FN Thomson Reuters Web of Science™
VR 1.0
PT J
AU Bagatell, N
AF Bagatell, Nancy
TI Engaged Moments: Mediated Action and Children With Autism in the
   Classroom Setting
SO OTJR-OCCUPATION PARTICIPATION AND HEALTH
LA English
DT Article
DE autism spectrum disorder; engagement; participation
ID SPECTRUM DISORDERS; OCCUPATIONAL-THERAPY; SOCIAL ENGAGEMENT;
   PARTICIPATION; DISABILITIES
AB The purpose of this microethnographic study is to explore ways to better understand engagement in occupation of children with autism spectrum disorder. Using video data, moments of engagement were examined in a child with autism spectrum disorder during the daily classroom activity of Circle Time. The interpretive frame focused on mediated action, the interaction between the agent, and cultural tools. Three scenes were analyzed using narrative and micro-analytic strategies. Analyses of two scenes highlighted how social and material mediators offer opportunities for engagement. Other children with autism provided appropriate scaffolds and demonstrated evidence of intersubjectivity, whereas material tools provided proximal prompts that enabled the child to engage. The third scene suggests that engagement may not always be observable (i.e., engagement may be a subjective state). Implications for practice and methodological insights are offered.
C1 Quinnipiac Univ, Hamden, CT 06518 USA.
RP Bagatell, N (reprint author), Quinnipiac Univ, Hamden, CT 06518 USA.
EM Nancy.Bagatell@quinnipiac.edu
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NR 39
TC 2
Z9 2
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 1539-4492
J9 OTJR-OCCUP PART HEAL
JI OTJR-Occup. Particip. Health
PD WIN
PY 2012
VL 32
IS 1
BP 258
EP 265
DI 10.3928/15394492-20110722-01
PG 8
WC Rehabilitation
SC Rehabilitation
GA 877WE
UT WOS:000299212600006
ER

PT J
AU Martin, LA
   Horriat, NL
AF Martin, Loren A.
   Horriat, Narges L.
TI The Effects of Birth Order and Birth Interval on the Phenotypic
   Expression of Autism Spectrum Disorder
SO PLOS ONE
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; RECEPTOR
   GENE OXTR; FETAL-BRAIN; DIAGNOSTIC INTERVIEW; BEHAVIORAL TREATMENT;
   REPETITIVE BEHAVIOR; SYMPTOM DOMAINS; SOCIAL-BEHAVIOR; NONVERBAL IQ
AB A rise in the prevalence of diagnosed cases of autism spectrum disorder (ASD) has been reported in several studies in recent years. While this rise in ASD prevalence is at least partially related to increased awareness and broadened diagnostic criteria, the role of environmental factors cannot be ruled out, especially considering that the cause of most cases of ASD remains unknown. The study of families with multiple affected children can provide clues about ASD etiology. While the majority of research on ASD multiplex families has focused on identifying genetic anomalies that may underlie the disorder, the study of symptom severity across ASD birth order may provide evidence for environmental factors in ASD. We compared social and cognitive measures of behavior between over 300 first and second affected siblings within multiplex autism families obtained from the Autism Genetic Resource Exchange dataset. Measures included nonverbal IQ assessed with the Ravens Colored Progressive Matrices, verbal IQ assessed with the Peabody Picture Vocabulary Test, and autism severity assessed with the Social Responsiveness Scale (SRS), an instrument established as a quantitative measure of autism. The results indicated that females were more severely impacted by ASD than males, especially first affected siblings. When first and second affected siblings were compared, significant declines in nonverbal and verbal IQ scores were observed. In addition, SRS results demonstrated a significant increase in autism severity between first and second affected siblings consistent with an overall decline in function as indicated by the IQ data. These results remained significant after controlling for the age and sex of the siblings. Surprisingly, the SRS scores were found to only be significant when the age difference between siblings was less than 2 years. These results suggest that some cases of ASD are influenced by a dosage effect involving unknown epigenetic, environmental, and/or immunological factors.
C1 [Martin, Loren A.] Azusa Pacific Univ, Dept Grad Psychol, Azusa, CA 91702 USA.
   [Horriat, Narges L.] Azusa Pacific Univ, Dept Biol & Chem, Azusa, CA USA.
RP Martin, LA (reprint author), Azusa Pacific Univ, Dept Grad Psychol, Azusa, CA 91702 USA.
EM lamartin@apu.edu
FU Faculty Research Council at Azusa Pacific University; National Institute
   of Mental Health [1U24MH081810]
FX This research was funded by a grant from the Faculty Research Council at
   Azusa Pacific University. The Autism Genetic Resource Exchange 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). 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 70
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 30
PY 2012
VL 7
IS 11
AR e51049
DI 10.1371/journal.pone.0051049
PG 12
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 054WM
UT WOS:000312376100265
ER

PT J
AU Pillai, D
   Sheppard, E
   Mitchell, P
AF Pillai, Dhanya
   Sheppard, Elizabeth
   Mitchell, Peter
TI Can People Guess What Happened to Others from Their Reactions?
SO PLOS ONE
LA English
DT Article
ID FIXATION PATTERNS; MIND; AUTISM; BELIEFS; ADULTS
AB Are we able to infer what happened to a person from a brief sample of his/her behaviour? It has been proposed that mentalising skills can be used to retrodict as well as predict behaviour, that is, to determine what mental states of a target have already occurred. The current study aimed to develop a paradigm to explore these processes, which takes into account the intricacies of real-life situations in which reasoning about mental states, as embodied in behaviour, may be utilised. A novel task was devised which involved observing subtle and naturalistic reactions of others in order to determine the event that had previously taken place. Thirty-five participants viewed videos of real individuals reacting to the researcher behaving in one of four possible ways, and were asked to judge which of the four 'scenarios' they thought the individual was responding to. Their eye movements were recorded to establish the visual strategies used. Participants were able to deduce successfully from a small sample of behaviour which scenario had previously occurred. Surprisingly, looking at the eye region was associated with poorer identification of the scenarios, and eye movement strategy varied depending on the event experienced by the person in the video. This suggests people flexibly deploy their attention using a retrodictive mindreading process to infer events. Citation: Pillai D, Sheppard E, Mitchell P (2012) Can People Guess What Happened to Others from Their Reactions? PLoS ONE 7(11): e49859. doi:10.1371/journal.pone.0049859
C1 [Pillai, Dhanya; Sheppard, Elizabeth; Mitchell, Peter] Univ Nottingham, Sch Psychol, Selangor, Malaysia.
RP Pillai, D (reprint author), Univ Nottingham, Sch Psychol, Malaysia Campus, Selangor, Malaysia.
EM khpx9dkr@nottingham.edu.my
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NR 18
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 30
PY 2012
VL 7
IS 11
AR e49859
DI 10.1371/journal.pone.0049859
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 054WM
UT WOS:000312376100035
PM 23226227
ER

PT J
AU Billeci, L
   Calderoni, S
   Tosetti, M
   Catani, M
   Muratori, F
AF Billeci, Lucia
   Calderoni, Sara
   Tosetti, Michela
   Catani, Marco
   Muratori, Filippo
TI White matter connectivity in children with autism spectrum disorders: a
   tract-based spatial statistics study
SO BMC NEUROLOGY
LA English
DT Article
DE ASD; TBSS; Tractography; Arcuate fasciculs; Language
ID CORPUS-CALLOSUM; YOUNG-CHILDREN; FRACTIONAL ANISOTROPY; FRONTAL-LOBE;
   DIFFUSION; BRAIN; LANGUAGE; CHILDHOOD; AGENESIS; IMPAIRMENTS
AB Background: Autism spectrum disorders (ASD) are associated with widespread alterations in white matter (WM) integrity. However, while a growing body of studies is shedding light on microstructural WM alterations in high-functioning adolescents and adults with ASD, literature is still lacking in information about whole brain structural connectivity in children and low-functioning patients with ASD. This research aims to investigate WM connectivity in ASD children with and without mental retardation compared to typically developing controls (TD).
   Methods: Diffusion tensor imaging (DTI) was performed in 22 young children with ASD (mean age: 5.54 years) and 10 controls (mean age: 5.25 years). Data were analysed both using the tract-based spatial statistics (TBSS) and the tractography. Correlations were investigated between the WM microstructure in the identified altered regions and the productive language level.
   Results: The TBSS analysis revealed widespread increase of fractional anisotropy (FA) in major WM pathways. The tractographic approach showed an increased fiber length and FA in the cingulum and in the corpus callosum and an increased mean diffusivity in the indirect segments of the right arcuate and the left cingulum. Mean diffusivity was also correlated with expressive language functioning in the left indirect segments of the arcuate fasciculus.
   Conclusions: Our study confirmed the presence of several structural connectivity abnormalities in young ASD children. In particular, the TBSS profile of increased FA that characterized the ASD patients extends to children a finding previously detected in ASD toddlers only. The WM integrity abnormalities detected may be relevant to the pathophysiology of ASD, since the structures involved participate in some core atypical characteristics of the disorder.
C1 [Billeci, Lucia] Natl Council Res CNR, Inst Clin Physiol, Pisa, Italy.
   [Calderoni, Sara; Tosetti, Michela; Muratori, Filippo] IRCCS Stella Maris Fdn, Pisa, Italy.
   [Catani, Marco] Kings Coll London, Inst Psychiat, NatBrainLab, London WC2R 2LS, England.
   [Muratori, Filippo] Univ Pisa, Dept Dev Med, Pisa, Italy.
RP Muratori, F (reprint author), IRCCS Stella Maris Fdn, Pisa, Italy.
EM filippo.muratori@inpe.unipi.it
FU European Union; Italian Ministry of Health
FX This study has been financially supported by the European Union (The
   MICHELANGELO Project) and by the Italian Ministry of Health (Strategic
   Program: Inquiry into Disruption of Intersubjective Equipment in Autism
   Spectrum Disorder in Childhood -IDIA-).
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NR 68
TC 19
Z9 20
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2377
J9 BMC NEUROL
JI BMC Neurol.
PD NOV 29
PY 2012
VL 12
AR 148
DI 10.1186/1471-2377-12-148
PG 16
WC Clinical Neurology
SC Neurosciences & Neurology
GA 111ZP
UT WOS:000316561300001
PM 23194030
ER

PT J
AU McFadden, KL
   Hepburn, S
   Winterrowd, E
   Schmidt, GL
   Rojas, DC
AF McFadden, Kristina L.
   Hepburn, Susan
   Winterrowd, Erin
   Schmidt, Gwenda L.
   Rojas, Donald C.
TI Abnormalities in gamma-band responses to language stimuli in
   first-degree relatives of children with autism spectrum disorder: an MEG
   study
SO BMC PSYCHIATRY
LA English
DT Article
ID MULTIPLE-INCIDENCE; SELECTIVE ATTENTION; BRAIN OSCILLATIONS; FAMILIES;
   MEMORY; EEG; LATERALIZATION; PHENOTYPE; PARENTS; HUMANS
AB Background: Synchronous neural oscillatory activity in the gamma range (30-80 Hz) has been shown to be abnormal in individuals with autism spectrum disorders (ASD) and their first-degree relatives in response to simple auditory stimuli. Gamma-band abnormalities in ASD probands have been seen in response to language stimuli, but this has not been investigated in first-degree relatives. This is of particular interest given that language impairments are a core symptom of ASD and may be part of the broad autism phenotype (BAP) seen in relatives.
   Methods: Magnetoencephalography recordings during a continuous word recognition task were obtained for 23 parents of a child with ASD (pASD) and 28 adult control participants. Total and evoked gamma-band activity, as well as inter-trial phase-locking factor (PLF), were measured in response to the task. Beta-band activity was also measured, due to its suggested role in language processing. Participants completed a series of language measures to assess the relationship between brain activity and language function, and lateralization of task-related activity was assessed.
   Results: The pASD group showed increased evoked gamma and beta activity, while controls had decreased evoked activity. Additionally, while both groups showed a reduction in total gamma power (commonly seen in language tasks), this reduction was more prominent in the control group. The pASD group demonstrated significantly worse performance on a measure of phonology compared to controls. Significant but distinct relationships were found between gamma/beta activity and language measures within the two groups. In addition, while the overall task generally elicited left lateralized responses, pASD showed greater left lateralization than controls in some regions of interest.
   Conclusions: Abnormalities in oscillatory responses to language were seen in pASD that are consistent with previous findings in ASD probands. Gamma-band responses to language stimuli have not previously been assessed in first-degree relatives of ASD probands and these findings are supportive of gamma-band activity as a heritable, neurophysiological biomarker of ASD. The possible relationship seen between language function and neural activity in the current study should be investigated further to assess if oscillatory response abnormalities may contribute to behavioural manifestations of the BAP.
C1 [McFadden, Kristina L.; Hepburn, Susan; Rojas, Donald C.] Univ Colorado, Dept Psychiat, Aurora, CO 80045 USA.
   [Hepburn, Susan] Univ Colorado, JFK Partners, Aurora, CO 80045 USA.
   [Winterrowd, Erin] Univ Wisconsin Oshkosh, Dept Psychol, Oshkosh, WI 54901 USA.
   [Schmidt, Gwenda L.] Hope Coll, Dept Psychol, Holland, MI 49423 USA.
RP Rojas, DC (reprint author), Univ Colorado, Dept Psychiat, Denver Anschutz Med Campus,13001 E 17th Pl, Aurora, CO 80045 USA.
EM don.rojas@ucdenver.edu
FU Cure Autism Now Foundation; Autism Speaks; PHS grant [R01 MH082820]; NIH
   [T32 MH015442]
FX This work was supported by a grant from the Cure Autism Now Foundation
   (to DCR), Autism Speaks, and PHS grant R01 MH082820 (to DCR) and in part
   under NIH grant T32 MH015442, institutional postdoctoral research
   training program for KLM.
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NR 83
TC 7
Z9 8
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 NOV 29
PY 2012
VL 12
AR 213
DI 10.1186/1471-244X-12-213
PG 18
WC Psychiatry
SC Psychiatry
GA 081FU
UT WOS:000314303700001
PM 23194079
ER

PT J
AU Severance, EG
   Kannan, G
   Gressitt, KL
   Xiao, JC
   Alaedini, A
   Pletnikov, MV
   Yolken, RH
AF Severance, Emily G.
   Kannan, Geetha
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   Alaedini, Armin
   Pletnikov, Mikhail V.
   Yolken, Robert H.
TI Anti-Gluten Immune Response following Toxoplasma gondii Infection in
   Mice
SO PLOS ONE
LA English
DT Article
ID CELIAC-DISEASE; GENE-EXPRESSION; INTESTINAL PERMEABILITY; GLIADIN
   PEPTIDES; DIETARY ANTIGENS; BIPOLAR DISORDER; GUT PERMEABILITY; ORAL
   INFECTION; C57BL/6 MICE; 2 PARTS
AB Gluten sensitivity may affect disease pathogenesis in a subset of individuals who have schizophrenia, bipolar disorder or autism. Exposure to Toxoplasma gondii is a known risk factor for the development of schizophrenia, presumably through a direct pathological effect of the parasite on brain and behavior. A co-association of antibodies to wheat gluten and to T. gondii in individuals with schizophrenia was recently uncovered, suggesting a coordinated gastrointestinal means by which T. gondii and dietary gluten might generate an immune response. Here, we evaluated the connection between these infectious- and food-based antigens in mouse models. BALB/c mice receiving a standard wheat-based rodent chow were infected with T. gondii via intraperitoneal, peroral and prenatal exposure methods. Significant increases in the levels of anti-gluten IgG were documented in all infected mice and in offspring from chronically infected dams compared to uninfected controls ( repetitive measures ANOVAs, two-tailed t-tests, all p <= 0.00001). Activation of the complement system accompanied this immune response (p <= 0.002-0.00001). Perorally-infected females showed higher levels of anti-gluten IgG than males (p <= 0.009) indicating that T. gondii-generated gastrointestinal infection led to a significant anti-gluten immune response in a sex-dependent manner. These findings support a gastrointestinal basis by which two risk factors for schizophrenia, T. gondii infection and sensitivity to dietary gluten, might be connected to produce the immune activation that is becoming an increasingly recognized pathology of psychiatric disorders. Citation: Severance EG, Kannan G, Gressitt KL, Xiao J, Alaedini A, et al. (2012) Anti-Gluten Immune Response following Toxoplasma gondii Infection in Mice. PLoS ONE 7(11): e50991. doi:10.1371/journal.pone.0050991
C1 [Severance, Emily G.; Gressitt, Kristin L.; Xiao, Jianchun; Yolken, Robert H.] Johns Hopkins Univ, Sch Med, Dept Pediat, Stanley Div Dev Neurovirol, Baltimore, MD 21205 USA.
   [Kannan, Geetha; Pletnikov, Mikhail V.] Johns Hopkins Univ, Sch Med, Dept Psychiat, Div Neurobiol, Baltimore, MD 21205 USA.
   [Alaedini, Armin] Columbia Univ, Dept Med, Med Ctr, New York, NY USA.
RP Severance, EG (reprint author), Johns Hopkins Univ, Sch Med, Dept Pediat, Stanley Div Dev Neurovirol, Baltimore, MD 21205 USA.
EM eseverance@jhmi.edu
FU National Institute of Mental Health (NIMH) P50 Silvio O. Conte Center at
   Johns Hopkins [MH-94268]; Brain and Behavior Research Foundation;
   Scott-Gentle Foundation Young Investigator; Stanley Medical Research
   Institute
FX This work was supported by a National Institute of Mental Health (NIMH)
   P50 Silvio O. Conte Center at Johns Hopkins (grant# MH-94268;
   http://www.nimh.nih.gov/); by the Brain and Behavior Research Foundation
   where Dr. Severance is a Scott-Gentle Foundation Young Investigator
   (http://bbrfoundation.org/); and by the Stanley Medical Research
   Institute (www.stanleyresearch.org/). These funders played no role in
   study design, data collection and analysis, decision to publish, or
   preparation of the manuscript.
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NR 68
TC 9
Z9 9
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 2012
VL 7
IS 11
AR e50991
DI 10.1371/journal.pone.0050991
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 051DI
UT WOS:000312104900093
PM 23209841
ER

PT J
AU Nelson, TH
   Jung, JY
   DeLuca, TF
   Hinebaugh, BK
   St Gabriel, KC
   Wall, DP
AF Nelson, Tristan H.
   Jung, Jae-Yoon
   DeLuca, Todd F.
   Hinebaugh, Byron K.
   St Gabriel, Kristian Che
   Wall, Dennis P.
TI Autworks: a cross-disease network biology application for Autism and
   related disorders
SO BMC MEDICAL GENOMICS
LA English
DT Article
DE Autism; Autistic disorder; Autism spectrum disorders; Autism genetics;
   Autism genomics; Network biology; Network medicine; Translational
   bioinformatics; Protein-protein interactions
ID SPECTRUM DISORDERS; HUMAN GENOME; GENETICS; DATABASE; EPIDEMIOLOGY;
   ASSOCIATION; COMPLEX; TWIN
AB Background: The genetic etiology of autism is heterogeneous. Multiple disorders share genotypic and phenotypic traits with autism. Network based cross-disorder analysis can aid in the understanding and characterization of the molecular pathology of autism, but there are few tools that enable us to conduct cross-disorder analysis and to visualize the results.
   Description: We have designed Autworks as a web portal to bring together gene interaction and gene-disease association data on autism to enable network construction, visualization, network comparisons with numerous other related neurological conditions and disorders. Users may examine the structure of gene interactions within a set of disorder-associated genes, compare networks of disorder/disease genes with those of other disorders/diseases, and upload their own sets for comparative analysis.
   Conclusions: Autworks is a web application that provides an easy-to-use resource for researchers of varied backgrounds to analyze the autism gene network structure within and between disorders. Availability: http://autworks.hms.harvard.edu/
C1 [Nelson, Tristan H.; Jung, Jae-Yoon; DeLuca, Todd F.; Hinebaugh, Byron K.; St Gabriel, Kristian Che; Wall, Dennis P.] Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA 02115 USA.
   [Nelson, Tristan H.; Wall, Dennis P.] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02115 USA.
RP Wall, DP (reprint author), Harvard Univ, Sch Med, Ctr Biomed Informat, Boston, MA 02115 USA.
EM dpwall@hms.harvard.edu
FU National Science Foundation [0543480, 0640809]; National Institutes of
   Health [LM009261]
FX Funding: This work was supported by the National Science Foundation
   [0543480 to D.P.W, 0640809 to D.P.W]; and the National Institutes of
   Health [LM009261 to D.P.W].
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NR 35
TC 1
Z9 1
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1755-8794
J9 BMC MED GENOMICS
JI BMC Med. Genomics
PD NOV 28
PY 2012
VL 5
AR 56
DI 10.1186/1755-8794-5-56
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 064AR
UT WOS:000313043800001
PM 23190929
ER

PT J
AU Henry, FE
   McCartney, AJ
   Neely, R
   Perez, AS
   Carruthers, CJL
   Stuenkel, EL
   Inoki, K
   Sutton, MA
AF Henry, Fredrick E.
   McCartney, Amber J.
   Neely, Ryan
   Perez, Amanda S.
   Carruthers, Cynthia J. L.
   Stuenkel, Edward L.
   Inoki, Ken
   Sutton, Michael A.
TI Retrograde Changes in Presynaptic Function Driven by Dendritic mTORC1
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID LOCAL PROTEIN-SYNTHESIS; BDNF MESSENGER-RNA; HOMEOSTATIC SYNAPTIC
   PLASTICITY; LONG-TERM DEPRESSION; MAMMALIAN TARGET; HIPPOCAMPAL-NEURONS;
   TUBEROUS-SCLEROSIS; TRANSLATIONAL CONTROL; SIGNALING PATHWAY; RETINOIC
   ACID
AB Mutations that alter signaling through the mammalian target of rapamycin complex 1 (mTORC1), a well established regulator of neuronal protein synthesis, have been linked to autism and cognitive dysfunction. Although previous studies have established a role for mTORC1 as necessary for enduring changes in postsynaptic function, here we demonstrate that dendritic mTORC1 activation in rat hippocampal neurons also drives a retrograde signaling mechanism promoting enhanced neurotransmitter release from apposed presynaptic terminals. This novel mode of synaptic regulation conferred by dendritic mTORC1 is locally implemented, requires downstream synthesis of brain-derived neurotrophic factor as a retrograde messenger, and is engaged in an activity-dependent fashion to support homeostatic trans-synaptic control of presynaptic function. Our findings thus reveal that mTORC1-dependent translation in dendrites subserves a unique mode of synaptic regulation, highlighting an alternative regulatory pathway that could contribute to the social and cognitive dysfunction that accompanies dysregulated mTORC1 signaling.
C1 [Henry, Fredrick E.; McCartney, Amber J.; Neely, Ryan; Perez, Amanda S.; Carruthers, Cynthia J. L.; Sutton, Michael A.] Univ Michigan, Mol & Behav Neurosci Inst, Ann Arbor, MI 48109 USA.
   [Henry, Fredrick E.; McCartney, Amber J.; Stuenkel, Edward L.; Sutton, Michael A.] Univ Michigan, Grad Program Neurosci, Ann Arbor, MI 48109 USA.
   [Inoki, Ken] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA.
   [Stuenkel, Edward L.; Inoki, Ken; Sutton, Michael A.] Univ Michigan, Dept Mol & Integrat Physiol, Ann Arbor, MI 48109 USA.
RP Sutton, MA (reprint author), Univ Michigan, Mol & Behav Neurosci Inst, 5067 BSRB,109 Zina Pitcher Pl, Ann Arbor, MI 48109 USA.
EM masutton@umich.edu
FU National Institute of Mental Health [F31MH093112, RO1MH085798]; Pew
   Biomedical Scholars Program
FX This work was supported by Grants F31MH093112 (F. E. H.) and RO1MH085798
   (M. A. S.) from The National Institute of Mental Health and a grant from
   the Pew Biomedical Scholars Program (M. A. S.). We thank Robert Edwards
   for generously providing vglut1-pHluorin. We also thank Hisashi Umemori
   and members of the Sutton laboratory for many helpful discussions.
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NR 75
TC 13
Z9 13
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 28
PY 2012
VL 32
IS 48
BP 17128
EP 17142
DI 10.1523/JNEUROSCI.2149-12.2012
PG 15
WC Neurosciences
SC Neurosciences & Neurology
GA 046WI
UT WOS:000311794700010
PM 23197706
ER

PT J
AU Xia, HW
   Wu, N
   Su, YJ
AF Xia, Haiwei
   Wu, Nan
   Su, Yanjie
TI Investigating the Genetic Basis of Theory of Mind (ToM): The Role of
   Catechol-O-Methyltransferase (COMT) Gene Polymorphisms
SO PLOS ONE
LA English
DT Article
ID ASPERGER-SYNDROME; METHYL-TRANSFERASE; SCHIZOPHRENIA; BRAIN; AUTISM;
   ASSOCIATION; DISORDERS; DOPAMINE; STORIES; ABILITY
AB The ability to deduce other persons' mental states and emotions which has been termed 'theory of mind (ToM)' is highly heritable. First molecular genetic studies focused on some dopamine-related genes, while the genetic basis underlying different components of ToM (affective ToM and cognitive ToM) remain unknown. The current study tested 7 candidate polymorphisms (rs4680, rs4633, rs2020917, rs2239393, rs737865, rs174699 and rs59938883) on the catechol-O-methyltransferase (COMT) gene. We investigated how these polymorphisms relate to different components of ToM. 101 adults participated in our study; all were genetically unrelated, non-clinical and healthy Chinese subjects. Different ToM tasks were applied to detect their theory of mind ability. The results showed that the COMT gene rs2020917 and rs737865 SNPs were associated with cognitive ToM performance, while the COMT gene rs5993883 SNP was related to affective ToM, in which a significant gender-genotype interaction was found (p = 0.039). Our results highlighted the contribution of DA-related COMT gene on ToM performance. Moreover, we found out that the different SNP at the same gene relates to the discriminative aspect of ToM. Our research provides some preliminary evidence to the genetic basis of theory of mind which still awaits further studies.
C1 [Xia, Haiwei; Wu, Nan; Su, Yanjie] Peking Univ, Dept Psychol, Beijing 100871, Peoples R China.
RP Su, YJ (reprint author), Peking Univ, Dept Psychol, Beijing 100871, Peoples R China.
EM yjsu@pku.edu.cn
FU National Natural Science Foundation of China [30970907, 31170995];
   National Basic Research Program (973 Program) [2010CB833904]
FX This work was supported by the National Natural Science Foundation of
   China (Project 30970907, 31170995) and National Basic Research Program
   (973 Program: 2010CB833904).
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NR 38
TC 5
Z9 6
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 2012
VL 7
IS 11
AR e49768
DI 10.1371/journal.pone.0049768
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048BS
UT WOS:000311885800022
PM 23209597
ER

PT J
AU Lavezzi, AM
   Matturri, L
AF Lavezzi, Anna M.
   Matturri, Luigi
TI Neuroanatomical dysmorphology of the medial superior olivary nucleus in
   sudden fetal and infant death
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE sudden infant death syndrome; sudden intrauterine unexplained death
   syndrome; medial superior olivary nucleus; superior olivary complex;
   neuropathology
ID INTRAUTERINE UNEXPLAINED DEATH; AUTISM SPECTRUM DISORDERS; TOBACCO-SMOKE
   EXPOSURE; BRAIN-STEM; CIGARETTE-SMOKING; PERINATAL DEATH; COMPLEX;
   CYTOARCHITECTURE; HINDBRAIN; NEURONS
AB This study expands our understanding of the organization of the human caudal pons, providing a morphologic characterization of the medial superior olivary nucleus (MSO), component of the superior olivary complex (SOC) that plays an important role in the processing of acoustic information. We examined victims of sudden unexplained fetal and infant death and controls (n=75), from 25 gestational weeks to 8 months of postnatal age, by complete autopsy and in-depth autonomic nervous system histological examination, particularly of the MSO nucleus, the focus of this study. Peculiar cytoarchitectural features of the MSO nucleus were found in sudden death cases, such as hypoplasia/agenesis and immature hypercellularity, frequently related to dysgenesis of contiguous structures involved in respiratory rhythm-generating circuit, in particular to hypoplasia of the retrotrapezoid and the facial nuclei. We propose the involvement of this nucleus in more important functions than those related to hearing, as breathing and, more extensively, all the vital activities. Besides, we highlight the fundamental role of the maternal smoking in pregnancy as etiological factor in the dysmorphic neuroanatomical development of the MSO nucleus.
C1 [Lavezzi, Anna M.; Matturri, Luigi] Univ Milan, Dept Biomed Surg & Dent Sci, Lino Rossi Res Ctr Study & Prevent Unexpected Per, I-20122 Milan, Italy.
RP Lavezzi, AM (reprint author), Univ Milan, Dept Biomed Surg & Dent Sci, Lino Rossi Res Ctr Study & Prevent Sudden Perinat, Via Commenda 19, I-20122 Milan, Italy.
EM anna.lavezzi@unimi.it
FU Italian Health's Ministry; Italian Ministry of University (PRIN)
   [2009KE5N9K]
FX The authors wish to express their gratitude to Dr. Graziella Alfonsi for
   her skillful technical cooperation. This study was supported by the
   Italian Health's Ministry in accordance with the Law 31/2006
   "Regulations for Diagnostic Post Mortem Investigation in Victims of
   Sudden Infant Death Syndrome (SIDS) and Unexpected Fetal Death" and by
   the project "Investigating the genetic and environmental basis of sudden
   infant death syndrome (SIDS) and sudden intrauterine unexplained death
   (SIUD)" founded by the Italian Ministry of University (PRIN 2009, grant
   no. 2009KE5N9K).
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NR 50
TC 3
Z9 3
PU FRONTIERS RESEARCH FOUNDATION
PI LAUSANNE
PA PO BOX 110, LAUSANNE, 1015, SWITZERLAND
SN 1662-5161
J9 FRONT HUM NEUROSCI
JI Front. Hum. Neurosci.
PD NOV 27
PY 2012
VL 6
AR 322
DI 10.3389/fnhum.2012.00322
PG 7
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 045TH
UT WOS:000311719200001
PM 23205011
ER

PT J
AU Volman, I
   Noordzij, ML
   Toni, I
AF Volman, Inge
   Noordzij, Matthijs L.
   Toni, Ivan
TI Sources of variability in human communicative skills
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE social cognition; joint action; tacit communication game; interactive
   intelligence; cooperation
ID PROGRESSIVE MATRICES; EMPATHY QUOTIENT; EMERGENCE; COGNITION; LANGUAGE;
   NEED; SYSTEMS; AUTISM
AB When established communication systems cannot be used, people rapidly create novel systems to modify the mental state of another agent according to their intentions. However, there are dramatic inter-individual differences in the implementation of this human competence for communicative innovation. Here we characterize psychological sources of inter-individual variability in the ability to build a shared communication system from scratch. We consider two potential sources of variability in communicative skill. Cognitive traits of two individuals could independently influence their joint ability to establish a communication system. Another possibility is that the overlap between those individual traits influences the communicative performance of a dyad. We assess these possibilities by quantifying the relationship between cognitive traits and behavior of communicating dyads. Cognitive traits were assessed with psychometric scores quantifying cooperative attitudes and fluid intelligence. Competence for implementing successful communicative innovations was assessed by using a non-verbal communicative task. Individual capacities influence communicative success when communicative innovations are generated. Dyadic similarities and individual traits modulate the type of communicative strategy chose. The ability to establish novel communicative actions was influenced by a combination of the communicator's ability to understand intentions and the addressee's ability to recognize patterns. Communicative pairs with comparable systemizing abilities or behavioral inhibition were more likely to explore the search space of possible communicative strategies by systemically adding new communicative behaviors to those already available. No individual psychometric measure seemed predominantly responsible for communicative success. These findings support the notion that the human ability for fast communicative innovations represents a special type of complex collaborative activity.
C1 [Volman, Inge; Noordzij, Matthijs L.; Toni, Ivan] Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
   [Volman, Inge] Radboud Univ Nijmegen, Inst Behav Sci, NL-6525 ED Nijmegen, Netherlands.
   [Noordzij, Matthijs L.] Univ Twente, Dept Cognit Psychol & Ergon, NL-7500 AE Enschede, Netherlands.
RP Toni, I (reprint author), Radboud Univ Nijmegen, Donders Inst Brain Cognit & Behav, Kapitellweg 29, NL-6525 ED Nijmegen, Netherlands.
EM ivan.toni@donders.ru.nl
RI Volman, Inge/E-1317-2012
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NR 39
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 22
PY 2012
VL 6
AR 310
DI 10.3389/fnhum.2012.00310
PG 11
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 045SV
UT WOS:000311718000001
PM 23189048
ER

PT J
AU Gong, T
   Shuai, L
AF Gong, Tao
   Shuai, Lan
TI Modelling the coevolution of joint attention and language
SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE joint attention; language origin; coevolution; ratchet effect; computer
   simulation
ID EVOLUTION; PROTOLANGUAGE; EMERGENCE; COGNITION; COMMUNICATION;
   ADAPTATION; CATEGORIES; CHILDREN; ORIGINS; AUTISM
AB Joint attention (JA) is important to many social, communicative activities, including language, and humans exhibit a considerably high level of JA compared with non-human primates. We propose a coevolutionary hypothesis to explain this degree-difference in JA: once JA started to aid linguistic comprehension, along with language evolution, communicative success (CS) during cultural transmission could enhance the levels of JA among language users. We illustrate this hypothesis via a multi-agent computational model, where JA boils down to a genetically transmitted ability to obtain non-linguistic cues aiding comprehension. The simulation results and statistical analysis show that: (i) the level of JA is correlated with the understandability of the emergent language; and (ii) CS can boost an initially low level of JA and 'ratchet' it up to a stable high level. This coevolutionary perspective helps explain the degree-difference in many language-related competences between humans and non-human primates, and reflects the importance of biological evolution, individual learning and cultural transmission to language evolution.
C1 [Gong, Tao] Univ Hong Kong, Dept Linguist, Hong Kong, Hong Kong, Peoples R China.
   [Shuai, Lan] Johns Hopkins Univ, Dept Elect & Comp Engn, Baltimore, MA USA.
RP Gong, T (reprint author), Univ Hong Kong, Dept Linguist, Pokfulam Rd, Hong Kong, Hong Kong, Peoples R China.
EM gtojty@gmail.com
RI Gong, Tao/H-9685-2014
FU Society of Scholars in the Humanities in the University of Hong Kong
FX This work was supported in part by the Society of Scholars in the
   Humanities in the University of Hong Kong. We thank Morten Christiansen
   from Cornell University for valuable comments on this work.
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NR 64
TC 7
Z9 7
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8452
J9 P ROY SOC B-BIOL SCI
JI Proc. R. Soc. B-Biol. Sci.
PD NOV 22
PY 2012
VL 279
IS 1747
BP 4643
EP 4651
DI 10.1098/rspb.2012.1431
PG 9
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
   Ecology; Evolutionary Biology
GA 025TU
UT WOS:000310218400017
PM 22977146
ER

PT J
AU El-Ansary, A
   Al-Ayadhi, L
AF El-Ansary, Afaf
   Al-Ayadhi, Laila
TI Lipid mediators in plasma of autism spectrum disorders
SO LIPIDS IN HEALTH AND DISEASE
LA English
DT Article
DE Autism; Inflammation; Prostaglandins; Leukotrienes; Isoprostane;
   Arachidonic acid
ID IN-VIVO; SYNAPTIC PLASTICITY; OXIDATIVE STRESS; SAUDI-ARABIA;
   FATTY-ACIDS; BRAIN; PROSTAGLANDINS; LEUKOTRIENES; INHIBITORS; EMERGENCE
AB Background: Inflammation is increasingly recognized as being of both physiological and pathological importance in the immature brain. Cerebellar pathology occurs in autism, as a neurodevelopmental disorder with genetic and environmental origins. The genesis of this disorder is still not understood but inflammation in utero or early in childhood is an environmental risk factor.
   Methods: Prostaglandin E2 (PGE2), cysteinyl leukotriene as two important lipid mediators together with 8 isoprostane as marker of oxidative stress were measured using ELISA in plasma of 20 male autistic patients compared to 19 age and gender matching control participants.
   Results: PGE2, leukotrienes and isoprostanes recorded significantly elevated levels in autistics compared to controls. Role of these measured parameters in inflammation and autoimmunity as two etiological factors in autism were discussed in details.
   Conclusion: Receiver Operating Characteristic (ROC) curve analysis shows satisfactory values of area under the curve (AUC) which could reflect the high degree of specificity and sensitivity of the altered PGE2, leukotrienes and isoprostanes as predictive biomarkers in autistic patients from Saudi Arabia.
C1 [El-Ansary, Afaf] King Saud Univ, Coll Sci, Dept Biochem, Riyadh 11451, Saudi Arabia.
   [Al-Ayadhi, Laila] King Saud Univ, Dept Physiol, Fac Med, Riyadh, Saudi Arabia.
   [El-Ansary, Afaf; Al-Ayadhi, Laila] Autism Res & Treatment Ctr, Riyadh, Saudi Arabia.
   [El-Ansary, Afaf; Al-Ayadhi, Laila] King Saud Univ, Shaik AL Amodi Autism Res Chair, Riyadh, Saudi Arabia.
RP El-Ansary, A (reprint author), King Saud Univ, Coll Sci, Dept Biochem, Riyadh 11451, Saudi Arabia.
EM elansary@ksu.edu.sa
FU King Abdul Aziz City for Science and Technology (KACST)
FX The authors would like to thank Shaik AL-Amodi Autism Research Chair,
   NPST - Medical Centers and the parents of autistic children, without
   whom this work was not possible. This work was supported by King Abdul
   Aziz City for Science and Technology (KACST).
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NR 55
TC 6
Z9 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-511X
J9 LIPIDS HEALTH DIS
JI Lipids Health Dis.
PD NOV 21
PY 2012
VL 11
AR 160
DI 10.1186/1476-511X-11-160
PG 9
WC Biochemistry & Molecular Biology; Nutrition & Dietetics
SC Biochemistry & Molecular Biology; Nutrition & Dietetics
GA 092HD
UT WOS:000315110000001
PM 23170784
ER

PT J
AU Gil, S
   Chambres, P
   Hyvert, C
   Fanget, M
   Droit-Volet, S
AF Gil, Sandrine
   Chambres, Patrick
   Hyvert, Charlotte
   Fanget, Muriel
   Droit-Volet, Sylvie
TI Children with Autism Spectrum Disorders Have "The Working Raw Material"
   for Time Perception
SO PLOS ONE
LA English
DT Article
ID INTERNAL CLOCK; TEMPORAL INFORMATION; ASSESSING ATTENTION; BISECTION;
   MEMORY; PERFORMANCE; DEFICIT; INTELLIGENCE; EXPECTANCY; COGNITION
AB The aim of the present study was to investigate whether children with Autism Spectrum Disorders (ASD) have a deficit in time perception. Twelve ASD children of normal intelligence and twelve typically developing children (TD) - matched on sex, chronological age, and mental age - performed four temporal bisection tasks that were adapted to the population. Two short (0.5 to 1 s and 1.25 to 2.5 s) and two long duration ranges (3.12 to 6.25 s and 7.81 to 16.62 s) were thus examined. The findings suggested that the perception of time in bisection is not impaired in ASD.
C1 [Gil, Sandrine] Univ Poitiers, Ctr Rech Cognit & Apprentissage, UMR 7295, CNRS, Poitiers, France.
   [Chambres, Patrick; Hyvert, Charlotte; Fanget, Muriel; Droit-Volet, Sylvie] Univ Clermont Ferrand, Lab Psychol Sociale & Cognit, UMR 6024, CNRS, Clermont Ferrand, France.
RP Gil, S (reprint author), Univ Poitiers, Ctr Rech Cognit & Apprentissage, UMR 7295, CNRS, Poitiers, France.
EM sandrine.gil@univ-poitiers.fr
FU Agence Nationale de la Recherche (ANR: Emotion(s), Cognition,
   Comportement (EMCO)), France
FX This work was supported by a grant from the Agence Nationale de la
   Recherche (ANR: Emotion(s), Cognition, Comportement (EMCO)), France. 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 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 21
PY 2012
VL 7
IS 11
AR e49116
DI 10.1371/journal.pone.0049116
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 047ER
UT WOS:000311821000029
PM 23185299
ER

PT J
AU Zielinski, BA
   Anderson, JS
   Froehlich, AL
   Prigge, MBD
   Nielsen, JA
   Cooperrider, JR
   Cariello, AN
   Fletcher, PT
   Alexander, AL
   Lange, N
   Bigler, ED
   Lainhart, JE
AF Zielinski, Brandon A.
   Anderson, Jeffrey S.
   Froehlich, Alyson L.
   Prigge, Molly B. D.
   Nielsen, Jared A.
   Cooperrider, Jason R.
   Cariello, Annahir N.
   Fletcher, P. Thomas
   Alexander, Andrew L.
   Lange, Nicholas
   Bigler, Erin D.
   Lainhart, Janet E.
TI scMRI Reveals Large-Scale Brain Network Abnormalities in Autism
SO PLOS ONE
LA English
DT Article
ID VOXEL-BASED MORPHOMETRY; FUNCTIONAL CONNECTIVITY; SPECTRUM DISORDERS;
   DEFAULT-MODE; CORPUS-CALLOSUM; FRONTAL-CORTEX; COMMUNICATION DEFICITS;
   CORTICAL CONNECTIVITY; STRUCTURAL COVARIANCE; MRI
AB Autism is a complex neurological condition characterized by childhood onset of dysfunction in multiple cognitive domains including socio-emotional function, speech and language, and processing of internally versus externally directed stimuli. Although gross brain anatomic differences in autism are well established, recent studies investigating regional differences in brain structure and function have yielded divergent and seemingly contradictory results. How regional abnormalities relate to the autistic phenotype remains unclear. We hypothesized that autism exhibits distinct perturbations in network-level brain architecture, and that cognitive dysfunction may be reflected by abnormal network structure. Network-level anatomic abnormalities in autism have not been previously described. We used structural covariance MRI to investigate network-level differences in gray matter structure within two large-scale networks strongly implicated in autism, the salience network and the default mode network, in autistic subjects and age-, gender-, and IQ-matched controls. We report specific perturbations in brain network architecture in the salience and default-mode networks consistent with clinical manifestations of autism. Extent and distribution of the salience network, involved in social-emotional regulation of environmental stimuli, is restricted in autism. In contrast, posterior elements of the default mode network have increased spatial distribution, suggesting a 'posteriorization' of this network. These findings are consistent with a network-based model of autism, and suggest a unifying interpretation of previous work. Moreover, we provide evidence of specific abnormalities in brain network architecture underlying autism that are quantifiable using standard clinical MRI.
C1 [Zielinski, Brandon A.] Univ Utah, Dept Pediat, Salt Lake City, UT 84112 USA.
   [Zielinski, Brandon A.] Univ Utah, Dept Neurol, Salt Lake City, UT USA.
   [Anderson, Jeffrey S.] Univ Utah, Dept Neuroradiol, Salt Lake City, UT USA.
   [Anderson, Jeffrey S.; Nielsen, Jared A.; Cooperrider, Jason R.; Lainhart, Janet E.] Univ Utah, Interdept Program Neurosci, Salt Lake City, UT USA.
   [Anderson, Jeffrey S.; Bigler, Erin D.; Lainhart, Janet E.] Univ Utah, Inst Brain, Salt Lake City, UT USA.
   [Froehlich, Alyson L.; Prigge, Molly B. D.; Nielsen, Jared A.; Cooperrider, Jason R.; Cariello, Annahir N.; Lainhart, Janet E.] Univ Utah, Sch Med, Dept Psychiat, Salt Lake City, UT 84112 USA.
   [Fletcher, P. Thomas] Univ Utah, Sch Comp, Salt Lake City, UT USA.
   [Fletcher, P. Thomas] Univ Utah, Sci Comp & Imaging Inst, Salt Lake City, UT USA.
   [Alexander, Andrew L.] Univ Wisconsin, Waisman Lab Brain Imaging & Behav, Madison, WI USA.
   [Alexander, Andrew L.] Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA.
   [Alexander, Andrew L.] Univ Wisconsin, Dept Psychiat, Madison, WI 53706 USA.
   [Lange, Nicholas] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA.
   [Lange, Nicholas] Harvard Univ, Sch Med, Dept Biostat, Boston, MA USA.
   [Lange, Nicholas] McLean Hosp, Neurostat Lab, Belmont, MA 02178 USA.
   [Bigler, Erin D.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
   [Bigler, Erin D.] Brigham Young Univ, Ctr Neurosci, Provo, UT 84602 USA.
RP Zielinski, BA (reprint author), Univ Utah, Dept Pediat, Salt Lake City, UT 84112 USA.
EM brandon.zielinski@utah.edu
FU NIH CHRCDA [5K12HD001410-10]; NIMH [RO1MH080826, P50MH60450]; NINDS
   [R01NS34783]; NIDCD [1F31 DC10143-01, T32DC008553]; Primary Children's
   Medical Center Foundation; Autism Speaks Mentor-based Predoctoral
   Fellowship [1677]; Ben B. and Iris M. Margolis Foundation
FX This study was supported by NIH CHRCDA 5K12HD001410-10; NIMH
   RO1MH080826, P50MH60450; NINDS R01NS34783; NIDCD 1F31 DC10143-01,
   T32DC008553; Primary Children's Medical Center Foundation; Autism Speaks
   Mentor-based Predoctoral Fellowship (1677); Ben B. and Iris M. Margolis
   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 79
TC 10
Z9 10
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 2012
VL 7
IS 11
AR e49172
DI 10.1371/journal.pone.0049172
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 047ER
UT WOS:000311821000032
PM 23185305
ER

PT J
AU Lombardo, MV
   Chakrabarti, B
   Lai, MC
   Baron-Cohen, S
AF Lombardo, Michael V.
   Chakrabarti, Bhismadev
   Lai, Meng-Chuan
   Baron-Cohen, Simon
CA MRC AIMS Consortium
TI Self-referential and social cognition in a case of autism and agenesis
   of the corpus callosum
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism; Agenesis of the corpus callosum; Self; Theory of mind;
   Mentalizing; Social cognition
ID HIGH-FUNCTIONING AUTISM; DE-NOVO MUTATIONS; ASPERGER-SYNDROME; SPECTRUM
   DISORDER; WHITE-MATTER; INDIVIDUAL-DIFFERENCES; YOUNG-CHILDREN; ADULTS;
   DEFICITS; ALEXITHYMIA
AB Background: While models of autism spectrum conditions (ASC) are emerging at the genetic level of analysis, clear models at higher levels of analysis, such as neuroanatomy, are lacking. Here we examine agenesis of the corpus callosum (AgCC) as a model at the level of neuroanatomy that may be relevant for understanding self-referential and social-cognitive difficulties in ASC.
   Methods: We examined performance on a wide array of tests in self-referential and social-cognitive domains in a patient with both AgCC and a diagnosis of ASC. Tests included a depth-of-processing memory paradigm with self-referential and social-cognitive manipulations, self-report measures of self-consciousness, alexithymia, and empathy, as well as performance measures of first-person pronoun usage and mentalizing ability. The performance of the AgCC patient was compared to a group of individuals with ASC but without AgCC and with neurotypical controls. These comparison groups come from a prior study where group differences were apparent across many measures. We used bootstrapping to assess whether the AgCC patient exhibited scores that were within or outside the 95% bias-corrected and accelerated bootstrap confidence intervals observed in both comparison groups.
   Results: Within the depth-of-processing memory paradigm, the AgCC patient showed decreased memory sensitivity that was more extreme than both comparison groups across all conditions. The patient's most pronounced difficulty on this task emerged in the social-cognitive domain related to information-processing about other people. The patient was similar to the ASC group in benefiting less from self-referential processing compared to the control group. Across a variety of other self-referential (i.e. alexithymia, private self-consciousness) and social-cognitive measures (i.e. self-reported imaginative and perspective-taking subscales of empathy, mentalizing), the AgCC patient also showed more extreme scores than those observed for both of the comparison groups. However, the AgCC patient scored within the range observed in the comparison groups on measures of first-person pronoun usage and self-reported affective empathy subscales.
   Conclusions: We conclude that AgCC co-occurring with a diagnosis of ASC may be a relevant model at the level of neuroanatomy for understanding mechanisms involved in self-referential and high-level social-cognitive difficulties in ASC.
C1 [Lombardo, Michael V.; Chakrabarti, Bhismadev; Lai, Meng-Chuan; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England.
   [Chakrabarti, Bhismadev] Univ Reading, Sch Psychol & Clin Language Sci, Ctr Integrat Neurosci & Neurodynam, Whiteknights RG6 6AL, England.
RP Lombardo, MV (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England.
EM ml437@cam.ac.uk
RI Ecker, Christine/E-5194-2010; Bolton, Patrick/E-8501-2010
OI Bolton, Patrick/0000-0002-5270-6262
FU Medical Research Council (MRC) Autism Imaging Multi-Centre Study (AIMS)
   Consortium; Shirley Foundation; Cambridge Overseas Trust, Jesus College
   Cambridge; British Academy
FX We acknowledge support from the Medical Research Council (MRC) Autism
   Imaging Multi-Centre Study (AIMS) Consortium. We thank Jennifer Barnes,
   Liliana Ruta, Greg Pasco, Sally Wheelwright, and Erin Ingudomnukul for
   help with data collection for the comparison groups. MVL was supported
   by the Shirley Foundation, the Cambridge Overseas Trust, Jesus College
   Cambridge, and the British Academy during this period of work. This work
   was conducted in association with the NIHR CLAHRC for Cambridgeshire and
   Peterborough NHS Foundation Trust. All funding bodies had no role in
   study design, data collection, analysis, and interpretation of the data.
   The MRC AIMS Consortium is a UK collaboration between the Institute of
   Psychiatry at Kings College, London, the Autism Research Centre and
   Brain Mapping Unit at the University of Cambridge, and the Autism
   Research Group at the University of Oxford. The Consortium members are,
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NR 102
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 21
PY 2012
VL 3
AR 14
DI 10.1186/2040-2392-3-14
PG 15
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254TH
UT WOS:000327189500001
PM 23171505
ER

PT J
AU Srinivasan, K
   Leone, DP
   Bateson, RK
   Dobreva, G
   Kohwi, Y
   Kohwi-Shigematsu, T
   Grosschedl, R
   McConnell, SK
AF Srinivasan, Karpagam
   Leone, Dino P.
   Bateson, Rosalie K.
   Dobreva, Gergana
   Kohwi, Yoshinori
   Kohwi-Shigematsu, Terumi
   Grosschedl, Rudolf
   McConnell, Susan K.
TI A network of genetic repression and derepression specifies projection
   fates in the developing neocortex
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE cell fate; cerebral cortex; axon guidance; transcription factor
ID DEVELOPING CEREBRAL-CORTEX; AUTISM SPECTRUM DISORDER; CORTICOSPINAL
   TRACT; NEURON IDENTITY; TBR1; DIFFERENTIATION; NETRIN-1; CALLOSAL;
   GUIDANCE; SPECIFICATION
AB Neurons within each layer in the mammalian cortex have stereotypic projections. Four genes-Fezf2, Ctip2, Tbr1, and Satb2-regulate these projection identities. These genes also interact with each other, and it is unclear how these interactions shape the final projection identity. Here we show, by generating double mutants of Fezf2, Ctip2, and Satb2, that cortical neurons deploy a complex genetic switch that uses mutual repression to produce subcortical or callosal projections. We discovered that Tbr1, EphA4, and Unc5H3 are critical downstream targets of Satb2 in callosal fate specification. This represents a unique role for Tbr1, implicated previously in specifying corticothalamic projections. We further show that Tbr1 expression is dually regulated by Satb2 and Ctip2 in layers 2-5. Finally, we show that Satb2 and Fezf2 regulate two disease-related genes, Auts2 (Autistic Susceptibility Gene2) and Bhlhb5 (mutated in Hereditary Spastic Paraplegia), providing a molecular handle to investigate circuit disorders in neurodevelopmental diseases.
C1 [Srinivasan, Karpagam; Leone, Dino P.; Bateson, Rosalie K.; McConnell, Susan K.] Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
   [Dobreva, Gergana; Grosschedl, Rudolf] Max Planck Inst Immunobiol & Epigenet, D-79108 Freiburg, Germany.
   [Kohwi, Yoshinori; Kohwi-Shigematsu, Terumi] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, Berkeley, CA 94720 USA.
RP McConnell, SK (reprint author), Stanford Univ, Dept Biol, Stanford, CA 94305 USA.
EM suemcc@stanford.edu
FU National Institutes of Health [EY08411, K99 MH086720]
FX We thank Bin Chen and William McKenna (University of California, Santa
   Cruz) for sharing reagents; Geetu Tuteja, Lee Shoa Long Clarke, and
   Bruce Schaar (Stanford University) for help and advice with ChIP
   experiments; Jeffrey Macklis (Harvard University) for Ctip2 mutant mice;
   Avraham Yaron (Weizmann Institute) for EphA4 and PlxnA4 expression
   constructs; and Robert Nechanitzky and Thomas Manke (laboratory of R.
   G.) for helping with in silico analyses of Satb2 binding sites. This
   study was funded by National Institutes of Health Grants EY08411 (to S.
   K. M.) and K99 MH086720 (to K.S.).
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NR 31
TC 28
Z9 28
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 20
PY 2012
VL 109
IS 47
BP 19071
EP 19078
DI 10.1073/pnas.1216793109
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 049PZ
UT WOS:000311997200020
PM 23144223
ER

PT J
AU Robertson, CE
   Martin, A
   Baker, CI
   Baron-Cohen, S
AF Robertson, Caroline E.
   Martin, Alex
   Baker, Chris I.
   Baron-Cohen, Simon
TI Atypical Integration of Motion Signals in Autism Spectrum Conditions
SO PLOS ONE
LA English
DT Article
ID DORSAL VISUAL PATHWAY; BIOLOGICAL MOTION; PARIETAL CORTEX; PERCEPTUAL
   DECISION; DOUBLE DISSOCIATION; TRANSPARENT MOTION; ASPERGER SYNDROME;
   JOINT ATTENTION; REACTION-TIME; NEURAL BASIS
AB Vision in Autism Spectrum Conditions (ASC) is characterized by enhanced perception of local elements, but impaired perception of global percepts. Deficits in coherent motion perception seem to support this characterization, but the roots and robustness of such deficits remain unclear. We aimed to investigate the dynamics of the perceptual decision-making network known to support coherent motion perception. In a series of forced-choice coherent motion perception tests, we parametrically varied a single stimulus dimension, viewing duration, to test whether the rate at which evidence is accumulated towards a global decision is atypical in ASC. 40 adult participants (20 ASC) performed a classic motion discrimination task, manually indicating the global direction of motion in a random-dot kinematogram across a range of coherence levels (2-75%) and stimulus-viewing durations (200-1500 ms). We report a deficit in global motion perception at short viewing durations in ASC. Critically, however, we found that increasing the amount of time over which motion signals could be integrated reduced the magnitude of the deficit, such that at the longest duration there was no difference between the ASC and control groups. Further, the deficit in motion integration at the shortest duration was significantly associated with the severity of autistic symptoms in our clinical population, and was independent from measures of intelligence. These results point to atypical integration of motion signals during the construction of a global percept in ASC. Based on the neural correlates of decision-making in global motion perception our findings suggest the global motion deficit observed in ASC could reflect a slower or more variable response from the primary motion area of the brain or longer accumulation of evidence towards a decision-bound in parietal areas.
C1 [Robertson, Caroline E.; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
   [Robertson, Caroline E.; Martin, Alex; Baker, Chris I.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Robertson, CE (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
EM cr419@cam.ac.uk
FU Intramural Research Program of the National Institute of Mental Health;
   Medical Research Council (UK); Gates-Cambridge Trust; NIH-Cambridge
   Fellowship
FX This work was supported by the Intramural Research Program of the
   National Institute of Mental Health and the Medical Research Council
   (UK) (http://www.mrc.ac.uk). CER was supported by the Gates-Cambridge
   Trust and the NIH-Cambridge 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 64
TC 9
Z9 9
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 2012
VL 7
IS 11
AR e48173
DI 10.1371/journal.pone.0048173
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 043II
UT WOS:000311535700008
PM 23185249
ER

PT J
AU Murdaugh, DL
   Shinkareva, SV
   Deshpande, HR
   Wang, J
   Pennick, MR
   Kana, RK
AF Murdaugh, Donna L.
   Shinkareva, Svetlana V.
   Deshpande, Hrishikesh R.
   Wang, Jing
   Pennick, Mark R.
   Kana, Rajesh K.
TI Differential Deactivation during Mentalizing and Classification of
   Autism Based on Default Mode Network Connectivity
SO PLOS ONE
LA English
DT Article
ID EVENT-RELATED FMRI; FUNCTIONAL CONNECTIVITY; ASPERGER-SYNDROME;
   PREFRONTAL CORTEX; SOCIAL COGNITION; SELF-REFLECTION; BRAIN-FUNCTION;
   MINDS; ATTRIBUTION; ABNORMALITIES
AB The default mode network (DMN) is a collection of brain areas found to be consistently deactivated during task performance. Previous neuroimaging studies of resting state have revealed reduced task-related deactivation of this network in autism. We investigated the DMN in 13 high-functioning adults with autism spectrum disorders (ASD) and 14 typically developing control participants during three fMRI studies (two language tasks and a Theory-of-Mind (ToM) task). Each study had separate blocks of fixation/resting baseline. The data from the task blocks and fixation blocks were collated to examine deactivation and functional connectivity. Deficits in the deactivation of the DMN in individuals with ASD were specific only to the ToM task, with no group differences in deactivation during the language tasks or a combined language and self-other discrimination task. During rest blocks following the ToM task, the ASD group showed less deactivation than the control group in a number of DMN regions, including medial prefrontal cortex (MPFC), anterior cingulate cortex, and posterior cingulate gyrus/precuneus. In addition, we found weaker functional connectivity of the MPFC in individuals with ASD compared to controls. Furthermore, we were able to reliably classify participants into ASD or typically developing control groups based on both the whole-brain and seed-based connectivity patterns with accuracy up to 96.3%. These findings indicate that deactivation and connectivity of the DMN were altered in individuals with ASD. In addition, these findings suggest that the deficits in DMN connectivity could be a neural signature that can be used for classifying an individual as belonging to the ASD group.
C1 [Murdaugh, Donna L.; Deshpande, Hrishikesh R.; Pennick, Mark R.; Kana, Rajesh K.] Univ Alabama Birmingham, Dept Psychol, Birmingham, AL 35294 USA.
   [Shinkareva, Svetlana V.; Wang, Jing] Univ S Carolina, Dept Psychol, Columbia, SC 29208 USA.
RP Kana, RK (reprint author), Univ Alabama Birmingham, Dept Psychol, Birmingham, AL 35294 USA.
EM rkana@uab.edu
FU UAB College of Arts and Sciences Faculty Development Grant;
   McNulty-Civitan Scientist Award
FX This research was supported by the UAB College of Arts and Sciences
   Faculty Development Grant and the McNulty-Civitan Scientist Award to RK.
   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 52
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 NOV 19
PY 2012
VL 7
IS 11
AR e50064
DI 10.1371/journal.pone.0050064
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040PB
UT WOS:000311333800067
PM 23185536
ER

PT J
AU Corbett, BA
   Schupp, CW
   Lanni, KE
AF Corbett, Blythe A.
   Schupp, Clayton W.
   Lanni, Kimberly E.
TI Comparing biobehavioral profiles across two social stress paradigms in
   children with and without autism spectrum disorders
SO MOLECULAR AUTISM
LA English
DT Article
DE Cortisol; Autism; Stress; Novelty; Peer; Age
ID HIGH-FUNCTIONING CHILDREN; COMPLEX DEVELOPMENTAL DISORDER;
   CORTICOTROPIN-RELEASING FACTOR; CORTISOL CIRCADIAN-RHYTHMS; PSYCHOSOCIAL
   STRESS; SALIVARY CORTISOL; ALPHA-AMYLASE; ANXIETY; RESPONSES; AMYGDALA
AB Background: Autism spectrum disorders (ASD) are defined by impairment in reciprocal social interaction and flexible adaptation to the environment. This study compared physiological stress in children with and without ASD exposed to two social stress protocols. We hypothesized that the ASD group would show heightened initial and enduring cortisol levels to the social stressors, which would be moderated by age and intelligence.
   Methods: Twenty-seven children with ASD and 32 with typical development (TYP) completed a standardized social-evaluative performance task and a validated paradigm of social play with peers. Physiological stress was measured by salivary cortisol at nine time points. Statistical approaches included repeated-measures linear mixed models and correlation analyses.
   Results: The average cortisol level of both groups during initial exposure to social situations was significantly greater than baseline levels (ASD, P = 0.018; TYP, P = 0.006). Stress responsivity was significantly different between the groups; the TYP group showed a significant reduction in cortisol over time (P = 0.023), whereas the ASD group maintained an elevated cortisol level (P > 0.05). The ASD group evidenced greater variability in between-group, within-group and intra-individual analyses. Age was a positive moderator of stress for the ASD group (P = 0.047), whereas IQ was a negative moderator for the TYP group (P = 0.061).
   Conclusions: Initial stress to novel social scenarios is idiosyncratic and predictive of subsequent exposure. Amidst significant variability in cortisol, children with ASD show enhanced and sustained social stress that increases with age. Developmental and cognitive factors differentially moderate stress in children with ASD and TYP, respectively. A model of neuroendocrine reactivity is proposed.
C1 [Corbett, Blythe A.] Vanderbilt Univ, Vanderbilt Kennedy Ctr, Dept Psychiat, Nashville, TN 37203 USA.
   [Schupp, Clayton W.] Canc Prevent Inst Calif, Fremont, CA 94538 USA.
   [Lanni, Kimberly E.] Vet Affairs Northern Calif Healthcare Syst, Mather, CA 95655 USA.
RP Corbett, BA (reprint author), Vanderbilt Univ, Vanderbilt Kennedy Ctr, Dept Psychiat, PMB 40,230 Appleton Pl, Nashville, TN 37203 USA.
EM blythe.corbett@vanderbilt.edu
FU National Institute of Health (NIH) [5K08NMH072958]; NIH [NIMH
   R01MH085717]
FX This study was supported by a National Institute of Health (NIH) Career
   Development Award (grant number 5K08NMH072958) and NIH Award (grant
   number NIMH R01MH085717) to BAC. The authors appreciate the valuable
   comments provided by Karoly Mirnics, MD pertaining to our manuscript.
   They are grateful to the children and families who participated in and
   continue to support this research.
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NR 57
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 NOV 17
PY 2012
VL 3
AR 13
DI 10.1186/2040-2392-3-13
PG 10
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254TG
UT WOS:000327189400001
PM 23158965
ER

PT J
AU Sun, W
   Deng, AC
   Jayaram, A
   Gibson, B
AF Sun, Wei
   Deng, Anchun
   Jayaram, Aditi
   Gibson, Brittany
TI Noise exposure enhances auditory cortex responses related to hyperacusis
   behavior
SO BRAIN RESEARCH
LA English
DT Article
DE Noise exposure; Hyperacusis; Tinnitus; Auditory cortex; Startle reflex
ID SALICYLATE-INDUCED TINNITUS; AWAKE GUINEA-PIGS; ACOUSTIC TRAUMA;
   HEARING-LOSS; EVOKED-RESPONSES; NEURAL ACTIVITY; RATS; MIGRAINE;
   STIMULATION; INHIBITION
AB Hyperacusis, a marked intolerance to normal environmental sound, is a common symptom in patients with tinnitus, Williams syndrome, autism, and other neurologic diseases. It has been suggested that an imbalance of excitation and inhibition in the central auditory system (CAS) may play an important role in hyperacusis. Recent studies found that noise exposure, one of the most common causes of hearing loss and tinnitus, can increase the auditory cortex (AC) response, presumably by increasing the gain of the AC. However, it is not clear whether the increased cortical response will affect sound sensitivity and induce hyperacusis. In this experiment, we studied the effects of noise exposure (narrow band noise, 12 kHz, 120 dB SPL, 1 hour) on the physiological response of the inferior colliculus (IC) and the AC, and the behavioral sound reaction in conscious Sprague Dawley rats. Noise exposure induced a decrease of sound evoked potential in the IC. However, significant increases of AC response including sound evoked potentials and the spike firing rates of AC neurons were recorded right after the noise exposure. These results suggest that noise exposure induces hyperexcitability of AC presumably by increasing the post-synaptic response of AC neurons. The behavioral consequence of the noise exposure on sound perception was measured by the amplitude of the acoustic startle response before and after noise exposure in a separate group of rats. Although noise exposure caused a moderate hearing loss, the acoustic startle amplitude at the super-threshold level was significantly increased. These results suggest that noise exposure can cause exaggerated the sound reaction which may be related with the enhanced responsiveness of the AC neurons. This phenomenon may be related with noise induced hyperacusis. This article is part of a Special Issue entitled: Tinnitus Neuroscience. Published by Elsevier B.V.
C1 [Sun, Wei; Deng, Anchun; Jayaram, Aditi; Gibson, Brittany] SUNY Buffalo, Ctr Hearing & Deafness, Buffalo, NY 14214 USA.
   [Sun, Wei; Jayaram, Aditi; Gibson, Brittany] SUNY Buffalo, Dept Communicat Disorders & Sci, Buffalo, NY 14214 USA.
RP Sun, W (reprint author), SUNY Buffalo, Ctr Hearing & Deafness, 137 Cary Hall, Buffalo, NY 14214 USA.
EM weisun@buffalo.edu
FU Action on Hearing Loss [G42]
FX We want thank Dr. Brian Allman for his critical comments on the
   manuscript. We also want to thank the reviewers for their suggestive
   criticism. This experiment was supported by grants from Action on
   Hearing Loss (G42).
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NR 35
TC 21
Z9 23
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD NOV 16
PY 2012
VL 1485
SI SI
BP 108
EP 116
DI 10.1016/j.brainres.2012.02.008
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 049LE
UT WOS:000311983700011
PM 22402030
ER

PT J
AU Chen, YK
   Chen, CY
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   Hsueh, YP
AF Chen, Yi-Kai
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TI CTTNBP2, but not CTTNBP2NL, regulates dendritic spinogenesis and
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SO MOLECULAR BIOLOGY OF THE CELL
LA English
DT Article
ID PROTEIN PHOSPHATASE 2A; BINDING PROTEIN; SPINES; CORTACTIN; ACTIN;
   AUTISM; DOMAIN; FAMILY; PP2A; GENE
AB Cortactin-binding protein 2 (CTTNBP2) interacts with cortactin to regulate cortactin mobility and control dendritic spine formation. CTTNBP2 has also been associated with autistic spectrum disorder. The regulation of dendritic spinogenesis could explain the association of CTTNBP2 with autism. Sequence comparison has indicated that CTTNBP2 N-terminal-like protein (CTTNBP2NL) is a CTTNBP2 homologue. To confirm the specific effect of CTTNBP2 on dendritic spinogenesis, here we investigate whether CTTNBP2NL has a similar function to CTTNBP2. Although both CTTNBP2 and CTTNBP2NL interact with cortactin, CTTNBP2NL is associated with stress fibers, whereas CTTNBP2 is distributed to the cortex and intracellular puncta. We also provide evidence that CTTNBP2, but not CTTNBP2NL, is predominantly expressed in the brain. CTTNBP2NL does not show any activity in the regulation of dendritic spinogenesis. In addition to spine morphology, CTTNBP2 is also found to regulate the synaptic distribution of striatin and zinedin (the regulatory B subunits of protein phosphatase 2A [PP2A]), which interact with CTTNBP2NL in HEK293 cells. The association between CTTNBP2 and striatin/zinedin suggests that CTTNBP2 targets the PP2A complex to dendritic spines. Thus we propose that the interactions of CTTNBP2 and cortactin and the PP2A complex regulate spine morphogenesis and synaptic signaling.
C1 [Chen, Yi-Kai; Chen, Chiung-Ya; Hu, Hsiao-Tang; Hsueh, Yi-Ping] Acad Sinica, Inst Mol Biol, Taipei 11529, Taiwan.
   [Hu, Hsiao-Tang; Hsueh, Yi-Ping] Natl Def Med Ctr, Grad Inst Life Sci, Taipei 161, Taiwan.
RP Hsueh, YP (reprint author), Acad Sinica, Inst Mol Biol, Taipei 11529, Taiwan.
EM yph@gate.sinica.edu.tw
FU Academia Sinica [AS-100-TP-B09]; National Science Council [NSC
   100-2321-B-001-022, 101-2321-B-001-010]
FX We thank Morgan Sheng and David Pallas for DNA constructs. This work was
   supported through grants from the Academia Sinica (AS-100-TP-B09) and
   National Science Council (NSC 100-2321-B-001-022 and 101-2321-B-001-010)
   to Y.P.H.
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NR 23
TC 8
Z9 14
PU AMER SOC CELL BIOLOGY
PI BETHESDA
PA 8120 WOODMONT AVE, STE 750, BETHESDA, MD 20814-2755 USA
SN 1059-1524
J9 MOL BIOL CELL
JI Mol. Biol. Cell
PD NOV 15
PY 2012
VL 23
IS 22
BP 4383
EP 4392
DI 10.1091/mbc.E12-05-0365
PG 10
WC Cell Biology
SC Cell Biology
GA 082PP
UT WOS:000314404700005
PM 23015759
ER

PT J
AU Ahmadlou, M
   Adeli, H
   Adeli, A
AF Ahmadlou, Mehran
   Adeli, Hojjat
   Adeli, Amir
TI Fuzzy Synchronization Likelihood-wavelet methodology for diagnosis of
   autism spectrum disorder
SO JOURNAL OF NEUROSCIENCE METHODS
LA English
DT Article
DE Autism; EEG; Fuzzy synchronization likelihood; Wavelet
ID EEG-BASED DIAGNOSIS; BRAIN CONNECTIVITY; NEURAL-NETWORKS; COHERENCE
AB This paper presents a methodology for investigation of functional connectivity in patients with autism spectrum disorder (ASD) using Fuzzy Synchronization Likelihood (Fuzzy SL). Fuzzy SLs between and within brain regions are calculated in all EEG sub-bands produced by the wavelet decomposition as well as in the full-band EEG. Then, discriminative Fuzzy SLs between and within different regions and different EEG sub-bands or full-band EEG for distinguishing autistic children from healthy control children are determined based on Analysis of Variation (ANOVA). Finally, the selected features are used as input to an Enhanced Probabilistic Neural Network classifier to make an accurate diagnosis of ASD based on the detected differences in the regional functional connectivity of autistic and healthy EEGs. The methodology is validated using EEG data obtained from 9 autistic and 9 healthy children. The ANOVA test showed high ability of the regional Fuzzy SLs in low frequency bands, delta and theta, as well as alpha band for discriminating the two groups. A high classification accuracy of 95.5% was achieved for distinguishing autistic EEGs from healthy EEGs. It is concluded that the methodology presented in this paper can be used as an effective tool for diagnosis of the autism. Further, the regional Fuzzy SLs discovered in this research can be used as reliable markers in neurofeedback treatments to improve neuronal plasticity and connectivity in autistic patients. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Adeli, Hojjat] Ohio State Univ, Dept Biomed Engn, Columbus, OH 43210 USA.
   [Ahmadlou, Mehran] Dynam Brain Res Off, Tehran, Iran.
   [Adeli, Hojjat] Ohio State Univ, Dept Biomed Informat, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Civil & Environm Engn & Geodet Sci, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Elect & Comp Engn, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Neurol Surg, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Neurosci, Columbus, OH 43210 USA.
   [Adeli, Amir] Ohio State Univ, Dept Neurol, Columbus, OH 43210 USA.
RP Adeli, H (reprint author), Ohio State Univ, Dept Biomed Engn, 470 Hitchcock Hall,2070 Neil Ave, Columbus, OH 43210 USA.
EM adeli.1@osu.edu
RI adeli, hojjat/D-1430-2010
OI adeli, hojjat/0000-0001-5718-1453
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NR 41
TC 32
Z9 32
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-0270
J9 J NEUROSCI METH
JI J. Neurosci. Methods
PD NOV 15
PY 2012
VL 211
IS 2
BP 203
EP 209
DI 10.1016/j.jneumeth.2012.08.020
PG 7
WC Biochemical Research Methods; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 060CG
UT WOS:000312753500004
PM 22968137
ER

PT J
AU Smith, J
AF Smith, Julianne
TI Party Planning for Children and Teens on the Autism Spectrum: How To
   Avoid Meltdowns and Have Fun!
SO LIBRARY JOURNAL
LA English
DT Book Review
CR REYNOLDS KE, 2012, PARTY PLANNING CHILD
NR 1
TC 0
Z9 0
PU REED BUSINESS INFORMATION
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA
SN 0363-0277
J9 LIBR J
JI Libr. J.
PD NOV 15
PY 2012
VL 137
IS 19
BP 74
EP 75
PG 2
WC Information Science & Library Science
SC Information Science & Library Science
GA 044WD
UT WOS:000311655000068
ER

PT J
AU Braunschweig, D
   Golub, MS
   Koenig, CM
   Qi, LH
   Pessah, IN
   Van de Water, J
   Berman, RF
AF Braunschweig, Daniel
   Golub, Mari S.
   Koenig, Claire M.
   Qi, Lihong
   Pessah, Isaac N.
   Van de Water, Judy
   Berman, Robert F.
TI Maternal autism-associated IgG antibodies delay development and produce
   anxiety in a mouse gestational transfer model
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Article
DE Autism; Maternal antibodies; Passive transfer; Immune; Mouse behavior
ID FETAL-BRAIN; MICE; DISORDERS; CHILDREN; BEHAVIOR; MOTHERS; SYSTEM;
   IMPAIRMENT; TRANSPORT; LUPUS
AB A murine passive transfer model system was employed to ascertain the effects of gestational exposure to a single, intravenous dose of purified, brain-reactive IgG antibodies from individual mothers of children with autism (MAU) or mothers with typically developing children (MTD). Growth and behavioral outcomes in offspring were measured from postnatal days 8 to 65 in each group. Comparisons revealed alterations in early growth trajectories, significantly impaired motor and sensory development, and increased anxiety. This report demonstrates for the first time the effects of a single, low dose gestational exposure of IgG derived from individual MAU on their offspring's physical and social development. Published by Elsevier BM.
C1 [Braunschweig, Daniel; Pessah, Isaac N.; Van de Water, Judy] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
   [Braunschweig, Daniel; Van de Water, Judy] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
   [Braunschweig, Daniel; Koenig, Claire M.; Qi, Lihong; Pessah, Isaac N.; Van de Water, Judy; Berman, Robert F.] Univ Calif Davis, NIEHS Ctr Childrens Environm Hlth, Davis, CA 95616 USA.
   [Qi, Lihong] Univ Calif Davis, Sch Med, Div Biostat, Dept Publ Hlth Sci, Davis, CA 95616 USA.
   [Golub, Mari S.] Univ Calif Davis, Dept Environm Toxicol, Davis, CA 95616 USA.
   [Pessah, Isaac N.] Univ Calif Davis, Dept Vet Mol Biosci, Davis, CA 95616 USA.
   [Koenig, Claire M.; Berman, Robert F.] Univ Calif Davis, Sch Med, Dept Neurol Surg, Davis, CA 95616 USA.
RP Braunschweig, D (reprint author), Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
EM dnau@ucdavis.edu
FU NIEHS [1P01ES11269-0]; U.S. EPA [R829388]; Autism Speaks; JB Johnson
   Foundation
FX This work was supported in part by NIEHS 1P01ES11269-0 and U.S. EPA
   Grant R829388, a Targeted Research Grant from Autism Speaks and an
   unrestricted research grant from the JB Johnson Foundation.
CR Arakawa H, 2008, NEUROSCI BIOBEHAV R, V32, P1236, DOI 10.1016/j.neubiorev.2008.05.012
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NR 36
TC 9
Z9 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-5728
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD NOV 15
PY 2012
VL 252
IS 1-2
BP 56
EP 65
DI 10.1016/j.jneuroim.2012.08.002
PG 10
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 037UR
UT WOS:000311132500007
PM 22951357
ER

PT J
AU Abdallah, MW
   Larsen, N
   Mortensen, EL
   Atladottir, HO
   Norgaard-Pedersen, B
   Bonefeld-Jorgensen, EC
   Grove, J
   Hougaard, DM
AF Abdallah, Morsi W.
   Larsen, Nanna
   Mortensen, Erik L.
   Atladottir, Hjordis O.
   Norgaard-Pedersen, Bent
   Bonefeld-Jorgensen, Eva Cecilie
   Grove, Jakob
   Hougaard, David M.
TI Neonatal levels of cytokines and risk of autism spectrum disorders: An
   exploratory register-based historic birth cohort study utilizing the
   Danish Newborn Screening Biobank
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Article
DE Autistic disorder; Cytokines; Newborn Screening Biobank; Population
   registers
ID INFECTION; CHILDREN; HOSPITALIZATION; SCHIZOPHRENIA; NEUROTROPHINS;
   BRAIN; BLOOD
AB The aim of the study was to analyze cytokine profiles in neonatal dried blood samples (n-DBSS) retrieved from The Danish Newborn Screening Biobank of children developing Autism Spectrum Disorders (ASD) later in life and controls. Samples of 359 ASD cases and 741 controls were analyzed using Luminex xMAP technology and clinical data were retrieved from nationwide registers. Findings showed that children developing ASD were more likely to have decreased levels of both T helper-1(Th-1)-like cytokines (i.e. IFN-gamma) and Th-2like cytokines (i.e. IL-4, IL-10) which may suggest a depressed or hypoactive immune cell activity during neonatal period in ASD. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Abdallah, Morsi W.] Univ Rostock, Rostock Univ Hosp, Dept Psychiat & Psychotherapy, D-18147 Rostock, Germany.
   [Abdallah, Morsi W.; Larsen, Nanna; Norgaard-Pedersen, Bent; Hougaard, David M.] Statens Serum Inst, Dept Clin Biochem & Immunol, DK-2300 Copenhagen S, Denmark.
   [Abdallah, Morsi W.; Atladottir, Hjordis O.] Aarhus Univ, Epidemiol Sect, HEALTH, DK-8000 Aarhus C, Denmark.
   [Mortensen, Erik L.] Univ Copenhagen, Inst Publ Hlth, DK-1353 Copenhagen K, Denmark.
   [Mortensen, Erik L.] Univ Copenhagen, Ctr Hlth Aging, DK-1353 Copenhagen K, Denmark.
   [Bonefeld-Jorgensen, Eva Cecilie] Aarhus Univ, Fac Hlth Sci, Ctr Arctic Environm Med, DK-8000 Aarhus C, Denmark.
   [Bonefeld-Jorgensen, Eva Cecilie] Aarhus Univ, Fac Hlth Sci, Unit Cellular & Mol Toxicol, DK-8000 Aarhus C, Denmark.
   [Grove, Jakob] Aarhus Univ, HEALTH, Dept Biomed, DK-8000 Aarhus C, Denmark.
   [Grove, Jakob] Aarhus Univ, HEALTH, Bioinformat Res Ctr BiRC, DK-8000 Aarhus C, Denmark.
RP Abdallah, MW (reprint author), Univ Rostock, Rostock Univ Hosp, Dept Psychiat & Psychotherapy, Gehlsheimer Str 20, D-18147 Rostock, Germany.
EM morsi.abdallah@med.uni-rostock.de
RI Bonefeld-Jorgensen, Eva Cecilie/A-1682-2015
FU Danish Medical Research Foundation; Danish Ministry of the Interior and
   Health [0523/09-060179]; Aarhus University Faculty of Health Sciences,
   Aarhus, Denmark and Statens Serum Institute; Department of Clinical
   Biochemistry and Immunology, Copenhagen, Denmark [494028]
FX The authors thank Lasse S. Jonsson and Jun Riis from Statens Serum
   Institute (SSI) and Maria Pryds for their assistance in data retrieval
   and also Vibeke Munk from University of Copenhagen for her
   administrative assistance. We also thank SSI Luminex Lab technical staff
   for their time and efforts and Dr. Poul Thorsen for his input and
   suggestions. The Danish Historic Birth Cohort was established at Statens
   Serum Institute in Copenhagen with a grant from The Danish Medical
   Research Foundation and The Danish Ministry of the Interior and Health
   (Project no. 271-05-0523/09-060179). This study is funded jointly by
   Aarhus University Faculty of Health Sciences, Aarhus, Denmark and
   Statens Serum Institute, Department of Clinical Biochemistry and
   Immunology, Copenhagen, Denmark (Project Title: Intrauterine Exposures
   and Childhood Psychiatric Disorders, Project ID: 494028).
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NR 56
TC 13
Z9 14
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-5728
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD NOV 15
PY 2012
VL 252
IS 1-2
BP 75
EP 82
DI 10.1016/j.jneuroim.2012.07.013
PG 8
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 037UR
UT WOS:000311132500009
PM 22917523
ER

PT J
AU de Ligt, J
   Willemsen, MH
   van Bon, BWM
   Kleefstra, T
   Yntema, HG
   Kroes, T
   Vulto-van Silfhout, AT
   Koolen, DA
   de Vries, P
   Gilissen, C
   del Rosario, M
   Hoischen, A
   Scheffer, H
   de Vries, BBA
   Brunner, HG
   Veltman, JA
   Vissers, LELM
AF de Ligt, Joep
   Willemsen, Marjolein H.
   van Bon, Bregje W. M.
   Kleefstra, Tjitske
   Yntema, Helger G.
   Kroes, Thessa
   Vulto-van Silfhout, Anneke T.
   Koolen, David A.
   de Vries, Petra
   Gilissen, Christian
   del Rosario, Marisol
   Hoischen, Alexander
   Scheffer, Hans
   de Vries, Bert B. A.
   Brunner, Han G.
   Veltman, Joris A.
   Vissers, Lisenka E. L. M.
TI Diagnostic Exome Sequencing in Persons with Severe Intellectual
   Disability
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID DE-NOVO MUTATIONS; MENTAL-RETARDATION; CONGENITAL-ANOMALIES; AUTISM;
   DISORDERS; GENETICS; SPECTRUM
AB Background
   The causes of intellectual disability remain largely unknown because of extensive clinical and genetic heterogeneity.
   Methods
   We evaluated patients with intellectual disability to exclude known causes of the disorder. We then sequenced the coding regions of more than 21,000 genes obtained from 100 patients with an IQ below 50 and their unaffected parents. A data-analysis procedure was developed to identify and classify de novo, autosomal recessive, and X-linked mutations. In addition, we used high-throughput resequencing to confirm new candidate genes in 765 persons with intellectual disability (a confirmation series). All mutations were evaluated by molecular geneticists and clinicians in the context of the patients' clinical presentation.
   Results
   We identified 79 de novo mutations in 53 of 100 patients. A total of 10 de novo mutations and 3 X-linked (maternally inherited) mutations that had been previously predicted to compromise the function of known intellectual-disability genes were found in 13 patients. Potentially causative de novo mutations in novel candidate genes were detected in 22 patients. Additional de novo mutations in 3 of these candidate genes were identified in patients with similar phenotypes in the confirmation series, providing support for mutations in these genes as the cause of intellectual disability. We detected no causative autosomal recessive inherited mutations in the discovery series. Thus, the total diagnostic yield was 16%, mostly involving de novo mutations.
   Conclusions
   De novo mutations represent an important cause of intellectual disability; exome sequencing was used as an effective diagnostic strategy for their detection. (Funded by the European Union and others.)
C1 [de Ligt, Joep; Willemsen, Marjolein H.; van Bon, Bregje W. M.; Kleefstra, Tjitske; Yntema, Helger G.; Kroes, Thessa; Vulto-van Silfhout, Anneke T.; Koolen, David A.; de Vries, Petra; Gilissen, Christian; del Rosario, Marisol; Hoischen, Alexander; Scheffer, Hans; de Vries, Bert B. A.; Brunner, Han G.; Veltman, Joris A.; Vissers, Lisenka E. L. M.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen Ctr Mol Life Sci,Inst Genet & Metab Dis, NL-6500 HB Nijmegen, Netherlands.
RP Veltman, JA (reprint author), Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen Ctr Mol Life Sci,Inst Genet & Metab Dis, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM j.veltman@gen.umcn.nl
RI Gilissen, Christian/E-5246-2012; Scheffer, Hans/E-4644-2012; Brunner,
   Han/C-9928-2013; van Bon, Bregje/D-3720-2013; Willemsen,
   Marjolein/G-9491-2013; Kleefstra, Tjitske/G-2619-2012; Vissers,
   Lisenka/A-2598-2015; Veltman, Joris/F-5128-2010
OI Gilissen, Christian/0000-0003-1693-9699; Scheffer,
   Hans/0000-0002-2986-0915; 
FU European Union; consortium Stronger on Your Own Feet; Netherlands
   Organization for Health Research and Development [ZonMW 907-00-365,
   917-86-319, 916-12-095, 917-66-363, 916-86-016]; European Union-funded
   TECHGENE project [Health-F5-2009-223143]; GEUVADIS project
   [Health-F7-2010-261123]; European Research Council [DENOVO 281964]; 
   [EU-7th-2010-241995]
FX Funded by the European Union and others.Supported by grants from the
   consortium Stronger on Your Own Feet (to Drs. Willemsen and Kleefstra),
   the Netherlands Organization for Health Research and Development (ZonMW
   907-00-365, to Dr. Kleefstra; 917-86-319, to Ms. de Vries; 916-12-095,
   to Dr. Hoischen; 917-66-363, to Dr. Veltman; and 916-86-016, to Dr.
   Vissers), the GENCODYS project (EU-7th-2010-241995, to Drs. Vulto-van
   Silfout and Kleefstra), the European Union-funded TECHGENE project
   (Health-F5-2009-223143, to Mr. de Ligt and Drs. Brunner, Scheffer, and
   Veltman), the GEUVADIS project (Health-F7-2010-261123, to Dr. Veltman),
   and the European Research Council (DENOVO 281964, to Dr. Veltman).
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NR 30
TC 240
Z9 298
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD NOV 15
PY 2012
VL 367
IS 20
BP 1921
EP 1929
DI 10.1056/NEJMoa1206524
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 036MB
UT WOS:000311029300008
PM 23033978
ER

PT J
AU Joseph, JE
   Swearingen, JE
   Clark, JD
   Benca, CE
   Collins, HR
   Corbly, CR
   Gathers, AD
   Bhatt, RS
AF Joseph, Jane E.
   Swearingen, Joshua E.
   Clark, Jonathan D.
   Benca, Chelsie E.
   Collins, Heather R.
   Corbly, Christine R.
   Gathers, Ann D.
   Bhatt, Ramesh S.
TI The changing landscape of functional brain networks for face processing
   in typical development
SO NEUROIMAGE
LA English
DT Article
DE Face processing; Development; Functional connectivity; Social
   neuroscience
ID EVENT-RELATED FMRI; OBJECT RECOGNITION; EFFECTIVE CONNECTIVITY; FACIAL
   IDENTITY; INFORMATION; PERCEPTION; EXPERTISE; AUTISM; MEMORY;
   REPRESENTATION
AB Greater expertise for faces in adults than in children may be achieved by a dynamic interplay of functional segregation and integration of brain regions throughout development The present study examined developmental changes in face network functional connectivity in children (5-12 years) and adults (18-43 years) during face-viewing using a graph-theory approach. A face-specific developmental change involved connectivity of the right occipital face area. During childhood, this node increased in strength and within-module clustering based on positive connectivity. These changes reflect an important role of the ROFA in segregation of function during childhood. In addition, strength and diversity of connections within a module that included primary visual areas (left and right calcarine) and limbic regions (left hippocampus and right inferior orbitofrontal cortex) increased from childhood to adulthood, reflecting increased visuo-limbic integration. This integration was pronounced for faces but also emerged for natural objects. Taken together, the primary face-specific developmental changes involved segregation of a posterior visual module during childhood, possibly implicated in early stage perceptual face processing, and greater integration of visuo-limbic connections from childhood to adulthood, which may reflect processing related to development of perceptual expertise for individuation of faces and other visually homogenous categories. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Joseph, Jane E.; Swearingen, Joshua E.; Benca, Chelsie E.; Collins, Heather R.] Med Univ S Carolina, Dept Neurosci, Charleston, SC 29425 USA.
   [Joseph, Jane E.; Clark, Jonathan D.; Benca, Chelsie E.; Collins, Heather R.; Corbly, Christine R.; Gathers, Ann D.] Univ Kentucky, Coll Med, Dept Anat & Neurobiol, Lexington, KY 40536 USA.
   [Bhatt, Ramesh S.] Univ Kentucky, Coll Arts & Sci, Dept Psychol, Lexington, KY 40506 USA.
RP Joseph, JE (reprint author), Med Univ S Carolina, Dept Neurosci, 19 Hagood Ave,Harborview Off Tower,Suite 806,POB, Charleston, SC 29425 USA.
EM josep@musc.edu
FU National Institutes of Health [R01-MH063817, R01-HD052724, R01-HD042451,
   F31-MH067461, P20-RR015592, P50-DA005312]; National Science Foundation
   [BCS-0224240]
FX This research was supported by the National Institutes of Health
   (R01-MH063817; R01-HD052724; R01-HD042451; F31-MH067461; P20-RR015592;
   P50-DA005312) and the National Science Foundation (BCS-0224240). We
   thank C. Butler, F. Davies, R. Ellison, N. Johnson, X. Liu and S.
   Whitaker for their technical assistance and S. Heydinger for his help
   with participant recruitment. We thank O. Sporns and M. Rubinov for
   their helpful input on the connectivity analyses. We also thank the
   volunteers and their families.
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NR 63
TC 7
Z9 7
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 2012
VL 63
IS 3
BP 1223
EP 1236
DI 10.1016/j.neuroimage.2012.08.021
PG 14
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 027UK
UT WOS:000310379100025
PM 22906788
ER

PT J
AU Nowaczyk, MJM
   Irons, MB
AF Nowaczyk, Malgorzata J. M.
   Irons, Mira B.
TI Smith-Lemli-Opitz syndrome: Phenotype, natural history, and epidemiology
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE Smith-Lemli-Opitz syndrome; DHCR7; 7-dehydrocholesterol; 2-3 toe
   syndactyly
ID 7-DEHYDROCHOLESTEROL REDUCTASE DEFICIENCY; DEFECTIVE
   CHOLESTEROL-BIOSYNTHESIS; MULTIPLE CONGENITAL-ANOMALIES; AUTISM SPECTRUM
   DISORDERS; PRENATAL-DIAGNOSIS; DELTA-7-STEROL REDUCTASE;
   HIRSCHSPRUNG-DISEASE; STEROL BIOSYNTHESIS; CARRIER FREQUENCY;
   AMNIOTIC-FLUID
AB SmithLemliOpitz syndrome (SLOS) is a congenital multiple anomaly/intellectual disability syndrome caused by a deficiency of cholesterol synthesis resulting from a deficiency of 7-dehydrocholesterol (7DHC) reductase encoded by DHCR7. SLOS is inherited in an autosomal recessive pattern. It is characterized by prenatal and postnatal growth retardation, microcephaly, a variable degree of intellectual disability that encompasses normal intelligence to severe intellectual deficiency, and multiple major and minor malformations. External malformations include distinctive facial features, cleft palate, postaxial polydactyly, 23 syndactyly of the toes, and underdeveloped external genitalia in males, while internal anomalies may affect every organ system. The clinical spectrum is wide, and rare individuals have been described with normal development and only minor malformations. The clinical diagnosis of SLOS is confirmed by demonstrating an abnormally elevated concentration of the cholesterol precursor, 7DHC, in serum or other tissues, or by the presence of two DHCR7 mutations. The enzymatic deficiency results in decreased cholesterol and increased 7DHC levels, both during embryonic development and after birth. The malformations found in SLOS may result from decreased cholesterol, increased 7DHC or a combination of these two factors. This review discusses the physical and behavioral phenotype of SLOS, the diagnostic approaches, the natural history from the prenatal period to adulthood, and current understanding of the pathophysiology of SLOS. (C) 2012 Wiley Periodicals, Inc.
C1 [Nowaczyk, Malgorzata J. M.] McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Hamilton, ON L8S 4J9, Canada.
   [Irons, Mira B.] Childrens Hosp Boston, Div Genet, Clin Programs, Boston, MA USA.
   [Irons, Mira B.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
RP Nowaczyk, MJM (reprint author), McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Room 3N16,1200 Main St W, Hamilton, ON L8S 4J9, Canada.
EM nowaczyk@hhsc.ca
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NR 132
TC 12
Z9 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2012
VL 160C
IS 4
SI SI
BP 250
EP 262
DI 10.1002/ajmg.c.31343
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 023YB
UT WOS:000310072700003
PM 23059950
ER

PT J
AU Svoboda, MD
   Christie, JM
   Eroglu, Y
   Freeman, KA
   Steiner, RD
AF Svoboda, Melissa D.
   Christie, Jill M.
   Eroglu, Yasemen
   Freeman, Kurt A.
   Steiner, Robert D.
TI Treatment of Smith-Lemli-Opitz Syndrome and Other Sterol Disorders
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE Smith-Lemli-Opitz syndrome; sterol disorders; cholesterol
   supplementation; simvastatin; behavior
ID ABNORMAL CHOLESTEROL-METABOLISM; MULTIPLE CONGENITAL-ANOMALIES; AUTISM
   SPECTRUM DISORDERS; PLASMA CHOLESTANOL LEVELS; CEREBROTENDINOUS
   XANTHOMATOSIS; CHENODEOXYCHOLIC ACID; 7-DEHYDROCHOLESTEROL-DERIVED
   OXYSTEROLS; SIMVASTATIN TREATMENT; RETINAL DEGENERATION;
   DIETARY-CHOLESTEROL
AB Smith-Lemli-Opitz syndrome (SLOS) is an autosomal recessive genetic condition with a broad phenotype that results from deficiency of the final enzyme of the cholesterol synthesis pathway. This defect causes low or low-normal plasma cholesterol levels and increased 7- and 8-dehydrocholesterol (DHC) levels. Many therapies for SLOS and other disorders of sterol metabolism have been proposed, and a few of them have been undertaken in selected patients, but robust prospective clinical trials with validated outcome measures are lacking. We review the current literature and expert opinion on treatments for SLOS and other selected sterol disorders, including dietary cholesterol therapy, statin treatment, bile acid supplementation, medical therapies, and surgical interventions, as well as directions for future therapies and treatment research. (C) 2012 Wiley Periodicals, Inc.
C1 [Steiner, Robert D.] Oregon Hlth & Sci Univ, Dept Pediat, Fac Pediat Mol & Med Genet, Portland, OR 97239 USA.
   [Eroglu, Yasemen] Oregon Hlth & Sci Univ, Div Pediat Gastroenterol, Portland, OR 97239 USA.
   [Steiner, Robert D.] Oregon Hlth & Sci Univ, Program Mol & Cellular Biosci, Portland, OR 97239 USA.
   [Steiner, Robert D.] NIH, Sterol & Isoprenoid Res Consortium, STAIR, Rare Dis Clin Res Consortium RDCRC, Bethesda, MD 20892 USA.
RP Steiner, RD (reprint author), Oregon Hlth & Sci Univ, Dept Pediat, Fac Pediat Mol & Med Genet, 707 SW Gaines St CDRC P, Portland, OR 97239 USA.
EM steinerr@ohsu.edu
FU NIH Rare Diseases Clinical Research Network (RDCRN) via the Sterol and
   Isoprenoid Research (STAIR) consortium; HHS [U54 HD 061939, R01 HL
   073980];  [HHS U54 HD061939];  [HHS R01 HL 073980]
FX Grant sponsor: HHS U54 HD061939.Grant sponsor: HHS R01 HL 073980.The
   authors thank Mary Lou Oster-Granite for her review of the manuscript.
   R. D. S. is supported by the NIH Rare Diseases Clinical Research Network
   (RDCRN) via the Sterol and Isoprenoid Research (STAIR) consortium, HHS
   grant U54 HD 061939, and by HHS grant R01 HL 073980. The authors thank
   Jean-Baptiste Roullet for creation of the figure.
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NR 87
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
EI 1552-4876
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2012
VL 160C
IS 4
SI SI
BP 285
EP 294
DI 10.1002/ajmg.c.31347
PG 10
WC Genetics & Heredity
SC Genetics & Heredity
GA 023YB
UT WOS:000310072700005
PM 23042642
ER

PT J
AU Diaz-Stransky, A
   Tierney, E
AF Diaz-Stransky, Andrea
   Tierney, Elaine
TI Cognitive and behavioral aspects of Smith-Lemli-Opitz syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS
LA English
DT Article
DE intellectual disability; language deficits; motor deficits;
   opisthokinesis; self-injury behavior; autism; hyperactivity; sensory
   hypersensitivity; affect dysregulation; sleep disturbances; suicidal
   risk; behavioral response to cholesterol supplementation
ID AUTISM SPECTRUM DISORDERS; DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; SENSORY
   PROFILE; SLEEP PROBLEMS; RSH SYNDROME; CHILDREN; METABOLISM; PHENOTYPE;
   DISABILITIES; PERFORMANCE
AB The brain's high concentrations of cholesterol make it especially vulnerable to the cholesterol biosynthetic defect that characterizes SmithLemliOpitz syndrome (SLOS). An attempt to characterize the cognitive and behavioral phenotype of SLOS has identified increased rates of intellectual disability, language and motor developmental delay, repeated self-injury behaviors, sensory hyperreactivity, hyperactivity, affect dysregulation, and sleep disturbances. Some research has suggested that carriers of the gene mutation that results in SLOS display increased risk of suicidal behavior. Cholesterol dysregulation impairs neuroplasticity, which may be a mechanism underlying some of the mentioned abnormalities. Discrete positive effects have been reported with the use of cholesterol supplementation in the treatment of SLOS. Research has been limited by the small number of subjects available, and a limited understanding of lipid metabolism in the brain. Hopefully future research will help clarify the role that cholesterol plays in cognitive and behavioral abnormalities like the ones associated with SLOS. This would accelerate the development of treatments for SLOS, and perhaps also further understanding of non-syndromic psychiatric disorders such as autism and attention deficit hyperactivity disorder. (C) 2012 Wiley Periodicals, Inc.
C1 [Tierney, Elaine] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21218 USA.
RP Tierney, E (reprint author), KKI Psychiat, Rm 227A,716 North Broadway, Baltimore, MD 21205 USA.
EM tierney@kennedykrieger.org
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NR 56
TC 11
Z9 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4868
EI 1552-4876
J9 AM J MED GENET C
JI Am. J. Med. Genet. C
PD NOV 15
PY 2012
VL 160C
IS 4
SI SI
BP 295
EP 300
DI 10.1002/ajmg.c.31342
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 023YB
UT WOS:000310072700006
PM 23042585
ER

PT J
AU Balestrieri, E
   Arpino, C
   Matteucci, C
   Sorrentino, R
   Pica, F
   Alessandrelli, R
   Coniglio, A
   Curatolo, P
   Rezza, G
   Macciardi, F
   Garaci, E
   Gaudi, S
   Sinibaldi-Vallebona, P
AF Balestrieri, Emanuela
   Arpino, Carla
   Matteucci, Claudia
   Sorrentino, Roberta
   Pica, Francesca
   Alessandrelli, Riccardo
   Coniglio, Antonella
   Curatolo, Paolo
   Rezza, Giovanni
   Macciardi, Fabio
   Garaci, Enrico
   Gaudi, Simona
   Sinibaldi-Vallebona, Paola
TI HERVs Expression in Autism Spectrum Disorders
SO PLOS ONE
LA English
DT Article
ID HUMAN ENDOGENOUS RETROVIRUSES; LYMPHOBLASTOID CELL-LINES; HUMAN TISSUES;
   L1 RETROTRANSPOSITION; HUMAN BRAIN; GENOME; SCHIZOPHRENIA; ASSOCIATION;
   IDENTIFICATION; POLYMORPHISMS
AB Background: Autistic Spectrum Disorder (ASD) is a heterogeneous neurodevelopmental disorder, resulting from complex interactions among genetic, genomic and environmental factors. Here we have studied the expression of Human Endogenous Retroviruses (HERVs), non-coding DNA elements with potential regulatory functions, and have tested their possible implication in autism.
   Methods: The presence of retroviral mRNAs from four HERV families (E, H, K and W), widely implicated in complex diseases, was evaluated in peripheral blood mononuclear cells (PBMCs) from ASD patients and healthy controls (HCs) by qualitative RT-PCR. We also analyzed the expression of the env sequence from HERV-H, HERV-W and HERV-K families in PBMCs at the time of sampling and after stimulation in culture, in both ASD and HC groups, by quantitative Real-time PCR. Differences between groups were evaluated using statistical methods.
   Results: The percentage of HERV-H and HERV-W positive samples was higher among ASD patients compared to HCs, while HERV-K was similarly represented and HERV-E virtually absent in both groups. The quantitative evaluation shows that HERV-H and HERV-W are differentially expressed in the two groups, with HERV-H being more abundantly expressed and, conversely, HERV-W, having lower abundance, in PBMCs from ASDs compared to healthy controls. PMBCs from ASDs also showed an increased potential to up-regulate HERV-H expression upon stimulation in culture, unlike HCs. Furthermore we report a negative correlation between expression levels of HERV-H and age among ASD patients and a statistically significant higher expression in ASD patients with Severe score in Communication and Motor Psychoeducational Profile-3.
   Conclusions: Specific HERV families have a distinctive expression profile in ASD patients compared to HCs. We propose that HERV-H expression be explored in larger samples of individuals with autism spectrum in order to determine its utility as a novel biological trait of this complex disorder.
C1 [Balestrieri, Emanuela; Matteucci, Claudia; Sorrentino, Roberta; Pica, Francesca; Garaci, Enrico; Sinibaldi-Vallebona, Paola] Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00173 Rome, Italy.
RP Balestrieri, E (reprint author), Univ Roma Tor Vergata, Dept Expt Med & Biochem Sci, I-00173 Rome, Italy.
EM Sinibaldi-Vallebona@med.uniroma2.it
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NR 43
TC 4
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 14
PY 2012
VL 7
IS 11
AR e48831
DI 10.1371/journal.pone.0048831
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038CD
UT WOS:000311151900045
PM 23155411
ER

PT J
AU Rauch, A
   Wieczorek, D
   Graf, E
   Wieland, T
   Endele, S
   Schwarzmayr, T
   Albrecht, B
   Bartholdi, D
   Beygo, J
   Di Donato, N
   Dufke, A
   Cremer, K
   Hempel, M
   Horn, D
   Hoyer, J
   Joset, P
   Ropke, A
   Moog, U
   Riess, A
   Thiel, CT
   Tzschach, A
   Wiesener, A
   Wohlleber, E
   Zweier, C
   Ekici, AB
   Zink, AM
   Rump, A
   Meisinger, C
   Grallert, H
   Sticht, H
   Schenck, A
   Engels, H
   Rappold, G
   Schrock, E
   Wieacker, P
   Riess, O
   Meitinger, T
   Reis, A
   Strom, TM
AF Rauch, Anita
   Wieczorek, Dagmar
   Graf, Elisabeth
   Wieland, Thomas
   Endele, Sabine
   Schwarzmayr, Thomas
   Albrecht, Beate
   Bartholdi, Deborah
   Beygo, Jasmin
   Di Donato, Nataliya
   Dufke, Andreas
   Cremer, Kirsten
   Hempel, Maja
   Horn, Denise
   Hoyer, Juliane
   Joset, Pascal
   Ropke, Albrecht
   Moog, Ute
   Riess, Angelika
   Thiel, Christian T.
   Tzschach, Andreas
   Wiesener, Antje
   Wohlleber, Eva
   Zweier, Christiane
   Ekici, Arif B.
   Zink, Alexander M.
   Rump, Andreas
   Meisinger, Christa
   Grallert, Harald
   Sticht, Heinrich
   Schenck, Annette
   Engels, Hartmut
   Rappold, Gudrun
   Schrock, Evelin
   Wieacker, Peter
   Riess, Olaf
   Meitinger, Thomas
   Reis, Andre
   Strom, Tim M.
TI Range of genetic mutations associated with severe non-syndromic sporadic
   intellectual disability: an exome sequencing study
SO LANCET
LA English
DT Article
ID DE-NOVO MUTATIONS; AUTISM SPECTRUM DISORDERS; MENTAL-RETARDATION;
   DEVELOPMENTAL DELAY; NONSENSE MUTATION; DELINEATION; VARIANTS; EPILEPSY;
   RECEPTOR; PATIENT
AB Background The genetic cause of intellectual disability in most patients is unclear because of the absence of morphological clues, information about the position of such genes, and suitable screening methods. Our aim was to identify de-novo variants in individuals with sporadic non-syndromic intellectual disability.
   Methods In this study, we enrolled children with intellectual disability and their parents from ten centres in Germany and Switzerland. We compared exome sequences between patients and their parents to identify de-novo variants. 20 children and their parents from the KORA Augsburg Diabetes Family Study were investigated as controls.
   Findings We enrolled 51 participants from the German Mental Retardation Network. 45 (88%) participants in the case group and 14 (70%) in the control group had de-novo variants. We identified 87 de-novo variants in the case group, with an exomic mutation rate of 1.71 per individual per generation. In the control group we identifi ed 24 de-novo variants, which is 1.2 events per individual per generation. More participants in the case group had loss-of-function variants than in the control group (20/51 vs 2/20; p=0.022), suggesting their contribution to disease development. 16 patients carried de-novo variants in known intellectual disability genes with three recurrently mutated genes (STXBP1, SYNGAP1, and SCN2A). We deemed at least six loss-of-function mutations in six novel genes to be disease causing. We also identifi ed several missense alterations with potential pathogenicity.
   Interpretation After exclusion of copy-number variants, de-novo point mutations and small indels are associated with severe, sporadic non-syndromic intellectual disability, accounting for 45-55% of patients with high locus heterogeneity. Autosomal recessive inheritance seems to contribute little in the outbred population investigated. The large number of de-novo variants in known intellectual disability genes is only partially attributable to known non-specific phenotypes. Several patients did not meet the expected syndromic manifestation, suggesting a strong bias in present clinical syndrome descriptions.
C1 [Rauch, Anita; Joset, Pascal] Univ Zurich, Inst Med Genet, Zurich, Switzerland.
   [Rauch, Anita] Univ Zurich, Neurosci Ctr Zurich, Zurich, Switzerland.
   [Rauch, Anita] Univ Zurich, Zurich Ctr Integrat Human Physiol, Zurich, Switzerland.
   [Rauch, Anita; Endele, Sabine; Hoyer, Juliane; Thiel, Christian T.; Wiesener, Antje; Zweier, Christiane; Ekici, Arif B.; Riess, Olaf] Univ Erlangen Nurnberg, Inst Human Genet, D-91054 Erlangen, Germany.
   [Wieczorek, Dagmar; Albrecht, Beate; Beygo, Jasmin; Cremer, Kirsten] Univ Klinikum Essen, Inst Human Genet, Essen, Germany.
   [Graf, Elisabeth; Wieland, Thomas; Schwarzmayr, Thomas; Meitinger, Thomas; Strom, Tim M.] Helmholtz Zentrum Munchen, Inst Human Genet, D-85764 Neuherberg, Germany.
   [Di Donato, Nataliya; Rump, Andreas; Schrock, Evelin] Tech Univ Dresden, Inst Clin Genet, D-01062 Dresden, Germany.
   [Dufke, Andreas; Riess, Angelika; Tzschach, Andreas; Riess, Olaf] Univ Tubingen, Inst Human Genet, Tubingen, Germany.
   [Hempel, Maja; Meitinger, Thomas; Strom, Tim M.] Tech Univ Munich, Inst Human Genet, Munich, Germany.
   [Horn, Denise] Univ Med Berlin, Charite, Inst Med Genet, Berlin, Germany.
   [Ropke, Albrecht; Wieacker, Peter] Univ Munster, Inst Human Genet, D-4400 Munster, Germany.
   [Moog, Ute; Rappold, Gudrun] Univ Heidelberg, Inst Human Genet, Heidelberg, Germany.
   [Wohlleber, Eva; Zink, Alexander M.; Engels, Hartmut] Univ Bonn, Inst Human Genet, Bonn, Germany.
   [Meisinger, Christa] Helmholtz Zentrum Munchen, Inst Epidemiol 2, D-85764 Neuherberg, Germany.
   [Grallert, Harald] Helmholtz Zentrum Munchen, Res Unit Mol Epidemiol, D-85764 Neuherberg, Germany.
   [Sticht, Heinrich] Univ Erlangen Nurnberg, Inst Biochem, D-91054 Erlangen, Germany.
   [Schenck, Annette] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, Nijmegen Ctr Mol Life Sci,Donders Inst Brain Cogn, NL-6525 ED Nijmegen, Netherlands.
RP Strom, TM (reprint author), Helmholtz Zentrum Munchen, Inst Human Genet, Ingolstadter Landstr 1, D-85764 Neuherberg, Germany.
EM timstrom@helmholtz-muenchen.de
RI Zink, Alexander/B-2305-2013; Grallert, Harald/B-3424-2013; Ekici,
   Arif/C-3971-2013; Schenck, Annette/E-4514-2012; Thiel,
   Christian/H-8964-2012; Meisinger, Christine/B-5358-2014; Rauch,
   Anita/C-5568-2014; Reis, Andre/D-2309-2009; Zweier,
   Christiane/F-2202-2015
OI Schenck, Annette/0000-0002-6918-3314; Thiel,
   Christian/0000-0003-3817-7277; Rauch, Anita/0000-0003-2930-3163; Reis,
   Andre/0000-0002-6301-6363; 
FU German Ministry of Education and Research [01GS08160, 01GR0802,
   01GM0867]; European Commission 7th Framework Program [261123]; Swiss
   National Science Foundation [320030_135669]
FX We thank all patients and their families for participating in this
   study. This work was supported by the German Ministry of Education and
   Research (01GS08160, 01GR0802, and 01GM0867), the European Commission
   7th Framework Program (261123, GEUVADIS), and the Swiss National Science
   Foundation (320030_135669).
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NR 40
TC 175
Z9 177
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0140-6736
J9 LANCET
JI Lancet
PD NOV 10
PY 2012
VL 380
IS 9854
BP 1674
EP 1682
DI 10.1016/S0140-6736(12)61480-9
PG 9
WC Medicine, General & Internal
SC General & Internal Medicine
GA 035MN
UT WOS:000310951400029
PM 23020937
ER

PT J
AU Hoddenbach, E
   Koot, HM
   Clifford, P
   Gevers, C
   Clauser, C
   Boer, F
   Begeer, S
AF Hoddenbach, Elske
   Koot, Hans M.
   Clifford, Pamela
   Gevers, Carolien
   Clauser, Cassandra
   Boer, Frits
   Begeer, Sander
TI Individual differences in the efficacy of a short theory of mind
   intervention for children with autism spectrum disorder: a randomized
   controlled trial
SO TRIALS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; SOCIAL-SKILLS; PSYCHOSOCIAL
   INTERVENTIONS; DISRUPTIVE BEHAVIOR; QUESTIONNAIRE; INSTRUMENT
AB Background: Having a 'theory of mind', or having the ability to attribute mental states to oneself or others, is considered one of the most central domains of impairment among children with an autism spectrum disorder (ASD). Many interventions focus on improving theory of mind skills in children with ASD. Nonetheless, the empirical evidence for the effect of these interventions is limited. The main goal of this study is to examine the effectiveness of a short theory of mind intervention for children with ASD. A second objective is to determine which subgroups within the autism spectrum profit most from the intervention.
   Methods: This study is a randomized controlled trial. One hundred children with ASD, aged 7 to 12 years will be randomly assigned to an intervention or a waiting list control group. Outcome measures include the completion of theory of mind and emotion understanding tasks, and parent and teacher questionnaires on children's social skills. Follow-up data for the intervention group will be collected 6 months after the interventions.
   Discussion: This study evaluates the efficacy of a theory of mind intervention for children with ASD. Hypotheses, strengths, and limitations of the study are discussed.
C1 [Hoddenbach, Elske; Koot, Hans M.; Begeer, Sander] Vrije Univ Amsterdam, Amsterdam, Netherlands.
   [Clifford, Pamela; Gevers, Carolien] Wei43, Amsterdam, Netherlands.
   [Clauser, Cassandra] De Bascule, Amsterdam, Netherlands.
   [Boer, Frits] AMC De Bacule, Amsterdam, Netherlands.
   [Begeer, Sander] Univ Sydney, Sch Psychol, Sydney, NSW 2006, Australia.
RP Begeer, S (reprint author), Vrije Univ Amsterdam, Amsterdam, Netherlands.
EM Sander.begeer@sydney.edu.au
FU Fonds Psychische Gezondheid [2009 6442]
FX The study is funded by Fonds Psychische Gezondheid, (project number 2009
   6442). We wish to thank all the children, parents, and clinicians who
   were involved in the study.
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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NR 38
TC 0
Z9 0
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1745-6215
J9 TRIALS
JI Trials
PD NOV 9
PY 2012
VL 13
AR 206
DI 10.1186/1745-6215-13-206
PG 7
WC Medicine, Research & Experimental
SC Research & Experimental Medicine
GA 078MP
UT WOS:000314103400001
PM 23140338
ER

PT J
AU Clement, JP
   Aceti, M
   Creson, TK
   Ozkan, ED
   Shi, YL
   Reish, NJ
   Almonte, AG
   Miller, BH
   Wiltgen, BJ
   Miller, CA
   Xu, XM
   Rumbaugh, G
AF Clement, James P.
   Aceti, Massimiliano
   Creson, Thomas K.
   Ozkan, Emin D.
   Shi, Yulin
   Reish, Nicholas J.
   Almonte, Antoine G.
   Miller, Brooke H.
   Wiltgen, Brian J.
   Miller, Courtney A.
   Xu, Xiangmin
   Rumbaugh, Gavin
TI Pathogenic SYNGAP1 Mutations Impair Cognitive Development by Disrupting
   Maturation of Dendritic Spine Synapses
SO CELL
LA English
DT Article
ID GTPASE-ACTIVATING PROTEIN; NMDA RECEPTOR; SYNAPTIC PLASTICITY;
   MENTAL-RETARDATION; SILENT SYNAPSES; IN-VIVO; CRITICAL PERIOD;
   VISUAL-CORTEX; ANIMAL-MODEL; AUTISM
AB Mutations that cause intellectual disability (ID) and autism spectrum disorder (ASD) are commonly found in genes that encode for synaptic proteins. However, it remains unclear how mutations that disrupt synapse function impact intellectual ability. In the SYNGAP1 mouse model of ID/ASD, we found that dendritic spine synapses develop prematurely during the early postnatal period. Premature spine maturation dramatically enhanced excitability in the developing hippocampus, which corresponded with the emergence of behavioral abnormalities. Inducing SYNGAP1 mutations after critical developmental windows closed had minimal impact on spine synapse function, whereas repairing these pathogenic mutations in adulthood did not improve behavior and cognition. These data demonstrate that SynGAP protein acts as a critical developmental repressor of neural excitability that promotes the development of life-long cognitive abilities. We propose that the pace of dendritic spine synapse maturation in early life is a critical determinant of normal intellectual development.
C1 [Clement, James P.; Aceti, Massimiliano; Creson, Thomas K.; Ozkan, Emin D.; Miller, Brooke H.; Miller, Courtney A.; Rumbaugh, Gavin] Scripps Res Inst, Dept Neurosci, Jupiter, FL 33458 USA.
   [Miller, Courtney A.] Scripps Res Inst, Dept Metab & Aging, Jupiter, FL 33458 USA.
   [Shi, Yulin; Xu, Xiangmin] Univ Calif Irvine, Dept Anat & Neurobiol, Irvine, CA 92697 USA.
   [Reish, Nicholas J.; Almonte, Antoine G.] Univ Alabama Birmingham, Dept Neurobiol, Birmingham, AL 35294 USA.
   [Wiltgen, Brian J.] Univ Virginia, Dept Psychol, Charlottesville, VA 22904 USA.
RP Rumbaugh, G (reprint author), Scripps Res Inst, Dept Neurosci, Jupiter, FL 33458 USA.
EM grumbaug@scripps.edu
RI Wiltgen, Brian/D-2947-2013; Ozkan, Emin Deniz/A-5752-2009; Miller,
   Courtney/E-8651-2010
OI Ozkan, Emin Deniz/0000-0002-1073-6703; Miller,
   Courtney/0000-0001-8628-4902
FU National Institute for Neurological Disorders and Stroke [R01NS064079];
   Eunice Kennedy Shriver National Institute for Child Health and Human
   Development [R03HD060672]; National Alliance for Research on
   Schizophrenia and Depression (NARSAD); National Institute for Drug Abuse
   [DA023700-04S1]
FX We thank Drs. Ronald Davis, Damon Page, and Fadi Hamdan, as well as
   members of the Rumbaugh Laboratory, for their helpful comments on this
   manuscript. We also thank Zachary Collier, Samuel Bacharach, Bryce
   Grier, and Gopi Patel for assistance in context discrimination studies.
   This work was supported by grants to G. R. from the National Institute
   for Neurological Disorders and Stroke (R01NS064079), The Eunice Kennedy
   Shriver National Institute for Child Health and Human Development
   (R03HD060672), and the National Alliance for Research on Schizophrenia
   and Depression (NARSAD). The laser photostimulation and
   voltage-sensitive dye imaging part of this work was performed in X.X.'s
   laboratory, supported by a grant from the National Institute for Drug
   Abuse (DA023700-04S1). J.P.C. and E.D.O. performed electrophysiological
   recordings; M. A. performed multiphoton imaging studies and spine
   analysis; T. K. C., N.J.R., A. G. A., and B.J.W. performed behavioral
   studies; Y.S. and X. X. performed laser photo-stimulation and imaging
   studies; G. R., C. A. M., T. K. C., J.P.C., M. A., B.J.W., X. X.
   designed experiments; B. M. and T. K. C. performed protein/mRNA studies;
   G. R. conceived the study and wrote the manuscript; G. R., C. A. M.,
   J.P.C., and T. K. C. edited the manuscript.
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NR 56
TC 36
Z9 37
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0092-8674
J9 CELL
JI Cell
PD NOV 9
PY 2012
VL 151
IS 4
BP 709
EP 723
DI 10.1016/j.cell.2012.08.045
PG 15
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 035CV
UT WOS:000310921200005
PM 23141534
ER

PT J
AU Baez, S
   Rattazzi, A
   Gonzalez-Gadea, ML
   Torralva, T
   Vigliecca, NS
   Decety, J
   Manes, F
   Ibanez, A
AF Baez, Sandra
   Rattazzi, Alexia
   Gonzalez-Gadea, Maria L.
   Torralva, Teresa
   Silvana Vigliecca, Nora
   Decety, Jean
   Manes, Facundo
   Ibanez, Agustin
TI Integrating intention and context: assessing social cognition in adults
   with Asperger syndrome
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE Asperger syndrome; contextual social cognition; executive functions;
   individual variability
ID HIGH-FUNCTIONING AUTISM; SELF-MONITORING SCALE; FRONTAL-LOBE LESIONS;
   MULTIPLE CASE SERIES; FRONTOTEMPORAL DEMENTIA; SPECTRUM DISORDERS; FLUID
   INTELLIGENCE; IMPAIRED RECOGNITION; BEHAVIORAL VARIANT; HEALTHY
   RELATIVES
AB Deficits in social cognition are an evident clinical feature of the Asperger syndrome (AS). Although many daily life problems of adults with AS are related to social cognition impairments, few studies have conducted comprehensive research in this area. The current study examined multiple domains of social cognition in adults with AS assessing the executive functions (EF) and exploring the intra and inter-individual variability. Fifteen adult's diagnosed with AS and 15 matched healthy controls completed a battery of social cognition tasks. This battery included measures of emotion recognition, theory of mind (ToM), empathy, moral judgment, social norms knowledge, and self-monitoring behavior in social settings. We controlled for the effect of EF and explored the individual variability. The results indicated that adults with AS had a fundamental deficit in several domains of social cognition. We also found high variability in the social cognition tasks. In these tasks, AS participants obtained mostly subnormal performance. EF did not seem to play a major role in the social cognition impairments. Our results suggest that adults with AS present a pattern of social cognition deficits characterized by the decreased ability to implicitly encode and integrate contextual information in order to access to the social meaning. Nevertheless, when social information is explicitly presented or the situation can be navigated with abstract rules, performance is improved. Our findings have implications for the diagnosis and treatment of individuals with AS as well as for the neurocognitive models of this syndrome.
C1 [Ibanez, Agustin] Favaloro Univ, Inst Cognit Neurol, Lab Expt Psychol & Neurosci, Buenos Aires, DF, Argentina.
   [Baez, Sandra; Gonzalez-Gadea, Maria L.; Torralva, Teresa; Manes, Facundo; Ibanez, Agustin] Favaloro Univ, Inst Neurosci, Buenos Aires, DF, Argentina.
   [Baez, Sandra; Gonzalez-Gadea, Maria L.; Silvana Vigliecca, Nora; Ibanez, Agustin] Natl Sci & Tech Res Council, Buenos Aires, DF, Argentina.
   [Baez, Sandra] Pontifical Catholic Univ Argentina, Buenos Aires, DF, Argentina.
   [Rattazzi, Alexia] Argentinean Program Children Adolescents & Adults, Buenos Aires, DF, Argentina.
   [Silvana Vigliecca, Nora] Natl Univ Cordoba, Fac Philosophy & Humanities, Res Ctr, Cordoba, Spain.
   [Decety, Jean] Univ Chicago, Dept Psychol, Chicago, IL 60637 USA.
   [Decety, Jean] Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA.
   [Decety, Jean] Univ Chicago, Ctr Cognit & Social Neurosci, Chicago, IL 60637 USA.
   [Ibanez, Agustin] Univ Diego Portales, Cognit Neurosci Lab, Santiago, Chile.
RP Ibanez, A (reprint author), Favaloro Univ, Inst Cognit Neurol, Lab Expt Psychol & Neurosci, Pacheco de Melo 1860, Buenos Aires, DF, Argentina.
EM aibanez@ineco.org.ar
FU CONICET; FONDECYT [1130920]; INECO Foundation
FX The authors thank Ralph Adolphs and Phil Baker for their helpful and
   insightful comments in an earlier version of the paper. This research
   was partially supported by CONICET, FONDECYT (1130920) and INECO
   Foundation Grants. Any opinions, findings, and conclusions or
   recommendations expressed in this material are those of the authors and
   do not necessarily reflect the views of those grants.
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NR 103
TC 20
Z9 20
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 2012
VL 6
AR 302
DI 10.3389/fnhum.2012.00302
PG 21
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 039ET
UT WOS:000311227600001
PM 23162450
ER

PT J
AU Anagnostou, E
AF Anagnostou, Evdokia
TI TRANSLATIONAL MEDICINE Mice and men show the way
SO NATURE
LA English
DT Editorial Material
ID FRAGILE-X-SYNDROME; AUTISM
C1 Univ Toronto, Dept Pediat, Bloorview Res Inst, Toronto, ON M4G 1R8, Canada.
RP Anagnostou, E (reprint author), Univ Toronto, Dept Pediat, Bloorview Res Inst, Toronto, ON M4G 1R8, Canada.
EM eanagnostou@hollandbloorview.ca
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NR 12
TC 2
Z9 3
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 0028-0836
J9 NATURE
JI Nature
PD NOV 8
PY 2012
VL 491
IS 7423
BP 196
EP 197
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 033DP
UT WOS:000310774300026
PM 23135462
ER

PT J
AU Tayama, M
   Tateno, M
   Park, TW
   Ukai, W
   Hashimoto, E
   Saito, T
AF Tayama, Masaya
   Tateno, Masaru
   Park, Tae Woo
   Ukai, Wataru
   Hashimoto, Eri
   Saito, Toshikazu
TI The Study of Cognitive Characteristics in Asperger's Disorder by Using a
   Modified Prisoner's Dilemma Game with a Variable Payoff Matrix
SO PLOS ONE
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM SPECTRUM; INFANTILE-AUTISM;
   SOCIAL DILEMMAS; COOPERATION; MIND; PREVALENCE; JAPAN; EPIDEMIOLOGY;
   CHILDREN
AB Individuals with Asperger's Disorder (ASP) have difficulties in social reciprocity and in providing appropriate cooperative behavior. The Prisoner's Dilemma (PD) is a well-known model in game theory that illustrates the paradoxical disposition of interaction between two individuals with opposing interests, and may be a useful tool in the diagnosis of ASP in early childhood. In this study, we investigated the cognitive characteristics of ASP by using a modified PD game. The subjects were 29 individuals with ASP and 28 age-and IQ-matched controls. In the PD game, each of two players has two cards: card 1 represents cooperation and card 2 betrayal. The score each player obtains is decided according to a 2 x 2 payoff matrix and depends on the combination of their selections. The P-score ("P" for punishment) is defined as the score that is given when they both select betrayal. Comparing the two groups, the mean P-score at the end of the game and the mean total score were significantly higher in the ASP group, while the rate of selection of cooperative choice in both groups did not differ significantly. The classification of the shape of the graph according to fluctuation of the P-score revealed that in the ASP group only 2 cases (6.9%) showed continuous decrease of P-score compared to 8 control cases (28.6%) demonstrating similar results. However, the reasons were thought to be different: ASP subjects presumably selected card 2 because of a preference for the number itself, whereas control subjects preferentially chose this card to enhance their chance of winning the competition. It is often difficult to diagnose ASP in the young especially when they lack the distinctive clinical features of ASD in early childhood. Given the limited number of objective tools to evaluate the cognitive characteristics of ASP subjects, the PD game might be a useful diagnostic support tool for ASP.
C1 [Tayama, Masaya; Tateno, Masaru; Ukai, Wataru; Hashimoto, Eri; Saito, Toshikazu] Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Sapporo, Hokkaido, Japan.
   [Park, Tae Woo] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02118 USA.
   [Park, Tae Woo] Vet Affairs Boston Healthcare Syst, Boston, MA USA.
RP Tateno, M (reprint author), Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Sapporo, Hokkaido, Japan.
EM tatema@sapmed.ac.jp
FU  [22791133]
FX This study was supported by a Grant-in-Aid for Young Scientists (B) for
   Masaru Tateno (22791133). 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 41
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 7
PY 2012
VL 7
IS 11
AR e48794
DI 10.1371/journal.pone.0048794
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 048TK
UT WOS:000311935800137
PM 23144975
ER

PT J
AU He, HB
   Mahnke, AH
   Doyle, S
   Fan, N
   Wang, CC
   Hall, BJ
   Tang, YP
   Inglis, FM
   Chen, C
   Erickson, JD
AF He, Hongbo
   Mahnke, Amanda H.
   Doyle, Sukhjeevan
   Fan, Ni
   Wang, Chih-Chieh
   Hall, Benjamin J.
   Tang, Ya-Ping
   Inglis, Fiona M.
   Chen, Chu
   Erickson, Jeffrey D.
TI Neurodevelopmental Role for VGLUT2 in Pyramidal Neuron Plasticity,
   Dendritic Refinement, and in Spatial Learning
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID VESICULAR GLUTAMATE TRANSPORTER; LONG-TERM POTENTIATION; HIPPOCAMPAL
   SYNAPTIC PLASTICITY; ACTIVITY-DEPENDENT REGULATION; ASPARTATE RECEPTOR
   BLOCKADE; AUTISM SPECTRUM DISORDERS; EXCITATORY NEURONS; PREFRONTAL
   CORTEX; RETT-SYNDROME; QUANTAL SIZE
AB The level and integrity of glutamate transmission during critical periods of postnatal development plays an important role in the refinement of pyramidal neuron dendritic arbor, synaptic plasticity, and cognition. Presently, it is not clear how excitatory transmission via the two predominant isoforms of the vesicular glutamate transporter (VGLUT1 and VGLUT2) participate in this process. To assess a neurodevelopmental role for VGLUT2 in pyramidal neuron maturation, we generated recombinant VGLUT2 knock-out mice and inactivated VGLUT2 throughout development using Emx1-Cre(+/+) knock-in mice. We show that VGLUT2 deficiency in corticolimbic circuits results in reduced evoked glutamate transmission, release probability, and LTD at hippocampal CA3-CA1 synapses during a formative developmental period (postnatal days 11-14). In adults, we find a marked reduction in the amount of dendritic arbor across the span of the dendritic tree of CA1 pyramidal neurons and reduced long-term potentiation and levels of synaptic markers spinophilin and VGLUT1. Loss of dendritic arbor is accompanied by corresponding reductions in the number of dendritic spines, suggesting widespread alterations in synaptic connectivity. Conditional VGLUT2 knock-out mice exhibit increased open-field exploratory activity yet impaired spatial learning and memory, endophenotypes similar to those of NMDA receptor knock-down mice. Remarkably, the impairment in learning can be partially restored by selectively increasing NMDA receptor-mediated glutamate transmission in adult mice by prolonged treatment with D-serine and a D-amino acid oxidase inhibitor. Our data indicate that VGLUT2 expression is pivotal to the proper development of mature pyramidal neuronal architecture and plasticity, and that such glutamatergic deficiency leads to cognitive malfunction as observed in several neurodevelopmental psychiatric disorders.
C1 [He, Hongbo; Doyle, Sukhjeevan; Fan, Ni; Chen, Chu; Erickson, Jeffrey D.] Louisiana State Univ, Hlth Sci Ctr, Neurosci Ctr Excellence, New Orleans, LA 70112 USA.
   [Tang, Ya-Ping] Louisiana State Univ, Hlth Sci Ctr, Dept Cell Biol & Anat, New Orleans, LA 70112 USA.
   [Mahnke, Amanda H.; Wang, Chih-Chieh; Hall, Benjamin J.; Inglis, Fiona M.] Tulane Univ, Dept Cell & Mol Biol, New Orleans, LA 70118 USA.
RP Erickson, JD (reprint author), Louisiana State Univ, Med Ctr, Ctr Neurosci, 2020 Gravier St,Suite D, New Orleans, LA 70112 USA.
EM jerick@lsuhsc.edu
RI Tang, Ya-Ping/A-1035-2011
FU National Institutes of Health [R01 NS036936, R01 NS076815, P20RR016816];
   NARSAD Independent Investigator Award from the Brain and Behavior
   Research Foundation; Research Enhancement Fund Grant from Louisiana
   State University Health Science Center; National Science Foundation
   [0952455]
FX This work was supported by National Institutes of Health Grant R01
   NS036936, a NARSAD Independent Investigator Award from the Brain and
   Behavior Research Foundation, and a Research Enhancement Fund Grant from
   Louisiana State University Health Science Center to J.D.E. National
   Institute of Health Grant R01 NS076815 supported C. C. National
   Institute of Health COBRE Grant P20RR016816 supported F. M. I. National
   Science Foundation CAREER Award 0952455 supported B.J.H. We thank Dr.
   Hilary Thompson (Department of Biostatistics, Louisiana State University
   Health Sciences Center, New Orleans, LA) for extensive consultation and
   assistance with the statistical analyses.
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NR 115
TC 8
Z9 8
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 7
PY 2012
VL 32
IS 45
BP 15886
EP U425
DI 10.1523/JNEUROSCI.4505-11.2012
PG 17
WC Neurosciences
SC Neurosciences & Neurology
GA 034AH
UT WOS:000310842000023
PM 23136427
ER

PT J
AU Chen, YC
   Lin, YQ
   Banerjee, S
   Venken, K
   Li, JJ
   Ismat, A
   Chen, KC
   Duraine, L
   Bellen, HJ
   Bhat, MA
AF Chen, Yu-Chi
   Lin, Yong Qi
   Banerjee, Swati
   Venken, Koen
   Li, Jingjun
   Ismat, Afshan
   Chen, Kuchuan
   Duraine, Lita
   Bellen, Hugo J.
   Bhat, Manzoor A.
TI Drosophila Neuroligin 2 is Required Presynaptically and Postsynaptically
   for Proper Synaptic Differentiation and Synaptic Transmission
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID TUMOR-SUPPRESSOR GENE; ACTIVE ZONE; NEUROMUSCULAR-JUNCTION; NEUREXIN-I;
   SYNAPSES; EXPRESSION; MELANOGASTER; MATURATION; PLASTICITY; GROWTH
AB Trans-synaptic adhesion between Neurexins (Nrxs) and Neuroligins (Nlgs) is thought to be required for proper synapse organization and modulation, and mutations in several human Nlgs have shown association with autism spectrum disorders. Here we report the generation and phenotypic characterization of Drosophila neuroligin 2 (dnlg2) mutants. Loss of dnlg2 results in reduced bouton numbers, aberrant presynaptic and postsynaptic development at neuromuscular junctions (NMJs), and impaired synaptic transmission. In dnlg2 mutants, the evoked responses are decreased in amplitude, whereas the total active zone (AZ) numbers at the NMJ are comparable to wild type, suggesting a decrease in the release probability. Ultrastructurally, the presynaptic AZ number per bouton area and the postsynaptic density area are both increased in dnlg2 mutants, whereas the subsynaptic reticulum is reduced in volume. We show that both presynaptic and postsynaptic expression of Dnlg2 is required to restore synaptic growth and function in dnlg2 mutants. Postsynaptic expression of Dnlg2 in dnlg2 mutants and wild type leads to reduced bouton growth whereas presynaptic and postsynaptic overexpression in wild-type animals results in synaptic overgrowth. Since Nlgs have been shown to bind to Nrxs, we created double mutants. These mutants are viable and display phenotypes that closely resemble those of dnlg2 and dnrx single mutants. Our results provide compelling evidence that Dnlg2 functions both presynaptically and postsynaptically together with Neurexin to determine the proper number of boutons as well as the number of AZs and size of synaptic densities during the development of NMJs.
C1 [Chen, Yu-Chi; Bhat, Manzoor A.] Univ N Carolina, Sch Med, Curriculum Genet & Mol Biol, Chapel Hill, NC 27599 USA.
   [Chen, Yu-Chi; Banerjee, Swati; Li, Jingjun; Ismat, Afshan; Bhat, Manzoor A.] Univ N Carolina, Sch Med, Dept Cell & Mol Physiol, Chapel Hill, NC 27599 USA.
   [Bhat, Manzoor A.] Univ N Carolina, Sch Med, Curriculum Neurobiol, Chapel Hill, NC 27599 USA.
   [Li, Jingjun; Bhat, Manzoor A.] Univ N Carolina, Sch Med, UNC Neurosci Ctr, Chapel Hill, NC 27599 USA.
   [Li, Jingjun; Bhat, Manzoor A.] Univ N Carolina, Sch Med, Carolina Inst Dev Disabil, Chapel Hill, NC 27599 USA.
   [Lin, Yong Qi; Venken, Koen; Chen, Kuchuan; Duraine, Lita; Bellen, Hugo J.] Baylor Coll Med, Howard Hughes Med Inst, Dept Mol & Human Genet, Dept Neurosci,Program Dev Biol,Neurol Res Inst, Houston, TX 77030 USA.
RP Bhat, MA (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Sch Med, Dept Physiol, 7703 Floyd Curl Dr, San Antonio, TX 78229 USA.
EM bhatm@uthscsa.edu
RI Venken, Koen/B-9909-2013
OI Venken, Koen/0000-0003-0741-4698
FU Simons Foundation [SF-177037]; National Institutes of Health [NS050356];
    [T32 GM007526]
FX K.V. was supported by training grant T32 GM007526 to the Molecular and
   Human Genetics Department at Baylor College of Medicine. H.J.B. is an
   investigator of the Howard Hughes Medical Institute. This work was
   supported by the Simons Foundation Grant (SF-177037) and in part by the
   National Institutes of Health Grant NS050356 (M. A. B.). We are grateful
   to Aaron DiAntonio for anti-GluRIII, Gabrielle L. Boulianne, and Wei Xie
   for dnlg2<SUP>KO70</SUP> and UAS-dnlg2, and Vivian Budnik for isogenized
   w<SUP>1118</SUP> fly stocks. We thank the Bloomington Stock Center for
   fly stocks, the Developmental Studies Hybridoma Bank, and the University
   of Iowa for monoclonal antibodies; Michael Chua for assistance with GluR
   quantification; Rosa Mino for assistance with dnlg2 in situ
   hybridization; and Alan Fanning and past and current members of the Bhat
   laboratory for technical assistance and helpful discussions.
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NR 64
TC 13
Z9 13
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 7
PY 2012
VL 32
IS 45
BP 16018
EP 16030
DI 10.1523/JNEUROSCI.1685-12.2012
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 034AH
UT WOS:000310842000034
PM 23136438
ER

PT J
AU Kane, MJ
   Angoa-Perez, M
   Briggs, DI
   Sykes, CE
   Francescutti, DM
   Rosenberg, DR
   Kuhn, DM
AF Kane, Michael J.
   Angoa-Perez, Mariana
   Briggs, Denise I.
   Sykes, Catherine E.
   Francescutti, Dina M.
   Rosenberg, David R.
   Kuhn, Donald M.
TI Mice Genetically Depleted of Brain Serotonin Display Social Impairments,
   Communication Deficits and Repetitive Behaviors: Possible Relevance to
   Autism
SO PLOS ONE
LA English
DT Article
ID FAMILY-BASED ASSOCIATION; COPY-NUMBER VARIATION; RARE DE-NOVO; MOUSE
   MODEL; SPECTRUM DISORDERS; TRYPTOPHAN HYDROXYLASE-2; ULTRASONIC
   VOCALIZATIONS; INBRED STRAINS; CORTICAL DEVELOPMENT; AGGRESSIVE-BEHAVIOR
AB Autism is a complex neurodevelopmental disorder characterized by impaired reciprocal social interaction, communication deficits and repetitive behaviors. A very large number of genes have been linked to autism, many of which encode proteins involved in the development and function of synaptic circuitry. However, the manner in which these mutated genes might participate, either individually or together, to cause autism is not understood. One factor known to exert extremely broad influence on brain development and network formation, and which has been linked to autism, is the neurotransmitter serotonin. Unfortunately, very little is known about how alterations in serotonin neuronal function might contribute to autism. To test the hypothesis that serotonin dysfunction can contribute to the core symptoms of autism, we analyzed mice lacking brain serotonin (via a null mutation in the gene for tryptophan hydroxylase 2 (TPH2)) for behaviors that are relevant to this disorder. Mice lacking brain serotonin (TPH2-/-) showed substantial deficits in numerous validated tests of social interaction and communication. These mice also display highly repetitive and compulsive behaviors. Newborn TPH2-/- mutant mice show delays in the expression of key developmental milestones and their diminished preference for maternal scents over the scent of an unrelated female is a forerunner of more severe socialization deficits that emerge in weanlings and persist into adulthood. Taken together, these results indicate that a hypo-serotonin condition can lead to behavioral traits that are highly characteristic of autism. Our findings should stimulate new studies that focus on determining how brain hyposerotonemia during critical neurodevelopmental periods can alter the maturation of synaptic circuits known to be mis-wired in autism and how prevention of such deficits might prevent this disorder.
C1 [Kane, Michael J.; Angoa-Perez, Mariana; Briggs, Denise I.; Sykes, Catherine E.; Francescutti, Dina M.; Kuhn, Donald M.] John D Dingell VA Med Ctr, Res & Dev Serv, Detroit, MI USA.
   [Kane, Michael J.; Angoa-Perez, Mariana; Briggs, Denise I.; Sykes, Catherine E.; Francescutti, Dina M.; Rosenberg, David R.; Kuhn, Donald M.] Wayne State Univ, Sch Med, Dept Psychiat & Behav Neurosci, Detroit, MI USA.
RP Kuhn, DM (reprint author), John D Dingell VA Med Ctr, Res & Dev Serv, Detroit, MI USA.
EM donald.kuhn@wayne.edu
FU Department of Veterans Affairs
FX This work was supported by the Department of Veterans Affairs. 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 106
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 NOV 6
PY 2012
VL 7
IS 11
AR e48975
DI 10.1371/journal.pone.0048975
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300066
PM 23139830
ER

PT J
AU Ronconi, L
   Gori, S
   Ruffino, M
   Franceschini, S
   Urbani, B
   Molteni, M
   Facoetti, A
AF Ronconi, Luca
   Gori, Simone
   Ruffino, Milena
   Franceschini, Sandro
   Urbani, Barbara
   Molteni, Massimo
   Facoetti, Andrea
TI Decreased Coherent Motion Discrimination in Autism Spectrum Disorder:
   The Role of Attentional Zoom-Out Deficit
SO PLOS ONE
LA English
DT Article
ID CORTICAL MAGNIFICATION FACTOR; VISUAL-ATTENTION; PERCEPTION;
   INFORMATION; CORTEX; FIELD; FORM; PSYCHOPHYSICS; CONNECTIVITY;
   SENSITIVITY
AB Autism spectrum disorder (ASD) has been associated with decreased coherent dot motion (CDM) performance, a task that measures magnocellular sensitivity as well as fronto-parietal attentional integration processing. In order to clarify the role of spatial attention in CDM tasks, we measured the perception of coherently moving dots displayed in the central or peripheral visual field in ASD and typically developing children. A dorsal-stream deficit in children with ASD should predict a generally poorer performance in both conditions. In our study, however, we show that in children with ASD, CDM perception was selectively impaired in the central condition. In addition, in the ASD group, CDM efficiency was correlated to the ability to zoom out the attentional focus. Importantly, autism symptoms severity was related to both the CDM and attentional zooming-out impairment. These findings suggest that a dysfunction in the attentional network might help to explain decreased CDM discrimination as well as the "core'' social cognition deficits of ASD.
C1 [Ronconi, Luca; Gori, Simone; Franceschini, Sandro; Facoetti, Andrea] Univ Padua, Dev & Cognit Neurosci Lab, Dept Gen Psychol, Padua, Italy.
   [Gori, Simone; Ruffino, Milena; Urbani, Barbara; Molteni, Massimo; Facoetti, Andrea] Sci Inst Eugenio Medea, Dev Neuropsychol Unit, Bosisio Parini, Italy.
RP Facoetti, A (reprint author), Univ Padua, Dev & Cognit Neurosci Lab, Dept Gen Psychol, Padua, Italy.
EM andreafacoetti@unipd.it
RI Facoetti, Andrea/C-2876-2009
FU University of Padova
FX This study was made possible through two grants of the University of
   Padova ("Progetto di Ateneo 2009'' and "Progetto di Ateneo 2011'' to
   AF). 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 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 NOV 6
PY 2012
VL 7
IS 11
AR e49019
DI 10.1371/journal.pone.0049019
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300068
PM 23139831
ER

PT J
AU Seibt, J
   Armant, O
   Le Digarcher, A
   Castro, D
   Ramesh, V
   Journot, L
   Guillemot, F
   Vanderhaeghen, P
   Bouschet, T
AF Seibt, Julie
   Armant, Olivier
   Le Digarcher, Anne
   Castro, Diogo
   Ramesh, Vidya
   Journot, Laurent
   Guillemot, Francois
   Vanderhaeghen, Pierre
   Bouschet, Tristan
TI Expression at the Imprinted Dlk1-Gtl2 Locus Is Regulated by Proneural
   Genes in the Developing Telencephalon
SO PLOS ONE
LA English
DT Article
ID MOUSE TELENCEPHALON; PROGENITOR CELLS; STEM-CELLS; GTL2 GENE; BRAIN;
   SPECIFICATION; NEURONS; DIFFERENTIATION; NEUROGENESIS; NETWORK
AB Imprinting is an epigenetic mechanism that restrains the expression of about 100 genes to one allele depending on its parental origin. Several imprinted genes are implicated in neurodevelopmental brain disorders, such as autism, Angelman, and Prader-Willi syndromes. However, how expression of these imprinted genes is regulated during neural development is poorly understood. Here, using single and double KO animals for the transcription factors Neurogenin2 (Ngn2) and Achaete-scute homolog 1 (Ascl1), we found that the expression of a specific subset of imprinted genes is controlled by these proneural genes. Using in situ hybridization and quantitative PCR, we determined that five imprinted transcripts situated at the Dlk1-Gtl2 locus (Dlk1, Gtl2, Mirg, Rian, Rtl1) are upregulated in the dorsal telencephalon of Ngn2 KO mice. This suggests that Ngn2 influences the expression of the entire Dlk1-Gtl2 locus, independently of the parental origin of the transcripts. Interestingly 14 other imprinted genes situated at other imprinted loci were not affected by the loss of Ngn2. Finally, using Ngn2/Ascl1 double KO mice, we show that the upregulation of genes at the Dlk1-Gtl2 locus in Ngn2 KO animals requires a functional copy of Ascl1. Our data suggest a complex interplay between proneural genes in the developing forebrain that control the level of expression at the imprinted Dlk1-Gtl2 locus (but not of other imprinted genes). This raises the possibility that the transcripts of this selective locus participate in the biological effects of proneural genes in the developing telencephalon.
C1 [Seibt, Julie; Vanderhaeghen, Pierre; Bouschet, Tristan] Univ Libre Bruxelles ULB, IRIBHM Inst Interdisciplinary Res, Brussels, Belgium.
   [Seibt, Julie] Campus Charite Mitte, Neurosci Res Ctr NWFZ, Berlin, Germany.
   [Armant, Olivier; Castro, Diogo; Ramesh, Vidya; Guillemot, Francois] Natl Inst Med Res, Div Mol Neurobiol, London NW7 1AA, England.
   [Le Digarcher, Anne; Journot, Laurent; Bouschet, Tristan] Inst Genom Fonct, CNRS, UMR 5203, Montpellier, France.
   [Le Digarcher, Anne; Journot, Laurent; Bouschet, Tristan] INSERM, U661, Montpellier, France.
   [Le Digarcher, Anne; Journot, Laurent; Bouschet, Tristan] Univ Montpellier I, UMR 5203, Montpellier, France.
   [Le Digarcher, Anne; Journot, Laurent; Bouschet, Tristan] Univ Montpellier 2, UMR 5203, Montpellier, France.
   [Vanderhaeghen, Pierre] Univ Libre Bruxelles ULB, Welbio, Brussels, Belgium.
RP Vanderhaeghen, P (reprint author), Univ Libre Bruxelles ULB, IRIBHM Inst Interdisciplinary Res, Brussels, Belgium.
EM pvdhaegh@ulb.ac.be; Tristan.Bouschet@igf.cnrs.fr
FU Belgian Queen Elizabeth Medical Foundation; Fondation Universite Libre
   de Bruxelles (ULB); Fondation Pierre Clerdent; Fondation Roger de
   Spoelberch; Action de Recherches Concertees (ARC) Programs;
   Interuniversity Attraction Poles Program (IUAP), Belgian State, Federal
   Office for Scientific, Technical and Cultural Affairs; Belgian National
   Fund for Scientific Research (FNRS and FRSM); Marie Curie Fellowship;
   European Molecular Biology Organization (EMBO); Medical Research Council
FX This work was funded by grants from the Belgian Queen Elizabeth Medical
   Foundation, the Fondations Universite Libre de Bruxelles (ULB), Pierre
   Clerdent, and Roger de Spoelberch, the Action de Recherches Concertees
   (ARC) Programs, the Interuniversity Attraction Poles Program (IUAP),
   Belgian State, Federal Office for Scientific, Technical and Cultural
   Affairs, the Belgian National Fund for Scientific Research (FNRS and
   FRSM) (to P.V), a Marie Curie Fellowship (to T.B.) and a Short-Term
   Fellowship from European Molecular Biology Organization (EMBO) (to J.S).
   The work in F.G.'s lab was supported by institutional funds from the
   Medical Research Council. 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
SN 1932-6203
J9 PLOS ONE
JI PLoS One
PD NOV 6
PY 2012
VL 7
IS 11
AR e48675
DI 10.1371/journal.pone.0048675
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 040IE
UT WOS:000311315300052
PM 23139813
ER

PT J
AU Meechan, DW
   Tucker, ES
   Maynard, TM
   LaMantia, AS
AF Meechan, Daniel W.
   Tucker, Eric S.
   Maynard, Thomas M.
   LaMantia, Anthony-Samuel
TI Cxcr4 regulation of interneuron migration is disrupted in 22q11.2
   deletion syndrome
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; CARDIO-FACIAL SYNDROME; GABAERGIC
   INTERNEURONS; CORTICAL INTERNEURONS; MOUSE MODEL; GANGLIONIC EMINENCE;
   SCHIZOPHRENIA; NEURONS; SUBTYPES; ADULTS
AB Interneurons are thought to be a primary pathogenic target for several behavioral disorders that arise during development, including schizophrenia and autism. It is not known, however, whether genetic lesions associated with these diseases disrupt established molecular mechanisms of interneuron development. We found that diminished 22q11.2 gene dosage-the primary genetic lesion in 22q11.2 deletion syndrome (22q11.2 DS)-specifically compromises the distribution of early-generated parvalbumin-expressing interneurons in the Large Deletion (LgDel) 22q11.2DS mouse model. This change reflects cell-autonomous disruption of interneuron migration caused by altered expression of the cytokine C-X-C chemokine receptor type 4 (Cxcr4), an established regulator of this process. Cxcr4 is specifically reduced in LgDel migrating interneurons, and genetic analysis confirms that diminished Cxcr4 alters interneuron migration in LgDel mice. Thus, diminished 22q11.2 gene dosage disrupts cortical circuit development by modifying a critical molecular signaling pathway via Cxcr4 that regulates cortical interneuron migration and placement.
C1 [Meechan, Daniel W.; Maynard, Thomas M.; LaMantia, Anthony-Samuel] George Washington Univ, Dept Pharmacol & Physiol, Washington, DC 20037 USA.
   [Meechan, Daniel W.; Maynard, Thomas M.; LaMantia, Anthony-Samuel] George Washington Univ, George Washington Inst Neurosci, Washington, DC 20037 USA.
   [Tucker, Eric S.] W Virginia Univ, Sch Med, Dept Neurobiol & Anat, Morgantown, WV 26506 USA.
   [Tucker, Eric S.] W Virginia Univ, Sch Med, Ctr Neurosci, Morgantown, WV 26506 USA.
RP LaMantia, AS (reprint author), George Washington Univ, Dept Pharmacol & Physiol, Washington, DC 20037 USA.
EM lamantia@gwu.edu
RI Maynard, Thomas/I-9039-2012
OI Maynard, Thomas/0000-0001-6976-3936
FU National Institutes of Health (NIH)National Institute of Child Health
   and Human Development [042182]; NIH/National Institute of Mental Health
   [64065, S10RR025565]; National Institute of Neurological Disorders and
   Stroke [NS031768]; National Alliance for Research on Schizophrenia and
   Depression Young Investigator Award from the Brain and Behavior Research
   Foundation
FX We thank Thomas Harrigan for technical support. We thank Teresa Hawley
   for FACS analysis. This work was supported by National Institutes of
   Health (NIH)National Institute of Child Health and Human Development
   Grant 042182 and NIH/National Institute of Mental Health Grant 64065 (to
   A-S. L.), Grant S10RR025565 for microscopic analysis, and National
   Institute of Neurological Disorders and Stroke Grant NS031768 for the
   University of North Carolina at Chapel Hill Neuroscience Center core
   facility. D. W. M. was funded by a National Alliance for Research on
   Schizophrenia and Depression Young Investigator Award from the Brain and
   Behavior Research Foundation.
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NR 44
TC 22
Z9 22
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 6
PY 2012
VL 109
IS 45
BP 18601
EP 18606
DI 10.1073/pnas.1211507109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038DZ
UT WOS:000311156700076
PM 23091025
ER

PT J
AU Gringras, P
   Gamble, C
   Jones, AP
   Wiggs, L
   Williamson, PR
   Sutcliffe, A
   Montgomery, P
   Whitehouse, WP
   Choonara, I
   Allport, T
   Edmond, A
   Appleton, R
AF Gringras, P.
   Gamble, C.
   Jones, A. P.
   Wiggs, L.
   Williamson, P. R.
   Sutcliffe, A.
   Montgomery, P.
   Whitehouse, W. P.
   Choonara, I.
   Allport, T.
   Edmond, A.
   Appleton, R.
CA MENDS Study Grp
TI Melatonin for sleep problems in children with neurodevelopmental
   disorders: randomised double masked placebo controlled trial
SO BRITISH MEDICAL JOURNAL
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; EXOGENOUS MELATONIN; METAANALYSIS; EFFICACY;
   SAFETY
AB Objective To assess the effectiveness and safety of melatonin in treating severe sleep problems in children with neurodevelopmental disorders.
   Design 12 week double masked randomised placebo controlled phase III trial.
   Setting 19 hospitals across England and Wales.
   Participants 146 children aged 3 years to 15 years 8 months were randomised. They had a range of neurological and developmental disorders and a severe sleep problem that had not responded to a standardised sleep behaviour advice booklet provided to parents four to six weeks before randomisation. A sleep problem was defined as the child not falling asleep within one hour of lights out or having less than six hours' continuous sleep.
   Interventions Immediate release melatonin or matching placebo capsules administered 45 minutes before the child's bedtime for a period of 12 weeks. All children started with a 0.5 mg capsule, which was increased through 2 mg, 6 mg, and 12 mg depending on their response to treatment.
   Main outcome measures Total sleep time at night after 12 weeks adjusted for baseline recorded in sleep diaries completed by the parent. Secondary outcomes included sleep onset latency, assessments of child behaviour, family functioning, and adverse events. Sleep was measured with diaries and actigraphy.
   Results Melatonin increased total sleep time by 22.4 minutes (95% confidence interval 0.5 to 44.3 minutes) measured by sleep diaries (n=110) and 13.3 (-15.5 to 42.2) measured by actigraphy (n=59). Melatonin reduced sleep onset latency measured by sleep diaries (-37.5 minutes, -55.3 to -19.7 minutes) and actigraphy (-45.3 minutes, -68.8 to -21.9 minutes) and was most effective for children with the longest sleep latency (P=0.009). Melatonin was associated with earlier waking times than placebo (29.9 minutes, 13.6 to 46.3 minutes). Child behaviour and family functioning outcomes showed some improvement and favoured use of melatonin. Adverse events were mild and similar between the two groups.
   Conclusions Children gained little additional sleep on melatonin; though they fell asleep significantly faster, waking times became earlier. Child behaviour and family functioning outcomes did not significantly improve. Melatonin was tolerable over this three month period. Comparisons with slow release melatonin preparations or melatonin analogues are required.
C1 [Gringras, P.] Kings Coll London, London SE1 7EH, England.
   [Gringras, P.] St Thomas Hosp, Evelina Childrens Hosp, London SE1 7EH, England.
   [Gamble, C.; Jones, A. P.; Williamson, P. R.] Univ Liverpool, Alder Hey Childrens NHS Fdn Trust, Med Children Res Network Clin Trials Unit, Liverpool L12 2AP, Merseyside, England.
   [Wiggs, L.] Oxford Brookes Univ, Dept Psychol, Oxford OX3 0BP, England.
   [Sutcliffe, A.] UCL, Inst Child Hlth, GAP Unit, London WC1N 1EH, England.
   [Montgomery, P.] Univ Oxford, Ctr Evidence Based Intervent, Oxford OX1 2ER, England.
   [Whitehouse, W. P.] Univ Nottingham, Nottingham NG7 2RD, England.
   [Whitehouse, W. P.] Nottingham Univ Hosp NHS Trust, Nottingham Childrens Hosp, Nottingham, England.
   [Choonara, I.] Derbyshire Childrens Hosp, Sch Med, Acad Div Child Hlth, Derby DE22 3DT, England.
   [Allport, T.; Edmond, A.] Univ Bristol, Ctr Child & Adolescent Hlth, Bristol BS8 2BN, Avon, England.
   [Appleton, R.] Alder Hey Childrens NHS Fdn Trust, Paediat Neurosci Fdn, Roald Dahl EEG Dept, Liverpool, Merseyside, England.
RP Gringras, P (reprint author), Kings Coll London, London SE1 7EH, England.
EM Paul.Gringras@gstt.nhs.uk
FU NIHR Health Technology Assessment programme [05/14/02]
FX This project was funded by the NIHR Health Technology Assessment
   programme (project number 05/14/02) and will be published in full in
   Health Technology Assessment journal. See the HTA programme website for
   further project information. This report presents independent research
   commissioned by the National Institute for Health Research (NIHR). The
   views and opinions expressed therein are those of the authors and do not
   necessarily reflect those of the NHS, the NIHR, NETSCC, the HTA
   programme, or the Department of Health.
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NR 33
TC 24
Z9 24
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 1756-1833
J9 BRIT MED J
JI Br. Med. J.
PD NOV 5
PY 2012
VL 345
AR e6664
DI 10.1136/bmj.e6664
PG 16
WC Medicine, General & Internal
SC General & Internal Medicine
GA 036KY
UT WOS:000311026000001
PM 23129488
ER

PT J
AU Cheshire, WP
AF Cheshire, William P.
TI HIGHLIGHTS IN CLINICAL AUTONOMIC NEUROSCIENCE: NEW INSIGHTS INTO
   AUTONOMIC DYSFUNCTION IN AUTISM
SO AUTONOMIC NEUROSCIENCE-BASIC & CLINICAL
LA English
DT Article
DE Autistic Disorder; Autonomic Nervous System Diseases; Vagus Nerve;
   Pupil, Questionnaires
ID RETT-SYNDROME; SPECTRUM DISORDER; CHILDREN; ATTENTION; PATTERNS;
   OBJECTS; MECP2; MODEL
AB Investigations of autonomic nervous system biomarkers in autism have been sparse relative to its prevalence. Recent studies of children with autism spectrum disorders (ASD) have increasingly drawn correlations between autonomic findings and psychosocial behavior. Studies of heart rate variability, pupil size, salivary alpha-amylase, and electrodermal responsiveness have shown that children with ASD differ from normally developing children in their autonomic responsiveness to visualizing human faces and other mental tasks. While some results have conflicted, much of the data appears to support the theory of a hypersympathetic state in autism insufficiently attenuated by vagal parasympathetic influences. To what degree these differences in autonomic physiology might influence cognitive processing and behavior rather than simply being epiphenomena of a pervasive disorder of brain development is as yet unclear. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Cheshire, William P.] Mayo Clin, Coll Med, Rochester, MN 55905 USA.
RP Cheshire, WP (reprint author), Mayo Clin, Coll Med, Rochester, MN 55905 USA.
EM cheshire@mayo.edu
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NR 19
TC 4
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1566-0702
J9 AUTON NEUROSCI-BASIC
JI Auton. Neurosci-Basic Clin.
PD NOV 2
PY 2012
VL 171
IS 1-2
BP 4
EP 7
DI 10.1016/j.autneu.2012.08.003
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 055LF
UT WOS:000312417100002
PM 23040840
ER

PT J
AU Arechavaleta-Velasco, ME
   Alcala-Escamilla, K
   Robles-Rios, C
   Tsuruda, JM
   Hunt, GJ
AF Arechavaleta-Velasco, Miguel E.
   Alcala-Escamilla, Karla
   Robles-Rios, Carlos
   Tsuruda, Jennifer M.
   Hunt, Greg J.
TI Fine-Scale Linkage Mapping Reveals a Small Set of Candidate Genes
   Influencing Honey Bee Grooming Behavior in Response to Varroa Mites
SO PLOS ONE
LA English
DT Article
ID QUANTITATIVE TRAIT LOCI; APIS-MELLIFERA COLONIES; POPULATION-GROWTH;
   NEUREXIN-I; DESTRUCTOR; RESISTANCE; JACOBSONI; LOSSES; MEXICO;
   HERITABILITY
AB Populations of honey bees in North America have been experiencing high annual colony mortality for 15-20 years. Many apicultural researchers believe that introduced parasites called Varroa mites (V. destructor) are the most important factor in colony deaths. One important resistance mechanism that limits mite population growth in colonies is the ability of some lines of honey bees to groom mites from their bodies. To search for genes influencing this trait, we used an Illumina Bead Station genotyping array to determine the genotypes of several hundred worker bees at over a thousand single-nucleotide polymorphisms in a family that was apparently segregating for alleles influencing this behavior. Linkage analyses provided a genetic map with 1,313 markers anchored to genome sequence. Genotypes were analyzed for association with grooming behavior, measured as the time that individual bees took to initiate grooming after mites were placed on their thoraces. Quantitative-trait-locus interval mapping identified a single chromosomal region that was significant at the chromosome-wide level (p<.05) on chromosome 5 with a LOD score of 2.72. The 95% confidence interval for quantitative trait locus location contained only 27 genes (honey bee official gene annotation set 2) including Atlastin, Ataxin and Neurexin-1 (AmNrx1), which have potential neurodevelopmental and behavioral effects. Atlastin and Ataxin homologs are associated with neurological diseases in humans. AmNrx1 codes for a presynaptic protein with many alternatively spliced isoforms. Neurexin-1 influences the growth, maintenance and maturation of synapses in the brain, as well as the type of receptors most prominent within synapses. Neurexin-1 has also been associated with autism spectrum disorder and schizophrenia in humans, and self-grooming behavior in mice.
C1 [Tsuruda, Jennifer M.; Hunt, Greg J.] Purdue Univ, Dept Entomol, W Lafayette, IN 47907 USA.
   [Arechavaleta-Velasco, Miguel E.; Robles-Rios, Carlos] Inst Nacl Invest Forestales Agr & Pecuarias, Ajuchitlan, Queretaro, Mexico.
   [Alcala-Escamilla, Karla] Inst Nacl Invest Forestales Agr & Pecuarias, Etla, Oaxaca, Mexico.
RP Hunt, GJ (reprint author), Purdue Univ, Dept Entomol, W Lafayette, IN 47907 USA.
EM ghunt@purdue.edu
FU USDA-NRI [2008-35302-18803]; Managed Pollinator Coordinated Agricultural
   Project [USDA-NIFA 2009-8511805718]; CONACYT [SEP-C02-45528]; INIFAP
   research project [2276977P]
FX This research was funded by a USDA-NRI award (2008-35302-18803) and the
   Managed Pollinator Coordinated Agricultural Project (USDA-NIFA
   2009-8511805718) to GJH, and by CONACYT award (SEP-C02-45528) and the
   INIFAP research project (2276977P) to MEAV. 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 72
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 NOV 2
PY 2012
VL 7
IS 11
AR e47269
DI 10.1371/journal.pone.0047269
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 032GO
UT WOS:000310702400008
PM 23133594
ER

PT J
AU Wojciak, P
   Remlinger-Molenda, A
   Rybakowski, J
AF Wojciak, Pawel
   Remlinger-Molenda, Agnieszka
   Rybakowski, Janusz
TI The role of oxytocin and vasopressin in central nervous system activity
   and mental disorders
SO PSYCHIATRIA POLSKA
LA Polish
DT Article
DE oxytocin; vasopressin; schizophrenia; depression; autism; social
   behaviours
ID SOCIAL-PERCEPTION; AUTOANTIBODIES; ATTACHMENT; DEPRESSION; LOVE;
   NEUROENDOCRINE; SCHIZOPHRENIA; CLOZAPINE; SECRETION; SYMPTOMS
AB Oxytocin and vasopressin, "peptides of love and fear", except for their classic role in control of labor and breastfeeding and blood pressure regulation, are also implicated in various processes like sexual behaviours, social recognition and stress response. These hormones seems to be essential for appropriate and beneficial social interactions, play a very important role in maternal care and closeness, promote general trust and cooperation and prolong social memory. They also play a very important role in modulating fear and anxiety response, especially by regulating the hypothalamic-pituitary-adrenal axis and amygdala activity by its projections to the brain stem and hypothalamic structures. Both hormones, particularly oxytocin, appears to be activating sexual behaviour or is responsible for increased sexual arousal. Evidence from clinical trials suggests their potential role in pathogenesis of schizophrenia, depression, autism and addiction together with possible therapeutic use in the above conditions. In schizophrenia, patients with higher peripheral oxytocin levels showed less severe positive, general and social symptoms and better prosocial behaviours. Literature suggests that exogenous oxytocin may be effective as an adjunctive therapy for that illness. Some data suggest that naturally occurring autoantibodies reacting with oxytocin and vasopressin are involved in depression, eating disorders and conduct disorder genesis.
C1 [Wojciak, Pawel; Remlinger-Molenda, Agnieszka; Rybakowski, Janusz] Klin Psychiat Doroslych UM, Poznaniu, Poland.
RP Wojciak, P (reprint author), Uniwersytet Med Karola Marcinkowskiego, Klin Psychiat Doroslych, Ul Szpitalna 27-33, PL-60572 Poznan, Poland.
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NR 48
TC 2
Z9 5
PU WYDAWNICZY POLSKIEGO TOWARZYSTWA
PI CRACOW
PA LENARTOWICZA 14 STRREET,, CRACOW, 31-138, POLAND
SN 0033-2674
J9 PSYCHIATR POL
JI Psychiatr. Pol.
PD NOV-DEC
PY 2012
VL 46
IS 6
BP 1043
EP 1052
PG 10
WC Psychiatry
SC Psychiatry
GA 094IG
UT WOS:000315255600010
PM 23479945
ER

PT J
AU Brynska, A
AF Brynska, Anita
TI Seeking the aetiology of autistic spectrum disorder. Part 1: structural
   neuroimaging
SO PSYCHIATRIA POLSKA
LA Polish
DT Article
DE autistic spectrum disorder; aetiology; neuroimaging
ID CORTICAL THICKNESS; BRAIN VOLUME; MRI; METAANALYSIS; AGE; ABNORMALITIES;
   NEUROANATOMY; ADOLESCENTS; ENLARGEMENT; MORPHOMETRY
AB Although the aetiology of autistic-spectrum disorder (ASD) remains unclear, great advances have been made to clarify the underlying neuroanatomical abnormalities and brain-behaviour relationships in autism. There is variability in the literature on structural neuroimaging findings in ASD. Early brain overgrowth is probably the most replicated finding in this subgroup. Additionally some specific brain regions are particularly implicated, including the frontal, limbic, basal ganglia and cerebellar regions. There is also evidence of volume abnormalities in both grey and white matter. New techniques, such as cortical-thickness measurements, surface morphometry and diffusion tensor imaging help to understand in more detail the patterns of abnormalities. More work is required, involving the use of large and homogeneous samples, to investigate the neuroanatomical determinants and their role in aetiology of ASD. The goal of this review is to summarise the available structural neuroimaging data and examine their implication for understanding of the neurobiology of ASD.
C1 Klin Psychiat Wieku Rozwojowego WUM, PL-00576 Warsaw, Poland.
RP Brynska, A (reprint author), Klin Psychiat Wieku Rozwojowego WUM, Ul Marszalkowska 24, PL-00576 Warsaw, Poland.
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NR 35
TC 3
Z9 3
PU WYDAWNICZY POLSKIEGO TOWARZYSTWA
PI CRACOW
PA LENARTOWICZA 14 STRREET,, CRACOW, 31-138, POLAND
SN 0033-2674
J9 PSYCHIATR POL
JI Psychiatr. Pol.
PD NOV-DEC
PY 2012
VL 46
IS 6
BP 1053
EP 1060
PG 8
WC Psychiatry
SC Psychiatry
GA 094IG
UT WOS:000315255600011
PM 23479946
ER

PT J
AU Brynska, A
AF Brynska, Anita
TI Seeking the aetiology of autistic spectrum disorder. Part 2: functional
   neuroimaging
SO PSYCHIATRIA POLSKA
LA Polish
DT Article
DE autistic spectrum disorder; aetiology; neuroimaging
ID CEREBRAL-BLOOD-FLOW; CHILDHOOD AUTISM; WHITE-MATTER; CHILDREN;
   ACTIVATION; LANGUAGE; FMRI; UNDERCONNECTIVITY; SYNCHRONIZATION;
   ABNORMALITIES
AB Multiple functional imaging techniques help to a better understanding of the neurobiological basis of autism-spectrum disorders (ASD). The early functional imaging studies on ASD focused on task-specific methods related to core symptom domains and explored patterns of activation in response to face processing, theory of mind tasks, language processing and executive function tasks. On the other hand, fMRI research in ASD focused on the development of functional connectivity methods and has provided evidence of alterations in cortical connectivity in ASD and establish autism as a disorder of under-connectivity among the brain regions participating in cortical networks. This atypical functional connectivity in ASD results in inefficiency and poor integration of processing in network connections to achieve task performance. The goal of this review is to summarise the actual neuroimaging functional data and examine their implication for understanding of the neurobiology of ASD.
C1 Klin Psychiat Wieku Rozwojowego WUM, PL-00576 Warsaw, Poland.
RP Brynska, A (reprint author), Klin Psychiat Wieku Rozwojowego WUM, Ul Marszalkowska 24, PL-00576 Warsaw, Poland.
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NR 36
TC 2
Z9 2
PU WYDAWNICZY POLSKIEGO TOWARZYSTWA
PI CRACOW
PA LENARTOWICZA 14 STRREET,, CRACOW, 31-138, POLAND
SN 0033-2674
J9 PSYCHIATR POL
JI Psychiatr. Pol.
PD NOV-DEC
PY 2012
VL 46
IS 6
BP 1061
EP 1071
PG 11
WC Psychiatry
SC Psychiatry
GA 094IG
UT WOS:000315255600012
PM 23479947
ER

PT J
AU Talarowska, M
   Florkowski, A
   Orzechowska, A
   Zboralski, K
   Lechanska, J
   Galecki, P
AF Talarowska, Monika
   Florkowski, Antoni
   Orzechowska, Agata
   Zboralski, Krzysztof
   Lechanska, Joanna
   Galecki, Piotr
TI The use of RHLB battery for the evaluation of the lingual and social
   skills among psychiatric patients - case study
SO PSYCHIATRIA POLSKA
LA Polish
DT Article
DE right hemisphere; schizophrenia; lingual and social skills
ID PARANOID SCHIZOPHRENIA; EMOTIONAL PROSODY; AMYGDALA VOLUME; RECOGNITION;
   MIND; LANGUAGE; DEFICITS; AUTISM
AB Prosody plays an important role in the process of verbal communication, complementing and emphasising the linguistic and emotional aspects of language. Disturbances of speech prosody are rarely recognised, although aprosodia occurs frequently in patients with schizophrenia. Prosodic disturbance of speech can significantly impair verbal communication and social functioning of patients with schizophrenia. Right-hemisphere is connected with emotional prosody deficits and left-hemisphere with linguistic prosody. The aim of the study is to describe. The Right Hemisphere Language Battery by Karen L. Bryan in the examination of patients with schizophrenia.
C1 [Talarowska, Monika; Florkowski, Antoni; Orzechowska, Agata; Zboralski, Krzysztof; Lechanska, Joanna; Galecki, Piotr] Klin Psychiat Doroslych UM Lodzi, PL-91229 Lodz, Poland.
RP Talarowska, M (reprint author), Klin Psychiat Doroslych UM Lodzi, Ul Aleksandrowska 159, PL-91229 Lodz, Poland.
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NR 29
TC 1
Z9 1
PU WYDAWNICZY POLSKIEGO TOWARZYSTWA
PI CRACOW
PA LENARTOWICZA 14 STRREET,, CRACOW, 31-138, POLAND
SN 0033-2674
J9 PSYCHIATR POL
JI Psychiatr. Pol.
PD NOV-DEC
PY 2012
VL 46
IS 6
BP 1089
EP 1098
PG 10
WC Psychiatry
SC Psychiatry
GA 094IG
UT WOS:000315255600014
PM 23479949
ER

PT J
AU van Steensel, FJA
   Bogels, SM
   Dirksen, CD
AF van Steensel, Francisca J. A.
   Bogels, Susan M.
   Dirksen, Carmen D.
TI Anxiety and Quality of Life: Clinically Anxious Children With and
   Without Autism Spectrum Disorders Compared
SO JOURNAL OF CLINICAL CHILD AND ADOLESCENT PSYCHOLOGY
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; DSM-IV; SYMPTOMS;
   ADOLESCENTS; PREVALENCE; INTERVIEW; EUROQOL; TRIAL; EQ-5D
AB Comorbid anxiety disorders are common in children with autism spectrum disorders (ASD). However, studies comparing children with ASD to clinically anxious children are rare. This study investigated anxiety problems and health-related quality of life in children with high-functioning ASD and comorbid anxiety disorders (referred to as the ASD group), compared with children with anxiety disorders (referred to as the AD group). In total, 237 families participated; 115 children were in the ASD group (90 boys and 25 girls, M age = 11.37 years), and 122 children were in the AD group (62 boys and 60 girls, M age = 12.79 years). Anxiety disorders, anxiety symptoms, ASD-like symptoms, and health-related quality of life were assessed with the ADIS-C/P, SCARED-71, CSBQ, and EuroQol-5D, respectively. The number and types of anxiety disorders, as well as their severity, were similar in the ASD and AD groups; however, specific phobias were more common in the ASD group than in the AD group. As compared to the AD group, parents from the ASD group reported their children to have higher scores for total anxiety, social anxiety disorder, and panic disorder. More ASD-like behaviors and higher anxiety severity predicted a lower quality of life, irrespective of group. The results of this study support a highly similar phenotype of anxiety disorders in children with ASD; however, additional research is needed to examine the etiology and treatment effectiveness of anxiety disorders in children with ASD.
C1 [van Steensel, Francisca J. A.; Bogels, Susan M.] Univ Amsterdam, Res Inst Child Dev & Educ, NL-1018 VZ Amsterdam, Netherlands.
   [Dirksen, Carmen D.] Maastricht Univ, Dept Clin Epidemiol & Med Technol Assessment, Med Ctr, Maastricht, 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
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NR 29
TC 14
Z9 14
PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD
PI ABINGDON
PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND
SN 1537-4416
J9 J CLIN CHILD ADOLESC
JI J. Clin. Child Adolesc. Psychol.
PD NOV 1
PY 2012
VL 41
IS 6
BP 731
EP 738
DI 10.1080/15374416.2012.698725
PG 8
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA 093UQ
UT WOS:000315218600002
PM 22775580
ER

PT J
AU Wagnon, JL
   Briese, M
   Sun, WZ
   Mahaffey, CL
   Curk, T
   Rot, G
   Ule, J
   Frankel, WN
AF Wagnon, Jacy L.
   Briese, Michael
   Sun, Wenzhi
   Mahaffey, Connie L.
   Curk, Tomaz
   Rot, Gregor
   Ule, Jernej
   Frankel, Wayne N.
TI CELF4 Regulates Translation and Local Abundance of a Vast Set of mRNAs,
   Including Genes Associated with Regulation of Synaptic Function
SO PLOS GENETICS
LA English
DT Article
ID MENTAL-RETARDATION PROTEIN; FRAGILE-X-SYNDROME; JUVENILE MYOCLONIC
   EPILEPSY; BINDING PROTEINS; DEPENDENT TRANSLATION; FAMILY; MUTATIONS;
   GRANULES; AUTISM; NEURONS
AB RNA-binding proteins have emerged as causal agents of complex neurological diseases. Mice deficient for neuronal RNA-binding protein CELF4 have a complex neurological disorder with epilepsy as a prominent feature. Human CELF4 has recently been associated with clinical features similar to those seen in mutant mice. CELF4 is expressed primarily in excitatory neurons, including large pyramidal cells of the cerebral cortex and hippocampus, and it regulates excitatory but not inhibitory neurotransmission. We examined mechanisms underlying neuronal hyperexcitability in Celf4 mutants by identifying CELF4 target mRNAs and assessing their fate in the absence of CELF4 in view of their known functions. CELF4 binds to at least 15%-20% of the transcriptome, with striking specificity for the mRNA 3' untranslated region. CELF4 mRNA targets encode a variety of proteins, many of which are well established in neuron development and function. While the overall abundance of these mRNA targets is often dysregulated in Celf4 deficient mice, the actual expression changes are modest at the steady-state level. In contrast, by examining the transcriptome of polysome fractions and the mRNA distribution along the neuronal cell body-neuropil axis, we found that CELF4 is critical for maintaining mRNA stability and availability for translation. Among biological processes associated with CELF4 targets that accumulate in neuropil of mutants, regulation of synaptic plasticity and transmission are the most prominent. Together with a related study of the impact of CELF4 loss on sodium channel Na(v)1.6 function, we suggest that CELF4 deficiency leads to abnormal neuronal function by combining a specific effect on neuronal excitation with a general impairment of synaptic transmission. These results also expand our understanding of the vital roles RNA-binding proteins play in regulating and shaping the activity of neural circuits.
C1 [Wagnon, Jacy L.; Sun, Wenzhi; Mahaffey, Connie L.; Frankel, Wayne N.] Jackson Lab, Bar Harbor, ME 04609 USA.
   [Briese, Michael; Ule, Jernej] MRC Lab Mol Biol, Cambridge, England.
   [Curk, Tomaz; Rot, Gregor] Univ Ljubljana, Fac Comp & Informat Sci, Ljubljana, Slovenia.
RP Wagnon, JL (reprint author), Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA.
EM wayne.frankel@jax.org
RI Ule, Jernej/C-6315-2013
OI Ule, Jernej/0000-0002-2452-4277
FU NIH; Epilepsy Foundation of America; Relf Family Gift; Medical Research
   Council; Slovenian Research Agency; European Research Council
FX This work was supported by the NIH, Epilepsy Foundation of America, Relf
   Family Gift, Medical Research Council, Slovenian Research Agency, and
   the European Research Council. 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 75
TC 10
Z9 10
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 NOV
PY 2012
VL 8
IS 11
AR e1003067
DI 10.1371/journal.pgen.1003067
PG 19
WC Genetics & Heredity
SC Genetics & Heredity
GA 048DY
UT WOS:000311891600051
PM 23209433
ER

