 246DJ
UT WOS:000326517100018
PM 23841484
ER
PT J
AU Kothari, R
Skuse, D
Wakefield, J
Micali, N
AF Kothari, Radha
Skuse, David
Wakefield, Justin
Micali, Nadia
TI Gender Differences in the Relationship Between Social Communication and
Emotion Recognition
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE autism spectrum disorder (ASD); Avon Longitudinal Study of Parents and
Children (ALSPAC); emotion recognition; gender; social communication
ID AUTISM SPECTRUM DISORDERS; GENERAL-POPULATION; TRAITS; CHILDREN;
IMPAIRMENT; DEFICITS; PARENTS
AB Objective: To investigate the association between autistic traits and emotion recognition in a large community sample of children using facial and social motion cues, additionally stratifying by gender. Method: A general population sample of 3,666 children from the Avon Longitudinal Study of Parents and Children (ALSPAC) were assessed on their ability to correctly recognize emotions using the faces subtest of the Diagnostic Analysis of Non-Verbal Accuracy, and the Emotional Triangles Task, a novel test assessing recognition of emotion from social motion cues. Children with autistic-like social communication difficulties, as assessed by the Social Communication Disorders Checklist, were compared with children without such difficulties. Results: Autistic-like social communication difficulties were associated with poorer recognition of emotion from social motion cues in both genders, but were associated with poorer facial emotion recognition in boys only (odds ratio = 1.9, 95% CI = 1.4, 2.6, p = .0001). This finding must be considered in light of lower power to detect differences in girls. Conclusions: In this community sample of children, greater deficits in social communication skills are associated with poorer discrimination of emotions, implying there may be an underlying continuum of liability to the association between these characteristics. As a similar degree of association was observed in both genders on a novel test of social motion cues, the relatively good performance of girls on the more familiar task of facial emotion discrimination may be due to compensatory mechanisms. Our study might indicate the existence of a cognitive process by which girls with underlying autistic traits can compensate for their covert deficits in emotion recognition, although this would require further investigation.
C1 [Kothari, Radha; Skuse, David; Wakefield, Justin; Micali, Nadia] UCL, London WC1N 1EH, England.
RP Kothari, R (reprint author), UCL, 30 Guilford St, London WC1N 1EH, England.
EM Radha.kothari.10@ucl.ac.uk
RI Micali, nadia/E-6829-2010
OI Micali, nadia/0000-0001-5571-2273
FU National Institute of Health Research (NIHR) clinician scientist award
[DHCS/08/08/012]; Wellchild project grant; Wellcome Trust [092731]
FX This research was funded by a National Institute of Health Research
(NIHR) clinician scientist award (DHCS/08/08/012) to Dr. Micali and by a
Wellchild project grant.The authors are extremely grateful to all of the
families who took part in this study, the midwives for their help in
recruiting them, and the whole Avon Longitudinal Study of Parents and
Children (ALSPAC) team. The UK Medical Research Council and the Wellcome
Trust (grant 092731) and the University of Bristol provide core support
for ALSPAC. This publication is the work of the authors, and Drs.
Kothari, Skuse, Wakefield, and Micah will serve as guarantors for the
contents The views expressed in this publication are those of the
author(s) and not necessarily those of the National Health Service
(NHS), NIHR, or the Department of Health.
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NR 32
TC 4
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2013
VL 52
IS 11
BP 1148
EP 1157
DI 10.1016/j.jaac.2013.08.006
PG 10
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 245RF
UT WOS:000326480800006
PM 24157389
ER
PT J
AU Green, SA
Rudie, JD
Colich, NL
Wood, JJ
Shirinyan, D
Hernandez, L
Tottenham, N
Dapretto, M
Bookheimer, SY
AF Green, Shulamite A.
Rudie, Jeffrey D.
Colich, Natalie L.
Wood, Jeffrey J.
Shirinyan, David
Hernandez, Leanna
Tottenham, Nim
Dapretto, Mirella
Bookheimer, Susan Y.
TI Overreactive Brain Responses to Sensory Stimuli in Youth With Autism
Spectrum Disorders
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE amygdala; anxiety; autism spectrum disorders; functional magnetic
resonance imaging (fMRI); sensory over-responsivity
ID OVER-RESPONSIVITY; ANXIETY DISORDERS; YOUNG-CHILDREN; AMYGDALA;
ADOLESCENTS; FEAR; ABNORMALITIES; INDIVIDUALS; HIPPOCAMPUS; MECHANISMS
AB Objectives: Sensory over-responsivity (SOR), defined as a negative response to or avoidance of sensory stimuli, is both highly prevalent and extremely impairing in youth with autism spectrum disorders (ASD), yet little is known about the neurological bases of SOR. This study aimed to examine the functional neural correlates of SOR by comparing brain responses to sensory stimuli in youth with and without ASD. Method: A total of 25 high-functioning youth with ASD and 25 age- and IQ-equivalent typically developing (IT)) youth were presented with mildly aversive auditory and visual stimuli during a functional magnetic resonance imaging (fMRI) scan. Parents provided ratings of children's SOR and anxiety symptom severity. Results: Compared to TD participants, ASD participants displayed greater activation in primary sensory cortical areas as well as amygdala, hippocampus, and orbital-frontal cortex. In both groups, the level of activity in these areas was positively correlated with level of SOR severity as rated by parents, over and above behavioral ratings of anxiety. Conclusions: This study demonstrates that youth with ASD show neural hyper-responsivity to sensory stimuli, and that behavioral symptoms of SOR may be related to both heightened responsivity in primary sensory regions as well as areas related to emotion processing and regulation.
C1 [Green, Shulamite A.; Wood, Jeffrey J.; Tottenham, Nim] Univ Calif Los Angeles, Los Angeles, CA 90095 USA.
[Rudie, Jeffrey D.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
[Colich, Natalie L.] Stanford Univ, Stanford, CA 94305 USA.
[Shirinyan, David] Santa Monica Coll, Santa Monica, CA USA.
[Hernandez, Leanna; Dapretto, Mirella; Bookheimer, Susan Y.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA.
RP Green, SA (reprint author), Univ Calif Los Angeles, Dept Psychol, 1285 Franz Hall, Los Angeles, CA 90095 USA.
EM shulamite@ucla.edu
FU National Institute of Child Health and Human Development [P50 HD055784];
National Institute of Mental Health [1R01 HD065280-01]; National
Research Service Award predoctoral fellowship [F31 MH093999-01A1]
FX This work was supported in part by grants from the National Institute of
Child Health and Human Development (P50 HD055784) and the National
Institute of Mental Health (1R01 HD065280-01) as well as a National
Research Service Award predoctoral fellowship to S.G. (F31
MH093999-01A1)
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Wechsler D, 1999, WECHSLER ABBREVIATED
Weng SJ, 2011, J CHILD PSYCHOL PSYC, V52, P296, DOI 10.1111/j.1469-7610.2010.02317.x
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NR 50
TC 12
Z9 12
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
EI 1527-5418
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2013
VL 52
IS 11
BP 1158
EP 1172
DI 10.1016/j.jaac.2013.08.004
PG 15
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 245RF
UT WOS:000326480800007
PM 24157390
ER
PT J
AU Doughty, AH
Giorno, KG
Miller, HL
AF Doughty, Adam H.
Giorno, Kenneth G.
Miller, Hannah L.
TI EFFECTS OF REINFORCER MAGNITUDE ON REINFORCED BEHAVIORAL VARIABILITY
SO JOURNAL OF THE EXPERIMENTAL ANALYSIS OF BEHAVIOR
LA English
DT Article
DE behavioral variability; reinforcer magnitude; induction; pigeon; key
peck
ID RESPONSE VARIABILITY; OPERANT VARIABILITY; SCHEDULE; AUTISM; FOOD;
PROBABILITY; PERFORMANCE; CONTINGENCY; REPETITION; INTERVAL
AB Eight pigeons were exposed to a two-component multiple schedule. In each component, four-peck sequences across left and right keys were reinforced according to a variability threshold contingency. In one condition, only infrequently occurring response sequences were reinforced in each component, thereby generating highly variable sequences. In a separate condition, when the variability threshold contingency was lenient in each component, sequences were much less variable. In each condition, reinforcer magnitude was manipulated across components, and the larger reinforcer magnitude produced less variability than the smaller reinforcer magnitude. These results suggest that larger reinforcers hinder the reinforcement of behavioral variability. The results are interpretable in terms of the larger reinforcer inducing a greater level of behavioral repetition, particularly as the time to reinforcement was approached. This effect may have implications for reinforcing behavioral variability in humans.
C1 [Doughty, Adam H.; Giorno, Kenneth G.; Miller, Hannah L.] Coll Charleston, Charleston, SC 29424 USA.
RP Doughty, AH (reprint author), Coll Charleston, Dept Psychol, 57 Coming St, Charleston, SC 29424 USA.
EM doughtya@cofc.edu
FU SURF (Summer Undergraduate Research with Faculty) grant; Faculty
Research and Development grant; College of Charleston
FX Portions of this research were supported by a SURF (Summer Undergraduate
Research with Faculty) grant as well as a Faculty Research and
Development grant, both through the College of Charleston. The authors
thank several students for their contributions to this research,
particularly Nina Deese.
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NR 35
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-5002
EI 1938-3711
J9 J EXP ANAL BEHAV
JI J. Exp. Anal. Behav.
PD NOV
PY 2013
VL 100
IS 3
BP 355
EP 369
DI 10.1002/jeab.50
PG 15
WC Psychology, Biological; Behavioral Sciences; Psychology, Experimental
SC Psychology; Behavioral Sciences
GA 246AR
UT WOS:000326508500006
PM 24122484
ER
PT J
AU Delli, K
Reichart, PA
Bornstein, MM
Livas, C
AF Delli, Konstantina
Reichart, Peter A.
Bornstein, Michael M.
Livas, Christos
TI Management of children with autism spectrum disorder in the dental
setting: Concerns, behavioural approaches and recommendations
SO MEDICINA ORAL PATOLOGIA ORAL Y CIRUGIA BUCAL
LA English
DT Article
DE Autism spectrum disorder; dental management; children
ID ORAL-HEALTH STATUS; CARIES EXPERIENCE; CARE NEEDS; DENTISTRY; EDUCATION;
PARENTS; SCHOOLS
AB Objectives: This article reviews the present literature on the issues encountered while coping with children with autistic spectrum disorder from the dental perspective. The autistic patient profile and external factors affecting the oral health status of this patient population are discussed upon the existing body of evidence.
Material and Methods: The MEDLINE database was searched using the terms 'Autistic Disorder', 'Behaviour Control/methods', 'Child', 'Dental care for disabled', 'Education', 'Oral Health', and 'Pediatric Dentistry' to locate related articles published up to January 2013.
Results: Most of the relevant studies indicate poor oral hygiene whereas they are inconclusive regarding the caries incidence in autistic individuals. Undergraduate dental education appears to determine the competence of dental professionals to treat developmentally disabled children and account partly for compromised access to dental care. Dental management of an autistic child requires in-depth understanding of the background of the autism and available behavioural guidance theories. The dental professional should be flexible to modify the treatment approach according to the individual patient needs.
C1 [Delli, Konstantina] Univ Groningen, Univ Med Ctr Groningen, Dept Oral & Maxillofacial Surg, NL-9700 RB Groningen, Netherlands.
[Bornstein, Michael M.] Univ Bern, Sch Dent Med, Dept Oral Surg & Stomatol, CH-3012 Bern, Switzerland.
[Livas, Christos] Univ Groningen, Univ Med Ctr Groningen, Dept Orthodont, NL-9700 RB Groningen, Netherlands.
RP Livas, C (reprint author), Univ Groningen, Univ Med Ctr Groningen, Dept Orthodont, Hanzepl 1 Postbus 30-001, NL-9700 RB Groningen, Netherlands.
EM c.livas@umcg.nl
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NR 40
TC 0
Z9 0
PU MEDICINA ORAL S L
PI VALENCIA
PA CALLE DANIEL BALACIART N 4 PTA 17, VALENCIA, 46020, SPAIN
SN 1698-6946
J9 MED ORAL PATOL ORAL
JI Med. Oral Patol. Oral Cir. Bucal
PD NOV
PY 2013
VL 18
IS 6
BP E862
EP E868
AR 19084
DI 10.4317/medoral.19084
PG 7
WC Dentistry, Oral Surgery & Medicine
SC Dentistry, Oral Surgery & Medicine
GA 249QA
UT WOS:000326790500007
PM 23986012
ER
PT J
AU Bertelsen, B
Debes, NM
Hjermind, LE
Skov, L
Brondum-Nielsen, K
Tumer, Z
AF Bertelsen, Birgitte
Debes, Nanette Mol
Hjermind, Lena E.
Skov, Liselotte
Brondum-Nielsen, Karen
Tumer, Zeynep
TI Chromosomal rearrangements in Tourette syndrome: implications for
identification of candidate susceptibility genes and review of the
literature
SO NEUROGENETICS
LA English
DT Review
DE Chromosome rearrangement; Cytogenetics; Tourette syndrome
ID AUTISM SPECTRUM DISORDERS; COPY NUMBER VARIANTS; LA-TOURETTE;
TRANSLOCATION BREAKPOINT; LANGUAGE DISORDER; LINKAGE ANALYSIS; MENKES
DISEASE; MULTIPLE TICS; FAMILY; DISRUPTION
AB Tourette syndrome (TS) is a childhood-onset complex neurobiological disorder characterized by a combination of persistent motor and vocal tics and frequent presence of other neuropsychiatric comorbidities. TS shares the fate of other complex disorders, where the genetic etiology is largely unknown, and identification of susceptibility genes through linkage and association studies has been complicated due to inherent difficulties such as no clear mode of inheritance, genetic heterogeneity, and apparently incomplete penetrance. Positional cloning through mapping of disease-related chromosome rearrangements has been an efficient tool for the cloning of disease genes in several Mendelian disorders and in a number of complex disorders. Through cytogenetic investigation of 205 TS patients, we identified three possibly disease-associated chromosome rearrangements rendering this approach relevant in chasing TS susceptibility genes.
C1 [Bertelsen, Birgitte; Brondum-Nielsen, Karen; Tumer, Zeynep] Copenhagen Univ Hosp, Rigshosp, Kennedy Ctr, DK-2600 Glostrup, Denmark.
[Debes, Nanette Mol; Skov, Liselotte] Herlev Univ Hosp, Tourette Clin, Dept Pediat, DK-2730 Herlev, Denmark.
[Hjermind, Lena E.] Copenhagen Univ Hosp, Rigshosp, Dept Neurol, Memory Disorders Res Grp,Neurogenet Clin, Copenhagen, Denmark.
[Hjermind, Lena E.] Univ Copenhagen, Panum Inst, Dept Cellular & Mol Med, Neurogenet Sect, DK-2200 Copenhagen, Denmark.
RP Tumer, Z (reprint author), Copenhagen Univ Hosp, Rigshosp, Kennedy Ctr, DK-2600 Glostrup, Denmark.
EM zeynep.tumer@regionh.dk
FU The Lundbeck Foundation [R24-A219]; University of Copenhagen
FX The study is supported by The Lundbeck Foundation (R24-A219), and BB is
currently funded by a scholarship from the University of Copenhagen.
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NR 48
TC 1
Z9 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1364-6745
EI 1364-6753
J9 NEUROGENETICS
JI Neurogenetics
PD NOV
PY 2013
VL 14
IS 3-4
BP 197
EP 203
DI 10.1007/s10048-013-0372-y
PG 7
WC Genetics & Heredity; Clinical Neurology
SC Genetics & Heredity; Neurosciences & Neurology
GA 247SQ
UT WOS:000326641000005
PM 23989977
ER
PT J
AU Izquierdo, PG
Calahorro, F
Ruiz-Rubio, M
AF Izquierdo, Patricia G.
Calahorro, Fernando
Ruiz-Rubio, Manuel
TI Neuroligin modulates the locomotory dopaminergic and serotonergic
neuronal pathways of C. elegans
SO NEUROGENETICS
LA English
DT Article
DE Neuroligins; Dopamine; Serotonin; Methylphenidate; Fluoxetine;
Caenorhabditis elegans
ID CAENORHABDITIS-ELEGANS; DEFICIENT MUTANTS; AUTISM; TRANSPORTER; NLGN4;
GENE; METHYLPHENIDATE; DISORDERS; RECEPTOR; SYNAPSE
AB Neuroligins are neuronal and neuromuscular transmembrane proteins that have been implicated in autism spectrum disorder and other cognitive diseases. The nlg-1 gene from Caenorhabditis elegans is orthologous to human neuroligin genes. In the nematode, the locomotory rate is mediated by dopaminergic and serotonergic pathways, which result in two different behavioral responses known as basal slowing response (BSR) and enhanced slowing response (ESR), respectively. We report that nlg-1-deficient mutants are defective in both the BSR and ESR behaviors. In addition, we demonstrate that methylphenidate (a dopamine reuptake inhibitor) and fluoxetine (a serotonin reuptake inhibitor), two drugs widely used for the treatment of behavioral disorders in humans, are able to restore the BSR and ESR wild type phenotypes, respectively, in nlg-1 defective mutant nematodes. The abnormal locomotory behavior patterns were rescued in nlg-1-deficient mutant by expressing a cDNA from the human NLGN1 gene under the C. elegans nlg-1 promoter. However, human NLGN1 (R453C) and NLGN1 (D432X) mutant alleles did not rescue any of the two mutant phenotypes. The results indicate that neuroligin is involved in modulating the action of dopamine and serotonin in the nematode and suggest that the functional mechanism underpinning both methylphenidate and fluoxetine in C. elegans might be comparable to that in humans. The neuroligin-deficient mutants may undergo inefficient synaptic transmissions which could affect different traits in the nervous system. In particular, neuroligin might be required for normal neurotransmitters release. The understanding of the mechanisms by which methylphenidate and fluoxetine are able to restore the behavior of these mutants could help to explain the etiology of some human neurological diseases.
C1 [Izquierdo, Patricia G.; Calahorro, Fernando; Ruiz-Rubio, Manuel] Univ Cordoba, Dept Genet, E-14071 Cordoba, Spain.
[Izquierdo, Patricia G.; Calahorro, Fernando; Ruiz-Rubio, Manuel] Hosp Univ Reina Sofia, Cordoba, Spain.
[Izquierdo, Patricia G.; Calahorro, Fernando; Ruiz-Rubio, Manuel] Inst Maimonides Invest Biomed Cordoba IMIBIC, Cordoba, Spain.
RP Ruiz-Rubio, M (reprint author), Univ Cordoba, Dept Genet, E-14071 Cordoba, Spain.
EM ge1rurum@uco.es
FU Consejeria de Salud, Junta de Andalucia, Spain [PI0197]
FX We thank the Caenorhabditis Genetics Center, the Japanese National
Bioresource Project, Antonio Miranda-Vizuete, Julian Ceron, Thomas
Dresbach, Peter Askjaer, Juan Cabello, Noemi Cabrera-Poch, Rosina
Giordano, and Denis Dupuy for sharing worm strains and plasmids. We are
thankful to Jim Rand for the information about the C. elegans nlg-1
promoter, to Randy Blakely for the SWIP assay protocol, and to Antonio
Miranda-Vizuete and Elena P. Nadales for critical reading of the
manuscript. We also thank Justo P. Castano for giving us the opportunity
to use the microinjection station in his lab. Comments from Encarna
Alejandre and assistance from Isabel Caballero are sincerely
acknowledged. This work was supported by grant PI0197 from the
Consejeria de Salud, Junta de Andalucia, Spain.
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NR 30
TC 3
Z9 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1364-6745
EI 1364-6753
J9 NEUROGENETICS
JI Neurogenetics
PD NOV
PY 2013
VL 14
IS 3-4
BP 233
EP 242
DI 10.1007/s10048-013-0377-6
PG 10
WC Genetics & Heredity; Clinical Neurology
SC Genetics & Heredity; Neurosciences & Neurology
GA 247SQ
UT WOS:000326641000009
PM 24100941
ER
PT J
AU Weber, A
Kohler, A
Hahn, A
Neubauer, B
Muller, U
AF Weber, Axel
Koehler, Angelika
Hahn, Andreas
Neubauer, Bernd
Mueller, Ulrich
TI Benign infantile convulsions (IC) and subsequent paroxysmal kinesigenic
dyskinesia (PKD) in a patient with 16p11.2 microdeletion syndrome
SO NEUROGENETICS
LA English
DT Article
DE Paroxysmal kinesigenic dyskinesia; PKD; PKD/IC; Infantile convulsions;
16p11.2 deletion syndrome; THAPBS; THAP1; PRRT2
ID MUTATIONS; ORIGIN; PRRT2; GENE
AB Paroxysmal kinesigenic dyskinesia with infantile convulsions (PKD/IC) is caused by mutations in the gene PRRT2 located in 16p11.2. A deletion syndrome 16p11.2 is well established and is characterized by intellectual disability, speech delay, and autism. PKD/IC, however, is extremely rare in this syndrome. We describe a case of PKD/IC and 16p11.2 deletion syndrome and discuss modifiers of PRRT2 activity to explain the rare concurrence of both syndromes.
C1 [Weber, Axel; Koehler, Angelika; Mueller, Ulrich] Univ Giessen, Inst Humangenet, D-35390 Giessen, Germany.
[Hahn, Andreas; Neubauer, Bernd] Zentrum Kinderheilkunde & Jugendmed, Abt Neuropadiatrie Sozialpadiatrie & Epileptol, Giessen, Germany.
RP Weber, A (reprint author), Univ Giessen, Inst Humangenet, D-35390 Giessen, Germany.
EM axel.weber@humangenetik.med.uni-giessen.de;
ulrich.mueller@humangenetik.med.uni-giessen.de
CR Ballif BC, 2007, NAT GENET, V39, P1071, DOI 10.1038/ng2107
Bhatia KP, 2011, MOVEMENT DISORD, V26, P1157, DOI 10.1002/mds.23765
Chen WJ, 2011, NAT GENET, V43, P1252, DOI 10.1038/ng.1008
Dale RC, 2012, DEV MED CHILD NEUROL, V54, P618, DOI 10.1111/j.1469-8749.2012.04287.x
Dale RC, 2011, NEUROLOGY, V77, P1401, DOI 10.1212/WNL.0b013e31823152d7
Gavarini S, 2010, ANN NEUROL, V68, P456
Glaser RL, 2006, NUCLEIC ACIDS RES, V34, pD29, DOI 10.1093/nar/gkj101
Kaiser FJ, 2010, ANN NEUROL, V68, P462
Lee HY, 2012, CELL REP, V1, P2, DOI 10.1016/j.celrep.2011.11.001
Lipton J, 2009, NEUROLOGY, V73, P479, DOI 10.1212/WNL.0b013e3181b16393
Morison IM, 1998, HUM MOL GENET, V7, P1599, DOI 10.1093/hmg/7.10.1599
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Wang Jun-Ling, 2011, Brain, V134, P3493, DOI 10.1093/brain/awr289
NR 13
TC 1
Z9 2
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1364-6745
EI 1364-6753
J9 NEUROGENETICS
JI Neurogenetics
PD NOV
PY 2013
VL 14
IS 3-4
BP 251
EP 253
DI 10.1007/s10048-013-0376-7
PG 3
WC Genetics & Heredity; Clinical Neurology
SC Genetics & Heredity; Neurosciences & Neurology
GA 247SQ
UT WOS:000326641000012
PM 24100940
ER
PT J
AU Benros, ME
Laursen, TM
Dalton, SO
Nordentoft, M
Mortensen, PB
AF Benros, Michael Eriksen
Laursen, Thomas Munk
Dalton, Susanne Oksbjerg
Nordentoft, Merete
Mortensen, Preben Bo
TI The Risk of Schizophrenia and Child Psychiatric Disorders in Offspring
of Mothers with Lung Cancer and Other Types of Cancer: A Danish
Nationwide Register Study
SO PLOS ONE
LA English
DT Article
ID NERVOUS-SYSTEM; HU ANTIBODIES; AUTOANTIBODIES; PREGNANCY; PSYCHOSIS;
DISEASES; PARENTS; AUTISM; HYPERACTIVITY; INFECTIONS
AB Background: Maternal immune responses and brain-reactive antibodies have been proposed as possible causal mechanisms for schizophrenia and some child psychiatric disorders. According to this hypothesis maternal antibodies may cross the placenta and interact with the developing CNS of the fetus causing future neurodevelopmental disorders. Therefore, we investigated if children of mothers with cancer might be at higher risk of developing psychiatric disorders, with particular focus on small-cell lung cancer, which is known to induce production of antibodies binding to CNS elements.
Methods: Nationwide population-based registers were linked, including the Danish Psychiatric Central Register and The Danish Cancer Registry. Data were analyzed as a cohort study using survival analysis techniques. Incidence rate ratios (IRRs) and accompanying 95% confidence intervals (CIs) were used as measures of relative risk.
Results: In general, parental cancer was not associated with schizophrenia in the offspring (IRR, 0.98; 95% CI, 0.95-1.01). Furthermore, we found no temporal associations with maternal cancer in general; neither around the pregnancy period. However, maternal small-cell lung cancer increased the risk of early-onset schizophrenia and maternal small-cell lung cancer diagnosed within 20 years after childbirth increased the risk of schizophrenia. Parental cancer was not associated with child psychiatric disorders (IRR, 1.01; 95% CI, 0.98-1.05) except for the smoking related cancers. There was a significantly increased risk of child psychiatric disorders in offspring of both mothers (IRR, 1.35; 95% CI, 1.16-1.58) and fathers (IRR, 1.47; 95% CI, 1.30-1.66) with lung cancer of all types.
Conclusions: In general, parental cancer did not increase the risk of schizophrenia nor of child psychiatric disorders. However, maternal small-cell lung cancer increased the risk of schizophrenia in subgroups; and lung cancer in general increased the risk of child psychiatric disorders, which could be due to risk factors associated with parental smoking.
C1 [Benros, Michael Eriksen; Laursen, Thomas Munk; Mortensen, Preben Bo] Aarhus Univ, Natl Ctr Register Based Res, Aarhus, Denmark.
[Benros, Michael Eriksen; Nordentoft, Merete] Univ Copenhagen, Fac Hlth Sci, Mental Hlth Ctr Copenhagen, Copenhagen, Denmark.
[Benros, Michael Eriksen; Laursen, Thomas Munk; Nordentoft, Merete; Mortensen, Preben Bo] Lundbeck Fdn Initiat Integrat Psychiat Res, iPSYCH, Aarhus, Denmark.
[Dalton, Susanne Oksbjerg] Danish Canc Soc, Inst Canc Epidemiol, Copenhagen, Denmark.
RP Benros, ME (reprint author), Aarhus Univ, Natl Ctr Register Based Res, Aarhus, Denmark.
EM Benros@ncrr.dk
FU Stanley Medical Research Institute; ERC [294838]; Lundbeck Foundation
Initiative for Integrative Psychiatric Research, iPSYCH
FX The study was supported financially by a grant from the Stanley Medical
Research Institute, ERC Advanced Grant Project no. 294838 and the
Lundbeck Foundation Initiative for Integrative Psychiatric Research,
iPSYCH. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
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NR 56
TC 0
Z9 0
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 1
PY 2013
VL 8
IS 11
DI 10.1371/journal.pone.0079031
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 245XZ
UT WOS:000326499300048
PM 24223877
ER
PT J
AU Hiller, R
Pellicano, L
AF Hiller, Rachel
Pellicano, Liz
TI Anorexia and autism - a cautionary note
SO PSYCHOLOGIST
LA English
DT Letter
C1 [Hiller, Rachel] Flinders Univ S Australia, Adelaide, SA, Australia.
RP Hiller, R (reprint author), Flinders Univ S Australia, Adelaide, SA, Australia.
CR Baron-Cohen S, 2013, MOL AUTISM, V4, DOI 10.1186/2040-2392-4-24
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Wade TD, 2011, EUR EAT DISORD REV, V19, P382, DOI 10.1002/erv.1078
NR 5
TC 0
Z9 0
PU BRITISH PSYCHOLOGICAL SOC
PI LEICESTER
PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND
SN 0952-8229
J9 PSYCHOLOGIST
JI Psychologist
PD NOV
PY 2013
VL 26
IS 11
BP 780
EP 780
PG 1
WC Psychology, Multidisciplinary
SC Psychology
GA 245UD
UT WOS:000326488400003
ER
PT J
AU Singh, GK
Yu, SM
Kogan, MD
AF Singh, Gopal K.
Yu, Stella M.
Kogan, Michael D.
TI Health, Chronic Conditions, and Behavioral Risk Disparities Among US
Immigrant Children and Adolescents
SO PUBLIC HEALTH REPORTS
LA English
DT Article
ID CAUSE-SPECIFIC MORTALITY; UNITED-STATES; OVERWEIGHT PREVALENCE;
ETHNIC-IMMIGRANT; NONCOVERAGE BIAS; OBESITY; ACCULTURATION;
ASSOCIATIONS; BORN; DETERMINANTS
AB Objective. We examined differentials in the prevalence of 23 parent-reported health, chronic condition, and behavioral indicators among 91,532 children of immigrant and U.S.-born parents.
Methods. We used the 2007 National Survey of Children's Health to estimate health differentials among 10 ethnic-nativity groups. Logistic regression yielded adjusted differentials.
Results. Immigrant children in each racial/ethnic group had a lower prevalence of depression and behavioral problems than native-born children. The prevalence of autism varied from 0.3% among immigrant Asian children to 1.3%-1.4% among native-born non-Hispanic white and Hispanic children. Immigrant children had a lower prevalence of asthma, attention deficit disorder/attention deficit hyperactivity disorder; developmental delay; learning disability; speech, hearing, and sleep problems; school absence; and chronic condition than native-born children, with health risks increasing markedly in relation to mother's duration of residence in the U.S. Immigrant children had a substantially lower exposure to environmental tobacco smoke, with the odds of exposure being 60%-95% lower among immigrant non-Hispanic black, Asian, and Hispanic children compared with native non-Hispanic white children. Obesity prevalence ranged from 7.7% for native-born Asian children to 24.9%-25.1% for immigrant Hispanic and native-born non-Hispanic black children. Immigrant children had higher physical inactivity levels than native-horn children; however, inactivity rates declined with each successive generation of immigrants. Immigrant Hispanic children were at increased risk of obesity and sedentary behaviors. Ethnic-nativity differentials in health and behavioral indicators remained marked after covariate adjustment.
Conclusions. Immigrant patterns in child health and health-risk behaviors vary substantially by ethnicity, generational status, and length of time since immigration. Public health programs must target at-risk children of both immigrant and U.S.-born parents.
C1 [Singh, Gopal K.; Yu, Stella M.; Kogan, Michael D.] US Hlth Resources & Serv Adm, US Dept HHS, Maternal & Child Hlth Bur, Rockville, MD 20857 USA.
RP Singh, GK (reprint author), US Hlth Resources & Serv Adm, US Dept HHS, Maternal & Child Hlth Bur, 5600 Fishers Ln,Room 18-41, Rockville, MD 20857 USA.
EM gsingh@hrsa.gov
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NR 46
TC 3
Z9 3
PU ASSOC SCHOOLS PUBLIC HEALTH
PI WASHINGTON
PA 1900 M ST NW, STE 710, WASHINGTON, DC 20036 USA
SN 0033-3549
J9 PUBLIC HEALTH REP
JI Public Health Rep.
PD NOV-DEC
PY 2013
VL 128
IS 6
BP 463
EP 479
PG 17
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 247IP
UT WOS:000326611400006
PM 24179258
ER
PT J
AU Horovitz, M
Matson, JL
AF Horovitz, Max
Matson, Johnny L.
TI The Baby and Infant Screen for Children with aUtIsm Traits-Part 3: The
development of age-based scoring procedures
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE BISCUIT; Autism; ASD; Challenging behaviors; Cutoffs; Psychometric
properties
ID SELF-INJURIOUS-BEHAVIOR; SPECTRUM DISORDERS; YOUNG-CHILDREN; CHALLENGING
BEHAVIORS; INTELLECTUAL DISABILITY; PDD-NOS; MENTAL-RETARDATION; EARLY
INTERVENTION; COMMUNICATION DEVELOPMENT; FUNCTIONAL-ANALYSIS
AB The objective of the current study was to develop age-based scoring procedures for the BISCUIT-Part 3, an assessment measure of challenging behaviors in infants and toddlers aged 17-37 months. Separate age-based cutoffs were developed for those with an autism spectrum disorder (ASD) and those with non-ASD related developmental delays, using the standard deviation from the mean method. The sample consisted of 3022 infants and toddlers and their parents. As age increased in those with ASD, higher cutoff scores were required. Less variation was seen in the cutoff scores established for those with non-ASD related delays. The findings suggest that as children with ASD grow older, challenging behaviors become more frequent and severe. Additionally, they become easier to detect in comparison to same-aged peers. The implications of these results are discussed. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Horovitz, Max; Matson, Johnny L.] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Matson, JL (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM johnmatson@aol.com
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NR 87
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1291
EP 1299
DI 10.1016/j.rasd.2013.07.019
PG 9
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500001
ER
PT J
AU Hay-Hansson, AW
Eldevik, S
AF Hay-Hansson, Aina W.
Eldevik, Sigmund
TI Training discrete trials teaching skills using videoconference
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Discrete trials teaching; Videoconference; Staff training; Autism
ID INTENSIVE BEHAVIORAL TREATMENT; FUNCTIONAL-ANALYSIS;
DEVELOPMENTAL-DISABILITIES; SELF-INJURY; AUTISM; ASSESSMENTS; CHILDREN;
INTERVENTION; TELEMEDICINE; STUDENTS
AB This study investigated the effect of videoconferencing in training staff to implement discrete trial teaching in real life settings with children with autism. Fourteen participants were randomly assigned to two groups. One group received training on-site and the other group received training via videoconference. The participants in both groups received 3x 15 min of training on three different teaching programs: matching, receptive and expressive labeling. The results showed no significant differences between the groups in the post-test whilst both groups improved significantly following training. Although preliminary, these results suggest that videoconferencing can be a cost-saving way to train staff in how to implement discrete trial teaching. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
C1 [Hay-Hansson, Aina W.] Vestre Viken Hosp Trust, Drammen Hosp, Ctr Habilitat Rehabil, N-3019 Drammen, Norway.
[Eldevik, Sigmund] Oslo & Akershus Univ Coll Appl Sci, NO-0130 Oslo, Norway.
RP Hay-Hansson, AW (reprint author), Vestre Viken Hosp Trust, Drammen Hosp, Ctr Habilitat Rehabil, Konggata 51, N-3019 Drammen, Norway.
EM ainahay@gmail.com
CR Allen KD, 2000, J APPL BEHAV ANAL, V33, P373, DOI 10.1901/jaba.2000.33-373
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NR 35
TC 2
Z9 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1300
EP 1309
DI 10.1016/j.rasd.2013.07.022
PG 10
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500002
ER
PT J
AU Weiss, JA
Robinson, S
Fung, S
Tint, A
Chalmers, P
Lunsky, Y
AF Weiss, Jonathan A.
Robinson, Suzanne
Fung, Stephanie
Tint, Ami
Chalmers, Philip
Lunsky, Yona
TI Family hardiness, social support, and self-efficacy in mothers of
individuals with Autism Spectrum Disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Family hardiness; Mothers; Social support; Self-efficacy; Autism
Spectrum Disorders; Stress
ID FRAGILE-X-SYNDROME; DOUBLE ABCX MODEL; DEVELOPMENTAL-DISABILITIES;
INTELLECTUAL DISABILITIES; MENTAL-HEALTH; BEHAVIOR PROBLEMS;
DOWN-SYNDROME; POSITIVE PSYCHOLOGY; CHILDREN; STRESS
AB Family hardiness is an important construct to understand coping in parents of individuals with Autism Spectrum Disorders (ASD), who are often at risk for considerable distress in the face of multiple stressors. The current study examined family hardiness, perceived social support and parent self-efficacy as predictors of family distress in 138 mothers of individuals with ASD, 4-41 years of age. Using a multiple mediation analysis, we demonstrated that perceived self-efficacy and social support mediated the link between the pile-up of stressors and family hardiness, and that hardiness was a partial mediator in explaining how stressors were associated with family distress. Researchers and clinicians should consider the role that perceived social support and parent self-efficacy play in explaining family hardiness, and how the perception of such hardiness is associated with less distress. (C) 2013 The Authors. Published by Elsevier Ltd. All rights reserved.
C1 [Weiss, Jonathan A.; Robinson, Suzanne; Fung, Stephanie; Tint, Ami; Chalmers, Philip] York Univ, Dept Psychol, N York, ON M3J 1P3, Canada.
[Lunsky, Yona] Ctr Addict & Mental Hlth, Dual Diag Program, Toronto, ON, Canada.
RP Weiss, JA (reprint author), York Univ, Dept Psychol, 4700 Keele St, N York, ON M3J 1P3, Canada.
EM jonweiss@yorku.ca
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NR 64
TC 4
Z9 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1310
EP 1317
DI 10.1016/j.rasd.2013.07.016
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500003
ER
PT J
AU Matson, JL
Cervantes, PE
AF Matson, Johnny L.
Cervantes, Paige E.
TI Comorbidity among persons with intellectual disabilities
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Review
DE Comorbid; Intellectual disabilities; Challenging behaviors; Health
problems; Psychopathology
ID AUTISM SPECTRUM DISORDERS; SEVERE RETARDATION MESSIER; PROFOUND
MENTAL-RETARDATION; SELF-INJURIOUS-BEHAVIOR; II DASH-II; SOCIAL-SKILLS;
MATSON EVALUATION; DIAGNOSTIC-ASSESSMENT; INDIVIDUALS; ADULTS
AB Within the last three decades, the study of conditions that co-occur with intellectual disabilities has flourished. The present paper provides an analysis of the content of 405 papers that were reviewed on the topic. From these papers, trends emerged. The papers fell into one of three broad categories; comorbid psychopathology, comorbid medical problems, and comorbid challenging behaviors. Also, the volume of studies has been increasing rapidly. Implications of these and related issues are discussed. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Matson, Johnny L.; Cervantes, Paige E.] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Cervantes, PE (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM pcerva2@tigers.lsu.edu
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NR 35
TC 6
Z9 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1318
EP 1322
DI 10.1016/j.rasd.2013.07.018
PG 5
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500004
ER
PT J
AU Hesse, TL
Danko, CM
Budd, KS
AF Hesse, Tessa L.
Danko, Christina M.
Budd, Karen S.
TI Siblings of children with autism: Predictors of adjustment
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Adjustment; Siblings; Autism spectrum disorder; Parents; Sibling
adjustment; Parent satisfaction
ID MATERNAL SELF-EFFICACY; BEHAVIORAL INTERVENTION; DIFFICULTIES
QUESTIONNAIRE; SPECTRUM DISORDERS; PARENTING STRESS; SATISFACTION;
MOTHERS; STRATEGIES; STRENGTHS; PROGRAMS
AB As the prevalence of autism increases, so does the need to examine the effects of autism on family members of children with autism. The current study evaluated possible predictors of adjustment in siblings of children with autism. Aspects of the parents' functioning as caregivers for a child with autism were examined to determine whether they predicted the adjustment of the child's sibling. Two hundred caregivers of 4-10-year-old children with autism who had at least one sibling without autism participated by filling out questionnaires online. Parental satisfaction with the role of caregiver for the child with autism was negatively correlated with difficulties in sibling adjustment, and it was the only significant predictor of sibling adjustment in a hierarchical regression analysis. Parental stress and parental self-efficacy were not unique contributors to sibling adjustment when other parental variables were considered. No significant relationship was found between parental therapy involvement and sibling adjustment, or between parental educational involvement and sibling adjustment. The lack of parental involvement as a predictor of sibling adjustment adds new findings to the current literature, which had found such a relationship in a previous study with a smaller sample. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Hesse, Tessa L.] Univ Calif Davis, Dept Human Ecol, Davis, CA 95616 USA.
[Danko, Christina M.; Budd, Karen S.] Depaul Univ, Dept Psychol, Chicago, IL 60614 USA.
RP Hesse, TL (reprint author), Univ Calif Davis, Dept Human Ecol, 1 Shields Ave, Davis, CA 95616 USA.
EM thesse@ucdavis.edu
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NR 30
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1323
EP 1331
DI 10.1016/j.rasd.2013.07.024
PG 9
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500005
ER
PT J
AU Akoury-Dirani, L
Alameddine, M
Salamoun, M
AF Akoury-Dirani, Leyla
Alameddine, Maysam
Salamoun, Mariana
TI Validation of the Lebanese Childhood Autism Rating Scale - Second
Edition - High Functioning Version
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE CARS2; Validation; High Functioning Autism; Lebanon
ID SPECTRUM DISORDERS; ASPERGERS-DISORDER; CRITERIA; DSM-5; CHILDREN
AB This paper presents the psychometric properties of the Lebanese version of the Childhood Autism Rating Scale Second Edition, High Functioning Version (CARS2-HF). The participants consisted of 30 children aged 6-18 years among which 24 had a clinical diagnosis of Asperger disorder or Pervasive Developmental Disorder-Not Otherwise Specified and 6 had a clinical diagnosis of Attention Deficit Hyperactivity Disorder (ADHD). All participants were verbally fluent and had IQ estimates of 80 or higher, determined with the Wechsler Nonverbal Scale of Ability (WNV). Forward and backward translation of the CARS2-HF and the Childhood Autism Rating Scale Second Edition, Questionnaire for Parents or Caregivers (CARS2-QPC) was completed before the administration of the scales. The results of this study showed that the Lebanese CARS2-HF has a high degree of internal consistency (.92), inter-rater reliability (.97), and test-retest reliability (.99). Receiver Operating Characteristic (ROC) analysis determined that individuals with total raw scores below 26 are less likely - to be in the autism spectrum. This instrument can be used in screening and assessing for ASD in high-functioning Lebanese and Arab speaking individuals. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Akoury-Dirani, Leyla; Alameddine, Maysam; Salamoun, Mariana] Amer Univ Beirut, Dept Psychiat, Beirut 11072020, Lebanon.
RP Akoury-Dirani, L (reprint author), Amer Univ Beirut, Dept Psychiat, Mail Box Riad El Solh, Beirut 11072020, Lebanon.
EM l55@aub.edu.lb; mma72@aub.edu.lb; mariana.salamoun@gmail.com
CR Akoury-Dirani L, 2013, EARLY CHILD DEV CARE, DOI [10.1080/03004430.2013.772992, DOI 10.1080/03004430.2013.772992]
Akoury-Dirani L, 2013, RES AUTISM SPECT DIS, V7, P1097, DOI 10.1016/j.rasd.2013.05.004
Alameddine M., 2013, INT J ED PSYCHOL ASS, V13, P64
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World Health Organization, 2010, WHO AIMS REP MENT HL
World Health Organization, 2010, ICD 10 INT STAT CLAS
NR 30
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1332
EP 1338
DI 10.1016/j.rasd.2013.08.001
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500006
ER
PT J
AU Konst, MJ
Matson, JL
Turygin, N
AF Konst, Matthew J.
Matson, Johnny L.
Turygin, Nicole
TI Comparing the rates of tantrum behavior in children with ASD and ADHD as
well as children with comorbid ASD and ADHD diagnoses
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorders; Tantrum behavior; Autism Spectrum
Disorders-Comorbidity for Children (ASD-CC); Comorbidity
ID AUTISM SPECTRUM DISORDERS; PERVASIVE DEVELOPMENTAL DISORDERS;
CHALLENGING BEHAVIORS; INTELLECTUAL DISABILITY; DIFFERENTIAL-DIAGNOSIS;
PSYCHIATRIC-DISORDERS; FUNCTIONAL ASSESSMENT; TRAITS BISCUIT;
SOCIAL-SKILLS; INFANT SCREEN
AB The current study investigated the presentation of tantrum behaviors in individuals with an autism spectrum disorder (ASD) diagnosis with and without a comorbid diagnosis of attention deficit hyperactivity disorder (ADHD). Participants included 347 children ranging in age from 2 to 18 years old. Diagnostic categories in the current study were based upon clinical diagnosis. The severity of ASD symptomology was measured by the Autism Spectrum Disorder-Diagnostic Child Version (ASD-DC). The presence and severity of tantrum behaviors were measured by the Tantrum behavior subscale of the Autism Spectrum Disorders-Comorbidity for Children (ASD-CC). The influence of diagnosis and ASD symptomology had upon the expression of tantrum behaviors were examined, controlling for participant age. Initial analysis revealed significant differences in the expression of tantrum behavior between the ASD, ADHD and ASD/ADHD groups. However, age did not have a significant influence on the exhibition of tantrum behaviors. Follow-up analyses demonstrated that those individuals diagnosed with an ASD and a comorbid ADHD diagnosis exhibited significantly greater tantrum behavior. Post hoc analyses identified a significant positive correlation between increases in ASD symptomology and elevations of the severity of tantrum behaviors for each group. The observed correlation for the ADHD group was found to be significantly greater than the ASD group. Correlations for individual item responses of the ASD-CC were also computed and discussed for each diagnostic group. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Konst, Matthew J.; Matson, Johnny L.; Turygin, Nicole] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Konst, MJ (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM mkonst1@tigers.lsu.edu
CR American Psychiatric Association, 2013, DIAGNOSTIC AND STATI
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NR 60
TC 4
Z9 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1339
EP 1345
DI 10.1016/j.rasd.2013.07.023
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500007
ER
PT J
AU Alexander, JL
Ayres, KM
Smith, KA
Shepley, SB
Mataras, TK
AF Alexander, Jennifer L.
Ayres, Kevin M.
Smith, Katie A.
Shepley, Sally B.
Mataras, Theologia K.
TI Using video modeling on an iPad to teach generalized matching on a
sorting mail task to adolescents with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Generalized matching; Technology; Video modeling; Vocational
skills
ID MODERATE INTELLECTUAL DISABILITIES; CHILDREN; INDIVIDUALS; INSTRUCTION;
STUDENTS; SELF; INTERVENTION; BEHAVIOR; SKILLS; DISCRIMINATION
AB Two multiple probe designs across three and four participants evaluated the effects of video modeling to teach a matching response (sorting mail) to seven adolescents with autism. Participants were instructed on one set of responses (five mail pieces) using video modeling, while concurrently monitoring two other sets for generalization effects. Results indicated that three participants learned their target set and generalized to the untrained sets, and two participants required an error correction procedure to achieve or approach mastery on their target set. Two participants did not acquire target sets with video based instruction. Data on setting generalization and maintenance are also provided for the participants who reached mastery. Participant variables that may relate to responding, limitations to the study, and directions for future research on video based instruction are discussed. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Alexander, Jennifer L.; Ayres, Kevin M.; Smith, Katie A.; Shepley, Sally B.; Mataras, Theologia K.] Univ Georgia, Athens, GA 30606 USA.
RP Alexander, JL (reprint author), Univ Georgia, 516 Aderhold Hall, Athens, GA 30606 USA.
EM jenlenz@uga.edu
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Wolery M., 1990, EFFICIENCY INSTRUCTI
NR 42
TC 3
Z9 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1346
EP 1357
DI 10.1016/j.rasd.2013.07.021
PG 12
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500008
ER
PT J
AU Vasa, RA
Kalb, L
Mazurek, M
Kanne, S
Freedman, B
Keefer, A
Clemons, T
Murray, D
AF Vasa, Roma A.
Kalb, Luther
Mazurek, Micah
Kanne, Stephen
Freedman, Brian
Keefer, Amy
Clemons, Traci
Murray, Donna
TI Age-related differences in the prevalence and correlates of anxiety in
youth with autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Anxiety; Prevalence; Correlate; Age group
ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILD-BEHAVIOR CHECKLIST;
HIGH-FUNCTIONING AUTISM; PROSPECTIVE-LONGITUDINAL COMMUNITY; SENSORY
OVER-RESPONSIVITY; ASPERGER-SYNDROME; INTELLECTUAL DISABILITIES;
PSYCHIATRIC-DISORDERS; ADOLESCENTS; SYMPTOMS
AB Age-related differences in the prevalence and correlates of anxiety were cross-sectionally examined in 1316 children and adolescents with autism spectrum disorder (ASD) who presented for initial evaluation at 14 outpatient autism centers around the country and in Canada. The prevalence of clinical and subclinical anxiety as well as the correlates of anxiety were examined in three age groups of children: preschool, school age and adolescents. Findings showed that the prevalence of anxiety in each age group exceeded the prevalence of anxiety in the general population. Adolescents and school age children had the highest prevalence of clinical (40%) and subclinical anxiety (26%), respectively. Higher IQ and less ASD severity were each weakly correlated with more anxiety in preschool and school age children. Affective symptoms were strongly associated with anxiety in each age group. Age specific psychiatric comorbidities were also present. Anxiety was associated with attention deficit hyperactivity disorder (ADHD) and oppositional defiant disorder (ODD) symptoms in the preschool group, ODD and somatic symptoms in the school age children, and ADHD symptoms in adolescents. These data underscore the need for prevention and treatment of anxiety as well as research examining the characteristics of anxiety in children with ASD using a developmental framework. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Vasa, Roma A.] Johns Hopkins Univ, Sch Med, Ctr Autism & Related Disorders, Kennedy Krieger Inst,Dept Psychiat, Baltimore, MD 21211 USA.
[Kalb, Luther; Keefer, Amy] Ctr Autism & Related Disorders, Kennedy Krieger Inst, Baltimore, MD 21211 USA.
[Mazurek, Micah; Kanne, Stephen] Univ Missouri, Thompson Ctr Autism & Neurodev Disorders, Dept Hlth Psychol, Columbia, MO 65201 USA.
[Freedman, Brian] Univ Delaware, Ctr Disabil Studies, Newark, DE 19716 USA.
[Clemons, Traci] EMMES Corp, Rockville, MD 20850 USA.
[Murray, Donna] Univ Cincinnati, Coll Med, Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
RP Vasa, RA (reprint author), Johns Hopkins Univ, Sch Med, Ctr Autism & Related Disorders, Kennedy Krieger Inst,Dept Psychiat, 3901 Greenspring Ave, Baltimore, MD 21211 USA.
EM vasa@kennedykrieger.org; kalb@kennedykrieger.org; mazurekm@missouri.edu;
kannest@health.missouri.edu; brianf@udel.edu; keefer@kennedykrieger.org;
tclemons@emmes.com; donna.murray@cchmc.org
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NR 96
TC 6
Z9 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1358
EP 1369
DI 10.1016/j.rasd.2013.07.005
PG 12
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500009
ER
PT J
AU Kornacki, LT
Ringdahl, JE
Sjostrom, A
Nuernberger, JE
AF Kornacki, Lisa T.
Ringdahl, Joel E.
Sjostrom, Anna
Nuernberger, Jodi E.
TI A component analysis of a behavioral skills training package used to
teach conversation skills to young adults with autism spectrum and other
developmental disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Social skills; Conversation; Behavioral skills training; Task
analysis
ID DISABILITIES; MODEL
AB We conducted a component analysis of a behavioral skills training (BST) package to teach conversation skills to young adults with autism and/or developmental disorders. Performance following each component of the package was compared to a task analysis that included both vocal and non-vocal conversation skills, such as making comments related to the conversation topic, maintaining eye contact, maintaining and appropriate distance from the conversation partner. The components of the BST package included instructions, modeling of an appropriate conversation, rehearsal, rehearsal with feedback, in situ training with feedback provided to the participants in a private training room, and in situ training with feedback plus reinforcement. Results suggested unique components were correlated with acquisition of the conversation skills across participants. Results are presented as they relate to effective components of BST and implications for providing BST to individuals in clinical contexts. (C) 2013 Published by Elsevier Ltd.
C1 [Kornacki, Lisa T.; Ringdahl, Joel E.; Sjostrom, Anna; Nuernberger, Jodi E.] So Illinois Univ, Carbondale, IL 62901 USA.
RP Ringdahl, JE (reprint author), So Illinois Univ, Inst Rehabil, 1025 Lincoln Dr Rehn Hall, Carbondale, IL 62901 USA.
EM joelringdahl@siu.edu
CR American Psychiatric Association, 2000, DIAGNOSTIC AND STATI
Cooper J. O., 2007, APPLIED BEHAVIOR ANA, V2nd
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NR 13
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1370
EP 1376
DI 10.1016/j.rasd.2013.07.012
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500010
ER
PT J
AU Tureck, K
Matson, JL
Turygin, N
Macmillan, K
AF Tureck, Kim
Matson, Johnny L.
Turygin, Nicole
Macmillan, Katie
TI Rates of psychotropic medication use in children with ASD compared to
presence and severity of problem behaviors
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Psychotropic medication; Autism spectrum disorder; Externalizing
behaviors; Autism Spectrum Disorders - Behavior; Problem Child (ASD-BPC)
ID AUTISM-SPECTRUM DISORDERS; PERVASIVE DEVELOPMENTAL DISORDER;
SOCIAL-SKILLS; ADULTS; PSYCHOPATHOLOGY; SYMPTOMS; DISABILITIES;
ADOLESCENTS; RELIABILITY; MANAGEMENT
AB There is a scarcity of research on the relationship between presence of problem behaviors and psychotropic medication use in children with autism spectrum disorder (ASD). Participants in the current study were children and adolescents ages 3-17 years who were sorted into four groups: ASD on psychotropic medication (N = 100), ASD not on psychotropic medication (N = 147), typically developing on medication (N = 48), and typically developing not on medication (N = 168). A one-way multivariate analysis of covariance (MANCOVA) was conducted to determine the relationship between medication use and rates of internalizing and externalizing behaviors. Post hoc analyses revealed that children with ASD on psychotropic medication evinced significantly more externalizing behaviors than children with ASD not on medication. However, the two groups did not significantly differ on rates of internalizing behaviors. These results suggest that psychotropic medications may often be prescribed to manage externalizing behaviors. Implications of these findings are discussed in relation to the existing literature. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Tureck, Kim; Matson, Johnny L.; Turygin, Nicole; Macmillan, Katie] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Tureck, K (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM kturec1@lsu.edu
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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World Health Organization, 1992, INT CLASS DIS
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NR 52
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1377
EP 1382
DI 10.1016/j.rasd.2013.08.003
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500011
ER
PT J
AU MacDonald, M
Lord, C
Ulrich, D
AF MacDonald, Megan
Lord, Catherine
Ulrich, Dale
TI The relationship of motor skills and adaptive behavior skills in young
children with autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Motor skills; Young children; Adaptive behavior
ID DIAGNOSTIC OBSERVATION SCHEDULE; INFANTS; INTERVENTIONS; TODDLERS
AB Objective: To determine the relationship of motor skills and adaptive behavior skills in young children with autism.
Design: A multiple regression analysis tested the relationship of motor skills on the adaptive behavior composite, daily living, adaptive social and adaptive communicative skills holding constant age, non-verbal problem solving, and calibrated autism severity.
Setting: Majority of the data collected took place in an autism clinic.
Participants: A cohort of 233 young children with ASD (n = 172), PDD-NOS (n = 22) and non-ASD (developmental delay, n = 39) between the ages of 14-49 months were recruited from early intervention studies and clinical referrals. Children with non-ASD (developmental delay) were included in this study to provide a range of scores indicted through calibrated autism severity.
Interventions: Not applicable.
Main outcome measures: The primary outcome measures in this study were adaptive behavior skills.
Results: Fine motor skills significantly predicted all adaptive behavior skills (p <0.01). Gross motor skills were predictive of daily living skills (p <0.05). Children with weaker motor skills displayed greater deficits in adaptive behavior skills.
Conclusions: The fine and gross motor skills are significantly related to adaptive behavior skills in young children with autism spectrum disorder. There is more to focus on and new avenues to explore in the realm of discovering how to implement early intervention and rehabilitation for young children with autism and motor skills need to be a part of the discussion. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [MacDonald, Megan] Oregon State Univ, Sch Biol & Populat Hlth Sci, Corvallis, OR 97331 USA.
[Lord, Catherine] New York Presbyterian Hosp, Weill Cornell Med Coll, Ctr Autism & Dev Brain, White Plains, NY 10605 USA.
[Ulrich, Dale] Univ Michigan, Sch Kinesiol, Ann Arbor, MI 48109 USA.
RP MacDonald, M (reprint author), Oregon State Univ, Sch Biol & Populat Hlth Sci, 202 Womens Bldg, Corvallis, OR 97331 USA.
EM megan.macdonald@oregonstate.edu
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American Psychological Association (APA), 1994, DIAGN STAT MAN MENT
APA, 2013, DIAGNOSTIC AND STATI
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National Research Council (NRC), 2001, EDUCATING CHILDREN W
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Staples KL, 2012, INT REV RES DEV DISA, V42, P179, DOI 10.1016/B978-0-12-394284-5.00007-3
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Ulrich D., 2013, ADAPTED PHYSICAL ACT
Vernazza-Martin S, 2005, J AUTISM DEV DISORD, V35, P91, DOI 10.1007/s10803-004-1037-3
Wong VCN, 2010, J AUTISM DEV DISORD, V40, P677, DOI 10.1007/s10803-009-0916-z
Yirmiya N, 2007, J AUTISM DEV DISORD, V37, P1, DOI 10.1007/s10803-006-0329-1
NR 52
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1383
EP 1390
DI 10.1016/j.rasd.2013.07.020
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500012
ER
PT J
AU Nordahl-Hansen, A
Kaale, A
Ulvund, SE
AF Nordahl-Hansen, Anders
Kaale, Anett
Ulvund, Stein Erik
TI Inter-rater reliability of parent and preschool teacher ratings of
language in children with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Language; Autism; Inter-rater reliability; MacArthur CDI; Parents;
Preschool teachers
ID COMMUNICATIVE DEVELOPMENT INVENTORIES; SPECTRUM DISORDERS;
PREDICTIVE-VALIDITY; VOCABULARY SPURT; YOUNG-CHILDREN; COMPREHENSION;
ACQUISITION; ABILITY; CDI
AB Parent reports such as MacArthur-Bates Communicative Development Inventories (CDIs) have been suggested as a measure of language in young children with autism since this group often score below base levels of direct tests. However, questions have been raised concerning the reliability of report-based assessments. Parents and preschool teachers filled out the CDI-Words & Gestures for 55 children diagnosed with autistic disorder. Inter-rater reliability analyses were done for the whole sample and a subgroup of minimally verbal children (n = 28). Further, potential over- or under-estimation, comparing the raters was analyzed. Results suggested excellent to fair inter-rater reliability between parent and preschool teacher. Parents tended to rate the children slightly higher than preschool teachers. However, the differences were small, and most likely due to contextual variations. These findings suggest that parents can be reliable sources of information about language abilities in children with autism. Therefore, when children are difficult to assess through direct tests, parent reports such as the CDI can be a good alternative.(C) 2013 Elsevier Ltd. All rights reserved.
C1 [Nordahl-Hansen, Anders; Ulvund, Stein Erik] Univ Oslo, Dept Educ, N-0317 Oslo, Norway.
[Kaale, Anett] Oslo Univ Hosp, Div Mental Hlth & Addict, N-0424 Oslo, Norway.
RP Nordahl-Hansen, A (reprint author), Univ Oslo, Dept Educ, POB 1092, N-0317 Oslo, Norway.
EM a.j.n.hansen@ped.uio.no
CR Adamson LB, 2009, J AUTISM DEV DISORD, V39, P84, DOI 10.1007/s10803-008-0601-7
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NR 30
TC 3
Z9 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1391
EP 1396
DI 10.1016/j.rasd.2013.08.006
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500013
ER
PT J
AU Zachor, DA
Ben-Shachar, S
Ben-Itzchak, E
AF Zachor, Ditza A.
Ben-Shachar, Shay
Ben-Itzchak, Esther
TI Do risk factors for autism spectrum disorders affect gender
representation?
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Gender; Male:female ratio; Risk factors; Low
birth weight; Multiplex families
ID BIRTH-WEIGHT; PATERNAL AGE; CHILDREN; PSYCHOPATHOLOGY; COMPLICATIONS;
EPIDEMIOLOGY; PREVALENCE; RECURRENCE; TWIN
AB To examine the M:F ratio in several known risk factors to demonstrate insights regarding autism spectrum disorders (ASD) etiology and sex. The study included 615 participants aged 18 months to 18 years age (mean = 49.8 months, SD = 28.4 months) diagnosed with ASD. Cognitive, adaptive and assessment of ASD were obtained using standardized tests. Detailed birth, familial, medical and developmental histories were obtained from the parents. Risk factors included ASD in the family (having a first-order family member with ASD); advanced maternal age (>= 35 years); advanced paternal age (>= 38 years); birth order (first-born versus third-born); low birth weight (LBW) (<2500 g); prematurity (gestational age <36 weeks). The M:F ratio (4.4:1) in the LBW group was lower than the M:F ratio (7.1:1) in the >2500 g group; however the difference showed only a statistical trend. No significant differences in M:F ratio were found between the ASD groups with and without the other examined risk factors. It is possible that the absence of a major association between most of the examined risk factors and sex representation points to the relatively minor role of these risk factors in ASD. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Zachor, Ditza A.; Ben-Itzchak, Esther] Assaf Harofeh Med Ctr, Autism Ctr, Dept Pediat, IL-70300 Zerifin, Israel.
[Zachor, Ditza A.] Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel.
[Ben-Shachar, Shay] Sourasky Med Ctr, Genet Inst, IL-64238 Tel Aviv, Israel.
[Ben-Itzchak, Esther] Ariel Univ Ctr Samaria, Dept Commun Disorders, IL-40700 Ariel, Israel.
RP Zachor, DA (reprint author), Assaf Harofeh Med Ctr, Autism Ctr, IL-70300 Zerifin, Israel.
EM dzachor@smile.net.il
CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th
Anello A, 2009, J AUTISM DEV DISORD, V39, P1487, DOI 10.1007/s10803-009-0755-y
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Bayley N, 1993, BAYLEY SCALES INFANT
Ben-Itzchak E, 2013, AUTISM RES, V6, P596, DOI 10.1002/aur.1319
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Constantino JN, 2010, AM J PSYCHIAT, V167, P1349, DOI 10.1176/appi.ajp.2010.09101470
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Tsai L. Y., 1983, J AUTISM DEV DISORD, V13, P57
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Wechsler D., 1989, WECHSLER PRESCHOOL P
NR 40
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1397
EP 1402
DI 10.1016/j.rasd.2013.08.008
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500014
ER
PT J
AU Inokuchi, E
Kamio, Y
AF Inokuchi, Eiko
Kamio, Yoko
TI Qualitative analyses of verbal fluency in adolescents and young adults
with high-functioning autism spectrum disorder
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE High-functioning autism spectrum disorders; Verbal fluency; Action
fluency; Semantic strategy; Cognitive flexibility; Generativity
ID EXECUTIVE DYSFUNCTION; PARKINSONS-DISEASE; WORD FLUENCY; FRONTAL-LOBE;
CHILDREN; INDIVIDUALS; PERFORMANCE; LANGUAGE; DEFICITS; MEMORY
AB Systematic qualitative analyses of verbal fluency might aid our understanding of the characteristic cognitive processes in individuals with autism spectrum disorder (ASD). In this study, we compared through qualitative and quantitative analyses performance on letter fluency (LF), category fluency (CF), and action fluency (AF) in adolescents and young adults with high-functioning autism spectrum disorders (HFASD) with that of an age-, gender-, and IQ-matched control group. Quantitative analyses revealed significantly fewer correct responses on category and action fluency and significantly more intrusions on category fluency in individuals with HFASD than in control participants. Qualitative analyses revealed significantly fewer semantic clusters and significantly more phonemic clusters during action fluency in individuals with HFASD compared to control participants. With respect to action fluency, the number of correct responses and clusters were related to verbal IQ for individuals with HFASD but not for control participants. We discuss these results in terms of abnormalities in semantic/phonemic strategy choice, cognitive flexibility, and generativity in ASD. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Inokuchi, Eiko; Kamio, Yoko] Natl Ctr Neurol & Psychiat, Natl Inst Mental Hlth, Dept Child & Adolescent Mental Hlth, Kodaira, Tokyo 1878553, Japan.
RP Kamio, Y (reprint author), Natl Ctr Neurol & Psychiat, Natl Inst Mental Hlth, Dept Child & Adolescent Mental Hlth, 4-1-1 Ogawa Higashi, Kodaira, Tokyo 1878553, Japan.
EM kamio@ncnp.go.jp
CR Abwender DA, 2001, ASSESSMENT, V8, P323, DOI 10.1177/107319110100800308
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NR 37
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1403
EP 1410
DI 10.1016/j.rasd.2013.08.010
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500015
ER
PT J
AU Yi, L
Fan, YB
Zhao, J
Huang, D
Li, YY
Zou, XB
AF Yi, Li
Fan, Yuebo
Zhao, Jing
Huang, Dan
Li, Yunyi
Zou, Xiaobing
TI Atypical understanding of mental terms in Chinese-speaking children with
autism spectrum disorder
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Mental terms; Verb factivity; Theory of mind; Autism spectrum disorder;
Chinese
ID EXECUTIVE FUNCTION; INDIVIDUAL-DIFFERENCES; YOUNG-CHILDREN; FALSE
BELIEFS; MIND; ACQUISITION; LANGUAGE; STATES; PRESCHOOLERS; ABILITY
AB The present study investigated how Chinese children with autism spectrum disorder (ASD) understand mental terms, especially their knowledge of verb factivity. We examined these children's ability to understand mental terms representing true belief (i.e., zhi1dao4, know) and false belief (i.e., yi3wei2, thought) and compared their ability with that of typically developing (TD) children matched with age, and TD children matched with verbal mental age (VMA). Children were asked to participate in a game to find a toy according to the experimenter's testimony, which involved these mental terms. Results showed that all children from these three groups understood zhi1dao4 better than yi3wei2. Particularly, children with ASD performed statistically significantly worse in understanding mental terms than their age-matched TO children, but not differently from VMA-matched TD children. The understanding of mental verbs was correlated with the language ability of children with ASD, and with age, language ability and executive function of TO children. After controlling for the effects of age, general language ability, and executive functions, the group difference of mental verb understanding still existed. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Yi, Li; Li, Yunyi] Sun Yat Sen Univ, Dept Psychol, Guangzhou 510275, Guangdong, Peoples R China.
[Fan, Yuebo; Huang, Dan] Guangzhou Cana Sch, Guangzhou, Guangdong, Peoples R China.
[Fan, Yuebo; Huang, Dan] Guangzhou Rehabil & Res Ctr Children ASD, Guangzhou, Guangdong, Peoples R China.
[Zhao, Jing] Sun Yat Sen Univ, Dept English, Guangzhou 510275, Guangdong, Peoples R China.
[Zou, Xiaobing] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou 510275, Guangdong, Peoples R China.
RP Yi, L (reprint author), Sun Yat Sen Univ, Dept Psychol, 135 Xingang West Rd, Guangzhou 510275, Guangdong, Peoples R China.
EM yili5@mail.sysu.edu.cn
CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th
Astington J. W., 2005, WHY LANGUAGE MATTERS
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NR 37
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1411
EP 1417
DI 10.1016/j.rasd.2013.08.009
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500016
ER
PT J
AU Reitzel, J
Summers, J
Lorv, B
Szatmari, P
Zwaigenbaum, L
Georgiades, S
Duku, E
AF Reitzel, J.
Summers, J.
Lorv, B.
Szatmari, P.
Zwaigenbaum, L.
Georgiades, S.
Duku, E.
TI Pilot randomized controlled trial of a Functional Behavior Skills
Training program for young children with Autism Spectrum Disorder who
have significant early learning skill impairments and their families
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism Spectrum Disorder; Functional behavior skills; Early learning
skill impairment; Parent training; Randomized controlled trial
ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE EARLY INTERVENTION; PROFOUND
MENTAL-RETARDATION; INDEPENDENT-LIVING SKILLS; CHALLENGING BEHAVIORS;
INTELLECTUAL DISABILITY; FOLLOW-UP; INDIVIDUALS; STRESS; METAANALYSIS
AB Many children with Autism Spectrum Disorder (ASD) possess early learning skill deficits and, do not achieve significant cognitive and adaptive gains following intensive behavioral intervention. This pilot randomized controlled trial investigated the effectiveness of a Functional Behavior Skills Training (FBST) program in improving children's performance on functional skills and communication, mitigating children's problem behaviors, and improving parents' strain, sense of competence, and, knowledge of Applied Behavior Analysis (ABA). Fifteen children with ASD who demonstrated early, learning skill impairments (ages between 38 and 82 months) were recruited from a community-based, IBI program or its waitlist. Children and their parents were randomized to a treatment group who, received FBST for four months or a control group who received their treatment as usual. Children who, received FBST improved on targeted functional skills and communication and demonstrated lower, levels of disruptive behavior. Meanwhile, parents who received FBST improved in their knowledge of, ABA. Overall, preliminary findings suggest that FBST is a feasible and promising behavioral, intervention for children with ASD who have early learning skill impairments. FBST promotes the, development of functional behavior and communication which can direct children onto a path of, appropriate skill development and meaningful interactions in the real world. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Reitzel, J.; Summers, J.] McMaster Univ, Hamilton, ON, Canada.
[Reitzel, J.; Summers, J.; Lorv, B.] McMaster Childrens Hosp, Hamilton, ON, Canada.
[Georgiades, S.; Duku, E.] McMaster Univ, Offord Ctr Child Studies, Hamilton, ON, Canada.
[Szatmari, P.] Univ Toronto, Toronto, ON, Canada.
[Zwaigenbaum, L.] Univ Alberta, Edmonton, AB, Canada.
RP Reitzel, J (reprint author), 555 Sanat Rd, Hamilton, ON L9C 0C4, Canada.
EM reitzel@hhsc.ca
CR American Psychiatric Association, 2000, DIAGNOSTIC AND STATI
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NR 83
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1418
EP 1432
DI 10.1016/j.rasd.2013.07.025
PG 15
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500017
ER
PT J
AU Jang, J
Matson, JL
Cervantes, PE
Goldin, RL
AF Jang, Jina
Matson, Johnny L.
Cervantes, Paige E.
Goldin, Rachel L.
TI The relationship between race and comorbid symptoms in infants and
toddlers with autism spectrum disorder
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Comorbidity; The Baby and Infant Screen for
Children with aUtIsm Traits - Part 2; Race
ID CHALLENGING BEHAVIORS; PSYCHIATRIC-DISORDERS; INTELLECTUAL DISABILITY;
TRAITS BISCUIT; DSM-5 CRITERIA; SOCIAL-SKILLS; PDD-NOS; CHILDREN; ASD;
PSYCHOPATHOLOGY
AB Researchers have indicated that persons with autism spectrum disorder (ASD) population evince higher rates of comorbid symptoms. While the relationship between comorbid symptoms and factors such as autism symptom severity, IQ level, age, communication abilities, and degree of social impairment were previously examined, there has been limited research on the effect of race in this area. The current study examined the potential role of race in comorbid symptoms in toddlers with ASD and atypically developing toddlers without a diagnosis of ASD using The Baby and Infant Screen for Children with aUtIsm Traits Part 2 (BISCUIT-Part 2). Based on the current findings, African-American toddlers evinced higher rates of comorbid symptoms than Caucasian toddlers and toddlers of other races. In addition, toddlers with ASD evinced higher rates of comorbid symptoms than atypically developing toddlers without a diagnosis of ASD. Implications regarding these findings are discussed. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Jang, Jina; Matson, Johnny L.; Cervantes, Paige E.; Goldin, Rachel L.] Louisiana State Univ, Baton Rouge, LA 70803 USA.
RP Jang, J (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
EM jinajang87@gmail.com
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NR 48
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1433
EP 1438
DI 10.1016/j.rasd.2013.08.011
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500018
ER
PT J
AU McDonald, TA
Machalicek, W
AF McDonald, T. A.
Machalicek, Wendy
TI Systematic review of intervention research with adolescents with autism
spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Adolescent; Autism; Intervention; Literature review; Treatment
ID PERVASIVE DEVELOPMENTAL DISORDERS; VIDEO MODELING INTERVENTIONS; SOCIAL
STORY INTERVENTION; ON-TASK BEHAVIOR; ASPERGER-SYNDROME; SEVERE
DISABILITIES; PSYCHOSOCIAL INTERVENTIONS; DIFFERENTIAL REINFORCEMENT;
EPIDEMIOLOGIC SURVEYS; DESTRUCTIVE BEHAVIOR
AB A growing body of research provides effective interventions to address the core symptoms of autism spectrum disorders (ASD). However, adolescents with ASDs may face age-specific challenges necessitating the need for contextually relevant and effective interventions. This systematic review examined peer-reviewed intervention research for adolescents (ages 12-21) with ASD. Electronic database searches and ancestral searches were used to identify studies published between 1980 and 2011. 102 studies were identified. A variety of interventions were implemented in these studies to address a wide range of targeted skills and behaviors. Reviewed studies were categorized into seven domains based on the skills and behaviors targeted: (a) social skills; (b) communication skills; (c) challenging behavior; (d) academic skills; (e) vocational skills; (f) independence and self-care; and (g) physical development. Results indicate that effective interventions exist in each category. These results are discussed in relation to participant characteristics, intervention effectiveness, social validity, generalization and maintenance. Generalization, maintenance, and social validity data were gathered in only 34%, 43%, and 31% of the articles, respectively. Additionally, few studies investigated interventions addressing communication, vocational or academic skills. Recommendations for future research are provided. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [McDonald, T. A.] Univ Wisconsin, Madison, WI 53706 USA.
[Machalicek, Wendy] 5261 Univ Oregon, Univ Oregon, Coll Educ, Dept Special Educ & Clin Sci, Eugene, OR 97403 USA.
RP Machalicek, W (reprint author), 5261 Univ Oregon, Univ Oregon, Coll Educ, Dept Special Educ & Clin Sci, Eugene, OR 97403 USA.
EM wmachali@uoregon.edu
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Zanden J. W. V., 2003, HUMAN DEV UPDATED 7
NR 154
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1439
EP 1460
DI 10.1016/j.rasd.2013.07.015
PG 22
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500019
ER
PT J
AU Kadey, HJ
Roane, HS
Diaz, JC
McCarthy, CM
AF Kadey, Heather J.
Roane, Henry S.
Diaz, Janet C.
McCarthy, Christie M.
TI Using a Nuk (R) brush to increase acceptance of solids and liquids for
two children diagnosed with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Feeding disorders; Escape extinction; Physical guidance; Autism
ID FOOD REFUSAL; ESCAPE EXTINCTION; POSITIVE REINFORCEMENT;
FUNCTIONAL-ANALYSIS; VARIETY
AB Escape extinction (EE) procedures, such as non-removal of the spoon (NRS) and physical guidance, have been shown to be effective for increasing the acceptance of previously refused foods in children with feeding disorders. NRS typically involves presenting a utensil at a child's lips until he/she accepts a bite/drink or until an arbitrary meal duration is met. As a result, some children may learn to "wait out" the meal duration thus avoiding bites/drinks altogether. Physical guidance procedures are implemented in a similar manner but also include physically guiding the child's mouth open by applying pressure on the mandibular joint (i.e., jaw prompt). In some cases, the jaw prompt may harm the child if too much pressure is applied to his/her face. Due to the limitations of these procedures we evaluated an alternative PG strategy by using a Nuk (R) brush to increase the acceptance of bites and drinks in two participants. Published by Elsevier Ltd.
C1 [Kadey, Heather J.; Roane, Henry S.] SUNY Upstate Med Univ, Syracuse, NY 13210 USA.
[Diaz, Janet C.; McCarthy, Christie M.] Kelherman Behav & Feeding Program, Utica, NY 13501 USA.
RP Kadey, HJ (reprint author), SUNY Upstate Med Univ, 600 East Genesee St,Suite 124, Syracuse, NY 13210 USA.
EM kadeyh@upstate.edu
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Volkert VM, 2010, J APPL BEHAV ANAL, V43, P155, DOI 10.1901/jaba.2010.43-155
NR 29
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1461
EP 1480
DI 10.1016/j.rasd2013.07.017
PG 20
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500020
ER
PT J
AU Murray, C
Healy, O
AF Murray, Clodagh
Healy, Olive
TI Increasing response variability in children with autism spectrum
disorder using lag schedules of reinforcement
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Response variability; Lag schedules; Reinforcement; U-Value statistic
ID CONTINGENCY; EXTINCTION
AB Individuals with autism spectrum disorder (ASD) often present with deficits in variability in responding across multiple repertoires. However, research to date has resulted in little empirical evaluation of remediation strategies for such deficits. We investigated the effects of lag schedules of reinforcement on response variability using a computer-based task designed for the purpose of the study. The U-value statistic was used as a measure of variability in responding to determine if increasing the lag criterion would correspondingly increase levels of variability. Participants included children with ASD (Group 1) and neurotypical children (Group 2). Results showed that U-values were higher when reinforcement was contingent on increased variability, indicating the effectiveness of higher lag values on response variability. A significant difference in response variability between groups provided evidence for the disparity in such responding in children with ASD compared to their neurotypical peers. Group 1 showed consistently lower U-values than Group 2 indicating lower response variability. However, data from this study clearly show that lag schedules of reinforcement may be employed to increase response variability in ASD. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Murray, Clodagh; Healy, Olive] Natl Univ Ireland Galway, Galway, Ireland.
RP Healy, O (reprint author), Natl Univ Ireland, Sch Psychol, Univ Rd, Galway, Ireland.
EM olive.healy@nuigalway.ie
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Susa Carrie, 2012, Anal Verbal Behav, V28, P125
NR 15
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
EI 1878-0237
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD NOV
PY 2013
VL 7
IS 11
BP 1481
EP 1488
DI 10.1016/j.rasd.2013.08.004
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 247JK
UT WOS:000326613500021
ER
PT J
AU Meyers, OI
AF Meyers, O., I
TI THE IMPACT OF DSM-5 ON THE DEVELOPMENT OF DRUGS TO TREAT AUTISM SPECTRUM
DISORDER
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Meyers, O., I] Truven Hlth Analyt, Cleveland, OH USA.
NR 0
TC 0
Z9 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
EI 1524-4733
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2013
VL 16
IS 7
BP A607
EP A607
PG 1
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 242MY
UT WOS:000326247602337
ER
PT J
AU Vohra, R
Madhavan, S
Sambamoorthi, U
AF Vohra, R.
Madhavan, S.
Sambamoorthi, U.
TI IMPACT OF AUTISM SPECTRUM DISORDERS ON THE FAMILY - A NATIONAL
PERSPECTIVE
SO VALUE IN HEALTH
LA English
DT Meeting Abstract
C1 [Vohra, R.; Madhavan, S.; Sambamoorthi, U.] W Virginia Univ, Sch Pharm, Morgantown, WV 26506 USA.
NR 0
TC 0
Z9 0
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1098-3015
EI 1524-4733
J9 VALUE HEALTH
JI Value Health
PD NOV
PY 2013
VL 16
IS 7
BP A553
EP A554
PG 2
WC Economics; Health Care Sciences & Services; Health Policy & Services
SC Business & Economics; Health Care Sciences & Services
GA 242MY
UT WOS:000326247602044
ER
PT J
AU Mohiuddin, S
Ghaziuddin, M
AF Mohiuddin, Sarah
Ghaziuddin, Mohammad
TI Psychopharmacology of autism spectrum disorders: A selective review
SO AUTISM
LA English
DT Article
DE autism; psychopharmacology; comorbidity
ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; ATYPICAL
ANTIPSYCHOTICS; SCHIZOPHRENIC CHILDREN; REPETITIVE BEHAVIORS; ADOLESCENT
AUTISM; CROSSOVER TRIAL; PLACEBO; IRRITABILITY; RISPERIDONE
AB While there is no cure for autism spectrum disorder, psychopharmacologic agents are often used with behavioral and educational approaches to treat its comorbid symptoms of hyperactivity, irritability, and aggression. Studies suggest that at least 50% of persons with autism spectrum disorder receive psychotropic medications during their life span. This selective review examines recent studies about the use of psychotropic medications in persons with autism spectrum disorder. The aim was to focus on randomized controlled trials conducted from 1990 to 2010 on this topic. A comprehensive literature search was performed using PubMed and Cochrane databases. Out of 105 studies identified for the review, only 24 were randomized controlled trials. Thus, despite the common use of these medications in autism spectrum disorder, more controlled studies are needed to determine their long-term efficacy and safety.
C1 [Mohiuddin, Sarah; Ghaziuddin, Mohammad] Univ Michigan, Ann Arbor, MI 48109 USA.
RP Ghaziuddin, M (reprint author), Univ Michigan, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA.
EM mghaziud@umich.edu
CR Aman MG, 2010, J CHILD ADOL PSYCHOP, V20, P415, DOI 10.1089/cap.2009.0120
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NR 45
TC 1
Z9 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 645
EP 654
DI 10.1177/1362361312453776
PG 10
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100002
PM 22892891
ER
PT J
AU Sasson, NJ
Nowlin, RB
Pinkham, AE
AF Sasson, Noah J.
Nowlin, Rachel B.
Pinkham, Amy E.
TI Social cognition, social skill, and the broad autism phenotype
SO AUTISM
LA English
DT Article
DE broad autism phenotype; social cognition; social functioning; social
skill
ID GENERAL-POPULATION; SPECTRUM DISORDERS; FUNCTIONING AUTISM; TRAITS;
SCHIZOPHRENIA; INDIVIDUALS; RECOGNITION; ASSOCIATION; PREDICTORS; FAMILY
AB Social-cognitive deficits differentiate parents with the broad autism phenotype from non-broad autism phenotype parents more robustly than other neuropsychological features of autism, suggesting that this domain may be particularly informative for identifying genetic and brain processes associated with the phenotype. The current study examined whether the social-cognitive deficits associated with the broad autism phenotype extend to the general population and relate to reduced social skill. A total of 74 undergraduates completed the Broad Autism Phenotype Questionnaire, three standardized social-cognitive tasks, and a live social interaction with an unfamiliar research assistant. Social broad autism phenotype traits were significantly associated with deficits in social cognition and reduced social skill. In addition, the relationship between social broad autism phenotype traits and social skill was partially mediated by social cognition, suggesting that the reduced interpersonal ability associated with the broad autism phenotype occurs in part because of poorer social-cognitive ability. Together, these findings indicate that the impairments in social cognition and social skill that characterize autism spectrum disorder extend in milder forms to the broad autism phenotype in the general population and suggest a framework for understanding how social broad autism phenotype traits may manifest in diminished social ability.
C1 [Sasson, Noah J.; Nowlin, Rachel B.] Univ Texas Dallas, Richardson, TX 75080 USA.
[Pinkham, Amy E.] So Methodist Univ, Dallas, TX 75275 USA.
RP Sasson, NJ (reprint author), Univ Texas Dallas, Sch Behav & Brain Sci, GR41,800 W Campbell Rd, Richardson, TX 75080 USA.
EM nsasson@utdallas.edu
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NR 42
TC 4
Z9 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 655
EP 667
DI 10.1177/1362361312455704
PG 13
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100003
PM 22987889
ER
PT J
AU Poljac, E
Poljac, E
Wagemans, J
AF Poljac, Ervin
Poljac, Edita
Wagemans, Johan
TI Reduced accuracy and sensitivity in the perception of emotional facial
expressions in individuals with high autism spectrum traits
SO AUTISM
LA English
DT Article
DE Autism spectrum quotient; Broader autistic phenotype; Face perception;
Emotion recognition; Facial expression
ID RECOGNITION ABILITY; FUNCTIONING AUTISM; FACE RECOGNITION; BASIC
EMOTIONS; QUOTIENT AQ; DISORDERS; CHILDREN; PHENOTYPE
AB Autism spectrum disorder (ASD) is among other things characterized by specific impairments in emotion processing. It is not clear, however, to what extent the typical decline in affective functioning is related to the specific autistic traits. We employed The Autism Spectrum-Quotient (AQ) to quantify autistic traits in a group of 500 healthy individuals and investigate whether we could detect similar difficulties in the perception of emotional expressions in a broader autistic phenotype. The group with high AQ score was less accurate and needed higher emotional content to recognize emotions of anger, disgust, and sadness. Our findings demonstrate a selective impairment in identification of emotional facial expressions in healthy individuals that is primarily related to the extent of autistic traits.
C1 [Poljac, Ervin; Wagemans, Johan] Univ Leuven, Louvain, Belgium.
[Poljac, Edita] Univ Oxford, Oxford OX1 2JD, England.
RP Poljac, E (reprint author), Univ Leuven KU Leuven, Expt Psychol Lab, Tiensestr 102,Bus 3711, BE-3000 Louvain, Belgium.
EM Ervin.Poljac@psy.kuleuven.be
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Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49
NR 49
TC 3
Z9 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 668
EP 680
DI 10.1177/1362361312455703
PG 13
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100004
PM 22987888
ER
PT J
AU van Steensel, FJA
Deutschman, AACG
Bogels, SM
AF van Steensel, Francisca J. A.
Deutschman, Amber A. C. G.
Bogels, Susan M.
TI Examining the Screen for Child Anxiety-Related Emotional Disorder-71 as
an assessment tool for anxiety in children with high-functioning autism
spectrum disorders
SO AUTISM
LA English
DT Article
DE ASD; anxiety; self-report; child-parent agreement
ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS;
RANDOMIZED-TRIAL; ADOLESCENTS; INTERVIEW; SYMPTOMS; RELIABILITY;
THERAPY; SAMPLE; YOUTH
AB The psychometric properties of a questionnaire developed to assess symptoms of anxiety disorders (SCARED-71) were compared between two groups of children: children with high-functioning autism spectrum disorder and comorbid anxiety disorders (ASD-group; n = 115), and children with anxiety disorders (AD-group; n = 122). Anxiety disorders were established with a semi-structured interview (ADIS-C/P), using child- as well as parent-report. Internal consistency, construct validity, sensitivity, specificity, and discriminant validity of the SCARED-71 was investigated. Results revealed that the psychometric properties of the SCARED-71 for the ASD-group were quite comparable to the AD-group, however, the discriminant validity of the SCARED-71 child-report was less in the ASD-group. Raising the parental cutoffs of the SCARED-71 resulted in higher specificity rates, which suggests that research should focus more on establishing alternative cutoffs for the ASD-population.
C1 [van Steensel, Francisca J. A.; Deutschman, Amber A. C. G.; Bogels, Susan M.] Univ Amsterdam, NL-1018 VZ Amsterdam, Netherlands.
RP van Steensel, FJA (reprint author), Univ Amsterdam, Res Inst Child Dev & Educ, Nieuwe Prinsengracht 130, NL-1018 VZ Amsterdam, Netherlands.
EM f.j.a.vansteensel@uva.nl
CR (APA) APA, 2000, DIAGN STAT MAN MENT
Birhamer B, 1999, J AM ACAD CHILD ADOL, V38, P1230
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NR 31
TC 10
Z9 10
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 681
EP 692
DI 10.1177/1362361312455875
PG 12
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100005
PM 23045220
ER
PT J
AU Warren, Z
Vehorn, A
Dohrmann, E
Newsom, C
Taylor, JL
AF Warren, Zachary
Vehorn, Alison
Dohrmann, Elizabeth
Newsom, Cassandra
Taylor, Julie Lounds
TI Brief report: Service implementation and maternal distress surrounding
evaluation recommendations for young children diagnosed with autism
SO AUTISM
LA English
DT Article
DE adherence; autism spectrum disorders; caregiver distress; diagnosis;
service implementation
ID SPECTRUM DISORDERS; BEHAVIOR PROBLEMS; PARENTING STRESS; INTERVENTION;
MOTHERS
AB There is limited evidence surrounding the ability of families of children with autism spectrum disorders to access and implement recommended interventions following diagnosis. The distress a family may encounter with regard to inability to access recommended services is also poorly understood. In this study, we present preliminary data regarding implementation of clinical recommendations following autism spectrum disorder diagnosis as well as associations of implementation with maternal functioning. In total, 75 mothers of young children diagnosed with autism spectrum disorder through a university-based preschool autism clinic returned surveys regarding access to recommended services as well as maternal mental health and distress. Results indicate that while families were able to implement numerous recommendations, specific categories of intervention were less likely to be received. Challenges implementing recommended services were not related to increased maternal distress. These results suggest that despite potential barriers toward accessing some specific recommended services following diagnosis of autism spectrum disorder, many families may be quite successful in implementing many other core recommended services and that failure to access such services may not necessarily negatively impact maternal mental health and distress.
C1 [Warren, Zachary; Vehorn, Alison; Dohrmann, Elizabeth; Newsom, Cassandra; Taylor, Julie Lounds] Vanderbilt Univ, Nashville, TN 37203 USA.
RP Warren, Z (reprint author), Vanderbilt Univ, Vanderbilt Kennedy Ctr, MRL Bldg,Peabody Box 74,230 Appleton Pl, Nashville, TN 37203 USA.
EM zachary.warren@vanderbilt.edu
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NR 24
TC 0
Z9 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 693
EP 700
DI 10.1177/1362361312453881
PG 8
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100006
PM 23045221
ER
PT J
AU Yudell, M
Tabor, HK
Dawson, G
Rossi, J
Newschaffer, C
AF Yudell, Michael
Tabor, Holly K.
Dawson, Geraldine
Rossi, John
Newschaffer, Craig
CA Working Grp Autism Risk Commun Eth
TI Priorities for autism spectrum disorder risk communication and ethics
SO AUTISM
LA English
DT Article
DE autism; ethics; risk communication
ID RESEARCH PARTICIPANTS; UNDERSTANDING AUTISM; WORKING GROUP; HEALTH;
PREVALENCE; PERCEPTION; CHILDREN; ISSUES; ASSOCIATION; INFORMATION
AB Autism spectrum disorders are an issue of increasing public health significance. The incidence of autism spectrum disorders has been increasing in recent years, and they are associated with significant personal and financial impacts for affected persons and their families. In recent years, a large number of scientific studies have been undertaken, which investigate genetic and environmental risk factors for autism, with more studies underway. At present, much remains unknown regarding autism spectrum disorder risk factors, but the emerging picture of causation is in many cases complex, with multiple genes and gene-environment interactions being at play. The complexity and uncertainty surrounding autism spectrum disorder risk factors raise a number of questions regarding the ethical considerations that should be taken into account when undertaking autism spectrum disorder risk communication. At present, however, little has been written regarding autism spectrum disorder risk communication and ethics. This article summarizes the findings of a recent conference investigating ethical considerations and policy recommendations in autism spectrum disorder risk communication, which to the authors' knowledge is the first of its kind. Here, the authors discuss a number of issues, including uncertainty; comprehension; inadvertent harm; justice; and the appropriate roles of clinicians, scientists, and the media in autism spectrum disorder risk communication.
