FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Liu, XD Solehdin, F Cohen, IL Gonzalez, MG Jenkins, EC Lewis, MES Holden, JJA AF Liu, Xudong Solehdin, Fatima Cohen, Ira L. Gonzalez, Maripaz G. Jenkins, Edmund C. Lewis, M. E. Suzanne Holden, Jeanette J. A. TI Population- and Family-Based Studies Associate the MTHFR Gene with Idiopathic Autism in Simplex Families SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism spectrum disorders (ASDs); Gene association; Methylenetetrahydrofolate reductase (MTHFR); Functional polymorphism; Epigenetics; Methylation ID METHYLENETETRAHYDROFOLATE REDUCTASE GENE; GENOMIC DNA METHYLATION; SPECTRUM DISORDERS; COMMON MUTATION; RETT-SYNDROME; HUMAN-LYMPHOCYTES; RISK-FACTOR; CHILDREN; HYPOMETHYLATION; POLYMORPHISMS AB Two methylenetetrahydrofolate reductase gene (MTHFR) functional polymorphisms were studied in 205 North American simplex (SPX) and 307 multiplex (MPX) families having one or more children with an autism spectrum disorder. Case-control comparisons revealed a significantly higher frequency of the low-activity 677T allele, higher prevalence of the 677TT genotype and higher frequencies of the 677T-1298A haplotype and double homozygous 677TT/1298AA genotype in affected individuals relative to controls. Family-based association testing demonstrated significant preferential transmission of the 677T and 1298A alleles and the 677T-1298A haplotype to affected offspring. The results were not replicated in MPX families. The results associate the MTHFR gene with autism in SPX families only, suggesting that reduced MTHFR activity is a risk factor for autism in these families. C1 [Liu, Xudong; Holden, Jeanette J. A.] Queens Univ, Dept Psychiat & Physiol, Autism Res Program, Ongwanada Resource Ctr, Kingston, ON K7M 8A6, Canada. [Solehdin, Fatima; Lewis, M. E. Suzanne] Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada. [Lewis, M. E. Suzanne] BC Child & Family Res Inst, Vancouver, BC, Canada. [Cohen, Ira L.; Gonzalez, Maripaz G.] New York State Inst Basic Res Dev Disabil, Dept Psychol, Staten Isl, NY 10314 USA. [Jenkins, Edmund C.] New York State Inst Basic Res Dev Disabil, Dept Human Genet, Staten Isl, NY 10314 USA. [Liu, Xudong; Solehdin, Fatima; Cohen, Ira L.; Gonzalez, Maripaz G.; Jenkins, Edmund C.; Lewis, M. E. Suzanne; Holden, Jeanette J. A.] ASD CARC, Kingston, ON, Canada. RP Holden, JJA (reprint author), Queens Univ, Dept Psychiat & Physiol, Autism Res Program, Ongwanada Resource Ctr, 191 Portsmouth Ave, Kingston, ON K7M 8A6, Canada. 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TI Brief Report: Attachment Security in Infants At-Risk for Autism Spectrum Disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Attachment; Autism; Infant-sibling; Risk; Strange-situation procedure ID STRANGE SITUATION; DEVELOPMENTAL DISORDERS; FAMILY-HISTORY; CHILDREN; SIBLINGS; PHENOTYPE; COMMUNICATION; SENSITIVITY; IMPAIRMENT; TODDLERS AB Little is known about attachment security and disorganization in children who are at genetic risk for an Autism Spectrum Disorder (ASD) prior to a possible diagnosis. The present study examined distributions of attachment security and disorganization at 15-months of age in a sample of infant siblings of older children with (ASD-sibs; n = 51) or without (COMP-sibs; n = 34) an ASD. ASD-sibs were not more or less likely to evince attachment insecurity or disorganization than COMP-sibs. However, relative to COMP-sibs, the rate of B1-B2 secure subclassifications was disproportionately larger in the ASD-sib group. 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Schultz, Robert T. TI Multi-voxel pattern analysis of fMRI data predicts clinical symptom severity SO NEUROIMAGE LA English DT Article DE MVPA; fMRI; Multivariate; Pattern; Patient; Autism ID FUSIFORM FACE AREA; AUTISM SPECTRUM DISORDER; DIAGNOSTIC OBSERVATION SCHEDULE; VENTRAL TEMPORAL CORTEX; DISTRIBUTED REPRESENTATIONS; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; CORTICAL ACTIVITY; SOCIAL COGNITION; FUNCTIONAL MRI AB Multi-voxel pattern analysis (MVPA) has been applied successfully to a variety of fMRI research questions in healthy participants. The full potential of applying MVPA to functional data from patient groups has yet to be fully explored. Our goal in this study was to investigate whether MVPA might yield a sensitive predictor of patient symptoms. We also sought to demonstrate that this benefit can be realized from existing datasets, even when they were not designed with MVPA in mind. We analyzed data from an fMRI study of the neural basis for face processing in individuals with an Autism Spectrum Disorder (ASD), who often show fusiform gyrus hypoactivation when presented with unfamiliar faces, compared to controls. We found reliable correlations between MVPA classification performance and standardized measures of symptom severity that exceeded those observed using a univariate measure; a relation that was robust across variations in ROI definition. A searchlight analysis across the ventral temporal lobes identified regions with relationships between classification performance and symptom severity that were not detected using mean activation. These analyses illustrate that MVPA has the potential to act as a sensitive functional biomarker of patient severity. (C) 2011 Elsevier Inc. All rights reserved. C1 [Coutanche, Marc N.; Thompson-Schill, Sharon L.] Univ Penn, Dept Physiol, Philadelphia, PA 19104 USA. [Schultz, Robert T.] Childrens Hosp Philadelphia, Ctr Autism Res, Philadelphia, PA 19104 USA. RP Coutanche, MN (reprint author), Univ Penn, Dept Physiol, 3720 Walnut St, Philadelphia, PA 19104 USA. EM coumarc@psych.upenn.edu RI Thompson-Schill, Sharon/M-1788-2013 FU NIMH [R01MH073084]; NIH [R01MH070850] FX This work was supported by NIMH grant R01MH073084 (R.T. Schultz), with further support from NIH grant R01MH070850 (S.L. Thompson-Schill). We thank members of the Thompson-Schill lab and CHOP Center for Autism Research for helpful discussions. We thank Lauren Hallion for valuable comments on an earlier version of the manuscript, and the anonymous reviewers for their insightful suggestions. 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We integrate this knowledge to emphasize how inappropriate SERT expression or its dysregulation may be linked to the pathophysiology of psychiatric, cardiovascular and gastrointestinal diseases. (C) 2011 Elsevier Inc. All rights reserved. C1 [Daws, Lynette C.; Gould, Georgianna G.] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA. RP Daws, LC (reprint author), Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, 7703 Floyd Curl Dr,MC 7756, San Antonio, TX 78229 USA. EM daws@uthscsa.edu; gouldg@uthscsa.edu FU USPHS [MH64489, MH064489-07S1]; NARSAD; San Antonio Area Foundation FX Supported in part from USPHS grant MH64489 (LCD), MH064489-07S1, (LCD), NARSAD (LCD) and the San Antonio Area Foundation (GGG). 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Ther. PD JUL PY 2011 VL 131 IS 1 BP 61 EP 79 DI 10.1016/j.pharmthera.2011.03.013 PG 19 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 779IL UT WOS:000291771200006 PM 21447358 ER PT J AU Radua, J Via, E Catani, M Mataix-Cols, D AF Radua, J. Via, E. Catani, M. Mataix-Cols, D. TI Voxel-based meta-analysis of regional white-matter volume differences in autism spectrum disorder versus healthy controls SO PSYCHOLOGICAL MEDICINE LA English DT Article DE Arcuate fasciculus; Asperger; autism; meta-analysis; uncinate fasciculus; voxel-based morphometry; white matter ID HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; ASPERGER-SYNDROME; HUMAN BRAIN; NEUROIMAGING DATA; CORPUS-CALLOSUM; IN-VIVO; HEAD CIRCUMFERENCE; CHILDHOOD AUTISM; MORPHOMETRY AB Background. We conducted a meta-analysis of voxel-based morphometry (VBM) studies in autism spectrum disorder (ASD) to clarify the changes in regional white-matter volume underpinning this condition, and generated an online database to facilitate replication and further analyses by other researchers. Method. PubMed, ScienceDirect, Web of Knowledge and Scopus databases were searched between 2002 (the date of the first white-matter VBM study in ASD) and 2010. Manual searches were also conducted. Authors were contacted to obtain additional data. Coordinates were extracted from clusters of significant white-matter difference between patients and controls. A new template for white matter was created for the signed differential mapping (SDM) meta-analytic method. A diffusion tensor imaging (DTI)-derived atlas was used to optimally localize the changes in white-matter volume. Results. Thirteen datasets comprising 246 patients with ASD and 237 healthy controls met inclusion criteria. No between-group differences were found in global white-matter volumes. ASD patients showed increases of white-matter volume in the right arcuate fasciculus and also in the left inferior fronto-occipital and uncinate fasciculi. These findings remained unchanged in quartile and jackknife sensitivity analyses and also in subgroup analyses (pediatric versus adult samples). Conclusions. Patients with ASD display increases of white-matter volume in tracts known to be important for language and social cognition. Whether the results apply to individuals with lower IQ or younger age and whether there are meaningful neurobiological differences between the subtypes of ASD remain to be investigated. C1 [Radua, J.; Via, E.; Mataix-Cols, D.] Kings Coll London, Inst Psychiat, Dept Psychosis Studies, London SE5 8AF, England. [Radua, J.] Hosp Benito Menni Complex Assistencial Salut Ment, CIBERSAM, St Boi De Llobregat, Spain. [Via, E.] Hosp Univ Bellvitge, IDIBELL, Lhospitalet De Llobregat, Spain. 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Med. PD JUL PY 2011 VL 41 IS 7 BP 1539 EP 1550 DI 10.1017/S0033291710002187 PG 12 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 780KL UT WOS:000291854700021 PM 21078227 ER PT J AU Bale, TL AF Bale, Tracy L. TI Sex differences in prenatal epigenetic programing of stress pathways SO STRESS-THE INTERNATIONAL JOURNAL ON THE BIOLOGY OF STRESS LA English DT Review DE Brain; masculinization; neurodevelopmental disorders; placenta; prenatal stress; sex differences ID PITUITARY-ADRENAL AXIS; CORTICOTROPIN-RELEASING HORMONE; ANTENATAL MATERNAL EXPOSURE; FOLIC-ACID SUPPLEMENTATION; JUVENILE RHESUS-MONKEYS; GENE-EXPRESSION; FEMALE RAT; GLUCOCORTICOID-RECEPTOR; PLACENTAL DEVELOPMENT; BEHAVIORAL-RESPONSES AB Maternal stress experience is associated with neurodevelopmental disorders including schizophrenia and autism. Recent studies have examined mechanisms by which changes in the maternal milieu may be transmitted to the developing embryo and potentially translated into programing of the epigenome. Animal models of prenatal stress have identified important sex- and temporal-specific effects on offspring stress responsivity. As dysregulation of stress pathways is a common feature in most neuropsychiatric diseases, molecular and epigenetic analyses at the maternal--embryo interface, especially in the placenta, may provide unique insight into identifying much-needed predictive biomarkers. In addition, as most neurodevelopmental disorders present with a sex bias, examination of sex differences in the inheritance of phenotypic outcomes may pinpoint gene targets and specific windows of vulnerability in neurodevelopment, which have been disrupted. 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Kononen, Eija Gottfried, Carmem TI A dental look at the autistic patient through orofacial pain SO ACTA ODONTOLOGICA SCANDINAVICA LA English DT Review DE Amalgam fillings; autism; behavioral symptoms; dental intervention; oral health ID MERCURY EXPOSURE; MEDICAL-MANAGEMENT; MENTAL-RETARDATION; CHEMICAL-COMPOUNDS; AMALGAM FILLINGS; NEUROPATHIC PAIN; FACIAL-PAIN; CHILDREN; DISORDER; PATHOPHYSIOLOGY AB Autism is a neurodevelopmental disorder characterized by impaired social interaction and restricted interests, compromised communication skills, and repetitive patterns of behavior. Both social and behavioral problems, which may include hyperactivity and quick frustration, may hinder the detection of other important pathologies such as orofacial pain. This is aggravated by the invasive nature of oral exploration, which may trigger violent and self-injurious responses, such as temper tantrums and/or head banging, which make the work of professionals extremely difficult during diagnoses, follow-up examinations, and dental treatments. In addition, mercury-containing amalgams used to treat dental caries (the most common form of acute orofacial pain) have been associated with higher rates of severe autism in children. The purpose of this review is to describe the current state of the art regarding the co-occurrence of orofacial pain and autism spectrum disorder, and how these conditions may interrelate clinically and neurobiologically. C1 [Zeidan-Chulia, Fares; Gottfried, Carmem] Univ Fed Rio Grande do Sul, Inst Basic Hlth Sci, Dept Biochem, Neuroglial Plast Lab,Postgrad Program Biol Sci, BR-90035003 Porto Alegre, RS, Brazil. [Zeidan-Chulia, Fares; Gottfried, Carmem] Univ Fed Rio Grande do Sul, Clin Hosp Porto Alegre, Pervas Dev Disorders Program ProTID, BR-90035003 Porto Alegre, RS, Brazil. [Gursoy, Ulvi K.; Kononen, Eija] Univ Turku, Inst Dent, Turku, Finland. RP Gottfried, C (reprint author), Univ Fed Rio Grande do Sul, Inst Basic Hlth Sci, Dept Biochem, Neuroglial Plast Lab,Postgrad Program Biol Sci, Rua Ramiro Barcelos 2600, BR-90035003 Porto Alegre, RS, Brazil. EM cgottfried@ufrgs.br RI Zeidan Chulia, Fares/E-5605-2015 FU National Council for Scientific and Technological Development (CNPq) of the Federal Republic of Brazil; Marie Curie Early Stage Research Training (EST) program FX This work was supported by the National Council for Scientific and Technological Development (CNPq) of the Federal Republic of Brazil. F. Z.-C. is grateful to the Marie Curie Early Stage Research Training (EST) program for his previous funding. 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PD JUL PY 2011 VL 124 IS 1 BP 74 EP 75 DI 10.1111/j.1600-0447.2011.01689.x PG 3 WC Psychiatry SC Psychiatry GA 784IE UT WOS:000292149500012 ER PT J AU Okamoto, N Hatsukawa, Y Shimojima, K Yamamoto, T AF Okamoto, Nobuhiko Hatsukawa, Yoshikazu Shimojima, Keiko Yamamoto, Toshiyuki TI Submicroscopic Deletion in 7q31 Encompassing CADPS2 and TSPAN12 in a Child With Autism Spectrum Disorder and PHPV SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE CADPS2; TSPAN12; autism; PHPV; CGH ID FAMILIAL EXUDATIVE VITREORETINOPATHY; RETINAL VASCULAR DEVELOPMENT; CHROMOSOME 7Q; CADPS2-KNOCKOUT MICE; MENTAL-RETARDATION; MUTATIONS; PATIENT; LINKAGE; GENES; ASSOCIATION AB We performed array comparative genomic hybridization utilizing a whole genome oligonucleotide microarray in a patient with the autism spectrum disorders (ASDs) and persistent hyperplastic primary vitreous (PHPV). Submicroscopic deletions in 7q31 encompassing CADPS2 (Ca(2+)-dependent activator protein for secretion 2) and TSPAN12 (one of the members of the tetraspanin superfamily) were confirmed. The CADPS2 plays important roles in the release of neurotrophin-3 and brain-derived neurotrophic factor. Mutations in TSPAN12 are a relatively frequent cause of familial exudative vitreoretinopathy. We speculate that haploinsufficiency of CADPS2 and TSPAN12 contributes to ASDs and PHPV, respectively. (C) 2011 Wiley-Liss, Inc. C1 [Okamoto, Nobuhiko] Osaka Med Ctr, Dept Med Genet, Izumi Ku, Osaka 5941101, Japan. [Okamoto, Nobuhiko] Res Inst Maternal & Child Hlth, Izumi Ku, Osaka 5941101, Japan. [Hatsukawa, Yoshikazu] Osaka Med Ctr, Dept Ophthalmol, Osaka 5941101, Japan. [Shimojima, Keiko; Yamamoto, Toshiyuki] Tokyo Womens Med Univ, Inst Integrated Med Sci, Tokyo, Japan. RP Okamoto, N (reprint author), Osaka Med Ctr, Dept Med Genet, Izumi Ku, 840 Murodocho, Osaka 5941101, Japan. EM okamoto@osaka.email.ne.jp FU Ministry of Health, Labour and Welfare of Japan FX Grant sponsor: Ministry of Health, Labour and Welfare of Japan. 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J. Med. Genet. A PD JUL PY 2011 VL 155A IS 7 BP 1568 EP 1573 DI 10.1002/ajmg.a.34028 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 781OZ UT WOS:000291944700013 PM 21626674 ER PT J AU Soysal, Y Vermeesch, J Davani, NA Hekimler, K Imirzalioglu, N AF Soysal, Yasemin Vermeesch, Joris Davani, Nooshin Ardeshir Hekimler, Kuyas Imirzalioglu, Necat TI A 10.46 Mb 12p11.1-12.1 Interstitial Deletion Coincident With a 0.19 Mb NRXN1 Deletion Detected by Array CGH in a Girl With Scoliosis and Autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE interstitial deletion; chromosome 12p; array CGH; NRXN1 (neurexin-1); autism; developmental disorders; scoliosis ID LACTICO-DEHYDROGENASE-B; SHORT ARM; 12P; GENE; CHROMOSOME-12; DISORDERS; VARIANTS; SPECTRUM; PATIENT AB We present a 12-year-old girl with de novo karyotype 46, XX, del(12)(p11.1p12.1). Array CGH revealed in addition to a 10.466Mb interstitial deletion on 12p11.1 -> 12p12.1 a 0.191Mb deletion on 2p16.3. The girl presented with mild facial dysmorphism consisting of microcephaly, hypertelorism, downslanting palpebral fissures, strabismus, broad nasal base, bulbous nose, short philtrum, micro/retrognathia, irregular tooth arrangement, phalangeal deformity in distal phalanges of hands, 5th finger camptodactyly, brachydactyly in feet, history of joint hypermobility, and scoliosis. She was considered to have mild to moderate mental retardation and ascertained for an autism spectrum disorder(ASD). Short arm of chromosome 12 interstitial deletions are rarely reported whereas point mutations and deletions of NRXN1, which is located on chromosome 2p16.3, are associated with ASDs. In this article we present and discuss the phenotypic consequences of a patient who was affected by deletions of two different chromosomal regions. (C) 2011 Wiley-Liss, Inc. C1 [Soysal, Yasemin; Hekimler, Kuyas; Imirzalioglu, Necat] Afyon Kocatepe Univ, Fac Med, Dept Med Genet, Dekanlik Binasi, Afyonkarahisar, Turkey. 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Children were randomly assigned to an experimental or delayed-treatment control group. Results: From pre- to post-treatment, all children had less parent reported negativity/lability, better parent reported emotion regulation, and shorter outbursts, and also generated more coping strategies in response to vignettes. Parents also reported increases in their own confidence and their child's ability to deal with anger and anxiety. Conclusions: This study suggests that young children with high functioning ASD may benefit from CBT to improve regulation of anger and anxiety, and parent training may improve parental self-efficacy. Future studies are needed to make conclusions about its efficacy. C1 [Scarpa, Angela; Reyes, Nuri M.] Virginia Polytech Inst & State Univ, Blacksburg, VA 24061 USA. RP Scarpa, A (reprint author), Virginia Tech Psychol, 3110 Prices Fork Rd, Blacksburg, VA 24061 USA. 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PD JUL PY 2011 VL 39 IS 4 BP 495 EP 500 DI 10.1017/S1352465811000063 PG 6 WC Psychology, Clinical SC Psychology GA 782BK UT WOS:000291982400010 PM 21457605 ER PT J AU Thomas, C Humphreys, K Jung, KJ Minshew, N Behrmann, M AF Thomas, Cibu Humphreys, Kate Jung, Kwan-Jin Minshew, Nancy Behrmann, Marlene TI The anatomy of the callosal and visual-association pathways in high-functioning autism: A DTI tractography study SO CORTEX LA English DT Article DE Autism; White matter; Inferior fronto-occipito fasciculus; Inferior longitudinal fasciculus; Diffusion tensor tractography ID DIFFUSION-TENSOR MRI; CORPUS-CALLOSUM; WHITE-MATTER; SPECTRUM DISORDER; HEMISPHERIC ASYMMETRIES; AXONAL PROJECTIONS; ARCUATE FASCICULUS; ASPERGER-SYNDROME; BRAIN; CONNECTIVITY AB There is increasing recognition that many of the core behavioral impairments that characterize autism potentially emerge from poor neural synchronization across nodes comprising dispersed cortical networks. A likely candidate for the source of this atypical functional connectivity in autism is an alteration in the structural integrity of intra- and inter-hemispheric white matter (VIM) tracts that form large-scale cortical networks. To test this hypothesis, in a group of adults with high-functioning autism (HFA) and matched control participants, we used diffusion tensor tractography to compare the structural integrity of three intra-hemispheric visual-association VIM tracts, the inferior longitudinal fasciculus (ILF), the inferior fronto-occipito fasciculus (IFOF) and the uncinate fasciculus (UF), with the integrity of three sub-portions of the major inter-hemispheric fiber tract, the corpus callosum. Compared with the control group, the HFA group evinced an increase in the volume of the intra-hemispheric fibers, particularly in the left hemisphere, and a reduction in the volume of the forceps minor (F-Mi) and body of the corpus callosum. The reduction in the volume of the F-Mi also correlated with an increase in repetitive and stereotypical behavior as measured by the Autism Diagnostic Interview. These findings suggest that the abnormalities in the integrity of key inter- and intra-hemispheric VIM tracts may underlie the atypical information processing observed in these individuals. (C) 2010 Elsevier Srl. All rights reserved. C1 [Thomas, Cibu; Humphreys, Kate; Behrmann, Marlene] Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. [Thomas, Cibu; Behrmann, Marlene] Carnegie Mellon Univ, Ctr Neural Basis Cognit, Pittsburgh, PA 15213 USA. [Jung, Kwan-Jin] Univ Pittsburgh, Brain Imaging Res Ctr, Pittsburgh, PA 15260 USA. [Minshew, Nancy] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15260 USA. [Minshew, Nancy] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15260 USA. RP Thomas, C (reprint author), Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. EM thomascp@mail.nih.gov FU NICHD/NIDCD [PO1/U19]; National Alliance of Autism Research (Autism Speaks); Cure Autism Now foundation FX This research was funded by a grant from the NICHD/NIDCD PO1/U19 to Marlene Behrmann (PI: Nancy Minshew), which is part of the NICHD/NIDCD Collaborative Programs for Excellence in Autism and by awards from the National Alliance of Autism Research (Autism Speaks) to CT and KH and from the Cure Autism Now foundation to KH. We thank Scott Kurdilla and Debbie Viszlay of the Brain Imaging Research Center for their help in the acquisition of the imaging data. 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Dapretto, Mirella TI An fMRI investigation of responses to peer rejection in adolescents with autism spectrum disorders SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE LA English DT Article DE Autism spectrum disorders; Peer rejection; Social exclusion; Adolescence; Functional magnetic resonance imaging AB Peer rejection is particularly pervasive among adolescents with autism spectrum disorders (ASD). However, how adolescents with ASD differ from typically developing adolescents in their responses to peer rejection is poorly understood. The goal of the current investigation was to examine neural responses to peer exclusion among adolescents with ASD compared to typically developing adolescents. Nineteen adolescents with ASD and 17 typically developing controls underwent fMRI as they were ostensibly excluded by peers during an online game called Cyberball. Afterwards, participants reported their distress about the exclusion. Compared to typically developing adolescents, those with ASD displayed less activity in regions previously linked with the distressing aspect of peer exclusion, including the subgenual anterior cingulate and anterior insula, as well as less activity in regions previously linked with the regulation of distress responses during peer exclusion, including the ventrolateral prefrontal cortex and ventral striatum. Interestingly, however, both groups self-reported equivalent levels of distress. This suggests that adolescents with ASD may engage in differential processing of social experiences at the neural level, but be equally aware of, and concerned about, peer rejection. Overall, these findings contribute new insights about how this population may differentially experience negative social events in their daily lives. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Masten, Carrie L.] Univ Calif Davis, Ctr Mind & Brain, Davis, CA 95616 USA. [Colich, Natalie L.; Rudie, Jeffrey D.; Dapretto, Mirella] Univ Calif Los Angeles, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA USA. [Rudie, Jeffrey D.; Bookheimer, Susan Y.; Dapretto, Mirella] Univ Calif Los Angeles, Interdept Neurosci Program, Los Angeles, CA USA. [Rudie, Jeffrey D.] Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA. [Bookheimer, Susan Y.; Dapretto, Mirella] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. [Eisenberger, Naomi I.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. [Dapretto, Mirella] Univ Calif Los Angeles, FPR UCLA Ctr Culture Brain & Dev, Los Angeles, CA USA. RP Masten, CL (reprint author), Univ Calif Davis, Ctr Mind & Brain, 267 Cousteau Pl, Davis, CA 95616 USA. EM clmasten@ucdavis.edu FU National Institute of Child Health and Human Development [P50 HD055784]; Ruth L. Kirschstein National Research Service Award; National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) [RR12169, RR13642, RR00865] FX The authors wish to thank Deanna Greene. This work was supported by the National Institute of Child Health and Human Development [P50 HD055784], and a Ruth L. Kirschstein National Research Service Award (awarded to C.L. Masten). For generous support the authors also wish to thank the Brain Mapping Medical Research Organization, Brain Mapping Support Foundation, Pierson-Lovelace Foundation, Ahmanson Foundation, Tamkin Foundation, Jennifer Jones-Simon Foundation, Capital Group Companies Charitable Foundation, Robson Family, William M. and Linda R. Dietel Philanthropic Fund at the Northern Piedmont Community Foundation, and Northstar Fund. 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PD JUL PY 2011 VL 1 IS 3 BP 260 EP 270 DI 10.1016/j.dcn.2011.01.004 PG 11 WC Neurosciences SC Neurosciences & Neurology GA V28AK UT WOS:000208653500006 PM 22318914 ER PT J AU McPartland, JC Crowley, MJ Perszyk, DR Naples, AJ Mukerji, CE Wu, J Molfese, P Bolling, DZ Pelphrey, KA Mayes, LC AF McPartland, James C. Crowley, Michael J. Perszyk, Danielle R. Naples, Adam J. Mukerji, Cora E. Wu, Jia Molfese, Peter Bolling, Danielle Z. Pelphrey, Kevin A. Mayes, Linda C. TI Temporal dynamics reveal atypical brain response to social exclusion in autism SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE LA English DT Article DE ERP; EEG; Autism spectrum disorder; Social exclusion; Social neuroscience AB Despite significant social difficulties, children with autism spectrum disorder (ASD) are vulnerable to the effects of social exclusion. We recorded EEG while children with ASD and typical peers played a computerized game involving peer rejection. Children with ASD reported ostracism-related distress comparable to typically developing children. Event-related potentials (ERPs) indicated a distinct pattern of temporal processing of rejection events in children with ASD. While typically developing children showed enhanced response to rejection at a late slow wave indexing emotional arousal and regulation, those with autism showed attenuation at an early component, suggesting reduced engagement of attentional resources in the aversive social context. Results emphasize the importance of studying the time course of social information processing in ASD; they suggest distinct mechanisms subserving similar overt behavior and yield insights relevant to development and implementation of targeted treatment approaches and objective measures of response to treatment. (C) 2011 Elsevier Ltd. All rights reserved. C1 [McPartland, James C.; Crowley, Michael J.; Perszyk, Danielle R.; Naples, Adam J.; Mukerji, Cora E.; Wu, Jia; Molfese, Peter; Bolling, Danielle Z.; Pelphrey, Kevin A.; Mayes, Linda C.] Yale Child Study Ctr, New Haven, CT 06520 USA. RP McPartland, JC (reprint author), Yale Child Study Ctr, 230 South Frontage Rd, New Haven, CT 06520 USA. EM james.mcpartland@yale.edu FU NIMH [K23MH086785, MH071284]; NARSAD Young Investigator Awards; NIH [NIH 2T32MH018268-26]; Bial Foundation; NIDA [K05DA020091]; CTSA from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) [UL1 RR024139]; NIH roadmap for Medical Research (USA) FX This work was supported by NIMH K23MH086785 (JM), NARSAD Young Investigator Awards (JM, MC), the NIH 2T32MH018268-26 (AN) Bial Foundation (MC), NIMH MH071284 (KP), NIDA K05DA020091 (LCM), and CTSA Grant number UL1 RR024139 (JM, LCM) from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH), and NIH roadmap for Medical Research (USA). Its contents are solely the responsibility of the authors and do not necessarily represent the official view of NCRR or NIH. 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Cogn. Neurosci. PD JUL PY 2011 VL 1 IS 3 BP 271 EP 279 DI 10.1016/j.dcn.2011.02.003 PG 9 WC Neurosciences SC Neurosciences & Neurology GA V28AK UT WOS:000208653500007 PM 21731598 ER PT J AU Bolling, DZ Pitskel, NB Deen, B Crowley, MJ McPartland, JC Kaiser, MD Vander Wyk, BC Wu, J Mayes, LC Pelphrey, KA AF Bolling, Danielle Z. Pitskel, Naomi B. Deen, Ben Crowley, Michael J. McPartland, James C. Kaiser, Martha D. Vander Wyk, Brent C. Wu, Jia Mayes, Linda C. Pelphrey, Kevin A. TI Enhanced neural responses to rule violation in children with autism: A comparison to social exclusion SO DEVELOPMENTAL COGNITIVE NEUROSCIENCE LA English DT Article DE Social exclusion; Rule violation; Autism Spectrum Disorder; Right insula; Functional magnetic resonance imaging AB The present study aimed to explore the neural correlates of two characteristic deficits in Autism Spectrum Disorders (ASDs): social impairment and restricted, repetitive behavior patterns. To this end, we used comparable experiences of social exclusion and rule violation to probe potentially atypical neural networks in ASD. In children and adolescents with and without ASD, we used the interactive ball-toss game (Cyberball) to elicit social exclusion and a comparable game (Cybershape) to elicit a non-exclusive rule violation. Using functional magnetic resonance imaging (fMRI), we identified group differences in brain responses to social exclusion and rule violation. Though both groups reported equal distress following exclusion, the right insula and ventral anterior cingulate cortex were hypoactive during exclusion in children with ASD. In rule violation, right insula and dorsal prefrontal cortex were hyperactive in ASD. Right insula showed a dissociation in activation; it was hypoactive to social exclusion and hyperactive to rule violation in the ASD group. Further probed, different regions of right insula were modulated in each game, highlighting differences in regional specificity for which subsequent analyses revealed differences in patterns of functional connectivity. These results demonstrate neurobiological differences in processing social exclusion and rule violation in children with ASD. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Bolling, Danielle Z.; Pitskel, Naomi B.; Deen, Ben; Crowley, Michael J.; McPartland, James C.; Kaiser, Martha D.; Vander Wyk, Brent C.; Wu, Jia; Mayes, Linda C.; Pelphrey, Kevin A.] Yale Univ, Yale Child Study Ctr, New Haven, CT 06520 USA. [Pitskel, Naomi B.] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15261 USA. [Deen, Ben] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. RP Pelphrey, KA (reprint author), Yale Univ, Yale Child Study Ctr, 230 South Frontage Rd, New Haven, CT 06520 USA. EM kevin.pelphrey@yale.edu FU National Institute of Mental Health; John Merck Scholars Fund; Bial Foundation; Simons Foundation; National Institutes of Health (NIMH) [MH071284]; Doris Duke Charitable Foundation; [NIDA K05 DA020091]; [NIMH K23 MH086785] FX The research presented herein was supported by grants from the National Institute of Mental Health, the John Merck Scholars Fund, the Bial Foundation (M.J.C.), and the Simons Foundation. Kevin Pelphrey was supported by a Career Development Award from the National Institutes of Health (NIMH Grant MH071284). Linda Mayes was also supported by a Career Development Award (NIDA K05 DA020091). Naomi Pitskel was supported by a grant from the Doris Duke Charitable Foundation to Yale University. James McPartland was supported by a Career Development Award (NIMH K23 MH086785). 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A Propensity Score Analysis SO FAMILY RELATIONS LA English DT Article DE disability-related studies; families with children who have disabilities; families with disabled members; siblings; sibling relationships ID DOWN-SYNDROME; BEHAVIORAL-ADJUSTMENT; CHILDREN; AUTISM; FAMILY; PERSPECTIVES; INDIVIDUALS; COMPETENCE; STRATEGIES; DISORDERS AB This study examined whether siblings of children with disabilities have increased mental health problems, behavioral difficulties, or greater mental health service use as compared to siblings of children without disabilities. Data come from the 2006 National Health Interview Survey. Propensity score matching was used to complete the analysis. Twelve siblings and family demographic characteristics were used to create the propensity score. Hierarchical greedy matching without replacement was used to match siblings. Prior to the match, significant differences were present between sibling groups on all outcome variables. After the match, no significant differences remained. Effect sizes were compared and were smaller postmatch for all the three measured outcomes. Findings suggest that differences in siblings' mental health are not likely due to the presence of a brother or sister with a disability, but it is more likely that the co-occurring risk factors (e.g., living in a lower income household) contribute to the observed sibling differences. C1 [Neely-Barnes, Susan L.] Univ Memphis, Div Social Work, Memphis, TN 38152 USA. [Graff, J. Carolyn] Univ Tennessee, Hlth Sci Ctr, Coll Nursing, Memphis, TN 38163 USA. RP Neely-Barnes, SL (reprint author), Univ Memphis, Div Social Work, Memphis, TN 38152 USA. EM snlybrns@memphis.edu CR Barr J, 2010, INT J SPEECH-LANG PA, V12, P162, DOI 10.3109/17549500903434133 Barth RP, 2008, RES SOCIAL WORK PRAC, V18, P212, DOI 10.1177/1049731507307791 Bellin MH, 2009, J FAM PSYCHOL, V23, P39, DOI 10.1037/a0014381 Blackford JU, 2009, INTELLECT DEV DISAB, V47, P348, DOI 10.1352/1934-9556-47.5.348 Brehaut JC, 2009, AM J PUBLIC HEALTH, V99, P1254, DOI 10.2105/AJPH.2007.129817 Cox A., 2003, J FAMILY NURSING, V9, P397, DOI 10.1177/1074840703258328 Cuskelly M, 2006, J INTELL DISABIL RES, V50, P917, DOI 10.1111/j.1365-2788.2006.00922.x Dauz Williams P., 2010, ISSUES COMPREHENSIVE, V33, P39, DOI 10.3109/01460860903486515 Dew A, 2008, J DEV PHYS DISABIL, V20, P485, DOI 10.1007/s10882-008-9109-5 Dowling M, 2001, DISABIL SOC, V16, P21, DOI 10.1080/713662027 Dunn J, 1999, J CHILD PSYCHOL PSYC, V40, P1025, DOI 10.1017/S0021963099004369 Fisman S, 2000, CAN J PSYCHIAT, V45, P369 Fujiura GT, 2000, EXCEPT CHILDREN, V66, P187 FUJIURA GT, 1998, J DISABILITY POLICY, V0009 Giallo R, 2006, J INTELL DISABIL RES, V50, P937, DOI 10.1111/j.1365-2788.2006.00928.x Goodman R, 1997, J CHILD PSYCHOL PSYC, V38, P581, DOI 10.1111/j.1469-7610.1997.tb01545.x Graff JC, 2008, INT REV RES MENT RET, V36, P233, DOI 10.1016/S0074-7750(08)00007-4 Grissom MO, 2002, AM J MENT RETARD, V107, P79 Guo S., 2010, PROPENSITY SCORE ANA Hannah ME, 1999, AM J MENT RETARD, V104, P22, DOI 10.1352/0895-8017(1999)104<0022:CAAOSO>2.0.CO;2 Hastings RP, 2007, J AUTISM DEV DISORD, V37, P1485, DOI 10.1007/s10803-006-0230-y Hastings RP, 2003, J AUTISM DEV DISORD, V33, P141, DOI 10.1023/A:1022983209004 Hodapp RM, 2005, MENT RETARD, V43, P334 Hodapp RM, 2007, J INTELL DISABIL RES, V51, P1018, DOI 10.1111/j.1365-2788.2007.00994.x Hummer RA, 1999, SOC SCI QUART, V80, P136 *INT CONS POL SOC, 2006, NATL HLTH INT SURV 2 Kaminsky L, 2002, J CHILD PSYCHOL PSYC, V43, P225, DOI 10.1111/1469-7610.00015 LECROY CW, 2007, SOCIAL WORK RES, V313, P243 Luellen JK, 2005, EVALUATION REV, V29, P530, DOI 10.1177/0193841X05275596 McMahon MA, 2001, J HEAD TRAUMA REHAB, V16, P587 Meyers MK, 1998, SOC SERV REV, V72, P209, DOI 10.1086/515751 Mulroy S, 2008, J INTELL DISABIL RES, V52, P216, DOI 10.1111/j.1365-2788.2007.01005.x Myers S. 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Relat. PD JUL PY 2011 VL 60 IS 3 BP 331 EP 341 DI 10.1111/j.1741-3729.2011.00652.x PG 11 WC Family Studies; Social Work SC Family Studies; Social Work GA 784XJ UT WOS:000292191600007 ER PT J AU Scherer, SW Dawson, G AF Scherer, Stephen W. Dawson, Geraldine TI Risk factors for autism: translating genomic discoveries into diagnostics SO HUMAN GENETICS LA English DT Review ID COPY NUMBER VARIATION; SCAFFOLDING PROTEIN SHANK3; DE-NOVO MUTATIONS; SPECTRUM DISORDERS; PSYCHIATRIC-DISORDERS; STRUCTURAL VARIATION; MENTAL-RETARDATION; CHROMOSOMAL REARRANGEMENTS; RECURRENT REARRANGEMENTS; INTELLECTUAL DISABILITY AB Autism spectrum disorders (ASDs) are a group of conditions characterized by impairments in communication and reciprocal social interaction, and the presence of restricted and repetitive behaviors. The spectrum of autistic features is variable, with severity of symptoms ranging from mild to severe, sometimes with poor clinical outcomes. Twin and family studies indicate a strong genetic basis for ASD susceptibility. Recent progress in defining rare highly penetrant mutations and copy number variations as ASD risk factors has prompted early uptake of these research findings into clinical diagnostics, with microarrays becoming a 'standard of care' test for any ASD diagnostic work-up. The ever-changing landscape of the generation of genomic data coupled with the vast heterogeneity in cause and expression of ASDs (further influenced by issues of penetrance, variable expressivity, multigenic inheritance and ascertainment) creates complexity that demands careful consideration of how to apply this knowledge. Here, we discuss the scientific, ethical, policy and communication aspects of translating the new discoveries into clinical and diagnostic tools for promoting the well-being of individuals and families with ASDs. C1 [Scherer, Stephen W.] Hosp Sick Children, McLaughlin Ctr, Toronto, ON M5G 1L7, Canada. [Scherer, Stephen W.] Hosp Sick Children, Ctr Appl Genom, Toronto, ON M5G 1L7, Canada. [Scherer, Stephen W.] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 1A1, Canada. [Dawson, Geraldine] Univ N Carolina, Autism Speaks & Dept Psychiat, Chapel Hill, NC 27599 USA. RP Scherer, SW (reprint author), Hosp Sick Children, McLaughlin Ctr, Toronto, ON M5G 1L7, Canada. EM stephen.scherer@sickkids.ca; gdawson@autismspeaks.org RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 FU Autism Speaks; Autism Speaks Canada; Canadian Institutes of Health Research (CIHR); Institute of Genetics; Institute of Neurosciences; Mental Health and Addiction, Genome Canada; Hospital for Sick Children; Medical Research Council (UK); National Institute of Child Health and Human Development, NeuroDevNet; Ontario Genomics Institute; Ontario Ministry of Research and Innovation; Robarts Institute (Dr. Robert Hegele-Genome Canada) FX We thank Janet A. Buchanan for her contributions to all aspects of this manuscript as well as Anath C. Lionel for his technical assistance. Much of the content of this review was drawn from conversations at a meeting called 'Genetic Risk Factors for Autism: Translating Discoveries into Diagnostics' held 1-2 September 2010 in Toronto. We wish to thank Andy Shih for initiating and helping to shape the Toronto meeting. The sponsor organizations were Autism Speaks, Autism Speaks Canada, the Canadian Institutes of Health Research (CIHR), Institute of Genetics and Institute of Neurosciences, Mental Health and Addiction, Genome Canada, the Hospital for Sick Children, the Medical Research Council (UK), the National Institute of Child Health and Human Development, NeuroDevNet, the Ontario Genomics Institute, the Ontario Ministry of Research and Innovation, the Robarts Institute (Dr. Robert Hegele-Genome Canada grant), The Centre for Applied Genomics and the University of Toronto McLaughlin Centre. S. W. S. holds the GlaxoSmithKline-CIHR Endowed Chair in Genetics and Genomics at the Hospital for Sick Children and University of Toronto. 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Genet. PD JUL PY 2011 VL 130 IS 1 SI SI BP 123 EP 148 DI 10.1007/s00439-011-1037-2 PG 26 WC Genetics & Heredity SC Genetics & Heredity GA 786MR UT WOS:000292313000013 PM 21701786 ER PT J AU Kushner, D AF Kushner, David TI the autism defense SO IEEE SPECTRUM LA English DT Article NR 0 TC 0 Z9 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA SN 0018-9235 J9 IEEE SPECTRUM JI IEEE Spectr. PD JUL PY 2011 VL 48 IS 7 BP 32 EP 37 PG 6 WC Engineering, Electrical & Electronic SC Engineering GA 783SO UT WOS:000292104500011 ER PT J AU Silva, K Correia, R Lima, M Magalhaes, A de Sousa, L AF Silva, Karine Correia, Rita Lima, Mariely Magalhaes, Ana de Sousa, Liliana TI Can Dogs Prime Autistic Children for Therapy? Evidence from a Single Case Study SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE LA English DT Article AB Background and objectives: Canine-assisted therapy has been receiving growing attention as a means of aiding children with autism spectrum disorder (ASD). Yet, only limited studies have been done and a great deal of literature related to this intervention is anecdotal. The present study aims at providing additional quantitative evidence on the potential of dogs to positively modulate the behavior of children with ASD. Settings/location, subjects, and interventions: A 12-year-old boy diagnosed with ASD was exposed, at his usual treatment location (the Portuguese Association for Developmental Disorders and Autism at Vila Nova de Gaia, Portugal), to the following treatment conditions: (1) one-to-one structured activities with a therapist assisted by a certified therapy dog, and (2) one-to-one structured activities with the same therapist alone (as a control). To accurately assess differences in the behavior of the participant between these treatment conditions, the therapist followed a strict research protocol. The behavior of the participant was continuously video-recorded during both treatment conditions for further analysis and comparison. Treatment outcomes: In the presence of the dog, the participant exhibited more frequent and longer durations of positive behaviors (such as smiling and positive physical contacting) as well as less frequent and shorter durations of negative behaviors (such as aggressive manifestations). Conclusions: These findings are in accordance with previous experimental work and provide additional support for the assertion that dogs can prime autistic children for therapy. Ultimately, this study may contribute toward a change for full acceptance of canine-assisted therapy programs within the medical milieu. Additional studies using a similar research protocol on more autistic children will certainly help professionals to work on the most effective methods to individually serve this population through canine-assisted interventions. C1 [Silva, Karine; Lima, Mariely; de Sousa, Liliana] Inst Ciencias Biomed Abel Salazar, Dept Ciencias Comportamento, P-4400003 Oporto, Portugal. [Silva, Karine; Lima, Mariely; de Sousa, Liliana] Animas, Oporto, Portugal. [Correia, Rita] Inst Super Psicol Aplicada, Dept Psicol Clin, Lisbon, Portugal. [Magalhaes, Ana] Inst Biol Mol & Celular, Oporto, Portugal. RP Silva, K (reprint author), Inst Ciencias Biomed Abel Salazar, Dept Ciencias Comportamento, Largo Prof Abel Salazar 2, P-4400003 Oporto, Portugal. EM karine_silva_24@hotmail.com RI de Sousa, Liliana/K-9756-2014 OI de Sousa, Liliana/0000-0001-6656-4595 FU Fundacao para a Ciencia e a Tecnologia [FCT-SFRH/BD/44748/2008, FCT-SFRH/BPD/37017/2007, FCT-SFRH/BPD/19200/2004] FX The authors are grateful to Dr. Helena Vidal for videotaping and to the Portuguese Association for Developmental Disorders and Autism for the permission to conduct the study. Also, the authors are grateful to the members of Animas, especially Sebastiao Castro Lemos and Scooby. Fundacao para a Ciencia e a Tecnologia funded the participation of Mariely Lima (FCT-SFRH/BD/44748/2008), Karine Silva (FCT-SFRH/BPD/37017/2007), and Ana Magalhaes (FCT-SFRH/BPD/19200/2004). CR Beck A. M., 1996, PETS PEOPLE IMPORTAN Braun Carie, 2009, Complement Ther Clin Pract, V15, P105, DOI 10.1016/j.ctcp.2009.02.008 Edgington ES, 1996, BEHAV RES THER, V34, P567, DOI 10.1016/0005-7967(96)00012-5 Fine A. 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PD JUL PY 2011 VL 17 IS 7 BP 655 EP 659 DI 10.1089/acm.2010.0436 PG 5 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 784UL UT WOS:000292183600013 PM 21689015 ER PT J AU Chien, IC Lin, CH Chou, YJ Chou, P AF Chien, I-Chia Lin, Ching-Heng Chou, Yiing-Jenq Chou, Pesus TI Prevalence and Incidence of Autism Spectrum Disorders Among National Health Insurance Enrollees in Taiwan from 1996 to 2005 SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE prevalence; incidence; autism; National Health Insurance; Taiwan ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; CHILDREN; SCHEDULE; IMPACT AB The authors used a national database to examine the prevalence and incidence of autism spectrum disorders. The National Health Research Institute provided a database of 1 000 000 random participants for study. A population-based sample of 372 642 aged younger than 18 was obtained as a dynamic cohort. Those study participants who had at least one service claim from 1996 to 2005 with a principal diagnosis of autism spectrum disorders were identified. The cumulative prevalence of autism spectrum disorders increased from 1.79 to 28.72 per 10 000 from 1996 to 2005. The annual incidence of autism spectrum disorders increased from 0.91 to 4.41 per 10 000 per year from 1997 to 2005. Higher incidence was detected in the 0 to 5 age group, in males, and in those who lived in northern, southern, and eastern regions and urban areas. Our findings suggest increases in the prevalence and incidence of treated autism spectrum disorders in Taiwan. C1 [Chien, I-Chia; Chou, Yiing-Jenq; Chou, Pesus] Natl Yang Ming Univ, Community Med Res Ctr, Dept Publ Hlth, Taipei 112, Taiwan. [Chien, I-Chia; Chou, Yiing-Jenq; Chou, Pesus] Natl Yang Ming Univ, Inst Publ Hlth, Taipei 112, Taiwan. [Chien, I-Chia] Taoyuan Mental Hosp, Dept Hlth, Tao Yuan, Taiwan. [Lin, Ching-Heng] Taichung Vet Gen Hosp, Taichung, Taiwan. RP Chou, P (reprint author), Natl Yang Ming Univ, Community Med Res Ctr, Dept Publ Hlth, Taipei 112, Taiwan. 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Child Neurol. PD JUL PY 2011 VL 26 IS 7 BP 830 EP 834 DI 10.1177/0883073810393964 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 785DK UT WOS:000292207400005 PM 21460178 ER PT J AU Antshel, KM Polacek, C McMahon, M Dygert, K Spenceley, L Dygert, L Miller, L Faisal, F AF Antshel, Kevin M. Polacek, Carol McMahon, Michele Dygert, Karen Spenceley, Laura Dygert, Lindsay Miller, Laura Faisal, Fatima TI Comorbid ADHD and Anxiety Affect Social Skills Group Intervention Treatment Efficacy in Children With Autism Spectrum Disorders SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism spectrum; social skills; ADHD ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDER; ASPERGER-SYNDROME; CONTROLLED-TRIAL; FOLLOW-UP; ADOLESCENTS; ATTENTION; SCHEDULE; SYMPTOMS; OUTCOMES AB Objective: To assess the influence of psychiatric comorbidity on social skill treatment outcomes for children with autism spectrum disorders (ASDs). Methods: A community sample of 83 children (74 males, 9 females) with an ASD (mean age = 9.5 yr; SD = 1.2) and common comorbid disorders participated in 10-week social skills training groups. The first 5 weeks of the group focused on conversation skills and the second 5 weeks focused on social problem solving skills. A concurrent parent group was also included in the treatment. Social skills were assessed using the Social Skills Rating System. Ratings were completed by parents at pre- and posttreatment time periods. Results: Children with ASD and children with an ASD and comorbid anxiety disorder improved in their parent reported social skills. Children with ASD and comorbid attention deficit/hyperactivity disorder failed to improve. Conclusion: Psychiatric comorbidity affects social skill treatment gains in the ASD population. 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Dev. Behav. Pediatr. PD JUL-AUG PY 2011 VL 32 IS 6 BP 439 EP 446 DI 10.1097/DBP.0b013e318222355d PG 8 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 784CN UT WOS:000292131500001 PM 21654508 ER PT J AU Nelson, ED Bal, M Kavalali, ET Monteggia, LM AF Nelson, Erika D. Bal, Manjot Kavalali, Ege T. Monteggia, Lisa M. TI Selective impact of MeCP2 and associated histone deacetylases on the dynamics of evoked excitatory neurotransmission SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article DE Rett syndrome; transcriptional repression; synaptic neurotransmission; knockout; methyl-CpG-binding protein 2 ID CPG-BINDING PROTEIN-2; SYNAPTIC CIRCUIT ABNORMALITIES; 2/3 PYRAMIDAL NEURONS; RETT-SYNDROME; MOUSE MODEL; DOWN-SYNDROME; TRANSCRIPTIONAL REPRESSION; NETWORK HYPEREXCITABILITY; HIPPOCAMPAL SYNAPSES; GLUTAMATE RELEASE AB Nelson ED, Bal M, Kavalali ET, Monteggia LM. Selective impact of MeCP2 and associated histone deacetylases on the dynamics of evoked excitatory neurotransmission. J Neurophysiol 106: 193-201, 2011. First published April 20, 2011; doi:10.1152/jn.00751.2010.-An imbalance between the strengths of excitatory and inhibitory synaptic inputs has been proposed as the cellular basis of autism and related neurodevelopmental disorders. Previous studies examining spontaneous levels of excitatory and inhibitory neurotransmission in the forebrain regions of methyl-CpG-binding protein 2 (Mecp2) mutant mice, models of the autism spectrum disorder Rett syndrome, have identified a decrease in excitatory drive, in some cases coupled with an increase in inhibitory synaptic strength, as a major source of this imbalance. Here, we reevaluated this question by examining the short-term dynamics of evoked neurotransmission between hippocampal neurons cultured from MeCP2 knockout mice and found a marked increase in evoked excitatory neurotransmission that is consistent with an increase in presynaptic release probability. This increase in evoked excitatory drive was not matched with alterations in evoked inhibitory neurotransmission. Moreover, we observed similar excitatory drive specific changes after the loss of key histone deacetylases (histone deacetylase 1 and 2) that form a complex with MeCP2 and mediate transcriptional regulation. These findings suggest a distinct role for MeCP2 and its cofactors in the regulation of evoked excitatory neurotransmission compared with their essential role in basal synaptic activity. C1 [Nelson, Erika D.; Monteggia, Lisa M.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA. [Bal, Manjot; Kavalali, Ege T.] Univ Texas SW Med Ctr Dallas, Dept Neurosci, Dallas, TX 75390 USA. RP Monteggia, LM (reprint author), Univ Texas SW Med Ctr Dallas, Dept Psychiat, 5323 Harry Hines Blvd, Dallas, TX 75390 USA. EM lisa.monteggia@utsouthwestern.edu FU National Institute for Mental Health [MH-081060, MH-066198]; University of Texas Southwestern Medical Center FX This work was supported by National Institute for Mental Health Grants MH-081060 (to L. M. Monteggia) and MH-066198 (to E. T. Kavalali) as well as the Division of Basic Sciences Training Program of University of Texas Southwestern Medical Center (to E. D. Nelson). E. T. Kavalali is an Established Investigator of the American Heart Association. 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Neurophysiol. PD JUL PY 2011 VL 106 IS 1 BP 193 EP 201 DI 10.1152/jn.00751.2010 PG 9 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA 786PC UT WOS:000292319400020 PM 21511710 ER PT J AU Kim, HS Lee, JJ Cho, AR Kim, DH Choi, CW AF Kim, Hyun Soo Lee, Jae Jin Cho, Ah Rang Kim, Dae Hyun Choi, Cheon Woong TI Squamous Cell Carcinoma of the Lung in an Autistic Child Who has Never Smoked SO JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article DE squamous cell carcinoma of lung; child; smoking; autism; carboplatin; gemcitabine ID CANCER NSCLC; CHEMOTHERAPY; CISPLATIN; EPIDEMIOLOGY; SURVEILLANCE; CARBOPLATIN; TRIAL; GENE; IV AB Primary bronchogenic carcinoma of the lung is extremely rare in childhood, particularly the squamous cell type. Only 13 cases have been reported in the literature. We report a case of squamous cell carcinoma in an autistic, 16-year-old boy who presented with a productive cough. Interestingly, he was a never-smoker, but had been exposed to environmental tobacco smoking by his father for 13 years. The diagnosis was delayed by approximately 1 month due to his young age. He was diagnosed with squamous cell carcinoma of the lung by video-assisted thoracoscopic surgery, and chemotherapy was arranged. Considering his age, autism, and good performance status, a combined chemotherapeutic regimen with gemcitabine plus carboplatin was planned. After the second cycle of chemotherapy, the cough resolved and a computed tomography scan showed a partial response of the central conglomerated mass with the absence of the malignant pleural effusion. C1 [Choi, Cheon Woong] Kyung Hee Univ, E W Neo Med Ctr, Dept Resp & Crit Care Med, Seoul, South Korea. [Kim, Hyun Soo; Lee, Jae Jin] Kyung Hee Univ, E W Neo Med Ctr, Dept Med Oncol & Hematol, Seoul, South Korea. [Cho, Ah Rang] Kyung Hee Univ, E W Neo Med Ctr, Dept Psychiat, Seoul, South Korea. 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Pediatr. Hematol. Oncol. PD JUL PY 2011 VL 33 IS 5 BP E216 EP E219 DI 10.1097/MPH.0b013e318211836a PG 4 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA 781IS UT WOS:000291924700012 PM 21617565 ER PT J AU Liu, XQ Georgiades, S Duku, E Thompson, A Devlin, B Cook, EH Wijsman, EM Paterson, AD Szatmari, P AF Liu, Xiao-Qing Georgiades, Stelios Duku, Eric Thompson, Ann Devlin, Bernie Cook, Edwin H. Wijsman, Ellen M. Paterson, Andrew D. Szatmari, Peter TI Identification of Genetic Loci Underlying the Phenotypic Constructs of Autism Spectrum Disorders SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; ADI-R; factor analysis; linkage analysis; quantitative trait ID QUANTITATIVE TRAIT LOCUS; LINKAGE ANALYSIS; GENOME SCAN; REPETITIVE BEHAVIOR; BIPOLAR DISORDER; SAVANT SKILLS; SCHIZOPHRENIA; ASSOCIATION; 15Q11-Q13; FAMILIES AB Objective: To investigate the underlying phenotypic constructs in autism spectrum disorders (ASD) and to identify genetic loci that are linked to these empirically derived factors. Method: Exploratory factor analysis was applied to two datasets with 28 selected Autism Diagnostic Interview-Revised (ADI-R) algorithm items. The first dataset was from the Autism Genome Project (AGP) phase I (1,236 ASD subjects from 618 families); the second was from the AGP phase II (804 unrelated ASD subjects). Variables derived from the factor analysis were then used as quantitative traits in genome-wide variance components linkage analyses. Results: Six factors, namely, joint attention, social interaction and communication, nonverbal communication, repetitive sensory-motor behavior, peer interaction, and compulsion/restricted interests, were retained for both datasets. There was good agreement between the factor loading patterns from the two datasets. All factors showed familial aggregation. Suggestive evidence for linkage was obtained for the joint attention factor on 11q23. Genome-wide significant evidence for linkage was obtained for the repetitive sensory-motor behavior factor on 19q13.3. Conclusions: This study demonstrates that the underlying phenotypic constructs based on the ADT-R algorithm items are replicable in independent datasets, and that the empirically derived factors are suitable and informative in genetic studies of ASD. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(7): 687-696. C1 [Georgiades, Stelios; Duku, Eric; Thompson, Ann; Szatmari, Peter] McMaster Univ, Offord Ctr Child Studies, Hamilton, ON L8S 4K1, Canada. [Liu, Xiao-Qing] Univ Manitoba, Winnipeg, MB R3T 2N2, Canada. [Devlin, Bernie] Univ Pittsburgh, Sch Med, Pittsburgh, PA 15260 USA. [Cook, Edwin H.] Univ Illinois, Inst Juvenile Res, Chicago, IL USA. [Wijsman, Ellen M.] Univ Washington, Seattle, WA 98195 USA. [Paterson, Andrew D.] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON, Canada. RP Szatmari, P (reprint author), McMaster Univ, Offord Ctr Child Studies, Patterson Bldg,Chedoke Site,1280 Main St W, Hamilton, ON L8S 4K1, Canada. EM szatmar@mcmaster.ca FU Autism Speaks (USA); Health Research Board (HRB; Ireland); Medical Research Council (MRC; UK); Genome Canada/Ontario Genomics Institute; Hilibrand Foundation (USA); US National Institutes of Health [HD055782, HD055751]; Canada Research Chair in Genetics of Complex Diseases; Canadian Institutes for Health Research (CIHR) FX The authors gratefully acknowledge the families participating in this study, the Autism Genome Project (AGP) Consortium, and the main funders of AGP: Autism Speaks (USA), the Health Research Board (HRB; Ireland), the Medical Research Council (MRC; UK), Genome Canada/Ontario Genomics Institute, and the Hilibrand Foundation (USA). Additional support for the authors was provided by the US National Institutes of Health (HD055782, HD055751), the Canada Research Chair in Genetics of Complex Diseases, and the Canadian Institutes for Health Research (CIHR). 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Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 2011 VL 50 IS 7 BP 687 EP 696 DI 10.1016/j.jaac.2011.05.002 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 786CC UT WOS:000292279100009 PM 21703496 ER PT J AU Motwani, J Marshall, D Nyatunga, P Emitt, S Denver, L Williams, M AF Motwani, J. Marshall, D. Nyatunga, P. Emitt, S. Denver, L. Williams, M. TI Challenges in treating children with severe bleeding disorders and severe autism: a single centre experience SO JOURNAL OF THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 [Motwani, J.; Marshall, D.; Nyatunga, P.; Emitt, S.; Denver, L.; Williams, M.] Birmingham Childrens Hosp, Haemophilia Comprehens Care Ctr, Birmingham, W Midlands, England. NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1538-7933 EI 1538-7836 J9 J THROMB HAEMOST JI J. Thromb. Haemost. PD JUL PY 2011 VL 9 SU 2 SI SI MA P-WE-564 BP 698 EP 698 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA V33AX UT WOS:000208992802461 ER PT J AU Srivastava, DP Woolfrey, KM Penzes, P AF Srivastava, Deepak P. Woolfrey, Kevin M. Penzes, Peter TI Analysis of Dendritic Spine Morphology in Cultured CNS Neurons SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS LA English DT Article DE Neuroscience; Issue 53; Excitatory synapse; neuroscience; brain; cortex; cortical neurons; primary culture; confocal microscopy; timelapse imaging; remodeling AB Dendritic spines are the sites of the majority of excitatory connections within the brain, and form the post-synaptic compartment of synapses. These structures are rich in actin and have been shown to be highly dynamic. In response to classical Hebbian plasticity as well as neuromodulatory signals, dendritic spines can change shape and number, which is thought to be critical for the refinement of neural circuits and the processing and storage of information within the brain. Within dendritic spines, a complex network of proteins link extracellular signals with the actin cyctoskeleton allowing for control of dendritic spine morphology and number. Neuropathological studies have demonstrated that a number of disease states, ranging from schizophrenia to autism spectrum disorders, display abnormal dendritic spine morphology or numbers. Moreover, recent genetic studies have identified mutations in numerous genes that encode synaptic proteins, leading to suggestions that these proteins may contribute to aberrant spine plasticity that, in part, underlie the pathophysiology of these disorders. In order to study the potential role of these proteins in controlling dendritic spine morphologies/ number, the use of cultured cortical neurons offers several advantages. Firstly, this system allows for high-resolution imaging of dendritic spines in fixed cells as well as time-lapse imaging of live cells. Secondly, this in vitro system allows for easy manipulation of protein function by expression of mutant proteins, knockdown by shRNA constructs, or pharmacological treatments. These techniques allow researchers to begin to dissect the role of disease-associated proteins and to predict how mutations of these proteins may function in vivo. C1 [Srivastava, Deepak P.; Woolfrey, Kevin M.; Penzes, Peter] Northwestern Univ, Feinberg Sch Med, Dept Physiol, Evanston, IL 60208 USA. [Penzes, Peter] Northwestern Univ, Feinberg Sch Med, Dept Psychiat & Behav Sci, Evanston, IL 60208 USA. RP Penzes, P (reprint author), Northwestern Univ, Feinberg Sch Med, Dept Physiol, Evanston, IL 60208 USA. EM p-penzes@northwestern.edu FU NIH [R01MH 071316]; Alzheimer's Association; National Alliance for Research on Schizophrenia and Depression (NARSAD); National Alliance for Autism Research (NAAR); American Heart Association Postdoctoral Fellowship; American Heart Association Predoctoral Fellowship FX We thank Kelly Jones for careful editing. This work was supported by NIH grant R01MH 071316, Alzheimer's Association, the National Alliance for Research on Schizophrenia and Depression (NARSAD), and the National Alliance for Autism Research (NAAR) (P.P.); American Heart Association Postdoctoral Fellowship (D.P.S.); American Heart Association Predoctoral Fellowship (K.M.W.). 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These "friend or foe" judgements are often based on first impressions, which in turn may affect our decisions to "approach or avoid". Previous studies investigating the neural correlates of social cognition tended to use static facial stimuli (2). Here, we illustrate an experimental design in which whole-body animated characters were used in conjunction with functional magnetic resonance imaging (fMRI) recordings. Fifteen participants were presented with short movie-clips of guest-host interactions in a business setting, while fMRI data were recorded; at the end of each movie, participants also provided ratings of the host behaviour. This design mimics more closely real-life situations, and hence may contribute to better understanding of the neural mechanisms of social interactions in healthy behaviour, and to gaining insight into possible causes of deficits in social behaviour in such clinical conditions as social anxiety and autism C1 [Sung, Keen] Univ Alberta, Dept Comp Sci, Edmonton, AB T6G 2M7, Canada. [Dolcos, Sanda; Dolcos, Florin] Univ Illinois, Dept Psychol, Chicago, IL 60680 USA. [Flor-Henry, Sophie; Zhou, Crystal] Univ Alberta, Ctr Neurosci, Edmonton, AB T6G 2M7, Canada. [Gasior, Claudia] Univ Alberta, Dept Psychol, Edmonton, AB T6G 2M7, Canada. [Argo, Jennifer] Univ Alberta, Dept Mkt Business Econ & Law, Edmonton, AB T6G 2M7, Canada. [Dolcos, Florin] Univ Illinois, Neurosci Program, Champaign, IL USA. [Dolcos, Florin] Univ Illinois, Beckman Inst, Champaign, IL USA. RP Dolcos, F (reprint author), Univ Illinois, Dept Psychol, Chicago, IL 60680 USA. EM fdolcos@illinois.edu FU start-up funds; Alberta Heritage Foundation for Medical Research; National Alliance for Research on Schizophrenia and Depression; Canadian Psychiatric Research Foundation FX This research was supported by start-up funds to FD. KS was supported by a summer studentship from the Alberta Heritage Foundation for Medical Research. FD was supported by a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression, and a CPRF Award from the Canadian Psychiatric Research Foundation. The authors wish to thank Peter Seres for assistance with data collection and Kristina Suen for assistance with data analysis. CR Adolphs R, 2009, ANNU REV PSYCHOL, V60, P693, DOI 10.1146/annurev.psych.60.110707.163514 Costa P. T., 1992, REVISED NEO PERSONAL Eddington KM, 2007, J COGNITIVE NEUROSCI, V19, P1152, DOI 10.1162/jocn.2007.19.7.1152 Eddington KM, 2009, SOC COGN AFFECT NEUR, V4, P238, DOI 10.1093/scan/nsp016 Friston K. 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PD JUL PY 2011 IS 53 AR e2379 DI 10.3791/2379 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA V36MC UT WOS:000209215000002 PM 21775952 ER PT J AU Nielsen, CMB AF Nielsen, Charlotte Marie Bisgaard TI Towards applied integrationism - integrating autism in teaching and coaching sessions SO LANGUAGE SCIENCES LA English DT Article DE Autism research; Applied integrationism; Methodology; Self-reflection; Contextualization AB At present, Denmark counts numerous cases of youngsters with Aspergers syndrome and the implementation of separate project classrooms for Asperger-students has proved beneficial (EVA-report January 2010). Today, Asperger-students at project schools have the opportunity to receive an education whereas before they often ended up as psychiatric cases. The few participating schools offer one class of approximately 10 persons each per year. Unfortunately, this covers only a small percentage of a growing need. Indeed, some students are struck with more severe Autism than Aspergers. In 1994, autistic psychopathy was put on the list of psychiatric diagnoses as "Aspergers syndrome" by the World Health Organization (WHO) (Asperger and Kanner, 1996). For traditional teachers, Asperger-students often seem difficult to teach because they perform differently in social settings. They are often perceived as problematic and marginalized by teachers and peers when integrated in conventional classes. As a high school teacher, language psychologist and mentor, I have been closely involved with Asperger-students at schools in my hometown outside of the classroom. The Danish government has recently granted four additional project classes nationwide and is considering an expansion of the project: http://www.uvm.dk/Aktuelt/similar to/media/C9D1SAE89C54449C9E3A325B76F2E987.ashx (last visited June 6th 2010). Suggestions will be needed for the long term and guidance will be necessary for teachers to deal professionally with Asperger-students. My main purpose here is to discuss the potential application of integrationism towards the design of an integrational case-study. This contribution suggests a way to analyze why teachers and Asperger-individuals experience communicational problems. Several related questions are important to consider: How does society improve the general integration of Asperger-students in educational institutions? What can teachers and coaches do to enhance the integration of Asperger-students in their daily practice according to an integrational approach? This study suggests that teachers and institutions must understand that Asperger-diagnosed students are agents in the world just as are ordinary students. They perform as anyone else in verbal and non-verbal ways. Contextualization is therefore a keyword to this investigation and its suggestions. Focusing on how to enhance integration working explicitly with self-observation in communication may be a tool for teachers to contribute to change the way people experience and face Asperger-students. (C) 2011 Elsevier Ltd. All rights reserved. C1 Hasseris Gymnasium & IB World Sch, DK-9100 Aalborg, Denmark. RP Nielsen, CMB (reprint author), Hasseris Gymnasium & IB World Sch, Hasserisvej 300,Postbox 70, DK-9100 Aalborg, Denmark. EM charimbn@yahoo.dk CR ASPERGER H, 1996, VIDENSCENTER AUTISME Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BJORNE P, 2007, POSSIBLE WORLD AUTIS Drew Paul, 1992, TALK WORK INTERACTIO Frith U., 2003, AUTISM EXPLAINING EN Grandin T., 2008, WAY SEE IT PERSONAL Grandin Temple, 2006, THINKING PICTURES MY, Vrev Grice H. 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SO PEDIATRICS LA English DT Article DE child development disorder; pervasive screening programs; early diagnosis; health care ID RANDOMIZED CONTROLLED-TRIAL; GROSS MOTOR FUNCTION; SPECTRUM DISORDERS; YOUNG-CHILDREN; CEREBRAL-PALSY; DEVELOPMENTAL DISORDERS; MODIFIED CHECKLIST; FOLLOW-UP; INTERVENTION; COMMUNICATION AB BACKGROUND. Autism is a serious neurodevelopmental disorder that has a reportedly rising prevalence rate. The American Academy of Pediatrics recommends that screening for autism be incorporated into routine practice. It is important to consider the pros and cons of conducting autism screening as part of routine practice and its implications on the community. We have explored this question in the context of screening from a scientific point of view. METHOD: A literature search was conducted to assess the effectiveness of community screening programs for autism. RESULTS: Judged against critical questions about autism, screening programs failed to fulfill most criteria. 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Lima-Ojeda, Juan M. Pfeiffer, Natascha Schneider, Miriam Gass, Peter TI Lack of long-term behavioral alterations after early postnatal treatment with tropisetron: Implications for developmental psychobiology SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE 5-HT(3) receptors; Schizophrenia; Autism; Anxiety; Depression ID GATED ION-CHANNEL; RADIAL-ARM MAZE; ACETYLCHOLINE-RELEASE; 5-HT3 RECEPTORS; CORTICAL DEVELOPMENT; BRAIN-DEVELOPMENT; 5HT3 RECEPTOR; ADULT MICE; SEROTONIN; ANXIETY AB The early postnatal period represents a critical time window for brain development. Transient Cajal-Retzius cells in layer I of the cortex play an important role in cortical lamination by modulating neuronal migration and maturation. Recent data have demonstrated that the 5-HT(3) receptor antagonist and alpha7 nicotinic receptor partial agonist tropisetron, acting via 5-HT(3) receptors expressed on Cajal-Retzius cells, can disturb the formation of cortical columns at perinatal stages. This process is thought to be involved in several neuropsychiatric disorders. Here we investigated the possible long-term behavioral effects of exposure to tropisetron at early postnatal stages in mice. We found that the administration of 1 mg/kg, intraperitoneal (i.p.) tropisetron from postnatal days 2-12 (P2-P12) did not induce significant cognitive, schizophrenia-like or emotional alterations in tropisetron-treated animals as compared to controls, when tested in multiple behavioral assays. These results may be of relevance regarding the possible protracted deleterious neuropsychiatric effects of tropisetron during early life. (C) 2011 Elsevier Inc. All rights reserved. C1 [Inta, Dragos; Vogt, Miriam A.; Lima-Ojeda, Juan M.; Pfeiffer, Natascha; Gass, Peter] Univ Heidelberg, Cent Inst Mental Hlth Mannheim, RG Anim Models Psychiat, Dept Psychiat & Psychotherapy, D-68159 Mannheim, Germany. 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Ther. PD JUL PY 2011 VL 91 IS 7 BP 1116 EP 1129 DI 10.2522/ptj.20100294 PG 14 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA 786FL UT WOS:000292288700015 PM 21546566 ER PT J AU Furman, DJ Chen, MC Gotlib, IH AF Furman, Daniella J. Chen, Michael C. Gotlib, Ian H. TI Variant in oxytocin receptor gene is associated with amygdala volume SO PSYCHONEUROENDOCRINOLOGY LA English DT Article DE Oxytocin receptor; Genetics; Amygdala; MRI; Risk factor; Depression; Autism ID OBSESSIVE-COMPULSIVE DISORDER; NEURAL CIRCUITRY; BINDING-SITES; HUMAN BRAIN; AUTISM; BEHAVIOR; ANXIETY; ADOLESCENTS; DEPRESSION; CHILDREN AB The oxytocin system plays a significant role in modulating stress responses in animals and humans; perturbations in this system may contribute to the pathogenesis of psychiatric disorder. Attempts to identify clinically relevant genetic variants in the oxytocin system have yielded associations between polymorphisms of the oxytocin receptor (OXTR) gene and both autism and major depression. To date, however, little is known about how such variants affect brain structures implicated in these disorders. Applying a manual tracing procedure to high-resolution structural magnetic resonance images, amygdala volumes were measured in 51 girls genotyped on OXTR rs2254298(G>A), a single nucleotide polymorphism associated with psychopathology. Results of this study indicate that despite having greater gray matter volume, participants homozygous for the G allele were characterized by smaller volumes of both left and right amygdala than were carriers of the A allele. A subsequent whole-brain voxel-based morphometry analysis revealed additional genotype-mediated volumetric group differences in the posterior brain stem and dorsomedial anterior cingulate cortex. These findings highlight one neurobiological pathway by which oxytocin gene variants may increase risk for psychopathology. Further research is needed to characterize the mechanism by which this polymorphism contributes to anatomical variability and to identify functional correlates of these alterations in regional brain volume. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Furman, Daniella J.; Chen, Michael C.; Gotlib, Ian H.] Stanford Univ, Dept Psychol, Stanford, CA 94305 USA. RP Furman, DJ (reprint author), Stanford Univ, Dept Psychol, Jordan Hall,Bldg 420,450 Serra Mall, Stanford, CA 94305 USA. EM dfurman@stanford.edu FU National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD); National Institute of Mental Health [MH74849] FX This research was supported by grants from the National Alliance for Research in Schizophrenia and Affective Disorders (NARSAD) and the National Institute of Mental Health (MH74849) to IHG; funding sources had no further role in the design of the study or in the collection, analysis or interpretation of data. 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Stigler, Kimberly A. Wink, Logan K. Mullett, Jennifer E. Kohn, Arlene Posey, David J. McDougle, Christopher J. TI A prospective open-label study of aripiprazole in fragile X syndrome SO PSYCHOPHARMACOLOGY LA English DT Article DE Fragile X syndrome; Irritability; Aripiprazole ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM DIAGNOSTIC INTERVIEW; PARTIAL AGONIST; BEHAVIOR; CHILDREN; RISPERIDONE; SCALE; IRRITABILITY; ADOLESCENTS AB Rationale Fragile X syndrome (FXS) is the most common inherited form of developmental disability and most common single gene cause of autism. Persons with FXS frequently exhibit irritable behavior marked by aggression, self-injury, and severe tantrums. Despite frequent clinical use of atypical antipsychotic drugs to target this behavioral cluster, no systematic trials to date have assessed the efficacy and safety of these drugs in persons with FXS. Methods We conducted a prospective open-label 12-week trial of aripiprazole in 12 persons aged 6-25 years (mean age, 14.3 years) with FXS who were free of concomitant psychoactive drugs. Results Aripiprazole use (mean dose, 9.8 mg/day) was associated with treatment response (defined by a Clinical Global Impressions-Improvement scale score of much improved or very much improved and a >= 25% improvement on the Aberrant Behavior Checklist-Irritability subscale) in 10 of 12 (87%) persons. Two individuals (13%) discontinued aripiprazole prior to study completion due to adverse events. One discontinuation was due to akathisia, mild drooling, and mild tiredness and the other due to moderate tiredness and moderate drooling. No significant changes in vital signs including weight or laboratory measures occurred during treatment with aripiprazole. Conclusions Aripiprazole was generally safe and well tolerated and was associated with significant improvement in irritable behavior. Given these findings, a double-blind, placebo-controlled study of aripiprazole in FXS is warranted. C1 [Erickson, Craig A.; Stigler, Kimberly A.; Wink, Logan K.; Mullett, Jennifer E.; Kohn, Arlene; Posey, David J.; McDougle, Christopher J.] Indiana Univ Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. [Erickson, Craig A.; Stigler, Kimberly A.; Wink, Logan K.; Mullett, Jennifer E.; Kohn, Arlene; Posey, David J.; McDougle, Christopher J.] Christian Sarkine Autism Treatment Ctr, Indianapolis, IN USA. [Erickson, Craig A.; Stigler, Kimberly A.; Wink, Logan K.; Mullett, Jennifer E.; Kohn, Arlene; Posey, David J.; McDougle, Christopher J.] Fragile X Res & Treatment Ctr, Indianapolis, IN USA. [Erickson, Craig A.; Stigler, Kimberly A.; Wink, Logan K.; Mullett, Jennifer E.; Kohn, Arlene; Posey, David J.; McDougle, Christopher J.] James Whitcomb Riley Hosp Children, Indianapolis, IN 46202 USA. RP Erickson, CA (reprint author), Indiana Univ Sch Med, Dept Psychiat, 702 Barnhill Dr,Room 4300, Indianapolis, IN 46202 USA. EM crericks@iupui.edu FU FRAXA Research Foundation; The Division of Disability and Rehabilitative Services; Indiana Family and Social Services Administration; National Institute of Health [KL2 UL1 RR025761]; Daniel X. and Mary Freedman Fellowship in Academic Psychiatry; NIMH [K23 MH082119, R01 MH072964, R01 MH077600, R01 MH083739] FX This work is supported by a grant from the FRAXA Research Foundation (Drs. McDougle and Erickson). The work is also supported in part by The Division of Disability and Rehabilitative Services, Indiana Family and Social Services Administration (Drs. Erickson, Wink, McDougle); National Institute of Health grant KL2 UL1 RR025761 Indiana University Clinical and Translational Sciences Institute Career Development Award (Dr. Erickson); Daniel X. and Mary Freedman Fellowship in Academic Psychiatry (Dr. Stigler); NIMH grant K23 MH082119 (Dr. Stigler); and NIMH grants R01 MH072964, R01 MH077600, R01 MH083739 (Dr. McDougle). Bristol Myers Squibb provided drug for use in this study. 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Cross-species co-expression and protein interaction network analyses identified glycogen synthase kinase 3 beta (GSK3B) as one of the most consistent and conserved covariates of NRXN1. By using the Molecular Genetics of Schizophrenia data set, we were able to test and confirm that markers in NRXN1 and GSK3B have epistatic interactions in human populations that can jointly modulate risk of schizophrenia. C1 [Mozhui, K.; Wang, X.; Mulligan, M. K.; Li, Z.; Ingles, J.; Lu, L.; Williams, R. W.] Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, Ctr Integrat & Translat Genom, Memphis, TN 38163 USA. [Chen, J.; Chen, X.] Virginia Common Wealth Univ, Dept Psychiat, Richmond, VA USA. RP Mozhui, K (reprint author), Univ Tennessee, Ctr Hlth Sci, Dept Anat & Neurobiol, 855 Monroe Ave,Suite 515, Memphis, TN 38163 USA. 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Psychiatr. PD JUL PY 2011 VL 1 AR e25 DI 10.1038/tp.2011.24 PG 11 WC Psychiatry SC Psychiatry GA V29SS UT WOS:000208768700009 PM 22832527 ER PT J AU Spencer, MD Holt, RJ Chura, LR Suckling, J Calder, AJ Bullmore, ET Baron-Cohen, S AF Spencer, M. D. Holt, R. J. Chura, L. R. Suckling, J. Calder, A. J. Bullmore, E. T. Baron-Cohen, S. TI A novel functional brain imaging endophenotype of autism: the neural response to facial expression of emotion SO TRANSLATIONAL PSYCHIATRY LA English DT Article DE autism; endophenotype; fMRI; genetic; sibling AB Siblings of individuals with autism have over 20 times the population risk of autism. Evidence of comparable, but less marked, cognitive and social communication deficits in siblings suggests a role for these traits in the search for biomarkers of familial risk. However, no neuroimaging biomarkers of familial risk have been identified to date. Here we show, for the first time, that the neural response to facial expression of emotion differs between unaffected siblings and healthy controls with no family history of autism. Strikingly, the functional magnetic resonance imaging (fMRI) response to happy versus neutral faces was significantly reduced in unaffected siblings compared with controls within a number of brain areas implicated in empathy and face processing. The response in unaffected siblings did not differ significantly from the response in autism. Furthermore, investigation of the response to faces versus fixation crosses suggested that, within the context of this study, an atypical response specifically to happy faces, rather than to faces in general, accounts for the observed sibling versus controls difference and is a clear biomarker of familial risk. Our findings suggest that an atypical implicit response to facial expression of emotion may form the basis of impaired emotional reactivity in autism and in the broader autism phenotype in relatives. These results demonstrate that the fMRI response to facial expression of emotion is a candidate neuroimaging endophenotype for autism, and may offer far-reaching insights into the etiology of autism. C1 [Spencer, M. D.; Holt, R. J.; Chura, L. R.; Baron-Cohen, S.] Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 8AH, England. [Suckling, J.; Bullmore, E. T.] Univ Cambridge, Dept Psychiat, Cambridge CB2 8AH, England. [Calder, A. J.] MRC Cognit & Brain Sci Unit, Cambridge, England. RP Spencer, MD (reprint author), Univ Cambridge, Autism Res Ctr, Dept Psychiat, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England. EM mds1003@cam.ac.uk FU MRC Clinician Scientist Fellowship; UK Medical Research Council [G0701919]; Gates Cambridge Scholarship Trust FX We are grateful to all participants and their families for their participation in our study and to all autism support organizations that helped with recruitment. We are grateful for the technical assistance of Dr Cinly Ooi. This research was funded by an MRC Clinician Scientist Fellowship to MDS from the UK Medical Research Council (G0701919). LRC is supported by the Gates Cambridge Scholarship Trust. 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Psychiatr. PD JUL PY 2011 VL 1 AR e19 DI 10.1038/tp.2011.18 PG 7 WC Psychiatry SC Psychiatry GA V29SS UT WOS:000208768700003 PM 22832521 ER PT J AU De Jong, M Punt, M De Groot, E Minderaa, RB Hadders-Algra, M AF De Jong, Marianne Punt, Marja De Groot, Erik Minderaa, Ruud B. Hadders-Algra, Mijna TI Minor neurological dysfunction in children with autism spectrum disorder SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CONNECTIVITY; VOLUME; ABNORMALITIES; BEHAVIOR; CORTEX AB Aim The aim of this study was to improve the understanding of brain function in children with autism spectrum disorder (ASD) in relation to minor neurological dysfunctions (MNDs). Method We studied MNDs in 122 children (93 males, 29 females; mean age 8y 1mo, SD 2y 6mo) who, among a total cohort of 705 children (513 males, 192 females; mean age 9y, SD 2y 0.5mo) referred to a regional outpatient non-academic psychiatric centre in the Netherlands, were diagnosed with ASD after an extensive multidisciplinary psychiatric assessment. Children with clear neurological abnormalities (e.g. cerebral palsy or spina bifida) were excluded from the study. MNDs were assessed in all 705 children using the Touwen examination method. Special attention was paid to the severity and type of MND. Data of the children with ASD were compared with neurological morbidity data of children with other psychiatric disorders and with children in the general population, who were born at Groningen University Hospital between 1975 and 1978. Results Seventy-four percent of the children with ASD showed complex MNDs compared with 52% of the children with other psychiatric disorders and 6% of the reference group (chi 2=18.0, p < 0.001; chi 2=937.5, p < 0.001 respectively). Specific dysfunctions frequently encountered in ASD were dysfunctional posture and muscle tone, fine manipulative disability, dyscoordination, and excessive associated movements. Conclusion These findings suggest a contribution of dysfunctional supraspinal networks involving multiple parts of the brain in the pathogenesis of ASD. This is consistent with findings from neuroimaging studies, and highlights the importance of neurological examinations in paediatric psychiatric assessments. C1 [De Jong, Marianne; Punt, Marja] Dept Child & Adolescent Psychiat Fornhese, Symfora Grp, Amersfoort, Netherlands. [De Groot, Erik] Ctr Mental Hlth Care, Deventer, Netherlands. [Minderaa, Ruud B.] Univ Groningen, Univ Med Ctr Groningen, Dept Child & Adolescent Psychiat, NL-9713 AV Groningen, Netherlands. [Hadders-Algra, Mijna] Univ Groningen, Univ Med Ctr Groningen, Dept Paediat, NL-9713 AV Groningen, Netherlands. RP De Jong, M (reprint author), Regentesselaan 10, NL-3762 DS Soest, Netherlands. EM marjapunt@planet.nl FU Open Ankh Foundation, Soesterberg, the Netherlands FX The Open Ankh Foundation, Soesterberg, the Netherlands, provided financial support for this study. 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Gupta, Varsha Chan, Wai Yen Sitoh, Yih-Yian Sim, Kang TI Use of normative distribution of gray to white matter ratio in orthogonal planes in human brain studies and computer-assisted neuroradiology SO INTERNATIONAL JOURNAL OF COMPUTER ASSISTED RADIOLOGY AND SURGERY LA English DT Article DE MRI brain scans; Gray to white matter ratio; Aging; Autism; Neuroimage quantification; Data explosion; Brain characterization; Brain landmarks ID VOXEL-BASED MORPHOMETRY; MAGNETIC-RESONANCE NEUROIMAGES; TALAIRACH TRANSFORMATION; SEX-DIFFERENCES; ADULT BRAIN; AGE; VOLUMETRY; SEGMENTATION; VALIDATION; GENDER AB Purpose Although the brain has been extensively studied, relationships of gray (GM) to white (WM) matters in individual sections as typically acquired and read radiologically have not yet been examined. A novel GM/WM-based approach with a compact whole brain representation is introduced and applied to study the brain and perform neuroimage processing. Methods The gray to white matter ratio GWR defined as GM/(GM+WM) was calculated for 3T T1-weighted axial, coronal, and sagittal sections of 75 normal subjects. The mean (normative) GWR curves were employed to describe the normal brain and quantify aging and to illustrate pathology detection and characterization. Results The mean GWR curves characterize the normal brain by only six, neuroanatomy-related numbers. The regions with a significant GWR decline with age surround the ventricular system. The GWR decline rate in males is higher (-0.17%/year) than females (-0.14%/year); moreover, males show a significantly higher decline in middle to elder group. The GWR decline from young (<= 25 years) to middle (26-40 years) age group (males/females -0.31%/-0.34%/year) is significantly higher than that from middle to elder (>40 years) group (males/females -0.13/-0.07%/year). Conclusion The GWR-based analysis is useful to characterize normal brain, determine significant regions of interest, and quantify healthy aging. It has potential applications in brain compression, comparison, morphometry, normalization, and detecting and quantifying pathologies, which open new avenues in computer-assisted neuroradiology from screening to large brain databases searching. C1 [Nowinski, Wieslaw L.; Gupta, Varsha] Agcy Sci Technol & Res, Biomed Imaging Lab, Singapore 138671, Singapore. [Chan, Wai Yen; Sim, Kang] Woodbridge Hosp, Inst Mental Hlth, Dept Adult Psychiat 3, Singapore 539747, Singapore. [Sitoh, Yih-Yian] Natl Inst Neurosci, Dept Neuroradiol, Singapore 308433, Singapore. RP Nowinski, WL (reprint author), Agcy Sci Technol & Res, Biomed Imaging Lab, 30 Biopolis St,07-01 Matrix, Singapore 138671, Singapore. 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TI The relationship between syntactic development and Theory of Mind: Evidence from a small-population study of a developmental language disorder SO JOURNAL OF NEUROLINGUISTICS LA English DT Article DE Developmental language disorder; Theory of Mind; False belief; Syntactic complexity; Syntactic development; Sentential complementation ID FALSE-BELIEF; WORKING-MEMORY; INHIBITORY CONTROL; EXECUTIVE FUNCTION; CHILDRENS THEORY; DEAF-CHILDREN; IMPAIRMENT; COGNITION; AUTISM; STATES AB We investigated whether performance on false belief understanding tasks is related to language ability by looking at Russian-speaking children enrolled in a study of a developmental language disorder in a geographically isolated small population characterized by a high prevalence of developmental language disorders. All consenting children between the ages of 6 and 12 (n = 54) were given the Assessment of the Development of Russian Language (ORRIA), nonverbal IQ short-term memory measures, a narrative task, and the Unexpected Transfer task of false belief. We found that language development scores were related to success on the false belief task even when controlled for IQ and short-term memory. Also, the group who succeeded on the false belief task had significantly higher syntactic complexity scores for narratives than those who failed it. References to mental states, manifested by the children's use of mental, psychological and perception verbs, were not related to performance on the false belief task. These findings support the hypothesis that developed representations of false belief are tied to syntactic development, not general cognitive functioning or the acquisition of mental-state verbs. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Grigorenko, Elena L.] Yale Univ, Ctr Child Study, New Haven, CT 06519 USA. [Kornilov, Sergey A.] Univ Connecticut, Storrs, CT USA. [Kornilov, Sergey A.; Grigorenko, Elena L.] Moscow MV Lomonosov State Univ, Moscow, Russia. [Koposov, Roman A.] Univ Tromso, Tromso, Norway. [Koposov, Roman A.] No State Med Univ, Arkhangelsk, Russia. [Grigorenko, Elena L.] Columbia Univ, New York, NY USA. RP Grigorenko, EL (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06519 USA. EM natalia.rakhlin@yale.edu; sa.kornilov@gmail.com; jodi.reich@yale.edu; maria.babyonyshev@yale.edu; roman.koposov@uit.no; elena.grigorenko@yale.edu FU [DC007665] FX The first two authors have contributed equally to this article. This research was supported by DC007665. Grantees undertaking such projects are encouraged to express freely their professional judgment. 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TI Gender-Specific Effect of Mthfr Genotype and Neonatal Vigabatrin Interaction on Synaptic Proteins in Mouse Cortex SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE sociability; cerebral cortex; FMR1; reelin; GluR1 ID FRAGILE-X-SYNDROME; METHYLENETETRAHYDROFOLATE REDUCTASE MTHFR; FETAL ANTICONVULSANT SYNDROME; GENETIC RISK-FACTOR; GAMMA-VINYL-GABA; AMPA RECEPTOR; COMMON MUTATION; GLUTAMATE RECEPTORS; HIPPOCAMPAL-NEURONS; PLASMA HOMOCYSTEINE AB The enzyme methylenetetrahydrofolate reductase (MTHFR) is a part of the homocysteine and folate metabolic pathways, affecting the methylations of DNA, RNA, and proteins. Mthfr deficiency was reported as a risk factor for neurodevelopmental disorders such as autism spectrum disorder and schizophrenia. Neonatal disruption of the GABAergic system is also associated with behavioral outcomes. The interaction between the epigenetic influence of Mthfr deficiency and neonatal exposure to the GABA potentiating drug vigabatrin (GVG) in mice has been shown to have gender-dependent effects on mice anxiety and to have memory impairment effects in a gender-independent manner. Here we show that Mthfr deficiency interacts with neonatal GABA potentiation to alter social behavior in female, but not male, mice. This impairment was associated with a gender-dependent enhancement of proteins implicated in excitatory synapse plasticity in the female cortex. Reelin and fragile X mental retardation 1 protein (FMRP) levels and membrane GluR1/GluR2 ratios were elevated in wild-type mice treated neonatally with GVG and in Mthfr +/- mice treated with saline, but not in Mthfr +/- mice treated with GVG, compared with control groups (wild type treated with saline). A minor influence on the levels of these proteins was observed in male mice cortices, possibly due to high basal protein levels. Interaction between gender, genotype, and treatment was also observed in the GABA pathway. In female mice, GABA A alpha 2/gephyrin ratios were suppressed in all test groups; in male mice, a genotype-specific enhancement of GABA A alpha 2/gephyrin was observed. The lack of an effect on either reln or Fmr1 transcription suggests post-transcriptional regulation of these genes. Taken together, these findings suggest that Mthfr deficiency may interact with neonatal GABA potentiation in a gender-dependent manner to interrupt synaptic function. This may illustrate a possible mechanism for the epigenetic involvement of Mthfr deficiency in neurodevelopmental disorders. Neuropsychopharmacology (2011) 36, 1714-1728; doi:10.1038/npp.2011.52; published online 13 April 2011 C1 [Blumkin, Elinor; Levav-Rabkin, Tamar; Melamed, Osnat; Galron, Dalia; Golan, Hava M.] Ben Gurion Univ Negev, Fac Hlth Sci, Dept Dev Mol Genet, IL-84105 Beer Sheva, Israel. [Blumkin, Elinor; Levav-Rabkin, Tamar; Melamed, Osnat; Golan, Hava M.] Ben Gurion Univ Negev, Zlotowski Ctr Neurosci, IL-84105 Beer Sheva, Israel. RP Golan, HM (reprint author), Ben Gurion Univ Negev, Fac Hlth Sci, Dept Dev Mol Genet, IL-84105 Beer Sheva, Israel. EM havag@bgu.ac.il RI GOLAN, HAVA/F-2121-2012 FU Israel Ministry of Health [3_4030]; Israeli Ministry of Science, Culture, and Sport FX This work was supported by the Israel Ministry of Health (No. 3_4030). We thank the Israeli Ministry of Science, Culture, and Sport for the Eshkol Fellowship to Mrs Tamar Levav-Rabkin. Gratitude is also extended to Prof. Rima Rozen from McGill University, Canada, for kindly providing the Mthfr knockout mice, and to Prof. Ruth Parvari and Ms Sofia Borokovsky from the Department of Developmental Genetics, Faculty of Health Sciences, Ben-Gurion University of the Negev, Israel, for their help with the protein methylation assay. 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Kuban, Karl C. K. O'Shea, T. Michael Paneth, Nigel Allred, Elizabeth N. Leviton, Alan CA ELGAN Study Investigators TI The Modified Checklist for Autism in Toddlers in extremely low gestational age newborns: individual items associated with motor, cognitive, vision and hearing limitations SO PAEDIATRIC AND PERINATAL EPIDEMIOLOGY LA English DT Article DE M-CHAT; autistic spectrum disorder; very preterm; cerebral palsy; motor impairment; vision; hearing ID SPECTRUM DISORDERS; RISK-FACTORS; CEREBRAL-PALSY; CHILDREN; INFANTS; BIRTH AB P>Luyster RJ, Kuban KCK, O'Shea TM, Paneth N, Allred EN, Leviton A for ELGAN Study investigators. The Modified Checklist for Autism in Toddlers in extremely low gestational age newborns: Individual items associated with motor, cognitive, vision and hearing limitations. Paediatric and Perinatal Epidemiology 2011; 25: 366-376. The Modified Checklist for Autism in Toddlers (M-CHAT) has yielded elevated rates of screening failure for children born preterm or with low birthweight. We extended these findings with a detailed examination of M-CHAT items in a large sample of children born at extremely low gestational age. The sample was grouped according to children's current limitations and degree of impairment. The aim was to better understand how disabilities might influence M-CHAT scores. Fourteen participating institutions of the Extremely Low Gestational Age Newborns (ELGAN) Study prospectively collected information about 1086 infants who were born before the 28th week of gestation and had an assessment at age 24-months. The 24-month visit included a neurological assessment, the Bayley Scales of Infant Development, Second edition (BSID-II), M-CHAT and a medical history form. Outcome measures included the distribution of failed M-CHAT items among groups classified according to cerebral palsy diagnosis, gross motor function, BSID-II scores and vision or hearing impairments. M-CHAT items were failed more frequently by children with concurrently identified impairments (motor, cognitive, vision and hearing). In addition, the frequency of item failure increased with the severity of impairment. The failed M-CHAT items were often, but not consistently, related to children's specific impairments. Importantly, four of the six M-CHAT 'critical items' were commonly affected by presence and severity of concurrent impairments. The strong association between impaired sensory or motor function and M-CHAT results among extremely low gestational age children suggests that such impairments might give rise to false positive M-CHAT screening. C1 [Luyster, Rhiannon J.] Harvard Univ, Sch Med, Div Dev Med, Labs Cognit Neurosci, Boston, MA 02215 USA. [Allred, Elizabeth N.; Leviton, Alan] Harvard Univ, Sch Med, Childrens Hosp Boston, Neuroepidemiol Unit,Dept Neurol, Boston, MA 02215 USA. [Kuban, Karl C. K.] Boston Univ, Boston Med Ctr, Dept Pediat, Div Pediat Neurol, Boston, MA 02215 USA. [O'Shea, T. Michael] Wake Forest Univ, Dept Neonatol, Winston Salem, NC 27109 USA. [Paneth, Nigel] Michigan State Univ, Sparrow Med Ctr, E Lansing, MI 48824 USA. RP Luyster, RJ (reprint author), Harvard Univ, Sch Med, Div Dev Med, Labs Cognit Neurosci, 1 Autumn St, Boston, MA 02215 USA. EM rhiannon.luyster@childrens.harvard.edu FU National Institute of Neurological Disorders and Stroke [1 U01 NS 40069-01A2]; National Institute of Child Health and Human Development [5P30HD018655-28] FX Financial support for this research was provided by the National Institute of Neurological Disorders and Stroke (cooperative agreement 1 U01 NS 40069-01A2) and a centre grant award from the National Institute of Child Health and Human Development (5P30HD018655-28). The authors gratefully acknowledge the contributions of their subjects, and their subjects' families, as well as those of their colleagues. There are no conflicts of interest. 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PD JUL PY 2011 VL 75 IS 4 BP 341 EP 349 DI 10.1007/s00426-010-0311-6 PG 9 WC Psychology, Experimental SC Psychology GA 777GK UT WOS:000291603700008 PM 20941504 ER PT J AU Chonchaiya, W Nuntnarumit, P Pruksananonda, C AF Chonchaiya, Weerasak Nuntnarumit, Prapasri Pruksananonda, Chandhita TI Comparison of television viewing between children with autism spectrum disorder and controls SO ACTA PAEDIATRICA LA English DT Article DE Autism spectrum disorder; Language development; Media; Screen time; Television viewing ID LANGUAGE-DEVELOPMENT; MEDIA AB Aim: To examine the pattern and extent of television viewing in children with autism spectrum disorder (ASD) compared with typically developing controls and those with delayed language development (DLD). Methods: Fifty-four individuals with ASD (mean age 2.56 +/- 0.66 years) and 84 controls (mean age 2.43 +/- 0.81 years) were enrolled. Fifty-six individuals with DLD, who had language developmental levels similar to those with ASD, were enrolled in our previous study. Main outcome measures included onset and frequency of television viewing, in addition to the type of programme and whether a caregiver cowatched television. Results: Those with ASD began to watch television significantly earlier than controls (6.44 +/- 6.35 vs. 12.41 +/- 6.00 months of age, p < 0.0001*) and spent more time watching television than those with DLD (4.60 +/- 1.91 vs. 3.05 +/- 1.90 h/day, p < 0.0001*) and controls (4.60 +/- 1.91 vs. 2.06 +/- 1.21 h/day, p < 0.0001*). Those with ASD appeared to watch more adult programmes than normal controls, and they were less likely to watch television with caregivers than both control groups. Conclusion: There is an earlier onset and higher frequency of television viewing in autistic children compared with children with typical development. 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PD JUL PY 2011 VL 37 IS 4 BP 459 EP 461 DI 10.1111/j.1365-2214.2011.01218.x PG 3 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 773ML UT WOS:000291311300001 PM 21426369 ER PT J AU Crowe, LM Beauchamp, MH Catroppa, C Anderson, V AF Crowe, L. M. Beauchamp, M. H. Catroppa, C. Anderson, V. TI Social function assessment tools for children and adolescents: A systematic review from 1988 to 2010 SO CLINICAL PSYCHOLOGY REVIEW LA English DT Review DE Social skills; Social function; Child; Psychometrics; Assessment ID PROBLEM-SOLVING SKILLS; INITIAL VALIDATION; AUTISM SPECTRUM; PSYCHOMETRIC PROPERTIES; SELF-CONCEPT; INDIVIDUAL-DIFFERENCES; FRIENDSHIP QUALITY; PEER INTERACTIONS; COMPETENCE SCALE; MIDDLE CHILDHOOD AB Advances in neuroscience have added to the understanding of social functioning which has become an increasing area of focus in the psychology and neuropsychology literature. 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PD JUL PY 2011 VL 31 IS 5 BP 767 EP 785 DI 10.1016/j.cpr.2011.03.008 PG 19 WC Psychology, Clinical SC Psychology GA 771VM UT WOS:000291188800007 PM 21513693 ER PT J AU Zerbo, O Iosif, AM Delwiche, L Walker, C Hertz-Picciotto, I AF Zerbo, Ousseny Iosif, Ana-Maria Delwiche, Lora Walker, Cheryl Hertz-Picciotto, Irva TI Month of Conception and Risk of Autism SO EPIDEMIOLOGY LA English DT Article ID SPECTRUM DISORDERS; INFANTILE-AUTISM; CONGENITAL RUBELLA; BIRTH; SEASON; CHILDREN; CALIFORNIA; EXPOSURE; POPULATION; INFLUENZA AB Background: Studies of season of birth or season of conception can provide clues about etiology. We investigated whether certain months or seasons of conception are associated with increased risk of autism spectrum disorders, for which etiology is particularly obscure. Methods: The study population comprises 6,604,975 children born from 1990 to 2002 in California. Autism cases (n = 19,238) were identified from 1990 through 2008 in databases of the California Department of Developmental Services, which coordinates services for people with developmental disorders. The outcome in this analysis was autism diagnosed before the child's sixth birth date. The main independent variables were month of conception and season of conception (winter, spring, summer, and fall). Multivariate logistic regression models were used to estimate odds ratios (ORs) with their 95% confidence intervals (CIs) for autism by month of conception. Results: Children conceived in December (OR = 1.09 [95% CI = 1.02-1.17]), January (1.08 [1.00-1.17]), February (1.12 [1.041.20]), or March (1.16 [1.08-1.24]) had higher risk of developing autism compared with those conceived in July. Conception in the winter season (December, January, and February) was associated with a 6% (OR = 1.06, 95% CI = 1.02-1.10) increased risk compared with summer. Conclusions: Higher risks for autism among those conceived in winter months suggest the presence of environmental causes of autism that vary by season. C1 [Zerbo, Ousseny; Iosif, Ana-Maria; Delwiche, Lora; Walker, Cheryl; Hertz-Picciotto, Irva] Univ Calif Davis, Dept Publ Hlth Sci, Sch Med, Davis, CA 95616 USA. [Hertz-Picciotto, Irva] UC Davis Med Invest Neurodev Disorders MIND Inst, Sacramento, CA USA. RP Zerbo, O (reprint author), Univ Calif Davis, Dept Publ Hlth Sci, Sch Med, MS1C, Davis, CA 95616 USA. EM ozerbo@ucdavis.edu FU National Institute of Environmental Health Sciences [R01-ES015359, P01-ES11269]; U.S. Environmental Protection Agency STAR (Science to Achieve Results) [R-829388, R833292] FX Supported by grants from the National Institute of Environmental Health Sciences: R01-ES015359 and P01-ES11269 and from the U.S. Environmental Protection Agency STAR (Science to Achieve Results) #R-829388 & R833292. 