PT J
AU Byiers, BJ
   Reichle, J
   Symons, FJ
AF Byiers, Breanne J.
   Reichle, Joe
   Symons, Frank J.
TI Single-Subject Experimental Design for Evidence-Based Practice
SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY
LA English
DT Article
DE single-subject experimental designs; tutorial; research methods;
   evidence-based practice
ID ALTERNATING TREATMENTS DESIGN; QUANTITATIVE SYNTHESIS; RANDOMIZATION
   TESTS; FLEXIBILITY; PERCENTAGE; CHILDREN; VALIDITY; AUTISM
AB Purpose: Single-subject experimental designs (SSEDs) represent an important tool in the development and implementation of evidence-based practice in communication sciences and disorders. The purpose of this article is to review the strategies and tactics of SSEDs and their application in speech-language pathology research.
   Method: The authors discuss the requirements of each design, followed by advantages and disadvantages. The logic and methods for evaluating effects in SSED are reviewed as well as contemporary issues regarding data analysis with SSED data sets. Examples of challenges in executing SSEDs are included. Specific exemplars of how SSEDs have been used in speech-language pathology research are provided throughout.
   Conclusion: SSED studies provide a flexible alternative to traditional group designs in the development and identification of evidence-based practice in the field of communication sciences and disorders.
C1 [Byiers, Breanne J.; Reichle, Joe; Symons, Frank J.] Univ Minnesota, Minneapolis, MN 55455 USA.
RP Byiers, BJ (reprint author), Univ Minnesota, Minneapolis, MN 55455 USA.
EM byier001@umn.edu
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NR 58
TC 9
Z9 9
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1058-0360
J9 AM J SPEECH-LANG PAT
JI Am. J. Speech-Lang. Pathol.
PD NOV 1
PY 2012
VL 21
IS 4
BP 397
EP 414
DI 10.1044/1058-0360(2012/11-0036)
PG 18
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 083JY
UT WOS:000314460700011
PM 23071200
ER

PT J
AU Mormann, M
   Gilbertson, C
   Milavetz, G
   Vos, S
AF Mormann, Megan
   Gilbertson, Carolyn
   Milavetz, Gary
   Vos, Susan
TI Dispelling vaccine myths: MMR and considerations for practicing
   pharmacists
SO JOURNAL OF THE AMERICAN PHARMACISTS ASSOCIATION
LA English
DT Editorial Material
DE Pediatric; immunizations; MMR; autism spectrum disorders
ID MUMPS-RUBELLA VACCINATION; AUTISM; MEASLES; CHILDREN; POPULATION;
   ASSOCIATION; DISORDERS
AB Objectives: To discuss information surrounding the erroneous association between the measles-mumps-rubella (MMR) vaccine and autism spectrum disorders (ASDs) and to provide pharmacists with information to dispel vaccine myths.
   Data sources: Pharmaceutical and medical literature and public media (e.g., newspapers).
   Summary: The diagnosis of ASDs is on the rise, and many speculations have been made as to the cause, including the MMR vaccine. A small case series article published in The Lancet in 1998 and later retracted has been the center of the controversy over whether the MMR vaccine causes ASDs. New definitive research demonstrates no link, and medical organizations state that evidence does not support a link between the MMR vaccine and ASDs.
   Conclusion: Pharmacists can play a role in providing up-do-date information to patients to dispel myths concerning vaccine safety. Accurate peer review remains an important step to ensure correct information is given to health care providers and the public.
C1 [Mormann, Megan] NE Iowa Family Practice Ctr, Waterloo, IA USA.
   [Gilbertson, Carolyn; Milavetz, Gary; Vos, Susan] Univ Iowa, Coll Pharm, Iowa City, IA 52242 USA.
RP Vos, S (reprint author), Univ Iowa, Coll Pharm, 115 S Grand Ave,S413 PHAR, Iowa City, IA 52242 USA.
EM susan-vos@uiowa.edu
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NR 28
TC 1
Z9 1
PU AMER PHARMACEUTICAL ASSOC
PI WASHINGTON
PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 USA
SN 1544-3191
J9 J AM PHARM ASSOC
JI J. Am. Pharm. Assoc.
PD NOV-DEC
PY 2012
VL 52
IS 6
BP E282
EP E286
DI 10.1331/JAPhA.2012.11239
PG 5
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA 082OM
UT WOS:000314401500020
PM 23229992
ER

PT J
AU King, M
AF King, Marissa
TI Understanding Autism: Parents, Doctors, and the History of a Disorder
SO AMERICAN JOURNAL OF SOCIOLOGY
LA English
DT Book Review
C1 [King, Marissa] Yale Univ, New Haven, CT 06520 USA.
RP King, M (reprint author), Yale Univ, New Haven, CT 06520 USA.
CR Silverman C, 2012, UNDERSTANDING AUTISM: PARENTS, DOCTORS, AND THE HISTORY OF A DISORDER, P1
NR 1
TC 0
Z9 0
PU UNIV CHICAGO PRESS
PI CHICAGO
PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA
SN 0002-9602
EI 1537-5390
J9 AM J SOCIOL
JI Am. J. Sociol.
PD NOV
PY 2012
VL 118
IS 3
BP 827
EP 829
DI 10.1086/667393
PG 5
WC Sociology
SC Sociology
GA 073CU
UT WOS:000313721800013
ER

PT J
AU Kalnak, N
   Peyrard-Janvid, M
   Sahlen, B
   Forssberg, H
AF Kalnak, N.
   Peyrard-Janvid, M.
   Sahlen, B.
   Forssberg, H.
TI Family history interview of a broad phenotype in specific language
   impairment and matched controls
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE ADHD; attention; autism spectrum disorders; dyslexia; heredity;
   prevalence rates; reading; SLI; social communication; Swedish population
ID ATTENTION-DEFICIT/HYPERACTIVITY; READING OUTCOMES; CHILDREN; SPEECH;
   DISORDERS; RISK; PREVALENCE; SLI; AGGREGATION; GENETICS
AB The aim was to study a broader phenotype of language-related diagnoses and problems in three generations of relatives of children with specific language impairment (SLI). Our study is based on a family history interview of the parents of 59 children with SLI and of 100 matched control children, exploring the prevalence of problems related to language, reading, attention, school achievement and social communication as well as diagnoses such as attention-deficit hyperactivity disorder (ADHD), autism, Asperger syndrome, dyslexia, mental retardation, cleft palate and stuttering. The results show a spectrum of language-related problems in families of SLI children. In all three generations of SLI relatives, we found significantly higher prevalence rates of language, literacy and social communication problems. The risk of one or both parents having language-related diagnoses or problems was approximately six times higher for the children with SLI (85%) than for the control children (13%) (odds ratio=37.2). We did not find a significantly higher prevalence of the diagnoses ADHD, autism or Asperger syndrome in the relatives of the children with SLI. However, significantly more parents of the children with SLI had problems with attention/hyperactivity when compared with the parents of controls. Our findings suggest common underlying mechanisms for problems with language, literacy and social communication, and possibly also for attention/hyperactivity symptoms.
C1 [Kalnak, N.] Astrid Lindgren Childrens Hosp, Neuropediat Unit, Dept Womens & Childrens Hlth, SE-17176 Stockholm, Sweden.
   [Peyrard-Janvid, M.] Karolinska Inst, Dept Biosci & Nutr, Stockholm, Sweden.
   [Sahlen, B.] Lund Univ, Dept Logoped Phoniatr & Audiol, Lund, Sweden.
RP Kalnak, N (reprint author), Astrid Lindgren Childrens Hosp, Neuropediat Unit, Dept Womens & Childrens Hlth, H2 07, SE-17176 Stockholm, Sweden.
EM Nelli.Kalnak@karolinska.se
RI Sahlen, Birgitta/O-1245-2014
OI Sahlen, Birgitta/0000-0002-8468-0546
FU foundation Olle Engkvist Byggmastare; foundation Frimurarna Barnhuset;
   foundation Sunnerdahls Handikappfond; foundation Clas Groschinskys
   Minnesfond; foundation Promobilia; foundation Sallskapet Barnavard;
   Swedish Research Council; Swedish Foundation for Strategic Research;
   VINNOVA; Karolinska Institutet
FX We are grateful to the study participants, their families and schools
   for their cooperation. We would like to thank Viktoria Akerlund and
   Kerstin Andersson for their help with the recruitment of participants
   and with data collection, Professor Anders Lofqvist and the Linneus
   environment for Cognition, Communication and Learning at Lund University
   for advice. This work was supported by grants from the foundations Olle
   Engkvist Byggmastare, Frimurarna Barnhuset, Sunnerdahls Handikappfond,
   Clas Groschinskys Minnesfond, Promobilia and Sallskapet Barnavard,
   Swedish Research Council, Swedish Foundation for Strategic Research,
   VINNOVA and Strategic Neuroscience Program at Karolinska Institutet.
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NR 39
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD NOV
PY 2012
VL 11
IS 8
BP 921
EP 927
DI 10.1111/j.1601-183X.2012.00841.x
PG 7
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 076YE
UT WOS:000313994300004
PM 22928858
ER

PT J
AU Ey, E
   Yang, M
   Katz, AM
   Woldeyohannes, L
   Silverman, JL
   Leblond, CS
   Faure, P
   Torquet, N
   Le Sourd, AM
   Bourgeron, T
   Crawley, JN
AF Ey, E.
   Yang, M.
   Katz, A. M.
   Woldeyohannes, L.
   Silverman, J. L.
   Leblond, C. S.
   Faure, P.
   Torquet, N.
   Le Sourd, A. -M.
   Bourgeron, T.
   Crawley, J. N.
TI Absence of deficits in social behaviors and ultrasonic vocalizations in
   later generations of mice lacking neuroligin4
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Adult social interaction; autism; juvenile social interaction; mouse
   models; neuroligin4; resident-intruder; three-chambered social approach
   task; ultrasonic vocalizations
ID AUTISM SPECTRUM DISORDERS; DE-NOVO MUTATIONS; MENTAL-RETARDATION;
   TOURETTE-SYNDROME; MOUSE MODEL; NLGN4; PHENOTYPES; GENES; NETWORK
AB Mutations in NLGN4X have been identified in individuals with autism spectrum disorders and other neurodevelopmental disorders. A previous study reported that adult male mice lacking neuroligin4 (Nlgn4) displayed social approach deficits in the three-chambered test, altered aggressive behaviors and reduced ultrasonic vocalizations. To replicate and extend these findings, independent comprehensive analyses of autism-relevant behavioral phenotypes were conducted in later generations of the same line of Nlgn4 mutant mice at the National Institute of Mental Health in Bethesda, MD, USA and at the Institut Pasteur in Paris, France. Adult social approach was normal in all three genotypes of Nlgn4 mice tested at both sites. Reciprocal social interactions in juveniles were similarly normal across genotypes. No genotype differences were detected in ultrasonic vocalizations in pups separated from the nest or in adults during reciprocal social interactions. Anxiety-like behaviors, self-grooming, rotarod and open field exploration did not differ across genotypes, and measures of developmental milestones and general health were normal. Our findings indicate an absence of autism-relevant behavioral phenotypes in subsequent generations of Nlgn4 mice tested at two locations. Testing environment and methods differed from the original study in some aspects, although the presence of normal sociability was seen in all genotypes when methods taken from Jamain et al. (2008) were used. The divergent results obtained from this study indicate that phenotypes may not be replicable across breeding generations, and highlight the significant roles of environmental, generational and/or procedural factors on behavioral phenotypes.
C1 [Ey, E.; Leblond, C. S.; Torquet, N.; Le Sourd, A. -M.; Bourgeron, T.] Inst Pasteur, CNRS, URA Genes Synapses & Cognit 2182, Paris, France.
   [Ey, E.; Leblond, C. S.; Torquet, N.; Le Sourd, A. -M.; Bourgeron, T.] Univ Paris Diderot, Sorbonne Paris Cite, Paris, France.
   [Yang, M.; Katz, A. M.; Woldeyohannes, L.; Silverman, J. L.; Crawley, J. N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA.
   [Faure, P.] Univ Paris 06, CNRS, UMR 7702, Paris, France.
RP Yang, M (reprint author), Univ Calif Davis, Sch Med, Dept Psychiat & Behav Sci, Room 1001 Res 2 Bldg 96,4625 2nd Ave, Sacramento, CA 95817 USA.
EM mu.yang@ucdmc.udavis.edu
FU National Institute of Mental Health; Fondation de France; ANR FLEXNEURIM
   [ANR09BLAN034003]; ANR [ANR-08-MNPS-037-01 - SynGen]; Neuron-ERANET
   (EUHF-AUTISM); Fondation Orange; Fondation FondaMentale; Fondation
   Bettencourt-Schueller
FX We are grateful to Professor Nils Brose at the Max Planck Institute for
   generously contributing breeding pairs of the Nlgn4 mice which were used
   to generate the mice in this study, and for encouraging our in-depth
   analyses of the behavioral consequences of Nlgn4 mutations in mice. We
   thank Sandrine Vandormael-Pournin (Genetique Fonctionnelle de la Souris,
   Institut Pasteur) for the protocol to detect oestrus status in female
   mice. M. Y., A. M. K., L. W., J. L. S. and J. N. C. were supported by
   the National Institute of Mental Health Intramural Research Program. E.
   E. was supported by Fondation de France, ANR FLEXNEURIM
   (ANR09BLAN034003), C. S. L., N. T., A. L. S. and T. B. by ANR
   (ANR-08-MNPS-037-01 - SynGen), Neuron-ERANET (EUHF-AUTISM), Fondation
   Orange and the Fondation FondaMentale. P. F. was supported by the
   Fondation Bettencourt-Schueller.
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NR 40
TC 18
Z9 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD NOV
PY 2012
VL 11
IS 8
BP 928
EP 941
DI 10.1111/j.1601-183X.2012.00849.x
PG 14
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 076YE
UT WOS:000313994300005
PM 22989184
ER

PT J
AU Kim, JJ
   Freeman, SFN
   Paparella, T
   Forness, SR
AF Kim, Joanne J.
   Freeman, Stephanny F. N.
   Paparella, Tanya
   Forness, Steven R.
TI Five-Year Follow-up of Preschoolers with Autism and Comorbid Psychiatric
   Disorders
SO BEHAVIORAL DISORDERS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; ATTENTION-DEFICIT/HYPERACTIVITY
   DISORDER; SPECTRUM DISORDERS; EMOTIONAL DISTURBANCES; COMPARISON
   SAMPLES; YOUNG-CHILDREN; PREVALENCE; ADOLESCENTS; POPULATION; SYMPTOMS
AB Although several studies have examined the prevalence of comorbid psychiatric disorders in children with autism spectrum disorders, there are no current longitudinal studies of such children regarding the impact of comorbidity. In this study, 44 of an original sample of 175 preschoolers were located after 5 1/2 years, at an average chronological age of 10 years 3 months, and reassessed for comorbid disorders; a subsample was surveyed regarding use of special education and mental health services. Findings not only suggest continued comorbidity but also somewhat higher than expected use of behavioral services, often requiring out-of-school funding. The differential impact of comorbidity is discussed in relation to special education and access to related services.
C1 [Kim, Joanne J.; Freeman, Stephanny F. N.; Paparella, Tanya; Forness, Steven R.] Univ Calif Los Angeles, Resnick Neuropsychiat Hosp, Los Angeles, CA 90024 USA.
RP Kim, JJ (reprint author), Univ Calif Los Angeles, Resnick Neuropsychiat Hosp, 760 Westwood Plaza,Rm 78-222B, Los Angeles, CA 90024 USA.
EM jjkim@mednet.ucla.edu
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NR 64
TC 0
Z9 0
PU COUNCIL CHILDREN BEHAVIORAL DISORDERS
PI ARLINGTON
PA COUNCIL EXCEPTIONAL CHILDREN, 1110 NORTH GLEBE RD, ARLINGTON, VA
   22201-5704 USA
SN 0198-7429
J9 BEHAV DISORDERS
JI Behav. Disord.
PD NOV
PY 2012
VL 38
IS 1
BP 57
EP 70
PG 14
WC Psychology, Clinical; Psychology, Educational
SC Psychology
GA 072UA
UT WOS:000313697300004
ER

PT J
AU Kalkman, HO
AF Kalkman, Hans O.
TI Potential opposite roles of the extracellular signal-regulated kinase
   (ERK) pathway in autism spectrum and bipolar disorders
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE Timothy syndrome; SYNGAP1; ERK1; Circadian rhythm
ID LONG-TERM POTENTIATION; GLYCOGEN-SYNTHASE KINASE-3; ACTIVATED
   PROTEIN-KINASES; CACNA1C RISK ALLELE; NMDA RECEPTOR; SYNAPTIC
   PLASTICITY; DENDRITIC ARBORIZATION; PSYCHIATRIC-DISORDERS; ASSOCIATION
   ANALYSIS; GENETIC ASSOCIATION
AB Signal transduction from the synapse to the nucleus subsequently involves transient increases in synaptic Ca2+, activation of CaM kinases, activation of the GTPase Ras, activation of the ERK mitogen-activated protein kinase pathway, and finally GSK3 inhibition and CREB-activation. Genetic studies in autism have identified mutations and copy number variations in a number of genes involved in this synapse to nucleus signaling path. In particular, a gain of function mutation in the CACNA1C gene, deletions and disruption of the SYNGAP1 gene, a copy number variation encompassing the MAPK3 gene and a duplication of YWHAE indicate that in a subset of autism patients the ERK cascade is inappropriately activated. Predicted functional consequences of this hyperactivation would be an increase in complexity of the dendritic tree, and via inhibition of GSK3, a delayed circadian phase. The latter effect indeed fits the frequent sleep disturbances observed in autistic patients. Interestingly, the sleep disturbances in bipolar disorder patients are frequently characterized as phase advanced. A selective evaluation of genetic mutations in bipolar patients indicates that the activity of the ERK cascade, at least in a subset of patients, presumably is hypoactive. Thus, with respect to the ERK pathway, autism and bipolar disorder seem each other's counter pole. (C) 2012 Elsevier Ltd. All rights reserved.
C1 Novartis Inst Biomed Res, Neurosci Dept, CH-4002 Basel, Switzerland.
RP Kalkman, HO (reprint author), Novartis Inst Biomed Res, Neurosci Dept, Bldg 386-14-22-15, CH-4002 Basel, Switzerland.
EM hans.kalkman@novartis.com
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NR 118
TC 12
Z9 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD NOV
PY 2012
VL 36
IS 10
BP 2206
EP 2213
DI 10.1016/j.neubiorev.2012.07.008
PG 8
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 071SC
UT WOS:000313613500003
PM 22884480
ER

PT J
AU Blanchard, DC
   Defensor, EB
   Meyza, KZ
   Pobbe, RLH
   Pearson, BL
   Bolivar, VJ
   Blanchard, RJ
AF Blanchard, D. Caroline
   Defensor, Erwin B.
   Meyza, Ksenia Z.
   Pobbe, Roger L. H.
   Pearson, Brandon L.
   Bolivar, Valerie J.
   Blanchard, Robert J.
TI BTBR T+tf/J mice: Autism-relevant behaviors and reduced
   fractone-associated heparan sulfate (vol 36, pg 285, 2012)
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Correction
C1 [Blanchard, D. Caroline] Univ Hawaii, Pacific Biosci Res Ctr, Honolulu, HI 96822 USA.
   [Defensor, Erwin B.; Meyza, Ksenia Z.; Pobbe, Roger L. H.; Pearson, Brandon L.; Blanchard, Robert J.] Univ Hawaii, Dept Psychol, Honolulu, HI 96822 USA.
   [Bolivar, Valerie J.] SUNY Albany, Wadsworth Ctr, New York State Dept Hlth, Albany, NY 12208 USA.
   [Bolivar, Valerie J.] SUNY Albany, Dept Biomed Sci, Sch Publ Hlth, Albany, NY 12208 USA.
RP Blanchard, DC (reprint author), Univ Hawaii, Pacific Biosci Res Ctr, 1993 East West Rd, Honolulu, HI 96822 USA.
EM blanchar@hawaii.edu
CR Blanchard DC, 2012, NEUROSCI BIOBEHAV R, V36, P285, DOI 10.1016/j.neubiorev.2011.06.008
NR 1
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD NOV
PY 2012
VL 36
IS 10
BP 2370
EP 2370
DI 10.1016/j.neubiorev.2012.09.005
PG 1
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 071SC
UT WOS:000313613500016
PM 23320265
ER

PT J
AU Milovancevic, MP
   Vesic, M
   Jelisavcic, M
   Niksic, S
   Pilic, GR
   Maravic, VM
AF Milovancevic, Milica Pejovic
   Vesic, Marija
   Jelisavcic, Marko
   Niksic, Snezana
   Pilic, Gordana Radivojevic
   Maravic, Vanja Mandic
TI Family Paracentric Inversion of the Short Arm of Chromosome X
   (Xp21.2p11.23) and Connection with Autism Spectrum Disorders
SO SRPSKI ARHIV ZA CELOKUPNO LEKARSTVO
LA Serbian
DT Article
DE paracentric inversion; short arm of chromosome X; autism spectrum
   disorders
ID MENTAL-RETARDATION; FISH
AB Introduction Autism spectrum disorders (ASDs) are a group of complex pervasive developmental disorders characterized by impairments in communication, social interaction and behavior. In most cases autism is caused by a combination of genetic factors and environmental risk factors. In 10% to 20% of cases it has been shown that the cause of ASD is genetic.
   Case Outline We are describing a 2-year-old boy who was referred to genetic counseling because of speech delay and certain autism-like behavior. By cytogenetic analysis the karyotype 46, inv(X),Y was obtained. The boy was a carrier of a paracentric inversion of the short arm of the chromosome X. After cytogenetic analysis of parental blood, it was detected that mother was a carrier of identical aberration, but had no clinical signs. The method of fluorescent in situ hybridization (FISH) yielded the precise breakpoint in the region (p21.2p11.23). Mother and son were carriers of identical X chromosome.
   Conclusion Breakpoints are located in the regions that have already been linked to autism, which indicates that the positional effect of the gene could have been a possible cause of the patient's genotype. In addition to positional effects, in order to better understand the etiology of autism other genetic and environmental factors should be always taken into consideration.
C1 [Milovancevic, Milica Pejovic] Univ Belgrade, Sch Med, Belgrade, Serbia.
   [Milovancevic, Milica Pejovic; Vesic, Marija; Jelisavcic, Marko; Niksic, Snezana; Pilic, Gordana Radivojevic; Maravic, Vanja Mandic] Inst Mentalno Zdravlje, Belgrade 11000, Serbia.
RP Milovancevic, MP (reprint author), Inst Mentalno Zdravlje, Palmoticeva 37, Belgrade 11000, Serbia.
EM mpejovic@eunet.rs
CR Amir RE, 1999, NAT GENET, V23, P185
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NR 22
TC 0
Z9 0
PU SRPSKO LEKARSKO DRUSTVO
PI BEOGRAD
PA UREDNISTVO CASOPISA SRPSKI ARHIV, UL DZORDZA VASINGTONA 19, BEOGRAD,
   11000, SERBIA
SN 0370-8179
J9 SRP ARK CELOK LEK
JI Srp. Ark. Celok. Lek.
PD NOV-DEC
PY 2012
VL 140
IS 11-12
BP 760
EP 764
DI 10.2298/SARH1212760P
PG 5
WC Medicine, General & Internal
SC General & Internal Medicine
GA 070RI
UT WOS:000313527900014
PM 23350252
ER

PT J
AU McGovern, RJ
   McGovern, JJ
AF McGovern, R. J.
   McGovern, J. J.
TI NEW FRONTIERS IN AGING: INSIGHTS FROM AUTISM APPLIED TO ELDERLY BASED ON
   "GREEN CARE" FARMS IN EUROPE
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [McGovern, R. J.] Argosy Univ, Arizona Sch Profess Psychol, Phoenix, AZ USA.
   [McGovern, R. J.] Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA.
   [McGovern, J. J.] AT Still Univ, Kirksville, MO USA.
NR 0
TC 0
Z9 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 39
EP 39
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888201200
ER

PT J
AU Wright, SD
   D' Astous, V
   Wright, C
   Diener, M
AF Wright, S. D.
   D' Astous, V.
   Wright, C.
   Diener, M.
TI GRANDPARENTS OF GRANDCHILDREN WITH AUTISM SPECTRUM DISORDER (ASD):
   STRENGTHENING RELATIONSHIPS THROUGH TECHNOLOGY ACTIVITIES
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wright, S. D.; D' Astous, V.; Wright, C.; Diener, M.] Univ Utah, Gerontol Program, Salt Lake City, UT USA.
NR 0
TC 0
Z9 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 72
EP 72
PG 1
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888201342
ER

PT J
AU Wright, SD
   D'Astous, V
   Grandin, T
AF Wright, S. D.
   D'Astous, V.
   Grandin, T.
TI THE CHALLENGE AND THE PROMISE OF AUTISM SPECTRUM DISORDERS IN ADULTHOOD
   AND AGING: A SYSTEMATIC REVIEW OF THE LITERATURE (1990-2012)
SO GERONTOLOGIST
LA English
DT Meeting Abstract
C1 [Wright, S. D.; D'Astous, V.] Univ Utah, Gerontol Program, Salt Lake City, UT USA.
   [Grandin, T.] Colorado State Univ, Ft Collins, CO 80523 USA.
NR 0
TC 0
Z9 0
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 0016-9013
J9 GERONTOLOGIST
JI Gerontologist
PD NOV
PY 2012
VL 52
SU 1
BP 606
EP 607
PG 2
WC Gerontology
SC Geriatrics & Gerontology
GA 061ZG
UT WOS:000312888204252
ER

PT J
AU Higashida, H
   Yokoyama, S
   Huang, JJ
   Liu, L
   Ma, WJ
   Akther, S
   Higashida, C
   Kikuchi, M
   Minabe, Y
   Munesue, T
AF Higashida, Haruhiro
   Yokoyama, Shigeru
   Huang, Jian-Jun
   Liu, Li
   Ma, Wen-Jie
   Akther, Shirin
   Higashida, Chiharu
   Kikuchi, Mitsuru
   Minabe, Yoshio
   Munesue, Toshio
TI Social memory, amnesia, and autism: Brain oxytocin secretion is
   regulated by NAD(+) metabolites and single nucleotide polymorphisms of
   CD38
SO NEUROCHEMISTRY INTERNATIONAL
LA English
DT Article
DE CD38; cADPR; TRPM2 channels; Oxytocin secretion; Social behavior; Autism
ID CYCLIC-ADP-RIBOSE; HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; KNOCKOUT
   MICE; SUPRAOPTIC NUCLEUS; INSULIN-SECRETION; GENETIC-VARIANTS;
   RAT-BRAIN; BEHAVIOR; RECEPTOR
AB Previously, we demonstrated that CD38, a transmembrane protein with ADP-ribosyl cyclase activity, plays a critical role in mouse social behavior by regulating the release of oxytocin (OXT), which is essential for mutual recognition. When CD38 was disrupted, social amnesia was observed in Cd38 knockout mice. The autism spectrum disorders (ASDs), characterized by defects in reciprocal social interaction and communication, occur either sporadically or in a familial pattern. However, the etiology of ASDs remains largely unknown. Therefore, the theoretical basis for pharmacological treatments has not been established. Hence, there is a rationale for investigating single nucleotide polymorphisms (SNPs) in the human CD38 gene in ASD subjects. We found several SNPs in this gene. The SNP rs3796863 (C>A) was associated with high-functioning autism (HFA) in American samples from the Autism Gene Resource Exchange. Although this finding was partially confirmed in low-functioning autism subjects in Israel, it has not been replicated in Japanese HFA subjects. The second SNP of interest, rs1800561 (4693C > T), leads to the substitution of an arginine (R) at codon 140 by tryptophan (W; R140W) in CD38. This mutation was found in four probands of ASD and in family members of three pedigrees with variable levels of ASD or ASD traits. The plasma levels of OXT in ASD subjects with the R140W allele were lower than those in ASD subjects lacking this allele. The OXT levels were unchanged in healthy subjects with or without this mutation. One proband with the R140W allele receiving intranasal OXT for approximately 3 years showed improvement in areas of social approach, eye contact and communication behaviors, emotion, irritability, and aggression. Five other ASD subjects with mental deficits received nasal OXT for various periods; three subjects showed improved symptoms, while two showed little or no effect. These results suggest that SNPs in CD38 may be possible risk factors for ASD by abrogating OXT function and that some ASD subjects can be treated with OXT in preliminary clinical trials. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Higashida, Haruhiro; Yokoyama, Shigeru; Huang, Jian-Jun; Liu, Li; Ma, Wen-Jie; Akther, Shirin; Higashida, Chiharu] Kanazawa Univ, Grad Sch Med, Dept Biophys Genet, Kanazawa, Ishikawa 9208640, Japan.
   [Higashida, Haruhiro; Yokoyama, Shigeru; Higashida, Chiharu; Kikuchi, Mitsuru; Minabe, Yoshio; Munesue, Toshio] Kanazawa Univ, Ctr Child Mental Dev, Kanazawa, Ishikawa 9208640, Japan.
   [Higashida, Haruhiro; Yokoyama, Shigeru; Huang, Jian-Jun; Liu, Li; Ma, Wen-Jie; Akther, Shirin; Higashida, Chiharu; Kikuchi, Mitsuru; Munesue, Toshio] Core Res Evolut Sci & Technol CRESTO, Tokyo 1020075, Japan.
   [Higashida, Haruhiro; Yokoyama, Shigeru; Kikuchi, Mitsuru; Minabe, Yoshio; Munesue, Toshio] MEXT Strateg Res Program Brain Sci SRPBS, Okazaki, Aichi 4440840, Japan.
RP Higashida, H (reprint author), Kanazawa Univ, Grad Sch Med, Dept Biophys Genet, 13-1 Takaramachi, Kanazawa, Ishikawa 9208640, Japan.
EM haruhiro@med.kanazawa-u.ac.jp
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NR 89
TC 12
Z9 12
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0197-0186
J9 NEUROCHEM INT
JI Neurochem. Int.
PD NOV
PY 2012
VL 61
IS 6
BP 828
EP 838
DI 10.1016/j.neuint.2012.01.030
PG 11
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 068NY
UT WOS:000313374600005
PM 22366648
ER

PT J
AU Tian, P
AF Tian, Peichao
TI RELN gene polymorphisms and susceptibility to autism in Chinese Han
   population
SO NEUROLOGY INDIA
LA English
DT Article
DE Association; autism; RELN gene; single nucleotide polymorphisms;
   susceptibility
ID REELIN GENE; SPECTRUM DISORDER; CANDIDATE GENE; SEROTONIN TRANSPORTER;
   ASSOCIATION ANALYSIS; ALLELES; LINKAGE; OXTR; REPEAT; REGION
AB Background: Single nucleotide polymorphisms (SNPs) in the Reelin gene (RELN) are likely candidates to confer risk for autism. The objective of the present study is to investigate the association of RELN gene SNPs with autism. Materials and Methods: A total of 367 Chinese Han subjects were recruited, including 186 autism patients and 181 unrelated healthy controls. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing methods were used to detect RELN gene polymorphisms. The association between SNPs and autism was analyzed in this study. Results: The g.333509A>C in intron12 and g.504742G>A in exon60 were detected in the RELN gene and a significant association was found between the g.504742G>A polymorphism and autism. Allele and genotype frequencies for the g.504742G>A polymorphism in autistic patients were significantly different for healthy subjects. There was no significantly difference in g.333509A>C polymorphism and autism in the studied populations. Conclusions: Our findings indicated that g.333509A>C was not significantly associated with autism. The g.504742G>A polymorphic variant in the RELN gene might affect subjects susceptibility toward autism in Chinese Han population.
C1 Zhengzhou Univ, Affiliated Hosp 1, Dept Pediat, Zhengzhou, Peoples R China.
RP Tian, P (reprint author), Zhengzhou Univ, Affiliated Hosp 1, Dept Pediat, 1 Jianshe E Rd, Zhengzhou, Peoples R China.
EM peichaotian@sina.com
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NR 29
TC 1
Z9 2
PU MEDKNOW PUBLICATIONS & MEDIA PVT LTD
PI MUMBAI
PA B-9, KANARA BUSINESS CENTRE, OFF LINK RD, GHAKTOPAR-E, MUMBAI, 400075,
   INDIA
SN 0028-3886
J9 NEUROL INDIA
JI Neurol. India
PD NOV-DEC
PY 2012
VL 60
IS 6
BP 581
EP 584
DI 10.4103/0028-3886.105190
PG 4
WC Neurosciences
SC Neurosciences & Neurology
GA 068FH
UT WOS:000313350900005
PM 23287318
ER

PT J
AU Krahn, TM
   Fenton, A
AF Krahn, Timothy M.
   Fenton, Andrew
TI Funding Priorities: Autism and the Need for a More Balanced Research
   Agenda in Canada
SO PUBLIC HEALTH ETHICS
LA English
DT Article
ID PUBLIC-HEALTH ETHICS; SPECTRUM DISORDERS; CHILDREN; PARENTS; QUALITY
AB The public purse is responsible for funding almost all autism spectrum disorders (ASD) research in Canada (as per Canadian Institutes of Health Research [CIHR]) and for providing some of the existing services and supports for this population. In this article, we consider various reasons why Canada should be concerned to ensure a more equitable distribution of relevant public funding for ASD research than is currently the case to meet the express needs and interests of the diversity of autism stakeholders. As such, we report data to show that CIHR-supported ASD research from the period of 2000-2010 demonstrates a bias focussed on the aetiology of the condition revealing a disproportionate emphasis on only two (Biomedical and Clinical) out of the four research pillars avowed by CIHR, with a comparative lack of fiscal resources committed to Health Systems and Services and Population and Public Health research. We advance certain normative and prudential reasons for funding more Health Systems and Services and Population and Public Health ASD research in Canada. In our view, this would seem to follow from CIHR's official mandate 'as a flexible mechanism that will continually align health research funding with changes in the manner in which health problems and opportunities are identified, understood and addressed'.
C1 [Krahn, Timothy M.] Dalhousie Univ, Novel Tech Eth, Fac Med, Halifax, NS B3H 3M6, Canada.
   [Fenton, Andrew] Calif State Univ Fresno, Dept Philosophy, Fresno, CA 93740 USA.
RP Krahn, TM (reprint author), Dalhousie Univ, Novel Tech Eth, Fac Med, 1379 Seymour St, Halifax, NS B3H 3M6, Canada.
EM timothykrahn@gmail.com
FU Canadian Institutes of Health Research States of Mind: Emerging Issues
   in Neuroethics [NNF 80045]
FX This work was supported by Canadian Institutes of Health Research [NNF
   80045] States of Mind: Emerging Issues in Neuroethics.
CR AMAT, 2010, AUT MAN ADV TEAM REP
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   CIHR [Canadian Institutes of Health Research], 2004, STRENGTH PILL 4 RES
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NR 71
TC 1
Z9 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1754-9973
J9 PUBLIC HEALTH ETH-UK
JI Public Health Ethics
PD NOV
PY 2012
VL 5
IS 3
BP 296
EP 310
DI 10.1093/phe/phs027
PG 15
WC Ethics; Public, Environmental & Occupational Health; Medical Ethics
SC Social Sciences - Other Topics; Public, Environmental & Occupational
   Health; Medical Ethics
GA 067MW
UT WOS:000313299600009
ER

PT J
AU Atzori, M
   Garcia-Oscos, F
   Mendez, JA
AF Atzori, Marco
   Garcia-Oscos, Francisco
   Alfredo Mendez, Jose
TI Role of IL-6 in the etiology of hyperexcitable neuropsychiatric
   conditions: experimental evidence and therapeutic implications
SO FUTURE MEDICINAL CHEMISTRY
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; BLOOD-BRAIN-BARRIER; N-ACETYL-CYSTEINE;
   INFLAMMATORY CYTOKINE RESPONSES; MATERNAL IMMUNE ACTIVATION; POSSIBLE
   CENTRAL MECHANISM; PHOSPHO-DEPENDENT BINDING; PITUITARY-ADRENAL AXIS;
   CENTRAL-NERVOUS-SYSTEM; DOUBLE-HIT HYPOTHESIS
AB Many neuropsychiatric conditions are primed or triggered by different types of stressors. The mechanisms through which stress induces neuropsychiatric disease are complex and incompletely understood. A 'double hit' hypothesis of neuropsychiatric disease postulates that stress induces maladaptive behavior in two phases separated by a dormant period. Recent research shows that the pleiotropic cytokine IL-6 is released centrally and peripherally following physical and psychological stress. In this article, we analyze evidence from clinics and animal models suggesting that stress-induced elevation in the levels of IL-6 may play a key role in the etiology of a heterogeneous family of hyperexcitable central conditions including epilepsy, schizophrenic psychoses, anxiety and disorders of the autistic spectrum. The cellular mechanism leading to hyperexcitable conditions might be a decrease in inhibitory/excitatory synaptic balance in either or both temporal phases of the conditions. Following these observations, we discuss how they may have important implications for optimal prophylactic and therapeutic pharmacological treatment.
C1 [Atzori, Marco; Garcia-Oscos, Francisco] Univ Texas Dallas, Sch Behav & Brain Sci, Richardson, TX 75080 USA.
   [Alfredo Mendez, Jose] Univ Autonoma San Luis Potosi, Inst Fis, San Luis Potosi, Mexico.
RP Atzori, M (reprint author), Univ Texas Dallas, Sch Behav & Brain Sci, Richardson, TX 75080 USA.
EM marco.atzori@utdallas.edu
RI Mendez, J Alfredo/E-2031-2015
OI Mendez, J Alfredo/0000-0002-2859-7086
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NR 197
TC 3
Z9 3
PU FUTURE SCI LTD
PI LONDON
PA UNITED HOUSE, 2 ALBERT PL, LONDON, N3 1QB, ENGLAND
SN 1756-8919
J9 FUTURE MED CHEM
JI Future Med. Chem.
PD NOV
PY 2012
VL 4
IS 17
BP 2177
EP 2192
DI 10.4155/FMC.12.156
PG 16
WC Chemistry, Medicinal
SC Pharmacology & Pharmacy
GA 059AG
UT WOS:000312676200016
PM 23190106
ER

PT J
AU Quintana, DS
   Guastella, AJ
   Outhred, T
   Hickie, IB
   Kemp, AH
AF Quintana, Daniel S.
   Guastella, Adam J.
   Outhred, Tim
   Hickie, Ian B.
   Kemp, Andrew H.
TI Heart rate variability is associated with emotion recognition: Direct
   evidence for a relationship between the autonomic nervous system and
   social cognition
SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY
LA English
DT Article
DE Heart rate variability; Emotion recognition; Autonomic nervous system;
   Social cognition; Polyvagal theory; Neurovisceral integration model
ID GENDER-RELATED DIFFERENCES; ANXIETY STRESS SCALES; ALCOHOL-ABUSE;
   DEPRESSION; WOMEN; MIND; MEN; SCHIZOPHRENIA; PERSPECTIVE; AUTISM
AB It is well established that heart rate variability (HRV) plays an important role in social communication. Polyvagal theory suggests that HRV may provide a sensitive marker of one's ability to respond and recognize social cues. The aim of the present study was to directly test this hypothesis. Resting-state HRV was collected and performance on the Reading the Mind in the Eyes Test was assessed in 65 volunteers. HRV was positively associated with performance on this emotion recognition task confirming our hypothesis and these findings were retained after controlling for a variety of confounding variables known to influence HRV - sex, BMI, smoking habits, physical activity levels, depression, anxiety, and stress. Our data suggests that increased HRV may provide a novel marker of one's ability to recognize emotions in humans. Implications for understanding the biological basis of emotion recognition, and social impairment in humans are discussed. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Quintana, Daniel S.; Outhred, Tim; Kemp, Andrew H.] Univ Sydney, Sch Psychol, SCAN Res & Teaching Unit, Sydney, NSW 2006, Australia.
   [Quintana, Daniel S.; Guastella, Adam J.; Hickie, Ian B.] Univ Sydney, Brain & Mind Res Inst, Sydney, NSW 2006, Australia.
   [Kemp, Andrew H.] Univ Sydney, Sydney Med Sch, Discipline Psychiat, CADE Clin, Sydney, NSW 2006, Australia.
RP Kemp, AH (reprint author), Univ Sydney, Sch Psychol, SCAN Res & Teaching Unit, Brennan MacCallum Bldg A18, Sydney, NSW 2006, Australia.
EM andrew.kemp@sydney.edu.au
RI Kemp, Andrew/C-7984-2012
OI Kemp, Andrew/0000-0003-1146-3791
FU Australian Rotary Health/Hooton family scholarship; Australian
   Postgraduate Award (APA); NHMRC Career Development Fellowship [571101]
FX The authors DSQ TO and AHK are supported by an Australian Rotary
   Health/Hooton family scholarship, an Australian Postgraduate Award
   (APA), and a NHMRC Career Development Fellowship (571101) respectively.
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NR 42
TC 10
Z9 11
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0167-8760
J9 INT J PSYCHOPHYSIOL
JI Int. J. Psychophysiol.
PD NOV
PY 2012
VL 86
IS 2
BP 168
EP 172
DI 10.1016/j.ijpsycho.2012.08.012
PG 5
WC Psychology, Biological; Neurosciences; Physiology; Psychology;
   Psychology, Experimental
SC Psychology; Neurosciences & Neurology; Physiology
GA 056EB
UT WOS:000312470100006
PM 22940643
ER

PT J
AU Perkins, EA
   Berkman, KA
AF Perkins, Elizabeth A.
   Berkman, Karen A.
TI Into the Unknown: Aging with Autism Spectrum Disorders
SO AJIDD-AMERICAN JOURNAL ON INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE older adults; health; quality of life; age-related changes; autism
ID GASTROINTESTINAL SYMPTOMS; DIAGNOSTIC INTERVIEW; UNITED-STATES;
   DOWN-SYNDROME; CHILDREN; ADULTS; PREVALENCE; EPILEPSY; INDIVIDUALS;
   ADOLESCENTS
AB Research investigation of older adults with autism spectrum disorders (ASD) noticeably lags behind studies of children and younger adults with ASD. This article reviews the current literature regarding a range of quality of life outcomes of aging adults with ASD. Studies that have addressed life expectancy, comorbid physical and mental health issues, ASD symptomatology, and social, residential, and vocational outcomes are reviewed. Research challenges in identifying older cohorts of adults with ASD are also discussed, and notable areas of concern are highlighted. Overall, aging with ASD does present challenges, but there is also evidence that positive outcomes are attainable. The article concludes with brief recommendations on how to optimize the aging process for individuals with ASD.
C1 [Perkins, Elizabeth A.] Univ S Florida, Florida Ctr Inclus Communities UCEDD, Tampa, FL 33612 USA.
RP Perkins, EA (reprint author), Univ S Florida, Florida Ctr Inclus Communities UCEDD, 13301 Bruce B Downs Blvd, Tampa, FL 33612 USA.
EM eperkins@mail.usf.edu
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NR 84
TC 6
Z9 6
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1944-7515
J9 AJIDD-AM J INTELLECT
JI AJIDD-Am. J. Intellect. Dev. Disabil.
PD NOV
PY 2012
VL 117
IS 6
BP 478
EP 496
DI 10.1352/1944-7558-117.6.478
PG 19
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 048RZ
UT WOS:000311931600005
PM 23167487
ER

PT J
AU Blaker-Lee, A
   Gupta, S
   McCammon, JM
   De Rienzo, G
   Sive, H
AF Blaker-Lee, Alicia
   Gupta, Sunny
   McCammon, Jasmine M.
   De Rienzo, Gianluca
   Sive, Hazel
TI Zebrafish homologs of genes within 16p11.2, a genomic region associated
   with brain disorders, are active during brain development, and include
   two deletion dosage sensor genes
SO DISEASE MODELS & MECHANISMS
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; COPY-NUMBER VARIATION; MAJOR VAULT PROTEIN;
   MENTAL-RETARDATION; DANIO-RERIO; ALDOLASE-A; CHROMOSOME 16P11.2;
   HEMOLYTIC-ANEMIA; DE-NOVO; SYNAPTIC-TRANSMISSION
AB Deletion or duplication of one copy of the human 16p11.2 interval is tightly associated with impaired brain function, including autism spectrum disorders (ASDs), intellectual disability disorder (IDD) and other phenotypes, indicating the importance of gene dosage in this copy number variant region (CNV). The core of this CNV includes 25 genes; however, the number of genes that contribute to these phenotypes is not known. Furthermore, genes whose functional levels change with deletion or duplication (termed 'dosage sensors'), which can associate the CNV with pathologies, have not been identified in this region. Using the zebrafish as a tool, a set of 16p11.2 homologs was identified, primarily on chromosomes 3 and 12. Use of 11 phenotypic assays, spanning the first 5 days of development, demonstrated that this set of genes is highly active, such that 21 out of the 22 homologs tested showed loss-of-function phenotypes. Most genes in this region were required for nervous system development impacting brain morphology, eye development, axonal density or organization, and motor response. In general, human genes were able to substitute for the fish homolog, demonstrating orthology and suggesting conserved molecular pathways. In a screen for 16p11.2 genes whose function is sensitive to hemizygosity, the aldolase a (aldoaa) and kinesin family member 22 (kif22) genes were identified as giving clear phenotypes when RNA levels were reduced by similar to 50%, suggesting that these genes are deletion dosage sensors. This study leads to two major findings. The first is that the 16p11.2 region comprises a highly active set of genes, which could present a large genetic target and might explain why multiple brain function, and other, phenotypes are associated with this interval. The second major finding is that there are (at least) two genes with deletion dosage sensor properties among the 16p11.2 set, and these could link this CNV to brain disorders such as ASD and IDD.
C1 [Blaker-Lee, Alicia; Gupta, Sunny; McCammon, Jasmine M.; De Rienzo, Gianluca; Sive, Hazel] Whitehead Inst Biomed Res, Cambridge, MA 02142 USA.
   [Sive, Hazel] MIT, Cambridge, MA 02139 USA.
RP Sive, H (reprint author), Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142 USA.
EM sive@wi.mit.edu
FU Simons Foundation Autism Research Initiative [95091]
FX This work was supported by the Simons Foundation Autism Research
   Initiative [grant 95091].
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NR 112
TC 11
Z9 11
PU COMPANY OF BIOLOGISTS LTD
PI CAMBRIDGE
PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE CB4 4DL,
   CAMBS, ENGLAND
SN 1754-8403
J9 DIS MODEL MECH
JI Dis. Model. Mech.
PD NOV
PY 2012
VL 5
IS 6
BP 834
EP 851
DI 10.1242/dmm.009944
PG 18
WC Cell Biology; Pathology
SC Cell Biology; Pathology
GA 047RT
UT WOS:000311859700016
PM 22566537
ER

PT J
AU Dombret, C
   Nguyen, T
   Schakman, O
   Michaud, JL
   Hardin-Pouzet, H
   Bertrand, MJM
   De Backer, O
AF Dombret, Carlos
   Tuan Nguyen
   Schakman, Olivier
   Michaud, Jacques L.
   Hardin-Pouzet, Helene
   Bertrand, Mathieu J. M.
   De Backer, Olivier
TI Loss of Maged1 results in obesity, deficits of social interactions,
   impaired sexual behavior and severe alteration of mature oxytocin
   production in the hypothalamus
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID PRADER-WILLI-SYNDROME; AUTISM SPECTRUM DISORDERS; AROMATASE-KNOCKOUT
   MICE; RECEPTOR GENE OXTR; PARAVENTRICULAR NUCLEUS; NECDIN GENE;
   SUPRAOPTIC NUCLEI; FEEDING-BEHAVIOR; MEDIAL AMYGDALA; CANDIDATE GENE
AB MAGED1, NECDIN and MAGEL2 are members of the MAGE gene family. The latter two of these genes have been involved in PraderWilli syndrome (PWS), which includes hyperphagia, repetitive and compulsive behaviors, and cognitive impairment. Here, we show that Maged1-deficient mice develop progressive obesity associated with hyperphagia and reduced motor activity. Loss of Maged1 also results in a complex behavioral syndrome that includes reduced social interactions and memory, deficient sexual behavior, as well as increased anxiety and self-grooming. Oxytocin (OT), which is produced in the hypothalamus, can act as a neurotransmitter that reduces anxiety, promotes social behaviors and regulates food intake. Growing evidences indicate that OT is involved in autism. We found that Maged1 mutants showed a severe reduction in the levels of mature OT, but not of its precursors, in the hypothalamus. Moreover, the administration of OT rescued the deficit in social memory of these mice. We conclude that Maged1 is required for OT processing or stability. A decrease in mature OT levels in Maged1 mutants affects social interactions and possibly other behavioral processes. Our observations suggest that, in human, MAGED1 could play a role in autism or cause a neurodevelopmental condition that is reminiscent of the PWS.
C1 [Dombret, Carlos; Tuan Nguyen; De Backer, Olivier] Univ Namur, FUNDP Sch Med, NARILIS Namur Res Inst Life Sci, URPHYM Unite Rech Physiol Mol, B-5000 Namur, Belgium.
   [Schakman, Olivier] Catholic Univ Louvain, Inst Neurosci IoNS, Lab Cell Physiol, B-1200 Brussels, Belgium.
   [Michaud, Jacques L.] Univ Montreal, Hop St Justine, Res Ctr, Ctr Excellence Neurosci, Montreal, PQ H3T 1C5, Canada.
   [Hardin-Pouzet, Helene] UPMC Paris 6 Univ, PMSNC Lab, CNRS UMR 7224, INSERM UMRS 952, F-75005 Paris, France.
   [Bertrand, Mathieu J. M.] VIB, Dept Mol Biomed Res, Mol Signaling & Cell Death Unit, B-9052 Ghent, Belgium.
   [Bertrand, Mathieu J. M.] Univ Ghent, Dept Biomed Mol Biol, B-9052 Ghent, Belgium.
RP De Backer, O (reprint author), Univ Namur, FUNDP Sch Med, NARILIS Namur Res Inst Life Sci, URPHYM Unite Rech Physiol Mol, 61 Rue Bruxelles, B-5000 Namur, Belgium.
EM olivier.debacker@fundp.ac.be
FU Fonds de la Recherche Scientifique et Medicale of the Fonds National de
   la Recherche Scientifique of Belgium [3.4527.04]; 'Programme
   d'excellence Marshall' (DIANE convention) from the 'Region Wallonne';
   Commission Universitaire pour le Developpement of the Communaute
   Francaise de Belgique; FWO
FX This work was supported by the Fonds de la Recherche Scientifique et
   Medicale (grant no 3.4527.04) of the Fonds National de la Recherche
   Scientifique of Belgium (to O.B.) and by grants from the 'Programme
   d'excellence Marshall' (DIANE convention) from the 'Region Wallonne' (to
   O.S.). H.N.T.N. was supported by the Commission Universitaire pour le
   Developpement of the Communaute Francaise de Belgique. M.J.M.B. has a
   tenure track position within the Multidisciplinary Research Program from
   the Ghent University (GROUP-ID) and holds a postdoctoral fellowship from
   the FWO.
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NR 107
TC 10
Z9 10
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 1
PY 2012
VL 21
IS 21
BP 4703
EP 4717
DI 10.1093/hmg/dds310
PG 15
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 025DN
UT WOS:000310165500010
PM 22865874
ER

PT J
AU Falivelli, G
   De Jaco, A
   Favaloro, FL
   Kim, H
   Wilson, J
   Dubi, N
   Ellisman, MH
   Abrahams, BS
   Taylor, P
   Comoletti, D
AF Falivelli, Giulia
   De Jaco, Antonella
   Favaloro, Flores Lietta
   Kim, Hyuck
   Wilson, Jennifer
   Dubi, Noga
   Ellisman, Mark H.
   Abrahams, Brett S.
   Taylor, Palmer
   Comoletti, Davide
TI Inherited genetic variants in autism-related CNTNAP2 show perturbed
   trafficking and ATF6 activation
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID UNFOLDED PROTEIN RESPONSE; ENDOPLASMIC-RETICULUM; SPECTRUM DISORDERS;
   NEUREXIN SUPERFAMILY; MYELINATED FIBERS; K+ CHANNELS; MUTATIONS; CASPR2;
   EXPRESSION; EPILEPSY
AB Although genetic variations in several genes encoding for synaptic adhesion proteins have been found to be associated with autism spectrum disorders, one of the most consistently replicated genes has been CNTNAP2, encoding for contactin-associated protein-like 2 (CASPR2), a multidomain transmembrane protein of the neurexin superfamily. Using immunofluorescence confocal microscopy and complementary biochemical techniques, we compared wild-type CASPR2 to 12 point mutations identified in individuals with autism. In contrast to the wild-type protein, localized to the cell surface, some of the mutants show altered cellular disposition. In particular, CASPR2-D1129H is largely retained in the endoplasmic reticulum (ER) in HEK-293 cells and in hippocampal neurons. BiP/Grp78, Calnexin and ERp57, key ER chaperones, appear to be responsible for retention of this mutant and activation of one signaling pathway of the unfolded protein response (UPR). The presence of this mutation also lowers expression and activates proteosomal degradation. A frame-shift mutation that causes a form of syndromic epilepsy (CASPR2-1253), results in a secreted protein with seemingly normal folding and oligomerization. Taken together, these data indicate that CASPR2-D1129H has severe trafficking abnormalities and CASPR2-1253 is a secreted soluble protein, suggesting that the structural or signaling functions of the membrane tethered form are lost. Our data support a complex genetic architecture in which multiple distinct risk factors interact with others to shape autism risk and presentation.
C1 [Kim, Hyuck; Comoletti, Davide] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Child Hlth Inst New Jersey, New Brunswick, NJ 08901 USA.
   [Kim, Hyuck; Comoletti, Davide] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurosci & Cell Biol, New Brunswick, NJ 08901 USA.
   [Falivelli, Giulia; Wilson, Jennifer; Dubi, Noga; Taylor, Palmer; Comoletti, Davide] Univ Calif San Diego, Skaggs Sch Pharm & Pharmaceut Sci, Dept Pharmacol, La Jolla, CA 92093 USA.
   [Ellisman, Mark H.] Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA.
   [Falivelli, Giulia] Univ Bologna, Dept Pharmacol, I-40100 Bologna, Italy.
   [De Jaco, Antonella; Favaloro, Flores Lietta] Univ Roma La Sapienza, Dept Biol & Biotechnol Charles Darwin, Daniel Bovet Neurobiol Res Ctr, I-00185 Rome, Italy.
   [De Jaco, Antonella] Univ Roma La Sapienza, Ist Pasteur, Fdn Cenci Bolognetti, I-00185 Rome, Italy.
   [Abrahams, Brett S.] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10461 USA.
   [Abrahams, Brett S.] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA.
RP Comoletti, D (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Child Hlth Inst New Jersey, 89 French St, New Brunswick, NJ 08901 USA.
EM comoleda@umdnj.edu
FU Robert Wood Johnson Foundation [67038]; National Institutes of Health
   [P42-ES10337-08, RO1-GM18360-39, RO1-MH092906-01]; Autism Speaks [2617];
   Compagnia San Paolo Bando in Neuroscienze; NIH [P41 RR004050,
   P41GM103412]; New Investigator Development Award; Human Genetics Pilot
   Award; Rose F. Kennedy Intellectual and Developmental Disabilities
   Research Center [P30HD071593]; Albert Einstein College of Medicine
FX We are grateful to Dr Giudo Gaietta for helpful advice in the use of the
   confocal microscope and to Ms Eva N. Rubio-Marrero for the technical
   help during the resubmission process. We would like to thank the Robert
   Wood Johnson Foundation (grant # 67038) for their support of the Child
   Health Institute of New Jersey.This work was supported by National
   Institutes of Health grants, P42-ES10337-08 and RO1-GM18360-39 to P. T.;
   RO1-MH092906-01 and Autism Speaks # 2617 to D. C.; Compagnia San Paolo
   Bando in Neuroscienze to ADJ; Confocal microscopy employed the
   facilities of the National Center for Imaging and Microscopy (NCMIR) at
   UCSD supported by NIH P41 RR004050 and P41GM103412 (MHE). BSA was
   supported by a New Investigator Development Award, a Human Genetics
   Pilot Award and a Rose F. Kennedy Intellectual and Developmental
   Disabilities Research Center (P30HD071593) Pilot Award from the Albert
   Einstein College of Medicine.
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NR 53
TC 6
Z9 6
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 1
PY 2012
VL 21
IS 21
BP 4761
EP 4773
DI 10.1093/hmg/dds320
PG 13
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 025DN
UT WOS:000310165500014
PM 22872700
ER

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   Volkmar, Fred
   Vorstman, J. A. S.
   Wallace, Simon
   Wing, Kirsty
   Wittemeyer, Kerstin
   Wood, Shawn
   Zurawiecki, Danielle
   Zwaigenbaum, Lonnie
   Bailey, Anthony J.
   Battaglia, Agatino
   Cantor, Rita M.
   Coon, Hilary
   Cuccaro, Michael L.
   Dawson, Geraldine
   Ennis, Sean
   Freitag, Christine M.
   Geschwind, Daniel H.
   Haines, Jonathan L.
   Klauck, Sabine M.
   McMahon, William M.
   Maestrini, Elena
   Miller, Judith
   Monaco, Anthony P.
   Nelson, Stanley F.
   Nurnberger, John I., Jr.
   Oliveira, Guiomar
   Parr, Jeremy R.
   Pericak-Vance, Margaret A.
   Piven, Joseph
   Schellenberg, Gerard D.
   Scherer, StephenW.
   Vicente, Astrid M.
   Wassink, Thomas H.
   Wijsman, Ellen M.
   Betancur, Catalina
   Buxbaum, Joseph D.
   Cook, Edwin H.
   Gallagher, Louise
   Gill, Michael
   Hallmayer, Joachim
   Paterson, Andrew D.
   Sutcliffe, James S.
   Szatmari, Peter
   Vieland, Veronica J.
   Hakonarson, Hakon
   Devlin, Bernie
TI Individual common variants exert weak effects on the risk for autism
   spectrum disorderspi
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID GENOME-WIDE ASSOCIATION; DE-NOVO MUTATIONS; COPY NUMBER VARIATION;
   DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; LINKAGE ANALYSES; GENE;
   LOCI; DELETIONS; CNTNAP2
AB While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm 1). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
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RP Devlin, B (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, 3811 OHara St, Pittsburgh, PA 15232 USA.
EM devlinbj@upmc.edu
RI Scherer, Stephen /B-3785-2013; Haines, Jonathan/C-3374-2012; Rutter,
   Michael/C-8570-2013; Melhem, Nadine/G-1510-2013; Howe,
   Jennifer/I-9013-2012; Oliveira, Guiomar/I-7255-2013; Maestrini,
   Elena/K-7508-2012; Sutcliffe, James/C-1348-2012; Duque,
   Frederico/H-3692-2014; Monaco, Anthony/A-4495-2010; Bolton,
   Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014; Pickles,
   Andrew/A-9625-2011
OI Scherer, Stephen /0000-0002-8326-1999; Sutcliffe,
   James/0000-0001-5200-6007; Duque, Frederico/0000-0001-5684-1472; Monaco,
   Anthony/0000-0001-7480-3197; Bolton, Patrick/0000-0002-5270-6262;
   Bailey, Anthony/0000-0003-4257-972X; Pickles, Andrew/0000-0003-1283-0346
FU AGP: Autism Speaks (USA); Health Research Board (HRB; Ireland)
   [AUT/2006/1, AUT/2006/2, PD/2006/48]; Medical Research Council (MRC;
   UK); Genome Canada/Ontario Genomics Institute; Hilibrand Foundation
   (USA); US National Institutes of Health (NIH) [HD035469, HD055748,
   HD055751, HD055782, HD055784, MH52708, MH55284, MH057881, MH061009,
   MH06359, MH066673, MH080647, MH081754, MH66766, NS026630, NS042165,
   NS049261]; Cnadian Institutes for Health Research (CIHR); Assistance
   Publique - Hopitaux de Paris (France); Autism Speaks UK; Canada
   Foundation for Innovation/Ontario Innovation Trust; Deutsche
   Forschungsgemeinschaft (Germany) [Po 255/17-4]; EC Sixth FP AUTISM
   MOLGEN; National Childrens Research Centre (Ireland); Fundacao Calouste
   Gulbenkian (Portugal); Fondation de France; Fondation FondaMental
   (France); Fondation Orange (France); Fondation pour la Recherche
   Medicale (France); Fundacao para a Ciencia e Tecnologia (Portugal);
   Hospital for Sick Children Foundation; University of Toronto (Canada);
   INSERM (France); Institut Pasteur (France); Italian Ministry of Health;
   John P Hussman Foundation (USA); McLaughlin Centre (Canada); Ontario
   Ministry of Research and Innovation (Canada); Seaver Foundation (USA);
   Swedish Science Council; Centre for Applied Genomics (Canada); Utah
   Autism Foundation (USA); Wellcome Trust (UK) [075491/Z/04]; Royal
   Netherlands Academy of Arts and Sciences [TMF/DA/5801]; Netherlands
   Organization for Scientific Research [825.06.031]; Trinity Centre for
   High Performance Computing; Science Foundation Ireland; Autism Speaks
FX The authors thank the main funders of the AGP: Autism Speaks (USA), the
   Health Research Board (HRB; Ireland; AUT/2006/1, AUT/2006/2,
   PD/2006/48), The Medical Research Council (MRC; UK), Genome
   Canada/Ontario Genomics Institute and the Hilibrand Foundation (USA).
   Additional support for individual groups was provided by the US National
   Institutes of Health (NIH grants: HD035469, HD055748, HD055751,
   HD055782, HD055784, MH52708, MH55284, MH057881, MH061009, MH06359,
   MH066673, MH080647, MH081754, MH66766, NS026630, NS042165, NS049261),
   the Canadian Institutes for Health Research (CIHR), Assistance Publique
   - Hopitaux de Paris (France), Autism Speaks UK, Canada Foundation for
   Innovation/Ontario Innovation Trust, Deutsche Forschungsgemeinschaft
   (grant: Po 255/17-4) (Germany), EC Sixth FP AUTISM MOLGEN, The National
   Childrens Research Centre (Ireland), Fundacao Calouste Gulbenkian
   (Portugal), Fondation de France, Fondation FondaMental (France),
   Fondation Orange (France), Fondation pour la Recherche Medicale
   (France), Fundacao para a Ciencia e Tecnologia (Portugal), the Hospital
   for Sick Children Foundation and University of Toronto (Canada), INSERM
   (France), Institut Pasteur (France), the Italian Ministry of Health
   (convention 181 of 19.10.2001), the John P Hussman Foundation (USA),
   McLaughlin Centre (Canada), Ontario Ministry of Research and Innovation
   (Canada), the Seaver Foundation (USA), the Swedish Science Council, The
   Centre for Applied Genomics (Canada), the Utah Autism Foundation (USA)
   and the Wellcome Trust core award 075491/Z/04 (UK). D. P. is supported
   by fellowships from the Royal Netherlands Academy of Arts and Sciences
   (TMF/DA/5801) and the Netherlands Organization for Scientific Research
   (Rubicon 825.06.031). S. W. S. holds the GlaxoSmithKline-CIHR Pathfinder
   Chair in Genetics and Genomics at the University of Toronto and the
   Hospital for Sick Children (Canada). Computational infrastructure for
   RJLA was supported by the Trinity Centre for High Performance Computing
   (http://www.tchpc.tcd.ie/) funded through grants from Science Foundation
   Ireland. Funding to pay the Open Access publication charges for this
   article was provided by Autism Speaks.
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NR 68
TC 90
Z9 94
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD NOV 1
PY 2012
VL 21
IS 21
BP 4781
EP 4792
DI 10.1093/hmg/dds301
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 025DN
UT WOS:000310165500016
PM 22843504
ER

PT J
AU Qian, XQ
   Reichle, J
   Bogenschutz, M
AF Qian, Xueqin
   Reichle, Joe
   Bogenschutz, Matthew
TI Chinese Parents' Perceptions of Early Development of Their Children
   Diagnosed with Autism Spectrum Disorders
SO JOURNAL OF COMPARATIVE FAMILY STUDIES
LA English
DT Article
ID EARLY IDENTIFICATION; EARLY INTERVENTION; TODDLERS; ABNORMALITIES;
   RECOGNITION; FAMILIES; CULTURE; PROGRAM
AB This study investigated parental perceptions of the early signs, age of initial concern, age of diagnosis, and age of initial intervention for children with Autism Spectrum Disorders (ASD) in mainland China. A sample of 146 Chinese parents of children with ASD responded to an online survey. The findings suggested that parents were concerned about their child's development at a mean age of approximately three years, obtained an initial diagnosis at an average age of four years, and procured intervention for their child at an average age of four years-three months. The results also revealed that early indicators of ASD validated in the United States were among those used by Chinese parents, though some early signs may gain particular salience in the Chinese context. Additionally, educational implications and areas of future research are discussed.
C1 [Qian, Xueqin] Univ Minnesota, Inst Community Integrat, Minneapolis, MN 55455 USA.
   [Bogenschutz, Matthew] Adelphi Univ, Sch Social Work, Garden City, NY 11530 USA.
RP Qian, XQ (reprint author), Univ Minnesota, Inst Community Integrat, 204 Pattee Hall,150 Pillsbury Dr SE, Minneapolis, MN 55455 USA.
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NR 39
TC 0
Z9 0
PU J COMPARATIVE FAMILY STUDIES
PI CALGARY
PA UNIV CALGARY-DEPT SOCIOLOGY 2500 UNIVERSITY DRIVE NW, CALGARY, AB T2N
   1N4, CANADA
SN 0047-2328
J9 J COMP FAM STUD
JI J. Comp. Fam. Stud.
PD NOV-DEC
PY 2012
VL 43
IS 6
BP 903
EP +
PG 12
WC Family Studies
SC Family Studies
GA 050JZ
UT WOS:000312050900006
ER

PT J
AU Ghosh, S
   Greenberg, JS
   Seltzer, MM
AF Ghosh, Subharati
   Greenberg, Jan S.
   Seltzer, Marsha Mailick
TI Adaptation to a Spouse's Disability by Parents of Adult Children With
   Mental Illness or Developmental Disability
SO PSYCHIATRIC SERVICES
LA English
DT Article
ID AGING PARENTS; HEALTH; SCHIZOPHRENIA; TRANSITIONS; SERVICES; MIDLIFE;
   MOTHERS; IMPACTS; AUTISM; CARE
AB Objective: This study examined the effects on well-being of a spouse's disability among aging parents already serving as caregivers of adult children with severe mental illness or a developmental disability. Methods: The study sample consisted of two groups of participants in the Wisconsin Longitudinal Study of 1957 high school graduates and their randomly selected siblings-those who had a child with a disability (N=227) and a matched comparison group of parents who did not have a child with a disability (N=1,463). The participants were surveyed in 1992-1994 and 2004-2006, and participants with a spouse with a disability in 1992-1994 were excluded from the analysis. The effect of multiple caregiving roles was investigated by using regression analysis. Results: Parents of adult children with severe mental illness were more likely than either parents of adult children with developmental disabilities or the comparison group to report that their spouse developed a disability in the early retirement years. The experience of caring for a spouse with a disability and the experience of caring for an adult child with disabilities had additive effects in eroding the well-being of older adults. Parents of adult children with severe mental illness in general had the lowest levels of well-being. Conclusions: As they move into their retirement years, aging parents who care for children with long-term disabilities are likely to experience multiple caregiving responsibilities. Service providers must address the needs of these aging parents and develop interventions to help them cope and plan for their future. (Psychiatric Services 63:1118-1124, 2012; doi: 10.1176/appi.ps.201200014)
C1 [Ghosh, Subharati] Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02453 USA.
   [Ghosh, Subharati] Brandeis Univ, Lurie Inst Disabil Policy, Waltham, MA 02453 USA.
   [Greenberg, Jan S.; Seltzer, Marsha Mailick] Univ Wisconsin Madison, Waisman Ctr, Madison, WI USA.
   [Greenberg, Jan S.; Seltzer, Marsha Mailick] Univ Wisconsin Madison, Sch Social Work, Madison, WI USA.
RP Ghosh, S (reprint author), Brandeis Univ, Heller Sch Social Policy & Management, 415 South St, Waltham, MA 02453 USA.
EM subharati@gmail.com
FU National Institute on Aging [R01 AG20558, R01 AG08768, P01 AG21079];
   National Institute of Child Health and Human Development [P30 HD03352]
FX This study was supported by grants R01 AG20558, R01 AG08768, and P01
   AG21079 from the National Institute on Aging and by grant P30 HD03352
   from the National Institute of Child Health and Human Development.
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NR 33
TC 4
Z9 4
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 1075-2730
J9 PSYCHIAT SERV
JI Psychiatr. Serv.
PD NOV
PY 2012
VL 63
IS 11
BP 1118
EP 1124
DI 10.1176/appi.ps.201200014
PG 7
WC Health Policy & Services; Public, Environmental & Occupational Health;
   Psychiatry
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health; Psychiatry
GA 049KF
UT WOS:000311981200010
PM 22948898
ER

PT J
AU Megargel, E
   Broder-Fingert, S
AF Megargel, Eve
   Broder-Fingert, Sarabeth
TI Autism and Hospitals: A Difficult Match
SO ACADEMIC PEDIATRICS
LA English
DT Editorial Material
AB As a resident, you always have that one patient who sticks out in your mind-the one who had some profound impact on your practice of medicine and your life outside of medicine. For me, though, it wasn't just one patient. It was one patient after another with the same challenge: autism. Having worked in the school system before medical school, I immediately recognized what was missing in the way physicians and the medical establishment approached children with autism. The hospital staff had no real understanding of these children and how their worlds worked. I first met Billy's mother on a crisp spring afternoon. I had been thinking about and searching for a way to provide the best care for children with autism when in the hospital. I wanted to hear what Eve, the mother of a ywung man with autism, thought about the issue. The following is Eve's story, in her own words.
C1 [Broder-Fingert, Sarabeth] MassGen Hosp Children, Ctr Child & Adolescent Hlth Res & Policy, Boston, MA 02114 USA.
RP Broder-Fingert, S (reprint author), MassGen Hosp Children, Ctr Child & Adolescent Hlth Res & Policy, 100 Cambridge St,15th Fl, Boston, MA 02114 USA.
EM sbroderfingert@gmail.com
NR 0
TC 1
Z9 1
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1876-2859
J9 ACAD PEDIATR
JI Acad. Pediatr.
PD NOV-DEC
PY 2012
VL 12
IS 6
BP 469
EP 470
PG 2
WC Pediatrics
SC Pediatrics
GA 048OA
UT WOS:000311920600001
PM 23159035
ER

PT J
AU Mueller, S
   Keeser, D
   Reiser, MF
   Teipel, S
   Meindl, T
AF Mueller, S.
   Keeser, D.
   Reiser, M. F.
   Teipel, S.
   Meindl, T.
TI Functional and Structural MR Imaging in Neuropsychiatric Disorders, Part
   1: Imaging Techniques and Their Application in Mild Cognitive Impairment
   and Alzheimer Disease
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Review
ID DEFAULT-MODE NETWORK; RESTING-STATE NETWORKS; VOXEL-BASED MORPHOMETRY;
   GRAY-MATTER LOSS; INDEPENDENT COMPONENT ANALYSIS; HUMAN BRAIN;
   WHITE-MATTER; HIPPOCAMPAL ACTIVATION; POSTEROMEDIAL CORTEX; DIAGNOSTIC
   UTILITY
AB During the past decade, the application of advanced MR imaging techniques in neuropsychiatric disorders has seen a rapid increase. Disease-specific alterations in brain function can be assessed by fMRI. Structural GM and WM properties are increasingly investigated by DTI and voxel-based approaches like VBM. These methods provide neurobiologic correlates for brain architecture and function, evaluation tools for therapeutic approaches, and potential early markers for diagnosis. The aim of this review was to provide insight into the principles of functional and structural imaging and to delineate major findings in MCI, AD (Part 1), autism, and schizophrenia (Part 2), which are common psychiatric disorders covering different stages of the life span. Part 2 will conclude by summarizing current applications, limitations, and future prospects in the field of MR imaging based neuroimaging.
C1 [Mueller, S.; Keeser, D.; Reiser, M. F.; Meindl, T.] Univ Munich, Inst Clin Radiol, Munich, Germany.
   [Keeser, D.] Univ Munich, Dept Psychiat & Psychotherapy, Munich, Germany.
   [Teipel, S.] Univ Rostock, Dept Psychiat, Rostock, Germany.
RP Mueller, S (reprint author), Univ Hosp Munich, Inst Clin Radiol, Marchioninistr 15, D-81377 Munich, Germany.
EM sophia.muel-lermed@uni-muenchen.de
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NR 98
TC 8
Z9 8
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD NOV
PY 2012
VL 33
IS 10
BP 1845
EP 1850
DI 10.3174/ajnr.A2799
PG 6
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 045QH
UT WOS:000311711400003
PM 22173754
ER

PT J
AU Fabricius, T
AF Fabricius, Thomas
TI On neural systems for speech and song in autism
SO BRAIN
LA English
DT Letter
C1 Family Med Agnesian Healthcare Syst, Fond Du Lac, WI 54935 USA.
RP Fabricius, T (reprint author), Family Med Agnesian Healthcare Syst, 420 E Div St, Fond Du Lac, WI 54935 USA.
EM tjafab@gmail.com
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NR 9
TC 1
Z9 1
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD NOV
PY 2012
VL 135
AR e222
DI 10.1093/brain/aws179
PN 11
PG 2
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 044SV
UT WOS:000311644800006
PM 22945968
ER

PT J
AU Spencer, MD
   Holt, RJ
   Chura, LR
   Calder, AJ
   Suckling, J
   Bullmore, ET
   Baron-Cohen, S
AF Spencer, Michael D.
   Holt, Rosemary J.
   Chura, Lindsay R.
   Calder, Andrew J.
   Suckling, John
   Bullmore, Edward T.
   Baron-Cohen, Simon
TI Atypical activation during the Embedded Figures Task as a functional
   magnetic resonance imaging endophenotype of autism
SO BRAIN
LA English
DT Article
DE autism; Embedded Figures Task; siblings; functional MRI; endophenotype
ID LOCAL VISUAL-SEARCH; SPECTRUM DISORDERS; COGNITIVE PHENOTYPE;
   ASPERGER-SYNDROME; EXECUTIVE DYSFUNCTION; CHILDREN; PARENTS; BRAIN;
   FMRI; PERFORMANCE
AB Atypical activation during the Embedded Figures Task has been demonstrated in autism, but has not been investigated in siblings or related to measures of clinical severity. We identified atypical activation during the Embedded Figures Task in participants with autism and unaffected siblings compared with control subjects in a number of temporal and frontal brain regions. Autism and sibling groups, however, did not differ in terms of activation during this task. This suggests that the pattern of atypical activation identified may represent a functional endophenotype of autism, related to familial risk for the condition shared between individuals with autism and their siblings. We also found that reduced activation in autism relative to control subjects in regions including associative visual and face processing areas was strongly correlated with the clinical severity of impairments in reciprocal social interaction. Behavioural performance was intact in autism and sibling groups. Results are discussed in terms of atypical information processing styles or of increased activation in temporal and frontal regions in autism and the broader phenotype. By separating the aspects of atypical activation as markers of familial risk for the condition from those that are autism-specific, our findings offer new insight into the factors that might cause the expression of autism in families, affecting some children but not others.
C1 [Spencer, Michael D.; Holt, Rosemary J.; Chura, Lindsay R.; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England.
   [Calder, Andrew J.] MRC, Cognit & Brain Sci Unit, Cambridge CB2 7EF, England.
   [Suckling, John; Bullmore, Edward T.] Univ Cambridge, Dept Psychiat, Cambridge CB2 0SZ, England.
RP Spencer, MD (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18 B Trumpington Rd, Cambridge CB2 8AH, England.
EM mds1003@cam.ac.uk
RI Bullmore, Edward/C-1706-2012
OI Bullmore, Edward/0000-0002-8955-8283
FU Medical Research Council, UK [G0701919]; Gates Cambridge Scholarship
   Trust
FX Clinician Scientist Fellowship from the Medical Research Council, UK
   [grant number G0701919] (to M. D. S.) and the Gates Cambridge
   Scholarship Trust (to L.R.C.).
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NR 59
TC 16
Z9 17
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0006-8950
J9 BRAIN
JI Brain
PD NOV
PY 2012
VL 135
BP 3469
EP 3480
DI 10.1093/brain/aws229
PN 11
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 044SV
UT WOS:000311644800030
PM 23065480
ER

PT J
AU Kokubo, N
   Inagaki, M
   Gunji, A
   Kobayashi, T
   Ohta, H
   Kajimoto, O
   Kaga, M
AF Kokubo, Naomi
   Inagaki, Masumi
   Gunji, Atsuko
   Kobayashi, Tomoka
   Ohta, Hidenobu
   Kajimoto, Osami
   Kaga, Makiko
TI Developmental change of visuo-spatial working memory in children:
   Quantitative evaluation through an Advanced Trail Making Test
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Working Memory; Trail making test; Visuo-spatial; Development; Child
ID INDIVIDUAL-DIFFERENCES; TASK; CAPACITY; AGE; IMPAIRMENT; AUTISM; SPAN
AB Aim: The present study aimed to investigate the developmental change in Visuo-Spatial Working Memory (VSWM) in typically developed children using a specially designed Advanced Trail Making Test for children (ATMT-C). Methods: We developed a new method for evaluating VSWM efficiency in children using a modified version ATMT to suit their shorter sustained attention. The ATMT-C consists of two parts; a number-based ATMT and a hiragana (Japanese phonogram)-based ATMT, both employing symbols familiar to young children. A total of 94 healthy participants (6-28 years of age) were enrolled in this study. Results: A non-linear developmental change of VSWM efficiency was observed in the results from the ATMT-C. In the number-based ATMT, children under 8 years of age showed a relatively rapid increase in VSWM efficiency while older children (9-12 years) had a more gradual increase in VSWM efficiency. Results from the hiragana-based ATMT-C showed a slightly delayed increase pattern in VSWM efficiency compared to the pattern from the number-based ATMT. There were no significant differences in VSWM efficiency for gender, handedness and test order. Interpretation: VSWM in children gradually matures in a non steady-state manner and there is an important stage for VSWM maturation before reaching 12 years of age. VSWM efficiency may also vary depending on developmental condition of its cognitive subsystems. (C) 2012 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Kokubo, Naomi; Inagaki, Masumi; Gunji, Atsuko; Kobayashi, Tomoka; Ohta, Hidenobu; Kaga, Makiko] NCNP, Natl Inst Mental Hlth, Dept Dev Disorders, Kodaira, Tokyo 1878553, Japan.
   [Kajimoto, Osami] Osaka City Univ, Grad Sch Med, Dept Med Sci Fatigue, Abeno Ku, Osaka 5458585, Japan.
RP Inagaki, M (reprint author), NCNP, Natl Inst Mental Hlth, Dept Dev Disorders, 4-1-1 Ogawa Higashi Machi, Kodaira, Tokyo 1878553, Japan.
EM inagaki@ncnp.go.jp
RI Gunji, Atsuko/O-6323-2014
OI Gunji, Atsuko/0000-0001-8908-8739
FU National Institute of Mental Health, National Center of Neurology and
   Psychiatry (NCNP) in Japan [22-6]
FX This study was supported in part by Intramural Research Grant (22-6;
   Clinical Research for Diagnostic and Therapeutic Innovations in
   Developmental Disorders) for Neurological and Psychiatric Disorders of
   National Institute of Mental Health, National Center of Neurology and
   Psychiatry (NCNP) in Japan. We also thank Mr. David Egginton for his
   editorial advice.
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NR 30
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD NOV
PY 2012
VL 34
IS 10
BP 799
EP 805
DI 10.1016/j.braindev.2012.02.001
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 042IX
UT WOS:000311466000001
PM 22398277
ER

PT J
AU Seneff, S
   Davidson, RM
   Liu, JJ
AF Seneff, Stephanie
   Davidson, Robert M.
   Liu, Jingjing
TI Empirical Data Confirm Autism Symptoms Related to Aluminum and
   Acetaminophen Exposure
SO ENTROPY
LA English
DT Review
DE autism; vaccines; MMR; HEP-B; glutathione; sulfate; cholesterol sulfate;
   aluminum; mercury; acetaminophen
ID HUMAN-PAPILLOMAVIRUS; VACCINE ADJUVANTS; MOLECULAR-MECHANISMS;
   CHOLESTEROL SULFATE; SPECTRUM DISORDERS; PARTICLE VACCINE; OXIDATIVE
   STRESS; SERUM-ALBUMIN; YOUNG-WOMEN; HEPATITIS-B
AB Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC Vaccine Adverse Events Reporting System (VAERS) database. Our results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever.
C1 [Seneff, Stephanie; Liu, Jingjing] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
   [Davidson, Robert M.] PhyNet Inc, Internal Med Grp Practice, Longview, TX 75604 USA.
RP Seneff, S (reprint author), MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM seneff@csail.mit.edu; patrons99@yahoo.com; jingl@csail.mit.edu
FU Quanta Computer under the Qmulus Initiative
FX This work was funded in part by Quanta Computer under the Qmulus
   Initiative. The authors are grateful to three anonymous reviewers who
   provided outstanding comments that led to a greatly improved quality of
   the document.
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NR 120
TC 9
Z9 9
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1099-4300
J9 ENTROPY-SWITZ
JI Entropy
PD NOV
PY 2012
VL 14
IS 11
BP 2227
EP 2253
DI 10.3390/e14112227
PG 27
WC Physics, Multidisciplinary
SC Physics
GA 041TB
UT WOS:000311423000010
ER

PT J
AU Seneff, S
   Davidson, RM
   Liu, JJ
AF Seneff, Stephanie
   Davidson, Robert M.
   Liu, Jingjing
TI Is Cholesterol Sulfate Deficiency a Common Factor in Preeclampsia,
   Autism, and Pernicious Anemia?
SO ENTROPY
LA English
DT Review
DE encephalitis; preeclampsia; autism; cobalamin; pernicious anemia; nitric
   oxide; cholesterol sulfate; aluminum; seizures
ID NITRIC-OXIDE SYNTHASE; DISSEMINATED INTRAVASCULAR COAGULATION; SOLUBLE
   GUANYLATE-CYCLASE; SPECTRUM DISORDERS; WHITE-MATTER; MACROPHAGIC
   MYOFASCIITIS; ANAPHYLACTIC SHOCK; NEONATAL JAUNDICE; REDUCING BACTERIA;
   VACCINE ADJUVANTS
AB In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed to a severe depletion of cholesterol sulfate. Through studies on the Vaccine Adverse Event Reporting System (VAERS) database, we demonstrate a strong statistical relationship among the signs and symptoms associated with autism and those associated with preeclampsia, pernicious anemia, and serious adverse reactions to vaccines. We show that VAERS reports associated with symptoms typical of pernicious anemia produce both a set of symptoms that are highly correlated with preeclampsia and another set highly correlated with autism. We explain this observation via an argument that, in a severe reaction, the cascade of events subsequent to vaccination reflects a profuse production of nitric oxide (NO) and consequential destruction of both red blood cells (RBCs) and cobalamin. This may explain the diverse signs and symptoms associated with both preeclampsia and severe vaccine adverse reactions. We argue that excess NO synthesis, induced by the aluminum and antigen in vaccines, results in hemolysis of RBCs, which allows hemoglobin to scavenge the excess NO, converting it to nitrate. The NO is also scavenged by cobalamin, leading to its inactivation and contributing to subsequent pernicious anemia. Finally, we demonstrate that severe adverse reactions to vaccines can be associated with life-threatening conditions related to the heart and brain, as well as stillbirth, when the vaccine is administered to a woman in the third-trimester of pregnancy, as demonstrated by statistical analysis of the Gardasil records.
C1 [Seneff, Stephanie; Liu, Jingjing] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
   [Davidson, Robert M.] PhyNet Inc, Internal Med Grp Practice, Longview, TX 75604 USA.
RP Seneff, S (reprint author), MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM Seneff@csail.mit.edu; patrons99@yahoo.com; jingl@csail.mit.edu
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NR 122
TC 3
Z9 3
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1099-4300
J9 ENTROPY-SWITZ
JI Entropy
PD NOV
PY 2012
VL 14
IS 11
BP 2265
EP 2290
DI 10.3390/e14112265
PG 26
WC Physics, Multidisciplinary
SC Physics
GA 041TB
UT WOS:000311423000012
ER

PT J
AU Crespo-Eguilaz, N
   Narbona, J
   Magallon, S
AF Crespo-Eguilaz, Nerea
   Narbona, Juan
   Magallon, Sara
TI Dysfunction of central coherence in schoolchildren with procedural
   learning disorder
SO REVISTA DE NEUROLOGIA
LA Spanish
DT Article
DE Central coherence function; Coordination disorder; Non verbal learning
   disability; Procedural disorder; Simultagnosia; Strange images; Visual
   extinction
ID AUTISM; ATTENTION; ACCOUNT
AB Introduction. Children with coordination disorder-non verbal learning disorder, procedural learning disorder (PLD)-have difficulties in understanding complex simultaneous visual information.
   Aim. Validation of two different visual tasks to measure central coherence function of children with PLD.
   Subjects and methods. A chimeric image and a complex visual story are showed to 200 schoolchildren: 20 of them have PLD, 60 have PLD plus attention deficit/hyperactivity disorder (PLD + ADHD), 60 have non comorbid ADHD, and 60 subjects are typical control children. A chi square test and a discriminant analysis are used to study the performances of the different groups in verbal description of both images.
   Results. Performance is lower in children with PLD and PLD + ADHD than in those with non-comorbid ADHD or controls. Moreover 93% and 92% of children with poor performance in, respectively, chimeric and complex images, have PLD or PLD + ADHD. Eighty seven per cent of subjects with PLD + ADHD fail in some of the tasks and, by contrast only 15% of children with ADHD do.
   Conclusions. Children with PLD have disability in quick understanding of simultaneous complex information and central coherence. The two tasks used in this research are useful to detect these difficulties, with high sensibility and specificity.
C1 [Crespo-Eguilaz, Nerea; Narbona, Juan; Magallon, Sara] Clin Univ Navarra, Dept Pediat, Unidad Neurol Pediat, E-31080 Pamplona, Navarra, Spain.
RP Crespo-Eguilaz, N (reprint author), Clin Univ Navarra, Dept Pediat, Unidad Neuropediat, Avda Pio 12 S-N, E-31080 Pamplona, Navarra, Spain.
EM necrespo@unav.es
CR American Psychiatric Association, 2012, DSM 5 DEV
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NR 25
TC 4
Z9 4
PU REVISTA DE NEUROLOGIA
PI BARCELONA
PA C/O CESAR VIGUERA, EDITOR, APDO 94121, 08080 BARCELONA, SPAIN
SN 0210-0010
J9 REV NEUROLOGIA
JI Rev. Neurologia
PD NOV 1
PY 2012
VL 55
IS 9
BP 513
EP 519
PG 7
WC Clinical Neurology
SC Neurosciences & Neurology
GA 047UR
UT WOS:000311867500001
PM 23111989
ER

PT J
AU Leopold, A
   Krueger, F
   dal Monte, O
   Pardini, M
   Pulaski, SJ
   Solomon, J
   Grafman, J
AF Leopold, Anne
   Krueger, Frank
   dal Monte, Olga
   Pardini, Matteo
   Pulaski, Sarah J.
   Solomon, Jeffrey
   Grafman, Jordan
TI Damage to the left ventromedial prefrontal cortex impacts affective
   theory of mind
SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE
LA English
DT Article
DE affective theory of mind; ventromedial prefrontal cortex; traumatic
   brain injury; emotional intelligence; empathy
ID EMOTIONAL INTELLIGENCE; BRAIN-LESIONS; RHESUS-MONKEY; FALSE BELIEF;
   HEAD-INJURY; DISSOCIATION; IMPAIRMENTS; EMPATHY; DEPRESSION; AUTISM
AB Studies investigating theory of mind (ToM) abilities (i.e. ability to understand and predict others' mental states) have revealed that affective and cognitive functions play a significant role and that each of those functions are associated with distinct neural networks. Cognitive facets of ToM have implicated the medial prefrontal cortex, temporo-parietal junction and the anterior paracingulate cortex, whereas affective facets have implicated the ventromedial prefrontal cortex (vmPFC). Although the vmPFC has repeatedly shown to be critical for affective functions, knowledge regarding the exact role of the left and right vmPFC in affective ToM is still obscure. Here, we compared performances of 30 patients with left, right and bilateral vmPFC lesions to two comparison groups (one without and one with brain injuries) on the Faux Pas Recognition task measuring the facets of ToM. We also investigated whether any deficits may be associated with other emotional measures, namely emotional empathy and emotional intelligence. Our results extend earlier findings by showing that the vmPFC is associated with abilities in affective ToM. More importantly, our results revealed that the left, and not the right vmPFC as indicated previously, is involved in affective ToM and that this deficit is associated with emotional intelligence.
C1 [Krueger, Frank] George Mason Univ, Dept Mol Neurosci, Fairfax, VA 22030 USA.
   [Grafman, Jordan] Kessler Fdn Res Ctr, Traumat Brain Injury Res Lab, W Orange, NJ 07052 USA.
   [Krueger, Frank] George Mason Univ, Dept Psychol, Fairfax, VA 22030 USA.
   [dal Monte, Olga] Univ Turin, Dept Neuropsychol, Turin, Italy.
   [dal Monte, Olga] Henry M Jackson Fdn, Rockville, MD USA.
   [Pardini, Matteo] Univ Genoa, Dept Neurosci Ophthalmol & Genet, Genoa, Italy.
   [Solomon, Jeffrey] Med Numer, Germantown, MD USA.
   [Leopold, Anne; dal Monte, Olga; Pulaski, Sarah J.] NINDS, Cognit Neurosci Sect, NIH, Bethesda, MD 20892 USA.
   [Leopold, Anne] Univ Utrecht, Dept Social & Hlth Psychol, Utrecht, Netherlands.
RP Krueger, F (reprint author), George Mason Univ, Dept Mol Neurosci, 4400 Univ Dr,Mail Stop 2A1, Fairfax, VA 22030 USA.
EM FKrueger@gmu.edu; jgrafman@kesslerfoundation.org
RI Pardini, Matteo/F-8414-2010
OI Pardini, Matteo/0000-0002-4740-1982
FU National Naval Medical Center; U.S. National Institute of Neurological
   Disorders and Stroke; U.S. Army Medical Research and Material Command
   [DAMD17-01-1-0675]
FX The views expressed in this article are those of the authors and do not
   necessarily reflect the official policy or position of the Department of
   the Navy, the Department of Defense, or the U. S. Government. The
   authors are grateful to all the Vietnam veterans who participated in
   this study. Without their long-term commitment to improving the health
   care of veterans, this study could not have been completed. We thank the
   National Naval Medical Center for their support and provision of their
   facilities. We are grateful to S. Bonifant, B. Cheon, C. Ngo, A.
   Greathouse, K. Reding and G. Tasick for their invaluable help with the
   testing of participants and organization of this study. The work was
   supported by the U.S. National Institute of Neurological Disorders and
   Stroke intramural research program and a project grant from the U.S.
   Army Medical Research and Material Command administrated by the Henry M.
   Jackson Foundation (Vietnam Head Injury Study Phase III: a 30-year
   post-injury follow-up study), grant number: DAMD17-01-1-0675.
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NR 72
TC 16
Z9 16
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 1749-5016
J9 SOC COGN AFFECT NEUR
JI Soc. Cogn. Affect. Neurosci.
PD NOV
PY 2012
VL 7
IS 8
BP 871
EP 880
DI 10.1093/scan/nsr071
PG 10
WC Neurosciences; Psychology; Psychology, Experimental
SC Neurosciences & Neurology; Psychology
GA 045BZ
UT WOS:000311671100001
PM 22021651
ER

PT J
AU Gutman, SA
AF Gutman, Sharon A.
TI FROM THE DESK OF THE EDITOR State of the Journal, 2012
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Editorial Material
DE journal impact factor; occupational therapy; periodicals; publishing;
   research
ID RANDOMIZED CONTROLLED-TRIAL; DWELLING OLDER-ADULTS; AUTISM SPECTRUM
   DISORDERS; DRIVING BEHAVIOR MEASURE; TEST-RETEST RELIABILITY;
   OCCUPATIONAL-THERAPY; DEVELOPMENTAL-DISABILITIES; COGNITIVE PERFORMANCE;
   ACTIVITY ENGAGEMENT; CEREBRAL-PALSY
C1 Columbia Univ, Programs Occupat Therapy, New York, NY 10027 USA.
RP Gutman, SA (reprint author), Columbia Univ, Programs Occupat Therapy, New York, NY 10027 USA.
EM ajoteditor@aota.org
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   Yang CL, 2012, AM J OCCUP THER, V66, P198, DOI 10.5014/ajot.2012.003103
   Yuen HK, 2012, AM J OCCUP THER, V66, P110, DOI 10.5014/ajot.2012.001594
NR 82
TC 0
Z9 0
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2012
VL 66
IS 6
BP 636
EP 643
PG 8
WC Rehabilitation
SC Rehabilitation
GA 038RV
UT WOS:000311192700001
PM 23106984
ER

PT J
AU Clark, F
AF Clark, Florence
TI PRESIDENTIAL ADDRESS, 2012 Beyond High Definition: Attitude and Evidence
   Bringing OT in HD-3D
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Editorial Material
DE evidence-based practice; health policy; interdisciplinary communication;
   occupational therapy; research
ID CHILDREN; AUTISM
C1 [Clark, Florence] Amer Occupat Therapy Assoc, Los Angeles, CA 90089 USA.
   [Clark, Florence] Univ So Calif, Los Angeles, CA 90089 USA.
RP Clark, F (reprint author), Amer Occupat Therapy Assoc, 1540 Alcazar St,CHP 133, Los Angeles, CA 90089 USA.
EM fclark@usc.edu
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NR 20
TC 1
Z9 1
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2012
VL 66
IS 6
BP 644
EP 651
DI 10.5014/ajot.2012.666002
PG 8
WC Rehabilitation
SC Rehabilitation
GA 038RV
UT WOS:000311192700002
PM 23106985
ER

PT J
AU Palsbo, SE
   Hood-Szivek, P
AF Palsbo, Susan E.
   Hood-Szivek, Pamela
TI Effect of Robotic-Assisted Three-Dimensional Repetitive Motion to
   Improve Hand Motor Function and Control in Children With Handwriting
   Deficits: A Nonrandomized Phase 2 Device Trial
SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY
LA English
DT Article
DE handwriting; motor skills; motor skills disorders; robotics; therapy,
   computer-assisted
ID ELEMENTARY STUDENTS; CEREBRAL-PALSY; REHABILITATION; THERAPY; STROKE;
   FEEDBACK; OUTCOMES; INTERVENTION; PERFORMANCE; INTEGRATION
AB OBJECTIVE. We explored the efficacy of robotic technology in improving handwriting in children with impaired motor skills.
   METHOD. Eighteen participants had impairments arising from cerebral palsy (CP), autism spectrum disorder (ASD), attention deficit disorder (ADD), attention deficit hyperactivity disorder (ADHD), or other disorders. The intervention was robotic-guided three-dimensional repetitive motion in 15-20 daily sessions of 25-30 min each over 4-8 wk.
   RESULTS. Fine motor control improved for the children with learning disabilities and those ages 9 or older but not for those with CP or under age 9. All children with ASD or ADHD referred for slow writing speed were able to increase speed while maintaining legibility.
   CONCLUSION. Three-dimensional, robot-assisted, repetitive motion training improved handwriting fluidity in children with mild to moderate fine motor deficits associated with ASD or ADHD within 10 hr of training. This dosage may not be sufficient for children with CP.
C1 [Palsbo, Susan E.] George Mason Univ, Coll Hlth & Human Serv, Fairfax, VA 22030 USA.
   [Hood-Szivek, Pamela] Corvallis Childrens Therapy, Corvallis, OR USA.
RP Palsbo, SE (reprint author), 3130 Summit Sky Blvd, Eugene, OR 97405 USA.
EM InnovAbility@comcast.net
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NR 47
TC 2
Z9 2
PU AMER OCCUPATIONAL THERAPY ASSOC, INC
PI BETHESDA
PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA
SN 0272-9490
J9 AM J OCCUP THER
JI Am. J. Occup. Ther.
PD NOV-DEC
PY 2012
VL 66
IS 6
BP 682
EP 690
DI 10.5014/ajot.2012.004556
PG 9
WC Rehabilitation
SC Rehabilitation
GA 038RV
UT WOS:000311192700005
PM 23106988
ER

PT J
AU Scerbina, T
   Chatterjee, D
   Gerlai, R
AF Scerbina, Tanya
   Chatterjee, Diptendu
   Gerlai, Robert
TI Dopamine receptor antagonism disrupts social preference in zebrafish: a
   strain comparison study
SO AMINO ACIDS
LA English
DT Article
DE Dopamine; Serotonin; Shoaling; Social behavior; Strain differences;
   Zebrafish
ID DANIO-RERIO; IMMUNOCYTOCHEMICAL LOCALIZATION; ALCOHOL EXPOSURE; D1
   RECEPTORS; BEHAVIOR; AUTISM; BRAIN; MODEL; VERTEBRATE; DISORDERS
AB Zebrafish form shoals in nature and in the laboratory. The sight of conspecifics has been found reinforcing in zebrafish learning tasks. However, the mechanisms of shoaling, and those of its reinforcing properties, are not known. The dopaminergic system has been implicated in reward among other functions and it is also engaged by drugs of abuse as shown in a variety of vertebrates including zebrafish. The ontogenetic changes in dopamine levels and, to a lesser degree, in serotonin levels, have been found to accompany the maturation of shoaling in zebrafish. Thus, we hypothesized that the dopaminergic system may contribute to shoaling in zebrafish. To test this we employed a D1-receptor antagonist and quantified behavioral responses of our subjects using a social preference (shoaling) paradigm. We found significant reduction of social preference induced by the D1-R antagonist, SCH23390, in the AB strain of zebrafish, an alteration that was not accompanied by changes in motor function or vision. We also detected D1-R antagonist-induced changes in the level of dopamine, DOPAC, serotonin and 5HIAA, respectively, in the brain of AB zebrafish as quantified by HPLC with electrochemical detection. We found the antagonist-induced behavioral changes to be absent and the levels of these neurochemicals to be lower in another zebrafish population, SF, demonstrating naturally occurring genetic variability in these traits. We conclude that this variability may be utilized to unravel the mechanisms of social behavior in zebrafish, a line of research that may be extended to other vertebrates including our own species.
C1 [Scerbina, Tanya; Chatterjee, Diptendu; Gerlai, Robert] Univ Toronto, Dept Psychol, Mississauga, ON L5L 1C6, Canada.
RP Gerlai, R (reprint author), Univ Toronto, Dept Psychol, 3359 Mississauga Rd N,Rm 4020C, Mississauga, ON L5L 1C6, Canada.
EM robert_gerlai@yahoo.com
FU NIH/NIAAA (USA); NSERC (CANADA)
FX This study was supported by an NIH/NIAAA R01 (USA) grant awarded to
   Robert Gerlai, and an NSERC (CANADA) summer undergraduate research
   scholarship awarded to Tanya Scerbina.
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NR 52
TC 14
Z9 14
PU SPRINGER WIEN
PI WIEN
PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA
SN 0939-4451
J9 AMINO ACIDS
JI Amino Acids
PD NOV
PY 2012
VL 43
IS 5
BP 2059
EP 2072
DI 10.1007/s00726-012-1284-0
PG 14
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 021CR
UT WOS:000309863400023
PM 22491827
ER

PT J
AU Esperger, Z
   Bereczkei, T
AF Esperger, Zsofia
   Bereczkei, Tamas
TI Machiavellianism and Spontaneous Mentalization: One Step Ahead of Others
SO EUROPEAN JOURNAL OF PERSONALITY
LA English
DT Article
DE manipulation; theory of mind; social cognition
ID EMOTIONAL INTELLIGENCE; BRAIN MECHANISMS; MIND; PSYCHOPATHY;
   PERSONALITY; PERCEPTION; PATTERNS; DEFICITS; EMPATHY; AUTISM
AB In spite of the Machiavellians' successful strategies in exploitation of others, they show cognitive deficiencies, especially reduced mind-reading skill. Theory of mind is usually regarded as an ability to make inferences about the mental states of others and thus to predict their behaviour. In our study, we have instead emphasized a motivation-based approach, using the concept of spontaneous mentalization. This concept is construed solely in a motivational context and not in relation to the automaticity of mind-reading ability. It entails that people in their social relations make efforts to explore the thoughts and intentions of others and are motivated to make hypotheses about the mental state of the other person. We assumed that what is peculiar to Machiavellianism is spontaneous mentalization as a kind of motivation rather than mind-reading as an ability. To measure spontaneous mentalization, we created a set of image stimuli and asked our participants to describe their impressions of the pictures. The results show that individual differences in spontaneous mentalization correlate positively with the scores of Machiavellianism. These results suggest that those who have a stronger motivation for putting themselves into the mind of others can be more successful in misleading and exploiting them. Further research should be carried out to clarify how spontaneous mentalization and mind-reading ability relate to each other. Copyright (C) 2011 John Wiley & Sons, Ltd.
C1 [Esperger, Zsofia; Bereczkei, Tamas] Univ Pecs, Inst Psychol, H-7624 Pecs, Hungary.
RP Bereczkei, T (reprint author), Univ Pecs, Inst Psychol, Ifjusag U 6, H-7624 Pecs, Hungary.
EM bereczkei.tamas@pte.hu
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NR 37
TC 1
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0890-2070
J9 EUR J PERSONALITY
JI Eur. J. Personal.
PD NOV-DEC
PY 2012
VL 26
IS 6
BP 580
EP 587
DI 10.1002/per.859
PG 8
WC Psychology, Social
SC Psychology
GA 041RL
UT WOS:000311418800003
ER

PT J
AU Weedon, D
   Carbone, P
   Bilder, D
   O'Brien, S
   Dorius, J
AF Weedon, Dean
   Carbone, Paul
   Bilder, Deborah
   O'Brien, Stephanie
   Dorius, Josette
TI Building a Person-Centered Medical Home: Lessons from a Program for
   People with Developmental Disabilities
SO JOURNAL OF HEALTH CARE FOR THE POOR AND UNDERSERVED
LA English
DT Article
DE Medical home; developmental disabilities; case management; care
   coordination; intellectual disabilities; autism
ID HEALTH-CARE NEEDS; CHILDREN; COORDINATION; SERVICES; AUTISM; OUTCOMES;
   ACCESS; IMPACT; YOUTH; COSTS
AB The HOME Program provides medical and behavioral health care for people with developmental disabilities across the lifespan. Its unique funding structure provides a fiscally viable, and replicable, means of supporting case management in a medical home setting, addressing system-level barriers that typically impede the implementation of the patient-centered medical home.
C1 [Weedon, Dean; Carbone, Paul; Bilder, Deborah; O'Brien, Stephanie; Dorius, Josette] Univ Utah, HOME Program, Salt Lake City, UT 84108 USA.
   [Carbone, Paul] Univ Utah, Dept Pediat, Salt Lake City, UT 84108 USA.
   [Bilder, Deborah] Univ Utah, Dept Psychiat, Salt Lake City, UT 84108 USA.
RP Weedon, D (reprint author), Univ Utah, HOME Program, 650 Komas Dr,200, Salt Lake City, UT 84108 USA.
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NR 22
TC 6
Z9 6
PU JOHNS HOPKINS UNIV PRESS
PI BALTIMORE
PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD
   21218-4363 USA
SN 1049-2089
J9 J HEALTH CARE POOR U
JI J. Health Care Poor Underserved
PD NOV
PY 2012
VL 23
IS 4
BP 1600
EP 1608
PG 9
WC Health Policy & Services; Public, Environmental & Occupational Health
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health
GA 036CF
UT WOS:000311003300022
PM 23698674
ER

PT J
AU Thomas, KC
   Parish, SL
   Rose, RA
   Kilany, M
AF Thomas, Kathleen C.
   Parish, Susan L.
   Rose, Roderick A.
   Kilany, Mona
TI Access to care for children with autism in the context of state Medicaid
   reimbursement
SO MATERNAL AND CHILD HEALTH JOURNAL
LA English
DT Article
DE Autism; Medicaid; Access to care
ID HEALTH-CARE; SPECTRUM DISORDERS; UNITED-STATES; MANAGED CARE; NEEDS;
   SERVICES; DIAGNOSIS; INSURANCE; SHORTAGE; PROGRAM
AB This paper examines the role of state residence and Medicaid reimbursement rates in explaining the relationship between having autism and access to care for children. Three questions are addressed: (1) Is there variation across states in the relationship between having autism and access to care? (2) Does taking account of state residence explain a significant amount of the variation in this relationship? (3) Does accounting for Medicaid reimbursement rates enhance our understanding of this relationship? Data from the 2005 National Survey of Children with Special Health Care Needs were combined with state characteristics to estimate a hierarchical generalized linear model of the association between state residence, Medicaid reimbursement rate and problems accessing care for children with special health care needs with and without autism. Findings indicate there is significant variation between states in the relationship between having autism and problems accessing care, and accounting for state residence explains a significant amount of variation in the model. Medicaid reimbursement rates have an independent effect on access to care for children with autism: when families raising children with autism live in states with higher reimbursement rates, they have lower odds of experiencing problems accessing care. The state context in which families live impacts access to care for children with autism. Moreover, when families live in states with higher Medicaid reimbursement rates, they are less likely to experience problems getting care. The value of this analysis is that it helps identify where to look for strategies to improve access.
C1 [Thomas, Kathleen C.; Rose, Roderick A.; Kilany, Mona] Univ N Carolina, Chapel Hill, NC 27515 USA.
   [Parish, Susan L.] Brandeis Univ, Waltham, MA USA.
RP Thomas, KC (reprint author), Univ N Carolina, Chapel Hill, NC 27515 USA.
EM thomas@schsr.unc.edu
RI Rose, Roderick/A-3558-2013
OI Rose, Roderick/0000-0001-5309-4547
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NR 47
TC 5
Z9 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1092-7875
J9 MATERN CHILD HLTH J
JI Matern. Child Health J.
PD NOV
PY 2012
VL 16
IS 8
BP 1636
EP 1644
DI 10.1007/s10995-011-0862-1
PG 9
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 042YN
UT WOS:000311508900010
PM 21833759
ER

PT J
AU Kennedy, DP
   Adolphs, R
AF Kennedy, Daniel P.
   Adolphs, Ralph
TI The social brain in psychiatric and neurological disorders
SO TRENDS IN COGNITIVE SCIENCES
LA English
DT Review
ID AUTISM SPECTRUM DISORDERS; VENTROMEDIAL PREFRONTAL CORTEX;
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   WILLIAMS-SYNDROME; HUMAN AMYGDALA; FUNCTIONAL CONNECTIVITY; COGNITIVE
   NEUROSCIENCE; CORPUS-CALLOSUM; NEURAL BASIS
AB Psychiatric and neurological disorders have historically provided key insights into the structure-function relationships that subserve human social cognition and behavior, informing the concept of the 'social brain'. In this review, we take stock of the current status of this concept, retaining a focus on disorders that impact social behavior. We discuss how the social brain, social cognition, and social behavior are interdependent, and emphasize the important role of development and compensation. We suggest that the social brain, and its dysfunction and recovery, must be understood not in terms of specific structures, but rather in terms of their interaction in large-scale networks.
C1 [Kennedy, Daniel P.; Adolphs, Ralph] CALTECH, Pasadena, CA 91125 USA.
RP Kennedy, DP (reprint author), Indiana Univ, 1101 E 10th St, Bloomington, IN 47405 USA.
EM dpk@indiana.edu; radolphs@caltech.edu
FU NIMH [R01MH080721, P50MH094258, K99 MH094409]
FX We thank Jed Elison, John Constantino, Bob Spunt, and three anonymous
   reviewers for comments. Supported by grants from the NIMH to R.A.
   (R01MH080721; P50MH094258) and D.P.K. (K99 MH094409).
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NR 156
TC 68
Z9 68
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1364-6613
J9 TRENDS COGN SCI
JI TRENDS COGN. SCI.
PD NOV
PY 2012
VL 16
IS 11
BP 559
EP 572
DI 10.1016/j.tics.2012.09.006
PG 14
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 042LY
UT WOS:000311473900008
PM 23047070
ER

PT J
AU AL-Ayadhi, L
   Mostfa, G
AF AL-Ayadhi, L.
   Mostfa, G.
TI The possible link between the elevated levels of neurokinin A and
   anti-ribosomal P protein antibodies in children with autism
SO ALLERGY
LA English
DT Meeting Abstract
CT 31st Congress of the European-Academy-of-Allergy-and-Clinical-Immunology
   (EAACI)
CY JUN 16-20, 2012
CL Geneva, SWITZERLAND
SP European Acad Allergy & Clin Immunol (EAACI)
C1 [AL-Ayadhi, L.; Mostfa, G.] King Saud Univ, Autism Res & Treatment Ctr, Al Amodi Autism Res Chair, Dept Physiol,Fac Med, Riyadh, Saudi Arabia.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0105-4538
J9 ALLERGY
JI Allergy
PD NOV
PY 2012
VL 67
SU 96
SI SI
MA 682
BP 270
EP 271
PG 2
WC Allergy; Immunology
SC Allergy; Immunology
GA 026CA
UT WOS:000310247701289
ER

PT J
AU Casalonga, S
AF Casalonga, Sabine
TI Screening A genetic test to diagnose autism
SO BIOFUTUR
LA French
DT News Item
CR Skafidas E, 2014, MOL PSYCHIATR, V19, P504, DOI 10.1038/mp.2012.126
NR 1
TC 0
Z9 0
PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
PI PARIS
PA 23 RUE LINOIS, 75724 PARIS, FRANCE
SN 0294-3506
J9 BIOFUTUR
JI Biofutur
PD NOV
PY 2012
IS 337
BP 7
EP 7
PG 1
WC Biotechnology & Applied Microbiology
SC Biotechnology & Applied Microbiology
GA 031WK
UT WOS:000310673100004
ER

PT J
AU Gonzalez-Fraguela, ME
   Hung, MLD
   Vera, H
   Robinson, M
   Gottfried, C
AF Gonzalez-Fraguela, Maria Elena
   Hung, Mei-Li Diaz
   Vera, Hector
   Robinson, Maria
   Gottfried, Carmem
TI Oxidative Stress Markers in Children with Autism Spectrum Disorders
SO FREE RADICAL BIOLOGY AND MEDICINE
LA English
DT Meeting Abstract
CT 19th Annual Meeting of the Society-for-Free-Radical-Biology-and-Medicine
   (SFRBM)
CY NOV 14-18, 2012
CL San Diego, CA
SP Soc Free Rad Biol & Med (SFRBM)
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 0891-5849
J9 FREE RADICAL BIO MED
JI Free Radic. Biol. Med.
PD NOV 1
PY 2012
VL 53
SU 2
BP S21
EP S21
DI 10.1016/j.freeradbiomed.2012.10.048
PG 1
WC Biochemistry & Molecular Biology; Endocrinology & Metabolism
SC Biochemistry & Molecular Biology; Endocrinology & Metabolism
GA 031RS
UT WOS:000310660600044
ER

PT J
AU Wei, HE
   Mori, S
   Hua, KG
   Li, XH
AF Wei, Hongen
   Mori, Susumu
   Hua, Kegang
   Li, Xiaohong
TI Alteration of brain volume in IL-6 overexpressing mice related to autism
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Article
DE Autism; Interleukin-6; Volume measurement; Brain; Magnetic resonance
   imaging
ID FUTURE-DIRECTIONS; SPECTRUM DISORDER; GENE DELIVERY; MOUSE MODEL;
   IMMUNE; ABNORMALITIES; INTERLEUKIN-6; ACTIVATION; CHILDREN; THERAPY
AB Abnormal neuroimmune responses have been reported to be associated with autism and could be appropriate targets for pharmacologic intervention. Our previous studies showed that neuroimmune factor, interleukin (IL)-6, was significantly elevated in the fontal cortex and cerebellum of autistic subjects. The IL-6 overexpressing mice displayed several autism-like features as well as an abnormal dendritic spine morphology and synaptic function. The purpose of this study was to examine the volumetric differences in the brain of IL-6 overexpressing mice and compare with corresponding control mice using magnetic resonance imaging. Here we show that IL-6 overexpressing mice display an increase in the total brain volume. In addition, the lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. These results indicate that IL-6 elevation in the brain could mediate neuroanatomical abnormalities. Taking together with our previous findings, a mechanism by which IL-6 may be involved in the pathogenesis of autism is proposed. (C) 2012 ISDN. Published by Elsevier Ltd. All rights reserved.
C1 [Wei, Hongen] Shanxi Prov Peoples Hosp, Cent Lab, Taiyuan 030012, Peoples R China.
   [Mori, Susumu; Hua, Kegang] Johns Hopkins Univ, Sch Med, Russell H Morgan Dept Radiol & Radiol Sci, Baltimore, MD USA.
   [Li, Xiaohong] NY State Inst Basic Res Dev Disabil, Dept Neurochem, New York, NY 10314 USA.
RP Wei, HE (reprint author), Shanxi Prov Peoples Hosp, Cent Lab, 29 Shuangta Rd, Taiyuan 030012, Peoples R China.
EM hongenwei@gmail.com; xiaohongli99@gmail.com
FU Rural India Charitable Trust
FX This work was partially supported by the Rural India Charitable Trust.
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NR 36
TC 6
Z9 6
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD NOV
PY 2012
VL 30
IS 7
BP 554
EP 559
DI 10.1016/j.ijdevneu.2012.08.007
PG 6
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 036VD
UT WOS:000311059400002
PM 22940293
ER

PT J
AU Tu, WJ
   Chen, H
   He, J
AF Tu, Wen-Jun
   Chen, Hui
   He, Jian
TI Application of LC-MS/MS analysis of plasma amino acids profiles in
   children with autism
SO JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION
LA English
DT Letter
DE autism; Chinese; amino Acids profiles; liquid chromatography-tandem mass
   spectrometry
C1 [Tu, Wen-Jun; Chen, Hui] China Rehabil Res Ctr, Dept Clin Lab, Beijing 100068, Peoples R China.
   [He, Jian] Chinese Acad Med Sci, Ctr Clin Lab Dev, Beijing 102206, Peoples R China.
   [He, Jian] Peking Union Med Coll, Beijing 102206, Peoples R China.
RP Tu, WJ (reprint author), China Rehabil Res Ctr, Dept Clin Lab, Beijing 100068, Peoples R China.
EM twjun1983@gamil.com
CR Arnold GL, 2003, J AUTISM DEV DISORD, V33, P449, DOI 10.1023/A:1025071014191
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NR 6
TC 4
Z9 4
PU JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION
PI KYOTO
PA KYOTO PREFECTURAL UNIV MED, GRAD SCH MEDICAL SCIENCE, DEPT MOLECULAR
   GASTROENTEROLOGY & HEPATOLOGY, KYOTO, 602-8566, JAPAN
SN 0912-0009
EI 1880-5086
J9 J CLIN BIOCHEM NUTR
JI J. Clin. Biochem. Nutr.
PD NOV 1
PY 2012
VL 51
IS 3
BP 248
EP 249
DI 10.3164/jcbn.12-45
PG 2
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 037TK
UT WOS:000311129200014
PM 23170055
ER

PT J
AU Kraus, N
AF Kraus, Nina
TI Biological impact of music and software-based auditory training
SO JOURNAL OF COMMUNICATION DISORDERS
LA English
DT Article
DE Learning; Training; Brainstem; Communication
ID SPEECH-IN-NOISE; AUTISM SPECTRUM DISORDERS; DEVELOPMENTAL DYSLEXIA;
   EXECUTIVE FUNCTION; BACKGROUND-NOISE; NORMAL-HEARING; BRAIN; CHILDREN;
   PLASTICITY; MEMORY
AB Auditory-based communication skills are developed at a young age and are maintained throughout our lives. However, some individuals - both young and old - encounter difficulties in achieving or maintaining communication proficiency. Biological signals arising from hearing sounds relate to real-life communication skills such as listening to speech in noisy environments and reading, pointing to an intersection between hearing and cognition. Musical experience, amplification, and software-based training can improve these biological signals. These findings of biological plasticity, in a variety of subject populations, relate to attention and auditory memory, and represent an integrated auditory system influenced by both sensation and cognition.
   Learning outcomes: The reader will (1) explain that the auditory system is malleable to experience and training, (2) identify the ingredients necessary for auditory learning to successfully be applied to communication, (3) recognize that the auditory brainstem response to complex sounds (cABR) is a window into the integrated auditory system, and (4) identify examples of how cABR can be used to track the outcome of experience and training. (C) 2012 Elsevier Inc. All rights reserved.
C1 Northwestern Univ, Dept Commun Sci Neurobiol & Physiol, Evanston, IL 60208 USA.
RP Kraus, N (reprint author), Northwestern Univ, Dept Commun Sci Neurobiol & Physiol, 2240 Campus Dr, Evanston, IL 60208 USA.
EM nkraus@northwestern.edu
FU National Science Foundation [BCS-0921275, BCS-1057556]; National
   Institutes of Health [R01-DC010016]; Hugh Knowles Hearing Center; Phonak
   Corporation
FX This work was supported by grants from the National Science Foundation
   (BCS-0921275 and BCS-1057556), the National Institutes of Health
   (R01-DC010016), the Hugh Knowles Hearing Center, and the Phonak
   Corporation.
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NR 70
TC 6
Z9 6
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0021-9924
J9 J COMMUN DISORD
JI J. Commun. Disord.
PD NOV-DEC
PY 2012
VL 45
IS 6
BP 403
EP 410
DI 10.1016/j.jcomdis.2012.06.005
PG 8
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 038LK
UT WOS:000311176000003
PM 22789822
ER

PT J
AU Shield, A
   Meier, RP
AF Shield, Aaron
   Meier, Richard P.
TI Palm reversal errors in native-signing children with autism
SO JOURNAL OF COMMUNICATION DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Sign language
ID SPECTRUM DISORDERS; MOTOR IMPAIRMENT; POLYGLOT SAVANT; LANGUAGE;
   IMITATION; INDIVIDUALS; IDENTIFICATION; COMMUNICATION; CONSEQUENCES;
   DYSFUNCTION
AB Children with autism spectrum disorder (ASD) who have native exposure to a sign language such as American Sign Language (ASL) have received almost no scientific attention. This paper reports the first studies on a sample of five native-signing children (four deaf children of deaf parents and one hearing child of deaf parents; ages 4;6 to 7;5) diagnosed with ASD. A domain-general deficit in the ability of children with ASD to replicate the gestures of others is hypothesized to be a source of palm orientation reversal errors in sign. In Study 1, naturalistic language samples were collected from three native-signing children with ASD and were analyzed for errors in handshape, location, movement and palm orientation. In Study 2, four native-signing children with ASD were compared to 12 typically developing deaf children (ages 3;7 to 6;9, all born to deaf parents) on a fingerspelling task. In both studies children with ASD showed a tendency to reverse palm orientation on signs specified for inward/outward orientation. Typically developing deaf children did not produce any such errors in palm orientation. We conclude that this kind of palm reversal has a perceptual rather than a motoric source, and is further evidence of a "self-other mapping" deficit in ASD.
   Learning outcomes: Educational objectives: The reader will: (1) recognize the gesture imitation deficit in autism; (2) recall the four parameters of sign language articulation; and (3) discuss how autism affects these parameters in native-signing children. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Shield, Aaron; Meier, Richard P.] Univ Texas Austin, Dept Linguist, Austin, TX 78712 USA.
RP Shield, A (reprint author), Boston Univ, Dept Psychol, 64 Cummington Mall, Boston, MA 02215 USA.
EM ashield@bu.edu
FU Autism Speaks grant [4721]; NSF [BCS-0746009]; National Institute on
   Deafness and Other Communication Disorders of the National Institutes of
   Health [F32DC011219]
FX Funding for this research was provided by Autism Speaks grant number
   4721 to the first author and by NSF dissertation improvement grant
   BCS-0746009 to both authors. Support for this research was also provided
   by the National Institute on Deafness and Other Communication Disorders
   of the National Institutes of Health under Award Number F32DC011219. The
   content is solely the responsibility of the authors and does not
   necessarily represent the official views of the National Institutes of
   Health. The authors thank A. Rebecca Neal and Helen Tager-Flusberg for
   feedback on earlier versions of this manuscript, Lynn Hou for assistance
   with the coding of data, Annie Marks for creating and editing the sign
   photographs, Franky Ramont for serving as the model, and all of the
   parents, children, teachers, and school administrators at the Texas,
   Indiana, Ohio, and Iowa Schools for the Deaf, the Minnesota State
   Academy for the Deaf, and the Learning Center for Deaf Children.
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NR 80
TC 7
Z9 7
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0021-9924
J9 J COMMUN DISORD
JI J. Commun. Disord.
PD NOV-DEC
PY 2012
VL 45
IS 6
BP 439
EP 454
DI 10.1016/j.jcomdis.2012.08.004
PG 16
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 038LK
UT WOS:000311176000007
PM 22981637
ER

PT J
AU Dinstein, I
   Heeger, D
   Lorenzi, L
   Minshew, N
   Malach, R
   Behrmann, M
AF Dinstein, I
   Heeger, D.
   Lorenzi, L.
   Minshew, N.
   Malach, R.
   Behrmann, M.
TI Poor sensory reliability in autism
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 20th Annual Meeting of the Israel-Society-for-Neuroscience
CY DEC 11-13, 2011
CL Eilat, ISRAEL
SP Israel Soc Neurosci
C1 [Dinstein, I; Malach, R.] Weizmann Inst Sci, IL-76100 Rehovot, Israel.
   [Heeger, D.] NYU, New York, NY 10003 USA.
   [Lorenzi, L.; Behrmann, M.] Carnegie Mellon Univ, Pittsburgh, PA 15213 USA.
   [Minshew, N.] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
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
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2012
VL 48
SU 1
BP S27
EP S27
PG 1
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 030BC
UT WOS:000310541600062
ER

PT J
AU Remington, A
   Swettenham, J
   Lavie, N
AF Remington, A.
   Swettenham, J.
   Lavie, N.
TI Inattentional blindness and perceptual capacity in children with Autism
   Spectrum Disorder
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Meeting Abstract
CT 20th Annual Meeting of the Israel-Society-for-Neuroscience
CY DEC 11-13, 2011
CL Eilat, ISRAEL
SP Israel Soc Neurosci
C1 [Remington, A.; Lavie, N.] UCL, Inst Cognit Neurosci, London WC1E 6BT, England.
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
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2012
VL 48
SU 1
BP S95
EP S96
PG 2
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 030BC
UT WOS:000310541600246
ER

PT J
AU Szatmari, P
   Charman, T
   Constantino, JN
AF Szatmari, Peter
   Charman, Tony
   Constantino, John N.
TI Into, and Out of, the "Valley of Death": Research in Autism Spectrum
   Disorders
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID FRAGILE-X; CHILDREN; PATHOPHYSIOLOGY; INTERVENTIONS; TRAJECTORIES;
   TRANSITION; ADULTHOOD; ATTENTION; MODEL
C1 [Szatmari, Peter] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4K1, Canada.
   [Charman, Tony] Univ London, London WC1E 7HU, England.
   [Constantino, John N.] Washington Univ, St Louis, MO 63130 USA.
RP Szatmari, P (reprint author), McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4K1, Canada.
EM szatmar@mcmaster.ca
RI Charman, Tony/A-2085-2014
OI Charman, Tony/0000-0003-1993-6549
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NR 21
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1108
EP 1112
DI 10.1016/j.jaac.2012.08.027
PG 5
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 035IF
UT WOS:000310939300002
PM 23101736
ER

PT J
AU Bregman, JD
AF Bregman, Joel D.
TI Evidence-Based Integrated Treatment in Autism Spectrum Disorders
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Editorial Material
ID CHILDREN
C1 Ctr Autism, Philadelphia, PA 19131 USA.
RP Bregman, JD (reprint author), Ctr Autism, 3905 Ford Rd,Suite 5, Philadelphia, PA 19131 USA.
EM JBregman@thecenterforautism.org
CR Aman MG, 2009, J AM ACAD CHILD PSY, V48, P1143, DOI 10.1097/CHI.0b013e3181bfd669
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   Warren Z, 2011, COMP EFFECT REV, P26
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NR 9
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1113
EP 1115
DI 10.1016/j.jaac.2012.08.022
PG 3
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 035IF
UT WOS:000310939300003
PM 23101737
ER

PT J
AU Dawson, G
   Jones, EJH
   Merkle, K
   Venema, K
   Lowy, R
   Faja, S
   Kamara, D
   Murias, M
   Greenson, J
   Winter, J
   Smith, M
   Rogers, SJ
   Webb, SJ
AF Dawson, Geraldine
   Jones, Emily J. H.
   Merkle, Kristen
   Venema, Kaitlin
   Lowy, Rachel
   Faja, Susan
   Kamara, Dana
   Murias, Michael
   Greenson, Jessica
   Winter, Jamie
   Smith, Milani
   Rogers, Sally J.
   Webb, Sara J.
TI Early Behavioral Intervention Is Associated With Normalized Brain
   Activity in Young Children With Autism
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE autism; early behavioral intervention; Early Start Denver Model;
   event-related potentials; brain activity
ID TYPICAL DEVELOPMENT; SPECTRUM DISORDERS; INFANTS; FACE; OSCILLATIONS;
   POTENTIALS; ATTENTION; MEMORY; SYNCHRONIZATION; PERCEPTION
AB Objective: A previously published randomized clinical trial indicated that a developmental behavioral intervention, the Early Start Denver Model (ESDM), resulted in gains in IQ, language, and adaptive behavior of children with autism spectrum disorder. This report describes a secondary outcome measurement from this trial, EEG activity. Method: Forty-eight 18- to 30-month-old children with autism spectrum disorder were randomized to receive the ESDM or referral to community intervention for 2 years. After the intervention (age 48 to 77 months), EEG activity (event-related potentials and spectral power) was measured during the presentation of faces versus objects. Age-matched typical children were also assessed. Results: The ESDM group exhibited greater improvements in autism symptoms, IQ language, and adaptive and social behaviors than the community intervention group. The ESDM group and typical children showed a shorter Nc latency and increased cortical activation (decreased a power and increased 0 power) when viewing faces, whereas the community intervention group showed the opposite pattern (shorter latency event-related potential [ERP] and greater cortical activation when viewing objects). Greater cortical activation while viewing faces was associated with improved social behavior. Conclusions: This was the first trial to demonstrate that early behavioral intervention is associated with normalized patterns of brain activity, which is associated with improvements in social behavior, in young children with autism spectrum disorder. J. Am. Acad. Child Adolesc. Psychiatry; 2012; 51(11): 1150-1159. Clinical trial registration information-Early Characteristics of Autism; http://www.clinicaltrials.gov; NCT00090415.
C1 [Dawson, Geraldine] Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA.
   [Jones, Emily J. H.; Venema, Kaitlin; Lowy, Rachel; Faja, Susan; Kamara, Dana; Murias, Michael; Greenson, Jessica; Winter, Jamie; Smith, Milani; Webb, Sara J.] Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA.
   [Merkle, Kristen] Vanderbilt Univ, Nashville, TN USA.
RP Dawson, G (reprint author), Univ N Carolina, Sch Med, Dept Psychiat, 4120 Bioinformat Bldg,3366, Chapel Hill, NC 27599 USA.
EM gdawson@autismspeaks.org
FU National Institute of Mental Health [U54MH066399]; Autism Speaks
FX This study was supported by grant U54MH066399 from the National
   Institute of Mental Health (G.W.), and a postdoctoral fellowship from
   Autism Speaks (E.J.H.J.).
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NR 31
TC 57
Z9 59
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1150
EP 1159
DI 10.1016/j.jaac.2012.08.018
PG 10
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 035IF
UT WOS:000310939300007
PM 23101741
ER

PT J
AU van der Meer, JMJ
   Oerlemans, AM
   van Steijn, DJ
   Lappenschaar, MGA
   de Sonneville, LMJ
   Buitelaar, JK
   Rommelse, NNJ
AF van der Meer, Jolanda M. J.
   Oerlemans, Anoek M.
   van Steijn, Daphne J.
   Lappenschaar, Martijn G. A.
   de Sonneville, Leo M. J.
   Buitelaar, Jan K.
   Rommelse, Nanda N. J.
TI Are Autism Spectrum Disorder and Attention-Deficit/Hyperactivity
   Disorder Different Manifestations of One Overarching Disorder? Cognitive
   and Symptom Evidence From a Clinical and Population-Based Sample
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE autism spectrum disorder (ASD); attention-deficit/hyperactivity disorder
   (ADHD); latent class analysis (LCA); heterogeneity; cognition
ID DEFICIT HYPERACTIVITY DISORDER; INTRAINDIVIDUAL VARIABILITY; NONVERBAL
   INFORMATION; EMOTION RECOGNITION; TWIN SAMPLE; ADHD; CHILDREN;
   PSYCHOPATHOLOGY; INHIBITION; BEHAVIOR
AB Objective: Autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD) frequently co-occur. Given the heterogeneity of both disorders, several more homogeneous ASD ADHD comorbidity subgroups may exist. The current study examined whether such subgroups exist, and whether their overlap or distinctiveness in associated comorbid symptoms and cognitive profiles gives support for a gradient overarching disorder hypothesis or a separate disorders hypothesis. Method: Latent class analysis was performed on Social Communication Questionnaire (SCQ) and Conners' Parent Rating Scale (CPRS-R:L) data for 644 children and adolescents (5 through 17 years of age). Classes were compared for comorbid symptoms and cognitive profiles of motor speed and variability, executive functioning, attention, emotion recognition, and detail-focused processing style. Results: Latent class analysis revealed five classes: two without behavioral problems, one with only ADHD behavior, and two with both clinical symptom levels of ASD and ADHD but with one domain more prominent than the other (ADHD[+ASD] and ASD[+ADHD]). In accordance with the gradient overarching disorder hypothesis were the presence of an ADHD class without ASD symptoms and the absence of an ASD class without ADHD symptoms, as well as cognitive functioning of the simple ADHD class being less impaired than that of both comorbid classes. In conflict with this hypothesis was that there was some specificity of cognitive deficits across classes. Conclusions: The overlapping cognitive deficits may be used to further unravel the shared etiological underpinnings of ASD and ADHD, and the nonoverlapping deficits may indicate why some children develop ADHD despite their enhanced risk for ASD. The two subtypes of children with both ASD and ADHD behavior will most likely benefit from different clinical approaches. J. Am. Acad. Child Adolesc. Psychiatry, 2012;51(11): 1160-1172.
C1 [van der Meer, Jolanda M. J.; Oerlemans, Anoek M.; van Steijn, Daphne J.; Buitelaar, Jan K.; Rommelse, Nanda N. J.] Univ Ctr Nijmegen, Karakter Child & Adolescent Psychiat, Nijmegen, Netherlands.
   [van der Meer, Jolanda M. J.; Oerlemans, Anoek M.; Buitelaar, Jan K.; Rommelse, Nanda N. J.] Radboud Univ Nijmegen Med Ctr, Donders Inst Brain Cognit & Behav, Nijmegen, Netherlands.
   [Lappenschaar, Martijn G. A.] Radboud Univ Nijmegen, Inst Comp & Informat Sci, Nijmegen, Netherlands.
   [de Sonneville, Leo M. J.] Leiden Univ, Leiden Inst Brain & Cognit, NL-2300 RA Leiden, Netherlands.
RP van der Meer, JMJ (reprint author), Univ Med Ctr Nijmegen, Donders Inst Brain Cognit & Behav, Reinier Postlaan 12, NL-6525 GC Nijmegen, Netherlands.
EM J.vanderMeer@psy.umcn.nl
RI Rommelse, Nanda/D-4872-2009
OI Rommelse, Nanda/0000-0002-1711-0359
FU Netherlands Organisation for Scientific Research (NWO) [91610024,
   056-13-015]; Neurotechnology Solutions Ltd.
FX This study was partly funded by the Netherlands Organisation for
   Scientific Research (NWO) by grants 91610024 (N.N.J.R.), 056-13-015
   (J.K.B.), and by Neurotechnology Solutions Ltd.
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NR 54
TC 26
Z9 26
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1160
EP 1172
DI 10.1016/j.jaac.2012.08.024
PG 13
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 035IF
UT WOS:000310939300008
PM 23101742
ER

PT J
AU Arnold, LE
   Aman, MG
   Li, XB
   Butter, E
   Humphries, K
   Scahill, L
   Lecavalier, L
   McDougle, CJ
   Swiezy, NB
   Handen, B
   Wilson, K
   Stigler, KA
AF Arnold, L. Eugene
   Aman, Michael G.
   Li, Xiaobai
   Butter, Eric
   Humphries, Kristina
   Scahill, Lawrence
   Lecavalier, Luc
   McDougle, Christopher J.
   Swiezy, Naomi B.
   Handen, Benjamin
   Wilson, Krystina
   Stigler, Kimberly A.
TI Research Units of Pediatric Psychopharmacology (RUPP) Autism Network
   Randomized Clinical Trial of Parent Training and Medication: One-Year
   Follow-Up
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE autism; antipsychotic; parent training; follow-up; clinical trial
ID PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST;
   ATTENTION-DEFICIT/HYPERACTIVITY-DISORDER; TREATMENT STRATEGIES; CHILDREN
AB Objective: To follow up on a three-site, 24-week randomized clinical trial (N = 124) comparing antipsychotic medication alone (MED) with antipsychotic medication plus parent training in the behavior management (COMB) of children with autism spectrum disorders and severe behavior problems. The COMB treatment had shown a significant advantage for child behavioral noncompliance (p = .006, d = 0.34), irritability (p = .01, d = 0.48), and hyperactivity/noncompliance (p = .04, d = 0.55) with a lower medication dose. Method: One year after each participant's termination, the authors mailed an assessment packet with a return-addressed envelope; a telephone call alerted the family. Failure to return packets within 1 month elicited another contact and offers to resend. Results: Eighty-seven of 124 families (70.2%) participated in the follow-up. The improvement difference between treatments attenuated from after treatment to follow-up for noncompliance (d = 0.32 to 0.12) and irritability (d = 0.46 to 0.03). The follow-up differences were nonsignificant (the noncompliance difference also was nonsignificant after treatment for these 87 families). Sixty-seven percent of the COMB group and 53% of the MED group were still taking risperidone, the original study medication. Most needed dose adjustments or additional medication, and the COMB group no longer had a significantly lower dose. All COMB families but only 39% of MED families reported seeking parent training after treatment. Improvements in daily living skills during treatment predicted noncompliance improvement at follow-up for the COMB children, but noncompliance deterioration and especially hyperactivity/noncompliance deterioration for the MED children. Conclusions: The study treatment experience/familiarity greatly influenced the follow-up treatment: those who had received parent training reported seeking it, whereas those who had not received it tended not to seek it. The superiority of COMB over MED after treatment attenuated by more than half at follow-up. J. Am. Acad. Child Adolesc. Psychiatry, 2012;51(11): 1173-1184.
C1 [Arnold, L. Eugene; Aman, Michael G.; Lecavalier, Luc; Wilson, Krystina] Ohio State Univ, Nisonger Ctr, Sunbury, OH 43074 USA.
   [Li, Xiaobai] Ohio State Univ, Ctr Biostat, Sunbury, OH 43074 USA.
   [Humphries, Kristina] Ohio State Univ, Clin Trials Off, Sunbury, OH 43074 USA.
   [Scahill, Lawrence] Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA.
   [McDougle, Christopher J.] Harvard Univ, Sch Med, Cambridge, MA 02138 USA.
   [McDougle, Christopher J.] Lurie Ctr Autism, Austin, TX USA.
   [Swiezy, Naomi B.; Stigler, Kimberly A.] Indiana Univ, Bloomington, IN 47405 USA.
   [Handen, Benjamin] Univ Pittsburgh, Pittsburgh, PA 15260 USA.
RP Arnold, LE (reprint author), Ohio State Univ, Nisonger Ctr, 479 S Galena Rd, Sunbury, OH 43074 USA.
EM l.arnold@osumc.edu
FU National Institute of Mental Health (NIMH) through Pediatric
   Psychopharmacology (RUPP); National Institute of Mental Health (NIMH)
   through Ohio State University [U10MH66768]; National Institute of Mental
   Health (NIMH) through Indiana University [U10MH66766]; National
   Institute of Mental Health (NIMH) through Yale University [U10MH66764];
   National Center for Research Resources [UI1RR025755]; Autism Speaks
FX The original study was supported by the National Institute of Mental
   Health (NIMH) through the following Research Units of Pediatric
   Psychopharmacology (RUPP) grants: Ohio State University, U10MH66768
   (M.G.A., PI); Indiana University, U10MH66766 (C.J.M., PI); and Yale
   University, U10MH66764 (LS., PI). It was further supported by award
   UL1RR025755 from the National Center for Research Resources. This
   follow-up study was supported by a grant from Autism Speaks (L.E.A.).
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NR 18
TC 6
Z9 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1173
EP 1184
DI 10.1016/j.jaac.2012.08.028
PG 12
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 035IF
UT WOS:000310939300009
PM 23101743
ER

PT J
AU Sullivan, PF
   Magnusson, C
   Reichenberg, A
   Boman, M
   Dalman, C
   Davidson, M
   Fruchter, E
   Hultman, CM
   Lundberg, M
   Langstrom, N
   Weiser, M
   Svensson, AC
   Lichtenstein, P
AF Sullivan, Patrick F.
   Magnusson, Cecilia
   Reichenberg, Abraham
   Boman, Marcus
   Dalman, Christina
   Davidson, Michael
   Fruchter, Eyal
   Hultman, Christina M.
   Lundberg, Michael
   Langstrom, Niklas
   Weiser, Mark
   Svensson, Anna C.
   Lichtenstein, Paul
TI Family History of Schizophrenia and Bipolar Disorder as Risk Factors for
   Autism
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID CHILDHOOD-ONSET SCHIZOPHRENIA; SPECTRUM DISORDERS;
   PSYCHIATRIC-DISORDERS; ASSOCIATION; TWIN; DUPLICATIONS; HERITABILITY;
   DIAGNOSES; 16P11.2; ILLNESS
AB Context: The clinical and etiologic relation between autism spectrum disorders (ASDs) and schizophrenia is unclear. The degree to which these disorders share a basis in etiology has important implications for clinicians, researchers, and those affected by the disorders.
   Objective: To determine whether a family history of schizophrenia and/or bipolar disorder is a risk factor for ASD.
   Design, Setting, and Participants: We conducted a case-control evaluation of histories of schizophrenia or bipolar disorder in first-degree relatives of probands in 3 samples-population registers in Sweden, Stockholm County (in Sweden), and Israel. Probands met criteria for ASD, and affection status of parents and siblings for schizophrenia and bipolar disorder were established.
   Results: The presence of schizophrenia in parents was associated with an increased risk for ASD in a Swedish national cohort (odds ratio [OR], 2.9; 95% CI, 2.5-3.4) and a Stockholm County cohort (OR, 2.9; 95% CI, 2.0-4.1). Similarly, schizophrenia in a sibling was associated with an increased risk for ASD in a Swedish national cohort (OR, 2.6; 95% CI, 2.0-3.2) and an Israeli conscription cohort (OR, 12.1; 95% CI, 4.5-32.0). Bipolar disorder showed a similar pattern of associations but of lesser magnitude.
   Conclusions: Findings from these 3 registers along with consistent findings from a similar study in Denmark suggest that ASD, schizophrenia, and bipolar disorder share common etiologic factors. Arch Gen Psychiatry. 2012; 69(11): 1099-1103. Published online July 2, 2012. doi:10.1001/archgenpsychiatry.2012.730
C1 [Sullivan, Patrick F.] Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA.
   [Sullivan, Patrick F.; Boman, Marcus; Hultman, Christina M.; Langstrom, Niklas; Lichtenstein, Paul] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Magnusson, Cecilia; Dalman, Christina; Lundberg, Michael; Svensson, Anna C.] Karolinska Inst, Dept Publ Hlth Sci, Stockholm, Sweden.
   [Reichenberg, Abraham] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
   [Davidson, Michael; Weiser, Mark] Tel Aviv Univ, IL-69978 Tel Aviv, Israel.
   [Davidson, Michael; Weiser, Mark] Chaim Sheba Med Ctr, Dept Psychiat, Tel Aviv, Israel.
   [Fruchter, Eyal] Israeli Def Force Med Corp, Dept Mental Hlth, Ramat Gan, Israel.
RP Sullivan, PF (reprint author), Univ N Carolina, Dept Genet, CB 7264, Chapel Hill, NC 27599 USA.
EM pfsulliv@med.unc.edu
FU Swedish Council for Working Life and Social Research; Swedish Research
   Council; Beatrice and Samuel A. Seaver Foundation
FX The Swedish Council for Working Life and Social Research, the Swedish
   Research Council, and the Beatrice and Samuel A. Seaver Foundation
   funded this study.
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NR 48
TC 33
Z9 34
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD NOV
PY 2012
VL 69
IS 11
BP 1099
EP 1103
DI 10.1001/archgenpsychiatry.2012.730
PG 5
WC Psychiatry
SC Psychiatry
GA 032CI
UT WOS:000310689200002
PM 22752149
ER

PT J
AU Sterzing, PR
   Shattuck, PT
   Narendorf, SC
   Wagner, M
   Cooper, BP
AF Sterzing, Paul R.
   Shattuck, Paul T.
   Narendorf, Sarah C.
   Wagner, Mary
   Cooper, Benjamin P.
TI Bullying Involvement and Autism Spectrum Disorders Prevalence and
   Correlates of Bullying Involvement Among Adolescents With an Autism
   Spectrum Disorder
SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE
LA English
DT Article
ID SPECIAL-EDUCATION; CHILDREN; VICTIMIZATION; SCHOOL; STUDENTS; YOUTH;
   DISABILITIES; EXPERIENCES; POPULATION; TRANSITION
AB Objectives: To produce nationally representative estimates for rates of bullying involvement among adolescents with an autism spectrum disorder (ASD), to compare population estimates with adolescents who have other developmental disabilities, and to identify social ecological correlates of bullying involvement.
   Design: Nationally representative surveys from 2001.
   Setting: United States.
   Participants: Parents of adolescents with an ASD, principals of the schools they attended, and staff members most familiar with their school programs.
   Main Exposure: Autism spectrum disorders.
   Main Outcome Measures: Parent report of victimization, perpetration, and victimization/perpetration within the past school year.
   Results: The prevalence rates of bullying involvement for adolescents with an ASD were 46.3% for victimization, 14.8% for perpetration, and 8.9% for victimization/perpetration. Victimization was related to having a non-Hispanic ethnicity, attention-deficit/hyperactivity disorder, lower social skills, some form of conversational ability, and more classes in general education. Correlates of perpetration included being white, having attention-deficit/hyperactivity disorder, and getting together with friends at least once a week. Victimization/perpetration was associated with being white non-Hispanic, having attention-deficit/hyperactivity disorder, and getting together with friends at least once a week.
   Conclusions: School-based bullying interventions need to target the core deficits of ASD (conversational ability and social skills) and comorbid conditions (eg, attention-deficit/hyperactivity disorder). Future bullying interventions also need to address the higher rates of victimization that occur in general education settings by increasing social integration into protective peer groups and increasing the empathy and social skills of typically developing students toward their peers with an ASD.
C1 [Sterzing, Paul R.; Shattuck, Paul T.; Narendorf, Sarah C.; Cooper, Benjamin P.] Washington Univ, George Warren Brown Sch Social Work, St Louis, MO 63130 USA.
   [Wagner, Mary] SRI Int, Menlo Pk, CA 94025 USA.
   [Narendorf, Sarah C.] Univ Houston, Grad Sch Social Work, Houston, TX 77204 USA.
RP Sterzing, PR (reprint author), Univ Calif Berkeley, Sch Social Welf, 120 Haviland Hall, Berkeley, CA 94720 USA.
EM sterzing@berkeley.edu
FU Organization for Autism Research; Autism Speaks; National Institute of
   Mental Health [R01 MH086489]
FX This study was supported by the Organization for Autism Research (Dr
   Shattuck), by Autism Speaks (Dr Shattuck), and by grant R01 MH086489
   from the National Institute of Mental Health (Dr Shattuck).
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NR 40
TC 8
Z9 8
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 1072-4710
J9 ARCH PEDIAT ADOL MED
JI Arch. Pediatr. Adolesc. Med.
PD NOV
PY 2012
VL 166
IS 11
BP 1058
EP 1064
DI 10.1001/archpediatrics.2012.790
PG 7
WC Pediatrics
SC Pediatrics
GA 032BI
UT WOS:000310686400010
PM 22945284
ER

PT J
AU Mandell, DS
   Lawer, LJ
   Branch, K
   Brodkin, ES
   Healey, K
   Witalec, R
   Johnson, DN
   Gur, RE
AF Mandell, David S.
   Lawer, Lindsay J.
   Branch, Kira
   Brodkin, Edward S.
   Healey, Kristin
   Witalec, Robert
   Johnson, Donielle N.
   Gur, Raquel E.
TI Prevalence and correlates of autism in a state psychiatric hospital
SO AUTISM
LA English
DT Article
DE autism; schizophrenia; hospitalization; adults; differential diagnosis
ID SPECTRUM DISORDERS; ASPERGER-SYNDROME; DSM-III; SCHIZOPHRENIA; CHILDREN;
   ADULTS; ADOLESCENTS; DIAGNOSIS
AB This study estimated the ASD prevalence in a psychiatric hospital and evaluated the Social Responsiveness Scale (SRS) combined with other information for differential diagnosis. Chart review, SRS and clinical interviews were collected for 141 patients at one hospital. Diagnosis was determined at case conference. Receiver operating characteristic (ROC) curves were used to evaluate the SRS as a screening instrument. Chi-squared Automatic Interaction Detector (CHAID) analysis estimated the role of other variables, in combination with the SRS, in separating cases and non-cases. Ten percent of the sample had ASD. More than other patients, their onset was prior to 12 years of age, they had gait problems and intellectual disability, and were less likely to have a history of criminal involvement or substance abuse. Sensitivity (0.86) and specificity (0.60) of the SRS were maximized at a score of 84. Adding age of onset <12 years and cigarette use among those with SRS <80 increased sensitivity to 1.00 without lowering specificity. Adding a history substance abuse among those with SRS >80 increased specificity to 0.90 but dropped sensitivity to 0.79. Undiagnosed ASD may be common in psychiatric hospitals. The SRS, combined with other information, may discriminate well between ASD and other disorders.
C1 [Mandell, David S.] Univ Penn, Sch Med, Dept Psychiat, Ctr Autism Res, Philadelphia, PA 19104 USA.
   [Johnson, Donielle N.] Univ Penn, Sch Arts & Sci, Philadelphia, PA 19104 USA.
RP Mandell, DS (reprint author), Univ Penn, Sch Med, Dept Psychiat, Ctr Autism Res, 3535 Market St,8th Floor, Philadelphia, PA 19104 USA.
EM mandelld@upenn.edu
RI Mandell, David/H-2730-2012
OI Mandell, David/0000-0001-8240-820X
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NR 43
TC 4
Z9 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 557
EP 567
DI 10.1177/1362361311412058
PG 11
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600002
PM 21846667
ER

PT J
AU Venker, CE
   McDuffie, A
   Weismer, SE
   Abbeduto, L
AF Venker, Courtney E.
   McDuffie, Andrea
   Weismer, Susan Ellis
   Abbeduto, Leonard
TI Increasing verbal responsiveness in parents of children with autism: a
   pilot study
SO AUTISM
LA English
DT Article
DE autism; caregiver responsiveness; language intervention; parent-mediated
   intervention; verbal responsiveness
ID YOUNG-CHILDREN; SPECTRUM DISORDER; CONTROLLED-TRIAL; LANGUAGE;
   COMMUNICATION; INTERVENTION; BEHAVIORS; PREDICT
AB Correlational studies have revealed a positive relationship between parent verbal responsiveness and language outcomes in children with autism. We investigated whether parents of young children on the autism spectrum could learn and implement the specific categories of verbal responsiveness that have been suggested to facilitate language development. Parents were taught to increase their verbal responsiveness in the context of a short-term language intervention that included group parent education sessions, as well as individual and small-group coaching sessions of parent-child play interactions. Parents in the treatment group increased their use of comments that: described their child's focus of attention; interpreted or expanded child communication acts; and prompted child communication. Preliminary treatment effects were also noted in children's prompted and spontaneous communication. These results support the use of parent-mediated interventions targeting verbal responsiveness to facilitate language development and communication in young children with autism.
C1 [Venker, Courtney E.; McDuffie, Andrea; Weismer, Susan Ellis; Abbeduto, Leonard] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
   [Venker, Courtney E.; Weismer, Susan Ellis] Univ Wisconsin, Dept Commun Disorders, Madison, WI 53705 USA.
   [Abbeduto, Leonard] Univ Wisconsin, Dept Educ Psychol, Madison, WI 53705 USA.
RP Venker, CE (reprint author), Univ Wisconsin, Waisman Ctr, Room 441,1500 Highland Ave, Madison, WI 53705 USA.
EM cgerickson@wisc.edu
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NR 31
TC 9
Z9 9
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 568
EP 585
DI 10.1177/1362361311413396
PG 18
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600003
PM 21846665
ER

PT J
AU Minne, EP
   Semrud-Clikeman, M
AF Minne, Elizabeth Portman
   Semrud-Clikeman, Margaret
TI A social competence intervention for young children with high
   functioning autism and Asperger syndrome: a pilot study
SO AUTISM
LA English
DT Article
DE Autism; Asperger Syndrome; Social Competence; Group Intervention
ID SKILLS
AB The key features of Asperger Syndrome (AS) and high functioning autism (HFA) include marked and sustained impairment in social interactions. A multi-session, small group program was developed to increase social perception based on the assumption perceptual or interpretive problems underlying these social difficulties. Additionally, the group format espoused a play therapy orientation and the use of sociodramatic play was the primary therapeutic modality used. Qualitative analyses of the data resulted in an explanation of the key changes in social interactions that took place through the course of the intervention. Although each participant's experience in this group was unique, all children in this program demonstrated improvements in their social interactions, as they experienced development both emotionally and behaviorally. Findings suggest that, despite their rigid interests and behavior patterns, the social limitations of these children improved when provided with the necessary environmental resources.
C1 [Semrud-Clikeman, Margaret] Univ Minnesota, Sch Med, Minneapolis, MN 55455 USA.
RP Minne, EP (reprint author), 4009 Banister Ln,Suite 368, Austin, TX 78704 USA.
EM Liz@Minne.org
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NR 26
TC 0
Z9 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 586
EP 602
DI 10.1177/1362361311423384
PG 17
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600004
PM 22087045
ER

PT J
AU Boucher, J
   Mayes, A
AF Boucher, Jill
   Mayes, Andrew
TI Memory in ASD: have we been barking up the wrong tree?
SO AUTISM
LA English
DT Article
DE autism spectrum disorder; memory; hippocampus; prefrontal cortex;
   parietal cortex; default network
ID HIGH-FUNCTIONING AUTISM; LONG-TERM-MEMORY; EPISODIC MEMORY;
   ASPERGER-SYNDROME; AUTOBIOGRAPHICAL MEMORY; DEVELOPMENTAL AMNESIA;
   RECOGNITION MEMORY; SPECTRUM DISORDER; IMPAIRED MEMORY; SEMANTIC MEMORY
AB In this theoretical note, possible neural causes of episodic memory impairment in individuals with ASD and currently normal intellectual and linguistic function are considered. The neural causes most commonly argued for are hippocampal or prefrontal cortex dysfunction, associated with impaired neural connectivity. It is argued here that a hippocampal dysfunction hypothesis is weakened by differences in cued recall and paired associate learning in individuals with ASD compared with individuals with developmental or acquired hippocampus-related amnesia, and that recent findings on patients with posterior parietal lesions (PPC) offer a better fit with the dissociation between free and cued recall observed in ASD. The PPC forms part of the default system subserving mindreading, among other functions, and an association between PPC dysfunction and memory impairment in ASD is consistent with recent suggestions that neural disconnectivity within the default system underlies behaviours diagnostic of ASD.
C1 [Boucher, Jill] City Univ London, Autism Res Grp, London EC1V 0HB, England.
   [Mayes, Andrew] Univ Manchester, Manchester M13 9PL, Lancs, England.
RP Boucher, J (reprint author), City Univ London, Autism Res Grp, Northampton Sq, London EC1V 0HB, England.
EM Jill.Boucher.1@city.ac.uk
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NR 78
TC 4
Z9 4
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 603
EP 611
DI 10.1177/1362361311417738
PG 9
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600005
PM 22332184
ER

PT J
AU Luke, L
   Clare, IC
   Ring, H
   Redley, M
   Watson, P
AF Luke, Lydia
   Clare, Isabel C. H.
   Ring, Howard
   Redley, Marcus
   Watson, Peter
TI Decision-making difficulties experienced by adults with autism spectrum
   conditions
SO AUTISM
LA English
DT Article
DE Autism spectrum conditions; decision-making; experiences; general
   decision making style
ID IOWA GAMBLING TASK; FUNCTIONING AUTISM; PREFRONTAL CORTEX; ANXIETY;
   DISORDERS; AMYGDALA; CHOICE; STYLE
AB Autobiographical and clinical accounts, as well as a limited neuropsychological research literature, suggest that, in some situations, men and women with autism spectrum conditions (ASCs) may have difficulty making decisions. Little is known, however, about how people with ASCs experience decision-making or how they might best be supported to make decisions for themselves. In this study, we compared the decision-making experiences of adults with and without ASCs (n=38 and n=40, respectively) using a novel questionnaire and the General Decision Making Style inventory (GDMS, Scott & Bruce, 1995). The participants with ASCs reported experiencing several problems in decision-making more frequently than the comparison group, and were more likely to report avoidance of decision-making, as measured using the GDMS. The findings highlight areas of potential future research and inform suggestions for supporting adults with ASCs during decision-making
C1 [Luke, Lydia] Univ Cambridge, Cambridge Intellectual & Dev Disabil Res Grp, Dept Psychiat, Cambridge CB2 8AH, England.
   [Watson, Peter] MRC, Cognit & Brain Sci Unit, Cambridge, England.
RP Luke, L (reprint author), Univ Cambridge, Cambridge Intellectual & Dev Disabil Res Grp, Dept Psychiat, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England.
EM lrl25@cantab.net
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NR 32
TC 10
Z9 10
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 612
EP 621
DI 10.1177/1362361311415876
PG 10
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600006
PM 21846664
ER

PT J
AU Falter, CM
   Bailey, AJ
AF Falter, Christine M.
   Bailey, Anthony J.
TI Perception of mirror symmetry in autism spectrum disorders
SO AUTISM
LA English
DT Article
DE autism; symmetry; Gestalt
ID ATTENTION; FORM
AB Gestalt grouping in autism spectrum disorders (ASD) is selectively impaired for certain organization principles but for not others. Symmetry is a fundamental Gestalt principle characterizing many biological shapes. Sensitivity to symmetry was tested using the Picture Symmetry Test, which requires finding symmetry lines on pictures. Individuals with ASD showed decreased sensitivity to symmetry and a correlation of test performance with performance IQ. Decreased sensitivity for symmetry in ASD is discussed in relation to reduced visual experience of faces in early development.
C1 [Falter, Christine M.] Univ Oxford, Dept Psychiat, Oxford OX3 7JX, England.
   [Bailey, Anthony J.] Univ British Columbia, Dept Psychiat, Vancouver, BC, Canada.
RP Falter, CM (reprint author), Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford OX3 7JX, England.
EM christine.falter@psych.ox.ac.uk
RI Bailey, Anthony/J-2860-2014
OI Bailey, Anthony/0000-0003-4257-972X
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NR 15
TC 2
Z9 2
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 622
EP 626
DI 10.1177/1362361311407353
PG 5
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600007
PM 21610185
ER

PT J
AU Papadopoulos, N
   McGinley, J
   Tonge, B
   Bradshaw, J
   Saunders, K
   Murphy, A
   Rinehart, N
AF Papadopoulos, Nicole
   McGinley, Jennifer
   Tonge, Bruce
   Bradshaw, John
   Saunders, Kerryn
   Murphy, Anna
   Rinehart, Nicole
TI Motor proficiency and emotional/behavioural disturbance in autism and
   Asperger's disorder: another piece of the neurological puzzle?
SO AUTISM
LA English
DT Article
DE Asperger's disorder; autism; behavioural disturbance; communication;
   emotional disturbance; motor performance
ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS;
   MOVEMENT-RELATED POTENTIALS; SPECTRUM DISORDERS; CHILDREN; IMPAIRMENT;
   COORDINATION; PERFORMANCE; CLUMSINESS; DIAGNOSIS
AB The relationship of motor proficiency with emotional/behavioural disturbance, autistic symptoms and communication disturbance was investigated in children diagnosed with autism and Asperger's disorder (AD). The Movement Assessment Battery for Children was used as a measure of motor impairment, and the Developmental Behavioural Checklist was used as a measure of emotional/behavioural disturbance in the following groups: AD (n = 22), high functioning autism (HFA) (n = 23), LFA (n = 8) and typically developing children (n = 20). The HFA group had more difficulty with motor items, such as ball skills and balance, than did the AD group. There were significant positive correlations between impairments in motor proficiency (in particular ball skills and balance) and emotional/behavioural disturbance, autistic symptoms and communication disturbance. These findings are consistent with the hypothesis that there are qualitative and quantitative differences in the motor profile between autism and AD. In addition, the association between motor proficiency impairment and emotional/behavioural disturbance in autism and AD emphasizes the importance for screening of co-occurring emotional/behavioural symptoms in individuals with motor difficulties. These findings have implications for the potential use of adjunct motor measures in the diagnosis and definition of autism spectrum disorders.
C1 [Papadopoulos, Nicole; Bradshaw, John; Rinehart, Nicole] Monash Univ, Sch Psychol & Psychiat, Ctr Dev Psychiat & Psychol, Clayton, Vic 3800, Australia.
   [McGinley, Jennifer] Univ Melbourne, Cheltenham, Vic, Australia.
   [Murphy, Anna] So Hlth, Clin Res Ctr Movement Disorders & Gait, Kingston Ctr, Cheltenham, Vic, Australia.
   [Tonge, Bruce] Monash Med Ctr, Sch Psychol & Psychiat, Ctr Dev Psychiat & Psychol, Clayton, Vic, Australia.
   [Saunders, Kerryn] Monash Univ, Dept Med Nursing & Hlth Sci, Monash Med Ctr, Clayton, Vic 3800, Australia.
RP Papadopoulos, N (reprint author), Monash Univ, Sch Psychol & Psychiat, Ctr Dev Psychiat & Psychol, Clayton, Vic 3800, Australia.
EM Nicole.Papadopoulos@monash.edu
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NR 50
TC 7
Z9 7
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 627
EP 640
DI 10.1177/1362361311418692
PG 14
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600008
PM 21949004
ER

PT J
AU Hudenko, WJ
   Magenheimer, MA
AF Hudenko, William J.
   Magenheimer, Michael A.
TI Listeners prefer the laughs of children with autism to those of
   typically developing children
SO AUTISM
LA English
DT Article
DE affect; autism; emotion; laughs; laughter; perception
ID HIGH-FUNCTIONING CHILDREN; DOWN-SYNDROME; SPECTRUM DISORDERS; FACIAL
   EXPRESSIONS; PARENTS; MOTHERS; STRESS; RECOGNITION; VOLUNTARY; ATTENTION
AB The purpose of this study was to investigate the impact of laugh sounds produced by 8-to 10-year-old children with and without autism on naive listeners, and to evaluate if listeners could distinguish between the laughs of the two groups. Results showed that listeners rated the laughs of children with autism more positively than the laughs of typically developing children, and that they were slightly above chance levels at judging which group produced the laugh. A subset of participants who reported listening for "uncontrolled" or "longer" laughs were significantly better at discriminating between the laughs of the two groups. Our results suggest that the laughs of children with autism have the potential to promote the formation of relationships.
C1 [Hudenko, William J.] Ithaca Coll, Dept Psychol, Ithaca, NY 14850 USA.
RP Hudenko, WJ (reprint author), Ithaca Coll, Dept Psychol, 953 Danby Rd, Ithaca, NY 14850 USA.
EM whudenko@ithaca.edu
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NR 55
TC 1
Z9 1
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1362-3613
J9 AUTISM
JI Autism
PD NOV
PY 2012
VL 16
IS 6
BP 641
EP 655
DI 10.1177/1362361311402856
PG 15
WC Psychology, Developmental
SC Psychology
GA 032SY
UT WOS:000310740600009
PM 21810911
ER

PT J
AU Wentz, E
   Nyden, A
   Krevers, B
AF Wentz, Elisabet
   Nyden, A.
   Krevers, B.
TI Development of an internet-based support and coaching model for
   adolescents and young adults with ADHD and autism spectrum disorders: a
   pilot study
SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorder; ADHD; Internet-based support; Coaching;
   Intervention; Self-esteem
ID DEFICIT-HYPERACTIVITY DISORDER; QUALITY-OF-LIFE;
   ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; MANCHESTER SHORT ASSESSMENT;
   REHABILITATION PROCESS; DEPRESSION SCALE; SOCIAL SKILLS; COHERENCE;
   SYMPTOMS; CHILDREN
AB The aims of this paper were to develop an internet-based support and coaching model for young people with autism spectrum disorder (ASD) and/or attention-deficit/hyperactivity disorder (ADHD), and to validate the model. A user-centred design was applied to develop a model for internet-based support and coaching, where individuals received 8-week support via internet (chat). The model was validated by 10 individuals, 15-26 years of age, with ASD and/or ADHD. Self-report questionnaires [Sense of Coherence (SOC), the Rosenberg Self Esteem Scale, the Manchester Short Assessment of Quality of Life, Montgomery sberg Depression Rating Scale, and the Hospital Anxiety and Depression Scale] were distributed before and after intervention. A structured interview regarding the quality of the model, the Patient perspective of Care and Rehabilitation process (POCR), was used after the intervention. The validation showed significant improvement of SOC, self-esteem and subjective Quality of Life at follow-up and the majority perceived high fulfilment/importance on the POCR. In conclusion, The model can be an important complement to other interventions for young people with ASD and/or ADHD.
C1 [Wentz, Elisabet; Nyden, A.] Univ Gothenburg, Gillberg Neuropsychiat Ctr, Inst Neurosci & Physiol, S-41119 Gothenburg, Sweden.
   [Wentz, Elisabet; Krevers, B.] Swedish Inst Hlth Sci, Vardal Inst, Lund, Sweden.
   [Krevers, B.] Linkoping Univ, Fac Hlth Sci, Dept Med & Hlth Sci, Linkoping, Sweden.
RP Wentz, E (reprint author), Univ Gothenburg, Gillberg Neuropsychiat Ctr, Inst Neurosci & Physiol, Kungsgatan 12, S-41119 Gothenburg, Sweden.
EM elisabet.wentz@vgregion.se
FU Vardal Institute; Swedish Institute for Health Sciences; ALF; Wilhelm
   and Martina Lundgren foundation; Vinnvard
FX The authors gratefully acknowledge the young adults who participated. We
   also like to thank the coaches Lena Niklasson, Louise Hakenas-Plate, Eva
   Billstedt and Marie Lindstrom, and the coordinator Helena
   Osmar-Swerkersdotter. We are grateful to Mikael Elf for conducting the
   POCR interviews. This work was supported by The Vardal Institute, the
   Swedish Institute for Health Sciences, government grants under the ALF
   agreement, the Wilhelm and Martina Lundgren foundation and Vinnvard.
   Parts of the manuscript have been presented at The IX International
   Congress Autism Europe, Catania 2010.
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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 1018-8827
J9 EUR CHILD ADOLES PSY
JI Eur. Child Adolesc. Psych.
PD NOV
PY 2012
VL 21
IS 11
BP 611
EP 622
DI 10.1007/s00787-012-0297-2
PG 12
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 034RR
UT WOS:000310891100003
PM 22736195
ER

PT J
AU Daily, J
   Smith, AG
   Weeber, EJ
AF Daily, Jennifer
   Smith, Amanda G.
   Weeber, Edwin J.
TI Spatial and temporal silencing of the human maternal UBE3A gene
SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY
LA English
DT Article
DE Angelman syndrome; UBE3A; E6-AP; Mouse model; Post-mortem
ID UBIQUITIN-PROTEIN LIGASE; ANGELMAN-SYNDROME; MOUSE MODEL; PRADER-WILLI;
   AUTISM; SUSCEPTIBILITY; IDENTIFICATION; CHROMOSOME-15; DUPLICATION;
   EXPRESSION
AB Angelman syndrome (AS) is characterized by severe cognitive disruption, seizures, difficulty speaking and ataxia. Nearly all cases are attributed to the disruption or absence of the imprinted maternal copy of UBE3A, transcribing an E3-type ubiquitin ligase. Much of what is known about the molecular and biochemical changes in the CNS associated with AS has been obtained through this murine model. This widely used mouse model created by a null mutation of the maternal UBE3A gene recapitulates the major phenotypes characteristic of AS patients. The imprinting of maternal UBE3A was originally believed to be brain region specific; however recent reports using the AS mouse model have revealed a more widespread absence of the protein. The present study is the first to determine that the Ube3a protein ablation seen in the AS mouse model is also characteristic of AS patients and the silencing of the paternal UBE3A allele appears to be lifelong. (C) 2012 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.
C1 [Daily, Jennifer; Weeber, Edwin J.] Univ S Florida, Dept Mol Pharmacol & Physiol, Tampa, FL USA.
   [Daily, Jennifer; Smith, Amanda G.; Weeber, Edwin J.] Univ S Florida, USF Hlth Byrd Alzheimers Inst, Tampa, FL USA.
RP Weeber, EJ (reprint author), 12901 Bruce B Downs Blvd,MDC 36, Tampa, FL 33612 USA.
EM eweeber@health.usf.edu
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NR 27
TC 2
Z9 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1090-3798
J9 EUR J PAEDIATR NEURO
JI Eur. J. Paediatr. Neurol.
PD NOV
PY 2012
VL 16
IS 6
BP 587
EP 591
DI 10.1016/j.ejpn.2012.03.006
PG 5
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 034HF
UT WOS:000310862800004
PM 22560727
ER

PT J
AU Isaksen, J
   Diseth, TH
   Schjolberg, S
   Skjeldal, OH
AF Isaksen, Jorn
   Diseth, Trond H.
   Schjolberg, Synnve
   Skjeldal, Ola H.
TI Observed prevalence of autism spectrum disorders in two Norwegian
   counties
SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY
LA English
DT Article
DE Autism; Autism spectrum disorder; Prevalence; Multi method approach
ID PERVASIVE DEVELOPMENTAL DISORDERS; SCREENING QUESTIONNAIRE; TOTAL
   POPULATION; EPIDEMIOLOGY; CHILDREN
AB Background: The prevalence of autism spectrum disorders (ASD) has previously been reported to be increasing dramatically in European and non-European countries. No similar increase in prevalence rates has been documented in Norway to date. The current study reports on ASD prevalence rates in two Norwegian counties.
   Methods: The population comprised 31 015 children, ages six to 12. Information about special needs services was provided by the school authorities and the public health service. Multiple search strategies were applied to identify children at risk of ASD or diagnosed with ASD. Hospital registers were searched and a mapping tool was used in all local schools.
   Results: The total number of patients with ASD found in the population was 158. This gives a prevalence of 51 per 10 000 (95% CI, 0.43-0.59).
   Conclusion: Compared with the previously reported prevalence of ASD in Norway, there has been almost a fourfold increase in the occurrence of childhood autism and a tenfold increase in the occurrence of all ASD groups. These findings have significant implications for designing and dimensioning appropriate intervention programmes for children with ASD and their families. (C) 2012 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.
C1 [Isaksen, Jorn] Innlandet Hosp Trust, Dept Habilitat, N-2609 Lillehammer, Norway.
   [Diseth, Trond H.] Oslo Univ Hosp, Dept Clin Neurosci & Children, Women & Childrens Div, Oslo, Norway.
   [Schjolberg, Synnve] Norwegian Inst Publ Hlth, Div Mental Hlth, Oslo, Norway.
   [Skjeldal, Ola H.] Vestre Viken Hosp Trust, Women & Childrens Clin, Drammen, Norway.
   [Diseth, Trond H.] Univ Oslo, N-0316 Oslo, Norway.
RP Isaksen, J (reprint author), Innlandet Hosp Trust, Dept Habilitat, Maihaugveien 4, N-2609 Lillehammer, Norway.
EM jorn.isaksen@sykehuset-innlandet.no
FU Innlandet Hospital Trust research foundation; Oslo University Hospital -
   Regional academic community for autism
FX The authors gratefully acknowledge the assistance of paediatricians Dr.
   Vesna Bryn and Dr. Pernille Tryli, research nurses Janne Fossnes and,
   Bente Grondalen and Romain Mertz, and the rest of the diagnostic teams
   at CHS's at Ottestad and Lillehammer. This study was supported by
   Innlandet Hospital Trust research foundation and Oslo University
   Hospital - Regional academic community for autism.
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NR 32
TC 7
Z9 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1090-3798
J9 EUR J PAEDIATR NEURO
JI Eur. J. Paediatr. Neurol.
PD NOV
PY 2012
VL 16
IS 6
BP 592
EP 598
DI 10.1016/j.ejpn.2012.01.014
PG 7
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 034HF
UT WOS:000310862800005
PM 22342070
ER

PT J
AU Laffin, JJS
   Raca, G
   Jackson, CA
   Strand, EA
   Jakielski, KJ
   Shriberg, LD
AF Laffin, Jennifer J. S.
   Raca, Gordana
   Jackson, Craig A.
   Strand, Edythe A.
   Jakielski, Kathy J.
   Shriberg, Lawrence D.
TI Novel candidate genes and regions for childhood apraxia of speech
   identified by array comparative genomic hybridization
SO GENETICS IN MEDICINE
LA English
DT Article
DE 16p11.2; apraxia; dyspraxia; FOXP2; speech disorder
ID LANGUAGE IMPAIRMENT; DISORDERS; FOXP2; AUTISM; DELETION; 7Q31;
   TRANSLOCATION; LOCALIZATION; PHENOTYPE; DYSPRAXIA
AB Purpose: The goal of this study was to identify new candidate genes and genomic copy-number variations associated with a rare, severe, and persistent speech disorder termed childhood apraxia of speech. Childhood apraxia of speech is the speech disorder segregating with a mutation in FOXP2 in a multigenerational London pedigree widely studied for its role in the development of speech-language in humans.
   Methods: A total of 24 participants who were suspected to have childhood apraxia of speech were assessed using a comprehensive protocol that samples speech in challenging contexts. All participants met clinical-research criteria for childhood apraxia of speech. Array comparative genomic hybridization analyses were completed using a customized 385K Nimblegen array (Roche Nimblegen, Madison, WI) with increased coverage of genes and regions previously associated with childhood apraxia of speech.
   Results: A total of 16 copy-number variations with potential consequences for speech-language development were detected in 12 or half of the 24 participants. The copy-number variations occurred on 10 chromosomes, 3 of which had two to four candidate regions. Several participants were identified with copy-number variations in two to three regions. In addition, one participant had a heterozygous FOXP2 mutation and a copy-number variation on chromosome 2, and one participant had a 16p11.2 microdeletion and copy-number variations on chromosomes 13 and 14.
   Conclusion: Findings support the likelihood of heterogeneous genomic pathways associated with childhood apraxia of speech.
C1 [Laffin, Jennifer J. S.; Jackson, Craig A.; Shriberg, Lawrence D.] Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA.
   [Raca, Gordana] Univ Chicago, Chicago, IL 60637 USA.
   [Strand, Edythe A.] Mayo Clin, Rochester, MN USA.
   [Jakielski, Kathy J.] Augustana Coll, Rock Isl, IL 61201 USA.
   [Shriberg, Lawrence D.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
RP Shriberg, LD (reprint author), Univ Wisconsin, Wisconsin State Lab Hyg, Madison, WI 53706 USA.
EM shriberg@waisman.wisc.edu
RI Jackson, Craig/K-6908-2014
OI Jackson, Craig/0000-0003-4023-0276
FU National Institute on Deafness and Other Communicative Disorders
   [DC000496]; National Institute of Health and Development [HD03352]
FX This work was supported by a grant from the National Institute on
   Deafness and Other Communicative Disorders (DC000496) to L. D. S. and a
   core grant from the National Institute of Health and Development
   (HD03352) to the Waisman Center. We thank each of the participants and
   their families and Leah Frater-Rubsam, Sheryl Hall, Heather Karlsson,
   Heather Lohmeier, Maureen McCormack, Jane McSweeny, Christie Tilkens,
   and the University of Wisconsin Biotechnology Sequencing Center for
   their contributions to this research.
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NR 46
TC 10
Z9 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD NOV
PY 2012
VL 14
IS 11
BP 928
EP 936
DI 10.1038/gim.2012.72
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 033ZQ
UT WOS:000310840300006
PM 22766611
ER