C1 [Yudell, Michael; Rossi, John; Newschaffer, Craig] Drexel Univ, Philadelphia, PA 19102 USA.
[Tabor, Holly K.] Univ Washington, Seattle, WA 98195 USA.
[Tabor, Holly K.] Seattle Childrens Res Inst, Seattle, WA USA.
[Dawson, Geraldine] Univ N Carolina, Chapel Hill, NC 27515 USA.
RP Yudell, M (reprint author), Drexel Univ, Sch Publ Hlth, 1505 Race St,MS 1032, Philadelphia, PA 19102 USA.
EM may27@drexel.edu
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NR 77
TC 3
Z9 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 701
EP 722
DI 10.1177/1362361312453511
PG 22
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100007
PM 22917844
ER
PT J
AU Eussen, MLJM
Van Gool, AR
Verheij, F
De Nijs, PFA
Verhulst, FC
Greaves-Lord, K
AF Eussen, Mart L. J. M.
Van Gool, Arthur R.
Verheij, Fop
De Nijs, Pieter F. A.
Verhulst, Frank C.
Greaves-Lord, Kirstin
TI The association of quality of social relations, symptom severity and
intelligence with anxiety in children with autism spectrum disorders
SO AUTISM
LA English
DT Article
DE anxiety; autism spectrum disorders; intelligence; social relations;
symptom severity
ID PERVASIVE DEVELOPMENTAL DISORDERS; PDD-NOS; INTERNALIZING SYMPTOMS;
PSYCHIATRIC-DISORDERS; ADOLESCENTS; VALIDITY; IV; DISABILITIES;
CHILDHOOD; DIAGNOSES
AB Limited quality of social relations, milder symptom severity and higher intelligence were shown to account for higher anxiety levels in autism spectrum disorders. The current study replicated and extended earlier findings by combining these three determinants of anxiety in autism spectrum disorders in one study. The sample consisted of 134 school-aged children with autism spectrum disorders, of whom 58 (43%) had a co-morbid anxiety disorder according to the Diagnostic Interview Schedule for Children-Parent version. In this sample, we tested associations between these determinants and anxiety univariately and multivariately to clarify the unique contribution of all determinants. Since we hypothesized that the association between limited quality of social relations and anxiety would be amplified by low symptom severity and/or high intelligence, we additionally tested for moderating effects. We found that higher anxiety levels were associated with a lower quality of social relations and lower symptom severity. In this mainly high-functioning sample, intelligence was not related to anxiety levels. No moderation effects were found. Since lower quality of social relations and lower symptom severity are associated with higher anxiety levels in children with autism spectrum disorders, therapeutic interventions aimed at reducing anxiety in autism spectrum disorders should pay attention to improving social relations, and presumably children with a lower symptom severity could benefit most from such interventions.
C1 [Verheij, Fop; De Nijs, Pieter F. A.; Verhulst, Frank C.; Greaves-Lord, Kirstin] Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, NL-3015 GJ Rotterdam, Netherlands.
RP Greaves-Lord, K (reprint author), Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, Dr Molewaterpl 60, NL-3015 GJ Rotterdam, Netherlands.
EM k.greaves-lord@erasmusmc.nl
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American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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NR 46
TC 2
Z9 3
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 723
EP 735
DI 10.1177/1362361312453882
PG 13
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100008
PM 22917843
ER
PT J
AU Pearl, AM
Murray, MJ
Smith, LA
Arnold, M
AF Pearl, Amanda M.
Murray, Michael J.
Smith, Laura A.
Arnold, Mariah
TI Assessing adolescent social competence using the Social Responsiveness
Scale: Should we ask both parents or will just one do?
SO AUTISM
LA English
DT Article
DE assessment; autism spectrum disorder; interrater reliability; parent
agreement; Social Responsiveness Scale
ID AGREEMENT
AB There is a paucity of instruments designed to measure social competence of adolescents with autism spectrum disorders. The Social Responsiveness Scale is one of a few that can be used. This study compared differences between mother and father reports of social competence of adolescents. Data were collected from parents of 50 adolescents with and without an autism spectrum disorder diagnosis between the ages of 12 and 17 years. The Social Responsiveness Scale demonstrated high interrater reliability between parents. These results suggest that the Social Responsiveness Scale is an efficient and valuable tool for researchers and clinicians to obtain a more comprehensive understanding of an individual's social skills deficits. Additionally, given the extremely high agreement between mothers and fathers on the ratings of their children's social competence, obtaining data from either parent is sufficient to provide an accurate reflection of social competence at home.
C1 [Pearl, Amanda M.; Murray, Michael J.; Arnold, Mariah] Penn State Univ, Coll Med, University Pk, PA 16802 USA.
[Smith, Laura A.] Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA.
RP Pearl, AM (reprint author), Penn State Coll Med, Dept Psychiat, Penn State Milton S Hershey Med Ctr, 500 Univ Dr, Hershey, PA 17033 USA.
EM apearl@hmc.psu.edu
CR ACHENBACH TM, 1987, PSYCHOL BULL, V101, P213, DOI 10.1037/0033-2909.101.2.213
[Anonymous], 2009, MMWR SURVEILL SUMM, V58, P1
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Constantino JN, 2005, SOCIAL RESPONSIVENES
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Pearl AM, 2010, PENNS PSYCH ASS HARR
Posserud MB, 2006, J CHILD PSYCHOL PSYC, V47, P167, DOI 10.1111/j.1469-7610.2005.01462.x
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NR 13
TC 1
Z9 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 736
EP 742
DI 10.1177/1362361312453349
PG 7
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100009
PM 22914777
ER
PT J
AU Milne, SL
McDonald, JL
Comino, EJ
AF Milne, Susan L.
McDonald, Jenny L.
Comino, Elizabeth J.
TI Adaptive function in preschoolers in relation to developmental delay and
diagnosis of autism spectrum disorders: Insights from a clinical sample
SO AUTISM
LA English
DT Article
DE adaptive behaviour; Adaptive Behaviour Assessment System-Second Edition;
autism; developmental disability; preschoolers
ID BEHAVIOR DOMAINS; DOWN-SYNDROME; CHILDREN; VINELAND; INDIVIDUALS; SCALES
AB This study aims to explore the relationship between developmental ability, autism and adaptive skills in preschoolers. Adaptive function was assessed in 152 preschoolers with autism, with and without developmental delay, and without autism, with and without developmental delay. Their overall adaptive function, measured by the general adaptive composite on the Adaptive Behaviour Assessment System, was closely correlated to developmental ability as measured by the general quotient on the Griffith Mental Development Scales. Children with autism performed significantly less well on both scales. Domain scores discriminated between children with and without autism, with poorer performance on both the social and practical domain scores for children with autism, even when controlling for the effects of development. Children with average development, both with and without autism, had lower adaptive skills than expected for their developmental level. The importance of considering domain scores as well as the general adaptive composite when determining support needs is emphasised.
C1 [Milne, Susan L.; McDonald, Jenny L.] Campbelltown Hosp, Campbelltown, NSW 2560, Australia.
[Comino, Elizabeth J.] Univ NSW, Sydney, NSW, Australia.
RP Milne, SL (reprint author), Campbelltown Hosp, Paediat Allied Hlth Unit, POB 149, Campbelltown, NSW 2560, Australia.
EM susan.milne@sswahs.nsw.gov.au
CR Achenbach T, 2000, MANUAL ASEBA PRESCHO
American Association on Mental Retardation, 1992, MENTAL RETARDATION D
American Association on Mental Retardation, 2002, MENT RET DEF CLASS S
American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
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NR 25
TC 0
Z9 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 743
EP 753
DI 10.1177/1362361312453091
PG 11
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100010
PM 22987892
ER
PT J
AU Hanley, M
McPhillips, M
Mulhern, G
Riby, DM
AF Hanley, Mary
McPhillips, Martin
Mulhern, Gerry
Riby, Deborah M.
TI Spontaneous attention to faces in Asperger syndrome using ecologically
valid static stimuli
SO AUTISM
LA English
DT Article
DE Asperger syndrome; Autism; eye tracking; face perception; social
attention
ID WILLIAMS-SYNDROME; AUTISM; FIXATION; CHILDREN; INDIVIDUALS; COMPETENCE;
DISORDERS; PATTERNS
AB Previous eye tracking research on the allocation of attention to social information by individuals with autism spectrum disorders is equivocal and may be in part a consequence of variation in stimuli used between studies. The current study explored attention allocation to faces, and within faces, by individuals with Asperger syndrome using a range of static stimuli where faces were either viewed in isolation or viewed in the context of a social scene. Results showed that faces were viewed typically by the individuals with Asperger syndrome when presented in isolation, but attention to the eyes was significantly diminished in comparison to age and IQ-matched typical viewers when faces were viewed as part of social scenes. We show that when using static stimuli, there is evidence of atypicality for individuals with Asperger syndrome depending on the extent of social context. Our findings shed light on the previous explanations of gaze behaviour that have emphasised the role of movement in atypicalities of social attention in autism spectrum disorders and highlight the importance of consideration of the realistic portrayal of social information for future studies.
C1 [Hanley, Mary; McPhillips, Martin; Mulhern, Gerry] Queens Univ Belfast, Belfast BT7 1NN, Antrim, North Ireland.
[Riby, Deborah M.] Newcastle Univ, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
RP Hanley, M (reprint author), Queens Univ Belfast, Sch Psychol, Belfast BT7 1NN, Antrim, North Ireland.
EM m.hanley@qub.ac.uk
CR Baron-Cohen S., 2004, MIND READING INTERAC
Birmingham W, 2008, Q J EXPT PSYCHOL, V61, P986
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Wechsler D, 1999, WECHSLER ABBREVIATED
WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288
NR 19
TC 6
Z9 6
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 754
EP 761
DI 10.1177/1362361312456746
PG 8
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100011
PM 22987893
ER
PT J
AU Williams, BT
Gray, KM
AF Williams, Beth T.
Gray, Kylie M.
TI The relationship between emotion recognition ability and social skills
in young children with autism
SO AUTISM
LA English
DT Article
DE Autism; emotion recognition; social skills
ID SPECTRUM DISORDERS
AB This study assessed the relationship between emotion recognition ability and social skills in 42 young children with autistic disorder aged 4-7 years. The analyses revealed that accuracy in recognition of sadness, but not happiness, anger or fear, was associated with higher ratings on the Vineland-II Socialization domain, above and beyond the influence of chronological age, cognitive ability and autism symptom severity. These findings extend previous research with adolescents and adults with autism spectrum disorders, suggesting that sadness recognition is also associated with social skills in children with autism.
C1 [Williams, Beth T.; Gray, Kylie M.] Monash Univ, Sch Psychol & Psychiat, Ctr Dev Psychiat & Psychol, Clayton, Vic 3800, Australia.
RP Gray, KM (reprint author), Monash Med Ctr, ELMHS, 246 Clayton Rd, Melbourne, Vic 3168, Australia.
EM kylie.gray@monash.edu
RI Gray, Kylie/H-3345-2014
OI Gray, Kylie/0000-0001-6518-4240
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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Harrison P., 2003, ADAPTIVE BEHAV ASSES, V2nd
Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947
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Sparrow SS, 2005, VINELAND ADAPTIVE BE
Wallace GL, 2011, J AUTISM DEV DISORD, V41, P1475, DOI 10.1007/s10803-010-1170-0
Wechsler D., 2002, WECHSLER PRESCHOOL P, V3rd
Wright B, 2008, AUTISM, V12, P607, DOI 10.1177/1362361308097118
NR 16
TC 2
Z9 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 762
EP 768
DI 10.1177/1362361312465355
PG 7
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100012
PM 23175751
ER
PT J
AU [Anonymous]
AF [Anonymous]
TI Psychopharmacology of autism spectrum disorders: A selective review
SO AUTISM
LA English
DT Meeting Abstract
NR 0
TC 0
Z9 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
EI 1461-7005
J9 AUTISM
JI Autism
PD NOV
PY 2013
VL 17
IS 6
BP 769
EP 774
DI 10.1177/1362361313508671
PG 6
WC Psychology, Developmental
SC Psychology
GA 241FF
UT WOS:000326151100013
ER
PT J
AU Grigg-Damberger, M
Ralls, F
AF Grigg-Damberger, Madeleine
Ralls, Frank
TI Treatment strategies for complex behavioral insomnia in children with
neurodevelopmental disorders
SO CURRENT OPINION IN PULMONARY MEDICINE
LA English
DT Review
DE circadian rhythm; clock genes; insomnia; melatonin; neurodevelopmental
disorders
ID AUTISM SPECTRUM DISORDERS; SMITH-MAGENIS-SYNDROME; PLACEBO-CONTROLLED
TRIAL; RETT-SYNDROME; SLEEP PROBLEMS; ANGELMAN-SYNDROME;
WILLIAMS-SYNDROME; BETA(1)-ADRENERGIC ANTAGONISTS; REPETITIVE BEHAVIORS;
TYPICAL DEVELOPMENT
AB Purpose of reviewThis review describes recent research in pediatric behavioral insomnias in neurodevelopmental disorders and their treatment.Recent findingsInsomnia in children with autism spectrum disorder (ASD) and other neurodevelopmental disorders (NDDs) is typically complex, chronic, and difficult to adequately control. Abnormalities in genetic and/or epigenetic regulation of sleep/wakefulness and its timing predispose patients with NDD to insomnia, although poor sleep hygiene, maladaptive associations, and limit-setting are likely to contribute. Parents are agents for change in problematic sleep behaviors in patients with NDD. We review the benefits of behavioral therapies and melatonin to treat sleep problems in children with NDD. Problematic sleep is so prevalent in some neurodevelopmental syndromes (Rett, Angelman, Williams, and Smith-Magenis) that it is part of their diagnostic criteria.SummaryChildren and adolescents with neurological disorders frequently have complex sleep disorders that require treatment. Understanding the basic pathology and treatment strategies provides an opportunity to improve well being and quality of life in those affected by NDD and their families.
C1 [Grigg-Damberger, Madeleine] Univ New Mexico, Sch Med, Dept Neurol, Albuquerque, NM 87131 USA.
[Grigg-Damberger, Madeleine] Univ New Mexico, Med Ctr, Univ Hosp Sleep Disorders Ctr, Pediatr Sleep Med Serv, Albuquerque, NM 87131 USA.
[Grigg-Damberger, Madeleine] Univ New Mexico, Med Ctr, Clin Neurodiagnost Lab, Albuquerque, NM 87131 USA.
[Ralls, Frank] Univ New Mexico Hosp, Sleep Disorders Ctr, Dept Internal Med, Albuquerque, NM USA.
[Ralls, Frank] Univ New Mexico Hosp, Adult Sleep Med Serv, Sleep Disorders Ctr, Albuquerque, NM USA.
[Ralls, Frank] Univ New Mexico Hosp, Program Sleep Med, Sleep Disorders Ctr, Albuquerque, NM USA.
RP Grigg-Damberger, M (reprint author), One Univ New Mexico, Dept Neurol, MSC10 5620, Albuquerque, NM 87131 USA.
EM MGriggD@salud.unm.edu
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NR 87
TC 2
Z9 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1070-5287
EI 1531-6971
J9 CURR OPIN PULM MED
JI Curr. Opin. Pulm. Med.
PD NOV
PY 2013
VL 19
IS 6
BP 616
EP 625
DI 10.1097/MCP.0b013e328365ab89
PG 10
WC Respiratory System
SC Respiratory System
GA 247FW
UT WOS:000326602900005
PM 24055857
ER
PT J
AU Karanth, P
Chandhok, T
AF Karanth, Prathibha
Chandhok, Tanushree Saxena
TI Impact of Early Intervention on Children with Autism Spectrum Disorders
as Measured by Inclusion and Retention in Mainstream Schools
SO INDIAN JOURNAL OF PEDIATRICS
LA English
DT Article
DE Autism; Early intervention; Impact; Mainstreaming
ID YOUNG-CHILDREN
AB To follow up the school/educational status of children with a primary diagnosis of Autism Spectrum Disorders (ASD), who had been enrolled in an Early Intervention (EI) program for 1-3 y, before the age of 6.
Data was collected through a questionnaire covering three specific areas-the families' success in following the recommendation given on completion of the EI program, issues in schooling and feedback on the EI program. The contact modes included email, post, telephonic interviews and face-to-face interviews.
One hundred and two of the 296 children responded to the questionnaire. The responses were analyzed to identify, the number of families who had completed the program and were able to follow through with the recommendation given on completion of the EI program, difficulties faced if any, family feedback on the program and the additional help that they would have liked to receive. The reasons for failure to comply with the recommendations were analyzed. Of the 102 children who responded seven had dropped out midway through the program and 10 had discontinued after one year. Of the remaining 85 who completed the program, 71 were advised mainstreaming (83.5 %) and 14 were advised special school (16.5 %). Sixty-five of the 71 children, who were advised to enroll their child in the mainstream, were in regular school. 76.5 % of the children who completed the EI program were integrated in regular schools, 2 to 7 y after having completed the program.
EI helps in enrolment and retention of substantial numbers of children with ASD in mainstream schools.
C1 [Karanth, Prathibha; Chandhok, Tanushree Saxena] Com DEALL Trust, Dept Speech Language Pathol, Bangalore 560084, Karnataka, India.
RP Karanth, P (reprint author), Com DEALL Trust, Dept Speech Language Pathol, 47 Hutchins Rd II Cross, Bangalore 560084, Karnataka, India.
EM communicationdeall@gmail.com
FU Navajbai Ratan Tata Trust
FX The authors would like to thank Navajbai Ratan Tata Trust for providing
the financial support to employ a research assistant for this study.
They would like to thank Lathina Lawrence who served as the Research
Assistant for collection of data, Dr Subbakrishna for guidance in
statistical analysis and all of the staff of Com DEALL at Bangalore-past
and present for their contribution to the success of the children.
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NR 14
TC 0
Z9 0
PU ALL INDIA INST MEDICAL SCIENCES
PI NEW DELHI
PA ANSARI NAGAR, NEW DELHI 110 029, INDIA
SN 0019-5456
EI 0973-7693
J9 INDIAN J PEDIATR
JI Indian J. Pediatr.
PD NOV
PY 2013
VL 80
IS 11
BP 911
EP 919
DI 10.1007/s12098-013-1014-y
PG 9
WC Pediatrics
SC Pediatrics
GA 244GY
UT WOS:000326376900006
PM 23686797
ER
PT J
AU Yi, L
Pan, JH
Fan, YB
Zou, XB
Wang, XM
Lee, K
AF Yi, Li
Pan, Junhao
Fan, Yuebo
Zou, Xiaobing
Wang, Xianmai
Lee, Kang
TI Children with autism spectrum disorder are more trusting than typically
developing children
SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY
LA English
DT Article
DE Autism spectrum disorder; Trust Distrust; Deception; Selective trust;
Children; Development
ID OF-MIND DEVELOPMENT; FALSE-BELIEF; MENTAL MODELS; DECEPTION; ABILITY;
BEHAVIOR; PRESCHOOLERS; METAANALYSIS; INDIVIDUALS; DEAFNESS
AB The current study examined whether children with autism spectrum disorder (ASD) had an indiscriminate trust bias whereby they would believe any information provided by an unfamiliar adult with whom they had no interactive history. Young school-aged children with ASD and their age- and ability-matched typically developing (TD) peers participated in a simple hide-and-seek game. In the game, an experimenter with whom the children had no previous interactive history pointed to or left a marker on a box to indicate the whereabouts of a hidden reward. Results showed that although young school-aged ASD children did not blindly trust any information provided by the unfamiliar adult, they appeared to be more trusting in the adult informant than did their age- and ability-matched TO children. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Yi, Li; Pan, Junhao] Sun Yat Sen Univ, Dept Psychol, Guangzhou 510275, Guangdong, Peoples R China.
[Fan, Yuebo] Guangzhou Cana Sch, Guangzhou 510540, Guangdong, Peoples R China.
[Fan, Yuebo] Guangzhou Rehabil & Res Ctr Children ASD, Guangzhou 510540, Guangdong, Peoples R China.
[Zou, Xiaobing] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China.
[Wang, Xianmai] Jinan Univ, Sch Management, Guangzhou 510632, Guangdong, Peoples R China.
[Lee, Kang] Univ Toronto, Dr Eric Jackman Inst Child Study, Toronto, ON M5R 2X2, Canada.
[Lee, Kang] Univ Calif San Diego, Dept Psychol, La Jolla, CA 92093 USA.
RP Yi, L (reprint author), Sun Yat Sen Univ, Dept Psychol, 135 Xingang West Rd, Guangzhou 510275, Guangdong, Peoples R China.
EM yili5@mail.sysu.edu.cn; kang.lee@utoronto.ca
CR American Psychiatric Association, 1994, DIAGNOSTIC AND STATI
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NR 33
TC 1
Z9 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0022-0965
EI 1096-0457
J9 J EXP CHILD PSYCHOL
JI J. Exp. Child Psychol.
PD NOV
PY 2013
VL 116
IS 3
BP 755
EP 761
DI 10.1016/j.jecp.2013.05.005
PG 7
WC Psychology, Developmental; Psychology, Experimental
SC Psychology
GA 243KP
UT WOS:000326315600014
PM 23810631
ER
PT J
AU Pinto, WBVD
Pedroso, JL
de Souza, PVS
Oliveira, ASB
Barsottini, OGP
AF Vieira de Rezende Pinto, Wladimir Bocca
Pedroso, Jose Luiz
Sgobbi de Souza, Paulo Victor
Bulle Oliveira, Acary Souza
Povoas Barsottini, Orlando Graziani
TI Phelan-McDermid syndrome presenting with autistic spectrum: are we
underdiagnosing chromosomal diseases in patients with autism?
SO JOURNAL OF NEUROLOGY
LA English
DT Letter
ID 22Q13 DELETION SYNDROME; DISORDERS; SPEECH; DELAY
C1 [Vieira de Rezende Pinto, Wladimir Bocca; Pedroso, Jose Luiz; Sgobbi de Souza, Paulo Victor; Bulle Oliveira, Acary Souza; Povoas Barsottini, Orlando Graziani] Univ Fed Sao Paulo, Dept Neurol, Sao Paulo, Brazil.
RP Pinto, WBVD (reprint author), Univ Fed Sao Paulo, Dept Neurol, Botucatu St,740,Vila Clementino, Sao Paulo, Brazil.
EM wladimirbvrpinto@gmail.com
RI Barsottini, O/E-9117-2010; Pedroso, Jose/F-1757-2013; Souza, Paulo
Victor Sgobbi /N-2958-2014; Pinto, Wladimir/J-6555-2014
OI Souza, Paulo Victor Sgobbi /0000-0002-7416-7108; Pinto,
Wladimir/0000-0002-0150-525X
CR Cusmano-Ozog K, 2007, AM J MED GENET C, V145C, P393, DOI 10.1002/ajmg.c.30155
Leung Alexander K C, 2007, J Pediatr Health Care, V21, P108, DOI 10.1016/j.pedhc.2006.05.004
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Phelan MC, 2008, ORPHANET J RARE DIS, V3, DOI 10.1186/1750-1172-3-14
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Verhoeven WMA, 2013, AM J MED GENET A, V161A, P158, DOI 10.1002/ajmg.a.35597
Zafeiriou DI, 2013, AM J MED GENET B, V162B, P327, DOI 10.1002/ajmg.b.32152
NR 12
TC 0
Z9 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-5354
EI 1432-1459
J9 J NEUROL
JI J. Neurol.
PD NOV
PY 2013
VL 260
IS 11
BP 2900
EP 2902
DI 10.1007/s00415-013-7127-4
PG 3
WC Clinical Neurology
SC Neurosciences & Neurology
GA 244PF
UT WOS:000326400800028
ER
PT J
AU Knapp, C
Woodworth, L
Fernandez-Baca, D
Baron-Lee, J
Thompson, L
Hinojosa, M
AF Knapp, Caprice
Woodworth, Lindsey
Fernandez-Baca, Daniel
Baron-Lee, Jacqueline
Thompson, Lindsay
Hinojosa, Melanie
TI Factors Associated with a Patient-Centered Medical Home Among Children
with Behavioral Health Conditions
SO MATERNAL AND CHILD HEALTH JOURNAL
LA English
DT Article
DE ADHD; Autism; Depression; Medical home; Child health outcomes; Survey
ID UNITED-STATES; ACCESS; CARE; SERVICES; DISPARITIES; INSURANCE
AB At some point in their lives, nearly one-half of all American children will have a behavioral health condition. Many will not receive the care they need from a fragmented health delivery system. The patient-centered medical home is a promising model to improve their care; however, little evidence exists. Our study aim was to examine the association between several behavioral health indicators and having a patient-centered medical home. 91,642 children's parents or guardians completed the 2007 National Survey of Children's Health. An indicator for patient-centered medical home was included in the dataset. Descriptive statistics, bivariate tests, and multivariate regression models were used in the analyses. Children in the sample were mostly Male (52 %), White (78 %), non-Hispanic (87 %), and did not have a special health care need (80 %). 6.2 % of the sample had at least one behavioral health condition. Conditions ranged from ADHD (6 %) to Autism Spectrum Disorder (ASD) (1 %). Frequency of having a patient-centered medical home also varied for children with a behavioral health condition (49 % of children with ADHD and 33 % of children with ASD). Frequency of having a patient-centered medical home decreased with multiple behavioral health conditions. Higher severity of depression, anxiety, and conduct disorder were associated with a decreased likelihood of a patient-centered medical home. Results from our study can be used to target patient-centered medical home interventions toward children with one or more behavioral health conditions and consider that children with depression, anxiety, and conduct disorder are more vulnerable to these disparities.
C1 [Knapp, Caprice; Woodworth, Lindsey; Fernandez-Baca, Daniel; Baron-Lee, Jacqueline; Hinojosa, Melanie] Univ Florida, Dept Hlth Outcomes & Policy, Gainesville, FL 32610 USA.
[Thompson, Lindsay] Univ Florida, Dept Pediat, Gainesville, FL USA.
RP Knapp, C (reprint author), Univ Florida, Dept Hlth Outcomes & Policy, 1329 SW 16th St, Gainesville, FL 32610 USA.
EM caprice1@ufl.edu
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Merikangas KR, 2010, PEDIATRICS, V125, P75
National Survey of Children's Health, 2007, METH REP NAT SURV CH
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NR 13
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1092-7875
EI 1573-6628
J9 MATERN CHILD HLTH J
JI Matern. Child Health J.
PD NOV
PY 2013
VL 17
IS 9
BP 1658
EP 1664
DI 10.1007/s10995-012-1179-4
PG 7
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 243EJ
UT WOS:000326299300016
PM 23108741
ER
PT J
AU Schafer, G
Williams, TI
Smith, PT
AF Schafer, Graham
Williams, Tim I.
Smith, Philip T.
TI Which Words are Hard for Autistic Children to Learn?
SO MIND & LANGUAGE
LA English
DT Article
ID COMMUNICATIVE DEVELOPMENT INVENTORY; SPECTRUM DISORDERS;
ASPERGERS-SYNDROME; INFANTILE-AUTISM; LANGUAGE-DEVELOPMENT; FREE-RECALL;
COMPREHENSION; VOCABULARY; ACQUISITION; CATEGORIZATION
AB Motivated by accounts of concept use in autistic spectrum disorder (ASD) and a computational model of weak central coherence (O'Loughlin and Thagard, 2000) we examined comprehension and production vocabulary in typically-developing children and those with ASD and Down syndrome (DS). Controlling for frequency, familiarity, length and imageability, Colorado Meaningfulness played a hitherto unremarked role in the vocabularies of children with ASD. High Colorado Meaningful words were underrepresented in the comprehension vocabularies of 2- to 12-year-olds with ASD. The Colorado Meaningfulness of a word is a measure of how many words can be associated with it. Situations in which high Colorado Meaningfulness words are encountered are typically highly variable, and words with High Colorado Meaningfulness often involve extensive use of context. Our data suggest that the number of contexts in which a particular word can appear has a role in determining vocabulary in ASD. This suggestion is consistent with the weak central coherence theory of autism.
C1 [Schafer, Graham; Williams, Tim I.; Smith, Philip T.] Univ Reading, Dept Psychol, Reading RG6 6AL, Berks, England.
RP Schafer, G (reprint author), Univ Reading, Dept Psychol, Reading RG6 6AL, Berks, England.
EM g.w.schafer@reading.ac.uk
RI Williams, Timothy/D-3512-2011
OI Williams, Timothy/0000-0003-0072-3316
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NR 64
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0268-1064
EI 1468-0017
J9 MIND LANG
JI Mind Lang.
PD NOV
PY 2013
VL 28
IS 5
BP 661
EP 698
DI 10.1111/mila.12038
PG 38
WC Linguistics; Psychology, Experimental
SC Linguistics; Psychology
GA 244LK
UT WOS:000326389700004
ER
PT J
AU Schaaf, CP
Gonzalez-Garay, ML
Xia, F
Potocki, L
Gripp, KW
Zhang, BL
Peters, BA
McElwain, MA
Drmanac, R
Beaudet, AL
Caskey, CT
Yang, YP
AF Schaaf, Christian P.
Gonzalez-Garay, Manuel L.
Xia, Fan
Potocki, Lorraine
Gripp, Karen W.
Zhang, Baili
Peters, Brock A.
McElwain, Mark A.
Drmanac, Radoje
Beaudet, Arthur L.
Caskey, C. Thomas
Yang, Yaping
TI Truncating mutations of MAGEL2 cause Prader-Willi phenotypes and autism
SO NATURE GENETICS
LA English
DT Article
ID DE-NOVO MUTATIONS; SPECTRUM DISORDERS; GENE; DELETION; CLUSTER; MODELS
AB Prader-Willi syndrome (PWS) is caused by the absence of paternally expressed, maternally silenced genes at 15q11-q13. We report four individuals with truncating mutations on the paternal allele of MAGEL2, a gene within the PWS domain. The first subject was ascertained by whole-genome sequencing analysis for PWS features. Three additional subjects were identified by reviewing the results of exome sequencing of 1,248 cases in a clinical laboratory. All four subjects had autism spectrum disorder (ASD), intellectual disability and a varying degree of clinical and behavioral features of PWS. These findings suggest that MAGEL2 is a new gene causing complex ASD and that MAGEL2 loss of function can contribute to several aspects of the PWS phenotype.
C1 [Schaaf, Christian P.; Xia, Fan; Potocki, Lorraine; Zhang, Baili; Beaudet, Arthur L.; Caskey, C. Thomas; Yang, Yaping] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
[Schaaf, Christian P.] Texas Childrens Hosp, Jan & Dan Duncan Neurol Res Inst, Houston, TX 77030 USA.
[Gonzalez-Garay, Manuel L.] Univ Texas Hlth Sci Ctr Houston, Brown Fdn Inst Mol Med Prevent Human Dis, Houston, TX 77030 USA.
[Gripp, Karen W.] Alfred I duPont Hosp Children, Div Med Genet, Wilmington, DC USA.
[Peters, Brock A.; McElwain, Mark A.; Drmanac, Radoje] Complete Genom Inc, Mountain View, CA USA.
RP Schaaf, CP (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
EM schaaf@bcm.edu; manuel.l.gonzalezgaray@uth.tmc.edu
FU US National Institutes of Health grant [HD037283]; Joan and Stanford
Alexander family; Doris Duke Charitable Foundation; Cullen Foundation
for Higher Education; Houston Foundation
FX We are indebted to the patients and their families for their willingness
to participate in our research study. We thank P. Zimmerman and E.
Austin for clinical assistance. C.P.S. is generously supported by the
Joan and Stanford Alexander family. C.P.S. is a recipient of a Clinical
Scientist Development Award from the Doris Duke Charitable Foundation.
M.L.G.- G. and C.T.C. are generously supported by the Cullen Foundation
for Higher Education and the Houston Foundation. A.L.B. is supported by
US National Institutes of Health grant HD037283.
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NR 27
TC 13
Z9 13
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
EI 1546-1718
J9 NAT GENET
JI Nature Genet.
PD NOV
PY 2013
VL 45
IS 11
BP 1405
EP +
DI 10.1038/ng.2776
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 244JL
UT WOS:000326384100025
PM 24076603
ER
PT J
AU Smith, LN
Cowan, CW
AF Smith, Laura N.
Cowan, Christopher W.
TI Striking a balance in fragile X
SO NATURE MEDICINE
LA English
DT Editorial Material
ID MENTAL-RETARDATION; MESSENGER-RNAS; MOUSE MODEL; PROTEIN; TRANSLATION;
AUTISM
C1 [Smith, Laura N.; Cowan, Christopher W.] Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat, Belmont, MA USA.
RP Smith, LN (reprint author), Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat, Belmont, MA USA.
EM cwcowan@mclean.harvard.edu
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PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD NOV
PY 2013
VL 19
IS 11
BP 1370
EP 1371
DI 10.1038/nm.3383
PG 2
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 251IF
UT WOS:000326920300012
PM 24202383
ER
PT J
AU Udagawa, T
Farny, NG
Jakovcevski, M
Kaphzan, H
Alarcon, JM
Anilkumar, S
Ivshina, M
Hurt, JA
Nagaoka, K
Nalavadi, VC
Lorenz, LJ
Bassell, GJ
Akbarian, S
Chattarji, S
Klann, E
Richter, JD
AF Udagawa, Tsuyoshi
Farny, Natalie G.
Jakovcevski, Mira
Kaphzan, Hanoch
Alarcon, Juan Marcos
Anilkumar, Shobha
Ivshina, Maria
Hurt, Jessica A.
Nagaoka, Kentaro
Nalavadi, Vijayalaxmi C.
Lorenz, Lori J.
Bassell, Gary J.
Akbarian, Schahram
Chattarji, Sumantra
Klann, Eric
Richter, Joel D.
TI Genetic and acute CPEB1 depletion ameliorate fragile X pathophysiology
SO NATURE MEDICINE
LA English
DT Article
ID MENTAL-RETARDATION PROTEIN; XENOPUS OOCYTE MATURATION; LONG-TERM
POTENTIATION; CAMKII MESSENGER-RNA; T-MAZE ALTERNATION; CYTOPLASMIC
POLYADENYLATION; SYNAPTIC PLASTICITY; TRANSLATIONAL CONTROL;
WORKING-MEMORY; MOUSE MODEL
AB Fragile X syndrome (FXS), the most common cause of inherited mental retardation and autism, is caused by transcriptional silencing of FMR1, which encodes the translational repressor fragile X mental retardation protein (FMRP). FMRP and cytoplasmic polyadenylation element-binding protein (CPEB), an activator of translation, are present in neuronal dendrites, are predicted to bind many of the same mRNAs and may mediate a translational homeostasis that, when imbalanced, results in FXS. Consistent with this possibility, Fmr1(-/y); Cpeb1(-/-) double-knockout mice displayed amelioration of biochemical, morphological, electrophysiological and behavioral phenotypes associated with FXS. Acute depletion of CPEB1 in the hippocampus of adult Fmr1(-/y) mice rescued working memory deficits, demonstrating reversal of this FXS phenotype. Finally, we find that FMRP and CPEB1 balance translation at the level of polypeptide elongation. Our results suggest that disruption of translational homeostasis is causal for FXS and that the maintenance of this homeostasis by FMRP and CPEB1 is necessary for normal neurologic function.
C1 [Udagawa, Tsuyoshi; Farny, Natalie G.; Ivshina, Maria; Nagaoka, Kentaro; Lorenz, Lori J.; Richter, Joel D.] Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
[Jakovcevski, Mira; Akbarian, Schahram] Univ Massachusetts, Sch Med, Brudnik Neuropsychiat Res Inst, Dept Psychiat, Worcester, MA USA.
[Kaphzan, Hanoch; Klann, Eric] NYU, Ctr Neural Sci, New York, NY 10003 USA.
[Alarcon, Juan Marcos] Suny Downstate Med Ctr, Dept Pathol, Brooklyn, NY 11203 USA.
[Anilkumar, Shobha; Chattarji, Sumantra] Inst Stem Cell Biol & Regenerat Med, Ctr Brain Dev & Repair, Bangalore, Karnataka, India.
[Anilkumar, Shobha; Chattarji, Sumantra] Natl Ctr Biol Sci, Bangalore, Karnataka, India.
[Hurt, Jessica A.] MIT, Dept Biol, Cambridge, MA USA.
[Nalavadi, Vijayalaxmi C.; Bassell, Gary J.] Emory Univ, Sch Med, Dept Cell Biol, Atlanta, GA USA.
RP Richter, JD (reprint author), Univ Massachusetts, Sch Med, Program Mol Med, Worcester, MA 01605 USA.
EM joel.richter@umassmed.edu
RI Nagaoka, Kentaro/C-2019-2013
OI Nagaoka, Kentaro/0000-0003-1038-1380
FU FRAXA Research Foundation; US National Institutes of Health NRSA
[F32GM095060]; NIH [GM46779, NS079415, MH086509]
FX We thank N. Dawra for technical assistance, P. Lombroso (Yale
University) and C. Proud (University of Southampton) for kind gifts of
antibodies (STEP and eEF2, respectively), J. Pelletier (McGill
University) for the kind gift of hippuristanol and members of the
Richter lab for helpful discussions. T.U. and N.G.F. gratefully
acknowledge fellowships from the FRAXA Research Foundation. J.A.H. was
supported by US National Institutes of Health NRSA Postdoctoral
Fellowship F32GM095060. This work was supported by NIH grants GM46779
and NS079415 to J.D.R. and MH086509 to S. Akbarian.
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TC 12
Z9 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1078-8956
EI 1546-170X
J9 NAT MED
JI Nat. Med.
PD NOV
PY 2013
VL 19
IS 11
BP 1473
EP +
DI 10.1038/nm.3353
PG 7
WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research &
Experimental
SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental
Medicine
GA 251IF
UT WOS:000326920300024
PM 24141422
ER
PT J
AU von Gontard, A
AF von Gontard, Alexander
TI Urinary incontinence in children with special needs
SO NATURE REVIEWS UROLOGY
LA English
DT Article
ID DEFICIT-HYPERACTIVITY DISORDER; SPINAL MUSCULAR-ATROPHY;
FRAGILE-X-SYNDROME; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER;
PRADER-WILLI-SYNDROME; NOCTURNAL ENURESIS; ELIMINATION DISORDERS;
RETT-SYNDROME; VELOCARDIOFACIAL SYNDROME; LEARNING-DISABILITIES
AB Nocturnal enuresis, daytime urinary incontinence, lower urinary tract symptoms and faecal incontinence are more common in children with special needs than in typically developing children. Children with intellectual disability, which can be attributed to a range of causes, are particularly affected. Indeed, the epidemiological and clinical studies conducted to date show clear associations that children with special needs have higher rates of urinary (and faecal) incontinence than children without development, physical or cognitive impairments. For example, low intelligence quotient (IQ)-associated physical disability and conditions such as Fragile X and Rett syndromes increase the risk for incontinence, which can persist into adulthood if left untreated. Although the association of attention deficit hyperactivity disorder and incontinence has been shown in many studies, further research is needed on other specific disorders, such as autism. As many children are not receiving adequate care, specific multimodal treatments based on rigorous assessment of the incontinence, underlying condition and associated comorbid disorders should be actively offered.
C1 Saarland Univ Hosp, Dept Child & Adolescent Psychiat, D-66421 Homburg, Germany.
RP von Gontard, A (reprint author), Saarland Univ Hosp, Dept Child & Adolescent Psychiat, D-66421 Homburg, Germany.
EM alexander.von.gontard@uks.eu
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NR 68
TC 2
Z9 2
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1759-4812
EI 1759-4820
J9 NAT REV UROL
JI Nat. Rev. Urol.
PD NOV
PY 2013
VL 10
IS 11
BP 667
EP 674
DI 10.1038/nrurol.2013.213
PG 8
WC Urology & Nephrology
SC Urology & Nephrology
GA 247PS
UT WOS:000326631700013
PM 24080904
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PT J
AU Frith, U
AF Frith, Uta
TI Autism and Dyslexia: A Glance Over 25 Years of Research
SO PERSPECTIVES ON PSYCHOLOGICAL SCIENCE
LA English
DT Article
DE developmental disorders; Asperger syndrome; cognitive neuroscience
ID ASPERGER-SYNDROME; LECTURE
AB Autism and dyslexia are wrongly classified as childhood disorders: They are lifelong and therefore have to be studied in adults as well as in children. Individual variability is enormous, and, as a result, behavioral diagnosis remains problematic. The study of the underlying cognitive abilities in autism and dyslexia has acted as a gateway for the emergence of developmental cognitive neuroscience.
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[Frith, Uta] Univ Aarhus, Ctr Funct Integrat Neurosci, DK-8000 Aarhus C, Denmark.
RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England.
EM u.frith@ucl.ac.uk
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Penn, DL
Perkins, D
Woods, SW
Addington, J
AF Healey, Kristin M.
Penn, David L.
Perkins, Diana
Woods, Scott W.
Addington, Jean
TI Theory of mind and social judgments in people at clinical high risk of
psychosis
SO SCHIZOPHRENIA RESEARCH
LA English
DT Article
DE Clinical high risk; Schizophrenia; Social cognition; Theory of mind;
Social judgments; Longitudinal study
ID ULTRA-HIGH-RISK; HIGH-FUNCTIONING AUTISM; PERSECUTORY DELUSIONS;
SCHIZOPHRENIA; COGNITION; INDIVIDUALS; PREDICTORS; RELATIVES; AMYGDALA
AB Background: Social cognitive deficits are consistently reported in psychotic populations. Few studies have longitudinally investigated social cognition in clinical high-risk (CHR) populations.
Aims: Longitudinally examine theory of mind (ToM) and social judgments in a CHR sample to investigate the stability of performance over time and potential ability to predict conversion to psychosis.
Method: 147 CHR individuals and 85 help seeking controls (HSC) were assessed for up to 2 years; 28 participants developed psychosis across both groups. Generalized linear mixed models for repeated measures were used to examine change over time for ratings on the three social cognitive indices of ToM, trustworthiness, and approachability. Hierarchical regression was used to test whether social cognitive variables explain more variance in conversion than IQ.
Results: CHR individuals showed a positive bias in approachability judgments over time compared to HSC. Baseline ToM performance significantly (p < .05) predicted later conversion beyond IQ scores. These results were attenuated when controlling for baseline symptom level.
Conclusions: Although ToM deficits might predate conversion to psychosis, one must consider initial symptoms as well. Social judgments were not associated with conversion to schizophrenia. (C) 2013 Elsevier B. V. All rights reserved.
C1 [Healey, Kristin M.; Penn, David L.] Univ N Carolina, Dept Psychol, Chapel Hill, NC 27599 USA.
[Perkins, Diana] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA.
[Woods, Scott W.] Yale Univ, Dept Psychiat, New Haven, CT 06520 USA.
[Addington, Jean] Univ Calgary, Fac Med, Dept Psychiat, Calgary, AB, Canada.
RP Penn, DL (reprint author), Univ N Carolina, Dept Psychol, 250 Davie Hall, Chapel Hill, NC 27599 USA.
EM kmhealey@email.unc.edu; dpenn@email.unc.edu; diana_perkins@unc.edu;
scott.woods@yale.edu; jmadding@ucalgary.ca
FU NIMH [U01U01MH066134-02, U01 MH066069-04, U01MH066160]
FX This study was supported by the following NIMH grants: U01U01MH066134-02
to J. Addington, U01 MH066069-04 to D. Perkins, and U01MH066160 to S.
Woods.
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Wechsler D, 1997, WECHSLER ADULT INTEL, P3
NR 36
TC 2
Z9 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0920-9964
EI 1573-2509
J9 SCHIZOPHR RES
JI Schizophr. Res.
PD NOV
PY 2013
VL 150
IS 2-3
BP 498
EP 504
DI 10.1016/j.schres.2013.08.038
PG 7
WC Psychiatry
SC Psychiatry
GA 241PY
UT WOS:000326180700028
PM 24055202
ER
PT J
AU Shaw, CA
Li, Y
Tomljenovic, L
AF Shaw, C. A.
Li, Y.
Tomljenovic, L.
TI Administration of aluminium to neonatal mice in vaccine-relevant amounts
is associated with adverse long term neurological outcomes
SO JOURNAL OF INORGANIC BIOCHEMISTRY
LA English
DT Article
DE Autism; Aluminium; Adjuvants; Vaccines; Neurotoxicity;
Neurodevelopmental disorders
ID AUTISM SPECTRUM DISORDERS; CHRONIC-FATIGUE-SYNDROME; HEPATITIS-B
VACCINATION; MACROPHAGIC MYOFASCIITIS; ALZHEIMERS-DISEASE; IMMUNE
CHALLENGE; ADJUVANTS; INFLAMMASOME; AUTOIMMUNITY; PREVALENCE
AB Our previous ecological studies of autism spectrum disorder (ASD) has demonstrated a correlation between increasing ASD rates and aluminium (Al) adjuvants in common use in paediatric vaccines in several Western countries. The correlation between ASD rate and Al adjuvant amounts appears to be dose-dependent and satisfies 8 of 9 Hill criteria for causality. We have now sought to provide an animal model to explore potential behavioural phenotypes and central nervous system (CNS) alterations using s.c. injections of Al hydroxide in early postnatal CD-1 mice of both sexes. Injections of a "high" and "low" Al adjuvant levels were designed to correlate to either the U.S. or Scandinavian paediatric vaccine schedules vs. control saline-injected mice. Both male and female mice in the "high Al" group showed significant weight gains following treatment up to sacrifice at 6 months of age. Male mice in the "high Al" group showed significant changes in light-dark box tests and in various measures of behaviour in an open field. Female mice showed significant changes in the light-dark box at both doses, but no significant changes in open field behaviours. These current data implicate Al injected in early postnatal life in some CNS alterations that may be relevant for a better understanding of the aetiology of ASD. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Shaw, C. A.; Li, Y.; Tomljenovic, L.] Univ British Columbia, Dept Ophthalmol & Visual Sci, Vancouver, BC V5Z 1M9, Canada.
[Shaw, C. A.] Univ British Columbia, Program Expt Med, Vancouver, BC V5Z 1M9, Canada.
[Shaw, C. A.] Univ British Columbia, Program Neurosci, Vancouver, BC V5Z 1M9, Canada.
RP Shaw, CA (reprint author), Neural Dynam Res Grp, 828 W 10th Ave, Vancouver, BC V5Z1L8, Canada.
EM cashawlab@gmail.com
FU Dwoskin Family Foundation; Katlyn Fox Foundation
FX The authors thank the Dwoskin Family Foundation and the Katlyn Fox
Foundation for their financial support. We are also grateful to Agripina
Suarez and other laboratory members for their assistance.
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NR 89
TC 7
Z9 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0162-0134
EI 1873-3344
J9 J INORG BIOCHEM
JI J. Inorg. Biochem.
PD NOV
PY 2013
VL 128
SI SI
BP 237
EP 244
DI 10.1016/j.jinorgbio.2013.07.022
PG 8
WC Biochemistry & Molecular Biology; Chemistry, Inorganic & Nuclear
SC Biochemistry & Molecular Biology; Chemistry
GA 239YB
UT WOS:000326060800030
PM 23932735
ER
PT J
AU Gogolinska, A
Nowak, W
AF Gogolinska, Anna
Nowak, Wieslaw
TI Molecular basis of lateral force spectroscopy nano-diagnostics:
computational unbinding of autism related chemokine MCP-1 from IgG
antibody
SO JOURNAL OF MOLECULAR MODELING
LA English
DT Article
DE Atomic force microscopy; Bionanomechanics; IgG antibody;
Monocyte-chemoatractant protein-1; Steered molecular dynamics
ID CHEMOATTRACTANT PROTEIN-1 MCP-1; MONOCYTE CHEMOATTRACTANT; RECOGNITION
EVENTS; ALIGNMENT EDITOR; MICROSCOPY; DYNAMICS; ELECTROSTATICS; PDB2PQR;
BRAIN; CCR2
AB Monocyte-chemoattractant protein-1 (MCP-1), also known as CCL2, is a potent chemoattractant of T cells and monocytes, involved in inflammatory and angio-proliferative brain and retinal diseases. Higher expression of MCP-1 is observed in metastatic tumors. Unusual levels of MCP-1 in the brain may be correlated with autism. Immunochemistry where atomic force microscope (AFM) tips functionalized with appropriate antibodies against MCP-1 are used could in principle support medical diagnostics. Useful signals from single molecule experiments may be generated if interaction forces are large enough. The chemokine-antibody unbinding force depends on a relative motion of the interacting fragments of the complex. In this paper the stability of the medically important MCP-1- immunoglobulin G antibody Fab fragment complex has been studied using steered molecular dynamics (SMD) computer simulations with the aim to model possible arrangements of nano-diagnostics experiments. Using SMD we confirm that molecular recognition in MCP1-IgG is based mainly on six pairs of residues: Glu39A - Arg98H, Lys56A - Asp52H, Asp65A - Arg32L, Asp68A - Arg32L, Thr32A - Glu55L, Gln61A - Tyr33H. The minimum external force required for mechanical dissociation of the complex depends on a direction of the force. The pulling of the MCP-1 antigen in the directions parallel to the antigen-antibody contact plane requires forces about 20 %-40 % lower than in the perpendicular one. Fortunately, these values are large enough that the fast lateral force spectroscopy may be used for effective nano-diagnostics purposes. We show that molecular modeling is a useful tool in planning AFM force spectroscopy experiments.
C1 [Gogolinska, Anna; Nowak, Wieslaw] Nicholas Copernicus Univ, Fac Phys Astron & Informat, PL-87100 Torun, Poland.
[Gogolinska, Anna] Nicholas Copernicus Univ, Fac Math & Comp Sci, PL-87100 Torun, Poland.
[Nowak, Wieslaw] Inst Fizyki UMK, PL-87100 Torun, Poland.
RP Nowak, W (reprint author), Inst Fizyki UMK, Ul Grudziadzka 5, PL-87100 Torun, Poland.
EM wiesiek@fizyka.umk.pl
FU Polish Funds for Science [N519 578138, N202 262038]
FX This work was supported by Polish Funds for Science - grant no. N519
578138 and grant no. N202 262038.
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NR 52
TC 1
Z9 1
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1610-2940
EI 0948-5023
J9 J MOL MODEL
JI J. Mol. Model.
PD NOV
PY 2013
VL 19
IS 11
BP 4773
EP 4780
DI 10.1007/s00894-013-1972-z
PG 8
WC Biochemistry & Molecular Biology; Biophysics; Chemistry,
Multidisciplinary; Computer Science, Interdisciplinary Applications
SC Biochemistry & Molecular Biology; Biophysics; Chemistry; Computer
Science
GA 241UH
UT WOS:000326193200017
PM 24061853
ER
PT J
AU Helander, A
Stodberg, T
Jaeken, J
Matthijs, G
Eriksson, M
Eggertsen, G
AF Helander, Anders
Stodberg, Tommy
Jaeken, Jaak
Matthijs, Gert
Eriksson, Maud
Eggertsen, Gosta
TI Dolichol kinase deficiency (DOLK-CDG) with a purely neurological
presentation caused by a novel mutation
SO MOLECULAR GENETICS AND METABOLISM
LA English
DT Article
DE Congenital disorder of glycosylation; Dolichol kinase; DOLK-CDG;
Transferrin glycosylation; Carbohydrate-deficient transferrin
ID CAPILLARY-ZONE-ELECTROPHORESIS; CONGENITAL DISORDERS; SERUM TRANSFERRIN;
GLYCOSYLATION; DIAGNOSIS
AB A 4-month old boy presented with multiple epileptic seizure types including West syndrome. Screening for infectious and structural etiologies showed normal results. A metabolic investigation was undertaken to investigate the cause of his neurological disease.
Screening for congenital disorders of glycosylation (CDG) by HPLC analysis of serum carbohydrate-deficient transferrin (CDT) showed a type 1 pattern with 18% disialotransferrin (reference < 2%) and 2% asialotransferrin (reference 0). An undiagnosed 10-year old sister with a similar clinical history with infantile spasms at age 4 months, intellectual disability and an autism spectrum disorder, also showed a type 1 CDT pattern. Both siblings lacked dysmorphic features and extra-cerebral symptoms. The boy had cytotoxic edema of the thalamus and mesencephalon on MRI at age 7 months, whereas the girl had normal MM at age 8 months. Phosphomannomutase (PMM) and phosphomannose isomerase (MPI) activities in cultured fibroblasts were normal, excluding PMM2-CDG and MPI-CDG. Fibroblast lipid-linked oligosaccharide analysis was also normal, suggesting an early defect in glycan assembly. Sequence analysis of the dolichol kinase gene revealed a homozygous new missense mutation (p.M1?; c.2 T>C) in both siblings.
In conclusion, two siblings were demonstrated to suffer from DOLK-CDG (MIM 610768) and to be homozygous for a new mutation. They presented with West syndrome and so far show a purely neurological phenotype. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Helander, Anders; Eggertsen, Gosta] Karolinska Inst, Dept Lab Med, Stockholm, Sweden.
[Helander, Anders; Eggertsen, Gosta] Karolinska Univ Lab, SE-14186 Stockholm, Sweden.
[Stodberg, Tommy; Eriksson, Maud] Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Neuropediat Unit, Stockholm, Sweden.
[Jaeken, Jaak] Univ Hosp Gasthuisberg, Ctr Metabol Dis, B-3000 Louvain, Belgium.
[Matthijs, Gert] Univ Hosp Gasthuisberg, Ctr Human Genet, B-3000 Louvain, Belgium.
RP Helander, A (reprint author), Karolinska Univ Lab, C1-74, SE-14186 Stockholm, Sweden.
EM anders.helander@ki.se
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NR 21
TC 3
Z9 3
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1096-7192
EI 1096-7206
J9 MOL GENET METAB
JI Mol. Genet. Metab.
PD NOV
PY 2013
VL 110
IS 3
BP 342
EP 344
DI 10.1016/j.ymgme.2013.07.002
PG 3
WC Biochemistry & Molecular Biology; Genetics & Heredity; Medicine,
Research & Experimental
SC Biochemistry & Molecular Biology; Genetics & Heredity; Research &
Experimental Medicine
GA 239WZ
UT WOS:000326058000023
PM 23890587
ER
PT J
AU Ruiz-Robledillo, N
Moya-Albiol, L
AF Ruiz-Robledillo, N.
Moya-Albiol, L.
TI Self-reported health and cortisol awakening response in parents of
people with asperger syndrome: The role of trait anger and anxiety,
coping and burden
SO PSYCHOLOGY & HEALTH
LA English
DT Article
DE family caregivers; ASPERGER syndrome; health; cortisol awakening
response
ID AUTISM SPECTRUM DISORDER; QUALITY-OF-LIFE; SALIVARY CORTISOL; SOCIAL
SUPPORT; DEPRESSIVE SYMPTOMS; BEHAVIORAL-PROBLEMS; PERCEIVED STRESS;
CHILDREN; CAREGIVERS; STRATEGIES
AB Caring for offspring with autism spectrum disorders entails high levels of stress for a long period of time and is associated with several types of health complaints. Few studies have focused on specific effects of particular disorders in the spectrum. This study was carried out with the aim of evaluating the global health of parents of people with Asperger syndrome (N=53) compared to those of typically developing children (N=54) through self-reported measures (medication consumption and somatic symptoms) and biological markers (cortisol awakening response [CAR]). Additionally, we analysed various psychological variables as potential predictors of caregiver health. We found that caregivers take more medication and have worse self-reported health than controls, but there were no significant differences in CAR between the groups. However, after controlling for negative affect, differences between groups in CAR reached significance. With regards to predictor variables, anxiety trait, cognitive-coping style, burden and anger temperament were significantly associated with caregiver's self-reported health. These findings underline the need to develop interventions that foster improvements in the health of caregivers, reduce their burden and enhance their quality of life.
C1 [Ruiz-Robledillo, N.; Moya-Albiol, L.] Univ Valencia, Fac Psychol, Dept Psychobiol, Valencia, Spain.
RP Moya-Albiol, L (reprint author), Univ Valencia, Fac Psychol, Dept Psychobiol, Valencia, Spain.
EM Luis.Moya@uv.es
RI Moya-Albiol, Luis/C-6078-2011
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NR 60
TC 5
Z9 5
PU TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND
SN 0887-0446
EI 1476-8321
J9 PSYCHOL HEALTH
JI Psychol. Health
PD NOV 1
PY 2013
VL 28
IS 11
BP 1246
EP 1264
DI 10.1080/08870446.2013.800517
PG 19
WC Public, Environmental & Occupational Health; Psychology,
Multidisciplinary
SC Public, Environmental & Occupational Health; Psychology
GA 242DU
UT WOS:000326218400002
PM 23713979
ER
PT J
AU Mason, RA
Davis, HS
Boles, MB
Goodwyn, F
AF Mason, Rose A.
Davis, Heather S.
Boles, Margot B.
Goodwyn, Fara
TI Efficacy of Point-of-View Video Modeling: A Meta-Analysis
SO REMEDIAL AND SPECIAL EDUCATION
LA English
DT Article
DE autism; exceptionalities; meta-analysis; research methodology; video
modeling; point-of-view modeling; developmental disabilities
ID AUTISM SPECTRUM DISORDERS; DAILY LIVING SKILLS; SINGLE-CASE-RESEARCH;
MODERATE INTELLECTUAL DISABILITIES; DEVELOPMENTAL-DISABILITIES;
QUANTITATIVE SYNTHESIS; CONFIDENCE-INTERVALS; SUBJECT RESEARCH;
THE-LITERATURE; STUDENTS
AB Point-of-view video modeling (POV), a variation of video-based modeling interventions, involves creating a video exemplar from a first-person perspective. The advantage is a significant reduction in extraneous stimuli, as well as increased efficiency in production. However, the lack of systematic analysis to evaluate differential impact on targeted outcomes for individuals with disabilities limits the identification of the population for whom POV is most appropriate, as well as the most efficacious implementation procedure. Through meta-analysis of single-subject studies using POV to improve targeted outcomes, this study identifies differential effects of participant characteristics, implementation procedures, and targeted outcomes. Results of the systematic search reveal that POV has only been implemented with individuals with developmental disabilities or an autism spectrum disorder. Analysis yielded an overall improvement rate difference (IRD) effect size of .78 (83.4% confidence interval [CI] = [.76, .80]). Furthermore, age, disability, and implementation variables moderate outcomes. Areas of future research and implications for practice are discussed.
C1 [Mason, Rose A.] Univ Kansas, Kansas City, KS 66101 USA.
[Davis, Heather S.; Boles, Margot B.; Goodwyn, Fara] Texas A&M Univ, College Stn, TX USA.
RP Mason, RA (reprint author), Univ Kansas, Juniper Gardens Childrens Project, 444 Minnesota Ave, Kansas City, KS 66101 USA.
EM rmason519@ku.edu
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NR 60
TC 1
Z9 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0741-9325
EI 1538-4756
J9 REM SPEC EDUC
JI Remedial Spec. Educ.
PD NOV
PY 2013
VL 34
IS 6
BP 333
EP 345
DI 10.1177/0741932513486298
PG 13
WC Education, Special
SC Education & Educational Research
GA 242KR
UT WOS:000326240500002
ER
PT J
AU Mechling, LC
Ayres, KM
Foster, AL
Bryant, KJ
AF Mechling, Linda C.
Ayres, Kevin M.
Foster, Ashley L.
Bryant, Kathryn J.
TI Comparing the Effects of Commercially Available and Custom-Made Video
Prompting for Teaching Cooking Skills to High School Students With
Autism
SO REMEDIAL AND SPECIAL EDUCATION
LA English
DT Article
DE special education; classroom; life skills; curriculum; education; adults
ID DAILY LIVING SKILLS; MODERATE INTELLECTUAL DISABILITIES;
DEVELOPMENTAL-DISABILITIES; MODELING INTERVENTIONS; SPECTRUM DISORDERS;
TASK COMPLETION; YOUNG-ADULTS; INDIVIDUALS; SELF; INSTRUCTION
AB The study compared the effects of using commercially available and custom-made video prompts on the completion of cooking recipes by four high school age males with a diagnosis of autism. An adapted alternating treatments design with continuous baseline, comparison, final treatment, and best treatment condition was used to compare the two procedures. Gains were made by each participant when using both video procedures. However, results indicate that all students performed more steps independently correct when completing recipes with the custom-made video prompts during the comparison condition. During the best treatment condition, recipes initially prepared using the commercially available video prompts in the comparison condition were performed at criterion levels when completed with the custom-made videos prompts. Implications for use and development of commercial and customized video products with attention to the salient features of video prompts are presented.
C1 [Mechling, Linda C.; Foster, Ashley L.; Bryant, Kathryn J.] Univ N Carolina, Wilmington, NC 28403 USA.
[Ayres, Kevin M.] Univ Georgia, Athens, GA 30602 USA.
RP Mechling, LC (reprint author), Univ N Carolina, Dept Early Childhood & Special Educ, 601 S Coll Rd, Wilmington, NC 28403 USA.
EM mechlingl@uncw.edu
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NR 42
TC 2
Z9 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0741-9325
EI 1538-4756
J9 REM SPEC EDUC
JI Remedial Spec. Educ.
PD NOV
PY 2013
VL 34
IS 6
BP 371
EP 383
DI 10.1177/0741932513494856
PG 13
WC Education, Special
SC Education & Educational Research
GA 242KR
UT WOS:000326240500005
ER
PT J
AU Selten, JP
van der Ven, E
Rutten, BPF
Cantor-Graae, E
AF Selten, Jean-Paul
van der Ven, Elsje
Rutten, Bart P. F.
Cantor-Graae, Elizabeth
TI The Social Defeat Hypothesis of Schizophrenia: An Update
SO SCHIZOPHRENIA BULLETIN
LA English
DT Article
DE genetics; epidemiology; dopamine; social exclusion; migration;
intelligence
ID INDUCED DOPAMINE RELEASE; PSYCHOTIC-DISORDERS; RISK-FACTOR; PSYCHOMETRIC
PROPERTIES; PSYCHOLOGICAL STRESS; ETHNIC DENSITY; COHORT; METAANALYSIS;
IMMIGRANTS; MIGRATION
AB According to the social defeat (SD) hypothesis, published in 2005, long-term exposure to the experience of SD may lead to sensitization of the mesolimbic dopamine (DA) system and thereby increase the risk for schizophrenia. The hypothesis posits that SD (ie, the negative experience of being excluded from the majority group) is the common denominator of 5 major schizophrenia risk factors: urban upbringing, migration, childhood trauma, low intelligence, and drug abuse. The purpose of this update of the literature since 2005 is to answer 2 questions: (1) What is the evidence that SD explains the association between schizophrenia and these risk factors? (2) What is the evidence that SD leads to sensitization of the mesolimbic DA system? The evidence for SD as the mechanism underlying the increased risk was found to be strongest for migration and childhood trauma, while the evidence for urban upbringing, low intelligence, and drug abuse is suggestive, but insufficient. Some other findings that may support the hypothesis are the association between risk for schizophrenia and African American ethnicity, unemployment, single status, hearing impairment, autism, illiteracy, short stature, Klinefelter syndrome, and, possibly, sexual minority status. While the evidence that SD in humans leads to sensitization of the mesolimbic DA system is not sufficient, due to lack of studies, the evidence for this in animals is strong. The authors argue that the SD hypothesis provides a parsimonious and plausible explanation for a number of epidemiological findings that cannot be explained solely by genetic confounding.
C1 [Selten, Jean-Paul; van der Ven, Elsje; Rutten, Bart P. F.] Maastricht Univ, Sch Mental Hlth & Neurosci, Maastricht, Netherlands.
[Selten, Jean-Paul; van der Ven, Elsje] Rivierduinen Psychiat Inst, Leiden, Netherlands.
[Cantor-Graae, Elizabeth] Lund Univ, Sect Social Med & Global Hlth, Malmo, Sweden.
[Cantor-Graae, Elizabeth] Lund Univ, Skane Univ Hosp, Dept Clin Sci, Clin Res Ctr, Malmo, Sweden.
RP Selten, JP (reprint author), GGZ Leiden, Sandifortdreef 19, NL-2333 ZZ Leiden, Netherlands.
EM j.selten@ggzleiden.nl
FU European Community's Seventh Framework Programme [HEALTH-F2-2010-241909]
FX European Community's Seventh Framework Programme under grant agreement
no. HEALTH-F2-2010-241909 (Project EU-GEI).
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NR 62
TC 19
Z9 19
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0586-7614
EI 1745-1701
J9 SCHIZOPHRENIA BULL
JI Schizophr. Bull.
PD NOV
PY 2013
VL 39
IS 6
BP 1180
EP 1186
DI 10.1093/schbul/sbt134
PG 7
WC Psychiatry
SC Psychiatry
GA 241TC
UT WOS:000326189700003
PM 24062592
ER
PT J
AU Gordon, I
Eilbott, JA
Feldman, R
Pelphrey, KA
Vander Wyk, BC
AF Gordon, Ilanit
Eilbott, Jeffrey A.
Feldman, Ruth
Pelphrey, Kevin A.
Vander Wyk, Brent C.
TI Social, reward, and attention brain networks are involved when online
bids for joint attention are met with congruent versus incongruent
responses
SO SOCIAL NEUROSCIENCE
LA English
DT Article
DE Joint attention; fMRI; Eye tracking
ID ANTERIOR CINGULATE CORTEX; TEMPORO-PARIETAL JUNCTION; NEURAL BASIS;
FUSIFORM GYRUS; COGNITION; AUTISM; FMRI; FACE; MIND; CONTRIBUTE
AB Joint attention (JA) is a cornerstone of adaptive human social functioning. Little functional magnetic resonance imaging (fMRI) research has examined, in interactive paradigms, neural activation underlying bids for JA, met with a congruent or an incongruent social response. We developed a highly naturalistic fMRI paradigm utilizing eye-tracking to create real-time, contingent social responses to participant-initiated JA. During congruent responses to JA bids, we observed increased activation in the right amygdala, the right fusiform gyrus, anterior and dorsal anterior cingulate cortices, striatum, ventral tegmental area, and posterior parietal cortices. Incongruent responses to JA bids elicited increased activity localized to the right temporoparietal junction (TPJ) and bilateral cerebellum. No differences in eye-gaze patterns were observed during congruent or incongruent trials. Our results highlight the importance of utilizing interactive fMRI paradigms in social neuroscience and the impact of congruency in recruiting integrated social, reward, and attention circuits for processing JA.
C1 [Gordon, Ilanit; Eilbott, Jeffrey A.; Pelphrey, Kevin A.; Vander Wyk, Brent C.] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[Feldman, Ruth] Bar Ilan Univ, Dept Psychol, IL-52900 Ramat Gan, Israel.
[Feldman, Ruth] Bar Ilan Univ, Gonda Brain Res Ctr, IL-52900 Ramat Gan, Israel.
RP Gordon, I (reprint author), Yale Univ, Ctr Child Study, 230 South Frontage Rd, New Haven, CT 06520 USA.
EM ilanit.gordon@yale.edu
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NR 50
TC 5
Z9 5
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 1747-0919
EI 1747-0927
J9 SOC NEUROSCI-UK
JI Soc. Neurosci.
PD NOV 1
PY 2013
VL 8
IS 6
BP 544
EP 554
DI 10.1080/17470919.2013.832374
PG 11
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 243YE
UT WOS:000326353500003
PM 24044427
ER
PT J
AU Tunc-Ozcan, E
Ullmann, TM
Shukla, PK
Redei, EE
AF Tunc-Ozcan, Elif
Ullmann, Timothy M.
Shukla, Pradeep K.
Redei, Eva E.
TI Low-Dose Thyroxine Attenuates Autism-Associated Adverse Effects of Fetal
Alcohol in Male Offspring's Social Behavior and Hippocampal Gene
Expression
SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH
LA English
DT Article
DE Fetal Alcohol Spectrum Disorders; Autism Spectrum Disorders; Social
Interaction; Social Memory; Thyroxine
ID THYROID-HORMONE LEVELS; SPECTRUM DISORDERS; ANIMAL-MODELS; PRENATAL
EXPOSURE; ETHANOL EXPOSURE; RECEPTOR; BRAIN; RATS; POPULATION; PROFILES
AB Background Fetal alcohol spectrum disorder (FASD) is characterized by neurodevelopmental anomalies manifesting in cognitive and behavioral deficits in the offspring with diverse severities. Social behavior is affected in FASD, and these deficits overlap with those of autism spectrum disorder (ASD). Identifying some of the molecular characteristics related to ASD in an animal model of FASD could ultimately provide details on the underlying molecular mechanisms of both disorders that could lead to novel treatments.
MethodsPregnant Sprague-Dawley rats received the following diets: control (C; ad libitum standard laboratory chow), nutritional control pair-fed (PF), ethanol (EtOH), or an EtOH diet supplemented with 0.3, 1.5, or 7.5mg thyroxine (T4)/l in the diet. Social behavior and memory were tested in the adult offspring. Plasma total T4, free T3 (fT3), and thyroid-stimulating hormone (TSH) levels were measured. Hippocampal expression of Gabrb3,Ube3a,Nr2b, Rasgrf1, and Dio3 were measured by RT-qPCR and protein levels of Mecp2 and Slc25a12 by Western blotting.
ResultsAdult male offspring of EtOH dams showed elevated fT3 and low TSH levels. Adult male, but not female, offspring of EtOH dams exhibited social behavior and memory deficits. Expression of autism candidates, Gabrb3,Ube3a, Mecp2, and Slc25a12, was significantly increased in the hippocampus of male offspring of EtOH dams. Hippocampal Nr2b and Dio3 were also increased, while Rasgrf1 was decreased in the same population. Peripheral thyroid function, social behavioral deficits, and altered expression of the above genes were normalized by simultaneous administration of 0.3mg/l T4 in the EtOH diet.
ConclusionsOur data suggest that social interaction deficits of FASD share molecular mechanism with ASD by showing altered hippocampal expression of several ASD candidate genes. Social interaction deficits as well as the gene expression changes in the offspring of EtOH-consuming dams can be reversed by low dose of thyroid hormone supplementation to the mothers.
C1 [Tunc-Ozcan, Elif; Ullmann, Timothy M.; Shukla, Pradeep K.; Redei, Eva E.] Northwestern Univ, Feinberg Sch Med, Asher Ctr, Dept Psychiat & Behav Sci, Chicago, IL 60611 USA.
RP Redei, EE (reprint author), Northwestern Univ, Feinberg Sch Med, Asher Ctr, Dept Psychiat & Behav Sci, Chicago, IL 60611 USA.
EM e-redei@northwestern.edu
FU NIH [AA013452, AA017978]
FX This study was funded by NIH AA013452 and AA017978 to EER.
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NR 55
TC 7
Z9 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0145-6008
EI 1530-0277
J9 ALCOHOL CLIN EXP RES
JI Alcoholism (NY)
PD NOV
PY 2013
VL 37
IS 11
BP 1986
EP 1995
DI 10.1111/acer.12183
PG 10
WC Substance Abuse
SC Substance Abuse
GA 239QB
UT WOS:000326039400021
PM 23763370
ER
PT J
AU O'Keefe, N
Lindell, AK
AF O'Keefe, Natalie
Lindell, Annukka K.
TI Reduced interhemispheric interaction in non-autistic individuals with
normal but high levels of autism traits
SO BRAIN AND COGNITION
LA English
DT Article
DE Autism; AQ; Weak central coherence; Interhemispheric interaction
ID EMBEDDED FIGURES TASK; PERVASIVE DEVELOPMENTAL DISORDERS; WEAK CENTRAL
COHERENCE; SPECTRUM QUOTIENT AQ; CORPUS-CALLOSUM; FUNCTIONING AUTISM;
CHILDREN; HEMISPHERES; PERFORMANCE; DEFICITS
AB People with autism spectrum disorder (ASD) show superior performance for tasks requiring detail-focused processing. Atypical neural connectivity and reduced interhemispheric communication are posited to underlie this cognitive advantage. Given recent conceptualization of autism as a continuum, we sought to investigate whether people with normal but high levels of autism like traits (AQ) also exhibit reduced hemispheric interaction. Sixty right-handed participants completed the AQ questionnaire (Baron-Cohen, Wheelwright, Skinner, Martin, & Clubley, 2001) and a lateralised letter matching task that assessed unilateral and bilateral performance in response to simple (physical) and complex (identity) matches. Whereas people with low self-rated AQ scores showed a bilateral advantage for the more complex task, indicating normal interhemispheric interaction, people in the high AQ group failed to show a bilateral gain for the computationally demanding stimuli. This finding of disrupted interhemispheric interaction converges with a dimensional conceptualisation of ASD, suggesting that the structural anomalies of ASD extend to non-autistic individuals with high levels of autism traits. (c) 2013 Elsevier Inc. All rights reserved.
C1 [O'Keefe, Natalie; Lindell, Annukka K.] La Trobe Univ, Sch Psychol Sci, Melbourne, Vic, Australia.
RP O'Keefe, N (reprint author), 30 McNamara St, Preston, Vic 3072, Australia.
EM natalie.okeefe@uqconnect.edu.au; a.lindell@latrobe.edu.au
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NR 46
TC 1
Z9 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0278-2626
EI 1090-2147
J9 BRAIN COGNITION
JI Brain Cogn.
PD NOV
PY 2013
VL 83
IS 2
BP 183
EP 189
DI 10.1016/j.bandc.2013.08.005
PG 7
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 235SI
UT WOS:000325740600004
PM 24056118
ER
PT J
AU Kenworthy, L
Wallace, GL
Birn, R
Milleville, SC
Case, LK
Bandettini, PA
Martin, A
AF Kenworthy, Lauren
Wallace, Gregory L.
Birn, Rasmus
Milleville, Shawn C.
Case, Laura K.
Bandettini, Peter A.
Martin, Alex
TI Aberrant neural mediation of verbal fluency in autism spectrum disorders
SO BRAIN AND COGNITION
LA English
DT Article
DE Autism; Verbal fluency; fMRI; Executive function; Left inferior frontal
gyrus
ID HIGH-FUNCTIONING AUTISM; VENTROLATERAL PREFRONTAL CORTEX; FRONTAL-LOBE
LESIONS; WORKING-MEMORY TASK; EXECUTIVE FUNCTIONS; REPETITIVE BEHAVIOR;
BRAIN ACTIVATION; SENTENCE COMPREHENSION; ASPERGERS-DISORDER; COGNITIVE
CONTROL
AB Objective: Contrasts of verbal fluency and automatic speech provide an opportunity to evaluate the neural underpinnings of generativity and flexibility in autism spectrum disorders (ASD).
Method: We used functional magnetic resonance imaging (fMRI) to contrast brain activity in high functioning ASD (n = 17, mean verbal IQ = 117) and neurotypical (NT; n = 20, mean verbal IQ = 112) adolescent and young adult males (12-23 years). Participants responded to three word generation conditions: automatic speech (reciting months), category fluency, and letter fluency.
Results: Our paradigm closely mirrored behavioral fluency tasks by requiring overt, free recall word generation while controlling for differences in verbal output between the groups and systematically increasing the task demand. The ASD group showed reduced neural response compared to the NT participants during fluency tasks in multiple regions of left anterior and posterior cortices, and sub-cortical structures. Six of these regions fell in cortico-striatal circuits previously linked to repetitive behaviors (Langen, Durston, Kas, van Engeland, & Staal, 2011), and activity in two of them (putamen and thalamus) was negatively correlated with autism repetitive behavior symptoms in the ASD group. In addition, response in left inferior frontal gyrus was differentially modulated in the ASD, relative to the NT, group as a function of task demand.
Conclusions: These data indicate a specific, atypical brain response in ASD to demanding generativity tasks that may have relevance to repetitive behavior symptoms in ASD as well as to difficulties generating original verbal responses. Published by Elsevier Inc.
C1 [Kenworthy, Lauren; Wallace, Gregory L.; Birn, Rasmus; Milleville, Shawn C.; Case, Laura K.; Bandettini, Peter A.; Martin, Alex] NIMH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Kenworthy, Lauren] Childrens Natl Med Ctr, Ctr Autism Spectrum Disorders, Rockville, MD 20850 USA.
RP Kenworthy, L (reprint author), NIMH, Lab Brain & Cognit, 10 Ctr Dr,Room 4C104,MSC 1366, Bethesda, MD 20892 USA.
EM lkenwort@cnmc.org; gregwallace@mail.nih.-gov; rbirn@wisc.edu;
millevis@mail.nih.gov; lkcase@gmail.com; bandettp@mail.nih.gov;
alexmar-tin@mail.nih.gov
FU National Institute of Mental Health, National Institutes of Health,
Division of Intramural Research under National Institutes of Health
[10-M-0027]; Guldelsky Family Foundation
FX This study was supported by the National Institute of Mental Health,
National Institutes of Health, Division of Intramural Research, and it
was conducted under National Institutes of Health Clinical Study
Protocol 10-M-0027 (ClinicalTrials.gov ID NCT01031407). In addition,
Lauren Kenworthy received support from the Guldelsky Family Foundation.
The authors thank the children and their families who participated in
the investigation, Ben Yerys for valuable feedback regarding the
manuscript, and Eunice Dixon for editorial assistance.
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NR 82
TC 1
Z9 1
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0278-2626
EI 1090-2147
J9 BRAIN COGNITION
JI Brain Cogn.
PD NOV
PY 2013
VL 83
IS 2
BP 218
EP 226
DI 10.1016/j.bandc.2013.08.003
PG 9
WC Neurosciences; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 235SI
UT WOS:000325740600007
PM 24056237
ER
PT J
AU Stevens, SA
Nash, K
Koren, G
Rovet, J
AF Stevens, Sara A.
Nash, Kelly
Koren, Gideon
Rovet, Joanne
TI Autism characteristics in children with fetal alcohol spectrum disorders
SO CHILD NEUROPSYCHOLOGY
LA English
DT Article
DE Fetal alcohol spectrum disorders; Autism spectrum disorder
ID HYPERACTIVITY DISORDER; BEHAVIORAL-PHENOTYPE; ATTENTION-DEFICIT;
EXPOSURE; MOTHERS; SKILLS
AB Background: Children with fetal alcohol spectrum disorders (FASD) exhibit difficulties in many cognitive and behavioral domains and also have high comorbidity with other disorders such as attention deficit/hyperactivity disorder (ADHD) and conduct disorder as well as autism. Although the FASD profile is shown to be distinct from ADHD and conduct disorder, far less is known about the commonalities with autism. The current study used a parent-rated questionnaire containing an autism subscale to explore the autistic-like features that children with FASD exhibit. Methods: Studied were 25 children with FASD (age: M = 10.3 years) and 17 normal controls (NCs; age: M = 10.2 years). As part of a larger study, all parents/caregivers completed the Social Skills Improvement System (SSIS; Gresham & Elliot, 2008), which in addition to evaluating social skills and behavior problems globally, includes an Autism subscale. Results: Between-group comparisons showed the FASD group not only scored significantly lower in social skills and significantly higher in behavior problems than the NC group but children with FASD also scored significantly higher on the Autism subscale. Item analysis revealed they showed the most difficulty in terms of social and communicative functioning and the least in repetitive and restrictive behaviors. Conclusion: Current findings signify that FASD and autism share similarities with regard to social and communicative functioning. These findings, which further our knowledge of the FASD phenotype, may be useful in specifying the particular interventions these children need.
C1 [Stevens, Sara A.; Nash, Kelly; Rovet, Joanne] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Stevens, Sara A.; Rovet, Joanne] Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada.
[Nash, Kelly] Univ Toronto, Ontario Inst Studies Educ, Toronto, ON, Canada.
[Koren, Gideon; Rovet, Joanne] Univ Toronto, Dept Pediat, Toronto, ON, Canada.
[Koren, Gideon] Hosp Sick Children, Motherisk Program, Toronto, ON M5G 1X8, Canada.
RP Stevens, SA (reprint author), Hosp Sick Children, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM sara.stevens@utoronto.ca
FU Canadian Institutes of Health Research (CIHR); Canadian Foundation on
Fetal Alcohol Research (CFFAR)
FX The authors gratefully appreciate the FASD diagnostic clinics staff for
assistance in recruiting. We also wish to acknowledge the anonymous
reviewers for their insightful comments and suggestions. This work was
supported by the Canadian Institutes of Health Research (CIHR) and
Canadian Foundation on Fetal Alcohol Research (CFFAR).
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NR 30
TC 1
Z9 1
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 0929-7049
EI 1744-4136
J9 CHILD NEUROPSYCHOL
JI Child Neuropsychol.
PD NOV 1
PY 2013
VL 19
IS 6
BP 579
EP 587
DI 10.1080/09297049.2012.727791
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 240BY
UT WOS:000326070900002
PM 23030694
ER
PT J
AU Vetter, NC
Leipold, K
Kliegel, M
Phillips, LH
Altgassen, M
AF Vetter, Nora C.
Leipold, Kristina
Kliegel, Matthias
Phillips, Louise H.
Altgassen, Mareike
TI Ongoing development of social cognition in adolescence
SO CHILD NEUROPSYCHOLOGY
LA English
DT Article
DE Adolescence; Puberty; Social cognition; Emotion; Basic cognitive
abilities
ID HIGH-FUNCTIONING AUTISM; WORKING-MEMORY; ASPERGER-SYNDROME; FACIAL
EXPRESSIONS; DEVELOPING-CHILDREN; PUBERTAL STATUS; LATE CHILDHOOD;
FALSE-BELIEF; MIND; RECOGNITION
AB Age differences in social cognition between adolescents and young adults were investigated. Two large groups of adolescents and young adults were given tasks of theory of mind and emotion recognition. In addition, to control for possibly related basic cognitive development, working memory, speed of processing, and verbal ability were assessed. A strong age effect was revealed across both measures of social cognition. Adolescents performed with a lower accuracy than adults. Further analyses indicated that those age differences remained significant even after controlling for basic cognitive abilities. Exploratory analyses indicated no influence of pubertal phase on social cognition. Results suggest ongoing development of social cognition across adolescence, independent of individual differences in more basic cognitive abilities.
C1 [Vetter, Nora C.; Altgassen, Mareike] Tech Univ Dresden, Dept Psychol, D-01062 Dresden, Germany.
[Leipold, Kristina] Tech Univ Dresden, Dept Business & Econ, D-01062 Dresden, Germany.
[Kliegel, Matthias] Univ Geneva, Dept Psychol, Geneva, Switzerland.
[Phillips, Louise H.] Univ Aberdeen, Sch Psychol, Aberdeen, Scotland.
RP Vetter, NC (reprint author), Tech Univ Dresden, Dept Psychol, D-01062 Dresden, Germany.
EM vetter@psychologie.tu-dresden.de
RI Phillips, Louise/A-7952-2008; Altgassen, Mareike/J-3048-2012
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NR 58
TC 3
Z9 3
PU PSYCHOLOGY PRESS
PI HOVE
PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND
SN 0929-7049
EI 1744-4136
J9 CHILD NEUROPSYCHOL
JI Child Neuropsychol.
PD NOV 1
PY 2013
VL 19
IS 6
BP 615
EP 629
DI 10.1080/09297049.2012.718324
PG 15
WC Clinical Neurology
SC Neurosciences & Neurology
GA 240BY
UT WOS:000326070900005
PM 22934659
ER
PT J
AU Young, WS
AF Young, W. Scott
TI Shedding Heat on Oxytocin
SO ENDOCRINOLOGY
LA English
DT Editorial Material
ID RECEPTOR-DEFICIENT MICE; SOCIAL RECOGNITION; AUTISM LOCI; GENOME-WIDE;
PARTURITION; MOUSE; BEHAVIOR; IMPAIRS; SEARCH; GENES
C1 NIMH, NIH, Dept Hlth & Human Serv, Sect Neural Gene Express, Bethesda, MD 20892 USA.
RP Young, WS (reprint author), NIMH, NIH, Dept Hlth & Human Serv, Sect Neural Gene Express, Bethesda, MD 20892 USA.
EM wsy@mail.nih.gov
RI Young, W/A-9333-2009
OI Young, W/0000-0001-6614-5112
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NR 32
TC 0
Z9 0
PU ENDOCRINE SOC
PI CHEVY CHASE
PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA
SN 0013-7227
EI 1945-7170
J9 ENDOCRINOLOGY
JI Endocrinology
PD NOV
PY 2013
VL 154
IS 11
BP 3961
EP 3962
DI 10.1210/en.2013-1885
PG 2
WC Endocrinology & Metabolism
SC Endocrinology & Metabolism
GA 238HI
UT WOS:000325935200004
PM 24141993
ER
PT J
AU Maguire, S
O'Dell, A
Touyz, L
Russell, J
AF Maguire, Sarah
O'Dell, Adrienne
Touyz, Lauren
Russell, Janice
TI Oxytocin and AnorexiaNervosa: A Review of the Emerging Literature
SO EUROPEAN EATING DISORDERS REVIEW
LA English
DT Review
DE oxytocin; anorexia nervosa; eating disorders; treatment; neuropeptide
ID BULIMIA-NERVOSA; CSF OXYTOCIN; DISORDERS; HUMANS; VASOPRESSIN; BEHAVIOR;
AUTISM; STRESS
AB Anorexia nervosa (AN) is an intractable illness that is difficult to treat. The identification of neural correlates and novel agents to transform treatment has become priority avenues for research. Oxytocin (OT) is a neuropeptide whose emerging sphere of influence on mammalian behaviour and demonstrated impact on psychiatric illness suggest it may have potential in AN. In this paper, we undertake a targeted summary of the existing literature on OT research as it pertains to brain based behaviour and psychiatric dysfunction. Then, we conduct a systematic review of OT in AN. Papers that addressed any aspect of the OT system in AN were examined. The existing literature, although limited and based on small sample sizes, suggests a derangement of the OT system in AN that may normalise upon recovery. Preliminary pilot data from unpublished studies suggest a potential effect of OT administration on eating-related indices. Copyright (c) 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
C1 [Maguire, Sarah; O'Dell, Adrienne; Touyz, Lauren; Russell, Janice] Univ Sydney, Boden Inst, Ctr Eating & Dieting Disorders, Sydney, NSW 2006, Australia.
[Russell, Janice] Northside Clin, Eating Disorders Unit, Sydney, NSW, Australia.
RP Maguire, S (reprint author), Univ Sydney, Boden Inst, Ctr Eating & Dieting Disorders, Med Fdn Bldg,K25, Sydney, NSW 2006, Australia.
EM sarah.maguire@email.cs.nsw.gov.au
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NR 33
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-4133
EI 1099-0968
J9 EUR EAT DISORD REV
JI Eur. Eat. Disord. Rev.
PD NOV
PY 2013
VL 21
IS 6
SI SI
BP 475
EP 478
DI 10.1002/erv.2252
PG 4
WC Psychology, Clinical
SC Psychology
GA 239LS
UT WOS:000326026600006
PM 24115458
ER
PT J
AU de Sampaio, FTP
Soneira, S
Aulicino, A
Allegri, RF
AF Tapajoz Pereira de Sampaio, Fernanda
Soneira, Sebastian
Aulicino, Alfredo
Allegri, Ricardo F.
TI Theory of Mind in Eating Disorders and Their Relationship to Clinical
Profile
SO EUROPEAN EATING DISORDERS REVIEW
LA English
DT Article
DE anorexia; bulimia; theory of mind; social cognition; clinical profile
ID OBSESSIVE-COMPULSIVE INVENTORY; HIGH-FUNCTIONING AUTISM;
ANOREXIA-NERVOSA; BULIMIA-NERVOSA; COGNITIVE REMEDIATION; EMOTION
RECOGNITION; ASPERGER-SYNDROME; CENTRAL COHERENCE; CASE-SERIES; VERSION
AB ObjectiveThis study aimed to assess cognitive and affective theory of mind (ToM) in patients with eating disorders and to explore its relationship with the clinical and psychopathological profile.
MethodTheory of mind was assessed in 65 women, consisting of 22 with anorexia nervosa (AN), 19 with bulimia nervosa (BN), and 24 healthy controls (HC), using the Reading the Mind in the Eyes Test and the Faux Pas Test. These tasks evaluate affective and cognitive ToM, respectively. We also examined the correlations between performance on ToM tasks and the clinical psychopathological profile, which was extensively evaluated through self-report instruments and clinical interviews.
ResultsPatients with AN had poorer performance than BN patients and HCs had in the affective ToM task, particularly in recognizing negative emotions and emotions in male eyes. Moreover, this deficit showed no correlation with the psychopathological profile. Performance in the BN group was equivalent to that of HCs in both tasks.
ConclusionsIn this study, patients with AN showed an impairment in affective ToM, independent of their clinical status. Consistent with other studies, our findings demonstrate a specific difficulty in social cognition in patients with AN. This may be a trait marker in this population and should be considered in treatment. Furthermore, patients with AN and BN have different difficulty profiles in this domain of social cognition. Copyright (c) 2013 John Wiley & Sons, Ltd and Eating Disorders Association.
C1 [Tapajoz Pereira de Sampaio, Fernanda; Allegri, Ricardo F.] Consejo Nacl Invest Cient & Tecn, RA-1033 Buenos Aires, DF, Argentina.
[Tapajoz Pereira de Sampaio, Fernanda; Allegri, Ricardo F.] Inst Invest Neurol Raul Carrea FLENI, Dept Cognit Neurol Neuropsychol & Neuropsychiat, Buenos Aires, DF, Argentina.