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Hansen, Robin L. Hartiala, Jaana Allayee, Hooman Schmidt, Linda C. Tancredi, Daniel J. Tassone, Flora Hertz-Picciotto, Irva TI Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism SO EPIDEMIOLOGY LA English DT Article ID NEURAL-TUBE DEFECTS; O-METHYL TRANSFERASE; FOLIC-ACID; SPECTRUM DISORDERS; METHYLENETETRAHYDROFOLATE REDUCTASE; FUNCTIONAL POLYMORPHISM; METHIONINE SYNTHASE; EARLY-PREGNANCY; FOLATE; HOMOCYSTEINE AB Background: Causes of autism are unknown. Associations with maternal nutritional factors and their interactions with gene variants have not been reported. Methods: Northern California families were enrolled from 2003 to 2009 in the CHARGE (CHildhood Autism Risks from Genetics and Environment) population-based case-control study. Children aged 24-60 months were evaluated and confirmed to have autism (n = 288), autism spectrum disorder (n = 141), or typical development (n = 278) at the University of California-Davis Medical Investigation of Neurodevelopmental Disorders Institute using standardized clinical assessments. We calculated adjusted odds ratios (ORs) for associations between autism and retrospectively collected data on maternal vitamin intake before and during pregnancy. We explored interaction effects with functional genetic variants involved in one-carbon metabolism (MTHFR, COMT, MTRR, BHMT, FOLR2, CBS, and TCN2) as carried by the mother or child. Results: Mothers of children with autism were less likely than those of typically developing children to report having taken prenatal vitamins during the 3 months before pregnancy or the first month of pregnancy (OR = 0.62 [95% confidence interval = 0.42-0.93]). Significant interaction effects were observed for maternal MTHFR 677 TT, CBS rs234715 GT + TT, and child COMT 472 AA genotypes, with greater risk for autism when mothers did not report taking prenatal vitamins periconceptionally (4.5 [1.4-14.6]; 2.6 [1.2-5.4]; and 7.2 [2.3-22.4], respectively). Greater risk was also observed for children whose mothers had other one-carbon metabolism pathway gene variants and reported no prenatal vitamin intake. Conclusions: Periconceptional use of prenatal vitamins may reduce the risk of having children with autism, especially for genetically susceptible mothers and children. Replication and mechanistic investigations are warranted. C1 [Schmidt, Rebecca J.; Hertz-Picciotto, Irva] Univ Calif Davis, Dept Publ Hlth Sci, 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, Sacramento, CA 95817 USA. [Hansen, Robin L.; Tancredi, Daniel J.] Univ Calif Davis, Dept Pediat, Sch Med, Davis, CA 95616 USA. [Hartiala, Jaana; Allayee, Hooman] Univ So Calif, Keck Sch Med, Inst Genet Med, Dept Prevent Med, Los Angeles, CA 90033 USA. [Schmidt, Linda C.; Tassone, Flora] Univ Calif Davis, Dept Biochem & Mol Med, Sch Med, Davis, CA 95616 USA. [Tancredi, Daniel J.] Univ Calif Davis, Ctr Healthcare Policy & Res, Sch Med, Davis, CA 95616 USA. RP Schmidt, RJ (reprint author), Univ Calif Davis, Dept Publ Hlth Sci, Sch Med, 123 MS1C,1 Shields Ave, Davis, CA 95616 USA. EM rjschmidt@ucdavis.edu FU National Institutes of Health [1R01-ES015359, P01-11269, T32-MH073124]; U.S. EPA [R-829388, R-833292]; UC Davis Medical Investigations of Neurodevelopmental Disorders Institute FX Supported by grants 1R01-ES015359, P01-11269, and T32-MH073124 from the National Institutes of Health; grants #R-829388 & R-833292 from the U.S. EPA STAR program; and by the UC Davis Medical Investigations of Neurodevelopmental Disorders Institute. 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TI Loss of the tuberous sclerosis complex protein tuberin causes Purkinje cell degeneration SO NEUROBIOLOGY OF DISEASE LA English DT Article DE Purkinje cell; Tsc2; Tuberin; Tuberous sclerosis complex; Neurodegeneration ID ENDOPLASMIC-RETICULUM STRESS; OXIDATIVE STRESS; NEURODEGENERATIVE DISEASES; SIGNALING PATHWAY; IMPROVED SURVIVAL; MAMMALIAN TARGET; RAPAMYCIN; TSC2; CEREBELLUM; MOUSE AB Tuberous sclerosis complex (TSC) is a neurogenetic disorder that often causes brain abnormalities leading to epilepsy, developmental delay, and autism. TSC is caused by inactivating mutations in either of the genes encoding the proteins hamartin (TSC1) and tuberin (TSC2). These proteins form a heterodimer that inhibits the mammalian target of rapamycin complex 1 (mTORC1) pathway, controlling translation and cell growth. Loss of either protein results in dysregulated mTORC1 activation, an important aspect of TSC pathogenesis. About thirty percent of TSC patients have cerebellar pathology that is poorly understood. To investigate the effects of TSC on the cerebellum, we created a mouse model in which the Tsc2 gene was selectively deleted from Purkinje cells starting at postnatal day 6 (P6). The loss of Tsc2 caused a progressive increase in Purkinje cell size and subsequent death from apoptosis. Purkinje cell loss was predominantly cell type specific and associated with motor deficits. Immunohistochemical analysis showed that both endoplasmic reticulum (ER) and oxidative stress were increased in Tsc2-null Purkinje cells. The cell death and ER stress phenotypes were rescued by treatment with the mTORC1 inhibitor rapamycin. To assess whether the murine Purkinje cell loss has a correlate to the human TSC, we analyzed postmortem cerebellum samples from TSC patients and detected Purkinje cell loss in half of the samples. Our results establish a critical role for the TSC complex in Purkinje cell survival by regulating ER and oxidative stress and reveal a novel aspect of TSC neuropathology. (C) 2011 Elsevier Inc. All rights reserved. C1 [Reith, R. Michelle; Way, Sharon; McKenna, James, III; Haines, Katherine; Gambello, Michael J.] Univ Texas Houston, Hlth Sci Ctr, Dept Pediat, Div Med Genet, Houston, TX 77030 USA. RP Gambello, MJ (reprint author), 6431 Fannin St,MSB 3-144, Houston, TX 77030 USA. EM Michael.j.gambello@uth.tmc.edu FU NIH/NINDS [RO1NS060804]; DOD [W81XWH-07-1-0275]; NIH/NCRR [TL1RR024147] FX We thank Drs. Seonhee Kim, Seo-Hee Cho, Karen Posey, and S. Shahrukh Hashmi for their advice on experiments and comments on our manuscript. Human tissue was obtained from the NICHD Brain and Tissue Bank for Developmental Disorders at the University of Maryland, Baltimore, MD. "The role of the NICHD Brain and Tissue Bank is to distribute tissue, and, therefore, cannot endorse the studies performed or the interpretation of results." The project described was supported by NIH/NINDS grant RO1NS060804 and DOD grant W81XWH-07-1-0275 to MJG and NIH/NCRR award TL1RR024147 to RMR. "The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health." 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KCNJ10, encoding Kir4.1, has been recently linked to seizure susceptibility in humans and mice, and is a possible candidate gene for Autism Spectrum Disorders (ASD). In this study, we performed a mutational screening of KCNJ10 in 52 patients with epilepsy of "unknown cause" associated with impairment of either cognitive or communicative abilities, or both. Among them, 14 patients fitted the diagnostic criteria for ASD. We identified two heterozygous KCNJ10 mutations (p.R18Q and p.V84M) in three children (two unrelated families) with seizures, ASD, and intellectual disability. The mutations replaced amino acid residues that are highly conserved throughout evolution and were undetected in about 500 healthy chromosomes. The effects of mutations on channel activity were functionally assayed using a heterologous expression system. These studies indicated that the molecular mechanism contributing to the disorder relates to an increase in either surface-expression or conductance of the Kir4.1 channel. Unlike previous syndromic associations of genetic variants in KCNJ10, the pure neuropsychiatric phenotype in our patients suggests that the new mutations affect K+ homeostasis mainly in the brain, by acting through gain-of-function defects. Dysfunction in astrocytic-dependent K+ buffering may contribute to autism/epilepsy phenotype, by altering neuronal excitability and synaptic function, and may represent a new target for novel therapeutic approaches. (C) 2011 Elsevier Inc. All rights reserved. C1 [Sicca, Federico; Brovedani, Paola; Guerrini, Renzo] IRCCS Stella Maris Fdn, Epilepsy Neurophysiol & Neurogenet Unit, I-56128 Pisa, Italy. [Imbrici, Paola; D'Adamo, Maria Cristina; Pessia, Mauro] Univ Perugia, Sch Med, Sect Human Physiol, I-06126 Perugia, Italy. [Moro, Francesca; Bonatti, Fabrizia; Santorelli, Filippo Maria] IRCCS Stella Maris Fdn, Mol Med Unit, I-56128 Pisa, Italy. [Grottesi, Alessandro] CASPUR Interuniv Consortium Applicat Super Comp U, Computat Chem & Biol Grp, I-00185 Rome, Italy. [Guerrini, Renzo] Univ Florence, Child Neurol Unit, A Meyer Pediat Hosp, I-50139 Florence, Italy. [Masi, Gabriele] IRCCS Stella Maris Fdn, Child Psychiat & Psychopharmacol Unit, I-56128 Pisa, Italy. RP Sicca, F (reprint author), IRCCS Stella Maris Fdn, Epilepsy Neurophysiol & Neurogenet Unit, Via Giacinti 2, I-56128 Pisa, Italy. EM federico.sicca@inpe.unipi.it; pimbrici@unipg.it; cdadamo@unipg.it; fmoro@inpe.unipi.it; fabrizia.bonatti@tiscali.it; pbrovedani@inpe.unipi.it; A.Grottesi@caspur.it; r.guerrini@meyer.it; gmasi@inpe.unipi.it; fsantorelli@inpe.unipi.it; pessia@unipg.it FU COMPAGNIA di San Paolo (Turin); MIUR (Italian Ministry of Instruction, University and Research); Fondazione Cassa di Risparmio di Perugia FX This work was partially supported by the COMPAGNIA di San Paolo (Turin) "Programma Neuroscienze," MIUR (Italian Ministry of Instruction, University and Research)-PRIN, and the Fondazione Cassa di Risparmio di Perugia. 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Modificat. PD JUL PY 2011 VL 35 IS 4 BP 347 EP 369 DI 10.1177/0145445511405184 PG 23 WC Psychology, Clinical SC Psychology GA 768NG UT WOS:000290941100003 PM 21613240 ER PT J AU Rivet, TT Matson, JL AF Rivet, Tessa Taylor Matson, Johnny L. TI Review of gender differences in core symptomatology in autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Autism; Gender; Females; Girls; Intellectual disability ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; MALE BRAIN THEORY; X-LINKED GENES; CONGENITAL ADRENAL-HYPERPLASIA; EARLY-CHILDHOOD AUTISM; SEX-DIFFERENCES; FOLLOW-UP; INFANTILE-AUTISM; TURNER-SYNDROME AB A preponderance of males with autism spectrum disorders (ASD) has been evident since the initial writings on the topic. This male predominance has consistently emerged in all ASD research to date in epidemiological as well as clinical populations. Despite this long recognized gender disparity in ASD, surprisingly there is a paucity of research addressing gender as it relates to core ASD symptom presentation. Gender differences may manifest with regard to symptom domains, severity, breadth, and so forth. The present review will discuss background (e.g., history, prevalence), assessment issues, gender differences in typically developing individuals in domains relevant to ASD, an in depth review of the literature base on the nature and etiology of gender differences in ASD, as well as future research directions and implications. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Rivet, Tessa Taylor; Matson, Johnny L.] Louisiana State Univ, Baton Rouge, LA 70803 USA. RP Rivet, TT (reprint author), 59460 Highway 1148, Plaquemine, LA 70764 USA. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 957 EP 976 DI 10.1016/j.rasd.2010.12.003 PG 20 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200001 ER PT J AU Duffy, C Healy, O AF Duffy, Cormac Healy, Olive TI Spontaneous communication in autism spectrum disorder: A review of topographies and interventions SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Autism spectrum disorder; Spontaneous communication; Communicative topographies; Behavioral interventions ID SCRIPT-FADING PROCEDURE; SOCIAL-INTERACTION SKILLS; YOUNG-CHILDREN; DEVELOPMENTAL-DISABILITIES; MULTIPLE DISABILITIES; TEACHING LANGUAGE; SIGN LANGUAGE; MANUAL SIGNS; TIME-DELAY; SPEECH AB Lack of spontaneous communicative initiations appears to be a consistent problem in individuals with a diagnosis of autism spectrum disorder (ASD: Fujiki & Brinton, 2009). Spontaneous communication is emitted at a much lower frequency compared to individuals with language impairment and typically developing persons. Deficits of spontaneity in social interaction have been identified explicitly in the diagnostic criteria for autism, regardless of communication level or ability (American Psychiatric Association, 1994). In addition, without intervention 21-66% of children with ASD do not develop communicative speech (Lord & McGee, 2001). Individuals with autism rarely initiate appropriate speech and often fail to engage in typical social interactions such as asking questions, requesting information, expressing affection or requesting interactions (Carr & Kologinsky, 1983). This paper provides a review of the communicative topographies used to ameliorate spontaneous communication functions in individuals with autism and addresses the behavioral interventions that are used to induce such spontaneity. (C) 2010 Elsevier Ltd. All rights reserved. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 977 EP 983 DI 10.1016/j.rasd.2010.12.005 PG 7 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200002 ER PT J AU Kaland, N AF Kaland, Nils TI Brief report: Should Asperger syndrome be excluded from the forthcoming DSM-V? SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Asperger syndrome; High-functioning autism; Diagnosis; Differences; DSM-V ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; EXTERNAL VALIDITY; CHILDREN; DIAGNOSIS; MIND; ADOLESCENTS; INDIVIDUALS; PROFILE AB Asperger syndrome (AS) is a pervasive developmental disorder, characterized by social impairments and focused, circumscribed interests and activities in the absence of significant language impairment and cognitive delay. Since its inclusion in the DSM-IV, there has been a dramatic increase in its recognition both in children and adults. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 984 EP 989 DI 10.1016/j.rasd.2011.01.011 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200003 ER PT J AU Gould, E Dixon, DR Najdowski, AC Smith, MN Tarbox, J AF Gould, Evelyn Dixon, Dennis R. Najdowski, Adel C. Smith, Marlena N. Tarbox, Jonathan TI A review of assessments for determining the content of early intensive behavioral intervention programs for autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Autism; Assessment; Curriculum; Early intensive behavioral intervention ID MENTAL-RETARDATION; CHILDREN; PREDICTORS; SYMPTOMS; SCALES; ISSUES AB A large proportion of national education and treatment centers for persons with autism spectrum disorders (ASD), including those providing applied behavior analysis (ABA)-based services, show a relatively high percentage of agreement among practitioners on the instruments they routinely use for a variety of purposes, including curriculum design and treatment evaluation. In this paper, several assessments are reviewed and evaluated in terms of their utility for designing comprehensive early intensive behavioral intervention (EIBI) curriculum programs for children with ASD. 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TI Applications of technology to teach social skills to children with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Social skills; Technology; Autism ID SPECTRUM DISORDERS; TREATMENT INTEGRITY; YOUNG-CHILDREN; PERSPECTIVE-TAKING; BEHAVIOR-ANALYSIS; PRETEND PLAY; VIDEO; INTERVENTIONS; INITIATIONS; INSTRUCTION AB Children with autism spectrum disorder show deficits in social skills such as initiating conversation, responding in social situations, social problem-solving, and others. These deficits are targeted through the use of social skills interventions, some of which use a technology-based approach as a resource-efficient alternative to common forms of instruction. The current literature review aims to (a) determine the number of empirical studies using a technology-based social skills intervention, (b) explore the features of social skills targeted in these studies, and (c) analyze the number of studies reporting reliability of the dependent and independent variables. Results indicate that a majority of the studies relied on a video or DVD to deliver the intervention (modeling or feedback), were conducted in school settings, and targeted more than one social skill. The most common social skill addressed was initiating conversation followed by play skills. All but one study included standardized assessment before treatment; however, none of the studies used a published social skills assessment. Like previous research, reliability of the dependent variables was common; however, reliability of the independent variables was infrequent. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Reed, Florence D. DiGennaro; Hyman, Sarah R.; Hirst, Jason M.] Univ Kansas, Dept Appl Behav Sci, Dole Human Dev Ctr 4001, Lawrence, KS 66044 USA. RP Reed, FDD (reprint author), Univ Kansas, Dept Appl Behav Sci, Dole Human Dev Ctr 4001, 1000 Sunnyside Ave, Lawrence, KS 66044 USA. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1003 EP 1010 DI 10.1016/j.rasd.2011.01.022 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200005 ER PT J AU Kern, JK Geier, DA Adams, JB Troutman, MR Davis, G King, PG Young, JL Geier, MR AF Kern, Janet K. Geier, David A. Adams, James B. Troutman, Melissa R. Davis, Georgia King, Paul G. Young, John L. Geier, Mark R. TI Autism severity and muscle strength: A correlation analysis SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Autism severity; Muscle strength; Grip strength ID HAND-HELD DYNAMOMETER; CARNITINE DEFICIENCY; SPECTRUM DISORDERS; CHILDREN; RELIABILITY; PERFORMANCE; IMPAIRMENT AB The current study examined the relationship between muscle strength, as measured by hand grip strength, and autism severity, as measured by the Childhood Autism Rating Scale (CARS). Thirty-seven (37) children with a diagnosis of autism spectrum disorder (ASD) were evaluated using the CARS and then tested for hand muscle strength using a hand grip dynamometer. Statistical analysis was then conducted to examine the relationship between autism severity and hand muscle strength. The model generated in the present study showed that the CARS score is a significant predictor of Max Hand Muscle Score after adjustment for age, race, gender, year of birth, and a history of prior chelation therapy. Evidence suggests that hand grip strength in children with ASD is related to the severity of the disorder. Further research is needed to determine the extent and consistency of the muscle weakness and possible treatments. (C) 2010 Published by Elsevier Ltd. C1 [Kern, Janet K.] Genet Consultants Dallas ASD Ctr LLC, Allen, TX 75013 USA. [Kern, Janet K.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA. [Geier, David A.] CoMeD Inc, Silver Spring, MD USA. [Geier, David A.] Inst Chron Illnesses Inc, Silver Spring, MD USA. [Adams, James B.] Arizona State Univ, Tempe, AZ USA. [Troutman, Melissa R.] Genet Consultants Indiana, Indianapolis, IN USA. [Davis, Georgia] Genet Consultants So Illinois, Springfield, IL USA. [King, Paul G.] Genet Consultants New Jersey, Parsippany, NJ USA. [Young, John L.] Genet Consultants Maryland, Rockville, MD USA. [Geier, Mark R.] LLC, ASD Ctr, Silver Spring, MD USA. RP Kern, JK (reprint author), Genet Consultants Dallas ASD Ctr LLC, 408 N Allen Dr, Allen, TX 75013 USA. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1011 EP 1015 DI 10.1016/j.rasd.2010.11.002 PG 5 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200006 ER PT J AU Magiati, I Moss, J Charman, T Howlin, P AF Magiati, Iliana Moss, Joanna Charman, Tony Howlin, Patricia TI Patterns of change in children with Autism Spectrum Disorders who received community based comprehensive interventions in their pre-school years: A seven year follow-up study SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism Spectrum Disorder; Intervention; Longitudinal; Follow-up ID INTENSIVE BEHAVIORAL INTERVENTION; PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; ADAPTIVE-BEHAVIOR; AGE; INDIVIDUALS; LANGUAGE; COMMUNICATION; METAANALYSIS; PREDICTORS AB There are few long-term follow-up studies of children with Autism Spectrum Disorders (ASD) who attended intensive intervention programmes in their pre-school years. Thirty-six children with ASD enrolled in relatively intensive, specialist pre-school programmes (minimum of 15 h intervention per week for 2 years at a mean age of 3.4 years) were assessed after 2 years (mean age 5.5 years) and again after a further 5 years (mean age 10.3 years). Cognitive, language and adaptive behaviour skills and severity of autism symptoms were assessed at intake (Time 1) and subsequent follow-ups (Times 2 and 3). Children made significant increases in raw and age equivalent scores in most areas of development assessed, although mean standard scores remained stable or decreased over time. Time 1 IQ language and adaptive behaviour skills were predictive of outcome at Time 3. Although there were marked individual differences in the rate and patterns of change over time, many children continued to show increases in test scores over the course of the study. This study highlights that whilst overall group improvements may be evident, the rate and nature of these improvements is highly variable across individual children. Further investigation of the specific child characteristics that affect treatment effectiveness is required. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Magiati, Iliana] Natl Univ Singapore, Dept Psychol, Singapore 117570, Singapore. [Magiati, Iliana; Moss, Joanna; Howlin, Patricia] Kings Coll London, Inst Psychiat, Dept Psychol, London, England. [Moss, Joanna] Univ Birmingham, Cerebra Ctr Neurodev Disorders, Birmingham B15 2TT, W Midlands, England. [Charman, Tony] Ctr Res Autism & Educ, Inst Educ, Dept Psychol & Human Dev, London, England. RP Magiati, I (reprint author), Natl Univ Singapore, Dept Psychol, Blk AS4 02-24,9 Arts Link, Singapore 117570, Singapore. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1016 EP 1027 DI 10.1016/j.rasd.2010.11.007 PG 12 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200007 ER PT J AU Jang, JN Dixon, DR Tarbox, J Granpeesheh, D AF Jang, Jina Dixon, Dennis R. Tarbox, Jonathan Granpeesheh, Doreen TI Symptom severity and challenging behavior in children with ASD SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Challenging behavior; Autism spectrum disorders; Children; Early intensive behavioral intervention ID AUTISM SPECTRUM DISORDERS; YOUNG-CHILDREN; RISK MARKERS; INTERVENTIONS; DISABILITIES; RELIABILITY; DC AB The prevalence of challenging behaviors in the autism spectrum disorders (ASD) population is often assumed to be high but relatively little research has actually been published on it. Furthermore, challenging behaviors are likely to impede progress in evidence-based treatment programs, such as early intensive behavioral intervention (EIBI). Little or no previous research has evaluated the prevalence of various topographies of challenging behavior in a population of children with ASD receiving EIBI services, nor evaluated the relationship between such behaviors and the severity of ASD symptoms. Using data from the ASD-DC and the ASD-BPC in 84 children with autism receiving EIBI services, the current study conducted a regression analysis of relations between endorsement of challenging behaviors and ASD symptom severity. Results indicated that 94% of the sample reported the presence of challenging behavior, stereotypical behaviors were the most commonly reported, and that the presence of challenging behavior was predicted by ASD severity. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Jang, Jina; Dixon, Dennis R.; Tarbox, Jonathan; Granpeesheh, Doreen] Ctr Autism & Related Disorders, Tarzana, CA 91356 USA. RP Dixon, DR (reprint author), Ctr Autism & Related Disorders, 19019 Ventura Blvd, Tarzana, CA 91356 USA. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1028 EP 1032 DI 10.1016/j.rasd.2010.11.008 PG 5 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200008 ER PT J AU Carter, M Roberts, J Williams, K Evans, D Parmenter, T Silove, N Clark, T Warren, A AF Carter, Mark Roberts, Jacqueline Williams, Katrina Evans, David Parmenter, Trevor Silove, Natalie Clark, Trevor Warren, Anthony TI Interventions used with an Australian sample of preschool children with autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Parents; Survey; Treatment; Education; Complementary and alternative medicine ID YOUNG-CHILDREN; COMPLEMENTARY AB This study examined the previous and current range of educational, therapy, medical and CAM interventions used by a clearly described Australian sample of 84 families of preschool-aged children with autism spectrum disorders who were enrolled in a controlled trial of early intervention services. With regard to educational and therapy interventions, the most frequently used services were speech language pathology, preschool and childcare, generic early intervention, and occupational therapy. With the exception of preschool and childcare, the access frequency for most of these services indicated they were used at relatively low intensity. Exclusion diets, oils/fatty acids and vitamin and mineral supplements were the primary CAM interventions used by families. There was no clear evidence of a relationship between the number of interventions used by families and developmental status although this may have been due to the relatively recent diagnoses. Implications of these findings and directions for future research are discussed. Crown Copyright (C) 2010 Published by Elsevier Ltd. All rights reserved. C1 [Carter, Mark] Macquarie Univ, Macquarie Univ Special Educ Ctr, N Ryde, NSW 2109, Australia. [Roberts, Jacqueline] Univ Canberra, Fac Educ, Canberra, ACT 2601, Australia. [Williams, Katrina] Univ New S Wales, Fac Med, Sydney, NSW 2052, Australia. [Evans, David] Univ Sydney, Fac Educ, Sydney, NSW 2006, Australia. [Parmenter, Trevor] Univ Sydney, Sydney Sch Med, Sydney, NSW 2006, Australia. [Silove, Natalie] Childrens Hosp, Westmead, NSW, Australia. RP Carter, M (reprint author), Macquarie Univ, Macquarie Univ Special Educ Ctr, N Ryde, NSW 2109, Australia. EM mark.carter.mq@gmail.com RI Williams, Katrina/B-6828-2015 OI Williams, Katrina/0000-0002-1686-4458 CR American Psychiatric Association (APA), 2000, DSM 4 DIAGN STAT MAN Arnold GL, 2003, J AUTISM DEV DISORD, V33, P449, DOI 10.1023/A:1025071014191 *AUSTR BUR STAT, 2007, GEN SOC SURV SUMM RE Australian Bureau of Statistics, 2008, CENS POP HOUS SOC IN Bent S, 2009, J AUTISM DEV DISORD, V39, P1145, DOI 10.1007/s10803-009-0724-5 Milllward C, 2008, COCHRANE DB SYST REV, DOI 10.1002/14651858.CD003498.pub3 Cornish E, 2002, J HUM NUTR DIET, V15, P261, DOI 10.1046/j.1365-277X.2002.00372.x Goin-Kochel RP, 2007, RES AUTISM SPECT DIS, V1, P195, DOI 10.1016/j.rasd.2006.08.006 Green VA, 2006, RES DEV DISABIL, V27, P70, DOI 10.1016/j.ridd.2004.12.002 Green VA, 2007, J DEV PHYS DISABIL, V19, P91, DOI 10.1007/s10882-007-9035-y Hediger ML, 2008, J AUTISM DEV DISORD, V38, P848, DOI 10.1007/s10803-007-0453-6 Herndon AC, 2009, J AUTISM DEV DISORD, V39, P212, DOI 10.1007/s10803-008-0606-2 Kohler F. 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M., 2004, REV RES IDENTIFY MOS Smith T, 2000, BEHAV INTERVENT, V15, P83, DOI 10.1002/(SICI)1099-078X(200004/06)15:2<83::AID-BIN47>3.0.CO;2-W Summers JA, 2005, J INTELL DISABIL RES, V49, P777, DOI 10.1111/j.1365-2788.2005.00751.x Thomas KC, 2007, J AUTISM DEV DISORD, V37, P818, DOI 10.1007/s10803-006-0208-9 Williams K, 2005, MED J AUSTRALIA, V182, P108 Wong HHL, 2006, J AUTISM DEV DISORD, V36, P901, DOI 10.1007/s10803-006-0131-0 Wong VCN, 2009, J AUTISM DEV DISORD, V39, P454, DOI 10.1007/s10803-008-0644-9 NR 34 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 JUL-SEP PY 2011 VL 5 IS 3 BP 1033 EP 1041 DI 10.1016/j.rasd.2010.11.009 PG 9 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200009 ER PT J AU Pan, CY Tsai, CL Hsieh, KW Chu, CH Li, YL Huang, ST AF Pan, Chien-Yu Tsai, Chia-Liang Hsieh, Kai-Wen Chu, Chia-Hua Li, Ya-Lin Huang, Shih-Tse TI Accelerometer-determined physical activity among elementary school-aged children with autism spectrum disorders in Taiwan SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Physical activity; Accelerometry; Autism; Children ID ACTIVITY PATTERNS; COMPUTER-SCIENCE; YOUTH; ADOLESCENTS; PROGRAM; RECESS; SKILLS AB To examine age-related physical activity (PA) patterns between- and within-day in elementary school-aged children with autism spectrum disorders (ASD). PA was recorded every 5-s by uniaxial accelerometry in 35 children (grades 1-2, n = 13; grades 3-4, n = 13; grades 5-6, n = 9) for up to five weekdays and two weekend days. Younger children were more active during weekend days compared with weekdays, while the opposite was observed in older children. Age variation also exists in children's PA levels within a weekday, with this effect being most evident during recess and after school. Weekend days and free time within school days seem appropriate targets when promoting PA in older children with ASD. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Pan, Chien-Yu; Chu, Chia-Hua; Li, Ya-Lin; Huang, Shih-Tse] Natl Kaohsiung Normal Univ, Dept Phys Educ, Kaohsiung 802, Taiwan. [Tsai, Chia-Liang; Hsieh, Kai-Wen] Natl Cheng Kung Univ, Inst Phys Educ Hlth & Leisure Studies, Tainan 701, Taiwan. RP Pan, CY (reprint author), Natl Kaohsiung Normal Univ, Dept Phys Educ, 116 He Ping 1st Rd, Kaohsiung 802, Taiwan. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1042 EP 1052 DI 10.1016/j.rasd.2010.11.010 PG 11 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200010 ER PT J AU Davis, TN Durand, S Chan, JM AF Davis, Tonya N. Durand, Shannon Chan, Jeffrey M. TI The effects of a brushing procedure on stereotypical behavior SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Stereotypy; Sensory integration; Body brushing; Wilbarger Protocol; Autism; Developmental disabilities ID SELF-INJURIOUS-BEHAVIOR; MENTAL-RETARDATION; DASH-II; AUTISM; CHILDREN; ADULTS; INTERVENTION; STIMULATION; REINFORCER; OPERATION AB In this study we analyzed the effects of a brushing protocol on stereotyped behavior of a young boy with autism. First, a functional analysis was conducted which showed that the participant's stereotypy was maintained by automatic reinforcement. Next, the Wilbarger Protocol, a brushing intervention, was implemented. An ABA design was implemented in which the participant was observed during four phases: (a) baseline, prior to the administration of the brushing protocol; (b) week 3 of implementation of the brushing protocol; (c) week 5 of implementation; and (d) 6 months after the discontinuation of the brushing protocol. Findings suggest that the brushing protocol had no marked affect on levels of stereotypy. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Davis, Tonya N.; Durand, Shannon] Baylor Univ, Waco, TX 76798 USA. [Chan, Jeffrey M.] No Illinois Univ, De Kalb, IL 60115 USA. RP Davis, TN (reprint author), Baylor Univ, 1 Bear Pl 97031, Waco, TX 76798 USA. EM Tonya_Davis@baylor.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MET D AYLLON T, 1968, J APPL BEHAV ANAL, V1, P13, DOI 10.1901/jaba.1968.1-13 BODFISH JW, 1995, AM J MENT RETARD, V100, P183 Champagne T, 2004, J PSYCHOSOC NURS MEN, V42, P35 Conroy M. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1053 EP 1058 DI 10.1016/j.rasd.2010.11.011 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200011 ER PT J AU Kodak, T Fisher, WW Clements, A Paden, AR Dickes, NR AF Kodak, Tiffany Fisher, Wayne W. Clements, Andrea Paden, Amber R. Dickes, Nitasha R. TI Functional assessment of instructional variables: Linking assessment and treatment SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Academic interventions; Auditory-visual conditional discrimination; Functional assessment; Instructional variables ID YOUNG-CHILDREN; SELF-INJURY; DISABILITIES; DISCRIMINATION; AUTISM; SKILLS AB The purpose of the present investigation was to refine and validate an assessment procedure to identify instructional variables influencing acquisition of conditional discriminations in children diagnosed with autism. An assessment was implemented with eleven individuals to identify the specific instructional variables influencing the individual's responding. A prescribed academic intervention was selected for participants based on the results of the functional assessment. The prescribed intervention was compared to an alternative treatment and control condition. The functional assessment identified several different patterns of responding to instructional variables across participants. The treatment evaluation demonstrated that the prescribed academic intervention was effective in teaching conditional discriminations. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Kodak, Tiffany; Fisher, Wayne W.; Clements, Andrea; Paden, Amber R.; Dickes, Nitasha R.] Univ Nebraska Med Ctr, Ctr Autism Spectrum Disorders, Munroe Meyer Inst, Nebraska Med Ctr, Omaha, NE 68198 USA. RP Kodak, T (reprint author), Univ Nebraska Med Ctr, Ctr Autism Spectrum Disorders, Munroe Meyer Inst, Nebraska Med Ctr, 985450 Nebraska Med Ctr, Omaha, NE 68198 USA. EM tkodak@unmc.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bourret J, 2004, J APPL BEHAV ANAL, V37, P129, DOI 10.1901/jaba.2004.37-129 Carr EG, 1997, J APPL BEHAV ANAL, V30, P673, DOI 10.1901/jaba.1997.30-673 CHARLOP MH, 1985, J APPL BEHAV ANAL, V18, P155, DOI 10.1901/jaba.1985.18-155 Dale PS, 1996, BEHAV RES METH INS C, V28, P125, DOI 10.3758/BF03203646 Daly EJ, 1997, SCHOOL PSYCHOL REV, V26, P554 DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Fisher WW, 2007, J APPL BEHAV ANAL, V40, P489, DOI 10.1901/jaba.2007.40-489 Green G., 1996, BEHAV INTERVENTIONS Hanley GP, 2003, J APPL BEHAV ANAL, V36, P147, DOI 10.1901/jaba.2003.36-147 Iwata B A, 1994, J Appl Behav Anal, V27, P131, DOI 10.1901/jaba.1994.27-131 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Lerman DC, 2004, J APPL BEHAV ANAL, V37, P11, DOI 10.1901/jaba.2004.37-11 Matson JL, 1999, RES DEV DISABIL, V20, P163, DOI 10.1016/S0891-4222(98)00039-0 McComas J. J., 2009, J BEHAV ED, V18, P56, DOI DOI 10.1007/S10864-009-9080-Y RODGERS TA, 1991, J APPL BEHAV ANAL, V24, P775, DOI 10.1901/jaba.1991.24-775 SAUNDERS KJ, 1990, J EXP ANAL BEHAV, V54, P239, DOI 10.1901/jeab.1990.54-239 Sindelar P. T., 1985, ED TREATMENT CHILDRE, V8, P67 Spradlin J.E., 1999, AUTISM BEHAV ANAL PE Wolery M, 1997, J SPEC EDUC, V31, P61 NR 21 TC 7 Z9 7 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 JUL-SEP PY 2011 VL 5 IS 3 BP 1059 EP 1077 DI 10.1016/j.rasd.2010.11.012 PG 19 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200012 ER PT J AU Ingersoll, B Meyer, K AF Ingersoll, Brooke Meyer, Katherine TI Examination of correlates of different imitative functions in young children with autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Imitation; Social communication ID JOINT ATTENTION; SYMBOLIC PLAY; MOTOR IMITATION; LANGUAGE; SKILLS; COMMUNICATION; PREDICTORS; INFANTS AB Children with autism spectrum disorders (ASD) have difficulties with social-communication skills, including imitation, language, joint attention, and play. This study investigated whether imitation performance in two different contexts (structured-elicited vs. social-interactive) was differentially related to attention-following, social reciprocity, language, and play in children with ASD. This study used a concurrent, correlational design to investigate the relationships between these skills in 23, 2-4-year-old children with autism. Participants imitated more actions on the structured-elicited than social-interactive task. After controlling for developmental level, imitation in the structured-elicited condition was correlated with vocabulary size and imitation in the social-interactive condition was correlated with vocabulary size, social reciprocity, and symbolic play. These findings suggest different skills may underlie imitation in different contexts. In addition, while imitation in both contexts appears to be important for vocabulary development at this age, imitation in a social context may be more important in the development of symbolic play skills. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Ingersoll, Brooke; Meyer, Katherine] Michigan State Univ, Dept Psychol, E Lansing, MI 48824 USA. RP Ingersoll, B (reprint author), Michigan State Univ, Dept Psychol, 105B Psychol Bldg, E Lansing, MI 48824 USA. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1078 EP 1085 DI 10.1016/j.rasd.2010.12.001 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200013 ER PT J AU Worley, JA Matson, JL AF Worley, Julie A. Matson, Johnny L. TI Psychiatric symptoms in children diagnosed with an Autism Spectrum Disorder: An examination of gender differences SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Psychopathology; Gender; Autism Spectrum Disorders-Comorbid for Children (ASD-CC) ID SEX-DIFFERENCES; PDD-NOS; PSYCHOPATHOLOGY; PREVALENCE; ADULTS; DEPRESSION; POPULATION; VALIDITY AB In addition to the triad of impairments experienced by children and adolescents diagnosed with Autism Spectrum Disorders (ASD), they often present with symptoms of psychiatric disorders. To date, very few studies have examined gender differences in regards to psychiatric symptoms in children and adolescents diagnosed with an ASD. Thus, the current study compared male and female children and adolescents (n = 129) who were diagnosed with an ASD or who were typically developing psychiatric symptoms. The Autism Spectrum Disorders-Comorbid for Children (ASD-CC) was utilized to assess for symptoms of psychopathology. Males and females diagnosed with an ASD did not significantly differ from each other in total psychiatric symptoms or on any of the specific factors of psychiatric symptoms examined (i.e., tantrum behavior, repetitive behavior, worry/depressed, avoidant behavior, under-eating, conduct, and over-eating). Similarly, males and females who were typically developing did not differ from each other on any factors examined. A discussion including future directions of research is included. (C) 2010 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. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1086 EP 1091 DI 10.1016/j.rasd.2010.12.002 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200014 ER PT J AU Tsai, CL Pan, CY Wang, CH Tseng, YT Hsieh, KW AF Tsai, Chia-Liang Pan, Chien-Yu Wang, Chun-Hao Tseng, Yu-Ting Hsieh, Kai-Wen TI An event-related potential and behavioral study of impaired inhibitory control in children with autism spectrum disorder SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Inhibitory control; Endogenous Posner paradigm; Autism; Event-related potentials; Visuospatial attention ID HIGH-FUNCTIONING AUTISM; DEFICIT HYPERACTIVITY DISORDER; CORPUS CALLOSAL SIZE; EXECUTIVE FUNCTIONS; CHILDHOOD AUTISM; ANTICIPATORY MECHANISMS; VISUOSPATIAL ATTENTION; REPETITIVE BEHAVIORS; RESPONSE-INHIBITION; ANTERIOR CINGULATE AB Autism spectrum disorders (ASD) are characterized by a deficit of dorsal visual stream processing as well as the impairment of inhibitory control capability. However, the cognitive processing mechanisms of executive dysfunction have not been addressed. In the present study, the endogenous Posner paradigm task was administered to 15 children with ASD and 16 typically developing (TD) children to simultaneously investigate and compare the behavioral performance and event-related potentials (ERPs) measures. Children with ASD showed slower reaction time in the incongruent condition but did not significantly differ in the overall conditions and in response accuracy as compared to TD children. The ASD group also exhibited significant impairment on measures of inhibitory control. In terms of ERPs regarding early and late inhibition, there were no significant differences found with regard to N2 latency, N2 amplitude, and P3 amplitude in children with ASD relative to TD children, but the ASD group manifested prolonged latency on the P3 component to target stimuli, especially in the incongruent condition, which is indicative of slow and inefficient stimulus classification speed as compared to TD children. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Tsai, Chia-Liang] Natl Cheng Kung Univ, Inst Phys Educ Hlth & Leisure Studies, Lab Cognit Neurophysiol, Tainan 701, Taiwan. [Pan, Chien-Yu] Natl Kaohsiung Normal Univ, Dept Phys Educ, Kaohsiung, Taiwan. RP Tsai, CL (reprint author), Natl Cheng Kung Univ, Inst Phys Educ Hlth & Leisure Studies, Lab Cognit Neurophysiol, 1 Univ Rd, Tainan 701, Taiwan. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1092 EP 1102 DI 10.1016/j.rasd.2010.12.004 PG 11 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200015 ER PT J AU Jennett, H Hagopian, LP Beaulieu, L AF Jennett, Heather Hagopian, Louis P. Beaulieu, Lauren TI Analysis of heart rate and self-injury with and without restraint in an individual with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Self-injury; Heart rate; Physiological measurement; Restraint; Anxiety ID BEHAVIOR AB The relation between self-injury and heart rate was analyzed for an individual who appeared anxious while engaging in self-injury. The analysis involved manipulating the presence or absence of restraint while simultaneously measuring heart rate. The following findings were obtained and replicated: (a) when some form of restraint was applied, heart rate was typically within or close to the range of resting heart rate; (b) when restraint was removed or signaled to be removed, heart rate increased dramatically within a short time period; and (c) when restraint was re-applied, heart rate decreased and eventually returned to resting range within a couple of minutes. Recommendations for the assessment of anxiety in individuals with limited verbal skills are discussed. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Jennett, Heather] Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD 21205 USA. [Jennett, Heather; Hagopian, Louis P.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RP Jennett, H (reprint author), Kennedy Krieger Inst, Neurobehav Unit, 707N Broadway, Baltimore, MD 21205 USA. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1110 EP 1118 DI 10.1016/j.rasd.2010.12.007 PG 9 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200017 ER PT J AU Dillenburger, K AF Dillenburger, Karola TI The Emperor's new clothes: Eclecticism in autism treatment SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism Spectrum Disorders; Eclectic; ABA; Applied Behaviour Analysis; Government reports ID INTENSIVE BEHAVIORAL INTERVENTION; YOUNG-CHILDREN; SOCIAL VALIDITY; DISORDER AB Increasingly, Applied Behaviour Analysis (ABA) is internationally recognised as the scientific basis for teaching and treatment in Autism Spectrum Disorders. Yet, many governments and professionals across Europe promote an eclectic model as more child-centred and pragmatic. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1119 EP 1128 DI 10.1016/j.rasd.2010.12.008 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200018 ER PT J AU Lin, JD Hung, WJ Lin, LP Lai, CI AF Lin, Jin-Ding Hung, Wen-Jiu Lin, Lan-Ping Lai, Chia-Im TI Utilization and expenditure of hospital admission in patients with autism spectrum disorder: National Health Insurance claims database analysis SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism spectrum disorder; Hospital admission; Medical expenditure ID CARE EXPENDITURES; CHILDREN AB There were not many studies to provide information on health access and health utilization of people with autism spectrum disorders (ASD). The present study describes a general profile of hospital admission and the medical cost among people with ASD, and to analyze the determinants of medical cost. A retrospective study was employed to analyze medical fee of 397 individuals with ASD based on population-based National Health Insurance (NHI) claims data in Taiwan. The average frequency of hospital admission in the respondents was 3.5 annually, mean of hospital stay was 111.9 days, and the mean medical expenditure was 94,293 NTD in the year of 2005. Those autistic individuals with characteristics of younger age (OR = 31.085, 95% CI = 12.772-75.659), hold a serious illness card (OR = 4.980, 95% CI = 1.690-14.673), more frequent in inpatient care (OR = 7.636, 95% Cl = 2.643-22.066), longer days in acute ward (OR = 3.840, 95% CI = 1.989-7.416), and days in acute + chronic wards (OR = 3.804, 95% CI = 1.334-10.846) were more likely to consume more medical expenditure than their counterparts. The present study provides valuable medical care utilization information to health care decision makers to initiate a supportive healing environment for people with ASD. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Lin, Jin-Ding; Hung, Wen-Jiu] Natl Def Med Ctr, Sch Publ Hlth, Taipei, Taiwan. [Lin, Lan-Ping] Natl Def Med Ctr, Grad Inst Life Sci, Taipei, Taiwan. [Lai, Chia-Im] Natl Def Med Ctr, Triserv Gen Hosp, Off Med Serv, Taipei, Taiwan. RP Lin, JD (reprint author), Natl Def Med Ctr, Sch Publ Hlth, 161,Min Chun E Rd,Sect 6, Taipei, Taiwan. EM a530706@ndmctsgh.edu.tw CR Bauman ML, 2010, NEUROTHERAPEUTICS, V7, P320, DOI 10.1016/j.nurt.2010.06.001 Brooks R., 2004, CURRENT PAEDIAT, V14, P208, DOI 10.1016/j.cupe.2004.02.002 Brown HK, 2010, RES AUTISM SPECT DIS, V4, P539, DOI 10.1016/j.rasd.2009.12.009 CDC (Cent. Dis. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1138 EP 1142 DI 10.1016/j.rasd.2010.12.010 PG 5 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200020 ER PT J AU Lambrechts, G Van Leeuwen, K Boonen, H Maes, B Noens, I AF Lambrechts, Greet Van Leeuwen, Karla Boonen, Hannah Maes, Bea Noens, Ilse TI Parenting behaviour among parents of children with autism spectrum disorder SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Parenting behaviour; Autism spectrum disorder ID PRESCHOOL-CHILDREN; COGNITIVE-STYLE; WEAK COHERENCE; MOTHERS; STRESS; FATHERS; MIND AB Contrary to the extensive amount of empirical findings about parental perceptions, parenting cognitions, and coping in families with a child with autism spectrum disorder (ASD), research about parenting itself is very scarce. A first goal of this study was to examine the factor structure and internal consistency of two scales to measure parenting behaviour: the Parental Behaviour Scale-short version (PBS, Van Leeuwen, 2002; Van Leeuwen & Vermulst, 2004, 2010) and a new scale to measure parenting behaviours more specifically relevant to children with ASD. A second goal was to compare general and more specific parenting behaviour among parents of children with and without ASD. The participants were 305 parents of a child with ASD between 8 and 18 years old and 325 parents of a typically developing child between 8 and 18 years old. Parents completed both scales. Exploratory factor analysis of the new scale resulted in two factors: Stimulating the Development and Adapting the Environment. Multisample confirmatory factor analyses showed good fit indices for the noninvariant model of both the PBS and the new scale. Mean level analyses revealed significant main effects of group with higher mean scores for the control group in comparison with the experimental group for the subscale Harsh Punishment and the reversed effect for the subscale Stimulating the Development. We concluded that it is possible to use the parenting constructs of the PBS-short version to investigate parenting behaviour of parents with and without children with ASD. Furthermore, the new scale showed a relatively stable two factor structure for the control group as well as for the experimental group. The two factors 'Stimulating the child's Development' and 'Adapting the child's Environment' were also convincing as regards content. A first indication was found that parents of children with ASD indeed use more specifically relevant parenting behaviours. It is self-evident that more research is needed to gain further insight into the nature of these behaviours. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Lambrechts, Greet; Van Leeuwen, Karla; Boonen, Hannah; Maes, Bea; Noens, Ilse] Katholieke Univ Leuven, Parenting & Special Educ Res Grp, B-3000 Louvain, Belgium. [Lambrechts, Greet; Boonen, Hannah; Noens, Ilse] Katholieke Univ Leuven, Leuven Autism Res Consortium LAuRes, B-3000 Louvain, Belgium. [Noens, Ilse] Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA. RP Lambrechts, G (reprint author), Katholieke Univ Leuven, Parenting & Special Educ Res Grp, Vesaliusstr 2,POB 3765, B-3000 Louvain, Belgium. EM Greet.Lambrechts@ped.kuleuven.be; Karla.Vanleeuwen@ped.kuleuven.be; Hannah.Boonen@ped.kuleuven.be; Bea.Maes@ped.kuleuven.be; Ilse.Noens@ped.kuleuven.be CR Bentler P. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1143 EP 1152 DI 10.1016/j.rasd.2010.12.011 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200021 ER PT J AU Singh, NN Lancioni, GE Manikam, R Winton, ASW Singh, ANA Singh, J Singh, ADA AF Singh, Nirbhay N. Lancioni, Giulio E. Manikam, Ramasamy Winton, Alan S. W. Singh, Ashvind N. A. Singh, Judy Singh, Angela D. A. TI A mindfulness-based strategy for self-management of aggressive behavior in adolescents with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Aggression; Meditation on the Soles of the Feet; Treatment for aggression ID INTELLECTUAL DISABILITIES; CHALLENGING BEHAVIORS; MENTAL-RETARDATION; CHILDREN; INTERVENTIONS; INDIVIDUALS; ILLNESS; SUPPORT; PEOPLE; ANGER AB Some individuals with autism engage in physical aggression to an extent that interferes with not only their quality of life, but also that of their parents and siblings. Behavioral and psychopharmacological treatments have been the mainstay of treatments for aggression in children and adolescents with autism. We evaluated the effectiveness of a mindfulness-based procedure, Meditation on the Soles of the Feet, in helping three adolescents to manage their physical aggression. This procedure required the adolescents to rapidly shift the focus of their attention from the aggression-triggering event to a neutral place on their body, the soles of their feet. Incidents of aggression across the three adolescents ranged from a mean of 14-20 per week during baseline, 4-6 per week during mindfulness training, including zero rates during the last 4 weeks of intervention. Aggression occurred a rate of about 1 per year during a 3-year follow-up. Our results suggest adolescents with autism can learn, and effectively use, a mindfulness-based procedure to self-manage their physical aggression over several years. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Singh, Nirbhay N.; Manikam, Ramasamy; Singh, Ashvind N. A.; Singh, Judy; Singh, Angela D. A.] Amer Hlth & Wellness Inst, Verona, VA USA. [Lancioni, Giulio E.] Univ Bari, I-70121 Bari, Italy. [Winton, Alan S. W.] Massey Univ, Palmerston North, New Zealand. RP Singh, NN (reprint author), Amer Hlth & Wellness Inst, POB 5419, Midlothian, VA USA. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1153 EP 1158 DI 10.1016/j.rasd.2010.12.012 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200022 ER PT J AU Lanovaz, MJ Sladeczek, IE AF Lanovaz, Marc J. Sladeczek, Ingrid E. TI Vocal stereotypy in children with autism: Structural characteristics, variability, and effects of auditory stimulation SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Matched stimulation; Music; Structural characteristics; Variability; Vocal stereotypy ID MENTAL-RETARDATION; MATCHED STIMULATION; YOUNG-CHILDREN; BODY-ROCKING; BEHAVIOR; SKILLS; INTERVENTION AB Two experiments were conducted to examine (a) the relationship between the structural characteristics (i.e., bout duration, inter-response time [IRT], pitch, and energy) and overall duration of vocal stereotypy, and (b) the effects of auditory stimulation on the duration and temporal structure of the behavior. In the first experiment, we measured the structural characteristics of vocal stereotypy in five children with autism during five 30-min free-operant sessions. The results suggested that the structure of vocal stereotypy varied considerably within and across participants. Furthermore, the overall duration of vocal stereotypy was positively correlated with bout duration and negatively correlated with IRT. In the second experiment, reversal designs were used to examine the effects of noncontingent access to auditory stimulation (i.e., music) on the vocal stereotypy of three participants. Music decreased engagement in vocal stereotypy for two of the participants. The reductions were mostly associated with a considerable increase in IRT. The implications of the results are discussed in terms of measuring the structural characteristics of vocal stereotypy to identify more effective matched stimuli and using music to facilitate the implementation of other interventions. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Lanovaz, Marc J.; Sladeczek, Ingrid E.] McGill Univ, Dept Educ & Counselling Psychol, Montreal, PQ H3A 1Y2, Canada. RP Lanovaz, MJ (reprint author), McGill Univ, Dept Educ & Counselling Psychol, 3700 McTavish St, Montreal, PQ H3A 1Y2, Canada. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1159 EP 1168 DI 10.1016/j.rasd.2011.01.001 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200023 ER PT J AU Wouters, SGM Spek, AA AF Wouters, Saskia G. M. Spek, Annelies A. TI The use of the Autism-spectrum Quotient in differentiating high-functioning adults with autism, adults with schizophrenia and a neurotypical adult control group SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Schizophrenia; Autism-spectrum Quotient ID DSM-III-R; WAIS-III; ONSET SCHIZOPHRENIA; SOCIAL COMPETENCE; AQ; RELIABILITY; DISORDER; INTERVIEW; INSIGHT; SAMPLE AB The present study compared 21 high functioning individuals with autism, 21 individuals with schizophrenia and 21 healthy individuals in self-reported features of autism, as measured by the Autism-spectrum Quotient (AQ). The individuals with autism reported impairment on all AQ subscales, compared to the neurotypical group. The schizophrenia group reported deficits on all subscales except Attention to Detail, compared to the neurotypical group. The autism group reported more impairment than the individuals with schizophrenia in Social skill, Communication and Attention switching. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Wouters, Saskia G. M.] Open Univ, NL-5612 AB Eindhoven, Netherlands. [Spek, Annelies A.] Mental Hlth Inst GGZ Eindhoven, NL-5600 WC Eindhoven, Netherlands. RP Wouters, SGM (reprint author), Open Univ, John F Kennedylaan 2, NL-5612 AB Eindhoven, Netherlands. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1169 EP 1175 DI 10.1016/j.rasd.2011.01.002 PG 7 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200024 ER PT J AU Dewrang, P Sandberg, AD AF Dewrang, Petra Sandberg, Annika Dahlgren TI Repetitive behaviour and obsessive-compulsive features in Asperger syndrome: Parental and self-reports SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Asperger syndrome; Ritualistic behaviour; Obsessive-compulsive features; Self-evaluation; Parental evaluation ID HIGH-FUNCTIONING AUTISM; YOUNG-CHILDREN; PSYCHOMETRIC PROPERTIES; DISORDER; ANXIETY; RITUALS; SCALE; PSYCHOPATHOLOGY; INDIVIDUALS; IMPAIRMENT AB Symptoms of repetitive, obsessive and compulsive behaviour were explored in a group of adolescents and young adults with Asperger syndrome and compared to a typically developing group. By means of self-evaluations and an interview regarding such symptoms with the adolescents and young adults and parental evaluations, the parents retrospectively assessed the behaviour of their children from preschool years to middle teens, and the young participants assessed their own behaviour from school years until present time. An anxiety scale was also used. The results revealed no significant differences between the groups on the interview and the anxiety scale. There were, however, significant differences on both the parental and the self-evaluations. Thus, the parents reported that their children had difficulties with repetitive, obsessive-compulsive behaviour, and social interaction from preschool years, and both the parents and the adolescents and young adults reported considerable difficulties in those areas during school years. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1176 EP 1186 DI 10.1016/j.rasd.2011.01.003 PG 11 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200025 ER PT J AU Iwanami, A Okajima, Y Ota, H Tani, M Yamada, T Hashimoro, R Kanai, C Watanabe, H Yamasue, H Kawakubo, Y Kato, N AF Iwanami, Akira Okajima, Yuka Ota, Haruhisa Tani, Masayuki Yamada, Takashi Hashimoro, Ryuichiro Kanai, Chieko Watanabe, Hiromi Yamasue, Hidenori Kawakubo, Yuki Kato, Nobumasa TI Task dependent prefrontal dysfunction in persons with Asperger's disorder investigated with multi-channel near-infrared spectroscopy SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Asperger's disorder; PDD; NIRS; Prefrontal dysfunction; Verbal fluency task ID PERVASIVE DEVELOPMENTAL DISORDERS; VERBAL FLUENCY TASK; REDUCED FRONTOPOLAR ACTIVATION; EXECUTIVE FUNCTION DEFICITS; AUTISM SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; BRAIN ACTIVATION; JAPANESE VERSION; QUOTIENT AQ; ADULTS AB Dysfunction of the prefrontal cortex has been previously reported in individuals with Asperger's disorder. In the present study, we used multi-channel near-infrared spectroscopy (NIRS) to detect changes in the oxygenated hemoglobin concentration ([oxy-Hb]) during two verbal fluency tasks. The subjects were 20 individuals with Asperger's disorder and 18 age- and IQ-matched healthy controls. The relative [oxy-Hb] in the prefrontal cortex was measured during the category and letter fluency tasks. The mean total [oxy-Hb] during the category fluency task did not differ significantly between the groups; however, during the letter fluency task, the mean [oxy-Hb] in persons with Asperger's disorder was significantly lower than that in controls. These results suggested task-relevant or task-specific prefrontal dysfunction in persons with Asperger's disorder. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Iwanami, Akira; Okajima, Yuka; Ota, Haruhisa; Tani, Masayuki; Yamada, Takashi; Hashimoro, Ryuichiro; Kanai, Chieko; Watanabe, Hiromi; Kato, Nobumasa] Showa Univ, Sch Med, Dept Psychiat, Shinagawa Ku, Tokyo 1428655, Japan. [Yamasue, Hidenori; Kawakubo, Yuki] Univ Tokyo, Grad Sch, Dept Neuropsychiat, Tokyo 1130033, Japan. RP Iwanami, A (reprint author), Showa Univ, Sch Med, Dept Psychiat, Shinagawa Ku, 1-5-8 Hatanodai, Tokyo 1428655, Japan. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1187 EP 1193 DI 10.1016/j.rasd.2011.01.005 PG 7 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200026 ER PT J AU Sanefuji, W Ohgami, H AF Sanefuji, Wakako Ohgami, Hidehiro TI Children's responses to the image of self, peer, and adult: Autism and typical development SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Self-other understanding; Preference; Similarity; Autism ID SPECTRUM DISORDER; SOCIAL COGNITION; INTENTIONAL ATTUNEMENT; EARLY RECOGNITION; HOME VIDEOTAPES; JOINT ATTENTION; IMITATION; INFANCY; PREFERENCE; STIMULI AB The typical development (TD) of social cognition could be rooted in the implicit notion that others are like the self. Although many studies show their impairment of social orienting, such a primary notion in children with autistic disorder (AD) has not been known. The present paper examined the responses of children with AD to stimuli such as others with similar features as the self. The preferential looking paradigm was used to assess the responses of children with AD to others of the same or different age (i.e., peer or adult), and compare these responses to those of children with TD. Subsequently, the same participants' responses to the self and peer were also examined. The results revealed that children with AD did not show preferential responses to peer nor adult, but showed a looking preference for their own images: on the other hand, children with TD preferred to look at both peer and the self. It could be interpreted that children with AD might not be able to generalize their understanding of the self to that of others at least at the visual level, whereas children with TD should, on the basis of self-recognition, detect similarity and perceive familiarity with others of the same age as themselves. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Sanefuji, Wakako] Osaka Univ, Mol Res Ctr Childrens Mental Dev, Suita, Osaka 5650871, Japan. [Ohgami, Hidehiro] Kyushu Univ, Fac Human Environm Studies, Higashi Ku, Fukuoka 8128581, Japan. RP Sanefuji, W (reprint author), Osaka Univ, Mol Res Ctr Childrens Mental Dev, 2-2 Yamadaoka, Suita, Osaka 5650871, Japan. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1194 EP 1200 DI 10.1016/j.rasd.2011.01.006 PG 7 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200027 ER PT J AU Kowalski, RM Fedina, C AF Kowalski, Robin M. Fedina, Cristin TI Cyber bullying in ADHD and Asperger Syndrome populations SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Bullying; Cyber bullying; Asperger's Syndrome; Attention deficit hyperactivity disorder (ADHD); Peer victimization ID HEALTH-CARE NEEDS; SPECTRUM DISORDERS; PEER VICTIMIZATION; CHILDREN; AUTISM; STUDENTS; SCHOOL; EXPERIENCES; ADOLESCENTS; PREVALENCE AB Cyber bullying or electronic bullying refers to bullying that occurs through the Internet or cellular phones. With the rise of technology, researchers have shown a keen interest in the topic of cyber bullying. However, that interest has not extended to individuals with special needs. To address this gap in the literature, the current study examined the prevalence of both "traditional" bullying and cyber bullying in youth with ADHD and/or Asperger's Syndrome, and assessed the social, psychological, and health effects of bullying on participants. In addition, the study addressed the disconnect between parents' understanding of their child's online experiences and their child's actual experiences in the virtual world. Forty-two children and youth reported high rates of bullying victimization through both traditional and electronic means. Individuals not involved with bullying showed greater levels of physical and psychological health relative to those involved with bullying. Parents and children disagreed on a number of issues related to use of the Internet, indicating the need for more clear communication between parents and their children. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1201 EP 1208 DI 10.1016/j.rasd.2011.01.007 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200028 ER PT J AU Stauder, JEA Cornet, LJM Ponds, RWHM AF Stauder, J. E. A. Cornet, L. J. M. Ponds, R. W. H. M. TI The Extreme Male Brain theory and gender role behaviour in persons with an autism spectrum condition SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Extreme Male Brain theory; Gender role behaviour; Psychosexual behaviour ID ADRENAL-HYPERPLASIA CAH; HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; QUOTIENT; ANDROGEN; MIND; TESTOSTERONE; IDENTITY; ADULTS AB According to the Extreme Male Brain theory persons with autism possess masculinised cognitive traits. In this study masculinisation of gender role behaviour is evaluated in 25 persons with an autism spectrum condition (ASC) and matched controls with gender role behaviour as part of a shortened version of the Minnesota Multiphasic Personality Inventory-2 and the Empathizing Quotient and Systemizing Quotient. Both males and females with an ASC showed minimum male role behaviour. It is suggested that the minimum male gender role could be related to an underdeveloped Theory of Mind, a well-known feature of autism. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Stauder, J. E. A.; Cornet, L. J. M.] Maastricht Univ, Dept Neurocognit, Fac Psychol & Neurosci, NL-6200 MD Maastricht, Netherlands. [Ponds, R. W. H. M.] Maastricht Univ, Fac Hlth Med & Life Sci, Sch Mental Hlth & Neurosci, NL-6200 MD Maastricht, Netherlands. RP Stauder, JEA (reprint author), Maastricht Univ, Dept Neurocognit, Fac Psychol & Neurosci, POB 616, NL-6200 MD Maastricht, Netherlands. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1209 EP 1214 DI 10.1016/j.rasd.2011.01.008 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200029 ER PT J AU McTiernan, A Leader, G Healy, O Mannion, A AF McTiernan, Aoife Leader, Geraldine Healy, Olive Mannion, Arlene TI Analysis of risk factors and early predictors of challenging behavior for children with autism spectrum disorder SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Challenging behavior; Risk factors; IQ; Stereotyped behavior; Aggression; Self-injurious behavior ID YOUNG-CHILDREN; TOTAL POPULATION; INTERVENTION; PREVALENCE; SYMPTOMS AB The current study evaluated risk factors for the occurrence, frequency and severity of challenging behavior among a sample of individuals with a diagnosis of autism, under the age of eighteen, in Ireland. Age, gender, hours of intervention received, age at diagnosis, presence of challenging behavior at diagnosis and treatment type at diagnosis were not found to be significant predictors for the frequency or severity of challenging behavior. The participants' IQ was found to be a significant predictor of the frequency and severity of the behaviors measured. Lower IQ predicted greater frequencies of stereotyped behavior, aggression and self-injurious behavior along with increased severity of stereotyped behavior and self-injurious behavior. The intervention participants were currently receiving was not significant in predicting the frequency of challenging behavior, nor the severity of aggressive or self-injurious behaviors. However, this variable was a significant predictor of severity of stereotyped behaviors with individuals currently in Applied Behavior Analysis interventions presenting with more severe stereotyped behavior than those currently in "eclectic" interventions. Additional findings and implications in relation to these variables are discussed. (C) 2011 Published by Elsevier Ltd. C1 [McTiernan, Aoife; Leader, Geraldine; Healy, Olive; Mannion, Arlene] Natl Univ Ireland, Sch Psychol, Galway, Ireland. RP Leader, G (reprint author), Natl Univ Ireland, Sch Psychol, Galway, Ireland. EM geraldine.leader@nuigalway.ie CR Baghdadli A, 2003, J INTELL DISABIL RES, V47, P622, DOI 10.1046/j.1365-2788.2003.00507.x Cunningham AB, 2008, RES AUTISM SPECT DIS, V2, P469, DOI 10.1016/j.rasd.2007.09.006 Eikeseth S, 2002, BEHAV MODIF, V26, P49, DOI 10.1177/0145445502026001004 Emerson E, 2001, RES DEV DISABIL, V22, P77, DOI 10.1016/S0891-4222(00)00061-5 Emerson E, 2001, RES DEV DISABIL, V22, P67, DOI 10.1016/S0891-4222(00)00062-7 Filipek PA, 2000, NEUROLOGY, V55, P468 Foxx RM, 2007, BEHAV INTERVENT, V22, P69, DOI 10.1002/bin.232 Holden B, 2006, RES DEV DISABIL, V27, P456, DOI 10.1016/j.ridd.2005.06.001 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 Matson JL, 2008, RES AUTISM SPECT DIS, V2, P60, DOI 10.1016/j.rasd.2007.03.003 Matson JL, 2007, RES DEV DISABIL, V28, P567, DOI 10.1016/j.ridd.2006.08.001 Moss S, 2000, BRIT J PSYCHIAT, V177, P452, DOI 10.1192/bjp.177.5.452 Murphy O., 2009, RES AUTISM SPECT DIS, V3, P291 Remington B, 2007, AM J MENT RETARD, V112, P418, DOI 10.1352/0895-8017(2007)112[418:EIBIOF]2.0.CO;2 Rojahn J, 2001, J AUTISM DEV DISORD, V31, P577, DOI 10.1023/A:1013299028321 Zachor DA, 2007, RES AUTISM SPECT DIS, V1, P304, DOI 10.1016/j.rasd.2006.12.001 NR 16 TC 22 Z9 22 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 JUL-SEP PY 2011 VL 5 IS 3 BP 1215 EP 1222 DI 10.1016/j.rasd.2011.01.009 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200030 ER PT J AU Goldman, SE McGrew, S Johnson, KP Richdale, AL Clemons, T Malow, BA AF Goldman, Suzanne E. McGrew, Susan Johnson, Kyle P. Richdale, Amanda L. Clemons, Traci Malow, Beth A. TI Sleep is associated with problem behaviors in children and adolescents with Autism Spectrum Disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Sleep problems; Behavior problems; Parental Concerns Checklist; Children's Sleep Habits Questionnaire; Autism Spectrum Disorder ID SELF-INJURIOUS-BEHAVIOR; PRESCHOOL-AGE CHILDREN; DEVELOPMENTAL DELAYS; ASPERGERS-DISORDER; QUESTIONNAIRE; DISTURBANCES; PREVALENCE; SYMPTOMS; HABITS; ADULTS AB Multiple sleep problems have been reported in children with Autism Spectrum Disorder (ASD). The association of poor sleep with problematic daytime behaviors has been shown in small studies of younger children. We assessed the relationship between sleep and behavior in 1784 children, ages 2-18, with confirmed diagnosis of ASD participating in the Autism Treatment Network. Sleep problems were identified using the Children's Sleep Habits Questionnaire (CSHQ). The Parental Concerns Questionnaire (PCQ) was used to evaluate behavioral concerns and to define good or poor sleepers. Poor sleepers had a higher percentage of behavioral problems on all PCQ scales than good sleepers. Over three-fourths had problems with attention span and social interactions. Further delineation of this phenotype will help guide future interventions. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Goldman, Suzanne E.; Malow, Beth A.] Vanderbilt Univ, Med Ctr, Dept Neurol, Sleep Disorders Program, Nashville, TN 37232 USA. [McGrew, Susan] Vanderbilt Univ, Med Ctr, Ctr Child Dev, Nashville, TN 37203 USA. [Johnson, Kyle P.] Oregon Hlth & Sci Univ, Portland, OR 97239 USA. [Richdale, Amanda L.] La Trobe Univ, Olga Tennison Autism Res Ctr, Sch Psychol Sci, Bundoora, Vic, Australia. [Clemons, Traci] EMMES Corp, Rockville, MD USA. RP Goldman, SE (reprint author), Vanderbilt Univ, Med Ctr, Dept Neurol, Sleep Disorders Program, 1161 21st Ave S,Room AA0232B, Nashville, TN 37232 USA. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1223 EP 1229 DI 10.1016/j.rasd.2011.01.010 PG 7 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200031 ER PT J AU Akechi, H Senju, A Kikuchi, Y Tojo, Y Osanai, H Hasegawa, T AF Akechi, Hironori Senju, Atsushi Kikuchi, Yukiko Tojo, Yoshikuni Osanai, Hiroo Hasegawa, Toshikazu TI Do children with ASD use referential gaze to learn the name of an object? An eye-tracking study SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism spectrum disorder; Gaze reference; Word learning; Eye tracking; Children; Social cognition ID AUTISM SPECTRUM DISORDER; JOINT ATTENTION; 2-YEAR-OLD CHILDREN; DIRECTION; INFANTS; CUES; FACES; AGE AB Children with autism spectrum disorder (ASD) are reported to have difficulty in learning novel word-object associations in case of discrepancy between objects in the speaker's focus and their focus (the discrepant condition). Two eye-tracking experiments investigated this difficulty by controlling and recording children's gaze fixation. In Experiment Vs discrepant condition, typically developing (TD) children (age: 6-11 years) mapped the novel word to the novel object in the speaker's focus more frequently than children with ASD (age: 6-11 years). Additionally, the former looked at the object in the speaker's focus longer than the object in their own focus, while the latter looked at these objects for the same duration. In Experiment 2, the saliency of the object in the speaker's focus was enhanced and children with ASD (age: 6-12 years) mapped the word to the object in the speaker's focus as well as TD children (age: 6-12 years). Moreover, they looked at the object in the speaker's focus longer than the object in their focus. Comparison between experiments also confirmed improvement in performance, suggesting that the duration of gaze at an object in the speaker's focus is related to difficulty in referential word learning in children with ASD. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Akechi, Hironori; Kikuchi, Yukiko; Hasegawa, Toshikazu] Univ Tokyo, Dept Cognit & Behav Sci, Meguro Ku, Tokyo, Japan. [Senju, Atsushi] Univ London, Ctr Brain & Cognit Dev, London, England. [Tojo, Yoshikuni] Ibaraki Univ, Dept Educ Children Disabil, Ibaraki, Japan. [Osanai, Hiroo] Musashino Higashi Ctr Educ & Res, Tokyo, Japan. RP Akechi, H (reprint author), Univ Tokyo, Dept Cognit & Behav Sci, Meguro Ku, 3-8-1 Komaba, Tokyo, Japan. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1230 EP 1242 DI 10.1016/j.rasd.2011.01.013 PG 13 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200032 ER PT J AU Pry, R Petersen, AF Baghdadli, AM AF Pry, Rene Petersen, Arne F. Baghdadli, A. Maria TI On general and specific markers of lexical development in children with autism from 5 to 8 years of age SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism spectrum disorder; Prediction of language production; Phonological and lexical development; Developmental trajectories ID COMMUNICATIVE DEVELOPMENT INVENTORY; MENTALLY-RETARDED SUBJECTS; LANGUAGE-ACQUISITION; PHONOLOGICAL DEVELOPMENT; SPECTRUM DISORDER; ASPERGER-SYNDROME; INFANTILE-AUTISM; DEFICITS; OUTCOMES; SKILLS AB Delays in language production in children with autism (ASD) are now well known. For parents and clinicians, the possibility of using the first vocal productions as prognostic indications has been tempting. However, such an approach implies questions of predictability and the development of language. To describe and analyze certain relationships between phonological and lexical development with the aim of determining a simple prognostic indicator, 60 children were observed twice, at 5 years of age (T1) and three years later (T2). Linguistic data were obtained in a semi-standardized situation (ADDS-G) and from parents (ADI-R, Item 19), and analyzed with CHILDES. At Ti, the sample was distributed into a 'verbal' and a 'non-verbal' group. From Ti to T2, the sample replicated the four trajectories known from pathological development characterized by stability, progression and regression. A multiple regression analysis for predicting morpheme production at T2 showed that two general markers (CARS and DLS, being 'risk factors') and one specific marker (phoneme production, a 'protection' factor) were significantly related to lexical development. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Pry, Rene] Univ Montpellier III, Dept Psychol, Montpellier, France. [Petersen, Arne F.] CHU Montpellier, Ctr Resource Autism, Montpellier, France. RP Pry, R (reprint author), Univ Montpellier III, Dept Psychol, Montpellier, France. 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PD JUL-SEP PY 2011 VL 5 IS 3 BP 1243 EP 1252 DI 10.1016/j.rasd.2011.01.014 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200033 ER PT J AU Osborne, LA Reed, P AF Osborne, Lisa A. Reed, Phil TI School factors associated with mainstream progress in secondary education for included pupils with Autism Spectrum Disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE School inclusion; Mainstream education; School characteristics; Behavior problems; Teacher training; School belonging ID BEHAVIOR CHECKLIST; DIFFICULTIES QUESTIONNAIRE; YOUNG-CHILDREN; STUDENTS; MEMBERSHIP; STRENGTHS; VALIDITY; OUTCOMES; SCALE; SIZE AB This research examined the factors promoting inclusion of young people with Autism Spectrum Disorders (ASD) in mainstream secondary schools, and noted high levels of behavioral difficulties in these pupils. The size of the secondary school, and the class size, impacted positively on the pupils with Autism, and the number of other pupils with Special Educational Needs (SEN) statements and the number of support staff per pupil were both positive factors in school progress for children with Autism, but not Asperger's Syndrome. Support teachers and assistants helped to reduce emotional and behavioral difficulties, but also reduced improvements in pro-social behavior. Good staff-training promoted the pupils' social behaviors and their sense of school belonging. In summary, social-emotional behaviors are better facilitated in mainstream secondary schools with larger numbers of other children with SEN statements, individual support, which helps emotional and behavioral difficulties, but does not facilitate social behaviors, good teacher-training, which facilitates social behaviors, and a sense of school belonging. (C) 2011 Elsevier Ltd. All rights reserved. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1253 EP 1263 DI 10.1016/j.rasd.2011.01.016 PG 11 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200034 ER PT J AU Senju, A Kikuchi, Y Akechi, H Hasegawa, T Tojo, Y Osanai, H Johnson, MH AF Senju, Atsushi Kikuchi, Yukiko Akechi, Hironori Hasegawa, Toshikazu Tojo, Yoshikuni Osanai, Hiroo Johnson, Mark H. TI Atypical modulation of face-elicited saccades in autism spectrum disorder in a double-step saccade paradigm SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism spectrum disorder; Face processing; Subcortical route; Superior colliculus; Double saccade; Eye tracking ID EARLY INFANCY; STIMULI; EYE; TODDLERS; AMYGDALA; CHILDREN; FRAMES AB Atypical development of face processing is a major characteristic in autism spectrum disorder (ASD), which could be due to atypical interactions between subcortical and cortical face processing. The current study investigated the saccade planning towards faces in ASD. Seventeen children with ASD and 17 typically developing (TD) children observed a pair of upright or inverted face configurations flashed sequentially in two different spatial positions. The reactive saccades of participants were recorded by eye-tracking. The results did not provide evidence of overall impairment of subcortical route in ASD, However, the upright, but not the inverted, face configuration modulated the frequency of vector sum saccades (an index of subcortical control) in TD, but not in ASD. The current results suggest that children with ASD do not have overall impairment of the subcortical route, but the subcortical route may not be specialized to face processing. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Senju, Atsushi; Johnson, Mark H.] Univ London, Ctr Brain & Cognit Dev, London WC1E 7HX, England. [Kikuchi, Yukiko; Akechi, Hironori; Hasegawa, Toshikazu] Univ Tokyo, Dept Cognit & Behav Sci, Tokyo, Japan. [Tojo, Yoshikuni] Ibaraki Univ, Sch Educ, Ibaraki, Japan. [Osanai, Hiroo] Ctr Educ & Res, Tokyo, Japan. RP Senju, A (reprint author), Univ London, Ctr Brain & Cognit Dev, Malet St, London WC1E 7HX, England. 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Autism Spectr. Disord. PD JUL-SEP PY 2011 VL 5 IS 3 BP 1264 EP 1269 DI 10.1016/j.rasd.2011.01.021 PG 6 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA 747NR UT WOS:000289327200035 ER PT J AU Lukose, R Schmidt, E Wolski, TP Murawski, NJ Kulesza, RJ AF Lukose, Richard Schmidt, Elise Wolski, Thomas P., Jr. Murawski, Nathen J. Kulesza, Randy J., Jr. TI Malformation of the superior olivary complex in an animal model of autism SO BRAIN RESEARCH LA English DT Article DE Development; Olive; Trapezoid body; Hearing; Auditory ID BRAIN-STEM RESPONSES; FETAL VALPROATE SYNDROME; EARLY INFANTILE-AUTISM; SPECTRUM DISORDER; PRENATAL EXPOSURE; MOUSE MODEL; DEVELOPMENTAL NEUROBIOLOGY; MORPHOLOGICAL FEATURES; BEHAVIORAL ALTERATIONS; ANTIEPILEPTIC DRUGS AB Autism is a neurodevelopmental disorder characterized by social difficulties, impaired communication skills and repetitive behavioral patterns. Additionally, there is evidence that auditory deficits are a common feature of the autism spectrum disorders. Despite the prevalence of autism, the neurobiology of this disorder is poorly understood. However, abnormalities in neuronal morphology, cell number and connectivity have been described throughout the autistic brain. Indeed, we have demonstrated significant dysmorphology in the superior olivary complex (SOC), a collection of auditory brainstem nuclei, in the autistic brain. Prenatal exposure to valproic acid (VPA) in humans has been associated with autism and in rodents prenatal VPA exposure produces many neuroanatomical and behavioral deficits associated with autism. Thus, in an effort to devise an animal model of the autistic auditory brainstem, we have investigated neuronal number and morphology in animals prenatally exposed to valproic acid (VPA). In VPA exposed rats, we find significantly fewer neurons and significant alterations in neuronal morphology. Thus, prenatal VPA exposure in rats appears to produce similar dysmorphology as we have reported in the autistic human brain. (C) 2011 Elsevier B.V. All rights reserved. C1 [Schmidt, Elise; Wolski, Thomas P., Jr.; Kulesza, Randy J., Jr.] Lake Erie Coll Osteopath Med, Auditory Res Ctr, Erie, PA 16509 USA. [Lukose, Richard] Hamot Med Ctr, Dept Neurol, Erie, PA USA. [Murawski, Nathen J.] Univ Delaware, Dept Psychol, Newark, DE 19716 USA. RP Kulesza, RJ (reprint author), Lake Erie Coll Osteopath Med, Auditory Res Ctr, 1858 W Grandview Blvd, Erie, PA 16509 USA. 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For gamma to function as a clock, it must be autocoherent: phase and frequency conserved over a period of time. We computed phase and frequency trajectories of gamma-band bursts, using time-frequency analysis of LFPs recorded in macaque primary visual cortex (V1) during visual stimulation. The data were compared with simulations of random networks and clock signals in noise. Gamma-band bursts in LFP data were statistically indistinguishable from those found in filtered broadband noise. Therefore, V1 LFP data did not contain clock-like gamma-band signals. We consider possible functions for stochastic gamma-band activity, such as a synchronizing pulse signal. C1 [Burns, Samuel P.; Xing, Dajun; Shapley, Robert M.] NYU, Ctr Neural Sci, New York, NY 10012 USA. [Burns, Samuel P.; Xing, Dajun; Shapley, Robert M.] NYU, Courant Inst Math Sci, New York, NY 10012 USA. RP Burns, SP (reprint author), Johns Hopkins Univ, Dept Biomed Engn, Baltimore, MD 21218 USA. EM sburns9@jhu.edu RI Xing, Dajun/F-4217-2011 FU Swartz Foundation; NIH [T32-EY007158, R01 EY-01472]; National Science Foundation [IOS-745253] FX This work was supported by the Swartz Foundation and NIH Training Grant T32-EY007158. Robert M. Shapley and Dajun Xing were also supported by NIH Grant R01 EY-01472 and National Science Foundation Grant IOS-745253. CR Atallah BV, 2009, NEURON, V62, P566, DOI 10.1016/j.neuron.2009.04.027 Baker SN, 2000, J NEUROPHYSIOL, V84, P1770 Bracewell R. 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A deficit in oxytocin (OT)-producing neurons of the hypothalamic paraventricular nucleus has been reported in these patients. Methods: In a double-blind, randomised, placebo-controlled study, 24 adult patients with PWS received a single intranasal administration of 24 IU of OT or placebo and were tested 45 min later on social skills. Behaviours were carefully monitored and scored using an in-house grid as follows: over the two days before drug administration, on the half-day following administration, and over the subsequent two days. All patients were in a dedicated PWS centre with more than ten years of experience. Patients are regularly admitted to this controlled environment. Results: Patients with PWS who received a single intranasal administration of OT displayed significantly increased trust in others (P = 0.02) and decreased sadness tendencies (P = 0.02) with less disruptive behaviour (P = 0.03) in the two days following administration than did patients who received placebo. 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Here, we show that disrupted synchronization is evident in the spontaneous cortical activity of naturally sleeping toddlers with autism, but not in toddlers with language delay or typical development. Toddlers with autism exhibited significantly weaker interhemispheric synchronization (i.e., weak "functional connectivity" across the two hemispheres) in putative language areas. The strength of synchronization was positively correlated with verbal ability and negatively correlated with autism severity, and it enabled identification of the majority of autistic toddlers (72%) with high accuracy (84%). Disrupted cortical synchronization, therefore, appears to be a notable characteristic of autism neurophysiology that is evident at very early stages of autism development. C1 [Dinstein, Ilan; Pierce, Karen; Eyler, Lisa; Solso, Stephanie; Courchesne, Eric] Univ Calif San Diego, Autism Ctr Excellence, La Jolla, CA 92037 USA. [Eyler, Lisa] Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92037 USA. [Pierce, Karen; Courchesne, Eric] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92037 USA. [Dinstein, Ilan; Malach, Rafael] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel. [Behrmann, Marlene] Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. RP Dinstein, I (reprint author), Univ Calif San Diego, Autism Ctr Excellence, La Jolla, CA 92037 USA. EM ilan.dinstein@weizmann.ac.il FU NIMH Autism Center of Excellence [P50-MH081755]; NIMH [R01-MH080134, R01-MH036840]; NIH [F31-MH080457]; ISF and Bikura grants; Pennsylvania Department of Health SAP [4100047862]; NICHD/NIDCD [PO1/U19]; Simons Foundation SFARI FX Supported by NIMH Autism Center of Excellence grant P50-MH081755 (E.C.), NIMH grants R01-MH080134 (K.P.) and R01-MH036840 (E.C.), NIH grant F31-MH080457 (ID.), ISF and Bikura grants (R.M.), Pennsylvania Department of Health SAP grant 4100047862, NICHD/NIDCD PO1/U19, and Simons Foundation SFARI grant (M.B.). 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Eyles, Darryl W. Flatscher-Bader, Traute McGrath, John J. Burne, Thomas H. J. TI New perspectives on rodent models of advanced paternal age: relevance to autism SO FRONTIERS IN BEHAVIORAL NEUROSCIENCE LA English DT Article DE advanced paternal age; mouse; behavior; epigenetics; autism AB Offspring of older fathers have an increased risk of various adverse health outcomes, including autism and schizophrenia. With respect to biological mechanisms for this association, there are many more germline cell divisions in the life history of a sperm relative to that of an oocyte. This leads to more opportunities for copy error mutations in germ cells from older fathers. Evidence also suggests that epigenetic patterning in the sperm from older men is altered. Rodent models provide an experimental platform to examine the association between paternal age and brain development. Several rodent models of advanced paternal age (APA) have been published with relevance to intermediate phenotypes related to autism. All four published APA models vary in key features creating a lack of consistency with respect to behavioral phenotypes. A consideration of common phenotypes that emerge from these APA-related mouse models may be informative in the exploration of the molecular and neurobiological correlates of APA. C1 [Foldi, Claire J.; Eyles, Darryl W.; Flatscher-Bader, Traute; McGrath, John J.; Burne, Thomas H. J.] Univ Queensland, Queensland Brain Inst, St Lucia, Qld 4076, Australia. [Eyles, Darryl W.; McGrath, John J.; Burne, Thomas H. J.] Queensland Ctr Mental Hlth Res, Pk Ctr Mental Hlth, Richlands, Qld, Australia. [Flatscher-Bader, Traute] Queensland Inst Med Res, Herston, Qld 4006, Australia. [McGrath, John J.] Univ Queensland, Discipline Psychiat, St Lucia, Qld, Australia. RP Burne, THJ (reprint author), Univ Queensland, Queensland Brain Inst, St Lucia, Qld 4076, Australia. EM t.burne@uq.edu.au RI Burne, Thomas/C-5656-2009 OI Burne, Thomas/0000-0003-3502-9789 FU Queensland Health; National Health and Medical Research Council of Australia FX The authors are grateful for support from Queensland Health and the National Health and Medical Research Council of Australia. We thank Prof. E. Whitelaw and Dr S. Chong for valuable comments on the manuscript. 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Behav. Neurosci. PD JUN 23 PY 2011 VL 5 AR 32 DI 10.3389/fnbeh.2011.00032 PG 7 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA V29WL UT WOS:000208778400001 PM 21734873 ER PT J AU Holmes, AB Hawson, A Liu, F Friedman, C Khiabanian, H Rabadan, R AF holmes, Antony B. Hawson, Alexander Liu, Feng Friedman, Carol Khiabanian, Hossein Rabadan, Raul TI Discovering Disease Associations by Integrating Electronic Clinical Data and Medical Literature SO PLOS ONE LA English DT Article ID KAWASAKI-DISEASE; HEALTH RECORDS; TRAUMATIC STRESS; KAPOSIS-SARCOMA; VACCINATION; SYSTEM; AUTISM; PATHOGENESIS; CHALLENGES; INFECTION AB Electronic health record (EHR) systems offer an exceptional opportunity for studying many diseases and their associated medical conditions within a population. The increasing number of clinical record entries that have become available electronically provides access to rich, large sets of patients' longitudinal medical information. By integrating and comparing relations found in the EHRs with those already reported in the literature, we are able to verify existing and to identify rare or novel associations. Of particular interest is the identification of rare disease co-morbidities, where the small numbers of diagnosed patients make robust statistical analysis difficult. Here, we introduce ADAMS, an Application for Discovering Disease Associations using Multiple Sources, which contains various statistical and language processing operations. We apply ADAMS to the New York-Presbyterian Hospital's EHR to combine the information from the relational diagnosis tables and textual discharge summaries with those from PubMed and Wikipedia in order to investigate the co-morbidities of the rare diseases Kaposi sarcoma, toxoplasmosis, and Kawasaki disease. In addition to finding well-known characteristics of diseases, ADAMS can identify rare or previously unreported associations. In particular, we report a statistically significant association between Kawasaki disease and diagnosis of autistic disorder. C1 [holmes, Antony B.; Liu, Feng; Friedman, Carol; Khiabanian, Hossein; Rabadan, Raul] Columbia Univ Coll Phys & Surg, Dept Biomed Informat, New York, NY 10032 USA. [holmes, Antony B.; Hawson, Alexander; Khiabanian, Hossein; Rabadan, Raul] Columbia Univ Coll Phys & Surg, Ctr Computat Biol & Bioinformat, New York, NY 10032 USA. [Hawson, Alexander] Columbia Univ Coll Phys & Surg, Dept Med, New York, NY 10032 USA. RP Holmes, AB (reprint author), Columbia Univ Coll Phys & Surg, Dept Biomed Informat, 630 W 168th St, New York, NY 10032 USA. EM hossein@c2b2.columbia.edu FU Northeast Biodefense Center [U54-AI057158]; National Library of Medicine Eureka [1R01LM010140-01]; National Library of Medicine [LM008635] FX This work was supported by awards from the Northeast Biodefense Center grant U54-AI057158, the National Library of Medicine Eureka grant 1R01LM010140-01 and the National Library of Medicine grant LM008635. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Immune abnormalities, including autoimmunity with production of brain specific auto-antibodies, are also commonly observed in this disorder. Hyperserotonemia may be one of the contributing factors to autoimmunity in some patients with autism through the reduction of T-helper (Th) 1-type cytokines. We are the first to investigate the possible role of hyperserotonemia in the induction of autoimmunity, as indicated by serum anti-myelin-basic protein (anti-MBP) auto-antibodies, in autism. Methods: Serum levels of serotonin and anti-MBP auto-antibodies were measured, by ELISA, in 50 autistic patients, aged between 5 and 12 years, and 30 healthy-matched children. Results: Autistic children had significantly higher serum levels of serotonin and anti-MBP auto-antibodies than healthy children (P < 0.001 and P < 0.001, respectively). Increased serum levels of serotonin and anti-MBP auto-antibodies were found in 92% and 80%, respectively of autistic patients. Patients with severe autism had significantly higher serum serotonin levels than children with mild to moderate autism (P < 0.001). Serum serotonin levels had no significant correlations with serum levels of anti-MBP auto-antibodies in autistic patients (P = 0.39). Conclusions: Hyperserotonemia may not be one of the contributing factors to the increased frequency of serum anti-MBP auto-antibodies in some autistic children. These data should be treated with caution until further investigations are performed. However, inclusion of serum serotonin levels as a correlate may be useful in other future immune studies in autism to help unravel the long-standing mystery of hyperserotonemia and its possible role in the pathophysiology of this disorder. C1 [Mostafa, Gehan Ahmed; AL-Ayadhi, Laila Yousef] King Saud Univ, Dept Physiol, Autism Res & Treatment Ctr, AL Amodi Autism Res Chair,Fac Med, Riyadh, Saudi Arabia. [Mostafa, Gehan Ahmed] Ain Shams Univ, Fac Med, Dept Pediat, Cairo, Egypt. RP Mostafa, GA (reprint author), King Saud Univ, Dept Physiol, Autism Res & Treatment Ctr, AL Amodi Autism Res Chair,Fac Med, Riyadh, Saudi Arabia. EM hafezg@softhome.net FU King Abdulaziz City for Science and Technology, Riyadh, Saudi Arabia FX This work was financially supported by the King Abdulaziz City for Science and Technology, Riyadh, Saudi Arabia. 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Sokol, Deborah K. Lahiri, Debomoy K. TI Increased Secreted Amyloid Precursor Protein-alpha (sAPP alpha) in Severe Autism: Proposal of a Specific, Anabolic Pathway and Putative Biomarker SO PLOS ONE LA English DT Article ID FRAGILE-X-SYNDROME; NEURAL STEM-CELLS; AMINO-TERMINAL REGION; NEUROTROPHIC FACTOR; ALZHEIMERS-DISEASE; MESSENGER-RNA; DIAGNOSTIC INTERVIEW; HIPPOCAMPAL-NEURONS; MENTAL-RETARDATION; NEURITE OUTGROWTH AB Autism is a neurodevelopmental disorder characterized by deficits in verbal communication, social interactions, and the presence of repetitive, stereotyped and compulsive behaviors. Excessive early brain growth is found commonly in some patients and may contribute to disease phenotype. Reports of increased levels of brain-derived neurotrophic factor (BDNF) and other neurotrophic-like factors in autistic neonates suggest that enhanced anabolic activity in CNS mediates this overgrowth effect. We have shown previously that in a subset of patients with severe autism and aggression, plasma levels of the secreted amyloid-beta (A beta) precursor protein-alpha form (sAPP alpha) were significantly elevated relative to controls and patients with mild-to-moderate autism. Here we further tested the hypothesis that levels of sAPP alpha and sAPP beta (proteolytic cleavage products of APP by alpha-and beta-secretase, respectively) are deranged in autism and may contribute to an anabolic environment leading to brain overgrowth. We measured plasma levels of sAPP alpha, sAPP beta, A beta peptides and BDNF by corresponding ELISA in a well characterized set of subjects. We included for analysis 18 control, 6 mild-to-moderate, and 15 severely autistic patient plasma samples. We have observed that sAPPa levels are increased and BDNF levels decreased in the plasma of patients with severe autism as compared to controls. 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Green, Steven Morris, James P. Kragel, Philip Pelphrey, Kevin A. Bulik, Cynthia M. LaBar, Kevin S. TI Hemodynamic signals of mixed messages during a social exchange SO NEUROREPORT LA English DT Article DE anorexia nervosa; autism; biological motion; emotional expression; functional magnetic resonance imaging; multisensory integration; social cognition; social rejection ID SUPERIOR TEMPORAL SULCUS; PERCEPTION; EXPRESSIONS; EXCLUSION; REJECTION; EMOTIONS; GAZE; RECOGNITION; HURT; EYE AB This study used functional magnetic resonance imaging to characterize hemodynamic activation patterns recruited when the participants viewed mixed social communicative messages during a common interpersonal exchange. Mixed messages were defined as conflicting sequences of biological motion and facial affect signals that are unexpected within a particular social context (e. g. observing the reception of a gift). Across four social vignettes, valenced facial expressions were crossed with rejecting and accepting gestures in a virtual avatar responding to presentation of a gift from the participant. The results indicate that conflicting facial affect and gesture activated superior temporal sulcus, a region implicated in expectancy violations, as well as inferior frontal gyrus and putamen. Scenarios conveying rejection differentially activated the insula and putamen, regions implicated in embodied cognition, and motivated learning, as well as frontoparietal cortex. Characterizing how meaning is inferred from integration of conflicting nonverbal communicative cues is essential to understand nuances and complexities of human exchange. NeuroReport 22:413-418 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins. C1 [Zucker, Nancy L.; LaBar, Kevin S.] Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC 27705 USA. [Zucker, Nancy L.; Green, Steven; Kragel, Philip; LaBar, Kevin S.] Duke Univ, Ctr Cognit Neurosci, Durham, NC 27705 USA. [Morris, James P.] Univ Virginia, Dept Psychol, Chapel Hill, NC USA. [Pelphrey, Kevin A.] Yale Univ, Yale Child Study Ctr, Chapel Hill, NC USA. [Bulik, Cynthia M.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. RP Zucker, NL (reprint author), Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, POB 3842, Durham, NC 27705 USA. EM zucke001@mc.duke.edu RI X, Simon/F-4678-2011 FU NIH [K23 MH070418, R01 MH078211]; Duke Institute for Brain Sciences FX This study was supported by NIH grants K23 MH070418 and R01 MH078211 awarded to Dr Zucker, and a Duke Institute for Brain Sciences Research Incubator awarded to Drs Zucker and LaBar. There are no conflicts of interest to report. 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Tian, Yuan Horvath, Steve Mill, Jonathan Cantor, Rita M. Blencowe, Benjamin J. Geschwind, Daniel H. TI Transcriptomic analysis of autistic brain reveals convergent molecular pathology SO NATURE LA English DT Article ID COMMON GENETIC-VARIANTS; SPECTRUM DISORDERS; NETWORK ANALYSIS; CANDIDATE GENE; COPY NUMBER; ASSOCIATION; EXPRESSION; PATHWAYS; PACKAGE; DISEASE AB Autism spectrum disorder (ASD) is a common, highly heritable neurodevelopmental condition characterized by marked genetic heterogeneity(1-3). Thus, a fundamental question is whether autism represents an aetiologically heterogeneous disorder in which the myriad genetic or environmental risk factors perturb common underlying molecular pathways in the brain(4). Here, we demonstrate consistent differences in transcriptome organization between autistic and normal brain by gene co-expression network analysis. Remarkably, regional patterns of gene expression that typically distinguish frontal and temporal cortex are significantly attenuated in the ASD brain, suggesting abnormalities in cortical patterning. We further identify discrete modules of co-expressed genes associated with autism: a neuronal module enriched for known autism susceptibility genes, including the neuronal specific splicing factor A2BP1 (also known as FOX1), and a module enriched for immune genes and glial markers. Using high-throughput RNA sequencing we demonstrate dysregulated splicing of A2BP1-dependent alternative exons in the ASD brain. Moreover, using a published autism genome-wide association study (GWAS) data set, we show that the neuronal module is enriched for genetically associated variants, providing independent support for the causal involvement of these genes in autism. In contrast, the immune-glial module showed no enrichment for autism GWAS signals, indicating a non-genetic aetiology for this process. 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Takasaki, Kevin T. Saulnier, Jessica L. Denefrio, Cassandra L. Sabatini, Bernardo L. TI Loss of Tsc1 In Vivo Impairs Hippocampal mGluR-LTD and Increases Excitatory Synaptic Function SO JOURNAL OF NEUROSCIENCE LA English DT Article ID LONG-TERM DEPRESSION; FRAGILE-X-SYNDROME; TUBEROUS SCLEROSIS COMPLEX; MOUSE MODEL; PROTEIN-SYNTHESIS; MENTAL-RETARDATION; SIGNALING PATHWAY; TSC1-TSC2 COMPLEX; MAMMALIAN TARGET; AMPA RECEPTORS AB The autism spectrum disorder tuberous sclerosis complex (TSC) is caused by mutations in the Tsc1 or Tsc2 genes, whose protein products form a heterodimeric complex that negatively regulates mammalian target of rapamycin-dependent protein translation. Although several forms of synaptic plasticity, including metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD), depend on protein translation at the time of induction, it is unknown whether these forms of plasticity require signaling through the Tsc1/2 complex. To examine this possibility, we postnatally deleted Tsc1 in vivo in a subset of hippocampal CA1 neurons using viral delivery of Cre recombinase in mice. We found that hippocampal mGluR-LTD was abolished by loss of Tsc1, whereas a protein synthesis-independent form of NMDA receptor-dependent LTD was preserved. Additionally, AMPA and NMDA receptor-mediated EPSCs and miniature spontaneous EPSC frequency were enhanced in Tsc1 KO neurons. These changes in synaptic function occurred in the absence of alterations in spine density, morphology, or presynaptic release probability. Our findings indicate that signaling through Tsc1/2 is required for the expression of specific forms of hippocampal synaptic plasticity as well as the maintenance of normal excitatory synaptic strength. Furthermore, these data suggest that perturbations of synaptic signaling may contribute to the pathogenesis of TSC. C1 [Bateup, Helen S.; Takasaki, Kevin T.; Saulnier, Jessica L.; Denefrio, Cassandra L.; Sabatini, Bernardo L.] Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Neurobiol, Boston, MA 02115 USA. RP Sabatini, BL (reprint author), Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Neurobiol, 220 Longwood Ave, Boston, MA 02115 USA. EM bsabatini@hms.harvard.edu FU NINDS [NS052707]; Nancy Lurie Marks Postdoctoral Fellowship FX This work was supported by NINDS Grant NS052707 to B. L. S. H. S. B. is supported by a Nancy Lurie Marks Postdoctoral Fellowship. We thank the members of the Sabatini laboratory for helpful discussions and constructive comments, Caroline Johnson for technical support, and Jessica Hauser for pilot experiments. The CreEGFP viral construct was kindly provided by Matthew During. 