PT J
AU Brock, ME
   Freuler, A
   Baranek, GT
   Watson, LR
   Poe, MD
   Sabatino, A
AF Brock, M. E.
   Freuler, A.
   Baranek, G. T.
   Watson, L. R.
   Poe, M. D.
   Sabatino, A.
TI Temperament and Sensory Features of Children with Autism
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Developmental delay; Temperament; Sensory processing and
   reactivity
ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; YOUNG-CHILDREN;
   SPECTRUM DISORDERS; EXPERIENCES QUESTIONNAIRE; REPETITIVE BEHAVIORS;
   TYPICAL DEVELOPMENT; OVER-RESPONSIVITY; TODDLERS; AMYGDALA
AB This study sought to characterize temperament traits in a sample of children with autism spectrum disorder (ASD), ages 3-7 years old, and to determine the potential association between temperament and sensory features in ASD. Individual differences in sensory processing may form the basis for aspects of temperament and personality, and aberrations in sensory processing may inform why some temperamental traits are characteristic of specific clinical populations. Nine dimensions of temperament from the Behavioral Style Questionnaire (McDevitt and Carey in Manual for the behavioral style questionnaire, Behavioral-Developmental Initiatives, Scottsdale, AZ, 1996) were compared among groups of children with ASD (n = 54), developmentally delayed (DD; n = 33), and the original normative sample of typically developing children (McDevitt and Carey in J Child Psychol Psychiatr 19(3):245-253, 1978; n = 350) using an ANOVA to determine the extent to which groups differed in their temperament profiles. The hypothesized overlap between three sensory constructs (hyperresponsiveness, hyporesponsivness, and seeking) and the nine dimensions of temperament was analyzed in children with ASD using regression analyses. The ASD group displayed temperament scores distinct from norms for typically developing children on most dimensions of temperament (activity, rhythmicity, adaptability, approach, distractibility, intensity, persistence, and threshold) but differed from the DD group on only two dimensions (approach and distractibility). Analyses of associations between sensory constructs and temperament dimensions found that sensory hyporesponsiveness was associated with slowness to adapt, low reactivity, and low distractibility; a combination of increased sensory features (across all three patterns) was associated with increased withdrawal and more negative mood. Although most dimensions of temperament distinguished children with ASD as a group, not all dimensions appear equally associated with sensory response patterns. Shared mechanisms underlying sensory responsiveness, temperament, and social withdrawal may be fruitful to explore in future studies.
C1 [Brock, M. E.] Vanderbilt Univ, Nashville, TN 37203 USA.
   [Brock, M. E.; Poe, M. D.] Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC USA.
   [Freuler, A.; Baranek, G. T.] Univ N Carolina, Dept Allied Hlth Sci, Div Occupat Sci, Chapel Hill, NC 27599 USA.
   [Watson, L. R.] Univ N Carolina, Dept Allied Hlth Sci, Div Speech & Hearing Sci, Chapel Hill, NC 27599 USA.
   [Sabatino, A.] Univ N Carolina, Dept Psychol, Chapel Hill, NC USA.
RP Brock, ME (reprint author), Vanderbilt Univ, 230 Appleton Pl,Peabody Box 228, Nashville, TN 37203 USA.
EM matthew.e.brock@vanderbilt.edu
RI Poe, Michele/K-6615-2012
OI Poe, Michele/0000-0001-9693-3638
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NR 73
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2271
EP 2284
DI 10.1007/s10803-012-1472-5
PG 14
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600001
PM 22366913
ER

PT J
AU Gadow, KD
   DeVincent, CJ
AF Gadow, Kenneth D.
   DeVincent, Carla J.
TI Comparison of Children with Autism Spectrum Disorder with and Without
   Schizophrenia Spectrum Traits: Gender, Season of Birth, and Mental
   Health Risk Factors
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Schizophrenia spectrum disorder; Season of
   birth; Gender
ID PERVASIVE DEVELOPMENTAL DISORDERS; OPPOSITIONAL DEFIANT DISORDER;
   CHILDHOOD-ONSET SCHIZOPHRENIA; PSYCHIATRIC-DISORDERS; SYMPTOM
   INVENTORY-4; POSITIVE SCHIZOTYPY; SCORING ALGORITHMS; PSYCHOTIC
   SYMPTOMS; CLINICAL UTILITY; SEX-DIFFERENCES
AB Children with autism spectrum disorder (ASD) with and without co-occurring schizophrenia spectrum traits (SST) were examined for differences in co-occurring psychiatric symptoms, background characteristics, and mental health risk factors. Participating mothers and teachers completed a DSM-IV-referenced rating scale and a background questionnaire (mothers only) describing 147 children (6-12 years) with ASD. There was a clear pattern of group differences in co-occurring psychiatric symptom severity (+SST > SST-) and background characteristics. Children with impairing SST had more mental health risk factors. Girls were more likely to be classified SST according to mothers' ratings. Children born in spring-summer were more likely to be classified non-SST by teachers' ratings. Findings provide tentative evidence that SST may be a useful marker of behavioral heterogeneity within the ASD clinical phenotype.
C1 [Gadow, Kenneth D.] SUNY Stony Brook, Cody Ctr Autism & Dev Disabil Pediat, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
   [DeVincent, Carla J.] SUNY Stony Brook, Dept Radiol, Stony Brook, NY 11794 USA.
RP Gadow, KD (reprint author), SUNY Stony Brook, Cody Ctr Autism & Dev Disabil Pediat, Dept Psychiat & Behav Sci, Putnam Hall,South Campus, Stony Brook, NY 11794 USA.
EM kenneth.gadow@stonybrook.edu
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NR 99
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2285
EP 2296
DI 10.1007/s10803-012-1473-4
PG 12
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600002
PM 22361923
ER

PT J
AU Morsanyi, K
   Handley, SJ
AF Morsanyi, Kinga
   Handley, Simon J.
TI Reasoning on the Basis of Fantasy Content: Two Studies with
   High-Functioning Autistic Adolescents
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Cognitive development; Developmental disorders; Executive
   functioning; Fantasy context; Syllogistic reasoning
ID TYPICALLY DEVELOPING-CHILDREN; ASPERGER-SYNDROME; WORKING-MEMORY; FALSE
   PREMISES; SPECTRUM DISORDERS; CENTRAL COHERENCE; MIND; RETRIEVAL;
   ABILITY; ADULTS
AB Reasoning about problems with empirically false content can be hard, as the inferences that people draw are heavily influenced by their background knowledge. However, presenting empirically false premises in a fantasy context helps children and adolescents to disregard their beliefs, and to reason on the basis of the premises. The aim of the present experiments was to see if high-functioning adolescents with autism are able to utilize fantasy context to the same extent as typically developing adolescents when they reason about empirically false premises. The results indicate that problems with engaging in pretence in autism persist into adolescence, and this hinders the ability of autistic individuals to disregard their beliefs when empirical knowledge is irrelevant.
C1 [Morsanyi, Kinga] Univ Cambridge, Dept Expt Psychol, Ctr Neurosci Educ, Cambridge CB2 3EB, England.
   [Handley, Simon J.] Univ Plymouth, Sch Psychol, Plymouth PL4 8AA, Devon, England.
RP Morsanyi, K (reprint author), Univ Cambridge, Dept Expt Psychol, Ctr Neurosci Educ, Downing St, Cambridge CB2 3EB, England.
EM km574@cam.ac.uk
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NR 66
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2297
EP 2311
DI 10.1007/s10803-012-1477-0
PG 15
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600003
PM 22391809
ER

PT J
AU Frazier, TW
   Keshavan, MS
   Minshew, NJ
   Hardan, AY
AF Frazier, Thomas W.
   Keshavan, Matcheri S.
   Minshew, Nancy J.
   Hardan, Antonio Y.
TI A Two-Year Longitudinal MRI Study of the Corpus Callosum in Autism
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Magnetic resonance imaging; Autism; Corpus callosum; Rostral body
ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; WHITE-MATTER; FOLLOW-UP;
   EXECUTIVE FUNCTION; INTENTIONAL ATTUNEMENT; AMYGDALA VOLUME; BRAIN
   VOLUME; CHILDREN; SIZE
AB A growing body of literature has identified size reductions of the corpus callosum (CC) in autism. However, to our knowledge, no published studies have reported on the growth of CC volumes in youth with autism. Volumes of the total CC and its sub-divisions were obtained from 23 male children with autism and 23 age- and gender-matched controls at baseline and 2-year follow-up. Persistent reductions in total CC volume were observed in participants with autism relative to controls. Only the rostral body subdivision showed a normalization of size over time. Persistent reductions are consistent with the diagnostic stability and life-long impairment observed in many individuals with autism. Multi-modal imaging studies are needed to identify specific fiber tracks contributing to CC reductions.
C1 [Frazier, Thomas W.] Cleveland Clin, Ctr Autism & Pediat Behav Hlth CRS10, Cleveland, OH 44104 USA.
   [Keshavan, Matcheri S.] Harvard Univ, Sch Med, Dept Psychiat, Beth Israel & Deaconess Med Ctr, Boston, MA 02115 USA.
   [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Pittsburgh, PA USA.
   [Hardan, Antonio Y.] Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
RP Frazier, TW (reprint author), Cleveland Clin, Ctr Autism & Pediat Behav Hlth CRS10, 2801 Martin Luther King Jr Dr, Cleveland, OH 44104 USA.
EM fraziet2@ccf.org
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NR 76
TC 13
Z9 13
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2312
EP 2322
DI 10.1007/s10803-012-1478-z
PG 11
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600004
PM 22350341
ER

PT J
AU McCanlies, EC
   Fekedulegn, D
   Mnatsakanova, A
   Burchfiel, CM
   Sanderson, WT
   Charles, LE
   Hertz-Picciotto, I
AF McCanlies, Erin C.
   Fekedulegn, Desta
   Mnatsakanova, Anna
   Burchfiel, Cecil M.
   Sanderson, Wayne T.
   Charles, Luenda E.
   Hertz-Picciotto, Irva
TI Parental Occupational Exposures and Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Autism spectrum disorder; Parental exposures; Parent;
   Occupation; Exposure
ID HAZARDOUS AIR-POLLUTANTS; ORGANIC-SOLVENT EXPOSURE; INCREASED
   PREVALENCE; PERINATAL FACTORS; DIAGNOSTIC CHANGE; POPULATION; CHILDREN;
   OUTCOMES; EPIDEMIOLOGY; METAANALYSIS
AB Both self-report and industrial hygienist (IH) assessed parental occupational information were used in this pilot study in which 174 families (93 children with ASD and 81 unaffected children) enrolled in the Childhood Autism Risks from Genetics and Environment study participated. IH results indicated exposures to lacquer, varnish, and xylene occurred more often in the parents of children with ASD compared to the parents of unaffected children. Parents of children with ASD were more likely to report exposures to asphalt and solvents compared to parents of unaffected children. This study was limited by the small sample size, but results suggest that workplace exposures to some chemicals may be important in the etiology of ASD and deserve further investigation.
C1 [McCanlies, Erin C.; Fekedulegn, Desta; Mnatsakanova, Anna; Burchfiel, Cecil M.; Charles, Luenda E.] NIOSH, Morgantown, WV 26505 USA.
   [Sanderson, Wayne T.] Univ Kentucky, Coll Publ Hlth, Lexington, KY 40536 USA.
   [Hertz-Picciotto, Irva] Univ Calif Davis, Davis, CA 95616 USA.
RP McCanlies, EC (reprint author), NIOSH, MS L4050,1095 Willowdale Rd, Morgantown, WV 26505 USA.
EM Eim4@cdc.gov
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NR 52
TC 11
Z9 11
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2323
EP 2334
DI 10.1007/s10803-012-1468-1
PG 12
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600005
PM 22399411
ER

PT J
AU John, A
   Morris, AS
   Halliburton, AL
AF John, Aesha
   Morris, Amanda Sheffield
   Halliburton, Amy L.
TI Looking beyond Maternal Sensitivity: Mother-Child Correlates of
   Attachment Security among Children with Intellectual Disabilities in
   Urban India
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Intellectual disability; Attachment security; India; Emotional
   availability; Mother-child interaction; Child functioning
ID AUTISM SPECTRUM DISORDER; DOWN-SYNDROME; EMOTIONAL AVAILABILITY;
   MENTAL-RETARDATION; STRANGE SITUATION; DEVELOPMENTAL DISORDERS;
   INCLUSIVE EDUCATION; INFANT ATTACHMENT; YOUNG-CHILDREN; BEHAVIOR
AB This study examined correlates of attachment security among children with intellectual disabilities in urban India. Survey and observational data were gathered from 47 children, mothers, and teachers on children's attachment security, adaptive functioning, and mother-child emotional availability. The data were analyzed to examine whether child emotional availability mediates the links between maternal emotional availability and child attachment security, and between child functioning and attachment security. The results supported full mediation, indicating that children's emotional availability was a primary mechanism through which maternal emotional availability and child functioning were linked to attachment security among children in our sample. The study findings are discussed in the context of implications for family interventions and research on socio-emotional development among children with intellectual disabilities.
C1 [John, Aesha] Pittsburg State Univ, Dept Hist Philosophy & Social Sci, Pittsburg, KS 66762 USA.
   [Morris, Amanda Sheffield; Halliburton, Amy L.] Oklahoma State Univ, Dept Human Dev & Family Sci, Tulsa, OK 74106 USA.
RP John, A (reprint author), Pittsburg State Univ, Dept Hist Philosophy & Social Sci, Russ Hall 323, Pittsburg, KS 66762 USA.
EM ajohn@pittstate.edu
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NR 65
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2335
EP 2345
DI 10.1007/s10803-012-1479-y
PG 11
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600006
PM 22371146
ER

PT J
AU Bishop, SL
   Seltzer, MM
AF Bishop, Somer L.
   Seltzer, Marsha Mailick
TI Self-Reported Autism Symptoms in Adults with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum quotient; Adults; Assessment; Self-report
ID PERVASIVE DEVELOPMENTAL DISORDERS; QUOTIENT AQ; PHENOTYPE; INDIVIDUALS;
   POPULATION; VALIDITY; VERSION; ADOLESCENCE; RELIABILITY; IMPAIRMENT
AB Scores on the autism spectrum quotient (AQ) were examined in 65 adults with ASD. Maternal reports of symptoms were collected simultaneously using the autism diagnostic interview-revised (ADI-R) and the Vineland Screener. A slightly revised AQ administration procedure was used to accommodate adults with below average IQ. AQ scores were lower than in the original validation study, with only 11 adults (17%) scoring above the proposed diagnostic cut-off and 24 (27%) exceeding the screening cut-off. Adults with higher IQs endorsed more symptoms than those with below average intelligence, but even when analyses were restricted to the 39 adults with at least average IQ, only 44% met the screening cut-off. AQ scores were not significantly correlated with ADI-R or Vineland scores.
C1 [Bishop, Somer L.] Cincinnati Childrens Hosp Med Ctr, Div Dev & Behav Pediat, Cincinnati, OH 45229 USA.
   [Seltzer, Marsha Mailick] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
RP Bishop, SL (reprint author), Cincinnati Childrens Hosp Med Ctr, Div Dev & Behav Pediat, MLC 4002, Cincinnati, OH 45229 USA.
EM somer.bishop@cchmc.org
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   Taylor JL, 2010, J AUTISM DEV DISORD, V40, P1431, DOI 10.1007/s10803-010-1005-z
   Wakabayashi A, 2006, PERS INDIV DIFFER, V41, P873, DOI 10.1016/j.paid.2006.04.003
   Wakabayashi Akio, 2004, Shinrigaku Kenkyu, V75, P78
   Wheelwright S, 2010, MOL AUTISM, V1, DOI 10.1186/2040-2392-1-10
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   Woodbury-Smith MR, 2005, J AUTISM DEV DISORD, V35, P331, DOI 10.1007/s10803-005-3300-7
NR 37
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2354
EP 2363
DI 10.1007/s10803-012-1483-2
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600008
PM 22361924
ER

PT J
AU Mechling, LC
   Ayres, KM
AF Mechling, Linda C.
   Ayres, Kevin M.
TI A Comparative Study: Completion of Fine Motor Office Related Tasks by
   High School Students with Autism Using Video Models on Large and Small
   Screen Sizes
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Personal digital assistant; Video modeling; Autism; Screen size
   comparison
ID MODERATE INTELLECTUAL DISABILITIES; GENERAL-EDUCATION CLASSROOM;
   PERSONAL DIGITAL ASSISTANT; COMPUTER; PROMPTS; PEOPLE; SYSTEM; IPOD
AB The purpose of this investigation was to compare fine motor task completion when using video models presented on a smaller screen size (Personal Digital Assistant) compared to a larger laptop screen size. The investigation included four high school students with autism spectrum disorders and mild to moderate intellectual disabilities and used an adapted alternating treatments design with baseline, extended baseline, comparison, and final treatment conditions. Results showed that although independent completion of fine motor office related tasks increased under both procedures, use of video models on the larger screen resulted in a higher percentage of correct responses across all four students.
C1 [Mechling, Linda C.] Univ N Carolina, Dept Early Childhood & Special Educ, 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 22
TC 3
Z9 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2364
EP 2373
DI 10.1007/s10803-012-1484-1
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600009
PM 22354709
ER

PT J
AU Storch, EA
   Wood, JJ
   Ehrenreich-May, J
   Jones, AM
   Park, JM
   Lewin, AB
   Murphy, TK
AF Storch, Eric A.
   Wood, Jeffrey J.
   Ehrenreich-May, Jill
   Jones, Anna M.
   Park, Jennifer M.
   Lewin, Adam B.
   Murphy, Tanya K.
TI Convergent and Discriminant Validity and Reliability of the Pediatric
   Anxiety Rating Scale in Youth with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorders; Anxiety; Children; Pediatric Anxiety Rating
   Scale; Validity; Reliability
ID PERVASIVE DEVELOPMENTAL DISORDERS; COGNITIVE-BEHAVIORAL THERAPY;
   CONTROLLED-TRIAL; PSYCHIATRIC-DISORDERS; ASPERGER-SYNDROME; CHILDREN;
   SYMPTOMS; ADOLESCENTS; PREVALENCE; SERTRALINE
AB The psychometric properties of the Pediatric Anxiety Rating Scale (PARS), a clinician-administered measure for assessing severity of anxiety symptoms, were examined in 72 children and adolescents diagnosed with an autism spectrum disorder (ASD). The internal consistency of the PARS was 0.59, suggesting that the items were related but not repetitive. The PARS showed high 26-day test-retest (ICC = 0.83) and inter-rater reliability (ICC = 0.86). The PARS was strongly correlated with clinician-ratings of overall anxiety severity and parent-report anxiety measures, supporting convergent validity. Results for divergent validity were mixed. Although the PARS was not associated with the sum of the Social and Communication items on the Autism Diagnostic Observation System, it was moderately correlated with parent-reported inattention, aggression and externalizing behavior. Overall, these results suggest that the psychometric properties of the PARS are adequate for assessing anxiety symptoms in youth with ASD, although additional clarification of divergent validity is needed.
C1 [Storch, Eric A.; Jones, Anna M.; Park, Jennifer M.; Lewin, Adam B.; Murphy, Tanya K.] Univ S Florida, Dept Pediat, St Petersburg, FL 33701 USA.
   [Wood, Jeffrey J.] Univ Calif Los Angeles, Dept Educ Psychol, Los Angeles, CA USA.
   [Ehrenreich-May, Jill] Univ Miami, Dept Psychol, Coral Gables, FL 33124 USA.
RP Storch, EA (reprint author), Univ S Florida, Dept Pediat, 880 6th St S Box 7523, St Petersburg, FL 33701 USA.
EM estorch@health.usf.edu
RI Lewin, Adam/A-9832-2013
CR Achenbach TM, 2001, MANUAL ASEBA SCH AGE
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NR 40
TC 16
Z9 16
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2374
EP 2382
DI 10.1007/s10803-012-1489-9
PG 9
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600010
PM 22395820
ER

PT J
AU Hayward, DA
   Shore, DI
   Ristic, J
   Kovshoff, H
   Iarocci, G
   Mottron, L
   Burack, JA
AF Hayward, Dana A.
   Shore, David I.
   Ristic, Jelena
   Kovshoff, Hanna
   Iarocci, Grace
   Mottron, Laurent
   Burack, Jacob A.
TI Flexible Visual Processing in Young Adults with Autism: The Effects of
   Implicit Learning on a Global-Local Task
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE High-functioning autism; Visual attention; Hierarchical figures;
   Implicit learning
ID EXECUTIVE DYSFUNCTION; SPECTRUM DISORDERS; CHILDREN; PRECEDENCE;
   ATTENTION; INTERFERENCE; PERFORMANCE; ACCOUNT; STIMULI; DETAIL
AB We utilized a hierarchical figures task to determine the default level of perceptual processing and the flexibility of visual processing in a group of high-functioning young adults with autism (n = 12) and a typically developing young adults, matched by chronological age and IQ (n = 12). In one task, participants attended to one level of the figure and ignored the other in order to determine the default level of processing. In the other task, participants attended to both levels and the proportion of trials in which a target would occur at either level was manipulated. Both groups exhibited a global processing bias and showed similar flexibility in performance, suggesting that persons with autism may not be impaired in flexible shifting between task levels.
C1 [Shore, David I.] McMaster Univ, Dept Psychol Neurosci & Behav PNB, Hamilton, ON L8S 4K1, Canada.
   [Hayward, Dana A.; Ristic, Jelena] McGill Univ, Dept Psychol, Montreal, PQ, Canada.
   [Kovshoff, Hanna] Univ Southampton, Sch Psychol, Southampton, Hants, England.
   [Iarocci, Grace] Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada.
   [Mottron, Laurent; Burack, Jacob A.] Hop Riviere des Praries, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ, Canada.
   [Burack, Jacob A.] McGill Univ, Dept Educ & Counselling Psychol, Montreal, PQ H3A 1Y2, Canada.
RP Shore, DI (reprint author), McMaster Univ, Dept Psychol Neurosci & Behav PNB, Psychol Bldg PC,Room 409,1280 Main St W, Hamilton, ON L8S 4K1, Canada.
EM jake.burack@mcgill.ca
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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NR 27
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2383
EP 2392
DI 10.1007/s10803-012-1485-0
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600011
PM 22391810
ER

PT J
AU Reed, P
   Hawthorn, R
   Bolger, S
   Meredith, K
   Bishop, R
AF Reed, Phil
   Hawthorn, Rose
   Bolger, Sam
   Meredith, Katie
   Bishop, Ruth
TI Disrupted Stimulus Control But Not Reward Sensitivity in Individuals
   with Autism Spectrum Disorders: A Matching Law Analysis
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Stimulus control; Reward sensitivity; Matching
ID CONCURRENT-SCHEDULE PERFORMANCE; REINFORCER RATE; FUNCTIONING CHILDREN;
   BEHAVIOR CHECKLIST; AUDITORY-STIMULI; CHOICE; MAGNITUDE; EXTINCTION;
   DIMENSIONS; FREQUENCY
AB The matching law suggests that behavior is emitted in proportion to the level of reinforcement available. The current study investigated this effect in individuals with autism spectrum disorders (ASD), and focused on the effects of magnitude of reinforcement (Study 1), and rate of reinforcement (Studies 2 and 3), on matching performance. Studies 1 and 2 employed lower functioning children with ASD, and demonstrated matching in both groups, but that the group with ASD displayed greater levels of stimulus bias. Study 3 employed higher functioning children with ASD, and found little evidence of matching, but higher stimulus bias in the group with ASD. These effects suggest a disruption of stimulus control, but not reward sensitivity, in individuals with ASD.
C1 [Reed, Phil; Hawthorn, Rose; Bolger, Sam; Meredith, Katie; Bishop, Ruth] Swansea Univ, Dept Psychol, Swansea SA2 8PP, W Glam, Wales.
RP Reed, P (reprint author), Swansea Univ, Dept Psychol, Singleton Pk, Swansea SA2 8PP, W Glam, Wales.
EM p.reed@swansea.ac.uk
CR ALSOP B, 1988, J EXP ANAL BEHAV, V49, P21, DOI 10.1901/jeab.1988.49-21
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NR 45
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2393
EP 2403
DI 10.1007/s10803-012-1494-z
PG 11
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600012
PM 22407578
ER

PT J
AU Rodgers, J
   Glod, M
   Connolly, B
   McConachie, H
AF Rodgers, J.
   Glod, M.
   Connolly, B.
   McConachie, H.
TI The Relationship Between Anxiety and Repetitive Behaviours in Autism
   Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Repetitive behaviours; Anxiety; Insistence on sameness; Autism spectrum
ID ASPERGER-SYNDROME; CHILDREN; ADOLESCENTS; SYMPTOMS; ADULTS
AB Children with Autism Spectrum Disorder are vulnerable to anxiety. Repetitive behaviours are a core feature of Autism Spectrum Disorder (ASD) and have been associated anxiety. This study examined repetitive behaviours and anxiety in two groups of children with autism spectrum disorder, those with high anxiety and those with lower levels of anxiety. Children with high anxiety had more repetitive behaviours than those without anxiety. Within the anxiety sample, higher levels of insistence on sameness were associated with more anxiety. No association was found between sensory motor repetitive behaviours and anxiety in this group. In the non-anxious sample, anxiety was associated with sensory motor repetitive behaviours. These findings indicate a differential relationship for repetitive behaviours in relation to anxious and non-anxious children with ASD.
C1 [Rodgers, J.; Glod, M.] Univ Newcastle, Inst Neurosci, Fac Med Sci, Newcastle NE1 7RU, Tyne & Wear, England.
   [Connolly, B.] Univ Newcastle, Sch Psychol, Fac Med Sci, Newcastle NE1 7RU, Tyne & Wear, England.
   [McConachie, H.] Univ Newcastle, Inst Hlth & Soc, Fac Med Sci, Newcastle NE1 7RU, Tyne & Wear, England.
RP Rodgers, J (reprint author), Univ Newcastle, Inst Neurosci, Fac Med Sci, Ridley Bldg, Newcastle NE1 7RU, Tyne & Wear, England.
EM Jacqui.rodgers@ncl.ac.uk
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
   Cath DC, 2008, PSYCHOPATHOLOGY, V41, P101, DOI 10.1159/000111555
   Chalfant A., 2006, J AUTISM DEV DISORD, V33, P283
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   Honey E, 2012, RES AUTISM SPECT DIS, V6, P355, DOI 10.1016/j.rasd.2011.06.009
   Hurtig T, 2009, AUTISM, V13, P583, DOI 10.1177/1362361309335719
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   Le Couteur A. S., 2003, NATL AUTISM PLAN CHI
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   MacNeil BM, 2009, RES AUTISM SPECT DIS, V3, P1, DOI 10.1016/j.rasd.2008.06.001
   McConachie R., 2008, ARCH DIS CHILD, V94, P38
   Nauta MH, 2004, BEHAV RES THER, V42, P813, DOI 10.1016/S0005-7967(03)00200-6
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   Rodgers J., MEASURING ANXI UNPUB
   Russell E, 2005, AUST NZ J PSYCHIAT, V39, P633, DOI 10.1080/j.1440-1614.2005.01637.x
   Rutter M., 2003, SOCIAL COMMUNICATION
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   White SW, 2009, CLIN PSYCHOL REV, V29, P216, DOI 10.1016/j.cpr.2009.01.003
NR 34
TC 20
Z9 20
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2404
EP 2409
DI 10.1007/s10803-012-1531-y
PG 6
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600013
PM 22527704
ER

PT J
AU Allen, KD
   Burke, RV
   Howard, MR
   Wallace, DP
   Bowen, SL
AF Allen, Keith D.
   Burke, Raymond V.
   Howard, Monica R.
   Wallace, Dustin P.
   Bowen, Scott L.
TI Use of Audio Cuing to Expand Employment Opportunities for Adolescents
   with Autism Spectrum Disorders and Intellectual Disabilities
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Intellectual disability; Employment; Job skills; Audio cuing
ID ASPERGER-SYNDROME; YOUNG-ADULTS; FOLLOW-UP; OUTCOMES; PERFORMANCE;
   INDIVIDUALS; IMPACT; YOUTH
AB We evaluated audio cuing to facilitate community employment of individuals with autism and intellectual disability. The job required promoting products in retail stores by wearing an air-inflated WalkAround(A (R)) costume of a popular commercial character. Three adolescents, ages 16-18, were initially trained with video modeling. Audio cuing was then used by an attendant who delivered prompts regarding when to perform job skills. The two interventions were evaluated in an interrupted time series withdrawal design during training and then again in an actual job setting. Results show video modeling was not effective. However, the audio cuing produced job performances well above the designated criteria during training and when on the job. These changes were replicated with each participant, demonstrating clear experimental control. The changes proved statistically significant as well. Participants and parents reported high job satisfaction. The challenges of competitive employment for individuals with autism and intellectual disabilities are discussed.
C1 [Allen, Keith D.; Howard, Monica R.] Univ Nebraska Med Ctr, Munroe Meyer Inst Genet & Rehabil, Omaha, NE 68198 USA.
   [Burke, Raymond V.; Bowen, Scott L.] Prevent Grp LLC, Omaha, NE USA.
   [Burke, Raymond V.] Univ Nebraska, Lincoln, NE USA.
   [Wallace, Dustin P.] Univ Missouri, Kansas City, MO 64110 USA.
   [Bowen, Scott L.] Signs & Shapes Int Inc, Omaha, NE USA.
RP Allen, KD (reprint author), Univ Nebraska Med Ctr, Munroe Meyer Inst Genet & Rehabil, Omaha, NE 68198 USA.
EM kdallen@unmc.edu; ray@thepreventiongroup.org
CR ALBERTO PA, 1986, J ASSOC PERS SEVERE, V11, P85
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NR 36
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2410
EP 2419
DI 10.1007/s10803-012-1519-7
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600014
PM 22456818
ER

PT J
AU Russell-Smith, SN
   Maybery, MT
   Bayliss, DM
   Sng, AAH
AF Russell-Smith, Suzanna N.
   Maybery, Murray T.
   Bayliss, Donna M.
   Sng, Adelln A. H.
TI Support for a Link Between the Local Processing Bias and Social Deficits
   in Autism: An Investigation of Embedded Figures Test Performance in
   Non-Clinical Individuals
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Local-global processing; Embedded figures; Social deficits;
   Attention-to-detail
ID WEAK CENTRAL COHERENCE; SPECTRUM QUOTIENT AQ; HIGH-FUNCTIONING ADULTS;
   COGNITIVE PHENOTYPE; ASPERGER-SYNDROME; GENERAL-POPULATION; REPETITIVE
   BEHAVIORS; EXECUTIVE CONTROL; CHILDREN; TRAITS
AB The aim of this investigation was to explore the degree to which specific subsets of autistic-like traits relate to performance on the Embedded Figures Test (Witkin et al. in A manual for the embedded figures test. Consulting Psychologists Press, Palo Alto, CA, 1971). In the first group-based investigation with this focus, students were selected for their extreme scores (either high or low) on each of the 'Social Skills' and 'Details/Patterns' factors of the Autism Spectrum Quotient (Baron-Cohen et al. in J Austim Dev Disord 31:5-17, 2001). The resulting 2 x 2 factorial design permitted examination of the degree to which the social and non-social autistic-like traits separately relate to EFT performance. Surprisingly, in two studies, superior EFT performance was found to relate only to greater social difficulty, suggesting that the local processing bias in autism may be linked specifically to the social deficits.
C1 [Russell-Smith, Suzanna N.; Maybery, Murray T.; Bayliss, Donna M.; Sng, Adelln A. H.] Univ Western Australia, Sch Psychol, Neurocognit Dev Unit, Perth, WA 6009, Australia.
RP Russell-Smith, SN (reprint author), Univ Western Australia, Sch Psychol, Neurocognit Dev Unit, 35 Stirling Highway, Perth, WA 6009, Australia.
EM srussell-smith@graduate.uwa.edu.au
RI Maybery, Murray/H-5390-2014; Bayliss, Donna/H-8810-2014
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NR 59
TC 9
Z9 9
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2420
EP 2430
DI 10.1007/s10803-012-1506-z
PG 11
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600015
PM 22434280
ER

PT J
AU Movsas, TZ
   Paneth, N
AF Movsas, Tammy Z.
   Paneth, Nigel
TI The Effect of Gestational Age on Symptom Severity in Children with
   Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism Spectrum Disorder symptoms; Preterm; Post-term; Post-mature; SCQ;
   SRS
ID PERVASIVE DEVELOPMENTAL DISORDERS; NEUROANATOMICAL OBSERVATIONS;
   POSTTERM DELIVERY; BIRTH-WEIGHT; RISK-FACTORS; TWIN PAIRS; ADOLESCENTS;
   PREVALENCE; CHILDHOOD; BRAIN
AB Between 2006 and 2010, two research-validated instruments, Social Communication Questionnaire (SCQ) and Social Responsiveness Scale (SRS) were filled out online by 4,188 mothers of Autism Spectrum Disorder (ASD) children, aged 4-21, as part of voluntary parental participation in a large web-based registry. Univariate and multivariate linear regression analysis (adjusted for child's sex, ability to verbalize, categorical IQ score, and fetal growth rate) demonstrated significantly higher SCQ and SRS scores for ASD children of both preterm (< 37 weeks) and post-term (> 42 weeks) gestational age (GA) compared to ASD children of normal GA, thus indicating that both preterm and post-term children manifest increased ASD symptomatology. Normal GA at birth appears to mitigate the severity of autistic social impairment in ASD children.
C1 [Movsas, Tammy Z.] Michigan State Univ, Dept Epidemiol, Coll Human Med, E Lansing, MI 48824 USA.
   [Paneth, Nigel] Michigan State Univ, Coll Human Med, Dept Epidemiol & Pediat & Human Dev, E Lansing, MI 48824 USA.
RP Movsas, TZ (reprint author), Michigan State Univ, Dept Epidemiol, Coll Human Med, B601 W Fee Hall, E Lansing, MI 48824 USA.
EM tmovsas@epi.msu.edu
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NR 23
TC 4
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2431
EP 2439
DI 10.1007/s10803-012-1501-4
PG 9
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600016
PM 22422339
ER

PT J
AU Pijnacker, J
   Vervloed, MPJ
   Steenbergen, B
AF Pijnacker, Judith
   Vervloed, Mathijs P. J.
   Steenbergen, Bert
TI Pragmatic Abilities in Children with Congenital Visual Impairment: An
   Exploration of Non-literal Language and Advanced Theory of Mind
   Understanding
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Visual impairment; Children; Pragmatic language; Advanced theory of
   mind; Non-literal stories
ID AUTISM SPECTRUM DISORDER; BLIND-CHILDREN; ASPERGER-SYNDROME;
   FALSE-BELIEF; PERFORMANCE; ADULTS; TASKS; ADOLESCENTS; MEMORY
AB Children with congenital visual impairment have been reported to be delayed in theory of mind development. So far, research focused on first-order theory of mind, and included mainly blind children, whereas the majority of visually impaired children is not totally blind. The present study set out to explore whether children with a broader range of congenital visual impairments have a delay in more advanced theory of mind understanding, in particular second-order theory of mind (i.e. awareness that other people have beliefs about beliefs) and non-literal language (e.g. irony or figure of speech). Twenty-four children with congenital visual impairment and 24 typically developing sighted children aged between 6 and 13 were included. All children were presented with a series of stories involving understanding of theory of mind and non-literal language. When compared with sighted children of similar age and verbal intelligence, performance of children with congenital visual impairment on advanced theory of mind and non-literal stories was alike. The ability to understand the motivations behind non-literal language was associated with age, verbal intelligence and theory of mind skills, but was not associated with visual ability.
C1 [Pijnacker, Judith; Vervloed, Mathijs P. J.; Steenbergen, Bert] Radboud Univ Nijmegen, Inst Behav Sci, NL-6500 HE Nijmegen, Netherlands.
RP Pijnacker, J (reprint author), Radboud Univ Nijmegen, Inst Behav Sci, POB 9104, NL-6500 HE Nijmegen, Netherlands.
EM j.pijnacker@pwo.ru.nl; m.vervloed@pwo.ru.nl; steenbergen@pwo.ru.nl
RI Vervloed, Mathijs/D-6094-2012
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NR 38
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2440
EP 2449
DI 10.1007/s10803-012-1500-5
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600017
PM 22437442
ER

PT J
AU Wang, J
   Lee, LC
   Chen, YS
   Hsu, JW
AF Wang, Jessica
   Lee, Li-Ching
   Chen, Ying-Sheue
   Hsu, Ju-Wei
TI Assessing Autistic Traits in a Taiwan Preschool Population:
   Cross-Cultural Validation of the Social Responsiveness Scale (SRS)
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE SRS; Taiwan; Cross-cultural; Validity; Autism spectrum disorder
ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT-HYPERACTIVITY DISORDER;
   ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; LANGUAGE IMPAIRMENT;
   QUANTITATIVE ASSESSMENT; ANXIETY DISORDERS; SPECTRUM DISORDER; ADHD
   COMORBIDITY; FAMILIAL TRAIT; CHILDREN
AB The cross-cultural validity of the Mandarin-adaptation of the social responsiveness scale (SRS) was examined in a sample of N = 307 participants in Taiwan, 140 typically developing and 167 with clinically-diagnosed developmental disorders. This scale is an autism assessment tool that provides a quantitative rather than categorical measure of social impairment in the general population. SRS total and subscale scores distinguished significantly between autism spectrum disorder and other developmental disorders (p < 0.01). Total SRS scores and sensitivity and specificity of the scale for diagnosing developmental disorders in the Taiwan study were similar to those observed in Western studies. These findings support the cross-cultural validity of the SRS scale for detecting autistic traits and for distinguishing between autism and other neuropsychiatric conditions.
C1 [Chen, Ying-Sheue; Hsu, Ju-Wei] Taipei Vet Gen Hosp, Dept Psychiat, Taipei, Taiwan.
   [Wang, Jessica] Weill Cornell Med Coll, New York, NY USA.
   [Wang, Jessica] New York Presbyterian Hosp, Dept Pediat, New York, NY USA.
   [Lee, Li-Ching] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD USA.
RP Hsu, JW (reprint author), Taipei Vet Gen Hosp, Dept Psychiat, 201,Sec 2 Shih Pai Rd, Taipei, Taiwan.
EM jwhsu@vghtpe.gov.tw
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NR 49
TC 4
Z9 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2450
EP 2459
DI 10.1007/s10803-012-1499-7
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600018
PM 22407579
ER

PT J
AU Duerden, EG
   Oatley, HK
   Mak-Fan, KM
   McGrath, PA
   Taylor, MJ
   Szatmari, P
   Roberts, SW
AF Duerden, Emma G.
   Oatley, Hannah K.
   Mak-Fan, Kathleen M.
   McGrath, Patricia A.
   Taylor, Margot J.
   Szatmari, Peter
   Roberts, S. Wendy
TI Risk Factors Associated with Self-Injurious Behaviors in Children and
   Adolescents with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Pain; Sensory; Self-injury; Autism; Human
ID NALTREXONE TREATMENT; YOUNG-CHILDREN; INTELLECTUAL DISABILITY;
   MALADAPTIVE BEHAVIORS; CHALLENGING BEHAVIORS; REPETITIVE BEHAVIORS;
   LANGUAGE IMPAIRMENT; PHARMACOLOGICAL TREATMENT; MENTAL-RETARDATION;
   ADULTS
AB While self-injurious behaviors (SIB) can cause significant morbidity for children with autism spectrum disorders (ASD), little is known about its associated risk factors. We assessed 7 factors that may influence self-injury in a large cohort of children with ASD: (a) atypical sensory processing; (b) impaired cognitive ability; (c) abnormal functional communication; (d) abnormal social functioning; (e) age; (f) the need for sameness; (g) rituals and compulsions. Half (52.3%, n = 126) of the children (n = 241, aged 2-19 years) demonstrated SIB. Abnormal sensory processing was the strongest single predictor of self-injury followed by sameness, impaired cognitive ability and social functioning. Since atypical sensory processing and sameness have a greater relative impact on SIB, treatment approaches that focus on these factors may be beneficial in reducing self-harm in children with ASD.
C1 [Duerden, Emma G.; Mak-Fan, Kathleen M.; Taylor, Margot J.] Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada.
   [Oatley, Hannah K.; Mak-Fan, Kathleen M.; Taylor, Margot J.] Univ Toronto, Dept Psychol, Toronto, ON M5S 1A1, Canada.
   [McGrath, Patricia A.] Univ Toronto, Dept Anesthesia, Toronto, ON, Canada.
   [Szatmari, Peter] McMaster Univ, Fac Hlth Sci, Dept Psychiat & Behav Neurosci, Offord Ctr Child Studies, Hamilton, ON, Canada.
   [Roberts, S. Wendy] Holland Bloorview Childrens Rehabil Ctr, Toronto, ON, Canada.
RP Duerden, EG (reprint author), Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada.
EM emma.duerden@sickkids.ca
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NR 71
TC 19
Z9 19
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2460
EP 2470
DI 10.1007/s10803-012-1497-9
PG 11
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600019
PM 22422338
ER

PT J
AU Mayo, J
   Eigsti, IM
AF Mayo, Jessica
   Eigsti, Inge-Marie
TI Brief Report: A Comparison of Statistical Learning in School-Aged
   Children with High Functioning Autism and Typically Developing Peers
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Language; Implicit learning; Statistical learning; Speech
   segmentation
ID PERVASIVE DEVELOPMENTAL DISORDERS; DECLARATIVE/PROCEDURAL MODEL;
   LANGUAGE DISCRIMINATION; SPECTRUM DISORDERS; FLUENT SPEECH; INFANTS;
   SEGMENTATION; IMPLICIT; MEMORY; ADULTS
AB Individuals with autism spectrum disorders have impairments in language acquisition, but the underlying mechanism of these deficits is poorly understood. Implicit learning is potentially relevant to language development, particularly in speech segmentation, which relies on sensitivity to transitional probabilities between speech sounds. This study investigated the relationship between implicit learning and current language abilities in school-aged children with high functioning autism and a history of language delay (n = 17) and in children with typical development (n = 24) using a well-studied artificial language learning task. Results suggest that high functioning children with autism (HFA) and TD groups were equally able to implicitly learn transitional probabilities from a lengthy stimulus stream. Furthermore, task performance was not strongly associated with current language abilities. Implications for implicit learning research in HFA are discussed.
C1 [Mayo, Jessica; Eigsti, Inge-Marie] Univ Connecticut, Dept Psychol, Unit 1020, Storrs, CT 06269 USA.
RP Eigsti, IM (reprint author), Univ Connecticut, Dept Psychol, Unit 1020, 406 Babbidge Rd, Storrs, CT 06269 USA.
EM inge-marie.eigsti@uconn.edu
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   Ullman MT, 2004, COGNITION, V92, P231, DOI 10.1016/j.cognition.2003.10.008
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NR 63
TC 10
Z9 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2476
EP 2485
DI 10.1007/s10803-012-1493-0
PG 10
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600021
PM 22382606
ER

PT J
AU Scattone, D
   Raggio, DJ
   May, W
AF Scattone, Dorothy
   Raggio, Donald J.
   May, Warren
TI Brief Report: Concurrent Validity of the Leiter-R and KBIT-2 Scales of
   Nonverbal Intelligence for Children with Autism and Language Impairments
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Leiter International Performance Scale-Revised; Kaufman Brief
   Intelligence Test, Second Edition
ID AGREEMENT
AB The concurrent validity of the KBIT-2 Nonverbal IQ and Leiter-R Brief IQ was evaluated for two groups of children: those with high functioning autism and those with language impairments without autism. Fifty-three children between the ages of 4 and 13 years of age participated in the study. The correlation between the scales was large (r = .62) and no statistical difference was found between the means. However, large intraindividual differences were found for 11 children who received scores at least 10 points higher on the Leiter-R Brief IQ, 5 of those scored beyond 20 points higher than nonverbal scores on the KBIT-2. Conversely, 11 children scored at least 10 points higher on the KBIT-2 than on the Leiter-R with 4 of those scoring 20 points higher. These findings highlight the importance of using multiple measures when assessing individuals with autism or language disorders.
C1 [Scattone, Dorothy; Raggio, Donald J.] Univ Mississippi, Med Ctr, Dept Pediat, Jackson, MS 39216 USA.
   [May, Warren] Univ Mississippi, Med Ctr, Dept Prevent Med, Jackson, MS 39216 USA.
RP Scattone, D (reprint author), Univ Mississippi, Med Ctr, Dept Pediat, 2500 N State St, Jackson, MS 39216 USA.
EM DScattone@umc.edu
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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NR 16
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2486
EP 2490
DI 10.1007/s10803-012-1495-y
PG 5
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600022
PM 22430361
ER

PT J
AU Brosnan, MJ
   Gwilliam, LR
   Walker, I
AF Brosnan, Mark J.
   Gwilliam, Lucy R.
   Walker, Ian
TI Brief Report: The Relationship Between Visual Acuity, the Embedded
   Figures Test and Systemizing in Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Visual acuity; Embedded Figures Test (EFT); Systemizing
ID MALE BRAIN THEORY; ENHANCED DISCRIMINATION; ADULTS; PERCEPTION; ABILITY;
   VISION; TRAITS; SEARCH
AB Enhanced performance upon the Embedded Figures Test (EFT) in individuals with autism spectrum disorder (ASD) has informed psychological theories of the non-social aspects that characterise ASD. The Extreme Male Brain theory of autism proposes that enhanced visual acuity underpins greater attention to detail (assessed by the EFT) which is a prerequisite for Systemizing. To date, however, no study has empirically examined these relationships. 13 males with ASD and 13 male controls were assessed upon tasks argued to reflect these levels of processing. The ASD group were found to have significantly greater visual acuity, EFT performance and Systemizing ability than the control group. However, regression analysis revealed that the strongest relationship was between visual acuity and EFT performance.
C1 [Brosnan, Mark J.; Gwilliam, Lucy R.; Walker, Ian] Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England.
RP Brosnan, MJ (reprint author), Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England.
EM M.J.Brosnan@Bath.ac.uk
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NR 32
TC 8
Z9 8
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2491
EP 2497
DI 10.1007/s10803-012-1505-0
PG 7
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600023
PM 22450702
ER

PT J
AU Bruder, MB
   Kerins, G
   Mazzarella, C
   Sims, J
   Stein, N
AF Bruder, Mary Beth
   Kerins, Gerard
   Mazzarella, Cynthia
   Sims, Jessica
   Stein, Neil
TI Brief Report: The Medical Care of Adults with Autism Spectrum Disorders:
   Identifying the Needs
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Adults with autism; Medical needs; Characteristics of adults with ASD;
   Training of physicians
ID HEALTH-CARE; INTELLECTUAL DISABILITY; DEVELOPMENTAL-DISABILITIES;
   SYNDROME SPECIFICITY; CHILDREN; HOME; INDIVIDUALS; MANAGEMENT; SERVICES;
   PARENTS
AB There is a lack of information concerning adults with autism spectrum disorder (ASD), especially with regards to their access to health care. A paper and electronic survey was sent to 1,580 primary care physicians in Connecticut. 346 respondents returned a survey and provided care to adults with an ASD. This physician survey provides data on adults with ASD such as: reasons for physician visits, living arrangements, employment status, and any services they are receiving. Responses revealed inadequate training in the care of adults with an ASD and physicians interest in obtaining additional training. The ability to provide a medical home for adults with autism will need to address effective strategies to train current and future physicians.
C1 [Bruder, Mary Beth; Kerins, Gerard; Mazzarella, Cynthia; Sims, Jessica] Univ Connecticut, AJ Pappanikou Ctr Excellence Dev Disabil Educ Res, Farmington, CT 06030 USA.
   [Kerins, Gerard] Hosp St Raphael, New Haven, CT 06511 USA.
   [Sims, Jessica] Child Care Aware Missouri, St Louis, MO USA.
   [Stein, Neil] Univ Connecticut, Ctr Hlth, Farmington, CT USA.
RP Bruder, MB (reprint author), Univ Connecticut, AJ Pappanikou Ctr Excellence Dev Disabil Educ Res, 263 Farmington Ave,MC6222, Farmington, CT 06030 USA.
EM bruder@nso1.uchc.edu
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NR 38
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2498
EP 2504
DI 10.1007/s10803-012-1496-x
PG 7
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600024
PM 22427260
ER

PT J
AU Sivaratnam, CS
   Cornish, K
   Gray, KM
   Howlin, P
   Rinehart, NJ
AF Sivaratnam, Carmel S.
   Cornish, Kim
   Gray, Kylie M.
   Howlin, Patricia
   Rinehart, Nicole J.
TI Brief Report: Assessment of the Social-Emotional Profile in Children
   with Autism Spectrum Disorders using a Novel Comic Strip Task
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Theory of Mind; Early to middle childhood; Belief understanding;
   Intention understanding; Emotion understanding
ID MIND; LANGUAGE; RECOGNITION; INTENTION; METAANALYSIS; PERFORMANCE;
   KNOWLEDGE; ABILITY; STATES
AB This study investigated whether the novel Comic Strip Task (CST) could be used to detect Theory-of-Mind impairments (ToM) in 4- to 8-year-old children with high functioning Autism Spectrum Disorders (ASD). Twelve children with either high-functioning autism or Asperger's Disorder and 12 typically-developing children completed the 21-item measure. The overall CST demonstrated moderate internal consistency but the Belief-understanding subscale was excluded from the test due to poor reliability. As predicted, the ASD group performed significantly more poorly than controls on the overall 2-subscale CST and on the intention-understanding subscale. No group differences were found in emotion-understanding subscale performance. Controlling for age, verbal ability was positively correlated with overall CST performance across groups. CST performance in the ASD group positively correlated with parent-reports of communication difficulties. Despite some limitations with the belief-understanding subscale, the CST has promising psychometric features warranting further development of this measure.
C1 [Sivaratnam, Carmel S.; Cornish, Kim; Gray, Kylie M.; Rinehart, Nicole J.] Monash Univ, Sch Psychol & Psychol, Ctr Dev Psychiat & Psychol, Notting Hill, Vic 3168, Australia.
   [Cornish, Kim] Monash Univ, Monash Inst Brain Dev & Repair, Notting Hill, Vic 3168, Australia.
   [Howlin, Patricia] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
RP Rinehart, NJ (reprint author), Monash Univ, Sch Psychol & Psychol, Ctr Dev Psychiat & Psychol, Bldg 1,270 Ferntree Gully Rd, Notting Hill, Vic 3168, Australia.
EM Nicole.Rinehart@monash.edu
RI Howlin, Patricia/A-7622-2011; Gray, Kylie/H-3345-2014
OI Gray, Kylie/0000-0001-6518-4240
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   Wechsler D., 2002, WECHSLER PRESCHOOL P, V3rd
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NR 33
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2505
EP 2512
DI 10.1007/s10803-012-1498-8
PG 8
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600025
PM 22419380
ER

PT J
AU d'Arc, BF
   Dawson, M
   Soulieres, I
   Mottron, L
AF d'Arc, Baudouin Forgeot
   Dawson, Michelle
   Soulieres, Isabelle
   Mottron, Laurent
TI Self-Injury in Autism is Largely Unexplained: Now What?
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Letter
ID SPECTRUM; CHILDREN
C1 [d'Arc, Baudouin Forgeot; Soulieres, Isabelle; Mottron, Laurent] Hop Riviere des Prairies, Pervas Dev Disorders Specialized Clin, Montreal, PQ H1E 1A4, Canada.
   [d'Arc, Baudouin Forgeot; Dawson, Michelle; Soulieres, Isabelle; Mottron, Laurent] Univ Montreal CETEDUM, Montreal, PQ, Canada.
   [d'Arc, Baudouin Forgeot; Soulieres, Isabelle; Mottron, Laurent] Univ Montreal, Dept Psychiat, Ctr Rech Fernand Seguin, Montreal, PQ H3C 3J7, Canada.
   [Soulieres, Isabelle] Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada.
RP d'Arc, BF (reprint author), Hop Riviere des Prairies, Pervas Dev Disorders Specialized Clin, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada.
EM b.forgeot@gmail.com
CR Bodfish J. W., 1999, W CAROLINA CTR RES R
   Cappadocia MC, 2012, J AUTISM DEV DISORD, V42, P266, DOI 10.1007/s10803-011-1241-x
   Caron MJ, 2006, BRAIN, V129, P1789, DOI 10.1093/brain/awl072
   Duerden EG, 2012, J AUTISM DEV DISORD, V42, P2460, DOI 10.1007/s10803-012-1497-9
   Giletta M, 2012, PSYCHIAT RES, V197, P66, DOI 10.1016/j.psychres.2012.02.009
   Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947
   Mottron L, 2009, PHILOS T R SOC B, V364, P1385, DOI 10.1098/rstb.2008.0333
   Rowley E, 2012, RES AUTISM SPECT DIS, V6, P1126, DOI 10.1016/j.rasd.2012.03.004
   Soulieres I, 2009, HUM BRAIN MAPP, V30, P4082, DOI 10.1002/hbm.20831
NR 9
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2513
EP 2514
DI 10.1007/s10803-012-1628-3
PG 2
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600026
ER

PT J
AU Duerden, EG
   Szatmari, P
   Roberts, SW
AF Duerden, Emma G.
   Szatmari, Peter
   Roberts, S. Wendy
TI Toward a Better Understanding of Self Injurious Behaviors in Children
   and Adolescents with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Letter
ID HOSPITALIZATION; PAIN
C1 [Duerden, Emma G.] Hosp Sick Children, Dept Diagnost Imaging, Toronto, ON M5G 1X8, Canada.
   [Duerden, Emma G.; Roberts, S. Wendy] Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada.
   [Szatmari, Peter] McMaster Univ, Fac Hlth Sci, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada.
   [Szatmari, Peter] McMaster Univ, Offord Ctr Child Studies, Hamilton, ON, Canada.
   [Roberts, S. Wendy] Holland Bloorview Childrens Rehabil Ctr, Toronto, ON, Canada.
RP Duerden, EG (reprint author), Hosp Sick Children, Dept Diagnost Imaging, 555 Univ Ave, Toronto, ON M5G 1X8, Canada.
EM emma.duerden@sickkids.ca
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NR 15
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2515
EP 2518
DI 10.1007/s10803-012-1600-2
PG 4
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600027
PM 22798052
ER

PT J
AU Butterly, FR
AF Butterly, Felicity Ruth
TI Book Review for the Socially Included Child: A Parent's Guide to
   Successful Playdates, Recreation, and Family Events for Children with
   Autism
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Book Review
DE Autism; Challenging behaviour; Parents' guide
AB This review critiqued 'L. LeComer, The Socially Included Child: A Parent's Guide to Successful Playdates, Recreation, and Family Events for Children with Autism'. New York, Jessica Kingsley Publishers, 2009, 230 pp., ISBN 978-0-425-22965-1, $14.00 (paper)'. The book was found to be useful for parents as a means of training them to be more aware of their child's behaviour leading up to challenging behaviours. However, the recommendations for behaviour management are based on explaining all challenging behaviour as a hypersensitivity to a particular aspect of the child's environment.
C1 Coventry Univ, Coventry, W Midlands, England.
RP Butterly, FR (reprint author), Coventry Univ, Coventry, W Midlands, England.
EM butterlf@uni.coventry.ac.uk
CR BUTTER FR, BOOK REVIER SOCIALLY
   LeComer L., 2009, SOCIALLY INCLUDED CH
NR 2
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD NOV
PY 2012
VL 42
IS 11
BP 2519
EP 2520
DI 10.1007/s10803-011-1429-0
PG 2
WC Psychology, Developmental
SC Psychology
GA 024DQ
UT WOS:000310088600028
ER

PT J
AU Kalb, LG
   Freedman, B
   Foster, C
   Menon, D
   Landa, R
   Kishfy, L
   Law, P
AF Kalb, Luther G.
   Freedman, Brian
   Foster, Catherine
   Menon, Deepa
   Landa, Rebecca
   Kishfy, Louis
   Law, Paul
TI Determinants of Appointment Absenteeism at an Outpatient Pediatric
   Autism Clinic
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE autism; no-show; wait time; services; outpatient
ID MISSED APPOINTMENTS; SPECTRUM DISORDERS; ATTENDANCE; TELEPHONE;
   DIAGNOSIS; REMINDERS; SERVICES; CHILDREN; INFANTS; RATES
AB Objective: Two widely discussed yet highly understudied factors that obstruct timely diagnosis and intervention among children with an autism spectrum disorder (ASD) are missed scheduled appointments and wait time for outpatient services. Research surrounding outpatient appointment no-show and cancellation rates as well as predictors of such would shed light on the barriers to community-based clinical care. Methods: In this study, data from 8049 children and adolescents (mean = 6.97 years, SD = 4.81) with scheduled appointments at a multidisciplinary pediatric outpatient autism center were examined. A total of 43,504 appointments, scheduled between June 2003 and April 2012, were analyzed. Random and fixed effects multinomial logistic regression models were employed to explore the child-, clinician-, and appointment-related determinants of no-show and cancellation for initial and follow-up appointments. Results: A no-show rate of 9% and 15%, and a cancellation rate of 11% and 10% was observed for initial (n = 8049) and follow-up (n = 35,455) appointments, respectively. Different predictors were found for both no-show and cancellation at the initial and follow-up appointments. In the multivariate analyses, the most consistent and robust predictors of no-show were African-American child race, medical assistance, provider type and appointment type, and evening appointments. For cancellation, these included increased wait time and provider type. Importantly, cancellation and no-show at the initial evaluation increased the risk for these same outcomes at follow-up. Conclusion: As ASD prevalence figures continue to increase in the United States, findings surrounding wait time, appointment absenteeism, and clinical models of care are important to improving public health. (J Dev Behav Pediatr 33:685-697, 2012)
C1 [Kalb, Luther G.; Foster, Catherine; Menon, Deepa; Landa, Rebecca] Kennedy Krieger Inst, Ctr Autism & Related Disorders, Baltimore, MD USA.
   [Freedman, Brian] Univ Delaware, Ctr Disabil Studies, Newark, DE USA.
   [Landa, Rebecca] Johns Hopkins Univ, Dept Psychiat, Baltimore, MD USA.
   [Kishfy, Louis] Johns Hopkins Univ, Dept Biol, Baltimore, MD 21218 USA.
   [Law, Paul] Kennedy Krieger Inst, Dept Med Informat, Baltimore, MD USA.
   [Law, Paul] Johns Hopkins Univ, Dept Pediat, Baltimore, MD 21218 USA.
RP Kalb, LG (reprint author), 3901 Greenspring Ave, Baltimore, MD 21211 USA.
EM kalb@kennedykrieger.org
FU ROAR (Ride on for Autism Research)
FX The authors thank ROAR (Ride on for Autism Research) for the funding to
   conduct this research.
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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NR 21
TC 3
Z9 3
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 2012
VL 33
IS 9
BP 685
EP 697
DI 10.1097/DBP.0b013e31826c66ef
PG 13
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 033JZ
UT WOS:000310793100001
PM 23095496
ER

PT J
AU Emrick, BB
AF Emrick, Beth Bloom
TI Individualized Autism Intervention for Young Children: Blending Discrete
   Trial & Naturalistic Strategies
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Book Review
C1 [Emrick, Beth Bloom] Akron Childrens Hosp, NeuroDev Sci Ctr, Akron, OH USA.
RP Emrick, BB (reprint author), Akron Childrens Hosp, NeuroDev Sci Ctr, Akron, OH USA.
CR Thompson T., 2011, INDIVIDUALIZED AUTIS
NR 1
TC 0
Z9 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD NOV-DEC
PY 2012
VL 33
IS 9
BP 697
EP 697
DI 10.1097/DBP.0b013e31827b1468
PG 1
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 033JZ
UT WOS:000310793100002
ER

PT J
AU Kranz, TM
   Ekawardhani, S
   Lin, MK
   Witzmann, SR
   Streit, F
   Schuelter, U
   Bauer, H
   Henseler, D
   Turner, JD
   Muller, CP
   Reif, A
   Schote, AB
   Meyer, J
AF Kranz, Thorsten M.
   Ekawardhani, Savira
   Lin, Michelle K.
   Witzmann, Simone R.
   Streit, Fabian
   Schuelter, Ulrike
   Bauer, Hans
   Henseler, Darja
   Turner, Jonathan D.
   Muller, Claude P.
   Reif, Andreas
   Schote, Andrea B.
   Meyer, Jobst
TI The chromosome 15q14 locus for bipolar disorder and schizophrenia: Is
   C15orf53 a major candidate gene?
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Bipolar disorder; Schizophrenia; C15orf53; Segregation; Gene expression;
   Periodic catatonia
ID GENOME-WIDE ASSOCIATION; FULL-LENGTH HUMAN; PERIODIC CATATONIA; LARGE
   FAMILY; HETEROGENEITY; AUTISM; REGION; POLYMORPHISMS; METAANALYSIS;
   PREVALENCE
AB Bipolar disorder (BD) and schizophrenia are complexly inherited and highly heritable disorders with currently unknown etiologies. Recently, two independent genome-wide association studies for BD identified a small region on chromosome 15q14-15.1, pointing to a locus close to the gene C15orf53. Previously, this genomic region was also found to co-segregate with periodic catatonia (SCZD10, OMIM %605419), an unsystematic schizophrenia according to Leonhard's classification, in several multiplex families, thus pointing to overlapping etiologies of both conditions. A susceptibility locus on chromosome 15q14-15.1 was narrowed down to a 4.38 Mb region in these affected families followed by mutation and segregation analyses of C15orf53. Association analysis of individuals affected by BD and/or SCZD10 (n = 274) and controls (n = 230) and expression analyses in distinct post-mortem human limbic brain tissues were conducted. C15orf53 revealed no mutations in our SCZD10 family members, but segregation of two common haplotypes was found. No association of identified haplotypes was found in our case control samples. Gene expression could be demonstrated for immune-system-derived cells but not for the post-mortem human limbic brain tissue. Our results indicate that C15orf53 is probably neither causative for the etiology of BD nor for SCZD10 in our samples. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Kranz, Thorsten M.; Ekawardhani, Savira; Lin, Michelle K.; Schuelter, Ulrike; Bauer, Hans; Henseler, Darja; Schote, Andrea B.; Meyer, Jobst] Univ Trier, Inst Psychobiol, Dept Neurobehav Genet, D-54290 Trier, Germany.
   [Witzmann, Simone R.; Turner, Jonathan D.; Muller, Claude P.] Ctr Rech Publ Sante, Lab Natl Sante, Inst Immunol, L-1950 Luxembourg, Luxembourg.
   [Witzmann, Simone R.; Turner, Jonathan D.; Muller, Claude P.] Univ Trier, Inst Psychobiol, Dept Immunol, D-54290 Trier, Germany.
   [Streit, Fabian] Cent Inst Mental Hlth, Dept Genet Epidemiol Psychiat, D-68159 Mannheim, Germany.
   [Reif, Andreas] Univ Wurzburg, Dept Psychiat Psychosomat & Psychotherapy, D-97080 Wurzburg, Germany.
RP Meyer, J (reprint author), Univ Trier, Inst Psychobiol, Dept Neurobehav Genet, Johanniterufer 15, D-54290 Trier, Germany.
EM thorsten.m.kranz@googlemail.com; meyerjo@uni-trier.de
FU Deutsche Forschungsgemeinschaft [ME 1923/5-1, ME 1632/5-3, GRK 1389/1,
   RE1632/5-1, KFO 125, SFB TRR 58 Z02]; BMBF
FX This research was supported by grants from the Deutsche
   Forschungsgemeinschaft (ME 1923/5-1, ME 1632/5-3 and GRK 1389/1 to JM;
   RE1632/5-1, KFO 125, SFB TRR 58 Z02 to AR) and BMBF (Panic-Net to AR).
   The funding sources had no role in study design; in the collection,
   analysis and interpretation of data; in the writing of the report; or in
   the decision to submit the paper for publication.
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NR 56
TC 3
Z9 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD NOV
PY 2012
VL 46
IS 11
BP 1414
EP 1420
DI 10.1016/j.jpsychires.2012.08.008
PG 7
WC Psychiatry
SC Psychiatry
GA 031VO
UT WOS:000310670800005
PM 22944046
ER

PT J
AU Nightingale, S
AF Nightingale, Sarah
TI Autism spectrum disorders (vol 11, pg 745, 2012)
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Correction
CR Nightingale S, 2012, NAT REV DRUG DISCOV, V11, P745, DOI 10.1038/nrd3771
NR 1
TC 0
Z9 0
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD NOV
PY 2012
VL 11
IS 11
DI 10.1038/nrd3892
PG 1
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 033HW
UT WOS:000310786000024
ER

PT J
AU Murphy, D
   Spooren, W
AF Murphy, Declan
   Spooren, Will
TI EU-AIMS: a boost to autism research
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Editorial Material
C1 [Spooren, Will] CNS DTA, F Hoffmann La Roche, CH-4070 Basel, Switzerland.
   [Murphy, Declan] Kings Coll London, Dept Forens & Neurodev Sci, Inst Psychiat, London SE5 8AF, England.
RP Spooren, W (reprint author), CNS DTA, F Hoffmann La Roche, Bldg 72-141, CH-4070 Basel, Switzerland.
EM will.spooren@roche.com
CR Baudouin SJ, 2012, SCIENCE, V338, P128, DOI 10.1126/science.1224159
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NR 4
TC 16
Z9 16
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD NOV
PY 2012
VL 11
IS 11
BP 815
EP 816
DI 10.1038/nrd3881
PG 2
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 033HW
UT WOS:000310786000001
PM 23123927
ER

PT J
AU Anderson, C
   Law, JK
   Daniels, A
   Rice, C
   Mandell, DS
   Hagopian, L
   Law, PA
AF Anderson, Connie
   Law, J. Kiely
   Daniels, Amy
   Rice, Catherine
   Mandell, David S.
   Hagopian, Louis
   Law, Paul A.
TI Occurrence and Family Impact of Elopement in Children With Autism
   Spectrum Disorders
SO PEDIATRICS
LA English
DT Article
DE autism spectrum disorders; elopement; wandering
ID CANCER CLINICAL-TRIALS; CHALLENGING BEHAVIORS; FUNCTIONAL-ANALYSIS;
   VALIDATION; QUESTIONNAIRE; PARTICIPATION; DEATH
AB OBJECTIVES: Anecdotal reports suggest that elopement behavior in children with autism spectrum disorders (ASDs) increases risk of injury or death and places a major burden on families. This study assessed parent-reported elopement occurrence and associated factors among children with ASDs.
   METHODS: Information on elopement frequency, associated characteristics, and consequences was collected via an online questionnaire. The study sample included 1218 children with ASD and 1076 of their siblings without ASD. The association among family sociodemographic and child clinical characteristics and time to first elopement was estimated by using a Cox proportional hazards model.
   RESULTS: Forty-nine percent (n = 598) of survey respondents reported their child with an ASD had attempted to elope at least once after age 4 years; 26% (n = 316) were missing long enough to cause concern. Of those who went missing, 24% were in danger of drowning and 65% were in danger of traffic injury. Elopement risk was associated with autism severity, increasing, on average, 9% for every 10-point increase in Social Responsiveness Scale T score (relative risk 1.09, 95% confidence interval: 1.02, 1.16). Unaffected siblings had significantly lower rates of elopement across all ages compared with children with ASD.
   CONCLUSIONS: Nearly half of children with ASD were reported to engage in elopement behavior, with a substantial number at risk for bodily harm. These results highlight the urgent need to develop interventions to reduce the risk of elopement, to support families coping with this issue, and to train child care professionals, educators, and first responders who are often involved when elopements occur. Pediatrics 2012;130:870-877
C1 [Law, Paul A.] Kennedy Krieger Inst, Dept Med Informat, Baltimore, MD 21211 USA.
   [Law, J. Kiely; Hagopian, Louis; Law, Paul A.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA.
   [Daniels, Amy] Autism Speaks, New York, NY USA.
   [Rice, Catherine] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA.
   [Mandell, David S.] Univ Penn, Perelman Sch Med, Ctr Mental Hlth Policy & Serv Res, Philadelphia, PA 19104 USA.
RP Law, PA (reprint author), Kennedy Krieger Inst, Dept Med Informat, 3825 Greenspring Ave,Painter Bldg,1st Floor, Baltimore, MD 21211 USA.
EM lawp@kennedykrieger.org
RI Mandell, David/H-2730-2012
OI Mandell, David/0000-0001-8240-820X
FU Autism Research Institute; Autism Science Foundation, Autism Speaks;
   Global Autism Collaboration; National Autism Association; Autism Speaks
FX Supported by the Autism Research Institute, the Autism Science
   Foundation, Autism Speaks, the Global Autism Collaboration, and the
   National Autism Association.Dr Daniels was employed by Kennedy Krieger
   Institute through the submission of the manuscript. On February 26, she
   started a position with Autism Speaks. Autism Speaks is a financial
   supporter of the IAN Project, the study through which the elopement
   survey was implemented. The other authors have indicated they have no
   financial relationships relevant to this article to disclose.
CR Algase DL, 2009, J AM GERIATR SOC, V57, P2037, DOI 10.1111/j.1532-5415.2009.02491.x
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NR 34
TC 7
Z9 7
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2012
VL 130
IS 5
BP 870
EP 877
DI 10.1542/peds.2012-0762
PG 8
WC Pediatrics
SC Pediatrics
GA 029OT
UT WOS:000310505900056
PM 23045563
ER

PT J
AU Gotham, K
   Pickles, A
   Lord, C
AF Gotham, Katherine
   Pickles, Andrew
   Lord, Catherine
TI Trajectories of Autism Severity in Children Using Standardized ADOS
   Scores
SO PEDIATRICS
LA English
DT Article
DE autism spectrum disorders; severity; trajectory; Autism Diagnostic
   Observation Schedule Comparison Score
ID DIAGNOSTIC-OBSERVATION-SCHEDULE; SPECTRUM DISORDER; REVISED ALGORITHMS;
   ADOLESCENTS
AB OBJECTIVES: To plot longitudinal trajectories of autism spectrum disorder (ASD) severity from early childhood to early adolescence. In line with reported trajectories in toddlers, we hypothesize that a substantial minority of children will show marked changes in ASD severity over time, with "Improvers" demonstrating the highest mean baseline and rate of growth in verbal IQ (VIQ).
   METHODS: Patients included 345 clinic referrals and research participants with best-estimate clinical diagnoses of ASD at 1 or more time points, and repeated Autism Diagnostic Observation Schedule (ADOS), VIQ, and nonverbal IQ scores. Standardized ADOS severity scores were applied to 1026 assessments collected longitudinally between the ages of 2 and 15 (VIQ at most recent assessment: mean = 58, SD = 35). Scores were fitted for latent severity trajectory classes with and without covariates. Adaptive behavior and VIQ trajectories over time were modeled within each of the best-fit latent classes.
   RESULTS: A 4-class model best represented the observed data. Over 80% of participants were assigned to persistent (stable) high or moderately severe classes; 2 small classes respectively increased or decreased in severity over time. Age, gender, race, and nonverbal IQ did not predict class membership; VIQ was a significant predictor. Baseline VIQ was highest in the improving and worsening classes; it increased at the greatest rate in the improving class. Adaptive behavior declined in all but the improving class, with consistent impairment in all classes.
   CONCLUSIONS: If replicated, identified trajectory classes of ADOS severity may contribute to clinical prognosis and to subtyping samples for neurobiological and genetic research. Pediatrics 2012;130:e1278-e1284
C1 [Gotham, Katherine] Univ Michigan Autism & Commun Disorders Ctr, Ann Arbor, MI USA.
   [Pickles, Andrew] Kings Coll London, Inst Psychiat, Dept Biostat, London WC2R 2LS, England.
   [Lord, Catherine] Weill Cornell Med Coll, Ctr Autism & Dev Brain, White Plains, NY USA.
RP Gotham, K (reprint author), PMB74,230 Appleton Pl, Nashville, TN 37203 USA.
EM katherine.gotham@vanderbilt.edu
RI Pickles, Andrew/A-9625-2011
OI Pickles, Andrew/0000-0003-1283-0346
FU ADOS-2; National Institute of Mental Health [NIMH R01 MH57167, MH066469,
   T32-MH18921]; National Institute of Child Health and Human Development
   [HD 35482-01, P30HD15052]; Autism Speaks Pre-doctoral Training
   Fellowship; National Institutes of Health (NIH)
FX Dr Lord receives royalties for the ADOS; profits related to this study
   were donated to charity; Dr Gotham will receive royalties from the
   ADOS-2, the second edition of the measure described here and plans to
   donate all proceeds from research use to charity. and Dr Pickles has
   indicated that he has no financial relationships relevant to this
   article to disclose.This study was funded by the National Institute of
   Mental Health (NIMH R01 MH57167, MH066469, and T32-MH18921), the
   National Institute of Child Health and Human Development (HD 35482-01
   and P30HD15052), and an Autism Speaks Pre-doctoral Training Fellowship.
   Funded by the National Institutes of Health (NIH).
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NR 25
TC 17
Z9 18
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD NOV
PY 2012
VL 130
IS 5
BP E1278
EP E1284
DI 10.1542/peds.2011-3668
PG 7
WC Pediatrics
SC Pediatrics
GA 029OT
UT WOS:000310505900028
PM 23090336
ER

PT J
AU Heaton, P
   Reichenbacher, L
   Sauter, D
   Allen, R
   Scott, S
   Hill, E
AF Heaton, P.
   Reichenbacher, L.
   Sauter, D.
   Allen, R.
   Scott, S.
   Hill, E.
TI Measuring the effects of alexithymia on perception of emotional
   vocalizations in autistic spectrum disorder and typical development
SO PSYCHOLOGICAL MEDICINE
LA English
DT Article
DE Alexithymia; autism; emotional vocalizations
ID FUNCTIONING AUTISM; ASPERGER-SYNDROME; RECOGNITION; EXPRESSIONS;
   CHILDREN; VALIDITY; SELF; INTENSITIES; PREVALENCE; DEFICITS
AB Background. The results from recent studies suggest that alexithymia, a disorder characterized by impairments in understanding personal experiences of emotion, is frequently co-morbid with autism spectrum disorder (ASD). However, the extent that alexithymia is associated with primary deficits in recognizing external emotional cues, characteristic in ASD, has yet to be determined.
   Method. Twenty high-functioning adults with ASD and 20 age-and intelligence-matched typical controls categorized vocal and verbal expressions of emotion and completed an alexithymia assessment.
   Results. Emotion recognition scores in the ASD group were significantly poorer than in the control group and performance was influenced by the severity of alexithymia and the psycho-acoustic complexity of the presented stimuli. For controls, the effect of complexity was significantly smaller than for the ASD group, although the association between total emotion recognition scores and alexithymia was still strong.
   Conclusions. Higher levels of alexithymia in the ASD group accounted for some, but not all, of the group difference in emotion recognition ability. However, alexithymia was insufficient to explain the different sensitivities of the two groups to the effects of psycho-acoustic complexity on performance. The results showing strong associations between emotion recognition and alexithymia scores in controls suggest a potential explanation for variability in emotion recognition in non-clinical populations.
C1 [Heaton, P.; Reichenbacher, L.; Sauter, D.; Allen, R.; Scott, S.; Hill, E.] Univ London Goldsmiths Coll, London SE14 6NW, England.
RP Heaton, P (reprint author), Univ London Goldsmiths Coll, London SE14 6NW, England.
EM p.heaton@gold.ac.uk
RI Allen, Rory/E-8660-2011; Scott, Sophie/A-1843-2010
OI Allen, Rory/0000-0003-3434-9772; 
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NR 47
TC 6
Z9 6
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0033-2917
J9 PSYCHOL MED
JI Psychol. Med.
PD NOV
PY 2012
VL 42
IS 11
BP 2453
EP 2459
DI 10.1017/S0033291712000621
PG 7
WC Psychology, Clinical; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 031HI
UT WOS:000310629600019
PM 22475181
ER

PT J
AU Sebastian, C
AF Sebastian, Catherine
TI Don't leave me out!
SO PSYCHOLOGIST
LA English
DT Article
ID NEUROSCIENCE PERSPECTIVE; SOCIAL NEUROSCIENCE; ASPERGER-SYNDROME; PEER
   REJECTION; SELF-ESTEEM; ADOLESCENCE; DISORDERS; OSTRACISM; AUTISM;
   PREVALENCE
AB Adolescents are anecdotally sensitive to peer rejection. Many people can vividly recall, even as adults, instances during their teenage years in which they were excluded by a particular clique or left 'out of the loop' about parties or social plans. Rejection is undoubtedly part of the social landscape in adolescence, but why do young people find it quite so distressing? One possibility is that ongoing brain development in regions involved in emotional processing, emotion regulation, and social cognition may contribute to this phenomenon. This development could have far-reaching implications, not just for how adolescents respond to rejection, but for mental health during this crucial and formative stage of development.
C1 Univ London, Dept Psychol, London WC1E 7HU, England.
RP Sebastian, C (reprint author), Univ London, Dept Psychol, London WC1E 7HU, England.
EM catherine.sebastian@rhul.ac.uk
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NR 37
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 2012
VL 25
IS 11
BP 820
EP 823
PG 4
WC Psychology, Multidisciplinary
SC Psychology
GA 033TF
UT WOS:000310823300030
ER

PT J
AU Sall, JW
   Stratmann, G
   Leong, J
   Woodward, E
   Bickler, PE
AF Sall, Jeffrey W.
   Stratmann, Greg
   Leong, Jason
   Woodward, Elliott
   Bickler, Philip E.
TI Propofol at Clinically Relevant Concentrations Increases Neuronal
   Differentiation But Is Not Toxic to Hippocampal Neural Precursor Cells
   In Vitro
SO ANESTHESIOLOGY
LA English
DT Article
ID BRAIN; NEUROAPOPTOSIS; ACTIVATION; ANESTHESIA; MECHANISM; BINDING;
   AUTISM
AB Background: Propofol in the early postnatal period has been shown to cause brain cell death. One proposed mechanism for cognitive dysfunction after anesthesia is alteration of neural stem cell function and neurogenesis. We examined the effect of propofol on neural precursor or stem cells (NPCs) grown in vitro.
   Methods: Hippocampal-derived NPCs from postnatal day 2 rats were exposed to propofol or Diprivan. NPCs were then analyzed for bromodeoxyuridine incorporation to measure proliferation. Cell death was measured by lactate dehydrogenase release. Immunocytochemistry was used to evaluate the expression of neuronal and glial markers in differentiating NPCs exposed to propofol.
   Results: Propofol dose dependently increases the release of lactate dehydrogenase from NPCs under both proliferating and differentiating conditions at supraclinical concentrations (more than 7.1 mu m). Both Diprivan and propofol had the same effect on NPCs. Propofol-mediated release of lactate dehydrogenase is not inhibited by blocking the gamma-aminobutyric acid type A receptor or extracellular calcium influx and is not mediated by caspase-3/7. Direct gamma-aminobutyric acid type A receptor activation did not have the same effect. In differentiating NPCs, 6 h of propofol at 2.1 mu m increased the number neurons but not glial cells 4 days later. Increased neuronal differentiation was not blocked by bicuculline.
   Conclusions: Only supraclinical concentrations of propofol or Diprivan kill NPCs in culture by a non-gamma-aminobutyric acid type A, noncaspase-3 mechanism. Clinically relevant doses of propofol increase neuronal fate choice by a non-gamma-aminobutyric acid type A mechanism.
C1 [Sall, Jeffrey W.; Stratmann, Greg; Leong, Jason; Bickler, Philip E.] Univ Calif San Francisco, Dept Anesthesia & Perioperat Care, San Francisco, CA 94143 USA.
RP Sall, JW (reprint author), Univ Calif San Francisco, Dept Anesthesia & Perioperat Care, S-257,Box 0542,513 Parnassus Ave, San Francisco, CA 94143 USA.
EM sallj@anesthesia.ucsf.edu
FU National Institutes of Health, Bethesda, Maryland [K08 GM086511];
   Department of Anesthesia and Perioperative Care, University of
   California, San Francisco; Clinical and Translational Science Institute,
   University of California, San Francisco
FX Supported by grant No. K08 GM086511 (to Dr. Sall) from the National
   Institutes of Health, Bethesda, Maryland; by the Department of
   Anesthesia and Perioperative Care, University of California, San
   Francisco (to Dr. Sall and Dr. Stratmann), and by the Clinical and
   Translational Science Institute, University of California, San Francisco
   (to Dr. Sall).
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NR 24
TC 3
Z9 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0003-3022
J9 ANESTHESIOLOGY
JI Anesthesiology
PD NOV
PY 2012
VL 117
IS 5
BP 1080
EP 1090
DI 10.1097/ALN.0b013e31826f8d86
PG 11
WC Anesthesiology
SC Anesthesiology
GA 027DN
UT WOS:000310332100023
PM 23001052
ER

PT J
AU Pizzo, B
   Coyle, M
   Seiverling, L
   Williams, K
AF Pizzo, Bianca
   Coyle, Molly
   Seiverling, Laura
   Williams, Keith
TI PLATE A-PLATE B: USE OF SEQUENTIAL PRESENTATION IN THE TREATMENT OF FOOD
   SELECTIVITY
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID CHILDHOOD FEEDING PROBLEMS; REPEATED TASTE EXPOSURE; INTERVENTION;
   EXTINCTION; BEHAVIOR
AB This study examined the effects of sequential presentation of foods on increasing acceptance of novel foods in a 16-year-old boy with autism spectrum disorder residing in a short-term behavioral stabilization unit. The participant ate only 10 foods and one beverage prior to treatment. The intervention involved presenting a plate containing pea-sized bites of novel foods (Plate A) and a plate containing spoonful-sized bites of highly preferred foods (Plate B). After the participant consumed a bite from Plate A, he chose a bite from Plate B and was given a preferred beverage. The intervention, involving sequential presentation and establishing operations without the use of escape extinction, was successful in increasing the number of foods eaten from 10 to 24 while not increasing his maladaptive behaviors. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Pizzo, Bianca] Bancroft, Haddonfield, NJ USA.
   [Seiverling, Laura] Penn State Univ, University Pk, PA 16802 USA.
RP Pizzo, B (reprint author), Rowan Univ, 201 Mullica Hill Rd, Glassboro, NJ 08028 USA.
EM ColemanB@rowan.edu
CR Ahearn WH, 2002, BEHAV INTERVENT, V17, P111, DOI 10.1002/bin.112
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   Levin L, 2001, BEHAV MODIF, V25, P443, DOI 10.1177/0145445501253004
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   Patel M, 2007, BEHAV INTERVENT, V22, P305, DOI 10.1002/bin.251
   Paul C, 2007, APPETITE, V49, P708, DOI 10.1016/j.appet.2007.07.012
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   Seiverling L, 2012, J APPL BEHAV ANAL, V45, P197, DOI 10.1901/jaba.2012.45-197
   Williams KE, 2008, APPETITE, V51, P739, DOI 10.1016/j.appet.2008.05.063
NR 14
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2012
VL 27
IS 4
BP 175
EP 184
DI 10.1002/bin.1347
PG 10
WC Psychology, Clinical
SC Psychology
GA 029FT
UT WOS:000310480900001
ER

PT J
AU Dickman, SE
   Bright, CN
   Montgomery, DH
   Miguel, CF
AF Dickman, Sarah E.
   Bright, Candice N.
   Montgomery, Dawn H.
   Miguel, Caio F.
TI THE EFFECTS OF RESPONSE INTERRUPTION AND REDIRECTION (RIRD) AND
   DIFFERENTIAL REINFORCEMENT ON VOCAL STEREOTYPY AND APPROPRIATE
   VOCALIZATIONS
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID AUTISM; DISABILITIES; REPLICATION; CHILDREN
AB The relation between contextually appropriate vocalizations (AV) and vocal stereotypy (VS) has yet to be established within the response interruption and redirection (RIRD) literature. RIRD may promote AV by suppressing VS and/or by functioning as incompatible responses. The occurrence of VS and AV was assessed during baseline, RIRD alone, and RIRD combined with a differential reinforcement system for AV (RIRD + DRI) for a 5-year-old child with autism. Results showed an increase in AV once RIRD was implemented and further increases in AV and decreases in stereotypy when the token system of reinforcement for AV was implemented. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Miguel, Caio F.] Calif State Univ Sacramento, Dept Psychol, Sacramento, CA 95819 USA.
   [Dickman, Sarah E.; Bright, Candice N.; Montgomery, Dawn H.] HOPE Consulting LLC, Sacramento, CA USA.
RP Miguel, CF (reprint author), Calif State Univ Sacramento, Dept Psychol, 6000 J St, Sacramento, CA 95819 USA.
EM miguelc@csus.edu
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   Liu-Gitz L, 2010, BEHAV INTERVENT, V25, P77, DOI 10.1002/bin.297
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   Richman DM, 2001, J APPL BEHAV ANAL, V34, P73, DOI 10.1901/jaba.2001.34-73
   Skinner B. F., 1957, VERBAL BEHAV
NR 12
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2012
VL 27
IS 4
BP 185
EP 192
DI 10.1002/bin.1348
PG 8
WC Psychology, Clinical
SC Psychology
GA 029FT
UT WOS:000310480900002
ER

PT J
AU Lanovaz, MJ
   Sladeczek, IE
   Rapp, JT
AF Lanovaz, Marc J.
   Sladeczek, Ingrid E.
   Rapp, John T.
TI EFFECTS OF NONCONTINGENT MUSIC ON VOCAL STEREOTYPY AND TOY MANIPULATION
   IN CHILDREN WITH AUTISM SPECTRUM DISORDERS
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
ID RESPONSE DEPRIVATION; MATCHED STIMULATION; PROBLEM BEHAVIOR; MULTIPLE
   FORMS; ACCESS; REINFORCEMENT; INTERVENTION; PREFERENCE
AB Noncontingent music has been shown to reduce engagement in vocal stereotypy in children with autism spectrum disorders, but its effects on appropriate collateral behavior remain unknown. Given that noncontingent music is typically implemented during periods of free play, clinicians may be concerned with the effects of the intervention on toy manipulation. Thus, we examined the immediate and subsequent effects of noncontingent music on engagement in vocal stereotypy and toy manipulation in four children with autism spectrum disorders by using a three-component multiple schedule combined with a multi-element design. The results suggest that noncontingent music (i) reduced immediate engagement in vocal stereotypy for three of four participants, (ii) never increased subsequent engagement in vocal stereotypy, and (iii) produced idiosyncratic effects on immediate and subsequent engagement in toy manipulation for two participants. The clinical implications of the results are discussed in terms of improving the treatment of vocal stereotypy using noncontingent music. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 [Lanovaz, Marc J.; Sladeczek, Ingrid E.] McGill Univ, Dept Educ & Counseling Psychol, Montreal, PQ H3A 1Y2, Canada.
   [Rapp, John T.] St Cloud State Univ, Dept Community Psychol & Educ Leadership, St Cloud, MN 56301 USA.
RP Lanovaz, MJ (reprint author), Univ Montreal, Ecole Psychoeduc, CP 6128,Succursale Ctr Ville, Montreal, PQ H3C 3J7, Canada.
EM marc.lanovaz@umontreal.ca
CR Ahearn WH, 2005, J APPL BEHAV ANAL, V38, P247, DOI 10.1901/jaba.2005.36-04
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   Piazza CC, 2000, J APPL BEHAV ANAL, V33, P13, DOI 10.1901/jaba.2000.33-13
   Rapp JT, 2007, J APPL BEHAV ANAL, V40, P73, DOI 10.1901/jaba.2007.142-05
   Rapp JT, 2005, RES DEV DISABIL, V26, P527, DOI 10.1016/j.ridd.2004.11.005
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   Saylor S, 2012, J APPL BEHAV ANAL, V45, P185, DOI 10.1901/jaba.2012.45-185
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NR 30
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2012
VL 27
IS 4
BP 207
EP 223
DI 10.1002/bin.1345
PG 17
WC Psychology, Clinical
SC Psychology
GA 029FT
UT WOS:000310480900004
ER

PT J
AU Madzharova, MS
   Sturmey, P
   Jones, EA
AF Madzharova, Maya S.
   Sturmey, Peter
   Jones, Emily A.
TI TRAINING STAFF TO INCREASE MANDING IN STUDENTS WITH AUTISM: TWO
   PRELIMINARY CASE STUDIES
SO BEHAVIORAL INTERVENTIONS
LA English
DT Article
AB Two case studies evaluated two versions of behavioral skills training on peer-to-peer manding. Case Study 1 evaluated the full package of instructions, modeling, rehearsal, and feedback, and Case Study 2 used modeling and feedback only. Both case studies employed AB designs. In both case studies, staff increased correct teaching responses, and students increased the number of independent peer-to peer mands. These pilot data suggest that staff can readily acquire teaching skills to increase peer-to-peer manding and that modeling and feedback may be sufficient to train staff to do so. Copyright (c) 2012 John Wiley & Sons, Ltd.
C1 CUNY, Grad Ctr, Dept Psychol, New York, NY USA.
   CUNY, Queens Coll, New York, NY 10021 USA.
RP Madzharova, MS (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY 11367 USA.
EM maya.madzharova@qc.cuny.edu
CR Graff RB, 2012, J APPL BEHAV ANAL, V45, P69, DOI 10.1901/jaba.2012.45-69
   Gutierrez A, 2007, J APPL BEHAV ANAL, V40, P645, DOI 10.1901/jaba.2007.645-658
   Lavie T, 2002, J APPL BEHAV ANAL, V35, P209, DOI 10.1901/jaba.2002.35-209
   Nigro-Bruzzi D, 2010, J APPL BEHAV ANAL, V43, P757, DOI 10.1901/jaba.2010.43-757
   Sarokoff RA, 2004, J APPL BEHAV ANAL, V37, P535, DOI 10.1901/jaba.2004.37-535
   Skinner B. F., 1957, VERBAL BEHAV
   Ward-Horner J, 2012, BEHAV INTERVENT, V27, P75, DOI 10.1002/bin.1339
   Winborn L, 2002, J APPL BEHAV ANAL, V35, P295, DOI 10.1901/jaba.2002.35-295
NR 8
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1072-0847
J9 BEHAV INTERVENT
JI Behav. Intervent.
PD NOV
PY 2012
VL 27
IS 4
BP 224
EP 235
DI 10.1002/bin.1349
PG 12
WC Psychology, Clinical
SC Psychology
GA 029FT
UT WOS:000310480900005
ER

PT J
AU Ratnayake, U
   Quinn, TA
   Castillo-Melendez, M
   Dickinson, H
   Walker, DW
AF Ratnayake, Udani
   Quinn, Tracey A.
   Castillo-Melendez, Margie
   Dickinson, Hayley
   Walker, David W.
TI Behaviour and hippocampus-specific changes in spiny mouse neonates after
   treatment of the mother with the viral-mimetic Poly I:C at mid-pregnancy
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Spiny mouse; Poly I:C; Microglia; Reelin; Astrocytes; Schizophrenia;
   Autism; GFAP; Iba1
ID FIBRILLARY ACIDIC PROTEIN; MATERNAL IMMUNE ACTIVATION;
   NEURODEVELOPMENTAL ANIMAL-MODEL; ADULT SCHIZOPHRENIA; PRENATAL EXPOSURE;
   ACOMYS-CAHIRINUS; DOPAMINERGIC HYPERFUNCTION; PERINATAL-DEVELOPMENT;
   IMMUNOLOGICAL STRESS; OBJECT RECOGNITION
AB Epidemiological studies have suggested a link between prenatal exposure to bacterial or viral infections and subsequent development of mental disorders such as schizophrenia and autism. Animal models to study the prenatal origin of such outcomes of pregnancy have largely used conventional rodents which are immature at birth compared to the human neonate, and doses of the infective agent (i.e., lipopolysaccharide, Poly I:C) have been large enough to cause sickness behaviour in the mother. In this study we have used the spiny mouse (Acomys cahirinus) whose offspring have completed organogenesis at birth, and a single subcutaneous injection of a low (0.5 mg/kg) dose of polyriboinosinic-polyribocytidilic acid (Poly I:C) at mid gestation (20 days, term is 39 days). The treatment had no effect on maternal, fetal or neonatal survival, or postnatal growth of the offspring. However, offspring showed significant impairments in non-spatial memory and learning tasks, and motor activity. Brain histology examined at 1 and 100 days of age revealed significant decreases in reelin, increased GFAP expression, and increased numbers of activated microglia, specifically in the hippocampus. This study provides evidence that a prenatal subclinical infection can have profound effects on brain development that are long-lasting. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Ratnayake, Udani; Quinn, Tracey A.; Castillo-Melendez, Margie; Dickinson, Hayley; Walker, David W.] Monash Univ, Monash Inst Med Res, Ritchie Ctr, Melbourne, Vic 3168, Australia.
RP Ratnayake, U (reprint author), Monash Univ, Monash Inst Med Res, Ritchie Ctr, 27-31 Wright St, Melbourne, Vic 3168, Australia.
EM Udani.Ratnayake@monash.edu
FU ANZ Trustees; National Health and Medical Research Council; Victorian
   Government
FX This research has been undertaken in the authors' capacity as a staff
   member, student or affiliate of Monash Institute of Medical Research,
   Monash University. This work is supported by funding from the ANZ
   Trustees, National Health and Medical Research Council and the Victorian
   Government's Operational Infrastructure Support Program.
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NR 66
TC 26
Z9 27
PU ACADEMIC PRESS INC ELSEVIER SCIENCE
PI SAN DIEGO
PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
SN 0889-1591
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD NOV
PY 2012
VL 26
IS 8
BP 1288
EP 1299
DI 10.1016/j.bbi.2012.08.011
PG 12
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 025JV
UT WOS:000310186000014
PM 22960545
ER

PT J
AU Nowakowski, ME
   Tasker, SL
   Schmidt, LA
AF Nowakowski, Matilda E.
   Tasker, Susan L.
   Schmidt, Louis A.
TI Joint Attention in Toddlerhood Predicts Internalizing Problems at Early
   School Age
SO CLINICAL PEDIATRICS
LA English
DT Article
DE socioemotional development; internalizing behaviors; externalizing
   behaviors; mother-child interactions; joint attention
ID INFANT TEMPERAMENT; PRESCHOOL-CHILDREN; MOTHER-INFANT; BEHAVIOR; DEAF;
   HEARING; AUTISM; DYADS; COMPETENCE; RATINGS
AB The authors examined the longitudinal relation between joint attention and socioemotional functioning in a low-risk, typically developing sample of children when the children were toddlers and again during the early school-age years. Fifty-eight mothers and their children were observed in the home or laboratory engaging in 1 unstructured and 4 semistructured tasks designed to assess joint attention episodes when the children were toddlers. Approximately 4 years later, the mother-child dyads were contacted again and mothers completed the Child Behavior Checklist as a measure of their children's socioemotional outcome at the early school years. The authors found that lower frequencies of joint attention episodes at toddlerhood predicted higher internalizing behaviors at early school age. Preliminary findings are discussed in terms of their theoretical implications for work on early mother-child interactions and children's typical and atypical sociemotional development.
C1 [Nowakowski, Matilda E.] Ryerson Univ, Dept Psychol, Toronto, ON M5B 2K3, Canada.
   [Nowakowski, Matilda E.; Schmidt, Louis A.] McMaster Univ, Hamilton, ON, Canada.
   [Tasker, Susan L.] Univ Victoria, Victoria, BC, Canada.
RP Nowakowski, ME (reprint author), Ryerson Univ, Dept Psychol, 350 Victoria St, Toronto, ON M5B 2K3, Canada.
EM mnowakowski@psych.ryerson.ca
FU Social Sciences and Humanities Research Council (SSHRC) of Canada;
   Ontario Graduate Scholarship
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This research
   was supported by a graduate scholarship from the Social Sciences and
   Humanities Research Council (SSHRC) of Canada and an Ontario Graduate
   Scholarship awarded to the first and second author and an operating
   grant from SSHRC to the third author.
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NR 40
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0009-9228
J9 CLIN PEDIATR
JI Clin. Pediatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1032
EP 1040
DI 10.1177/0009922812441670
PG 9
WC Pediatrics
SC Pediatrics
GA 027UB
UT WOS:000310378200004
PM 22511189
ER

PT J
AU Williams, PG
   Tomchek, S
   Grau, R
   Bundy, MB
   Davis, DW
   Kleinert, H
AF Williams, Patricia Gail
   Tomchek, Scott
   Grau, Rebecca
   Bundy, Myra Beth
   Davis, Deborah Winders
   Kleinert, Harold
TI Parent and Physician Perceptions of Medical Home Care for Children With
   Autism Spectrum Disorders in the State of Kentucky
SO CLINICAL PEDIATRICS
LA English
DT Article
DE autism spectrum disorders; medical home
ID HEALTH; NEEDS; SERVICES; EXPERIENCES
AB The medical home model of care is widely accepted as the ideal for children with autism spectrum disorders (ASDs) but may be very difficult to implement. In this study, parents of children with autism and pediatricians caring for children with autism in Kentucky were surveyed to determine the current status of primary care services for children with ASDs. Results indicated that the majority of families and physicians were comfortable with the routine health care provided to children with ASDs, but had concerns about physician ability to provide information regarding community resources, address comorbid conditions associated with autism, and discuss treatment options. The need for physician education regarding available national and regional autism resources is clear. Creative strategies involving collaboration across medical, educational, and community systems appear to be essential for establishing effective medical homes for children with ASDs.
C1 [Williams, Patricia Gail; Tomchek, Scott; Grau, Rebecca; Davis, Deborah Winders] Univ Louisville, Louisville, KY 40202 USA.
   [Bundy, Myra Beth] Eastern Kentucky Univ, Richmond, KY 40475 USA.
   [Kleinert, Harold] Univ Kentucky, Lexington, KY USA.
RP Williams, PG (reprint author), Univ Louisville, 571 S Floyd St, Louisville, KY 40202 USA.
EM pgwill01@louisville.edu
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NR 22
TC 0
Z9 0
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0009-9228
J9 CLIN PEDIATR
JI Clin. Pediatr.
PD NOV
PY 2012
VL 51
IS 11
BP 1071
EP 1078
DI 10.1177/0009922812460333
PG 8
WC Pediatrics
SC Pediatrics
GA 027UB
UT WOS:000310378200009
PM 22984194
ER

PT J
AU Martorell, L
   Tondo, M
   Garcia-Fructuoso, F
   Naudo, M
   Alegre, C
   Gamez, J
   Genoves, J
   Poo, P
AF Martorell, Loreto
   Tondo, Mireia
   Garcia-Fructuoso, Ferran
   Naudo, Montserrat
   Alegre, Cayetano
   Gamez, Josep
   Genoves, Jordi
   Poo, Pilar
TI Screening for the presence of FMR1 premutation alleles in a Spanish
   population with fibromyalgia
SO CLINICAL RHEUMATOLOGY
LA English
DT Article
DE Autoimmune disease; CGG repeat; Fibromyalgia, chronic pain; FMR1 gene;
   Genetic counseling; Premutation
ID FRAGILE-X-SYNDROME; CENTRAL SENSITIVITY SYNDROMES; CGG REPEAT; GENE;
   CARRIERS; WOMEN; PREVALENCE; PHENOTYPE; PARADOX
AB Fragile X mental retardation 1 (FMR1) premutation carriers, who are at risk of having children with fragile X Syndrome, were initially considered as clinically unaffected. However, recent clinical and molecular studies have shifted this point of view. The incidence of premutation in the general population is substantial. Apart from the well-documented fragile X-associated tremor-ataxia and fragile X premature ovarian insufficiency, there is a broad constellation of symptoms including depression, anxiety, muscle pain, autoimmune and thyroid disease, chronic fatigue, and fibromyalgia that has been described, particularly in females with the premutation (55-200 repeats). Fibromyalgia (FM) is the most common cause of widespread pain and comprises a heterogeneous group of patients, affecting 2-3 % of the general population. We analyzed the FMR1 gene in a cohort of females diagnosed with fibromyalgia in order to assess the incidence of premutated alleles. CGG repeat size was determined in 353 females suffering from FM and results were compared with a control group. Four premutated carriers in the FM group were detected. The observed incidence is higher than that described for a normal female population (1/88 vs 1/250). The early detection of premutation carriers for the FMR1 gene among individuals diagnosed with fibromyalgia is important and would be helpful in correct genetic counseling of patients and their families, who may be at risk of having children with fragile X syndrome, the most common known cause of inherited intellectual disability and autism. Our data should be cautiously interpreted based on just this study; nevertheless, screening for the FMR1 gene in FM patients at least with presentations suggestive of FMR1 gene-related disease seems recommendable.
C1 [Martorell, Loreto; Tondo, Mireia; Naudo, Montserrat; Genoves, Jordi] Hosp St Joan de Deu, Mol Genet Sect, Barcelona 08950, Spain.
   [Garcia-Fructuoso, Ferran] CIMA Clin, Dept Rheumatol, Barcelona, Spain.
   [Alegre, Cayetano] Hosp Valle De Hebron, Rehumatol Dept, Barcelona, Spain.
   [Gamez, Josep] Hosp Valle De Hebron, Dept Neurol, Barcelona, Spain.
   [Poo, Pilar] Hosp St Joan de Deu, Dept Neurol, Barcelona 08950, Spain.
   [Alegre, Cayetano] Inst Univ Dexeus, Barcelona, Spain.
RP Martorell, L (reprint author), Hosp St Joan de Deu, Mol Genet Sect, Edifici Docent C Santa Rosa 39, Barcelona 08950, Spain.
EM lmartorell@hsjdbcn.org
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NR 25
TC 1
Z9 1
PU SPRINGER LONDON LTD
PI LONDON
PA 236 GRAYS INN RD, 6TH FLOOR, LONDON WC1X 8HL, ENGLAND
SN 0770-3198
J9 CLIN RHEUMATOL
JI Clin. Rheumatol.
PD NOV
PY 2012
VL 31
IS 11
BP 1611
EP 1615
DI 10.1007/s10067-012-2052-y
PG 5
WC Rheumatology
SC Rheumatology
GA 027UO
UT WOS:000310379500012
PM 22903700
ER

PT J
AU Demurie, E
   Roeyers, H
   Baeyens, D
   Sonuga-Barke, EJS
AF Demurie, Ellen
   Roeyers, Herbert
   Baeyens, Dieter
   Sonuga-Barke, Edmund J. S.
TI Temporal discounting of monetary rewards in children and adolescents
   with ADHD and autism spectrum disorders
SO DEVELOPMENTAL SCIENCE
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT-HYPERACTIVITY
   DISORDER; PERVASIVE DEVELOPMENTAL DISORDER; DELAYED REWARDS; SUSTAINED
   ATTENTION; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; BEHAVIOR; SYMPTOMS;
   TASK
AB It has been difficult to differentiate attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) in terms of some aspects of their cognitive profile. While both show deficits in executive functions, it has been suggested that they may differ in their response to monetary reward. For instance, children with ADHD prefer small immediate over large delayed rewards more than typically developing controls. One explanation for this is that they discount the value of rewards to a higher degree as they are moved into the future. The current study investigated whether children with ADHD can be differentiated from those with ASD in terms of reward discounting. Thirty-nine children (8-16 y) with ADHD, 34 children with ASD and 46 typically developing controls performed a hypothetical monetary temporal discounting task. Participants were instructed to make repeated choices between small variable rewards (0, 5, 10, 20, 30(sic)) delivered immediately and large rewards delivered after a variable delay. Children with ADHD but not ASD discounted future rewards at a higher rate than typically developing controls. These data confirm steeper discounting of future rewards in ADHD and add to a small but growing literature showing that the psychological profile of ADHD can be distinguished from that of ASD in terms of disrupted motivational processes.
C1 [Demurie, Ellen; Roeyers, Herbert; Sonuga-Barke, Edmund J. S.] Univ Ghent, Dept Expt Clin & Hlth Psychol, B-9000 Ghent, Belgium.
   [Baeyens, Dieter] Lessius Univ Coll, Dept Appl Psychol, Antwerp, Belgium.
   [Sonuga-Barke, Edmund J. S.] Univ Southampton, Dept Psychol, Southampton SO9 5NH, Hants, England.
RP Demurie, E (reprint author), Univ Ghent, Dept Expt Clin & Hlth Psychol, Henri Dunantlaan 2, B-9000 Ghent, Belgium.
EM ellen.demurie@ugent.be
RI Sonuga-Barke, Edmund/D-9137-2011
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NR 67
TC 17
Z9 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1363-755X
EI 1467-7687
J9 DEVELOPMENTAL SCI
JI Dev. Sci.
PD NOV
PY 2012
VL 15
IS 6
BP 791
EP 800
DI 10.1111/j.1467-7687.2012.01178.x
PG 10
WC Psychology, Developmental; Psychology, Experimental
SC Psychology
GA 029SO
UT WOS:000310516200008
PM 23106733
ER

PT J
AU Isrie, M
   Froyen, G
   Devriendt, K
   de Ravel, T
   Fryns, JP
   Vermeesch, JR
   Van Esch, H
AF Isrie, M.
   Froyen, G.
   Devriendt, K.
   de Ravel, T.
   Fryns, J. P.
   Vermeesch, J. R.
   Van Esch, H.
TI Sporadic male patients with intellectual disability: Contribution of
   X-chromosome copy number variants
SO EUROPEAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE X-chromosome; Copy number variation; Intellectual disability;
   Comparative genome hybridization; HTR2C
ID LINKED MENTAL-RETARDATION; ARRAY-CGH; VCX-A; GENE; DELETION;
   DUPLICATIONS; AUTISM; MUTATIONS; ICHTHYOSIS; PHENOTYPE
AB Genome-wide array comparative genome hybridization has become the first in line diagnostic tool in the clinical work-up of patients presenting with intellectual disability. As a result, chromosome X-copy number variations are frequently being detected in routine diagnostics. We retrospectively reviewed genome wide array-CGH data in order to determine the frequency and nature of chromosome X-copy number variations (X-CNV) in a cohort of 2222 sporadic male patients with intellectual disability (ID) referred to us for diagnosis. In this cohort, 68 males were found to have at least one X-CNV (3.1%). However, correct interpretation of causality remains a challenging task, and is essential for proper counseling, especially when the CNV is inherited. On the basis of these data, earlier experience and literature data we designed and propose an algorithm that can be used to evaluate the clinical relevance of X-CNVs detected in sporadic male ID patients. Applied to our cohort, 19 male ID patients (0.85%) were found to carry a (likely) pathogenic X-CNV. (C) 2012 Elsevier Masson SAS. All rights reserved.
C1 [Isrie, M.; Devriendt, K.; de Ravel, T.; Fryns, J. P.; Vermeesch, J. R.; Van Esch, H.] Katholieke Univ Leuven, Univ Hosp Leuven, Ctr Human Genet, B-3000 Louvain, Belgium.
   [Froyen, G.] Katholieke Univ Leuven VIB, Ctr Human Genet, Human Genome Lab, B-3000 Louvain, Belgium.
RP Van Esch, H (reprint author), Katholieke Univ Leuven, Univ Hosp Leuven, Ctr Human Genet, Herestr 49, B-3000 Louvain, Belgium.
EM Hilde.VanEsch@med.kuleuven.be
FU Geconcerteerde Onderzoeks Actie (GOA)
FX We are grateful to the patients and their families for their cooperation
   and participation. H. V. E. and K. D. are clinical investigators of the
   Fund for Scientific Research-Flanders, Belgium (FWO-Vlaanderen). This
   work was funded by the Geconcerteerde Onderzoeks Actie (GOA 2011-2015).
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NR 55
TC 8
Z9 8
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1769-7212
J9 EUR J MED GENET
JI Eur. J. Med. Genet.
PD NOV
PY 2012
VL 55
IS 11
BP 577
EP 585
DI 10.1016/j.ejmg.2012.05.005
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 019MK
UT WOS:000309743700001
PM 22659343
ER

PT J
AU Willemsen, MH
   de Leeuw, N
   de Brouwer, APM
   Pfundt, R
   Hehir-Kwa, JY
   Yntema, HG
   Nillesen, WM
   de Vries, BBA
   van Bokhoven, H
   Kleefstra, T
AF Willemsen, Marjolein H.
   de Leeuw, Nicole
   de Brouwer, Arjan P. M.
   Pfundt, Rolph
   Hehir-Kwa, Jayne Y.
   Yntema, Helger G.
   Nillesen, Willy M.
   de Vries, Bert B. A.
   van Bokhoven, Hans
   Kleefstra, Tjitske
TI Interpretation of clinical relevance of X-chromosome copy number
   variations identified in a large cohort of individuals with cognitive
   disorders and/or congenital anomalies
SO EUROPEAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE X-linked; Intellectual disability; Autism; X-chromosome; Copy number
   variation; Clinical interpretation
ID LINKED MENTAL-RETARDATION; COMPARATIVE GENOMIC HYBRIDIZATION; AUTISM
   SPECTRUM DISORDER; ARRAY-CGH; INTELLECTUAL DISABILITY; CYTOGENETIC
   ANALYSIS; DEVELOPMENTAL DELAY; DYSMORPHIC FEATURES; MICROARRAY ANALYSIS;
   GENE DELETION
AB Genome-wide array studies are now routinely being used in the evaluation of patients with cognitive disorders (CD) and/or congenital anomalies (CA). Therefore, inevitably each clinician is confronted with the challenging task of the interpretation of copy number variations detected by genome-wide array platforms in a diagnostic setting. Clinical interpretation of autosomal copy number variations is already challenging, but assessment of the clinical relevance of copy number variations of the X-chromosome is even more complex. This study provides an overview of the X-Chromosome copy number variations that we have identified by genome-wide array analysis in a large cohort of 4407 male and female patients. We have made an interpretation of the clinical relevance of each of these copy number variations based on well-defined criteria and previous reports in literature and databases. The prevalence of X-chromosome copy number variations in this cohort was 57/4407 (similar to 1.3%), of which 15 (0.3%) were interpreted as (likely) pathogenic. (C) 2012 Elsevier Masson SAS. All rights reserved.
C1 [Willemsen, Marjolein H.; de Leeuw, Nicole; de Brouwer, Arjan P. M.; Pfundt, Rolph; Hehir-Kwa, Jayne Y.; Yntema, Helger G.; Nillesen, Willy M.; de Vries, Bert B. A.; van Bokhoven, Hans; Kleefstra, Tjitske] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet 849, NL-6500 HB Nijmegen, Netherlands.
RP Willemsen, MH (reprint author), Radboud Univ Nijmegen, Med Ctr, Dept Human Genet 849, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM m.willemsen@gen.umcn.nl
RI van Bokhoven, Hans/D-8764-2012; Willemsen, Marjolein/G-9491-2013;
   Kleefstra, Tjitske/G-2619-2012
FU Consortium VG Oost-Nederland "Stronger on your own feet"; Netherlands
   Organization for Health Research and Development (ZonMw) [907-00-365];
   GENCODYS, an EU FP7 large-scale integrating project grant [241995]
FX This work was supported by grants from the Consortium VG Oost-Nederland
   "Stronger on your own feet" (to T. K and M. H. W), The Netherlands
   Organization for Health Research and Development (ZonMw grant number
   907-00-365 to T. K.) and GENCODYS, an EU FP7 large-scale integrating
   project grant (grant number 241995 to H. v. B. and T.K.).
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NR 79
TC 4
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1769-7212
J9 EUR J MED GENET
JI Eur. J. Med. Genet.
PD NOV
PY 2012
VL 55
IS 11
BP 586
EP 598
DI 10.1016/j.ejmg.2012.05.001
PG 13
WC Genetics & Heredity
SC Genetics & Heredity
GA 019MK
UT WOS:000309743700002
PM 22796527
ER

PT J
AU Vucurovic, K
   Landais, E
   Delahaigue, C
   Eutrope, J
   Schneider, A
   Leroy, C
   Kabbaj, H
   Motte, J
   Gaillard, D
   Rolland, AC
   Doco-Fenzy, M
AF Vucurovic, Ksenija
   Landais, Emilie
   Delahaigue, Cecile
   Eutrope, Julien
   Schneider, Anouck
   Leroy, Camille
   Kabbaj, Hamza
   Motte, Jacques
   Gaillard, Dominique
   Rolland, Anne-Catherine
   Doco-Fenzy, Martine
TI Bipolar affective disorder and early dementia onset in a male patient
   with SHANK3 deletion
SO EUROPEAN JOURNAL OF MEDICAL GENETICS
LA English
DT Article
DE SHANK3 deletion; Bipolar affective disorder; 22q13 deletion syndrome;
   Dementia onset; Dementia of Alzheimer's type
ID EXPRESSION; SYNAPSES; PROTEIN; SLEEP
AB The SHANK3 protein is a scaffold protein known to stabilize metabotropic glutamate receptor mGluR5 in the post-synaptic membrane of neurons. It is associated with genetic vulnerability in autism and schizophrenia. Here we report the case of an 18 year-old male patient who displayed psychiatric features of bipolar affective disorder associated with early setting of dementia. This mental status is related to sporadic occurrence of SHANK3 gene complex multiple deletions. A low beta amyloid protein rate (479 mg/L) found in cerebrospinal fluid suggests a possible link between SHANK3 deletion syndrome-associated regression and dementia of Alzheimers's type. In addition, we propose an overview of the phenotype related to SHANK3 deletion. (C) 2012 Elsevier Masson SAS. All rights reserved.
C1 [Vucurovic, Ksenija; Delahaigue, Cecile; Eutrope, Julien; Kabbaj, Hamza; Rolland, Anne-Catherine] Univ Hosp Reims, Dept Child & Adolescent Psychiat, Reims, France.
   [Landais, Emilie; Schneider, Anouck; Leroy, Camille; Gaillard, Dominique; Doco-Fenzy, Martine] Univ Hosp Reims, Dept Genet, Biol Sect, Reims, France.
   [Schneider, Anouck] CHU Montpellier, Dept Genet, Montpellier, France.
   [Motte, Jacques] SFR CAP SANTE REIMS, CHU REIMS, Amer Mem Hosp, Dept Pediat, Reims, France.
   [Doco-Fenzy, Martine] SFR CAP SANTE REIMS, EA 3801, Reims, France.
RP Vucurovic, K (reprint author), CHU Reims, Serv Psychotherapie Enfant & Adolescent, Ave Gen Koenig, F-51100 Reims, France.
EM vksenija@yahoo.com
CR Benington JH, 2003, PROG NEUROBIOL, V69, P71, DOI 10.1016/S0301-0082(03)00018-2
   Blennow K, 2006, LANCET, V368, P387, DOI 10.1016/S0140-6736(06)69113-7
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NR 17
TC 4
Z9 5
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 1769-7212
J9 EUR J MED GENET
JI Eur. J. Med. Genet.
PD NOV
PY 2012
VL 55
IS 11
BP 625
EP 629
DI 10.1016/j.ejmg.2012.07.009
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 019MK
UT WOS:000309743700008
PM 22922660
ER

PT J
AU Ladd-Acosta, C
   Lee, BK
   Bonner, J
   Sheppard, B
   Gidaya, N
   Weiss, L
   Quinn, J
   Windham, G
   Reynolds, A
   Croen, L
   Schendel, D
   Newschaffer, C
   Fallin, D
AF Ladd-Acosta, Christine
   Lee, Brian K.
   Bonner, Joseph
   Sheppard, Brooke
   Gidaya, Nicole
   Weiss, Lauren
   Quinn, Jeffrey
   Windham, Gayle
   Reynolds, Ann
   Croen, Lisa
   Schendel, Diana
   Newschaffer, Craig
   Fallin, Daniele
TI Application of Genome-wide Gene-environment Interaction Methods: The
   SEED Autism Study
SO GENETIC EPIDEMIOLOGY
LA English
DT Meeting Abstract
CT Annual Meeting of the International-Genetic-Epidemiology-Society (IGES)
CY OCT 18-20, 2012
CL Stevenson, WA
SP Int Genet Epidemiol Soc (IGES)
C1 [Ladd-Acosta, Christine; Sheppard, Brooke; Fallin, Daniele] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Lee, Brian K.; Gidaya, Nicole; Newschaffer, Craig] Drexel Univ, Sch Publ Hlth, Philadelphia, PA 19104 USA.
   [Bonner, Joseph] Michigan State Univ, Biomed Res Informat Core, E Lansing, MI 48824 USA.
   [Weiss, Lauren; Quinn, Jeffrey] Univ Calif San Francisco, San Francisco, CA 94143 USA.
   [Windham, Gayle; Croen, Lisa] Kaiser Permanente No California, Div Res, Oakland, CA USA.
   [Reynolds, Ann] Univ Colorado, Denver Sch Med, Boulder, CO 80309 USA.
   [Schendel, Diana] Ctr Dis Control & Prevent, Atlanta, GA 30329 USA.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0741-0395
J9 GENET EPIDEMIOL
JI Genet. Epidemiol.
PD NOV
PY 2012
VL 36
IS 7
MA 131
BP 757
EP 757
PG 1
WC Genetics & Heredity; Public, Environmental & Occupational Health
SC Genetics & Heredity; Public, Environmental & Occupational Health
GA 021VJ
UT WOS:000309913200136
ER

PT J
AU Lampi, KM
   Lehtonen, L
   Tran, PL
   Suominen, A
   Lehti, V
   Banerjee, PN
   Gissler, M
   Brown, AS
   Sourander, A
AF Lampi, Katja M.
   Lehtonen, Liisa
   Phuong Lien Tran
   Suominen, Auli
   Lehti, Venla
   Banerjee, P. Nina
   Gissler, Mika
   Brown, Alan S.
   Sourander, Andre
TI Risk of Autism Spectrum Disorders in Low Birth Weight and Small for
   Gestational Age Infants
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDER; PERINATAL FACTORS; OBSTETRIC
   COMPLICATIONS; ASPERGER-SYNDROME; NEONATAL FACTORS; CHILDREN;
   POPULATION; PRETERM; OUTCOMES; DISABILITIES
AB Objective To examine the relationship between birth weight, gestational age, small for gestational age (SGA), and 3 of the most common autism spectrum disorder (ASD) subtypes.
   Study design In this population-based case-control study conducted in Finland, 4713 cases born between 1987 and 2005 with International Classification of Diseases-diagnoses of childhood autism, Asperger syndrome, or pervasive developmental disorder (PDD), were ascertained from the Finnish Hospital Discharge Register. Four controls, individually matched on sex, date of birth, and place of birth, were selected from the Finnish Medical Birth Register for each case. Conditional logistic regression models were used to assess whether birth weight and gestational age information predicted ASD after controlling for maternal age, parity, smoking during pregnancy, and psychiatric history, as well as for infant's major congenital anomalies.
   Results Very low (< 1500 g) and moderately low (< 2500 g) birth weight, very low gestational age (less than 32 weeks), and SGA increased risk of childhood autism (adjusted OR 3.05, 95% CI 1.4-6.5; 1.57, 1.1-2.3; 2.51, 1.3-5.0; and 1.72, 1.1-2.6, respectively). Very low and moderately low birth weight, very low gestational age, and SGA were also associated with increase in PDD risk (OR 3.44, 95% CI 1.9-6.3; 1.81, 1.4-2.4; 2.46, 1.4-2.3; and 2.24, 1.7-3.0, respectively). No associations were found between the perinatal characteristics and Asperger syndrome. The increased risks persisted after controlling for selected potential confounders.
   Conclusions The finding that low birth weight, prematurity, and SGA were related to childhood autism and PDD but not to Asperger syndrome suggests that prenatal factors related to these exposures may differ for these ASD subtypes, which may have preventive implications. (J Pediatr 2012;161:830-6).
C1 [Sourander, Andre] Univ Turku, Child Psychiat Res Ctr, Dept Child Psychiat, Turku 20014, Finland.
   [Lehtonen, Liisa] Univ Turku, Dept Pediat, Turku 20014, Finland.
   [Lehtonen, Liisa] Turku Univ Hosp, Dept Pediat, FIN-20520 Turku, Finland.
   [Phuong Lien Tran] Univ Grenoble 1, Grenoble, France.
   [Banerjee, P. Nina; Brown, Alan S.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
   [Gissler, Mika] Natl Inst Hlth & Welf THL, Helsinki, Finland.
   [Gissler, Mika] Nord Sch Publ Hlth, Gothenburg, Sweden.
   [Brown, Alan S.; Sourander, Andre] Columbia Univ, Coll Phys & Surg, New York State Psychiat Inst, Dept Psychiat, New York, NY USA.
   [Sourander, Andre] Turku Univ Hosp, Dept Child Psychiat, FIN-20520 Turku, Finland.
RP Sourander, A (reprint author), Univ Turku, Child Psychiat Res Ctr, Dept Child Psychiat, Itainen Pitkakatu 1, Turku 20014, Finland.
EM katja.lampi@utu.fi
FU NIMH [1K02-MH65422, R01 MH 069819]; National Institute of Environmental
   Health Sciences [1R01ES019004]; Sigrid Juselius Foundation (Finland);
   Foundation for Pediatric Research (Finland); NIH/NIEHS
   [1R01ES019004-01]; NIH/NIMH [1R01MH082052-01, R01 MH073080,
   1P50MH090966-01, 2 K02 MH065422-06]
FX Supported by Autism Speaks, NIMH (1K02-MH65422), National Institute of
   Environmental Health Sciences (1R01ES019004), Sigrid Juselius Foundation
   (Finland), and Foundation for Pediatric Research (Finland). A.B.
   received the following grants, which do not conflict with the current
   study: NIH/NIEHS (1R01ES019004-01; PI: A.B.), NIH/NIMH (1R01MH082052-01
   [PI: A.B.], R01 MH073080 [PI: A.B.], 1P50MH090966-01, and 2 K02
   MH065422-06), and NIMH (R01 MH 069819). The authors declare no conflicts
   of interest.
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NR 44
TC 28
Z9 28
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD NOV
PY 2012
VL 161
IS 5
BP 830
EP 836
DI 10.1016/j.jpeds.2012.04.058
PG 7
WC Pediatrics
SC Pediatrics
GA 027RJ
UT WOS:000310370600015
PM 22677565
ER

PT J
AU Matsuzaki, M
   Matsushita, H
   Tomizawa, K
   Matsui, H
AF Matsuzaki, Mitsuhiro
   Matsushita, Hiroaki
   Tomizawa, Kazuhito
   Matsui, Hideki
TI Oxytocin: a therapeutic target for mental disorders
SO JOURNAL OF PHYSIOLOGICAL SCIENCES
LA English
DT Review
DE Oxytocin; Depression; Sildenafil; CREB; MAP kinase
ID MAP KINASE; MAJOR DEPRESSION; ANTIDEPRESSANT; PLASMA; BEHAVIOR; STRESS;
   MEMORY; RATS; DYSFUNCTION; SILDENAFIL
AB We review here that oxytocin (OT) is released into blood and within distinct brain regions in response to stressful and social stimuli, and has been shown to have an antidepressant-like effect in animal studies. Clinical reports suggest OT to be a promising drug for psychiatric diseases such as depression, anxiety disorders, schizophrenia, and autism. OT may also have therapeutic potential in the treatment of major depressive disorders, even though OT administered into blood does not readily cross the blood-brain barrier. Physiological functions such as sexual activity and mating induce the release of OT in the central nervous system. A drug for the treatment of sexual dysfunction, sildenafil, enhances the electrically evoked release of OT from the posterior pituitary. This drug has antidepressant-like effects through activation of an OT signaling pathway. These results suggest that sildenafil may have promise as a potential antidepressant.
C1 [Matsuzaki, Mitsuhiro; Matsushita, Hiroaki; Matsui, Hideki] Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol, Kita Ku, Okayama 7008558, Japan.
   [Tomizawa, Kazuhito] Kumamoto Univ, Dept Mol Physiol, Fac Life Sci, Kumamoto 8608556, Japan.
RP Matsui, H (reprint author), Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol, Kita Ku, 2-5-1 Shikata Cho, Okayama 7008558, Japan.
EM matsuihi@cc.okayama-u.ac.jp
RI Tomizawa, Kazuhito/F-2405-2015
OI Tomizawa, Kazuhito/0000-0002-5663-2627
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NR 43
TC 14
Z9 15
PU SPRINGER JAPAN KK
PI TOKYO
PA CHIYODA FIRST BLDG EAST, 3-8-1 NISHI-KANDA, CHIYODA-KU, TOKYO, 101-0065,
   JAPAN
SN 1880-6546
J9 J PHYSIOL SCI
JI J. Physiol. Sci.
PD NOV
PY 2012
VL 62
IS 6
BP 441
EP 444
DI 10.1007/s12576-012-0232-9
PG 4
WC Physiology
SC Physiology
GA 030AX
UT WOS:000310541100002
PM 23007624
ER

PT J
AU [Anonymous]
AF [Anonymous]
TI High demands of the Autism Centers of Excellence programme
SO LANCET NEUROLOGY
LA English
DT Editorial Material
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 1474-4422
J9 LANCET NEUROL
JI Lancet Neurol.
PD NOV
PY 2012
VL 11
IS 11
BP 929
EP 929
PG 1
WC Clinical Neurology
SC Neurosciences & Neurology
GA 028KW
UT WOS:000310422200001
ER

PT J
AU Lind, SE
   Williams, DM
AF Lind, Sophie E.
   Williams, David M.
TI The association between past and future oriented thinking: Evidence from
   autism spectrum disorder
SO LEARNING AND MOTIVATION
LA English
DT Article
DE Autism spectrum disorder; Episodic memory; Episodic future thinking;
   Mental time travel; Planning; Prospective memory
ID SHORT-TERM-MEMORY; AUTOBIOGRAPHICAL MEMORY; EPISODIC MEMORY;
   ASPERGER-SYNDROME; AUTONOETIC CONSCIOUSNESS; WORKING-MEMORY; INNER
   SPEECH; ADULTS; MIND; ABILITY
AB A number of recently developed theories (e.g., the constructive episodic simulation, self-projection, and scene construction hypotheses) propose that the ability to simulate possible future events (sometimes referred to as episodic future thinking, prospection, or foresight) depends on the same neurocognitive system that is implicated in the recall of past events (episodic memory). In this paper, we argue that autism spectrum disorder (ASD) offers an ideal test of such theories, given that it is a developmental disorder that is characterized by impairments in episodic memory. Each of these theories would predict concomitant impairments in episodic future thinking among individuals with ASD. We review evidence concerning episodic future thinking in ASD, as well as studies of prospective memory (remembering to do something in the future), planning, navigation, and theory of mind, which some theories suggest also rely on the same mechanism as episodic future thinking. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Lind, Sophie E.; Williams, David M.] Univ Durham, Dept Psychol, Durham DH1 3LE, England.
RP Williams, DM (reprint author), Univ Durham, Dept Psychol, Sci Site,South Rd, Durham DH1 3LE, England.
EM sophie.lind@durham.ac.uk; david.williams@durham.ac.uk
RI Williams, David/B-9804-2013
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NR 76
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 0023-9690
J9 LEARN MOTIV
JI Learn. Motiv.
PD NOV
PY 2012
VL 43
IS 4
SI SI
BP 231
EP 240
DI 10.1016/j.lmot.2012.05.004
PG 10
WC Psychology, Biological; Psychology, Experimental
SC Psychology
GA 024ND
UT WOS:000310115000008
ER

PT J
AU Barcia, G
   Fleming, MR
   Deligniere, A
   Gazula, VR
   Brown, MR
   Langouet, M
   Chen, HJ
   Kronengold, J
   Abhyankar, A
   Cilio, R
   Nitschke, P
   Kaminska, A
   Boddaert, N
   Casanova, JL
   Desguerre, I
   Munnich, A
   Dulac, O
   Kaczmarek, LK
   Colleaux, L
   Nabbout, R
AF Barcia, Giulia
   Fleming, Matthew R.
   Deligniere, Aline
   Gazula, Valeswara-Rao
   Brown, Maile R.
   Langouet, Maeva
   Chen, Haijun
   Kronengold, Jack
   Abhyankar, Avinash
   Cilio, Roberta
   Nitschke, Patrick
   Kaminska, Anna
   Boddaert, Nathalie
   Casanova, Jean-Laurent
   Desguerre, Isabelle
   Munnich, Arnold
   Dulac, Olivier
   Kaczmarek, Leonard K.
   Colleaux, Laurence
   Nabbout, Rima
TI De novo gain-of-function KCNT1 channel mutations cause malignant
   migrating partial seizures of infancy
SO NATURE GENETICS
LA English
DT Article
ID ACTIVATED POTASSIUM CHANNELS; AUTISM SPECTRUM DISORDERS; EPILEPTIC
   ENCEPHALOPATHY; SCN1A MUTATIONS; FOCAL SEIZURES; ION CHANNELS; K+
   CHANNELS; SLACK; SODIUM; LEVETIRACETAM
AB Malignant migrating partial seizures of infancy (MMPSI) is a rare epileptic encephalopathy of infancy that combines pharmacoresistant seizures with developmental delay(1). We performed exome sequencing in three probands with MMPSI and identified de novo gain-of-function mutations affecting the C-terminal domain of the KCNT1 potassium channel. We sequenced KCNT1 in 9 additional individuals with MMPSI and identified mutations in 4 of them, in total identifying mutations in 6 out of 12 unrelated affected individuals. Functional studies showed that the mutations led to constitutive activation of the channel, mimicking the effects of phosphorylation of the C-terminal domain by protein kinase C. In addition to regulating ion flux, KCNT1 has a non-conducting function, as its C terminus interacts with cytoplasmic proteins involved in developmental signaling pathways. These results provide a focus for future diagnostic approaches and research for this devastating condition.
C1 [Barcia, Giulia; Deligniere, Aline; Desguerre, Isabelle; Dulac, Olivier; Nabbout, Rima] Hop Necker Enfants Malad, AP HP, Ctr Reference Epilepsies Rares, Dept Pediat Neurol, Paris, France.
   [Barcia, Giulia; Dulac, Olivier; Nabbout, Rima] Univ Paris 05, Hop Necker Enfants Malad, INSERM, U663, Paris, France.
   [Fleming, Matthew R.; Gazula, Valeswara-Rao; Brown, Maile R.; Kronengold, Jack; Kaczmarek, Leonard K.] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06510 USA.
   [Fleming, Matthew R.; Kaczmarek, Leonard K.] Yale Univ, Sch Med, Dept Cellular & Mol Physiol, New Haven, CT 06510 USA.
   [Langouet, Maeva; Munnich, Arnold; Colleaux, Laurence] Univ Paris 05, Hop Necker Enfants Malad, INSERM, U781,Inst Imagine, Paris, France.
   [Chen, Haijun] SUNY Albany, Dept Biol Sci, Albany, NY 12222 USA.
   [Abhyankar, Avinash; Casanova, Jean-Laurent] Rockefeller Univ, Rockefeller Branch, St Giles Lab Human Genet Infect Dis, New York, NY 10021 USA.
   [Cilio, Roberta] Bambino Gesu Pediat Hosp, Div Neurol, Rome, Italy.
   [Nitschke, Patrick] Hop Necker Enfants Malad, Dept Biostat, Paris, France.
   [Kaminska, Anna] Hop Necker Enfants Malad, AP HP, Clin Electrophysiol Unit, Paris, France.
   [Boddaert, Nathalie] Hop Necker Enfants Malad, AP HP, Dept Paediat Radiol, Paris, France.
RP Nabbout, R (reprint author), Hop Necker Enfants Malad, AP HP, Ctr Reference Epilepsies Rares, Dept Pediat Neurol, Paris, France.
EM rimanabbout@yahoo.com
FU Centre National de la Recherche Scientifique; French National Research
   Agency [ANR-08-MNP-010]; US National Institutes of Health (NIH)
   [HD067517, DC01919, NS073943]; FRAXA foundation; St. Giles Foundation;
   Rockefeller University Center for Clinical and Translational Science
   [5UL1RR024143]; Rockefeller University
FX We are grateful to the affected individuals and their families for their
   participation in the study. The team of L.C. was supported in part by
   the Centre National de la Recherche Scientifique and the French National
   Research Agency (ANR-08-MNP-010). Work by the team of L.K.K. is
   supported by the US National Institutes of Health (NIH) grants HD067517,
   DC01919 and NS073943 and a grant from the FRAXA foundation. The
   Laboratory of Human Genetics of Infectious Diseases is supported in part
   by grants from the St. Giles Foundation, the Rockefeller University
   Center for Clinical and Translational Science grant 5UL1RR024143 and the
   Rockefeller University.
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NR 39
TC 62
Z9 65
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1061-4036
J9 NAT GENET
JI Nature Genet.
PD NOV
PY 2012
VL 44
IS 11
BP 1255
EP 1259
DI 10.1038/ng.2441
PG 5
WC Genetics & Heredity
SC Genetics & Heredity
GA 029KZ
UT WOS:000310495800019
PM 23086397
ER

PT J
AU Garcia, MJM
   Becerra, IG
   Espin, MJG
AF Martin Garcia, Maria Jesus
   Gomez Becerra, Inmaculada
   Garro Espin, Maria Jose
TI Theory of Mind in a child with autism: How to train her?
SO PSICOTHEMA
LA Spanish
DT Article
ID PERSPECTIVE-TAKING; INDIVIDUALS; PERFORMANCE; ADULTS; BELIEF
AB Theory of Mind in a child with autism: How to train her? Theory of Mind is a metacognitive skill that, in many cases, is deficient in autism. In this paper, we present a clinical study conducted with a child diagnosed with autism, which verifies the effectiveness of a training protocol testing false beliefs, which has been considered to measure the Theory of Mind. Basically, the protocol incorporates a number of verbal prompts (such as emphasizing the elements of the narratives that indicate situational or temporary changes), trains many examples, extending the tests incorporating some games with more familiar objects from the child's daily life, applies differential contingencies to discriminate right from wrong in each child's responses and provides descriptive feedback. The results show that the training protocol achieved the highest level of correct trials and the child generalizes the ability to take the perspective of her natural context.
C1 [Gomez Becerra, Inmaculada] Univ Almeria, Escuela Super Politecn, Almeria 04120, Spain.
RP Becerra, IG (reprint author), Univ Almeria, Escuela Super Politecn, Almeria 04120, Spain.
EM igomez@ual.es
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NR 28
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
J9 PSICOTHEMA
JI Psicothema
PD NOV
PY 2012
VL 24
IS 4
BP 542
EP 547
PG 6
WC Psychology, Multidisciplinary
SC Psychology
GA 020YM
UT WOS:000309852500006
ER

PT J
AU Heck, DH
   Gu, WL
   Cao, Y
   Qi, SH
   Lacaria, M
   Lupski, JR
AF Heck, Detlef H.
   Gu, Wenli
   Cao, Ying
   Qi, Shuhua
   Lacaria, Melanie
   Lupski, James R.
TI Opposing phenotypes in mice with Smith-Magenis deletion and
   Potocki-Lupski duplication syndromes suggest gene dosage effects on
   fluid consumption behavior
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE copy number variation (CNV); fluid consumption behavior; gene dosage
   effect; mouse licking assay
ID COPY NUMBER VARIATION; SYNDROME DEL 17P11.2; CRANIOFACIAL ANOMALIES;
   MOUSE MODELS; HUMAN GENOME; AUTISM; DUP(17)(P11.2P11.2); SCHIZOPHRENIA;
   LICKING; 16P11.2
AB A quantitative long-term fluid consumption and fluid-licking assay was performed in two mouse models with either an similar to 2?Mb genomic deletion, Df(11)17, or the reciprocal duplication copy number variation (CNV), Dp(11)17, analogous to the human genomic rearrangements causing either SmithMagenis syndrome [SMS; OMIM #182290] or PotockiLupski syndrome [PTLS; OMIM #610883], respectively. Both mouse strains display distinct quantitative alterations in fluid consumption compared to their wild-type littermates; several of these changes are diametrically opposing between the two chromosome engineered mouse models. Mice with duplication versus deletion showed longer versus shorter intervals between visits to the waterspout, generated more versus less licks per visit and had higher versus lower variability in the number of licks per lick-burst as compared to their respective wild-type littermates. These findings suggest that copy number variation can affect long-term fluid consumption behavior in mice. Other behavioral differences were unique for either the duplication or deletion mutants; the deletion CNV resulted in increased variability of the licking rhythm, and the duplication CNV resulted in a significant slowing of the licking rhythm. Our findings document a readily quantitated complex behavioral response that can be directly and reciprocally influenced by a gene dosage effect. (c) 2012 Wiley Periodicals, Inc.
C1 [Heck, Detlef H.; Cao, Ying; Qi, Shuhua] Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, Memphis, TN 38163 USA.
   [Gu, Wenli; Lacaria, Melanie; Lupski, James R.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Lupski, James R.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
   [Lupski, James R.] Texas Childrens Hosp, Houston, TX 77030 USA.
RP Heck, DH (reprint author), Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, Memphis, TN 38163 USA.
EM dheck@uthsc.edu; jlupski@bcm.edu
FU National Institutes of Health [R01NS060887, R01NS067201, R01NS063009];
   National Institutes of Neurological Diseases and Stroke [R01NS058529]
FX This research was supported by grants from the National Institutes of
   Health to D.H.H. (R01NS060887, R01NS067201, and R01NS063009) and from
   the National Institutes of Neurological Diseases and Stroke
   (R01NS058529) to J.R.L. The content of this publication is solely the
   responsibility of the authors and does not necessarily represent the
   official views of the NIH.
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NR 49
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD NOV
PY 2012
VL 158A
IS 11
BP 2807
EP 2814
DI 10.1002/ajmg.a.35601
PG 8
WC Genetics & Heredity
SC Genetics & Heredity
GA 023XT
UT WOS:000310071700026
PM 22991245
ER

PT J
AU Gilmore, JH
   Shi, F
   Woolson, SL
   Knickmeyer, RC
   Short, SJ
   Lin, WL
   Zhu, HT
   Hamer, RM
   Styner, M
   Shen, DG
AF Gilmore, John H.
   Shi, Feng
   Woolson, Sandra L.
   Knickmeyer, Rebecca C.
   Short, Sarah J.
   Lin, Weili
   Zhu, Hongtu
   Hamer, Robert M.
   Styner, Martin
   Shen, Dinggang
TI Longitudinal Development of Cortical and Subcortical Gray Matter from
   Birth to 2 Years
SO CEREBRAL CORTEX
LA English
DT Article
DE amygdala; cerebral cortex; hippocampus; lateral ventricle; magnetic
   resonace imaging
ID NEONATAL BRAIN STRUCTURE; HUMAN PREFRONTAL CORTEX; HUMAN
   CEREBRAL-CORTEX; PATH-INTEGRATION; EARLY ADULTHOOD; WHITE-MATTER; INFANT
   BRAIN; LIFE-SPAN; AUTISM; CHILDHOOD
AB Very little is known about cortical development in the first years of life, a time of rapid cognitive development and risk for neurodevelopmental disorders. We studied regional cortical and subcortical gray matter volume growth in a group of 72 children who underwent magnetic resonance scanning after birth and at ages 1 and 2 years using a novel longitudinal registration/parcellation approach. Overall, cortical gray matter volumes increased substantially (106%) in the first year of life and less so in the second year (18%). We found marked regional differences in developmental rates, with primary motor and sensory cortices growing slower in the first year of life with association cortices growing more rapidly. In the second year of life, primary sensory regions continued to grow more slowly, while frontal and parietal regions developed relatively more quickly. The hippocampus grew less than other subcortical structures such as the amygdala and thalamus in the first year of life. It is likely that these patterns of regional gray matter growth reflect maturation and development of underlying function, as they are consistent with cognitive and functional development in the first years of life.
C1 [Gilmore, John H.; Woolson, Sandra L.; Knickmeyer, Rebecca C.; Short, Sarah J.; Hamer, Robert M.; Styner, Martin] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA.
   [Gilmore, John H.; Shi, Feng; Lin, Weili; Zhu, Hongtu; Shen, Dinggang] Univ N Carolina, Biomed Res Imaging Ctr, Chapel Hill, NC 27599 USA.
   [Shi, Feng; Lin, Weili; Shen, Dinggang] Univ N Carolina, Dept Radiol, Chapel Hill, NC 27599 USA.
   [Zhu, Hongtu; Hamer, Robert M.] Univ N Carolina, Dept Biostat, Chapel Hill, NC 27599 USA.
   [Styner, Martin] Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA.
RP Gilmore, JH (reprint author), 10522 Neurosci Hosp, UNC Sch Med, Dept Psychiat, CB 7160, Chapel Hill, NC 27599 USA.
EM jgilmore@med.unc.edu
RI Shi, Feng/G-3247-2012; Knickmeyer, Rebecca/G-8128-2014
OI Knickmeyer, Rebecca/0000-0001-7708-1388
FU National Institutes of Health [P50 MH064065, HD053000, MH070890]
FX National Institutes of Health (grant P50 MH064065, HD053000, and
   MH070890 to J.H.G).
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NR 62
TC 41
Z9 42
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD NOV
PY 2012
VL 22
IS 11
BP 2478
EP 2485
DI 10.1093/cercor/bhr327
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 018XH
UT WOS:000309700700003
PM 22109543
ER

PT J
AU Howlin, P
AF Howlin, Patricia
TI Autism Spectrum Disorders
SO CHILD AND ADOLESCENT MENTAL HEALTH
LA English
DT Book Review
C1 [Howlin, Patricia] Inst Psychiat, London, England.
RP Howlin, P (reprint author), Inst Psychiat, London, England.
CR Amaral D., 2011, AUTISM SPECTRUM DISO
NR 1
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1475-357X
J9 CHILD ADOL MENT H-UK
JI Child Adolesc. Ment. Health
PD NOV
PY 2012
VL 17
IS 4
BP 256
EP 256
DI 10.1111/camh.12008_3
PG 1
WC Psychology, Clinical; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 023UX
UT WOS:000310063000012
ER

PT J
AU Hock, RM
   Timm, TM
   Ramisch, JL
AF Hock, Robert M.
   Timm, Tina M.
   Ramisch, Julie L.
TI Parenting children with autism spectrum disorders: a crucible for couple
   relationships
SO CHILD & FAMILY SOCIAL WORK
LA English
DT Article
DE autism spectrum disorder (ASD); autism; couples; marriage; parenting;
   relationship
ID COPING STRATEGIES; BEHAVIOR PROBLEMS; MOTHERS; STRESS; FAMILY; FATHERS;
   IMPACT; DISABILITIES; PERCEPTIONS; ADJUSTMENT
AB As the incidence of autism spectrum disorders (ASDs) continues to rise, there is a growing need to understand how ASDs impact family life. This qualitative study explored the ways in which parenting a child with ASD impacts marriages. Using modified grounded theory, nine couples and one wife (n= 19) were interviewed. The dominant finding that emerged is that parenting a child with ASD acts as a crucible for couple relationships, exerting extraordinary pressure on partners that forces qualitative adaptations in their relationship. Two relationship phases emerged from the analysis: tag team and deeper intimacy and commitment. The resulting theoretical model can help clinicians tailor assessment and intervention for couples who are parenting a child with ASD.
C1 [Hock, Robert M.] Univ S Carolina, Coll Social Work, Columbia, SC 29208 USA.
   [Timm, Tina M.] Michigan State Univ, Sch Social Work, E Lansing, MI 48824 USA.
RP Hock, RM (reprint author), Univ S Carolina, Coll Social Work, Columbia, SC 29208 USA.
EM roberth@sc.edu
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NR 37
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1356-7500
J9 CHILD FAM SOC WORK
JI Child Fam. Soc. Work
PD NOV
PY 2012
VL 17
IS 4
BP 406
EP 415
DI 10.1111/j.1365-2206.2011.00794.x
PG 10
WC Family Studies; Social Work
SC Family Studies; Social Work
GA 023VQ
UT WOS:000310065400003
ER

PT J
AU Pavone, V
   Pratico, AD
   Parano, E
   Pavone, P
   Verrotti, A
   Falsaperla, R
AF Pavone, Vito
   Pratico, Andrea Domenico
   Parano, Enrico
   Pavone, Piero
   Verrotti, Alberto
   Falsaperla, Raffaele
TI Spine and brain malformations in a patient obligate carrier of MTHFR
   with autism and mental retardation
SO CLINICAL NEUROLOGY AND NEUROSURGERY
LA English
DT Article
DE Autism; Diastematomyelia; Mental retardation; MTHFR; Spinal malformation
C1 [Pavone, Piero] Univ Catania, Dept Pediat, Div Orthoped, Orthoped Clin, I-95124 Catania, Italy.
   [Pratico, Andrea Domenico; Pavone, Piero; Falsaperla, Raffaele] Univ Hosp Vittorio Emanuele Policlin, Unit Pediat & Pediat Emergency Costanza Gravina, Catania, Italy.
   [Parano, Enrico] CNR, Inst Neurol Sci, Catania, Italy.
   [Verrotti, Alberto] Univ G dAnnunzio, Chair Pediat Neurol, Chieti, Italy.
RP Pavone, P (reprint author), Univ Catania, Dept Pediat, Div Orthoped, Orthoped Clin, Via Plebiscito 767, I-95124 Catania, Italy.
EM ppavone@unict.it
CR Martinez CA, 2009, AM J OBSTET GYNECOL, V201, P1
   Moretti P, 2005, NEUROLOGY, V64, P1088
   Rossi A, 2004, J NEURORADIOLOGY, V31, P3, DOI 10.1016/S0150-9861(04)96875-7
   Sadler TW, 2005, AM J MED GENET C, V135C, P2, DOI 10.1002/ajmg.c.30049
   Troen AM, 2008, J NUTR, V138, P2502, DOI 10.3945/jn.108.093641
NR 5
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0303-8467
J9 CLIN NEUROL NEUROSUR
JI Clin. Neurol. Neurosurg.
PD NOV
PY 2012
VL 114
IS 9
BP 1280
EP 1282
DI 10.1016/j.clineuro.2012.03.008
PG 3
WC Clinical Neurology; Surgery
SC Neurosciences & Neurology; Surgery
GA 024NJ
UT WOS:000310115600017
PM 22498705
ER

PT J
AU Roberson, D
   Kikutani, M
   Doge, P
   Whitaker, L
   Majid, A
AF Roberson, Debi
   Kikutani, Mariko
   Doege, Paula
   Whitaker, Lydia
   Majid, Asifa
TI Shades of emotion: What the addition of sunglasses or masks to faces
   reveals about the development of facial expression processing
SO COGNITION
LA English
DT Article
DE Facial expression; Emotion; Child-development; Categories
ID UPSIDE-DOWN FACES; EYE CONTACT; RECOGNITION; AUTISM; PERCEPTION;
   CHILDREN; INTENSITIES; LANGUAGE; DISORDER; INFANTS
AB Three studies investigated developmental changes in facial expression processing, between 3 years-of-age and adulthood. For adults and older children, the addition of sunglasses to upright faces caused an equivalent decrement in performance to face inversion. However, younger children showed better classification of expressions of faces wearing sunglasses than children who saw the same faces un-occluded. When the mouth area was occluded with a mask, children under nine years showed no impairment in expression classification, relative to un-occluded faces. An early selective focus of attention on the eyes may be optimal for socialization, but mediate against accurate expression classification. The data support a model in which a threshold level of attentional control must be reached before children can develop adult-like configural processing skills and be flexible in their use of face- processing strategies. (c) 2012 Elsevier B.V. All rights reserved.
C1 [Roberson, Debi; Kikutani, Mariko; Whitaker, Lydia] Univ Essex, Colchester CO4 3SQ, Essex, England.
   [Doege, Paula] Univ Osnabruck, D-49069 Osnabruck, Germany.
   [Majid, Asifa] Max Planck Inst Psycholinguist, NL-6500 AH Njimegen, Netherlands.
   [Majid, Asifa] Radboud Univ Nijmegen, Donders Ctr Brain Cognit & Behav, NL-6525 ED Nijmegen, Netherlands.
RP Roberson, D (reprint author), Univ Essex, Colchester CO4 3SQ, Essex, England.
EM robedd@essex.ac.uk
RI Roberson, Debi/C-1612-2009; Majid, Asifa/A-7906-2008
OI Roberson, Debi/0000-0002-6778-8547; 
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NR 39
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0010-0277
J9 COGNITION
JI Cognition
PD NOV
PY 2012
VL 125
IS 2
BP 195
EP 206
DI 10.1016/j.cognition.2012.06.018
PG 12
WC Psychology, Experimental
SC Psychology
GA 022HR
UT WOS:000309949300006
PM 22892280
ER

PT J
AU Holt, R
   Sykes, NH
   Conceicao, IC
   Cazier, JB
   Anney, RJL
   Oliveira, G
   Gallagher, L
   Vicente, A
   Monaco, AP
   Pagnamenta, AT
AF Holt, Richard
   Sykes, Nuala H.
   Conceicao, Ines C.
   Cazier, Jean-Baptiste
   Anney, Richard J. L.
   Oliveira, Guiomar
   Gallagher, Louise
   Vicente, Astrid
   Monaco, Anthony P.
   Pagnamenta, Alistair T.
TI CNVs leading to fusion transcripts in individuals with autism spectrum
   disorder
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE CNV; MAPKAPK5; ACAD10; ALDH2; KIAA0319; dyslexia
ID COPY NUMBER VARIATION; ALCOHOL-CONSUMPTION; PROSTATE-CANCER; GENE;
   EXPRESSION; DYSLEXIA; SUSCEPTIBILITY; KIAA0319; GENOME; SHANK3
AB There is strong evidence that rare copy number variants (CNVs) have a role in susceptibility to autism spectrum disorders (ASDs). Much research has focused on how CNVs mediate a phenotypic effect by altering gene expression levels. We investigated an alternative mechanism whereby CNVs combine the 5' and 3' ends of two genes, creating a 'fusion gene'. Any resulting mRNA with an open reading frame could potentially alter the phenotype via a gain-of-function mechanism. We examined 2382 and 3096 rare CNVs from 996 individuals with ASD and 1287 controls, respectively, for potential to generate fusion transcripts. There was no increased burden in individuals with ASD; 122/996 cases harbored at least one rare CNV of this type, compared with 179/1287 controls (P = 0.89). There was also no difference in the overall frequency distribution between cases and controls. We examined specific examples of such CNVs nominated by case-control analysis and a candidate approach. Accordingly, a duplication involving REEP1-POLR1A (found in 3/996 cases and 0/1287 controls) and a single occurrence CNV involving KIAA0319-TDP2 were tested. However, no fusion transcripts were detected by RT-PCR. Analysis of additional samples based on cell line availability resulted in validation of a MAPKAPK5-ACAD10 fusion transcript in two probands. However, this variant was present in controls at a similar rate and is unlikely to influence ASD susceptibility. In summary, although we find no evidence that fusion-gene generating CNVs lead to ASD susceptibility, discovery of a MAPKAPK5-ACAD10 transcript with an estimated frequency of similar to 1/200 suggests that gain-of-function mechanisms should be considered in future CNVs studies. European Journal of Human Genetics (2012) 20, 1141-1147; doi: 10.1038/ejhg.2012.73; published online 2 May 2012
C1 [Holt, Richard; Sykes, Nuala H.; Cazier, Jean-Baptiste; Monaco, Anthony P.; Pagnamenta, Alistair T.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England.
   [Conceicao, Ines C.; Vicente, Astrid] Inst Nacl Saude Dr Ricardo Jorge, Lisbon, Portugal.
   [Conceicao, Ines C.; Vicente, Astrid] Inst Gulbenkian Ciencias, Oeiras, Portugal.
   [Conceicao, Ines C.; Vicente, Astrid] Ctr Biodivers Funct & Integrat Genom BIOFIG, Lisbon, Portugal.
   [Anney, Richard J. L.; Gallagher, Louise] Trinity Coll Dublin, Dept Psychiat, Sch Med, Autism Genet Grp, Dublin, Ireland.
   [Oliveira, Guiomar] Hosp Pediat Coimbra, Ctr Desenvolvimento Cri Crianca, Unidade Neurodesenvolvimento & Autismo, Coimbre, Portugal.
   [Oliveira, Guiomar] Hosp Pediat Coimbra, Ctr Invest & Formacao Clin, Coimbra, Portugal.
   [Oliveira, Guiomar] Univ Coimbra, Fac Med, Coimbra, Portugal.
RP Pagnamenta, AT (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England.
EM alistair@well.ox.ac.uk
RI Oliveira, Guiomar/I-7255-2013; Monaco, Anthony/A-4495-2010
OI Monaco, Anthony/0000-0001-7480-3197
FU Autism Speaks; Wellcome Trust [090532/Z/09/Z]; NIHR Biomedical Research
   Centre; National Institute of Mental Health [1U24MH081810]
FX We gratefully acknowledge the families participating in the study,
   Dalila Pinto and members of the international Autism Genome Project
   consortium for sharing data, ideas and comments on the manuscript.
   Funding was from Autism Speaks and a Wellcome Trust core award
   090532/Z/09/Z. ATP is currently supported by the NIHR Biomedical
   Research Centre. We gratefully acknowledge the resources provided by the
   Autism Genetic Resource Exchange (AGRE) Consortium and the participating
   AGRE families. The Autism Genetic Resource Exchange 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).
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NR 31
TC 7
Z9 7
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD NOV
PY 2012
VL 20
IS 11
BP 1141
EP 1147
DI 10.1038/ejhg.2012.73
PG 7
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 025TW
UT WOS:000310218600007
PM 22549408
ER

PT J
AU Vengoechea, J
   Parikh, AS
   Zhang, SL
   Tassone, F
AF Vengoechea, Jaime
   Parikh, Aditi S.
   Zhang, Shulin
   Tassone, Flora
TI De novo microduplication of the FMR1 gene in a patient with
   developmental delay, epilepsy and hyperactivity
SO EUROPEAN JOURNAL OF HUMAN GENETICS
LA English
DT Article
DE microduplication; fragile X; developmental delay; epilepsy;
   hyperactivity; copy number variation
ID FRAGILE-X-SYNDROME; MENTAL-RETARDATION; CGG REPEAT; SYNAPTIC PLASTICITY;
   MESSENGER-RNA; MALES; AUTISM; REGION; IDENTIFICATION; PREMUTATION
AB Loss-of-function due to expansion of a CGG repeat located in the 5'UTR of the FMR1 gene is the most frequent cause of fragile X syndrome. Less than 1% of individuals with fragile X syndrome have been reported to have a partial or full deletion or point mutation of the FMR1 gene. However, whether a copy number gain of the FMR1 gene could result in certain clinical phenotypes has not been fully investigated. Here, we report the case of a child who presented with developmental delay starting at 9 months of age, fine motor and speech delay, progressive seizures since 18 months of age and hyperactivity. Molecular workup identified a de novo microduplication in the Xq27.3 region, including the FMR1 gene and the ASFMR1 gene. The expression level of the FMR1 gene in peripheral blood did not differ from that of the controls. In addition, an inherited 363-kb duplication on the chromosome 1q44 region and an inherited deletion of 168 kb on the chromosome 4p15.31 region were detected. It is not clear whether these inherited copy number variations (CNVs) also have a modifying role in the clinical phenotype of this patient. European Journal of Human Genetics (2012) 20, 1197-1200; doi: 10.1038/ejhg.2012.78; published online 2 May 2012
C1 [Vengoechea, Jaime; Parikh, Aditi S.; Zhang, Shulin] Univ Hosp Cleveland, Ctr Human Genet, Case Med Ctr, Cleveland, OH 44106 USA.
   [Vengoechea, Jaime; Parikh, Aditi S.] Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA.
   [Vengoechea, Jaime] Case Western Reserve Univ, Dept Internal Med, Cleveland, OH 44106 USA.
   [Parikh, Aditi S.] Case Western Reserve Univ, Dept Pediat, Cleveland, OH 44106 USA.
   [Zhang, Shulin] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA.
   [Tassone, Flora] Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Sacramento, CA 95817 USA.
   [Tassone, Flora] Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA.
RP Vengoechea, J (reprint author), Univ Hosp Cleveland, Ctr Human Genet, Case Med Ctr, 11100 Euclid Ave, Cleveland, OH 44106 USA.
EM jaimevengoechea@gmail.com
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NR 34
TC 5
Z9 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1018-4813
J9 EUR J HUM GENET
JI Eur. J. Hum. Genet.
PD NOV
PY 2012
VL 20
IS 11
BP 1197
EP 1200
DI 10.1038/ejhg.2012.78
PG 4
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 025TW
UT WOS:000310218600016
PM 22549406
ER

PT J
AU Bacon, C
   Rappold, GA
AF Bacon, Claire
   Rappold, Gudrun A.
TI The distinct and overlapping phenotypic spectra of FOXP1 and FOXP2 in
   cognitive disorders
SO HUMAN GENETICS
LA English
DT Review
ID ESSENTIAL TRANSCRIPTIONAL REGULATOR; DEVELOPMENTAL VERBAL DYSPRAXIA;
   AUTISM-SUSCEPTIBILITY GENE; DE-NOVO MUTATIONS; LANGUAGE DISORDER;
   INHERITED SPEECH; INTELLECTUAL DISABILITY; DIAGNOSTIC BOUNDARIES;
   BIPOLAR DISORDER; CHROMOSOME 3P
AB Rare disruptions of FOXP2 have been strongly implicated in deficits in language development. Research over the past decade has suggested a role in the formation of underlying neural circuits required for speech. Until recently no evidence existed to suggest that the closely related FOXP1 gene played a role in neurodevelopmental processes. However, in the last few years, novel rare disruptions in FOXP1 have been reported in multiple cases of cognitive dysfunction, including intellectual disability and autism spectrum disorder, together with language impairment. As FOXP1 and FOXP2 form heterodimers for transcriptional regulation, one may assume that they co-operate in common neurodevelopmental pathways through the co-regulation of common targets. Here we compare the phenotypic consequences of FOXP1 and FOXP2 impairment, drawing on well-known studies from the past as well as recent exciting findings and consider what these tell us regarding the functions of these two genes in neural development.
C1 [Bacon, Claire; Rappold, Gudrun A.] Univ Heidelberg, Dept Human Mol Genet, D-69120 Heidelberg, Germany.
RP Rappold, GA (reprint author), Univ Heidelberg, Dept Human Mol Genet, Neuenheimer Feld 366, D-69120 Heidelberg, Germany.
EM claire.bacon@med.uni-heidelberg.de; gudrun.rappold@med.uni-heidelberg.de
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NR 83
TC 21
Z9 22
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0340-6717
J9 HUM GENET
JI Hum. Genet.
PD NOV
PY 2012
VL 131
IS 11
BP 1687
EP 1698
DI 10.1007/s00439-012-1193-z
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 021GQ
UT WOS:000309873700001
PM 22736078
ER

PT J
AU Low, H
   Crane, FL
   Morre, DJ
AF Low, Hans
   Crane, Frederick L.
   Morre, D. James
TI Putting together a plasma membrane NADH oxidase: A tale of three
   laboratories
SO INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
LA English
DT Article
DE Cell growth; ENOX; CNOX; PMOR; Anti-cancer drugs; Coenzyme Q; NADH;
   Hormone; Transferrin; Insulin; Protein disulfide isomerase; Cancer
   diagnosis; Sirtuin; Autism; Apoptosis
ID ELECTRON-TRANSPORT; FERRICYANIDE REDUCTION; CELL-SURFACE; REDOX SYSTEM;
   COENZYME-Q; RAT-LIVER; GROWTH; DEHYDROGENASE; PROTEINS; TNOX
AB The observation that high cellular concentrations of NADH were associated with low adenylate cyclase activity led to a search for the mechanism of the effect. Since cyclase is in the plasma membrane, we considered the membrane might have a site for NADH action, and that NADH might be oxidized at that site. A test for NADH oxidase showed very low activity, which could be increased by adding growth factors. The plasma membrane oxidase was not inhibited by inhibitors of mitochondria! NADH oxidase such as cyanide, rotenone or antimycin. Stimulation of the plasma membrane oxidase by iso-proterenol or triiodothyronine was different from lack of stimulation in endoplasmic reticulum. After 25 years of research, three components of a trans membrane NADH oxidase have been discovered. Flavoprotein NADH coenzyme Q reductases (NADH cytochrome b reductase) on the inside, coenzyme Q in the middle, and a coenzyme Q oxidase on the outside as a terminal oxidase. The external oxidase segment is a copper protein with unique properties in timekeeping, protein disulfide isomerase and endogenous NADH oxidase activity, which affords a mechanism for control of cell growth by the overall NADH oxidase and the remarkable inhibition of oxidase activity and growth of cancer cells by a wide range of anti-tumor drugs. A second trans plasma membrane electron transport system has been found in voltage dependent anion channel (VDAC), which has NADH ferricyanide reductase activity. This activity must be considered in relation to ferricyanide stimulation of growth and increased VDAC antibodies in patients with autism. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Crane, Frederick L.] Purdue Univ, Dept Biol Sci, W Lafayette, IN 47907 USA.
   [Low, Hans] Karolinska Inst, Dept Mol Med, Stockholm, Sweden.
   [Morre, D. James] Purdue Univ, Dept Med Chem, W Lafayette, IN 47907 USA.
RP Crane, FL (reprint author), Purdue Univ, Dept Biol Sci, W Lafayette, IN 47907 USA.
EM flccoq10@aol.com
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NR 52
TC 3
Z9 3
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 1357-2725
J9 INT J BIOCHEM CELL B
JI Int. J. Biochem. Cell Biol.
PD NOV
PY 2012
VL 44
IS 11
BP 1834
EP 1838
DI 10.1016/j.biocel.2012.06.032
PG 5
WC Biochemistry & Molecular Biology; Cell Biology
SC Biochemistry & Molecular Biology; Cell Biology
GA 020DF
UT WOS:000309788200013
PM 22750028
ER

PT J
AU Fornasari, L
   Garzitto, M
   Fabbro, F
   Londero, D
   Zago, D
   Desinano, C
   Rigo, S
   Molteni, M
   Brambilla, P
AF Fornasari, L.
   Garzitto, M.
   Fabbro, F.
   Londero, D.
   Zago, D.
   Desinano, C.
   Rigo, S.
   Molteni, M.
   Brambilla, P.
TI Twelve months of TEACCH-oriented habilitation on an Italian population
   of children with autism
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Rehabilitation; Psychiatry; Disability; Psychoeducation; PEP-R
ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM-DISORDERS; YOUNG-CHILDREN;
   PRESCHOOL-CHILDREN; PROGRAM; INTERVENTION; EPILEPSY
AB Autism is a severe disorder and it is important to implement targeted interventions designed on the strengths and needs of affected children in order to improve their daily life. In this sense, the TEACCH program (Treatment and Education of Autistic and related Communication handicapped CHildren) may be useful in autism. A longitudinal study was conducted in Italy to evaluate the effectiveness of our treatment and the best age to start a low-intensive TEACCH-oriented intervention. Twenty-eight children with autism were treated twice a week following the guidelines inspired by the TEACCH intervention. Developmental abilities were rated at baseline and after six and 12 months with the Psychoeducational Profile-Revised (PEP-R) scale. Developmental abilities significantly improved during the first 6 months with progressive amelioration throughout the 12-month follow-up period, particularly for children under 40 months of age. Specifically perception, motor skills, and cognition improved only in patients who begun the program before 60 months of age. This study shows that early low-intensive TEACCH habilitation is effective in improving developmental abilities in autism even after 6 months, particularly in patients at the very early stages of the disease. It is therefore crucial to begin the habilitation program in autism at the very early stage of the illness in order to maximize the effectiveness of the treatment.
C1 [Fornasari, L.; Brambilla, P.] Univ Udine, Dept Expt & Clin Med DISM, Interuniv Ctr Behav Neurosci, I-33100 Udine, Italy.
   [Fornasari, L.; Garzitto, M.; Fabbro, F.] Univ Udine, Dept Human Sci DISU, I-33100 Udine, Italy.
RP Brambilla, P (reprint author), AOU, Dipartimento Med Sperimentali & Sci Clin, Ple Kolbe 3, I-33100 Udine, Italy.
EM paolo.brambilla@uniud.it
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NR 53
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
J9 INT J DEV DISABIL
JI Int. J. Dev. Disabil.
PD NOV
PY 2012
VL 58
IS 3
BP 145
EP 158
DI 10.1179/2047386912Z.00000000018
PG 14
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 027NF
UT WOS:000310358700004
ER

PT J
AU Brown, HK
   Ouellette-Kuntz, H
   Hunter, D
   Kelley, E
   Cobigo, V
AF Brown, Hilary K.
   Ouellette-Kuntz, Helene
   Hunter, Duncan
   Kelley, Elizabeth
   Cobigo, Virginie
TI Unmet Needs of Families of School-Aged Children with an Autism Spectrum
   Disorder
SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES
LA English
DT Article
DE autism; parents; perceived need; school-aged children
ID TRAUMATIC BRAIN INJURY; YOUNG-CHILDREN; HEALTH; SERVICE; CARE; PARENTS;
   ACCESS; DIAGNOSIS
AB Background To aid decision making regarding the allocation of limited resources, information is needed on the perceived unmet needs of parents of school-aged children with an autism spectrum disorder. Materials and Methods A cross-sectional survey was conducted of 101 Canadian families of school-aged children with an autism spectrum disorder. Results Commonly reported unmet needs were for social activities for the child (78.2%), information about services (77.2%) and continuous service provision (74.3%). Conclusions This study provides insight into needs which have not been met by the service system. Information about the unmet needs of children with an autism spectrum disorder and their families may help policy makers and service providers to develop resources and services that are responsive to their client group.
C1 [Brown, Hilary K.; Ouellette-Kuntz, Helene; Hunter, Duncan; Cobigo, Virginie] Queens Univ, Dept Community Hlth & Epidemiol, Kingston, ON, Canada.
   [Brown, Hilary K.; Ouellette-Kuntz, Helene] Natl Epidemiol Database Study Autism Canada, Kingston, ON, Canada.
   [Ouellette-Kuntz, Helene] Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada.
   [Ouellette-Kuntz, Helene] Ongwanada, Kingston, ON, Canada.
   [Kelley, Elizabeth] Queens Univ, Dept Psychol, Kingston, ON K7L 3N6, Canada.
RP Ouellette-Kuntz, H (reprint author), 191 Portsmouth Ave, Kingston, ON K7M 8A6, Canada.
EM helene.kuntz@queensu.ca
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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 1360-2322
J9 J APPL RES INTELLECT
JI J. Appl. Res. Intellect. Disabil.
PD NOV
PY 2012
VL 25
IS 6
BP 497
EP 508
DI 10.1111/j.1468-3148.2012.00692.x
PG 12
WC Psychology, Educational; Rehabilitation
SC Psychology; Rehabilitation
GA 019QA
UT WOS:000309753200002
PM 23055284
ER

PT J
AU McGill, P
   Poynter, J
AF McGill, Peter
   Poynter, Jo
TI High Cost Residential Placements for Adults with Intellectual
   Disabilities
SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES
LA English
DT Article
DE high cost placements; out-of-area placements; residential care;
   supported living
ID CHALLENGING BEHAVIOR; PEOPLE
AB Background Concern has been expressed repeatedly about the cost and quality of residential placements for adults with learning disabilities and additional needs. This study sought to identify characteristics of the highest cost placements in the South-East of England. Method Lead learning disability commissioners in the South-East of England were asked to provide information about the five highest cost residential placements that they commissioned for adults with learning disabilities. Results The average placement cost of 172k pound per annum disguised wide variation. Individuals placed were mainly young and male with high rates of challenging behaviour and/or autism spectrum disorder. Most placements were in out-of-area residential care. The highest costs were associated with hospital placements and placements for people presenting challenging behaviour. Conclusions Young, male adults with learning disability, challenging behaviour and/or autism continue to receive very high cost residential support, often in out-of-area residential care. There remains limited evidence of plans to redirect resources to more local service developments.
C1 [McGill, Peter] Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England.
RP McGill, P (reprint author), Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England.
EM p.mcgill@kent.ac.uk
CR Allen DG, 2007, J INTELL DISABIL RES, V51, P409, DOI 10.1111/j.1365-2788.2006.00877.x
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NR 11
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1360-2322
J9 J APPL RES INTELLECT
JI J. Appl. Res. Intellect. Disabil.
PD NOV
PY 2012
VL 25
IS 6
BP 584
EP 587
DI 10.1111/j.1468-3148.2012.00689.x
PG 4
WC Psychology, Educational; Rehabilitation
SC Psychology; Rehabilitation
GA 019QA
UT WOS:000309753200009
PM 23055291
ER

PT J
AU Kaplan, ES
   Cao, ZY
   Hulsizer, S
   Tassone, F
   Berman, RF
   Hagerman, PJ
   Pessah, IN
AF Kaplan, Eitan S.
   Cao, Zhengyu
   Hulsizer, Susan
   Tassone, Flora
   Berman, Robert F.
   Hagerman, Paul J.
   Pessah, Isaac N.
TI Early mitochondrial abnormalities in hippocampal neurons cultured from
   Fmr1 pre-mutation mouse model
SO JOURNAL OF NEUROCHEMISTRY
LA English
DT Article
DE autism; Fmr1; FXTAS; fragile-X; mitochondria; OCR
ID FRAGILE-X PREMUTATION; CEREBELLAR-TREMOR/ATAXIA-SYNDROME; CGG-REPEAT
   LENGTH; KNOCK-IN MICE; MESSENGER-RNA; AXONAL-TRANSPORT; SYNDROME FXTAS;
   FULL MUTATION; DEFICITS; GENE
AB Pre-mutation CGG repeat expansions (55200 CGG repeats; pre-CGG) within the fragile-X mental retardation 1 (FMR1) gene cause fragile-X-associated tremor/ataxia syndrome in humans. Defects in neuronal morphology, early migration, and electrophysiological activity have been described despite appreciable expression of fragile-X mental retardation protein (FMRP) in a pre-CGG knock-in (KI) mouse model. The triggers that initiate and promote pre-CGG neuronal dysfunction are not understood. The absence of FMRP in a Drosophila model of fragile-X syndrome was shown to increase axonal transport of mitochondria. In this study, we show that dissociated hippocampal neuronal culture from pre-CGG KI mice (average 170 CGG repeats) express 42.6% of the FMRP levels and 3.8-fold higher Fmr1 mRNA than that measured in wild-type neurons at 4days in vitro. Pre-CGG hippocampal neurons show abnormalities in the number, mobility, and metabolic function of mitochondria at this early stage of differentiation. Pre-CGG hippocampal neurites contained significantly fewer mitochondria and greatly reduced mitochondria mobility. In addition, pre-CGG neurons had higher rates of basal oxygen consumption and proton leak. We conclude that deficits in mitochondrial trafficking and metabolic function occur despite the presence of appreciable FMRP expression and may contribute to the early pathophysiology in pre-CGG carriers and to the risk of developing clinical fragile-X-associated tremor/ataxia syndrome.
C1 [Kaplan, Eitan S.; Cao, Zhengyu; Hulsizer, Susan; Pessah, Isaac N.] Univ Calif Davis, Dept Mol Biosci, Sch Vet Med, Davis, CA 95616 USA.
   [Tassone, Flora; Hagerman, Paul J.] Univ Calif Davis, Dept Biochem & Mol Med, Sch Med, Davis, CA 95616 USA.
   [Berman, Robert F.] Univ Calif Davis, Dept Neurol Surg, Sch Med, Davis, CA 95616 USA.
   [Tassone, Flora; Berman, Robert F.; Hagerman, Paul J.; Pessah, Isaac N.] Univ Calif Davis, Med Invest Neurodev Disorders MIND Inst, Davis, CA 95616 USA.
RP Pessah, IN (reprint author), Univ Calif Davis, Dept Mol Biosci, Sch Vet Med, 1 Shields Ave, Davis, CA 95616 USA.
EM inpessah@ucdavis.edu
RI cao, zhengyu/G-2527-2012
FU NIH [DE019583, AG032119, ES04699, ES011269]; J.B. Johnson Foundation
   [NS062411]
FX We thank Yucui Chen for her guidance regarding dissociated hippocampal
   cultures and Diptiman Bose for helpful discussions regarding imaging. We
   thank Binh Ta for carrying out all of the genotyping and Lee
   Rognlie-Howes for coordinating the breeding of mice used in this study.
   This work was supported by NIH grants DE019583 (PJH), AG032119 (PJH,
   INP), ES04699, ES011269 and the J.B. Johnson Foundation (INP), and
   NS062411 (RFB). Eitan S. Kaplan, Zhengyu Cao, Susan Hulsizer, and Flora
   Tassone performed experiments; all authors analyzed the data and drafted
   the manuscript. Isaac N. Pessah and Paul J. Hagerman designed the
   experiments, evaluated raw data and data summaries. Robert Berman
   laboratory supplied the time-mated mice. All authors edited the
   manuscripts. The authors have no interest to declare.
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NR 54
TC 15
Z9 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3042
J9 J NEUROCHEM
JI J. Neurochem.
PD NOV
PY 2012
VL 123
IS 4
BP 613
EP 621
DI 10.1111/j.1471-4159.2012.07936.x
PG 9
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 021WU
UT WOS:000309916900015
PM 22924671
ER

PT J
AU Elamin, M
   Pender, N
   Hardiman, O
   Abrahams, S
AF Elamin, Marwa
   Pender, Niall
   Hardiman, Orla
   Abrahams, S.
TI Social cognition in neurodegenerative disorders: a systematic review
SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY
LA English
DT Review
ID AMYOTROPHIC-LATERAL-SCLEROSIS; FRONTOTEMPORAL LOBAR DEGENERATION;
   PROGRESSIVE SUPRANUCLEAR PALSY; EMOTIONAL FACIAL EXPRESSIONS;
   PRECLINICAL HUNTINGTONS-DISEASE; HIGH-FUNCTIONING AUTISM; MILD
   ALZHEIMER-DISEASE; PARKINSONS-DISEASE; IMPAIRED RECOGNITION; PREFRONTAL
   CORTEX
AB Social cognitive neuroscience is the study of the neurobiological systems underlying effective social behaviour. The neural processes supporting effective social interactions in everyday life and the consequences of dysfunction in these processes have been the focus of intense research over the last two decades. It is becoming increasingly apparent that the identification of social cognitive deficits in neurodegenerative conditions and their neural basis may provide a better understanding of the behavioural changes observed in these disorders. In addition, accumulating data suggest that detection of early impairment in social cognitive skills may aid in the early diagnosis of cognitive or behavioural impairment in some of these disorders, and may even play a role in the investigation of new therapeutic options. In this review, we outline the basic components of social cognitive processing, provide a systematic review of the literature pertaining to common neurodegenerative conditions, discuss current controversies and make recommendations for future research.
C1 [Elamin, Marwa; Hardiman, Orla] Trinity Coll Dublin, Inst Neurosci, Dublin D2, Ireland.
   [Pender, Niall] Beaumont Hosp, Dept Psychol, Dublin 9, Ireland.
   [Hardiman, Orla] Beaumont Hosp, Dept Neurol, Dublin 9, Ireland.
   [Abrahams, S.] Univ Edinburgh, Euan MacDonald Ctr MND Res, Ctr Cognit Ageing & Epidemiol, Edinburgh, Midlothian, Scotland.
RP Elamin, M (reprint author), Trinity Coll Dublin, Inst Neurosci, Dublin D2, Ireland.
EM marwaelamin08@gmail.com
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NR 157
TC 11
Z9 11
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-3050
J9 J NEUROL NEUROSUR PS
JI J. Neurol. Neurosurg. Psychiatry
PD NOV
PY 2012
VL 83
IS 11
BP 1071
EP 1079
DI 10.1136/jnnp-2012-302817
PG 9
WC Clinical Neurology; Psychiatry; Surgery
SC Neurosciences & Neurology; Psychiatry; Surgery
GA 020MG
UT WOS:000309813600009
PM 22869923
ER