[Soneira, Sebastian] Inst Dr Cormillot, Nutr & Hlth Clin, Buenos Aires, DF, Argentina.
[Tapajoz Pereira de Sampaio, Fernanda; Aulicino, Alfredo] Hosp Gen Cosme Argerich, Sect Eating Disorders, Buenos Aires, DF, Argentina.
RP de Sampaio, FTP (reprint author), Inst Invest Neurol Raul Carrea FLENI, Dept Cognit Neurol Neuropsychol & Neuropsychiat, Montaneses 2325 8th Floor,C1428AQK, Buenos Aires, DF, Argentina.
EM fetapajoz@hotmail.com
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NR 51
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-4133
EI 1099-0968
J9 EUR EAT DISORD REV
JI Eur. Eat. Disord. Rev.
PD NOV
PY 2013
VL 21
IS 6
SI SI
BP 479
EP 487
DI 10.1002/erv.2247
PG 9
WC Psychology, Clinical
SC Psychology
GA 239LS
UT WOS:000326026600007
ER
PT J
AU Zhang, T
Zhang, Q
Li, YY
Long, CQ
Li, H
AF Zhang, Ting
Zhang, Qin
Li, Yiyuan
Long, Changquan
Li, Hong
TI Belief and sign, true and false: the unique of false belief reasoning
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Article
DE False belief reasoning; True belief reasoning; False sign reasoning; N2;
Late slow wave
ID MIND; BRAIN; CHILDREN; ERP; CATEGORIZATION; COMPONENT; AUTISM; TASK
AB For a long time, a controversy has been proposed that whether the process of theory of mind is a result of domain-specific or domain-general changes (Wellman in The handbook of childhood cognitive development. Blackwell Publication, New Jersey, 2011). This event-related potential study explored the neural time course of domain-general and domain-specific components in belief reasoning. Fourteen participants completed location transfer false belief (FB), true belief (TB), false sign (FS) and true sign (TS) tasks, in which two pictures told a story related to a dog that ran from a green into a red box. In the TB and FB tasks, a boy saw or did not see the transfer of the dog, respectively. In the FS and TS tasks, an arrow that pointed to the green box either altered its direction to the red box or did not alter following the transfer of the dog. Participants then inferred where the boy thought of, or the arrow indicated the location of the dog. FB and TB reasoning elicited lower N2 amplitudes than FS and TS reasoning, which is associated with domain-general components, the detection, and classification. The late slow wave (LSW) for FB was more positive at frontal, central, and parietal sites than FS because of the domain-specific component involved in FB reasoning. However, the LSW was less positive for TB than for FB but did not differ from the TS condition, which implies that mental representation might not be involved in TB reasoning.
C1 [Zhang, Ting; Li, Yiyuan; Long, Changquan; Li, Hong] Southwest Univ, Fac Psychol, Chongqing 400715, Peoples R China.
[Zhang, Qin] Univ Elect Sci & Technol China, Sch Polit Sci & Publ Adm, Chengdu 610054, Peoples R China.
[Li, Yiyuan] Mianyang Normal Univ, Sch Educ Sci, Mianyang, Peoples R China.
[Li, Hong] Niaoning Normal Univ, Sch Psychol, Niaoning, Peoples R China.
RP Zhang, T (reprint author), Southwest Univ, Fac Psychol, Chongqing 400715, Peoples R China.
EM scarletl312@gmail.com; lihongwrm@vip.sina.com
FU Fundamental Research Funds for University [SWU 1009098]; [NSFC31200780]
FX This study was supported by the Fundamental Research Funds for
University (SWU 1009098) and NSFC31200780. We would like to appreciate
Dr. Qu Li from Nanyang Technological University for her valuable
suggestion.
CR Aichhorn M, 2009, J COGNITIVE NEUROSCI, V21, P1179, DOI 10.1162/jocn.2009.21082
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NR 27
TC 0
Z9 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0014-4819
EI 1432-1106
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD NOV
PY 2013
VL 231
IS 1
BP 27
EP 36
DI 10.1007/s00221-013-3661-7
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 238SQ
UT WOS:000325969600004
PM 23975150
ER
PT J
AU Hirata, S
Okuzumi, H
Kitajima, Y
Hosobuchi, T
Kokubun, M
AF Hirata, Shogo
Okuzumi, Hideyuki
Kitajima, Yoshio
Hosobuchi, Tomio
Kokubun, Mitsuru
TI Speed and accuracy of motor and cognitive control in children with
intellectual disabilities
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE motor control; cognitive control; intellectual disability; speed and
accuracy
ID 6-YEAR-OLD CHILDREN; MENTAL-RETARDATION; RETARDED-CHILDREN;
DOWN-SYNDROME; PERFORMANCE; DISORDER; ATTENTION; HYPERACTIVITY;
PROFICIENCY; PERCEPTION
AB Objectives: The purpose of this study was to investigate the relationship between motor and cognitive control in children with intellectual disabilities (ID), focusing on the two aspects of speed and accuracy.
Methods: The subjects were 39 children with ID aged 8-15 years. Their Intelligence Quotient (IQ) ranged from 13 to 71. The children with ID included 12 children with Down's syndrome and 10 children with autism. We conducted three tasks: seal affixation task, tray-carrying task, and the Matching Familiar Figures Test (MFFT). The seal affixation and tray-carrying tasks are motor tasks we devised that can separately measure the speed and accuracy of motor control. MFFT is a cognitive control task that can be used to evaluate cognitive styles, such as impulsive-reflective.
Results: In the children with ID in this study, motor speed and accuracy were related to cognitive speed and accuracy. Moreover, these children could be classified into four groups based on their MFFT performance, with the motor performances of each group corresponding to the characteristics of that group seen on MFFT.
Discussion: These results suggest the possibility that a motor-cognitive control link exists in children with ID.
C1 [Hirata, Shogo; Kitajima, Yoshio] Chiba Univ, Fac Educ, Chiba 2638522, Japan.
[Hirata, Shogo] Japan Soc Promot Sci, Tokyo, Japan.
[Okuzumi, Hideyuki; Kokubun, Mitsuru] Tokyo Gakugei Univ, Fac Educ, Tokyo, Japan.
[Hosobuchi, Tomio] Saitama Univ, Fac Educ, Saitama, Japan.
RP Hirata, S (reprint author), Chiba Univ, Dept Educ, Inage Ku, Yayoi Machi, Chiba 2638522, Japan.
EM r093002g@st.u-gakugei.ac.jp
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NR 40
TC 0
Z9 0
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 2047-3869
EI 2047-3877
J9 INT J DEV DISABIL
JI Int. J. Dev. Disabil.
PD NOV
PY 2013
VL 59
IS 3
BP 166
EP 178
DI 10.1179/2047387712Y.0000000010
PG 13
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 239JD
UT WOS:000326017900003
ER
PT J
AU Zahid, S
AF Zahid, Sofia
TI A Brief Guide to Autism Treatments
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL DISABILITIES
LA English
DT Book Review
CR SANDBERG E, 2012, BRIEF GUIDE AUTISM T
NR 1
TC 0
Z9 0
PU MANEY PUBLISHING
PI LEEDS
PA STE 1C, JOSEPHS WELL, HANOVER WALK, LEEDS LS3 1AB, W YORKS, ENGLAND
SN 2047-3869
EI 2047-3877
J9 INT J DEV DISABIL
JI Int. J. Dev. Disabil.
PD NOV
PY 2013
VL 59
IS 3
BP 192
EP 192
PG 1
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 239JD
UT WOS:000326017900006
ER
PT J
AU Godbee, K
Porter, M
AF Godbee, Kali
Porter, Melanie
TI Comprehension of sarcasm, metaphor and simile in Williams syndrome
SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS
LA English
DT Article
DE Williams syndrome; sarcasm; metaphor; simile; cognition
ID FRENCH-SPEAKING CHILDREN; VERBAL IRONY; LANGUAGE; AUTISM; ADOLESCENTS;
DISORDERS; IDIOMS; MIND; HYPERSOCIABILITY; PRAGMATICS
AB BackgroundAlthough people with Williams syndrome (WS) are often characterized as friendly and sociable with relatively good general language abilities, there is emerging evidence of pragmatic difficulties and trouble comprehending aspects of non-literal language.
AimsThe main aim was to investigate the comprehension of sarcasm, metaphor and simile in WS relative to typically developing controls. A secondary aim was to examine the association between non-literal language comprehension and a range of other cognitive abilities, both in WS and in the typically developing population.
Methods & ProceduresTwenty-six participants with WS were compared with 26 typically developing chronological age-matched controls (TDCA) and 26 typically developing mental age-matched controls (TDMA). Participants listened to stories in which characters made non-literal comments. They were then asked what each character meant by their comment. In order to investigate the second aim of the study, cognitive abilities were also assessed using the Woodcock-Johnson (Revised) Tests of Cognitive Ability, including expressive vocabulary, verbal working memory, perceptual integration, inferential reasoning and overall cognitive ability.
Outcomes & ResultsComprehension of non-literal language in WS was significantly below TDCA levels, but was not significantly different to TDMA levels. For typically developing controls, each of the cognitive measures was strongly correlated with each of the measures of non-literal language comprehension. The same relationships were not always found for participants with WS. In particular, sarcasm comprehension in WS was not significantly correlated with any of the assessed cognitive abilities, and expressive vocabulary was not significantly correlated with any measure of non-literal comprehension.
Conclusions & ImplicationsComprehension of simile in WS is below TDCA levels but seems on par with their mental age level. It appears that comprehension of sarcasm and metaphors is above the cognitive capabilities and mental age level of most individuals with WS. Further, the pattern of correlations between non-literal comprehension and cognitive abilities in WS relative to controls suggests that perhaps the linguistic and cognitive systems that underpin non-literal language comprehension in typically developing individuals interact and integrate in different ways in WS.
C1 [Godbee, Kali; Porter, Melanie] Macquarie Univ, Dept Psychol, Sydney, NSW 2109, Australia.
RP Porter, M (reprint author), Macquarie Univ, Dept Psychol, Sydney, NSW 2109, Australia.
EM melanie.porter@mq.edu.au
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NR 67
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1368-2822
EI 1460-6984
J9 INT J LANG COMM DIS
JI Int. J. Lang. Commun. Disord.
PD NOV
PY 2013
VL 48
IS 6
BP 651
EP 665
DI 10.1111/1460-6984.12037
PG 15
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 239WU
UT WOS:000326057500005
PM 24165362
ER
PT J
AU Tadic, V
Pring, L
Dale, N
AF Tadic, Valerija
Pring, Linda
Dale, Naomi
TI Story discourse and use of mental state language between mothers and
school-aged children with and without visual impairment
SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS
LA English
DT Article
DE visual impairment; mental state language; mother-child discourse
ID MATERNAL MIND-MINDEDNESS; YOUNG-CHILDREN; BLIND-CHILDREN; FALSE BELIEF;
COMMUNICATION; DIRECTIVES; INFANTS; AUTISM; INPUT; TALK
AB BackgroundLack of sight compromises insight into other people's mental states. Little is known about the role of maternal language in assisting the development of mental state language in children with visual impairment (VI).
AimsTo investigate mental state language strategies of mothers of school-aged children with VI and to compare these with mothers of comparable children with typically developing vision. To investigate whether the characteristics of mother-child discourse were associated with the child's socio-communicative competence.
Methods & ProceduresMother-child discourse with twelve 6-12-year-old children with VI was coded during a shared book-reading narrative and compared with 14 typically sighted children matched in age and verbal ability.
Outcomes & ResultsMothers of children with VI elaborated more and made significantly more references to story characters' mental states and descriptive elaborations than mothers of sighted children. Mental state elaborations of mothers in the VI group related positively with the level produced by their children, with the association remaining after mothers' overall verbosity and children's developmental levels were controlled for. Frequency of maternal elaborations, including their mental state language, was related to socio-communicative competence of children with VI.
Conclusions & ImplicationsThe findings offer insights into the potential contribution of maternal verbal scaffolding to mentalistic language and social-communicative competences of children with VI.
C1 [Tadic, Valerija] UCL Inst Child Hlth, MRC Ctr Epidemiol Child Hlth, Ctr Paediat Epidemiol & Biostat, London WC1N 1EH, England.
[Pring, Linda] Univ London, Dept Psychol, London, England.
[Dale, Naomi] Great Ormond St Hosp Children NHS Fdn Trust, Wolfson Neurodisabil Serv, London, England.
RP Tadic, V (reprint author), UCL Inst Child Hlth, MRC Ctr Epidemiol Child Hlth, Ctr Paediat Epidemiol & Biostat, 30 Guilford St, London WC1N 1EH, England.
EM v.tadic@ucl.ac.uk
FU Economic and Social Research Council (ESRC) [PTA-031-2004-00211]
FX The study was supported by an Economic and Social Research Council
(ESRC) PhD studentship award (PTA-031-2004-00211). The authors thank the
children and their parents who participated in this research; Dr Laura
Crane for reliability coding; and Dr Ian Tharp for statistical advice.
Declaration of interest: The authors report no conflicts of interest.
The authors alone are responsible for the content and writing of the
paper.
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NR 38
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1368-2822
EI 1460-6984
J9 INT J LANG COMM DIS
JI Int. J. Lang. Commun. Disord.
PD NOV
PY 2013
VL 48
IS 6
BP 679
EP 688
DI 10.1111/1460-6984.12040
PG 10
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 239WU
UT WOS:000326057500007
PM 24165364
ER
PT J
AU Andres-Roqueta, C
Adrian, JE
Clemente, RA
Katsos, N
AF Andres-Roqueta, Clara
Adrian, Juan E.
Clemente, Rosa A.
Katsos, Napoleon
TI Which are the best predictors of theory of mind delay in children with
specific language impairment?
SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS
LA English
DT Article
DE theory of mind (ToM); specific language impairment (SLI); pragmatic
language impairment (PLI); information processing; language disorder
ID FALSE-BELIEF; SOCIAL COGNITION; PSYCHOLINGUISTIC MARKERS; EXECUTIVE
FUNCTION; AUTISM; SLI; DISORDER; DIFFICULTIES; METAANALYSIS
AB BackgroundThe relationship between language and theory of mind (ToM) development in participants with specific language impairment (SLI) it is far from clear due to there were differences in study design and methodologies of previous studies.
AimsThis research consisted of an in-depth investigation of ToM delay in children with SLI during the typical period of acquisition, and it studied whether linguistic or information-processing variables were the best predictors of this process. It also took into account whether there were differences in ToM competence due to the degree of pragmatic impairment within the SLI group.
Methods & ProceduresThirty-one children with SLI (3;5-7;5 years old) and two control groups (age matched and language matched) were assessed with False Belief (FB) tasks, a wide battery of language measures and additional information-processing measures.
Outcomes & ResultsThe members of the SLI group were less competent than their age-matched peers at solving FB tasks, but they performed similarly to the language-matched group. Regression analysis showed that overall linguistic skills of children with SLI were the best predictor of ToM performance, and especially grammar abilities. No differences between SLI subgroups were found according to their pragmatic level.
Conclusions & ImplicationsA delay in ToM development in children with SLI around the critical period of acquisition is confirmed more comprehensively, and it is shown to be more strongly related to their general linguistic level than to their age and other information-processing faculties. This finding stresses the importance of early educational and clinical programmes aimed at reducing deleterious effects in later development.
C1 [Andres-Roqueta, Clara; Adrian, Juan E.; Clemente, Rosa A.] Univ Jaume I Castello, Dept Educ & Dev Psychol, Castellon de La Plana 12071, Spain.
[Katsos, Napoleon] Univ Cambridge, Dept Theoret & Appl Linguist, Cambridge, England.
RP Andres-Roqueta, C (reprint author), Univ Jaume I Castello, Dept Educ & Dev Psychol, Av Sos Baynat S-N, Castellon de La Plana 12071, Spain.
EM candres@uji.es
FU Fundacio Caixa-Castello [P1-1B2010-16]; Spanish Ministerio de Ciencia e
Innovacion [EDU2010-21791]
FX The authors would like to thank the children who took part in this
study; and also express their gratitude for financial support provided
by Grant Number P1-1B2010-16 from Fundacio Caixa-Castello, and Grant
Number EDU2010-21791 from the Spanish Ministerio de Ciencia e
Innovacion. Declaration of interest: The authors report no conflicts of
interest. The authors alone are responsible for the content and writing
of the paper.
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NR 53
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1368-2822
EI 1460-6984
J9 INT J LANG COMM DIS
JI Int. J. Lang. Commun. Disord.
PD NOV
PY 2013
VL 48
IS 6
BP 726
EP 737
DI 10.1111/1460-6984.12045
PG 12
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 239WU
UT WOS:000326057500011
PM 24165368
ER
PT J
AU Hani, HB
Gonzalez-Barrero, AM
Nadig, AS
AF Hani, Hanady Bani
Gonzalez-Barrero, Ana Maria
Nadig, Aparna S.
TI Children's referential understanding of novel words and parent labeling
behaviors: similarities across children with and without autism spectrum
disorders
SO JOURNAL OF CHILD LANGUAGE
LA English
DT Article
ID JOINT ATTENTION; COMMUNICATIVE DEVELOPMENT; PRESCHOOL-CHILDREN;
TASK-PERFORMANCE; EARLY LANGUAGE; ACQUISITION; ABILITY; PREDICTORS;
VOCABULARY; PICTURES
AB This study examined two facets of the use of social cues for early word learning in parent-child dyads, where children had an Autism Spectrum Disorder (ASD) or were typically developing. In Experiment 1, we investigated word learning and generalization by children with ASD (age range: 3; 01-6; 02) and typically developing children (age range: 1; 02-4; 09) who were matched on language ability. In Experiment 2, we examined verbal and non-verbal parental labeling behaviors. First, we found that both groups were similarly able to learn a novel label using social cues alone, and to generalize this label to other representations of the object. Children who utilized social cues for word learning had higher language levels. Second, we found that parental cues used to introduce object labels were strikingly similar across groups. Moreover, parents in both groups adapted labeling behavior to their child's language level, though this surfaced in different ways across groups.
C1 [Hani, Hanady Bani; Gonzalez-Barrero, Ana Maria; Nadig, Aparna S.] McGill Univ, Sch Commun Sci & Disorders, Montreal, PQ H3A 2T5, Canada.
RP Gonzalez-Barrero, AM (reprint author), McGill Univ, Sch Commun Sci & Disorders, Montreal, PQ H3A 2T5, Canada.
EM aparna.nadig@mcgill.ca
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NR 58
TC 1
Z9 1
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0305-0009
EI 1469-7602
J9 J CHILD LANG
JI J. Child Lang.
PD NOV
PY 2013
VL 40
IS 5
BP 971
EP 1002
DI 10.1017/S0305000912000426
PG 32
WC Psychology, Developmental; Linguistics; Psychology, Experimental
SC Psychology; Linguistics
GA 237EV
UT WOS:000325852300003
PM 23021075
ER
PT J
AU Bagozzi, RP
Verbeke, WJMI
Dietvorst, RC
Belschak, FD
van den Berg, WE
Rietdijk, WJR
AF Bagozzi, Richard P.
Verbeke, Willem J. M. I.
Dietvorst, Roeland C.
Belschak, Frank D.
van den Berg, Wouter E.
Rietdijk, Wim J. R.
TI Theory of Mind and Empathic Explanations of Machiavellianism: A
Neuroscience Perspective
SO JOURNAL OF MANAGEMENT
LA English
DT Article
DE Machiavellianism; theory of mind; empathy; functional magnetic resonance
imaging; neuroscience; organizational behavior
ID ORGANIZATIONAL COGNITIVE NEUROSCIENCE; TEMPORO-PARIETAL JUNCTION; MIRROR
NEURON SYSTEM; ASPERGER-SYNDROME; SOCIAL COGNITION; EMOTIONAL
INTELLIGENCE; CITIZENSHIP BEHAVIOR; NORMAL ADULTS; MECHANISMS; AUTISM
AB We study theory of mind (ToM) and empathic underpinnings of Machiavellianism by use of functional magnetic resonance imaging, where account managers are used as participants in 3 studies. Study 1 finds evidence for activation of the medial prefrontal cortex, left and right temporo-parietal junction, and left and right precuneus regions; all five regions are negatively correlated with Machiavellianism, suggesting that Machiavellians are less facile than non-Machiavellians with ToM skills. Study 2 presents evidence for activation of the left and right pars opercularis, left and right insula, and left precuneus regions; the former four regions of the motor neuron system were positively associated, and the latter negatively associated, with Machiavellianism, implying that Machiavellians resonate more readily with the emotions of others than non-Machiavellians. This is the first study to our knowledge to show a negative correlation between perspective taking and emotional sharing in empathic processes in general and Machiavellianism in particular. Study 3 tests implications of managerial control on both performance and organizational citizenship behaviors, as moderated by Machiavellianism in the field. Our study grounds the functioning of Machiavellianism in organizations in basic neuroscience processes, resolves some long-standing ambiguities with self-report investigations, and points to conditions under which Machiavellianism both inhibits and promotes performance and citizenship behavior.
C1 [Bagozzi, Richard P.] Univ Michigan, Ann Arbor, MI 48109 USA.
[Verbeke, Willem J. M. I.; van den Berg, Wouter E.; Rietdijk, Wim J. R.] Erasmus Univ, NL-3000 DR Rotterdam, Netherlands.
[Belschak, Frank D.] Univ Amsterdam, NL-1012 WX Amsterdam, Netherlands.
RP Bagozzi, RP (reprint author), Univ Michigan, Ross Sch, 701 Tappan St, Ann Arbor, MI 48109 USA.
EM bagozzi@umich.edu
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NR 124
TC 8
Z9 8
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0149-2063
EI 1557-1211
J9 J MANAGE
JI J. Manag.
PD NOV
PY 2013
VL 39
IS 7
BP 1760
EP 1798
DI 10.1177/0149206312471393
PG 39
WC Business; Psychology, Applied; Management
SC Business & Economics; Psychology
GA 229JG
UT WOS:000325258500007
ER
PT J
AU Hiroi, N
Takahashi, T
Hishimoto, A
Izumi, T
Boku, S
Hiramoto, T
AF Hiroi, N.
Takahashi, T.
Hishimoto, A.
Izumi, T.
Boku, S.
Hiramoto, T.
TI Copy number variation at 22q11.2: from rare variants to common
mechanisms of developmental neuropsychiatric disorders
SO MOLECULAR PSYCHIATRY
LA English
DT Review
DE autism; copy number variant; intellectual disability; mouse model;
schizophrenia; ADHD
ID CARDIO-FACIAL-SYNDROME; AUTISM SPECTRUM DISORDERS; DEFICIT HYPERACTIVITY
DISORDER; CHILDHOOD-ONSET SCHIZOPHRENIA; CATECHOL-O-METHYLTRANSFERASE;
MICRORNA MACHINERY GENES; DELETION SYNDROME; VELOCARDIOFACIAL SYNDROME;
WORKING-MEMORY; MICRODUPLICATION 22Q11.2
AB Recently discovered genome-wide rare copy number variants (CNVs) have unprecedented levels of statistical association with many developmental neuropsychiatric disorders, including schizophrenia, autism spectrum disorders, intellectual disability and attention deficit hyperactivity disorder. However, as CNVs often include multiple genes, causal genes responsible for CNV-associated diagnoses and traits are still poorly understood. Mouse models of CNVs are in use to delve into the precise mechanisms through which CNVs contribute to disorders and associated traits. Based on human and mouse model studies on rare CNVs within human chromosome 22q11.2, we propose that alterations of a distinct set of multiple, noncontiguous genes encoded in this chromosomal region, in concert with modulatory impacts of genetic background and environmental factors, variably shift the probabilities of phenotypes along a predetermined developmental trajectory. This model can be further extended to the study of other CNVs and may serve as a guide to help characterize the impact of genes in developmental neuropsychiatric disorders.
C1 [Hiroi, N.; Takahashi, T.; Hishimoto, A.; Izumi, T.; Boku, S.; Hiramoto, T.] Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Bronx, NY 10461 USA.
[Hiroi, N.] Albert Einstein Coll Med, Dominick P Purpura Dept Neurosci, Bronx, NY 10461 USA.
[Hiroi, N.] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10461 USA.
RP Hiroi, N (reprint author), Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Dominick P Purpura Dept Neurosci, Dept Genet, Golding 104,1300 Morris Pk Ave, Bronx, NY 10461 USA.
EM noboru.hiroi@einstein.yu.edu
FU NIH [R21HD05311, R01MH099660]; NARSAD Independent Investigator Award;
Maltz Foundation; Ministry of Defense, Japan; Uehara fellowship; Senshin
Medical Research Foundation fellowship, Japan; Kobe University Graduate
School of Medicine; Society for Promotion of Science, Japan [24591674]
FX We thank Drs Herb Lachman, Santhosh Girirajan and Edward Brodkin for
their invaluable comments on an early draft of this paper. This work was
supported by the NIH (R21HD05311 and R01MH099660), NARSAD Independent
Investigator Award and the Maltz Foundation to NH; funds from the
Ministry of Defense, Japan, to TT; the Uehara fellowship and a Senshin
Medical Research Foundation fellowship, Japan, to SB; funds from Kobe
University Graduate School of Medicine to AH; and Grants-in-Aid for
Scientific Research (24591674) from the Society for Promotion of
Science, Japan, to TI.
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NR 205
TC 11
Z9 11
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD NOV
PY 2013
VL 18
IS 11
BP 1153
EP 1165
DI 10.1038/mp.2013.92
PG 13
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 240KN
UT WOS:000326094800004
PM 23917946
ER
PT J
AU Brimberg, L
Sadiq, A
Gregersen, PK
Diamond, B
AF Brimberg, L.
Sadiq, A.
Gregersen, P. K.
Diamond, B.
TI Brain-reactive IgG correlates with autoimmunity in mothers of a child
with an autism spectrum disorder
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE anti-brain antibodies; ASD; autoimmunity; maternal
ID FETAL-BRAIN; ANTIBODIES; DISEASES; AUTOANTIBODIES; AUTOANTIGENS;
RESOURCE; GENETICS; PROTEIN; FAMILY; LUPUS
AB It is believed that in utero environmental factors contribute to autism spectrum disorder (ASD). The goal of this study was to demonstrate, using the largest cohort reported so far, that mothers of an ASD child have an elevated frequency of anti-brain antibodies and to assess whether brain reactivity is associated with an autoimmune diathesis of the mother. We screened plasma of 2431 mothers of an ASD child from Simon Simplex Collection and plasma of 653 unselected women of child-bearing age for anti-brain antibodies using immunohistology on mouse brain. Positive and negative plasma from mothers with an ASD child were analyzed for anti-nuclear antibodies and for autoimmune disorders. Mothers of an ASD child were four times more likely to harbor anti-brain antibodies than unselected women of child-bearing age (10.5 vs 2.6%). A second cohort from The Autism Genetic Resource Exchange with multiplex families displayed an 8.8% prevalence of anti-brain antibodies in the mothers of these families. Fifty-three percent of these mothers with anti-brain antibodies also exhibited anti-nuclear autoantibodies compared with 13.4% of mothers of an ASD child without anti-brain antibodies and 15% of control women of child-bearing age. The analysis of ASD mothers with brain-reactive antibodies also revealed an increased prevalence of autoimmune diseases, especially rheumatoid arthritis and systemic lupus erythematosus. This study provides robust evidence that brain-reactive antibodies are increased in mothers of an ASD child and may be associated with autoimmunity. The current study serves as a benchmark and justification for studying the potential pathogenicity of these antibodies on the developing brain. The detailed characterization of the specificity of these antibodies will provide practical benefits for the management and prevention of this disorder.
C1 [Brimberg, L.; Sadiq, A.; Diamond, B.] Ctr Autoimmune & Musculoskeletal Dis, Manhasset, NY USA.
[Gregersen, P. K.] Feinstein Inst Med Res, Ctr Genom & Human Genet, Manhasset, NY 11030 USA.
RP Diamond, B (reprint author), Feinstein Inst Med Res, Ctr Autoimmune & Musculoskeletal Dis, 350 Community Dr, Manhasset, NY 11030 USA.
EM bdiamond@nshs.edu
FU Bradley; Simons Foundation, Autism Speaks
FX We thank Dr Marta Benedetti at the Simons Foundation and William Jensen
at Prometheus Research for assistance with obtaining and analyzing
clinical data on the Simons collection. We also thank Matt State for
access to genetic data on mothers in the Simons Collection; Bradley and
Jennifer Marsh for seed funding for this project. This work was
supported by Simons Foundation, Autism Speaks.
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NR 38
TC 13
Z9 13
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD NOV
PY 2013
VL 18
IS 11
BP 1171
EP 1177
DI 10.1038/mp.2013.101
PG 7
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 240KN
UT WOS:000326094800006
PM 23958959
ER
PT J
AU Szatkiewicz, JP
Neale, BM
O'Dushlaine, C
Fromer, M
Goldstein, JI
Moran, JL
Chambert, K
Kahler, A
Magnusson, PKE
Hultman, CM
Sklar, P
Purcell, S
McCarroll, SA
Sullivan, PF
AF Szatkiewicz, J. P.
Neale, B. M.
O'Dushlaine, C.
Fromer, M.
Goldstein, J. I.
Moran, J. L.
Chambert, K.
Kahler, A.
Magnusson, P. K. E.
Hultman, C. M.
Sklar, P.
Purcell, S.
McCarroll, S. A.
Sullivan, P. F.
TI Detecting large copy number variants using exome genotyping arrays in a
large Swedish schizophrenia sample
SO MOLECULAR PSYCHIATRY
LA English
DT Article
DE copy number variation; exome array; genotyping; Illumina; schizophrenia;
structural variation
ID CHROMOSOME 16P11.2; ASSOCIATION; GENOME; DUPLICATIONS; DELETIONS;
DISEASE; AUTISM
AB Although copy number variants (CNVs) are important in genomic medicine, CNVs have not been systematically assessed for many complex traits. Several large rare CNVs increase risk for schizophrenia (SCZ) and autism and often demonstrate pleiotropic effects; however, their frequencies in the general population and other complex traits are unknown. Genotyping large numbers of samples is essential for progress. Large cohorts from many different diseases are being genotyped using exome-focused arrays designed to detect uncommon or rare protein-altering sequence variation. Although these arrays were not designed for CNV detection, the hybridization intensity data generated in each experiment could, in principle, be used for gene-focused CNV analysis. Our goal was to evaluate the extent to which CNVs can be detected using data from one particular exome array (the Illumina Human Exome Bead Chip). We genotyped 9100 Swedish subjects (3962 cases with SCZ and 5138 controls) using both standard genome-wide association study (GWAS) and exome arrays. In comparison with CNVs detected using GWAS arrays, we observed high sensitivity and specificity for detecting genic CNVs >= 400 kb including known pathogenic CNVs along with replicating the literature finding that cases with SCZ had greater enrichment for genic CNVs. Our data confirm the association of SCZ with 16p11.2 duplications and 22q11.2 deletions, and suggest a novel association with deletions at 11q12.2. Our results suggest the utility of exome-focused arrays in surveying large genic CNVs in very large samples; and thereby open the door for new opportunities such as conducting well-powered CNV assessment and comparisons between different diseases. The use of a single platform also minimizes potential confounding factors that could impact accurate detection.
C1 [Szatkiewicz, J. P.; Sullivan, P. F.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
[Neale, B. M.; Goldstein, J. I.; Purcell, S.] Harvard Univ, Sch Med, Analyt & Translat Genet Unit, Boston, MA USA.
[Neale, B. M.; O'Dushlaine, C.; Fromer, M.; Moran, J. L.; Chambert, K.; McCarroll, S. A.] Broad Inst MIT & Harvard, Stanley Ctr Psychiat Res, Cambridge, MA USA.
[Fromer, M.; Sklar, P.; Purcell, S.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Kahler, A.; Magnusson, P. K. E.; Hultman, C. M.; Sullivan, P. F.] Karolinska Inst, Dept Med Epidemiol, Stockholm, Sweden.
[McCarroll, S. A.] Harvard Univ, Sch Med, Dept Genet, Boston, MA USA.
RP Sullivan, PF (reprint author), Univ N Carolina, Dept Genet, CB 7264,5097 Genom Med Bldg, Chapel Hill, NC 27599 USA.
EM pfsulliv@med.unc.edu
RI Kahler, Anna/J-2874-2012
FU Stanley Center for Psychiatric Research; Karolinska Institutet;
Karolinska University Hospital,; Swedish Research Council; Swedish
County Council; Soderstrom Konigska Foundation; Sylvan Herman
Foundation; [K01 MH093517]; [R01 MH077139]
FX Funding was from K01 MH093517 (JPS), R01 MH077139 (PFS), the Stanley
Center for Psychiatric Research, the Karolinska Institutet, Karolinska
University Hospital, the Swedish Research Council, an ALF grant from
Swedish County Council, the Soderstrom Konigska Foundation and the
Sylvan Herman Foundation. This study makes use of data generated by the
DECIPHER Consortium. A full list of centers who contributed to the
generation of the data is available from http://decipher.sanger.ac.uk or
from decipher@sanger.ac.uk. Funding for the project was provided by the
Wellcome Trust. We thank two anonymous reviewers for their helpful
comments. All authors reviewed and approved the final version of the
manuscript. The corresponding authors had access to the full data set.
CR Bergen SE, 2012, MOL PSYCHIATR, V17, P880, DOI 10.1038/mp.2012.73
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NR 22
TC 3
Z9 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
EI 1476-5578
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD NOV
PY 2013
VL 18
IS 11
BP 1178
EP 1184
DI 10.1038/mp.2013.98
PG 7
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 240KN
UT WOS:000326094800007
PM 23938935
ER
PT J
AU Bernard, PB
Castano, AM
O'Leary, H
Simpson, K
Browning, MD
Benke, TA
AF Bernard, Paul B.
Castano, Anna M.
O'Leary, Heather
Simpson, Kameron
Browning, Michael D.
Benke, Tim A.
TI Phosphorylation of FMRP and alterations of FMRP complex underlie
enhanced mLTD in adult rats triggered by early life seizures
SO NEUROBIOLOGY OF DISEASE
LA English
DT Article
DE Seizure; Long-term depression (LTD); Metabotropic glutamate receptor
(mGluR); Fragile X Mental Retardation Protein (FMRP); Protein
phosphatase 2A (PP2A); Striatal-enriched tyrosine protein phosphatase
(STEP)
ID LONG-TERM DEPRESSION; FRAGILE-X-SYNDROME; MENTAL-RETARDATION PROTEIN;
TYROSINE PHOSPHATASE STEP; KINASE ANCHORING PROTEIN; MESSENGER-RNA
GRANULES; BRAIN DAMAGE SYNDROME; MOUSE MODEL; NEONATAL SEIZURES; NMDA
RECEPTOR
AB Outside of Fragile X syndrome (FXS), the role of Fragile-X Mental Retardation Protein (FMRP) in mediating neuropsychological abnormalities is not clear. FMRP, p70-S6 kinase (S6K) and protein phosphatase 2A (PP2A) are thought to cooperate as a dynamic signaling complex. In our prior work, adult rats have enhanced CA1 hippocampal long-term depression (LTD) following an early life seizure (ELS). We now show that mGluR-mediated LTD (mLTD) is specifically enhanced following ELS, similar to FMRP knock-outs. Total FMRP expression is unchanged but S6K is hyperphosphorylated, consistent with S6K overactivation. We postulated that either disruption of the FMRP-S6K-PP2A complex and/or removal of this complex from synapses could explain our findings. Using subcellular fractionation, we were surprised to find that concentrations of FMRP and PP2A were undisturbed in the synaptosomal compartment but reduced in parallel in the cytosolic compartment. Following ELS FMRP phosphorylation was reduced in the cytosolic compartment and increased in the synaptic compartment, in parallel with the compartmentalization of S6K activation. Furthermore, FMRP and PP2A remain bound following ELS. In contrast, the interaction of S6K with FMRP is reduced by ELS. Blockade of PP2A results in enhanced mLTD; this is occluded by ELS. This suggests a critical role for the location and function of the FMRP-S6K-PP2A signaling complex in limiting the amount of mLTD. Specifically, non-synaptic targeting and the function of the complex may influence the "set-point" for regulating mLTD. Consistent with this, striatal-enriched protein tyrosine phosphatase (STEP), an FMRP "target" which regulates mLTD expression, is specifically increased in the synaptosomar compai Unent following ELS. Further, we provide behavioral data to suggest that FMRP complex dysfunction may underlie altered socialization, a symptom associated and observed in other rodent models of autism, including FXS. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Bernard, Paul B.; Castano, Anna M.; O'Leary, Heather; Benke, Tim A.] Univ Colorado, Sch Med, Dept Pediat, Denver, CO 80202 USA.
[Benke, Tim A.] Univ Colorado, Sch Med, Grad Program Neurosci, Denver, CO 80202 USA.
[Simpson, Kameron; Browning, Michael D.] PhosphoSolutions, Aurora, CO USA.
[Benke, Tim A.] Univ Colorado, Sch Med, Dept Neurol, Denver, CO 80202 USA.
[Benke, Tim A.] Univ Colorado, Sch Med, Dept Pharmacol, Denver, CO 80262 USA.
[Benke, Tim A.] Univ Colorado, Sch Med, Dept Otolaryngol, Denver, CO 80202 USA.
RP Benke, TA (reprint author), Univ Colorado, Sch Med, 12800 E 19th,MS8102, Denver, CO 80045 USA.
EM tim.benke@ucdenver.edu
FU Children's Hospital Colorado Research Institute; Epilepsy Foundation;
NIH-NINDS [R01 NS076577]
FX Special thanks to, Ulli Bayer, Mark Dell'Acqua, Steve Coultrap and other
members of the Benke, Bayer and Dell'Acqua labs, Ms. Vivian Carlson and
Ms. Christy Beitzel for behavioral analysis, Dr. Yogi Raol and the UC
Rodent In Vivo Neurophysiology Core, the IDDRC behavior core, the UC
Pharmacology Microscopy Core and Dr Tom Finger and the UC CDB Microscopy
core. Thanks to Dr. Stephen Warren, Emory University, for supplying the
FMRP-wild-type and S499A-FMR1 plasmids. Funding provided by the
Children's Hospital Colorado Research Institute, Epilepsy Foundation,
and NIH-NINDS (R01 NS076577). The content is solely the responsibility
of the authors and does not necessarily represent the official views of
NINDS or NIH.
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NR 87
TC 8
Z9 8
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0969-9961
EI 1095-953X
J9 NEUROBIOL DIS
JI Neurobiol. Dis.
PD NOV
PY 2013
VL 59
BP 1
EP 17
DI 10.1016/j.nbd.2013.06.013
PG 17
WC Neurosciences
SC Neurosciences & Neurology
GA 221MV
UT WOS:000324663900001
PM 23831253
ER
PT J
AU Nilsen, RM
Suren, P
Gunnes, N
Alsaker, ER
Bresnahan, M
Hirtz, D
Hornig, M
Lie, KK
Lipkin, WI
Reichborn-Kjennerud, T
Roth, C
Schjolberg, S
Smith, GD
Susser, E
Vollset, SE
Oyen, AS
Magnus, P
Stoltenberg, C
AF Nilsen, Roy M.
Suren, Pal
Gunnes, Nina
Alsaker, Elin R.
Bresnahan, Michaeline
Hirtz, Deborah
Hornig, Mady
Lie, Kari Kveim
Lipkin, W. Ian
Reichborn-Kjennerud, Ted
Roth, Christine
Schjolberg, Synnve
Smith, George Davey
Susser, Ezra
Vollset, Stein Emil
Oyen, Anne-Siri
Magnus, Per
Stoltenberg, Camilla
TI Analysis of Self-selection Bias in a Population-based Cohort Study of
Autism Spectrum Disorders
SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY
LA English
DT Article
DE Autism; cohort; Norway; pregnancy; selection bias
ID FOLIC-ACID SUPPLEMENTS; PERINATAL RISK-FACTORS; INFANTILE-AUTISM;
CHILDREN; PARTICIPATION; ASSOCIATION; PREVALENCE; REGISTRY; CHARGE;
DELAY
AB BackgroundThis study examined potential self-selection bias in a large pregnancy cohort by comparing exposure-outcome associations from the cohort to similar associations obtained from nationwide registry data. The outcome under study was specialist-confirmed diagnosis of autism spectrum disorders (ASDs).
MethodsThe cohort sample (n=89836) was derived from the population-based prospective Norwegian Mother and Child Cohort Study and its substudy of ASDs, the Autism Birth Cohort (ABC) study. The nationwide registry data were derived from the Medical Birth Registry of Norway (n=507856). The children were born in 1999-2007, and seven prenatal and perinatal exposures were selected for analyses.
ResultsASDs were reported for 234 (0.26%) children in the cohort and 2072 (0.41%) in the nationwide population. Compared with the nationwide population, the cohort had an under-representation of the youngest women (<25 years), those who had single status, mothers who smoked during pregnancy, and non-users of prenatal folic acid supplements. The ratios of the adjusted odds ratios (ORs) in the cohort over the adjusted ORs in the nationwide population were as follows; primipara pregnancy: 1.39/1.22, prenatal folic acid use: 0.85/0.86, prenatal smoking: 1.20/1.17, preterm birth (<37 weeks): 1.48/1.42, low birthweight (<2500g): 1.60/1.58, male sex: 4.39/4.59 (unadjusted only); and caesarean section history: 1.03/1.04.
ConclusionsAssociations estimated between ASDs and perinatal and prenatal exposures in the cohort are close to those estimated in the nationwide population. Self-selection does not appear to compromise validity of exposure-outcome associations in the ABC study.
C1 [Nilsen, Roy M.; Vollset, Stein Emil; Stoltenberg, Camilla] Univ Bergen, Dept Global Publ Hlth & Primary Care, N-5018 Bergen, Norway.
[Reichborn-Kjennerud, Ted] Univ Oslo, Inst Psychiat, N-0316 Oslo, Norway.
[Oyen, Anne-Siri] Lovisenberg Hosp, Nic Waals Inst, Oslo, Norway.
[Bresnahan, Michaeline; Hornig, Mady; Lipkin, W. Ian; Susser, Ezra] Columbia Univ, Mailman Sch Publ Hlth, New York, NY USA.
[Hirtz, Deborah] NINDS, Bethesda, MD 20892 USA.
[Smith, George Davey] Univ Bristol, MRC Integrat Epidemiol Unit IEU, Bristol, Avon, England.
RP Nilsen, RM (reprint author), Univ Bergen, Dept Global Publ Hlth & Primary Care, Kalfarveien 31, N-5018 Bergen, Norway.
EM roy.nilsen@uib.no
FU Norwegian Ministry of Health and Care Services; Norwegian Ministry of
Education and Research; Research Council of Norway/FUGE [151918];
National Institute of Neurological Disorders and Stroke (NIH/NINDS),
Bethesda, MD, USA [NS47537]; National Institute of Environmental Health
Sciences (NIH/NIEHS), Research Triangle Park, NC, USA [NO-ES-75558];
NINDS [NS47537]; Faculty of Medicine and Dentistry, University of
Bergen, Norway
FX The authors are indebted to Ane Johannessen for her valuable comments on
previous versions of this manuscript. The Norwegian Mother and Child
Cohort Study is supported by the Norwegian Ministry of Health and Care
Services, the Norwegian Ministry of Education and Research, the Research
Council of Norway/FUGE (grant 151918), the National Institute of
Neurological Disorders and Stroke (NIH/NINDS), Bethesda, MD, USA [grant
NS47537 (Lipkin)], and the National Institute of Environmental Health
Sciences (NIH/NIEHS), Research Triangle Park, NC, USA (contract
NO-ES-75558). The Autism Birth Cohort study is funded by the NINDS
[grant NS47537 (Lipkin)]. The current work was supported by the Faculty
of Medicine and Dentistry, University of Bergen, Norway.
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NR 30
TC 10
Z9 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0269-5022
EI 1365-3016
J9 PAEDIATR PERINAT EP
JI Paediatr. Perinat. Epidemiol.
PD NOV
PY 2013
VL 27
IS 6
BP 553
EP 563
DI 10.1111/ppe.12077
PG 11
WC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
SC Public, Environmental & Occupational Health; Obstetrics & Gynecology;
Pediatrics
GA 238WZ
UT WOS:000325983800006
PM 23919580
ER
PT J
AU Dolique, T
Favereaux, A
Roca-Lapirot, O
Roques, V
Leger, C
Landry, M
Nagy, F
AF Dolique, Tiphaine
Favereaux, Alexandre
Roca-Lapirot, Olivier
Roques, Virginie
Leger, Claire
Landry, Marc
Nagy, Frederic
TI Unexpected association of the "inhibitory" neuroligin 2 with excitatory
PSD95 in neuropathic pain
SO PAIN
LA English
DT Article
DE Dorsal horn; Neuroligin; Neuropathic pain; Painful sensitization; Spinal
cord
ID CELL-ADHESION MOLECULE; SYNAPSE FORMATION; GLUTAMATERGIC SYNAPSES;
VARIABLE PHENOTYPE; SPINAL MOTONEURONS; ALPHA-NEUREXINS; BETA-NEUREXINS;
EXPRESSION; PSD-95; AUTISM
AB In the spinal nerve ligation (SNL) model of neuropathic pain, synaptic plasticity shifts the excitation/inhibition balance toward excitation in the spinal dorsal horn. We investigated the deregulation of the synaptogenic neuroligin (NL) molecules, whose NL1 and NL2 isoforms are primarily encountered at excitatory and inhibitory synapses, respectively. In the dorsal horn of SNL rats, NL2 was overexpressed whereas NL1 remained unchanged. In control animals, intrathecal injections of small interfering RNA (siRNA) targeting NL2 increased mechanical sensitivity, which confirmed the association of NL2 with inhibition. By contrast, siRNA application produced antinociceptive effects in SNL rats. Regarding NL partners, expression of the excitatory postsynaptic scaffolding protein PSD95 unexpectedly covaried with NL2 overexpression, and NL2/PSD95 protein interaction and colocalization increased. Expression of the inhibitory scaffolding protein gephyrin remained unchanged, indicating a partial change in NL2 postsynaptic partners in SNL rats. This phenomenon appears to be specific to the NL2(-) isoform. Our data showed unexpected upregulation and pronociceptive effects of the "inhibitory" NL2 in neuropathic pain, suggesting a functional shift of NL2 from inhibition to excitation that changed the synaptic ratio toward higher excitation. (C) 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
C1 [Dolique, Tiphaine; Favereaux, Alexandre; Roca-Lapirot, Olivier; Landry, Marc; Nagy, Frederic] CNRS, UMR5297, IINS, F-33077 Bordeaux, France.
[Dolique, Tiphaine; Favereaux, Alexandre; Roca-Lapirot, Olivier; Roques, Virginie; Leger, Claire; Landry, Marc; Nagy, Frederic] Univ Bordeaux, F-33077 Bordeaux, France.
[Roques, Virginie; Leger, Claire] INSERM, U862, Neuroctr Magendie, F-33077 Bordeaux, France.
[Dolique, Tiphaine] Inst Rech Clin Montreal, Montreal, PQ H2W 1R7, Canada.
RP Landry, M (reprint author), Univ Bordeaux 2, CNRS UMR5297, IINS, 146 Rue Leo Saignat, F-33077 Bordeaux, France.
EM marc.landry@u-bordeaux2.fr
FU ARC-INCa [07/3D1616/IABC-23-7/NC-NG]; Agence Nationale pour la Recherche
[ANR-07-NEURO-015-01]; Conseil Regional d'Aquitaine [2008/30/023];
French Ministry for Research; Fondation pour la Recherche Medicale
FX We are very grateful to Dr F. Varoqueaux (Max-Planck-Institute,
Goettingen, Germany) for providing us with the anti-NL2 antibody and for
helpful scientific discussion. We thank the Bordeaux Imaging Center and
especially C. Poujol for help in image analysis. This work was supported
by ARC-INCa (07/3D1616/IABC-23-7/NC-NG), Agence Nationale pour la
Recherche (ANR-07-NEURO-015-01), Conseil Regional d'Aquitaine
(2008/30/023), and studentships from the French Ministry for Research
and Fondation pour la Recherche Medicale to TD.
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NR 77
TC 1
Z9 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0304-3959
EI 1872-6623
J9 PAIN
JI Pain
PD NOV
PY 2013
VL 154
IS 11
BP 2529
EP 2546
DI 10.1016/j.pain.2013.07.035
PG 18
WC Anesthesiology; Clinical Neurology; Neurosciences
SC Anesthesiology; Neurosciences & Neurology
GA 238FG
UT WOS:000325927500037
PM 23891900
ER
PT J
AU Ibanez, JMG
Ristol, JEGA
AF Gavilan Ibanez, Jose M.
Garcia-Albea Ristol, Jose E.
TI Theory of mind and language comprehension in schizophrenia
SO PSICOTHEMA
LA English
DT Article
DE schizophrenia; theory of mind; language comprehension; executive
functions
ID PEOPLE; DEFICITS; IMPAIRMENTS; METAANALYSIS; PSYCHOSIS; SYMPTOMS;
CHILDREN; ORIGINS; ADULTS
AB Background: Theory of mind (ToM) is the natural ability to attribute/infer mental states about ourselves and others. The study of the limits of this capacity in autism-spectrum disorders has been projected more recently to the case of schizophrenia. Method: We review the studies on ToM deficiency in schizophrenia, based on the link observed by Chris Frith between psychotic symptoms and mentalizing anomalies, with particular attention to the implications of ToM in linguistic communication in the field of figurative language comprehension. Results: The data support a connection between ToM deficits and psychotic symptoms. In schizophrenia, the deficit in ToM appears to be specific and not dependent on more general cognitive abilities, and according to the evidence examined, it resembles a trait more than a state condition. The analysis of results shows that anomalies in ToM have projections on pragmatic aspects of language comprehension. Conclusions: ToM deficits showed by schizophrenic patients are especially linked to difficulties in understanding figurative language, beyond the influence of intelligence and executive functions.
C1 [Gavilan Ibanez, Jose M.; Garcia-Albea Ristol, Jose E.] Univ Rovira & Virgili, Res Ctr Behav Assessment CRAMC, E-43007 Tarragona, Spain.
RP Ibanez, JMG (reprint author), Univ Rovira & Virgili, Fac Ciencias Educ & Psicol, E-43007 Tarragona, Spain.
EM jm.gavilan@urv.cat
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NR 44
TC 0
Z9 0
PU COLEGIO OFICIAL DE PSICOLOGOS DE ASTURIAS
PI OVIEDO
PA ILDEFONSO S. DEL RIO, 4-1 B, 33001 OVIEDO, SPAIN
SN 0214-9915
EI 1886-144X
J9 PSICOTHEMA
JI Psicothema
PD NOV
PY 2013
VL 25
IS 4
BP 440
EP 445
DI 10.7334/psicothema2012.357
PG 6
WC Psychology, Multidisciplinary
SC Psychology
GA 236GJ
UT WOS:000325783200004
ER
PT J
AU Sundaramoorthy, R
Rao, KM
Abilash, VG
AF Sundaramoorthy, Rajiv
Rao, Kavya M.
Abilash, Valsala Gopalakrishnan
TI Genetic damage analysis of Autism Spectrum Disorder (ASD) patients of
Tamilnadu, South India using Cytokinesis-block micronucleus cytome (CBMN
cyt) assay
SO RESEARCH JOURNAL OF BIOTECHNOLOGY
LA English
DT Article
DE Autism; Human lymphocyte; CBMN; Cytochalasin-B; DNA damage
ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT HYPERACTIVITY DISORDER;
MENTAL-RETARDATION; IN-VITRO; GENOTOXICITY; PREVALENCE; CHILDREN;
ADOLESCENTS
AB The frequency of micronuclei in peripheral blood lymphocytes of ASD patients were monitored with the CBMN Assay. We have evaluated a random population of 46 children and 5 adults aged 2-24 years with appropriate age and sex matched controls. The patients were first clinically pre-screened with help of physician. Peripheral blood samples were collected from antecubital vein, cultured using RPMI-1640medium and treated with Cytochalasin-B. Harvested cells were stained using giemsa and a total of 1000 BN cells were scored for all the subjects. All the patients were analyzed cytogenetically and categorized clinically using the DSM-IV manual. Patients with PDD, ADHD, MR, AS and both PDD/ADHD, showed significant proportion of DNA damage which was statistically significant when compared with age and sex matched controls.
This study shows a significant level of DNA damage in ASD patients when compared to controls. To an extent, environmental, occupational exposures, lifestyle factors, dietary deficiencies and different diseases have also added up to the rise. Important knowledge gap still remains about the characteristics of micronuclei and other nuclear abnormalities, including the basic biology explaining the appearance of various cell types in autism patients which may be addressed by further studies.
C1 [Sundaramoorthy, Rajiv; Rao, Kavya M.; Abilash, Valsala Gopalakrishnan] VIT Univ, Div Biomol & Genet, Sch Biosci & Technol, Vellore 632014, Tamil Nadu, India.
RP Abilash, VG (reprint author), VIT Univ, Div Biomol & Genet, Sch Biosci & Technol, Vellore 632014, Tamil Nadu, India.
EM abilash.vg@vit.ac.in
FU VIT University
FX The authors are indebted to patients and family members for providing us
with blood samples. The authors would also like to thank the management
of VIT University for providing the facilities to carry out this work.
The author S.Rajiv is grateful to VIT University for providing the
financial assistance during this tenure.
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NR 40
TC 0
Z9 0
PU RESEARCH JOURNAL BIOTECHNOLOGY
PI INDORE
PA SECTOR A-80, SCHEME NO 54, VIJAY NAGAR, A B ROAD, INDORE, 452 010 MP,
INDIA
SN 0973-6263
J9 RES J BIOTECHNOL
JI Res. J. Biotechnol.
PD NOV
PY 2013
VL 8
IS 11
BP 78
EP 86
PG 9
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 237VX
UT WOS:000325900100014
ER
PT J
AU Falcomata, TS
Muething, CS
Gainey, S
Hoffman, K
Fragale, C
AF Falcomata, Terry S.
Muething, Colin S.
Gainey, Summer
Hoffman, Katherine
Fragale, Christina
TI Further Evaluations of Functional Communication Training and Chained
Schedules of Reinforcement to Treat Multiple Functions of Challenging
Behavior
SO BEHAVIOR MODIFICATION
LA English
DT Article
DE Asperger syndrome; autism; chained schedule of reinforcement;
challenging behavior; functional communication training
ID NEGATIVE REINFORCEMENT; ESCAPE; INTERVENTION; AUTISM
AB We evaluated functional communication training (FCT) combined with a chained schedule of reinforcement procedure for the treatment of challenging behavior exhibited by two individuals diagnosed with Asperger syndrome and autism. Following functional analyses that suggested that challenging behavior served multiple functions for both participants, we implemented FCT in which mands for a discriminative stimulus (S-D; wristband) were reinforced with access to the S-D and all three functional reinforcers. Next, we modified the procedure by incorporating delays to increase ease of implementation and promote toleration of delays to reinforcement. Last, we made additional modifications to the procedure by incorporating a chained schedule of reinforcement such that (a) mands for the wristband were reinforced with access to the wristband and (b) specific mands for respective functional reinforcers were reinforced in the presence of the wristband. The results showed that the procedure successfully treated challenging behavior with multiple functions. Future directions in the evaluation and development of treatments that simultaneously address multiple functions are discussed.
C1 [Falcomata, Terry S.; Gainey, Summer; Hoffman, Katherine] Univ Texas Austin, Dept Special Educ, Austin, TX 78712 USA.
[Muething, Colin S.] Univ Texas Austin, Dept Educ Psychol, Austin, TX 78712 USA.
RP Falcomata, TS (reprint author), Univ Texas Austin, Dept Special Educ, 1 Univ Stn D5300, Austin, TX 78712 USA.
EM falcomata@mail.utexas.edu
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NR 27
TC 1
Z9 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0145-4455
EI 1552-4167
J9 BEHAV MODIF
JI Behav. Modificat.
PD NOV
PY 2013
VL 37
IS 6
BP 723
EP 746
DI 10.1177/0145445513500785
PG 24
WC Psychology, Clinical
SC Psychology
GA 234PW
UT WOS:000325657400002
PM 23990645
ER
PT J
AU Giannopulu, I
AF Giannopulu, Irini
TI Multimodal interactions in typically and atypically developing children:
natural versus artificial environments
SO COGNITIVE PROCESSING
LA English
DT Review
DE Multimodal interactions; Verbal/nonverbal development; Autism; Mobile
toy robot; Free game play; Positive emotion; Neural mediator
ID PERVASIVE DEVELOPMENTAL DISORDERS; POSITRON-EMISSION-TOMOGRAPHY; ROBOT
INTERACTION; DECISION-MAKING; AUTISM; BRAIN; IMITATION; LANGUAGE;
CHILDHOOD; CORTEX
AB This review addresses the central role played by multimodal interactions in neurocognitive development. We first analyzed our studies of multimodal verbal and nonverbal cognition and emotional interactions within neuronal, that is, natural environments in typically developing children. We then tried to relate them to the topic of creating artificial environments using mobile toy robots to neurorehabilitate severely autistic children. By doing so, both neural/natural and artificial environments are considered as the basis of neuronal organization and reorganization. The common thread underlying the thinking behind this approach revolves around the brain's intrinsic properties: neuroplasticity and the fact that the brain is neurodynamic. In our approach, neural organization and reorganization using natural or artificial environments aspires to bring computational perspectives into cognitive developmental neuroscience.
C1 Univ Paris 06, F-75005 Paris, France.
RP Giannopulu, I (reprint author), Univ Paris 06, 4 Pl Jussieu, F-75005 Paris, France.
EM igiannopulu@psycho-prat.fr
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NR 96
TC 0
Z9 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1612-4782
EI 1612-4790
J9 COGN PROCESS
JI Cogn. Process.
PD NOV
PY 2013
VL 14
IS 4
BP 323
EP 331
DI 10.1007/s10339-013-0566-0
PG 9
WC Psychology, Experimental
SC Psychology
GA 235FM
UT WOS:000325702200001
PM 23689878
ER
PT J
AU LeBarton, ES
Iverson, JM
AF LeBarton, Eve Sauer
Iverson, Jana M.
TI Fine motor skill predicts expressive language in infant siblings of
children with autism
SO DEVELOPMENTAL SCIENCE
LA English
DT Article
ID COMMUNICATIVE DEVELOPMENT INVENTORY; SPECTRUM DISORDERS; IMPAIRMENT;
DYSPRAXIA; TODDLERS; DEFICITS; RISK
AB We investigated whether fine motor and expressive language skills are related in the later-born siblings of children with autism (heightened-risk, HR infants) who are at increased risk for language delays. We observed 34 HR infants longitudinally from 12 to 36months. We used parent report and standardized observation measures to assess fine motor skill from 12 to 24months in HR infants (Study 1) and its relation to later expressive vocabulary at 36months in HR infants (Study 2). In Study 1, we also included 25 infants without a family history of autism to serve as a normative comparison group for a parent-report fine motor measure. We found that HR infants exhibited fine motor delays between 12 and 24months and expressive vocabulary delays at 36months. Further, fine motor skill significantly predicted expressive language at 36months. Fine motor and expressive language skills are related early in development in HR infants, who, as a group, exhibit risk for delays in both. Our findings highlight the importance of considering fine motor skill in children at risk for language impairments and may have implications for early identification of expressive language difficulties.
C1 [LeBarton, Eve Sauer; Iverson, Jana M.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
RP LeBarton, ES (reprint author), Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
EM eal48@pitt.edu
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NR 44
TC 10
Z9 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1467-7687
J9 DEVELOPMENTAL SCI
JI Dev. Sci.
PD NOV
PY 2013
VL 16
IS 6
BP 815
EP 827
DI 10.1111/desc.12069
PG 13
WC Psychology, Developmental; Psychology, Experimental
SC Psychology
GA 233EP
UT WOS:000325549300003
PM 24118709
ER
PT J
AU Hermann, I
Haser, V
van Elst, LT
Ebert, D
Muller-Feldmeth, D
Riedel, A
Konieczny, L
AF Hermann, Ismene
Haser, Verena
van Elst, Ludger Tebartz
Ebert, Dieter
Mueller-Feldmeth, Daniel
Riedel, Andreas
Konieczny, Lars
TI Automatic metaphor processing in adults with Asperger syndrome: a
metaphor interference effect task
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Article
DE Asperger syndrome; Nonliteral language; Novel metaphors; Metaphor
comprehension; Metaphor interference effect; Autism spectrum disorders
(ASD); Pragmatic language
ID HIGH-FUNCTIONING AUTISM; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDER;
LITERAL LANGUAGE; RATING-SCALE; CHILDREN; COMPREHENSION; INDIVIDUALS;
COMMUNICATION; INFORMATION
AB This paper investigates automatic processing of novel metaphors in adults with Asperger Syndrome (AS) and typically developing controls. We present an experiment combining a semantic judgment task and a recognition task. Four types of sentences were compared: Literally true high-typical sentences, literally true low-typical sentences, apt metaphors, and scrambled metaphors (literally false sentences which are not readily interpretable as metaphors). Participants were asked to make rapid decisions about the literal truth of such sentences. The results revealed that AS and control participants showed significantly slower RTs for metaphors than for scrambled metaphors and made more mistakes in apt metaphoric sentences than in scrambled metaphors. At the same time, there was higher recognition of apt metaphors compared with scrambled metaphors. The findings indicate intact automatic metaphor processing in AS and replicate previous findings on automatic metaphor processing in typically developing individuals.
C1 [Hermann, Ismene; van Elst, Ludger Tebartz; Ebert, Dieter; Riedel, Andreas] Univ Med Ctr Freiburg, Dept Psychiat & Psychotherapy, D-79104 Freiburg, Germany.
[Haser, Verena] Univ Freiburg, Dept English Linguist, D-79106 Freiburg, Germany.
[Mueller-Feldmeth, Daniel; Konieczny, Lars] Univ Freiburg, Ctr Cognit Sci, D-79106 Freiburg, Germany.
RP Riedel, A (reprint author), Univ Med Ctr Freiburg, Dept Psychiat & Psychotherapy, Hauptstr 5, D-79104 Freiburg, Germany.
EM andreas.riedel@uniklinik-freiburg.de
FU German Association for Psychiatry and Psychotherapy (DGPPN)
FX This article is part of the supplement "Bridging the gap between
Neurobiology and Psychosocial Medicine". This supplement was not
sponsored by outside commercial interests. It was funded by the German
Association for Psychiatry and Psychotherapy (DGPPN).
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NR 50
TC 2
Z9 2
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
EI 1433-8491
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD NOV
PY 2013
VL 263
SU 2
BP S177
EP S187
DI 10.1007/s00406-013-0453-9
PG 11
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 238KC
UT WOS:000325944100007
PM 24081827
ER
PT J
AU Montag, C
Sauer, C
Reuter, M
Kirsch, P
AF Montag, Christian
Sauer, Carina
Reuter, Martin
Kirsch, Peter
TI An interaction between oxytocin and a genetic variation of the oxytocin
receptor modulates amygdala activity toward direct gaze: evidence from a
pharmacological imaging genetics study
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Article
DE Oxytocin; Gaze; Amygdala; Oxytocin receptor gene; Imaging genetics
ID INTRANASAL OXYTOCIN; SOCIAL COGNITION; NEURAL CIRCUITRY; AUTISM; HUMANS;
VASOPRESSIN; FACES; OXTR; ASSOCIATION; BEHAVIOR
AB The neuropeptide oxytocin plays an important role in social cognition. One valuable tool to study social cognition in healthy and autistic humans in a neuroscientific context is the investigation of gaze toward another person. Of importance, it has been demonstrated that pronounced amygdala activation could be observed, when participants are confronted with direct gaze pictures in an fMRI setting, an effect that can be particularly observed in autistic individuals. In the present study, a combined pharmacological imaging genetics study has been conducted to further investigate the biological basis of direct gaze processing. N = 55 healthy males were invited to an oxytocin challenge study administered while watching direct vs. averted gaze pictures in an fMRI setting. In addition, the promoter region of the oxytocin receptor (OXTR) gene of the participants was investigated to search for individual differences in the recorded BOLD signal. The main result revealed that a genetic variation of the OXTR gene (rs401015) modulated the right amygdala activity for the fMRI contrast "direct < averted gaze" under the influence of the neuropeptide oxytocin. Here, carriers of the heterozygous CT variant showed higher activity compared to the TT group. The present study highlights the role of individual differences in a genetic variant of the OXTR gene for amygdala activation during processing of direct gaze pictures after intranasal oxytocin administration. In sum, the study shows the importance of combining a pharmacological challenge with genetic imaging to better understand the biological basis of social cognition.
C1 [Montag, Christian; Reuter, Martin] Univ Bonn, Dept Psychol, Bonn, Germany.
[Montag, Christian; Reuter, Martin] Univ Bonn, Neurogenet Lab, Bonn, Germany.
[Montag, Christian; Reuter, Martin] Univ Bonn, Ctr Econ & Neurosci, Bonn, Germany.
[Sauer, Carina; Kirsch, Peter] Heidelberg Univ, Cent Inst Mental Hlth, Med Fac Mannheim, Dept Clin Psychol, D-68159 Mannheim, Germany.
RP Kirsch, P (reprint author), Heidelberg Univ, Cent Inst Mental Hlth, Med Fac Mannheim, Dept Clin Psychol, J5, D-68159 Mannheim, Germany.
EM peter.kirsch@zi-mannheim.de
FU Deutsche Forschungsgemeinschaft (German Research Association, DFG) [KI
576/10-1, RE 1692/4-1]
FX This research was supported by a research grant from the Deutsche
Forschungsgemeinschaft (German Research Association, DFG) to PK (KI
576/10-1) and MR (RE 1692/4-1). We thank Christiane Worner, Andre
Spachmann and Dagmar Gass for their assistance during data collection
and analysis.
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NR 36
TC 1
Z9 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
EI 1433-8491
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD NOV
PY 2013
VL 263
SU 2
BP S169
EP S175
DI 10.1007/s00406-013-0452-x
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 238KC
UT WOS:000325944100006
PM 24071915
ER
PT J
AU van Elst, LT
Pick, M
Biscaldi, M
Fangmeier, T
Riedel, A
AF van Elst, Ludger Tebartz
Pick, Marion
Biscaldi, Monica
Fangmeier, Thomas
Riedel, Andreas
TI High-functioning autism spectrum disorder as a basic disorder in adult
psychiatry and psychotherapy: psychopathological presentation, clinical
relevance and therapeutic concepts
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Review
DE Autism; High-functioning autism; Asperger's syndrome; Classification;
Adults; Therapy; Comorbidity
ID ASPERGER SYNDROME; DIAGNOSIS; CHILDHOOD; COMMUNITY; ETIOLOGY; GENETICS
AB Autism spectrum disorder (ASD) is characterized by deficits in social cognition and competence, communication, highly circumscribed interests and a strong desire for routines. Besides, there are specific abnormalities in perception and language. Typical symptoms are already present in early childhood. Traditionally autism has been regarded as a severe form of neurodevelopmental disorder which goes along with overtly abnormal language, learning difficulties and low IQ in the majority of cases. However, over the last decades, it has become clear that there are also many patients with high-functioning variants of ASD. These are patients with normal language at a superficial level of description and normal and sometimes above average intelligence. In high-functioning variants of the disease, they may run unrecognized until late in adult life. High-functioning ASD is associated with a very high prevalence of comorbid classical psychiatric disorders such as depression, anxiety, ADHD, tics, psychotic symptoms or emotionally unstable syndromes. In many such cases, there is a causal relationship between ASD and the comorbid psychiatric conditions in that the specific ASD symptoms result in chronic conflicts, misunderstandings and failure in private and vocational relationships. These problems in turn often lead to depression, anxiety and sometimes psychosis-like stress reactions. In this constellation, ASD has to be regarded as a basic disorder with causal relevance for secondary psychiatric syndromes. In this paper, we summarize the classical presentation of high-functioning ASD in adult psychiatry and psychotherapy and suggest a nosological model to classify different ASD conditions instead. To conclude, we outline first treatment concepts in out-and in-patient settings.
C1 [van Elst, Ludger Tebartz; Pick, Marion; Fangmeier, Thomas; Riedel, Andreas] Univ Med Ctr Freiburg, Dept Psychiat & Psychotherapy, D-79104 Freiburg, Germany.
[Biscaldi, Monica] Univ Med Ctr Freiburg, Dept Child & Adolescent Psychiat & Psychotherapy, D-79104 Freiburg, Germany.
RP van Elst, LT (reprint author), Univ Med Ctr Freiburg, Dept Psychiat & Psychotherapy, Hauptstr 5, D-79104 Freiburg, Germany.
EM tebartzvanelst@uniklinik-freiburg.de;
andreas.riedel@uniklinik-freiburg.de
FU UCB; GSK; Lilly; Janssen CilAG; Lundbeck; German Association for
Psychiatry and Psychotherapy (DGPPN)
FX LTvE has given lectures and workshops on the issues of autism,
schizophrenia, depression, brain imaging, psychotherapy, epilepsy, etc.
which were at least in part supported by the following companies: UCB,
GSK, Lilly, Janssen CilAG, Lundbeck. He has been advisor to UCB with
respect to psychiatric aspects in epilepsy. The other authors declare
that they have no conflict of interest.This article is part of the
supplement "Bridging the gap between Neurobiology and Psychosocial
Medicine." This supplement was not sponsored by outside commercial
interests. It was funded by the German Association for Psychiatry and
Psychotherapy (DGPPN).
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NR 38
TC 7
Z9 7
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
EI 1433-8491
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD NOV
PY 2013
VL 263
SU 2
BP S189
EP S196
DI 10.1007/s00406-013-0459-3
PG 8
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 238KC
UT WOS:000325944100008
ER
PT J
AU Vogeley, K
Kirchner, JC
Gawronski, A
van Elst, LT
Dziobek, I
AF Vogeley, K.
Kirchner, J. C.
Gawronski, A.
van Elst, L. Tebartz
Dziobek, I.
TI Toward the development of a supported employment program for individuals
with high-functioning autism in Germany
SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE
LA English
DT Review
DE High-functioning autism (HFA); Asperger syndrome; Supported employment
program
ID QUALITY-OF-LIFE; SPECTRUM DISORDERS; ASPERGER-SYNDROME; VIRTUAL-REALITY;
YOUNG-ADULTS; DISABILITIES; SERVICES; CHILDREN
AB Human-human interactions are of central relevance for the success in professional and occupational environments, which also substantially influence quality of life. This is especially true in the case of individuals with high-functioning autism (HFA), who experience deficits in social cognition that often lead to social exclusion and unemployment. Despite good education and high motivation, individuals with HFA do not reach employment rates that are substantially higher than 50 %. This is an alarmingly high rate of unemployment considering that the United Nations have recently emphasized the inclusion of handicapped persons as a mandatory human right. To date, the specific needs of autistic persons with respect to their working environment are largely unexplored. It remains moreover an open question how support systems and activities, including newly developed communication devices for professional environments of individuals with HFA, should look like. The German health and social care systems are not adequately prepared for the proper support of this population. This leads us to suggest that supported employment programs should be developed for adults with HFA that specifically address their needs and requirements. Such programs should comprise (1) the adequate assessment of HFA, including a neuropsychological profile and an individual matching of persons' preferences with requirements of the working place, (2) on-the-job coaching activities that include systematic communication and interaction training, and (3) instruction of non-autistic peers, including colleagues and supervisors, about weaknesses and strengths of HFA.
C1 [Vogeley, K.; Gawronski, A.] Univ Hosp Cologne, Dept Psychiat, D-50924 Cologne, Germany.
[Vogeley, K.] Res Ctr Juelich, Inst Neurosci & Med, Julich, Germany.
[Kirchner, J. C.; Dziobek, I.] Free Univ Berlin, Cluster Excellence Languages Emot, Berlin, Germany.
[van Elst, L. Tebartz] Univ Hosp Freiburg, Clin Psychiat & Psychotherapy, Freiburg, Germany.
RP Vogeley, K (reprint author), Univ Hosp Cologne, Dept Psychiat, Kerpener Str 62, D-50924 Cologne, Germany.
EM kai.vogeley@uk-koeln.de
RI Vogeley, K/E-4860-2012
OI Vogeley, K/0000-0002-5891-5831
FU German Association for Psychiatry and Psychotherapy (DGPPN)
FX This article is part of the supplement "Bridging the gap between
Neurobiology and Psychosocial Medicine." This supplement was not
sponsored by outside commercial interests. It was funded by the German
Association for Psychiatry and Psychotherapy (DGPPN).
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NR 57
TC 1
Z9 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0940-1334
EI 1433-8491
J9 EUR ARCH PSY CLIN N
JI Eur. Arch. Psych. Clin. Neurosci.
PD NOV
PY 2013
VL 263
SU 2
BP S197
EP S203
DI 10.1007/s00406-013-0455-7
PG 7
WC Clinical Neurology; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 238KC
UT WOS:000325944100009
PM 24077909
ER
PT J
AU Mizutani, S
Tsunemi, T
Mizutani, E
Hattori, A
Tsujimoto, M
Kobayashi, H
AF Mizutani, Shigehiko
Tsunemi, Taihei
Mizutani, Eita
Hattori, Akira
Tsujimoto, Masafumi
Kobayashi, Hiroshi
TI New insights into the role of aminopeptidases in the treatment for both
preeclampsia and preterm labor
SO EXPERT OPINION ON INVESTIGATIONAL DRUGS
LA English
DT Review
DE aminopeptidase A; angiotensin; autism; beta-2 stimulant; cardiomyopathy;
fetal peptide hormone; magnesium sulfate; oxytocin; placental leucine
aminopeptidase; preeclampsia; preterm labor; vasopressin
ID SPONTANEOUSLY HYPERTENSIVE-RATS; PURIFIED PLACENTAL AMINOPEPTIDASES;
REGULATED MEMBRANE AMINOPEPTIDASE; ANGIOTENSIN-II RECEPTOR; IN-VITRO
DEGRADATION; P-LAP; SUBCELLULAR-FRACTIONS; ANTAGONIST ATOSIBAN;
PREGNANCY SERUM; DEFICIENT MICE
AB Introduction: Evidence elucidating the pathophysiology and pharmacology of conventional drugs, beta-2 stimulants and magnesium sulfate, on safety and effectiveness for preeclampsia and preterm labor are rarely found. Both compounds pass through the placental barrier and could exert their adverse effects on the fetus. Exposure to these agents could be problematic long after the birth, and possibly result in diseases such as autism and cardiomyopathy. Since 1970 the possible roles of placental aminopeptidases, which degrade peptide hormones, in preeclampsia and preterm labor have been studied.
Areas covered: Many studies reveal that the fetus secretes peptide hormones, such as angiotensin II, vasopressin, and oxytocin, under hypoxia (stress) during the course of its growth, suggesting the critical effects these hormones have during pregnancy. The roles of placental aminopeptidases, the enzymes which degrade fetal hormones without passing through the placental barrier, were clarified. A first-step production system for recombinant aminopeptidases was established, by which engineered recombinant aminopeptidases were used for further experiments testing expected efficacy on controlling the level of hormones.
Expert opinion: The authors conclude that both aminopeptidase A and placental leucine aminopeptidase could be potentially safe and effective drugs for patients and their babies in the treatment of preeclampsia and preterm labor.
C1 [Mizutani, Shigehiko; Mizutani, Eita] Daiya Bldg Ladys Clin, Nakamura Ku, Nagoya, Aichi 4500002, Japan.
[Mizutani, Shigehiko] Protect Neonates & Mother Preterm Birth & Preecla, Nakamura Ku, Nagoya, Aichi 4500002, Japan.
[Tsunemi, Taihei; Kobayashi, Hiroshi] Nara Med Univ, Dept Obstet & Gynecol, Kashihara, Nara 6348522, Japan.
[Hattori, Akira] Kyoto Univ, Sch Pharmaceut Sci, Div Bioinformat & Chem Genom Grad, Dept Syst Chemotherapy & Mol Sci,Sakyo Ku, Kyoto 6068501, Japan.
[Tsujimoto, Masafumi] Teikyo Heisei Univ, Fac Pharmaceut Sci, Nakano Ku, Tokyo 1648530, Japan.
RP Kobayashi, H (reprint author), Nara Med Univ, Dept Obstet & Gynecol, 840 Shijo Cho, Kashihara, Nara 6348522, Japan.
EM hirokoba@naramed-u.ac.jp
FU ministry of Education, Science and Culture of Japan
FX The paper was supported by a grant in aid of scientific research from
the ministry of Education, Science and Culture of Japan.
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NR 71
TC 1
Z9 1
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1354-3784
EI 1744-7658
J9 EXPERT OPIN INV DRUG
JI Expert Opin. Investig. Drugs
PD NOV
PY 2013
VL 22
IS 11
BP 1425
EP 1436
DI 10.1517/13543784.2013.825248
PG 12
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 235YV
UT WOS:000325760400007
PM 23931642
ER
PT J
AU Bolte, EE
Diehl, JJ
AF Bolte, Erin Elizabeth
Diehl, Joshua John
TI Measurement Tools and Target Symptoms/Skills Used to Assess Treatment
Response for Individuals with Autism Spectrum Disorder
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LA English
DT Article
DE Autism; Intervention; Treatment; Behavior; Symptoms; Measures
ID PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST; EARLY
INTERVENTION PROGRAMS; RATING-SCALE; VALIDITY; CHILDREN; RELIABILITY;
ADOLESCENTS; INVENTORY; ISSUES
AB This study examined the measurement tools and target symptoms/skills used to assess treatment response during Autism Spectrum Disorder (ASD) intervention trials from 2001 through 2010. Data from 195 prospective trials were analyzed. There were 289 unique measurement tools, of which 61.6 % were used only once, and 20.8 % were investigator-designed. Only three tools were used in more than 2 % of the studies, and none were used in more than 7 % of studies. Studies investigated an average of 11.4 tool-symptom combinations per trial, with as many as 45 in one study. These results represent a lack of consistency in outcome measurements in ASD intervention trials. These findings highlight the need to set guidelines for appropriate outcome measurement in the ASD field.
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RP Diehl, JJ (reprint author), Univ Notre Dame, Ctr Children & Families, 1602 N Ironwood Dr, South Bend, IN 46635 USA.
EM erinbolte@gmail.com; joshua.diehl@nd.edu
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NR 36
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2491
EP 2501
DI 10.1007/s10803-013-1798-7
PG 11
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000001
PM 23479074
ER
PT J
AU Green, J
Wan, MW
Guiraud, J
Holsgrove, S
McNally, J
Slonims, V
Elsabbagh, M
Charman, T
Pickles, A
Johnson, M
AF Green, Jonathan
Wan, Ming Wai
Guiraud, Jeanne
Holsgrove, Samina
McNally, Janet
Slonims, Vicky
Elsabbagh, Mayada
Charman, Tony
Pickles, Andrew
Johnson, Mark
CA BASIS Team
TI Intervention for Infants at Risk of Developing Autism: A Case Series
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Intervention; Prodromal; Infancy; Parent-child interaction
ID FUNCTIONAL BRAIN-DEVELOPMENT; DOWN-SYNDROME; SPECTRUM DISORDERS;
AT-RISK; CHILDREN; COMMUNICATION; LANGUAGE; ATTENTION; SIBLINGS;
PREDICTORS
AB Theory and evidence suggest the potential value of prodromal intervention for infants at risk of developing autism. We report an initial case series (n = 8) of a parent-mediated, video-aided and interaction-focused intervention with infant siblings of autistic probands, beginning at 8-10 months of age. We outline the theory and evidence base behind this model and present data on feasibility, acceptability and measures ranging from parent-infant social interaction, to infant atypical behaviors, attention and cognition. The intervention proves to be both feasible and acceptable to families. Measurement across domains was successful and on larger samples promise to be an effective test of whether such an intervention in infancy will modify emergent atypical developmental trajectories in infants at risk for autism.
C1 [Green, Jonathan; Wan, Ming Wai; Holsgrove, Samina; McNally, Janet] Univ Manchester, Inst Brain Behav & Mental Hlth, Manchester M13 9PL, Lancs, England.
[Guiraud, Jeanne; Elsabbagh, Mayada; Johnson, Mark] Univ London, Ctr Brain & Cognit Dev, Dept Psychol Sci, London WC1E 7HX, England.
[Slonims, Vicky] Guys & St Thomas NHS Fdn Trust, Kings Coll London, London SE1 9RT, England.
[Charman, Tony] Kings Coll London, Inst Psychiat, Dept Psychol, London SE5 8AF, England.
[Pickles, Andrew] Kings Coll London, Inst Psychiat, Dept Biostat, London SE5 8AF, England.
RP Green, J (reprint author), Univ Manchester, Inst Brain Behav & Mental Hlth, Room 4-308,Jean McFarlane Bldg,Oxford Rd, Manchester M13 9PL, Lancs, England.
EM jonathan.green@manchester.ac.uk
RI Charman, Tony/A-2085-2014; Bolton, Patrick/E-8501-2010; Pickles,
Andrew/A-9625-2011
OI Charman, Tony/0000-0003-1993-6549; Bolton, Patrick/0000-0002-5270-6262;
Pickles, Andrew/0000-0003-1283-0346
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NR 55
TC 10
Z9 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2502
EP 2514
DI 10.1007/s10803-013-1797-8
PG 13
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000002
PM 23532347
ER
PT J
AU Wilson, CE
Gillan, N
Spain, D
Robertson, D
Roberts, G
Murphy, CM
Maltezos, S
Zinkstok, J
Johnston, K
Dardani, C
Ohlsen, C
Deeley, PQ
Craig, M
Mendez, MA
Happe, F
Murphy, DGM
AF Wilson, C. Ellie
Gillan, Nicola
Spain, Deborah
Robertson, Dene
Roberts, Gedeon
Murphy, Clodagh M.
Maltezos, Stefanos
Zinkstok, Janneke
Johnston, Katie
Dardani, Christina
Ohlsen, Chris
Deeley, P. Quinton
Craig, Michael
Mendez, Maria A.
Happe, Francesca
Murphy, Declan G. M.
TI Comparison of ICD-10R, DSM-IV-TR and DSM-5 in an Adult Autism Spectrum
Disorder Diagnostic Clinic
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism Spectrum Disorder; Diagnosis; Prevalence; DSM-5
ID PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE INVENTORY;
CRITERIA; VALIDATION; INTERVIEW; VERSION; SAMPLE
AB An Autism Spectrum Disorder (ASD) diagnosis is often used to access services. We investigated whether ASD diagnostic outcome varied when DSM-5 was used compared to ICD-10R and DSM-IV-TR in a clinical sample of 150 intellectually able adults. Of those diagnosed with an ASD using ICD-10R, 56 % met DSM-5 ASD criteria. A further 19 % met DSM-5 (draft) criteria for Social Communication Disorder. Of those diagnosed with Autistic Disorder/Asperger Syndrome on DSM-IV-TR, 78 % met DSM-5 ASD criteria. Sensitivity of DSM-5 was significantly increased by reducing the number of criteria required for a DSM-5 diagnosis, or by rating 'uncertain' criteria as 'present', without sacrificing specificity. Reduced rates of ASD diagnosis may mean some ASD individuals will be unable to access clinical services.
C1 [Wilson, C. Ellie; Gillan, Nicola; Spain, Deborah; Roberts, Gedeon; Murphy, Clodagh M.; Maltezos, Stefanos; Zinkstok, Janneke; Dardani, Christina; Deeley, P. Quinton; Craig, Michael; Mendez, Maria A.; Murphy, Declan G. M.] Kings Coll London, Dept Forens & Neurodev Sci, Inst Psychiat, London SE5 8AF, England.
[Wilson, C. Ellie; Gillan, Nicola; Spain, Deborah; Robertson, Dene; Roberts, Gedeon; Murphy, Clodagh M.; Maltezos, Stefanos; Zinkstok, Janneke; Johnston, Katie; Ohlsen, Chris; Deeley, P. Quinton; Craig, Michael; Mendez, Maria A.; Murphy, Declan G. M.] South London & Maudsley NHS Fdn Trust, Behav Genet Clin, Maudsley Hosp, London SE5 8AZ, England.
[Happe, Francesca] Kings Coll London, Dept Social Genet Dev & Psychiat Ctr, Inst Psychiat, London SE5 8AF, England.
RP Wilson, CE (reprint author), Kings Coll London, Dept Forens & Neurodev Sci, Inst Psychiat, London SE5 8AF, England.
EM ellie.wilson@kcl.ac.uk
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NR 28
TC 9
Z9 9
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2515
EP 2525
DI 10.1007/s10803-013-1799-6
PG 11
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000003
PM 23504376
ER
PT J
AU Lampi, KM
Hinkka-Yli-Salomaki, S
Lehti, V
Helenius, H
Gissler, M
Brown, AS
Sourander, A
AF Lampi, Katja M.
Hinkka-Yli-Salomaki, Susanna
Lehti, Venla
Helenius, Hans
Gissler, Mika
Brown, Alan S.
Sourander, Andre
TI Parental Age and Risk of Autism Spectrum Disorders in a Finnish National
Birth Cohort
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Epidemiology; Autism spectrum disorders; Parental age
ID PERVASIVE DEVELOPMENTAL DISORDER; DE-NOVO MUTATIONS; PERINATAL FACTORS;
PATERNAL AGE; ASPERGER-SYNDROME; CONDUCT DISORDER; POPULATION;
SCHIZOPHRENIA; EPIGENETICS; PREGNANCY
AB Aim of the study was to examine the associations between parental age and autism spectrum disorders (ASD). Data were based on the FIPS-A (Finnish Prenatal Study of Autism and Autism Spectrum Disorders), a case-control study with a total of 4,713 cases with childhood autism (n = 1,132), Asperger's syndrome (n = 1,785) or other pervasive developmental disorder (PDD) (n = 1,796), which were ascertained from the Finnish Hospital Discharge Register. Controls were selected from the Finnish Medical Birth Register. Conditional logistic regression models were used for statistical analyses. Advanced paternal age (35-49 years) was associated with childhood autism in offspring, whereas advanced maternal age was associated with both Asperger's syndrome and PDD in offspring (35 years or more and 40 years or more, respectively). Teenage motherhood (19 years or less) was associated with PDD in offspring. The main finding was that maternal and paternal ages were differentially associated with ASD subtypes. In addition to advanced parental age, teenage pregnancy seems to incur a risk for PDD in offspring.
C1 [Lampi, Katja M.; Hinkka-Yli-Salomaki, Susanna; Lehti, Venla; Gissler, Mika; Sourander, Andre] Univ Turku, Dept Child Psychiat, Turku, Finland.
[Helenius, Hans] Univ Turku, Dept Biostat, Turku, Finland.
[Gissler, Mika] Natl Inst Hlth & Welf THL, Helsinki, Finland.
[Gissler, Mika] Nord Sch Publ Hlth, Gothenburg, Sweden.
[Brown, Alan S.] Columbia Univ Coll Phys & Surg, New York State Psychiat Inst, Dept Psychiat, New York, NY 10032 USA.
[Brown, Alan S.] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Sourander, Andre] Turku Univ Hosp, Dept Child Psychiat, Turku 20014, Finland.
RP Sourander, A (reprint author), Turku Univ Hosp, Dept Child Psychiat, Itainen Pitkakatu 1 Varia, Turku 20014, Finland.
EM andre.sourander@utu.fi
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NR 58
TC 11
Z9 11
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2526
EP 2535
DI 10.1007/s10803-013-1801-3
PG 10
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000004
PM 23479075
ER
PT J
AU Vida, MD
Maurer, D
Calder, AJ
Rhodes, G
Walsh, JA
Pachai, MV
Rutherford, MD
AF Vida, Mark D.
Maurer, Daphne
Calder, Andrew J.
Rhodes, Gillian
Walsh, Jennifer A.
Pachai, Matthew V.
Rutherford, M. D.
TI The Influences of Face Inversion and Facial Expression on Sensitivity to
Eye Contact in High-Functioning Adults with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Gaze; Eye contact; Cone of gaze; Facial expression; Face
inversion
ID FINE-GRAINED SENSITIVITY; GAZE-DIRECTION; ASPERGER-SYNDROME; BIOLOGICAL
MOTION; NEURAL CIRCUITRY; PERCEPTION; CHILDREN; LOOKING; AMYGDALA; ME
AB We examined the influences of face inversion and facial expression on sensitivity to eye contact in high-functioning adults with and without an autism spectrum disorder (ASD). Participants judged the direction of gaze of angry, fearful, and neutral faces. In the typical group only, the range of directions of gaze leading to the perception of eye contact (the cone of gaze) was narrower for upright than inverted faces. In both groups, the cone of gaze was wider for angry faces than for fearful or neutral faces. These results suggest that in high-functioning adults with ASD, the perception of eye contact is not tuned to be finer for upright than inverted faces, but that information is nevertheless integrated across expression and gaze direction.
C1 [Vida, Mark D.; Maurer, Daphne; Walsh, Jennifer A.; Pachai, Matthew V.; Rutherford, M. D.] McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada.
[Maurer, Daphne; Calder, Andrew J.; Rhodes, Gillian; Rutherford, M. D.] Univ Western Australia, Sch Psychol, ARC Ctr Excellence Cognit & Its Disorders, Crawley, WA, Australia.
[Calder, Andrew J.] MRC Cognit & Brain Sci Unit, Cambridge, England.
RP Vida, MD (reprint author), McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada.
EM vidamd@mcmaster.ca; maurer@mcmaster.ca; andy.calder@mrc-cbu.cam.ac.uk;
gillian.rhodes@uwa.edu.au; walshj5@mcmaster.ca; pachaim@mcmaster.ca;
rutherm@mcmaster.ca
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NR 70
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2536
EP 2548
DI 10.1007/s10803-013-1802-2
PG 13
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000005
PM 23471478
ER
PT J
AU Cashon, CH
Ha, OR
DeNicola, CA
Mervis, CB
AF Cashon, Cara H.