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In this fMRI study, 39 participants completed a face recognition task. 11 participants underwent the same experiment approximately four months later. Robust face-selective activation of FG, amygdala, and lateral occipital cortex were observed. Dynamic causal modeling and Bayesian Model Selection (BMS) were used to test the intrinsic connections between these structures, and their modulation by face perception. BMS results strongly favored a dynamic causal model with bidirectional, face-modulated amygdala-FG connections. However, the right hemisphere connections diminished at time 2, with the face modulation parameter no longer surviving Bonferroni correction. These findings suggest that amygdala strongly influences FG function during face perception, and that this influence is shaped by experience and stimulus salience. (C) 2011 Elsevier Inc. All rights reserved. C1 [Herrington, John D.; Taylor, James M.; Schultz, Robert T.] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. [Grupe, Daniel W.] Univ Wisconsin, Madison, WI 53706 USA. [Curby, Kim M.] Temple Univ, Philadelphia, PA 19122 USA. [Schultz, Robert T.] Univ Penn, Philadelphia, PA 19104 USA. RP Herrington, JD (reprint author), Childrens Hosp Philadelphia, 3535 Market St,Suite 860, Philadelphia, PA 19104 USA. EM herringtonj@email.chop.edu FU NIMH [R01MH073084] FX We would like to thank Elinora Hunyadi, Mikle South and Julie Wolf for their roles in recruiting and testing research participants for this study. Funding for this project was provided by an award from NIMH (R01MH073084) to R. Schultz. 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TI Spatial Attention, Feature-Based Attention, and Saccades: Three Sides of One Coin? SO BIOLOGICAL PSYCHIATRY LA English DT Article DE Autism; feature-based attention; neurophysiology; premotor theory; spatial attention; top-down modulation ID DEFICIT HYPERACTIVITY DISORDER; VISUAL RECEPTIVE-FIELDS; EXTRASTRIATE AREA V4; FRONTAL EYE FIELDS; DEFICIT/HYPERACTIVITY DISORDER; SELECTIVE ATTENTION; NORMALIZATION MODEL; FEATURE-INTEGRATION; NEURONAL RESPONSES; NEURAL MECHANISMS AB The last three decades has seen a steady growth of neuroscience research aimed at understanding the functions and sources of top-down attentional modulation in the brain. This correlates with recognition that attention may be a necessary component of sensory systems to support natural behaviors in natural environments. Complexity and clutter are two of the most recognizable hallmarks of natural environments, which can simultaneously contain vitally important and completely irrelevant stimuli. 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It began with puzzlement about and the flaring of research on the decline of wildlife, particularly avian species. The proposed causes accented pesticides, especially persistent organochlorines such as DDT. Its scope gradually widened beyond pesticides, and, as endocrine disruption offered an explanation for the wildlife phenomena, it seemed to explain, as well, changes in fertility and disorders of male reproduction such as testicular cancer. Once disturbed gonadal hormone function became the most likely explanation, it provoked other questions. The most challenging arose because of how critical gonadal hormones are to brain function, especially as determinants of brain sexual differentiation. Pursuit of such connections has generated a robust literature embracing a broad swath of chemical classes. How endocrine disrupting chemicals influence the adult and aging brain is a question, so far mostly ignored because of the emphasis on early development, that warrants vigorous investigation. Gonadal hormones are crucial to optimal brain function during maturity and even senescence. They are pivotal to the processes of neurogenesis. They exert protective actions against neurodegenerative disorders such as dementia and support smoothly functioning cognitive activities. The limited research conducted so far on endocrine disruptors, aging, and neurogenesis argues that they should be overlooked no longer. (C) 2011 Elsevier B.V. All rights reserved. C1 Univ Rochester, Med Ctr, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USA. RP Weiss, B (reprint author), Univ Rochester, Med Ctr, Sch Med & Dent, Dept Environm Med, 610 Elmwood Ave, Rochester, NY 14642 USA. 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Benfenati, Fabio Cossette, Patrick TI SYN1 loss-of-function mutations in autism and partial epilepsy cause impaired synaptic function SO HUMAN MOLECULAR GENETICS LA English DT Article ID SYNAPSIN DOMAIN-E; I-DEFICIENT MICE; SPECTRUM DISORDER; NEUROTRANSMITTER RELEASE; PRESYNAPTIC TERMINALS; MENTAL-RETARDATION; VESICLE PROTEIN; GENE; TRANSMISSION; CONTACTIN-ASSOCIATED-PROTEIN-LIKE-2 AB Several genes predisposing to autism spectrum disorders (ASDs) with or without epilepsy have been identified, many of which are implicated in synaptic function. Here we report a Q555X mutation in synapsin 1 (SYN1), an X-linked gene encoding for a neuron-specific phosphoprotein implicated in the regulation of neurotransmitter release and synaptogenesis. This nonsense mutation was found in all affected individuals from a large French-Canadian family segregating epilepsy and ASDs. Additional mutations in SYN1 (A51G, A550T and T567A) were found in 1.0 and 3.5% of French-Canadian individuals with autism and epilepsy, respectively. The majority of these SYN1 mutations were clustered in the proline-rich D-domain which is substrate of multiple protein kinases. When expressed in synapsin I (SynI) knockout (KO) neurons, all the D-domain mutants failed in rescuing the impairment in the size and trafficking of synaptic vesicle pools, whereas the wild-type human SynI fully reverted the KO phenotype. Moreover, the nonsense Q555X mutation had a dramatic impact on phosphorylation by MAPK/Erk and neurite outgrowth, whereas the missense A550T and T567A mutants displayed impaired targeting to nerve terminals. These results demonstrate that SYN1 is a novel predisposing gene to ASDs, in addition to epilepsy, and strengthen the hypothesis that a disturbance of synaptic homeostasis underlies the pathogenesis of both diseases. C1 [Patry, Lysanne; Piton, Amelie; Gauthier, Julie; Lapointe, Line; St-Onge, Judith; Meloche, Caroline; Mottron, Laurent; Dang Khoa Nguyen; Rouleau, Guy A.; Cossette, Patrick] Univ Montreal, CHUM Hop Notre Dame, Dept Med, Ctr Excellence Neur, Montreal, PQ H2L 4M1, Canada. [Fassio, Anna; Congia, Sonia; Onofri, Franco; Messa, Mirko; Fadda, Manuela; Corradi, Anna; Baldelli, Pietro; Benfenati, Fabio] Univ Genoa, Natl Inst Neurosci, Dept Expt Med, I-16132 Genoa, Italy. [Congia, Sonia; Pozzi, Davide; Messa, Mirko; Defranchi, Enrico; Fadda, Manuela; Baldelli, Pietro; Benfenati, Fabio] Italian Inst Technol, Dept Neurosci & Brain Technol, I-16163 Genoa, Italy. [Valtorta, Flavia] Univ Vita Salute San Raffaele, San Raffaele Sci Inst, I-20132 Milan, Italy. RP Cossette, P (reprint author), Univ Montreal, CHUM Hop Notre Dame, Dept Med, Ctr Excellence Neur, 1560 Sherbrooke E, Montreal, PQ H2L 4M1, Canada. EM fabio.benfenati@iit.it; patrick.cossette@umontreal.ca RI Valtorta, flavia/F-3450-2012; piton, amelie/F-1201-2013; fassio, anna/K-4482-2014 OI fassio, anna/0000-0002-8801-038X FU Canadian Institute for Health Research and Genome Canada; Savoy Foundation; Italian Ministry of Research; Italian Ministry of Health; Compagnia di San Paolo-Torino; Quebec Ministry of International Relationships; Italian Ministry of Foreign Affairs; Telethon-Italy [GGP09134] FX This work was supported by grants from the Canadian Institute for Health Research and Genome Canada (to P.C. and G.A.R.), the Savoy Foundation (to L.P.), the Italian Ministry of Research (to F.B., F.O. and F.V.), the Italian Ministry of Health (to A.F. and P.B.), Compagnia di San Paolo-Torino (to F.B., A.F., P.B. and F.V.), the Quebec Ministry of International Relationships and Italian Ministry of Foreign Affairs (to P.C. and F.B.). The support of Telethon-Italy (GGP09134 to F.B and F.V.) is also acknowledged. 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However, within ASC it is unclear if there are phenotypic sex differences. Testing for similarities and differences between the sexes is important not only for clinical assessment but also has implications for theories of typical sex differences and of autism. Using cognitive and behavioral measures, we investigated similarities and differences between the sexes in age-and IQ-matched adults with ASC (high-functioning autism or Asperger syndrome). Of the 83 (45 males and 38 females) participants, 62 (33 males and 29 females) met Autism Diagnostic Interview-Revised (ADI-R) cut-off criteria for autism in childhood and were included in all subsequent analyses. The severity of childhood core autism symptoms did not differ between the sexes. Males and females also did not differ in self-reported empathy, systemizing, anxiety, depression, and obsessive-compulsive traits/symptoms or mentalizing performance. However, adult females with ASC showed more lifetime sensory symptoms (p = 0.036), fewer current socio-communication difficulties (p = 0.001), and more self-reported autistic traits (p = 0.012) than males. In addition, females with ASC who also had developmental language delay had lower current performance IQ than those without developmental language delay (p < 0.001), a pattern not seen in males. The absence of typical sex differences in empathizing-systemizing profiles within the autism spectrum confirms a prediction from the extreme male brain theory. Behavioral sex differences within ASC may also reflect different developmental mechanisms between males and females with ASC. We discuss the importance of the superficially better socio-communication ability in adult females with ASC in terms of why females with ASC may more often go under-recognized, and receive their diagnosis later, than males. C1 [Lai, Meng-Chuan; Lombardo, Michael V.; Pasco, Greg; Ruigrok, Amber N. V.; Wheelwright, Sally J.; Sadek, Susan A.; Chakrabarti, Bhismadev; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. [Chakrabarti, Bhismadev] Univ Reading, Sch Psychol & Clin Language Sci, Ctr Integrat Neurosci & Neurodynam, 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; daly, eileen/B-6716-2011; Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014; Williams, Steve/D-6979-2011 OI Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X; FU Medical Research Council, United Kingdom FX This study was funded by the Medical Research Council, United Kingdom. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Zoghbi, Huda Y. TI Solving the Autism Puzzle a Few Pieces at a Time SO NEURON LA English DT Editorial Material ID RARE DE-NOVO; SPECTRUM DISORDERS AB In this issue, a pair of studies (Levy et al. and Sanders et al.) identify several de novo copy-number variants that together account for 5%-8% of cases of simplex autism spectrum disorders. These studies suggest that several hundreds of loci are likely to contribute to the complex genetic heterogeneity of this group of disorders. An accompanying study in this issue (Gilman et al.), presents network analysis implicating these CNVs in neural processes related to synapse development, axon targeting, and neuron motility. C1 [Schaaf, Christian P.; Zoghbi, Huda Y.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. [Zoghbi, Huda Y.] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA. [Zoghbi, Huda Y.] Baylor Coll Med, Program Dev Biol, Dept Pediat, Houston, TX 77030 USA. 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Ercan-Sencicek, A. Gulhan Hus, Vanessa Luo, Rui Murtha, Michael T. Moreno-De-Luca, Daniel Chu, Su H. Moreau, Michael P. Gupta, Abha R. Thomson, Susanne A. Mason, Christopher E. Bilguvar, Kaya Celestino-Soper, Patricia B. S. Choi, Murim Crawford, Emily L. Davis, Lea Wright, Nicole R. Davis Dhodapkar, Rahul M. DiCola, Michael DiLullo, Nicholas M. Fernandez, Thomas V. Fielding-Singh, Vikram Fishman, Daniel O. Frahm, Stephanie Garagaloyan, Rouben Goh, Gerald S. Kammela, Sindhuja Klei, Lambertus Lowe, Jennifer K. Lund, Sabata C. McGrew, Anna D. Meyer, Kyle A. Moffat, William J. Murdoch, John D. O'Roak, Brian J. Ober, Gordon T. Pottenger, Rebecca S. Raubeson, Melanie J. Song, Youeun Wang, Qi Yaspan, Brian L. Yu, Timothy W. Yurkiewicz, Liana R. Beaudet, Arthur L. Cantor, Rita M. Curland, Martin Grice, Dorothy E. Guenel, Murat Lifton, Richard P. Mane, Shrikant M. Martin, Donna M. Shaw, Chad A. Sheldon, Michael Tischfield, Jay A. Walsh, Christopher A. Morrow, Eric M. Ledbetter, David H. Fombonne, Eric Lord, Catherine Martin, Christa Lese Brooks, Andrew I. Sutcliffe, James S. Cook, Edwin H., Jr. Geschwind, Daniel Roeder, Kathryn Devlin, Bernie State, Matthew W. TI Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism SO NEURON LA English DT Article ID COPY NUMBER VARIATION; RARE CHROMOSOMAL DELETIONS; HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA; SPECTRUM DISORDERS; GENETIC DISORDER; BEUREN-SYNDROME; INCREASE RISK; EARLY-ONSET; GENOME AB We have undertaken a genome-wide analysis of rare copy-number variation (CNV) in 1124 autism spectrum disorder (ASD) families, each comprised of a single proband, unaffected parents, and, in most kindreds, an unaffected sibling. We find significant association of ASD with de novo duplications of 7q11.23, where the reciprocal deletion causes Williams-Beuren syndrome, characterized by a highly social personality. We identify rare recurrent de novo CNVs at five additional regions, including 16p13.2 (encompassing genes USP7 and C16orf72) and Cadherin 13, and implement a rigorous approach to evaluating the statistical significance of these observations. Overall, large de novo CNVs, particularly those encompassing multiple genes, confer substantial risks (OR = 5.6; CI = 2.6-12.0, p = 2.4 x 10(-7)). We estimate there are 130-234 ASD-related CNV regions in the human genome and present compelling evidence, based on cumulative data, for association of rare de novo events at 7q11.23, 15q11.2-13.1, 16p11.2, and Neurexin 1. C1 [Sanders, Stephan J.; Ercan-Sencicek, A. Gulhan; Murtha, Michael T.; Bilguvar, Kaya; Guenel, Murat; State, Matthew W.] Yale Univ, Sch Med, Program Neurogenet, New Haven, CT 06520 USA. [Sanders, Stephan J.; Ercan-Sencicek, A. Gulhan; Murtha, Michael T.; Gupta, Abha R.; Wright, Nicole R. Davis; Dhodapkar, Rahul M.; DiLullo, Nicholas M.; Fernandez, Thomas V.; Kammela, Sindhuja; Moffat, William J.; Ober, Gordon T.; Song, Youeun; Yurkiewicz, Liana R.; State, Matthew W.] Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. [Sanders, Stephan J.; Ercan-Sencicek, A. Gulhan; Murtha, Michael T.; State, Matthew W.] Yale Univ, Sch Med, Dept Psychiat, New Haven, CT 06520 USA. [Sanders, Stephan J.; Ercan-Sencicek, A. Gulhan; Murtha, Michael T.; Bilguvar, Kaya; Choi, Murim; Goh, Gerald S.; Murdoch, John D.; Guenel, Murat; Lifton, Richard P.; State, Matthew W.] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA. [Hus, Vanessa; Lund, Sabata C.; Lord, Catherine] Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. [Luo, Rui; Cantor, Rita M.] Univ Calif Los Angeles, Dept Human Genet, David Geffen Sch Med, Los Angeles, CA 90095 USA. [Moreno-De-Luca, Daniel; Martin, Christa Lese] Emory Univ, Sch Med, Dept Human Genet, Atlanta, GA 30322 USA. [Chu, Su H.; Roeder, Kathryn] Carnegie Mellon Univ, Dept Stat, Pittsburgh, PA 15213 USA. [Moreau, Michael P.; DiCola, Michael; Frahm, Stephanie; Wang, Qi; Brooks, Andrew I.] Rutgers State Univ, Environm & Occupat Hlth Sci Inst, Piscataway, NJ 08854 USA. [Gupta, Abha R.] Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA. [Thomson, Susanne A.; Crawford, Emily L.; McGrew, Anna D.; Yaspan, Brian L.; Sutcliffe, James S.] Vanderbilt Univ, Ctr Mol Neurosci, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. [Mason, Christopher E.] Weill Cornell Med Coll, Dept Physiol Biophys, New York, NY 10021 USA. [Mason, Christopher E.] Weill Cornell Med Coll, Inst Computat Biomed, New York, NY 10021 USA. [Bilguvar, Kaya; Guenel, Murat] Yale Univ, Sch Med, Dept Neurosurg, New Haven, CT 06510 USA. [Bilguvar, Kaya; Guenel, Murat] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06510 USA. [Celestino-Soper, Patricia B. S.; Beaudet, Arthur L.; Shaw, Chad A.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. [Davis, Lea; Cook, Edwin H., Jr.] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60608 USA. [Fielding-Singh, Vikram] Stanford Univ, Sch Med, Stanford, CA 94305 USA. [Fishman, Daniel O.] Vanderbilt Univ, Sch Med, Nashville, TN 37232 USA. [Garagaloyan, Rouben; Curland, Martin] Microangelo Associates LLC, Pacific Palisades, CA 90272 USA. [Klei, Lambertus; Devlin, Bernie] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA. [Lowe, Jennifer K.; Geschwind, Daniel] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Neurogenet Program, Los Angeles, CA 90095 USA. [Meyer, Kyle A.] Yale Univ, Interdept Neurosci Program, New Haven, CT 06510 USA. [O'Roak, Brian J.; Raubeson, Melanie J.] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. [Pottenger, Rebecca S.] Princeton Univ, Princeton, NJ 08544 USA. [Yu, Timothy W.] Harvard Univ, Sch Med, Massachusetts Gen Hosp, Childrens Hosp Boston,Dept Neurol,Div Genet, Boston, MA 02115 USA. [Cantor, Rita M.] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA. [Grice, Dorothy E.] Columbia Univ, Dept Psychiat, Div Child & Adolescent Psychiat, New York, NY 10032 USA. [Grice, Dorothy E.] New York State Psychiat Inst & Hosp, New York, NY 10032 USA. [Choi, Murim; Lifton, Richard P.] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06510 USA. [Mane, Shrikant M.] Yale Ctr Genome Anal, Orange, CT 06477 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. [Sheldon, Michael; Tischfield, Jay A.] Rutgers State Univ, Dept Genet, Piscataway, NJ 08854 USA. [Sheldon, Michael; Tischfield, Jay A.] Rutgers State Univ, Inst Human Genet, Piscataway, NJ 08854 USA. [Walsh, Christopher A.] Harvard Univ, Sch Med, Ctr Life Sci, Howard Hughes Med Inst, Boston, MA 02115 USA. [Walsh, Christopher A.] Harvard Univ, Sch Med, Ctr Life Sci, Div Genet,Childrens Hosp Boston, Boston, MA 02115 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. [Ledbetter, David H.] Geisinger Hlth Syst, Danville, PA 17822 USA. [Fombonne, Eric] McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3Z 1P2, Canada. [Lord, Catherine] Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA. [Lord, Catherine] Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA. [Lord, Catherine] Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA. [Lord, Catherine] Univ Michigan, Ctr Human Growth & Dev, Ann Arbor, MI 48109 USA. RP State, MW (reprint author), Yale Univ, Sch Med, Program Neurogenet, 230 S Frontage Rd, New Haven, CT 06520 USA. EM matthew.state@yale.edu RI Morrow, Eric/J-2767-2013; Sutcliffe, James/C-1348-2012; Goh, Gerald/E-9158-2014; Fernandez, Thomas/D-4295-2009 OI Sutcliffe, James/0000-0001-5200-6007; Goh, Gerald/0000-0002-3832-6466; Fernandez, Thomas/0000-0003-0830-022X FU Simons Foundation [SFARI 124827] FX We are most grateful to all of the families at the participating Simons Foundation Autism Research Initiative (SFARI) Simplex Collection (SSC) sites. This work was supported by a grant from the Simons Foundation (SFARI 124827). C.A. Walsh and R.P. Lifton are Investigators of the Howard Hughes Medical Institute. 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 (M. Greenup and S. Johnson); R. Smith and Z. Galfayan at Microangelo Associates for bioinformatics support; Prometheus Research; the Yale Center of Genomic Analysis staff, in particular S. Umlauf and C. Castaldi; T. Brooks-Boone and M. Wojciechowski for their help in administering the project at Yale; and J. Krystal, G.D. Fischbach, A. Packer, J. Spiro, and M. Benedetti for their suggestions throughout and very helpful comments during the preparation of this manuscript. Approved researchers can obtain the SSC population data set described in this study by applying at https://base.sfari.org. D.H. Ledbetter acts as a consultant for Roche Diagnostics and BioReference Laboratories; M.W. State, R.P. Lifton, and B.J. O'Roak hold a patent relating to the gene CNTNAP2. 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Pai, Deepa Ye, Kenny Buja, Andreas Krieger, Abba Yoon, Seungtai Troge, Jennifer Rodgers, Linda Lossifov, Ivan Wigler, Michael TI Rare De Novo and Transmitted Copy-Number Variation in Autistic Spectrum Disorders SO NEURON LA English DT Article ID RECURRENT MICRODELETIONS; ASSOCIATION; MUTATIONS; VARIANTS; MICRODUPLICATION; IDENTIFICATION; SCHIZOPHRENIA; PREDISPOSE; EXPRESSION; DELETIONS AB To explore the genetic contribution to autistic spectrum disorders (ASDs), we have studied genomic copy-number variation in a large cohort of families with a single affected child and at least one unaffected sibling. We confirm a major contribution from de novo deletions and duplications but also find evidence of a role for inherited "ultrarare" duplications. Our results show that, relative to males, females have greater resistance to autism from genetic causes, which raises the question of the fate of female carriers. By analysis of the proportion and number of recurrent loci, we set a lower bound for distinct target loci at several hundred. We find many new candidate regions, adding substantially to the list of potential gene targets, and confirm several loci previously observed. The functions of the genes in the regions of de novo variation point to a great diversity of genetic causes but also suggest functional convergence. C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. [Ye, Kenny] Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA. [Buja, Andreas; Krieger, Abba] Univ Penn, Wharton Sch, Dept Stat, Philadelphia, PA 19104 USA. RP Wigler, M (reprint author), Cold Spring Harbor Lab, POB 100, Cold Spring Harbor, NY 11724 USA. EM wigler@cshl.edu FU Simons Foundation [SF51] FX This work was supported by a grant from the Simons Foundation (SFARI award number SF51 to MW). 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Iossifov, Ivan Levy, Dan Ronemus, Michael Wigler, Michael Vitkup, Dennis TI Rare De Novo Variants Associated with Autism Implicate a Large Functional Network of Genes Involved in Formation and Function of Synapses SO NEURON LA English DT Article ID CORTICAL PYRAMIDAL NEURONS; DENDRITIC SPINE DENSITY; SPECTRUM DISORDERS; GENOMEWIDE ASSOCIATION; COMPLEX DISEASES; PATHWAYS; PATHOLOGY; PROTEIN; MTOR; WNT AB Identification of complex molecular networks underlying common human phenotypes is a major challenge of modern genetics. In this study, we develop a method for network-based analysis of genetic associations (NETBAG). We use NETBAG to identify a large biological network of genes affected by rare de novo CNVs in autism. The genes forming the network are primarily related to synapse development, axon targeting, and neuron motility. The identified network is strongly related to genes previously implicated in autism and intellectual disability phenotypes. Our results are also consistent with the hypothesis that significantly stronger functional perturbations are required to trigger the autistic phenotype in females compared to males. Overall, the presented analysis of de novo variants supports the hypothesis that perturbed synaptogenesis is at the heart of autism. More generally, our study provides proof of the principle that networks underlying complex human phenotypes can be identified by a network-based functional analysis of rare genetic variants. C1 [Gilman, Sarah R.; Vitkup, Dennis] Columbia Univ, Ctr Computat Biol & Bioinformat, New York, NY 10032 USA. [Gilman, Sarah R.; Vitkup, Dennis] Columbia Univ, Dept Biomed Informat, New York, NY 10032 USA. [Iossifov, Ivan; Levy, Dan; Ronemus, Michael; Wigler, Michael] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. RP Iossifov, I (reprint author), Columbia Univ, Ctr Computat Biol & Bioinformat, 1130 St Nicolas Ave, New York, NY 10032 USA. EM iossifov@cshl.edu; dv2121@columbia.edu FU Simons Foundation [SF51]; National Centers for Biomedical Computing (MAGNet) [U54CA121852]; Simons Foundation Autism Research Initiative; [T32 GM082797] FX This work was supported in part by a grant from the Simons Foundation (SFARI award number SF51 to M.W.), the National Centers for Biomedical Computing (MAGNet) grant U54CA121852 to Columbia University. S.R.G. was supported by the training grant T32 GM082797. We are grateful to all of the families at the participating SFARI Simplex Collection (SSC) sites, as well as the principal investigators (A. Beaudet, R. Bernier, J. Constantino, E. Cook, E. Fombonne, D. Geschwind, D. Grice, A. Klin, R. Kochel, D. Ledbetter, C. Lord, C. Martin, D. Martin, R. Maxim, J. Miles, O. Ousley, B. Pelphrey, B. Peterson, J. Piggot, C. Saulnier, M. State, W. Stone, J. Sutcliffe, C. Walsh, E. 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Wenderoth, Nicole TI Action and Emotion Recognition from Point Light Displays: An Investigation of Gender Differences SO PLOS ONE LA English DT Article ID BIOLOGICAL MOTION PERCEPTION; HIGH-FUNCTIONING AUTISM; MIRROR-NEURON SYSTEM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; SPECTRUM DISORDERS; MAGNETIC STIMULATION; EMPATHY QUOTIENT; NORMAL ADULTS; MOTOR CORTEX AB Folk psychology advocates the existence of gender differences in socio-cognitive functions such as 'reading' the mental states of others or discerning subtle differences in body-language. A female advantage has been demonstrated for emotion recognition from facial expressions, but virtually nothing is known about gender differences in recognizing bodily stimuli or body language. The aim of the present study was to investigate potential gender differences in a series of tasks, involving the recognition of distinct features from point light displays (PLDs) depicting bodily movements of a male and female actor. Although recognition scores were considerably high at the overall group level, female participants were more accurate than males in recognizing the depicted actions from PLDs. Response times were significantly higher for males compared to females on PLD recognition tasks involving (i) the general recognition of 'biological motion' versus 'non-biological' (or 'scrambled' motion); or (ii) the recognition of the 'emotional state' of the PLD-figures. No gender differences were revealed for a control test (involving the identification of a color change in one of the dots) and for recognizing the gender of the PLD-figure. In addition, previous findings of a female advantage on a facial emotion recognition test (the 'Reading the Mind in the Eyes Test' (Baron-Cohen, 2001)) were replicated in this study. Interestingly, a strong correlation was revealed between emotion recognition from bodily PLDs versus facial cues. This relationship indicates that inter-individual or gender-dependent differences in recognizing emotions are relatively generalized across facial and bodily emotion perception. Moreover, the tight correlation between a subject's ability to discern subtle emotional cues from PLDs and the subject's ability to basically discriminate biological from non-biological motion provides indications that differences in emotion recognition may - at least to some degree - be related to more basic differences in processing biological motion per se. C1 [Alaerts, Kaat; Nackaerts, Evelien; Meyns, Pieter; Swinnen, Stephan P.; Wenderoth, Nicole] Katholieke Univ Leuven, Grp Biomed Sci, Dept Biomed Kinesiol, Motor Control Lab,Res Ctr Movement Control & Neur, B-3001 Heverlee, Belgium. RP Alaerts, K (reprint author), Katholieke Univ Leuven, Grp Biomed Sci, Dept Biomed Kinesiol, Motor Control Lab,Res Ctr Movement Control & Neur, B-3001 Heverlee, Belgium. EM Kaat.Alaerts@faber.kuleuven.be RI Wenderoth, Nicole/D-7262-2015 OI Wenderoth, Nicole/0000-0002-3246-9386 FU Flanders Fund for Scientific Research [G.0749.09, 1.2.060.10.N.00]; Belgian federal government [P6/29] FX Support for this study was provided through grants from the Flanders Fund for Scientific Research (Project Grant G.0749.09 and Fellowship Grant 1.2.060.10.N.00)(http://www.fwo.be). This work was also supported by Grant P6/29 from the Interuniversity Attraction Poles program of the Belgian federal government. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Hung, Albert Y. Sheng, Morgan Crawley, Jacqueline N. TI Communication Impairments in Mice Lacking Shank1: Reduced Levels of Ultrasonic Vocalizations and Scent Marking Behavior SO PLOS ONE LA English DT Article ID AUTISM SPECTRUM DISORDERS; MUS-DOMESTICUS RUTTY; FEMALE HOUSE MICE; POSTSYNAPTIC DENSITY PROTEINS; TF/J MOUSE MODEL; DEVELOPMENTAL INFLUENCES; URINE MARKING; GENETIC INFLUENCES; UNUSUAL REPERTOIRE; SYNAPTIC PROTEINS AB Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK gene family, as mutations in SHANK2 and SHANK3 have been detected in several autistic individuals. SHANK genes code for a family of scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that a mutation in SHANK1 contributes to the symptoms of autism, we evaluated Shank1(-/-) null mutant mice for behavioral phenotypes with relevance to autism, focusing on social communication. Ultrasonic vocalizations and the deposition of scent marks appear to be two major modes of mouse communication. Our findings revealed evidence for low levels of ultrasonic vocalizations and scent marks in Shank1(-/-) mice as compared to wildtype Shank1(+/+) littermate controls. Shank1(-/-) pups emitted fewer vocalizations than Shank1(+/+) pups when isolated from mother and littermates. In adulthood, genotype affected scent marking behavior in the presence of female urinary pheromones. Adult Shank1(-/-) males deposited fewer scent marks in proximity to female urine than Shank1(+/+) males. Call emission in response to female urinary pheromones also differed between genotypes. Shank1(+/+) mice changed their calling pattern dependent on previous female interactions, while Shank1(-/-) mice were unaffected, indicating a failure of Shank1(-/-) males to learn from a social experience. The reduced levels of ultrasonic vocalizations and scent marking behavior in Shank1(-/-) mice are consistent with a phenotype relevant to social communication deficits in autism. C1 [Woehr, Markus; Roullet, Florence I.; Crawley, Jacqueline N.] NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA. [Hung, Albert Y.; Sheng, Morgan] MIT, Picower Inst Learning & Memory, Cambridge, MA 02139 USA. RP Wohr, M (reprint author), NIMH, Lab Behav Neurosci, Bethesda, MD 20892 USA. EM markus.woehr@staff.uni-marburg.de; crawleyj@mail.nih.gov FU National Institute of Mental Health; Simons Foundation FX This work was supported by the National Institute of Mental Health Intramural Research Program and Simons Foundation (M. S. & A. H.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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TI Protein Interactome Reveals Converging Molecular Pathways Among Autism Disorders SO SCIENCE TRANSLATIONAL MEDICINE LA English DT Article ID COPY NUMBER VARIATION; POSTSYNAPTIC DENSITY PROTEINS; TUBEROUS SCLEROSIS GENE; SPECTRUM DISORDERS; MENTAL-RETARDATION; INTERACTION NETWORK; MOUSE MODEL; IDENTIFICATION; MECP2; MUTATIONS AB To uncover shared pathogenic mechanisms among the highly heterogeneous autism spectrum disorders (ASDs), we developed a protein interaction network that identified hundreds of new interactions among proteins encoded by ASD-associated genes. We discovered unexpectedly high connectivity between SHANK and TSC1, previously implicated in syndromic autism, suggesting that common molecular pathways underlie autistic phenotypes in distinct syndromes. ASD patients were more likely to harbor copy number variations that encompass network genes than were control subjects. We also identified, in patients with idiopathic ASD, three de novo lesions (deletions in 16q23.3 and 15q22 and one duplication in Xq28) that involve three network genes (NECAB2, PKM2, and FLNA). The protein interaction network thus provides a framework for identifying causes of idiopathic autism and for understanding molecular pathways that underpin both syndromic and idiopathic ASDs. C1 [Sakai, Yasunari; Shaw, Chad A.; Dawson, Brian C.; Dugas, Diana V.; Al-Mohtaseb, Zaina; Zoghbi, Huda Y.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. [Sakai, Yasunari; Dawson, Brian C.; Zoghbi, Huda Y.] Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA. [Hill, David E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Ctr Canc Syst Biol, Boston, MA 02115 USA. [Hill, David E.] Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Canc Biol, Boston, MA 02115 USA. [Hill, David E.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. [Zoghbi, Huda Y.] Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. [Zoghbi, Huda Y.] Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. [Zoghbi, Huda Y.] Texas Childrens Hosp, Jan & Dan Duncan Neurol Res Inst, Houston, TX 77030 USA. RP Shaw, CA (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. EM cashaw@bcm.tmc.edu; hzoghbi@bcm.tmc.edu RI Hill, David/B-6617-2011 FU Howard Hughes Medical Institute; Simons Foundation Autism Research Initiative (SFARI); Ellison Foundation FX Funding: Supported by the Howard Hughes Medical Institute (H.Y.Z.), the Simons Foundation Autism Research Initiative (SFARI award to H.Y.Z.), and the Ellison Foundation (D. E. H.; awarded to M. Vidal). We are grateful to all of the families at the participating SFARI 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, D. Grice, A. Klin, D. Ledbetter, C. Lord, C. Martin, D. Martin, R. Maxim, J. Miles, O. Ousley, B. Peterson, J. Piggot, C. Saulnier, M. State, W. Stone, J. Sutcliffe, C. Walsh, and E. Wijsman). We appreciate obtaining access to phenotypic data on SFARI Base. Approved researchers can obtain the SSC population data set described in this study by applying at https://base.sfari.org. The array CGH data for the probands analyzed in the study have been deposited in National Center for Biotechnology Information's Gene Expression Omnibus (GEO) and are accessible through GEO Series accession number GSE29576 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE29576). 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Transl. Med. PD JUN 8 PY 2011 VL 3 IS 86 AR 86ra49 DI 10.1126/scitranslmed.3002166 PG 10 WC Cell Biology; Medicine, Research & Experimental SC Cell Biology; Research & Experimental Medicine GA 795NG UT WOS:000292980300002 PM 21653829 ER PT J AU Adams, JB Audhya, T McDonough-Means, S Rubin, RA Quig, D Geis, E Gehn, E Loresto, M Mitchell, J Atwood, S Barnhouse, S Lee, W AF Adams, James B. Audhya, Tapan McDonough-Means, Sharon Rubin, Robert A. Quig, David Geis, Elizabeth Gehn, Eva Loresto, Melissa Mitchell, Jessica Atwood, Sharon Barnhouse, Suzanne Lee, Wondra TI Nutritional and metabolic status of children with autism vs. neurotypical children, and the association with autism severity SO NUTRITION & METABOLISM LA English DT Article ID TANDEM MASS-SPECTROMETRY; S-ADENOSYLHOMOCYSTEINE HYDROLASE; STABLE-ISOTOPE-DILUTION; REDUCED SERUM-LEVELS; AMINO-ACID LEVELS; LIQUID-CHROMATOGRAPHY; OXIDATIVE STRESS; SPECTRUM DISORDERS; MITOCHONDRIAL DYSFUNCTION; ELECTROCHEMICAL DETECTION AB Background: The relationship between relative metabolic disturbances and developmental disorders is an emerging research focus. This study compares the nutritional and metabolic status of children with autism with that of neurotypical children and investigates the possible association of autism severity with biomarkers. Method: Participants were children ages 5-16 years in Arizona with Autistic Spectrum Disorder (n = 55) compared with non-sibling, neurotypical controls (n = 44) of similar age, gender and geographical distribution. Neither group had taken any vitamin/mineral supplements in the two months prior to sample collection. Autism severity was assessed using the Pervasive Development Disorder Behavior Inventory (PDD-BI), Autism Treatment Evaluation Checklist (ATEC), and Severity of Autism Scale (SAS). Study measurements included: vitamins, biomarkers of vitamin status, minerals, plasma amino acids, plasma glutathione, and biomarkers of oxidative stress, methylation, sulfation and energy production. Results: Biomarkers of children with autism compared to those of controls using a t-test or Wilcoxon test found the following statistically significant differences (p < 0.001): Low levels of biotin, plasma glutathione, RBC SAM, plasma uridine, plasma ATP, RBC NADH, RBC NADPH, plasma sulfate (free and total), and plasma tryptophan; also high levels of oxidative stress markers and plasma glutamate. Levels of biomarkers for the neurotypical controls were in good agreement with accessed published reference ranges. In the Autism group, mean levels of vitamins, minerals, and most amino acids commonly measured in clinical care were within published reference ranges. A stepwise, multiple linear regression analysis demonstrated significant associations between several groups of biomarkers with all three autism severity scales, including vitamins (adjusted R(2) of 0.25-0.57), minerals (adj. R(2) of 0.22-0.38), and plasma amino acids (adj. R(2) of 0.22-0.39). Conclusion: The autism group had many statistically significant differences in their nutritional and metabolic status, including biomarkers indicative of vitamin insufficiency, increased oxidative stress, reduced capacity for energy transport, sulfation and detoxification. Several of the biomarker groups were significantly associated with variations in the severity of autism. These nutritional and metabolic differences are generally in agreement with other published results and are likely amenable to nutritional supplementation. Research investigating treatment and its relationship to the co-morbidities and etiology of autism is warranted. C1 [Adams, James B.; Geis, Elizabeth; Gehn, Eva; Loresto, Melissa; Atwood, Sharon; Barnhouse, Suzanne; Lee, Wondra] Arizona State Univ, Tempe, AZ 85287 USA. [Audhya, Tapan] Hlth Diagnost, S Amboy, NJ USA. [McDonough-Means, Sharon] Integrat Dev Pediat, Tucson, AZ USA. [Rubin, Robert A.] Whittier Coll, Dept Math, Whittier, CA USA. [Quig, David] Doctors Data, St Charles, IL USA. [Mitchell, Jessica] SW Coll Naturopath Med, Tempe, AZ USA. RP Adams, JB (reprint author), Arizona State Univ, Tempe, AZ 85287 USA. EM jim.adams@asu.edu FU Autism Research Institute; Legacy Foundation FX First and foremost, we thank the many autism families and their friends who volunteered as participants in this research study. We thank the Autism Research Institute and the Legacy Foundation for financial support of this study. We thank the Autism Society of Greater Phoenix and the Arizona Division of Developmental Disabilities for assistance with advertising this study. We thank the staff of the Southwest College of Naturopathic Medicine (N. Foster, M. Harland, B. Peterson, N. Tkacenko) for help with phlebotomy, and we thank ICDRC for providing use of their offices for participant evaluations. We thank Vitamin Diagnostics and Doctor's Data for providing testing for this study. 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Fung, Germaine Yu, Kevin K. Tai, Kin-Shing Sham, Pak C. Chua, Siew E. TI MRI Study of Minor Physical Anomaly in Childhood Autism Implicates Aberrant Neurodevelopment in Infancy SO PLOS ONE LA English DT Article ID GENERALIZED SOCIAL PHOBIA; VOXEL-BASED MRI; CONGENITAL-RUBELLA; BRAIN-DEVELOPMENT; AMYGDALA VOLUME; WHITE-MATTER; SCHIZOPHRENIA; DISORDER; CHILDREN; GROWTH AB Background: MPAs (minor physical anomalies) frequently occur in neurodevelopmental disorders because both face and brain are derived from neuroectoderm in the first trimester. Conventionally, MPAs are measured by evaluation of external appearance. Using MRI can help overcome inherent observer bias, facilitate multi-centre data acquisition, and explore how MPAs relate to brain dysmorphology in the same individual. Optical MPAs exhibit a tightly synchronized trajectory through fetal, postnatal and adult life. As head size enlarges with age, inter-orbital distance increases, and is mostly completed before age 3 years. We hypothesized that optical MPAs might afford a retrospective 'window' to early neurodevelopment; specifically, inter-orbital distance increase may represent a biomarker for early brain dysmaturation in autism. Methods: We recruited 91 children aged 7-16; 36 with an autism spectrum disorder and 55 age- and gender-matched typically developing controls. All children had normal IQ. Inter-orbital distance was measured on T1-weighted MRI scans. This value was entered into a voxel-by-voxel linear regression analysis with grey matter segmented from a bimodal MRI data-set. Age and total brain tissue volume were entered as covariates. Results: Intra-class coefficient for measurement of the inter-orbital distance was 0.95. Inter-orbital distance was significantly increased in the autism group (p = 0.03, 2-tailed). The autism group showed a significant relationship between inter-orbital distance grey matter volume of bilateral amygdalae extending to the unci and inferior temporal poles. Conclusions: Greater inter-orbital distance in the autism group compared with healthy controls is consistent with infant head size expansion in autism. Inter-orbital distance positively correlated with volume of medial temporal lobe structures, suggesting a link to "social brain" dysmorphology in the autism group. We suggest these data support the role of optical MPAs as a "fossil record" of early aberrant neurodevelopment, and potential biomarker for brain dysmaturation in autism. C1 [Cheung, Charlton; McAlonan, Grainne M.; Fung, Germaine; Yu, Kevin K.; Sham, Pak C.; Chua, Siew E.] Univ Hong Kong, Dept Psychiat, Pokfulam, Hong Kong, Peoples R China. [Tai, Kin-Shing] Univ Hong Kong, Dept Radiol, Pokfulam, Hong Kong, Peoples R China. [McAlonan, Grainne M.; Sham, Pak C.; Chua, Siew E.] Univ Hong Kong, State Key Lab Cognit Neurosci, Hong Kong, Hong Kong, Peoples R China. [Fung, Yee Y.] Harvard Univ, Harvard Sch Dent Med, Boston, MA 02115 USA. RP Cheung, C (reprint author), Univ Hong Kong, Dept Psychiat, Pokfulam, Hong Kong, Peoples R China. EM mcalonan@hkucc.hku.hk FU ING Asia-Pacific; University of Hong Kong FX Dr G McAlonan received funding donation for autism research from ING Asia-Pacific. The authors acknowledge a generous donation from ING Asia Pacific to support autism research in Department of Psychiatry, University of Hong Kong and University of Hong Kong funding support. No other external funding exists for this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Lett, Tristram A. P. Lerch, Jason P. Tiwari, Arun K. Ameis, Stephanie H. Rajji, Tarek K. Mueller, Daniel J. Mulsant, Benoit H. Kennedy, James L. TI Neurexin-1 and Frontal Lobe White Matter: An Overlapping Intermediate Phenotype for Schizophrenia and Autism Spectrum Disorders SO PLOS ONE LA English DT Article ID COPY NUMBER VARIATION; ADOLESCENT-ONSET SCHIZOPHRENIA; EXCITATORY SYNAPSE FORMATION; DEVELOPMENTAL DISORDERS; STRUCTURAL VARIANTS; NICOTINE DEPENDENCE; ASPERGERS-SYNDROME; PREFRONTAL CORTEX; BIPOLAR DISORDER; BRAIN ANATOMY AB Background: Structural variation in the neurexin-1 (NRXN1) gene increases risk for both autism spectrum disorders (ASD) and schizophrenia. However, the manner in which NRXN1 gene variation may be related to brain morphology to confer risk for ASD or schizophrenia is unknown. Method/Principal Findings: 53 healthy individuals between 18-59 years of age were genotyped at 11 single nucleotide polymorphisms of the NRXN1 gene. All subjects received structural MRI scans, which were processed to determine cortical gray and white matter lobar volumes, and volumes of striatal and thalamic structures. Each subject's sensorimotor function was also assessed. The general linear model was used to calculate the influence of genetic variation on neural and cognitive phenotypes. Finally, in silico analysis was conducted to assess potential functional relevance of any polymorphisms associated with brain measures. A polymorphism located in the 39 untranslated region of NRXN1 significantly influenced white matter volumes in whole brain and frontal lobes after correcting for total brain volume, age and multiple comparisons. Follow-up in silico analysis revealed that this SNP is a putative microRNA binding site that may be of functional significance in regulating NRXN1 expression. This variant also influenced sensorimotor performance, a neurocognitive function impaired in both ASD and schizophrenia. Conclusions: Our findings demonstrate that the NRXN1 gene, a vulnerability gene for SCZ and ASD, influences brain structure and cognitive function susceptible in both disorders. In conjunction with our in silico results, our findings provide evidence for a neural and cognitive susceptibility mechanism by which the NRXN1 gene confers risk for both schizophrenia and ASD. C1 [Voineskos, Aristotle N.; Lett, Tristram A. P.; Tiwari, Arun K.; Rajji, Tarek K.; Mueller, Daniel J.; Mulsant, Benoit H.; Kennedy, James L.] Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON, Canada. [Lerch, Jason P.; Ameis, Stephanie H.] Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada. RP Voineskos, AN (reprint author), Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON, Canada. EM Aristotle_Voineskos@camh.net RI Voineskos, Aristotle/J-5014-2013 FU Canadian Institutes of Health Research; APA/APIRE Astra-Zeneca; NARSAD; Centre for Addiction and Mental Health; Ontario Mental Health Foundation; Bristo-Meyers Squibb; Eli-Lilly; Pfizer FX This work was supported by the Canadian Institutes of Health Research Clinician Scientist Award (ANV); APA/APIRE Astra-Zeneca Young Minds in Psychiatry Award (ANV), NARSAD (ANV, AKT, TKR) and the Centre for Addiction and Mental Health (AKT). Dr. Muller is supported by the Canadian Institutes of Health Research, Ontario Mental Health Foundation, and NARSAD. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.The authors have read the journal's policy and have the following conflicts: JKL: one time honorarium from Eli Lilly Corporation. BHM: research support (medications for federally-funded clinical trials) from Bristo-Meyers Squibb, Eli-Lilly, and Pfizer. This does not alter the authors' adherence to all the PLoS ONE policies on sharing data and materials. 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Mileni, Mauro Comoletti, Davide Stevens, Raymond C. Harel, Michel Taylor, Palmer TI The Crystal Structure of the alpha-Neurexin-1 Extracellular Region Reveals a Hinge Point for Mediating Synaptic Adhesion and Function SO STRUCTURE LA English DT Article ID ALPHA-NEUREXINS; LIGAND-BINDING; BETA-NEUREXINS; CELL-ADHESION; LNS DOMAIN; CA2+ CHANNELS; AUTISM; COMPLEX; NEUROLIGIN; PROTEIN AB alpha- and beta-neurexins (NRXNs) are transmembrane cell adhesion proteins that localize to presynaptic membranes in neurons and interact with the postsynaptic neuroligins (NLGNs). Their gene mutations are associated with the autism spectrum disorders. The extracellular region of alpha-NRXNs, containing nine independently folded domains, has structural complexity and unique functional characteristics, distinguishing it from the smaller beta-NRXNs. We have solved the X-ray crystal structure of seven contiguous domains of the alpha-NRXN-1 extracellular region at 3.0 angstrom resolution. The structure reveals an arrangement where the N-terminal five domains adopt a more rigid linear conformation and the two C-terminal domains form a separate arm connected by a flexible hinge. In an extended conformation the molecule is suitably configured to accommodate a bound NLGN molecule, as supported by structural comparison and surface plasmon resonance. These studies provide the structural basis for a multifunctional synaptic adhesion complex mediated by alpha-NRXN-1. C1 [Miller, Meghan T.; Comoletti, Davide; Harel, Michel; Taylor, Palmer] Univ Calif San Diego, Dept Pharmacol, Skaggs Sch Pharm & Pharmaceut Sci, La Jolla, CA 92093 USA. [Mileni, Mauro; Stevens, Raymond C.] Scripps Res Inst, Dept Mol Biol, La Jolla, CA 92037 USA. [Harel, Michel] Weizmann Inst Sci, Dept Struct Biol, IL-76100 Rehovot, Israel. RP Miller, MT (reprint author), Univ Calif San Diego, Dept Pharmacol, Skaggs Sch Pharm & Pharmaceut Sci, La Jolla, CA 92093 USA. EM m4miller@ucsd.edu; pwtaylor@ucsd.edu FU NIH [RO1-GM18360-39, P42ES 10337, GM 07752, P50 GM073197] FX We are grateful to Drs. Yves Bourne and Pascale Marchot for helpful comments on the manuscript. This work was supported by NIH grants RO1-GM18360-39 and P42ES 10337 to P.T., Training Grant GM 07752 to M.T.M., NIH Common Fund Grant P50 GM073197 for technology development to R.C.S, and Autism Speaks #2617 to D.C. X-ray data were collected at that the BL11-1 beamline of the Stanford Synchrotron Radiation Lightsource (SSRL, Menlo Park, CA). 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The alpha-neurexin extracellular domain consists of six LNS domains interspersed by three EGF-like repeats and interacts with many different proteins in the synaptic cleft. To understand how alpha-neurexins might function as synaptic organizers, we solved the structure of the neurexin la extracellular domain (nl alpha) to 2.65 angstrom. The L-shaped molecule can be divided into a flexible repeat I (LNS1-EGF-A-LNS2), a rigid horseshoe-shaped repeat II (LNS5-EGF-B-LNS4) with structural similarity to so-called reelin repeats, and an extended repeat Ill (LNS5-EGF-B-LNS6) with controlled flexibility. A 2.95 angstrom structure of n1 alpha carrying splice insert SS#3 in LNS4 reveals that SS#3 protrudes as a loop and does not alter the rigid arrangement of repeat II. The global architecture imposed by conserved structural features enables alpha-neurexins to recruit and organize proteins in distinct and variable ways, influenced by splicing, thereby promoting synaptic function. C1 [Chen, Fang; Venugopal, Vandavasi; Murray, Beverly; Rudenko, Gabby] Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA. [Rudenko, Gabby] Univ Michigan, Dept Pharmacol, Ann Arbor, MI 48109 USA. RP Rudenko, G (reprint author), Univ Michigan, Inst Life Sci, Ann Arbor, MI 48109 USA. EM rudenko@umich.edu FU NIMH [RO1 MH077303]; American Recovery and Reinvestment Act [3R01MH077303-04S1] FX This work was funded by NIMH RO1 MH077303 and would not have been possible without funds from the American Recovery and Reinvestment Act 3R01MH077303-04S1. We thank Dr. T. Sudhof for the n1 alpha cDNA, Dr. D. Borek for advice on data processing, Dr. S. Anderson for excellent beamline support, I. Wu for initial crystallization experiments, and Dr. C. Brown for reagents. Diffraction data were collected at LS-CAT (beam-line 21-ID-D) at the Advanced Photon Source, Argonne National Laboratories. F.C. performed molecular biology, protein purification, and crystallization. V.V. performed crystallization, and structure determination of n1 alpha+SS#3. B.M. performed molecular biology. G.R. conceived the research plan, performed protein purification, crystallization, structure determination of n1 alpha and wrote the manuscript. 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Mankuta, David Yirmiya, Nurit Malavasi, Fabio TI Are retinoids potential therapeutic agents in disorders of social cognition including autism? SO FEBS LETTERS LA English DT Review DE Autism spectrum disorder (ASD); All-trans retinoic acid (ATRA); CD38; Oxytocin; Polymorphism ID OXYTOCIN RECEPTOR OXTR; LYMPHOBLASTOID CELL-LINES; PERVASIVE DEVELOPMENTAL DISORDERS; GENE-EXPRESSION PROFILES; HIGH-FUNCTIONING AUTISM; ADP-RIBOSYL CYCLASE; BIPOLAR DISORDER; ARGININE-VASOPRESSIN; SPECTRUM DISORDERS; GENOME-WIDE AB Increasing evidence suggests that the nonapeptide, oxytocin (OT), helps shape social and affiliative behaviors not only in lower mammals but also in humans. Recently, an essential mediator of brain OT release has been discovered, ADP-ribosyl cyclase and/or CD38. We have subsequently shown that polymorphisms across the CD38 gene are associated with autism spectrum disorders (ASD). 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CR Bertone A, 2004, BEHAV BRAIN SCI, V27, P592 Crick F., 1990, Seminars in the Neurosciences, V2, P263 Nieoullon A, 2002, PROG NEUROBIOL, V67, P53, DOI 10.1016/S0301-0082(02)00011-4 Seth AK, 2009, CONSCIOUSNESS COMPLE Seth AK, 2008, TRENDS COGN SCI, V12, P314, DOI 10.1016/j.tics.2008.04.008 NR 5 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 2011 VL 23 IS 3 BP E25 EP E25 PG 1 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 924XF UT WOS:000302723900018 PM 21948914 ER PT J AU Oriel, KN George, CL Peckus, R Semon, A AF Oriel, Kathryn N. George, Cheryl L. Peckus, Rebecca Semon, Amanda TI The Effects of Aerobic Exercise on Academic Engagement in Young Children With Autism Spectrum Disorder SO PEDIATRIC PHYSICAL THERAPY LA English DT Article DE aerobic exercise; attention; autism spectrum disorder; child; educational activities; physical therapy/methods; special education; stereotypic movement disorder/therapy ID SELF-STIMULATORY BEHAVIOR; STEREOTYPIC BEHAVIORS; PHYSICAL EXERCISE; CLASSROOMS; STUDENTS AB Purpose: To determine whether participation in aerobic exercise before classroom activities improves academic engagement and reduces stereotypic behaviors in young children with autism spectrum disorder. Methods: This study employed a within-subjects crossover design, using a treatment condition (aerobic exercise) and a control condition, across 4 classrooms. The treatment condition included 15 minutes of running/jogging followed by a classroom task. The control condition included a classroom task not preceded by exercise. The number of stereotypic behaviors, percentage of on-task behavior, and correct/incorrect responses were measured. The Wilcoxon signed rank test was used to compare differences between conditions. Results: Statistically significant improvements were found in correct responding following exercise (P < .05). No significant differences were found for on-task behavior or stereotypic behaviors. Conclusions: Consistent with findings in older children, these results indicate that aerobic exercise prior to classroom activities may improve academic responding in young children with autism spectrum disorder. (Pediatr Phys Ther 2011;23:187-193) C1 [Oriel, Kathryn N.; George, Cheryl L.; Peckus, Rebecca; Semon, Amanda] Lebanon Valley Coll, Dept Phys Therapy, Annville, PA 17003 USA. RP Oriel, KN (reprint author), Lebanon Valley Coll, Dept Phys Therapy, 101 N Coll Ave, Annville, PA 17003 USA. 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Phys. Ther. PD SUM PY 2011 VL 23 IS 2 BP 187 EP 193 DI 10.1097/PEP.0b013e318218f149 PG 7 WC Pediatrics; Rehabilitation SC Pediatrics; Rehabilitation GA 896HD UT WOS:000300555400014 PM 21552085 ER PT J AU vander Net, J Sprong, M AF vander Net, Janjaap Sprong, Maaike TI Commentary on "The Effects of Aerobic Exercise on Academic Engagement in Young Children With Autism Spectrum Disorder" SO PEDIATRIC PHYSICAL THERAPY LA English DT Editorial Material C1 [vander Net, Janjaap; Sprong, Maaike] Univ Childrens Hosp UMC, Utrecht, Netherlands. RP vander Net, J (reprint author), Univ Childrens Hosp UMC, Utrecht, Netherlands. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0898-5669 J9 PEDIATR PHYS THER JI Pediatr. Phys. Ther. PD SUM PY 2011 VL 23 IS 2 BP 193 EP 193 DI 10.1097/PEP.0b013e3182193630 PG 1 WC Pediatrics; Rehabilitation SC Pediatrics; Rehabilitation GA 896HD UT WOS:000300555400015 PM 21552086 ER PT J AU Mieres, AC Smallwood, V Nicholson, SK AF Mieres, Ana C. Smallwood, Varina Nicholson, Sheila K. TI Retrospective Case Report: Evaluation of Pain in a Child With Pervasive Developmental Disorder SO PEDIATRIC PHYSICAL THERAPY LA English DT Article DE autism spectrum disorder; child; interdisciplinary health team; interdisciplinary health team/jurisprudence; nursing; pain assessment; pain measurement; periodontal abscess; physical therapy; primary health care; school health services; special education ID AUTISM; HEALTH AB Purpose: To describe how a nurse and a physical therapist in an interprofessional (IP) school-based clinic collaborated to meet the needs of a child with pervasive developmental disorder-not otherwise specified, with atypical classroom behaviors and declining student performance. Summary: The IP team sought answers for atypical classroom behaviors with declining student performance. Student sensory perceptions masked and delayed the ability to recognize infection. Observations: Cumulative observations by the team generated serial referrals until a diagnosis of dental abscess was identified. Conclusions: An IP team in this school setting generated a positive outcome for a student demonstrating absence of clear indicators of pain or infection, with additional positive outcomes for the clinic. Recommendations for clinical practice: Further studies are needed to recognize illness earlier in the absence of pain or pain perception in children with a form of autism spectrum disorder and to develop reliable and valid metrics for pain identification. (Pediatr Phys Ther 2011;23:194-200) C1 [Mieres, Ana C.] Univ S Florida, Coll Med, Sch Phys Therapy & Rehabil Sci, Tampa, FL 33612 USA. [Smallwood, Varina] Tampa Gen Hosp, Specialty Clin, Tampa, FL 33606 USA. 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PD SUM PY 2011 VL 23 IS 2 BP 194 EP 200 DI 10.1097/PEP.0b013e318218f35f PG 7 WC Pediatrics; Rehabilitation SC Pediatrics; Rehabilitation GA 896HD UT WOS:000300555400016 PM 21552087 ER PT J AU Bruneau, N Szepetowski, P AF Bruneau, Nadine Szepetowski, Pierre TI The Role of the Urokinase Receptor in Epilepsy, in Disorders of Language, Cognition, Communication and Behavior, and in the Central Nervous System SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review DE uPAR; PLAUR; SRPX2; sushi domain; epilepsy; language; speech; cognition; autism; brain development ID PLASMINOGEN-ACTIVATOR RECEPTOR; ROLANDIC EPILEPSY; INTERNEURON DEVELOPMENT; INCREASED EXPRESSION; CORTICAL INTERNEURONS; CELL-MIGRATION; DEFICIENT MICE; GROWTH-FACTOR; SPEECH; GENE AB As a key component of the plasminogen activation system, uPAR, the receptor for the plasminogen activator of the urokinase type, is involved in many physiological and pathological processes. Besides its classical roles, there has been increased evidence that uPAR or uPAR-associated pathways, participate in the development, in the functioning and in the pathology of the central nervous system. Qualitative and quantitative changes in the expressions of uPAR and of its canonical ligand uPA have been observed in a large variety of epileptic disorders, either in human or in animal models, as well as in other brain diseases (stroke and brain trauma, multiple sclerosis, Alzheimer's disease, cerebral malaria, HIV-associated leukoencephalopathy and encephalitis). The variety of such pathological conditions and the different brain areas and cell types involved, likely reflects the wide range and the complexity of the multiple and somehow intertwined pathophysiological mechanisms related with uPAR. In the mouse, the knock-out of the Upar-encoding gene (Plaur) leads to significant and nearly complete loss in parvalbumin-containing interneurons during brain development. This is associated with increased susceptibility to spontaneous and chemically-induced seizures and with increased anxiety and impaired social interactions. The recent identification of the novel uPAR ligand SRPX2 (Sushi repeat protein, X-linked 2) and the regulation of both the SRPX2 and PLAUR genes by transcription factor FOXP2 has shed novel and exciting insights into the role of uPAR-related molecular networks in rolandic epilepsy, in developmental verbal dyspraxia, in perisylvian polymicrogyria, and generally in disorders of the speech areas and circuits. uPAR, its regulators and partners, as well as other proteins containing Ly-6/uPAR/alpha-neurotoxin domains, represent key entry points for present and future studies not only on speech-related disorders but also on epilepsy and autism spectrum disorders. C1 [Szepetowski, Pierre] INSERM, Inst Neurobiol Mediterranee INMED, GEIA Grp, UMRS901, F-13273 Marseille 09, France. [Bruneau, Nadine; Szepetowski, Pierre] Univ Aix Marseille 2, UMR S901, Aix Marseille 2, France. RP Szepetowski, P (reprint author), INSERM, Inst Neurobiol Mediterranee INMED, GEIA Grp, UMRS901, Parc Sci Luminy,BP 13, F-13273 Marseille 09, France. EM szepetowski@inmed.univ-mrs.fr FU INSERM (Institut National de la Sante et de la Recherche Medicale); ANR (Agence Nationale de la Recherche) FX This work was supported by INSERM (Institut National de la Sante et de la Recherche Medicale) and by an ANR (Agence Nationale de la Recherche) grant (EPILAND project). 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Pharm. Design PD JUN PY 2011 VL 17 IS 19 BP 1914 EP 1923 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 883GK UT WOS:000299622000005 PM 21711233 ER PT J AU Carpentier, PA Dingman, AL Palmer, TD AF Carpentier, Pamela A. Dingman, Andra L. Palmer, Theo D. TI Placental TNF-alpha Signaling in Illness-Induced Complications of Pregnancy SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID NECROSIS-FACTOR-ALPHA; TOLL-LIKE RECEPTORS; RECURRENT SPONTANEOUS-ABORTION; AUTISM SPECTRUM DISORDERS; MATERNAL INFLAMMATION; AUTOIMMUNE-DISEASES; PRENATAL INFECTION; GROWTH RESTRICTION; BRAIN-DEVELOPMENT; INFANTILE-AUTISM AB Maternal infections are implicated in a variety of complications during pregnancy, including pregnancy loss, prematurity, and increased risk of neurodevelopmental disorders in the child. Here, we show in mice that even mild innate immune activation by low-dose lipopolysaccharide in early pregnancy causes hemorrhages in the placenta and increases the risk of pregnancy loss. Surviving fetuses exhibit hypoxia in the brain and impaired fetal neurogenesis. Maternal Toll-like receptor 4 signaling is a critical mediator of this process, and its activation is accompanied by elevated proinflammatory cytokines in the placenta. We evaluated the role of tumor necrosis factor-alpha (TNF-alpha) signaling and show that TNF receptor 1 (TNFR1) is necessary for the illnessinduced placental pathology, accompanying fetal hypoxia, and neuroproliferative defects in the fetal brain. We also show that placental TNFR1 in the absence of maternal TNFR1 is sufficient for placental pathology to develop and that a clinically relevant TNT-a antagonist prevents placental pathology and fetal loss. Our observations suggest that the placenta is highly sensitive to proinflammatory signaling in early pregnancy and that TNT-a is an effective target for preventing illness-related placental defects and related risks to the fetus and fetal brain development. (Am J Pathol 2011, 178:2802-2810; DOL. 10.1016/j.ajpath.2011.02.042) C1 [Palmer, Theo D.] Stanford Univ, Inst Stem Cell Biol & Regenerat Med, Stanford, CA 94305 USA. Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA. RP Palmer, TD (reprint author), Stanford Univ, Inst Stem Cell Biol & Regenerat Med, 265 Campus Dr,G1141B, Stanford, CA 94305 USA. EM tpalmer@stanford.edu FU March of Dimes, Autism Speaks; Blume Foundation; Lucile Packard Foundation; NIH [F32 NS060427-01A1, 5T90DK070103-04]; Howard Hughes Medical Foundation FX Supported by grants from the March of Dimes, Autism Speaks, and the Blume Foundation (T.D.P.); by fellowship support from the Lucile Packard Foundation and NIH F32 NS060427-01A1 and NIH 5T90DK070103-04 (P.A.C.); and by fellowship support from the Howard Hughes Medical Foundation (A.L.D.). 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TI ABOVE GENETICS: LESSONS FROM CEREBRAL DEVELOPMENT IN AUTISM SO TRANSLATIONAL NEUROSCIENCE LA English DT Article DE Beta catenin; Minicolumns; Neural stem cells; Rett syndrome; Fragile X syndrome; Tuberous sclerosis; Valproic acid; Pten phosphohydrolase; Ultrasonography; Cell adhesion molecules, neuronal ID FRAGILE-X-SYNDROME; TUBEROUS SCLEROSIS COMPLEX; CONGENITAL ADRENAL-HYPERPLASIA; MENTAL-RETARDATION PROTEIN; POLYCYSTIC-OVARY-SYNDROME; FETAL VALPROATE SYNDROME; CELL-ADHESION MOLECULE; NEURAL STEM-CELLS; GROWTH-FACTOR-I; BETA-CATENIN AB While a distinct minicolumnar phenotype seems to be an underlying factor in a significant portion of cases of autism, great attention is being paid not only to genetics but to epigenetic factors which may lead to development of the conditions. Here we discuss the indivisible role the molecular environment plays in cellular function, particularly the pivotal position which the transcription factor and adhesion molecule, beta-catenin, occupies in cellular growth. In addition, the learning environment is not only integral to postnatal plasticity, but the prenatal environment plays a vital role during corticogenesis, neuritogenesis, and synaptogenesis as well. To illustrate these points in the case of autism, we review important findings in genetics studies (e.g., PTEN, TSC1/2, FMRP, MeCP2, Neurexin-Neuroligin) and known epigenetic factors ( e. g., valproic acid, estrogen, immune system, ultrasound) which may predispose towards the minicolumnar and connectivity patterns seen in the conditions, showing how one-gene mutational syndromes and exposure to certain CNS teratogens may ultimately lead to comparable phenotypes. This in turn may shed greater light on how environment and complex genetics combinatorially give rise to a heterogenetic group of conditions such as autism. C1 [Williams, Emily L.] Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA. [Casanova, Manuel F.] Univ Louisville, Dept Psychiat & Behav Sci, Louisville, KY 40202 USA. RP Williams, EL (reprint author), Univ Louisville, Dept Anat Sci & Neurobiol, Louisville, KY 40202 USA. 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Neurosci. PD JUN PY 2011 VL 2 IS 2 BP 106 EP 120 DI 10.2478/s13380-011-0016-3 PG 15 WC Neurosciences SC Neurosciences & Neurology GA 873ME UT WOS:000298886600003 ER PT J AU Battaglia, A AF Battaglia, A. TI Sensory impairment in mental retardation: a potential role for NGF SO ARCHIVES ITALIENNES DE BIOLOGIE LA English DT Article DE Mental retardation; Autism spectrum disorder; Sensory impairment; Eph receptors; Pain; NGF; TrkA; Rett syndrome; Familial dysautonomia; Prader-Willi; Williams syndrome ID NERVE GROWTH-FACTOR; TUBEROUS SCLEROSIS COMPLEX; CONGENITAL INSENSITIVITY; AUTISTIC DISORDER; RETT-SYNDROME; DELETION SYNDROME; NEONATAL BLOOD; YOUNG-CHILDREN; DOWN-SYNDROME; PAIN AB Sensory impairment is defined as the inability to interpret outside stimuli such as visual, auditory, verbal, sense of touch, taste or smell or feelings of pain. This leads to absence of sensation and neuronal coordination. The impairment may be caused by ageing and other physiological changes, accident or injuries or can be found in some cases of mental retardation (MR) also referred to as intellectual disability. Known cases of MR involving inability to accurately interpret an outside source or stimuli are: Fragile-X syndrome; Tuberous sclerosis complex (TSC) with associated autism spectrum disorder (ASD); Rett syndrome; Autism and ASD with or without MR; Chromosome 22q13.3 deletion syndrome; familial dysautonomia, Prader-Willi's syndrome, Williams syndrome. In this review we will discuss in particular form of ASD and altered sensory sensitivity. The role of NGF in causing pro-nociceptive activity and its role in peripheral sensitisation is discussed under the light of its involvement in forms of MR where loss of pain perception is a main feature due to mutations to NGF receptors or NGF genes during development. Other forms of MR with altered sensory impairment will be considered as well as additional potential mechanisms involved. C1 Kings Coll London, Sch Biomed Sci, Dept Anat & Human Sci, London, England. RP Battaglia, A (reprint author), Kings Coll London, Sch Biomed Sci, Dept Anat & Human Sci, London, England. 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Ital. Biol. PD JUN PY 2011 VL 149 IS 2 SI SI BP 193 EP 203 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 853OC UT WOS:000297434600003 PM 21701991 ER PT J AU Rapin, I AF Rapin, Isabelle TI Child Neurologists as Evaluators of Developmental Disorders SO SEMINARS IN PEDIATRIC NEUROLOGY LA English DT Review AB Child neurologists are required to evaluate and care for an increasing number of children with developmental disorders; therefore they need to be familiar with the more prevalent ones, in particular the autism spectrum disorders which may masquerade as others. Their assessment needs to include a screening mental status evaluation and reviewing a recent definitive test of hearing in all children with defective speech. Neurologists' responsibility is to make sure that there is no likely underlying problem like epilepsy, neurologic, or genetic condition that requires specific medical intervention or genetic counseling. They need to discuss with the parents how deeply to test for neurologic, neuropsychologic, or genetic underlying causes in children with "idiopathic" developmental problem. There is no routine work-up, thus neurologists need to be aware of and to protect children from many almost certainly uninformative, expensive tests like EEGs, brain imaging, metabolic tests, and genetic micro-array unless there is a specific indication, or testing is being performed with parents' consent for research and paid for by research, not clinical, funds. Child neurologists-in-training need to have observed psychologic/neuropsychologic testing so that they have at least a superficial understanding of the content, indications, and limitations of major tests. I do not recommend that child neurologists administer standardized tests or questionnaires, but they need to know enough about them to be able to judge their appropriateness and review recommendations with parents. Neurologists need to protect children from unnecessary testing, ineffective and in some cases potentially dangerous exploitative treatments. They must be aware of what legitimate therapies are likely to be offered, that early appropriate education is most effective long-term because it influences brain development and is superior to symptomatic pharmacotherapy. If pills are needed, child psychiatrists are likely to be better informed than neurologists and need to be consulted whenever medications familiar to neurologists are not adequately effective. Semin Pediatr Neurol 18:104-109 (C) 2011 Elsevier Inc. All rights reserved. C1 [Rapin, Isabelle] Albert Einstein Coll Med, Rose F Kennedy Ctr Intellectual & Dev Disabil Res, Bronx, NY 10461 USA. [Rapin, Isabelle] Albert Einstein Coll Med, Saul R Korey Dept Neurol, Dept Pediat, Bronx, NY 10461 USA. RP Rapin, I (reprint author), Albert Einstein Coll Med, Rose F Kennedy Ctr Intellectual & Dev Disabil Res, Room 807 Kennedy Ctr,1410 Pelham Pkwy S, Bronx, NY 10461 USA. EM isabelle.rapin@einstein.yu.edu CR Baron IS, 2004, NEUROPSYCHOLOGICAL E Deonna T, 2010, BRAIN DEV-JPN, V32, P746, DOI 10.1016/j.braindev.2010.06.011 Martin R, 2010, DEV MED CHILD NEUROL, V52, pe188, DOI 10.1111/j.1469-8749.2010.03670.x Perkins FF, 2008, J CHILD NEUROL, V23, P389, DOI 10.1177/0883073807309239 NR 4 TC 0 Z9 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 1071-9091 J9 SEMIN PEDIATR NEUROL JI Semin. Pediatr. Neurol. PD JUN PY 2011 VL 18 IS 2 BP 104 EP 109 DI 10.1016/j.spen.2011.05.004 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 849CS UT WOS:000297103700014 PM 22036491 ER PT J AU Johnston, MV AF Johnston, Michael V. TI Education of a Child Neurologist: Developmental Neuroscience Relevant to Child Neurology SO SEMINARS IN PEDIATRIC NEUROLOGY LA English DT Review ID WHITE-MATTER INJURY; NEONATAL ENCEPHALOPATHY; CELLULAR MECHANISMS; TUBEROUS SCLEROSIS; DEVELOPING BRAIN; BASAL GANGLIA; PLASTICITY; DYSFUNCTION; HYPOTHERMIA; STROKE AB Developmental neuroscience is increasingly relevant to clinical child neurology, and study of advances in neurobiology, neurochemistry and neurogenetics should be part of the curriculum of residency training. The profile of synaptic development is especially relevant to neurodevelopmental disorders such as autism, Fragile X syndrome, and early epileptic encephalopathies. This knowledge is increasingly being translated into therapies for previously untreatable disorders. Semin Pediatr Neurol 18:133-138 (C) 2011 Elsevier Inc. All rights reserved. C1 [Johnston, Michael V.] Kennedy Krieger Inst, Baltimore, MD 21205 USA. [Johnston, Michael V.] Johns Hopkins Univ, Sch Med, Baltimore, MD USA. RP Johnston, MV (reprint author), Kennedy Krieger Inst, 707 N Broadway, Baltimore, MD 21205 USA. 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Pediatr. Neurol. PD JUN PY 2011 VL 18 IS 2 BP 133 EP 138 DI 10.1016/j.spen.2011.06.009 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 849CS UT WOS:000297103700024 PM 22036501 ER PT J AU Kurt, O AF Kurt, Onur TI A Comparison of Discrete Trial Teaching with and without Gestures/Signs in Teaching Receptive Language Skills to Children with Autism SO KURAM VE UYGULAMADA EGITIM BILIMLERI LA English DT Article DE Discrete Trial Teaching; Autism; Language and Communication; Receptive Language Skills ID ALTERNATIVE COMMUNICATION; SIGN LANGUAGE; ACQUISITION; INTERVENTION; RATIONALE; SPEECH AB The present study was designed to compare the effectiveness and efficiency of two discrete trial teaching procedures for teaching receptive language skills to children with autism. While verbal instructions were delivered alone during the first procedure, all verbal instructions were combined with simple gestures and/or signs during the second procedure when teaching receptive language skills by using discrete trial teaching. A parallel treatments design was used to compare the differential effects of the two procedures on the acquisition of the receptive language skills. Two students with autism participated in the study. The results of the study showed that the discrete trial teaching procedure in which verbal instructions were combined with simple gestures and/or signs was slightly more effective and efficient on promoting the acquisition of receptive language skills for both students. Discrete trial teaching procedure in which verbal instructions were delivered alone was not effective for any of the training sets across students. C1 Anadolu Univ, Res Inst Handicapped, Eskisehir, Turkey. 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PD SUM PY 2011 VL 11 IS 3 BP 1436 EP 1444 PG 9 WC Education & Educational Research SC Education & Educational Research GA 826FA UT WOS:000295336000016 ER PT J AU Odluyurt, S AF Odluyurt, Serhat TI The Effects of Constant Time Delay Embedded Into Teaching Activities for Teaching the Names of Clothes for Preschool Children with Developmental Disabilities SO KURAM VE UYGULAMADA EGITIM BILIMLERI LA English DT Article DE Developmental Disabilities; Embedded Instruction; Constant Time Delay; Single Subject Design ID EARLY-CHILDHOOD PROGRAMS; SKILLS; INSTRUCTION; OUTCOMES; AUTISM AB The general purpose of this study was to examine the effectiveness of constant time delay embedded in activities for teaching clothes name for preschool children with developmental disabilities. This study included four participants having Down syndrome with an age range of 43-46 months. All experimental sessions were conducted in one to one teaching style. All sessions were conducted in a classroom of the university unit where the participants are every day. A multiple probe design across behaviors and replicated across subjects was used. The dependent variable of the study was teaching the names of clothes name and the independent variable of the study was constant time delay procedure. There were, full probe, intervention, generalization and maintenance sessions in the study. The results concerning effectiveness revealed that all three participants acquired the target skills at criterion level. Furthermore, participants maintained acquired skills at criterion level and generalized acquired skills to another person at criterion level. C1 Anadolu Univ, Res Inst Handicapped, Dept Special Educ, Program Educ Mentally Disabled, Eskisehir, Turkey. RP Odluyurt, S (reprint author), Anadolu Univ, Res Inst Handicapped, Dept Special Educ, Program Educ Mentally Disabled, Eskisehir, Turkey. 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PD SUM PY 2011 VL 11 IS 3 BP 1457 EP 1460 PG 4 WC Education & Educational Research SC Education & Educational Research GA 826FA UT WOS:000295336000017 ER PT J AU Toret, G Acarlar, F AF Toret, Gokhan Acarlar, Funda TI Gestures in Prelinguistic Turkish children with Autism, Down Syndrome, and Typically Developing Children SO KURAM VE UYGULAMADA EGITIM BILIMLERI LA English DT Article DE Prelinguistic Communication; Gesture Development; Autism; Down Syndrome ID JOINT ATTENTION; LANGUAGE-DEVELOPMENT; EARLY RECOGNITION; YOUNG-CHILDREN; PRETEND PLAY; INFANTS; DISORDER; PROFILES; LIFE; 1ST AB The purpose of this study was to examine gesture use in Turkish children with autism, Down syndrome, and typically developing children. Participants included 30 children in three groups: Ten children with Down syndrome, ten children with autism between 24-60 months of age, and ten typically developing children between 12-18 months of age. Principal Caregiver-child and researcher-child interactions were video-recorded in this descriptive study. Significant group differences were found for total gesture use, communicative functions, and types of gestures. Results revealed significant differences for gestures within the category of behavior regulation between the groups. The typically developing children used gestures more frequently than other groups. The lowest frequency of gesture use have been found for children with autism. It was found that children with autism have more difficulties in gesture use within the category of Social interaction and joint attention than Down syndrome and typically developing groups. Children with Down syndrome have become more successful in the use of these gestures than other two groups. It was found that researcher-child interaction provides more information about the frequency of gestures than parent-child interaction. 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Bilim. PD SUM PY 2011 VL 11 IS 3 BP 1471 EP 1478 PG 8 WC Education & Educational Research SC Education & Educational Research GA 826FA UT WOS:000295336000018 ER PT J AU Weil, TM Hayes, SC Capurro, P AF Weil, Timothy M. Hayes, Steven C. Capurro, Philip TI ESTABLISHING A DEICTIC RELATIONAL REPERTOIRE IN YOUNG CHILDREN SO PSYCHOLOGICAL RECORD LA English DT Article DE Relational Frame Theory; deictic relations; perspective taking; Theory of Mind ID PERSPECTIVE-TAKING; MIND DEVELOPMENT; FALSE BELIEF; PREFERENCES; COMPLEXITY; BEHAVIOR; OPERANT; AUTISM; CATCH AB Perspective-taking skills have been shown to be pivotal in a variety of social and interpersonal interactions. A better understanding of the process involved in building such a repertoire could be beneficial in a wide variety of language and social skills training programs. A relational frame theory approach to perspective taking involves a focus on deictic relations, such as I-You, Here-There, and Now-Then. The present study examined the effect of operant contingencies on deictic relational responding in 3 normally developing young (57 to 68 months old) children. In a multiple baseline across persons and tasks format, I-You, Here-There, and Now-Then deictic relational frames were successfully shaped as operant behavior. As the children acquired deictic relational frames at the Reversed and Double-Reversed levels, the children's performance on traditional perspective-taking measures generally increased. C1 [Weil, Timothy M.] Univ S Florida, Tampa, FL 33620 USA. [Hayes, Steven C.; Capurro, Philip] Univ Nevada, Reno, NV 89557 USA. RP Weil, TM (reprint author), Univ S Florida, Tampa, FL 33620 USA. 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PD SUM PY 2011 VL 61 IS 3 BP 371 EP 390 PG 20 WC Psychology, Multidisciplinary SC Psychology GA 836IT UT WOS:000296105900005 ER PT J AU Reyna, VF Brainerd, CJ AF Reyna, Valerie F. Brainerd, Charles J. TI Dual processes in decision making and developmental neuroscience: A fuzzy-trace model SO DEVELOPMENTAL REVIEW LA English DT Article DE Autism; Aging; Adolescence; Decision making; Framing effects; Biases; Heuristics; Neurodevelopment; Prospect theory; Risk taking ID RISK-TAKING; CONJUNCTION FALLACY; INDIVIDUAL-DIFFERENCES; AGE-DIFFERENCES; PROSPECT-THEORY; EXPECTED VALUE; FALSE-MEMORY; OLDER-ADULTS; INTERTEMPORAL CHOICE; PREFRONTAL CORTEX AB From Piaget to the present, traditional and dual-process theories have predicted improvement in reasoning from childhood to adulthood, and improvement has been observed. However, developmental reversals-that reasoning biases emerge with development-have also been observed in a growing list of paradigms. We explain how fuzzy-trace theory predicts both improvement and developmental reversals in reasoning and decision making. Drawing on research on logical and quantitative reasoning, as well as on risky decision making in the laboratory and in life, we illustrate how the same small set of theoretical principles apply to typical neurodevelopment, encompassing childhood, adolescence, and adulthood, and to neurological conditions such as autism and Alzheimer's disease. For example, framing effects that risk preferences shift when the same decisions are phrased in terms of gains vs. losses-emerge in early adolescence as gist-based intuition develops. In autistic individuals, who rely less on gist-based intuition and more on verbatim-based analysis, framing biases are attenuated (i.e., they outperform typically developing control subjects). In adults, simple manipulations based on fuzzy-trace theory can make framing effects appear and disappear depending on whether gist-based intuition or verbatim-based analysis is induced. These theoretical principles are summarized and integrated in a new mathematical model that specifies how dual modes of reasoning combine to produce predictable variability in performance. In particular, we show how the most popular and extensively studied model of decision making-prospect theory-can be derived from fuzzy-trace theory by combining analytical (verbatim-based) and intuitive (gist-based) processes. (C) 2011 Elsevier Inc. All rights reserved. C1 [Reyna, Valerie F.] Cornell Univ, Dept Human Dev, Ctr Behav Econ & Decis Res, Ithaca, NY 14853 USA. [Reyna, Valerie F.] Cornell Univ, Dept Psychol, Ctr Behav Econ & Decis Res, Ithaca, NY 14853 USA. [Brainerd, Charles J.] Cornell Univ, Dept Human Dev, Coll Law, Ithaca, NY 14853 USA. 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Feirsen, Nicole Tanel, Nadia Hollander, Eric TI Factor Analysis of Repetitive Behaviors in Autism as Measured by the Y-BOCS SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; MENTAL-RETARDATION; SYMPTOM; SCALE; CHILDREN; PLACEBO; ADULTS AB The authors carried out a factor analysis of the Yale-Brown Obsessive-Compulsive Scale checklist at the category level in order to reduce the number of variables in this domain and ultimately identify possible endophenotypes; 181 children with autism were enrolled. The authors estimated a tetrachoric correlation matrix among the dichotomous symptom categories and then used exploratory and confirmatory factor analyses to identify a clinically meaningful factor structure for this correlation matrix. Their analysis supported a four-factor solution: obsessions, higher-order repetitive behaviors, lower-order repetitive behaviors, and hoarding. These findings are another step in the effort to identify genetically and biologically distinct groups within this population. (The Journal of Neuropsychiatry and Clinical Neurosciences 2011; 23:332-339) C1 [Anagnostou, Evdokia] Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. St Johns Univ, Dept Psychol, Jamaica, NY 11439 USA. Univ Toronto, Dept Pediat, Toronto, ON M5S 1A1, Canada. Albert Einstein Coll Med, Dept Psychiat, New York, NY USA. Montefiore Med Ctr, New York, NY USA. RP Anagnostou, E (reprint author), Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. 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Neuropsychiatr. Clin. Neurosci. PD SUM PY 2011 VL 23 IS 3 BP 332 EP 339 PG 8 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 822BI UT WOS:000295018300011 PM 21948895 ER PT J AU Wolery, M Dunlap, G Ledford, JR AF Wolery, Mark Dunlap, Glen Ledford, Jennifer R. TI Single-Case Experimental Methods Suggestions for Reporting SO JOURNAL OF EARLY INTERVENTION LA English DT Editorial Material DE autism spectrum disorders; preschoolers; effective intervention; single case methods; mental retardation; preschool inclusion; disabilities and development delays ID SPECIAL-EDUCATION; SUBJECT RESEARCH; RELIABILITY AB This editorial describes important issues in the reporting of studies using single case experimental methods. The intent is to provide authors with a short description of information that should be included in manuscripts using single case experimental methods and submitted to the Journal of Early Intervention. The editorial is organized by several questions, and these questions refer to the major sections of research reports. References are provided to give authors more detailed descriptions of single case methods and the reporting of studies using those methods. C1 [Wolery, Mark] Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. [Dunlap, Glen] Univ S Florida, Tampa, FL USA. RP Wolery, M (reprint author), Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. EM mark.wolery@vanderbilt.edu RI Ledford, Jennifer/G-7455-2014 CR ARTMAN K, REMEDIAL SP IN PRESS, DOI DOI 10.1177/0741932510381653 Barlow D. H., 2008, SINGLE CASE EXPT DES BILLINGSLEY F, 1980, BEHAV ASSESS, V2, P229 BIRNBRAUER JS, 1981, ANAL INTERVEN DEVEL, V1, P117, DOI 10.1016/0270-4684(81)90026-4 Campbell D. T., 1963, EXPT QUASIEXPERIMENT Campbell J. M., 2010, SINGLE SUBJECT RES M, P417 CHRISTENSEN LB, 1991, EXPT METHODOLOGY Durand VM, 2005, J POSIT BEHAV INTERV, V7, P186, DOI 10.1177/10983007050070030801 Gast D. 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PD JUN PY 2011 VL 33 IS 2 BP 103 EP 109 DI 10.1177/1053815111418235 PG 7 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 818GM UT WOS:000294739700001 ER PT J AU Smith, AL Romski, MA Sevcik, RA Adamson, LB Bakeman, R AF Smith, Ashlyn L. Romski, Mary Ann Sevcik, Rose A. Adamson, Lauren B. Bakeman, Roger TI Parent Stress and Its Relation to Parent Perceptions of Communication Following Parent-Coached Language Intervention SO JOURNAL OF EARLY INTERVENTION LA English DT Article DE disabilities and developmental delays; early language intervention; parent stress; parent perceptions ID DEVELOPMENTAL DELAYS; HANDICAPPED-CHILDREN; POSITIVE PERCEPTIONS; BEHAVIOR PROBLEMS; FAMILIES; DISABILITIES; TODDLERS; AUTISM; SKILLS AB The effects of a parent-coached language intervention on parent stress and its relation to parent perceptions of communication development were examined in 60 parents of toddlers with developmental delays. Results indicated that overall parent stress was not high prior to or following language intervention. Parents' perceptions about the severity of their children's communication deficits partially mediated the relationship between expressive language at preintervention and parent stress at postintervention. Parents of children who had better expressive language at the beginning of intervention perceived their children's communication difficulties as less severe and had less parent stress following language intervention. C1 [Smith, Ashlyn L.; Sevcik, Rose A.; Adamson, Lauren B.; Bakeman, Roger] Georgia State Univ, Dept Psychol, Atlanta, GA 30303 USA. [Romski, Mary Ann] Georgia State Univ, Dept Commun, Atlanta, GA 30303 USA. [Romski, Mary Ann] Georgia State Univ, Dept Psychol, Atlanta, GA 30303 USA. RP Smith, AL (reprint author), Georgia State Univ, Dept Psychol, Univ Plaza, Atlanta, GA 30303 USA. 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Early Interv. PD JUN PY 2011 VL 33 IS 2 BP 135 EP 150 DI 10.1177/1053815111405526 PG 16 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 818GM UT WOS:000294739700003 ER PT J AU Sasson, NJ Pinkham, AE Carpenter, KLH Belger, A AF Sasson, Noah J. Pinkham, Amy E. Carpenter, Kimberly L. H. Belger, Aysenil TI The benefit of directly comparing autism and schizophrenia for revealing mechanisms of social cognitive impairment SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Social cognition; Face processing; Emotion; Amygdala; Superior temporal sulcus; Fusiform gyrus ID HIGH-FUNCTIONING AUTISM; FACIAL-AFFECT RECOGNITION; EARLY INFANTILE-AUTISM; HUMAN NEURAL SYSTEM; FUSIFORM FACE AREA; CLINICAL HIGH-RISK; ASPERGER-SYNDROME; PERSECUTORY DELUSIONS; BEHAVIORAL EVIDENCE; SPECTRUM DISORDERS AB Autism and schizophrenia share a history of diagnostic conflation that was not definitively resolved until the publication of the DSM-III in 1980. Though now recognized as heterogeneous disorders with distinct developmental trajectories and dissociative features, much of the early nosological confusion stemmed from apparent overlap in certain areas of social dysfunction. In more recent years, separate but substantial literatures have accumulated for autism and schizophrenia demonstrating that abnormalities in social cognition directly contribute to the characteristic social deficits of both disorders. The current paper argues that direct comparison of social cognitive impairment can highlight shared and divergent mechanisms underlying pathways to social dysfunction, a process that can provide significant clinical benefit by informing the development of tailored treatment efforts. Thus, while the history of diagnostic conflation between autism and schizophrenia may have originated in similarities in social dysfunction, the goal of direct comparisons is not to conflate them once again but rather to reveal distinctions that illuminate disorder-specific mechanisms and pathways that contribute to social cognitive impairment. C1 [Sasson, Noah J.] Univ Texas Dallas, Sch Behav & Brain Sci, Richardson, TX 75080 USA. [Pinkham, Amy E.] So Methodist Univ, Dept Psychol, Dallas, TX 75275 USA. [Carpenter, Kimberly L. H.; Belger, Aysenil] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. [Carpenter, Kimberly L. H.] Univ N Carolina, Curriculum Neurobiol, Chapel Hill, NC USA. RP Sasson, NJ (reprint author), Univ Texas Dallas, Sch Behav & Brain Sci, GR41,800 W Campbell Rd, Richardson, TX 75080 USA. 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Neurodev. Disord. PD JUN PY 2011 VL 3 IS 2 BP 87 EP 100 DI 10.1007/s11689-010-9068-x PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 817XP UT WOS:000294711300001 PM 21484194 ER PT J AU Campbell, DB Datta, D Jones, ST Lee, EB Sutcliffe, JS Hammock, EAD Levitt, P AF Campbell, Daniel B. Datta, Dibyadeep Jones, Shaine T. Lee, Evon Batey Sutcliffe, James S. Hammock, Elizabeth A. D. Levitt, Pat TI Association of oxytocin receptor (OXTR) gene variants with multiple phenotype domains of autism spectrum disorder SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Oxytocin; Autism; ADI-R; ADOS; SRS; Association ID GENOME-WIDE SCAN; MATERNAL-BEHAVIOR; SOCIAL-BEHAVIOR; HUMANS; SCREEN; VASOPRESSIN; RESPONSES; ETIOLOGY; LINKAGE; TWINS AB Autism spectrum disorder (ASD) is characterized by core deficits in social behavior, communication, and behavioral flexibility. Several lines of evidence indicate that oxytocin, signaling through its receptor (OXTR), is important in a wide range of social behaviors. In attempts to determine whether genetic variations in the oxytocin signaling system contribute to ASD susceptibility, seven recent reports indicated association of common genetic polymorphisms in the OXTR gene with ASD. Each involved relatively small sample sizes (57 to 436 families) and, where it was examined, failed to identify association of OXTR polymorphisms with measures of social behavior in individuals with ASD. We report genetic association analysis of 25 markers spanning the OXTR locus in 1,238 pedigrees including 2,333 individuals with ASD. Association of three markers previously implicated in ASD susceptibility, rs2268493 (P=0.043), rs1042778 (P=0.037), and rs7632287 (P=0.016), was observed. Further, these genetic markers were associated with multiple core ASD phenotypes, including social domain dysfunction, measured by standardized instruments used to diagnose and describe ASD. The data suggest association of OXTR genetic polymorphisms with ASD, although the results should be interpreted with caution because none of the significant associations would survive appropriate correction for multiple comparisons. However, the current findings of association in a large independent cohort are consistent with previous results, and the biological plausibility of participation of the oxytocin signaling system in modulating social disruptions characteristic of ASD, suggest that functional polymorphisms of OXTR may contribute to ASD risk in a subset of families. C1 [Campbell, Daniel B.] Univ So Calif, Dept Psychiat & Behav Sci, Keck Sch Med, Zilkha Neurogenet Inst 213, Los Angeles, CA 90089 USA. [Campbell, Daniel B.; Levitt, Pat] Univ So Calif, Zilkha Neurogenet Inst, Keck Sch Med, Los Angeles, CA 90089 USA. [Datta, Dibyadeep; Jones, Shaine T.] Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37232 USA. [Lee, Evon Batey; Hammock, Elizabeth A. D.] Vanderbilt Univ, Dept Pediat, Nashville, TN 37232 USA. [Lee, Evon Batey; Sutcliffe, James S.; Hammock, Elizabeth A. D.] Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, Nashville, TN 37232 USA. [Sutcliffe, James S.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. [Levitt, Pat] Univ So Calif, Dept Cell & Neurobiol, Keck Sch Med, Los Angeles, CA 90089 USA. RP Campbell, DB (reprint author), Univ So Calif, Dept Psychiat & Behav Sci, Keck Sch Med, Zilkha Neurogenet Inst 213, 1501 San Pablo St, Los Angeles, CA 90089 USA. EM dbcampbe@usc.edu RI Hammock, Elizabeth/G-1897-2011 FU National Institutes of Mental Health [MH080759] FX The Vanderbilt University Center for Human Genetics Research, Computational Genomics Core provided computational and/or analytical support for this work. The Vanderbilt University Center for Human Genetics DNA Resources Core provided technical assistance for this work. This work was funded by National Institutes of Mental Health grant MH080759. 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Szatmari, Peter CA Autism Genome Project AGP TI Novel method for combined linkage and genome-wide association analysis finds evidence of distinct genetic architecture for two subtypes of autism SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Linkage analysis; Genome-wide association; PPL; PPLD; IQ ID RECURRENT REARRANGEMENTS; POSTERIOR PROBABILITY; LOCUS HETEROGENEITY; SPECTRUM DISORDER; PHENOTYPE; MODEL; RISK; IDENTIFICATION; SCHIZOPHRENIA; STATISTICS AB The Autism Genome Project has assembled two large datasets originally designed for linkage analysis and genome-wide association analysis, respectively: 1,069 multiplex families genotyped on the Affymetrix 10 K platform, and 1,129 autism trios genotyped on the Illumina 1 M platform. We set out to exploit this unique pair of resources by analyzing the combined data with a novel statistical method, based on the PPL statistical framework, simultaneously searching for linkage and association to loci involved in autism spectrum disorders (ASD). Our analysis also allowed for potential differences in genetic architecture for ASD in the presence or absence of lower IQ, an important clinical indicator of ASD subtypes. We found strong evidence of multiple linked loci; however, association evidence implicating specific genes was low even under the linkage peaks. Distinct loci were found in the lower IQ families, and these families showed stronger and more numerous linkage peaks, while the normal IQ group yielded the strongest association evidence. It appears that presence/absence of lower IQ (LIQ) demarcates more genetically homogeneous subgroups of ASD patients, with not just different sets of loci acting in the two groups, but possibly distinct genetic architecture between them, such that the LIQ group involves more major gene effects (amenable to linkage mapping), while the normal IQ group potentially involves more common alleles with lower penetrances. The possibility of distinct genetic architecture across subtypes of ASD has implications for further research and perhaps for research approaches to other complex disorders as well. C1 [Vieland, Veronica J.; Huang, Yungui] Ohio State Univ, Battelle Ctr Math Med, Nationwide Childrens Hosp, Res Inst, Columbus, OH 43205 USA. [Hallmayer, Joachim] Stanford Univ, Sch Med, Dept Psychiat, Div Child & Adolescent Psychiat & Child Dev, Palo Alto, CA 94304 USA. [Pagnamenta, Alistair T.; Monaco, Anthony P.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. [Pinto, Dalila; Khan, Hameed; Paterson, Andrew D.; Scherer, Stephen W.] Univ Toronto, Ctr Appl Genom, Hosp Sick Children, Toronto, ON M5G 1L7, Canada. [Pinto, Dalila; Khan, Hameed; Paterson, Andrew D.; Scherer, Stephen W.] Univ Toronto, Program Genet & Genom Biol, Hosp Sick Children, Toronto, ON M5G 1L7, Canada. [Pinto, Dalila; Khan, Hameed; Paterson, Andrew D.; Scherer, Stephen W.] Univ Toronto, Dept Mol Genet, Toronto, ON M5G 1L7, Canada. [Sutcliffe, James S.] Vanderbilt Univ, Dept Mol Physiol & Biophys, Vanderbilt Kennedy Ctr, Nashville, TN 37232 USA. [Sutcliffe, James S.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN 37232 USA. [Sutcliffe, James S.] Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN 37232 USA. [Szatmari, Peter] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. RP Vieland, VJ (reprint author), Ohio State Univ, Battelle Ctr Math Med, Nationwide Childrens Hosp, Res Inst, Columbus, OH 43205 USA. EM Veronica.Vieland@nationwidechildrens.org RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013; Monaco, Anthony/A-4495-2010; Bailey, Anthony/J-2860-2014 OI Scherer, Stephen /0000-0002-8326-1999; Monaco, Anthony/0000-0001-7480-3197; Bailey, Anthony/0000-0003-4257-972X FU NIH [MH086117, NS042165]; Autism Speaks (USA); Health Research Board (HRB, Ireland); The Medical Research Council (MRC, UK); Genome Canada/Ontario Genomics Institute; Hilibrand Foundation (USA); US National Institutes of Health (NIH) [HD055751, HD055782, HD055784, HD35465, MH52708, MH55284, MH061009, MH06359, MH066673, MH080647, MH081754, MH66766, NS026630, NS049261]; Canadian Institutes for Health Research (CIHR); AP-HP Autism Speaks UK; Canada Foundation for Innovation/Ontario Innovation Trust; Deutsche Forschungsgemeinschaft (Germany) [Po 255/17-4]; EC; 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); GlaxoSmithKline-CIHR Pathfinder Chair (Canada); 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); Netherlands Organization; Ontario Ministry of Research and Innovation (Canada); Royal Netherlands Academy of Arts and Sciences [TMF/DA/5801]; Seaver Foundation (USA); Swedish Science Council; The Centre for Applied Genomics (Canada); Utah Autism Foundation (USA) FX This work was funded in part by NIH grant MH086117 (VJV) and NS042165 to the Autism Genetics Collaborative. The authors gratefully acknowledge the families participating in the study and the main funders of the AGP: Autism Speaks (USA), the Health Research Board (HRB, Ireland), 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: HD055751, HD055782, HD055784, HD35465, MH52708, MH55284, MH061009, MH06359, MH066673, MH080647, MH081754, MH66766, NS026630, NS049261), the Canadian Institutes for Health Research (CIHR), AP-HP Autism Speaks UK, Canada Foundation for Innovation/Ontario Innovation Trust, Deutsche Forschungsgemeinschaft (grant: Po 255/17-4) (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), GlaxoSmithKline-CIHR Pathfinder Chair (Canada), 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), Netherlands Organization for Scientific Research (Rubicon 825.06.031), Ontario Ministry of Research and Innovation (Canada), Royal Netherlands Academy of Arts and Sciences (TMF/DA/5801), the Seaver Foundation (USA), the Swedish Science Council, The Centre for Applied Genomics (Canada) and the Utah Autism Foundation (USA). 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Neurodev. Disord. PD JUN PY 2011 VL 3 IS 2 BP 113 EP 123 DI 10.1007/s11689-011-9072-9 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 817XP UT WOS:000294711300003 PM 21484201 ER PT J AU Pagnamenta, AT Holt, R Yusuf, M Pinto, D Wing, K Betancur, C Scherer, SW Volpi, EV Monaco, AP AF Pagnamenta, Alistair T. Holt, Richard Yusuf, Mohammed Pinto, Dalila Wing, Kirsty Betancur, Catalina Scherer, Stephen W. Volpi, Emanuela V. Monaco, Anthony P. TI A family with autism and rare copy number variants disrupting the Duchenne/Becker muscular dystrophy gene DMD and TRPM3 SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Becker; Duchenne; CNV; Comorbid; DMD ID SPECTRUM DISORDERS; KABUKI SYNDROME; RISK LOCI; CHROMOSOMES; LINKAGE; GENOME; CANCER; MALES AB Autism spectrum disorder is a genetically complex and clinically heterogeneous neurodevelopmental disorder. A recent study by the Autism Genome Project (AGP) used 1M single-nucleotide polymorphism arrays to show that rare genic copy number variants (CNVs), possibly acting in tandem, play a significant role in the genetic aetiology of this condition. In this study, we describe the phenotypic and genomic characterisation of a multiplex autism family from the AGP study that was found to harbour a duplication of exons 31-44 of the Duchenne/Becker muscular dystrophy gene DMD and also a rare deletion involving exons 1-9 of TRPM3. Further characterisation of these extremely rare CNVs was carried out using quantitative PCR, fluorescent in situ hybridisation, long-range PCR amplification and sequencing of junction fragments. The maternal chrX:32,097,213-32,321,945 tandem duplication and paternal chr9:72,480,413-73,064,196 deletion (NCBI build 36 coordinates) were transmitted to both affected boys, potentially signifying a multi-hit mechanism. The DMD reading frame rule predicts a Becker phenotype, characterised by later onset and milder symptoms. When last evaluated, neither child had developed signs of muscular dystrophy. These data are consistent with a degree of comorbidity between autism and muscular dystrophy and suggest that genomic background as well as the position of the mutation within the DMD gene may impact on the neurological correlates of Duchenne/Becker muscular dystrophy. Finally, communicating unexpected findings such as these back to families raises a number of ethical questions, which are discussed. C1 [Pagnamenta, Alistair T.; Holt, Richard; Yusuf, Mohammed; Wing, Kirsty; Volpi, Emanuela V.; Monaco, Anthony P.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. [Pinto, Dalila; Scherer, Stephen W.] Univ Toronto, Ctr Appl Genom, Hosp Sick Children, Toronto, ON M5G 1L7, Canada. [Pinto, Dalila; Scherer, Stephen W.] Univ Toronto, McLaughlin Ctr, Toronto, ON M5G 1L7, Canada. [Pinto, Dalila; Scherer, Stephen W.] Univ Toronto, Dept Mol Genet, Toronto, ON M5G 1L7, Canada. [Betancur, Catalina] Univ Paris 06, INSERM, U952, F-75005 Paris, France. [Betancur, Catalina] Univ Paris 06, CNRS, UMR 7224, F-75005 Paris, France. [Betancur, Catalina] Univ Paris 06, UPMC, F-75005 Paris, France. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. EM anthony.monaco@well.ox.ac.uk RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013; Monaco, Anthony/A-4495-2010 OI Scherer, Stephen /0000-0002-8326-1999; Monaco, Anthony/0000-0001-7480-3197 FU Nancy Lurie Marks Family Foundation; Simons Foundation; Autistica; Wellcome Trust [075491/Z/04]; NIHR Biomedical Research Centre; Royal Netherlands Academy of Arts and Sciences [TMF/DA/5801]; Netherlands Organization for Scientific Research [Rubicon 825.06.031] FX Funding for this work was from the Nancy Lurie Marks Family Foundation, the Simons Foundation, Autistica and the Wellcome Trust (core award, grant number 075491/Z/04). BAC and fosmid clones were obtained as a gift from the Wellcome Trust Sanger Institute. The authors gratefully acknowledge the families participating in the study and the international Autism Genome Project consortium for sharing data and ideas. ATP is currently supported by the NIHR Biomedical Research Centre. DP 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) and SWS is the GlaxoSmithKline Pathfinder Chair in Genetics and Genomics at the University of Toronto and the Hospital for Sick Children. We also thank Samantha Knight (NIHR Biomedical Research Centre, Oxford and The Wellcome Trust Centre for Human Genetics, Oxford) and Jane Kaye (Centre for Health, Law and Emerging Technologies, University of Oxford) for useful discussions. Raw genotype data for family 3019 is available from the NCBI Gene Omnibus Expression and dbGaP (accession codes GSE6754: for Affymetrix 10K and phs000267.v1.p1: for 1M SNP data). 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Neurodev. Disord. PD JUN PY 2011 VL 3 IS 2 BP 124 EP 131 DI 10.1007/s11689-011-9076-5 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 817XP UT WOS:000294711300004 PM 21484199 ER PT J AU Bowers, K Li, Q Bressler, J Avramopoulos, D Newschaffer, C Fallin, MD AF Bowers, Katherine Li, Qing Bressler, Joseph Avramopoulos, Dimitrios Newschaffer, Craig Fallin, M. Daniele TI Glutathione pathway gene variation and risk of autism spectrum disorders SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Oxidative stress; Gene-gene interaction ID ALCOHOL-DEHYDROGENASE; OXIDATIVE STRESS; ASSOCIATION; CHILDREN; ANTIOXIDANTS; METABOLISM; MECHANISMS; VARIANTS; ETIOLOGY; DISEASE AB Despite evidence that autism is highly heritable with estimates of 15 or more genes involved, few studies have directly examined associations of multiple gene interactions. Since inability to effectively combat oxidative stress has been suggested as a mechanism of autism, we examined genetic variation 42 genes (308 single-nucleotide polymorphisms (SNPs)) related to glutathione, the most important antioxidant in the brain, for both marginal association and multi-gene interaction among 318 case-parent trios from The Autism Genetic Resource Exchange. Models of multi-SNP interactions were estimated using the trio Logic Regression method. A three-SNP joint effect was observed for genotype combinations of SNPs in glutaredoxin, glutaredoxin 3 (GLRX3), and cystathione gamma lyase (CTH); OR=3.78, 95% CI: 2.36, 6.04. Marginal associations were observed for four genes including two involved in the three-way interaction: CTH, alcohol dehydrogenase 5, gamma-glutamylcysteine synthetase, catalytic subunit and GLRX3. These results suggest that variation in genes involved in counterbalancing oxidative stress may contribute to autism, though replication is necessary. C1 [Li, Qing; Fallin, M. Daniele] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, Baltimore, MD 21205 USA. [Bowers, Katherine; Fallin, M. Daniele] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA. [Bressler, Joseph] Johns Hopkins Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA. [Bressler, Joseph] Kennedy Krieger Inst, Baltimore, MD 21205 USA. [Avramopoulos, Dimitrios] Johns Hopkins Univ, McKusick Nathans Inst Genet Med, Sch Med, Baltimore, MD 21205 USA. [Avramopoulos, Dimitrios] Johns Hopkins Univ, Dept Psychiat, Sch Med, Baltimore, MD 21205 USA. [Newschaffer, Craig] Drexel Univ, Dept Epidemiol & Biostat, Sch Publ Hlth, Philadelphia, PA 19102 USA. RP Fallin, MD (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Biostat, 615 N Wolfe St, Baltimore, MD 21205 USA. EM dfallin@jhsph.edu RI Avramopoulos, Dimitrios/J-4392-2012 FU National Institute of Mental Health [1U24MH081810] FX 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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Neurodev. Disord. PD JUN PY 2011 VL 3 IS 2 BP 132 EP 143 DI 10.1007/s11689-011-9077-4 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 817XP UT WOS:000294711300005 PM 21484198 ER PT J AU Okerlund, ND Cheyette, BNR AF Okerlund, Nathan D. Cheyette, Benjamin N. R. TI Synaptic Wnt signaling-a contributor to major psychiatric disorders? SO JOURNAL OF NEURODEVELOPMENTAL DISORDERS LA English DT Article DE Wnt; Synapse; Schizophrenia; Bipolar disorder; Autism spectrum disorders ID ADENOMATOUS POLYPOSIS-COLI; PITT-HOPKINS-SYNDROME; FRAGILE-X-SYNDROME; KNOCK-OUT MICE; BETA-CATENIN; BIPOLAR DISORDER; HIPPOCAMPAL-NEURONS; MENTAL-RETARDATION; AXON GUIDANCE; VERTEBRATE GASTRULATION AB Wnt signaling is a key pathway that helps organize development of the nervous system. It influences cell proliferation, cell fate, and cell migration in the developing nervous system, as well as axon guidance, dendrite development, and synapse formation. Given this wide range of roles, dysregulation of Wnt signaling could have any number of deleterious effects on neural development and thereby contribute in many different ways to the pathogenesis of neurodevelopmental disorders. Some major psychiatric disorders, including schizophrenia, bipolar disorder, and autism spectrum disorders, are coming to be understood as subtle dysregulations of nervous system development, particularly of synapse formation and maintenance. This review will therefore touch on the importance of Wnt signaling to neurodevelopment generally, while focusing on accumulating evidence for a synaptic role of Wnt signaling. These observations will be discussed in the context of current understanding of the neurodevelopmental bases of major psychiatric diseases, spotlighting schizophrenia, bipolar disorder, and autism spectrum disorder. In short, this review will focus on the potential role of synapse formation and maintenance in major psychiatric disorders and summarize evidence that defective Wnt signaling could contribute to their pathogenesis via effects on these late neural differentiation processes. C1 [Okerlund, Nathan D.; Cheyette, Benjamin N. R.] Univ Calif San Francisco, Nina Ireland Lab Dev Neurobiol, Dept Psychiat, San Francisco, CA 94158 USA. [Okerlund, Nathan D.; Cheyette, Benjamin N. R.] Univ Calif San Francisco, Neurosci Program, San Francisco, CA 94158 USA. [Cheyette, Benjamin N. R.] Univ Calif San Francisco, Program Dev & Stem Cell Biol, San Francisco, CA 94158 USA. RP Cheyette, BNR (reprint author), Univ Calif San Francisco, Nina Ireland Lab Dev Neurobiol, Dept Psychiat, 1550 4th St, San Francisco, CA 94158 USA. EM bc@ucsf.edu RI Cheyette, Benjamin/K-5535-2014 OI Cheyette, Benjamin/0000-0001-9934-7941 FU US National Institutes of Health [R21MH085995]; Autism Speaks [4654]; Simons Foundation Autism Research Initiative FX This work was supported by the US National Institutes of Health R21MH085995 (B.N.R.C), Autism Speaks (N.D.O.: Predoctoral Fellowship 4654), and Simons Foundation Autism Research Initiative (B.N.R.C.). 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Neurodev. Disord. PD JUN PY 2011 VL 3 IS 2 BP 162 EP 174 DI 10.1007/s11689-011-9083-6 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 817XP UT WOS:000294711300008 PM 21533542 ER PT J AU Cetin, M AF Cetin, Mesut TI Psychotropic drug use in pregnancy: An update SO KLINIK PSIKOFARMAKOLOJI BULTENI-BULLETIN OF CLINICAL PSYCHOPHARMACOLOGY LA Turkish DT Review DE Drug use in pregnancy; teratogenicity; psychotropic drugs; antidepressants; antipsychotics ID SEROTONIN-REUPTAKE INHIBITORS; PERSISTENT PULMONARY-HYPERTENSION; PRENATAL ANTIDEPRESSANT EXPOSURE; NEONATAL WITHDRAWAL SYNDROME; ONSET MAJOR DEPRESSION; LONG-TERM TREATMENT; IN-UTERO EXPOSURE; ANTIEPILEPTIC DRUGS; BIPOLAR DISORDER; MATERNAL USE AB Pregnancy is a turbulent period, during which hormonal and psychosocial lifestyle changes occur. Hence depression, anxiety disorders, or obsessive-compulsive disorders can be triggered and chronic psychiatric disorders can be exacerbated, particularly, due to limitations on the use of psychotropic drugs. Considering a large percentage of pregnancies are not planned, overcoming these challenges creates difficulties for both the pregnant women and the team providing health care services. There are contradictory findings about the safety of psychotropic drugs and their use in the treatment of psychiatric disorders during pregnancy. The benefits and risks of psychopharmacological treatment during pregnancy should be considered carefully. When psychotropic drugs are given to pregnant women they easily reach fetus, as there are no barriers between maternal and placental blood. Generally higher serum drug levels are detected in newborns than in maternal serum. Therefore in deciding on psychotropic drug use during pregnancy, the risks of neonatal toxicity, premature and still births, and morphological and behavioral teratogenicity must be taken into account. In addition not only anatomical malformations, but also long-term behavioral teratogenicity of the drugs must be considered while evaluating the safety of drug use during pregnancy. The classical antipsychotics and tricyclic antidepressants (except chlomipramine) are relatively safe for the fetus. Antidepressant use is associated with the risk of anomalies during almost all of the prenatal period; however, the risk appears to be especially increased in fetuses that have been exposed to paroxetine and chlomipramine. There are significant findings that many atypical antipschotics cause an increase in the rate of fetal malformations by provoking gestational diabetes. Therefore, women who wish to become pregnant, who have been on ongoing atypical antipsychotic treatment before pregnancy, should always be switched to conventional antipsychotics upon the beginning of pregnancy. Benzodiazepines used during the first trimester can be teratogenic and can cause withdrawal symptoms in high doses in newborns, hypotonia, and agitation. The mood stabilizers (carbamazepine, valproate, similar anticonvulsants, and lithium) have been known to possess high teratogenic risk for a long time. However, the teratogenicity risk for lithium has recently been decreased. On the other hand, the use of valproate during pregnancy has a strong association with the risk of fetal abnormalities and autism-spectrum disorders. For these reasons, the uses of clomipramine, paroxetine, valproate, and atypical antipsychotics are recommended to be avoided during pregnancy. If there is a need for long-term use of psychotropic drugs during pregnancy, a full assessment should be conducted, polypharmacy and unnecessary medication use should be avoided, and the doses of psychotropic drugs should be kept to a minimum, because there are rarely valid reasons to discontinue medications that are necessary during pregnancy. In this paper, we aimed to update psychotropic drug use during pregnancy, an important and common issue in daily psychiatry practice, in the light of recent data. C1 [Cetin, Mesut] Klin Psikofarmakol Bulteni Editoru, Istanbul, Turkey. RP Cetin, M (reprint author), GATA Haydarpasa Egitim Hastanesi Psikiyatri Ogret, TR-34668 Istanbul, Turkey. 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TI AN INNOVATIVE APPROACH TO COGNITIVE INTER VIEWING FOR CULTURALLY ADAPTING AUTISM SCREENING INSTRUMENTS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract CT 3rd North American Congress of Epidemiology CY JUN 21-24, 2010 CL Montreal, CANADA C1 [Yucel, F.; Kudumu, M.; Barker-Cummings, C.; Wetherby, A.] Social & Sci Syst Inc, Durham, NC 27703 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 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD JUN 1 PY 2011 VL 173 SU 11 BP S225 EP S225 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 810GU UT WOS:000294114601177 ER PT J AU West, AE Greenberg, ME AF West, Anne E. Greenberg, Michael E. TI Neuronal Activity-Regulated Gene Transcription in Synapse Development and Cognitive Function SO COLD SPRING HARBOR PERSPECTIVES IN BIOLOGY LA English DT Article ID CPG-BINDING-PROTEIN; LONG-TERM POTENTIATION; SERUM RESPONSE FACTOR; IMMEDIATE-EARLY GENES; CHROMATIN-REMODELING COMPLEXES; NEUROTROPHIC FACTOR EXPRESSION; ACTIVITY-DEPENDENT REGULATION; DENDRITIC ARBOR DEVELOPMENT; AUTISM SPECTRUM DISORDERS; DEVELOPING NERVOUS-SYSTEM AB Activity-dependent plasticity of vertebrate neurons allows the brain to respond to its environment. During brain development, both spontaneous and sensory-driven neural activity are essential for instructively guiding the process of synapse development. These effects of neuronal activity are transduced in part through the concerted regulation of a set of activity-dependent transcription factors that coordinate a program of gene expression required for the formation and maturation of synapses. 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Here we describe recent findings from mouse models of FXS that have identified synaptic defects in the basolateral amygdala that are in many respects distinct from those reported earlier in the hippocampus. Long-term potentiation and surface expression of AMPA-receptors are impaired. Further, presynaptic defects are seen at both excitatory and inhibitory synapses. Remarkably, some of these synaptic defects in the amygdala are also amenable to pharmacological rescue. These results also underscore the need to modify the current hippocampus-centric framework to better explain FXS-related synaptic dysfunction in the amygdala. C1 [Suvrathan, Aparna; Chattarji, Sumantra] Natl Ctr Biol Sci, Bangalore 560065, Karnataka, India. RP Chattarji, S (reprint author), Natl Ctr Biol Sci, Bangalore 560065, Karnataka, India. 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Opin. Neurobiol. PD JUN PY 2011 VL 21 IS 3 BP 509 EP 515 DI 10.1016/j.conb.2011.04.005 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 810AF UT WOS:000294097100021 PM 21555214 ER PT J AU Suto, K AF Suto, Kunihiko TI Helping Behavior in Children With Autism Spectrum Disorders : Present Behavior and Helping Behavior SO JAPANESE JOURNAL OF EDUCATIONAL PSYCHOLOGY LA Japanese DT Article DE present behavior; helping behavior; context of helping; conditioned discrimination; children with autism spectrum disorders AB The present study tests the effect of discriminative stimuli for the helping behavior of two 10-year-old boys with autism spectrum disorders who had been trained in helping behavior and present behavior. The participants were exposed to 2 or 3 conditions. In Task 1. in a non-discriminative context of helping, 2 objects and verbal stimuli were presented. In Task 2, in a non-discriminative context of helping, only a verbal stimulus was presented. In Task 3. in a discriminative context of helping, an object and a verbal stimulus were presented. The target behaviors in Tasks 1 and 2 were appropriate present behavior and helping behavior, whereas in Task 3, the target behavior was only helping behavior. Both participants showed the target behaviors on the tasks. One of them also generalized present behavior and helping behavior to tasks not involved in the intervention and also at his home. The present results suggest that present behavior clarifies the discriminative stimulus and prevents inappropriate behavior from autism-related stimulus overselectivity. C1 Yamaguchi Univ, Fac Educ, Yamaguchi, Japan. RP Suto, K (reprint author), Yamaguchi Univ, Fac Educ, Yamaguchi, Japan. 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TI Attention-deficit/hyperactivity disorder in autism spectrum disorders SO INVESTIGACION CLINICA LA Spanish DT Review DE attention-deficit/hyperactivity disorder; autism spectrum disorders; pervasive developmental disorders; autism; ASD; ADHD; comorbidity ID DEFICIT HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDER; CHILDREN; COMORBIDITY; PDD; SYMPTOMS; ADHD; PSYCHOPATHOLOGY; SAMPLES AB According to the DSM-IV-TR, symptoms of inattention and hyperactivity are frequent in children with Autism Spectrum Disorders (ASD). This statement is supported by clinical observation and formal assessment. However, ASD diagnosis is still among the exclusion criteria for the Attention-Deficit/Hyperactivity Disorder (ADHD). Such exclusion generates controversy and questions regarding the need and benefits of maintening or not these separations; so much so, that the proposed criteria for the DSM-V eliminate that exclusion condition. It is necessary a better understanding of the comorbidity between both entities in order to be able to have an appropriate sequence of the intervention goals. For that reason, if inattention and hyperactivity in individuals with ASD are considered as a representation of a comorbid diagnosis of ADHD, treatment plans for this group would be better adjusted and more likely to offer a real benefit in the outcome of their adaptive functioning. C1 [Montiel-Nava, Cecilia] Univ Zulia, Dept Psicol, Escuela Educ, Fac Humanidades & Educ, Maracaibo 4011, Venezuela. [Montiel-Nava, Cecilia] Univ Zulia, Clin Trastornos Espectro Autista, Maracaibo 4011, Venezuela. [Pena, Joaquin A.] Univ Zulia, Fac Med, Dept Clin Pediat, Maracaibo 4011, Venezuela. RP Montiel-Nava, C (reprint author), Calle 79 3E-31,Sect La Lago, Maracaibo 4002A, Venezuela. 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PD JUN PY 2011 VL 52 IS 2 BP 195 EP 204 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 806OS UT WOS:000293818100009 PM 21866791 ER PT J AU Zhu, HP Sun, YR Duan, WY AF Zhu, Huaping Sun, Yaoru Duan, Wenya TI Electroencephalogram evidence for mirror neuron activity during the observation of drawn hand motion SO NEURAL REGENERATION RESEARCH LA English DT Article DE drawn hand motion; human mirror neuron; direct matching hypothesis; mu rhythm; event-related desynchronization ID NONLINEAR EEG SYNCHRONIZATION; SEQUENTIAL FINGER MOVEMENTS; POSTERIOR PARIETAL CORTEX; AUTISM SPECTRUM DISORDERS; LIGHT BIOLOGICAL MOTION; PREMOTOR CORTEX; MU-RHYTHMS; MOTOR; HUMANS; SYSTEM AB The present study used electroencephalography to examine mu rhythm suppression (a putative index of human mirror neuron system activation) at frontal sites (F3, Fz and F4), central sites (C3, Cz and C4), parietal sites (P3, Pz and P4) and occipital sites (O1 and O2), while subjects observed real hand motion (real hand motion condition) and illustrative depictions of hand motion (drawn hand motion condition). Experimental data revealed that mu rhythm suppression was exhibited in the mirror neuron system when subjects observed both real and drawn hand motion. Moreover, the mu rhythm recorded at the F3, Fz, F4, and Pz poles was significantly suppressed while observing both stimulus types, but no obvious mu suppression occurred at the O1, O2 and O3 poles. These results suggest that the observation of drawings of human hand actions can activate the human mirror neuron system. This evidence supports the hypothesis that the mirror neuron system may be involved in intransitively abstract action understanding. C1 [Zhu, Huaping; Sun, Yaoru] Tongji Univ, Minist Educ, Key Lab Embedded Syst & Serv Comp, Shanghai 200092, Peoples R China. [Duan, Wenya] Jiangxi Normal Univ, Sch Comp & Informat Engn, Nanchang 330022, Jiangxi Prov, Peoples R China. RP Sun, YR (reprint author), Tongji Univ, Minist Educ, Key Lab Embedded Syst & Serv Comp, Shanghai 200092, Peoples R China. EM yaoru@tongji.edu.cn FU National Natural Science Foundation of China [60775019, 60970062]; Shanghai Pujiang Program [09PJ1410200]; SRF for ROCS, SEM FX This work was supported by the Grants from the National Natural Science Foundation of China, No. 60775019, 60970062; the Shanghai Pujiang Program, No. 09PJ1410200; and the Project-sponsored by SRF for ROCS, SEM. 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Res. PD JUN PY 2011 VL 6 IS 18 BP 1398 EP 1403 DI 10.3969/j.issn.1673-5374.2011.18.007 PG 6 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 806IN UT WOS:000293801200007 ER PT J AU Rousselot-Pailley, B Fortin, C Golse, B Falissard, B Robel, L AF Rousselot-Pailley, B. Fortin, C. Golse, B. Falissard, B. Robel, L. TI The FAQ self-report is a valid instrument to characterize endophenotypes of the autistic spectrum in parents of children with autism SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE Autism; Parents; Endophenotype self-report; Validation ID PERVASIVE DEVELOPMENTAL DISORDERS; GENERAL-POPULATION; INFANTILE-AUTISM; PHENOTYPE; TRAITS; SIBLINGS; QUOTIENT AB Background. - We have previously developed the FAQ self-report, an adaptation of the Baron-Cohen's Autism Quotient self-report, in order to detect traits of the autistic spectrum in the parents and siblings of children with autism. We have previously shown that parents of children with autism show significant differences in their global scores and in their social functioning scores according to their answers to the FAQ self-report. Objective. - Our aim was to validate the FAQ self-report in a population of control parents, and to confirm our previous results concerning parents of children with autism. Methodology. - Hundred and twenty-seven adults (67 female, 60 male), parents of children with normal development were recruited in the general population. They were asked to fulfill the 40 questions of the FAQ self-report at two different times. Sixty-six parents of children with autism were asked to fulfill the FAQ self-report, for group comparisons. Statistical factor analysis and test-retest reliability analysis was performed with the Matlab toolbox (c) software. Results. - Statistical factor analysis and test-retest reliability show that the FAQ is structured in two main factors, socialization and communication on one hand, rigidity and imagination on the other, with good test-retest reliability. Further comparison between parents of children with autism and control parents shows a significant difference between the two groups for the socialization and communication domain, and for the global score. We show for the first time that scores of the parents of children with autism remain unchanged from infancy to adulthood. Conclusion. - The FAQ is the first French validated self-report focused on the detection of traits of the autistic spectrum in parents and siblings of children with autism. It is structured in two main factors, corresponding to imagination/rigidity, which are negatively correlated, and communication and socialization, which are positively correlated. The FAQ is therefore a reliable instrument to measure endophenotypes associated with the autistic spectrum in parents of children with autism, and may be useful in genetic studies. (C) L'Encephale, Paris, 2010. C1 [Rousselot-Pailley, B.; Fortin, C.; Golse, B.; Robel, L.] Hop Necker Enfants Malad, Serv Pedopsychiat Enfant & Adolescent, F-75015 Paris, France. [Golse, B.; Falissard, B.; Robel, L.] PSIGIAM, INSERM, U669, F-75014 Paris, France. RP Robel, L (reprint author), Hop Necker Enfants Malad, Serv Pedopsychiat Enfant & Adolescent, 149-162 Rue Sevres, F-75015 Paris, France. 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PD JUN PY 2011 VL 37 IS 3 BP 191 EP 198 DI 10.1016/j.encep.2010.08.014 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 801FF UT WOS:000293422800005 PM 21703434 ER PT J AU Hubert, A Szoke, A Leboyer, M Schurhoff, F AF Hubert, A. Szoeke, A. Leboyer, M. Schuerhoff, F. TI Influence of paternal age in schizophrenia SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE Paternal age; De novo mutations; Genetic; Schizophrenia ID POPULATION-BASED COHORT; DE-NOVO MUTATIONS; PARENTAL AGE; RISK-FACTORS; BIRTH-DEFECTS; AUTISM; DISORDERS; AUSTRALIA; CANCER AB Background. - Schizophrenia is an aetiologically heterogeneous syndrome, with a strong genetic component. Despite a reduced fertility in this disorder, its prevalence is maintained and could be explained by de novo genetic mutations. Advanced paternal age (APA) is a major source of new mutations in human beings and could thus be associated with an increased risk of developing schizophrenia in offspring. New mutations related to APA have been implicated as a cause of sporadic cases in several autosomal dominant diseases and also in neurodevelopmental diseases, autism, intellectual disabilities, and social functioning. The aim of the present study was to summarize the results of studies investigating the role of APA, and to discuss some interpretations. Methods. - All relevant studies were identified through the National Library of Medicine (PubMed (R) database). Keywords used for research were "age" and "schizophrenia" linked to "paternal or father". We have identified and analysed eight cohort studies, five case-control studies, two meta-analyses, and one review concerning different father's mutations potentially transmitted, two studies comparing paternal age at conception between sporadic versus familial cases of schizophrenia. All studies selected have been published between 2000 and 2009. Results. - After controlling for several confounding factors including maternal age, the relative risk of schizophrenia increased from 1.84 to 4.62 in offspring of fathers with an older age of fatherhood. Mother's age showed no significant effects after adjusting for paternal age. There was a significant association between paternal age and risk of developing schizophrenia, there was a weaker association with psychosis. Discussion. - The results of these different studies are confirmed by two recent meta-analyses which found an increased risk of schizophrenia in offspring of fathers older than 35 years. Two main hypotheses could explain these results. The first one is based on the presence of new mutations in the spermatogonia, possibly because of accumulating replication errors in spermatogonial cell lines. This hypothesis is confirmed by Malaspina et al. (2002) [19], who found that patients without a family history of schizophrenia had significantly older fathers than probands with a positive family history of schizophrenia. However, this result has not been confirmed by other studies, and paternal age effect could be also explained by a mechanism called imprinting, which is a form of gene regulation. The second hypothesis is based on the fact that fathers with schizophrenia spectrum personality disorder, known to be genetically related to schizophrenia, could have an advanced age at conception. However, regarding this hypothesis, advanced maternal age at conception should be a risk factor for schizophrenia, and this is not the case. Thus, the first hypothesis seems more plausible than the second. APA has been identified as a risk factor for other psychiatric disorders such as autism, bipolar disorder, obsessive-compulsive disorder, and phobia, and thus seems to be a non-specific risk factor. Furthermore, its association with impaired neurocognitive outcomes during infancy and childhood in normal populations raises the question of the phenotype linked to APA. Conclusion. - APA at conception appears to be a risk factor for schizophrenia. This risk factor probably interacts with genetic factors in a gene-environment interaction. To date, there is no validated cut-off at which the risk is significantly increased in offspring. In the future, studies could benefit from analyzing the phenotype related to APA. (C) L'Encephale, Paris, 2010. C1 [Hubert, A.; Szoeke, A.; Leboyer, M.; Schuerhoff, F.] Grp Hosp Henri Mondor Albert Chenevier, CHU Creteil, AP HP, F-94000 Creteil, France. [Hubert, A.; Szoeke, A.; Leboyer, M.; Schuerhoff, F.] IMRB, INSERM, U955, Dept Genet,Equipe 15, F-94000 Creteil, France. [Hubert, A.; Szoeke, A.; Leboyer, M.; Schuerhoff, F.] Univ Paris Est Creteil, Fac Med, IFR10, F-94000 Creteil, France. [Hubert, A.] Hop Chenevier, Fdn Cooperat Sci, Fdn Fondamental, F-94000 Creteil, France. RP Schurhoff, F (reprint author), Grp Hosp Henri Mondor Albert Chenevier, CHU Creteil, AP HP, 40 Rue Mesly, F-94000 Creteil, France. 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Psychiatr. Clin. Biol. Ther. PD JUN PY 2011 VL 37 IS 3 BP 199 EP 206 DI 10.1016/j.encep.2010.12.005 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 801FF UT WOS:000293422800006 PM 21703435 ER PT J AU Reed, P Clark, C AF Reed, Phil Clark, Charlotte TI Impact of intervening learning on resurgence in humans with Autism Spectrum Disorders SO LEARNING & BEHAVIOR LA English DT Article DE Resurgence; Humans; Autism ID ALTERNATIVE BEHAVIOR; EXTINCTION; REINFORCEMENT; RELAPSE AB In the present study, we investigated the degree to which responding would resurge in children diagnosed with Autism Spectrum Disorders (ASD) following an intervening training period comprising different schedules of reinforcement. Twenty-four children of the ages 7-15, with a diagnosis of an ASD, were taught a play a sequence on a variable ratio(VR) 3 schedule of reinforcement, during a 30-min session. The play sequence was then extinguished before the participants were taught a second play sequence, using a VR-4 schedule for 30 min, a VR-4 schedule for 60 min, or a VR-2 schedule for 30 min. A 5-min extinction session was then conducted to determine the impact that the intervening schedules had on the resurgence of the original behavior. The original sequence resurged to a greater extent for Group VR-4 30 min than it did for the other two groups. The results provide evidence that the length of time between initial training and testing is not a prime determinant of the level of resurgence, but that the amount of conditioning may play a stronger role: The greater the number of reinforcers received, the smaller the resurgence effect. C1 [Reed, Phil; Clark, Charlotte] 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. 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PD JUN PY 2011 VL 39 IS 2 BP 163 EP 170 DI 10.3758/s13420-010-0014-2 PG 8 WC Psychology, Biological; Behavioral Sciences; Psychology, Experimental; Zoology SC Psychology; Behavioral Sciences; Zoology GA 798MU UT WOS:000293212600007 PM 21264565 ER PT J AU Lobanenkov, V Loukinov, D Pugacheva, E AF Lobanenkov, Victor Loukinov, Dmitry Pugacheva, Elena TI Conference Scene Environmental epigenomics and disease susceptibility SO EPIGENOMICS LA English DT Article AB The main objective of this conference was to provide solid evidence that environmental exposures during early development can affect faithful reproduction of individual parental epigenomes without changing DNA sequence in the offspring. No doubt, this important goal has been successfully achieved owing to the high quality of presented epidemiological and experimental studies and engaging discussions of many yet to be published results. Compelling data suggested a strong causal link between prenatal vulnerability of future parental epigenomes to damaging environmental factors aggravated by abnormal socio-cultural conditions (including, for instance, malnutrition and chronic stress) and the alarming risk of developing heritable complex medical conditions later in life, such as asthma, autism, cancer, cardiovascular disease, diabetes, obesity, schizophrenia and a whole range of rare neuromuscular pathologies. It was concluded that modern epigenetic research promises to markedly improve our ability to diagnose, prevent and treat these and other pathological conditions of humans. However, the complex heritability pattern of 'epigenetic syndromes' also introduces unique legal and ethical issues that were discussed at the end of this outstanding meeting. C1 [Lobanenkov, Victor; Loukinov, Dmitry; Pugacheva, Elena] NIAID, Mol Pathol Sect, Immunopathol Lab, Rockville, MD 20852 USA. RP Lobanenkov, V (reprint author), NIAID, Mol Pathol Sect, Immunopathol Lab, Twinbrook 1,Room 1417,MSC-8152,5640 Fishers Lane, Rockville, MD 20852 USA. EM vlobanenkov@niaid.nih.gov NR 0 TC 4 Z9 6 PU FUTURE MEDICINE LTD PI LONDON PA UNITEC HOUSE, 3RD FLOOR, 2 ALBERT PLACE, FINCHLEY CENTRAL, LONDON, N3 1QB, ENGLAND SN 1750-1911 J9 EPIGENOMICS-UK JI Epigenomics PD JUN PY 2011 VL 3 IS 3 BP 261 EP 266 DI 10.2217/EPI.11.25 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 798XV UT WOS:000293246400007 PM 22122336 ER PT J AU Badcock, C AF Badcock, Christopher TI The imprinted brain: how genes set the balance between autism and psychosis SO EPIGENOMICS LA English DT Article DE autism spectrum disorder; diametric model of the mind; extreme male brain theory; genetic conflict; genius; genomic imprinting; hypermentalism; kinship theory of imprinting; mechanistic cognition; mentalistic cognition; nurture via nature; psychotic spectrum disorder; savant; X chromosome ID PRADER-WILLI-SYNDROME; POSTTRAUMATIC-STRESS-DISORDER; ANGELMAN-SYNDROME; SPECTRUM DISORDERS; BEHAVIORAL-PHENOTYPE; PRENATAL EXPOSURE; SEXUAL-DIMORPHISM; SOCIAL BRAIN; MOUSE-BRAIN; SCHIZOPHRENIA AB The imprinted brain theory proposes that autism spectrum disorder (ASD) represents a paternal bias in the expression of imprinted genes. This is reflected in a preference for mechanistic cognition and in the corresponding mentalistic deficits symptomatic of ASD. Psychotic spectrum disorder (PSD) would correspondingly result from an imbalance in favor of maternal and/or X-chromosome gene expression. If differences in gene expression were reflected locally in the human brain as mouse models and other evidence suggests they are, ASD would represent not so much an 'extreme male brain' as an extreme paternal one, with PSD correspondingly representing an extreme maternal brain. To the extent that copy number variation resembles imprinting and aneuploidy in nullifying or multiplying the expression of particular genes, it has been found to conform to the diametric model of mental illness peculiar to the imprinted brain theory. The fact that nongenetic factors such as nutrition in pregnancy can mimic and/or interact with imprinted gene expression suggests that the theory might even be able to explain the notable effect of maternal starvation on the risk of PSD - not to mention the 'autism epidemic' of modern affluent societies. Finally, the theory suggests that normality represents balanced cognition, and that genius is an extraordinary extension of cognitive configuration in both mentalistic and mechanistic directions. Were it to be proven correct, the imprinted brain theory would represent one of the biggest single advances in our understanding of the mind and of mental illness that has ever taken place, and would revolutionize psychiatric diagnosis, prevention and treatment - not to mention our understanding of epigenomics. C1 London Sch Econ, London WC2A 2AE, England. RP Badcock, C (reprint author), London Sch Econ, Houghton St, London WC2A 2AE, England. 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Controversial issues in hyperbaric oxygen therapy: a European College of Hyperbaric Medicine Workshop. Diving and Hyperbaric Medicine. 2011;41(2):101-4.) Every few years, the European Committee for Hyperbaric Medicine (ECHM) publishes its recommendations concerning the clinical indications for hyperbaric oxygen therapy (HBOT). The last recommendations were issued during the 7th European Consensus Conference on Hyperbaric Medicine in 2004. Since then, several publications have reported on the use of HBOT in some indications in which it has not yet been recommended routinely, namely aseptic bone necrosis, global brain ischaemia and autism. Patients or their families push physicians and staff of hyperbaric facilities to use hyperbaric treatment regardless of the quality of the scientific evidence. Therefore, the ECHM Workshop "Controversial issues in hyperbaric oxygen therapy" was convened as a satellite meeting of the 2010 European Underwater and Baromedical Society Annual Scientific Meeting in Istanbul, Turkey in 2010. For each topic, a set procedure was used: first came a general report by specialists in the topic, incorporating a review of current pathophysiological, experimental and clinical evidence. Then, there were reports from hyperbaric facilities that had gained clinical experience in that condition, followed by a general discussion with specialists present in the audience. Finally, statements regarding each topic were proposed and voted on by the audience and these were presented to the ECHM Executive Board for consideration and possible approval. In conclusion, the use of HBOT in femoral head necrosis will be proposed during the next ECHM Consensus Conference to become an 'accepted' indication; whilst the use of HBOT in global brain ischaemia and autism should retain its current ECHM recommendations, that it should be 'optional' and 'non-accepted' respectively. C1 [Kot, Jacek] Med Univ Gdansk, Natl Ctr Hyperbar Med, Inst Maritime & Trop Med, PL-81519 Gdynia, Poland. [Mathieu, Daniel] Hop Calmette, Serv Urgences Resp Reanimat Med & Med Hyperbare, Lille, France. RP Kot, J (reprint author), Med Univ Gdansk, Natl Ctr Hyperbar Med, Inst Maritime & Trop Med, Powstania Styczniowego 9B, PL-81519 Gdynia, Poland. 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Formation of a functional synapse is a complex process requiring stabilization of initial synaptic contacts by adhesive protein interactions, organization of presynaptic and postsynaptic specializations by scaffolding proteins, regulation of growth by intercellular signaling pathways, reorganization of the actin cytoskeleton, and proper endosomal trafficking of synaptic growth signaling complexes. Many neuropsychiatric disorders, including autism, schizophrenia, and intellectual disability, have been linked to inherited mutations which perturb these processes. Our understanding of the basic biology of synaptogenesis is therefore critical to unraveling the pathogenesis of neuropsychiatric disorders. C1 [Littleton, J. Troy] MIT, Dept Biol, Picower Inst Learning & Memory, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. RP Littleton, JT (reprint author), MIT, Dept Biol, Picower Inst Learning & Memory, Dept Brain & Cognit Sci, 43 Vassar St,46-3251, Cambridge, MA 02139 USA. 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Methods: We retrospectively reviewed clinical and laboratory data of patients with idiopathic autism evaluated at NYU Epilepsy Center during a 20-year period. Key Findings: One hundred twenty-seven patients had idiopathic autism and at least one epileptic seizure; 33.9% had TRE and 27.5% were seizure free. The remaining 38.6% of patients had infrequent seizures or insufficient data to categorize. Patients with TRE had a significantly earlier onset of seizures than seizure-free patients, and a trend for more developmental regression and motor and language delays. Three patients had surgical resection (two had limited improvement and one had no improvement) and one had an anterior callosotomy (no improvement). Vagus nerve stimulator (VNS) implantation provided limited improvement (2 patients) and no improvement (7). Significance: This study found that TRE is common in idiopathic autism and more common with early age of seizure onset. Relatively few patients underwent surgical resection due to multifocal partial epilepsy, comorbid generalized epilepsy, or limited impact of ongoing partial seizures given other problems related to autism. Our small sample suggests that surgical and VNS outcomes in this group are less favorable than in other TRE populations. C1 [Sansa, Gemma; Carlson, Chad; Bluvstein, Judith; Barr, William; Devinsky, Orrin] NYU, Langone Sch Med, Dept Neurol, New York, NY 10016 USA. [Doyle, Werner; Weiner, Howard L.; Devinsky, Orrin] NYU, Langone Sch Med, Dept Neurosurg, New York, NY 10016 USA. RP Devinsky, O (reprint author), NYU, Epilepsy Ctr, 223 E 34 St, New York, NY 10016 USA. 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Molholm, Sophie Blanco, Daniella Gomez-Ramirez, Manuel Saint-Amour, Dave Foxe, John J. TI The development of multisensory speech perception continues into the late childhood years SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE audiovisual; children; crossmodal; intersensory; sensory integration; speech-in-noise ID AUDITORY-VISUAL INTEGRATION; SUPERIOR TEMPORAL SULCUS; AUDIOVISUAL SPEECH; INTERMODAL REPRESENTATION; CHILDRENS PERCEPTION; CORTICAL THICKNESS; SEEING VOICES; RECOGNITION; INFANTS; NOISE AB Observing a speaker's articulations substantially improves the intelligibility of spoken speech, especially under noisy listening conditions. This multisensory integration of speech inputs is crucial to effective communication. Appropriate development of this ability has major implications for children in classroom and social settings, and deficits in it have been linked to a number of neurodevelopmental disorders, especially autism. It is clear from structural imaging studies that there is a prolonged maturational course within regions of the perisylvian cortex that persists into late childhood, and these regions have been firmly established as being crucial to speech and language functions. Given this protracted maturational timeframe, we reasoned that multisensory speech processing might well show a similarly protracted developmental course. Previous work in adults has shown that audiovisual enhancement in word recognition is most apparent within a restricted range of signal-to-noise ratios (SNRs). Here, we investigated when these properties emerge during childhood by testing multisensory speech recognition abilities in typically developing children aged between 5 and 14 years, and comparing them with those of adults. By parametrically varying SNRs, we found that children benefited significantly less from observing visual articulations, displaying considerably less audiovisual enhancement. The findings suggest that improvement in the ability to recognize speech-in-noise and in audiovisual integration during speech perception continues quite late into the childhood years. The implication is that a considerable amount of multisensory learning remains to be achieved during the later schooling years, and that explicit efforts to accommodate this learning may well be warranted. C1 [Ross, Lars A.; Molholm, Sophie; Blanco, Daniella; Foxe, John J.] Albert Einstein Coll Med Van Etten Bldg, Cognit Neurophysiol Lab, CERC, Dept Pediat, Bronx, NY 10461 USA. [Ross, Lars A.; Molholm, Sophie; Blanco, Daniella; Foxe, John J.] Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA. [Molholm, Sophie; Foxe, John J.] Nathan S Kline Inst Psychiat Res, Cognit Neurophysiol Lab, Orangeburg, NY 10962 USA. [Molholm, Sophie; Blanco, Daniella; Foxe, John J.] CUNY City Coll, Program Cognit Neurosci, Dept Psychol, New York, NY 10031 USA. 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This article will focus on the most significant applications of high-throughput oligonucleotide microarrays, both in genetic diagnosis and research. In genetic diagnosis, the method is becoming a standard tool for investigating patients with unexplained developmental delay/intellectual disability, autism spectrum disorders and/or with multiple congenital anomalies. Oligonucleotide microarray have also been recently applied to the detection of genomic imbalances in prenatal diagnosis either to characterize a chromosomal rearrangement that has previously been identified by standard prenatal karyotyping or to detect a cryptic genomic imbalance in a fetus with ultrasound abnormalities and a normal standard prenatal karyotype. In research, oligonucleotide microarrays have been used for a wide range of applications, such as the identification of new genes responsible for monogenic disorders and the association of a copy-number variant as a predisposing factor to a common disease. Despite its widespread use, the interpretation of results is not always straightforward. We will discuss several unexpected results and ethical issues raised by these new methods. C1 [Le Caignec, Cedric] CHU, Serv Genet Med, F-44093 Nantes, France. [Le Caignec, Cedric] Inst Thorax, INSERM, UMR915, Nantes, France. [Le Caignec, Cedric] Univ Nantes, Nantes, France. [Le Caignec, Cedric] CNRS, ERL3147, Nantes, France. [Keren, Boris] Grp Hosp Pitie Salpetriere, AP HP, Dept Genet & Cytogenet, F-75634 Paris, France. [Keren, Boris] Inst Cerveau & Moelle Epiniere, Ctr Rech, INSERM, UMR S975, Paris, France. [Keren, Boris] Univ Paris 05, Paris, France. RP Le Caignec, C (reprint author), CHU, Serv Genet Med, 9 Quai Moncousu, F-44093 Nantes, France. EM cedric.lecaignec@chu-nantes.fr FU Direction Generale de l'Organisation des Soins (DGOS); Centre Hospitalier Universitaire de Nantes; University de Nantes, France FX This research was funded by the Direction Generale de l'Organisation des Soins (DGOS). Cedric Le Caignec is supported by the Centre Hospitalier Universitaire de Nantes and the University de Nantes, France. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. 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Mol. Diagn. PD JUN PY 2011 VL 11 IS 5 BP 521 EP 532 DI 10.1586/ERM.11.32 PG 12 WC Pathology SC Pathology GA 788BN UT WOS:000292420500013 PM 21707460 ER PT J AU Pagan, C Goubran-Botros, H Fauchereau, F Huguet, G Lemiere, N Delorme, R Chaste, P Leboyer, M Herbrecht, E Callebert, J Jean-Marie, L Bourgeron, T AF Pagan, C. Goubran-Botros, H. Fauchereau, F. Huguet, G. Lemiere, N. Delorme, R. Chaste, P. Leboyer, M. Herbrecht, E. Callebert, J. Jean-Marie, L. Bourgeron, T. TI Alterations of the Melatonin Pathway as a susceptibility factor to Autism SO FEBS JOURNAL LA English DT Meeting Abstract CT 36th FEBS Congress of the Biochemistry for Tomorrows Medicine CY JUN 25-30, 2011 CL Torino, ITALY SP Federat Soc Biochem & Mol Biol C1 Inst Pasteur, Paris, France. Univ Paris 05, Paris, France. NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1742-464X J9 FEBS J JI FEBS J. PD JUN PY 2011 VL 278 SU 1 SI SI BP 146 EP 146 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 786UJ UT WOS:000292333101231 ER PT J AU Kuang, SQ Guo, DC Prakash, SK McDonald, MLN Johnson, RJ Wang, M Regalado, ES Russell, L Cao, JM Kwartler, C Fraivillig, K Coselli, JS Safi, HJ Estrera, AL Leal, SM LeMaire, SA Belmont, JW Milewicz, DM AF Kuang, Shao-Qing Guo, Dong-Chuan Prakash, Siddharth K. McDonald, Merry-Lynn N. Johnson, Ralph J. Wang, Min Regalado, Ellen S. Russell, Ludivine Cao, Jiu-Mei Kwartler, Callie Fraivillig, Kurt Coselli, Joseph S. Safi, Hazim J. Estrera, Anthony L. Leal, Suzanne M. LeMaire, Scott A. Belmont, John W. Milewicz, Dianna M. CA GenTAC Investigators TI Recurrent Chromosome 16p13.1 Duplications Are a Risk Factor for Aortic Dissections SO PLOS GENETICS LA English DT Article ID COPY NUMBER VARIANTS; SMOOTH-MUSCLE; MUTATIONS; ANEURYSMS; GENOME; DISORDERS; DELETIONS; EVOLUTION; 1Q21.1; AUTISM AB Chromosomal deletions or reciprocal duplications of the 16p13.1 region have been implicated in a variety of neuropsychiatric disorders such as autism, schizophrenia, epilepsies, and attention-deficit hyperactivity disorder (ADHD). In this study, we investigated the association of recurrent genomic copy number variants (CNVs) with thoracic aortic aneurysms and dissections (TAAD). By using SNP arrays to screen and comparative genomic hybridization microarrays to validate, we identified 16p13.1 duplications in 8 out of 765 patients of European descent with adult-onset TAAD compared with 4 of 4,569 controls matched for ethnicity (P = 5.0 x 10(-5), OR = 12.2). The findings were replicated in an independent cohort of 467 patients of European descent with TAAD (P = 0.005, OR = 14.7). Patients with 16p13.1 duplications were more likely to harbor a second rare CNV (P = 0.012) and to present with aortic dissections (P = 0.010) than patients without duplications. Duplications of 16p13.1 were identified in 2 of 130 patients with familial TAAD, but the duplications did not segregate with TAAD in the families. MYH11, a gene known to predispose to TAAD, lies in the duplicated region of 16p13.1, and increased MYH11 expression was found in aortic tissues from TAAD patients with 16p13.1 duplications compared with control aortas. These data suggest chromosome 16p13.1 duplications confer a risk for TAAD in addition to the established risk for neuropsychiatric disorders. It also indicates that recurrent CNVs may predispose to disorders involving more than one organ system, an observation critical to the understanding of the role of recurrent CNVs in human disease and a finding that may be common to other recurrent CNVs involving multiple genes. C1 [Kuang, Shao-Qing; Guo, Dong-Chuan; Prakash, Siddharth K.; Johnson, Ralph J.; Wang, Min; Regalado, Ellen S.; Cao, Jiu-Mei; Kwartler, Callie; Fraivillig, Kurt; Milewicz, Dianna M.] Univ Texas Hlth Sci Ctr Houston, Dept Internal Med, Houston, TX 77225 USA. [McDonald, Merry-Lynn N.; Leal, Suzanne M.; Belmont, John W.] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. [Russell, Ludivine; Coselli, Joseph S.; LeMaire, Scott A.] Baylor Coll Med, Michael E DeBakey Dept Surg, Div Cardiothorac Surg, Houston, TX 77030 USA. [Milewicz, Dianna M.] St Lukes Episcopal Hosp, Texas Heart Inst, Internal Med Serv, Houston, TX USA. [Safi, Hazim J.; Estrera, Anthony L.] Univ Texas Hlth Sci Ctr Houston, Dept Cardiothorac & Vasc Surg, Houston, TX USA. RP Kuang, SQ (reprint author), Univ Texas Hlth Sci Ctr Houston, Dept Internal Med, Houston, TX 77225 USA. EM Dianna.M.Milewicz@uth.tmc.edu FU National Institute of Health [R21 HL091509, P50HL083794-01, RO1 HL62594]; Vivian L. Smith Foundation; TexGen Foundation; Doris Duke Charitable Trust FX The following sources provided funding for these studies: National Institute of Health grants R21 HL091509, P50HL083794-01 (DMM), and RO1 HL62594 (DMM); the Vivian L. Smith Foundation; the TexGen Foundation; and the Doris Duke Charitable Trust grant (DMM). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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PD JUN PY 2011 VL 7 IS 6 AR e1002118 DI 10.1371/journal.pgen.1002118 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 787OJ UT WOS:000292386300034 PM 21698135 ER PT J AU Park, BY Lee, BC Jung, KH Jung, MH Park, BL Chai, YG Choi, IG AF Park, Byung-Yang Lee, Boung-Chul Jung, Kyoung Hwa Jung, Myung Hun Park, Byung Lae Chai, Young Gyu Choi, Ihn-Geun TI Epigenetic Changes of Serotonin Transporter in the Patients with Alcohol Dependence: Methylation of an Serotonin Transporter Promoter CpG Island SO PSYCHIATRY INVESTIGATION LA English DT Article DE Serotonin transporter region (5-HTTLPR); Methylation; Alcohol dependence ID GENE POLYMORPHISMS; METAANALYSIS; ASSOCIATION; DEPRESSION; DISORDERS; GENOTYPE; AUTISM; DNA AB Objective Psychiatric disorders such as depression, anxiety and alcohol dependence are associated with serotonin metabolism. We assessed the methylation level of the serotonin transporter (5-HTT) promoter region in control and alcohol dependent patients. Methods Twenty seven male patients who met the Diagnostic and Statistical Manual of Mental Disorder W (DSM-IV) criteria for alcohol dependence were compared with fifteen controls. Polymerase chain reaction (PCR) assays of bisulfate-modified DNA were designed to amplify a part of the CpG island in the 5HTT gene. Pyrosequencing was performed and the methylation level at seven CpG island sites was measured. Results We found no differences in the methylation patterns of the serotonin transporter linked promoter region (5-HTTLPR) between alcohol-dependent and control subjects. Conclusion Our negative finding may be because 5-HTT epigenetic variation may not affect the expression for 5-HTT or there may be other methylation site critical for its expression. To find out more conclusive result, repeating the study in more methylation sites with a larger number of samples in a well-controlled setting is needed. Psychiatry Investig 2011;8:130-133 C1 [Lee, Boung-Chul; Jung, Myung Hun; Choi, Ihn-Geun] Hallym Univ, Dept Neuropsychiat, Hangang Sacred Heart Hosp, Seoul 150719, South Korea. [Park, Byung-Yang] Hallym Univ, Dept Neuropsychiat, Chunchon, South Korea. [Jung, Kyoung Hwa; Chai, Young Gyu] Hanyang Univ, Div Mol & Life Sci, Ansan, South Korea. [Park, Byung Lae] SNP Genet Inc, Dept Genet Epidemiol, Seoul, South Korea. RP Choi, IG (reprint author), Hallym Univ, Dept Neuropsychiat, Hangang Sacred Heart Hosp, 94-200 Yeongdeungpo Dong, Seoul 150719, South Korea. EM ihngeun@hallym.or.kr FU Korean Neuropsychiatric Association, Republic of Korea FX This study was supported by a grant from the Korean Neuropsychiatric Association, Republic of Korea. 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PD JUN PY 2011 VL 8 IS 2 BP 130 EP 133 DI 10.4306/pi.2011.8.2.130 PG 4 WC Psychiatry SC Psychiatry GA 788AC UT WOS:000292416800008 PM 21852989 ER PT J AU Paradis, M AF Paradis, Michel TI Principles underlying the Bilingual Aphasia Test (BAT) and its uses SO CLINICAL LINGUISTICS & PHONETICS LA English DT Article DE equivalence criteria; contrastive features; procedural memory; declarative memory; multilingualism; aphasia ID SUBTHALAMIC NUCLEUS STIMULATION; COMPLEX COGNITIVE DISRUPTION; REMITTING MULTIPLE-SCLEROSIS; SPANISH-ENGLISH BILINGUALS; MOTOR-NEURON DISEASE; LANGUAGE IMPAIRMENT; PARKINSONS-DISEASE; TRILINGUAL APHASIA; PARALLEL RECOVERY; NAMING TREATMENT AB The Bilingual Aphasia Test (BAT) is designed to be objective (so it can be administered by a lay native speaker of the language) and equivalent across languages (to allow for a comparison between the languages of a given patient as well as across patients from different institutions). 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Linguist. Phon. PD JUN PY 2011 VL 25 IS 6-7 BP 427 EP 443 DI 10.3109/02699206.2011.560326 PG 17 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 777YU UT WOS:000291661900001 PM 21675824 ER PT J AU Schneider, HD Hopp, JP AF Schneider, Harry D. Hopp, Jenna P. TI The use of the Bilingual Aphasia Test for assessment and transcranial direct current stimulation to modulate language acquisition in minimally verbal children with autism SO CLINICAL LINGUISTICS & PHONETICS LA English DT Article DE syntax; first language acquisition; neuromodulation; multilingual; bilingual children with autism; modified Bilingual Aphasia Test ID PRIMARY MOTOR CORTEX; SPECTRUM DISORDERS; PREFRONTAL CORTEX; JOINT ATTENTION; YOUNG-CHILDREN; MEMORY; BRAIN; SAFETY; EXCITABILITY; FACILITATION AB Minimally verbal children with autism commonly demonstrate language dysfunction, including immature syntax acquisition. We hypothesised that transcranial direct current stimulation (tDCS) should facilitate language acquisition in a cohort (n = 10) of children with immature syntax. We modified the English version of the Bilingual Aphasia Test (BAT) to test only basic canonical subject-verb-object sentences. We tested syntactic accuracy after teaching then testing all vocabulary from the subsequent syntax test to ensure validity of syntactic scoring. We used scaffolding sentences for syntax training. All procedures were performed both before and after tDCS. Results demonstrated a large effect size of the difference between pre-/post-tDCS groups (p < 0.0005, d = 2.78), indicating syntax acquisition. Combining a modified BAT with tDCS constitutes effective modalities for assessment and treatment of immature syntax in children with autism. Future studies should explore the BAT for patients with an inability to use or understand language, in particular bilingual children with autism. C1 [Schneider, Harry D.] Columbia Univ, Med Ctr, Program Cognit Sci PICS, New York, NY 10032 USA. [Schneider, Harry D.; Hopp, Jenna P.] Ctr Med & Brain Sci, Plainview, NY USA. RP Schneider, HD (reprint author), Columbia Univ, Med Ctr, Program Cognit Sci PICS, 710 W 168th St Suite B-41 Box 108, New York, NY 10032 USA. 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Okamura, Kelsie Starace, Nicole TI Evidence-Based Treatments for Children and Adolescents: An Updated Review of Indicators of Efficacy and Effectiveness SO CLINICAL PSYCHOLOGY-SCIENCE AND PRACTICE LA English DT Review DE children; dissemination; evidence-based; services ID LARGE-SCALE IMPLEMENTATION; EVIDENCE-BASED SERVICES; PSYCHOSOCIAL TREATMENTS; MENTAL-HEALTH; PSYCHOTHERAPIES; INTERVENTIONS; METAANALYSIS; DISORDERS; THERAPIES; KNOWLEDGE AB This updated review of evidence-based treatments follows the original review performed by the Hawaii Task Force. Over 750 treatment protocols from 435 studies were coded and rated on a 5-level strength of evidence system. Results showed large numbers of evidence-based treatments applicable to anxiety, attention, autism, depression, disruptive behavior, eating problems, substance use, and traumatic stress. Treatments were reviewed in terms of diversity of client characteristics, treatment settings and formats, therapist characteristics, and other variables potentially related to feasibility and generalizability. Overall, the literature has expanded considerably since the previous review, yielding a growing list of options and information available to guide decisions about treatment selection. C1 [Chorpita, Bruce F.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. [Young, John; Trent, Lindsay] Univ Mississippi, University, MS 38677 USA. [Nakamura, Brad J.; Lynch, Roxanna; Okamura, Kelsie] Univ Hawaii, Honolulu, HI 96822 USA. [Smith, Rita L.] Univ Calif San Francisco, San Francisco, CA 94143 USA. RP Chorpita, BF (reprint author), Univ Calif Los Angeles, Dept Psychol, Box 951563, Los Angeles, CA 90095 USA. 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Psychol.-Sci. Pract. PD JUN PY 2011 VL 18 IS 2 BP 154 EP 172 PG 19 WC Psychology, Clinical SC Psychology GA 779CO UT WOS:000291755900009 ER PT J AU Tomljenovic, L Shaw, CA AF Tomljenovic, L. Shaw, C. A. TI Aluminum Vaccine Adjuvants: Are they Safe? SO CURRENT MEDICINAL CHEMISTRY LA English DT Review DE Aluminum adjuvants; adjuvant safety; autoimmunity; autism; Gulf War Syndrome; multiple sclerosis; macrophagic myofasciitis; neurotoxicity; seizures; Th2 immune response; vaccines ID DIALYSIS ENCEPHALOPATHY SYNDROME; VARICELLA-ZOSTER-VIRUS; MACROPHAGIC MYOFASCIITIS; HUMAN-PAPILLOMAVIRUS; NEUROFIBRILLARY DEGENERATION; MONOCLONAL-ANTIBODY; ALZHEIMERS-DISEASE; PARTICLE VACCINE; GENE-EXPRESSION; ADVERSE EVENTS AB Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science's understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. In particular, aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences. In our opinion, the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community. We hope that the present paper will provide a framework for a much needed and long overdue assessment of this highly contentious medical issue. C1 [Tomljenovic, L.] Univ British Columbia, Dept Ophthalmol & Visual Sci, Neural Dynam Res Grp, Vancouver, BC V5Z 1L8, Canada. [Shaw, C. A.] Univ British Columbia, Grad Program Neurosci, Dept Ophthalmol & Visual Sci, Vancouver, BC V5Z 1L8, Canada. [Shaw, C. A.] Univ British Columbia, Grad Program Neurosci, Dept Expt Med, Vancouver, BC V5Z 1L8, Canada. RP Tomljenovic, L (reprint author), Univ British Columbia, Dept Ophthalmol & Visual Sci, Neural Dynam Res Grp, 828 W 10th Ave, Vancouver, BC V5Z 1L8, Canada. EM lucijat77@gmail.com FU Katlyn Fox Foundation; Dwoskin Family Foundation; Lotus Foundation FX This work was supported by the Katlyn Fox Foundation, the Dwoskin Family Foundation and the Lotus Foundation. 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PD JUN PY 2011 VL 18 IS 17 BP 2630 EP 2637 PG 8 WC Biochemistry & Molecular Biology; Chemistry, Medicinal; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy GA 777SQ UT WOS:000291645700011 PM 21568886 ER PT J AU Barbato, M Maiella, G Di Camillo, C Guida, S Valitutti, F Lastrucci, G Mainiero, F Cucchiara, S AF Barbato, Maria Maiella, Giulia Di Camillo, Chiara Guida, Sofia Valitutti, Francesco Lastrucci, Ginevra Mainiero, Fabrizio Cucchiara, Salvatore TI The anti-deamidated gliadin peptide antibodies unmask celiac disease in small children with chronic diarrhoea SO DIGESTIVE AND LIVER DISEASE LA English DT Article DE Antigliadin antibodies; Celiac disease; Deamidated gliadin peptides; Food allergy ID TISSUE TRANSGLUTAMINASE; GLUTEN SENSITIVITY; DIAGNOSIS; AUTOANTIBODIES; RECOGNITION; ENTEROPATHY; INTOLERANCE; PROTEIN; MUCOSA; AUTISM AB Objectives: To assess the usefulness of a new class of antibodies, the anti-deamidated gliadin peptides, in the diagnostic approach to children less than 2 years with suspected celiac disease. Patients and methods: We investigated 40 children (median age: 16.8 months; age range: 4-24 months), with symptoms and signs of chronic enteropathy and high serum levels of conventional anti-gliadin antibodies, but normal values of anti-transglutaminase and anti-endomysial antibodies; all underwent measurement of anti-deamidated gliadin peptides serum levels, upper gastrointestinal endoscopy with biopsies and HLA typing; 40 subjects served as controls. Results: In 29 patients (group A) serum levels of anti-deamidated gliadin peptides were normal and duodenal histology showed a spectrum of abnormalities ranging from mucosal inflammatory infiltrates to villous damage (in almost all cases compatible with Marsh 1-to-2 lesions). All improved on a cow's and soy milk free diet containing gluten. In 11 patients (group B) there were high serum levels of anti-deamidated gliadin peptides and histology showed features suggestive of celiac disease (Marsh 2-to-3 lesions) in all; furthermore, human leucocyte antigen typing was consistent with a celiac disease genetic pattern in all. Group B patients significantly improved on a gluten free diet containing cow's and soy milk proteins. None of the control group was anti-deamidated gliadin peptides positive. Conclusions: In children younger than 2 years with signs of chronic enteropathy and normal values of classical serum markers of celiac disease, the latter can be predicted by high serum levels of anti-deamidated gliadin peptides. (C) 2011 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved. C1 [Barbato, Maria; Maiella, Giulia; Di Camillo, Chiara; Valitutti, Francesco; Lastrucci, Ginevra; Cucchiara, Salvatore] Univ Roma La Sapienza, Pediat Gastroenterol & Liver Unit, Dept Pediat, I-00161 Rome, Italy. [Guida, Sofia; Mainiero, Fabrizio] Univ Roma La Sapienza, Dept Expt Med, I-00161 Rome, Italy. RP Cucchiara, S (reprint author), Univ Roma La Sapienza, Pediat Gastroenterol & Liver Unit, Dept Pediat, Viale Regina Elena 324, I-00161 Rome, Italy. 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This study examined how to improve the knowledge and understanding of sleep quality and sleep problems in people with ID among care staff at a residential facility and, consequently, to reduce extrinsic sleep problems. Using a variation on a crossover design with two groups, sleep efficiency and sleep latency in people with ID (not suspected of having sleep problems) were measured four times. One group (Group A) of staff was offered a lecture after the first measurement and a workshop after the second one. A second group (Group B) of staff was only offered a lecture, between the second and third measurements. In both groups, sleep efficiency rose significantly. The time spent in bed by residents overseen by Group A was reduced significantly, and there was a significant reduction of daily napping time among group A's residents. In Group B, there was a significant increase of daily napping time and in the number of naps. 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Vis. Impair. Blind. PD JUN PY 2011 VL 105 IS 6 BP 334 EP 338 PG 5 WC Rehabilitation SC Rehabilitation GA 779EG UT WOS:000291760300004 ER PT J AU Lin, LY AF Lin, Ling-Yi TI Factors Associated with Caregiving Burden and Maternal Pessimism in Mothers of Adolescents with an Autism Spectrum Disorder in Taiwan SO OCCUPATIONAL THERAPY INTERNATIONAL LA English DT Article DE autism; caregiving burden; paediatric occupational therapy; Taiwan ID DOWN-SYNDROME; STRESS; ADULTS; CHILDREN; PARENTS; QUESTIONNAIRE; RESOURCES; QUALITY AB Relative to the United States and other western countries, less research has focused on factors associated with caregiving burden and maternal pessimism in Taiwanese mothers of adolescents with an autism spectrum disorder (ASD). The characteristics of 50 adolescents with an ASD living at home in Taiwan and its association with caregiving burden and maternal pessimism were examined. The age range of adolescents with an ASD was from 10 to 18. Mothers, aged 35 to 55 years, completed self-report written questionnaires regarding their child's adaptive functioning and their own perceptions of caregiving burdens and concerns. Findings indicated that functional independence, severe maladaptive behaviours and severity of autism were predictive of maternal caregiving burden. Maternal pessimism was associated with functional independence and severity of autism. The findings of this study indicated that occupational therapy practitioners could focus on training functional independence of the individual with an ASD to meet the family's need in Taiwan. Researchers should pay significant attention to the lifespan issues of autism in Taiwanese families. The major limitations of this study were small sample size and without a comparison group. Future research using larger samples with a comparison group is needed. Copyright (C) 2010 John Wiley & Sons, Ltd. C1 Natl Cheng Kung Univ, Dept Occupat Therapy, Tainan 701, Taiwan. RP Lin, LY (reprint author), Natl Cheng Kung Univ, Dept Occupat Therapy, 1 Univ Rd, Tainan 701, Taiwan. EM lingyi@mail.ncku.edu.tw FU College of Health and Rehabilitation Sciences at Boston University, Boston, Massachusetts, USA FX Support for this research was provided by a grant from the Dudley Allen Sargent Research Fund at the College of Health and Rehabilitation Sciences at Boston University, Boston, Massachusetts, USA. I thank the families who participated in this research, the Autism Society Taiwan, Republic of China and the parents associations of autism in Taiwan. 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PD JUN PY 2011 VL 18 IS 2 BP 96 EP 105 DI 10.1002/oti.305 PG 10 WC Rehabilitation SC Rehabilitation GA 780MC UT WOS:000291860100003 PM 20925134 ER PT J AU Kita, Y Gunji, A Inoue, Y Goto, T Sakihara, K Kaga, M Inagaki, M Hosokawa, T AF Kita, Yosuke Gunji, Atsuko Inoue, Yuki Goto, Takaaki Sakihara, Kotoe Kaga, Makiko Inagaki, Masumi Hosokawa, Toru TI Self-face recognition in children with autism spectrum disorders: A near-infrared spectroscopy study SO BRAIN & DEVELOPMENT LA English DT Article DE Autism spectrum disorders (ASD); Self-face recognition; Inferior frontal gyrus; Near-infrared spectroscopy (NIRS); Eye-movement; ASD severity; Self-consciousness ID RIGHT PREFRONTAL CORTEX; GAZE; FIXATION; NIRS; FMRI; AM AB It is assumed that children with autism spectrum disorders (ASD) have specificities for self-face recognition, which is known to be a basic cognitive ability for social development. In the present study, we investigated neurological substrates and potentially influential factors for self-face recognition of ASD patients using near-infrared spectroscopy (NIRS). The subjects were 11 healthy adult men, 13 normally developing boys, and 10 boys with ASD. Their hemodynamic activities in the frontal area and their scanning strategies (eye-movement) were examined during self-face recognition. Other factors such as ASD severities and self-consciousness were also evaluated by parents and patients, respectively. Oxygenated hemoglobin levels were higher in the regions corresponding to the right inferior frontal gyrus than in those corresponding to the left inferior frontal gyrus. In two groups of children these activities reflected ASD severities, such that the more serious ASD characteristics corresponded with lower activity levels. Moreover, higher levels of public self-consciousness intensified the activities, which were not influenced by the scanning strategies. These findings suggest that dysfunction in the right inferior frontal gyrus areas responsible for self-face recognition is one of the crucial neural substrates underlying ASD characteristics, which could potentially be used to evaluate psychological aspects such as public self-consciousness. (C) 2010 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved. C1 [Kita, Yosuke] Tohoku Univ, Grad Sch Educ, Aoba Ku, Sendai, Miyagi 9818576, Japan. [Kita, Yosuke] Japan Soc Promot Sci, Tokyo, Japan. [Gunji, Atsuko; Inoue, Yuki; Goto, Takaaki; Sakihara, Kotoe; Kaga, Makiko; Inagaki, Masumi] Natl Ctr Neurol & Psychiat, Natl Inst Mental Hlth, Dept Dev Disorders, Tokyo, Japan. RP Kita, Y (reprint author), Tohoku Univ, Grad Sch Educ, Aoba Ku, 27-1 Kawauchi, Sendai, Miyagi 9818576, Japan. EM yosuke@s.tohoku.ac.jp RI Gunji, Atsuko/O-6323-2014 OI Gunji, Atsuko/0000-0001-8908-8739 FU JSPS [20-8503]; MEXT [4002] FX This work was done as a partial requirement for the dissertation of Y.K. at Tohoku University, Japan. We thank Toshihide Koike, Wataru Shoji, Asako Mashima and Yasuyuki Takeshima for their assistance. The study was supported in part by a JSPS Grant-in-Aid for the Japan Society for the Promotion of Science Fellows (20-8503 to Y.K.) and a MEXT Grant-in-Aid for Scientific Research on Innovative Areas (4002 to Ryusuke Kakigi (P.I.) and M.I.). 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PD JUN PY 2011 VL 33 IS 6 BP 494 EP 503 DI 10.1016/j.braindev.2010.11.007 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 774UY UT WOS:000291413300009 PM 21168985 ER PT J AU Silva, LMT Schalock, M Ayres, R AF Silva, Louisa M. T. Schalock, Mark Ayres, Robert TI A Model and Treatment for Autism at the Convergence of Chinese Medicine and Western Science: First 130 Cases SO CHINESE JOURNAL OF INTEGRATIVE MEDICINE LA English DT Article DE Kai Qiao Tuina; Qigong sensory training; autism treatment for children; sensory impairment; abnormal sensory responses; autism; early intervention for autism ID SOMATOTOPIC MAP; YOUNG-CHILDREN AB Objective: To present a model for autism showing that impairment of sensory and self-regulation is the core deficit that underlies delays in social/language skills and abnormal behavior in autism; and to demonstrate the efficacy of a treatment for autism based on Chinese medicine. Methods: Children with autism under 6 years of age were assigned to treatment or wait-list conditions. A total of 130 children were treated and the results compared with 45 wait-list controls. Treatment is a tuina methodology directed at sensory impairment-Kai Qiao Tuina. The treatment was a five-month protocol that was implemented daily by trained parents via trained support staff. The effects of treatment on the main symptoms, autistic behavior, social/language delay, sensory and self-regulatory impairment, as well as on parenting stress, were observed and compared. Results: The treatment had a large effect size (P<0.0001) on measures of sensory and self-regulation. The evaluations done by pre-school teachers demonstrated improvement in the measures of autism (P<0.003), and were confirmed by evaluations done by parents (P<0.0001). There was a large decrease (P<0.0001) in parenting stress. 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Hertz-Picciotto, Irva Delwiche, Lora Lurmann, Fred McConnell, Rob TI Residential Proximity to Freeways and Autism in the CHARGE Study SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE autism; epidemiology; gene-environment interaction; roadway proximity; traffic emissions ID POLYCYCLIC AROMATIC-HYDROCARBONS; HAZARDOUS AIR-POLLUTANTS; SPECTRUM DISORDERS; PRENATAL EXPOSURE; CHILDHOOD ASTHMA; OXIDATIVE STRESS; MULTIETHNIC POPULATION; ULTRAFINE PARTICLES; NITROGEN-DIOXIDE; GENE-EXPRESSION AB BACKGROUND: Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects. OBJECTIVES: We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure. METHODS: Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls. RESULTS: Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (<= 309 m) for cases than for controls [odds ratio (OR) = 1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR = 2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism. CONCLUSIONS: Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed. C1 [Volk, Heather E.; McConnell, Rob] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA 90033 USA. [Volk, Heather E.] Univ So Calif, Keck Sch Med, Childrens Hosp Los Angeles, Dept Prevent Med,Zilkha Neurogenet Inst, Los Angeles, CA 90033 USA. 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TI Heads-Up: New Roles for the Fragile X Mental Retardation Protein in Neural Stem and Progenitor Cells SO GENESIS LA English DT Review DE fate specification; neural tissue; proliferation; differentiation; neurogenesis; fragile X syndrome ID FMR1 KNOCKOUT MICE; CENTRAL-NERVOUS-SYSTEM; MESSENGER-RNA TRANSPORT; DROSOPHILA-MELANOGASTER; MOUSE MODEL; GENE-EXPRESSION; DENDRITIC SPINES; IN-VIVO; POSTEMBRYONIC NEUROBLASTS; COGNITIVE DYSFUNCTION AB Fragile X syndrome (FXS) is the most common form of inherited mental retardation and is caused by the loss of function for Fragile X Mental Retardation Protein (FMRP), a selective RNA-binding protein with a demonstrated role in the localized translation of target mRNAs at synapses. Several recent studies provide compelling evidence for a new role of FMRP in the development of the nervous system, during neurogenesis. Using a multi-faceted approach and a variety of model systems ranging from cultured neurospheres and progenitor cells to in vivo Drosophila and mouse models these reports indicate that FMRP is required for neural stem and progenitor cell proliferation, differentiation, survival, as well as regulation of gene expression. Here we compare and contrast these recent reports and discuss the implications of FMRP's new role in embryonic and adult neurogenesis, including the development of novel therapeutic approaches to FXS and related neurological disorders such as autism. genesis 49:424-440, 2011. (C) 2011 Wiley-Liss, Inc. C1 [Callan, Matthew A.; Zarnescu, Daniela C.] Univ Arizona, Dept Mol & Cellular Biol, Tucson, AZ 85721 USA. [Zarnescu, Daniela C.] Univ Arizona, Dept Neurosci, Tucson, AZ 85721 USA. [Zarnescu, Daniela C.] Univ Arizona, Dept Neurol, Tucson, AZ 85721 USA. RP Zarnescu, DC (reprint author), Univ Arizona, Dept Mol & Cellular Biol, Rm 552, Tucson, AZ 85721 USA. 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07030-5774, NJ USA SN 1526-954X J9 GENESIS JI Genesis PD JUN PY 2011 VL 49 IS 6 BP 424 EP 440 DI 10.1002/dvg.20745 PG 17 WC Developmental Biology; Genetics & Heredity SC Developmental Biology; Genetics & Heredity GA 777CE UT WOS:000291590400001 PM 21404421 ER PT J AU Chen, LJ Hadd, AG Sah, S Houghton, JF Filipovic-Sadic, S Zhang, WT Hagerman, PJ Tassone, F Latham, GJ AF Chen, Liangjing Hadd, Andrew G. Sah, Sachin Houghton, Jeffrey F. Filipovic-Sadic, Stela Zhang, Wenting Hagerman, Paul J. Tassone, Flora Latham, Gary J. TI High-resolution methylation polymerase chain reaction for fragile X analysis: Evidence for novel FMR1 methylation patterns undetected in Southern blot analyses SO GENETICS IN MEDICINE LA English DT Article DE fragile X; autism; FMR1 gene; PCR; methylation ID CHROMOSOME INACTIVATION; EXPANDED ALLELES; FULL-MUTATION; CGG REPEAT; TREMOR/ATAXIA SYNDROME; BISULFITE CONVERSION; FEMALE CARRIERS; PCR; DNA; GENE AB Fragile X syndrome is associated with the expansion of CGG trinucleotide repeats and subsequent methylation of the FMR1 gene. Molecular diagnosis of fragile X currently requires Southern blot analysis to assess methylation. This study describes the evaluation of a polymerase chain reaction-only workflow for the determination of methylation status across a broad range of FMR1 genotypes in male and female specimens. Methods: We evaluated a novel method that combines allele-specific methylation polymerase chain reaction and capillary electrophoresis with eight cell line and 80 clinical samples, including 39 full mutations. Methylation status was determined using a three-step workflow: (1) differential treatment of genomic DNA using a methylation-sensitive restriction enzyme; (2) polymerase chain reaction with two sets of dye-tagged primers; and (3) amplicon sizing by capillary electrophoresis. All samples were analyzed by both methylation polymerase chain reaction and Southern blot analysis. Results: FMR1 methylation status and CGG repeat sizing were accurately and reproducibly determined in a set of methylation controls and genomic DNA samples representing a spectrum of CGG repeat lengths and methylation states. Moreover, methylation polymerase chain reaction revealed allele-specific methylation patterns in premutation alleles that were unobtainable using Southern blot analysis. Conclusions: Methylation polymerase chain reaction enabled high throughput, high resolution, and semiquantitative methylation assessments of FMR1 alleles, as well as determinations of CGG repeat length. Results for all samples were concordant with corresponding Southern blot analyses. As a result, this study presents a polymerase chain reaction-based method for comprehensive FMR1 analysis. In addition, the identification of novel methylation mosaic patterns revealed after polymerase chain reaction and capillary electrophoresis may be relevant to several FMR1 disorders. Genet Med 2011:13(6):528-538. C1 [Chen, Liangjing; Hadd, Andrew G.; Sah, Sachin; Houghton, Jeffrey F.; Filipovic-Sadic, Stela; Latham, Gary J.] Asuragen Inc, Diagnost Res & Technol Dev, Austin, TX USA. [Zhang, Wenting; Hagerman, Paul J.; Tassone, Flora] Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA. [Zhang, Wenting; Hagerman, Paul J.; Tassone, Flora] Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. RP Latham, GJ (reprint author), 2150 Woodward St, Austin, TX 78744 USA. EM glatham@asuragen.com FU Eunice Kennedy Shriver National Institute of Child Health & Human Development [R43HD060450, R44HD060450, HD02274, HD040661] FX This project was supported, in part, by awards from the Eunice Kennedy Shriver National Institute of Child Health & Human Development, including R43HD060450 and R44HD060450 to A. G. H., HD02274 to F. T., and HD040661 to P.J.H. The authors acknowledge Dr. Timothy Stenzel and Dr. Stephen Brown for helpful discussions. 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Med. PD JUN PY 2011 VL 13 IS 6 BP 528 EP 538 DI 10.1097/GIM.0b013e31820a780f PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 774ZX UT WOS:000291426800006 PM 21430544 ER PT J AU Blacher, J Christensen, L AF Blacher, Jan Christensen, Lisa TI Sowing the Seeds of the Autism Field: Leo Kanner (1943) SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY INFANTILE-AUTISM; AFFECTIVE CONTACT; JOINT ATTENTION; FAMILY-HISTORY; CHILDHOOD; PARENTS; DISTURBANCES; METAANALYSIS; INDIVIDUALS AB More than 65 years after Leo Kanner published his seminal article, research on autism continues to be an area of increasing interest. Although much progress has been made, this field is still in its infancy, and many avenues of research are just beginning to be pursued. Despite the time that has passed, the syndrome Kanner identified and his comments about the children he observed continue to have meaning today, and although some of his suggestions about the etiology and presentation of autism were grounded in the thinking of his clay, many of his observations were quite prescient. In this paper we explore Kanner's contributions to the field of autism, discuss how the field has changed, and suggest ways that research on autism spectrum disorders can continue to move forward. C1 [Blacher, Jan] Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. [Christensen, Lisa] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Blacher, J (reprint author), Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. 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PD JUN PY 2011 VL 49 IS 3 BP 172 EP 191 DI 10.1352/1934-9556-49.3.172 PG 20 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 777NC UT WOS:000291627400005 PM 21639744 ER PT J AU Tashiro, Y Oyabu, A Imura, Y Uchida, A Narita, N Narita, M AF Tashiro, Yasura Oyabu, Akiko Imura, Yoshio Uchida, Atsuko Narita, Naoko Narita, Masaaki TI Morphological abnormalities of embryonic cranial nerves after in utero exposure to valproic acid: implications for the pathogenesis of autism with multiple developmental anomalies SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE Autism; Cranial nerve; Facial motor nerve; Valproic acid; Rat embryo; Whole mount immunostaining ID RETINOIC ACID; HISTONE DEACETYLASE; THALIDOMIDE; BRAIN; ORGANIZATION; PATHWAYS; GANGLIA; NEURONS; NUCLEI; SYSTEM AB Autism is often associated with multiple developmental anomalies including asymmetric facial palsy. In order to establish the etiology of autism with facial palsy, research into developmental abnormalities of the peripheral facial nerves is necessary. In the present study, to investigate the development of peripheral cranial nerves for use in an animal model of autism, rat embryos were treated with valproic acid (VPA) in utero and their cranial nerves were visualized by immunostaining. Treatment with VPA after embryonic day 9 had a significant effect on the peripheral fibers of several cranial nerves. Following VPA treatment, immunoreactivity within the trigeminal, facial, glossopharyngeal and vagus nerves was significantly reduced. Additionally, abnormal axonal pathways were observed in the peripheral facial nerves. Thus, the morphology of several cranial nerves, including the facial nerve, can be affected by prenatal VPA exposure as early as E13. Our findings indicate that disruption of early facial nerve development is involved in the etiology of asymmetric facial palsy, and may suggest a link to the etiology of autism. (C) 2011 ISDN. Published by Elsevier Ltd. All rights reserved. C1 [Tashiro, Yasura; Oyabu, Akiko; Imura, Yoshio; Uchida, Atsuko; Narita, Masaaki] Mie Univ, Grad Sch Med, Dept Anat 2, Tsu, Mie 514, Japan. [Narita, Naoko] Bunkyo Univ, Dept Educ, Tsu, Mie, Japan. RP Tashiro, Y (reprint author), Mie Univ, Grad Sch Med, Dept Anat 2, 2-174 Edobashi, Tsu, Mie 514, Japan. EM ytashiro@doc.medic.mie-u.ac.jp RI Uchida, Atsuko /E-3081-2010 OI Uchida, Atsuko /0000-0002-4658-1504 FU Ministry of Education, Culture, Sports, Science and Technology, Japan; KAKENHI [19700323]; School of Medicine, Mie University FX The 2H3 monoclonal antibody developed by Thomas M. Jessell and Jane Dodd was obtained from the Developmental Studies Hybridoma Bank developed under the auspices of the NICHD and maintained by The University of Iowa, Department of Biology, Iowa City, IA 52242. This study was supported by a Grant-in-Aid for Young Scientists (B) from the Ministry of Education, Culture, Sports, Science and Technology, Japan. KAKENHI (19700323) and a Grand-in-Aid from the School of Medicine, Mie University. 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J. Dev. Neurosci. PD JUN PY 2011 VL 29 IS 4 BP 359 EP 364 DI 10.1016/j.ijdevneu.2011.03.008 PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 776AD UT WOS:000291506000001 PM 21458558 ER PT J AU Tanimura, Y King, MA Williams, DK Lewis, MH AF Tanimura, Yoko King, Michael A. Williams, Dustin K. Lewis, Mark H. TI Development of repetitive behavior in a mouse model: Roles of indirect and striosomal basal ganglia pathways SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE Autism; Stereotypy; Subthalamic nucleus; Neurodevelopmental disorders; Deer mice; Animal models ID HIGH-FREQUENCY STIMULATION; SUBTHALAMIC NUCLEUS; PREFRONTAL CORTEX; TOPOGRAPHICAL ORGANIZATION; ORBITOFRONTAL CORTEX; HUNTINGTONS-DISEASE; METABOLIC-ACTIVITY; CORTICAL INPUTS; SAS PROCEDURE; ANIMAL-MODEL AB Restricted repetitive behaviors (stereotypy, compulsions, rituals) are diagnostic for autism spectrum disorder and common in related neurodevelopmental disorders. Despite their prevalence in clinical populations, underlying mechanisms associated with the development of these behaviors remain poorly understood. We examined the role of the indirect basal ganglia pathway in the development of stereotypy using deer mice. We measured neuronal metabolic activity in the subthalamic nucleus (STN) and other relevant brain regions using cytochrome oxidase (CO) histochemistry at three developmental time-points. Although no differences were observed in STN across development, significant differences were found when mice were grouped by developmental trajectory. At 6 weeks post-weaning, significantly lower CO activity in STN was found in those trajectory groups that developed high levels of repetitive behavior versus the trajectory group that did not, suggesting the development of stereotypy is associated with decreased indirect basal ganglia pathway activity. In addition, we tested the hypothesis that preferential activation of striatal striosomes relative to surrounding matrix would be associated with the development of stereotypy. No differences in the relative activation of these striatal compartments were observed across development or among trajectory groups. Our results point to dynamic changes in the indirect pathway associated with the development of repetitive behavior and extends our prior work linking reduced indirect pathway activation to stereotypy in adult deer mice. (C) 2011 ISDN. Published by Elsevier Ltd. All rights reserved. C1 [Tanimura, Yoko; Lewis, Mark H.] Univ Florida, McKnight Brain Inst, Dept Psychol, Gainesville, FL 32611 USA. [Tanimura, Yoko; Lewis, Mark H.] Univ Florida, McKnight Brain Inst, Dept Psychiat, Gainesville, FL 32611 USA. [King, Michael A.; Williams, Dustin K.] Univ Florida, McKnight Brain Inst, Dept Neurosci, Gainesville, FL 32611 USA. RP Lewis, MH (reprint author), Univ Florida, McKnight Brain Inst, Dept Psychol, 100 S Newell Dr,L4-116, Gainesville, FL 32611 USA. EM marklewis@ufl.edu RI Tanimura, Yoko/D-3141-2014 FU NIH [MH080055] FX This work was supported by NIH grant MH080055. 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J. Dev. Neurosci. PD JUN PY 2011 VL 29 IS 4 BP 461 EP 467 DI 10.1016/j.ijdevneu.2011.02.004 PG 7 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 776AD UT WOS:000291506000012 PM 21329752 ER PT J AU Wang, LW Tancredi, DJ Thomas, DW AF Wang, Lulu W. Tancredi, Daniel J. Thomas, Dan W. TI The Prevalence of Gastrointestinal Problems in Children Across the United States With Autism Spectrum Disorders From Families With Multiple Affected Members SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism spectrum disorders; gastrointestinal problems; constipation; diarrhea; AGRE ID PERVASIVE DEVELOPMENTAL DISORDERS; REGRESSIVE AUTISM; SYMPTOMS; MET; ASSOCIATION; POPULATION; DISTINCT; MEASLES; DISEASE; VARIANT AB Objective: To perform a large registry-based study to determine the relative prevalence of gastrointestinal (GI) problems in children with an autism spectrum disorder (ASD) from families with multiple affected members compared with their unaffected sibling(s). Methods: In-home structured retrospective medical history interviews by parent recall were conducted by a pediatric neurologist. Our analysis sample included information about GI health of 589 subjects with idiopathic, familial ASD and 163 of their unaffected sibling controls registered with Autism Genetic Resource Exchange. Individuals with ASD were subgrouped into 3 autism severity groups (Full Autism, Almost Autism, and Spectrum) based on their Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Scale scores. Results: Parents reported significantly more GI problems in children with ASD (249/589; 42%) compared with their unaffected siblings (20/163; 12%) (p < .001). The 2 most common Gl problems in children with ASD were constipation (116/589; 20%) and chronic diarrhea (111/589; 19%). Conditional logistic regression analysis showed that having Full Autism (adjusted odds ratio [AOR] = 14.28, 95% confidence interval [CI]: 6.22-32.77) or Almost Autism (AOR = 5.16, 95% CI 2.02-13.21) was most highly associated with experiencing GI problems. Increased autism symptom severity was associated with higher odds of GI problems (AOR for trend = 2.63, 95% CI: 1.56-4.45). Conclusions: Parents report significantly more GI problems in children with familial ASD, especially those with Full Autism, than in their unaffected children. Increased autism symptom severity is associated with increased odds of having GI problems. C1 [Wang, Lulu W.] Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. [Wang, Lulu W.; Tancredi, Daniel J.] Univ Calif Davis, Sch Med, Dept Pediat, Sacramento, CA 95817 USA. [Thomas, Dan W.] Univ So Calif, Keck Sch Med, Div Pediat Gastroenterol & Nutr, Childrens Hosp Los Angeles, Los Angeles, CA 90033 USA. RP Wang, LW (reprint author), Univ Calif Davis, Med Ctr, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. EM wang@ucdmc.ucdavis.edu FU American Academy of Pediatrics; Celiac Foundation of America; Children's Hospital Los Angeles, Department of Pediatrics; National Institute of Mental Health [1U24MH081810]; Autism Speaks FX This work was supported by grants from the American Academy of Pediatrics, Celiac Foundation of America, and the Children's Hospital Los Angeles, Department of Pediatrics. The Autism Genetic Resource Exchange (AGRE) is a program of Autism Speaks and is supported, in part, by grant 1U24MH081810 from the National Institute of Mental Health to Clara M. Lajonchere (PI).We acknowledge support from the Autism Genetic Resource Exchange (AGRE) and Autism Speaks. We acknowledge the resources provided by the AGRE consortium and the participating AGRE families. We thank Prometheus Laboratories for supporting this research by running some exploratory laboratory testing. We thank Dr. Fred Dorey for aid in the initial power calculations and statistical analyses. We thank Dr. Robin Hansen for discussions and insights on the interpretation and presentation of our findings. 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Dev. Behav. Pediatr. PD JUN PY 2011 VL 32 IS 5 BP 351 EP 360 DI 10.1097/DBP.0b013e31821bd06a PG 10 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 774ZJ UT WOS:000291425200001 PM 21555957 ER PT J AU Reschke-Hernandez, AE AF Reschke-Hernandez, Alaine E. TI History of Music Therapy Treatment Interventions for Children with Autism SO JOURNAL OF MUSIC THERAPY LA English DT Article ID SPECTRUM DISORDER; SCERTS MODEL; BEHAVIORS; CLIENTS; RESPONSIVENESS; INDIVIDUALS; MEDICINE; PROGRAM; GOALS AB The purpose of this paper is to provide a systematic review of the history of music therapy research and treatment of children with autism. Understanding such history is important in order to improve clinical efficacy and inform future research. 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Music Ther. PD SUM PY 2011 VL 48 IS 2 BP 169 EP 207 PG 39 WC Music; Rehabilitation SC Music; Rehabilitation GA 776XV UT WOS:000291575200003 PM 21938891 ER PT J AU Buehler, MR AF Buehler, M. R. TI A proposed mechanism for autism: an aberrant neuroimmune response manifested as a psychiatric disorder SO MEDICAL HYPOTHESES LA English DT Article ID NECROSIS-FACTOR-ALPHA; INFLAMMATORY RESPONSE; SPECTRUM DISORDERS; BRAIN-DAMAGE; TNF-ALPHA; SCHIZOPHRENIA; CYTOKINES; INTERLEUKIN-1; INFECTION; PREGNANCY AB Autism, an incurable neurodevelopmental brain disorder, is a complex psychopathology in which the affected individual cannot effectively self-regulate their sensory inputs toward coherent and focused motor outputs. There have been many hypotheses as to the etiology of autism - genetics, neurotransmitter imbalances, early childhood immunizations, xenobiotic and teratogenic agents, and maternal infection; the disorder can perhaps be studied best under the field of "Psychoneuroimmunology", which analyzes systemic and psychopathologies from an integrated approach through the combined effects of the nervous, immune, and endocrine systems. Using principles of psychoneuroimmunology along with previously established but yet un-linked scientific principles and observations, this paper proposes a neuroimmune-based mechanistic hypothesis for the etiology of autism that connects elevated levels of maternal pro-inflammatory cytokines to autistic symptoms in her offspring through a logical sequence of events. While both researchers and clinicians often note correlations between pro-inflammatory cytokine levels and autistic symptoms in affected individuals, no specific mechanism has been documented that logically and directly connects the two. I propose that pro-inflammatory cytokines arising from maternal inflammation, infection, and, possibly, autoimmunity, pass through the placenta; enter the fetal circulation; cross the fetal blood-brain barrier (BBB); and cause aberrant neuronal growth and plasticity within the fetal brain via a "cytokine-storm". Microglia and astrocyte stimulation lead to a positive-feedback loop that also facilitates the development of a chronic inflammatory environment within the fetus, pre-disposing it to lifelong comorbid psychiatric and systemic pathologies. Such a mechanism could account for many of the observed symptoms and behaviors of autistic individuals such as hyper-sensitivity to environmental stimuli, object fixation, echolalia, repetitive physical behaviors, chronic enterocolitis, autoimmune disease, and, at the extreme, savantism. The thiazolidinedione pioglitazone (and possibly rosiglitazone), a non-steroidal anti-inflammatory drug (NSAID), which is commonly used to lower blood glucose levels and associated inflammatory markers in patients with diabetes, and histamine receptor blockers, as well as monitoring and limiting sucrose-containing foods, might prove to be effective preventative therapies for the development of autism in the fetus for pregnant women displaying either a cytokine-induced depression or other elevated systemic inflammatory state conditions. Published by Elsevier Ltd. C1 USAF Acad, HQ USAFA DFB, Colorado Springs, CO 80840 USA. RP Buehler, MR (reprint author), USAF Acad, HQ USAFA DFB, 2355 Fac Dr,Suite 2P389, Colorado Springs, CO 80840 USA. EM matthew.buehler@usafa.edu FU United States Air Force; United States Air Force Academy FX Thank you to the United States Air Force and the United States Air Force Academy for funding the advanced degree program under which this mechanism was developed. I would also like to thank my advisor, Dr. Kenneth Hunter, Sc.D., of the University of Nevada School of Medicine, who introduced me to the field of "psychoneuroimmunology" and felt that maternal inflammation could play a role in autism development within the fetus, with the outward sign potentially being a cytokine-induced depression in the mother based on the JHU IAN data included in this paper. He noticed the high rate of diagnosed depression in mothers who had children with autism in the JHU IAN study. In addition to Dr. Hunter's mentorship and insights, I sincerely appreciate the insights of the following faculty from various departments and schools at the University of Nevada, Reno and the United States Air Force Academy: Grant Mastick, Ph.D., Jeffrey Hutsler, Ph.D., Debra Vigil, Ph.D., Fiona Britton, Ph.D., Patricia Berninsone, Ph.D., and Mike Wilcox, Ph.D. All of their assistance was of great help in developing this mechanism. 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Hypotheses PD JUN PY 2011 VL 76 IS 6 BP 863 EP 870 DI 10.1016/j.mehy.2011.02.038 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 776HE UT WOS:000291524300023 PM 21421290 ER PT J AU Geier, DA Kern, JK Davis, G King, PG Adams, JB Young, JL Geier, MR AF Geier, David A. Kern, Janet K. Davis, Georgia King, Paul G. Adams, James B. Young, John L. Geier, Mark R. TI A prospective double-blind, randomized clinical trial of levocarnitine to treat autism spectrum disorders SO MEDICAL SCIENCE MONITOR LA English DT Article DE autism spectrum disorder; carnitine; mitochondrial dysfunction ID L-CARNITINE; CHILDREN AB Background: L-carnitine was proposed as a potential treatment for patients diagnosed with an autism spectrum disorder to improve mitochondrial dysfunction, but no prior randomized controlled trials have been conducted. Material/Methods: Thirty subjects diagnosed with an ASD were randomly assigned to receive a standardized regimen (50 mg L-carnitine/kg bodyweight/day) of liquid L-carnitine (n=19) or placebo (n=11) for 3-months. Measures included changes in professionally completed Childhood Autism Rating Scale (CARS), hand muscle testing, and modified clinical global impression (CGI) forms; parent completed Autism Treatment Evaluation Checklist (ATEC), treatment adherence measurement (TAM), frequency and intensity of side effect rating (FISER)/global rating of side effect burden (GRSEB)/patient report of incidence of side effects (PRISE) forms; and lab testing. Results: Significant improvements were observed in CARS (-2.03, 95% CI=-3.7 to -0.31), CGI (-0.69, 95% CI=-1.1 to -0.06), and ATEC scores. Significant correlations between changes in serum free-carnitine levels and positive clinical changes were observed for hand muscle strength (R(2)=0.23, P=0.046), cognitive scores (R(2)=0.27, P=0.019), and CARS scores (R(2)=0.20, P=0.047). Study subjects were protocol-compliant (average adherence was >85%) and generally well-tolerated the L-carnitine therapy given. Conclusions: L-carnitine therapy (50 mg/kilogram-bodyweight/day) administered for 3-months significantly improved several clinical measurements of ASD severity, but subsequent studies are recommended. C1 [Geier, David A.] Inst Chron Illnesses Inc, Silver Spring, MD USA. [Geier, David A.] CoMeD Inc, Silver Spring, MD USA. [Kern, Janet K.] Genet Consultants Dallas, Allen, TX USA. [Kern, Janet K.] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA. [Davis, Georgia] Genet Consultants So Illinois, Springfield, IL USA. [King, Paul G.] Genet Consultants New Jersey, Parsippany, NJ USA. [Adams, James B.] Arizona State Univ, Tempe, AZ USA. [Young, John L.] Genet Consultants Maryland, Rockville, MD USA. [Geier, Mark R.] ASD Ctr LLC, Silver Spring, MD USA. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. EM mgeier@comcast.net FU Autism Research Institute; CoMeD, Inc.; Institute of Chronic Illnesses, Inc; Brenen Hornstein Autism Research and Education (BHARE) Foundation; Yates Foundation for Autism; Sandra Gray Memorial Fund FX This research was funded by a grant from the Autism Research Institute, non-profit CoMeD, Inc., and by the non-profit Institute of Chronic Illnesses, Inc from grants received from the Brenen Hornstein Autism Research and Education (BHARE) Foundation, the Yates Foundation for Autism, and the Sandra Gray Memorial Fund. None of the authors owned a financial interest in the production of L-carnitine prior to conducting the present study. Since, the completion of the study Mark Geier and David Geier have a patent pending for the use of L-carnitine for the treatment of autism spectrum disorders. 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TI Medicaid's Increasing Role in Treating Youths With Autism Spectrum Disorders SO PSYCHIATRIC SERVICES LA English DT Editorial Material C1 [Semansky, Rafael M.; Xie, Ming; Mandell, David S.] Univ Penn, Sch Med, Philadelphia, PA 19104 USA. RP Semansky, RM (reprint author), Univ Penn, Sch Med, 3535 Market St,3rd Floor, Philadelphia, PA 19104 USA. EM semansky@upenn.edu RI Mandell, David/H-2730-2012 OI Mandell, David/0000-0001-8240-820X CR ROWLAND D, 2009, CHILDRENS COVERAGE R *US DEP ED, 2006, CHILDR DIS REC SPEC NR 2 TC 3 Z9 3 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 JUN PY 2011 VL 62 IS 6 BP 588 EP 588 PG 1 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 774SL UT WOS:000291406600002 PM 21632723 ER PT J AU Dionne, M Martini, R AF Dionne, Maryse Martini, Rose TI Floor Time Play with a child with autism: A single-subject study SO CANADIAN JOURNAL OF OCCUPATIONAL THERAPY-REVUE CANADIENNE D ERGOTHERAPIE LA English DT Article DE Autistic disorder; Paediatric occupational therapy; Play ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; DISORDERS; PROGRAM AB Background. Children with autism exhibit difficulties with social interaction and communication skills, and they present with restricted interests and stereotyped patterns of behaviour that affect their daily lives. Floor time play (FTP) is an intervention approach that addresses these issues; however, there are few published studies on its effectiveness. Purpose. This study determines the effectiveness of FTP intervention with a child diagnosed with autism. Methods. A single subject AB design was used with circles of communication as the behaviour indicator for improvement. Visual and statistical analyses were completed. The child's mother kept a daily journal describing FTP intervention sessions at home. Findings. Despite variability in the data, statistical analyses indicate a significant difference between the numbers of circles of communication during the intervention phase as compared with the observation phase. Implications. This study provides preliminary evidence for the use of the FTP approach with a child with autism. C1 [Martini, Rose] Univ Ottawa, Fac Hlth Sci, Sch Rehabil Sci, Occupat Therapy Program, Ottawa, ON K1H 8M5, Canada. RP Dionne, M (reprint author), 92 Boul St Raymond,Suite 205, Gatineau, PQ J8Y 1S7, Canada. 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J. Occup. Ther. PD JUN PY 2011 VL 78 IS 3 BP 196 EP 203 DI 10.2182/cjot.2011.78.3.8 PG 8 WC Rehabilitation SC Rehabilitation GA 773RT UT WOS:000291328200011 PM 21699014 ER PT J AU Whitehouse, AJO Bishop, DVM Ang, QW Pennell, CE Fisher, SE AF Whitehouse, A. J. O. Bishop, D. V. M. Ang, Q. W. Pennell, C. E. Fisher, S. E. TI CNTNAP2 variants affect early language development in the general population SO GENES BRAIN AND BEHAVIOR LA English DT Article DE Autism; CNTNAP2; language delay; language development; Raine study; SLI ID AT-RISK INFANTS; AUTISM; GENOME; ASSOCIATION; IMPAIRMENT; DISORDERS; ETIOLOGY; VALIDITY; DELAY AB Early language development is known to be under genetic influence, but the genes affecting normal variation in the general population remain largely elusive. Recent studies of disorder reported that variants of the CNTNAP2 gene are associated both with language deficits in specific language impairment (SLI) and with language delays in autism. We tested the hypothesis that these CNTNAP2 variants affect communicative behavior, measured at 2 years of age in a large epidemiological sample, the Western Australian Pregnancy Cohort (Raine) Study. Singlepoint analyses of 1149 children (606 males and 543 females) revealed patterns of association which were strikingly reminiscent of those observed in previous investigations of impaired language, centered on the same genetic markers and with a consistent direction of effect (rs2710102, P = 0.0239; rs759178, P = 0.0248). On the basis of these findings, we performed analyses of four-marker haplotypes of rs2710102-rs759178-rs17236239-rs2538976 and identified significant association (haplotype TTAA, P = 0.049; haplotype GCAG, P = .0014). Our study suggests that common variants in the exon 13-15 region of CNTNAP2 influence early language acquisition, as assessed at age 2, in the general population. We propose that these CNTNAP2 variants increase susceptibility to SLI or autism when they occur together with other risk factors. C1 [Whitehouse, A. J. O.] Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6009, Australia. [Whitehouse, A. J. O.; Bishop, D. V. M.] Univ Western Australia, Sch Psychol, Neurocognit Dev Unit, Perth, WA 6009, Australia. [Bishop, D. V. M.] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. [Ang, Q. W.; Pennell, C. E.] Univ Western Australia, Sch Womens & Infants Hlth, Perth, WA 6009, Australia. [Fisher, S. E.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. [Fisher, S. E.] Max Planck Inst Psycholinguist, Language & Genet Dept, Nijmegen, Netherlands. RP Whitehouse, AJO (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, 100 Roberts Rd, Subiaco, WA, Australia. EM awhitehouse@ichr.uwa.edu.au RI Fisher, Simon/E-9130-2012 OI Fisher, Simon/0000-0002-3132-1996 FU National Health and Medical Research Council (NHMRC) [572613]; University of Western Australia (UWA); UWA Faculty of Medicine, Dentistry and Health Sciences; Raine Medical Research Foundation; Telethon Institute for Child Health Research; Women's and Infants Research Foundation; Royal Society; Simons Foundation Autism Research Initiative; Max Planck Society; Wellcome Trust FX The authors would like to acknowledge the National Health and Medical Research Council (NHMRC) for their long-term contribution to funding the Raine study over the last 20 years. Core Management of the Raine study has been funded by the University of Western Australia (UWA), 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. The genotyping of the Raine cohort was funded by a project grant from the NHMRC (572613). The authors are extremely grateful to the study participants and their families as well as the Raine study team for cohort co-ordination and data collection. A.J.O.W. is supported by the NHMRC. S.E.F. is supported by the Royal Society, the Simons Foundation Autism Research Initiative and the Max Planck Society. D.V.M.B. is supported by the Wellcome Trust. 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PD JUN PY 2011 VL 10 IS 4 BP 451 EP 456 DI 10.1111/j.1601-183X.2011.00684.x PG 6 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 772XF UT WOS:000291270700009 PM 21310003 ER PT J AU Cox, KH Rissman, EF AF Cox, K. H. Rissman, E. F. TI Sex differences in juvenile mouse social behavior are influenced by sex chromosomes and social context SO GENES BRAIN AND BEHAVIOR LA English DT Article DE Autism; adolescent; juvenile; play; sex chromosomes; social behavior ID BTBR-T+TF/J MICE; INBRED STRAINS; PLAY-BEHAVIOR; FEMALE RATS; DIFFERENTIATION; PHENOTYPES; RECEPTOR; AUTISM; TESTOSTERONE; ORGANIZATION AB Play behavior in juvenile primates, rats and other species is sexually dimorphic, with males showing more play than females. In mice, sex differences in juvenile play have only been examined in out-bred CD-1 mice. In this strain, contrary to other animals, male mice display less play soliciting than females. Using an established same-sex dyadic interaction test, we examined play in in-bred C57BL/6J (B6) 21-day-old mice. When paired with non-siblings, males tended to be more social than females, spending more time exploring the test cage. Females displayed significantly more anogenital sniffing and solicited play more frequently than did males. To determine if the origin of the sex difference was sex chromosome genes or gonadal sex, next we used the four core genotype mouse. We found significant interactions between gonadal sex and genotype for several behaviors. Finally, we asked if sibling pairs (as compared to non-siblings) would display qualitatively or quantitatively different behavior. In fact, XX females paired with a sibling were more social and less exploratory or investigative, whereas XY males exhibited less investigative and play soliciting behaviors in tests with siblings. Many neurobehavioral disorders, like autism spectrum disorder (ASD), are sexually dimorphic in incidence and patients interact less than normal with other children. Our results suggest that sex chromosome genes interact with gonadal hormones to shape the development of juvenile social behavior, and that social context can drastically alter sex differences. These data may have relevance for understanding the etiology of sexually dimorphic disorders such as ASD. C1 [Rissman, E. F.] Univ Virginia, Dept Biochem & Mol Genet, Charlottesville, VA 22908 USA. [Rissman, E. F.] Univ Virginia, Grad Program Neurosci, Charlottesville, VA 22908 USA. RP Rissman, EF (reprint author), Univ Virginia, Dept Biochem & Mol Genet, POB 800733, Charlottesville, VA 22908 USA. EM Rissman@virginia.edu FU NIH [RO1 MH086711, T32 HD007323]; Eunice Kennedy Shriver NICHD/NIH (SCCPIR) [U54-HD28934] FX The authors thank Aileen Wills and Savera Shetty for their assistance in genotyping the mice. This work was supported by NIH RO1 MH086711. KHC was supported by NIH T32 HD007323. The University of Virginia Center for Reproduction Ligand Assay and Analysis Core is supported by the Eunice Kennedy Shriver NICHD/NIH (SCCPIR) Grant U54-HD28934. 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The present study explored this question in the context of a particularly salient form of perceived animacy: chasing, in which one shape (the "wolf") pursues another shape (the "sheep"). Here the participants themselves controlled the movement of the sheep, and the perception of chasing was assessed in terms of their ability to avoid being caught by the wolf-which looked identical to many moving distractors, and so could be identified only by its motion. The wolf's pursuit was frequently interrupted by periods in which it was static, jiggling in place, or moving randomly (amidst distractors that behaved similarly). Only the latter condition greatly impaired the detection of chasing-and only when the random motion was grouped into temporally extended chunks. These results reveal (1) how the detection of chasing is determined by the character and temporal grouping (rather than just the brute amount) of "pursuit" over time; and (2) how these temporal dynamics can lead the visual system to either construct or actively reject interpretations of chasing. C1 [Gao, Tao; Scholl, Brian J.] Yale Univ, Dept Psychol, New Haven, CT 06520 USA. RP Gao, T (reprint author), Yale Univ, Dept Psychol, Box 208205, New Haven, CT 06520 USA. EM tao.gao@yale.edu; brian.scholl@yale.edu CR Abell F, 2000, COGNITIVE DEV, V15, P1, DOI 10.1016/S0885-2014(00)00014-9 Adelson E. 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Exp. Psychol.-Hum. Percept. Perform. PD JUN PY 2011 VL 37 IS 3 BP 669 EP 684 DI 10.1037/a0020735 PG 16 WC Psychology; Psychology, Experimental SC Psychology GA 771CN UT WOS:000291134900006 PM 21639674 ER PT J AU Davis, TE Hess, JA Matthews, RA Fodstad, JC Dempsey, T Jenkins, WS Moree, BN Matson, JL AF Davis, Thompson E., III Hess, Julie A. Matthews, Russell A. Fodstad, Jill C. Dempsey, Tim Jenkins, Whitney S. Moree, Brittany N. Matson, Johnny L. TI The Moderating Effect of Anxiety on Development in Atypically Developing Toddlers SO JOURNAL OF PSYCHOPATHOLOGY AND BEHAVIORAL ASSESSMENT LA English DT Article DE Anxiety; Toddlers; Development; Atypically developing ID COMORBIDITY SURVEY REPLICATION; DSM-IV DISORDERS; PSYCHIATRIC-DISORDERS; INTELLECTUAL ABILITY; CHILDREN; AUTISM; ACHIEVEMENT; PREVALENCE AB In typically developing children, researchers have found that anxiety disorders are associated with poorer intellectual abilities (Davis et al. Journal of Psychopathology and Behavioral Assessment 30:43-51, 2008). The aim of the current study was to examine the impact anxiety symptoms had on the developmental quotients of toddlers. A total of 170 toddlers ranging in age from 17 to 37 months were selected for inclusion in this study, all of whom were at risk for or had a developmental delay. Two factors indicative of behavioral symptoms of anxiety from the Baby and Infant Screen for Children with aUtIsm Traits-Part2 were utilized as the independent variables and the total developmental quotient from the Battelle Developmental Inventory, 2nd Edition was utilized for the dependent variable. Examination of results revealed that atypically developing toddlers with symptoms of anxiety had significantly lower developmental quotients when compared to toddlers without any anxiety symptoms. A discussion of the implications and limitations of this study are included. C1 [Davis, Thompson E., III; Hess, Julie A.; Matthews, Russell A.; Fodstad, Jill C.; Dempsey, Tim; Jenkins, Whitney S.; Moree, Brittany N.; Matson, Johnny L.] Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA. RP Davis, TE (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA. EM ted@lsu.edu CR BARON RM, 1986, J PERS SOC PSYCHOL, V51, P1173, DOI 10.1037/0022-3514.51.6.1173 Bryant B. J., 2005, CHILD ADOL PSYCH CL, P111 CLEARY PD, 1982, J HEALTH SOC BEHAV, V23, P159, DOI 10.2307/2136512 Davis III T. 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PD JUN PY 2011 VL 33 IS 2 BP 171 EP 177 DI 10.1007/s10862-010-9194-5 PG 7 WC Psychology, Clinical SC Psychology GA 771OF UT WOS:000291169600003 ER PT J AU Happe, F AF Happe, Francesca TI Criteria, Categories, and Continua: Autism and Related Disorders in DSM-5 SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Editorial Material C1 Kings Coll London, Inst Psychiat, MRC SGDP Ctr, London SE5 8AF, England. RP Happe, F (reprint author), Kings Coll London, Inst Psychiat, MRC SGDP Ctr, POB 80,Denmark Hill, London SE5 8AF, England. EM Francesca.happe@kcl.ac.uk RI Happe, Francesca/D-5544-2012 CR *AM PSYCH ASS, SOC COMM DIS PROP RE American Psychiatric Association, PROP DRAFT REV DSM D Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Howlin P, 2003, J AUTISM DEV DISORD, V33, P3, DOI 10.1023/A:1022270118899 LORD C, 2011, MULTISITE STUD UNPUB Mandy W, 2011, AUTISM RES, V4, P121, DOI 10.1002/aur.178 Mattila ML, 2011, J AM ACAD CHILD PSY, V50, P583, DOI 10.1016/j.jaac.2011.04.001 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 Williams K, 2008, J PAEDIATR CHILD H, V44, P108, DOI 10.1111/j.1440-1754.2007.01232.x Wing L, 2011, RES DEV DISABIL, V32, P768, DOI 10.1016/j.ridd.2010.11.003 Witwer AN, 2008, J AUTISM DEV DISORD, V38, P1611, DOI 10.1007/s10803-008-0541-2 NR 11 TC 27 Z9 27 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 JUN PY 2011 VL 50 IS 6 BP 540 EP 542 DI 10.1016/j.jaac.2011.03.015 PG 3 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 773DZ UT WOS:000291288500004 PM 21621137 ER PT J AU Mattila, ML Kielinen, M Linna, SL Jussila, K Ebeling, H Bloigu, R Joseph, RM Moilanen, I AF Mattila, Marja-Leena Kielinen, Marko Linna, Sirkka-Liisa Jussila, Katja Ebeling, Hanna Bloigu, Risto Joseph, Robert M. Moilanen, Irma TI Autism Spectrum Disorders According to DSM-IV-TR and Comparison With DSM-5 Draft Criteria: An Epidemiological Study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE Autism spectrum disorder; autism; prevalence; DSM-IV; DSM-5 ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; CHILDREN AB Objective: The latest definitions of autism spectrum disorders (ASDs) were specified in DSM-IV-TR in 2000. DSM-5 criteria are planned for 2013. Here, we estimated the prevalence of ASDs and autism according to DSM-IV-TR, clarified confusion concerning diagnostic criteria, and evaluated DSM-5 draft criteria for ASD posted by the American Psychiatry Association (APA) in February 2010. Method: This was an epidemiological study of 5,484 eight-year-old children in Finland, 4,472 (81%) of them rated via the Autism Spectrum Screening Questionnaire by parents and/or teachers, and 110 examined by using a structured interview, semi-structured observation, IQ measurement, school-day observation, and patient records. Diagnoses were assigned according to DSM-IV-TR criteria and DSM-5 draft criteria in children with a full-scale IQ (FSIQ) >= 50. Patient records were evaluated in children with an FSIQ < 50 to discover diagnoses of ASDs. Results: The prevalence of ASDs was 8.4 in 1,000 and that of autism 4.1 in 1,000 according to DSM-IV-TR. Of the subjects with ASDs and autism, 65% and 61% were high-functioning (FSIQ >= 70), respectively. The prevalence of pervasive developmental disorder not otherwise specified was not estimated because of inconsistency in DSM-IV-TR criteria. DSM-5 draft criteria were shown to be less sensitive in regard to identification of subjects with ASDs, particularly those with Asperger's syndrome and some high-functioning subjects with autism. Conclusions: DSM-IV-TR helps with the definition of ASDs only up to a point. We suggest modifications to five details of DSM-5 draft criteria posted by the APA in February 2010. Completing revision of DSM criteria for ASDs is a challenging task. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(6): 583-592. C1 [Mattila, Marja-Leena; Linna, Sirkka-Liisa; Jussila, Katja; Ebeling, Hanna; Moilanen, Irma] Univ Hosp Oulu, FIN-90029 Oulu, Finland. [Mattila, Marja-Leena; Linna, Sirkka-Liisa; Jussila, Katja; Ebeling, Hanna; Moilanen, Irma] Univ Oulu, Clin Child Psychiat, Oulu, Finland. [Joseph, Robert M.] Boston Univ, Sch Med, Boston, MA 02215 USA. RP Mattila, ML (reprint author), Univ Hosp Oulu, POB 26, FIN-90029 Oulu, Finland. EM marja-leena.mattila@fimnet.fi RI Edwards, chacola /A-7127-2012; Joseph, Roy/D-8530-2015 FU Finland's Slot Machine Association; Eija and Veikko Lesonen Foundation, Oulu, Finland; Alma and K.A. Snellman Foundation, Oulu, Finland; Rinnekoti Research Foundation, Espoo, Finland; Child Psychiatric Research Foundation, Finland; Child Psychiatric Research Foundation, Oulu Area, Finland; Oulu Medical Research Foundation, Oulu, Finland; Emil Aaltonen Foundation, Finland; Thule Institute, University of Oulu, Finland; Juselius Foundation, Finland FX This study was supported by research grants from Finland's Slot Machine Association, the Eija and Veikko Lesonen Foundation, Oulu, Finland, the Alma and K.A. Snellman Foundation, Oulu, Finland, the Rinnekoti Research Foundation, Espoo, Finland, the Child Psychiatric Research Foundation, Finland, the Child Psychiatric Research Foundation, Oulu Area, Finland, the Oulu Medical Research Foundation, Oulu, Finland, the Emil Aaltonen Foundation, Finland, the Thule Institute, University of Oulu, Finland, and the Juselius Foundation, Finland. The sponsors had no role in the design of the study or the manner in which it was conducted. 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This article explores the depiction of physically and mentally disabled characters in Borges' Funes the Memorious (1942)-a story about an Uruguayan gaucho who has been left paralysed after a fall from a horse which simultaneously endowed him with an infallible memory and perception-and Beckett's Trilogy: Molloy (1951), Malone Dies (1951) and The Unnamable (1953). It examines the prodigious memory of Funes and the forgetful minds of Molloy and Malone with reference to influential neuropsychological studies such as Alexander Luria's twofold exploration of memory and forgetfulness in The Mind of a Mnemonist (1968) and The Man with a Shattered World (1972). The article demonstrates that in contrast to Beckett's amnesiacs and Luria's brain-damaged patient, who are able to transcend their circumstances through cathartic writing, Borges' and Luria's mnemonic prodigies fail to achieve anything significant with their unlimited memories and remain imprisoned within their cognitive disabilities. It reveals that medical discourses can provide invaluable insights and lead to a deeper understanding of the minds and bodily afflictions of literary characters. C1 Univ Kent, Canterbury CT2 7NF, Kent, England. RP Novillo-Corvalan, P (reprint author), Univ Kent, Cornwallis Bldg, Canterbury CT2 7NF, Kent, England. EM p.novillo-corvalan@kent.ac.uk CR ACKERLEY CJ, 2006, FABER COMPANION S BE, P361 BECKETT S, 1976, BECKETT TRILOGY MOLL Beckett Samuel, 2009, MURPHY, P106 BELLVILLADA G, 1981, BORGES HIS FICTION, P100 BORGES JL, 1998, COLLECTED FICTIONS J, P129 BORGES JL, 1984, 24 CONVERSATIONS BOR, P28 Borges Jorge Luis, 2000, LABYRINTHS CASEY E, 1987, REMEMBERING PHENOMEN, P7 CORDINGLEY A, 2004, BECKETT APRES BECKET, P131 DOWN JL, 1887, SOME MENTAL AFFECTIO, P102 FIFIELD P, 2009, BECKETT DEATH, P131 FIFIELD P, 2009, BECKETT DEATH, P128 JAMES W, 1890, PRINCIPLES PSYCHOL, V1, P660 KNOWLSON J, 2006, BECKETT REMEMBERING, P116 KNOWLSON J, 1996, DAMNED FAME LIFE S B, P208 KNOWLSON J, 1996, DAMNED FAME LIFE S B, P175 KNOWLSON J, 2006, BECKETT REMEMBERING, P47 LURIA AR, 1987, MAN SHATTERED WORLD, P86 LURIA AR, 1969, MIND MNEMONIST, P31 MONEGAL ER, 1988, JL BORGES LIT BIOGRA, P100 Nietzsche F, 1997, UNTIMELY MEDITATIONS Nietzsche Friedrich, 1997, UNTIMELY MEDITATIONS, P62 NOVILLOCORVALAN P, 2011, BORGES JOYCE INFINIT, P81 QUAYSON A, 2007, DISABILITY CRISIS RE, P35 Quiroga RQ, 2010, NATURE, V463, P611, DOI 10.1038/463611a RICOEUR P, 1995, MEMORY FORGETFULNESS, V2, P1 Ricoeur Paul, 2004, MEMORY HIST FORGETTI Slote S, 2010, J BECKETT STUD, V19, P15, DOI 10.3366/E0309520709000429 TREFFERT DA, 2010, AUTISM TALENT, P1 VEBERNE T, 1976, AUST NZ J PSYCHIAT, P255 VERBERNE T, 1976, AUST NZ J PSYCHIAT, V10, P253, DOI 10.3109/00048677609159507 2008, JOBS, V17, P78 NR 32 TC 1 Z9 1 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 1468-215X J9 MED HUMANIT JI Med. Humanit. PD JUN PY 2011 VL 37 IS 1 BP 38 EP 43 DI 10.1136/jmh.2011.007476 PG 6 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 765LT UT WOS:000290708500013 PM 21593247 ER PT J AU Wharff, EA Ginnis, KB Ross, AM Blood, EA AF Wharff, Elizabeth A. Ginnis, Katherine B. Ross, Abigail M. Blood, Emily A. TI Predictors of Psychiatric Boarding in the Pediatric Emergency Department Implications for Emergency Care SO PEDIATRIC EMERGENCY CARE LA English DT Article DE emergency psychiatry; crisis intervention; inpatient hospitalization; psychiatric care delivery ID LENGTH-OF-STAY AB Objectives: Patients who present to the emergency department (ED) and require psychiatric hospitalization may wait in the ED or be admitted to a medical service because there are no available inpatient psychiatric beds. These patients are psychiatric "boarders.'' This study describes the extent of the boarder problem in a large, urban pediatric ED, compares characteristics of psychiatrically hospitalized patients with boarders, and compares predictors of boarding in 2 ED patient cohorts. Methods: A retrospective cohort study was conducted in 2007-2008. The main outcome measure was placement into a psychiatric facility or boarding. Predictors of boarding in the present analysis were compared with predictors from a similar study conducted in the same ED in 1999-2000. Results: Of 461 ED patient encounters requiring psychiatric admission, 157 (34.1%) boarded. Mean and median boarding duration for the sample were 22.7(SD, 8.08) and 21.18 hours, respectively. Univariate generalized estimating equations demonstrated increased boarding odds for patients carrying Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition diagnoses of autism, mental retardation, and/or developmental delay (P = 0.01), presenting during the weekend (P = 0.03) or presenting during months without school vacation (P = 0.02). Suicidal ideation (SI) significantly predicted boarding status, with increased likelihood of boarding for severe SI (P = 0.02). Age, race, insurance status, and homicidal ideation did not significantly predict boarding in the 2007-2008 patient cohort, although they did in the earlier study. Systemic factors and SI predicted boarding status in both cohorts. Conclusions: Suicidal patients continue to board. Limits within the system, including timing of ED presentation and a dearth of specialized services, still exist, elevating the risk of boarding for some populations. Implications for pediatric ED psychiatric care delivery are discussed. C1 [Wharff, Elizabeth A.] Childrens Hosp, Dept Psychiat, Emergency Psychiat Serv, Boston, MA 02115 USA. [Wharff, Elizabeth A.; Ginnis, Katherine B.; Blood, Emily A.] Harvard Univ, Sch Med, Boston, MA USA. [Blood, Emily A.] Childrens Hosp, Div Adolescent Med, Boston, MA 02115 USA. RP Wharff, EA (reprint author), Childrens Hosp, Dept Psychiat, Emergency Psychiat Serv, Fegan 8,300 Longwood Ave, Boston, MA 02115 USA. EM Elizabeth.wharff@childrens.harvard.edu FU Cohasset Tennis Association FX Support for this research was provided by the Cohasset Tennis Association. CR *ACEP, ACEP PSYCH SUBST AB BENDER D, 2008, LIT REV PSYCHIAT BOA Bernstein SL, 2009, ACAD EMERG MED, V16, P1, DOI 10.1111/j.1553-2712.2008.00295.x Camilli V., 2005, TOPICS EMERGENCY MED, V27, P313 Falvo T, 2007, ACAD EMERG MED, V14, P332, DOI 10.1197/j.aem.2006.11.011 Gorelick MH, 2005, ANN EMERG MED, V45, P128, DOI 10.1016/j.annemergmed.2004.08.041 Hart BG, 2008, J EMERG NURS, V34, P359, DOI 10.1016/j.jen.2008.04.028 Hoot NR, 2008, ANN EMERG MED, V52, P126, DOI 10.1016/j.annemergmed.2008.03.014 Institute of Medicine, 2001, CROSS QUAL CHASM NEW KATZ A, 2006, PATIENTS WAIT HOURS *MA HLTH POL FOR, 2001, ISSUE BRIEF, V12 Mansbach JM, 2003, PEDIATRICS, V111, pE693, DOI 10.1542/peds.111.6.e693 Nelson KA, 2009, PEDIATR EMERG CARE, V25, P835, DOI 10.1097/PEC.0b013e3181c330c4 OLSHAKER JS, 2005, J EMERGENCY MED, V30, P351 OSHEA J, 2007, CRISIS AM EMERGENCY SHARFSTEIN J, 2000, CLIN FISCAL IMPLICAT Stefan S, 2006, EMERGENCY DEP TREATM TRAFFORD A, 2000, BOARDER KIDS EDGE TUTTLE G, 2008, ACCESS PSYCHIAT BEDS Young D, 2007, AM J HEALTH-SYST PH, V64, P1255, DOI 10.2146/news070057 2004, MENTAL HLTH CRISIS N NR 21 TC 7 Z9 7 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0749-5161 J9 PEDIATR EMERG CARE JI Pediatr. Emerg. Care PD JUN PY 2011 VL 27 IS 6 BP 483 EP 489 DI 10.1097/PEC.0b013e31821d8571 PG 7 WC Emergency Medicine; Pediatrics SC Emergency Medicine; Pediatrics GA 772PX UT WOS:000291247800004 PM 21629148 ER PT J AU Boyle, CA Boulet, S Schieve, LA Cohen, RA Blumberg, SJ Yeargin-Allsopp, M Visser, S Kogan, MD AF Boyle, Coleen A. Boulet, Sheree Schieve, Laura A. Cohen, Robin A. Blumberg, Stephen J. Yeargin-Allsopp, Marshalyn Visser, Susanna Kogan, Michael D. TI Trends in the Prevalence of Developmental Disabilities in US Children, 1997-2008 SO PEDIATRICS LA English DT Article DE developmental disabilities; prevalence; autism; attention deficit hyperactivity disorder ID ATTENTION-DEFICIT/HYPERACTIVITY-DISORDER; AUTISM SPECTRUM DISORDER; UNITED-STATES; IDENTIFYING INFANTS; MENTAL-RETARDATION; HEALTH; IMPACT; DIAGNOSIS; GIRLS AB OBJECTIVE: To fill gaps in crucial data needed for health and educational planning, we determined the prevalence of developmental disabilities in US children and in selected populations for a recent 12-year period. PARTICIPANTS AND METHODS: We used data on children aged 3 to 17 years from the 1997-2008 National Health Interview Surveys, which are ongoing nationally representative samples of US households. Parent-reported diagnoses of the following were included: attention deficit hyperactivity disorder; intellectual disability; cerebral palsy; autism; seizures; stuttering or stammering; moderate to profound hearing loss; blindness; learning disorders; and/or other developmental delays. RESULTS: Boys had a higher prevalence overall and for a number of select disabilities compared with girls. Hispanic children had the lowest prevalence for a number of disabilities compared with non-Hispanic white and black children. Low income and public health insurance were associated with a higher prevalence of many disabilities. Prevalence of any developmental disability increased from 12.84% to 15.04% over 12 years. Autism, attention deficit hyperactivity disorder, and other developmental delays increased, whereas hearing loss showed a significant decline. These trends were found in all of the sociodemographic subgroups, except for autism in non-Hispanic black children. CONCLUSIONS: Developmental disabilities are common and were reported in similar to 1 in 6 children in the United States in 2006-2008. The number of children with select developmental disabilities (autism, attention deficit hyperactivity disorder, and other developmental delays) has increased, requiring more health and education services. Additional study of the influence of risk-factor shifts, changes in acceptance, and benefits of early services is needed. Pediatrics 2011; 127:1034-1042 C1 [Boyle, Coleen A.; Boulet, Sheree; Schieve, Laura A.; Yeargin-Allsopp, Marshalyn; Visser, Susanna] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30333 USA. [Cohen, Robin A.; Blumberg, Stephen J.] Ctr Dis Control & Prevent, Natl Ctr Hlth Stat, Atlanta, GA 30333 USA. [Kogan, Michael D.] Maternal & Child Hlth Bur, US Hlth Resources & Serv Adm, Rockville, MD USA. RP Boyle, CA (reprint author), Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, 1600 Clifton Rd, Atlanta, GA 30333 USA. EM cboyle@cdc.gov FU Centers for Disease Control and Prevention, Atlanta, Georgia FX The National Health Interview Study is supported by the Centers for Disease Control and Prevention, Atlanta, Georgia. CR ACKLAND MJ, 1995, J PAEDIATR CHILD H, V31, P423, DOI 10.1111/j.1440-1754.1995.tb00851.x Atladottir HO, 2007, ARCH PEDIAT ADOL MED, V161, P193, DOI 10.1001/archpedi.161.2.193 *AUT OTH DEV DIS M, 2009, MMWR-MORBID MORTAL W, V58, P2 Boulet SL, 2009, ARCH PEDIAT ADOL MED, V163, P19, DOI 10.1001/archpediatrics.2008.506 BOULET SL, 2009, MATERN CHILD HLTH J BOYLE CA, 1994, PEDIATRICS, V93, P399 Brosco JP, 2006, ARCH PEDIAT ADOL MED, V160, P302, DOI 10.1001/archpedi.160.3.302 Gaffney M., 2010, Morbidity and Mortality Weekly Report, V59, P220 Visser S. N., 2010, Morbidity and Mortality Weekly Report, V59, P1439 Duby JC, 2006, PEDIATRICS, V118, P405, DOI 10.1542/peds.2006-1231 Daniel K L, 2009, Public Health, V123 Suppl 1, pe11, DOI 10.1016/j.puhe.2009.06.002 DEHAAS PA, 1986, J ABNORM CHILD PSYCH, V14, P457, DOI 10.1007/BF00915438 Froehlich TE, 2007, ARCH PEDIAT ADOL MED, V161, P857, DOI 10.1001/archpedi.161.9.857 GRINKER RR, AUTISM SPEC IN PRESS Gurney JG, 2003, ARCH PEDIAT ADOL MED, V157, P622, DOI 10.1001/archpedi.157.7.622 *INT LEAG EP, 2009, REV TERM CONC ORG EP Karapurkar-Bhasin T, 2006, MMWR-MORBID MORTAL W, V55, P1 Kogan MD, 2009, PEDIATRICS, V124, P1395, DOI 10.1542/peds.2009-1522 Larson K, 2010, MATERN CHILD HLTH J, V14, P332, DOI 10.1007/s10995-009-0477-y Larson SA, 2005, PROBLEMS DEFINING ME, V7 Miller JE, 2001, VITAL HLTH STAT, V2, P1 Jensen PS, 2004, PEDIATRICS, V113, P754 MURPHY CC, 1995, EPILEPSIA, V36, P866, DOI 10.1111/j.1528-1157.1995.tb01629.x National Center for Health Statistics, 2009, NAT HLTH INT SURV NEWSCHAFFER CJ, PEDIATRICS, V115 Petrini JR, 2009, J PEDIATR-US, V154, P169, DOI 10.1016/j.jpeds.2008.08.020 Robison LM, 2002, CNS DRUGS, V16, P129, DOI 10.2165/00023210-200216020-00005 Rowland AS, 2002, MENT RETARD DEV D R, V8, P162, DOI 10.1002/mrdd.10036 Schalock RL, 2007, INTELLECT DEV DISAB, V45, P116, DOI 10.1352/1934-9556(2007)45[116:TROMRU]2.0.CO;2 SCHECHTER R, 2008, ARCH GEN PSYCHIAT, V65, P15 SCHENKER N, 2009, MULT IMP FAM INC PER Schieve L. A., 2006, Morbidity and Mortality Weekly Report, V55, P481 Schieve LA, 2009, AM J EPIDEMIOL, V170, P1396, DOI 10.1093/aje/kwp281 Shin M, 2009, PEDIATRICS, V124, P1565, DOI 10.1542/peds.2009-0745 The national sports colleges and universities teaching material committee, 1999, VITAL HLTH STAT, P1 *US DOE, 1999, CLAR POL ADDR NEEDS Van Cleave J, 2010, JAMA-J AM MED ASSOC, V303, P623, DOI 10.1001/jama.2010.104 Wilcken B, 2009, PEDIATRICS, V124, pE241, DOI 10.1542/peds.2008-0586 Yeargin-Allsopp M, 2008, PEDIATRICS, V121, P547, DOI 10.1542/peds.2007-1270 NR 39 TC 196 Z9 200 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 JUN PY 2011 VL 127 IS 6 BP 1034 EP 1042 DI 10.1542/peds.2010-2989 PG 9 WC Pediatrics SC Pediatrics GA 771GV UT WOS:000291146100043 PM 21606152 ER PT J AU Manning, SE Davin, CA Barfield, WD Kotelchuck, M Clements, K Diop, H Osbahr, T Smith, LA AF Manning, Susan E. Davin, Carol A. Barfield, Wanda D. Kotelchuck, Milton Clements, Karen Diop, Hafsatou Osbahr, Tracy Smith, Lauren A. TI Early Diagnoses of Autism Spectrum Disorders in Massachusetts Birth Cohorts, 2001-2005 SO PEDIATRICS LA English DT Article DE autism spectrum disorders; ASD; early diagnoses; early intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; PREVALENCE TRENDS; UNITED-STATES; PATERNAL AGE; CHILDREN; POPULATION; RISK; CALIFORNIA; MINNESOTA AB OBJECTIVE: We examined trends in autism spectrum disorder diagnoses by age 36 months (early diagnoses) and identified characteristics associated with early diagnoses. METHODS: Massachusetts birth certificate and early-intervention program data were linked to identify infants born between 2001 and 2005 who were enrolled in early intervention and receiving autism-related services before age 36 months (through December 31, 2008). Trends in early autism spectrum disorders were examined using Cochran-Armitage trend tests. chi(2) Statistics were used to compare distributions of selected characteristics for children with and without autism spectrum disorders. Multivariate logistic regression analyses were conducted to identify independent predictors of early diagnoses. RESULTS: A total of 3013 children (77.5 per 10 000 study population births) were enrolled in early intervention for autism spectrum disorder by age 36 months. Autism spectrum disorder incidence increased from 56 per 10 000 infants among the 2001 birth cohort to 93 per 10 000 infants in 2005. Infants of mothers younger than 24 years of age, whose primary language was not English or who were foreign-born had lower odds of an early autism spectrum disorder diagnosis. Maternal age older than 30 years was associated with increased odds of an early autism spectrum disorder diagnosis. Odds of early autism spectrum disorders were 4.5 (95% confidence interval: 4.1-5.0) times higher for boys than girls. CONCLUSIONS: Early autism spectrum disorder diagnoses are increasing in Massachusetts, reflecting the national trend observed among older children. Linkage of early-intervention program data with population-based vital statistics is valuable for monitoring autism spectrum disorder trends and planning developmental and educational service needs. Pediatrics 2011; 127:1043-1051 C1 [Manning, Susan E.; Barfield, Wanda D.] Ctr Dis Control & Prevent, Atlanta, GA USA. [Manning, Susan E.; Davin, Carol A.; Diop, Hafsatou; Osbahr, Tracy; Smith, Lauren A.] Bur Family Hlth & Nutr, Massachusetts Dept Publ Hlth, Boston, MA USA. [Kotelchuck, Milton] Harvard Univ, Sch Med, Boston, MA USA. [Clements, Karen] I3 Innovus, Medford, MA USA. RP Manning, SE (reprint author), Ctr Dis Control & Prevent, 286 Water St,8th Floor, Augusta, ME 04333 USA. EM aci6@cdc.gov CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Barbaresi WJ, 2005, ARCH PEDIAT ADOL MED, V159, P37, DOI 10.1001/archpedi.159.1.37 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 BURD L, 1987, J AM ACAD CHILD PSY, V26, P700, DOI 10.1097/00004583-198709000-00014 Campbell JM, 2003, RES DEV DISABIL, V24, P120, DOI 10.1016/S0891-4222(03)00014-3 Centers for Disease Control and Prevention, 2007, MMWR-MORBID MORTAL W, V56, P1 Centers for Disease Control and Prevention, 2009, MMWR-MORBID MORTAL W, V58, P1 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Cohen H, 2006, J DEV BEHAV PEDIATR, V27, pS145, DOI 10.1097/00004703-200604002-00013 DEMYER MK, 1981, SCHIZOPHRENIA BULL, V7, P388 Eikeseth S, 2002, BEHAV MODIF, V26, P49, DOI 10.1177/0145445502026001004 Eldevik S, 2006, J AUTISM DEV DISORD, V36, P211, DOI 10.1007/s10803-005-0058-x Fombonne E, 2009, PEDIATR RES, V65, P591, DOI 10.1203/PDR.0b013e31819e7203 Fombonne E, 2006, PEDIATRICS, V118, pE139, DOI 10.1542/peds.2005-2993 Grether JK, 2009, AM J EPIDEMIOL, V170, P1118, DOI 10.1093/aje/kwp247 Gurney JG, 2003, ARCH PEDIAT ADOL MED, V157, P622, DOI 10.1001/archpedi.157.7.622 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 Johnson CP, 2007, PEDIATRICS, V120, P1183, DOI 10.1542/peds.2007-2361 Kogan MD, 2009, PEDIATRICS, V124, P1395, DOI 10.1542/peds.2009-1522 KUBAN KC, 2009, J PEDIAT, V154, pE531 Kuban KCK, 2009, J PEDIATR-US, V154, P535, DOI 10.1016/j.jpeds.2008.10.011 Limperopoulos C, 2008, PEDIATRICS, V121, P758, DOI 10.1542/peds.2007-2158 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 McEachin JJ, 1993, AM J MENT RETARD, V97, P373 *NAT RES COUNC COM, 2001, ED CHILDR AUT PERV D Newschaffer CJ, 2005, PEDIATRICS, V115, pE277, DOI 10.1542/peds.2004-1958 Nicholas JS, 2009, ANN EPIDEMIOL, V19, P808, DOI 10.1016/j.annepidem.2009.04.005 Parner ET, 2008, ARCH PEDIAT ADOL MED, V162, P1150, DOI 10.1001/archpedi.162.12.1150 Reichenberg A, 2006, ARCH GEN PSYCHIAT, V63, P1026, DOI 10.1001/archpsyc.63.9.1026 RITVO ER, 1989, AM J PSYCHIAT, V146, P194 Rogers SJ, 2008, J CLIN CHILD ADOLESC, V37, P8, DOI 10.1080/15374410701817808 Sallows GO, 2005, AM J MENT RETARD, V110, P417, DOI 10.1352/0895-8017(2005)110[417:IBTFCW]2.0.CO;2 Schechter R, 2008, ARCH GEN PSYCHIAT, V65, P19, DOI 10.1001/archgenpsychiatry.2007.1 Schendel D, 2008, PEDIATRICS, V121, P1155, DOI 10.1542/peds.2007-1049 Schieve L. 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The current study evaluates cognitive functioning in adolescents and adults diagnosed with Autism or Asperger's syndrome using the Wechsler Adult Intelligence Scale-Fourth Edition (WAIS-IV) and the Social Perception subtest from the Advanced Clinical Solutions. Deficits in social perception, verbal comprehension, and processing speed were found in the Autism sample. Additionally, they exhibited inconsistent performance on auditory working memory and perceptual reasoning tasks. The Asperger's syndrome group had better overall cognitive skills than the Autism group, but compared with controls, they had weaknesses in processing speed, social perception, and components of auditory working memory. Both groups had relatively low scores on the WAIS-IV Comprehension subtest compared with the other verbal comprehension subtests. Clinical application and utility of the WAIS-IV and Social Perception in Autism Spectrum Disorders are discussed. C1 [Holdnack, James; Drozdick, Lisa] Pearson Inc, San Antonio, TX USA. [Goldstein, Gerald] VA Pittsburgh Healthcare Ctr, Pittsburgh, PA USA. RP Holdnack, J (reprint author), 5 Rose Hill Dr, Bear, DE 19701 USA. 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The aim of this study was to find out potential differences between the levels of organic acids in the urine of autistic and non-autistic children. Design and methods: The organic acids in the urine were determined by capillary gas chromatography/mass spectrometry (GC/MS). All overnight urine samples were collected from 35 autistic children and 36 neurologically normal children as healthy controls (4-10 years). Results: Significant differences were found between the autistic children and the control group in organic acids: 2-oxoglutaric, isocitric, citric, 4-hydroxybenzoic, 4-hydroxyphenylacetic, hippuric, adipic, suberic (all with p<0.05). Conclusion: Organic acids test can be used to assess an individual need for nutrient and biochemical abnormalities, especially important for autistic children. (C) 2011 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. C1 Tech Univ Lodz, Dept Chem, Inst Gen & Ecol Chem, PL-90924 Lodz, Poland. RP Kaluzna-Czaplinska, J (reprint author), Tech Univ Lodz, Dept Chem, Inst Gen & Ecol Chem, 116 Zeromskiego Str, PL-90924 Lodz, Poland. EM jkaluzna@p.lodz.pl FU Ministry of Science and Higher Education [NN 204 316234] FX The work was supported by means of Ministry of Science and Higher Education: NN 204 316234. 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Biochem. PD JUN PY 2011 VL 44 IS 8-9 BP 686 EP 691 DI 10.1016/j.clinbiochem.2011.01.015 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA 770IY UT WOS:000291081400022 PM 21300048 ER PT J AU Duch, W Dobosz, K AF Duch, Wlodzislaw Dobosz, Krzysztof TI Visualization for understanding of neurodynamical systems SO COGNITIVE NEURODYNAMICS LA English DT Article DE Neurodynamics; Symbolic dynamics; Visualization of multidimensional time series; Attractor networks; Attractor dynamics; Recurrence plots ID RECURRENCE PLOTS; AUTISM; ATTENTION; CONCRETE AB Complex neurodynamical systems are quite difficult to analyze and understand. New type of plots are introduced to help in visualization of high-dimensional trajectories and show global picture of the phase space, including relations between basins of attractors. Color recurrence plots (RPs) display distances from each point on the trajectory to all other points in a two-dimensional matrix. Fuzzy Symbolic Dynamics (FSD) plots enhance this information mapping the whole trajectory to two or three dimensions. Each coordinate is defined by the value of a fuzzy localized membership function, optimized to visualize interesting features of the dynamics, showing to which degree a point on the trajectory belongs to some neighborhood. The variance of the trajectory within the attraction basin plotted against the variance of the synaptic noise provides information about sizes and shapes of these basins. Plots that use color to show the distance between each trajectory point and a larger number of selected reference points (for example centers of attractor basins) are also introduced. Activity of 140 neurons in the semantic layer of dyslexia model implemented in the Emergent neural simulator is analyzed in details showing different aspects of neurodynamics that may be understood in this way. Influence of connectivity and various neural properties on network dynamics is illustrated using visualization techniques. A number of interesting conclusions about cognitive neurodynamics of lexical concept activations are drawn. Changing neural accommodation parameters has very strong influence on the dwell time of the trajectories. This may be linked to attention deficits disorders observed in autism in case of strong enslavement, and to ADHD-like behavior in case of weak enslavement. C1 [Duch, Wlodzislaw] Nicholas Copernicus Univ, Dept Informat, Torun, Poland. [Dobosz, Krzysztof] Nicholas Copernicus Univ, Fac Math & Comp Sci, Torun, Poland. [Duch, Wlodzislaw] Nanyang Technol Univ, Sch Comp Sci, Singapore, Singapore. RP Duch, W (reprint author), Nicholas Copernicus Univ, Dept Informat, Torun, Poland. EM wduch@is.umk.pl; kdobosz@mat.umk.pl FU Polish Ministry of Education and Science [N519 578138] FX We are grateful for the support of the Polish Ministry of Education and Science through Grant No N519 578138. CR Aisa B, 2008, NEURAL NETWORKS, V21, P1146, DOI 10.1016/j.neunet.2008.06.016 Bilder RM, 2009, NEUROSCIENCE, V164, P30, DOI 10.1016/j.neuroscience.2009.01.027 Cox T., 2001, MULTIDIMENSIONAL SCA Dawkins R., 1989, SELFISH GENE Distin K., 2005, SELFISH MEME CRITICA Dobosz K, 2010, NEURAL NETWORKS, V23, P487, DOI 10.1016/j.neunet.2009.12.005 Duch W, 2005, IEEE T NEURAL NETWOR, V16, P10, DOI 10.1109/TNN.2004.836200 DUCH W, 2009, SAT S 13 ANN M ASS S, P46 ECKMANN JP, 1987, EUROPHYS LETT, V4, P973, DOI 10.1209/0295-5075/4/9/004 Freeman W. 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Neurodynamics PD JUN PY 2011 VL 5 IS 2 BP 145 EP 160 DI 10.1007/s11571-011-9153-1 PG 16 WC Neurosciences SC Neurosciences & Neurology GA 768LE UT WOS:000290935300003 PM 22654987 ER PT J AU Pelphrey, KA Shultz, S Hudac, CM Wyk, BCV AF Pelphrey, Kevin A. Shultz, Sarah Hudac, Caitlin M. Wyk, Brent C. Vander TI Research Review: Constraining heterogeneity: the social brain and its development in autism spectrum disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE Social perception; social cognition; autism; functional neuroimaging; social brain ID HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; HUMAN VISUAL-CORTEX; BIOLOGICAL MOTION; TEMPORAL CORTEX; CHILDHOOD AUTISM; WHITE-MATTER; SENTENCE COMPREHENSION; CORTICAL ACTIVATION; FACIAL EXPRESSIONS AB The expression of autism spectrum disorder (ASD) is highly heterogeneous, owing to the complex interactions between genes, the brain, and behavior throughout development. Here we present a model of ASD that implicates an early and initial failure to develop the specialized functions of one or more of the set of neuroanatomical structures involved in social information processing (i.e., the 'social brain'). From this early and primary disruption, abnormal brain development is canalized because the individual with an ASD must develop in a highly social world without the specialized neural systems that would ordinarily allow him or her to partake in the fabric of social life, which is woven from the thread of opportunities for social reciprocity and the tools of social engagement. This brain canalization gives rise to other characteristic behavioral deficits in ASD including deficits in communication, restricted interests, and repetitive behaviors. We propose that focused efforts to explore the brain mechanisms underlying the core, pathognomic deficits in the development of mechanisms for social engagement in ASD will greatly elucidate our understanding and treatment of this complex, devastating family of neurodevelopmental disorders. In particular, developmental studies (i.e., longitudinal studies of young children with and without ASD, as well as infants at increased risk for being identified with ASD) of the neural circuitry supporting key aspects of social information processing are likely to provide important insights into the underlying components of the full-syndrome of ASD. These studies could also contribute to the identification of developmental brain endophenotypes to facilitate genetic studies. The potential for this kind of approach is illustrated via examples of functional neuroimaging research from our own laboratory implicating the posterior superior temporal sulcus (STS) as a key player in the set of neural structures giving rise to ASD. C1 [Pelphrey, Kevin A.] Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06520 USA. [Pelphrey, Kevin A.; Shultz, Sarah] Yale Univ, Dept Psychol, New Haven, CT 06520 USA. RP Pelphrey, KA (reprint author), Yale Univ, Sch Med, Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. EM kevin.pelphrey@yale.edu FU Simons Foundation; National Institute of Mental Health; National Institute of Child Health and Development; John Merck Scholars Fund; US Veterans Affairs Administration; Autism Speaks; National Institutes of Health (NIMH) [MH071284] FX The research reviewed herein was supported by grants from the Simons Foundation, the National Institute of Mental Health, the National Institute of Child Health and Development, the John Merck Scholars Fund, the US Veterans Affairs Administration, and Autism Speaks. Kevin Pelphrey was supported by a Career Development Award from the National Institutes of Health (NIMH Grant MH071284). We gratefully acknowledge our collaborators, especially Gregory McCarthy, James Morris, and Truett Allison. We are deeply grateful to the families, adults, and children who participate in our research. We confirm that all of the research from our laboratory presented in this review meets the ethical guidelines, including adherence to the legal requirements, of the USA. Informed consent was obtained from each of the study participants or their parents. 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Child Psychol. Psychiatry PD JUN PY 2011 VL 52 IS 6 BP 631 EP 644 DI 10.1111/j.1469-7610.2010.02349.x PG 14 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 765EG UT WOS:000290685600002 PM 21244421 ER PT J AU Brock, J AF Brock, Jon TI Commentary: Complementary approaches to the developmental cognitive neuroscience of autism - reflections on Pelphrey et al. (2011) SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Editorial Material C1 [Brock, Jon] Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia. [Brock, Jon] Macquarie Univ, ARC Ctr Excellence Cognit & Disorders, Sydney, NSW 2109, Australia. RP Brock, J (reprint author), Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia. EM jon.brock@mq.edu.au CR Brock J, 2002, DEV PSYCHOPATHOL, V14, P209 Hoffman RE, 1997, AM J PSYCHIAT, V154, P1683 Norbury CF, 2009, J CHILD PSYCHOL PSYC, V50, P834, DOI 10.1111/j.1469-7610.2009.02073.x Passingham RE, 2002, NAT REV NEUROSCI, V3, P606, DOI 10.1038/nrn893 Pelphrey KA, 2011, J CHILD PSYCHOL PSYC, V52, P631, DOI 10.1111/j.1469-7610.2010.02349.x NR 5 TC 8 Z9 8 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JUN PY 2011 VL 52 IS 6 BP 645 EP 646 DI 10.1111/j.1469-7610.2011.02414.x PG 2 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 765EG UT WOS:000290685600003 PM 21574994 ER PT J AU Lobato, D Kao, B Plante, W Seifer, R Grullon, E Cheas, L Canino, G AF Lobato, Debra Kao, Barbara Plante, Wendy Seifer, Ronald Grullon, Edicta Cheas, Lydia Canino, Glorisa TI Psychological and school functioning of Latino siblings of children with intellectual disability SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Siblings; intellectual disability; Latino; culture ID BEHAVIORAL-ADJUSTMENT; AMERICAN FAMILIES; MEXICAN-AMERICAN; ANXIETY; PARENTS; AUTISM; SCALE AB Background: Siblings of children with disabilities are at risk for internalizing psychological disorders; however, little is known about how culture influences this effect. This study examined the psychological and school functioning of Latino siblings of children with intellectual disability (ID). Methods: Participants were 100 Latino (L) and nonLatino (NL) siblings (8-15 years) of children with ID (50 LID, 50 NLID) and 100 Latino and nonLatino control siblings (50 LC, 50 NLC). Siblings, parents, and teachers completed standard questionnaires regarding sibling emotional and behavioral functioning; sibling school report cards were obtained. Analyses of variance were conducted, controlling for parent age and family income; planned contrasts compared LID siblings to the other sibling groups. Results: LID siblings reported significantly more internalizing (t(1) = 2.41, p < .05) and emotional t(1) = 3.06, p < .05) symptoms, poorer awareness of (t(1) = 2.26, p < .01) and greater reluctance to express (t(1) = 3.12, p < .01) their emotions, and more problems in personal adjustment and relationships with parents (t(1) = -2.50, p < .05). Significantly higher percentages of LID siblings scored in the at-risk or clinical range for internalizing and emotional symptoms, and were more likely to score above the clinical cut-off for separation anxiety disorder and to endorse global impairment. LID siblings experienced more school absences and lower academic performance. There were no group differences in externalizing behavior problems, somatic symptoms, or teacher-reported internalizing symptoms. Conclusions: Latino siblings of children with ID are at greater risk for internalizing psychological disorders and greater impairment in personal and school functioning. Results are discussed in terms of their sociocultural significance and clinical implications. C1 [Lobato, Debra] Brown Univ, Alpert Med Sch, Rhode Isl Hosp, Dept Pediat,Bradley Hasbro Childrens Res Ctr, Providence, RI 02903 USA. [Lobato, Debra; Plante, Wendy; Seifer, Ronald] Brown Univ, Alpert Med Sch, Dept Psychiat & Human Behav, Providence, RI 02903 USA. [Canino, Glorisa] Univ Puerto Rico, Behav Sci Res Inst, San Juan, PR 00936 USA. [Canino, Glorisa] Univ Puerto Rico, Dept Pediat, San Juan, PR 00936 USA. [Lobato, Debra; Plante, Wendy; Seifer, Ronald] Brown Univ, Alpert Med Sch, Bradley Hasbro Childrens Res Ctr, Providence, RI 02903 USA. RP Lobato, D (reprint author), Brown Univ, Alpert Med Sch, Rhode Isl Hosp, Dept Pediat,Bradley Hasbro Childrens Res Ctr, Coro W 2,1 Hoppin St, Providence, RI 02903 USA. EM debra_lobato@brown.edu FU National Institute of Child Health and Human Development [1RO1HD050557] FX This work was supported by the National Institute of Child Health and Human Development (1RO1HD050557/Lobato). The authors are grateful to the families and community agencies who participated in this project. 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TI Sibling influences on theory of mind development for children with ASD SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Autism spectrum disorders; siblings; theory of mind ID FALSE-BELIEF; AUTISM SPECTRUM; DISABILITIES; METAANALYSIS; CATCH; OLDER AB Background: Research indicates that having child siblings is positively associated with theory of mind (ToM) in typically developing children. As ToM is important to everyday social behaviours it is important to extend this research to examine whether there are similar sibling effects for children with autism spectrum disorders (ASD). Methods: Theory of mind and executive functioning abilities of 60 children clinically diagnosed with ASD were assessed with batteries of standard tasks. Verbal mental age (VMA) and severity of autism symptoms were also measured together with number of child-aged siblings (1 to 12 years) and position in the sibling constellation. Results: Having older siblings was a significant negative predictor of ToM performance for children with ASD, even after controlling for age, VMA, executive function and autism symptom severity. A weaker ToM benefit of younger siblings was not statistically significant independently of control variables. Conclusions: In sharp contrast to findings for typically developing preschoolers, having an older sibling was a disadvantage for ToM development in children with ASD. Conceivably, older siblings may over-compensate for their younger ASD siblings in social interactions, thereby limiting opportunities for social-cognitive growth. Parental attitudes, family resources, cultural norms and access to educational interventions may also conceivably be relevant and clearly warrant further research. C1 [O'Brien, Karen] Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP O'Brien, K (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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Child Psychol. Psychiatry PD JUN PY 2011 VL 52 IS 6 BP 713 EP 719 DI 10.1111/j.1469-7610.2011.02389.x PG 7 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 765EG UT WOS:000290685600016 PM 21418062 ER PT J AU Kortum, F Das, S Flindt, M Morris-Rosendahl, DJ Stefanova, I Goldstein, A Horn, D Klopocki, E Kluger, G Martin, P Rauch, A Roumer, A Saitta, S Walsh, LE Wieczorek, D Uyanik, G Kutsche, K Dobyns, WB AF Kortuem, Fanny Das, Soma Flindt, Max Morris-Rosendahl, Deborah J. Stefanova, Irina Goldstein, Amy Horn, Denise Klopocki, Eva Kluger, Gerhard Martin, Peter Rauch, Anita Roumer, Agathe Saitta, Sulagna Walsh, Laurence E. Wieczorek, Dagmar Uyanik, Goekhan Kutsche, Kerstin Dobyns, William B. TI The core FOXG1 syndrome phenotype consists of postnatal microcephaly, severe mental retardation, absent language, dyskinesia, and corpus callosum hypogenesis SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID HELIX TRANSCRIPTION FACTOR; PITT-HOPKINS-SYNDROME; HEAD GENE FAMILY; BRAIN FACTOR-I; RETT-SYNDROME; CONGENITAL VARIANT; ANGELMAN-SYNDROME; VENTRAL TELENCEPHALON; CEREBRAL HEMISPHERES; MUTATIONS AB Background Submicroscopic deletions in 14q12 spanning FOXG1 or intragenic mutations have been reported in patients with a developmental disorder described as a congenital variant of Rett syndrome. This study aimed to further characterise and delineate the phenotype of FOXG1 mutation positive patients. Method The study mapped the breakpoints of a 2; 14 translocation by fluorescence in situ hybridisation and analysed three chromosome rearrangements in 14q12 by cytogenetic analysis and/or array comparative genomic hybridisation. The FOXG1 gene was sequenced in 210 patients, including 129 patients with unexplained developmental disorders and 81 MECP2 mutation negative individuals. Results One known mutation, seen in two patients, and nine novel mutations of FOXG1 including two deletions, two chromosome rearrangements disrupting or displacing putative cis-regulatory elements from FOXG1, and seven sequence changes, are reported. Analysis of 11 patients in this study, and a further 15 patients reported in the literature, demonstrates a complex constellation of features including mild postnatal growth deficiency, severe postnatal microcephaly, severe mental retardation with absent language development, deficient social reciprocity resembling autism, combined stereotypies and frank dyskinesias, epilepsy, poor sleep patterns, irritability in infancy, unexplained episodes of crying, recurrent aspiration, and gastro-oesophageal reflux. Brain imaging studies reveal simplified gyral pattern and reduced white matter volume in the frontal lobes, corpus callosum hypogenesis, and variable mild frontal pachgyria. Conclusions These findings have significantly expanded the number of FOXG1 mutations and identified two affecting possible cis-regulatory elements. While the phenotype of the patients overlaps both classic and congenital Rett syndrome, extensive clinical evaluation demonstrates a distinctive and clinically recognisable phenotype which the authors suggest designating as the FOXG1 syndrome. C1 [Kortuem, Fanny; Flindt, Max; Uyanik, Goekhan; Kutsche, Kerstin] Univ Klinikum Hamburg Eppendorf, Inst Humangenet, D-20246 Hamburg, Germany. [Das, Soma] Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. [Morris-Rosendahl, Deborah J.] Univ Clin Freiburg, Inst Human Genet, Freiburg, Germany. [Stefanova, Irina] Univ Lubeck, Inst Humangenet, Lubeck, Germany. [Goldstein, Amy] Childrens Hosp Pittsburgh, Div Child Neurol, Pittsburgh, PA 15213 USA. [Horn, Denise; Klopocki, Eva] Charite, Inst Med Genet, D-13353 Berlin, Germany. [Kluger, Gerhard] Epilepsy Ctr Children & Adolescents, Neuropediat Clin & Clin Neurorehabil, Vogtareuth, Germany. [Martin, Peter] Epilepsy Ctr Kork, Seguin Clin, Kehl, Germany. [Rauch, Anita] Univ Hosp Erlangen, Inst Human Genet, Erlangen, Germany. [Rauch, Anita] Univ Zurich, Inst Med Genet, CH-8603 Schwerzenbach, Switzerland. [Roumer, Agathe] Sozialpadiatr Zentrum Frankfurt Mitte, Frankfurt, Germany. [Saitta, Sulagna] Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. [Walsh, Laurence E.] Indiana Univ, Dept Med Genet, Indianapolis, IN 46204 USA. [Wieczorek, Dagmar] Univ Klinikum Essen, Inst Humangenet, Essen, Germany. [Uyanik, Goekhan] Univ Regensburg, Neurol Klin & Poliklin, Regensburg, Germany. [Dobyns, William B.] Univ Washington, Dept Pediat, Seattle, WA 98101 USA. [Dobyns, William B.] Seattle Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA 98101 USA. RP Kutsche, K (reprint author), Univ Klinikum Hamburg Eppendorf, Inst Humangenet, Campus Forsch,Martinistr 52, D-20246 Hamburg, Germany. EM kkutsche@uke.de; wbd@uw.edu RI Rauch, Anita/C-5568-2014 OI Rauch, Anita/0000-0003-2930-3163 FU Werner Otto-Stiftung [WOS 3/76]; Deutsche Forschungsgemeinschaft (DFG) [GRK1459]; National Institutes of Health (NIH) [1R01-NS058721]; German Ministry of Research and Education [01GS08160, 01GS08164] FX This work was supported by grants from the Werner Otto-Stiftung (WOS 3/76 to GU); the Deutsche Forschungsgemeinschaft (DFG) (GRK1459 to KK); and the National Institutes of Health (NIH) (1R01-NS058721 to WBD). This work was part of the German Mental Retardation Network (MRNET) funded through a grant from the German Ministry of Research and Education to A Rauch (01GS08160) and DW (01GS08164). 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Med. Genet. PD JUN PY 2011 VL 48 IS 6 BP 396 EP 406 DI 10.1136/jmg.2010.087528 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 768SL UT WOS:000290958600006 PM 21441262 ER PT J AU Neves-Pereira, M Muller, B Massie, D Williams, JHG O'Brien, PCM Hughes, A Shen, SB St Clair, D Miedzybrodzka, Z AF Neves-Pereira, M. Mueller, B. Massie, D. Williams, J. H. G. O'Brien, P. C. M. Hughes, A. Shen, S-B St Clair, D. Miedzybrodzka, Z. TI Deregulation of EIF4E: a novel mechanism for autism (vol 46, pg 759, 2009) SO JOURNAL OF MEDICAL GENETICS LA English DT Correction C1 [St Clair, D.] Univ Aberdeen, Inst Med Sci, Aberdeen, Scotland. [Miedzybrodzka, Z.] Univ Aberdeen, Dept Genet, Aberdeen, Scotland. RP St Clair, D (reprint author), Univ Aberdeen, Inst Med Sci, Aberdeen, Scotland. EM d.stclair@abdn.ac.uk; zosia@abdn.ac.uk RI Shen, Sanbing/E-3750-2015 CR NEVESPEREIRA M, 2009, MIEDZYBRODZKA Z DERE, V46, P759 NR 1 TC 0 Z9 0 PU B M J 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 JUN PY 2011 VL 48 IS 6 BP 421 EP 421 DI 10.1136/jmg.2009.066852corr1 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 768SL UT WOS:000290958600010 ER PT J AU Hunsaker, MR Greco, CM Tassone, F Berman, RF Willemsen, R Hagerman, RJ Hagerman, PJ AF Hunsaker, Michael R. Greco, Claudia M. Tassone, Flora Berman, Robert F. Willemsen, Rob Hagerman, Randi J. Hagerman, Paul J. TI Rare Intranuclear Inclusions in the Brains of 3 Older Adult Males With Fragile X Syndrome: Implications for the Spectrum of Fragile X-Associated Disorders SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE Autism; FMR1; Fragile X syndrome; FXTAS; Neurodegeneration; Parkinson ID FMR1 MESSENGER-RNA; TREMOR/ATAXIA SYNDROME; MOUSE MODEL; CGG-REPEAT; PREMUTATION CARRIERS; SPANISH PATIENTS; ELEVATED LEVELS; FXTAS; GENE; ALLELES AB The FMR1 gene is polymorphic for the length of CGG trinucleotide repeat expansions in the 5' untranslated region. Premutation (55-200 CGG repeats) and full-mutation (>200 CGG repeats) alleles give rise to their respective disorders by different pathogenic mechanisms: RNA gain-of-function toxicity leads to fragile X-associated tremor/ataxia syndrome in the premutation range, and transcriptional silencing and absence of fragile X mental retardation protein (FMRP) lead to fragile X syndrome in the full-mutation range. However, for the latter, incomplete silencing and/or size-mosaicism might result in some contribution to the disease process from residual messenger RNA production. To address this possibility, we examined the brains of 3 cases of fragile X syndrome for the presence of intranuclear inclusions in the hippocampal dentate gyrus. We identified low levels (0.1%-1.3%) of intranuclear inclusions in all 3 cases. Quantitative reverse transcription-polymerase chain reaction for FMR1 messenger RNA and immunofluorescence for FMRP revealed low but detectable levels of both RNA and protein in the 3 cases, consistent with the presence of small numbers of inclusions. The intranuclear inclusions were only present in FMRP-immunoreactive cells. The small numbers of inclusions and very low levels of both FMR1 RNA and protein suggest that the clinical course in these 3 subjects would not have been influenced by contributions from RNA toxicity. C1 [Tassone, Flora; Hagerman, Paul J.] Univ Calif Davis, Davis Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA. [Hunsaker, Michael R.; Berman, Robert F.] Univ Calif Davis, Sch Med, Dept Neurol Surg, Davis, CA 95616 USA. [Hunsaker, Michael R.; Berman, Robert F.] Univ Calif Davis, Sch Med, NeuroTherapeut Res Inst, Davis, CA 95616 USA. [Greco, Claudia M.] Calif State Univ Sacramento, Dept Pathol & Lab Med, Sacramento, CA 95819 USA. [Greco, Claudia M.; Tassone, Flora; Berman, Robert F.; Hagerman, Randi J.; Hagerman, Paul J.] Univ Calif Davis, Davis Hlth Syst, MIND Inst, Sacramento, CA 95817 USA. [Willemsen, Rob] Erasmus MC, Dept Med Genet, Rotterdam, Netherlands. [Hagerman, Randi J.] Calif State Univ Sacramento, Davis Sch Med, Dept Pediat, Sacramento, CA 95819 USA. RP Hagerman, PJ (reprint author), Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA. EM pjhagerman@ucdavis.edu FU National Institutes of Health (NIH) [HD036071, HD056031, NS044299, AG024488, HD002274, MH077554, MH078041, RL1 AG032115, RL1 NS062411, RL1 AG032119]; National Fragile X Foundation; Medical Investigation of Neurodevelopmental Disorders Institute; National Institute of Dental and Craniofacial Research, NeuroTherapeutics Research Institute consortium [UL1 DE019583]; National Center for Research Resources, a component of the NIH [UL1 RR024146]; NIH Roadmap for Medical Research FX This work was supported by National Institutes of Health (NIH) Grant Nos. HD036071, HD056031, NS044299, AG024488, HD002274, MH077554, MH078041, RL1 AG032115, RL1 NS062411, and RL1 AG032119; the National Fragile X Foundation, and the Medical Investigation of Neurodevelopmental Disorders Institute. This work was also made possible by a Roadmap Initiative grant (UL1 DE019583) from the National Institute of Dental and Craniofacial Research in support of the NeuroTherapeutics Research Institute consortium; and by a grant (UL1 RR024146) from the National Center for Research Resources, a component of the NIH, and NIH Roadmap for Medical Research. 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TI Exome sequencing in sporadic autism spectrum disorders identifies severe de novo mutations SO NATURE GENETICS LA English DT Article ID HUMAN-GENOME; RECURRENT MICRODELETIONS; SEGMENTAL DUPLICATIONS; MENTAL-RETARDATION; LANGUAGE DISORDER; GENE; SPEECH; SCN1A; FOXP1; RISK AB Evidence for the etiology of autism spectrum disorders (ASDs) has consistently pointed to a strong genetic component complicated by substantial locus heterogeneity(1,2). We sequenced the exomes of 20 individuals with sporadic ASD (cases) and their parents, reasoning that these families would be enriched for de novo mutations of major effect. We identified 21 de novo mutations, 11 of which were protein altering. Protein-altering mutations were significantly enriched for changes at highly conserved residues. We identified potentially causative de novo events in 4 out of 20 probands, particularly among more severely affected individuals, in FOXP1, GRIN2B, SCN1A and LAMC3. In the FOXP1 mutation carrier, we also observed a rare inherited CNTNAP2 missense variant, and we provide functional support for a multi-hit model for disease risk(3). Our results show that trio-based exome sequencing is a powerful approach for identifying new candidate genes for ASDs and suggest that de novo mutations may contribute substantially to the genetic etiology of ASDs. C1 [O'Roak, Brian J.; Lee, Choli; Vives, Laura; Schwartz, Jerrod J.; Girirajan, Santhosh; Karakoc, Emre; MacKenzie, Alexandra P.; Ng, Sarah B.; Baker, Carl; Rieder, Mark J.; Nickerson, Deborah A.; Shendure, Jay; Eichler, Evan E.] Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA. [Deriziotis, Pelagia; Fisher, Simon E.] Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. [Bernier, Raphael] Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. [Fisher, Simon E.] Max Planck Inst Psycholinguist, Language & Genet Dept, Nijmegen, Netherlands. [Eichler, Evan E.] Howard Hughes Med Inst, Washington, DC USA. RP Eichler, EE (reprint author), Univ Washington, Sch Med, Dept Genome Sci, Seattle, WA 98195 USA. EM shendure@uw.edu; eee@gs.washington.edu RI Fisher, Simon/E-9130-2012; Derizioti, Pelagia/C-3857-2015 OI Fisher, Simon/0000-0002-3132-1996; Derizioti, Pelagia/0000-0001-5544-8345 FU US National Institutes of Health [HD065285]; Wellcome Trust [075491/Z/04]; Max Planck Society; Simons Foundation Autism Research Initiative (SFARI) [191889, 137578] FX We would like to thank and recognize the following ongoing studies that produced and provided exome variant calls for comparison: National Heart, Lung, and Blood Institute (NHBLI) Lung Cohort Sequencing Project (HL 1029230), NHLBI Women's Health Initiative (WHI) Sequencing Project (HL 102924), National Institute of Environmental Health Sciences (NIEHS) SNPs (HHSN273200800010C), NHLBI/National Human Genome Research Institute (NHGRI) SeattleSeq (HL 094976), NHGRI Next Generation Mendelian Genetics (HG 005608) and the Northwest Genomics Center (HL 102926). We also thank M.-C. King and S. Stray for processing and managing DNA samples, B. H. King and E. Bliss for their work in subject recruitment and phenotype collection, E. Turner, C. Igartua, I. Stanaway, M. Dennis and B. Coe for thoughtful discussions, M. State for providing SNP genotyping data and especially the families that volunteered their time to participate in this research. This work was supported by US National Institutes of Health grant HD065285 (E. E. E. and J.S.), Wellcome Trust core award 075491/Z/04 (S. E. F. and P. D.), the Max Planck Society (S. E. F.) and grants from the Simons Foundation Autism Research Initiative (SFARI) (191889 and 137578) (E. E. E., R. B., S. E. F. and P. D.). E. E. E. is an Investigator of the Howard Hughes Medical Institute. 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Of 110 Sturge-Weber syndrome patients, 14 demonstrated bilateral brain involvement, with an asymmetric pattern on glucose metabolism positron emission tomography. Although most patients manifested frequent seizures initially, associated with frontal hypometabolism on positron emission tomography, six (43%) had achieved good seizure control during follow-up. Bilateral frontal hypometabolism was associated with severe developmental impairment. Two children with bitemporal hypometabolism exhibited autistic features. Hemiparesis was associated with superior frontal (motor cortex) hypometabolism. Three patients underwent resective surgery, resulting in improved seizure control and developmental outcomes. The severity of neurologic complications and clinical course depend on the extent of cortical dysfunction in bilateral Sturge-Weber syndrome. Bilateral frontal and temporal hypometabolism is associated with poor developmental outcomes. Good seizure control and only mild/moderate developmental impairment can be achieved in about 50% of patients with bilateral Sturge-Weber syndrome, with or without resective surgery. (C) 2011 Elsevier Inc. All rights reserved. C1 [Alkonyi, Balint; Chugani, Harry T.; Karia, Samir; Behen, Michael E.; Juhasz, Csaba] Wayne State Univ, Sch Med, Carman & Ann Adams Dept Pediat, Detroit, MI 48201 USA. [Alkonyi, Balint; Chugani, Harry T.; Juhasz, Csaba] Childrens Hosp Michigan, Positron Emiss Tomog Ctr, Detroit, MI 48201 USA. [Chugani, Harry T.; Karia, Samir; Behen, Michael E.; Juhasz, Csaba] Wayne State Univ, Sch Med, Dept Neurol, Detroit, MI 48201 USA. [Karia, Samir] Med Univ S Carolina, Div Pediat Neurol, Dept Neurosci, Charleston, SC 29425 USA. RP Juhasz, C (reprint author), Wayne State Univ, Sch Med, Dept Pediat, 3901 Beaubien Blvd, Detroit, MI 48201 USA. EM juhasz@pet.wayne.edu FU National Institutes of Health [R01 NS041922] FX This study was partly supported by grant R01 NS041922 from the National Institutes of Health to C.J. The authors thank the Sturge-Weber Foundation for referring patients to us. The authors are grateful to the families and children who participated in the study. 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Neurol. PD JUN PY 2011 VL 44 IS 6 BP 443 EP 449 DI 10.1016/j.pediatrneurol.2011.01.005 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 768YZ UT WOS:000290977400007 PM 21555056 ER PT J AU Glatt, SJ Cohen, OS Faraone, SV Tsuang, MT AF Glatt, Stephen J. Cohen, Ori S. Faraone, Stephen V. Tsuang, Ming T. TI Dysfunctional Gene Splicing as a Potential Contributor to Neuropsychiatric Disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE alternative splicing; mRNA; pre-mRNA; RNA processing; spliceosome ID NMDA RECEPTOR SUBUNIT; MESSENGER-RNA; BIPOLAR DISORDER; MAMMALIAN NUMB; SYNAPTIC PLASTICITY; FUNCTIONAL VARIANTS; PREFRONTAL CORTEX; MOLECULAR-CLONING; PROTEIN ISOFORMS; MOOD DISORDERS AB Alternative pre-mRNA splicing is a major mechanism by which the proteomic diversity of eukaryotic genomes is amplified. 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Lastly, we suggest potentially fruitful lines for future research that should illuminate the nature, extent, causes, and consequences of alternative splicing abnormalities in neuropsychiatric disorders. (C) 2011 Wiley-Liss, Inc. C1 [Glatt, Stephen J.; Cohen, Ori S.; Faraone, Stephen V.] SUNY Upstate Med Univ, Psychiat Genet Epidemiol & Neurobiol Lab, Dept Psychiat & Behav Sci, Med Genet Res Ctr, Syracuse, NY 13210 USA. [Glatt, Stephen J.; Cohen, Ori S.; Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Neurosci, Med Genet Res Ctr, Syracuse, NY 13210 USA. [Glatt, Stephen J.; Cohen, Ori S.; Faraone, Stephen V.] SUNY Upstate Med Univ, Dept Physiol, Med Genet Res Ctr, Syracuse, NY 13210 USA. [Tsuang, Ming T.] Univ Calif San Diego, Dept Psychiat, Inst Genom Med, Ctr Behav Genom, San Diego, CA 92103 USA. [Tsuang, Ming T.] Vet Affairs San Diego Healthcare Syst, San Diego, CA USA. [Tsuang, Ming T.] Harvard Inst Psychiat Epidemiol & Genet, Harvard Dept Epidemiol, Boston, MA USA. 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J. Med. Genet. B PD JUN PY 2011 VL 156B IS 4 BP 382 EP 392 DI 10.1002/ajmg.b.31181 PG 11 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 766FA UT WOS:000290765200002 PM 21438146 ER PT J AU Scheuerle, A Wilson, K AF Scheuerle, Angela Wilson, Kathleen TI PARK2 Copy Number Aberrations in Two Children Presenting With Autism Spectrum Disorder: Further Support of an Association and Possible Evidence for a New Microdeletion/Microduplication Syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE asperger; chromosome 6; 6q26; parkinsonism; pharmacogenetic ID PARKINSON-DISEASE; JUVENILE PARKINSONISM; HUMAN GENOME; GENE; MUTATIONS; UBIQUITIN; DELETION; PROMOTER; REVEALS; LINKAGE AB Microdeletions of PARK2 have been reported previously in seven patients with autism spectrum disorder. There are no reports of PARK2 microduplications in this population. Presented are two patients, one with deletion and the other with duplication, both with autism spectrum disorder, though their syndromic phenotypes vary. The deletion patient is cognitively normal and ectomorphic: the duplication patient is cognitively impaired, underweight and short. Further, the microduplication patient has demonstrated adverse medication reactions to psychotropic medications active in the dopamine metabolic pathway: cyclopentolate, lisdexamfetamine, methylphenidate. These patients support an association between PARK2 mutations and autism spectrum disorder and suggest that duplications may be equally causative. It is hypothesized that the disparate patient phenotypes may represent a deletion/duplication syndrome and that the adverse medication reactions may be a pharmacogenetic phenomenon. (C) 2011 Wiley-Liss, Inc. C1 [Scheuerle, Angela] Tesserae Genet, Dallas, TX 75230 USA. [Wilson, Kathleen] Univ Texas SW, McDermott Ctr Human Growth & Dev, Dallas, TX USA. RP Scheuerle, A (reprint author), Tesserae Genet, Forest Lane,Suite B240, Dallas, TX 75230 USA. 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Nestadt, Gerald TI Comprehensive Family-Based Association Study of the Glutamate Transporter Gene SLC1A1 in Obsessive-Compulsive Disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE obsessive-compulsive disorder; glutamate transporter; candidate gene ID OCD COLLABORATIVE GENETICS; O-METHYLTRANSFERASE COMT; LINKAGE ANALYSIS; SEX; SCHIZOPHRENIA; SUPPORTS; AUTISM; SAMPLE AB SLC1A1 encodes a neuronal glutamate transporter and is a promising candidate gene for obsessive-compulsive disorder (OCD). Several independent research groups have reported significant associations between OCD and single nucleotide polymorphisms (SNPs) in this gene. Previously, we evaluated 13 SNPs in, or near, SLC1A1 and reported a strong association signal with rs301443, a SNP 7.5 kb downstream of the gene [Shugart et al. (2009); Am J Med Genet Part B 150B:886-892]. Theaims of the current study were first, to further investigate this finding by saturating the region around rs301443; and second, to explore the entire gene more thoroughly with a dense panel of SNP markers. We genotyped an additional 111 SNPs in or near SLC1A1, covering from 9 kb upstream to 84 kb downstream of the gene at average spacing of 1.7 kb per SNP, and conducted family-based association analyses in 1,576 participants in 377 families. We found that none of the surrounding markers were in linkage disequilibrium with rs301443, nor were any associated with OCD. We also found that SNP rs4740788, located about 8.8 kb upstream of the gene, was associated with OCD in all families (P = 0.003) and in families with male affecteds (P = 0.002). A three-SNP haplotype (rs4740788-rs10491734-rs10491733) was associated with OCD in the total sample (P = 0.00015) and in families with male affecteds (P = 0.0007). Although of nominal statistical significance considering the number of comparisons, these findings provide further support for the involvement of SLC1A1 in the pathogenesis of OCD. (C) 2011 Wiley-Liss, Inc. C1 [Samuels, Jack; Wang, Ying; Riddle, Mark A.; Grados, Marco A.; Cullen, Bernadette; Bienvenu, O. Joseph, III; Nestadt, Gerald] Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21231 USA. [Greenberg, Benjamin D.; Rasmussen, Steven A.] Butler Hosp, Brown Med Sch, Dept Psychiat & Human Behav, Providence, RI 02906 USA. [Fyer, Abby J.] Columbia Univ, New York State Psychiat Inst, Dept Psychiat, Coll Phys & Surg, New York, NY USA. [McCracken, James T.; Piacentini, John] Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. [Rauch, Scott L.; Geller, Daniel] Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. [Murphy, Dennis L.] NIMH, Clin Sci Lab, NIH, Bethesda, MD 20892 USA. [Knowles, James A.] Univ So Calif, Sch Med, Dept Psychiat, Los Angeles, CA USA. [Pauls, David L.] Massachusetts Gen Hosp, Dept Psychiat, Psychiat & Neurodev Genet Unit, Boston, MA 02114 USA. [Liang, Kung-Yee] Johns Hopkins Univ, Dept Biostat, Bloomberg Sch Publ Hlth, Baltimore, MD 21205 USA. [Shugart, Yin Y.] NIMH, Genom Res Branch, Div Neurosci & Basic Behav Sci, Bethesda, MD 20892 USA. RP Samuels, J (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, 1629 Thames St,Suite 401, Baltimore, MD 21231 USA. EM jacks@jhmi.edu RI Liang, Kung-Yee/F-8299-2011 FU National Institute of Mental Health [RO1MH50214, R01MH071507, NIH/NCRR/OPD-GCRC RR00052] FX Grant sponsor: National Institute of Mental Health; Grant numbers: RO1MH50214, R01MH071507, NIH/NCRR/OPD-GCRC RR00052. 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J. Med. Genet. B PD JUN PY 2011 VL 156B IS 4 BP 472 EP 477 DI 10.1002/ajmg.b.31184 PG 6 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 766FA UT WOS:000290765200012 PM 21445956 ER PT J AU Cukier, HN Salyakina, D Blankstein, SF Robinson, JL Sacharow, S Ma, DQ Wright, HH Abramson, RK Menon, R Williams, SM Haines, JL Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Cukier, Holly N. Salyakina, Daria Blankstein, Sarah F. Robinson, Joycelyn L. Sacharow, Stephanie Ma, Deqiong Wright, Harry H. Abramson, Ruth K. Menon, Ramkumar Williams, Scott M. Haines, Jonathan L. Cuccaro, Michael L. Gilbert, John R. Pericak-Vance, Margaret A. TI Microduplications in an Autism Multiplex Family Narrow the Region of Susceptibility for Developmental Disorders on 15q24 and Implicate 7p21 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism spectrum disorder (ASD); copy number variation (CNV); low-copy repeat (LCR); non-allelic homologous recombination ID COPY NUMBER VARIATION; HUMAN GENOME; MICRODELETION SYNDROME; STRUCTURAL VARIATION; INTERSTITIAL DELETION; SPECTRUM DISORDER; ARRAY-CGH; IDENTIFICATION; ASSOCIATION; DUPLICATION AB Copy number variations (CNVs) play a crucial role in the intricate genetics of autism spectrum disorders. A region on chromosome 15q24 vulnerable to both deletions and duplications has been previously implicated in a range of phenotypes including autism, Asperger's syndrome, delayed development, and mild to severe mental retardation. Prior studies have delineated a minimal critical region of approximately 1.33 Mb. In this study, a multiplex autism family was evaluated for CNVs using genotyping data from the Illumina 1 M BeadChip and analyzed with the PennCNV algorithm. Variants were then identified that co-segregate with autism features in this family. Here, we report autistic first cousins who carry two microduplications concordant with disease. Both duplications were inherited maternally and found to be identical by descent. The first is an approximately 10,000 base pair microduplication within the minimal region on 15q24 that falls across a single gene, ubiquitin-like 7. This is the smallest duplication in the region to result in a neuropsychiatric disorder, potentially narrowing the critical region for susceptibility to developmental and autism spectrum disorders. The second is a novel, 352 kb tandem duplication on 7p21 that replicates part of the neurexophilin 1 and islet cell autoantigen 1 genes. The breakpoint junction falls within the intronic regions of these genes and demonstrates a microhomology of four base pairs. Each of these microduplications may contribute to the complex etiology of autism spectrum disorders. (C) 2011 Wiley-Liss, Inc. C1 [Cukier, Holly N.; Salyakina, Daria; Blankstein, Sarah F.; Robinson, Joycelyn L.; Sacharow, Stephanie; Ma, Deqiong; Cuccaro, Michael L.; Gilbert, John R.; Pericak-Vance, Margaret A.] Univ Miami, Miller Sch Med, John P Hussman Inst Human Genom, Miami, FL 33136 USA. [Sacharow, Stephanie; Ma, Deqiong; Cuccaro, Michael L.; Gilbert, John R.; Pericak-Vance, Margaret A.] Univ Miami, Miller Sch Med, Dr John T Macdonald Fdn, Dept Human Genet, Miami, FL 33136 USA. [Wright, Harry H.; Abramson, Ruth K.] Univ S Carolina, Sch Med, Dept Neuropsychiat, Columbia, SC USA. [Menon, Ramkumar] Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA. [Menon, Ramkumar] Emory Univ, Rollins Sch Publ Hlth, Dept Obstet & Gynecol, Atlanta, GA 30322 USA. [Williams, Scott M.; Haines, Jonathan L.] Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN USA. RP Pericak-Vance, MA (reprint author), Univ Miami, Miller Sch Med, John P Hussman Inst Human Genom, 1501 NW 10th Ave,BRB-314,M860, Miami, FL 33136 USA. EM mpericak@med.miami.edu RI Williams, Scott/B-9491-2012; Haines, Jonathan/C-3374-2012 FU National Institute of Neurological Disorders and Stroke [7P01NS026630, 9R01MH080647]; Hussman Foundation FX Grant sponsor: National Institute of Neurological Disorders and Stroke; Grant numbers: 7P01NS026630, 9R01MH080647; Grant sponsor: Hussman Foundation. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Andrieux J, 2009, AM J MED GENET A, V149A, P2813, DOI 10.1002/ajmg.a.33097 Cao M, 2007, J NEUROSCI, V27, P12945, DOI 10.1523/JNEUROSCI.2040-07.2007 Cushman LJ, 2005, AM J MED GENET A, V137A, P65, DOI 10.1002/ajmg.a.30836 El-Hattab AW, 2010, GENET MED, V12, P573, DOI 10.1097/GIM.0b013e3181eb9b4a El-Hattab AW, 2009, HUM GENET, V126, P589, DOI 10.1007/s00439-009-0706-x GAI X, 2011, MOL PSYCH Hedges DJ, 2007, MUTAT RES-FUND MOL M, V616, P46, DOI 10.1016/j.mrfmmm.2006.11.021 Kidd JM, 2008, NATURE, V453, P56, DOI 10.1038/nature06862 Kim HG, 2008, AM J HUM GENET, V82, P199, DOI 10.1016/j.ajhg.2007.09.011 Klopocki E, 2008, EUR J PEDIATR, V167, P903, DOI 10.1007/s00431-007-0616-7 Liu SX, 2003, IMMUNOL LETT, V86, P169, DOI 10.1016/S0165-2478(03)00004-X Locke DP, 2006, AM J HUM GENET, V79, P275, DOI 10.1086/505653 Lord C., 1999, AUTISM DIAGNOSTIC OB Lund ABK, 2008, EUR J MED GENET, V51, P520, DOI 10.1016/j.ejmg.2008.07.008 Ma DQ, 2009, ANN HUM GENET, V73, P263, DOI 10.1111/j.1469-1809.2009.00523.x Marshall CR, 2008, AM J HUM GENET, V82, P477, DOI 10.1016/j.ajhg.2007.12.009 Masurel-Paulet A, 2009, AM J MED GENET A, V149A, P1504, DOI 10.1002/ajmg.a.32904 McInnes LA, 2010, MOL AUTISM, V1, DOI 10.1186/2040-2392-1-5 Melin M, 2006, NEUROPSYCHOBIOLOGY, V54, P64, DOI 10.1159/000096040 Missler M, 1998, J NEUROSCI, V18, P3630 Pasterkamp RJ, 2003, NATURE, V424, P398, DOI 10.1038/nature01790 Pinto D, 2010, NATURE, V466, P368, DOI 10.1038/nature09146 Redon R, 2006, NATURE, V444, P444, DOI 10.1038/nature05329 Rutter M., 2003, AUTISM DIAGNOSTIC IN Rutter M., 2003, SOCIAL COMMUNICATION Sharp AJ, 2006, NAT GENET, V38, P1038, DOI 10.1038/ng1862 Sharp AJ, 2007, HUM MOL GENET, V16, P567, DOI 10.1093/hmg/ddm016 Smith M, 2000, AM J MED GENET, V96, P765, DOI 10.1002/1096-8628(20001204)96:6<765::AID-AJMG13>3.0.CO;2-L Stankiewicz P, 2010, ANNU REV MED, V61, P437, DOI 10.1146/annurev-med-100708-204735 Velez DR, 2009, AM J OBSTET GYNECOL, V200 Wang K, 2007, GENOME RES, V17, P1665, DOI 10.1101/gr.6861907 Weiss LA, 2009, NATURE, V461, P802, DOI 10.1038/nature08490 Yan J, 2008, NEUROSCI LETT, V438, P368, DOI 10.1016/j.neulet.2008.04.074 Zhang F, 2009, TRENDS GENET, V25, P298, DOI 10.1016/j.tig.2009.05.005 NR 35 TC 4 Z9 4 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD JUN PY 2011 VL 156B IS 4 BP 493 EP 501 DI 10.1002/ajmg.b.31188 PG 9 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 766FA UT WOS:000290765200016 PM 21480499 ER PT J AU Marquenie, K Rodger, S Mangohig, K Cronin, A AF Marquenie, Kylie Rodger, Sylvia Mangohig, Kim Cronin, Anne TI Dinnertime and bedtime routines and rituals in families with a young child with an autism spectrum disorder SO AUSTRALIAN OCCUPATIONAL THERAPY JOURNAL LA English DT Article DE ASD; early intervention; qualitative research; rituals; routines ID INTERVENTION AB Background/aim: Routines are thought to be critical in laying the foundation for ritual development, and in turn rituals are considered important for forming a strong and healthy family unit. This article provides a description of the experiences of dinnertime and bedtime routines and rituals in Australian families with a young child with an Autism Spectrum Disorder (ASD), as well as common challenges experienced. Methods: Fourteen Australian mothers with a young child with an ASD between the ages of two and five years were interviewed about their performance of dinnertime and bedtime routines and rituals and their perceptions of both occupations. Descriptive qualitative interviews were audio taped and transcribed. Transcripts were analysed using thematic content analysis. Results: Two overarching themes emerged, including 'centred on ASD' and 'ASD alters meaning'. Mothers' descriptions revealed that families with a young child with an ASD experienced unstructured and chaotic routines at dinnertime. In contrast, bedtime involved the performance of more structured, and at times, non-functional routines. Moreover, dinnertime was bereft of meaningful interactions and rituals, whereas bedtime contained some positive meaningful interactions and rituals. Conclusions: Occupational therapists need to consider supporting mothers and the child with an ASD in enhancing their participation within all aspects of family life, by encouraging them to develop structured and more predictable dinnertime and bedtime routines inclusive of all family members. In doing so, this action will support mothers to develop a strong and cohesive family unit. C1 [Marquenie, Kylie; Rodger, Sylvia; Mangohig, Kim; Cronin, Anne] Univ Queensland, Sch Hlth Sci, Div Occupat Therapy, Brisbane, Qld, Australia. [Cronin, Anne] W Virginia Univ, Sch Med, Div Occupat Therapy, Morgantown, WV 26506 USA. RP Marquenie, K (reprint author), Care of Radger S, Univ Queensland, Sch Hlth & Rehabil Sci, Div Occupat Therapy, St Lucia, Qld 4072, Australia. EM kmarquenie.ot@gmail.com CR (APA) APA, 2000, DIAGN STAT MAN MENT *AUSTR GOV, IND INC TAX RAT RES BOYCE WT, 1983, SOC SCI MED, V17, P193, DOI 10.1016/0277-9536(83)90116-8 CHEAL D, 1988, AM BEHAV SCI, V31, P632, DOI 10.1177/0002764288031006003 DEGRACE W, 2004, AM J OCCUPATIONAL TH, V58, P543 FIESE BH, 1993, J MARRIAGE FAM, V55, P633, DOI 10.2307/353344 Gray DE, 1997, SOC SCI MED, V44, P1097, DOI 10.1016/S0277-9536(96)00237-7 Higgins DJ, 2005, AUTISM, V9, P125, DOI 10.1177/1362361305051403 Imber-Black E., 1992, RITUALS OUR TIMES CE KREFTING L, 1991, AM J OCCUP THER, V45, P214 Larson E, 2006, OTJR-OCCUP PART HEAL, V26, P69 Patton M. 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TI Missing voices: representations of autism in British newspapers, 1999-2008 SO BRITISH JOURNAL OF LEARNING DISABILITIES LA English DT Article DE Austism; newspaper representations; discourse analysis ID MENTAL-ILLNESS; MEDIA; DISABILITY; RISK; COMMUNICATION; INFORMATION; TELEVISION; DEPICTIONS; PORTRAYAL; SPECTRUM AB Accessible summary This study examines how autism is portrayed in newspapers in the United Kingdom. The findings indicate that many of the stories about autism are not based on interviews with individuals with autism. Newspaper accounts tend to focus on stories about children with autism, rather than on adults. Summary Past research indicates that newspaper representations of developmental disability reinforce negative stereotypes. The aim of this study was to examine depictions of autism in British newspapers. A qualitative content and discourse analysis of newspaper accounts of autism was conducted over four 1-month time points, every 3 years, between May 1999 and May 2008. The analysis indicated that conceptualisations of autism could be categorised under three themes: missing voices; the burden of autism; and, sensationalising, misconceptions and misuse of a label. Autism was also portrayed in a standardised and homogenised way that failed to recognise human diversity, and the focus predominated on childhood and third-hand accounts of autism. C1 [Huws, Jaci C.] Bangor Univ, Sch Healthcare Sci, Bangor, Gwynedd, Wales. [Jones, Robert S. P.] Bangor Univ, Sch Psychol, Bangor, Gwynedd, Wales. RP Huws, JC (reprint author), Bangor Univ, Sch Healthcare Sci, Bangor, Gwynedd, Wales. 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J. Learn. Disabil. PD JUN PY 2011 VL 39 IS 2 BP 98 EP 104 DI 10.1111/j.1468-3156.2010.00624.x PG 7 WC Education, Special SC Education & Educational Research GA 759GA UT WOS:000290227500004 ER PT J AU Langan, M AF Langan, Mary TI GAP Good Autism Practice: Celebrating the First 10 Years of the Journal SO BRITISH JOURNAL OF LEARNING DISABILITIES LA English DT Book Review EM m.langan@open.ac.uk CR JONES G, 2010, GAP GOOD AUTISM PRAC, P179 NR 1 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1354-4187 J9 BRIT J LEARN DISABIL JI Brit. J. Learn. Disabil. PD JUN PY 2011 VL 39 IS 2 BP 168 EP 168 DI 10.1111/j.1468-3156.2011.00687.x PG 1 WC Education, Special SC Education & Educational Research GA 759GA UT WOS:000290227500014 ER PT J AU Lindsay, G AF Lindsay, Geoff TI The collection and analysis of data on children with speech, language and communication needs: The challenge to education and health services SO CHILD LANGUAGE TEACHING & THERAPY LA English DT Article DE Bercow Report; data analysis; school census; collaborative practice; speech language and communication needs ID SPECTRUM; AUTISM; DIFFICULTIES; DISORDERS AB The Bercow Report (Bercow, 2008) commissioned by the UK government provided a high status impetus to improve services for children and young people with the full range of speech, language and communication needs (SLCN). A research study commissioned to provide evidence to Bercow (2008) identified both limitations and potential benefits regarding the collection, analysis and use of data on children and young people with SLCN. This article draws on that study of six local authorities and their partner primary care trusts, and on analyses of national statistics. The term 'speech, language and communication needs' (SLCN) is shown to be used in England for two different populations: all children with some form of SLCN, whatever the cause, and the more specific group comprising children and young people with primary language difficulties. The article focuses mainly on the latter group and those with autistic spectrum disorder to explore the use of data available on children and the use of these data to aid collaborative planning by education and speech therapy services. It is concluded that local authorities are 'data rich' with child level information, but effective use of these data for children with SLCN is limited. Collaborative data collection, analysis and use for policy or individual child level action by education and speech and language therapy services are even less common. Data are necessary to support the evaluation of interventions and provide an appropriate accountability framework. It is argued that effective data use by local authorities and primary care trusts, especially if working collaboratively, has the potential to improve services for children with SLCN. C1 Univ Warwick, CEDAR, Coventry CV4 7AL, W Midlands, England. RP Lindsay, G (reprint author), Univ Warwick, CEDAR, Coventry CV4 7AL, W Midlands, England. 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E., 1998, PREVENTING READING D Strand S, 2009, J SPEC EDUC, V43, P174, DOI 10.1177/0022466908320461 *TRAIN DEV AG SCH, SCH IMPR PLANN FRAM World Health Organization, 2007, INT STAT CLASS DIS R, V10th NR 31 TC 4 Z9 4 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0265-6590 J9 CHILD LANG TEACH THE JI Child Lang. Teach. Ther. PD JUN PY 2011 VL 27 IS 2 SI SI BP 135 EP 150 DI 10.1177/0265659010396608 PG 16 WC Education, Special; Linguistics; Language & Linguistics SC Education & Educational Research; Linguistics GA 765XZ UT WOS:000290744000002 ER PT J AU Worth, S AF Worth, Sarah TI Autism and the edges of the known world: Sensitivities, language and constructed reality SO CHILD LANGUAGE TEACHING & THERAPY LA English DT Book Review C1 [Worth, Sarah] Cheshire Autism Support & Dev Team, Nr Northwich CW8 4QP, Cheshire, England. RP Worth, S (reprint author), Cheshire Autism Support & Dev Team, Townfield Lane, Nr Northwich CW8 4QP, Cheshire, England. EM Sarah.Worth@cheshirewestandchester.gov.uk CR Bogdashina O., 2010, AUTISM EDGES KNOWN W Hobson R. P., 2002, CRADLE THOUGHT EXPLO Hobson R. Peter, 1993, AUTISM DEV MIND NR 3 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0265-6590 J9 CHILD LANG TEACH THE JI Child Lang. Teach. Ther. PD JUN PY 2011 VL 27 IS 2 SI SI BP 239 EP 240 PG 2 WC Education, Special; Linguistics; Language & Linguistics SC Education & Educational Research; Linguistics GA 765XZ UT WOS:000290744000008 ER PT J AU Cashion, L Van Roden, A AF Cashion, Larry Van Roden, Angela TI Asperger's Disorder in an Adolescent With 47, XYY Chromosomal Syndrome SO CLINICAL PEDIATRICS LA English DT Article ID AUTISM; CHILDHOOD; CHILDREN; 47,XYY; DIAGNOSIS; GENOTYPE; MALES C1 [Cashion, Larry] Dev Assessment NT, Bishopsbourne, Tas 7301, Australia. 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Pediatr. PD JUN PY 2011 VL 50 IS 6 BP 562 EP 566 DI 10.1177/0009922810380453 PG 5 WC Pediatrics SC Pediatrics GA 763US UT WOS:000290585800015 PM 20837608 ER PT J AU Southall, CM Gast, DL AF Southall, Candice M. Gast, David L. TI Self-Management Procedures: A Comparison across the Autism Spectrum SO EDUCATION AND TRAINING IN AUTISM AND DEVELOPMENTAL DISABILITIES LA English DT Article ID HIGH-FUNCTIONING AUTISM; GENERAL-EDUCATION; ASPERGERS-DISORDER; TREATMENT PROGRAM; HIGH-SCHOOL; CHILDREN; BEHAVIOR; STUDENTS; DISABILITIES; STRATEGIES AB Individuals with autism spectrum disorders (ASD) have difficulty generalizing learned behavior to varied environments with independence. This review of 24 empirical studies compares self-management as a systematic procedure for modifying one's own behavior, to increase target behaviors in students with either autistic disorder (AD) or high-functioning autism/Asperger's syndrome (HFA/AS). Twenty-four single subject research studies are included in the review comparing methodological, demographic, procedural, and outcome aspects of self-management studies between the two disorders under the umbrella of Pervasive Developmental Disorder (PDD). Results show that self-management procedures, regardless of components and age of child, are effective in teaching social, vocational, and communication skills, or decreasing restrictive and repetitive patterns of behaviors for individuals with a PDD. General conclusions are made on how the procedures are used differently across levels of functioning within the autism spectrum and PDD. This literature should encourage researchers and practitioners to continue interventions using self-management procedures with this population to broaden the research base and improve methodological adequacy. C1 [Southall, Candice M.] Univ Georgia, Dept Commun Sci & Special Educ, Athens, GA 30602 USA. 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A., 2005, ED PSYCHOL PRACTICE, V21, P307, DOI 10.1080/02667360500344914 Wilkinson LA, 2008, INTERV SCH CLIN, V43, P150, DOI 10.1177/1053451207311613 WING L, 1981, PSYCHOL MED, V11, P115 Witwer AN, 2008, J AUTISM DEV DISORD, V38, P1611, DOI 10.1007/s10803-008-0541-2 Wolery M., 2010, SINGLE SUBJECT RES M, P57 WOLF MM, 1978, J APPL BEHAV ANAL, V11, P203, DOI 10.1901/jaba.1978.11-203 NR 59 TC 7 Z9 7 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 2154-1647 J9 EDUC TRAIN AUTISM DE JI Educ. Train. Autism Dev. Disabil. PD JUN PY 2011 VL 46 IS 2 BP 155 EP 171 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 763IE UT WOS:000290549200001 ER PT J AU Leaf, JB Oppenheim-Leaf, ML Dotson, WH Johnson, VA Courtemanche, AB Sheldon, JB Sherman, JA AF Leaf, Justin B. Oppenheim-Leaf, Misty L. Dotson, Wesley H. Johnson, Valerie A. Courtemanche, Andrea B. Sheldon, Jan B. Sherman, James A. TI Effects of No-No Prompting on Teaching Expressive Labeling of Facial Expressions to Children with and without a Pervasive Developmental Disorder SO EDUCATION AND TRAINING IN AUTISM AND DEVELOPMENTAL DISABILITIES LA English DT Article ID SMALL-GROUP INSTRUCTION; BEHAVIORAL TREATMENT; AUTISTIC-CHILDREN; TIME-DELAY; DISABILITIES; PRESCHOOLERS; EXCLUSION; SKILLS AB Discrete trial teaching is a systematic form of instruction found to be effective for children diagnosed with autism. Three areas of discrete trial teaching warranting more research are the effectiveness and efficiency of various prompting procedures, the effectiveness of implementing teaching in a group instructional format, and the ability of children with autism to observationally learn from their peers. This study evaluated the effectiveness of a no-no prompting procedure implemented in a group instructional format to teach five children, four of whom were diagnosed with an autism spectrum disorder, to correctly label facial expressions. Additionally, this study evaluated whether participants observationally learned to expressively label facial expressions not directly taught to them but taught to their peers. Using a multiple baseline design, results of this study indicated that all participants learned to expressively label facial expressions taught to them directly with a no-no prompting procedure. The participants also learned through observation to expressively label facial expressions taught only to their peers using the same procedure. C1 [Leaf, Justin B.; Oppenheim-Leaf, Misty L.; Dotson, Wesley H.; Johnson, Valerie A.; Courtemanche, Andrea B.; Sheldon, Jan B.; Sherman, James A.] Univ Kansas, Lawrence, KS 66045 USA. RP Leaf, JB (reprint author), 8799 Old Sappington Rd, St Louis, MO 63126 USA. EM leafku@ku.edu CR Akmanoglu N, 2004, EDUC TRAIN DEV DISAB, V39, P326 Carr D, 2003, J APPL BEHAV ANAL, V36, P507, DOI 10.1901/jaba.2003.36-507 CHARLOP MH, 1986, J APPL BEHAV ANAL, V19, P307, DOI 10.1901/jaba.1986.19-307 deRose JC, 1996, J APPL BEHAV ANAL, V29, P451, DOI 10.1901/jaba.1996.29-451 Fickel K. 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S., 1991, LANG SPEECH HEAR SER, V22, P123 SOLUAGA D, 2008, RES AUTIMS SPECTRUM, V2, P735 Taubman M, 2001, RES DEV DISABIL, V22, P205, DOI 10.1016/S0891-4222(01)00068-3 TRYON AS, 1986, J ABNORM CHILD PSYCH, V14, P537, DOI 10.1007/BF01260522 VARNI JW, 1979, J ABNORM CHILD PSYCH, V7, P31, DOI 10.1007/BF00924508 NR 27 TC 3 Z9 3 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 2154-1647 J9 EDUC TRAIN AUTISM DE JI Educ. Train. Autism Dev. Disabil. PD JUN PY 2011 VL 46 IS 2 BP 186 EP 203 PG 18 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 763IE UT WOS:000290549200003 ER PT J AU Dogoe, MS Banda, DR Lock, RH Feinstein, R AF Dogoe, Maud S. Banda, Devender R. Lock, Robin H. Feinstein, Rita TI Teaching Generalized Reading of Product Warning Labels to Young Adults with Autism Using the Constant Time Delay Procedure SO EDUCATION AND TRAINING IN AUTISM AND DEVELOPMENTAL DISABILITIES LA English DT Article ID SAFETY SKILLS; MENTAL-RETARDATION; SIGHT WORDS; STUDENTS; DISABILITIES; MODERATE; INSTRUCTION; ADOLESCENTS; CHILDREN AB This study examined the effectiveness of the constant timed delay procedure for teaching two young adults with autism to read, define, and state the contextual meaning of keywords on product warning labels of common household products. Training sessions were conducted in the dyad format using flash cards. Results indicated that both participants successfully acquired the skills and generalized them across materials. Even though participants could not attain criterion on generalization across setting probes before the study ended, there were improvements in performance. The implications of the findings for future research and practice are discussed. C1 [Dogoe, Maud S.] Cent Michigan Univ, Dept Counseling & Special Educ, Coll Edu & Human Serv, Mt Pleasant, MI 48859 USA. [Banda, Devender R.; Lock, Robin H.; Feinstein, Rita] Texas Tech Univ, Lubbock, TX 79409 USA. RP Dogoe, MS (reprint author), Cent Michigan Univ, Dept Counseling & Special Educ, Coll Edu & Human Serv, 353 EHS Bldg, Mt Pleasant, MI 48859 USA. EM dogoe1ms@cmich.edu CR Alig-Cybriwsky C., 1990, J EARLY INTERVENTION, V14, P99 AULT MJ, 1988, J AUTISM DEV DISORD, V18, P627 Collins B., 2007, FOCUS AUTISM OTHER D, V22, P220, DOI DOI 10.1177/10883576070220040401 Collins B., 1996, ED TREATMENT CHILDRE, V19, P30 Collins B. C., 1994, EXCEPTIONALITY, V5, P163 COLLINS BC, 1995, EDUC TRAIN MENT RET, V30, P65 COLLINS BC, 1993, EDUC TRAIN MENT RET, V28, P128 CUVO AJ, 1992, J APPL BEHAV ANAL, V25, P499, DOI 10.1901/jaba.1992.25-499 DURAN E, 1985, ADOLESCENCE, V20, P433 DURAN E, 1996, TEACHING STUDENTS MO, P140 FLETCHER D, 1988, EDUC TRAIN MENT RET, V23, P224 GAST DL, 1988, EDUC TRAIN MENT RET, V23, P117 GAST DL, 1994, PROMOTING HLTH SAFET Himle MB, 2004, J APPL BEHAV ANAL, V37, P1, DOI 10.1901/jaba.2004.37-1 Knight MG, 2003, EDUC TRAIN MENT RET, V38, P179 ORZEN A, 2008, INT J SPECIAL ED, V23, P85 SCHOEN SF, 1989, J AUTISM DEV DISORD, V19, P57, DOI 10.1007/BF02212718 Self T, 2007, TOP LANG DISORD, V27, P242 WINTERLING V, 1992, J APPL BEHAV ANAL, V25, P217, DOI 10.1901/jaba.1992.25-217 Wolery M., 1992, TEACHING STUDENTS MO NR 20 TC 3 Z9 3 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 2154-1647 J9 EDUC TRAIN AUTISM DE JI Educ. Train. Autism Dev. Disabil. PD JUN PY 2011 VL 46 IS 2 BP 204 EP 213 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 763IE UT WOS:000290549200004 ER PT J AU Yokotani, K AF Yokotani, Kenji TI Avoidant Attachment Style Indicates Job Adaptation of People with High Functional Autistic Spectrum Disorders SO EDUCATION AND TRAINING IN AUTISM AND DEVELOPMENTAL DISABILITIES LA English DT Article ID QUOTIENT AQ AB The aim of the present study was to investigate whether or not the avoidant attachment style indicates job adaptation of people with High Functional Autistic Spectrum Disorders (HFASD). HFASD are groups of developmental disorders characterized by impairment of social interaction and normal level of intelligence. Twenty-two people with HFASD answered questionnaires, including the Autism Spectrum Quotient, Perceived Emotional Support Network Scales in a family, Avoidant scale of the Internal Working Model Scales, and queries about their employment years. Results revealed that people with HFASD who had obtained better job adaptation had a more avoidant style, regardless of their perceived support and autistic tendencies. The avoidant style might be the optimal coping style for people with HFASD who obtained competitive employment. C1 Tohoku Univ, Grad Sch Educ, Sendai, Miyagi 9808576, Japan. RP Yokotani, K (reprint author), Tohoku Univ, Grad Sch Educ, Kawauchi 27-1, Sendai, Miyagi 9808576, Japan. EM yokotanikenji@m.tains.tohoku.ac.jp CR Ainsworth M. S., 1978, PATTERNS ATTACHMENT American Psychiatric Association, 2000, DIAGN STAT MAN MENT Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARTHOLOMEW K, 1991, J PERS SOC PSYCHOL, V61, P226, DOI 10.1037//0022-3514.61.2.226 Bowlby J., 1969, ATTACHMENT LOSS, V1 Cederlund M, 2008, J AUTISM DEV DISORD, V38, P72, DOI 10.1007/s10803-007-0364-6 Compas BE, 2001, PSYCHOL BULL, V127, P87, DOI 10.1037//0033-2909.127.1.87 Ebata A. 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A., 1994, ADV PERSONAL RELATIO, V5, P181 Sprong M, 2008, SCHIZOPHR RES, V99, P38, DOI 10.1016/j.schres.2007.10.031 TAKUMA T., 1988, J SOCIAL SCI HUMANIT, V196, P1 Wakabayashi A, 2006, J AUTISM DEV DISORD, V36, P263, DOI 10.1007/s10803-005-0061-2 Williams K, 2008, J PAEDIATR CHILD H, V44, P504, DOI 10.1111/j.1440-1754.2008.01331.x NR 24 TC 0 Z9 0 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 2154-1647 J9 EDUC TRAIN AUTISM DE JI Educ. Train. Autism Dev. Disabil. PD JUN PY 2011 VL 46 IS 2 BP 291 EP 296 PG 6 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 763IE UT WOS:000290549200011 ER PT J AU Alexander, MGF Dummer, GM Smeltzer, A Denton, SJ AF Alexander, Melissa G. F. Dummer, Gail M. Smeltzer, Ashley Denton, Stephen J. TI Developing the Social Skills of Young Adult Special Olympics Athletes SO EDUCATION AND TRAINING IN AUTISM AND DEVELOPMENTAL DISABILITIES LA English DT Article ID MENTAL-RETARDATION; CHILDREN; INTERVENTION; AUTISM; SPECTRUM; PROGRAM AB The purpose of the study was to determine if young adult Special Olympics participants could develop, generalize, and maintain target social skills (eye contact, contributing relevant information, and turn taking) as a result of a 14-week Social Skills and Sports (S(3)) Program that combined classroom instruction with soccer activities. Data were collected through direct observation during soccer practices, parent interviews, and parent rating forms. Visual analysis and qualitative methodology were applied to analyze the four case studies. All of the participants increased their ability to demonstrate at least one of the targeted skills, generalized the skill(s) to other settings, and maintained the skill(s) five weeks after completing the intervention. Participants also developed social skills that were not targeted in S(3). C1 [Alexander, Melissa G. F.] Montclair State Univ, Dept Exercise Sci & Phys Educ, Montclair, NJ 07043 USA. [Dummer, Gail M.] Michigan State Univ, E Lansing, MI 48824 USA. [Smeltzer, Ashley] Univ Rochester, Rochester, NY 14627 USA. [Denton, Stephen J.] Univ New England, Armidale, NSW 2351, Australia. RP Alexander, MGF (reprint author), Montclair State Univ, Dept Exercise Sci & Phys Educ, 1 Normal Ave,4113 Univ Hall, Montclair, NJ 07043 USA. EM alexanderm@mail.montclair.edu CR ALEXANDER MGF, 2008, THESIS MICHIGAN STAT Asher S. R., 1998, CO THEY KEEP FRIENDS, P366 Baker J. 