PT J
AU Tanoue, K
   Matsui, K
   Takamasu, T
AF Tanoue, Koji
   Matsui, Kiyoshi
   Takamasu, Tetsuya
TI Fried-Potato Diet Causes Vitamin A Deficiency in an Autistic Child
SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION
LA English
DT Article
DE eating disorders; long-term care; pediatrics; vitamins
AB A 5-year-old boy with autism developed dry eye and xerophthalmia. Serum vitamin A was undetectable. Dietary history revealed a markedly altered intake consisting of only fried potatoes and rice balls for 2 years. Fried potatoes contain no vitamin A. Autism is a multifaceted developmental disorder infrequently accompanied by abnormal eating practices. To the authors' knowledge, most children with autism who develop dietary vitamin A deficiency have consumed an excess of fried potatoes. Attention to possible vitamin A deficiency is essential when fried potatoes are consumed exclusively. (JPEN J Parenter Enteral Nutr. 2012; 36: 753-755)
C1 [Tanoue, Koji] Kanagawa Childrens Med Ctr, Dept Gen Med, Minami Ku, Yokohama, Kanagawa 2328555, Japan.
   [Takamasu, Tetsuya] Kanagawa Childrens Med Ctr, Dept Allergy, Yokohama, Kanagawa 2328555, Japan.
RP Tanoue, K (reprint author), Kanagawa Childrens Med Ctr, Dept Gen Med, Minami Ku, 2-138-4 Mutukawa, Yokohama, Kanagawa 2328555, Japan.
EM ktanoue@kcmc.jp
CR Arnold GL, 2003, J AUTISM DEV DISORD, V33, P449, DOI 10.1023/A:1025071014191
   CLARK JH, 1993, JPEN-PARENTER ENTER, V17, P284, DOI 10.1177/0148607193017003284
   Fugazzi P, 2003, J AM COLL NUTR, V22, P481
   McAbee GN, 2009, J CHILD NEUROL, V24, P1288, DOI 10.1177/0883073809333541
   RAITEN DJ, 1986, J AUTISM DEV DISORD, V16, P133, DOI 10.1007/BF01531725
   Steinemann TL, 1998, ARCH OPHTHALMOL-CHIC, V116, P392
   Uyanik O, 2006, CHILD CARE HLTH DEV, V32, P601, DOI 10.1111/j.1365-2214.2006.00586.x
NR 7
TC 3
Z9 3
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0148-6071
J9 JPEN-PARENTER ENTER
JI J. Parenter. Enter. Nutr.
PD NOV
PY 2012
VL 36
IS 6
BP 753
EP 755
DI 10.1177/0148607111436280
PG 3
WC Nutrition & Dietetics
SC Nutrition & Dietetics
GA 022EF
UT WOS:000309937600017
PM 22318966
ER

PT J
AU Bressler, JP
   Gillin, PK
   O'Driscoll, C
   Kiihl, S
   Solomon, M
   Zimmerman, AW
AF Bressler, Joseph P.
   Gillin, Pam K.
   O'Driscoll, Cliona
   Kiihl, Samara
   Solomon, Megan
   Zimmerman, Andrew W.
TI Maternal Antibody Reactivity to Lymphocytes of Offspring With Autism
SO PEDIATRIC NEUROLOGY
LA English
DT Article
ID FETAL-BRAIN; CHILDREN; MOTHERS
AB The study examined whether maternal serum antibodies from mothers of autistic children preferentially bind to lymphocytes of their autistic children compared with unaffected siblings. In a previous study, maternal serum antibodies from mothers mediated cytotoxicity with complement to lymphocytes of their autistic children. Here, maternal serum antibody binding was examined by flow cytometry. We compared levels of mothers' serum binding against peripheral blood monocytes of their autistic children vs unaffected siblings. Because the level of binding to peripheral blood monocytes could be low, binding was examined in specific lymphocyte subpopulations. In 19 samples, the mean level of maternal serum immunoglobulin G binding to CD4 and CD8 T cells, B cells, natural killer cells, and macro-phages was not significantly different from the mean level of binding to unaffected siblings. The percentages of different subpopulations were not significantly different between autistic children and unaffected siblings, although a trend (P < 0.1) emerged, i.e., autistic children displayed a higher percentage of natural killer cells and a lower percentage of B cells. These findings cast doubt on a direct effect of maternal antibodies, but do not preclude potential intrauterine pathogenic immune mechanisms in autism. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Bressler, Joseph P.; Gillin, Pam K.; O'Driscoll, Cliona; Solomon, Megan; Zimmerman, Andrew W.] Kennedy Krieger Inst, Dept Neurol, Baltimore, MD 21205 USA.
   [Bressler, Joseph P.; O'Driscoll, Cliona] Johns Hopkins Univ, Dept Environm Hlth Sci, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
   [Kiihl, Samara] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA.
   [Zimmerman, Andrew W.] Massachusetts Gen Hosp Children, Lurie Ctr Autism, Lexington, MA USA.
RP Bressler, JP (reprint author), Kennedy Krieger Inst, Dept Neurol, 707 N Broadway, Baltimore, MD 21205 USA.
EM bressler@kennedykrieger.org
RI kiihl, samara/E-3109-2012
FU Hussman Foundation
FX The authors thank the families who participated in the study, including
   the parents, their children with autism, and unaffected siblings. This
   study was funded by the Hussman Foundation. The authors also thank
   Christina M. Morris, MS, and Harvey S. Singer, MD, for contributing data
   on maternal antibodies.
CR Ashwood P, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0019299
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   Zimmerman AW, 2005, IMMUNE SYSTEM, P371
NR 12
TC 4
Z9 4
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0887-8994
J9 PEDIATR NEUROL
JI Pediatr. Neurol.
PD NOV
PY 2012
VL 47
IS 5
BP 337
EP 340
DI 10.1016/j.pediatrneurol.2012.06.017
PG 4
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 023OJ
UT WOS:000310044000004
PM 23044014
ER

PT J
AU Katsnelson, A
AF Katsnelson, Alla
TI The Autism Pill A new crop of drugs aim, for the first time, at the core
   symptoms of this disorder
SO SCIENTIFIC AMERICAN
LA English
DT Editorial Material
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 0036-8733
J9 SCI AM
JI Sci.Am.
PD NOV
PY 2012
VL 307
IS 5
BP 16
EP 16
PG 1
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 023NG
UT WOS:000310041100016
PM 23120883
ER

PT J
AU Baron-Cohen, S
AF Baron-Cohen, Simon
TI AUTISM AND THE TECHNICAL MIND
SO SCIENTIFIC AMERICAN
LA English
DT Article
C1 [Baron-Cohen, Simon] Univ Cambridge, Cambridge CB2 1TN, England.
RP Baron-Cohen, S (reprint author), Univ Cambridge, Cambridge CB2 1TN, England.
CR Baron-Cohen S, 2005, SCIENCE, V310, P819, DOI 10.1126/science.1115455
   Baron-Cohen S., 2008, AUTISM ASPERGER SYND
   Baron-Cohen S, 2004, ESSENTIAL DIFFERENCE
   Baron-Cohen S, 2011, PLOS BIOL, V9, DOI 10.1371/journal.pbio.1001081
NR 4
TC 4
Z9 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 0036-8733
J9 SCI AM
JI Sci.Am.
PD NOV
PY 2012
VL 307
IS 5
BP 72
EP 75
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 023NG
UT WOS:000310041100038
PM 23120898
ER

PT J
AU Ahmedani, BK
   Hock, RM
AF Ahmedani, Brian K.
   Hock, Robert M.
TI Health care access and treatment for children with co-morbid autism and
   psychiatric conditions
SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY
LA English
DT Article
DE Autism; Developmental disability; Treatment; Access; Psychiatric
   comorbidity
ID SPECTRUM DISORDERS; COMORBIDITY; POPULATION; YOUTH
AB To characterize the rate of comorbid psychiatric conditions (CPC) among children with autism spectrum disorders (ASD), to examine their treatment utilization, and to investigate treatment delay or non-delivery.
   Lifetime ASD and CPC in children, aged 2-17, were investigated using data from the 2007-2008 National Survey of Children's Health (NSCH). The NSCH surveyed parents and guardians regarding the health and well being, including treatment, of their child(ren) under age 18 (n = 91,642). Children with health conditions were defined by parent report that a doctor or other health professional had ever said their child had that condition. Factors related to overall health, treatment utilization, and barriers to access variables were investigated among this group.
   Children with ASD/CPC had poorer overall health outcomes than children with ASD alone. They more often were dissatisfied with their between-provider communication and less often had insurance cover needed services. Nonetheless, they did tend to use care coordination and mental health services to a greater degree. Families were more likely to report the delay or non-receipt of needed services when they perceived a lack of communication and partnership with providers, when they lacked insurance coverage, and when they felt that health care costs were unreasonable.
   The presence of a CPC seems to shape the treatment utilization and health outcomes of children with ASD. Because of this, health professionals working with children with autism should give special attention to treatment of those with comorbid diagnoses.
C1 [Ahmedani, Brian K.] Henry Ford Hlth Syst, Ctr Hlth Policy & Hlth Serv Res, Detroit, MI 48202 USA.
   [Hock, Robert M.] Univ S Carolina, Coll Social Work, Columbia, SC 29208 USA.
RP Ahmedani, BK (reprint author), Henry Ford Hlth Syst, Ctr Hlth Policy & Hlth Serv Res, 1 Ford Pl 3A, Detroit, MI 48202 USA.
EM bahmeda1@hfhs.org; roberth@sc.edu
FU Health Resources and Services Administration's Maternal and Child Health
   Bureau of the Department of Health and Human Services
FX The NSCH was funded by the Health Resources and Services
   Administration's Maternal and Child Health Bureau of the Department of
   Health and Human Services. The Center for Disease Control's National
   Center for Health Statistics (NCHS) administered the overall study
   protocol.
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NR 24
TC 6
Z9 6
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 0933-7954
J9 SOC PSYCH PSYCH EPID
JI Soc. Psychiatry Psychiatr. Epidemiol.
PD NOV
PY 2012
VL 47
IS 11
BP 1807
EP 1814
DI 10.1007/s00127-012-0482-0
PG 8
WC Psychiatry
SC Psychiatry
GA 025RB
UT WOS:000310208800011
PM 22322982
ER

PT J
AU Taylor, M
   Charman, T
   Ronald, A
AF Taylor, Mark
   Charman, Tony
   Ronald, Angelica
TI Nonshared environmental influences on the association between traits of
   autism and attention-deficit/hyperactivity disorder: A monozygotic twin
   differences study
SO BEHAVIOR GENETICS
LA English
DT Meeting Abstract
CT 42nd Annual Meeting of the Behavior-Genetics-Association
CY JUN 22-25, 2012
CL Edinburgh, SCOTLAND
SP Behav Genet Assoc
RI Charman, Tony/A-2085-2014
OI Charman, Tony/0000-0003-1993-6549
NR 0
TC 0
Z9 0
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0001-8244
J9 BEHAV GENET
JI Behav. Genet.
PD NOV
PY 2012
VL 42
IS 6
BP 970
EP 970
PG 1
WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary
SC Behavioral Sciences; Genetics & Heredity; Psychology
GA 018KS
UT WOS:000309659800194
ER

PT J
AU Pratt, K
   Baird, G
   Gringras, P
AF Pratt, K.
   Baird, G.
   Gringras, P.
TI Ensuring successful admission to hospital for young people with learning
   difficulties, autism and challenging behaviour: a continuous quality
   improvement and change management programme
SO CHILD CARE HEALTH AND DEVELOPMENT
LA English
DT Article
DE autism; challenging behaviour; hospital admission; pre-admission
   planning
ID CHILDREN
AB Background Children and young people with autism spectrum conditions frequently have adverse experiences in accessing health care. Methods An audit of experiences of families known to our tertiary service and hospital staff was conducted. A checklist asking about particular aspects of behaviour and communication was developed and incorporated into pre-admission planning. Results Awareness of the child/young person's communication needs and behaviours, plus good preplanning by all staff involved and a team member allocated to ensure that the care plan is carried through, has resulted in a vastly improved patient experience from the perspective of family and staff. Conclusion Children and young people with autism spectrum disorder, often with co-existing learning difficulties, vary greatly in their reactions to hospital admission. Preplanning that involves the family with a dedicated informed staff member can dramatically reduce distress and improve the patient and staff experience.
C1 [Baird, G.] Guys & St Thomas NHS Fdn Trust, Newcomen Child Dev Ctr, London SE1 9RT, England.
   [Baird, G.; Gringras, P.] Kings Coll London, London WC2R 2LS, England.
RP Baird, G (reprint author), Guys & St Thomas NHS Fdn Trust, Newcomen Child Dev Ctr, London SE1 9RT, England.
EM gillian.baird@gstt.nhs.uk
CR Beadle-Brown J., 2009, TIZARD LEARNING DISA, V14, P18
   Department of Health, 2010, NHS OUTC FRAM 2011 1
   Department of Health, 2009, VAL PEOPL NOW NEW 3
   Hudson J., 2006, PRESCRIPTION SUCCESS
   MENCAP, 2007, DEATH IND
   Michael J., 2008, HEALTHC ALL
   Van der Walt JH, 2001, PAEDIATR ANAESTH, V11, P401, DOI 10.1046/j.1460-9592.2001.00688.x
   Vaz I, 2010, CHILD CARE HLTH DEV, V36, P753, DOI 10.1111/j.1365-2214.2010.01144.x
NR 8
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0305-1862
J9 CHILD CARE HLTH DEV
JI Child Care Health Dev.
PD NOV
PY 2012
VL 38
IS 6
BP 789
EP 797
DI 10.1111/j.1365-2214.2011.01335.x
PG 9
WC Psychology, Developmental; Pediatrics
SC Psychology; Pediatrics
GA 017OX
UT WOS:000309601000004
PM 22017703
ER

PT J
AU King, G
   Zwaigenbaum, L
   Bates, A
   Baxter, D
   Rosenbaum, P
AF King, G.
   Zwaigenbaum, L.
   Bates, A.
   Baxter, D.
   Rosenbaum, P.
TI Parent views of the positive contributions of elementary and high
   school-aged children with autism spectrum disorders and Down syndrome
SO CHILD CARE HEALTH AND DEVELOPMENT
LA English
DT Article
DE benefits; family; positive contributions; qualitative; resilience
ID CHRONIC DISABILITIES; FAMILIES; RESILIENCE; STRESS; PERCEPTIONS;
   ADJUSTMENT; PSYCHOLOGY; MOTHERS; PEOPLE
AB Background Much is known about the hardships associated with parenting a child with a disability, but few studies have examined the broader contributions of the child to family life or society. Methods The study involved qualitative analysis of interviews with 16 families of children with autism spectrum disorder or Down syndrome at critical transition periods (entry to elementary or high school), targeting their perceptions of benefits. Results Parents discussed a wide range of benefits beyond the personal level, including parental, family and societal benefits. Exploratory group comparisons indicated that parents of high school-aged children were more likely to mention family-level and societal benefits. Conclusions The findings suggest that raising a child with a disability can trigger role-related decisions that lead to a series of resiliency-related processes and cascading benefits. The findings inform practitioners about the nature of potential positive experiences that can be shared with families starting out on their journey, allowing parents to recognize the positive dimensions of raising a child with a disability in addition to the hardships.
C1 [King, G.] Bloorview Res Inst, Toronto, ON M4G 1R8, Canada.
   [Bates, A.] Parent Informant, Hamilton, ON, Canada.
   [Rosenbaum, P.] McMaster Univ, Hamilton, ON, Canada.
   [Baxter, D.] City London, London, ON, Canada.
   [Zwaigenbaum, L.] Glenrose Rehabil Hosp, Edmonton, AB, Canada.
RP King, G (reprint author), Bloorview Res Inst, 150 Kilgour Rd, Toronto, ON M4G 1R8, Canada.
EM gking27@uwo.ca
FU Canadian Institutes of Health Research; Jack and Ina Pollock Foundation
FX We acknowledge the Canadian Institutes of Health Research for funding
   the study and the Jack and Ina Pollock Foundation for supporting pilot
   work. Appreciation is extended to: the participating parents and service
   providers, Susanne King for her assistance with the project and the
   organizations assisting with recruitment (Autism Society of Ontario,
   London and District; Autism Society of Ontario, Niagara District;
   Hamilton Family Network; Hamilton Down Syndrome Association; London Down
   Syndrome Association; Niagara Down Syndrome Association; Chedoke site of
   McMaster University, PDD Program; Thames Valley Children's Centre).
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NR 42
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0305-1862
J9 CHILD CARE HLTH DEV
JI Child Care Health Dev.
PD NOV
PY 2012
VL 38
IS 6
BP 817
EP 828
DI 10.1111/j.1365-2214.2011.01312.x
PG 12
WC Psychology, Developmental; Pediatrics
SC Psychology; Pediatrics
GA 017OX
UT WOS:000309601000008
PM 21916929
ER

PT J
AU Gill, M
AF Gill, Michael
TI Developmental psychopathology: The role of structural variation in the
   genome
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID COPY-NUMBER VARIATION; CARDIO-FACIAL SYNDROME; AUTISM SPECTRUM
   DISORDERS; DE-NOVO CNVS; MENTAL-RETARDATION; CHROMOSOMAL REARRANGEMENTS;
   CYTOGENETIC ABNORMALITIES; X-CHROMOSOME; ARRAY CGH; RECURRENT
   MICRODELETIONS
AB A wide range of developmental disorders present with characteristic psychopathologies and behaviors, with diagnoses including, inter alia, cognitive disorders and learning disabilities, epilepsies, autism, and schizophrenia. Each, to varying extent, has a genetic component to etiology and is associated with cytogenetic abnormalities. Technological developments, particularly array-based comparative genome hybridization and single nucleotide polymorphism chips, has revealed a wide range of rare recurrent and de novo copy number variants (CNVs) to be associated with disorder and psychopathology. It is surprising that many apparently similar CNVs are identified across two or more disorders hitherto considered unrelated. This article describes the characteristics of CNVs and current technological restrictions that make accurately identifying small events difficult. It summarizes the latest discoveries for individual diagnostic categories and considers the implications for a shared neurobiology. It examines likely developments in the knowledge base as well as addressing the clinical implications going forward.
C1 [Gill, Michael] Trinity Coll Dublin, Dublin, Ireland.
RP Gill, M (reprint author), St James Hosp, Dept Psychiat, Trinity Ctr, Dublin 8, Ireland.
EM mgill@tcd.ie
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NR 103
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
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2012
VL 24
IS 4
SI SI
BP 1319
EP 1334
DI 10.1017/S0954579412000739
PG 16
WC Psychology, Developmental
SC Psychology
GA 021ZX
UT WOS:000309925800013
PM 23062300
ER

PT J
AU Rucker, JJH
   McGuffin, P
AF Rucker, James J. H.
   McGuffin, Peter
TI Genomic structural variation in psychiatric disorders
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID COPY-NUMBER VARIATION; MAJOR DEPRESSIVE DISORDER; RARE CHROMOSOMAL
   DELETIONS; AUTISM SPECTRUM DISORDER; CASE-CONTROL SAMPLE;
   BIPOLAR-DISORDER; MENTAL-RETARDATION; WIDE ASSOCIATION;
   SCHIZOPHRENIA-PATIENTS; MICRODELETION SYNDROME
AB Copy number variants (CNVs) are submicroscopic deletions and duplications of genomic material that were previously thought to be rare phenomena. They have now been robustly associated with a variety of disorders such as autism, schizophrenia, and attention-deficit/hyperactivity disorder through an emerging research base in affective disorders. A complex picture is emerging of a polygenic, heterogeneous model of disease, with CNVs conferring broad susceptibility to a variety of neurodevelopmental disorders, rather than specific disorders per se. Although the insights gleaned thus far only represent a small piece of a much larger puzzle, progress has been rapid and new technologies promise even more insights into these hitherto opaque brain disorders. We will discuss CNVs, the current state of evidence for their role in the pathogenesis of classical psychiatric disorders, and the application of such knowledge in clinical settings.
C1 [Rucker, James J. H.] Kings Coll London, MRC Social Genet & Dev Psychiat Ctr, Inst Psychiat, London SE5 8AF, England.
RP Rucker, JJH (reprint author), Kings Coll London, MRC Social Genet & Dev Psychiat Ctr, Inst Psychiat, 16 De Crespigny Pk, London SE5 8AF, England.
EM james.rucker@kcl.ac.uk
RI McGuffin, Peter/A-1565-2012
OI McGuffin, Peter/0000-0002-9888-2907
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NR 100
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
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2012
VL 24
IS 4
SI SI
BP 1335
EP 1344
DI 10.1017/S0954579412000740
PG 10
WC Psychology, Developmental
SC Psychology
GA 021ZX
UT WOS:000309925800014
PM 23062301
ER

PT J
AU Stevens, HE
   Mariani, J
   Coppola, G
   Vaccarino, FM
AF Stevens, Hanna E.
   Mariani, Jessica
   Coppola, Gianfilippo
   Vaccarino, Flora M.
TI Neurobiology meets genomic science: The promise of human-induced
   pluripotent stem cells
SO DEVELOPMENT AND PSYCHOPATHOLOGY
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; CORTICAL SURFACE-AREA; HEAD CIRCUMFERENCE;
   CEREBRAL-CORTEX; NEURON NUMBER; PREFRONTAL CORTEX; BRAIN OVERGROWTH;
   WIDE ASSOCIATION; PROGENITOR CELLS; GENE-EXPRESSION
AB The recent introduction of the induced pluripotent stem cell technology has made possible the derivation of neuronal cells from somatic cells obtained from human individuals. This in turn has opened new areas of investigation that can potentially bridge the gap between neuroscience and psychopathology. For the first time we can study the cell biology and genetics of neurons derived from any individual. Furthermore, by recapitulating in vitro the developmental steps whereby stem cells give rise to neuronal cells, we can now hope to understand factors that control typical and atypical development. We can begin to explore how human genes and their variants are transcribed into messenger RNAs within developing neurons and how these gene transcripts control the biology of developing cells. Thus, human-induced pluripotent stem cells have the potential to uncover not only what aspects of development are uniquely human but also variations in the series of events necessary for normal human brain development that predispose to psychopathology.
C1 [Vaccarino, Flora M.] Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA.
RP Vaccarino, FM (reprint author), Yale Univ, Ctr Child Study, Sch Med, POB 207900,230 S Frontage Rd, New Haven, CT 06520 USA.
EM flora.vaccarino@yale.edu
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NR 103
TC 1
Z9 2
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0954-5794
J9 DEV PSYCHOPATHOL
JI Dev. Psychopathol.
PD NOV
PY 2012
VL 24
IS 4
SI SI
BP 1443
EP 1451
DI 10.1017/S095457941200082X
PG 9
WC Psychology, Developmental
SC Psychology
GA 021ZX
UT WOS:000309925800022
PM 23062309
ER

PT J
AU Gori, M
   Squeri, V
   Sciutti, A
   Masia, L
   Sandini, G
   Konczak, J
AF Gori, Monica
   Squeri, Valentina
   Sciutti, Alessandra
   Masia, Lorenzo
   Sandini, Giulio
   Konczak, Juergen
TI Motor commands in children interfere with their haptic perception of
   objects
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Article
DE Forward models; Human development; Haptic; Active perception; Passive
   perception
ID JOINT TORQUE; MOVEMENT; MODELS; CURVATURE; AUTISM; TRANSFORMATIONS;
   RECOGNITION; INFANTS; BLIND
AB Neural processes of sensory-motor- and motor-sensory integration link perception and action, forming the basis for human interaction with the environment. Haptic perception, the ability to extract object features through action, is based on these processes. To study the development of motor-sensory integration, children judged the curvature of virtual objects after exploring them actively or while guided passively by a robot. Haptic acuity reached adult levels only at early adolescence. Unlike in adults, haptic precision in children was consistently lower during active exploration when compared to passive motion. Thus, the exploratory movements themselves constitute a form of noise for the developing haptic system that younger brains cannot compensate until mid-adolescence. Computationally, this is consistent with a noisy efference copy mechanism producing imprecise predicted sensory feedback, which compromises haptic precision in children, while the mature mechanism aids the adult brain to account for the effect of self-generated motion on perception.
C1 [Gori, Monica; Squeri, Valentina; Sciutti, Alessandra; Masia, Lorenzo; Sandini, Giulio; Konczak, Juergen] Ist Italiano Tecnol, Dept Robot Brain & Cognit Sci, Genoa, Italy.
   [Konczak, Juergen] Univ Minnesota, Human Sensorimotor Control Lab, Ctr Clin Movement Sci, Minneapolis, MN USA.
RP Gori, M (reprint author), Ist Italiano Tecnol, Dept Robot Brain & Cognit Sci, Genoa, Italy.
EM monica.gori@iit.it
RI MASIA, LORENZO/D-9385-2014
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NR 43
TC 4
Z9 4
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0014-4819
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD NOV
PY 2012
VL 223
IS 1
BP 149
EP 157
DI 10.1007/s00221-012-3248-8
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 021EU
UT WOS:000309868900014
PM 23064882
ER

PT J
AU Simonoff, E
   Jones, CRG
   Pickles, A
   Happe, F
   Baird, G
   Charman, T
AF Simonoff, Emily
   Jones, Catherine R. G.
   Pickles, Andrew
   Happe, Francesca
   Baird, Gillian
   Charman, Tony
TI Severe mood problems in adolescents with autism spectrum disorder
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Severe mood dysregulation; mood disorders; childhood autism; autism
   spectrum disorder; SNAP
ID PEDIATRIC BIPOLAR DISORDER; PSYCHIATRIC-DISORDERS; DIFFICULTIES
   QUESTIONNAIRE; DIAGNOSTIC INTERVIEW; LABELING DEFICITS; CHILDREN;
   PREVALENCE; POPULATION; YOUTH; DYSREGULATION
AB Introduction: Severe mood dysregulation and problems (SMP) in otherwise typically developing youth are recognized as an important mental health problem with a distinct set of clinical features, family history and neurocognitive characteristics. SMP in people with autism spectrum disorders (ASDs) have not previously been explored. Method: We studied a longitudinal, population-based cohort of adolescents with ASD in which we collected parent-reported symptoms of SMP that included rage, low and labile mood and depressive thoughts. Ninety-one adolescents with ASD provided data at age 16 years, of whom 79 had additional data from age 12. We studied whether SMP have similar correlates to those seen in typically developing youth. Results: Severe mood problems were associated with current (parent-rated) and earlier (parent- and teacher-rated) emotional problems. The number of prior psychiatric diagnoses increased the risk of subsequent SMP. Intellectual ability and adaptive functioning did not predict to SMP. Maternal mental health problems rated at 12 and 16 years were associated with SMP. Autism severity as rated by parents was associated with SMP, but the relationship did not hold for clinician ratings of autistic symptoms or diagnosis. SMP were associated with difficulty in identifying the facial expression of surprise, but not with performance recognizing other emotions. Relationships between SMP and tests of executive function (card sort and trail making) were not significant after controlling for IQ. Conclusions: This is the first study of the behavioural and cognitive correlates of severe mood problems in ASD. As in typically developing youth, SMP in adolescents with ASD are related to other affective symptoms and maternal mental health problems. Previously reported links to deficits in emotion recognition and cognitive flexibility were not found in the current sample. Further research is warranted using categorical and validated measures of SMP.
C1 [Simonoff, Emily] Kings Coll London, Dept Child & Adolescent Psychiat, Inst Psychiat, London SE5 8AF, England.
   [Simonoff, Emily] NIHR Biomed Res Ctr Mental Hlth, London SE5 8AF, England.
   [Jones, Catherine R. G.] Univ Essex, Dept Psychol, Colchester CO4 3SQ, Essex, England.
   [Pickles, Andrew] Kings Coll London, Inst Psychiat, Dept Biostat, London SE5 8AF, England.
   [Happe, Francesca] Kings Coll London, Inst Psychiat, MRC SDGP Res Ctr, London SE5 8AF, England.
   [Baird, Gillian] Guys & St Thomas NHS Fdn Trust, Newcomen Ctr, London, England.
   [Charman, Tony] Univ London, Inst Educ, Ctr Res Autism & Educ, London WC1N 1AZ, England.
RP Simonoff, E (reprint author), Kings Coll London, Dept Child & Adolescent Psychiat, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England.
EM emily.simonoff@kcl.ac.uk
RI Simonoff, Emily/B-7593-2011; Jones, Catherine/E-4956-2013; Charman,
   Tony/A-2085-2014; Pickles, Andrew/A-9625-2011
OI Charman, Tony/0000-0003-1993-6549; Pickles, Andrew/0000-0003-1283-0346
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NR 47
TC 12
Z9 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD NOV
PY 2012
VL 53
IS 11
BP 1157
EP 1166
DI 10.1111/j.1469-7610.2012.02600.x
PG 10
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 022AP
UT WOS:000309927700008
PM 22909395
ER

PT J
AU Burkett, JP
   Young, LJ
AF Burkett, James P.
   Young, Larry J.
TI The behavioral, anatomical and pharmacological parallels between social
   attachment, love and addiction
SO PSYCHOPHARMACOLOGY
LA English
DT Review
DE Social attachment; Love; Addiction; Substance dependence; Dopamine;
   Opioids; CRF; Oxytocin; Vasopressin; Pair bond
ID CORTICOTROPIN-RELEASING-FACTOR; MU-OPIOID-RECEPTOR; FEMALE PRAIRIE
   VOLES; CONDITIONED PLACE PREFERENCE; VENTRAL TEGMENTAL AREA;
   NUCLEUS-ACCUMBENS DOPAMINE; MESSENGER-RNA EXPRESSION; INCREASE
   EXTRACELLULAR DOPAMINE; AUTISM SPECTRUM DISORDERS; ETHANOL-DEPENDENT
   RATS
AB Love has long been referred to as an addiction in literature and poetry. Scientists have often made comparisons between social attachment processes and drug addiction, and it has been suggested that the two may share a common neurobiological mechanism. Brain systems that evolved to govern attachments between parents and children and between monogamous partners may be the targets of drugs of abuse and serve as the basis for addiction processes.
   Here, we review research on drug addiction in parallel with research on social attachments, including parent-offspring attachments and social bonds between mating partners. This review focuses on the brain regions and neurochemicals with the greatest overlap between addiction and attachment and, in particular, the mesolimbic dopamine (DA) pathway.
   Significant overlap exists between these two behavioral processes. In addition to conceptual overlap in symptomatology, there is a strong commonality between the two domains regarding the roles and sites of action of DA, opioids, and corticotropin-releasing factor. The neuropeptides oxytocin and vasopressin are hypothesized to integrate social information into attachment processes that is not present in drug addiction.
   Social attachment may be understood as a behavioral addiction, whereby the subject becomes addicted to another individual and the cues that predict social reward. Understandings from both fields may enlighten future research on addiction and attachment processes.
C1 [Burkett, James P.; Young, Larry J.] Emory Univ, Yerkes Natl Primate Res Ctr, Div Behav Neurosci & Psychiat Disorders, Ctr Translat Social Neurosci,Dept Psychiat & Beha, Atlanta, GA 30329 USA.
RP Young, LJ (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, Div Behav Neurosci & Psychiat Disorders, Ctr Translat Social Neurosci,Dept Psychiat & Beha, 954 Gatewood Rd, Atlanta, GA 30329 USA.
EM james.p.burkett@gmail.com; Lyoun03@emory.edu
FU NIH [P51OD011132]; Emory Scholars Program in Interdisciplinary
   Neuroscience Research;  [MH64692]
FX We acknowledge the funding from MH64692 to LJY, NIH P51OD011132 to
   YNPRC, and the Emory Scholars Program in Interdisciplinary Neuroscience
   Research to JPB.
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NR 380
TC 34
Z9 35
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
EI 1432-2072
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD NOV
PY 2012
VL 224
IS 1
BP 1
EP 26
DI 10.1007/s00213-012-2794-x
PG 26
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 018SB
UT WOS:000309681900001
PM 22885871
ER

PT J
AU Braun, JM
AF Braun, Joe M.
TI Endocrine disrupting compounds, gonadal hormones, and autism
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Letter
C1 Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
RP Braun, JM (reprint author), Harvard Univ, Sch Publ Hlth, Dept Environm Hlth, Boston, MA 02115 USA.
EM jbraun@hsph.harvard.edu
RI Braun, Joseph/H-8649-2014
CR Engel SM, 2010, ENVIRON HEALTH PERSP, V118, P565, DOI 10.1289/ehp.0901470
   Howdeshell KL, 2008, TOXICOL SCI, V105, P153, DOI 10.1093/toxsci/kfn077
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   Woodruff TJ, 2011, ENVIRON HEALTH PERSP, V119, P878, DOI 10.1289/ehp.1002727
NR 6
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1622
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD NOV
PY 2012
VL 54
IS 11
BP 1068
EP 1068
DI 10.1111/j.1469-8749.2012.04372.x
PG 1
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 017OB
UT WOS:000309598500026
PM 22788982
ER

PT J
AU Milley, A
   Machalicek, W
AF Milley, Allison
   Machalicek, Wendy
TI Decreasing Students' Reliance on Adults: A Strategic Guide for Teachers
   of Students With Autism Spectrum Disorders
SO INTERVENTION IN SCHOOL AND CLINIC
LA English
DT Article
DE activity schedules; autism; peer supports; tactile prompts
ID PERVASIVE DEVELOPMENTAL DISORDER; APPLIED BEHAVIOR ANALYSIS; ACTIVITY
   SCHEDULES; SOCIAL INTERACTIONS; SELF-MANAGEMENT; CURRENT DIMENSIONS;
   TACTILE PROMPT; CHILDREN; INTERVENTIONS; DISABILITIES
AB Students with autism spectrum disorders (ASD) often lack independent task initiation skills, have difficulty staying actively engaged in academic tasks, and may require prompting to complete and transition between tasks or activities. In response to these difficulties, teachers often provide additional attention to students in the form of frequent verbal prompts and individual support. Unfortunately, these instructional strategies may have negative academic and social implications as students become dependent on adults for prompts and social supports. This article highlights the importance of fostering student independence for students with ASD and presents three evidence-based strategies to improve student task engagement and decrease reliance on adult prompts: activity schedules, tactile prompting, and peer support interventions.
C1 [Machalicek, Wendy] Univ Oregon, Coll Educ, Eugene, OR 97403 USA.
   [Milley, Allison] Univ Wisconsin, Madison, WI USA.
RP Machalicek, W (reprint author), Univ Oregon, Coll Educ, 5261 Univ Oregon, Eugene, OR 97403 USA.
EM wmachali@uoregon.edu
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NR 42
TC 1
Z9 1
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 2012
VL 48
IS 2
BP 67
EP 75
DI 10.1177/1053451212449739
PG 9
WC Education, Special
SC Education & Educational Research
GA 018SR
UT WOS:000309684000001
ER

PT J
AU Giles, AF
   St Peter, CC
   Pence, ST
   Gibson, AB
AF Giles, Aimee F.
   St Peter, Claire C.
   Pence, Sacha T.
   Gibson, Alexandra B.
TI Preference for blocking or response redirection during stereotypy
   treatment
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Punishment; Automatic reinforcement; Concurrent chain; Social validity
ID SELF-INJURIOUS-BEHAVIOR; VOCAL STEREOTYPY; FUNCTIONAL-ANALYSIS;
   CHILDREN; EXTINCTION; PUNISHMENT; AUTISM; REINFORCEMENT; INTERRUPTION;
   REPLICATION
AB Response redirection and response blocking reduce stereotypy maintained by automatic reinforcement. The current study evaluated the effects of redirection and response blocking on the stereotypic responding of three elementary-age children diagnosed with autism. During the treatment evaluation, redirection and response blocking were evaluated using an alternating treatment embedded in a reversal design. Both procedures resulted in comparably low levels of motor stereotypy. Following treatment evaluation, a concurrent chain was conducted to evaluate participant preference for redirection or response blocking. All three participants preferred redirection. Practitioners may wish to consider participant preference when developing and implementing treatments for stereotypy. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Giles, Aimee F.; St Peter, Claire C.; Pence, Sacha T.; Gibson, Alexandra B.] W Virginia Univ, Dept Psychol, Morgantown, WV 26506 USA.
RP St Peter, CC (reprint author), W Virginia Univ, Dept Psychol, POB 6040, Morgantown, WV 26506 USA.
EM Aimee.Giles@mail.wvu.edu; Claire.StPeter@mail.wvu.edu;
   Sacha.Pence@mail.wvu.edu; agibso11@mix.wvu.edu
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NR 27
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-DEC
PY 2012
VL 33
IS 6
BP 1691
EP 1700
DI 10.1016/j.ridd.2012.05.008
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000001
PM 22695072
ER

PT J
AU Marschik, PB
   Sigafoos, J
   Kaufmann, WE
   Wolin, T
   Talisa, VB
   Bartl-Pokorny, KD
   Budimirovic, DB
   Vollmann, R
   Einspieler, C
AF Marschik, Peter B.
   Sigafoos, Jeff
   Kaufmann, Walter E.
   Wolin, Thomas
   Talisa, Victor B.
   Bartl-Pokorny, Katrin D.
   Budimirovic, Dejan B.
   Vollmann, Ralf
   Einspieler, Christa
TI Peculiarities in the gestural repertoire: An early marker for Rett
   syndrome?
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Communication; Gesture; Interaction; Language; Language impairment;
   Pointing; Rett; Speech; Video analysis
ID AUTISM SPECTRUM DISORDERS; PRESERVED SPEECH VARIANT; COMMUNICATIVE
   DEVELOPMENT; LANGUAGE-DEVELOPMENT; PRESCHOOL-CHILDREN; YOUNG-CHILDREN;
   HOME MOVIES; DIAGNOSIS; ABILITIES; FEMALES
AB We studied the gestures used by children with classic Rett syndrome (RTT) to provide evidence as to how this essential aspect of communicative functions develops. Seven participants with RTT were longitudinally observed between 9 and 18 months of life. The gestures used by these participants were transcribed and coded from a retrospective analysis of a video footage. Gestures were classified as deictic gestures, play schemes, and representational gestures. Results of the analysis showed that the majority of gestures observed were of deictic character. There were no gestures that could be classified as play schemes and only two (e.g., head nodding and waving bye bye) that were coded as representational or symbolic gestures. The overall repertoire of gestures, even though not necessarily delayed in it's onset, was characterized by little variability and a restricted pragmatic functionality. We conclude that the gestural abilities in girls with RTT appear to remain limited and do not constitute a compensatory mechanism for the verbal language modality. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Marschik, Peter B.; Wolin, Thomas; Bartl-Pokorny, Katrin D.; Einspieler, Christa] Med Univ Graz, Ctr Physiol Med, Inst Physiol Dev Physiol & Dev Neurosci INspired, A-8010 Graz, Austria.
   [Marschik, Peter B.; Kaufmann, Walter E.; Talisa, Victor B.; Budimirovic, Dejan B.] Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Ctr Genet Disorders Cognit & Behav, Baltimore, MD USA.
   [Sigafoos, Jeff] Victoria Univ Wellington, Wellington, New Zealand.
   [Kaufmann, Walter E.] Harvard Univ, Sch Med, Childrens Hosp Boston, Boston, MA USA.
   [Vollmann, Ralf] Karl Franzens Univ Graz, Dept Linguist, Graz, Austria.
RP Marschik, PB (reprint author), Med Univ Graz, Ctr Physiol Med, Inst Physiol, Harrachgasse 21-5, A-8010 Graz, Austria.
EM peter.marschik@medunigraz.at
RI Budimirovic, Dejan/O-7885-2014
OI Budimirovic, Dejan/0000-0001-7263-5134
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NR 68
TC 7
Z9 7
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-DEC
PY 2012
VL 33
IS 6
BP 1715
EP 1721
DI 10.1016/j.ridd.2012.05.014
PG 7
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000004
PM 22699245
ER

PT J
AU Bourke-Taylor, H
   Pallant, JF
   Law, M
   Howie, L
AF Bourke-Taylor, Helen
   Pallant, Julie F.
   Law, Mary
   Howie, Linsey
TI Predicting mental health among mothers of school-aged children with
   developmental disabilities: The relative contribution of child, maternal
   and environmental factors
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Caring; Developmental disability; Maternal health
ID QUALITY-OF-LIFE; CEREBRAL-PALSY; PRIMARY CAREGIVERS; LEISURE ACTIVITIES;
   PARTICIPATION; STRESS; EMPOWERMENT; PARENTS; IMPACT; CARE
AB Aim: Many mothers of children with developmental disabilities are known to experience high levels of stress, and compromised mental health. Research is crucial to better understand and assist mothers with compromised mental health, and ultimately better service families raising and supporting a child with a disability.
   Method: Data were collected using cross sectional mail-out survey with follow up phone call. Instruments included the Short Form 36 version 2 (SF-36v2) and instruments that measured maternal, child and environmental factors. Descriptive statistics examined characteristics of participants. Correlation, t-tests, and multiple regression analyses were used to identify factors associated with mothers' mental health.
   Results: Mothers (N = 152) cared for a school-aged child (aged 5-18 years) with high care needs and developmental disabilities including autism spectrum disorder (n = 94); cerebral palsy (n = 29); attention deficit hyperactivity disorder (n = 19). Factors associated with maternal mental health included the child's psychosocial health (r = .36) and challenging behaviour (r = -.33); maternal empowerment (r = .40); maternal participation in health promoting activities (r = .43); and the child's unmet service needs (r = -.29). The strongest predictors of maternal mental health in this cross sectional study were maternal participation in healthy activity and empowerment, the child's emotional functioning and unmet service needs.
   Conclusion: This study identified maternal factors as the most important influence on self reported mental health among this sample of mothers. Findings suggest that service changes that provide mothers with information about their own health and need for health enhancing activities, as well as education that empowers mothers to manage and master their child's disability and needs, may contribute to maternal mental health and well being. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bourke-Taylor, Helen] Monash Univ, Fac Med Nursing & Hlth Sci, Sch Primary Hlth Care, Dept Occupat Therapy, Frankston, Vic 3199, Australia.
   [Pallant, Julie F.] Univ Melbourne, Rural Hlth Acad Ctr, Shepparton, Vic 3630, Australia.
   [Law, Mary] McMaster Univ, CanChild Ctr Childhood Disabil Res, Hamilton, ON, Canada.
   [Howie, Linsey] La Trobe Univ, Dept Occupat Therapy, Bundoora, Vic 3086, Australia.
RP Bourke-Taylor, H (reprint author), Monash Univ, Fac Med Nursing & Hlth Sci, Sch Primary Hlth Care, Dept Occupat Therapy, Peninsula Campus,POB 527, Frankston, Vic 3199, Australia.
EM Helen.Bourke-Taylor@monash.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 0891-4222
J9 RES DEV DISABIL
JI Res. Dev. Disabil.
PD NOV-DEC
PY 2012
VL 33
IS 6
BP 1732
EP 1740
DI 10.1016/j.ridd.2012.04.011
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000006
PM 22699247
ER

PT J
AU Marschik, PB
   Kaufmann, WE
   Einspieler, C
   Bartl-Pokorny, KD
   Wolin, T
   Pini, G
   Budimirovic, DB
   Zappella, M
   Sigafoos, J
AF Marschik, Peter B.
   Kaufmann, Walter E.
   Einspieler, Christa
   Bartl-Pokorny, Katrin D.
   Wolin, Thomas
   Pini, Giorgio
   Budimirovic, Dejan B.
   Zappella, Michele
   Sigafoos, Jeff
TI Profiling early socio-communicative development in five young girls with
   the preserved speech variant of Rett syndrome
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Communicative forms and functions; Preserved speech; Speech-language
   development; Rett syndrome; Video analysis
ID RISK-FACTORS; HOME MOVIES; AUTISM; CHILDREN; PERCEPTION; DIAGNOSIS;
   DISORDER; FEMALES; MECP2; VIDEO
AB Rett syndrome (WIT) is a developmental disorder characterized by regression of purposeful hand skills and spoken language, although some affected children retain some ability to speech. We assessed the communicative abilities of five young girls, who were later diagnosed with the preserved speech variant of RTT, during the pre-regression period (aged 12-24 months). Videotapes, obtained by parents during routine family situations and celebrations, were analyzed to identify communicative forms and functions used by these toddlers. Non-verbal communicative forms dominated over verbal-communicative forms for six of the eight identified communication functions. Although the girls used various non-verbal forms to make requests, for example, none of the individuals were observed to make choices or request information. Early peculiarities in the speech-language domain during the first year of life became more prominent and evident during the second year of life as general differences between typical development and atypical development become more obvious in RTT These findings highlight the importance of assessing socio-communicative forms and functions at early age in children with RTT. The results suggest that speech-language functions did not appear to play a major role in the children's communicative attempts. We conclude that, even among children with the preserved speech variant, socio-communicative deficits are present before regression and persist after this period. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Marschik, Peter B.; Einspieler, Christa; Bartl-Pokorny, Katrin D.; Wolin, Thomas] Med Univ Graz, Ctr Physiol Med, Inst Physiol Dev Physiol & Dev Neurosci Inspired, A-8010 Graz, Austria.
   [Kaufmann, Walter E.] Harvard Univ, Sch Med, Childrens Hosp Boston, Boston, MA USA.
   [Marschik, Peter B.; Kaufmann, Walter E.; Budimirovic, Dejan B.] Johns Hopkins Univ, Sch Med, Fragile X Clin, Ctr Genet Disorders Cognit & Behav,Kennedy Kriege, Baltimore, MD USA.
   [Pini, Giorgio; Zappella, Michele] Versilia Hosp, Tuscany Rett Ctr, Lido Di Camaiore, Italy.
   [Sigafoos, Jeff] Victoria Univ Wellington, Wellington, New Zealand.
RP Einspieler, C (reprint author), Med Univ Graz, Ctr Physiol Med, Inst Physiol, Harrachgasse 21-5, A-8010 Graz, Austria.
EM christa.einspieler@medunigraz.at
RI Budimirovic, Dejan/O-7885-2014
OI Budimirovic, Dejan/0000-0001-7263-5134
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NR 59
TC 10
Z9 10
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-DEC
PY 2012
VL 33
IS 6
BP 1749
EP 1756
DI 10.1016/j.ridd.2012.04.012
PG 8
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000008
PM 22699249
ER

PT J
AU Peters-Scheffer, N
   Didden, R
   Korzilius, H
   Matson, J
AF Peters-Scheffer, Nienke
   Didden, Robert
   Korzilius, Hubert
   Matson, Johnny
TI Cost comparison of early intensive behavioral intervention and treatment
   as usual for children with autism spectrum disorder in the Netherlands
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Early intensive behavioral intervention; Special education; Cost-offset
   study; Autism spectrum disorder
ID PERVASIVE DEVELOPMENTAL DISORDER; YOUNG-CHILDREN; PRESCHOOL-CHILDREN;
   FOLLOW-UP; MENTAL-RETARDATION; PREVALENCE; METAANALYSIS; INDIVIDUALS;
   PREDICTORS; MORTALITY
AB Early intensive behavioral intervention (EIBI) may result in improved cognitive, adaptive and social functioning and reductions in autism severity and behavioral problems in children with Autism Spectrum Disorder (ASD). For a subset of children, normal functioning may be the result. However, due to the intensity (20-40 h per week for 3 years with a low child staff ratio) implementation costs are high and can be controversial. Estimated costs for education, (supported) work and (sheltered) living for individuals with ASD in the Netherlands are applied in a cost-offset model. A compelling argument for the provision of EIBI is long term savings which are approximately (sic) 1,103,067 from age 3 to 65 years per individual with ASD. Extending these costs to the whole Dutch ASD population, cost savings of (sic) 109.2-(sic) 182 billion have been estimated, excluding costs associated with inflation. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Peters-Scheffer, Nienke; Didden, Robert] Radboud Univ Nijmegen, Inst Behav Sci, NL-6500 HE Nijmegen, Netherlands.
   [Peters-Scheffer, Nienke] Stichting Driestroom, NL-6660 AC Elst, Netherlands.
   [Didden, Robert] Trajecturn Zutphen, NL-7200 AH Zutphen, Netherlands.
   [Korzilius, Hubert] Radboud Univ Nijmegen, Inst Management Res, NL-6500 HE Nijmegen, Netherlands.
   [Matson, Johnny] Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
RP Peters-Scheffer, N (reprint author), Radboud Univ Nijmegen, Inst Behav Sci, POB 9104, NL-6500 HE Nijmegen, Netherlands.
EM n.peters@pwo.ru.nl
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NR 82
TC 16
Z9 16
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-DEC
PY 2012
VL 33
IS 6
BP 1763
EP 1772
DI 10.1016/j.ridd.2012.04.006
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000010
PM 22705454
ER

PT J
AU Bossaert, G
   Colpin, H
   Pijl, SJ
   Petry, K
AF Bossaert, Goele
   Colpin, Hilde
   Pijl, Sip Jan
   Petry, Katja
TI Loneliness among students with special educational needs in mainstream
   seventh grade
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Inclusive education; Special educational needs; Loneliness; Autism;
   Early adolescence
ID HIGH-FUNCTIONING CHILDREN; AUTISM; TRANSITION; SCHOOL
AB The goals of this study were twofold. The first aim was to explore loneliness prevalence in typically developing students, students with ASD and students with motor and/or sensory disabilities in mainstream 7th grade in Belgium. The second aim was to explore the relations between number of friends, friendship quality, social self-concept on the one hand and loneliness on the other for each of these three groups, and to compare them across groups. In this study, 108 students with special educational needs (SEN: i.e., 58 students with ASD and 50 students with motor and/or sensory disabilities) were matched to 108 typically developing classmates. Students with ASD reported more loneliness than typically developing students and students with motor and/or sensory disabilities. Loneliness prevalence for typically developing students and students with motor and/or sensory disabilities did not differ significantly. Factors related with loneliness differed between typically developing students and students with SEN (i.e., students with ASD and students with motor and/or sensory disabilities). For students with SEN, same-sex social self-concept was related with loneliness, but not, as for typically developing students, number of friends and opposite-sex social self-concept. Also friendship quality had a marginally significant effect on loneliness feelings for students with SEN. Implications for further research and practice are discussed. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bossaert, Goele; Petry, Katja] Katholieke Univ Leuven, Res Unit, Res Grp Parenting & Special Educ, B-3000 Louvain, Belgium.
   [Colpin, Hilde] Katholieke Univ Leuven, Sch Psychol & Child & Adolescent Dev, Res Grp, B-3000 Louvain, Belgium.
   [Pijl, Sip Jan] Univ Groningen, Dept Special Educ, NL-9700 AB Groningen, Netherlands.
   [Pijl, Sip Jan] Norwegian Univ Sci & Technol, Dept Educ, Trondheim, Norway.
RP Bossaert, G (reprint author), Katholieke Univ Leuven, Res Unit, Res Grp Parenting & Special Educ, Leopold Vanderkelenstr 32,Box 3765, B-3000 Louvain, Belgium.
EM goele.bossaert@ppw.kuleuven.be; hilde.colpin@ppw.kuleuven.be;
   s.j.pijl@rug.nl; katja.petry@ppw.kuleuven.be
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NR 21
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-DEC
PY 2012
VL 33
IS 6
BP 1888
EP 1897
DI 10.1016/j.ridd.2012.05.010
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000022
PM 22705912
ER

PT J
AU Lin, YH
   Su, CY
   Guo, WY
   Wuang, YP
AF Lin, Yueh-Hsien
   Su, Chwen-Yng
   Guo, Wei-Yuan
   Wuang, Yee-Pay
TI Psychometric validation and normative data of a second Chinese version
   of the Hooper Visual Organization Test in children
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Hooper Visual Organization Test; Psychometrics; Normative tables; Rasch
   model; Children
ID INDIVIDUALS; ATTENTION
AB The Hooper Visual Organization Test (HVOT) is a measure of visuosynthetic ability. Previously, the psychometric properties of the HVOT have been evaluated for Chinese-speaking children aged 5-11 years. This study reports development and further evidence of reliability and validity for a second version involving an extended age range of healthy children and children with developmental disabilities (DD) from 5 to 14 years of age. Rasch analysis revealed that after deletion of 6 items, a 24-item version conformed to a unidimensional scale. The test showed satisfactory internal consistency; 3-week test-retest coefficients all exceeded .85 for three DD subsamples. The second version was able to successfully differentiate between the three DD subgroups (attention-deficit hyperactivity disorder, autism spectrum disorders, and mental retardation) and the healthy control group, with correct classification rates ranging from 86.6% to 94.1%. Its construct validity was supported by expected correlations. Accordingly, age-based normative data were established as a basis for interpretation of performance. In sum, the second Chinese version of the HVOT has good psychometric properties and norms that are suited for use in clinical practice. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Su, Chwen-Yng; Guo, Wei-Yuan; Wuang, Yee-Pay] Kaohsiung Med Univ, Dept Occupat Therapy, Kaohsiung 807, Taiwan.
   [Lin, Yueh-Hsien] Natl Taiwan Normal Univ, Special Educ Ctr, Taipei, Taiwan.
RP Wuang, YP (reprint author), Kaohsiung Med Univ, Dept Occupat Therapy, 100 Shih Chuan 1st Rd, Kaohsiung 807, Taiwan.
EM yeepwu@cc.kmu.edu.tw
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NR 35
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-DEC
PY 2012
VL 33
IS 6
BP 1919
EP 1927
DI 10.1016/j.ridd.2012.05.016
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000026
PM 22728603
ER

PT J
AU Clarke, MT
   Loganathan, D
   Swettenham, J
AF Clarke, Michael T.
   Loganathan, Deborah
   Swettenham, John
TI Assessing true and false belief in young children with cerebral palsy
   through anticipatory gaze behaviours: A pilot study
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Cerebral palsy; Theory of mind; Children; Severe speech and physical
   impairments; Anticipatory gaze
ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; SPECTRUM DISORDERS; MIND;
   ATTRIBUTION; DECEPTION; LANGUAGE; TASK; REPRESENTATION; RECOGNITION
AB Children with a clinical description of cerebral palsy (CP) commonly experience cognitive and sensory difficulties that co-occur with motor impairment, and for some children this can include impairments in social communication. While research has begun to examine theory of mind abilities in children with CP, relatively little is known about social communication difficulties in this population. Assessing theory of mind abilities in children with CP using traditional procedures such as the classic Sally-Anne task can be problematic if performance is affected by physical difficulties in signalling responses and/or by cognitive and language demands inherent to the task itself. The central aim of this study therefore was to examine the potential of using a new action anticipation task and eye-tracking technique to assess implicit true and false belief understanding in four developmentally young children with quadriplegic cerebral palsy who had little or no functional speech, and one language age matched child with Down syndrome who did not have severe motor impairment. All children in this study consistently demonstrated anticipatory gaze behaviours in the context of the true belief task. One child with CP and the child with Down syndrome demonstrated anticipatory gaze behaviours indicative of an ability to attribute false belief. The findings are discussed in relation to the application of action anticipation and eye-tracking paradigms in research and clinical practice. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Clarke, Michael T.; Loganathan, Deborah; Swettenham, John] UCL, London WC1N 1PF, England.
RP Clarke, MT (reprint author), UCL, Chandler House,2 Wakefield St, London WC1N 1PF, England.
EM m.clarke@ucl.ac.uk
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NR 47
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-DEC
PY 2012
VL 33
IS 6
BP 2058
EP 2066
DI 10.1016/j.ridd.2012.05.009
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000042
PM 22750668
ER

PT J
AU Brossard-Racine, M
   Shevell, M
   Snider, L
   Belanger, SA
   Majnemer, A
AF Brossard-Racine, Marie
   Shevell, Michael
   Snider, Laurie
   Belanger, Stacey Ageranioti
   Majnemer, Annette
TI Motor skills of children newly diagnosed with Attention Deficit
   Hyperactivity Disorder prior to and following treatment with stimulant
   medication
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Attention Deficit Hyperactivity Disorder; Motor skill disorder; Motor
   performance; Methylphenidate; Stimulant medication
ID DEVELOPMENTAL COORDINATION DISORDER; ADHD; METHYLPHENIDATE; MOVEMENTS;
   FINE; INTERVENTION; TEACHERS; PARENTS; AUTISM; SCHOOL
AB Motor difficulties are common in children with Attention Deficit Hyperactivity Disorder (ADHD). Although preliminary evidence has suggested that methylphenidate can improve the motor skills in children with ADHD and Developmental Coordination Disorder (DCD), the effect of stimulant medication on motor performance in children newly diagnosed with ADHD with or without motor impairment remains unclear. A cohort study of 49 medication-naive children (39 male; mean age 8.4 +/- 1.3 years) with ADHD was conducted. Children were evaluated using the Movement Assessment Battery for Children and the developmental test of visual motor integration at diagnosis and again three months following daily treatment with a stimulant medication. Motor difficulties were highly present at baseline (73.5%) but resolved in a subset after treatment with stimulant medication, suggesting that their motor difficulties may be attributed in part to their attentional problems. Nevertheless, motor impairment persisted in 55.1% of the sample. The severity of the behavioural symptoms was significantly associated with balance skills in children without motor impairments (r(2) = 0.30, p < 0.01) and with visual motor integration skills in children with persisting motor difficulties (r(2) = 0.27, p < 0.01). Attentional difficulties negatively affect the motor skills of children with ADHD. Following the use of stimulant medication, an important subset continued to demonstrate motor difficulties. The improvement in behaviour was insufficient to resolve motor problems and these children should therefore be targeted for rehabilitation services. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Majnemer, Annette] McGill Univ, Montreal Childrens Hosp, Div Paediat Neurol, Sch Phys & Occupat Therapy,MUHC, Montreal, PQ H3H 1P, Canada.
   [Brossard-Racine, Marie] Childrens Natl Med Ctr, Adv Pediat Brain Imaging Res Lab Diagnost Imaging, Washington, DC 20010 USA.
   [Belanger, Stacey Ageranioti] CHU St Justine, Montreal, PQ, Canada.
RP Majnemer, A (reprint author), McGill Univ, Montreal Childrens Hosp, Div Paediat Neurol, Sch Phys & Occupat Therapy,MUHC, 2300 Tupper,Room A-509, Montreal, PQ H3H 1P, Canada.
EM annette.majnemer@mcgill.ca
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NR 41
TC 9
Z9 9
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-DEC
PY 2012
VL 33
IS 6
BP 2080
EP 2087
DI 10.1016/j.ridd.2012.06.003
PG 8
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000045
PM 22796639
ER

PT J
AU Gardiner, E
   Iarocci, G
AF Gardiner, Emily
   Iarocci, Grace
TI Unhappy (and happy) in their own way: A developmental psychopathology
   perspective on quality of life for families living with developmental
   disability with and without autism
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Review
DE Family quality of life; Developmental disabilities; Autism spectrum
   disorder; Developmental psychopathology
ID INTELLECTUAL DISABILITY; SPECTRUM DISORDER; PARENTING STRESS; MENTAL
   RETARDATION; EARLY INTERVENTION; EMOTIONAL-PROBLEMS; UNITED-STATES;
   CHILDREN; OUTCOMES; SUPPORT
AB Research on families living with developmental disability generally and autism specifically is dominated by a deficit view that elicits an elaborate representation of problems and risks without the benefit of considering families' potential for adaptation and resilience. A central tenet of developmental psychopathology is that the study of adaptive and maladaptive development is mutually informative. Specifically, one can examine resilience within the context of adversity and the multiple processes and pathways to adaptive and maladaptive developmental outcomes. We believe these concepts can also be extended to the study of families living with developmental disability as they transition through the family lifecycle. This paper provides an overview of the family quality of life (FQOL) construct, including its conceptualization and measurement, and a review of studies on FQOL among families of children with various developmental disabilities. Special attention is given to families of children with autism, as this is a circumstance characterized by unique adversity. We suggest benefits from adopting a developmental psychopathology perspective, and illustrate how relevant concepts can inform our methodologies as we move forward. We will demonstrate how such an integrated, systemic, and temporal approach will help generate more refined questions on FQOL among families caring for a child with developmental disability in order to provide the specific answers needed to directly inform policy and clinical practice. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Gardiner, Emily] Simon Fraser Univ, Dept Psychol, Autism & Dev Disorders Lab, Burnaby, BC V5A 1S6, Canada.
RP Gardiner, E (reprint author), Simon Fraser Univ, Dept Psychol, Autism & Dev Disorders Lab, 8888 Univ Dr, Burnaby, BC V5A 1S6, Canada.
EM emily_gardiner@sfu.ca; giarocci@sfu.ca
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NR 114
TC 15
Z9 16
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-DEC
PY 2012
VL 33
IS 6
BP 2177
EP 2192
DI 10.1016/j.ridd.2012.06.014
PG 16
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000053
PM 22789702
ER

PT J
AU Dyches, TT
   Smith, TB
   Korth, BB
   Roper, SO
   Mandleco, B
AF Dyches, Tina Taylor
   Smith, Timothy B.
   Korth, Byran B.
   Roper, Susanne Olsen
   Mandleco, Barbara
TI Positive parenting of children with developmental disabilities: A
   meta-analysis
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Developmental disabilities; Down syndrome; Autism; Developmental delay;
   Parenting styles; Meta-analysis
ID TYPICALLY DEVELOPING-CHILDREN; DOWN-SYNDROME; YOUNG-CHILDREN;
   PRESCHOOL-CHILDREN; ADOLESCENT MOTHERS; AUTISM; FAMILY; PREDICTORS;
   CHILDHOOD; BEHAVIORS
AB Although a large body of literature exists supporting the relationship between positive parenting and child outcomes for typically developing children, there are reasons to analyze separately the relevant literature specific to children with developmental disabilities. However, that literature has not been synthesized in any systematic review. This study examined the association between positive parenting attributes and outcomes of young children with developmental disabilities through meta-analytic aggregation of effect sizes across 14 studies including 576 participants. The random effects weighted average effect size was r = .22 (SE = .06, p < .001), indicative of a moderate association between positive parenting attributes and child outcomes. Publication bias did not appear to be a substantial threat to the results. There was a trend for studies with more mature parents to have effect sizes of higher magnitude than studies with young parents. The results provide support for efforts to evaluate and promote effective parenting skills when providing services for young children with disabilities. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Dyches, Tina Taylor; Smith, Timothy B.] Brigham Young Univ, Dept Counseling Psychol & Special Educ, Provo, UT 84602 USA.
   [Korth, Byran B.] Brigham Young Univ, Dept Teacher Educ, Provo, UT 84602 USA.
   [Roper, Susanne Olsen] Brigham Young Univ, Sch Family Life, Provo, UT 84602 USA.
   [Mandleco, Barbara] Brigham Young Univ, Coll Nursing, 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 Tina_dyches@byu.edu; Tim_smith@byu.edu; Byran_korth@byu.edu;
   Susanne_olsen@byu.edu; Barbara_Mandleco@byu.edu
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NR 61
TC 10
Z9 10
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-DEC
PY 2012
VL 33
IS 6
BP 2213
EP 2220
DI 10.1016/j.ridd.2012.06.015
PG 8
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000056
PM 22820061
ER

PT J
AU de Campos, AC
   Savelsbergh, GJP
   Rocha, NACF
AF de Campos, Ana Carolina
   Savelsbergh, Geert J. P.
   Cicuto Ferreira Rocha, Nelci Adriana
TI What do we know about the atypical development of exploratory actions
   during infancy?
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Review
DE Infants at risk; Exploratory behavior; Perception; Infant development
ID FULL-TERM INFANTS; MOTOR DEVELOPMENT; OBJECT EXPLORATION; PRETERM
   INFANTS; BLIND INFANTS; DOWN-SYNDROME; BEHAVIOR; ATTENTION; MOTHERS;
   MANIPULATION
AB Recent theoretical approaches to infant development have highlighted the importance of exploratory actions to motor, perceptual and cognitive development in infancy. However, the performance of infants exposed to risk factors when exploring objects has been frequently overlooked as a variable of interest. The aim of this study was to review scientific publications investigating the role of developmental risk factors on the development of exploratory actions over objects. Electronic databases (Medline and Science Direct) were searched for papers by using for the following key-words in combination: "exploration", "exploratory", "infants". Eighteen papers were included in the review. The performance of infants exposed to various risk conditions such as prematurity, blindness, Down syndrome, autism and low socioeconomic level have been addressed in the literature. Each risk condition has influenced infants' behaviors in particular ways. Considerations for further research were made based on issues raised by the review that still need to be further understood. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [de Campos, Ana Carolina; Cicuto Ferreira Rocha, Nelci Adriana] Fed Univ Sao Carlos UFSCar, Neuropediat Sect, Dept Physiotherapy, Sao Carlos, Brazil.
   [Savelsbergh, Geert J. P.] Vrije Univ Amsterdam, Fac Human Movement Sci, Res Inst MOVE, Amsterdam, Netherlands.
RP de Campos, AC (reprint author), 6010 Calif Circle,Apt 207, Rockville, MD 20852 USA.
EM campos.anacarol@gmail.com
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NR 45
TC 6
Z9 6
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-DEC
PY 2012
VL 33
IS 6
BP 2228
EP 2235
DI 10.1016/j.ridd.2012.06.016
PG 8
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000058
PM 22820063
ER

PT J
AU Venuti, P
   Caria, A
   Esposito, G
   De Pisapia, N
   Bornstein, MH
   de Falco, S
AF Venuti, Paola
   Caria, Andrea
   Esposito, Gianluca
   De Pisapia, Nicola
   Bornstein, Marc H.
   de Falco, Simona
TI Differential brain responses to cries of infants with autistic disorder
   and typical development: An fMRI study
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE Autism; Infant cry; fMRI; Autistic disorder; Brain imaging; Parenting;
   Typical development
ID PHYSIOLOGICAL CONDITION; ACOUSTIC FEATURES; CORTICAL ACTIVITY;
   YOUNG-CHILDREN; HUMAN AMYGDALA; PERCEPTION; CRY; DISTRESS; BEHAVIOR;
   EMPATHY
AB This study used fMRI to measure brain activity during adult processing of cries of infants with autistic disorder (AD) compared to cries of typically developing (TD) infants. Using whole brain analysis, we found that cries of infants with AD compared to those of TD infants elicited enhanced activity in brain regions associated with verbal and prosodic processing, perhaps because altered acoustic patterns of AD cries render them especially difficult to interpret, and increased activity in brain regions associated with emotional processing, indicating that AD cries also elicit more negative feelings and may be perceived as more aversive and/or arousing. Perceived distress engendered by AD cries related to increased activation in brain regions associated with emotional processing. This study supports the hypothesis that cry is an early and meaningful anomaly displayed by children with AD. It could be that cries associated with AD alter parent-child interactions much earlier than the time that reliable AD diagnosis normally occurs. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Venuti, Paola; Caria, Andrea; Esposito, Gianluca; De Pisapia, Nicola; de Falco, Simona] Univ Trent, Dept Cognit Sci & Educ, Trento, Italy.
   [Caria, Andrea] Univ Tubingen, Inst Med Psychol & Behav Neurobiol, Tubingen, Germany.
   [Esposito, Gianluca] RIKEN Brain Sci Inst, Unit Affiliat Social Behav, Saitama, Japan.
   [Bornstein, Marc H.] Eunice Kennedy Shriver Natl Inst Child Hlth & Hum, NIH, Dept Hlth & Human Serv, Eunice, LA USA.
RP Venuti, P (reprint author), Dept Cognit Sci & Educ, Via Matteo Del Ben 5, I-38068 Rovereto, TN, Italy.
EM paola.venuti@unitn.it
RI Esposito, Gianluca/B-1374-2012; Esposito, Gianluca/K-9353-2013
OI Esposito, Gianluca/0000-0002-9442-0254; Esposito,
   Gianluca/0000-0002-9442-0254
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NR 77
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-DEC
PY 2012
VL 33
IS 6
BP 2255
EP 2264
DI 10.1016/j.ridd.2012.06.011
PG 10
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000061
PM 22835685
ER

PT J
AU Allely, CS
   Doolin, O
   Gillberg, C
   Gillberg, IC
   Puckering, C
   Smillie, M
   McConnachie, A
   Heron, J
   Golding, J
   Wilson, P
AF Allely, C. S.
   Doolin, O.
   Gillberg, C.
   Gillberg, I. C.
   Puckering, C.
   Smillie, M.
   McConnachie, A.
   Heron, J.
   Golding, J.
   Wilson, P.
TI Can psychopathology at age 7 be predicted from clinical observation at
   one year? Evidence from the ALSPAC cohort
SO RESEARCH IN DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE ALSPAC; Clinical observation; Infants; ADHD; Pervasive developmental
   disorder; Disruptive behaviour disorder
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; AUTISM SPECTRUM DISORDER;
   FAMILY HOME MOVIES; PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIOR
   PROBLEMS; MIDDLE CHILDHOOD; YOUNG-CHILDREN; INFANT ATTACHMENT; ANXIETY
   DISORDERS; 1ST YEAR
AB One of the challenges of developmental psychopathology is to determine whether identifiable pathways to developmental disorders exist in the first months or years of life. Early identification of such disorders poses a similar challenge for clinical services. Using data from a large contemporary birth cohort, we examined whether psychopathology at age seven can be predicted from clinician observation at one year. Two groups of clinical raters observed videos of caregiver-infant interaction. Neither group of raters could reliably identify any precursors of later development of psychopathology in the one-year-old infants in this setting. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Allely, C. S.; Gillberg, C.; Puckering, C.; Wilson, P.] Univ Glasgow, RHSC Yorkhill, Inst Hlth & Wellbeing, Glasgow G3 8SJ, Lanark, Scotland.
   [Doolin, O.; McConnachie, A.] Univ Glasgow, Robertson Ctr Biostat, Glasgow G12 8QQ, Lanark, Scotland.
   [Gillberg, I. C.] Univ Gothenburg, Sahlgren Univ Hosp, Dept Child & Adolescent Psychiat, Annedals Clin, S-41345 Gothenburg, Sweden.
   [Heron, J.; Golding, J.] Univ Bristol, Sch Social & Community Med, Bristol BS8 1TH, Avon, England.
RP Wilson, P (reprint author), Univ Glasgow, Royal Hosp Sick Children, Inst Hlth & Wellbeing, Caledonia House, Glasgow G3 8SJ, Lanark, Scotland.
EM Clare.allely@glasgow.ac.uk; Orla.doolin@glasgow.ac.uk;
   Christopher.gillberg@pediat.gu.se; Carina.gillberg@gnc.gu.se;
   Christine.puckering@glasgow.ac.uk; maureensmillie@tiscali.co.uk;
   alex.mcconnachie@glasgow.ac.uk; Jon.heron@bristol.ac.uk;
   jean.golding@bristol.ac.uk; Philip.wilson@glasgow.ac.uk
RI Heron, Jon/D-5884-2011
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NR 107
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-DEC
PY 2012
VL 33
IS 6
BP 2292
EP 2300
DI 10.1016/j.ridd.2012.07.009
PG 9
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 009JL
UT WOS:000309022000065
PM 22853888
ER

PT J
AU Brown, HD
   Amodeo, DA
   Sweeney, JA
   Ragozzino, ME
AF Brown, Holden D.
   Amodeo, Dionisio A.
   Sweeney, John A.
   Ragozzino, Michael E.
TI The selective serotonin reuptake inhibitor, escitalopram, enhances
   inhibition of prepotent responding and spatial reversal learning
SO JOURNAL OF PSYCHOPHARMACOLOGY
LA English
DT Article
DE Anxiety; escitalopram; rats; reversal learning; reward; serotonin
ID OBSESSIVE-COMPULSIVE DISORDER; AUTISM SPECTRUM DISORDERS; ELEVATED
   T-MAZE; DOUBLE-BLIND; FRONTAL-CORTEX; BEHAVIORAL FLEXIBILITY;
   ORBITOFRONTAL CORTEX; DORSOMEDIAL STRIATUM; ACETYLCHOLINE-RELEASE;
   TRYPTOPHAN DEPLETION
AB Previous findings indicate treatment with a selective serotonin reuptake inhibitor (SSRI) facilitates behavioral flexibility when conditions require inhibition of a learned response pattern. The present experiment investigated whether acute treatment with the SSRI, escitalopram, affects behavioral flexibility when conditions require inhibition of a naturally biased response pattern (elevated conflict test) and/or reversal of a learned response pattern (spatial reversal learning). An additional experiment was carried out to determine whether escitalopram, at doses that affected behavioral flexibility, also reduced anxiety as tested in the elevated plus-maze. In each experiment, Long-Evans rats received an intraperitoneal injection of either saline or escitalopram (0.03, 0.3 or 1.0 mg/kg) 30 min prior to behavioral testing. Escitalopram, at all doses tested, enhanced acquisition in the elevated conflict test, but did not affect performance in the elevated plus-maze. Escitalopram (0.3 and 1.0 mg/kg) did not alter acquisition of the spatial discrimination, but facilitated reversal learning. In the elevated conflict and spatial reversal learning test, escitalopram enhanced the ability to maintain the relevant strategy after being initially selected. The present findings suggest that enhancing serotonin transmission with an SSRI facilitates inhibitory processes when conditions require a shift away from either a naturally biased response pattern or a learned choice pattern.
C1 [Brown, Holden D.; Amodeo, Dionisio A.; Sweeney, John A.; Ragozzino, Michael E.] Univ Illinois, Dept Psychol, Chicago, IL 60607 USA.
   [Brown, Holden D.] Univ Illinois, Grad Program Neurosci, Chicago, IL 60607 USA.
   [Sweeney, John A.; Ragozzino, Michael E.] Univ Illinois, Ctr Cognit Med, Chicago, IL 60607 USA.
RP Ragozzino, ME (reprint author), Univ Illinois, Dept Psychol, Chicago, IL 60607 USA.
EM mrago@uic.edu
FU NIH [P50 HD055751]; Janssen Pharmaceuticals; Epix Pharmaceuticals
FX This research was supported by NIH grant P50 HD055751 (JAS, MER).John A
   Sweeney serves a consultant for Pfizer Pharmaceuticals and has an
   investigator initiated grant from Janssen Pharmaceuticals. Michael E
   Ragozzino has received an investigator initiated grant from Epix
   Pharmaceuticals.
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NR 80
TC 5
Z9 5
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 0269-8811
EI 1461-7285
J9 J PSYCHOPHARMACOL
JI J. Psychopharmacol.
PD NOV
PY 2012
VL 26
IS 11
BP 1443
EP 1455
DI 10.1177/0269881111430749
PG 13
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 020UC
UT WOS:000309839100006
PM 22219222
ER

PT J
AU Bekhet, AK
   Johnson, NL
   Zauszniewski, JA
AF Bekhet, Abir K.
   Johnson, Norah L.
   Zauszniewski, Jaclene A.
TI Effects on Resilience of Caregivers of Persons With Autism Spectrum
   Disorder: The Role of Positive Cognitions
SO JOURNAL OF THE AMERICAN PSYCHIATRIC NURSES ASSOCIATION
LA English
DT Article
DE autism spectrum disorder; caregivers; positive cognitions;
   resourcefulness; burden
AB BACKGROUND : Approximately 2.8 million people in the United States are diagnosed with autism spectrum disorder (ASD). Family caregivers manage many aspects of their care, which is demanding, overwhelming, and can affect their mental health. OBJECTIVE: This study examined the effects of caregiver burden (risk factor) and positive cognitions (protective factors) on resourcefulness (resilience indicator) in 95 caregivers of persons with ASD. DESIGN: Descriptive, correlational, and cross-sectional. RESULTS : Positive cognitions explained 32% of the variance in resourcefulness, F(1, 93) = 44.49, p < .001, and as positive cognitions increased, caregivers' resourcefulness increased. A substantial drop in the beta weight of caregiver burden from B = -.36 to -.04 when positive cognitions was entered the equation suggested that positive cognitions mediated the effect of caregiver burden on resourcefulness. CONCLUSION: The results support resilience theory and suggest a need for developing interventions to strengthen positive thinking among caregivers of persons with ASD.
C1 [Bekhet, Abir K.; Johnson, Norah L.] Marquette Univ, Coll Nursing, Milwaukee, WI 53233 USA.
   [Zauszniewski, Jaclene A.] Case Western Reserve Univ, Cleveland, OH 44106 USA.
RP Bekhet, AK (reprint author), Marquette Univ, Coll Nursing, Clark Hall 530 N 16th St, Milwaukee, WI 53233 USA.
EM abir.bekhet@marquette.edu
FU The American Psychiatric Nurses Foundation (APNF) [74614]
FX The author(s) disclosed receipt of the following financial support for
   the research, authorship, and/or publication of this article: This
   research is funded by The American Psychiatric Nurses Foundation (APNF),
   Research Grant No. 74614.
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NR 43
TC 7
Z9 7
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1078-3903
EI 1532-5725
J9 J AM PSYCHIAT NURSES
JI J. Am. Psych. Nurses Assoc.
PD NOV-DEC
PY 2012
VL 18
IS 6
BP 337
EP 344
DI 10.1177/1078390312467056
PG 8
WC Nursing; Psychiatry
SC Nursing; Psychiatry
GA V32PP
UT WOS:000208963400003
PM 23139377
ER

PT J
AU Anitha, A
   Nakamura, K
   Thanseem, I
   Yamada, K
   Iwayama, Y
   Toyota, T
   Matsuzaki, H
   Miyachi, T
   Yamada, S
   Tsujii, M
   Tsuchiya, KJ
   Matsumoto, K
   Iwata, Y
   Suzuki, K
   Ichikawa, H
   Sugiyama, T
   Yoshikawa, T
   Mori, N
AF Anitha, Ayyappan
   Nakamura, Kazuhiko
   Thanseem, Ismail
   Yamada, Kazuo
   Iwayama, Yoshimi
   Toyota, Tomoko
   Matsuzaki, Hideo
   Miyachi, Taishi
   Yamada, Satoru
   Tsujii, Masatsugu
   Tsuchiya, Kenji J.
   Matsumoto, Kaori
   Iwata, Yasuhide
   Suzuki, Katsuaki
   Ichikawa, Hironobu
   Sugiyama, Toshiro
   Yoshikawa, Takeo
   Mori, Norio
TI Brain region-specific altered expression and association of
   mitochondria-related genes in autism
SO MOLECULAR AUTISM
LA English
DT Article
DE Autism; Mitochondria; Postmortem brain; NEFL; Uncoupling protein;
   Metaxin
ID ANTERIOR CINGULATE CORTEX; CARRIER SLC25A12 GENE; PERVASIVE
   DEVELOPMENTAL DISORDERS; MARIE-TOOTH DISEASE; SPECTRUM DISORDERS;
   UNCOUPLING PROTEINS; ENERGY-METABOLISM; OUTER-MEMBRANE; PROPIONIC-ACID;
   CELL-DEATH
AB Background: Mitochondrial dysfunction (MtD) has been observed in approximately five percent of children with autism spectrum disorders (ASD). MtD could impair highly energy-dependent processes such as neurodevelopment, thereby contributing to autism. Most of the previous studies of MtD in autism have been restricted to the biomarkers of energy metabolism, while most of the genetic studies have been based on mutations in the mitochondrial DNA (mtDNA). Despite the mtDNA, most of the proteins essential for mitochondrial replication and function are encoded by the genomic DNA; so far, there have been very few studies of those genes. Therefore, we carried out a detailed study involving gene expression and genetic association studies of genes related to diverse mitochondrial functions.
   Methods: For gene expression analysis, postmortem brain tissues (anterior cingulate gyrus (ACG), motor cortex (MC) and thalamus (THL)) from autism patients (n=8) and controls (n=10) were obtained from the Autism Tissue Program (Princeton, NJ, USA). Quantitative real-time PCR arrays were used to quantify the expression of 84 genes related to diverse functions of mitochondria, including biogenesis, transport, translocation and apoptosis. We used the delta delta Ct (Delta Delta Ct) method for quantification of gene expression. DNA samples from 841 Caucasian and 188 Japanese families were used in the association study of genes selected from the gene expression analysis. FBAT was used to examine genetic association with autism.
   Results: Several genes showed brain region-specific expression alterations in autism patients compared to controls. Metaxin 2 (MTX2), neurofilament, light polypeptide (NEFL) and solute carrier family 25, member 27 (SLC25A27) showed consistently reduced expression in the ACG, MC and THL of autism patients. NEFL (P = 0.038; Z-score 2.066) and SLC25A27 (P = 0.046; Z-score 1.990) showed genetic association with autism in Caucasian and Japanese samples, respectively. The expression of DNAJC19, DNM1L, LRPPRC, SLC25A12, SLC25A14, SLC25A24 and TOMM20 were reduced in at least two of the brain regions of autism patients.
   Conclusions: Our study, though preliminary, brings to light some new genes associated with MtD in autism. If MtD is detected in early stages, treatment strategies aimed at reducing its impact may be adopted.
C1 [Anitha, Ayyappan; Matsuzaki, Hideo; Miyachi, Taishi; Tsujii, Masatsugu; Tsuchiya, Kenji J.; Matsumoto, Kaori; Suzuki, Katsuaki; Mori, Norio] Hamamatsu Univ Sch Med, Res Ctr Child Mental Dev, Hamamatsu, Shizuoka 4313192, Japan.
   [Nakamura, Kazuhiko; Thanseem, Ismail; Iwata, Yasuhide; Mori, Norio] Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan.
   [Yamada, Kazuo; Iwayama, Yoshimi; Toyota, Tomoko; Yoshikawa, Takeo] RIKEN, Brain Sci Inst, Lab Mol Psychiat, Wako, Saitama 3510198, Japan.
   [Yamada, Satoru; Ichikawa, Hironobu] Tokyo Metropolitan Childrens Med Ctr, Fuchu, Tokyo 1838561, Japan.
   [Tsujii, Masatsugu] Chukyo Univ, Fac Sociol, Toyota 4700393, Japan.
   [Sugiyama, Toshiro] Hamamatsu Univ Sch Med, Dept Child & Adolescent Psychiat, Hamamatsu, Shizuoka 4313192, Japan.
RP Nakamura, K (reprint author), Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, 1-20-1 Handayama, Hamamatsu, Shizuoka 4313192, Japan.
EM nakamura@hama-med.ac.jp
FU PHS [R 24 MH 068855]; Ministry of Education, Culture, Sports, Science,
   and Technology of Japan [23591700, 23390288]
FX We thank Dr. Jane Pickett, Director of Brain Resources and Data, Autism
   Tissue Program, for facilitating brain tissue collection. Human tissue
   was obtained from the NICHD Brain and Tissue Bank for Developmental
   Disorders at the University of Maryland, Baltimore, Maryland. Tissue
   samples were also provided by the Harvard Brain Tissue Resource Center,
   which is supported in part by PHS grant number R 24 MH 068855. This work
   was supported by Grants-in-Aid for Scientific Research from the Ministry
   of Education, Culture, Sports, Science, and Technology of Japan
   (23591700 to AA and 23390288 to KN). A part of this study is the result
   of "Integrated research on neuropsychiatric disorders" carried out under
   the Strategic Research Program for Brain Sciences by the Ministry of
   Education, Culture, Sports, Science and Technology of Japan. We thank
   Tae Takahashi and Mika Oyaizu for technical assistance.
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NR 87
TC 13
Z9 13
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 2012
VL 3
AR 12
DI 10.1186/2040-2392-3-12
PG 12
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254TE
UT WOS:000327189100001
PM 23116158
ER

PT J
AU Weil, TN
   Inglehart, MR
AF Weil, Taryn N.
   Inglehart, Marita Rohr
TI Three- to 21-year-old Patients with Autism Spectrum Disorders: Parents'
   Perceptions of Severity of Symptoms, Oral Health, and Oral
   Health-related Behavior
SO PEDIATRIC DENTISTRY
LA English
DT Article
DE AUTISM SPECTRUM DISORDERS; ORAL HEALTH; TOOTHBRUSHING; ACCESS TO HEALTH
   CARE
AB Purpose: The purpose was to explore the relationship between the level of functioning (listening/talking/reading/daily self-care/care at home/social skills) of three to 21-year-old patients with autism spectrum disorders (ASDs) and their oral health and oral health-related behavior (brushing, flossing, dental visits). Methods: Survey data were collected from 85 parents of ASD patients. Patients' level of functioning was determined with a short version of the Survey Interview Form of the Vineland Adaptive Behavior Scales (2nd edition). Results: The patients ranged from very low to high levels of functioning. Oral health correlated with the ability to: listen (r=.53; P<.001); talk (r=.40; P<.001); read (r=.30; P<.01); engage in daily self-care (r=.36; P<.001); engage in care at home (r=.44; P<.001); and demonstrate social skills (r=.36; P<.001). The parents' comfort levels concerning brushing and flossing their children's teeth and taking their children to the dentist varied considerably and correlated with children's level of functioning. Frequency of tooth-brushing correlated with listening skills (r=.31; P<.01); the frequency of flossing correlated with the ability to talk (r=.31; P<.01). Conclusions: Understanding the relationships between level of functioning of children with ASDs and their oral health and oral health-related behavior could increase dentists' ability to provide the best possible care for these patients.
C1 [Inglehart, Marita Rohr] Univ Michigan, Sch Dent, Dept Periodont & Oral Med, Ann Arbor, MI 48109 USA.
   [Inglehart, Marita Rohr] Univ Michigan, Dept Psychol, Coll Literature Sci & Arts, Ann Arbor, MI USA.
RP Inglehart, MR (reprint author), Univ Michigan, Sch Dent, Dept Periodont & Oral Med, Ann Arbor, MI 48109 USA.
EM mri@umich.edu
FU School of Dentistry, University of Michigan, Ann Arbor, Mich;
   Interactive Autism Network
FX This research was supported by a student research fellowship awarded by
   the School of Dentistry, University of Michigan, Ann Arbor, Mich. The
   authors wish to thank the Interactive Autism Network for its support for
   this research and all respondents for taking the time to participate in
   this study.
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NR 33
TC 1
Z9 1
PU AMER ACAD PEDIATRIC DENTISTRY
PI CHICAGO
PA 211 E CHICAGO AVENUE SUITE 1036, CHICAGO, IL 60611-2616 USA
SN 0164-1263
EI 1942-5473
J9 PEDIATR DENT
JI Pediatr. Dent.
PD NOV-DEC
PY 2012
VL 34
IS 7
BP 473
EP 479
PG 7
WC Dentistry, Oral Surgery & Medicine; Pediatrics
SC Dentistry, Oral Surgery & Medicine; Pediatrics
GA V34GX
UT WOS:000209076000004
PM 23265164
ER

PT J
AU Capozza, LE
   Bimstein, E
AF Capozza, Lauren E.
   Bimstein, Enrique
TI Preferences of Parents of Children with Autism Spectrum Disorders
   Concerning Oral Health and Dental Treatment
SO PEDIATRIC DENTISTRY
LA English
DT Article
DE AUTISTIC DISORDER; DENTAL MATERIALS; DENTAL CARE; DENTAL AMALGAM;
   PARENTAL CONSENT
AB Purpose: The purpose of this study was to describe the preferences of parents of children with or without autism spectrum disorders (ASDs) concerning oral health and dental treatment. Methods: A questionnaire that queried demographics, dental needs, perceptions of dental materials and treatments, and parental concerns regarding relevant ASD issues in medicine and dentistry was distributed in the waiting rooms of a pediatric dental Clinic and an autism clinic to parents or legal guardians of children undergoing treatment. The responses for the children with or without ASDs were compared. Results: Statistically significant differences between the ASDs (N=23 and non-ASDS (N=33) groups existed for: parental age; frequency of dental visits per year; supervision of tooth-brushing; and use of a fluoridated toothpaste. Statistically insignificant differences were found in attitudes toward: amalgam; composite; fluoride products; or behavior guidance techniques. Conclusions: Parents or legal guardians of children with autism spectrum disorders are likely to have special beliefs and preferences regarding dental materials and dental behavior guidance.
C1 [Capozza, Lauren E.] Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA.
   [Bimstein, Enrique] Univ Kentucky, Coll Dent, Div Pediat Dent, Lexington, KY 40506 USA.
RP Bimstein, E (reprint author), Univ Kentucky, Coll Dent, Div Pediat Dent, Lexington, KY 40506 USA.
EM ebi223@uky.edu
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NR 26
TC 2
Z9 2
PU AMER ACAD PEDIATRIC DENTISTRY
PI CHICAGO
PA 211 E CHICAGO AVENUE SUITE 1036, CHICAGO, IL 60611-2616 USA
SN 0164-1263
EI 1942-5473
J9 PEDIATR DENT
JI Pediatr. Dent.
PD NOV-DEC
PY 2012
VL 34
IS 7
BP 480
EP 484
PG 5
WC Dentistry, Oral Surgery & Medicine; Pediatrics
SC Dentistry, Oral Surgery & Medicine; Pediatrics
GA V34GX
UT WOS:000209076000005
PM 23265165
ER

PT J
AU Sanders, BK
AF Sanders, Bryan K.
TI Flowers for Algernon: steroid dysgenesis, epigenetics and brain
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SO PHARMACOLOGICAL REPORTS
LA English
DT Review
DE autism; antidepressants; behavior; epigenetic; rodents; serotonin; sex
   differences; valproic acid
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C1 Univ Calif Berkeley, Coll Letters & Sci Alumnus, Berkeley, CA 94720 USA.
RP Sanders, BK (reprint author), Univ Calif Berkeley, Coll Letters & Sci Alumnus, Durant Hall,MC 2920, Berkeley, CA 94720 USA.
EM bksanders@cal.berkeley.edu
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PU POLISH ACAD SCIENCES INST PHARMACOLOGY
PI KRAKOW
PA SMETNA 12, 31-343 KRAKOW, POLAND
SN 1734-1140
J9 PHARMACOL REP
JI Pharmacol. Rep.
PD NOV-DEC
PY 2012
VL 64
IS 6
BP 1285
EP 1290
PG 6
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA V30VR
UT WOS:000208844000001
PM 23406739
ER

PT J
AU Kumar, B
   Prakash, A
   Sewal, RK
   Medhi, B
   Modi, M
AF Kumar, Baldeep
   Prakash, Ajay
   Sewal, Rakesh K.
   Medhi, Bikash
   Modi, Manish
TI Drug therapy in autism: a present and future perspective
SO PHARMACOLOGICAL REPORTS
LA English
DT Review
DE autism; ASD; behavior; clinical studies; drugs
ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT-HYPERACTIVITY DISORDER;
   PLACEBO-CONTROLLED CROSSOVER; OPEN-LABEL TRIAL; SEROTONIN-REUPTAKE
   INHIBITORS; HYPERBARIC-OXYGEN THERAPY; CEREBRAL-BLOOD-FLOW; SPECTRUM
   DISORDERS; DOUBLE-BLIND; OXIDATIVE STRESS
AB Autism is a neurodevelopmental disorder, with a multifactorial etiology, characterized by severe abnormalities in communications, social awareness and skills, and the presence of restrictive and stereotyped patterns of behaviors. It is traditionally considered a "static" encephalopathic disorder without any specific cure and few effective biomedical interventions. There are various factors which are involved in the etiopathogenesis of autism or autism spectrum disorder (ASD) such as impaired immune responses, neuroinflammation, abnormal neurotransmission, oxidative stress, mitochondrial dysfunction, environmental toxins and stressors. The autism is often associated with a number of genetic disorders such as fragile X syndrome, tuberous sclerosis, epilepsy and Down syndrome. The recent approaches to autism treatment included various non-pharmacological and pharmacological therapy such as food supplementation, detoxification, treatment of neuroinflammation, immunologic treatments and psychotropic medications, which are found to be effective in treating various behavioral symptoms of autism. In current practice, there is no curative treatment for autism but the recommended treatment for autism involves educational therapies: speech therapy, sensory integration therapy, auditory therapy. There are classes of different pharmacological agents which are found to be effective in improving behavioral symptoms of ASD such as neurotransmitter reuptake inhibitors (fluoxetine), tricyclic antidepressants (imipramine), anticonvulsants (lamotrigine), atypical antipsychotics (clozapine), acetylcholinesterase inhibitors (rivastigmine), etc. New classes of drugs with novel mechanisms of action should be there so that this disorder will become less prevalent in the future.
C1 [Kumar, Baldeep; Prakash, Ajay; Sewal, Rakesh K.; Medhi, Bikash] Postgrad Inst Med Educ & Res, Dept Pharmacol, Chandigarh 160012, India.
   [Modi, Manish] Postgrad Inst Med Educ & Res, Dept Neurol, Chandigarh 160012, India.
RP Medhi, B (reprint author), Postgrad Inst Med Educ & Res, Dept Pharmacol, Chandigarh 160012, India.
EM drbikashus@yahoo.com
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NR 133
TC 8
Z9 8
PU POLISH ACAD SCIENCES INST PHARMACOLOGY
PI KRAKOW
PA SMETNA 12, 31-343 KRAKOW, POLAND
SN 1734-1140
J9 PHARMACOL REP
JI Pharmacol. Rep.
PD NOV-DEC
PY 2012
VL 64
IS 6
BP 1291
EP 1304
PG 14
WC Pharmacology & Pharmacy
SC Pharmacology & Pharmacy
GA V30VR
UT WOS:000208844000002
PM 23406740
ER

PT J
AU Morsanyi, K
   Primi, C
   Handley, SJ
   Chiesi, F
   Galli, S
AF Morsanyi, Kinga
   Primi, Caterina
   Handley, Simon J.
   Chiesi, Francesca
   Galli, Silvia
TI Are systemizing and autistic traits related to talent and interest in
   mathematics and engineering? Testing some of the central claims of the
   empathizing-systemizing theory
SO BRITISH JOURNAL OF PSYCHOLOGY
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; STATISTICAL ANXIETY SCALE; NORMAL
   SEX-DIFFERENCES; SPECTRUM QUOTIENT AQ; MALE BRAIN THEORY; FETAL
   TESTOSTERONE; GENDER-DIFFERENCES; ASPERGER-SYNDROME; SPATIAL ABILITY;
   MEASUREMENT INVARIANCE
AB In two experiments, we tested some of the central claims of the empathizingsystemizing (E-S) theory. Experiment 1 showed that the systemizing quotient (SQ) was unrelated to performance on a mathematics test, although it was correlated with statistics-related attitudes, self-efficacy, and anxiety. In Experiment 2, systemizing skills, and gender differences in these skills, were more strongly related to spatial thinking styles than to SQ. In fact, when we partialled the effect of spatial thinking styles, SQ was no longer related to systemizing skills. Additionally, there was no relationship between the Autism Spectrum Quotient (AQ) and the SQ, or skills and interest in mathematics and mechanical reasoning. We discuss the implications of our findings for the E-S theory, and for understanding the autistic cognitive profile.
C1 [Morsanyi, Kinga; Handley, Simon J.] Univ Plymouth, Sch Psychol, Plymouth PL4 8AA, Devon, England.
   [Primi, Caterina; Chiesi, Francesca; Galli, Silvia] Univ Florence, Dept Psychol, I-50121 Florence, Italy.
RP Morsanyi, K (reprint author), Univ Plymouth, Sch Psychol, Plymouth PL4 8AA, Devon, England.
EM kinga.morsanyi@plymouth.ac.uk
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NR 80
TC 3
Z9 3
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0007-1269
J9 BRIT J PSYCHOL
JI Br. J. Psychol.
PD NOV
PY 2012
VL 103
BP 472
EP 496
DI 10.1111/j.2044-8295.2011.02089.x
PN 4
PG 25
WC Psychology, Multidisciplinary
SC Psychology
GA 014YB
UT WOS:000309410700003
PM 23034108
ER

PT J
AU Loui, P
   Zamm, A
   Schlaug, G
AF Loui, Psyche
   Zamm, Anna
   Schlaug, Gottfried
TI Enhanced functional networks in absolute pitch
SO NEUROIMAGE
LA English
DT Article
DE Pitch; Emotion; Music; fMRI; Small-world network
ID SMALL-WORLD NETWORKS; GRAPHEME-COLOR SYNESTHESIA; HUMAN BRAIN; DOPAMINE
   RELEASE; WORKING-MEMORY; RELATIVE PITCH; CONNECTIVITY; AUTISM;
   MUSICIANS; EMOTION
AB Functional networks in the human brain give rise to complex cognitive and perceptual abilities. While the decrease of functional connectivity is linked to neurological and psychiatric disorders, less is known about the consequences of increased functional connectivity. One population that has exceptionally enhanced perceptual abilities is people with absolute pitch (AP) - an ability to categorize tones into pitch classes without reference. AP has been linked to exceptional talent as well as to psychiatric and neurological conditions. Here we show that AP possessors have increased functional activation during music listening, as well as increased degrees, clustering, and local efficiency of functional correlations, with the difference being highest around the left superior temporal gyrus. Our results provide the first evidence that increased functional connectivity in a small-world brain network is related to exceptional perceptual abilities in a healthy population. (C) 2012 Published by Elsevier Inc.
C1 [Schlaug, Gottfried] Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA.
   Harvard Univ, Sch Med, Boston, MA 02215 USA.
RP Schlaug, G (reprint author), Beth Israel Deaconess Med Ctr, Dept Neurol, 330 Brookline Ave,Palmer 127, Boston, MA 02215 USA.
EM gschlaug@bidmc.harvard.edu
FU NIH [R01 DC 009823]; Templeton Foundation for Positive Neuroscience
FX We thank Robert Rowe and Sourcetone, LLC for providing us with sound
   samples used in this study. We thank Robert J. Ellis for useful
   discussions and two anonymous reviewers for helpful suggestions on a
   previous version of the manuscript. This research was made possible by
   support from NIH R01 DC 009823 and the Templeton Foundation for Positive
   Neuroscience.
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NR 64
TC 16
Z9 16
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 2012
VL 63
IS 2
BP 632
EP 640
DI 10.1016/j.neuroimage.2012.07.030
PG 9
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 013VY
UT WOS:000309335200002
PM 22836173
ER

PT J
AU Go, HS
   Kim, KC
   Choi, CS
   Jeon, SJ
   Kwon, KJ
   Han, SH
   Lee, J
   Cheong, JH
   Ryu, JH
   Kim, CH
   Ko, KH
   Shin, CY
AF Go, Hyo Sang
   Kim, Ki Chan
   Choi, Chang Soon
   Jeon, Se Jin
   Kwon, Kyung Ja
   Han, Seol-Heui
   Lee, Jongmin
   Cheong, Jae Hoon
   Ryu, Jong Hoon
   Kim, Chong-Hyun
   Ko, Kwang Ho
   Shin, Chan Young
TI Prenatal exposure to valproic acid increases the neural progenitor cell
   pool and induces macrocephaly in rat brain via a mechanism involving the
   GSK-3 beta/beta-catenin pathway
SO NEUROPHARMACOLOGY
LA English
DT Article
DE Nestin; GSK-3 beta; beta-Catenin; Macrocephaly; Autism
ID AUTISM SPECTRUM DISORDERS; MOOD-STABILIZING DRUGS; CEREBRAL CORTICAL
   SIZE; PROTEIN-KINASE-C; MINICOLUMNAR PATHOLOGY; NEURITE OUTGROWTH;
   PREFRONTAL CORTEX; SIGNALING PATHWAY; UP-REGULATION; SELF-RENEWAL
AB Autism is a spectrum of neurodevelopmental disorders characterized by social isolation and lack of interaction. Anatomically, autism patients often show macrocephaly and high neuronal density. To investigate the mechanism underlying the higher neuronal populations seen in ASD, we subcutaneously injected VPA (400 mg/kg) into pregnant Sprague-Dawley rats on E12, an animal model often used in ASD study. Alternatively, cultured rat neural progenitor cells were treated with VPA. Until E18, VPA induced NPC proliferation and delayed neurogenesis in fetal brain, but the subsequent differentiation of NPCs to neurons increased brain neuronal density afterward. Similar findings were observed with NPCs treated with VPA in vitro. At a molecular level, VPA enhanced Wnt1 expression and activated the GSK-3 beta/beta-catenin pathway. Furthermore, inhibition of this pathway attenuated the effects of VPA. The findings of this study suggest that an altered developmental process underlies the macrocephaly and abnormal brain structure observed in the autistic brain. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Choi, Chang Soon; Shin, Chan Young] Konkuk Univ, Sch Med, Dept Pharmacol, Seoul 143701, South Korea.
   [Go, Hyo Sang; Kim, Ki Chan; Ko, Kwang Ho] Seoul Natl Univ, Coll Pharm, Dept Pharmacol, Seoul, South Korea.
   [Go, Hyo Sang; Kim, Ki Chan; Choi, Chang Soon; Jeon, Se Jin; Kwon, Kyung Ja; Han, Seol-Heui; Lee, Jongmin; Shin, Chan Young] Konkuk Univ, SMART IABS, Neurosci Res Ctr, Seoul 143701, South Korea.
   [Han, Seol-Heui] Konkuk Univ, Sch Med, Dept Neurol, Seoul 143701, South Korea.
   [Cheong, Jae Hoon] Sahmyook Univ, Coll Pharm, Seoul, South Korea.
   [Ryu, Jong Hoon] Kyung Hee Univ, Coll Pharm, Dept Oriental Pharmaceut Sci, Seoul 130701, South Korea.
   [Kim, Chong-Hyun] Korea Inst Sci & Technol, Ctr Neural Sci, Seoul, South Korea.
   [Kim, Chong-Hyun] Univ Sci & Technol, Dept Neurosci, Taejon, South Korea.
RP Shin, CY (reprint author), Konkuk Univ, Sch Med, Dept Pharmacol, 1 Hwayang Dong, Seoul 143701, South Korea.
EM chanyshin@kku.ac.kr
FU NRF; Ministry of Education, Science and Technology, Republic of Korea
   (MEST) [2011-0014258]
FX This work was supported by the Mid-career Researcher Program by a NRF
   grant funded by Ministry of Education, Science and Technology, Republic
   of Korea (MEST) (CY Shin, grant no. 2011-0014258).
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NR 69
TC 14
Z9 15
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3908
J9 NEUROPHARMACOLOGY
JI Neuropharmacology
PD NOV
PY 2012
VL 63
IS 6
BP 1028
EP 1041
DI 10.1016/j.neuropharm.2012.07.028
PG 14
WC Neurosciences; Pharmacology & Pharmacy
SC Neurosciences & Neurology; Pharmacology & Pharmacy
GA 015IC
UT WOS:000309438600012
PM 22841957
ER

PT J
AU Russell, G
   Kelly, SE
   Ford, T
   Steer, C
AF Russell, Ginny
   Kelly, Susan E.
   Ford, Tamsin
   Steer, Colin
TI Diagnosis as a social determinant: The development of prosocial
   behaviour before and after an autism spectrum diagnosis
SO SOCIAL SCIENCE & MEDICINE
LA English
DT Article
DE UK; ALSPAC; Autism; ASD; Sociology of diagnosis; Diagnosis; Social
   determinant; Child health; Developmental trajectory; Pervasive
   developmental disorder
ID DIFFICULTIES QUESTIONNAIRE; GENERAL-POPULATION; ASPERGER-SYNDROME;
   DISORDER; CHILDREN; STRENGTHS; INTERVENTIONS; REFLECTIONS; INFORMATION;
   AGGRESSION
AB Jutel and Nettleton (2011) discuss diagnosis as not only a major classification tool for medicine but also an interactive social process that itself may have ramifications for health. Consideration of diagnosis as a social determinant of health outcomes led to the formulation of our research question: Can we detect a change in the development of prosocial symptoms before and after an Autism Spectrum Disorder (ASD) diagnosis? we examined the developmental trajectory of prosocial skills of children, as impairment in social skills is given as a core symptom for children with ASD. We used a validated scale measuring prosocial behaviour for a sample of 57 children where the measure was repeatedly recorded over ten years. We plotted the developmental trajectory of the prosocial trait in this sample who were enrolled in a longitudinal birth cohort study based in South West England. Multi-factorial fixed effect modelling suggests that the developmental trajectory of this measure of behaviour was not significantly altered by ASD diagnosis, or the consequences of diagnosis, either for better or worse. Further analysis was conducted on a subset of 33 of the children who had both pre-diagnosis and post-diagnosis information, and the same result obtained. The results indicate that prosocial behaviours may be resistant to typical 'treatments': provision of educational and specialist health services triggered by a clinical ASD diagnosis. The implications of this for considering diagnosis as a social determinant are discussed. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Russell, Ginny; Ford, Tamsin] Univ Exeter, Peninsula Coll Med & Dent, Inst Hlth Serv Res, Exeter EX2 4SN, Devon, England.
   [Russell, Ginny; Kelly, Susan E.] Univ Exeter, ESRC Ctr Genom Soc Egenis, Exeter EX2 4SN, Devon, England.
   [Steer, Colin] Univ Bristol, Ctr Child & Adolescent Hlth, Bristol BS8 1TH, Avon, England.
RP Russell, G (reprint author), Univ Exeter, Peninsula Coll Med & Dent, Inst Hlth Serv Res, Veysey Bldg,Salmon Pool Lane, Exeter EX2 4SN, Devon, England.
EM g.russell@ex.ac.uk
FU UK Economic and Social Research Council (ESRC); Medical Research Council
   (MRC)
FX We are extremely grateful to all the families who took part in this
   study, the midwives for their help in recruiting them, and the whole
   ALSPAC team. The Medical Research Council, The Wellcome Trust and the
   University of Bristol provide core support for ALSPAC. The work of the
   first author was funded by the UK Economic and Social Research Council
   (ESRC) and Medical Research Council (MRC).
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NR 53
TC 2
Z9 2
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 2012
VL 75
IS 9
BP 1642
EP 1649
DI 10.1016/j.socscimed.2012.06.019
PG 8
WC Public, Environmental & Occupational Health; Social Sciences, Biomedical
SC Public, Environmental & Occupational Health; Biomedical Social Sciences
GA 013IS
UT WOS:000309299700013
PM 22841319
ER

PT J
AU Heinzlmann, A
   Kiss, G
   Toth, ZE
   Dochnal, R
   Pal, A
   Sipos, I
   Manczinger, M
   Szabo, G
   Hashimoto, H
   Koves, K
AF Heinzlmann, Andrea
   Kiss, Gusztav
   Toth, Zsuzsanna E.
   Dochnal, Roberta
   Pal, Agnes
   Sipos, Ildiko
   Manczinger, Mate
   Szabo, Gyula
   Hashimoto, Hitoshi
   Koeves, Katalin
TI Intranasal Application of Secretin, Similarly to Intracerebroventricular
   Administration, Influences the Motor Behavior of Mice Probably Through
   Specific Receptors
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Article
DE Japanese waltzing mouse; Rat; Open field test; Ambulation distance;
   Rearing
ID RAT-BRAIN; NERVOUS-SYSTEM; DEFICIENT MICE; AUTISM; CEREBELLUM;
   EXPRESSION; CHOLECYSTOKININ; TRANSPORT; BINDING; MOUSE
AB Secretin and its receptors show wide distribution in the central nervous system. It was demonstrated previously that intravenous (i.v.) and intracerebroventricular (i.c.v.) application of secretin influenced the behavior of rat, mouse, and human. In our previous experiment, we used a special animal model, Japanese waltzing mice (JWM). These animals run around without stopping (the ambulation distance is very limited) and they do not bother with their environment. The i.c.v. secretin attenuated this hyperactive repetitive movement. In the present work, the effect of i.c.v. and intranasal (i.n.) application of secretin was compared. We have also looked for the presence of secretin receptors in the brain structures related to motor functions. Two micrograms of i.c.v. secretin improved the horizontal movement of JWM, enhancing the ambulation distance. It was nearly threefold higher in treated than in control animals. The i.n. application of secretin to the left nostril once or twice a day or once for 3 days more effectively enhanced the ambulation distance than i.c.v. administration. When secretin was given twice a day for 3 days it had no effect. Secretin did not improve the explorative behavior (the rearing), of JWM. With the use of in situ hybridization, we have found very dense secretin receptor labeling in the cerebellum. In the primary motor cortex and in the striatum, only a few labeled cells were seen. It was supposed that secretin exerted its effect through specific receptors, mainly present in the cerebellum.
C1 [Heinzlmann, Andrea; Koeves, Katalin] Semmelweis Univ, Dept Human Morphol & Dev Biol, Fac Med, H-1094 Budapest, Hungary.
   [Kiss, Gusztav; Dochnal, Roberta; Pal, Agnes; Sipos, Ildiko; Manczinger, Mate; Szabo, Gyula] Albert Szent Gyorgyi Univ, Dept Pathophysiol, Fac Med, Szeged, Hungary.
   [Toth, Zsuzsanna E.] Semmelweis Univ, Neuromorphol & Neuroendocrine Res Lab, Dept Anat Histol & Embryol, H-1094 Budapest, Hungary.
   [Toth, Zsuzsanna E.] Hungarian Acad Sci, Budapest, Hungary.
   [Hashimoto, Hitoshi] Osaka Univ, Lab Med Pharmacol, Grad Sch Pharmaceut Sci, Osaka, Japan.
RP Koves, K (reprint author), Semmelweis Univ, Dept Human Morphol & Dev Biol, Fac Med, Tuzolto U 58, H-1094 Budapest, Hungary.
EM koves.katalin@med.semmelweis-univ.hu
RI Hashimoto, Hitoshi/D-1209-2010
OI Hashimoto, Hitoshi/0000-0001-6548-4016
FU Department of Human Morphology and Developmental Biology, Semmelweis
   University; ETT Grant [355-08]
FX This work was partially supported by the Department of Human Morphology
   and Developmental Biology, Semmelweis University and ETT Grant (355-08)
   to Gyula Szabo. We say thanks to Anna Takacs and Kerti Judit for their
   technical assistance.
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NR 32
TC 2
Z9 2
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD NOV
PY 2012
VL 48
IS 3
BP 558
EP 564
DI 10.1007/s12031-012-9839-9
PG 7
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 008LS
UT WOS:000308959100010
PM 22752505
ER

PT J
AU Morrier, MJ
   Gallagher, PA
AF Morrier, Michael J.
   Gallagher, Peggy A.
TI Racial Disparities in Preschool Special Education Eligibility for Five
   Southern States
SO JOURNAL OF SPECIAL EDUCATION
LA English
DT Article
DE disproportionate representation; preschoolers; diversity; eligibility
ID CROSS-CULTURAL PERSPECTIVES; DISPROPORTIONATE REPRESENTATION;
   MINORITY-STUDENTS; BEHAVIORAL-DISORDERS; AFRICAN-AMERICAN; REFERRAL
   RATES; HEAD-START; DISABILITIES; CHILDREN; ETHNICITY
AB More than 67,000 preschoolers with disabilities across five states were examined for disproportionate special education eligibilities using risk ratios (RRs). Results indicated children classified as American Indian (RR = 2.25) and Black (RR = 1.64) were disproportionate in one state, whereas children classified as Asian, Hispanic, and White showed no disproportionality. Significant differences were found for preschoolers under orthopedic impairment (F = 43.99, p = .002, eta(2) = .971). Child ethnicity was significant for speech or language impairments (F = 3.313, p = .034, eta(2) = .424), mental retardation (F = 65.215, p = .001, eta(2) = .963), multiple disabilities (F = 5.244, p = .048, eta(2) = .636), hearing impairments (F = 4.181, p = .047, eta(2) = .611), other health impairments (F = 24.148, p = .003, eta(2) = .906), autism (F = 48.570, p = .001, eta(2) = .930), and developmental delay (F = 6.407, p = .003, eta(2) = .631).
C1 [Morrier, Michael J.] Emory Univ, Sch Med, Emory Autism Ctr, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA.
   [Gallagher, Peggy A.] Georgia State Univ, Atlanta, GA 30303 USA.
RP Morrier, MJ (reprint author), Emory Univ, Sch Med, Emory Autism Ctr, Dept Psychiat & Behav Sci, 1551 Shoup Court, Atlanta, GA 30322 USA.
EM michae.j.morrier@emory.edu
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NR 76
TC 1
Z9 1
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 2012
VL 46
IS 3
BP 152
EP 169
DI 10.1177/0022466910380465
PG 18
WC Education, Special
SC Education & Educational Research
GA 011CZ
UT WOS:000309142300003
ER

PT J
AU Odluyurt, S
   Tekin-Iftar, E
   Adalioglu, I
AF Odluyurt, Serhat
   Tekin-Iftar, Elif
   Adalioglu, Iclal
TI Does Treatment Integrity Matter in Promoting Learning Among Children
   With Developmental Disabilities?
SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION
LA English
DT Article
DE autistic spectrum disorders; mental retardation; treatment integrity;
   simultaneous prompting; applied behavior analysis
ID SIMULTANEOUS PROMPTING PROCEDURE; INSTRUCTIVE FEEDBACK; COGNITIVE
   IMPAIRMENT; MENTAL-RETARDATION; SCHOOL-STUDENTS; SKILLS; INDIVIDUALS;
   AUTISM; ADULTS; TEACH
AB The purpose of this study was to compare the effects of simultaneous prompting instruction with high and low treatment integrity on the learning of children with developmental disabilities. Low treatment integrity was defined as not delivering a controlling prompt during 30% of the teaching trials. Three preschool children with autism and intellectual disabilities were taught to identify objects and professions in the study. An adapted alternating treatments design was used to compare the effectiveness and efficiency of simultaneous prompting instruction conducted with high versus low treatment integrity. The results showed that both conditions were effective in promoting learning. However, consistent data were not obtained for efficiency measures across children. The results, implications, and future research are discussed.
C1 [Tekin-Iftar, Elif] Anadolu Univ, Engelliler Arastirma Enstitusu, TR-26470 Eskisehir, Turkey.
RP Tekin-Iftar, E (reprint author), Anadolu Univ, Engelliler Arastirma Enstitusu, TR-26470 Eskisehir, Turkey.
EM eltekin@anadolu.edu.tr
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NR 32
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 2012
VL 32
IS 3
BP 143
EP 150
DI 10.1177/0271121410394208
PG 8
WC Education, Special
SC Education & Educational Research
GA 012KY
UT WOS:000309236300002
ER

PT J
AU Hohmann, CF
   Beard, NA
   Kari-Kari, P
   Jarvis, N
   Simmons, Q
AF Hohmann, C. F.
   Beard, N. A.
   Kari-Kari, P.
   Jarvis, N.
   Simmons, Q.
TI Effects of brief stress exposure during early postnatal development in
   Balb/CByJ mice: II. Altered cortical morphology
SO DEVELOPMENTAL PSYCHOBIOLOGY
LA English
DT Article
DE early experience; stress; neocortex; rodent; sex differences
ID PITUITARY-ADRENAL AXIS; LONG-EVANS RATS; MATERNAL-CARE; ENVIRONMENTAL
   ENRICHMENT; GENE-EXPRESSION; INFANT RAT; PROTEIN EXPRESSION; TIME
   WINDOWS; ADULT-RATS; BRAIN
AB Early life experience can significantly determine later mental health status and cognitive function. Neonatal stress, in particular, has been linked to the etiology of mental health disorders as divergent as mood disorder, schizophrenia, and autism. Our study uses a Balb/CByJ mouse model to test the hypothesis, that neonatal stress will alter development and subsequent environmental modulation of neocortex. Using a split litter design, we generated stressed mice (STR) and within litter controls (LMC) along with age-matched, untreated animals (AMC), to serve as across litter controls. Short, daily exposure to a psychosocial/physical stressor, during the first week of life, resulted by adulthood in significant changes in neocortical thickness and architecture, which were further modulated by exposure to behavioral testing. Surprisingly, cortical size in LMC mice was also affected. These observations were compared to the effects of environmental enrichment in the same mouse strain. Our data indicate that LMC and STR males share with environmentally enriched males, an increase in thickness in infra-granular cortical layers, while STR also display a stress selective decrease in supragranular layers, in response to behavioral training as adults. (C) 2012 Wiley Periodicals,Inc. Dev Psychobiol 54: 723735, 2012.
C1 [Hohmann, C. F.; Beard, N. A.; Kari-Kari, P.; Jarvis, N.; Simmons, Q.] Morgan State Univ, Dept Biol, Baltimore, MD 21251 USA.
RP Hohmann, CF (reprint author), Morgan State Univ, Dept Biol, 1700 E Cold Spring Lane, Baltimore, MD 21251 USA.
EM christine.hohmann@morgan.edu
FU  [SO6GM51971];  [R25GM058904]
FX We want to express our appreciation to Dr. D. E. Carlson, Department of
   Surgery, University of Maryland Baltimore, School of Medicine, for
   helping us to establish the radioimmunoassay procedure for CORT
   measurements in our mice. This work was supported by SO6GM51971 to Dr.
   Christine Hohmann and R25GM058904 training support to MSU undergraduate
   students N. Beard and P. Kari-Kari.
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NR 80
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1630
J9 DEV PSYCHOBIOL
JI Dev. Psychobiol.
PD NOV
PY 2012
VL 54
IS 7
BP 723
EP 735
DI 10.1002/dev.21028
PG 13
WC Developmental Biology; Psychology
SC Developmental Biology; Psychology
GA 008CJ
UT WOS:000308934600006
PM 22488100
ER

PT J
AU Akins, MR
   LeBlanc, HF
   Stackpole, EE
   Chyung, E
   Fallon, JR
AF Akins, Michael R.
   LeBlanc, Hannah F.
   Stackpole, Emily E.
   Chyung, Eunice
   Fallon, Justin R.
TI Systematic mapping of fragile X granules in the mouse brain reveals a
   potential role for presynaptic FMRP in sensorimotor functions
SO JOURNAL OF COMPARATIVE NEUROLOGY
LA English
DT Article
DE RNA binding proteins; local translation; axonal protein synthesis
ID MENTAL-RETARDATION PROTEIN; SYNAPTIC PLASTICITY; TERM PLASTICITY;
   OLFACTORY-BULB; MOTOR CORTEX; MODEL; ORGANIZATION; AUTISM; EXPRESSION;
   AXONS
AB Loss of Fragile X mental retardation protein (FMRP) leads to Fragile X syndrome (FXS), the most common form of inherited intellectual disability and autism. Although the functions of FMRP and its homologs FXR1P and FXR2P are well studied in the somatodendritic domain, recent evidence suggests that this family of RNA binding proteins also plays a role in the axonal and presynaptic compartments. Fragile X granules (FXGs) are morphologically and genetically defined structures containing Fragile X proteins that are expressed axonally and presynaptically in a subset of circuits. To further understand the role of presynaptic Fragile X proteins in the brain, we systematically mapped the FXG distribution in the mouse central nervous system. This analysis revealed both the circuits and the neuronal types that express FXGs. FXGs are enriched in circuits that mediate sensory processing and motor planningfunctions that are particularly perturbed in FXS patients. Analysis of FXG expression in the hippocampus suggests that CA3 pyramidal neurons use presynaptic Fragile X proteins to modulate recurrent but not feedforward processing. Neuron-specific FMRP mutants revealed a requirement for neuronal FMRP in the regulation of FXGs. Finally, conditional FMRP ablation demonstrated that FXGs are expressed in axons of thalamic relay nuclei that innervate cortex, but not in axons of thalamic reticular nuclei, striatal nuclei, or cortical neurons that innervate thalamus. Together, these findings support the proposal that dysregulation of axonal and presynaptic Fragile X proteins contribute to the neurological symptoms of FXS. J. Comp. Neurol. 520:36873706, 2012. (C) 2012 Wiley Periodicals, Inc.
C1 [Akins, Michael R.; LeBlanc, Hannah F.; Stackpole, Emily E.; Chyung, Eunice; Fallon, Justin R.] Brown Univ, Dept Neurosci, Providence, RI 02912 USA.
RP Fallon, JR (reprint author), Brown Univ, Dept Neurosci, Box G-LN, Providence, RI 02912 USA.
EM Justin_Fallon@brown.edu
RI Akins, Michael/C-6712-2008
FU NIH [HD052083, MH090237]
FX Grant sponsor: NIH Grants; Grant number: HD052083 (to J.R.F.), MH090237
   (to M.R.A.).
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NR 48
TC 15
Z9 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9967
J9 J COMP NEUROL
JI J. Comp. Neurol.
PD NOV 1
PY 2012
VL 520
IS 16
BP 3687
EP 3706
DI 10.1002/cne.23123
PG 20
WC Neurosciences; Zoology
SC Neurosciences & Neurology; Zoology
GA 000RT
UT WOS:000308406400008
PM 22522693
ER

PT J
AU Hoffman, K
   Kalkbrenner, AE
   Vieira, VM
   Daniels, JL
AF Hoffman, Kate
   Kalkbrenner, Amy E.
   Vieira, Veronica M.
   Daniels, Julie L.
TI The spatial distribution of known predictors of autism spectrum
   disorders impacts geographic variability in prevalence in central North
   Carolina
SO ENVIRONMENTAL HEALTH
LA English
DT Article
DE Autism spectrum disorders (ASD); Intellectual disability (ID); Spatial
   analysis; Disease mapping; Generalized additive models (GAMs);
   Geographic information systems (GIS)
ID HAZARDOUS AIR-POLLUTANTS; RISK-FACTORS; CALIFORNIA; AGE; EPIDEMIOLOGY;
   AREA
AB Background: The causes of autism spectrum disorders (ASD) remain largely unknown and widely debated; however, evidence increasingly points to the importance of environmental exposures. A growing number of studies use geographic variability in ASD prevalence or exposure patterns to investigate the association between environmental factors and ASD. However, differences in the geographic distribution of established risk and predictive factors for ASD, such as maternal education or age, can interfere with investigations of ASD etiology. We evaluated geographic variability in the prevalence of ASD in central North Carolina and the impact of spatial confounding by known risk and predictive factors.
   Methods: Children meeting a standardized case definition for ASD at 8 years of age were identified through records-based surveillance for 8 counties biennially from 2002 to 2008 (n=532). Vital records were used to identify the underlying cohort (15% random sample of children born in the same years as children with an ASD, n=11,034), and to obtain birth addresses. We used generalized additive models (GAMs) to estimate the prevalence of ASD across the region by smoothing latitude and longitude. GAMs, unlike methods used in previous spatial analyses of ASD, allow for extensive adjustment of individual-level risk factors (e.g. maternal age and education) when evaluating spatial variability of disease prevalence.
   Results: Unadjusted maps revealed geographic variation in surveillance-recognized ASD. Children born in certain regions of the study area were up to 1.27 times as likely to be recognized as having ASD compared to children born in the study area as a whole (prevalence ratio (PR) range across the study area 0.57-1.27; global P=0.003). However, geographic gradients of ASD prevalence were attenuated after adjusting for spatial confounders (adjusted PR range 0.72-1.12 across the study area; global P= 0.052).
   Conclusions: In these data, spatial variation of ASD in central NC can be explained largely by factors impacting diagnosis, such as maternal education, emphasizing the importance of adjusting for differences in the geographic distribution of known individual-level predictors in spatial analyses of ASD. These results underscore the critical importance of accounting for such factors in studies of environmental exposures that vary across regions.
C1 [Hoffman, Kate; Kalkbrenner, Amy E.; Daniels, Julie L.] Univ N Carolina, Gillings Sch Global Publ Hlth, Chapel Hill, NC 27599 USA.
   [Kalkbrenner, Amy E.] Univ Wisconsin, Zilber Sch Publ Hlth, Milwaukee, WI 53211 USA.
   [Vieira, Veronica M.] Boston Univ, Sch Publ Hlth, Boston, MA 02118 USA.
   [Vieira, Veronica M.] Univ Calif Irvine, Sch Ecol, Irvine, CA 92617 USA.
RP Hoffman, K (reprint author), Univ N Carolina, Gillings Sch Global Publ Hlth, CB 7435, Chapel Hill, NC 27599 USA.
EM katehoff@email.unc.edu
FU CDC [5-UR3-DD000089-03]; NIEHS [T32ES007018]
FX The Autism and Developmental Disabilities Network is funded by the CDC
   (5-UR3-DD000089-03). Kate Hoffman was funded by NIEHS T32ES007018. We
   gratefully acknowledge Amy Herring for her statistical advice in
   conceptualizing this research. The findings and conclusions in this
   report are those of the authors and do not necessarily represent the
   official position of the Centers for Disease Control and Prevention or
   the National Institute of Environmental Health Sciences.
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NR 39
TC 6
Z9 6
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-069X
J9 ENVIRON HEALTH-GLOB
JI Environ. Health
PD OCT 31
PY 2012
VL 11
AR 80
DI 10.1186/1476-069X-11-80
PG 10
WC Environmental Sciences; Public, Environmental & Occupational Health
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health
GA 040HK
UT WOS:000311313100001
PM 23113973
ER

PT J
AU Coughlin, CR
   Scharer, GH
   Shaikh, TH
AF Coughlin, Curtis R., III
   Scharer, Gunter H.
   Shaikh, Tamim H.
TI Clinical impact of copy number variation analysis using high-resolution
   microarray technologies: advantages, limitations and concerns
SO GENOME MEDICINE
LA English
DT Review
DE Comparative genomic hybridization; CGH; copy number variation; CNV;
   genetic counseling; microarray; single nucleotide polymorphism; SNP
ID COMPARATIVE GENOMIC HYBRIDIZATION; DEPENDENT PROBE AMPLIFICATION;
   ARRAY-CGH ANALYSIS; MULTIPLE CONGENITAL-ANOMALIES; ABNORMAL ULTRASOUND
   FINDINGS; AUTISM SPECTRUM DISORDERS; DOMINANT ROBINOW-SYNDROME;
   LOW-LEVEL MOSAICISM; MENTAL-RETARDATION; STRUCTURAL VARIATION
AB Copy number variation (CNV) analysis has had a major impact on the field of medical genetics, providing a mechanism to identify disease-causing genomic alterations in an unprecedented number of diseases and phenotypes. CNV analysis is now routinely used in the clinical diagnostic laboratory, and has led to a significant increase in the detection of chromosomal abnormalities. These findings are used for prenatal decision making, clinical management and genetic counseling. Although a powerful tool to identify genomic alterations, CNV analysis may also result in the detection of genomic alterations that have unknown clinical significance or reveal unintended information. This highlights the importance of informed consent and genetic counseling for clinical CNV analysis. This review examines the advantages and limitations of CNV discovery in the clinical diagnostic laboratory, as well as the impact on the clinician and family.
C1 [Coughlin, Curtis R., III; Scharer, Gunter H.; Shaikh, Tamim H.] Univ Colorado Denver, Sect Clin Genet & Metab, Dept Pediat, Aurora, CO 80045 USA.
   [Scharer, Gunter H.; Shaikh, Tamim H.] Univ Colorado Denver, Intellectual & Dev Disabil Res Ctr, Aurora, CO 80045 USA.
RP Shaikh, TH (reprint author), Univ Colorado Denver, Sect Clin Genet & Metab, Dept Pediat, Aurora, CO 80045 USA.
EM Tamim.Shaikh@ucdenver.edu
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NR 153
TC 4
Z9 4
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1756-994X
J9 GENOME MED
JI Genome Med.
PD OCT 30
PY 2012
VL 4
AR 80
DI 10.1186/gm381
PG 12
WC Genetics & Heredity
SC Genetics & Heredity
GA 084YW
UT WOS:000314578400003
PM 23114084
ER

PT J
AU Dadds, MR
   Cauchi, AJ
   Wimalaweera, S
   Hawes, DJ
   Brennan, J
AF Dadds, Mark Richard
   Cauchi, Avril Jessica
   Wimalaweera, Subodha
   Hawes, David John
   Brennan, John
TI Outcomes, moderators, and mediators of empathic-emotion recognition
   training for complex conduct problems in childhood
SO PSYCHIATRY RESEARCH
LA English
DT Article
DE Emotion recognition; Child psychopathology; Conduct problems; Randomized
   controlled trial; Callous-unemotional traits; Trans-diagnostic models
ID CALLOUS-UNEMOTIONAL TRAITS; DISRUPTIVE BEHAVIOR DISORDERS; PSYCHOPATHIC
   TRAITS; SOCIAL INFORMATION; CHILDREN; DEFICITS; AUTISM; AMYGDALA; FACES;
   DIMENSIONS
AB Impairments in emotion recognition skills are a trans-diagnostic indicator of early mental health problems and may be responsive to intervention. We report on a randomized controlled trial of "Emotion-recognition-training" (ERT) versus treatment-as-usual (TAU) with N=195 mixed diagnostic children (mean age 10.52 years) referred for behavioral/emotional problems measured at pre- and 6 months post-treatment. We tested overall outcomes plus moderation and mediation models, whereby diagnostic profile was tested as a moderator of change. ERT had no impact on the group as a whole. Diagnostic status of the child did not moderate outcomes: however, levels of callous-unemotional (CU) traits moderated outcomes such that children with high CU traits responded less well to TAU, while ERT produced significant improvements in affective empathy and conduct problems in these children. Emotion recognition training has potential as an adjunctive intervention specifically for clinically referred children with high CU traits, regardless of their diagnostic status. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
C1 [Dadds, Mark Richard; Cauchi, Avril Jessica; Wimalaweera, Subodha] Univ New S Wales, Sch Psychol, Sydney, NSW, Australia.
   [Hawes, David John] Univ Sydney, Sch Psychol, Sydney, NSW 2006, Australia.
   [Brennan, John] Univ New S Wales, Sch Psychiat, Sydney, NSW, Australia.
RP Dadds, MR (reprint author), Univ New S Wales, Sch Psychol, Sydney, NSW, Australia.
EM m.dadds@unsw.edu.au
FU Australian Research Council
FX Funding was received as a Linkage Grant from the Australian Research
   Council. The authors wish to thank Royal Far West, especially Jann
   Kingston and Jane Less lie, and the participating families, for their
   support.
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NR 52
TC 22
Z9 22
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0165-1781
J9 PSYCHIAT RES
JI Psychiatry Res.
PD OCT 30
PY 2012
VL 199
IS 3
BP 201
EP 207
DI 10.1016/j.psychres.2012.04.033
PG 7
WC Psychiatry
SC Psychiatry
GA 058IR
UT WOS:000312627800009
PM 22703720
ER

PT J
AU Whitehouse, AJO
   Mattes, E
   Maybery, MT
   Dissanayake, C
   Sawyer, M
   Jones, RM
   Pennell, CE
   Keelan, JA
   Hickey, M
AF Whitehouse, Andrew J. O.
   Mattes, Eugen
   Maybery, Murray T.
   Dissanayake, Cheryl
   Sawyer, Michael
   Jones, Rachel M.
   Pennell, Craig E.
   Keelan, Jeffrey A.
   Hickey, Martha
TI Perinatal testosterone exposure and autistic-like traits in the general
   population: a longitudinal pregnancy-cohort study
SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Testosterone; Prenatal; Perinatal; Autistic-like traits
ID SPECTRUM QUOTIENT AQ; ANDROGEN RECEPTOR GENE; 4TH DIGIT RATIO; FETAL
   TESTOSTERONE; STEROID-HORMONES; CAG REPEAT; DISORDERS; SERUM; SEX;
   CHILDREN
AB Background: Increased prenatal testosterone exposure has been hypothesized as a mechanism underlying autism spectrum disorders (ASD). However, no studies have prospectively measured prenatal testosterone exposure and ASD. The current study sought to determine whether testosterone concentrations in umbilical cord blood are associated with a clinical diagnosis of ASD in a small number of children and with autistic-like traits in the general population.
   Methods: Umbilical cord blood was collected from 707 children. Samples were analyzed for total (TT) and bioavailable (BioT) testosterone concentrations. Parent report indicated that five individuals had a clinical diagnosis of ASD. Those participants without a diagnosis were approached in early adulthood to complete the Autism-Spectrum Quotient (AQ), a self-report measure of autistic-like traits, with 184 males (M = 20.10 years; SD= 0.65 years) and 190 females (M = 19.92 years; SD=0.68 years) providing data.
   Results: The BioT and TT concentrations of the five children diagnosed with ASD were within one standard-deviation of the sex-specific means. Spearman's rank-order coefficients revealed no significant correlations between TT levels and scores on any AQ scale among males (rho range: -.01 to .06) or females (rho value range: -.07 to .01). There was also no significant association between BioT or TT concentrations and AQ scores among males (rho value range: -.07 to .08) or females (rho value range: -.06 to .12). Males were more likely than females to have 'high' scores (upper decile) on the AQ scale relating pattern and detail processing. However, the likelihood of a high score on this scale was unrelated to BioT and TT concentrations in both males and females.
   Conclusions: These findings indicate that testosterone concentrations from umbilical cord blood are unrelated to autistic-like traits in the general population. However, the findings do not exclude an association between testosterone exposure in early intrauterine life and ASD.
C1 [Whitehouse, Andrew J. O.; Mattes, Eugen; Jones, Rachel M.] Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, Subiaco, WA 6008, Australia.
   [Maybery, Murray T.] Univ Western Australia, Sch Psychol, Crawley, WA 6009, Australia.
   [Dissanayake, Cheryl] La Trobe Univ, Sch Psychol Sci, Melbourne, Vic 3086, Australia.
   [Sawyer, Michael] Univ Adelaide, Discipline Paediat, Adelaide, SA 5005, Australia.
   [Pennell, Craig E.; Keelan, Jeffrey A.] Univ Western Australia, Sch Womens & Infants Hlth, Crawley, WA 6009, Australia.
   [Hickey, Martha] Univ Melbourne, Royal Womens Hosp, Dept Obstet & Gynaecol, Parkville, Vic 3052, Australia.
RP Whitehouse, AJO (reprint author), Univ Western Australia, Ctr Child Hlth Res, Telethon Inst Child Hlth Res, 100 Roberts Rd, Subiaco, WA 6008, Australia.
EM awhitehouse@ichr.uwa.edu.au
RI Keelan, Jeffrey/G-2170-2011; Maybery, Murray/H-5390-2014
OI Keelan, Jeffrey/0000-0002-5403-6266; 
FU national Health and Medical Research Council (NHMRC); University of
   Western Australia (UWA); Curtin University; UWA Faculty of Medicine,
   Dentistry and Health Sciences; Raine Medical Research Foundation;
   Telethon Institute for Child Health Research; Women's and Infants
   Research Foundation; NHMRC [1003424, 1004065]; Australian Rotary Health;
   Women and Infants' Research Foundation
FX Core Management of the Raine Study has been funded by the national
   Health and Medical Research Council (NHMRC), University of Western
   Australia (UWA), Curtin University, the UWA Faculty of Medicine,
   Dentistry and Health Sciences, the Raine Medical Research Foundation,
   the Telethon Institute for Child Health Research, and the Women's and
   Infants Research Foundation. This study was funded by the NHMRC (#
   1003424) and Australian Rotary Health. AJOW (# 1004065) and MH are
   funded by Career Development Fellowships from the NHMRC; JAK is funded
   by the Women and Infants' Research Foundation. These funders had no
   further role in study design; in the collection, analysis and
   interpretation of data; in the writing of the report; and in the
   decision to submit the paper for publication. The authors are extremely
   grateful to all of the families who took part in this study and the
   whole Raine Study team, which includes the Cohort Manager, Data Manager
   and data collection team.
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NR 48
TC 3
Z9 3
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1866-1947
J9 J NEURODEV DISORD
JI J. Neurodev. Disord.
PD OCT 30
PY 2012
VL 4
AR 25
DI 10.1186/1866-1955-4-25
PG 12
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 047FY
UT WOS:000311825200001
PM 23110806
ER

PT J
AU Anderson, GR
   Galfin, T
   Xu, W
   Aoto, J
   Malenka, RC
   Sudhof, TC
AF Anderson, Garret R.
   Galfin, Timothy
   Xu, Wei
   Aoto, Jason
   Malenka, Robert C.
   Suedhof, Thomas C.
TI Candidate autism gene screen identifies critical role for cell-adhesion
   molecule CASPR2 in dendritic arborization and spine development
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE dendrite; synaptogenesis
ID LA-TOURETTE-SYNDROME; MYELINATED AXONS; SPECTRUM DISORDERS; CNTNAP2
   GENE; NEUREXIN IV; LANGUAGE DISORDERS; K+ CHANNELS; DE-NOVO; CONTACTIN;
   RECEPTOR
AB Mutations in the contactin-associated protein 2 (CNTNAP2) gene encoding CASPR2, a neurexin-related cell-adhesion molecule, predispose to autism, but the function of CASPR2 in neural circuit assembly remains largely unknown. In a knockdown survey of autism candidate genes, we found that CASPR2 is required for normal development of neural networks. RNAi-mediated knockdown of CASPR2 produced a cell-autonomous decrease in dendritic arborization and spine development in pyramidal neurons, leading to a global decline in excitatory and inhibitory synapse numbers and a decrease in synaptic transmission without a detectable change in the properties of these synapses. Our data suggest that in addition to the previously described role of CASPR2 in mature neurons, where CASPR2 organizes nodal microdomains of myelinated axons, CASPR2 performs an earlier organizational function in developing neurons that is essential for neural circuit assembly and operates coincident with the time of autism spectrum disorder (ASD) pathogenesis.
C1 [Anderson, Garret R.; Galfin, Timothy; Xu, Wei; Aoto, Jason; Suedhof, Thomas C.] Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA.
   [Anderson, Garret R.; Galfin, Timothy; Malenka, Robert C.] Stanford Univ, Sch Med, Nancy Pritzker Lab, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA.
   [Xu, Wei; Suedhof, Thomas C.] Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA.
RP Sudhof, TC (reprint author), Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA.
EM tcs1@stanford.edu
FU National Institute of Mental Health [MH052804, MH089054]; National
   Institute of Neurological Disorders and Stroke [R01 NS077906]; National
   Institutes of Health [2T32 NS007280-26A1]; Autism Speaks Translational
   Postdoctoral Fellowship [7953]; American Heart Association Award
   [11POST7360078]
FX This study was supported by National Institute of Mental Health Grants
   MH052804 and MH089054 and National Institute of Neurological Disorders
   and Stroke Grant R01 NS077906. G.R.A. is supported by National
   Institutes of Health Training Grant 2T32 NS007280-26A1 and Autism Speaks
   Translational Postdoctoral Fellowship Grant 7953. J.A. is supported by
   American Heart Association Award 11POST7360078.
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NR 45
TC 25
Z9 25
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 30
PY 2012
VL 109
IS 44
BP 18120
EP 18125
DI 10.1073/pnas.1216398109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038BJ
UT WOS:000311149900087
PM 23074245
ER

PT J
AU Iwata, K
   Izumo, N
   Matsuzaki, H
   Manabe, T
   Ishibashi, Y
   Ichitani, Y
   Yamada, K
   Thanseem, I
   Anitha, A
   Vasu, MM
   Shimmura, C
   Wakuda, T
   Kameno, Y
   Takahashi, T
   Iwata, Y
   Suzuki, K
   Nakamura, K
   Mori, N
AF Iwata, Keiko
   Izumo, Nobuo
   Matsuzaki, Hideo
   Manabe, Takayuki
   Ishibashi, Yukiko
   Ichitani, Yukio
   Yamada, Kazuo
   Thanseem, Ismail
   Anitha, Ayyappan
   Vasu, Mahesh Mundalil
   Shimmura, Chie
   Wakuda, Tomoyasu
   Kameno, Yosuke
   takahashi, Taro
   Iwata, Yasuhide
   Suzuki, Katsuaki
   Nakamura, Kazuhiko
   Mori, Norio
TI Vldlr overexpression causes hyperactivity in rats
SO MOLECULAR AUTISM
LA English
DT Article
DE Hyperactivity; Neurodevelopmental disorder; Psychiatric disorder;
   Reelin; Transgenic rat; Vldlr
ID HETEROZYGOUS REELER MOUSE; DENSITY LIPOPROTEIN RECEPTOR; CAJAL-RETZIUS
   NEURONS; LOCOMOTOR-ACTIVITY; SYNAPTIC PLASTICITY; NUCLEUS-ACCUMBENS;
   BIPOLAR DISORDER; TYROSINE PHOSPHORYLATION; EXTRACELLULAR-MATRIX;
   BEHAVIORAL-PHENOTYPE
AB Background: Reelin regulates neuronal positioning in cortical brain structures and neuronal migration via binding to the lipoprotein receptors Vldlr and Lrp8. Reeler mutant mice display severe brain morphological defects and behavioral abnormalities. Several reports have implicated reelin signaling in the etiology of neurodevelopmental and psychiatric disorders, including autism, schizophrenia, bipolar disorder, and depression. Moreover, it has been reported that VLDLR mRNA levels are increased in the post-mortem brain of autistic patients.
   Methods: We generated transgenic (Tg) rats overexpressing Vldlr, and examined their histological and behavioral features.
   Results: Spontaneous locomotor activity was significantly increased in Tg rats, without detectable changes in brain histology. Additionally, Tg rats tended to show performance deficits in the radial maze task, suggesting that their spatial working memory was slightly impaired. Thus, Vldlr levels may be involved in determining locomotor activity and memory function.
   Conclusions: Unlike reeler mice, patients with neurodevelopmental or psychiatric disorders do not show striking neuroanatomical aberrations. Therefore, it is notable, from a clinical point of view, that we observed behavioral phenotypes in Vldlr-Tg rats in the absence of neuroanatomical abnormalities.
C1 [Iwata, Keiko; Matsuzaki, Hideo; Anitha, Ayyappan; takahashi, Taro; Suzuki, Katsuaki] Hamamatsu Univ, Sch Med, Res Ctr Child Mental Dev, Hamamatsu, Shizuoka, Japan.
   [Izumo, Nobuo] Yokohama Coll Pharm, Dept Clin Pharmacol, Yokohama, Kanagawa, Japan.
   [Manabe, Takayuki] Fujita Hlth Univ, Inst Comprehens Med Sci, Div Gene Express Mech, Toyoake, Aichi, Japan.
   [Ishibashi, Yukiko] Yokohama Coll Pharm, Dept Synthet Organ Chem, Yokohama, Kanagawa, Japan.
   [Ichitani, Yukio; Yamada, Kazuo] Univ Tsukuba, Inst Psychol & Behav Neurosci, Tsukuba, Ibaraki, Japan.
   [Thanseem, Ismail; Vasu, Mahesh Mundalil; Shimmura, Chie; Wakuda, Tomoyasu; Kameno, Yosuke; Iwata, Yasuhide; Nakamura, Kazuhiko; Mori, Norio] Hamamatsu Univ, Sch Med, Dept Psychiat, Hamamatsu, Shizuoka, Japan.
RP Matsuzaki, H (reprint author), Hamamatsu Univ, Sch Med, Res Ctr Child Mental Dev, Hamamatsu, Shizuoka, Japan.
EM matsu@hama-med.ac.jp
FU Ministry of Education, Culture, Sports, Science, and Technology of Japan
FX We thank Tae Takahashi, Mika Oyaizu and Erina Sakamoto for excellent
   technical assistance. This study was supported by a Grant-in-Aid for
   Scientific Research (B) from the Ministry of Education, Culture, Sports,
   Science, and Technology of Japan (to NM), and a Grant-in-Aid for Young
   Scientists (B) from the Ministry of Education, Culture, Sports, Science,
   and Technology of Japan (to KI).
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NR 48
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 30
PY 2012
VL 3
AR 11
DI 10.1186/2040-2392-3-11
PG 9
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254TD
UT WOS:000327189000001
PM 23110844
ER

PT J
AU Gavrilov, Y
   Rotem, S
   Ofek, R
   Geva, R
AF Gavrilov, Yana
   Rotem, Sarit
   Ofek, Renana
   Geva, Ronny
TI Socio-cultural effects on children's initiation of joint attention
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE joint attention; cross-cultural differences; tradition; gender; affect;
   play; exploration; social
ID INDIVIDUAL-DIFFERENCES; YOUNG-CHILDREN; FOLLOW GAZE; INFANT; AUTISM;
   MODEL; PARTICIPATION; MATURATION; INFERENCES; COGNITION
AB Exchanging gazes with a social partner in response to an event in the environment is considered an effective means to direct attention, share affective experiences, and highlight a target in the environment. This behavior appears during infancy and plays an important role in children's learning and in shaping their socio-emotional development. It has been suggested that cultural values of the community affect socio-emotional development through attentional dynamics of social reference (Rogoff et al., 1993). Maturational processes of brain-circuits have been found to mediate socio-cultural learning and the behavioral manifestation of cultural norms starting at preschool age (Nelson and Guyer, 2011). The aim of the current study was to investigate the relations between cultural ecology levels and children's joint attention (JA). Initiation of JA bids was studied empirically as a function of the level of social load of the target toy (3 levels), the community level of adherence to traditional values (3 levels), parental education (2 levels), and gender. Sixty-two kindergarten aged children were enrolled in a structured toy-exploration task, during which they were presented with toys of various social loads, with social agents (i.e., mother and experimenter) present nearby, and non-social distracters presented intermittently. Measurements included the child's number of JA bids and the extent of positive affect. Analysis of variance indicated that the child's initiation of JA toward the social partner was affected by all levels of cultural ecology (i.e., toy's social load, adherence to tradition values, parental education, gender), thus supporting the study's hypotheses. The effects were such that overall, children, particularly girls' JA initiation was augmented in social toys and moderated by the socio-cultural variables. These results suggest that cultural ecology is related to children's JA, thereby scaffolding initiation of social sharing cues between children and adults. JA plays a role in adjusting children's internal representations of their respective ecological environment.
C1 [Gavrilov, Yana; Rotem, Sarit; Ofek, Renana; Geva, Ronny] Bar Ilan Univ, Dept Psychol, Dev Neuropsychol Lab, Gonda Multidisciplinary Brain Res Ctr, IL-52900 Ramat Gan, Israel.
RP Geva, R (reprint author), Bar Ilan Univ, Dept Psychol, Dev Neuropsychol Lab, Gonda Multidisciplinary Brain Res Ctr, IL-52900 Ramat Gan, Israel.
EM ronny.geva@biu.ac.il
FU Israel Science Foundation [1518-2007]
FX The authors thank the participating families for their cooperation and
   gratefully acknowledge Ms. Jessica Schreiber for her editorial input.
   This research was funded by The Israel Science Foundation grant
   #1518-2007 awarded to Ronny Geva.
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NR 81
TC 2
Z9 2
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 25
PY 2012
VL 6
AR 286
DI 10.3389/fnhum.2012.00286
PG 10
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 025RP
UT WOS:000310210500001
PM 23112768
ER

PT J
AU Arons, MH
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AF Arons, Magali H.
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   Li, Dong
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TI Autism-Associated Mutations in ProSAP2/Shank3 Impair Synaptic
   Transmission and Neurexin-Neuroligin-Mediated Transsynaptic Signaling
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID DENDRITIC SPINE MORPHOLOGY; POSTSYNAPTIC DENSITY; SPECTRUM DISORDER;
   MOLECULAR-MECHANISMS; MENTAL-RETARDATION; CELL-ADHESION; ACTIVE ZONE;
   PROTEIN; GLUTAMATE; SHANK3
AB Mutations in several postsynaptic proteins have recently been implicated in the molecular pathogenesis of autism and autism spectrum disorders (ASDs), including Neuroligins, Neurexins, and members of the ProSAP/Shank family, thereby suggesting that these genetic forms of autism may share common synaptic mechanisms. Initial studies of ASD-associated mutations in ProSAP2/Shank3 support a role for this protein in glutamate receptor function and spine morphology, but these synaptic phenotypes are not universally penetrant, indicating that other core facets of ProSAP2/Shank3 function must underlie synaptic deficits in patients with ASDs. In the present study, we have examined whether the ability of ProSAP2/Shank3 to interact with the cytoplasmic tail of Neuroligins functions to coordinate pre/postsynaptic signaling through the Neurexin-Neuroligin signaling complex in hippocampal neurons of Rattus norvegicus. Indeed, we find that synaptic levels of ProSAP2/Shank3 regulate AMPA and NMDA receptor-mediated synaptic transmission and induce widespread changes in the levels of presynaptic and postsynaptic proteins via Neurexin-Neuroligin transsynaptic signaling. ASD-associated mutations in ProSAP2/Shank3 disrupt not only postsynaptic AMPA and NMDA receptor signaling but also interfere with the ability of ProSAP2/Shank3 to signal across the synapse to alter presynaptic structure and function. These data indicate that ASD-associated mutations in a subset of synaptic proteins may target core cellular pathways that coordinate the functional matching and maturation of excitatory synapses in the CNS.
C1 [Garner, Craig C.] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Palo Alto, CA 94304 USA.
   [Thynne, Charlotte J.; Li, Dong; Cheyne, Juliette E.; Montgomery, Johanna M.] Univ Auckland, Dept Physiol, Auckland 1142, New Zealand.
   [Grabrucker, Andreas M.; Schoen, Michael; Boeckers, Tobias M.] Univ Ulm, Inst Anat & Cell Biol, D-89081 Ulm, Germany.
   Univ Ulm, Dept Neurol, D-89081 Ulm, Germany.
RP Garner, CC (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, 1201 Welch Rd, Palo Alto, CA 94304 USA.
EM cgarner@stanford.edu
FU National Institute of Neurological Disorders and Stroke; National
   Research Service Award [5F31NS066786-025]; German Research Foundation;
   National Institutes of Health [P01 NS053862, R21 MH091471]; United
   States Israel Binational Science Foundation Grant [2007425];
   Neurological Foundation of New Zealand; Auckland Medical Research
   Foundation
FX This work was supported by National Institute of Neurological Disorders
   and Stroke National Research Service Award Fellowship Grant
   5F31NS066786-025 (M.H.A.), a fellowship from the German Research
   Foundation (A.M.G.), National Institutes of Health Grants P01 NS053862
   and R21 MH091471 (C.C.G.), United States Israel Binational Science
   Foundation Grant 2007425 (C.C.G.), and the Neurological Foundation of
   New Zealand and the Auckland Medical Research Foundation (C.J.T., D.L.
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NR 71
TC 29
Z9 30
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 24
PY 2012
VL 32
IS 43
BP 14966
EP 14978
DI 10.1523/JNEUROSCI.2215-12.2012
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 029VD
UT WOS:000310523900013
PM 23100419
ER

PT J
AU Kos, M
   van den Brink, D
   Snijders, TM
   Rijpkema, M
   Franke, B
   Fernandez, G
   Hagoort, P
AF Kos, Miriam
   van den Brink, Danielle
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   Rijpkema, Mark
   Franke, Barbara
   Fernandez, Guillen
   Hagoort, Peter
TI CNTNAP2 and Language Processing in Healthy Individuals as Measured with
   ERPs
SO PLOS ONE
LA English
DT Article
ID STRUCTURAL BRAIN ABNORMALITIES; SENTENCE COMPREHENSION; INHERITED
   SPEECH; FOXP2 GENE; POTENTIALS; DISORDER; AUTISM; N400; ASSOCIATION;
   INTEGRATION
AB The genetic FOXP2-CNTNAP2 pathway has been shown to be involved in the language capacity. We investigated whether a common variant of CNTNAP2 (rs7794745) is relevant for syntactic and semantic processing in the general population by using a visual sentence processing paradigm while recording ERPs in 49 healthy adults. While both AA homozygotes and T-carriers showed a standard N400 effect to semantic anomalies, the response to subject-verb agreement violations differed across genotype groups. T-carriers displayed an anterior negativity preceding the P600 effect, whereas for the AA group only a P600 effect was observed. These results provide another piece of evidence that the neuronal architecture of the human faculty of language is shaped differently by effects that are genetically determined.
C1 [Kos, Miriam; van den Brink, Danielle; Snijders, Tineke M.; Rijpkema, Mark; Franke, Barbara; Fernandez, Guillen; Hagoort, Peter] Radboud Univ Nijmegen, Donders Inst Brain, NL-6525 ED Nijmegen, Netherlands.
   [van den Brink, Danielle] Radboud Univ Nijmegen, Inst Behav Sci, NL-6525 ED Nijmegen, Netherlands.
   [Snijders, Tineke M.] Univ Utrecht, Helmholtz Inst, Dept Expt Psychol, Utrecht, Netherlands.
   [Snijders, Tineke M.] Univ Med Ctr Utrecht, Rudolf Magnus Inst Neuroscience, Dept Child & Adolescent Psychiat, Utrecht, Netherlands.
   [Franke, Barbara] Radboud Univ Nijmegen, Med Ctr, Dept Genet, NL-6525 ED Nijmegen, Netherlands.
   [Franke, Barbara] Radboud Univ Nijmegen, Med Ctr, Dept Psychiat, NL-6525 ED Nijmegen, Netherlands.
   [Fernandez, Guillen] Radboud Univ Nijmegen, Med Ctr, Dept Cognit Neurosci, NL-6525 ED Nijmegen, Netherlands.
   [Hagoort, Peter] Max Planck Inst Psycholinguist, Nijmegen, Netherlands.
RP Kos, M (reprint author), Radboud Univ Nijmegen, Donders Inst Brain, NL-6525 ED Nijmegen, Netherlands.
EM m.kos@donders.ru.nl; p.hagoort@donders.ru.nl
RI Rijpkema, Mark/D-1974-2010; Snijders, Tineke/A-3431-2013; Hagoort,
   Peter/B-7417-2012; Franke, Barbara/D-4836-2009; van den Brink,
   Danielle/D-6485-2012; Fernandez, Guillen/B-3771-2009
OI Snijders, Tineke/0000-0002-2442-0451; Franke,
   Barbara/0000-0003-4375-6572; Fernandez, Guillen/0000-0002-5522-0604
FU SPINOZA prize from the Netherlands Organization for Scientific Research
   (NWO)
FX This research was supported by a SPINOZA prize from the Netherlands
   Organization for Scientific Research (NWO) to Peter Hagoort. 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 61
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 24
PY 2012
VL 7
IS 10
AR e46995
DI 10.1371/journal.pone.0046995
PG 8
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 026VC
UT WOS:000310310200022
PM 23115634
ER

PT J
AU Li, SY
   Wang, YN
   Xu, PF
   Pu, F
   Li, DY
   Fan, YB
   Gong, GL
   Luo, YJ
AF Li, Shuyu
   Wang, Yanan
   Xu, Pengfei
   Pu, Fang
   Li, Deyu
   Fan, Yubo
   Gong, Gaolang
   Luo, Yuejia
TI Surface Morphology of Amygdala Is Associated with Trait Anxiety
SO PLOS ONE
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; FUNCTIONAL CONNECTIVITY; SHAPE-ANALYSIS;
   HIPPOCAMPUS; DEPRESSION; FEAR; MODULATION; CHILDREN; NETWORK;
   VARIABILITY
AB Previous neuroimaging studies have suggested a role of amygdala in trait anxiety level, in which amygdala was typically treated as a whole. To date, it remains unknown whether the morphology of specific subregions of amygdala are associated with trait anxiety. Here, we employed a shape analysis approach to locate the association between its morphology and trait anxiety on the surface of amygdala. 24 healthy young participants were included. The boundary of amygdala for each subject was first manually outlined using high-resolution magnetic resonance (MR) image, followed by 3D surface reconstruction and parameterization using spherical harmonic description. Two point-wise metrics, direct displacement between the individual surface and atlas surface and its normal projection, were used to quantify the surface morphology of amygdala. Statistical analysis revealed significant correlations between the two surface metrics and trait anxiety levels, which were located around the lateral and central nucleus of right amygdala. Our results provided localized information for the association between amygdala and trait anxiety, and suggested a central role of the lateral and central nucleus of right amygdala on trait anxiety.
C1 [Xu, Pengfei; Gong, Gaolang; Luo, Yuejia] Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
   [Li, Shuyu] Beihang Univ, Sch Biol Sci & Med Engn, State Key Lab Software Dev Environm, Beijing, Peoples R China.
   [Li, Shuyu; Wang, Yanan; Pu, Fang; Li, Deyu; Fan, Yubo] Beihang Univ, Sch Biol Sci & Med Engn, Minist Educ, Key Lab Biomech & Mechanobiol, Beijing, Peoples R China.
RP Gong, GL (reprint author), Beijing Normal Univ, State Key Lab Cognit Neurosci & Learning, Beijing 100875, Peoples R China.
EM gaolang.gong@bnu.edu.cn; luoyj@bnu.edu.cn
FU National Science Foundation of China [81171403, 81071212, 30700182,
   31000499, 91132704]; 973 program [2013CB837300]; State Key Laboratory of
   Software Development Environment [SKLSDE-2011ZX-10]; Global Research
   Initiative Program, NIH [1R01TW007897]
FX This work was supported by the National Science Foundation of China
   (81171403, 81071212, 30700182, 31000499, and 91132704), the 973 program
   (2013CB837300), State Key Laboratory of Software Development Environment
   (SKLSDE-2011ZX-10), and Global Research Initiative Program, NIH
   (1R01TW007897).
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NR 51
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 2012
VL 7
IS 10
AR e47817
DI 10.1371/journal.pone.0047817
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 026VC
UT WOS:000310310200086
PM 23112851
ER

PT J
AU Avinun, R
   Ebstein, RP
   Knafo, A
AF Avinun, Reut
   Ebstein, Richard P.
   Knafo, Ariel
TI Human maternal behaviour is associated with arginine vasopressin
   receptor 1A gene
SO BIOLOGY LETTERS
LA English
DT Article
DE arginine vasopressin receptor 1A; maternal behaviour; control; warmth;
   structuring
ID OXYTOCIN; QUALITY
AB Parenting is one of the main influences on children's early development, and yet its underlying genetic mechanisms have only recently begun to be explored, with many studies neglecting to control for possible child effects. This study focuses on maternal behaviour and on an allele at the RS3 promoter region of the arginine vasopressin receptor 1A (AVPR1A) gene, previously associated with autism and with higher amygdala activation in a face-matching task. Mothers were observed during a free-play session with each of their 3.5-year-old twins. Multilevel regression analyses revealed that mothers who are carriers of the AVPR1A RS3 allele tend to show less structuring and support throughout the interaction independent of the child's sex and RS3 genotype. This finding advances our understanding of the genetic influences on human maternal behaviour.
C1 [Avinun, Reut; Knafo, Ariel] Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel.
   [Ebstein, Richard P.] Natl Univ Singapore, Dept Psychol, Singapore 117570, Singapore.
RP Knafo, A (reprint author), Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel.
EM msarielk@huji.ac.il
RI Knafo, Ariel/E-8067-2011
FU European Research Council [240994]
FX This study was supported by a European Research Council Starting grant
   (no. 240994) to A.K.
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NR 21
TC 6
Z9 6
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 1744-9561
J9 BIOL LETTERS
JI Biol. Lett.
PD OCT 23
PY 2012
VL 8
IS 5
BP 894
EP 896
DI 10.1098/rsbl.2012.0492
PG 3
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
   Ecology; Evolutionary Biology
GA 005ZP
UT WOS:000308789200056
PM 22764113
ER

PT J
AU Goodbourn, PT
   Bosten, JM
   Hogg, RE
   Bargary, G
   Lawrance-Owen, AJ
   Mollon, JD
AF Goodbourn, Patrick T.
   Bosten, Jenny M.
   Hogg, Ruth E.
   Bargary, Gary
   Lawrance-Owen, Adam J.
   Mollon, J. D.
TI Do different 'magnocellular tasks' probe the same neural substrate?
SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
LA English
DT Article
DE magnocellular; dorsal stream; psychophysics; vision; hearing; individual
   differences
ID AUTISM-SPECTRUM CONDITIONS; CONTRAST SENSITIVITY; MOTION COHERENCE;
   DEVELOPMENTAL DYSLEXIA; INDIVIDUAL-DIFFERENCES; VISUAL FUNCTIONS;
   PERCEPTION; PATHWAYS; CHILDREN; DEFICIT
AB The sensory abnormalities associated with disorders such as dyslexia, autism and schizophrenia have often been attributed to a generalized deficit in the visual magnocellular-dorsal stream and its auditory homologue. To probe magnocellular function, various psychophysical tasks are often employed that require the processing of rapidly changing stimuli. But is performance on these several tasks supported by a common substrate? To answer this question, we tested a cohort of 1060 individuals on four 'magnocellular tasks': detection of low-spatial-frequency gratings reversing in contrast at a high temporal frequency (so-called frequency-doubled gratings); detection of pulsed low-spatial-frequency gratings on a steady luminance pedestal; detection of coherent motion; and auditory discrimination of temporal order. Although all tasks showed test-retest reliability, only one pair shared more than 4 per cent of variance. Correlations within the set of 'magnocellular tasks' were similar to the correlations between those tasks and a 'non-magnocellular task', and there was little consistency between 'magnocellular deficit' groups comprising individuals with the lowest sensitivity for each task. Our results suggest that different 'magnocellular tasks' reflect different sources of variance, and thus are not general measures of 'magnocellular function'.
C1 [Goodbourn, Patrick T.; Bosten, Jenny M.; Hogg, Ruth E.; Bargary, Gary; Lawrance-Owen, Adam J.; Mollon, J. D.] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England.
   [Hogg, Ruth E.] Queens Univ Belfast, Royal Victoria Hosp, Ctr Vis & Vasc Sci, Belfast BT12 6BA, Antrim, North Ireland.
   [Bargary, Gary] City Univ London, Dept Optometry & Visual Sci, London EC1V 0HB, England.
RP Goodbourn, PT (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England.
EM p.goodbourn@psychol.cam.ac.uk
FU Gatsby Charitable Foundation; Cambridge Commonwealth and Overseas
   Trusts; Overseas Research Studentship; Gonville and Caius College,
   Cambridge
FX This work was supported by the Gatsby Charitable Foundation. P.T.G. was
   supported by a scholarship from the Cambridge Commonwealth and Overseas
   Trusts, and by an Overseas Research Studentship. J.M.B. was supported by
   a research fellowship from Gonville and Caius College, Cambridge.
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NR 51
TC 17
Z9 17
PU ROYAL SOC
PI LONDON
PA 6-9 CARLTON HOUSE TERRACE, LONDON SW1Y 5AG, ENGLAND
SN 0962-8452
J9 P ROY SOC B-BIOL SCI
JI Proc. R. Soc. B-Biol. Sci.
PD OCT 22
PY 2012
VL 279
IS 1745
BP 4263
EP 4271
DI 10.1098/rspb.2012.1430
PG 9
WC Biology; Ecology; Evolutionary Biology
SC Life Sciences & Biomedicine - Other Topics; Environmental Sciences &
   Ecology; Evolutionary Biology
GA 005JZ
UT WOS:000308748000022
PM 22896642
ER

PT J
AU Beaudet, AL
AF Beaudet, Arthur L.
TI Preventable Forms of Autism?
SO SCIENCE
LA English
DT Editorial Material
ID AMINO-ACID TRANSPORTER; SPECTRUM DISORDERS; MUTATIONS; CARNITINE;
   ATB(0,+); DISEASE; RISK; AGE
C1 Baylor Coll Med, Dept Human & Mol Genet, Houston, TX 77030 USA.
RP Beaudet, AL (reprint author), Baylor Coll Med, Dept Human & Mol Genet, Houston, TX 77030 USA.
EM abeaudet@bcm.edu
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NR 15
TC 8
Z9 8
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 19
PY 2012
VL 338
IS 6105
BP 342
EP 343
PG 2
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 022JS
UT WOS:000309955800031
PM 23087240
ER

PT J
AU Novarino, G
   El-Fishawy, P
   Kayserili, H
   Meguid, NA
   Scott, EM
   Schroth, J
   Silhavy, JL
   Kara, M
   Khalil, RO
   Ben-Omran, T
   Ercan-Sencicek, AG
   Hashish, AF
   Sanders, SJ
   Gupta, AR
   Hashem, HS
   Matern, D
   Gabriel, S
   Sweetman, L
   Rahimi, Y
   Harris, RA
   State, MW
   Gleeson, JG
AF Novarino, Gaia
   El-Fishawy, Paul
   Kayserili, Hulya
   Meguid, Nagwa A.
   Scott, Eric M.
   Schroth, Jana
   Silhavy, Jennifer L.
   Kara, Majdi
   Khalil, Rehab O.
   Ben-Omran, Tawfeg
   Ercan-Sencicek, A. Gulhan
   Hashish, Adel F.
   Sanders, Stephan J.
   Gupta, Abha R.
   Hashem, Hebatalla S.
   Matern, Dietrich
   Gabriel, Stacey
   Sweetman, Larry
   Rahimi, Yasmeen
   Harris, Robert A.
   State, Matthew W.
   Gleeson, Joseph G.
TI Mutations in BCKD-kinase Lead to a Potentially Treatable Form of Autism
   with Epilepsy
SO SCIENCE
LA English
DT Article
ID SYRUP-URINE-DISEASE; DEHYDROGENASE KINASE; AMINO-ACIDS; METABOLISM;
   EXPRESSION; TRANSPORT; MICE
AB Autism spectrum disorders are a genetically heterogeneous constellation of syndromes characterized by impairments in reciprocal social interaction. Available somatic treatments have limited efficacy. We have identified inactivating mutations in the gene BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) in consanguineous families with autism, epilepsy, and intellectual disability. The encoded protein is responsible for phosphorylation-mediated inactivation of the E1 alpha subunit of branched-chain ketoacid dehydrogenase (BCKDH). Patients with homozygous BCKDK mutations display reductions in BCKDK messenger RNA and protein, E1 alpha phosphorylation, and plasma branched-chain amino acids. Bckdk knockout mice show abnormal brain amino acid profiles and neurobehavioral deficits that respond to dietary supplementation. Thus, autism presenting with intellectual disability and epilepsy caused by BCKDK mutations represents a potentially treatable syndrome.
C1 [Novarino, Gaia; Scott, Eric M.; Schroth, Jana; Silhavy, Jennifer L.; Gleeson, Joseph G.] Univ Calif San Diego, Howard Hughes Med Inst, Neurogenet Lab, Dept Neurosci, La Jolla, CA 92093 USA.
   [Ercan-Sencicek, A. Gulhan; Sanders, Stephan J.; State, Matthew W.] Yale Univ, Ctr Child Study, Sch Med, Program Neurogenet,Dept Psychiat, New Haven, CT 06520 USA.
   [Kayserili, Hulya] Istanbul Univ, Istanbul Fac Med, Dept Med Genet, TR-34093 Faith Istanbul, Turkey.
   [Meguid, Nagwa A.; Khalil, Rehab O.; Hashish, Adel F.; Hashem, Hebatalla S.] Natl Res Ctr, Dept Res Children Special Needs, Cairo, Egypt.
   [Kara, Majdi] Tripoli Childrens Hosp, Dept Pediat, Tripoli, Libya.
   [Ben-Omran, Tawfeg] Hamad Med Corp, Dept Pediat, Clin & Metab Genet Div, Doha, Qatar.
   [Ercan-Sencicek, A. Gulhan; Sanders, Stephan J.; State, Matthew W.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA.
   [Gupta, Abha R.] Yale Univ, Sch Med, Dept Pediat, Ctr Child Study, New Haven, CT 06520 USA.
   [Matern, Dietrich] Mayo Clin, Dept Lab Med & Pathol, Biochem Genet Lab, Rochester, MN 55905 USA.
   [Gabriel, Stacey] Broad Inst Harvard & MIT, Cambridge, MA 02142 USA.
   [Sweetman, Larry] Baylor Res Inst, Inst Metab Dis, Dallas, TX 75226 USA.
   [Rahimi, Yasmeen; Harris, Robert A.] Indiana Univ Sch Med, Roudebush VA Med Ctr, Indianapolis, IN 46202 USA.
   [Rahimi, Yasmeen; Harris, Robert A.] Indiana Univ Sch Med, Dept Biochem & Mol Biol, Indianapolis, IN 46202 USA.
RP Novarino, G (reprint author), Univ Calif San Diego, Howard Hughes Med Inst, Neurogenet Lab, Dept Neurosci, La Jolla, CA 92093 USA.
EM gnovarino@ucsd.edu; jogleeson@ucsd.edu
FU NIH [P01HD070494, R01NS048453, P30NS047101, RC2MH089956, K08MH087639,
   T32MH018268]; Broad Institute [U54HG003067]; Center for Inherited
   Disease Research for genotyping; Simons Foundation Autism Research
   Initiative; Veterans Administration Merit Award; German Research
   Foundation; American Academy of Child and Adolescent Psychiatry Pilot
   Research Award/Elaine Schlosser Lewis Fund; American Psychiatric
   Association/Lilly Research Fellowship
FX We thank the families for their participation; R. Weavers and E. Morava
   (Nijmegen Medical Center, Netherlands) and B. Barshop for providing
   patients; M. Kara's colleague for arranging shipment during the Libyan
   revolution; C. Lynch for the pSer293 antibody; the S. Taylor lab (UCSD)
   for help in protein modeling; M. Seashore, W. MacLean Jr., T. Cowan, and
   A. El-Gharabawy for suggestions; N. Wright-Davis, M. Murtha, M.
   Raubeson, N. DiLullo, M. Walker, Y. Song, N. Lifton, K. Bilguvar, A.
   Caglayan, Z. Omay, M. Choi, N. Carriero, R. D. Bjornson, P. Ventola, K.
   Koenig, and A. Bozik for technical assistance; the Yale Center for
   Genome Analysis (S. Mane); and the Sanford Burnham Institute. Supported
   by NIH grants P01HD070494, R01NS048453, and P30NS047101 (J.G.G.),
   RC2MH089956 (M. W. S.), K08MH087639 (A. R. G.), T32MH018268 and
   (P.E.-F.); Broad Institute grant U54HG003067 (E. L.); the Center for
   Inherited Disease Research for genotyping; the Simons Foundation Autism
   Research Initiative (J.G.G. and M. W. S.); a Veterans Administration
   Merit Award (R. A. H.); the German Research Foundation (G. N.); the
   American Academy of Child and Adolescent Psychiatry Pilot Research
   Award/Elaine Schlosser Lewis Fund (P.E.-F.); and the American
   Psychiatric Association/Lilly Research Fellowship (P.E.-F.). J.G.G. is
   an investigator of the Howard Hughes Medical Institute. Data have been
   deposited into dbGap (phs000288) and the NCBI Sequence Read Archive
   (SRS351252) (whole exome sequencing) and into GEO (GSE39447)
   (microarrays). J.G.G. is a consultant for Halozyme Therapeutics, a
   biopharmaceutical company that develops products targeting the
   extracellular matrix. M. W. S. is a consultant to Synapdx, that is
   developing diagnostic tests for autism, and to Pfizer Pharmaceuticals
   that is working to develop autism therapeutics. Bckdk gene trap mice are
   available for noncommercial research from R. A. H. under MTA agreement
   with Lexicon. J.G.G. and M. W. S. are inventors on a patent application
   filed 17 July 2012 by UCSD covering diagnostic and therapeutic
   strategies for patients with autism and epilepsy.
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NR 21
TC 39
Z9 41
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 19
PY 2012
VL 338
IS 6105
BP 394
EP 397
DI 10.1126/science.1224631
PG 4
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 022JS
UT WOS:000309955800044
PM 22956686
ER

PT J
AU Kalkman, HO
AF Kalkman, Hans Otto
TI A review of the evidence for the canonical Wnt pathway in autism
   spectrum disorders
SO MOLECULAR AUTISM
LA English
DT Review
DE WNT2; FZD9; BCL9; DOCK4; DISC1; ADAM10; Valproate; SSRI
ID ADENOMATOUS POLYPOSIS-COLI; REGULATES DENDRITIC DEVELOPMENT;
   RUBINSTEIN-TAYBI SYNDROME; HEPATOCYTE GROWTH-FACTOR; MAJOR
   MENTAL-ILLNESS; BETA-CATENIN; SIGNALING PATHWAY; WILLIAMS-SYNDROME;
   JOUBERT-SYNDROME; BEHAVIORAL ABNORMALITIES
AB Microdeletion and microduplication copy number variations are found in patients with autism spectrum disorder and in a number of cases they include genes that are involved in the canonical Wnt signaling pathway (for example, FZD9, BCL9 or CDH8). Association studies investigating WNT2, DISC1, MET, DOCK4 or AHI1 also provide evidence that the canonical Wnt pathway might be affected in autism. Prenatal medication with sodium-valproate or antidepressant drugs increases autism risk. In animal studies, it has been found that these medications promote Wnt signaling, including among others an increase in Wnt2 gene expression. Notably, the available genetic information indicates that not only canonical Wnt pathway activation, but also inhibition seems to increase autism risk. The canonical Wnt pathway plays a role in dendrite growth and suboptimal activity negatively affects the dendritic arbor. In principle, this provides a logical explanation as to why both hypo-and hyperactivity may generate a similar set of behavioral and cognitive symptoms. However, without a validated biomarker to stratify for deviant canonical Wnt pathway activity, it is probably too dangerous to treat patients with compounds that modify pathway activity.
C1 Novartis Inst Biomed Res, Neurosci Dept, CH-4002 Basel, Switzerland.
RP Kalkman, HO (reprint author), Novartis Inst Biomed Res, Neurosci Dept, Bldg 386-14-22-15, CH-4002 Basel, Switzerland.
EM hans.kalkman@novartis.com
FU Novartis
FX At the time of writing, the author's salary was paid by Novartis. The
   author owns Novartis stock.
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NR 130
TC 13
Z9 14
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 19
PY 2012
VL 3
AR 10
DI 10.1186/2040-2392-3-10
PG 12
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254TA
UT WOS:000327188700001
PM 23083465
ER

PT J
AU Bhattacharya, A
   Kaphzan, H
   Alvarez-Dieppa, AC
   Murphy, JP
   Pierre, P
   Klann, E
AF Bhattacharya, Aditi
   Kaphzan, Hanoch
   Alvarez-Dieppa, Amanda C.
   Murphy, Jaclyn P.
   Pierre, Philippe
   Klann, Eric
TI Genetic Removal of p70 S6 Kinase 1 Corrects Molecular, Synaptic, and
   Behavioral Phenotypes in Fragile X Syndrome Mice
SO NEURON
LA English
DT Article
ID MENTAL-RETARDATION PROTEIN; LONG-TERM DEPRESSION; PHOSPHOINOSITIDE
   3-KINASE-AKT-MAMMALIAN TARGET; RAPAMYCIN SIGNALING PATHWAY; FMR1
   KNOCKOUT MOUSE; MESSENGER-RNA; MAMMALIAN TARGET; TRANSLATION; MTOR;
   MEMORY
AB Fragile X syndrome (FXS) is the leading inherited cause of autism and intellectual disability. Aberrant synaptic translation has been implicated in the etiology of FXS, but most lines of research on therapeutic strategies have targeted protein synthesis indirectly, far upstream of the translation machinery. We sought to perturb p70 ribosomal S6 kinase 1 (S6K1), a key translation initiation and elongation regulator, in FXS model mice. We found that genetic reduction of S6K1 prevented elevated phosphorylation of translational control molecules, exaggerated protein synthesis, enhanced mGluR-dependent long-term depression (LTD), weight gain, and macro-orchidism in FXS model mice. In addition, S6K1 deletion prevented immature dendritic spine morphology and multiple behavioral phenotypes, including social interaction deficits, impaired novel object recognition, and behavioral inflexibility. Our results support the model that dysregulated protein synthesis is the key causal factor in FXS and that restoration of normal translation can stabilize peripheral and neurological function in FXS.
C1 [Bhattacharya, Aditi; Kaphzan, Hanoch; Alvarez-Dieppa, Amanda C.; Murphy, Jaclyn P.; Klann, Eric] NYU, Ctr Neural Sci, New York, NY 10003 USA.
   [Pierre, Philippe] Univ Aix Marseille 2, CNRS, INSERM, Ctr Immunol Marseille Luminy, F-13288 Marseille 09, France.
   [Pierre, Philippe] INSERM, U1104, F-13288 Marseille, France.
   [Pierre, Philippe] CNRS, UMR 7280, F-13288 Marseille, France.
RP Klann, E (reprint author), NYU, Ctr Neural Sci, New York, NY 10003 USA.
EM eklann@cns.nyu.edu
FU NIH [NS034007, NS047384]; FRAXA Research Foundation; FRAXA Postdoctoral
   Fellowship; NSF REU Site Grant in Neural Science [DBI 1004172]
FX This work was supported by NIH grants NS034007 and NS047384 (E.K.),
   FRAXA Research Foundation (E.K.), and a FRAXA Postdoctoral Fellowship
   (A.B). J.P.M. was supported by a summer training grant, NSF REU Site
   Grant in Neural Science DBI 1004172.
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NR 63
TC 49
Z9 50
PU CELL PRESS
PI CAMBRIDGE
PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA
SN 0896-6273
J9 NEURON
JI Neuron
PD OCT 18
PY 2012
VL 76
IS 2
BP 325
EP 337
DI 10.1016/j.neuron.2012.07.022
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 028LV
UT WOS:000310424700009
PM 23083736
ER