Ha, Oh-Ryeong
DeNicola, Christopher A.
Mervis, Carolyn B.
TI Toddlers with Williams Syndrome Process Upright but not Inverted Faces
Holistically
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Face perception; Holistic processing; Inversion effect; Perceptual
expertise; Williams syndrome; Developmental disability
ID RECOGNITION; INVERSION; INFANTS; AUTISM; HYPERSOCIABILITY; INFORMATION;
PERCEPTION; CHILDREN
AB Holistic processing of upright, but not inverted, faces is a marker of perceptual expertise for faces. This pattern is shown by typically developing individuals beginning at age 7 months. Williams syndrome (WS) is a rare neurogenetic developmental disorder characterized by extreme interest in faces from a very young age. Research on the effects of inversion on holistic processing of faces by older children and adults with WS has produced mixed results. Younger children with WS were not included in these previous studies. Using the habituation switch paradigm, we demonstrated that 15-35-month-olds with WS process upright, but not inverted, faces holistically. This study provides evidence of perceptual expertise for faces in individuals with WS early in life.
C1 [Cashon, Cara H.; Ha, Oh-Ryeong; DeNicola, Christopher A.; Mervis, Carolyn B.] Univ Louisville, Dept Psychol & Brain Sci, Louisville, KY 40292 USA.
RP Cashon, CH (reprint author), Univ Louisville, Dept Psychol & Brain Sci, Louisville, KY 40292 USA.
EM cara.cashon@louisville.edu
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NR 34
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2549
EP 2557
DI 10.1007/s10803-013-1804-0
PG 9
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000006
PM 23494560
ER
PT J
AU Terrett, G
Rendell, PG
Raponi-Saunders, S
Henry, JD
Bailey, PE
Altgassen, M
AF Terrett, Gill
Rendell, Peter G.
Raponi-Saunders, Sandra
Henry, Julie D.
Bailey, Phoebe E.
Altgassen, Mareike
TI Episodic Future Thinking in Children with Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Episodic future thinking; Imagining the
future; Episodic memory; Executive functioning; Children
ID MENTAL TIME-TRAVEL; AUTOBIOGRAPHICAL MEMORY; EXECUTIVE CONTROL; ADULTS;
CONSTRUCTION; SIMULATION; EVOLUTION; EVENTS
AB The capacity to imagine oneself experiencing future events has important implications for effective daily living but investigation of this ability in autism spectrum disorder (ASD) is limited. This study investigated future thinking in 30 children with high functioning ASD (IQ > 85) and 30 typically developing children. They completed the Adapted Autobiographical Interview, a measure which required participants to describe personal past events (indexing episodic memory) and plausible future events (indexing episodic future thinking). The results showed that there are ASD-related deficits in future thinking, and also provided preliminary evidence regarding cognitive mechanisms that may (and may not) contribute to these difficulties. The theoretical and practical implications of these results are discussed.
C1 [Terrett, Gill; Rendell, Peter G.; Raponi-Saunders, Sandra] Australian Catholic Univ, Sch Psychol, Fitzroy, Vic 3065, Australia.
[Henry, Julie D.] Univ Queensland, Sch Psychol, Brisbane, Qld, Australia.
[Bailey, Phoebe E.] Univ Western Sydney, Sch Social Sci & Psychol, Sydney, NSW, Australia.
[Altgassen, Mareike] Tech Univ Dresden, Dept Psychol, D-01062 Dresden, Germany.
[Altgassen, Mareike] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
RP Terrett, G (reprint author), Australian Catholic Univ, Sch Psychol, Melbourne Campus,Locked Bag 4115, Fitzroy, Vic 3065, Australia.
EM gill.terrett@acu.edu.au
RI Altgassen, Mareike/J-3048-2012
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NR 46
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2558
EP 2568
DI 10.1007/s10803-013-1806-y
PG 11
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000007
PM 23504377
ER
PT J
AU Freeth, M
Sheppard, E
Ramachandran, R
Milne, E
AF Freeth, Megan
Sheppard, Elizabeth
Ramachandran, Rajani
Milne, Elizabeth
TI A Cross-Cultural Comparison of Autistic Traits in the UK, India and
Malaysia
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Culture; Autistic traits; Western; Eastern; India; Malaysia; UK
ID SPECTRUM QUOTIENT AQ; STATES-OF-AMERICA; UNITED-STATES; COGNITIVE
PHENOTYPE; NONCLINICAL SAMPLE; EMPATHY QUOTIENT; SOUTH-KOREA; DISORDERS;
CHILDREN; RELIABILITY
AB The disorder of autism is widely recognised throughout the world. However, the diagnostic criteria and theories of autism are based on research predominantly conducted in Western cultures. Here we compare the expression of autistic traits in a sample of neurotypical individuals from one Western culture (UK) and two Eastern cultures (India and Malaysia), using the Autism-spectrum Quotient (AQ) in order to identify possible cultural differences in the expression of autistic traits. Behaviours associated with autistic traits were reported to a greater extent in the Eastern cultures than the Western culture. Males scored higher than females and science students scored higher than non-science students in each culture. Indian students scored higher than both other groups on the Imagination sub-scale, Malaysian students scored higher than both other groups on the Attention Switching sub-scale. The underlying factor structures of the AQ for each population were derived and discussed.
C1 [Freeth, Megan; Milne, Elizabeth] Univ Sheffield, Dept Psychol, Western Bank, Sheffield S10 2TP, S Yorkshire, England.
[Sheppard, Elizabeth] Univ Nottingham, Sch Psychol, Semenyih 43500, Selangor Darul, Malaysia.
[Ramachandran, Rajani] Univ Calicut, Dept Psychol, Malappuram 673635, Kerala, India.
RP Freeth, M (reprint author), Univ Sheffield, Dept Psychol, Western Bank, Sheffield S10 2TP, S Yorkshire, England.
EM m.freeth@sheffield.ac.uk
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NR 63
TC 3
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2569
EP 2583
DI 10.1007/s10803-013-1808-9
PG 15
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000008
PM 23494561
ER
PT J
AU Kirkovski, M
Enticott, PG
Fitzgerald, PB
AF Kirkovski, Melissa
Enticott, Peter G.
Fitzgerald, Paul B.
TI A Review of the Role of Female Gender in Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Review
DE Gender; Symptomatology; Diagnosis; Etiology
ID PERVASIVE DEVELOPMENTAL DISORDERS; X-CHROMOSOME INACTIVATION; RARE
DE-NOVO; SEX-DIFFERENCES; FETAL TESTOSTERONE; ANOREXIA-NERVOSA;
INTELLECTUAL DISABILITY; CHILDHOOD-AUTISM; FAMILY-HISTORY;
NEUROPSYCHIATRIC DISORDERS
AB This paper reviews the literature exploring gender differences associated with the clinical presentation of autism spectrum disorders (ASD). The potentially mediating effect of comorbid psychopathology, biological and neurodevelopmental implications on these gender differences is also discussed. A vastly heterogeneous condition, while females on the lower-functioning end of the spectrum appear to be more severely affected, an altered clinical manifestation of the disorder among high-functioning females may consequently result in many being un or misdiagnosed. To date, there is strong bias in the literature towards the clinical presentation of ASD in males. It is imperative that future research explores gender differences across the autism spectrum, in order to improve researchers', clinicians' and the publics' understanding of this debilitating disorder.
C1 [Kirkovski, Melissa; Enticott, Peter G.; Fitzgerald, Paul B.] Monash Univ, Alfred & Cent Clin Sch, Monash Alfred Psychiat Res Ctr, Melbourne, Vic 3004, Australia.
RP Kirkovski, M (reprint author), Monash Univ, Alfred & Cent Clin Sch, Monash Alfred Psychiat Res Ctr, Level 4,607 St Kilda Rd, Melbourne, Vic 3004, Australia.
EM melissa.kirkovski@monash.edu
RI Fitzgerald, Paul/A-1225-2008
OI Fitzgerald, Paul/0000-0003-4217-8096
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NR 159
TC 14
Z9 14
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2584
EP 2603
DI 10.1007/s10803-013-1811-1
PG 20
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000009
PM 23525974
ER
PT J
AU Harper, A
Dyches, TT
Harper, J
Roper, SO
South, M
AF Harper, Amber
Dyches, Tina Taylor
Harper, James
Roper, Susanne Olsen
South, Mikle
TI Respite Care, Marital Quality, and Stress in Parents of Children with
Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorders; Marital quality; Respite; Social support;
Stress; Mothers and fathers
ID HIGH-FUNCTIONING AUTISM; PRESCHOOL-CHILDREN; HEALTH-CARE; MOTHERS;
FAMILIES; IMPACT; PERCEPTIONS; ADJUSTMENT; FATHERS; DISABILITIES
AB Parents of children with autism spectrum disorders (ASD) are at risk for having higher stress and lower marital quality than other parents. Survey data regarding respite care, marital quality, and daily hassles and uplifts were obtained from 101 mother-father dyads who were together raising at least one child with ASD (total # of children = 118). Number of hours of respite care was positively related to improved marital quality for both husbands and wives, such that a 1-h increase in weekly respite care was associated with a one-half standard deviation increase in marital quality. This relationship was significantly mediated by perceived daily stresses and uplifts in both husbands and wives. More respite care was associated with increased uplifts and reduced stress; increased uplifts were associated with improved marital quality; and more stress was associated with reduced marital quality. The number of children in the family was associated with greater stress, and reduced relational quality and daily uplifts. Results suggest policymakers and practitioners should develop supports for providing respite for families raising children with ASD.
C1 [Harper, Amber] Wasatch Mental Hlth, Giant Steps, Orem, UT 84097 USA.
[Dyches, Tina Taylor] Brigham Young Univ, Dept Counseling Psychol & Special Educ, Provo, UT 84602 USA.
[Harper, James; Roper, Susanne Olsen] Brigham Young Univ, Sch Family Life, Provo, UT 84602 USA.
[South, Mikle] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
[South, Mikle] Brigham Young Univ, Ctr Neurosci, Provo, UT 84602 USA.
RP Dyches, TT (reprint author), Brigham Young Univ, Dept Counseling Psychol & Special Educ, 340 F McKay Bldg, Provo, UT 84602 USA.
EM aharper@wasatch.org; Tina_Dyches@byu.edu; james_harper@byu.edu;
Susanne_olsen_roper@byu.edu; south@byu.edu
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NR 55
TC 4
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2604
EP 2616
DI 10.1007/s10803-013-1812-0
PG 13
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000010
PM 23529841
ER
PT J
AU Byers, ES
Nichols, S
Voyer, SD
AF Byers, E. Sandra
Nichols, Shana
Voyer, Susan D.
TI Challenging Stereotypes: Sexual Functioning of Single Adults with High
Functioning Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Sexuality; Autism spectrum disorder; Asperger syndrome
ID GENDER-DIFFERENCES; ASPERGER-SYNDROME; RESPONSE RATES; HELP-SEEKING;
ADOLESCENTS; SATISFACTION; EXPERIENCE; CHILDREN; BEHAVIOR; SAMPLE
AB This study examined the sexual functioning of single adults (61 men, 68 women) with high functioning autism and Asperger syndrome living in the community with and without prior relationship experience. Participants completed an on-line questionnaire assessing autism symptoms, psychological functioning, and various aspects of sexual functioning. In general participants reported positive sexual functioning. Participants without prior relationship experience were significantly younger and more likely to be male and identify as heterosexual. They reported significantly higher sexual anxiety, lower sexual arousability, lower dyadic desire, and fewer positive sexual cognitions. The men reported better sexual function than did the women in a number of areas. These results counter negative societal perceptions about the sexuality of high functioning individuals on the autism spectrum.
C1 [Byers, E. Sandra; Voyer, Susan D.] Univ New Brunswick, Dept Psychol, Fredericton, NB E3B 5A3, Canada.
[Nichols, Shana] Fay J Lindner Ctr Autism, Bethpage, NY USA.
RP Byers, ES (reprint author), Univ New Brunswick, Dept Psychol, POB 4400, Fredericton, NB E3B 5A3, Canada.
EM byers@unb.ca
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NR 56
TC 5
Z9 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2617
EP 2627
DI 10.1007/s10803-013-1813-z
PG 11
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000011
PM 23526036
ER
PT J
AU Knight, V
McKissick, BR
Saunders, A
AF Knight, Victoria
McKissick, Bethany R.
Saunders, Alicia
TI A Review of Technology-Based Interventions to Teach Academic Skills to
Students with Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Review
DE Technology; Evidence-based practices; Individuals with autism spectrum
disorder
ID MODERATE INTELLECTUAL DISABILITIES; COMPUTER-ASSISTED-INSTRUCTION;
SPECIAL-EDUCATION; ANIMATED TUTOR; CHILDREN; VOCABULARY; PROGRAM;
CONSTRUCTION; ACQUISITION; MULTIMEDIA
AB A comprehensive review of the literature was conducted for articles published between 1993 and 2012 to determine the degree to which technology-based interventions can be considered an evidence-based practice to teach academic skills to individuals with Autism Spectrum Disorder (ASD). Criteria developed by Horner et al. (Except Child 71:165-178, 2005) and Gersten et al. (Except Child 71:149-164, 2005) were used to determine the quality of single-subject research studies and group experimental research studies respectively. A total of 25 studies met inclusion criteria. Of these studies, only three single-subject studies and no group studies met criteria for quality or acceptable studies. Taken together, the results suggest that practitioners should use caution when teaching academic skills to individuals with ASD using technology-based interventions. Limitations and directions for future research are discussed.
C1 [Knight, Victoria] Vanderbilt Univ, Peabody Coll, Nashville, TN 37203 USA.
[McKissick, Bethany R.] Mississippi State Univ, Starkville, MS 39762 USA.
[Saunders, Alicia] Univ N Carolina, Charlotte, NC 28223 USA.
RP McKissick, BR (reprint author), Mississippi State Univ, 310 Allen Hall,Box 9705, Starkville, MS 39762 USA.
EM bmckissick@colled.msstate.edu
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NR 55
TC 8
Z9 8
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2628
EP 2648
DI 10.1007/s10803-013-1814-y
PG 21
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000012
PM 23543292
ER
PT J
AU Schendel, DE
Bresnahan, M
Carter, KW
Francis, RW
Gissler, M
Gronborg, TK
Gross, R
Gunnes, N
Hornig, M
Hultman, CM
Langridge, A
Lauritsen, MB
Leonard, H
Parner, ET
Reichenberg, A
Sandin, S
Sourander, A
Stoltenberg, C
Suominen, A
Suren, P
Susser, E
AF Schendel, Diana E.
Bresnahan, Michaeline
Carter, Kim W.
Francis, Richard W.
Gissler, Mika
Gronborg, Therese K.
Gross, Raz
Gunnes, Nina
Hornig, Mady
Hultman, Christina M.
Langridge, Amanda
Lauritsen, Marlene B.
Leonard, Helen
Parner, Erik T.
Reichenberg, Abraham
Sandin, Sven
Sourander, Andre
Stoltenberg, Camilla
Suominen, Auli
Suren, Pal
Susser, Ezra
TI The International Collaboration for Autism Registry Epidemiology
(iCARE): Multinational Registry-Based Investigations of Autism Risk
Factors and Trends
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Epidemiology; Study methods; Risk factors; Multinational
ID TWIN PAIRS; DISORDERS; DATABASE; EUROPE
AB The International Collaboration for Autism Registry Epidemiology (iCARE) is the first multinational research consortium (Australia, Denmark, Finland, Israel, Norway, Sweden, USA) to promote research in autism geographical and temporal heterogeneity, phenotype, family and life course patterns, and etiology. iCARE devised solutions to challenges in multinational collaboration concerning data access security, confidentiality and management. Data are obtained by integrating existing national or state-wide, population-based, individual-level data systems and undergo rigorous harmonization and quality control processes. Analyses are performed using database federation via a computational infrastructure with a secure, web-based, interface. iCARE provides a unique, unprecedented resource in autism research that will significantly enhance the ability to detect environmental and genetic contributions to the causes and life course of autism.
C1 [Schendel, Diana E.] Univ Aarhus, Dept Publ Hlth, DK-8000 Aarhus C, Denmark.
[Schendel, Diana E.] Univ Aarhus, Dept Econ & Business, DK-8000 Aarhus C, Denmark.
[Bresnahan, Michaeline; Hornig, Mady; Susser, Ezra] Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA.
[Bresnahan, Michaeline; Susser, Ezra] New York State Psychiat Inst & Hosp, New York, NY 10032 USA.
[Carter, Kim W.; Francis, Richard W.; Langridge, Amanda; Leonard, Helen] Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6009, Australia.
[Gissler, Mika] Natl Inst Hlth & Welf, Helsinki, Finland.
[Gissler, Mika] Nord Sch Publ Hlth, Gothenburg, Sweden.
[Gissler, Mika] Turku Univ, Turku, Finland.
[Gronborg, Therese K.; Parner, Erik T.] Univ Aarhus, Dept Publ Hlth, Aarhus, Denmark.
[Gross, Raz] Chaim Sheba Med Ctr, Div Psychiat, IL-52621 Tel Hashomer, Israel.
[Gross, Raz] Tel Aviv Univ, Dept Epidemiol & Prevent Med, Sackler Fac Med, Ramat Aviv, Israel.
[Gunnes, Nina; Stoltenberg, Camilla; Suren, Pal] Norwegian Inst Publ Hlth, Oslo, Norway.
[Hornig, Mady] Columbia Univ, Ctr Infect & Immun, Mailman Sch Publ Hlth, New York, NY USA.
[Hultman, Christina M.; Sandin, Sven] Karolinska Inst, Stockholm, Sweden.
[Lauritsen, Marlene B.] Aarhus Univ Hosp, Res Unit Child & Adolescent Psychiat, Aalborg Psychiat Hosp, Aalborg, Denmark.
[Reichenberg, Abraham] Kings Coll London, Inst Psychiat, Dept Psychosis Studies, London, England.
[Reichenberg, Abraham] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Sourander, Andre] Turku Univ, Dept Child Psychiat, Child Psychiat Res Ctr, Turku, Finland.
[Sourander, Andre] Turku Univ Hosp, FIN-20520 Turku, Finland.
[Suominen, Auli] Turku Univ, Dept Child Psychiat, Turku, Finland.
RP Schendel, DE (reprint author), Univ Aarhus, Dept Publ Hlth, DK-8000 Aarhus C, Denmark.
EM diana.schendel@folkesundhed.au.dk
RI Leonard, Helen/A-1010-2013
OI Leonard, Helen/0000-0001-6405-5834
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Bettelheim B., 1972, EMPTY FORTRESS INFAN
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NR 18
TC 4
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2650
EP 2663
DI 10.1007/s10803-013-1815-x
PG 14
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000013
PM 23563868
ER
PT J
AU Teatero, ML
Netley, C
AF Teatero, Missy L.
Netley, Charles
TI A Critical Review of the Research on the Extreme Male Brain Theory and
Digit Ratio (2D:4D)
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Review
DE Extreme male brain; Autism spectrum; Empathizing; Systemizing; Digit
ratio; 2D:4D
ID HIGH-FUNCTIONING AUTISM; FINGER LENGTH RATIO; CONGENITAL
ADRENAL-HYPERPLASIA; NORMAL SEX-DIFFERENCES; SPECTRUM QUOTIENT AQ; FETAL
TESTOSTERONE; ASPERGER-SYNDROME; SYSTEMATIZING QUOTIENT; EMPATHY
QUOTIENT; EYES TEST
AB Boys are more likely than girls to be diagnosed with an autism spectrum disorder (ASD). The extreme male brain (EMB) theory of ASD suggests that fetal testosterone (FT) exposure may underlie sex differences in autistic traits. A link between the organizational effects of FT on the brain and ASD is often drawn based on research using digit ratio (2D:4D), a putative biomarker, without a full survey of the findings. This paper critically and quantitatively reviews the research on the relationship between 2D:4D and ASD as well as autism spectrum, empathizing, and systemizing measures in neurotypical populations. Overall, there is some support for the EMB theory in all four areas, particularly the 2D:4D-ASD relationship. Recommendations for future research are provided.
C1 [Teatero, Missy L.] Lakehead Univ, Dept Psychol, Hlth Hormones & Behav Lab, Thunder Bay, ON P7B 5E1, Canada.
[Netley, Charles] Lakehead Univ, Dept Psychol, Thunder Bay, ON P7B 5E1, Canada.
RP Teatero, ML (reprint author), Lakehead Univ, Dept Psychol, Hlth Hormones & Behav Lab, 995 Oliver Rd, Thunder Bay, ON P7B 5E1, Canada.
EM mteatero@lakeheadu.ca
CR Auyeung B, 2006, EUR J ENDOCRINOL, V155, pS123, DOI 10.1530/eje.1.02260
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NR 85
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2664
EP 2676
DI 10.1007/s10803-013-1819-6
PG 13
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000014
PM 23575643
ER
PT J
AU Stein, TP
Schluter, MD
Steer, RA
Ming, X
AF Stein, T. Peter
Schluter, Margaret D.
Steer, Robert A.
Ming, Xue
TI Autism and Phthalate Metabolite Glucuronidation
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Diethylhexyl phthalate; Phthalates; Autism; Glucuronidation
ID HAZARDOUS AIR-POLLUTANTS; SPECTRUM DISORDERS; DI(2-ETHYLHEXYL)PHTHALATE
DEHP; UDP-GLUCURONOSYLTRANSFERASES; URINARY CONCENTRATIONS; PERINATAL
EXPOSURE; UNITED-STATES; BISPHENOL-A; CHILDREN; PHYTOESTROGENS
AB Exposure to environmental chemicals may precipitate autism spectrum disorders (ASD) in genetically susceptible children. Differences in the efficiency of the glucuronidation process may substantially modulate substrate concentrations and effects. To determine whether the efficiency of this pathway is compromised in children with ASD, we measured the efficiency of glucuronidation for a series of metabolites derived from the commonly used plasticizer, diethylhexyl phthalate. Spot urines were collected and analyzed for the fraction of each metabolite conjugated by isotope dilution-liquid chromatography mass spectrometry-mass spectrometry. The degree of glucuronidation was lower with the ASD group. The glucuronidation pathway may differ in some children with ASD.
C1 [Stein, T. Peter; Schluter, Margaret D.] Univ Med & Dent New Jersey, Dept Surg, Sch Osteopath Med, Stratford, NJ 08084 USA.
[Steer, Robert A.] Univ Med & Dent New Jersey, Dept Psychiat, Sch Osteopath Med, Stratford, NJ 08084 USA.
[Ming, Xue] Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol, Newark, NJ 07103 USA.
[Ming, Xue] JFK Med Ctr, New Jersey Neurosci Inst, Dept Neurol, Edison, NJ 08817 USA.
RP Stein, TP (reprint author), Univ Med & Dent New Jersey, Dept Surg, Sch Osteopath Med, 2 Med Ctr Dr, Stratford, NJ 08084 USA.
EM tpstein@umdnj.edu
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NR 43
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2677
EP 2685
DI 10.1007/s10803-013-1822-y
PG 9
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000015
PM 23575644
ER
PT J
AU Siniscalco, D
Sapone, A
Giordano, C
Cirillo, A
de Magistris, L
Rossi, F
Fasano, A
Bradstreet, JJ
Maione, S
Antonucci, N
AF Siniscalco, Dario
Sapone, Anna
Giordano, Catia
Cirillo, Alessandra
de Magistris, Laura
Rossi, Francesco
Fasano, Alessio
Bradstreet, James Jeffrey
Maione, Sabatino
Antonucci, Nicola
TI Cannabinoid Receptor Type 2, but not Type 1, is Up-Regulated in
Peripheral Blood Mononuclear Cells of Children Affected by Autistic
Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autistic disorders; Cannabinoid system; Gene expression; PBMCs
ID MESSENGER-RNA TURNOVER; ENDOCANNABINOID SYSTEM; SPECTRUM DISORDERS;
IMMUNE-RESPONSE; GENE-EXPRESSION; CB2; PROTEIN; MODULATION; ACTIVATION;
ACETAMINOPHEN
AB Autistic disorders (ADs) are heterogeneous neurodevelopmental disorders arised by the interaction of genes and environmental factors. Dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and non-verbal behaviours are common features of ADs. There are no defined mechanisms of pathogenesis, rendering curative therapy very difficult. Indeed, the treatments for autism presently available can be divided into behavioural, nutritional and medical approaches, although no defined standard approach exists. Autistic children display immune system dysregulation and show an altered immune response of peripheral blood mononuclear cells (PBMCs). In this study, we investigated the involvement of cannabinoid system in PBMCs from autistic children compared to age-matched normal healthy developing controls (age ranging 3-9 years; mean age: 6.06 +/- A 1.52 vs. 6.14 +/- A 1.39 in autistic children and healthy subjects, respectively). The mRNA level for cannabinoid receptor type 2 (CB2) was significantly increased in AD-PBMCs as compared to healthy subjects (mean +/- A SE of arbitrary units: 0.34 +/- A 0.03 vs. 0.23 +/- A 0.02 in autistic children and healthy subjects, respectively), whereas CB1 and fatty acid amide hydrolase mRNA levels were unchanged. mRNA levels of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D gene were slightly decreased. Protein levels of CB-2 were also significantly increased in autistic children (mean +/- A SE of arbitrary units: 33.5 +/- A 1.32 vs. 6.70 +/- A 1.25 in autistic children and healthy subjects, respectively). Our data indicate CB2 receptor as potential therapeutic target for the pharmacological management of the autism care.
C1 [Siniscalco, Dario; Giordano, Catia; Rossi, Francesco; Maione, Sabatino] Univ Naples 2, Div Pharmacol, Dept Expt Med, I-80138 Naples, Italy.
[Siniscalco, Dario] La Forza del Silenzio, Ctr Autism, Caserta, Italy.
[Sapone, Anna; de Magistris, Laura] Univ Naples 2, Dept Internal & Expt Med Magrassi Lanzara, I-80138 Naples, Italy.
[Sapone, Anna; Fasano, Alessio] Massachusetts Gen Hosp E, Ctr Celiac Res, Charlestown, MA USA.
[Sapone, Anna; Fasano, Alessio] Massachusetts Gen Hosp E, Mucosal Immunol & Biol Res Ctr, Charlestown, MA USA.
[Cirillo, Alessandra] Univ Naples 2, Div Biotechnol & Mol Biol A Cascino, Dept Expt Med, I-80138 Naples, Italy.
[Fasano, Alessio] MassGen Hosp Children, Boston, MA USA.
[Bradstreet, James Jeffrey] Int Child Dev Resource Ctr, Cumming, GA USA.
[Antonucci, Nicola] Biomed Ctr Autism Res & Treatment, Bari, Italy.
RP Siniscalco, D (reprint author), Univ Naples 2, Div Pharmacol, Dept Expt Med, Via S Maria Costantinopoli 16, I-80138 Naples, Italy.
EM dariosin@uab.edu
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NR 65
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2686
EP 2695
DI 10.1007/s10803-013-1824-9
PG 10
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000016
PM 23585028
ER
PT J
AU Kover, ST
McDuffie, AS
Hagerman, RJ
Abbeduto, L
AF Kover, Sara T.
McDuffie, Andrea S.
Hagerman, Randi J.
Abbeduto, Leonard
TI Receptive Vocabulary in Boys with Autism Spectrum Disorder:
Cross-Sectional Developmental Trajectories
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Language development; Comprehension; Production; Vocabulary;
Trajectory
ID EARLY LANGUAGE; COMMUNICATIVE DEVELOPMENT; METHODOLOGICAL ISSUES;
EXPRESSIVE LANGUAGE; PRESCHOOL-CHILDREN; IMPAIRMENT; PREDICTORS;
ACQUISITION; PHENOTYPES; TODDLERS
AB In light of evidence that receptive language may be a relative weakness for individuals with autism spectrum disorder (ASD), this study characterized receptive vocabulary profiles in boys with ASD using cross-sectional developmental trajectories relative to age, nonverbal cognition, and expressive vocabulary. Participants were 49 boys with ASD (4-11 years) and 80 typically developing boys (2-11 years). Receptive vocabulary, assessed with the Peabody Picture Vocabulary Test, was a weakness for boys with ASD relative to age and nonverbal cognition. Relative to expressive vocabulary, assessed with the Expressive Vocabulary Test, receptive vocabulary increased at a lower rate for boys with ASD. Vocabulary trajectories in ASD are distinguished from typical development; however, nonverbal cognition largely accounts for the patterns observed.
C1 [Kover, Sara T.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
[McDuffie, Andrea S.; Hagerman, Randi J.; Abbeduto, Leonard] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
[McDuffie, Andrea S.; Abbeduto, Leonard] Univ Calif Davis, Dept Psychiat & Behav Sci, Davis, CA 95616 USA.
[Hagerman, Randi J.] Univ Calif Davis, Dept Pediat, Davis, CA 95616 USA.
RP Kover, ST (reprint author), Univ Wisconsin, Waisman Ctr, Room 475,1500 Highland Ave, Madison, WI 53705 USA.
EM kover@wisc.edu; andrea.mcduffie@ucdmc.ucdavis.edu;
randi.hagerman@ucdmc.ucdavis.edu; leonard.abbeduto@ucdmc.ucdavis.edu
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NR 51
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2696
EP 2709
DI 10.1007/s10803-013-1823-x
PG 14
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000017
PM 23588510
ER
PT J
AU Orsmond, GI
Shattuck, PT
Cooper, BP
Sterzing, PR
Anderson, KA
AF Orsmond, Gael I.
Shattuck, Paul T.
Cooper, Benjamin P.
Sterzing, Paul R.
Anderson, Kristy A.
TI Social Participation Among Young Adults with an Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Social participation; Young adulthood
ID ASPERGER-SYNDROME; CHILDREN; ADOLESCENTS; OUTCOMES; FRIENDSHIP;
PREVALENCE; COMMUNITY; EDUCATION; SYMPTOMS; YOUTH
AB Investigating social participation of young adults with an autism spectrum disorder (ASD) is important given the increasing number of youth aging into young adulthood. Social participation is an indicator of life quality and overall functioning. Using data from the National Longitudinal Transition Study 2, we examined rates of participation in social activities among young adults who received special education services for autism (ASD group), compared to young adults who received special education for intellectual disability, emotional/behavioral disability, or a learning disability. Young adults with an ASD were significantly more likely to never see friends, never get called by friends, never be invited to activities, and be socially isolated. Among those with an ASD, lower conversation ability, lower functional skills, and living with a parent were predictors of less social participation.
C1 [Orsmond, Gael I.] Boston Univ, Dept Occupat Therapy, Boston, MA 02215 USA.
[Shattuck, Paul T.; Cooper, Benjamin P.] Washington Univ, George Warren Brown Sch Social Work, St Louis, MO 63130 USA.
[Sterzing, Paul R.] Univ Calif Berkeley, Sch Social Welf, Berkeley, CA 94720 USA.
[Anderson, Kristy A.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
RP Orsmond, GI (reprint author), Boston Univ, Dept Occupat Therapy, Boston, MA 02215 USA.
EM gorsmond@bu.edu
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NR 30
TC 3
Z9 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2710
EP 2719
DI 10.1007/s10803-013-1833-8
PG 10
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000018
PM 23615687
ER
PT J
AU Butterly, F
Percy, C
Ward, G
AF Butterly, Felicity
Percy, Carol
Ward, Gillian
TI Brief Report: Do Service Dog Providers Placing Dogs with Children with
Developmental Disabilities Use Outcome Measures and, If So, What Are
they?
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Assistance Dogs; Service providers; Outcome measures; Developmental
disability
ID FAMILIES; HEALTH
AB The aim of this study was to identify the outcomes expected and assessed by those providing service dogs to children with developmental disabilities. Seventeen registered service dog providers were invited to complete a mixed methods online survey. Five providers, who prepared dogs to work with a wide range of conditions and behaviours, mainly Asperger's syndrome, autism and communication disorders, completed the survey. All five participants reported that they expected to see positive changes as a consequence of the service dog placement, in both the recipient child and their family, including improvements in attention span and language skills, as well as increased familial cohesion. Survey responses indicated that not all desired outcomes were routinely assessed. The range of assessments used were interviews, intake conversations, pre-placement questionnaires, child social dairies filled in by parents, follow up surveys after placement, and child observation by parents. No specifically named valid and reliable clinical or research measures were referred to, showing an emphasis on assessments from parents and service dog providers. It is not clear whether pre-intervention assessments are repeated systematically at follow-up, which could show robust intervention effects. There is scope for professionals in developmental disability to work with service dog providers to improve the evidence base in this field.
C1 [Butterly, Felicity] Coventry Univ, Fac Hlth & Life Sci, Occupat Therapy & Psychol Dept, Coventry CV1 5FB, W Midlands, England.
[Percy, Carol; Ward, Gillian] Coventry Univ, Coventry CV1 5FB, W Midlands, England.
RP Butterly, F (reprint author), Coventry Univ, Fac Hlth & Life Sci, Occupat Therapy & Psychol Dept, Priory St, Coventry CV1 5FB, W Midlands, England.
EM butterlf@uni.coventry.ac.uk; c.percy@coventry.ac.uk;
g.ward@coventry.ac.uk
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Davis D., 2006, CHALLENGED AUTISM OT
Esposito L, 2011, CHILD DEV PERSPECT, V5, P205, DOI 10.1111/j.1750-8606.2011.00175.x
Eva KW, 2005, ACAD MED, V80, pS46, DOI 10.1097/00001888-200510001-00015
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Fombonne E., 2006, PEDIATRICS, V118, P139
Gardner D., 2007, FRIEND HENRY
Slevin E., 2010, LEARNING DISABILITY, V13, P12
Thomas KC, 2007, J AUTISM DEV DISORD, V37, P818, DOI 10.1007/s10803-006-0208-9
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NR 13
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2720
EP 2725
DI 10.1007/s10803-013-1803-1
PG 6
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000019
PM 23479076
ER
PT J
AU Brock, J
Bzishvili, S
Reid, M
Hautus, M
Johnson, BW
AF Brock, Jon
Bzishvili, Samantha
Reid, Melanie
Hautus, Michael
Johnson, Blake W.
TI Brief Report: Atypical Neuromagnetic Responses to Illusory Auditory
Pitch in Children with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Auditory evoked potentials; Auditory perception; Autism; MEG
ID SPEECH; POTENTIALS; PERCEPTION; DISCRIMINATION; CORTEX
AB Atypical auditory perception is a widely recognised but poorly understood feature of autism. In the current study, we used magnetoencephalography to measure the brain responses of 10 autistic children as they listened passively to dichotic pitch stimuli, in which an illusory tone is generated by sub-millisecond inter-aural timing differences in white noise. Relative to control stimuli that contain no inter-aural timing differences, dichotic pitch stimuli typically elicit an object related negativity (ORN) response, associated with the perceptual segregation of the tone and the carrier noise into distinct auditory objects. Autistic children failed to demonstrate an ORN, suggesting a failure of segregation; however, comparison with the ORNs of age-matched typically developing controls narrowly failed to attain significance. More striking, the autistic children demonstrated a significant differential response to the pitch stimulus, peaking at around 50 ms. This was not present in the control group, nor has it been found in other groups tested using similar stimuli. This response may be a neural signature of atypical processing of pitch in at least some autistic individuals.
C1 [Brock, Jon; Bzishvili, Samantha; Reid, Melanie; Johnson, Blake W.] Macquarie Univ, Dept Cognit Sci, Sydney, NSW 2109, Australia.
[Brock, Jon; Johnson, Blake W.] Australian Res Council, Ctr Excellence Cognit & Its Disorders, Sydney, NSW, Australia.
[Hautus, Michael] Univ Auckland, Dept Psychol, Auckland, New Zealand.
RP Brock, J (reprint author), Macquarie Univ, Dept Cognit Sci, Sydney, NSW 2109, Australia.
EM jon.brock@mq.edu.au
RI Hautus, Michael/B-5077-2008
OI Hautus, Michael/0000-0003-2936-9023
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NR 28
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2726
EP 2731
DI 10.1007/s10803-013-1805-z
PG 6
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000020
PM 23543291
ER
PT J
AU Staples, KL
AF Staples, Kerri L.
TI Commentary: The Motor Skills of 7-10 Year Old Children Diagnosed with
ASD. Are the Comparison Groups and Assessments Being Used Appropriate
for the Research Questions Being Asked?
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Editorial Material
ID AUTISM SPECTRUM DISORDER; IMPAIRMENT
C1 Univ Regina, Fac Kinesiol & Hlth Studies, Regina, SK S4S 0A2, Canada.
RP Staples, KL (reprint author), Univ Regina, Fac Kinesiol & Hlth Studies, Regina, SK S4S 0A2, Canada.
EM kerri.staples@uregina.ca
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Pan CY, 2009, J AUTISM DEV DISORD, V39, P1694, DOI 10.1007/s10803-009-0813-5
Shaked M, 2004, J AUTISM DEV DISORD, V34, P35, DOI 10.1023/B:JADD.0000018072.42845.83
Staples KL, 2012, INT REV RES DEV DISA, V42, P179, DOI 10.1016/B978-0-12-394284-5.00007-3
Staples KL, 2010, J AUTISM DEV DISORD, V40, P209, DOI 10.1007/s10803-009-0854-9
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Whyatt CP, 2012, J AUTISM DEV DISORD, V42, P1799, DOI 10.1007/s10803-011-1421-8
NR 23
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
EI 1573-3432
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2013
VL 43
IS 11
BP 2732
EP 2736
DI 10.1007/s10803-013-1809-8
PG 5
WC Psychology, Developmental
SC Psychology
GA 234HH
UT WOS:000325633000021
PM 23504378
ER
PT J
AU Hallett, V
Ronald, A
Colvert, E
Ames, C
Woodhouse, E
Lietz, S
Garnett, T
Gillan, N
Rijsdijk, F
Scahill, L
Bolton, P
Happe, F
AF Hallett, Victoria
Ronald, Angelica
Colvert, Emma
Ames, Catherine
Woodhouse, Emma
Lietz, Stephanie
Garnett, Tracy
Gillan, Nicola
Rijsdijk, Fruhling
Scahill, Lawrence
Bolton, Patrick
Happe, Francesca
TI Exploring anxiety symptoms in a large-scale twin study of children with
autism spectrum disorders, their co-twins and controls
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorders; anxiety; twin; siblings; comorbidity
ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME TEST;
SCHOOL-AGE-CHILDREN; PSYCHIATRIC-DISORDERS; BEHAVIOR PROBLEMS;
DEPRESSION SCALE; CHILDHOOD; ASSOCIATION; PREVALENCE; LANGUAGE
AB BackgroundAlthough many children with autism spectrum disorders (ASDs) experience difficulties with anxiety, the manifestation of these difficulties remains unresolved. The current study assessed anxiety in a large population-based twin sample, aged 10-15years. Phenotypic analyses were used to explore anxiety symptoms in children with ASDs, their unaffected co-twins and a control sample.
MethodsParticipants included 146 families from the Twins Early Development Study (TEDS) where one or both children had a suspected ASD. Eighty control families were also included. The Revised Child Anxiety and Depression scale (Chorpita, Yim, Moffitt, Umemoto & Francis, 2000) was completed (self- and parent-report), along with diagnostic and cognitive tests. Children were categorized into four groups (a) ASD (b) Broader Autism Phenotype (BAP: mainly co-twins of children with ASDs, with high subclinical autistic traits) (c) unaffected co-twins (with neither ASDs nor BAP) (d) controls.
ResultsChildren in the ASD and BAP groups scored significantly higher than controls for all parent-rated (although not child-rated) anxiety subscales. There were no significant differences between the ASD and BAP groups for any of the parent-rated anxiety subscales. Compared with controls, unaffected co-twins showed significantly heightened Social Anxiety, Generalized Anxiety, and Panic symptoms. Significant associations were observed between certain anxiety subscales and both IQ and ASD symptoms. For example, greater parent-rated Social Anxiety was associated with higher IQ and increased social and communicative impairments. Significant interrater correlations were observed for anxiety reports in children with ASDs (r=.27-.54; p<.01), their unaffected co-twins (r=.32-.63; p<.01) and controls (r=.23-.43; p<.01) suggesting that children in this sample with and without ASD symptoms were able to report on their anxiety symptoms with some accuracy.
ConclusionsThese findings support previous reports of heightened anxiety in children with ASDs, at least on parent-reported measures. Unaffected co-twins of children with ASDs also showed increased anxiety, generating questions about the potential etiological overlap between ASDs and anxiety. Progress in this area now depends on more refined anxiety measurement in ASDs and continued investigation of interrater differences.
C1 [Hallett, Victoria; Ames, Catherine] Kings Coll London, Inst Psychiat, Dept Psychol, London, England.
[Ronald, Angelica] Univ London, Dept Psychol Sci, London, England.
[Colvert, Emma; Woodhouse, Emma; Lietz, Stephanie; Rijsdijk, Fruhling; Bolton, Patrick; Happe, Francesca] Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London, England.
[Garnett, Tracy; Gillan, Nicola] South London & Maudsley NHS Fdn Trust, Denmark Hill, England.
[Scahill, Lawrence] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
RP Hallett, V (reprint author), Inst Psychiat, Addiction Sci Bldg,4 Windsor Walk, Denmark Hill SE5 8AF, England.
EM victoria.v.hallett@kcl.ac.uk
RI Ronald, Angelica/C-7812-2009; Bolton, Patrick/E-8501-2010
OI Ronald, Angelica/0000-0002-9576-2176; Bolton,
Patrick/0000-0002-5270-6262
FU National Institute of Health Research (UK); Biomedical Research Centre
in Mental Health at the South London & Maudsley NHS Trust Hospital,
London; Shire; Roche; Pfizer; Autism Speaks
FX The authors would also like to thank Hannah Wiltshire, Rosemary Jessop,
Bethan Corlett, and Jana Caemmerer for data collection and input
assistance. This research was supported by a grant to P. B. from Autism
Speaks. P. B. is supported by a National Institute of Health Research
(UK) Senior Investigator award and the Biomedical Research Centre in
Mental Health at the South London & Maudsley NHS Trust Hospital, London.
L. S. acts as a consultant for Roche, Pfizer, Brachet, and BioMarin. He
also receives research support from Shire, Roche, and Pfizer. The other
authors have no conflicts of interests to declare.
CR Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004
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NR 41
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
EI 1469-7610
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD NOV
PY 2013
VL 54
IS 11
BP 1176
EP 1185
DI 10.1111/jcpp.12068
PG 10
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 234DT
UT WOS:000325621700003
PM 24273800
ER
PT J
AU Gibson, J
Adams, C
Lockton, E
Green, J
AF Gibson, Jenny
Adams, Catherine
Lockton, Elaine
Green, Jonathan
TI Social communication disorder outside autism? A diagnostic
classification approach to delineating pragmatic language impairment,
high functioning autism and specific language impairment
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Social communication disorder; high functioning autism; language
impairment; pragmatics; restricted and repetitive behaviours and
interests; social functioning; diagnosis
ID SPECTRUM DISORDER; REPETITIVE BEHAVIOR; CHILDREN; INTERVENTION;
PRESCHOOLERS; BORDERLANDS; CRITERIA; OUTCOMES; SLI; AGE
AB BackgroundDevelopmental disorders of language and communication present considerable diagnostic challenges due to overlapping of symptomatology and uncertain aetiology. We aimed to further elucidate the behavioural and linguistic profile associated with impairments of social communication occurring outside of an autism diagnosis.
MethodsSix to eleven year olds diagnosed with pragmatic language impairment (PLI), high functioning autism (HFA) or specific language impairment (SLI) were compared on measures of social interaction with peers (PI), restricted and repetitive behaviours/interests (RRBIs) and language ability. Odds ratios (OR) from a multinomial logistic regression were used to determine the importance of each measure to diagnostic grouping. MANOVA was used to investigate differences in subscale scores for the PI measure.
ResultsGreater degrees of PI difficulties (OR=1.22, 95% CI=1.05-1.41), RRBI (OR=1.23, 95% CI=1.06-1.42) and expressive language ability (OR=1.16, 95% CI=1.03-1.30) discriminated HFA from PLI. PLI was differentiated from SLI by elevated PI difficulties (OR=0.82, 95% CI=0.70-0.96) and higher expressive language ability (OR=0.88, 95% CI=0.77-0.98), but indistinguishable from SLI using RRBI (OR=1.01, 95% CI=0.94-1.09). A significant effect of group on PI subscales was observed (=1.38, F(4, 56)=19.26, p<.01) and PLI and HFA groups shared a similar PI subscale profile.
ConclusionsResults provide empirical support for a conceptualisation of PLI as a developmental impairment distinguishable from HFA by absence of RRBIs and by the presence of expressive language difficulties. PI difficulties appear elevated in PLI compared with SLI, but may be less pervasive than in HFA. Findings are discussed with reference to the proposed new category of social communication disorder' in DSM-5.
C1 [Gibson, Jenny] Univ Cambridge, Dept Dev Psychiat, Cambridge, England.
[Adams, Catherine; Lockton, Elaine; Green, Jonathan] Univ Manchester, Inst Brain Behav & Mental Hlth, Manchester, Lancs, England.
RP Gibson, J (reprint author), Dept Dev Psychiat, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England.
EM jlg53@medschl.cam.ac.uk
FU MRC/ESRC; Kids Company charity
FX Jenny Gibson carried out this research at University of Manchester while
supported by an MRC/ESRC interdisciplinary PhD studentship. Thanks to
all participating children and families. Thanks to children and staff at
Moor House School. Jenny Gibson is currently supported by a grant made
by Kids Company charity to University of Cambridge.
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NR 46
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
EI 1469-7610
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD NOV
PY 2013
VL 54
IS 11
BP 1186
EP 1197
DI 10.1111/jcpp.12079
PG 12
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 234DT
UT WOS:000325621700004
PM 23639107
ER
PT J
AU Gadow, KD
Kaat, AJ
Lecavalier, L
AF Gadow, Kenneth D.
Kaat, Aaron J.
Lecavalier, Luc
TI Relation of symptom-induced impairment with other illness parameters in
clinic-referred youth
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Psychiatric disorder; impairment; diagnosis; children; ADHD
ID OPPOSITIONAL DEFIANT DISORDER; AUTISM SPECTRUM DISORDER; MULTIPLE TIC
DISORDER; FUNCTIONAL IMPAIRMENT; SCHIZOPHRENIA SPECTRUM;
PSYCHIATRIC-SYMPTOMS; CHILDREN; ADHD; METHYLPHENIDATE; ADOLESCENTS
AB ObjectiveTo examine the relation of caregiver ratings of psychiatric symptom-induced impairment with number and severity of symptoms and informant agreement in consecutive child psychiatry outpatient referrals.
MethodsParents and teachers completed a broadband DSM-IV-referenced rating scale with disorder-specific impairment for 636 youth (6-18years). Illness parameters included impairment, number and severity of symptoms, and their combination (symptom+impairment) as well as categorical (cut-off) and dimensional scoring.
ResultsAgreement between impairment and other illness parameters showed considerable variation as a function of type of parameter, disorder, and informant, but to lesser extent age and gender. Many youth who met impairment cut-off for specific disorders did not meet symptom cut-off. Conversely, most youth who met symptom cut-off were impaired. Symptom cut-off evidenced greater convergence with impairment cut-off than combined symptom+impairment cut-offs. Severity of impairment was moderately to highly correlated with number and severity of symptoms. Parents' and teachers' ratings indicated little disorder-specific agreement about youth who met impairment cut-off, symptom cut-off, or combined symptom+impairment cut-off. Therefore, sole reliance on one informant greatly underestimates the pervasiveness of impairment.
ConclusionFindings are consistent with the notion that each illness parameter represents a unique conceptual construct, which has important clinical and research implications.
C1 [Gadow, Kenneth D.] SUNY Stony Brook, Dept Psychiat & Behav Sci, New York, NY USA.
[Kaat, Aaron J.; Lecavalier, Luc] Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA.
[Kaat, Aaron J.; Lecavalier, Luc] Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA.
[Lecavalier, Luc] Ohio State Univ, Dept Psychiat, Columbus, OH 43210 USA.
RP Gadow, KD (reprint author), SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
EM kenneth.gadow@stonybrook.edu
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NR 35
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
EI 1469-7610
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD NOV
PY 2013
VL 54
IS 11
BP 1198
EP 1207
DI 10.1111/jcpp.12077
PG 10
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 234DT
UT WOS:000325621700005
PM 23586345
ER
PT J
AU Kent, RG
Carrington, SJ
Le Couteur, A
Gould, J
Wing, L
Maljaars, J
Noens, I
van Berckelaer-Onnes, I
Leekam, SR
AF Kent, Rachel G.
Carrington, Sarah J.
Le Couteur, Ann
Gould, Judith
Wing, Lorna
Maljaars, Jarymke
Noens, Ilse
van Berckelaer-Onnes, Ina
Leekam, Susan R.
TI Diagnosing Autism Spectrum Disorder: who will get a DSM-5 diagnosis?
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE DSM-5; diagnosis; ASD; DISCO
ID COMMUNICATION DISORDERS; INTERVIEW; CRITERIA; CHILDREN; IV;
ABNORMALITIES; VALIDATION
AB BackgroundIntroduction of proposed criteria for DSM-5 Autism Spectrum Disorder (ASD) has raised concerns that some individuals currently meeting diagnostic criteria for Pervasive Developmental Disorder (PDD; DSM-IV-TR/ICD-10) will not qualify for a diagnosis under the proposed changes. To date, reports of sensitivity and specificity of the new criteria have been inconsistent across studies. No study has yet considered how changes at the sub domain' level might affect overall sensitivity and specificity, and few have included individuals of different ages and ability levels.
MethodsA set of DSM-5 ASD algorithms were developed using items from the Diagnostic Interview for Social and Communication Disorders (DISCO). The number of items required for each DSM-5 subdomain was defined either according to criteria specified by DSM-5 (Initial Algorithm), a statistical approach (Youden J Algorithm), or to minimise the number of false positives while maximising sensitivity (Modified Algorithm). The algorithms were designed, tested and compared in two independent samples (Sample 1, N=82; Sample 2, N=115), while sensitivity was assessed across age and ability levels in an additional dataset of individuals with an ICD-10 PDD diagnosis (Sample 3, N=190).
ResultsSensitivity was highest in the Initial Algorithm, which had the poorest specificity. Although Youden J had excellent specificity, sensitivity was significantly lower than in the Modified Algorithm, which had both good sensitivity and specificity. Relaxing the domain A rules improved sensitivity of the Youden J Algorithm, but it remained less sensitive than the Modified Algorithm. Moreover, this was the only algorithm with variable sensitivity across age. All versions of the algorithm performed well across ability level.
ConclusionsThis study demonstrates that good levels of both sensitivity and specificity can be achieved for a diagnostic algorithm adhering to the DSM-5 criteria that is suitable across age and ability level.
C1 [Kent, Rachel G.; Carrington, Sarah J.; Leekam, Susan R.] Cardiff Univ, Sch Psychol, Wales Autism Res Ctr, Cardiff CF10 3AT, S Glam, Wales.
[Le Couteur, Ann] Newcastle Univ, Inst Hlth & Soc, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England.
[Gould, Judith; Wing, Lorna] Natl Autist Soc, Lorna Wing Ctr, Bromley, England.
[Maljaars, Jarymke; Noens, Ilse] Univ Leuven KU Leuven, Louvain, Belgium.
[Maljaars, Jarymke; van Berckelaer-Onnes, Ina] Leiden Univ, Leiden, Netherlands.
RP Leekam, SR (reprint author), Cardiff Univ, Sch Psychol, Wales Autism Res Ctr, Tower Bldg,Pk Pl, Cardiff CF10 3AT, S Glam, Wales.
EM LeekamSR@cardiff.ac.uk
RI Carrington, Sarah/C-1246-2010
OI Carrington, Sarah/0000-0001-5548-8793
FU Economic and Social Research Council [ES/G039399/1]; Wales Autism
Research Centre; Autism Cymru; Autistica
FX This research was supported by an Economic and Social Research Council
PhD award ES/G039399/1 to R. K. and by Wales Autism Research Centre
funding led by Autism Cymru and Autistica that supported S. C. and S. L.
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NR 34
TC 6
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
EI 1469-7610
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD NOV
PY 2013
VL 54
IS 11
BP 1242
EP 1250
DI 10.1111/jcpp.12085
PG 9
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 234DT
UT WOS:000325621700010
PM 23701321
ER
PT J
AU Trofimova, I
AF Trofimova, Ira
TI Understanding misunderstanding: a study of sex differences in meaning
attribution
SO PSYCHOLOGICAL RESEARCH-PSYCHOLOGISCHE FORSCHUNG
LA English
DT Article
ID PERSONALITY-DISORDERS; GENDER DIFFERENCES; COMMUNITY SAMPLE; DEPRESSION;
PREVALENCE; LANGUAGE; AUTISM; AGE
AB There are biologically based sex differences in verbal abilities and in neuropsychological systems of verbal processing. Measurement of observable behaviour, however, does not say much about sex differences in the internal, semantic processing of verbal material. The present study, which was conducted in Canada, China and Russia, investigated sex differences in connotative meaning attribution to the most common concepts using an object scale symmetry in the choice of the nouns and bipolar adjectives (projective semantic method). The results showed that males had a tendency to estimate reality- and work-related concepts more negatively and social- and physical attractors more positively than women. The paper hypothesizes that at the level of the most fundamental semantic processing men favour more exceptional objects than women, and women favour more predictable objects, including rules and routines.
C1 McMaster Univ, Dept Psychiat & Neurosci, Collect Intelligence Lab, Hamilton, ON L8S 2T6, Canada.
RP Trofimova, I (reprint author), McMaster Univ, Dept Psychiat & Neurosci, Collect Intelligence Lab, 92 Bowman St, Hamilton, ON L8S 2T6, Canada.
EM iratrofimov@gmail.com
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NR 42
TC 0
Z9 0
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0340-0727
EI 1430-2772
J9 PSYCHOL RES-PSYCH FO
JI Psychol. Res.-Psychol. Forsch.
PD NOV
PY 2013
VL 77
IS 6
BP 748
EP 760
DI 10.1007/s00426-012-0462-8
PG 13
WC Psychology, Experimental
SC Psychology
GA 235IV
UT WOS:000325712300008
PM 23179581
ER
PT J
AU Wilczynski, SM
AF Wilczynski, Susan M.
TI INTRODUCTION TO THE SPECIAL ISSUE: ADOLESCENTS AND ADULTS ON THE AUTISM
SPECTRUM
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Editorial Material
C1 [Wilczynski, Susan M.] Ball State Univ, Muncie, IN 47306 USA.
RP Wilczynski, SM (reprint author), Ball State Univ, Teachers Coll, Dept Special Educ, Room 722, Muncie, IN 47306 USA.
EM smwilczynski@bsu.edu
CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT
American Psychiatric Association, 2013, DIAGN STAT MAN MENT
Carter EW, 2012, J DISABIL POLICY STU, V23, P50, DOI 10.1177/1044207311414680
Centers for Disease Control and Prevention, 2012, AUTISM SPECTRUM DISO
Nation Autism Center, 2009, NAT STAND REP NAT ST
Sheridan S. M., 2007, CONJOINT BEHAV CONSU
NR 6
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 863
EP 865
DI 10.1002/pits.21714
PG 3
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300001
ER
PT J
AU Tullis, CA
Zangrillo, AN
AF Tullis, Christopher A.
Zangrillo, Amanda N.
TI SEXUALITY EDUCATION FOR ADOLESCENTS AND ADULTS WITH AUTISM SPECTRUM
DISORDERS
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; SOCIAL STORIES; INTELLECTUAL DISABILITIES;
SKILLS; INDIVIDUALS; ATTITUDES; BEHAVIOR
AB As people with autism spectrum disorders (ASD) mature from adolescents into adults, social deficits may become more pronounced and apparent in new areas (e.g., social functioning and sexuality). Like neurotypicals, sexuality may be directly related to quality of life for people with ASD. Current practice for addressing sexuality in the ASD population includes some curricula that may be beneficial for teaching skills related to sexuality, but the scientific support for such curricula is absent. Typically sexuality education is only implemented when a behavior is demonstrated that is considered deviant or problematic. Although reactive education may be a common practice, a strategy that includes proactive sexuality education may be more beneficial for the long-term quality of life for people with ASD. The current paper will highlight some of the areas for further investigation and program development for adolescents and adults with ASD. (C) 2013 Wiley Periodicals, Inc.
C1 [Tullis, Christopher A.; Zangrillo, Amanda N.] Ball State Univ, Muncie, IN 47306 USA.
RP Tullis, CA (reprint author), Ball State Univ, 2000 West Univ Ave, Muncie, IN 47306 USA.
EM catullis@bsu.edu
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NR 37
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 866
EP 875
DI 10.1002/pits.21713
PG 10
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300002
ER
PT J
AU Wilczynski, SM
Trammell, B
Clarke, LS
AF Wilczynski, Susan M.
Trammell, Beth
Clarke, Laura S.
TI IMPROVING EMPLOYMENT OUTCOMES AMONG ADOLESCENTS AND ADULTS ON THE AUTISM
SPECTRUM
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID INDEPENDENT TASK-PERFORMANCE; COMPUTER-AIDED SYSTEM; INTELLECTUAL
DISABILITIES; SUPPORTED EMPLOYMENT; YOUNG-ADULTS;
DEVELOPMENTAL-DISABILITIES; MENTAL-RETARDATION; PROMPTING SYSTEM;
DISORDERS; JOB
AB As the number of diagnosed cases of ASD increases, school professionals must consider not only efficacious teaching approaches for improving academic goals, but also what systems must be in place to address one of the most important jobs of the school systems: preparing capable citizens. For more than 160 years, schools have been tasked with preparing good citizens who are capable of contributing to society through work. Given the fact that schools have been required to provide appropriate educational programming to students with disabilities for decades and that this includes planning for the transition to adulthood, the staggeringly poor employment outcomes of individuals on the autism spectrum should be a cause for concern. The present article reviews the significant problem of unemployment as well as employment supports for individuals with ASD. These supports include both the natural supports (scaffolding to enhance success in obtaining and maintaining employment) as well as technological advances that may minimize ostracization in the workplace. Lastly, recommendations for school psychologists who seek to play a vital role in this critical area are offered. (C) 2013 Wiley Periodicals, Inc.
C1 [Wilczynski, Susan M.; Clarke, Laura S.] Ball State Univ, Muncie, IN 47306 USA.
RP Wilczynski, SM (reprint author), Ball State Univ, Teachers Coll, Dept Special Educ, Room 722, Muncie, IN 47306 USA.
EM smwilczynski@bsu.edu
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Spence-Cochran K., 2011, ED STUDENTS AUTISM S, P295
Storey K, 2003, INT J REHABIL RES, V26, P79, DOI 10.1097/01.mrr.0000070757.63544.c8
Taber T. A., 1999, FOCUS AUTISM OTHER D, V14, P159, DOI 10.1177/108835769901400305
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Trach JS, 1997, J REHABIL, V63, P43
NR 66
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 876
EP 887
DI 10.1002/pits.21718
PG 12
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300003
ER
PT J
AU Carter, EW
Harvey, MN
Taylor, JL
Gotham, K
AF Carter, Erik W.
Harvey, Michelle N.
Taylor, Julie Lounds
Gotham, Katherine
TI CONNECTING YOUTH AND YOUNG ADULTS WITH AUTISM SPECTRUM DISORDERS TO
COMMUNITY LIFE
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID NATIONAL LONGITUDINAL TRANSITION; HIGH-FUNCTIONING CHILDREN;
POSTSECONDARY EDUCATION; INTELLECTUAL DISABILITY; EMPLOYMENT; STUDENTS;
INDIVIDUALS; ADOLESCENTS; OUTCOMES; SCHOOL
AB Equipping youth with autism spectrum disorders (ASD) to flourish during and after high school is central to the purpose and practice of special education. However, many students with ASD are leaving high school without the preparation and connections needed to engage meaningfully in their communities. This article reviews research-based approaches for connecting adolescents with ASD to life beyond the classroom by describing promising practices for fostering inclusion in postsecondary education and community activities. Recognizing that relationships are at the core of community life, emphasis is placed on fostering social connections as an essential aspect of helping young people with ASD thrive in these settings. We conclude with suggestions for school staff to support the successful transitions of young people with ASD. (C) 2013 Wiley Periodicals, Inc.
C1 [Carter, Erik W.; Harvey, Michelle N.; Taylor, Julie Lounds; Gotham, Katherine] Vanderbilt Univ, Nashville, TN 37072 USA.
RP Carter, EW (reprint author), Vanderbilt Univ, Nashville, TN 37072 USA.
EM erik.carter@vanderbilt.edu
CR Adreon D, 2007, INTERV SCH CLIN, V42, P271, DOI 10.1177/10534512070420050201
Aud S., 2011, AM YOUTH TRANSITIONS
Ault MJ, 2013, INTELLECT DEV DISAB, V51, P48, DOI 10.1352/1934-9556-51.01.048
Baum S., 2010, ED PAYS 2010 BENEFIT
Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156
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Carter EW, 2010, INTERV SCH CLIN, V45, P275, DOI 10.1177/1053451209359077
Chiang HM, 2012, J AUTISM DEV DISORD, V42, P685, DOI 10.1007/s10803-011-1297-7
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McGovern CW, 2005, J CHILD PSYCHOL PSYC, V46, P401, DOI 10.1111/j.1469-7610.2004.00361.x
Migliore A, 2012, REHABIL COUNS BULL, V55, P176, DOI 10.1177/0034355212438943
National Collaborative on Workforce and Disability for Youth, 2009, GUID SUCC
Newman L., 2009, POSTHIGH SCH OUTCOME
Orsmond GI, 2004, J AUTISM DEV DISORD, V34, P245, DOI 10.1023/B:JADD.0000029547.96610.df
Papay CK, 2011, EDUC TRAIN AUTISM DE, V46, P78
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Sanford C., 2011, POSTHIGH SCH OUTCOME
Shattuck PT, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0027176
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Swedeen B., 2010, TEACHING EXCEPTIONAL, V43, P38
Taylor JL, 2011, J AUTISM DEV DISORD, V41, P566, DOI 10.1007/s10803-010-1070-3
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Trainor AA, 2008, J SPEC EDUC, V42, P148, DOI 10.1177/0022466907313346
Veenstra-VanderWeele J., 2012, AGENCY HEALTHCARE RE
Wagner M., 2004, NLTS2 DATA BRIEF, V3, P1
Walton KM, 2013, J AUTISM DEV DISORD, V43, P594, DOI 10.1007/s10803-012-1601-1
NR 41
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 888
EP 898
DI 10.1002/pits.21716
PG 11
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300004
ER
PT J
AU Koegel, LK
Ashbaugh, K
Koegel, RL
Detar, WJ
Regester, A
AF Koegel, Lynn Kern
Ashbaugh, Kristen
Koegel, Robert L.
Detar, Whitney J.
Regester, April
TI INCREASING SOCIALIZATION IN ADULTS WITH ASPERGER'S SYNDROME
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; CHILDREN; DISABILITIES; ADOLESCENTS
AB Difficulties engaging in social activities are considered to be a core symptom of individuals with autism spectrum disorder (ASD). Both the literature and our clinical observations suggest that most individuals with ASD have a desire to engage in social activities, but social skill deficits make social interaction challenging, and in turn can lead to feelings of loneliness and isolation. Currently there are few resources to support adult students with ASD in forming friendships and involvement in the college community. Using a multiple baseline design over a 33-week period, this study evaluated the effectiveness of structured social planning for college students with ASD. Intervention included weekly sessions that included providing step-by-step social planning related to their interests, and feedback regarding their participation in social activities. In addition, training in specific organizational skills was implemented, such as determining activities, using a planner to ensure participation in the activities, inviting peers to activities, arranging for transportation, and so on. Results demonstrated that participants were not attending any social events throughout the baseline period. Following intervention, all participants increased the number of social events attended per week. Further, quality of life and satisfaction questionnaires all reported a higher satisfaction with their college experience and peer interactions following intervention. Finally, improvements were seen in other untargeted areas, including increases in non-structured social interactions, improvements in grade point averages, and employment. Results are discussed in regards to a creating a social support program for college students with ASD. (C) 2013 Wiley Periodicals, Inc.
C1 [Koegel, Lynn Kern; Ashbaugh, Kristen; Koegel, Robert L.; Detar, Whitney J.] Univ Calif Santa Barbara, Eli & Edythe L Broad Asperger Res Ctr, Santa Barbara, CA 93106 USA.
[Regester, April] Univ Missouri, St Louis, MO 63121 USA.
RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Koegel Autism Ctr, Clin & Sch Psychol Dept, Santa Barbara, CA 93106 USA.
EM Lynnk@education.ucsb.edu
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
Baker MJ, 1998, J ASSOC PERS SEVERE, V23, P300, DOI 10.2511/rpsd.23.4.300
Barnhill G., 2001, FOCUS AUTISM OTHER D, V22, P116
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Dillon M. R., 2007, COLL STUDENT J, V41, P499
Fitzgerald M., 2004, AUTISM CREATIVITY IS
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Koegel LK, 2012, J POSIT BEHAV INTERV, V14, P220, DOI 10.1177/1098300712437042
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Koegel RL, 2012, J POSIT BEHAV INTERV, V14, P133, DOI 10.1177/1098300712437043
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Stewart ME, 2006, AUTISM, V10, P103, DOI 10.1177/1362361306062013
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WEST M, 1993, EXCEPT CHILDREN, V59, P456
NR 20
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 899
EP 909
DI 10.1002/pits.21715
PG 11
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300005
ER
PT J
AU Rubenstein, LD
Pierson, EE
Wilczynski, SM
Connolly, SC
AF Rubenstein, Lisa Davia
Pierson, Eric E.
Wilczynski, Susan M.
Connolly, Sarah C.
TI FITTING THE HIGH ABILITY PROGRAM TO THE NEEDS OF INDIVIDUALS WITH AUTISM
SPECTRUM DISORDERS
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID ASPERGER SYNDROME; GIFTED STUDENTS; CHILDREN
AB As the number of individuals diagnosed with Autism Spectrum Disorders grows, leaders are increasingly recognizing the limitations of the existing literature base to serve unique subsets of students on the spectrum. To date, there is a dearth of research regarding individuals who are both diagnosed on the spectrum and identified as gifted or high ability. This article provides a theoretical structure to guide professionals working with this population, as well as recommendations for further research. The High Ability/Autism puzzle includes three interlocking pieces that must be connected. First, this population must be appropriately defined, and then second, that definition must guide how professionals identify members of this population. Third, identification methods must inform the educational programming decisions to best serve the High Ability/Autism population. The definition, identification, and available programs must be interrelated to provide appropriate support and guidance for this unique population. This article will outline this process and make recommendations for both practitioners and researchers committed to gifted individuals on the spectrum. (C) 2013 Wiley Periodicals, Inc.
C1 [Rubenstein, Lisa Davia; Pierson, Eric E.; Wilczynski, Susan M.; Connolly, Sarah C.] Ball State Univ, Muncie, IN 47306 USA.
RP Rubenstein, LD (reprint author), Ball State Univ, Teachers Coll, Room 524, Muncie, IN 47306 USA.
EM lmrubenstein@bsu.edu
CR Amend E. R., 2009, GIFTED CHILD TODAY, V32, P57
American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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YOUNG JM, 1994, J APPL BEHAV ANAL, V27, P685, DOI 10.1901/jaba.1994.27-685
NR 67
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 910
EP 922
DI 10.1002/pits.21719
PG 13
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300006
ER
PT J
AU Scattone, D
Mong, M
AF Scattone, Dorothy
Mong, Michael
TI COGNITIVE BEHAVIOR THERAPY IN THE TREATMENT OF ANXIETY FOR ADOLESCENTS
AND ADULTS WITH AUTISM SPECTRUM DISORDERS
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; CHILDREN; SYMPTOMS; TRIAL; QUESTIONNAIRE;
REPLICATION; PARENT
AB Important areas of treatment for individuals with autism spectrum disorders (ASD) have only begun to be explored empirically in the last decade. Fortunately, there has been growing interest in identifying how to best adapt treatments that have been demonstrated to be efficacious with broader populations to individuals with ASD. This article provides a review of the literature for cognitive behavior therapy (CBT) in the treatment of anxiety and mood disorders with modifications for adolescents and adults diagnosed with ASD. The majority of these studies incorporated manualized procedures, structured sessions, visual aids, use of worksheets, and an opportunity for social engagement, in addition to regular practice and feedback within a supportive environment. Treatment has been provided primarily in groups; however, researchers are beginning to explore the advantages of individualized treatment. Although only a handful of studies have been published on the use of CBT with adolescents or adults with ASD, results are promising. School psychologists will want to familiarize themselves with this literature to best meet the needs of students in their care. Implications and directions for future research are discussed. (C) 2013 Wiley Periodicals, Inc.
C1 [Scattone, Dorothy] Univ Mississippi, Med Ctr, Jackson, MS 39216 USA.
[Mong, Michael] Univ So Mississippi, Hattiesburg, MS 39406 USA.
RP Scattone, D (reprint author), Univ Mississippi, Med Ctr Child Dev, Jackson, MS 39216 USA.
EM dscattone@umc.edu
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NR 52
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 923
EP 935
DI 10.1002/pits.21717
PG 13
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300007
ER
PT J
AU Trammell, B
Wilczynski, SM
Dale, B
Mcintosh, DE
AF Trammell, Beth
Wilczynski, Susan M.
Dale, Brittany
Mcintosh, David E.
TI ASSESSMENT AND DIFFERENTIAL DIAGNOSIS OF COMORBID CONDITIONS IN
ADOLESCENTS AND ADULTS WITH AUTISM SPECTRUM DISORDERS
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID ASPERGER-SYNDROME; INTELLECTUAL DISABILITY; PSYCHIATRIC-DISORDERS;
INDIVIDUALS; POPULATION; CHILDREN; SCALE; CHALLENGES; PREVALENCE; RATES
AB Successful treatment of individuals with autism spectrum disorders (ASD) is entirely contingent on an accurate diagnosis. Although many resources exist to help the clinician with differential diagnosis of children, particularly in early childhood, the resources available for evaluating adolescents and adults is far less prevalent. Clinicians often rely on multiple forms of data from numerous sources to make accurate diagnoses, which for adults is a complex process. Lack of availability of instruments that have been normed with individuals with ASD creates limitations for the clinician. In addition, gathering background information from adolescents and adults on the spectrum can be challenging for a number of reasons, including poor self-reporting and poor memory for events from parents or caregivers. To further complicate the matter, comorbid conditions become more and more common as the individual with ASD goes through adolescence and adulthood. This article aims to identify the challenges related to the evaluation of adolescents and adults with ASD, noting particular attention to the differential diagnosis of common comorbid conditions. Recommendations for how to conduct a thorough psychological evaluation with an adolescent or adult with an ASD are made. (C) 2013 Wiley Periodicals, Inc.
C1 [Trammell, Beth] Indiana Univ East, Richmond, IN 47374 USA.
[Wilczynski, Susan M.; Dale, Brittany; Mcintosh, David E.] Ball State Univ, Muncie, IN 47306 USA.
RP Trammell, B (reprint author), Indiana Univ East, Dept Social Sci, 2325 Chester Blvd, Richmond, IN 47374 USA.
EM batramme@iue.edu
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
American Psychiatric Association, 2013, DIAGN STAT MAN MENT
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NR 49
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 936
EP 946
DI 10.1002/pits.21720
PG 11
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300008
ER
PT J
AU Rue, HC
Knox, M
AF Rue, Hanna C.
Knox, Maria
TI CAPACITY BUILDING: EVIDENCE-BASED PRACTICE AND ADOLESCENTS ON THE AUTISM
SPECTRUM
SO PSYCHOLOGY IN THE SCHOOLS
LA English
DT Article
ID IMPLEMENTATION INTEGRITY; TEACHER; PERFORMANCE; DISORDERS; EDUCATION;
MEDICINE; FEEDBACK; STUDENTS; BEHAVIOR; CHILDREN
AB Empirical research in the treatment of autism spectrum disorders (ASDs) has resulted in the identification of numerous evidence-based interventions (EBIs). Adolescents with an ASD are faced with unique academic challenges, complex social environments, and physiological changes. They often require interventions to aid in acclimating to their evolving social environments and physical changes. One of the many challenges for practitioners working with adolescents is turning research findings into practice. We provide a framework to build capacity within a middle or high-school setting to implement EBIs for adolescent students with an ASD. Key elements of implementing EBIs in the school setting include: developing a team of professionals dedicated to achieving a system change, a systematic plan, monitoring progress, and a plan for sustainability. Teacher training is an essential part of implementing EBIs in an educational setting. Empirical evidence suggests that teacher training consists of different strategies including in-vivo training. Accessing resources outside of the school system, such as professionals at universities and teaching hospitals, can aid in training and other aspects of implementing EBIs in the classroom. (C) 2013 Wiley Periodicals, Inc.
RP Rue, HC (reprint author), May Inst, 41 Pacella Pk Dr, Randolph, MA 02368 USA.
EM hrue@mayinstitute.org
CR Albuquerque Kevin V, 2011, J Oncol Pract, V7, P222, DOI 10.1200/JOP.2011.000237
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NR 46
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0033-3085
EI 1520-6807
J9 PSYCHOL SCHOOLS
JI Psychol. Schools
PD NOV
PY 2013
VL 50
IS 9
SI SI
BP 947
EP 956
DI 10.1002/pits.21712
PG 10
WC Psychology, Educational
SC Psychology
GA 234HK
UT WOS:000325633300009
ER
PT J
AU de Boer, A
Pijl, SJ
Post, W
Minnaert, A
AF de Boer, Anke
Pijl, Sip Jan
Post, Wendy
Minnaert, Alexander
TI Peer Acceptance and Friendships of Students with Disabilities in General
Education: The Role of Child, Peer, and Classroom Variables
SO SOCIAL DEVELOPMENT
LA English
DT Article
DE peer acceptance; attitudes; behaviour disorders; autistic spectrum
disorders
ID SPECIAL NEEDS; SOCIAL-PARTICIPATION; INCLUSIVE EDUCATION; REGULAR
SCHOOLS; PUPILS; ATTITUDES; QUESTIONNAIRE; ATTENTION; AUTISM; GENDER
AB To understand the difficulties students with disabilities experience in their social participation in general education, this study examined which child, peer, and class variables relate to peer acceptance and friendships. In a cross-sectional study, sociometric data were gathered for students without disabilities (N = 985) and students with disabilities (N = 65), together with personal related variables of students with disabilities, attitudes of peers towards students with disabilities, and classroom information. Using separate social networks for both boys and girls, the findings of the logistic multilevel regression analyses showed different outcomes for peer acceptance of boys and girls with disabilities. The implications of the findings are discussed in the light of possible interventions to improve peer acceptance and friendships of students with disabilities in general primary education.
C1 [de Boer, Anke; Pijl, Sip Jan; Post, Wendy; Minnaert, Alexander] Univ Groningen, NL-9712 TJ Groningen, Netherlands.
[Pijl, Sip Jan] Norwegian Univ Sci & Technol, Trondheim, Norway.
RP de Boer, A (reprint author), Univ Groningen, Dept Special Educ, Grote Rozenstr 38, NL-9712 TJ Groningen, Netherlands.
EM anke.de.boer@rug.nl
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NR 52
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0961-205X
EI 1467-9507
J9 SOC DEV
JI Soc. Dev.
PD NOV
PY 2013
VL 22
IS 4
BP 831
EP 844
DI 10.1111/j.1467-9507.2012.00670.x
PG 14
WC Psychology, Developmental
SC Psychology
GA 232NM
UT WOS:000325500700011
ER
PT J
AU Pignatelli, M
Feligioni, M
Piccinin, S
Molinaro, G
Nicoletti, F
Nistico, R
AF Pignatelli, Marco
Feligioni, Marco
Piccinin, Sonia
Molinaro, Gemma
Nicoletti, Ferdinando
Nistico, Robert
TI Synaptic Plasticity as a Therapeutic Target in the Treatment of
Autism-related Single-gene Disorders
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Article
DE Synaptic plasticity; long-term potentiation; long-term depression;
monogenic autism; mGLURs
ID FRAGILE-X-SYNDROME; METABOTROPIC GLUTAMATE-RECEPTOR; TUBEROUS SCLEROSIS
COMPLEX; LONG-TERM POTENTIATION; MENTAL-RETARDATION PROTEIN; CPG-BINDING
PROTEIN-2; MOUSE MODEL; RETT-SYNDROME; ANGELMAN-SYNDROME; UBIQUITIN
LIGASE
AB The term "Autism Spectrum" is often used to describe disorders that are currently classified as Pervasive Developmental Disorders. These disorders are typically characterized by social deficits, communication difficulties, stereotyped or repetitive behaviors and/or cognitive delays or mental retardation; sometimes they present high comorbidity rates with epilepsy. Although these diagnoses share some common features, individuals with these disorders are thought to be "on the spectrum" because of differences in severity across these domains.
Recent advances in the genetics of autism spectrum disorders (ASDs) are offering new valuable insights into molecular and cellular mechanisms of pathology. Of particular interest are transgenic technologies that allowed the engineering of several mouse models mimicking different kinds of monogenic heritable forms of ASDs. These transgenic models provide excellent opportunities to explore in detail cellular and molecular mechanisms underlying disease pathology and to identify novel targets for therapeutic intervention.
Increasing evidence suggests that the pathophysiological core of the murine model is primarily due to changes in normal synaptic transmission and plasticity.
Here, we will extensively review the synaptic alterations across different animal models of ASDs and recapitulate the pharmacological strategies aimed at rescuing hippocampal plasticity phenotypes. We describe how pharmacological modulation of mGlu5 receptor, through the use of positive or negative allosteric modulators (depending on the specific disorder), may represent a promising therapeutic strategy for ASDs treatment.
C1 [Pignatelli, Marco; Feligioni, Marco; Piccinin, Sonia] European Brain Res Inst, Pharmacol Synapt Plast Unit, I-00143 Rome, Italy.
[Pignatelli, Marco; Piccinin, Sonia; Nicoletti, Ferdinando; Nistico, Robert] Univ Roma La Sapienza, Dept Physiol & Pharmacol, I-00185 Rome, Italy.
[Molinaro, Gemma; Nicoletti, Ferdinando] IRCCS Neuromed, I-86077 Pozzilli, Italy.
[Nistico, Robert] IRCCS S Lucia Fdn, I-00143 Rome, Italy.
RP Pignatelli, M (reprint author), Univ Roma La Sapienza, Dept Physiol & Pharmacol, Piazzale Aldo Moro 5, I-00185 Rome, Italy.
EM marco.pignatelli@hotmail.it; robert.nistico@uniroma1.it
FU PRIN
FX This work was supported by PRIN 2009 to RN.
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NR 153
TC 3
Z9 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
EI 1873-4286
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD NOV
PY 2013
VL 19
IS 36
BP 6480
EP 6490
PG 11
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 227YT
UT WOS:000325152300008
PM 23432715
ER
PT J
AU Fanelli, F
Marino, R
Keller, F
AF Fanelli, Francesca
Marino, Ramona
Keller, Flavio
TI Focusing on the Interactions between the GABAergic System and
Neurosteroids in Neurodevelopmental Disorders
SO CURRENT PHARMACEUTICAL DESIGN
LA English
DT Article
DE Brain sexual dimorphism; neurosteroids; neurodevelopmental disorders;
GABA receptors; autism; synaptic plasticity; estrogen; androgen
ID CA1 HIPPOCAMPAL SUBFIELD; OVARIECTOMIZED FEMALE RATS; NORMAL
SEXUAL-DIMORPHISM; SPINE SYNAPSE FORMATION; GAD65 MESSENGER-RNA;
NEUROACTIVE STEROIDS; PREFRONTAL CORTEX; SUBSTANTIA-NIGRA; BIPOLAR
DISORDER; BASAL GANGLIA
AB Neurosteroids play essential roles in the control of central nervous system functions during physiological and pathological conditions. Increasing evidences show gender differences in the pathogenesis and clinical manifestations of several neurodevelopmental conditions, including Autism Spectrum Disorders (ASD), possibly due to the action of sex hormones during critical periods of brain development. Furthermore, it is known that neuroactive steroids contribute to neuroprotection, spinogenesis, synaptogenesis, as well as to modulation of neuronal excitability via their interaction with GABA receptors. Dysfunctions of GABAergic signaling early in development lead to a severe excitation-inhibition unbalance in neuronal circuits, which may contribute to the pathophysiology of autism.
In this review, we summarize recent data concerning the functional role of neurosteroids and their relationship with the GABAergic system, focusing on GABA-mediated neurotrasmission alterations characterizing some neurodevelopmental disorders.
C1 [Fanelli, Francesca; Marino, Ramona; Keller, Flavio] Univ Campus Biomed, Lab Dev Neurosci & Neural Plast, I-00128 Rome, Italy.
RP Keller, F (reprint author), Univ Campus Biomed, Lab Dev Neurosci & Neural Plast, Via Alvaro Portillo 21, I-00128 Rome, Italy.
EM f.keller@unicampus.it
FU Autism Speaks [4191]; MIUR [PRIN 2009P9CE2R]
FX The preparation of this manuscript was partly supported by grants from
Autism Speaks (4191) and MIUR (PRIN 2009P9CE2R) to F. K.
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NR 87
TC 3
Z9 3
PU BENTHAM SCIENCE PUBL LTD
PI SHARJAH
PA EXECUTIVE STE Y-2, PO BOX 7917, SAIF ZONE, 1200 BR SHARJAH, U ARAB
EMIRATES
SN 1381-6128
J9 CURR PHARM DESIGN
JI Curr. Pharm. Design
PD NOV
PY 2013
VL 19
IS 36
BP 6491
EP 6498
PG 8
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 227YT
UT WOS:000325152300009
PM 23432713
ER
PT J
AU Cohen, MJ
Meador, KJ
Browning, N
May, R
Baker, GA
Clayton-Smith, J
Kalayjian, LA
Kanner, A
Liporace, JD
Pennell, PB
Privitera, M
Loring, DW
AF Cohen, Morris J.
Meador, Kimford J.
Browning, Nancy
May, Ryan
Baker, Gus A.
Clayton-Smith, Jill
Kalayjian, Laura A.
Kanner, Andres
Liporace, Joyce D.
Pennell, Page B.
Privitera, Michael
Loring, David W.
CA NEAD Study Grp
TI Fetal antiepileptic drug exposure: Adaptive and emotional/behavioral
functioning at age 6 years
SO EPILEPSY & BEHAVIOR
LA English
DT Article
DE Antiepileptic drugs; Child development; Behavioral neurology; Epilepsy;
Pregnancy; Valproate
ID DEVELOPING RAT-BRAIN; SPECTRUM DISORDERS; OUTCOMES; CHILDREN; AUTISM;
PREGNANCY; EPILEPSY
AB The Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study is a prospective observational multicenter study in the USA and UK, which enrolled pregnant women with epilepsy on antiepileptic drug (AED) monotherapy from 1999 to 2004. The study aimed to determine if differential long-term neurodevelopmental effects exist across four commonly used AEDs (carbamazepine, lamotrigine, phenytoin, and valproate). In this report, we examine fetal AED exposure effects on adaptive and emotional/behavioral functioning at 6 years of age in 195 children (including three sets of twins) whose parent (in most cases, the mother) completed at least one of the rating scales. Adjusted mean scores for the four AED groups were in the low average to average range for parent ratings of adaptive functioning on the Adaptive Behavior Assessment System-Second Edition (ABAS-II) and for parent and teacher ratings of emotional/behavioral functioning on the Behavior Assessment System for Children (BASC). However, children whose mothers took valproate during pregnancy had significantly lower General Adaptive Composite scores than the lamotrigine and phenytoin groups. Further, a significant dose-related performance decline in parental ratings of adaptive functioning was seen for both valproate and phenytoin. Children whose mothers took valproate were also rated by their parents as exhibiting significantly more a typical behaviors and inattention than those in the lamotrigine and phenytoin groups. Based upon BASC parent and teacher ratings of attention span and hyperactivity, children of mothers who took valproate during their pregnancy were at a significantly greater risk for a diagnosis of ADHD. The increased likelihood of difficulty with adaptive functioning and ADHD with fetal valproate exposure should be communicated to women with epilepsy who require antiepileptic medication. Finally, additional research is needed to confirm these findings in larger prospective study samples, examine potential risks associated with other AEDs, better define the risks to the neonate that are associated with AEDs for treatment of seizures, and understand the underlying mechanisms of adverse AED effects on the immature brain. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Cohen, Morris J.] Georgia Regents Univ, Augusta, GA 30912 USA.
[Meador, Kimford J.; Loring, David W.] Emory Univ, Atlanta, GA 30322 USA.
[Browning, Nancy; May, Ryan] EMMES Corp, Rockville, MD USA.
[Baker, Gus A.] Univ Liverpool, Walton Ctr Neurol & Neurosurg, Liverpool L69 3BX, Merseyside, England.
[Clayton-Smith, Jill] St Marys Hosp, Manchester M13 0JH, Lancs, England.
[Kalayjian, Laura A.] Univ So Calif, Los Angeles, CA USA.
[Kanner, Andres] Rush Univ, Med Ctr, Chicago, IL 60612 USA.
[Liporace, Joyce D.] Riddle Hlth Care, Media, PA USA.
[Pennell, Page B.] Brigham & Womens Hosp, Boston, MA 02115 USA.
[Privitera, Michael] Univ Cincinnati, Cincinnati, OH USA.
RP Cohen, MJ (reprint author), Georgia Regents Univ, Childrens Med Ctr, Dept Neurol, BT-2601,1446 Harper St, Augusta, GA 30912 USA.
EM mcohen@gru.edu
FU National Institutes of Health [2RO1-NS038455, R01NS050659]; United
Kingdom Epilepsy Research Foundation [RB219738]
FX This work was supported by the National Institutes of Health
[2RO1-NS038455 to K. M., R01NS050659 to N.B.] and the United Kingdom
Epilepsy Research Foundation [RB219738 to G.B.].
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NR 36
TC 6
Z9 6
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1525-5050
J9 EPILEPSY BEHAV
JI Epilepsy Behav.
PD NOV
PY 2013
VL 29
IS 2
BP 308
EP 315
DI 10.1016/j.yebeh.2013.08.001
PG 8
WC Behavioral Sciences; Clinical Neurology; Psychiatry
SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry
GA 231NB
UT WOS:000325422500010
PM 24012508
ER
PT J
AU Francis, GL
McMullen, VB
Blue-Banning, M
Haines, S
AF Francis, Grace L.
McMullen, Victoria B.
Blue-Banning, Martha
Haines, Shana
TI Increasing the Social Skills of a Student With Autism Through a
Literacy-Based Behavioral Intervention
SO INTERVENTION IN SCHOOL AND CLINIC
LA English
DT Article
DE autism; social skills; behavioral intervention
ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; CHILDREN; STORIES
AB Social skills instruction is as important for many students with disabilities as instruction in core academic subjects. Frequently, students with autism require individualized social skills instruction to experience success in general education settings. Literacy-based behavioral Interventions (LBBIs) are an effective intervention that instructors may use to increase positive social skills among students. This article describes LBBIs, provides step-by-step instructions for creating an LBBI, and describes the benefits of LBBIs.
C1 [Francis, Grace L.; Blue-Banning, Martha; Haines, Shana] Univ Kansas, Lawrence, KS 66045 USA.
[McMullen, Victoria B.] Webster Univ, St Louis, MO USA.
RP Francis, GL (reprint author), Univ Kansas, 1200 Sunnyside Ave,3125 Haworth Hall, Lawrence, KS 66045 USA.
EM glucyf@ku.edu
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NR 16
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1053-4512
J9 INTERV SCH CLIN
JI Interv. Sch. Clin.
PD NOV
PY 2013
VL 49
IS 2
BP 77
EP 83
DI 10.1177/1053451213493168
PG 7
WC Education, Special
SC Education & Educational Research
GA 225VX
UT WOS:000324994200002
ER
PT J
AU Ghanizadeh, A
AF Ghanizadeh, Ahmad
TI Atomoxetine for Treating ADHD Symptoms in Autism: A Systematic Review
SO JOURNAL OF ATTENTION DISORDERS
LA English
DT Article
DE ADHD; autism; atomoxetine; treatment
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL
DISORDERS; SPECTRUM DISORDERS; TOURETTE SYNDROME; EXTRACELLULAR LEVELS;
PREFRONTAL CORTEX; OPEN-LABEL; CHILDREN; ADOLESCENTS; EFFICACY
AB Objective: This study systematically reviews the current literature on the administration of atomoxetine for treating children and adolescents with comorbidity on autism spectrum disorder (ASD) and ADHD. Method: PubMed/Medline and Google Scholar databases were electronically searched to find the published trials on atomoxetine and ASD. Results: Six articles reported the clinical trials of atomoxetine for treatment of ADHD symptoms in patients with autism or pervasive development disorders. Only one study that was placebo-controlled crossover pilot trial reported that it is effective. Atomoxetine may be effective in high-functioning patients with autism or patients with low severity. Those with high severity of ASD may be more vulnerable to the adverse effects of atomoxetine. Conclusion: There are not enough controlled clinical trials for showing the efficacy of atomoxetine for treatment of ADHD symptoms in autism. Although evidence suggests potential efficacy of atomoxetine, the current evidences are not conclusive.
C1 [Ghanizadeh, Ahmad] Shiraz Univ Med Sci, Sch Med, Hafez Hosp, Shiraz, Iran.
RP Ghanizadeh, A (reprint author), Shiraz Univ Med Sci, Sch Med, Res Ctr Psychiat & Behav Sci, Hafez Hosp, Shiraz, Iran.
EM ghanizad@sina.tums.ac.ir
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NR 36
TC 5
Z9 5
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1087-0547
J9 J ATTEN DISORD
JI J. Atten. Disord.