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E., 1982, SINGLE CASE RES DESI Kohler FW, 2001, TOP EARLY CHILD SPEC, V21, P93, DOI 10.1177/027112140102100203 Laushey KM, 2000, J AUTISM DEV DISORD, V30, P183, DOI 10.1023/A:1005558101038 O'Reilly MF, 2000, EDUC TRAIN MENT RET, V35, P250 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Patton MQ., 1990, QUALITATIVE EVALUATI QUINN MM, 1995, PREVENTING SCH FAILU, V39, P26 SCHAEFER CE, 1989, HDB PARENT TRAINING Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SISSON LA, 1988, BEHAV MODIF, V12, P497, DOI 10.1177/01454455880124002 STRAIN PS, 1986, EXCEPT CHILDREN, V52, P543 Sugai G, 1996, FOCUS EXCEPT CHILD, V29, P1 TIEDEMANN GL, 1992, BEHAV THER, V23, P299, DOI 10.1016/S0005-7894(05)80387-9 TOWBIN KE, 2002, CHILDREN DISABILITIE, P407 WEBSTERSTRATTON C, 1990, BEHAV THER, V21, P319, DOI 10.1016/S0005-7894(05)80334-X WEHMAN P, 1981, LEISURE PROGRAMS HAN Woods JJ, 2003, LANG SPEECH HEAR SER, V34, P180, DOI 10.1044/0161-1461(2003/015) ZWALD L, 1982, SCH PSYCHOL REV, V11, P428 NR 41 TC 1 Z9 1 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 2154-1647 J9 EDUC TRAIN AUTISM DE JI Educ. Train. Autism Dev. Disabil. PD JUN PY 2011 VL 46 IS 2 BP 297 EP 310 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 763IE UT WOS:000290549200012 ER PT J AU Patel, C Cooper-Charles, L McMullan, DJ Walker, JM Davison, V Morton, J AF Patel, Chirag Cooper-Charles, Lisa McMullan, Dominic J. Walker, Judith M. Davison, Val Morton, Jenny TI Translocation breakpoint at 7q31 associated with tics: further evidence for IMMP2L as a candidate gene for Tourette syndrome SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE Tourette syndrome; IMMP2L; 7q31.1 region; array CGH; FOXP2; breakpoint mapping ID LANGUAGE DISORDER; AUTISM; REGION; SPEECH; IDENTIFICATION; FAMILY; SCHIZOPHRENIA; INVOLVEMENT; DELETIONS; COMPLEX AB Gilles de la Tourette syndrome is a complex neuropsychiatric disorder with a strong genetic basis. We identified a male patient with Tourette syndrome-like tics and an apparently balanced de novo translocation [46, XY, t(2; 7)(p24.2; q31)]. Further analysis using array comparative genomic hybridisation (CGH) revealed a cryptic deletion at 7q31.1-7q31.2. Breakpoints disrupting this region have been reported in one isolated and one familial case of Tourette syndrome. In our case, IMMP2L, a gene coding for a human homologue of the yeast inner mitochondrial membrane peptidase subunit 2, was disrupted by the breakpoint on 7q31.1, with deletion of exons 1-3 of the gene. The IMMP2L gene has previously been proposed as a candidate gene for Tourette syndrome, and our case provides further evidence of its possible role in the pathogenesis. The deleted region (7q31.1-7q31.2) of 7.2Mb of genomic DNA also encompasses numerous genes, including FOXP2, associated with verbal dyspraxia, and the CFTR gene. European Journal of Human Genetics (2011) 19, 634-639; doi:10.1038/ejhg.2010.238; published online 9 March 2011 C1 [Patel, Chirag; Morton, Jenny] Birmingham Womens Hosp NHS Fdn Trust, Dept Clin Genet, Birmingham, W Midlands, England. [Cooper-Charles, Lisa; McMullan, Dominic J.; Walker, Judith M.; Davison, Val] Birmingham Womens Hosp NHS Fdn Trust, W Midlands Reg Genet Lab, Birmingham, W Midlands, England. RP Patel, C (reprint author), Birmingham Womens Hosp, Dept Clin Genet, Metchley Pk Rd, Birmingham B15 2TG, W Midlands, England. 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CA STAART Psychopharmacology Network TI Reduced transcript expression of genes affected by inherited and de novo CNVs in autism SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE autism; CNV; aCGH; expression; deletion; duplication ID COPY NUMBER VARIATION; SPECTRUM DISORDER; SCHIZOPHRENIA; CNTNAP2; GENOME; REARRANGEMENTS; MICRODELETION; ASSOCIATION; DISRUPTION; PATHWAYS AB Individuals with autism are more likely to carry rare inherited and de novo copy number variants (CNVs). However, further research is needed to establish which CNVs are causal and the mechanisms by which these CNVs influence autism. We examined genomic DNA of children with autism (N=41) and healthy controls (N=367) for rare CNVs using a high-resolution array comparative genomic hybridization platform. We show that individuals with autism are more likely to harbor rare CNVs as small as similar to 10 kb, a threshold not previously detectable, and that CNVs in cases disproportionately affect genes involved in transcription, nervous system development, and receptor activity. We also show that a subset of genes that have known or suspected allele-specific or imprinting effects and are within rare-case CNVs may undergo loss of transcript expression. In particular, expression of CNTNAP2 and ZNF214 are decreased in probands compared with their unaffected transmitting parents. Furthermore, expression of PRODH and ARID1B, two genes affected by de novo CNVs, are decreased in probands compared with controls. These results suggest that for some genes affected by CNVs in autism, reduced transcript expression may be a mechanism of pathogenesis during neurodevelopment. European Journal of Human Genetics (2011) 19, 727-731; doi:10.1038/ejhg.2011.24; published online 30 March 2011 C1 [Nord, Alex S.; Dickel, Diane E.; O'Connor, Kristen Lewis; King, Mary-Claire] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA. [Roeb, Wendy; Walsh, Tom; Stray, Sunday M.; Taylor, Susan M.; King, Mary-Claire] Univ Washington, Dept Med, Seattle, WA 98195 USA. [Kusenda, Mary; McCarthy, Shane E.] Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. [Kusenda, Mary] SUNY Stony Brook, Grad Program Genet, Stony Brook, NY 11794 USA. [Malhotra, Dheeraj; Sebat, Jonathan] Univ Calif San Diego, Inst Genom Med, Dept Cellular & Mol Med, Dept Psychiat, La Jolla, CA 92093 USA. [King, Bryan; McClellan, Jon M.] Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RP Nord, AS (reprint author), Univ Washington, Dept Genome Sci, Hlth Sci Room K-160, Seattle, WA 98195 USA. EM nordalex@u.washington.edu FU National Institutes of Health [R01MH083989, R01MH076431, R01HG004222, U54MH066398, U01HD045023, U54MH066673, U54MH068172, U54MH066418, U54MH066494, 5T32ES007032, T32ES015459] FX This work was supported by the National Institutes of Health grants R01MH083989, R01MH076431, R01HG004222, U54MH066398, U01HD045023, U54MH066673, U54MH068172, U54MH066418, U54MH066494, 5T32ES007032, and T32ES015459. 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PD JUN PY 2011 VL 26 IS 2 BP 67 EP 74 DI 10.1177/1088357610397345 PG 8 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 760FW UT WOS:000290311100001 ER PT J AU Barnhill, GP Polloway, EA Sumutka, BM AF Barnhill, Gena P. Polloway, Edward A. Sumutka, Bianca M. TI A Survey of Personnel Preparation Practices in Autism Spectrum Disorders SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES LA English DT Article DE autism spectrum disorders; personnel preparation; qualified teachers ID CHILDREN AB Researchers indicate that special education is grappling with many issues and challenges that point to the need to examine the nature and type of personnel preparation for educators working with individuals with autism spectrum disorders (ASD). The purpose of this study was to survey teacher educators at colleges and universities to (a) determine the prevalence of programs training teachers in this area; (b) identify the nature of the autism-specific coursework and programs currently being offered (e.g., the motivation for developing these courses, the number of such courses offered); and (c) ascertain the topics included in ASD coursework and the depth at which these topics are addressed. Survey forms were mailed to personnel at 184 institutions of higher education (IHEs) in 43 states; responses were received from faculty members at 87 IHEs in 34 states. Current patterns in personnel preparation are discussed and followed by recommendations for future action. C1 [Barnhill, Gena P.; Polloway, Edward A.; Sumutka, Bianca M.] Lynchburg Coll, Lynchburg, VA 24501 USA. RP Barnhill, GP (reprint author), Lynchburg Coll, 1501 Lakeside Dr, Lynchburg, VA 24501 USA. 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TI Schema-Based Strategy Instruction in Mathematics and the Word Problem-Solving Performance of a Student With Autism SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES LA English DT Article DE autism; mathematics; problem solving; schema-based instruction ID LEARNING-DISABILITIES; DRAWINGS; DEFICITS; CHILDREN AB The purpose of this study was to provide preliminary results on the use of schema-based strategy instruction to teach addition and subtraction word problem solving to a fourth grade student with autism. The student was taught to use schematic diagrams to solve three types of addition and subtraction word problems. A multiple probes across behaviors single-case design was used, with solving each of the three problem types treated as a separate behavior. Interpretation of results indicated that the participant's ability to solve all types of one-step addition and subtraction word problems improved following instruction. 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S., 2007, WHY IS MATH SO HARD, P219 NR 33 TC 5 Z9 5 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1088-3576 J9 FOCUS AUTISM DEV DIS JI Focus Autism Dev. Disabil. PD JUN PY 2011 VL 26 IS 2 BP 87 EP 95 DI 10.1177/1088357611405039 PG 9 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 760FW UT WOS:000290311100003 ER PT J AU Schultz, TR Schmidt, CT Stichter, JP AF Schultz, Tia R. Schmidt, Carla T. Stichter, Janine P. TI A Review of Parent Education Programs for Parents of Children With Autism Spectrum Disorders SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES LA English DT Article DE autism spectrum disorders; training; parent ID NATURAL-LANGUAGE PARADIGM; YOUNG-CHILDREN; EARLY INTERVENTION; TRAINING-PROGRAM; PSYCHOSOCIAL INTERVENTIONS; TEACHING SKILLS; NONCOMPLIANCE; AGGRESSION; FAMILIES; INCREASE AB Benefits of parent education have been demonstrated for decades. However, there exists a lack of formative evaluation of parent education for parents of children with autism spectrum disorders (ASD), limiting the interpretation of ongoing and future research. To understand the current status, key characteristics, and evaluation methods of parent education specific to ASD, relevant research was reviewed with an emphasis on presentation format, evaluation methods, and participant demographics. Of the 30 articles that met inclusion criteria, more than half included descriptions of programs for parents of children with ASD ages 3-5 years, 76% involved a one-on-one training approach, 40% relied on a manual or curriculum, 86% included data on parent and child outcomes, and 70% used single-case designs to evaluate program effectiveness. None of the researchers reported data on fidelity of implementation. Suggestions for further evaluation and next-generation research are provided. C1 [Schultz, Tia R.; Stichter, Janine P.] Univ Missouri, Columbia, MO 65211 USA. [Schmidt, Carla T.] Univ Kansas, Juniper Gardens Childrens Project, Lawrence, KS 66045 USA. RP Schultz, TR (reprint author), Univ Missouri, 303 Townsend, Columbia, MO 65211 USA. EM trs4g2@mail.missouri.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson S. 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PD JUN PY 2011 VL 26 IS 2 BP 96 EP 104 DI 10.1177/1088357610397346 PG 9 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 760FW UT WOS:000290311100004 ER PT J AU Robinson, SE AF Robinson, Suzanne Elaine TI Teaching Paraprofessionals of Students With Autism to Implement Pivotal Response Treatment in Inclusive School Settings Using a Brief Video Feedback Training Package SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES LA English DT Article DE paraprofessionals; autism; Pivotal Response Treatment; social communication; inclusion; video feedback ID SPECIAL-EDUCATION TEACHERS; YOUNG-CHILDREN; SOCIAL VALIDITY; SEVERE DISABILITIES; PREPARING TEACHERS; DISCRETE-TRIAL; BEHAVIOR; INTERVENTION; FAMILY; SKILLS AB Given that students with autism spend the majority of their days in school settings, largely supported by paraprofessionals, it is important that these paraprofessionals receive adequate training. The author investigated a training package consisting of modeling and video-based feedback as a means of enabling paraprofessionals to implement Pivotal Response Treatment (PRT) in the inclusive school setting. A multiple baseline design across four paraprofessional -focal student pairs was employed. The findings suggest that the training package was effective and efficient in improving paraprofessional PRT implementation and levels of involvement as well as social communication target behaviors of the students with autism. Generalization across activities and students, maintenance, and social validity were also assessed. C1 Calif State Univ, Fullerton, CA 92834 USA. RP Robinson, SE (reprint author), Calif State Univ, POB 6868, Fullerton, CA 92834 USA. EM srobinson@fullerton.edu CR Albin R. W., 1996, POSITIVE BEHAV SUPPO, P81 Arco L, 1996, BEHAV MODIF, V20, P300, DOI 10.1177/01454455960203004 Armstrong KJ, 1997, J DEV PHYS DISABIL, V9, P359, DOI 10.1023/A:1024982112859 Barlow D. 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S., 1995, J BEHAV ED, V5, P281, DOI 10.1007/BF02110316 NR 66 TC 10 Z9 10 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1088-3576 J9 FOCUS AUTISM DEV DIS JI Focus Autism Dev. Disabil. PD JUN PY 2011 VL 26 IS 2 BP 105 EP 118 DI 10.1177/1088357611407063 PG 14 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 760FW UT WOS:000290311100005 ER PT J AU Jantz, KM AF Jantz, Kathryn Mederise TI Support Groups for Adults With Asperger Syndrome SO FOCUS ON AUTISM AND OTHER DEVELOPMENTAL DISABILITIES LA English DT Article DE adults; Asperger syndrome; support groups; loneliness ID AUTISM; ADOLESCENTS; LONELINESS AB A total of 35 adults (24-77 years; 24 males and 11 females) with Asperger syndrome (AS) who were in, were waiting to get in, or had been in support groups participated in the study. In general, the adults were highly educated but unemployed or underemployed and living alone with family members as friends. The participants were interviewed, completed the Autism-Spectrum Quotient questionnaire and the UCLA Loneliness Scale, and rated group experiences. The results of qualitative and quantitative analyses can be interpreted to conclude that participants were lonely and perceived support groups as beneficial for providing (a) social skills and interaction, (b) information and advice, and (c) structure. Participants also reported that someone had encouraged them to attend a support group. This information can help practitioners gain insight into the content and structure of support groups for individuals with AS and may aid in the design of future research on services for adults with AS. RP Jantz, KM (reprint author), 374 Congress St, Boston, MA 02210 USA. EM kjantz1@gmail.com CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Barnhill G. 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P., 1998, FOCUS AUTISM OTHER D, V13, P45 SZIVOS SE, 1990, MENT RETARD, V28, P333 U. S. Census Bureau, 2000, AM COMM SURV Volkmar F. R., 2000, ASPERGER SYNDROME, P340 WING L, 1981, PSYCHOL MED, V11, P115 NR 25 TC 2 Z9 2 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1088-3576 J9 FOCUS AUTISM DEV DIS JI Focus Autism Dev. Disabil. PD JUN PY 2011 VL 26 IS 2 BP 119 EP 128 DI 10.1177/1088357611406903 PG 10 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 760FW UT WOS:000290311100006 ER PT J AU Mechling, LC Savidge, EJ AF Mechling, Linda C. Savidge, Erin J. TI Using a Personal Digital Assistant to Increase Completion of Novel Tasks and Independent Transitioning by Students with Autism Spectrum Disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Personal digital assistant; Video prompting; Hand held self-prompting system; Autism; TEACCH ID DAILY LIVING SKILLS; MODERATE INTELLECTUAL DISABILITIES; HELD PROMPTING SYSTEM; ACTIVITY SCHEDULES; DEVELOPMENTAL-DISABILITIES; SELF-MANAGEMENT; COOKING SKILLS; TEACCH PROGRAM; ON-SCHEDULE; CHILDREN AB The purpose of this study was to evaluate the use of a Personal Digital Assistant with multiple prompt levels to increase completion of novel task boxes and transitioning within and between tasks. The study used a multiple probe design across three sets of task boxes replicated with three students with a diagnosis of autism spectrum disorder. 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PD JUN PY 2011 VL 41 IS 6 BP 687 EP 704 DI 10.1007/s10803-010-1088-6 PG 18 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200001 PM 20714798 ER PT J AU Gomot, M Blanc, R Clery, H Roux, S Barthelemy, C Bruneau, N AF Gomot, Marie Blanc, Romuald Clery, Helen Roux, Sylvie Barthelemy, Catherine Bruneau, Nicole TI Candidate Electrophysiological Endophenotypes of Hyper-Reactivity to Change in Autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Change processing; Auditory evoked potential (AEP); Mismatch negativity (MMN); P3a; Children ID EVENT-RELATED POTENTIALS; MISMATCH NEGATIVITY MMN; ASPERGER-SYNDROME; SENSORY MEMORY; REPETITIVE BEHAVIORS; AUDITORY-PERCEPTION; TYPICAL DEVELOPMENT; NOVELTY DETECTION; CENTRAL COHERENCE; BRAIN POTENTIALS AB Although resistance to change is a main feature of autism, the brain processes underlying this aspect of the disorder remain poorly understood. The aims of this study were to examine neural basis of auditory change-detection in children with autism spectrum disorders (ASD; N = 27) through electrophysiological patterns (MMN, P3a) and to test whether these are quantitatively related to intolerance of change (using the BSE-R scale). ASD displayed significantly shorter MMN latency and larger P3a than controls, indicating a greater tendency to switch attention to deviant events. These electrophysiological abnormalities were significantly more marked in children who displayed greater difficulties in tolerating change. The atypical neurophysiological mechanism of change perception identified might thus be associated with one of the hallmark behavioural manifestations of autism. C1 [Gomot, Marie] CHU Bretonneau, INSERM, Ctr Pedopsychiat, U930, F-37044 Tours 9, France. [Gomot, Marie; Clery, Helen; Roux, Sylvie; Barthelemy, Catherine; Bruneau, Nicole] Univ Francois Rabelais Tours, CNRS, CHRU, INSERM,UMRS Imagerie & Cerveau,FRE 2448,U930, Tours, France. [Blanc, Romuald] Univ Paris 05, Lab Psychopathol & Neuropsychol Clin, Inst Psychol, Paris V, France. RP Gomot, M (reprint author), CHU Bretonneau, INSERM, Ctr Pedopsychiat, U930, 2 Bd Tonnelle, F-37044 Tours 9, France. 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Autism Dev. Disord. PD JUN PY 2011 VL 41 IS 6 BP 732 EP 740 DI 10.1007/s10803-010-1092-x PG 9 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200004 PM 20730560 ER PT J AU Butler, RC Gillis, JM AF Butler, Robert C. Gillis, Jennifer M. TI The Impact of Labels and Behaviors on the Stigmatization of Adults with Asperger's Disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger's Disorder; Stigmatization; Social Distance Scale; Adults ID FORMER MENTAL-PATIENTS; SOCIAL DISTANCE; CHILDRENS ATTITUDES; ILLNESS; PEOPLE; REJECTION; AUTISM; COMMUNITY; STIGMA; SCHIZOPHRENIA AB Currently, there is a paucity of literature on stigmatization of adults with Asperger's Disorder (AD). Therefore, this study examined whether young adults hold stigmatizing views towards individuals with AD and if that stigmatization is elicited by behaviors or labels. College students (N = 195) read one of six vignettes. A modified Social Distance Scale (Link et al. 1987) was used to assess stigmatization. A 2 x 3 analysis of variance revealed that the social behaviors commonly observed in AD significantly impacted stigmatization scores, while the label, "Asperger's Disorder," did not. These findings have important implications for future research, educating the public, providing support services, and treatment recommendations for individuals with AD. C1 [Butler, Robert C.; Gillis, Jennifer M.] Auburn Univ, Dept Psychol, Auburn, AL 36849 USA. RP Butler, RC (reprint author), Auburn Univ, Dept Psychol, 226 Thach Hall, Auburn, AL 36849 USA. 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Autism Dev. Disord. PD JUN PY 2011 VL 41 IS 6 BP 741 EP 749 DI 10.1007/s10803-010-1093-9 PG 9 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200005 PM 20811769 ER PT J AU Ben-Yizhak, N Yirmiya, N Seidman, I Alon, R Lord, C Sigman, M AF Ben-Yizhak, Noa Yirmiya, Nurit Seidman, Ifat Alon, Raaya Lord, Catherine Sigman, Marian TI Pragmatic Language and School Related Linguistic Abilities in Siblings of Children with Autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Siblings; Broad autism phenotype; Language; Pragmatics; Learning difficulties ID SPECTRUM DISORDERS; BROADER PHENOTYPE; 1ST-DEGREE RELATIVES; PARENTS; INDIVIDUALS; COMMUNICATION; IMPAIRMENT; ADJUSTMENT; COGNITION; PATTERNS AB Siblings of probands with autism spectrum disorders are at higher risk for developing the broad autism phenotype (BAP). We compared the linguistic abilities (i.e., pragmatic language, school achievements, and underling reading processes) of 35 school-age siblings of children with autism (SIBS-A) to those of 42 siblings of children with typical development. Results indicated lower pragmatic abilities in a subgroup of SIBS-A identified with BAP related difficulties (SIBS-A-BAP) whereas school achievements and reading processes were intact. Furthermore, among SIBS-A-BAP, significant negative correlations emerged between the severity scores on the Autism Diagnostic Observation Schedule and full and verbal IQ scores. These results are discussed in the context of the developmental trajectories of SIBS-A and in relation to the BAP. C1 [Ben-Yizhak, Noa; Yirmiya, Nurit; Seidman, Ifat] Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. [Alon, Raaya] Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. [Lord, Catherine] Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. 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PD JUN PY 2011 VL 41 IS 6 BP 750 EP 760 DI 10.1007/s10803-010-1096-6 PG 11 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200006 PM 20844942 ER PT J AU Gjevik, E Eldevik, S Fjaeran-Granum, T Sponheim, E AF Gjevik, Elen Eldevik, Sigmund Fjaeran-Granum, Torill Sponheim, Eili TI Kiddie-SADS Reveals High Rates of DSM-IV Disorders in Children and Adolescents with Autism Spectrum Disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE ASD; Children-adolescents; Comorbid psychiatric disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PSYCHIATRIC-DISORDERS; INTELLECTUAL DISABILITY; ANXIETY SYMPTOMS; PREVALENCE; HYPERACTIVITY; ASSOCIATION; CHILDHOOD; PSYCHOPATHOLOGY AB Prevalence of current comorbid DSM-IV disorders was assessed in a special school population of children and adolescents with ASD (N = 71, age 6.0-17.9 years), representing all cognitive levels and main ASD subgroups. Symptoms were assessed through parent interview and association to child characteristics was explored. Seventy-two percent was diagnosed with at least one comorbid disorder. Anxiety disorders (41%) and attention deficit/hyperactivity disorder (31%) were most prevalent. Obsessive-compulsive disorder was more common in older children, and oppositional defiant disorder/conduct disorder more prevalent in pervasive developmental disorder, not otherwise specified. Our results show high rates of comorbid DSM-IV disorders and underscore the importance of such evaluation in children ASD. However, diagnostic challenges are present and future research on the diagnostic validity of comorbid psychiatric disorders is needed. C1 [Gjevik, Elen; Sponheim, Eili] Oslo Univ Hosp, Div Mental Hlth & Addict, N-0319 Oslo, Norway. [Gjevik, Elen] Univ Oslo, Inst Clin Med, Oslo, Norway. [Eldevik, Sigmund; Fjaeran-Granum, Torill] Nordvoll Sch, Oslo, Norway. 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TI Automated Detection of Stereotypical Motor Movements SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Stereotypical motor movement; Accelerometry; Pattern recognition ID AUTISM SPECTRUM DISORDERS; SELF-STIMULATORY-BEHAVIOR; MENTALLY-RETARDED PERSONS; TARDIVE-DYSKINESIA; REPETITIVE BEHAVIORS; BODY-ROCKING; PERCEPTUAL REINFORCEMENT; AMBULATORY ACCELEROMETRY; DEVELOPMENTAL DISORDERS; POSTURAL STABILITY AB To overcome problems with traditional methods for measuring stereotypical motor movements in persons with Autism Spectrum Disorders (ASD), we evaluated the use of wireless three-axis accelerometers and pattern recognition algorithms to automatically detect body rocking and hand flapping in children with ASD. Findings revealed that, on average, pattern recognition algorithms correctly identified approximately 90% of stereotypical motor movements repeatedly observed in both laboratory and classroom settings. 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PD JUN PY 2011 VL 41 IS 6 BP 770 EP 782 DI 10.1007/s10803-010-1102-z PG 13 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200008 PM 20839042 ER PT J AU Wang, PS Michaels, CA Day, MS AF Wang, Peishi Michaels, Craig A. Day, Matthew S. TI Stresses and Coping Strategies of Chinese Families with Children with Autism and Other Developmental Disabilities SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Family stress; Family coping; China; Autism ID REPUBLIC-OF-CHINA; DOWN-SYNDROME; HONG-KONG; INTELLECTUAL DISABILITY; MENTAL-RETARDATION; PARENTING STRESS; MOTHERS; THERAPY; PREDICTORS; PRESCHOOL AB Data from 368 families of children with autism and other developmental disabilities in the People's Republic of China were gathered to understand the stresses that families experience and the coping strategies they employ. Chinese families of children with developmental disabilities perceived high levels of stress related to pessimism, child characteristics, and parent and family problems. Regarding coping strategies, acceptance, active coping, positive reinterpretation and growth, suppression of competing activities, and planning were the most frequently employed coping strategies. Parents of children with autism experienced more stress and used planning as a coping strategy to a greater degree than parents of children with other developmental disabilities. The implications and limitations of these findings are discussed. C1 [Wang, Peishi; Michaels, Craig A.; Day, Matthew S.] CUNY, Dept Educ & Community Programs, Queens Coll, Flushing, NY 11367 USA. RP Wang, PS (reprint author), CUNY, Dept Educ & Community Programs, Queens Coll, 65-30 Kissena Blvd, Flushing, NY 11367 USA. 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Autism Dev. Disord. PD JUN PY 2011 VL 41 IS 6 BP 783 EP 795 DI 10.1007/s10803-010-1099-3 PG 13 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200009 PM 20859670 ER PT J AU Krebs, JF Biswas, A Pascalis, O Kamp-Becker, I Remschmidt, H Schwarzer, G AF Krebs, Julia F. Biswas, Ajanta Pascalis, Olivier Kamp-Becker, Inge Remschmidt, Helmuth Schwarzer, Gudrun TI Face Processing in Children with Autism Spectrum Disorder: Independent or Interactive Processing of Facial Identity and Facial Expression? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Face processing; Facial identity; Emotional expression ID HIGH-FUNCTIONING AUTISM; EMOTION RECOGNITION; ASPERGER-SYNDROME; FAMILIAR FACES; BASIC EMOTIONS; PERCEPTION; INFORMATION; ATTENTION; SPEECH; PEOPLE AB The current study investigated if deficits in processing emotional expression affect facial identity processing and vice versa in children with autism spectrum disorder. Children with autism and IQ and age matched typically developing children classified faces either by emotional expression, thereby ignoring facial identity or by facial identity disregarding emotional expression. Typically developing children processed facial identity independently from facial expressions but processed facial expressions in interaction with identity. Children with autism processed both facial expression and identity independently of each other. They selectively directed their attention to one facial parameter despite variations in the other. Results indicate that there is no interaction in processing facial identity and emotional expression in autism spectrum disorder. C1 [Krebs, Julia F.; Schwarzer, Gudrun] Univ Giessen, Dept Dev Psychol, D-35394 Giessen, Germany. [Biswas, Ajanta; Pascalis, Olivier] Univ Sheffield, Dept Cognit Neurosci, Western Bank, Sheffield S10 2TP, S Yorkshire, England. 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Autism Dev. Disord. PD JUN PY 2011 VL 41 IS 6 BP 796 EP 804 DI 10.1007/s10803-010-1098-4 PG 9 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200010 PM 20839043 ER PT J AU Hodgetts, S Magill-Evans, J Misiaszek, JE AF Hodgetts, Sandra Magill-Evans, Joyce Misiaszek, John E. TI Weighted Vests, Stereotyped Behaviors and Arousal in Children with Autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; Stereotyped behaviors; Weighted vests; Arousal; Sensory modulation ID SINGLE-SUBJECT RESEARCH; HEART-RATE; TASK; DISORDERS; PRESSURE; EFFICACY AB The homeostatic theory of stereotyped behaviors assumes that these behaviors modulate arousal. Weighted vests are used to decrease stereotyped behaviors in persons with autism because the input they provide is thought to serve the same homeostatic function. This small-n, randomized and blinded study measured the effects of wearing a weighted vest on stereotyped behaviors and heart rate for six children with autism in the classroom. Weighted vests did not decrease motoric stereotyped behaviors in any participant. Verbal stereotyped behaviors decreased in one participant. Weighted vests did not decrease heart rate. Heart rate increased in one participant. Based on this protocol, the use of weighted vests to decrease stereotyped behaviors or arousal in children with autism in the classroom was not supported. C1 [Hodgetts, Sandra; Magill-Evans, Joyce; Misiaszek, John E.] Univ Alberta, Dept Occupat Therapy, Fac Rehabil Med, Edmonton, AB T6G 2G4, Canada. RP Hodgetts, S (reprint author), Univ Alberta, Dept Pediat, Fac Med, Edmonton, AB, Canada. EM sandra.hodgetts@ualberta.ca CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bailey J. S., 2002, RES METHODS APPL BEH Baranek G. 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Autism Dev. Disord. PD JUN PY 2011 VL 41 IS 6 BP 805 EP 814 DI 10.1007/s10803-010-1104-x PG 10 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200011 PM 20839040 ER PT J AU Maras, K Bowler, DM AF Maras, Katie Bowler, Dermot M. TI Brief Report: Schema Consistent Misinformation Effects in Eyewitnesses with Autism Spectrum Disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism spectrum disorder; Schema; Typicality; Misinformation; Eyewitness; Memory ID ASPERGERS-SYNDROME; MEMORY; ADOLESCENTS; COHERENCE; INTERVIEW; IMPLICIT; ACCOUNT; SCRIPTS; ADULTS AB A number of studies have demonstrated schema-related misinformation effects in typical individuals, but no research to date has examined this with witnesses with autism spectrum disorder (ASD), despite their impaired ability to generate core elements that define everyday events. After witnessing slides depicting a bank robbery, 16 adults with ASD and 16 matched comparison individuals were exposed to post-event misinformation that was either schema typical or atypical. Consistent with previous work, the comparison group went onto report more schema typical misinformation than atypical misinformation. However, so too did the ASD group, suggesting that individuals with ASD do have understanding of the causal links between events, persons and actions, an important finding from both theoretical and applied perspectives. C1 [Maras, Katie; Bowler, Dermot M.] City Univ London, Autism Res Grp, Dept Psychol, London EC1V 0HB, England. RP Maras, K (reprint author), City Univ London, Autism Res Grp, Dept Psychol, London EC1V 0HB, England. EM Katie.Maras.1@city.ac.uk RI Maras, Katie/F-9283-2013 CR Abelson R., 1977, SCRIPTS PLANS GOALS Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x BIEDERMAN I, 1981, PERCEPTION, V10, P573, DOI 10.1068/p100573 Bowler DM, 2004, J AUTISM DEV DISORD, V34, P533, DOI 10.1007/s10803-004-2548-7 Bowler DM, 2000, J ABNORM PSYCHOL, V109, P663, DOI 10.1037//0021-843X.109.4.663 Fisher R. 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A., 1993, UNDERSTANDING OTHER, P247 Luna K, 2008, PSICOLOGICA, V29, P171 MARAS KL, J AUTISM DE IN PRESS Renner P, 2000, J AUTISM DEV DISORD, V30, P3, DOI 10.1023/A:1005487009889 Roediger HL, 2001, PSYCHON B REV, V8, P365, DOI 10.3758/BF03196174 Tuckey MR, 2003, J EXP PSYCHOL-APPL, V9, P101, DOI 10.1037/1076-898X.9.2.101 Tuckey MR, 2003, APPL COGNITIVE PSYCH, V17, P785, DOI 10.1002/acp.906 Volden J, 1999, J AUTISM DEV DISORD, V29, P203, DOI 10.1023/A:1023028021580 Wechsler D, 1981, WECHSLER ADULT INTEL NR 25 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 JUN PY 2011 VL 41 IS 6 BP 815 EP 820 DI 10.1007/s10803-010-1089-5 PG 6 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200012 PM 20734225 ER PT J AU Al-Farsi, YM Al-Sharbati, MM Al-Farsi, OA Al-Shafaee, MS Brooks, DR Waly, MI AF Al-Farsi, Yahya M. Al-Sharbati, Marwan M. Al-Farsi, Omar A. Al-Shafaee, Mohammed S. Brooks, Daniel R. Waly, Mostafa I. TI Brief Report: Prevalence of Autistic Spectrum Disorders in the Sultanate of Oman SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism; ASD; Prevalence; Symptoms; Oman AB Prevalence of autistic spectrum disorders (ASD) in Oman is unknown. We conducted a cross-sectional study to estimate the prevalence of ASD among 0-14 year old children. Diagnoses were made as per DSM-IV-TR criteria and supplemented with information collected with the standard Childhood Autism Rating Scale (CARS) questionnaire. A total 113 cases of ASD were enumerated nationwide, indicating an overall prevalence of 1.4 (95% CI 1.2, 1.7) cases per 10,000 children aged 0-14 years. More prevalent cases were among boys (75%) and among low-income families. Ritualistic interests were more common among girls as an onset-symptom compared to boys (p = 0.03). The reported low prevalence of ASD in Oman is likely due to under-diagnosis and under-reporting. C1 [Al-Farsi, Yahya M.; Al-Farsi, Omar A.; Al-Shafaee, Mohammed S.] Sultan Qaboos Univ, Dept Family Med & Publ Hlth, Coll Med & Hlth Sci, Al Khoud 123, Oman. [Al-Sharbati, Marwan M.] Sultan Qaboos Univ, Dept Behav Med, Coll Med & Hlth Sci, Al Khoud 123, Oman. [Brooks, Daniel R.] Boston Univ, Sch Publ Hlth, Boston, MA 02215 USA. [Waly, Mostafa I.] Sultan Qaboos Univ, Coll Agr & Marine Sci, Al Khoud 123, Oman. RP Al-Farsi, YM (reprint author), Sultan Qaboos Univ, Dept Family Med & Publ Hlth, Coll Med & Hlth Sci, POB 35, Al Khoud 123, Oman. EM ymfarsi@squ.edu.om CR Al-Salehi SM, 2009, TRANSCULT PSYCHIATRY, V46, P340, DOI 10.1177/1363461509105823 Al-Sharbati MM, 2003, SAUDI MED J, V24, P391 ALSHOMARI T, 2002, J SPECIAL ED ACAD, V1, P1 American Psychiatric Association, 2000, DIAGN STAT MAN MENT, P70 [Anonymous], 2005, 7 5 YEAR PLAN HLTH D Cannell JJ, 2008, MED HYPOTHESES, V70, P750, DOI 10.1016/j.mehy.2007.08.016 *DIR GEN SOC STAT, 2009, STAT YB DIR GEN SOC, V37, P65 Eldin AS, 2008, INT REV PSYCHIATR, V20, P281, DOI 10.1080/09540260801990324 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 2009, PEDIATR RES, V65, P591, DOI 10.1203/PDR.0b013e31819e7203 JAJU S, 2009, BMC CHILD ADOLESCENT, V3, P29 Lenoir P, 2009, ENCEPHALE, V35, P36, DOI 10.1016/j.encep.2007.12.011 *MINS HLTH, 2008, ANN HLTH REP Rutter M, 2005, ACTA PAEDIATR, V94, P2, DOI 10.1080/08035250410023124 Rutter M, 2005, J AUTISM DEV DISORD, V35, P241, DOI 10.1007/s10803-005-2003-4 SCHOPLER E, 1985, CHILDHOOD AUTISM RAT Selvin S, 1996, STAT ANAL EPIDEMIOLO, V2nd Yazbak FE, 2004, BRIT MED J, V328, P226, DOI 10.1136/bmj.328.7433.226-c NR 18 TC 22 Z9 23 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 JUN PY 2011 VL 41 IS 6 BP 821 EP 825 DI 10.1007/s10803-010-1094-8 PG 5 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200013 PM 20809376 ER PT J AU Lane, AE Dennis, SJ Geraghty, ME AF Lane, Alison E. Dennis, Simon J. Geraghty, Maureen E. TI Brief Report: Further Evidence of Sensory Subtypes in Autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Sensory processing; Subtypes; Autism; Model-based cluster analysis ID CHILDREN AB Distinct sensory processing (SP) subtypes in autism have been reported previously. This study sought to replicate the previous findings in an independent sample of thirty children diagnosed with an Autism Spectrum Disorder. Model-based cluster analysis of parent-reported sensory functioning (measured using the Short Sensory Profile) confirmed the triad of sensory subtypes reported earlier. Subtypes were differentiated from each other based on degree of SP dysfunction, taste/smell sensitivity and vestibular/proprioceptive processing. Further elucidation of two of the subtypes was also achieved in this study. Children with a primary pattern of sensory-based inattention could be further described as sensory seekers or non-seekers. Children with a primary pattern of vestibular/proprioceptive dysfunction were also differentiated on movement and tactile sensitivity. C1 [Lane, Alison E.] Ohio State Univ, Div Occupat Therapy, Sch Allied Med Profess, Columbus, OH 43210 USA. [Dennis, Simon J.] Ohio State Univ, Sch Psychol, Columbus, OH 43210 USA. [Geraghty, Maureen E.] Ohio State Univ, Div Med Dietet, Sch Allied Med Profess, Columbus, OH 43210 USA. [Geraghty, Maureen E.] Abbott Labs, Columbus, OH 43219 USA. RP Lane, AE (reprint author), Ohio State Univ, Div Occupat Therapy, Sch Allied Med Profess, 406C Atwell Hall,453 W 10th Ave, Columbus, OH 43210 USA. EM lane.350@osu.edu RI Lane, Alison/E-3460-2011 CR Baranek GT, 2007, AM J MENT RETARD, V112, P233, DOI 10.1352/0895-8017(2007)112[233:HSPIYC]2.0.CO;2 Baranek GT, 2002, J AUTISM DEV DISORD, V32, P397, DOI 10.1023/A:1020541906063 Ben-Sasson A, 2009, J AUTISM DEV DISORD, V39, P1, DOI 10.1007/s10803-008-0593-3 Dawson G, 2002, DEV PSYCHOPATHOL, V14, P581, DOI 10.1017/S0954579402003103 Koenig K. P., 2008, SPECIAL INTEREST SEC, V31, P3 Koomar J. A., 2002, SENSORY INTEGRATION, P261 Lane AE, 2010, J AUTISM DEV DISORD, V40, P112, DOI 10.1007/s10803-009-0840-2 Lane SL, 2002, SENSORY INTEGRATION, P101 McIntosh D. N., 1999, SENSORY PROFILE EXAM, P59 Miller L. J., 2005, FINAL REPORT QUANTIT Miller LJ, 2007, AM J OCCUP THER, V61, P135 Murray E. A., 2002, SENSORY INTEGRATION, P71 Reynolds S, 2008, J AUTISM DEV DISORD, V38, P516, DOI 10.1007/s10803-007-0418-9 *US DEP HHS, 2009, INT AUT COORD COMM S Zhong S, 2003, J MACHINE LEARNING R, V4, P1001, DOI 10.1162/jmlr.2003.4.6.1001 NR 15 TC 18 Z9 18 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 JUN PY 2011 VL 41 IS 6 BP 826 EP 831 DI 10.1007/s10803-010-1103-y PG 6 WC Psychology, Developmental SC Psychology GA 763RK UT WOS:000290577200014 PM 20839041 ER PT J AU Elder, JH Donaldson, SO Kairalla, J Valcante, G Bendixen, R Ferdig, R Self, E Walker, J Palau, C Serrano, M AF Elder, Jennifer H. Donaldson, Susan O. Kairalla, John Valcante, Gregory Bendixen, Roxanna Ferdig, Richard Self, Erica Walker, Jeffrey Palau, Christina Serrano, Michele TI In-Home Training for Fathers of Children with Autism: A Follow up Study and Evaluation of Four Individual Training Components SO JOURNAL OF CHILD AND FAMILY STUDIES LA English DT Article DE Autism; Fathers; Parent training ID BEHAVIORAL TREATMENT; JOINT ATTENTION; LANGUAGE; MOTHERS AB Literature regarding fathers of children with autism remains sparse, and because mothers are the more common intervening parent, few training methods have focused on fathers. Thus, we sought to evaluate effects of in-home training directed at fathers and their ability to train mothers in the same manner in which they were trained. Fathers were taught four skills commonly associated with in-home training interventions for parents of children with autism: following the child's lead, imitation with animation, commenting on the child, and expectant waiting. Father skills were evaluated twice a week for 12 weeks during videotaped in-home father-child play sessions. Analyses included visual inspection of graphed data and statistical analyses of father skill acquisition, mother skill acquisition, and child behaviors with both parents. A multivariate repeated measures analysis of 18 dyads revealed significant increases in frequencies of fathers' imitation with animation, expectant waiting, and commenting on the child. Child initiating rates increased significantly as did frequencies of child non-speech vocalizations. Analysis of mothers revealed significant increases in frequencies of imitation with animation, expectant waiting, and following the child's lead. Child behaviors had similar results for father and mother sessions. Findings are consistent with those from our first study indicating that fathers can effectively implement skills that promote father-child social interactions and that children respond positively to this approach. C1 [Elder, Jennifer H.; Donaldson, Susan O.; Kairalla, John; Valcante, Gregory; Bendixen, Roxanna; Ferdig, Richard; Self, Erica; Walker, Jeffrey; Palau, Christina; Serrano, Michele] Univ Florida, Gainesville, FL 32610 USA. RP Elder, JH (reprint author), Univ Florida, 101 S Newell Rd,Box 100187, Gainesville, FL 32610 USA. EM elderjh@ufl.edu CR Ainsworth M. S., 1978, PATTERNS ATTACHMENT American Psychiatric Association, 2000, DIAGN STAT MAN MENT BARNARD K, 1983, J MATERNAL CHILD NUR, V8, P36 BELSKY J, 1984, CHILD DEV, V55, P718, DOI 10.1111/j.1467-8624.1984.tb03810.x Booth A., 1998, MEN FAMILIES DO THEY BRAZELTON TB, 1974, EFFECT INFANT ITS CA, V1, P49 BRUNER JS, 1975, COGNITION, V3, P255, DOI 10.1016/0010-0277(74)90012-2 CALHOUN M L, 1991, Physical and Occupational Therapy in Pediatrics, V11, P45, DOI 10.1300/J006v11n03_03 CUNNINGHAM CE, 1981, CHILD DEV, V52, P62 Damon W., 1998, HDB CHILD PSYCHOL SO Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 Donnellan A. 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PD JUN PY 2011 VL 20 IS 3 BP 263 EP 271 DI 10.1007/s10826-010-9387-2 PG 9 WC Family Studies; Psychology, Developmental; Psychiatry SC Family Studies; Psychology; Psychiatry GA 759IB UT WOS:000290232800002 ER PT J AU Elsabbagh, M Cohen, H Cohen, M Rosen, S Karmiloff-Smith, A AF Elsabbagh, M. Cohen, H. Cohen, M. Rosen, S. Karmiloff-Smith, A. TI Severity of hyperacusis predicts individual differences in speech perception in Williams Syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE hyperacusis; language; speech perception in noise; Williams Syndrome ID METHODOLOGICAL ISSUES; DISORDERS; PHENOTYPE; TODDLERS; CHILDREN; AUTISM; MEMORY; NOISE AB Background Williams Syndrome (WS) is a neurodevelopmental disorder of genetic origin, characterised by relative proficiency in language in the face of serious impairment in several other domains. Individuals with WS display an unusual sensitivity to noise, known as hyperacusis. Methods In this study, we examined the extent to which hyperacusis interferes with the perception of speech in children and adults with WS. Participants were required to discriminate words which differed in one consonant of a cluster when these contrasts were embedded in a background of noise. Results Although the introduction of noise interfered with performance on a consonant cluster discrimination task equally in the WS and control groups, the severity of hyperacusis significantly predicted individual variability in speech perception within the WS group. Conclusions These results suggest that alterations in sensitivity to input mediate atypical pathways for language development in WS, where hyperacusis exerts an important influence together with other non-auditory factors. C1 [Elsabbagh, M.; Cohen, M.; Karmiloff-Smith, A.] Univ London, Ctr Brain & Cognit Dev, London WC1E 7HX, England. [Cohen, H.] Univ Quebec, Cognit Neurosci Ctr, Montreal, PQ H3C 3P8, Canada. 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Intell. Disabil. Res. PD JUN PY 2011 VL 55 BP 563 EP 571 DI 10.1111/j.1365-2788.2011.01411.x PN 6 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 762PH UT WOS:000290491400003 PM 21557785 ER PT J AU Goldstein, TR AF Goldstein, Thalia R. TI Correlations Among Social-Cognitive Skills in Adolescents Involved in Acting or Arts Classes SO MIND BRAIN AND EDUCATION LA English DT Article ID THEORY-OF-MIND; EMOTION-RELATED REGULATION; HIGH-FUNCTIONING AUTISM; INDIVIDUAL-DIFFERENCES; ASPERGER-SYNDROME; EMPATHY; BEHAVIOR; TEMPERAMENT; PERSONALITY; PERSPECTIVE AB Empathy, theory of mind, and adaptive emotion regulation are critical skills for social functioning. However, the ways in which these skills may co- or differentially develop has thus far been understudied. We explored how these social-cognitive skills converge and diverge across a year of development in early adolescence, and with different kinds of arts training: the visual arts or music, and acting. Results show differential effects of acting versus other arts training, with the expected convergence for the artists and musicians but less convergence than predicted for the actors. Results are discussed in light of the cognitive effects of arts and acting training and social cognition as a field. C1 [Goldstein, Thalia R.] Yale Univ, Dept Psychol, New Haven, CT 06520 USA. [Goldstein, Thalia R.] Boston Coll, Dept Psychol, Chestnut Hill, MA 02167 USA. RP Goldstein, TR (reprint author), Yale Univ, Dept Psychol, Box 208205, New Haven, CT 06520 USA. 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PD JUN PY 2011 VL 5 IS 2 BP 97 EP 103 DI 10.1111/j.1751-228X.2011.01115.x PG 7 WC Education & Educational Research; Psychology, Developmental SC Education & Educational Research; Psychology GA 766EI UT WOS:000290763400006 ER PT J AU Saygin, ZM Osher, DE Augustinack, J Fischl, B Gabrieli, JDE AF Saygin, Zeynep M. Osher, David E. Augustinack, Jean Fischl, Bruce Gabrieli, John D. E. TI Connectivity-based segmentation of human amygdala nuclei using probabilistic tractography SO NEUROIMAGE LA English DT Article DE Diffusion imaging; DTI; DWI; Tractography; Amygdala; Structural connectivity ID MEDIAL PREFRONTAL CORTEX; MACAQUE MONKEY AMYGDALA; CORTICAL AREAS TE; RHESUS-MONKEY; TOPOGRAPHIC ORGANIZATION; AFFERENT CONNECTIONS; EXTENDED AMYGDALA; LATERAL NUCLEUS; MACACA-MULATTA; PROJECTIONS AB The amygdala plays an important role in emotional and social functions, and amygdala dysfunction has been associated with multiple neuropsychiatric disorders, including autism, anxiety, and depression. Although the amygdala is composed of multiple anatomically and functionally distinct nuclei, typical structural magnetic resonance imaging (MRI) sequences are unable to discern them. Thus, functional MRI (fMRI) studies typically average the BOLD response over the entire structure, which reveals some aspects of amygdala function as a whole but does not distinguish the separate roles of specific nuclei in humans. We developed a method to segment the human amygdala into its four major nuclei using only diffusion-weighted imaging and connectivity patterns derived mainly from animal studies. We refer to this new method as Tractography-based Segmentation, or TractSeg. The segmentations derived from TractSeg were topographically similar to their corresponding amygdaloid nuclei, and were validated against a high-resolution scan in which the nucleic boundaries were visible. In addition, nuclei topography was consistent across subjects. TractSeg relies on short scan acquisitions and widely accessible software packages, making it attractive for use in healthy populations to explore normal amygdala nucleus function, as well as in clinical and pediatric populations. Finally, it paves the way for implementing this method in other anatomical regions which are also composed of functional subunits that are difficult to distinguish with standard structural MRI. (C) 2011 Elsevier Inc. All rights reserved. C1 [Saygin, Zeynep M.; Osher, David E.; Gabrieli, John D. E.] MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. [Augustinack, Jean; Fischl, Bruce] Harvard Univ, MIT, Dept Radiol,MGH, Med Sch,Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. RP Saygin, ZM (reprint author), MIT, Dept Brain & Cognit Sci, 43 Vassar St,Room 46-4033E, Cambridge, MA 02139 USA. EM zsaygin@mit.edu FU PHS [DA023427]; Poitras Center for Affective Disorders Research; National Center for Research Resources [P41-RR14075]; NCRR [BIRN002, U24 RR021382]; National Institute for Biomedical Imaging and Bioengineering [R01EB006758]; National Institute on Aging [AG022381]; National Institute for Neurological Disorders and Stroke [R01 NS052585-01, 1R21NS072652-01]; Ellison Medical Foundation; [1S10RR023401]; [1S10RR019]; [1S10RR023043] FX We are grateful to S. Ghosh and R. R. Saxe for valuable discussions and revisions, A. Kouwe, F. Polli, S. Sabhlok, and G. Reynolds for help with acquisition, and M. Reuter for help with high-resolution registration methods. This work was supported by PHS grant DA023427 (Z.M.S) and by the Poitras Center for Affective Disorders Research (J.D.E.G.). Support was also provided in part by: the National Center for Research Resources (P41-RR14075, and the NCRR BIRN Morphometric Project BIRN002, U24 RR021382), the National Institute for Biomedical Imaging and Bioengineering (R01EB006758), the National Institute on Aging (AG022381), the National Institute for Neurological Disorders and Stroke (R01 NS052585-01, 1R21NS072652-01), Shared Instrumentation Grants (1S10RR023401, 1S10RR019, and 1S10RR023043), and the Ellison Medical Foundation (B.F.). 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Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 764RF UT WOS:000290649300048 PM 21396459 ER PT J AU Marsh, LE Hamilton, AFD AF Marsh, Lauren E. Hamilton, Antonia F. de C. TI Dissociation of mirroring and mentalising systems in autism SO NEUROIMAGE LA English DT Article DE Autism; Social cognition; Theory of mind; Mirror neuron system; Action understanding ID ANTERIOR INTRAPARIETAL SULCUS; SPECTRUM DISORDERS; ASPERGER-SYNDROME; NEURON SYSTEM; SOCIAL COGNITION; ANIMATED SHAPES; HUMAN BRAIN; IMITATION; MIND; REPRESENTATION AB The role of mirror neuron systems and mentalising systems in causing poor social and communication skills in individuals with autistic spectrum conditions is hotly debated. We studied 18 adults with autistic spectrum conditions in comparison to 19 age and IQ matched typical individuals. Behavioural assessments revealed difficulties in mental state attribution and action comprehension in the autism sample. We examined brain responses when observing rational and irrational hand actions, because these actions engage mirror and mentalising components of the social brain respectively. Both typical and autistic participants activated the left anterior intraparietal sulcus component of the mirror system when viewing hand actions compared to moving shapes. The typical but not autistic participants activated the posterior mid cingulate cortex/supplementary motor area and bilateral fusiform cortex when viewing hand actions. When viewing irrational hand actions, the medial prefrontal cortex of typical participants deactivated but this region did not distinguish the different stimuli in autistic participants. These results suggest that parietal mirror regions function normally in autism, while differences in action understanding could be due to abnormal function of cingulate, fusiform and medial prefrontal regions. Thus, brain regions associated with mirroring and mentalising functions are differentially affected in autistic spectrum conditions. (C) 2011 Elsevier Inc. All rights reserved. C1 [Marsh, Lauren E.; Hamilton, Antonia F. de C.] Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Hamilton, AFD (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. EM antonia.hamilton@nottingham.ac.uk RI Hamilton, Antonia/B-3612-2008 OI Hamilton, Antonia/0000-0001-8000-0219 FU Autism Speaks [1925]; School of Psychology, University of Nottingham FX This work is supported by a pilot grant from Autism Speaks (#1925) and by the School of Psychology, University of Nottingham. 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Chakrabarti, Bhismadev Bullmore, Edward T. Baron-Cohen, Simon CA MRC AIMS Consortium TI Specialization of right temporo-parietal junction for mentalizing and its relation to social impairments in autism SO NEUROIMAGE LA English DT Article DE Autism; Mentalizing; Theory of mind; Right temporo-parietal junction; fMRI ID MEDIAL PREFRONTAL CORTEX; SPECTRUM DISORDERS; ASPERGER-SYNDROME; FUNCTIONING AUTISM; NEURAL MECHANISMS; BRAIN-REGIONS; MIND; SELF; COMPREHENSION; ATTENTION AB Over the last 25 years, "mindblindness" (deficits in representing mental states) has been one of the primary explanations behind the hallmark social-communication difficulties in autism spectrum conditions (ASC). However, highlighting neural systems responsible for mindblindness and their relation to variation in social impairments has remained elusive. In this study we show that one of the neural systems responsible for mindblindness in ASC and its relation to social impairments is the right temporo-parietal junction (RTPJ). Twenty-nine adult males with ASC and 33 age and IQ-matched Controls were scanned with fMRI while making reflective mentalizing or physical judgments about themselves or another person. Regions of interest within mentalizing circuitry were examined for between-group differences in activation during mentalizing about self and other and correlations with social symptom severity. RTPJ was the only mentalizing region that responded atypically in ASC. In Controls. RTPJ was selectively more responsive to mentalizing than physical judgments. This selectivity for mentalizing was not apparent in ASC and generalized across both self and other. Selectivity of RTPJ for mentalizing was also associated wills the degree of reciprocal social impairment in ASC. These results lend support to the idea that RTPJ is one important neural system behind mindblindness in ASC. Understanding the contribution of RTPJ in conjunction with other neural systems responsible for other component processes involved in social cognition will be illuminating in fully explaining the hallmark social-communication difficulties of autism. (C) 2011 Elsevier Inc. All rights reserved. C1 [Lombardo, Michael V.; Chakrabarti, Bhismadev; Baron-Cohen, Simon] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England. [Chakrabarti, Bhismadev] Univ Reading, Sch Psychol & Clin Language Sci, Reading RG6 2AH, Berks, England. [Bullmore, Edward T.] Univ Cambridge, Dept Psychiat, Brain Mapping Unit, Cambridge CB2 1TN, 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; daly, eileen/B-6716-2011; Bullmore, Edward/C-1706-2012; Williams, Steve/D-6979-2011; Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Bullmore, Edward/0000-0002-8955-8283; Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X FU Medical Research Council (MRC) Autism Imaging Multi-Centre Study (AIMS) Consortium; Shirley Foundation; Cambridge Overseas Trust; MRC FX We thank Jason Mitchell and Adrianna Jenkins for generously letting us use their stimuli, and Uta Frith, Andy Calder, Kevin Pelphrey, and two anonymous reviewers for their valuable discussion and comments. We also acknowledge financial support from the Medical Research Council (MRC) Autism Imaging Multi-Centre Study (AIMS) Consortium, a doctoral studentship to MVL by the Shirley Foundation and the Cambridge Overseas Trust, and from an MRC program grant to SBC. This work was conducted in association with the NIHR CLAHRC for Cambridgeshire and Peterborough NHS Mental Health Trust. 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Hossein Folsom, Timothy D. TI The role of fragile X mental retardation protein in major mental disorders SO NEUROPHARMACOLOGY LA English DT Review DE Fragile X mental retardation protein; Brain; Autism; Schizophrenia; Dendrite; Metabotropic glutamate receptor ID GLUTAMIC-ACID DECARBOXYLASE; MGLUR5 ANTAGONIST MPEP; GABA(A) RECEPTOR; MOUSE MODEL; MESSENGER-RNAS; TREMOR/ATAXIA SYNDROME; HIPPOCAMPAL-NEURONS; DENDRITIC SPINES; GENE-EXPRESSION; KNOCKOUT MICE AB Fragile X mental retardation protein (FMRP) is highly enriched in neurons and binds to approximately 4% of mRNAs in mammalian brain. Its loss is a hallmark of fragile X syndrome (FXS), the most common form of mental retardation. In this review we discuss the mutation in the fragile X mental retardation-1 gene (FMR1), that leads to FXS, the role FMRP plays in neuronal cells, experiments from our own laboratory that demonstrate reductions of FMRP in additional psychiatric disorders (autism, schizophrenia, bipolar disorder, and major depressive disorder), and potential therapies to ameliorate the loss of FMRP. This article is part of a Special Issue entitled 'Trends in Neuropharmacology: In Memory of Erminio Costa'. (C) 2010 Elsevier Ltd. All rights reserved. C1 [Fatemi, S. Hossein; Folsom, Timothy D.] Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. [Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Pharmacol, Minneapolis, MN 55455 USA. [Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, MMC 392,420 Delaware St SE, Minneapolis, MN 55455 USA. EM fatem002@umn.edu; folso013@umn.edu FU NICHD; NIMH [1R015HD052074-04, 3R01HD052074-03S1, 1R01MH086000-01A2]; PHS [R24 MH068855]; National Parkinson Foundation, Inc., Miami, Florida; Autism Tissue Program FX Grant support from NICHD and NIMH for SHF (1R015HD052074-04, 3R01HD052074-03S1, 1R01MH086000-01A2) is greatly appreciated. Human tissue was obtained from the NICHD Brain and Tissue Bank for Developmental Disorders, University of Maryland, Baltimore, MD (The role of the NICHD Brain and Tissue Bank is to distribute tissue, and therefore, cannot endorse the studies performed or the interpretation of results); the Harvard Brain Tissue Resource Center, which is supported in part by PHS grant number R24 MH068855; the Brain Endowment Bank, which is funded in part by the National Parkinson Foundation, Inc., Miami, Florida; the Autism Tissue Program; and The Stanley Medical Research Institute's brain collection are gratefully acknowledged. Reviews of results of FMRP in autism, schizophrenia, bipolar disorder, and major depressive disorder are summarized from the following articles: 1) Fatemi, S.H., Folsom, T.D., Kneeland, R.E., Liesch, S.B., Metabotropic glutamate receptor 5 upregulation in children with autism is associated with underexpression of both Fragile X mental retardation protein and GABAA receptor beta 3 in adults with autism, Anatomical Record, in press, copyright (2011) with permission from John Wiley and Sons and 2) Fatemi, S.H., Kneeland, R.E., Liesch, S.B., Folsom, T.D., Fragile X mental retardation protein levels are decreased in major psychiatric disorders, Schizophrenia Research, 124(1-3):246-247, copyright (2010) with permission from Elsevier. 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Singh, Jorawer S. Whitaker-Azmitia, Patricia M. TI Increased serotonin axons (immunoreactive to 5-HT transporter) in postmortem brains from young autism donors SO NEUROPHARMACOLOGY LA English DT Article DE Cerebral cortex; Stress; Morphometrics; Medial forebrain bundle; Ansa lenticularis ID TRYPTOPHAN-HYDROXYLASE; PERINATAL FACTORS; RAT HIPPOCAMPUS; RISK-FACTORS; CHILDREN; DISORDER; STRESS; SYSTEM; CORTISOL; RECEPTOR AB Imaging studies of serotonin transporter binding or tryptophan retention in autistic patients suggest that the brain serotonin system is decreased. However, treatment with drugs which increase serotonin (5-HT) levels, specific serotonin reuptake inhibitors (SSRIs), commonly produce a worsening of the symptoms. In this study we examined 5-HT axons that were immunoreactive to a serotonin transporter (5-HTT) antibody in a number of postmortem brains from autistic patients and controls with no known diagnosis who ranged in age from 2 to 29 years. Fine, highly branched, and thick straight fibers were found in forebrain pathways (e.g. medial forebrain bundle, stria terminalis and ansa lenticularis). Many immunoreactive varicose fine fibers were seen in target areas (e.g. globus pallidus, amygdala and temporal cortex). Morphometric analysis of the stained axons at all ages studied indicated that the number of serotonin axons was increased in both pathways and terminal regions in cortex from autism donors. Our findings provide morphological evidence to warrant caution when using serotonin enhancing drugs (e.g. SSRIs and receptor agonist) to treat autistic children. This article is part of a Special Issue entitled 'Trends in Neuropharmacology: In Memory of Erminio Costa'. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Azmitia, Efrain C.; Singh, Jorawer S.] NYU, Dept Biol, New York, NY 11791 USA. [Azmitia, Efrain C.; Singh, Jorawer S.] NYU, Dept Psychiat, New York, NY 11791 USA. [Whitaker-Azmitia, Patricia M.] SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. RP Azmitia, EC (reprint author), NYU, Dept Biol, 100 Washington Sq E, New York, NY 11791 USA. 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Stevens, Hanna E. Kocabas, Arif Palejev, Dean Szekely, Anna Grigorenko, Elena L. Weissman, Sherman TI Induced pluripotent stem cells: A new tool to confront the challenge of neuropsychiatric disorders SO NEUROPHARMACOLOGY LA English DT Review DE Neural stem cells; Human; Development; Induced pluripotent stem cell; Neural differentiation; Psychiatry ID COPY NUMBER VARIATION; HUMAN SOMATIC-CELLS; REPROGRAMMING FACTORS; PARKINSONS-DISEASE; HUMAN GENOME; DIRECTED DIFFERENTIATION; NEURAL DIFFERENTIATION; L1 RETROTRANSPOSITION; FAMILIAL DYSAUTONOMIA; STRUCTURAL VARIATION AB Studies in the area of human brain development are critical as research on neurological and psychiatric disorders has advanced, revealing the origins of pathophysiology to be in the earliest developmental stages. Only with a more precise understanding of the genes and environments that influence the brain in these early stages can we address questions about the pathology, diagnosis, prevention and treatment of neuropsychiatric disorders of developmental origin, like autism, schizophrenia, and burette syndrome. A new approach for studying early developmental events is the use of induced pluripotent stem cells (iPSCs). These are cells with wide potential, similar to that of embryonic stem cells, derived from mature somatic cells. We review the protocols used to create iPSCs, including the most efficient and reliable reprogramming strategies available to date for generating iPSCs. In addition, we discuss how this new tool can be applied to neuropsychiatric research. The use of iPSCs can advance our understanding of how genes and gene products are dynamically involved in the formation of unique features of the human brain, and how aberrant genetic variation may interfere with its typical formation. The iPSC technology, if properly applied, can also address basic questions about neural differentiation such as how stem cells can be guided into general and specific neuro-developmental pathways. Current work in neuropsychiatry with iPSCs derived from patients has focused on disorders with specific genetics deficits and those with less-defined origins; it has revealed previously unknown aspects of pathology and potential pharmacological interventions. These exciting advances based on the use of iPSCs hold promise for improving early diagnosis and, possibly, treatment of psychiatric disorders. This article is part of a Special Issue entitled "Special Issue in honor of Dr. Erminio Costa". This article is part of a Special Issue entitled 'Trends in Neuropharmacology: In Memory of Erminio Costa'. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Vaccarino, Flora M.; Stevens, Hanna E.; Kocabas, Arif; Palejev, Dean; Grigorenko, Elena L.] Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. [Vaccarino, Flora M.] Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA. [Vaccarino, Flora M.; Stevens, Hanna E.; Kocabas, Arif; Szekely, Anna; Grigorenko, Elena L.; Weissman, Sherman] Yale Univ, Program Neurodev & Regenerat, New Haven, CT 06520 USA. [Szekely, Anna; Weissman, Sherman] Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA. [Grigorenko, Elena L.] Yale Univ, Sch Med, Dept Psychol, New Haven, CT 06520 USA. [Grigorenko, Elena L.] Yale Univ, Sch Med, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA. RP Vaccarino, FM (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. 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TI 11p14.1 Microdeletions Associated With ADHD, Autism, Developmental Delay, and Obesity SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE microdeletion; developmental delay; ADHD; autism; obesity; WAGR; BDNF; 11p14.1 ID NEUROTROPHIC FACTOR BDNF; IDIOPATHIC MENTAL-RETARDATION; WAGR SYNDROME; ARRAY CGH; CONGENITAL-ANOMALIES; DOWN-REGULATION; ONSET OBESITY; BRAIN; DELETION; MICE AB Genomic copy number imbalances are being increasingly identified as an important cause of intellectual disability and behavioral abnormalities. The typical deletion in WAGR syndrome encompasses the PAX6 andWT1 genes, but larger deletions have been associated with neurobehavioral abnormalities and obesity. We identified four patients with overlapping interstitial deletions on 11p14.1 and extending telomeric to the WAGR critical domain. The minimal overlapping critical chromosomal region was 2.3 Mb at 11p14.1. 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J. Med. Genet. A PD JUN PY 2011 VL 155A IS 6 BP 1472 EP 1475 DI 10.1002/ajmg.a.33977 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 781OV UT WOS:000291944200041 PM 21567917 ER PT J AU Poussaint, TY AF Poussaint, T. Y. TI Hot Topics in Pediatric Neuroradiology SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article ID TRAUMATIC BRAIN-INJURY; DIFFUSION TENSOR; TUBEROUS SCLEROSIS; RESPONSES; AUTISM; CT AB Advances in brain imaging technologies allow a more comprehensive means to investigate pediatric neurological disorders and diseases. This article highlights 5 unique projects in pediatric neuroradiology which may improve our understanding of these disorders. C1 Childrens Hosp, Dept Radiol, Div Neuroradiol, Boston, MA 02115 USA. RP Poussaint, TY (reprint author), Childrens Hosp, Dept Radiol, Div Neuroradiol, 300 Longwood Ave, Boston, MA 02115 USA. 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Rapin, Isabelle Goldman, Sylvie TI Male Predominance in Autism: Neuroendocrine Influences on Arousal and Social Anxiety SO AUTISM RESEARCH LA English DT Review DE behavioral analysis of animal models; developmental neurobiology; sex differences; testosterone; androgen receptor ID PERVASIVE DEVELOPMENTAL DISORDERS; INDUCED NORADRENERGIC ACTIVATION; RIBONUCLEIC-ACID EXPRESSION; NEONATAL AMYGDALA LESIONS; ESTROGEN-RECEPTOR-ALPHA; PLASMA OXYTOCIN LEVELS; BASOLATERAL AMYGDALA; SEROTONIN TRANSPORTER; SPECTRUM DISORDERS; FETAL TESTOSTERONE AB We offer a neurobiologic theory based on animal work that helps account for the conspicuous male predominance in autism spectrum disorders (ASD). In young male animals, testosterone (TST) binds to androgen receptors (AR) in brainstem neurons responsible for enhancing brain arousal. As a consequence, arousal-related neurotransmitters bombard the amygdala hypersensitized by TST acting though AR. Arousal-related inputs are known to prime amygdaloid mechanisms for fear and anxiety, with resultant social avoidance. We hypothesize that similar mechanisms contribute to autism's male predominance and to its defining impaired social skills. The theory rests on two key interacting factors: the molecular effects of TST in genetically vulnerable boys in combination with environmental stresses they experienced in utero, neonatally, or during the first years. We postulate that higher TST levels and, therefore, higher amounts of arousal-related inputs to the amygdala sensitize these genetically vulnerable male infants to very early stresses. In sharp contrast to boys, girls not only do not have high levels of TST-facilitated arousal-causing inputs to the amygdala but they also enjoy the protection afforded by estrogenic hormones, oxytocin, and the oxytocin receptor. This theory suggests that novel technologies applied to the molecular endocrinology of TST's actions through AR will offer new avenues of enquiry into ASD. Since the high male preponderance in autism is important yet understudied, we offer our theory, which is based on detailed neurobehavioral research with animals, to stimulate basic and clinical research in animals and humans and hopefully help develop novel more effective medical treatments for autism. Autism Res 2011,4:163-176. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Goldman, Sylvie] Albert Einstein Coll Med, Kennedy Ctr, Dept Pediat, Bronx, NY 10461 USA. [Pfaff, Donald W.] Rockefeller Univ, New York, NY 10021 USA. [Rapin, Isabelle; Goldman, Sylvie] Yeshiva Univ Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10461 USA. [Rapin, Isabelle; Goldman, Sylvie] Rose F Kennedy Ctr Res Mental Retardat & Human De, Bronx, NY USA. 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PD JUN PY 2011 VL 4 IS 3 BP 163 EP 176 DI 10.1002/aur.191 PG 14 WC Behavioral Sciences; Psychology, Developmental SC Behavioral Sciences; Psychology GA 781CO UT WOS:000291908400001 PM 21465671 ER PT J AU Schoen, E Paul, R Chawarska, K AF Schoen, Elizabeth Paul, Rhea Chawarska, Katarzyna TI Phonology and Vocal Behavior in Toddlers With Autism Spectrum Disorders SO AUTISM RESEARCH LA English DT Article DE autism; phonology; autism spectrum disorders; atypical; vocalizations ID HIGH-FUNCTIONING AUTISM; 2ND YEAR; PRESCHOOL-CHILDREN; ASPERGER-SYNDROME; LANGUAGE; SPEECH; COMMUNICATION; DIAGNOSIS; STABILITY; PROFILES AB The purpose of this study is to examine the phonological and other vocal productions of children, 18-36 months, with autism spectrum disorder (ASD) and to compare these productions to those of age-matched and language-matched controls. Speech samples were obtained from 30 toddlers with ASD, 11 age-matched toddlers and 23 language-matched toddlers during either parent-child or clinician-child play sessions. Samples were coded for a variety of speech-like and nonspeech vocalization productions. Toddlers with ASD produced speech-like vocalizations similar to those of language-matched peers, but produced significantly more atypical nonspeech vocalizations when compared to both control groups. Toddlers with ASD show speech-like sound production that is linked to their language level, in a manner similar to that seen in typical development. The main area of difference in vocal development in this population is in the production of atypical vocalizations. Findings suggest that toddlers with ASDs do not tune into the language model of their environment. Failure to attend to the ambient language environment negatively impacts the ability to acquire spoken language. Autism Res 2011,4:177-188. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Schoen, Elizabeth; Paul, Rhea; Chawarska, Katarzyna] Yale Univ, Yale Child Study Ctr, New Haven, CT 06510 USA. RP Schoen, E (reprint author), Yale Univ, Yale Child Study Ctr, 40 Temple St 7D, New Haven, CT 06510 USA. EM elizabeth.schoen@yale.edu FU National Institute of Mental Health [P50 MH81756]; National Institute of Environmental Health Sciences; National Institute of Child Health and Human Development; National Institute of Neurological Disorders and Stroke [U54 MH66494]; NIDCD [K24 HD045576]; NIMH Autism Center of Excellence [P50 MH81756] FX Grant sponsor: National Institute of Mental Health; Grant number: P50 MH81756; Grant sponsors: National Institute of Environmental Health Sciences; National Institute of Child Health and Human Development; National Institute of Neurological Disorders and Stroke; Grant number: U54 MH66494; Grant sponsor: NIDCD MidCareer Development Award; Grant number: K24 HD045576; Grant sponsor: NIMH Autism Center of Excellence Grant; Grant number: # P50 MH81756. 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TI Contactin 4 as an Autism Susceptibility Locus SO AUTISM RESEARCH LA English DT Article DE contactin 4; autism; autism spectrum disorder; 3p26 deletion; contactins; susceptibility locus ID 3P DELETION SYNDROME; SPECTRUM DISORDERS; HUMAN GENOME; MOLECULAR CHARACTERIZATION; DEVELOPMENTAL DELAY; GENE-EXPRESSION; MUTATIONS; REARRANGEMENTS; ASSOCIATION; SUPERFAMILY AB Structural and sequence variation have been described in several members of the contactin (CNTN) and contactin-associated protein (CNTNAP) gene families in association with neurodevelopmental disorders, including autism. Using array comparative genome hybridization (CGH), we identified a maternally inherited similar to 535 kb deletion at 3p26.3 encompassing the 5' end of the contactin 4 gene (CNTN4) in a patient with autism. Based on this finding and previous reports implicating genomic rearrangements of CNTN4 in autism spectrum disorders (ASDs) and 3p(-) microdeletion syndrome, we undertook sequencing of the coding regions of the gene in a local ASD cohort in comparison with a set of controls. Unique missense variants were identified in 4 of 75 unrelated individuals with ASD, as well as in 1 of 107 controls. All of the amino acid substitutions were nonsynonomous, occurred at evolutionarily conserved positions, and were, thus, felt likely to be deleterious. However, these data did not reach statistical significance, nor did the variants segregate with disease within all of the ASD families. Finally, there was no detectable difference in binding of two of the variants to the interacting protein PTPRG in vitro. Thus, additional larger studies will be necessary to determine whether CNTN4 functions as an autism susceptibility locus in combination with other genetic and/or environmental factors. Autism Res 2011,4:189-199. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Bir, Natalie; Varga, Elizabeth; Alvarez, Carlos E.; Evans, Johnna; Trimarchi, Michael; Cunningham, David; McBride, Kim L.; Herman, Gail E.] Nationwide Childrens Hosp, Ctr Mol & Human Genet, Res Inst, Columbus, OH 43205 USA. [Cottrell, Catherine E.; Thrush, Devon L.; Gastier-Foster, Julie M.] Nationwide Childrens Hosp, Dept Pathol & Lab Med, Columbus, OH 43205 USA. [Alvarez, Carlos E.; Thrush, Devon L.; Butter, Eric M.; Cunningham, David; Gastier-Foster, Julie M.; McBride, Kim L.; Herman, Gail E.] Ohio State Univ, Dept Pediat, Columbus, OH 43205 USA. [Gastier-Foster, Julie M.] Ohio State Univ, Dept Pathol, Columbus, OH 43205 USA. [Bouyain, Samuel] Univ Missouri, Div Mol Biol & Biochem, Sch Biol Sci, Kansas City, MO 64110 USA. [Zernzach, Randall] Dept Pediat, Wright Patterson AFB, OH USA. RP Herman, GE (reprint author), Nationwide Childrens Hosp, Ctr Mol & Human Genet, Res Inst, 700 Childrens Dr,Room W403, Columbus, OH 43205 USA. EM Gail.Herman@nationwidechildrens.org RI Gastier-Foster, Julie/E-3105-2011; McBride, Kim/A-5879-2008 OI McBride, Kim/0000-0002-8407-8942 FU USAF Department of Defense [FA7014-09-2-0004]; NIH [R21 HG004663, R01 GM088806] FX Grant sponsor: USAF Department of Defense grant/Cooperative Agreement; Grant number: FA7014-09-2-0004; Grant sponsor: NIH; Grant numbers: R21 HG004663; R01 GM088806. 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Social-emotional deficits are a hallmark of autism and early neuropathology studies have indicated involvement of the limbic system. Imaging studies demonstrate abnormal activation of the posterior cingulate cortex (PCC), a component of the limbic system. Abnormal activation has also been noted in the fusiform gyrus (FFG), a region important for facial recognition and a key element in social interaction. A potential imbalance between excitatory and inhibitory interneurons in the cortex may contribute to altered information processing in autism. Furthermore, reduced numbers of GABA receptors have previously been reported in the autistic brain. Thionin-stained sections were used to qualitatively assess cytoarchitectonic patterning and quantitatively determine the density of neurons and immunohistochemistry was used to determine the densities of a subset of GABAergic interneurons utilizing parvalbumin- and calbindin-immunoreactivity. In autism, the PCC displayed altered cytoarchitecture with irregularly distributed neurons, poorly demarcated layers IV and V. and increased presence of white matter neurons. In contrast, no neuropathology was observed in the FFG. There was no significant difference in the density of thionin, parvalbumin, or calbindin interneurons in either region and there was a trend towards a reduced density of calbindin neurons in the PCC. This study highlights the presence of abnormal findings in the PCC, which appear to be developmental in nature and could affect the local processing of social-emotional behaviors as well as functioning of interrelated areas. Autism Res 2011,4:200-211. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Oblak, Adrian L.; Rosene, Douglas L.; Kemper, Thomas L.; Bauman, Margaret L.; Blatt, Gene J.] Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. 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PD JUN PY 2011 VL 4 IS 3 BP 200 EP 211 DI 10.1002/aur.188 PG 12 WC Behavioral Sciences; Psychology, Developmental SC Behavioral Sciences; Psychology GA 781CO UT WOS:000291908400004 PM 21360830 ER PT J AU Estes, A Shaw, DWW Sparks, BF Friedman, S Giedd, JN Dawson, G Bryan, M Dager, SR AF Estes, Annette Shaw, Dennis W. W. Sparks, Bobbi F. Friedman, Seth Giedd, Jay N. Dawson, Geraldine Bryan, Matthew Dager, Stephen R. TI Basal Ganglia Morphometry and Repetitive Behavior in Young Children with Autism Spectrum Disorder SO AUTISM RESEARCH LA English DT Article DE neuroimaging; preschoolers < pediatrics; clinical psychology; repetitive behavior; autism spectrum disorders ID HIGH-FUNCTIONING AUTISM; CAUDATE-NUCLEUS; BRAIN SIZE; AGE; PATTERNS; VOLUME; INTERESTS; INFANCY; LIFE; MRI AB We investigated repetitive and stereotyped behavior (RSB) and its relationship to morphometric measures of the basal ganglia and thalami in 3- to 4-year-old children with autism spectrum disorder (ASD; n = 77) and developmental delay without autism (DD; n = 34). Children were assessed through clinical evaluation and parent report using RSB-specific scales extracted from the Autism Diagnostic Observation Schedule (ADOS), the Autism Diagnostic Interview, and the Aberrant Behavior Checklist. A subset of children with ASD (n = 45), DD (n = 14), and a group of children with typical development (TD; n = 25) were also assessed by magnetic resonance imaging. Children with ASD demonstrated elevated RSB across all measures compared to children with DD. Enlargement of the left and right striatum, more specifically the left and right putamen, and left caudate, was observed in the ASD compared to the TD group. However, nuclei were not significantly enlarged after controlling for cerebral volume. The DD group, in comparison to the ASD group, demonstrated smaller thalami and basal ganglia regions even when scaled for cerebral volume, with the exception of the left striatum, left putamen, and right putamen. Elevated RSB, as measured by the ADOS, was associated with decreased volumes in several brain regions: left thalamus, right globus pallidus, left and right putamen, right striatum and a trend for left globus pallidus and left striatum within the ASD group. These results confirm earlier reports that RSB is common early in the clinical course of ASD and, furthermore, demonstrate that such behaviors may be associated with decreased volumes of the basal ganglia and thalamus. Autism Res 2011,4:212-220. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Estes, Annette] Univ Washington, UW Autism Ctr, Dept Speech & Hearing Sci, Seattle, WA 98195 USA. [Estes, Annette; Dager, Stephen R.] Univ Washington, Autism Ctr, Seattle, WA 98195 USA. [Shaw, Dennis W. W.; Sparks, Bobbi F.; Friedman, Seth; Dager, Stephen R.] Univ Washington, Dept Radiol, Seattle, WA 98195 USA. [Giedd, Jay N.] NIMH, Bethesda, MD 20892 USA. [Dawson, Geraldine] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. [Dawson, Geraldine] Autism Speaks, New York, NY USA. [Bryan, Matthew] Univ Washington, Dept Biostat, Seattle, WA 98195 USA. RP Estes, A (reprint author), Univ Washington, UW Autism Ctr, Dept Speech & Hearing Sci, Box 357920, Seattle, WA 98195 USA. EM estesa@u.washington.edu RI Giedd, Jay/A-3080-2008; Giedd, Jay/B-7302-2012 OI Giedd, Jay/0000-0003-0827-3460 FU National Institute of Child Health and Human Development; National Institute on Deafness and Communication Disorders [U19HD34565]; National Institute of Child Health and Human Development [P50HD55782]; National Institute of Child Health and Human Development which is part of the Autism Centers of Excellence (ACE) [P50HD55782] FX Grant sponsors: National Institute of Child Health and Human Development; National Institute on Deafness and Communication Disorders; Grant number: U19HD34565; Grant sponsor: National Institute of Child Health and Human Development; Grant number: P50HD55782.This research was funded by a program project grant from the National Institute of Child Health and Human Development and the National Institute on Deafness and Communication Disorders (U19HD34565) which is part of the NICHD Collaborative Program of Excellence in Autism (CPEA) and a program project grant from the National Institute of Child Health and Human Development (P50HD55782) which is part of the Autism Centers of Excellence (ACE). 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PD JUN PY 2011 VL 4 IS 3 BP 212 EP 220 DI 10.1002/aur.193 PG 9 WC Behavioral Sciences; Psychology, Developmental SC Behavioral Sciences; Psychology GA 781CO UT WOS:000291908400005 PM 21480545 ER PT J AU Griswold, AJ Ma, DQ Sacharow, SJ Robinson, JL Jaworski, JM Wright, HH Abramson, RK Lybaek, H Oyen, N Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Griswold, Anthony J. Ma, Deqiong Sacharow, Stephanie J. Robinson, Joycelyn L. Jaworski, James M. Wright, Harry H. Abramson, Ruth K. Lybaek, Helle Oyen, Nina Cuccaro, Michael L. Gilbert, John R. Pericak-Vance, Margaret A. TI A De Novo 1.5 Mb Microdeletion on Chromosome 14q23.2-23.3 in a Patient With Autism and Spherocytosis SO AUTISM RESEARCH LA English DT Article DE genetics; copy number variation < molecular genetics; molecular genetics ID COPY NUMBER VARIATION; NUCLEOTIDE EXCHANGE-FACTOR; LINKED MENTAL-RETARDATION; HEREDITARY SPHEROCYTOSIS; SPECTRUM DISORDERS; BETA-SPECTRIN; RETT-SYNDROME; MUTATIONS; GENE; IDENTIFICATION AB Autism is a neuro-developmental disorder characterized by deficits in social interaction and communication as well as restricted interests or repetitive behaviors. Cytogenetic studies have implicated large chromosomal aberrations in the etiology of approximately 5-7% of autism patients, and the recent advent of array-based techniques allows the exploration of submicroscopic copy number variations (CNVs). We genotyped a 14-year-old boy with autism, spherocytosis and other physical dysmorphia, his parents, and two non-autistic siblings with the Illumina Human 1M Beadchip as part of a study of the molecular genetics of autism and determined copy number variants using the PennCNV algorithm. We identified and validated a de novo 1.5 Mb microdeletion of 14q23.2-23.3 in our autistic patient. This region contains 15 genes, including spectrin beta (SPTB), encoding a cytoskeletal protein previously associated with spherocytosis, methylenetetrahydrofolate dehydrogenase 1 (MTHED1), a folate metabolizing enzyme previously associated with bipoloar disorder and schizophrenia, pleckstrin homology domain-containing family G member 3 (PLEKHG3), a guanide nucleotide exchange enriched in the brain, and churchill domain containing protein 1 (CHURC1), homologs of which regulate neuronal development in model organisms. While a similar deletion has previously been reported in a family with spherocytosis, severe learning disabilities, and mild mental retardation, this is the first implication of chr14q23.2-23.3 in the etiology of autism and points to MTHED1, PLEKHG3, and CHURC1 as potential candidate genes contributing to autism risk. Autism Res 2011,4:221-227. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Griswold, Anthony J.; Ma, Deqiong; Robinson, Joycelyn L.; Jaworski, James M.; Cuccaro, Michael L.; Gilbert, John R.; Pericak-Vance, Margaret A.] Univ Miami, John P Hussman Inst Human Genom, Miami, FL 33136 USA. [Sacharow, Stephanie J.] Univ Miami, Dept Human Genet, Miller Sch Med, Miami, FL 33136 USA. [Wright, Harry H.; Abramson, Ruth K.] Univ S Carolina, Sch Med, Columbia, SC USA. [Lybaek, Helle; Oyen, Nina] Haukeland Hosp, Ctr Med Genet & Mol Med, N-5021 Bergen, Norway. RP Pericak-Vance, MA (reprint author), Univ Miami, John P Hussman Inst Human Genom, 1501 NW 10th Ave, Miami, FL 33136 USA. EM mpericak@med.miami.edu RI Griswold, Anthony/B-7507-2012 FU National Institute of Mental Health [5R01MH080647-13]; National Institute of Neurological Disorders and Stroke [5P01NS026630-20]; Hussman Foundation FX Grant sponsor: National Institute of Mental Health; Grant number: 5R01MH080647-13; Grant sponsor: National Institute of Neurological Disorders and Stroke; Grant number: 5P01NS026630-20; Grant sponsor: The Hussman Foundation. 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PD JUN PY 2011 VL 4 IS 3 BP 221 EP 227 DI 10.1002/aur.186 PG 7 WC Behavioral Sciences; Psychology, Developmental SC Behavioral Sciences; Psychology GA 781CO UT WOS:000291908400006 PM 21360829 ER PT J AU Kantojarvi, K Kotala, I Rehnstrom, K Ylisaukko-oja, T Vanhala, R von Wendt, TN von Wendt, L Jarvela, I AF Kantojarvi, Katri Kotala, Ilona Rehnstrom, Karola Ylisaukko-oja, Tero Vanhala, Raija von Wendt, Taina Nieminen von Wendt, Lennart Jarvela, Irma TI Fine Mapping of Xq11.1-q21.33 and Mutation Screening of RPS6KA6, ZNF711, ACSL4, DLG3, and IL1RAPL2 for Autism Spectrum Disorders (ASD) SO AUTISM RESEARCH LA English DT Article DE ACSL4; autism spectrum disorders; DLG3; gene; IL1RAPL2; linkage; RPS6KA6; single nucleotide polymorphism; ZNF711; XLMR ID LINKED MENTAL-RETARDATION; X-CHROMOSOME; GENOMEWIDE SCREEN; SUSCEPTIBILITY LOCI; LINKAGE ANALYSIS; GENETIC-LINKAGE; FAMILY; REARRANGEMENTS; VARIANTS; KINASE AB About 80% of cases with autism express intellectual disability. Both in autism and in mental retardation without autism the majority of the cases are males, suggesting a X-chromosomal effect. In fact, some molecular evidence has been obtained for a common genetic background for autism spectrum disorders (ASD) and X-linked mental retardation (XLMR). In several genome-wide scans (GWS), evidence for linkage at X-chromosome has been reported including the GWS of Finnish ASD families with the highest multipoint lod score (MLS) of 2.75 obtained close to DXS7132 at Xq11.1. To further dissect the relationship between autism and genes implicated in XLMR, we have fine-mapped Xq11.1-q21.33 and analyzed five candidate genes in the region. We refined the region using 26 microsatellite markers and linkage analysis in 99 Finnish families with ASD. The most significant evidence for linkage was observed at DXS1225 on Xq21.1 with a nonparametric multipoint NPL(all) value of 3.43 (P = 0.0004). We sequenced the coding regions and splice sites of RPS6KA6 and ZNF711 residing at the peak region in 42 male patients from families contributing to the linkage. We also analyzed ACSL4 and DLG3, which have previously been known to cause XLMR and IL1RAPL2, a homologous gene for IL1RAPL1 that is mutated in autism and XLMR. A total of six novel and 11 known single nucleotide polymorphisms were identified. Further studies are warranted to analyze the candidate genes at Xq11.1-q21.33. Autism Res 2011,4:228-233. (c) 2011 International Society for Autism Research, Wiley Periodicals, Inc. C1 [Kantojarvi, Katri; Kotala, Ilona; Rehnstrom, Karola; Ylisaukko-oja, Tero; Jarvela, Irma] Univ Helsinki, Dept Med Genet, Haartman Inst, Helsinki 00251, Finland. [Rehnstrom, Karola; Ylisaukko-oja, Tero] Inst Welf & Hlth, Dept Mol Med, Helsinki, Finland. [Vanhala, Raija; von Wendt, Taina Nieminen; von Wendt, Lennart] Hosp Children & Adolescents, Dept Child Neurol, Helsinki, Finland. [Jarvela, Irma] Univ Helsinki, Cent Hosp, Mol Genet Lab, Helsinki, Finland. RP Jarvela, I (reprint author), Univ Helsinki, Dept Med Genet, Haartman Inst, PL104, Helsinki 00251, Finland. EM irma.jarvela@kolumbus.fi RI Jarvela, Irma/L-5836-2013 FU Helsinki University [TYH7227]; Academy of Finland Helsinki Finland; Medical Society of Finland, Helsinki, Finland; Cure Autism Now; European Union [512158] FX Grant sponsor: Helsinki University Hospital Research Funding; Grant number: #TYH7227; Grant sponsors: The Academy of Finland Helsinki Finland; The Medical Society of Finland, Helsinki, Finland; Cure Autism Now; European Union; Grant number: #512158. 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PD JUN PY 2011 VL 4 IS 3 BP 228 EP 233 DI 10.1002/aur.187 PG 6 WC Behavioral Sciences; Psychology, Developmental SC Behavioral Sciences; Psychology GA 781CO UT WOS:000291908400007 PM 21384559 ER PT J AU Miyajima, T Kimura, N Kumada, T Oda, N Shimomura, H Fujii, T AF Miyajima, Tomoko Kimura, Nobusuke Kumada, Tomohiro Oda, Nozomi Shimomura, Hideki Fujii, Tatsuya TI Epilepsy in pervasive developmental disorder without brain MRI abnormalities SO BRAIN & DEVELOPMENT LA English DT Article DE Epilepsy; Pervasive developmental disorder; Autism; Mental retardation; MRI abnormalities ID AUTISM SPECTRUM DISORDERS; ACTIVE EPILEPSY; CHILDREN AB Background: Epilepsy has been reported in patients with pervasive developmental disorder (PDD), with an incidence ranging from 5% to 40%; however most of the studies included patients with brain magnetic resonance imaging (MRI) abnormalities (e.g., tuberous sclerosis) and patients with epilepsy whose seizure onset was in the first year of life. Methods: We retrospectively examined 67 patients (45 males, 22 females) with PDD and epilepsy, who did not have brain MRI abnormalities. Patients who had seizures in the first year of life were excluded. We divided the patients into two groups: group A included 34 patients with an IQ < 50, and group B included 33 patients with an IQ >= 50. Results: The median age of epilepsy onset was higher in group A than group B (8.8 vs. 5.2 years, P < 0.01). Only one patient (3%) in group A and nine patients (27%) in group B were classified with generalized epilepsy (P < 0.05). At the last observation, 16 patients (47%) in group A and 25 patients (76%) in group B were seizure-free for >= 1 year (not statistically significant). Conclusion: The relationship between PDD and epilepsy may be different between patients with lower (group A) and higher (group B) IQs in patients who do not have brain MRI abnormalities. (C) 2010 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved. C1 [Miyajima, Tomoko; Kimura, Nobusuke; Kumada, Tomohiro; Oda, Nozomi; Shimomura, Hideki; Fujii, Tatsuya] Shiga Med Ctr Children, Dept Pediat, Shiga, Japan. RP Miyajima, T (reprint author), Shiga Med Ctr Children, Dept Pediat, Shiga, Japan. 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PD JUN PY 2011 VL 33 IS 6 BP 504 EP 507 DI 10.1016/j.braindev.2010.08.014 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 774UY UT WOS:000291413300010 PM 20863637 ER PT J AU Ghafoor, M Halsnad, M Grew, N Asokan, S Ajit, P AF Ghafoor, M. Halsnad, M. Grew, N. Asokan, S. Ajit, P. TI RESTORATION FRAGMENTS SO BRITISH DENTAL JOURNAL LA English DT Letter ID OCCUPATIONAL-THERAPY; INTERVENTIONS; AUTISM CR Case-Smith J, 2008, AM J OCCUP THER, V62, P416 Gordon C. Y., 1996, OCCUPATIONAL THERAPY, P141 ORNITZ EM, 1973, CALIF MED, V118, P21 Polatajko HJ, 2010, AM J OCCUP THER, V64, P415, DOI 10.5014/ajot.2010.09072 NR 4 TC 1 Z9 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0610 J9 BRIT DENT J JI Br. Dent. J. PD JUN PY 2011 VL 210 IS 12 BP 558 EP 559 DI 10.1038/sj.bdj.2011.491 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 782RJ UT WOS:000292027400009 PM 21701452 ER PT J AU Marzullo-Kerth, D Reeve, SA Reeve, KF Townsend, DB AF Marzullo-Kerth, Denise Reeve, Sharon A. Reeve, Kenneth F. Townsend, Dawn B. TI USING MULTIPLE-EXEMPLAR TRAINING TO TEACH A GENERALIZED REPERTOIRE OF SHARING TO CHILDREN WITH AUTISM SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; generalization; multiple-exemplar training; social behavior; sharing; video modeling ID PRESCHOOL-CHILDREN; VIDEO; PREFERENCE; BEHAVIOR; SKILLS AB The current study examined the utility of multiple-exemplar training to teach children with autism to share. Stimuli from 3 of 4 categories were trained using a treatment package of video modeling, prompting, and reinforcement. Offers to share increased for all 3 children following the introduction of treatment, with evidence of skill maintenance. In addition, within-stimulus-category generalization of sharing was evident for all participants, although only 1 participant demonstrated across-category generalization of sharing. Offers to share occurred in a novel setting, with familiar and novel stimuli, and in the presence of novel adults and peers for all participants during posttreatment probes. C1 [Reeve, Sharon A.] Caldwell Coll, Dept Appl Behav Anal, Caldwell, NJ 07006 USA. RP Reeve, SA (reprint author), Caldwell Coll, Dept Appl Behav Anal, 120 Bloomfield Ave, Caldwell, NJ 07006 USA. 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PD SUM PY 2011 VL 44 IS 2 BP 279 EP 294 DI 10.1901/jaba.2011.44-279 PG 16 WC Psychology, Clinical SC Psychology GA 782LW UT WOS:000292012200004 PM 21709784 ER PT J AU Reichow, B Wolery, M AF Reichow, Brian Wolery, Mark TI COMPARISON OF PROGRESSIVE PROMPT DELAY WITH AND WITHOUT INSTRUCTIVE FEEDBACK SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism spectrum disorders; progressive prompt delay; instructive feedback; instructional efficiency; response prompting ID CHILDREN; AUTISM AB We examined the effectiveness and efficiency of 2 instructional arrangements using progressive prompt delay (PPD) with 3 young children with autism and 1 child with developmental delays. Specifically, we compared PPD with instructive feedback (IF) to PPD without IF in an adapted alternating treatment design. The results suggested that (a) children with autism and developmental delays can learn when PPD is used with IF, (b) IF can be an effective method of instruction for young children with autism and developmental delays, and (c) the combination of PPD and IF can increase the efficiency of instruction. Data collected 8 to 9 weeks after instruction ended showed that participants maintained mastery of 58% to 92% of the acquired behaviors. We discuss these results within the constraints and limitations of the data and recommend areas for future research. C1 [Reichow, Brian; Wolery, Mark] Vanderbilt Univ, Nashville, TN 37235 USA. RP Reichow, B (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06520 USA. 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PD SUM PY 2011 VL 44 IS 2 BP 327 EP 340 DI 10.1901/jaba.2011.44-327 PG 14 WC Psychology, Clinical SC Psychology GA 782LW UT WOS:000292012200008 PM 21709788 ER PT J AU Dittlinger, LH Lerman, DC AF Dittlinger, Laura Harper Lerman, Dorothea C. TI FURTHER ANALYSIS OF PICTURE INTERFERENCE WHEN TEACHING WORD RECOGNITION TO CHILDREN WITH AUTISM SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE blocking; extrastimulus prompts; overshadowing; picture prompts; sight-word recognition ID OVER-SELECTED STIMULI; BLOCKING; EXTINCTION; ATTENTION; OVERSELECTIVITY; ASSOCIATION; PIGEON AB Previous research indicates that pairing pictures with associated words when teaching sight-word reading may hinder acquisition (e.g., Didden, Prinsen, & Sigafoos, 2000; Singh & Solman, 1990; Solman & Singh, 1992). The purpose of the current study was to determine whether this phenomenon was due to a previously learned association between the spoken word and picture (i.e., blocking) or due to the mere presence of a picture as an extrastimulus prompt (i.e., overshadowing). Three participants were taught to recognize words that were presented alone or paired with pictures that the participants either could or could not identify prior to training. All participants learned the words more quickly when they were presented alone rather than with pictures, regardless of their prior learning history with respect to pictures representing the words. This finding is consistent with the phenomenon of overshadowing. Nonetheless, consistent with blocking, all participants also acquired the words presented alone more quickly if they could not identify the associated pictures prior to training. Together, these findings have important implications for using prompts when teaching skills to individuals with developmental disabilities. C1 [Lerman, Dorothea C.] Univ Houston Clear Lake, Dept Psychol, Houston, TX 77058 USA. RP Lerman, DC (reprint author), Univ Houston Clear Lake, Dept Psychol, 2700 Bay Area Blvd,Box 245, Houston, TX 77058 USA. 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Appl. Behav. Anal. PD SUM PY 2011 VL 44 IS 2 BP 341 EP 349 DI 10.1901/jaba.2011.44-341 PG 9 WC Psychology, Clinical SC Psychology GA 782LW UT WOS:000292012200009 PM 21709789 ER PT J AU Betz, AM Higbee, TS Kelley, KN Sellers, TP Pollard, JS AF Betz, Alison M. Higbee, Thomas S. Kelley, Kristen N. Sellers, Tyra P. Pollard, Joy S. TI INCREASING RESPONSE VARIABILITY OF MAND FRAMES WITH SCRIPT TRAINING AND EXTINCTION SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE extinction; mands; script training; variability; verbal behavior ID MECHANISMS; DIVERSITY; AUTISM AB We examined the effects of script training and extinction on response variability of mand frames used by children with autism. Results demonstrated that extinction following script training was effective for increasing variability for 2 of the 3 participants. C1 [Higbee, Thomas S.] Utah State Univ, Dept Special Educ & Rehabil, Logan, UT 84322 USA. RP Higbee, TS (reprint author), Utah State Univ, Dept Special Educ & Rehabil, 2865 Old Main Hill, Logan, UT 84322 USA. EM tom.higbee@usu.edu RI Higbee, Thomas/F-5157-2010 CR Carr JE, 2000, J APPL BEHAV ANAL, V33, P353, DOI 10.1901/jaba.2000.33-353 FRITH U, 1972, J AUTISM CHILD SCHIZ, V2, P160, DOI 10.1007/BF01537569 GOETZ EM, 1973, J APPL BEHAV ANAL, V6, P209, DOI 10.1901/jaba.1973.6-209 Harding JW, 2004, J APPL BEHAV ANAL, V37, P185, DOI 10.1901/jaba.2004.37-185 LALLI JS, 1994, J APPL BEHAV ANAL, V27, P735, DOI 10.1901/jaba.1994.27-735 Lee R, 2007, PSYCHOL REC, V57, P429 McClannahan L. E., 2005, TEACHING CONVERSATIO Napolitano DA, 2010, J APPL BEHAV ANAL, V43, P265, DOI 10.1901/jaba.2010.43-265 NR 8 TC 3 Z9 3 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2011 VL 44 IS 2 BP 357 EP 362 DI 10.1901/jaba.2011.44-357 PG 6 WC Psychology, Clinical SC Psychology GA 782LW UT WOS:000292012200012 PM 21709793 ER PT J AU Schiff, A Tarbox, J Lanagan, T Farag, P AF Schiff, Averil Tarbox, Jonathan Lanagan, Taira Farag, Peter TI ESTABLISHING COMPLIANCE WITH LIQUID MEDICATION ADMINISTRATION IN A CHILD WITH AUTISM SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE liquid medication; autism; stimulus fading ID FOOD REFUSAL; REINFORCEMENT AB Children with autism often display difficulty with swallowing pills and liquid medications. In the current study, stimulus fading and positive reinforcement established compliance with liquid medication administration in a young boy with autism. The boy's mother eventually administered liquid medication on her own. RP Tarbox, J (reprint author), 19019 Ventura Blvd,3rd Floor, Tarzana, CA 91356 USA. EM j.tarbox@centerforautism.com CR Andersen Ornulf, 1995, Tidsskrift for den Norske Laegeforening, V115, P947 DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 Ghuman JK, 2004, J CHILD ADOL PSYCHOP, V14, P601, DOI 10.1089/cap.2004.14.601 Kerwin ME, 1999, J PEDIATR PSYCHOL, V24, P193, DOI 10.1093/jpepsy/24.3.193 Patel MR, 2001, J APPL BEHAV ANAL, V34, P357, DOI 10.1901/jaba.2001.34-357 Piazza CC, 2003, J APPL BEHAV ANAL, V36, P309, DOI 10.1901/jaba.2003.36-309 Schopler E., 1988, CHILDHOOD AUTISM RAT Shabani DB, 2006, J APPL BEHAV ANAL, V39, P449, DOI 10.1901/jaba.2006.30-05 Wilder DA, 2005, J APPL BEHAV ANAL, V38, P549, DOI 10.1901/jaba.2005.132-04 NR 9 TC 2 Z9 2 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2011 VL 44 IS 2 BP 381 EP 385 DI 10.1901/jaba.2011.44-381 PG 5 WC Psychology, Clinical SC Psychology GA 782LW UT WOS:000292012200016 PM 21709797 ER PT J AU Simpson, RL Mundschenk, NA Heflin, LJ AF Simpson, Richard L. Mundschenk, Nancy A. Heflin, L. Juane TI Issues, Policies, and Recommendations for Improving the Education of Learners With Autism Spectrum Disorders SO JOURNAL OF DISABILITY POLICY STUDIES LA English DT Article DE autism policy; autism issues; autism recommendations ID YOUNG-CHILDREN; BEHAVIORAL TREATMENT; ACADEMIC ENGAGEMENT; INCLUSIVE SETTINGS; REGULAR CLASSROOMS; SERVICE DELIVERY; SCHOOL STUDENTS; LEGAL ANALYSIS; DISABILITIES; TEACHERS AB Children and youth with autism spectrum disorders (ASD) create significant challenges to educators and the educational system not only based on their ever-increasing numbers but also because of the questions and debates surrounding how best to provide them an appropriate and effective education. These issues include the skills, knowledge, and professional credentials of educators who teach learners with ASD, which settings are best suited for their educational experiences, and what and how children and youth with ASD should be taught. In this article the authors address these three core elements that underpin the education of pupils with ASD and offer recommendations for improving the present system. C1 [Simpson, Richard L.] Univ Kansas, Dept Special Educ, Lawrence, KS 66045 USA. [Mundschenk, Nancy A.] So Illinois Univ, Carbondale, IL 62901 USA. [Heflin, L. Juane] Georgia State Univ, Teacher Preparat Program ASD, Atlanta, GA 30303 USA. RP Simpson, RL (reprint author), Univ Kansas, Dept Special Educ, JR Pearson Hall,1122 W Campus Rd, Lawrence, KS 66045 USA. 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PD JUN PY 2011 VL 22 IS 1 BP 3 EP 17 DI 10.1177/1044207310394850 PG 15 WC Rehabilitation SC Rehabilitation GA 054TS UT WOS:000312367500001 ER PT J AU Bhat, A Palatinus, K Menacherry, P Mhadeshwar, A Marsh, K AF Bhat, Anjana Palatinus, Kinga Menacherry, Phoebe Mhadeshwar, Ashish Marsh, Kerry TI Self- and social coordination in typically developing children and children with autism spectrum disorders (ASDs)/ADHD SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 [Bhat, Anjana; Palatinus, Kinga; Menacherry, Phoebe; Mhadeshwar, Ashish; Marsh, Kerry] Univ Connecticut, Storrs, CT 06269 USA. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2011 VL 33 SU S BP S26 EP S27 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 777LN UT WOS:000291619700049 ER PT J AU Julie, G Hamdan, FF Rouleau, GA AF Julie, Gauthier Hamdan, Fadi F. Rouleau, Guy A. TI A Strategy to Identify de Novo Mutations in Common Disorders such as Autism and Schizophrenia SO JOVE-JOURNAL OF VISUALIZED EXPERIMENTS LA English DT Article DE Medicine; Issue 52; de novo mutation; complex diseases; schizophrenia; autism; rare variations; DNA sequencing AB There are several lines of evidence supporting the role of de novo mutations as a mechanism for common disorders, such as autism and schizophrenia. First, the de novo mutation rate in humans is relatively high, so new mutations are generated at a high frequency in the population. However, de novo mutations have not been reported in most common diseases. Mutations in genes leading to severe diseases where there is a strong negative selection against the phenotype, such as lethality in embryonic stages or reduced reproductive fitness, will not be transmitted to multiple family members, and therefore will not be detected by linkage gene mapping or association studies. The observation of very high concordance in monozygotic twins and very low concordance in dizygotic twins also strongly supports the hypothesis that a significant fraction of cases may result from new mutations. Such is the case for diseases such as autism and schizophrenia. Second, despite reduced reproductive fitness(1) and extremely variable environmental factors, the incidence of some diseases is maintained worldwide at a relatively high and constant rate. This is the case for autism and schizophrenia, with an incidence of approximately 1% worldwide. Mutational load can be thought of as a balance between selection for or against a deleterious mutation and its production by de novo mutation. Lower rates of reproduction constitute a negative selection factor that should reduce the number of mutant alleles in the population, ultimately leading to decreased disease prevalence. These selective pressures tend to be of different intensity in different environments. Nonetheless, these severe mental disorders have been maintained at a constant relatively high prevalence in the worldwide population across a wide range of cultures and countries despite a strong negative selection against them(2). This is not what one would predict in diseases with reduced reproductive fitness, unless there was a high new mutation rate. Finally, the effects of paternal age: there is a significantly increased risk of the disease with increasing paternal age, which could result from the age related increase in paternal de novo mutations. This is the case for autism and schizophrenia(3). The male-to-female ratio of mutation rate is estimated at about 4-6:1, presumably due to a higher number of germ-cell divisions with age in males. Therefore, one would predict that de novo mutations would more frequently come from males, particularly older males(4). A high rate of new mutations may in part explain why genetic studies have so far failed to identify many genes predisposing to complexes diseases genes, such as autism and schizophrenia, and why diseases have been identified for a mere 3% of genes in the human genome. Identification for de novo mutations as a cause of a disease requires a targeted molecular approach, which includes studying parents and affected subjects. The process for determining if the genetic basis of a disease may result in part from de novo mutations and the molecular approach to establish this link will be illustrated, using autism and schizophrenia as examples. C1 [Julie, Gauthier] Univ Montreal, CHUM Res Ctr, Ctr Excellence Neur, Montreal, PQ H3C 3J7, Canada. [Julie, Gauthier] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada. [Hamdan, Fadi F.] Univ Montreal, CHU St Justine, Ctr Excellence Neur, Montreal, PQ H3C 3J7, Canada. [Hamdan, Fadi F.] Univ Montreal, CHUM Notre Dame Res Ctr, Montreal, PQ H3C 3J7, Canada. [Rouleau, Guy A.] Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada. RP Rouleau, GA (reprint author), Univ Montreal, CHUM Res Ctr, Ctr Excellence Neur, Montreal, PQ H3C 3J7, Canada. EM guy.rouleau@umontreal.ca FU Genome Canada; Genome Quebec; Universite de Montreal; Canadian Foundation for Innovation FX We thanks our funding sources Genome Canada and Genome Quebec, and Universite de Montreal as well as funding from the Canadian Foundation for Innovation for funding our 'Synapse to Disease' (S2D) project. CR Bassett AS, 1996, SCHIZOPHR RES, V21, P151, DOI 10.1016/0920-9964(96)00018-7 DeLisi LE, 2002, AM J PSYCHIAT, V159, P803, DOI 10.1176/appi.ajp.159.5.803 Gauthier J., 2010, P NATL ACAD IN PRESS Jablensky A, 1992, Psychol Med Monogr Suppl, V20, P1 Krawczak M, 1998, AM J HUM GENET, V63, P474, DOI 10.1086/301965 Malaspina Dolores, 2002, CNS Spectr, V7, P26 Piton A, 2008, HUM MOL GENET, V17, P3965, DOI 10.1093/hmg/ddn300 NR 7 TC 1 Z9 1 PU JOURNAL OF VISUALIZED EXPERIMENTS PI CAMBRIDGE PA 1 ALEWIFE CENTER, STE 200, CAMBRIDGE, MA 02140 USA SN 1940-087X J9 JOVE-J VIS EXP JI J. Vis. Exp. PD JUN PY 2011 IS 52 DI 10.3791/2534 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA V36MB UT WOS:000209214900002 ER PT J AU Yanardag, M Birkan, B Yilmaz, I Konukman, F Agbuga, B Lieberman, L AF Yanardag, Mehmet Birkan, Bunyamin Yilmaz, Ilker Konukman, Ferman Agbuga, Bulent Lieberman, Lauren TI THE EFFECTS OF LEAST-TO-MOST PROMPTING PROCEDURE IN TEACHING BASIC TENNIS SKILLS TO CHILDREN WITH AUTISM SO KINESIOLOGY LA English DT Article DE autism; least-to-most prompt; basic tennis skills ID CONSTANT-TIME DELAY; SPECTRUM DISORDERS; RETARDED-ADULTS; LEISURE SKILLS; PLAY; COORDINATION; DISABILITIES; EXERCISE; BEHAVIOR; AGE AB In the present study, the effects of a least-to-most prompting procedure in teaching basic tennis skills (i.e. tennis ball dribble, air dribble and dribble the lines drills) to children with autism were investigated. A single-subject multiple-probe design with probe conditions across behaviors was used. Participants were four male children with autism, aged 7-9 years. Data were collected over the course of 6 weeks, five times a week, an hour per session. Inter-observer reliability data of the study was determined as 93% on probes and 100% on teaching sessions for participant one, 96% on probes and 100% on teaching sessions for participant two, 90% on probes and 100% on teaching sessions for participant three, and 93% on probes and 100% on teaching sessions for participant four. Procedural reliability showed that the trainer implemented the planned steps with 100% accuracy for all participants. Results revealed that least to most prompting was an effective instructional approach and all subjects increased their basic tennis skills considerably during intervention. C1 [Yanardag, Mehmet] Anadolu Univ, Res Inst Handicapped, TR-26140 Eskisehir, Turkey. [Yilmaz, Ilker] Anadolu Univ, Sch Phys Educ & Sports, Eskisehir, Turkey. 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Minshew, Nancy J. Just, Marcel Adam TI Autonomy of lower-level perception from global processing in autism: Evidence from brain activation and functional connectivity SO NEUROPSYCHOLOGIA LA English DT Article DE Autism; Local; Global; fMRI; Functional connectivity ID EMBEDDED FIGURES TASK; MEDIAL FRONTAL-CORTEX; WORKING-MEMORY; VISUAL-SEARCH; CORTICAL UNDERCONNECTIVITY; SENTENCE COMPREHENSION; SPECTRUM DISORDERS; WEAK COHERENCE; PERFORMANCE; FMRI AB Previous behavioral studies have shown that individuals with autism are less hindered by interference from global processing during the performance of lower-level perceptual tasks, such as finding embedded figures. The primary goal of this study was to examine the brain manifestation of such atypicality in high-functioning autism using fMRI. Fifteen participants with high-functioning autism and fifteen age-and IQ-matched typical controls were asked to perform a lower-level perceptual line-counting task in the presence of a distracting depiction of a 3-D object, in which participants counted whether there were more red or more green contours (In a contrasting 3-D task, participants judged whether the same 3-D stimulus objects (but without color in any contours) depicted a possible or impossible 3-D object). We hypothesized that individuals with autism would be less likely than controls to process the global 3-D information (and would hence show fewer neural signs of such interfering 3-D processing) during the lower-level line-counting task. The fMRI results revealed that in the line-counting task, the autism group did not show the increased medial frontal activity (relative to the possibility task), or the increased functional connectivity between the medial frontal region and posterior visual-spatial regions, demonstrated by the control group. Both findings are indices of lesser effort and difficulty in the line-counting task for the autism group than for the control group, attributed to less interference from the 3-D processing in the autism group. In addition, in the line-counting task, the control group showed a positive correlation between a measure of spatial ability (Vandenberg scores) and activation in the medial frontal region, suggesting that more spatially able control participants did more suppression of the irrelevant 3-D background information in order to focus on the line-counting task. The findings collectively indicate that the global 3-D structure of the figure had a smaller effect, if any, on local processing in the group with autism compared to the control group. The results from this study provide the first direct neural evidence of reduced global-to-local interference in autism. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Liu, Yanni; Cherkassky, Vladimir L.; Just, Marcel Adam] Carnegie Mellon Univ, Dept Psychol, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. [Minshew, Nancy J.] Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA. RP Liu, YN (reprint author), Carnegie Mellon Univ, Dept Psychol, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. EM yanniliu.cmu@gmail.com RI Liu, Yanni/B-8557-2013 OI Liu, Yanni/0000-0003-3198-6987 FU National Institute of Child Health and Human Development [HD055748] FX This research was supported by the Autism Centers of Excellence Grant (HD055748) from the National Institute of Child Health and Human Development. We appreciate the assistance of current and former members of the Center for help in conducting the experiments. In particular, we would like to thank Justin Abernethy for his assistance in preparing materials, Jennifer Moore for editorial comments, Diane Williams for extensive discussions, and Tim Keller for his excellent technical support and comments on earlier versions of the manuscript. We would also like to express our sincere appreciation for the time and effort of the participants and their families in making this research possible. 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The ability to integrate correlated information from multiple senses reduces processing load and underlies the perception of a multimodal and unified world. Perceiving biological motion facilitates filial attachment and detection of predators/prey. In the literature, these mechanisms are discussed in isolation. In this eye-tracking study, we tested their relative strengths in young human infants. We showed five-month-old infants point-light animation pairs of human motion, accompanied by a soundtrack. We found that audiovisual synchrony was a strong determinant of attention when it was embedded in biological motion (two upright animations). However, when biological motion was shown together with distorted biological motion (upright animation and inverted animation, respectively), infants looked at the upright animation and disregarded audiovisual synchrony. Thus, infants oriented to biological motion rather than multimodally unified physical events. These findings have important implications for understanding the developmental trajectory of brain specialization in early human infancy. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Falck-Ytter, Terje; Bakker, Marta] Uppsala Univ, Dept Psychol, S-75142 Uppsala, Sweden. [Falck-Ytter, Terje] Karolinska Inst KIND, Astrid Lindgren Childrens Hosp, Ctr Neurodev Disorders, Dept Womens & Childrens Hlth Q2 07, SE-17176 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; marta.bakker@psyk.uu.se; claes.von_hofsten@psyk.uu.se FU Bank of Sweden [P09-0933:1]; ESF COST Action [BM1004] FX This study was supported by grants to CvH from the Tercentennial Fund of the Bank of Sweden (P09-0933:1). The work of TFY and CvH was supported by the ESF COST Action BM1004 Enhancing the Scientific Study of Early Autism (ESSEA). 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INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD JUN PY 2011 VL 58 IS 3 BP 685 EP + DI 10.1016/j.pcl.2011.03.009 PG 15 WC Pediatrics SC Pediatrics GA 780YC UT WOS:000291896300010 PM 21600349 ER PT J AU Baron-Cohen, S Lombardo, MV Auyeung, B Ashwin, E Chakrabarti, B Knickmeyer, R AF Baron-Cohen, Simon Lombardo, Michael V. Auyeung, Bonnie Ashwin, Emma Chakrabarti, Bhismadev Knickmeyer, Rebecca TI Why Are Autism Spectrum Conditions More Prevalent in Males? SO PLOS BIOLOGY LA English DT Editorial Material ID DEFICIT HYPERACTIVITY DISORDER; HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; MAJOR SUSCEPTIBILITY LOCUS; FIGURES TASK-PERFORMANCE; CAST CHILDHOOD ASPERGER; ANDROGEN RECEPTOR GENE; REGIONAL GRAY-MATTER AB Autism Spectrum Conditions (ASC) are much more common in males, a bias that may offer clues to the etiology of this condition. Although the cause of this bias remains a mystery, we argue that it occurs because ASC is an extreme manifestation of the male brain. The extreme male brain (EMB) theory, first proposed in 1997, is an extension of the Empathizing-Systemizing (E-S) theory of typical sex differences that proposes that females on average have a stronger drive to empathize while males on average have a stronger drive to systemize. In this first major update since 2005, we describe some of the evidence relating to the EMB theory of ASC and consider how typical sex differences in brain structure may be relevant to ASC. One possible biological mechanism to account for the male bias is the effect of fetal testosterone (fT). We also consider alternative biological theories, the X and Y chromosome theories, and the reduced autosomal penetrance theory. None of these theories has yet been fully confirmed or refuted, though the weight of evidence in favor of the fT theory is growing from converging sources (longitudinal amniocentesis studies from pregnancy to age 10 years old, current hormone studies, and genetic association studies of SNPs in the sex steroid pathways). Ultimately, as these theories are not mutually exclusive and ASC is multi-factorial, they may help explain the male prevalence of ASC. C1 [Baron-Cohen, Simon; Lombardo, Michael V.; Auyeung, Bonnie; Ashwin, Emma; Chakrabarti, Bhismadev; Knickmeyer, Rebecca] 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. [Knickmeyer, Rebecca] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. EM sb205@cam.ac.uk RI Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 FU MRC; Wellcome Trust; Nancy Lurie Marks Foundation; NIHR CLAHRC for Cambridgeshire and Peterborough FX MRC, Wellcome Trust, Nancy Lurie Marks Foundation, NIHR CLAHRC for Cambridgeshire and Peterborough. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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PD JUN PY 2011 VL 9 IS 6 AR e1001081 DI 10.1371/journal.pbio.1001081 PG 10 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA 784XF UT WOS:000292191200008 PM 21695109 ER PT J AU Nicolaidis, C Raymaker, D McDonald, K Dern, S Ashkenazy, E Boisclair, C Robertson, S Baggs, A AF Nicolaidis, Christina Raymaker, Dora McDonald, Katherine Dern, Sebastian Ashkenazy, Elesia Boisclair, Cody Robertson, Scott Baggs, Amanda TI Collaboration Strategies in Nontraditional Community-Based Participatory Research Partnerships: Lessons From an Academic-Community Partnership With Autistic Self-Advocates SO PROGRESS IN COMMUNITY HEALTH PARTNERSHIPS-RESEARCH EDUCATION AND ACTION LA English DT Article DE Community-based participatory research; process issues; autism; autistic community; self-advocacy; disability; remote collaboration; atypical communication AB Background: Most community-based participatory research (CBPR) projects involve local communities defined by race, ethnicity, geography, or occupation. Autistic self-advocates, a geographically dispersed community defined by disability, experience issues in research similar to those expressed by more traditional minorities. Objectives: We sought to build an academic community partnership that uses CBPR to improve the lives of people on the autistic spectrum. Methods: The Academic Autistic Spectrum Partnership in Research and Education (AASPIRE) includes representatives from academic, self-advocate, family, and professional communities. We are currently conducting several studies about the health care experiences and well-being of autistic adults. Lessons Learned: We have learned a number of strategies that integrate technology and process to successfully equalize power and accommodate diverse communication and collaboration needs. Conclusions: CBPR can be conducted successfully with autistic self-advocates. 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TI Presynaptic function in health and disease SO TRENDS IN NEUROSCIENCES LA English DT Review ID UBIQUITIN-PROTEASOME SYSTEM; SYNAPTIC VESICLE PROTEIN; SYNAPSIN-III GENE; CLATHRIN-MEDIATED ENDOCYTOSIS; STIFF-PERSON SYNDROME; ALZHEIMERS-DISEASE; ACTIVE ZONE; BEHAVIORAL ABNORMALITIES; NEUROTRANSMITTER RELEASE; INHIBITORY SYNAPSES AB Neurons communicate with one another at specialized contact sites called synapses, composed of pre- and postsynaptic compartments. Presynaptic compartments, or 'boutons', signal to the postsynaptic compartment by releasing chemical neurotransmitter in response to incoming electrical impulses. Recent studies link defects in the function of presynaptic boutons to the etiology of several neurodevelopmental and neurodegenerative diseases, including autism, schizophrenia and Alzheimer's disease. 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CLW and CCG are supported by grants from the National Institutes of Health (MH085954, NS053862, MH091471), the Fidelity Foundation, the Down Syndrome Research and Treatment Foundation as well as the US-Israel Binational Science Foundation. 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PD JUN PY 2011 VL 34 IS 6 BP 326 EP 337 DI 10.1016/j.tins.2011.03.004 PG 12 WC Neurosciences SC Neurosciences & Neurology GA 785OM UT WOS:000292238300005 PM 21596448 ER PT J AU Tasdemiroglu, E Kaya, M Yildirim, CH Firat, L AF Tasdemiroglu, Erol Kaya, Miktat Yildirim, Can Hakan Firat, Levent TI Postoperative cerebellar mutism and autistic spectrum disorder SO CHILDS NERVOUS SYSTEM LA English DT Review DE Ataxic dysarthria; Autistic spectrum disorder; Cerebellar tumor; Cerebellar mutism; Risk factors ID POSTERIOR-FOSSA SYNDROME; SUBSEQUENT DYSARTHRIA; CHILDREN; SURGERY; VERMIS; ANTIBODIES; RESECTION; SYMPTOMS; DISEASE; TUMORS AB Purpose I read the article "An Inside View of Autism" written by a 44-year-old autistic woman who had a successful international career designing livestock equipment. In this article, she wrote about her life, disease, and experiences as an autistic individual. She stated that "It is interesting that my speech resembled the stressed speech in young children who have had tumors removed from the cerebellum". Methods In this article, we intend to review and extensively document both postoperative cerebellar mutism and autistic spectrum disorder. Results We reviewed the clinical and neurological findings, etio-pathogenesis, neuroanatomy, mechanisms of development, and similarities between the etio-pathogenesis of both diseases. Conclusions Cerebellar lesions can produce mutism and dysarthria, symptoms sometimes seen in autistic spectrum disorder. In mammals, cerebellar lesions disturb motivated behavior and reduce social interactions, functions that are disturbed in autistic spectrum disorder and cerebellar mutism. The cerebellum and two regions within the frontal lobes are active in certain language tasks. Language is abnormal in autistic spectrum disorder and cerebellar mutism. 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The majority of RTT patients carry missense and nonsense mutations leading to a hypomorphic MECP2, while null mutations leading to the complete absence of a functional protein are rare. MECP2 is an X-linked gene subject to random X-chromosome inactivation resulting in mosaic expression of mutant MECP2. The lack of human brain tissue motivates the need for alternative human cellular models to study RTT. Here we report the characterization of a MECP2 mutation in a classic female RTT patient involving rearrangements that remove exons 3 and 4 creating a functionally null mutation. To generate human neuron models of RTT, we isolated human induced pluripotent stem (hiPS) cells from RTT patient fibroblasts. RTT-hiPS cells retained the MECP2 mutation, are pluripotent and fully reprogrammed, and retained an inactive X-chromosome in a nonrandom pattern. Taking advantage of the latter characteristic, we obtained a pair of isogenic wild-type and mutant MECP2 expressing RTT-hiPS cell lines that retained this MECP2 expression pattern upon differentiation into neurons. Phenotypic analysis of mutant RTT-hiPS cell-derived neurons demonstrated a reduction in soma size compared with the isogenic control RTT-hiPS cell-derived neurons from the same RTT patient. Analysis of isogenic control and mutant hiPS cell-derived neurons represents a promising source for understanding the pathogenesis of RTT and the role of MECP2 in human neurons. C1 [Ellis, James] Hosp Sick Children, Program Dev & Stem Cell Biol, MaRS Ctr, Toronto, ON M5G 1L7, Canada. [Grafodatskaya, Daria; Weksberg, Rosanna] Hosp Sick Children, Program Genet & Genome Biol, Toronto, ON M5G 1L7, Canada. [Cheung, Aaron Y. L.; Ellis, James] Univ Toronto, Dept Mol Genet, Toronto, ON M5S 1A8, Canada. [Horvath, Lindsay M.; Carrel, Laura] Penn State Coll Med, Dept Biochem & Mol Biol, Hershey, PA 17033 USA. [Hotta, Akitsu; Ellis, James] Ontario Human Induced Pluripotent Stem Cell Facil, Toronto, ON M5G 1L7, Canada. RP Ellis, J (reprint author), Hosp Sick Children, Program Dev & Stem Cell Biol, MaRS Ctr, Room 13-310,Toronto Med Discovery Tower,101 Coll, Toronto, ON M5G 1L7, Canada. EM jellis@sickkids.ca RI Ellis, James/F-4789-2011 FU Canadian Institute for Health [MOP102649, IG194505, RMF92090]; Ontario Ministry for Research and Innovation; Beta Sigma Phi International Endowment Fund; National Institutes of Health [HD056452]; McGill University; Natural Sciences and Engineering Research Council of Canada FX This work was supported by the Canadian Institute for Health Research (MOP102649, IG194505, RMF92090 to J.E.); the Ontario Ministry for Research and Innovation to J.E.; the Beta Sigma Phi International Endowment Fund to J.E.; the National Institutes of Health (HD056452 to L. 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PD JUN 1 PY 2011 VL 20 IS 11 BP 2103 EP 2115 DI 10.1093/hmg/ddr093 PG 13 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 763WG UT WOS:000290589800003 PM 21372149 ER PT J AU Bavaro, SL Calabro, M Kanduc, D AF Bavaro, Simona Lucia Calabro, Michele Kanduc, Darja TI Pentapeptide sharing between Corynebacterium diphtheria toxin and the human neural protein network SO IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY LA English DT Article DE Comparative peptidomics; corynebacterium diphtheria; diphtheria toxin; neural protein network; peptide sharing; cross-reactivity ID BARDET-BIEDL-SYNDROME; AUTISM SPECTRUM DISORDER; WILLIAMS-BEUREN-SYNDROME; RECEPTOR GENE OXTR; DUCHENNE MUSCULAR-DYSTROPHY; TUBEROUS SCLEROSIS COMPLEX; CHINESE HAN POPULATION; HIGH-FUNCTIONING LEVEL; LEMLI-OPITZ-SYNDROME; CANDIDATE GENES AB We describe the pentapeptides shared between the Corynebacterium diphtheria toxin and the human proteins associated with fundamental neural functions. We report that diphtheria toxin pentapeptides are spread among human antigens such as tuberous sclerosis proteins 1 and 2, reelin, contactin-4, neuroligins, semaphorin-5A, sodium channel protein type 1 subunit alpha, Williams-Beuren syndrome chromosomal region 1 protein, Williams-Beuren syndrome chromosomal region 20A protein. Williams-Beuren syndrome chromosomal region 8 protein, Bardet-Biedl syndrome 9 protein, Bardet-Biedl syndrome 10 protein, oligodendrocyte-myelin glycoprotein, neurofibromin-2, and periaxin. The data are discussed in relation to the bacterial immune escape phenomenon, and in the context of potential cross-reactions in diagnostic tests and immune therapies. C1 [Bavaro, Simona Lucia; Calabro, Michele; Kanduc, Darja] Univ Bari, Dept Biochem & Mol Biol, I-70126 Bari, Italy. RP Kanduc, D (reprint author), Univ Bari, Dept Biochem & Mol Biol, I-70126 Bari, Italy. 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Oude TI Diagnosing autism spectrum disorders in elderly people SO INTERNATIONAL PSYCHOGERIATRICS LA English DT Review DE aged; autism; autism spectrum disorders; diagnosis; elderly; old age ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; OBSERVATION SCHEDULE; BRAIN MECHANISMS; REVISED VERSION; QUOTIENT AQ; ADULTS; MIND; CHILDREN AB Background: As autism spectrum disorders (ASD) have largely been neglected in old-age psychiatry, the objective of the present paper is to describe the diagnostic process in elderly patients. Methods: A systematic review of the literature on ASD in older age was undertaken and illustrated by a case series of three elderly patients first diagnosed with ASD in later life by a tertiary mental health clinic. Results: The search of the literature only yielded three papers on late-life ASD, while the review of the available diagnostic procedures among adults suggests some relevance for screening instruments (Autism Questionnaire), diagnostic instruments (Module 4, Autism Diagnostic Observation Schedule), and neuropsychological examination to profile impairments. Nonetheless, the case reports clearly showed that taking a thorough history with the patient, corroborated and supplemented by a close relative or caregiver who has known the patient for at least ten years, still remains the most important diagnostic tool. Conclusion: The three case studies show that in clinical practice ASD can easily be missed in elderly individuals presenting with comorbid psychiatric disorders, potentially causing iatrogenic damage. Although further research on phenotyping and diagnosing ASD in older people is warranted, the most important step at this point is to create a greater awareness of the possibility of ASD in old age among health-care professionals working with people in this age group. C1 [van Niekerk, Maarten E. H.; Groen, Wouter; Vissers, Constance Th. W. M.; Kan, Cees C.; Voshaar, Richard C. Oude] Radboud Univ Nijmegen Med Ctr, Dept Psychiat, Nijmegen, Netherlands. [van Niekerk, Maarten E. H.; van Driel-de Jong, Dorine] Pro Persona, Nijmegen Mental Hlth Ctr, Nijmegen, Netherlands. [Vissers, Constance Th. W. M.] Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Psychiat, NL-6525 ED Nijmegen, Netherlands. [Vissers, Constance Th. W. M.] Vincent van Gogh Inst Psychiat, Ctr Excellence Neuropsychiat, Venray, Netherlands. [Voshaar, Richard C. Oude] Univ Groningen, Univ Med Ctr Groningen, Univ Ctr Psychiat, NL-9713 AV Groningen, Netherlands. RP van Niekerk, MEH (reprint author), Univ Med Ctr Nijmegen, Dept Psychiat 333, POB 9101, NL-6500 HB Nijmegen, Netherlands. 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Psychogeriatr. PD JUN PY 2011 VL 23 IS 5 BP 700 EP 710 DI 10.1017/S1041610210002152 PG 11 WC Psychology, Clinical; Geriatrics & Gerontology; Gerontology; Psychiatry; Psychology SC Psychology; Geriatrics & Gerontology; Psychiatry GA 757TB UT WOS:000290109500002 PM 21110908 ER PT J AU Bopp, KD Mirenda, P AF Bopp, Karen D. Mirenda, Pat TI Prelinguistic predictors of language development in children with autism spectrum disorders over four-five years SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID COMMUNICATIVE DEVELOPMENT INVENTORY; CHILDHOOD AUTISM; RATING-SCALE; INDIVIDUAL GROWTH; VOCABULARY GROWTH; OUTCOMES; MODELS; ALPHA; SAS; AGE AB This study examined relationships between prelinguistic variables from the MacArthur-Bates CDI and the development of language comprehension and production in children with autism. Forty-four children were assessed at baseline and 6, 12, 24, 33 and 53 months later. Growth Curve Modeling was used to examine the extent to which three composite CDI variables and three CDI item groupings predicted language development over 4-5 years. When examined individually, prespeech and early gestures were significant predictors of change for both comprehension and production, but late gestures were not. In addition, initiating joint attention and games and routines predicted comprehension and production over 4-5 years, and conventional gestures also predicted production. When all factors were considered simultaneously, children's ability to participate in games and routines was the only significant predictor of language production over time. The results are discussed with regard to their implications for understanding the complex factors that affect developmental outcomes. C1 [Bopp, Karen D.; Mirenda, Pat] Univ British Columbia, Vancouver, BC V6T 1Z4, Canada. RP Bopp, KD (reprint author), Univ British Columbia, 2125 Main Mall, Vancouver, BC V6T 1Z4, Canada. 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PD JUN PY 2011 VL 38 IS 3 BP 485 EP 503 DI 10.1017/S0305000910000140 PG 19 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 757TY UT WOS:000290111800002 PM 20609280 ER PT J AU Hvidtjorn, D Grove, J Schendel, D Schieve, LA Svaerke, C Ernst, E Thorsen, P AF Hvidtjorn, D. Grove, J. Schendel, D. Schieve, L. A. Svaerke, C. Ernst, E. Thorsen, P. TI Risk of autism spectrum disorders in children born after assisted conception: a population-based follow-up study SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH LA English DT Article ID IN-VITRO FERTILIZATION; OBSTETRIC COMPLICATIONS; NEUROLOGICAL SEQUELAE; PERINATAL FACTORS; INFANTILE-AUTISM; NATIONAL COHORT; CEREBRAL-PALSY; BIRTH-WEIGHT; IVF; REGISTER AB Objectives To assess the risk of autism spectrum disorders (ASD) in children born after assisted conception compared with children born after natural conception. Design Population-based follow-up study. Setting All children born alive in Denmark 1995-2003. Participants 588 967 children born in Denmark from January 1995 to December 2003. Assisted conception was defined as in vitro fertilisation (IVF) with or without intracytoplasmic sperm injection and ovulation induction (OI) with or without subsequent insemination. Children exposed to IVF or OI were identified in the IVF Register and in the Danish Drug Prescription Register. Main outcome measures A diagnosis of ASD in the Danish Psychiatric Central Register. Results 33 139 (5.6%) of all children born in Denmark in 1995-2003 resulted from assisted conception, 225 of whom (0.68%) had a diagnosis of ASD. Of the 555 828 children born in this period after natural conception, 3394 (0.61%) had a diagnosis of ASD. The follow-up time was 4-13 years (median 9 years). In crude analyses, children born after assisted conception had an increased risk of a diagnosis of ASD: crude hazard rate ratio (HRR) 1.25 (95% CI 1.09 to 1.43). In analyses adjusting for maternal age, educational level, parity, smoking, birth weight and multiplicity, the risk disappeared: adjusted HRR 1.13. (95% CI 0.97 to 1.31). However, subgroup analyses that suggest possible associations in women who received follicle stimulating hormone indicate the need for further study. Discussion This population-based follow-up study found no risk of ASD in children born after assisted conception. C1 [Hvidtjorn, D.; Grove, J.; Svaerke, C.; Thorsen, P.] Univ Aarhus, Dept Epidemiol, Inst Publ Hlth, DK-8000 Aarhus C, Denmark. [Schendel, D.; Schieve, L. A.] Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA. [Ernst, E.] Aarhus Univ Hosp, Dept Obstet & Gynaecol, Fertil Sect, DK-8000 Aarhus, Denmark. RP Hvidtjorn, D (reprint author), Univ Aarhus, Dept Epidemiol, Inst Publ Hlth, Paludan Mullers Vej 17, DK-8000 Aarhus C, Denmark. EM dh@soci.au.dk FU Danish Agency for Science, Technology and Innovation, University of Aarhus; Elsass Foundation; Sofiefonden; Health Insurance Foundation; Augustinus Foundation; Julie von Mullens Foundation; Direktor Jacob Madsen and Hustru Olga Madsens Fond; Aase and Ejnar Danielsen Foundation FX The study was funded as a co-financed PhD project by The Danish Agency for Science, Technology and Innovation, University of Aarhus and The Elsass Foundation. Further funding was supplied by Sofiefonden, The Health Insurance Foundation, The Augustinus Foundation, Julie von Mullens Foundation, Direktor Jacob Madsen and Hustru Olga Madsens Fond and Aase and Ejnar Danielsen Foundation. CR Andersen AN, 1999, DAN MED BULL, V46, P357 Auyeung B, 2009, BRIT J PSYCHOL, V100, P1, DOI 10.1348/000712608X311731 Baron IS, 2008, NEUROPSYCHOL REV, V18, P271, DOI 10.1007/s11065-008-9070-1 Bhasin TK, 2007, J AUTISM DEV DISORD, V37, P667, DOI 10.1007/s10803-006-0194-y Centers for Disease Control and Prevention, 2007, MMWR-MORBID MORTAL W, V56, P1 Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Durkin MS, 2008, AM J EPIDEMIOL, V168, P1268, DOI 10.1093/aje/kwn250 Eaton WW, 2001, J AUTISM DEV DISORD, V31, P279, DOI 10.1023/A:1010743203048 Ericson A, 2002, HUM REPROD, V17, P929, DOI 10.1093/humrep/17.4.929 Gardener H, 2009, BRIT J PSYCHIAT, V195, P7, DOI 10.1192/bjp.bp.108.051672 Gaudoin M, 2003, AM J OBSTET GYNECOL, V188, P611, DOI 10.1067/mob.2003.5 Geier DA, 2006, HORM RES, V66, P182, DOI 10.1159/000094467 Glasson EJ, 2004, ARCH GEN PSYCHIAT, V61, P618, DOI 10.1001/archpsyc.61.6.618 Helmerhorst FM, 2004, BRIT MED J, V328, P261, DOI 10.1136/bmj.37957.560278.EE Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 Hvidtjorn D, 2009, ARCH PEDIAT ADOL MED, V163, P72, DOI 10.1001/archpediatrics.2008.507 Hvidtjorn D, 2006, PEDIATRICS, V118, P475, DOI 10.1542/peds.2005-2585 Ingudomnuku E, 2007, HORM BEHAV, V51, P597, DOI 10.1016/j.yhbeh.2007.02.001 Kallen B, 2002, OBSTET GYNECOL, V100, P414, DOI 10.1016/S0029-7844(02)02069-0 Klemetti R, 2006, PEDIATRICS, V118, P1819, DOI 10.1542/peds.2006-0735 Knudsen LB, 1998, DAN MED BULL, V45, P320 Larsson HJ, 2005, AM J EPIDEMIOL, V161, P916, DOI 10.1093/aje/kwi123 Lauritsen MB, 2005, J CHILD PSYCHOL PSYC, V46, P963, DOI 10.1111/j.1469-7610.2004.00391.x Lauritsen MB, 2010, J AUTISM DEV DISORD, V40, P139, DOI 10.1007/s10803-009-0818-0 Lidegaard O, 2005, HUM REPROD, V20, P950, DOI 10.1093/humrep/deh714 Maimburg RD, 2007, HUM REPROD, V22, P1841, DOI 10.1093/humrep/dem082 MunkJorgensen P, 1997, DAN MED BULL, V44, P82 NYBOEANDERSEN A, 2007, HUM REPROD, V22, P1513, DOI DOI 10.1093/HUMREP/DEM053 OLIVENNES F, 1993, HUM REPROD, V8, P1297 Ombelet W, 2006, HUM REPROD, V21, P1025, DOI 10.1093/humrep/dei419 Pinborg A, 2004, BRIT MED J, V329, P311, DOI 10.1136/bmj.38156.715694.3A Pinborg A, 2003, HUM REPROD, V18, P1234, DOI 10.1093/humrep/deg257 Reichenberg A, 2006, ARCH GEN PSYCHIAT, V63, P1026, DOI 10.1001/archpsyc.63.9.1026 Schendel D, 2008, PEDIATRICS, V121, P1155, DOI 10.1542/peds.2007-1049 Stein D, 2006, COMPR PSYCHIAT, V47, P69, DOI 10.1016/j.comppsych.2005.01.001 Stromberg B, 2002, LANCET, V359, P461, DOI 10.1016/S0140-6736(02)07674-2 Tebruegge Marc, 2004, BMC Pediatr, V4, P4, DOI 10.1186/1471-2431-4-4 Wang JX, 2002, HUM REPROD, V17, P945, DOI 10.1093/humrep/17.4.945 Wright Victoria Clay, 2006, Morbidity and Mortality Weekly Report, V55, P1 NR 40 TC 33 Z9 35 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0143-005X J9 J EPIDEMIOL COMMUN H JI J. Epidemiol. Community Health PD JUN PY 2011 VL 65 IS 6 BP 497 EP 502 DI 10.1136/jech.2009.093823 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 758ZW UT WOS:000290209400006 PM 20584728 ER PT J AU Fountain, C King, MD Bearman, PS AF Fountain, Christine King, Marissa D. Bearman, Peter S. TI Age of diagnosis for autism: individual and community factors across 10 birth cohorts SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH LA English DT Article ID SPECTRUM DISORDERS; CHILDREN; PREVALENCE; IDENTIFICATION; INTERVENTION AB Background The incidence of autism rose dramatically between 1992 and 2001, while the age at which children were first diagnosed declined. During this period the size and composition of the autism caseload has changed, but little is known about whether the factors associated with the timing of diagnosis may also have shifted. Using a multilevel analysis strategy, the individual and community-level factors associated with age of diagnosis were modelled across 10 birth cohorts of California children. Methods Linked birth and administrative records on 17 185 children with diagnoses of autistic disorder born in California between 1992 and 2001 and enrolled with the California Department of Developmental Services (DDS) were analysed. Information on cases, their parents and their residential location were extracted from birth and DDS records. Zip codes of residence were matched to census data to create community-level measures. Multilevel linear models were estimated for each birth cohort, with individual-level effects for sex, race, parental characteristics, poverty status, birth order and symptom expression. At the community level measures of educational and economic composition, local autism prevalence and the presence of a child psychiatrist were included. Results Children with highly educated parents are diagnosed earlier, and this effect has strengthened over time. There is a persistent gap in the age of diagnosis between high and low socioeconomic status (SES) children that has shrunk but not disappeared over time. Conclusion Routine screening for autism in early childhood for all children, particularly those of low SES, is necessary to eliminate disparities in early intervention. C1 [Fountain, Christine; King, Marissa D.; Bearman, Peter S.] Columbia Univ, Paul Lazarsfeld Ctr Social Sci, New York, NY 10027 USA. RP Bearman, PS (reprint author), Columbia Univ, Paul Lazarsfeld Ctr Social Sci, 803 Int Affairs Bldg,Mail Code 3355, New York, NY 10027 USA. EM psb17@columbia.edu FU NIH; NIH Roadmap for Medical Research [1 DP1 OD003635-01] FX This research was supported by the NIH Director's Pioneer Award program, part of the NIH Roadmap for Medical Research, through grant number 1 DP1 OD003635-01. 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Epidemiol. Community Health PD JUN PY 2011 VL 65 IS 6 BP 503 EP 510 DI 10.1136/jech.2009.104588 PG 8 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 758ZW UT WOS:000290209400007 PM 20974836 ER PT J AU Fields, C AF Fields, Chris TI From "Oh, OK" to "Ah, yes" to "Aha!": Hyper-systemizing and the rewards of insight SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Review DE Systemizing; Mentalizing; Development; Insight; Default network; Sensitization; Analogy; ASD ID ANTERIOR CINGULATE CORTEX; INCENTIVE-SENSITIZATION THEORY; HIGH-FUNCTIONING AUTISM; INTRINSIC MOTIVATION; PREFRONTAL CORTEX; SOCIAL COGNITION; DEFAULT-MODE; NEUROCOGNITIVE MECHANISMS; DECISION-MAKING; NEURAL ACTIVITY AB Hyper-systemizers are individuals displaying an unusually strong bias toward systemizing, i.e. toward explaining events and solving problems by appeal to mechanisms that do not involve intentions or agency. 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PD JUN PY 2011 VL 50 IS 8 BP 1159 EP 1167 DI 10.1016/j.paid.2011.02.010 PG 9 WC Psychology, Social SC Psychology GA 757IR UT WOS:000290079200001 ER PT J AU Barnard-Brak, L AF Barnard-Brak, Lucy TI The difference between autism and ADHD is in the eye of the cognitive task? SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE Autism; Autism spectrum disorders; Attention Deficit Hyperactivity Disorder (ADHD) ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; CHILDREN; PERFORMANCE; SYMPTOMS; VALIDITY AB A body of literature has indicated shared characteristics of children with autism spectrum disorders (ASDs) and Attention Deficit Hyperactivity Disorder (ADHD). The purpose of the current study was to demonstrate how different cognitive-attentional tasks may distinguish between children with ASDs and ADHD dependent upon the cognitive-attentional task. Multivariate analyses of covariance (MANCOVAs) were performed to determine whether the Leiter-R sustained attention subscale task and a rapid letter naming task distinguished between children with ADHD and ASDs, respectively in Study 1 and Study 2. Leiter-R sustained attention subscale task scores did not distinguish between children with ADHD and ASDs. Rapid letter naming performance, however, did appear to distinguish between children with ADHD and ASDs. Different cognitive-attentional tasks may distinguish differently between children with ADHD and ASDs. (C) 2011 Elsevier Ltd. All rights reserved. C1 Baylor Univ, Dept Educ Psychol, Waco, TX 76798 USA. RP Barnard-Brak, L (reprint author), Baylor Univ, Dept Educ Psychol, 1 Bear Pl 97301, Waco, TX 76798 USA. 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Petersen, M. B. TI Clinical variability of genetic isolates of Cohen syndrome SO CLINICAL GENETICS LA English DT Article DE clinical variability; COH1; Cohen syndrome; founder mutation; genetic isolate; mental retardation; migration ID FINNISH-DISEASE HERITAGE; DIAGNOSTIC-CRITERIA; NATURAL-HISTORY; HETEROGENEITY; POPULATION; MUTATIONS; DELETIONS; SPECTRUM; OBESITY AB Cohen syndrome (CS) (OMIM#216550) is an uncommon autosomal recessive developmental disorder that has been attributed to mutations in the COH1 gene in at least 200 patients of diverse ethnic background so far. The clinical heterogeneity of CS is evident when comparing patients of different ethnic backgrounds, especially when evaluating specific system phenotypes separately, such as the ophthalmic and central nervous systems. We reviewed the available clinical data on CS cohorts of patients who share a founder effect and demonstrated that most features associated so far with CS are less than those always present in the patients who share a founder mutation thus representing clinical heterogeneity. Furthermore, there is a wide clinical variability of CS in the distinct founder mutation cohorts, the Finnish, Greek/Mediterranean, Amish and Irish travelers. The Greek/Mediterranean founder mutation is correlated to a CS phenotype characterized by specific and persistent skeletal features, corneal changes, periodontal disease, a distinct neurocognitive phenotype for the high recurrence of autism and non-verbal communication and inconstant microcephaly. C1 [Douzgou, S.; Petersen, M. B.] Aghia Sophia Childrens Hosp, Inst Child Hlth, Dept Genet, Athens 11527, Greece. RP Douzgou, S (reprint author), Aghia Sophia Childrens Hosp, Inst Child Hlth, Dept Genet, Athens 11527, Greece. 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Genet. PD JUN PY 2011 VL 79 IS 6 BP 501 EP 506 DI 10.1111/j.1399-0004.2011.01669.x PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 759TJ UT WOS:000290271100001 PM 21418059 ER PT J AU Chasson, GS Timpano, KR Greenberg, JL Shaw, A Singer, T Wilhelm, S AF Chasson, Gregory S. Timpano, Kiara R. Greenberg, Jennifer L. Shaw, Ashley Singer, Tracy Wilhelm, Sabine TI Shared social competence impairment: Another link between the obsessive-compulsive and autism spectrums? SO CLINICAL PSYCHOLOGY REVIEW LA English DT Review DE Obsessive-Compulsive Spectrum Disorders; Autism Spectrum Disorders; Social Competence Impairment; Obsessive-Compulsive Disorder; Autism ID BODY DYSMORPHIC DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; EMOTION RECOGNITION DEFICITS; HIGH-FUNCTIONING CHILDREN; ASPERGER-SYNDROME; GLUTAMATE-RECEPTOR-6 GENE; PSYCHIATRIC-DISORDERS; CHRONIC-SCHIZOPHRENIA; SYMPTOM PROVOCATION; FACIAL EXPRESSIONS AB Recently, there has been a growing interest in the phenotypic, pathogenic, and pathophysiological overlap between autism spectrum disorders (ASD) and obsessive-compulsive spectrum disorders (OCSD). However, social competence impairment is one domain of overlap that has received less attention. Codified as one of three diagnostic categories in ASD, pathological social processing has also been demonstrated in OCSD. Yet, to date no reviews have synthesized the research literature on social competence impairments in OCSD, especially impairments that may parallel those found in ASD. The current review set out to examine the extant literature in this area in the service of advancing understanding of shared phenomenology between these two spectrums of conditions. Further, delineation of shared social competence impairments between ASD and OCSD might highlight candidate endophenotypes for further investigation. Ultimately, understanding the links between OCSD and ASD may aid in development of better intervention and prevention strategies, some of which may directly target maladaptive social processing. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Chasson, Gregory S.; Singer, Tracy] Towson Univ, Dept Psychol, Towson, MD 21254 USA. [Timpano, Kiara R.] Univ Miami, Dept Psychol, Coral Gables, FL 33124 USA. 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Psychol. Rev. PD JUN PY 2011 VL 31 IS 4 BP 653 EP 662 DI 10.1016/j.cpr.2011.02.006 PG 10 WC Psychology, Clinical SC Psychology GA 755HY UT WOS:000289920900012 PM 21482323 ER PT J AU Bartzokis, G AF Bartzokis, George TI Neuroglialpharmacology: white matter pathophysiologies and psychiatric treatments SO FRONTIERS IN BIOSCIENCE-LANDMARK LA English DT Article DE White matter; oligodendrocyte; neuregulin; ErbB; DISC1; nardilysin; apolipoprotein; secretase; medication; degeneration; MRI; Review ID CATECHOL-O-METHYLTRANSFERASE; CENTRAL-NERVOUS-SYSTEM; N-ACETYL-CYSTEINE; NICOTINIC ACETYLCHOLINE-RECEPTOR; FATTY-ACID-COMPOSITION; POSTMORTEM ORBITOFRONTAL CORTEX; MILD COGNITIVE IMPAIRMENT; PLACEBO-CONTROLLED-TRIAL; OLIGODENDROCYTE PRECURSOR CELLS; DORSOLATERAL PREFRONTAL CORTEX AB Psychotropic treatments such as second generation or "atypical" antipsychotics are efficacious in a wide spectrum of psychiatric disorders ranging from schizophrenia to depression, bipolar disorder, and autism. These treatments are associated with peripheral metabolic derangements that are often also present in drug-naive patients. Furthermore, altering lipid composition/levels (with omega 3 fatty acids) and ameliorating oxidative toxicities may treat/prevent disease. The above observations are reexamined from the perspective of a myelin-centered model of the human brain. The model proposes that the human brain's extensive myelination required higher metabolic resources that caused evolutionary adaptations resulting in our quadratic (inverted U) myelination trajectory that peaks in the sixth decade of life. It further proposes that optimal brain function depends on exquisite action potential synchronization that myelin makes possible and that myelin's exceptional vulnerability to subtle metabolic/oxidative abnormalities may promote both developmental and degenerative diseases. Available data are integrated herein to suggest that widely used psychotropic treatments have under-appreciated CNS metabolic and neurotransmitter effects on myelination, its plasticity, and repair that may substantially contribute to their mechanisms of action. C1 [Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat, Los Angeles, CA 90095 USA. [Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Div Brain Mapping, Lab Neuroimaging,Dept Neurol, Los Angeles, CA 90095 USA. [Bartzokis, George] Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst, Los Angeles, CA 90095 USA. [Bartzokis, George] Greater Los Angeles VA Healthcare Syst, Los Angeles, CA 90073 USA. RP Bartzokis, G (reprint author), 300 UCLA Med Plaza,Suite 2200, Los Angeles, CA 90095 USA. EM gbar@ucla.edu RI Bartzokis, George/K-2409-2013 FU NIH [MH 0266029, AG027342]; Research and Psychiatry Services of the Department of Veterans Affairs; RCS Foundation FX This work was supported in part by NIH grants (MH 0266029; AG027342), Research and Psychiatry Services of the Department of Veterans Affairs, and the RCS Foundation. The author thanks Lori L. Altshuler, M.D., and Keith H. Nuechterlein, Ph.D. for reading the manuscript and providing suggestions for improving it. 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Biosci. PD JUN 1 PY 2011 VL 16 BP 2695 EP 2733 DI 10.2741/3881 PG 39 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 757OK UT WOS:000290097400020 PM 21622204 ER PT J AU Wright, GJ Washbourne, P AF Wright, Gavin J. Washbourne, Philip TI Neurexins, Neuroligins and LRRTMs: synaptic adhesion getting fishy SO JOURNAL OF NEUROCHEMISTRY LA English DT Review DE autism; cell adhesion; development; neurodevelopmental disorder; synapse; zebrafish ID LEUCINE-RICH REPEATS; CELL-SURFACE PROTEINS; CRYSTAL-STRUCTURE; EXCITATORY SYNAPSES; VESICLE EXOCYTOSIS; NERVOUS-SYSTEM; BETA-NEUREXINS; GENE FAMILY; TRANSMEMBRANE PROTEINS; RIBONUCLEASE INHIBITOR AB P>Recent studies have identified the leucine rich repeat protein LRRTM2 as a post-synaptic ligand of Neurexins. Neurexins also bind the post-synaptic adhesion molecules, Neuroligins. All three families of genes have been implicated in the etiologies of neurodevelopmental disorders, specifically autism spectrum disorders and schizophrenia. Does the binding promiscuity of Neurexins now suggest complex cooperativity or redundancy at the synapse? While recent studies in primary neuronal cultures and also systematic extracellular protein interaction screens suggest summative effects of these systems, we propose that studying these interactions in the developing zebrafish embryo or larvae may shed more light on their functions during synaptogenesis in vivo. These gene families have recently been extensively characterized in zebrafish, demonstrating high sequence conservation with the human genes. The simpler circuitry of the zebrafish, together with the characterization of the expression patterns down to single, identifiable neurons and the ability to knock-down or over-express multiple genes in a rapid way lend themselves to dissecting complex interaction pathways. Furthermore, the capability of performing high-throughput drug screens suggests that these small vertebrates may prove extremely useful in identifying pharmacological approaches to treating autism spectrum disorders. C1 [Wright, Gavin J.] Wellcome Trust Sanger Inst, Cambridge, England. [Washbourne, Philip] Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA. RP Washbourne, P (reprint author), 1254 Univ Oregon, Inst Neurosci, Eugene, OR 97403 USA. EM pwash@uoneuro.uoregon.edu FU National Institute of Neurological Disorders and Stroke (NINDS) [R01NS065795]; Wellcome Trust [077108/Z/05/Z]; NIH [RO1NS063400] FX We would like to thank Alexandra Tallafuss for critical reading of the manuscript. Work in the Washbourne laboratory is funded by an R01 federal grant R01NS065795 from the National Institute of Neurological Disorders and Stroke (NINDS). Relevant work in the Wright lab was sponsored by the Wellcome Trust (grant No. 077108/Z/05/Z) and NIH grant RO1NS063400. 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Neurochem. PD JUN PY 2011 VL 117 IS 5 BP 765 EP 778 DI 10.1111/j.1471-4159.2010.07141.x PG 14 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 759FB UT WOS:000290225000001 PM 21155806 ER PT J AU Bishop, DVM Scerif, G AF Bishop, Dorothy V. M. Scerif, Gaia TI Klinefelter syndrome as a window on the aetiology of language and communication impairments in children: the neuroligin-neurexin hypothesis SO ACTA PAEDIATRICA LA English DT Article DE Autism; Klinefelter syndrome; Language impairment; Neurexin; Neuroligin; Sex chromosome trisomy ID FINE MOTOR DEVELOPMENT; Y-CHROMOSOME; AUTISM; DISORDERS; 47,XXY; GENES; BOYS; INDIVIDUALS; PHENOTYPES; CHILDHOOD AB Aim: To compare the phenotype in Klinefelter syndrome (KS) with (i) specific language impairment (SLI) and (ii) XXX and XYY trisomies. Methods: Phenotypes of KS, XXX and XYY were based on data from a systematic review of neurodevelopmental outcomes plus a recent parent survey. Phenotype of SLI was based on a published survey of children attending a special school. Results: There are close similarities between the KS phenotype and SLI. Furthermore, a minority of children with KS have features of autistic spectrum disorder. Similar language and communication problems are seen in the other two sex chromosome trisomies (SCTs), XXX and XYY. Conclusion: We propose the neurexin-neuroligin hypothesis, based on the observation that neuroligin genes, which occur on both X and Y chromosomes, are involved in the same synaptic networks as neurexin genes with common variants that affect risk for SLI and autism. According to our hypothesis, the effect of a triple dose of neuroligin gene product will be particularly detrimental when it occurs in conjunction with specific variants of neurexin genes on other chromosomes. This speculative proposal demonstrates the potential of illuminating the aetiology of common neurodevelopmental disorders by studying children with SCTs. C1 [Bishop, Dorothy V. M.; Scerif, Gaia] Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. EM dorothy.bishop@psy.ox.ac.uk FU Newlife Foundation [06-19]; Wellcome Trust [082498/Z/07/Z] FX This paper reports some novel data from a study supported by grant number 06-19 from Newlife Foundation. We gratefully acknowledge the families who gave their time to participate in this study, the staff at Unique (http://www.rarechromo.org), and the invaluable input to the study from our colleagues Katherine Lachlan, Diana Wellesley, Angela Barnicoat, Patricia A. Boyd, Alan Fryer, Prisca Middlemiss, Sarah Smithson, Kay Metcalfe, Deborah Shears, Victoria Leggett and Kate Nation. Special thanks are due to Patricia A. Jacobs, who first alerted us to the potential role of neuroligins in aetiology of autistic features in children with sex chromosome trisomies. DVMB is funded by a Principal Research Fellowship from the Wellcome Trust (ref 082498/Z/07/Z). 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Methods: A total of 73 subjects with KS (25 children and 48 adults) and 93 age-matched controls (53 children and 40 adults) participated in the study. The discrepancy between verbal IQ (VIQ) and performance IQ (PIQ) was assessed using the Wechsler Intelligence Scales. IQ data were only measured in the Klinefelter group. All participants completed the Autism Questionnaire and Schizotypal Personality Questionnaire. Results: Increased levels of autism traits and schizotypal traits were observed in individuals with KS, with schizotypal traits increasing with age. The VIQ < PIQ group (n = 33) showed significantly increased levels of autism traits compared to the PIQ < VIQ group (n = 12) and controls. The PIQ < VIQ group showed significantly increased levels of schizotypal traits compared to the VIQ < PIQ group and controls. The VIQ-PIQ discrepancy significantly correlated with schizotypal traits and autism traits, in opposite directions. Conclusion: Risk for psychopathology in KS may be age specific as well as dependent on cognitive profile. Relative deficits in verbal abilities seem more strongly associated with increased autism traits, whereas relative deficits in visuospatial abilities seem more strongly associated with increased schizotypal traits. C1 [van Rijn, Sophie; Swaab, Hanna] Leiden Univ, NL-2333 AK Leiden, Netherlands. [van Rijn, Sophie; Swaab, Hanna] Leiden Inst Brain & Cognit, Leiden, Netherlands. RP van Rijn, S (reprint author), Leiden Univ, Wassenaarseweg 52, NL-2333 AK Leiden, Netherlands. EM srijn@fsw.leidenuniv.nl FU Netherlands Organization for Scientific Research (NWO) [016.095.060] FX This work was supported by a personal grant (grant number 016.095.060) to SvR from the Netherlands Organization for Scientific Research (NWO). 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We hypothesized that children with regressive autism would demonstrate a greater degree of sleep disruption either at a macrostructural or microstructural level and a more problematic sleep as reported by parents. Twenty-two children with non-regressive autism, 18 with regressive autism without comorbid pathologies and 12 with TD, aged 5-10 years, underwent standard overnight multi-channel polysomnographic evaluation. Parents completed a structured questionnaire (Childrens' Sleep Habits Questionnaire-CSHQ). The initial hypothesis, that regressed children have more disrupted sleep, was supported by our findings that they scored significantly higher on CSHQ, particularly on bedtime resistance, sleep onset delay, sleep duration and night wakings CSHQ subdomains than non-regressed peers, and both scored more than typically developing controls. 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TI Reverse-translational biomarker validation of Abnormal Repetitive Behaviors in mice: An illustration of the 4P's modeling approach SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE Autism; OCD; Trichotillomania; Stereotypy; Perservation; Executive; Prefrontal cortex; Orbitofrontal cortex; Basal ganglia ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; LABORATORY MICE; FUNCTIONAL-ANATOMY; PREFRONTAL CORTEX; ANIMAL-MODELS; TRICHOTILLOMANIA; STEREOTYPIES; AUTISM; NEUROPSYCHOLOGY AB The NIMH's new strategic plan, with its emphasis on the "4P's" (Prediction, Pre-emption, Personalization, and Populations) and biomarker-based medicine requires a radical shift in animal modeling methodology. In particular 4P's models will be non-determinant (i.e. disease severity will depend on secondary environmental and genetic factors); and validated by reverse-translation of animal homologues to human biomarkers. A powerful consequence of the biomarker approach is that different closely related disorders have a unique fingerprint of biomarkers. Animals can be validated as a highly specific model of a single disorder by matching this 'fingerprint'; or as a model of a symptom seen in multiple disorders by matching common biomarkers. Here we illustrate this approach with two Abnormal Repetitive Behaviors (ARBs) in mice: stereotypies and barbering (hair pulling). We developed animal versions of the neuropsychological biomarkers that distinguish human ARBs, and tested the fingerprint of the different mouse ARBs. As predicted, the two mouse ARBs were associated with different biomarkers. Both barbering and stereotypy could be discounted as models of OCD (even though they are widely used as such), due to the absence of limbic biomarkers which are characteristic of OCD and hence are necessary for a valid model. Conversely barbering matched the fingerprint of trichotillomania (i.e. selective deficits in set-shifting), suggesting it may be a highly specific model of this disorder. In contrast stereotypies were correlated only with a biomarker (deficits in response shifting) correlated with stereotypies in multiple disorders, suggesting that animal stereotypies model stereotypies in multiple disorders. (C) 2011 Elsevier B.V. All rights reserved. C1 [Garner, Joseph P.; Thogerson, Collette M.; Dufour, Brett D.] Purdue Univ, Dept Anim Sci, W Lafayette, IN 47907 USA. [Wuerbel, Hanno] Univ Giessen, Div Anim Welf & Ethol, D-35392 Giessen, Germany. [Murray, James D.; Mench, Joy A.] Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA. RP Garner, JP (reprint author), Purdue Univ, Dept Anim Sci, 125 S Russell St, W Lafayette, IN 47907 USA. EM jgarner@purdue.edu RI Citations, TLC SAB/C-4006-2011; Wurbel, Hanno/D-6281-2012; Garner, Joseph/C-8422-2009 OI Wurbel, Hanno/0000-0002-2934-3010; FU NIMH [5 R03 MH 63907-2] FX We thank undergraduate interns, and Aria Prater and Sandra Weisker. Project design and infrastructure: JPG, JAM and JDM. Bias-corrected gambling task, barbering scoring, and supporting software: JPG. IDED task and stereotypy scoring: HW and JPG. Project management: CMT and BD. Funding: NIMH grant # 5 R03 MH 63907-2. 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TI Perceived Barriers and Facilitators of Participation in After-School Physical Activity by Children with Autism Spectrum Disorders SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE Autism spectrum disorders; Physical activity; Photovoice; Barriers; Ecological model ID ADOLESCENTS; PHOTOVOICE; UNIVERSITY; EXERCISE; STUDENTS; OBESITY; YOUTH AB This study used Photovoice methodology to assess barriers to and facilitators of after-school participation in moderate to vigorous physical activity as perceived by children with ASD and determine if physical activity patterns exist in relation to these barriers. Participants were a convenience sample of 12 boys and two girls with autism spectrum disorders (ASD), ages 8-14 years. Participants wore an accelerometer and completed an activity log for 7 days. Data were analyzed using qualitative techniques and fitted in a socio-ecological model. Participants reported 143 (44%) barriers and 181 (56%) facilitators. The most frequently cited barriers were intrapersonal, followed by interpersonal, physical, community, and institutional. The most frequent facilitators were physical, followed by intrapersonal and interpersonal, community, and institutional. The study gives support to the use of a multipronged approach when designing physical activity interventions for children and adolescents with ASD. C1 [Obrusnikova, Iva; Cavalier, Albert R.] Univ Delaware, Sch Educ, Newark, DE 19716 USA. RP Obrusnikova, I (reprint author), Univ Delaware, Sch Educ, 26 N Coll Ave, Newark, DE 19716 USA. 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Zimmer, Michelle Sacco, Kelley Turner, Kylan TI Effects of Gluten Free/Casein Free Diet in Young Children with Autism: A Pilot Study SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE Gluten-fee; Casein-free diet; Autism; Dietary restrictions ID PERVASIVE DEVELOPMENTAL DISORDERS; BLIND CLINICAL-TRIAL; CASEIN-FREE DIET; SPECTRUM DISORDERS AB With reports of the growing incidence of autism spectrum disorder ASD in the United States, a large number of families of affected children is seeking alternative or complementary forms of treatment. One of the more popular interventions has been use of elimination regimes, such as the gluten and casein free (GFCF) diet. This pilot study involved a three-month, prospective, open label, randomized, parallel groups design of a GFCF diet compared to a healthy, low sugar diet (attention control) for young children with ASD. Both treatment groups evidenced some gains across a range of variables, including measures of behavior, language, and ratings of the core features of ASD. No statistically significant differences were noted between treatment groups. While our results do not support use of a GFCF diet in ASD, it is possible that a greater period of time is required for treatment before gains can be observed. Moreover, no significant nutritional differences or side effects were observed on the GFCF diet compared to the control diet. However, adherence to the GFCF diet proved difficult based on our adherence data. C1 [Johnson, Cynthia R.] Univ Pittsburgh, Sch Med, Childrens Hosp Pittsburgh, Autism Ctr, Pittsburgh, PA 15213 USA. [Zimmer, Michelle] Univ Cincinnati, Cincinnati, OH USA. [Turner, Kylan] Univ Pittsburgh, Sch Educ, Pittsburgh, PA 15260 USA. RP Johnson, CR (reprint author), Univ Pittsburgh, Sch Med, Childrens Hosp Pittsburgh, Autism Ctr, 3420 5th Ave, Pittsburgh, PA 15213 USA. 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Dev. Phys. Disabil. PD JUN PY 2011 VL 23 IS 3 BP 213 EP 225 DI 10.1007/s10882-010-9217-x PG 13 WC Rehabilitation SC Rehabilitation GA 753SQ UT WOS:000289800400004 ER PT J AU Hodge, D Hoffman, CD Sweeney, DP AF Hodge, Danelle Hoffman, Charles D. Sweeney, Dwight P. TI Increased Psychopathology in Parents of Children with Autism: Genetic Liability or Burden of Caregiving? SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE Autism; Parenting; Genetics; Caregiver burden; Mental health ID PSYCHIATRIC-DISORDERS; MENTAL-HEALTH; BEHAVIOR PROBLEMS; FAMILY STRESS; DOWN-SYNDROME; MOTHERS; WELL; FATHERS; INDIVIDUALS; PERCEPTIONS AB The goals of this research were to identify which psychopathologies are common in parents of children with autistic spectrum disorders (ASD) and to explore competing hypotheses regarding mechanisms contributing to this risk. 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Dev. Phys. Disabil. PD JUN PY 2011 VL 23 IS 3 BP 227 EP 239 DI 10.1007/s10882-010-9218-9 PG 13 WC Rehabilitation SC Rehabilitation GA 753SQ UT WOS:000289800400005 ER PT J AU Hillier, AJ Fish, T Siegel, JH Beversdorf, DQ AF Hillier, Ashleigh J. Fish, Tom Siegel, Jeffrey H. Beversdorf, David Q. TI Social and Vocational Skills Training Reduces Self-reported Anxiety and Depression Among Young Adults on the Autism Spectrum SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE Asperger's syndrome; Vocational support; Social skills, anxiety, depression, peer relationships ID HIGH-FUNCTIONING CHILDREN; ASPERGER-SYNDROME; DISORDERS; ADOLESCENTS; SYMPTOMATOLOGY; ABILITIES; SYMPTOMS AB Those with autism spectrum disorders (ASD) frequently experience high levels of anxiety and depression. These psychological factors may be related to some of the core challenges seen among those with ASD, including social difficulties. We examined whether a social and vocational skills intervention program for adolescents and young adults on the autism spectrum would yield a broader impact that partially alleviated these psychological factors. Following the intervention program participants reported significantly lower depression and anxiety. Responses on a measure of peer relationships were also improved post-intervention, although this did not reach significance. Although preliminary, our findings demonstrate the broader, positive impact that such programs may have. C1 [Hillier, Ashleigh J.] Univ Massachusetts Lowell, Dept Psychol, Lowell, MA 01854 USA. [Fish, Tom; Siegel, Jeffrey H.] Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. [Beversdorf, David Q.] Univ Missouri, Dept Radiol, Dept Neurol, Dept Psychol Sci, Columbia, MO USA. [Beversdorf, David Q.] Univ Missouri, Thompson Ctr, Columbia, MO USA. 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TI Summaries from the XVIII World Congress of Psychiatric Genetics, Athens, Greece, 3-7 October 2010 SO PSYCHIATRIC GENETICS LA English DT Editorial Material DE autism; DNA; International Society of Psychiatric Genetics; schizophrenia; sequencing; World Congress of Psychiatric Genetics ID GENOME-WIDE ASSOCIATION; DEFICIT HYPERACTIVITY DISORDER; COPY NUMBER VARIATION; FRAGILE-X-SYNDROME; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; HIDDEN-MARKOV MODEL; SNP GENOTYPING DATA; BIPOLAR-DISORDER; ALCOHOL DEPENDENCE; MAJOR DEPRESSION AB The XVIIIth World Congress of Psychiatric Genetics, sponsored by The International Society of Psychiatric Genetics took place in Athens, Greece on October 3-7, 2010. Approximately 950 participants gathered to discuss the latest findings in this rapidly advancing field. The following report was written by junior travel awardees, as well as others who were volunteers from student meeting attendees. Each was assigned sessions as rapporteurs. This report represents some of the areas covered in oral presentation during the conference, and reports on some of the notable major new findings described at this 2010 World Congress of Psychiatric Genetics. Psychiatr Genet 21: 136-172 (C) 2011 Wolters Kluwer Health | Lippincott Williams & Wilkins. C1 [O'Shea, Anne; DeLisi, Lynn E.] Harvard Univ, Sch Med, Brockton VA Boston Healthcare Syst, Brockton, MA 02301 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Neurodev Genet Unit, Boston, MA USA. [Ozomaro, Uzoezi] Univ Miami Miller Sch Med, John P Hussman Inst Human Genom, Miami, FL USA. [Balhara, Yatan Pal Singh] Lady Hardinge Med Coll & Associated Hosp, Dept Psychiat, New Delhi, India. [Balhara, Yatan Pal Singh] Lady Hardinge Med Coll & Associated Hosp, Deaddict Ctr, New Delhi, India. [Christoforou, Andrea] Univ Bergen, Bergen Mental Hlth Res Ctr, Labbygget, Norway. [Christoforou, Andrea] Univ Bergen, Sect Med Genet & Mol Med, Dept Clin Med, Labbygget, Norway. [Christoforou, Andrea] Haukeland Hosp, Dr Einar Martens Res Grp Biol Psychiat, Ctr Med Genet & Mol Med, Helse Bergen HF, N-5021 Bergen, Norway. [Dempster, Emma] Kings Coll London, Psychiat Epigenet Grp, Inst Psychiat, London WC2R 2LS, England. [Cole, James; Lysenko, Laura; Nymberg, Charlotte] Kings Coll London, MRC SGDP Res Ctr, Inst Psychiat, London WC2R 2LS, England. [Lopez, Lorna M.] Univ Edinburgh, Dept Psychol, Ctr Cognit Ageing & Cognit Epidemiol, Edinburgh, Midlothian, Scotland. [Degenhardt, Franziska; Muehleisen, Thomas W.] Univ Bonn, Inst Human Genet, Life & Brain Ctr, D-5300 Bonn, Germany. [Degenhardt, Franziska; Muehleisen, Thomas W.] Univ Bonn, Dept Genom, Life & Brain Ctr, D-5300 Bonn, Germany. [Fatjo-Vilas, Mar] Univ Barcelona, Fac Biol, Dept Biol Anim, IBUB,CIBERSAM, Barcelona, Spain. [Khedr, Yara] Heliopolis, Cairo, Egypt. [Neves, Fernando S.] Univ Fed Minas Gerais, Dept Psiquiatria, Fac Med, Belo Horizonte, MG, Brazil. [Verweij, Karin J. 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Spanagel, Rainer Heberlein, Ulrike A. Jarvelin, Marjo-Riitta Elliott, Paul TI Genome-wide association and genetic functional studies identify autism susceptibility candidate 2 gene (AUTS2) in the regulation of alcohol consumption (vol 108, pg 7119, 2011) SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Correction RI Desrivieres, Sylvane/B-7399-2011; Onland-Moret, N. Charlotte/G-9185-2011; Aliev, Fazil/D-7172-2013; Palkovits, Miklos/F-2707-2013; Lourdusamy, Anbarasu/G-3387-2011; Aulchenko, Yurii/M-8270-2013; Grobbee, Diederick/C-7651-2014 OI Desrivieres, Sylvane/0000-0002-9120-7060; Aliev, Fazil/0000-0001-8357-4699; Aulchenko, Yurii/0000-0002-7899-1575; Grobbee, Diederick/0000-0003-4472-4468 CR Schumann G, 2011, P NATL ACAD SCI USA, V108, P7119, DOI 10.1073/pnas.1017288108 NR 1 TC 0 Z9 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 31 PY 2011 VL 108 IS 22 BP 9316 EP 9316 DI 10.1073/pnas.1106917108 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 770RM UT WOS:000291106200078 ER PT J AU Enticott, PG Kennedy, HA Bradshaw, JL Rinehart, NJ Fitzgerald, PB AF Enticott, Peter G. Kennedy, Harley A. Bradshaw, John L. Rinehart, Nicole J. Fitzgerald, Paul B. TI Motor corticospinal excitability during the observation of interactive hand gestures SO BRAIN RESEARCH BULLETIN LA English DT Article DE Emotion; Mirror neurons; Transcranial magnetic stimulation; Premotor cortex; Primary motor cortex; Empathy ID MIRROR-NEURON SYSTEM; TRANSCRANIAL MAGNETIC STIMULATION; AUTISM SPECTRUM DISORDERS; CORTICAL EXCITABILITY; EMPATHY QUOTIENT; MODULATION; FACILITATION; PERCEPTION; HUMANS; CORTEX AB The observation of other's behaviour results in increased corticospinal excitability (CSE) within the primary motor cortex, a phenomenon that has typically been interpreted in the context of motor resonance and human "mirror systems". Mirror systems are implicated in empathy, and may therefore show a preferential response to the observation of interactive behaviour. Participants were administered transcranial magnetic stimulation (TMS) to the primary motor cortex while viewing matched hand movements with or without (1) an interactive context and (2) an interactive context with an implied heightened emotional aspect. CSE was not enhanced when viewing interactive (compared with individual) hand movements. There was, however, some evidence for an enhanced response when viewing hand movements with an emotional component. There was no association between mirror systems and self-reported empathy. Mirror systems may not be more responsive to interactive behaviour, but the inclusion of a strong emotional element could be of significance to mirror neurons. (C) 2011 Elsevier Inc. All rights reserved. C1 [Enticott, Peter G.] The Alfred, Monash Alfred Psychiat Res Ctr, Melbourne, Vic 3004, Australia. [Enticott, Peter G.; Kennedy, Harley A.; Fitzgerald, Paul B.] Monash Univ, Monash Alfred Psychiat Res Ctr, Sch Psychol & Psychiat, Melbourne, Vic 3004, Australia. [Enticott, Peter G.; Bradshaw, John L.; Rinehart, Nicole J.] Monash Univ, Monash Med Ctr, Sch Psychol & Psychiat, Ctr Dev Psychiat & Psychol, Clayton, Vic 3168, Australia. RP Enticott, PG (reprint author), The Alfred, Monash Alfred Psychiat Res Ctr, Level 1,Old Baker Bldg, Melbourne, Vic 3004, Australia. EM peter.enticott@monash.edu RI Fitzgerald, Paul/A-1225-2008 OI Fitzgerald, Paul/0000-0003-4217-8096 FU National Health and Medical Research Council (NHMRC) [545811] FX This study was supported by a National Health and Medical Research Council (NHMRC) Project Grant (#545811). PGE is supported by a NHMRC Training Fellowship. PBF is supported by a NHMRC Practitioner Fellowship. 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Bull. PD MAY 30 PY 2011 VL 85 IS 3-4 BP 89 EP 95 DI 10.1016/j.brainresbull.2011.03.018 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 788FQ UT WOS:000292431200002 PM 21457764 ER PT J AU Jacome, LF Burket, JA Herndon, AL Deutsch, SI AF Jacome, Luis F. Burket, Jessica A. Herndon, Amy L. Deutsch, Stephen I. TI D-Cycloserine enhances social exploration in the Balb/c mouse SO BRAIN RESEARCH BULLETIN LA English DT Article DE Balb/c mouse strain; Sociability; Anxiety; D-Cycloserine; Autism spectrum disorders ID NMDA RECEPTOR ANTAGONIST; STRAINS DIFFER; PLUS-MAZE; MK-801; MICE; SENSITIVITY; BEHAVIOR; MEMORY; SCHIZOPHRENIA; AGONISTS AB Inbred Balb/c mice show deficits of sociability. The endogenous tone of NMDA receptor-mediated neurotransmission is altered in Balb/c mice, which may explain the beneficial effect of D-cycloserine on impaired sociability. In the current study, Balb/c mice spent more time than the Swiss Webster comparator strain in the open arms of an elevated plus maze (EPM), suggesting that they are not more anxious or fearful in the absence of a social stimulus mouse. Moreover, Balb/c and Swiss Webster mice did not differ in the amount of time they spent exploring an inanimate object in an open field. Differences in exploratory activity between strains emerged only when a salient social stimulus mouse was enclosed in the open field. D-Cycloserine increased the amount of time Balb/c mice spent exploring the enclosed stimulus mouse to levels observed in vehicle-treated Swiss Webster mice. Finally, irrespective of strain, D-cycloserine increased exploratory activity as measured in open arm entries in the EPM, when no enclosed stimulus mouse was present. The data show that mouse strain influences D-cycloserine's effect on exploration in the presence of a salient social stimulus mouse. In the absence of an enclosed stimulus mouse, D-cycloserine increased open arm entries significantly in both the sociability-impaired Balb/c and comparator Swiss Webster strains. Thus, D-cycloserine positively affects exploratory activity in general, but strain differences emerge when the stimulus eliciting exploration is a salient social stimulus mouse versus an inanimate object. Further, the sociability deficit of the Balb/c mouse is not an epiphenomenon of increased generalized anxiety. (C) 2011 Elsevier Inc. All rights reserved. C1 [Jacome, Luis F.; Burket, Jessica A.; Herndon, Amy L.; Deutsch, Stephen I.] Eastern Virginia Med Sch, Dept Psychiat & Behav Sci, Norfolk, VA 23507 USA. RP Deutsch, SI (reprint author), Eastern Virginia Med Sch, Dept Psychiat & Behav Sci, 825 Fairfax Ave,Suite 710, Norfolk, VA 23507 USA. 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Bull. PD MAY 30 PY 2011 VL 85 IS 3-4 BP 141 EP 144 DI 10.1016/j.brainresbull.2011.03.004 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 788FQ UT WOS:000292431200009 PM 21396991 ER PT J AU He, YQ Xun, GL Xia, K Hu, ZM Lv, LX Deng, ZM Zhao, JP AF He, Yiqun Xun, Guanglei Xia, Kun Hu, Zhengmao Lv, Luxian Deng, Zemin Zhao, Jingping TI No significant association between RELN polymorphism and autism in case-control and family-based association study in Chinese Han population SO PSYCHIATRY RESEARCH LA English DT Article DE Autism; Reelin gene; Polymorphism ID REELIN GENE ALLELES; SPECTRUM DISORDER; GENOMEWIDE SCREEN; SUSCEPTIBILITY; LINKAGE; REPEAT; TRIADS; RISK; APOE AB The present study genotyped four SNPs (rs736707, rs2229864, rs362691, and rs2073559) of the Reelin gene (RELN) in 165 autistic trios, 67 sporadic autistic children and 283 healthy controls with Chinese Han pedigree. Both case-control analysis and transmission disequilibrium test (TDT) found no evidence of significant association. The results do not support previous positive findings and suggest that the four single-nucleotide polymorphisms (SNP) of RELN are unlikely to be associated with childhood autism in Chinese Han population. (C) 2010 Elsevier Ireland Ltd. All rights reserved. C1 [He, Yiqun; Xun, Guanglei; Zhao, Jingping] Cent S Univ, Xiangya Hosp 2, Mental Hlth Inst, Changsha 410011, Hunan, Peoples R China. [He, Yiqun; Lv, Luxian] Second Affiliated Hosp, XinXiang Med Coll, Xinxiang, Hunan, Peoples R China. [Xia, Kun; Hu, Zhengmao] Natl Lab Med Genet China, Changsha, Hunan, Peoples R China. [Deng, Zemin] Univ So Calif, Keck Sch Med, Zilkha Neurogenet Inst, Los Angeles, CA 90033 USA. RP Zhao, JP (reprint author), Cent S Univ, Xiangya Hosp 2, Mental Hlth Inst, 139 Renmin Middle Rd, Changsha 410011, Hunan, Peoples R China. EM zhaojingpinghunan@yahoo.com.cn FU National Natural Science Foundation of China [30630062] FX This work was supported by grants from the National Natural Science Foundation of China (Grant No. 30630062). 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Methods: A total of 100 well-treated and compliant CD patients (65 females/35 males; age mean +/- SD: 10.38 +/- 2.71) were compared to 100 normal controls (58 females/42 males; age mean +/- SD: 11.47 +/- 2.61). Emotional and behavioral problems were assessed by the Child Behavior Checklist (CBCL), the Children's Depression Inventory (CDI) and the Multidimensional Anxiety Scale for Children (MASC). Results: Subjects with CD self-reported an increased rate of anxiety and depression symptoms and showed higher scores in "harm avoidance" and "somatic complaints", in the CBCL parent-report questionnaire, as compared to healthy control subjects. Furthermore, gender differences could be observed in the group of CD patients, with males displaying significantly higher CBCL externalizing scores, in social, thought and attention problems, as compared to female, who in turns showed more prominent internalizing symptoms such as depression. 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PD MAY 27 PY 2011 VL 11 AR 46 DI 10.1186/1471-2431-11-46 PG 6 WC Pediatrics SC Pediatrics GA 801YX UT WOS:000293477600001 PM 21619651 ER PT J AU Bangash, MA Park, JM Melnikova, T Wang, DH Jeon, SK Lee, D Syeda, S Kim, J Kouser, M Schwartz, J Cui, YY Zhao, X Speed, HE Kee, SE Tu, JC Hu, JH Petralia, RS Linden, DJ Powell, CM Savonenko, A Xiao, B Worley, PF AF Bangash, M. Ali Park, Joo Min Melnikova, Tatiana Wang, Dehua Jeon, Soo Kyeong Lee, Deidre Syeda, Sbaa Kim, Juno Kouser, Mehreen Schwartz, Joshua Cui, Yiyuan Zhao, Xia Speed, Haley E. Kee, Sara E. Tu, Jian Cheng Hu, Jia-Hua Petralia, Ronald S. Linden, David J. Powell, Craig M. Savonenko, Alena Xiao, Bo Worley, Paul F. TI Enhanced Polyubiquitination of Shank3 and NMDA Receptor in a Mouse Model of Autism (Retracted article. See vol. 152, pg. 367, 2013) SO CELL LA English DT Article ID SCAFFOLDING PROTEIN SHANK3; X MENTAL-RETARDATION; SPECTRUM DISORDERS; SCHIZOPHRENIA; MUTATIONS; HOMER; GENE; MICE; RECOGNITION; EXPRESSION AB We have created a mouse genetic model that mimics a human mutation of Shank3 that deletes the C terminus and is associated with autism. Expressed as a single copy [Shank3(+/Delta C) mice], Shank3 Delta C protein interacts with the wild-type (WT) gene product and results in >90% reduction of Shank3 at synapses. This "gain-of-function" phenotype is linked to increased polyubiquitination of WT Shank3 and its redistribution into proteasomes. Similarly, the NR1 subunit of the NMDA receptor is reduced at synapses with increased polyubiquitination. Assays of postsynaptic density proteins, spine morphology, and synapse number are unchanged in Shank3(+/Delta C) mice, but the amplitude of NMDAR responses is reduced together with reduced NMDAR-dependent LTP and LTD. Reciprocally, mGluR-dependent LTD is markedly enhanced. Shank3(+/Delta C) mice show behavioral deficits suggestive of autism and reduced NMDA receptor function. These studies reveal a mechanism distinct from haploinsufficiency by which mutations of Shank3 can evoke an autism-like disorder. C1 [Bangash, M. Ali; Park, Joo Min; Jeon, Soo Kyeong; Kim, Juno; Schwartz, Joshua; Tu, Jian Cheng; Hu, Jia-Hua; Linden, David J.; Xiao, Bo; Worley, Paul F.] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. [Melnikova, Tatiana; Lee, Deidre; Syeda, Sbaa; Savonenko, Alena] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA. [Melnikova, Tatiana; Lee, Deidre; Syeda, Sbaa; Savonenko, Alena] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. [Kouser, Mehreen; Speed, Haley E.; Kee, Sara E.; Powell, Craig M.] Univ Texas SW Med Ctr Dallas, Dept Neurol, Dallas, TX 75390 USA. [Kouser, Mehreen; Speed, Haley E.; Kee, Sara E.; Powell, Craig M.] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA. [Wang, Dehua; Cui, Yiyuan; Zhao, Xia; Xiao, Bo] Sichuan Univ, State Key Lab Biotherapy, W China Hosp, Chengdu 610065, Peoples R China. [Petralia, Ronald S.] Natl Inst Deafness & Other Commun Disorders, Neurochem Lab, NIH, Bethesda, MD 20892 USA. RP Worley, PF (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. EM pworley@jhmi.edu FU National Institute of Neurological Disorders and Stroke [5R01NS070301-02]; National Institute of Mental Health [5P50MH084020-03]; National 973 Basic Research Program of China [20009CB941400, R21HD065290, R01MH081164]; Autism Speaks; Autism Science Foundation; Hartwell Foundation; NIDCD FX M.A.B., A. S., B. X., and P. F. W. designed the study. M. A. B. executed and analyzed all the biochemistry, immunocytochemistry, and DiI experiments. B. X., M. A. B., D. W., Y.C., and X.Z. created the Shank3 mouse. J.M.P., S.K.J., and J.K. did the electrophysiology experiments and analysis supervised by P. F. W. and D.J.L. R. S. P. did the electron microscopy. T. M., D. L., S. S., M. K., H. E. S., and S. E. K. did the behavior experiments and analysis supervised by A. S. and C. M. P. J.C.T. and J.-H.H. provided reagents. M. A. B., A. S., and P. F. W. wrote the manuscript and P. F. W. supervised the overall project. We thank Maria Papapavlou for administrative assistance; Holly Wellington, Ann Lawler, Johnisha Witherspoon, and Charles Hawkins for assistance in generating the Shank3(+/Delta C) mice; Uejin Kim, Jasmin Harpe, Matt Jo, Pennson Wang, Dakim Gaines, Olivia Tong, Julia Wynne, and Eugenia Cho for help with behavioral testing and data handling; Ya-Xian Wang for help with the electron microscopy preparation. This work was supported by National Institute of Neurological Disorders and Stroke grant 5R01NS070301-02 (P. F. W.), National Institute of Mental Health Core grant 5P50MH084020-03 (P. F. W.), National 973 Basic Research Program of China 20009CB941400 (B. X.), R21HD065290 (C. M. P.), R01MH081164 (C. M. P.), Autism Speaks (C. M. P. and M. K.), The Autism Science Foundation (C. M. P. and H. S.), The Hartwell Foundation (C. M. P.), NIDCD Intramural Program (R. S. P.), and Weatherstone predoctoral fellowship from Autism Speaks (M.A.B.). CR Bear MF, 2004, TRENDS NEUROSCI, V27, P370, DOI 10.1016/j.tins.2004.04.009 Beneken J, 2000, NEURON, V26, P143, DOI 10.1016/S0896-6273(00)81145-9 Bonaglia MC, 2001, AM J HUM GENET, V69, P261, DOI 10.1086/321293 Brakeman PR, 1997, NATURE, V386, P284, DOI 10.1038/386284a0 Condra JA, 2007, PSYCHIAT GENET, V17, P292, DOI 10.1097/YPG.0b013e3281ac2345 DeLisi LE, 2002, AM J PSYCHIAT, V159, P803, DOI 10.1176/appi.ajp.159.5.803 Durand CM, 2007, NAT GENET, V39, P25, DOI 10.1038/ng1933 Ehlers MD, 2003, NAT NEUROSCI, V6, P231, DOI 10.1038/nn1013 Ferguson JN, 2002, FRONT NEUROENDOCRIN, V23, P200, DOI 10.1006/frne.2002.0229 Gauthier J, 2010, P NATL ACAD SCI USA, V107, P7863, DOI 10.1073/pnas.0906232107 Geschwind DH, 2008, CELL, V135, P391, DOI 10.1016/j.cell.2008.10.016 Hayashi MK, 2009, CELL, V137, P159, DOI 10.1016/j.cell.2009.01.050 Huber KM, 2002, P NATL ACAD SCI USA, V99, P7746, DOI 10.1073/pnas.122205699 Kanne SM, 2011, J AUTISM DEV DISORD, V41, P926, DOI 10.1007/s10803-010-1118-4 Kato A, 2005, P NATL ACAD SCI USA, V102, P5600, DOI 10.1073/pnas.0501769102 Marshall CR, 2008, AM J HUM GENET, V82, P477, DOI 10.1016/j.ajhg.2007.12.009 Moessner R, 2007, AM J HUM GENET, V81, P1289, DOI 10.1086/522S90 Mohn AR, 1999, CELL, V98, P427, DOI 10.1016/S0092-8674(00)81972-8 NESSLINGER NJ, 1994, AM J HUM GENET, V54, P464 Powell CM, 2006, BIOL PSYCHIAT, V59, P1198, DOI 10.1016/j.biopsych.2006.05.008 Rampon C, 2000, NAT NEUROSCI, V3, P238 Rapoport J, 2009, J AM ACAD CHILD PSY, V48, P10, DOI 10.1097/CHI.0b013e31818b1c63 Roussignol G, 2005, J NEUROSCI, V25, P3560, DOI 10.1523/JNEUROSCI.4354-04.2005 Sebat J, 2007, SCIENCE, V316, P445, DOI 10.1126/science.1138659 Szumlinski KK, 2005, GENES BRAIN BEHAV, V4, P273, DOI 10.1111/j.1601-183X.2005.00120x NR 25 TC 68 Z9 71 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0092-8674 J9 CELL JI Cell PD MAY 27 PY 2011 VL 145 IS 5 BP 758 EP 772 DI 10.1016/j.cell.2011.03.052 PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 769MR UT WOS:000291018600015 PM 21565394 ER PT J AU Suda, M Takei, Y Aoyama, Y Narita, K Sakurai, N Fukuda, M Mikuni, M AF Suda, Masashi Takei, Yuichi Aoyama, Yoshiyuki Narita, Kosuke Sakurai, Noriko Fukuda, Masato Mikuni, Masahiko TI Autistic Traits and Brain Activation during Face-to-Face Conversations in Typically Developed Adults SO PLOS ONE LA English DT Article ID NEAR-INFRARED SPECTROSCOPY; SPECTRUM QUOTIENT AQ; SOCIAL BRAIN; ASPERGER-SYNDROME; CHILDHOOD AUTISM; PERCEPTION; REACTIVITY; DISORDERS; FLUENCY AB Background: Autism spectrum disorders (ASD) are characterized by impaired social interaction and communication, restricted interests, and repetitive behaviours. The severity of these characteristics is posited to lie on a continuum that extends into the general population. Brain substrates underlying ASD have been investigated through functional neuroimaging studies using functional magnetic resonance imaging (fMRI). However, fMRI has methodological constraints for studying brain mechanisms during social interactions (for example, noise, lying on a gantry during the procedure, etc.). In this study, we investigated whether variations in autism spectrum traits are associated with changes in patterns of brain activation in typically developed adults. We used near-infrared spectroscopy (NIRS), a recently developed functional neuroimaging technique that uses near-infrared light, to monitor brain activation in a natural setting that is suitable for studying brain functions during social interactions. Methodology: We monitored regional cerebral blood volume changes using a 52-channel NIRS apparatus over the prefrontal cortex (PFC) and superior temporal sulcus (STS), 2 areas implicated in social cognition and the pathology of ASD, in 28 typically developed participants (14 male and 14 female) during face-to-face conversations. This task was designed to resemble a realistic social situation. We examined the correlations of these changes with autistic traits assessed using the Autism-Spectrum Quotient (AQ). Principal Findings: Both the PFC and STS were significantly activated during face-to-face conversations. AQ scores were negatively correlated with regional cerebral blood volume increases in the left STS during face-to-face conversations, especially in males. Conclusions: Our results demonstrate successful monitoring of brain function during realistic social interactions by NIRS as well as lesser brain activation in the left STS during face-to-face conversations in typically developed participants with higher levels of autistic traits. C1 [Suda, Masashi; Takei, Yuichi; Aoyama, Yoshiyuki; Narita, Kosuke; Sakurai, Noriko; Fukuda, Masato; Mikuni, Masahiko] Gunma Univ, Grad Sch Med, Dept Psychiat & Neurosci, Gunma, Japan. RP Suda, M (reprint author), Gunma Univ, Grad Sch Med, Dept Psychiat & Neurosci, Gunma, Japan. EM fkdpsy@med.gunma-u.ac.jp FU Gunma University; Hitachi Group (Advanced Research Laboratory, Hitachi Ltd, and the Research and Developmental Center, Hitachi Medical Corporation) FX Gunma University (Drs. Fukuda and Mikuni) and the Hitachi Group (Advanced Research Laboratory, Hitachi Ltd, and the Research and Developmental Center, Hitachi Medical Corporation) have had an official contract for a collaborative study of the clinical application of near-infrared spectroscopy in psychiatric disorders since 2002. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Iwata, Yasuhide Nakamura, Kazuhiko Tsujii, Masatsugu Sugiyama, Toshirou Mori, Norio TI Plasma Cytokine Profiles in Subjects with High-Functioning Autism Spectrum Disorders SO PLOS ONE LA English DT Article ID T-CELLS; INTERFERON-GAMMA; IMMUNE-RESPONSE; CHILDREN; SERUM; INTERLEUKIN-12; INFLAMMATION; ACTIVATION; INNATE; BRAIN AB Background: Accumulating evidence suggests that dysregulation of the immune system is involved in the pathophysiology of autism spectrum disorders (ASD). The aim of the study was to explore immunological markers in peripheral plasma samples from non-medicated subjects with high-functioning ASD. Methodology/Principal Findings: A multiplex assay for cytokines and chemokines was applied to plasma samples from male subjects with high-functioning ASD (n = 28) and matched controls (n = 28). Among a total of 48 analytes examined, the plasma concentrations of IL-1 beta, IL-1RA, IL-5, IL-8, IL-12(p70), IL-13, IL-17 and GRO-alpha were significantly higher in subjects with ASD compared with the corresponding values of matched controls after correction for multiple comparisons. Conclusion/Significance: The results suggest that abnormal immune responses as assessed by multiplex analysis of cytokines may serve as one of the biological trait markers for ASD. C1 [Suzuki, Katsuaki; Matsuzaki, Hideo; Iwata, Keiko; Takebayashi, Kiyokazu; Matsumoto, Kaori; Tsuchiya, Kenji J.; Mori, Norio] Hamamatsu Univ Sch Med, Res Ctr Child Mental Dev, Hamamatsu, Shizuoka 4313192, Japan. [Kameno, Yosuke; Shimmura, Chie; Wakuda, Tomoyasu; Takagai, Shu; Iwata, Yasuhide; Nakamura, Kazuhiko; Mori, Norio] Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan. [Kawai, Satomi] Natl Hosp Org Tenryu Hosp, Dept Psychiat, Hamamatsu, Shizuoka, Japan. [Yoshihara, Yujiro] Koujin Hosp, Dept Psychiat, Nagoya, Aichi, Japan. [Tsujii, Masatsugu] Chukyo Univ, Fac Sociol, Toyota, Japan. [Sugiyama, Toshirou] Hamamatsu Univ Sch Med, Dept Child & Adolescent Psychiat, Hamamatsu, Shizuoka 4313192, Japan. RP Suzuki, K (reprint author), Hamamatsu Univ Sch Med, Res Ctr Child Mental Dev, Hamamatsu, Shizuoka 4313192, Japan. EM k-suzuki@hama-med.ac.jp FU Ministry of Education, Culture, Sports, Science, and Technology of Japan [22390221] FX This work was supported by a Grant-in-Aid for Scientific Research (B) from the Ministry of Education, Culture, Sports, Science, and Technology of Japan to KS (#22390221). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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Takami, Satoshi Kishino, Hirohisa TI A scan statistic to extract causal gene clusters from case-control genome-wide rare CNV data SO BMC BIOINFORMATICS LA English DT Article ID COPY NUMBER VARIATION; AUTISM SPECTRUM DISORDERS; COMMON DISEASES; ASSOCIATION; SCHIZOPHRENIA; VARIANTS; MICRODELETIONS; EXPRESSION; UBIQUITIN; SEQUENCE AB Background: Several statistical tests have been developed for analyzing genome-wide association data by incorporating gene pathway information in terms of gene sets. Using these methods, hundreds of gene sets are typically tested, and the tested gene sets often overlap. This overlapping greatly increases the probability of generating false positives, and the results obtained are difficult to interpret, particularly when many gene sets show statistical significance. Results: We propose a flexible statistical framework to circumvent these problems. Inspired by spatial scan statistics for detecting clustering of disease occurrence in the field of epidemiology, we developed a scan statistic to extract disease-associated gene clusters from a whole gene pathway. Extracting one or a few significant gene clusters from a global pathway limits the overall false positive probability, which results in increased statistical power, and facilitates the interpretation of test results. In the present study, we applied our method to genome-wide association data for rare copy-number variations, which have been strongly implicated in common diseases. Application of our method to a simulated dataset demonstrated the high accuracy of this method in detecting disease-associated gene clusters in a whole gene pathway. Conclusions: The scan statistic approach proposed here shows a high level of accuracy in detecting gene clusters in a whole gene pathway. This study has provided a sound statistical framework for analyzing genome-wide rare CNV data by incorporating topological information on the gene pathway. C1 [Nishiyama, Takeshi] Natl Inst Publ Hlth, Publ Hlth Program Biostat, Wako, Saitama 3510197, Japan. [Nishiyama, Takeshi] Nagoya City Univ Hosp, Clin Trial Management Ctr, Nagoya, Aichi 4678601, Japan. [Takahashi, Kunihiko; Tango, Toshiro] Natl Inst Publ Hlth, Dept Technol Assessment & Biostat, Wako, Saitama 3510197, Japan. [Tango, Toshiro] Ctr Med Stat, Tokyo 1050021, Japan. [Pinto, Dalila; Scherer, Stephen W.] Hosp Sick Children, Ctr Appl Genom, Toronto, ON M5G 1L7, Canada. [Pinto, Dalila; Scherer, Stephen W.] Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1L7, Canada. [Takami, Satoshi; Kishino, Hirohisa] Univ Tokyo, Lab Biometry & Bioinformat, Grad Sch Agr & Life Sci, Tokyo 1138657, Japan. RP Nishiyama, T (reprint author), Natl Inst Publ Hlth, Publ Hlth Program Biostat, Wako, Saitama 3510197, Japan. EM nishiyama@minos.ocn.ne.jp RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013 OI Scherer, Stephen /0000-0002-8326-1999 FU Ministry of Education, Science, Sports and Culture [22300095] FX The authors acknowledge the families participating in the Autism Genome Project Consortium (AGP) and the Study of Addiction: Genetics and Environment (SAGE). This work was supported by the Grant-in-Aid for Scientific Research (B) 22300095 from the Ministry of Education, Science, Sports and Culture. 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SO BMC MEDICINE LA English DT Editorial Material ID RECURRENCE; MOTHERS; RISK AB The ability to determine an infant's likelihood of developing autism via a relatively simple neurological measure would constitute an important scientific breakthrough. In their recent publication in this journal, Bosl and colleagues claim that a measure of EEG complexity can be used to detect, with very high accuracy, infants at high risk for autism (HRA). On the surface, this appears to be that very scientific breakthrough and as such the paper has received widespread media attention. But a close look at how these high accuracy rates were derived tells a very different story. This stems from a conflation between "high risk" as a population-level property and "high risk" as a property of an individual. We describe the approach of Bosl et al. and examine their results with respect to baseline prevalence rates, the inclusion of which is necessary to distinguish infants with a biological risk of autism from typically developing infants with a sibling with autism. This is an important distinction that should not be overlooked. Please see research article: http://www.biomedcentral.com/1741-7015/9/18 and correspondence article: http://www.biomedcentral. com/1741-7015/9/60 C1 [Griffin, Richard] Tufts Univ, Dept Psychol, Medford, MA 02155 USA. [Griffin, Richard] Tufts Univ, Ctr Cognit Studies, Medford, MA 02155 USA. [Westbury, Chris] Univ Alberta, Dept Psychol, Edmonton, AB, Canada. RP Griffin, R (reprint author), Tufts Univ, Dept Psychol, Medford, MA 02155 USA. 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PD MAY 20 PY 2011 VL 9 AR 61 DI 10.1186/1741-7015-9-61 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 778XT UT WOS:000291743400001 PM 21599952 ER PT J AU Bosl, W Tierney, A Tager-Flusberg, H Nelson, C AF Bosl, William Tierney, Adrienne Tager-Flusberg, Helen Nelson, Charles TI Response: Infant EEG activity as a biomarker for autism: A promising approach or a false promise? SO BMC MEDICINE LA English DT Letter ID NETWORKS; BRAIN; CONNECTIVITY C1 [Bosl, William; Nelson, Charles] Harvard Univ, Sch Med, Boston, MA 02115 USA. [Bosl, William] Childrens Hosp Boston, Informat Program, Harvard MIT Div Hlth Sci & Technol, Boston, MA USA. [Tierney, Adrienne] Harvard Univ, Grad Sch Educ, Cambridge, MA 02138 USA. [Tierney, Adrienne; Nelson, Charles] Childrens Hosp Boston, Dept Dev Med, Boston, MA USA. [Tager-Flusberg, Helen] Boston Univ, Dept Psychol, Boston, MA 02215 USA. RP Bosl, W (reprint author), Harvard Univ, Sch Med, Boston, MA 02115 USA. 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PD MAY 20 PY 2011 VL 9 AR 60 DI 10.1186/1741-7015-9-60 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 786IQ UT WOS:000292298700001 PM 21599951 ER PT J AU Wei, HG Zou, H Sheikh, AM Malik, M Dobkin, C Brown, WT Li, XH AF Wei, Hongen Zou, Hua Sheikh, Ashfaq M. Malik, Mazhar Dobkin, Carl Brown, W. Ted Li, Xiaohong TI IL-6 is increased in the cerebellum of autistic brain and alters neural cell adhesion, migration and synaptic formation SO JOURNAL OF NEUROINFLAMMATION LA English DT Article DE Autism cytokines; synapse development; neural adhesion and migration; apoptosis; inflammation ID CENTRAL-NERVOUS-SYSTEM; SPECTRUM DISORDER; CYTOKINE PRODUCTION; NEURONAL MIGRATION; INTERFERON-GAMMA; INTERLEUKIN-6; APOPTOSIS; CHILDREN; ACTIVATION; DIFFERENTIATION AB Background: Although the cellular mechanisms responsible for the pathogenesis of autism are not understood, a growing number of studies have suggested that localized inflammation of the central nervous system (CNS) may contribute to the development of autism. Recent evidence shows that IL-6 has a crucial role in the development and plasticity of CNS. Methods: Immunohistochemistry studies were employed to detect the IL-6 expression in the cerebellum of study subjects. In vitro adenoviral gene delivery approach was used to over-express IL-6 in cultured cerebellar granule cells. Cell adhesion and migration assays, Dil labeling, TO-PRO-3 staining and immunofluorescence were used to examine cell adhesion and migration, dendritic spine morphology, cell apoptosis and synaptic protein expression respectively. Results: In this study, we found that IL-6 was significantly increased in the cerebellum of autistic subjects. We investigated how IL-6 affects neural cell development and function by transfecting cultured mouse cerebellar granule cells with an IL-6 viral expression vector. We demonstrated that IL-6 over-expression in granule cells caused impairments in granule cell adhesion and migration but had little effect on the formation of dendritic spines or granule cell apoptosis. However, IL-6 over-expression stimulated the formation of granule cell excitatory synapses, without affecting inhibitory synapses. Conclusions: Our results provide further evidence that aberrant IL-6 may be associated with autism. In addition, our results suggest that the elevated IL-6 in the autistic brain could alter neural cell adhesion, migration and also cause an imbalance of excitatory and inhibitory circuits. Thus, increased IL-6 expression may be partially responsible for the pathogenesis of autism. C1 [Wei, Hongen; Zou, Hua; Sheikh, Ashfaq M.; Malik, Mazhar; Li, Xiaohong] NY State Inst Basic Res Dev Disabil, Dept Neurochem, New York, NY USA. [Dobkin, Carl; Brown, W. Ted] NY State Inst Basic Res Dev Disabil, Dept Human Genet, New York, NY USA. [Wei, Hongen] Shanghai Jiao Tong Univ, Sch Med, Shanghai Mental Hlth Ctr, Shanghai 200030, Peoples R China. [Zou, Hua] Nanfang Hosp, Dept Obstet & Gynecol, Guangzhou, Guangdong, Peoples R China. RP Li, XH (reprint author), NY State Inst Basic Res Dev Disabil, Dept Neurochem, New York, NY USA. EM xiaohongli99@gmail.com FU NYS Office for People with Developmental Disabilities; Rural India Charitable Trust; Northfield Bank Foundation FX This work was supported by the NYS Office for People with Developmental Disabilities, the Rural India Charitable Trust, and Northfield Bank Foundation. 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Neuroinflamm. PD MAY 19 PY 2011 VL 8 AR 52 DI 10.1186/1742-2094-8-52 PG 10 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 777CM UT WOS:000291591500001 PM 21595886 ER PT J AU Berger, BE Navar-Boggan, AM Omer, SB AF Berger, Brynn E. Navar-Boggan, Ann Marie Omer, Saad B. TI Congenital rubella syndrome and autism spectrum disorder prevented by rubella vaccination - United States, 2001-2010 SO BMC PUBLIC HEALTH LA English DT Article ID DEVELOPING-COUNTRIES; MEASLES; MUMPS; POPULATION; VACCINES; CHILDREN; BURDEN AB Background: Congenital rubella syndrome (CRS) is associated with several negative outcomes, including autism spectrum disorders (ASDs). The objective of this study was to estimate the numbers of CRS and ASD cases prevented by rubella vaccination in the United States from 2001 through 2010. Methods: Prevention estimates were calculated through simple mathematical modeling, with values of model parameters determined from published literature. Model parameters included pre-vaccine era CRS incidence, vaccine era CRS incidence, the number of live births per year, and the percentage of CRS cases presenting with an ASD. Results: Based on our estimates, 16,600 CRS cases (range: 8300-62,250) were prevented by rubella vaccination from 2001 through 2010 in the United States. An estimated 1228 ASD cases were prevented by rubella vaccination in the United States during this time period. Simulating a slight expansion in ASD diagnostic criteria in recent decades, we estimate that a minimum of 830 ASD cases and a maximum of 6225 ASD cases were prevented. Conclusions: We estimate that rubella vaccination prevented substantial numbers of CRS and ASD cases in the United States from 2001 through 2010. These findings provide additional incentive to maintain high measles-mumps-rubella (MMR) vaccination coverage. C1 [Berger, Brynn E.] Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, Atlanta, GA 30322 USA. [Navar-Boggan, Ann Marie] Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. [Navar-Boggan, Ann Marie] Duke Univ, Med Ctr, Dept Internal Med, Durham, NC 27710 USA. [Omer, Saad B.] Emory Univ, Rollins Sch Publ Hlth, Hubert Dept Global Hlth, Atlanta, GA 30322 USA. [Omer, Saad B.] Emory Univ, Sch Med, Dept Pediat, Atlanta, GA 30322 USA. [Omer, Saad B.] Emory Vaccine Ctr, Atlanta, GA USA. RP Berger, BE (reprint author), Emory Univ, Rollins Sch Publ Hlth, Dept Epidemiol, 1518 Clifton Rd NE,Room 7017,CNR Bldg, Atlanta, GA 30322 USA. EM brynn.e.berger@gmail.com RI Omer, Saad/K-1182-2012 OI Omer, Saad/0000-0002-5383-3474 FU Emory University Global Health Institute FX This study was partially funded through the Emory University Global Health Institute which had no role in the design and conduct of the study; management, analysis, and interpretation of the data; and preparation and submission of the final manuscript. No honorarium, grant, or other form of payment was given to anyone to produce this manuscript. 