PT J
AU Carter, EJ
   Williams, DL
   Minshew, NJ
   Lehman, JF
AF Carter, Elizabeth J.
   Williams, Diane L.
   Minshew, Nancy J.
   Lehman, Jill F.
TI Is He Being Bad? Social and Language Brain Networks during Social
   Judgment in Children with Autism
SO PLOS ONE
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; SPECTRUM DISORDERS;
   ASPERGER-SYNDROME; PEER INTERACTION; MORAL JUDGMENT; WORKING-MEMORY;
   MIND REGIONS; FMRI; COMPREHENSION
AB Individuals with autism often violate social rules and have lower accuracy in identifying and explaining inappropriate social behavior. Twelve children with autism (AD) and thirteen children with typical development (TD) participated in this fMRI study of the neurofunctional basis of social judgment. Participants indicated in which of two pictures a boy was being bad (Social condition) or which of two pictures was outdoors (Physical condition). In the within-group Social-Physical comparison, TD children used components of mentalizing and language networks [bilateral inferior frontal gyrus (IFG), bilateral medial prefrontal cortex (mPFC), and bilateral posterior superior temporal sulcus (pSTS)], whereas AD children used a network that was primarily right IFG and bilateral pSTS, suggesting reduced use of social and language networks during this social judgment task. A direct group comparison on the Social-Physical contrast showed that the TD group had greater mPFC, bilateral IFG, and left superior temporal pole activity than the AD group. No regions were more active in the AD group than in the group with TD in this comparison. Both groups successfully performed the task, which required minimal language. The groups also performed similarly on eyetracking measures, indicating that the activation results probably reflect the use of a more basic strategy by the autism group rather than performance disparities. Even though language was unnecessary, the children with TD recruited language areas during the social task, suggesting automatic encoding of their knowledge into language; however, this was not the case for the children with autism. These findings support behavioral research indicating that, whereas children with autism may recognize socially inappropriate behavior, they have difficulty using spoken language to explain why it is inappropriate. The fMRI results indicate that AD children may not automatically use language to encode their social understanding, making expression and generalization of this knowledge more difficult.
C1 [Carter, Elizabeth J.] Carnegie Mellon Univ, Inst Robot, Pittsburgh, PA 15213 USA.
   [Carter, Elizabeth J.] Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA.
   [Williams, Diane L.] Duquesne Univ, Dept Speech Language Pathol, Pittsburgh, PA 15219 USA.
   [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA.
   [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA.
   [Lehman, Jill F.] Carnegie Mellon Univ, Dept Comp Sci, Pittsburgh, PA 15213 USA.
RP Carter, EJ (reprint author), Carnegie Mellon Univ, Inst Robot, Pittsburgh, PA 15213 USA.
EM ejcarter@gmail.com
FU National Institute of Child Health and Human Development Autism Center
   of Excellence [P50HD055748]; National Institute on Deafness and Other
   Communication Disorders [DC006691]
FX This work was supported by a National Institute of Child Health and
   Human Development Autism Center of Excellence grant (P50HD055748, PI:
   NJM) and a National Institute on Deafness and Other Communication
   Disorders K23 award (DC006691, PI: DLW). 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 80
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 OCT 17
PY 2012
VL 7
IS 10
AR e47241
DI 10.1371/journal.pone.0047241
PG 9
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038AF
UT WOS:000311146900047
PM 23082151
ER

PT J
AU Lai, MC
   Lombardo, MV
   Ruigrok, ANV
   Chakrabarti, B
   Wheelwright, SJ
   Auyeung, B
   Allison, C
   Baron-Cohen, S
AF Lai, Meng-Chuan
   Lombardo, Michael V.
   Ruigrok, Amber N. V.
   Chakrabarti, Bhismadev
   Wheelwright, Sally J.
   Auyeung, Bonnie
   Allison, Carrie
   Baron-Cohen, Simon
CA MRC AIMS Consortium
TI Cognition in Males and Females with Autism: Similarities and Differences
SO PLOS ONE
LA English
DT Article
ID HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; SPECTRUM DISORDERS;
   SEX-DIFFERENCES; ASPERGER-SYNDROME; EXECUTIVE DYSFUNCTION;
   INFANTILE-AUTISM; DIAGNOSTIC INTERVIEW; FACIAL EXPRESSION; CHILDHOOD
   AUTISM
AB The male bias in autism spectrum conditions (ASC) has led to females with ASC being under-researched. This lack of attention to females could hide variability due to sex that may explain some of the heterogeneity within ASC. In this study we investigate four key cognitive domains (mentalizing and emotion perception, executive function, perceptual attention to detail, and motor function) in ASC, to test for similarities and differences between males and females with and without ASC (n = 128 adults; n = 32 per group). In the mentalizing and facial emotion perception domain, males and females with ASC showed similar deficits compared to neurotypical controls. However, in attention to detail and dexterity involving executive function, although males with ASC showed poorer performance relative to neurotypical males, females with ASC performed comparably to neurotypical females. We conclude that performance in the social-cognitive domain is equally impaired in male and female adults with ASC. However, in specific non-social cognitive domains, performance within ASC depends on sex. This suggests that in specific domains, cognitive profiles in ASC are modulated by sex.
C1 [Lai, Meng-Chuan; Lombardo, Michael V.; Ruigrok, Amber N. V.; Chakrabarti, Bhismadev; Wheelwright, Sally J.; Auyeung, Bonnie; Allison, Carrie; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
   [Chakrabarti, Bhismadev] Univ Reading, Ctr Integrat Neurosci & Neurodynam, Sch Psychol & Clin Language Sci, Reading, Berks, England.
RP Lai, MC (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England.
EM mcl45@cam.ac.uk
RI Ecker, Christine/E-5194-2010; Bolton, Patrick/E-8501-2010; Bailey,
   Anthony/J-2860-2014
OI Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X
FU United Kingdom Medical Research Council [GO 400061]; Waterloo Foundation
   [921/1247]; Wellcome Trust; British Academy
FX The project was funded by the United Kingdom Medical Research Council
   (GO 400061, http://www.mrc.ac.uk/index.html). MCL was supported by the
   Waterloo Foundation during the period of this study (921/1247,
   http://www.waterloofoundation.org.uk/index.html), MVL was supported by
   the Wellcome Trust (http://www.wellcome.ac.uk/) and the British Academy
   (http://www.britac.ac.uk/), and SBC was supported by the Wellcome Trust
   (http://www.wellcome.ac.uk/). 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 137
TC 17
Z9 17
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 17
PY 2012
VL 7
IS 10
AR e47198
DI 10.1371/journal.pone.0047198
PG 15
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038AF
UT WOS:000311146900042
PM 23094036
ER

PT J
AU Lopez-Rodriguez, A
   Holmgren, M
AF Lopez-Rodriguez, Angelica
   Holmgren, Miguel
TI Restoration of Proper Trafficking to the Cell Surface for Membrane
   Proteins Harboring Cysteine Mutations
SO PLOS ONE
LA English
DT Article
ID NUCLEOTIDE-GATED CHANNELS; SHAKER K+ CHANNEL; RENAL TUBULAR-ACIDOSIS;
   ION CHANNELS; FUNCTIONAL EXPRESSION; CHEMICAL CHAPERONES; POTASSIUM
   CHANNEL; COMPLEMENTARY-DNA; GAUCHER-DISEASE; CNGA3 MUTATIONS
AB A common phenotype for many genetic diseases is that the cell is unable to deliver full-length membrane proteins to the cell surface. For some forms of autism, hereditary spherocytosis and color blindness, the culprits are single point mutations to cysteine. We have studied two inheritable cysteine mutants of cyclic nucleotide-gated channels that produce achromatopsia, a common form of severe color blindness. By taking advantage of the reactivity of cysteine's sulfhydryl group, we modified these mutants with chemical reagents that attach moieties with similar chemistries to the wild-type amino acids' side chains. We show that these modifications restored proper delivery to the cell membrane. Once there, the channels exhibited normal functional properties. This strategy might provide a unique opportunity to assess the chemical nature of membrane protein traffic problems.
C1 [Lopez-Rodriguez, Angelica; Holmgren, Miguel] NINDS, Neurophysiol Sect, Porter Neurosci Res Ctr, NIH, Bethesda, MD 20892 USA.
RP Holmgren, M (reprint author), NINDS, Neurophysiol Sect, Porter Neurosci Res Ctr, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA.
EM holmgren@ninds.nih.gov
FU National Institutes of Health, National Institute Neurological Disorders
   and Stroke
FX This work was supported by the Intramural Research Program of the
   National Institutes of Health, National Institute Neurological Disorders
   and Stroke. The funders had no role in study design, data collection and
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NR 43
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 OCT 17
PY 2012
VL 7
IS 10
AR e47693
DI 10.1371/journal.pone.0047693
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 038AF
UT WOS:000311146900090
PM 23082193
ER

PT J
AU Karmiloff-Smith, A
   D'Souza, D
   Dekker, TM
   Van Herwegen, J
   Xu, F
   Rodic, M
   Ansari, D
AF Karmiloff-Smith, Annette
   D'Souza, Dean
   Dekker, Tessa M.
   Van Herwegen, Jo
   Xu, Fei
   Rodic, Maja
   Ansari, Daniel
TI Genetic and environmental vulnerabilities in children with
   neurodevelopmental disorders
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE autism; Down syndrome; infant development; number development; social
   cognition; Williams syndrome
ID FUNCTIONAL BRAIN-DEVELOPMENT; LARGE-NUMBER DISCRIMINATION;
   WILLIAMS-SYNDROME; DEVELOPMENTAL DISORDERS; DOWN-SYNDROME; INFANTS;
   AUTISM; ORIGINS; REPRESENTATIONS; COMPREHENSION
AB One might expect that children with varying genetic mutations or children raised in low socioeconomic status environments would display different deficits. Although this expectation may hold for phenotypic outcomes in older children and adults, cross-syndrome comparisons in infancy reveal many common neural and sociocognitive deficits. The challenge is to track dynamic trajectories over developmental time rather than focus on end states like in adult neuropsychological studies. We contrast the developmental and adult approaches with examples from the cognitive and social domains, and we conclude that static models of adult brain lesions cannot be used to account for the dynamics of change in genetic and environmentally induced disorders in children.
C1 [Karmiloff-Smith, Annette; D'Souza, Dean; Dekker, Tessa M.; Rodic, Maja] Birkbeck Ctr Brain & Cognit Dev, Dept Psychol Sci, London WC1N 7HX, England.
   [Van Herwegen, Jo] Kingston Univ, Dept Psychol, Kingston Upon Thames KT1 2EE, Surrey, England.
   [Xu, Fei] Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA.
   [Ansari, Daniel] Univ Western Ontario, Dept Psychol, London, ON NA6 3K7, Canada.
RP Karmiloff-Smith, A (reprint author), Birkbeck Ctr Brain & Cognit Dev, Dept Psychol Sci, London WC1N 7HX, England.
EM a.karmiloff-smith@bbk.ac.uk
RI Ansari, Daniel/B-2832-2009
OI Ansari, Daniel/0000-0002-7625-618X
FU Medical Research Council [G0800554]; Economic and Social Research
   Council (ESRC)
FX We thank the Down's Syndrome Association UK, Down Syndrome Education
   International, and the Williams Syndrome Foundation for their assistance
   with the recruitment of infants/toddlers as well as the families of the
   participants in the studies. The experimental studies reported here were
   supported by Medical Research Council Grant G0800554 (to A.K.-S.) as
   well as a studentship (to D. D.) funded by the Economic and Social
   Research Council (ESRC).
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NR 48
TC 16
Z9 16
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 16
PY 2012
VL 109
SU 2
BP 17261
EP 17265
DI 10.1073/pnas.1121087109
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 029QL
UT WOS:000310510500019
PM 23045661
ER

PT J
AU Lee, AY
   Chen, W
   Stippec, S
   Self, J
   Yang, F
   Ding, XJ
   Chen, S
   Juang, YC
   Cobb, MH
AF Lee, A-Young
   Chen, Wei
   Stippec, Steve
   Self, Jon
   Yang, Fan
   Ding, Xiaojun
   Chen, She
   Juang, Yu-Chi
   Cobb, Melanie H.
TI Protein kinase WNK3 regulates the neuronal splicing factor Fox-1
SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF
   AMERICA
LA English
DT Article
DE cytoplasmic retention; FMNL3
ID PRE-MESSENGER-RNA; AUTISM; GENE; XP11.22-P11.23; RECOGNITION; HOMOLOGS;
   BRAIN
AB We report an action of the protein kinase WNK3 on the neuronal mRNA splicing factor Fox-1. Fox-1 splices mRNAs encoding proteins important in synaptic transmission and membrane excitation. WNK3, implicated in the control of neuronal excitability through actions on ion transport, binds Fox-1 and inhibits its splicing activity in a kinase activity-dependent manner. Phosphorylation of Fox-1 by WNK3 does not change its RNA binding capacity; instead, WNK3 increases the cytoplasmic localization of Fox-1, thereby suppressing Fox-1-dependent splicing. These findings demonstrate a role of WNK3 in RNA processing. Considering the implication of WNK3 and Fox-1 in disorders of neuronal development such as autism, WNK3 may offer a target for treatment of Fox-1-induced disease.
C1 [Lee, A-Young; Chen, Wei; Stippec, Steve; Self, Jon; Juang, Yu-Chi; Cobb, Melanie H.] Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
   [Yang, Fan; Ding, Xiaojun; Chen, She] Natl Inst Biol Sci, Beijing 102206, Peoples R China.
RP Cobb, MH (reprint author), Univ Texas SW Med Ctr Dallas, Dept Pharmacol, Dallas, TX 75390 USA.
EM melanie.cobb@utsouthwestern.edu
FU National Institutes of Health [GM53032]; Robert A. Welch Foundation
   [I1243]
FX We thank Kristen Lynch and Lynch laboratory members Jason Jackson, Laura
   Motta-Mena, and Alan Tong for the gift of the pcAT-Glo1 construct, human
   genomic DNA, and their help setting up splicing assays. This work was
   supported by National Institutes of Health Grant GM53032 and Robert A.
   Welch Foundation Grant I1243.
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NR 27
TC 4
Z9 4
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 16
PY 2012
VL 109
IS 42
BP 16841
EP 16846
DI 10.1073/pnas.1215406109
PG 6
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 029SK
UT WOS:000310515800027
PM 23027929
ER

PT J
AU Tateno, M
   Park, TW
   Kato, TA
   Umene-Nakano, W
   Saito, T
AF Tateno, Masaru
   Park, Tae Woo
   Kato, Takahiro A.
   Umene-Nakano, Wakako
   Saito, Toshikazu
TI Hikikomori as a possible clinical term in psychiatry: a questionnaire
   survey
SO BMC PSYCHIATRY
LA English
DT Article
DE Hikikomori; Social withdrawal; School refusal; Psychiatric diagnosis;
   Developmental disorders
ID CULTURE-BOUND SYNDROME; SOCIAL WITHDRAWAL; AUTISM-SPECTRUM; COMMUNITY
   POPULATION; YOUNG-PEOPLE; JAPAN; DEPRESSION; PREVALENCE; DISORDERS
AB Background: The word hikikomori, the abnormal avoidance of social contact, has become increasingly well-known. However, a definition of this phenomenon has not been discussed thoroughly. The aim of this study is to gain a better understanding of the perception of hikikomori amongst health-related students and professionals and to explore possible psychiatric conditions underlying hikikomori.
   Methods: A total of 1,038 subjects were requested to complete a questionnaire regarding hikikomori phenomenon.
   Results: While some differences in the perception of hikikomori do exist, all subjects tended to disagree with the statement, "hikikomori is NOT a disorder". Regarding the underlying psychiatric disorders of hikikomori, approximately 30% of psychiatrists chose schizophrenia as the most applicable ICD-10 diagnosis for hikikomori, whereas 50% of pediatricians chose neurotic or stress-related disorders.
   Conclusions: An argument still exists regarding the relationship between hikikomori and psychiatric disorders. We propose that the term hikikomori could be used to describe severe social withdrawal in the setting of a number of psychiatric disorders.
C1 [Tateno, Masaru; Saito, Toshikazu] Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Chuo Ku, Sapporo, Hokkaido 0608543, Japan.
   [Park, Tae Woo] Boston Univ, Sch Med, Dept Psychiat, Boston, MA 02114 USA.
   [Park, Tae Woo] VA Boston Healthcare Syst, Boston, MA 02114 USA.
   [Kato, Takahiro A.] Kyushu Univ, Grad Sch Med Sci, Dept Neuropsychiat, Higashi Ku, Fukuoka 8128582, Japan.
   [Umene-Nakano, Wakako] Univ Occupat & Environm Hlth, Sch Med, Dept Psychiat, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan.
RP Tateno, M (reprint author), Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Chuo Ku, South 1,West 16, Sapporo, Hokkaido 0608543, Japan.
EM tatema@sapmed.ac.jp
FU World Psychiatric Association (WPA)
FX The authors thank Yasuyo Suzuki, Kiyoji Matsuyama (Sapporo Medical
   University), Takeshi Ujiie (Hokkaido Ujiie Clinic for Psychosomatic
   Children) for their contributions for data collection, and Ryuji Sasaki
   (Sapporo Medical University) for his technical assistance for on-line
   questionnaire. This study was partially supported by the World
   Psychiatric Association (WPA) Research Fund 2010 to TAK.
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NR 35
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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 15
PY 2012
VL 12
AR 169
DI 10.1186/1471-244X-12-169
PG 7
WC Psychiatry
SC Psychiatry
GA 044RJ
UT WOS:000311640400001
PM 23061675
ER

PT J
AU Lupski, JR
AF Lupski, James R.
TI Brain Copy Number Variants and Neuropsychiatric Traits
SO BIOLOGICAL PSYCHIATRY
LA English
DT Editorial Material
ID AUTISM; SCHIZOPHRENIA; GENOMICS; 16P11.2
C1 [Lupski, James R.] Texas Childrens Hosp, Baylor Coll Med, Dept Mol Genet, Houston, TX 77030 USA.
   [Lupski, James R.] Dept Human Genet, Houston, TX USA.
   [Lupski, James R.] Dept Pediat, Houston, TX USA.
   [Lupski, James R.] Human Genome Sequencing Ctr, Houston, TX USA.
RP Lupski, JR (reprint author), Texas Childrens Hosp, Baylor Coll Med, Dept Mol Genet, 1 Baylor Plaza,Room 604B, Houston, TX 77030 USA.
EM jlupski@bcm.tmc.edu
CR Conrad DF, 2010, NATURE, V464, P704, DOI 10.1038/nature08516
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   Lupski JR, 2008, NATURE, V455, P178, DOI 10.1038/455178a
   Lupski JR, 2011, CELL, V147, P32, DOI 10.1016/j.cell.2011.09.008
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NR 10
TC 6
Z9 6
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 2012
VL 72
IS 8
BP 617
EP 619
DI 10.1016/j.biopsych.2012.08.007
PG 3
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 016UQ
UT WOS:000309545400002
PM 22999336
ER

PT J
AU Ye, TZ
   Lipska, BK
   Tao, R
   Hyde, TM
   Wang, LQ
   Li, C
   Choi, KH
   Straub, RE
   Kleinman, JE
   Weinberger, DR
AF Ye, Tianzhang
   Lipska, Barbara K.
   Tao, Ran
   Hyde, Thomas M.
   Wang, Liqin
   Li, Chao
   Choi, Kwang H.
   Straub, Richard E.
   Kleinman, Joel E.
   Weinberger, Daniel R.
TI Analysis of Copy Number Variations in Brain DNA from Patients with
   Schizophrenia and Other Psychiatric Disorders
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Autism; copy number variations; gene expression; major depressive
   disorder; postmortem brain; prefrontal cortex; schizophrenia
ID HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA; GENE-EXPRESSION; MICROARRAY;
   RISK
AB Background: Clinical studies have identified several regions of the genome with copy number variations (CNVs) associated with diverse neurodevelopmental behavioral disorders.
   Methods: We analyzed 1 million (M) single nucleotide polymorphism genotype arrays for evidence of previously reported recurrent CNVs and enriched genome-wide CNV burden in DNA from 600 brains, including 441 individuals with various psychiatric diagnoses. We explored gene expression in the dorsolateral prefrontal cortex in selected cases with CNVs and in other subjects with Illumina BeadArrays (568 subjects in total) and additionally in 66-92 subjects with quantitative real-time polymerase chain reaction.
   Results: The CNVs in previously reported genomic regions were identified in 4 of 193 patients with the diagnosis of schizophrenia (1q21.1, 11q25, 15q11.2, 22q11), 4 of 238 patients with mood disorders (11q25, 15q11.2, 22q11), and 1 of 10 patients with autism (2p16.3). No evidence of increased genome-wide CNV burden was observed in cases with schizophrenia or mood disorders, although the study is underpowered to observe rare events. Messenger RNA expression patterns suggested incomplete molecular penetrance of observed CNVs.
   Conclusions: Our data confirm in brain DNA the presence of certain recurrent CNVs in a small percentage of patients with psychiatric diagnoses.
C1 [Ye, Tianzhang; Hyde, Thomas M.; Straub, Richard E.; Weinberger, Daniel R.] Johns Hopkins Univ, Lieber Inst Brain Dev, Baltimore, MD 21205 USA.
   [Lipska, Barbara K.; Tao, Ran; Wang, Liqin; Li, Chao; Kleinman, Joel E.] NIMH, Clin Brain Disorders Branch, Genes Cognit & Psychosis Program, Intramural Res Program,NIH, Bethesda, MD 20892 USA.
   [Choi, Kwang H.] Uniformed Serv Univ Hlth Sci, Dept Psychiat, Bethesda, MD 20814 USA.
   [Choi, Kwang H.] Uniformed Serv Univ Hlth Sci, Program Neurosci, Bethesda, MD 20814 USA.
RP Weinberger, DR (reprint author), Johns Hopkins Univ, Lieber Inst Brain Dev, Med Campus,855 N Wolfe St, Baltimore, MD 21205 USA.
EM drweinberger@libd.org
RI Tao, Ran/C-2662-2013; Tao, Ran/L-3460-2014
CR Burnside R, 2011, HUM GENET, V130, P517, DOI 10.1007/s00439-011-0970-4
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NR 17
TC 9
Z9 10
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 2012
VL 72
IS 8
BP 651
EP 654
DI 10.1016/j.biopsych.2012.06.014
PG 4
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 016UQ
UT WOS:000309545400007
PM 22795968
ER

PT J
AU Bartlett, CW
   Flax, JF
   Fermano, Z
   Hare, A
   Hou, LP
   Petrill, SA
   Buyske, S
   Brzustowicz, LM
AF Bartlett, Christopher W.
   Flax, Judy F.
   Fermano, Zena
   Hare, Abby
   Hou, Liping
   Petrill, Stephen A.
   Buyske, Steven
   Brzustowicz, Linda M.
TI Gene x Gene Interaction in Shared Etiology of Autism and Specific
   Language Impairment
SO BIOLOGICAL PSYCHIATRY
LA English
DT Article
DE Autism; epistasis; gene-gene interaction; heritability; shared etiology;
   specific language impairment
ID DIAGNOSTIC OBSERVATION SCHEDULE; SPECTRUM DISORDERS; CNTNAP2 GENE;
   PHENOTYPE; CHILDREN; TWIN; LINKAGE; TRAITS; HERITABILITY; ADOLESCENTS
AB Background: To examine the relationship between autism spectrum disorders (ASD) and specific language impairment (SLI), family studies typically take a comparative approach where families with one disease are examined for traits of the other disease. In contrast, the present report is the first study with both disorders required to be present in each family to provide a more direct test of the hypothesis of shared genetic etiology.
   Methods: We behaviorally assessed 51 families including at least one person with ASD and at least one person with SLI (without ASD). Pedigree members were tested with 22 standardized measures of language and intelligence. Because these extended families include a nonshared environmental contrast, we calculated heritability, not just familiality, for each measure twice: 1) baseline heritability analysis, compared with; 2) heritability estimates after statistically removing ASD subjects from pedigrees.
   Results: Significant increases in heritability on four supra-linguistic measures (including Pragmatic Judgment) and a composite language score but not on any other measures were observed when removing ASD subjects from the analysis, indicating differential genetic effects that are unique to ASD. Nongenetic explanations such as effects of ASD severity or measurement error or low score variability in ASD subjects were systematically ruled out, leaving the hypothesis of nonadditive genetics effects as the potential source of the heritability change caused by ASD.
   Conclusions: Although the data suggest genetic risk factors common to both SLI and ASD, there are effects that seem unique to ASD, possibly caused by nonadditive gene-gene interactions of shared risk loci.
C1 [Bartlett, Christopher W.; Hou, Liping; Petrill, Stephen A.] Nationwide Childrens Hosp, Res Inst, Battelle Ctr Math Med, Columbus, OH 43205 USA.
   [Petrill, Stephen A.] Ohio State Univ, Dept Pediat, Columbus, OH 43205 USA.
   [Petrill, Stephen A.] Ohio State Univ, Dept Human Dev & Family Sci, Columbus, OH 43205 USA.
   [Flax, Judy F.] Rutgers State Univ, Ctr Mol & Behav Neurosci, Piscataway, NJ USA.
   [Flax, Judy F.; Fermano, Zena; Hare, Abby; Buyske, Steven; Brzustowicz, Linda M.] Rutgers State Univ, Dept Genet, Piscataway, NJ USA.
   [Buyske, Steven] Rutgers State Univ, Dept Stat & Biostat, Piscataway, NJ USA.
RP Bartlett, CW (reprint author), Nationwide Childrens Hosp, Res Inst, Battelle Ctr Math Med, JW3926,700 Childrens Dr, Columbus, OH 43205 USA.
EM bartletc@ccri.net
RI Bartlett, Christopher/B-4958-2009; Petrill, Stephen/J-3040-2013; Hou,
   Liping/G-1648-2011
OI Bartlett, Christopher/0000-0001-7837-6348; Hou,
   Liping/0000-0003-3972-245X
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NR 54
TC 6
Z9 6
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 2012
VL 72
IS 8
BP 692
EP 699
DI 10.1016/j.biopsych.2012.05.019
PG 8
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 016UQ
UT WOS:000309545400013
PM 22704665
ER

PT J
AU Kleinhans, NM
   Pauley, G
   Richards, T
   Neuhaus, E
   Martin, N
   Corrigan, NM
   Shaw, DW
   Estes, A
   Dager, SR
AF Kleinhans, Natalia M.
   Pauley, Gregory
   Richards, Todd
   Neuhaus, Emily
   Martin, Nathalie
   Corrigan, Neva M.
   Shaw, Dennis W.
   Estes, Annette
   Dager, Stephen R.
TI Age-related abnormalities in white matter microstructure in autism
   spectrum disorders
SO BRAIN RESEARCH
LA English
DT Article
DE Autism; White matter; DTI; Age; Interaction
ID HIGH-FUNCTIONING AUTISM; CORPUS-CALLOSUM; ASPERGER-SYNDROME; BRAIN SIZE;
   SENTENCE COMPREHENSION; FRACTIONAL ANISOTROPY; INFANTILE-AUTISM;
   FRONTAL-CORTEX; YOUNG-CHILDREN; HEAD GROWTH
AB Abnormalities in structural and functional connectivity have been reported in autism spectrum disorders (ASD) across a wide age range. However, developmental changes in white matter microstructure are poorly understood. We used a cross-sectional design to determine whether white matter abnormalities measured using diffusion tensor imaging (DTI) were present in adolescents and adults with ASD and whether age-related changes in white matter microstructure differed between ASD and typically developing (TD) individuals. Participants included 28 individuals with ASD and 33 TD controls matched on age and IQ and assessed at one time point. Widespread decreased fractional anisotropy (FA), and increased radial diffusivity (RaD) and mean diffusivity (MD) were observed in the ASD group compared to the TD group. In addition, significant group-by-age interactions were observed in FA, RaD, and MD in all major tracts except the brain stem, indicating that age-related changes in white matter microstructure differed between the groups. We propose that white matter microstructural changes in ASD may reflect myelination and/or other structural differences including differences in axonal density/arborization. In addition, we suggest that white matter microstuctural impairments may be normalizing during young adulthood in ASD. Future longitudinal studies that include a wider range of ages and more extensive clinical characterization will be critical for further uncovering the neurodevelopmental processes unfolding during this dynamic time in development. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Kleinhans, Natalia M.; Pauley, Gregory; Richards, Todd; Martin, Nathalie; Corrigan, Neva M.; Shaw, Dennis W.; Dager, Stephen R.] Univ Washington, Dept Radiol, Seattle, WA 98195 USA.
   [Neuhaus, Emily; Estes, Annette] Univ Washington, Dept Psychol, Seattle, WA 98195 USA.
   [Estes, Annette] Univ Washington, Dept Speech & Hearing Sci, Seattle, WA 98195 USA.
   [Dager, Stephen R.] Univ Washington, Dept Bioengn, Seattle, WA 98195 USA.
   [Kleinhans, Natalia M.; Pauley, Gregory; Richards, Todd; Martin, Nathalie] Univ Washington, Integrated Brain Imaging Ctr, Seattle, WA 98195 USA.
   [Kleinhans, Natalia M.; Richards, Todd; Estes, Annette; Dager, Stephen R.] Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA.
   [Kleinhans, Natalia M.; Richards, Todd; Neuhaus, Emily; Shaw, Dennis W.; Estes, Annette; Dager, Stephen R.] Univ Washington, UW Autism Ctr, Seattle, WA 98195 USA.
RP Kleinhans, NM (reprint author), Univ Washington, Dept Radiol, Box 357115, Seattle, WA 98195 USA.
EM nkleinha@u.washington.edu
FU NINDS/NIH [5K01NS059675]; NICHD/NIH [5P50HD055782]
FX This work was supported by NINDS/NIH 5K01NS059675 and NICHD/NIH
   5P50HD055782. We would like to thank Drs. Paul Borghesani and Kurt
   Weaver for their input on background and interpretation of DTI scalars
   and Dr. Edith Sullivan for her input on the DTI preprocessing pipeline
   and methods for evaluating data quality.
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NR 87
TC 13
Z9 13
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD OCT 15
PY 2012
VL 1479
BP 1
EP 16
DI 10.1016/j.brainres.2012.07.056
PG 16
WC Neurosciences
SC Neurosciences & Neurology
GA 028HV
UT WOS:000310414300001
PM 22902768
ER

PT J
AU Spotorno, N
   Koun, E
   Prado, J
   Van Der Henst, JB
   Noveck, IA
AF Spotorno, Nicola
   Koun, Eric
   Prado, Jerome
   Van Der Henst, Jean-Baptiste
   Noveck, Ira A.
TI Neural evidence that utterance-processing entails mentalizing: The case
   of irony
SO NEUROIMAGE
LA English
DT Article
DE Theory of Mind; Language; Irony; fMRI; PPI; Pragmatics
ID SOCIAL COGNITION; VERBAL IRONY; BRAIN; SARCASM; MIND; COMPREHENSION;
   METAANALYSIS; FMRI; REPRESENTATION; AUTISM
AB It is now well established that communicators interpret others' mental states through what has been called "Theory of Mind" (ToM). From a linguistic-pragmatics perspective, this mentalizing ability is considered critical because it is assumed that the linguistic code in all utterances underdetermines the speaker's meaning, leaving a vital role for ToM to fill the gap. From a neuroscience perspective, understanding others' intentions has been shown to activate a neural ToM network that includes the right and left temporal parietal junction (rTPJ, ITPJ), the medial prefrontal cortex (MPFC) and the precuneus (PC). Surprisingly, however, there are no studies - to our knowledge - that aim to uncover a direct, on-line link between language processing and ToM through neuroimaging. This is why we focus on verbal irony, an obviously pragmatic phenomenon that compels a listener to detect the speaker's (dissociated, mocking) attitude (Wilson, 2009). In the present fMRI investigation, we compare participants' comprehension of 18 target sentences as contexts make them either ironic or literal. Consider an opera singer who tells her interlocutor: "Tonight we gave a superb performance!" when the performance in question was clearly awful (making the statement ironic) or very good (making the statement literal). We demonstrate that the ToM network becomes active while a participant is understanding verbal irony. Moreover, we demonstrate - through Psychophysiological Interactions (PPI) analyses - that ToM activity is directly linked with language comprehension processes. The paradigm, its predictions, and the reported results contrast dramatically with those from seven prior fMRI studies on irony. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Spotorno, Nicola; Koun, Eric; Prado, Jerome; Van Der Henst, Jean-Baptiste; Noveck, Ira A.] Univ Lyon 1, CNRS, Lab L2C2, FRE3406, F-69675 Bron, France.
   [Noveck, Ira A.] Ctr Rech Francais Jerusalem, MAEE CNRS UMIFRE 7, IL-91004 Jerusalem, Israel.
RP Spotorno, N (reprint author), Univ Lyon 1, L2C2 CNRS, Inst Cognit Sci, 67 Bd Pinel, F-69675 Bron, France.
EM nicola.spotorno@isc.cnrs.fr
RI Prado, Jerome /D-5581-2013
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NR 52
TC 12
Z9 13
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 OCT 15
PY 2012
VL 63
IS 1
BP 25
EP 39
DI 10.1016/j.neuroimage.2012.06.046
PG 15
WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 005SN
UT WOS:000308770300003
PM 22766167
ER

PT J
AU Madrigal, I
   Rodriguez-Revenga, L
   Xuncla, M
   Mila, M
AF Madrigal, Irene
   Rodriguez-Revenga, Laia
   Xuncla, Mar
   Mila, Montserrat
TI 15q11.2 microdeletion and FMR1 premutation in a family with intellectual
   disabilities and autism
SO GENE
LA English
DT Article
DE 15q11.2 deletion; Autism; Intellectual disabilities; CYFIPI; FMR1
ID HEREDITARY SPASTIC PARAPLEGIA; PRADER-WILLI-SYNDROME;
   FRAGILE-X-SYNDROME; SEGMENTAL DUPLICATIONS; SPECTRUM DISORDERS; MG2+
   TRANSPORTER; CRITICAL REGION; 4 GENES; REARRANGEMENTS; EXPRESSION
AB Genomic rearrangements of chromosome 15q11-q13 are responsible for diverse phenotypes including intellectual disabilities and autism. 15q11.2 deletion, implicating common PWS/AS breakpoints BP1-BP2, has been described in patients with delayed motor and speech development and behavioural problems. Here we report the clinical and molecular characterisation of a maternally inherited BP1-BP2 deletion in two siblings with intellectual, motor and speech delay, autistic syndrome disorder and several dysmorphic features. One of the patients was also a carrier of an FMR1 allele in the low premutation range. The four genes within the deletion were under-expressed in all deletion carriers but FMR1 mRNA levels remained normal. Our results suggest that BP1-BP2 deletion could be considered as a risk factor for neuropsychological phenotypes and that it presents with variable clinical expressivity. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Madrigal, Irene; Rodriguez-Revenga, Laia; Xuncla, Mar; Mila, Montserrat] Hosp Clin Barcelona, Biochem & Mol Genet Dept, Barcelona 08014, Spain.
   [Madrigal, Irene; Rodriguez-Revenga, Laia; Xuncla, Mar; Mila, Montserrat] IDIBAPS, Barcelona, Spain.
   [Madrigal, Irene; Rodriguez-Revenga, Laia; Xuncla, Mar; Mila, Montserrat] CIBER Enfermedades Raras CIBERER, Barcelona, Spain.
RP Mila, M (reprint author), Hosp Clin Barcelona, Biochem & Mol Genet Dept, Villarroel 170,Esc 7 Pis 5, Barcelona 08014, Spain.
EM mmila@clinic.ub.es
FU Fundacion Esther Koplowitz [DN40533]; CIBER de Enfermedades Raras
FX We are grateful to the patients and their families for participating in
   this study. This work was supported by Fundacion Esther Koplowitz
   (DN40533) and the CIBER de Enfermedades Raras, which is an initiative of
   the ISCIII.
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NR 24
TC 6
Z9 6
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-1119
J9 GENE
JI Gene
PD OCT 15
PY 2012
VL 508
IS 1
BP 92
EP 95
DI 10.1016/j.gene.2012.07.023
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 012PS
UT WOS:000309249600013
PM 22842191
ER

PT J
AU Heuer, LS
   Rose, M
   Ashwood, P
   Van de Water, J
AF Heuer, Luke S.
   Rose, Melissa
   Ashwood, Paul
   Van de Water, Judy
TI Decreased levels of total immunoglobulin in children with autism are not
   a result of B cell dysfunction
SO JOURNAL OF NEUROIMMUNOLOGY
LA English
DT Article
DE Autism; B cell; Immunoglobulin; Immune system
ID LYMPHOCYTE CYTOKINE PROFILES; SPECTRUM DISORDERS; IMMUNE ACTIVATION;
   GASTROINTESTINAL SYMPTOMS; T-CELLS; BRAIN; PREGNANCY; RESPONSES;
   GLOBULIN; INNATE
AB Autism spectrum disorders are a heterogeneous group of behaviorally defined disorders having complex etiologies. We previously reported a direct correlation between lower plasma levels of the immunoglobulins (Ig) IgG and IgM and increased severity of behavioral symptoms in children with autism. Our current objective was to determine if these reduced plasma levels of IgG and IgM are the result of defective B cell development, activation, or function. Results suggest no differences in the B cell parameters measured, indicating that decreased Ig in autism is not a result of B cell dysfunction and other immune cells might be involved. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Heuer, Luke S.; Van de Water, Judy] Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA.
   [Rose, Melissa] Univ Calif Davis, Dept Publ Hlth Sci, Davis, CA 95616 USA.
   [Ashwood, Paul] Univ Calif Davis, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
   [Heuer, Luke S.; Rose, Melissa; Ashwood, Paul; Van de Water, Judy] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA.
   [Heuer, Luke S.; Rose, Melissa; Ashwood, Paul; Van de Water, Judy] Univ Calif Davis, NIEHS Ctr Childrens Environm Hlth, Davis, CA 95616 USA.
RP Van de Water, J (reprint author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, 451 E Hlth Sci Dr, Davis, CA 95616 USA.
EM javandewater@ucdavis.edu
FU NIEHS [1P01ES11269-01]; U.S. EPA [R829388]
FX Sponsors: NIEHS 1P01ES11269-01 and U.S. EPA Grant R829388.
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NR 37
TC 3
Z9 4
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0165-5728
J9 J NEUROIMMUNOL
JI J. Neuroimmunol.
PD OCT 15
PY 2012
VL 251
IS 1-2
BP 94
EP 102
DI 10.1016/j.jneuroim.2012.07.001
PG 9
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 013OM
UT WOS:000309314700014
PM 22854260
ER

PT J
AU 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
   Melhem, NM
   Chaste, P
   Sutcliffe, JS
   State, MW
   Cook, EH
   Roeder, K
   Devlin, B
AF 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.
   Melhem, Nadine M.
   Chaste, Pauline
   Sutcliffe, James S.
   State, Matthew W.
   Cook, Edwin H., Jr.
   Roeder, Kathryn
   Devlin, Bernie
TI Common genetic variants, acting additively, are a major source of risk
   for autism
SO MOLECULAR AUTISM
LA English
DT Article
DE Narrow-sense heritability; Multiplex; Simplex; Quantitative genetics
ID DE-NOVO MUTATIONS; COPY-NUMBER VARIATION; SPECTRUM DISORDERS; LINKAGE
   DISEQUILIBRIUM; FAMILIAL AGGREGATION; ASSOCIATION; HERITABILITY;
   DISEASE; TWIN; SCHIZOPHRENIA
AB Background: Autism spectrum disorders (ASD) are early onset neurodevelopmental syndromes typified by impairments in reciprocal social interaction and communication, accompanied by restricted and repetitive behaviors. While rare and especially de novo genetic variation are known to affect liability, whether common genetic polymorphism plays a substantial role is an open question and the relative contribution of genes and environment is contentious. It is probable that the relative contributions of rare and common variation, as well as environment, differs between ASD families having only a single affected individual (simplex) versus multiplex families who have two or more affected individuals.
   Methods: By using quantitative genetics techniques and the contrast of ASD subjects to controls, we estimate what portion of liability can be explained by additive genetic effects, known as narrow-sense heritability. We evaluate relatives of ASD subjects using the same methods to evaluate the assumptions of the additive model and partition families by simplex/multiplex status to determine how heritability changes with status.
   Results: By analyzing common variation throughout the genome, we show that common genetic polymorphism exerts substantial additive genetic effects on ASD liability and that simplex/multiplex family status has an impact on the identified composition of that risk. As a fraction of the total variation in liability, the estimated narrow-sense heritability exceeds 60% for ASD individuals from multiplex families and is approximately 40% for simplex families. By analyzing parents, unaffected siblings and alleles not transmitted from parents to their affected children, we conclude that the data for simplex ASD families follow the expectation for additive models closely. The data from multiplex families deviate somewhat from an additive model, possibly due to parental assortative mating.
   Conclusions: Our results, when viewed in the context of results from genome-wide association studies, demonstrate that a myriad of common variants of very small effect impacts ASD liability.
C1 [Klei, Lambertus; Melhem, Nadine M.; Chaste, Pauline; Devlin, Bernie] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
   [Sanders, Stephan J.; Murtha, Michael T.; State, Matthew W.] Yale Univ, Sch Med, Program Neurogenet, New Haven, CT USA.
   [Sanders, Stephan J.; Willsey, A. Jeremy; State, Matthew W.] Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA.
   [Sanders, Stephan J.; State, Matthew W.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT USA.
   [Sanders, Stephan J.; 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.] Univ Calif Los Angeles, Dept Neurol, Neurogenet Program, Los Angeles, CA 90024 USA.
   [Lowe, Jennifer K.] Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst, Ctr Autism Res & Treatment, Los Angeles, CA 90095 USA.
   [Moreno-De-Luca, Daniel; Martin, Christa Lese] Univ Pittsburgh, Sch Med, Dept Human Genet, Pittsburgh, PA USA.
   [Yu, Timothy W.] Harvard Univ, Sch Med, Childrens Hosp Boston, Div Genet, Boston, MA USA.
   [Fombonne, Eric] McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3Z 1P2, Canada.
   [Grice, Dorothy E.] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA.
   [Ledbetter, David H.] Geisinger Hlth Syst, Danville, PA USA.
   Weill Cornell Med Coll, Ctr Autism & Dev Brain, White Plains, NY USA.
   [Mane, Shrikant M.] Yale Ctr Genome Anal, Orange, CT USA.
   [Martin, Donna M.] Univ Michigan, Sch Med, Dept Pediat, Ann Arbor, MI USA.
   [Martin, Donna M.] Univ Michigan, Sch Med, Dept Human Genet, Ann Arbor, MI 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.
   [Walsh, Christopher A.] Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA.
   [Walsh, Christopher A.] Childrens Hosp, Div Genet, Boston, MA 02115 USA.
   [Walsh, Christopher A.] Harvard Univ, Sch Med, Ctr Life Sci, Boston, MA USA.
   [Sutcliffe, James S.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Ctr Mol Neurosci, Nashville, TN 37232 USA.
   [Cook, Edwin H., Jr.] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA.
   [Roeder, Kathryn] Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA.
RP Devlin, B (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA.
EM devlinbj@upmc.edu
RI Melhem, Nadine/G-1510-2013
FU Simons Foundation [MH057881]; National Institutes of Health [HD055751,
   HD055782, HD055784, HD35465, MH52708, MH55284, MH57881, MH061009,
   MH06359, MH066673, MH080647, MH081754, MH66766, NS026630, NS042165,
   NS049261, HHSN268200782096C, HHSN268201100011I]; Canadian Institutes for
   Health Research (CIHR); Assistance Publique - Hopitaux de Paris, France;
   Autism Speaks UK; Canada Foundation for Innovation/Ontario Innovation
   Trust [Po 255/17-4]; Deutsche Forschungsgemeinschaft, Germany; EC Sixth
   FP AUTISM MOLGEN; Fundacao Calouste Gulbenkian, Portugal; Fondation de
   France; Fondation FondaMental, France; Fondation Orange, France;;
   Fondation pour la Recherche Medicale, France; Fundacao para a Ciencia e
   Tecnologia, Portugal; Hospital for Sick Children Foundation and
   University of Toronto, Canada; INSERM, France; Institut Pasteur, France;
   Italian Ministry of Health; John P Hussman Foundation, USA; McLaughlin
   Centre, Canada; Netherlands Organization for Scientific Research
   [TMF/DA/5801]; Royal Netherlands Academy of Arts and Sciences; Ontario
   Ministry of Research and Innovation, Canada; Seaver Foundation, USA;
   Swedish Science Council; Centre for Applied Genomics, Canada; Utah
   Autism Foundation, USA; Core [075491/Z/04]; Wellcome Trust, UK; Division
   of Aging Biology, NIA; Division of Geriatrics and Clinical Gerontology,
   NIA; NIH [R01 NS36960]; Michael J Fox Foundation
FX Research supported by grants from the Simons Foundation and MH057881.
   SSC: We are grateful to all of the families participating in the Simons
   Foundation Autism Research Initiative (SFARI) Simplex Collection (SSC).
   This work was supported by a grant from the Simons Foundation. We wish
   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; the coordinators and
   staff at the SSC sites; the SFARI staff, in particular M. Benedetti;
   Prometheus Research; the Yale Center of Genomic Analysis staff, in
   particular M. Mahajan, S. Umlauf, I. Tikhonova and A. Lopez; T.
   Brooks-Boone, N. Wright-Davis and M. Wojciechowski for their help in
   administering the project at Yale; I. Hart for support; and G.D.
   Fischbach, A. Packer, J. Spiro, M. Benedetti and M. Carlson for their
   helpful suggestions throughout. Approved researchers can obtain the SSC
   population data set described in this study by applying at
   https://base.sfari.org.AGP: We used data from the Autism Genome Project
   (AGP) Consortium Whole Genome Association and Copy Number Variation
   Study of over 1,500 Parent-Offspring Trios - Stage I (dbGaP Study
   Accession: phs000267.v1.p1). Funding for AGP was provided from National
   Institutes of Health (HD055751, HD055782, HD055784, HD35465, MH52708,
   MH55284, MH57881, MH061009, MH06359, MH066673, MH080647, MH081754,
   MH66766, NS026630, NS042165, NS049261); The Canadian Institutes for
   Health Research (CIHR); Assistance Publique - Hopitaux de Paris, France;
   Autism Speaks UK; Canada Foundation for Innovation/Ontario Innovation
   Trust; Grant: Po 255/17-4. Deutsche Forschungsgemeinschaft, Germany; EC
   Sixth FP AUTISM MOLGEN; Fundacao Calouste Gulbenkian, Portugal;
   Fondation de France; Fondation FondaMental, France; Fondation Orange,
   France; Fondation pour la Recherche Medicale, France; Fundacao para a
   Ciencia e Tecnologia, Portugal; The Hospital for Sick Children
   Foundation and University of Toronto, Canada; INSERM, France; Institut
   Pasteur, France; Convention 181 of 19.10.2001. Italian Ministry of
   Health; John P Hussman Foundation, USA; McLaughlin Centre, Canada;
   Rubicon 825.06.031. Netherlands Organization for Scientific Research;
   TMF/DA/5801. Royal Netherlands Academy of Arts and Sciences; Ontario
   Ministry of Research and Innovation, Canada; Seaver Foundation, USA;
   Swedish Science Council; The Centre for Applied Genomics, Canada; Utah
   Autism Foundation, USA; Core award 075491/Z/04. Wellcome Trust,
   UK.Genotype and phenotype data were obtained from dbGap, as provided by
   AGP Study Investigators.HealthABC: These controls were obtained from
   Database for Genotypes and Phenotypes (dbGap) at
   http://www.ncbi.nlm.nih.gov/gap. Funding support for the "CIDR Visceral
   Adiposity Study" (Study accession number: phs000169.v1.p1) was provided
   through the Division of Aging Biology and the Division of Geriatrics and
   Clinical Gerontology, NIA. The CIDR Visceral Adiposity Study includes a
   genome-wide association study funded as part of the Division of Aging
   Biology and the Division of Geriatrics and Clinical Gerontology, NIA.
   Assistance with phenotype harmonization and genotype cleaning, as well
   as with general study coordination, was provided by Heath ABC Study
   Investigators.NGRC: We also used the NINDS dbGaP database from the CIDR:
   NGRC Parkinson's Disease Study (dbGap accession number phs000196.v2.p1).
   The genetic arm of the study has been funded by NIH since 1998 (R01
   NS36960, Haydeh Payami, PI). In 2004, the consortium was formalized as a
   Michael J Fox Foundation Funded Global Genetic Consortium, and an
   epidemiologic arm was implemented. Genotype and phenotype data were
   obtained from dbGap, as provided by NGRC Parkinson's Disease Study
   Investigators. For both the HealthABC and NGRC studies, genotyping
   services were provided by the Center for Inherited Disease Research
   (CIDR). CIDR is funded through a federal contract from the National
   Institutes of Health to The Johns Hopkins University, contract number
   HHSN268200782096C and HHSN268201100011I.
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NR 68
TC 72
Z9 73
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 15
PY 2012
VL 3
AR 9
DI 10.1186/2040-2392-3-9
PG 13
WC Genetics & Heredity; Neurosciences
SC Genetics & Heredity; Neurosciences & Neurology
GA 254SX
UT WOS:000327188400001
PM 23067556
ER

PT J
AU Ahmadlou, M
   Adeli, H
   Adeli, A
AF Ahmadlou, Mehran
   Adeli, Hojjat
   Adeli, Amir
TI Improved visibility graph fractality with application for the diagnosis
   of Autism Spectrum Disorder
SO PHYSICA A-STATISTICAL MECHANICS AND ITS APPLICATIONS
LA English
DT Article
DE Visibility graph; Time series; Chaos; Fractal; EEG analysis
ID NEURAL NETWORK METHODOLOGY; WAVELET-CHAOS METHODOLOGY; EEG-BASED
   DIAGNOSIS; ALZHEIMERS-DISEASE; DIMENSION; EPILEPSY; SEIZURE
AB Recently, the visibility graph (VG) algorithm was proposed for mapping a time series to a graph to study complexity and fractality of the time series through investigation of the complexity of its graph. The visibility graph algorithm converts a fractal time series to a scale-free graph. VG has been used for the investigation of fractality in the dynamic behavior of both artificial and natural complex systems. However, robustness and performance of the power of scale-freeness of VG (PSVG) as an effective method for measuring fractality has not been investigated. Since noise is unavoidable in real life time series, the robustness of a fractality measure is of paramount importance. To improve the accuracy and robustness of PSVG to noise for measurement of fractality of time series in biological time-series, an improved PSVG is presented in this paper. The proposed method is evaluated using two examples: a synthetic benchmark time series and a complicated real life Electroencephalograms (EEG)-based diagnostic problem, that is distinguishing autistic children from non-autistic children. It is shown that the proposed improved PSVG is less sensitive to noise and therefore more robust compared with PSVG. Further, it is shown that using improved PSVG in the wavelet-chaos neural network model of Adeli and c-workers in place of the Katz fractality dimension results in a more accurate diagnosis of autism, a complicated neurological and psychiatric disorder. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Adeli, Hojjat] Ohio State Univ, Dept Biomed Engn, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Biomed Informat, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Biomed Informat, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Civil & Environm Engn & Geodet Sci, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Elect & Comp Engn, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Neurol Surg, Columbus, OH 43210 USA.
   [Adeli, Hojjat] Ohio State Univ, Dept Neurosci, Columbus, OH 43210 USA.
   [Ahmadlou, Mehran] Amirkabir Univ, Dept Biomed Engn, Tehran 158754413, Iran.
   [Ahmadlou, Mehran] Dynam Brain Res Off, Tehran, Iran.
   [Adeli, Amir] Ohio State Univ, Dept Neurol, Columbus, OH 43210 USA.
RP Adeli, H (reprint author), Ohio State Univ, Dept Biomed Engn, 470 Hitchcock Hall,2070 Neil Ave, Columbus, OH 43210 USA.
EM adeli.1@osu.edu
RI adeli, hojjat/D-1430-2010
OI adeli, hojjat/0000-0001-5718-1453
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NR 22
TC 28
Z9 28
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0378-4371
J9 PHYSICA A
JI Physica A
PD OCT 15
PY 2012
VL 391
IS 20
BP 4720
EP 4726
DI 10.1016/j.physa.2012.04.025
PG 7
WC Physics, Multidisciplinary
SC Physics
GA 979MY
UT WOS:000306825300018
ER

PT J
AU St-Hilaire, S
   Ezike, VO
   Stryhn, H
   Thomas, MA
AF St-Hilaire, Sophie
   Ezike, Victor O.
   Stryhn, Henrik
   Thomas, Michael A.
TI An ecological study on childhood autism
SO INTERNATIONAL JOURNAL OF HEALTH GEOGRAPHICS
LA English
DT Article
DE Idiopathic autism; Environmental factors; Drinking water; Air
   pollutants; Precipitation
ID TROUT ONCORHYNCHUS-MYKISS; HAZARDOUS AIR-POLLUTANTS; MESSENGER-RNA
   EXPRESSION; HEALTH-RISK ASSESSMENT; SURFACE WATERS;
   POLYCHLORINATED-BIPHENYLS; ORGANOCHLORINE COMPOUNDS; SPECTRUM DISORDERS;
   DRINKING-WATER; BRAIN
AB Background and methods: Idiopathic autism, suspected to be caused by exposure of genetically susceptible individuals to unknown environmental triggers, has increased dramatically in the past 25 years. The objectives of our study were to determine, using a linear regression model, whether the county prevalence of autism in the Pacific Northwest of the United States was associated with the source of drinking water for that county and whether this relationship was dependent on the level of environmental pollutants and meteorological factors in the county.
   Results: We found the previously reported relationship between precipitation and autism in a county was dependent on the amount of drinking water derived from surface sources in the county. We also found a positive association between the EPA's risk of neurological disease and autism, but this relationship was only present in warm areas.
   Conclusions: Our study provides evidence for the hypothesis that environmental factors are associated with autism and that meteorological factors play a role in this relationship.
C1 [St-Hilaire, Sophie; Stryhn, Henrik] Univ Prince Edward Isl, Atlantic Vet Coll, Dept Hlth Management, Charlottetown, PE C1A 4P3, Canada.
   [Ezike, Victor O.; Thomas, Michael A.] Idaho State Univ, Dept Biol Sci, Pocatello, ID 83209 USA.
RP St-Hilaire, S (reprint author), Univ Prince Edward Isl, Atlantic Vet Coll, Dept Hlth Management, 550 Univ Ave, Charlottetown, PE C1A 4P3, Canada.
EM ssthilaire@upei.ca
RI Thomas, Michael/B-7489-2008
OI Thomas, Michael/0000-0003-2982-0291
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NR 50
TC 2
Z9 2
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1476-072X
J9 INT J HEALTH GEOGR
JI Int. J. Health Geogr.
PD OCT 11
PY 2012
VL 11
AR 44
DI 10.1186/1476-072X-11-44
PG 8
WC Public, Environmental & Occupational Health
SC Public, Environmental & Occupational Health
GA 044NM
UT WOS:000311626700001
PM 23051560
ER

PT J
AU Lapenta, OM
   Fregni, F
   Oberman, LM
   Boggio, PS
AF Lapenta, Olivia Morgan
   Fregni, Felipe
   Oberman, Lindsay M.
   Boggio, Paulo Sergio
TI Bilateral temporal cortex transcranial direct current stimulation
   worsens male performance in a multisensory integration task
SO NEUROSCIENCE LETTERS
LA English
DT Article
DE Multisensory integration; tDCS; Superior temporal sulcus; Gender;
   Extreme male brain theory
ID DC STIMULATION; BRAIN; MODULATION; AUTISM
AB Somatosensory integration is a critical cognitive function for human social interaction. Though somatosensory integration has been highly explored in cognitive studies: only a few studies have explored focal modulation of cortical excitability using a speech perception paradigm. In the current study, we aimed to investigate the effects of tDCS applied over the temporal cortex of healthy subjects during a go-no-go task in which stimuli were shapes and non-words. Twenty-eight subjects were randomized to receive cathodal, anodal or sham tDCS bilaterally over the superior temporal cortex (the reference electrode was on deltoid) in a counterbalanced order. The effects on judgment of congruency between shapes and non-words in healthy volunteers were measured by a go-no-go task. Our findings show a significant modification of performance according to the polarity of stimulation, task and subject gender. We found that men performed worse on the no-go condition for congruent stimuli during cathodal tDCS. For reaction time, on the other hand, there was a similar effect for anodal and cathodal stimulation. There were significantly faster responses on incongruent trials during both anodal and cathodal tDCS. Along with previous literature showing gender differences in tasks associated with speech perception, the findings of this study provide additional evidence suggesting that men may have a more focal and restricted neural processing in this multisensory integration task. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
C1 [Lapenta, Olivia Morgan; Boggio, Paulo Sergio] Univ Prebiteriana Mackenzie, Ctr Hlth & Biol Sci, Social & Cognit Neurosci Lab, BR-01241001 Sao Paulo, Brazil.
   [Lapenta, Olivia Morgan; Boggio, Paulo Sergio] Univ Prebiteriana Mackenzie, Ctr Hlth & Biol Sci, Dev Disorders Program, BR-01241001 Sao Paulo, Brazil.
   [Fregni, Felipe] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Boston, MA USA.
   [Fregni, Felipe] Spaulding Rehabil Hosp, Dept Phys Med & Rehabil, Lab Neuromodulat, Boston, MA USA.
   [Fregni, Felipe; Oberman, Lindsay M.] Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Berenson Allen Ctr Noninvas Brain Stimulat, Boston, MA 02215 USA.
RP Boggio, PS (reprint author), Univ Prebiteriana Mackenzie, Ctr Hlth & Biol Sci, Social & Cognit Neurosci Lab, Rua Piaui 181,10 Andar, BR-01241001 Sao Paulo, Brazil.
EM boggio@mackenzie.br
RI Boggio, Paulo/K-6272-2012
OI Boggio, Paulo/0000-0002-6109-0447
FU CNPq [305718/2009-6]; Master grant (CAPES-PROSUP-IES modality I)
FX PSB is supported by a CNPq researcher grant (305718/2009-6). OML was
   supported by a Master grant (CAPES-PROSUP-IES modality I).
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NR 15
TC 6
Z9 6
PU ELSEVIER IRELAND LTD
PI CLARE
PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000,
   IRELAND
SN 0304-3940
J9 NEUROSCI LETT
JI Neurosci. Lett.
PD OCT 11
PY 2012
VL 527
IS 2
BP 105
EP 109
DI 10.1016/j.neulet.2012.08.076
PG 5
WC Neurosciences
SC Neurosciences & Neurology
GA 024EP
UT WOS:000310091800008
PM 22985520
ER

PT J
AU Hammock, EAD
   Levitt, P
AF Hammock, E. A. D.
   Levitt, P.
TI MODULATION OF PARVALBUMIN INTERNEURON NUMBER BY DEVELOPMENTALLY
   TRANSIENT NEOCORTICAL VASOPRESSIN RECEPTOR 1A (V1AR)
SO NEUROSCIENCE
LA English
DT Article
DE C57BL/6J; post-natal development; sex difference; parvalbumin;
   calbindin; vasopressin 1a receptor
ID BINDING-SITES; RAT-BRAIN; SCHIZOPHRENIC-PATIENTS; MONTANE VOLES;
   PSYCHIATRIC-PATIENTS; WATER-INTOXICATION; PROMOTER REGION; AUTISM;
   OXYTOCIN; AVPR1A
AB Arginine-vasopressin (AVP) and the vasopressin la receptor (V1aR) modulate social behavior and learning and memory in adult animals. Both functions depend upon the normal emergence of the balance of excitation and inhibition (E/I balance) in the neocortex. Here, we tested the hypothesis that V1aR signaling and E/I balance converge through the influence of the neuropeptide on interneuron number achieved in the neocortex. Postnatal mapping of forebrain V1aR binding in male and female mice revealed a transient expression of high levels of receptor in the neocortex and hippocampus in the second and third post-natal weeks. Receptor binding levels in these cortical structures fell dramatically in the adult, maintaining high levels of expression subcortically. Surprisingly, we observed sex differences in the number of calbindin interneurons, and a contribution of V1aR to the number of parvalbumin-immunoreactive neurons in the adult mouse neocortex. These data suggest that individual differences in developmentally transient V1aR signaling and even sex may alter the development of E/I balance in the neocortex, with long-lasting influence on information processing. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
C1 [Hammock, E. A. D.] Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37232 USA.
   [Hammock, E. A. D.] Vanderbilt Univ, Vanderbilt Kennedy Ctr, Nashville, TN 37232 USA.
   [Levitt, P.] Univ So Calif, Keck Sch Med, Zilkha Neurogenet Inst, Dept Cell & Neurobiol, Los Angeles, CA 90089 USA.
RP Hammock, EAD (reprint author), Vanderbilt Univ, Sch Med, Dept Pediat, 2215 Garland Ave,Light Hall,Room 1115, Nashville, TN 37232 USA.
EM liz.hammock@vanderbilt.edu; plevitt@med.usc.edu
FU NIMH [080759, T32 MH075883]; NICHD [P30HD15052]
FX Acknowledgements We thank Larry Young, Ph.D. of Emory University for the
   founder mice we used to establish fully congenic Avpr1a mice on a
   C57BL/6J background. We also acknowledge the gifted technical support of
   Caitlin Law, Jennifer Fletcher, Lisa McFayden-Ketchum, Paula Woods,
   Deborah Gregory, Danielle Sganga, Donte Smith and Shelby Smith. Further,
   we would like to thank Louis Muglia, M.D., Ph.D. for facilitating the
   completion of the studies at Vanderbilt University. This work was
   supported by NIMH 080759 (P.L.), T32 MH075883 (E.A.D.H) and NICHD
   P30HD15052 to Vanderbilt University.
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NR 61
TC 4
Z9 5
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 11
PY 2012
VL 222
BP 20
EP 28
DI 10.1016/j.neuroscience.2012.07.025
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 010HM
UT WOS:000309085500003
PM 22820266
ER

PT J
AU Weiss, A
   Neuringer, A
AF Weiss, Alison
   Neuringer, Allen
TI Reinforced variability enhances object exploration in shy and bold rats
SO PHYSIOLOGY & BEHAVIOR
LA English
DT Article
DE Reinforced variability; Shy-bold; Foraging; Novel objects; Enrichment;
   Open field
ID RATTUS-NORVEGICUS; OPEN-FIELD; ANIMALS; BEHAVIOR; DIVERSITY; EXERCISE;
   AUTISM; PEOPLE; STRAIN
AB In an open-field test, the Long-Evans (LE) strain of rats was identified as "bold" and the PVG strain as "shy." Some members of each strain then experienced 14 sessions of a common enrichment procedure, namely exposure to a series of novel objects (Exposed). Others in each strain were explicitly reinforced with food pellets for variable interactions with the same objects (Reinforced). Both experience and strain influenced object interactions. In particular, Reinforced rats interacted more variably with the objects - contacting, probing, pushing and so forth - than did the Exposed; and LEs interacted more variably than PVGs. Foraging proficiency in the same rats was then studied in a transfer-of-training test. Food pellets were hidden among never-before experienced objects and the rats were permitted to explore freely. Reinforced rats discovered and consumed more pellets than Exposed; and LEs discovered and consumed more than PVGs. Thus a bold genetic strain and reinforcement of variability independently contributed to successful foraging behavior. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Weiss, Alison; Neuringer, Allen] Reed Coll, Dept Psychol, Portland, OR 97202 USA.
RP Neuringer, A (reprint author), Reed Coll, Dept Psychol, 3203 SE Woodstock Blvd, Portland, OR 97202 USA.
EM alison.weiss@gmail.com; allen.neuringer@reed.edu
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NR 25
TC 1
Z9 1
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0031-9384
J9 PHYSIOL BEHAV
JI Physiol. Behav.
PD OCT 10
PY 2012
VL 107
IS 3
BP 451
EP 457
DI 10.1016/j.physbeh.2012.07.012
PG 7
WC Psychology, Biological; Behavioral Sciences
SC Psychology; Behavioral Sciences
GA 067PQ
UT WOS:000313308000025
PM 22885121
ER

PT J
AU Jack, A
   Connelly, JJ
   Morris, JP
AF Jack, Allison
   Connelly, Jessica J.
   Morris, James P.
TI DNA methylation of the oxytocin receptor gene predicts neural response
   to ambiguous social stimuli
SO FRONTIERS IN HUMAN NEUROSCIENCE
LA English
DT Article
DE oxytocin receptor gene; functional magnetic resonance imaging (fMRI);
   DNA methylation; epigenetics; social cognition
ID BIOLOGICAL-MOTION; BRAIN IMAGES; HUMANS; PERCEPTION; OXTR; AUTISM;
   TISSUE; ROBUST; FMRI; MIND
AB Oxytocin and its receptor (OXTR) play an important role in a variety of social perceptual and affiliative processes. Individual variability in social information processing likely has a strong heritable component, and as such, many investigations have established an association between common genetic variants of OXTR and variability in the social phenotype. However, to date, these investigations have primarily focused only on changes in the sequence of DNA without considering the role of epigenetic factors. DNA methylation is an epigenetic mechanism by which cells control transcription through modification of chromatin structure. DNA methylation of OXTR decreases expression of the gene and high levels of methylation have been associated with autism spectrum disorders (ASD). This link between epigenetic variability and social phenotype allows for the possibility that social processes are under epigenetic control. We hypothesized that the level of DNA methylation of OXTR would predict individual variability in social perception. Using the brain's sensitivity to displays of animacy as a neural endophenotype of social perception, we found significant associations between the degree of OXTR methylation and brain activity evoked by the perception of animacy. Our results suggest that consideration of DNA methylation may substantially improve our ability to explain individual differences in imaging genetic association studies.
C1 [Connelly, Jessica J.] Univ Virginia, Robert M Berne Cardiovasc Res Ctr, Charlottesville, VA 22908 USA.
   [Connelly, Jessica J.] Univ Virginia, Dept Med, Charlottesville, VA 22908 USA.
   [Connelly, Jessica J.] Univ Virginia, Div Cardiovasc Med, Charlottesville, VA 22908 USA.
   [Jack, Allison; Morris, James P.] Univ Virginia, Dept Psychol, Charlottesville, VA 22908 USA.
RP Connelly, JJ (reprint author), Univ Virginia, Robert M Berne Cardiovasc Res Ctr, 415 Lane Rd, Charlottesville, VA 22908 USA.
EM jessica.connelly@virginia.edu; jpmorris@virginia.edu
FU University of Virginia; NIMH; NHLBI
FX This research was supported by funds provided to Drs. Morris and
   Connelly by the University of Virginia. Dr. Morris was supported by an
   NIMH Pathway to Independence Award Career Development Award. Dr.
   Connelly was supported by an NHLBI Pathway to Independence Career
   Development Award. The authors wish to thank Zoe Englander, Meghan
   Cronk, Themistoclis Karaoli, and Travis Lillard for assistance with this
   project.
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NR 55
TC 26
Z9 26
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 10
PY 2012
VL 6
AR 280
DI 10.3389/fnhum.2012.00280
PG 7
WC Neurosciences; Psychology
SC Neurosciences & Neurology; Psychology
GA 025RK
UT WOS:000310209900001
PM 23087634
ER

PT J
AU Yamasue, H
   Yee, JR
   Hurlemann, R
   Rilling, JK
   Chen, FS
   Meyer-Lindenberg, A
   Tost, H
AF Yamasue, Hidenori
   Yee, Jason R.
   Hurlemann, Rene
   Rilling, James K.
   Chen, Frances S.
   Meyer-Lindenberg, Andreas
   Tost, Heike
TI Integrative Approaches Utilizing Oxytocin to Enhance Prosocial Behavior:
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SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID RECEPTOR GENE OXTR; RANDOMIZED CONTROLLED-TRIAL; HEALTHY CAUCASIAN
   ADULTS; PITUITARY-ADRENAL AXIS; EXTENDED LIMBIC SYSTEM; INTRANASAL
   OXYTOCIN; SPECTRUM DISORDERS; CENTRAL AMYGDALA; BRAIN OXYTOCIN;
   AFFILIATIVE BEHAVIOR
AB The prevalence of autism spectrum disorder (ASD) is as high as 1 in 100 individuals and is a heavy burden to society. Thus, identifying causes and treatments is imperative. Here, we briefly review the topics covered in our 2012 Society for Neuroscience Mini-Symposium entitled "Integrative Approaches Using Oxytocin to Enhance Prosocial Behavior: From Animal and Human Social Behavior to ASD's Social Dysfunction." This work is not meant to be a comprehensive review of oxytocin and prosocial behavior. Instead, we wish to share the newest findings on the effects of oxytocin on social behavior, the brain, and the social dysfunction of ASD at the molecular, genetic, systemic, and behavior levels, in varied subjects ranging from animal models to humans suffering from autism for the purpose of promoting further study for developing the clinical use of oxytocin in treating ASD.
C1 [Yamasue, Hidenori] Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1138655, Japan.
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RP Yamasue, H (reprint author), Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM yamasue-tky@umin.ac.jp
RI Meyer-Lindenberg, Andreas/H-1076-2011; Hurlemann, Rene/G-4164-2012
OI Meyer-Lindenberg, Andreas/0000-0001-5619-1123; Hurlemann,
   Rene/0000-0003-2628-565X
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NR 155
TC 51
Z9 51
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 10
PY 2012
VL 32
IS 41
BP 14109
EP +
DI 10.1523/JNEUROSCI.3327-12.2012
PG 10
WC Neurosciences
SC Neurosciences & Neurology
GA 022MO
UT WOS:000309963700010
PM 23055480
ER

PT J
AU Hyman, SE
AF Hyman, Steven E.
TI Revolution Stalled
SO SCIENCE TRANSLATIONAL MEDICINE
LA English
DT Article
ID PSYCHIATRIC-DISORDERS; NEUROPSYCHIATRIC DISORDERS;
   CHRONIC-SCHIZOPHRENIA; ANTIPSYCHOTIC-DRUGS; ANIMAL-MODELS; DEPRESSION;
   MEDICINE; BRAIN; TRIAL
AB Drug discovery is at a near standstill for treating psychiatric disorders such as schizophrenia, bipolar disorder, depression, and common forms of autism. Despite high prevalence and unmet medical need, major pharmaceutical companies are deemphasizing or exiting psychiatry, thus removing significant capacity from efforts to discover new medicines. In this Commentary, I develop a view of what has gone wrong scientifically and ask what can be done to address this parlous situation.
C1 Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
RP Hyman, SE (reprint author), Broad Inst MIT & Harvard, Cambridge, MA 02142 USA.
EM seh@harvard.edu
FU Stanley Foundation
FX Funding: This work was supported by the Stanley Foundation.
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NR 32
TC 16
Z9 16
PU AMER ASSOC ADVANCEMENT SCIENCE
PI WASHINGTON
PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA
SN 1946-6234
J9 SCI TRANSL MED
JI Sci. Transl. Med.
PD OCT 10
PY 2012
VL 4
IS 155
AR 155cm11
DI 10.1126/scitranslmed.3003142
PG 5
WC Cell Biology; Medicine, Research & Experimental
SC Cell Biology; Research & Experimental Medicine
GA 022NT
UT WOS:000309966800001
PM 23052291
ER

PT J
AU Uematsu, A
   Matsui, M
   Tanaka, C
   Takahashi, T
   Noguchi, K
   Suzuki, M
   Nishijo, H
AF Uematsu, Akiko
   Matsui, Mie
   Tanaka, Chiaki
   Takahashi, Tsutomu
   Noguchi, Kyo
   Suzuki, Michio
   Nishijo, Hisao
TI Developmental Trajectories of Amygdala and Hippocampus from Infancy to
   Early Adulthood in Healthy Individuals
SO PLOS ONE
LA English
DT Article
ID NORMAL BRAIN-DEVELOPMENT; TEMPORAL-LOBE; GRAY-MATTER; VOLUME; CHILDREN;
   AUTISM; MRI; ADOLESCENCE; METABOLISM; MATURATION
AB Knowledge of amygdalar and hippocampal development as they pertain to sex differences and laterality would help to understand not only brain development but also the relationship between brain volume and brain functions. However, few studies investigated development of these two regions, especially during infancy. The purpose of this study was to examine typical volumetric trajectories of amygdala and hippocampus from infancy to early adulthood by predicting sexual dimorphism and laterality. We performed a cross-sectional morphometric MRI study of amygdalar and hippocampal growth from 1 month to 25 years old, using 109 healthy individuals. The findings indicated significant non-linear age-related volume changes, especially during the first few years of life, in both the amygdala and hippocampus regardless of sex. The peak ages of amygdalar and hippocampal volumes came at the timing of preadolescence (9-11 years old). The female amygdala reached its peak age about one year and a half earlier than the male amygdala did. In addition, its rate of growth change decreased earlier in the females. Furthermore, both females and males displayed rightward laterality in the hippocampus, but only the males in the amygdala. The robust growth of the amygdala and hippocampus during infancy highlight the importance of this period for neural and functional development. The sex differences and laterality during development of these two regions suggest that sex-related factors such as sex hormones and functional laterality might affect brain development.
C1 [Uematsu, Akiko; Matsui, Mie] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Psychol, Toyama 930, Japan.
   [Tanaka, Chiaki] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Pediat, Toyama 930, Japan.
   [Takahashi, Tsutomu; Suzuki, Michio] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Neuropsychiat, Toyama 930, Japan.
   [Noguchi, Kyo] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Radiol, Toyama 930, Japan.
   [Nishijo, Hisao] Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Syst Emot Sci, Toyama 930, Japan.
RP Matsui, M (reprint author), Toyama Univ, Grad Sch Med & Pharmaceut Sci, Dept Psychol, Toyama 930, Japan.
EM mmatsui@las.u-toyama.ac.jp
FU Japan Society for the Promotion of Science (JSPS) [20330141, 21243040];
   JSPS Asian Core Program
FX This study was supported by a Grant-in-Aid for Scientific Research (B)
   20330141 and (A) 21243040 from the Japan Society for the Promotion of
   Science (JSPS) and JSPS Asian Core Program. 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 37
TC 27
Z9 28
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 2012
VL 7
IS 10
AR e46970
DI 10.1371/journal.pone.0046970
PG 10
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 021MR
UT WOS:000309889400040
PM 23056545
ER

PT J
AU Xiao, T
   Xiao, Z
   Ke, XY
   Hong, SS
   Yang, HY
   Su, YL
   Chu, KK
   Xiao, X
   Shen, JY
   Liu, YJ
AF Xiao, Ting
   Xiao, Zhou
   Ke, Xiaoyan
   Hong, Shanshan
   Yang, Hongyu
   Su, Yanli
   Chu, Kangkang
   Xiao, Xiang
   Shen, Jiying
   Liu, Yijun
TI Response Inhibition Impairment in High Functioning Autism and Attention
   Deficit Hyperactivity Disorder: Evidence from Near-Infrared Spectroscopy
   Data
SO PLOS ONE
LA English
DT Article
ID INFERIOR PREFRONTAL CORTEX; SPECTRUM DISORDER; EXECUTIVE FUNCTIONS;
   COGNITIVE CONTROL; MOTOR INHIBITION; STROOP TASK; CHILDREN; ACTIVATION;
   ADHD; COMMON
AB Background: Response inhibition, an important domain of executive function (EF), involves the ability to suppress irrelevant or interfering information and impulses. Previous studies have shown impairment of response inhibition in high functioning autism (HFA) and attention deficit hyperactivity disorder (ADHD), but more recent findings have been inconsistent. To date, almost no studies have been conducted using functional imaging techniques to directly compare inhibitory control between children with HFA and those with ADHD.
   Method: Nineteen children with HFA, 16 age-and intelligence quotient (IQ)-matched children with ADHD, and 16 typically developing (TD) children were imaged using functional near-infrared spectroscopy (NIRS) while performing Go/No-go and Stroop tasks.
   Results: Compared with the TD group, children in both the HFA and ADHD groups took more time to respond during the No-go blocks, with reaction time longest for HFA and shortest for TD. Children in the HFA and ADHD groups also made a greater number of reaction errors in the No-go blocks than those in the TD group. During the Stroop task, there were no significant differences between these three groups in reaction time and omission errors. Both the HFA and ADHD groups showed a higher level of inactivation in the right prefrontal cortex (PFC) during the No-go blocks, relative to the TD group. However, no significant differences were found between groups in the levels of oxyhemoglobin concentration in the PFC during the Stroop task.
   Conclusion: Functional brain imaging using NIRS showed reduced activation in the right PFC in children with HFA or ADHD during an inhibition task, indicating that inhibitory dysfunction is a shared feature of both HFA and ADHD.
C1 [Xiao, Ting; Xiao, Zhou; Ke, Xiaoyan; Su, Yanli; Chu, Kangkang; Xiao, Xiang; Shen, Jiying] Nanjing Med Univ, Nanjing Brain Hosp, Child Mental Hlth Res Ctr, Nanjing, Jiangsu, Peoples R China.
   [Hong, Shanshan; Yang, Hongyu] Southeast Univ, Key Lab Child Dev & Learning Sci, Nanjing, Jiangsu, Peoples R China.
   [Liu, Yijun] Univ Florida, Dept Psychiat, Gainesville, FL 32611 USA.
   [Liu, Yijun] Univ Florida, McKnight Brain Inst, Gainesville, FL USA.
RP Ke, XY (reprint author), Nanjing Med Univ, Nanjing Brain Hosp, Child Mental Hlth Res Ctr, Nanjing, Jiangsu, Peoples R China.
EM kexynj@hotmail.com
FU Health Research Projects of JiangSu [H200948]; National Natural Science
   Foundation of China [81071111]; Key Program of Medical Development of
   Nanjing [ZKX10023]
FX The work was supported by the Health Research Projects of JiangSu (No.
   H200948), the National Natural Science Foundation of China (No.
   81071111) and the Key Program of Medical Development of Nanjing (No.
   ZKX10023). 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 36
TC 15
Z9 16
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 2012
VL 7
IS 10
AR e46569
DI 10.1371/journal.pone.0046569
PG 7
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 021MR
UT WOS:000309889400018
PM 23056348
ER

PT J
AU Hui, W
   Chen, C
   Hsieh, FS
AF Hui Wang
   Chen Chen
   Hsieh Fushing
TI Extracting Multiscale Pattern Information of fMRI Based Functional Brain
   Connectivity with Application on Classification of Autism Spectrum
   Disorders
SO PLOS ONE
LA English
DT Article
ID COGNITIVE CONTROL; TASK; SCHIZOPHRENIA; NETWORKS; CHILDREN;
   UNDERCONNECTIVITY; DISCONNECTION; DIAGNOSIS; STATE; MRI
AB We employed a multi-scale clustering methodology known as "data cloud geometry" to extract functional connectivity patterns derived from functional magnetic resonance imaging (fMRI) protocol. The method was applied to correlation matrices of 106 regions of interest (ROIs) in 29 individuals with autism spectrum disorders (ASD), and 29 individuals with typical development (TD) while they completed a cognitive control task. Connectivity clustering geometry was examined at both "fine" and "coarse" scales. At the coarse scale, the connectivity clustering geometry produced 10 valid clusters with a coherent relationship to neural anatomy. A supervised learning algorithm employed fine scale information about clustering motif configurations and prevalence, and coarse scale information about intra-and inter-regional connectivity; the algorithm correctly classified ASD and TD participants with sensitivity of 82.8% and specificity of 82.8%. Most of the predictive power of the logistic regression model resided at the level of the fine-scale clustering geometry, suggesting that cellular versus systems level disturbances are more prominent in individuals with ASD. This article provides validation for this multi-scale geometric approach to extracting brain functional connectivity pattern information and for its use in classification of ASD.
C1 [Hui Wang; Chen Chen; Hsieh Fushing] Univ Calif Davis, Dept Stat, Davis, CA 95616 USA.
RP Hsieh, FS (reprint author), Univ Calif Davis, Dept Stat, Davis, CA 95616 USA.
EM fushing@wald.ucdavis.edu
FU National Science Foundation (NSF) [DMS-1007219]
FX This research was partly supported by National Science Foundation (NSF)
   grant: DMS-1007219. The funders had no role in study design, data
   collection and analysis, decision to publish, or preparation of the
   manuscript. No additional external funding received for this study.
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NR 34
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 OCT 8
PY 2012
VL 7
IS 10
AR e45502
DI 10.1371/journal.pone.0045502
PG 14
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 020RP
UT WOS:000309831500019
ER

PT J
AU Baudouin, SJ
   Gaudias, J
   Gerharz, S
   Hatstatt, L
   Zhou, KK
   Punnakkal, P
   Tanaka, KF
   Spooren, W
   Hen, R
   De Zeeuw, CI
   Vogt, K
   Scheiffele, P
AF Baudouin, Stephane J.
   Gaudias, Julien
   Gerharz, Stefan
   Hatstatt, Laetitia
   Zhou, Kuikui
   Punnakkal, Pradeep
   Tanaka, Kenji F.
   Spooren, Will
   Hen, Rene
   De Zeeuw, Chris I.
   Vogt, Kaspar
   Scheiffele, Peter
TI Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent
   Models of Autism
SO SCIENCE
LA English
DT Article
ID LONG-TERM DEPRESSION; RARE DE-NOVO; NEUROLIGINS; MUTATIONS; MICE;
   CEREBELLUM; SYNAPSES; RECEPTOR; DISEASE; PROTEIN
AB The genetic heterogeneity of autism poses a major challenge for identifying mechanism-based treatments. A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their multifaceted symptoms and have revealed specific defects in synaptic plasticity. We discovered an unexpected convergence of synaptic pathophysiology in a nonsyndromic form of autism with those in fragile X syndrome. Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor-dependent synaptic plasticity, a hallmark of fragile X. These phenotypes could be rescued by reexpression of neuroligin-3 in juvenile mice, highlighting the possibility of reverting neuronal circuit alterations in autism after the completion of development.
C1 [Baudouin, Stephane J.; Gaudias, Julien; Gerharz, Stefan; Hatstatt, Laetitia; Punnakkal, Pradeep; Vogt, Kaspar; Scheiffele, Peter] Univ Basel, Biozentrum, Basel, Switzerland.
   [Zhou, Kuikui; De Zeeuw, Chris I.] Erasmus MC, Dept Neurosci, Rotterdam, Netherlands.
   [Tanaka, Kenji F.; Hen, Rene] Columbia Univ, Dept Neurosci, New York, NY USA.
   [Tanaka, Kenji F.] Keio Univ, Sch Med, Dept Neuropsychiat, Tokyo, Japan.
   [Spooren, Will] Hoffmann La Roche AG, Basel, Switzerland.
   [De Zeeuw, Chris I.] Royal Netherlands Acad Arts & Sci, Netherlands Inst Neurosci, Amsterdam, Netherlands.
RP Scheiffele, P (reprint author), Univ Basel, Biozentrum, Basel, Switzerland.
EM peter.scheiffele@unibas.ch
RI baudouin, stephane/I-4372-2012
FU Dutch Organization for Medical Sciences (ZonMw); Life Sciences (ALW);
   Senter (NeuroBasic); Prinses Beatrix Fonds; European Research Council
   (European Community); SystemsX grant; EU-AIMS (European Autism
   Interventions); Innovative Medicines Initiative [115300]; European
   Union; European Federation of Pharmaceutical Industries and Associations
   companies'; NCCR Synapsy; Swiss National Science Foundation; Kanton
   Basel-Stadt
FX We are grateful to our colleagues Arber, Barde, Gosh, Sylwestrak, Witte,
   and Xiao for comments on the manuscript; to Ponti, Genoud, Sauder,
   Ahrne, Ehrenfeuchter, and Stiefvater for technical help; and Zeilhofer,
   Fritschy, Brose, and Sans for sharing reagents. C.D.Z. was supported by
   the Dutch Organization for Medical Sciences (ZonMw); Life Sciences
   (ALW); Senter (NeuroBasic); Prinses Beatrix Fonds; and the European
   Research Council-advanced, CEREBNET, and C7 programs (European
   Community). This work was supported by a SystemsX grant (P.S. and W.S.);
   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 FP7/2007-2013), 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; by NCCR
   Synapsy; the Swiss National Science Foundation; and Kanton Basel-Stadt.
CR American Psychiatric Association Task Force on DSM-IV, 2000, DIAGN STAT MAN MENT, V4th
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NR 30
TC 69
Z9 69
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 5
PY 2012
VL 338
IS 6103
BP 128
EP 132
DI 10.1126/science.1224159
PG 5
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 015PC
UT WOS:000309457400069
PM 22983708
ER

PT J
AU Capra, V
   Mirabelli-Badenier, M
   Stagnaro, M
   Rossi, A
   Tassano, E
   Gimelli, S
   Gimelli, G
AF Capra, Valeria
   Mirabelli-Badenier, Marisol
   Stagnaro, Michela
   Rossi, Andrea
   Tassano, Elisa
   Gimelli, Stefania
   Gimelli, Giorgio
TI Identification of a rare 17p13.3 duplication including the BHLHA9 and
   YWHAE genes in a family with developmental delay and behavioural
   problems
SO BMC MEDICAL GENETICS
LA English
DT Article
DE Familial 17p13.3 duplication syndrome; PAFAH1B1 and YWHAE genes;
   Array-CGH
ID MICRODUPLICATIONS; MICRODELETIONS; DELINEATION
AB Background: Deletions and duplications of the PAFAH1B1 and YWHAE genes in 17p13.3 are associated with different clinical phenotypes. In particular, deletion of PAFAH1B1 causes isolated lissencephaly while deletions involving both PAFAH1B1 and YWHAE cause Miller-Dieker syndrome. Isolated duplications of PAFAH1B1 have been associated with mild developmental delay and hypotonia, while isolated duplications of YWHAE have been associated with autism. In particular, different dysmorphic features associated with PAFAH1B1 or YWHAE duplication have suggested the need to classify the patient clinical features in two groups according to which gene is involved in the chromosomal duplication.
   Methods: We analyze the proband and his family by classical cytogenetic and array-CGH analyses. The putative rearrangement was confirmed by fluorescence in situ hybridization.
   Results: We have identified a family segregating a 17p13.3 duplication extending 329.5 kilobases by FISH and array-CGH involving the YWHAE gene, but not PAFAH1B1, affected by a mild dysmorphic phenotype with associated autism and mental retardation. We propose that BHLHA9, YWHAE, and CRK genes contribute to the phenotype of our patient. The small chromosomal duplication was inherited from his mother who was affected by a bipolar and borderline disorder and was alcohol addicted.
   Conclusions: We report an additional familial case of small 17p13.3 chromosomal duplication including only BHLHA9, YWHAE, and CRK genes. Our observation and further cases with similar microduplications are expected to be diagnosed, and will help better characterise the clinical spectrum of phenotypes associated with 17p13.3 microduplications.
C1 [Tassano, Elisa; Gimelli, Giorgio] Ist Giannina Gaslini, Lab Citogenet, I-16148 Genoa, Italy.
   [Capra, Valeria] Ist Giannina Gaslini, UO Neurochirurg, I-16148 Genoa, Italy.
   [Mirabelli-Badenier, Marisol; Stagnaro, Michela] Ist Giannina Gaslini, UO Neuropsichiatria, I-16148 Genoa, Italy.
   [Rossi, Andrea] Ist Giannina Gaslini, Dipartimento Neuroradiol, I-16148 Genoa, Italy.
   [Gimelli, Stefania] Univ Hosp Geneva, Serv Genet Med, Geneva, Switzerland.
RP Gimelli, G (reprint author), Ist Giannina Gaslini, Lab Citogenet, I-16148 Genoa, Italy.
EM giorgio.gimelli@gmail.com
RI Rossi, Andrea/A-4146-2011
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NR 12
TC 8
Z9 8
PU BIOMED CENTRAL LTD
PI LONDON
PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND
SN 1471-2350
J9 BMC MED GENET
JI BMC Med. Genet.
PD OCT 4
PY 2012
VL 13
AR 93
DI 10.1186/1471-2350-13-93
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 037ZO
UT WOS:000311145200001
PM 23035971
ER

PT J
AU Lesch, KP
   Waider, J
AF Lesch, Klaus-Peter
   Waider, Jonas
TI Serotonin in the Modulation of Neural Plasticity and Networks:
   Implications for Neurodevelopmental Disorders
SO NEURON
LA English
DT Review
ID DEFICIT HYPERACTIVITY DISORDER; AUTISM SPECTRUM DISORDERS; CELL-ADHESION
   MOLECULES; DE-NOVO MUTATIONS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER;
   5-HT1A RECEPTOR EXPRESSION; TRANSPORTER KNOCKOUT MICE; MONKEY PREFRONTAL
   CORTEX; LOCAL PROTEIN-SYNTHESIS; LONG-TERM FACILITATION
AB Serotonin (5-HT) shapes brain networks during development and modulates a wide spectrum of essential neuronal functions ranging from perception and cognitive appraisal to emotional responses in the mature brain. Deficits in 5-HT-moderated synaptic signaling fundamentally impact the pathophysiology and long-term outcome of neurodevelopmental disorders. Our understanding of how 5-HT-dependent modulation of circuit configuration influences social cognition and emotional learning has been enhanced by recent insight into the molecular and cellular mechanisms of synapse formation and plasticity. In this review, we discuss emerging concepts as to how defects in synaptic plasticity impact our biosocial brain and how recent findings regarding 5-HT's role in brain development and function provide insight into the cellular and physiological basis of neurodevelopmental disorders.
C1 [Lesch, Klaus-Peter; Waider, Jonas] Univ Wurzburg, Dept Psychiat Psychosomat & Psychotherapy, ADHD Clin Res Network, Div Mol Psychiat,Lab Translat Neurosci, D-97080 Wurzburg, Germany.
   [Lesch, Klaus-Peter] Maastricht Univ, Sch Mental Hlth & Neurosci, Dept Neurosci, NL-6211 LK Maastricht, Netherlands.
RP Lesch, KP (reprint author), Univ Wurzburg, Dept Psychiat Psychosomat & Psychotherapy, ADHD Clin Res Network, Div Mol Psychiat,Lab Translat Neurosci, D-97080 Wurzburg, Germany.
EM kplesch@mail.uni-wuerzburg.de
RI Lesch, Klaus-Peter/J-4906-2013
OI Lesch, Klaus-Peter/0000-0001-8348-153X
FU Deutsche Forschungsgemeinschaft [SFB 581/B9, SFB TRR 58/A1, SFB TRR
   58/A5, KFO 125]
FX We apologize to colleagues whose work could not be cited due to space
   limitations. The writing of this article and the authors' related
   research were supported by the Deutsche Forschungsgemeinschaft (SFB
   581/B9, SFB TRR 58/A1 and A5, KFO 125). The authors thank J. Stilla and
   G. Lesch for assistance in generating graphical material. The authors
   are also grateful to C. Gross for his critical comments.
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NR 166
TC 51
Z9 52
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 4
PY 2012
VL 76
IS 1
BP 175
EP 191
DI 10.1016/j.neuron.2012.09.013
PG 17
WC Neurosciences
SC Neurosciences & Neurology
GA 020HG
UT WOS:000309799000013
PM 23040814
ER

PT J
AU Girirajan, S
   Rosenfeld, JA
   Coe, BP
   Parikh, S
   Friedman, N
   Goldstein, A
   Filipink, RA
   McConnell, JS
   Angle, B
   Meschino, WS
   Nezarati, MM
   Asamoah, A
   Jackson, KE
   Gowans, GC
   Martin, JA
   Carmany, EP
   Stockton, DW
   Schnur, RE
   Penney, LS
   Martin, DM
   Raskin, S
   Leppig, K
   Thiese, H
   Smith, R
   Aberg, E
   Niyazov, DM
   Escobar, LF
   El-Khechen, D
   Johnson, KD
   Lebel, RR
   Siefkas, K
   Ball, S
   Shur, N
   McGuire, M
   Brasington, CK
   Spence, JE
   Martin, LS
   Clericuzio, C
   Ballif, BC
   Shaffer, LG
   Eichler, EE
AF Girirajan, Santhosh
   Rosenfeld, Jill A.
   Coe, Bradley P.
   Parikh, Sumit
   Friedman, Neil
   Goldstein, Amy
   Filipink, Robyn A.
   McConnell, Juliann S.
   Angle, Brad
   Meschino, Wendy S.
   Nezarati, Marjan M.
   Asamoah, Alexander
   Jackson, Kelly E.
   Gowans, Gordon C.
   Martin, Judith A.
   Carmany, Erin P.
   Stockton, David W.
   Schnur, Rhonda E.
   Penney, Lynette S.
   Martin, Donna M.
   Raskin, Salmo
   Leppig, Kathleen
   Thiese, Heidi
   Smith, Rosemarie
   Aberg, Erika
   Niyazov, Dmitriy M.
   Escobar, Luis F.
   El-Khechen, Dima
   Johnson, Kisha D.
   Lebel, Robert R.
   Siefkas, Kiana
   Ball, Susie
   Shur, Natasha
   McGuire, Marianne
   Brasington, Campbell K.
   Spence, J. Edward
   Martin, Laura S.
   Clericuzio, Carol
   Ballif, Blake C.
   Shaffer, Lisa G.
   Eichler, Evan E.
TI Phenotypic Heterogeneity of Genomic Disorders and Rare Copy-Number
   Variants
SO NEW ENGLAND JOURNAL OF MEDICINE
LA English
DT Article
ID SMITH-MAGENIS-SYNDROME; MICRODELETION SYNDROME; DEVELOPMENTAL DELAY;
   MENTAL-RETARDATION; MULTIPLE GENES; AUTISM; SCHIZOPHRENIA; 16P11.2;
   MICRODUPLICATIONS; REARRANGEMENTS
AB Background
   Some copy-number variants are associated with genomic disorders with extreme phenotypic heterogeneity. The cause of this variation is unknown, which presents challenges in genetic diagnosis, counseling, and management.
   Methods
   We analyzed the genomes of 2312 children known to carry a copy- number variant associated with intellectual disability and congenital abnormalities, using array comparative genomic hybridization.
   Results
   Among the affected children, 10.1% carried a second large copy-number variant in addition to the primary genetic lesion. We identified seven genomic disorders, each defined by a specific copy-number variant, in which the affected children were more likely to carry multiple copy-number variants than were controls. We found that syndromic disorders could be distinguished from those with extreme phenotypic heterogeneity on the basis of the total number of copy-number variants and whether the variants are inherited or de novo. Children who carried two large copy-number variants of unknown clinical significance were eight times as likely to have developmental delay as were controls (odds ratio, 8.16; 95% confidence interval, 5.33 to 13.07; P = 2.11x10(-38)). Among affected children, inherited copy-number variants tended to co-occur with a second-site large copy-number variant (Spearman correlation coefficient, 0.66; P < 0.001). Boys were more likely than girls to have disorders of phenotypic heterogeneity (P < 0.001), and mothers were more likely than fathers to transmit second-site copy-number variants to their offspring (P = 0.02).
   Conclusions
   Multiple, large copy-number variants, including those of unknown pathogenic significance, compound to result in a severe clinical presentation, and secondary copy-number variants are preferentially transmitted from maternal carriers. (Funded by the Simons Foundation Autism Research Initiative and the National Institutes of Health.)
C1 [Eichler, Evan E.] Univ Washington, Sch Med, Howard Hughes Med Inst, Dept Genome Sci, Seattle, WA 98195 USA.
   [Rosenfeld, Jill A.; Ballif, Blake C.; Shaffer, Lisa G.] PerkinElmer, Signature Genom Labs, Spokane, WA USA.
   [Martin, Judith A.] Providence Sacred Heart Hosp, Spokane, WA USA.
   [Leppig, Kathleen; Thiese, Heidi] Grp Hlth Cooperat Puget Sound, Seattle, WA USA.
   [Siefkas, Kiana; Ball, Susie] Yakima Valley Mem Hosp, Yakima, WA USA.
   [Parikh, Sumit; Friedman, Neil] Cleveland Clin, Cleveland, OH USA.
   [Goldstein, Amy; Filipink, Robyn A.] Univ Pittsburgh, Childrens Hosp Pittsburgh, Div Child Neurol, Med Ctr, Pittsburgh, PA 15213 USA.
   [McConnell, Juliann S.; McGuire, Marianne] Univ Pittsburgh, Childrens Hosp Pittsburgh, Dept Pediat, Med Ctr, Pittsburgh, PA 15213 USA.
   [McGuire, Marianne] Univ Pittsburgh, Sch Med, Dept Pediat, Pittsburgh, PA 15261 USA.
   [Angle, Brad] Rush Univ, Med Ctr, Ann & Robert H Lurie Childrens Hosp, Chicago, IL 60612 USA.
   [Johnson, Kisha D.] Rush Univ, Med Ctr, Dept Pediat, Chicago, IL 60612 USA.
   [Meschino, Wendy S.; Nezarati, Marjan M.] N York Gen Hosp, Toronto, ON, Canada.
   [Penney, Lynette S.] Dalhousie Univ, Dept Pediat, Halifax, NS, Canada.
   [Aberg, Erika] Izaak Walton Killam Hlth Ctr, Halifax, NS, Canada.
   [Asamoah, Alexander; Jackson, Kelly E.; Gowans, Gordon C.] Univ Louisville, Dept Pediat, Weisskopf Child Evaluat Ctr, Louisville, KY 40292 USA.
   [Carmany, Erin P.; Stockton, David W.] Childrens Hosp Michigan, Detroit, MI 48201 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.
   [Schnur, Rhonda E.] Rowan Univ, Cooper Med Sch, Dept Pediat, Div Genet, Camden, NJ USA.
   [Raskin, Salmo] Pontificia Univ Catolica Parana, Ctr Biol & Hlth Sci, Grad Program Hlth Sci, Grp Adv Mol Invest, Curitiba, Parana, Brazil.
   [Raskin, Salmo] Ctr Aconselhamento & Lab Genet, Curitiba, Parana, Brazil.
   [Niyazov, Dmitriy M.] Ochsner Clin Fdn, Dept Pediat, New Orleans, LA USA.
   [Escobar, Luis F.; El-Khechen, Dima] Peyton Manning Childrens Hosp St Vincent, Indianapolis, IN USA.
   [Lebel, Robert R.] SUNY Upstate Med Univ, Syracuse, NY USA.
   [Shur, Natasha] Rhode Isl Hosp, Hasbro Childrens Hosp, Providence, RI USA.
   [Brasington, Campbell K.; Spence, J. Edward] Carolinas Med Ctr, Levine Childrens Hosp, Dept Pediat, Charlotte, NC 28203 USA.
   [Martin, Laura S.] Nemours Childrens Clin, Jacksonville, FL USA.
   [Clericuzio, Carol] Univ New Mexico, Div Pediat Genet, Hlth Sci Ctr, Div Clin Genet Dysmorphol, Albuquerque, NM 87131 USA.
RP Eichler, EE (reprint author), Univ Washington, Sch Med, Howard Hughes Med Inst, Dept Genome Sci, Foege S-413A,Box 355065,3720 15th Ave NE, Seattle, WA 98195 USA.
EM eee@gs.washington.edu
FU Simons Foundation Autism Research Initiative; National Institutes of
   Health
FX Funded by the Simons Foundation Autism Research Initiative and the
   National Institutes of Health.
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NR 38
TC 128
Z9 131
PU MASSACHUSETTS MEDICAL SOC
PI WALTHAM
PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA
SN 0028-4793
J9 NEW ENGL J MED
JI N. Engl. J. Med.
PD OCT 4
PY 2012
VL 367
IS 14
BP 1321
EP 1331
DI 10.1056/NEJMoa1200395
PG 11
WC Medicine, General & Internal
SC General & Internal Medicine
GA 014WJ
UT WOS:000309406100008
PM 22970919
ER

PT J
AU Marley, A
   von Zastrow, M
AF Marley, Aaron
   von Zastrow, Mark
TI A Simple Cell-Based Assay Reveals That Diverse Neuropsychiatric Risk
   Genes Converge on Primary Cilia
SO PLOS ONE
LA English
DT Article
ID CANDIDATE GENE; SCHIZOPHRENIA; PROTEIN; CILIOGENESIS; MUTATIONS;
   INTERACTS; DISEASE; DISRUPTED-IN-SCHIZOPHRENIA-1; TRANSLOCATION;
   CILIOPATHY
AB Human genetic studies are beginning to identify a large number of genes linked to neuropsychiatric disorders. It is increasingly evident that different genes contribute to risk for similar syndromes and, conversely, the same genes or even the same alleles cross over traditional diagnostic categories. A current challenge is to understand the cellular biology of identified risk genes. However, most genes associated with complex neuropsychiatric phenotypes are not related through a known biochemical pathway, and many have an entirely unknown cellular function. One possibility is that diverse disease-linked genes converge at a higher-level cellular structure. The synapse is already known to be one such convergence, and emerging evidence suggests the primary cilium as another. Because many genes associated with neuropsychiatric illness are expressed also outside the nervous system, as are cilia, we tested the hypothesis that such genes affect conserved features of the primary cilium. Using RNA interference to test 41 broadly expressed candidate genes associated with schizophrenia, bipolar affective disorder, autism spectrum disorder and intellectual disability, we found 20 candidates that reduce ciliation in NIH3T3 cells when knocked down, and three whose manipulation increases cilia length. Three of the candidate genes were previously implicated in cilia formation and, altogether, approximately half of the candidates tested produced a ciliary phenotype. Our results support the hypothesis that primary cilia indeed represent a conserved cellular structure at which the effects of diverse neuropsychiatric risk genes converge. More broadly, they suggest a relatively simple cell-based approach that may be useful for exploring the complex biological underpinnings of neuropsychiatric disease.
C1 [von Zastrow, Mark] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
   Univ Calif San Francisco, Dept Cellular & Mol Pharmacol, San Francisco, CA 94143 USA.
RP von Zastrow, M (reprint author), Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA.
EM mark.vonzastrow@ucsf.edu
FU National Institutes of Health (NIH) [DA010154]; Friends of Langley
   Porter Endowed Chair for Research in Schizophrenia and Depression
FX These studies were supported by the National Institutes of Health (NIH)
   (DA010154) and the Friends of Langley Porter Endowed Chair for Research
   in Schizophrenia and Depression. 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 34
TC 6
Z9 6
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 2012
VL 7
IS 10
AR e46647
DI 10.1371/journal.pone.0046647
PG 11
WC Multidisciplinary Sciences
SC Science & Technology - Other Topics
GA 015NU
UT WOS:000309454000068
PM 23056384
ER

PT J
AU Kron, M
   Howell, CJ
   Adams, IT
   Ransbottom, M
   Christian, D
   Ogier, M
   Katz, DM
AF Kron, Miriam
   Howell, C. James
   Adams, Ian T.
   Ransbottom, Michael
   Christian, Diana
   Ogier, Michael
   Katz, David M.
TI Brain Activity Mapping in Mecp2 Mutant Mice Reveals Functional Deficits
   in Forebrain Circuits, Including Key Nodes in the Default Mode Network,
   that are Reversed with Ketamine Treatment
SO JOURNAL OF NEUROSCIENCE
LA English
DT Article
ID CPG-BINDING PROTEIN-2; NUCLEUS-TRACTUS-SOLITARIUS; MIDBRAIN
   PERIAQUEDUCTAL GRAY; 2/3 PYRAMIDAL NEURONS; C-FOS EXPRESSION;
   RETT-SYNDROME; MOUSE MODEL; RETROSPLENIAL CORTICES;
   SYNAPTIC-TRANSMISSION; POSTERIOR CINGULATE
AB Excitatory-inhibitory imbalance has been identified within specific brain microcircuits in models of Rett syndrome (RTT) and other autism spectrum disorders (ASDs). However, macrocircuit dysfunction across the RTT brain as a whole has not been defined. To approach this issue, we mapped expression of the activity-dependent, immediate-early gene product Fos in the brains of wild-type (Wt) and methyl-CpG-binding protein 2 (Mecp2)-null (Null) mice, a model of RTT, before and after the appearance of overt symptoms (3 and 6 weeks of age, respectively). At 6 weeks, Null mice exhibit significantly less Fos labeling than Wt in limbic cortices and subcortical structures, including key nodes in the default mode network. In contrast, Null mice exhibit significantly more Fos labeling than Wt in the hindbrain, most notably in cardiorespiratory regions of the nucleus tractus solitarius (nTS). Using nTS as a model, whole-cell recordings demonstrated that increased Fos expression in Nulls at 6 weeks of age is associated with synaptic hyperexcitability, including increased frequency of spontaneous and miniature EPSCs and increased amplitude of evoked EPSCs in Nulls. No such effect of genotype on Fos or synaptic function was seen at 3 weeks. In the mutant forebrain, reduced Fos expression, as well as abnormal sensorimotor function, were reversed by the NMDA receptor antagonist ketamine. In light of recent findings that the default mode network is hypoactive in autism, our data raise the possibility that hypofunction within this meta-circuit is a shared feature of RTT and other ASDs and is reversible.
C1 [Kron, Miriam; Howell, C. James; Adams, Ian T.; Ransbottom, Michael; Christian, Diana; Ogier, Michael; Katz, David M.] Case Western Reserve Univ, Sch Med, Dept Neurosci, Cleveland, OH 44106 USA.
RP Katz, DM (reprint author), Case Western Reserve Univ, Sch Med, Dept Neurosci, 10900 Euclid Ave, Cleveland, OH 44106 USA.
EM david.katz@case.edu
FU NINDS; International Rett Syndrome Foundation; Autism Speaks
FX This work was supported by grants from NINDS (D. M. K.), the
   International Rett Syndrome Foundation (D. M. K., M. K.) and Autism
   Speaks (D. M. K.). We thank Dr. Dan Wesson for reading the manuscript,
   Dr. Roberto Galan for helpful discussions regarding the ketamine
   experiments, Dr. Diana Kunze for help with the electrophysiology, and
   Elizabeth Shick and Alex Kreger for their skilled technical assistance.
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NR 76
TC 23
Z9 23
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 3
PY 2012
VL 32
IS 40
BP 13860
EP 13872
DI 10.1523/JNEUROSCI.2159-12.2012
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 016GU
UT WOS:000309506600020
PM 23035095
ER

PT J
AU Wang, XM
   Carlen, M
AF Wang, Xinming
   Carlen, Marie
TI Optogenetic dissection of cortical information processing-shining light
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SO BRAIN RESEARCH
LA English
DT Review
DE Optogenetics; Information processing; Cortex; Schizophrenia; Gamma
   oscillations; Synchrony; Parvalbumin; Intemeurons
ID PREFRONTAL CORTEX; GAMMA-OSCILLATIONS; PSYCHIATRIC-DISORDERS; INHIBITORY
   NEURONS; PYRAMIDAL CELLS; GENE-EXPRESSION; CEREBRAL-CORTEX;
   WORKING-MEMORY; NEURAL SYSTEMS; INTERNEURONS
AB Since optogenetics was introduced in 2005, fundamental progress has been made in our understanding of the neural processes central to higher-order functions such as perception, cognition and emotion. Until the inception of optogenetics, science was lacking neuromodulatory tools that could target specific populations of neurons with the spatial and temporal precision necessary for casually linking neural activity patterns to behavior. Optogenetics has also provided invaluable insights on the neural circuit elements affected in psychiatric disorders such as schizophrenia, anxiety, depression and autism. Here we review experiments where optogenetics has been instrumental in adding new information about functions governing cognition, such as information processing. In addition, we review optogenetic findings shedding light on how changed information processing could underlie cognitive dysfunction in schizophrenia.
   This article is part of a Special Issue entitled: Brain Integration. (c) 2012 Published by Elsevier B.V.
C1 [Wang, Xinming; Carlen, Marie] Karolinska Inst, Dept Neurosci, S-17177 Stockholm, Sweden.
RP Carlen, M (reprint author), Karolinska Inst, Dept Neurosci, Retzius Vag 8, S-17177 Stockholm, Sweden.
EM marie.carlen@ki.se
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   Yizhar O, 2011, NATURE, V477, P171, DOI 10.1038/nature10360
   Yizhar O., 2012, BIOL PSYCHIAT
   Yizhar O, 2011, NEURON, V71, P9, DOI 10.1016/j.neuron.2011.06.004
NR 59
TC 3
Z9 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0006-8993
J9 BRAIN RES
JI Brain Res.
PD OCT 2
PY 2012
VL 1476
SI SI
BP 31
EP 37
DI 10.1016/j.brainres.2012.04.015
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 035JV
UT WOS:000310943600004
PM 22578471
ER

PT J
AU Dudova, I
   Hrdlicka, M
AF Dudova, I.
   Hrdlicka, M.
TI Relationship of olfactory functions and psychopathology in patients with
   autism spectrum disorders
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 25th Congress of the European-College-of-Neuropsychopharmacology (ECNP)
CY OCT 13-17, 2012
CL Vienna, AUSTRIA
SP European Coll Neuropsychopharmacol (ECNP)
C1 [Dudova, I.; Hrdlicka, M.] Charles Univ Prague, Sch Med 2, Dept Child Psychiat, Prague, Czech Republic.
CR Bennetto L, 2007, BIOL PSYCHIAT, V62, P1015, DOI 10.1016/j.biopsych.2007.04.019
   Dudova I, 2011, EUR CHILD ADOLES PSY, V20, P333, DOI 10.1007/s00787-011-0177-1
   Hrdlicka M, 2011, J AUTISM DEV DISORD, V41, P524, DOI 10.1007/s10803-010-1084-x
NR 3
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2012
VL 22
SU 2
BP S416
EP S417
PG 2
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 130VQ
UT WOS:000317948600543
ER

PT J
AU Magnano, F
   Crisafulli, G
   Petralia, A
   Aguglia, E
AF Magnano, F.
   Crisafulli, G.
   Petralia, A.
   Aguglia, E.
TI Autism spectrum disorders in adults affected by schizophrenia and
   obsessive compulsive disorders
SO EUROPEAN NEUROPSYCHOPHARMACOLOGY
LA English
DT Meeting Abstract
CT 25th Congress of the European-College-of-Neuropsychopharmacology (ECNP)
CY OCT 13-17, 2012
CL Vienna, AUSTRIA
SP European Coll Neuropsychopharmacol (ECNP)
C1 [Magnano, F.; Crisafulli, G.; Petralia, A.; Aguglia, E.] UOPI Psychiat, AOU Policlin Vittorio Emanuele, Catania, Italy.
CR Goldstein G, 2002, ARCH CLIN NEUROPSYCH, V17, P461, DOI 10.1016/S0887-6177(01)00129-9
   Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947
   Woodbury-Smith MR, 2005, J AUTISM DEV DISORD, V35, P331, DOI 10.1007/s10803-005-3300-7
NR 3
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0924-977X
J9 EUR NEUROPSYCHOPHARM
JI Eur. Neuropsychopharmacol.
PD OCT
PY 2012
VL 22
SU 2
BP S205
EP S205
PG 1
WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 130VQ
UT WOS:000317948600188
ER

PT J
AU Feczko, E
   Miezin, FM
   Constantino, JN
   Schlaggar, BL
   Petersen, SE
   Pruett, JR
AF Feczko, Eric
   Miezin, Francis M.
   Constantino, John N.
   Schlaggar, Bradley L.
   Petersen, Steven E.
   Pruett, John R., Jr.
TI The hemodynamic response in children with Simplex Autism
SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE
LA English
DT Article
DE Functional magnetic resonance imaging; Visuomotor; Autism spectrum
   disorders; Event-related; Neurovascular coupling; Medication effects
ID HIGH-FUNCTIONING AUTISM; SEPARATING PROCESSES; BRAIN; FMRI;
   CONNECTIVITY; ACTIVATION; DEFICITS; TRIAL; MRI
AB Background: Numerous functional magnetic resonance imaging (fMRI) studies of the brain-bases of autism have demonstrated altered cortical responses in subjects with autism, relative to typical subjects, during a variety of tasks. These differences may reflect altered neuronal responses or altered hemodynamic response. This study searches for evidence of hemodynamic response differences by using a simple visual stimulus and elementary motor actions, which should elicit similar neuronal responses in patients and controls.
   Methods: We acquired fMRI data from two groups of 16 children, a typical group and a group with Simplex Autism, during a simple visuomotor paradigm previously used to assess this question in other cross-group comparisons. A general linear model estimated the blood-oxygen-level-dependent (BOLD) signal time course, and repeated-measures analysis of variance tested for potential cross-group differences in the BOLD signal.
   Results: The hemodynamic response in Simplex Autism is similar to that found in typical children. Although the sample size was small for a secondary analysis, medication appeared to have no effect on the hemodynamic response within the Simplex Autism group.
   Conclusions: When fMRI studies show BOLD response differences between autistic and typical subjects, these results likely reflect between-group differences in neural activity and not an altered hemodynamic response. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Feczko, Eric; Constantino, John N.; Pruett, John R., Jr.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA.
   [Miezin, Francis M.; Schlaggar, Bradley L.; Petersen, Steven E.] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA.
   [Miezin, Francis M.; Schlaggar, Bradley L.; Petersen, Steven E.] Washington Univ, Sch Med, Dept Radiol, St Louis, MO 63110 USA.
   [Constantino, John N.; Schlaggar, Bradley L.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA.
   [Schlaggar, Bradley L.; Petersen, Steven E.] Washington Univ, Sch Med, Dept Anat & Neurobiol, St Louis, MO 63110 USA.
   [Petersen, Steven E.] Washington Univ, Dept Psychol, St Louis, MO 63130 USA.
   [Petersen, Steven E.] Washington Univ, Dept Biomed Engn, St Louis, MO 63130 USA.
RP Feczko, E (reprint author), Washington Univ, Sch Med, Campus Box 8134,660 S Euclid St, St Louis, MO 63110 USA.
EM ericf@npg.wustl.edu
FU Simons Foundation Autism Research Initiative ("Brain Circuitry in
   Simplex Autism,");  [K12 EY16336]
FX This work was supported by a grant from the Simons Foundation Autism
   Research Initiative ("Brain Circuitry in Simplex Autism," Steven
   Petersen - PI). John Pruett's effort was supported by K12 EY16336. We
   thank Sarah Hoertel, for coordinating recruitment, scheduling, and
   assessments of the subjects. We also thank Kelly McVey for help with
   recruitment, scheduling, assessing, and scanning subjects. We thank Jen
   Simmons, Anna Abbacchi, Teddi Gray and others from the Constantino lab
   for assessing and/or recruiting subjects. We would also like to thank
   Dan Marcus and his lab for database support.
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NR 31
TC 3
Z9 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1878-9293
J9 DEV COGN NEUROS-NETH
JI Dev. Cogn. Neurosci.
PD OCT
PY 2012
VL 2
IS 4
BP 396
EP 408
DI 10.1016/j.dca.2012.06.001
PG 13
WC Neurosciences
SC Neurosciences & Neurology
GA 095ER
UT WOS:000315318000002
PM 22795455
ER

PT J
AU Vander Wyk, BC
   Voos, A
   Pelphrey, KA
AF Vander Wyk, Brent C.
   Voos, Avery
   Pelphrey, Kevin A.
TI Action representation in the superior temporal sulcus in children and
   adults: An fMRI study
SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE
LA English
DT Article
DE fMRI; Action observation; Development
ID BIOLOGICAL-MOTION; SOCIAL-PERCEPTION; BRAIN; ACTIVATION; MECHANISMS;
   OTHERS; INTENTIONS; CHILDHOOD; BEHAVIOR; AUTISM
AB The superior temporal sulcus (STS) plays an important role in the perception of biological motion and in the representation of higher order information about other's goals and intentions. Using a rapid event related functional magnetic resonance imaging paradigm (fMRI), children (n = 37, mean age 11.0) and adults (n = 17, mean age 25.3) viewed congruent or incongruent actions. Congruency (and incongruency) of a reach toward an object was a function of whether the object had just previously received positive or negative regard. Relative to congruent trials, both children and adults showed an increase in activation in the posterior STS bilaterally, in response to incongruent trials. In children, these STS regions exhibited developmental changes. Specifically, the differential response to incongruent trials relative to congruent trials was larger in older children in both hemispheres. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Vander Wyk, Brent C.; Voos, Avery; Pelphrey, Kevin A.] Yale Univ, Ctr Child Study, New Haven, CT 06520 USA.
RP Vander Wyk, BC (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA.
EM Brent.vanderwyk@yale.edu; Avery.voos@yale.edu; Kevin.pelphrey@yale.edu
FU National Institute of Mental Health [R01MH084080]
FX We thank Randi Bennett, Allison Berken, Benjamin Deen, Moira Dillon,
   Jeffery Eilbott, and Daniel Sugrue for valuable contributions to the
   study. We would also like to thank Alex Ahmed and Federica Riva for
   helpful comments on the manuscript. This work was funded by National
   Institute of Mental Health grant R01MH084080.
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NR 31
TC 7
Z9 7
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1878-9293
J9 DEV COGN NEUROS-NETH
JI Dev. Cogn. Neurosci.
PD OCT
PY 2012
VL 2
IS 4
BP 409
EP 416
DI 10.1016/j.dcn.2012.04.004
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 095ER
UT WOS:000315318000003
PM 22727762
ER

PT J
AU Zaccagnino, M
   Mattei, P
   Merlini, A
   Rossi, A
   Fazzi, E
AF Zaccagnino, M.
   Mattei, P.
   Merlini, A.
   Rossi, A.
   Fazzi, E.
TI CLASSIFICATION OF THE INSTRUMENT OF ASSESSMENT OF CHILDREN BETWEEN 0 AND
   3 YEARS OF AGE
SO MINERVA PEDIATRICA
LA Italian
DT Review
DE Self-assessment; Psychopathology; Growth and development
ID MOTHER-INFANT INTERACTION; POSTNATAL DEPRESSION; BRAIN-DEVELOPMENT;
   ATTACHMENT THEORY; MENTAL-HEALTH; AUTISM; VALIDITY; BEHAVIOR;
   PSYCHOPATHOLOGY; CAREGIVERS
AB CLASSIFICATION OF THE INSTRUMENT OF ASSESSMENT OF CHILDREN BETWEEN 0 AND 3 YEARS OF AGE One of the difficulties described in epidemiological studies about psychopathology in children 0-3 years of age appears during the assessment phase. In fact, the assessment of indicators of particular difficulties in children is hampered by the rapid processes of transformation of behavior that cross all areas of child development. The aim of this article was to provide an overview as complete as possible of all instruments used in the assessment phase of children 0-3 years. The literature shows a number of tools for evaluation and diagnosis of psychopathology that have been divided into four categories: mental development tests, interviews with parents, questionnaires and rating scales, evaluation of the parent-child assessment of specific diagnostic entities. The main features of each instrument are described.
C1 [Zaccagnino, M.; Rossi, A.; Fazzi, E.] Spedali Civil Brescia, Unita Neuroriabilitaz Precoce, I-25123 Brescia, Italy.
   [Zaccagnino, M.; Rossi, A.; Fazzi, E.] Spedali Civil Brescia, Unita Operat Neuropsichiat Infanzia & Adolescenza, I-25123 Brescia, Italy.
   [Mattei, P.; Merlini, A.; Rossi, A.; Fazzi, E.] Univ Brescia, Brescia, Italy.
RP Zaccagnino, M (reprint author), Spedali Civil Brescia, Unita Neuroriabilitaz Precoce, Piazzale Spedali Civili 1, I-25123 Brescia, Italy.
EM mariazaccagnino@hotmail.com
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NR 75
TC 0
Z9 0
PU EDIZIONI MINERVA MEDICA
PI TURIN
PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY
SN 0026-4946
J9 MINERVA PEDIATR
JI Minerva Pediat.
PD OCT
PY 2012
VL 64
IS 5
BP 521
EP 540
PG 20
WC Pediatrics
SC Pediatrics
GA 095EJ
UT WOS:000315317200007
PM 22992534
ER

PT J
AU Ingersoll, B
   Meyer, K
   Bonter, N
   Jelinek, S
AF Ingersoll, Brooke
   Meyer, Katherine
   Bonter, Nicole
   Jelinek, Sara
TI A Comparison of Developmental Social-Pragmatic and Naturalistic
   Behavioral Interventions on Language Use and Social Engagement in
   Children With Autism
SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH
LA English
DT Article
DE autism; language intervention; behavioral; developmental
ID COMMUNICATION INTERVENTION; SPECTRUM DISORDERS
AB Purpose: Developmental social-pragmatic and naturalistic behavioral interventions share a number of features, but they differ in their use of facilitative strategies and direct elicitation of child language. In this study, the authors investigated whether these approaches produce different language and social outcomes in young children with autism.
   Method: The authors used an ABACAD design to compare the effects of a developmental social-pragmatic, naturalistic behavioral, and combined intervention on language type and function and social engagement in 5 children with autism.
   Results: Milieu teaching and the combined intervention produced higher rates of language targets than did responsive interaction. An analysis of the type and function of language targets suggested that differences between conditions were driven primarily by prompted-and, to a lesser extent, spontaneous-requests. Social engagement ratings were higher during each intervention than at baseline, but differences between treatment conditions were not consistent across children.
   Conclusions: For children with autism, naturalistic interventions that use direct elicitation of child language lead to greater short-term gains in the use of expressive language targets-in particular, prompted requests-than interventions that use facilitative strategies only. All 3 naturalistic language interventions can promote social engagement. For some children, the combined use of direct elicitation and responsiveness-based strategies may enhance treatment response.
C1 [Ingersoll, Brooke; Meyer, Katherine; Bonter, Nicole; Jelinek, Sara] Michigan State Univ, E Lansing, MI 48824 USA.
RP Ingersoll, B (reprint author), Michigan State Univ, E Lansing, MI 48824 USA.
EM ingers19@msu.edu
RI Ingersoll, Brooke/A-9117-2012
FU Autism Speaks
FX This study was supported by a grant from Autism Speaks to the first
   author. We are grateful to the children and their families who
   participated in this research. We also thank the research assistants who
   worked on this project.
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NR 34
TC 4
Z9 4
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 1092-4388
J9 J SPEECH LANG HEAR R
JI J. Speech Lang. Hear. Res.
PD OCT 1
PY 2012
VL 55
IS 5
BP 1301
EP 1313
DI 10.1044/1092-4388(2012/10-0345)
PG 13
WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation
GA 084HQ
UT WOS:000314529800005
PM 22361104
ER

PT J
AU Clegg, J
   Ansorge, L
   Stackhouse, J
   Donlan, C
AF Clegg, Judy
   Ansorge, Lydia
   Stackhouse, Joy
   Donlan, Chris
TI Developmental Communication Impairments in Adults: Outcomes and Life
   Experiences of Adults and Their Parents
SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS
LA English
DT Article
DE developmental communication impairments; psychosocial outcomes; life
   experiences
ID RECEPTIVE LANGUAGE DISORDER; QUALITY-OF-LIFE; COMPARATIVE FOLLOW-UP;
   PSYCHOSOCIAL OUTCOMES; SOCIAL COGNITION; INFANTILE-AUTISM; YOUNG-PEOPLE;
   CHILDREN; HISTORY; SPEECH
AB Purpose: This study identifies the outcomes and documents the longitudinal life experiences of adults who attended a specialist residential school for children with pervasive and complex developmental communication impairments.
   Method: Semistructured interviews were carried out with 26 adult ex-pupils who had attended the school and the parents of 15 of the ex-pupils.
   Results: Seven key themes were identified from the data, including (a) lack of appropriate support and the impact of this in early childhood, (b) advantages and disadvantages of specialist educational provision compared to mainstream and other provision, (c) changing impact of developmental communication impairments over time, (d) challenging transition away from specialist educational provision, (e) absence of appropriate support for adults with developmental communication impairments, (f) persisting impact of developmental communication impairments on social and emotional functioning in adult life, and (g) differences in perspective between the adult ex-pupils and their parents.
   Conclusion: Across the adult ex-pupils and their parents, the perceived reported benefits of early intervention, parental support, specialist educational provision, and guidance at times of transitions should inform current service provision for this vulnerable group of individuals and their families.
C1 [Clegg, Judy; Ansorge, Lydia; Stackhouse, Joy] Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England.
   [Donlan, Chris] UCL, London WC1E 6BT, England.
RP Clegg, J (reprint author), Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England.
EM j.clegg@sheffield.ac.uk
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NR 39
TC 3
Z9 3
PU AMER SPEECH-LANGUAGE-HEARING ASSOC
PI ROCKVILLE
PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA
SN 0161-1461
J9 LANG SPEECH HEAR SER
JI Lang. Speech Hear. Serv. Sch.
PD OCT 1
PY 2012
VL 43
IS 4
BP 521
EP 535
DI 10.1044/0161-1461(2012/11-0068)
PG 15
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA 083YG
UT WOS:000314501900011
PM 22826372
ER

PT J
AU Ghanizadeh, A
   Derakhshan, N
AF Ghanizadeh, Ahmad
   Derakhshan, Nima
TI N-acetylcysteine for treatment of autism, a case report
SO JOURNAL OF RESEARCH IN MEDICAL SCIENCES
LA English
DT Article
DE Autism; children; glutathione; oxidative stress; treatment
ID OXIDATIVE STRESS; CHILDREN; BIOMARKERS; TRANSSULFURATION; NEUROTENSIN;
   DISORDERS
AB There are a limited number of Food and Drug Administration (FDA)-approved medications for the treatment of autism. Meanwhile, oxidative stress and neuroinflammation are supposed to play a causative role in autism. N-acetylcysteine may provide cystine, a precursor for glutathione (GSH), which is an important antioxidant factor in the brain. We here report a child with autism, whose symptoms were markedly decreased after taking oral N-acetylcysteine 800 mg/day, in three divided doses. His social interaction was significantly increased. The score of social impairment on a visual analog scale decreased from 10 to 6 in the two-month trial. The aggressive behaviors decreased from 10 to 3. This case suggests that N-acetylcysteine may decrease some symptoms of autism.
C1 [Ghanizadeh, Ahmad; Derakhshan, Nima] Shiraz Univ Med Sci, Dept Psychiat, Res Ctr Psychiat & Behav Sci, Sch Med, Shiraz, Iran.
   [Ghanizadeh, Ahmad] Shiraz Univ Med Sci, Dept Psychiat, Sch Med, Shiraz, Iran.
RP Ghanizadeh, A (reprint author), Hafez Hosp, Dept Psychiat, Res Ctr Psychiat & Behav, Shiraz, Iran.
EM ghanizad@sina.tums.ac.ir
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
   Dean O, 2011, J PSYCHIATR NEUROSCI, V36, P78, DOI 10.1503/jpn.100057
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NR 21
TC 8
Z9 8
PU ISFAHAN UNIV MED SCIENCES
PI ISFAHAN
PA HEZARJERIB AVE, PO BOX 81745-319, ISFAHAN, 00000, IRAN
SN 1735-1995
J9 J RES MED SCI
JI J. Res. Med. Sci.
PD OCT
PY 2012
VL 17
IS 10
BP 985
EP 987
PG 3
WC Medicine, General & Internal
SC General & Internal Medicine
GA 080FN
UT WOS:000314226800018
PM 23826003
ER

PT J
AU Shulman, ST
AF Shulman, Stanford T.
TI The Many Faces of Autism
SO PEDIATRIC ANNALS
LA English
DT Editorial Material
C1 [Shulman, Stanford T.] Northwestern Univ, Feinberg Sch Med, Evanston, IL 60208 USA.
   [Shulman, Stanford T.] Ann & Robert H Lurie Childrens Hosp, Div Infect Dis, Chicago, IL USA.
RP Shulman, ST (reprint author), Northwestern Univ, Feinberg Sch Med, Evanston, IL 60208 USA.
EM Pediatrics@Healio.com
CR Newburger JW, 2004, PEDIATRICS, V114, P1708, DOI 10.1542/peds.2004-2182
NR 1
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP 388
EP 389
DI 10.3928/00904481-20120924-01
PG 2
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300007
PM 23052138
ER

PT J
AU Lohr, WD
   Tanguay, P
AF Lohr, W. David
   Tanguay, Peter
TI Case Challenges in Autism Spectrum Disorder: The Role of the
   Pediatrician
SO PEDIATRIC ANNALS
LA English
DT Editorial Material
ID DSM-5; CRITERIA; CHILDREN
C1 [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
   [Lohr, W. David] Univ Louisville, Sch Med, Louisville, KY 40292 USA.
   [Tanguay, Peter] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Louisville, KY 40292 USA.
RP Lohr, WD (reprint author), Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
CR Autism and Developmental Disabilities Monitoring Network Surveillance Year 2008 Principal Investigators Centers for Disease Control and Prevention, 2012, MMWR SURVEILLANCE SU, V61, P1
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NR 12
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP 408
EP 409
DI 10.3928/00904481-20120924-07
PG 2
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300018
PM 23052144
ER

PT J
AU Le, JF
   Lohr, WD
AF Le, Jennifer F.
   Lohr, W. David
TI Pharmacology in the Treatment of Severe Autism Spectrum Disorder
SO PEDIATRIC ANNALS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; CROSSOVER TRIAL; CHILDREN;
   RISPERIDONE; IRRITABILITY; ARIPIPRAZOLE; ADOLESCENTS; FLUOXETINE
C1 [Le, Jennifer F.; Lohr, W. David] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Emergency Psychiat Serv, Louisville, KY USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
RP Le, JF (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM Jennifer.Le@louisville.edu
CR DeLong GR, 1998, DEV MED CHILD NEUROL, V40, P551
   Hollander E, 2005, NEUROPSYCHOPHARMACOL, V30, P582, DOI 10.1038/sj.npp.1300627
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   Nagaraj R, 2006, J CHILD NEUROL, V21, P450, DOI 10.2310/7010.2006.00099
   Owen R, 2009, PEDIATRICS, V124, P1533, DOI 10.1542/peds.2008-3782
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   Aman MG, 2005, ARCH GEN PSYCHIAT, V62, P1266
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NR 9
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E201
EP E203
DI 10.3928/00904481-20120924-11
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300004
ER

PT J
AU Le, JF
   Lohr, WD
AF Le, Jennifer F.
   Lohr, W. David
TI Aggression and Self-Injury in a Patient with Severe Autism
SO PEDIATRIC ANNALS
LA English
DT Article
ID DISORDERS
C1 [Le, Jennifer F.; Lohr, W. David] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Emergency Psychiat Serv, Louisville, KY USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
RP Le, JF (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM Jennifer.Le@louisville.edu
CR Burke LM, 2010, J PEDIATR ADOL GYNEC, V23, P11, DOI 10.1016/j.jpag.2009.04.005
   Jeste SS, 2011, CURR OPIN NEUROL, V24, P132, DOI 10.1097/WCO.0b013e3283446450
   Kuddo T, 2003, CURR OPIN PEDIATR, V15, P339, DOI 10.1097/00008480-200306000-00020
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   Rossignol DA, 2011, DEV MED CHILD NEUROL, V53, P783, DOI 10.1111/j.1469-8749.2011.03980.x
NR 5
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E207
EP E209
DI 10.3928/00904481-20120924-13
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300006
ER

PT J
AU Lohr, WD
   Le, JF
AF Lohr, W. David
   Le, Jennifer F.
TI Outpatient Diagnosis of Autism Spectrum Disorder
SO PEDIATRIC ANNALS
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; RECIPROCAL SOCIAL-BEHAVIOR;
   FUNCTIONING AUTISM; ASPERGER-SYNDROME; DEFICITS; CHILDREN; SCALE
C1 [Lohr, W. David; Le, Jennifer F.] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
RP Lohr, WD (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM wdlohr01@louisville.edu
CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444
   Constantino JN, 2003, J AM ACAD CHILD PSY, V42, P458, DOI 10.1097/01.CHI.0000046811.95464.21
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NR 12
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E192
EP E194
DI 10.3928/00904481-20120924-08
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300001
ER

PT J
AU Lohr, WD
   Le, JF
AF Lohr, W. David
   Le, Jennifer F.
TI An 11-Year-Old Boy with Tantrums and Head Banging
SO PEDIATRIC ANNALS
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; CHILDREN; ANXIETY; SYMPTOMS; PDD
C1 [Lohr, W. David; Le, Jennifer F.] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Emergency Psychiat Serv, Louisville, KY USA.
RP Lohr, WD (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM wdlohr01@louisville.edu
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NR 10
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E204
EP E206
DI 10.3928/00904481-20120924-12
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300005
ER

PT J
AU Lohr, WD
   Le, JF
AF Lohr, W. David
   Le, Jennifer F.
TI Proposed DSM-5 Changes for Autism Spectrum Disorder
SO PEDIATRIC ANNALS
LA English
DT Article
ID CRITERIA
C1 [Lohr, W. David; Le, Jennifer F.] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Emergency Psychiat Serv, Louisville, KY USA.
RP Lohr, WD (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM wdlohr01@louisville.edu
CR American Psychiatric Association, 2012, DSM 5 DEV AUT SPECTR
   American Psychiatric Association, 2000, EL DSM IV TR PLUS 1
   Constantino JN, 2003, J AM ACAD CHILD PSY, V42, P458, DOI 10.1097/01.CHI.0000046811.95464.21
   Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524
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   Tanguay PE, 2011, AM J PSYCHIAT, V168, P1142, DOI 10.1176/appi.ajp.2011.11071024
NR 8
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E195
EP E197
DI 10.3928/00904481-20120924-09
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300002
ER

PT J
AU Lohr, WD
   Le, JF
AF Lohr, W. David
   Le, Jennifer F.
TI Treatment Plan for a Patient with an Autism Spectrum Disorder
SO PEDIATRIC ANNALS
LA English
DT Article
ID ASPERGER-SYNDROME; CROSSOVER TRIAL; CHILDREN; HYPERACTIVITY;
   IRRITABILITY; ARIPIPRAZOLE; ADOLESCENTS
C1 [Lohr, W. David; Le, Jennifer F.] Univ Louisville, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA.
   [Lohr, W. David] Univ Louisville, Autism Ctr, Louisville, KY 40292 USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Inpatient Child & Adolescent Psychiat Unit, Louisville, KY USA.
   [Le, Jennifer F.] Kosair Childrens Hosp, Emergency Psychiat Serv, Louisville, KY USA.
RP Lohr, WD (reprint author), Bingham Clin, 200 E Chestnut St, Louisville, KY 40202 USA.
EM wdlohr01@louisville.edu
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NR 17
TC 0
Z9 0
PU SLACK INC
PI THOROFARE
PA 6900 GROVE RD, THOROFARE, NJ 08086 USA
SN 0090-4481
EI 1938-2359
J9 PEDIATR ANN
JI Pediatr. Annu.
PD OCT
PY 2012
VL 41
IS 10
BP E198
EP E200
DI 10.3928/00904481-20120924-10
PG 3
WC Pediatrics
SC Pediatrics
GA 082NS
UT WOS:000314399300003
ER

PT J
AU Badoni, M
AF Badoni, Marta
TI ON THE AUTISM GUIDELINES PUT FORWARD BY THE MINISTRY OF HEALTH AND
   SUBSEQUENT DEBATES
SO RIVISTA DI PSICOANALISI
LA Italian
DT Article
DE Autism; guidelines; multidisciplinary approach; psychoanalysis
AB ON THE AUTISM GUIDELINES PUT FORWARD BY THE MINISTRY OF HEALTH AND SUBSEQUENT DEBATES. Starting from the challenge that the autistic subject poses for the therapist and society, the necessity of an accurate methodological study is emphasized - a study within psychoanalysis viewed as an institution and as a research community. A broad, courageous, and rigorous multidisciplinary comparison is urgently called for. In particular, the nature of the family's suffering is discussed.
RP Badoni, M (reprint author), Via Cosimo del Fante 3, I-20122 Milan, Italy.
CR Asperger H., 1991, AUTISM ASPERGERS SYN
   BALLERINI A., 2006, AUTISMO UMANITA NASC
   BETTELHEIM B., 1976, FORTEZZA VUOTA AUTIS
   CAVENAGHI R., 2007, STORIE AUTISTICHE AL
   Kanner L, 1943, NERV CHILD, V2, P217
   Maestro S, 2005, CHILD PSYCHIAT HUM D, V35, P383, DOI 10.1007/s10578-005-2695-x
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   MURATORI F., 2003, GIORNALE PSICHIATRIA, V23, P72
   PAGNONI A., 2000, ESSERE NON
   RESNIK S., 2004, ABITARE ASSENZA SCRI
   RHODE M., 2011, RICHARD PIGGLE, V1, P1
   Winnicott D.W., 1970, SVILUPPO AFFETTIVO A
NR 12
TC 0
Z9 0
PU EDIZIONI BORLA SRL
PI ROME
PA VIA DELLE FORNACI 50, ROME, 00165, ITALY
SN 0035-6492
J9 RIV PSICOANAL
JI Riv. Psicoanal.
PD OCT-DEC
PY 2012
VL 58
IS 4
BP 977
EP 986
PG 10
WC Psychology, Psychoanalysis
SC Psychology
GA 074VO
UT WOS:000313843000010
ER

PT J
AU Battistini, A
AF Battistini, Angelo
TI AUTISM AND THE THERAPEUTIC ENVIRONMENT: SOME NOTES ON THE EXPERIENCE AT
   "I TIGLI" IN RIMINI - BIOGRAPHY AND CLINICAL CONSIDERATION
SO RIVISTA DI PSICOANALISI
LA Italian
DT Article
DE Autism; institutional countertransference; psychosis; therapeutic
   environment
AB AUTISM AND THE THERAPEUTIC ENVIRONMENT: SOME NOTES ON THE EXPERIENCE AT "I TIGLI" IN RIMINI - BIOGRAPHY AND CLINICAL CONSIDERATION. The Author refers to an eight year experience of community therapy with psychotic and autistic children in a semi-residential structure called "I Tigli", in the city of Rimini.
RP Battistini, A (reprint author), Via Bastioni Orientali 70, I-47900 Rimini, Italy.
CR BALLERINI A., 2006, AUTISMO UMANITA NASC
   BATTISTINI A., 2007, SGUARDO PSICOANALITI
   BATTISTINI A., 1981, NEUROPSICHIATRIA INF, P238
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   MANNONI M., 1976, LIEU VIVRE
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   TUSTIN F., 1975, AUTISMO PSICOSI INFA
NR 7
TC 0
Z9 0
PU EDIZIONI BORLA SRL
PI ROME
PA VIA DELLE FORNACI 50, ROME, 00165, ITALY
SN 0035-6492
J9 RIV PSICOANAL
JI Riv. Psicoanal.
PD OCT-DEC
PY 2012
VL 58
IS 4
BP 987
EP 999
PG 13
WC Psychology, Psychoanalysis
SC Psychology
GA 074VO
UT WOS:000313843000011
ER

PT J
AU Cattelan, C
AF Cattelan, Chiara
TI WHAT WE TALK ABOUT WHEN WE TALK ABOUT AUTISM
SO RIVISTA DI PSICOANALISI
LA Italian
DT Article
DE Autism; autism and mental development; bifocal child/adult vision;
   psychoanalytic method and autism
AB WHAT WE TALK ABOUT WHEN WE TALK ABOUT AUTISM. This paper tries to highlight the role of the psychoanalyst in autistic states. The author wants to demonstrate how the principles of the psychoanalytic method may be respected in working with these patients, though with some technical adaptations, and that these principles are suitable to work in these areas. She emphasizes the necessity of more accurate diagnostic distinctions during consultation through the careful use of counter-transference, and she tries to show how work with the autistic child, as well as with the adult who has pockets of autistic functioning, may be complementary to understanding. Considering autism a privileged field of observation for knowledge of the mind's development, the author hopes that a space for teaching these subjects will be identified within both child and adult training programs, and that in the future, the exchange that has begun with those on the mailing list within our society will go on.
RP Cattelan, C (reprint author), S Croce 914, I-30135 Venice, Italy.
CR BION W.R., 1972, APPRENDERE ESPERIENZ
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NR 24
TC 0
Z9 0
PU EDIZIONI BORLA SRL
PI ROME
PA VIA DELLE FORNACI 50, ROME, 00165, ITALY
SN 0035-6492
J9 RIV PSICOANAL
JI Riv. Psicoanal.
PD OCT-DEC
PY 2012
VL 58
IS 4
BP 1001
EP 1015
PG 15
WC Psychology, Psychoanalysis
SC Psychology
GA 074VO
UT WOS:000313843000012
ER

PT J
AU Chailangkarn, T
   Acab, A
   Muotri, AR
AF Chailangkarn, Thanathom
   Acab, Allan
   Muotri, Alysson Renato
TI Modeling neurodevelopmental disorders using human neurons
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID PLURIPOTENT STEM-CELLS; PRADER-WILLI-SYNDROME; FRAGILE-X-SYNDROME;
   RETT-SYNDROME; L1 RETROTRANSPOSITION; ANGELMAN SYNDROME; TIMOTHY
   SYNDROME; DEFINED FACTORS; MECP2; MUTATIONS
AB The cellular and molecular mechanisms of neurodevelopmental conditions such as autism spectrum disorders have been studied intensively for decades. The unavailability of live patient neurons for research, however, has represented a major obstacle in the elucidation of the disease etiologies. Recently, the development of induced pluripotent stem cell (iPSC) technology allows for the generation of human neurons from somatic cells of patients. We review ongoing studies using iPSCs as an approach to model neurodevelopmental disorders, the promise and caveats of this technique and its potential for drug screening. The reproducible findings of relevant phenotypes in Rett syndrome iPSC-derived neurons suggest that iPSC technology offers a novel and unique opportunity for the understanding of and the development of therapeutics for other autism spectrum disorders.
C1 [Chailangkarn, Thanathom; Acab, Allan; Muotri, Alysson Renato] Univ Calif San Diego, Sch Med, Dept Pediat,Stem Cell Program, Rady Childrens Hosp San Diego,Dept Cellular & Mol, La Jolla, CA 92093 USA.
RP Muotri, AR (reprint author), Univ Calif San Diego, Sch Med, Dept Pediat,Stem Cell Program, Rady Childrens Hosp San Diego,Dept Cellular & Mol, MC 0695, La Jolla, CA 92093 USA.
EM muotri@ucsd.edu
FU California Institute for Regenerative Medicine (CIRM) [TR2-01814];
   National Institutes of Health through the NIH Director's New Innovator
   Award Program from NIMH [1-DP2-OD006495-01, 1R21MH093954]; National
   Institutes of Health through the NIH Director's New Innovator Award
   Program from NIH [P01 HD33113, NS22343]; Royal Thai Government
   Scholarship; NIH predoctoral training grant [T32 GM008666]; Emerald
   Foundation
FX The work was supported by grants from the California Institute for
   Regenerative Medicine (CIRM) TR2-01814, the National Institutes of
   Health through the NIH Director's New Innovator Award Program,
   1-DP2-OD006495-01, 1R21MH093954 from NIMH, P01 HD33113 and NS22343 from
   NIH, the Royal Thai Government Scholarship to T.C., the NIH predoctoral
   training grant T32 GM008666 to A.A and the Emerald Foundation. We would
   like to thank members of the Muotri laboratory for critical comments on
   the manuscript. This is a brief review on the fast growing field of
   disease modeling, we apologize for the omission of important work from
   colleagues that could not be described or cited here.
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NR 47
TC 13
Z9 13
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 785
EP 790
DI 10.1016/j.conb.2012.04.004
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000008
PM 22717528
ER

PT J
AU Coe, BP
   Girirajan, S
   Eichler, EE
AF Coe, Bradley P.
   Girirajan, Santhosh
   Eichler, Evan E.
TI A genetic model for neurodevelopmental disease
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID COPY-NUMBER VARIATION; AUTISM SPECTRUM DISORDERS; IDIOPATHIC GENERALIZED
   EPILEPSY; DE-NOVO CNVS; MENTAL-RETARDATION; STRUCTURAL VARIATION; HUMAN
   GENOME; DEVELOPMENTAL DELAY; 15Q13.3 MICRODELETIONS; INTRAGENIC
   DELETIONS
AB The genetic basis of neurodevelopmental and neuropsychiatric diseases has been advanced by the discovery of large and recurrent copy number variants significantly enriched in cases when compared to controls. The pattern of this variation strongly implies that rare variants contribute significantly to neurological disease; that different genes will be responsible for similar diseases in different families; and that the same 'primary' genetic lesions can result in a different disease outcome depending potentially on the genetic background. Next-generation sequencing technologies are beginning to broaden the spectrum of disease-causing variation and provide specificity by pinpointing both genes and pathways for future diagnostics and therapeutics.
C1 [Coe, Bradley P.; Girirajan, Santhosh; Eichler, Evan E.] Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA.
   [Eichler, Evan E.] Univ Washington, Howard Hughes Med Inst, Seattle, WA 98195 USA.
RP Eichler, EE (reprint author), Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA.
EM eee@gs.washington.edu
FU Canadian Institutes of Health Research; Simons Foundation Autism
   Research Initiative [SFARI 137578, 191889]
FX We also thank Tonia Brown and Brian O'Roak for useful discussions and
   editing the manuscript. BPC is supported by a fellowship from the
   Canadian Institutes of Health Research. EEE is an Investigator of the
   Howard Hughes Medical Institute. This work was supported by the Simons
   Foundation Autism Research Initiative (SFARI 137578 & 191889) to EEE.
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NR 67
TC 11
Z9 11
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 829
EP 836
DI 10.1016/j.conb.2012.04.007
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000014
PM 22560351
ER

PT J
AU Peca, J
   Feng, GP
AF Peca, Joao
   Feng, Guoping
TI Cellular and synaptic network defects in autism
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID FRAGILE-X-SYNDROME; POSTSYNAPTIC DENSITY PROTEINS; DENDRITIC SPINE
   MORPHOLOGY; TUBEROUS SCLEROSIS GENE; COPY NUMBER VARIATION;
   MENTAL-RETARDATION; ANGELMAN-SYNDROME; SPECTRUM DISORDERS; SHANK FAMILY;
   MOUSE MODEL
AB Many candidate genes are now thought to confer susceptibility to autism spectrum disorders (ASDs). Here we review four interrelated complexes, each composed of multiple families of genes that functionally coalesce on common cellular pathways. We illustrate a common thread in the organization of glutamatergic synapses and suggest a link between genes involved in Tuberous Sclerosis Complex, Fragile X syndrome, Angelman syndrome and several synaptic ASD candidate genes. When viewed in this context, progress in deciphering the molecular architecture of cellular protein-protein interactions together with the unraveling of synaptic dysfunction in neural networks may prove pivotal to advancing our understanding of ASDs.
C1 [Peca, Joao; Feng, Guoping] MIT, Dept Brain & Cognit Sci, McGovern Inst Brain Res, Cambridge, MA 02139 USA.
   [Feng, Guoping] Broad Inst, Stanley Ctr Psychiat Res, Cambridge, MA 02142 USA.
RP Feng, GP (reprint author), MIT, Dept Brain & Cognit Sci, McGovern Inst Brain Res, E25-618, Cambridge, MA 02139 USA.
EM fengg@mit.edu
RI Peca, Joao/K-7900-2013
OI Peca, Joao/0000-0003-4989-2129
FU National Institutes of Health [NIMH R01MH081201]; Hartwell Foundation;
   Stanley Center for Psychiatric Research; SPARC program from Broad
   Institute of MIT; Autism Speaks Translational Postdoctoral Fellowship
   [7649]; Simons Foundation Autism Research Initiative (SFARI); SPARC
   program from Broad Institute of Harvard
FX We thank Dr. Jonathan Ting for critical comments on this manuscript. GF
   is supported by grants from the National Institutes of Health (NIMH
   R01MH081201), The Hartwell Foundation, Simons Foundation Autism Research
   Initiative (SFARI), Stanley Center for Psychiatric Research, and the
   SPARC program from Broad Institute of MIT and Harvard. JP is funded by
   an Autism Speaks Translational Postdoctoral Fellowship (#7649).
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NR 72
TC 14
Z9 14
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 866
EP 872
DI 10.1016/j.conb.2012.02.015
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000019
PM 22440525
ER

PT J
AU Zhou, J
   Parada, LF
AF Zhou, Jing
   Parada, Luis F.
TI PTEN signaling in autism spectrum disorders
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; RILEY-RUVALCABA-SYNDROME;
   GLYCOGEN-SYNTHASE KINASE-3; LHERMITTE-DUCLOS-DISEASE; DE-NOVO MUTATIONS;
   TUBEROUS-SCLEROSIS; MOUSE MODEL; IN-VIVO; GASTROINTESTINAL SYMPTOMS;
   NEURONAL POLARITY
AB PTEN germline mutations are found in a small subset of children diagnosed with autism spectrum disorder (ASD) and accompanying macrocephaly. In this review, we discuss recent advances that offer insight into the pathogenesis of this subgroup of autism patients. We provide an overview of how disrupting PTEN function influences neuronal cells, and describe efforts to decipher the cellular mechanisms associated with altered social behaviors. We discuss the PTEN downstream signaling pathways that likely mediate these cellular and behavioral effects. In addition, emerging data suggest that PTEN mutation can synergize with mutations in other autism susceptibility genes to contribute to the development of autistic behaviors. These studies extend our knowledge of PTEN and the PTEN signaling pathway, and offer molecular and cellular clues to better understand the etiology of ASDs.
C1 [Zhou, Jing; Parada, Luis F.] Univ Texas SW Med Ctr Dallas, Dept Dev Biol, Dallas, TX 75390 USA.
RP Parada, LF (reprint author), Univ Texas SW Med Ctr Dallas, Dept Dev Biol, Dallas, TX 75390 USA.
EM luis.parada@utsouthwestern.edu
RI Parada, luis/B-9400-2014
FU Simons Foundation
FX We thank Dr. Renee McKay for critical advice during preparation of this
   manuscript. Grant support: Simons Foundation (LFP). LFP is an American
   Cancer Society Research Professor.
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NR 55
TC 32
Z9 33
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 873
EP 879
DI 10.1016/j.conb.2012.05.004
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000020
PM 22664040
ER

PT J
AU Lee, HY
   Jan, LY
AF Lee, Hye Young
   Jan, Lily Yeh
TI Fragile X syndrome: mechanistic insights and therapeutic avenues
   regarding the role of potassium channels
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID MENTAL-RETARDATION PROTEIN; LONG-TERM POTENTIATION; CA1 PYRAMIDAL
   NEURONS; FMR1 KNOCKOUT MICE; MESSENGER-RNA; MOUSE MODEL; SYNAPTIC
   PLASTICITY; GLUTAMATE RECEPTORS; HIPPOCAMPAL-NEURONS; DENDRITIC SPINES
AB Fragile X syndrome (FXS) is a common form of mental disability and one of the known causes of autism. The mutation responsible for FXS is a large expansion of the trinucleotide CGG repeats that leads to DNA methylation of the fragile X mental retardation gene 1 (FMR1) and transcriptional silencing, resulting in the absence of fragile X mental retardation protein (FMRP), an mRNA binding protein. Although it is widely known that FMRP is critical for metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), which has provided a general theme for developing pharmacological drugs for FXS, specific downstream targets of FMRP may also be of therapeutic value. Since alterations in potassium channel expression level or activity could underlie neuronal network defects in FXS, here we describe recent findings on how these channels might be altered in mouse models of FXS and the possible therapeutic avenues for treating FXS.
C1 [Jan, Lily Yeh] Univ Calif San Francisco, Dept Physiol, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
   Univ Calif San Francisco, Dept Biochem, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
   Univ Calif San Francisco, Dept Biophys, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
RP Jan, LY (reprint author), Univ Calif San Francisco, Dept Physiol, Howard Hughes Med Inst, San Francisco, CA 94158 USA.
EM lily.jan@ucsf.edu
FU NIH [MH065334]
FX We thank Dr. Shi-Bing Yang, David Gorczyca and Dr. Desiree Thayer for
   discussions, Dr. Kaczamarek for the generous permission and providing
   high-resolution figures for the use of Kv3.1b tonotopicity results, and
   the NIH grant MH065334 for support. LYJ is an HHMI investigator.
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NR 97
TC 5
Z9 6
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 887
EP 894
DI 10.1016/j.conb.2012.03.010
PG 8
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000022
PM 22483378
ER

PT J
AU Sahin, M
AF Sahin, Mustafa
TI Targeted treatment trials for tuberous sclerosis and autism: no longer a
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SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID IMPAIRED SYNAPTIC PLASTICITY; FACIAL-ANGIOFIBROMAS; 3-KINASE/AKT
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AB Genetic disorders that present with a high incidence of autism spectrum disorders (ASD) offer tremendous potential both for elucidating the underlying neurobiology of ASD and identifying therapeutic drugs and/or drug targets. As a result, clinical trials for genetic disorders associated with ASD are no longer a hope for the future but rather an exciting reality whose time has come. Tuberous sclerosis complex (TSC) is one such genetic disorder that presents with ASD, epilepsy, and intellectual disability. Cell culture and mouse model experiments have identified the mTOR pathway as a therapeutic target in this disease. This review summarizes the advantages of using TSC as model of ASD and the recent advances in the translational and clinical treatment trials in TSC.
C1 Harvard Univ, Sch Med, Dept Neurol, FM Kirby Neurobiol Ctr,Childrens Hosp Boston, Boston, MA 02115 USA.
RP Sahin, M (reprint author), Harvard Univ, Sch Med, Dept Neurol, FM Kirby Neurobiol Ctr,Childrens Hosp Boston, Boston, MA 02115 USA.
EM mustafa.sahin@childrens.harvard.edu
FU Novartis; Autism Speaks; Tuberous Sclerosis Alliance; NIH [R01
   NS058956]; John Merck Fund; Nancy Lurie Marks Family Foundation;
   Children's Hospital Boston Translational Research Program; Manton Family
   Foundation
FX I am grateful to Kira Dies for assistance with the figure/table and Drs.
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   Family Foundation, Children's Hospital Boston Translational Research
   Program and the Manton Family Foundation.
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NR 59
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Z9 23
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 895
EP 901
DI 10.1016/j.conb.2012.04.008
PG 7
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000023
PM 22560338
ER

PT J
AU Smith, DG
   Ehlers, MD
AF Smith, Daniel G.
   Ehlers, Michael D.
TI Mining and modeling human genetics for autism therapeutics
SO CURRENT OPINION IN NEUROBIOLOGY
LA English
DT Article
ID FRAGILE-X-SYNDROME; IPSC-DERIVED NEURONS; SPECTRUM DISORDERS; MOUSE
   MODEL; L1 RETROTRANSPOSITION; MENTAL-RETARDATION; DELETION SYNDROME;
   ANGELMAN-SYNDROME; RETT-SYNDROME; HUMAN BRAIN
AB A growing understanding of the genetic origins of autism spectrum disorders (ASDs) and the impact of ASD risk genes on synaptic function presents new opportunities for drug discovery. Large-scale human genetics studies have begun to reveal molecular pathways and potential therapeutic drug targets. Subsequent validation and characterization of ASD risk genes in mouse models holds promise for defining relevant cellular mechanisms and brain circuits associated with the core behavioral symptoms of autism. Here We review recent advances in the molecular therapeutics in ASDs and discuss opportunities and obstacles for converting emerging biology into new medicines. We present emerging concepts on the impact of risk genes during development and adulthood that define points of intervention. We further highlight ongoing clinical trials in patients with syndromic forms of autism. These clinical studies will be an important test of the utility of human genetics as a starting point for drug discovery in ASDs.
C1 [Smith, Daniel G.; Ehlers, Michael D.] Pfizer Worldwide Res & Dev, Neurosci Res Unit, Groton, CT 06340 USA.
RP Smith, DG (reprint author), Pfizer Worldwide Res & Dev, Neurosci Res Unit, Groton, CT 06340 USA.
EM daniel.g.smith@pfizer.com; Michael.Ehlers@pfizer.com
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NR 70
TC 5
Z9 5
PU CURRENT BIOLOGY LTD
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 0959-4388
J9 CURR OPIN NEUROBIOL
JI Curr. Opin. Neurobiol.
PD OCT
PY 2012
VL 22
IS 5
BP 902
EP 910
DI 10.1016/j.conb.2012.03.004
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 060FN
UT WOS:000312762000024
PM 22483267
ER

PT J
AU Aoki, Y
   Abe, O
   Yahata, N
   Kuwabara, H
   Natsubori, T
   Iwashiro, N
   Takano, Y
   Inoue, H
   Kawakubo, Y
   Gonoi, W
   Sasaki, H
   Murakami, M
   Katsura, M
   Nippashi, Y
   Takao, H
   Kunimatsu, A
   Matsuzaki, H
   Tsuchiya, KJ
   Kato, N
   Kasai, K
   Yamasue, H
AF Aoki, Y.
   Abe, O.
   Yahata, N.
   Kuwabara, H.
   Natsubori, T.
   Iwashiro, N.
   Takano, Y.
   Inoue, H.
   Kawakubo, Y.
   Gonoi, W.
   Sasaki, H.
   Murakami, M.
   Katsura, M.
   Nippashi, Y.
   Takao, H.
   Kunimatsu, A.
   Matsuzaki, H.
   Tsuchiya, K. J.
   Kato, N.
   Kasai, K.
   Yamasue, H.
TI Absence of age-related prefrontal NAA change in adults with autism
   spectrum disorders
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE anterior cingulate; Asperger syndrome; autistic disorder; case-control;
   human; pervasive developmental disorder
ID MAGNETIC-RESONANCE-SPECTROSCOPY; N-ACETYLASPARTATE; ASPERGER-SYNDROME;
   IN-VIVO; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; MR SPECTROSCOPY;
   RATING-SCALE; WHITE-MATTER; METABOLITE CONCENTRATIONS
AB Atypical trajectory of brain growth in autism spectrum disorders (ASDs) has been recognized as a potential etiology of an atypical course of behavioral development. Numerous neuroimaging studies have focused on childhood to investigate atypical age-related change of brain structure and function, because it is a period of neuron and synapse maturation. Recent studies, however, have shown that the atypical age-related structural change of autistic brain expands beyond childhood and constitutes neural underpinnings for lifelong difficulty to behavioral adaptation. Thus, we examined effects of aging on neurochemical aspects of brain maturation using 3-T proton magnetic resonance spectroscopy (H-1-MRS) with single voxel in the medial prefrontal cortex (PFC) in 24 adult men with non-medicated high-functioning ASDs and 25 age-, IQ-and parental-socioeconomic- background-matched men with typical development (TD). Multivariate analyses of covariance demonstrated significantly high N-acetylaspartate (NAA) level in the ASD subjects compared with the TD subjects (F = 4.83, P = 0.033). The low NAA level showed a significant positive correlation with advanced age in the TD group (r = -0.618, P = 0.001), but was not evident among the ASD individuals (r = -0.258, P = 0.223). Fisher's r-to-z transformation showed a significant difference in the correlations between the ASD and TD groups (Z = -3.23, P = 0.001), which indicated that the age-NAA relationship was significantly specific to people with TD. The current H-1-MRS study provided new evidence that atypical age-related change of neurochemical aspects of brain maturation in ASD individuals expands beyond childhood and persists during adulthood. Translational Psychiatry (2012) 2, e178; doi:10.1038/tp.2012.108; published online 23 October 2012
C1 [Yamasue, H.] Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1138655, Japan.
   [Abe, O.] Nihon Univ, Sch Med, Dept Radiol, Tokyo, Japan.
   [Yahata, N.] Univ Tokyo, GCOE, Tokyo 1138655, Japan.
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   [Yamasue, H.] Japan Sci & Technol Agcy, CREST, Tokyo, Japan.
RP Yamasue, H (reprint author), Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan.
EM yamasue-tky@umin.ac.jp
FU CREST (Japan Science and Technology Agency); KAKENHI [22689034,
   20591378]; 'Development of biomarker candidates for social behavior'
   project
FX This study was supported in part by CREST (Japan Science and Technology
   Agency), and was also supported by KAKENHI (22689034 to HY; 20591378 to
   NY), the 'Development of biomarker candidates for social behavior'
   project carried out under the Strategic Research Program for Brain
   Sciences by the MEXT and the Global Center of Excellence (COE) Program
   'Comprehensive Center of Education and Research for Chemical Biology of
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NR 71
TC 12
Z9 12
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD OCT
PY 2012
VL 2
AR e178
DI 10.1038/tp.2012.108
PG 8
WC Psychiatry
SC Psychiatry
GA 062EB
UT WOS:000312900800014
PM 23092982
ER

PT J
AU Favre, G
   Lavenex, PB
   Lavenex, P
AF Favre, G.
   Lavenex, P. Banta
   Lavenex, P.
TI Developmental regulation of expression of schizophrenia susceptibility
   genes in the primate hippocampal formation
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE Alzheimer; autism spectrum disorder; epilepsy; hippocampus;
   schizophrenia; Williams
ID MAJOR DEPRESSIVE DISORDER; TEMPORAL-LOBE EPILEPSY; BIPOLAR-DISORDER;
   BEHAVIORAL-GENETICS; ALZHEIMERS-DISEASE; WILLIAMS-SYNDROME; ALLELE
   FREQUENCY; NMDA RECEPTORS; VERBAL MEMORY; DOWN-SYNDROME
AB The hippocampal formation is essential for normal memory function and is implicated in many neurodevelopmental, neurodegenerative and neuropsychiatric disorders. In particular, abnormalities in hippocampal structure and function have been identified in schizophrenic subjects. Schizophrenia has a strong polygenic component, but the role of numerous susceptibility genes in normal brain development and function has yet to be investigated. Here we described the expression of schizophrenia susceptibility genes in distinct regions of the monkey hippocampal formation during early postnatal development. We found that, as compared with other genes, schizophrenia susceptibility genes exhibit a differential regulation of expression in the dentate gyrus, CA3 and CA1, over the course of postnatal development. A number of these genes involved in synaptic transmission and dendritic morphology exhibit a developmental decrease of expression in CA3. Abnormal CA3 synaptic organization observed in schizophrenics might be related to some specific symptoms, such as loosening of association. Interestingly, changes in gene expression in CA3 might occur at a time possibly corresponding to the late appearance of the first clinical symptoms. We also found earlier changes in expression of schizophrenia susceptibility genes in CA1, which might be linked to prodromal psychotic symptoms. A number of schizophrenia susceptibility genes including APOE, BDNF, MTHFR and SLC6A4 are involved in other disorders, and thus likely contribute to nonspecific changes in hippocampal structure and function that must be combined with the dysregulation of other genes in order to lead to schizophrenia pathogenesis. Translational Psychiatry (2012) 2, e173; doi:10.1038/tp.2012.105; published online 23 October 2012
C1 [Lavenex, P. Banta; Lavenex, P.] Univ Lausanne, Inst Psychol, Quartier UNIL Dorigny, Lab Expt Res Behav, CH-1015 Lausanne, Switzerland.
   [Favre, G.; Lavenex, P. Banta; Lavenex, P.] Univ Fribourg, Dept Med, Lab Brain & Cognit Dev, CH-1700 Fribourg, Switzerland.
RP Lavenex, P (reprint author), Univ Lausanne, Inst Psychol, Quartier UNIL Dorigny, Lab Expt Res Behav, CH-1015 Lausanne, Switzerland.
EM pierre.lavenex@unil.ch
FU Swiss National Science Foundation [PP00A-106701, PP00P3-124536/1];
   National Alliance for Research on Schizophrenia and Depression (NARSAD)
FX This work was supported by the Swiss National Science Foundation
   (PP00A-106701, PP00P3-124536/1) and the National Alliance for Research
   on Schizophrenia and Depression (NARSAD). We thank Jeff Gregg, Ryan
   Davis and Steven Sugden for their contribution to the early stages of
   this research program.
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NR 80
TC 4
Z9 4
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD OCT
PY 2012
VL 2
AR e173
DI 10.1038/tp.2012.105
PG 9
WC Psychiatry
SC Psychiatry
GA 062EB
UT WOS:000312900800009
PM 23092977
ER

PT J
AU Ishima, T
   Iyo, M
   Hashimoto, K
AF Ishima, T.
   Iyo, M.
   Hashimoto, K.
TI Neurite outgrowth mediated by the heat shock protein Hsp90 alpha: a
   novel target for the antipsychotic drug aripiprazole
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE aripirazole; Ca2+ signaling; heat shock protein; IP3 receptors; neurite
   outgrowth
ID NERVE GROWTH-FACTOR; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; SEROTONIN
   5-HT1A RECEPTORS; PC12 CELLS; IP3 RECEPTORS; MOLECULAR CHAPERONES;
   SIGNAL-TRANSDUCTION; SIGMA-1 RECEPTORS; CONTROLLED-TRIALS; BIPOLAR
   DISORDER
AB Aripiprazole is an atypical antipsychotic drug approved for the treatment of psychiatric disorders such as schizophrenia, bipolar disorder, major depressive disorder and autism. The drug shows partial agonistic activity at dopamine D-2 receptors and 5-hydroxytryptamine (5-HT) 5-HT1A receptors, and antagonistic activity at 5-HT2A receptors. However, the precise mechanistic pathways remain unclear. In this study, we examined the effects of aripiprazole on neurite outgrowth. Aripiprazole significantly potentiated nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells, in a concentration-dependent manner. The 5-HT1A receptor antagonist WAY-100635, but not the dopamine D-2 receptor antagonist sulpiride, blocked the effects of aripiprazole, although, only partially. Specific inhibitors of inositol 1,4,5-triphosphate (IP3) receptors and BAPTA-AM, a chelator of intracellular Ca2+, blocked the effects of aripiprazole. Moreover, specific inhibitors of several common signaling pathways phospholipase C-gamma (PLC-gamma), phosphatidylinositol-3 kinase (PI3K), mammalian target of rapamycin, p38 MAPK, c-Jun N-terminal kinase, Akt, Ras, Raf, ERK, MAPK) also blocked the effects of aripiprazole. Using proteomic analysis, we found that aripiprazole significantly increased levels of the heat shock protein Hsp90 alpha in cultured cells. The effects of aripiprazole on NGF-induced neurite outgrowth were significantly attenuated by treatment with Hsp90 alpha RNA interference, but not by the negative control of Hsp90 alpha. These findings suggest that both 5-HT1A receptor activation and Ca2+ signaling via IP3 receptors, as well as their downstream cellular signaling pathways play a role in the promotion of aripiprazole-induced neurite outgrowth. Furthermore, aripiprazole-induced increases in Hsp90 alpha protein expression may form part of the therapeutic mechanism for this drug. Translational Psychiatry (2012) 2, e170; doi:10.1038/tp.2012.97; published online 16 October 2012
C1 [Ishima, T.; Hashimoto, K.] Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, Chiba 2608670, Japan.
   [Iyo, M.] Chiba Univ, Grad Sch Med, Dept Psychiat, Chiba 2608670, Japan.
RP Hashimoto, K (reprint author), Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, 1-8-1 Inohana, Chiba 2608670, Japan.
EM hashimoto@faculty.chiba-u.jp
FU Japan Society for the Promotion of Science (JSPS); Ministry of
   Education, Culture, Sports, Science and Technology (MEXT), Japan
FX This study was supported by a Grant-in-Aid for Young Scientists (B) (to
   TI), a Grant-in-Aid for Scientific Research (B) (to KH) from Japan
   Society for the Promotion of Science (JSPS), and a Grant-in-Aid for
   Scientific Research on Innovative Areas (to KH) from the Ministry of
   Education, Culture, Sports, Science and Technology (MEXT), Japan.
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NR 62
TC 10
Z9 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD OCT
PY 2012
VL 2
AR e170
DI 10.1038/tp.2012.97
PG 8
WC Psychiatry
SC Psychiatry
GA 062EB
UT WOS:000312900800006
PM 23047241
ER

PT J
AU Nava, C
   Lamari, F
   Heron, D
   Mignot, C
   Rastetter, A
   Keren, B
   Cohen, D
   Faudet, A
   Bouteiller, D
   Gilleron, M
   Jacquette, A
   Whalen, S
   Afenjar, A
   Perisse, D
   Laurent, C
   Dupuits, C
   Gautier, C
   Gerard, M
   Huguet, G
   Caillet, S
   Leheup, B
   Leboyer, M
   Gillberg, C
   Delorme, R
   Bourgeron, T
   Brice, A
   Depienne, C
AF Nava, C.
   Lamari, F.
   Heron, D.
   Mignot, C.
   Rastetter, A.
   Keren, B.
   Cohen, D.
   Faudet, A.
   Bouteiller, D.
   Gilleron, M.
   Jacquette, A.
   Whalen, S.
   Afenjar, A.
   Perisse, D.
   Laurent, C.
   Dupuits, C.
   Gautier, C.
   Gerard, M.
   Huguet, G.
   Caillet, S.
   Leheup, B.
   Leboyer, M.
   Gillberg, C.
   Delorme, R.
   Bourgeron, T.
   Brice, A.
   Depienne, C.
TI Analysis of the chromosome X exome in patients with autism spectrum
   disorders identified novel candidate genes, including TMLHE
SO TRANSLATIONAL PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorders; carnitine; chromosome X; male excess;
   next-generation sequencing; TMLHE
ID LINKED MENTAL-RETARDATION; CLEFT LIP/CLEFT PALATE; DE-NOVO MUTATIONS;
   UBIQUITIN LIGASE HUWE1; COPY NUMBER VARIATION; CARNITINE BIOSYNTHESIS;
   PHF8 GENE; DIFFERENTIATION; VARIANTS; BRAIN
AB The striking excess of affected males in autism spectrum disorders (ASD) suggests that genes located on chromosome X contribute to the etiology of these disorders. To identify new X-linked genes associated with ASD, we analyzed the entire chromosome X exome by next-generation sequencing in 12 unrelated families with two affected males. Thirty-six possibly deleterious variants in 33 candidate genes were found, including PHF8 and HUWE1, previously implicated in intellectual disability (ID). A nonsense mutation in TMLHE, which encodes the epsilon-N-trimethyllysine hydroxylase catalyzing the first step of carnitine biosynthesis, was identified in two brothers with autism and ID. By screening the TMLHE coding sequence in 501 male patients with ASD, we identified two additional missense substitutions not found in controls and not reported in databases. Functional analyses confirmed that the mutations were associated with a loss-of-function and led to an increase in trimethyllysine, the precursor of carnitine biosynthesis, in the plasma of patients. This study supports the hypothesis that rare variants on the X chromosome are involved in the etiology of ASD and contribute to the sex-ratio disequilibrium. Translational Psychiatry (2012) 2, e179; doi:10.1038/tp.2012.102; published online 23 October 2012
C1 [Nava, C.; Rastetter, A.; Bouteiller, D.; Laurent, C.; Dupuits, C.; Gautier, C.; Brice, A.; Depienne, C.] Hop La Pitie Salpetriere, Inst Cerveau & Moelle Epiniere ICM, INSERM, U975,CRICM, F-75013 Paris, France.
   [Nava, C.; Rastetter, A.; Bouteiller, D.; Laurent, C.; Gautier, C.; Brice, A.; Depienne, C.] Hop La Pitie Salpetriere, CNRS 7225, CRICM, F-75013 Paris, France.
   [Nava, C.; Rastetter, A.; Bouteiller, D.; Brice, A.; Depienne, C.] Univ Paris 06, UMR S 975, Paris, France.
   [Nava, C.; Heron, D.; Mignot, C.; Faudet, A.; Jacquette, A.; Whalen, S.; Afenjar, A.; Brice, A.] Hop La Pitie Salpetriere, AP HP, Dept Genet & Cytogenet, Unite Fonct Genet Clin, F-75013 Paris, France.
   [Lamari, F.; Gilleron, M.] Hop La Pitie Salpetriere, AP HP, Dept Biochim, F-75013 Paris, France.
   [Heron, D.; Mignot, C.; Afenjar, A.] Hop Trousseau, AP HP, Serv Neuropediat, F-75571 Paris, France.
   [Heron, D.; Mignot, C.; Jacquette, A.; Afenjar, A.] Ctr Reference Deficiences Intellectuelles Causes, Paris, France.
   [Heron, D.; Mignot, C.; Jacquette, A.; Afenjar, A.] GRC Deficience Intellectuelle & Autisme UPMC, Grp Rech Clin, Paris, France.
   [Keren, B.] Hop La Pitie Salpetriere, AP HP, Dept Genet & Cytogenet, Unite Fonct Cytogenet, F-75013 Paris, France.
   [Cohen, D.; Perisse, D.; Laurent, C.] Hop La Pitie Salpetriere, AP HP, Serv Psychiat Enfant & Adolescent, F-75013 Paris, France.
   [Cohen, D.] UPMC Paris 6, CNRS UMR 7222, Inst Syst Intelligents & Robot, Paris, France.
   [Bouteiller, D.] Hop La Pitie Salpetriere, PFGS Platform, ICM, F-75013 Paris, France.
   [Afenjar, A.] Hop Trousseau, Ctr Reference Anomalies Dev & Syndromes Malformat, F-75571 Paris, France.
   [Perisse, D.] Ctr Referent Autisme, Paris, France.
   [Dupuits, C.; Caillet, S.] Hop La Pitie Salpetriere, AP HP, Serv Dietet & Unite Fonct Neurormetabolise, F-75013 Paris, France.
   [Gerard, M.] CHU Cote Nacre, Paris, France.
   [Huguet, G.; Bourgeron, T.] Inst Pasteur, Human Genet & Cognit Funct Unit, Paris, France.
   [Huguet, G.; Bourgeron, T.] Inst Pasteur, CNRS URA Genes Synapses & Cogn 2182, Paris, France.
   [Huguet, G.; Bourgeron, T.] Univ Paris Diderot, Paris, France.
   [Leheup, B.] CHU Nancy Pole Enfants, Serv Med Infantile & Genet Clin, Ctr Reference Anomalies Dev & Syndromes Malformat, Vandoeuvre Les Nancy, France.
   [Leheup, B.] Univ Lorraine, EA 4368, Vandoeuvre Les Nancy, France.
   [Leboyer, M.] Univ Paris Est, Fac Med, Creteil, France.
   [Leboyer, M.] Hop H Mondor A Chenevier, AP HP, Creteil, France.
   [Leboyer, M.] Fondat FondaMental, Creteil, France.
   [Leboyer, M.] Gothenburg Univ, Dept Child & Adolescent Psychiat, Gothenburg, Sweden.
   [Gillberg, C.] Hop Robert Debre, AP HP, Serv Pedopsychiat, Paris, France.
   [Delorme, R.] Hop La Pitie Salpetriere, AP HP, Dept Genet & Cytogenet, Unite Fonct Neurogenet Mol Cullulaire, Paris, France.
   [Depienne, C.] Hop Henri Mondor, INSERM, U955, F-94010 Creteil, France.
RP Depienne, C (reprint author), Hop La Pitie Salpetriere, Inst Cerveau & Moelle Epiniere, INSERM, Cricm U975, F-75013 Paris, France.
EM alexis.brice@upmc.fr; christel.depienne@upmc.fr
FU GIS-Maladies Rares; Fondation de France; ERA-NET NEURON EUHFAUTISM;
   INSERM; AP-HP
FX We thank the patients for their participation in the study, the P3S
   platform and the genotyping and sequencing platform of the ICM for
   technical assistance and the DNA and cell bank of CRICM for DNA
   extraction and cell culture. We also thank Dr Merle Ruberg for critical
   reading of the manuscript and Pr Andre Megarbane for kindly providing
   DNA of controls individuals from Lebanon. This study was financially
   supported by GIS-Maladies Rares, Fondation de France, ERA-NET NEURON
   EUHFAUTISM, INSERM and AP-HP.
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NR 52
TC 17
Z9 17
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 2158-3188
J9 TRANSL PSYCHIAT
JI Transl. Psychiatr.
PD OCT
PY 2012
VL 2
AR e179
DI 10.1038/tp.2012.102
PG 12
WC Psychiatry
SC Psychiatry
GA 062EB
UT WOS:000312900800015
PM 23092983
ER

PT J
AU Ku, CS
   Roukos, DH
AF Ku, Chee-Seng
   Roukos, Dimitrios H.
TI De novo mutations, protein-protein interactions and functional
   regulatory networks toward novel diagnostics in autism
SO EXPERT REVIEW OF PROTEOMICS
LA English
DT Editorial Material
DE autism; de novo mutations; heterogeneity; protein-protein interactions;
   whole-exome sequencing
ID COPY NUMBER VARIATION; SPECTRUM DISORDERS; REVEALS; GENES; RESISTANCE;
   MEDICINE; CANCER
C1 [Ku, Chee-Seng] Univ Ioannina, Ctr Biosyst & Genom Network Med CBS GenNetMed, GR-45110 Ioannina, Greece.
   [Ku, Chee-Seng] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
   [Roukos, Dimitrios H.] Ioannina Univ Hosp, Dept Surg, Ioannina, Greece.
RP Roukos, DH (reprint author), Univ Ioannina, Ctr Biosyst & Genom Network Med CBS GenNetMed, GR-45110 Ioannina, Greece.
EM droukos@uoi.gr
CR Barabasi AL, 2011, NAT REV GENET, V12, P56, DOI 10.1038/nrg2918
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   Devlin B, 2012, CURR OPIN GENET DEV, V22, P229, DOI 10.1016/j.gde.2012.03.002
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NR 27
TC 0
Z9 0
PU EXPERT REVIEWS
PI LONDON
PA UNITEC HOUSE, 3RD FL, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON N3 1QB,
   ENGLAND
SN 1478-9450
J9 EXPERT REV PROTEOMIC
JI Expert Rev. Proteomics
PD OCT
PY 2012
VL 9
IS 5
BP 473
EP 476
DI 10.1586/EPR.12.43
PG 4
WC Biochemical Research Methods
SC Biochemistry & Molecular Biology
GA 057ZX
UT WOS:000312604600002
PM 23194261
ER