PD NOV
PY 2013
VL 17
IS 8
BP 635
EP 640
DI 10.1177/1087054712443154
PG 6
WC Psychology, Developmental; Psychiatry
SC Psychology; Psychiatry
GA 231LZ
UT WOS:000325419400001
PM 22544388
ER
PT J
AU Kenny, MC
Bennett, KD
Dougery, J
Steele, F
AF Kenny, Maureen C.
Bennett, Kyle D.
Dougery, Jonelle
Steele, Francesca
TI Teaching General Safety and Body Safety Training Skills to a Latino
Preschool Male with Autism
SO JOURNAL OF CHILD AND FAMILY STUDIES
LA English
DT Article
DE Childhood sexual abuse prevention; Autism; Disabilities; Body safety
training; Injuries
ID SEXUAL-ABUSE PREVENTION; YOUNG-CHILDREN; MENTAL-RETARDATION; PROGRAM;
DISABILITIES; PREVALENCE; PARENTS; INSTRUCTORS; DISORDERS; EDUCATION
AB This case study describes the implementation of a safety training program with a 5-year-old Latino boy diagnosed with Autism Spectrum Disorder. The program focused on teaching him general safety rules and body safety in an effort to reduce his likelihood of sexual victimization and injury. The boy was treated in conjunction with another child by two therapists, while his caretakers participated in a caretaker group. Both groups consisted of 10 h of safety education instruction. Results show that the boy was able to learn a few safety concepts as well as increase his knowledge of personal safety. Caregiver data revealed a minor increase in knowledge of general safety and an increase in family communication regarding safety issues. However, upon a 3-month follow-up, the boy appeared to lose some knowledge. Recommendations for implementing the Body Safety Training program with children with disabilities and providing their caretakers with information regarding the risk of child sexual abuse is provided.
C1 [Kenny, Maureen C.; Bennett, Kyle D.; Dougery, Jonelle; Steele, Francesca] Florida Int Univ, Coll Educ, Miami, FL 33199 USA.
RP Kenny, MC (reprint author), Florida Int Univ, Coll Educ, Miami, FL 33199 USA.
EM kennym@fiu.edu
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NR 64
TC 0
Z9 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1062-1024
J9 J CHILD FAM STUD
JI J. Child Fam. Stud.
PD NOV
PY 2013
VL 22
IS 8
BP 1092
EP 1102
DI 10.1007/s10826-012-9671-4
PG 11
WC Family Studies; Psychology, Developmental; Psychiatry
SC Family Studies; Psychology; Psychiatry
GA 229FP
UT WOS:000325247500007
ER
PT J
AU Carr, A
AF Carr, Alan
TI Thematic review of Family Therapy Journals 2012
SO JOURNAL OF FAMILY THERAPY
LA English
DT Article
ID INTIMATE PARTNER VIOLENCE; EMOTIONALLY FOCUSED THERAPY; RANDOMIZED
CONTROLLED-TRIAL; COUPLE-BASED INTERVENTIONS; MENTAL-HEALTH RECOVERY;
TREATMENT FOSTER-CARE; RELATIONSHIP EDUCATION; COMMON FACTORS;
MULTISYSTEMIC THERAPY; FUTURE-DIRECTIONS
AB In this article the contents of the principal English-language family therapy journals, and key family therapy articles published in other journals in 2012 are reviewed under these headings: therapy processes in the treatment of child-focused problems, autism, adolescent substance use, human immunodeficiency virus, depression and grief, fragile families, mental health recovery, medical family therapy, family business and systemic practice, couple therapy, intimate partner violence, key issues in theory and practice, research, diversity, international perspectives, interviews, and deaths.
C1 Univ Coll Dublin, Sch Psychol, Dublin 4, Ireland.
RP Carr, A (reprint author), Univ Coll Dublin, Sch Psychol, Newman Bldg, Dublin 4, Ireland.
EM alan.carr@ucd.ie
CR Abbott BV, 2012, J FAM THER, V34, P306, DOI 10.1111/j.1467-6427.2012.00597.x
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NR 97
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0163-4445
J9 J FAM THER
JI J. Fam. Ther.
PD NOV
PY 2013
VL 35
IS 4
BP 407
EP 426
DI 10.1111/1467-6427.12021
PG 20
WC Psychology, Clinical; Family Studies
SC Psychology; Family Studies
GA 232LC
UT WOS:000325494300005
ER
PT J
AU Braam, W
Keijzer, H
Boudier, HS
Didden, R
Smits, M
Curfs, L
AF Braam, W.
Keijzer, H.
Boudier, H. Struijker
Didden, R.
Smits, M.
Curfs, L.
TI CYP1A2 polymorphisms in slow melatonin metabolisers: a possible
relationship with autism spectrum disorder?
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE autism; CYP1A2; melatonin; polymorphism; poor metaboliser
ID CAFFEINE URINARY METABOLITES; PLACEBO-CONTROLLED TRIAL; SLEEP-ONSET
INSOMNIA; INTELLECTUAL DISABILITY; EXOGENOUS MELATONIN; CYTOCHROME-P450
1A2; CHILDREN; GENE; EXPRESSION; HUMANS
AB Background In some of our patients with intellectual disabilities (ID) and sleep problems, the initial good response to melatonin disappeared within a few weeks after starting treatment. In these patients melatonin levels at noon were extremely high (>50pg/ml). We hypothesise that the disappearing effectiveness is associated with slow metabolisation of melatonin because of a single nucleotide polymorphism (SNP) of CYP1A2. Method In this pilot study we analysed DNA extracted from saliva samples of 15 consecutive patients with disappearing effectiveness of melatonin. Saliva was collected at noon and 4 pm for measuring melatonin levels. Results In all patients' salivary melatonin levels at noon were >50 or melatonin half time was >5h. A SNP was found in eight of 15 patients. The allele *1C was found in two patients and in six patients the *1F allele was found. Conclusions Of 15 patients with disappearing effectiveness of melatonin, seven were diagnosed with autism spectrum disorder, and in four of them a SNP was found. The other eight patients were known with a genetic syndrome. In six of them behaviour was considered to be autistic-type and in three of them a SNP was found. This finding may give a new direction for research into the genetic background of autism.
C1 [Braam, W.] S Heeren Loo Zuid Veluwe, Dept Advisium, Wekerom, Netherlands.
[Keijzer, H.] Rijnstate Hosp, Dept Clin Chem, Arnhem, Netherlands.
[Boudier, H. Struijker] Maastricht Univ, Dept Pharmacol & Toxicol, Maastricht, Netherlands.
[Didden, R.] Radboud Univ Nijmegen, Inst Behav Sci, NL-6525 ED Nijmegen, Netherlands.
[Smits, M.] Gelderse Vallei Hosp, Dept Neurol, Ede, Netherlands.
[Curfs, L.] Univ Maastricht, Acad Hosp, Dept Clin Genet, Maastricht, Netherlands.
RP Braam, W (reprint author), S Heeren Loo Midden Nederland, Lokatie Wekerom, POB 75, NL-6710 BB Ede, Netherlands.
EM wiebe.braam@sheerenloo.nl
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NR 38
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD NOV
PY 2013
VL 57
IS 11
BP 993
EP 1000
DI 10.1111/j.1365-2788.2012.01595.x
PG 8
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA 224VV
UT WOS:000324920100001
PM 22823064
ER
PT J
AU Cascio, C
Gribbin, M
Gouttard, S
Smith, RG
Jomier, M
Field, S
Graves, M
Hazlett, HC
Muller, K
Gerig, G
Piven, J
AF Cascio, C.
Gribbin, M.
Gouttard, S.
Smith, R. G.
Jomier, M.
Field, S.
Graves, M.
Hazlett, H. C.
Muller, K.
Gerig, G.
Piven, J.
TI Fractional anisotropy distributions in 2-to 6-year-old children with
autism
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE autism; brain; developmental; diffusion tensor imaging; fractional
anisotropy; white matter
ID VOXEL-BASED MORPHOMETRY; WHITE-MATTER; SPECTRUM DISORDER;
SPATIAL-STATISTICS; ASPERGER-SYNDROME; CORPUS-CALLOSUM; FRONTAL-CORTEX;
YOUNG-CHILDREN; DIFFUSION; BRAIN
AB Background Increasing evidence suggests that autism is a disorder of distributed neural networks that may exhibit abnormal developmental trajectories. Characterisation of white matter early in the developmental course of the disorder is critical to understanding these aberrant trajectories. Methods A cross-sectional study of 2- to 6-year-old children with autism was conducted using diffusion tensor imaging combined with a novel statistical approach employing fractional anisotropy distributions. Fifty-eight children aged 18-79 months were imaged: 33 were diagnosed with autism, 8 with general developmental delay, and 17 were typically developing. Fractional anisotropy values within global white matter, cortical lobes and the cerebellum were measured and transformed to random F distributions for each subject. Each distribution of values for a region was summarised by estimating , the estimated mean and standard deviation of the approximating F for each distribution. Results The estimated delta parameter, delta d, was significantly decreased in individuals with autism compared to the combined control group. This was true in all cortical lobes, as well as in the cerebellum, but differences were most robust in the temporal lobe. Predicted developmental trajectories of delta d across the age range in the sample showed patterns that partially distinguished the groups. Exploratory analyses suggested that the variability, rather than the central tendency, component of delta was the driving force behind these results. Conclusions While preliminary, our results suggest white matter in young children with autism may be abnormally homogeneous, which may reflect poorly organised or differentiated pathways, particularly in the temporal lobe, which is important for social and emotional cognition.
C1 [Cascio, C.] Vanderbilt Univ, Nashville, TN 37235 USA.
[Cascio, C.] Vanderbilt Univ, Kennedy Ctr Res Human Dev, Nashville, TN 37235 USA.
[Gribbin, M.] Human Genome Sci, Dept Biostat, Rockville, MD USA.
[Gouttard, S.] Univ Utah, Dept Comp Sci, Salt Lake City, UT 84112 USA.
[Smith, R. G.; Graves, M.; Hazlett, H. C.; Piven, J.] Univ N Carolina, Psychiat Carolina Inst Dev Disabil, Chapel Hill, NC 27599 USA.
[Jomier, M.] Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA.
[Field, S.] Univ N Carolina, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC USA.
[Muller, K.] Univ Florida, Dept Epidemiol & Hlth Policy Res, Gainesville, FL USA.
RP Piven, J (reprint author), Univ N Carolina, Psychiat Carolina Inst Dev Disabil, Chapel Hill, NC 27599 USA.
EM joe_piven@med.unc.edu
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Shukla DK, 2011, J CHILD PSYCHOL PSYC, V52, P286, DOI 10.1111/j.1469-7610.2010.02342.x
Sparks BF, 2002, NEUROLOGY, V59, P184
Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515
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Yushkevich PA, 2006, NEUROIMAGE, V31, P1116, DOI 10.1016/j.neuroimage.2006.01.015
NR 54
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD NOV
PY 2013
VL 57
IS 11
BP 1037
EP 1049
DI 10.1111/j.1365-2788.2012.01599.x
PG 13
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA 224VV
UT WOS:000324920100005
PM 22998325
ER
PT J
AU Vemuri, M
AF Vemuri, Murali
TI Autism Spectrum Disorders Through the Life Span
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Book Review
C1 [Vemuri, Murali] Brooklands Hosp, New York, NY USA.
RP Vemuri, M (reprint author), Brooklands Hosp, New York, NY USA.
CR Deb S, 2009, WORLD PSYCHIATRY, V8, P181
TANTAM D, 2012, AUTISM SPECTRUM DISO
NR 2
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD NOV
PY 2013
VL 57
IS 11
BP 1088
EP 1090
DI 10.1111/j.1365-2788.2012.01622.x
PG 3
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA 224VV
UT WOS:000324920100010
ER
PT J
AU Richman, DM
Barnard-Brak, L
Bosch, A
Thompson, S
Grubb, L
Abby, L
AF Richman, D. M.
Barnard-Brak, L.
Bosch, A.
Thompson, S.
Grubb, L.
Abby, L.
TI Predictors of self-injurious behaviour exhibited by individuals with
autism spectrum disorder (vol 57, pg 429, 2013)
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Correction
CR Richman DM, 2013, J INTELL DISABIL RES, V57, P429, DOI 10.1111/j.1365-2788.2012.01628.x
NR 1
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD NOV
PY 2013
VL 57
IS 11
BP 1091
EP 1091
DI 10.1111/jir.12094
PG 1
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
Neurology; Psychiatry; Rehabilitation
GA 224VV
UT WOS:000324920100011
ER
PT J
AU Mechling, LC
Swindle, CO
AF Mechling, Linda C.
Swindle, Catherine O.
TI Fine and Gross Motor Task Performance When Using Computer-Based Video
Models by Students With Autism and Moderate Intellectual Disability
SO JOURNAL OF SPECIAL EDUCATION
LA English
DT Article
DE video modeling; fine motor; gross motor; autism spectrum disorders;
moderate intellectual disability
ID OF-THE-LITERATURE; SPECTRUM DISORDERS; CHILDREN; INTERVENTION;
INDIVIDUALS; INSTRUCTION; SKILLS
AB This investigation examined the effects of video modeling on the fine and gross motor task performance by three students with a diagnosis of moderate intellectual disability (Group 1) and by three students with a diagnosis of autism spectrum disorder (Group 2). Using a multiple probe design across three sets of tasks, the study examined the effectiveness of video modeling across differing types of motor response requirements (fine and gross motor) and whether effects would differ across disability groups. Results indicate an increase in the number of fine and gross motor tasks correctly performed following the introduction of video modeling. As a whole, students across both groups performed more gross motor than fine motor tasks independently correct and students in Group 1 performed more tasks independently correct than those in Group 2. Implications are discussed concerning evaluation of task requirements and the development of video models.
C1 [Mechling, Linda C.; Swindle, Catherine O.] Univ N Carolina, Wilmington, NC 28403 USA.
RP Mechling, LC (reprint author), Univ N Carolina, Dept Early Childhood & Special Educ, 601 S Coll Rd, Wilmington, NC 28403 USA.
EM mechlingl@uncw.edu
CR ALCANTARA PR, 1994, EXCEPT CHILDREN, V61, P40
Ayres Kevin M., 2007, Journal of Special Education Technology, V22
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Mechling L., 2005, Journal of Special Education Technology, V20
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NR 24
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-4669
J9 J SPEC EDUC
JI J. Spec. Educ.
PD NOV
PY 2013
VL 47
IS 3
BP 135
EP 147
DI 10.1177/0022466911433859
PG 13
WC Education, Special
SC Education & Educational Research
GA 227SG
UT WOS:000325133800001
ER
PT J
AU Cho, HJ
Kingston, N
AF Cho, Hyun-Jeong
Kingston, Neal
TI Why IEP Teams Assign Low Performers With Mild Disabilities to the
Alternate Assessment Based on Alternate Achievement Standards
SO JOURNAL OF SPECIAL EDUCATION
LA English
DT Article
DE alternate assessment based on alternate achievement standards; test-type
misassignment; eligibility guidelines; accountability system;
significant cognitive disability; IEP team
ID MENTALLY-RETARDED CHILDREN; INTELLECTUAL DISABILITY; ACTIVE EPILEPSY;
STUDENTS; AUTISM; DIAGNOSIS; ACCOMMODATIONS; PARTICIPATION;
INTERVENTIONS; RETARDATION
AB The purpose of this case study was to determine teachers' rationales for assigning students with mild disabilities to alternate assessment based on alternate achievement standards (AA-AAS). In interviews, special educators stated that their primary considerations in making the assignments were low academic performance, student use of extended standard modifications, and the inflexible 1% cap. None of the teachers provided their students with grade-level content or appropriate modifications. Some students were competent in grade-level reading, but were assigned to the 2010 AA-AAS because read-aloud accommodation is not permitted in the reading passages of the general assessment. Findings raised concerns about the susceptibility of eligibility guidelines to lead to subjective decisions. Future research, implications of these findings, and limitations of the study are discussed.
C1 [Cho, Hyun-Jeong; Kingston, Neal] Univ Kansas, Lawrence, KS 66047 USA.
RP Cho, HJ (reprint author), Univ Kansas, Ctr Educ Testing & Evaluat, 1122 West Campus Rd,735 Joseph R Pearson Hall, Lawrence, KS 66047 USA.
EM chohj@ku.edu
CR American Association on Intellectual and Developmental Disabilities, 2010, INTELLECTUAL DISABIL
American Psychiatric Association, 2000, DIAGN STAT MAN MENT
American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
Cascella PW, 1999, CHILD ADOL PSYCH CL, V8, P61
Cho H.-J., 2011, EXAMINING IEP TEAM D
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NR 39
TC 3
Z9 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0022-4669
J9 J SPEC EDUC
JI J. Spec. Educ.
PD NOV
PY 2013
VL 47
IS 3
BP 162
EP 174
DI 10.1177/0022466911435416
PG 13
WC Education, Special
SC Education & Educational Research
GA 227SG
UT WOS:000325133800003
ER
PT J
AU Hodgetts, S
Nicholas, D
Zwaigenbaum, L
McConnell, D
AF Hodgetts, Sandra
Nicholas, David
Zwaigenbaum, Lonnie
McConnell, David
TI Parents' and professionals' perceptions of family-centered care for
children with autism spectrum disorder across service sectors
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE Autism; Family-centered care; Services; Lifespan; Access; Canada
AB Family-centered care (FCC) has been linked with improved parent and child outcomes, yet its implementation can be challenging due to family, professional, organizational and systemic factors and policies. This study aims to increase knowledge and understanding of how families with children with autism spectrum disorder (ASD) experience FCC in Alberta, Canada. 152 parents with a child with ASD completed the Measure of Processes of Care, separately for each utilized service sector, and 146 professionals working with persons with ASD completed the Measure of Processes of Care Service Providers. Additionally, in-depth interviews were conducted with a sub-sample of 19 parents, purposefully sampled for diversity in child and family characteristics. Data were collected in 2011. Descriptive and inferential statistics were used to analyze quantitative data. Interview transcripts were analyzed using grounded theory constant comparison methods, yielding a data generated theoretical model depicting families' experiences with FCC over time and across service sectors. There were no statistically significant differences in FCC scores across service sectors, but statistically significant differences in FCC scores between parents' and professionals' were found. Qualitative data revealed positive experiences and perceptions of receiving FCC from professionals "on the ground" across sectors, but negative experiences and perceptions of FCC at the systems level (i.e., administration, funders). These broad experiences emerged as a core theme "System of Exclusion", which integrated the key themes: (1) "The Fight", (2) "Roles and Restrictions of Care", and (3) "Therapeutic Rapport". Professionals and service providers can use findings to ensure that services reflect current conceptualizations of FCC, and decision and policy makers can use findings to recognize systemic barriers to implementing FCC and inform policy change. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Hodgetts, Sandra; McConnell, David] Univ Alberta, Dept Occupat Therapy, Edmonton, AB T6G 2G4, Canada.
[Nicholas, David] Univ Calgary Edmonton Reg, Fac Social Work, Edmonton, AB, Canada.
[Zwaigenbaum, Lonnie] Univ Alberta, Dept Pediat, Edmonton, AB T6G 2G4, Canada.
RP Hodgetts, S (reprint author), Univ Alberta, Dept Occupat Therapy, 2-64 Corbett Hall, Edmonton, AB T6G 2G4, Canada.
EM sandra.hodgetts@ualberta.ca
FU Alberta Centre for Child, Family and Community Research (ACCFCR)
FX We thank the parents for taking the time in their busy lives to
participate in this study, and the Autism Clinic at the Glenrose
Rehabilitation Hospital, Autism Society of Edmonton and Area, Autism
Calgary Association, and Foothills SNAPS for their assistance with
participant recruitment. This study was supported by a grant from the
Alberta Centre for Child, Family and Community Research (ACCFCR). Sandra
Hodgetts was a Postdoctoral trainee in the CIHR Canadian Child Health
Clinician Scientist Training Program.
CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, VIV
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NR 24
TC 4
Z9 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0277-9536
J9 SOC SCI MED
JI Soc. Sci. Med.
PD NOV
PY 2013
VL 96
SI SI
BP 138
EP 146
DI 10.1016/j.socscimed.2013.07.012
PG 9
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 225LN
UT WOS:000324964500017
PM 24034961
ER
PT J
AU Katz, E
Girolametto, L
AF Katz, Esther
Girolametto, Luigi
TI Peer-Mediated Intervention for Preschoolers With ASD Implemented in
Early Childhood Education Settings
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE peer interactions; autism spectrum disorder; preschoolers; peer-mediated
intervention; single-subject design
ID AUTISM SPECTRUM DISORDERS; YOUNG-CHILDREN; SOCIAL-SKILLS; COMMUNICATION
INTERVENTION; DISABILITIES; VALIDITY; ISSUES; PLAY; COMPETENCE;
CONCURRENT
AB The purpose of this study was to investigate the effects of peer intervention on the social interactions of children with autism spectrum disorder (ASD). In this model, a speech-language pathologist and three early childhood educators trained typically developing peers to engage children with ASD in play. Three preschool children with ASD and six peers participated. The peer intervention took place in early childhood classrooms during play sessions with blocks and play dough. A single-subject multiple baseline design across subjects was used to determine the effects of the intervention. All three children with ASD demonstrated significant gains in the number and length of their interactions with peers, and maintained their gains. The results provided preliminary evidence supporting this model of intervention. Treatment fidelity and social validation measures are documented.
C1 [Katz, Esther; Girolametto, Luigi] Univ Toronto, Toronto, ON M5G 1V7, Canada.
RP Katz, E (reprint author), Univ Toronto, Dept Speech Language Pathol, 160-500 Univ Ave, Toronto, ON M5G 1V7, Canada.
EM esther.katz@utoronto.ca
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NR 48
TC 3
Z9 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-1214
J9 TOP EARLY CHILD SPEC
JI Top. Early Child. Spec. Educ.
PD NOV
PY 2013
VL 33
IS 3
BP 133
EP 143
DI 10.1177/0271121413484972
PG 11
WC Education, Special
SC Education & Educational Research
GA 227SM
UT WOS:000325134600003
ER
PT J
AU Turner, KS
Johnson, CR
AF Turner, Kylan S.
Johnson, Cynthia R.
TI Behavioral Interventions to Address Sleep Disturbances in Children With
Autism Spectrum Disorders: A Review
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE sleep; autism; ASD; behavioral intervention
ID DEVELOPMENTAL-DISABILITIES; BEDTIME; PREVALENCE; PATTERNS
AB Sleep problems are a common occurrence among children with autism spectrum disorders (ASD). In addition to the adverse effects that sleep problems present for children's neurodevelopment, learning, and daytime behaviors, these sleep problems also present significant challenges for the entire family. This article outlines the results of a comprehensive review of behavioral intervention literature to address sleep problems in young children with ASD using the National Autism Center (NAC) criteria. Results indicate that a variety of antecedent- and consequence-based interventions have been evaluated with young children with ASD to address sleep disturbances. The empirical strength of the literature reviewed reveals an emerging evidence base. These findings suggest the need for more research evaluating behavioral interventions with young children with ASD to contribute to best practices for early childhood special educators and practitioners working with these children.
C1 [Turner, Kylan S.; Johnson, Cynthia R.] Univ Pittsburgh, Pittsburgh, PA 15213 USA.
RP Turner, KS (reprint author), Univ Pittsburgh, Autism Ctr, 3420 5th Ave,2nd Floor, Pittsburgh, PA 15213 USA.
EM kylan.turner@chp.edu
CR Albin R. W., 1996, POSITIVE BEHAV SUPPO, P81
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NR 45
TC 4
Z9 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-1214
J9 TOP EARLY CHILD SPEC
JI Top. Early Child. Spec. Educ.
PD NOV
PY 2013
VL 33
IS 3
BP 144
EP 152
DI 10.1177/0271121412446204
PG 9
WC Education, Special
SC Education & Educational Research
GA 227SM
UT WOS:000325134600004
ER
PT J
AU Pizur-Barnekow, K
Muusz, M
McKenna, C
O'Connor, E
Cutler, A
AF Pizur-Barnekow, Kris
Muusz, Marta
McKenna, Catherine
O'Connor, Emily
Cutler, Ann
TI Service Coordinators' Perceptions of Autism-Specific Screening and
Referral Practices in Early Intervention
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE screening; assessment; autism spectrum disorder (ASD); disability
populations; personnel; survey methodologies; descriptive studies;
research methodologies
ID SPECTRUM DISORDERS; YOUNG-CHILDREN; DEVELOPMENTAL DISORDERS; MODIFIED
CHECKLIST; IDENTIFICATION; SURVEILLANCE; DIAGNOSIS; TODDLERS
AB Service coordinators in a statewide early intervention program were surveyed to develop an understanding of screening and referral practices to identify children on the autism spectrum. Quantitative and qualitative data summarizing autism-specific screening and referral practices are reported. More than 50% of the respondents reported that they had never received a referral from a physician or another early intervention provider because a child has failed an autism-specific screening. While service coordinators identified that early intervention providers have a role in conducting autism-specific screening, more than 50% of the respondents indicated that they do not see autism-specific screening completed in early intervention settings. More than 80% of the respondents identified a lack of knowledge as the most significant barrier to autism-specific screening. Together, these findings suggest that early intervention providers may benefit from professional development that imparts knowledge, teaches skills, and addresses potential concerns of parents related to autism.
C1 [Pizur-Barnekow, Kris] Univ Wisconsin, Milwaukee, WI 53221 USA.
[Muusz, Marta; McKenna, Catherine; O'Connor, Emily; Cutler, Ann] Univ Illinois, Chicago, IL USA.
RP Pizur-Barnekow, K (reprint author), Univ Wisconsin, Dept Occupat Sci & Technol, Milwaukee, WI 53221 USA.
EM krisb@uwm.edu
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NR 23
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-1214
J9 TOP EARLY CHILD SPEC
JI Top. Early Child. Spec. Educ.
PD NOV
PY 2013
VL 33
IS 3
BP 153
EP 161
DI 10.1177/0271121412463086
PG 9
WC Education, Special
SC Education & Educational Research
GA 227SM
UT WOS:000325134600005
ER
PT J
AU Jeans, LM
Santos, RM
Laxman, DJ
McBride, BA
Dyer, WJ
AF Jeans, Laurie M.
Santos, Rosa Milagros
Laxman, Daniel J.
McBride, Brent A.
Dyer, W. Justin
TI Examining ECLS-B: Maternal Stress and Depressive Symptoms When Raising
Children With ASD
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE Autism Spectrum Disorder; maternal stress; depression; ECLS-B
ID AUTISM SPECTRUM DISORDERS; PERVASIVE DEVELOPMENTAL DISORDERS; PARENTING
STRESS; PRESCHOOL-CHILDREN; MENTAL-HEALTH; BEHAVIOR PROBLEMS; SOCIAL
SUPPORT; DOWN-SYNDROME; MOTHERS; TODDLERS
AB Using the Early Childhood Longitudinal Study-Birth Cohort (ECLS-B), a nationally representative data set, we examined the extent to which mothers of preschool children with and without the diagnosis of an Autism Spectrum Disorder (ASD) reported stress and depressive symptoms prior to and following diagnosis of ASD. At 4 years, approximately 100 children were parent-identified as diagnosed with ASD. Mothers of children with ASD at 9 months and 4 years had significantly higher incidence of depressive symptoms and stress than mothers of typically developing children. Mothers of children with ASD experienced higher levels of depressive symptoms than mothers of children with disabilities, but the difference was not statistically significant. Using linear regression, a within-group comparison of depressive symptoms of mothers of children with ASD indicated no differences based on child gender, ethnicity, number of children in the family, or partnership status. Implications are presented.
C1 [Jeans, Laurie M.; Santos, Rosa Milagros; Laxman, Daniel J.; McBride, Brent A.] Univ Illinois, Urbana, IL 61801 USA.
[Dyer, W. Justin] Brigham Young Univ, Provo, UT 84602 USA.
RP Jeans, LM (reprint author), Univ Illinois, 1310 South 6th St,MC 288, Champaign, IL 61820 USA.
EM ljeans2@illinois.edu
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WHO, 2001, DEPR
Woodgate RL, 2008, QUAL HEALTH RES, V18, P1075, DOI 10.1177/1049732308320112
NR 50
TC 2
Z9 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-1214
EI 1538-4845
J9 TOP EARLY CHILD SPEC
JI Top. Early Child. Spec. Educ.
PD NOV
PY 2013
VL 33
IS 3
BP 162
EP 171
DI 10.1177/0271121413481680
PG 10
WC Education, Special
SC Education & Educational Research
GA 227SM
UT WOS:000325134600006
ER
PT J
AU McDuffie, A
Machalicek, W
Oakes, A
Haebig, E
Weismer, SE
Abbeduto, L
AF McDuffie, Andrea
Machalicek, Wendy
Oakes, Ashley
Haebig, Eileen
Weismer, Susan Ellis
Abbeduto, Leonard
TI Distance Video-Teleconferencing in Early Intervention: Pilot Study of a
Naturalistic Parent-Implemented Language Intervention
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE parent-child interaction; autism spectrum disorder; language;
communication intervention; parent education; naturalistic;
video-teleconference
ID VERBAL RESPONSIVENESS; YOUNG-CHILDREN; AUTISM; COMMUNICATION;
PRESCHOOLERS; ACQUISITION; STRATEGIES; PREDICT
AB Maternal verbal responsiveness in naturally occurring interactions is known to facilitate language development for children with neurodevelopmental disorders. The present study used a series of A-B replications to examine proximal effects of a naturalistic language intervention on the use of specific language support strategies by mothers of eight young children with an autism spectrum disorder (ASD). Distal effects on child communication also were examined. The intervention consisted of four monthly parent education lessons, each paired with face-to-face clinician coaching of a play-based parent-child interaction. In addition, 12 distance coaching sessions were implemented via desktop video-teleconferencing (VTC). Parents increased their use of verbal responses that followed into their child's focus of attention and responded to child communication acts. Parents also increased the frequency with which they prompted child communication. Increases in parent strategy use were observed during both on-site and distance coaching sessions. Implications for future research are discussed.
C1 [McDuffie, Andrea; Oakes, Ashley; Abbeduto, Leonard] Univ Calif Davis, Sacramento, CA 95817 USA.
[Machalicek, Wendy] Univ Oregon, Eugene, OR 97403 USA.
[Haebig, Eileen; Weismer, Susan Ellis] Univ Wisconsin, Madison, WI 53706 USA.
RP McDuffie, A (reprint author), Univ Calif Davis, MIND Inst, 2625 50th St, Sacramento, CA 95817 USA.
EM andrea.mcduffie@ucdmc.ucdavis.edu
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Zimmerman I., 2007, PRESCHOOL LANGUAGE S
NR 33
TC 1
Z9 1
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0271-1214
J9 TOP EARLY CHILD SPEC
JI Top. Early Child. Spec. Educ.
PD NOV
PY 2013
VL 33
IS 3
BP 172
EP 185
DI 10.1177/0271121413476348
PG 14
WC Education, Special
SC Education & Educational Research
GA 227SM
UT WOS:000325134600007
ER
PT J
AU Wang, JP
Qin, W
Liu, B
Wang, DW
Zhang, YT
Jiang, TZ
Yu, CS
AF Wang, Junping
Qin, Wen
Liu, Bing
Wang, Dawei
Zhang, Yunting
Jiang, Tianzi
Yu, Chunshui
TI Variant in OXTR gene and functional connectivity of the hypothalamus in
normal subjects
SO NEUROIMAGE
LA English
DT Article
DE Oxytocin receptor; Single nucleotide polymorphism; Autism; Hypothalamus;
Functional connectivity
ID AUTISM SPECTRUM DISORDERS; OXYTOCIN RECEPTOR OXTR; VASOPRESSIN; MRI;
THERAPEUTICS; ASSOCIATION; POPULATION; BEHAVIOR; MATTER; MEMORY
AB The oxytocin receptor gene (OXTR) rs53576A has been associated with autism spectrum disorders (ASDs). A smaller hypothalamic volume has been reported in healthy male A-allele carriers than in male GG homozygotes and in patients with ASDs than in healthy controls. These findings prompt the hypothesis that male AA homozygotes may have weaker hypothalamic functional connectivity when compared to male G-allele carriers. We calculated local functional connectivity density (FCD) using a voxel-wise data-driven approach based on resting-state functional MRI data in 270 young healthy subjects. Both the main effect of genotype and the gender-by-genotype interaction were considered. Of the whole brain, only the local FCD of the hypothalamus exhibited the main effect of genotype. Post-hoc testing revealed significantly lower local FCD in male AA homozygotes compared to male G-allele carriers although there was only a trend of significance in the gender-by-genotype interaction. We further analyzed the resting-state functional connectivity (rsFC) of the hypothalamic region that demonstrating significant genotype differences in local FCD. We found a significant gender-by-genotype interaction in rsFC between the hypothalamic region and the left dorsolateral prefrontal cortex, but no significant main effect of genotype was found. Post-hoc testing revealed that this rsFC was significantly weaker in male AA homozygotes compared to male G-allele carriers. Our findings identify gender-dependent mechanisms of OXTR rs53576 gene variation impacting the functional connectivity of the hypothalamus in healthy individuals and suggest that these mechanisms are important for understanding ASDs. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Wang, Junping; Qin, Wen; Wang, Dawei; Zhang, Yunting; Yu, Chunshui] Tianjin Med Univ, Gen Hosp, Dept Radiol, Tianjin 300052, Peoples R China.
[Liu, Bing; Jiang, Tianzi] Chinese Acad Sci, Inst Automat, Natl Lab Pattern Recognit, LIAMA Ctr Computat Med, Beijing 100190, Peoples R China.
RP Jiang, TZ (reprint author), Chinese Acad Sci, Inst Automat, Natl Lab Pattern Recognit, Beijing 100190, Peoples R China.
EM jiangtz@nlpr.ia.ac.cn; chunshuiyu@yahoo.cn
RI Liu, Bing/C-5758-2014; Jiang, Tianzi/I-4256-2012
FU Natural Science Foundation of China [81271551]; National Basic Research
Program of China (973 Program) [2011CB707801]; International Cooperation
and Exchanges NSFC [81061120533]
FX This work was supported by the Natural Science Foundation of China (No.
81271551), the National Basic Research Program of China (973 Program,
No. 2011CB707801), and the International Cooperation and Exchanges NSFC
(No. 81061120533).
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NR 38
TC 5
Z9 5
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 1053-8119
J9 NEUROIMAGE
JI Neuroimage
PD NOV 1
PY 2013
VL 81
BP 199
EP 204
DI 10.1016/j.neuroimage.2013.05.029
PG 6
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 198PI
UT WOS:000322934400019
PM 23684879
ER
PT J
AU Jung, EL
Zadbood, A
Lee, SH
Tomarken, AJ
Blake, R
AF Jung, Eunice L.
Zadbood, Asieh
Lee, Sang-Hun
Tomarken, Andrew J.
Blake, Randolph
TI Individual differences in the perception of biological motion and
fragmented figures are not correlated
SO FRONTIERS IN PSYCHOLOGY
LA English
DT Article
DE perceptual grouping; biological motion; fragmented figures; individual
differences
ID AUTISM SPECTRUM DISORDERS; LATERAL OCCIPITAL COMPLEX; OBJECT-RECOGNITION
AREAS; VISUAL RECOGNITION; BRAIN-AREAS; CORRELATION-COEFFICIENT; SOCIAL
COGNITION; FORM; CHILDREN; CORTEX
AB We live in a cluttered, dynamic visual environment that poses a challenge for the visual system: for objects, including those that move about, to be perceived, information specifying those objects must be integrated over space and over time. Does a single, omnibus mechanism perform this grouping operation, or does grouping depend on separate processes specialized for different feature aspects of the object? To address this question, we tested a large group of healthy young adults on their abilities to perceive static fragmented figures embedded in noise and to perceive dynamic point-light biological motion figures embedded in dynamic noise. There were indeed substantial individual differences in performance on both tasks, but none of the statistical tests we applied to this data set uncovered a significant correlation between those performance measures. These results suggest that the two tasks, despite their superficial similarity, require different segmentation and grouping processes that are largely unrelated to one another. Whether those processes are embodied in distinct neural mechanisms remains an open question.
C1 [Jung, Eunice L.; Zadbood, Asieh; Lee, Sang-Hun; Blake, Randolph] Seoul Natl Univ, Dept Brain & Cognit Sci, Seoul, South Korea.
[Jung, Eunice L.; Zadbood, Asieh; Tomarken, Andrew J.; Blake, Randolph] Vanderbilt Univ, Dept Psychol, Nashville, TN 37240 USA.
RP Blake, R (reprint author), Vanderbilt Univ, Dept Psychol, 111 21st Ave South,301 Wilson Hall, Nashville, TN 37240 USA.
EM randolph.blake@vanderbilt.edu
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NR 114
TC 1
Z9 1
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-1078
J9 FRONT PSYCHOL
JI Front. Psychol.
PD OCT 30
PY 2013
VL 4
AR 795
DI 10.3389/fpsyg.2013.00795
PG 15
WC Psychology, Multidisciplinary
SC Psychology
GA AA6VK
UT WOS:000331236100001
PM 24198799
ER
PT J
AU Kohane, IS
Eran, A
AF Kohane, Isaac S.
Eran, Alal
TI Can We Measure Autism?
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Editorial Material
C1 [Kohane, Isaac S.] Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA 02115 USA.
[Kohane, Isaac S.] Childrens Hosp, Boston, MA 02115 USA.
[Eran, Alal] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA.
[Eran, Alal] Boston Childrens Hosp, Childrens Hosp Informat Program, Boston, MA 02115 USA.
RP Kohane, IS (reprint author), Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA 02115 USA.
EM isaac_kohane@harvard.edu; alal@mit.edu
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NR 10
TC 0
Z9 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
EI 1946-6242
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD OCT 30
PY 2013
VL 5
IS 209
AR 209ed18
DI 10.1126/scitranslmed.3007340
PG 2
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 245YR
UT WOS:000326501700001
PM 24174324
ER
PT J
AU McCarroll, SA
Hyman, SE
AF McCarroll, Steven A.
Hyman, Steven E.
TI Progress in the Genetics of Polygenic Brain Disorders: Significant New
Challenges for Neurobiology
SO NEURON
LA English
DT Review
ID DE-NOVO MUTATIONS; AUTISM SPECTRUM DISORDERS; RETT-SYNDROME; HUMAN
GENOME; INTELLECTUAL DISABILITY; PSYCHIATRIC-DISORDERS;
POPULATION-SCALE; BIPOLAR DISORDER; COMMON SNPS; RISK LOCI
AB Advances in genome analysis, accompanied by the assembly of large patient cohorts, are making possible successful genetic analyses of polygenic brain disorders. If the resulting molecular clues, previously hidden in the genomes of affected individuals, are to yield useful information about pathogenesis and inform the discovery of new treatments, neurobiology will have to rise to many difficult challenges. Here we review the underlying logic of the genetic investigations, describe in more detail progress in schizophrenia and autism, and outline the challenges for neurobiology that lie ahead. We argue that technologies at the disposal of neuroscience are adequately advanced to begin to study the biology of common and devastating polygenic disorders.
C1 [McCarroll, Steven A.; Hyman, Steven E.] Broad Inst Harvard & MIT, Stanley Ctr Psychiat Res, Cambridge, MA 02141 USA.
[McCarroll, Steven A.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA.
[Hyman, Steven E.] Harvard Univ, Dept Stem Cell & Regenerat Biol, Cambridge, MA 02138 USA.
RP McCarroll, SA (reprint author), Broad Inst Harvard & MIT, Stanley Ctr Psychiat Res, Cambridge, MA 02141 USA.
EM mccarroll@genetics.med.harvard.edu; seh@harvard.edu
FU Stanley Medical Research Institute; NIH [R01 HG006855]
FX This work was made possible by funding from the Stanley Medical Research
Institute and by NIH grant R01 HG006855 to S.A.M. We also thank Janet
Theurer and Pat Rossi for the artwork. S.E.H. discloses that he serves
on the Novartis Science Board and has advised AstraZeneca.
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NR 70
TC 17
Z9 17
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD OCT 30
PY 2013
VL 80
IS 3
BP 578
EP 587
DI 10.1016/j.neuron.2013.10.046
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 247IA
UT WOS:000326609900005
PM 24183011
ER
PT J
AU Paul, SM
Doherty, JJ
Robichaud, AJ
Belfort, GM
Chow, BY
Hammond, RS
Crawford, DC
Linsenbardt, AJ
Shu, HJ
Izumi, Y
Mennerick, SJ
Zorumski, CF
AF Paul, Steven M.
Doherty, James J.
Robichaud, Albert J.
Belfort, Gabriel M.
Chow, Brian Y.
Hammond, Rebecca S.
Crawford, Devon C.
Linsenbardt, Andrew J.
Shu, Hong-Jin
Izumi, Yukitoshi
Mennerick, Steven J.
Zorumski, Charles F.
TI The Major Brain Cholesterol Metabolite 24(S)-Hydroxycholesterol Is a
Potent Allosteric Modulator of N-Methyl-D-Aspartate Receptors
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LONG-TERM POTENTIATION; PREGNENOLONE SULFATE; NMDA RECEPTORS;
HIPPOCAMPAL-NEURONS; SYNAPTIC TRANSMISSION; GABA(A) RECEPTOR;
MOUSE-BRAIN; IN-VITRO; STEROIDS; RAT
AB N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are critical to the regulation of excitatory synaptic function in the CNS. NMDARs govern experience-dependent synaptic plasticity and have been implicated in the pathophysiology of various neuropsychiatric disorders including the cognitive deficits of schizophrenia and certain forms of autism. Certain neurosteroids modulate NMDARs experimentally but their low potency, poor selectivity, and very low brain concentrations make them poor candidates as endogenous ligands or therapeutic agents. Here we show that the major brain-derived cholesterol metabolite 24(S)-hydroxycholesterol (24(S)-HC) is a very potent, direct, and selective positive allosteric modulator of NMDARs with a mechanism that does not overlap that of other allosteric modulators. At submicromolar concentrations 24(S)-HC potentiates NMDAR-mediated EPSCs in rat hippocampal neurons but fails to affect AMPAR or GABA(A) receptors (GABA(A)Rs)-mediated responses. Cholesterol itself and other naturally occurring oxysterols present in brain do not modulate NMDARs at concentrations <= 10 mu M. In hippocampal slices, 24(S)-HC enhances the ability of subthreshold stimuli to induce long-term potentiation (LTP). 24(S)-HC also reverses hippocampal LTP deficits induced by the NMDAR channel blocker ketamine. Finally, we show that synthetic drug-like derivatives of 24(S)-HC, which potently enhance NMDAR-mediated EPSCs and LTP, restore behavioral and cognitive deficits in rodents treated with NMDAR channel blockers. Thus, 24(S)-HC may function as an endogenous modulator of NMDARs acting at a novel oxysterol modulatory site that also represents a target for therapeutic drug development.
C1 [Paul, Steven M.; Doherty, James J.; Robichaud, Albert J.; Belfort, Gabriel M.; Chow, Brian Y.; Hammond, Rebecca S.] Sage Therapeut, Cambridge, MA 02142 USA.
[Paul, Steven M.] Weill Cornell Med Coll, Dept Psychiat, Brain & Mind Res Inst, Appel Alzheimers Dis Res Inst, New York, NY 10065 USA.
[Paul, Steven M.] Weill Cornell Med Coll, Dept Pharmacol, Brain & Mind Res Inst, Appel Alzheimers Dis Res Inst, New York, NY 10065 USA.
[Crawford, Devon C.; Linsenbardt, Andrew J.; Shu, Hong-Jin; Izumi, Yukitoshi; Mennerick, Steven J.; Zorumski, Charles F.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
[Crawford, Devon C.; Linsenbardt, Andrew J.; Shu, Hong-Jin; Izumi, Yukitoshi; Mennerick, Steven J.; Zorumski, Charles F.] Washington Univ, Sch Med, Taylor Family Inst Innovat Psychiat Res, St Louis, MO 63110 USA.
RP Paul, SM (reprint author), Cornell Univ, Weill Cornell Med Coll, Brain & Mind Res Inst, Appel Alzheimers Dis Res Inst, 1300 York Ave, New York, NY 10065 USA.
EM smpaulmd@med.cornell.edu
FU Sage Therapeutics; National Institutes of Health [MH078823, MH077791,
GM47969, AA017413]; Bantly Foundation
FX This work was supported by Sage Therapeutics and National Institutes of
Health Grants MH078823, MH077791, GM47969, and AA017413, and the Bantly
Foundation. We thank J.C. Dodart, Frank Salituro, Gabriel Botella, Kiran
Reddy, Carlos Loya, Ann Benz, and Amanda Taylor for their technical
support and suggestions.
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NR 59
TC 18
Z9 18
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 30
PY 2013
VL 33
IS 44
BP 17290
EP 17300
DI 10.1523/JNEUROSCI.2619-13.2013
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 246BB
UT WOS:000326509800007
PM 24174662
ER
PT J
AU Guariglia, SR
Chadman, KK
AF Guariglia, Sara Rose
Chadman, Kathryn K.
TI Water T-maze: A useful assay for determination of repetitive behaviors
in mice
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Reversal learning; Water T-maze; Repetitive behavior; Autism; BTBR
T(+)tf/J
ID AUTISTIC-LIKE BEHAVIORS; TF/J MOUSE MODEL; PLUS TF/J; REVERSAL;
CHILDREN; STRAINS; HIPPOCAMPAL; DYSFUNCTION; PHENOTYPES; C57BL/6J
AB Background: Repetitive behavior is a term used to describe a wide variety of invariant and inappropriate behaviors that occur in many diverse conditions, including autism. It is necessary to utilize and/or design rodent behavioral assays that exploit individual types of repetitive behavior so that underlying pathology and therapeutic measures can be determined. A variety of high-throughput assays to investigate lower order repetitive behaviors are available for rodents, whereas, fewer assays are available to investigate higher order repetitive behaviors, such as perseverative behavior. BTBR T(+)tf/J (BTBR) mice, harbor behavioral deficits that share similarity to the core deficits found in autism, yet have not conclusively demonstrated deficits in conventional reversal learning tasks (i.e. Morris water maze (MWM), T-maze) which are typically used to examine perseverance.
New method: By combining elements of both the MWM and T-maze, we designed a water T-maze assay to determine if perseverative behavior could become perceptible in BTBR mice.
Results: We found that BTBR mice show a significant impairment in reversal learning as compared to C57BL/6J (B6) mice in our water-T-maze reversal learning assay.
Comparison of existing methods: Our water T-maze is sensitive, simple to perform, inexpensive and less time intensive than other tasks that can be used to measure higher order repetitive behaviors.
Conclusions: Our findings suggest that our water T-maze assay is effective for determining perseverance, which is not readily revealed by using conventional methods. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Guariglia, Sara Rose; Chadman, Kathryn K.] New York State Inst Basic Res Dev Disabil, Dept Dev Neurobiol, Staten Isl, NY 10314 USA.
RP Guariglia, SR (reprint author), Columbia Univ, Mailman Sch Publ Hlth, 722 W 168th St, New York, NY 10032 USA.
EM srg2156@columbia.edu; kathryn.chadmanibr@gmail.com
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NR 31
TC 3
Z9 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
EI 1872-678X
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD OCT 30
PY 2013
VL 220
IS 1
BP 24
EP 29
DI 10.1016/j.jneumeth.2013.08.019
PG 6
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 244ZY
UT WOS:000326429900004
PM 23994357
ER
PT J
AU Lenroot, RK
Yeung, PK
AF Lenroot, Rhoshel K.
Yeung, Pui Ka
TI Heterogeney within autism spectrum disorders: what have we learned from
neuroimaging studies?
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Review
DE autism; psychiatry and developmental disabilities; intellectual
disability; functional magnetic resonance imaging; structural magnetic
resonance imaging
ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM;
FRAGILE-X-SYNDROME; CARDIO-FACIAL SYNDROME; OBSESSIVE-COMPULSIVE
DISORDER; TYPICALLY DEVELOPING-CHILDREN; LANGUAGE-ASSOCIATION CORTEX;
RESONANCE-IMAGING MRI; WHOLE-BRAIN ANALYSIS; SEX-DIFFERENCES
AB Autism spectrum disorders (ASD) display significant heterogeneity. Although most neuroimaging studies in ASD have been designed to identify commonalities among affected individuals, rather than differences, some studies have explored variation within ASD. There have been two general types of approaches used for this in the neuroimaging literature to date: comparison of subgroups within ASD, and analyses using dimensional measures to link clinical variation to brain differences. This review focuses on structural and functional magnetic resonance imaging studies that have used these approaches to begin to explore heterogeneity between individuals with ASD. Although this type of data is yet sparse, recognition is growing of the limitations of behaviorally defined categorical diagnoses for understanding neurobiology. Study designs that are more informative regarding the sources of heterogeneity in ASD have the potential to improve our understanding of the neurobiological processes underlying ASD.
C1 [Lenroot, Rhoshel K.; Yeung, Pui Ka] Univ New S Wales, Sch Psychiat, Sydney, NSW, Australia.
[Lenroot, Rhoshel K.; Yeung, Pui Ka] Neurosci Res Australia, Sydney, NSW 2031, Australia.
RP Lenroot, RK (reprint author), Neurosci Res Australia, Hosp Rd, Sydney, NSW 2031, Australia.
EM r.lenroot@unsw.edu.au
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NR 200
TC 8
Z9 8
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 30
PY 2013
VL 7
AR 733
DI 10.3389/fnhum.2013.00733
PG 16
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 242UU
UT WOS:000326269100001
PM 24198778
ER
PT J
AU Tuchman, R
Hirtz, D
Mamounas, LA
AF Tuchman, Roberto
Hirtz, Deborah
Mamounas, Laura A.
TI NINDS epilepsy and autism spectrum disorders workshop report
SO NEUROLOGY
LA English
DT Review
ID FRAGILE-X-SYNDROME; TUBEROUS SCLEROSIS COMPLEX; TARGETED TREATMENT
TRIALS; RETT-SYNDROME; INTELLECTUAL DISABILITY; CHILDREN; BRAIN;
DYSFUNCTION; SEIZURES; MECP2
AB The association of epilepsy and autism spectrum disorders (ASD), although well-recognized, is poorly understood. The purpose of this report is to summarize the discussion of a workshop sponsored by the National Institute of Neurological Disorders and Stroke, with support from the National Institute of Child Health and Human Development, Autism Speaks, and Citizens United for Research in Epilepsy, that took place in Bethesda, Maryland, on May 29 and 30, 2012. The goals of this workshop were to highlight the clinical and biological relationships between ASD and epilepsy, to determine both short- and long-term goals that address research and treatment conundrums in individuals with both ASD and epilepsy, and to identify resources that can further both clinical and basic research. Topics discussed included epidemiology, genetics, environmental factors, common mechanisms, neuroimaging, neuropathology, neurophysiology, treatment, and research gaps and challenges in this unique population.
C1 [Tuchman, Roberto] Miami Childrens Hosp Dan Marino Ctr, Dept Neurol, Weston, FL 33331 USA.
[Hirtz, Deborah; Mamounas, Laura A.] NINDS, NIH, Bethesda, MD 20892 USA.
RP Tuchman, R (reprint author), Miami Childrens Hosp Dan Marino Ctr, Dept Neurol, Weston, FL 33331 USA.
EM roberto.tuchman@gmail.com
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NR 60
TC 3
Z9 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD OCT 29
PY 2013
VL 81
IS 18
BP 1630
EP 1636
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA AA0FB
UT WOS:000330769800020
PM 24089385
ER
PT J
AU Moeller, S
Lau, NM
Green, PHR
Hellberg, D
Higgins, JJ
Rajadhyaksha, AM
Alaedini, A
AF Moeller, Sina
Lau, Nga M.
Green, Peter H. R.
Hellberg, Dan
Higgins, Joseph J.
Rajadhyaksha, Anjali M.
Alaedini, Armin
TI LACK OF ASSOCIATION BETWEEN AUTISM AND ANTI-GM1 GANGLIOSIDE ANTIBODY
SO NEUROLOGY
LA English
DT Editorial Material
ID NEUROPATHY
C1 [Moeller, Sina; Lau, Nga M.; Green, Peter H. R.; Alaedini, Armin] Columbia Univ, Dept Med, Med Ctr, New York, NY 10027 USA.
[Hellberg, Dan] Uppsala Univ, Clin Res Ctr, Falun, Sweden.
[Higgins, Joseph J.; Rajadhyaksha, Anjali M.] Weill Cornell Med Coll, Dept Pediat, New York, NY USA.
[Rajadhyaksha, Anjali M.] Weill Cornell Med Coll, Dept Neurol & Neurosci, New York, NY USA.
RP Alaedini, A (reprint author), Columbia Univ, Dept Med, Med Ctr, New York, NY 10027 USA.
EM aa819@columbia.edu
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Yuki N, 2004, P NATL ACAD SCI USA, V101, P11404, DOI 10.1073/pnas.0402391101
NR 7
TC 1
Z9 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0028-3878
EI 1526-632X
J9 NEUROLOGY
JI Neurology
PD OCT 29
PY 2013
VL 81
IS 18
BP 1640
EP 1641
PG 2
WC Clinical Neurology
SC Neurosciences & Neurology
GA AA0FB
UT WOS:000330769800023
PM 24068789
ER
PT J
AU Egawa, K
Fukuda, A
AF Egawa, Kiyoshi
Fukuda, Atsuo
TI Pathophysiological power of improper tonic GABA(A) conductances in
mature and immature models
SO FRONTIERS IN NEURAL CIRCUITS
LA English
DT Review
DE GABA; GAT; extrasynaptic; ambient; transporter; tonic inhibition;
neurological disease; GABA(A) receptor
ID FRAGILE-X-SYNDROME; HIPPOCAMPAL PYRAMIDAL NEURONS; AUTISM-SPECTRUM
DISORDERS; RECEPTOR INVERSE AGONIST; CEREBELLAR GRANULE CELLS; LONG-TERM
POTENTIATION; ALPHA-5 SUBUNIT; MOUSE MODEL; A RECEPTORS; PREFRONTAL
CORTEX
AB High-affinity extrasynaptic gamma-aminobutyric acid A (GABA(A)) receptors are tonically activated by low and consistent levels of ambient GABA, mediating chronic inhibition against neuronal excitability (tonic inhibition) and the modulation of neural development. Synaptic (phasic) inhibition is spatially and temporally precise compared with tonic inhibition, which provides blunt yet strong integral inhibitory force by shunting electrical signaling. Although effects of acute modification of tonic inhibition are known, its pathophysiological significance remains unclear because homeostatic regulation of neuronal excitability can compensate for long-term deficit of extrasynaptic GABA(A) receptor activation. Nevertheless, tonic inhibition is of great interest for its pathophysiological involvement in central nervous system (CNS) diseases and thus as a therapeutic target. Together with the development of experimental models for various pathological states, recent evidence demonstrates such pathological involvements of tonic inhibition in neuronal dysfunction. This review focuses on the recent progress of tonic activation of GABA(A) conductance on the development and pathology of the CNS. Findings indicate that neuronal function in various brain regions are exacerbated with a gain or loss of function of tonic inhibition by GABA spillover. Disturbance of tonic GABA(A) conductance mediated by non-synaptic ambient GABA may result in brain mal-development. Therefore, various pathological states (epilepsy, motor dysfunctions, psychiatric disorders, and neurodevelopmental disorders) may be partly attributable to abnormal tonic GABA(A) conductances. Thus, the tone of tonic conductance and level of ambient GABA may be precisely tuned to maintain the regular function and development of the CNS. Therefore, receptor expression and factors for regulating the ambient GABA concentration are highlighted to gain a deeper understanding of pathology and therapeutic strategy for CNS diseases.
C1 [Egawa, Kiyoshi] Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA USA.
[Egawa, Kiyoshi] Hokkaido Univ, Grad Sch Med, Dept Pediat, Sapporo, Hokkaido, Japan.
[Fukuda, Atsuo] Hamamatsu Univ Sch Med, Dept Neurophysiol, Hamamatsu, Shizuoka 4313192, Japan.
RP Fukuda, A (reprint author), Hamamatsu Univ Sch Med, Dept Neurophysiol, Higashi Ku, 20-1 Handayama 1 Chome, Hamamatsu, Shizuoka 4313192, Japan.
EM axfukuda@hama-med.ac.jp
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NR 178
TC 6
Z9 6
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5110
J9 FRONT NEURAL CIRCUIT
JI Front. Neural Circuits
PD OCT 24
PY 2013
VL 7
AR 170
DI 10.3389/fncir.2013.00170
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 269XG
UT WOS:000328276500001
PM 24167475
ER
PT J
AU Rivest, JB
Jemel, B
Bertone, A
McKerral, M
Mottron, L
AF Rivest, Jessica B.
Jemel, Boutheina
Bertone, Armando
McKerral, Michelle
Mottron, Laurent
TI Luminance- and Texture-Defined Information Processing in School-Aged
Children with Autism
SO PLOS ONE
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDER; TRAUMATIC BRAIN-INJURY; HUMAN
VISUAL-CORTEX; 2ND-ORDER MOTION; SPECTRUM DISORDER; 1ST-ORDER MOTION;
SELECTIVE IMPAIRMENT; CONTRAST MODULATIONS; PERCEPTION; VEP
AB According to the complexity-specific hypothesis, the efficacy with which individuals with autism spectrum disorder (ASD) process visual information varies according to the extensiveness of the neural network required to process stimuli. Specifically, adults with ASD are less sensitive to texture-defined (or second-order) information, which necessitates the implication of several cortical visual areas. Conversely, the sensitivity to simple, luminance-defined (or first-order) information, which mainly relies on primary visual cortex (V1) activity, has been found to be either superior (static material) or intact (dynamic material) in ASD. It is currently unknown if these autistic perceptual alterations are present in childhood. In the present study, behavioural (threshold) and electrophysiological measures were obtained for static luminance-and texture-defined gratings presented to school-aged children with ASD and compared to those of typically developing children. Our behavioural and electrophysiological (P140) results indicate that luminance processing is likely unremarkable in autistic children. With respect to texture processing, there was no significant threshold difference between groups. However, unlike typical children, autistic children did not show reliable enhancements of brain activity (N230 and P340) in response to texture-defined gratings relative to luminance-defined gratings. This suggests reduced efficiency of neuro-integrative mechanisms operating at a perceptual level in autism. These results are in line with the idea that visual atypicalities mediated by intermediate-scale neural networks emerge before or during the school-age period in autism.
C1 [Rivest, Jessica B.; Bertone, Armando; Mottron, Laurent] Univ Montreal, Ctr Excellence Pervas Dev Disorders CETEDUM, Montreal, PQ, Canada.
[Rivest, Jessica B.; McKerral, Michelle] Univ Montreal, Ctr Rech Neuropsychol & Cognit CERNEC, Montreal, PQ, Canada.
[Rivest, Jessica B.; McKerral, Michelle] Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada.
[Jemel, Boutheina] Univ Montreal, Riviere des Prairies Hosp, Res Lab Neurosci & Cognit Electrophysiol, Montreal, PQ, Canada.
RP Mottron, L (reprint author), Univ Montreal, Ctr Excellence Pervas Dev Disorders CETEDUM, Montreal, PQ, Canada.
EM Laurent.mottron@gmail.com
FU Canadian Institutes of Health Research (CIHR)
[200703MOP-171795-BSB-CFCA-4239]; Natural Sciences and Engineering
Research Council of Canada (NSERC) [327504-2006 RGPIN]; NSCERC; Autism
Research Training (ART) program in Canada
FX This work was supported by a grant to LM from the Canadian Institutes of
Health Research (CIHR) (grant number 200703MOP-171795-BSB-CFCA-4239), by
a grant to MM from the Natural Sciences and Engineering Research Council
of Canada (NSERC) (grant number 327504-2006 RGPIN), as well as
scholarships to JBR from NSCERC and the Autism Research Training (ART)
program in Canada. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 73
TC 1
Z9 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 24
PY 2013
VL 8
IS 10
AR e78978
DI 10.1371/journal.pone.0078978
PG 16
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 241FR
UT WOS:000326152300087
PM 24205355
ER
PT J
AU Tsang, KM
Croen, LA
Torres, AR
Kharrazi, M
Delorenze, GN
Windham, GC
Yoshida, CK
Zerbo, O
Weiss, LA
AF Tsang, Kathryn M.
Croen, Lisa A.
Torres, Anthony R.
Kharrazi, Martin
Delorenze, Gerald N.
Windham, Gayle C.
Yoshida, Cathleen K.
Zerbo, Ousseny
Weiss, Lauren A.
TI A Genome-Wide Survey of Transgenerational Genetic Effects in Autism
SO PLOS ONE
LA English
DT Article
ID SPECTRUM DISORDERS; FETAL MICROCHIMERISM; EARLY MARKERS; RISK-FACTORS;
TWIN PAIRS; BRAIN; ASSOCIATION; VARIANTS; PROGENITOR; PREGNANCY
AB Effects of parental genotype or parent-offspring genetic interaction are well established in model organisms for a variety of traits. However, these transgenerational genetic models are rarely studied in humans. We have utilized an autism case-control study with 735 mother-child pairs to perform genome-wide screening for maternal genetic effects and maternal-offspring genetic interaction. We used simple models of single locus parent-child interaction and identified suggestive results (P<10(-4)) that cannot be explained by main effects, but no genome-wide significant signals. Some of these maternal and maternal-child associations were in or adjacent to autism candidate genes including: PCDH9, FOXP1, GABRB3, NRXN1, RELN, MACROD2, FHIT, RORA, CNTN4, CNTNAP2, FAM135B, LAMA1, NFIA, NLGN4X, RAPGEF4, and SDK1. We attempted validation of potential autism association under maternal-specific models using maternal-paternal comparison in family-based GWAS datasets. Our results suggest that further study of parental genetic effects and parent-child interaction in autism is warranted.
C1 [Tsang, Kathryn M.; Weiss, Lauren A.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
[Tsang, Kathryn M.; Weiss, Lauren A.] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
[Croen, Lisa A.; Delorenze, Gerald N.; Yoshida, Cathleen K.; Zerbo, Ousseny] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
[Torres, Anthony R.] Utah State Univ, Ctr Persons Disabil, Logan, UT 84322 USA.
[Kharrazi, Martin] Calif Dept Hlth Serv, Genet Dis Screening Program, Richmond, CA USA.
[Windham, Gayle C.] Calif Dept Hlth Serv, Div Environm & Occupat Dis Control, Richmond, CA USA.
RP Weiss, LA (reprint author), Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
EM Lauren.Weiss@ucsf.edu
FU National Institute of environmental Health Sciences [R01-ES016669];
National Institute of Health [MH52708, MH39437, MH00219, MH00980,
MH64547]; National Health Medical Research Council [0034328]; Scottish
Rite; Spunk Fund, Inc.; Rebecca and Solomon Baker Fund; APEX Foundation;
National Alliance for Research in Schizophrenia and Affective Disorders;
Nancy Pritzker Laboratory (Stanford); Cure Autism Now Foundation;
National Institute of Mental Health [1U24MH081810]; Medical Research
Council [G0601030]; Wellcome Trust [075491/Z/04]
FX This study was supported by the National Institute of environmental
Health Sciences (http://www.niehs.nih.gov/- R01-ES016669). The
collection of data and biomaterials that participated in the National
Institute of Mental Health Autism Genetics Initiative has been supported
by National Institute of Health grants MH52708, MH39437, MH00219 and
MH00980; National Health Medical Research Council grant 0034328; and by
grants from the Scottish Rite, the Spunk Fund, Inc., the Rebecca and
Solomon Baker Fund, the APEX Foundation, the National Alliance for
Research in Schizophrenia and Affective Disorders, the endowment fund of
the Nancy Pritzker Laboratory (Stanford), by gifts from the Autism
Society of America, the Janet M. Grace Pervasive Developmental Disorders
Fund, and families and friends of individuals with autism. The
collection data and biomaterials also come from the Autism Genetic
Resource Exchange (AGRE) collection supported by a National Institute of
Health grant MH64547 and the Cure Autism Now Foundation. AGRE is a
program of Autism Speaks and is supported, in part, by grant
1U24MH081810 from the National Institute of Mental Health to Clara M.
Lajonchere (PI). Collection and submission of the data to dbGaP were
supported by a grant from the Medical Research Council (G0601030) and
the Wellcome Trust (075491/Z/04), Anthony P. Monaco, P. I., University
of Oxford. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
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NR 65
TC 3
Z9 3
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 24
PY 2013
VL 8
IS 10
AR e76978
DI 10.1371/journal.pone.0076978
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 241FR
UT WOS:000326152300012
PM 24204716
ER
PT J
AU Carpentier, PA
Haditsch, U
Braun, AE
Cantu, AV
Moon, HM
Price, RO
Anderson, MP
Saravanapandian, V
Ismail, K
Rivera, M
Weimann, JM
Palmer, TD
AF Carpentier, Pamela A.
Haditsch, Ursula
Braun, Amy E.
Cantu, Andrea V.
Moon, Hyang Mi
Price, Robin O.
Anderson, Matthew P.
Saravanapandian, Vidya
Ismail, Khadija
Rivera, Moises
Weimann, James M.
Palmer, Theo D.
TI Stereotypical Alterations in Cortical Patterning Are Associated with
Maternal Illness-Induced Placental Dysfunction
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID DEVELOPING CEREBRAL-CORTEX; PRENATAL IMMUNE CHALLENGE; CAJAL-RETZIUS
CELLS; PROJECTION NEURON IDENTITY; AUTISM SPECTRUM DISORDERS; MOUSE;
PREGNANCY; BRAIN; SCHIZOPHRENIA; EXPRESSION
AB We have previously shown in mice that cytokine-mediated damage to the placenta can temporarily limit the flow of nutrients and oxygen to the fetus. The placental vulnerability is pronounced before embryonic day 11, when even mild immune challenge results in fetal loss. As gestation progresses, the placenta becomes increasingly resilient to maternal inflammation, but there is a narrow window in gestation when the placenta is still vulnerable to immune challenge yet resistant enough to allow for fetal survival. This gestational window correlates with early cortical neurogenesis in the fetal brain. Here, we show that maternal illness during this period selectively alters the abundance and laminar positioning of neuronal subtypes influenced by the Tbr1, Satb2, and Ctip2/Fezf2 patterning axis. The disturbances also lead to a laminar imbalance in the proportions of projection neurons and interneurons in the adult and are sufficient to cause changes in social behavior and cognition. These data illustrate how the timing of an illness-related placental vulnerability causes developmental alterations in neuroanatomical systems and behaviors that are relevant to autism spectrum disorders.
C1 [Carpentier, Pamela A.; Haditsch, Ursula; Braun, Amy E.; Cantu, Andrea V.; Moon, Hyang Mi; Price, Robin O.; Anderson, Matthew P.; Saravanapandian, Vidya; Ismail, Khadija; Rivera, Moises; Weimann, James M.; Palmer, Theo D.] Stanford Univ, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA.
RP Palmer, TD (reprint author), Stanford Univ, Inst Stem Cell Biol & Regenerat Med, 265 Campus Dr,Room 1141, Stanford, CA 94305 USA.
EM tpalmer@stanford.edu
FU March of Dimes; Autism Speaks; Simons Foundation; National Institutes of
Health (NIH)/National Institute of Mental Health [1R01MH096815]; NIH
(National Institute of Neurological Disorders and Stroke) [5F32NS60427];
Lucile Packard Foundation
FX This work was supported by grants to T.D.P. from the March of Dimes,
Autism Speaks, Simons Foundation, and National Institutes of Health
(NIH)/National Institute of Mental Health (1R01MH096815) and grants to
P.A.C. from the NIH (National Institute of Neurological Disorders and
Stroke, 5F32NS60427) and the Lucile Packard Foundation. We thank
Elizabeth Alcamo and Susan McConnell for experimental advice and helpful
comments. We also thank the Stanford Behavioral and Functional
Neuroscience Service Center for technical assistance with PPI and Social
Interaction paradigms.
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NR 44
TC 4
Z9 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 23
PY 2013
VL 33
IS 43
BP 16874
EP 16888
DI 10.1523/JNEUROSCI.4654-12.2013
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 240II
UT WOS:000326088500003
PM 24155294
ER
PT J
AU Robertson, CE
Kravitz, DJ
Freyberg, J
Baron-Cohen, S
Baker, CI
AF Robertson, Caroline E.
Kravitz, Dwight J.
Freyberg, Jan
Baron-Cohen, Simon
Baker, Chris I.
TI Slower Rate of Binocular Rivalry in Autism
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID STIMULUS COMPLEXITY; BISTABLE PERCEPTION; SPECTRUM DISORDERS;
VISUAL-PERCEPTION; MODEL; EXCITATION/INHIBITION; SENSITIVITY;
ADAPTATION; ATTENTION; DYNAMICS
AB An imbalance between cortical excitation and inhibition is a central component of many models of autistic neurobiology. We tested a potential behavioral footprint of this proposed imbalance using binocular rivalry, a visual phenomenon in which perceptual experience is thought to mirror the push and pull of excitatory and inhibitory cortical dynamics. In binocular rivalry, two monocularly presented images compete, leading to a percept that alternates between them. In a series of trials, we presented separate images of objects (e.g., a baseball and a broccoli) to each eye using a mirror stereoscope and asked human participants with autism and matched control subjects to continuously report which object they perceived, or whether they perceived a mixed percept. Individuals with autism demonstrated a slower rate of binocular rivalry alternations than matched control subjects, with longer durations of mixed percepts and an increased likelihood to revert to the previously perceived object when exiting a mixed percept. Critically, each of these findings was highly predictive of clinical measures of autistic symptomatology. Control "playback" experiments demonstrated that differences in neither response latencies nor response criteria could account for the atypical dynamics of binocular rivalry we observed in autistic spectrum conditions. Overall, these results may provide an index of atypical cortical dynamics that may underlie both the social and nonsocial symptoms of autism.
C1 [Robertson, Caroline E.; Kravitz, Dwight J.; Baker, Chris I.] NIMH, NIH, Lab Brain & Cognit, Bethesda, MD 20892 USA.
[Robertson, Caroline E.; Freyberg, Jan; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England.
RP Robertson, CE (reprint author), Harvard Soc Fellows, 78 Mt Auburn St, Cambridge, MA 02138 USA.
EM carolinerobertson@fas.harvard.edu
FU National Institute of Mental Health; Gates-Cambridge Trust; National
Institutes of Health-Cambridge Fellowship; Medical Research Council;
Wellcome Trust
FX This work was supported in part by the Intramural Research Program of
the National Institute of Mental Health, and was conducted in
association with the National Institute for Health Research
Collaboration for Leadership in Applied Health Research and Care for
Cambridgeshire and Peterborough NHS Foundation Trust. This work was also
supported by the Gates-Cambridge Trust and the National Institutes of
Health-Cambridge Fellowship (C.E.R.). S.B.-C. was supported by the
Medical Research Council and the Wellcome Trust during the period of
this work. We thank John Mollon for the use of his mirror stereoscope;
David Leopold, Carson Chow, Shashaank Vattikuti, Alex Martin, and Kate
Plaisted-Grant for comments; and Carrie Allison for help with
recruitment.
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NR 41
TC 11
Z9 11
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 23
PY 2013
VL 33
IS 43
BP 16983
EP 16991
DI 10.1523/JNEUROSCI.0448-13.2013
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 240II
UT WOS:000326088500012
PM 24155303
ER
PT J
AU Lukoshe, A
White, T
Schmidt, MN
van der Lugt, A
Hokken-Koelega, AC
AF Lukoshe, Akvile
White, Tonya
Schmidt, Marcus N.
van der Lugt, Aad
Hokken-Koelega, Anita C.
TI Divergent structural brain abnormalities between different genetic
subtypes of children with Prader-Willi syndrome
SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS
LA English
DT Article
DE Prader-Willi syndrome; Neurodevelopmental disorder; Chromosome
15q11-q13; Structural MRI
ID GROWTH-HORMONE TREATMENT; HUMAN CEREBRAL-CORTEX; MAGNETIC-RESONANCE
IMAGES; DEFAULT-MODE NETWORK; BIPOLAR DISORDER; AUTISM SPECTRUM;
NERVOUS-SYSTEM; MRI; SCHIZOPHRENIA; ANGELMAN
AB Background: Prader-Willi syndrome (PWS) is a complex neurogenetic disorder with symptoms that indicate not only hypothalamic, but also a global, central nervous system (CNS) dysfunction. However, little is known about developmental differences in brain structure in children with PWS. Thus, our aim was to investigate global brain morphology in children with PWS, including the comparison between different genetic subtypes of PWS. In addition, we performed exploratory cortical and subcortical focal analyses.
Methods: High resolution structural magnetic resonance images were acquired in 20 children with genetically confirmed PWS (11 children carrying a deletion (DEL), 9 children with maternal uniparental disomy (mUPD)), and compared with 11 age-and gender-matched typically developing siblings as controls. Brain morphology measures were obtained using the FreeSurfer software suite.
Results: Both children with DEL and mUPD showed smaller brainstem volume, and a trend towards smaller cortical surface area and white matter volume. Children with mUPD had enlarged lateral ventricles and larger cortical cerebrospinal fluid (CSF) volume. Further, a trend towards increased cortical thickness was found in children with mUPD. Children with DEL had a smaller cerebellum, and smaller cortical and subcortical grey matter volumes. Focal analyses revealed smaller white matter volumes in left superior and bilateral inferior frontal gyri, right cingulate cortex, and bilateral precuneus areas associated with the default mode network (DMN) in children with mUPD.
Conclusions: Children with PWS show signs of impaired brain growth. Those with mUPD show signs of early brain atrophy. In contrast, children with DEL show signs of fundamentally arrested, although not deviant brain development and presented few signs of cortical atrophy. Our results of global brain measurements suggest divergent neurodevelopmental patterns in children with DEL and mUPD.
C1 [Lukoshe, Akvile; Hokken-Koelega, Anita C.] Dutch Growth Res Fdn, NL-3001 KB Rotterdam, Netherlands.
[Lukoshe, Akvile; Hokken-Koelega, Anita C.] Sophia Childrens Hosp Rotterdam, Erasmus Med Ctr Rotterdam, Dept Pediat, NL-3000 CB Rotterdam, Netherlands.
[White, Tonya; Schmidt, Marcus N.] Sophia Childrens Hosp Rotterdam, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, NL-3000 CB Rotterdam, Netherlands.
[White, Tonya; van der Lugt, Aad] Erasmus MC, Dept Radiol, NL-3000 CA Rotterdam, Netherlands.
RP Lukoshe, A (reprint author), Dutch Growth Res Fdn, Postbus 23068, NL-3001 KB Rotterdam, Netherlands.
EM a.lukose@kindengroei.nl
FU Foundation for Prader-Willi Research, Los Angeles, CA, USA; Dutch Growth
Research Foundation, Rotterdam, The Netherlands
FX We would like to thank parents and children for their participation. We
also thank Afzal Bechan and Marielle van Eekelen for their assistance
with the MRI acquisition, and Zyrhea Troeman for conducting the biannual
IQ tests. This study was financially supported by the Foundation for
Prader-Willi Research, Los Angeles, CA, USA, and Dutch Growth Research
Foundation, Rotterdam, The Netherlands.
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NR 65
TC 3
Z9 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1866-1947
EI 1866-1955
J9 J NEURODEV DISORD
JI J. Neurodev. Disord.
PD OCT 22
PY 2013
VL 5
AR 31
DI 10.1186/1866-1955-5-31
PG 11
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 242ZX
UT WOS:000326287000001
PM 24144356
ER
PT J
AU McFadden, K
Minshew, NJ
AF McFadden, Kathryn
Minshew, Nancy J.
TI Evidence for dysregulation of axonal growth and guidance in the etiology
of ASD
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Review
DE autism spectrum disorders; connectivity; neuritic outgrowth; axonal
guidance; subplate
ID AUTISM SPECTRUM DISORDERS; RECEPTOR TYROSINE KINASE; WHITE-MATTER
COMPROMISE; HIGH-FUNCTIONING AUTISM; COPY NUMBER VARIATION;
CEREBRAL-CORTEX; FRONTAL-CORTEX; DYNAMIC GENE; HUMAN BRAIN; SUBPLATE
AB Current theories concerning the cause of autism spectrum disorders (ASDs) have converged on the concept of abnormal development of brain connectivity. This concept is supported by accumulating evidence from functional imaging, diffusion tensor imaging, and high definition fiber tracking studies which suggest altered microstructure in the axonal tracts connecting cortical areas may underly many of the cognitive manifestations of ASD. Additionally, large-scale genomic studies implicate numerous gene candidates known or suspected to mediate neuritic outgrowth and axonal guidance in fetal and perinatal life. Neuropathological observations in postmortem ASD brain samples further support this model and include subtle disturbances of cortical lamination and subcortical axonal morphology. Of note is the relatively common finding of poor differentiation of the gray-white junction associated with an excess superficial white matter or "interstitial" neurons (INs). INs are thought to be remnants of the fetal subplate, a transient structure which plays a key role in the guidance and morphogenesis of thalamocortical and cortico-cortical connections and the organization of cortical columnar architecture. While not discounting the importance of synaptic dysfunction in the etiology of ASD, this paper will briefly review the cortical abnormalities and genetic evidence supporting a model of dysregulated axonal growth and guidance as key developmental processes underlying the clinical manifestations of ASD.
C1 [McFadden, Kathryn] Univ Pittsburgh, Dept Neurobiol, Pittsburgh, PA 15213 USA.
[Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Psychiat & Neurol, Pittsburgh, PA 15213 USA.
RP Minshew, NJ (reprint author), Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Webster Hall,Suite 300,3811 OHara St, Pittsburgh, PA 15213 USA.
EM minshewnj@upmc.edu
FU Pennsylvania Department of Health [4100047862]; Eunice Kennedy Shriver
National Institute of Child Health and Human Development (NICHD)
[HD055748]
FX The authors gratefully acknowledge support by the Pennsylvania
Department of Health, grant 4100047862 (Kathryn McFadden and Nancy J.
Minshew), and Eunice Kennedy Shriver National Institute of Child Health
and Human Development (NICHD), grant HD055748 (Nancy J. Minshew).
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NR 87
TC 9
Z9 9
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 22
PY 2013
VL 7
AR 671
DI 10.3389/fnhum.2013.00671
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 238BZ
UT WOS:000325917000001
PM 24155705
ER
PT J
AU Wong, M
Guo, D
AF Wong, M.
Guo, D.
TI DENDRITIC SPINE PATHOLOGY IN EPILEPSY: CAUSE OR CONSEQUENCE?
SO NEUROSCIENCE
LA English
DT Article
DE seizure; epilepsy; epileptogenesis; dendrite; actin
ID TEMPORAL-LOBE EPILEPSY; DENTATE GRANULE CELLS; LASER-SCANNING
MICROSCOPY; RAT PILOCARPINE MODEL; STATUS EPILEPTICUS; RETT-SYNDROME;
IN-VIVO; SYNAPTIC PLASTICITY; TUBEROUS SCLEROSIS; HIPPOCAMPAL DENDRITES
AB Abnormalities in dendritic spines have commonly been observed in brain specimens from epilepsy patients and animal models of epilepsy. However, the functional implications and clinical consequences of this dendritic pathology for epilepsy are uncertain. Dendritic spine abnormalities may promote hyperexcitable circuits and seizures in some types of epilepsy, especially in specific genetic syndromes with documented dendritic pathology, but in these cases it is difficult to differentiate their effects on seizures versus other comorbidities, such as cognitive deficits and autism. In other situations, seizures themselves may cause damage to dendrites and dendritic spines and this seizure-induced brain injury may then contribute to progressive epileptogenesis, memory problems and other neurological deficits in epilepsy patients. The mechanistic basis of dendritic spine abnormalities in epilepsy has begun to be elucidated and suggests novel therapeutic strategies for treating epilepsy and its complications.
This article is part of a Special Issue entitled: Dendritic Spine Plasticity in Brain Disorders. (c) 2012 IBRO Published by Elsevier Ltd. All rights reserved.
C1 [Wong, M.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
Washington Univ, Sch Med, Hope Ctr Neurol Disorders, St Louis, MO 63110 USA.
RP Wong, M (reprint author), Washington Univ, Sch Med, Dept Neurol, Box 8111,660 South Euclid Ave, St Louis, MO 63110 USA.
EM wong_m@wustl.edu
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NR 87
TC 6
Z9 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0306-4522
J9 NEUROSCIENCE
JI Neuroscience
PD OCT 22
PY 2013
VL 251
SI SI
BP 141
EP 150
DI 10.1016/j.neuroscience.2012.03.048
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 230ZR
UT WOS:000325383300012
PM 22522469
ER
PT J
AU Brogaard, B
AF Brogaard, Berit
TI Serotonergic hyperactivity as a potential factor in developmental,
acquired and drug-induced synesthesia
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE acquired synesthesia; autism spectrum disorder; drug-induced
synaesthesia; left-hemisphere injuries; multisensory perception; savant
syndrome; serotonin hypothesis; traumatic brain injury
ID TRAUMATIC BRAIN-INJURY; GRAPHEME-COLOR SYNESTHESIA; AUDITORY-VISUAL
SYNESTHESIA; FRONTOTEMPORAL DEMENTIA; STRUCTURAL CONNECTIVITY;
ASPERGER-SYNDROME; THALAMIC LESION; SAVANT MEMORY; IN-VITRO;
SYNAESTHESIA
AB Though synesthesia research has seen a huge grow thin recent decades, and tremendous progress has been made in terms of understanding the mechanism and cause of synesthesia, we are still left mostly in the dark when it comes to the mechanistic commonalities (if any) among developmental, acquired and drug-induced synesthesia. We know that many forms of synesthesia involve aberrant structural or functional brain connectivity. Proposed mechanisms include direct projection and disinhibited feedback mechanisms, in which information from two otherwise structurally or functionally separate brain regions mix. We also know that synesthesia sometimes runs in families. However, it is unclear what causes its on set. Studies of psychedelic drugs, such as psilocybin, LSD and mescaline, reveal that exposure to these drugs can induce synesthesia. One neurotransmitter suspected to be central to the perceptual changes is serotonin. Excessive serotonin in the brain may cause many of the characteristics of psychedelic in toxication. Excessive serotonin levels may also play a role in synesthesia acquired after brain injury. In brain injury sudden cell death floods local brain regions with serotonin and glutamate. This neurotransmitter flooding could perhaps result in unusual feature binding. Finally, developmental synesthesia that occurs in individuals with autism may be a result of alterations in the serotonergic system, leading to a blockage of regular gating mechanisms. I conclude on these grounds that one commonality among at least some cases of acquired, developmental and drug-induced synesthesia may be the presence of excessive levels of serotonin, which increases the excitability and connectedness of sensory brain regions.
C1 [Brogaard, Berit] Univ Missouri, Dept Philosophy, St Louis, MO 63121 USA.
[Brogaard, Berit] Univ Missouri, Ctr Neurodynam, St Louis, MO 63121 USA.
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NR 141
TC 6
Z9 6
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 21
PY 2013
VL 7
AR 657
DI 10.3389/fnhum.2013.00657
PG 13
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 238BV
UT WOS:000325916500001
PM 24155703
ER
PT J
AU Lehti, V
Hinkka-Yli-Salomaki, S
Cheslack-Postava, K
Gissler, M
Brown, AS
Sourander, A
AF Lehti, Venla
Hinkka-Yli-Salomaki, Susanna
Cheslack-Postava, Keely
Gissler, Mika
Brown, Alan S.
Sourander, Andre
TI The risk of childhood autism among second-generation migrants in
Finland: a case-control study
SO BMC PEDIATRICS
LA English
DT Article
DE Autism; Risk factor; Parental; Migration; Epidemiology
ID SPECTRUM DISORDERS; INFANTILE-AUTISM; VITAMIN-D; EPIDEMIOLOGY;
ENVIRONMENT; EXPOSURE; ORIGIN
AB Background: Studying second-generation immigrants can help in identifying genetic or environmental risk factors for childhood autism. Most previous studies have focused on maternal region of birth and showed inconsistent results. No previous study has been conducted in Finland.
Methods: The study was a nested case-control study based on a national birth cohort. Children born in 1987-2005 and diagnosed with childhood autism by the year 2007 were identified from the Finnish Hospital Discharge Register. Controls were selected from the Finnish Medical Birth Register. Information on maternal and paternal country of birth and mother tongue was collected from the Finnish Central Population Register. There were 1132 cases and 4515 matched controls. The statistical test used was conditional logistic regression analysis.
Results: Compared with children with two Finnish parents, the risk of childhood autism was increased for those whose parents are both immigrants (adjusted odds ratio [aOR] 1.8, 95% confidence interval [CI] 1.2-2.7) and for those with only an immigrant mother (aOR 1.8, 95% CI 1.2-2.7), but not for those with only an immigrant father. The risk was increased for those with a mother born in the former Soviet Union or Yugoslavia and for those with a mother or a father born in Asia. Specific parental countries of birth associated with an increased risk were the former Soviet Union, the former Yugoslavia and Vietnam.
Conclusions: In Finland, children who are born to immigrant mothers with or without an immigrant partner, have an increased risk of childhood autism. The risk varies with immigrant parents' region of birth. The findings may help in identifying possible risk factors, which can be examined in future studies.
C1 [Lehti, Venla; Hinkka-Yli-Salomaki, Susanna; Gissler, Mika; Sourander, Andre] Univ Turku, Dept Child Psychiat, Turku 20014, Finland.
[Cheslack-Postava, Keely; Brown, Alan S.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY 10032 USA.
[Gissler, Mika] Natl Inst Hlth & Welf THL, Helsinki 00271, Finland.
[Gissler, Mika] Nord Sch Publ Hlth, SE-40242 Gothenburg, Sweden.
[Brown, Alan S.; Sourander, Andre] Columbia Univ Coll Phys & Surg, Dept Psychiat, New York State Psychiat Inst, Unit 23, New York, NY 10032 USA.
RP Sourander, A (reprint author), Univ Turku, Dept Child Psychiat, Lemminkaisenkatu 3 Teutori, Turku 20014, Finland.
EM andre.sourander@utu.fi
FU Autism Speaks; National Institute of Mental Health (NIMH)
[1K02-MH65422]; National Institute of Environmental Health Sciences
[1R01ES019004]
FX This study was supported by Autism Speaks, National Institute of Mental
Health (NIMH) 1K02-MH65422, and National Institute of Environmental
Health Sciences 1R01ES019004. The funding bodies had no role in the
collection, analysis and interpretation of data, in the writing of the
manuscript or in the decision to submit the manuscript for publication.
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LA English
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ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; SIMULATION; EXPOSURE;
EMPATHY; OTHERS; ADULTS
AB Understanding others' mental states is a crucial skill that enables the complex social relationships that characterize human societies. Yet little research has investigated what fosters this skill, which is known as Theory of Mind (ToM), in adults. We present five experiments showing that reading literary fiction led to better performance on tests of affective ToM (experiments 1 to 5) and cognitive ToM (experiments 4 and 5) compared with reading nonfiction (experiments 1), popular fiction (experiments 2 to 5), or nothing at all (experiments 2 and 5). Specifically, these results show that reading literary fiction temporarily enhances ToM. More broadly, they suggest that ToM may be influenced by engagement with works of art.
C1 [Kidd, David Comer; Castano, Emanuele] New Sch Social Res, New York, NY 10011 USA.
RP Kidd, DC (reprint author), New Sch Social Res, 80 5th Ave, New York, NY 10011 USA.
EM kiddd305@newschool.edu; castanoe@newschool.edu
FU New School for Social Research
FX Data are available in spreadsheet format from authors by request. This
research was funded by a Prize Fellowship and a Dissertation Fellowship
by the New School for Social Research to the first author, and a Faculty
Development Award by the New School for Social Research to the second
author. We are grateful to Andrew Marzoni for his insight into literary
criticism and pointing us toward Barthes's S/Z (19).
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NR 36
TC 35
Z9 35
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
EI 1095-9203
J9 SCIENCE
JI Science
PD OCT 18
PY 2013
VL 342
IS 6156
BP 377
EP 380
DI 10.1126/science.1239918
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 235XG
UT WOS:000325755100050
PM 24091705
ER
PT J
AU Skwerer, DP
Tager-Flusberg, H
AF Skwerer, Daniela Plesa
Tager-Flusberg, Helen
TI Innovative approaches to the study of social phenotypes in
neurodevelopmental disorders: an introduction to the research topic
SO FRONTIERS IN PSYCHOLOGY
LA English
DT Editorial Material
DE neurodevelopmental disorders; social phenotypes; cross-syndrome and
longitudinal approaches; autism spectrum disorders; Williams syndrome
C1 [Skwerer, Daniela Plesa; Tager-Flusberg, Helen] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
RP Skwerer, DP (reprint author), Boston Univ, Dept Psychol, 64 Cummington St, Boston, MA 02215 USA.
EM dplesas@bu.edu
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TC 0
Z9 0
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-1078
J9 FRONT PSYCHOL
JI Front. Psychol.
PD OCT 17
PY 2013
VL 4
AR 747
DI 10.3389/fpsyg.2013.00747
PG 3
WC Psychology, Multidisciplinary
SC Psychology
GA AA6VT
UT WOS:000331237000001
ER
PT J
AU Sampath, S
Bhat, S
Gupta, S
O'Connor, A
West, AB
Arking, DE
Chakravarti, A
AF Sampath, Srirangan
Bhat, Shambu
Gupta, Simone
O'Connor, Ashley
West, Andrew B.
Arking, Dan E.
Chakravarti, Aravinda
TI Defining the Contribution of CNTNAP2 to Autism Susceptibility
SO PLOS ONE
LA English
DT Article
ID DE-NOVO MUTATIONS; PERVASIVE DEVELOPMENTAL DISORDERS; CARRIER SLC25A12
GENE; SPECTRUM DISORDERS; GENOMIC SCREEN; CHROMOSOME 7Q;
GENOTYPE-IMPUTATION; GENOMEWIDE SCREEN; UNIFIED APPROACH; ASSOCIATION
AB Multiple lines of genetic evidence suggest a role for CNTNAP2 in autism. To assess its population impact we studied 2148 common single nucleotide polymorphisms (SNPs) using transmission disequilibrium test (TDT) across the entire similar to 3.3 Mb CNTNAP2 locus in 186 (408 trios) multiplex and 323 simplex families with autistic spectrum disorder (ASD). This analysis yielded two SNPs with nominal statistical significance (rs17170073, p = 2.0 x 10(-4); rs2215798, p = 1.6 x 10(-4)) that did not survive multiple testing. In a combined analysis of all families, two highly correlated (r(2) = 0.99) SNPs in intron 14 showed significant association with autism (rs2710093, p = 9.0 x 10(-6); rs2253031, p = 2.5 x 10(-5)). To validate these findings and associations at SNPs from previous autism studies (rs7794745, rs2710102 and rs17236239) we genotyped 2051 additional families (572 multiplex and 1479 simplex). None of these variants were significantly associated with ASD after corrections for multiple testing. The analysis of Mendelian errors within each family did not indicate any segregating deletions. Nevertheless, a study of CNTNAP2 gene expression in brains of autistic patients and of normal controls, demonstrated altered expression in a subset of patients (p = 1.9 x 10(-5)). Consequently, this study suggests that although CNTNAP2 dysregulation plays a role in some cases, its population contribution to autism susceptibility is limited.
C1 [Sampath, Srirangan; Bhat, Shambu; Gupta, Simone; O'Connor, Ashley; Arking, Dan E.; Chakravarti, Aravinda] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Ctr Complex Dis Genom, Baltimore, MD 21218 USA.
[West, Andrew B.] Univ Alabama Birmingham, Dept Neurol & Neurobiol, Ctr Neurodegenerat & Expt Therapeut, Birmingham, AL USA.
RP Sampath, S (reprint author), Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Ctr Complex Dis Genom, Baltimore, MD 21218 USA.
EM aravinda@jhmi.edu
FU Simons Foundation [SFARI 102882]; National Institutes of Health (ACE
Genetics Consortium) [MH081754]
FX This work was supported by grants from the Simons Foundation (SFARI
102882 to AC) and the National Institutes of Health (ACE Genetics
Consortium, MH081754) to AC. The funders had no role in study design,
data collection and analysis, decision to publish, or preparation of the
manuscript.
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PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 17
PY 2013
VL 8
IS 10
DI 10.1371/journal.pone.0077906
PG 13
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 239KL
UT WOS:000326022200085
PM 24147096
ER
PT J
AU Deshpande, G
Libero, LE
Sreenivasan, KR
Deshpande, HD
Kana, RK
AF Deshpande, Gopikrishna
Libero, Lauren E.
Sreenivasan, Karthik R.
Deshpande, Hrishikesh D.
Kana, Rajesh K.
TI Identification of neural connectivity signatures of autism using machine
learning
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE autism; effective connectivity; fMRI; classification; machine learning;
theory-of-mind
ID GRANGER CAUSALITY ANALYSIS; HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDER;
WHITE-MATTER; CORTICAL UNDERCONNECTIVITY; SENTENCE COMPREHENSION;
SOCIAL-PERCEPTION; CORPUS-CALLOSUM; HEAD MOTION; FMRI DATA
AB Alterations in interregional neural connectivity have been suggested as a signature of the pathobiology of autism. There have been many reports of functional and anatomical connectivity being altered while individuals with autism are engaged in complex cognitive and social tasks. Although disrupted instantaneous correlation between cortical regions observed from functional MRI is considered to be an explanatory model for autism, the causal influence of a brain area on another (effective connectivity) is a vital link missing in these studies. The current study focuses on addressing this in an fMRI study of Theory-of-Mind (ToM) in 15 high-functioning adolescents and adults with autism and 15 typically developing control participants. Participants viewed a series of comic strip vignettes in the MRI scanner and were asked to choose the most logical end to the story from three alternatives, separately for trials involving physical and intentional causality. The mean time series, extracted from 18 activated regions of interest, were processed using a multivariate autoregressive model (MVAR) to obtain the causality matrices for each of the 30 participants. These causal connectivity weights, along with assessment scores, functional connectivity values, and fractional anisotropy obtained from DTI data for each participant, were submitted to a recursive cluster elimination based support vector machine classifier to determine the accuracy with which the classifier can predict a novel participant's group membership (autism or control). We found a maximum classification accuracy of 95.9% with 19 features which had the highest discriminative ability between the groups. All of the 19 features were effective connectivity paths, indicating that causal information may be critical in discriminating between autism and control groups. These effective connectivity paths were also found to be significantly greater in controls as compared to ASD participants and consisted predominantly of outputs from the fusiform face area and middle temporal gyrus indicating impaired connectivity in ASD participants, particularly in the social brain areas. These findings collectively point toward the fact that alterations in causal connectivity in the brain in ASD could serve as a potential non-invasive neuroimaging signature for autism.
C1 [Deshpande, Gopikrishna; Sreenivasan, Karthik R.] Auburn Univ, Dept Elect & Comp Engn, AU MRI Res Ctr, Auburn, AL 36849 USA.
[Deshpande, Gopikrishna] Auburn Univ, Dept Psychol, Auburn, AL 36849 USA.
[Libero, Lauren E.; Deshpande, Hrishikesh D.; Kana, Rajesh K.] Univ Alabama Birmingham, Dept Psychol, Birmingham, AL 35294 USA.
RP Kana, RK (reprint author), Univ Alabama Birmingham, Dept Psychol, CIRC 235G,1719 6th Ave South, Birmingham, AL 35294 USA.
EM rkana@uab.edu
FU Auburn University MRI Research Center
FX The authors would like to thank the UAB department of Psychology and the
Civitan-McNulty Scientist Award to Rajesh K. Kana as well as support
from Auburn University MRI Research Center to Gopikrishna Deshpande as
sources of funding support for this study.
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NR 87
TC 9
Z9 9
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 17
PY 2013
VL 7
AR 670
DI 10.3389/fnhum.2013.00670
PG 15
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 235UO
UT WOS:000325746400001
PM 24151458
ER
PT J
AU Jamadar, SD
Fielding, J
Egan, GF
AF Jamadar, Sharna D.
Fielding, Joanne
Egan, Gary F.
TI Quantitative meta-analysis of fMRI and PET studies reveals consistent
activation in fronto-striatal-parietal regions and cerebellum during
antisaccades and prosaccades
SO FRONTIERS IN PSYCHOLOGY
LA English
DT Article
DE antisaccade; oculomotor; functional magnetic resonance imaging; positron
emission tomography; meta-analysis; activation likelihood estimation
ID ANTERIOR CINGULATE CORTEX; EVENT-RELATED FMRI;
POSITRON-EMISSION-TOMOGRAPHY; SUPPLEMENTARY EYE FIELD; AUTISM SPECTRUM
DISORDERS; HUMAN SUPERIOR COLLICULUS; VISUALLY-GUIDED SACCADES;
INHIBITORY CONTROL; COGNITIVE CONTROL; FUNCTIONAL NEUROANATOMY
AB The antisaccade task is a classic task of oculomotor control that requires participants to inhibit a saccade to a target and instead make a voluntary saccade to the mirror opposite location. By comparison, the prosaccade task requires participants to make a visually-guided saccade to the target. These tasks have been studied extensively using behavioral oculomotor, electrophysiological, and neuroimaging in both non-human primates and humans. In humans, the antisaccade task is under active investigation as a potential endophenotype or biomarker for multiple psychiatric and neurological disorders. A large and growing body of literature has used functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) to study the neural correlates of the antisaccade and prosaccade tasks. We present a quantitative meta-analysis of all published voxel-wise fMRI and PET studies (18) of the antisaccade task and show that consistent activation for antisaccades and prosaccades is obtained in a fronto-subcortical-parietal network encompassing frontal and supplementary eye fields (SEFs), thalamus, striatum, and intraparietal cortex. This network is strongly linked to oculomotor control and was activated to a greater extent for antisaccade than prosaccade trials. Antisaccade but not prosaccade trials additionally activated dorsolateral and ventrolateral prefrontal cortices. We also found that a number of additional regions not classically linked to oculomotor control were activated to a greater extent for antisaccade vs. prosaccade trials; these regions are often reported in antisaccade studies but rarely commented upon. While the number of studies eligible to be included in this meta-analysis was small, the results of this systematic review reveal that antisaccade and prosaccade trials consistently activate a distributed network of regions both within and outside the classic definition of the oculomotor network.
C1 [Jamadar, Sharna D.; Egan, Gary F.] Monash Univ, Monash Biomed Imaging, Melbourne, Vic 3004, Australia.
[Jamadar, Sharna D.; Fielding, Joanne; Egan, Gary F.] Monash Univ, Sch Psychol & Psychiat, Melbourne, Vic 3004, Australia.
RP Jamadar, SD (reprint author), Monash Univ, Sch Psychol & Psychiat, Monash Biomed Imaging, 770 Blackburn Rd, Clayton, Vic 3800, Australia.
EM sharna.jamadar@monash.edu
RI Egan, Gary/A-1381-2013
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NR 146
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1664-1078
J9 FRONT PSYCHOL
JI Front. Psychol.
PD OCT 16
PY 2013
VL 4
DI 10.3389/fpsyg.2013.00749
PG 15
WC Psychology, Multidisciplinary
SC Psychology
GA AA6WH
UT WOS:000331238400001
PM 24137150
ER
PT J
AU Wolfe, D
Dudek, S
Ritchie, MD
Pendergrass, SA
AF Wolfe, Daniel
Dudek, Scott
Ritchie, Marylyn D.
Pendergrass, Sarah A.
TI Visualizing genomic information across chromosomes with PhenoGram
SO BIODATA MINING
LA English
DT Article
DE Data visualization; Bioinformatics; Genome-wide association study; GWAS;
Copy-number variants; CNV; SNP; Ideogram
ID WIDE ASSOCIATION; AUTISM
AB Background: With the abundance of information and analysis results being collected for genetic loci, user-friendly and flexible data visualization approaches can inform and improve the analysis and dissemination of these data. A chromosomal ideogram is an idealized graphic representation of chromosomes. Ideograms can be combined with overlaid points, lines, and/or shapes, to provide summary information from studies of various kinds, such as genome-wide association studies or phenome-wide association studies, coupled with genomic location information. To facilitate visualizing varied data in multiple ways using ideograms, we have developed a flexible software tool called PhenoGram which exists as a web-based tool and also a command-line program.
Results: With PhenoGram researchers can create chomosomal ideograms annotated with lines in color at specific base-pair locations, or colored base-pair to base-pair regions, with or without other annotation. PhenoGram allows for annotation of chromosomal locations and/or regions with shapes in different colors, gene identifiers, or other text. PhenoGram also allows for creation of plots showing expanded chromosomal locations, providing a way to show results for specific chromosomal regions in greater detail. We have now used PhenoGram to produce a variety of different plots, and provide these as examples herein. These plots include visualization of the genomic coverage of SNPs from a genotyping array, highlighting the chromosomal coverage of imputed SNPs, copy-number variation region coverage, as well as plots similar to the NHGRI GWA Catalog of genome-wide association results.
Conclusions: PhenoGram is a versatile, user-friendly software tool fostering the exploration and sharing of genomic information. Through visualization of data, researchers can both explore and share complex results, facilitating a greater understanding of these data.
C1 [Wolfe, Daniel; Dudek, Scott; Ritchie, Marylyn D.; Pendergrass, Sarah A.] Penn State Univ, Eberly Coll Sci, Huck Inst Life Sci, Ctr Syst Genom,Dept Biochem & Mol Biol, University Pk, PA 16802 USA.
RP Ritchie, MD (reprint author), Penn State Univ, Eberly Coll Sci, Huck Inst Life Sci, Ctr Syst Genom,Dept Biochem & Mol Biol, 512 Wartik Lab, University Pk, PA 16802 USA.
EM marylyn.ritchie@psu.edu
FU [5U01 HG004798-03]; [5R01 LM010040-02]; [U19 HL065962-10]
FX We would like to thank everyone who has had suggestions for improvements
and additions to this software. This work was supported by the following
funding agencies and grants: 5U01 HG004798-03, 5R01 LM010040-02, and U19
HL065962-10.
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TC 2
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PI LONDON
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SN 1756-0381
J9 BIODATA MIN
JI BioData Min.
PD OCT 16
PY 2013
VL 6
AR 18
DI 10.1186/1756-0381-6-18
PG 12
WC Mathematical & Computational Biology
SC Mathematical & Computational Biology
GA 279IY
UT WOS:000328954800001
PM 24131735
ER
PT J
AU Dodero, L
Damiano, M
Galbusera, A
Bifone, A
Tsaftsaris, SA
Scattoni, ML
Gozzi, A
AF Dodero, Luca
Damiano, Mario
Galbusera, Alberto
Bifone, Angelo
Tsaftsaris, Sotirios A.
Scattoni, Maria Luisa
Gozzi, Alessandro
TI Neuroimaging Evidence of Major Morpho-Anatomical and Functional
Abnormalities in the BTBR T plus TF/J Mouse Model of Autism
SO PLOS ONE
LA English
DT Article
ID VOXEL-BASED MORPHOMETRY; CEREBRAL BLOOD-VOLUME; CORPUS-CALLOSUM;
CORTICAL THICKNESS; SPECTRUM DISORDERS; CHILDHOOD AUTISM; IMAGE
REGISTRATION; SOCIAL COGNITION; INBRED STRAINS; PROBST BUNDLE
AB BTBR T+tf/J (BTBR) mice display prominent behavioural deficits analogous to the defining symptoms of autism, a feature that has prompted a widespread use of the model in preclinical autism research. Because neuro-behavioural traits are described with respect to reference populations, multiple investigators have examined and described the behaviour of BTBR mice against that exhibited by C57BL/6J (B6), a mouse line characterised by high sociability and low self-grooming. In an attempt to probe the translational relevance of this comparison for autism research, we used Magnetic Resonance Imaging (MRI) to map in both strain multiple morpho-anatomical and functional neuroimaging readouts that have been extensively used in patient populations. Diffusion tensor tractography confirmed previous reports of callosal agenesis and lack of hippocampal commissure in BTBR mice, and revealed a concomitant rostro-caudal reorganisation of major cortical white matter bundles. Intact inter-hemispheric tracts were found in the anterior commissure, ventro-medial thalamus, and in a strain-specific white matter formation located above the third ventricle. BTBR also exhibited decreased fronto-cortical, occipital and thalamic gray matter volume and widespread reductions in cortical thickness with respect to control B6 mice. Foci of increased gray matter volume and thickness were observed in the medial prefrontal and insular cortex. Mapping of resting-state brain activity using cerebral blood volume weighted fMRI revealed reduced cortico-thalamic function together with foci of increased activity in the hypothalamus and dorsal hippocampus of BTBR mice. Collectively, our results show pronounced functional and structural abnormalities in the brain of BTBR mice with respect to control B6 mice. The large and widespread white and gray matter abnormalities observed do not appear to be representative of the neuroanatomical alterations typically observed in autistic patients. The presence of reduced fronto-cortical metabolism is of potential translational relevance, as this feature recapitulates previously-reported clinical observations.
C1 [Dodero, Luca; Damiano, Mario; Galbusera, Alberto; Bifone, Angelo; Gozzi, Alessandro] Ctr Neurosci & Cognit Syst UniTn, Ist Italiano Tecnol, Rovereto, Italy.
[Tsaftsaris, Sotirios A.] Northwestern Univ, Dept Elect Engn & Comp Sci, Evanston, IL USA.
[Scattoni, Maria Luisa] Ist Super Sanita, Neurotoxicol & Neuroendocrinol Sect, Dept Cell Biol & Neurosci, I-00161 Rome, Italy.
RP Gozzi, A (reprint author), Ctr Neurosci & Cognit Syst UniTn, Ist Italiano Tecnol, Rovereto, Italy.
EM alessandro.gozzi@iit.it
FU Istituto Italiano di Tecnologia
FX The study was funded by the Istituto Italiano di Tecnologia. The funders
had no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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NR 76
TC 13
Z9 13
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 16
PY 2013
VL 8
IS 10
AR e76655
DI 10.1371/journal.pone.0076655
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 239JR
UT WOS:000326019400078
PM 24146902
ER
PT J
AU Yang, Y
Vasylyev, DV
Dib-Hajj, F
Veeramah, KR
Hammer, MF
Dib-Hajj, SD
Waxman, SG
AF Yang, Yang
Vasylyev, Dmytro V.
Dib-Hajj, Fadia
Veeramah, Krishna R.
Hammer, Michael F.
Dib-Hajj, Sulayman D.
Waxman, Stephen G.
TI Multistate Structural Modeling and Voltage-Clamp Analysis of
Epilepsy/Autism Mutation Kv10.2-R327H Demonstrate the Role of This
Residue in Stabilizing the Channel Closed State
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID MOLECULAR-DYNAMICS SIMULATIONS; GO POTASSIUM CHANNELS; K+ CHANNEL;
SODIUM-CHANNEL; SEIZURE LOCUS; EAG FAMILY; SENSOR; ACTIVATION; CHARGE;
EXPRESSION
AB Voltage-gated potassium channel Kv10.2 (KCNH5) is expressed in the nervous system, but its functions and involvement in human disease are poorly understood. We studied a human Kv10.2 channel mutation (R327H) recently identified in a child with epileptic encephalopathy and autistic features. Using multistate structural modeling, we demonstrate that the Arg327 residue in the S4 helix of voltage-sensing domain has strong ionic interactions with negatively charged residues within the S1-S3 helices in the resting (closed) and early-activation state but not in the late-activation and fully-activated (open) state. The R327H mutation weakens ionic interactions between residue 327 and these negatively charged residues, thus favoring channel opening. Voltage-clamp analysis showed a strong hyperpolarizing (similar to 70 mV) shift of voltage dependence of activation and an acceleration of activation. Our results demonstrate the critical role of the Arg327 residue in stabilizing the channel closed state and explicate for the first time the structural and functional change of a Kv10.2 channel mutation associated with neurological disease.
C1 [Yang, Yang; Vasylyev, Dmytro V.; Dib-Hajj, Fadia; Dib-Hajj, Sulayman D.; Waxman, Stephen G.] Yale Univ, Sch Med, Dept Neurol, New Haven, CT 06510 USA.
[Yang, Yang; Vasylyev, Dmytro V.; Dib-Hajj, Fadia; Dib-Hajj, Sulayman D.; Waxman, Stephen G.] Yale Univ, Sch Med, Ctr Neurosci & Regenerat Res, New Haven, CT 06510 USA.
[Yang, Yang; Vasylyev, Dmytro V.; Dib-Hajj, Fadia; Dib-Hajj, Sulayman D.; Waxman, Stephen G.] Vet Affairs Connecticut Healthcare Syst, Rehabil Res Ctr, West Haven, CT 06516 USA.
[Veeramah, Krishna R.; Hammer, Michael F.] Univ Arizona, Arizona Res Labs, Div Biotechnol, Tucson, AZ 85721 USA.
RP Waxman, SG (reprint author), Vet Affairs Connecticut Healthcare Syst, Neurosci & Regenerat Res Ctr, 950 Campbell Ave,Bldg 34, West Haven, CT 06516 USA.
EM stephen.waxman@yale.edu
FU Medical Research Service, Department of Veterans Affairs; Rehabilitation
Research Service, Department of Veterans Affairs; Connecticut Stem Cell
Research Grants Program
FX This work was supported by the Medical Research Service and
Rehabilitation Research Service, Department of Veterans Affairs (S. G.
W.). Y.Y. is supported by Connecticut Stem Cell Research Grants Program.
The Center for Neuroscience and Regeneration Research is a Collaboration
of the Paralyzed Veterans of America with Yale University. We thank Dr.
Mark Estacion, Dr. Chongyang Han, and Dr. Jianying Huang for valuable
comments. We thank Dr. David E. Shaw and Dr. Morten Jensen of D. E. Shaw
Research for providing coordinates of their molecular dynamics
simulation results and helpful discussion.
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NR 45
TC 4
Z9 4
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 16
PY 2013
VL 33
IS 42
BP 16586
EP 16593
DI 10.1523/JNEUROSCI.2307-13.2013
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 236OY
UT WOS:000325809800016
PM 24133262
ER
PT J
AU Burgess, JD
Arnold, SL
Fitzgibbon, BM
Fitzgerald, PB
Enticott, PG
AF Burgess, Jed D.
Arnold, Sara L.
Fitzgibbon, Bernadette M.
Fitzgerald, Paul B.
Enticott, Peter G.
TI A transcranial magnetic stimulation study of the effect of visual
orientation on the putative human mirror neuron system
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE mirror neurons; transcranial magnetic stimulation; electromyography;
associative learning; action observation; visual perspective
ID AUTISM SPECTRUM DISORDERS; CORTICOSPINAL EXCITABILITY; MOTOR
FACILITATION; MODULATION; IMITATION; OTHERS; DYSFUNCTION; EMOTIONS;
CHILDREN; BIRTH
AB Mirror neurons are a class of motor neuron that are active during both the performance and observation of behavior, and have been implicated in interpersonal understanding. There is evidence to suggest that the mirror response is modulated by the perspective from which an action is presented (e.g., egocentric or allocentric). Most human research, however, has only examined this when presenting intransitive actions. Twenty-three healthy adult participants completed a transcranial magnetic stimulation experiment that assessed corticospinal excitability whilst viewing transitive hand gestures from both egocentric (i.e., self) and allocentric (i.e., other) viewpoints. Although action observation was associated with increases in corticospinal excitability (reflecting putative human mirror neuron activity), there was no effect of visual perspective. These findings are discussed in the context of contemporary theories of mirror neuron ontogeny, including models concerning associative learning and evolutionary adaptation.
C1 [Burgess, Jed D.; Arnold, Sara L.; Fitzgibbon, Bernadette M.; Fitzgerald, Paul B.; Enticott, Peter G.] Monash Univ, Monash Alfred Psychiat Res Ctr, Alfred & Cent Clin Sch, Fac Med Nursing & Hlth Sci, Melbourne, Vic 3004, Australia.
RP Enticott, PG (reprint author), Monash Univ, Monash Alfred Psychiat Res Ctr, Alfred & Cent Clin Sch, Fac Med Nursing & Hlth Sci, Level 4,607 St Kilda Rd, Melbourne, Vic 3004, Australia.
EM peter.enticott@monash.edu
FU National Health and Medical Research Council (NHMRC) Career Development
Fellowship; NHMRC Practitioner Fellowship; Australian Research Council
(ARC) Discovery Project [DP120101738]
FX Peter G. Enticott is supported by a National Health and Medical Research
Council (NHMRC) Career Development Fellowship. Paul B. Fitzgerald is
supported by a NHMRC Practitioner Fellowship. This research was
supported by an Australian Research Council (ARC) Discovery Project
awarded to Peter G. Enticott (DP120101738).
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NR 37
TC 1
Z9 1
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 16
PY 2013
VL 7
AR 679
DI 10.3389/fnhum.2013.00679
PG 6
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 234ZI
UT WOS:000325683000001
PM 24137125
ER
PT J
AU Panoutsopoulou, K
Tachmazidou, I
Zeggini, E
AF Panoutsopoulou, Kalliope
Tachmazidou, Ioanna
Zeggini, Eleftheria
TI In search of low-frequency and rare variants affecting complex traits
SO HUMAN MOLECULAR GENETICS
LA English
DT Review
ID DE-NOVO MUTATIONS; GENOME-WIDE ASSOCIATION; AUTISM SPECTRUM DISORDERS;
CANCER SUSCEPTIBILITY; GENETIC-VARIATION; COMMON DISEASES; SEQUENCING
DATA; CROHNS-DISEASE; CONTRIBUTE; SCHIZOPHRENIA
AB The allelic architecture of complex traits is likely to be underpinned by a combination of multiple common frequency and rare variants. Targeted genotyping arrays and next-generation sequencing technologies at the whole-genome sequencing (WGS) and whole-exome scales (WES) are increasingly employed to access sequence variation across the full minor allele frequency (MAF) spectrum. Different study design strategies that make use of diverse technologies, imputation and sample selection approaches are an active target of development and evaluation efforts. Initial insights into the contribution of rare variants in common diseases and medically relevant quantitative traits point to low-frequency and rare alleles acting either independently or in aggregate and in several cases alongside common variants. Studies conducted in population isolates have been successful in detecting rare variant associations with complex phenotypes. Statistical methodologies that enable the joint analysis of rare variants across regions of the genome continue to evolve with current efforts focusing on incorporating information such as functional annotation, and on the meta-analysis of these burden tests. In addition, population stratification, defining genome-wide statistical significance thresholds and the design of appropriate replication experiments constitute important considerations for the powerful analysis and interpretation of rare variant association studies. Progress in addressing these emerging challenges and the accrual of sufficiently large data sets are poised to help the field of complex trait genetics enter a promising era of discovery.
C1 [Panoutsopoulou, Kalliope; Tachmazidou, Ioanna; Zeggini, Eleftheria] Wellcome Trust Sanger Inst, Hinxton, England.
RP Zeggini, E (reprint author), Wellcome Trust Sanger Inst, Morgan Bldg,Wellcome Trust Genome Campus, Cambridge CB10 1HH, England.
EM eleftheria@sanger.ac.uk
FU Wellcome Trust [098051]; Arthritis Research UK [19542]
FX K.P., I.T. and E.Z. are funded by the Wellcome Trust (098051). K.P. is
funded by Arthritis Research UK (19542). Funding to pay the Open Access
publication charges for this article was provided by The Wellcome Trust
(098051).
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NR 66
TC 18
Z9 18
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
EI 1460-2083
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 15
PY 2013
VL 22
SI 1
BP R16
EP R21
DI 10.1093/hmg/ddt376
PG 6
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 230LH
UT WOS:000325340500003
PM 23922232
ER
PT J
AU Abrams, DA
Uddin, LQ
Menon, V
AF Abrams, Daniel A.
Uddin, Lucina Q.
Menon, Vinod
TI Reply to Brock: Renewed focus on the voice and social reward in children
with autism
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Letter
C1 [Abrams, Daniel A.; Uddin, Lucina Q.; Menon, Vinod] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Palo Alto, CA 94304 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Program Neurosci, Palo Alto, CA 94304 USA.
[Menon, Vinod] Stanford Univ, Sch Med, Stanford Inst Neuroinnovat & Translat Neurosci, Palo Alto, CA 94304 USA.
RP Abrams, DA (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.
EM daa@stanford.edu; menon@stanford.edu
CR Abrams DA, 2013, P NATL ACAD SCI USA, V110, P12060, DOI 10.1073/pnas.1302982110
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NR 6
TC 0
Z9 0
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 15
PY 2013
VL 110
IS 42
BP E3974
EP E3974
DI 10.1073/pnas.1313455110
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 234HT
UT WOS:000325634200002
PM 24278966
ER
PT J
AU Brock, J
AF Brock, Jon
TI Connectivity and cognition in autism spectrum disorders: Where are the
links?
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Letter
C1 [Brock, Jon] Macquarie Univ, Dept Cognit Sci, Sydney, NSW 2109, Australia.
EM jon.brock@mq.edu.au
CR Abrams DA, 2013, P NATL ACAD SCI USA, V110, P12060, DOI 10.1073/pnas.1302982110
Pelphrey KA, 2011, J CHILD PSYCHOL PSYC, V52, P631, DOI 10.1111/j.1469-7610.2010.02349.x
NR 2
TC 1
Z9 1
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 15
PY 2013
VL 110
IS 42
BP E3973
EP E3973
DI 10.1073/pnas.1311907110
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 234HT
UT WOS:000325634200001
PM 24101453
ER
PT J
AU Raznahan, A
Wallace, GL
Antezana, L
Greenstein, D
Lenroot, R
Thurm, A
Gozzi, M
Spence, S
Martin, A
Swedo, SE
Giedd, JN
AF Raznahan, Armin
Wallace, Gregory L.
Antezana, Ligia
Greenstein, Dede
Lenroot, Rhoshel
Thurm, Audrey
Gozzi, Marta
Spence, Sarah
Martin, Alex
Swedo, Susan E.
Giedd, Jay N.
TI Compared to What? Early Brain Overgrowth in Autism and the Perils of
Population Norms
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Autism; bias; CDC; head circumference; systematic review; WHO
ID HEAD CIRCUMFERENCE GROWTH; PERVASIVE DEVELOPMENTAL DISORDERS; AGE 2
YEARS; SPECTRUM DISORDERS; 1ST YEAR; BIRTH COHORT; CHILDREN; LIFE;
INFANTS; SIZE
AB Background: Early brain overgrowth (EBO) in autism spectrum disorder (ASD) is among the best replicated biological associations in psychiatry. Most positive reports have compared head circumference (HC) in ASD (an excellent proxy for early brain size) with well-known reference norms. We sought to reappraise evidence for the EBO hypothesis given 1) the recent proliferation of longitudinal HC studies in ASD, and 2) emerging reports that several of the reference norms used to define EBO in ASD may be biased toward detecting HC overgrowth in contemporary samples of healthy children.
Methods: Systematic review of all published HC studies in children with ASD. Comparison of 330 longitudinally gathered HC measures between birth and 18 months from male children with autism (n = 35) and typically developing control subjects (n = 22).
Results: In systematic review, comparisons with locally recruited control subjects were significantly less likely to identify EBO in ASD than norm-based studies (p < .001). Through systematic review and analysis of new data, we replicate seminal reports of EBO in ASD relative to classical HC norms but show that this overgrowth relative to norms is mimicked by patterns of HC growth age in a large contemporary community-based sample of US children (n similar to 75,000). Controlling for known HC norm biases leaves inconsistent support for a subtle, later emerging and subgroup specific pattern of EBO in clinically ascertained ASD versus community control subjects.
Conclusions: The best-replicated aspects of EBO reflect generalizable HC norm biases rather than disease-specific biomarkers. The potential HC norm biases we detail are not specific to ASD research but apply throughout clinical and academic medicine.
C1 [Raznahan, Armin; Greenstein, Dede; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
[Wallace, Gregory L.; Antezana, Ligia; Martin, Alex] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
[Lenroot, Rhoshel] Univ New S Wales, Dept Psychiat, Sydney, NSW, Australia.
[Thurm, Audrey; Gozzi, Marta; Swedo, Susan E.] NIMH, Pediat Dev Neurosci Branch, NIH, Bethesda, MD 20892 USA.
[Spence, Sarah] Harvard Univ, Sch Med, Dept Neurol, Childrens Hosp Boston, Boston, MA 02115 USA.
RP Raznahan, A (reprint author), NIMH, NIH, Child Psychiat Branch, Room 4C108,Bldg 10,10 Ctr Dr, Bethesda, MD 20892 USA.
EM raznahana@mail.nih.gov
RI Giedd, Jay/B-7302-2012
OI Giedd, Jay/0000-0003-0827-3460
FU National Institutes of Health Intramural Research Program
FX Financial support for this work was provided by the National Institutes
of Health Intramural Research Program.
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NR 81
TC 22
Z9 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 15
PY 2013
VL 74
IS 8
BP 563
EP 575
DI 10.1016/j.biopsych.2013.03.022
PG 13
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 223OH
UT WOS:000324814900003
PM 23706681
ER
PT J
AU Chaste, P
Klei, L
Sanders, SJ
Murtha, MT
Hus, V
Lowe, JK
Willsey, AJ
Moreno-De-Luca, D
Yu, TW
Fombonne, E
Geschwind, D
Grice, DE
Ledbetter, DH
Lord, C
Mane, SM
Martin, CL
Martin, DM
Morrow, EM
Walsh, CA
Sutcliffe, JS
State, MW
Devlin, B
Cook, EH
Kim, SJ
AF Chaste, Pauline
Klei, Lambertus
Sanders, Stephan J.
Murtha, Michael T.
Hus, Vanessa
Lowe, Jennifer K.
Willsey, A. Jeremy
Moreno-De-Luca, Daniel
Yu, Timothy W.
Fombonne, Eric
Geschwind, Daniel
Grice, Dorothy E.
Ledbetter, David H.
Lord, Catherine
Mane, Shrikant M.
Martin, Christa Lese
Martin, Donna M.
Morrow, Eric M.
Walsh, Christopher A.
Sutcliffe, James S.
State, Matthew W.
Devlin, Bernie
Cook, Edwin H., Jr.
Kim, Soo-Jeong
TI Adjusting Head Circumference for Covariates in Autism: Clinical
Correlates of a Highly Heritable Continuous Trait
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE ASD; autism spectrum disorder; body metrics; genetic ancestry; head
circumference; IQ
ID SPECTRUM DISORDERS; BRAIN VOLUME; 1ST YEAR; CHILDREN; GROWTH; BIRTH;
AGE; SIZE; LIFE; ENLARGEMENT
AB Background: Brain development follows a different trajectory in children with autism spectrum disorders (ASD) than in typically developing children. A proxy for neurodevelopment could be head circumference (HC), but studies assessing HC and its clinical correlates in ASD have been inconsistent. This study investigates HC and clinical correlates in the Simons Simplex Collection cohort.
Methods: We used a mixed linear model to estimate effects of covariates and the deviation from the expected HC given parental HC (genetic deviation). After excluding individuals with incomplete data, 7225 individuals in 1891 families remained for analysis. We examined the relationship between HC/genetic deviation of HC and clinical parameters.
Results: Gender, age, height, weight, genetic ancestry, and ASD status were significant predictors of HC (estimate of the ASD effect = .2 cm). HC was approximately normally distributed in probands and unaffected relatives, with only a few outliers. Genetic deviation of HC was also normally distributed, consistent with a random sampling of parental genes. Whereas larger HC than expected was associated with ASD symptom severity and regression, IQ decreased with the absolute value of the genetic deviation of HC.
Conclusions: Measured against expected values derived from covariates of ASD subjects, statistical outliers for HC were uncommon. HC is a strongly heritable trait, and population norms for HC would be far more accurate if covariates including genetic ancestry, height, and age were taken into account. The association of diminishing IQ with absolute deviation from predicted HC values suggests HC could reflect subtle underlying brain development and warrants further investigation.
C1 [Chaste, Pauline; Klei, Lambertus; Devlin, Bernie] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
[Chaste, Pauline] FondaMental Fdn, Creteil, France.
[Sanders, Stephan J.; Murtha, Michael T.; Moreno-De-Luca, Daniel; State, Matthew W.] Yale Univ, Sch Med, Program Neurogenet, New Haven, CT USA.
[Sanders, Stephan J.; Willsey, A. Jeremy; State, Matthew W.] Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA.
[Sanders, Stephan J.; Moreno-De-Luca, Daniel; State, Matthew W.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
[Sanders, Stephan J.; Willsey, A. Jeremy; State, Matthew W.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
[Hus, Vanessa] Univ Michigan, Dept Psychol, Ann Arbor, MI USA.
[Lowe, Jennifer K.; Geschwind, Daniel] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Dept Neurol,Neurogenet Program, Los Angeles, CA 90095 USA.
[Lowe, Jennifer K.; Geschwind, Daniel] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Ctr Autism Res & Treatment, Los Angeles, CA 90095 USA.
[Yu, Timothy W.] Harvard Univ, Childrens Hosp, Sch Med, Div Genet, Boston, MA 02115 USA.
[Fombonne, Eric] Oregon Hlth & Sci Univ, Dept Psychiat, Portland, OR 97201 USA.
[Grice, Dorothy E.] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY USA.
[Grice, Dorothy E.] Icahn Sch Med Mt Sinai, Friedman Brain Inst, New York, NY USA.
[Ledbetter, David H.; Martin, Christa Lese] Geisinger Hlth Syst, Autism & Dev Med Inst, Danville, PA USA.
[Lord, Catherine] Weill Cornell Med Coll, Ctr Autism & Developing Brain, White Plains, NY USA.
[Mane, Shrikant M.] Yale Ctr Genome Anal, Orange, CT USA.
[Martin, Donna M.] Univ Michigan, Med Ctr, Dept Pediat, Ann Arbor, MI 48109 USA.
[Martin, Donna M.] Univ Michigan, Med Ctr, Dept Human Genet, Ann Arbor, MI 48109 USA.
[Morrow, Eric M.] Brown Univ, Mol Med Lab, Dept Mol Biol, Providence, RI 02912 USA.
[Morrow, Eric M.] Brown Univ, Mol Med Lab, Inst Brain Sci, Providence, RI 02912 USA.
[Morrow, Eric M.] Brown Univ, Sch Med, Emma Pendleton Bradley Hosp, Dev Disorders Genet Res Program, East Providence, RI USA.
[Morrow, Eric M.] Brown Univ, Sch Med, Dept Psychiat & Human Behav, East Providence, RI USA.
[Walsh, Christopher A.] Harvard Univ, Sch Med, Howard Hughes Med Inst, Childrens Hosp Boston, Boston, MA 02115 USA.
[Walsh, Christopher A.] Harvard Univ, Childrens Hosp, Sch Med, Div Genet, Boston, MA 02115 USA.
[Walsh, Christopher A.] Harvard Univ, Sch Med, Boston, MA USA.
[Sutcliffe, James S.] Vanderbilt Univ, Vanderbilt Brain Inst, Dept Mol Physiol & Biophys, Nashville, TN 37235 USA.
[Sutcliffe, James S.] Vanderbilt Univ, Vanderbilt Brain Inst, Dept Psychiat, Nashville, TN 37235 USA.
[State, Matthew W.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Cook, Edwin H., Jr.] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA.
[Kim, Soo-Jeong] Univ Washington, Seattle Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA 98195 USA.
[Kim, Soo-Jeong] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
RP Kim, SJ (reprint author), Seattle Childrens Res Inst, Ctr Integrat Brain Res, 1900 9th Ave, Seattle, WA 98101 USA.
EM kimsooj@uw.edu
RI Sutcliffe, James/C-1348-2012
OI Sutcliffe, James/0000-0001-5200-6007
FU Simons Foundation [SFARI 124827]; National Institutes of Health (NIH)
[K23MH082883, NIH R01HD065272, NIH R01MH089390]; Fondamental Foundation
FX We are grateful to all of the families at the participating Simons
Simplex Collection (SSC) sites, as well as the principal investigators
(A. Beaudet, R. Bernier, J. Constantino, E. Cook, E. Fombonne, D.
Geschwind, R. Goin-Kochel, E. Hanson, D. Grice, A. Klin, D. Ledbetter,
C. Lord, C. Martin, D. Martin, R. Maxim, J. Miles, O. Ousley, K.
Pelphrey, B. Peterson, J. Piggot, C. Saulnier, M. State, W. Stone, J.
Sutcliffe, C. Walsh, Z. Warren, E. Wijsman). We appreciate obtaining
access to phenotypic data on the Simons Foundation Autism Research
Initiative (SFARI) Base. Approved researchers can obtain the SSC
population data set described in this study
(http://sfari.org/resources/sfari-base) by applying at
https://base.sfari.org. This work was supported by a grant from the
Simons Foundation (Grant No. SFARI 124827 to the investigators of the
SSC Genetic Consortium), National Institutes of Health (NIH; Grant No.
K23MH082883 (SJK), NIH R01HD065272 (CL), NIH R01MH089390 (CL), and
Fondamental Foundation (PC).
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NR 58
TC 14
Z9 14
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 15
PY 2013
VL 74
IS 8
BP 576
EP 584
DI 10.1016/j.biopsych.2013.04.018
PG 9
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 223OH
UT WOS:000324814900004
PM 23746936
ER
PT J
AU Arns, M
van der Heijden, KB
Arnold, LE
Kenemans, JL
AF Arns, Martijn
van der Heijden, Kristiaan B.
Arnold, L. Eugene
Kenemans, J. Leon
TI Geographic Variation in the Prevalence of
Attention-Deficit/Hyperactivity Disorder: The Sunny Perspective
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE ADHD; chronobiological; circadian; light; prevalence; solar intensity
ID DEFICIT HYPERACTIVITY DISORDER; SLEEP ONSET INSOMNIA; SUBSEQUENT
RECOVERY; LIGHT THERAPY; INTERNET USE; CHILDREN; ADHD; RESTRICTION;
PERFORMANCE; ADULTS
AB Background: Attention-deficit/hyperactivity disorder (ADHD) is the most common psychiatric disorder of childhood, with average worldwide prevalence of 5.3%, varying by region.
Methods: We assessed the relationship between the prevalence of ADHD and solar intensity (SI) (kilowatt hours/square meters/day) on the basis of multinational and cross-state studies. Prevalence data for the U.S. were based on self-report of professional diagnoses; prevalence data for the other countries were based on diagnostic assessment. The SI data were obtained from national institutes.
Results: In three datasets (across 49 U.S. states for 2003 and 2007, and across 9 non-U.S. countries) a relationship between SI and the prevalence of ADHD was found, explaining 34%-57% of the variance in ADHD prevalence, with high SI having an apparent preventative effect. Controlling for low birth weight, infant mortality, average income (socioeconomic status), latitude, and other relevant factors did not change these findings. Furthermore, these findings were specific to ADHD, not found for the prevalence of autism spectrum disorders or major depressive disorder.
Conclusions: In this study we found a lower prevalence of ADHD in areas with high SI for both U.S. and non-U.S. data. This association has not been reported before in the literature. The preventative effect of high SI might be related to an improvement of circadian clock disturbances, which have recently been associated with ADHD. These findings likely apply to a substantial subgroup of ADHD patients and have major implications in our understanding of the etiology and possibly prevention of ADHD by medical professionals, schools, parents, and manufacturers of mobile devices.
C1 [Arns, Martijn; Kenemans, J. Leon] Univ Utrecht, Dept Expt Psychol, Utrecht, Netherlands.
[Arns, Martijn] Res Inst Brainclin, NL-6524 AD Nijmegen, Netherlands.
[van der Heijden, Kristiaan B.] Leiden Univ, Dept Clin Child & Adolescent Studies, Leiden Inst Brain & Cognit, Leiden, Netherlands.
[Arnold, L. Eugene] Ohio State Univ, Columbus, OH 43210 USA.
RP Arns, M (reprint author), Res Inst Brainclin, Dept Expt Psychol, Bijleveldsingel 34, NL-6524 AD Nijmegen, Netherlands.
EM martijn@brainclinics.com
FU AstraZeneca; Biomarin; CureMark; Lilly; Novartis; Noven; Seaside
Therapeutics; Shire
FX LEA has received research funding (to the university) or advisory board
honoraria from AstraZeneca, Biomarin, CureMark, Lilly, Novartis, Noven,
Seaside Therapeutics, and Shire and travel support from Noven.
CR Arns M., 2012, NEUROSCI BIOBEHAV RE
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NR 39
TC 11
Z9 11
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 15
PY 2013
VL 74
IS 8
BP 585
EP 590
DI 10.1016/j.biopsych.2013.02.010
PG 6
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 223OH
UT WOS:000324814900005
PM 23523340
ER
PT J
AU Di Martino, A
Zuo, XN
Kelly, C
Grzadzinski, R
Mennes, M
Schvarcz, A
Rodman, J
Lord, C
Castellanos, FX
Milham, MP
AF Di Martino, Adriana
Zuo, Xi-Nian
Kelly, Clare
Grzadzinski, Rebecca
Mennes, Maarten
Schvarcz, Ariel
Rodman, Jennifer
Lord, Catherine
Castellanos, F. Xavier
Milham, Michael P.
TI Shared and Distinct Intrinsic Functional Network Centrality in Autism
and Attention-Deficit/Hyperactivity Disorder
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE ADHD; amygdala; autism; caudate; functional connectivity; network
centrality; precuneus; resting state fMRI
ID RESTING-STATE FMRI; PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT
HYPERACTIVITY DISORDER; DEFAULT-MODE NETWORK; SPECTRUM DISORDERS;
CONNECTIVITY MRI; HUMAN BRAIN; PSYCHIATRIC-DISORDERS; DIAGNOSTIC
INTERVIEW; YOUNG-CHILDREN
AB Background: Individuals with autism spectrum disorders (ASD) often exhibit symptoms of attention-deficit/hyperactivity disorder (ADHD). Across both disorders, observations of distributed functional abnormalities suggest aberrant large-scale brain network connectivity. Yet, common and distinct network correlates of ASD and ADHD remain unidentified. Here, we aimed to examine patterns of dysconnection in school-age children with ASD and ADHD and typically developing children who completed a resting state functional magnetic resonance imaging scan.
Methods: We measured voxelwise network centrality, functional connectivity metrics indexing local (degree centrality [DC]) and global (eigenvector centrality) functional relationships across the entire brain connectome, in resting state functional magnetic resonance imaging data from 56 children with ASD, 45 children with ADHD, and 50 typically developing children. A one-way analysis of covariance, with group as fixed factor (whole-brain corrected), was followed by post hoc pairwise comparisons.
Results: Cortical and subcortical areas exhibited centrality abnormalities, some common to both ADHD and ASD, such as in precuneus. Others were disorder-specific and included ADHD-related increases in DC in right striatum/pallidum, in contrast with ASD-related increases in bilateral temporolimbic areas. Secondary analyses differentiating children with ASD into those with or without ADHD-like comorbidity (ASD(+) and ASD(-), respectively) revealed that the ASD(+) group shared ADHD-specific abnormalities in basal ganglia. By contrast, centrality increases in temporolimbic areas characterized children with ASD regardless of ADHD-like comorbidity. At the cluster level, eigenvector centrality group patterns were similar to DC.
Conclusions: ADHD and ASD are neurodevelopmental disorders with distinct and overlapping clinical presentations. This work provides evidence for both shared and distinct underlying mechanisms at the large-scale network level.
C1 [Di Martino, Adriana; Kelly, Clare; Grzadzinski, Rebecca; Mennes, Maarten; Schvarcz, Ariel; Castellanos, F. Xavier] Langone Med Ctr, Inst Pediat Neurosci, Ctr Child Study, New York, NY USA.
[Zuo, Xi-Nian] Chinese Acad Sci, Key Lab Behav Sci, Inst Psychol, Lab Funct Connectome & Dev, Beijing, Peoples R China.
[Castellanos, F. Xavier] Chinese Acad Sci, Inst Psychol, Beijing 100101, Peoples R China.
[Schvarcz, Ariel] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA USA.
[Grzadzinski, Rebecca; Lord, Catherine] Weill Cornell Med Coll, Ctr Autism & Developing Brain, New York, NY USA.
[Castellanos, F. Xavier; Milham, Michael P.] Nathan S Kline Inst Psychiat Res, Orangeburg, NY USA.
[Milham, Michael P.] Child Mind Inst, Ctr Developing Brain, New York, NY USA.
RP Milham, MP (reprint author), Child Mind Inst, Ctr Developing Brain, 445 Pk Ave, New York, NY 10022 USA.
EM michael.milham@childmind.org
RI Mennes, Maarten/C-9924-2011; Milham, Michael/K-9501-2014; Di Martino,
Adriana/L-2497-2014
OI Mennes, Maarten/0000-0002-7279-3439;
FU Brain & Behavior Research Foundation; National Institute of Mental
Health [K23MH087770, R01MH081218]; National Institute of Child Health
and Human Development [R01HD065282]; Autism Speaks; Stavros Niarchos
Foundation; Leon Levy Foundation; Natural Science Foundation of China
[81171409, 81220108014]; Chinese Academy of Sciences [KSZD-EW-TZ-002,
Y0CX492S03, Y2CX112006]
FX This work was supported by grants from the Brain & Behavior Research
Foundation (previously known as National Alliance for Research in
Schizophrenia and Affective Disorders) to ADM and National Institute of
Mental Health (K23MH087770 to ADM; R01MH081218 to FXC); from the
National Institute of Child Health and Human Development (R01HD065282),
Autism Speaks, and the Stavros Niarchos Foundation, awarded to FXC; the
Leon Levy Foundation awarded to MPM, ADM, and CK; the Natural Science
Foundation of China (81171409, 81220108014) and the Chinese Academy of
Sciences (KSZD-EW-TZ-002, Y0CX492S03, Y2CX112006) to X-NZ; and gifts
from Joseph P. Healey and the Stavros Niarchos Foundation to the Child
Mind Institute (MPM).
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NR 106
TC 24
Z9 24
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0006-3223
J9 BIOL PSYCHIAT
JI Biol. Psychiatry
PD OCT 15
PY 2013
VL 74
IS 8
BP 623
EP 632
DI 10.1016/j.biopsych.2013.02.011
PG 10
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 223OH
UT WOS:000324814900010
PM 23541632
ER
PT J
AU Sarachana, T
Hu, VW
AF Sarachana, Tewarit
Hu, Valerie W.
TI Differential recruitment of coregulators to the RORA promoter adds
another layer of complexity to gene (dys) regulation by sex hormones in
autism
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism; RORA; Sex hormones; Nuclear receptor; Coregulator; Coactivator;
Corepressor
ID ESTROGEN-RECEPTOR-ALPHA; STAGGERER MUTANT MICE; SPECTRUM DISORDERS;
FETAL TESTOSTERONE; ANDROGEN RECEPTOR; NUCLEAR RECEPTORS; SIGNALING
ATLAS; DSM-IV; BRAIN; BETA
AB Background: Our independent cohort studies have consistently shown the reduction of the nuclear receptor RORA (retinoic acid-related orphan receptor-alpha) in lymphoblasts as well as in brain tissues from individuals with autism spectrum disorder (ASD). Moreover, we have found that RORA regulates the gene for aromatase, which converts androgen to estrogen, and that male and female hormones regulate RORA in opposite directions, with androgen suppressing RORA, suggesting that the sexually dimorphic regulation of RORA may contribute to the male bias in ASD. However, the molecular mechanisms through which androgen and estrogen differentially regulate RORA are still unknown.
Methods: Here we use functional knockdown of hormone receptors and coregulators with small interfering RNA (siRNA) to investigate their involvement in sex hormone regulation of RORA in human neuronal cells. Luciferase assays using a vector containing various RORA promoter constructs were first performed to identify the promoter regions required for inverse regulation of RORA by male and female hormones. Sequential chromatin immunoprecipitation methods followed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) analyses of RORA expression in hormone-treated SH-SY5Y cells were then utilized to identify coregulators that associate with hormone receptors on the RORA promoter. siRNA-mediated knockdown of interacting coregulators was performed followed by qRT-PCR analyses to confirm the functional requirement of each coregulator in hormone-regulated RORA expression.
Results: Our studies demonstrate the direct involvement of androgen receptor (AR) and estrogen receptor (ER) in the regulation of RORA by male and female hormones, respectively, and that the promoter region between -10055 bp and -2344 bp from the transcription start site of RORA is required for the inverse hormonal regulation. We further show that AR interacts with SUMO1, a reported suppressor of AR transcriptional activity, whereas ER alpha interacts with the coactivator NCOA5 on the RORA promoter. siRNA-mediated knockdown of SUMO1 and NCOA5 attenuate the sex hormone effects on RORA expression.
Conclusions: AR and SUMO1 are involved in the suppression RORA expression by androgen, while ER alpha and NCOA5 collaborate in the up-regulation of RORA by estrogen. While this study offers a better understanding of molecular mechanisms involved in sex hormone regulation of RORA, it also reveals another layer of complexity with regard to gene regulation in ASD. Inasmuch as coregulators are capable of interacting with a multitude of transcription factors, aberrant expression of coregulator proteins, as we have seen previously in lymphoblasts from individuals with ASD, may contribute to the polygenic nature of gene dysregulation in ASD.
C1 [Sarachana, Tewarit; Hu, Valerie W.] George Washington Univ, Dept Biochem & Mol Med, Sch Med & Hlth Sci, Washington, DC 20037 USA.
[Sarachana, Tewarit] Chulalongkorn Univ, Fac Allied Hlth Sci, Dept Clin Chem, Bangkok 10330, Thailand.
RP Hu, VW (reprint author), George Washington Univ, Dept Biochem & Mol Med, Sch Med & Hlth Sci, 2300 1 St NW, Washington, DC 20037 USA.
EM valhu@gwu.edu
RI nakham, kwanphat/F-4661-2014
FU Simons Foundation [221192]; George Washington University; Office of the
Commission on Higher Education of the Royal Thai Government, Thailand,
through the Faculty of Allied Health Sciences, Chulalongkorn University
FX We wish to thank Mr. Bren Belovarac for his assistance with the qRT-PCR
analysis of siAR- and siER alpha-transfected cells. This study was
supported in part by a generous gift from the LIFE Foundation (Aspen,
CO, USA), a Simons Foundation grant number 221192 (VWH), and an
intramural grant from The George Washington University (Medical Faculty
Associates award). We also thank Turner Biosystems (now Promega,
Madison, WI, USA) for the gift of the Veritas microplate luminometer to
VWH for her research on autism. None of the funding sources played any
role in the study design, collection, analysis, and interpretation of
data, writing of the manuscript, or decision to submit this study for
publication. TS was a predoctoral student in the Institute for
Biomedical Sciences at the George Washington University, who was
supported by the Higher Educational Strategic Scholarship for Frontier
Research Network (SFR scholarship) from the Office of the Commission on
Higher Education of the Royal Thai Government, Thailand, through the
Faculty of Allied Health Sciences, Chulalongkorn University.
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NR 69
TC 4
Z9 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD OCT 11
PY 2013
VL 4
AR 39
DI 10.1186/2040-2392-4-39
PG 16
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254YK
UT WOS:000327205800001
PM 24119295
ER
PT J
AU Jones, RM
Cadby, G
Melton, PE
Abraham, LJ
Whitehouse, AJ
Moses, EK
AF Jones, Rachel Maree
Cadby, Gemma
Melton, Phillip E.
Abraham, Lawrence J.
Whitehouse, Andrew J.
Moses, Eric K.
TI Genome-wide association study of autistic-like traits in a general
population study of young adults
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE autistic-like traits; genome-wide association; PRKCB1; autism spectrum
disorder; autism spectrum quotient; CBLN1
ID SPECTRUM QUOTIENT AQ; COPY NUMBER VARIANTS; TOURETTE-SYNDROME;
DISORDERS; PREVALENCE; BEHAVIORS; PHENOTYPE; CHILDREN; NEUREXIN; EMPATHY
AB It has been proposed that autistic-like traits in the general population lie on a continuum, with clinical Autism Spectrum Disorder (ASD), representing the extreme end of this distribution. The current study undertook a genome-wide association (GWA) scan of 965 young Western Australian adults to identify novel risk variants associated with autistic-like traits. No associations reached genome-wide significance; however, a review of nominally associated single nucleotide polymorphisms (SNPs) indicated two positional candidate loci that have been previously implicated in autistic-like trait etiology.
Research has proposed that autistic-like traits in the general population lie on a continuum, with clinical ASD representing the extreme end of this distribution. Inherent in this proposal is that biological mechanisms associated with clinical ASD may also underpin variation in autistic-like traits within the general population. A GWA study using 2,462,046 SNPs was undertaken for ASD in 965 individuals from the Western Australian Pregnancy Cohort (Raine) Study. No SNP associations reached genome-wide significance (p < 5.0 x 10-8). However, investigations into nominal observed SNP associations (p < 1.0 x 10-5) add support to two positional candidate genes previously implicated in ASD etiology, PRKCB1, and CBLN1. The rs198198 SNP (p = 9.587 x 10-6), is located within an intron of the protein kinase C, beta 1 (PRKCB1) gene on chromosome 16p11. The PRKCB1 gene has been previously reported in linkage and association studies for ASD, and its mRNA expression has been shown to be significantly down regulated in ASD cases compared with controls. The rs16946931 SNP (p = 1.78 x 10-6) is located in a region flanking the Cerebellin 1 (CBLN1) gene on chromosome 16q12.1. The CBLN1 gene is involved with synaptogenesis and is part of a gene family previously implicated in ASD. This GWA study is only the second to examine SNPs associated with autistic-like traits in the general population, and provides evidence to support roles for the PRKCB1 and CBLN1 genes in risk of clinical ASD.
C1 [Jones, Rachel Maree; Cadby, Gemma; Melton, Phillip E.; Abraham, Lawrence J.; Moses, Eric K.] Univ Western Australia, Ctr Genet Origins Hlth & Dis, Perth, WA 6009, Australia.
[Abraham, Lawrence J.] Univ Western Australia, Sch Chem & Biochem, Perth, WA 6009, Australia.
[Whitehouse, Andrew J.] Telethon Inst Child Hlth Res, Perth, WA, Australia.
RP Moses, EK (reprint author), Univ Western Australia, Ctr Genet Origins Hlth & Dis, 35 Stirling Highway, Perth, WA 6009, Australia.
EM eric.moses@uwa.edu.au
RI Melton, Phillip/A-5012-2013
OI Melton, Phillip/0000-0003-4026-2964
FU National Health and Medical Research Council [572613]
FX Grant sponsor: National Health and Medical Research Council; Grant
number: 572613.
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NR 54
TC 6
Z9 6
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 11
PY 2013
VL 7
AR 658
DI 10.3389/fnhum.2013.00658
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 232XE
UT WOS:000325527000001
PM 24133439
ER
PT J
AU Schmidt, C
AF Schmidt, Charles
TI PSYCHIATRIC RESEARCH Severe Autism, Often Slighted, Now Targeted for
Study
SO SCIENCE
LA English
DT News Item
NR 0
TC 0
Z9 0
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 0036-8075
J9 SCIENCE
JI Science
PD OCT 11
PY 2013
VL 342
IS 6155
BP 179
EP 179
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 232EV
UT WOS:000325475200015
PM 24115416
ER
PT J
AU De Angelis, M
Piccolo, M
Vannini, L
Siragusa, S
De Giacomo, A
Serrazzanetti, DI
Cristofori, F
Guerzoni, ME
Gobbetti, M
Francavilla, R
AF De Angelis, Maria
Piccolo, Maria
Vannini, Lucia
Siragusa, Sonya
De Giacomo, Andrea
Serrazzanetti, Diana Isabella
Cristofori, Fernanda
Guerzoni, Maria Elisabetta
Gobbetti, Marco
Francavilla, Ruggiero
TI Fecal Microbiota and Metabolome of Children with Autism and Pervasive
Developmental Disorder Not Otherwise Specified
SO PLOS ONE
LA English
DT Article
ID HUMAN INTESTINAL BACTERIA; GUT MICROBIOTA; SPECTRUM DISORDERS;
REGRESSIVE AUTISM; ONSET AUTISM; BEHAVIOR; DISEASE; HEALTH; MODEL; FLORA
AB This study aimed at investigating the fecal microbiota and metabolome of children with Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and autism (AD) in comparison to healthy children (HC). Bacterial tag-encoded FLX-titanium amplicon pyrosequencing (bTEFAP) of the 16S rDNA and 16S rRNA analyses were carried out to determine total bacteria (16S rDNA) and metabolically active bacteria (16S rRNA), respectively. The main bacterial phyla (Firmicutes, Bacteroidetes, Fusobacteria and Verrucomicrobia) significantly (P<0.05) changed among the three groups of children. As estimated by rarefaction, Chao and Shannon diversity index, the highest microbial diversity was found in AD children. Based on 16S-rRNA and culture-dependent data, Faecalibacterium and Ruminococcus were present at the highest level in fecal samples of PDD-NOS and HC children. Caloramator, Sarcina and Clostridium genera were the highest in AD children. Compared to HC, the composition of Lachnospiraceae family also differed in PDD-NOS and, especially, AD children. Except for Eubacterium siraeum, the lowest level of Eubacteriaceae was found on fecal samples of AD children. The level of Bacteroidetes genera and some Alistipes and Akkermansia species were almost the highest in PDD-NOS or AD children as well as almost all the identified Sutterellaceae and Enterobacteriaceae were the highest in AD. Compared to HC children, Bifidobacterium species decreased in AD. As shown by Canonical Discriminant Analysis of Principal Coordinates, the levels of free amino acids and volatile organic compounds of fecal samples were markedly affected in PDD-NOS and, especially, AD children. If the gut microbiota differences among AD and PDD-NOS and HC children are one of the concomitant causes or the consequence of autism, they may have implications regarding specific diagnostic test, and/or for treatment and prevention.
C1 [De Angelis, Maria; Piccolo, Maria; Siragusa, Sonya; Gobbetti, Marco] Univ Bari Aldo Moro, Dept Soil Plant & Food Sci, Bari, Italy.
[Vannini, Lucia; Serrazzanetti, Diana Isabella] Univ Cesena, Interdept Ctr Ind Agri Food Res, Cesena, Italy.
[Vannini, Lucia; Guerzoni, Maria Elisabetta] Univ Bologna, Dept Agr & Food Sci, Bologna, Italy.
[De Giacomo, Andrea] Univ Bari Aldo Moro, Child Neurol & Psychiat Unit, Dept Neurol & Psychiat Sci, Bari, Italy.
[Cristofori, Fernanda; Francavilla, Ruggiero] Univ Bari Aldo Moro, Dept Interdisciplinary Med, Bari, Italy.
RP De Angelis, M (reprint author), Univ Bari Aldo Moro, Dept Soil Plant & Food Sci, Bari, Italy.
EM maria.deangelis@uniba.it
FU Department of Soil, Plant and Food Science
FX The work was funded by the Department of Soil, Plant and Food Science.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.
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NR 77
TC 20
Z9 20
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 9
PY 2013
VL 8
IS 10
AR e76993
DI 10.1371/journal.pone.0076993
PG 18
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 236PJ
UT WOS:000325810900114
PM 24130822
ER
PT J
AU Lieblein-Boff, JC
Mckim, DB
Shea, DT
Wei, P
Deng, Z
Sawicki, C
Quan, N
Bilbo, SD
Bailey, MT
McTigue, DM
Godbout, JP
AF Lieblein-Boff, Jacqueline C.
Mckim, Daniel B.
Shea, Daniel T.
Wei, Ping
Deng, Zhen
Sawicki, Caroline
Quan, Ning
Bilbo, Staci D.
Bailey, Michael T.
McTigue, Dana M.
Godbout, Jonathan P.
TI Neonatal E. Coli Infection Causes Neuro-Behavioral Deficits Associated
with Hypomyelination and Neuronal Sequestration of Iron
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID CENTRAL-NERVOUS-SYSTEM; REGULATORY HORMONE HEPCIDIN; B STREPTOCOCCAL
MENINGITIS; AUTISM SPECTRUM DISORDERS; EARLY-LIFE INFECTION;
WHITE-MATTER; RAT-BRAIN; MATERNAL SEPARATION; MEMORY IMPAIRMENT;
ESCHERICHIA-COLI
AB Recent evidence indicates that inflammatory insults in neonates significantly influenced white matter development and caused behavioral deficits that manifest in young adulthood. The mechanisms underlying these developmental and behavioral complications, however, are not well understood. We hypothesize that acute brain inflammation caused by neonatal infection reduces the bioavailability of iron required for oligodendrocyte maturation and white matter development. Here, we confirm that peripheral Escherichia coli infection in neonates at postnatal day 3 (P3) caused acute brain inflammation that was resolved within 72 h. Nonetheless, transient early life infection (ELI) profoundly influenced behavior, white matter development, and iron homeostasis in the brain. For instance, mice exposed to E. coli as neonates had increased locomotor activity and impaired motor coordination as juveniles (P35) and young adults (P60). In addition, these behavioral deficits were associated with marked hypomyelination and a reduction of oligodendrocytes in subcortical white matter and motor cortex. Moreover, ELI altered transcripts related to cellular sequestration of iron in the brain including hepcidin, ferroportin, and L-ferritin. For example, ELI increased hepcidin mRNA and decreased ferroportin mRNA and protein in the brain at P4, which preceded increased L-ferritin mRNA at P12. Consistent with the mRNA results, L-ferritin protein was robustly increased at P12 specifically in neurons of E. coli infected mice. We interpret these data to indicate that neonatal infection causes significant neuronal sequestration of iron at a time point before myelination. Together, these data indicate a possible role for aberrant neuronal iron storage in neonatal infection-induced disturbances in myelination and behavior.
C1 [Lieblein-Boff, Jacqueline C.; Mckim, Daniel B.; Wei, Ping; Deng, Zhen; Sawicki, Caroline; McTigue, Dana M.; Godbout, Jonathan P.] Ohio State Univ, Dept Neurosci, Columbus, OH 43210 USA.
[Mckim, Daniel B.; Shea, Daniel T.; Sawicki, Caroline; Quan, Ning; Bailey, Michael T.] Ohio State Univ, Div Oral Biol, Columbus, OH 43210 USA.
[Quan, Ning; Bailey, Michael T.; Godbout, Jonathan P.] Ohio State Univ, Inst Behav Med Res, Columbus, OH 43210 USA.
[McTigue, Dana M.; Godbout, Jonathan P.] Ohio State Univ, Ctr Brain & Spinal Cord Repair, Columbus, OH 43210 USA.
[Lieblein-Boff, Jacqueline C.] Abbott Nutr, Columbus, OH 43219 USA.
[Bilbo, Staci D.] Duke Univ, Dept Psychol & Neurosci, Durham, NC 27708 USA.
RP Godbout, JP (reprint author), 259 IBMR Bldg,460 Med Ctr Dr, Columbus, OH 43210 USA.
EM Jonathan.Godbout@osumc.edu
FU Abbott Nutrition Contract [ANUS1011]; NIH [R01-AG-033028]; Abbott
Nutrition
FX This work was supported by an Abbott Nutrition Contract (ANUS1011) and
NIH Grant R01-AG-033028 to J.P.G. We thank Todd Lash for his technical
assistance on this project.J.C. Lieblein-Boff is employed by Abbott
Nutrition. J.P. Godbout received funding from Abbott Nutrition in
support of this work.
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NR 58
TC 6
Z9 6
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 9
PY 2013
VL 33
IS 41
BP 16334
EP 16345
DI 10.1523/JNEUROSCI.0708-13.2013
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 234LE
UT WOS:000325644800027
PM 24107964
ER
PT J
AU Delattre, V
La Mendola, D
Meystre, J
Markram, H
Markram, K
AF Delattre, V.
La Mendola, D.
Meystre, J.
Markram, H.
Markram, K.
TI Nlgn4 knockout induces network hypo-excitability in juvenile mouse
somatosensory cortex in vitro
SO SCIENTIFIC REPORTS
LA English
DT Article
ID CELL-ADHESION MOLECULE; INHIBITORY SYNAPSES; PRENATAL EXPOSURE; NMDA
RECEPTOR; VALPROIC ACID; AUTISM; NEUROLIGINS; MICE; MATURATION;
PLASTICITY
AB Neuroligins (Nlgns) are postsynaptic cell adhesion molecules that form transynaptic complexes with presynaptic neurexins and regulate synapse maturation and plasticity. We studied the impact of the loss of Nlgn4 on the excitatory and inhibitory circuits in somatosensory cortical slices of juvenile mice by electrically stimulating these circuits using a multi-electrode array and recording the synaptic input to single neurons using the patch-clamp technique. We detected a decreased network response to stimulation in both excitatory and inhibitory circuits of Nlgn4 knock-out animals as compared to wild-type controls, and a decreased excitation-inhibition ratio. These data indicate that Nlgn4 is involved in the regulation of excitatory and inhibitory circuits and contributes to a balanced circuit response to stimulation.
C1 [Delattre, V.; La Mendola, D.; Meystre, J.; Markram, H.; Markram, K.] Ecole Polytech Fed Lausanne, Brain Mind Inst, Lab Neural Microcircuitry, CH-1015 Lausanne, Switzerland.
RP Markram, K (reprint author), Ecole Polytech Fed Lausanne, Brain Mind Inst, Lab Neural Microcircuitry, CH-1015 Lausanne, Switzerland.
EM kamila.markram@epfl.ch
FU EPFL; Asterion Foundation
FX We would like to thank N. Brose, O. Hagens, M. Telefont, M. Pezzoli and
S. Muralidhar for comments and helpful discussions. This work was
supported by the EPFL and Asterion Foundation.
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NR 35
TC 1
Z9 1
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 2045-2322
J9 SCI REP-UK
JI Sci Rep
PD OCT 9
PY 2013
VL 3
AR 2897
DI 10.1038/srep02897
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 231EM
UT WOS:000325396800002
PM 24104404
ER
PT J
AU Rose'Meyer, R
AF Rose'Meyer, Roselyn
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development of autism spectrum disorders
SO MOLECULAR AUTISM
LA English
DT Review
DE Autism spectrum disorder; Cortisol; Serotonin; SERT
ID GESTATIONAL-DIABETES-MELLITUS; 11-BETA-HYDROXYSTEROID DEHYDROGENASE
TYPE-1; CORTICOTROPIN-RELEASING HORMONE; BETA-HYDROXYSTEROID
DEHYDROGENASE; ACTIVATED PROTEIN-KINASE; PITUITARY-ADRENAL AXIS;
GLUCOCORTICOID-RESPONSIVE ELEMENTS; CORTICOSTEROID-BINDING GLOBULIN;
IRRITABLE-BOWEL-SYNDROME; RISK-FACTORS
AB The diagnosis of autism spectrum disorder (ASD) during early childhood has a profound effect not only on young children but on their families. Aside from the physical and behavioural issues that need to be dealt with, there are significant emotional and financial costs associated with living with someone diagnosed with ASD. Understanding how autism occurs will assist in preparing families to deal with ASD, if not preventing or lessening its occurrence. Serotonin plays a vital role in the development of the brain during the prenatal and postnatal periods, yet very little is known about the serotonergic systems that affect children with ASD. This review seeks to provide an understanding of the biochemistry and physiological actions of serotonin and its termination of action through the serotonin reuptake transporter (SERT). Epidemiological studies investigating prenatal conditions that can increase the risk of ASD describe a number of factors which elevate plasma cortisol levels causing such symptoms during pregnancy such as hypertension, gestational diabetes and depression. Because cortisol plays an important role in driving dysregulation of serotonergic signalling through elevating SERT production in the developing brain, it is also necessary to investigate the physiological functions of cortisol, its action during gestation and metabolic syndromes.
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RP Rose'Meyer, R (reprint author), Griffith Univ, Sch Med Sci, Gold Coast Campus,Parklands Dr, Southport, Qld 4222, Australia.
EM r.rosemeyer@griffith.edu.au
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NR 259
TC 1
Z9 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD OCT 8
PY 2013
VL 4
AR 37
DI 10.1186/2040-2392-4-37
PG 16
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254YJ
UT WOS:000327205700001
PM 24103554
ER
PT J
AU Yoshimura, Y
Kikuchi, M
Shitamichi, K
Ueno, S
Munesue, T
Ono, Y
Tsubokawa, T
Haruta, Y
Oi, M
Niida, Y
Remijn, GB
Takahashi, T
Suzuki, M
Higashida, H
Minabe, Y
AF Yoshimura, Yuko
Kikuchi, Mitsuru
Shitamichi, Kiyomi
Ueno, Sanae
Munesue, Toshio
Ono, Yasuki
Tsubokawa, Tsunehisa
Haruta, Yasuhiro
Oi, Manabu
Niida, Yo
Remijn, Gerard B.
Takahashi, Tsutomu
Suzuki, Michio
Higashida, Haruhiro
Minabe, Yoshio
TI Atypical brain lateralisation in the auditory cortex and language
performance in 3-to 7-year-old children with high-functioning autism
spectrum disorder: a child-customised magnetoencephalography (MEG) study
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism spectrum disorder (ASD); Laterality index; Magnetoencephalography
(MEG); P50m; Young children
ID 2-TO 5-YEAR-OLD CHILDREN; HUMAN CEREBRAL-CORTEX; EVOKED FIELDS;
DEVELOPMENTAL-CHANGES; MAGNETIC-FIELDS; YOUNG-CHILDREN; SPEECH;
IMPAIRMENT; MATURATION; RESPONSES
AB Background: Magnetoencephalography (MEG) is used to measure the auditory evoked magnetic field (AEF), which reflects language-related performance. In young children, however, the simultaneous quantification of the bilateral auditory-evoked response during binaural hearing is difficult using conventional adult-sized MEG systems. Recently, a child-customised MEG device has facilitated the acquisition of bi-hemispheric recordings, even in young children. Using the child-customised MEG device, we previously reported that language-related performance was reflected in the strength of the early component (P50m) of the auditory evoked magnetic field (AEF) in typically developing (TD) young children (2 to 5 years old) [Eur J Neurosci 2012, 35:644-650]. The aim of this study was to investigate how this neurophysiological index in each hemisphere is correlated with language performance in autism spectrum disorder (ASD) and TD children.
Methods: We used magnetoencephalography (MEG) to measure the auditory evoked magnetic field (AEF), which reflects language-related performance. We investigated the P50m that is evoked by voice stimuli (/ne/) bilaterally in 33 young children (3 to 7 years old) with ASD and in 30 young children who were typically developing (TD). The children were matched according to their age (in months) and gender. Most of the children with ASD were high-functioning subjects.
Results: The results showed that the children with ASD exhibited significantly less leftward lateralisation in their P50m intensity compared with the TD children. Furthermore, the results of a multiple regression analysis indicated that a shorter P50m latency in both hemispheres was specifically correlated with higher language-related performance in the TD children, whereas this latency was not correlated with non-verbal cognitive performance or chronological age. The children with ASD did not show any correlation between P50m latency and language-related performance; instead, increasing chronological age was a significant predictor of shorter P50m latency in the right hemisphere.
Conclusions: Using a child-customised MEG device, we studied the P50m component that was evoked through binaural human voice stimuli in young ASD and TD children to examine differences in auditory cortex function that are associated with language development. Our results suggest that there is atypical brain function in the auditory cortex in young children with ASD, regardless of language development.
C1 [Yoshimura, Yuko; Kikuchi, Mitsuru; Munesue, Toshio; Oi, Manabu; Niida, Yo; Higashida, Haruhiro; Minabe, Yoshio] Kanazawa Univ, Res Ctr Child Mental Dev, Kanazawa, Ishikawa, Japan.
[Yoshimura, Yuko; Kikuchi, Mitsuru; Shitamichi, Kiyomi; Ueno, Sanae; Munesue, Toshio; Ono, Yasuki; Minabe, Yoshio] Kanazawa Univ, Grad Sch Med Sci, Dept Psychiat & Neurobiol, Kanazawa, Ishikawa, Japan.
[Kikuchi, Mitsuru; Munesue, Toshio; Oi, Manabu; Higashida, Haruhiro; Minabe, Yoshio] Kanazawa Univ, Osaka Univ, United Grad Sch Child Dev, Dept Child Dev, Osaka, Japan.
[Kikuchi, Mitsuru; Munesue, Toshio; Oi, Manabu; Higashida, Haruhiro; Minabe, Yoshio] Osaka Univ, Hamamatsu Univ Sch Med, Osaka, Japan.
[Remijn, Gerard B.] Kyushu Univ, Int Educ Ctr, Fukuoka 812, Japan.
[Tsubokawa, Tsunehisa] Kanazawa Univ, Grad Sch Med Sci, Dept Anaesthesiol, Kanazawa, Ishikawa, Japan.
[Haruta, Yasuhiro] Yokogawa Elect Corp, Dept MEG, Tokyo, Japan.
[Takahashi, Tsutomu; Suzuki, Michio] Toyama Univ, Dept Neuropsychiat, Toyama 930, Japan.
RP Kikuchi, M (reprint author), Kanazawa Univ, Res Ctr Child Mental Dev, Kanazawa, Ishikawa, Japan.
EM mitsuru@zc4.so-net.ne.jp
FU MEXT, Japan [24000012]
FX This study was supported by Grant-in-Aid for Specially Promoted
(research no. 24000012), the Hokuriku Innovation Cluster for Health
Science (MEXT Program for Fostering Regional Innovation) and the
Strategic Research Program for Brain Sciences from MEXT, Japan.
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NR 67
TC 5
Z9 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD OCT 8
PY 2013
VL 4
AR 38
DI 10.1186/2040-2392-4-38
PG 14
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254YJ
UT WOS:000327205700002
PM 24103585
ER
PT J
AU Sawa, T
Kodaira, M
Oiji, A
Sasayama, D
Iwadare, Y
Ushijima, H
Usami, M
Watanabe, K
Saito, K
AF Sawa, Tetsuji
Kodaira, Masaki
Oiji, Arata
Sasayama, Daimei
Iwadare, Yoshitaka
Ushijima, Hirokage
Usami, Masahide
Watanabe, Kyota
Saito, Kazuhiko
TI Dysfunction of orbitofrontal and dorsolateral prefrontal cortices in
children and adolescents with high-functioning pervasive developmental
disorders
SO ANNALS OF GENERAL PSYCHIATRY
LA English
DT Article
DE Pervasive developmental disorders; Childhood; Adolescence; Iowa gambling
task; Wisconsin card sorting test; Orbitofrontal cortex; Dorsolateral
prefrontal cortex
ID IOWA GAMBLING TASK; CARD SORTING TEST; DECISION-MAKING; AUTISM; CORTEX;
PERFORMANCE; ACTIVATION
AB Background: Several lines of evidence suggest that dysfunction of the dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC) contributes to the pathophysiology of pervasive developmental disorders (PDD). The purpose of this study was to investigate neuropsychological dysfunctions in both the DLPFC and OFC of children and adolescents with high-functioning PDD.
Methods: The Iowa gambling task (IGT), which reflects OFC function, and the Wisconsin Card Sorting Test (WCST), which reflects DLPFC function, were assigned to 19 children and early adolescents with high-functioning PDD and 19 healthy controls matched for gender, age, and intelligence.
Results: Compared to healthy controls, patients with high-functioning PDD displayed poorer performance on the IGT and the WCST.
Conclusions: These results indicate that both the DLPFC and OFC could be impaired in children and early adolescents with high-functioning PDD.
C1 [Sawa, Tetsuji; Oiji, Arata] Kitasato Univ, Grad Sch Med Sci, Dept Dev Psychiat, Minami Ku, Sagamihara, Kanagawa 2520374, Japan.
[Kodaira, Masaki; Saito, Kazuhiko] Aiiku Hosp, Dept Child & Adolescent Mental Hlth, Minato Ku, Tokyo 1068580, Japan.
[Sasayama, Daimei] Shinshu Univ, Sch Med, Dept Neuropsychiat, Matsumoto, Nagano 3908621, Japan.
[Iwadare, Yoshitaka; Ushijima, Hirokage; Usami, Masahide; Watanabe, Kyota] Kohnodai Hosp, Natl Ctr Global Hlth & Med, Dept Child & Adolescent Psychiat, Ichikawa, Chiba 2720836, Japan.
RP Oiji, A (reprint author), Kitasato Univ, Grad Sch Med Sci, Dept Dev Psychiat, Minami Ku, 1-15-1 Kitasato, Sagamihara, Kanagawa 2520374, Japan.
EM pah00652@gmail.com
RI Usami, Masahide/G-1404-2015
OI Usami, Masahide/0000-0002-1145-9971
FU Japanese Ministry of Health, Labour, and Welfare [20B-6]
FX This study was funded by a research grant for Nervous and Mental
Disorders (20B-6) of the Japanese Ministry of Health, Labour, and
Welfare. We would like to express our deep gratitude to Professor
Katsutoshi Tanaka, Professor Hirokuni Tagaya, and Professor Yumi
Iwamitsu for giving us good opinions and advice. Moreover, we feel
deeply grateful for the children, caregivers, and staff members who
participated in this study.
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Paradigm for Autism-Like Behavioral Responses
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LA English
DT Article
ID DANIO-RERIO; CIRCLING BEHAVIOR; NEGATIVE SYMPTOMS; MK-801; ANTAGONIST;
BUSPIRONE; MODEL; RATS; SCHIZOPHRENIA; DISRUPTION
AB Because of its highly developed social character, zebrafish is a promising model system for the study of the genetic and neurochemical basis of altered social engagement such as is common in autism and schizophrenia. The traditional shoaling paradigm investigates social cohesion in homogeneous groups of zebrafish. However, the social dynamics of mixed groups is gaining interest from a therapeutic point of view and thus warrants animal modeling. Furthermore, mutant zebrafish are not always available in large numbers. Therefore, we developed a new paradigm that allows exploring shoaling in heterogeneous groups. The effects of MK-801, a non-competitive antagonist of the glutamate N-methyl-D-aspartate (NMDA) receptor, on social cohesion were studied to evaluate the paradigm. The drug has previously been shown to mimic aspects of autism and schizophrenia. Our results show that a single MK-801-treated zebrafish reduced social cohesion of the entire shoal drastically. Preliminary observations suggest that the social dynamics of the shoal as a whole was altered.
C1 [Maaswinkel, Hans; Zhu, Liqun; Weng, Wei] XyZfish, Res & Dev, Ronkonkoma, NY USA.
RP Maaswinkel, H (reprint author), XyZfish, Res & Dev, Ronkonkoma, NY USA.
EM hmaaswinkel@xyzfish.com
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TC 7
Z9 7
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 8
PY 2013
VL 8
IS 10
AR e75955
DI 10.1371/journal.pone.0075955
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 233FK
UT WOS:000325552200044
PM 24116082
ER
PT J
AU Maximo, JO
Keown, CL
Nair, A
Muller, RA
AF Maximo, Jose O.
Keown, Christopher L.
Nair, Aarti
Mueller, Ralph-Axel
TI Approaches to local connectivity in autism using resting state
functional connectivity MRI
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE autism; local connectivity; functional MRI; regional homogeneity;
graphtheory; BOLD signal; intrinsic connectivity
ID SPECTRUM DISORDERS; BRAIN CONNECTIVITY; DEFAULT MODE; REGIONAL
HOMOGENEITY; NEURAL SYSTEMS; NETWORKS; MOTION; CORTEX; PERCEPTION;
IMAGES
AB While the literature on aberrant long-distance connectivity in autism spectrum disorder (ASD) has grown fast over the past decade, little is known about local connectivity. We used regional homogeneity and local density approaches at different spatial scales to examine local connectivity in 29 children and adolescents with ASD and 29 matched typically developing participants, using resting state functional magnetic resonance imaging data. Across a total of 12 anlysis pipelines the gross pattern of between-group findings was overall stable, with local overconnectivity in the ASD group in occipital and posterior tempporal regions and underconnectivity in middle/posterior cingulate, and medial prefrontal regions. This general patern was confirmed in secondary anlyses for low-mention subsamples (n= 20 per group), in which time series segments with >0.25 mm head motion were censored, as well as in an analysis including global signal regression. Local overconnectivity in visual regions appears in ASD, whereas cingulate and medial frontal underconnnectivity may relate to aberrant function within the defalut mode network.
C1 [Maximo, Jose O.; Keown, Christopher L.; Nair, Aarti; Mueller, Ralph-Axel] San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA.
[Keown, Christopher L.] San Diego State Univ, Computat Sci Res Ctr, San Diego, CA 92120 USA.
[Nair, Aarti] San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA 92120 USA.
[Nair, Aarti] Univ Calif San Diego, San Diego, CA 92103 USA.
RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, 6363 Alvarado Court,Suite 200, San Diego, CA 92120 USA.
EM rmueller@mail.sdsu.edu
FU National Institutes of Health [R01MH081023]; NIH/NIGMS IMSD
[5R25GM058906-13]; Autism Speaks (Dennis Weatherstone Predoctoral
Fellowship) [7850]
FX This study was supported by the National Institutes of Health
R01MH081023, with additional funding from NIH/NIGMS IMSD 5R25GM058906-13
(Jose O. Maximo) and Autism Speaks (Dennis Weatherstone Predoctoral
Fellowship# 7850; to Aarti Nair). Special thanks to the participants and
their families.
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NR 74
TC 6
Z9 6
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 8
PY 2013
VL 7
AR 605
DI 10.3389/fnhum.2013.00605
PG 13
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 230GM
UT WOS:000325325100001
PM 24155702
ER
PT J
AU Pearson, A
Ropar, D
Hamilton, AFD
AF Pearson, Amy
Ropar, Danielle
Hamilton, Antonia F. de C.
TI A review of visual perspective taking in autism spectrum disorder
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Review
DE visual perspective taking; autism spectrum disorder; spatial
transformations; social cognition; spatial cognition; theory of mind
ID ASPERGER-SYNDROME; FUNCTIONING AUTISM; JOINT ATTENTION; MIND; CHILDREN;
ADULTS; TRANSFORMATIONS; SKILLS; BRAIN; ATTRIBUTION
AB Impairments in social cognition are a key symptom of autism spectrum disorder (ASD). People with autism have great difficulty with understanding the beliefs and desires of other people. In recent years literature has begun to examine the link between impairments in social cognition and abilities which demand the use of spatial and social skills, such as visual perspective taking (VPT). Flavell (1977) defined two levels of perspective taking: VPT level 1 is the ability to understand that other people have a different line of sight to ourselves, whereas VPT level 2 is the understanding that two people viewing the same item from different points in space may see different things. So far, literature on whether either level of VPT is impaired or intact in autism is inconsistent. Here we review studies which have examined VPT levels 1 and 2 in people with autism with a focus on their methods. We conclude the review with an evaluation of the findings into VPT in autism and give recommendations for future research which may give a clearer insight into whether perspective taking is truly impaired in autism.
C1 [Pearson, Amy] Univ Durham, Dept Psychol, Sci Labs, Durham DH1 3LE, England.
[Ropar, Danielle; Hamilton, Antonia F. de C.] Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England.
RP Pearson, A (reprint author), Univ Durham, Dept Psychol, Sci Labs, South Rd, Durham DH1 3LE, England.
EM amy.pearson@durham.ac.uk
RI Hamilton, Antonia/B-3612-2008
OI Hamilton, Antonia/0000-0001-8000-0219
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NR 56
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD OCT 8
PY 2013
VL 7
AR 652
DI 10.3389/fnhum.2013.00652
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 230HS
UT WOS:000325328900001
PM 24115930
ER
PT J
AU Chanda, S
Marro, S
Wernig, M
Sudhof, TC
AF Chanda, Soham
Marro, Samuele
Wernig, Marius
Suedhof, Thomas C.
TI Neurons generated by direct conversion of fibroblasts reproduce synaptic
phenotype caused by autism-associated neuroligin-3 mutation
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
AMERICA
LA English
DT Article
DE cellular reprogramming; stem cells; postsynaptic density; neurexin;
synapse
ID PLURIPOTENT STEM-CELLS; FUNCTIONAL-NEURONS; NEUROLOGICAL DISEASE;
DOPAMINERGIC-NEURONS; TRANSMISSION; INDUCTION; PROGRESS; BINDING; MODEL;
IPSCS
AB Recent studies suggest that induced neuronal (iN) cells that are directly transdifferentiated from nonneuronal cells provide a powerful opportunity to examine neuropsychiatric diseases. However, the validity of using this approach to examine disease-specific changes has not been demonstrated. Here, we analyze the phenotypes of iN cells that were derived from murine embryonic fibroblasts cultured from littermate wild-type and mutant mice carrying the autism-associated R704C substitution in neuroligin-3. We show that neuroligin-3 R704C-mutant iN cells exhibit a large and selective decrease in AMPA-type glutamate receptor-mediated synaptic transmission without changes in NMDA-type glutamate receptor-or in GABAA receptor-mediated synaptic transmission. Thus, the synaptic phenotype observed in R704C-mutant iN cells replicates the previously observed phenotype of R704C-mutant neurons. Our data show that the effect of the R704C mutation is applicable even to neurons transdifferentiated from fibroblasts and constitute a proof-of-concept demonstration that iN cells can be used for cellular disease modeling.
C1 [Chanda, Soham; Suedhof, Thomas C.] Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA.
[Chanda, Soham; Marro, Samuele; Wernig, Marius] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA.
[Chanda, Soham; Suedhof, Thomas C.] Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA.
[Chanda, Soham; Marro, Samuele; Wernig, Marius] Stanford Univ, Sch Med, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA.
RP Wernig, M (reprint author), Stanford Univ, Sch Med, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA.
EM wernig@stanford.edu; tcs1@stanford.edu
RI Marro, Samuele/I-4493-2014
OI Marro, Samuele/0000-0002-9326-6945
FU National Institutes of Health [R01 MH092931, AG010770-18A1]; Dean's
Postdoctoral Fellowship
FX We thank all members of the T.C.S. and M.W. laboratories for helpful
discussions. This study was supported by National Institutes of Health
Grants R01 MH092931 and AG010770-18A1 (to T.C.S. and M.W.), and a Dean's
Postdoctoral Fellowship (to S.M.). M.W. is a New York Stem Cell
Foundation-Robertson Investigator.
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NR 31
TC 9
Z9 9
PU NATL ACAD SCIENCES
PI WASHINGTON
PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA
SN 0027-8424
J9 P NATL ACAD SCI USA
JI Proc. Natl. Acad. Sci. U. S. A.
PD OCT 8
PY 2013
VL 110
IS 41
BP 16622
EP 16627
DI 10.1073/pnas.1316240110
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 231ED
UT WOS:000325395600075
PM 24046374
ER
PT J
AU Piven, J
Vieland, VJ
Parlier, M
Thompson, A
O'Conner, I
Woodbury-Smith, M
Huang, YG
Walters, KA
Fernandez, B
Szatmari, P
AF Piven, Joseph
Vieland, Veronica J.
Parlier, Morgan
Thompson, Ann
O'Conner, Irene
Woodbury-Smith, Mark
Huang, Yungui
Walters, Kimberly A.
Fernandez, Bridget
Szatmari, Peter
TI A molecular genetic study of autism and related phenotypes in extended
pedigrees
SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Genetics; Linkage; Pedigree; Phenotype; Posterior probability of
linkage
ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOME-WIDE LINKAGE; SPECTRUM
DISORDERS; BROAD AUTISM; MULTIPLE-INCIDENCE; FAMILY-HISTORY; REPETITIVE
BEHAVIOR; RECURRENCE RISK; INDIVIDUALS; SIBLINGS
AB Background: Efforts to uncover the risk genotypes associated with the familial nature of autism spectrum disorder (ASD) have had limited success. The study of extended pedigrees, incorporating additional ASD-related phenotypes into linkage analysis, offers an alternative approach to the search for inherited ASD susceptibility variants that complements traditional methods used to study the genetics of ASD.