PT J
AU Appleton, RE
   Jones, AP
   Gamble, C
   Williamson, PR
   Wiggs, L
   Montgomery, P
   Sutcliffe, A
   Barker, C
   Gringras, P
AF Appleton, R. E.
   Jones, A. P.
   Gamble, C.
   Williamson, P. R.
   Wiggs, L.
   Montgomery, P.
   Sutcliffe, A.
   Barker, C.
   Gringras, P.
TI The use of MElatonin in children with Neurodevelopmental Disorders and
   impaired Sleep: a randomised, double-blind, placebo-controlled, parallel
   study (MENDS)
SO HEALTH TECHNOLOGY ASSESSMENT
LA English
DT Article
ID AUTISM SPECTRUM DISORDERS; CONTROLLED-TRIAL; EXOGENOUS MELATONIN; ONSET
   INSOMNIA; HANDICAPPED-CHILDREN; SERUM MELATONIN; IMPROVES SLEEP; PHASE
   SYNDROME; RETT-SYNDROME; YOUNG-ADULTS
AB Background: Difficulties in initiating and maintaining sleep are common in children with neurodevelopmental disorders. Melatonin is unlicensed in children yet widely prescribed for sleep problems.
   Objective: To determine whether or not immediate-release melatonin is beneficial compared with placebo in improving total duration of night-time sleep in children with neurodevelopmental problems.
   Design: Randomised, double-blind, placebo-controlled, parallel study.
   Setting: Hospitals throughout England and Wales recruited patients referred by community paediatricians and other clinical colleagues.
   Participants: Children with neurodevelopmental problems aged from 3 years to 15 years 8 months who did not fall asleep within 1 hour of lights out or who had <6 hours of continuous sleep. Before randomisation, patients meeting eligibility criteria entered a 4- to 6-week behaviour therapy period in which a behaviour therapy advice booklet was provided. Sleep was measured using sleep diaries and actigraphy. After this period the sleep diaries were reviewed to determine if the sleep problem fulfilled the eligibility criteria. Eligible participants were randomised and followed for 12 weeks.
   Interventions: Melatonin or placebo capsules in doses of 0.5 mg, 2 mg, 6mg and 12 mg for a period of 12 weeks. The starting dose was 0.5 mg and the dose could be escalated through 2 mg and 6 mg to 12 mg during the first 4 weeks, at the end of which the child was maintained on that dose.
   Main outcome measures: The primary outcome was total night-time sleep time (TST) calculated using sleep diaries at 12 weeks compared with baseline. Secondary outcome measures included TST calculated using actigraphy data, sleep-onset latency (SOL) (time taken to fall asleep), sleep efficiency, Composite Sleep Disturbance Index score, global measure of child's sleep quality, Aberrant Behaviour Checklist, Family Impact Module of the Pediatric Quality of Life Inventory (PedsQL (TM)), the Epworth Sleepiness Scale, number and severity of seizures and adverse events. Salivary melatonin concentrations and association of genetic variants with abnormal melatonin production were also investigated.
   Results: A total of 275 children were screened to enter the trial; 263 (96%) children were registered and completed the 4- to 6-week behaviour therapy period and 146 (56%) children were randomised, of whom 110 (75%) contributed data for the primary outcome. The difference in TST time between the melatonin and placebo groups adjusted for baseline was 22.43 minutes [95% confidence interval (Cl) 0.52 to 44.34 minutes; p = 0.04] measured using sleep diaries. A reduction in SOL, adjusted for baseline, was seen for melatonin compared with placebo when measured by sleep diaries (-37.49 minutes, 95% CI -55.27 to -19.71 minutes; p < 0.0001) and actigraphy (-45.34 minutes, 95% CI -68.75 to -21.93 minutes; p=0.0003). There were no significant differences between the two groups in terms of the reporting of adverse events. The results of other secondary outcomes favoured melatonin but were not statistically significant.
   Conclusions: On average, the children treated with melatonin slept 23 minutes longer than those in the placebo group; however, the upper limit of the confidence interval was less than 1 hour, the minimum clinically worthwhile difference specified at the outset of the trial. Melatonin is effective in reducing SOL in children with neurodevelopmental delay by a mean of 45 minutes; a value of 30 minutes was specified a priori to be clinically important. Future studies should be conducted over longer periods and directly compare different formulations of melatonin with conventional hypnotic and sedative medications. It would also be important to study groups of children with specific neurological disorders.
   Trial registration: Current Controlled Trials ISRCTN05534585.
C1 [Appleton, R. E.; Barker, C.] Alder Hey Childrens NHS Fdn Trust, Liverpool, Merseyside, England.
   [Jones, A. P.; Gamble, C.; Williamson, P. R.] Univ Liverpool, Med Children Res Network, Clin Trials Unit, Liverpool L69 3BX, Merseyside, England.
   [Wiggs, L.] Oxford Brookes Univ, Dept Psychol, Oxford OX3 0BP, England.
   [Montgomery, P.] Univ Oxford, Ctr Evidence Based Intervent, Oxford, England.
   [Sutcliffe, A.] UCL, London, England.
   [Gringras, P.] Guys & St Thomas NHS Fdn Trust, London, England.
RP Appleton, RE (reprint author), Alder Hey Childrens NHS Fdn Trust, Liverpool, Merseyside, England.
EM Richard.Appleton@alderhey.nhs.uk
FU NIHR Health Technology Assessment programme
FX This project was funded by the NIHR Health Technology Assessment
   programme and will be published in full in Health Technology Assessment;
   Vol. 16, No. 40. See the HTA programme website for further project
   information.
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NR 88
TC 2
Z9 2
PU NATL COORDINATING CENTRE HEALTH TECHNOLOGY ASSESSMENT
PI SOUTHAMPTON
PA ALPHA HOUSE, UNIV SOUTHHAMPTON SCIENCE PARK, SOUTHAMPTON, SO16 7NS,
   ENGLAND
SN 1366-5278
J9 HEALTH TECHNOL ASSES
JI Health Technol. Assess.
PD OCT
PY 2012
VL 16
IS 40
BP 1
EP +
DI 10.3310/hta16400
PG 235
WC Health Care Sciences & Services
SC Health Care Sciences & Services
GA 058FG
UT WOS:000312618900001
ER

PT J
AU Rutherford, HJV
   Wareham, JD
   Vrouva, I
   Mayes, LC
   Fonagy, P
   Potenza, MN
AF Rutherford, Helena J. V.
   Wareham, Justin D.
   Vrouva, Ioanna
   Mayes, Linda C.
   Fonagy, Peter
   Potenza, Marc N.
TI Sex Differences Moderate the Relationship Between Adolescent Language
   and Mentalization
SO PERSONALITY DISORDERS-THEORY RESEARCH AND TREATMENT
LA English
DT Article
DE mentalization; language; adolescence; sex differences
ID BORDERLINE PERSONALITY-DISORDER; HIGH-FUNCTIONING AUTISM;
   ASPERGER-SYNDROME; BRAIN; MIND; CHILDREN; ADULTS; ASSOCIATIONS;
   ORGANIZATION; CHILDHOOD
AB Mentalization refers to the ability to infer mental states of self and others, and this capacity facilitates social interactions. Advances in mentalization theory have proposed that there are both explicit and implicit mentalizing capacities and language may be identified as being an important factor in differentiating these two components of mentalization. Moreover, given apparent sex differences in language and mentalization, we hypothesized that sex may moderate the relationship between language and mentalization. In this study, measures assessing implicit and explicit mentalization as well as language were examined in 49 adolescents (25 girls and 24 boys) aged 14 to 18 years. Participants were administered the Mentalizing Stories for Adolescents to assess explicit mentalization, and the Reading Mind in the Eyes Task to assess implicit mentalization. Language was assessed using the Clinical Evaluation of Language Fundamentals. Sex was found to moderate the relationship between language and explicit mentalization; while language and explicit mentalization were related in boys, these domains were unrelated in girls. There was no moderation of language and implicit mentalization by sex, and these two domains were also uncorrelated. These findings suggest an important role for language development in the capacity for explicit mentalization in boys, and we interpret this as a benefit in girls who may be more socially motivated and less limited by language in their efforts to mentalize.
C1 [Rutherford, Helena J. V.; Wareham, Justin D.; Mayes, Linda C.; Potenza, Marc N.] Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA.
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   [Potenza, Marc N.] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA.
RP Potenza, MN (reprint author), SAC, CMHC, Room S-104,34 Pk St, New Haven, CT 06519 USA.
EM marc.potenza@yale.edu
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NR 51
TC 8
Z9 8
PU EDUCATIONAL PUBLISHING FOUNDATION-AMERICAN PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST, NE, WASHINGTON, DC 20002-4242 USA
SN 1949-2715
J9 PERSONAL DISORD
JI Personal. Disord.
PD OCT
PY 2012
VL 3
IS 4
BP 393
EP 405
DI 10.1037/a0028938
PG 13
WC Psychology, Clinical
SC Psychology
GA 057MT
UT WOS:000312568400004
PM 22800178
ER

PT J
AU Ouimet, T
   Foster, NEV
   Hyde, KL
AF Ouimet, Tia
   Foster, Nicholas E. V.
   Hyde, Krista L.
TI Auditory global-local processing: Effects of attention and musical
   experience
SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA
LA English
DT Article
ID TEMPORAL INFORMATION; MELODIC CONTOUR; VISUAL ANGLE; MUSICIANS; BRAIN;
   PRECEDENCE; AUTISM; NONMUSICIANS; INTERVAL; FEATURES
AB In vision, global (whole) features are typically processed before local (detail) features ("global precedence effect"). However, the distinction between global and local processing is less clear in the auditory domain. The aims of the present study were to investigate: (i) the effects of directed versus divided attention, and (ii) the effect musical training on auditory global-local processing in 16 adult musicians and 16 non-musicians. Participants were presented with short nine-tone melodies, each comprised of three triplet sequences (three-tone units). In a "directed attention" task, participants were asked to focus on either the global or local pitch pattern and had to determine if the pitch pattern went up or down. In a "divided attention" task, participants judged whether the target pattern (up or down) was present or absent. Overall, global structure was perceived faster and more accurately than local structure. The global precedence effect was observed regardless of whether attention was directed to a specific level or divided between levels. Musicians performed more accurately than non-musicians overall, but non-musicians showed a more pronounced global advantage. This study provides evidence for an auditory global precedence effect across attention tasks, and for differences in auditory global-local processing associated with musical experience. (C) 2012 Acoustical Society of America. [http://dx.doi.org/10.1121/1.4747009]
C1 [Ouimet, Tia; Foster, Nicholas E. V.; Hyde, Krista L.] McGill Univ, Fac Med, Montreal Childrens Hosp, Montreal, PQ H3Z 2Z3, Canada.
RP Ouimet, T (reprint author), McGill Univ, Fac Med, Montreal Childrens Hosp, 4060 St Catherine W,Room 322, Montreal, PQ H3Z 2Z3, Canada.
EM ouimet.to@gmail.com
FU Canadian Institutes for Health Research
FX We thank T. Justus and A. List for sharing their stimulus framework with
   us from which we adapted our auditory material. We thank Lewis Hou for
   his assistance in data collection, and our participants for taking part
   in the study. This work was funded by a grant from the Canadian
   Institutes for Health Research to K.L.H.
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NR 44
TC 1
Z9 1
PU ACOUSTICAL SOC AMER AMER INST PHYSICS
PI MELVILLE
PA STE 1 NO 1, 2 HUNTINGTON QUADRANGLE, MELVILLE, NY 11747-4502 USA
SN 0001-4966
J9 J ACOUST SOC AM
JI J. Acoust. Soc. Am.
PD OCT
PY 2012
VL 132
IS 4
BP 2536
EP 2544
DI 10.1121/1.4747009
PN 1
PG 9
WC Acoustics; Audiology & Speech-Language Pathology
SC Acoustics; Audiology & Speech-Language Pathology
GA 018HJ
UT WOS:000309650600056
PM 23039447
ER

PT J
AU Tabares, C
   Vicente, F
   Sanchez, S
   Aparicio, A
   Alejo, S
   Cubero, J
AF Tabares, C.
   Vicente, F.
   Sanchez, S.
   Aparicio, A.
   Alejo, S.
   Cubero, J.
TI Quantification of hormonal changes by effects of hippotherapy in the
   autistic population
SO NEUROCHEMICAL JOURNAL
LA English
DT Article
DE autism; hippotherapy; oxytocin; cortisol and progesterone
ID SALIVARY CORTISOL; OXYTOCIN; IMMUNOASSAY; HUMANS
AB Zootherapy, more specifically in its equine form, has proliferated recently as a therapeutic activity and is one of the most common applications in the stimulation of autistic individuals. At the same time, the influence of certain hormones was recently revealed in the behavior of autistic spectrum disorders. We propose to objectify the influence of analyzing equestrian therapies through laboratory methods and non-invasive techniques (salivary samples), in the hormone levels of cortisol and progesterone, thus indirectly those of oxytocin, before and after hippotherapy sessions for people with Autism Spectrum Disorder (ASD). The main results indicated that equine therapy decreased (p a parts per thousand currency sign 0.05) the levels of salivary Cortisol in the rest of the sessions (before Hippotherapy 33.11 +/- 0.96 ng/mL vs. after Hippotherapy 2.23 +/- 0.75 ng/mL). And also the levels of salivary progesterone in the first session (before Hippotherapy 28.63 +/- 12.81 ng/mL vs. after Hippotherapy 51.59 +/- 33.11 ng/mL) and in the rest of the sessions (before hippotherapy 21.58 +/- 12 pg/mL vs. after Hippotherapy 26.03 +/- 11.98 pg/mL) which was always on the rise. These effective results were corroborated with the Cortisol/Progesterone Balance which reduced after equine therapy in the first session (before Hippotherapy 99.87 vs. after Hippotherapy 76.24) and the other sessions (before Hippotherapy 181.31 vs. after Hippotherapy 110.48). In conclusion, the Hippotherapy sessions for the population with ASD generated leads to an improvement in social attitudes, and it is confirmed with the effective modulation of the implicating hormones.
C1 [Tabares, C.; Vicente, F.; Sanchez, S.] Univ Extremadura, Dept Psychol & Anthropol, Res Grp Psyche Ex, Badajoz, Spain.
   [Cubero, J.] Univ Extremadura, Lab Lab Hlth Educ, Sci Educ Area, Badajoz, Spain.
   [Aparicio, A.; Alejo, S.] Univ Hosp Infanta Cristina, SES, Lab Clin Anal, Badajoz, Spain.
RP Tabares, C (reprint author), Av Elvas S-N, Badajoz 06006, Spain.
EM ktabsan@hotmail.com
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TC 1
Z9 1
PU MAIK NAUKA/INTERPERIODICA/SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013-1578 USA
SN 1819-7124
J9 NEUROCHEM J+
JI Neurochem. J.
PD OCT
PY 2012
VL 6
IS 4
BP 311
EP 316
DI 10.1134/S1819712412040125
PG 6
WC Neurosciences
SC Neurosciences & Neurology
GA 050PU
UT WOS:000312067300011
ER

PT J
AU Saitovitch, A
   Bargiacchi, A
   Chabane, N
   Brunelle, F
   Samson, Y
   Boddaert, N
   Zilbovicius, M
AF Saitovitch, A.
   Bargiacchi, A.
   Chabane, N.
   Brunelle, F.
   Samson, Y.
   Boddaert, N.
   Zilbovicius, M.
TI Social cognition and the superior temporal sulcus: Implications in
   autism
SO REVUE NEUROLOGIQUE
LA English
DT Article
DE Autism; Social perception; Social cognition; STS
ID PERVASIVE DEVELOPMENTAL DISORDERS; CEREBRAL-BLOOD-FLOW; BIOLOGICAL
   MOTION; CHILDHOOD AUTISM; HUMAN BRAIN; SPECTRUM DISORDERS; FUNCTIONING
   AUTISM; ASPERGER-SYNDROME; AUDITORY-CORTEX; PERCEPTION
AB The most common clinical sign of autism spectrum disorders (ASD) is social interaction impairment, which is associated with communication deficits and stereotyped behaviors. Based on brain-imaging results, our hypothesis is that abnormalities in the superior temporal sulcus (STS) are highly implicated in ASD. These abnormalities are characterized by decreased grey matter concentration, rest hypoperfusion and abnormal activation during social tasks. STS anatomofunctional anomalies occurring early across brain development could constitute the first step in the cascade of neural dysfunctions underlying autism. It is known that STS is highly implicated on social perception processing, from perception of biological movements, such as body movements or eye gaze, to more complex social cognition processes. Among the impairments that can be described in social perception processing, eye gaze perception is particularly relevant in autism. Gaze abnormalities can now be objectively measured using eye-tracking methodology. In the present work, we will review recent data on STS contributions to normal social cognition and its implication in autism, with particular focus on eye gaze perception. (C) 2012 Elsevier Masson SAS. All rights reserved.
C1 [Saitovitch, A.; Bargiacchi, A.; Chabane, N.; Brunelle, F.; Boddaert, N.; Zilbovicius, M.] Univ Paris 05, INSERM, Serv Radiol Pediat, Hop Necker Enfants Malad,AP HP,U1000, F-75015 Paris 15, France.
   [Bargiacchi, A.; Chabane, N.] Hop Robert Debre, AP HP, Serv Pedopsychiat, F-75019 Paris, France.
   [Samson, Y.] Univ Paris 06, Serv Urgences Cerebrovasc, Grp Hosp Pitie Salpetriere, AP HP, F-75013 Paris, France.
RP Saitovitch, A (reprint author), Univ Paris 05, INSERM, Serv Radiol Pediat, Hop Necker Enfants Malad,AP HP,U1000, 149 Rue Sevres, F-75015 Paris 15, France.
EM a.saitovitch@gmail.com
FU Fondation de France; Fondation Orange
FX To Fondation de France and Fondation Orange for funding the research.
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NR 75
TC 5
Z9 6
PU MASSON EDITEUR
PI MOULINEAUX CEDEX 9
PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE
SN 0035-3787
J9 REV NEUROL-FRANCE
JI Rev. Neurol.
PD OCT
PY 2012
VL 168
IS 10
BP 762
EP 770
DI 10.1016/j.neurol.2012.07.017
PG 9
WC Clinical Neurology
SC Neurosciences & Neurology
GA 050MM
UT WOS:000312057400014
PM 22981269
ER

PT J
AU Mitchell, MM
   Woods, R
   Chi, LH
   Schmidt, RJ
   Pessah, IN
   Kostyniak, PJ
   LaSalle, JM
AF Mitchell, Michelle M.
   Woods, Rima
   Chi, Lai-Har
   Schmidt, Rebecca J.
   Pessah, Isaac N.
   Kostyniak, Paul J.
   LaSalle, Janine M.
TI Levels of select PCB and PBDE congeners in human postmortem brain reveal
   possible environmental involvement in 15q11-q13 duplication autism
   spectrum disorder
SO ENVIRONMENTAL AND MOLECULAR MUTAGENESIS
LA English
DT Article
DE neurodevelopmental; environmental; copy number variation; autism;
   epigenetics; DNA methylation
ID POLYBROMINATED DIPHENYL ETHERS; PERSISTENT ORGANIC POLLUTANTS;
   PRADER-WILLI-SYNDROME; BROMINATED FLAME RETARDANTS;
   POLYCHLORINATED-BIPHENYLS; DEVELOPMENTAL EXPOSURE; DENDRITIC GROWTH;
   PROMOTER METHYLATION; DNA HYPOMETHYLATION; GENETIC SUBTYPES
AB Persistent organic pollutants (POPs), including polychlorinated biphenyls (PCBs) and polybrominated diphenylethers (PBDEs) that bioaccumulate in lipid-rich tissues are of concern as developmental neurotoxicants. Epigenetic mechanisms such as DNA methylation act at the interface of genetic and environmental factors implicated in autism-spectrum disorders. The relationship between POP levels and DNA methylation patterns in individuals with and without neurodevelopmental disorders has not been previously investigated. In this study, a total of 107 human frozen postmortem brain samples were analyzed for eight PCBs and seven PBDEs by GC-micro electron capture detector and GC/MS using negative chemical ionization. Human brain samples were grouped as neurotypical controls (n = 43), neurodevelopmental disorders with known genetic basis (n = 32, including Down, Rett, Prader-Willi, Angelman, and 15q11-q13 duplication syndromes), and autism of unknown etiology (n = 32). Unexpectedly, PCB 95 was significantly higher in the genetic neurodevelopmental group, but not idiopathic autism, as compared to neurotypical controls. Interestingly, samples with detectable PCB 95 levels were almost exclusively those with maternal 15q11-q13 duplication (Dup15q) or deletion in Prader-Willi syndrome. When sorted by birth year, Dup15q samples represented five out of six of genetic neurodevelopmental samples born after the 1976 PCB ban exhibiting detectable PCB 95 levels. Dup15q was the strongest predictor of PCB 95 exposure over age, gender, or year of birth. Dup15q brain showed lower levels of repetitive DNA methylation measured by LINE-1 pyrosequencing, but methylation levels were confounded by year of birth. These results demonstrate a novel paradigm by which specific POPs may predispose to genetic copy number variation of 15q11-q13. Environ. Mol. Mutagen., 2012. (c) 2012 Wiley Periodicals, Inc.
C1 [Mitchell, Michelle M.; Woods, Rima; LaSalle, Janine M.] Univ Calif Davis, Sch Med, Davis, CA 95616 USA.
   [Mitchell, Michelle M.; Woods, Rima; LaSalle, Janine M.] Univ Calif Davis, Genome Ctr, Davis, CA 95616 USA.
   [Mitchell, Michelle M.; Woods, Rima; Schmidt, Rebecca J.; LaSalle, Janine M.] Univ Calif Davis, Med Invest Neurodev Disorders Inst, Davis, CA 95616 USA.
   [Chi, Lai-Har; Kostyniak, Paul J.] SUNY Buffalo, Toxicol Res Ctr, Buffalo, NY 14260 USA.
   [Schmidt, Rebecca J.; Pessah, Isaac N.] Univ Calif Davis, Ctr Childrens Environm Hlth, Davis, CA 95616 USA.
   [Pessah, Isaac N.] Univ Calif Davis, Sch Vet Med, Davis, CA 95616 USA.
RP LaSalle, JM (reprint author), UC Davis Sch Med, Davis, CA 95616 USA.
EM jmlasalle@ucdavis.edu
RI LaSalle, Janine/A-4643-2008
OI LaSalle, Janine/0000-0002-3480-2031
FU NIH [R01ES015171, R01ES0210707, 2R01HD041462, R01 ES014901, R01
   ES017425, T32ES002321, 2K12HD051958-06]; NIEHS/EPA Center for Children's
   Environmental Health [PO1 ES11269]; US Environmental Protection Agency
   (US EPA) [R833292]; J.B. Johnson Foundation;  [R829388]
FX Grant sponsor: NIH; Grant Numbers: R01ES015171, R01ES0210707,
   2R01HD041462, R01 ES014901, R01 ES017425, T32ES002321, 2K12HD051958-06;
   Grant sponsor: NIEHS/EPA Center for Children's Environmental Health;
   Grant Number: PO1 ES11269; Grant sponsor: US Environmental Protection
   Agency (US EPA); Grant Number: R833292; Grant Number: R829388; Grant
   sponsor: J.B. Johnson Foundation.
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NR 70
TC 17
Z9 18
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0893-6692
EI 1098-2280
J9 ENVIRON MOL MUTAGEN
JI Environ. Mol. Mutagen.
PD OCT
PY 2012
VL 53
IS 8
BP 589
EP 598
DI 10.1002/em.21722
PG 10
WC Environmental Sciences; Genetics & Heredity; Toxicology
SC Environmental Sciences & Ecology; Genetics & Heredity; Toxicology
GA 017SK
UT WOS:000309611000002
PM 22930557
ER

PT J
AU Lionel, AC
   Marshall, CR
   Merico, D
   Fernandez, B
   Roberts, W
   Szatmari, P
   Schachar, R
   Bassett, AS
   Scherer, SW
AF Lionel, Anath C.
   Marshall, Christian R.
   Merico, Daniele
   Fernandez, Bridget
   Roberts, Wendy
   Szatmari, Peter
   Schachar, Russell
   Bassett, Anne S.
   Scherer, Stephen W.
TI Rare copy number variation discovery and cross-neuropsychiatric disorder
   comparisons identify risk genes for autism, ADHD, and schizophrenia
SO GENOME
LA English
DT Meeting Abstract
C1 [Lionel, Anath C.; Marshall, Christian R.; Scherer, Stephen W.] Univ Toronto, McLaughlin Ctr, 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.; Merico, Daniele; Scherer, Stephen W.] Hosp Sick Children, Ctr Appl Genom, Toronto, ON M5G 1L7, Canada.
   [Lionel, Anath C.; Marshall, Christian R.; Merico, Daniele; Scherer, Stephen W.] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1L7, Canada.
   [Fernandez, Bridget] Mem Univ Newfoundland, Discipline Genet, St John, NF A1B 3V6, Canada.
   [Fernandez, Bridget] Mem Univ Newfoundland, Discipline Med, St John, NF A1B 3V6, Canada.
   [Roberts, Wendy] Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada.
   [Szatmari, Peter] McMaster Univ, Offord Ctr Child Studies, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4K1, Canada.
   [Schachar, Russell] Hosp Sick Children, Dept Psychiat Neurosci & Mental Hlth, Toronto, ON M5G 1X8, Canada.
   [Bassett, Anne S.] Univ Toronto, Ctr Addict & Mental Hlth, Dept Psychiat, Clin Genet Res Program, Toronto, ON M5S 2S1, Canada.
NR 0
TC 0
Z9 0
PU CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
PI OTTAWA
PA 1200 MONTREAL ROAD, BUILDING M-55, OTTAWA, ON K1A 0R6, CANADA
SN 0831-2796
J9 GENOME
JI Genome
PD OCT
PY 2012
VL 55
IS 10
BP 732
EP 732
PG 1
WC Biotechnology & Applied Microbiology; Genetics & Heredity
SC Biotechnology & Applied Microbiology; Genetics & Heredity
GA 047HE
UT WOS:000311829100030
ER

PT J
AU Bultas, MW
AF Bultas, Margaret W.
TI The Health Care Experiences of the Preschool Child With Autism
SO JOURNAL OF PEDIATRIC NURSING-NURSING CARE OF CHILDREN & FAMILIES
LA English
DT Article
DE Autism; Health care; Preschool child; Mother
ID SPECTRUM DISORDERS; EXPENDITURES; PREVALENCE; MANAGEMENT; TRENDS;
   FAMILIES; PARENTS; MOTHERS; HOME; AGE
AB It is known that children with autism spectrum disorder (ASD) visit health care providers (HCPs) more frequently than typically developing peers, and mothers experience barriers in this process. The purpose of this interpretive phenomenological study was to gain a better understanding of a mother's experiences of taking her child with ASD to the HCP. Two themes related to the health care experience of the child surfaced from the study. These themes included feelings that HCPs do not "get" the complexity of caring for the child and marginalization of mothers by the HCP. The need for creation of child-specific profiles emerged from this study. (C) 2012 Elsevier Inc. All rights reserved.
C1 St Louis Univ, Sch Nursing, St Louis, MO 63103 USA.
RP Bultas, MW (reprint author), St Louis Univ, Sch Nursing, St Louis, MO 63103 USA.
EM mbultas@juno.com
FU Goldfarb School of Nursing at Barnes Jewish College; Tao Iota Chapter of
   Sigma Theta Tau
FX This research was funded by the Goldfarb School of Nursing at Barnes
   Jewish College and the Tao Iota Chapter of Sigma Theta Tau. I would like
   to acknowledge the following people for their support of this project:
   Jean Bachman, DSN, RN; Dawn Garzon, PhD, RN, PNP-BC, CPNP-PC, FAANP;
   Shawn Pohlman, PhD, RN; and Rebecca McCathren, PhD. Study results were
   disseminated at the 21st Annual Convention of the Society of Pediatric
   Nurses, April 2011, Las Vegas, NV.
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NR 45
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 OCT
PY 2012
VL 27
IS 5
BP 460
EP 470
DI 10.1016/j.pedn.2011.05.005
PG 11
WC Nursing; Pediatrics
SC Nursing; Pediatrics
GA 045OS
UT WOS:000311706800005
PM 22920657
ER

PT J
AU Kato, N
AF Kato, Nobumasa
TI Clinical manifestations and eye tracking patterns of adults with autism
   spectrum disorders (ASD)
SO ASIA-PACIFIC PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Kato, Nobumasa] Showa Univ, Karasuyama Hosp, Dept Psychiat, Tokyo, Japan.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1758-5864
J9 ASIA-PAC PSYCHIAT
JI Asia-Pac. Psychiatry
PD OCT
PY 2012
VL 4
SU 1
SI SI
BP 51
EP 52
PG 2
WC Psychiatry
SC Psychiatry
GA 029AK
UT WOS:000310467000120
ER

PT J
AU Chen, CH
AF Chen, Chia-Hsiang
TI Genomic structural variations in patients with autism spectrum disorders
   from Taiwan
SO ASIA-PACIFIC PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Chen, Chia-Hsiang] Natl Hlth Res Inst, Dept Mental Hlth & Addict Med, Miaoli, Taiwan.
RI Chen, Chia-Hsiang /E-3939-2010
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1758-5864
J9 ASIA-PAC PSYCHIAT
JI Asia-Pac. Psychiatry
PD OCT
PY 2012
VL 4
SU 1
SI SI
BP 52
EP 52
PG 1
WC Psychiatry
SC Psychiatry
GA 029AK
UT WOS:000310467000121
ER

PT J
AU Tan, YY
AF Tan, Yuyuan
TI Significance of family history in patients with autism spectrum
   disorders in Singapore
SO ASIA-PACIFIC PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Tan, Yuyuan] Inst Mental Hlth, Dept Psychiat, Singapore, Singapore.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1758-5864
J9 ASIA-PAC PSYCHIAT
JI Asia-Pac. Psychiatry
PD OCT
PY 2012
VL 4
SU 1
SI SI
BP 168
EP 168
PG 1
WC Psychiatry
SC Psychiatry
GA 029AK
UT WOS:000310467000353
ER

PT J
AU Singh, MK
   Chang, KD
AF Singh, Manpreet K.
   Chang, Kiki D.
TI The Neural Effects of Psychotropic Medications in Children and
   Adolescents
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Medication; Neuroimaging; Pediatric; Psychopathology; Magnetic resonance
   imaging
ID MAGNETIC-RESONANCE-SPECTROSCOPY; PEDIATRIC BIPOLAR DISORDER;
   CHILDHOOD-ONSET SCHIZOPHRENIA; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER;
   MAJOR DEPRESSIVE DISORDER; DEFICIT HYPERACTIVITY DISORDER; ANTERIOR
   CINGULATE CORTEX; AUTISM SPECTRUM DISORDER; N-ACETYL-ASPARTATE;
   FUNCTIONAL CONNECTIVITY
AB Little is known about the neurobiological effects of psychotropic medications used in the treatment of children and adolescents diagnosed with a psychiatric disorder. This review provides a synopsis of the literature demonstrating the neural effects associated with exposure to psychotropic medication in youth using multimodal neuroimaging. The article concludes by illustrating how, taken together, these studies suggest that pharmacological interventions during childhood do indeed affect brain structure and function in a detectable manner, and the effects appear to be ameliorative.
C1 [Singh, Manpreet K.; Chang, Kiki D.] Stanford Univ, Sch Med, Div Child & Adolescent Psychiat, Stanford, CA 94305 USA.
RP Singh, MK (reprint author), Stanford Univ, Sch Med, Div Child & Adolescent Psychiat, 401 Quarry Rd, Stanford, CA 94305 USA.
EM mksingh@stanford.edu
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NR 78
TC 6
Z9 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD OCT
PY 2012
VL 21
IS 4
BP 753
EP +
DI 10.1016/j.chc.2012.07.010
PG 21
WC Psychiatry
SC Psychiatry
GA 038SJ
UT WOS:000311194100005
PM 23040900
ER

PT J
AU Siegel, M
AF Siegel, Matthew
TI Psychopharmacology of Autism Spectrum Disorder: Evidence and Practice
SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA
LA English
DT Article
DE Autism spectrum disorder; Comorbid psychopathology; Psychopharmacology;
   Symptom-specific treatment
ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED CROSSOVER;
   ABERRANT BEHAVIOR CHECKLIST; DOUBLE-BLIND; PSYCHIATRIC-DISORDERS;
   REPETITIVE BEHAVIORS; ADOLESCENT AUTISM; CONTROLLED-TRIAL; CHILDREN;
   RISPERIDONE
AB Children with autism spectrum disorder present with a high rate of maladaptive behaviors and comorbid psychopathology. Psychopharmacologic treatment is frequently used in this population and is particularly associated with comorbid mental illness and increasing age. Successful treatment of presenting problems, however, is most likely achieved through consideration of multiple potential etiologic factors, only some of which may respond to pharmacologic intervention. The evidence base for targeting specific symptoms and disorders with psychopharmacology in children with autism spectrum disorder is expanding rapidly and offers guidance for practicing clinicians. The current evidence for symptom-specific treatment is presented.
C1 [Siegel, Matthew] Spring Harbor Hosp, Dev Disorders Program, Westbrook, ME 04092 USA.
   [Siegel, Matthew] Tufts Univ, Sch Med, Dept Psychiat, Boston, MA 02111 USA.
   [Siegel, Matthew] Maine Med Ctr, Res Inst, Ctr Outcomes Res & Evaluat, Portland, ME 04103 USA.
RP Siegel, M (reprint author), Spring Harbor Hosp, Dev Disorders Program, 123 Andover Rd, Westbrook, ME 04092 USA.
EM siegem@springharbor.org
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NR 70
TC 5
Z9 6
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 1056-4993
J9 CHILD ADOL PSYCH CL
JI Child Adolesc. Psychiatr. N. Am.
PD OCT
PY 2012
VL 21
IS 4
BP 957
EP +
DI 10.1016/j.chc.2012.07.006
PG 18
WC Psychiatry
SC Psychiatry
GA 038SJ
UT WOS:000311194100014
PM 23040909
ER

PT J
AU Blais, C
   Roy, C
   Fiset, D
   Arguin, M
   Gosselin, F
AF Blais, Caroline
   Roy, Cynthia
   Fiset, Daniel
   Arguin, Martin
   Gosselin, Frederic
TI The eyes are not the window to basic emotions
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Facial expression recognition; Facial features; Visual mechanisms;
   Classification image technique
ID SUPERIOR TEMPORAL SULCUS; FACIAL EXPRESSION; ACQUIRED PROSOPAGNOSIA;
   AMYGDALA DAMAGE; FACE; INFORMATION; AUTISM; RECOGNITION; PERCEPTION;
   ATTENTION
AB Facial expressions are one of the most important ways to communicate our emotional state. In popular culture and in the scientific literature on face processing, the eye area is often conceived as a very important - if not the most important - cue for the recognition of facial expressions. In support of this, an underutilization of the eye area is often observed in clinical populations with a deficit in the recognition of facial expressions of emotions. Here, we used the Bubbles technique to verify which facial cue is the most important when it comes to discriminating between eight static and dynamic facial expressions (i.e., six basic emotions, pain and a neutral expression). We found that the mouth area is the most important cue for both static and dynamic facial expressions. We conducted an ideal observer analysis on the static expressions and determined that the mouth area is the most informative. However, we found an underutilization of the eye area by human participants in comparison to the ideal observer. We then demonstrated that the mouth area contains the most discriminative motions across expressions. We propose that the greater utilization of the mouth area by the human participants might come from remnants of the strategy the brain has developed with dynamic stimuli, and/or from a strategy whereby the most informative area is prioritized due to the limited capacity of the visuo-cognitive system. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Blais, Caroline; Roy, Cynthia; Arguin, Martin; Gosselin, Frederic] Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada.
   [Blais, Caroline; Fiset, Daniel] Univ Quebec Outaouais, Dept Psychoeduc & Psychol, Gatineau, PQ J8X 3X7, Canada.
RP Gosselin, F (reprint author), Univ Montreal, Dept Psychol, CP 6128,Succ Ctr ville, Montreal, PQ H3C 3J7, Canada.
EM frederic.gosselin@umontreal.ca
FU Natural Sciences and Engineering Research Council of Canada (CRSNG);
   Fonds Quebecois de Recherche sur la Nature et les Technologies (FQRNT)
FX We would like to thank Marie Smith for kindly giving us access to her
   data. This work was supported by grants from the Natural Sciences and
   Engineering Research Council of Canada (CRSNG) to Frederic Gosselin and
   by a scholarship from the Fonds Quebecois de Recherche sur la Nature et
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NR 69
TC 8
Z9 8
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD OCT
PY 2012
VL 50
IS 12
BP 2830
EP 2838
DI 10.1016/j.neuropsychologia.2012.08.010
PG 9
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 035KQ
UT WOS:000310945900014
PM 22974675
ER

PT J
AU Fiorentini, C
   Gray, L
   Rhodes, G
   Jeffery, L
   Pellicano, E
AF Fiorentini, Chiara
   Gray, Laura
   Rhodes, Gillian
   Jeffery, Linda
   Pellicano, Elizabeth
TI Reduced face identity aftereffects in relatives of children with autism
SO NEUROPSYCHOLOGIA
LA English
DT Article
DE Autism; Endophenotype; Faces; Aftereffects; Adaptation
ID SPECTRUM DISORDERS; ENDOPHENOTYPE CONCEPT; MULTIPLE-INCIDENCE; BROADER
   PHENOTYPE; FACIAL IDENTITY; FAMILY-HISTORY; INDIVIDUALS; AMYGDALA; GAZE;
   RECOGNITION
AB Autism is a pervasive developmental condition with complex aetiology. To aid the discovery of genetic mechanisms, researchers have turned towards identifying potential endophenotypes - subtle neurobiological or neurocognitive traits present in individuals with autism and their "unaffected" relatives. Previous research has shown that relatives of individuals with autism exhibit face processing atypicalities, which are similar in nature albeit of lesser degree, to those found in children and adults with autism. Yet very few studies have examined the underlying mechanisms responsible for such atypicalities. Here, we investigated whether atypicalities in adaptive norm-based coding of faces are present in relatives of children with autism, similar to those previously reported in children with autism. To test this possibility, we administered a face identity aftereffect task in which adaptation to a particular face biases perception towards the opposite identity, so that a previously neutral face (i.e., the average face) takes on the computationally opposite identity. Parents and siblings of individuals with autism showed smaller aftereffects compared to parents and siblings of typically developing children, especially so when the adapting stimuli were located further away from the average face. In addition, both groups showed stronger aftereffects for adaptors far from the average than for adaptors closer to the average. These results suggest that, in relatives of children with autism, face-coding mechanism are similar (i.e., norm-based) but less efficient than in relatives of typical children. This finding points towards the possibility that diminished adaptive mechanisms might represent a neurocognitive endophenotype for autism. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Fiorentini, Chiara] Australian Natl Univ, Dept Psychol, Canberra, ACT 0200, Australia.
   [Fiorentini, Chiara] UCL, Inst Child Hlth, London WC1E 6BT, England.
   [Fiorentini, Chiara; Rhodes, Gillian; Jeffery, Linda; Pellicano, Elizabeth] Univ Western Australia, ARC Ctr Excellence Cognit & Its Disorders, Sch Psychol, Nedlands, WA 6009, Australia.
   [Gray, Laura; Pellicano, Elizabeth] Univ London, CRAE, Inst Educ, London WC1E 7HU, England.
RP Fiorentini, C (reprint author), Australian Natl Univ, Dept Psychol, GPO Box 4, Canberra, ACT 0200, Australia.
EM fiorentinichiara@gmail.com
FU Swiss National Science Foundation (FNS); Clothworkers' Foundation; Pears
   Foundation; Australian Research Council Centre of Excellence in
   Cognition and its Disorders [CE110001021]; Australian Research Council
   Professorial Fellowship; Australian Research Council Discovery Project
   [DP0770923]
FX We are extremely grateful to all of the families that generously took
   part in this research. C.F. was supported by a Swiss National Science
   Foundation (FNS) Fellowship for Young Researchers during the period of
   this research. Research at the Centre for Research in Autism and
   Education (CRAE) is supported by The Clothworkers' Foundation and Pears
   Foundation (LG. & E.P.). G.R., L.J. and E.P. were supported by the
   Australian Research Council Centre of Excellence in Cognition and its
   Disorders (project number CE110001021), an Australian Research Council
   Professorial Fellowship (G.R) and by Australian Research Council
   Discovery Project (DP0770923, L.J., G.R., E.P.). Many thanks to Mayu
   Nishimura and Daphne Maurer for co-creating the "Robbers Task", Libby
   Taylor for help setting up the task and Marc Stears for comments on a
   previous version of this manuscript.
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NR 51
TC 10
Z9 11
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0028-3932
J9 NEUROPSYCHOLOGIA
JI Neuropsychologia
PD OCT
PY 2012
VL 50
IS 12
BP 2926
EP 2932
DI 10.1016/j.neuropsychologia.2012.08.019
PG 7
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 035KQ
UT WOS:000310945900024
PM 22968036
ER

PT J
AU Matson, JL
   Neal, D
   Kozlowski, AM
AF Matson, Johnny L.
   Neal, Daniene
   Kozlowski, Alison M.
TI Treatments for the Challenging Behaviours of Adults With Intellectual
   Disabilities
SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE
LA English
DT Review
DE intellectual disabilities; adults; challenging behaviours; functional
   assessment; pharmacotherapy; applied behaviour analysis
ID AUTISM SPECTRUM DISORDERS; II DASH-II; FUNCTIONAL ASSESSMENT;
   DEVELOPMENTAL-DISABILITIES; DIAGNOSTIC-ASSESSMENT; MENTAL-RETARDATION;
   FUNCTION QABF; PSYCHOMETRIC PROPERTIES; DEPRESSIVE EQUIVALENTS; ABERRANT
   BEHAVIOR
AB Objective: To provide an overview and critical assessment of common problems and best evidence practice in treatments for the challenging behaviours (CBs) of adults with intellectual disabilities (IDs).
   Method: Commonly observed problems that present obstacles to successful treatment plans are discussed, followed by an analysis of available research on the efficacy of behavioural and pharmacological therapies.
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C1 [Matson, Johnny L.] Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA.
   [Neal, Daniene] Hammond Supports & Serv Ctr, Hammond, LA USA.
   [Kozlowski, Alison M.] Johns Hopkins Med Sch, Baltimore, MD 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 53
TC 3
Z9 3
PU CANADIAN PSYCHIATRIC ASSOC
PI OTTAWA
PA 141 LAURIER AVENUE WEST, STE 701, OTTAWA, ONTARIO K1P 5J3, CANADA
SN 0706-7437
J9 CAN J PSYCHIAT
JI Can. J. Psychiat.-Rev. Can. Psychiat.
PD OCT
PY 2012
VL 57
IS 10
BP 587
EP 592
PG 6
WC Psychiatry
SC Psychiatry
GA 033TP
UT WOS:000310824300002
PM 23072949
ER

PT J
AU Sturmey, P
AF Sturmey, Peter
TI Treatment of Psychopathology in People With Intellectual and Other
   Disabilities
SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE
LA English
DT Review
DE intellectual disabilities; mental retardation; autism spectrum
   disorders; psychopathology; applied behaviour analysis; psychosocial
   interventions; cognitive therapy; cognitive-behavioural therapy;
   psychopharmacology; randomized controlled trials
ID AUTISM SPECTRUM DISORDERS; PROFOUND MULTIPLE DISABILITIES; APPLIED
   BEHAVIOR ANALYSIS; MENTAL-RETARDATION; FUNCTIONAL-ANALYSIS;
   DEVELOPMENTAL-DISABILITIES; ANTIPSYCHOTIC MEDICATION;
   LEARNING-DISABILITIES; DESTRUCTIVE BEHAVIOR; CHALLENGING BEHAVIOR
AB Objective: To review the psychosocial, pharmacological, and other treatments of psychopathology in people with intellectual disabilities (IDs), autism, and other developmental disabilities (DDs).
   Method: Systematic reviews and meta-analyses of psychosocial, pharmacological, and other treatments for people with DDs are reviewed.
   Results: There is strong evidence for applied behaviour analysis (ABA) and other behavioural treatments of some forms of psychopathology. There is little good evidence to support the effectiveness of cognitive-behavioural therapy, cognitive therapy, sensory interventions, and other forms of psychosocial interventions. Recently, more randomized controlled trials (RCTs) of psychopharmacology have been published, especially with people with autism spectrum disorders. Most RCTs were for externalizing behaviour problems, rather than for psychopathology. These RCTs offer only preliminary support for the effectiveness of pharmacotherapy. No evidence was found for the effectiveness of other biological treatments.
   Conclusions: Current research supports the use of ABA and other behavioural interventions for some forms of psychopathology. Evidence for the effectiveness of other interventions is limited or absent.
C1 [Sturmey, Peter] CUNY, Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
   [Sturmey, Peter] CUNY, Grad Ctr, Flushing, NY 11367 USA.
RP Sturmey, P (reprint author), CUNY, Queens Coll, Dept Psychol, Flushing, NY 11367 USA.
EM psturmey@gmail.com
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NR 94
TC 1
Z9 1
PU CANADIAN PSYCHIATRIC ASSOC
PI OTTAWA
PA 141 LAURIER AVENUE WEST, STE 701, OTTAWA, ONTARIO K1P 5J3, CANADA
SN 0706-7437
J9 CAN J PSYCHIAT
JI Can. J. Psychiat.-Rev. Can. Psychiat.
PD OCT
PY 2012
VL 57
IS 10
BP 593
EP 600
PG 8
WC Psychiatry
SC Psychiatry
GA 033TP
UT WOS:000310824300003
PM 23072950
ER

PT J
AU Diken, IH
   Ardic, A
   Diken, O
   Gilliam, JE
AF Diken, Ibrahim H.
   Ardic, Avsar
   Diken, Ozlem
   Gilliam, James E.
TI Exploring the Validity and Reliability of Turkish Version of Gilliam
   Autism Rating Scale-2: Turkish Standardization Study
SO EGITIM VE BILIM-EDUCATION AND SCIENCE
LA English
DT Article
DE Autism; assessment; GARS-2; validity; reliability; Turkish sample
ID SPECTRUM DISORDERS; CHILDREN; DIAGNOSIS; UTILITY
AB This study aims at exploring the psychometric characteristics of the Turkish version of the Gilliam Autism Rating Scale-2 (TV-GARS-2) in order to standardize it into Turkish. Individuals diagnosed with autism, intellectual disability, hearing impairment and typically developing children were the participants of this standardization study (n=1191). After carrying out the Turkish translation procedure, the reliability and validity of TV-GARS-2 were examined by conducting a series of analyses such as construct validity, discriminant validity, item analysis, confirmatory factor analysis, internal consistency and test-retest reliability. Results yielded that TV-GARS-2 is a reliable and valid assessment tool that can be used with individuals with autism in Turkey.
C1 [Diken, Ibrahim H.; Diken, Ozlem] Anadolu Univ, Fac Educ, Dept Special Educ, TR-26470 Eskisehir, Turkey.
   [Ardic, Avsar] Pamukkale Univ, Fac Educ, Dept Special Educ, Denizli, Turkey.
RP Diken, IH (reprint author), Anadolu Univ, Fac Educ, Dept Special Educ, TR-26470 Eskisehir, Turkey.
EM ihdiken@anadolu.edu.tr; aardic@pamukkale.edu.tr;
   odogramaci@anadolu.edu.tr; jgilliam09@gmail.com
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NR 38
TC 0
Z9 0
PU TURKISH EDUCATION ASSOC
PI KOCATEPE
PA KIZILIRMAK CADDESI NO 8, KOCATEPE, ANKARA 00000, TURKEY
SN 1300-1337
J9 EGIT BILIM
JI Egit. Bilim
PD OCT
PY 2012
VL 37
IS 166
BP 318
EP 328
PG 11
WC Education & Educational Research
SC Education & Educational Research
GA 031WN
UT WOS:000310673400025
ER

PT J
AU Hartzell, S
   Seneff, S
AF Hartzell, Samantha
   Seneff, Stephanie
TI Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
SO ENTROPY
LA English
DT Review
DE autism; epigenetics; cholesterol sulfate; DNA methylation;
   sulfotransferases; heparan sulfate; folate; cobalamin; zinc
ID LONG-TERM POTENTIATION; WHOLE-BLOOD SEROTONIN; NITRIC-OXIDE SYNTHASE;
   SPECTRUM DISORDERS; DNA HYPOMETHYLATION; CHOLESTEROL SULFATE;
   HEPARAN-SULFATE; HOMOCYSTEINE METABOLISM; OXIDATIVE STRESS; VITAMIN-D
AB Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis.
C1 [Hartzell, Samantha; Seneff, Stephanie] MIT, Comp Sci & Artificial Intelligence Lab, Cambridge, MA 02139 USA.
RP Seneff, S (reprint author), MIT, Comp Sci & Artificial Intelligence Lab, 77 Massachusetts Ave, Cambridge, MA 02139 USA.
EM Seneff@csail.mit.edu
FU Quanta Computers, Taipei, Taiwan; Simons Foundation
FX This research was funded in part by Quanta Computers, Taipei, Taiwan,
   under the auspices of the Qmulus Project, and in part by a grant from
   the Simons Foundation to the Simons Center for the Social Brain at MIT.
   The authors are grateful to two reviewers whose efforts resulted in
   important augmentations from the research literature related to the
   topic of impaired sulfur metabolism in autism.
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NR 136
TC 4
Z9 4
PU MDPI AG
PI BASEL
PA POSTFACH, CH-4005 BASEL, SWITZERLAND
SN 1099-4300
J9 ENTROPY-SWITZ
JI Entropy
PD OCT
PY 2012
VL 14
IS 10
BP 1953
EP 1977
DI 10.3390/e14101953
PG 25
WC Physics, Multidisciplinary
SC Physics
GA 030CO
UT WOS:000310545800009
ER

PT J
AU Zhang, YB
   Bolivar, VJ
   Lawrence, DA
AF Zhang, Yubin
   Bolivar, Valerie J.
   Lawrence, David A.
TI Developmental exposure to mercury chloride does not impair social
   behavior of C57BL/6 x BTBR F-1 mice
SO JOURNAL OF IMMUNOTOXICOLOGY
LA English
DT Article; Proceedings Paper
CT 50th Annual Meeting of the Society-of-Toxicology (SOT)
CY MAR, 2011
CL Washington, DC
SP Soc Toxicol (SOT)
DE Mercury; mouse social behavior; IgG anti-brain antibodies
ID AUTISM SPECTRUM DISORDERS; INBRED MOUSE STRAINS; T-CELLS; PERINATAL
   EXPOSURE; ASPERGER-SYNDROME; PERIPHERAL-BLOOD; IMMUNE-RESPONSE;
   GENE-EXPRESSION; FETAL-BRAIN; CHILDREN
AB The effects of mercury (Hg) on social behavior and the mechanisms involved remain unknown. This study shows that Hg chloride (HgCl2) exposure during fetal development does not impair social behavior of a mouse strain susceptible to environment-induced autistic-like behavior based on the parental phenotype. On the contrary, Hg exposure elevated the sociability of females. Since B6 mice are behaviorally normal and BTBR mice display low levels of sociability, the F-1 offspring (B6BF(1)) of female B6 mice and male BTBR mice were used to investigate their social behavior and the effects of Hg. Developmental Hg-treatment increased the serum IgG levels of the post-natal day (pnd) 21 offspring, but not pnd70 offspring or the B6 dams. After Hg treatment, there were negligible levels of serum IgG anti-brain antibodies (Ab) in the pnd21 and pnd70 offspring as well as their dams. However, Hg did elevate IgG deposition in multiple assayed brain regions of the pnd21 offspring, but the higher levels were no longer present at pnd70. Cytokine levels were not changed in pnd21 or pnd70 brain by Hg exposure, suggesting neuroinflammation was not induced. Social behavior was assayed at pnd70. Surprisingly, Hg-treatment significantly enhanced sociability of female B6BF(1) offspring, but not that of the male offspring. Our data indicates that developmental exposure to HgCl2 did not impair social behavior of B6BF(1) offspring, but it enhanced the sociability of females, which was significantly lower in adult B6BF(1) females than B6BF(1) males in the absence of any Hg exposure.
C1 [Zhang, Yubin; Bolivar, Valerie J.; Lawrence, David A.] New York State Dept Hlth, Wadsworth Ctr, Immunol Lab, Albany, NY 12201 USA.
   [Zhang, Yubin; Bolivar, Valerie J.; Lawrence, David A.] SUNY Albany, Sch Publ Hlth, Albany, NY USA.
   [Zhang, Yubin] Albany Med Coll, Ctr Immunol & Microbial Dis, Albany, NY 12208 USA.
RP Lawrence, DA (reprint author), New York State Dept Hlth, Wadsworth Ctr, Immunol Lab, Albany, NY 12201 USA.
EM lawrencd@wadsworth.org
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NR 70
TC 0
Z9 0
PU INFORMA HEALTHCARE
PI NEW YORK
PA 52 VANDERBILT AVE, NEW YORK, NY 10017 USA
SN 1547-691X
J9 J IMMUNOTOXICOL
JI J. Immunotoxicol.
PD OCT-DEC
PY 2012
VL 9
IS 4
BP 401
EP 410
DI 10.3109/1547691X.2012.682663
PG 10
WC Toxicology
SC Toxicology
GA 033PA
UT WOS:000310808900009
PM 22657747
ER

PT J
AU Nagae, LM
   Zarnow, DM
   Blaskey, L
   Dell, J
   Khan, SY
   Qasmieh, S
   Levy, SE
   Roberts, TPL
AF Nagae, L. M.
   Zarnow, D. M.
   Blaskey, L.
   Dell, J.
   Khan, S. Y.
   Qasmieh, S.
   Levy, S. E.
   Roberts, T. P. L.
TI Elevated Mean Diffusivity in the Left Hemisphere Superior Longitudinal
   Fasciculus in Autism Spectrum Disorders Increases with More Profound
   Language Impairment
SO AMERICAN JOURNAL OF NEURORADIOLOGY
LA English
DT Article
ID WHITE-MATTER COMPROMISE; CORPUS-CALLOSUM; FRONTAL-LOBE; TENSOR;
   TRACTOGRAPHY; TRACTS; TRACKING; CHILDREN; STROKE; BRAINS
AB BACKGROUND AND PURPOSE: Language impairments are observed in a subset of individuals with ASD. To examine microstructurel brain white matter features associated with language ability in ASD, we measured the DTI parameters of language-related white matter tracts (SLF) as well as nonlanguage-related white matter tracts (CST) in children with ASD/+LI and ASD/-LI) and in TD.
   MATERIALS AND METHODS: Eighteen children with ASD/LI (age range, 6.7-17.5 years), 17 with ASD/+LI (age range, 6.8-14.8 years), and 25 TD (age range, 6.5-18 years) were evaluated with DTI and tractography. Primary DTI parameters considered for analysis were MD and FA.
   RESULTS: There was a main effect of diagnostic group on age-corrected MD (P < .05) with ASD/+LI significantly elevated compared with TD. This was most pronounced for left hemisphere SLF fiber tracts and for the temporal portion of the SLF. There was significant negative correlation between left hemisphere SLF MD values and the clinical assessment of language ability. There was no main effect of diagnostic group or diagnostic group X hemisphere interaction for FA. Although there was a main effect of diagnostic group on values of MD in the CST, this did not survive hemispheric subanalysis.
   CONCLUSIONS: Abnormal DTI parameters (specifically significantly elevated MD values in ASD) of the SLF appear to be associated with language impairment in ASD. These elevations are particularly pronounced in the left cerebral hemisphere, in the temporal portion of the SLF, and in children with clinical language impairment.
C1 [Nagae, L. M.; Zarnow, D. M.; Blaskey, L.; Dell, J.; Khan, S. Y.; Qasmieh, S.; Levy, S. E.; Roberts, T. P. L.] Childrens Hosp Philadelphia, Dept Radiol, Philadelphia, PA 19104 USA.
RP Roberts, TPL (reprint author), Childrens Hosp Philadelphia, Dept Radiol, 324 S 34th St,Room 2115,Wood Bldg, Philadelphia, PA 19104 USA.
EM robertstim@email.chop.edu
FU National Institutes of Health grant [R01DC008871]; Nancy Lurie Marks
   Family and Autism Speaks
FX This study was supported in part by a National Institutes of Health
   grant R01DC008871 (T.P.L.R.) and a grant from the Nancy Lurie Marks
   Family and Autism Speaks.
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NR 36
TC 10
Z9 10
PU AMER SOC NEURORADIOLOGY
PI OAK BROOK
PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA
SN 0195-6108
J9 AM J NEURORADIOL
JI Am. J. Neuroradiol.
PD OCT
PY 2012
VL 33
IS 9
BP 1720
EP 1725
DI 10.3174/ajnr.A3037
PG 6
WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical
   Imaging
SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging
GA 024PZ
UT WOS:000310122400015
PM 22492573
ER

PT J
AU Travers, BG
   Adluru, N
   Ennis, C
   Tromp, DPM
   Destiche, D
   Doran, S
   Bigler, ED
   Lange, N
   Lainhart, JE
   Alexander, AL
AF Travers, Brittany G.
   Adluru, Nagesh
   Ennis, Chad
   Tromp, Do P. M.
   Destiche, Dan
   Doran, Sam
   Bigler, Erin D.
   Lange, Nicholas
   Lainhart, Janet E.
   Alexander, Andrew L.
TI Diffusion Tensor Imaging in Autism Spectrum Disorder: A Review
SO AUTISM RESEARCH
LA English
DT Review
DE diffusion tensor imaging; neuroimaging; autism; white matter
ID WHITE-MATTER MICROSTRUCTURE; HIGH-FUNCTIONING AUTISM; SUPERIOR TEMPORAL
   SULCUS; VOXEL-BASED MORPHOMETRY; DEFAULT MODE NETWORK; CORPUS-CALLOSUM
   SIZE; HUMAN BRAIN; STRUCTURAL CONNECTIVITY; HEAD CIRCUMFERENCE; IN-VIVO
AB White matter tracts of the brain allow neurons and neuronal networks to communicate and function with high efficiency. The aim of this review is to briefly introduce diffusion tensor imaging methods that examine white matter tracts and then to give an overview of the studies that have investigated white matter integrity in the brains of individuals with autism spectrum disorder (ASD). From the 48 studies we reviewed, persons with ASD tended to have decreased fractional anisotropy and increased mean diffusivity in white matter tracts spanning many regions of the brain but most consistently in regions such as the corpus callosum, cingulum, and aspects of the temporal lobe. This decrease in fractional anisotropy was often accompanied by increased radial diffusivity. Additionally, the review suggests possible atypical lateralization in some white matter tracts of the brain and a possible atypical developmental trajectory of white matter microstructure in persons with ASD. Clinical implications and future research directions are discussed. Autism Res 2012, 5: 289313. (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Travers, Brittany G.] Univ Wisconsin, Waisman Ctr, Waisman Lab Brain Imaging & Behav, Madison, WI 53705 USA.
   [Bigler, Erin D.] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA.
   [Lange, Nicholas] Harvard Univ, Dept Psychiat, Boston, MA 02115 USA.
   [Lange, Nicholas] Harvard Univ, Dept Biostat, Boston, MA 02115 USA.
   [Lange, Nicholas] McLean Hosp, Neurostat Lab, Belmont, MA 02178 USA.
   [Lainhart, Janet E.] Univ Utah, Dept Psychiat, Salt Lake City, UT USA.
   [Lainhart, Janet E.] Univ Utah, Neurosci Program, Salt Lake City, UT USA.
   [Lainhart, Janet E.] Univ Utah, Inst Brain, Salt Lake City, UT USA.
   [Alexander, Andrew L.] Univ Wisconsin, Dept Med Phys, Madison, WI 53705 USA.
   [Alexander, Andrew L.] Univ Wisconsin, Dept Psychiat, Madison, WI 53705 USA.
RP Travers, BG (reprint author), Univ Wisconsin, Waisman Ctr, Waisman Lab Brain Imaging & Behav, 1500 Highland Ave, Madison, WI 53705 USA.
EM btravers@wisc.edu
FU National Institute of Child Health and Human Development (NICHD) [T32
   HD07 489, P30 HD003352]; National Institute of Mental Health (NIMH) [P50
   MH84051, RO1 MH080826]; Morgridge Institutes for Research
   (MIR-University of Wisconsin)
FX This work was supported by National Institute of Child Health and Human
   Development (NICHD) T32 HD07 489 Postdoctoral Training Award (BGT);
   NICHD P30 HD003352 (ALA); National Institute of Mental Health (NIMH) P50
   MH84051 (ALA), NIMH RO1 MH080826 (JEL, ALA, EDB, NL), the Morgridge
   Institutes for Research (MIR-University of Wisconsin; NA). The content
   is solely the responsibility of the authors and does not necessarily
   represent the official views of the NIMH, NICHD, or the NIH. The authors
   would also like to thank Frances Haeberli and Bimi Pangli for their
   assistance with selecting and reviewing the articles.
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NR 171
TC 61
Z9 64
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 289
EP 313
DI 10.1002/aur.1243
PG 25
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300001
PM 22786754
ER

PT J
AU McGrath, J
   Johnson, K
   Ecker, C
   O'Hanlon, E
   Gill, M
   Gallagher, L
   Garavan, H
AF McGrath, Jane
   Johnson, Katherine
   Ecker, Christine
   O'Hanlon, Erik
   Gill, Michael
   Gallagher, Louise
   Garavan, Hugh
TI Atypical Visuospatial Processing in Autism: Insights from Functional
   Connectivity Analysis
SO AUTISM RESEARCH
LA English
DT Review
DE autism; functional MRI; visuospatial processing; mental rotation;
   functional connectivity
ID EMBEDDED FIGURES TASK; TIME-RESOLVED FMRI; MENTAL ROTATION; SPECTRUM
   DISORDERS; EXECUTIVE FUNCTION; VISUAL-SEARCH; CORTICAL
   UNDERCONNECTIVITY; SENTENCE COMPREHENSION; ASPERGERS-DISORDER;
   WORKING-MEMORY
AB Atypical visuospatial processing is commonly described in autism spectrum disorders (ASDs); however the specific neurobiological underpinnings of this phenomenon are poorly understood. Given the extensive evidence suggesting ASDs are characterized by abnormal neural connectivity, this study aimed to investigate network connectivity during visuospatial processing in ASD. Twenty-two males with ASD without intellectual disability and 22 individually matched controls performed a mental rotation task during functional magnetic resonance imaging (MRI) in which two rotated stimuli were judged to be same (Same Trials) or mirror-imaged (Mirror Trials). Behavioral results revealed a relative advantage of mental rotation in the ASD groupcontrols were slower responding to the more difficult Mirror Trials than Same Trials whereas the ASD group completed Mirror Trials and Same-trials at similar speeds. In the ASD group, brain activity was reduced in frontal, temporal, occipital, striatal, and cerebellar regions and, consistent with previous literature, functional connectivity between a number of brain regions was reduced. However, some connections appeared to be conserved and were recruited in a qualitatively different way by the two groups. As task difficulty increased (on Mirror Trials), controls tended to increase connections between certain brain regions, whereas the ASD group appeared to suppress connections between these regions. There was an interesting exception to this pattern in the visual cortex, a finding that may suggest an advantage in early visual perceptual processing in ASD. Overall, this study has identified a relative advantage in mental rotation in ASD that is associated with aberrant neural connectivity and that may stem from enhanced visual perceptual processing. Autism Res 2012, 5: 314330. (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [McGrath, Jane; Johnson, Katherine; Gill, Michael; Gallagher, Louise] St James Hosp, Trinity Ctr Hlth Sci, Dept Psychiat, Dublin 8, Ireland.
   [Johnson, Katherine] Univ Melbourne, Parkville, Vic 3052, Australia.
   [Ecker, Christine] Inst Psychiat, Dept Forens & Neurodev Sci, London, England.
   [O'Hanlon, Erik] Beaumont Hosp, Royal Coll Surg Ireland, Dept Psychiat, Dublin 9, Ireland.
   [Garavan, Hugh] Univ Dublin Trinity Coll, Sch Psychol, Dublin 2, Ireland.
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   [Garavan, Hugh] Univ Vermont, Dept Psychiat, Burlington, VT USA.
   [Garavan, Hugh] Univ Vermont, Dept Psychol, Burlington, VT 05405 USA.
RP McGrath, J (reprint author), St James Hosp, Trinity Ctr Hlth Sci, Dept Psychiat, Dublin 8, Ireland.
EM jane.mcgrath@tcd.ie
RI Ecker, Christine/E-5194-2010
FU Molecular Medicine Ireland [4AA-G04005-S06]
FX Grant sponsor: Molecular Medicine IrelandGrant number: 4AA-G04005-S06
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NR 73
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 314
EP 330
DI 10.1002/aur.1245
PG 17
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300002
PM 22865697
ER

PT J
AU Sheinkopf, SJ
   Iverson, JM
   Rinaldi, ML
   Lester, BM
AF Sheinkopf, Stephen J.
   Iverson, Jana M.
   Rinaldi, Melissa L.
   Lester, Barry M.
TI Atypical Cry Acoustics in 6-Month-Old Infants at Risk for Autism
   Spectrum Disorder
SO AUTISM RESEARCH
LA English
DT Article
DE autism; infancy; cry; vocalizations; acoustic analysis
ID NEWBORN-INFANTS; EARLY IDENTIFICATION; 1ST YEAR; CHILDREN;
   COMMUNICATION; EXPOSURE; PRETERM; LIFE; TERM; CIRCUMCISION
AB This study examined differences in acoustic characteristics of infant cries in a sample of babies at risk for autism and a low-risk comparison group. Cry samples derived from vocal recordings of 6-month-old infants at risk for autism spectrum disorder (ASD; n?=?21) and low-risk infants (n?=?18) were subjected to acoustic analyses using analysis software designed for this purpose. Cries were categorized as either pain-related or non-pain-related based on videotape coding. At-risk infants produced pain-related cries with higher and more variable fundamental frequency (F 0) than low-risk infants. At-risk infants later classified with ASD at 36 months had among the highest F 0 values for both types of cries and produced cries that were more poorly phonated than those of nonautistic infants, reflecting cries that were less likely to be produced in a voiced mode. These results provide preliminary evidence that disruptions in cry acoustics may be part of an atypical vocal signature of autism in early life. Autism Res 2012, : . (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Sheinkopf, Stephen J.; Lester, Barry M.] Brown Univ, Women & Infants Hosp, Brown Alpert Med Sch, Ctr Study Children Risk,Dept Psychiat & Human Beh, Providence, RI 02905 USA.
   [Sheinkopf, Stephen J.; Lester, Barry M.] Brown Univ, Women & Infants Hosp, Brown Alpert Med Sch, Ctr Study Children Risk,Dept Pediat, Providence, RI 02905 USA.
   [Iverson, Jana M.] Univ Pittsburgh, Dept Psychol, Pittsburgh, PA 15260 USA.
   [Rinaldi, Melissa L.] EP Bradley Hosp, Brown Alpert Med Sch, Ctr Autism & Dev Disabil, Dept Psychiat & Human Behav, E Providence, RI USA.
RP Sheinkopf, SJ (reprint author), Brown Univ, Women & Infants Hosp, Brown Ctr Children, 101 Dudley St, Providence, RI 02905 USA.
EM Stephen_Sheinkopf@brown.edu
FU Autism Speaks; NICHD [R01-HD41677, R01-HD54979, R03-DC009301]
FX This study was supported by Autism Speaks and by NICHD; R01-HD41677,
   R01-HD54979, and NIDCD; R03-DC009301.
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NR 43
TC 11
Z9 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 331
EP 339
DI 10.1002/aur.1244
PG 9
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300003
PM 22890558
ER

PT J
AU Marco, EJ
   Khatibi, K
   Hill, SS
   Siegel, B
   Arroyo, MS
   Dowling, AF
   Neuhaus, JM
   Sherr, EH
   Hinkley, LNB
   Nagarajan, SS
AF Marco, Elysa J.
   Khatibi, Kasra
   Hill, Susanna S.
   Siegel, Bryna
   Arroyo, Monica S.
   Dowling, Anne F.
   Neuhaus, John M.
   Sherr, Elliott H.
   Hinkley, Leighton N. B.
   Nagarajan, Srikantan S.
TI Children With Autism Show Reduced Somatosensory Response: An MEG Study
SO AUTISM RESEARCH
LA English
DT Article
DE cognitive neuroscience; event related potential; school age; low-level
   perception; magnetoencephalography
ID TACTILE SENSITIVITY; EVOKED-POTENTIALS; SENSORY PROFILE; ABNORMALITIES;
   DISORDER; BRAINS; CORTEX; ADULTS; MODEL
AB The neural underpinnings of sensory processing differences in autism remain poorly understood. This prospective magnetoencephalography (MEG) study investigates whether children with autism show atypical cortical activity in the primary somatosensory cortex (S1) in comparison with matched controls. Tactile stimuli were clearly detectable, and painless taps were applied to the distal phalanx of the second (D2) and third (D3) fingers of the right and left hands. Three tactile paradigms were administered: an oddball paradigm (standard taps to D3 at an interstimulus interval (ISI) of 0.33 and deviant taps to D2 with ISI ranging from 1.32?s to 1.64?s); a slow-rate paradigm (D2) with an ISI matching the deviant taps in the oddball paradigm; and a fast-rate paradigm (D2) with an ISI matching the standard taps in the oddball. Study subjects were boys (age 711 years) with and without autism disorder. Sensory behavior was quantified using the Sensory Profile questionnaire. Boys with autism exhibited smaller amplitude left hemisphere S1 response to slow and deviant stimuli during the right-hand paradigms. In post-hoc analysis, tactile behavior directly correlated with the amplitude of cortical response. Consequently, the children were re-categorized by degree of parent-report tactile sensitivity. This regrouping created a more robust distinction between the groups with amplitude diminution in the left and right hemispheres and latency prolongation in the right hemisphere in the deviant and slow-rate paradigms for the affected children. This study suggests that children with autism have early differences in somatosensory processing, which likely influence later stages of cortical activity from integration to motor response. Autism Res 2012, 5: 340351. (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Marco, Elysa J.] Univ Calif San Francisco, Div Child Neurol, Dept Neurol Pediat & Psychiat, San Francisco, CA 94143 USA.
   [Khatibi, Kasra; Hill, Susanna S.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA.
   [Siegel, Bryna; Arroyo, Monica S.] Univ Calif San Francisco, Langley Porter Psychiat Inst, Dept Psychiat, San Francisco, CA USA.
   [Dowling, Anne F.; Hinkley, Leighton N. B.; Nagarajan, Srikantan S.] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94143 USA.
   [Neuhaus, John M.] Univ Calif San Francisco, Dept Biostat, San Francisco, CA 94143 USA.
   [Sherr, Elliott H.] Univ Calif San Francisco, Dept Neurol & Pediat, San Francisco, CA 94143 USA.
RP Marco, EJ (reprint author), Univ Calif San Francisco, Div Child Neurol, Dept Neurol Pediat & Psychiat, 350 Parnassus Ave,Ste 609, San Francisco, CA 94143 USA.
EM marcoe@neuropeds.ucsf.edu
FU National Institutes of Health [NSADA K12 NS01692-07, NIH-K23MH083890,
   NCRR UCSF-CTSI UL1 RR024131, RO1DC4855, RO1DC6435, R01NS066654,
   R01NS64060]; Cure Autism Now; Wallace Research Foundation
FX We appreciate the time and dedication of the children and their families
   who participated in this research. We thank John Rubenstein and Heidi
   Kirsch for their helpful comments, and Susanne Honma for her assistance
   with MEG data acquisition. This work was supported by the National
   Institutes of Health (E.J.M.: NSADA K12 NS01692-07, NIH-K23MH083890,
   NCRR UCSF-CTSI UL1 RR024131 and S.S.N.: RO1DC4855, RO1DC6435,
   R01NS066654, and R01NS64060), Cure Autism Now (grant to SSN), and the
   Wallace Research Foundation (Grant to EJM). Its contents are solely the
   responsibility of the authors and do not necessarily represent the
   official views of the NIH, and these funding organizations had no
   involvement in design, collection, analysis, or manuscript preparation
   or publication decisions. The authors have no conflicts of interest to
   declare.
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NR 39
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 340
EP 351
DI 10.1002/aur.1247
PG 12
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300004
PM 22933354
ER

PT J
AU Linkenauger, SA
   Lerner, MD
   Ramenzoni, VC
   Proffitt, DR
AF Linkenauger, Sally A.
   Lerner, Matthew D.
   Ramenzoni, Veronica C.
   Proffitt, Dennis R.
TI A Perceptual-Motor Deficit Predicts Social and Communicative Impairments
   in Individuals With Autism Spectrum Disorders
SO AUTISM RESEARCH
LA English
DT Article
DE autism spectrum disorders; social deficits; perception; perceptual;
   motor integration; action capability estimation; affordance perception
ID ATTENTION DEFICIT/HYPERACTIVITY DISORDER; BIOLOGICAL MOTION; PERCEIVING
   AFFORDANCES; SCALED INFORMATION; ASPERGERS SYNDROME; KINEMATIC ANALYSIS;
   VISUAL GUIDANCE; CHILDREN; MOVEMENTS; DISTANCE
AB Individuals with autism spectrum disorders (ASDs) have known impairments in social and motor skills. Identifying putative underlying mechanisms of these impairments could lead to improved understanding of the etiology of core social/communicative deficits in ASDs, and identification of novel intervention targets. The ability to perceptually integrate one's physical capacities with one's environment (affordance perception) may be such a mechanism. This ability has been theorized to be impaired in ASDs, but this question has never been directly tested. Crucially, affordance perception has shown to be amenable to learning; thus, if it is implicated in deficits in ASDs, it may be a valuable unexplored intervention target. The present study compared affordance perception in adolescents and adults with ASDs to typically developing (TD) controls. Two groups of individuals (adolescents and adults) with ASDs and age-matched TD controls completed well-established action capability estimation tasks (reachability, graspability, and aperture passability). Their caregivers completed a measure of their lifetime social/communicative deficits. Compared with controls, individuals with ASDs showed unprecedented gross impairments in relating information about their bodies' action capabilities to visual information specifying the environment. The magnitude of these deficits strongly predicted the magnitude of social/communicative impairments in individuals with ASDs. Thus, social/communicative impairments in ASDs may derive, at least in part, from deficits in basic perceptualmotor processes (e.g. action capability estimation). Such deficits may impair the ability to maintain and calibrate the relationship between oneself and one's social and physical environments, and present fruitful, novel, and unexplored target for intervention. Autism Res 2012,5:352362. (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Linkenauger, Sally A.] Max Planck Inst Biol Cybernet, Cognit & Computat Psychophys Dept, D-72012 Tubingen, Germany.
   [Lerner, Matthew D.; Proffitt, Dennis R.] Univ Virginia, Dept Psychol, Charlottesville, VA 22903 USA.
   [Ramenzoni, Veronica C.] Max Planck Inst Psycholinguist, Nijmegen, Netherlands.
RP Linkenauger, SA (reprint author), Max Planck Inst Biol Cybernet, Cognit & Computat Psychophys Dept, Postfach 21 69, D-72012 Tubingen, Germany.
EM sally.linkenauger@tuebingen.mpg.de
RI Ramenzoni, Veronica/J-8632-2012
OI Ramenzoni, Veronica/0000-0003-3003-5012
FU Jefferson Scholars Foundation; National Institute of Health
   [RO1MH075781]
FX Grant sponsor: Jefferson Scholars Foundation; Grant number: James H. and
   Elizabeth W. Wright Endowed Fellowship (Matthew D. Lerner).Grant
   sponsor: National Institute of Health; Grant number: RO1MH075781 (Dennis
   R. Proffitt).
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NR 84
TC 5
Z9 5
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 352
EP 362
DI 10.1002/aur.1248
PG 11
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300005
PM 22961977
ER

PT J
AU Hedley, D
   Young, R
   Brewer, N
AF Hedley, Darren
   Young, Robyn
   Brewer, Neil
TI Using Eye Movements as an Index of Implicit Face Recognition in Autism
   Spectrum Disorder
SO AUTISM RESEARCH
LA English
DT Article
DE face recognition; autism spectrum disorder; Asperger syndrome; face
   perception; eye movement-based memory effect
ID ASPERGER-SYNDROME; COVERT RECOGNITION; YOUNG-CHILDREN; MEMORY TEST;
   INDIVIDUALS; FAMILIARITY; PROSOPAGNOSIA; PERFORMANCE; ALGORITHMS;
   FIXATIONS
AB Individuals with an autism spectrum disorder (ASD) typically show impairment on face recognition tasks. Performance has usually been assessed using overt, explicit recognition tasks. Here, a complementary method involving eye tracking was used to examine implicit face recognition in participants with ASD and in an intelligence quotient-matched non-ASD control group. Differences in eye movement indices between target and foil faces were used as an indicator of implicit face recognition. Explicit face recognition was assessed using oldnew discrimination and reaction time measures. Stimuli were faces of studied (target) or unfamiliar (foil) persons. Target images at test were either identical to the images presented at study or altered by changing the lighting, pose, or by masking with visual noise. Participants with ASD performed worse than controls on the explicit recognition task. Eye movement-based measures, however, indicated that implicit recognition may not be affected to the same degree as explicit recognition. Autism Res 2012, 5: 363379. (C) 2012 International Society for Autism Research, Wiley Periodicals, Inc.
C1 [Hedley, Darren; Young, Robyn; Brewer, Neil] Flinders Univ S Australia, Sch Psychol, Adelaide, SA 5001, Australia.
RP Young, R (reprint author), Flinders Univ S Australia, Sch Psychol, GPO Box 2100, Adelaide, SA 5001, Australia.
EM robyn.young@flinders.edu.au
FU ARC [LE0882562, DP1093210]; Flinders University; DOD Counterdrug
   Technology Development Program Office
FX This research was supported by (a) ARC LE0882562 to Neil Brewer, Robyn
   Young et al., and ARC DP1093210 to Neil Brewer et al., (b) a Flinders
   University Research Grant to Robyn Young and Neil Brewer. Portions of
   this research used the FERET database of facial images collected under
   the FERET program, sponsored by the DOD Counterdrug Technology
   Development Program Office (Phillips et al., 1998, 2000). We are
   especially grateful to the individuals who participated in this study,
   to Jon Martin and Autism SA, to Paul Williamson, and particularly to Ben
   Maddock for technical support. The authors declare no financial or other
   potential conflicts of interest associated with this study.
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NR 54
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1939-3792
J9 AUTISM RES
JI Autism Res.
PD OCT
PY 2012
VL 5
IS 5
BP 363
EP 379
DI 10.1002/aur.1246
PG 17
WC Behavioral Sciences; Psychology, Developmental
SC Behavioral Sciences; Psychology
GA 023WI
UT WOS:000310067300006
PM 22865711
ER

PT J
AU Aitken, KJ
AF Aitken, Kenneth John
TI Clinicians learn less and less about more and more until they know
   nothing about everything; researchers learn more and more about less and
   less until they know everything about nothing: Discuss
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
ID RETT-SYNDROME; GENE-EXPRESSION; AUTISM; TWIN; CHORIONICITY; BEHAVIOR;
   HEALTH; DIET
AB A number of recent developments in our understanding of the biology of heritability question commonly held views on the immutability of genetic factors. These have numerous potential implications for improving understanding and practice in pre- and postconceptional care and for infant and child mental health, and they carry a cautionary message against overgeneralization.
C1 Dept Psychol, Aberdour KY3 0RH, Fife, Scotland.
RP Aitken, KJ (reprint author), Dept Psychol, Aberdour KY3 0RH, Fife, Scotland.
EM drken.aitken@btinternet.com
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NR 46
TC 0
Z9 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD OCT
PY 2012
VL 35
IS 5
BP 358
EP 359
DI 10.1017/S0140525X12001367
PG 2
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA 026WU
UT WOS:000310314600037
PM 23095379
ER

PT J
AU Deutsch, CK
   McIlvane, WJ
AF Deutsch, Curtis K.
   McIlvane, William J.
TI Non-Mendelian etiologic factors in neuropsychiatric illness: Pleiotropy,
   epigenetics, and convergence
SO BEHAVIORAL AND BRAIN SCIENCES
LA English
DT Editorial Material
ID DE-NOVO MUTATIONS; GENOMEWIDE ASSOCIATION; AUTISM; SCHIZOPHRENIA;
   DISORDERS; GENETICS; GENOMICS; 16P11.2; LINKAGE
AB The target article by Charney on behavior genetics/genomics discusses how numerous molecular factors can inform heritability estimations and genetic association studies. These factors find application in the search for genes for behavioral phenotypes, including neuropsychiatric disorders. We elaborate upon how single causal factors can generate multiple phenotypes, and discuss how multiple causal factors may converge on common neurodevelopmental mechanisms.
C1 [Deutsch, Curtis K.; McIlvane, William J.] Univ Massachusetts, Sch Med, Eunice Kennedy Shriver Ctr, Waltham, MA 02452 USA.
RP Deutsch, CK (reprint author), Univ Massachusetts, Sch Med, Eunice Kennedy Shriver Ctr, Waltham, MA 02452 USA.
EM curtis.deutsch@umassmed.edu; william.mcilvane@umassmed.edu
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NR 22
TC 0
Z9 0
PU CAMBRIDGE UNIV PRESS
PI NEW YORK
PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA
SN 0140-525X
EI 1469-1825
J9 BEHAV BRAIN SCI
JI Behav. Brain Sci.
PD OCT
PY 2012
VL 35
IS 5
BP 363
EP 364
DI 10.1017/S0140525X12001392
PG 2
WC Psychology, Biological; Behavioral Sciences; Neurosciences
SC Psychology; Behavioral Sciences; Neurosciences & Neurology
GA 026WU
UT WOS:000310314600042
PM 23095384
ER

PT J
AU Saunders, JA
   Gandal, MJ
   Roberts, TP
   Siegel, SJ
AF Saunders, John A.
   Gandal, Michael J.
   Roberts, Timothy P.
   Siegel, Steve J.
TI NMDA antagonist MK801 recreates auditory electrophysiology disruption
   present in autism and other neurodevelopmental disorders
SO BEHAVIOURAL BRAIN RESEARCH
LA English
DT Article
DE Autism; Electrophysiology; Endophenotype; Animal models; NMDA receptor
   antagonist
ID RECEPTOR ANTAGONIST; MICE; SCHIZOPHRENIA; MK-801; OSCILLATIONS;
   IMPAIRMENT; POTENTIALS; LOCOMOTION; STEREOTYPY; BIOMARKER
AB Autism is a highly disabling neurodevelopmental disorder characterized by social deficits, language impairment, and repetitive behaviors. There are few effective biological treatments for this disorder, partly due to the lack of translational biomarkers. However, recent data suggest that autism has reliable electrophysiological endophenotypes, along with evidence that some deficits may be caused by NMDA receptor (NMDAR) dysfunction. Similarly, the NMDAR antagonist MK801 has been used in behavioral animal models of autism. Since MK801 has also been used as a model of schizophrenia, this paper examines the independent and overlapping ways in which MK801 recreates the electrophysiogical changes present in both diseases. Mouse EEG was recorded in response to auditory stimuli after either vehicle or MK801 and the dose-response relationship for each measure was determined. ERP component amplitude and latency analysis was performed along with time-frequency analysis of gamma frequency inter-trial coherence and evoked power. Evoked gamma power and ITC were decreased by MK801 at the highest dose. P1, Ni latency and gamma baseline power were increased in dose dependent fashion following MK801. There were no amplitude changes in P1 or NI. MK801 caused alterations in evoked gamma activity, gamma ITC, gamma baseline power, P1 and Ni latency similar to findings in autism. These data provide evidence indicating that NMDAR dysfunction may contribute to deficits specific to autism and some that overlap with other disorders such as schizophrenia. Such observations could be important for developing novel therapeutics, as electrophysiological endophenotypes associate with functional measures and may provide early biomarkers for efficacy in clinical trials. (C) 2012 Published by Elsevier B.V.
C1 [Siegel, Steve J.] Univ Penn, Translat Res Labs, Dept Psychiat, Translat Neurosci Program, Philadelphia, PA 19104 USA.
   [Saunders, John A.; Gandal, Michael J.; Roberts, Timothy P.; Siegel, Steve J.] Univ Penn, Bioengn Grad Grp, Philadelphia, PA 19104 USA.
   [Roberts, Timothy P.] Childrens Hosp Philadelphia, Dept Radiol, Philadelphia, PA 19104 USA.
RP Siegel, SJ (reprint author), Univ Penn, Translat Res Labs, Dept Psychiat, Translat Neurosci Program, 125 S 31st St, Philadelphia, PA 19104 USA.
EM siegels@upenn.edu
FU Eli Lilly; AstraZeneca; NuPathe; Pfizer;  [5R01DA023210-02]; 
   [R01DC008871]
FX Steven Siegel reports having received grant support from Eli Lilly,
   AstraZeneca, NuPathe, and Pfizer that is unrelated to the content of
   this paper and consulting payments from NuPathe, Merck, Sanofi, and
   Wyeth that are unrelated to this work. Dr Roberts is a consultant for
   prism clinical imaging. All other authors report no biomedical financial
   interests or potential conflicts of interest.The study was supported by
   5R01DA023210-02 (SJS) R01DC008871 (TPR). The funding agencies had no
   further role in study design; in the collection, analysis and
   interpretation of data; in the writing of the report; and in the
   decision to submit the paper for publication
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NR 25
TC 9
Z9 10
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0166-4328
J9 BEHAV BRAIN RES
JI Behav. Brain Res.
PD OCT 1
PY 2012
VL 234
IS 2
BP 233
EP 237
DI 10.1016/j.bbr.2012.06.032
PG 5
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 002GY
UT WOS:000308521300013
PM 22771812
ER

PT J
AU Gouin, JP
   Carter, CS
   Pournajafi-Nazarloo, H
   Malarkey, WB
   Loving, TJ
   Stowell, J
   Kiecolt-Glaser, JK
AF Gouin, Jean-Philippe
   Carter, C. Sue
   Pournajafi-Nazarloo, Hossein
   Malarkey, William B.
   Loving, Timothy J.
   Stowell, Jeffrey
   Kiecolt-Glaser, Janice K.
TI Plasma vasopressin and interpersonal functioning
SO BIOLOGICAL PSYCHOLOGY
LA English
DT Article
DE Vasopressin; Social functioning; Couples; Social support; Marital
   quality
ID PSYCHOMETRIC PROPERTIES; PATERNAL BEHAVIOR; MAJOR DEPRESSION; PRAIRIE
   VOLES; OXYTOCIN; GENE; AVPR1A; AUTISM; SUSCEPTIBILITY; COMMUNICATION
AB The neuropeptide vasopressin has traditionally been associated with vasoconstriction and water reabsorption by the kidneys. However, data from experimental animal studies also implicate vasopressin in social bonding processes. Preliminary work suggests that vasopressin also plays a role in social behaviors in humans. The goal of this cross-sectional study was to evaluate associations among plasma vasopressin and self-reported interpersonal functioning in a sample of married couples. During a 24-h admission to a hospital-based research unit, 37 couples completed measures of interpersonal functioning and provided blood samples for neuropeptide analyses. Results showed that vasopressin was associated with markers of interpersonal functioning, but not with general psychological distress. Specifically, greater plasma vasopressin levels were related to a larger social network, fewer negative marital interactions, less attachment avoidance, more attachment security, and marginally greater spousal social support. These results indicate that vasopressin is likely implicated in different relationship maintenance processes in humans. (C) 2012 Elsevier B.V. All rights reserved.
C1 [Gouin, Jean-Philippe] Concordia Univ, Dept Psychol, Montreal, PQ H4B 1R6, Canada.
   [Carter, C. Sue; Pournajafi-Nazarloo, Hossein] Univ Illinois, Dept Psychiat, Brain & Body Ctr, Chicago, IL 60612 USA.
   [Carter, C. Sue; Kiecolt-Glaser, Janice K.] Res Triangle Inst Int, Res Triangle Pk, NC USA.
   [Malarkey, William B.] Ohio State Univ, Coll Med, Inst Behav Med Res, Columbus, OH 43210 USA.
   [Malarkey, William B.] Ohio State Univ, Coll Med, Dept Mol Virol Immunol & Med Genet, Columbus, OH 43210 USA.
   [Malarkey, William B.] Ohio State Univ, Coll Med, Dept Internal Med, Columbus, OH 43210 USA.
   [Loving, Timothy J.] Univ Texas Austin, Dept Human Dev & Family Sci, Austin, TX 78712 USA.
   [Stowell, Jeffrey] Eastern Illinois Univ, Dept Psychol, Charleston, IL USA.
   [Kiecolt-Glaser, Janice K.] Ohio State Univ, Coll Med, Dept Psychiat, Columbus, OH 43210 USA.
RP Gouin, JP (reprint author), Concordia Univ, Dept Psychol, 7141 Sherbrooke St W,PY 170-14, Montreal, PQ H4B 1R6, Canada.
EM jp.gouin@concordia.ca
RI Kiecolt-Glaser, Janice/A-3236-2009
OI Kiecolt-Glaser, Janice/0000-0003-4900-9578
FU National Institutes of Health (NIH) [DE13749, CA16058, UL1RR025755
   AG16321, CA158868]; NCRR [UL1RR025755]; Clinical Research Center; Ohio
   State Comprehensive Cancer Center Core Grant [CA16058];  [MH 072935]
FX This research was supported by National Institutes of Health (NIH)
   grants DE13749, CA16058, and UL1RR025755 AG16321 and CA158868, NCRR
   Grant UL1RR025755 which funds the Clinical Research Center, and by Ohio
   State Comprehensive Cancer Center Core Grant CA16058, and grant MH
   072935 to University of Illinois at Chicago.
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NR 38
TC 9
Z9 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0301-0511
EI 1873-6246
J9 BIOL PSYCHOL
JI Biol. Psychol.
PD OCT
PY 2012
VL 91
IS 2
BP 270
EP 274
DI 10.1016/j.biopsycho.2012.07.003
PG 5
WC Psychology, Biological; Behavioral Sciences; Psychology; Psychology,
   Experimental
SC Psychology; Behavioral Sciences
GA 028JM
UT WOS:000310418600013
PM 22820037
ER

PT J
AU Williams, PG
   Woods, C
   Stevenson, M
   Davis, DW
   Radmacher, P
   Smith, M
AF Williams, P. Gail
   Woods, Charles
   Stevenson, Michelle
   Davis, Deborah Winders
   Radmacher, Paula
   Smith, Michael
TI Psychotropic Medication Use in Children With Autism in the Kentucky
   Medicaid Population
SO CLINICAL PEDIATRICS
LA English
DT Article
DE autism; psychotropic drug; Kentucky Medicaid population
ID SPECTRUM DISORDERS; RUPP AUTISM; PATTERNS; ADOLESCENTS; PREVALENCE;
   RISPERIDONE
AB This study reviewed Kentucky Medicaid claims data for children with autism spectrum disorders to determine psychotropic drug (PTD) use in this population. Children with autism spectrum disorders (ICD-9 code 299.XX) in 3 different age-groups from 2005 to 2008 were identified; PTD use was defined as at least 1 prescription per year. PTD use in all age ranges was higher than in previously reported studies. High PTD use in children between 1 and 5 years is particularly of concern and may reflect perceived inadequacies of comprehensive educational/behavioral services for these children.
C1 [Williams, P. Gail] Univ Louisville, Dept Pediat, Weisskopff Child Evaluat Ctr, Louisville, KY 40202 USA.
RP Williams, PG (reprint author), Univ Louisville, Dept Pediat, Weisskopff Child Evaluat Ctr, Louisville, KY 40202 USA.
EM pgwill01@louisville.edu
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NR 22
TC 4
Z9 4
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0009-9228
J9 CLIN PEDIATR
JI Clin. Pediatr.
PD OCT
PY 2012
VL 51
IS 10
BP 923
EP 927
DI 10.1177/0009922812440837
PG 5
WC Pediatrics
SC Pediatrics
GA 027TZ
UT WOS:000310378000003
PM 22492834
ER

PT J
AU Sone, D
   Sugawara, T
   Sakakibara, E
   Tomioka, Y
   Taniguchi, G
   Murata, Y
   Watanabe, M
   Kaneko, S
AF Sone, Daichi
   Sugawara, Takayuki
   Sakakibara, Eisuke
   Tomioka, Yu
   Taniguchi, Go
   Murata, Yoshiko
   Watanabe, Masako
   Kaneko, Sunao
TI A case of autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE)
   coexisting with pervasive developmental disorder harboring SCN1A
   mutation in addition to CHRNB2 mutation
SO EPILEPSY & BEHAVIOR
LA English
DT Article
DE Autosomal dominant nocturnal frontal lobe epilepsy; Pervasive
   developmental disorder; Autistic spectrum disorder; SCN1A; CHRNB2;
   Refractory epilepsy; Genetic epilepsy
ID DE-NOVO MUTATIONS; AUTISM; CHILDREN
AB We report a case of autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) with several characteristics distinct from previously reported cases, in which genetic studies identified mutations in two different genes. This case differed from typical ADNFLE with respect to the following: (1) slightly younger onset and refractory to antiepileptic drugs and (2) borderline intellectual functioning and coexistence of pervasive developmental disorder from infancy. Genetic testing revealed a novel mutation and a silent substitution in SCN1A (c.4285G>T, A1429S and c.4371G>C, silent) in addition to a known mutation in CHRNB2 (c.1200C>G, I312M). SCN1A is a gene that codes for the voltage-dependent sodium channel alpha 1 subunit and has been implicated in generalized epilepsy with febrile seizures plus and severe myoclonic epilepsy in infancy. However, the relation between SCN1A and ADNFLE is unknown. We report the clinical course and symptomatic characteristics of this case although the relationship between ADNFLE mutation and SCN1A mutation remains to be elucidated. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Sone, Daichi; Sakakibara, Eisuke; Tomioka, Yu; Taniguchi, Go; Murata, Yoshiko; Watanabe, Masako] Natl Ctr Neurol & Psychiat, Dept Psychiat, Tokyo 1878551, Japan.
   [Sugawara, Takayuki; Kaneko, Sunao] Hirosaki Univ, Grad Sch Med, Dept Neuropsychiat, Hirosaki, Aomori, Japan.
RP Sone, D (reprint author), Natl Ctr Neurol & Psychiat, Dept Psychiat, 4-1-1 Ogawa Higashi, Tokyo 1878551, Japan.
EM daichisone@gmail.com
CR Aridon P, 2006, AM J HUM GENET, V79, P342, DOI 10.1086/506459
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NR 15
TC 2
Z9 3
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 OCT
PY 2012
VL 25
IS 2
BP 192
EP 195
DI 10.1016/j.yebeh.2012.07.027
PG 4
WC Behavioral Sciences; Clinical Neurology; Psychiatry
SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry
GA 028WZ
UT WOS:000310457100013
PM 23032131
ER

PT J
AU Hafizi, M
   Bakhshandeh, B
   Soleimani, M
   Atashi, A
AF Hafizi, Maryam
   Bakhshandeh, Behnaz
   Soleimani, Masoud
   Atashi, Amir
TI Exploring the enkephalinergic differentiation potential in adult stem
   cells for cell therapy and drug screening implications
SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
LA English
DT Article
DE Unrestricted somatic stem cells; Human mesenchymal stem cells;
   Enkephalinergic differentiation; Drug screening; Cell therapy
ID IN-VITRO DIFFERENTIATION; UMBILICAL-CORD BLOOD; BONE-MARROW;
   NEURODEGENERATIVE DISEASES; ALZHEIMERS-DISEASE; OPIOID SYSTEM;
   ANIMAL-MODEL; AUTISM; BRAIN; DOPAMINE
AB Stem cell therapy is one of the most promising treatments in neuroregenerative medicine. Considering the role of the endogenous opioid system in controlling the pathophysiology of neurological disorders and behavioral aberrations, current studies have focused on enkephalins as a part of the opioid system. Due to high capability of unrestricted somatic stem cells (USSCs) and human mesenchymal stem cells (hMSCs) for cell therapy and transplantation; here, we examined their enkephalinergic differentiation potential through Ikaros-related pathways in order to develop in vitro models to help drug screening and stem cell therapy for the opioid-related disorders. The authenticity of the stem cells was verified by differentiation experiments along with flow cytometry for surface markers. Later, we confirmed their neurogenic differentiation with semiquantitative and quantitative transcriptional and translational evaluations of the enkephalinergic-related genes such as proenkephalin, CREBZF, Ikaros, and prodynorphin. Our findings supported the enkephalinergic differentiation of these stem cells. Noteworthy, USSCs showed higher potential for differentiating into enkephalinergic neurons under Ikaros activation than hMSCs, which makes them appropriate for neurological therapeutic applications. In conclusion, this study suggests a powerful in vitro model for neurogenesis that may help clarification of enkephalinergic differentiation and related signaling networks along with neural drug screening. Such investigations may be beneficial to ameliorate the neural-related therapeutic approaches.
C1 [Soleimani, Masoud; Atashi, Amir] Tarbiat Modares Univ, Dept Hematol, Fac Med Sci, Tehran, Iran.
   [Bakhshandeh, Behnaz] Univ Tehran, Dept Biotechnol, Coll Sci, Tehran, Iran.
   [Hafizi, Maryam] Stem Cell Technol Res Ctr, Stem Cell Biol Dept, Tehran, Iran.
RP Soleimani, M (reprint author), Tarbiat Modares Univ, Dept Hematol, Fac Med Sci, POB 14115-111, Tehran, Iran.
EM soleim_m@modares.ac.ir; atashi@yahoo.com
FU Stem Cell Technology Research Center
FX This work was supported financially by Stem Cell Technology Research
   Center.
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NR 37
TC 6
Z9 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 1071-2690
J9 IN VITRO CELL DEV-AN
JI In Vitro Cell. Dev. Biol.-Anim.
PD OCT
PY 2012
VL 48
IS 9
BP 562
EP 569
DI 10.1007/s11626-012-9546-4
PG 8
WC Cell Biology; Developmental Biology
SC Cell Biology; Developmental Biology
GA 028MS
UT WOS:000310427000004
PM 23054438
ER

PT J
AU Jones, S
AF Jones, Sarah
TI Paternal age increases risk of autism and schizophrenia in children
SO NEUROPSYCHIATRY
LA English
DT News Item
NR 0
TC 0
Z9 0
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-2008
J9 NEUROPSYCHIATRY-LOND
JI Neuropsychiatry
PD OCT
PY 2012
VL 2
IS 5
BP 375
EP 375
PG 1
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 020YU
UT WOS:000309853300005
ER

PT J
AU Rapin, I
   Snodgrass, SR
AF Rapin, Isabelle
   Snodgrass, Samuel Robert
TI Classification issues in the developmental disorders: the case of autism
   and schizophrenia
SO NEUROPSYCHIATRY
LA English
DT Review
ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; INFANTILE-AUTISM;
   PSYCHIATRIC-DISORDERS; CHILDHOOD PSYCHOSES; SOCIAL COGNITION; NEURAL
   BASES; BRAIN; CHILDREN; GENETICS
AB New information continuously alters scientific classifications and their applications. A revision in progress of the DSM-IV-TR, which concerns classification of disorders, predominantly of behavioral symptoms, suggests reconsideration of overlaps and differences between two broad families of developmental disorders: autisms and schizophrenias. Developmental disorders are classified within two independent domains: behavioral/descriptive (level A) and biologic/etiologic (level C). Level A classification is syndromic and based on aggregates of mostly continuous, dimensional features with indistinct margins. Etiologic level C classification is based largely on categorical interacting genetic and environmental factors responsible for level A syndromes. Level B encompasses biologic mechanisms (pathogenesis) linking etiology (level C) to behavior (level A). Many level B hierarchical molecular and cellular networks contribute to the structure and function of the many brain networks responsible for level A behaviors. Autism and schizophrenia share some behavioral and cognitive characteristics, pathogenic mechanisms and etiologies, but major clinical disparities (level A) separate them.
C1 [Snodgrass, Samuel Robert] Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90502 USA.
   [Snodgrass, Samuel Robert] Harbor UCLA Med Ctr, Dept Neurol, Torrance, CA 90502 USA.
   [Rapin, Isabelle] Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10461 USA.
   [Rapin, Isabelle] Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA.
   [Rapin, Isabelle] Albert Einstein Coll Med, Rose F Kennedy Ctr Res Intellectual & Dev Disabil, Bronx, NY 10461 USA.
   [Snodgrass, Samuel Robert] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA.
RP Snodgrass, SR (reprint author), Harbor UCLA Med Ctr, Dept Pediat, Torrance, CA 90502 USA.
EM srsnodgrass@labiomed.ong
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NR 90
TC 1
Z9 1
PU FUTURE MEDICINE LTD
PI LONDON
PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3
   1QB, ENGLAND
SN 1758-2008
J9 NEUROPSYCHIATRY-LOND
JI Neuropsychiatry
PD OCT
PY 2012
VL 2
IS 5
BP 415
EP 427
DI 10.2217/NPY.12.46
PG 13
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 020YU
UT WOS:000309853300011
ER

PT J
AU Coghlan, S
   Horder, J
   Inkster, B
   Mendez, MA
   Murphy, DG
   Nutt, DJ
AF Coghlan, Suzanne
   Horder, Jamie
   Inkster, Becky
   Mendez, M. Andreina
   Murphy, Declan G.
   Nutt, David J.
TI GABA system dysfunction in autism and related disorders: From synapse to
   symptoms
SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
LA English
DT Review
DE GABA; Autism spectrum disorders; GABA(A) receptor; Inhibitory
   interneurons; Autism; Fragile X Syndrome; Rett Syndrome; Foetal
   Anticonvulsant Syndrome
ID FRAGILE-X-SYNDROME; MENTAL-RETARDATION PROTEIN; DE-NOVO MUTATIONS;
   ALCOHOL SPECTRUM DISORDER; CEREBELLAR PURKINJE-CELLS;
   GAMMA-AMINOBUTYRIC-ACID; RECEPTOR SUBUNIT GENES; RETT-SYNDROME; MOUSE
   MODEL; KNOCKOUT MICE
AB Autism spectrum disorders (ASDs) are neurodevelopmental syndromes characterised by repetitive behaviours and restricted interests, impairments in social behaviour and relations, and in language and communication. These symptoms are also observed in a number of developmental disorders of known origin, including Fragile X Syndrome, Rett Syndrome, and Foetal Anticonvulsant Syndrome. While these conditions have diverse etiologies, and poorly understood pathologies, emerging evidence suggests that they may all be linked to dysfunction in particular aspects of GABAergic inhibitory signalling in the brain. We review evidence from genetics, molecular neurobiology and systems neuroscience relating to the role of GABA in these conditions. We conclude by discussing how these deficits may relate to the specific symptoms observed. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Coghlan, Suzanne; Horder, Jamie; Mendez, M. Andreina; Murphy, Declan G.] Kings Coll London, Inst Psychiat, Dept Forens & Neurodev Sci, London SE5 8AF, England.
   [Inkster, Becky] Univ Cambridge, Dept Psychiat, Cambridge CB2 8AH, England.
   [Nutt, David J.] Univ London Imperial Coll Sci Technol & Med, Ctr Pharmacol & Therapeut, Neuropsychopharmacol Unit, Div Expt Med, London W12 0NN, England.
RP Horder, J (reprint author), Kings Coll London, Inst Psychiat, Dept Forens & Neurodev Sci, De Crespigny Pk, London SE5 8AF, England.
EM jamie.horder@kcl.ac.uk
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NR 185
TC 44
Z9 45
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0149-7634
J9 NEUROSCI BIOBEHAV R
JI Neurosci. Biobehav. Rev.
PD OCT
PY 2012
VL 36
IS 9
BP 2044
EP 2055
DI 10.1016/j.neubiorev.2012.07.005
PG 12
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 028LW
UT WOS:000310424800005
PM 22841562
ER

PT J
AU Bhat, S
   Dao, DT
   Terrillion, CE
   Arad, M
   Smith, RJ
   Soldatov, NM
   Gould, TD
AF Bhat, Shambhu
   Dao, David T.
   Terrillion, Chantelle E.
   Arad, Michal
   Smith, Robert J.
   Soldatov, Nikolai M.
   Gould, Todd D.
TI CACNA1C (Ca(v)1.2) in the pathophysiology of psychiatric disease
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
DE Calcium channel; CACNA1C; Genome wide association study; Bipolar
   disorder; Depression; Schizophrenia; Psychiatric genetics
ID CALCIUM-CHANNEL ANTAGONISTS; GENOME-WIDE ASSOCIATION; MAJOR DEPRESSIVE
   DISORDER; VENTRAL TEGMENTAL AREA; BIPOLAR-I-DISORDER; RANDOMIZED
   CLINICAL-TRIAL; LONG-TERM POTENTIATION; CA2+ CHANNELS; GENE-EXPRESSION;
   LINKAGE DISEQUILIBRIUM
AB One of the most consistent genetic findings to have emerged from bipolar disorder genome wide association studies (GWAS) is with CACNA1C, a gene that codes for the alpha(1C) subunit of the Ca(v)1.2 voltage-dependent L-type calcium channel (LTCC). Genetic variation in CACNA1C have also been associated with depression, schizophrenia, autism spectrum disorders, as well as changes in brain function and structure in control subjects who have no diagnosable psychiatric illness. These data are consistent with a continuum of shared neurobiological vulnerability between diverse Diagnostic and Statistical Manual (DSM) defined neuropsychiatric diseases. While involved in numerous cellular functions, Ca(v)1.2 is most frequently implicated in coupling of cell membrane depolarization to transient increase of the membrane permeability for calcium, leading to activation ani, potentially, changes in intracellular signaling pathway activity, gene transcription, and synaptic plasticity. Ca(v)1.2 is involved in the proper function of numerous neurological circuits including those involving the hippocampus, amygdala, and mesolimbic reward system, which are strongly implicated psychiatric disease pathophysiology. A number of behavioral effects of LTCC inhibitors have been described including antidepressant-like behavioral actions in rodent models. Clinical studies suggest possible treatment effects in a subset of patients with mood disorders. We review the genetic structure and variation of CACNA1C, discussing relevant human genetic and clinical findings, as well as the biological actions of Ca(v)1.2 that are most relevant to psychiatric illness. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bhat, Shambhu; Dao, David T.; Arad, Michal; Smith, Robert J.; Gould, Todd D.] Univ Maryland, Sch Med, Dept Psychiat, Baltimore, MD 21201 USA.
   [Terrillion, Chantelle E.; Gould, Todd D.] Univ Maryland, Program Neurosci, Baltimore, MD 21201 USA.
   [Gould, Todd D.] Univ Maryland, Sch Med, Dept Pharmacol, Baltimore, MD 21201 USA.
   [Soldatov, Nikolai M.] Humgenex Inc, Kensington, MD USA.
RP Gould, TD (reprint author), Univ Maryland, Sch Med, Dept Psychiat, Rm 934D,MSTF,685W Baltimore St, Baltimore, MD 21201 USA.
EM gouldlab@me.com
FU NARSAD; NIH [MH093967]
FX This work was supported by a NARSAD "Helen Lowenstein" Young
   Investigator Award and NIH MH093967 to TDG.
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NR 176
TC 36
Z9 39
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD OCT
PY 2012
VL 99
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BP 1
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SC Neurosciences & Neurology
GA 025FP
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PM 22705413
ER

PT J
AU Grayton, HM
   Fernandes, C
   Rujescu, D
   Collier, DA
AF Grayton, Hannah M.
   Fernandes, Cathy
   Rujescu, Dan
   Collier, David A.
TI Copy number variations in neurodevelopmental disorders
SO PROGRESS IN NEUROBIOLOGY
LA English
DT Review
DE Neurodevelopment; Schizophrenia; CNV; Copy number variant; GWA
ID CARDIO-FACIAL SYNDROME; AUTISM SPECTRUM DISORDER; PITT-HOPKINS-SYNDROME;
   COMPARATIVE GENOMIC HYBRIDIZATION; PROXIMAL 15Q DUPLICATION; 22Q11
   DELETION SYNDROME; MENTAL-RETARDATION; MICRODELETION SYNDROME;
   LEARNING-DISABILITY; DEVELOPMENTAL DELAY
AB Common neurodevelopmental disorders (including autism, speech and language delay, schizophrenia, epilepsy and intellectual disability) have complex aetiology, which is predominantly genomic, but also environmental in origin. They share a paradox, in that high heritability is matched by lowered fecundity, placing them under negative genetic selection. This implicates variants of recent origin, such as de nova mutations or common, very low-risk polymorphisms that escape negative selection. High or moderate risk variants have been discovered by chromosome analysis, genome sequencing and copy number variant (CNV) detection, including a 3Mb deletion causing 22q11.2 deletion syndrome (Velo-Cardio-Facial Syndrome) that has penetrance of up to 50% for schizophrenia. More recently, rare, recurrent and often de novo pathogenic CNVs, including deletions at NRXN1, 1q21.2, 15q11.2 and 15q13.3, 16p11.2 and duplications at VIPR2 and 16p13.11, have also been discovered. These have several unique features that differentiate them from Mendelian disease mutations in that they have incomplete penetrance, with moderate-to-high odds ratios for risk, and show diagnostic pleiotropy, increasing risk across the neurodevelopmental disorder spectrum. Some are also syndromic, with characteristic features such as facial dysmorphology, and other specific risks such as aortic dissection or obesity, implying that they might be better classified as distinct diagnoses. The discovery of pathogenic CNVs provide new opportunities for translation leading to patent benefit, including improvements in clinical genetic diagnosis and genetic counselling, the possibility of clinician decision-making tools for risk prediction, and the identification of drug targets and implementation of personalised medicine using stratification by genotype. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Collier, David A.] Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, MRC, London SE5 8AF, England.
   [Rujescu, Dan] Univ Munich, Dept Psychiat, Div Mol & Clin Neurobiol, D-80336 Munich, Germany.
RP Collier, DA (reprint author), Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, MRC, De Crespigny Pk,Denmark Hill, London SE5 8AF, England.
EM david.collier@kcl.ac.uk
RI Grayton, Hannah/A-9995-2013; Fernandes, Cathy/F-3422-2011
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NR 172
TC 35
Z9 35
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0301-0082
J9 PROG NEUROBIOL
JI Prog. Neurobiol.
PD OCT
PY 2012
VL 99
IS 1
BP 81
EP 91
DI 10.1016/j.pneurobio.2012.07.005
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 025FP
UT WOS:000310171800005
PM 22813947
ER

PT J
AU Rusconi, E
   McCrory, E
   Viding, E
AF Rusconi, Elena
   McCrory, Eamon
   Viding, Essi
TI Self-rated attention to detail predicts threat detection performance in
   security X-ray images
SO SECURITY JOURNAL
LA English
DT Article
DE attention to detail; autism-spectrum disorder; individual differences;
   psychological traits; threat detection
ID AUTISM; SEARCH; PERCEPTION; SIMON
AB Visual checks of thousands of X-ray images are carried out daily to detect and confiscate items that may compromise public security. Although technological advances are improving detection accuracy, screener-specific factors are also likely to matter. Here we investigated whether individual differences in self-rated attention to detail predicted performance on a simulated X-ray task with real small-vehicle images. An established measure of attention to detail was used to screen 124 naive adults; of these 29 high (n = 15) and low (n = 14) scoring individuals completed a detection task on unseen X-ray images. High scorers showed better performance than low scorers. The advantage emerged in both sensitivity (higher d') and localization, with high scorers unaffected by task-irrelevant correspondence between vehicle direction and response location. These findings suggest that greater attention to detail is associated with enhanced detection ability, and that recruitment processes for security officers may be improved by assessing Attention to Detail traits. Security Journal (2012) 25, 356-371. doi:10.1057/sj.2011.27; published online 10 October 2011
C1 [Rusconi, Elena] UCL, Dept Secur & Crime Sci, London WC1H 9EZ, England.
   [Rusconi, Elena] Univ Parma, Dept Neurosci, Physiol Sect, I-43100 Parma, Italy.
   [McCrory, Eamon; Viding, Essi] UCL, Div Psychol & Language Sci, London WC1H 0AP, England.
   [Viding, Essi] UCL, Inst Cognit Neurosci, London WC1N 3AR, England.
RP Rusconi, E (reprint author), UCL, Dept Secur & Crime Sci, 35 Tavistock Sq, London WC1H 9EZ, England.
EM elena.rusconi@gmail.com
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NR 43
TC 1
Z9 1
PU PALGRAVE MACMILLAN LTD
PI BASINGSTOKE
PA BRUNEL RD BLDG, HOUNDMILLS, BASINGSTOKE RG21 6XS, HANTS, ENGLAND
SN 0955-1662
J9 SECUR J
JI Secur. J.
PD OCT
PY 2012
VL 25
IS 4
BP 356
EP 371
DI 10.1057/sj.2011.27
PG 16
WC Criminology & Penology
SC Criminology & Penology
GA 024VD
UT WOS:000310136400005
ER

PT J
AU Staples, A
   Edmister, E
AF Staples, Amy
   Edmister, Evette
TI Evidence of Two Theoretical Models Observed in Young Children with
   Disabilities Who Are Beginning to Learn to Write
SO TOPICS IN LANGUAGE DISORDERS
LA English
DT Article
DE AAC; beginning writing; disabilities; early literacy; social
   interaction; writing processes
ID ALTERNATIVE COMMUNICATION; STUDENT; AUTISM; AAC
AB This study examined the composing process and communication of students aged 5-8 identified with intellectual disabilities. An open-ended writing activity called Big Paper was implemented at least once every 2 weeks for a 6-month period. Qualitative methods were utilized to analyze writing samples, videotapes of writing sessions, and transcripts of interactions during writing sessions. Students exhibited a range of communicative interactions during the writing sessions and varied improvement in writing quality along a scale of writing conventions. In addition, students demonstrated engagement in the cognitive process of writing (Flower & Hayes, 1981), and the community as a whole demonstrated engagement consistent with a social-interactive (Nystrand, 1989) composition model. Implications for defining composition, planning instruction, and assessing student growth are shared.
C1 [Staples, Amy] Univ No Iowa, Dept Special Educ, Schindler Educ Ctr 150A, Cedar Falls, IA 50614 USA.
   [Edmister, Evette] Univ No Iowa, Dept Commun Sci & Disorders, Cedar Falls, IA 50614 USA.
RP Staples, A (reprint author), Univ No Iowa, Dept Special Educ, Schindler Educ Ctr 150A, Cedar Falls, IA 50614 USA.
EM amy.staples@uni.edu; evette.edmister@uni.edu
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NR 40
TC 3
Z9 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-8294
J9 TOP LANG DISORD
JI Top. Lang. Disord.
PD OCT-DEC
PY 2012
VL 32
IS 4
SI SI
BP 319
EP 334
DI 10.1097/TLD.0b013e3182724d29
PG 16
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA 031MN
UT WOS:000310645400004
ER

PT J
AU Sturm, JM
AF Sturm, Janet M.
TI An Enriched Writers' Workshop for Beginning Writers with Developmental
   Disabilities
SO TOPICS IN LANGUAGE DISORDERS
LA English
DT Article
DE autism spectrum disorders; beginning writer; complex communication
   needs; developmental disabilities; writing instruction; writers'
   workshop
ID COGNITIVE STRATEGY INSTRUCTION; ALTERNATIVE COMMUNICATION; WRITING
   DEVELOPMENT; LITERACY; STUDENTS; CHILDREN; ADOLESCENTS; WRITTEN; AUTISM;
   MODEL
AB This article describes comprehensive, high-quality writing instruction for students with developmental disabilities. The Enriched Writers' Workshop combines differentiated writing process instruction with social communication instruction and cognitive strategy instruction for students with complex writing needs across a wide range of ages. It draws on research-based writing practices for all students, with reference to the U.S. Common Core State Standards for writing but with modifications for students with developmental disabilities. Appropriate populations include students with autism spectrum disorders, intellectual developmental disabilities, and complex communication needs, requiring augmentative and alternative communication supports. This article describes the Enriched Writers' Workshop framework of instruction, its tools, and the skills and strategies it targets. Illustrations are drawn from pilot implementation in special education classrooms team taught by special education teachers and speech-language pathologists. Case examples for 3 students show how the framework can be applied for beginning writers with varying profiles of abilities and needs, leading to measurable social communication and writing outcomes and other educational benefits for students with diverse developmental disabilities.
C1 Cent Michigan Univ, Dept Commun Disorders, Mt Pleasant, MI 48859 USA.
RP Sturm, JM (reprint author), Cent Michigan Univ, Dept Commun Disorders, 2167 Hlth Profess Bldg, Mt Pleasant, MI 48859 USA.
EM sturm1j@cmich.edu
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NR 76
TC 2
Z9 2
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-8294
J9 TOP LANG DISORD
JI Top. Lang. Disord.
PD OCT-DEC
PY 2012
VL 32
IS 4
SI SI
BP 335
EP 360
DI 10.1097/TLD.0b013e318272609b
PG 26
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA 031MN
UT WOS:000310645400005
ER

PT J
AU Asaro-Saddler, K
   Bak, N
AF Asaro-Saddler, Kristie
   Bak, Nicole
TI Teaching Children with High-Functioning Autism Spectrum Disorders to
   Write Persuasive Essays
SO TOPICS IN LANGUAGE DISORDERS
LA English
DT Article
DE autism spectrum disorders; persuasive essays; self-regulation; SRSD;
   writing
ID REGULATED STRATEGY-DEVELOPMENT; STRUGGLING YOUNG WRITERS;
   ASPERGER-SYNDROME; EXECUTIVE DYSFUNCTION; PLANNING INSTRUCTION;
   STUDENTS; SUPPORT; DISABILITIES; ADOLESCENTS; PERFORMANCE
AB In this single-subject design study, we examined the effects of an intervention targeting planning and self-regulation strategy use on the persuasive writing of children with high-functioning autism spectrum disorders (ASD). Three 8- to 9-year-old children with ASD in third and fourth grades learned a mnemonic-based strategy for planning and writing a persuasive essay using the self-regulated strategy development (SRSD) approach. The intervention was provided by the students' special education teachers following 2 professional development sessions, accompanied by weekly consultation by the authors. Comparison of 3 persuasive essay baseline probes with 3 postintervention probes revealed increases in holistic quality for all 3 participants, with mean increases from 3.2 to 7.0, 3.4 to 7.0, and 2.7 to 6.5 respectively. Word length decreased for 1 participant and increased for 2 participants, indicating that essay length in words was not directly correlated to improvements in overall quality. Evidence of planning and self-regulation was noted for all 3 participants on all 3 posttest probes, whereas planning was not evident on any of the pretest probes. Results of calculating the percentage of nonoverlapping data points from pre-/posttest holistic scores showed 100% posttest scores exceeding lowest baseline scores; this fell above the 90% effect-size threshold, providing evidence for the SRSD approach using POW + TREE as a "very effective" treatment option for improving the persuasive writing skills of students with high-functioning ASD. This study also showed that special education teachers could learn to implement the intervention with fidelity with limited training and consultation.
C1 [Asaro-Saddler, Kristie; Bak, Nicole] SUNY Albany, Albany, NY 12222 USA.
RP Asaro-Saddler, K (reprint author), SUNY Albany, ED 228, Albany, NY 12222 USA.
EM ksaddler@albany.edu
CR [Anonymous], 2007, NAT REP CARD
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NR 43
TC 6
Z9 6
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0271-8294
J9 TOP LANG DISORD
JI Top. Lang. Disord.
PD OCT-DEC
PY 2012
VL 32
IS 4
SI SI
BP 361
EP 378
DI 10.1097/TLD.0b013e318271813f
PG 18
WC Linguistics; Rehabilitation
SC Linguistics; Rehabilitation
GA 031MN
UT WOS:000310645400006
ER

PT J
AU Winarni, TI
   Chonchaiya, W
   Sumekar, TA
   Ashwood, P
   Morales, GM
   Tassone, F
   Nguyen, DV
   Faradz, SMH
   Van de Water, J
   Cook, K
   Hamlin, A
   Mu, Y
   Hagerman, PJ
   Hagerman, RJ
AF Winarni, Tri Indah
   Chonchaiya, Weerasak
   Sumekar, Tanjung Ayu
   Ashwood, Paul
   Morales, Guadalupe Mendoza
   Tassone, Flora
   Nguyen, Danh V.
   Faradz, Sultana M. H.
   Van de Water, Judy
   Cook, Kylee
   Hamlin, Alyssa
   Mu, Yi
   Hagerman, Paul J.
   Hagerman, Randi J.
TI Immune-Mediated Disorders Among Women Carriers of Fragile X Premutation
   Alleles
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE autoimmune; FXTAS; RNA toxicity; ovarian insufficiency
ID TREMOR/ATAXIA SYNDROME FXTAS; AUTISM SPECTRUM DISORDERS;
   IRRITABLE-BOWEL-SYNDROME; TOLL-LIKE RECEPTORS; FMR1 MESSENGER-RNA;
   AUTOIMMUNE-DISEASES; MULTIPLE-SCLEROSIS; RHEUMATOID-ARTHRITIS;
   MYOTONIC-DYSTROPHY; EXPANDED ALLELES
AB The relative risk of immune-mediated disorders (IMDs) among women carriers of premutation alleles is estimated by a survey for IMDs among 344 carrier women (age 19-81 years; mean 46.35 and SD 12.60) and 72 controls (age 18-87 years; mean 52.40 and SD 15.40). One hundred fifty four (44.77%) women carrier had at least one IMD, as did 20 controls (27.78%). Among women carriers, autoimmune thyroid disorder was the most common (24.4%), then fibromyalgia (10.2%), irritable bowel syndrome (IBS; 9.9%), Raynaud's phenomenon (7.6%), rheumatoid arthritis (RA; 3.8%), Sjogren syndrome (2.6%), systemic lupus erythematosus (SLE; 2.03%), multiple sclerosis (1.74%). Of 55 carriers age 40 or older with FXTAS, 72.73% had at least one IMD, compared to 46.54% of those without FXTAS (n = 159), and 31.58% of controls (n = 57). The estimated odds ratio (OR) for IMD is 2.6 (95% CI 1.2-5.6, P = 0.015) for women with FXTAS relative to those without FXTAS; the likelihood of IMD in carriers without or with FXTAS was also significantly higher than for controls (OR 2.1, 95% CI 1.1-4.2, P = 0.034; OR 5.5, 95% CI 2.4-12.5, P < 0.001, respectively). Similarly, the odds of having an IMD among carriers with FXPOI is about 2.4 times higher when compared to carriers without FXPOI (95% CI 1.1-5.0; P = 0.021). The likelihood of IMD in carriers with or without FXPOI is greater (OR 2.4, 95% CI 1.1-5.0; P = 0.021) compared to that of controls. (C) 2012 Wiley Periodicals, Inc.
C1 [Winarni, Tri Indah; Sumekar, Tanjung Ayu; Ashwood, Paul; Tassone, Flora; Van de Water, Judy; Cook, Kylee; Hamlin, Alyssa; Hagerman, Paul J.; Hagerman, Randi J.] Univ Calif Davis, Med Invest Neurodev Disorders MIND Inst, Sacramento, CA 95817 USA.
   [Winarni, Tri Indah; Sumekar, Tanjung Ayu; Faradz, Sultana M. H.] Diponegoro Univ Semarang, Fac Med, Ctr Biomed Res, Cent Java, Indonesia.
   [Chonchaiya, Weerasak] Chulalongkorn Univ, Fac Med, Bangkok 10330, Thailand.
   [Ashwood, Paul] Univ Calif Davis, Sch Med, Dept Med Microbiol & Immunol, Davis, CA 95616 USA.
   [Morales, Guadalupe Mendoza; Tassone, Flora; Hagerman, Paul J.] Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA.
   [Nguyen, Danh V.; Mu, Yi] Univ Calif Davis, Dept Publ Hlth Sci, Div Biostat, Davis, CA 95616 USA.
   [Van de Water, Judy] Univ Calif Davis, Dept Internal Med, Sacramento, CA 95817 USA.
   [Van de Water, Judy] Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA.
   [Hagerman, Randi J.] Univ Calif Davis, Sch Med, Dept Pediat, Sacramento, CA 95817 USA.
RP Hagerman, RJ (reprint author), UC Davis Hlth Syst, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA.
EM randi.hagerman@ucdmc.ucdavis.edu
FU National Institute of Health [HD036071, HD02274]; Neuro Therapeutics
   Research Institute (NTRI) [DE019583, DA024854]; National Institute on
   Aging [AG032119, AG032115]; National Institute of Mental Health
   [MH077554]; National Center for Research Resources [UL1 RR024146];
   Health and Human Services Administration on Developmental Disabilities
   [90DD05969]; Seaside Therapeutics; Roche; Novartis; Forest; Curemark
FX Grant sponsor: National Institute of Health; Grant numbers: HD036071,
   HD02274; Grant sponsor: Neuro Therapeutics Research Institute (NTRI);
   Grant numbers: DE019583, DA024854; Grant sponsor: National Institute on
   Aging; Grant numbers: AG032119, AG032115; Grant sponsor: National
   Institute of Mental Health; Grant number: MH077554; Grant sponsor:
   National Center for Research Resources; Grant number: UL1 RR024146;
   Grant sponsor: Health and Human Services Administration on Developmental
   Disabilities; Grant number: 90DD05969.Randi Hagerman has received
   funding from Seaside Therapeutics, Roche, Novartis, Forest, and Curemark
   to carry out treatment trials. Paul Hagerman and Flora Tassone are
   uncompensated collaborators with Asuragen, Inc., and hold a US patent
   for expanded-CGG screening. There are no other conflicts of interest
   from the authors.
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NR 61
TC 17
Z9 17
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2012
VL 158A
IS 10
BP 2473
EP 2481
DI 10.1002/ajmg.a.35569
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 023XK
UT WOS:000310070700015
PM 22903889
ER

PT J
AU Guerin, A
   Stavropoulos, DJ
   Diab, Y
   Chenier, S
   Christensen, H
   Kahr, WHA
   Babul-Hirji, R
   Chitayat, D
AF Guerin, Andrea
   Stavropoulos, Dimitri J.
   Diab, Yaser
   Chenier, Sebastien
   Christensen, Hilary
   Kahr, Walter H. A.
   Babul-Hirji, Riyana
   Chitayat, David
TI Interstitial Deletion of 11q-Implicating the KIRREL3 Gene in the
   Neurocognitive Delay Associated With Jacobsen Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE Jacobsen syndrome; 11q deletion; autism; speech delay
ID GTPASE-ACTIVATING-PROTEIN; CRITICAL REGION; MOLECULAR CHARACTERIZATION;
   KNOCKOUT MICE; STEM-CELLS; THROMBOCYTOPENIA; RECEPTOR; BARX2;
   DEFICIENCY; MICROARRAY
AB Jacobsen syndrome (JS) is a rare contiguous gene disorder characterized by a deletion within the distal part of the long arm of chromosome 11 ranging in size from 7 to 20 Mb. The clinical findings include characteristic dysmorphic features, growth and psychomotor delays and developmental anomalies involving the brain, eyes, heart, kidneys, immune, hematologic, endocrine, and gastrointestinal systems. The majority of cases are due to a terminal deletion of 11q; however interstitial deletions have also been reported. We report on a child with clinical manifestations consistent with JS who had a 2.899 Mb interstitial deletion at 11q24.2-q24.3 which is the smallest interstitial deletion reported so far to our knowledge. This deletion includes the KIRREL3 gene, and given our patient's history of neurocognitive delay and autism spectrum disorder, it raises the possibility that this gene is a candidate for the social and expressive language delay observed in our patient. (C) 2012 Wiley Periodicals, Inc.
C1 [Guerin, Andrea; Babul-Hirji, Riyana; Chitayat, David] Univ Toronto, Hosp Sick Children, Dept Pediat, Div Clin & Metab Genet, Toronto, ON M5G 1X8, Canada.
   [Stavropoulos, Dimitri J.] Univ Toronto, Dept Lab Med & Pathobiol, Toronto, ON, Canada.
   [Stavropoulos, Dimitri J.; Chenier, Sebastien] Hosp Sick Children, Dept Paediat Lab Med, Toronto, ON M5G 1X8, Canada.
   [Diab, Yaser; Christensen, Hilary; Kahr, Walter H. A.] Univ Toronto, Hosp Sick Children, Dept Pediat, Div Hematol, Toronto, ON M5G 1X8, Canada.
   [Kahr, Walter H. A.] Univ Toronto, Dept Biochem, Toronto, ON, Canada.
   [Chitayat, David] Univ Toronto, Mt Sinai Hosp, Prenatal Diag & Med Genet Program, Dept Obstet & Gynecol, Toronto, ON M5G 1X5, Canada.
RP Chitayat, D (reprint author), Dept Obstet & Genecol, Prenatal Diag & Med Genet Program, Ontario Power Generat Bldg,700 Univ Ave,Room 3292, Toronto, ON M5G 1X8, Canada.
EM dchitayat@mtsinai.on.ca
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NR 34
TC 9
Z9 9
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2012
VL 158A
IS 10
BP 2551
EP 2556
DI 10.1002/ajmg.a.35621
PG 6
WC Genetics & Heredity
SC Genetics & Heredity
GA 023XK
UT WOS:000310070700028
PM 22965935
ER

PT J
AU Burrage, LC
   Person, RE
   Flores, A
   Villanos, MTM
   Bi, WM
   Wiszniewska, J
   Bacino, CA
AF Burrage, Lindsay C.
   Person, Richard E.
   Flores, Angela
   Villanos, Maria Theresa M.
   Bi, Weimin
   Wiszniewska, Joanna
   Bacino, Carlos A.
TI De Novo Interstitial Duplication of 15q11.2-q13.1 With Complex Maternal
   Uniparental Trisomy for the 15q11-q13 Region in a Patient with
   Prader-Willi Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE uniparental trisomy; Prader-Willi Syndrome; 15q11-q13 duplication
ID PROXIMAL 15Q; ANGELMAN-SYNDROME; ARRAY CGH; RECOMBINATION; ORIGIN;
   DISOMY; CHROMOSOME-15; DIAGNOSIS
AB Prader-Willi syndrome is caused by the lack of paternal contribution for the imprinted 15q11-q13 region that originates through a number of mechanisms such as paternal deletion of 15q11-q13, maternal uniparental disomy, or by an imprinting defect due to epimutations in the paternal imprinting center. In the present report, we describe a female patient with complex maternal uniparental trisomy for the 15q11-q13 Prader-Willi syndrome critical region due to a de novo interstitial duplication of 15q11-q13 region that is present in one of the maternal homologs. As a result, the patient has three maternally derived copies of the Prader-Willi syndrome critical region and absence of paternal 15 contribution and thus, presents with a Prader-Willi syndrome phenotype with risk for developing additional phenotypes (e. g., autism and psychiatric phenotypes) characteristic of maternally derived duplications of this region. We suggest that this is a rather unique mechanism leading to Prader-Willi syndrome that has not been previously reported. (C) 2012 Wiley Periodicals, Inc.
C1 [Bacino, Carlos A.] Texas Childrens Hosp, Clin Care Ctr, Houston, TX 77030 USA.
   [Burrage, Lindsay C.; Person, Richard E.; Bi, Weimin; Wiszniewska, Joanna; Bacino, Carlos A.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Flores, Angela] Texas Tech Univ, Hlth Sci Ctr El Paso, Dept Pediat, Div Neonatol, El Paso, TX USA.
RP Bacino, CA (reprint author), Texas Childrens Hosp, Clin Care Ctr, 6701 Fannin St,Suite 1560, Houston, TX 77030 USA.
EM cbacino@bcm.edu
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NR 22
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2012
VL 158A
IS 10
BP 2557
EP 2563
DI 10.1002/ajmg.a.35549
PG 7
WC Genetics & Heredity
SC Genetics & Heredity
GA 023XK
UT WOS:000310070700029
PM 22903639
ER

PT J
AU Schroer, RJ
   Beaudet, AL
   Shinawi, M
   Sahoo, T
   Patel, A
   Sun, Q
   Skinner, C
   Stevenson, RE
AF Schroer, Richard J.
   Beaudet, Arthur L.
   Shinawi, Marwan
   Sahoo, Trilochan
   Patel, Ankita
   Sun, Qin
   Skinner, Cindy
   Stevenson, Roger E.
TI Duplication of OCRL and Adjacent Genes Associated With Autism but not
   Lowe Syndrome
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A
LA English
DT Article
DE X chromosome; autism; microduplication; OCRL; Lowe syndrome
AB Disturbances in the form of microduplications and microdeletions have been found throughout the genome and have been associated with autism, intellectual disability, and recognizable malformation syndromes. In our study of 187 probands with autism, we have identified a duplication in Xq25 including full gene duplication of OCRL and six flanking genes. Activity of the enzyme gene product in fibroblasts was elevated to over twice the level in control fibroblasts. The boy had no somatic or neurological findings reminiscent of Lowe syndrome. (C) 2012 Wiley Periodicals, Inc.
C1 [Schroer, Richard J.; Skinner, Cindy; Stevenson, Roger E.] Greenwood Genet Ctr, Greenwood, SC 29646 USA.
   [Beaudet, Arthur L.; Sahoo, Trilochan; Patel, Ankita; Sun, Qin] Baylor Coll Med, Houston, TX 77030 USA.
   [Shinawi, Marwan] Washington Univ, Sch Med, St Louis, MO USA.
RP Stevenson, RE (reprint author), Greenwood Genet Ctr, 113 Gregor Mendel Circle, Greenwood, SC 29646 USA.
EM res@ggc.org
FU South Carolina Department of Disabilities and Special Needs [MH 57840];
   National Institute of Mental Health [MH 57840]
FX Grant sponsor: South Carolina Department of Disabilities and Special
   Needs; Grant number: MH 57840; Grant sponsor: National Institute of
   Mental Health; Grant number: MH 57840.
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NR 5
TC 2
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4825
J9 AM J MED GENET A
JI Am. J. Med. Genet. A
PD OCT
PY 2012
VL 158A
IS 10
BP 2602
EP 2605
DI 10.1002/ajmg.a.35566
PG 4
WC Genetics & Heredity
SC Genetics & Heredity
GA 023XK
UT WOS:000310070700036
PM 22965764
ER

PT J
AU Plastow, M
AF Plastow, Michael
TI 'Theory of mind' III: the unbearable idea of other minds
SO AUSTRALASIAN PSYCHIATRY
LA English
DT Article
DE autism; mirror stage; narcissism; paranoid knowledge; theory of mind
AB Objective: In order to give an alternative explanation for the phenomena described by 'theory of mind', this topic is approached firstly by an examination of literary productions and then by reference to psychoanalysis.
   Conclusions: In literature there are many references to the apprehension of the other in terms of a mirror image of the self. The difficulty of grasping the other is described in a passage by the author Ian McEwan as 'the unbearable idea of other minds'. The notion that this difficulty can in part be overcome through both spoken and written language is also salient in the novels examined here. The concept of an entrapment within one's image of oneself was elaborated by Freud in his notion of narcissism. Lacan further developed this notion as foundational in one's relation to the other, but clarified that such mirroring relations to others are always imbued with jealousy and rivalry. Lacan's notion of "paranoid knowledge", an imagined knowledge of what the other is thinking, is precisely a 'theory of mind' that is able to account for the way one subject attempts, and ultimately fails, to read the mind of another.
C1 Alfred CYMHS, Moorabbin, Vic 3189, Australia.
RP Plastow, M (reprint author), Alfred CYMHS, 999 Nepean Hwy, Moorabbin, Vic 3189, Australia.
EM m.plastow@alfred.org.au
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NR 23
TC 0
Z9 0
PU SAGE PUBLICATIONS LTD
PI LONDON
PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND
SN 1039-8562
J9 AUSTRALAS PSYCHIATRY
JI Australas. Psychiatry
PD OCT
PY 2012
VL 20
IS 5
BP 369
EP 373
DI 10.1177/1039856212458330
PG 5
WC Psychiatry
SC Psychiatry
GA 023FQ
UT WOS:000310018700001
PM 23014127
ER

PT J
AU Carrillo-Santisteve, P
   Lopalco, PL
AF Carrillo-Santisteve, P.
   Lopalco, P. L.
TI Measles still spreads in Europe: who is responsible for the failure to
   vaccinate?
SO CLINICAL MICROBIOLOGY AND INFECTION
LA English
DT Review
DE Elimination; immunization; measles; public health; vaccination
ID RUBELLA VACCINATION; AUTISM; MUMPS; ASSOCIATION
AB Clin Microbiol Infect 2012; 18 (Suppl. 5): 5056 Abstract All countries in the European Region of the World Health Organization (WHO) have renewed their commitment to eliminate measles transmission by 2015. Measles elimination is a feasible target but requires vaccination coverage above 95% with two doses of a measles-mumps-rubella vaccine (MMR) in all population groups and in all geographical areas. Measles has re-emerged in the EU recently, due to suboptimal immunization levels that led to accumulation of susceptible populations over the last years. In fact, while an overall decreasing trend had been observed until 2009, the number of cases increased by a factor of four between2010 and 2011. According to vaccination coverage data reported to the WHO, between 2000 and 2010, almost 5 million individuals in the EU in the age group 212 had not had MMR vaccination. Catch-up vaccination activities for susceptible populations are paramount in order to reach the elimination goal, but only feasible if a multi-component approach is put in place quickly and efficiently. Advocacy and communication are key strategic areas.
C1 [Carrillo-Santisteve, P.; Lopalco, P. L.] European Ctr Dis Prevent & Control ECDC, Off Chief Scientist, Stockholm, Sweden.
RP Carrillo-Santisteve, P (reprint author), Tomtebodavagen 11, SE-17183 Stockholm, Sweden.
EM Paloma.carrillo@ecdc.europa.eu
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NR 29
TC 14
Z9 14
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1198-743X
J9 CLIN MICROBIOL INFEC
JI Clin. Microbiol. Infect.
PD OCT
PY 2012
VL 18
SU 5
SI SI
BP 50
EP 56
DI 10.1111/j.1469-0691.2012.03982.x
PG 7
WC Infectious Diseases; Microbiology
SC Infectious Diseases; Microbiology
GA 019DI
UT WOS:000309716900007
PM 23051058
ER

PT J
AU Stevenson, MT
   Soto, JA
   Adams, RB
AF Stevenson, Michael T.
   Soto, Jose A.
   Adams, Reginald B., Jr.
TI More Than Meets the Eye: The Role of Self-Identity in Decoding Complex
   Emotional States
SO EMOTION
LA English
DT Article
DE interpersonal communication; social categorization; self-identity;
   complex emotion decoding
ID FACIAL EXPRESSIONS; CULTURAL-DIFFERENCES; STEREOTYPE THREAT;
   RECOGNITION; IDENTIFICATION; ACCURACY; MIND
AB Folk wisdom asserts that "the eyes are the window to the soul," and empirical science corroborates a prominent role for the eyes in the communication of emotion. Herein we examine variation in the ability to "read" the eyes of others as a function of social group membership, employing a widely used emotional state decoding task: "Reading the Mind in Eyes." This task has documented impaired emotional state decoding across racial groups, with cross-race performance on par with that previously reported as a function of autism spectrum disorders. The present study extended this work by examining the moderating role of social identity in such impairments. For college students more highly identified with their university, cross-race performance differences were not found for judgments of "same-school" eyes but remained for "rival-school" eyes. These findings suggest that impaired emotional state decoding across groups may thus be more amenable to remediation than previously realized.
C1 [Stevenson, Michael T.; Soto, Jose A.; Adams, Reginald B., Jr.] Penn State Univ, Dept Psychol, University Pk, PA 16802 USA.
RP Stevenson, MT (reprint author), Penn State Univ, Dept Psychol, 366 Moore Bldg, University Pk, PA 16802 USA.
EM mts240@psu.edu; radams@psu.edu
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NR 31
TC 1
Z9 1
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1528-3542
J9 EMOTION
JI Emotion
PD OCT
PY 2012
VL 12
IS 5
BP 882
EP 886
DI 10.1037/a0028628
PG 5
WC Psychology, Experimental
SC Psychology
GA 022GQ
UT WOS:000309946200003
PM 22642348
ER

PT J
AU Maras, KL
   Gaigg, SB
   Bowler, DM
AF Maras, Katie L.
   Gaigg, Sebastian B.
   Bowler, Dermot M.
TI Memory for Emotionally Arousing Events Over Time in Autism Spectrum
   Disorder
SO EMOTION
LA English
DT Article
DE Autism Spectrum Disorder; emotion; arousal; eyewitness; memory; delay
ID HIGH-FUNCTIONING AUTISM; EYEWITNESS MEMORY; ASPERGER-SYNDROME; CARDIAC
   RESPONSES; YOUNG-CHILDREN; RECALL; ADULTS; INTACT; INFORMATION; DISTRESS
AB Emotionally arousing events are typically better remembered and more resistant to forgetting than neutral events. Findings from word list paradigms suggest that this may not hold for individuals with Autism Spectrum Disorder (ASD), who also tend to be less accurate as eyewitnesses under some circumstances. To test whether attenuated effects of arousal on memory may be responsible for poorer eyewitness testimonies in ASD, we asked adults with and without the disorder to view either arousing or neutral versions of a narrated slide sequence (Experiment 1) or video clip (Experiment 2) before assessing their memory for the material. Both groups exhibited increases in psychophysiological arousal during the arousing compared with the neutral version of the narratives, and both groups also demonstrated a memory advantage for the arousing events. Contrary to predictions, these observations indicate that stimulus induced arousal modulates memory for naturalistic events relatively typically in ASD.
C1 [Maras, Katie L.; Gaigg, Sebastian B.; Bowler, Dermot M.] City Univ London, Dept Psychol, London EC1V 0HB, England.
   [Maras, Katie L.; Gaigg, Sebastian B.; Bowler, Dermot M.] City Univ London, Autism Res Grp, London EC1V 0HB, England.
RP Maras, KL (reprint author), City Univ London, Dept Psychol, Northampton Sq, London EC1V 0HB, England.
EM Katie.Maras.1@city.ac.uk
RI Maras, Katie/F-9283-2013
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NR 40
TC 5
Z9 5
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 1528-3542
J9 EMOTION
JI Emotion
PD OCT
PY 2012
VL 12
IS 5
BP 1118
EP 1128
DI 10.1037/a0026679
PG 11
WC Psychology, Experimental
SC Psychology
GA 022GQ
UT WOS:000309946200031
PM 22309718
ER

PT J
AU Bell, CG
   Wilson, GA
   Butcher, LM
   Roos, C
   Walter, L
   Beck, S
AF Bell, Christopher G.
   Wilson, Gareth A.
   Butcher, Lee M.
   Roos, Christian
   Walter, Lutz
   Beck, Stephan
TI Human-specific CpG "beacons" identify loci associated with
   human-specific traits and disease
SO EPIGENETICS
LA English
DT Article
DE epigenetics; epigenomics; CpG islands; gene regulation; evolution; human
   disease
ID BIASED GENE CONVERSION; AUTISM SPECTRUM DISORDER; COPY NUMBER VARIATION;
   EMBRYONIC STEM-CELLS; DNA METHYLATION; HUMAN GENOME; MORPHOLOGICAL
   EVOLUTION; INTELLECTUAL DISABILITY; NONCODING SEQUENCES;
   CHROMATIN-STRUCTURE
AB Regulatory change has long been hypothesized to drive the delineation of the human phenotype from other closely related primates. Here we provide evidence that CpG dinucleotides play a special role in this process. CpGs enable epigenome variability via DNA methylation, and this epigenetic mark functions as a regulatory mechanism. Therefore, species-specific CpGs may influence species-specific regulation. We report non-polymorphic species-specific CpG dinucleotides (termed "CpG beacons") as a distinct genomic feature associated with CpG island (CGI) evolution, human traits and disease. Using an inter-primate comparison, we identified 21 extreme CpG beacon clusters (>= 20/kb peaks, empirical p < 1.0 x 10(-3)) in humans, which include associations with four monogenic developmental and neurological disease related genes (Benjamini-Hochberg corrected p = 6.03 x 10(-3)). We also demonstrate that beacon-mediated CpG density gain in CGIs correlates with reduced methylation in these species in orthologous CGIs over time, via human, chimpanzee and macaque MeDIP-seq. Therefore mapping into both the genomic and epigenomic space the identified CpG beacon clusters define points of intersection where a substantial two-way interaction between genetic sequence and epigenetic state has occurred. Taken together, our data support a model for CpG beacons to contribute to CGI evolution from genesis to tissue-specific to constitutively active CGIs.
C1 [Bell, Christopher G.; Wilson, Gareth A.; Butcher, Lee M.; Beck, Stephan] UCL, UCL Canc Inst, London, England.
   [Roos, Christian; Walter, Lutz] German Primate Ctr, Leibniz Inst Primate Res, Gene Bank Primates & Primate Genet Lab, Gottingen, Germany.
RP Bell, CG (reprint author), UCL, UCL Canc Inst, London, England.
EM christopher.bell@ucl.ac.uk; s.beck@ucl.ac.uk
RI Butcher, Lee/C-1540-2008
FU Wellcome Trust [084071]; Royal Society Wolfson Research Merit Award
   [WM100023]; EU [018883, 257082, 282510]
FX We thank the staff of the Tierpark Nordhorn, Basel Zoo, Leipzig Zoo and
   the German Primate Center for providing blood samples of chimpanzees and
   rhesus macaques. Work in the Beck lab was supported by the Wellcome
   Trust (084071), Royal Society Wolfson Research Merit Award (WM100023)
   and EU-FP7 projects HEROIC (018883), EPIGENESYS (257082) and BLUEPRINT
   (282510).
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NR 116
TC 11
Z9 11
PU LANDES BIOSCIENCE
PI AUSTIN
PA 1806 RIO GRANDE ST, AUSTIN, TX 78702 USA
SN 1559-2294
EI 1559-2308
J9 EPIGENETICS-US
JI Epigenetics
PD OCT
PY 2012
VL 7
IS 10
BP 1188
EP 1199
DI 10.4161/epi.22127
PG 12
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 022LJ
UT WOS:000309960600011
PM 22968434
ER

PT J
AU Dereu, M
   Roeyers, H
   Raymaekers, R
   Meirsschaut, M
   Warreyn, P
AF Dereu, Mieke
   Roeyers, Herbert
   Raymaekers, Ruth
   Meirsschaut, Mieke
   Warreyn, Petra
TI How useful are screening instruments for toddlers to predict outcome at
   age 4? General development, language skills, and symptom severity in
   children with a false positive screen for autism spectrum disorder
SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY
LA English
DT Article
DE Autism spectrum disorder; Screening; Toddlers; Language; General
   development; Symptom severity
ID DIAGNOSTIC-OBSERVATION-SCHEDULE; TRAITS QUESTIONNAIRE ESAT; MODIFIED
   CHECKLIST; REVISED ALGORITHMS; ADOS SCORES; POPULATION; VALIDITY; SIGNS;
   CHAT
AB Screening instruments for autism spectrum disorder (ASD) often generate many false positives. It is argued that these children may have other developmental difficulties and are also in need of thorough assessment and early intervention. The current study looked at the predictive validity of positive screens on the Checklist for Early Signs of Developmental Disorders (CESDD) and the Early Screening of Autistic Traits questionnaire (ESAT) at age 2 towards language, cognitive function, and symptom severity at age 4. Children who screened positive on the ESAT scored lower for both language and cognitive functioning at age 4 compared with children who screened negative on the ESAT. Also, the more signs of ASD that were recognized on the CESDD or ESAT, the lower the scores for language and cognitive functioning at age 4. False positive screens could be differentiated from true positive screens on the CESDD only in symptom severity score on the Autism Diagnostic Observation Schedule (ADOS). It seems that early screeners for ASD also detect children with other developmental disorders and that diagnostic instruments such as the ADOS are warranted to differentiate between children with ASD and other developmental problems.
C1 [Dereu, Mieke; Roeyers, Herbert; Raymaekers, Ruth; Meirsschaut, Mieke; Warreyn, Petra] Univ Ghent, Res Grp Dev Disorders, Dept Expt Clin & Hlth Psychol, B-9000 Ghent, Belgium.
RP Dereu, M (reprint author), Univ Ghent, Res Grp Dev Disorders, Dept Expt Clin & Hlth Psychol, Henri Dunantlaan 2, B-9000 Ghent, Belgium.
EM Mieke.Dereu@UGent.be
FU Steunpunt Expertisenetwerken; Vlaamse Vereniging Autisme
FX Partial funding for this research was provided by support from Steunpunt
   Expertisenetwerken and Vlaamse Vereniging Autisme. We thank the day-care
   centres, the children and their families for their participation to the
   study. Special thanks goes to the participating diagnostic centra across
   Flanders (COS and RCA Gent, COS and RCA Antwerpen, COS and RCA Brussel,
   COS and ECA Leuven).
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NR 40
TC 6
Z9 6
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 OCT
PY 2012
VL 21
IS 10
BP 541
EP 551
DI 10.1007/s00787-012-0280-y
PG 11
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 021GC
UT WOS:000309872300002
PM 22580987
ER

PT J
AU Fogel, BL
   Wexler, E
   Wahnich, A
   Friedrich, T
   Vijayendran, C
   Gao, FY
   Parikshak, N
   Konopka, G
   Geschwind, DH
AF Fogel, Brent L.
   Wexler, Eric
   Wahnich, Amanda
   Friedrich, Tara
   Vijayendran, Chandran
   Gao, Fuying
   Parikshak, Neelroop
   Konopka, Genevieve
   Geschwind, Daniel H.
TI RBFOX1 regulates both splicing and transcriptional networks in human
   neuronal development
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID MOLECULAR CHARACTERIZATION; EXPRESSION ANALYSIS; NEURAL PROGENITORS;
   BINDING PROTEINS; GENE-EXPRESSION; CANDIDATE GENES; HUMAN BRAIN;
   STEM-CELLS; RNA; AUTISM
AB RNA splicing plays a critical role in the programming of neuronal differentiation and, consequently, normal human neurodevelopment, and its disruption may underlie neurodevelopmental and neuropsychiatric disorders. The RNA-binding protein, fox-1 homolog (RBFOX1; also termed A2BP1 or FOX1), is a neuron-specific splicing factor predicted to regulate neuronal splicing networks clinically implicated in neurodevelopmental disease, including autism spectrum disorder (ASD), but only a few targets have been experimentally identified. We used RNA sequencing to identify the RBFOX1 splicing network at a genome-wide level in primary human neural stem cells during differentiation. We observe that RBFOX1 regulates a wide range of alternative splicing events implicated in neuronal development and maturation, including transcription factors, other splicing factors and synaptic proteins. Downstream alterations in gene expression define an additional transcriptional network regulated by RBFOX1 involved in neurodevelopmental pathways remarkably parallel to those affected by splicing. Several of these differentially expressed genes are further implicated in ASD and related neurodevelopmental diseases. Weighted gene co-expression network analysis demonstrates a high degree of connectivity among these disease-related genes, highlighting RBFOX1 as a key factor coordinating the regulation of both neurodevelopmentally important alternative splicing events and clinically relevant neuronal transcriptional programs in the development of human neurons.
C1 [Fogel, Brent L.; Wahnich, Amanda; Friedrich, Tara; Vijayendran, Chandran; Gao, Fuying; Parikshak, Neelroop; Konopka, Genevieve; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Program Neurogenet, Los Angeles, CA 90095 USA.
   [Wexler, Eric; Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA.
   [Geschwind, Daniel H.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA.
RP Fogel, BL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Program Neurogenet, 695 Charles Young Dr S,Gonda Room 2506, Los Angeles, CA 90095 USA.
EM bfogel@ucla.edu; dhg@mednet.ucla.edu
FU National Institute of Mental Health [K08MH86297, R37MH060233,
   R01MH081754, K08MH074362, R00MH090238, T32MH073526]; Eunice Kennedy
   Shriver National Institute of Child Health and Human Development
   [p30HD004612]; UCLA Caltech Medical Scientist Training Program; Dr
   Miriam and Sheldon G. Adelson Medical Research Foundation; John Douglas
   French Alzheimer's Research Foundation
FX This work was supported by the National Institute of Mental Health
   (grants K08MH86297 to B.L.F., R37MH060233 to D.H.G., R01MH081754 to
   D.H.G., K08MH074362 to E.W., R00MH090238 to G.K. and T32MH073526 to
   N.P.); the Eunice Kennedy Shriver National Institute of Child Health and
   Human Development (grant p30HD004612 to F.G. and D.H.G.); the UCLA
   Caltech Medical Scientist Training Program (to N.P.); the Dr Miriam and
   Sheldon G. Adelson Medical Research Foundation (to C.V.); and the John
   Douglas French Alzheimer's Research Foundation (to E.W.).
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NR 85
TC 44
Z9 45
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2012
VL 21
IS 19
BP 4171
EP 4186
DI 10.1093/hmg/dds240
PG 16
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 007KV
UT WOS:000308888100004
PM 22730494
ER

PT J
AU Yuan, E
   Tsai, PT
   Greene-Colozzi, E
   Sahin, M
   Kwiatkowski, DJ
   Malinowska, IA
AF Yuan, Elizabeth
   Tsai, Peter T.
   Greene-Colozzi, Emily
   Sahin, Mustafa
   Kwiatkowski, David J.
   Malinowska, Izabela A.
TI Graded loss of tuberin in an allelic series of brain models of TSC
   correlates with survival, and biochemical, histological and behavioral
   features
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID SCLEROSIS COMPLEX; MOUSE MODEL; GENE INACTIVATION; AUTISM; MICE;
   PHENOTYPE; SEIZURES; FAMILIES; MUTATION; LYMPHANGIOLEIOMYOMATOSIS
AB Tuberous sclerosis complex (TSC) is a neurodevelopmental disorder with prominent brain manifestations due to mutations in either TSC1 or TSC2. Here, we describe novel mouse brain models of TSC generated using conditional hypomorphic and null alleles of Tsc2 combined with the neuron-specific synapsin I cre (SynIcre) allele. This allelic series of homozygous conditional hypomorphic alleles (Tsc2(c-del3/c-del3)SynICre) and heterozygote null/conditional hypomorphic alleles (Tsc2(k/c-del3)SynICre) achieves a graded reduction in expression of Tsc2 in neurons in vivo. The mice demonstrate a progressive neurologic phenotype including hunchback, hind limb clasp, reduced survival and brain and cortical neuron enlargement that correlates with a graded reduction in expression of Tsc2 in the two sets of mice. Both models also showed behavioral abnormalities in anxiety, social interaction and learning assays, which correlated with Tsc2 protein levels as well. The observations demonstrate that there are graded biochemical, cellular and clinical/behavioral effects that are proportional to the extent of reduction in Tsc2 expression in neurons. Further, they suggest that some patients with milder manifestations of TSC may be due to persistent low-level expression of functional protein from their mutant allele. In addition, they point to the potential clinical benefit of strategies to raise TSC2 protein expression from the wild-type allele by even modest amounts.
C1 [Yuan, Elizabeth; Kwiatkowski, David J.; Malinowska, Izabela A.] Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA.
   [Tsai, Peter T.; Greene-Colozzi, Emily; Sahin, Mustafa] Childrens Hosp, Dept Neurol, FM Kirby Neurobiol Ctr, Boston, MA 02115 USA.
RP Kwiatkowski, DJ (reprint author), Brigham & Womens Hosp, Dept Med, 1 Blackfan Circle,Room 6-216, Boston, MA 02115 USA.
EM dk@rics.bwh.harvard.edu
RI Malinowska, Izabela/A-4816-2013
FU National Institutes of Health [1P01NS24279-16, 2R37NS031535-14];
   American Academy of Neurology [T32 NS007473]; Nancy Lurie Marks Family
   Foundation; John Merck Scholars Fund; Children's Hospital Boston
FX This work was supported by National Institutes of Health
   (1P01NS24279-16, 2R37NS031535-14). P.T.T. received support from the
   Developmental Neurology Training Grant (T32 NS007473), American Academy
   of Neurology and the Nancy Lurie Marks Family Foundation. M.S. was
   supported by the John Merck Scholars Fund and the Children's Hospital
   Boston Translational Research Program.
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NR 55
TC 8
Z9 8
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2012
VL 21
IS 19
BP 4286
EP 4300
DI 10.1093/hmg/dds262
PG 15
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 007KV
UT WOS:000308888100012
PM 22752306
ER

PT J
AU Mondal, K
   Ramachandran, D
   Patel, VC
   Hagen, KR
   Bose, P
   Cutler, DJ
   Zwick, ME
AF Mondal, Kajari
   Ramachandran, Dhanya
   Patel, Viren C.
   Hagen, Katie R.
   Bose, Promita
   Cutler, David J.
   Zwick, Michael E.
TI Excess variants in AFF2 detected by massively parallel sequencing of
   males with autism spectrum disorder
SO HUMAN MOLECULAR GENETICS
LA English
DT Article
ID COPY-NUMBER VARIATION; DE-NOVO MUTATIONS; MENTAL-RETARDATION;
   GENETIC-VARIATION; INTELLECTUAL DISABILITY; FMR2; GENOME; DELETION;
   ASSOCIATION; IDENTIFICATION
AB Autism spectrum disorder (ASD) is a heterogeneous disorder with substantial heritability, most of which is unexplained. ASD has a population prevalence of one percent and affects four times as many males as females. Patients with fragile X E (FRAXE) intellectual disability, which is caused by a silencing of the X-linked gene AFF2, display a number of ASD-like phenotypes. Duplications and deletions at the AFF2 locus have also been reported in cases with moderate intellectual disability and ASD. We hypothesized that other rare X-linked sequence variants at the AFF2 locus might contribute to ASD. We sequenced the AFF2 genomic region in 202 male ASD probands and found that 2.5 of males sequenced had missense mutations at highly conserved evolutionary sites. When compared with the frequency of missense mutations in 5545 X chromosomes from unaffected controls, we saw a statistically significant enrichment in patients with ASD (OR: 4.9; P 0.014). In addition, we identified rare AFF2 3 UTR variants at conserved sites which alter gene expression in a luciferase assay. These data suggest that rare variation in AFF2 may be a previously unrecognized ASD susceptibility locus and may help explain some of the male excess of ASD.
C1 [Mondal, Kajari; Ramachandran, Dhanya; Patel, Viren C.; Hagen, Katie R.; Bose, Promita; Cutler, David J.; Zwick, Michael E.] Emory Univ, Dept Human Genet, Sch Med, Atlanta, GA 30322 USA.
RP Zwick, ME (reprint author), Emory Univ, Dept Human Genet, Sch Med, Whitehead Biomed Res Bldg,Suite 301, Atlanta, GA 30322 USA.
EM mzwick@emory.edu
RI mondal, kajari/O-1791-2014
FU PHS from the Clinical and Translational Science Award program, National
   Institutes of Health, National Center for Research Resources [UL1
   RR025008]; National Institutes of Health/National Institutes of Mental
   Health (NIH/NIMH) and Gift Fund [MH076439]; Simons Foundation Autism
   Research Initiative; Training Program in Human Disease Genetics
   [1T32MH087977]
FX The Emory Custom Cloning Core facility generated constructs to our
   specifications for our expression analysis. We thank members of the
   Cutler and Zwick labs for comments on the manuscript, Jennifer Mulle and
   Stephen T. Warren for discussion, Cheryl T. Strauss for editing and the
   Emory-Georgia Research Alliance Genome Center (EGC), supported in part
   by PHS Grant UL1 RR025008 from the Clinical and Translational Science
   Award program, National Institutes of Health, National Center for
   Research Resources, for performing the Illumina sequencing runs. The
   ELLIPSE Emory High Performance Computing Cluster was used for this
   project. The authors would like to thank the NHLBI 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 WHI 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).This work
   was supported by the National Institutes of Health/National Institutes
   of Mental Health (NIH/NIMH) and Gift Fund (grant number: MH076439,
   M.E.Z.); the Simons Foundation Autism Research Initiative (M.E.Z.); and
   the Training Program in Human Disease Genetics (grant number:
   1T32MH087977, D.R.).
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NR 73
TC 9
Z9 9
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0964-6906
J9 HUM MOL GENET
JI Hum. Mol. Genet.
PD OCT 1
PY 2012
VL 21
IS 19
BP 4356
EP 4364
DI 10.1093/hmg/dds267
PG 9
WC Biochemistry & Molecular Biology; Genetics & Heredity
SC Biochemistry & Molecular Biology; Genetics & Heredity
GA 007KV
UT WOS:000308888100018
PM 22773736
ER

PT J
AU Zufferey, F
   Sherr, EH
   Beckmann, ND
   Hanson, E
   Maillard, AM
   Hippolyte, L
   Mace, A
   Ferrari, C
   Kutalik, Z
   Andrieux, J
   Aylward, E
   Barker, M
   Bernier, R
   Bouquillon, S
   Conus, P
   Delobel, B
   Faucett, W
   Goin-Kochel, RP
   Grant, E
   Harewood, L
   Hunter, JV
   Lebon, S
   Ledbetter, DH
   Martin, CL
   Mannik, K
   Martinet, D
   Mukherjee, P
   Ramocki, MB
   Spence, SJ
   Steinman, KJ
   Tjernagel, J
   Spiro, JE
   Reymond, A
   Beckmann, JS
   Chung, WK
   Jacquemont, S
AF Zufferey, Flore
   Sherr, Elliott H.
   Beckmann, Noam D.
   Hanson, Ellen
   Maillard, Anne M.
   Hippolyte, Loyse
   Mace, Aurelien
   Ferrari, Carina
   Kutalik, Zoltan
   Andrieux, Joris
   Aylward, Elizabeth
   Barker, Mandy
   Bernier, Raphael
   Bouquillon, Sonia
   Conus, Philippe
   Delobel, Bruno
   Faucett, WAndrew
   Goin-Kochel, Robin P.
   Grant, Ellen
   Harewood, Louise
   Hunter, Jill V.
   Lebon, Sebastien
   Ledbetter, David H.
   Martin, Christa Lese
   Maennik, Katrin
   Martinet, Danielle
   Mukherjee, Pratik
   Ramocki, Melissa B.
   Spence, Sarah J.
   Steinman, Kyle J.
   Tjernagel, Jennifer
   Spiro, John E.
   Reymond, Alexandre
   Beckmann, Jacques S.
   Chung, Wendy K.
   Jacquemont, Sebastien
CA Simons VIP Consortium
   16P11-2 European Consortium
TI A 600 kb deletion syndrome at 16p11.2 leads to energy imbalance and
   neuropsychiatric disorders
SO JOURNAL OF MEDICAL GENETICS
LA English
DT Article
ID PAROXYSMAL KINESIGENIC DYSKINESIA; COPY-NUMBER VARIATION; CHROMOSOME
   16P11.2; DE-NOVO; DIAGNOSTIC INTERVIEW; MENTAL-RETARDATION; AUTISM;
   MICRODELETION; OBESITY; INDIVIDUALS
AB Background The recurrent 600 kb 16p11.2 BP4-BP5 deletion is among the most frequent known genetic aetiologies of autism spectrum disorder (ASD) and related neurodevelopmental disorders.
   Objective To define the medical, neuropsychological, and behavioural phenotypes in carriers of this deletion.
   Methods We collected clinical data on 285 deletion carriers and performed detailed evaluations on 72 carriers and 68 intrafamilial non-carrier controls.
   Results When compared to intrafamilial controls, full scale intelligence quotient (FSIQ) is two standard deviations lower in carriers, and there is no difference between carriers referred for neurodevelopmental disorders and carriers identified through cascade family testing. Verbal IQ (mean 74) is lower than non-verbal IQ (mean 83) and a majority of carriers require speech therapy. Over 80% of individuals exhibit psychiatric disorders including ASD, which is present in 15% of the paediatric carriers. Increase in head circumference (HC) during infancy is similar to the HC and brain growth patterns observed in idiopathic ASD. Obesity, a major comorbidity present in 50% of the carriers by the age of 7 years, does not correlate with FSIQ or any behavioural trait. Seizures are present in 24% of carriers and occur independently of other symptoms. Malformations are infrequently found, confirming only a few of the previously reported associations.
   Conclusions The 16p11.2 deletion impacts in a quantitative and independent manner FSIQ, behaviour and body mass index, possibly through direct influences on neural circuitry. Although non-specific, these features are clinically significant and reproducible. Lastly, this study demonstrates the necessity of studying large patient cohorts ascertained through multiple methods to characterise the clinical consequences of rare variants involved in common diseases.
C1 [Chung, Wendy K.] Columbia Univ, Dept Pediat, Div Mol Genet, New York, NY 10032 USA.
   [Chung, Wendy K.] Columbia Univ, Dept Med, New York, NY 10032 USA.
   [Zufferey, Flore; Beckmann, Noam D.; Maillard, Anne M.; Hippolyte, Loyse; Martinet, Danielle; Jacquemont, Sebastien] CHU Vaudois, Serv Genet Med, CH-1011 Lausanne, Switzerland.
   [Sherr, Elliott H.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA USA.
   [Hanson, Ellen] Harvard Univ, Sch Med, Dept Psychiat, Boston Childrens Hosp, Boston, MA 02115 USA.
   [Mace, Aurelien; Kutalik, Zoltan; Beckmann, Jacques S.] Univ Lausanne, Dept Med Genet, Lausanne, Switzerland.
   [Mace, Aurelien; Kutalik, Zoltan; Beckmann, Jacques S.] Univ Lausanne, Swiss Inst Bioinformat, Lausanne, Switzerland.
   [Ferrari, Carina; Conus, Philippe] CHU Vaudois, Dept Psychiat, CH-1011 Lausanne, Switzerland.
   [Andrieux, Joris; Bouquillon, Sonia] CHRU Lille, Hop Jeanne Flandre, Inst Med Genet, Lille, France.
   [Aylward, Elizabeth] Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA USA.
   [Barker, Mandy] CHU Vaudois, SUPEA, Dept Child Psychiat, Lausanne, Switzerland.
   [Bernier, Raphael] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA.
   [Delobel, Bruno] Hop St Vincent de Paul, Ctr Genet Chromosom, GHICL, Lille, France.
   [Faucett, WAndrew; Ledbetter, David H.] Weis Ctr Res, Geisinger Clin, Genom Med Inst, Danville, PA 17822 USA.
   [Goin-Kochel, Robin P.] Baylor Coll Med, Dept Pediat, Psychol Sect, Houston, TX 77030 USA.
   [Grant, Ellen] Harvard Univ, Sch Med, Boston Childrens Hosp, Dept Radiol, Boston, MA USA.
   [Harewood, Louise; Maennik, Katrin; Reymond, Alexandre] Univ Lausanne, Ctr Integrat Genom, Lausanne, Switzerland.
   [Hunter, Jill V.] Baylor Coll Med, Dept Radiol, Houston, TX 77030 USA.
   [Lebon, Sebastien] CHU Vaudois, Dept Pediat, CH-1011 Lausanne, Switzerland.
   [Martin, Christa Lese] Emory Univ, Dept Human Genet, Atlanta, GA 30322 USA.
   [Mukherjee, Pratik] Univ Calif San Francisco, Dept Radiol & Biomed Imaging, San Francisco, CA 94143 USA.
   [Ramocki, Melissa B.] Baylor Coll Med, Dept Pediat, Sect Pediat Neurol & Dev Neurosci, Houston, TX 77030 USA.
   [Spence, Sarah J.] Harvard Univ, Sch Med, Dept Neurol, Boston Childrens Hosp, Boston, MA 02115 USA.
   [Steinman, Kyle J.] Seattle Childrens Res Inst, Dept Neurol, Seattle, WA USA.
   [Tjernagel, Jennifer; Spiro, John E.] Simons Fdn, New York, NY USA.
RP Chung, WK (reprint author), Columbia Univ, Dept Pediat, Div Mol Genet, Russ Berrie Pavil 1150,St Nicholas Ave,Rm 620, New York, NY 10032 USA.
EM alexandre.reymond@unil.ch; jacques.beckmann@unil.ch; wkc15@columbia.edu;
   sebastien.jacquemont@chuv.ch
RI Beckmann, Jacques/A-9772-2008
OI Beckmann, Jacques/0000-0002-9741-1900
FU bourse de releve academique de la Faculte de Biologie et Medecine de
   l'Universite de Lausanne; Swiss Scientific Exchange NMS Programme;
   Leenaards Foundation; Swiss National Science Foundation; SNSF; Estonian
   Government [SF0180142Cs08]; Centre of Translational Genomics
   [SP1GVARENG]; European Union; Simons Foundation Autism Research
   Initiative (SFARI)
FX We thank the participants, families, and referring providers for their
   contribution. SJ is recipient of a 'bourse de releve academique de la
   Faculte de Biologie et Medecine de l'Universite de Lausanne' and KM is a
   grantee of a scholarship from the Swiss Scientific Exchange NMS
   Programme. This work is supported by the Leenaards Foundation Prize (SJ
   and AR), the Swiss National Science Foundation (AR and JSB) and a
   specific SNSF Sinergia grant (AR). Phenotyping of EGC UT individuals was
   supported by Targeted Financing from Estonian Government grant
   SF0180142Cs08, Centre of Translational Genomics grant SP1GVARENG, and by
   the European Union through the European Regional Development Fund, in
   the frame of Centre of Excellence in Genomics. The Simons VIP work is
   supported by the Simons Foundation Autism Research Initiative (SFARI).
   We thank the coordinators and staff at the Simons Simplex Collection
   (SSC) sites. 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 SFARI Base. Approved researchers can obtain the SSC population
   dataset described in this study by applying at https://base.sfari.org
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NR 49
TC 33
Z9 35
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0022-2593
J9 J MED GENET
JI J. Med. Genet.
PD OCT
PY 2012
VL 49
IS 10
BP 660
EP 668
DI 10.1136/jmedgenet-2012-101203
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 022LN
UT WOS:000309961000009
PM 23054248
ER

PT J
AU Chiara, M
   Pesole, G
   Horner, DS
AF Chiara, Matteo
   Pesole, Graziano
   Horner, David S.
TI SVM2: an improved paired-end-based tool for the detection of small
   genomic structural variations using high-throughput single-genome
   resequencing data
SO NUCLEIC ACIDS RESEARCH
LA English
DT Article
ID COPY NUMBER VARIATION; POPULATION-SCALE; GENETIC-VARIATION; INSERTIONS;
   DELETIONS; IDENTIFICATION; POLYMORPHISM; 16P11.2; AUTISM; MAP
AB Several bioinformatics methods have been proposed for the detection and characterization of genomic structural variation (SV) from ultra high-throughput genome resequencing data. Recent surveys show that comprehensive detection of SV events of different types between an individual resequenced genome and a reference sequence is best achieved through the combination of methods based on different principles (split mapping, reassembly, read depth, insert size, etc.). The improvement of individual predictors is thus an important objective. In this study, we propose a new method that combines deviations from expected library insert sizes and additional information from local patterns of read mapping and uses supervised learning to predict the position and nature of structural variants. We show that our approach provides greatly increased sensitivity with respect to other tools based on paired end read mapping at no cost in specificity, and it makes reliable predictions of very short insertions and deletions in repetitive and low-complexity genomic contexts that can confound tools based on split mapping of reads.
C1 [Chiara, Matteo; Horner, David S.] Univ Milan, Dept Biomol Sci & Biotechnol, I-20133 Milan, Italy.
   [Pesole, Graziano] Univ Bari, Natl Res Council, Inst Biomembranes & Bioenerget, I-70125 Bari, Italy.
   [Pesole, Graziano] Univ Bari, Dept Biosci Biotechnol & Pharmacol Sci, I-70125 Bari, Italy.
   [Pesole, Graziano] Ctr Excellence Genom CEGBA, I-70125 Bari, Italy.
RP Chiara, M (reprint author), Univ Milan, Dept Biomol Sci & Biotechnol, I-20133 Milan, Italy.
EM matteo.chiara@unimi.it; david.horner@unimi.it
RI Pesole, Graziano/C-1408-2009; Pesole, Graziano/E-9051-2014
OI Pesole, Graziano/0000-0003-3663-0859; Pesole,
   Graziano/0000-0003-3663-0859
FU 'Ministero dell'Istruzione Universita e Ricerca' (MIUR, Italy):
   'Laboratorio Internazionale di Bioinformatica' [DM19410]; 'Ministero
   dell'Istruzione Universita e Ricerca' (MIUR, Italy): 'Laboratorio di
   Bioinformatica per la Biodiversita' Molecolare' [DM19410]; Center of
   Excellence in Genomics (CEGBA, Italy); MIUR/Laboratorio Internazionale
   di Bioinformatica
FX 'Ministero dell'Istruzione Universita e Ricerca' (MIUR, Italy):
   'Laboratorio Internazionale di Bioinformatica', 'Laboratorio di
   Bioinformatica per la Biodiversita' Molecolare' [Project DM19410] and by
   the Center of Excellence in Genomics (CEGBA, Italy). Funding for open
   access charge: MIUR/Laboratorio Internazionale di Bioinformatica.
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NR 40
TC 3
Z9 5
PU OXFORD UNIV PRESS
PI OXFORD
PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND
SN 0305-1048
J9 NUCLEIC ACIDS RES
JI Nucleic Acids Res.
PD OCT
PY 2012
VL 40
IS 18
DI 10.1093/nar/gks606
PG 11
WC Biochemistry & Molecular Biology
SC Biochemistry & Molecular Biology
GA 022AJ
UT WOS:000309927100009
PM 22735696
ER

PT J
AU Li, J
   Lin, ZM
   Zhu, LQ
AF Li Jing
   Lin Zhu-Mei
   Zhu Li-Qi
TI Genetic Basis and Neural Mechanism of Autism Spectrum Disorder
SO PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS
LA Chinese
DT Article
DE autism spectrum disorder; gene; brain function; brain function
   connectivity
ID HIGH-FUNCTIONING AUTISM; VOXEL-BASED MORPHOMETRY; CEREBRAL-BLOOD-FLOW;
   ASPERGER-SYNDROME; CHILDHOOD AUTISM; FUSIFORM GYRUS; FRONTAL-CORTEX;
   CHILDREN; CONNECTIVITY; ACTIVATION
AB Autism spectrum disorder (ASD) is a defective mental disease and its core impairments are social function defect, communication defect, restrictive and stereotyped behavior pattern. The paper introduces the genetic basis and neural mechanism of ASD. ASD has high genetic rate, and 5-HT and testosterone of ASD individual are both higher. Neuroimaging studies find that there are some differences between ASD and normal individuals in the structure and function of amygdala, cingulate gyrus, the fusiform gyrus, mirror neurons, prefrontal lobe and other brain areas, but it is inconsistent in the discrepancy direction of some areas' activation patterns. In addition, the results of functional connectivity studies also confirm the hypothesis that the ASD individuals are under-connection. Future research should focus more on how to use the basic research outcomes to put forward effective treatment and training for clinical research.
C1 [Li Jing; Lin Zhu-Mei; Zhu Li-Qi] Chinese Acad Sci, Inst Psychol, Key Lab Behav Sci, Beijing 100101, Peoples R China.
   [Li Jing; Lin Zhu-Mei] Univ Chinese Acad Sci, Beijing 100049, Peoples R China.
RP Zhu, LQ (reprint author), Chinese Acad Sci, Inst Psychol, Key Lab Behav Sci, Beijing 100101, Peoples R China.
EM zhulq@psych.ac.cn
FU National Basic Research Program of China [2010CB8339004]; The National
   Natural Science Foundation of China [30970911]
FX This work was supported by grants from National Basic Research Program
   of China (2010CB8339004) and The National Natural Science Foundation of
   China (30970911).
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NR 65
TC 0
Z9 2
PU CHINESE ACAD SCIENCES, INST BIOPHYSICS
PI BEIJING
PA 15 DATUN RD, CHAOYAND DISTRICT, BEIJING, 100101, PEOPLES R CHINA
SN 1000-3282
J9 PROG BIOCHEM BIOPHYS
JI Prog. Biochem. Biophys.
PD OCT
PY 2012
VL 39
IS 10
BP 952
EP 961
DI 10.3724/SP.J.1206.2011.00519
PG 10
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 024OK
UT WOS:000310118300003
ER