Methods: We examined evidence for linkage in 19 extended pedigrees ascertained through ASD cases spread across at least two (and in most cases three) nuclear families. Both compound phenotypes (i.e., ASD and, in non-ASD individuals, the broad autism phenotype) and more narrowly defined components of these phenotypes, e. g., social and repetitive behavior, pragmatic language, and anxiety, were examined. The overarching goal was to maximize the aggregate information available on the maximum number of individuals and to disaggregate syndromic phenotypes in order to examine the genetic underpinnings of more narrowly defined aspects of ASD behavior.
Results: Results reveal substantial between-family locus heterogeneity and support the importance of previously reported ASD loci in inherited, familial, forms of ASD. Additional loci, not seen in the ASD analyses, show evidence for linkage to the broad autism phenotype (BAP). BAP peaks are well supported by multiple subphenotypes (including anxiety, pragmatic language, and social behavior) showing linkage to regions overlapping with the compound BAP phenotype. Whereas 'repetitive behavior', showing the strongest evidence for linkage (Posterior Probability of Linkage = 62% at 6p25.2-24.3, and 69% at 19p13.3), appears to be linked to novel regions not detected with other compound or narrow phenotypes examined in this study.
Conclusions: These results provide support for the presence of key features underlying the complexity of the genetic architecture of ASD: substantial between-family locus heterogeneity, that the BAP appears to correspond to sets of subclinical features segregating with ASD within pedigrees, and that different features of the ASD phenotype segregate independently of one another. These findings support the additional study of larger, even more individually informative pedigrees, together with measurement of multiple, behavioral- and biomarker-based phenotypes, in both affected and non-affected individuals, to elucidate the complex genetics of familial ASD.
C1 [Piven, Joseph; Parlier, Morgan] Univ N Carolina, Sch Med, Carolina Inst Dev Disabil, Chapel Hill, NC 27599 USA.
[Vieland, Veronica J.; Huang, Yungui; Walters, Kimberly A.] Nationwide Childrens Hosp, Res Inst, Battelle Ctr Math Med, Columbus, OH 43215 USA.
[Vieland, Veronica J.] Ohio State Univ, Dept Pediat, Columbus, OH 43215 USA.
[Vieland, Veronica J.] Ohio State Univ, Dept Stat, Columbus, OH 43215 USA.
[Thompson, Ann; O'Conner, Irene; Woodbury-Smith, Mark; Szatmari, Peter] McMaster Dept Psychiat & Behav Neurosci, Hamilton, ON L9H 3Z5, Canada.
[Fernandez, Bridget] Hlth Sci Ctr, Prov Med Genet Program, St John, NF A1B 3V6, Canada.
[Szatmari, Peter] Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON, Canada.
RP Piven, J (reprint author), Univ N Carolina, Sch Med, Carolina Inst Dev Disabil, CB 3367, Chapel Hill, NC 27599 USA.
EM jpiven@med.unc.edu
FU NIH [MH076028, HD003110, R01 MH086117, U24 MH068457]
FX This project was supported by the following grants: NIH MH076028,
HD003110 (JP), R01 MH086117 (VJV); U24 MH068457 (J Tischfield, PI). We
also acknowledge the contributions of Molly Losh, Ph.D. to the design of
this study. Finally, we would like to thank all the families who
participated in this research.
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NR 73
TC 4
Z9 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1866-1947
EI 1866-1955
J9 J NEURODEV DISORD
JI J. Neurodev. Disord.
PD OCT 5
PY 2013
VL 5
AR 30
DI 10.1186/1866-1955-5-30
PG 15
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 281SR
UT WOS:000329121800001
PM 24093601
ER
PT J
AU Samuel, R
Attard, A
Kyriakopoulos, M
AF Samuel, Rani
Attard, Azizah
Kyriakopoulos, Marinos
TI Mental state deterioration after switching from brand-name to generic
olanzapine in an adolescent with bipolar affective disorder, autism and
intellectual disability: a case study
SO BMC PSYCHIATRY
LA English
DT Article
DE Olanzapine; Intellectual disability; Bioavailability; Generic
formulation; Adolescent
ID DRUG SUBSTITUTION
AB Background: The appropriateness of use of generic instead of brand-name medication remains unresolved and controversial in several areas of medicine. Some evidence suggestive of variations in bioavailability and clinical effectiveness between different formulations make policy decisions occasionally difficult. The use of generic olanzapine is a widely acceptable practice on the basis of quality, safety and efficacy data and has been adopted in several countries.
Case presentation: The case of a 14 year old boy with bipolar affective disorder, autism and intellectual disability who had brand-name to generic olanzapine switch associated with rapid deterioration of his mental state is described. This clinical change was not related to any physical illness or other medication adjustment and resolved as rapidly when generic olanzapine was switched back to the brand-name formulation.
Conclusions: Caution should be exercised when policy for switching from brand-name to generic psychotropic medications are made, especially when using medications off label, in extremes of age and in those patients with co-morbid complicating factors such as intellectual disability.
C1 [Samuel, Rani; Kyriakopoulos, Marinos] South London & Maudsley NHS Fdn Trust, Natl & Specialist Acorn Lodge Inpatient Childrens, London SE5 8AF, England.
[Attard, Azizah] South London & Maudsley NHS Fdn Trust, London SE5 8AF, England.
[Attard, Azizah; Kyriakopoulos, Marinos] Kings Coll London, Inst Psychiat PO66, London SE5 8AF, England.
RP Kyriakopoulos, M (reprint author), South London & Maudsley NHS Fdn Trust, Natl & Specialist Acorn Lodge Inpatient Childrens, De Crespigny Pk, London SE5 8AF, England.
EM marinos.kyriakopoulos@kcl.ac.uk
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NR 13
TC 0
Z9 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-244X
J9 BMC PSYCHIATRY
JI BMC Psychiatry
PD OCT 4
PY 2013
VL 13
AR 244
DI 10.1186/1471-244X-13-244
PG 3
WC Psychiatry
SC Psychiatry
GA 243CD
UT WOS:000326293300001
PM 24094081
ER
PT J
AU Witteveen, JS
Middelman, A
van Hulten, JA
Martens, GJM
Homberg, JR
Kolk, SM
AF Witteveen, Josefine S.
Middelman, Anthonieke
van Hulten, Josephus A.
Martens, Gerard J. M.
Homberg, Judith R.
Kolk, Sharon M.
TI Lack of serotonin reuptake during brain development alters rostral
raphe-prefrontal network formation
SO FRONTIERS IN CELLULAR NEUROSCIENCE
LA English
DT Article
DE explant assays; prefrontal cortex; serotonin transporter;
microdissection; axon guidance; depression; SERT; autism
ID DEVELOPING RAT-BRAIN; KNOCK-OUT MICE; CEREBRAL-CORTEX; TRANSIENT
EXPRESSION; CORTICAL DEVELOPMENT; AXON GUIDANCE; SSRI ANTIDEPRESSANTS;
NEUROTROPHIC FACTOR; PRENATAL EXPOSURE; GENETIC-VARIATION
AB Besides its classical neurotransmitter function, serotonin (5-HT) has been found to also act as a neurodevelopmental signal. During development, the 5-HT projection system, besides an external placental source, represents one of the earliest neurotransmitter systems to innervate the brain. One of the targets of the 5-HT projection system, originating in the brainstem raphe nuclei, is the medial prefrontal cortex (mPFC), an area involved in higher cognitive functions and important in the etiology of many neurodevelopmental disorders. Little is known, however, about the exact role of 5-HT and its signaling molecules in the formation of the raphe-prefrontal network. Using explant essays, we here studied the role of the 5-HT transporter (5-HTT), an important modulator of the 5-HT signal, in rostral raphe-prefrontal network formation. We found that the chemotrophic nature of the interaction between the origin (rostral raphe cluster) and a target (mPFC) of the 5-HT projection system was affected in rats lacking the 5-HTT (5-HTT-/-). While 5-HTT deficiency did not affect the dorsal raphe 5-HT-positive outgrowing neurites, the median raphe 5-HT neurites switched from a strong repulsive to an attractive interaction when co-cultured with the mPFC. Furthermore, the fasciculation of the mPFC outgrowing neurites was dependent on the amount of 5-HTT. In the mPFC of 5-HTT-/- pups, we observed clear differences in 5-HT innervation and the identity of a class of projection neurons of the mPFC. In the absence of the 5-HTT, the 5-HT innervation in all subareas of the early postnatal mPFC increased dramatically and the number of Satb2-positive callosal projection neurons was decreased. Together, these results suggest a 5-HTT dependency during early development of these brain areas and in the formation of the raphe-prefrontal network. The tremendous complexity of the 5-HT projection system and its role in several neurodevelopmental disorders highlights the need for further research in this largely unexplored area.
C1 [Witteveen, Josefine S.; van Hulten, Josephus A.; Martens, Gerard J. M.; Kolk, Sharon M.] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Dept Mol Anim Physiol, NL-6525 GA Nijmegen, Netherlands.
[Middelman, Anthonieke; Homberg, Judith R.] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Med Ctr, Dept Cognit Neurosci, NL-6525 GA Nijmegen, Netherlands.
RP Kolk, SM (reprint author), Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Nijmegen Ctr Mol Life Sci, Dept Mol Anim Physiol, Geert Grootepl Zuid 28, NL-6525 GA Nijmegen, Netherlands.
EM s.kolk@ncmls.ru.nl
RI Homberg, Judith/D-2473-2010; Kolk, Sharon/A-9055-2011; Martens,
Gerard/D-1925-2010
OI Kolk, Sharon/0000-0003-2116-5456;
FU Dutch Organization of Scientific Research (NWO) [433-09-311]
FX This work was supported by the Dutch Organization of Scientific Research
(NWO grant # 433-09-311) awarded to J. Homberg. We thank Stephanie
Miceli and the reviewers for critically reading this manuscript and
members of the Martens, Kolk, and Homber labs for helpful editing and
discussions. We thank the NCMLS microscopy platform
(http://ncmls.nl/technology-platform/microscope-imaging-centre/) for
excellent support and maintenance of the equipment.
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NR 121
TC 5
Z9 5
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5102
J9 FRONT CELL NEUROSCI
JI Front. Cell. Neurosci.
PD OCT 4
PY 2013
VL 7
AR 143
DI 10.3389/fncel.2013.00143
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 228FP
UT WOS:000325171500001
PM 24109430
ER
PT J
AU Abrahams, BS
Arking, DE
Campbell, DB
Mefford, HC
Morrow, EM
Weiss, LA
Menashe, I
Wadkins, T
Banerjee-Basu, S
Packer, A
AF Abrahams, Brett S.
Arking, Dan E.
Campbell, Daniel B.
Mefford, Heather C.
Morrow, Eric M.
Weiss, Lauren A.
Menashe, Idan
Wadkins, Tim
Banerjee-Basu, Sharmila
Packer, Alan
TI SFARI Gene 2.0: a community-driven knowledgebase for the autism spectrum
disorders (ASDs)
SO MOLECULAR AUTISM
LA English
DT Letter
AB New technologies enabling genome-wide interrogation have led to a large and rapidly growing number of autism spectrum disorder (ASD) candidate genes. Although encouraging, the volume and complexity of these data make it challenging for scientists, particularly non-geneticists, to comprehensively evaluate available evidence for individual genes. Described here is the Gene Scoring module within SFARI Gene 2.0 (https://gene.sfari.org/autdb/GS_Home.do), a platform developed to enable systematic community driven assessment of genetic evidence for individual genes with regard to ASD.
C1 [Abrahams, Brett S.] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA.
[Abrahams, Brett S.] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10467 USA.
[Arking, Dan E.] Johns Hopkins Univ, Sch Med, McKusick Nathans Inst Genet Med, Baltimore, MD USA.
[Campbell, Daniel B.] Univ So Calif, Keck Sch Med, Zilkha Neurogenet Inst, Los Angeles, CA 90033 USA.
[Campbell, Daniel B.] Univ So Calif, Keck Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA.
[Mefford, Heather C.] Univ Washington, Dept Pediat, Div Med Genet, Seattle, WA 98195 USA.
[Morrow, Eric M.] Brown Univ, Dept Mol Biol Cell Biol & Biochem, Providence, RI 02912 USA.
[Morrow, Eric M.] Brown Univ, Dept Psychiat & Human Behav, Providence, RI 02912 USA.
[Weiss, Lauren A.] UCSF, Ctr Neurobiol & Psychiat, Inst Human Genet, Dept Psychiat, San Francisco, CA USA.
[Menashe, Idan; Wadkins, Tim; Banerjee-Basu, Sharmila] MindSpec Inc, Mclean, VA USA.
[Menashe, Idan] Ben Gurion Univ Negev, Fac Hlth Sci, Dept Publ Hlth, IL-84105 Beer Sheva, Israel.
[Packer, Alan] Simons Fdn Autism Res Initiat, New York, NY USA.
RP Banerjee-Basu, S (reprint author), MindSpec Inc, 8280 Greensboro Dr,Suite 150, Mclean, VA USA.
EM sharmila@mindspec.org; apacker@simonsfoundation.org
CR Abrahams BS, 2009, VOGEL MOTULSKYS HUMA, P699
Abrahams BS, 2008, NAT REV GENET, V9, P341, DOI 10.1038/nrg2346
Basu SN, 2009, NUCLEIC ACIDS RES, V37, P832, DOI DOI 10.1093/NAR/GKN835
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NR 8
TC 10
Z9 10
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 2040-2392
J9 MOL AUTISM
JI Mol. Autism
PD OCT 3
PY 2013
VL 4
AR 36
DI 10.1186/2040-2392-4-36
PG 3
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254YH
UT WOS:000327205500001
PM 24090431
ER
PT J
AU Bendjilali, N
Kim, H
Weinsheimer, S
Guo, DE
Kwok, PY
Zaroff, JG
Sidney, S
Lawton, MT
McCulloch, CE
Koeleman, BPC
Klijn, CJM
Young, WL
Pawlikowska, L
AF Bendjilali, Nasrine
Kim, Helen
Weinsheimer, Shantel
Guo, Diana E.
Kwok, Pui-Yan
Zaroff, Jonathan G.
Sidney, Stephen
Lawton, Michael T.
McCulloch, Charles E.
Koeleman, Bobby P. C.
Klijn, Catharina J. M.
Young, William L.
Pawlikowska, Ludmila
TI A Genome-Wide Investigation of Copy Number Variation in Patients with
Sporadic Brain Arteriovenous Malformation
SO PLOS ONE
LA English
DT Article
ID HEREDITARY HEMORRHAGIC TELANGIECTASIA; AUTISM SPECTRUM DISORDERS; RISK;
POLYMORPHISMS; ASSOCIATION; GENE; SUSCEPTIBILITY; SCHIZOPHRENIA;
PATHOGENESIS; MUTATIONS
AB Background: Brain arteriovenous malformations (BAVM) are clusters of abnormal blood vessels, with shunting of blood from the arterial to venous circulation and a high risk of rupture and intracranial hemorrhage. Most BAVMs are sporadic, but also occur in patients with Hereditary Hemorrhagic Telangiectasia, a Mendelian disorder caused by mutations in genes in the transforming growth factor beta (TGF beta) signaling pathway.
Methods: To investigate whether copy number variations (CNVs) contribute to risk of sporadic BAVM, we performed a genome-wide association study in 371 sporadic BAVM cases and 563 healthy controls, all Caucasian. Cases and controls were genotyped using the Affymetrix 6.0 array. CNVs were called using the PennCNV and Birdsuite algorithms and analyzed via segment-based and gene-based approaches. Common and rare CNVs were evaluated for association with BAVM.
Results: A CNV region on 1p36.13, containing the neuroblastoma breakpoint family, member 1 gene (NBPF1), was significantly enriched with duplications in BAVM cases compared to controls (P = 2.2x10(-9)); NBPF1 was also significantly associated with BAVM in gene-based analysis using both PennCNV and Birdsuite. We experimentally validated the 1p36.13 duplication; however, the association did not replicate in an independent cohort of 184 sporadic BAVM cases and 182 controls (OR = 0.81, P = 0.8). Rare CNV analysis did not identify genes significantly associated with BAVM.
Conclusion: We did not identify common CNVs associated with sporadic BAVM that replicated in an independent cohort. Replication in larger cohorts is required to elucidate the possible role of common or rare CNVs in BAVM pathogenesis.
C1 [Bendjilali, Nasrine; Kim, Helen; Weinsheimer, Shantel; Guo, Diana E.; Young, William L.; Pawlikowska, Ludmila] Univ Calif San Francisco, Cerebrovasc Res Ctr, Dept Anesthesia & Perioperat Care, San Francisco, CA 94143 USA.
[Kim, Helen; Kwok, Pui-Yan; Pawlikowska, Ludmila] Univ Calif San Francisco, Inst Human Genet, San Francisco, CA 94143 USA.
[Kim, Helen; McCulloch, Charles E.] Univ Calif San Francisco, Dept Epidemiol & Biostat, San Francisco, CA 94143 USA.
[Kwok, Pui-Yan] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA.
[Zaroff, Jonathan G.; Sidney, Stephen] Kaiser Northern Calif Div Res, San Francisco, CA USA.
[Lawton, Michael T.; Young, William L.] Univ Calif San Francisco, Dept Neurol Surg, San Francisco, CA USA.
[Koeleman, Bobby P. C.] Univ Med Ctr, Dept Med Genet, Utrecht, Netherlands.
[Klijn, Catharina J. M.] Univ Med Ctr, Rudolf Magnus Inst Neurosci, Dept Neurol & Neurosurg, Utrecht, Netherlands.
[Young, William L.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
RP Pawlikowska, L (reprint author), Univ Calif San Francisco, Cerebrovasc Res Ctr, Dept Anesthesia & Perioperat Care, San Francisco, CA 94143 USA.
EM pawlikowskal@anesthesia.ucsf.edu
RI Kwok, Pui-Yan/F-7725-2014
OI Kwok, Pui-Yan/0000-0002-5087-3059
FU National Institutes of Health (NIH) [P01 NS044155, R01 NS034949, K23
NS058357]; private Dutch foundation; NIH [P50 NS2372, U19 AI063603]
FX This work was supported by National Institutes of Health (NIH) grants:
P01 NS044155 (WLY), R01 NS034949 (WLY), and K23 NS058357 (HK).
Additional support was provided by "Running for Nona,'' a private Dutch
foundation (CJMK). Control cohorts were supported by NIH grants P50
NS2372 (to E. Mignot) and U19 AI063603 (to D. Salomon). The funders had
no role in study design, data collection and analysis, decision to
publish, or preparation of the manuscript.
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NR 56
TC 1
Z9 1
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD OCT 3
PY 2013
VL 8
IS 10
AR e71434
DI 10.1371/journal.pone.0071434
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 232HM
UT WOS:000325483600001
PM 24098321
ER
PT J
AU Chen, J
Lin, MY
Foxe, JJ
Pedrosa, E
Hrabovsky, A
Carroll, R
Zheng, DY
Lachman, HM
AF Chen, Jian
Lin, Mingyan
Foxe, John J.
Pedrosa, Erika
Hrabovsky, Anastasia
Carroll, Reed
Zheng, Deyou
Lachman, Herbert M.
TI Transcriptome Comparison of Human Neurons Generated Using Induced
Pluripotent Stem Cells Derived from Dental Pulp and Skin Fibroblasts
SO PLOS ONE
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; BIPOLAR DISORDER; DEFINED FACTORS; IPS CELLS;
ASSOCIATION; INDUCTION; GENES; MODEL
AB Induced pluripotent stem cell (iPSC) technology is providing an opportunity to study neuropsychiatric disorders through the capacity to grow patient-specific neurons in vitro. Skin fibroblasts obtained by biopsy have been the most reliable source of cells for reprogramming. However, using other somatic cells obtained by less invasive means would be ideal, especially in children with autism spectrum disorders (ASD) and other neurodevelopmental conditions. In addition to fibroblasts, iPSCs have been developed from cord blood, lymphocytes, hair keratinocytes, and dental pulp from deciduous teeth. Of these, dental pulp would be a good source for neurodevelopmental disorders in children because obtaining material is non-invasive. We investigated its suitability for disease modeling by carrying out gene expression profiling, using RNA-seq, on differentiated neurons derived from iPSCs made from dental pulp extracted from deciduous teeth (T-iPSCs) and fibroblasts (F-iPSCs). This is the first RNA-seq analysis comparing gene expression profiles in neurons derived from iPSCs made from different somatic cells. For the most part, gene expression profiles were quite similar with only 329 genes showing differential expression at a nominally significant p-value (p<0.05), of which 63 remained significant after correcting for genome-wide analysis (FDR <0.05). The most striking difference was the lower level of expression detected for numerous members of the all four HOX gene families in neurons derived from T-iPSCs. In addition, an increased level of expression was seen for several transcription factors expressed in the developing forebrain (FOXP2, OTX1, and LHX2, for example). Overall, pathway analysis revealed that differentially expressed genes that showed higher levels of expression in neurons derived from T-iPSCs were enriched for genes implicated in schizophrenia (SZ). The findings suggest that neurons derived from T-iPSCs are suitable for disease-modeling neuropsychiatric disorder and may have some advantages over those derived from F-iPSCs.
C1 [Chen, Jian; Pedrosa, Erika; Hrabovsky, Anastasia; Lachman, Herbert M.] Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Bronx, NY 10467 USA.
[Lin, Mingyan; Zheng, Deyou; Lachman, Herbert M.] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA.
[Foxe, John J.; Carroll, Reed; Zheng, Deyou; Lachman, Herbert M.] Albert Einstein Coll Med, Dominick Purpura Dept Neurosci, Bronx, NY 10467 USA.
[Foxe, John J.] Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA.
[Zheng, Deyou] Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA.
[Lachman, Herbert M.] Albert Einstein Coll Med, Dept Med, Bronx, NY 10467 USA.
RP Lachman, HM (reprint author), Albert Einstein Coll Med, Dept Psychiat & Behav Sci, Bronx, NY 10467 USA.
EM Herb.Lachman@einstein.yu.edu
FU National Institutes of Health [MH087840, MH073164]; CTSA from the
National Center for Research Resources (NCRR), a component of the
National Institutes of Health (NIH) [UL1RR025750, KL2RR025749,
TL1RR025748]; NIH roadmap for Medical Research; Eunice Kennedy Shriver
National Institute of Child Health & Human Development (NICHD) at the
NIH [1P30HD071593-01]
FX This work was supported by the National Institutes of Health (MH087840
and MH073164 to HML). This publication was also supported in part by the
CTSA Grant UL1RR025750, KL2RR025749 and TL1RR025748 from the National
Center for Research Resources (NCRR), a component of the National
Institutes of Health (NIH), and NIH roadmap for Medical Research, and a
grant to The Rose F. Kennedy Intellectual and Developmental Disabilities
Research Center (RFK-IDDRC) from the Eunice Kennedy Shriver National
Institute of Child Health & Human Development (NICHD) at the NIH
(1P30HD071593-01). The contents of this paper are solely the
responsibility of the authors and do not necessarily represent the
official views of NCRR or NICHD. The funders had no role in study
design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
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J9 PLOS ONE
JI PLoS One
PD OCT 3
PY 2013
VL 8
IS 10
DI 10.1371/journal.pone.0075682
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 232HM
UT WOS:000325483600021
PM 24098394
ER
PT J
AU Krumm, N
O'Roak, BJ
Karakoc, E
Mohajeri, K
Nelson, B
Vives, L
Jacquemont, S
Munson, J
Bernier, R
Eichler, EE
AF Krumm, Niklas
O'Roak, Brian J.
Karakoc, Emre
Mohajeri, Kiana
Nelson, Ben
Vives, Laura
Jacquemont, Sebastien
Munson, Jeff
Bernier, Raphe
Eichler, Evan E.
TI Transmission Disequilibrium of Small CNVs in Simplex Autism
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID COPY-NUMBER VARIATION; DE-NOVO MUTATIONS; SPECTRUM DISORDERS; GENE;
ALGORITHM; UBIQUITIN; VARIANTS; RESOURCE; DELETION; ORIGIN
AB We searched for disruptive, genic rare copy-number variants (CNVs) among 411 families affected by sporadic autism spectrum disorder (ASD) from the Simons Simplex Collection by using available exome sequence data and CoNIFER (Copy Number Inference from Exome Reads). Compared to high-density SNP microarrays, our approach yielded similar to 2x more smaller genic rare CNVs. We found that affected probands inherited more CNVs than did their siblings (453 versus 394, p = 0.004; odds ratio [OR] = 1.19) and that the probands' CNVs affected more genes (921 versus 726, p = 0.02; OR = 1.30). These smaller CNVs (median size 18 kb) were transmitted preferentially from the mother (136 maternal versus 100 paternal, p = 0.02), although this bias occurred irrespective of affected status. The excess burden of inherited CNVs among probands was driven primarily by sibling pairs with discordant social-behavior phenotypes (p < 0.0002, measured by Social Responsiveness Scale [SRS] score), which contrasts with families where the phenotypes were more closely matched or less extreme (p > 0.5). Finally, we found enrichment of brain-expressed genes unique to probands, especially in the SRS-discordant group (p = 0.0035). In a combined model, our inherited CNVs, de novo CNVs, and de novo single-nucleotide variants all independently contributed to the risk of autism (p < 0.05). Taken together, these results suggest that small transmitted rare CNVs play a role in the etiology of simplex autism. Importantly, the small size of these variants aids in the identification of specific genes as additional risk factors associated with ASD.
C1 [Krumm, Niklas; O'Roak, Brian J.; Karakoc, Emre; Mohajeri, Kiana; Nelson, Ben; Vives, Laura; Eichler, Evan E.] Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA.
[Jacquemont, Sebastien] CHU Vaudois, Serv Med Genet, CH-1011 Lausanne, Vaud, Switzerland.
[Munson, Jeff; Bernier, Raphe] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
[Eichler, Evan E.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA.
RP Eichler, EE (reprint author), Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA.
EM eee@gs.washington.edu
FU National Institutes of Health (NIH) National Heart, Lung, and Blood
Institute [HL-102923, HL-102924, HL-102925, HL-102926, HL-103010];
Simons Foundation Autism Research Initiative [SFARI 137578, 191889]; NIH
[HD065285]
FX We thank the National Institutes of Health (NIH) National Heart, Lung,
and Blood Institute Grand Opportunity (GO) Exome Sequencing Project and
its ongoing studies, which produced and provided exome variant calls for
comparison: the Lung GO Sequencing Project (HL-102923), the Women's
Health Initiative Sequencing Project (HL-102924), the Broad GO
Sequencing Project (HL-102925), the Seattle GO Sequencing Project
(HL-102926), and the Heart GO Sequencing Project (HL-103010). We thank
all the families at the participating Simons Simplex Collection (SSC)
sites, as well as the principal investigators (A. Beaudet, R.B., J.
Constantino, E. Cook, E. Fombonne, D. Geschwind, E. Hanson, D. Grice, A.
Klin, R. Kochel, D. Ledbetter, C. Lord, C. Martin, D. Martin, R. Maxim,
S. Miles, O. Ousley, K. Pelphrey, B. Peterson, J. Piggot, C. Saulnier,
M. State, W. Stone, J. Sutcliffe, C. Walsh, Z. Warren, and E. Wijsman).
We also acknowledge M. State and the SSC Genetics Consortium for
providing Illumina genotyping data and T. Lehner and the Autism
Sequencing Consortium for data exchange among the participating groups.
We are grateful for helpful discussion and manuscript preparation from
T. Brown, P. Sudmant, and all members of the Eichler lab. This work was
supported by the Simons Foundation Autism Research Initiative (SFARI
137578 and 191889 to E.E.E., J.S., and R.B.) and NIH HD065285 (E.E.E.
and J.S.). E.B. is an Alfred P. Sloan Research Fellow. E.E.E. is an
Investigator of the Howard Hughes Medical Institute and is on the
scientific advisory boards for Pacific Biosciences, Inc., SynapDx Corp.,
and DNAnexus, Inc.
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Davidson J., 2012, J AUTISM DEV DISORD
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NR 34
TC 19
Z9 19
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD OCT 3
PY 2013
VL 93
IS 4
BP 595
EP 606
DI 10.1016/j.ajhg.2013.07.024
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 243GT
UT WOS:000326305600002
PM 24035194
ER
PT J
AU Poultney, CS
Goldberg, AP
Drapeau, E
Kou, Y
Harony-Nicolas, H
Kajiwara, Y
De Rubeis, S
Durand, S
Stevens, C
Rehnstrom, K
Palotie, A
Daly, MJ
Ma'ayan, A
Fromer, M
Buxbaum, JD
AF Poultney, Christopher S.
Goldberg, Arthur P.
Drapeau, Elodie
Kou, Yan
Harony-Nicolas, Hala
Kajiwara, Yuji
De Rubeis, Silvia
Durand, Simon
Stevens, Christine
Rehnstroem, Karola
Palotie, Aarno
Daly, Mark J.
Ma'ayan, Avi
Fromer, Menachem
Buxbaum, Joseph D.
TI Identification of Small Exonic CNV from Whole-Exome Sequence Data and
Application to Autism Spectrum Disorder
SO AMERICAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
ID COPY-NUMBER VARIATION; DE-NOVO MUTATIONS; HUMAN GENOME; GENE; TOOL;
REVEALS; DISCOVERY; NETWORK; 17P13.1; MAP
AB Copy number variation (CNV) is an important determinant of human diversity and plays important roles in susceptibility to disease. Most studies of CNV carried out to date have made use of chromosome microarray and have had a lower size limit for detection of about 30 kilobases (kb). With the emergence of whole-exome sequencing studies, we asked whether such data could be used to reliably call rare exonic CNV in the size range of 1-30 kilobases (kb), making use of the eXome Hidden Markov Model (XHMM) program. By using both transmission information and validation by molecular methods, we confirmed that small CNV encompassing as few as three exons can be reliably called from whole-exome data. We applied this approach to an autism case-control sample (n = 811, mean per-target read depth = 161) and observed a significant increase in the burden of rare (MAF <= 1%) 1-30 kb CNV, 1-30 kb deletions, and 1-10 kb deletions in ASD. CNV in the 1-30 kb range frequently hit just a single gene, and we were therefore able to carry out enrichment and pathway analyses, where we observed enrichment for disruption of genes in cytoskeletal and autophagy pathways in ASD. In summary, our results showed that XHMM provided an effective means to assess small exonic CNV from whole-exome data, indicated that rare 1-30 kb exonic deletions could contribute to risk in up to 7% of individuals with ASD, and implicated a candidate pathway in developmental delay syndromes.
C1 [Poultney, Christopher S.; Goldberg, Arthur P.; Drapeau, Elodie; Kou, Yan; Harony-Nicolas, Hala; Kajiwara, Yuji; De Rubeis, Silvia; Durand, Simon; Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Seaver Autism Ctr Res & Treatment, New York, NY 10029 USA.
[Poultney, Christopher S.; Goldberg, Arthur P.; Drapeau, Elodie; Harony-Nicolas, Hala; Kajiwara, Yuji; De Rubeis, Silvia; Durand, Simon; Fromer, Menachem; Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Dept Psychiat, New York, NY 10029 USA.
[Goldberg, Arthur P.; Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA.
[Kou, Yan; Ma'ayan, Avi] Icahn Sch Med Mt Sinai, Dept Pharmacol & Syst Therapeut, New York, NY 10029 USA.
[Kou, Yan; Ma'ayan, Avi] Icahn Sch Med Mt Sinai, Syst Biol Ctr New York, New York, NY 10029 USA.
[Stevens, Christine; Palotie, Aarno; Daly, Mark J.] Broad Inst MIT & Harvard, Program Med & Populat Genet, Cambridge, MA 02142 USA.
[Rehnstroem, Karola; Palotie, Aarno] Univ Helsinki, Inst Mol Med Finland FIMM, FIN-00290 Helsinki, Finland.
[Rehnstroem, Karola] Wellcome Trust Sanger Inst, Cambridge CB10 1SA, England.
[Daly, Mark J.] Massachusetts Gen Hosp, Dept Med, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Daly, Mark J.] Harvard Univ, Sch Med, Boston, MA 02114 USA.
[Fromer, Menachem; Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Dept Neurosci, Dept Genet & Genom Sci, New York, NY 10029 USA.
[Fromer, Menachem; Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Friedman Brain Inst, New York, NY 10029 USA.
[Buxbaum, Joseph D.] Icahn Sch Med Mt Sinai, Mindich Child Hlth & Dev Inst, New York, NY 10029 USA.
RP Buxbaum, JD (reprint author), Icahn Sch Med Mt Sinai, Seaver Autism Ctr Res & Treatment, New York, NY 10029 USA.
EM joseph.buxbaum@mssm.edu
FU National Institute of Mental Health, National Institutes of Health
[MH089025, MH097849, MH100233]; Seaver Foundation
FX This work was supported by the National Institute of Mental Health,
National Institutes of Health (grants MH089025, MH097849, and MH100233
to J.D.B.) and the Seaver Foundation. C.S.P. is a Seaver Fellow and
A.P.G. is a Seaver Fellow.
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NR 47
TC 24
Z9 24
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0002-9297
EI 1537-6605
J9 AM J HUM GENET
JI Am. J. Hum. Genet.
PD OCT 3
PY 2013
VL 93
IS 4
BP 607
EP 619
DI 10.1016/j.ajhg.2013.09.001
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 243GT
UT WOS:000326305600003
PM 24094742
ER
PT J
AU Yap, CC
Winckler, B
AF Yap, Chan Choo
Winckler, Bettina
TI Acid Indigestion in the Endosome: Linking Signaling Dysregulation to
Neurodevelopmental Disorders
SO NEURON
LA English
DT Editorial Material
ID NEURAL DEVELOPMENT
AB The sodium-proton exchanger NHE6 contributes to proper endosomal acidification. NHE6 mutations are also linked to autism-related disorders. In this issue of Neuron, using NHE6-knockout mice, Ouyang et al. (2013) uncover how dysregulation of endosomal pH leads to disturbances in BDNF signaling and neuronal morphogenesis defects.
C1 [Yap, Chan Choo; Winckler, Bettina] Univ Virginia, Dept Neurosci, Charlottesville, VA 22908 USA.
RP Winckler, B (reprint author), Univ Virginia, Dept Neurosci, 409 Lane Rd, Charlottesville, VA 22908 USA.
EM bwinckler@virginia.edu
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NR 15
TC 1
Z9 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD OCT 2
PY 2013
VL 80
IS 1
BP 4
EP 6
DI 10.1016/j.neuron.2013.09.018
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 243GQ
UT WOS:000326305300002
PM 24094097
ER
PT J
AU Novarino, G
Baek, ST
Gleeson, JG
AF Novarino, Gaia
Baek, Seung Tae
Gleeson, Joseph G.
TI The Sacred Disease: The Puzzling Genetics of Epileptic Disorders
SO NEURON
LA English
DT Editorial Material
ID DE-NOVO MUTATIONS; INTELLECTUAL DISABILITY; AUTISM
AB In the September 12, 2013 issue of Nature, the Epi4K Consortium (Allen et al., 2013) reported sequencing 264 patient trios with epileptic encephalopathies. The Consortium focused on genes exceptionally intolerant to sequence variations and found substantial interconnections with autism and intellectual disability gene networks.
C1 [Novarino, Gaia; Baek, Seung Tae; Gleeson, Joseph G.] Univ Calif San Diego, Dept Neurosci, Howard Hughes Med Inst, La Jolla, CA 92093 USA.
RP Gleeson, JG (reprint author), Univ Calif San Diego, Dept Neurosci, Howard Hughes Med Inst, La Jolla, CA 92093 USA.
EM jogleeson@ucsd.edu
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NR 11
TC 1
Z9 1
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD OCT 2
PY 2013
VL 80
IS 1
BP 9
EP 11
DI 10.1016/j.neuron.2013.09.019
PG 3
WC Neurosciences
SC Neurosciences & Neurology
GA 243GQ
UT WOS:000326305300004
PM 24094099
ER
PT J
AU Ouyang, Q
Lizarraga, SB
Schmidt, M
Yang, U
Gong, JY
Ellisor, D
Kauer, JA
Morrow, EM
AF Ouyang, Qing
Lizarraga, Sofia B.
Schmidt, Michael
Yang, Unikora
Gong, Jingyi
Ellisor, Debra
Kauer, Julie A.
Morrow, Eric M.
TI Christianson Syndrome Protein NHE6 Modulates TrkB Endosomal Signaling
Required for Neuronal Circuit Development
SO NEURON
LA English
DT Article
ID NA+/H+ EXCHANGER ISOFORM-6; MENTAL-RETARDATION; SODIUM/PROTON EXCHANGER;
NEUROTROPHIC FACTOR; ANGELMAN-SYNDROME; AUTISM; MECHANISMS; CELLS;
YEAST; PH
AB Neuronal arborization is regulated by cell-autonomous and nonautonomous mechanisms including endosomal signaling via BDNF/TrkB. The endosomal Na+/H+ exchanger 6 (NHE6) is mutated in a new autism-related disorder. NHE6 functions to permit proton leak from endosomes, yet the mechanisms causing disease are unknown. We demonstrate that loss of NHE6 results in overacidification of the endosomal compartment and attenuated TrkB signaling. Mouse brains with disrupted NHE6 display reduced axonal and dendritic branching, synapse number, and circuit strength. Site-directed mutagenesis shows that the proton leak function of NHE6 is required for neuronal arborization. We find that TrkB receptor colocalizes to NHE6-associated endosomes. TrkB protein and phosphorylation are reduced in NHE6 mutant neurons in response to BDNF signaling. Finally, exogenous BDNF rescues defects in neuronal arborization. We propose that NHE6 mutation leads to circuit defects that are in part due to impoverished neuronal arborization that may be treatable by enhanced TrkB signaling.
C1 [Ouyang, Qing; Lizarraga, Sofia B.; Schmidt, Michael; Yang, Unikora; Gong, Jingyi; Ellisor, Debra; Morrow, Eric M.] Brown Univ, Dept Mol Biol, Mol Med Lab, Providence, RI 02903 USA.
[Ouyang, Qing; Lizarraga, Sofia B.; Schmidt, Michael; Yang, Unikora; Gong, Jingyi; Ellisor, Debra; Morrow, Eric M.] Brown Univ, Dept Cell Biol, Mol Med Lab, Providence, RI 02903 USA.
[Ouyang, Qing; Lizarraga, Sofia B.; Schmidt, Michael; Yang, Unikora; Gong, Jingyi; Ellisor, Debra; Morrow, Eric M.] Brown Univ, Dept Biochem, Mol Med Lab, Providence, RI 02903 USA.
[Ouyang, Qing; Lizarraga, Sofia B.; Schmidt, Michael; Yang, Unikora; Gong, Jingyi; Ellisor, Debra; Morrow, Eric M.] Brown Univ, Inst Brain Sci, Mol Med Lab, Providence, RI 02903 USA.
[Kauer, Julie A.] Brown Univ, Dept Mol Pharmacol Physiol & Biotechnol, Providence, RI 02912 USA.
[Kauer, Julie A.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
[Morrow, Eric M.] Brown Univ, Sch Med, Emma Pendleton Bradley Hosp, Dev Disorders Genet Res Program, East Providence, RI 02915 USA.
[Morrow, Eric M.] Brown Univ, Sch Med, Dept Psychiat & Human Behav, East Providence, RI 02915 USA.
RP Morrow, EM (reprint author), Brown Univ, Dept Mol Biol, Mol Med Lab, 70 Ship St, Providence, RI 02903 USA.
EM eric_morrow@brown.edu
FU Career Award in Medical Science; Burroughs Wellcome Fund; NIH NIGMS
COBRE [8P20GM103537-10]; NIH [5T32MH019118-21]; Simons Foundation [SFARI
239834]; Nancy Lurie Marks Foundation
FX We thank Dr. Robbed Creton at Brown University Leduc Bioimaging Facility
for advice regarding microscopy and Dr. Peter Davies for the kind gift
of Phospho-Tau1 antibody. E.M.M. has received support from Career Award
in Medical Science, Burroughs Wellcome Fund, and NIH NIGMS COBRE
8P20GM103537-10. S.B.L. has received support from NIH 5T32MH019118-21.
This work was supported by a grant from the Simons Foundation (SFARI
239834 to E.M.M.) and also generous support to E.M.M. from the Nancy
Lurie Marks Foundation.
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NR 44
TC 13
Z9 13
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD OCT 2
PY 2013
VL 80
IS 1
BP 97
EP 112
DI 10.1016/j.neuron.2013.07.043
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 243GQ
UT WOS:000326305300011
PM 24035762
ER
PT J
AU Pettem, KL
Yokomaku, D
Luo, L
Linhoff, MW
Prasad, T
Connor, SA
Siddiqui, TJ
Kawabe, H
Chen, F
Zhang, L
Rudenko, G
Wang, YT
Brose, N
Craig, AM
AF Pettem, Katherine L.
Yokomaku, Daisaku
Luo, Lin
Linhoff, Michael W.
Prasad, Tuhina
Connor, Steven A.
Siddiqui, Tabrez J.
Kawabe, Hiroshi
Chen, Fang
Zhang, Ling
Rudenko, Gabby
Wang, Yu Tian
Brose, Nils
Craig, Ann Marie
TI The Specific alpha-Neurexin Interactor Calsyntenin-3 Promotes Excitatory
and Inhibitory Synapse Development
SO NEURON
LA English
DT Article
ID PROTEIN-TYROSINE PHOSPHATASES; MEMBRANE-PROTEINS; AXONAL-TRANSPORT; CA2+
CHANNELS; PTP-SIGMA; NEUROLIGINS; AUTISM; FAMILY; DELETIONS; SPECTRUM
AB Perturbations of cell surface synapse-organizing proteins, particularly alpha-neurexins, contribute to neurodevelopmental and psychiatric disorders. From an unbiased screen, we identify calsyntenin-3 (alcadein-beta) as a synapse-organizing protein unique in binding and recruiting alpha-neurexins, but not beta-neurexins. Calsyntenin-3 is present in many pyramidal neurons throughout cortex and hippocampus but is most highly expressed in interneurons. The transmembrane form of calsyntenin-3 can trigger excitatory and inhibitory presynapse differentiation in contacting axons. However, calsyntenin-3-shed ectodomain, which represents about half the calsyntenin-3 pool in brain, suppresses the ability of multiple alpha-neurexin partners including neuroligin 2 and LRRTM2 to induce presynapse differentiation. Cistn3(-/-) mice show reductions in excitatory and inhibitory synapse density by confocal and electron microscopy and corresponding deficits in synaptic transmission. These results identify calsyntenin-3 as an alpha-neurexin-specific binding partner required for normal functional GABAergic and glutamatergic synapse development.
C1 [Pettem, Katherine L.; Yokomaku, Daisaku; Luo, Lin; Linhoff, Michael W.; Prasad, Tuhina; Connor, Steven A.; Siddiqui, Tabrez J.; Zhang, Ling; Wang, Yu Tian; Craig, Ann Marie] Univ British Columbia, Brain Res Ctr, Vancouver, BC V6T 2B5, Canada.
[Pettem, Katherine L.; Yokomaku, Daisaku; Luo, Lin; Linhoff, Michael W.; Prasad, Tuhina; Connor, Steven A.; Siddiqui, Tabrez J.; Craig, Ann Marie] Univ British Columbia, Dept Psychiat, Vancouver, BC V6T 2B5, Canada.
[Connor, Steven A.; Zhang, Ling; Wang, Yu Tian] Univ British Columbia, Dept Med, Vancouver, BC V6T 2B5, Canada.
[Kawabe, Hiroshi; Brose, Nils] Max Planck Inst Expt Med, Dept Mol Neurobiol, D-37075 Gottingen, Germany.
[Chen, Fang; Rudenko, Gabby] Univ Michigan, Life Sci Inst, Ann Arbor, MI 48109 USA.
[Chen, Fang; Rudenko, Gabby] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA.
RP Craig, AM (reprint author), Univ British Columbia, Brain Res Ctr, Vancouver, BC V6T 2B5, Canada.
EM acraig@mail.ubc.ca
RI Craig, Ann Marie/M-2054-2014
FU National Institutes of Health [MH070860, MH077303]; Canada Research
Chair salary award; Natural Sciences and Engineering Research Council of
Canada Postgraduate Scholarship; Michael Smith Foundation for Health
Research Fellowships; German Research Foundation [SPP1365/KA3423/1-1];
Fritz Thyssen Foundation
FX We thank Xiling Zhou and Nazarine Fernandes for excellent technical
assistance, Vivian Lam and Sarah Au-Yeung for contributions for the
western blot analysis, Fergil Mills and Dr. Shernaz Bamji for
experimental advice and Derrick Home and Bradford Ross of the Bioimaging
Facility for technical assistance with electron microscopy, Michiko
Takeda for contributions to mouse colony management, Mika Kishimoto-Suga
for experimental advice with antibody generation, and Dr. Robert Holt
and team at the Michael Smith Genome Sciances Centre for arraying the
cDNA subpool and preparing DNA in 384-well format. This work was
supported by the National Institutes of Health (MH070860) and Canada
Research Chair salary award to A.M.C., a Natural Sciences and
Engineering Research Council of Canada Postgraduate Scholarship to
K.L.P., Michael Smith Foundation for Health Research Fellowships to
K.L.P. and T.J.S., the German Research Foundation (SPP1365/KA3423/1-1)
to H.K, and N.B., the Fritz Thyssen Foundation to H.K., and the National
Institutes of Health (MH077303) to G.R.
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NR 55
TC 10
Z9 10
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
EI 1097-4199
J9 NEURON
JI Neuron
PD OCT 2
PY 2013
VL 80
IS 1
BP 113
EP 128
DI 10.1016/j.neuron.2013.07.016
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 243GQ
UT WOS:000326305300012
PM 24094106
ER
PT J
AU Duerden, EG
Taylor, MJ
Soorya, LV
Wang, T
Fan, J
Anagnostou, E
AF Duerden, Emma G.
Taylor, Margot J.
Soorya, Latha V.
Wang, Ting
Fan, Jin
Anagnostou, Evdokia
TI Neural correlates of inhibition of socially relevant stimuli in adults
with autism spectrum disorder
SO BRAIN RESEARCH
LA English
DT Article
DE Autism; Emotion; Executive functioning; Brain; MRI; Human
ID HIGH-FUNCTIONING AUTISM; DORSOLATERAL PREFRONTAL CORTEX; INFERIOR
FRONTAL-CORTEX; RESPONSE-INHIBITION; EXECUTIVE FUNCTION; DELAYED
ALTERNATION; FACIAL EXPRESSIONS; ASPERGERS-DISORDER; BEHAVIORAL-CONTROL;
COGNITIVE CONTROL
AB Adults with autism spectrum disorder (ASD) can demonstrate difficulties with inhibiting inappropriate social responses. Presently, little research has utilized socially relevant stimuli to explore the modulatory effects of emotion on cognitive control in this population. To assess neural mechanisms of inhibiting social stimuli, we presented images of happy or sad facial expressions in a Go/NoGo task to unrnedicated adults with ASD and to controls during functional magnetic resonance imaging (fMRI). Groups did not differ on behavioral measures. Brain activation in response to NoGo vs. Go trials revealed differing regional patterns of activation within groups. Controls recruited brain regions involved in inhibition (dorsal- [DLPFC] and ventro-lateral prefrontal cortices [VLPFC], anterior cingulate cortex [ACC]), response suppression (parietal lobe), interoceptive awareness (insula), and also the fusiform and middle temporal gyri. Adults with ASD only recruited the VLPFC and right fusiform gyrus, and weakly activated the ACC and insula. Between-group comparisons indicated that controls activated the DLPFC, while adults with ASD relied on the VLPFC and the fusiform gyrus to inhibit responses. Adults with ASD may have relied more on visual association cortex, possibly as a means of recruiting additional neural processes that could act as a compensatory mechanism. (C) 2013 Elsevier B.V. All rights reserved.
C1 [Duerden, Emma G.; Taylor, Margot J.] Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada.
[Anagnostou, Evdokia] Bloorview Res Inst, Toronto, ON, Canada.
[Taylor, Margot J.; Anagnostou, Evdokia] Univ Toronto, Toronto, ON, Canada.
[Wang, Ting; Fan, Jin] Mt Sinai Sch Med, Seaver Autism Ctr Res & Treatment, New York, NY USA.
[Soorya, Latha V.] Rush Univ, Chicago, IL 60612 USA.
RP Duerden, EG (reprint author), Hosp Sick Children, Dept Diagnost Imaging, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM emma.duerden@sickkids.ca
FU Seaver Foundation; Research Training Competition Fellowship from the
Hospital for Sick Children; Reva Gerstein Fellowship in Pediatric
Psychology; Holland Bloorview Kids Rehabilitation Foundation
FX The authors would like to acknowledge the Seaver Foundation (EA), for
providing primary funding for this study. Additionally, support during
the data analysis and manuscript preparation process was provided by
Research Training Competition Fellowship from the Hospital for Sick
Children (ED), a Reva Gerstein Fellowship in Pediatric Psychology (ED)
and the Holland Bloorview Kids Rehabilitation Foundation (EA).
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NR 90
TC 7
Z9 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
EI 1872-6240
J9 BRAIN RES
JI Brain Res.
PD OCT 2
PY 2013
VL 1533
BP 80
EP 90
DI 10.1016/j.brainres.2013.08.021
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 233UL
UT WOS:000325594900009
PM 23962468
ER
PT J
AU Duffney, LJ
Wei, J
Cheng, J
Liu, WH
Smith, KR
Kittler, JT
Yan, Z
AF Duffney, Lara J.
Wei, Jing
Cheng, Jia
Liu, Wenhua
Smith, Katharine R.
Kittler, Josef T.
Yan, Zhen
TI Shank3 Deficiency Induces NMDA Receptor Hypofunction via an
Actin-Dependent Mechanism
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID RHO FAMILY GTPASES; POSTSYNAPTIC DENSITY PROTEINS; SMALL-MOLECULE
INHIBITOR; AUTISTIC-LIKE BEHAVIORS; DENDRITIC SPINES; P21-ACTIVATED
KINASE; MENTAL-RETARDATION; PREFRONTAL CORTEX; ALPHA-ACTININ;
GLUTAMATERGIC TRANSMISSION
AB Shank3, which encodes a scaffolding protein at glutamatergic synapses, is a genetic risk factor for autism. In this study, we examined the impact of Shank3 deficiency on the NMDA-type glutamate receptor, a key player in cognition and mental illnesses. We found that knockdown of Shank3 with a small interfering RNA (siRNA) caused a significant reduction of NMDAR-mediated ionic or synaptic current, as well as the surface expression of NR1 subunits, in rat cortical cultures. The effect of Shank3 siRNA on NMDAR currents was blocked by an actin stabilizer, and was occluded by an actin destabilizer, suggesting the involvement of actin cytoskeleton. Since actin dynamics is regulated by the GTPase Rac1 and downstream effector p21-activated kinase (PAK), we further examined Shank3 regulation of NMDARs when Rac1 or PAK was manipulated. We found that the reducing effect of Shank3 siRNA on NMDAR currents was mimicked and occluded by specific inhibitors for Rac1 or PAK, and was blocked by constitutively active Rac1 or PAK. Immunocytochemical data showed a strong reduction of F-actin clusters after Shank3 knockdown, which was occluded by a PAK inhibitor. Inhibiting cofilin, the primary downstream target of PAK and a major actin depolymerizing factor, prevented Shank3 siRNA from reducing NMDAR currents and F-actin clusters. Together, these results suggest that Shank3 deficiency induces NMDAR hypofunction by interfering with the Rac1/PAK/cofilin/actin signaling, leading to the loss of NMDAR membrane delivery or stability. It provides a potential mechanism for the role of Shank3 in cognitive deficit in autism.
C1 [Duffney, Lara J.; Wei, Jing; Cheng, Jia; Liu, Wenhua; Yan, Zhen] SUNY Buffalo, Sch Med & Biomed Sci, Dept Physiol & Biophys, Buffalo, NY 14214 USA.
[Smith, Katharine R.; Kittler, Josef T.] UCL, Dept Neurosci Physiol & Pharmacol, London WC1E 6BT, England.
RP Yan, Z (reprint author), SUNY Buffalo, Dept Physiol & Biophys, 124 Sherman Hall, Buffalo, NY 14214 USA.
EM zhenyan@buffalo.edu
RI Kittler, Josef/E-9113-2010
FU NIH [R01-MH085774, R21-MH101690]
FX This work was supported by NIH Grants (R01-MH085774 and R21-MH101690) to
Z.Y. We thank Xiaoqing Chen for her excellent technical support. We
thank Drs. Carlo Sala and Eunjoon Kim for providing Shank3 plasmids.
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NR 86
TC 9
Z9 12
PU SOC NEUROSCIENCE
PI WASHINGTON
PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA
SN 0270-6474
J9 J NEUROSCI
JI J. Neurosci.
PD OCT 2
PY 2013
VL 33
IS 40
BP 15767
EP 15778
DI 10.1523/JNEUROSCI.1175-13.2013
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 229RA
UT WOS:000325283600011
PM 24089484
ER
PT J
AU Shi, JX
Li, P
AF Shi, Jianxin
Li, Peng
TI TESTING ASSOCIATIONS OF COPY NUMBER VARIATIONS IN GENOME-WIDE
ASSOCIATION STUDIES
SO STATISTICA SINICA
LA English
DT Article
DE Copy number variation; family-based study; genome-wide association
study; Hidden Markov Model; TDT
ID HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA; SEGMENTATION; IMPUTATION
AB Copy number variations (CNVs) are a major source of genetic variation in humans. In large-scale genome-wide association studies (GWAS), CNVs have been detected from the intensity data generated by SNP genotyping arrays and then tested for association. This strategy lacks statistical power for detecting associations with short CNVs. In this article, we propose methods for testing the association for each probe, based on a Hidden Markov Model that leverages information from nearby probes in the same CNV region. Our methods do not require specifying CNV regions, are convenient for genome-wide scan data, and work for both population-based and family-based studies. Through simulation studies, we found that loss of efficiency due to CNV calling uncertainty was very small even for short CNVs covering as few as four probes in case-control studies. The efficiency loss was larger for short CNVs in family studies. We applied our methods to a large family-based GWAS of autism in 831 trios, and identified a genomic region on chromosome 17q22 harboring deletions that may contribute to the disease risk. Our methods are computationally efficient, requiring only two hours to analyze the genome-wide intensity data of all trios using a single Linux core.
C1 [Shi, Jianxin; Li, Peng] NCI, Div Canc Epidemiol & Genet, Biostat Branch, Rockville, MD 20852 USA.
RP Shi, JX (reprint author), NCI, Div Canc Epidemiol & Genet, Biostat Branch, 6120 Executive Blvd,RM8040, Rockville, MD 20852 USA.
EM Jianxin.Shi@nih.gov; lip4@mail.nih.gov
FU Intramural Research Program, Division of Cancer Epidemiology and
Genetics, National Cancer Institute at the National Institutes of Health
FX The authors are supported by the Intramural Research Program, Division
of Cancer Epidemiology and Genetics, National Cancer Institute at the
National Institutes of Health. This study utilized the high-performance
computational capabilities of the Biowulf Linux cluster at the National
Institutes of Health, Bethesda, Md. (http://biowulf.nih.gov).
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PU STATISTICA SINICA
PI TAIPEI
PA C/O DR H C HO, INST STATISTICAL SCIENCE, ACADEMIA SINICA, TAIPEI 115,
TAIWAN
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EI 1996-8507
J9 STAT SINICA
JI Stat. Sin.
PD OCT
PY 2013
VL 23
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SI SI
BP 1463
EP 1477
DI 10.5705/ss.2012.071s
PG 15
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SC Mathematics
GA AL4SU
UT WOS:000339125900003
ER
PT J
AU James, WH
AF James, William H.
TI Studies of Human Sex Ratios at Birth May Lead to the Understanding of
Several Forms of Pathology
SO HUMAN BIOLOGY
LA English
DT Review
DE HUMAN SEX RATIO; PATHOLOGY; HORMONAL HYPOTHESIS; BAYESIAN NETWORKS;
OBSTETRIC PATHOLOGIES; HEPATITIS B; AUTISM; TESTICULAR CANCER;
SEX-BIASED MALFORMATIONS; MANNING FINGER LENGTH RATIO
ID 4TH DIGIT RATIO; PARENTAL HORMONE-LEVELS; HEPATITIS-B-VIRUS; LATENT
ASYMPTOMATIC TOXOPLASMOSIS; AUTISM SPECTRUM DISORDERS; SELECTION
IN-UTERO; TESTICULAR CANCER; MAMMALIAN SEX; SERUM TESTOSTERONE; CYCLE
DAY
AB This article deals with the problem of the causes of the variation of sex ratio (proportion male) at birth. This problem is common to a number of areas in biology and medicine, for example, obstetrics, neurology/psychiatry, parasitology, virology, oncology, and teratology. It is established that there are significantly biased, but unexplained, sex ratios in each of these fields. Yet workers in them (with the possible exception of virology) have regarded the problem as a minor loose end, irrelevant to the field's major problems. However, as far as I know, no one has previously noted that unexplained biased sex ratios occur, and thus pose (perhaps similar) problems, in all these fields. Here it is suggested that similar sorts of solutions apply in each. Further research is proposed for testing each solution. If the argument here is substantially correct across this range of topics, it may lead to an improved understanding not only of sex ratio but also of some of the pathologies in these specialties.
C1 UCL, Dept Genet Evolut & Environm, London WC1E 6BT, England.
RP James, WH (reprint author), UCL, Dept Genet Evolut & Environm, Gower St, London WC1E 6BT, England.
EM w.james@ucl.ac.uk
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NR 125
TC 1
Z9 1
PU WAYNE STATE UNIV PRESS
PI DETROIT
PA 4809 WOODWARD AVE, DETROIT, MI 48201-1309 USA
SN 0018-7143
EI 1534-6617
J9 HUM BIOL
JI Hum. Biol.
PD OCT
PY 2013
VL 85
IS 5
BP 769
EP 787
PG 19
WC Anthropology; Biology; Genetics & Heredity
SC Anthropology; Life Sciences & Biomedicine - Other Topics; Genetics &
Heredity
GA AJ2QO
UT WOS:000337504300008
PM 25078960
ER
PT J
AU Berard, A
Sheehy, O
Boukris, T
AF Berard, Anick
Sheehy, Odile
Boukris, Takoua
TI Relation between the Prevalence of Attention Deficit and Hyperactivity
Disorders (ADHD) and Autism Spectrum Disorders (ASD), and Maternal
Depression and Antidepressant Use during Pregnancy
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
C1 [Berard, Anick; Boukris, Takoua] Univ Montreal, Fac Pharm, Montreal, PQ H3C 3J7, Canada.
[Berard, Anick; Boukris, Takoua] Univ Montreal, CHU Ste Justine, Montreal, PQ H3C 3J7, Canada.
[Sheehy, Odile] CHU Ste Justine, Res Ctr, Montreal, PQ, Canada.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD OCT
PY 2013
VL 22
SU 1
SI SI
MA 345
BP 167
EP 167
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AF7EJ
UT WOS:000334876100322
ER
PT J
AU Sirois, C
Gascon, H
Faubert, M
Gagnon, ME
AF Sirois, Caroline
Gascon, Hubert
Faubert, Mirella
Gagnon, Marie-Eve
TI Use of Medication by Young People with Autism-Spectrum Disorders in
Quebec
SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY
LA English
DT Meeting Abstract
C1 [Sirois, Caroline; Faubert, Mirella; Gagnon, Marie-Eve] Univ Quebec Rimouski, Dept Nursing, Levis, PQ, Canada.
[Gascon, Hubert] Univ Quebec Rimouski, Dept Educ, Levis, PQ, Canada.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1053-8569
EI 1099-1557
J9 PHARMACOEPIDEM DR S
JI Pharmacoepidemiol. Drug Saf.
PD OCT
PY 2013
VL 22
SU 1
SI SI
MA 1036
BP 516
EP 516
PG 1
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA AF7EJ
UT WOS:000334876102141
ER
PT J
AU Egiebor, E
Tulu, A
Abou-Zeid, N
Aighewi, IT
Ishaque, A
AF Egiebor, Egbe
Tulu, Adam
Abou-Zeid, Nadia
Aighewi, Isoken Tito
Ishaque, Ali
TI The Kinetic Signature of Toxicity of Four Heavy Metals and Their
Mixtures on MCF7 Breast Cancer Cell Line
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Article
DE heavy metals; real time electronic cell sensing; glutathione;
L-buthionine sulphoximine
ID MITOCHONDRIAL DYSFUNCTION; CARCINOMA-CELLS; GLUTATHIONE; CYTOTOXICITY;
MECHANISMS; CADMIUM; APOPTOSIS; STRESS; LEAD
AB This study evaluated the kinetic signature of toxicity of four heavy metals known to cause severe health and environmental issues-cadmium (Cd), mercury (Hg) lead (Pb) arsenic (As)-and the mixture of all four metals (Mix) on MCF7 cancer cells, in the presence and absence of the antioxidant glutathione (GSH). The study was carried out using real time cell electronic sensing (RT-CES). RT-CES monitors in real time the electrical impedance changes at the electrode/culture medium interface due to the number of adhered cells, which is used as an index of cell viability. Cells were seeded for 24 h before exposure to the metals and their mixtures. The results showed that in the presence and absence of cellular glutathione, arsenic was the most cytotoxic of all five treatments, inducing cell death after 5 h of exposure. Lead was the least cytotoxic in both scenarios. In the presence of cellular GSH, the cytotoxic trend was As > Cd > MIX > Hg > Pb, while in the absence of GSH, the cytotoxic trend was As > Hg > MIX > Cd > Pb. The findings from this study indicate the significance of glutathione-mediated toxicity of the metals examined-particularly for mercury-and may be clinically relevant for disorders such as autism spectrum disorder where decreased glutathione-based detoxification capacity is associated with increased mercury intoxication.
C1 [Egiebor, Egbe; Tulu, Adam; Abou-Zeid, Nadia; Ishaque, Ali] Univ Maryland Eastern Shore, Dept Nat Sci, Princess Anne, MD 21853 USA.
[Aighewi, Isoken Tito] Benedict Coll, Dept Biol Chem & Environm Hlth Sci, Columbia, SC 29204 USA.
RP Ishaque, A (reprint author), Univ Maryland Eastern Shore, Dept Nat Sci, Princess Anne, MD 21853 USA.
EM honeyspringsbv@yahoo.com; adamtulu@yahoo.com; nzeid06@yahoo.com;
aighewii@benedict.edu; abishaque@mail.umes.edu
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NR 19
TC 2
Z9 2
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD OCT
PY 2013
VL 10
IS 10
BP 5209
EP 5220
DI 10.3390/ijerph10105209
PG 12
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA 301GJ
UT WOS:000330520500041
PM 24157516
ER
PT J
AU Addae, C
Cheng, H
Martinez-Ceballos, E
AF Addae, Cynthia
Cheng, Henrique
Martinez-Ceballos, Eduardo
TI Effect of the Environmental Pollutant Hexachlorobenzene (HCB) on the
Neuronal Differentiation of Mouse Embryonic Stem Cells
SO INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
LA English
DT Article
DE hexachlorobenzene; retinoid acid; reactive oxygen species; antioxidant;
environmental pollutant; GABAergic; encapsulation; embryonic stem cells;
autism; ADD
ID OXIDATIVE STRESS; GROWTH-FACTORS; RAT; EXPOSURE; GENOTOXICITY;
ACTIVATION; APOPTOSIS; PATHWAYS; THERAPY; DISEASE
AB Exposure to persistent environmental pollutants may constitute an important factor on the onset of a number of neurological disorders such as autism, Parkinson's disease, and Attention Deficit Disorder (ADD), which have also been linked to reduced GABAergic neuronal function. GABAergic neurons produce gamma-aminobutyric acid (GABA), which is the main inhibitory neurotransmitter in the brain. However, the lack of appropriate models has hindered the study of suspected environmental pollutants on GABAergic function. In this work, we have examined the effect of hexachlorobenzene (HCB), a persistent and bioaccumulative environmental pollutant, on the function and morphology of GABAergic neurons generated in vitro from mouse embryonic stem (ES) cells. We observed that: (1) treatment with 0.5 nM HCB did not affect cell viability, but affected the neuronal differentiation of ES cells; (2) HCB induced the production of reactive oxygen species (ROS); and (3) HCB repressed neurite outgrowth in GABAergic neurons, but this effect was reversed by the ROS scavenger N-acetylcysteine (NAC). Our study also revealed that HCB did not significantly interfere with the function of K+ ion channels in the neuronal soma, which indicates that this pollutant does not affect the maturation of the GABAergic neuronal soma. Our results suggest a mechanism by which environmental pollutants interfere with normal GABAergic neuronal function and may promote the onset of a number of neurological disorders such as autism and ADD.
C1 [Addae, Cynthia; Martinez-Ceballos, Eduardo] Southern Univ, Dept Biol Sci, Baton Rouge, LA 70813 USA.
[Addae, Cynthia; Martinez-Ceballos, Eduardo] Southern Univ, Environm Toxicol Program, Baton Rouge, LA 70813 USA.
[Addae, Cynthia; Martinez-Ceballos, Eduardo] A&M Coll, Baton Rouge, LA 70813 USA.
[Cheng, Henrique] Louisiana State Univ, Sch Vet Med, Dept Comparat Biomed Sci, Baton Rouge, LA 70803 USA.
RP Martinez-Ceballos, E (reprint author), Southern Univ, Dept Biol Sci, Baton Rouge, LA 70813 USA.
EM cynaddae@yahoo.com; hcheng@vetmed.lsu.edu; eduardo_martinez@sube.edu
FU Institutional Development Award (IDeA) from the National Institute of
General Medical Sciences of the National Institutes of Health
[P20GM103424]
FX Research reported in this publication was supported by an Institutional
Development Award (IDeA) from the National Institute of General Medical
Sciences of the National Institutes of Health under grant number
P20GM103424.
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NR 31
TC 1
Z9 1
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1660-4601
J9 INT J ENV RES PUB HE
JI Int. J. Environ. Res. Public Health
PD OCT
PY 2013
VL 10
IS 10
BP 5244
EP 5256
DI 10.3390/ijerph10105244
PG 13
WC Environmental Sciences
SC Environmental Sciences & Ecology
GA 301GJ
UT WOS:000330520500044
PM 24157519
ER
PT J
AU Rawal, N
Saft, A
Malkani, A
Zawahir, S
Kader, H
Watkins, R
Blanchard, S
AF Rawal, Nidhi
Saft, Anca
Malkani, Anjali
Zawahir, Shamila
Kader, Howard
Watkins, Runa
Blanchard, Samra
TI A Systematic Review of Gluten-free, Casein-free Diet and Autism: What Do
We Know? Presidential Poster
SO AMERICAN JOURNAL OF GASTROENTEROLOGY
LA English
DT Meeting Abstract
CT 78th Annual Scientific Meeting of the
American-College-of-Gastroenterology
CY OCT 11-16, 2013
CL San Diego, CA
SP Amer Coll Gastroenterol
C1 [Rawal, Nidhi; Saft, Anca; Malkani, Anjali; Zawahir, Shamila; Kader, Howard; Watkins, Runa; Blanchard, Samra] Univ Maryland, Baltimore, MD 21201 USA.
NR 0
TC 0
Z9 0
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0002-9270
EI 1572-0241
J9 AM J GASTROENTEROL
JI Am. J. Gastroenterol.
PD OCT
PY 2013
VL 108
SU 1
MA 2052
BP S623
EP S623
PG 1
WC Gastroenterology & Hepatology
SC Gastroenterology & Hepatology
GA 296II
UT WOS:000330178102379
ER
PT J
AU Bauer, NS
Sturm, LA
Carroll, AE
Downs, SM
AF Bauer, Nerissa S.
Sturm, Lynne A.
Carroll, Aaron E.
Downs, Stephen M.
TI Computer Decision Support to Improve Autism Screening and Care in
Community Pediatric Clinics
SO INFANTS & YOUNG CHILDREN
LA English
DT Article
DE access and evaluation; autism; computerized; health care quality;
medical informatics; medical record systems; primary health care
ID SPECTRUM DISORDER; AMERICAN-ACADEMY; CHICA SYSTEM; CHILDREN; QUALITY;
IMPLEMENTATION; IDENTIFICATION; GUIDELINES; MANAGEMENT; TODDLERS
AB An autism module was added to an existing computer decision support system (CDSS) to facilitate adherence to recommended guidelines for screening for autism spectrum disorders in primary care pediatric clinics. User satisfaction was assessed by survey and informal feedback at monthly meetings between clinical staff and the software team. To assess outcomes, such as changes in identification and referrals, we reviewed data captured from the CDSS. Between November 15, 2010 and July 26, 2012, 857 patients were eligible for screening. Of these, 66% (567/857) were screened as determined by the number of forms scanned into the system, of which 30% (171/567) had concerning Modified Checklist for Autism in Toddlers. However, pediatricians failed to respond to alerts for 73 children. Of the remaining 98 children, pediatricians felt 50 (68%) did not have an Autism spectrum disorder, 23 (32%) were referred for autism evaluation, eight (11%) were suspected but not referred and two (3%) were referred for audiology. Seventy percent of all users agreed that automation of the screening process helped them to adhere to recommended guidelines. Automating autism care into a CDSS resulted in moderate adherence to guidelines. Health information technology can facilitate the implementation of autism guidelines in busy pediatric clinics.
C1 [Bauer, Nerissa S.; Sturm, Lynne A.; Carroll, Aaron E.; Downs, Stephen M.] Indiana Univ Sch Med, Dept Gen & Community Pediat, Indianapolis, IN 46202 USA.
[Bauer, Nerissa S.; Carroll, Aaron E.; Downs, Stephen M.] Indiana Univ Sch Med, Sect Childrens Hlth Serv Res, Indianapolis, IN 46202 USA.
RP Bauer, NS (reprint author), Indiana Univ Sch Med, Dept Gen & Community Pediat, 410 W 10th St,Suite 1000, Indianapolis, IN 46202 USA.
EM nsbauer@iupui.edu
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NR 38
TC 1
Z9 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0896-3746
EI 1550-5081
J9 INFANT YOUNG CHILD
JI Infants Young Child.
PD OCT-DEC
PY 2013
VL 26
IS 4
BP 306
EP 317
DI 10.1097/IYC.0b013e3182a4ec5e
PG 12
WC Education, Special; Psychology, Developmental; Rehabilitation
SC Education & Educational Research; Psychology; Rehabilitation
GA 299CK
UT WOS:000330372400004
ER
PT J
AU Lee, TY
Lin, FY
AF Lee, Tzu-Ying
Lin, Fang-Yi
TI Taiwanese Parents' Perceptions of Their Very Low-Birth-Weight Infant
With Developmental Disabilities
SO JOURNAL OF PERINATAL & NEONATAL NURSING
LA English
DT Article
DE developmental disability; infant; parent; Taiwan; very low-birth-weight
ID QUALITATIVE CONTENT-ANALYSIS; PREMATURE-INFANTS; YOUNG-CHILDREN;
MOTHERS; FAMILIES; CARE; EXPERIENCES; SERVICES; AUTISM; HEALTH
AB This study explores the perceptions and experiences of Taiwanese parents in coping with the unfolding evidence of a disability, their response to the official diagnosis, and their views about their child's developmental disability. This descriptive qualitative study is a partial analysis of data from a larger study including 19 Taiwanese parents of very low-birth-weight infants with developmental disability at 6 and 12 months of corrected age. Four themes were generated: uncertainty and worry about developmental progress, search for meaning and supernatural will, desire for normality and attitude toward services, and finding a balance point in family life and relationships. The parents of very low-birth-weight infants face uncertainty about developmental and other potential problems in the infant's early age. Adequate information related to infant development needs to be integrated into follow-up clinic and early intervention services. Early intervention programs should not only focus on the needs of these infants but also provide support and care to the whole family. Understanding parental beliefs and values toward developmental disabilities can help neonatal and pediatric professionals to provide optimal early intervention to these families.
C1 [Lee, Tzu-Ying; Lin, Fang-Yi] Natl Taipei Univ Nursing & Hlth Sci, Sch Nursing, Taipei 11219, Taiwan.
RP Lee, TY (reprint author), Natl Taipei Univ Nursing & Hlth Sci, Sch Nursing, 365 Ming Te Rd, Taipei 11219, Taiwan.
EM tzuying@ntunhs.edu.tw
FU National Science Council in Taiwan [NSC 94-2516-S-227-002]
FX Funded by the National Science Council in Taiwan (NSC
94-2516-S-227-002).
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Volpe JJ, 2003, PEDIATRICS, V112, P176, DOI 10.1542/peds.112.1.176
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NR 45
TC 0
Z9 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0893-2190
EI 1550-5073
J9 J PERINAT NEONAT NUR
JI J. Perinat. Neonatal Nurs.
PD OCT-DEC
PY 2013
VL 27
IS 4
BP 345
EP 352
DI 10.1097/JPN.0b013e3182a98408
PG 8
WC Nursing; Obstetrics & Gynecology; Pediatrics
SC Nursing; Obstetrics & Gynecology; Pediatrics
GA 300HG
UT WOS:000330454400011
PM 24164817
ER
PT J
AU Kutchko, KM
Frohlich, F
AF Kutchko, Katrina M.
Froehlich, Flavio
TI Emergence of Metastable State Dynamics in Interconnected Cortical
Networks with Propagation Delays
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID TRANSCRANIAL ELECTRICAL-STIMULATION; ALTERNATING-CURRENT STIMULATION;
HIGH-FREQUENCY OSCILLATIONS; FUNCTIONAL CONNECTIVITY; BRAIN-STIMULATION;
CORPUS-CALLOSUM; SPIKING NEURONS; VISUAL-CORTEX; SCHIZOPHRENIA;
SYNCHRONY
AB The importance of the large number of thin-diameter and unmyelinated axons that connect different cortical areas is unknown. The pronounced propagation delays in these axons may prevent synchronization of cortical networks and therefore hinder efficient information integration and processing. Yet, such global information integration across cortical areas is vital for higher cognitive function. We hypothesized that delays in communication between cortical areas can disrupt synchronization and therefore enhance the set of activity trajectories and computations interconnected networks can perform. To evaluate this hypothesis, we studied the effect of long-range cortical projections with propagation delays in interconnected large-scale cortical networks that exhibited spontaneous rhythmic activity. Long-range connections with delays caused the emergence of metastable, spatio-temporally distinct activity states between which the networks spontaneously transitioned. Interestingly, the observed activity patterns correspond to macroscopic network dynamics such as globally synchronized activity, propagating wave fronts, and spiral waves that have been previously observed in neurophysiological recordings from humans and animal models. Transient perturbations with simulated transcranial alternating current stimulation (tACS) confirmed the multistability of the interconnected networks by switching the networks between these metastable states. Our model thus proposes that slower long-range connections enrich the landscape of activity states and represent a parsimonious mechanism for the emergence of multistability in cortical networks. These results further provide a mechanistic link between the known deficits in connectivity and cortical state dynamics in neuropsychiatric illnesses such as schizophrenia and autism, as well as suggest non-invasive brain stimulation as an effective treatment for these illnesses.
C1 [Kutchko, Katrina M.; Froehlich, Flavio] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27515 USA.
[Kutchko, Katrina M.; Froehlich, Flavio] Univ N Carolina, Curriculum Bioinformat & Computat Biol, Chapel Hill, NC USA.
[Froehlich, Flavio] Univ N Carolina, Dept Cell Biol & Physiol, Chapel Hill, NC USA.
[Froehlich, Flavio] Univ N Carolina, Dept Biomed Engn, Chapel Hill, NC USA.
[Froehlich, Flavio] Univ N Carolina, Ctr Neurosci, Chapel Hill, NC USA.
RP Kutchko, KM (reprint author), Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27515 USA.
EM flavio_frohlich@med.unc.edu
FU UNC Department of Psychiatry; UNC School of Medicine; Foundation of Hope
FX This work was supported by the UNC Department of Psychiatry, UNC School
of Medicine, and the Foundation of Hope. The funders had no role in
study design, data collection and analysis, decision to publish, or
preparation of the manuscript.
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NR 83
TC 6
Z9 6
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD OCT
PY 2013
VL 9
IS 10
AR e1003304
DI 10.1371/journal.pcbi.1003304
PG 15
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 298WN
UT WOS:000330355300053
PM 24204238
ER
PT J
AU Lohrenz, T
Bhatt, M
Apple, N
Montague, PR
AF Lohrenz, Terry
Bhatt, Meghana
Apple, Nathan
Montague, P. Read
TI Keeping up with the Joneses: Interpersonal Prediction Errors and the
Correlation of Behavior in a Tandem Sequential Choice Task
SO PLOS COMPUTATIONAL BIOLOGY
LA English
DT Article
ID INFORMATION CASCADES; INVESTMENT TASK; CONFORMITY; MECHANISMS; STRIATUM;
DECISION; DISGUST; AUTISM; CORTEX; SIGNAL
AB In many settings, copying, learning from or assigning value to group behavior is rational because such behavior can often act as a proxy for valuable returns. However, such herd behavior can also be pathologically misleading by coaxing individuals into behaviors that are otherwise irrational and it may be one source of the irrational behaviors underlying market bubbles and crashes. Using a two-person tandem investment game, we sought to examine the neural and behavioral responses of herd instincts in situations stripped of the incentive to be influenced by the choices of one's partner. We show that the investments of the two subjects correlate over time if they are made aware of their partner's choices even though these choices have no impact on either player's earnings. We computed an "interpersonal prediction error", the difference between the investment decisions of the two subjects after each choice. BOLD responses in the striatum, implicated in valuation and action selection, were highly correlated with this interpersonal prediction error. The revelation of the partner's investment occurred after all useful information about the market had already been revealed. This effect was confirmed in two separate experiments where the impact of the time of revelation of the partner's choice was tested at 2 seconds and 6 seconds after a subject's choice; however, the effect was absent in a control condition with a computer partner. These findings strongly support the existence of mechanisms that drive correlated behavior even in contexts where there is no explicit advantage to do so.
C1 [Lohrenz, Terry; Bhatt, Meghana; Apple, Nathan; Montague, P. Read] Virginia Tech Carilion Res Inst, Roanoke, VA 24016 USA.
[Montague, P. Read] UCL, Wellcome Trust Ctr Neuroimaging, London, England.
RP Lohrenz, T (reprint author), Virginia Tech Carilion Res Inst, Roanoke, VA 24016 USA.
EM read@vt.edu
FU National Institutes of Health [1 RC4 AG039067, R01 DA11723, R01
MH085496, R01 DA030241]; Kane Foundation Fellowship; Wellcome Trust
FX This research was funded by the following grants: National Institutes of
Health grant # 1 RC4 AG039067, National Institutes of Health grant # R01
DA11723, National Institutes of Health grant # R01 MH085496, National
Institutes of Health grant # R01 DA030241, The Kane Foundation
Fellowship, and the Wellcome Trust. The funders had no role in the study
design, data collection and analysis, decision to publish or preparation
of the manuscript.
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NR 40
TC 2
Z9 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-734X
EI 1553-7358
J9 PLOS COMPUT BIOL
JI PLoS Comput. Biol.
PD OCT
PY 2013
VL 9
IS 10
AR e1003275
DI 10.1371/journal.pcbi.1003275
PG 8
WC Biochemical Research Methods; Mathematical & Computational Biology
SC Biochemistry & Molecular Biology; Mathematical & Computational Biology
GA 298WN
UT WOS:000330355300035
PM 24204226
ER
PT J
AU Davis, LK
Yu, DM
Keenan, CL
Gamazon, ER
Konkashbaev, AI
Derks, EM
Neale, BM
Yang, J
Lee, SH
Evans, P
Barr, CL
Bellodi, L
Benarroch, F
Berrio, GB
Bienvenu, OJ
Bloch, MH
Blom, RM
Bruun, RD
Budman, CL
Camarena, B
Campbell, D
Cappi, C
Silgado, JCC
Cath, DC
Cavallini, MC
Chavira, DA
Chouinard, S
Conti, DV
Cook, EH
Coric, V
Cullen, BA
Deforce, D
Delorme, R
Dion, Y
Edlund, CK
Egberts, K
Falkai, P
Fernandez, TV
Gallagher, PJ
Garrido, H
Geller, D
Girard, SL
Grabe, HJ
Grados, MA
Greenberg, BD
Gross-Tsur, V
Haddad, S
Heiman, GA
Hemmings, SMJ
Hounie, AG
Illmann, C
Jankovic, J
Jenike, MA
Kennedy, JL
King, RA
Kremeyer, B
Kurlan, R
Lanzagorta, N
Leboyer, M
Leckman, JF
Lennertz, L
Liu, C
Lochner, C
Lowe, TL
Macciardi, F
McCracken, JT
McGrath, LM
Restrepo, SCM
Moessner, R
Morgan, J
Muller, H
Murphy, DL
Naarden, AL
Ochoa, WC
Ophoff, RA
Osiecki, L
Pakstis, AJ
Pato, MT
Pato, CN
Piacentini, J
Pittenger, C
Pollak, Y
Rauch, SL
Renner, TJ
Reus, VI
Richter, MA
Riddle, MA
Robertson, MM
Romero, R
Rosario, MC
Rosenberg, D
Rouleau, GA
Ruhrmann, S
Ruiz-Linares, A
Sampaio, AS
Samuels, J
Sandor, P
Sheppard, B
Singer, HS
Smit, JH
Stein, DJ
Strengman, E
Tischfield, JA
Duarte, AVV
Vallada, H
Van Nieuwerburgh, F
Veenstra-VanderWeele, J
Walitza, S
Wang, Y
Wendland, JR
Westenberg, HGM
Shugart, YY
Miguel, EC
McMahon, W
Wagner, M
Nicolini, H
Posthuma, D
Hanna, GL
Heutink, P
Denys, D
Arnold, PD
Oostra, BA
Nestadt, G
Freimer, NB
Pauls, DL
Wray, NR
Stewart, SE
Mathews, CA
Knowles, JA
Cox, NJ
Scharf, JM
AF Davis, Lea K.
Yu, Dongmei
Keenan, Clare L.
Gamazon, Eric R.
Konkashbaev, Anuar I.
Derks, Eske M.
Neale, Benjamin M.
Yang, Jian
Lee, S. Hong
Evans, Patrick
Barr, Cathy L.
Bellodi, Laura
Benarroch, Fortu
Berrio, Gabriel Bedoya
Bienvenu, Oscar J.
Bloch, Michael H.
Blom, Rianne M.
Bruun, Ruth D.
Budman, Cathy L.
Camarena, Beatriz
Campbell, Desmond
Cappi, Carolina
Silgado, Julio C. Cardona
Cath, Danielle C.
Cavallini, Maria C.
Chavira, Denise A.
Chouinard, Sylvain
Conti, David V.
Cook, Edwin H.
Coric, Vladimir
Cullen, Bernadette A.
Deforce, Dieter
Delorme, Richard
Dion, Yves
Edlund, Christopher K.
Egberts, Karin
Falkai, Peter
Fernandez, Thomas V.
Gallagher, Patience J.
Garrido, Helena
Geller, Daniel
Girard, Simon L.
Grabe, Hans J.
Grados, Marco A.
Greenberg, Benjamin D.
Gross-Tsur, Varda
Haddad, Stephen
Heiman, Gary A.
Hemmings, Sian M. J.
Hounie, Ana G.
Illmann, Cornelia
Jankovic, Joseph
Jenike, Michael A.
Kennedy, James L.
King, Robert A.
Kremeyer, Barbara
Kurlan, Roger
Lanzagorta, Nuria
Leboyer, Marion
Leckman, James F.
Lennertz, Leonhard
Liu, Chunyu
Lochner, Christine
Lowe, Thomas L.
Macciardi, Fabio
McCracken, James T.
McGrath, Lauren M.
Restrepo, Sandra C. Mesa
Moessner, Rainald
Morgan, Jubel
Muller, Heike
Murphy, Dennis L.
Naarden, Allan L.
Ochoa, William Cornejo
Ophoff, Roel A.
Osiecki, Lisa
Pakstis, Andrew J.
Pato, Michele T.
Pato, Carlos N.
Piacentini, John
Pittenger, Christopher
Pollak, Yehuda
Rauch, Scott L.
Renner, Tobias J.
Reus, Victor I.
Richter, Margaret A.
Riddle, Mark A.
Robertson, Mary M.
Romero, Roxana
Rosario, Maria C.
Rosenberg, David
Rouleau, Guy A.
Ruhrmann, Stephan
Ruiz-Linares, Andres
Sampaio, Aline S.
Samuels, Jack
Sandor, Paul
Sheppard, Brooke
Singer, Harvey S.
Smit, Jan H.
Stein, Dan J.
Strengman, E.
Tischfield, Jay A.
Duarte, Ana V. Valencia
Vallada, Homero
Van Nieuwerburgh, Filip
Veenstra-VanderWeele, Jeremy
Walitza, Susanne
Wang, Ying
Wendland, Jens R.
Westenberg, Herman G. M.
Shugart, Yin Yao
Miguel, Euripedes C.
McMahon, William
Wagner, Michael
Nicolini, Humberto
Posthuma, Danielle
Hanna, Gregory L.
Heutink, Peter
Denys, Damiaan
Arnold, Paul D.
Oostra, Ben A.
Nestadt, Gerald
Freimer, Nelson B.
Pauls, David L.
Wray, Naomi R.
Stewart, S. Evelyn
Mathews, Carol A.
Knowles, James A.
Cox, Nancy J.
Scharf, Jeremiah M.
TI Partitioning the Heritability of Tourette Syndrome and Obsessive
Compulsive Disorder Reveals Differences in Genetic Architecture
SO PLOS GENETICS
LA English
DT Article
ID MISSING HERITABILITY; TIC DISORDERS; NEUROPSYCHIATRIC DISORDERS; COMPLEX
DISEASES; COMMON SNPS; GILLES; FAMILY; BRAIN; EXPRESSION; AUTISM
AB The direct estimation of heritability from genome-wide common variant data as implemented in the program Genome-wide Complex Trait Analysis (GCTA) has provided a means to quantify heritability attributable to all interrogated variants. We have quantified the variance in liability to disease explained by all SNPs for two phenotypically-related neurobehavioral disorders, obsessive-compulsive disorder (OCD) and Tourette Syndrome (TS), using GCTA. Our analysis yielded a heritability point estimate of 0.58 (se = 0.09, p = 5.64e-12) for TS, and 0.37 (se = 0.07, p = 1.5e-07) for OCD. In addition, we conducted multiple genomic partitioning analyses to identify genomic elements that concentrate this heritability. We examined genomic architectures of TS and OCD by chromosome, MAF bin, and functional annotations. In addition, we assessed heritability for early onset and adult onset OCD. Among other notable results, we found that SNPs with a minor allele frequency of less than 5% accounted for 21% of the TS heritability and 0% of the OCD heritability. Additionally, we identified a significant contribution to TS and OCD heritability by variants significantly associated with gene expression in two regions of the brain (parietal cortex and cerebellum) for which we had available expression quantitative trait loci (eQTLs). Finally we analyzed the genetic correlation between TS and OCD, revealing a genetic correlation of 0.41 (se = 0.15, p = 0.002). These results are very close to previous heritability estimates for TS and OCD based on twin and family studies, suggesting that very little, if any, heritability is truly missing (i.e., unassayed) from TS and OCD GWAS studies of common variation. The results also indicate that there is some genetic overlap between these two phenotypically-related neuropsychiatric disorders, but suggest that the two disorders have distinct genetic architectures.
C1 [Davis, Lea K.; Gamazon, Eric R.; Konkashbaev, Anuar I.; Evans, Patrick; Cox, Nancy J.] Univ Chicago, Dept Med, Med Genet Sect, Chicago, IL 60637 USA.
[Yu, Dongmei; Haddad, Stephen; Illmann, Cornelia; McGrath, Lauren M.; Osiecki, Lisa; Pauls, David L.; Scharf, Jeremiah M.] Harvard Univ, Massachusetts Gen Hosp, Dept Psychiat,Sch Med, Psychiat & Neurodev Genet Unit,Ctr Human Genet Re, Boston, MA USA.
[Yu, Dongmei; Neale, Benjamin M.; Scharf, Jeremiah M.] Broad Inst Harvard & MIT, Stanley Ctr Psychiat Res, Cambridge, MA USA.
[Keenan, Clare L.] Univ Chicago, Dept Med, Chicago, IL 60637 USA.
[Keenan, Clare L.] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
[Derks, Eske M.; Blom, Rianne M.; Denys, Damiaan] Univ Amsterdam, Acad Med Ctr, Dept Psychiat, NL-1105 AZ Amsterdam, Netherlands.
[Neale, Benjamin M.] Massachusetts Gen Hosp, Analyt & Translat Genet Unit, Boston, MA 02114 USA.
[Yang, Jian] Univ Queensland, Diamantina Inst, Brisbane, Qld 4072, Australia.
[Yang, Jian; Lee, S. Hong; Wray, Naomi R.] Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4072, Australia.
[Barr, Cathy L.] Univ Hlth Network, Toronto Western Res Inst, Toronto, ON, Canada.
[Barr, Cathy L.] Hosp Sick Children, Toronto, ON M5G 1X8, Canada.
[Bellodi, Laura] Univ Vita Salute San Raffaele, Milan, Italy.
[Benarroch, Fortu] Hadassah Hebrew Univ Med Ctr, Herman Dana Div Child & Adolescent Psychiat, Jerusalem, Israel.
[Berrio, Gabriel Bedoya; Silgado, Julio C. Cardona; Restrepo, Sandra C. Mesa; Ochoa, William Cornejo; Duarte, Ana V. Valencia] Univ Pontificia Bolivariana, Univ Antioquia, Medellin, Colombia.
[Bienvenu, Oscar J.; Cullen, Bernadette A.; Gallagher, Patience J.; Grados, Marco A.; Riddle, Mark A.; Samuels, Jack; Wang, Ying; Nestadt, Gerald] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
[Bloch, Michael H.; Coric, Vladimir] Yale Univ, Dept Psychiat, New Haven, CT 06520 USA.
[Bloch, Michael H.; Fernandez, Thomas V.] Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA.
[Bruun, Ruth D.] North Shore Long Isl Jewish Med Ctr, Manhasset, NY USA.
[Bruun, Ruth D.] NYU Med Ctr, New York, NY 10016 USA.
[Budman, Cathy L.] North Shore Long Isl Jewish Hlth Syst, Manhasset, NY USA.
[Budman, Cathy L.] Hofstra Univ, Sch Med, Hempstead, NY 11550 USA.
[Camarena, Beatriz] Inst Nacl Psiquiatria Ramon de la Fuente Muniz, Mexico City, DF, Mexico.
[Campbell, Desmond; Kremeyer, Barbara; Muller, Heike; Robertson, Mary M.; Ruiz-Linares, Andres] UCL, London, England.
[Campbell, Desmond] Univ Hong Kong, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China.
[Cappi, Carolina; Vallada, Homero; Miguel, Euripedes C.] Univ Sao Paulo, Sch Med, Dept Psychiat, Sao Paulo, Brazil.
[Cath, Danielle C.; Smit, Jan H.] Vrije Univ Amsterdam, Med Ctr, Dept Psychiat, Amsterdam, Netherlands.
[Cath, Danielle C.] Univ Utrecht, Dept Clin & Hlth Psychol, Utrecht, Netherlands.
[Cath, Danielle C.] Altrecht Acad Anxiety Ctr, Utrecht, Netherlands.
[Cavallini, Maria C.] Univ Milan, Osped San Raffaele, I-20127 Milan, Italy.
[Chavira, Denise A.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA.
[Chavira, Denise A.] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA.
[Chouinard, Sylvain; Girard, Simon L.] Univ Montreal, Montreal, PQ, Canada.
[Conti, David V.; Edlund, Christopher K.] Univ Calif Los Angeles, Keck Sch Med, Div Biostat, Dept Preventat Med, Los Angeles, CA USA.
[Cook, Edwin H.] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA.
[Deforce, Dieter; Van Nieuwerburgh, Filip] Univ Ghent, Lab Pharmaceut Biotechnol, B-9000 Ghent, Belgium.
[Delorme, Richard] Inst Pasteur, Paris, France.
[Delorme, Richard; Leboyer, Marion] French Natl Sci Fdn, Fondat Fondamental, Creteil, France.
[Delorme, Richard; Leboyer, Marion] Hop Robert Debre, AP HP, Dept Child & Adolescent Psychiat, F-75019 Paris, France.
[Dion, Yves] Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada.
[Egberts, Karin; Renner, Tobias J.] Univ Wurzburg, Dept Child & Adolescent Psychiat Psychosomat & Ps, D-97070 Wurzburg, Germany.
[Falkai, Peter] Univ Munich, Dept Psychiat & Psychotherapy, Munich, Germany.
[Fernandez, Thomas V.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
Harvard Univ, Sch Med, Dept Psychiat, Massachusetts Gen Hosp,OCD Program, Boston, MA 02115 USA.
[Grabe, Hans J.] Univ Med Greifswald, Helios Hosp Stralsund, Dept Psychiat & Psychotherapy, Greifswald, Germany.
[Garrido, Helena; Greenberg, Benjamin D.] Butler Hosp, Brown Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA.
[Geller, Daniel; Gross-Tsur, Varda; Pollak, Yehuda] Shaare Zedek Med Ctr, Neuropediatr Unit, Jerusalem, Israel.
[Heiman, Gary A.; Tischfield, Jay A.] Rutgers State Univ, Dept Genet, Human Genet Inst New Jersey, Piscataway, NJ USA.
[Hemmings, Sian M. J.] Univ Stellenbosch, Dept Psychiat, ZA-7600 Stellenbosch, South Africa.
[Hounie, Ana G.; Sampaio, Aline S.] Univ Sao Paulo, Fac Med, Dept Psychiat, BR-05508 Sao Paulo, Brazil.
[Jankovic, Joseph] Baylor Coll Med, Dept Neurol, Parkinsons Dis Ctr, Houston, TX 77030 USA.
[Jankovic, Joseph] Baylor Coll Med, Dept Neurol, Movement Disorders Clin, Houston, TX 77030 USA.
[Jenike, Michael A.; Stewart, S. Evelyn] Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA.
[Kennedy, James L.] Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON, Canada.
[Kennedy, James L.; Richter, Margaret A.; Arnold, Paul D.] Univ Toronto, Dept Psychiat, Toronto, ON, Canada.
[King, Robert A.] Yale Univ, Sch Med, Dept Genet, Yale Child Study Ctr, New Haven, CT 06510 USA.
[Kurlan, Roger] Overlook Hosp, Atlantic Neurosci Inst, Summit, NJ USA.
[Lanzagorta, Nuria] Carracci Med Grp, Mexico City, DF, Mexico.
[Leboyer, Marion] Inst Mondor Rech Biomed, Creteil, France.
[Leckman, James F.] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[Lennertz, Leonhard; Moessner, Rainald; Wagner, Michael] Univ Bonn, Dept Psychiat & Psychotherapy, Bonn, Germany.
[Liu, Chunyu] Univ Illinois, Dept Psychiat, Inst Human Genet, Chicago, IL 60612 USA.
[Lochner, Christine] Univ Stellenbosch, Dept Psychiat, MRC Unit Anxiety & Stress Disorders, ZA-7600 Stellenbosch, South Africa.
[Lowe, Thomas L.; Reus, Victor I.; Sheppard, Brooke; Mathews, Carol A.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
[Macciardi, Fabio; McCracken, James T.] UCI, Sch Med, Dept Psychiat & Human Behav, Irvine, CA USA.
[Morgan, Jubel] Univ Utah, Salt Lake City, UT USA.
[Murphy, Dennis L.; Wendland, Jens R.] NIMH Intramural Res Program, Clin Sci Lab, Bethesda, MD USA.
[Naarden, Allan L.] Med City Dallas Hosp, Dept Clin Res, Dallas, TX USA.
[Ophoff, Roel A.] Univ Med Ctr, Rudolf Magnus Inst Neurosci, Dept Psychiat, Utrecht, Netherlands.
[Ophoff, Roel A.; Freimer, Nelson B.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Ctr Neurobehav Genet, Los Angeles, CA 90024 USA.
[Pakstis, Andrew J.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA.
[Pato, Michele T.; Pato, Carlos N.; Knowles, James A.] Univ So Calif, Keck Sch Med, Zilkha Neurogenet Inst, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA.
[Piacentini, John] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA.
[Pittenger, Christopher] Yale Univ, Dept Psychiat, New Haven, CT 06520 USA.
[Pittenger, Christopher] Yale Univ, Dept Psychol, New Haven, CT 06520 USA.
[Pittenger, Christopher] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
[Rauch, Scott L.] Partners Psychiat & McLean Hosp, Boston, MA USA.
[Richter, Margaret A.] Sunnybrook Hlth Sci Ctr, Frederick W Thompson Anxiety Disorders Ctr, Toronto, ON M4N 3M5, Canada.
[Robertson, Mary M.] St George Hosp, London, England.
[Robertson, Mary M.] Sch Med, London, England.
[Romero, Roxana] Hosp Nacl Ninos Dr Carlos Saenz Herrera, San Jose, Costa Rica.
[Rosario, Maria C.] Univ Fed Sao Paulo, Dept Psychiat, Child & Adolescent Psychiat Unit UPIA, Sao Paulo, Brazil.
[Rosenberg, David] Wayne State Univ, Dept Psychiat & Behav Neurosci, Detroit, MI 48207 USA.
[Rosenberg, David] Detroit Med Ctr, Detroit, MI USA.
[Rouleau, Guy A.] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada.
[Ruhrmann, Stephan] Univ Cologne, Dept Psychiat & Psychotherapy, D-50931 Cologne, Germany.
[Sampaio, Aline S.] Univ Fed Bahia, Univ Hlth Care Serv SMURB, Salvador, BA, Brazil.
[Sandor, Paul] Univ Toronto, Dept Psychiat, Toronto, ON, Canada.
[Sandor, Paul] Univ Hlth Network, Toronto Western Res Inst, Toronto, ON, Canada.
[Sandor, Paul] Youthdale Treatment Ctr, Toronto, ON, Canada.
[Singer, Harvey S.] Johns Hopkins Univ Sch Med, Baltimore, MD USA.
[Stein, Dan J.] Univ Cape Town, ZA-7925 Cape Town, South Africa.
[Strengman, E.] Univ Med Ctr Utrecht, Dept Med Genet, Utrecht, Netherlands.
[Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Kennedy Ctr Res Human Dev, Dept Psychiat, Nashville, TN 37235 USA.
[Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Kennedy Ctr Res Human Dev, Dept Pediat & Pharmacol, Nashville, TN 37235 USA.
[Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Inst Brain, Nashville, TN 37235 USA.
[Walitza, Susanne] Univ Zurich, Dept Child & Adolescent Psychiat, Zurich, Switzerland.
[Walitza, Susanne] Univ Wurzburg, Dept Child & Adolescent Psychiat, D-97070 Wurzburg, Germany.
[Westenberg, Herman G. M.] Univ Amsterdam, Acad Med Ctr, Ctr Psychiat, NL-1105 BC Amsterdam, Netherlands.
[Westenberg, Herman G. M.; Denys, Damiaan] Inst Royal Netherlands Acad Arts & Sci NIN KNAW, Netherlands Inst Neurosci, Amsterdam, Netherlands.
[Shugart, Yin Yao] NIMH Intramural Res Program, Unit Stat Genom, Bethesda, MD USA.
[McMahon, William] Univ Utah, Dept Psychiat, Salt Lake City, UT USA.
[Nicolini, Humberto] Natl Inst Genom Med SAP, Carracci Med Grp, Mexico City, DF, Mexico.
[Posthuma, Danielle] Vrije Univ Amsterdam, Ctr Neurogen & Cognit Res, Dept Funct Genom, Amsterdam, Netherlands.
[Posthuma, Danielle] Vrije Univ Amsterdam Med Ctr, Dept Clin Genet, Amsterdam, Netherlands.
[Posthuma, Danielle] Erasmus Univ, Med Ctr, Dept Child & Adolescent Psychiat, Rotterdam, Netherlands.
[Hanna, Gregory L.] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA.
[Heutink, Peter] Vrije Univ Amsterdam, Med Ctr, Dept Clin Genet, Sect Med Genom, Amsterdam, Netherlands.
[Heutink, Peter] German Ctr Neurodegenerat Dis, Tubingen, Germany.
[Arnold, Paul D.] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1X8, Canada.
[Oostra, Ben A.] Erasmus MC, Dept Clin Genet, Rotterdam, Netherlands.
[Stewart, S. Evelyn] Univ British Columbia, British Columbia Mental Hlth & Addict Res Inst, Vancouver, BC V5Z 1M9, Canada.
[Scharf, Jeremiah M.] Brigham & Womens Hosp, Div Cognit & Behav Neurol, Boston, MA 02115 USA.
[Scharf, Jeremiah M.] Massachusetts Gen Hosp, Dept Neurol, Boston, MA 02114 USA.
RP Davis, LK (reprint author), Univ Chicago, Dept Med, Med Genet Sect, 5841 S Maryland Ave, Chicago, IL 60637 USA.
EM lea.k.davis@gmail.com; jscharf@partners.org
RI Vallada, Homero/D-1333-2014; Yang, Jian/A-5852-2010; Fernandez,
Thomas/D-4295-2009; Stein, Dan/A-1752-2008; Renner, Tobias/I-2120-2013;
Lee, Sang Hong/A-2569-2011; Wray, Naomi/C-8639-2015
OI Vallada, Homero/0000-0001-5123-8295; Yang, Jian/0000-0003-2001-2474;
Fernandez, Thomas/0000-0003-0830-022X; Stein, Dan/0000-0001-7218-7810;
Lee, Sang Hong/0000-0001-9701-2718; Wray, Naomi/0000-0001-7421-3357
FU Judah Foundation; NIH [NS40024, NS16648, MH079489, MH073250, NS037484,
1R01MH079487-01A1, K20 MH01065, R01 MH58376, MH085057, MH079494,
HHSN268200782096C]; Tourette Syndrome Association International
Consortium for Genetics (TSAICG); New Jersey Center for Tourette
Syndrome and Associated Disorders; NIMH [R01MH092293]; Obsessive
Compulsive Foundation; Ontario Mental Health Foundation; Tourette
Syndrome Association; American Academy of Child and Adolescent
Psychiatry (AACAP); Anxiety Disorders Association of America (ADAA);
University of British Columbia; Michael Smith Foundation; American
Recovery and Re-investment Act (ARRA) [NS40024-07S1, NS16648-29S1];
Australian Research Council [FT0991360, DE130100614]; Australian
National Health and Medical Research Council [1047956, 1052684]; German
Research Foundation [DFG GR 1912/1-1]; NIH Genes, Environment and Health
Initiative [GEI] [U01 HG004422]; Gene Environment Association Studies
(GENEVA) under GEI; NIH GEI [U01HG004438]; National Institute on Alcohol
Abuse and Alcoholism; National Institute on Drug Abuse; [R01 MH090937];
[P50MH094267]
FX This work was supported by a grant from the Judah Foundation, NIH grant
NS40024 to DLP/JMS and the Tourette Syndrome Association International
Consortium for Genetics (TSAICG), NIH grant NS16648, MH079489, and
MH073250 to DLP, NIH grant NS037484 to NBF, NIH grant 1R01MH079487-01A1
to JTM, New Jersey Center for Tourette Syndrome and Associated Disorders
and NIMH (R01MH092293) to GAH/RAK/JAT, NIH grant K20 MH01065 and R01
MH58376 and a grant from the Obsessive Compulsive Foundation to GLH,
Ontario Mental Health Foundation grant to PR and JLK, and a grant from
the Tourette Syndrome Association and NIH grant MH085057 to JMS,
MH079494 to JAK and the OCD Collaborative Genetics Association Study
which supported the imputation, by an American Academy of Child and
Adolescent Psychiatry (AACAP) Early Investigator Research Grant, an
Anxiety Disorders Association of America (ADAA) Junior Investigator
Research Grant, the University of British Columbia and a Michael Smith
Foundation Clinical Research Scholar Award to SES, and American Recovery
and Re-investment Act (ARRA) awards NS40024-07S1 to DLP/JMS and
NS16648-29S1 to DLP. Additional support for analysis was provided by R01
MH090937 and P50MH094267 awarded to NJC. Support was also provided by
the Australian Research Council FT0991360 (NRW), DE130100614 (SHL) and
the Australian National Health and Medical Research Council: 1047956
(NRW), 1052684 (JY), and the German Research Foundation (DFG GR
1912/1-1) to HJG and to PF, SR, MW. Funding support for the Study of
Addiction: Genetics and Environment (SAGE) was provided through the NIH
Genes, Environment and Health Initiative [GEI] (U01 HG004422). SAGE is
one of the genome-wide association studies funded as part of the Gene
Environment Association Studies (GENEVA) under GEI. Assistance with
phenotype harmonization and genotype cleaning, as well as with general
study coordination, was provided by the GENEVA Coordinating Center (U01
HG004446). Assistance with data cleaning was provided by the National
Center for Biotechnology Information. Support for collection of datasets
and samples was provided by the Collaborative Study on the Genetics of
Alcoholism (COGA; U10 AA008401), the Collaborative Genetic Study of
Nicotine Dependence (COGEND; P01 CA089392), and the Family Study of
Cocaine Dependence (FSCD; R01 DA013423), and R01-MH-50214 (GN). Funding
support for genotyping, which was performed at the Johns Hopkins
University Center for Inherited Disease Research, was provided by the
NIH GEI (U01HG004438), the National Institute on Alcohol Abuse and
Alcoholism, the National Institute on Drug Abuse, and the NIH contract
"High throughput genotyping for studying the genetic contributions to
human disease" (HHSN268200782096C). The datasets used for the analyses
described in this manuscript were obtained from dbGaP at
http://www.ncbi.nlm.nih.gov/projects/gap/cgibin/study.cgi?study_id=phs00
0092.v1.p1 through dbGaP accession number phs000092.v1.p. None of the
funding agencies for this project (NINDS, NIMH, the Tourette Syndrome
Association and the Judah Foundation) had any influence or played any
role in a) the design or conduct of the study; b) management, analysis
or interpretation of the data; c) preparation, review or approval of the
manuscript.
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NR 61
TC 25
Z9 25
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2013
VL 9
IS 10
AR e1003864
DI 10.1371/journal.pgen.1003864
PG 14
WC Genetics & Heredity
SC Genetics & Heredity
GA 299AR
UT WOS:000330367200041
PM 24204291
ER
PT J
AU Inoue, K
Rispoli, J
Yang, LC
MacLeod, D
Beal, MF
Klann, E
Abeliovich, A
AF Inoue, Keiichi
Rispoli, Joanne
Yang, Lichuan
MacLeod, David
Beal, M. Flint
Klann, Eric
Abeliovich, Asa
TI Coordinate Regulation of Mature Dopaminergic Axon Morphology by
Macroautophagy and the PTEN Signaling Pathway
SO PLOS GENETICS
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; LHERMITTE-DUCLOS-DISEASE; IN-VIVO; SELECTIVE
DELETION; MOUSE-BRAIN; SOMA SIZE; CELL-SIZE; AUTOPHAGY; MICE; NEURONS
AB Macroautophagy is a conserved mechanism for the bulk degradation of proteins and organelles. Pathological studies have implicated defective macroautophagy in neurodegeneration, but physiological functions of macroautophagy in adult neurons remain unclear. Here we show that Atg7, an essential macroautophagy component, regulates dopaminergic axon terminal morphology. Mature Atg7-deficient midbrain dopamine (DA) neurons harbored selectively enlarged axonal terminals. This contrasted with the phenotype of DA neurons deficient in Pten - a key negative regulator of the mTOR kinase signaling pathway and neuron size - that displayed enlarged soma but unaltered axon terminals. Surprisingly, concomitant deficiency of both Atg7 and Pten led to a dramatic enhancement of axon terminal enlargement relative to Atg7 deletion alone. Similar genetic interactions between Atg7 and Pten were observed in the context of DA turnover and DA-dependent locomotor behaviors. These data suggest a model for morphological regulation of mature dopaminergic axon terminals whereby the impact of mTOR pathway is suppressed by macroautophagy.
C1 [Inoue, Keiichi; Rispoli, Joanne; MacLeod, David; Abeliovich, Asa] Columbia Univ, Dept Pathol, Taub Inst, Med Ctr, New York, NY 10027 USA.
[Inoue, Keiichi; Rispoli, Joanne; MacLeod, David; Abeliovich, Asa] Columbia Univ, Dept Neurol, Taub Inst, Med Ctr, New York, NY USA.
[Yang, Lichuan; Beal, M. Flint] Cornell Univ, Weill Cornell Med Coll, Dept Neurol & Neurosci, New York, NY 10021 USA.
[Klann, Eric] NYU, Ctr Neural Sci, New York, NY 10003 USA.
RP Inoue, K (reprint author), Columbia Univ, Dept Pathol, Taub Inst, Med Ctr, New York, NY 10027 USA.
EM aa900@columbia.edu
FU NIH [NS064433-01, NS060876, NS082068-01]; Michael J. Fox Foundation;
Kanae Foundation for the Promotion of Medical Science and Research
Foundation ITSUU Laboratory
FX This work was supported by NIH grants NS064433-01, NS060876, and
NS082068-01 to AA; Michael J. Fox Foundation to AA; and the Kanae
Foundation for the Promotion of Medical Science and Research Foundation
ITSUU Laboratory to KI. The funders had no role in study design, data
collection and analysis, decision to publish, or preparation of the
manuscript.
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NR 59
TC 2
Z9 2
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2013
VL 9
IS 10
AR e1003845
DI 10.1371/journal.pgen.1003845
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 299AR
UT WOS:000330367200026
PM 24098148
ER
PT J
AU Sajan, SA
Fernandez, L
Nieh, SE
Rider, E
Bukshpun, P
Wakahiro, M
Christian, SL
Riviere, JB
Sullivan, CT
Sudi, J
Herriges, MJ
Paciorkowski, AR
Barkovich, AJ
Glessner, JT
Millen, KJ
Hakonarson, H
Dobyns, WB
Sherr, EH
AF Sajan, Samin A.
Fernandez, Liliana
Nieh, Sahar Esmaeeli
Rider, Eric
Bukshpun, Polina
Wakahiro, Mari
Christian, Susan L.
Riviere, Jean-Baptiste
Sullivan, Christopher T.
Sudi, Jyotsna
Herriges, Michael J.
Paciorkowski, Alexander R.
Barkovich, A. James
Glessner, Joseph T.
Millen, Kathleen J.
Hakonarson, Hakon
Dobyns, William B.
Sherr, Elliott H.
TI Both Rare and De Novo Copy Number Variants Are Prevalent in Agenesis of
the Corpus Callosum but Not in Cerebellar Hypoplasia or Polymicrogyria
SO PLOS GENETICS
LA English
DT Article
ID 17Q21.31 MICRODELETION SYNDROME; DANDY-WALKER MALFORMATION;
WHITE-MATTER; MENTAL-RETARDATION; DEVELOPMENTAL DELAY; SPECTRUM
DISORDERS; KANSL1 CAUSE; AUTISM; DELETION; MUTATIONS
AB Agenesis of the corpus callosum (ACC), cerebellar hypoplasia (CBLH), and polymicrogyria (PMG) are severe congenital brain malformations with largely undiscovered causes. We conducted a large-scale chromosomal copy number variation (CNV) discovery effort in 255 ACC, 220 CBLH, and 147 PMG patients, and 2,349 controls. Compared to controls, significantly more ACC, but unexpectedly not CBLH or PMG patients, had rare genic CNVs over one megabase (p = 1.48x10(-3); odds ratio [OR] = 3.19; 95% confidence interval [CI] = 1.89-5.39). Rare genic CNVs were those that impacted at least one gene in less than 1% of the combined population of patients and controls. Compared to controls, significantly more ACC but not CBLH or PMG patients had rare CNVs impacting over 20 genes (p = 0.01; OR = 2.95; 95% CI = 1.69-5.18). Independent qPCR confirmation showed that 9.4% of ACC patients had de novo CNVs. These, in comparison to inherited CNVs, preferentially overlapped de novo CNVs previously observed in patients with autism spectrum disorders (p = 3.06x10(-4); OR = 7.55; 95% CI = 2.40-23.72). Interestingly, numerous reports have shown a reduced corpus callosum area in autistic patients, and diminished social and executive function in many ACC patients. We also confirmed and refined previously known CNVs, including significantly narrowing the 8p23.1-p11.1 duplication present in 2% of our current ACC cohort. We found six novel CNVs, each in a single patient, that are likely deleterious: deletions of 1p31.3-p31.1, 1q31.2-q31.3, 5q23.1, and 15q11.2-q13.1; and duplications of 2q11.2-q13 and 11p14.3-p14.2. One ACC patient with microcephaly had a paternally inherited deletion of 16p13.11 that included NDE1. Exome sequencing identified a recessive maternally inherited nonsense mutation in the non-deleted allele of NDE1, revealing the complexity of ACC genetics. This is the first systematic study of CNVs in congenital brain malformations, and shows a much higher prevalence of large gene-rich CNVs in ACC than in CBLH and PMG.
C1 [Sajan, Samin A.] Baylor Coll Med, Dept Pediat, Neurol Sect, Houston, TX 77030 USA.
[Fernandez, Liliana; Nieh, Sahar Esmaeeli; Rider, Eric; Bukshpun, Polina; Wakahiro, Mari; Sherr, Elliott H.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
[Christian, Susan L.; Sullivan, Christopher T.; Millen, Kathleen J.; Dobyns, William B.] Seattle Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA USA.
[Riviere, Jean-Baptiste] Univ Bourgogne, Equipe Genet Anomalies Dev, Dijon, France.
[Sudi, Jyotsna] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA.
[Herriges, Michael J.] Univ Penn, Dept Cell & Dev Biol, Philadelphia, PA 19104 USA.
[Paciorkowski, Alexander R.] Univ Rochester, Med Ctr, Dept Neurol, Rochester, NY 14642 USA.
[Paciorkowski, Alexander R.] Univ Rochester, Med Ctr, Dept Pediat, Rochester, NY 14642 USA.
[Paciorkowski, Alexander R.] Univ Rochester, Med Ctr, Dept Biomed Genet, Rochester, NY 14642 USA.
[Barkovich, A. James] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, Div Neuroradiol, San Francisco, CA 94143 USA.
[Glessner, Joseph T.; Hakonarson, Hakon] Childrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USA.
[Millen, Kathleen J.; Dobyns, William B.] Univ Washington, Dept Pediat, Seattle, WA 98195 USA.
[Hakonarson, Hakon] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
[Dobyns, William B.] Univ Washington, Dept Neurol, Seattle, WA 98195 USA.
RP Sajan, SA (reprint author), Baylor Coll Med, Dept Pediat, Neurol Sect, Houston, TX 77030 USA.
EM SherrE@neuropeds.ucsf.edu
FU National Institute of Neurological Disorders and Stroke (NINDS) of the
National Institutes of Health [R01NS058721]
FX The research reported in this publication was supported by the National
Institute of Neurological Disorders and Stroke (NINDS) of the National
Institutes of Health under award number R01NS058721 (to WBD, EHS, and
KJM), and by a donation from Eric, Marnie, Alan and Patricia Baer. The
content is solely the responsibility of the authors and does not
necessarily represent the official views of the National Institutes of
Health. The funders had no role in study design, data collection and
analysis, decision to publish, or preparation of the manuscript.
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NR 69
TC 5
Z9 5
PU PUBLIC LIBRARY SCIENCE
PI SAN FRANCISCO
PA 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
SN 1553-7404
J9 PLOS GENET
JI PLoS Genet.
PD OCT
PY 2013
VL 9
IS 10
AR e1003823
DI 10.1371/journal.pgen.1003823
PG 16
WC Genetics & Heredity
SC Genetics & Heredity
GA 299AR
UT WOS:000330367200014
PM 24098143
ER
PT J
AU Botting, N
Psarou, P
Caplin, T
Nevin, L
AF Botting, Nicola
Psarou, Popi
Caplin, Tamara
Nevin, Laura
TI Short-Term Memory Skills in Children With Specific Language Impairment
The Effect of Verbal and Nonverbal Task Content
SO TOPICS IN LANGUAGE DISORDERS
LA English
DT Article
DE children; language impairment; nonverbal; short-term memory
ID NON-WORD REPETITION; WORKING-MEMORY; PSYCHOLINGUISTIC MARKERS; DYNAMIC
ASSESSMENT; SLI; VOCABULARY; CAPACITY; AUTISM
AB Background and Design: In recent years, evidence has emerged that suggests specific language impairment (SLI) does not exclusively affect linguistic skill. Studies have revealed memory difficulties, including those measured using nonverbal tasks. However, there has been relatively little research into the nature of the verbal/nonverbal boundaries either at a conceptual level or at a task-related level. This study explores the short-term memory performance of children with and without SLI on a series of tasks that involve varying degrees of verbal content, implied or explicit. In total, 14 children with SLI and 20 comparison peers participated. Results: Findings show that children with SLI performed more poorly than peers on all tasks except the purely nonverbal block recall task. Interestingly, a task that required no verbal processing or output was as problematic for the SLI group as a traditional nonword memory span task, suggesting that verbal encoding was used by the typical peers but less so by those with SLI. Furthermore, a verbal input picture span task (involving hearing a list of words but requiring a nonverbal response) correlated strongly with the block recall task for children with SLI. This may provide preliminary evidence that visual encoding was being used as a central strategy by the SLI group to aid performance. Discussion: The findings have implications for our understanding of the nature of SLI and also for the use of verbal and visual content in the classroom and other real-life settings.
C1 [Botting, Nicola; Psarou, Popi; Caplin, Tamara; Nevin, Laura] City Univ London, London EC1V 0HB, England.
RP Botting, N (reprint author), City Univ London, Northampton Sq, London EC1V 0HB, England.
EM nicola.botting.1@city.ac.uk
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NR 35
TC 2
Z9 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-8294
EI 1550-3259
J9 TOP LANG DISORD
JI Top. Lang. Disord.
PD OCT-DEC
PY 2013
VL 33
IS 4
BP 313
EP 327
DI 10.1097/01.TLD.0000437940.01237.51
PG 15
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA 299DY
UT WOS:000330376700005
ER
PT J
AU Ameis, SH
Fan, J
Rockel, C
Soorya, L
Wang, AT
Anagnostou, E
AF Ameis, Stephanie H.
Fan, Jin
Rockel, Conrad
Soorya, Latha
Wang, A. Ting
Anagnostou, Evdokia
TI Altered cingulum bundle microstructure in autism spectrum disorder
SO ACTA NEUROPSYCHIATRICA
LA English
DT Article
DE autism spectrum disorder; diffusion tensor imaging; limbic system
ID PERVASIVE DEVELOPMENTAL DISORDERS; WHITE-MATTER; IMAGING TRACTOGRAPHY;
DIFFUSION; BRAIN; CONNECTIVITY; CHILDREN; ADOLESCENTS; PATHOLOGY; ATLAS
AB Objective Here, we examined the cingulum bundle, a long-range white matter tract mediating dorsal limbic connectivity, using diffusion tensor imaging (DTI) tractography, in children and adolescents with autism spectrum disorder (ASD) versus controls. We hypothesised that cingulum bundle microstructure would be altered in ASD, based on evidence implicating abnormal white matter connectivity in this disorder.
Methods DTI data were acquired for 19 ASD participants (IQ 70; 7-18 years; mean = 12.4 3.1) and 16 age-matched controls (7-18 years; mean = 12.3 3.6) on a 3 T magnetic resonance imaging system. Deterministic tractography was used to isolate the cingulum bundle. Left and right cingulum bundles were examined for differences in several DTI metrics in ASD children/adolescents versus controls, including: fractional anisotropy (FA), mean, axial, and radial diffusivity.
Results Significant age x group interaction effects were found for all DTI metrics (mean diffusivity: F-1,F-28 = 9.5, p = 0.005, radial diffusivity: F-1,F-28 = 7.8, p = 0.009, axial diffusivity: F-1,F-28 = 5.2, p = 0.03, FA: F-1,F-28 = 4.4, p = 0.04). Interaction effects were driven by increases in cingulum bundle diffusivity (mean, radial, and axial diffusivity), and decreased FA, in younger ASD participants within our sample versus controls.
Conclusion Our results point to immature microstructural organisation of the cingulum bundle in ASD, particularly during the early years of life, with implications for limbic network synchronisation and complex socio-emotional performance.
C1 [Ameis, Stephanie H.; Rockel, Conrad] Univ Toronto, Hosp Sick Children, Dept Psychiat, Toronto, ON M4G 1R8, Canada.
[Fan, Jin] CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
[Fan, Jin; Soorya, Latha; Wang, A. Ting; Anagnostou, Evdokia] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
[Anagnostou, Evdokia] Univ Toronto, Bloorview Res Inst, Holland Bloorview Kids Rehabil Hosp, Dept Pediat, Toronto, ON M4G 1R8, Canada.
RP Anagnostou, E (reprint author), Univ Toronto, Bloorview Res Inst, Holland Bloorview Kids Rehabil Hosp, Dept Pediat, 150 Kilgour Rd, Toronto, ON M4G 1R8, Canada.
EM eanagnostou@hollandbloorview.ca
RI Fan, Jin/A-6716-2009
OI Fan, Jin/0000-0001-9630-8330
FU NARSAD; Autism Speaks; NIMH [MH083164]; Autism Research Training
Program; Canadian Institutes of Health Research (CIHR) Strategic
Training Initiative in Health Research (STIHR); Sinneave Family
Foundation
FX The research work presented here was carried out at: The Mount Sinai
School of Medicine (Department of Psychiatry), The Hospital for Sick
Children (Department of Psychiatry), and Holland Bloorview Kids
Rehabilitation Hospital. The authors would like to thank Ms. Nadia Tanel
(Holland Bloorview Kids Rehabilitation Hospital) for assistance with
data organisation. This work was supported by NARSAD (PI: Anagnostou),
Autism Speaks (PI: Anagnostou), NIMH MH083164 (PI: Fan), and the Autism
Research Training Program (salary support to S.H.A.), funded by the
Canadian Institutes of Health Research (CIHR) Strategic Training
Initiative in Health Research (STIHR), with supplemental funding from
the Sinneave Family Foundation.
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NR 44
TC 1
Z9 1
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 1601-5215
J9 ACTA NEUROPSYCHIATR
JI Acta Neuropsychiatr.
PD OCT
PY 2013
VL 25
IS 5
BP 275
EP 282
DI 10.1017/neu.2013.2
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 298YD
UT WOS:000330359700004
PM 25287727
ER
PT J
AU Orsucci, F
Paoloni, G
Conti, CM
Reda, M
Fulcheri, M
AF Orsucci, F.
Paoloni, G.
Conti, C. M.
Reda, M.
Fulcheri, M.
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SO JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
LA English
DT Editorial Material
DE oxytocin; vasopressin; plasticity; attachment; complexity; autism
ID PAIR BOND FORMATION; SOCIAL-BEHAVIOR; AFFILIATIVE BEHAVIOR; PRAIRIE
VOLES; VASOPRESSIN; DOPAMINE; RECEPTOR; BRAIN; AGGRESSION; FOREBRAIN
AB The peptide hormones oxytocin (OT) and arginine vasopressin (AVP) have been implicated in the regulation of mammalian social behavior. There is considerable evidence implicating both oxytocin and vasopressin in social recognition and social memory. This review explores their role in attachment dynamics. Oxytocin is one element in a complex network of interactions observed in natural phenomena ranging from molecular biology, etology, social behavior and human psychology.
C1 [Orsucci, F.] UCL, Div Psychol & Language Sci, London WC1E 6BT, England.
[Paoloni, G.; Conti, C. M.; Fulcheri, M.] Univ G dAnnunzio, Dept Psychol Humanist & Territorial Sci, Pescara, Italy.
[Reda, M.] Univ Siena, Dept Neurol & Behav Sci, I-53100 Siena, Italy.
RP Orsucci, F (reprint author), UCL, Div Psychol & Language Sci, Gower St, London WC1E 6BT, England.
EM f.orsucci@ucl.ac.uk
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Young LJ, 2005, J COMP NEUROL, V493, P51, DOI 10.1002/cne.20771
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Zanette DH, 2004, PHYSICA D, V194, P203, DOI 10.1016/j.physd.2004.03.002
NR 40
TC 0
Z9 0
PU BIOLIFE SAS
PI SILVA MARINA (TE)
PA VIA S STEFANO 39 BIS, 64029 SILVA MARINA (TE), ITALY
SN 0393-974X
EI 1724-6083
J9 J BIOL REG HOMEOS AG
JI J. Biol. Regul. Homeost. Agents
PD OCT-DEC
PY 2013
VL 27
IS 4
BP 947
EP 954
PG 8
WC Endocrinology & Metabolism; Immunology; Medicine, Research &
Experimental; Physiology
SC Endocrinology & Metabolism; Immunology; Research & Experimental
Medicine; Physiology
GA 292HO
UT WOS:000329893000003
PM 24382175
ER
PT J
AU Matsui, G
Ohtoshi, T
Takada, S
AF Matsui, Gakuyo
Ohtoshi, Taro
Takada, Satoshi
TI Imitation of 'bye-bye' in very low-birthweight infants
SO PEDIATRICS INTERNATIONAL
LA English
DT Article
DE bye-bye; development; imitation ability; very low-birthweight infant
ID MIRROR-NEURON SYSTEM; PRETERM INFANTS; AGE; MOVEMENTS; GESTURES; AUTISM
AB BackgroundThe aim of this study was to clarify the development of imitation skills in very low-birthweight (VLBW) infants compared with full-term infants with regard to the onset of bye-bye'.
MethodsA total of 597 full-term infants (age, 6-21 months) and 95 VLBW infants (corrected age, 6-21 months) participated in this study. The time at which the infants began to imitate bye-bye and how they moved their hands were investigated by direct observations of their behaviors.
ResultSome full-term infants began to imitate bye-bye at 9 months, and all full-term infants could imitate bye-bye by 16 months old. The imitation of bye-bye was delayed in VLBW infants, but all of them could imitate it at 17 months old. Bye-bye motions were divided into five types. The moving wrist up and down' motion was observed most frequently at the initial bye-bye in both groups, but it was more frequent in VLBW infants at the early stage. The motion types changed with age, with the palm facing others' motion observed exclusively at 16 months in full-term infants. All infants of both groups could imitate this type at 17 months old.
ConclusionThe development of the ability to imitate bye-bye was delayed in VLBW infants even after correction for gestational age. It was suspected that the fine motor development delay might contribute to the late appearance of bye-bye in VLBW infants. Further follow-up study is required to clarify the clinical significance.
C1 [Matsui, Gakuyo; Takada, Satoshi] Kobe Univ, Grad Sch Hlth Sci, Kobe, Hyogo 6540142, Japan.
[Ohtoshi, Taro] Kansai Univ Welf Sci, Osaka, Japan.
Kobe Univ, Grad Sch Hlth Sci, Suma Ku, Kobe, Hyogo 6540142, Japan.
RP Matsui, G (reprint author), Kobe Univ, Grad Sch Hlth Sci, Suma Ku, 7-10-2 Tomogaoka, Kobe, Hyogo 6540142, Japan.
EM 052m506m@stu.kobe-u.ac.jp
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NR 20
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1328-8067
EI 1442-200X
J9 PEDIATR INT
JI Pediatr. Int.
PD OCT
PY 2013
VL 55
IS 5
BP 561
EP 565
DI 10.1111/ped.12160
PG 5
WC Pediatrics
SC Pediatrics
GA 286ZL
UT WOS:000329507700014
PM 23773446
ER
PT J
AU Benson, AD
Burket, JA
Deutsch, SI
AF Benson, Andrew D.
Burket, Jessica A.
Deutsch, Stephen I.
TI Balb/c mice treated with D-cycloserine arouse increased social interest
in conspecifics
SO BRAIN RESEARCH BULLETIN
LA English
DT Article
DE D-Cycloserine; NMDA receptor; Sociability; Social preference; Balb/c
mouse
ID AUTISM SPECTRUM DISORDERS; INBRED MOUSE STRAINS; NMDA RECEPTOR
ANTAGONIST; STEREOTYPIC BEHAVIORS; IMPROVES SOCIABILITY; MK-801; MODEL;
SCHIZOPHRENIA; SENSITIVITY; DIFFER
AB The genetically inbred Balb/cJ (Balb/c) mouse with functional alteration of its endogenous tone of NMDA receptor-mediated neurotransmission displays impaired sociability in a standard paradigm; this mouse strain has been proposed as a model of autism spectrum disorders (ASDs). Prior work showed that treatment of the Balb/c mouse with a centrally effective dose of D-cycloserine, a partial glycine(B) NMDA receptor agonist, improved several measures of its sociability. Additionally, D-cycloserine-treated Balb/c mice show greater preference for a social stimulus mouse than an inanimate object. We wondered if treatment with D-cycloserine also improved the social salience of the Balb/c mouse for "normally" sociable comparator strains. The current experiments explored whether C578I/6J (B6) and ICR mouse strains prefer D-cycloserine-treated to vehicle-treated Balb/c stimulus mice in a paradigm that evaluated social preference. The results showed that B6 mice prefer D-cycloserine-treated Balb/c mice to vehicle-treated Balb/c mice, suggesting that treatment could have resulted in normalization of "emitted" social cues. (C) 2013 Elsevier Inc. All rights reserved.
C1 [Benson, Andrew D.; Burket, Jessica A.; Deutsch, Stephen I.] Eastern Virginia Med Sch, Dept Psychiat & Behav Sci, Norfolk, VA 23507 USA.
RP Deutsch, SI (reprint author), Eastern Virginia Med Sch, Dept Psychiat & Behav Sci, 825 Fairfax Ave,Suite 710, Norfolk, VA 23507 USA.
EM deutscsi@evms.edu
FU Eastern Virginia Medical School; Commonwealth Health Research Board of
the Commonwealth of Virginia; Office of the Dean of Eastern Virginia
Medical School
FX The authors acknowledge the support they received from the Office of the
Dean of Eastern Virginia Medical School, a Research Enhancement Grant
from Eastern Virginia Medical School, and a grant from the Commonwealth
Health Research Board of the Commonwealth of Virginia.
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NR 26
TC 4
Z9 4
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0361-9230
EI 1873-2747
J9 BRAIN RES BULL
JI Brain Res. Bull.
PD OCT
PY 2013
VL 99
BP 95
EP 99
DI 10.1016/j.brainresbull.2013.10.006
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 285TX
UT WOS:000329419000012
PM 24157954
ER
PT J
AU Chkhartishvili, D
Natriashvili, G
AF Chkhartishvili, D.
Natriashvili, G.
TI USEFULNESS OF NEEDLE ELECTROMYOGRAPHY IN CHILDREN WITH AUTISM
SO MUSCLE & NERVE
LA English
DT Meeting Abstract
CT 60th Annual Meeting of the
American-Association-of-Neuromuscular-and-Electrodiagnostic-Medicine
(AANEM)
CY OCT 16-19, 2013
CL San Antonio, TX
SP Amer Assoc Neuromuscular & Electrodiagnost Med
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0148-639X
EI 1097-4598
J9 MUSCLE NERVE
JI Muscle Nerve
PD OCT
PY 2013
VL 48
IS 4
BP 634
EP 634
DI 10.1002/mus.24071
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264NF
UT WOS:000327884200030
ER
PT J
AU Catassi, C
Bai, JC
Bonaz, B
Bouma, G
Calabro, A
Carroccio, A
Castillejo, G
Ciacci, C
Cristofori, F
Dolinsek, J
Francavilla, R
Elli, L
Green, P
Holtmeier, W
Koehler, P
Koletzko, S
Meinhold, C
Sanders, D
Schumann, M
Schuppan, D
Ullrich, R
Vecsei, A
Volta, U
Zevallos, V
Sapone, A
Fasano, A
AF Catassi, Carlo
Bai, Julio C.
Bonaz, Bruno
Bouma, Gerd
Calabro, Antonio
Carroccio, Antonio
Castillejo, Gemma
Ciacci, Carolina
Cristofori, Fernanda
Dolinsek, Jernej
Francavilla, Ruggiero
Elli, Luca
Green, Peter
Holtmeier, Wolfgang
Koehler, Peter
Koletzko, Sibylle
Meinhold, Christof
Sanders, David
Schumann, Michael
Schuppan, Detlef
Ullrich, Reiner
Vecsei, Andreas
Volta, Umberto
Zevallos, Victor
Sapone, Anna
Fasano, Alessio
TI Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related
Disorders
SO NUTRIENTS
LA English
DT Review
DE gluten sensitivity; celiac disease; wheat allergy; gluten-related
disorders; gluten-free diet
ID AUTISM SPECTRUM DISORDERS; CONTROLLED-TRIAL; FREE DIET; DISEASE;
CHILDREN; BLIND; WHEAT; PREVALENCE; CHALLENGE; SYMPTOMS
AB Non Celiac Gluten sensitivity (NCGS) was originally described in the 1980s and recently a re-discovered disorder characterized by intestinal and extra-intestinal symptoms related to the ingestion of gluten-containing food, in subjects that are not affected with either celiac disease (CD) or wheat allergy (WA). Although NCGS frequency is still unclear, epidemiological data have been generated that can help establishing the magnitude of the problem. Clinical studies further defined the identity of NCGS and its implications in human disease. An overlap between the irritable bowel syndrome (IBS) and NCGS has been detected, requiring even more stringent diagnostic criteria. Several studies suggested a relationship between NCGS and neuropsychiatric disorders, particularly autism and schizophrenia. The first case reports of NCGS in children have been described. Lack of biomarkers is still a major limitation of clinical studies, making it difficult to differentiate NCGS from other gluten related disorders. Recent studies raised the possibility that, beside gluten, wheat amylase-trypsin inhibitors and low-fermentable, poorly-absorbed, short-chain carbohydrates can contribute to symptoms (at least those related to IBS) experienced by NCGS patients. In this paper we report the major advances and current trends on NCGS.
C1 [Catassi, Carlo] Univ Politecn Marche, Dept Pediat, I-60121 Ancona, Italy.
[Bai, Julio C.] Hosp Gastroenterol Dr Carlos Bonorino Udaondo, Dept Med, RA-1264 Buenos Aires, DF, Argentina.
[Bonaz, Bruno] CHU Grenoble, Dept Gastroenterol & Liver Dis, F-38043 Grenoble, France.
[Bouma, Gerd] Vrije Univ Med Ctr, Dept Gastroenterol & Hepatol, NL-1081 HV Amsterdam, Netherlands.
[Calabro, Antonio] Univ Florence, Dept Expt & Clin Biomed Sci, Gastroenterol Unit, I-50134 Florence, Italy.
[Carroccio, Antonio] Giovanni Paolo II Hosp, Dept Internal Med, Sciacca, AG, Italy.
[Carroccio, Antonio] Univ Palermo, I-92019 Sciacca, Italy.
[Castillejo, Gemma] Univ Rovira & Virgili, Hosp Univ St Joan de Reus, Pediat Gastroenterol Unit, Tarragona 43204, Spain.
[Ciacci, Carolina] Univ Salerno, Dept Med & Surg, I-84081 Salerno, Italy.
[Cristofori, Fernanda; Francavilla, Ruggiero] Univ Bari, Interdisciplinary Dept Med, I-70124 Bari, Italy.
[Dolinsek, Jernej] Univ Med Ctr Maribor, Dept Pediat, Gastroenterol Unit, Maribor 2000, Slovenia.
[Elli, Luca] Ctr Prevenz & Diagnosi Malattia Celiaca Fdn IRCCS, I-20122 Milan, Italy.
[Green, Peter] Columbia Univ Med Ctr, Dept Med, Celiac Dis Ctr, New York, NY 10032 USA.
[Holtmeier, Wolfgang] Hosp Porz Rhein, Div Gastroenterol & Internal Med, D-51149 Cologne, Germany.
[Koehler, Peter] Leibniz Inst, German Res Ctr Food Chem, D-85354 Freising Weihenstephan, Germany.
[Koletzko, Sibylle] Univ Munich Med Ctr, Dr von Hauner Childrens Hosp, Div Pediat Gastroenterol & Hepatol, D-80337 Munich, Germany.
[Meinhold, Christof] Practice Nutr Therapy Meinhold & Team, D-50674 Cologne, Germany.
[Sanders, David] Royal Hallamshire Hosp, Dept Gastroenterol & Hepatol, Sheffield S10 2JF, S Yorkshire, England.
[Sanders, David] Univ Sheffield Med Sch, Sheffield S10 2JF, S Yorkshire, England.
[Schumann, Michael; Ullrich, Reiner] Charite, Dept Gastroenterol Rheumatol & Infectiol, D-10203 Berlin, Germany.
[Schuppan, Detlef; Zevallos, Victor] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Dept Med 1, D-55131 Mainz, Germany.
[Schuppan, Detlef] Beth Israel Deaconess Med Ctr, Div Gastroenterol, Boston, MA 02215 USA.
[Schuppan, Detlef] Beth Israel Deaconess Med Ctr, Celiac Ctr, Boston, MA 02215 USA.
[Schuppan, Detlef] Harvard Univ, Sch Med, Boston, MA 02215 USA.
[Vecsei, Andreas] St Anna Childrens Hosp, A-1090 Vienna, Austria.
[Volta, Umberto] Univ Bologna, Dept Med & Surg Sci, I-40138 Bologna, Italy.
[Sapone, Anna] Univ Naples 2, Dept Gastroenterol, I-80136 Naples, Italy.
[Fasano, Alessio] MassGen Hosp Children, Boston, MA 02129 USA.
RP Fasano, A (reprint author), MassGen Hosp Children, Boston, MA 02129 USA.
EM catassi@tin.it; jbai@intramed.net; bbonaz@chu-grenoble.fr;
g.bouma@vumc.nl; a.calabro@dfc.unifi.it; acarroccio@hotmail.com;
gcv@tinet.cat; cciacci@unisa.it; fernandacristofori@gmail.com;
jernej.dolinsek@ukc-mb.si; rfrancavilla@gmail.com; lucelli@yahoo.com;
pg11@columbia.edu; w.holtmeier@khporz.de; peter.koehler@tum.de;
sybille.koletzko@med.uni-muenchen.de; praxis@christof-meinhold.de;
david.sanders@sth.nhs.uk; michael.schumann@charite.de;
dschuppa@bidmc.harvard.edu; reiner.ullrich@charite.de;
andreas.vecsei@stanna.at; uvolt@yahoo.com; zevallos@uni-mainz.de;
annasapone@yahoo.it; afasano@partners.org
RI bouma, gerd/E-2520-2013
FU Schar; Menarini Diagnostics
FX Carlo Catassi received consulting fees from Schar and Menarini
Diagnostics. Luca Elli and Anna Sapone received consulting fees from
Schar. Peter Green is a member of the scientific advisory board of
Alvine Pharmaceuticals and Alba Therapeutics. Alessio Fasano owns stock
in Alba Therapeutics. The other authors declared no conflict of
interest.
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NR 40
TC 56
Z9 58
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 2072-6643
J9 NUTRIENTS
JI Nutrients
PD OCT
PY 2013
VL 5
IS 10
BP 3839
EP 3853
DI 10.3390/nu5103839
PG 15
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 274TA
UT WOS:000328627900003
PM 24077239
ER
PT J
AU Lee, RWY
Conley, SK
Gropman, A
Porter, FD
Baker, EH
AF Lee, Ryan W. Y.
Conley, Sandra K.
Gropman, Andrea
Porter, Forbes D.
Baker, Eva H.
TI Brain Magnetic Resonance Imaging Findings in Smith-Lemli-Opitz Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE Smith-Lemli-Opitz syndrome (SLOS); magnetic resonance imaging (MRI);
brain
ID DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; MULTIPLE CONGENITAL-ANOMALIES;
AUTISM SPECTRUM DISORDERS; SONIC-HEDGEHOG; LIPID RAFTS; SEPTI PELLUCIDI;
OPTIZ-SYNDROME; METABOLISM; FOREBRAIN; PHENOTYPE
AB Smith-Lemli-Opitz syndrome (SLOS) is a neurodevelopmental disorder caused by inborn errors of cholesterol metabolism resulting from mutations in 7-dehydrocholesterol reductase (DHCR7). There are only a few studies describing the brain imaging findings in SLOS. This study examines the prevalence of magnetic resonance imaging (MRI) abnormalities in the largest cohort of patients with SLOS to date. Fifty-five individuals with SLOS (27 M, 28 F) between age 0.17 years and 25.4 years (mean=6.2, SD=5.8) received a total of 173 brain MRI scans (mean=3.1 per subject) on a 1.5T GE scanner between September 1998 and December 2003, or on a 3T Philips scanner between October 2010 and September 2012; all exams were performed at the Clinical Center of the National Institutes of Health. We performed a retrospective review of these imaging studies for both major and minor brain anomalies. Aberrant MRI findings were observed in 53 of 55 (96%) SLOS patients, with abnormalities of the septum pellucidum the most frequent (42/55, 76%) finding. Abnormalities of the corpus callosum were found in 38 of 55 (69%) patients. Other findings included cerebral atrophy, cerebellar atrophy, colpocephaly, white matter lesions, arachnoid cysts, Dandy-Walker variant, and type I Chiari malformation. Significant correlations were observed when comparing MRI findings with sterol levels and somatic malformations. Individuals with SLOS commonly have anomalies involving the midline and para-midline structures of the brain. Further studies are required to examine the relationship between structural brain abnormalities and neurodevelopmental disability in SLOS. (c) 2013 Wiley Periodicals, Inc.
C1 [Lee, Ryan W. Y.] Kennedy Krieger Inst, Dept Neurol & Dev Med, Baltimore, MD 21205 USA.
[Lee, Ryan W. Y.; Conley, Sandra K.; Porter, Forbes D.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Bethesda, MD USA.
[Gropman, Andrea] Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA.
[Baker, Eva H.] NIH, Dept Radiol & Imaging Sci, Ctr Clin, Bethesda, MD 20892 USA.
RP Lee, RWY (reprint author), Kennedy Krieger Inst, Dept Neurol & Dev Med, 716 North Broadway St, Baltimore, MD 21205 USA.
EM leer@kennedykrieger.org
FU Eunice Kennedy Shriver National Institute of Child Health and Human
Development; NIH Clinical Center; NIH Office of Rare Diseases;
RSH/Smith-Lemli-Opitz Foundation
FX Grant sponsor: Eunice Kennedy Shriver National Institute of Child Health
and Human Development; Grant sponsor: NIH Clinical Center; Grant
sponsor: NIH Office of Rare Diseases; Grant sponsor:
RSH/Smith-Lemli-Opitz Foundation.
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NR 50
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2013
VL 161
IS 10
BP 2407
EP 2419
DI 10.1002/ajmg.a.36096
PG 13
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SC Genetics & Heredity
GA 264FP
UT WOS:000327862700002
PM 23918729
ER
PT J
AU Fisch, GS
AF Fisch, Gene S.
TI Autism and Epistemology IV: Does Autism Need a Theory of Mind?
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Editorial Material
DE theory of mind; autism; cognition; mirror neurons; mental states;
validity
ID FRAGILE-X-SYNDROME; MIRROR NEURON SYSTEM; THEORY-OF-MIND; FALSE-BELIEF;
SPECTRUM DISORDERS; EMOTION RECOGNITION; DEVELOPMENTAL DISORDERS;
CHILDRENS KNOWLEDGE; TYPICAL DEVELOPMENT; MENTAL-RETARDATION
AB In their article, Does the autistic child have a theory of mind'?, Baron-Cohen et al. [1985] proposed a novel paradigm to explain social impairment in children diagnosed as autistic (AD). Much research has been undertaken since their article went to print. The purpose of this commentary is to gauge whether Theory of Mind (ToM)or lack thereofis a valid model for explaining abnormal social behavior in children with AD. ToM is defined as the ability to impute mental states to oneself and to others and the ability to make inferences about what other people believe to be the case. The source for their model was provided by an article published earlier by Premack and Woodruff, Does the chimpanzee have a theory of mind? Later research in chimpanzees did not support a ToM in primates. From the outset, ToM as a neurocognitive model of autism has had many shortcomingsmethodological, logical, and empirical. Other ToM assumptions, for example, its universality in all children in all cultures and socioeconomic conditions, are not supported by data. The age at which a ToM emerges, or events that presage a ToM, are too often not corroborated. Recent studies of mirror neurons, their location and interconnections in brain, their relationship to social behavior and language, and the effect of lesions there on speech, language and social behavior, strongly suggests that a neurobiological as opposed to neurocognitive model of autism is a more parsimonious explanation for the social and behavioral phenotypes observed in autism. (c) 2013 Wiley Periodicals, Inc.
C1 [Fisch, Gene S.] NYU, Coll Dent, Dept Epidemiol & Hlth Promot, New York, NY 10003 USA.
[Fisch, Gene S.] NYU, Coll Nursing, Dept Epidemiol & Hlth Promot, New York, NY 10003 USA.
RP Fisch, GS (reprint author), NYU, Coll Dent, Dept Epidemiol & Hlth Promot, 250 Pk Ave S,6th Fl, New York, NY 10003 USA.
EM gene.fisch@nyu.edu
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NR 158
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2013
VL 161
IS 10
BP 2464
EP 2480
DI 10.1002/ajmg.a.36135
PG 17
WC Genetics & Heredity
SC Genetics & Heredity
GA 264FP
UT WOS:000327862700007
PM 23956150
ER
PT J
AU Dimassi, S
Andrieux, J
Labalme, A
Lesca, G
Cordier, MP
Boute, O
Neut, D
Edery, P
Sanlaville, D
Schluth-Bolard, C
AF Dimassi, Sarra
Andrieux, Joris
Labalme, Audrey
Lesca, Gaetan
Cordier, Marie-Pierre
Boute, Odile
Neut, Dorothee
Edery, Patrick
Sanlaville, Damien
Schluth-Bolard, Caroline
TI Interstitial 12p13.1 Deletion Involving GRIN2B in Three Patients With
Intellectual Disability
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE aCGH; 12p13; 1 deletion; GRIN2B; intellectual disability; NMDA receptor
ID AUTISM SPECTRUM DISORDERS; DE-NOVO MUTATIONS; NMDA RECEPTORS;
SCHIZOPHRENIA; SUBUNIT; MEMORY; PERFORMANCE; EXPRESSION; DIVERSITY;
CHANNEL
AB We report on three patients presenting moderate intellectual disability, delayed language acquisition, and mild facial dysmorphia. Array-CGH studies revealed overlapping interstitial 12p13.1 microdeletions encompassing all or part of GRIN2B. GRIN2B encodes the NR2B subunit of the N-methyl-D-aspartate (NMDA) receptor. This receptor is a heteromeric glutamate-activated ion channel, present throughout the central nervous system. It plays a critical role in corticogenesis, neuronal migration, and synaptogenesis during brain development. GRIN2B alterations, including mutation and gene disruption by apparently balanced chromosomal rearrangements, have been described in patients with intellectual disability and autism spectrum disorder. We report here on the first cases of GRIN2B deletion, enlarging the spectrum of GRIN2B abnormalities. Our findings confirm the involvement of this gene in neurodevelopmental disorders. (c) 2013 Wiley Periodicals, Inc.
C1 [Dimassi, Sarra; Labalme, Audrey; Lesca, Gaetan; Cordier, Marie-Pierre; Edery, Patrick; Sanlaville, Damien; Schluth-Bolard, Caroline] Hosp Civils Lyon, Serv Genet, Lab Cytogenet Constitut, Ctr Biol & Pathol Est, Lyon, France.
[Andrieux, Joris] Hop Jeanne de Flandre, Lab Genet Med, CHRU Lille, Lille, France.
[Lesca, Gaetan; Edery, Patrick; Sanlaville, Damien; Schluth-Bolard, Caroline] Univ Lyon 1, CNRL, INSERM U1028, CNRS UMR5292,Equipe TIGER, F-69365 Lyon, France.
[Boute, Odile] Hop Jeanne de Flandre, Serv Genet Clin, CHRU Lille, Lille, France.
RP Schluth-Bolard, C (reprint author), Ctr Biol & Pathol EST, Serv Genet, Lab Cytogenet Constitut, 59 Blvd Pinel, F-69677 Bron, France.
EM caroline.schluth-bolard@chu-lyon.fr
RI sanlaville, damien/M-4716-2014
OI sanlaville, damien/0000-0001-9939-2849
FU French Ministry of Health
FX Grant sponsor: French Ministry of Health.
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NR 24
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2013
VL 161
IS 10
BP 2564
EP 2569
DI 10.1002/ajmg.a.36079
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 264FP
UT WOS:000327862700020
PM 23918416
ER
PT J
AU Lacaze, E
Gruchy, N
Penniello-Valette, MJ
Plessis, G
Richard, N
Decamp, M
Mittre, H
Leporrier, N
Andrieux, J
Kottler, ML
Gerard, M
AF Lacaze, Elodie
Gruchy, Nicolas
Penniello-Valette, Marie-Jose
Plessis, Ghislaine
Richard, Nicolas
Decamp, Mathieu
Mittre, Herve
Leporrier, Nathalie
Andrieux, Joris
Kottler, Marie-Laure
Gerard, Marion
TI De Novo 15q13.3 Microdeletion With Cryptogenic West Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE West syndrome; epilepsy; CHRNA7; array-CGH; 15q13; 3 microdeletion
ID FRONTAL-LOBE EPILEPSY; AUTISM SPECTRUM DISORDERS; INFANTILE SPASMS;
MENTAL-RETARDATION; DEVELOPMENTAL DISORDER; GENE; MUTATIONS; DELETION;
ASSOCIATION; PHENOTYPES
AB West syndrome is a well-recognized form of epilepsy, defined by a triad of infantile spasms, hypsarrhythmia and developmental arrest. West syndrome is heterogenous, caused by mutations of genes ARX, STXBP1, KCNT1 among others; 16p13.11 and 17q21.31 microdeletions are less frequent, usually associated with intellectual disability and facial dysmorphism. So-called idiopathic West syndrome is of better prognostic, without prior intellectual deficiency and usually responsive to anti-epileptic treatment. We report on a boy falling within the scope of idiopathic West syndrome, with no dysmorphic features and normal development before the beginning of West syndrome, with a good resolution after treatment, bearing a de novo 15q13.3 microdeletion. Six genes are located in the deleted region, including CHRNA7, which encodes a subunit of a nicotinic acetylcholine receptor, and is frequently associated with epilepsy. Exploration of the 15q13.3 region should be proposed in idiopathic West syndrome. (c) 2013 Wiley Periodicals, Inc.
C1 [Lacaze, Elodie; Gruchy, Nicolas; Plessis, Ghislaine; Richard, Nicolas; Decamp, Mathieu; Mittre, Herve; Leporrier, Nathalie; Kottler, Marie-Laure; Gerard, Marion] Hop Cote Nacre, Dept Genet, Caen, France.
[Penniello-Valette, Marie-Jose] Hop Cote Nacre, Dept Neuropediat, Caen, France.
[Andrieux, Joris] CHRU Lille, Lab Genet Med, F-59037 Lille, France.
RP Gerard, M (reprint author), CHR Clemenceau, Caen, France.
EM gerard-m@chu-caen.fr
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NR 32
TC 3
Z9 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2013
VL 161
IS 10
BP 2582
EP 2587
DI 10.1002/ajmg.a.36085
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 264FP
UT WOS:000327862700023
PM 23929658
ER
PT J
AU Schwaibold, EMC
Zoll, B
Burfeind, P
Hobbiebrunken, E
Wilken, B
Funke, R
Shoukier, M
AF Schwaibold, Eva Maria Christina
Zoll, Barbara
Burfeind, Peter
Hobbiebrunken, Elke
Wilken, Bernd
Funke, Rudolf
Shoukier, Moneef
TI A 3p Interstitial Deletion in Two Monozygotic Twin Brothers and an
18-Year-Old Man: Further Characterization and Review
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE 3p interstitial deletion; intellectual disability; autistic features; 3p
proximal deletion
ID SEVERE SPEECH DELAY; PROXIMAL 3P; FOXP1 GENE; TUMOR; EXPRESSION;
PATIENT; PROTEIN; AUTISM
AB An increasing number of patients with 3p proximal deletions were reported in the previous decade, but the region responsible for the main features such as intellectual disability (ID) and developmental delay is not yet characterized. Here we report on two monozygotic twin brothers of 2 10/12 years and an 18-year-old man, all three of them displaying severe ID, psychomotoric delay, autistic features, and only mild facial dysmorphisms. Array CGH (aCGH), revealed a 6.55Mb de novo interstitial deletion of 3p14.1p14.3 in the twin brothers and a 4.76Mb interstitial deletion of 3p14.1p14.2 in the 18-year-old patient, respectively. We compared the malformation spectrum with previous molecularly well-defined patients in the literature and in the DECIPHER database (Database of Chromosomal Imbalance and Phenotype in Humans using Ensembl Resources; http://decipher.sanger.ac.uk/). In conclusion, the deletion of a region containing 3p14.2 seems to be associated with a relative concise phenotype including ID and developmental delay. Thus, we hypothesize that 3p14.2 is the potential core region in 3p proximal deletions. The knowledge of this potential core region could be helpful in the genetic counselling of patients with 3p proximal deletions, especially concerning their phenotype. (c) 2013 Wiley Periodicals, Inc.
C1 [Schwaibold, Eva Maria Christina; Zoll, Barbara; Burfeind, Peter] Univ Gottingen, Inst Human Genet, D-37073 Gottingen, Germany.
[Hobbiebrunken, Elke] Univ Gottingen, Dept Pediat & Pediat Neurol, D-37073 Gottingen, Germany.
[Wilken, Bernd; Funke, Rudolf] Sozialpadiatr Zentrum, Dept Neuropediat, Kassel, Germany.
[Shoukier, Moneef] Univ Gottingen, Dept Gynecol & Obstet, D-37073 Gottingen, Germany.
RP Schwaibold, EMC (reprint author), Inst Human Genet, Heinrich Duker Weg 12, D-37073 Gottingen, Germany.
EM eva.schwaibold@med.uni-goettingen.de
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NR 18
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
EI 1552-4833
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2013
VL 161
IS 10
BP 2634
EP 2640
DI 10.1002/ajmg.a.36129
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 264FP
UT WOS:000327862700032
PM 23949945
ER
PT J
AU Emerson, E
Felce, D
Stancliffe, RJ
AF Emerson, Eric
Felce, David
Stancliffe, Roger J.
TI Issues Concerning Self-Report Data and Population-Based Data Sets
Involving People With Intellectual Disabilities
SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE intellectual disabilities; self-report; proxy; response bias;
population-based data; secondary analysis
ID QUALITY-OF-LIFE; MATERNAL MENTAL-HEALTH; DEVELOPMENTAL-DISABILITIES;
WESTERN-AUSTRALIA; COGNITIVE DELAY; CHILDREN; PREVALENCE; RETARDATION;
AUTISM; SCALE
AB This article examines two methodological issues regarding ways of obtaining and analyzing outcome data for people with intellectual disabilities: (a) self-report and proxy-report data and (b) analysis of population-based data sets. Some people with intellectual disabilities have difficulties with self-reporting due to problems of understanding and communication. However, there are serious doubts about the validity of proxy data for subjective issues. One important challenge with secondary analysis of population-based data sets is the difficulty of accurately identifying survey participants with intellectual disabilities. In both areas examined, it is important to recognize these constraints when interpreting research based on such data.
C1 [Emerson, Eric; Stancliffe, Roger J.] Univ Sydney, Ctr Disabil Res & Policy, Lidcombe, NSW 1825, Australia.
[Emerson, Eric] Univ Lancaster, Ctr Disabil Res, Lancaster LA1 4YW, England.
[Felce, David] Cardiff Univ, Sch Med, Welsh Ctr Learning Disabil, Cardiff CF10 3AX, S Glam, Wales.
RP Emerson, E (reprint author), Univ Lancaster, Ctr Disabil Res, Lancaster LA1 4YW, England.
EM roger.stancliffe@sydney.edu.au
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NR 66
TC 2
Z9 2
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1934-9491
EI 1934-9556
J9 INTELLECT DEV DISAB
JI Intellect. Dev. Disabil.
PD OCT
PY 2013
VL 51
IS 5
SI SI
BP 333
EP 348
DI 10.1352/1934-9556-51.5.333
PG 16
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 272IO
UT WOS:000328453900004
PM 24303821
ER
PT J
AU Anderson, LL
Humphries, K
McDermott, S
Marks, B
Sisarak, J
Larson, S
AF Anderson, Lynda Lahti
Humphries, Kathy
McDermott, Suzanne
Marks, Beth
Sisarak, Jasmina
Larson, Sheryl
TI The State of the Science of Health and Wellness for Adults With
Intellectual and Developmental Disabilities
SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE health; health care; wellness; IDD
ID AUTISM SPECTRUM DISORDERS; MENTAL-RETARDATION; DOWN-SYNDROME;
NUTRITIONAL-STATUS; PHYSICAL-ACTIVITY; UNITED-STATES; PROMOTION PROGRAM;
PRIMARY-CARE; RISK-FACTORS; PEOPLE
AB Historically, people with intellectual and developmental disabilities (IDD) have experienced health disparities related to several factors including: a lack of access to high quality medical care, inadequate preparation of health care providers to meet their needs, the social determinants of health (e.g., poverty, race and gender), and the failure to include people with IDD in public health efforts and other prevention activities. Over the past decade, a greater effort has been made to both identify and begin to address myriad health disparities experienced by people with IDD through a variety of activities including programs that address health lifestyles and greater attention to the training of health care providers. Gaps in the literature include the lack of intervention trials, replications of successful approaches, and data that allow for better comparisons between people with IDD and without IDD living in the same communities. Implications for future research needed to reduce health disparities for people with IDD include: better monitoring and treatment for chronic conditions common in the general population that are also experienced by people with IDD, an enhanced understanding of how to promote health among those in the IDD population who are aging, addressing the health needs of people with IDD who are not part of the disability service system, developing a better understanding of how to include people with IDD in health and wellness programs, and improving methods for addressing the health care needs of members of this group in an efficient and cost-effective manner, either through better access to general medical care or specialized programs.
C1 [Anderson, Lynda Lahti; Larson, Sheryl] Univ Minnesota, Res & Training Ctr Community Living, Minneapolis, MN 55455 USA.
[Humphries, Kathy] Univ Montana, Montana Disabil & Hlth Program, Rural Inst, Missoula, MT 59812 USA.
[McDermott, Suzanne] Univ S Carolina, Dept Family & Prevent Med, Columbia, SC 29208 USA.
[Marks, Beth] Univ Illinois, Dep Disabil & Human Dev, Chicago, IL 60680 USA.
[Sisarak, Jasmina] Univ Illinois, Dept Disabil & Human Dev, Chicago, IL 60680 USA.
RP Anderson, LL (reprint author), Univ Minnesota, Res & Training Ctr Community Living, Minneapolis, MN 55455 USA.
EM LLA@UMN.EDU
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NR 90
TC 2
Z9 2
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1934-9491
EI 1934-9556
J9 INTELLECT DEV DISAB
JI Intellect. Dev. Disabil.
PD OCT
PY 2013
VL 51
IS 5
SI SI
BP 385
EP 398
DI 10.1352/1934-9556-51.5.385
PG 14
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 272IO
UT WOS:000328453900008
PM 24303825
ER
PT J
AU Tordjman, S
Najjar, I
Bellissant, E
Anderson, GM
Barburoth, M
Cohen, D
Jaafari, N
Schischmanoff, O
Fagard, R
Lagdas, E
Kermarrec, S
Ribardiere, S
Botbol, M
Fougerou, C
Bronsard, G
Vernay-Leconte, J
AF Tordjman, Sylvie
Najjar, Imen
Bellissant, Eric
Anderson, George M.
Barburoth, Marianne
Cohen, David
Jaafari, Nemat
Schischmanoff, Olivier
Fagard, Remi
Lagdas, Enas
Kermarrec, Solenn
Ribardiere, Sophie
Botbol, Michel
Fougerou, Claire
Bronsard, Guillaume
Vernay-Leconte, Julie
TI Advances in the Research of Melatonin in Autism Spectrum Disorders:
Literature Review and New Perspectives
SO INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
LA English
DT Review
DE melatonin; biological clocks; circadian rhythm; synchrony; autism
spectrum disorders; social communication; stereotyped behaviors
ID CONTROLLED-RELEASE MELATONIN; PARENT-INFANT SYNCHRONY; CIRCADIAN
ACTIVITY RHYTHMS; PLACEBO-CONTROLLED TRIAL; FRAGILE-X-SYNDROME;
SLEEP-WAKE RHYTHM; RETT-SYNDROME; NEURODEVELOPMENTAL DISABILITIES;
INTELLECTUAL DISABILITY; DEVELOPMENTAL OUTCOMES
AB Abnormalities in melatonin physiology may be involved or closely linked to the pathophysiology and behavioral expression of autistic disorder, given its role in neurodevelopment and reports of sleep-wake rhythm disturbances, decreased nocturnal melatonin production, and beneficial therapeutic effects of melatonin in individuals with autism. In addition, melatonin, as a pineal gland hormone produced from serotonin, is of special interest in autistic disorder given reported alterations in central and peripheral serotonin neurobiology. More specifically, the role of melatonin in the ontogenetic establishment of circadian rhythms and the synchronization of peripheral oscillators opens interesting perspectives to ascertain better the mechanisms underlying the significant relationship found between lower nocturnal melatonin excretion and increased severity of autistic social communication impairments, especially for verbal communication and social imitative play. In this article, first we review the studies on melatonin levels and the treatment studies of melatonin in autistic disorder. Then, we discuss the relationships between melatonin and autistic behavioral impairments with regard to social communication (verbal and non-verbal communication, social interaction), and repetitive behaviors or interests with difficulties adapting to change. In conclusion, we emphasize that randomized clinical trials in autism spectrum disorders are warranted to establish potential therapeutic efficacy of melatonin for social communication impairments and stereotyped behaviors or interests.
C1 [Tordjman, Sylvie; Najjar, Imen; Lagdas, Enas; Kermarrec, Solenn; Ribardiere, Sophie; Vernay-Leconte, Julie] Univ Rennes 1, Hosp Univ Dept Child & Adolescent Psychiat, Guillaume Regnier Hosp, F-35000 Rennes, France.
[Tordjman, Sylvie; Barburoth, Marianne] CNRS UMR 8158, Lab Psychol Percept, F-75270 Paris, France.
[Bellissant, Eric; Fougerou, Claire] Univ Rennes 1, Univ Hosp, Inserm CIC Clin Invest Ctr 0203, F-35033 Rennes, France.
[Bellissant, Eric; Fougerou, Claire] Univ Rennes 1, Univ Hosp, Dept Clin Pharmacol, F-35033 Rennes, France.
[Anderson, George M.] Yale Child Study Ctr, Lab Dev Neurochem, New Haven, CT 06519 USA.
[Anderson, George M.] Yale Univ, Dept Lab Med, Sch Med, New Haven, CT 06519 USA.
[Cohen, David] Univ Paris 06, Hosp Univ Dept Child & Adolescent Psychiat, Pitie Salpetriere Hosp, F-75013 Paris, France.
[Jaafari, Nemat] Ctr Hosp Henri Laborit, Unite Rech Clin Intersectorielle Psychiat, CHU Poitiers, CIC INSERM U802, F-86022 Poitiers, France.
[Schischmanoff, Olivier; Fagard, Remi] Univ Paris 13, INSERM UMR U978, F-93009 Bobigny, France.
[Schischmanoff, Olivier; Fagard, Remi] Hop Avicenne, APHP, Lab Biochim & Biol Mol, F-93009 Bobigny, France.
[Botbol, Michel] UBO, Serv Hosp Univ Psychiat Enfant & Adolescent Brest, F-29238 Brest, France.
[Bronsard, Guillaume] Conseil Gen Bouches Du Rhone, Maison Dept Adolescent, F-13256 Marseille, France.
[Bronsard, Guillaume] Conseil Gen Bouches Du Rhone, Ctr Medicopsychopedagog, F-13256 Marseille, France.
[Bronsard, Guillaume] Fac Med Timone, Lab Sante Publ EA3279, F-13256 Marseille, France.
RP Tordjman, S (reprint author), Univ Rennes 1, Hosp Univ Dept Child & Adolescent Psychiat, Guillaume Regnier Hosp, F-35000 Rennes, France.
EM s.tordjman@yahoo.fr; imen.najjar@gmail.com;
eric.bellissant@chu-rennes.fr; george.anderson@yale.edu;
marianne.barburoth@parisdescartes.fr; david.cohen@psl.aphp.fr;
nemat.jaafari@ch-poitiers.fr; olivier.schischmanoff@avc.aphp.fr;
remi.fagard@avc.aphp.fr; inas-lagdas@hotmail.com;
solennkermarrec@yahoo.fr; sophie.ribardiere@yahoo.fr;
michel.botbol@orange.fr; claire.fougerou@chu-rennes.fr;
guillaume.bronsard@free.fr; julie9175@hotmail.fr
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NR 161
TC 8
Z9 8
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1422-0067
J9 INT J MOL SCI
JI Int. J. Mol. Sci.
PD OCT
PY 2013
VL 14
IS 10
BP 20508
EP 20542
DI 10.3390/ijms141020508
PG 35
WC Biochemistry & Molecular Biology; Chemistry, Multidisciplinary
SC Biochemistry & Molecular Biology; Chemistry
GA 274QK
UT WOS:000328620900068
PM 24129182
ER
PT J
AU Reynell, C
Harris, JJ
AF Reynell, Clare
Harris, Julia J.
TI The BOLD signal and neurovascular coupling in autism
SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE
LA English
DT Article
DE BOLD fMRI; Autism; Blood flow; Neurovascular coupling; Energy; Glutamate
ID MENTAL-RETARDATION PROTEIN; CEREBRAL O-2 CONSUMPTION; GLUTAMATE-RECEPTOR
5; DEVELOPMENTAL-CHANGES; SPECTRUM DISORDERS; IMAGING SIGNALS;
BLOOD-FLOW; EKER RATS; BRAIN; CHILDREN
AB BOLD (blood oxygen level dependent) fMRI (functional magnetic resonance imaging) is commonly used to study differences in neuronal activity between human populations. As the BOLD response is an indirect measure of neuronal activity, meaningful interpretation of differences in BOLD responses between groups relies upon a stable relationship existing between neuronal activity and the BOLD response across these groups. However, this relationship can be altered by changes in neurovascular coupling or energy consumption, which would lead to problems in identifying differences in neuronal activity. In this review, we focus on fMRI studies of people with autism, and comparisons that are made of their BOLD responses with-those of-control groups. We examine neurophysiological-differences in autism that may alter neurovascular coupling or energy use, discuss recent studies that have used fMRI to identify differences between participants with autism and control participants, and explore experimental approaches that could help attribute between-group differences in BOLD signals to either neuronal or neurovascular factors. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [Reynell, Clare; Harris, Julia J.] UCL, Dept Neurosci Physiol & Pharmacol, London WC1E 6BT, England.
RP Reynell, C (reprint author), UCL, Dept Neurosci Physiol & Pharmacol, Gower St, London WC1E 6BT, England.
EM c.reynell@ucl.ac.uk
FU MRC; Wellcome Trust; Fondation Leducq; ERC
FX Supported by the MRC, Wellcome Trust, Fondation Leducq and ERC. We thank
David Attwell, Renaud jolivet and Anusha Mishra for comments on the
manuscript.
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NR 50
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1878-9293
EI 1878-9307
J9 DEV COGN NEUROS-NETH
JI Dev. Cogn. Neurosci.
PD OCT
PY 2013
VL 6
BP 72
EP 79
DI 10.1016/j.dcn.2013.07.003
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 270DI
UT WOS:000328298700008
PM 23917518
ER
PT J
AU O'Reilly, H
Thiebaut, FI
White, SJ
AF O'Reilly, Helen
Thiebaut, Flora I.
White, Sarah J.
TI Is macrocephaly a neural marker of a local bias in autism?
SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE
LA English
DT Article
DE Macrocephaly; Local bias; Central coherence; Connectivity; Autism
ID WEAK CENTRAL COHERENCE; EMBEDDED FIGURES TASK; SPECTRUM DISORDERS;
CORTICAL UNDERCONNECTIVITY; SELECTIVE ATTENTION; HEAD CIRCUMFERENCE;
ASPERGER-SYNDROME; COGNITIVE-STYLE; CHILDREN; PERFORMANCE
AB Previous research has suggested that the local processing bias often reported in studies of Autism Spectrum Condition may only be typical of a subgroup of individuals with autism also presenting with macrocephaly. The current study examined a group of children with autism, with and without macrocephaly, on the Children's Embedded Figures Test (CEFT), a well-established measure of local processing bias. The results demonstrated that the children with autism and macrocephaly performed significantly better on the CEFT than children with autism without macrocephaly, indicative of a local bias. These results lend support to the proposal that both macrocephaly in autism and a local processing bias may arise from the same underlying neural processes and these characteristics represent an endophenotype in a subgroup of individuals with ASC worthy of further investigation. (C) 2013 Elsevier Ltd. All rights reserved.
C1 [O'Reilly, Helen] Univ Cambridge, Autism Res Ctr, Cambridge CB2 1TN, England.
[Thiebaut, Flora I.; White, Sarah J.] UCL, Inst Cognit Neurosci, London WC1N 3AR, England.
RP White, SJ (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England.
EM s.white@ucl.ac.uk
RI White, Sarah/C-4084-2008
OI White, Sarah/0000-0001-6946-9155
FU British Academy [PDF/2009/213]
FX British Academy. Grant number: PDF/2009/213.
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NR 41
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1878-9293
EI 1878-9307
J9 DEV COGN NEUROS-NETH
JI Dev. Cogn. Neurosci.
PD OCT
PY 2013
VL 6
BP 149
EP 154
DI 10.1016/j.dcn.2013.09.002
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 270DI
UT WOS:000328298700015
PM 24161549
ER
PT J
AU Naushad, SM
Jain, JMN
Prasad, CK
Naik, U
Akella, RRD
AF Naushad, Shaik Mohammad
Jain, Jamal Md Nurul
Prasad, Chintakindi Krishna
Naik, Usha
Akella, Radha Rama Devi
TI Autistic children exhibit distinct plasma amino acid profile
SO INDIAN JOURNAL OF BIOCHEMISTRY & BIOPHYSICS
LA English
DT Article
DE Autism; Glutamate; Asparagine; Tryptophan; Methionine
ID BACTERIAL OVERGROWTH; SEROTONIN SYNTHESIS; GLUTAMATE; DISORDER;
SUSCEPTIBILITY; VITAMIN-B12; CAPACITY; FAMILIES; PATHWAY; MICE
AB In order to ascertain whether autistic children display characteristic metabolic signatures that are of diagnostic value, plasma amino acid analyses were carried out on a cohort Of 138 autistic children and 138 normal controls using reverse-phase HPLC. Pre-column derivatization of amino acids with phenyl isothiocyanate forms phenyl thio-carbamate derivates that have a lambda(max) of 254 nm, enabling their detection using photodiode array. Autistic children showed elevated levels of glutamic acid (120 +/- 89 vs. 83 +/- 35 mu mol/L) and asparagine (85 +/- 37 vs. 47 +/- 19 union); lower levels of phenylalanine (45 +/- 20 vs. 59 +/- 18 mu mol/L), tryptophan (24 +/- 11 vs. 41 +/- 16 mu mol/L), methionine (22 +/- 9 vs. 28 +/- 9 won) and histidine (45 +/- 21 vs. 58 +/- 15 mu mol/L). A low molar ratio of (tryptophan/large neutral amino acids) x 100 was observed in autism (5.4 vs 9.2), indicating lesser availability of tryptophan for neurotransmitter serotonin synthesis. To conclude, elevated levels of excitatory amino acids (glutamate and asparagine), decreased essential amino acids (phenylalanine, tryptophan and methionine) and decreased precursors of neurotransmitters (tyrosine and tryptophan) are the distinct characteristics of plasma amino acid profile of autistic children. Thus, such metabolic signatures might be useful tools for early diagnosis of autism.
C1 [Naushad, Shaik Mohammad] SASTRA Univ, Sch Chem & Biotechnol, Thanjavur, TN, India.
[Jain, Jamal Md Nurul; Prasad, Chintakindi Krishna] Ctr DNA Fingerprinting & Diagnost, Hyderabad, Andhra Pradesh, India.
[Naik, Usha] Niloufer Hosp, Inst Child Hlth, Hyderabad, Andhra Pradesh, India.
[Akella, Radha Rama Devi] Rainbow Childrens Hosp, Hyderabad, Andhra Pradesh, India.
RP Naushad, SM (reprint author), SASTRA Univ, Sch Chem & Biotechnol, Thanjavur, TN, India.
EM naushadsm@gmail.com
FU Department of Biotechnology (DBT), India
FX The research was supported by the core grant provided by Department of
Biotechnology (DBT), India. We thank all the families who participated
in this study.
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NR 33
TC 3
Z9 3
PU NATL INST SCIENCE COMMUNICATION-NISCAIR
PI NEW DELHI
PA DR K S KRISHNAN MARG, PUSA CAMPUS, NEW DELHI 110 012, INDIA
SN 0301-1208
EI 0975-0959
J9 INDIAN J BIOCHEM BIO
JI Indian J. Biochem. Biophys.
PD OCT
PY 2013
VL 50
IS 5
SI SI
BP 474
EP 478
PG 5
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 270FR
UT WOS:000328304800018
PM 24772971
ER
PT J
AU Brady, NC
Thiemann-Bourque, K
Fleming, K
Matthews, K
AF Brady, Nancy C.
Thiemann-Bourque, Kathy
Fleming, Kandace
Matthews, Kris
TI Predicting Language Outcomes for Children Learning Augmentative and
Alternative Communication: Child and Environmental Factors
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE children; augmentative and alternative communication; assessment;
outcomes; intellectual disabilities
ID AUTISM SPECTRUM DISORDERS; SYMBOLIC PLAY; DEVELOPMENTAL DELAYS;
YOUNG-CHILDREN; PRELINGUISTIC PREDICTORS; PRESCHOOL-CHILDREN;
MENTAL-RETARDATION; VOCABULARY GROWTH; JOINT ATTENTION; DOWN-SYNDROME
AB Purpose: To investigate a model of language development for nonverbal preschool-age children learning to communicate with augmentative or alternative communication.
Method: Ninety-three preschool children with intellectual disabilities were assessed at Time 1, and 82 of these children were assessed 1 year later, at Time 2. The outcome variable was the number of different words the children produced (with speech, sign, or speech-generating devices). Children's intrinsic predictor for language was modeled as a latent variable consisting of cognitive development, comprehension, play, and nonverbal communication complexity. Adult input at school and home, and amount of augmentative or alternative communication instruction, were proposed mediators of vocabulary acquisition.
Results: A confirmatory factor analysis revealed that measures converged as a coherent construct, and a structural equation model indicated that the intrinsic child predictor construct predicted different words children produced. The amount of input received at home, but not at school, was a significant mediator.
Conclusions: The hypothesized model accurately reflects a latent construct of Intrinsic Symbolic Factor (ISF). Children who evidenced higher initial levels of ISF and more adult input at home produced more words 1 year later. The findings support the need to assess multiple child variables and suggest interventions directed to the indicators of ISF and input.
C1 [Brady, Nancy C.; Thiemann-Bourque, Kathy; Fleming, Kandace; Matthews, Kris] Univ Kansas, Lawrence, KS 66045 USA.
RP Brady, NC (reprint author), Univ Kansas, Lawrence, KS 66045 USA.
EM nbrady@ku.edu
FU National Institutes of Health [DC007684, HD018955]
FX This research was supported by Grants DC007684 and HD018955 from the
National Institutes of Health. We thank the families and teachers who
participated in this research and the research assistants who helped
with data collection.
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NR 88
TC 1
Z9 1
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
EI 1558-9102
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD OCT 1
PY 2013
VL 56
IS 5
BP 1595
EP 1612
DI 10.1044/1092-4388(2013/12-0102)
PG 18
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 269UJ
UT WOS:000328267300021
PM 23785187
ER
PT J
AU Bay, MJ
Talisa, VB
Vaurio, RG
Kaufmann, WE
Capone, GT
AF Bay, M. J.
Talisa, V. B.
Vaurio, R. G.
Kaufmann, W. E.
Capone, G. T.
TI Using the Autism Diagnostic Interview-Revised (ADI-R) and the Autism
Diagnostic Observation Schedule (ADOS) in Diagnosing Autism Spectrum
Disorder (ASD) in Children with Down Syndrome (DS)
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Case studies/case series; Genetics
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S145
EP S145
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200425
ER
PT J
AU Brumback, AC
Sohal, VS
AF Brumback, A. C.
Sohal, V. S.
TI Mechanisms of Prefrontal Microcircuit Dysfunction in Animal Models of
Autism
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Translational/experimental therapeutics
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S186
EP S187
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200551
ER
PT J
AU Dy, ME
Ballantyne, AO
Trauner, DA
AF Dy, M. E.
Ballantyne, A. O.
Trauner, D. A.
TI Behavioral Profiles of Children and Adolescents with Specific Language
Impairment and High Functioning Autism
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Case studies/case series
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S138
EP S139
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200406
ER
PT J
AU Jeste, SS
Freeman, SN
Paparella, T
Senturak, D
Kupelian, C
Kirkham, N
Johnson, SP
AF Jeste, S. S.
Freeman, S. N.
Paparella, T.
Senturak, D.
Kupelian, C.
Kirkham, N.
Johnson, S. P.
TI Neural Correlates of Visual Statistical Learning in Young Children with
Autism Spectrum Disorder (ASD)
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Neuroimaging
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S178
EP S179
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200527
ER
PT J
AU Johnson, WG
Stenroos, ES
Buyske, S
AF Johnson, W. G.
Stenroos, E. S.
Buyske, S.
TI Maternally Acting Gene Alleles (MAGAs) in Autism, a GWAS Study with
Meta-analysis
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Genetics
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S165
EP S166
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200487
ER
PT J
AU Kaufmann, WE
Walton-Bowen, KL
Kuriyama, N
Cherubini, M
Carpenter, RL
Bear, MF
Wang, P
AF Kaufmann, W. E.
Walton-Bowen, K. L.
Kuriyama, N.
Cherubini, M.
Carpenter, R. L.
Bear, M. F.
Wang, P.
TI Randomized, Controlled, Phase2 Trial of STX209 (Arbaclofen) for Social
Function in Autism Spectrum Disorder
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Case studies/case series; Translational/experimental therapeutics
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S129
EP S130
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200378
ER
PT J
AU Letovsky, SI
Causey, ME
Aryee, M
Skoletsky, J
Proulx, C
Sharp, FR
Pessah, IN
Hansen, R
Gregg, J
Hertz-Picciotto, I
AF Letovsky, S., I
Causey, M. E.
Aryee, M.
Skoletsky, J.
Proulx, C.
Sharp, F. R.
Pessah, I. N.
Hansen, R.
Gregg, J.
Hertz-Picciotto, I
TI Distinguishing Autism Spectrum Disorders from Other Developmental Delays
Using Blood RNASeq
SO ANNALS OF NEUROLOGY
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Child-Neurology-Society
CY OCT 30-NOV 02, 2013
CL Austin, TX
SP Child Neurol Soc
DE Genetics
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0364-5134
EI 1531-8249
J9 ANN NEUROL
JI Ann. Neurol.
PD OCT
PY 2013
VL 74
SU 17
SI SI
BP S166
EP S166
PG 1
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 264XL
UT WOS:000327914200488
ER
EF