PT J
AU Hock, R
   Ahmedani, BK
AF Hock, Robert
   Ahmedani, Brian K.
TI Parent perceptions of autism severity: Exploring the social ecological
   context
SO DISABILITY AND HEALTH JOURNAL
LA English
DT Article
DE Autism spectrum disorders; Social ecology; Parental perception; Mental
   health; Social support
ID SELF-REPORTED HEALTH; SPECTRUM DISORDERS; RATED HEALTH; CHILDREN;
   BEHAVIORS; DIAGNOSIS; STRESS; LIFE; AGE
AB Background: Health professionals incorporate parent reports into the diagnosis and treatment of children with an autism spectrum disorder (ASD). Yet little is known about the contextual forces that may shape parents' perceptions of their child.
   Objectives: The current study seeks to: 1) compare the social ecological contexts of parents of children with ASD and parents of non-autistic children, and 2) explore the social ecological influences on parents' perception of their child's ASD severity.
   Methods: This study employed a cross-sectional analysis of data from the 2007-2008 National Survey of Children's Health (NSCH) in the United States. Social ecological factors of interest included variables depicting family physical environment, family social environment, and individual parent characteristics.
   Results: Results indicate that parents of children with ASD had increased odds of reporting poor neighborhood social capital, greater aggravation, more difficulty coping, and lower levels of relationship satisfaction and mental health. Parents' perceptions of their child's ASD severity were associated with several factors of their social ecological context. More severe parent-reported ASD was associated with aspects of the physical environment (rundown housing and garbage on the street), the social environment (parent relationship satisfaction) and individual parent characteristics (parent aggravation and mental health).
   Conclusions: Results suggest ways that professionals can contextualize parent reports to aid in the diagnosis and treatment of children with ASD. Findings also highlight a need for longitudinal research using well-characterized measures to determine the nature and direction of relationships between contextual factors and parents' perceptions. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Hock, Robert] Univ S Carolina, Coll Social Work, Columbia, SC 29208 USA.
   [Ahmedani, Brian K.] Henry Ford Hlth Syst, Ctr Hlth Serv Res, Detroit, MI 48202 USA.
RP Hock, R (reprint author), Univ S Carolina, Coll Social Work, 1731 Coll St,Rm 205, Columbia, SC 29208 USA.
EM roberth@sc.edu
FU Health Resources and Services Administration's Maternal and Child Health
   Bureau of the Department of Health and Human Services
FX The 2007 National Survey on Children's Health (NSCH) was funded by the
   Health Resources and Services Administration's Maternal and Child Health
   Bureau of the Department of Health and Human Services. The authors also
   wish to thank the field workers who collected the data for this project.
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NR 25
TC 2
Z9 2
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 1936-6574
J9 DISABIL HEALTH J
JI Disabil. Health J.
PD OCT
PY 2012
VL 5
IS 4
BP 298
EP 304
DI 10.1016/j.dhjo.2012.06.002
PG 7
WC Health Care Sciences & Services; Health Policy & Services; Public,
   Environmental & Occupational Health; Rehabilitation
SC Health Care Sciences & Services; Public, Environmental & Occupational
   Health; Rehabilitation
GA 016VQ
UT WOS:000309548300013
PM 23021742
ER

PT J
AU Halpert, J
AF Halpert, Julie
TI ALTERING THE PRIMAL ENVIRONMENT HEALTH EFFECTS ASSOCIATED WITH ASSISTED
   REPRODUCTIVE TECHNOLOGIES
SO ENVIRONMENTAL HEALTH PERSPECTIVES
LA English
DT Editorial Material
ID IN-VITRO FERTILIZATION; AUTISM SPECTRUM DISORDERS; VANISHING TWINS;
   GESTATIONAL-AGE; CEREBRAL-PALSY; BIRTH-DEFECTS; RISK; CONCEPTION;
   CHILDREN; METHYLATION
C1 Univ Michigan, Ann Arbor, MI 48109 USA.
RP Halpert, J (reprint author), Univ Michigan, Ann Arbor, MI 48109 USA.
CR [Anonymous], DAT 1990 WER PROV E
   ASRM, 2011, ASS REPR TECHN GUID
   ASRM, 2012, MED IND OV GUID PAT
   ASRM, 2012, FREQ ASK QUEST INF
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NR 28
TC 1
Z9 1
PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE
PI RES TRIANGLE PK
PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233,
   RES TRIANGLE PK, NC 27709-2233 USA
SN 0091-6765
J9 ENVIRON HEALTH PERSP
JI Environ. Health Perspect.
PD OCT
PY 2012
VL 120
IS 10
BP A390
EP A395
PG 6
WC Environmental Sciences; Public, Environmental & Occupational Health;
   Toxicology
SC Environmental Sciences & Ecology; Public, Environmental & Occupational
   Health; Toxicology
GA 018US
UT WOS:000309692600009
PM 23026346
ER

PT J
AU Gjorlund, MD
   Nielsen, J
   Pankratova, S
   Li, SZ
   Korshunova, I
   Bock, E
   Berezin, V
AF Gjorlund, Michelle D.
   Nielsen, Janne
   Pankratova, Stanislava
   Li, Shizhong
   Korshunova, Irina
   Bock, Elisabeth
   Berezin, Vladimir
TI Neuroligin-1 induces neurite outgrowth through interaction with
   neurexin-1 beta and activation of fibroblast growth factor receptor-1
SO FASEB JOURNAL
LA English
DT Article
DE synaptic cell adhesion molecules; neuritogenesis; hippocampal neurons
ID CELL-ADHESION MOLECULES; FGF-RECEPTOR; BETA-NEUREXINS; STRUCTURAL BASIS;
   NEURONAL SURVIVAL; CRYSTAL-STRUCTURE; SURFACE PROTEINS; N-CADHERIN;
   BINDING; EXPRESSION
AB Neurexin-1 (NRXN1) and neuroligin-1 (NLGN1) are synaptic cell adhesion molecules that connect pre- and postsynaptic neurons at synapses and mediate signaling across the synapse, which modulates synaptic activity and determines the properties of neuronal networks. Defects in the genes encoding NLGN1 have been linked to cognitive diseases such as autism. The roles of both NRXN1 and NLGN1 during synaptogenesis have been studied extensively, but little is known about the role of these molecules in neuritogenesis, which eventually results in neuronal circuitry formation. The present study investigated the neuritogenic effect of NLGN1 in cultures of hippocampal neurons. Our results show that NLGN1, both in soluble and membrane-bound forms, induces neurite outgrowth that depends on the interaction with NRXN1 beta and on activation of fibroblast growth factor receptor-1. In addition, we demonstrate that a synthetic peptide, termed neurolide, which is modeled after a part of the binding interface of NLGN1 for NRXN1 beta, can bind to NRXN1 beta and mimic the biological properties of NLGN1 in vitro.-Gjorlund, M. D., Nielsen, J., Pankratova, S., Li, S., Korshunova, I., Bock, B., Berezin, V. Neuroligin-1 induces neurite outgrowth through interaction with neurexin-1 beta and activation of fibroblast growth factor receptor-1. FASEB J. 26, 4174-4186 (2012). www.fasebj.org
C1 [Gjorlund, Michelle D.; Nielsen, Janne; Pankratova, Stanislava; Li, Shizhong; Korshunova, Irina; Bock, Elisabeth; Berezin, Vladimir] Univ Copenhagen, Dept Neurosci & Pharmacol, Fac Hlth Sci, Prot Lab, DK-2200 Copenhagen, Denmark.
RP Berezin, V (reprint author), Univ Copenhagen, Dept Neurosci & Pharmacol, Fac Hlth Sci, Prot Lab, Blegdamsvej 3B,Bldg 24-2, DK-2200 Copenhagen, Denmark.
EM berezin@sund.ku.dk
RI Nielsen, Janne/J-5987-2014
OI Nielsen, Janne/0000-0001-8521-7353
FU 7FP European Union collaborative project MemStick [201600]; Lundbeck
   Foundation; Danish Research Councils
FX This study was supported by the 7FP European Union collaborative project
   MemStick (grant agreement 201600), the Lundbeck Foundation, and the
   Danish Research Councils.
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NR 47
TC 9
Z9 9
PU FEDERATION AMER SOC EXP BIOL
PI BETHESDA
PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA
SN 0892-6638
J9 FASEB J
JI Faseb J.
PD OCT
PY 2012
VL 26
IS 10
BP 4174
EP 4186
DI 10.1096/fj.11-202242
PG 13
WC Biochemistry & Molecular Biology; Biology; Cell Biology
SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other
   Topics; Cell Biology
GA 018YM
UT WOS:000309704000023
PM 22750515
ER

PT J
AU Bohlen, MO
   Bailoo, JD
   Jordan, RL
   Wahlsten, D
AF Bohlen, M. O.
   Bailoo, J. D.
   Jordan, R. L.
   Wahlsten, D.
TI Hippocampal commissure defects in crosses of four inbred mouse strains
   with absent corpus callosum
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Complementation test; complex trait; four-way hybrid cross; inbred
   strains; reciprocal hybrid cross
ID BEHAVIORAL TASKS RELEVANT; GENETIC-VARIATION; MICE; BRAIN; PHENOTYPES;
   SYSTEM; AUTISM; GROWTH; DISC1; SIZE
AB It is known that four common inbred mouse strains show defects of the forebrain commissures. The BALB/cJ strain has a low frequency of abnormally small corpus callosum, whereas the 129 strains have many animals with deficient corpus callosum. The I/LnJ and BTBR T+ tf/J strains never have a corpus callosum, whereas half of I/LnJ and almost all BTBR show severely reduced size of the hippocampal commissure. Certain F1 hybrid crosses among these strains are known to be less severely abnormal than the inbred parents, suggesting that the parent strains have different genetic causes of commissure defects. In this study, all hybrid crosses among the four strains were investigated. The BTBR x I/Ln hybrid expressed almost no defects of the hippocampal commissure, unlike its inbred parent strains. Numerous three-way crosses among the four strains yielded many mice with no corpus callosum and severely reduced hippocampal commissure, which shows that the phenotypic defect can result from several different combinations of genetic alleles. The F2 and F3 hybrid crosses of BTBR and I/LnJ had almost 100% absence of the corpus callosum but about 50% frequency of deficient hippocampal commissure. The four-way hybrid cross among all four abnormal strains involved highly fertile parents and yielded a very wide phenotypic range of defects from almost no hippocampal commissure to totally normal forebrain commissures. The F2 and F3 crosses as well as the four-way cross provide excellent material for studies of genetic linkage and behavioral consequences of commissure defects.
C1 [Bohlen, M. O.; Bailoo, J. D.; Jordan, R. L.; Wahlsten, D.] Univ N Carolina, Dept Psychol, Greensboro, NC 27412 USA.
RP Wahlsten, D (reprint author), Univ N Carolina, Dept Psychol, EBER 275,1111 Spring Garden St, Greensboro, NC 27412 USA.
EM dlwahlst@uncg.edu
FU National Institute of Alcoholism and Alcohol Abuse [AA12714]
FX This research was supported by Grant AA12714 (Wahlsten, PI) from the
   National Institute of Alcoholism and Alcohol Abuse. Technical assistance
   of Erika Hayes is greatly appreciated. None of the authors has any
   conflict of interest with regard to the research reported here.
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NR 47
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
EI 1601-183X
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD OCT
PY 2012
VL 11
IS 7
BP 757
EP 766
DI 10.1111/j.1601-183X.2012.00802.x
PG 10
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 019QE
UT WOS:000309753600001
PM 22537318
ER

PT J
AU Johnson, C
   Lin, CCJ
   Stern, M
AF Johnson, C.
   Lin, C. Chun-Jen
   Stern, M.
TI Ras-dependent and Ras-independent effects of PI3K in Drosophila motor
   neurons
SO GENES BRAIN AND BEHAVIOR
LA English
DT Article
DE Autism spectrum disorders; Fragile X; metabotropic glutamate receptor;
   negative feedback; nerve terminal; Neurofibromatosis; neuronal
   excitability; Raf
ID LONG-TERM DEPRESSION; PROTEIN-KINASE-II; PHOSPHOINOSITIDE 3-KINASE;
   SIGNAL-TRANSDUCTION; SACCHAROMYCES-CEREVISIAE; NEUROMUSCULAR-JUNCTION;
   SYNAPTIC-TRANSMISSION; RAPAMYCIN PATHWAY; CELL-SURVIVAL; EXCITABILITY
AB The lipid kinase PI3K plays key roles in cellular responses to activation of receptor tyrosine kinases or G protein coupled receptors such as the metabotropic glutamate receptor (mGluR). Activation of the PI3K catalytic subunit p110 occurs when the PI3K regulatory subunit p85 binds to phosphotyrosine residues present in upstream activating proteins. In addition, Ras is uniquely capable of activating PI3K in a p85-independent manner by binding to p110 at amino acids distinct from those recognized by p85. Because Ras, like p85, is activated by phosphotyrosines in upstream activators, it can be difficult to determine if particular PI3K-dependent processes require p85 or Ras. Here, we ask if PI3K requires Ras activity for either of two different PI3K-regulated processes within Drosophila larval motor neurons. To address this question, we determined the effects on each process of transgenes and chromosomal mutations that decrease Ras activity, or mutations that eliminate the ability of PI3K to respond to activated Ras. We found that PI3K requires Ras activity to decrease motor neuron excitability, an effect mediated by ligand activation of the single Drosophila mGluR DmGluRA. In contrast, the ability of PI3K to increase nerve terminal growth is Ras-independent. These results suggest that distinct regulatory mechanisms underlie the effects of PI3K on distinct phenotypic outputs.
C1 [Johnson, C.; Lin, C. Chun-Jen; Stern, M.] Rice Univ, Dept Biochem & Cell Biol, Houston, TX 77005 USA.
RP Stern, M (reprint author), Rice Univ, Dept Biochem & Cell Biol MS 140, 6700 Main St, Houston, TX 77005 USA.
EM stern@rice.edu
FU Department of Defense Neurofibromatosis Research Program
   [W81XWH-09-1-0106]; National Science Foundation [IOS-0820660]
FX We are grateful to James McNew and Daniel S. Wagner for comments on the
   manuscript, Natalia Molinas for assistance in experiments, Sally
   Leevers, Gerald Rubin, Celeste Berg, Denise Montell, the Drosophila
   stock center at Bloomington, IN, and the National Institute of Genetics
   (Mishima, Japan) for providing fly stocks. Funded by grant
   W81XWH-09-1-0106 from the Department of Defense Neurofibromatosis
   Research Program and grant IOS-0820660 from the National Science
   Foundation (to M.S.).
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NR 64
TC 1
Z9 1
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1601-1848
J9 GENES BRAIN BEHAV
JI Genes Brain Behav.
PD OCT
PY 2012
VL 11
IS 7
BP 848
EP 858
DI 10.1111/j.1601-183X.2012.00822.x
PG 11
WC Behavioral Sciences; Neurosciences
SC Behavioral Sciences; Neurosciences & Neurology
GA 019QE
UT WOS:000309753600011
PM 22783951
ER

PT J
AU Soden, SE
   Garrison, CB
   Egan, AM
   Beckwith, AM
AF Soden, Sarah E.
   Garrison, Carol B.
   Egan, Anna M.
   Beckwith, Anna M.
TI Nutrition, Physical Activity, and Bone Mineral Density in Youth With
   Autistic Spectrum Disorders
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE autism; autistic spectrum disorders (ASD); osteopenia; vitamin D; low
   bone density
ID VITAMIN-D DEFICIENCY; CHILDREN; ADOLESCENTS; RICKETS; CHILDHOOD;
   INFANTS; HEALTH; MASS; DXA; SEX
AB Objective: Fractures and pain, secondary to low bone mineral density (BMD), have been reported in pediatric patients with autistic spectrum disorders (ASD). The purpose of this study was to assess the BMD of a clinical sample of 10- to 18-year olds with ASD, and the nutrition and physical activity correlates of skeletal health in this population. Methods: Twenty-six patients with ASD were recruited from an outpatient multidisciplinary child-development clinic. Lumbar bone density was measured using dual-energy x-ray absorptiometry. Data collection included anthropometries, serum nutrient levels, parent interview, and 72-hour diet, screen-time, and physical activity records. Results: Four patients (15%) met criteria for pediatric low BMD with z scores less than or equal to -2.0; another 4 were at risk with z scores less than or equal to -1.0. Approximately 54% of participants had insufficient serum 25-hydroxy vitamin D. Mean electronic media use was 251 minutes/day; mean physical activity 69 minutes/day. Fewer than 50% of participants met daily reference intake of vitamins A, B3, D, E, K, zinc, calcium, folate, potassium, and fiber. Bone density correlated positively with body mass (r = .47), calcium intake (r = .46), and calorie intake (r = .58). Conclusions: Children aged 10 to 18 years old with ASD are at risk for occult low bone density. In this study, those with low body mass index and insufficient calcium and calorie intake were at greater risk. Other unhealthy behaviors in this population included a high screen-time to physical activity ratio and multiple nutrient deficiencies.
C1 [Soden, Sarah E.; Garrison, Carol B.; Egan, Anna M.] Childrens Mercy Hosp & Clin, Dept Pediat, Sect Dev & Behav Sci, Kansas City, MO USA.
   [Beckwith, Anna M.] Childrens Specialized Hosp, Dept Neurodev Pediat, Mountainside, NJ USA.
RP Soden, SE (reprint author), Childrens Mercy Hosp, Dept Pediat, Sect Dev & Behav Sci, 2401 Gillham Rd, Kansas City, MO 64108 USA.
EM ssoden@cmh.edu
FU Katharine B. Richardson Associates Endowment Fund
FX This study was supported by the Katharine B. Richardson Associates
   Endowment Fund
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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
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD OCT
PY 2012
VL 33
IS 8
BP 618
EP 624
DI 10.1097/DBP.0b013e318260943c
PG 7
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 016VE
UT WOS:000309547000003
PM 23027134
ER

PT J
AU Soares, NS
   Langkamp, DL
AF Soares, Neelkamal S.
   Langkamp, Diane L.
TI Telehealth in Developmental-Behavioral Pediatrics
SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS
LA English
DT Article
DE telehealth; telemedicine; access to care; pediatrics
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; HEALTH-CARE; TELEMENTAL
   HEALTH; PALLIATIVE CARE; TELEMEDICINE; CHILDREN; PROGRAM; QUALITY;
   AUTISM; INTERVENTION
AB Developmental-behavioral pediatrics (DBP) is recognized as one of the fields with the greatest shortages of pediatric subspecialists. Families who access care often must travel great distances to tertiary academic medical centers or endure long waiting lists. While the shortages are likely to persist due to limited provider availability and an increasing number of children with developmental and behavioral disorders being identified, our field must look to innovative ways to reduce the barriers to access. One such way is telehealth, the use of videoconferencing to deliver DBP services to underserved populations. We aim to describe the practical uses of telehealth for the delivery of diagnostic and management clinical services in a variety of settings and for the additional educational and research benefits of the modality. We will highlight the obstacles to setting up a successful DBP telehealth practice and direct readers to resources to address these in their communities. Most of all, we will demonstrate the benefit to families and children, practitioners, and health care systems of supplementing traditional in-person DBP services with telehealth modalities to enhance outreach and engagement with communities.
C1 [Soares, Neelkamal S.] Univ Calif Los Angeles, David Geffen Sch Med, Mattel Childrens Hosp, Los Angeles, CA 90095 USA.
   [Langkamp, Diane L.] Akron Childrens Hosp, Div Dev Behav Pediat, Akron, OH USA.
   [Langkamp, Diane L.] NE Ohio Med Univ, Dept Pediat, Rootstown, OH USA.
RP Soares, NS (reprint author), 300 UCLA Med Plaza,Suite 3300, Los Angeles, CA 90095 USA.
EM nsoares@mednet.ucla.edu
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NR 63
TC 3
Z9 3
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0196-206X
J9 J DEV BEHAV PEDIATR
JI J. Dev. Behav. Pediatr.
PD OCT
PY 2012
VL 33
IS 8
BP 656
EP 665
DI 10.1097/DBP.0b013e3182690741
PG 10
WC Behavioral Sciences; Psychology, Developmental; Pediatrics
SC Behavioral Sciences; Psychology; Pediatrics
GA 016VE
UT WOS:000309547000009
PM 23027140
ER

PT J
AU Schmidt, RJ
   Hansen, RL
   Hartiala, J
   Allayee, H
   Schmidt, LC
   Tassone, F
   Hertz-Picciotto, I
AF Schmidt, Rebecca J.
   Hansen, Robin L.
   Hartiala, Jaana
   Allayee, Hooman
   Schmidt, Linda C.
   Tassone, Flora
   Hertz-Picciotto, Irva
TI Selected Vitamin D Metabolic Gene Variants and Risk for Autism Spectrum
   Disorders in the CHARGE Study
SO JOURNAL OF WOMENS HEALTH
LA English
DT Meeting Abstract
C1 [Schmidt, Rebecca J.; Hertz-Picciotto, Irva] Univ Calif Davis, Dept Publ Hlth Serv, Sch Med, Davis, CA 95616 USA.
   [Schmidt, Rebecca J.; Hansen, Robin L.; Tassone, Flora; Hertz-Picciotto, Irva] Univ Calif Davis, Med Invest Neurodev Disorders MIND Inst, Sch Med, Davis, CA 95616 USA.
   [Hansen, Robin L.] Univ Calif Davis, Dept Pediat, Sch Med, Davis, CA 95616 USA.
   [Schmidt, Linda C.; Tassone, Flora] Univ Calif Davis, Dept Biochem & Mol Med, Davis, CA 95616 USA.
   [Hartiala, Jaana; Allayee, Hooman] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA.
   [Hartiala, Jaana; Allayee, Hooman] Univ So Calif, Keck Sch Med, Inst Med Genet, Los Angeles, CA 90033 USA.
NR 0
TC 0
Z9 0
PU MARY ANN LIEBERT INC
PI NEW ROCHELLE
PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA
SN 1540-9996
J9 J WOMENS HEALTH
JI J. Womens Health
PD OCT
PY 2012
VL 21
IS 10
BP 1000
EP 1000
PG 1
WC Public, Environmental & Occupational Health; Medicine, General &
   Internal; Obstetrics & Gynecology; Women's Studies
SC Public, Environmental & Occupational Health; General & Internal
   Medicine; Obstetrics & Gynecology; Women's Studies
GA 018JF
UT WOS:000309655600048
ER

PT J
AU Nightingale, S
AF Nightingale, Sarah
TI Autism spectrum disorders
SO NATURE REVIEWS DRUG DISCOVERY
LA English
DT Editorial Material
C1 Datamonitor, London EC1R 3DA, England.
RP Nightingale, S (reprint author), Datamonitor, 119 Farringdon Rd, London EC1R 3DA, England.
EM snightingale@datamonitor.com
NR 0
TC 5
Z9 5
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1474-1776
J9 NAT REV DRUG DISCOV
JI Nat. Rev. Drug Discov.
PD OCT
PY 2012
VL 11
IS 10
BP 745
EP 746
DI 10.1038/nrd3771
PG 2
WC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
SC Biotechnology & Applied Microbiology; Pharmacology & Pharmacy
GA 016KD
UT WOS:000309515900013
PM 23000684
ER

PT J
AU Pellicano, E
   Burr, D
AF Pellicano, Elizabeth
   Burr, David
TI When the world becomes 'too real': a Bayesian explanation of autistic
   perception
SO TRENDS IN COGNITIVE SCIENCES
LA English
DT Review
ID SPECTRUM DISORDERS; VISUAL-PERCEPTION; OBJECT PERCEPTION; SAVANT
   SYNDROME; EYE GAZE; CHILDREN; DISCRIMINATION; MECHANISMS; COHERENCE;
   INFERENCE
AB Perceptual experience is influenced both by incoming sensory information and prior knowledge about the world, a concept recently formalised within Bayesian decision theory. We propose that Bayesian models can be applied to autism - a neurodevelopmental condition with atypicalities in sensation and perception - to pinpoint fundamental differences in perceptual mechanisms. We suggest specifically that attenuated Bayesian priors - 'hypo-priors' - may be responsible for the unique perceptual experience of autistic people, leading to a tendency to perceive the world more accurately rather than modulated by prior experience. In this account, we consider how hypo-priors might explain key features of autism - the broad range of sensory and other non-social atypicalities - in addition to the phenomenological differences in autistic perception.
C1 [Pellicano, Elizabeth] Univ London, Inst Educ, CRAE, London WC1N 1AZ, England.
   [Burr, David] Univ Florence, Dept Psychol, Florence, Italy.
   [Pellicano, Elizabeth; Burr, David] Univ Western Australia, Sch Psychol, Perth, WA 6009, Australia.
RP Pellicano, E (reprint author), Univ London, Inst Educ, CRAE, London WC1N 1AZ, England.
EM l.pellicano@ioe.ac.uk
FU UK's Medical Research Council [MR/J013145/1]; European Union;
   Clothworkers' Foundation; Pears Foundation
FX We are extremely grateful to Dorothy Bishop, Tom Griffiths, Rebecca
   Lawson, Kate Plaisted-Grant, Marc Stears, and Catherine Stoodley for
   helpful discussions and to Colin Clifford, Laurent Mottron, and three
   anonymous reviewers for constructive comments on a previous version of
   this manuscript. This work was supported by a grant from the UK's
   Medical Research Council (MR/J013145/1) and European Union FP7-ERC
   'STANIB'. Research at CRAE is also supported by The Clothworkers'
   Foundation and Pears Foundation.
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NR 69
TC 51
Z9 52
PU ELSEVIER SCIENCE LONDON
PI LONDON
PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND
SN 1364-6613
J9 TRENDS COGN SCI
JI TRENDS COGN. SCI.
PD OCT
PY 2012
VL 16
IS 10
BP 504
EP 510
DI 10.1016/j.tics.2012.08.009
PG 7
WC Behavioral Sciences; Neurosciences; Psychology, Experimental
SC Behavioral Sciences; Neurosciences & Neurology; Psychology
GA 020XA
UT WOS:000309848700007
PM 22959875
ER

PT J
AU Campbell, IM
   Yatsenko, SA
   Hixson, P
   Reimschisel, T
   Thomas, M
   Wilson, W
   Dayal, U
   Wheless, JW
   Crunk, A
   Curry, C
   Parkinson, N
   Fishman, L
   Riviello, JJ
   Nowaczyk, MJM
   Zeesman, S
   Rosenfeld, JA
   Bejjani, BA
   Shaffer, LG
   Cheung, SW
   Lupski, JR
   Stankiewicz, P
   Scaglia, F
AF Campbell, Ian M.
   Yatsenko, Svetlana A.
   Hixson, Patricia
   Reimschisel, Tyler
   Thomas, Matthew
   Wilson, William
   Dayal, Usha
   Wheless, James W.
   Crunk, Amy
   Curry, Cynthia
   Parkinson, Nicole
   Fishman, Leona
   Riviello, James J.
   Nowaczyk, Malgorzata J. M.
   Zeesman, Susan
   Rosenfeld, Jill A.
   Bejjani, Bassem A.
   Shaffer, Lisa G.
   Cheung, Sau Wai
   Lupski, James R.
   Stankiewicz, Pawel
   Scaglia, Fernando
TI Novel 9q34.11 gene deletions encompassing combinations of four Mendelian
   disease genes: STXBP1, SPTAN1, ENG, and TOR1A
SO GENETICS IN MEDICINE
LA English
DT Article
DE cis-genetics; dystonia; early infantile epileptic encephalopathy;
   hereditary hemorrhagic telangiectasia; intellectual disability
ID INFANTILE EPILEPTIC ENCEPHALOPATHY; HEREDITARY HEMORRHAGIC
   TELANGIECTASIA; SUPPRESSION-BURST PATTERN; ALPHA-II-SPECTRIN;
   MENTAL-RETARDATION; OHTAHARA-SYNDROME; TORSION DYSTONIA;
   BINDING-PROTEIN; WEST SYNDROME; MUTATIONS
AB Purpose: A number of genes in the 9q34.11 region may be haplo-insufficient. However, studies analyzing genotype phenotype correlations of deletions encompassing multiple dosage-sensitive genes in the region are lacking.
   Methods: We mapped breakpoints of 10 patients with 9q34.11 deletions using high-resolution 9q34-specific array comparative genomic hybridization (CGH) to determine deletion size and gene content.
   Results: The 9q34.11 deletions range in size from 67 kb to 2.8 Mb. Six patients exhibit intellectual disability and share a common deleted region including STXBP1; four manifest variable epilepsy. In five subjects, deletions include SPTAN1, previously associated with early infantile epileptic encephalopathy, infantile spasms, intellectual disability, and hypomyelination. In four patients, the deletion includes endoglin (ENG), causative of hereditary hemorrhagic telangiectasia. Finally, in four patients, deletions involve TOR1A, of which molecular defects lead to early-onset primary dystonia. Ninety-four other RefSeq genes also map to the genomic intervals investigated.
   Conclusion: STXBP1 haploinsufficiency results in progressive encephalopathy characterized by intellectual disability and may be accompanied by epilepsy, movement disorders, and autism. We propose that 9q34.11 genomic deletions involving ENG, TOR1A, STXBP1, and SPTAN1 are responsible for multisystemic vascular dysplasia, early-onset primary dystonia, epilepsy, and intellectual disability, therefore revealing cis-genetic effects leading to complex phenotypes.
C1 [Campbell, Ian M.; Yatsenko, Svetlana A.; Hixson, Patricia; Cheung, Sau Wai; Lupski, James R.; Stankiewicz, Pawel; Scaglia, Fernando] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Reimschisel, Tyler] Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA.
   [Thomas, Matthew; Wilson, William] Univ Virginia, Sch Med, Dept Pediat, Charlottesville, VA 22908 USA.
   [Dayal, Usha] Carolina Neurol Clin, Charlotte, NC USA.
   [Wheless, James W.] Univ Tennessee, Hlth Sci Ctr, Dept Pediat Neurol, Memphis, TN USA.
   [Crunk, Amy] Shodair Hosp, Helena, MT USA.
   [Curry, Cynthia] Univ Calif San Francisco, Fresno, CA USA.
   [Parkinson, Nicole; Fishman, Leona] Hosp Sick Children, Dept Pediat, Toronto, ON M5G 1X8, Canada.
   [Riviello, James J.] NYU, Dept Neurol, Langone Med Ctr, New York, NY 10016 USA.
   [Nowaczyk, Malgorzata J. M.; Zeesman, Susan] McMaster Univ, Dept Pathol & Mol Med & Pediat, Hamilton, ON, Canada.
   [Rosenfeld, Jill A.; Bejjani, Bassem A.; Shaffer, Lisa G.] PerkinElmer Inc, Signature Genom Labs, Spokane, WA USA.
   [Lupski, James R.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA.
   [Lupski, James R.; Scaglia, Fernando] Texas Childrens Hosp, Houston, TX 77030 USA.
RP Scaglia, F (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
EM fscaglia@bcm.edu
FU Intellectual and Developmental Disabilities Research Center [P30
   HD024064]; National Institute of Neurological Disorders and Stroke [R01
   NS058529]
FX We thank the families for their cooperation. This study was supported in
   part by grants from the Intellectual and Developmental Disabilities
   Research Center (P30 HD024064) and the National Institute of
   Neurological Disorders and Stroke (R01 NS058529) to J.R.L.
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NR 40
TC 9
Z9 10
PU NATURE PUBLISHING GROUP
PI NEW YORK
PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA
SN 1098-3600
J9 GENET MED
JI Genet. Med.
PD OCT
PY 2012
VL 14
IS 10
BP 868
EP 876
DI 10.1038/gim.2012.65
PG 9
WC Genetics & Heredity
SC Genetics & Heredity
GA 018FQ
UT WOS:000309645900006
PM 22722545
ER

PT J
AU Jordan, CJ
   Caldwell-Harris, CL
AF Jordan, Chloe Jennifer
   Caldwell-Harris, Catherine L.
TI Understanding Differences in Neurotypical and Autism Spectrum Special
   Interests Through Internet Forums
SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE autism spectrum disorder; Asperger syndrome; special interests; Internet
   discussion forums; adults
ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME;
   CIRCUMSCRIBED ATTENTION; YOUNG-CHILDREN; QUOTIENT; CLASSIFICATION;
   IMPAIRMENTS; VARIETIES; SUPPORT
AB Special interests are frequently developed by individuals with autism spectrum disorder, expressed as an intense focus on specific topics. Neurotypical individuals also develop special interests, often in the form of hobbies. Although past research has focused on special interests held by children with autism spectrum disorder, little is known about their role in adulthood. The current study investigated differences in the content, number, and specificity of the special interests held by adult individuals with autism spectrum disorder and neurotypical individuals, using Internet discussion forums as a data source. Quantitative analysis of forum posts revealed significant differences between the diagnostic groups. Individuals with autism spectrum disorder reported having more interests in systemizing domains, more specific interests, and a greater number of interests overall than neurotypical individuals. Understanding special interests can lead to the development of educational and therapeutic programs that facilitate the acquirement of other important social and communication skills.
C1 [Jordan, Chloe Jennifer; Caldwell-Harris, Catherine L.] Boston Univ, Dept Psychol, Boston, MA 02215 USA.
RP Jordan, CJ (reprint author), Boston Univ, Dept Psychol, 64 Cummington St, Boston, MA 02215 USA.
EM charris@bu.edu
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NR 47
TC 6
Z9 6
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1934-9491
J9 INTELLECT DEV DISAB
JI Intellect. Dev. Disabil.
PD OCT
PY 2012
VL 50
IS 5
BP 391
EP 402
DI 10.1352/1934-9556-50.5.391
PG 12
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 017RF
UT WOS:000309607600003
PM 23025641
ER

PT J
AU May, ME
   Brandt, RC
   Bohannan, JK
AF May, Michael E.
   Brandt, Rachel C.
   Bohannan, Joseph K.
TI Moderating Effects of Autism on Parent Views of Genetic Screening for
   Aggression
SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES
LA English
DT Article
DE aggression; autism; parents; genetic screening
ID FRAGILE-X-SYNDROME; MONOAMINE-OXIDASE; INTELLECTUAL DISABILITIES;
   CHALLENGING BEHAVIORS; ENVIRONMENTAL-INFLUENCES; PSYCHIATRIC CONDITIONS;
   RISK MARKERS; YOUNG-PEOPLE; CHILDHOOD; ATTITUDES
AB Advances in gene-environment interaction research have revealed genes that are associated with aggression. However, little is known about parent perceptions of genetic screening for behavioral symptoms like aggression as opposed to diagnosing disabilities. These perceptions may influence future research endeavors involving genetic linkage studies to behavior, including proactive approaches for parents to avoid events leading to aggression. The purpose of this study was to solicit the perspectives of parents who have children with autism about screening for genes associated with aggression, compared to responses from those who have children without disabilities and those planning to have children. Parents of children with autism were more likely to support screening and the use of the results to seek treatment if necessary. Results are discussed in the context of surveillance screening and systematic early intervention for behavioral symptoms related to autism. The results may provide insight for clincians, researchers, policymakers, and advocacy groups related to diagnosing and treating aggression in people with autism.
C1 [May, Michael E.; Brandt, Rachel C.; Bohannan, Joseph K.] So Illinois Univ, Carbondale, IL 62901 USA.
RP May, ME (reprint author), So Illinois Univ, Mailcode 4618, Carbondale, IL 62901 USA.
EM mayme@siu.edu
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NR 47
TC 0
Z9 0
PU AMER ASSOC INTELLECTUAL DEVELOPMENTAL DISABILITIES
PI WASHINGTON
PA 444 N CAPITOL ST, NW STE 846, WASHINGTON, DC 20001-1512 USA
SN 1934-9491
J9 INTELLECT DEV DISAB
JI Intellect. Dev. Disabil.
PD OCT
PY 2012
VL 50
IS 5
BP 415
EP 425
DI 10.1352/1934-9556-50.5.415
PG 11
WC Education, Special; Rehabilitation
SC Education & Educational Research; Rehabilitation
GA 017RF
UT WOS:000309607600005
PM 23025643
ER

PT J
AU Laidlaw, KEW
   Risko, EF
   Kingstone, A
AF Laidlaw, Kaitlin E. W.
   Risko, Evan F.
   Kingstone, Alan
TI A New Look at Social Attention: Orienting to the Eyes Is Not (Entirely)
   Under Volitional Control
SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-HUMAN PERCEPTION AND PERFORMANCE
LA English
DT Article
DE visual attention; attentional orienting; eye movements; face processing;
   reflexive versus volitional
ID FACE-INVERSION; HUMAN-BRAIN; GAZE; MOVEMENTS; PERCEPTION; VOLUNTARY;
   DIRECTION; MONKEYS; AUTISM; TASK
AB People tend to look at other people's eyes, but whether this bias is automatic or volitional is unclear. To discriminate between these two possibilities, we used a "don't look" (DL) paradigm. Participants looked at a series of upright or inverted faces. and were asked either to freely view the faces or to avoid looking at the eyes, or as a control, the mouth. As previously demonstrated, participants showed a bias to attend to both eyes and mouths during free viewing. In the DL condition, participants told to avoid the eyes of upright faces were unable to fully suppress the tendency to fixate on the faces' eyes, whereas participants told to avoid the mouth of upright faces successfully eliminated their bias to overtly attend to that feature. When faces were inverted, participants were equally able to suppress looks to the eyes and mouth. Together, these results suggest that the tendency to look at the eyes reflects orienting that is both volitional and automatic, and that the engagement of holistic or configural face processing mechanisms during upright face viewing has an influence in guiding gaze automatically to the eyes.
C1 [Laidlaw, Kaitlin E. W.; Kingstone, Alan] Univ British Columbia, Dept Psychol, Vancouver, BC V6T 1Z4, Canada.
   [Risko, Evan F.] Arizona State Univ, Tempe, AZ 85287 USA.
RP Laidlaw, KEW (reprint author), Univ British Columbia, Dept Psychol, 2136 W Mall, Vancouver, BC V6T 1Z4, Canada.
EM klaidlaw@psych.ubc.ca
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NR 40
TC 6
Z9 6
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0096-1523
J9 J EXP PSYCHOL HUMAN
JI J. Exp. Psychol.-Hum. Percept. Perform.
PD OCT
PY 2012
VL 38
IS 5
BP 1132
EP 1143
DI 10.1037/a0027075
PG 12
WC Psychology; Psychology, Experimental
SC Psychology
GA 014JH
UT WOS:000309371300009
PM 22686696
ER

PT J
AU Hartley, SL
   Barker, ET
   Baker, JK
   Seltzer, MM
   Greenberg, JS
AF Hartley, Sigan L.
   Barker, Erin T.
   Baker, Jason K.
   Seltzer, Marsha Mailick
   Greenberg, Jan S.
TI Marital Satisfaction and Life Circumstances of Grown Children With
   Autism Across 7 Years
SO JOURNAL OF FAMILY PSYCHOLOGY
LA English
DT Article
DE autism spectrum disorders; parents; marital satisfaction; parent child
   relationship
ID BEHAVIOR PROBLEMS; SPECTRUM DISORDERS; DIAGNOSTIC INTERVIEW;
   PRESCHOOL-CHILDREN; MENTAL-RETARDATION; FAMILY HISTORY; ADULTS; MOTHERS;
   ADOLESCENTS; FATHERS
AB We examined the extent to which marital satisfaction across 7 years in 199 mothers was associated with the characteristics (gender, age, and intellectual disability status) of their adolescent or adult child with an autism spectrum disorder (ASD) and whether fluctuations in marital satisfaction covaried with the child's autism symptoms, health, behavior problems, and closeness in the parent-child relationship. We also examined the impact of the departure of the adult child out of the family home on mothers' marital satisfaction. The effect of family context variables including the presence of an additional child with a disability, maternal education, and household income on marital satisfaction were also examined. We found that closeness in the mother-child relationship and household income had a significant effect on level of marital satisfaction, and that variability in the slope of mothers' marital satisfaction was significantly predicted by fluctuations in the behavior problems of the adolescent or adult child with an ASD. The grown child's departure out of the family home was not related to change in marital satisfaction. Interventions aimed at managing the behavior problems of adolescents and adults with ASDs may help strengthen parents' marital relationship.
C1 [Hartley, Sigan L.; Barker, Erin T.; Baker, Jason K.; Seltzer, Marsha Mailick; Greenberg, Jan S.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
   [Hartley, Sigan L.] Univ Wisconsin, Dept Human Dev & Family Studies, Madison, WI 53705 USA.
   [Seltzer, Marsha Mailick; Greenberg, Jan S.] Univ Wisconsin, Dept Social Work, 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
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NR 57
TC 2
Z9 2
PU AMER PSYCHOLOGICAL ASSOC
PI WASHINGTON
PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA
SN 0893-3200
J9 J FAM PSYCHOL
JI J. Fam. Psychol.
PD OCT
PY 2012
VL 26
IS 5
BP 688
EP 697
DI 10.1037/a0029354
PG 10
WC Psychology, Clinical; Family Studies
SC Psychology; Family Studies
GA 017CC
UT WOS:000309566700003
PM 22866933
ER

PT J
AU Pane, M
   Lombardo, ME
   Alfieri, P
   D'Amico, A
   Bianco, F
   Vasco, G
   Piccini, G
   Mallardi, M
   Romeo, DM
   Ricotti, V
   Ferlini, A
   Gualandi, F
   Vicari, S
   Bertini, E
   Berardinelli, A
   Mercuri, E
AF Pane, Marika
   Lombardo, Maria Elena
   Alfieri, Paolo
   D'Amico, Adele
   Bianco, Flaviana
   Vasco, Gessica
   Piccini, Giorgia
   Mallardi, Maria
   Romeo, Domenico M.
   Ricotti, Valeria
   Ferlini, Alessandra
   Gualandi, Francesca
   Vicari, Stefano
   Bertini, Enrico
   Berardinelli, Angela
   Mercuri, Eugenio
TI Attention Deficit Hyperactivity Disorder and Cognitive Function in
   Duchenne Muscular Dystrophy: Phenotype-Genotype Correlation
SO JOURNAL OF PEDIATRICS
LA English
DT Article
ID AUTISM SPECTRUM DISORDER; NEUROPSYCHOLOGICAL PROFILE; BOYS; ASSOCIATION;
   IMPAIRMENT; MEMORY; ADHD
AB Objectives To assess attention deficit hyperactivity disorder (ADHD) in boys affected by Duchenne muscular dystrophy (DMD) and to explore the relationship with cognitive abilities and genetic findings.
   Study design Boys with DMD (n = 103; 4-17 years of age, mean: 12.6) were assessed using a cognitive test (Wechsler scales). Assessment of ADHD was based on the Diagnostic Statistical Manual, Fourth Edition, Text Revision criteria and on the long version of the Conners Parents and Teachers Rating Scales.
   Results ADHD was found in 33 of the 103 boys with DMD. Attention problems together with hyperactivity (17/33) or in isolation (15/33) were more frequent than hyperactivity alone, which was found in 1 patient. Intellectual disability (ID) was found in 27/103 (24.6%). Sixty-two of the 103 boys had no ID and no ADHD, 9 had ID but no ADHD, 14 had ADHD but no ID, and 18 had both. ADHD occurred more frequently in association with mutations predicted to affect Dp140 expression (exon 45-55) and in those with mutations predicted to affect all dystrophin product, including Dp71 (ie, those that have promoter region and specific first exon between exons 62 and 63 but were also relatively frequent).
   Conclusions Our results suggest that ADHD is a frequent feature in DMD. The risk of ADHD appears to be higher in patients carrying mutations predicted to affect dystrophin isoforms expressed in the brain and are known to be associated with higher risk of cognitive impairment. (J Pediatr 2012;161:705-9).
C1 [Pane, Marika; Lombardo, Maria Elena; Bianco, Flaviana; Vasco, Gessica; Mallardi, Maria; Romeo, Domenico M.; Mercuri, Eugenio] Univ Cattolica Sacro Cuore, Dept Pediat Child Neurol & Psychiat, Rome, Italy.
   [Lombardo, Maria Elena] Univ Catania, Dept Physiol Sci, Catania, Italy.
   [Alfieri, Paolo; Piccini, Giorgia; Vicari, Stefano] Bambino Gesu Pediat Hosp, Dept Neurosci, Child Neuropsychiat Unit, Rome, Italy.
   [D'Amico, Adele; Bertini, Enrico] Bambino Gesu Pediat Hosp, Dept Lab Med, Mol Med Unit, Rome, Italy.
   [Ricotti, Valeria] UCL, Inst Child Hlth, Dubowitz Neuromuscular Ctr, London, England.
   [Ricotti, Valeria] Great Ormond St Hosp Sick Children, London WC1N 3JH, England.
   [Ferlini, Alessandra; Gualandi, Francesca] Univ Ferrara, Med Genet Sect, Dept Expt & Diagnost Med, I-44100 Ferrara, Italy.
   [Berardinelli, Angela] IRCCS C Mondino Fdn, Child Neurol & Psychiat Unit, Pavia, Italy.
RP Mercuri, E (reprint author), Policlin Gemelli, Dept Child Neurol, I-00168 Rome, Italy.
EM mercuri@rm.unicatt.it
RI Vicari, Stefano/J-3008-2012
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NR 29
TC 9
Z9 11
PU MOSBY-ELSEVIER
PI NEW YORK
PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0022-3476
J9 J PEDIATR-US
JI J. Pediatr.
PD OCT
PY 2012
VL 161
IS 4
BP 705
EP +
DI 10.1016/j.jpeds.2012.03.020
PG 6
WC Pediatrics
SC Pediatrics
GA 016KH
UT WOS:000309516400029
PM 22560791
ER

PT J
AU Rogers, SJ
   Estes, A
   Lord, C
   Vismara, L
   Winter, J
   Fitzpatrick, A
   Guo, MY
   Dawson, G
AF Rogers, Sally J.
   Estes, Annette
   Lord, Catherine
   Vismara, Laurie
   Winter, Jamie
   Fitzpatrick, Annette
   Guo, Mengye
   Dawson, Geraldine
TI Effects of a Brief Early Start Denver Model (ESDM)-Based Parent
   Intervention on Toddlers at Risk for Autism Spectrum Disorders: A
   Randomized Controlled Trial
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE Early Start Denver Model (ESDM); early intervention; toddler;
   parent-child interaction; autism
ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; COMMUNICATION;
   FAMILIES; SKILLS; PLAY
AB Objective: This study was carried out to examine the efficacy of a 12-week, low-intensity (1-hour/wk of therapist contact), parent-delivered intervention for toddlers at risk for autism spectrum disorders (ASD) aged 14 to 24 months and their families. Method: A randomized controlled trial involving 98 children and families was carried out in three different sites investigating the efficacy of a parent delivery of the Early Start Denver Model (P-ESDM), which fosters parental use of a child-centered responsive interaction style that embeds many teaching opportunities into play, compared to community treatment as usual. Assessments were completed at baseline and 12 weeks later, immediately after the end of parent coaching sessions. Results: There was no effect of group assignment on parent child interaction characteristics or on any child outcomes. Both groups of parents improved interaction skills, and both groups of children demonstrated progress. Parents receiving P-ESDM demonstrated significantly stronger working alliances with their therapists than did the community group. Children in the community group received significantly more intervention hours than those in the P-ESDM group. For the group as a whole, both younger child age at the start of intervention and a greater number of intervention hours were positively related to the degree of improvement in children's behavior for most variables. Conclusions: Parent-implemented intervention studies for early ASD thus far have not demonstrated the large effects seen in intensive-treatment studies. Evidence that both younger age and more intervention hours positively affect developmental rates has implications for clinical practice, service delivery, and public policy. J. Am. Acad. Child Adolesc. Psychiatry, 2012;51(10): 1052-1065.
C1 [Rogers, Sally J.; Vismara, Laurie] Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA.
   [Estes, Annette; Winter, Jamie; Fitzpatrick, Annette; Guo, Mengye] Univ Washington, Seattle, WA 98195 USA.
   [Lord, Catherine] Weill Cornell Med Coll, New York, NY USA.
   [Dawson, Geraldine] Univ N Carolina, Chapel Hill, NC 27515 USA.
RP Rogers, SJ (reprint author), Univ Calif Davis, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA.
EM sally.rogers@ucdmc.ucdavis.edu
FU Autism Speaks grants; National Institute of Mental Health (NIMH)/the
   National Institute of Child Health and Human Development (NICHD) [MH R01
   081757]
FX This research was funded by Autism Speaks grants (A.E., S.R.) and by the
   National Institute of Mental Health (NIMH)/the National Institute of
   Child Health and Human Development (NICHD) grant MH R01 081757 (S.R.).
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NR 44
TC 43
Z9 43
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2012
VL 51
IS 10
BP 1052
EP 1065
PG 14
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 017CJ
UT WOS:000309567400009
PM 23021480
ER

PT J
AU Gadow, KD
AF Gadow, Kenneth D.
TI Schizophrenia Spectrum and Attention-Deficit/Hyperactivity Disorder
   Symptoms in Autism Spectrum Disorder and Controls
SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY
LA English
DT Article
DE autism spectrum disorder; schizophrenia; schizophrenia spectrum
   disorder; attention-deficit/hyperactivity disorder; comorbidity
ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT HYPERACTIVITY DISORDER;
   CHILDHOOD-ONSET SCHIZOPHRENIA; OPPOSITIONAL DEFIANT DISORDER; FORMAL
   THOUGHT-DISORDER; RISK-FACTORS; CHILDREN; PSYCHOSIS; ADHD; ASSOCIATION
AB Objective: This study compared the differential severity of specific symptoms of schizophrenia spectrum disorder (SSD) in children with autism spectrum disorder (ASD) and child psychiatry outpatient referrals (controls). Each group was further subdivided into subgroups with and without co-occurring attention-deficit/hyperactivity disorder (ADHD). Method: Children with ASD (n = 147) and controls (n = 335) were evaluated with parent and teacher versions of a psychometrically established DSM-IV-referenced rating scale. Results: The two ASD groups (with and without ADHD) had a larger number of more severe SSD symptoms than their respective control groups (with and without ADHD), extending the observation of an association between ASD and SSD to subgroups with and without co-occurring ADHD. The ASD groups exhibited more severe schizoid personality symptoms than controls, but findings for schizophrenia symptoms were mixed. The ASD + ADHD group generally had more severe disorganized thought, disorganized behavior, and negative schizophrenia symptoms than controls (with and without ADHD); nevertheless, findings varied according to ADHD status (present versus absent), individual symptom (symptom specificity), and informant (informant specificity). Ratings of hallucinations and delusions indicated mild severity and few group differences. Negative symptoms such as inappropriate emotional reactions evidenced considerable group divergence. Conclusion: Findings provide additional support for an interrelation between ASD and SSD symptoms and the differential influence of neurobehavioral syndromes on co-occurring symptom severity, underscore the multidimensionality of SSD in children with ASD, and suggest how symptom phenotypes may contribute to a better understanding of the etiology, nosology, and possibly clinical management. J. Am. Acad. Child Adolesc. Psychiatry, 2012;51(10):1076-1084.
C1 SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
RP Gadow, KD (reprint author), SUNY Stony Brook, Dept Psychiat & Behav Sci, Putnam Hall, Stony Brook, NY 11794 USA.
EM kenneth.gadow@stonybrook.edu
FU Malt; Debra Cody Center for Autism and Developmental Disorders
FX This study was supported in port by the Malt and Debra Cody Center for
   Autism and Developmental Disorders.
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NR 50
TC 9
Z9 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0890-8567
J9 J AM ACAD CHILD PSY
JI J. Am. Acad. Child Adolesc. Psychiatr.
PD OCT
PY 2012
VL 51
IS 10
BP 1076
EP 1084
PG 9
WC Psychology, Developmental; Pediatrics; Psychiatry
SC Psychology; Pediatrics; Psychiatry
GA 017CJ
UT WOS:000309567400011
PM 23021482
ER

PT J
AU Hall, D
   Huerta, MF
   McAuliffe, MJ
   Farber, GK
AF Hall, Dan
   Huerta, Michael F.
   McAuliffe, Matthew J.
   Farber, Gregory K.
TI Sharing Heterogeneous Data: The National Database for Autism Research
SO NEUROINFORMATICS
LA English
DT Review
DE Autism; Database; Common data elements; Unique subject identifier; Data
   federation; Data repository
ID SPECTRUM DISORDERS; RISK-FACTORS; NEUROSCIENCE; LANDSCAPE; RESOURCE;
   DICOM; NIH
AB The National Database for Autism Research (NDAR) is a secure research data repository designed to promote scientific data sharing and collaboration among autism spectrum disorder investigators. The goal of the project is to accelerate scientific discovery through data sharing, data harmonization, and the reporting of research results. Data from over 25,000 research participants are available to qualified investigators through the NDAR portal. Summary information about the available data is available to everyone through that portal.
C1 [Farber, Gregory K.] NIMH, Off Technol Dev & Coordinat, NIH, Rockville, MD 20892 USA.
   [Hall, Dan] OMNITEC Solut Inc, Rockville, MD 20892 USA.
   [Huerta, Michael F.] Natl Lib Med, Off Hlth Informat Programs Dev, Bethesda, MD 20894 USA.
   [McAuliffe, Matthew J.] NIH, Ctr Informat Technol, Bethesda, MD 20892 USA.
RP Farber, GK (reprint author), NIMH, Off Technol Dev & Coordinat, NIH, 6001 Execut Blvd,Suite 7162, Rockville, MD 20892 USA.
EM halldan@mail.nih.gov; mike.huerta@nih.gov; matthew.mcauliffe@nih.gov;
   farberg@mail.nih.gov
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NR 28
TC 16
Z9 16
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 1539-2791
J9 NEUROINFORMATICS
JI Neuroinformatics
PD OCT
PY 2012
VL 10
IS 4
BP 331
EP 339
DI 10.1007/s12021-012-9151-4
PG 9
WC Computer Science, Interdisciplinary Applications; Neurosciences
SC Computer Science; Neurosciences & Neurology
GA 017AS
UT WOS:000309561700002
PM 22622767
ER

PT J
AU Bastidas, N
   Mackay, DDJ
   Taylor, JA
   Bartlett, SP
AF Bastidas, Nicholas
   Mackay, Duncan D. J.
   Taylor, Jesse A.
   Bartlett, Scott P.
TI Analysis of the Long-Term Outcomes of Nonsyndromic Bicoronal Synostosis
SO PLASTIC AND RECONSTRUCTIVE SURGERY
LA English
DT Article
ID SAETHRE-CHOTZEN-SYNDROME; FRONTO-ORBITAL ADVANCEMENT; GROWTH-FACTOR
   RECEPTOR-3; INTRACRANIAL HYPERTENSION; CORONAL CRANIOSYNOSTOSIS;
   CRANIOFACIAL SURGERY; NATURAL-HISTORY; MUTATION; PHENOTYPE; TWIST
AB Background: Isolated nonsyndromic bicoronal synostosis is a relatively rare entity that produces a characteristic turribrachycephalic skull shape. The purpose of this study was to evaluate the long-term outcomes of the isolated nonsyndromic bicoronal synostosis patients treated at the authors' institution.
   Methods: A retrospective chart review of all patients who underwent cranial vault remodeling for nonsyndromic bicoronal synostosis was performed at the Children's Hospital of Philadelphia from 1991 to 2011. Fifteen patients were identified for this study, and information regarding their demographic, perioperative, and postoperative details were analyzed.
   Results: Four boys and 11 girls were identified for inclusion in this study. The average age at the time of the initial surgery was 9 months, with an average follow-up of 13.4 years. There were no reported complications. Six patients with at least a 10-year follow-up (six of 10 patients) underwent revision for contour improvement in the forehead and temporal regions, and two patients required a repeated fronto-orbital advancement. Four patients underwent subsequent strabismus surgery. No patients were documented to have midface hypoplasia requiring orthognathic surgery. One patient with an associated diagnosis of autism was noted to have significant developmental delay.
   Conclusions: Isolated nonsyndromic bicoronal synostosis confers a high rate of revisions for contour deformities but is associated with a low risk of complications. Overall, nonsyndromic patients require less secondary fronto-orbital advancement when compared with syndromic patients. In contrast to the syndromic population, there were no instances of midface hypoplasia necessitating surgery. There did not appear to be significant correlation between bicoronal synostosis and developmental abnormalities or delays. (Plast. Reconstr. Surg. 130: 877, 2012.)
C1 [Bastidas, Nicholas; Mackay, Duncan D. J.; Taylor, Jesse A.; Bartlett, Scott P.] Childrens Hosp Philadelphia, Philadelphia, PA 19102 USA.
RP Bartlett, SP (reprint author), Childrens Hosp Philadelphia, 3400 Civ Ctr Blvd, Philadelphia, PA 19102 USA.
EM scott.bartlett@uphs.upenn.edu
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NR 28
TC 0
Z9 0
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0032-1052
J9 PLAST RECONSTR SURG
JI Plast. Reconstr. Surg.
PD OCT
PY 2012
VL 130
IS 4
BP 877
EP 883
DI 10.1097/PRS.0b013e318262f2fd
PG 7
WC Surgery
SC Surgery
GA 016UF
UT WOS:000309544300054
PM 22691840
ER

PT J
AU van der Vlugt, JJB
   van der Meulen, JJNM
   Creemers, HE
   Verhulst, FC
   Hovius, SER
   Okkerse, JME
AF van der Vlugt, Joris J. B.
   van der Meulen, Jacques J. N. M.
   Creemers, Hanneke E.
   Verhulst, Frank C.
   Hovius, Steven E. R.
   Okkerse, Jolanda M. E.
TI Cognitive and Behavioral Functioning in 82 Patients with Trigonocephaly
SO PLASTIC AND RECONSTRUCTIVE SURGERY
LA English
DT Article
ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; SOCIAL COMMUNICATION
   QUESTIONNAIRE; SINGLE-SUTURE CRANIOSYNOSTOSIS; PAST 10 YEARS;
   INTRACRANIAL-PRESSURE; DIAGNOSTIC INTERVIEW; DISRUPTIVE BEHAVIOR;
   METOPIC SYNOSTOSIS; MENTAL-RETARDATION; SHORT-FORM
AB Background: The main objective of the present study was to assess the prevalence rates of attention deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, and features of autism spectrum disorders in trigonocephalic patients, using validated instruments and by ruling out the confounding influence of IQ. The second aim was to assess the association between extracranial anomalies and cognitive and/or behavioral problems in patients with trigonocephaly.
   Methods: Objectives were studied in 82 trigonocephalic patients aged 4 to 18 years at the Erasmus Medical Center in Rotterdam, The Netherlands. Features of autism spectrum disorders were assessed using the Social Communication Questionnaire. Attention deficit hyperactivity disorder, oppositional defiant disorder, and conduct disorder were assessed with the Diagnostic Interview Schedule for Children-Parent Version. The presence and nature of extracranial anomalies were ascertained by a clinician.
   Results: Mental retardation (IQ < 70) was present in 9 percent of patients with trigonocephaly. Findings indicated a 70 percent versus 24 percent prevalence of psychopathology (attention deficit hyperactivity disorder, oppositional defiant disorder, conduct disorder, or features of autism spectrum disorder) in patients with IQ levels of, respectively, <85 and >= 85. In the latter group, psychopathology was not significantly more common than expected based on prevalence rates reported in community samples. Extracranial anomalies were significantly correlated with lower IQ levels. However, when adjusted for IQ, the presence of extracranial malformations was not associated with an increased risk of behavioral problems.
   Conclusion: The relatively high prevalence of behavioral problems in patients with trigonocephaly seems to be mainly attributable to the co-occurrence of trigonocephaly and low intelligence. (Plast. Reconstr. Surg. 130: 885, 2012.)
C1 Univ Amsterdam, Fac Behav & Social Sci, NL-1012 WX Amsterdam, Netherlands.
RP van der Vlugt, JJB (reprint author), Erasmus MC, Sophia Childrens Hosp, Dept Child & Adolescent Psychiat, POB 2060, NL-3000 CB Rotterdam, Netherlands.
EM j.vandervlugt@erasmusmc.nl
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NR 59
TC 1
Z9 1
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0032-1052
J9 PLAST RECONSTR SURG
JI Plast. Reconstr. Surg.
PD OCT
PY 2012
VL 130
IS 4
BP 885
EP 893
DI 10.1097/PRS.0b013e318262f21f
PG 9
WC Surgery
SC Surgery
GA 016UF
UT WOS:000309544300055
PM 23018698
ER

PT J
AU Tsai, LY
AF Tsai, Luke Y.
TI Sensitivity and Specificity: DSM-IV Versus DSM-5 Criteria for Autism
   Spectrum Disorder
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Editorial Material
C1 Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI 48109 USA.
RP Tsai, LY (reprint author), Univ Michigan, Sch Med, Dept Psychiat, Ann Arbor, MI 48109 USA.
EM lyctsai@umich.edu
CR Happe F, WHY FOLD ASPERGER SY
   Huerta M, 2012, AM J PSYCHIAT, V169, P1056, DOI 10.1176/appi.ajp.2012.12020276
   Mattila ML, 2011, J AM ACAD CHILD PSY, V50, P583, DOI 10.1016/j.jaac.2011.04.001
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   Tsai LY, 2010, CHIN MED J S2, V123, P9
NR 6
TC 6
Z9 6
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2012
VL 169
IS 10
BP 1009
EP 1011
DI 10.1176/appi.ajp.2012.12070922
PG 3
WC Psychiatry
SC Psychiatry
GA 015HS
UT WOS:000309437600001
PM 23032376
ER

PT J
AU Huerta, M
   Bishop, SL
   Duncan, A
   Hus, V
   Lord, C
AF Huerta, Marisela
   Bishop, Somer L.
   Duncan, Amie
   Hus, Vanessa
   Lord, Catherine
TI Application of DSM-5 Criteria for Autism Spectrum Disorder to Three
   Samples of Children With DSM-IV Diagnoses of Pervasive Developmental
   Disorders
SO AMERICAN JOURNAL OF PSYCHIATRY
LA English
DT Article
ID OBSERVATION-SCHEDULE; REVISED ALGORITHMS; SPECIFICITY; SENSITIVITY;
   VALIDITY
AB Objective: Substantial revisions to the DSM-IV criteria for autism spectrum disorders (ASDs) have been proposed in efforts to increase diagnostic sensitivity and specificity. This study evaluated the proposed DSM-5 criteria for the single diagnostic category of autism spectrum disorder in children with DSM-IV diagnoses of pervasive developmental disorders (PDDs) and non-PDD diagnoses.
   Method: Three data sets included 4,453 children with DSM-IV clinical PDD diagnoses and 690 with non-PDD diagnoses (e.g., language disorder). Items from a parent report measure of ASD symptoms (Autism Diagnostic Interview Revised) and clinical observation instrument (Autism Diagnostic Observation Schedule) were matched to DSM-5 criteria and used to evaluate the sensitivity and specificity of the proposed DSM-5 criteria and current DSM-IV criteria when compared with clinical diagnoses.
   Results: Based on just parent data, the proposed DSM-5 criteria identified 91% of children with clinical DSM-IV PDD diagnoses. Sensitivity remained high in specific subgroups, including girls and children under 4. The specificity of DSM-5 ASD was 0.53 overall, while the specificity of DSM-IV ranged from 0.24, for clinically diagnosed PDD not otherwise specified (PDD-NOS), to 0.53, for autistic disorder. When data were required from both parent and clinical observation, the specificity of the DSM-5 criteria increased to 0.63.
   Conclusions: These results suggest that most children with DSM-IV PDD diagnoses would remain eligible for an ASD diagnosis under the proposed DSM-5 criteria. Compared with the DSM-IV criteria for Asperger's disorder and PDD-NOS, the DSM-5 ASD criteria have greater specificity, particularly when abnormalities are evident from both parents and clinical observation. (Am Psychiatry 2012; 169:1056-1064)
C1 [Huerta, Marisela] Weill Cornell Med Coll, Dept Psychiat, New York, NY USA.
   Univ Michigan, Cincinnati Childrens Hosp Med Ctr, Div Dev & Behav Pediat, Ann Arbor, MI 48109 USA.
   Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA.
RP Huerta, M (reprint author), Weill Cornell Med Coll, Dept Psychiat, New York, NY USA.
EM mah2046@med.cornell.edu
FU NIMH [R01 MH-081873, RC1 MH-089721]; National Institute of Child Health
   and Human Development [R01 HD-065277]; Simons Foundation; Autism Speaks;
   Dennis Weatherstone Predoctoral Fellowship
FX Supported by NIMH grants R01 MH-081873 and RC1 MH-089721 to Dr. Lord,
   grant R01 HD-065277 from the National Institute of Child Health and
   Human Development to Dr. Bishop, and graduate fellowships from the
   Simons Foundation and Autism Speaks and a Dennis Weatherstone
   Predoctoral Fellowship to Ms. Hus.
CR Billstedt E, 2007, J CHILD PSYCHOL PSYC, V48, P1102, DOI 10.1111/j.1469-7610.2007.01774.x
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NR 20
TC 61
Z9 63
PU AMER PSYCHIATRIC PUBLISHING, INC
PI ARLINGTON
PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA
SN 0002-953X
J9 AM J PSYCHIAT
JI Am. J. Psychiat.
PD OCT
PY 2012
VL 169
IS 10
BP 1056
EP 1064
DI 10.1176/appi.ajp.2012.12020276
PG 9
WC Psychiatry
SC Psychiatry
GA 015HS
UT WOS:000309437600011
PM 23032385
ER

PT J
AU Daly, EM
   Deeley, Q
   Ecker, C
   Craig, M
   Hallahan, B
   Murphy, C
   Johnston, P
   Spain, D
   Gillan, N
   Brammer, M
   Giampietro, V
   Lamar, M
   Page, L
   Toal, F
   Cleare, A
   Surguladze, S
   Murphy, DGM
AF Daly, Eileen M.
   Deeley, Quinton
   Ecker, Christine
   Craig, Michael
   Hallahan, Brian
   Murphy, Clodagh
   Johnston, Patrick
   Spain, Debbie
   Gillan, Nicola
   Brammer, Michael
   Giampietro, Vincent
   Lamar, Melissa
   Page, Lisa
   Toal, Fiona
   Cleare, Anthony
   Surguladze, Simon
   Murphy, Declan G. M.
TI Serotonin and the Neural Processing of Facial Emotions in Adults With
   Autism An fMRI Study Using Acute Tryptophan Depletion
SO ARCHIVES OF GENERAL PSYCHIATRY
LA English
DT Article
ID PERVASIVE DEVELOPMENTAL DISORDERS; GENERIC BRAIN ACTIVATION;
   HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; ASPERGER-SYNDROME; BLOOD
   SEROTONIN; SPECTRUM DISORDER; INFANTILE-AUTISM; CHILDREN; PERCEPTION
AB Context: People with autism spectrum disorders (ASDs) have lifelong deficits in social behavior and differences in behavioral as well as neural responses to facial expressions of emotion. The biological basis to this is incompletely understood, but it may include differences in the role of neurotransmitters such as serotonin, which modulate facial emotion processing in health. While some individuals with ASD have significant differences in the serotonin system, to our knowledge, no one has investigated its role during facial emotion processing in adults with ASD and control subjects using acute tryptophan depletion (ATD) and functional magnetic resonance imaging.
   Objective: To compare the effects of ATD on brain responses to primary facial expressions of emotion in men with ASD and healthy control subjects.
   Design: Double-blind, placebo-controlled, crossover trial of ATD and functional magnetic resonance imaging to measure brain activity during incidental processing of disgust, fearful, happy, and sad facial expressions.
   Setting: Institute of Psychiatry, King's College London, and South London and Maudsley National Health Service Foundation Trust, England.
   Participants: Fourteen men of normal intelligence with autism and 14 control subjects who did not significantly differ in sex, age, or overall intelligence.
   Main Outcome Measures: Blood oxygenation level-dependent response to facial expressions of emotion.
   Results: Brain activation was differentially modulated by ATD depending on diagnostic group and emotion type within regions of the social brain network. For example, processing of disgust faces was associated with interactions in medial frontal and lingual gyri, whereas processing of happy faces was associated with interactions in middle frontal gyrus and putamen.
   Conclusions: Modulation of the processing of facial expressions of emotion by serotonin significantly differs in people with ASD compared with control subjects. The differences vary with emotion type and occur in social brain regions that have been shown to be associated with group differences in serotonin synthesis/receptor or transporter density.
   Arch Gen Psychiatry. 2012; 69(10): 1003-1013. Published online June 4, 2012. doi: 10.1001/archgenpsychiatry.2012.513
C1 [Daly, Eileen M.; Deeley, Quinton; Ecker, Christine; Craig, Michael; Murphy, Clodagh; Johnston, Patrick; Spain, Debbie; Gillan, Nicola; Page, Lisa; Toal, Fiona; Murphy, Declan G. M.] Kings Coll London, Inst Psychiat, Dept Forens & Neurodev Sci, London SE5 8AF, England.
   [Brammer, Michael; Giampietro, Vincent] Kings Coll London, Inst Psychiat, Dept Neuroimaging, London SE5 8AF, England.
   [Surguladze, Simon] Kings Coll London, Inst Psychiat, Dept Psychosis Studies, London SE5 8AF, England.
   [Cleare, Anthony] Kings Coll London, Inst Psychiat, Dept Psychol Med, London SE5 8AF, England.
   [Surguladze, Simon] Cygnet Hlth Care, London, England.
   [Hallahan, Brian] Natl Univ Ireland, Dept Psychiat, Galway, Ireland.
   [Lamar, Melissa] Univ Illinois, Dept Psychiat, Chicago, IL 60612 USA.
RP Daly, EM (reprint author), Kings Coll London, Inst Psychiat, Dept Forens Sci, DeCrespigny Pk, London SE5 8AF, England.
EM eileen.daly@kcl.ac.uk
RI Giampietro, Vincent/D-1279-2011; Ecker, Christine/E-5194-2010; Brammer,
   Michael/B-7128-2012
OI Giampietro, Vincent/0000-0002-9381-8201; Brammer,
   Michael/0000-0001-9800-2052
FU EU European Autism Interventions study
FX We thank all of the volunteers for their participation. We are also
   grateful for the assistance of the radiographers and physicists of the
   Centre for Neuroimaging Sciences and the National Institute for Health
   Research Biomedical Research Centre for Mental Health at the Institute
   of Psychiatry. We also acknowledge the support of the EU European Autism
   Interventions study. We also thank Roy Sherwood, PhD; Kate John, PhD;
   and Tracy Dew, PhD, in the Department of Clinical Biochemistry, King's
   College Hospital, London, for the analysis of the tryptophan levels and
   Mary L. Phillips, MD, Department of Psychiatry, University of Pittsburgh
   School of Medicine, for early work developing the functional magnetic
   resonance imaging paradigm.
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NR 90
TC 11
Z9 11
PU AMER MEDICAL ASSOC
PI CHICAGO
PA 515 N STATE ST, CHICAGO, IL 60654-0946 USA
SN 0003-990X
J9 ARCH GEN PSYCHIAT
JI Arch. Gen. Psychiatry
PD OCT
PY 2012
VL 69
IS 10
BP 1003
EP 1013
DI 10.1001/archgenpsychiatry.2012.513
PG 11
WC Psychiatry
SC Psychiatry
GA 014YV
UT WOS:000309412800003
PM 22638012
ER

PT J
AU Oruche, UM
   Gerkensmeyer, J
   Stephan, L
   Wheeler, CA
   Hanna, KM
AF Oruche, Ukamaka Marian
   Gerkensmeyer, Janis
   Stephan, Linda
   Wheeler, Corrine A.
   Hanna, Kathleen M.
TI The Described Experience of Primary Caregivers of Children With Mental
   Health Needs
SO ARCHIVES OF PSYCHIATRIC NURSING
LA English
DT Article
ID DEFICIT HYPERACTIVITY DISORDER; AUTISM SPECTRUM DISORDER; CARE NEEDS;
   INTELLECTUAL DISABILITY; MOTHERS; FAMILIES; INVOLVEMENT; PARENTS
AB About 10% of our nation's children have serious mental health needs that result in significant functional impairments. Although research has found that primary caregivers of children with mental health needs have high levels of depressive symptoms and distress, little is known about the challenges these caregivers face. Focus groups with 20 caregivers of children with mental health needs between 2 and 17 years of age revealed these themes: struggling with care systems, living in fear, being burdened and exhausted, worrying about the rest of the family, and having good things happen. Caregivers described extreme challenges and many unmet needs that are important to consider in efforts to improve both children's and caregivers' well-being. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Oruche, Ukamaka Marian; Gerkensmeyer, Janis; Stephan, Linda; Wheeler, Corrine A.; Hanna, Kathleen M.] Indiana Univ Sch Nursing Indianapolis, Indianapolis, IN 46202 USA.
RP Oruche, UM (reprint author), Indiana Univ Sch Nursing Indianapolis, 1111 Middle Dr Lane, Indianapolis, IN 46202 USA.
EM uoruche@iupui.edu; jgerkens@iupui.edu; cawheele@iupui.edu;
   kathanna@iupui.edu
RI Oruche, Ukamaka/J-2942-2013
OI Oruche, Ukamaka/0000-0003-1173-4109
FU Ethel Clarke Fellowship from Indiana University School of Nursing;
   National Institute of Nursing Research [2T32 NR007066]
FX This study was supported by a grant from the Ethel Clarke Fellowship
   from Indiana University School of Nursing. Preparation of the article
   for publication was made possible by Grant 2T32 NR007066 from the
   National Institute of Nursing Research. The authors wish to thank Dr.
   Melinda Swenson for guidance with qualitative research, Dr. Phyllis
   Dexter for her editorial suggestions, and the caregivers who
   participated in this study.
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NR 34
TC 3
Z9 3
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0883-9417
J9 ARCH PSYCHIAT NURS
JI Arch. Psychiatr. Nurs.
PD OCT
PY 2012
VL 26
IS 5
BP 382
EP 391
DI 10.1016/j.apnu.2011.12.006
PG 10
WC Nursing; Psychiatry
SC Nursing; Psychiatry
GA 015HT
UT WOS:000309437700007
PM 22999034
ER

PT J
AU Elwin, M
   Ek, L
   Schroder, A
   Kjellin, L
AF Elwin, Marie
   Ek, Lena
   Schroder, Agneta
   Kjellin, Lars
TI Autobiographical Accounts of Sensing in Asperger Syndrome and
   High-Functioning Autism
SO ARCHIVES OF PSYCHIATRIC NURSING
LA English
DT Article
ID QUALITATIVE CONTENT-ANALYSIS; SPECTRUM DISORDERS; ABNORMALITIES; ADULTS;
   CHILDHOOD; CHILDREN
AB Sensory experiences in Asperger syndrome (AS) or high-functioning autism (HFA) were explored by qualitative content analysis of autobiographical texts by persons with AS/HFA. Predetermined categories of hyper- and hyposensitivity were applied to texts. Hypersensitivity consists of strong reactions and heightened apprehension in reaction to external stimuli, sometimes together with overfocused or unselective attention. It was common in vision, hearing, and touch. In contrast, hyposensitivity was frequent in reaction to internal and body stimuli such as interoception, proprioception, and pain. It consists of less registration, discrimination, and recognition of stimuli as well as cravings for specific stimuli. Awareness of the strong impact of sensitivity is essential for creating good environments and encounters in the context of psychiatric and other health care. (C) 2012 Elsevier Inc. All rights reserved.
C1 [Elwin, Marie] Univ Orebro, Sch Hlth & Med Sci, Psychiat Res Ctr, SE-70116 Orebro, Sweden.
   Stockholm Univ, Dept Psychol, S-10691 Stockholm, Sweden.
RP Elwin, M (reprint author), Univ Orebro, Sch Hlth & Med Sci, Psychiat Res Ctr, POB 1613, SE-70116 Orebro, Sweden.
EM marie.elvin@orebroll.se; lena-birgitta.ek@telia.com;
   agneta.schroder@orebroll.se; lars.kjellin@orebroll.se
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NR 56
TC 4
Z9 4
PU W B SAUNDERS CO-ELSEVIER INC
PI PHILADELPHIA
PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA
SN 0883-9417
J9 ARCH PSYCHIAT NURS
JI Arch. Psychiatr. Nurs.
PD OCT
PY 2012
VL 26
IS 5
BP 420
EP 429
DI 10.1016/j.apnu.2011.10.003
PG 10
WC Nursing; Psychiatry
SC Nursing; Psychiatry
GA 015HT
UT WOS:000309437700011
PM 22999038
ER

PT J
AU Armstrong, T
AF Armstrong, Thomas
TI First, Discover Their Strengths
SO EDUCATIONAL LEADERSHIP
LA English
DT Article
ID AUTISM; TALENT
EM thomas@thomasarmstrong.com
CR Appleyard D, 1997, INDEPENDENT
   Armstrong T, NEURODIVERS IN PRESS
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NR 21
TC 0
Z9 0
PU ASSOC SUPERVISION CURRICULUM DEVELOPMENT
PI ALEXANDRIA
PA 1703 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA
SN 0013-1784
J9 EDUC LEADERSHIP
JI Educ. Leadership
PD OCT
PY 2012
VL 70
IS 2
BP 10
EP 16
PG 7
WC Education & Educational Research
SC Education & Educational Research
GA 013NG
UT WOS:000309311500002
ER

PT J
AU Malhi, P
   Singhi, P
AF Malhi, Prahbhjot
   Singhi, Pratibha
TI Regression in Children with Autism Spectrum Disorders
SO INDIAN JOURNAL OF PEDIATRICS
LA English
DT Article
DE ASD; Developmental regression; Young children
ID PERVASIVE DEVELOPMENTAL DISORDERS; CLINICAL CHARACTERISTICS; LANGUAGE
   REGRESSION; INFANTILE-AUTISM; SPEECH LOSS; COMMUNICATION; CPEA; AGE
AB To understand the characteristics of autistic regression and to compare the clinical and developmental profile of children with autism spectrum disorders (ASD) in whom parents report developmental regression with age matched ASD children in whom no regression is reported.
   Participants were 35 (Mean age = 3.57 y, SD = 1.09) children with ASD in whom parents reported developmental regression before age 3 y and a group of age and IQ matched 35 ASD children in whom parents did not report regression. All children were recruited from the outpatient Child Psychology Clinic of the Department of Pediatrics of a tertiary care teaching hospital in North India. Multi-disciplinary evaluations including neurological, diagnostic, cognitive, and behavioral assessments were done. Parents were asked in detail about the age at onset of regression, type of regression, milestones lost, and event, if any, related to the regression. In addition, the Childhood Autism Rating Scale (CARS) was administered to assess symptom severity.
   The mean age at regression was 22.43 mo (SD = 6.57) and large majority (66.7%) of the parents reported regression between 12 and 24 mo. Most (75%) of the parents of the regression-autistic group reported regression in the language domain, particularly in the expressive language sector, usually between 18 and 24 mo of age. Regression of language was not an isolated phenomenon and regression in other domains was also reported including social skills (75%), cognition (31.25%). In majority of the cases (75%) the regression reported was slow and subtle. There were no significant differences in the motor, social, self help, and communication functioning between the two groups as measured by the DP II.There were also no significant differences between the two groups on the total CARS score and total number of DSM IV symptoms endorsed. However, the regressed children had significantly (t = 2.36, P = .021) more social deficits as per the DSM IV as compared to the non-regressed children with autism.
   Autism with regression is not characterized by a distinctive developmental or symptom profile. Developmental regression may, however, be an early and reliable marker in a significant number of children with autism.
C1 [Malhi, Prahbhjot; Singhi, Pratibha] Post Grad Inst Med Educ & Res, Dept Pediat, Pediat Neurol Unit, Chandigarh 160012, India.
RP Malhi, P (reprint author), Post Grad Inst Med Educ & Res, Dept Pediat, Pediat Neurol Unit, Sect 12, Chandigarh 160012, India.
EM pmalhi18@hotmail.com
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NR 25
TC 1
Z9 1
PU ALL INDIA INST MEDICAL SCIENCES
PI NEW DELHI
PA ANSARI NAGAR, NEW DELHI 110 029, INDIA
SN 0019-5456
J9 INDIAN J PEDIATR
JI Indian J. Pediatr.
PD OCT
PY 2012
VL 79
IS 10
BP 1333
EP 1337
DI 10.1007/s12098-012-0683-2
PG 5
WC Pediatrics
SC Pediatrics
GA 014CV
UT WOS:000309353600005
PM 22350733
ER

PT J
AU Muneoka, K
   Funahashi, H
   Ogawa, T
   Whitaker-Azmitia, PM
   Shioda, S
AF Muneoka, Katsumasa
   Funahashi, Hisayuki
   Ogawa, Tetsuo
   Whitaker-Azmitia, Patricia M.
   Shioda, Seiji
TI Shared features of S100B immunohistochemistry and cytochrome oxidase
   histochemistry in the ventroposterior thalamus and lateral habenula in
   neonatal rats
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Article
DE S100B; Thalamus; Habenula; Astrocyte; Development
ID FIBRILLARY ACIDIC PROTEIN; VISUAL-CORTEX; SOMATOSENSORY CORTEX;
   S-100-BETA PROTEIN; CEREBRAL-CORTEX; SCHIZOPHRENIA; ASTROCYTES; AUTISM;
   CONNECTIVITY; NEURONS
AB The ventroposterior thalamus and the habenular nuclei of the epithalamus are relevant to the monoaminergic system functionally and anatomically. The glia-derived S100B protein plays a critical role in the development of the nervous system including the monoaminergic systems. In this study, we performed an immunohistochemical study of glia-related proteins including S100B, serotonin transporter, and microtubule-associated protein 2, as well as cytochrome oxidase histochemistry in neonatal rats. Results showed the same findings for S100B immunohistochemistry between the ventroposterior thalamus and the lateral habenula at postnatal day 7: intense staining in cell bodies of astrocytes, diffusely spread immunoproduct in the intercellular space, and S100B-free areas as well as a strong reaction to cytochrome oxidase histochemistry. Further common features were the scarcity of glial fibrillary acidic protein-positive astrocytes and the few apoptotic cells observed. The results of the cytochrome oxidase reaction suggested that S100B is released actively into intercellular areas in restricted brain regions showing high neuronal activity at postnatal day 7. Pathology of the ventroposterior thalamus and the habenula is suggested in mental disorders, and S100B might be a key factor for investigations in these areas. (C) 2012 ISDN. Published by Elsevier Ltd. All rights reserved.
C1 [Muneoka, Katsumasa; Funahashi, Hisayuki; Ogawa, Tetsuo; Shioda, Seiji] Showa Univ, Sch Med, Dept Anat 1, Shinagawa Ku, Tokyo 1428555, Japan.
   [Whitaker-Azmitia, Patricia M.] SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA.
RP Muneoka, K (reprint author), Showa Univ, Sch Med, Dept Anat 1, Shinagawa Ku, 1-5-8 Hatanodai, Tokyo 1428555, Japan.
EM kmuneoka@med.showa-u.ac.jp
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NR 49
TC 0
Z9 0
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0736-5748
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD OCT
PY 2012
VL 30
IS 6
BP 499
EP 505
DI 10.1016/j.ijdevneu.2012.05.003
PG 7
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 015ZN
UT WOS:000309487000013
PM 22627026
ER

PT J
AU Ogawa, T
   Kuwagata, M
   Muneoka, K
   Wakai, C
   Senuma, M
   Kubo, H
   Shioda, S
AF Ogawa, Tetsuo
   Kuwagata, Makiko
   Muneoka, Katsumasa
   Wakai, Chizu
   Senuma, Mika
   Kubo, Hiroko
   Shioda, Seiji
TI Abnormal brain function of the rat neonate in a prenatal 5-bromo-2
   '-deoxyuridine (BrdU)-induced developmental disorder model
SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
LA English
DT Article
DE BrdU; c-Fos; Home cage deprivation; Developmental neurotoxicity;
   Pre-weaning examination
ID INDIVIDUAL-DIFFERENCES; POLYCHLORINATED-BIPHENYLS; SPECTRUM DISORDERS;
   MATERNAL SMOKING; LOCUS-COERULEUS; VALPROIC ACID; ANIMAL-MODEL;
   AMYGDALA; EXPOSURE; AUTISM
AB Neonatal brain function was investigated in a prenatal BrdU-induced developmental disorder model, which has been reported to exhibit behavioral abnormalities such as locomotor hyperactivity, impaired learning and memory, and lower anxiety in offspring. After 1 h home cage deprivation we observed an increase in the number of c-Fos (neuronal activity marker) immunoreactive cells in several brain regions of the olfactory and stress-related areas in normal neonates at 11 days. Next, pregnant rats were exposed to 50 mg/kg of BrdU from gestation days 9-15, and their offspring at 11 days were home-cage deprived. Compared to vehicle control, the number of c-Fos immunoreactive cells in BrdU group was found to be decreased in the piriform cortex and locus coeruleus, which are known to play an important role in neonatal learning and memory. We also analyzed Pearson product-moment correlation coefficient of the number of c-Fos immunoreactive cells, focusing on the piriform cortex and locus coeruleus versus numerous other brain areas (11 areas including amygdala). Numerous significant correlations were observed in the vehicle control group, however, correlations of the locus coeruleus disappeared in the BrdU group. By observing c-Fos immunoreactivity after home cage deprivation our study uncovers abnormal brain functions as early as postnatal day 11 in this disorder model. Based on these results, we propose a new histological approach for functional characterization of developmental disorder models. (C) 2012 ISDN. Published by Elsevier Ltd. All rights reserved.
C1 [Ogawa, Tetsuo] Showa Univ, Sch Med, Dept Anat, Shinagawa Ku, Tokyo 1428555, Japan.
   [Kuwagata, Makiko; Senuma, Mika] FDSC, Hatano Res Inst, Div Toxicol, Pathol Lab, Kanagawa, Japan.
RP Ogawa, T (reprint author), Showa Univ, Sch Med, Dept Anat, Shinagawa Ku, 1-5-8 Hatanodai, Tokyo 1428555, Japan.
EM t.ogawa@med.showa-u.ac.jp
FU Japan Chemical Industry Association; MEXT (Ministry of Education,
   Culture, Sports, Science and Technology)
FX This research was supported by a grant for Long-range Research
   Initiative from the Japan Chemical Industry Association, and MEXT*-
   Supported Program for the Strategic Research Foundation at Private
   Universities, 2008-2012 (* Ministry of Education, Culture, Sports,
   Science and Technology). The authors are grateful to Dr. Randeep Rakwal
   (University of Tsukuba) for a critical reading of the manuscript.
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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 0736-5748
J9 INT J DEV NEUROSCI
JI Int. J. Dev. Neurosci.
PD OCT
PY 2012
VL 30
IS 6
BP 507
EP 515
DI 10.1016/j.ijdevneu.2012.05.002
PG 9
WC Developmental Biology; Neurosciences
SC Developmental Biology; Neurosciences & Neurology
GA 015ZN
UT WOS:000309487000014
PM 22609825
ER

PT J
AU Resta, N
   Memo, L
AF Resta, Nicoletta
   Memo, Luigi
TI Chromosomal microarray (CMA) analysis in infants with congenital
   anomalies: when is it really helpful?
SO JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
LA English
DT Article
DE Array-CGH; birth defects; copy-number variants (CNVs); SNP arrays
AB Background: Birth defects are very common, affecting two to three infants in every 100 births, and often represent a diagnostic and management challenge. The birth of a child with multiple malformations is the beginning of a complex diagnostic process, where the primary purpose is to determine a precise nosological definition. An accurate diagnosis is a key prerequisite in providing a care plan, a prognosis and genetic counselling. The poor specificity of birth defects, the aetiology and course of which can vary despite similar phenotypic patterns, often makes the diagnostic path problematic. The advent and application of high-resolution chromosomal microarray, encompassing array-based comparative genome hybridization and single-nucleotide polymorphism arrays, has led to the detection of genomic copy-number abnormalities in patients affected by multiple congenital anomalies, dysmorphisms, developmental delay and mental retardation, but who have a normal karyotype. Aim: We discuss current guidelines and recommendations for chromosomal microarray use and how its application can help clinicians make accurate diagnoses in order to appropriately manage and treat affected newborns. Conclusions: Current guidelines strongly support the application of chromosomal microarray analysis as a first-tier cytogenetic diagnostic test alternative to karyotyping for patients with multiple congenital anomalies, or developmental delay, intellectual disability and autism spectrum disorders.
C1 [Memo, Luigi] Osped San Martino, UOC Pediat, Paediat Unit, I-32100 Belluno, Italy.
   [Resta, Nicoletta] Univ Bari A Moro, Med Genet Sect, Interdisciplinary Med Dept, Bari, Italy.
RP Memo, L (reprint author), Osped San Martino, UOC Pediat, Paediat Unit, Viale Europa 21, I-32100 Belluno, Italy.
EM luigi.memo@ulss.belluno.it
CR Aase JM, 1990, DIAGNOSTIC DYSMORPHO
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NR 10
TC 2
Z9 2
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 1476-7058
J9 J MATERN-FETAL NEO M
JI J. Matern.-Fetal Neonatal Med.
PD OCT
PY 2012
VL 25
SU 4
BP 124
EP 126
DI 10.3109/14767058.2012.715004
PG 3
WC Obstetrics & Gynecology
SC Obstetrics & Gynecology
GA 005CA
UT WOS:000308726800039
PM 22958042
ER

PT J
AU Ehrlich, DE
   Ryan, SJ
   Rainnie, DG
AF Ehrlich, D. E.
   Ryan, S. J.
   Rainnie, D. G.
TI Postnatal development of electrophysiological properties of principal
   neurons in the rat basolateral amygdala
SO JOURNAL OF PHYSIOLOGY-LONDON
LA English
DT Review
ID CORTICOTROPIN-RELEASING-FACTOR; HYPERPOLARIZATION-ACTIVATED CURRENT;
   HIPPOCAMPAL PYRAMIDAL CELLS; BURSTING PACEMAKER NEURONS; PREFRONTAL
   CORTEX; SUBTHRESHOLD OSCILLATIONS; MEMBRANE RESONANCE; LATERAL AMYGDALA;
   FEAR MEMORY; I-H
AB Key points The amygdala mediates emotional processing, in particular fear learning, and disruption of its function is thought to contribute to the developmental origins of psychiatric disorders like depression, anxiety and autism spectrum disorders. It is difficult to identify the causes of these disorders or provide effective intervention because most of what is known of amygdala physiology is based on the adult. Using the whole-cell patch clamp technique, we show that neurons in the developing rat amygdala undergo drastic changes to their electrophysiology, including passive membrane properties, intrinsic currents and resonance. This provides the first evidence that amygdala neuron physiology is dynamic before adulthood, and likely to contribute to emotional development. The results help us better understand the normative development of emotional processing and identify critical periods of maturation that may be sensitive to insult. Abstract The basolateral amygdala (BLA) is critically involved in the pathophysiology of psychiatric disorders, which often emerge during brain development. Several studies have characterized postnatal changes to the morphology and biochemistry of BLA neurons, and many more have identified sensitive periods of emotional maturation. However, it is impossible to determine how BLA development contributes to emotional development or the aetiology of psychiatric disorders because no study has characterized the physiological maturation of BLA neurons. We addressed this critical knowledge gap for the first time using whole-cell patch clamp recording in rat BLA principal neurons to measure electrophysiological properties at postnatal day (P)7, P10, P14, P21, P28 and after P35. We show that intrinsic properties of these neurons undergo significant transitions before P21 and reach maturity around P28. Specifically, we observed significant reductions in input resistance and membrane time constant of nearly 10- and 4-fold, respectively, from P7 to P28. The frequency selectivity of these neurons to input also changed significantly, with peak resonance frequency increasing from 1.0 Hz at P7 to 5.7 Hz at P28. In the same period, maximal firing frequency significantly increased and doublets and triplets of action potentials emerged. Concomitantly, individual action potentials became significantly faster, firing threshold hyperpolarized 6.7 mV, the medium AHP became faster and shallower, and a fast AHP emerged. These results demonstrate neurons of the BLA undergo vast change throughout postnatal development, and studies of emotional development and treatments for juvenile psychiatric disorders should consider the dynamic physiology of the immature BLA.
C1 [Ehrlich, D. E.; Ryan, S. J.; Rainnie, D. G.] Emory Univ, Sch Med, Div Behav Neurosci & Psychiat Disorders, Dept Psychiat & Behav Sci,Yerkes Res Ctr, Atlanta, GA 30322 USA.
RP Rainnie, DG (reprint author), Emory Univ, Sch Med, Div Behav Neurosci & Psychiat Disorders, Dept Psychiat & Behav Sci,Yerkes Res Ctr, Atlanta, GA 30322 USA.
EM drainni@emory.edu
FU National Institutes of Health [MH 069852, RR 00165, MH 090729]
FX We would like to thank Professor Shannon L. Gourley for her constructive
   comments on the manuscript. We would also like to thank the National
   Institutes of Health (Grants MH 069852 to D. G. R., base grant RR 00165
   to the Yerkes National Primate Research centre, and MH 090729 to D. E.
   E.) for funding.
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NR 107
TC 8
Z9 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0022-3751
J9 J PHYSIOL-LONDON
JI J. Physiol.-London
PD OCT
PY 2012
VL 590
IS 19
BP 4819
EP 4838
DI 10.1113/jphysiol.2012.237453
PG 20
WC Neurosciences; Physiology
SC Neurosciences & Neurology; Physiology
GA 014UL
UT WOS:000309401100014
PM 22848043
ER

PT J
AU de Bartolomeis, A
   Tomasetti, C
AF de Bartolomeis, Andrea
   Tomasetti, Carmine
TI Calcium-Dependent Networks in Dopamine-Glutamate Interaction: The Role
   of Postsynaptic Scaffolding Proteins
SO MOLECULAR NEUROBIOLOGY
LA English
DT Article
DE Postsynaptic density; Homer; PSD95; Shank; Psychosis; Antipsychotics
ID ADENOSINE A(2A) RECEPTORS; METHYL-D-ASPARTATE; LONG-TERM POTENTIATION;
   RAT PREFRONTAL CORTEX; AUTISM SPECTRUM DISORDER; EARLY GENE-EXPRESSION;
   INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; ELECTRICALLY-EVOKED RESPONSES;
   STRIATAL SYNAPTIC PLASTICITY; PYRAMIDAL CELL EXCITABILITY
AB Dopamine and glutamate systems are both involved in cognitive, behavioral, and motor processes. Dysfunction of dopamine-glutamate interplay has been suggested in several psychotic diseases, above all in schizophrenia, for which there exists a need for novel medications. Intracellular calcium-dependent transduction pathways are key determinants of dopamine-glutamate interactions, which take place mainly, albeit not exclusively, in the postsynaptic density (PSD), a highly specialized postsynaptic ultrastructure. Stimulation of dopamine and glutamate receptors modulates the gene expression and the function of specific PSD proteins, the "scaffolding" proteins (Homer, Shank, and PSD95), belonging to a complex Ca2+-regulated network that integrates and converges dopamine and glutamate signaling to appropriate nuclear targets. Dysfunction of scaffolding proteins leads to severe impairment of Ca2+-dependent signaling, which may underlie the dopamine-glutamate aberrations putatively implicated in the pathogenesis of psychotic disorders. Antipsychotic therapy has been demonstrated to directly and indirectly affect the neuronal Ca2+-dependent pathways through the modulation of PSD scaffolding proteins, such as Homer, therefore influencing both dopaminergic and glutamatergic functions and enforcing Ca2+-mediated long-term synaptic changes. In this review, we will discuss the role of PSD scaffolding proteins in routing Ca2+-dependent signals to the nucleus. In particular, we will address the implication of PSD scaffolding proteins in the intracellular connections between dopamine and glutamate pathways, which involve both Ca2+-dependent and Ca2+-independent mechanisms. Finally, we will discuss how new strategies for the treatment of psychosis aim at developing antipsychotics that may impact both glutamate and dopamine signaling, and what should be the possible role of PSD scaffolding proteins.
C1 [de Bartolomeis, Andrea; Tomasetti, Carmine] Univ Sch Med Federico II, Dept Neurosci, Sect Psychiat, Lab Mol Psychiat & Psychopharmacotherapeut, I-80131 Naples, Italy.
RP de Bartolomeis, A (reprint author), Univ Sch Med Federico II, Dept Neurosci, Sect Psychiat, Lab Mol Psychiat & Psychopharmacotherapeut, Bldg 18,Via Pansini 5, I-80131 Naples, Italy.
EM adebarto@unina.it
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NR 238
TC 12
Z9 12
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0893-7648
J9 MOL NEUROBIOL
JI Mol. Neurobiol.
PD OCT
PY 2012
VL 46
IS 2
BP 275
EP 296
DI 10.1007/s12035-012-8293-6
PG 22
WC Neurosciences
SC Neurosciences & Neurology
GA 013YF
UT WOS:000309341500005
PM 22763587
ER

PT J
AU Franke, B
   Faraone, SV
   Asherson, P
   Buitelaar, J
   Bau, CHD
   Ramos-Quiroga, JA
   Mick, E
   Grevet, EH
   Johansson, S
   Haavik, J
   Lesch, KP
   Cormand, B
   Reif, A
AF Franke, B.
   Faraone, S. V.
   Asherson, P.
   Buitelaar, J.
   Bau, C. H. D.
   Ramos-Quiroga, J. A.
   Mick, E.
   Grevet, E. H.
   Johansson, S.
   Haavik, J.
   Lesch, K-P
   Cormand, B.
   Reif, A.
CA Int Multictr Persistent ADHD
TI The genetics of attention deficit/hyperactivity disorder in adults, a
   review
SO MOLECULAR PSYCHIATRY
LA English
DT Review
DE persistent ADHD; molecular genetics; heritability; endophenotype; IMpACT
ID DEFICIT-HYPERACTIVITY DISORDER; DOPAMINE TRANSPORTER GENE; GENOME-WIDE
   ASSOCIATION; TEST-RETEST RELIABILITY; 4 EUROPEAN POPULATIONS;
   AFRICAN-AMERICAN CHILDREN; AUTISM SPECTRUM DISORDER; AGE-DEPENDENT
   DECLINE; BETA-HYDROXYLASE GENE; NITRIC-OXIDE SYNTHASE
AB The adult form of attention deficit/hyperactivity disorder (aADHD) has a prevalence of up to 5% and is the most severe long-term outcome of this common neurodevelopmental disorder. Family studies in clinical samples suggest an increased familial liability for aADHD compared with childhood ADHD (cADHD), whereas twin studies based on self-rated symptoms in adult population samples show moderate heritability estimates of 30-40%. However, using multiple sources of information, the heritability of clinically diagnosed aADHD and cADHD is very similar. Results of candidate gene as well as genome-wide molecular genetic studies in aADHD samples implicate some of the same genes involved in ADHD in children, although in some cases different alleles and different genes may be responsible for adult versus childhood ADHD. Linkage studies have been successful in identifying loci for aADHD and led to the identification of LPHN3 and CDH13 as novel genes associated with ADHD across the lifespan. In addition, studies of rare genetic variants have identified probable causative mutations for aADHD. Use of endophenotypes based on neuropsychology and neuroimaging, as well as next-generation genome analysis and improved statistical and bioinformatic analysis methods hold the promise of identifying additional genetic variants involved in disease etiology. Large, international collaborations have paved the way for well-powered studies. Progress in identifying aADHD risk genes may provide us with tools for the prediction of disease progression in the clinic and better treatment, and ultimately may help to prevent persistence of ADHD into adulthood. Molecular Psychiatry (2012) 17, 960-987; doi:10.1038/mp.2011.138; published online 22 November 2011
C1 [Franke, B.] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6500 HB Nijmegen, Netherlands.
   [Franke, B.] Radboud Univ Nijmegen, Med Ctr, Dept Psychiat, Donders Inst Brain Cognit & Behav, NL-6500 HB Nijmegen, Netherlands.
   [Faraone, S. V.] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY USA.
   [Faraone, S. V.] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY USA.
   [Asherson, P.] Kings Coll London, Inst Psychiat, MRC Social Genet & Dev Psychiat, London WC2R 2LS, England.
   [Buitelaar, J.] Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Cognit Neurosci, NL-6500 HB Nijmegen, Netherlands.
   [Bau, C. H. D.] Univ Fed Rio Grande do Sul, Inst Biociencias, Dept Genet, BR-90049 Porto Alegre, RS, Brazil.
   [Bau, C. H. D.; Grevet, E. H.] Hosp Clin Porto Alegre, Adult ADHD Outpatient Clin, Porto Alegre, RS, Brazil.
   [Ramos-Quiroga, J. A.] Univ Autonoma Barcelona, Dept Psychiat, Hosp Univ Vall dHebron, CIBERSAM, E-08193 Barcelona, Catalonia, Spain.
   [Ramos-Quiroga, J. A.] Univ Autonoma Barcelona, Dept Psychiat & Legal Med, E-08193 Barcelona, Catalonia, Spain.
   [Mick, E.] Univ Massachusetts, Sch Med, Worcester, MA USA.
   [Johansson, S.] Haukeland Hosp, Ctr Med Genet & Mol Med, N-5021 Bergen, Norway.
   [Johansson, S.; Haavik, J.] Univ Bergen, Dept Biomed, KG Jebsen Ctr Res Neuropsychiat Disorders, Bergen, Norway.
   [Haavik, J.] Haukeland Hosp, Dept Psychiat, N-5021 Bergen, Norway.
   [Lesch, K-P] Univ Wurzburg, Dept Psychiat Psychosomat & Psychotherapy, ADHD Clin Res Network, Lab Translat Neurosci, Wurzburg, Germany.
   [Lesch, K-P] Maastricht Univ, Sch Mental Hlth & Neurosci MHENS, Dept Neurosci, Maastricht, Netherlands.
   [Cormand, B.] Univ Barcelona, Fac Biol, Dept Genet, Catalonia, Spain.
   [Cormand, B.] Biomed Network Res Ctr Rare Dis CIBERER, Barcelona, Catalonia, Spain.
   [Cormand, B.] Univ Barcelona, Inst Biomed, Catalonia, Spain.
RP Franke, B (reprint author), Radboud Univ Nijmegen, Med Ctr, Dept Human Genet 855, POB 9101, NL-6500 HB Nijmegen, Netherlands.
EM b.franke@antrg.umcn.nl
RI Bau, Claiton/C-9980-2013; Grevet, Eugenio/F-2007-2013; Franke,
   Barbara/D-4836-2009; Lesch, Klaus-Peter/J-4906-2013
OI Bau, Claiton/0000-0001-5644-3845; Grevet, Eugenio/0000-0002-6898-7126;
   Franke, Barbara/0000-0003-4375-6572; Lesch,
   Klaus-Peter/0000-0001-8348-153X
FU Deutsche Forschungsgemeinschaft [KFO 125, SFB 581, SFB TRR 58, GRK 1156,
   GRK 1253]; Bundesministerium fur Bildung und Forschung [BMBF 01GV0605];
   Agencia de Gestio d'Ajuts Universitaris i de Recerca-AGAUR
   [2009GR00971]; Health Department (Government of Catalonia); Alicia
   Koplowitz Foundation; Fundacio La Marato de TV3 [092330/31]; Instituto
   de Salud Carlos III-FIS [PI080519]; Netherlands Organization for
   Scientific Research (NWO) [433-09-229, 433-09-242]; CNPq; CAPES; PRONEX;
   FAPERGS-DECIT-PPSUS; Research Council of Norway; KG Jebsen Centre for
   Research on Neuropsychiatric Disorders; Western Norway Regional Health
   Authority
FX The work of KPL and AR was supported by the Deutsche
   Forschungsgemeinschaft (KFO 125, SFB 581, SFB TRR 58, GRK 1156, GRK
   1253) and the Bundesministerium fur Bildung und Forschung (KPL, BMBF
   01GV0605). BC is supported by the Agencia de Gestio d'Ajuts
   Universitaris i de Recerca-AGAUR (2009GR00971) and JAR-Q by Health
   Department (Government of Catalonia), Alicia Koplowitz Foundation,
   Fundacio La Marato de TV3 (092330/31) and Instituto de Salud Carlos
   III-FIS (PI080519). BF and JB are supported by the Netherlands
   Organization for Scientific Research (NWO, Brain and Cognition
   433-09-229 and 433-09-242). CHDB is supported by the Brazilian funding
   agencies CNPq, CAPES, PRONEX and FAPERGS-DECIT-PPSUS. JH and SJ receive
   support from the Research Council of Norway, the KG Jebsen Centre for
   Research on Neuropsychiatric Disorders and the Western Norway Regional
   Health Authority.
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NR 262
TC 48
Z9 48
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1359-4184
J9 MOL PSYCHIATR
JI Mol. Psychiatr.
PD OCT
PY 2012
VL 17
IS 10
BP 960
EP 987
DI 10.1038/mp.2011.138
PG 28
WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry
SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry
GA 012DB
UT WOS:000309214500003
PM 22105624
ER

PT J
AU Kotagal, S
   Broomall, E
AF Kotagal, Suresh
   Broomall, Eileen
TI Sleep in Children With Autism Spectrum Disorder
SO PEDIATRIC NEUROLOGY
LA English
DT Review
ID PERVASIVE DEVELOPMENTAL DISORDERS; UNFOLDED PROTEIN RESPONSE; BEHAVIOR
   DISORDER; MELATONIN TREATMENT; NEURODEVELOPMENTAL DISABILITIES; TUBEROUS
   SCLEROSIS; ADOLESCENTS; RESTRICTION; CHILDHOOD; PATTERNS
AB Children with autism spectrum disorder demonstrate an increased prevalence of difficulties with sleep initiation and maintenance. The consequences may include alterations in daytime behavior, memory, and learning in patients, and significant stress in caretakers. The dysregulation of melatonin synthesis, sensitization to environmental stimuli, behavioral insomnia syndromes, delayed sleep phase syndrome, rapid eye movement sleep behavior disorder, and comorbid anxiety, depression, and epilepsy comprise common etiologic factors. The clinical assessment of sleep problems in this population and a management algorithm are presented. (c) 2012 Elsevier Inc. All rights reserved.
C1 [Kotagal, Suresh; Broomall, Eileen] Mayo Clin, Div Child Neurol, Rochester, MN 55902 USA.
   [Kotagal, Suresh] Mayo Clin, Ctr Sleep Med, Rochester, MN 55902 USA.
RP Kotagal, S (reprint author), Mayo Clin, Div Child Neurol, 200 First St SW, Rochester, MN 55902 USA.
EM kotagal.suresh@mayo.edu
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NR 61
TC 22
Z9 22
PU ELSEVIER SCIENCE INC
PI NEW YORK
PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA
SN 0887-8994
J9 PEDIATR NEUROL
JI Pediatr. Neurol.
PD OCT
PY 2012
VL 47
IS 4
BP 242
EP 251
DI 10.1016/j.pediatrneurol.2012.05.007
PG 10
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 009NV
UT WOS:000309033400002
PM 22964437
ER

PT J
AU Dove, D
   Warren, Z
   McPheeters, ML
   Taylor, JL
   Sathe, NA
   Veenstra-VanderWeele, J
AF Dove, Dwayne
   Warren, Zachary
   McPheeters, Melissa L.
   Taylor, Julie Lounds
   Sathe, Nila A.
   Veenstra-VanderWeele, Jeremy
TI Medications for Adolescents and Young Adults With Autism Spectrum
   Disorders: A Systematic Review
SO PEDIATRICS
LA English
DT Review
DE autism spectrum disorders; antipsychotics; risperidone; serotonin
   reuptake inhibitors
ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; MENTAL-RETARDATION;
   CHILDREN; CLOMIPRAMINE; RISPERIDONE; FLUOXETINE; CROSSOVER
AB BACKGROUND AND OBJECTIVE: Although many treatments have been studied in children with autism spectrum disorders (ASDs), less attention has focused on interventions that may be helpful in adolescents and young adults with ASD. The goal of this study was to systematically review evidence regarding medication treatments for individuals between the ages of 13 and 30 years with ASD.
   METHODS: The Medline, PsycINFO, and ERIC databases were searched (1980-December 2011), as were reference lists of included articles. Two investigators independently assessed studies against predetermined inclusion/exclusion criteria. Two investigators independently extracted data regarding participant and intervention characteristics, assessment techniques, and outcomes and assigned overall quality and strength of evidence ratings on the basis of predetermined criteria.
   RESULTS: Eight studies of medications were identified that focused on 13- to 30-year-olds with ASD; 4 of the studies were of fair quality. The strength of evidence was insufficient for all outcomes associated with medications tested in this population; however, the 2 available studies of the atypical antipsychotic medication risperidone in this age range were consistent with the moderate evidence in children with ASD for treating problem behavior, including aggression, and high strength of evidence for adverse events, including sedation and weight gain.
   CONCLUSIONS: There is a marked lack of data on use of medication treatments for adolescents and young adults with ASD. The evidence on the use of risperidone in this age range is insufficient when considered alone but is consistent with the data in the population of children with ASD. Pediatrics 2012;130:717-726
C1 [Dove, Dwayne; Warren, Zachary; Taylor, Julie Lounds; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37212 USA.
   [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Psychiat, Med Ctr, Nashville, TN 37212 USA.
   [McPheeters, Melissa L.] Vanderbilt Univ, Dept Obstet & Gynecol, Med Ctr, Nashville, TN 37212 USA.
   [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pharmacol, Med Ctr, Nashville, TN 37212 USA.
   [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Vanderbilt Kennedy Ctr, Treatment & Res Inst Autism Spectrum Disorders, Med Ctr, Nashville, TN 37212 USA.
   [McPheeters, Melissa L.; Sathe, Nila A.] Vanderbilt Univ, Med Ctr, Vanderbilt Evidence Based Practice Ctr, Inst Med & Publ Hlth, Nashville, TN 37212 USA.
RP Veenstra-VanderWeele, J (reprint author), Vanderbilt Univ, Med Ctr, Dept Pediat, 465 21st Ave S,7158 MRB 3, Nashville, TN 37212 USA.
EM j.vvw@vanderbilt.edu
FU Agency for Healthcare Research and Quality, US Department of Health and
   Human Services [HHSA 290 2007 10065 I]; National Institute of Mental
   Health [K01 MH092598]; Eunice Kennedy Shriver National Institute of
   Child Health and Human Development; Autism Speaks; Marino Autism
   Research Institute; National Science Foundation; Agency for Healthcare
   Research and Quality [HHSA 290 2007 10065 I]; Simons Foundation;
   National Institute of Child Health and Human Development; American
   Academy of Child and Adolescent Psychiatry; NARSAD; Seaside
   Therapeutics; Roche Pharmaceuticals; Novartis
FX This project was funded under contract HHSA 290 2007 10065 I from the
   Agency for Healthcare Research and Quality, US Department of Health and
   Human Services. The authors of this report are responsible for its
   content. Statements in the report should not be construed as endorsement
   by the Agency for Healthcare Research and Quality or the US Department
   of Health and Human Services.Dr Dove has received training support from
   the National Institute of General Medical Sciences, the National Heart,
   Lung, and Blood Institute, the National Institute of Child Health and
   Human Development, the Maternal Child Health Bureau, the American Heart
   Association, and the Autism Speaks Autism Treatment Network; Dr Taylor
   has received research support from the National Institute of Mental
   Health, the Eunice Kennedy Shriver National Institute of Child Health
   and Human Development, Autism Speaks, and the Marino Autism Research
   Institute; Dr Warren has received research support from the National
   Institute of Mental Health, the Eunice Kennedy Shriver National
   Institute of Child Health and Human Development, the National Science
   Foundation, the Agency for Healthcare Research and Quality, Autism
   Speaks, the Marino Autism Research Institute, and the Simons Foundation;
   Dr Veenstra-VanderWeele has received research support from the National
   Institute of Mental Health, the National Institute of Child Health and
   Human Development, the Agency for Healthcare Research and Quality,
   Autism Speaks, the American Academy of Child and Adolescent Psychiatry,
   NARSAD, Seaside Therapeutics, Roche Pharmaceuticals, and Novartis. He
   has consulted for Novartis; and Dr McPheeters and Ms Sathe have
   indicated they have no financial relationships relevant to this article
   to disclose.The full review project was supported by the Agency for
   Healthcare Research and Quality (contract HHSA 290 2007 10065 I). Dr.
   Lounds Taylor was also supported by the National Institute of Mental
   Health through a K01 award (K01 MH092598) during participation on the
   project and preparation of the manuscript.
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NR 16
TC 23
Z9 25
PU AMER ACAD PEDIATRICS
PI ELK GROVE VILLAGE
PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA
SN 0031-4005
J9 PEDIATRICS
JI Pediatrics
PD OCT
PY 2012
VL 130
IS 4
BP 717
EP 726
DI 10.1542/peds.2012-0683
PG 10
WC Pediatrics
SC Pediatrics
GA 014YO
UT WOS:000309412100058
PM 23008452
ER

PT J
AU Waligorska, A
   Pisula, E
   Waligorski, M
   Letachowicz, M
AF Waligorska, Anna
   Pisula, Ewa
   Waligorski, Michal
   Letachowicz, Maciej
TI AutismPro system in supporting treatment of children with autism in
   Poland
SO PEDIATRICS INTERNATIONAL
LA English
DT Article
DE autism; home-based treatment; Internet resources; parents' satisfaction;
   therapy effectiveness
ID YOUNG-CHILDREN; EARLY INTERVENTION; SPECTRUM DISORDERS; PROGRAM;
   PATTERNS
AB Background: The efficacy of early intervention programs for children with autism has been emphasized in many studies. However, access for people with autism to professional services in Poland is very limited and the burden of supporting a child's development often falls on parents, especially in families with low socioeconomic status and families living far away from big cities. Using Internet resources in planning and delivering individualized intervention may be useful. This study examined the effects of a home program of intervention based on the AutismPro system with elements of consultative therapy. Methods: Ten families of children with a diagnosis of autism participated in the project; nine of them completed the 6-month program of intervention. Parents were taught to use the AutismPro system and implement the intervention techniques in a home setting. Modification of the intervention program to suit individual children's needs and evaluations of children's progress were performed during consultation meetings with therapists. The pre- and post-treatment measurement of child development was performed using the Psychoeducational Profile Revised (PEP-R). Results: Children involved in the study progressed in total PEP-R scores and on the PEP-R subtest of fine motor, gross motor, non-verbal and verbal cognitive skills and eyehand integration. Parents expressed positive opinions on the program. Conclusions: The results suggest that an intervention which combines the use of the Internet support tool and professional consultations may provide benefits to the children with autism. There are, however, methodological limitations of the study to be taken into account when interpreting the results.
C1 [Pisula, Ewa] Univ Warsaw, Fac Psychol, Dept Psychol, PL-00183 Warsaw, Poland.
   [Waligorska, Anna] Warsaw Sch Social Sci & Humanities, Dept Psychol, Warsaw, Poland.
   [Waligorski, Michal] SOTIS Therapy Ctr, Grojec, Poland.
   [Letachowicz, Maciej] Occupat Therapy Workshop Grojec, Grojec, Poland.
RP Pisula, E (reprint author), Univ Warsaw, Fac Psychol, Dept Psychol, Stawki 5-7, PL-00183 Warsaw, Poland.
EM ewa.pisula@psych.uw.edu.pl
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NR 32
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1328-8067
J9 PEDIATR INT
JI Pediatr. Int.
PD OCT
PY 2012
VL 54
IS 5
BP 693
EP 700
DI 10.1111/j.1442-200X.2012.03637.x
PG 8
WC Pediatrics
SC Pediatrics
GA 012KI
UT WOS:000309234600017
PM 22469462
ER

PT J
AU Barichello, T
   Generoso, JS
   Cipriano, AL
   Casagrande, R
   Collodel, A
   Savi, GD
   Scherer, EBS
   Kolling, J
   Wyse, ATS
AF Barichello, Tatiana
   Generoso, Jaqueline S.
   Cipriano, Andreza L.
   Casagrande, Renata
   Collodel, Allan
   Savi, Geovana D.
   Scherer, Emilene B. S.
   Kolling, Janaina
   Wyse, Angela T. S.
TI Increased Na plus ,K plus -ATPase activity in the rat brain after
   meningitis induction by Streptococcus pneumoniae
SO ACTA NEUROPSYCHIATRICA
LA English
DT Article
DE brain; meningitis; Na; K plus -ATPase; Streptococcus pneumoniae
ID PNEUMOCOCCAL MENINGITIS; BACTERIAL-MENINGITIS; MITOCHONDRIAL
   DYSFUNCTION; OXIDATIVE STRESS; TNF-ALPHA; HEART-FAILURE; CHILDREN;
   AUTISM; INJURY; PATHOGENESIS
AB Barichello T, Generoso JS, Cipriano AL, Casagrande R, Collodel A, Savi GD, Scherer EBS, Kolling J, Wyse ATS. Increase Na+,K+-ATPase activity in the rat brain after meningitis induction by Streptococcus pneumoniae. Background: Pneumococcal meningitis is the most severe infection of the central nervous system with a mortality rate up to 20% and an adverse neurological result in up to 50% of survivors. A complicated series of interactions among the host immune response and oxidants seems to be responsible for meningitis associated brain dysfunctions. Na+,K+-ATPase is an essential enzyme responsible for generating and maintaining the membrane potential necessary for neural excitability, however, the Na+,K+-ATPase activity is altered in several illness; Objective: The aim of this study is to evaluate the Na+,K+-ATPase activity in hippocampus and cortex of the rats submitted to pneumococcal meningitis. Methods: Animals received 10 mu l sterile saline as a placebo or an equivalent volume of Streptococcus pneumoniae to the concentration of 5 x 109cfu/ml and were killed at 24, 48, 72 and 96 h after meningitis induction. The brain structures, hippocampus and cortex, were immediately isolated on dry ice and stored at -80 degrees C to analyse Na+,K+-ATPase activity. Results: In the hippocampus, we verified the increase of Na+,K+-ATPase activity at 48, 72 and 96 h (p < 0.05) and in the cortex at 24 h (p < 0.05) after pneumococcal meningitis induction. Conclusion: The Na+,K+-ATPase activity is under the control of a diversity of intracellular messengers that are able to modulate the function of the particular isozymes in a precise way. Furthermore, we verified that pneumococcal meningitis increased the Na+,K+-ATPase activity in hippocampus and cortex; this increase can be correlated with a compensatory mechanism in illness pathophysiology.
C1 [Barichello, Tatiana] Univ Extremo Sul Catarinense, Lab Microbiol Expt, PPGCS, UNASAU,Unidade Acad Ciencias Saude, BR-88806000 Criciuma, SC, Brazil.
   [Barichello, Tatiana; Generoso, Jaqueline S.; Cipriano, Andreza L.; Casagrande, Renata; Collodel, Allan; Savi, Geovana D.] Univ Extremo Sul Catarinense, Inst Nacl Ciencia & Tecnol Translac Med, Programa Posgrad Ciencias Saude, Unidade Acad Ciencias Saude, BR-88806000 Criciuma, SC, Brazil.
   [Scherer, Emilene B. S.; Kolling, Janaina; Wyse, Angela T. S.] Univ Fed Rio Grande do Sul, Lab Neuroprotecao & Doencas Metab, ICBS, Porto Alegre, RS, Brazil.
RP Barichello, T (reprint author), Univ Extremo Sul Catarinense, Lab Microbiol Expt, PPGCS, UNASAU,Unidade Acad Ciencias Saude, BR-88806000 Criciuma, SC, Brazil.
EM tba@unesc.net
RI Barichello, Tatiana/E-2725-2013; Wyse, Angela/K-6104-2013; Generoso,
   Jaqueline/N-3142-2013; Collodel, Allan Minatto/B-8408-2015
OI Wyse, Angela/0000-0001-8769-1147; 
FU CNPq; FAPESC; UNESC; Instituto Nacional de Ciencia e Tecnologia
   Translacional em Medicina (INCT-TM); L'Oreal-UNESCO Brazil
FX This research was supported by grants from CNPq, FAPESC, UNESC,
   Instituto Nacional de Ciencia e Tecnologia Translacional em Medicina
   (INCT-TM) and L'Oreal-UNESCO Brazil Fellowship for Women in Science
   2011.
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NR 45
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0924-2708
J9 ACTA NEUROPSYCHIATR
JI Acta Neuropsychiatr.
PD OCT
PY 2012
VL 24
IS 5
BP 301
EP 305
DI 10.1111/j.1601-5215.2011.00635.x
PG 5
WC Neurosciences; Psychiatry
SC Neurosciences & Neurology; Psychiatry
GA 007IP
UT WOS:000308882300008
PM 25286995
ER

PT J
AU Bartnik, M
   Szczepanik, E
   Derwinska, K
   Wisniowiecka-Kowalnik, B
   Gambin, T
   Sykulski, M
   Ziemkiewicz, K
   Kedzior, M
   Gos, M
   Hoffman-Zacharska, D
   Mazurczak, T
   Jeziorek, A
   Antczak-Marach, D
   Rudzka-Dybala, M
   Mazurkiewicz, H
   Goszczanska-Ciuchta, A
   Zalewska-Miszkurka, Z
   Terczynska, I
   Sobierajewicz, M
   Shaw, CA
   Gambin, A
   Mierzewska, H
   Mazurczak, T
   Obersztyn, E
   Bocian, E
   Stankiewicz, P
AF Bartnik, Magdalena
   Szczepanik, Elzbieta
   Derwinska, Katarzyna
   Wisniowiecka-Kowalnik, Barbara
   Gambin, Tomasz
   Sykulski, Maciej
   Ziemkiewicz, Kamila
   Kedzior, Marta
   Gos, Monika
   Hoffman-Zacharska, Dorota
   Mazurczak, Tomasz
   Jeziorek, Anetta
   Antczak-Marach, Dorota
   Rudzka-Dybala, Mariola
   Mazurkiewicz, Hanna
   Goszczanska-Ciuchta, Alicja
   Zalewska-Miszkurka, Zofia
   Terczynska, Iwona
   Sobierajewicz, Malgorzata
   Shaw, Chad A.
   Gambin, Anna
   Mierzewska, Hanna
   Mazurczak, Tadeusz
   Obersztyn, Ewa
   Bocian, Ewa
   Stankiewicz, Pawel
TI Application of array comparative genomic hybridization in 102 patients
   with epilepsy and additional neurodevelopmental disorders
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE seizures; array CGH; copy-number variants; KCNJ3; WWOX; CDH15; IMMP2L
ID SEVERE MENTAL-RETARDATION; IDIOPATHIC GENERALIZED EPILEPSY; 1P36
   DELETION SYNDROME; COPY NUMBER VARIANTS; QUESTIONABLE PATHOGENICITY;
   15Q13.3 MICRODELETIONS; CONGENITAL-ANOMALIES; 16P13.11 PREDISPOSE; FOXG1
   DUPLICATION; TOURETTE-SYNDROME
AB Copy-number variants (CNVs) collectively represent an important cause of neurodevelopmental disorders such as developmental delay (DD)/intellectual disability (ID), autism, and epilepsy. In contrast to DD/ID, for which the application of microarray techniques enables detection of pathogenic CNVs in similar to 1020% of patients, there are only few studies of the role of CNVs in epilepsy and genetic etiology in the vast majority of cases remains unknown. We have applied whole-genome exon-targeted oligonucleotide array comparative genomic hybridization (array CGH) to a cohort of 102 patients with various types of epilepsy with or without additional neurodevelopmental abnormalities. Chromosomal microarray analysis revealed 24 non-polymorphic CNVs in 23 patients, among which 10 CNVs are known to be clinically relevant. Two rare deletions in 2q24.1q24.3, including KCNJ3 and 9q21.13 are novel pathogenic genetic loci and 12 CNVs are of unknown clinical significance. Our results further support the notion that rare CNVs can cause different types of epilepsy, emphasize the efficiency of detecting novel candidate genes by whole-genome array CGH, and suggest that the clinical application of array CGH should be extended to patients with unexplained epilepsies. (c) 2012 Wiley Periodicals, Inc.
C1 [Shaw, Chad A.; Stankiewicz, Pawel] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA.
   [Bartnik, Magdalena; Derwinska, Katarzyna; Wisniowiecka-Kowalnik, Barbara; Ziemkiewicz, Kamila; Kedzior, Marta; Gos, Monika; Hoffman-Zacharska, Dorota; Mazurczak, Tadeusz; Obersztyn, Ewa; Bocian, Ewa; Stankiewicz, Pawel] Inst Mother & Child Hlth, Dept Med Genet, Warsaw, Poland.
   [Szczepanik, Elzbieta; Mazurczak, Tomasz; Jeziorek, Anetta; Antczak-Marach, Dorota; Rudzka-Dybala, Mariola; Mazurkiewicz, Hanna; Goszczanska-Ciuchta, Alicja; Zalewska-Miszkurka, Zofia; Terczynska, Iwona; Mierzewska, Hanna] Inst Mother & Child Hlth, Clin Neurol Children & Adolescents, Warsaw, Poland.
   [Gambin, Tomasz] Warsaw Univ Technol, Inst Comp Sci, Warsaw, Poland.
   [Sykulski, Maciej; Gambin, Anna] Univ Warsaw, Inst Informat, Warsaw, Poland.
   [Sobierajewicz, Malgorzata] Child Neurol Outpatient Clin, Leszno, Poland.
   [Gambin, Anna] Polish Acad Sci, Mossakowski Med Res Ctr, Warsaw, Poland.
RP Stankiewicz, P (reprint author), Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Plaza,Rm R809, Houston, TX 77030 USA.
EM pawels@bcm.edu
RI Gambin, Anna/I-3580-2012
FU Polish Ministry of Science and Higher Education [R13-0005-04/2008];
   Foundation for Polish Science
FX Grant sponsor: Polish Ministry of Science and Higher Education; Grant
   number: R13-0005-04/2008; Grant sponsor: Foundation for Polish Science.
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NR 80
TC 13
Z9 13
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4841
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD OCT
PY 2012
VL 159B
IS 7
BP 760
EP 771
DI 10.1002/ajmg.b.32081
PG 12
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 007HR
UT WOS:000308879900002
PM 22825934
ER

PT J
AU Van Den Bossche, MJ
   Johnstone, M
   Strazisar, M
   Pickard, BS
   Goossens, D
   Lenaerts, AS
   De Zutter, S
   Nordin, A
   Norrback, KF
   Mendlewicz, J
   Souery, D
   De Rijk, P
   Sabbe, BG
   Adolfsson, R
   Blackwood, D
   Del-Favero, J
AF Van Den Bossche, Maarten J.
   Johnstone, Mandy
   Strazisar, Mojca
   Pickard, Benjamin S.
   Goossens, Dirk
   Lenaerts, An-Sofie
   De Zutter, Sonia
   Nordin, Annelie
   Norrback, Karl-Fredrik
   Mendlewicz, Julien
   Souery, Daniel
   De Rijk, Peter
   Sabbe, Bernard G.
   Adolfsson, Rolf
   Blackwood, Douglas
   Del-Favero, Jurgen
TI Rare copy number variants in neuropsychiatric disorders: Specific
   phenotype or not?
SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS
LA English
DT Article
DE copy number variants; schizophrenia; bipolar disorder; major depressive
   disorder; intellectual disability
ID IDIOPATHIC GENERALIZED EPILEPSY; AUTISM SPECTRUM DISORDER; CONGENITAL
   HEART-DISEASE; BIPOLAR-DISORDER; MENTAL-RETARDATION; CHROMOSOME 1Q21.1;
   INCREASE RISK; RECURRENT MICRODELETIONS; 15Q13.3 MICRODELETIONS;
   SCHIZOPHRENIA-PATIENTS
AB From a number of genome-wide association studies it was shown that de novo and/or rare copy number variants (CNVs) are found at an increased frequency in neuropsychiatric diseases. In this study we examined the prevalence of CNVs in six genomic regions (1q21.1, 2p16.3, 3q29, 15q11.2, 15q13.3, and 16p11.2) previously implicated in neuropsychiatric diseases. Hereto, a cohort of four neuropsychiatric disorders (schizophrenia, bipolar disorder, major depressive disorder, and intellectual disability) and control individuals from three different populations was used in combination with Multilpex Amplicon Quantifiaction (MAQ) assays, capable of high resolution (kb range) and custom-tailored CNV detection. Our results confirm the etiological candidacy of the six selected CNV regions for neuropsychiatric diseases. It is possible that CNVs in these regions can result in disturbed brain development and in this way lead to an increased susceptibility for different neuropsychiatric disorders, dependent on additional genetic and environmental factors. Our results also suggest that the neurodevelopmental component is larger in the etiology of schizophrenia and intellectual disability than in mood disorders. Finally, our data suggest that deletions are in general more pathogenic than duplications. Given the high frequency of the examined CNVs (12%) in patients of different neuropsychiatric disorders, screening of large cohorts with an affordable and feasible method like the MAQ assays used in this study is likely to result in important progress in unraveling the genetic factors leading to an increased susceptibility for several psychiatric disorders. (c) 2012 Wiley Periodicals, Inc.
C1 [Del-Favero, Jurgen] Univ Antwerp, Appl Mol Genom Grp, VIB Dept Mol Genet, B-2610 Antwerp, Belgium.
   [Van Den Bossche, Maarten J.; Strazisar, Mojca; Goossens, Dirk; Lenaerts, An-Sofie; De Zutter, Sonia; De Rijk, Peter; Del-Favero, Jurgen] Univ Antwerp VIB, Appl Mol Genom Grp, Dept Mol Genet, B-2610 Antwerp, Belgium.
   [Van Den Bossche, Maarten J.; Sabbe, Bernard G.] Univ Antwerp, Collaborat Antwerp Psychiat Res Inst, B-2610 Antwerp, Belgium.
   [Johnstone, Mandy; Pickard, Benjamin S.] Univ Edinburgh, Western Gen Hosp, Mol Med Ctr, Inst Genet & Mol Med, Edinburgh, Midlothian, Scotland.
   [Johnstone, Mandy; Blackwood, Douglas] Univ Edinburgh, Royal Edinburgh Hosp, Div Psychiat, Edinburgh, Midlothian, Scotland.
   [Nordin, Annelie; Norrback, Karl-Fredrik; Adolfsson, Rolf] Umea Univ, Dept Clin Sci, Div Psychiat, Umea, Sweden.
   [Souery, Daniel] Univ Libre Brussels, Lab Psychol Med, Brussels, Belgium.
   [Souery, Daniel] Ctr Europeen Psychol Med PsyPluriel, Brussels, Belgium.
   [Sabbe, Bernard G.] Psychiat Hosp Sint Norbertus, Duffel, Belgium.
RP Del-Favero, J (reprint author), Univ Antwerp, Appl Mol Genom Grp, VIB Dept Mol Genet, Campus Drie Eiken,Univ Pl 1, B-2610 Antwerp, Belgium.
EM jurgen.delfavero@molgen.vib-ua.be
RI Sabbe, Bernard/J-3598-2013
OI Sabbe, Bernard/0000-0002-1426-802X
FU Swedish Research Council [2006-4472, 2009-5269, 345-2003-3883,
   315-2004-6977]; County Council of Vasterbotten, Sweden; County Council
   of Norrbotten, Sweden; Fund for Scientific Research Flanders (FWO-F);
   Institute for the Promotion of Innovation Through Science and Technology
   in Flanders (IWT-F); Chief Scientist Office, Scotland [CZB_4_610];
   Academy of Medical Sciences/Wellcome Trust; RS MacDonald Charitable
   Trust
FX Grant sponsor: Swedish Research Council; Grant numbers: 2006-4472,
   2009-5269, 345-2003-3883, 315-2004-6977; Grant sponsor: County Councils
   of Vasterbotten and Norrbotten, Sweden; Grant sponsor: Fund for
   Scientific Research Flanders (FWO-F); Grant sponsor: Institute for the
   Promotion of Innovation Through Science and Technology in Flanders
   (IWT-F); Grant sponsor: Chief Scientist Office, Scotland; Grant number:
   CZB_4_610; Grant sponsor: Academy of Medical Sciences/Wellcome Trust;
   Grant sponsor: RS MacDonald Charitable Trust.
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NR 66
TC 12
Z9 12
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1552-4841
J9 AM J MED GENET B
JI Am. J. Med. Genet. B
PD OCT
PY 2012
VL 159B
IS 7
BP 812
EP 822
DI 10.1002/ajmg.b.32088
PG 11
WC Genetics & Heredity; Psychiatry
SC Genetics & Heredity; Psychiatry
GA 007HR
UT WOS:000308879900008
PM 22911887
ER

PT J
AU Rodger, S
   Ashburner, J
   Hinder, E
AF Rodger, Sylvia
   Ashburner, Jill
   Hinder, Elizabeth
TI Sensory interventions for children: Where does our profession stand?
SO AUSTRALIAN OCCUPATIONAL THERAPY JOURNAL
LA English
DT Editorial Material
ID AUTISM SPECTRUM DISORDERS
C1 [Rodger, Sylvia] Univ Queensland, Sch Hlth & Rehabil Sci, Div Occupat Therapy, Brisbane, Qld, Australia.
   [Ashburner, Jill] Sunnybank, Autism Queensland, Brisbane, Qld, Australia.
   [Hinder, Elizabeth] Dept Educ Training & Employment, Disabil Serv Support Unit, Woolloongabba, Qld, Australia.
RP Rodger, S (reprint author), Univ Queensland, Sch Hlth & Rehabil Sci, Div Occupat Therapy, Brisbane, Qld, Australia.
EM s.rodger@uq.edu.au
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NR 8
TC 7
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0045-0766
J9 AUST OCCUP THER J
JI Aust. Occup. Ther. J.
PD OCT
PY 2012
VL 59
IS 5
BP 337
EP 338
DI 10.1111/j.1440-1630.2012.01032.x
PG 2
WC Rehabilitation
SC Rehabilitation
GA 010AO
UT WOS:000309067000001
PM 22998510
ER

PT J
AU Torres, AR
   Westover, JB
   Gibbons, C
   Johnson, RC
   Ward, DC
AF Torres, Anthony R.
   Westover, Jonna B.
   Gibbons, Cole
   Johnson, Randall C.
   Ward, David C.
TI Activating killer-cell immunoglobulin-like receptors (KIR) and their
   cognate HLA ligands are significantly increased in autism
SO BRAIN BEHAVIOR AND IMMUNITY
LA English
DT Article
DE Killer-cell immunoglobulin-like receptor; KIR genes; KIR haplotypes;
   Human leukocyte antigen; HLA ligands; Leukocyte receptor complex;
   Autism; Immune dysfunction; Natural killer cells
ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; INCREASED
   PREVALENCE; AUTOIMMUNE-DISEASES; INCREASED FREQUENCY; DIAGNOSTIC CHANGE;
   FAMILY-HISTORY; NULL ALLELE; CHILDREN; ASSOCIATION
AB Killer-cell immunoglobulin-like receptor (KIR) proteins are expressed on natural killer (NK) cells and appear important in innate and adaptive immunity. There are about 14 KIR genes on chromosome 19q13.4, composed of those that inhibit and those that activate NK cell killing. Haplotypes have different combinations of these genes meaning that not all genes are present in a subject. There are two main classes of cognate human leukocyte antigen (HLA) ligands (HLA-Bw4 and HLA-C1/C2) that bind to the inhibitory/activating receptors. As a general rule, the inhibitory state is maintained except when virally infected or tumor cells are encountered; however, both increased activation and inhibition states have been associated with susceptibility and protection against numerous disease states including cancer, arthritis, and psoriasis.
   Utilizing DNA from 158 Caucasian subjects with autism and 176 KIR control subjects we show for the first time a highly significant increase in four activating KIR genes (2DS5, 3DS1, 2DS1 and 2DS4) as measured by chi square values and odds ratios. In addition, our data suggests a highly significant increase in the activating KIR gene 2DS1 and its cognate HLA-C2 ligand (2051 + C2; p = 0.00003 [Odds ratio = 2.87]). This information ties together two major immune gene complexes, the human leukocyte complex and the leukocyte receptor complex, and may partially explain immune abnormalities observed in many subjects with autism. (c) 2012 Elsevier Inc. All fights reserved.
C1 [Torres, Anthony R.; Westover, Jonna B.; Gibbons, Cole] Utah State Univ, Ctr Persons Disabil, Logan, UT 84322 USA.
   [Gibbons, Cole] Utah State Univ, Dept Bioengn, Logan, UT 84322 USA.
   [Johnson, Randall C.] SAIC Frederick Inc, Frederick Natl Lab Canc Res, BSP CCR Genet Core, Frederick, MD 21702 USA.
   [Johnson, Randall C.] Conservatoire Natl Arts & Metiers, Chaire Bioinformat, Paris, France.
   [Ward, David C.] Utah State Univ, Ctr Adv Nutr, Logan, UT 84322 USA.
RP Torres, AR (reprint author), Utah State Univ, Ctr Persons Disabil, 6804 Old Main Hill, Logan, UT 84322 USA.
EM Anthony.Torres@usu.edu
RI Johnson, Randall/B-1517-2014
OI Johnson, Randall/0000-0001-7754-0847
FU Early Markers for Autism NIH grant [RO1-ESO16669]; Utah Science
   Technology and Research (USTAR) initiative at Utah State University;
   Utah Autism Foundation (SLC, Utah); Frederick National Laboratory for
   Cancer Research; National Institutes of Health [HHSN261200800001E];
   Intramural Research Program of NIH; Frederick National Laboratory;
   Center for Cancer Research
FX We gratefully acknowledge the resources provided by the ACRE Consortium
   and the participating AGRE families. Funding was provided [in part] by
   the Early Markers for Autism NIH grant RO1-ESO16669, the Utah Science
   Technology and Research (USTAR) initiative at Utah State University, and
   the Utah Autism Foundation (SLC, Utah). This project also received
   Federal funding [in part] from the Frederick National Laboratory for
   Cancer Research, National Institutes of Health, under contract
   HHSN261200800001E. This research was also supported [in part] by the
   Intramural Research Program of NIH, Frederick National Laboratory,
   Center for Cancer Research. The content of this publication does not
   necessarily reflect the views of policies of the Department of Health
   and Human Services, nor does its mention of trade names, commercial
   products or organizations imply endorsement of the US Government.
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NR 46
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 0889-1591
J9 BRAIN BEHAV IMMUN
JI Brain Behav. Immun.
PD OCT
PY 2012
VL 26
IS 7
BP 1122
EP 1127
DI 10.1016/j.bbi.2012.07.014
PG 6
WC Immunology; Neurosciences
SC Immunology; Neurosciences & Neurology
GA 007PC
UT WOS:000308899600015
PM 22884899
ER

PT J
AU Zwaigenbaum, L
AF Zwaigenbaum, Lonnie
TI What's in a name: changing the terminology of autism diagnosis
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Editorial Material
ID SPECTRUM DISORDERS; DSM-5; CRITERIA
C1 Univ Alberta, Dept Pediat, Edmonton, AB, Canada.
RP Zwaigenbaum, L (reprint author), Univ Alberta, Dept Pediat, Edmonton, AB, Canada.
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NR 9
TC 4
Z9 4
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1622
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD OCT
PY 2012
VL 54
IS 10
BP 871
EP 872
DI 10.1111/j.1469-8749.2012.04424.x
PG 2
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 003UJ
UT WOS:000308636600001
PM 22963446
ER

PT J
AU Van Balkom, IDC
   Vuijk, PJ
   Franssens, M
   Hoek, HW
   Hennekam, RCM
AF Van Balkom, Ingrid D. C.
   Vuijk, Pieter Jelle
   Franssens, Marijke
   Hoek, Hans W.
   Hennekam, Raoul C. M.
TI Development, cognition, and behaviour in Pitt-Hopkins syndrome
SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY
LA English
DT Article
ID MENTAL-RETARDATION; INTELLECTUAL DISABILITY; INTERSTITIAL DELETION;
   TRANSCRIPTION FACTOR; TCF4 MUTATIONS; AUTISM; DISORDERS;
   HAPLOINSUFFICIENCY; PHENOTYPE; INTERVIEW
AB Aim The aim of the study was to collect detailed data on behavioural, adaptive, and psychological functioning in 10 individuals with PittHopkins syndrome (PTHS), with specific attention to manifestations of autism spectrum disorder (ASD). Method The participants (four females, six males), residing in the Netherlands and Belgium, were ascertained through the Dutch national PTHS support group. Median age of participants was 10 years, the age range was between 32 and 289 months. They underwent psychiatric examinations and neuropsychological measurements using a comprehensive assessment battery. Additionally, parental information was gathered through standardized interviews and questionnaires. Findings were compared with those from the literature. Results All participants showed profound intellectual disability, amiable demeanour with minimal maladaptive behaviours, severe impairments of communication and language, and intense, frequent motor stereotypies. Impairments in all participants were beyond what would be expected for cognitive abilities, fitting a classification of ASD. Interpretation Patients with PTHS are characterized not only by specific physical and genetic manifestations but also by specific behavioural and cognitive characteristics. Studying behaviour and cognition may improve diagnosis and prognosis, allows recognition of comorbidities, and contributes to adequate counselling of families.
C1 [Van Balkom, Ingrid D. C.; Franssens, Marijke] Lentis Psychiat Inst, Jonx Dept Youth Mental Hlth, NL-9470 AC Zuidlaren, Netherlands.
   [Van Balkom, Ingrid D. C.] Univ Groningen, Univ Med Ctr Groningen, Rob Giel Res Ctr, Groningen, Netherlands.
   [Vuijk, Pieter Jelle] Vrije Univ Amsterdam, Dept Clin Neuropsychol, Amsterdam, Netherlands.
   [Hoek, Hans W.] Parnassia Bavo Psychiat Inst, The Hague, Netherlands.
   [Hoek, Hans W.] Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA.
   [Hoek, Hans W.] Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, Groningen, Netherlands.
   [Hennekam, Raoul C. M.] Univ Amsterdam, Acad Med Ctr, Dept Pediat, NL-1105 AZ Amsterdam, Netherlands.
RP Van Balkom, IDC (reprint author), Lentis Psychiat Inst, Jonx Dept Youth Mental Hlth, POB 128, NL-9470 AC Zuidlaren, Netherlands.
EM idc.vanbalkom@lentis.nl
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NR 44
TC 8
Z9 8
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0012-1622
J9 DEV MED CHILD NEUROL
JI Dev. Med. Child Neurol.
PD OCT
PY 2012
VL 54
IS 10
BP 925
EP 931
DI 10.1111/j.1469-8749.2012.04339.x
PG 7
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 003UJ
UT WOS:000308636600015
PM 22712893
ER

PT J
AU Donohue, SE
   Darling, EF
   Mitroff, SR
AF Donohue, Sarah E.
   Darling, Elise F.
   Mitroff, Stephen R.
TI Links between multisensory processing and autism
SO EXPERIMENTAL BRAIN RESEARCH
LA English
DT Article
DE Multisensory; Autism; Auditory; Visual; Temporal
ID BRAIN-STEM RESPONSES; SPECTRUM DISORDERS; TEMPORAL WINDOW; CHILDREN;
   INTEGRATION; JUDGMENTS; SIMULTANEITY; PERCEPTION; EXPERIENCE; SYMPTOMS
AB Autism spectrum disorder is typically associated with social deficits and is often specifically linked to difficulty with processing faces and other socially relevant stimuli. Emerging research has suggested that children with autism might also have deficits in basic perceptual abilities including multisensory processing (e.g., simultaneously processing visual and auditory inputs). The current study examined the relationship between multisensory temporal processing (assessed via a simultaneity judgment task wherein participants were to report whether a visual stimulus and an auditory stimulus occurred at the same time or at different times) and self-reported symptoms of autism (assessed via the Autism Spectrum Quotient questionnaire). Data from over 100 healthy adults revealed a relationship between these two factors as multisensory timing perception correlated with symptoms of autism. Specifically, a stronger bias to perceive auditory stimuli occurring before visual stimuli as simultaneous was associated with greater levels of autistic symptoms. Additional data and analyses confirm that this relationship is specific to multisensory processing and symptoms of autism. These results provide insight into the nature of multisensory processing while also revealing a continuum over which perceptual abilities correlate with symptoms of autism and that this continuum is not just specific to clinical populations but is present within the general population.
C1 [Donohue, Sarah E.; Darling, Elise F.; Mitroff, Stephen R.] Duke Univ, Ctr Cognit Neurosci, LSRC, Durham, NC 27708 USA.
   [Donohue, Sarah E.] Duke Univ, Dept Neurobiol, Durham, NC USA.
   [Darling, Elise F.; Mitroff, Stephen R.] Duke Univ, Dept Psychol & Neurosci, Durham, NC USA.
RP Donohue, SE (reprint author), Duke Univ, Ctr Cognit Neurosci, LSRC, Box 90999, Durham, NC 27708 USA.
EM sarah.donohue@duke.edu
FU National Science Graduate Research Fellowship; Army Research Office
   [54528LS]; Institute for Homeland Security Solutions; Human Factors
   Division in the Department of Homeland Security (DHS); DHS
   [HSHQDC-08-C-00100]
FX We thank Matthew S. Cain for assistance with data analysis and helpful
   comments on this manuscript, Kait Clark for assistance with the
   visual-visual temporal-order judgment task, and Matthew Forester, Edward
   Liu, and Sylvia Nantier for assistance with data acquisition. This work
   was supported by a National Science Graduate Research Fellowship award
   to S. E. D. and was partially supported by the Army Research Office
   (#54528LS) and partially through a subcontract with the Institute for
   Homeland Security Solutions, a research consortium sponsored by the
   Human Factors Division in the Department of Homeland Security (DHS).
   This material is based upon work supported by the DHS under Contract No.
   HSHQDC-08-C-00100. Any opinions, findings, and conclusions or
   recommendations expressed in this material are those of the authors and
   do not necessarily reflect the official policy or position of DHS or of
   the US Government. The study is approved for public release.
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NR 48
TC 12
Z9 12
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0014-4819
J9 EXP BRAIN RES
JI Exp. Brain Res.
PD OCT
PY 2012
VL 222
IS 4
BP 377
EP 387
DI 10.1007/s00221-012-3223-4
PG 11
WC Neurosciences
SC Neurosciences & Neurology
GA 014DI
UT WOS:000309354900005
PM 22923209
ER

PT J
AU Matone, M
   Localio, R
   Huang, YS
   dosReis, S
   Feudtner, C
   Rubin, D
AF Matone, Meredith
   Localio, Russell
   Huang, Yuan-Shung
   dosReis, Susan
   Feudtner, Chris
   Rubin, David
TI The Relationship between Mental Health Diagnosis and Treatment with
   Second-Generation Antipsychotics over Time: A National Study of US
   Medicaid-Enrolled Children
SO HEALTH SERVICES RESEARCH
LA English
DT Article
DE Antipsychotics; mental health; pediatrics; Medicaid
ID PSYCHOTROPIC MEDICATIONS; ATYPICAL ANTIPSYCHOTICS; TRENDS; ADOLESCENTS;
   MANAGEMENT; SAFETY; YOUTH; RISPERIDONE; DISORDERS; PATTERNS
AB Objective To describe the relationship between mental health diagnosis and treatment with antipsychotics among U.S. Medicaid-enrolled children over time. Data Sources/Study Setting Medicaid Analytic Extract (MAX) files for 50 states and the District of Columbia from 2002 to 2007. Study Design Repeated cross-sectional design. Using logistic regression, outcomes of mental health diagnosis and filled prescriptions for antipsychotics were standardized across demographic and service use characteristics and reported as probabilities across age groups over time. Data Collection Center for Medicaid Services data extracted by means of age, ICD-9 codes, service use intensity, and National Drug Classification codes. Principal Findings Antipsychotic use increased by 62 percent, reaching 354,000 youth by 2007 (2.4 percent). Although youth with bipolar disorder, schizophrenia, and autism proportionally were more likely to receive antipsychotics, youth with attention deficit hyperactivity disorder (ADHD) and those with three or more mental health diagnoses were the largest consumers of antipsychotics over time; by 2007, youth with ADHD accounted for 50 percent of total antipsychotic use; 1 in 7 antipsychotic users were youth with ADHD as their only diagnosis. Conclusions In the context of safety concerns, disproportionate antipsychotic use among youth with nonapproved indications illustrates the need for more generalized efficacy data in pediatric populations.
C1 [Matone, Meredith; Feudtner, Chris; Rubin, David] Childrens Hosp Philadelphia, PolicyLab, Philadelphia, PA 19104 USA.
   [Localio, Russell] Univ Penn, Dept Biostat & Epidemiol, Perelman Sch Med, Philadelphia, PA 19104 USA.
   [Huang, Yuan-Shung; Feudtner, Chris; Rubin, David] Childrens Hosp Philadelphia, Div Gen Pediat, Philadelphia, PA 19104 USA.
   [dosReis, Susan] Univ Maryland, Sch Pharm, Dept Pharmaceut Hlth Serv Res, Baltimore, MD 21201 USA.
   [Feudtner, Chris; Rubin, David] Univ Penn, Dept Pediat, Perelman Sch Med, Philadelphia, PA 19104 USA.
RP Rubin, D (reprint author), Childrens Hosp Philadelphia, PolicyLab, CHOP N Room 1533,34th & Civ Ctr Blvd, Philadelphia, PA 19104 USA.
EM Rubin@email.chop.edu
FU Agency for Healthcare Research and Quality [5R01HS018550]; Stoneleigh
   Foundation
FX This study was funded by grant 5R01HS018550 from the Agency for
   Healthcare Research and Quality and a fellowship to Dr. David Rubin from
   the Stoneleigh Foundation. The findings have been presented at the June
   2012 Academy Health Annual Research Meeting, Orlando, FL.
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NR 32
TC 21
Z9 21
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0017-9124
J9 HEALTH SERV RES
JI Health Serv. Res.
PD OCT
PY 2012
VL 47
IS 5
BP 1836
EP 1860
DI 10.1111/j.1475-6773.2012.01461.x
PG 25
WC Health Care Sciences & Services; Health Policy & Services
SC Health Care Sciences & Services
GA 008PR
UT WOS:000308969500006
PM 22946905
ER

PT J
AU Szymanski, CA
   Brice, PJ
   Lam, KH
   Hotto, SA
AF Szymanski, Christen A.
   Brice, Patrick J.
   Lam, Kay H.
   Hotto, Sue A.
TI Deaf Children with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Hearing loss; Deaf; Annual Survey
ID PERVASIVE DEVELOPMENTAL DISORDERS; HEARING-LOSS; MULTIPLE DISABILITIES;
   LANGUAGE-DEVELOPMENT; COCHLEAR IMPLANTS; SIGN LANGUAGE; COMMUNICATION;
   EPIDEMIOLOGY; IMPAIRMENT; STUDENTS
AB Epidemiological studies investigating the prevalence of autism have increased in recent years, within the United States and abroad. However, statistics as to how many of those children may also have a comorbid hearing loss is lacking. The prevalence of school-administrator reported diagnosis of autism spectrum disorders (clinical diagnosis [DSM-IV] and/or IDEA classification) among children with hearing loss in the US was estimated from the 2009-2010 Annual Survey of Deaf and Hard of Hearing Children and Youth conducted by the Gallaudet Research Institute. Results indicate that during the 2009-2010 school year 1 in 59 children (specifically 8-year olds) with hearing loss were also receiving services for autism; considerably higher, than reported national estimates of 1 in 91 (Kogan et al. in Pediatrics 124(4):1-8, 2009) and 1 in 110 (CDC 2007) for hearing children. Significantly more children with profound hearing loss had a comorbid diagnosis of autism than those with milder forms of hearing loss. These results are discussed, while highlighting the need for increased awareness and research in a population that has thus far received little services or attention.
C1 [Szymanski, Christen A.] Gallaudet Univ, Laurent Clerc Natl Deaf Educ Ctr, Washington, DC 20002 USA.
   [Brice, Patrick J.] Gallaudet Univ, Dept Psychol, Washington, DC 20002 USA.
   [Lam, Kay H.; Hotto, Sue A.] Gallaudet Univ, Gallaudet Res Inst, Washington, DC 20002 USA.
RP Szymanski, CA (reprint author), Gallaudet Univ, Laurent Clerc Natl Deaf Educ Ctr, 800 Florida Ave NE, Washington, DC 20002 USA.
EM Christen.Szymanski@gallaudet.edu
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NR 60
TC 21
Z9 21
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2027
EP 2037
DI 10.1007/s10803-012-1452-9
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600001
PM 22290585
ER

PT J
AU Moore, DJ
   Heavey, L
   Reidy, J
AF Moore, David J.
   Heavey, Lisa
   Reidy, John
TI Attentional Processing of Faces in ASD: A Dot-Probe Study
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Attention; Social; Faces; Dot-Probe
ID AUTISM SPECTRUM DISORDER; ASPERGER-SYNDROME; SELECTIVE ATTENTION;
   EYE-MOVEMENTS; BIAS; ANXIETY; THREAT; INDIVIDUALS; PERCEPTION; AWARENESS
AB The present study used the Dot-Probe paradigm to explore attentional allocation to faces compared with non-social images in high-functioning individuals with autism spectrum disorder (ASD) and typically developing controls. There was no evidence of attentional bias in either group when stimuli were presented at individually calculated sub-threshold levels. However, at supra-threshold presentation (200 ms), a face bias was found for control participants but not for those with ASD. These results add to evidence of reduced social interest in ASD, relative to controls, and further demonstrate when atypical social processing arises in the attentional time course.
C1 [Moore, David J.; Heavey, Lisa; Reidy, John] Sheffield Hallam Univ, Dept Psychol Sociol & Polit, Fac Dev & Soc, Sheffield S10 2LD, S Yorkshire, England.
RP Heavey, L (reprint author), Sheffield Hallam Univ, Dept Psychol Sociol & Polit, Fac Dev & Soc, Collegiate Crescent Campus, Sheffield S10 2LD, S Yorkshire, England.
EM l.reidy@shu.ac.uk
CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
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NR 36
TC 4
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2038
EP 2045
DI 10.1007/s10803-012-1449-4
PG 8
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600002
PM 22278029
ER

PT J
AU Scheeren, AM
   Koot, HM
   Begeer, S
AF Scheeren, Anke M.
   Koot, Hans M.
   Begeer, Sander
TI Social Interaction Style of Children and Adolescents with
   High-Functioning Autism Spectrum Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Social subtype; Social interaction
ID PERVASIVE DEVELOPMENTAL DISORDER; QUALITY-OF-LIFE;
   INDIVIDUAL-DIFFERENCES; ASPERGER-SYNDROME; VALIDITY; SELF;
   SUBCLASSIFICATION; CLASSIFICATION; QUESTIONNAIRE; RELIABILITY
AB Qualitative differences in social interaction style exist within the autism spectrum. In this study we examined whether these differences are associated with (1) the severity of autistic symptoms and comorbid disruptive behavior problems, (2) the child's psycho-social health, and (3) executive functioning and perspective taking skills. The social interaction style of 156 children and adolescents (6-19 years) with high-functioning autism spectrum disorder (HFASD) was determined with the Wing Subgroups Questionnaire. An active-but-odd social interaction style was positively associated with symptoms of autism, attention deficit and hyperactivity. Furthermore, an active-but-odd social interaction style was negatively associated with children's psycho-social health and positively with executive functioning problems. Social interaction style explains part of the heterogeneity among children with HFASD.
C1 [Scheeren, Anke M.; Koot, Hans M.; Begeer, Sander] Vrije Univ Amsterdam, Dept Dev Psychol, NL-1081 BT Amsterdam, Netherlands.
RP Scheeren, AM (reprint author), Vrije Univ Amsterdam, Dept Dev Psychol, Van der Boechorststr 1, NL-1081 BT Amsterdam, Netherlands.
EM A.M.Scheeren@vu.nl
RI Begeer, Sander/I-3383-2012
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NR 40
TC 10
Z9 10
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2046
EP 2055
DI 10.1007/s10803-012-1451-x
PG 10
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600003
ER

PT J
AU Goodman, SJ
   Glenwick, DS
AF Goodman, Sabrina J.
   Glenwick, David S.
TI Correlates of Attachment Perceptions in Parents of Children with Autism
   Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorders; Attachment; Parenting stress; Parent
   cognitions; Parent perceptions
ID TO-INFANT ATTACHMENT; SOCIAL DESIRABILITY; CHILDHOOD AUTISM; FAMILY
   STRESS; DOWN-SYNDROME; MOTHERS; QUESTIONNAIRE; SCALE; EFFICACY; FATHERS
AB This study explored the relationship between parents' perceptions of their child's attachment to them and parents' own affective attachment to their child, as well the relationship of these constructs to parenting stress, parent-rated child functional impairment, and parenting sense of competence. Mothers (n = 76) and fathers (n = 30) of children ages 2-10 with autism spectrum disorders participated. Overall, parents' affective attachment to their child was more consistently related to other aspects of their parenting experiences than were their perceptions of their child's attachment to them. Also, perceptions of child-to-parent attachment were related to other aspects of parenting for fathers more than for mothers. Implications for parenting interventions and future research, such as longitudinal investigations, are discussed.
C1 [Goodman, Sabrina J.] Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA.
   [Goodman, Sabrina J.; Glenwick, David S.] Fordham Univ, Dept Psychol, Bronx, NY 10458 USA.
RP Goodman, SJ (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1160 5th Ave, New York, NY 10029 USA.
EM sagoodman@fordham.edu; glenwick@fordham.edu
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NR 57
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2056
EP 2066
DI 10.1007/s10803-012-1453-8
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600004
ER

PT J
AU Taylor, LJ
   Maybery, MT
   Whitehouse, AJO
AF Taylor, Lauren J.
   Maybery, Murray T.
   Whitehouse, Andrew J. O.
TI Do Children with Specific Language Impairment have a Cognitive Profile
   Reminiscent of Autism? A Review of the Literature
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Specific language impairment; Cognition; Etiological overlap
ID HIGH-FUNCTIONING AUTISM; WEAK CENTRAL COHERENCE; EARLY ADULT LIFE;
   SPECTRUM DISORDERS; EXECUTIVE FUNCTION; ASPERGER-SYNDROME; INNER SPEECH;
   SOCIAL COGNITION; FALSE-BELIEF; EMOTIONAL-REACTIONS
AB There is debate regarding the relationship between autism and specific language impairment (SLI), with some researchers proposing aetiological overlap between the conditions and others maintaining their aetiological distinction. Although considerable research has investigated the language phenotypes of these disorders, the relationship between the cognitive phenotypes has been left relatively unexplored. This paper reviews relevant literature on whether individuals with SLI exhibit cognitive characteristics reminiscent of autism. Overall, findings are inconsistent and there is a lack of substantive evidence supporting overlapping cognitive phenotypes in autism and SLI. Better powered and more rigorous experimental designs, as well as studies directly comparing the cognitive phenotype of children with SLI and those with autism will further elucidate the aetiological relationship between these two conditions.
C1 [Taylor, Lauren J.; Maybery, Murray T.; Whitehouse, Andrew J. O.] Univ Western Australia, Neurocognit Dev Unit, Sch Psychol, Crawley, WA 6009, Australia.
   [Taylor, Lauren J.; Whitehouse, Andrew J. O.] Univ Western Australia, Ctr Child Hlth Res, Crawley, WA 6009, Australia.
RP Taylor, LJ (reprint author), Univ Western Australia, Neurocognit Dev Unit, Sch Psychol, M304,35 Stirling Highway, Crawley, WA 6009, Australia.
EM lauren.taylor@uwa.edu.au
RI Maybery, Murray/H-5390-2014
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NR 101
TC 5
Z9 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2067
EP 2083
DI 10.1007/s10803-012-1456-5
PG 17
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600005
ER

PT J
AU Hume, K
   Plavnick, J
   Odom, SL
AF Hume, Kara
   Plavnick, Joshua
   Odom, Samuel L.
TI Promoting Task Accuracy and Independence in Students with Autism Across
   Educational Setting Through the Use of Individual Work Systems
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Work systems; Independence; Accuracy; Generalization; Division
   TEACCH
ID TEACHING-CHILDREN; DISABILITIES
AB Strategies that promote the independent demonstration of skills across educational settings are critical for improving the accessibility of general education settings for students with ASD. This research assessed the impact of an individual work system on the accuracy of task completion and level of adult prompting across educational setting. Student accuracy and adult prompting were measured in both special and general education settings during academic work periods. Work systems, an element of structured teaching developed by Division TEACCH, are organized sets of visual information that inform a student about participation in work areas. A multiple-probe-across-participants design was used to evaluate the effects of the individual work systems. All participants demonstrated increased accuracy yet required less adult support across special and general education settings. Results were maintained when measured during a 1-month follow-up probe.
C1 [Hume, Kara; Odom, Samuel L.] Univ N Carolina, Frank Porter Graham Child Dev Inst, Carrboro, NC 27510 USA.
   [Plavnick, Joshua] Michigan State Univ, Sch Educ, E Lansing, MI 48824 USA.
RP Hume, K (reprint author), Univ N Carolina, Frank Porter Graham Child Dev Inst, 517 S Greensboro St, Carrboro, NC 27510 USA.
EM kara.hume@unc.edu
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NR 45
TC 8
Z9 8
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2084
EP 2099
DI 10.1007/s10803-012-1457-4
PG 16
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600006
ER

PT J
AU Crane, L
   Pring, L
   Jukes, K
   Goddard, L
AF Crane, Laura
   Pring, Linda
   Jukes, Kaylee
   Goddard, Lorna
TI Patterns of Autobiographical Memory in Adults with Autism Spectrum
   Disorder
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Autobiographical memory; Sensory; Imageability; Frequency
ID ASPERGER-SYNDROME; EPISODIC MEMORY; AMNESIA; IMAGERY; EVENTS; SELF; AQ
AB Two studies are presented that explored the effects of experimental manipulations on the quality and accessibility of autobiographical memories in adults with autism spectrum disorder (ASD), relative to a typical comparison group matched for age, gender and IQ. Both studies found that the adults with ASD generated fewer specific memories than the comparison group, and took significantly longer to do so. Despite this, experimental manipulations affected two indices of autobiographical memory (specificity and retrieval latency) similarly in both groups. These results suggest that adults with ASD experience a quantitative reduction in the speed and specificity of autobiographical memory retrieval, but that when they do retrieve these memories, they do so in a way that is qualitatively similar to that of typical adults.
C1 [Crane, Laura; Pring, Linda; Jukes, Kaylee; Goddard, Lorna] Univ London, Dept Psychol, London SE14 6NW, England.
   [Crane, Laura] London S Bank Univ, London, England.
RP Crane, L (reprint author), Univ London, Dept Psychol, London SE14 6NW, England.
EM L.Crane@gold.ac.uk
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NR 41
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2100
EP 2112
DI 10.1007/s10803-012-1459-2
PG 13
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600007
PM 22322581
ER

PT J
AU Ray-Subramanian, CE
   Weismer, SE
AF Ray-Subramanian, Corey E.
   Weismer, Susan Ellis
TI Receptive and Expressive Language as Predictors of Restricted and
   Repetitive Behaviors in Young Children with Autism Spectrum Disorders
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Restricted and repetitive behaviors (RRBs); Language; Autism; Nonverbal
   cognitive skills; Toddlers; Preschoolers
ID DIAGNOSTIC-OBSERVATION-SCHEDULE; REVISED ALGORITHMS; TODDLERS; ADOS;
   PRESCHOOLERS; ASSOCIATION
AB This study examined whether language skills and nonverbal cognitive skills were associated with clinician-observed restricted and repetitive behaviors (RRBs) in a sample of 115 children with autism spectrum disorders (ASD) at ages 2 and 3. By age 3, RRBs were significantly negatively correlated with receptive and expressive language, as well as nonverbal cognitive skills. Increases in receptive and expressive language from age 2 to 3 significantly predicted decreases in RRBs, controlling for age in months, time between visits, and gains in nonverbal cognitive skills. This study contributes to the limited research that has examined early patterns and predictors of RRBs in young children with ASD.
C1 [Ray-Subramanian, Corey E.; Weismer, Susan Ellis] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
   [Weismer, Susan Ellis] Univ Wisconsin, Dept Commun Disorders, Madison, WI 53705 USA.
RP Ray-Subramanian, CE (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave, Madison, WI 53705 USA.
EM cray@wisc.edu
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NR 28
TC 6
Z9 6
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2113
EP 2120
DI 10.1007/s10803-012-1463-6
PG 8
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600008
PM 22350337
ER

PT J
AU Schendel, DE
   DiGuiseppi, C
   Croen, LA
   Fallin, MD
   Reed, PL
   Schieve, LA
   Wiggins, LD
   Daniels, J
   Grether, J
   Levy, SE
   Miller, L
   Newschaffer, C
   Pinto-Martin, J
   Robinson, C
   Windham, GC
   Alexander, A
   Aylsworth, AS
   Bernal, P
   Bonner, JD
   Blaskey, L
   Bradley, C
   Collins, J
   Ferretti, CJ
   Farzadegan, H
   Giarelli, E
   Harvey, M
   Hepburn, S
   Herr, M
   Kaparich, K
   Landa, R
   Lee, LC
   Levenseller, B
   Meyerer, S
   Rahbar, MH
   Ratchford, A
   Reynolds, A
   Rosenberg, S
   Rusyniak, J
   Shapira, SK
   Smith, K
   Souders, M
   Thompson, PA
   Young, L
   Yeargin-Allsopp, M
AF Schendel, Diana E.
   DiGuiseppi, Carolyn
   Croen, Lisa A.
   Fallin, M. Daniele
   Reed, Philip L.
   Schieve, Laura A.
   Wiggins, Lisa D.
   Daniels, Julie
   Grether, Judith
   Levy, Susan E.
   Miller, Lisa
   Newschaffer, Craig
   Pinto-Martin, Jennifer
   Robinson, Cordelia
   Windham, Gayle C.
   Alexander, Aimee
   Aylsworth, Arthur S.
   Bernal, Pilar
   Bonner, Joseph D.
   Blaskey, Lisa
   Bradley, Chyrise
   Collins, Jack
   Ferretti, Casara J.
   Farzadegan, Homayoon
   Giarelli, Ellen
   Harvey, Marques
   Hepburn, Susan
   Herr, Matthew
   Kaparich, Kristina
   Landa, Rebecca
   Lee, Li-Ching
   Levenseller, Brooke
   Meyerer, Stacey
   Rahbar, Mohammad H.
   Ratchford, Andria
   Reynolds, Ann
   Rosenberg, Steven
   Rusyniak, Julie
   Shapira, Stuart K.
   Smith, Karen
   Souders, Margaret
   Thompson, Patrick Aaron
   Young, Lisa
   Yeargin-Allsopp, Marshalyn
TI The Study to Explore Early Development (SEED): A Multisite Epidemiologic
   Study of Autism by the Centers for Autism and Developmental Disabilities
   Research and Epidemiology (CADDRE) Network
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Epidemiology; Study methods; Risk factors; Phenotype
ID PERINATAL RISK-FACTORS; SOCIAL COMMUNICATION QUESTIONNAIRE; DIAGNOSTIC
   OBSERVATION SCHEDULE; HAZARDOUS AIR-POLLUTANTS; SPECTRUM DISORDERS;
   INFANTILE-AUTISM; TWIN PAIRS; CYTOMEGALOVIRUS-INFECTION;
   GASTROINTESTINAL SYMPTOMS; ENVIRONMENTAL-FACTORS
AB The Study to Explore Early Development (SEED), a multisite investigation addressing knowledge gaps in autism phenotype and etiology, aims to: (1) characterize the autism behavioral phenotype and associated developmental, medical, and behavioral conditions and (2) investigate genetic and environmental risks with emphasis on immunologic, hormonal, gastrointestinal, and sociodemographic characteristics. SEED uses a case-control design with population-based ascertainment of children aged 2-5 years with an autism spectrum disorder (ASD) and children in two control groups-one from the general population and one with non-ASD developmental problems. Data from parent-completed questionnaires, interviews, clinical evaluations, biospecimen sampling, and medical record abstraction focus on the prenatal and early postnatal periods. SEED is a valuable resource for testing hypotheses regarding ASD characteristics and causes.
C1 [Schendel, Diana E.; Croen, Lisa A.; Wiggins, Lisa D.; Alexander, Aimee; Harvey, Marques; Shapira, Stuart K.; Yeargin-Allsopp, Marshalyn] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30333 USA.
   [DiGuiseppi, Carolyn] Univ Colorado, Dept Epidemiol, Colorado Sch Publ Hlth, Denver, CO 80202 USA.
   [Croen, Lisa A.; Collins, Jack] Kaiser Permanente No Calif, Div Res, Oakland, CA USA.
   [Fallin, M. Daniele; Farzadegan, Homayoon; Lee, Li-Ching; Meyerer, Stacey] Johns Hopkins Univ, Dept Epidemiol, Bloomberg Sch Publ Hlth, Baltimore, MD USA.
   [Reed, Philip L.; Bonner, Joseph D.; Thompson, Patrick Aaron] Michigan State Univ, Clin & Translat Sci Inst, E Lansing, MI 48824 USA.
   [Daniels, Julie; Bradley, Chyrise; Herr, Matthew] Univ N Carolina, Dept Epidemiol, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
   [Daniels, Julie] Univ N Carolina, Dept Maternal & Child Hlth, Gillings Sch Global Publ Hlth, Chapel Hill, NC USA.
   [Grether, Judith; Windham, Gayle C.; Smith, Karen] CA Dept Publ Hlth, Div Environm & Occupat Dis Control, Oakland, CA USA.
   [Levy, Susan E.; Blaskey, Lisa; Ferretti, Casara J.] Childrens Hosp Philadelphia, Ctr Autism, Philadelphia, PA 19104 USA.
   [Miller, Lisa; Ratchford, Andria] Colorado Dept Publ Hlth & Environm, Denver, CO USA.
   [Newschaffer, Craig] Drexel Univ, Dept Epidemiol & Biostat, Sch Publ Hlth, Philadelphia, PA 19104 USA.
   [Pinto-Martin, Jennifer; Giarelli, Ellen; Levenseller, Brooke; Souders, Margaret; Young, Lisa] Univ Penn, Sch Nursing, Philadelphia, PA 19104 USA.
   [Pinto-Martin, Jennifer] Sch Med, Philadelphia, PA USA.
   [Robinson, Cordelia; Hepburn, Susan; Kaparich, Kristina; Reynolds, Ann; Rosenberg, Steven] Univ Colorado, Sch Med, Denver, CO USA.
   [Aylsworth, Arthur S.] Univ N Carolina, Sch Med, Dept Pediat, Chapel Hill, NC USA.
   [Aylsworth, Arthur S.] Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC USA.
   [Bernal, Pilar] Kaiser Permanente No Calif, Autism Spectrum Disorders Ctr, San Jose Med Ctr, Oakland, CA USA.
   [Rahbar, Mohammad H.] Univ Texas Houston, Sch Publ Hlth, Div Epidemiol Human Genet & Environm Sci, Houston, TX USA.
   [Landa, Rebecca; Rusyniak, Julie] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA.
   [Landa, Rebecca; Rusyniak, Julie] Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD USA.
RP Schendel, DE (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, 1600 Clifton Rd,MS E-86, Atlanta, GA 30333 USA.
EM dschendel@cdc.gov
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NR 104
TC 3
Z9 4
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2121
EP 2140
DI 10.1007/s10803-012-1461-8
PG 20
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600009
PM 22350336
ER

PT J
AU Altgassen, M
   Koban, N
   Kliegel, M
AF Altgassen, Mareike
   Koban, Nancy
   Kliegel, Matthias
TI Do Adults with Autism Spectrum Disorders Compensate in Naturalistic
   Prospective Memory Tasks?
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Prospective memory; Executive functions; PDD; Monitoring
ID EXECUTIVE FUNCTION; ASPERGERS-SYNDROME; NONRETARDED-CHILDREN;
   OLDER-ADULTS; RECALL; AGE; RECOGNITION; PERFORMANCE; DYSFUNCTION;
   MANAGEMENT
AB The present study is the first to directly compare event- and time-based prospective memory in Autism Spectrum Disorders (ASD) using a contextual task mirroring real life demands of prospective memory. Twenty-five individuals with ASD and 25 age- and ability-matched controls completed the Dresden Breakfast task which required participants to prepare breakfast following a set of rules and time restrictions. Overall, adults with ASD had less correct time- and event-based prospective memory responses in comparison to controls, which is consistent with previous research in children with ASD. Moreover, ASD participants completed fewer tasks, followed rules less closely, and monitored the elapsing time less closely than controls. Individuals with ASD seem not to be compensating in naturalistic prospective memory tasks.
C1 [Altgassen, Mareike; Koban, Nancy; Kliegel, Matthias] Tech Univ Dresden, Dept Psychol, D-01062 Dresden, Germany.
   [Kliegel, Matthias] Univ Geneva, Dept Psychol, Geneva, Switzerland.
RP Altgassen, M (reprint author), Tech Univ Dresden, Dept Psychol, D-01062 Dresden, Germany.
EM altgassen@psychologie.tu-dresden.de
RI Altgassen, Mareike/J-3048-2012
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NR 72
TC 11
Z9 11
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2141
EP 2151
DI 10.1007/s10803-012-1466-3
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600010
PM 22350339
ER

PT J
AU Wong, C
   Kasari, C
AF Wong, Connie
   Kasari, Connie
TI Play and Joint Attention of Children with Autism in the Preschool
   Special Education Classroom
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Play; Joint attention; Engagement; Preschool special education
ID SYMBOLIC PLAY; SPECTRUM-DISORDER; YOUNG-CHILDREN; LANGUAGE;
   INTERVENTION; ENGAGEMENT; TODDLERS; BEHAVIOR; INFANT; SKILLS
AB The purpose of this study was to examine play and joint attention in children with autism (n=27) as compared to children with other developmental delays (n=28) in public preschool special education classrooms. The participants were observed in their classroom environment for 2 h over 3 separate days. Results show that children with autism spent more of their time unengaged and less time engaged in symbolic play and joint attention behaviors as compared to children with other developmental delays. Additionally, teachers seldom focused directly on symbolic play and joint attention in their teaching. These findings suggest the importance of educating teachers to target play and joint attention skills in their preschool special education classes, specifically for children with autism.
C1 [Wong, Connie] Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC 27510 USA.
   [Kasari, Connie] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA USA.
RP Wong, C (reprint author), Univ N Carolina, Frank Porter Graham Child Dev Inst, CB8040, Chapel Hill, NC 27510 USA.
EM connie.wong@unc.edu
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NR 47
TC 12
Z9 12
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2152
EP 2161
DI 10.1007/s10803-012-1467-2
PG 10
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600011
PM 22350340
ER

PT J
AU Mattila, ML
   Jussila, K
   Linna, SL
   Kielinen, M
   Bloigu, R
   Kuusikko-Gauffin, S
   Joskitt, L
   Ebeling, H
   Hurtig, T
   Moilanen, I
AF Mattila, Marja-Leena
   Jussila, Katja
   Linna, Sirkka-Liisa
   Kielinen, Marko
   Bloigu, Risto
   Kuusikko-Gauffin, Sanna
   Joskitt, Leena
   Ebeling, Hanna
   Hurtig, Tuula
   Moilanen, Irma
TI Validation of the Finnish Autism Spectrum Screening Questionnaire (ASSQ)
   for Clinical Settings and Total Population Screening
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Asperger's syndrome; Autism; Autism Spectrum
   Screening Questionnaire; ASSQ; Validation
ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM;
   ASPERGER-SYNDROME; CHILDREN; EPIDEMIOLOGY; DIAGNOSIS; CRITERIA
AB We assessed the validity and determined cut-off scores for the Finnish Autism Spectrum Screening Questionnaire (ASSQ). A population sample of 8-year-old children (n = 4,408) was rated via the ASSQ by parents and/or teachers, and a subgroup of 104 children was examined via structured interview, semi-structured observation, IQ measurement, school observation, and medical records. Autism spectrum disorders (ASDs) were diagnosed following DSM-IV-TR criteria. A search for hospital-registered ASDs was performed. For Finnish higher-functioning primary school-aged, 7- to 12-year-olds, the optimal cut-off score was 30 in clinical settings and 28 in total population screening using summed ASSQ scores of parents' and teachers' ratings. Determining appropriate cut-off scores in ASD screening in different languages and in different cultures is of utmost importance.
C1 [Mattila, Marja-Leena; Jussila, Katja; Kuusikko-Gauffin, Sanna; Joskitt, Leena; Ebeling, Hanna; Hurtig, Tuula; Moilanen, Irma] Univ & Univ Hosp Oulu, Clin Child Psychiat, Oulu 90029, Finland.
   [Linna, Sirkka-Liisa; Hurtig, Tuula] Univ Oulu, Inst Hlth Sci, Oulu 90014, Finland.
   [Kielinen, Marko] Univ Oulu, Dept Educ Sci & Teacher Educ, Oulu 90014, Finland.
   [Bloigu, Risto] Univ Oulu, Med Informat Grp, Oulu 90014, Finland.
RP Mattila, ML (reprint author), Univ & Univ Hosp Oulu, Clin Child Psychiat, POB 26, Oulu 90029, Finland.
EM marja-leena.mattila@fimnet.fi
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NR 31
TC 3
Z9 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2162
EP 2180
DI 10.1007/s10803-012-1464-5
PG 19
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600012
PM 22461223
ER

PT J
AU Maljaars, J
   Noens, I
   Scholte, E
   van Berckelaer-Onnes, I
AF Maljaars, Jarymke
   Noens, Ilse
   Scholte, Evert
   van Berckelaer-Onnes, Ina
TI Language in Low-Functioning Children with Autistic Disorder: Differences
   Between Receptive and Expressive Skills and Concurrent Predictors of
   Language
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Intellectual disability; Receptive language; Expressive
   language; Joint attention; Symbol understanding
ID SPECTRUM DISORDERS; YOUNG-CHILDREN; JOINT ATTENTION; COMMUNICATION
   DEVELOPMENT; PRELINGUISTIC PREDICTORS; CHALLENGING BEHAVIOR; PEOPLE;
   PLAY; DISABILITIES; ACQUISITION
AB Language profiles of children with autistic disorder and intellectual disability (n = 36) were significantly different from the comparison groups of children with intellectual disability (n = 26) and typically developing children (n = 34). The group low-functioning children with autistic disorder obtained a higher mean score on expressive than on receptive language, whereas both comparison groups showed the reverse pattern. Nonverbal mental age, joint attention, and symbolic understanding of pictures were analyzed in relation to concurrent receptive and expressive language abilities. In the group with autistic disorder and intellectual disability, symbol understanding and joint attention were most strongly related to language abilities. Nonverbal mental age was the most important predictor of language abilities in the comparison groups.
C1 [Maljaars, Jarymke; Noens, Ilse] Katholieke Univ Leuven, Parenting & Special Educ Res Unit, B-3000 Louvain, Belgium.
   [Maljaars, Jarymke; Scholte, Evert; van Berckelaer-Onnes, Ina] Leiden Univ, Leiden, Netherlands.
RP Maljaars, J (reprint author), Katholieke Univ Leuven, Parenting & Special Educ Res Unit, Leopold Vanderkelenstr 32 Bus 3765, B-3000 Louvain, Belgium.
EM jarymkemaljaars@hotmail.com
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NR 69
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2181
EP 2191
DI 10.1007/s10803-012-1476-1
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600013
PM 22350453
ER

PT J
AU Markoulakis, R
   Scharoun, SM
   Bryden, PJ
   Fletcher, PC
AF Markoulakis, R.
   Scharoun, S. M.
   Bryden, P. J.
   Fletcher, P. C.
TI An Examination of Handedness and Footedness in Children with High
   Functioning Autism and Asperger Syndrome
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Motor control; Footedness; High functioning autism; Asperger's syndrome
ID CHILDHOOD AUTISM; HAND PREFERENCE; MOTOR; SKILL; IQ; PERFORMANCE;
   LATERALITY; IMPAIRMENT; PROFILES; DISORDER
AB Motor control deficits have been documented in children with high functioning autism and Asperger syndrome (HFA/AS), but the extent to which these disorders affect the children's footedness must be delineated. Twelve typically developing (TD) children and 12 children with HFA/AS, ages 6-9 years, were recruited. Motor control skills were assessed through a variety of footedness tasks to determine location and nature of impairment, regarding motor dominance. Overall, greater inconsistencies in dominance arose in children with HFA/AS, through disparities in measures of preference. Results will have broader implications for understanding motor impairments in children with HFA/AS as determined by comparing performance on footedness tasks, as well as for the design of interventions to account for these deficits.
C1 [Markoulakis, R.; Scharoun, S. M.; Bryden, P. J.; Fletcher, P. C.] Wilfrid Laurier Univ, Dept Kinesiol & Phys Educ, Waterloo, ON N2L 3G5, Canada.
   [Markoulakis, R.] Univ Toronto, Grad Dept Rehabil Sci, Toronto, ON M5G 1V7, Canada.
RP Bryden, PJ (reprint author), Wilfrid Laurier Univ, Dept Kinesiol & Phys Educ, 75 Univ Ave W, Waterloo, ON N2L 3G5, Canada.
EM pbryden@wlu.ca
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NR 31
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2192
EP 2201
DI 10.1007/s10803-012-1469-0
PG 10
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600014
PM 22350451
ER

PT J
AU Mazzone, L
   Vassena, L
   Ruta, L
   Mugno, D
   Galesi, O
   Fichera, M
AF Mazzone, Luigi
   Vassena, Lia
   Ruta, Liliana
   Mugno, Diego
   Galesi, Ornella
   Fichera, Marco
TI Brief Report: Peculiar Evolution of Autistic Behaviors in Two Unrelated
   Children with Brachidactyly-Mental Retardation Syndrome
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; 2q37 region; BDMR; Evolutionary course
ID ALBRIGHT HEREDITARY OSTEODYSTROPHY; PERVASIVE DEVELOPMENTAL DISORDERS;
   CLINICAL PHENOTYPE; 2Q37.3 DELETION; INDIVIDUALS; DELINEATION; SPECTRUM
AB Brachidactyly-Mental Retardation (BDMR) Syndrome (MIM 600430) is associated with terminal deletions at chromosome 2q37 and a limited number of studies also reported an association between 2q37 -> qter deletion and autism. Herein we describe two cases of autism in unrelated children with BDMR Syndrome, showing physical, cognitive, behavioral, and disease natural history homologies, with a very prominent social impairment in the first 4 years of life. At follow-up evaluations, spanning a 5-years period, both children experienced a progressive reduction of the autistic symptoms, besides retaining compromised cognitive ability. This report supports the hypothesis that genes in the 2q37 region may contribute to the etiology of autism, leading, however, to a peculiar evolution of the disease, with symptoms severity decreasing over time.
C1 [Mazzone, Luigi; Ruta, Liliana; Mugno, Diego] Univ Catania, Div Child Neurol & Psychiat, Dept Pediat, I-95123 Catania, Italy.
   [Mazzone, Luigi] IRCCS Childrens Hosp Bambino Gesu, Dept Neurosci, Child Neuropsychiat Unit, Rome, Italy.
   [Vassena, Lia] Ist Sci San Raffaele, Dept Biol & Technol Res DIBIT, I-20132 Milan, Italy.
   [Galesi, Ornella; Fichera, Marco] IRCCS Oasi SS Maria, Lab Genet Diag, Troina, Italy.
RP Mazzone, L (reprint author), Univ Catania, Div Child Neurol & Psychiat, Dept Pediat, Via S Sofia 78, I-95123 Catania, Italy.
EM gigimazzone@yahoo.it
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NR 26
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2202
EP 2207
DI 10.1007/s10803-011-1432-5
PG 6
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600015
PM 22222775
ER

PT J
AU Bedford, R
   Elsabbagh, M
   Gliga, T
   Pickles, A
   Senju, A
   Charman, T
   Johnson, MH
AF Bedford, Rachael
   Elsabbagh, Mayada
   Gliga, Teodora
   Pickles, Andrew
   Senju, Atsushi
   Charman, Tony
   Johnson, Mark H.
CA BASIS Team
TI Precursors to Social and Communication Difficulties in Infants At-Risk
   for Autism: Gaze Following and Attentional Engagement
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; At-risk siblings; Broader autism phenotype; Joint attention;
   Gaze following
ID PERVASIVE DEVELOPMENTAL DISORDERS; JOINT VISUAL-ATTENTION; EYE GAZE;
   SPECTRUM DISORDERS; CHILDREN; COGNITION; MECHANISMS; DIAGNOSIS;
   SIBLINGS; SENSITIVITY
AB Whilst joint attention (JA) impairments in autism have been widely studied, little is known about the early development of gaze following, a precursor to establishing JA. We employed eye-tracking to record gaze following longitudinally in infants with and without a family history of autism spectrum disorder (ASD) at 7 and 13 months. No group difference was found between at-risk and low-risk infants in gaze following behaviour at either age. However, despite following gaze successfully at 13 months, at-risk infants with later emerging socio-communication difficulties (both those with ASD and atypical development at 36 months of age) allocated less attention to the congruent object compared to typically developing at-risk siblings and low-risk controls. The findings suggest that the subtle emergence of difficulties in JA in infancy may be related to ASD and other atypical outcomes.
C1 [Bedford, Rachael; Charman, Tony] Univ London, Ctr Res Autism & Educ, Inst Educ, London WC1H 0AA, England.
   [Elsabbagh, Mayada; Gliga, Teodora; Senju, Atsushi; Johnson, Mark H.] Univ London, Ctr Brain & Cognit Dev, London WC1H 0AA, England.
   [Pickles, Andrew] Kings Coll London, Inst Psychiat, London WC2R 2LS, England.
RP Bedford, R (reprint author), Univ London, Ctr Res Autism & Educ, Inst Educ, 25 Woburn Sq, London WC1H 0AA, England.
EM r.bedford@ioe.ac.uk
RI Bedford, Rachael/I-3939-2012; Pickles, Andrew/A-9625-2011; Charman,
   Tony/A-2085-2014; Bolton, Patrick/E-8501-2010
OI Pickles, Andrew/0000-0003-1283-0346; Charman, Tony/0000-0003-1993-6549;
   Bolton, Patrick/0000-0002-5270-6262
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NR 57
TC 23
Z9 26
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2208
EP 2218
DI 10.1007/s10803-012-1450-y
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600016
PM 22278030
ER

PT J
AU Dietrich, S
   Hertrich, I
   Riedel, A
   Ackermann, H
AF Dietrich, Susanne
   Hertrich, Ingo
   Riedel, Andreas
   Ackermann, Hermann
TI Brief Report: Impaired Differentiation of Vegetative/Affective and
   Intentional Nonverbal Vocalizations in a Subject with Asperger Syndrome
   (AS)
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Theory of mind; Affective system; Nonverbal vocalization
ID FUNCTIONING AUTISM; MIND; ADOLESCENTS; QUOTIENT; EMOTION; PROSODY
AB The Asperger syndrome (AS) includes impaired recognition of other people's mental states. Since language-based diagnostic procedures may be confounded by cognitive-linguistic compensation strategies, nonverbal test materials were created, including human affective and vegetative sounds. Depending on video context, each sound could be interpreted either as direct expression of an agent's affective/vegetative state or as result of intentional-executive mental operations. "Situational relevance" and "intentionality" ratings by a group of twelve healthy subjects nicely differentiated between context types. By contrast, an AS subject showed a systematic overinterpretation of vegetative/affective signals in terms of planned activities. Such overestimation of intentional motivation, leading to impaired social cognition, might be due to the inability to utilize "affective resonance" mechanisms for the interpretation of an individual's internal state.
C1 [Dietrich, Susanne; Hertrich, Ingo; Ackermann, Hermann] Univ Tubingen, Dept Gen Neurol, CIN, Hertie Inst Clin Brain Res, D-72076 Tubingen, Germany.
   [Riedel, Andreas] Univ Freiburg, Dept Psychiat & Psychotherapy, D-79104 Freiburg, Germany.
RP Dietrich, S (reprint author), Univ Tubingen, Dept Gen Neurol, CIN, Hertie Inst Clin Brain Res, Hoppe Seyler Str 3, D-72076 Tubingen, Germany.
EM susanne.dietrich@med.uni-tuebingen.de
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NR 18
TC 0
Z9 0
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2219
EP 2224
DI 10.1007/s10803-012-1455-6
PG 6
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600017
PM 22314575
ER

PT J
AU Auyeung, B
   Allison, C
   Wheelwright, S
   Baron-Cohen, S
AF Auyeung, Bonnie
   Allison, Carrie
   Wheelwright, Sally
   Baron-Cohen, Simon
TI Brief Report: Development of the Adolescent Empathy and Systemizing
   Quotients
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Empathy; Systemizing; Autism; Sex differences; Adolescents
ID CAST CHILDHOOD ASPERGER; HIGH-FUNCTIONING AUTISM; NORMAL
   SEX-DIFFERENCES; FETAL TESTOSTERONE; POPULATION; ADULTS; BRAIN; EQ
AB Adolescent versions of the Empathy Quotient (EQ) and Systemizing Quotient (SQ) were developed and administered to n = 1,030 parents of typically developing adolescents, aged 12-16 years. Both measures showed good test-retest reliability and high internal consistency. Girls scored significantly higher on the EQ, and boys scored significantly higher on the SQ. A sample of adolescents with Autism Spectrum Conditions (ASC) (n = 213) scored significantly lower on the EQ, and significantly higher on the SQ, compared to typical boys. Similar patterns of sex differences and cognitive brain types are observed in children, adolescents and adults, suggesting from cross-sectional studies that the behaviours measured by age-appropriate versions of the EQ and SQ are stable across time. Longitudinal studies would be useful to test this stability in the future. Finally, relative to typical sex differences, individuals with ASC, regardless of age, on average exhibit a 'hyper-masculinized' profile.
C1 [Auyeung, Bonnie; Allison, Carrie; Wheelwright, Sally; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England.
RP Auyeung, B (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England.
EM ba251@cam.ac.uk
CR American Psychiatric Association [APA], 1994, DSM 4 DIAGN STAT MAN
   Auyeung B, 2006, EUR J ENDOCRINOL, V155, pS123, DOI 10.1530/eje.1.02260
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   Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206
   Baron-Cohen SB, 2011, PLOS BIOL, V9, P1, DOI DOI 10.1371/JOURNAL.PBIO.1001081
   Carroll JM, 2006, J AUTISM DEV DISORD, V36, P949, DOI 10.1007/s10803-006-0127-9
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   World Health Organization (WHO ICD-10), 1994, ICD10 WHO
NR 19
TC 11
Z9 12
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2225
EP 2235
DI 10.1007/s10803-012-1454-7
PG 11
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600018
PM 22350450
ER

PT J
AU Falck-Ytter, T
   Fernell, E
   Hedvall, AL
   von Hofsten, C
   Gillberg, C
AF Falck-Ytter, Terje
   Fernell, Elisabeth
   Hedvall, Asa Lundholm
   von Hofsten, Claes
   Gillberg, Christopher
TI Gaze Performance in Children with Autism Spectrum Disorder when
   Observing Communicative Actions
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Joint attention; Eye-movements; Eye-tracking; Adaptive
   behaviour; Individual differences; Intelligence
ID JOINT ATTENTION; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; EYE GAZE; BEHAVIOR;
   DEFICITS
AB The main purpose of this eye tracking study was to map the correlates of gaze performance in a brief test of spontaneous gaze and point-gesture following in young children with autistic disorder (AD), Pervasive developmental disorder-not otherwise specified (PDD-NOS), or typical development (TD). Gaze measures included the children's spontaneous tendency to look at the correct (attended) toy, and the latency of their correct responses. In addition to group differences (AD vs. TD), we found that in AD, accuracy of performance was specifically related to adaptive communication skills. The study also indicated that the latency of correct gaze shifts is related to verbal intelligence. These results have direct implications for our understanding of (responsive) joint attention impairments in AD.
C1 [Falck-Ytter, Terje; von Hofsten, Claes] Uppsala Univ, Dept Psychol, S-75142 Uppsala, Sweden.
   [Falck-Ytter, Terje] Karolinska Inst KIND, Ctr Neurodev Disorders, Astrid Lindgren Childrens Hosp, Stockholm, Sweden.
   [Falck-Ytter, Terje; Fernell, Elisabeth; Hedvall, Asa Lundholm; Gillberg, Christopher] Gothenburg Univ, Gillberg Neuropsychiat Ctr, Sahlgrenska Acad, Gothenburg, Sweden.
   [Fernell, Elisabeth; Gillberg, Christopher] Autism Ctr Young Children Habilitat & Hlth, Stockholm, Sweden.
   [von Hofsten, Claes] Univ Oslo, Dept Psychol, N-0317 Oslo, Norway.
RP Falck-Ytter, T (reprint author), Uppsala Univ, Dept Psychol, Box 1225, S-75142 Uppsala, Sweden.
EM terje.falck-ytter@psyk.uu.se
CR Akechi H, 2011, RES AUTISM SPECT DIS, V5, P1230, DOI 10.1016/j.rasd.2011.01.013
   American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th
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   Coleman M., 2012, AUTISMS
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   Gliga T., CHILD DEV IN PRESS
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   Sparrow SS, 2005, VINELAND ADAPTIVE BE
   Sullivan M, 2007, J AUTISM DEV DISORD, V37, P37, DOI 10.1007/s10803-006-0335-3
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   Wing L, 2011, RES DEV DISABIL, V32, P768, DOI 10.1016/j.ridd.2010.11.003
NR 32
TC 7
Z9 7
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2236
EP 2245
DI 10.1007/s10803-012-1471-6
PG 10
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600019
PM 22354708
ER

PT J
AU Kirchner, JC
   Schmitz, F
   Dziobek, I
AF Kirchner, Jennifer Christina
   Schmitz, Florian
   Dziobek, Isabel
TI Brief Report: Stereotypes in Autism Revisited
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; Stereotypes; Attitudes; Implicit association test
ID IMPLICIT ASSOCIATION TEST; SOCIAL COGNITION; DIFFUSION-MODEL; CHILDREN;
   DISORDERS; PREJUDICE
AB Autism involves core impairments in social cognition. Given that social learning underlies the acquisition of stereotypes, it was hypothesized that use of stereotypes would be reduced in autism. Contrary to this prediction, previous studies found the same use of stereotypes in autistic individuals as in controls. Measurement of stereotypes, however, can be biased by effects of social desirability, which previous studies did not account for. In the current study we therefore employed an implicit approach, using the Implicit Association Test (IAT), which assesses more automatic components of stereotypes, in nineteen individuals with autism and nineteen controls. The data suggest that while both groups do show the use of stereotypes to some extent, autistic individuals have less stereotypical attitudes against the investigated minority.
C1 [Kirchner, Jennifer Christina; Dziobek, Isabel] Free Univ Berlin, D-14195 Berlin, Germany.
   [Kirchner, Jennifer Christina; Dziobek, Isabel] Max Planck Inst Human Dev, Berlin, Germany.
   [Schmitz, Florian] Univ Freiburg, D-79106 Freiburg, Germany.
RP Dziobek, I (reprint author), Free Univ Berlin, Habelschwerdter Allee 45, D-14195 Berlin, Germany.
EM isabel.dziobek@fu-berlin.de
CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT
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   Volkmar FR, 2011, DEV PSYCHOBIOL, V53, P428, DOI 10.1002/dev.20556
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NR 25
TC 2
Z9 2
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2246
EP 2251
DI 10.1007/s10803-012-1460-9
PG 6
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600020
PM 22322582
ER

PT J
AU Finkenauer, C
   Pollmann, M
   Begeer, S
   Kerkhof, P
AF Finkenauer, Catrin
   Pollmann, Monique M. H.
   Begeer, Sander
   Kerkhof, Peter
TI Brief Report: Examining the Link Between Autistic Traits and Compulsive
   Internet Use in a Non-Clinical Sample
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism; AQ; Compulsive internet use; Computer; Autistic traits
ID SPECTRUM DISORDERS; ADOLESCENTS; STUDENTS
AB Individuals with autism spectrum disorders or autistic traits may profit from Internet and computer-mediated interactions, but there is concern about their Internet use becoming compulsive. This study investigated the link between autistic traits and Internet use in a 2-wave longitudinal study with a non-clinical community sample (n = 390). As compared to people with less autistic traits, people with more autistic traits did not report a higher frequency of Internet use, but they were more prone to compulsive Internet use. For women, more autistic traits predicted an increase in compulsive Internet use over time. These results suggest that, despite its appeal for people with autistic traits, the Internet carries the risk of compulsive use.
C1 [Finkenauer, Catrin] Vrije Univ Amsterdam, Dept Clin Child & Family Studies, NL-1082 BT Amsterdam, Netherlands.
   [Begeer, Sander] Vrije Univ Amsterdam, Dept Dev Psychol, NL-1082 BT Amsterdam, Netherlands.
   [Begeer, Sander] Sch Psychol, Amsterdam, Netherlands.
   [Begeer, Sander] Univ Sydney, Sydney, NSW 2006, Australia.
   [Pollmann, Monique M. H.] Tilburg Univ, NL-5000 LE Tilburg, Netherlands.
RP Finkenauer, C (reprint author), Vrije Univ Amsterdam, Dept Clin Child & Family Studies, van der Boechorststr 1, NL-1082 BT Amsterdam, Netherlands.
EM c.finkenauer@vu.nl
RI Begeer, Sander/I-3383-2012; Kerkhof, Peter/B-5298-2008; Pollmann,
   Monique/C-6508-2011
CR Bauminger N, 2003, J AUTISM DEV DISORD, V33, P489, DOI 10.1023/A:1025827427901
   Burke M., 2010, ACM C COMP SUPP COOP
   Caplan SE, 2003, COMMUN RES, V30, P625, DOI 10.1177/0093650203257842
   Chou C, 2005, EDUC PSYCHOL REV, V17, P363, DOI 10.1007/s10648-005-8138-1
   Finkenauer C, 2009, PERS SOC PSYCHOL B, V35, P1410, DOI 10.1177/0146167209339629
   Hoekstra RA, 2011, J AUTISM DEV DISORD, V41, P589, DOI 10.1007/s10803-010-1073-0
   Kerkhof P., 2011, HUMAN COMMUNICATION, DOI [10.1111/j.1468-2958.2010.01397.x/pdf, DOI 10.1111/J.1468-2958.2010.01397.X/PDF]
   Meerkerk GJ, 2009, CYBERPSYCHOL BEHAV, V12, P1, DOI 10.1089/cpb.2008.0181
   Mineo BA, 2009, J AUTISM DEV DISORD, V39, P172, DOI 10.1007/s10803-008-0616-0
   Morahan-Martin J, 2000, COMPUT HUM BEHAV, V16, P13, DOI 10.1016/S0747-5632(99)00049-7
   Nally B, 2000, AUTISM, V4, P331, DOI DOI 10.1177/1362361300004003008
   Pollmann MMH, 2010, J AUTISM DEV DISORD, V40, P470, DOI 10.1007/s10803-009-0888-z
   Ramdoss S, 2011, RES AUTISM SPECT DIS, V5, P1306, DOI 10.1016/j.rasd.2011.03.004
   Schouten AP, 2007, MEDIA PSYCHOL, V10, P292, DOI 10.1080/15213260701375686
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   Trepagnier CY, 2006, CYBERPSYCHOL BEHAV, V9, P723
   Valkenburg PM, 2009, CURR DIR PSYCHOL SCI, V18, P1, DOI 10.1111/j.1467-8721.2009.01595.x
   van den Eijnden RJJM, 2008, DEV PSYCHOL, V44, P655, DOI 10.1037/0012-1649.44.3.655
   Wilkinson N, 2008, INT J SOC PSYCHIATR, V54, P370, DOI 10.1177/0020764008091659
NR 19
TC 5
Z9 5
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2252
EP 2256
DI 10.1007/s10803-012-1465-4
PG 5
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600021
PM 22350338
ER

PT J
AU Cox, NB
   Reeve, RE
   Cox, SM
   Cox, DJ
AF Cox, Neill Broderick
   Reeve, Ronald E.
   Cox, Stephany M.
   Cox, Daniel J.
TI Brief Report: Driving and Young Adults with ASD: Parents' Experiences
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Article
DE Autism and driving; Asperger's and driving; Autism spectrum disorders
   and driving; Driving and developmental disabilities; Parents'
   experiences of driving
ID AUTISM; CHILDREN
AB A paucity of research exists regarding driving skills and individuals with Autism Spectrum Disorders (ASD). The current study sought to gain a better understanding of driving and ASD by surveying parents/caregivers of adolescents/young adults with ASD who were currently attempting, or had previously attempted, to learn to drive. Respondents included 123 parents/caregivers of adolescents/young adults with ASD. The results indicate that learning to drive presents a substantial challenge for individuals with ASD; complex driving demands (e.g., multi-tasking) may be particularly problematic. Respondents provided suggestions that may be useful to others who seek to teach these skills. The survey results offer guidance for next steps in the study of driving with ASD.
C1 [Cox, Neill Broderick; Reeve, Ronald E.; Cox, Stephany M.] Univ Virginia, Curry Sch Educ, Charlottesville, VA 22904 USA.
   [Cox, Daniel J.] Univ Virginia, Dept Psychiat & Neurobehav Sci, Sch Med, Charlottesville, VA 22908 USA.
RP Cox, NB (reprint author), Univ Virginia, Curry Sch Educ, POB 400270, Charlottesville, VA 22904 USA.
EM nb5gs@virginia.edu
CR American Occupational Therapy Association (Producer), 2009, DRIV ASS TRAIN TECHN
   Baron-Cohen S, 2004, J NEUROL NEUROSUR PS, V75, P945, DOI 10.1136/jnnp.2003.018713
   Centers for Disease Control, 2007, PREV AUT SPECTR DIS
   Hofvander B, 2009, BMC PSYCHIATRY, V9, DOI 10.1186/1471-244X-9-35
   Iarocci G, 2006, J AUTISM DEV DISORD, V36, P117, DOI 10.1007/s10803-005-0045-2
   Klin A., 2005, DIAGNOSIS DEV NEUROB
   Sheppard E., 2009, J AUTISM DEV DISORD, V40, P504, DOI 10.1007/s10803-009-0890-5
   Sinzig J, 2008, ACTA NEUROPSYCHIATR, V20, P207, DOI 10.1111/j.1601-5215.2008.00292.x
   Weiner A., 2001, J DEV BEHAV PEDIATR, V22, P92
   Zalla T, 2010, EXP BRAIN RES, V201, P809, DOI 10.1007/s00221-009-2096-7
NR 10
TC 3
Z9 3
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2257
EP 2262
DI 10.1007/s10803-012-1470-7
PG 6
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600022
PM 22359179
ER

PT J
AU Chown, N
AF Chown, Nick
TI 'History and First Descriptions' of Autism: A response to Michael
   Fitzgerald
SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS
LA English
DT Letter
DE Academic ethics; Asperger; Asperger's syndrome; Autism; Kanner
AB Letter to the editor in response to Michael Fitzgerald's controversial allegation that one of the two pioneers of autism-Leo Kanner-may have been influenced by an earlier paper by the other autism pioneer-Hans Asperger-without acknowledging the debt, and that Kanner may even have been guilty of plagiarising Asperger. In correspondence, Professor Fitzgerald has suggested that I "consider doing my take on the matter". This is it.
C1 [Chown, Nick] Twin Elms, Market Harborough LE16 9SK, Leics, England.
   [Chown, Nick] Sheffield Hallam Univ, Sheffield S1 1WB, S Yorkshire, England.
RP Chown, N (reprint author), Twin Elms, Marston Lane, Market Harborough LE16 9SK, Leics, England.
EM nick@chown.fsbusiness.co.uk
CR Asperger H., 1938, WIEN KLIN WOCHENSCHR, V51, P1314
   Asperger H., 1944, AUTISM ASPERGER SYND
   Feinstein Adam, 2010, HIST AUTISM CONVERSA
   Fitzgerald M., 2008, ASPERGERS DISORDER
   Fitzgerald M., 2008, CREATIVITY PSYCHOSIS
   Kanner L, 1943, NERV CHILD, V2, P217
   Lyons V, 2007, J AUTISM DEV DISORD, V37, P2022, DOI 10.1007/s10803-007-0383-3
   Morgan H., SETTING SCENE INTRO
   Naylor M. L., 2011, HIST AUTISM
   Quayson A, 2010, U TORONTO QUART, V79, P838, DOI 10.3138/UTQ.79.2.838
   Skuse D. H., 2011, BRAIN, V134, P2436
NR 11
TC 1
Z9 1
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0162-3257
J9 J AUTISM DEV DISORD
JI J. Autism Dev. Disord.
PD OCT
PY 2012
VL 42
IS 10
BP 2263
EP 2265
DI 10.1007/s10803-012-1529-5
PG 3
WC Psychology, Developmental
SC Psychology
GA 010ZR
UT WOS:000309133600023
PM 22527702
ER

PT J
AU Ro, M
   Park, J
   Nam, M
   Bang, HJ
   Yang, J
   Choi, KS
   Kim, SK
   Chung, JH
   Kwack, K
AF Ro, MyungJa
   Park, JungWon
   Nam, Min
   Bang, Hee Jung
   Yang, JaeWon
   Choi, Kyung-Sik
   Kim, Su Kang
   Chung, Joo-Ho
   Kwack, KyuBum
TI Association Between Peroxisomal Biogenesis Factor 7 and Autism Spectrum
   Disorders in a Korean Population
SO JOURNAL OF CHILD NEUROLOGY
LA English
DT Article
DE autism spectrum disorder; PEX7; polymorphism; peroxisome
ID RHIZOMELIC CHONDRODYSPLASIA PUNCTATA; NEURONAL MIGRATION; PEX7 GENE;
   BIOSYNTHESIS; PLASMALOGENS; DISEASE; IMPORT; PHENOTYPE; PROTEINS;
   GENOTYPE
AB Autism spectrum disorder is a neurodevelopmental disorder characterized by deficits in social communication, impaired reciprocal social interaction, and repetitive patterns of behaviors or interests. Although the cause of autism spectrum disorder remains elusive, the present study identified peroxisomal biogenesis factor 7 (PEX7) as a gene associated with autism spectrum disorder, and this association was examined in a Korean population. PEX7 encodes a cytosolic receptor for peroxisome targeting signal 2 of peroxisomal matrix enzymes that are targeted to and translocated into the peroxisome. PEX7 defects are associated with rhizomelic chondrodysplasia punctata type 1 and Refsum disease. Mutations in PEX7 are related to a variety of mild to severe clinical symptoms, including mental retardation. The analysis of 9 intronic single nucleotide polymorphisms in 214 patients with autism spectrum disorder and 258 controls revealed the association of 2 single nucleotide polymorphisms and 1 haplotype with autism spectrum disorder (P < .05).
C1 [Ro, MyungJa; Park, JungWon; Kwack, KyuBum] CHA Univ, Dept Biomed Sci, Coll Life Sci, Songnam, South Korea.
   [Nam, Min] Seoul Metropolitan Childrens Hosp, Dept Psychiat, Seoul, South Korea.
   [Bang, Hee Jung] Ewha Womans Univ, Dept Psychol, Coll Social Sci, Seoul, South Korea.
   [Yang, JaeWon] Korea Univ, Coll Med, Ansan Hosp, Dept Psychiat, Ansan, South Korea.
   [Choi, Kyung-Sik] Joongbu Univ, Dept Elementary Special Educ, Coll Social Sci, Chungnam, South Korea.
   [Kim, Su Kang; Chung, Joo-Ho] Kyung Hee Univ, Kohwang Med Res Inst, Sch Med, Seoul, South Korea.
RP Kwack, K (reprint author), CHA Univ, Dept Biomed Sci, Coll Life Sci, 222 Yatapdong, Songnam 463836, Gyeonggido, South Korea.
EM kbkwack@cha.ac.kr
FU Ministry of Health and Welfare, Republic of Korea [A040002, A080734]
FX The authors disclosed receipt of the following financial support for the
   research, authorship, and/or publication of this article: This study was
   supported by grants from the Korea Health 21 R&D Project, Ministry of
   Health and Welfare, Republic of Korea (A040002, A080734).
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NR 31
TC 2
Z9 2
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 0883-0738
J9 J CHILD NEUROL
JI J. Child Neurol.
PD OCT
PY 2012
VL 27
IS 10
BP 1270
EP 1275
DI 10.1177/0883073811435507
PG 6
WC Clinical Neurology; Pediatrics
SC Neurosciences & Neurology; Pediatrics
GA 010EZ
UT WOS:000309078800005
PM 22378669
ER

PT J
AU Lee, NR
   Wallace, GL
   Adeyemi, EI
   Lopez, KC
   Blumenthal, JD
   Clasen, LS
   Giedd, JN
AF Lee, Nancy Raitano
   Wallace, Gregory L.
   Adeyemi, Elizabeth I.
   Lopez, Katherine C.
   Blumenthal, Jonathan D.
   Clasen, Liv S.
   Giedd, Jay N.
TI Dosage effects of X and Y chromosomes on language and social functioning
   in children with supernumerary sex chromosome aneuploidies: implications
   for idiopathic language impairment and autism spectrum disorders
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
DT Article
DE Chromosome anomalies; social cognition; language disorder; autistic
   disorder; sex differences
ID KLINEFELTER-SYNDROME; TRAITS; 47,XXY; BOYS; XXY; ABNORMALITIES;
   VALIDATION; EXPRESSION; SPEECH; XYY
AB Background: Supernumerary sex chromosome aneuploidies (X/Y-aneuploidies), the presence of extra X and/or Y chromosomes, are associated with heightened rates of language impairments and social difficulties. However, no single study has examined different language domains and social functioning in the same sample of children with tri-, tetra-, and pentasomy X/Y-aneuploidy. The current research sought to fill this gap in the literature and to examine dosage effects of X and Y chromosomes on language and social functioning. Methods: Participants included 110 youth with X/Y-aneuploidies (32 female) and 52 with typical development (25 female) matched on age (mean similar to 12 years; range 422) and maternal education. Participants completed the Wechsler intelligence scales, and parents completed the Childrens Communication Checklist-2 and the Social Responsiveness Scale to assess language skills and autistic traits, respectively. Results: Both supernumerary X and Y chromosomes were related to depressed structural and pragmatic language skills and increased autistic traits. The addition of a Y chromosome had a disproportionately greater impact on pragmatic language; the addition of one or more X chromosomes had a disproportionately greater impact on structural language. Conclusions: Given that we link extra X chromosomes with structural language impairments and an extra Y chromosome with pragmatic language impairments, X/Y-aneuploidies may provide clues to genetic mechanisms contributing to idiopathic language impairment and autism spectrum disorders.
C1 [Lee, Nancy Raitano; Wallace, Gregory L.; Adeyemi, Elizabeth I.; Lopez, Katherine C.; Blumenthal, Jonathan D.; Clasen, Liv S.; Giedd, Jay N.] NIMH, Child Psychiat Branch, NIH, Bethesda, MD 20892 USA.
   [Wallace, Gregory L.] NIMH, Lab Brain & Cognit, NIH, Bethesda, MD 20892 USA.
RP Lee, NR (reprint author), NIMH, Child Psychiat Branch, NIH, Bldg 10,MSC 1367, Bethesda, MD 20892 USA.
EM lnancy@mail.nih.gov
RI Giedd, Jay/B-7302-2012
OI Giedd, Jay/0000-0003-0827-3460
FU NIH, National Institute of Mental Health
FX This research was supported by the Intramural Research Program of the
   NIH, National Institute of Mental Health. We thank the families for
   their participation.
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NR 34
TC 9
Z9 10
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
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VL 53
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BP 1072
EP 1081
DI 10.1111/j.1469-7610.2012.02573.x
PG 10
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 012LQ
UT WOS:000309238100009
PM 22827287
ER

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   perspective and the need for change
SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY
LA English
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C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA.
RP Ozonoff, S (reprint author), Univ Calif Davis, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA.
EM sal-ly.ozonoff@ucdmc.ucdavis.edu
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NR 12
TC 6
Z9 7
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9630
J9 J CHILD PSYCHOL PSYC
JI J. Child Psychol. Psychiatry
PD OCT
PY 2012
VL 53
IS 10
BP 1092
EP 1094
DI 10.1111/j.1469-7610.2012.02614.x
PG 3
WC Psychology, Developmental; Psychiatry; Psychology
SC Psychology; Psychiatry
GA 012LQ
UT WOS:000309238100012
PM 22970941
ER

PT J
AU Kirkland, A
AF Kirkland, Anna
TI The Legitimacy of Vaccine Critics: What Is Left after the Autism
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SO JOURNAL OF HEALTH POLITICS POLICY AND LAW
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CR [Anonymous], 2009, WASHINGTON TIME 0315
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NR 4
TC 0
Z9 0
PU DUKE UNIV PRESS
PI DURHAM
PA 905 W MAIN ST, STE 18-B, DURHAM, NC 27701 USA
SN 0361-6878
J9 J HEALTH POLIT POLIC
JI J. Health Polit. Policy Law
PD OCT
PY 2012
VL 37
IS 5
BP 883
EP 883
DI 10.1215/03616878-1894011
PG 1
WC Health Care Sciences & Services; Health Policy & Services; Medicine,
   Legal; Social Issues; Social Sciences, Biomedical
SC Health Care Sciences & Services; Legal Medicine; Social Issues;
   Biomedical Social Sciences
GA 007OF
UT WOS:000308897300008
ER

PT J
AU Reilly, C
AF Reilly, C.
TI Behavioural phenotypes and special educational needs: is aetiology
   important in the classroom?
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE behavioural phenotypes; Down syndrome; fragile X; Prader-Willi syndrome;
   VCFS; Williams syndrome
ID FRAGILE-X-SYNDROME; PRADER-WILLI-SYNDROME; AUTISM SPECTRUM DISORDERS;
   CARDIO-FACIAL SYNDROME; MENTAL-RETARDATION SYNDROMES; 22Q11.2 DELETION
   SYNDROME; DEFICIT HYPERACTIVITY DISORDER; DOWN-SYNDROME;
   VELOCARDIOFACIAL SYNDROME; PSYCHIATRIC-DISORDERS
AB Background A number of genetic conditions with associated intellectual disability and/or special educational needs have increasingly well-defined behavioural phenotypes. Thus, the concept of 'behavioural phenotype' and aetiology of intellectual disability may be important with regard to school-based interventions.
   Method The evidence for distinctive cognitive and behavioural aspects of five of the most common genetic syndromes (Down syndrome, fragile X syndrome, Williams syndrome, Prader-Willi syndrome and velo-cardio-facial syndrome) associated with special educational needs is reviewed with respect to key studies and findings. The possible utility of aetiology-related interventions in education is discussed with reference to arguments for and against such approaches with respect to published guidelines and published research.
   Results Behavioural phenotypes are probabilistic and many children with a specific genetic syndrome will share commonalities with other children with other genetic syndromes and within syndrome variability is not uncommon. There is evidence that teachers and parents have limited knowledge of aspects of the proposed cognitive and behaviour profiles associated with the reviewed syndromes. While there are published guidelines in the area of learning and behaviour for each of the five reviewed syndromes there is a limited amount of evidence of the efficacy of such approaches in school settings.
   Conclusion It is likely that knowing the aetiology of a child's special educational needs will be helpful for staff who work in school settings in relation to cognitive and behavioural implications. However, how such knowledge might inform teaching practice or behavioural interventions has not been studied. A model is proposed that might help inform educators about the possible role of aetiology in the classroom.
C1 Univ Coll Dublin, Sch Educ, Dublin 4, Ireland.
RP Reilly, C (reprint author), Univ Coll Dublin, Sch Educ, Dublin 4, Ireland.
EM colin.reilly@ucdconnect.ie
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NR 135
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 OCT
PY 2012
VL 56
IS 10
BP 929
EP 946
DI 10.1111/j.1365-2788.2012.01542.x
PG 18
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
   Neurology; Psychiatry; Rehabilitation
GA 007ES
UT WOS:000308872200002
PM 22471356
ER

PT J
AU Povee, K
   Roberts, L
   Bourke, J
   Leonard, H
AF Povee, K.
   Roberts, L.
   Bourke, J.
   Leonard, H.
TI Family functioning in families with a child with Down syndrome: a mixed
   methods approach
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE Down syndrome; family functioning; maladaptive behaviour; marital
   adjustment
ID DYADIC ADJUSTMENT SCALE; SCHOOL-AGED CHILDREN; INTELLECTUAL DISABILITY;
   SPECTRUM DISORDERS; MARITAL ADJUSTMENT; WESTERN-AUSTRALIA; ASSESSMENT
   DEVICE; PARENTS; STRESS; AUTISM
AB Background This study aimed to explore the factors that predict functioning in families with a child with Down syndrome using a mixed methods design. The quantitative component examined the effect of maladaptive and autism-spectrum behaviours on the functioning of the family while the qualitative component explored the impact of having a child with Down syndrome on family holidays, family activities and general family functioning.
   Methods Participants in this study were 224 primary caregivers of children with Down syndrome aged 4-25 years (57.1% male; 42.9% female) currently residing in Western Australia (74.0% in metropolitan Perth and 26.0% in rural Western Australia).
   Results Maladaptive and autism-spectrum behaviour were associated with poorer family functioning. Mean total scores on the measures of family functioning and marital adjustment were comparable to that of families of typically developing children. Consistent with the quantitative findings, normality was the most common theme to emerge in the qualitative data. Child problem behaviours were also identified by parents/carers as having a negative impact on the family.
   Conclusions This study has implications for the development of programs to support families with a child with Down syndrome and may dispel some of the myths surrounding the impact of intellectual disability on the family.
C1 [Bourke, J.; Leonard, H.] Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6008, Australia.
   [Povee, K.; Roberts, L.] Curtin Univ Technol, Sch Psychol & Speech Pathol, Perth, WA, Australia.
RP Leonard, H (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, 100 Roberts Rd, Perth, WA 6008, Australia.
EM hleonard@ichr.uwa.edu.au
RI Leonard, Helen/A-1010-2013
OI Leonard, Helen/0000-0001-6405-5834
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NR 43
TC 9
Z9 9
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 OCT
PY 2012
VL 56
IS 10
BP 961
EP 973
DI 10.1111/j.1365-2788.2012.01561.x
PG 13
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
   Neurology; Psychiatry; Rehabilitation
GA 007ES
UT WOS:000308872200004
PM 22533693
ER

PT J
AU Sterling, A
   Abbeduto, L
AF Sterling, A.
   Abbeduto, L.
TI Language development in school-age girls with fragile X syndrome
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE cognitive behaviour; communication; fragile X; intellectual disability
ID WITHIN-SYNDROME DIFFERENCES; MENTAL-RETARDATION PROTEIN; DOWN-SYNDROME;
   EXPRESSIVE LANGUAGE; TURNER-SYNDROME; BOYS; COMMUNICATION; FEMALES;
   AUTISM; MALES
AB Background Girls with fragile X syndrome (FXS) have a wide range of cognitive and language abilities. The range of language outcomes experienced by girls with FXS, however, has been relatively unexplored. The purpose of this exploratory study was to examine receptive and expressive language, with a focus on vocabulary and syntax, in a group of school-age girls with FXS.
   Method Twenty-one girls with FXS aged 7-15 years participated in the study. The girls completed a receptive vocabulary test, non-verbal IQ test and an expressive language sample.
   Results The mean IQ for this group of girls was at the cut-off for intellectual disability. Vocabulary was an area of strength relative to non-verbal cognition. Age and non-verbal IQ were significant predictors of vocabulary performance.
   Conclusions The data suggest that a substantial portion of the sample would qualify for speech and language services. This study highlights the need for continued research in the area of language and cognitive development in girls with the full mutation of fragile X.
C1 [Sterling, A.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
   [Abbeduto, L.] Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA.
RP Sterling, A (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave,Room 529A, Madison, WI 53705 USA.
EM asterling@waisman.wisc.edu
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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 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD OCT
PY 2012
VL 56
IS 10
BP 974
EP 983
DI 10.1111/j.1365-2788.2012.01578.x
PG 10
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
   Neurology; Psychiatry; Rehabilitation
GA 007ES
UT WOS:000308872200005
PM 22676254
ER

PT J
AU Baker, JK
   Seltzer, MM
   Greenberg, JS
AF Baker, J. K.
   Seltzer, M. M.
   Greenberg, J. S.
TI Behaviour problems, maternal internalising symptoms and family relations
   in families of adolescents and adults with fragile X syndrome
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE behaviour problems; cohesion; family; fragile X syndrome; marital
   satisfaction
ID DEVELOPMENTAL-DISABILITIES; MENTAL-RETARDATION; PARENTING STRESS;
   ENVIRONMENT SCALE; MARITAL QUALITY; DOWN-SYNDROME; CHILDREN; MOTHERS;
   AUTISM; PREMUTATION
AB Background Studies have linked the behaviour problems of children with fragile X syndrome (FXS) to maternal well-being, but less is known about how behaviour problems relate to important family factors such as marital satisfaction and family cohesion.
   Methods Married mothers of 115 adolescents and adults with FXS completed questionnaires and interviews, and maternal CGG repeat length was obtained by medical/laboratory records or by blood analysis.
   Results Indirect effects were present between behaviour problems and family variables in that behaviour problems were positively related to maternal internalising symptoms which were, in turn, negatively associated with both family cohesion and marital satisfaction. Direct associations between behaviour problems and family relationship variables were not significant.
   Conclusions Findings suggest the importance of intervening with behaviour problems in individuals with FXS and identify maternal mental health as a potentially powerful conduit for the effects of child behaviour on relationships within these families. Implications for targeted interventions are discussed.
C1 [Baker, J. K.] Calif State Univ Fullerton, Dept Child & Adolescent Studies, Fullerton, CA 92831 USA.
   [Seltzer, M. M.; Greenberg, J. S.] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA.
RP Baker, JK (reprint author), Calif State Univ Fullerton, Dept Child & Adolescent Studies, Fullerton, CA 92831 USA.
EM jbaker@fullerton.edu
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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 0964-2633
J9 J INTELL DISABIL RES
JI J. Intell. Disabil. Res.
PD OCT
PY 2012
VL 56
IS 10
BP 984
EP 995
DI 10.1111/j.1365-2788.2012.01580.x
PG 12
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
   Neurology; Psychiatry; Rehabilitation
GA 007ES
UT WOS:000308872200006
PM 22676314
ER

PT J
AU Moshier, MS
   York, TP
   Silberg, JL
   Elsea, SH
AF Moshier, M. S.
   York, T. P.
   Silberg, J. L.
   Elsea, S. H.
TI Siblings of individuals with Smith-Magenis syndrome: an investigation of
   the correlates of positive and negative behavioural traits
SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH
LA English
DT Article
DE negative behavioural traits; positive behavioural traits; sibling;
   sibling relationships; Smith-Magenis syndrome
ID DOWN-SYNDROME; CHILDREN; DISABILITIES; AUTISM
AB Background Smith-Magenis syndrome (SMS) is a neurodevelopmental disorder that affects approximately one out of 25 000 births worldwide. To date, no research has been conducted to investigate how having an individual with SMS in a family is a positive or negative influence on siblings.
   Methods To investigate this question we conducted a study involving 79 siblings and 60 parents of individuals with SMS to assess perceptions of how having a sibling with SMS positively and negative influence siblings' behavioural traits.
   Results Our findings show that age of siblings of individuals with SMS was associated with a significant increase in positive behavioural traits and a significant decrease in negative behavioural traits. Additionally, siblings who perceive benefits from having a sibling with SMS demonstrate significantly more positive behavioural traits and significantly fewer negative behavioural traits. Parents accurately assess the changes in sibling behavioural traits with age, and parents who perceive their child as having experienced benefits from the sibling relationship report that siblings demonstrate significantly more positive behavioural traits and significantly fewer negative behavioural traits.
   Conclusions Our research shows that although individuals experience difficulties as a result of having a sibling with SMS, overall, siblings tend to fare well and parents appreciate both the positive and negative behavioural effects that result from having a sibling with SMS.
C1 [Elsea, S. H.] Virginia Commonwealth Univ, Dept Pediat, Richmond, VA 23298 USA.
   [Moshier, M. S.; York, T. P.; Silberg, J. L.; Elsea, S. H.] Virginia Commonwealth Univ, Dept Human & Mol Genet, Richmond, VA 23298 USA.
RP Elsea, SH (reprint author), Virginia Commonwealth Univ, Dept Pediat, 1101 E Marshall St,12-018 Sanger Hall, Richmond, VA 23298 USA.
EM selsea@vcu.edu
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NR 17
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 OCT
PY 2012
VL 56
IS 10
BP 996
EP 1007
DI 10.1111/j.1365-2788.2012.01581.x
PG 12
WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Genetics & Heredity; Neurosciences &
   Neurology; Psychiatry; Rehabilitation
GA 007ES
UT WOS:000308872200007
PM 22672270
ER

PT J
AU Cheng, J
   Dong, J
   Cui, YX
   Wang, LC
   Wu, B
   Zhang, C
AF Cheng, Juan
   Dong, Jie
   Cui, Yaxuan
   Wang, Liecheng
   Wu, Bei
   Zhang, Chen
TI Interacting Partners of AMPA-Type Glutamate Receptors
SO JOURNAL OF MOLECULAR NEUROSCIENCE
LA English
DT Article; Proceedings Paper
CT 16th International Symposium on Chromaffin Cell Biology (ISCCB)
CY JUL 11-15, 2011
CL Beijing, PEOPLES R CHINA
DE AMPA receptors; Protein-protein interactions; Synapses
ID LONG-TERM POTENTIATION; DOMAIN-CONTAINING PROTEIN; MEDIATED ACTIN
   DYNAMICS; SYNAPTIC PLASTICITY; EXCITATORY SYNAPSES; DENDRITIC SPINES;
   HIPPOCAMPAL-NEURONS; SURFACE EXPRESSION; KAINATE RECEPTORS; MOUSE
   STARGAZER
AB Glutamate is the principal excitatory neurotransmitter in the brain. The alpha-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic (AMPA) receptors, as one of several types of endogenous ionotropic glutamate receptors, mediate the fast excitatory synaptic transmission that is essential for information processing and integration in the mammalian brain. Modifications of AMPA receptors are assumed to be the molecular basis underlying learning and memory, and impairments of AMPA receptors cause certain neurological diseases, including epilepsy, autism spectrum disorders, and Alzheimer's disease. Thus, extensive studies have been conducted, and these have revealed a complex protein-protein network controlling the expression, trafficking, and function of AMPA receptors in neurons. Here, we summarize the interacting partners of AMPA-type glutamate receptors and the functional implications of these interactions.
C1 [Cheng, Juan; Dong, Jie; Cui, Yaxuan; Wu, Bei; Zhang, Chen] Peking Univ, Sch Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China.
   [Cheng, Juan; Wang, Liecheng] Anhui Med Univ, Dept Physiol, Hefei 230032, Anhui, Peoples R China.
RP Wu, B (reprint author), Peking Univ, Sch Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China.
EM beiwubeiwu@gmail.com; ch.zhang@pku.edu.cn
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NR 86
TC 3
Z9 3
PU HUMANA PRESS INC
PI TOTOWA
PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 USA
SN 0895-8696
J9 J MOL NEUROSCI
JI J. Mol. Neurosci.
PD OCT
PY 2012
VL 48
IS 2
BP 441
EP 447
DI 10.1007/s12031-012-9724-6
PG 7
WC Biochemistry & Molecular Biology; Neurosciences
SC Biochemistry & Molecular Biology; Neurosciences & Neurology
GA 008LO
UT WOS:000308958700019
PM 22361832
ER

PT J
AU van Rijn, S
   Bierman, M
   Bruining, H
   Swaab, H
AF van Rijn, Sophie
   Bierman, Marit
   Bruining, Hilgo
   Swaab, Hanna
TI Vulnerability for autism traits in boys and men with an extra X
   chromosome (47,XXY): The mediating role of cognitive flexibility
SO JOURNAL OF PSYCHIATRIC RESEARCH
LA English
DT Article
DE Klinefelter syndrome; XXY; Sex chromosomal aneuploidy; Autism; Executive
   functioning; Cognitive flexibility
ID KLINEFELTER-SYNDROME; EXECUTIVE FUNCTIONS; CHILDREN; BRAIN;
   ABNORMALITIES; ADOLESCENTS; DISORDERS; PROFILES; SAMPLE; SKILLS
AB The XXY chromosomal pattern (Klinefelter syndrome, KS) has been associated with specific effects on physical, neurobiological, endocrinological and psychological development. This study was focused on the described risk for autism in KS, and the cognitive mechanisms that mediate this risk. Our aim was to assess whether autistic features in KS result from impairments in executive functioning, more specifically difficulties in cognitive flexibility.
   In total, 71 boys and men with KS and 61 non-clinical controls participated in the study. Autistic features were assessed using the Autism-spectrum Quotient (AQ). Mental flexibility was measured using the Wisconsin Card Sorting Test (WCST).
   The level of autism traits was significantly increased in the KS group, the effect size for total AQ score was 1.6. The KS group also showed significantly more difficulties in cognitive flexibility, as indicated by and increased number of perseverative (but not non-perseverative) errors in the WCST. This effect was independent of intellectual functioning, age or testosterone supplements. Within the KS group, the number of perseverative errors was significantly (positively) correlated with total AQ score.
   Our findings suggest that KS can be associated with dysfunctions in mental flexibility, and that individuals with more mental flexibility problems also have more autism traits. This insight is relevant for diagnosis, prevention and treatment of severe problems in individuals with KS. Implications also extend beyond this specific syndrome. As executive dysfunctions in KS have also been linked to ADHD symptoms and thought disorder, this could be a shared mechanism contributing to overlap in symptoms and comorbidity between different psychiatric conditions. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [van Rijn, Sophie; Bierman, Marit; Swaab, Hanna] Leiden Univ, NL-2333 AK Leiden, Netherlands.
   [van Rijn, Sophie; Swaab, Hanna] Leiden Inst Brain & Cognit, NL-2300 RC Leiden, Netherlands.
   [Bierman, Marit; Bruining, Hilgo] Univ Med Ctr Utrecht, Dept Psychiat, NL-3584 CX Utrecht, Netherlands.
RP van Rijn, S (reprint author), Leiden Univ, Wassenaarseweg 52, NL-2333 AK Leiden, Netherlands.
EM srijn@fsw.leidenuniv.nl
FU VENI grant from the Netherlands Organization for Scientific Research
   (NWO) [016.095.060]
FX This work was supported by a VENI grant (grant number 016.095.060 to
   SvR) from the Netherlands Organization for Scientific Research (NWO).
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NR 44
TC 5
Z9 5
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0022-3956
J9 J PSYCHIATR RES
JI J. Psychiatr. Res.
PD OCT
PY 2012
VL 46
IS 10
BP 1300
EP 1306
DI 10.1016/j.jpsychires.2012.06.004
PG 7
WC Psychiatry
SC Psychiatry
GA 013GU
UT WOS:000309294700008
PM 22884425
ER

PT J
AU Benga, O
   Huber, VJ
AF Benga, Oana
   Huber, Vincent J.
TI Brain water channel proteins in health and disease
SO MOLECULAR ASPECTS OF MEDICINE
LA English
DT Review
DE Water channel proteins; Aquaporins; Brain water; Brain edema; Brain
   pathologies; Autism
ID CENTRAL-NERVOUS-SYSTEM; AQUAPORIN-4 MESSENGER-RNA; FIBRILLARY ACIDIC
   PROTEIN; FOCAL CEREBRAL-ISCHEMIA; NEUTRAL SOLUTE CHANNEL;
   CHOROID-PLEXUS; MOLECULAR CHARACTERIZATION; CEREBROSPINAL-FLUID;
   ALZHEIMER-DISEASE; INTRACEREBRAL HEMORRHAGE
AB The aim of this article is to describe the roles of water channel proteins (WCPs) in brain functionality. The fluid compartments of the brain, which include the brain parenchyma (with intracellular and extracellular spaces), the intravascular and the cerebrospinal fluid compartments are presented. Then the localization and functional roles of WCPs found in the brain are described: AQP1, AQP2, AQP3, AQP4, AQP5, AQP7, AQP8, AQP9 and AQP11. In subsequent chapters the involvement of brain WCPs in pathologies are discussed: brain edema, brain trauma, brain tumors, stroke, dementia (Alzheimer's disease, human immunodeficiency virus - HIV-dementia), autism, pain signal transduction and migraine, hydrocephalus and other pathologies with neurological implications: eclampsia, uremia. New WCP ligands for brain imaging are also discussed. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Benga, Oana] Univ Babes Bolyai, Dept Psychol, Cluj Napoca 400015, Romania.
   [Huber, Vincent J.] Niigata Univ, Ctr Integrated Human Brain Sci, Brain Res Inst, Niigata 95021, Japan.
RP Benga, O (reprint author), Univ Babes Bolyai, Dept Psychol, Republ St 37, Cluj Napoca 400015, Romania.
EM oanabenga@psychology.ro
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NR 189
TC 9
Z9 9
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0098-2997
J9 MOL ASPECTS MED
JI Mol. Asp. Med.
PD OCT-DEC
PY 2012
VL 33
IS 5-6
SI SI
BP 562
EP 578
DI 10.1016/j.mam.2012.03.008
PG 17
WC Biochemistry & Molecular Biology; Medicine, Research & Experimental
SC Biochemistry & Molecular Biology; Research & Experimental Medicine
GA 010LI
UT WOS:000309095500007
PM 22504060
ER

PT J
AU Cryan, JF
   Dinan, TG
AF Cryan, John F.
   Dinan, Timothy G.
TI Mind-altering microorganisms: the impact of the gut microbiota on brain
   and behaviour
SO NATURE REVIEWS NEUROSCIENCE
LA English
DT Review
ID IRRITABLE-BOWEL-SYNDROME; CENTRAL-NERVOUS-SYSTEM; ANXIETY-LIKE BEHAVIOR;
   PROBIOTIC BIFIDOBACTERIUM-INFANTIS; INDUCED VISCERAL HYPERSENSITIVITY;
   LACTOBACILLUS-REUTERI INGESTION; INTESTINAL BARRIER FUNCTION; AUTISM
   SPECTRUM DISORDERS; MATERNAL SEPARATION; ANIMAL-MODELS
AB Recent years have witnessed the rise of the gut microbiota as a major topic of research interest in biology. Studies are revealing how variations and changes in the composition of the gut microbiota influence normal physiology and contribute to diseases ranging from inflammation to obesity. Accumulating data now indicate that the gut microbiota also communicates with the CNS-possibly through neural, endocrine and immune pathways - and thereby influences brain function and behaviour. Studies in germ-free animals and in animals exposed to pathogenic bacterial infections, probiotic bacteria or antibiotic drugs suggest a role for the gut microbiota in the regulation of anxiety, mood, cognition and pain. Thus, the emerging concept of a microbiota-gut-brain axis suggests that modulation of the gut microbiota may be a tractable strategy for developing novel therapeutics for complex CNS disorders.
C1 [Cryan, John F.; Dinan, Timothy G.] Natl Univ Ireland Univ Coll Cork, Lab Neurogastroenterol, Alimentary Pharmabiot Ctr, Cork, Ireland.
   [Cryan, John F.] Natl Univ Ireland Univ Coll Cork, Dept Anat & Neurosci, Cork, Ireland.
   [Dinan, Timothy G.] Natl Univ Ireland Univ Coll Cork, Dept Psychiat, Cork, Ireland.
RP Cryan, JF (reprint author), Natl Univ Ireland Univ Coll Cork, Lab Neurogastroenterol, Alimentary Pharmabiot Ctr, Cork, Ireland.
EM j.cryan@ucc.ie
RI Cryan, John/A-6950-2013
OI Cryan, John/0000-0001-5887-2723
FU Science Foundation Ireland (SFI), through the Irish Government's
   National Development Plan; SFI [02/CE/B124, 07/CE/B1368]
FX The authors thank M. Julio-Pieper at Imagenes Ciencia for assistance
   with figures, and G. Clarke and L. Desbonnet for helpful comments on the
   paper. The Alimentary Pharmabiotic Centre is a research centre funded by
   Science Foundation Ireland (SFI), through the Irish Government's
   National Development Plan. The authors and their work were supported by
   SFI (grant numbers 02/CE/B124 and 07/CE/B1368).
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NR 137
TC 205
Z9 212
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1471-003X
EI 1471-0048
J9 NAT REV NEUROSCI
JI Nat. Rev. Neurosci.
PD OCT
PY 2012
VL 13
IS 10
BP 701
EP 712
DI 10.1038/nrn3346
PG 12
WC Neurosciences
SC Neurosciences & Neurology
GA 012CA
UT WOS:000309211800011
PM 22968153
ER

PT J
AU Ben-Ari, Y
   Khalilov, I
   Kahle, KT
   Cherubini, E
AF Ben-Ari, Yehezkel
   Khalilov, Ilgam
   Kahle, Kristopher T.
   Cherubini, Enrico
TI The GABA Excitatory/Inhibitory Shift in Brain Maturation and
   Neurological Disorders
SO NEUROSCIENTIST
LA English
DT Article
DE GABA; excitation/inhibition; neonatal neurons; epilepsies; bumetanide;
   NKCC1; KCC2; phenobarbital; diazepam; GABA-acting antiepileptic drugs
ID NEONATAL-RAT HIPPOCAMPUS; GIANT DEPOLARIZING POTENTIALS; TEMPORAL-LOBE
   EPILEPSY; LONG-TERM POTENTIATION; K-CL COTRANSPORTER; NEURONAL CHLORIDE
   ACCUMULATION; IN-VITRO; DEVELOPING NEOCORTEX; NETWORK ACTIVITY;
   EXCITATORY ACTIONS
AB Ionic currents and the network-driven patterns they generate differ in immature and adult neurons: The developing brain is not a "small adult brain." One of the most investigated examples is the developmentally regulated shift of actions of the transmitter GABA that inhibit adult neurons but excite immature ones because of an initially higher intracellular chloride concentration [Cl-](i), leading to depolarizing and often excitatory actions of GABA instead of hyperpolarizing and inhibitory actions. The levels of [Cl-](i) are also highly labile, being readily altered transiently or persistently by enhanced episodes of activity in relation to synaptic plasticity or a variety of pathological conditions, including seizures and brain insults. Among the plethora of channels, transporters, and other devices involved in controlling [Cl-](i), two have emerged as playing a particularly important role: the chloride importer NKCC1 and the chloride exporter KCC2. Here, the authors stress the importance of determining how [Cl-](i) is dynamically regulated and how this affects brain operation in health and disease. In a clinical perspective, agents that control [Cl-](i) and reinstate inhibitory actions of GABA open novel therapeutic perspectives in many neurological disorders, including infantile epilepsies, autism spectrum disorders, and other developmental disorders.
C1 [Ben-Ari, Yehezkel; Khalilov, Ilgam] INSERM, INMED, U901, F-13258 Marseille, France.
   [Ben-Ari, Yehezkel; Khalilov, Ilgam] Neurochlore, Marseille, France.
   [Kahle, Kristopher T.] Massachusetts Gen Hosp, Dept Neurosurg, Boston, MA 02114 USA.
   [Kahle, Kristopher T.] Harvard Univ, Sch Med, Boston, MA USA.
   [Cherubini, Enrico] Int Sch Adv Studies SISSA, Trieste, Italy.
RP Ben-Ari, Y (reprint author), INMED & CEO Neurochlore, INMED Campus Sci Luminy,163 Route Luminy, F-13273 Marseilles 09, France.
EM ben-ari@inmed.univ-mrs.fr
FU French Medical Research council (INSERM); French Medical Research (FRM)
   association; French Federation of Brain Research (FRC); European Union
   grants (EU No); Ministero Universita e Ricerca (MIUR, Italy); telethon
   grant [GGP11043]
FX The authors disclosed receipt of the following financial support for the
   research and/or authorship of this article: This work was supported by
   the French Medical Research council (INSERM), the French Medical
   Research (FRM) association, the French Federation of Brain Research
   (FRC), European Union grants (EU No), Ministero Universita e Ricerca
   (MIUR, Italy), and telethon grant GGP11043.
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NR 142
TC 67
Z9 68
PU SAGE PUBLICATIONS INC
PI THOUSAND OAKS
PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA
SN 1073-8584
J9 NEUROSCIENTIST
JI Neuroscientist
PD OCT
PY 2012
VL 18
IS 5
BP 467
EP 486
DI 10.1177/1073858412438697
PG 20
WC Clinical Neurology; Neurosciences
SC Neurosciences & Neurology
GA 011IC
UT WOS:000309157300005
PM 22547529
ER

PT J
AU Birman, CS
   Elliott, EJ
   Gibson, WPR
AF Birman, Catherine S.
   Elliott, Elizabeth J.
   Gibson, William P. R.
TI Pediatric Cochlear Implants: Additional Disabilities Prevalence, Risk
   Factors, and Effect on Language Outcomes
SO OTOLOGY & NEUROTOLOGY
LA English
DT Article
DE Additional disability; Cochlear implant; Language; Pediatric
ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; HEARING-LOSS; CHILDREN;
   PERFORMANCE; RECEIVE; SPEECH
AB Objective: To determine the prevalence of additional disabilities in a pediatric cochlear population, to identify medical and radiologic conditions associated with additional disabilities, and to identify the effect of additional disabilities on speech perception and language at 12 months postoperatively.
   Study Design: Retrospective case review.
   Setting: Tertiary referral center and cochlear implant program.
   Patients: Records were reviewed for children 0 to 16 years old inclusive, who had cochlear implant-related operations over a 12-month period.
   Interventions: Diagnostic and rehabilitative.
   Main Outcome Measures: Additional disabilities prevalence; medical history and radiologic abnormalities; and the effect on Categories of Auditory Performance (CAP) score at 12 months postoperatively.
   Results: Eighty-eight children having 96 operations were identified. The overall prevalence of additional disabilities (including developmental delay, cerebral palsy, visual impairment, autism and attention deficit disorder) was 33%. The main conditions associated with additional disabilities were syndromes and chromosomal abnormalities (87%), jaundice (86%), prematurity (62%), cytomegalovirus (60%), and inner ear abnormalities including cochlea nerve hypoplasia or aplasia (75%) and semicircular canal anomalies (56%). At 12 months postoperatively, almost all (96%) of the children without additional disabilities had a CAP score of 5 or greater (speech), compared with 52% of children with additional disabilities. Children with developmental delay had a median CAP score of 4, at 12 months compared with 6 for those without developmental delay.
   Conclusion: Additional disabilities are prevalent in approximately a third of pediatric cochlear implant patients. Additional disabilities significantly affect the outcomes of cochlear implants.
C1 [Birman, Catherine S.; Gibson, William P. R.] Sydney Cochlear Implant Ctr, Gladesville, NSW 1675, Australia.
   [Birman, Catherine S.; Elliott, Elizabeth J.; Gibson, William P. R.] Univ Sydney, Sydney Med Sch, Sydney, NSW 2006, Australia.
   [Birman, Catherine S.; Elliott, Elizabeth J.; Gibson, William P. R.] Sydney Childrens Network Westmead, Westmead, NSW, Australia.
RP Birman, CS (reprint author), Sydney Cochlear Implant Ctr, POB 188, Gladesville, NSW 1675, Australia.
EM Catherine.birman@gmail.com
FU National Health and Medical Research Council of Australia [457084,
   1021480]
FX E. J. E. is a Practitioner Fellow supported by the National Health and
   Medical Research Council of Australia (grants 457084 and 1021480).
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NR 22
TC 9
Z9 10
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 1531-7129
J9 OTOL NEUROTOL
JI Otol. Neurotol.
PD OCT
PY 2012
VL 33
IS 8
BP 1347
EP 1352
DI 10.1097/MAO.0b013e31826939cc
PG 6
WC Clinical Neurology; Otorhinolaryngology
SC Neurosciences & Neurology; Otorhinolaryngology
GA 010SH
UT WOS:000309113900014
PM 22975903
ER

PT J
AU Lit, L
   Sharp, FR
   Bertoglio, K
   Stamova, B
   Ander, BP
   Sossong, AD
   Hendren, RL
AF Lit, L.
   Sharp, F. R.
   Bertoglio, K.
   Stamova, B.
   Ander, B. P.
   Sossong, A. D.
   Hendren, R. L.
TI Gene expression in blood is associated with risperidone response in
   children with autism spectrum disorders
SO PHARMACOGENOMICS JOURNAL
LA English
DT Article
DE autism; risperidone; gene expression; atypical antipsychotic
ID PERVASIVE DEVELOPMENTAL DISORDERS; ANTIPSYCHOTIC TREATMENT; CANDIDATE
   GENES; SCHIZOPHRENIA; OLANZAPINE; SYMPTOMS; BEHAVIOR; RECEPTOR; TARGET
AB Children with autism spectrum disorders (ASDs) often have severe behavioral problems. Not all children with these problems respond to atypical antipsychotic medications; therefore, we investigated whether peripheral blood gene expression before treatment with risperidone, an atypical antipsychotic, was associated with improvements in severe behavioral disturbances 8 weeks following risperidone treatment in 42 ASD subjects (age 112.7 +/- 51.2 months). Exon expression levels in blood before risperidone treatment were compared with pre-post risperidone change in Aberrant Behavior Checklist-Irritability (ABC-I) scores. Expression of exons within five genes was correlated with change in ABC-I scores across all risperidone-treated subjects: GBP6, RABL5, RNF213, NFKBID and RNF40 (alpha < 0.001). RNF40 is located at 16p11.2, a region implicated in autism and schizophrenia. Thus, these genes expressed before treatment were associated with subsequent clinical response. Future studies will be needed to confirm these results and determine whether this expression profile is associated with risperidone response in other disorders, or alternative antipsychotic response within ASD. The Pharmacogenomics Journal (2012) 12, 368-371; doi:10.1038/tpj.2011.23; published online 7 June 2011
C1 [Lit, L.; Sharp, F. R.; Stamova, B.; Ander, B. P.] Univ Calif Davis, Dept Neurol, MIND Inst, Davis, CA 95817 USA.
   [Bertoglio, K.] Univ Calif Irvine, Sch Med, Irvine, CA 92717 USA.
   [Sossong, A. D.] Univ Calif San Francisco, Sch Med, San Francisco, CA USA.
   [Hendren, R. L.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA USA.
RP Lit, L (reprint author), Univ Calif Davis, Dept Neurol, MIND Inst, 2805 50th St,Room 2415, Davis, CA 95817 USA.
EM llit@ucdavis.edu
FU  [R21MH080026]
FX We appreciate the participation of study volunteers and their families.
   This study was supported by R21MH080026 (RLH).
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NR 28
TC 4
Z9 4
PU NATURE PUBLISHING GROUP
PI LONDON
PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND
SN 1470-269X
J9 PHARMACOGENOMICS J
JI Pharmacogenomics J.
PD OCT
PY 2012
VL 12
IS 5
BP 368
EP 371
DI 10.1038/tpj.2011.23
PG 4
WC Genetics & Heredity; Pharmacology & Pharmacy
SC Genetics & Heredity; Pharmacology & Pharmacy
GA 012CM
UT WOS:000309213000002
PM 21647175
ER

PT J
AU Yazdani, M
   Deogracias, R
   Guy, J
   Poot, RA
   Bird, A
   Barde, YA
AF Yazdani, Morteza
   Deogracias, Ruben
   Guy, Jacky
   Poot, Raymond A.
   Bird, Adrian
   Barde, Yves-Alain
TI Disease Modeling Using Embryonic Stem Cells: MeCP2 Regulates Nuclear
   Size and RNA Synthesis in Neurons
SO STEM CELLS
LA English
DT Article
DE Rett syndrome; Nuclear size; Transcription; Astrocytes; Brain-derived
   neurotrophic factor; Synaptophysin
ID CPG-BINDING PROTEIN-2; RETT-SYNDROME; GENE-EXPRESSION; CEREBRAL-CORTEX;
   DEFICIENCY; TRANSCRIPTION; MICE; PROGRESSION; MATURATION; MUTATIONS
AB Mutations in the gene encoding the methyl-CpG-binding protein MECP2 are the major cause of Rett syndrome, an autism spectrum disorder mainly affecting young females. MeCP2 is an abundant chromatin-associated protein, but how and when its absence begins to alter brain function is still far from clear. Using a stem cell-based system allowing the synchronous differentiation of neuronal progenitors, we found that in the absence of MeCP2, the size of neuronal nuclei fails to increase at normal rates during differentiation. This is accompanied by a marked decrease in the rate of ribonucleotide incorporation, indicating an early role of MeCP2 in regulating total gene transcription, not restricted to selected mRNAs. We also found that the levels of brain-derived neurotrophic factor (BDNF) were decreased in mutant neurons, while those of the presynaptic protein synaptophysin increased at similar rates in wild-type and mutant neurons. By contrast, nuclear size, transcription rates, and BDNF levels remained unchanged in astrocytes lacking MeCP2. Re-expressing MeCP2 in mutant neurons rescued the nuclear size phenotype as well as BDNF levels. These results reveal a new role of MeCP2 in regulating overall RNA synthesis in neurons during the course of their maturation, in line with recent findings indicating a reduced nucleolar size in neurons of the developing brain of mice lacking Mecp2. STEM Cells2012;30:21282139
C1 [Yazdani, Morteza; Deogracias, Ruben; Barde, Yves-Alain] Univ Basel, Biozentrum, CH-4056 Basel, Switzerland.
   [Guy, Jacky; Bird, Adrian] Univ Edinburgh, Wellcome Trust Ctr Cell Biol, Edinburgh, Midlothian, Scotland.
   [Poot, Raymond A.] Erasmus Med Ctr MC, Dept Cell Biol, Rotterdam, Netherlands.
RP Barde, YA (reprint author), Univ Basel, Biozentrum, 50-70 Klingelbergstr, CH-4056 Basel, Switzerland.
EM yves.barde@unibas.ch
FU Rett Syndrome Research Foundation; Swiss National Foundation
   [CRSI33_130441]; International Rett Syndrome Foundation
FX We would like to thank the Rett Syndrome Research Foundation for
   supporting the initial phase of this work, subsequently supported by a
   "Sinergia" program of the Swiss National Foundation, CRSI33_130441, and
   by the International Rett Syndrome Foundation.
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NR 39
TC 14
Z9 15
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1066-5099
J9 STEM CELLS
JI Stem Cells
PD OCT
PY 2012
VL 30
IS 10
BP 2128
EP 2139
DI 10.1002/stem.1180
PG 12
WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology;
   Oncology; Cell Biology; Hematology
SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology
GA 008AA
UT WOS:000308928300006
PM 22865604
ER

PT J
AU Reed, P
   Osborne, LA
AF Reed, Phil
   Osborne, Lisa A.
TI Diagnostic practice and its impacts on parental health and child
   behaviour problems in autism spectrum disorders
SO ARCHIVES OF DISEASE IN CHILDHOOD
LA English
DT Review
ID EARLY TEACHING INTERVENTIONS; SCHOOL-AGE-CHILDREN; QUALITY-OF-LIFE;
   YOUNG-CHILDREN; DEVELOPMENTAL DISABILITY; INTELLECTUAL DISABILITY;
   SYNDROME SPECIFICITY; ASPERGER-SYNDROME; INFANTILE-AUTISM; SELF-EFFICACY
AB Obtaining a diagnosis is a key point in developing a treatment plan for children with autism spectrum disorders (ASD), but little attention has been paid to the impacts of diagnostic practices on families, and the consequent impact on child outcomes. Parents' experiences during ASD diagnosis for their child can be stressful, and such stress can lead to parental ill health, child-behaviour problems, and poorer child outcomes following treatment. Thus, the conduct of diagnosis may be of particular importance for subsequent child outcomes and parental health. A lack of knowledge regarding best diagnostic practice may ultimately impair treatment efficacy and lead to increased health-and economic-burdens. Given this, the current article examines recent work concerning: parental experiences of ASD diagnoses; general health and psychological functioning of parents of newly-diagnosed children with ASD; aspects of the diagnostic process impacting on parental functioning; and the relationship of parental functioning to child outcomes. These are placed into the context of diagnostic best practice for ASD, and understanding the complex relationship between ASD and family variables.
C1 [Reed, Phil] Swansea Univ, Dept Psychol, Swansea SA2 8PP, W Glam, Wales.
   [Osborne, Lisa A.] Swansea Univ, Long Term & Chron Condit Ctr, Swansea SA2 8PP, W Glam, Wales.
RP Reed, P (reprint author), Swansea Univ, Dept Psychol, Singleton Pk, Swansea SA2 8PP, W Glam, Wales.
EM p.reed@swansea.ac.uk
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NR 74
TC 1
Z9 1
PU BMJ PUBLISHING GROUP
PI LONDON
PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND
SN 0003-9888
J9 ARCH DIS CHILD
JI Arch. Dis. Child.
PD OCT
PY 2012
VL 97
IS 10
BP 927
EP 931
DI 10.1136/archdischild-2012-301761
PG 5
WC Pediatrics
SC Pediatrics
GA 009WM
UT WOS:000309056100021
PM 22806234
ER

PT J
AU Smith, M
   Flodman, PL
   Gargus, JJ
   Simon, MT
   Verrell, K
   Haas, R
   Reiner, GE
   Naviaux, R
   Osann, K
   Spence, MA
   Wallace, DC
AF Smith, Moyra
   Flodman, Pamela L.
   Gargus, John J.
   Simon, Mariella T.
   Verrell, Kimberley
   Haas, Richard
   Reiner, Gail E.
   Naviaux, Robert
   Osann, Katherine
   Spence, M. Anne
   Wallace, Douglas C.
TI Mitochondrial and ion channel gene alterations in autism
SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS
LA English
DT Article
DE Autism; Mitochondria; OXPHOS; Copy number variants (CNVs); Calcium
   channel; Synapses
ID CARRIER SLC25A12 GENE; SPECTRUM DISORDERS; CALCIUM UNIPORTER; CANDIDATE
   GENES; ABNORMALITIES; DYSFUNCTION; NEUROBEACHIN; ASSOCIATION;
   DELINEATION; MUTATIONS
AB To evaluate the potential importance in autistic subjects of copy number variants (CNVs) that alter genes of relevance to bioenergetics, ionic metabolism, and synaptic function, we conducted a detailed microarray analysis of 69 autism probands and 35 parents, compared to 89 CEU HapMap controls. This revealed that the frequency CNVs of >= 100 kb and CNVs of >= 10 Kb were markedly increased in probands over parents and in probands and parents over controls. Evaluation of CNVs >= 1 Mb by chromosomal FISH confirmed the molecular identity of a subset of the CNVs, some of which were associated with chromosomal rearrangements. In a number of the cases, CNVs were found to alter the copy number of genes that are important in mitochondrial oxidative phosphorylation (OXPHOS), ion and especially calcium transport, and synaptic structure. Hence, autism might result from alterations in multiple bioenergetic and metabolic genes required for mental function. This article is part of a Special Issue entitled: 17th European Bioenergetics Conference (EBEC 2012). (C) 2012 Elsevier B.V. All rights reserved.
C1 [Wallace, Douglas C.] Univ Penn, Ctr Mitochondrial & Epigen Med, Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA.
   [Smith, Moyra; Flodman, Pamela L.; Gargus, John J.; Simon, Mariella T.; Verrell, Kimberley; Osann, Katherine; Spence, M. Anne] Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA.
   [Haas, Richard; Reiner, Gail E.; Naviaux, Robert] Univ Calif San Diego, San Diego, CA 92103 USA.
   [Wallace, Douglas C.] Univ Penn, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
RP Wallace, DC (reprint author), Univ Penn, Ctr Mitochondrial & Epigen Med, Childrens Hosp Philadelphia, Colket Translational Res Bldg,Room 6060,3501 Civ, Philadelphia, PA 19104 USA.
EM dmsmith@uci.edu; pflodman@uci.edu; jjgargus@uci.edu; simonm@uci.edu;
   kverrell@uci.edu; rhaas@ucsd.edu; gereiner@ucsd.edu; rnaviaux@ucsd.edu;
   kosann@uci.edu; maspence@uci.edu; wallaced1@email.chop.edu
FU Autism Speaks Foundation [5668]; Simons Foundation [205844]; NIH
   [NS070298, AG24373, NS21328, UL1 TR000153]
FX The work was supported by Autism Speaks Foundation grant 5668, Simons
   Foundation Grant # 205844, and NIH grants NS070298, AG24373, and NS21328
   awarded to DCW; and NIH UL1 TR000153 supporting MS and the overall
   project.
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NR 42
TC 6
Z9 7
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0005-2728
J9 BBA-BIOENERGETICS
JI Biochim. Biophys. Acta-Bioenerg.
PD OCT
PY 2012
VL 1817
IS 10
SI SI
BP 1796
EP 1802
DI 10.1016/j.bbabio.2012.04.004
PG 7
WC Biochemistry & Molecular Biology; Biophysics
SC Biochemistry & Molecular Biology; Biophysics
GA 994GF
UT WOS:000307918200012
PM 22538295
ER

PT J
AU Konishi, Y
   Okubo, K
   Kato, I
   Ijichi, S
   Nishida, T
   Kusaka, T
   Isobe, K
   Itoh, S
   Kato, M
   Konishi, Y
AF Konishi, Yukihiko
   Okubo, Kensuke
   Kato, Ikuko
   Ijichi, Sonoko
   Nishida, Tomoko
   Kusaka, Takashi
   Isobe, Kenichi
   Itoh, Susumu
   Kato, Masaharu
   Konishi, Yukuo
TI A developmental change of the visual behavior of the face recognition in
   the early infancy
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Visual function; Infant; Eye tracker
ID EXPLORATORY EYE-MOVEMENTS; AUTISM; MECHANISMS; PREFERENCE
AB The purpose of this study was to examine developmental changes in visuocognitive function, particularly face recognition, in early infancy. In this study, we measured eye movement in healthy infants with a preference gaze problem, particularly eye movement between two face stimulations. We used the eye tracker system (Tobii1750, Tobii Technologies, Sweden) to measure eye movement in infants. Subjects were 17 3-month-old infants and 16 4-month-old infants. The subjects looked two types of face stimulation (upright face/scrambled face) at the same time and we measured their visual behavior (preference/looking/eye movement). Our results showed that 4-month-old infants looked at an upright face longer than 3-month infants, and exploratory behavior while comparing two face stimulations significantly increased. In this study, 4-month-old infants showed a preference towards an upright face. The numbers of eye movements between two face stimuli significantly increased in 4-month-old infants. These results suggest that eye movements may be an important index in face cognitive function during early infancy. (C) 2012 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Konishi, Yukihiko; Okubo, Kensuke; Kato, Ikuko; Ijichi, Sonoko; Kusaka, Takashi; Isobe, Kenichi; Itoh, Susumu] Kagawa Univ, Dept Pediat, Fac Med, Kitagun, Kagawa 7610793, Japan.
   [Kato, Masaharu; Konishi, Yukuo] Doshisha Univ, Fac Psychol, Ctr Baby Sci, Kyoto, Japan.
   [Nishida, Tomoko] Kagawa Univ, Fac Educ, Dept Educ Children Special Needs, Kitagun, Kagawa 7610793, Japan.
RP Konishi, Y (reprint author), Kagawa Univ, Dept Pediat, Fac Med, Mikichol 750-1, Kitagun, Kagawa 7610793, Japan.
EM lilwest@med.kagawa-u.ac.jp; lilwest@med.kagawa-u.ac.jp
FU Ministry of Education of Japan (Science and culture Division) [22591202,
   22791031]
FX This research was supported by Grants-in-Aid for Scientific Research (C)
   No. 22591202 and Encouragement of Young Scientists No. 22791031 from the
   Ministry of Education of Japan (Science and culture Division).
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NR 14
TC 0
Z9 0
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2012
VL 34
IS 9
BP 719
EP 722
DI 10.1016/j.braindev.2012.01.004
PG 4
WC Clinical Neurology
SC Neurosciences & Neurology
GA 009HW
UT WOS:000309017900003
PM 22310452
ER

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   Kometani, Hiroshi
   Nakai, Akio
   Tsukahara, Hirokazu
   Tomoda, Akemi
   Mayumi, Mitsufumi
   Ohshima, Yusei
TI Focal EEG abnormalities might reflect neuropathological characteristics
   of pervasive developmental disorder and attention-deficit/hyperactivity
   disorder
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Pervasive developmental disorder; Attention-deficit/hyperactivity
   disorder; Electroencephalogram abnormality; Paroxysmal discharges
ID DEFICIT-HYPERACTIVITY DISORDER; ROLANDIC SPIKES; ADHD CHILDREN;
   FREQUENCY; AUTISM; ELECTROENCEPHALOGRAM; CHILDHOOD; BRAIN
AB Neurophysiological characteristics in electroencephalograms (EEG) were investigated for patients with pervasive developmental disorder (PDD) and for patients with attention-deficit/hyperactivity disorder (AD/HD). This study examined 64 PDD children and 22 AD/HD children with no history of epilepsy or progressive neurological or psychiatric disorder. We used multivariate analysis to compare EEG abnormalities, clinical symptoms, and intelligence levels between PDD and AD/AD patient groups. Paroxysmal discharges at the frontopolar-frontal (Fp-F) brain regions and background EEG abnormalities tended to be detected preferentially in the PDD group, although paroxysmal discharges at central temporal (C-T) regions tended to be detected preferentially in the AD/HD group. The paroxysmal discharges observed in patients expressing persistence and impulsivity are apparently localized respectively in the Fp-F and C-T regions. A combination of EEG abnormalities, including background EEG abnormalities and paroxysmal discharges at Fp-F and C-T regions, might be useful diagnostic hallmarks to distinguish PDD with AD/HD from AD/HD alone using a logistic regression model. The dysfunction of specific brain areas associated with EEG abnormalities might explain characteristics of clinical symptoms observed in PDD and AD/HD patients. (C) 2011 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Kawatani, Masao; Kometani, Hiroshi; Nakai, Akio; Tsukahara, Hirokazu; Mayumi, Mitsufumi; Ohshima, Yusei] Univ Fukui, Dept Pediat, Fac Med Sci, Yoshida, Fukui 9101193, Japan.
   [Kawatani, Masao; Hiratani, Michio] Hiratani Clin Dev Disorders Children, Fukui, Japan.
   [Tomoda, Akemi] Univ Fukui, Grad Sch Med Sci, Child Dev Res Ctr, Fukui 910, Japan.
RP Kawatani, M (reprint author), Univ Fukui, Dept Pediat, Fac Med Sci, Yoshida, Fukui 9101193, Japan.
EM kawatani@u-fukui.ac.jp
FU Japanese Ministry of Health, Labour and Welfare
FX This work was supported by Grants-in-Aid for Scientific Research from
   the Japanese Ministry of Health, Labour and Welfare.
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NR 22
TC 1
Z9 1
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2012
VL 34
IS 9
BP 723
EP 730
DI 10.1016/j.braindev.2011.11.009
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 009HW
UT WOS:000309017900004
PM 22225922
ER

PT J
AU Iwatani, Y
   Kagitani-Shimono, K
   Tominaga, K
   Okinaga, T
   Mohri, I
   Kishima, H
   Kato, A
   Sanefuji, W
   Yamamoto, T
   Tatsumi, A
   Murata, E
   Taniike, M
   Nagai, T
   Ozono, K
AF Iwatani, Yoshiko
   Kagitani-Shimono, Kuriko
   Tominaga, Koji
   Okinaga, Takeshi
   Mohri, Ikuko
   Kishima, Haruhiko
   Kato, Amami
   Sanefuji, Wakako
   Yamamoto, Tomoka
   Tatsumi, Aika
   Murata, Emi
   Taniike, Masako
   Nagai, Toshisaburo
   Ozono, Keiichi
TI Long-term developmental outcome in patients with West syndrome after
   epilepsy surgery
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE Autism; Developmental outcome; Epilepsy surgery; Spasms; West syndrome
ID INTRACTABLE INFANTILE SPASMS; SURGICAL-TREATMENT; CHILDREN; SEIZURE;
   HEMISPHERECTOMY; AUTISM; COMMUNICATION; INTERVENTION; DISORDERS;
   LANGUAGE
AB It has been hypothesized that early seizure control may prevent children with intractable epileptic spasms (ES) from developmental regression and may contribute to better developmental outcome. The effectiveness of surgery for ES has been reported. We investigated long-term post-operative outcomes of seizure control and development in patients with symptomatic West syndrome (S-WS) who underwent epilepsy surgery. Six children who underwent surgical intervention for intractable ES were retrospectively investigated. Cortical malformations were observed on pre-operative MRI in all patients, with hemispheric or multilobar involvement in four children and focal lesions in two. Following surgery, we measured motor function, developmental age (DA), language skills, and sociopsychological function for up to 7 years (mean, 4.9 years). Post-operative seizure outcome was Engel Class I (n = 4) or III (n = 2). Motor function and DA was increased following surgery in six and five patients, respectively. Two patients started to speak in sentences following focal resection. Autistic features were noted in four of the five examined patients post-operatively. None of the patients showed developmental regression following surgery. Epilepsy surgery for S-WS with ES may result in good seizure control and improvement in motor development. Improvement in cognitive function was modest in this small cohort of children and autistic features were noted post-operatively in a substantial proportion of the children. While seizure control can be obtained by epilepsy surgery, early intervention for sociopsychological comorbidities may be warranted in children with S-WS. (C) 2012 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Iwatani, Yoshiko; Kagitani-Shimono, Kuriko; Tominaga, Koji; Okinaga, Takeshi; Ozono, Keiichi] Osaka Univ, Dept Pediat, Grad Sch Med, Suita, Osaka 5650871, Japan.
   [Kagitani-Shimono, Kuriko; Mohri, Ikuko; Taniike, Masako] Osaka Univ, Grad Sch Med, United Grad Sch Child Dev, Osaka, Japan.
   [Tominaga, Koji; Mohri, Ikuko; Sanefuji, Wakako; Yamamoto, Tomoka; Tatsumi, Aika; Murata, Emi; Taniike, Masako] Osaka Univ, Grad Sch Med, Dept Mol Res, Ctr Childrens Mental Dev, Osaka, Japan.
   [Kishima, Haruhiko] Osaka Univ, Grad Sch Med, Dept Neurosurg, Osaka, Japan.
   [Kato, Amami] Kinki Univ, Fac Med, Dept Neurosurg, Osaka, Japan.
   [Nagai, Toshisaburo] Osaka Univ, Div Hlth Sci, Grad Sch Med, Osaka, Japan.
RP Kagitani-Shimono, K (reprint author), Osaka Univ, Dept Pediat, Grad Sch Med, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan.
EM kuriko@ped.med.osaka-u.ac.jp
FU Core Research for Evolutional Science and Technology (CREST) on
   Bio-medical-photonic LSI from Japan Science and Technology Agency (JST);
   Japan Society for the Promotion of Science (JSPS) [20300199]
FX This work was supported in part by the Core Research for Evolutional
   Science and Technology (CREST) on Bio-medical-photonic LSI from Japan
   Science and Technology Agency (JST), and a Grant-in-Aid for Scientific
   Research (20300199) from the Japan Society for the Promotion of Science
   (JSPS).
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NR 30
TC 3
Z9 3
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2012
VL 34
IS 9
BP 731
EP 738
DI 10.1016/j.braindev.2012.01.008
PG 8
WC Clinical Neurology
SC Neurosciences & Neurology
GA 009HW
UT WOS:000309017900005
PM 22336751
ER

PT J
AU Zvereff, V
   Carpenter, L
   Patton, D
   Cabral, H
   Rita, D
   Wilson, A
   Anyane-Yeboa, K
   White, L
   Friedman, KJ
AF Zvereff, Val
   Carpenter, Lori
   Patton, Dagny
   Cabral, Huong
   Rita, Debra
   Wilson, Ashley
   Anyane-Yeboa, Kwame
   White, Larry
   Friedman, Kenneth J.
TI Molecular diagnostic dilemmas in Rett syndrome
SO BRAIN & DEVELOPMENT
LA English
DT Article
DE MECP2; Rett syndrome; Autism; Mental retardation; Mutational analysis;
   XLMR
ID CPG-BINDING PROTEIN-2; MECP2 MUTATIONS; GENE; PHENOTYPE; LOCATION;
   SPECTRUM; POLYMORPHISMS; INACTIVATION; SEVERITY; SEQUENCE
AB Rett syndrome (OMIM 312750) is a progressive, X-linked neurodevelopmental disorder caused by mutations in the MECP2 gene located on chromosome Xq28. The disorder is characterized by a period of normal development during the first 6-18 months of life, followed by gradual loss of skills already gained, such as speech and purposeful movement of the hands. The majority of cases are sporadic and represent "de novo" mutations.
   In this study we summarize the results of diagnostic testing of 30 patients with Rett syndrome (RTT) or mental retardation of unknown etiology using bidirectional sequencing of the open reading frame of the MECP2 gene. Twenty different variants were identified in those patients including 12 missense (R133C, P152R, T158M, V300I, I303M, R306C, T311M, R344W, A358T, P384L, A443T, V481M), four nonsense (R168X, K192X, R255X, R270X), two deletion (E137_L386de1, 1293_S350de1), and two frameshift (S291QfsX26, G343AfsX6) mutations. Seven of the twenty variants identified were novel mutations (E137L386del, K192X, S291QfsX26, G343AfsX6, 1293_S350de1, P384L, and A443T). In the cases with novel or non-recurrent missense mutations, family studies were performed to investigate genotype-phenotype correlations. Our results demonstrate the importance of family studies and highlight the complexity of interpretation of MECP2 alterations, which may or may not be disease-associated. (C) 2012 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved.
C1 [Zvereff, Val; Carpenter, Lori; Patton, Dagny; Cabral, Huong; Friedman, Kenneth J.] Lab Corp Amer, Ctr Mol Biol & Pathol, Res Triangle Pk, NC 27709 USA.
   [Rita, Debra] Advocate Lutheran Gen Hosp, Park Ridge, IL USA.
   [Wilson, Ashley; Anyane-Yeboa, Kwame] Columbia Univ, Med Ctr, New York, NY 10027 USA.
   [White, Larry] Childrens Hosp Kings Daughters, Norfolk, VA USA.
RP Zvereff, V (reprint author), Lab Corp Amer, Ctr Mol Biol & Pathol, 1912 TW Alexander Dr, Res Triangle Pk, NC 27709 USA.
EM zverefv@labcorp.com
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NR 29
TC 1
Z9 2
PU ELSEVIER SCIENCE BV
PI AMSTERDAM
PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS
SN 0387-7604
J9 BRAIN DEV-JPN
JI Brain Dev.
PD OCT
PY 2012
VL 34
IS 9
BP 750
EP 755
DI 10.1016/j.braindev.2011.12.012
PG 6
WC Clinical Neurology
SC Neurosciences & Neurology
GA 009HW
UT WOS:000309017900008
PM 22277191
ER

PT J
AU Bzdok, D
   Schilbach, L
   Vogeley, K
   Schneider, K
   Laird, AR
   Langner, R
   Eickhoff, SB
AF Bzdok, Danilo
   Schilbach, Leonhard
   Vogeley, Kai
   Schneider, Karla
   Laird, Angela R.
   Langner, Robert
   Eickhoff, Simon B.
TI Parsing the neural correlates of moral cognition: ALE meta-analysis on
   morality, theory of mind, and empathy
SO BRAIN STRUCTURE & FUNCTION
LA English
DT Article
DE Moral cognition; Theory of mind (ToM); Empathy; Social cognition; Meta;
   analysis; ALE
ID VENTROMEDIAL PREFRONTAL CORTEX; RIGHT TEMPOROPARIETAL JUNCTION;
   TEMPORO-PARIETAL JUNCTION; HIGH-FUNCTIONING AUTISM; MENTAL TIME-TRAVEL;
   SOCIAL COGNITION; HUMAN AMYGDALA; INTERSUBJECT VARIABILITY;
   AUTOBIOGRAPHICAL MEMORY; PERSPECTIVE-TAKING
AB Morally judicious behavior forms the fabric of human sociality. Here, we sought to investigate neural activity associated with different facets of moral thought. Previous research suggests that the cognitive and emotional sources of moral decisions might be closely related to theory of mind, an abstract-cognitive skill, and empathy, a rapid-emotional skill. That is, moral decisions are thought to crucially refer to other persons' representation of intentions and behavioral outcomes as well as (vicariously experienced) emotional states. We thus hypothesized that moral decisions might be implemented in brain areas engaged in 'theory of mind' and empathy. This assumption was tested by conducting a large-scale activation likelihood estimation (ALE) meta-analysis of neuroimaging studies, which assessed 2,607 peak coordinates from 247 experiments in 1,790 participants. The brain areas that were consistently involved in moral decisions showed more convergence with the ALE analysis targeting theory of mind versus empathy. More specifically, the neurotopographical overlap between morality and empathy disfavors a role of affective sharing during moral decisions. Ultimately, our results provide evidence that the neural network underlying moral decisions is probably domain-global and might be dissociable into cognitive and affective sub-systems.
C1 [Eickhoff, Simon B.] Forschungszentrum Julich, Inst Neurowissensch & Med INM 2, D-52425 Julich, Germany.
   [Bzdok, Danilo; Schneider, Karla; Langner, Robert; Eickhoff, Simon B.] Rhein Westfal TH Aachen, Dept Psychiat Psychotherapy & Psychosomat, Sch Med, Aachen, Germany.
   [Bzdok, Danilo; Langner, Robert; Eickhoff, Simon B.] Res Ctr Julich, Inst Neurosci & Med INM 2, Julich, Germany.
   [Bzdok, Danilo; Schneider, Karla; Langner, Robert; Eickhoff, Simon B.] JARA, Aachen, Germany.
   [Schilbach, Leonhard] Max Planck Inst Neurol Res, D-50931 Cologne, Germany.
   [Schilbach, Leonhard; Vogeley, Kai] Univ Cologne, Dept Psychiat, D-50931 Cologne, Germany.
   [Laird, Angela R.] Univ Texas Hlth Sci Ctr San Antonio, Res Imaging Inst, San Antonio, TX 78229 USA.
   [Eickhoff, Simon B.] Univ Dusseldorf, Inst Clin Neurosci & Med Psychol, D-40225 Dusseldorf, Germany.
   [Vogeley, Kai] Res Ctr Julich, Inst Neurosci & Med INM 3, Julich, Germany.
RP Eickhoff, SB (reprint author), Forschungszentrum Julich, Inst Neurowissensch & Med INM 2, D-52425 Julich, Germany.
EM S.Eickhoff@fz-juelich.de
RI Laird, Angela/B-5800-2010; Schilbach, Leonhard/G-5832-2010; Vogeley,
   K/E-4860-2012
OI Schilbach, Leonhard/0000-0001-5547-8309; Vogeley, K/0000-0002-5891-5831
FU German Research Council (DFG) [IRTG 1328]; Human Brain Project
   [R01-MH074457-01A1]; Helmholtz Initiative on Systems Biology (Human
   Brain Model)
FX This study was supported by the German Research Council (DFG, IRTG 1328;
   KZ, SBE, DB), the Human Brain Project (R01-MH074457-01A1; ARL, SBE), and
   the Helmholtz Initiative on Systems Biology (Human Brain Model; KZ,
   SBE). The authors declare no conflict of interest.
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NR 138
TC 48
Z9 48
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1863-2653
J9 BRAIN STRUCT FUNCT
JI Brain Struct. Funct.
PD OCT
PY 2012
VL 217
IS 4
BP 783
EP 796
DI 10.1007/s00429-012-0380-y
PG 14
WC Anatomy & Morphology; Neurosciences
SC Anatomy & Morphology; Neurosciences & Neurology
GA 008NS
UT WOS:000308964300002
PM 22270812
ER

PT J
AU Quek, LH
   Sofronoff, K
   Sheffield, J
   White, A
   Kelly, A
AF Quek, Lake-Hui
   Sofronoff, Kate
   Sheffield, Jeanie
   White, Angela
   Kelly, Adrian
TI Co-Occurring Anger in Young People With Asperger's Syndrome
SO JOURNAL OF CLINICAL PSYCHOLOGY
LA English
DT Article
DE Asperger's syndrome; anger; anxiety; depression; adolescence
ID AUTISM SPECTRUM DISORDERS; RANDOMIZED CONTROLLED-TRIAL; HIGH-FUNCTIONING
   AUTISM; PSYCHOMETRIC PROPERTIES; CHILDRENS ANXIETY; PSYCHOPATHOLOGY;
   ADOLESCENTS; SAMPLE; INTERVENTION; INDIVIDUALS
AB Objectives The co-occurrence of anger in young people with Asperger's syndrome (AS) has received little attention despite aggression, agitation, and tantrums frequently being identified as issues of concern in this population. The present study investigated the occurrence of anger in young people with AS and explores its relationship with anxiety and depression. Method Sixty-two young people (1223 years old) diagnosed with AS were assessed using the Beck Anger Inventory for Youth, Spence Children's Anxiety Scale, and Reynolds Adolescent Depression Scale. Results Among young people with AS who participated in this study, 41% of participants reported clinically significant levels of anger (17%), anxiety (25.8%) and/or depression (11.5%). Anger, anxiety, and depression were positively correlated with each other. Depression, however, was the only significant predictor of anger. Conclusion Anger is commonly experienced by young people with AS and is correlated with anxiety and depression. These findings suggest that the emotional and behavioral presentation of anger could serve as a cue for further assessment, and facilitate earlier identification and intervention for anger, as well as other mental health problems.
C1 [Quek, Lake-Hui; Sofronoff, Kate; Sheffield, Jeanie; White, Angela; Kelly, Adrian] Univ Queensland, Brisbane, Qld 4072, Australia.
RP Quek, LH (reprint author), Univ Queensland, Royal Brisbane & Womens Hosp, Ctr Youth Subst Abuse Res, Herston, Qld 4029, Australia.
EM lh.quek@uq.edu.au
RI Quek, Lake-Hui/F-7720-2011; Kelly, Adrian/G-4531-2011
CR Attwood T., 2007, COMPLETE GUIDE ASPER
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NR 37
TC 11
Z9 11
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0021-9762
J9 J CLIN PSYCHOL
JI J. Clin. Psychol.
PD OCT
PY 2012
VL 68
IS 10
BP 1142
EP 1148
DI 10.1002/jclp.21888
PG 7
WC Psychology, Clinical
SC Psychology
GA 003WP
UT WOS:000308642400005
PM 22806337
ER

PT J
AU Jordan, I
   Robertson, D
   Catani, M
   Craig, M
   Murphy, D
AF Jordan, Iain
   Robertson, Dene
   Catani, Marco
   Craig, Michael
   Murphy, Declan
TI Aripiprazole in the treatment of challenging behaviour in adults with
   autism spectrum disorder
SO PSYCHOPHARMACOLOGY
LA English
DT Article
DE Autism; Autism spectrum disorders; Behavioural disorders;
   Antipsychotics; Aripiprazole; Neuropsychiatry
ID PERVASIVE DEVELOPMENTAL DISORDERS; ADOLESCENTS; CHILDREN; BRAIN;
   ANTIPSYCHOTICS; IRRITABILITY; MANAGEMENT; MRI
AB Autism spectrum disorders (ASD) are associated with repetitive behaviours and often also with hyperactivity, aggression, self-injurious behaviour, irritability and lability of mood. There is emerging evidence that aripiprazole, an antipsychotic with partial agonist dopaminergic effect, may be effective in the treatment of these challenging behaviours. Nevertheless, there is little evidence for their efficacy in adults with ASD.
   The aim of this article is to present preliminary data on the use of aripiprazole in the treatment of challenging behaviour in the setting of ASD.
   We present a consecutive series of five inpatients of normal intelligence with challenging behaviour associated with ASD, diagnosed according to ICD-10 criteria, which was resistant to treatment with other medical and behavioural interventions and which was treated with aripiprazole.
   Four out of five patients were classified as "much improved" or "very much improved" according to the Clinical Global Impression-Improvement scale. Aripiprazole caused akathisia, at a dose of 30 mg in the one patient who was not classified as a responder but was otherwise well tolerated.
   This is the first case series of adults with ASD presenting with challenging behaviour who have been treated with aripiprazole. While the results are promising, controlled trials are required to confirm the findings.
C1 [Jordan, Iain; Robertson, Dene; Catani, Marco; Craig, Michael; Murphy, Declan] Inst Psychiat, Dept Forens & Neurodev Sci, London SE5 8AF, England.
   [Jordan, Iain; Robertson, Dene; Catani, Marco; Craig, Michael; Murphy, Declan] Bethlem Royal & Maudsley Hosp, Behav Disorders Unit, Beckenham BR3 3BX, Kent, England.
RP Jordan, I (reprint author), Inst Psychiat, Dept Forens & Neurodev Sci, 16 De Crespigny Pk, London SE5 8AF, England.
EM iain_jordan@hotmail.com; dene.robertson@slam.nhs.uk;
   marco.catani@kcl.ac.uk; Michael.c.craig@kcl.ac.uk;
   declan.murphy@kcl.ac.uk
RI Catani, Marco/H-7801-2012
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NR 21
TC 6
Z9 6
PU SPRINGER
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0033-3158
J9 PSYCHOPHARMACOLOGY
JI Psychopharmacology
PD OCT
PY 2012
VL 223
IS 3
BP 357
EP 360
DI 10.1007/s00213-012-2723-z
PG 4
WC Neurosciences; Pharmacology & Pharmacy; Psychiatry
SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry
GA 003XW
UT WOS:000308645700010
PM 22535309
ER

PT J
AU van der Meer, L
   Sutherland, D
   O'Reilly, MF
   Lancioni, GE
   Sigafoos, J
AF van der Meer, Larah
   Sutherland, Dean
   O'Reilly, Mark F.
   Lancioni, Giulio E.
   Sigafoos, Jeff
TI A further comparison of manual signing, picture exchange, and
   speech-generating devices as communication modes for children with
   autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Augmentative and alternative communication; Autism spectrum disorders;
   Manual signing; Picture exchange communication; Preference assessment;
   Specific requesting; Speech-generating devices
ID OF-THE-LITERATURE; DEVELOPMENTAL-DISABILITIES; ALTERNATIVE
   COMMUNICATION; PECS; INTERVENTIONS; INDIVIDUALS; PREFERENCES; STUDENTS
AB We compared acquisition of, and preference for, manual signing (MS), picture exchange (PE), and speech-generating devices (SGDs) in four children with autism spectrum disorders (ASD). Intervention was introduced across participants in a non-concurrent multiple-baseline design and acquisition of the three communication modes was compared in an alternating treatments design. Children's preference for using MS. PE or the SGD was also assessed. With intervention, all four participants learned to make specific requests using at least one of the three communication modes. The children also showed a preference for one mode. These results extend previous studies by demonstrating (in four new children with ASD) differential acquisition of, and idiosyncratic preferences for, three commonly used alternative communication modes. The present results further suggest faster acquisition and better maintenance with the preferred mode. We conclude that children's preferences for MS. PE, and SGDs should be considered when designing and implementing augmentative and alternative communication interventions. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [van der Meer, Larah] Victoria Univ Wellington, Sch Educ Psychol, Wellington 6147, New Zealand.
   [Sutherland, Dean] Univ Canterbury, Canterbury, New Zealand.
   [O'Reilly, Mark F.] Univ Texas Austin, Meadows Ctr Preventing Educ Risk, Austin, TX 78712 USA.
   [Lancioni, Giulio E.] Univ Bari, I-70121 Bari, Italy.
RP van der Meer, L (reprint author), Victoria Univ Wellington, Sch Educ Psychol, POB 17-310, Wellington 6147, New Zealand.
EM larah.vandermeer@vuw.ac.nz
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   van der Meer L, 2011, RES DEV DISABIL, V32, P1422, DOI 10.1016/j.ridd.2011.02.003
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NR 39
TC 17
Z9 17
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1247
EP 1257
DI 10.1016/j.rasd.2012.04.005
PG 11
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700001
ER

PT J
AU Achmadi, D
   Kagohara, DM
   van der Meer, L
   O'Reilly, MF
   Lancioni, GE
   Sutherland, D
   Lang, R
   Marschik, PB
   Green, VA
   Sigafoos, J
AF Achmadi, Donna
   Kagohara, Debora M.
   van der Meer, Larah
   O'Reilly, Mark F.
   Lancioni, Giulio E.
   Sutherland, Dean
   Lang, Russell
   Marschik, Peter B.
   Green, Vanessa A.
   Sigafoos, Jeff
TI Teaching advanced operation of an iPod-based speech-generating device to
   two students with autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorders; iPod Touch (R); Multi-step requesting;
   Speech-generating device; Systematic instruction
ID CHILDREN
AB We evaluated a program for teaching two adolescents with autism spectrum disorders (ASD) to perform more advanced operations on an iPod-based speech-generating device (SGD). The effects of the teaching program were evaluated in a multiprobe multiple baseline across participants design that included two intervention phases. The first intervention focused on teaching the students to navigate between two screen pages and complete a multi-step response sequence to request preferred stimuli. The second intervention aimed to teach the students to turn on and unlock the device prior to navigating to the correct screen pages. Teaching procedures included response prompting, prompt fading, and differential reinforcement. Results showed that both interventions were effective in teaching the respective operations. Learning advanced operation of the iPod-based SGD could be seen as one way to promote greater independence in using such devices for multi-step communication. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Sigafoos, Jeff] Victoria Univ Wellington, Sch Educ Psychol, Wellington 6147, New Zealand.
   [O'Reilly, Mark F.; Lang, Russell] Univ Texas Austin, Meadows Ctr Preventing Educ Risk, Austin, TX 78712 USA.
   [Lancioni, Giulio E.] Univ Bari, Bari, Italy.
   [Sutherland, Dean] Univ Canterbury, Christchurch 1, New Zealand.
   [Lang, Russell] Texas State Univ San Marcos, Clin Autism Res Evaluat & Support, San Marcos, TX USA.
   [Marschik, Peter B.] Med Univ Graz, Graz, Austria.
RP Sigafoos, J (reprint author), Victoria Univ Wellington, Sch Educ Psychol, POB 17-310, Wellington 6147, New Zealand.
EM jeff.sigafoos@vuw.ac.nz
CR Bowker A., 2009, PERSPECTIVES AUGMENT, V18, P137, DOI DOI 10.1044/AAC18.4.137
   Duker P. C., 2004, ONE TO ONE TRAINING
   Flores M., 2012, AUGMENTATIVE ALTERNA, P1
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   Kagohara DM, 2012, RES AUTISM SPECT DIS, V6, P1224, DOI 10.1016/j.rasd.2012.04.001
   Kennedy C, 2005, SINGLE CASE DESIGNS
   Matson JL, 2010, DEV NEUROREHABIL, V13, P239, DOI 10.3109/17518423.2010.481299
   Mirenda P., 2009, PERSPECTIVES AUGMENT, V18, P112
   Schlosser RW, 2009, AUTISM SPECTRUM DISO, P141
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   Sparrow S., 2005, VINELAND 2 ADAPTIVE, V2nd
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NR 14
TC 12
Z9 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1258
EP 1264
DI 10.1016/j.rasd.2012.05.005
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700002
ER

PT J
AU Ito, H
   Tani, I
   Yukihiro, R
   Adachi, J
   Hara, K
   Ogasawara, M
   Inoue, M
   Kamio, Y
   Nakamura, K
   Uchiyama, T
   Ichikawa, H
   Sugiyama, T
   Hagiwara, T
   Tsujii, M
AF Ito, Hiroyuki
   Tani, Iori
   Yukihiro, Ryoji
   Adachi, Jun
   Hara, Koichi
   Ogasawara, Megumi
   Inoue, Masahiko
   Kamio, Yoko
   Nakamura, Kazuhiko
   Uchiyama, Tokio
   Ichikawa, Hironobu
   Sugiyama, Toshiro
   Hagiwara, Taku
   Tsujii, Masatsugu
TI Validation of an interview-based rating scale developed in Japan for
   pervasive developmental disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE PDD; Autism spectrum disorders; ADI-R; Psychometrics
ID AUTISM DIAGNOSTIC INTERVIEW; SCREENING QUESTIONNAIRE; OBSERVATION
   SCHEDULE; SPECTRUM DISORDERS; CHILDREN
AB The pervasive developmental disorders (PDDs) Autism Society Japan Rating Scale (PARS), an interview-based instrument for evaluating PDDs, has been developed in Japan with the aim of providing a method that (1) can be used to evaluate PDD symptoms and related support needs and (2) is simpler and easier than the currently used "gold standard" instruments such as the Autism Diagnostic Interview-Revised (ADI-R). We examined the reliability and validity of PARS on the basis of data from 572 participants (277 PDD patients and 295 nonclinical controls). Inter-rater reliability was sufficient at both the item and scale level. Factor analysis extracted four subscales, for which internal consistency was found to be high. The sub and total scores of PARS showed correlations with the domain and total scores of ADI-R, in line with theoretical prediction, indicating the convergent validity of PARS. A receiver operating characteristic analysis showed that PARS has good discriminative validity in differentiating between PDD patients and nonclinical controls, regardless of intellectual capacity. Considering that PARS can be easily implemented by professionals with appropriate knowledge regarding PDDs, PARS may be superior to the existing instruments in terms of cost performance. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Ito, Hiroyuki] Hamamatsu Univ Sch Med, Res Ctr Child Mental Dev, Higashi Ku, Hamamatsu, Shizuoka 4313192, Japan.
   [Yukihiro, Ryoji] Kyoto Gakuen Univ, Fac Human & Cultural Studies, Kyoto, Japan.
   [Adachi, Jun; Hagiwara, Taku] Hokkaido Univ, Sapporo, Hokkaido, Japan.
   [Hara, Koichi] Univ Tokushima, Fac Integrated Arts & Sci, Tokushima, Japan.
   [Ogasawara, Megumi] Tokyo Gakugei Univ, Sch Educ, Tokyo, Japan.
   [Inoue, Masahiko] Tottori Univ, Grad Sch Med Sci, Yonago, Tottori, Japan.
   [Nakamura, Kazuhiko] Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan.
   [Uchiyama, Tokio] Fukushirna Univ, Fac Human Dev & Culture, Fukushima, Japan.
   [Ichikawa, Hironobu] Tokyo Metropolitan Childrens Med Ctr, Tokyo, Japan.
   [Sugiyama, Toshiro] Hamamatsu Univ Sch Med, Dept Child & Adolescent Psychiat, Hamamatsu, Shizuoka 4313192, Japan.
   [Tsujii, Masatsugu] Chukyo Univ, Sch Contemporary Sociol, Nagoya, Aichi, Japan.
RP Ito, H (reprint author), Hamamatsu Univ Sch Med, Res Ctr Child Mental Dev, Higashi Ku, 1-20-1 Handayama, Hamamatsu, Shizuoka 4313192, Japan.
EM ito_hiroyuki@pd5.so-net.ne.jp
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NR 27
TC 8
Z9 8
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1265
EP 1272
DI 10.1016/j.rasd.2012.04.002
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700003
ER

PT J
AU Fava, L
   Vicari, S
   Valeri, G
   D'Elia, L
   Arima, S
   Strauss, K
AF Fava, Leonardo
   Vicari, Stefano
   Valeri, Giovanni
   D'Elia, Lidia
   Arima, Serena
   Strauss, Kristin
TI Intensive Behavioral Intervention for school-aged children with autism:
   Una Breccia nel Muro (UBM)-A Comprehensive Behavioral Model
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Intensive Behavioral Intervention; Parent inclusion; Inclusive
   settings; School-aged
ID HIGH-FUNCTIONING CHILDREN; YOUNG-CHILDREN; SPECTRUM DISORDERS;
   METHODOLOGICAL ISSUES; REPETITIVE BEHAVIOR; SOCIAL-INTERACTION; ACTIVITY
   SCHEDULES; FOLLOW-UP; PARENT; SKILLS
AB Although, reviews and outcome research supports empirical evidence for Early Intensive Behavior Intervention in pre-scholars, intensive behavioral service provision for school-aged children with autism spectrum disorders (ASD) are less subject to research studies. In order to provide effective behavioral interventions for school-aged children it was first necessary to comprehend key variables that are common to empirically validated programs and to tailor the to the needs of older children and their families in community settings. The proposed Comprehensive Behavioral Model "Una Breccia nel Muro" (UBM) includes individualized assessment and skill building, treatment provision in inclusive setting and cross-service collaboration, parent inclusion and support, and intensive training for parents, staff as well as school teachers. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Fava, Leonardo; Strauss, Kristin] Assoc Volontariato Breccia Nel Muro, Rome, Italy.
   [Fava, Leonardo; Vicari, Stefano; Valeri, Giovanni; D'Elia, Lidia; Strauss, Kristin] Autism Treatment & Res Ctr Breccia Nel Muro, Rome, Italy.
   [Vicari, Stefano; Valeri, Giovanni; D'Elia, Lidia] Childrens Hosp Bambino Gesu, Dept Neurosci, Rome, Italy.
   [Arima, Serena] Univ Roma La Sapienza, Dept Methods & Model Econ Terr & Finance, Rome, Italy.
RP Fava, L (reprint author), Assoc Volontariato Breccia Nel Muro, Rome, Italy.
EM supersghy@yahoo.it
RI Vicari, Stefano/J-3008-2012
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NR 120
TC 3
Z9 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1273
EP 1288
DI 10.1016/j.rasd.2012.03.011
PG 16
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700004
ER

PT J
AU Melogno, S
   Pinto, MA
   Levi, G
AF Melogno, Sergio
   Pinto, Maria Antonietta
   Levi, Gabriel
TI Metaphor and metonymy in ASD children: A critical review from a
   developmental perspective
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Review
DE Metaphor; Metonymy; ASD children; Development; Review
ID LANGUAGE DISORDERS; INFANTILE-AUTISM; COMPREHENSION; MIND; COMPETENCE;
   SPEAKERS; NAMES
AB The aim of the present article is to critically review the experimental research in the domain of metaphor and metonymy competencies in Autism Spectrum Disorders (ASD) children. After providing some basic definitions of metaphor and metonymy, we consider some major points emerging from studies on metaphorical and metonymical competencies in typical child development. Then, we review a number of emblematic studies concerning the relationship between autism and metaphor and metonymy, starting from the pioneering clinical studies by Kanner and Asperger in the 1940s, We also critically analyze experimental research on these same topics starting from the 1990s. The discussion highlights some major points emerging from recent experimental research and outlines possible perspectives for future research. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Melogno, Sergio; Levi, Gabriel] Univ Roma La Sapienza, Dept Paediat & Neuropsychiat, I-00185 Rome, Italy.
   [Pinto, Maria Antonietta] Univ Roma La Sapienza, Dept Psychol Dev & Socialisat Proc, I-00185 Rome, Italy.
RP Melogno, S (reprint author), Univ Roma La Sapienza, Dept Paediat & Neuropsychiat, 108 Via Sabelli, I-00185 Rome, Italy.
EM sergio.melogno@uniroma1.it; mariantonietta.pinto@uniroma1.it;
   Gabriel.levi@uniroma1.it
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NR 65
TC 2
Z9 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1289
EP 1296
DI 10.1016/j.rasd.2012.04.004
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700005
ER

PT J
AU Stampoltzis, A
   Papatrecha, V
   Polychronopoulou, S
   Mavronas, D
AF Stampoltzis, Aglaia
   Papatrecha, Virginia
   Polychronopoulou, Stavroula
   Mavronas, Dimitris
TI Developmental, familial and educational characteristics of a sample of
   children with Autism Spectrum Disorders in Greece
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Greece; Prevalence; Diagnosis
ID ASSISTED CONCEPTION; EXTREME PREMATURITY; SEX-DIFFERENCES;
   YOUNG-CHILDREN; PATERNAL AGE; RISK; DIAGNOSIS; PREVALENCE; INTERVENTION;
   PARENTS
AB The aim of this study is to describe the developmental, familial and educational characteristics of 91 children with a clinical diagnosis of autism spectrum disorders (ASDs), from one educational district of Athens, Greece. Records of the 91 children, aged 4-14 years old, were examined with respect to sex, age of diagnosis, type of ASDs, school placement, co-existing disorders, parental ages, type of conception, prematurity and birth order. The results indicated that the boy:girl ratio was 4.3:1 while the average age of diagnosis was 6 years which implies a delay in the early detection of ASDs. Children with typical autism constituted 80% of the sample, while the Asperger group constituted 20%. The majority of pupils were served in general education, and only a small percentage attended special schools. The preferable type of support was one-to-one support in the classroom (47%). Among the most common disorders that coexist with the ASDs was ADHD, epilepsy, dyslexia and learning difficulties. Interesting findings were obtained for the advanced parental age, birth order and the relationship of assisted conception and premature birth with the presence of autism. The present study offers some useful insights about the characteristics of ASDs in a Greek school-based sample. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Stampoltzis, Aglaia] Sch Pedag & Technol Educ ASPETE, Athens 14121, Greece.
   [Papatrecha, Virginia] 4th High Sch Argos, Argos 21200, Greece.
   [Polychronopoulou, Stavroula] Univ Athens, GR-10680 Athens, Greece.
   [Mavronas, Dimitris] KEDDY B Athinas, Athens 14231, Greece.
RP Stampoltzis, A (reprint author), Sch Pedag & Technol Educ ASPETE, Athens 14121, Greece.
EM lstamp@ambio.gr; gina85@windowslive.com; stavroula_poly@yahoo.com;
   dim.mavr@hotmail.com
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   Richdale AL, 2009, SLEEP MED REV, V13, P403, DOI 10.1016/j.smrv.2009.02.003
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NR 56
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1297
EP 1303
DI 10.1016/j.rasd.2012.05.004
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700006
ER

PT J
AU Bean, JL
   Eigsti, IM
AF Bean, Jessica L.
   Eigsti, Inge-Marie
TI Assessment of joint attention in school-age children and adolescents
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Review
DE Joint attention; Novel measure; Adolescents; Autism spectrum disorders
ID DISORDERS
AB Joint attention (JA), the ability to share attention to an object or event with another person, is one of the earliest identified deficits in autism spectrum disorders (ASD) and directly influences language and social development. There are several effective assessments of JA for young children (e.g., Mundy et al., 2003), but none are appropriate for school-age or adolescence. We developed a measure of response to JA and assessed individuals with ASD (n = 18) and typical development (n = 24), ages 7 to 17. Six naturalistic prompts were interleaved throughout a testing session. Discriminative validity was high: there was a broad range for both groups, though scores were lower for children with ASD. Scores in the ASD group were associated with receptive language, symptomatology, and theory of mind. Reliability across examiners was high (kappa = .875). This measure, which requires no special equipment and minimal training, was useful in capturing JA skills in older individuals with and without ASD. Further, scores were associated with theoretically related skills, indicating high external validity. Given the powerful developmental sequelae and numerous interventions for JA, this measure offers a longitudinal assessment opportunity. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Bean, Jessica L.; Eigsti, Inge-Marie] Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA.
RP Eigsti, IM (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd,Unit 1020, Storrs, CT 06269 USA.
EM inge-marie.eigsti@uconn.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
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1304
EP 1310
DI 10.1016/j.rasd.2012.04.003
PG 7
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700007
ER

PT J
AU Gukan, CK
   Hagerman, RJ
AF Gurkan, C. Kagan
   Hagerman, Randi J.
TI Targeted treatments in autism and fragile X syndrome
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Fragile X syndrome; Autism; mGluR; GABA; Treatment
ID SPECTRUM DISORDERS; D-CYCLOSERINE; PREMUTATION CARRIERS; REPETITIVE
   BEHAVIORS; TUBEROUS SCLEROSIS; PROTEIN-SYNTHESIS; SYNAPTIC FUNCTION;
   EXPOSURE THERAPY; TREATMENT TRIAL; SOCIAL ANXIETY
AB Autism is a neurodevelopmental disorder consisting of a constellation of symptoms that sometimes occur as part of a complex disorder characterized by impairments in social interaction, communication and behavioral domains. It is a highly disabling disorder and there is a need for treatment targeting the core symptoms. Although autism is accepted as highly heritable, there is no genetic cure at this time. Autism is shown to be linked to several genes and is a feature of some complex genetic disorders, including fragile X syndrome (FXS), fragile X premutation involvement, tuberous sclerosis and Rat syndrome. The term autism spectrum disorders (ASDs) covers autism, Asperger syndrome and pervasive developmental disorders (PDD-NOS) and the etiologies are heterogeneous. In recent years, targeted treatments have been developed for several disorders that have it known specific genetic cause leading to autism. Since there are significant molecular and neurobiological overlaps among disorders, targeted treatments developed for a specific disorder may be helpful in ASD of unknown etiology. Examples of this are two drug classes developed to treat FXS, Arbaclofen, a GABA(B) agonist, and mGluR5 antagonists, and both may be helpful in autism without FXS. The mGluR5 antagonists are also likely to have a benefit in the aging problems of fragile X premutation carriers, the fragile X-associated tremor ataxia syndrome (FXTAS) and the Parkinsonism that can occur in aging patients with fragile X syndrome. Targeted treatments in FXS which has a well known genetic etiology may lead to new targeted treatments in autism. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Gurkan, C. Kagan] Ankara Univ, Sch Med, Dept Child & Adolescent Psychiat, Cebeci Hosp, TR-06100 Ankara, Turkey.
   [Hagerman, Randi J.] UC Davis Med Center, Dept Pediat, Sacramento, CA 95817 USA.
   [Hagerman, Randi J.] UC Davis Med Center, MIND Inst, Sacramento, CA 95817 USA.
RP Gukan, CK (reprint author), Ankara Univ, Sch Med, Dept Child & Adolescent Psychiat, Cebeci Hosp, TR-06100 Ankara, Turkey.
EM kaganka@gmail.com; randi.hagerman@ucdmc.ucdavis.edu
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NR 110
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1311
EP 1320
DI 10.1016/j.rasd.2012.05.007
PG 10
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700008
ER

PT J
AU Young, KL
   Boris, AL
   Thomson, KM
   Martin, GL
   Yu, CT
AF Young, Kristen L.
   Boris, Ashley L.
   Thomson, Kendra M.
   Martin, Garry L.
   Yu, C. T.
TI Evaluation of a self-instructional package on discrete-trials teaching
   to parents of children with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Discrete-trials teaching; Autism; Self-instructional; Parent-training;
   Applied behavior analysis
ID ACQUISITION; SKILLS
AB The purpose of this research was to evaluate a self-instructional package (Fazzio & Martin, 2007) to train parents of children with autism to conduct discrete-trials teaching (DTT). In Study 1, we investigated the effectiveness of a self-instructional manual and a self-instructional video for teaching five parents of children with autism to correctly apply DTT to teach three tasks to a confederate who role-played a child with autism, and to their own child when possible. Following an average of 4.76 h of training, the package produced a strong effect with three parents and a weak effect with two parents. In Study 2, we investigated the effectiveness of the self-instructional manual combined with role-playing and feedback, plus the self-instructional video, for teaching an additional five parents. Following an average of 4.68 h of training, all five parents demonstrated large, clinically significant gains in their performance of DTT, both with a confederate as well as with their own child, with a minimal investment of one-on-one instructor time. These results suggest that the training package in Study 2 has considerable potential as an effective, efficient and acceptable method of training parents of children with autism to apply DTT. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Young, Kristen L.; Boris, Ashley L.; Thomson, Kendra M.; Martin, Garry L.; Yu, C. T.] Univ Manitoba, Dept Psychol, Winnipeg, MB R3T 2N6, Canada.
   [Yu, C. T.] St Amant Res Ctr, Winnipeg, MB R2M 3Z9, Canada.
RP Young, KL (reprint author), Selkirk Mental Hlth Ctr, Box 9600, Selkirk, MB R1A 2B5, Canada.
EM umcam224@cc.umanitoba.ca
RI Yu, C.T./D-1731-2014
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NR 16
TC 0
Z9 0
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1321
EP 1330
DI 10.1016/j.rasd.2012.05.001
PG 10
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700009
ER

PT J
AU Afshari, J
AF Afshari, Javad
TI The effect of perceptual-motor training on attention in the children
   with autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Children; Autism spectrum disorder; Perceptual-motor training; Attention
ID MANUAL RESPONSE PREPARATION; COGNITIVE FUNCTION; DEVELOPMENT SCALE;
   JOINT ATTENTION; ERP EVIDENCE; EXERCISE; BRAIN; PERFORMANCE; SHIFTS;
   STIMULATION
AB The present study attempted to investigate the effect of perceptual-motor training on attention in children with autism spectrum disorders. The participants (20 girls and 20 boys) were divided into experimental and control groups. They were selected from among 85 subjects after primary tests to be matched. The design of the study was quasi-experimental including an independent variable, a pretest and a posttest. After considering the research hypotheses using descriptive statistics and one-way Analysis of Covariance (ANCOVA), the results suggested a significant difference in posttest scores of experimental and control groups after independent variable being applied. The results also showed that perceptual-motor trainings for children with autism increase their attention because of the impact they have on increasing neurological and cognitive function. (C) 2012 Elsevier Ltd. All rights reserved.
C1 Univ Tehran, Tehran, Iran.
RP Afshari, J (reprint author), Univ Tehran, Kargar St, Tehran, Iran.
EM javadf76@gmail.com
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NR 46
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1331
EP 1336
DI 10.1016/j.rasd.2012.05.003
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700010
ER

PT J
AU Hodge, D
   Parnell, AMN
   Hoffman, CD
   Sweeney, DP
AF Hodge, Danelle
   Parnell, Andrea M. N.
   Hoffman, Charles D.
   Sweeney, Dwight P.
TI Methods for assessing sleep in children with autism spectrum disorders:
   A review
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Review
DE Autism; Sleep; Polysomnography; Actigraphy; Videosomnography
ID PERVASIVE DEVELOPMENTAL DISORDERS; HABITS QUESTIONNAIRE; BEHAVIORAL
   TREATMENT; TYPICAL DEVELOPMENT; SCHOOL PERFORMANCE; MENTAL-RETARDATION;
   CIRCADIAN-RHYTHMS; ASPERGER-SYNDROME; YOUNG-CHILDREN; WAKE PATTERNS
AB A literature review completed by Bauer and Blunden (2008) determined that compared to objective measures, subjective assessments of sleep for typically developing children (e.g., parental reports) were of limited utility. No comparable literature review has been undertaken to determine whether subjective measures are appropriate for assessing sleep in children with autism spectrum disorders (ASD). Such a review is necessary as children with ASD have more sleep problems than typically developing children and children's sleep difficulties can negatively affect the child and other family members. It is, therefore, important to have measures of sleep for children with ASD that can reliably detect sleep problems and track improvements in sleep. This literature review described frequently used measures of children's sleep and evaluated their utility for assessing sleep in children with ASD. It was determined that, with the exception of sleep latency, parents' reports of children's sleep are not consistently associated with objective measures of children's sleep. This was true for single-item parent-reports and for a widely used multi-item parent-report measure of children's sleep. Limitations of objective sleep measures (e.g., polysomnography, actigraphy), including the inability of children with ASD to tolerate such methods, are described. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Hodge, Danelle] Calif State Univ San Bernardino, Dept Psychol, San Bernardino, CA 92407 USA.
RP Hodge, D (reprint author), Calif State Univ San Bernardino, Dept Psychol, 5500 Univ Pkwy, San Bernardino, CA 92407 USA.
EM dhodge@csusb.edu
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NR 72
TC 3
Z9 3
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1337
EP 1344
DI 10.1016/j.rasd.2012.05.009
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700011
ER

PT J
AU Grondhuis, SN
   Aman, MG
AF Grondhuis, Sabrina N.
   Aman, Michael G.
TI Assessment of anxiety in children and adolescents with autism spectrum
   disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Review
DE Anxiety; Autism; Assessment
ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; COMORBID
   PSYCHIATRIC-DISORDERS; OBSESSIVE-COMPULSIVE DISORDER;
   COGNITIVE-BEHAVIORAL THERAPY; SCHOOL-AGE-CHILDREN; ASPERGER-SYNDROME;
   SOCIAL ANXIETY; INTELLECTUAL DISABILITY; CONTROLLED-TRIAL
AB Anxiety disorders are among the most common comorbid conditions in children and adolescents with autism spectrum disorders (ASDs), although assessment presents unique challenges. Many symptoms of anxiety appear to overlap with common presentations of autism. Furthermore, deficits in language and cognitive functioning make it difficult for such children to convey their emotional states accurately. A comprehensive review of the recent literature was conducted to assay the types and rates of use of tools for evaluating anxiety symptoms in children and adolescents with ASDs. We identified strengths and weaknesses in existing scales, identified instruments that (although imperfect) seem to have a good coverage for youngsters with ASDs, recommended strategies for studying anxiety in these youth, and offered suggestions for future scale development. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Grondhuis, Sabrina N.; Aman, Michael G.] Ohio State Univ, Columbus, OH 43210 USA.
RP Aman, MG (reprint author), Ohio State Univ, Columbus, OH 43210 USA.
EM sabrina.grondhuis@gmail.com; aman.1@osu.edu
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NR 115
TC 12
Z9 12
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1345
EP 1365
DI 10.1016/j.rasd.2012.04.006
PG 21
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700012
ER

PT J
AU Plavnick, JB
   Ferreri, SJ
AF Plavnick, Joshua B.
   Ferreri, Summer J.
TI Collateral effects of mand training for children with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism; Collateral effects; Mand training; Social skills; Verbal
   behavior
ID BEHAVIOR
AB Proponents of the verbal behavior approach to instruction for individuals with autism have identified mand training as a starting point for early intervention. Mand training is a process whereby the learner is taught to request highly preferred items under conditions when those items are most valuable. A hypothesized benefit of this approach is that mand training has a collateral effect on nontargeted behavior, though empirical support for this hypothesis is currently tenuous. The present investigation examined the collateral effects of vocal mand training compared to vocal request training for 3 previously nonvocal children with autism. Levels of orienting toward a speaker, compliance with instruction, and overall problem behavior were measured across experimental conditions and analyzed using an alternating treatment design. Results indicate that problem behavior for all participants occurred at lower levels during mand training than request training and that the level of nontargeted social behavior (i.e., orienting and compliance) was higher during mand training for 2 participants and was similar across both conditions for the final participant. The results support the hypothesis that mand training can have a collateral impact on nontargeted behavior, though explicit instruction of social behaviors may also need to be embedded within mand training procedures. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Plavnick, Joshua B.; Ferreri, Summer J.] Michigan State Univ, E Lansing, MI 48824 USA.
RP Plavnick, JB (reprint author), Michigan State Univ, E Lansing, MI 48824 USA.
EM plavnick@msu.edu
CR Brady N. C., 1994, ANAL VERBAL BEHAV, V12, P43
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   Tiger Jeffrey H, 2008, Behav Anal Pract, V1, P16
NR 18
TC 2
Z9 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1366
EP 1376
DI 10.1016/j.rasd.2012.05.008
PG 11
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700013
ER

PT J
AU Palmen, A
   Didden, R
AF Palmen, Annemiek
   Didden, Robert
TI Task engagement in young adults with high-functioning autism spectrum
   disorders: Generalization effects of behavioral skills training
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorder; High-functioning; Task engagement; Off-task
   behavior; Generalization
ID ACTIVITY SCHEDULES; CHILDREN; EMPLOYMENT; CHOICE
AB This study evaluated the effectiveness of a behavioral skills training package on task engagement in six young adults with high-functioning ASD who worked in a regular job-training setting. Experimental sessions were implemented in a small-group training format in a therapy room using unknown tasks. Data were collected on participant's off-task behavior and questions for help as well as on staffs behavior in the regular setting during regular job tasks (i.e.. generalization). Intervention consisted of discrimination training, self-management strategies, behavioral practice, corrective feedback, and reinforcement. Following intervention, a significant decrease was found in percentage off-task behavior in the regular setting while performing regular job tasks. No changes were found in questions for help by participants or in behavior of staff. Effects were maintained at 6-week follow-up and at 6-month follow-up outcomes were still beneath baseline levels. Findings are discussed in relation to future research. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Palmen, Annemiek] Radboud Univ Nijmegen, Dept Special Educ, NL-6500 HE Nijmegen, Netherlands.
   [Didden, Robert] Radboud Univ Nijmegen, Inst Behav Sci, NL-6500 HE Nijmegen, Netherlands.
RP Palmen, A (reprint author), Radboud Univ Nijmegen, Dept Special Educ, POB 9104, NL-6500 HE Nijmegen, Netherlands.
EM a.palmen@pwo.ru.nl
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NR 36
TC 2
Z9 2
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1377
EP 1388
DI 10.1016/j.rasd.2012.05.010
PG 12
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700014
ER

PT J
AU Cardon, TA
AF Cardon, Teresa A.
TI Teaching caregivers to implement video modeling imitation training via
   iPad for their children with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE iPad; Caregiver training; Imitation; Video modeling; Autism
ID YOUNG-CHILDREN; SPECTRUM DISORDERS; PRETEND PLAY; INTERVENTION;
   BEHAVIOR; SKILLS; COMMUNICATION; EFFICACY; SCALE
AB Children with autism fail to imitate from an early age and this lack of imitation is a salient diagnostic marker for the disorder. For children with Autism Spectrum Disorder (ASD), increased imitation skills appear to be related to increased skill development in a variety of areas. Video modeling was recently validated as a technique to support imitation acquisition in young children with autism. The purpose of this research was to determine if there is a functional relation between caregiver implemented Video Modeling Imitation Training (VMIT) via iPad and increased imitation skills in young children with autism. In addition, a secondary analysis of language development after exposure to VMIT was also conducted. A multiple baseline design across four caregivers and their children with autism was implemented. Results indicated that all four caregivers were able to successfully create video models on an iPad when provided with minimal training and implement VMIT with fidelity for their children. All four children made substantial gains in their imitation skills during caregiver implemented treatment. Imitation skills maintained post treatment and, to varying degrees, generalized to imitation of live models. Expressive language skills increased to varying degrees for all participants. (C) 2012 Elsevier Ltd. All rights reserved.
C1 Washington State Univ, Pullman, WA 99164 USA.
RP Cardon, TA (reprint author), Washington State Univ, Pullman, WA 99164 USA.
EM Teresa.cardon@wsu.edu
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NR 50
TC 6
Z9 6
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1389
EP 1400
DI 10.1016/j.rasd.2012.06.002
PG 12
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700015
ER

PT J
AU Tudor, ME
   DeVincent, CJ
   Gadow, KD
AF Tudor, Megan E.
   DeVincent, Carla J.
   Gadow, Kenneth D.
TI Prenatal pregnancy complications and psychiatric symptoms: Children with
   ASD versus clinic controls
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Autism spectrum disorder; Pregnancy complications; Psychiatric
   co-morbidity; Attention-deficit hyperactivity disorder; Generalized
   anxiety disorder; Depression
ID AUTISM SPECTRUM DISORDER; DEFICIT HYPERACTIVITY DISORDER; OPPOSITIONAL
   DEFIANT DISORDER; OBSTETRIC COMPLICATIONS; PERINATAL COMPLICATIONS;
   BIRTH COMPLICATIONS; RISK-FACTORS; PHENOTYPE; PSYCHOPATHOLOGY;
   SCHIZOPHRENIA
AB The current study examined the association between prenatal pregnancy complications (PPC) and childhood psychiatric symptoms in children with an autism spectrum disorder (ASD) and non-ASD children who were referred to a psychiatric clinic (Controls). Parents completed a DSM-IV-referenced rating scale and developmental history questionnaire. Participants were classified as having >= 1 PPC (+PPC) versus none (-PPC). Children with ASD were significantly more likely to have PPC than Controls. Intra-group comparisons demonstrated that children in the ASD + PPC group had more severe anxiety than ASD/-PPC group. The Control + PPC group obtained higher symptom ratings of inattention., hyperactivity, and oppositional behavior than Control/-PPC. Children in the ASD + PPC group were rated as having more severe anxiety and depression symptoms than Control + PPC. Dissimilar associations in ASD and non-ASD samples were found, suggesting divergent pathogenic processes in different clinical phenotypes. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Tudor, Megan E.] SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA.
   [DeVincent, Carla J.] SUNY Stony Brook, Dept Pediat, Med Ctr, Stony Brook, NY 11794 USA.
   [Gadow, Kenneth D.] SUNY Stony Brook, Med Ctr, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
RP Tudor, ME (reprint author), SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA.
EM metudor@notes.cc.sunysb.edu; Carla.Devincent@stonybrookmedicine.edu;
   Kenneth.Gadow@stonybrookmedicine.edu
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NR 38
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1401
EP 1405
DI 10.1016/j.rasd.2012.06.001
PG 5
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700016
ER

PT J
AU Horovitz, M
   Matson, JL
   Barker, A
AF Horovitz, Max
   Matson, Johnny L.
   Barker, Alyse
TI The relationship between symptoms of autism spectrum disorders and
   psychotropic medication use in infants and toddlers
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Psychotropic medication; ASD; BISCUIT; Infants; Toddlers
ID PERVASIVE DEVELOPMENTAL DISORDERS; SIDE-EFFECTS MEDS; INTELLECTUAL
   DISABILITY; MATSON EVALUATION; MENTAL-RETARDATION; SOCIAL-SKILLS;
   CHILDREN; PREVALENCE; PATTERNS; ADULTS
AB Little research has been conducted to date on the relationship between psychotropic medication use and autism spectrum disorders (ASDs). Participants in the current study were placed into one of four groups: ASD on psychotropic medications (N = 33), ASD off psychotropic medications (N = 45), atypically developing on psychotropic medications (N = 30) and atypically developing off psychotropic medications (N = 45). Severity of autistic symptoms were compared between the groups based on total scores on the Baby and Infant Screen for Children with aUtIsm Traits, Part 1(BISCUIT Part-1). Toddlers with ASD on psychotropic medications had significantly higher ratings than any other group. No such relationship was found within the atypically developing group. The results suggest a relationship between psychotropic medication use and severity of autistic symptoms in infants and toddlers. Implications of these results are discussed. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Matson, Johnny L.] Louisiana State Univ, Dept Psychol, 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 42
TC 1
Z9 1
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1406
EP 1411
DI 10.1016/j.rasd.2011.05.013
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700017
ER

PT J
AU Matson, JL
   Tureck, K
   Turygin, N
   Beighley, J
   Rieske, R
AF Matson, Johnny L.
   Tureck, Kimberly
   Turygin, Nicole
   Beighley, Jennifer
   Rieske, Robert
TI Trends and topics in Early Intensive Behavioral Interventions for
   toddlers with autism
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Early Intensive Behavioral Interventions; Autism; Applied behavior
   analysis
ID PROFOUND MENTAL-RETARDATION; SELF-INJURIOUS-BEHAVIOR; SPECTRUM
   DISORDERS; YOUNG-CHILDREN; SOCIAL-SKILLS; INTELLECTUAL DISABILITY;
   DIAGNOSTIC-ASSESSMENT; ASSESSMENT SCALE; PDD-NOS; DASH-II
AB The use of applied behavior analysis (ABA) to treat persons with autism goes back several decades. Many specific target behaviors and intervention strategies have been developed. In the last two decades the most heavily studied of these methods has been Early Intensive Behavioral Interventions (EIBI). This package of ABA methods is unique in two ways. First, a broad range of target behaviors are trained for 20-40 h per week. This training is much more treatment per week than what is described in most ABA studies. Second, the children treated are typically 2-3 years of age, which is younger than for most ABA research. Reviews of EIBI have typically focused on the efficacy of the methods. These are important, but at present we argue that these methods are effective. This paper is different in that it looks at current trends such as generalization, parent training, factors that mitigate against effective treatment and the need for follow-up and booster treatment. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Matson, Johnny L.] Louisiana State Univ, Dept Psychol, 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 78
TC 9
Z9 9
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1412
EP 1417
DI 10.1016/j.rasd.2012.02.010
PG 6
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700018
ER

PT J
AU Kasner, M
   Reid, G
   MacDonald, C
AF Kasner, Melanie
   Reid, Greg
   MacDonald, Cathy
TI Evidence-based practice: Quality indicator analysis of antecedent
   exercise in autism spectrum disorders
SO RESEARCH IN AUTISM SPECTRUM DISORDERS
LA English
DT Article
DE Antecedent exercise; Self-stimulatory behaviors; Autism spectrum
   disorders; Quality indicator; Group experimental; Single-subject
ID SELF-STIMULATORY-BEHAVIOR; SPECIAL-EDUCATION; STEREOTYPIC BEHAVIORS;
   PHYSICAL EXERCISE; CHILDREN; INDIVIDUALS
AB The purpose of the research was to conduct a quality indicator analysis of studies exploring the effects of antecedent exercise on self-stimulatory behaviors of individuals with autism spectrum disorders (ASD). Educational Resources Information Center (ERIC), Google Scholar, SPORTDiscus, PsychINFO, and PubMed/MedLine databases from 1980 to October 2010 and reference lists of included articles were searched. Twelve research studies employing group experimental (Gersten et al., 2005) or single-subject designs (Horner et al., 2005) met inclusion criteria. Each study was assessed for the presence and clarity of quality indicators. Group experimental and single-subject designs met 48% and 82% of quality indicators, respectively. This suggests that the effects of antecedent exercise on self-stimulatory behaviors of individuals with ASD is incomplete and claims of exercise being an evidence-based practice are premature. Several indicators were difficult to interpret or lacking clear definitions. Recommendations for clarifying and applying the quality indicators are offered. (C) 2012 Elsevier Ltd. All rights reserved.
C1 [Reid, Greg] McGill Univ, Dept Kinesiol & Phys Educ, Montreal, PQ H2W 1S4, Canada.
   [MacDonald, Cathy] SUNY Coll Cortland, Cortland, NY 13045 USA.
RP Reid, G (reprint author), McGill Univ, Dept Kinesiol & Phys Educ, 475 Pine Ave W, Montreal, PQ H2W 1S4, Canada.
EM gregory.reid@mcgill.ca
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NR 33
TC 4
Z9 4
PU ELSEVIER SCI LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND
SN 1750-9467
J9 RES AUTISM SPECT DIS
JI Res. Autism Spectr. Disord.
PD OCT-DEC
PY 2012
VL 6
IS 4
BP 1418
EP 1425
DI 10.1016/j.rasd.2012.02.001
PG 8
WC Education, Special; Psychology, Developmental; Psychiatry;
   Rehabilitation
SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation
GA 005DW
UT WOS:000308731700019
ER

PT J
AU Ustun, O
   Ongen, G
AF Ustun, Ozlem
   Ongen, Gaye
TI Production and separation of dipeptidyl peptidase IV from Lactococcus
   lactis: scale up for industrial production
SO BIOPROCESS AND BIOSYSTEMS ENGINEERING
LA English
DT Article
DE Lactococcus lactis spp. lactis; Lactococcus lactis spp. cremoris;
   Dipeptidyl Peptidase IV (DPP IV); Corn steep liquor (CSL); Scale up
   production and dietary supplement
ID PROLINE-SPECIFIC PEPTIDASES; LACTOBACILLUS-HELVETICUS; PURIFICATION;
   AMINOPEPTIDASE; AUTISM; SERUM
AB Lactococcus lactis spp. lactis and Lactococcus lactis spp. cremoris are widely used in the manufacture of fermented milk. These strains were compared for production of Dipeptidyl Peptidase IV (DPP IV) enzyme in terms of enzyme activity, specific growth rates and productivity. Lactococcus lactis spp. lactis was produced in 3 L bioreactor and scaled up to 30 and 150 L stirred tank bioreactors, and the enzyme activities were found as 110, 110 and 122 mU mL(-1), respectively. After 8 h of production, separation steps were performed. While purification fold was 127 and yield was 2.69 %, the molecular weight of the enzyme was estimated as 68 kDa. Partially purified enzyme was enteric coated with capsules and a 95.5 % of DPP IV enzyme passed into the artificial intestine. Results show that production of DPP IV enzyme by Lactococcus lactis spp. lactis strain in submerged culture is comparable with the productions by commercial strains, mostly Aspergillus, in solid state fermentations based on productivity.
C1 [Ustun, Ozlem] Pamukkale Univ, Fac Engn, Dept Food Engn, TR-20020 Kinikli, Denizli, Turkey.
   [Ongen, Gaye] Ege Univ, Dept Bioengn, Fac Engn, EBILTEM Binasi, TR-35100 Izmir, Turkey.
RP Ustun, O (reprint author), Pamukkale Univ, Fac Engn, Dept Food Engn, TR-20020 Kinikli, Denizli, Turkey.
EM drozlemustun@gmail.com
FU Scientific and Technological Research Council of Turkey (TUBITAK)
   [105T195]
FX This study was supported by The Scientific and Technological Research
   Council of Turkey (TUBITAK) with file number 105T195. We are grateful to
   Professor Erdal Bedir for his advice and valuable support, and Professor
   Fazilet Vardar Sukan for her guidance.
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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 1615-7591
J9 BIOPROC BIOSYST ENG
JI Bioprocess. Biosyst. Eng.
PD OCT
PY 2012
VL 35
IS 8
BP 1417
EP 1427
DI 10.1007/s00449-012-0730-4
PG 11
WC Biotechnology & Applied Microbiology; Engineering, Chemical
SC Biotechnology & Applied Microbiology; Engineering
GA 998MY
UT WOS:000308245200018
PM 22847360
ER

PT J
AU Verhoeven, JS
   Rommel, N
   Prodi, E
   Leemans, A
   Zink, I
   Vandewalle, E
   Noens, I
   Wagemans, J
   Steyaert, J
   Boets, B
   de Winckel, AV
   De Cock, P
   Lagae, L
   Sunaert, S
AF Verhoeven, Judith S.
   Rommel, Nathalie
   Prodi, Elena
   Leemans, Alexander
   Zink, Inge
   Vandewalle, Ellen
   Noens, Ilse
   Wagemans, Johan
   Steyaert, Jean
   Boets, Bart
   de Winckel, Ann Van
   De Cock, Paul
   Lagae, Lieven
   Sunaert, Stefan
TI Is There a Common Neuroanatomical Substrate of Language Deficit between
   Autism Spectrum Disorder and Specific Language Impairment?
SO CEREBRAL CORTEX
LA English
DT Article
DE autism spectrum disorder; diffusion tensor imaging; specific language
   impairment; superior longitudinal fascicle
ID WHITE-MATTER MATURATION; COMPARATIVE FOLLOW-UP; DIAGNOSTIC INTERVIEW;
   READING ABILITIES; INFANTILE-AUTISM; CHROMOSOME 7Q; HUMAN BRAIN;
   CHILDREN; CHILDHOOD; LINKAGE
AB Discussion of an overlap between specific language impairment (SLI) and autism spectrum disorder (ASD) is on going. The most intriguing overlap between both phenotypes is the similarity in the observed language deficits described in SLI and a subgroup of ASD with co-occurring linguistic impairment, ASD-LI. Examining whether a similar neuroanatomical substrate underlies this phenotypical linguistic overlap, we studied the white matter microstructural properties of the superior longitudinal fascicle (SLF) of 19 ASD-LI adolescents (mean age 13.8 +/- 1.6 years) and 21 age-matched controls and compared them with 13 SLI children (mean age 10.1 +/- 0.4 years) and 12 age-matched controls. A linguistic profile assessment and a diffusion tensor imaging analysis of the SLF were performed. Linguistic testing revealed a mixed receptive-expressive disorder profile in both groups, confirming their overlap at phenotypical level. At neuroanatomical level, no significant differences in mean SLF fractional anisotropy (FA) and mean SLF apparent diffusion coefficient values between ASD-LI participants and controls were seen. By contrast, the mean SLF FA was significantly reduced in the SLI children as compared with their controls. The observation of structural SLF disturbances in SLI but not in ASD-LI suggests the existence of a different neuroanatomical substrate for the language deficits in both disorders.
C1 [Verhoeven, Judith S.; Prodi, Elena; Sunaert, Stefan] Catholic Univ Louvain, Univ Hosp, Dept Radiol, B-3000 Louvain, Belgium.
   [Rommel, Nathalie; Zink, Inge; Vandewalle, Ellen] Catholic Univ Louvain, Univ Hosp, Dept Neurosci, Exp ORL, B-3000 Louvain, Belgium.
   [Verhoeven, Judith S.; Noens, Ilse; Wagemans, Johan; Steyaert, Jean; Boets, Bart; De Cock, Paul; Sunaert, Stefan] Catholic Univ Louvain, Leuven Autism Res Consortium, B-3000 Louvain, Belgium.
   [Verhoeven, Judith S.; De Cock, Paul; Lagae, Lieven] Catholic Univ Louvain, Univ Hosp, Dept Pediat, B-3000 Louvain, Belgium.
   [Prodi, Elena] Univ Milan, Dept Radiol, Ist Neurol Carlo Besta, Milan, Italy.
   [Leemans, Alexander] Univ Med Ctr Utrecht, Dept Radiol, Image Sci Inst, Utrecht, Netherlands.
   [Noens, Ilse; Boets, Bart] Univ Louvain, Dept Educ Sci, Parenting & Special Educ Res Grp, Louvain, Belgium.
   [Noens, Ilse] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA.
   [Wagemans, Johan] Univ Louvain, Lab Expt Psychol, Louvain, Belgium.
   [Steyaert, Jean; Boets, Bart] Catholic Univ Louvain, Univ Hosp, Dept Child & Adolescent Psychiat, B-3000 Louvain, Belgium.
   [Steyaert, Jean] Univ Maastricht, Dept Clin Genet, Maastricht, Netherlands.
   [de Winckel, Ann Van] Catholic Univ Louvain, Univ Hosp, Ctr Dev Disabil, B-3000 Louvain, Belgium.
   [De Cock, Paul] Univ Louvain, Fac Kinesiol & Rehabil Sci, Dept Rehabil Sci, Louvain, Belgium.
RP Sunaert, S (reprint author), Catholic Univ Louvain, Univ Hosp, Dept Radiol, Herestr 49, B-3000 Louvain, Belgium.
EM Stefan.sunaert@uzleuven.be
RI Leemans, Alexander/A-1784-2011; Rommel, Nathalie/D-6721-2014; Steyaert,
   Jean/B-5326-2015
OI Steyaert, Jean/0000-0003-2512-4694
FU Fund for Scientific Research-Flanders," FWO, Belgium [G.0354.06];
   IUAP-KUL (FWO fellowship) [asp/07]; Research Council [IDO/08/013]
FX "Fund for Scientific Research-Flanders," FWO, Belgium (G.0354.06);
   IUAP-KUL (FWO fellowship asp/07 to J.S.V.); the Research Council
   (IDO/08/013).
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NR 65
TC 20
Z9 20
PU OXFORD UNIV PRESS INC
PI CARY
PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA
SN 1047-3211
J9 CEREB CORTEX
JI Cereb. Cortex
PD OCT
PY 2012
VL 22
IS 10
BP 2263
EP 2271
DI 10.1093/cercor/bhr292
PG 9
WC Neurosciences
SC Neurosciences & Neurology
GA 002KI
UT WOS:000308530500005
PM 22047968
ER

PT J
AU Bandstra, NF
   Johnson, SA
   Filliter, JH
   Chambers, CT
AF Bandstra, Nancy F.
   Johnson, Shannon A.
   Filliter, Jillian H.
   Chambers, Christine T.
TI Self-reported and Parent-reported Pain for Common Painful Events in
   High-functioning Children and Adolescents With Autism Spectrum Disorder
SO CLINICAL JOURNAL OF PAIN
LA English
DT Article
DE pain; autism spectrum; self-report; parent-report
ID VENIPUNCTURE; TRIALS; MIND
AB Objectives: Previous research suggests that children with autism spectrum disorders (ASD) are at a higher risk for painful experiences, but there is limited research examining pain in children with ASD.
   Methods: The current study examined self-reported and parent-reported pain in 20 high-functioning youth with ASD (17 boys; 3 girls) and 20 typically developing controls (16 boys; 4 girls) ranging in age from 9 to 18 years and matched on age and IQ. Participants with and without ASD rated their hypothetical pain in a series of pictures depicting common childhood situations. They also rated the amount of pain they would expect to feel (using the Faces Pain Scale-Revised and a Numeric Rating Scale) in a series of validated hypothetical pain situations depicted in cartooned images (eg, scraping knee on sidewalk). Parents rated the amount of pain they would expect their child to show in each of the same cartoon stimuli.
   Results: There were no significant differences between pain vignette ratings of youth with ASD and their non-ASD peers or in the ratings provided by their parents. High-functioning youth with ASD were able to successfully use both of the self-report scales to rate pain.
   Discussion: This is the first study to successfully obtain self-report of pain from youth with ASD. Implications for the understanding of pain and pain assessment in high-functioning youth with ASD are discussed.
C1 [Bandstra, Nancy F.; Johnson, Shannon A.; Filliter, Jillian H.; Chambers, Christine T.] Dalhousie Univ, Dept Psychol, Halifax, NS B3H 4R2, Canada.
   Dalhousie Univ, Dept Pediat, Halifax, NS B3H 4R2, Canada.
   [Chambers, Christine T.] IWK Hlth Ctr, Halifax, NS, Canada.
RP Johnson, SA (reprint author), Dalhousie Univ, Dept Psychol, Halifax, NS B3H 4R2, Canada.
EM shannon.johnson@dal.ca
FU Dalhousie University (Halifax, Canada); IWK Health Centre Graduate
   Student Scholarship (Halifax, Canada); honorary Killam Predoctoral
   Scholarship (Halifax, Canada); Alexander Graham Bell Canada Graduate
   Scholarship from the National Science and Engineering Research Council
   (NSERC; Ottawa, Canada); honorary Killam Predoctoral Scholarship; Canada
   Research Chair (Ottawa, Canada)
FX This research was supported by funding to S.A.J. from Dalhousie
   University (Halifax, Canada). N.F.B. was supported by an IWK Health
   Centre Graduate Student Scholarship (Halifax, Canada) and an honorary
   Killam Predoctoral Scholarship (Halifax, Canada). She is a trainee
   member of Pain in Child Health, a Strategic Training Initiative in
   Health Research of the Canadian Institutes for Health Research (CIHR;
   Ottawa, Canada). J.H.F. is supported by an Alexander Graham Bell Canada
   Graduate Scholarship from the National Science and Engineering Research
   Council (NSERC; Ottawa, Canada) and an honorary Killam Predoctoral
   Scholarship. She is a trainee of the Autism Research Training program, a
   Strategic Training Initiative in Health Research of the CIHR. C.T.C. is
   supported by a Canada Research Chair (Ottawa, Canada). The authors
   declare no conflict of interest.
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NR 35
TC 4
Z9 4
PU LIPPINCOTT WILLIAMS & WILKINS
PI PHILADELPHIA
PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA
SN 0749-8047
J9 CLIN J PAIN
JI Clin. J. Pain
PD OCT
PY 2012
VL 28
IS 8
BP 715
EP 721
DI 10.1097/AJP.0b013e318243ecf6
PG 7
WC Anesthesiology; Clinical Neurology
SC Anesthesiology; Neurosciences & Neurology
GA 004HL
UT WOS:000308672100011
PM 22699139
ER

PT J
AU Poggi, I
   D'Errico, F
   Vinciarelli, A
AF Poggi, Isabella
   D'Errico, Francesca
   Vinciarelli, Alessandro
TI Social signals: from theory to applications
SO COGNITIVE PROCESSING
LA English
DT Editorial Material
DE Social signals; Theory of social signals; Applications
ID JOINT ACTION; THIN SLICES; COGNITION; AUTISM; IMITATION
AB The Special Issue Editorial introduces the research milieu in which Social Signal Processing originates, by merging computer scientists and social scientists and giving rise to this field in parallel with Human-Computer Interaction, Affective Computing, and Embodied Conversational Agents, all similarly characterized by high interdisciplinarity, stress on multimodality of communication, and the continuous loop from theory to simulation and application. Some frameworks of the cognitive and social processes underlying social signals are identified as reference points (Theory of Mind and Intersubjectivity, mirror neurons, and the ontogenesis and phylogenesis of communication), while three dichotomies (automatic vs. controlled, individualistic vs. intersubjective, and meaning vs. influence) are singled out as leads to navigate within the theoretical and applicative studies presented in the Special Issue.
C1 [Poggi, Isabella; D'Errico, Francesca; Vinciarelli, Alessandro] Roma Tre Univ, Rome, Italy.
RP D'Errico, F (reprint author), Roma Tre Univ, Rome, Italy.
EM poggi@uniroma3.it; fderrico@uniroma3.it; Vinciarelli@glasgow.ac.uk
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NR 50
TC 1
Z9 1
PU SPRINGER HEIDELBERG
PI HEIDELBERG
PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY
SN 1612-4782
J9 COGN PROCESS
JI Cogn. Process.
PD OCT
PY 2012
VL 13
SU 2
BP 389
EP 396
DI 10.1007/s10339-012-0514-4
PG 8
WC Psychology, Experimental
SC Psychology
GA 006NM
UT WOS:000308825900001
PM 22893010
ER

PT J
AU Miranda, JC
   Alvarez, X
   Orvalho, J
   Gutierrez, D
   Sousa, AA
   Orvalho, V
AF Miranda, Jose Carlos
   Alvarez, Xenxo
   Orvalho, Joao
   Gutierrez, Diego
   Augusto Sousa, A.
   Orvalho, Veronica
TI Sketch express: A sketching interface for facial animation
SO COMPUTERS & GRAPHICS-UK
LA English
DT Article
DE Sketching; Facial expression; Deformation; 3D mesh; Canvas; Billboard;
   Rig; User interface; Animation interface; Facial animation
AB One of the most challenging tasks for an animator is to quickly create convincing facial expressions. Finding an effective control interface to manipulate facial geometry has traditionally required experienced users (usually technical directors), who create and place the necessary animation controls. Here we present our sketching interface control system, designed to reduce the time and effort necessary to create facial animations. Inspired in the way artists draw, where simple strokes define the shape of an object, our approach allows the user to sketch such strokes either directly on the 3D mesh or on two different types of canvas: a 2D fixed canvas or more flexible 2.5D dynamic screen-aligned billboards. In all cases, the strokes do not control the geometry of the face, but the underlying animation rig instead, allowing direct manipulation of the rig elements. Additionally, we show how the strokes can be easily reused in different characters, allowing retargeting of poses on several models. We illustrate our interactive approach using varied facial models of different styles showing that first time users typically create appealing 3D poses and animations in just a few minutes. We also present in this article the results of a user study. We deploy our method in an application for an artistic purpose. Our system has also been used in a pioneer serious game context, where the goal was to teach people with Autism Spectrum Disorders (ASD) to recognize facial emotions, using real time synthesis and automatic facial expression analysis. (c) 2012 Elsevier Ltd. All rights reserved.
C1 [Alvarez, Xenxo; Orvalho, Veronica] Univ Porto, Fac Ciencias, Oporto, Portugal.
   [Gutierrez, Diego] Univ Zaragoza, E-50009 Zaragoza, Spain.
   [Augusto Sousa, A.] INESC Porto, Oporto, Portugal.
   [Miranda, Jose Carlos; Augusto Sousa, A.] Univ Porto, Fac Engn, Oporto, Portugal.
EM jcmira@ipg.pt
RI INESCTEC, USIG/H-9369-2012; FCUP, DCC/F-5042-2012
FU Instituto de Telecomunicacoes; Fundacao para a Ciencia e Tecnologia
   [SFRH/BD/46588/2008]; LIFEisGAME [UTA-Est/MAI/0009/2009]; VERE [257695];
   Golem [251415, FP7-PEOPLE-2009-IAPP]
FX This work is partially supported by Instituto de Telecomunicacoes,
   Fundacao para a Ciencia e Tecnologia (SFRH/BD/46588/2008), the projects
   LIFEisGAME (ref. UTA-Est/MAI/0009/2009), VERE (ref. 257695) and Golem
   (ref. 251415, FP7-PEOPLE-2009-IAPP). The 3D Human Head Scan used in the
   paper was created by Lee Perry-Smith and is licensed under a Creative
   Commons Attribution 3.0 Unported License. We specially thank Andrew
   Tucker for the cartoon models and Jacqueline Fernandes for the text
   revision.
CR Abirached B, 2011, IEEE INT C SER GAM A
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NR 28
TC 2
Z9 2
PU PERGAMON-ELSEVIER SCIENCE LTD
PI OXFORD
PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND
SN 0097-8493
J9 COMPUT GRAPH-UK
JI Comput. Graph.-UK
PD OCT
PY 2012
VL 36
IS 6
BP 585
EP 595
DI 10.1016/j.cag.2012.03.002
PG 11
WC Computer Science, Software Engineering
SC Computer Science
GA 003PA
UT WOS:000308622600003
ER

PT J
AU Angus, B
   Monson, K
AF Angus, Bethany
   Monson, Katherine
TI Autism spectrum disorders (ASDs) within EPPIC
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-7885
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2012
VL 6
SU 1
SI SI
BP 50
EP 50
PG 1
WC Psychiatry
SC Psychiatry
GA 003AI
UT WOS:000308580100185
ER

PT J
AU Khan, F
   Queenan, G
   Laganis, C
   Husain, N
   Constable, L
   Warburton, J
   Chaudhry, IB
AF Khan, Faria
   Queenan, Glynis
   Laganis, Christy
   Husain, Nusrat
   Constable, Lauren
   Warburton, Jeff
   Chaudhry, Imran B.
TI The prevalence of learning disabilities and autism spectrum conditions
   amongst service users of Lancashire Early Intervention Services
SO EARLY INTERVENTION IN PSYCHIATRY
LA English
DT Meeting Abstract
C1 [Khan, Faria; Queenan, Glynis; Laganis, Christy; Husain, Nusrat; Constable, Lauren; Warburton, Jeff; Chaudhry, Imran B.] Lancashire Care NHS Fdn Trust, Lancaster, England.
   [Husain, Nusrat; Chaudhry, Imran B.] Univ Manchester, Manchester M13 9PL, Lancs, England.
NR 0
TC 0
Z9 0
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 1751-7885
J9 EARLY INTERV PSYCHIA
JI Early Interv. Psychiatry
PD OCT
PY 2012
VL 6
SU 1
SI SI
BP 108
EP 108
PG 1
WC Psychiatry
SC Psychiatry
GA 003AI
UT WOS:000308580100409
ER

PT J
AU Capone, G
   Novello, G
   Bavaro, SL
   Fasano, C
   Delfino, AP
   Polito, AN
   Kanduc, D
AF Capone, Giovanni
   Novello, Giuseppe
   Bavaro, Simona Lucia
   Fasano, Candida
   Delfino, Antonella Pesce
   Polito, Anna Nunzia
   Kanduc, Darja
TI A qualitative description of the peptide sharing between poliovirus and
   Homo sapiens
SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY
LA English
DT Article
DE Poliovirus polyprotein; human proteome; peptide commonality; neural
   pathways; axon guidance
ID CELL-ADHESION MOLECULES; NEUROTROPIC VIRUSES; AUTISM RESEARCH; AXON
   GROWTH; PROTEIN; GUIDANCE; GENE; EXPRESSION; PROTEOMICS; DISORDER
AB In a companion paper, we reported that pentapeptides from human poliovirus 1, Mahoney strain, occur repeatedly in human proteins for a total of more than 18,000 overlaps. In the present study, we describe the distribution of the polio pentapeptides throughout biochemical pathways and networks characterizing functions and tissues in the human host. The present study might be of help to better define the poliovirus-host relationships as well as for designing peptide modules with anti-polio activity.
C1 [Capone, Giovanni; Novello, Giuseppe; Bavaro, Simona Lucia; Fasano, Candida; Kanduc, Darja] Univ Bari, Dept Biochem & Mol Biol, I-70126 Bari, Italy.
   [Delfino, Antonella Pesce] Univ Bari, Dept Hlth & Welf Anim, I-70126 Bari, Italy.
RP Kanduc, D (reprint author), Univ Bari, Dept Biochem & Mol Biol, I-70126 Bari, Italy.
EM d.kanduc@biologia.uniba.it
FU Ministry of University and Research of Italy
FX Partial funding for this work was provided by the Ministry of University
   and Research of Italy (60%).
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NR 82
TC 4
Z9 4
PU INFORMA HEALTHCARE
PI LONDON
PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND
SN 0892-3973
J9 IMMUNOPHARM IMMUNOT
JI Immunopharmacol. Immunotoxicol.
PD OCT
PY 2012
VL 34
IS 5
BP 779
EP 785
DI 10.3109/08923973.2012.654610
PG 7
WC Immunology; Pharmacology & Pharmacy; Toxicology
SC Immunology; Pharmacology & Pharmacy; Toxicology
GA 004EU
UT WOS:000308664000007
PM 22303874
ER

PT J
AU Gadow, KD
   Drabick, DAG
AF Gadow, Kenneth D.
   Drabick, Deborah A. G.
TI Anger and Irritability Symptoms among Youth with ODD: Cross-Informant
   Versus Source-Exclusive Syndromes
SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY
LA English
DT Article
DE Oppositional defiant disorder; Anger; Irritability; Informant; Nosology;
   DSM-5; Attention-deficit/hyperactivity disorder
ID OPPOSITIONAL DEFIANT DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER;
   AUTISM SPECTRUM DISORDER; PAST 10 YEARS; CONDUCT DISORDER;
   HYPERACTIVE-CHILDREN; PSYCHIATRIC-SYMPTOMS; BEHAVIORAL-DISORDERS;
   DISRUPTIVE BEHAVIOR; SPECIAL SECTION
AB We examined differences in co-occurring psychological symptoms and background characteristics among clinically referred youth with oppositional defiant disorder (ODD) with and without anger/irritability symptoms (AIS) according to either parent or teacher (source-exclusive) and both informants (cross-informant), youth with noncompliant symptoms (NS) of ODD, and non-ODD clinic controls. Parents and teachers evaluated 1127 youth (ages 6-18) with a DSM-IV-referenced rating scale to assess ODD and co-occurring psychological symptoms. Parents also completed a background questionnaire (demographic, developmental, treatment, relationship, and academic characteristics) and teachers rated school functioning. Source-exclusive AIS groups were associated with different clinical features, and there was some evidence that cross-informant youth had more mental health concerns than source-exclusive groups. Findings varied to some extent among older (12-18 years) versus younger (6-11 years) youth. In general, the NS group (youth without AIS) was the most similar to clinic controls. AIS and NS are likely candidates for component phenotypes in ODD and continued research into their pathogenesis may have important implications for nosology, etiology, and intervention.
C1 [Gadow, Kenneth D.] SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA.
   [Drabick, Deborah A. G.] Temple Univ, Dept Psychol, Philadelphia, PA 19122 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 68
TC 9
Z9 9
PU SPRINGER/PLENUM PUBLISHERS
PI NEW YORK
PA 233 SPRING ST, NEW YORK, NY 10013 USA
SN 0091-0627
J9 J ABNORM CHILD PSYCH
JI J. Abnorm. Child Psychol.
PD OCT
PY 2012
VL 40
IS 7
BP 1073
EP 1085
DI 10.1007/s10802-012-9637-4
PG 13
WC Psychology, Clinical; Psychology, Developmental
SC Psychology
GA 998LJ
UT WOS:000308240300004
PM 22581374
ER

PT J
AU Porter, S
   Holmes, V
   McLaughlin, K
   Lynn, F
   Cardwell, C
   Braiden, HJ
   Doran, J
   Rogan, S
AF Porter, Sam
   Holmes, Valerie
   McLaughlin, Katrina
   Lynn, Fiona
   Cardwell, Chris
   Braiden, Hannah-Jane
   Doran, Jackie
   Rogan, Sheelagh
TI Music in mind, a randomized controlled trial of music therapy for young
   people with behavioural and emotional problems: study protocol
SO JOURNAL OF ADVANCED NURSING
LA English
DT Article
DE child and adolescent mental health nursing; communication skills; music
   therapy; randomized controlled trial
ID CHILDREN; AUTISM; INTERVENTION; METAANALYSIS; ADOLESCENTS
AB porter s., holmes v., mclaughlin k., lynn f., cardwell c., braiden h.-j., doran j. & rogan s. (2012) Music in mind, a randomized controlled trial of music therapy for young people with behavioural and emotional problems: study protocol. Journal of Advanced Nursing68(10), 23492358. Abstract Aims. This article is a report of a trial protocol to determine if improvizational music therapy leads to clinically significant improvement in communication and interaction skills for young people experiencing social, emotional or behavioural problems. Background. Music therapy is often considered an effective intervention for young people experiencing social, emotional or behavioural difficulties. However, this assumption lacks empirical evidence. Study design. Music in mind is a multi-centred single-blind randomized controlled trial involving 200 young people (aged 816 years) and their parents. Eligible participants will have a working diagnosis within the ambit of International Classification of Disease 10 Mental and Behavioural Disorders and will be recruited over 15 months from six centres within the Child and Adolescent Mental Health Services of a large health and social care trust in Northern Ireland. Participants will be randomly allocated in a 1:1 ratio to receive standard care alone or standard care plus 12 weekly music therapy sessions delivered by the Northern Ireland Music Therapy Trust. Baseline data will be collected from young people and their parents using standardized outcome measures for communicative and interaction skills (primary endpoint), self-esteem, social functioning, depression and family functioning. Follow-up data will be collected 1 and 13 weeks after the final music therapy session. A cost-effectiveness analysis will also be carried out. Discussion. This study will be the largest trial to date examining the effect of music therapy on young people experiencing social, emotional or behavioural difficulties and will provide empirical evidence for the use of music therapy among this population. Trial registration.similar to This study is registered in the ISRCTN Register, ISRCTN96352204. Ethical approval was gained in October 2010.
C1 [Porter, Sam; Holmes, Valerie; Lynn, Fiona; Doran, Jackie] Queens Univ Belfast, Sch Nursing & Midwifery, Belfast BT7 1NN, Antrim, North Ireland.
   [Rogan, Sheelagh] Belfast Hlth & Social Care Trust, Child & Adolescent Mental Hlth Team, Belfast, Antrim, North Ireland.
   [Cardwell, Chris] Queens Univ Belfast, Sch Med Dent & Biomed Sci, Belfast BT7 1NN, Antrim, North Ireland.
   [McLaughlin, Katrina] Queens Univ Belfast, Inst Childcare Res, Belfast BT7 1NN, Antrim, North Ireland.
   [Braiden, Hannah-Jane] Western Educ & Lib Board, Omagh, North Ireland.
RP Porter, S (reprint author), Queens Univ Belfast, Sch Nursing & Midwifery, Belfast BT7 1NN, Antrim, North Ireland.
EM s.porter@qub.ac.uk
FU Big Lottery Fund [C984A1530]
FX Music in Mind is funded by a grant from The Big Lottery Fund
   (C984A1530).
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NR 22
TC 1
Z9 2
PU WILEY-BLACKWELL
PI HOBOKEN
PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA
SN 0309-2402
J9 J ADV NURS
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VL 68
IS 10
BP 2349
EP 2358
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PG 10
WC Nursing
SC Nursing
GA 002AQ
UT WOS:000308502600022
PM 22235808
ER

EF