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Sreenivasula, Swapna Adams, James B. TI Traditional and non-traditional treatments for autism spectrum disorder with seizures: an online survey SO BMC PEDIATRICS LA English DT Article ID LANDAU-KLEFFNER-SYNDROME; FRONTAL-LOBE EPILEPSY; KETOGENIC DIET; CHILDREN; EEG; ABNORMALITIES; PREVALENCE; MEDICATION; EFFICACY AB Background: Despite the high prevalence of seizure, epilepsy and abnormal electroencephalograms in individuals with autism spectrum disorder (ASD), there is little information regarding the relative effectiveness of treatments for seizures in the ASD population. In order to determine the effectiveness of traditional and non-traditional treatments for improving seizures and influencing other clinical factor relevant to ASD, we developed a comprehensive on-line seizure survey. Methods: Announcements (by email and websites) by ASD support groups asked parents of children with ASD to complete the on-line surveys. Survey responders choose one of two surveys to complete: a survey about treatments for individuals with ASD and clinical or subclinical seizures or abnormal electroencephalograms, or a control survey for individuals with ASD without clinical or subclinical seizures or abnormal electroencephalograms. Survey responders rated the perceived effect of traditional antiepileptic drug (AED), non-AED seizure treatments and non-traditional ASD treatments on seizures and other clinical factors (sleep, communication, behavior, attention and mood), and listed up to three treatment side effects. Results: Responses were obtained concerning 733 children with seizures and 290 controls. In general, AEDs were perceived to improve seizures but worsened other clinical factors for children with clinical seizure. Valproic acid, lamotrigine, levetiracetam and ethosuximide were perceived to improve seizures the most and worsen other clinical factors the least out of all AEDs in children with clinical seizures. Traditional non-AED seizure and non-traditional treatments, as a group, were perceived to improve other clinical factors and seizures but the perceived improvement in seizures was significantly less than that reported for AEDs. Certain traditional non-AED treatments, particularly the ketogenic diet, were perceived to improve both seizures and other clinical factors. For ASD individuals with reported subclinical seizures, other clinical factors were reported to be worsened by AEDs and improved by non-AED traditional seizure and non-traditional treatments. The rate of side effects was reportedly higher for AEDs compared to traditional non-AED treatments. Conclusion: Although this survey-based method only provides information regarding parental perceptions of effectiveness, this information may be helpful for selecting seizure treatments in individuals with ASD. C1 [Frye, Richard E.] Univ Texas Hlth Sci Ctr, Dept Pediat, Houston, TX 77225 USA. [Sreenivasula, Swapna] Univ Texas Hlth Sci Ctr, Sch Publ Hlth, Houston, TX USA. [Adams, James B.] Arizona State Univ, Sch Mech Aerosp Chem & Mat Engn, Tempe, AZ USA. RP Frye, RE (reprint author), Univ Texas Hlth Sci Ctr, Dept Pediat, Houston, TX 77225 USA. EM Richard.E.Frye@uth.tmc.edu FU Autism Research Institute; National Institutes of Health FX The Autism Research Institute provided partial funding for this study. The authors would like to thank Teri Arranga and Drs. Steve Edelson, Martha Herbert, Derrick MacFabe and Dan Rossignol for their advice and assistance with this project. We thank the members of the Elias Think Tank (See Additional file 1, Appendix A) for their advice on developing the survey. We also thank the Autism Research Institute, Autism Speaks, and many other ASD groups for their assistance in advertising the survey. We especially thank the many parents who volunteered their time to participate in this study.Dr. Richard E. Frye received his medical degree from Georgetown University. He completed his pediatric residency training at Jackson Memorial Hospital/University of Miami and child neurology residency training at Children's Hospital Boston/Harvard University. Following residency Dr. Frye completed concurrent fellowships, one in Behavioral Neurology and Learning Disabilities at Children's Hospital Boston/Harvard University and another in Psychology at Boston University. Dr. Frye completed a Ph.D. in Physiology and Biophysics at Georgetown University and a M. S. in Biomedical Science and Biostatistics at Drexel University. Dr. Frye is board certified in Pediatrics and in Neurology with special competency in Child Neurology. Dr. Frye has been funded by the National Institutes of Health to study brain function in individuals with neurodevelopmental disorders. Dr. Frye is the medical-director of the University of Texas medically-based autism clinic. The purpose of this unique clinic is to diagnose and treat medical disorders associated with autism in order to optimize remediation and recovery. Swapna Sreenivasula is currently a graduate student in the School of Public Health at University of Texas. She completed a Bachelor of Medicine and Bachelor of Surgery (M. B. B. S.) at Rangaraya Medical College, Kakinada Andhra Pradesh, India. 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The following research utilized a nonhuman primate;node] to investigate the potential impact of a mild endotoxemia during pregnancy on brain maturation and behavioral reactivity as well as the infants' hormone and immune physiology. Nine pregnant female rhesus monkeys (Macaca mulatto) were administered nanogram concentrations of lipopolysaccharide (LPS) on two consecutive days, 6 weeks before term, and their offspring were compared to nine control animals. When tested under arousing challenge conditions, infants from the LPS pregnancies were more behaviorally disturbed, including a failure to show a normal attenuation of startle responses on tests of prepulse inhibition. Examination of their brains at 1 year of age with magnetic resonance imaging (MRI) revealed the unexpected finding of a significant 8.8% increase in global white matter volume distributed across many cortical regions compared to controls. More selective changes in regional gray matter volume and cortical thickness were noted in parietal, medial temporal, and frontal areas. While inhibited neural growth has been described previously after prenatal infection and LPS administration at higher doses in rodents, this low dose endotoxemia in the monkey is the first paradigm to produce a neural phenotype associated with augmented gray and white matter growth. Published by Elsevier B.V. C1 [Willette, Auriel A.; Lubach, Gabriele R.; Short, Sarah J.; Coe, Christopher L.] Univ Wisconsin, Harlow Primate Lab, Madison, WI 53715 USA. [Knickmeyer, Rebecca C.; Styner, Martin; Gilmore, John H.] Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. [Styner, Martin] Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. RP Willette, AA (reprint author), Univ Wisconsin, Dept Med, 2500 Overlook Terrace, Madison, WI 53705 USA. EM AAWillette@medicine.wisc.edu RI Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 FU NIAID [A1067518]; NIMH (Conte Center) [MH064065]; NICHD (UNC Neurodevelopmental Disorders Research Center) [HD03110]; CTSA [IUL1RR025011] FX This research was supported by grants to CLC from the NIAID (A1067518), to JG from the NIMH (Conte Center, MH064065), and to MS from NICHD (UNC Neurodevelopmental Disorders Research Center (HD03110). Cortisol assays were conducted through the Endocrine Services unit of an NCRR-supported CTSA (IUL1RR025011). The assistance of A. Slukvina, H. Crispen, and other HPL staff with sample collection and assays is greatly appreciated. R. Bernstein provided valuable assistance in collecting peer behavior data. 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Brain Res. PD MAY 16 PY 2011 VL 219 IS 1 BP 108 EP 115 DI 10.1016/j.bbr.2010.12.023 PG 8 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 752BX UT WOS:000289664100016 PM 21192986 ER PT J AU Zheng, FF Wang, LF Jia, MX Yue, WH Ruan, Y Lu, TL Liu, J Li, J Zhang, D AF Zheng, Fanfan Wang, Lifang Jia, Meixiang Yue, Weihua Ruan, Yan Lu, Tianlan Liu, Jing Li, Jun Zhang, Dai TI Evidence for association between Disrupted-in-schizophrenia 1 (DISC1) gene polymorphisms and autism in Chinese Han population: a family-based association study SO BEHAVIORAL AND BRAIN FUNCTIONS LA English DT Article DE DISC1 autism; SNP; FBAT; association study ID ADULT BRAIN; SPECTRUM DISORDERS; NEURITE OUTGROWTH; MOTOR TASK; DISRUPTED-IN-SCHIZOPHRENIA-1; RISK; TWIN; TRANSLOCATION; PROTEIN; CORTEX AB Background: Disrupted-in-Schizophrenia 1 (DISC1) gene is one of the most promising candidate genes for major mental disorders. In a previous study, a Finnish group demonstrated that DISC1 polymorphisms were associated with autism and Asperger syndrome. However, the results were not replicated in Korean population. To determine whether DISC1 is associated with autism in Chinese Han population, we performed a family-based association study between DISC1 polymorphisms and autism. Methods: We genotyped seven tag single nucleotide polymorphisms (SNPs) in DISC1, spanning 338 kb, in 367 autism trios (singleton and their biological parents) including 1,101 individuals. Single SNP association and haplotype association analysis were performed using the family-based association test (FBAT) and Haploview software. Results: We found three SNPs showed significant associations with autism (rs4366301: G > C, Z = 2.872, p = 0.004; rs11585959: T > C, Z = 2.199, p = 0.028; rs6668845: A > G, Z = 2.326, p = 0.02). After the Bonferroni correction, SNP rs4366301, which located in the first intron of DISC1, remained significant. When haplotype were constructed with two-markers, three haplotypes displayed significant association with autism. These results were still significant after using the permutation method to obtain empirical p values. Conclusions: Our study provided evidence that the DISC1 may be the susceptibility gene of autism. It suggested DISC1 might play a role in the pathogenesis of autism. C1 [Zheng, Fanfan; Wang, Lifang; Yue, Weihua; Ruan, Yan; Lu, Tianlan; Li, Jun; Zhang, Dai] Minist Hlth, Key Lab Mental Hlth, Beijing, Peoples R China. [Zheng, Fanfan; Wang, Lifang; Jia, Meixiang; Yue, Weihua; Ruan, Yan; Lu, Tianlan; Liu, Jing; Li, Jun; Zhang, Dai] Peking Univ, Inst Mental Hlth, Beijing 100871, Peoples R China. RP Zhang, D (reprint author), Minist Hlth, Key Lab Mental Hlth, Beijing, Peoples R China. EM daizhang@bjmu.edu.cn FU National High Technology Research and Development Program of China [2010CB833905]; National Natural Science Foundation of China [30870897, 81071110]; Beijing Natural Science Foundation [7081005] FX We thank all the patients and their families for their support and participation. This work was supported by grants from the National High Technology Research and Development Program of China (2010CB833905), the National Natural Science Foundation of China (30870897, 81071110), and the Beijing Natural Science Foundation (7081005). 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The feedback-related negativity (FRN) is an event-related potential (ERP) that is more negative following losses than gains. We examined FRN amplitude in 25 individuals with Autism Spectrum Disorder (ASD) and 25 age- and IQ-matched typically developing control participants who completed a guessing task with monetary loss/gain feedback. Both groups demonstrated a robust FRN that was more negative to loss trials than gain trials; however, groups did not differ in FRN amplitude as a function of gain or loss trials. N1 and P300 amplitudes did not differentiate groups. FRN amplitude was positively correlated with age in individuals with ASD, but not measures of intelligence, anxiety, behavioral inhibition, or autism severity. Given previous findings of reduced-amplitude error-related negativity (ERN) in ASD, we propose that individuals with ASD may process external, concrete, feedback similar to typically developing individuals, but have difficulty with internal, more abstract, regulation of performance. (C) 2010 Elsevier Ireland Ltd. All rights reserved. C1 [Larson, Michael J.; South, Mikle; Krauskopf, Erin; Clawson, Ann] Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA. [Larson, Michael J.; South, Mikle] Brigham Young Univ, Ctr Neurosci, Provo, UT 84602 USA. [Crowley, Michael J.] Yale Child Study Ctr, New Haven, CT 06520 USA. RP Larson, MJ (reprint author), Brigham Young Univ, Dept Psychol, 244 TLRB, Provo, UT 84602 USA. EM michael_larson@byu.edu RI Larson, Michael/C-8543-2012; South, Mikle/H-4978-2013 OI South, Mikle/0000-0003-0152-1257 FU Brigham Young University College of Family, Home, and Social Sciences FX We gratefully acknowledge the assistance of Oliver Johnston and Peter Clayson in data collection. This study was supported by funds from the Brigham Young University College of Family, Home, and Social Sciences. 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PD MAY 15 PY 2011 VL 187 IS 1-2 BP 198 EP 203 DI 10.1016/j.psychres.2010.11.006 PG 6 WC Psychiatry SC Psychiatry GA 758RL UT WOS:000290183700034 PM 21122921 ER PT J AU McLaughlin, MR AF McLaughlin, Maura R. TI Speech and Language Delay in Children SO AMERICAN FAMILY PHYSICIAN LA English DT Article ID FOLLOW-UP; PRESCHOOL; DIFFICULTIES; INTELLIGENCE; RETARDATION; IMPAIRMENTS; OUTCOMES AB Speech and language delay in children is associated with increased difficulty with reading, writing, attention, and socialization. Although physicians should be alert to parental concerns and to whether children are meeting expected developmental milestones, there currently is insufficient evidence to recommend for or against routine use of formal screening instruments in primary care to detect speech and language delay. In children not meeting the expected milestones for speech and language, a comprehensive developmental evaluation is essential, because atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems. Types of primary speech and language delay include developmental speech and language delay, expressive language disorder, and receptive language disorder. Secondary speech and language delays are attributable to another condition such as hearing loss, intellectual disability, autism spectrum disorder, physical speech problems, or selective mutism. When speech and language delay is suspected, the primary care physician should discuss this concern with the parents and recommend referral to a speech-language pathologist and an audiologist. There is good evidence that speech-language therapy is helpful, particularly for children with expressive language disorder. 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Fam. Physician PD MAY 15 PY 2011 VL 83 IS 10 BP 1183 EP 1188 PG 6 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA 979ZS UT WOS:000306864000006 PM 21568252 ER PT J AU Ming, X Hashim, A Fleishman, S West, T Kang, N Chen, X Zimmerman-Bier, B AF Ming, Xue Hashim, Anjum Fleishman, Sharon West, Therese Kang, Ning Chen, Xiang Zimmerman-Bier, Barbie TI Access to specialty care in autism spectrum disorders-a pilot study of referral source SO BMC HEALTH SERVICES RESEARCH LA English DT Article ID CHILDREN AB Background: In the United States, a medical home model has been shown to improve the outcomes for children with special health care needs. As part of this model, primary care physicians provide comprehensive medical care that includes identification of delayed and/or atypical development in children and coordination of care with specialists. However, it is not clear if families of children with Autism Spectrum Disorder ( ASD) rely on the medical home model for care of their child to the same extent as families of children with other special health care needs. This study aims to add to the understanding of medical care for children with ASD by examining the referral source for specialty care. Methods: This retrospective study was accomplished by evaluating parent completed intake data for children with ASD compared to those with other neurological disorders in a single physician Pediatric Neurology Practice at a major urban medical center in Northern New Jersey. To account for referral bias, a similar comparison study was conducted using a multispecialty ASD practice at the same medical center. Parent reported "source of referral" and "reason for the referral" of 189 ASD children and 108 non-ASD neurological disordered children were analyzed. Results: The specialty evaluations of ASD were predominantly parent initiated. There were significantly less referrals received from primary care physicians for children with ASD compared to children with other neurodevelopmental disorders. Requirement of an insurance referral was not associated with a primary care physician prompted specialty visit. We identified different patterns of referral to our specialty clinics for children with ASD vs. children with other neurolodevelopmental disorders. Conclusion: The majority of the families of children with ASD evaluated at our autism center did not indicate that a primary care physician initiated the specialty referral. This study suggests that families of children with ASD interface differently with the primary care provider than families of children with other neurological disorders. C1 [Ming, Xue; West, Therese] UMDNJ New Jersey Med Sch, Dept Neurosci & Neurol, Newark, NJ 07103 USA. [Ming, Xue; Fleishman, Sharon; West, Therese] UMDNJ New Jersey Med Sch, Autism Ctr, Newark, NJ USA. [Hashim, Anjum] Newark Beth Israel Hosp, Dept Pediat, Newark, NJ USA. [Kang, Ning] Hlth Benchmarks Inc, IMS Hlth, Woodland Hills, CA USA. [Chen, Xiang] Yu Yin Childrens Hosp, WenZhou Med Coll, Dept Neurol, Wenzhou, Peoples R China. [Zimmerman-Bier, Barbie] St Peters Univ Hosp, Dept Pediat, New Brunswick, NJ USA. RP Ming, X (reprint author), UMDNJ New Jersey Med Sch, Dept Neurosci & Neurol, 185 S Orange Ave, Newark, NJ 07103 USA. EM mingxu@umdnj.edu CR Brachlow AE, 2007, ARCH PEDIAT ADOL MED, V161, P399, DOI 10.1001/archpedi.161.4.399 *CDCP, 2009, CDC MORBIDITY MORTAL, V58, P1 Sandler AD, 2001, PEDIATRICS, V107 Johnson CP, 2007, PEDIATRICS, V120, P1183, DOI 10.1542/peds.2007-2361 Kelley E, 2006, J AUTISM DEV DISORD, V36, P807, DOI 10.1007/s10803-006-0111-4 Levy SE, 2009, LANCET, V374, P1627, DOI 10.1016/S0140-6736(09)61376-3 Rhoades Rachel A, 2007, BMC Pediatr, V7, P37, DOI 10.1186/1471-2431-7-37 Sutera S, 2007, J AUTISM DEV DISORD, V37, P98, DOI 10.1007/s10803-006-0340-6 NR 8 TC 3 Z9 3 PU BIOMED CENTRAL LTD PI LONDON PA 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND SN 1472-6963 J9 BMC HEALTH SERV RES JI BMC Health Serv. Res. PD MAY 14 PY 2011 VL 11 AR 99 DI 10.1186/1472-6963-11-99 PG 6 WC Health Care Sciences & Services SC Health Care Sciences & Services GA 778GT UT WOS:000291692600001 PM 21569571 ER PT J AU Yu, JD He, X Yao, D Li, ZY Li, H Zhao, ZY AF Yu, Jindan He, Xue Yao, Dan Li, Zhongyue Li, Hui Zhao, Zhengyan TI A sex-specific association of common variants of neuroligin genes (NLGN3 and NLGN4X) with autism spectrum disorders in a Chinese Han cohort SO BEHAVIORAL AND BRAIN FUNCTIONS LA English DT Article ID MENTAL-RETARDATION; MUTATION; DIFFERENTIATION; GENETICS; BRAIN; NEUROBIOLOGY; EXPRESSION; PROBANDS; REVEALS; SYNAPSE AB Background: Synaptic genes, NLGN3 and NLGN4X, two homologous members of the neuroligin family, have been supposed as predisposition loci for autism spectrum disorders (ASDs), and defects of these two genes have been identified in a small fraction of individuals with ASDs. But no such rare variant in these two genes has as yet been adequately replicated in Chinese population and no common variant has been further investigated to be associated with ASDs. Methods: 7 known ASDs-related rare variants in NLGN3 and NLGN4X genes were screened for replication of the initial findings and 12 intronic tagging single nucleotide polymorphisms (SNPs) were genotyped for case-control association analysis in a total of 229 ASDs cases and 184 control individuals in a Chinese Han cohort, using matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry. Results: We found that a common intronic variant, SNP rs4844285 in NLGN3 gene, and a specific 3-marker haplotype X(A)-X(G)-X(T) (rs11795613-rs4844285-rs4844286) containing this individual SNP were associated with ASDs and showed a male bias, even after correction for multiple testing (SNP allele: P = 0.048, haplotype: P = 0.032). Simultaneously, none of these 7 known rare mutation of NLGN3 and NLGN4X genes was identified, neither in our patients with ASDs nor controls, giving further evidence that these known rare variants might be not enriched in Chinese Han cohort. Conclusion: The present study provides initial evidence that a common variant in NLGN3 gene may play a role in the etiology of ASDs among affected males in Chinese Han population, and further supports the hypothesis that defect of synapse might involvement in the pathophysiology of ASDs. C1 [Yu, Jindan; He, Xue; Yao, Dan; Zhao, Zhengyan] Zhejiang Univ, Sch Med, Childrens Hosp, Dept Pediat Hlth Care, Hangzhou 310003, Zhejiang, Peoples R China. [Li, Zhongyue] Zhejiang Univ, Sch Med, Childrens Hosp, Dept Gastroenterol, Hangzhou 310003, Zhejiang, Peoples R China. [Li, Hui] Zhejiang Univ, Sch Med, Childrens Hosp, Dept Cent Lab, Hangzhou 310003, Zhejiang, Peoples R China. RP Zhao, ZY (reprint author), Zhejiang Univ, Sch Med, Childrens Hosp, Dept Pediat Hlth Care, Hangzhou 310003, Zhejiang, Peoples R China. 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Brain Funct. PD MAY 14 PY 2011 VL 7 AR 13 DI 10.1186/1744-9081-7-13 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 781HS UT WOS:000291922100001 PM 21569590 ER PT J AU Priya, MDL Geetha, A AF Priya, Malarveni Damodaran Lakshmi Geetha, Arumugam TI A biochemical study on the level of proteins and their percentage of nitration in the hair and nail of autistic children SO CLINICA CHIMICA ACTA LA English DT Article DE Autism; Keratins; Low sulfur proteins (LS); High sulfur proteins (HS); Nitration; Oxidative stress ID SPECTRUM DISORDERS; CHILDHOOD AUTISM; RATING-SCALE; GLUTATHIONE; PREVALENCE; COMPLEMENT AB Background: Autism is a complex disorder which is heterogeneous in nature with varying degrees of severity for which no specific biological marker has been identified. Several studies are focused on the hair and nail protein pattern as a means to identify specific markers for the diagnosis of many childhood disorders like mental retardation, dyslexia, trichorrhexis nodosa, trichothiodystrophy, etc. The present study is one such approach in investigating the electrophoretic pattern of proteins in hard keratins and their percentage of nitration since nitric oxide production and nitration of tyrosine residues in proteins of autistic children are the emerging topic of research. Methods: We extracted and quantified the proteins from hair and nail samples of autistic children with different grades of severity, [low functioning autism (LFA), medium functioning autism (MFA), and high functioning autism (HFA)] and also from age- and sex-matched normal children. Protein pattern was evaluated by one-dimensional SDS-PAGE and the separated proteins were made to cross react with anti-nitro tyrosine antibody by Western blot analysis. Blood levels of TBARS, NO, GSH, vitamins A and C, SOD and GPx were also determined. Results: In the autistic groups, decreased concentration of protein in both hair and nail samples was observed. The SDS-PAGE analysis revealed that there was a significant decrease in both high and low sulfur proteins in the hair and nail extracts of autistic children and the Western blot analysis showed increased percentage of nitration of low sulfur proteins in autistic children when compared with normal children. Decreased levels of enzymatic and non-enzymatic antioxidants and increased concentration of TBARS and NO were also observed in the blood of autistic children. The LFA group showed more significant alteration (p < 0.001) in the concentration of proteins (in hair and nail) and percentage of nitration when compared with HFA and controls. Conclusion: Lower protein content and higher percentage of nitration in hair and nail of autistic children correlated with their degrees of severity. (C) 2011 Elsevier B.V. All rights reserved. C1 [Priya, Malarveni Damodaran Lakshmi; Geetha, Arumugam] Univ Madras, Dept Biochem, Bharathi Womens Coll, N Chennai 600108, Tamil Nadu, India. RP Geetha, A (reprint author), Univ Madras, Dept Biochem, Bharathi Womens Coll, N Chennai 600108, Tamil Nadu, India. EM geethav21@yahoo.co.in FU Indian Council of Medical Research, New Delhi FX The author M.D. Lakshmi Priya thanks the Indian Council of Medical Research, New Delhi for the financial assistance. The authors thank V-Excel Educational Trust (the school for special children), Mandaveli, Chennai, Tamil Nadu, India and the parents of autistic children for their cooperation. 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Chakraborty, Pranesh Kwong, Jeff Crowcroft, Natasha Rothwell, Deanna Manuel, Doug TI Patterns of emergency room visits, admissions and death following recommended pediatric vaccinations-A population based study of 969,519 vaccination events SO VACCINE LA English DT Article DE Immunization; Surveillance; Patient safety; Pediatric; Health services research ID SAFETY DATALINK PROJECT; ADVERSE-REACTIONS; CAUSAL ASSOCIATION; VACCINES; PERTUSSIS; MEASLES; MUMPS; IMMUNIZATION; AUTISM; MMR AB Background: The risk of immediate adverse events due to the inflammation created by a vaccine is a potential concern for pediatric vaccine programs. Methods: We analyzed data on children born between March 2006 and March 2009 in the province of Ontario. Using the self-controlled case series design, we examined the risk of the combined endpoint of emergency room visit and hospital admission in the immediate 3 days post vaccination to a control period 9-18 days after vaccination. We examined the end points of emergency room visits, hospital admissions and death separately as secondary outcomes. Results: We examined 969,519 separate vaccination events. The relative incidence of our combined end point was 0.85 (0.80-0.90) for vaccination at age 2 months, 0.74 (0.69-0.79) at age 4 months and 0.68 (0.63-0.72) at age 6 months. The relative incidence was reduced for the individual endpoints of emergency room visits, admissions and death. There were 5 or fewer deaths in the risk interval of all 969,519 vaccination events. In a post hoc analysis we observed a large reduction in events in the immediate 3 days prior to vaccination suggesting a large healthy vaccinee effect. Conclusion: There was no increased incidence of the combined end point of emergency room visits and hospitalizations in the 3-day period immediately following vaccination, nor for individual endpoints or death. The health vaccinee effect could create the perception of worsening health following vaccines in the absence of any vaccine adverse effect and could also mask an effect in the immediate post-vaccination period. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Wilson, Kumanan] Univ Ottawa, Res Inst, Ottawa Hosp, Dept Med, Ottawa, ON K1V 4E9, Canada. [Wilson, Kumanan; Hawken, Steven; Potter, Beth K.; Rothwell, Deanna; Manuel, Doug] Univ Ottawa, Res Inst, Ottawa Hosp, ICES Uottawa, Ottawa, ON K1V 4E9, Canada. [Wilson, Kumanan; Potter, Beth K.; Manuel, Doug] Univ Ottawa, Dept Epidemiol & Community Med, Ottawa, ON K1V 4E9, Canada. [Wilson, Kumanan; Chakraborty, Pranesh] Childrens Hosp Eastern Ontario, Ottawa, ON, Canada. [Chakraborty, Pranesh] Univ Ottawa, Dept Pediat, Ottawa, ON K1V 4E9, Canada. [Kwong, Jeff] Inst Clin Evaluat Sci, Toronto, ON, Canada. [Crowcroft, Natasha] Ontario Agcy Hlth Protect & Promot, Ottawa, ON, Canada. [Kwong, Jeff] Univ Ottawa, Lab Med & Pathobiol, Ottawa, ON K1V 4E9, Canada. [Kwong, Jeff] Univ Ottawa, Dalla Lana Sch Publ Hlth, Ottawa, ON K1V 4E9, Canada. [Manuel, Doug] Univ Ottawa, Dept Family Med, Ottawa, ON K1V 4E9, Canada. RP Wilson, K (reprint author), Univ Ottawa, Res Inst, Ottawa Hosp, Dept Med, Civ Campus,1053 Carling Ave,Adm Serv Bldg,Room 10, Ottawa, ON K1V 4E9, Canada. EM kwilson@ohri.ca FU Ontario Ministry of Health and Long-Term Care; Department of Family and Community Medicine, University of Toronto; Canadian Foundation for Innovation; Institute for Clinical Evaluative Sciences (ICES); Ontario Ministry of Health and Long-Term Care (MOHLTC) FX Dr. Kwong is supported by a Career Scientist award from the Ontario Ministry of Health and Long-Term Care and a Clinician Scientist award from the Department of Family and Community Medicine, University of Toronto. Professor Keelan is supported by a Career Scientist award from the Ontario Ministry of Health and Long-Term Care. Dr. Wilson holds the Canada Research Chair in Public Health Policy. Dr. Manuel holds the CIHR Chair in Applied Public Health.Source of funding/support: This study was supported by the Canadian Foundation for Innovation and by the Institute for Clinical Evaluative Sciences (ICES), which is funded by an annual grant from the Ontario Ministry of Health and Long-Term Care (MOHLTC). 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Yu, Liping Shea, Madeline A. TI Structural and Energetic Determinants of Apo Calmodulin Binding to the IQ Motif of the Na(v)1.2 Voltage-Dependent Sodium Channel SO STRUCTURE LA English DT Article ID GROUP HYDROGEN-EXCHANGE; C-TERMINAL DOMAIN; CRYSTAL-STRUCTURE; LABELED PROTEINS; CALCIUM AFFINITY; NMR STRUCTURE; PEPTIDE; INACTIVATION; COMPLEX; SYSTEM AB The neuronal voltage-dependent sodium channel (Na(v)1.2), essential for generation and propagation of action potentials, is regulated by calmodulin (CaM) binding to the IQ motif in its alpha subunit. A peptide (Na(v)1.2(IQp), KRKQEEVSAIVIQRAYRRYLLKQKVKK) representing the IQ motif had higher affinity for apo CaM than (Ca2+)(4)-CaM. Association was mediated solely by the C-domain of CaM. A solution structure (2KXW.pdb) of apo C-13,N-15-CaM C-domain bound to Na(v)1.2(IQp), was determined with NMR. The region of Na(v)1.2(IQp) bound to CaM was helical; R1902, an Na(v)1.2 residue implicated in familial autism, did not contact CaM. The apo C-domain of CaM in this complex shares features of the same domain bound to myosin V IQ motifs (2IX7) and bound to an SK channel peptide (1G4Y) that does not contain an IQ motif. Thermodynamic and structural studies of CaM-Na(v)1.2(IQp) interactions show that apo and (Ca2+)(4)-CaM adopt distinct conformations that both permit tight association with Na(v)1.2(IQp) during gating. C1 [Feldkamp, Michael D.; Yu, Liping; Shea, Madeline A.] Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Biochem, Iowa City, IA 52242 USA. [Yu, Liping] Univ Iowa, Roy J & Lucille A Carver Coll Med, NMR Facil, Iowa City, IA 52242 USA. RP Shea, MA (reprint author), Univ Iowa, Roy J & Lucille A Carver Coll Med, Dept Biochem, Iowa City, IA 52242 USA. EM madeline-shea@uiowa.edu FU National Institutes of Health [RO1 GM 57001]; Roy J. Carver Charitable Trust [01-224] FX Supported by the National Institutes of Health RO1 GM 57001 to M.A.S., and by the Roy J. Carver Charitable Trust Grant 01-224. 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The objective of this study was to investigate the underlying spatial localization and functional connectivity during voluntary movements of the right index finger. Adults with Down syndrome and healthy control adults participated in this study. Cortical responses were recorded with a 151-channel magnetoencephalographic system. In the Down syndrome group, we observed two distinct patterns of brain activation, an ipsilateral pattern and a contralateral pattern in the low-frequency band. The two distinct patterns of neural activation and the altered underlying network dynamics have not been reported previously, and may reflect differences in sensorimotor organization. NeuroReport 22:358-364 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins. C1 [Virji-Babul, Naznin] Univ British Columbia, Dept Phys Therapy, Vancouver, BC V6T 1Z3, Canada. 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In addition, we checked the extent to which the mu rhythm suppression depends on whether the observed and the imagined movement is performed by a human or is artificial. As a result of the experiment a significant difference in mu rhythm suppression between the conditions "Observation," "Imagery," and "White noise" was recorded. It did not matter whether the motion was carried out by a human being or performed by a machine. The results are discussed in the light of findings which relate to the mirror neuron system. (C) 2011 Elsevier Ireland Ltd. All rights reserved. C1 [Francuz, Piotr; Zapala, Dariusz] John Paul II Catholic Univ Lublin, Dept Expt Psychol, Lublin, Poland. RP Zapala, D (reprint author), John Paul II Catholic Univ Lublin, Dept Expt Psychol, Al Raclawickie 14, Lublin, Poland. 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Gangadharan, Charitha Abbagani, Kanakalatha Nagalla, Balakrishna Dasari, Niranjan Manna, Sunil K. TI A Study of Nuclear Transcription Factor-Kappa B in Childhood Autism SO PLOS ONE LA English DT Article ID FACTOR-INDUCED APOPTOSIS; CEREBROSPINAL-FLUID; SPECTRUM DISORDERS; ACTIVATION; CHILDREN; OVEREXPRESSION; INFLAMMATION; REGRESSION; PROTEIN-1; STRESS AB Background: Several children with autism show regression in language and social development while maintaining normal motor milestones. A clear period of normal development followed by regression and subsequent improvement with treatment, suggests a multifactorial etiology. The role of inflammation in autism is now a major area of study. Viral and bacterial infections, hypoxia, or medication could affect both foetus and infant. These stressors could upregulate transcription factors like nuclear factor kappa B (NF-kappa B), a master switch for many genes including some implicated in autism like tumor necrosis factor (TNF). On this hypothesis, it was proposed to determine NF-kappa B in children with autism. Methods: Peripheral blood samples of 67 children with autism and 29 control children were evaluated for NF-kappa B using electrophoretic mobility shift assay (EMSA). A phosphor imaging technique was used to quantify values. The fold increase over the control sample was calculated and statistical analysis was carried out using SPSS 15. Results: We have noted significant increase in NF-kappa B DNA binding activity in peripheral blood samples of children with autism. When the fold increase of NF-kappa B in cases (n = 67) was compared with that of controls (n = 29), there was a significant difference (3.14 vs. 1.40, respectively; p < 0.02). Conclusion: This finding has immense value in understanding many of the known biochemical changes reported in autism. As NF-kappa B is a response to stressors of several kinds and a master switch for many genes, autism may then arise at least in part from an NF-kappa B pathway gone awry. C1 [Naik, Usha S.; Abbagani, Kanakalatha; Dasari, Niranjan] Osmania Med Coll & Hosp, Dept Psychiat, Hyderabad, Andhra Pradesh, India. [Gangadharan, Charitha; Manna, Sunil K.] Ctr DNA Fingerprinting & Diagnost, Immunol Lab, Hyderabad, Andhra Pradesh, India. [Nagalla, Balakrishna] Natl Inst Nutr, Hyderabad 500007, Andhra Pradesh, India. RP Naik, US (reprint author), Osmania Med Coll & Hosp, Dept Psychiat, Hyderabad, Andhra Pradesh, India. EM manna@cdfd.org.in FU Department of Biotechnology, Ministry of Science and Technology, Government of India FX The study was funded by a Central Government Grant from the Department of Biotechnology, Ministry of Science and Technology, Government of India. The funders had no role in study design, data collection and analysis, decision to publish or preparation of the manuscript. 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Single photon emission computed tomography (SPECT) is a common technique used to measure regional cerebral blood flow (rCBF). Several studies have measured rCBF in children with ASD using SPECT, however, findings are discordant. In addition, the majority of subjects used in these studies were autistic. In this study, we aimed to investigate changes in rCBF in children with ASD using SPECT. Methods A Technetium-99m-ethyl cysteinate dimmer (Tc-99m-ECD) brain SPECT study was performed on an ASD group consisting of 23 children (3 girls and 20 boys; mean age (7.2 +/- 3.0) years) who were diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria and an age-matched control group with 8 children (1 girl and 7 boys, mean age (5.5 +/- 2.4) years). Image data were evaluated with Statistical Parametric Mapping, 5th version (SPM5). A Student's t test for unpaired data was used to compare rCBF and asymmetry in the autism and corresponding control group. The covariance analysis, taking age as covariance, was performed between the ASD and control group. Results There was a significant reduction in rCBF in the bilateral frontal lobe (frontal poles, arcula frontal gyrus) and the bilateral basal ganglia in the autism group, and a reduction in the bilateral frontal, temporal, parietal, legumina nucleus and cerebellum in the AS group compared to the control. In addition, asymmetry of hemispheric hypoperfusion in the ASD group was observed. Inner-group comparison analysis revealed that rCBF decreased significantly in the bilateral frontal lobe (42.7%), basal nucleus (24.9%) and temporal lobe (22.8%) in the autism group, and in the bilateral cerebellum (22.8%), basal nucleus (19.3%) and right thalamencephalon (16.6%) in the AS group (P <0.05). Conclusions The decrease in rCBF in ASD is a global event, which involves the bilateral frontal, temporal, limbic system and basal ganglias. Asymmetry of hemispheric hypoperfusion was more obvious in the AS group than the autism group, which indicates a different neurobiological mechanism from that of autism. Chin Med J 2011;124(9):1362-1366 C1 [Yang Wen-han; Jing Jin; Wang Xin; Bao Peng; Wang Qing-xiong] Sun Yat Sen Univ, Sch Publ Hlth, Fac Child & Maternal Hlth, Guangzhou 510080, Guangdong, Peoples R China. [Cheng Mu-hua] Sun Yat Sen Univ, Affiliated Hosp 3, Guangzhou 510080, Guangdong, Peoples R China. [Xiu Li-juan] Guangzhou Women & Childrens Med Ctr, Dept Hlth Care, Guangzhou 510623, Guangdong, Peoples R China. RP Jing, J (reprint author), Sun Yat Sen Univ, Sch Publ Hlth, Fac Child & Maternal Hlth, Guangzhou 510080, Guangdong, Peoples R China. EM jingjin@mail.sysu.edu.cn FU National Natural Science Foundation of China [30872130] FX This study was supported by a grant from the National Natural Science Foundation of China (No. 30872130). 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TI In Search of Cellular Immunophenotypes in the Blood of Children with Autism SO PLOS ONE LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; LYMPHOCYTE CYTOKINE PROFILES; DYE LABELING REAGENTS; SPECTRUM DISORDERS; GASTROINTESTINAL SYMPTOMS; SUCCINIMIDYL ESTERS; IMMUNE ACTIVATION; PERIPHERAL-BLOOD; T-CELLS; PLASMA AB Background: Autism is a neurodevelopmental disorder characterized by impairments in social behavior, communication difficulties and the occurrence of repetitive or stereotyped behaviors. There has been substantial evidence for dysregulation of the immune system in autism. Methods: We evaluated differences in the number and phenotype of circulating blood cells in young children with autism (n = 70) compared with age-matched controls (n = 35). Children with a confirmed diagnosis of autism (4-6 years of age) were further subdivided into low (IQ < 68, n = 35) or high functioning (IQ >= 68, n = 35) groups. Age- and gender-matched typically developing children constituted the control group. Six hundred and forty four primary and secondary variables, including cell counts and the abundance of cell surface antigens, were assessed using microvolume laser scanning cytometry. Results: There were multiple differences in immune cell populations between the autism and control groups. The absolute number of B cells per volume of blood was over 20% higher for children with autism and the absolute number of NK cells was about 40% higher. Neither of these variables showed significant difference between the low and high functioning autism groups. While the absolute number of T cells was not different across groups, a number of cellular activation markers, including HLA-DR and CD26 on T cells, and CD38 on B cells, were significantly higher in the autism group compared to controls. Conclusions: These results support previous findings that immune dysfunction may occur in some children with autism. 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Kas, Martien J. TI Identifying Human Disease Genes through Cross-Species Gene Mapping of Evolutionary Conserved Processes SO PLOS ONE LA English DT Article ID CORPUS-CALLOSUM ANOMALIES; MOUSE-BRAIN; INTERSTITIAL DELETION; MENTAL-RETARDATION; MB DELETION; MICRODELETION SYNDROME; DEVELOPMENTAL DELAY; REGION 1Q44; ARRAY-CGH; PHENOTYPE AB Background: Understanding complex networks that modulate development in humans is hampered by genetic and phenotypic heterogeneity within and between populations. Here we present a method that exploits natural variation in highly diverse mouse genetic reference panels in which genetic and environmental factors can be tightly controlled. The aim of our study is to test a cross-species genetic mapping strategy, which compares data of gene mapping in human patients with functional data obtained by QTL mapping in recombinant inbred mouse strains in order to prioritize human disease candidate genes. Methodology: We exploit evolutionary conservation of developmental phenotypes to discover gene variants that influence brain development in humans. We studied corpus callosum volume in a recombinant inbred mouse panel (C57BL/6J6 x DBA/2J, BXD strains) using high-field strength MRI technology. We aligned mouse mapping results for this neuro-anatomical phenotype with genetic data from patients with abnormal corpus callosum (ACC) development. Principal Findings: From the 61 syndromes which involve an ACC, 51 human candidate genes have been identified. Through interval mapping, we identified a single significant QTL on mouse chromosome 7 for corpus callosum volume with a QTL peak located between 25.5 and 26.7 Mb. Comparing the genes in this mouse QTL region with those associated with human syndromes (involving ACC) and those covered by copy number variations (CNV) yielded a single overlap, namely HNRPU in humans and Hnrpul1 in mice. 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EM m.j.h.kas@umcutrecht.nl RI Poot, Martin/F-9427-2010 FU Netherlands Organization for Scientific Research (NWO) [91786327]; NCRR [U24 RR021760, P41 RR005959]; NIAAA [U01AA13499, AA17590]; NIDA [P20DA21131]; NCI [U24 CA092656] FX This research was supported by a ZonMW VIDI-grant (91786327) from The Netherlands Organization for Scientific Research (NWO) to Dr. Martien Kas. The authors also benefited from support from NCRR U24 RR021760, NIAAA U01AA13499 and AA17590, NIDA P20DA21131, NCRR P41 RR005959 and NCI U24 CA092656. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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TI High functioning autism and Asperger's syndrome: The way they move - A video-based clinical study SO MOVEMENT DISORDERS LA English DT Meeting Abstract CT 15th International Congress of Parkinsons Disease and Movement Disorders CY 2011 CL Toronto, CANADA RI Engel, Andreas/C-7781-2012 OI Engel, Andreas/0000-0003-4899-8466 NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD MAY PY 2011 VL 26 SU 2 MA 1009 BP S336 EP S336 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 774CS UT WOS:000291359502223 ER PT J AU Pringsheim, TM Hammer, T Mitchell, BM AF Pringsheim, T. M. Hammer, T. Mitchell, B. Moshenko TI Comorbidity of tic disorders and autism spectrum disorder: A prevalence study SO MOVEMENT DISORDERS LA English DT Meeting Abstract CT 15th International Congress of Parkinsons Disease and Movement Disorders CY 2011 CL Toronto, CANADA NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD MAY PY 2011 VL 26 SU 2 MA 1110 BP S369 EP S370 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 774CS UT WOS:000291359502322 ER PT J AU Schunke, O Ganos, C Baumer, T Mall, V Jung, N Biscaldi-Schafer, M Munchau, A AF Schunke, O. Ganos, C. Baeumer, T. Mall, V. Jung, N. Biscaldi-Schaefer, M. Muenchau, A. TI Video-based analysis of tic phenomenology in patients with autism spectrum disorder SO MOVEMENT DISORDERS LA English DT Meeting Abstract CT 15th International Congress of Parkinsons Disease and Movement Disorders CY 2011 CL Toronto, CANADA NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0885-3185 J9 MOVEMENT DISORD JI Mov. Disord. PD MAY PY 2011 VL 26 SU 2 MA 1107 BP S368 EP S369 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 774CS UT WOS:000291359502319 ER PT J AU Sintes, A Arranz, B Ramirez, N Rueda, I San, L AF Sintes, Anna Arranz, Belen Ramirez, Nicolas Rueda, Isabel San, Luis TI Asperger Syndrome Can the disorder be diagnosed in the adult age? SO ACTAS ESPANOLAS DE PSIQUIATRIA LA English DT Article DE Asperger; autism; differential diagnosis; comorbidity; neuropsychology ID HIGH-FUNCTIONING AUTISM AB Introduction. Asperger Syndrome (AS) is characterized by a qualitative disorder of social interaction, a pattern of restrictive, repetitive and stereotyped behavior, interests and activities, with normal intellectual capacity and normal language skills in the areas of grammar and vocabulary. Since its inclusion in international taxonomies, there has been much controversy regarding its nosological validity. Clinical case. A patient with a diagnosis of AS in adulthood is described. Results from the psychopathological, personality and cognitive functioning assessment are included. Conclusions. Asperger Syndrome can also be diagnosed in adulthood and should be suspected whenever retrospective information and clinical assessment point to this diagnosis. C1 [Sintes, Anna; Rueda, Isabel; San, Luis] Hosp San Juan Dios, CIBERSAM, Psychiat & Psychol Serv, ES-08950 Barcelona, Spain. [Ramirez, Nicolas] Hosp Sant Rafael, Psychiat Serv, Barcelona, Spain. RP San, L (reprint author), Hosp San Juan Dios, CIBERSAM, Psychiat & Psychol Serv, Passeig Sant Joan de Des 2, ES-08950 Barcelona, Spain. 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To effectively communicate with vaccine-hesitant parents, HCPs must first understand the concerns of parents regarding immunization and understand influences that can lead to misinformation about the safety and effectiveness of vaccines. HCPs should establish an open, nonconfrontational dialogue with vaccine-hesitant parents at an early stage and provide unambiguous, easily comprehensible answers about known vaccine adverse events and provide accurate information about vaccination. Personal stories and visual images of patients and parents affected by vaccine-preventable diseases and reports of disease outbreaks serve as useful reminders of the need to maintain high immunization rates. Ongoing dialogue including provider recommendations may successfully reassure vaccine-hesitant parents that immunization is the best and safest option for their child. Pediatrics 2011;127:S127-S133 C1 [Pickering, Larry K.] Ctr Dis Control & Prevent, Natl Ctr Immunizat & Resp Dis, Atlanta, GA 30333 USA. 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SO PEDIATRIC RESEARCH LA English DT Article ID MATERNAL IMMUNE ACTIVATION; BRAIN-DEVELOPMENT; SPECTRUM DISORDERS; CYTOKINE LEVELS; CHILDHOOD PSYCHOSES; PRENATAL INFECTION; GENE-EXPRESSION; SERUM-LEVELS; SYSTEM; PREGNANCY AB Prenatal exposure to infection and subsequent inflammatory responses have been implicated in the etiology of schizophrenia and autism. In this review, we summarize current evidence from human and animal studies supporting the hypothesis that the pathogenesis of these two disorders is linked via exposure to inflammation at early stages of development. Moreover, we propose a hypothetical model in which inflammatory mechanisms may account for multiple shared and disorder-specific pathological characteristics of both entities. In essence, our model suggests that acute neuroinflammation during early fetal development may be relevant for the induction of psychopathological and neuropathological features shared by schizophrenia and autism, whereas postacute latent and persistent inflammation may contribute to schizophrenia- and autism-specific phenotypes, respectively, (Pediatr Res 69: 26R-33R, 2011) C1 [Meyer, Urs; Feldon, Joram] Swiss Fed Inst Technol, Lab Behav Neurobiol, CH-8603 Schwerzenbach, Switzerland. [Dammann, Olaf] Floating Hosp Children, Tufts Med Ctr, Div Newborn Med, Boston, MA 02111 USA. RP Meyer, U (reprint author), Swiss Fed Inst Technol, Lab Behav Neurobiol, Schorenstr 16, CH-8603 Schwerzenbach, Switzerland. EM urmeyer@ethz.ch FU Swiss National Science Foundation [3100AO-100309, 3100AO-116719]; ETH Zurich [11 07/03]; European Commission [LSHM-CT-2006-036534, HEALTH-F2-2009-241778]; NIH [1R21EY019253-01]; Richard Saltonstall Charitable Foundation FX The studies performed at the Laboratory of Behavioural Neurobiology, ETH Zurich, were supported by the Swiss National Science Foundation (grant 3100AO-100309 and grant 3100AO-116719) and ETH Zurich (grant 11 07/03). J.F. received additional support from a 2009 NARSAD Distinguished Investigator Award. O.D. is supported by the European Commission (NEOBRAIN, LSHM-CT-2006-036534: NEUROBID, HEALTH-F2-2009-241778), the NIH (1R21EY019253-01), and the Richard Saltonstall Charitable Foundation. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 26R EP 33R DI 10.1203/PDR.0b013e318212c196 PN 2 PG 8 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100005 PM 21289540 ER PT J AU Klein, S Wynn, K Ray, L Demeriez, L LaBerge, P Pei, J Pierre, CS AF Klein, Sheryl Wynn, Kerry Ray, Lynne Demeriez, Lori LaBerge, Patricia Pei, Jacqueline Pierre, Cherie St. TI Information Sharing During Diagnostic Assessments: What Is Relevant for Parents? SO PHYSICAL & OCCUPATIONAL THERAPY IN PEDIATRICS LA English DT Article DE Developmental delay; diagnostic assessment; family-centered care; information provision; neurodevelopment ID CENTERED CARE; DOWN-SYNDROME; PERSPECTIVES; DISABILITY; CHILDREN; AUTISM AB This descriptive qualitative study facilitates the application of family-centered care within a tertiary care interdisciplinary neurodevelopmental diagnostic assessment clinic by furthering an understanding of parent perceptions of the relevance of diagnostic information provision. An interdisciplinary assessment team completed an open-ended questionnaire to describe parent information provision. Parents from 9 families completed in-depth parent interviews following clinic attendance to discuss perceptions of information received. Interviews were audiotaped, transcribed, and coded by related themes. Parents did not perceive the information in the way professionals expected. Parents acknowledged receipt of comprehensive information relevant to the diagnosis but indicated that not all their needs were met. During the interviews, parents described the assessment process, preassessment information, and "steps in their journey." They noted that a strength-based approach and a focus on parental competency would support their coping efforts. Results underscore the need for professionals to be attentive to parents' individualized needs. C1 [Klein, Sheryl] Glenrose Rehabil Hosp, Occupat Therapy Serv, Edmonton, AB T5G 0B7, Canada. [Ray, Lynne] Univ Alberta, Fac Nursing, Edmonton, AB, Canada. [Pei, Jacqueline] Univ Alberta, Dept Pediat, Edmonton, AB, Canada. [Pei, Jacqueline] Univ Alberta, Dept Educ Psychol, Edmonton, AB T6G 2E1, Canada. RP Klein, S (reprint author), Glenrose Rehabil Hosp, Occupat Therapy Serv, 10230-111 Ave, Edmonton, AB T5G 0B7, Canada. EM Sh-eryl.Klein@albertahealthservices.ca FU Glenrose Rehabilitation Hospital Foundation FX Support for the study was provided by the Glenrose Rehabilitation Hospital Foundation. The authors would like to express their thanks to the families who participated in this study. 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PD MAY PY 2011 VL 49 IS 5 BP 13 EP 13 PG 1 WC Nursing SC Nursing GA 811ZH UT WOS:000294257000005 ER PT J AU Oexle, K Hempel, M Jauch, A Meitinger, T Rivera-Brugues, N Stengel-Rutkowski, S Strom, T AF Oexle, Konrad Hempel, Maja Jauch, Anna Meitinger, Thomas Rivera-Brugues, Nuria Stengel-Rutkowski, Sabine Strom, Tim TI 3.7 Mb tandem microduplication in chromosome 5p13.1-p13.2 associated with developmental delay, macrocephaly, obesity, and lymphedema. Further characterization of the dup(5p13) syndrome SO EUROPEAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Mental retardation; Autism; Low posterior hairline; Obesity; Lymphedema; Dup(5p) syndrome ID PARTIAL TRISOMY; COPY-NUMBER; SHORT ARM; DUPLICATION; LOCI AB In a male patient with developmental delay, autistic behaviour, obesity, lymphedema, hypertension, macrocephaly, and facial features of chromosome 5p duplication (trisomy 5p) a 3.7 Mb de novo tandem microduplication of 5p13.1-13.2 (rs4703415-rs261752, i.e., chr5:35.62-39.36 Mb) was identified. This observation contributes to the characterization and dissection of the 5p13 duplication syndrome. The possible role of increased NIPBL gene dosage is discussed. (C) 2010 Elsevier Masson SAS. All rights reserved. C1 [Oexle, Konrad; Hempel, Maja; Meitinger, Thomas] Tech Univ Munich, Inst Human Genet, D-81675 Munich, Germany. [Meitinger, Thomas; Rivera-Brugues, Nuria; Strom, Tim] Helmholtz Zentrum Munchen, Inst Human Genet, Neuherberg, Germany. [Jauch, Anna] Univ Heidelberg Hosp, Inst Human Genet, Heidelberg, Germany. [Stengel-Rutkowski, Sabine] Univ Munich, Inst Human Genet, Munich, Germany. RP Oexle, K (reprint author), Tech Univ Munich, Inst Human Genet, Trogerstr 32, D-81675 Munich, Germany. EM oexle@humangenetik.med.tum.de FU German Ministry for Education and Research [01GS08163] FX We are indebted to our patient for his permission to present his case to the scientific and medical community. The research was supported by a grant from the German Ministry for Education and Research (NGFNplus/www.ngfn.de/englisch/15.htm, project number 01GS08163) and participated in the MRNET consortium (http://www.german-mrnet.de/). The BAC clones from 5p13.2 were kindly provided by Joris Vermeesch, Center for Human Genetics, Leuven, Belgium. CR Avansino JR, 1999, AM J MED GENET, V87, P6 BLACKX L, 2008, MOL CYTOGENET, P1 BUSHBY KMD, 1992, ARCH DIS CHILD, V67, P1286 Cervera M, 2005, AM J MED GENET A, V136A, P381, DOI 10.1002/ajmg.a.30791 CHIA NL, 1987, CLIN GENET, V31, P65 Heid IM, 2010, NAT GENET, V42, P949, DOI 10.1038/ng.685 Iafrate AJ, 2004, NAT GENET, V36, P949, DOI 10.1038/ng1416 LEJEUNE J, 1964, CR HEBD ACAD SCI, V258, P5767 LordaSanchez I, 1997, AM J MED GENET, V68, P476, DOI 10.1002/(SICI)1096-8628(19970211)68:4<476::AID-AJMG21>3.0.CO;2-O Loscalzo ML, 2008, EUR J MED GENET, V51, P54, DOI 10.1016/j.ejmg.2007.09.006 RETHORE MO, 1989, HUM GENET, V82, P296, DOI 10.1007/BF00291177 Scherag A, 2010, PLOS GENET, V6, DOI 10.1371/journal.pgen.1000916 SCHINZEL A, 2001, CATALOGUE UNBALANCED, P242 Speliotes EK, 2010, NAT GENET, V42, P937, DOI 10.1038/ng.686 Teslovich TM, 2010, NATURE, V466, P707, DOI 10.1038/nature09270 Vera-Carbonell A, 2009, AM J MED GENET A, V149A, P2513, DOI 10.1002/ajmg.a.33055 Wagenstaller J, 2007, AM J HUM GENET, V81, P768, DOI 10.1086/521274 Yan J, 2009, J MED GENET, V46, P626, DOI 10.1136/jmg.2008.062471 ZABEL B, 1978, J MED GENET, V15, P143, DOI 10.1136/jmg.15.2.143 NR 19 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 MAY-JUN PY 2011 VL 54 IS 3 BP 225 EP 230 DI 10.1016/j.ejmg.2010.12.012 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 805QR UT WOS:000293744600005 PM 21211577 ER PT J AU Lo-Castro, A El-Malhany, N Galasso, C Verrotti, A Nardone, AM Postorivo, D Palmieri, C Curatolo, P AF Lo-Castro, Adriana El-Malhany, Nadia Galasso, Cinzia Verrotti, Alberto Nardone, Anna Maria Postorivo, Diana Palmieri, Cristina Curatolo, Paolo TI De novo mosaic ring chromosome 18 in a child with mental retardation, epilepsy and immunological problems SO EUROPEAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Developmental delay; Dysmorphisms; Epilepsy; Mental retardation; Immunological disorders; Ring chromosome 18 mosaicism ID 18Q-SYNDROME; AUTISM; R(18); GIRL; 18Q AB Ring chromosome 18 [r(18)] is a disorder in which one or both ends of chromosome 18 are lost and joined forming a ring-shaped figures. R(18) patients can therefore show features of 18q-, 18p- syndrome or a combination of both, depending on the size of the 18p and 18q deleted regions. The phenotype of the r(18) is characterized by developmental delay/mental retardation, typical facial dysmorphisms, major abnormalities and immunological problems. Here we report a case of de novo mosaic r(18) with a characterization by array-based comparative genomic hybridization analysis, and discuss the phenotypic correlation in r(18) also through a comparison with previously described cases of the literature. (C) 2011 Elsevier Masson SAS. All rights reserved. C1 [Lo-Castro, Adriana; El-Malhany, Nadia; Galasso, Cinzia; Curatolo, Paolo] Univ Roma Tor Vergata, Dept Neurosci, Paediat Neurol Unit, I-00133 Rome, Italy. [Verrotti, Alberto] Univ G dAnnunzio, Dept Paediat, I-66100 Chieti, Italy. [Nardone, Anna Maria; Postorivo, Diana; Palmieri, Cristina] Univ Roma Tor Vergata, Dept Med Genet, I-00133 Rome, Italy. RP Lo-Castro, A (reprint author), Univ Roma Tor Vergata, Dept Neurosci, Paediat Neurol Unit, Viale Oxford 81, I-00133 Rome, Italy. 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J. Med. Genet. PD MAY-JUN PY 2011 VL 54 IS 3 BP 329 EP 332 DI 10.1016/j.ejmg.2011.02.004 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 805QR UT WOS:000293744600026 PM 21333764 ER PT J AU Chaabane, A Aouam, K Ben Fredj, N Toumi, A Braham, D Boughattas, NA Chakroun, M AF Chaabane, Amel Aouam, Karim Ben Fredj, Nadia Toumi, Adnen Braham, Dorra Boughattas, Naceur A. Chakroun, Mohamed TI H1N1 Influenza Vaccines in Tunisia: Efficiency and Safety SO THERAPIE LA French DT Article DE adverse effect; efficiency; H1N1; influenza; vaccine ID GUILLAIN-BARRE-SYNDROME; A H1N1; MONOVALENT VACCINE; RANDOMIZED-TRIAL; IMMUNOGENICITY; CHILDREN; AUTISM; VIRUS; AGE AB H1N1 Influenza Vaccines in Tunisia: Efficiency and Safety. Objective. We carried out this study in order to evaluate the effectiveness and the safety of the two H1N1 vaccines available in Tunisia: Focetria (R) and Panenza (R). Methods. It's a prospective epidemiological study including 601 vaccinated subjects. The vaccine effectiveness was based on the occurrence of flu clinical symptoms after vaccination. The safety was based on the occurrence of unexpected events after vaccines administration. The vaccines imputability was established according to Begaud et al. method. Results. The number of subjects vaccinated by Focetria (R) is more important than Panenza (R). The efficiency of vaccines would be 93.6%. Neither the medical statue nor the type of the vaccine used influence the occurrence of a flu episode after vaccination. We recorded 406 adverse effects (32.4%) with a high score of imputability (I3). Focetria (R) adverse effects were more frequent than Panenza (R) ones (p=0.009). Almost all adverse events disappeared within few days. Conclusion. The two vaccines used in Tunisia remain enough efficient to face the influenza (H1N1) pandemia and are well tolerated independently of the demographic and pathological statue of the vaccinated person as well as nature of the vaccine used. 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Wilson, Kelly Dunlap, Glen TI Prevent-Teach-Reinforce: Addressing Problem Behaviors of Students with Autism in General Education Classrooms SO BEHAVIORAL DISORDERS LA English DT Article ID CHILDREN AB Children with autism and other disabilities are often prohibited from participating in inclusive educational environments due to the occurrence of problem behaviors. In this study, a standardized model for individualizing procedures of behavior support, Prevent-Teach-Reinforce (PTR), was evaluated in general education settings with three elementary school students with autism spectrum disorders and serious problem behaviors. A multiple baseline across students design was used to test the effects of PTR on the occurrence of problem behaviors and academic engagement. Results indicated that problem behaviors were reduced and engagement was increased for all of the participants. 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PD MAY PY 2011 VL 36 IS 3 BP 160 EP 171 PG 12 WC Psychology, Clinical; Psychology, Educational SC Psychology GA 802AB UT WOS:000293480600001 ER PT J AU Hughes, C AF Hughes, Claire TI Changes and Challenges in 20 Years of Research Into the Development of Executive Functions SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE executive function; neuroscience; autism; ADHD; social understanding ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; BEHAVIOR RATING INVENTORY; AUTISM SPECTRUM DISORDERS; PRENATAL ALCOHOL EXPOSURE; CONFIRMATORY FACTOR-ANALYSIS; AUTOMATED BATTERY CANTAB; LATENT VARIABLE ANALYSIS; INDIVIDUAL-DIFFERENCES; PRESCHOOL-CHILDREN; WORKING-MEMORY AB This review of 20 years of developmental research on Executive Functions (EF) offers a broad-brushstroke picture that touches on multiple issues including: (i) findings from typical and atypical groups, from infancy to adolescence; (ii) advances in assessment tools and in statistical analysis; (iii) the interplay between EF and other cognitive systems (e.g. those involved in children's developing understanding of mind, and in their processing of reward signals); (iv) integration of cognitive and neuroscience perspectives on EF; and (v) environmental factors that have either a positive influence (e.g. training/intervention programmes; parental scaffolding) or a negative influence (e.g. maltreatment, neglect, traumatic brain injury) on EF. Of the several themes to emerge from this review, two are particularly important; these concern the need to adopt developmental perspectives and the potential importance for intervention work of research on social influences on EF. Specifically, the review highlights both developmental continuities (e.g. in the correlates of EF) and contrasts (e.g. in the nature of EF and its neural substrates) and calls for research that compares developmental trajectories for EF in different groups (e.g. children with autism versus ADHD). In addition, findings from both family-based research and randomized controlled trials of school-based interventions highlight the importance of environmental influences on EF and so support the development of interventions to promote EF and hence improve children's academic and social outcomes. Copyright (C) 2011 John Wiley & Sons, Ltd. C1 Univ Cambridge, Ctr Family Res, Cambridge CB2 3RF, England. 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PD MAY-JUN PY 2011 VL 20 IS 3 BP 251 EP 271 DI 10.1002/icd.736 PG 21 WC Psychology, Developmental SC Psychology GA 789GE UT WOS:000292502300001 ER PT J AU Bapat, RS AF Bapat, Radhika S. TI THE EARLY START DENVER MODEL FOR YOUNG CHILDREN WITH AUTISM: PROMOTING LANGUAGE, LEARNING AND ENGAGEMENT. SO INFANT AND CHILD DEVELOPMENT LA English DT Book Review C1 [Bapat, Radhika S.] Sahyadri Specialty Hosp, Child Guidance Ctr, Pune, Maharashtra, India. RP Bapat, RS (reprint author), Sahyadri Specialty Hosp, Child Guidance Ctr, Pune, Maharashtra, India. CR Rogers S. J., 2009, EARLY START DENVER M NR 1 TC 0 Z9 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD MAY-JUN PY 2011 VL 20 IS 3 BP 351 EP 351 DI 10.1002/icd.707 PG 1 WC Psychology, Developmental SC Psychology GA 789GE UT WOS:000292502300009 ER PT J AU Anderberg, D Chevalier, A Wadsworth, J AF Anderberg, Dan Chevalier, Arnaud Wadsworth, Jonathan TI Anatomy of a health scare: Education, income and the MMR controversy in the UK SO JOURNAL OF HEALTH ECONOMICS LA English DT Article DE Childhood vaccinations; Health outcomes; Education ID INFLAMMATORY-BOWEL-DISEASE; TRACKING MOTHERS ATTITUDES; RUBELLA VACCINE; SOCIOECONOMIC-STATUS; CAUSAL ASSOCIATION; NO EVIDENCE; MEASLES; AUTISM; MUMPS; IMMUNIZATION AB The measles, mumps and rubella (MMR) controversy provides an interesting case where, for a short period of time, research publicized in the media, suggested a potential risk of serious side-effects associated with the vaccine, where there was also a sharp behavioral response from the public, and where the initial information was subsequently overturned. We consider the controversy from the perspective of health inequalities and the assimilation of information, focusing on whether and how vaccine uptake behavior in the wake of the controversy differed among groups of parents by education and income. Using panel data on the variation in the uptake of the MMR, and other childhood immunizations, across local Health Authority areas we find that the uptake rate of the MMR declined faster in areas where a larger fraction of parents had stayed in education past the age of 18 than in areas with less educated parents. We also find that the same areas reduced their relative uptake of other uncontroversial childhood immunizations, suggesting a "spillover" effect. Using a supplementary data source we find evidence of a corresponding positive income effect, indicating that wealthier parents avoided the MMR dilemma by purchasing single vaccines. (C) 2011 Elsevier B.V. All rights reserved. C1 [Anderberg, Dan] Royal Holloway Univ London, Dept Econ, Surrey, England. RP Anderberg, D (reprint author), Royal Holloway Univ London, Dept Econ, Surrey, England. 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Health Econ. PD MAY PY 2011 VL 30 IS 3 BP 515 EP 530 DI 10.1016/j.jhealeco.2011.01.009 PG 16 WC Economics; Health Care Sciences & Services; Health Policy & Services SC Business & Economics; Health Care Sciences & Services GA 788HH UT WOS:000292435500004 PM 21439663 ER PT J AU Hsiao, EY Patterson, PH AF Hsiao, Elaine Y. Patterson, Paul H. TI Activation of the maternal immune system induces endocrine changes in the placenta via IL-6 SO BRAIN BEHAVIOR AND IMMUNITY LA English DT Article DE Autism; Schizophrenia; Maternal immune activation; Inflammation; Growth hormone; Insulin-like growth factor; JAK/STAT3; Poly(I:C); Maternal infection ID IGF-BINDING PROTEIN-3; GROWTH-FACTOR-I; PRENATAL INFECTION; DOPAMINERGIC HYPERFUNCTION; OBSTETRIC COMPLICATIONS; PHARMACOLOGICAL CHANGES; INCREASED EXPRESSION; LATENT INHIBITION; BRAIN-DEVELOPMENT; TRANSGENIC MICE AB Activation of the maternal immune system in rodent models sets in motion a cascade of molecular pathways that ultimately result in autism- and schizophrenia-related behaviors in offspring. The finding that interleukin-6 (IL-6) is a crucial mediator of these effects led us to examine the mechanism by which this cytokine influences fetal development in vivo. Here we focus on the placenta as the site of direct interaction between mother and fetus and as a principal modulator of fetal development. We find that maternal immune activation (MIA) with a viral mimic, synthetic double-stranded RNA (poly(I:C)), increases IL-6 mRNA as well as maternally-derived IL-6 protein in the placenta. Placentas from MIA mothers exhibit increases in CD69+ decidual macrophages, granulocytes and uterine NK cells, indicating elevated early immune activation. Maternally-derived IL-6 mediates activation of the JAK/STAT3 pathway specifically in the spongiotrophoblast layer of the placenta, which results in expression of acute phase genes. Importantly, this parallels an IL-6-dependent disruption of the growth hormone-insulin-like growth factor (GH-IGF) axis that is characterized by decreased GH, IGFI and IGFBP3 levels. In addition, we observe an IL-6-dependent induction in pro-lactin-like protein-K (PLP-K) expression as well as MIA-related alterations in other placental endocrine factors. Together, these IL-6-mediated effects of MIA on the placenta represent an indirect mechanism by which MIA can alter fetal development. Published by Elsevier Inc. C1 [Hsiao, Elaine Y.; Patterson, Paul H.] CALTECH, Pasadena, CA 91125 USA. RP Hsiao, EY (reprint author), 1200 E Calif Blvd,Biol M-C 216-76, Pasadena, CA 91125 USA. EM ehsiao@caltech.edu FU Autism Speaks Dennis Weatherstone; National Institutes of Health (NIH/NRSA) [T32 GM07737] FX The authors acknowledge the kind assistance of B. Deverman and A. Bonnin with reviewing the manuscript; A. Colon, L Sandoval and R. Sauza with caring for and maintaining the animals; and N. Tetreault and D. Anderson with providing the LMD and qPCR equipment. This research was supported by an Autism Speaks Dennis Weatherstone Pre-Doctoral Fellowship and by a Caltech training grant from the National Institutes of Health (NIH/NRSA 5 T32 GM07737). 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Immun. PD MAY PY 2011 VL 25 IS 4 BP 604 EP 615 DI 10.1016/j.bbi.2010.12.017 PG 12 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 762GN UT WOS:000290463100003 PM 21195166 ER PT J AU Patterson, PH AF Patterson, Paul H. TI Modeling Autistic Features in Animals SO PEDIATRIC RESEARCH LA English DT Article ID MATERNAL IMMUNE ACTIVATION; SYNAPTIC-TRANSMISSION; VALPROIC ACID; NEURODEVELOPMENTAL DISORDERS; TUBEROUS SCLEROSIS; SPECTRUM DISORDERS; PRENATAL EXPOSURE; RETT-SYNDROME; BRAIN; SCHIZOPHRENIA AB A variety of features of autism can be simulated in rodents, including the core behavioral hallmarks of stereotyped and repetitive behaviors, and deficits in social interaction and communication. Other behaviors frequently found in autism spectrum disorders (ASDs) such as neophobia, enhanced anxiety, abnormal pain sensitivity and eye blink conditioning, disturbed sleep patterns, seizures, and deficits in sensorimotor gating are also present in some of the animal models. Neuropathology and some characteristic neurochemical changes that are frequently seen in autism, and alterations in the immune status in the brain and periphery are also found in some of the models. Several known environmental risk factors for autism have been successfully established in rodents, including maternal infection and maternal valproate administration. Also under investigation are a number of mouse models based on genetic variants associated with autism or on syndromic disorders with autistic features. This review briefly summarizes recent developments in this field, highlighting models with face and/or construct validity, and noting the potential for investigation of pathogenesis, and early progress toward clinical testing of potential therapeutics. Wherever possible, reference is made to reviews rather than to primary articles. (Pediatr Res 69: 34R-40R, 2011) C1 CALTECH, Div Biol, Pasadena, CA 91125 USA. RP Patterson, PH (reprint author), CALTECH, Div Biol, Pasadena, CA 91125 USA. EM php@caltech.edu FU National Institute of Mental Health [R01 MH079299, EUREKA MH086781, ARRA MH088879, P50 MH086383]; Binational Science Foundation; International Rett Syndrome Foundation; Simons Foundation; Autism Speaks Foundation FX Autism-related research in the author's laboratory is currently supported by the National Institute of Mental Health (R01 MH079299, EUREKA MH086781, ARRA MH088879, P50 MH086383), and the Binational Science, International Rett Syndrome, Simons, and Autism Speaks Foundations. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 34R EP 40R DI 10.1203/PDR.0b013e318212b80f PN 2 PG 7 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100006 PM 21289542 ER PT J AU Nobile, M Perego, P Piccinini, L Mani, E Rossi, A Bellina, M Molteni, M AF Nobile, Maria Perego, Paolo Piccinini, Luigi Mani, Elisa Rossi, Agnese Bellina, Monica Molteni, Massimo TI Further evidence of complex motor dysfunction in drug naive children with autism using automatic motion analysis of gait SO AUTISM LA English DT Article DE autism; gait analysis; jerk; locomotion system; motor dysfunction ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; PARKINSONS-DISEASE; ASPERGERS-DISORDER; SPECTRUM DISORDER; POSTURAL CONTROL; BASAL GANGLIA; MOVEMENT; IMITATION; ARM AB In order to increase the knowledge of locomotor disturbances in children with autism, and of the mechanism underlying them, the objective of this exploratory study was to reliably and quantitatively evaluate linear gait parameters (spatio-temporal and kinematic parameters), upper body kinematic parameters, walk orientation and smoothness using an automatic motion analyser (ELITE systems) in drug na < ve children with Autistic Disorder (AD) and healthy controls. The children with AD showed a stiffer gait in which the usual fluidity of walking was lost, trunk postural abnormalities, highly significant difficulties to maintain a straight line and a marked loss of smoothness (increase of jerk index), compared to the healthy controls. As a whole, these data suggest a complex motor dysfunction involving both the cortical and the subcortical area or, maybe, a possible deficit in the integration of sensory-motor information within motor networks (i.e., anomalous connections within the fronto-cerebello-thalamo-frontal network). Although the underlying neural structures involved remain to be better defined, these data may contribute to highlighting the central role of motor impairment in autism and suggest the usefulness of taking into account motor difficulties when developing new diagnostic and rehabilitation programs. C1 [Nobile, Maria] Eugenio Medea Sci Inst, Child Psychiat Unit, Child Psychiat Dept, I-23842 Bosisio Parini, LC, Italy. 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Lauwers, Gregory Y. Winter, Harland S. Buie, Timothy M. TI Intestinal disaccharidase activity in patients with autism Effect of age, gender, and intestinal inflammation SO AUTISM LA English DT Article DE autism; disaccharidases; inflammation; intestine ID GASTROINTESTINAL SYMPTOMS; LACTASE DEFICIENCY; SPECTRUM DISORDERS; ABDOMINAL-PAIN; CHILDREN; PREVALENCE; GENETICS AB Intestinal disaccharidase activities were measured in 199 individuals with autism to determine the frequency of enzyme deficiency. All patients had duodenal biopsies that were evaluated morphologically and assayed for lactase, sucrase, and maltase activity. Frequency of lactase deficiency was 58% in autistic children <= 5 years old and 65% in older patients. As would be expected, patients with autism at age 5 > years demonstrated significant decline in lactase activity (24%, p = .02) in comparison with <= 5 years old autistic patients. Boys <= 5 years old with autism had 1.7 fold lower lactase activity than girls with autism (p = .02). Only 6% of autistic patients had intestinal inflammation. Lactase deficiency not associated with intestinal inflammation or injury is common in autistic children and may contribute to abdominal discomfort, pain and observed aberrant behavior. Most autistic children with lactose intolerance are not identified by clinical history. C1 [Kushak, Rafail I.; Lauwers, Gregory Y.; Winter, Harland S.; Buie, Timothy M.] Harvard Univ, Sch Med, Boston, MA USA. RP Kushak, RI (reprint author), Massachusetts Gen Hosp Children, 175 Cambridge St,5th Floor, Boston, MA 02114 USA. 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Trivette, Carol M. Masiello, Tracy TI Exploratory investigation of the effects of interest-based learning on the development of young children with autism SO AUTISM LA English DT Article DE autism; child development; child interests; everyday learning ID INTENSE INTERESTS; EFFECT SIZES; BEHAVIORS; CHOICE AB The influences of child participation in interest-based learning activities on the development of 17 preschoolers with autism was the focus of this brief report. The children's mothers identified their children's interests and the everyday family and community activities that provided opportunities for interest-based learning. Parents then implemented intervention procedures for 14 to 16 weeks to increase child participation in the selected activities. Based on an investigator-administered interestingness scale, the children were divided into high and low interest-based learning groups. The children's language, cognitive, social, and motor development quotients obtained at the beginning, the middle, and the end of the intervention were the dependent measures. Results showed that the high interest-based group made considerably more developmental progress compared to the low interest-based group. Implications for practice and future research are discussed. C1 [Dunst, Carl J.; Trivette, Carol M.; Masiello, Tracy] Orelena Hawks Puckett Inst, Asheville, NC 28804 USA. RP Dunst, CJ (reprint author), Orelena Hawks Puckett Inst, 8 Elk Mt Rd, Asheville, NC 28804 USA. 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A., 1992, ROLE INTERESTS LEARN Rutter M., 2003, AUTISM DIAGNOSTIC IN Schopler E., 1993, CHILDHOOD AUTISM RAT Schraw G, 2001, EDUC PSYCHOL REV, V13, P23, DOI 10.1023/A:1009004801455 SCHWARTING G, 1998, 13 MENTAL MEASUREMEN, P356 Swanson J., 2006, CASETOOLS, V2, P1 Thompson B, 2001, J EXP EDUC, V70, P80 Vacha-Haase T, 2004, J COUNS PSYCHOL, V51, P473, DOI 10.1037/0022-0167.51.4.473 Valentine JC, 2003, EFFECT SIZE SUBSTANT Vismara LA, 2007, J POSIT BEHAV INTERV, V9, P214, DOI 10.1177/10983007070090040401 Warreyn P, 2007, J AUTISM DEV DISORD, V37, P501, DOI 10.1007/s10803-006-0184-0 NR 35 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 MAY PY 2011 VL 15 IS 3 BP 295 EP 305 DI 10.1177/1362361310370971 PG 11 WC Psychology, Developmental SC Psychology GA 776MY UT WOS:000291540600004 PM 21430019 ER PT J AU Speirs, S Yelland, G Rinehart, N Tonge, B AF Speirs, Samantha Yelland, Greg Rinehart, Nicole Tonge, Bruce TI Lexical processing in individuals with high-functioning autism and Asperger's disorder SO AUTISM LA English DT Article DE Asperger's disorder; autism; language; lexical processing; masked priming; word recognition ID SPECTRUM DISORDER; WORD RECOGNITION; READING-COMPREHENSION; DEVELOPING READERS; LANGUAGE; CHILDREN; ACCESS; ADULTS; SKILLS; IDENTIFICATION AB The presence or absence of clinically delayed language development prior to 3 years of age is a key, but contentious, clinical feature distinguishing autism from Asperger's disorder. The aim of this study was to examine language processing in children with high-functioning autism (HFA) and Asperger's disorder (AD) using a task which taps lexical processing, a core language ability. Eleven individuals with HFA, 11 with AD and 11 typically developing (TD) individuals completed a masked priming task, a psycholinguistic paradigm that directly examines lexical processes. Within-group analyses revealed the AD and TD groups had intact lexical processing systems and orthographic processing of the written word. The outcomes for the HFA group were ambiguous, suggesting that their lexical processing system is either delayed or is structurally different. This suggests that fundamental differences in lexical processing exist between HFA and AD and remain evident later in development. C1 [Yelland, Greg] Monash Univ, Sch Psychol & Psychiat, Clayton, Vic 3800, Australia. RP Yelland, G (reprint author), Monash Univ, Sch Psychol & Psychiat, Bldg 17, Clayton, Vic 3800, Australia. 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Stenning, Keith TI Visual/verbal-analytic reasoning bias as a function of self-reported autistic-like traits A study of typically developing individuals solving Raven's Advanced Progressive Matrices SO AUTISM LA English DT Article DE Autism-Spectrum Quotient; autistic-like traits; Raven's Advanced Progressive Matrices; strategies; typically developing individuals ID SPECTRUM QUOTIENT AQ; GENERAL-POPULATION; ASPERGER-SYNDROME; COGNITIVE-STYLE; MATRICES TEST; BLOCK DESIGN; EYES TEST; CHILDREN; INTELLIGENCE; PERFORMANCE AB People with autism spectrum condition (ASC) perform well on Raven's matrices, a test which loads highly on the general factor in intelligence. However, the mechanisms supporting enhanced performance on the test are poorly understood. Evidence is accumulating that milder variants of the ASC phenotype are present in typically developing individuals, and that those who are further along the autistic-like trait spectrum show similar patterns of abilities and impairments as people with clinically diagnosed ASC. We investigated whether self-reported autistic-like traits in a university student sample, assessed using the Autism-Spectrum Quotient (AQ; Baron-Cohen, Wheelwright, Skinner, et al., 2001), predict performance on Raven's Advanced Progressive Matrices. We found that reporting poorer social skills but better attention switching predicted a higher Advanced matrices score overall. DeShon, Chan, and Weissbein (1995) classified Advanced matrices items as requiring a visuospatial, or a verbal-analytic strategy. We hypothesised that higher AQ scores would predict better performance on visuospatial items than on verbal-analytic items. This prediction was confirmed. These results are consistent with the continuum view and can be explained by the enhanced perceptual functioning theory of performance peaks in ASC. The results also confirm a new prediction about Raven's Advanced Progressive Matrices performance in people with ASC. C1 [Fugard, Andrew J. B.] Salzburg Univ, ICT&S Ctr, A-5020 Salzburg, Austria. [Stewart, Mary E.] Heriot Watt Univ, Edinburgh, Midlothian, Scotland. [Stenning, Keith] Univ Edinburgh, Edinburgh EH8 9YL, Midlothian, Scotland. RP Fugard, AJB (reprint author), Salzburg Univ, ICT&S Ctr, Sigmund Haffner Gasse 18, A-5020 Salzburg, Austria. 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Twenty-eight SIBS-ANV (17 boys), ages 4-9 years, took part in the study. All children attended regular schools, and none had received a diagnosis of autism. Controls were 27 typically developing children (SIBS-TD; 16 boys) matched to the SIBS-ANV on age, family background, socioeconomic status and type of school they attended. Significant IQ differences, as well as language differences as measured on the Clinical Evaluation of Language Fundamentals (CELF), emerged between SIBS-ANV and SIBS-TD. However, differences in the language scores mostly disappeared when PIQ and FSIQ were controlled for. Furthermore, grammatical analysis of spontaneous speech samples produced in the course of testing did not reveal any significant differences between the groups. These results add to recent work suggesting that language deficits may not be part of the Broad Autism Phenotype (BAP). It further suggests that the cognitive deficit characteristic of nonverbal people with autism may be familial. C1 [Levy, Yonata] Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. RP Levy, Y (reprint author), Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. 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H., 1992, CLIN EVALUATION LANG Williams D, 2008, PSYCHOL BULL, V134, P944, DOI [10.1037/a0013743, 10.1037/0013743] Yirmiya N, 2007, J AUTISM DEV DISORD, V37, P218, DOI 10.1007/s10803-006-0163-5 Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 39 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 MAY PY 2011 VL 15 IS 3 BP 341 EP 354 DI 10.1177/1362361310386504 PG 14 WC Psychology, Developmental SC Psychology GA 776MY UT WOS:000291540600007 PM 21363870 ER PT J AU Sofronoff, K Dark, E Stone, V AF Sofronoff, Kate Dark, Elizabeth Stone, Valerie TI Social vulnerability and bullying in children with Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; bullying; social vulnerability ID CAST CHILDHOOD ASPERGER; SCHOOL-AGE-CHILDREN; SPECTRUM; ANXIETY; AUTISM; ADULTS AB Children with Asperger syndrome (AS) have IQ within the normal range but specific impairments in theory of mind, social interaction and communication skills. The majority receive education in mainstream schools and research suggests they are bullied more than typically developing peers. The current study aimed to evaluate factors that predict bullying for such children and also to examine a new measure, the Social Vulnerability Scale (SVS). One hundred and thirty three parents of children with AS completed the SVS and of these 92 parents completed both the SVS and questionnaires measuring anxiety, anger, behaviour problems, social skills and bullying. Regression analyses revealed that these variables together strongly predicted bullying, but that social vulnerability was the strongest predictor. Test-re-test and internal consistency analyses of the SVS demonstrated sound psychometric properties and factor analyses revealed two sub-scales: gullibility and credulity. Limitations of the study are acknowledged and suggestions for future research discussed. C1 [Sofronoff, Kate] Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Sofronoff, K (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. EM kate@psy.uq.edu.au CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Attwood T, 2004, BEHAV CHANGE, V21, P147, DOI 10.1375/bech.21.3.147.55995 Attwood T., 2007, COMPLETE GUIDE ASPER Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Cassidy T., 2009, SOC PSYCHOL EDUC, V12, P63, DOI [10.1007/s11218-008-9066-y, DOI 10.1007/S11218-008-9066-Y] Coakes S. J., 2001, SPSS ANAL ANGUISH Gadow KD, 2005, AUTISM, V9, P392, DOI 10.1177/1362361305056079 Golan O, 2006, SOC NEUROSCI-UK, V1, P111, DOI 10.1080/17470910600980986 GREENSPAN S, 1997, HDB MENTAL DEFICIENC, P311 Greenspan S, 2001, INT REV RES MENT RET, V 24, P101, DOI 10.1016/S0074-7750(01)80007-0 GUSTEIN SE, 2002, FOCUS AUTISM OTHER D, V17, P161 Heerey EA, 2005, J ABNORM CHILD PSYCH, V33, P55, DOI 10.1007/s10802-005-0934-z Humphrey N, 2008, AUTISM, V12, P23, DOI 10.1177/1362361307085267 Mishna F., 2004, CHILDREN SCH, V26, P234 Myles B. 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TI The everyday routines of families of children with autism Examining the impact of sensory processing difficulties on the family SO AUTISM LA English DT Article DE autism; family; qualitative research; routines; sensory processing ID ASPERGER-SYNDROME; PARENTS; ABNORMALITIES; DISORDERS; STRESS AB The purpose of this qualitative study was to explore the lived experience of how sensory-related behaviors of children with autism affected family routines. In-depth semi-structured interviews were conducted with four primary caregivers regarding the meaning and impact of their child's sensory-related behaviors on family routines that occurred inside and outside the home. Findings indicated that sensory behaviors are one factor that limited family participation in work, family and leisure activities; and that parents employed specific strategies to manage individual and family routines in light of the child's sensory-related behaviors. This information has important implications for professionals who work with families of children with autism to decrease caregiver stress and to increase life satisfaction for the child and family. C1 [Schaaf, Roseann C.; Toth-Cohen, Susan; Benevides, Teal W.] Thomas Jefferson Univ, Philadelphia, PA 19107 USA. [Johnson, Stephanie L.] Walter Reed Army Med Ctr, Washington, DC 20307 USA. [Outten, Gina] Therapy Serv Delaware, Wilmington, DE USA. RP Schaaf, RC (reprint author), Thomas Jefferson Univ, 130 S 9th St,Suite 810, Philadelphia, PA 19107 USA. EM roseann.schaaf@jefferson.edu CR Allik H, 2006, HEALTH QUAL LIFE OUT, V4, DOI 10.1186/1477-7525-4-1 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ashburner J, 2008, AM J OCCUP THER, V62, P564 Baranek GT, 2002, J AUTISM DEV DISORD, V32, P397, DOI 10.1023/A:1020541906063 Ben-Sasson A, 2009, J AUTISM DEV DISORD, V39, P1, DOI 10.1007/s10803-008-0593-3 Centers for Disease Control and Prevention, 2009, MMWR, P58 Creswell J. 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Hossein Folsom, Timothy D. Thuras, Paul D. TI Deficits in GABA(B) receptor system in schizophrenia and mood disorders: A postmortem study SO SCHIZOPHRENIA RESEARCH LA English DT Article DE GABA(B) receptor; Schizophrenia; Bipolar disorder; Major depression; Lateral cerebellum ID POSITRON-EMISSION-TOMOGRAPHY; MAJOR DEPRESSION; BIPOLAR DISORDER; IMMUNOHISTOCHEMICAL LOCALIZATION; PSYCHIATRIC-DISORDERS; PREFRONTAL CORTEX; PROTEIN-LEVELS; B-RECEPTOR; EXPRESSION; BRAIN AB Postmortem and genetic studies have clearly demonstrated changes in GABA(B) receptors in neuropsychiatric disorders such as autism, bipolar disorder, major depression, and schizophrenia. Moreover, a number of recent studies have stressed the importance of cerebellar dysfunction in these same disorders. In the current study, we examined protein levels of the two GABA(B) receptor subunits GABBR1 and GABBR2 in lateral cerebella from a well-characterized cohort of subjects with schizophrenia (n = 15), bipolar disorder (n = 14), major depression (n = 13) and healthy controls (n = 12). We found significant reductions in protein for both GABBR1 and GABBR2 in lateral cerebella from subjects with schizophrenia, bipolar disorder and major depression when compared with controls. These results provide further evidence of GABAergic dysfunction in these three disorders as well as identify potential targets for therapeutic intervention. (C) 2011 Elsevier B.V. All rights reserved. C1 [Fatemi, S. Hossein; Folsom, Timothy D.] Univ Minnesota, Dept Psychiat, Sch Med, Div Neurosci Res, Minneapolis, MN 55455 USA. [Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Pharmacol, Minneapolis, MN 55455 USA. [Fatemi, S. Hossein] Univ Minnesota, Sch Med, Dept Neurosci, Minneapolis, MN 55455 USA. [Thuras, Paul D.] VA Med Ctr, Dept Psychiat, Minneapolis, MN 55417 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Dept Psychiat, Sch Med, Div Neurosci Res, 420 Delaware St SE,MMC 392, Minneapolis, MN 55455 USA. EM fatem002@umn.edu; folso013@umn.edu; pthuras@yahoo.com FU National Institutes of Mental Health [1R01MH086000-01A2, 1R01-MH086000-01A2] FX Grant support by the National Institutes of Mental Health (Grant #1R01MH086000-01A2) to SHF is gratefully acknowledged. Tissue samples from the Stanley Medical Research Institute to SHF is gratefully acknowledged.Funding for this study was provided by the National Institutes of Mental Health (NIMH), Grant #1R01-MH086000-01A2 (SHF). NIMH 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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PD MAY PY 2011 VL 63 IS 2 BP 191 EP + PG 19 WC Theater SC Theater GA 772OC UT WOS:000291242200003 ER PT J AU Bethell, CD Kogan, MD Strickland, BB Schor, EL Robertson, J Newacheck, PW AF Bethell, Christina D. Kogan, Michael D. Strickland, Bonnie B. Schor, Edward L. Robertson, Julie Newacheck, Paul W. TI A National and State Profile of Leading Health Problems and Health Care Quality for US Children: Key Insurance Disparities and Across-State Variations SO ACADEMIC PEDIATRICS LA English DT Article DE children's health insurance; children's health services; chronic conditions in childhood; CSHCN medical home; national survey of children's health (NSCH); quality of care ID UNITED-STATES; NEEDS; ACCESS; COVERAGE; OBESITY AB BACKGROUND: Parent/consumer-reported data is valuable and necessary for population-based assessment of many key child health and health care quality measures relevant to both the Children's Health Insurance Program Reauthorization Act (CHIPRA) of 2009 and the Patient Protection and Affordable Care Act of 2010 (ACA). OBJECTIVES: The aim of this study was to evaluate national and state prevalence of health problems and special health care needs in US children; to estimate health care quality related to adequacy and consistency of insurance coverage, access to specialist, mental health and preventive medical and dental care, developmental screening, and whether children meet criteria for having a medical home, including care coordination and family centeredness; and to assess differences in health and health care quality for children by insurance type, special health care needs status, race/ethnicity, and/or state of residence. METHODS: National and state level estimates were derived from the 2007 National Survey of Children's Health (N = 91 642; children aged 0-17 years). Variations between children with public versus private sector health insurance, special health care needs, specific conditions, race/ethnicity, and across states were evaluated using multivariate logistic regression and/or standardized statistical tests. RESULTS: An estimated 43% of US children (32 million) currently have at least 1 of 20 chronic health conditions assessed, increasing to 54.1% when overweight, obesity, or being at risk for developmental delays are included; 19.2% (14.2 million) have conditions resulting in a special health care need, a 1.6 point increase since 2003. Compared with privately insured children, the prevalence, complexity, and severity of health problems were systematically greater for the 29.1% of all children who are publicly insured children after adjusting for variations in demographic and socioeconomic factors. Forty-five percent of all children in the United States scored positively on a minimal quality composite measure: 1) adequate insurance, 2) preventive care visit, and 3) medical home. A 22.2 point difference existed across states and there were wide variations by health condition (autism, 22.8, to asthma, 39.4). After adjustment for demographic and health status differences, quality of care varied between children with public versus private health insurance on all but the following 3 measures: not receiving needed mental health services, care coordination, and performance on the minimal quality composite. A 4.60 fold (gaps in insurance) to 1.27 fold (preventive dental and medical care visits) difference in quality scores was observed across states. Notable disparities were observed among publicly insured children according to race/ethnicity and across all children by special needs status and household income. CONCLUSIONS: Findings emphasize the importance of health care insurance duration and adequacy, health care access, chronic condition management, and other quality of care goals reflected in the 2009 CHIPRA legislation and the ACA. Despite disparities, similarities for public and privately insured children speak to the pervasive nature of availability, coverage, and access issues for mental health services in the United States, as well as the system-wide problem of care coordination and accessing specialist care for all children. Variations across states in key areas amenable to state policy and program management support cross-state learning and improvement efforts. C1 [Bethell, Christina D.; Robertson, Julie] Oregon Hlth & Sci Univ, Dept Pediat, Sch Med, Child & Adolescent Hlth Measurement Initiat, Portland, OR 97239 USA. [Kogan, Michael D.; Strickland, Bonnie B.] US Dept Hlth & Human Serv, Hlth Resources & Serv Adm, Maternal & Child Hlth Bur, Rockville, MD USA. [Schor, Edward L.] Commonwealth Fund, New York, NY USA. [Newacheck, Paul W.] Univ Calif San Francisco, Philip R Lee Inst Hlth Policy Studies, San Francisco, CA 94143 USA. RP Bethell, CD (reprint author), Oregon Hlth & Sci Univ, Dept Pediat, Sch Med, Child & Adolescent Hlth Measurement Initiat, 707 SW Gaines St,Mailcode CDRCP, Portland, OR 97239 USA. EM bethellc@ohsu.edu FU HHS Centers for Medicare & Medicaid Services; Maternal and Child Health Bureau [1-U59-MC06980-01] FX This paper is based on a report prepared for the Agency for Healthcare Research and Quality through purchase order HHSP233200900801P by the US Department of Health and Human Services (HHS), with funds provided by the HHS Centers for Medicare & Medicaid Services. This study was also supported by The Child and Adolescent Health Measurement Initiative's Data Resource Center for Child and Adolescent Health, which is funded by the Maternal and Child Health Bureau through Cooperative Agreement 1-U59-MC06980-01. 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In this special issue we bring together a range of papers where rare diseases were used as models to delineate specific aspects of learning and memory, or behaviour. In this introductory paper we summarize some of the lessons we can learn from rare diseases. Firstly, we learn that, collectively, rare diseases are not at all rare. As many as 1 in 20 individuals may be affected by a rare disease at some point in their life. Secondly, we learn that rare diseases may share common pathophysiological mechanisms. A discovery in one can therefore have direct relevance to many others. A third lesson is that the study of rare diseases can lead to an understanding of common disorders, as exemplified by the relationship between Trisomy 21 (Down syndrome) and Alzheimer's disease. A fourth lesson from rare diseases is that the 'one gene-one functional consequence' assumption is not correct. 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Genet. PD MAY PY 2011 VL 41 IS 3 SI SI BP 341 EP 348 DI 10.1007/s10519-011-9469-y PG 8 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 769RH UT WOS:000291035400001 PM 21541644 ER PT J AU Ehninger, D Silva, AJ AF Ehninger, Dan Silva, Alcino J. TI Increased Levels of Anxiety-related Behaviors in a Tsc2 Dominant Negative Transgenic Mouse Model of Tuberous Sclerosis SO BEHAVIOR GENETICS LA English DT Article DE Tuberous sclerosis; mTOR; Anxiety; Learning and memory; Behavior; Mouse ID ELEVATED PLUS-MAZE; COGNITIVE DEFICITS; COMPLEX TSC; RAT MODEL; POPULATION; PHENOTYPE; EPILEPSY; SEIZURES; AUTISM; SAMPLE AB Tuberous sclerosis (TSC) is a single-gene disorder caused by heterozygous mutations in the TSC1 or TSC2 gene. TSC is often associated with neurological (e.g., epilepsy), cognitive (intellectual disabilities, specific neuropsychological impairments) and behavioral pathologies (e.g., autism, attention deficit hyperactivity disorder). In addition, there is a high prevalence of psychiatric problems in TSC populations, including anxiety and mood disorders. To date, little is known about the pathogenetic bases of these associated psychiatric symptoms; for instance, it is unclear whether they are rooted in TSC-associated neurobiological alterations or whether they are secondary psychological phenomena (e.g., because individuals have to cope with the burden of the disease). Here, we report elevated levels of anxiety-related behaviors and mild deficits in two hippocampal-dependent learning tasks in a Tsc2 dominant negative transgenic mouse model of TSC. These findings establish a mouse model for TSC-related anxiety phenotypes and suggest that anxiety disorders in TSC have a biological foundation. C1 [Ehninger, Dan] German Ctr Neurodegenerat Dis DZNE, D-53175 Bonn, Germany. [Ehninger, Dan; Silva, Alcino J.] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA. [Ehninger, Dan; Silva, Alcino J.] Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA. [Ehninger, Dan; Silva, Alcino J.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. [Ehninger, Dan; Silva, Alcino J.] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Ehninger, D (reprint author), German Ctr Neurodegenerat Dis DZNE, Ludwig Erhard Allee 2, D-53175 Bonn, Germany. EM Dan.Ehninger@dzne.de FU DFG [EH223/2-1]; German Centre for Neurodegenerative Diseases (DZNE); NIH [R01 MH084315] FX Tsc2-DN mice were kindly provided by Jack L. Arbiser. This work was supported by DFG grant EH223/2-1 and funds of the German Centre for Neurodegenerative Diseases (DZNE) to D. E. and NIH R01 MH084315 to A.J.S. CR Bolton PF, 2002, BRAIN, V125, P1247, DOI 10.1093/brain/awf124 Crino PB, 2006, NEW ENGL J MED, V355, P1345, DOI 10.1056/NEJMra055323 Curatolo P, 2008, LANCET, V372, P657, DOI 10.1016/S0140-6736(08)61279-9 Dabora SL, 2002, AM J HUM GENET, V71, P750, DOI 10.1086/342718 de Vries PJ, 2007, EUR CHILD ADOLES PSY, V16, P16, DOI 10.1007/s00787-006-0570-3 de Vries P, 2005, EUR CHILD ADOLES PSY, V14, P183, DOI 10.1007/s00787-005-0443-1 de Vries PJ, 2009, AM J MED GENET A, V149A, P387, DOI 10.1002/ajmg.a.32690 de Vries PJ, 2007, NEW ENGL J MED, V356, P92 de Vries PJ, 2007, TRENDS MOL MED, V13, P319, DOI 10.1016/j.molmed.2007.06.003 Ehninger D, 2008, NAT MED, V14, P843, DOI 10.1038/nm1788 Goorden SMI, 2007, ANN NEUROL, V62, P648, DOI 10.1002/ana.21317 Govindarajan B, 2005, J BIOL CHEM, V280, P5870, DOI 10.1074/jbc.M411768200 Harrison JE, 1999, AM J MED GENET, V88, P642, DOI 10.1002/(SICI)1096-8628(19991215)88:6<642::AID-AJMG12>3.0.CO;2-O Hogg S, 1996, PHARMACOL BIOCHEM BE, V54, P21, DOI 10.1016/0091-3057(95)02126-4 Joinson C, 2003, PSYCHOL MED, V33, P335, DOI 10.1017/S0033291702007092 Kikuchi Y, 2004, INT J ONCOL, V24, P75 Lewis JC, 2004, J MED GENET, V41, P203, DOI 10.1136/jmg.2003.012757 Meikle L, 2007, J NEUROSCI, V27, P5546, DOI 10.1523/JNEUROSCI.5540-06.2007 Muzykewicz DA, 2007, EPILEPSY BEHAV, V11, P506, DOI 10.1016/j.yebeh.2007.07.010 Onda H, 1999, J CLIN INVEST, V104, P687, DOI 10.1172/JCI7319 Pasumarthi KBS, 2000, CIRC RES, V86, P1069 Prather P, 2004, J CHILD NEUROL, V19, P666 Pulsifer MB, 2007, EPILEPSY BEHAV, V10, P402, DOI 10.1016/j.yebeh.2007.02.004 Raznahan A, 2006, J INTELL DISABIL RES, V50, P561, DOI 10.1111/j.1365-2788.2006.00828.x Ridler K, 2007, CEREB CORTEX, V17, P261, DOI 10.1093/cercor/bhj144 Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 Uhlmann EJ, 2002, ANN NEUROL, V52, P285, DOI 10.1002/ana.10283 Walf AA, 2007, NAT PROTOC, V2, P322, DOI 10.1038/nprot.2007.44 Waltereit R, 2006, J NEUROCHEM, V96, P407, DOI 10.1111/j.1471-4159.2005.03538.x Way SW, 2009, HUM MOL GENET, V18, P1252, DOI 10.1093/hmg/ddp025 Webb DW, 1996, DEV MED CHILD NEUROL, V38, P146 Winterkorn EB, 2007, NEUROLOGY, V68, P62, DOI 10.1212/01.wnl.0000250330.44291.54 Yeung RS, 2001, GENOMICS, V78, P108, DOI 10.1006/geno.2001.6654 NR 33 TC 12 Z9 12 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD MAY PY 2011 VL 41 IS 3 SI SI BP 357 EP 363 DI 10.1007/s10519-010-9398-1 PG 7 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 769RH UT WOS:000291035400003 PM 20882401 ER PT J AU Waltereit, R Japs, B Schneider, M de Vries, PJ Bartsch, D AF Waltereit, Robert Japs, Birte Schneider, Miriam de Vries, Petrus J. Bartsch, Dusan TI Epilepsy and Tsc2 Haploinsufficiency Lead to Autistic-Like Social Deficit Behaviors in Rats SO BEHAVIOR GENETICS LA English DT Article DE Tuberous sclerosis; Autism; Mental retardation; Epilepsy; Animal models ID TUBEROUS SCLEROSIS COMPLEX; SPECTRUM DISORDERS; ANXIOLYTIC ACTION; ANIMAL-MODELS; RELEVANT; CHILDREN; MEMORY; SEIZURES; ANXIETY; GENE AB There is a strong association between autism spectrum disorders (ASD), epilepsy and intellectual disability in humans, but the nature of these correlations is unclear. The monogenic disorder Tuberous Sclerosis Complex (TSC) has high rates of ASD, epilepsy and cognitive deficits. Here we used the Tsc2 (+/-) (Eker) rat model of TSC and an experimental epilepsy paradigm to study the causal effect of seizures on learning and memory and social behavior phenotypes. Status epilepticus was induced by kainic acid injection at P7 and P14 in wild-type and Tsc2 (+/-) rats. At the age of 3-6 months, adult rats were assessed in the open field, light/dark box, fear conditioning, Morris water maze, novel object recognition and social interaction tasks. Learning and memory was unimpaired in na < ve Tsc2 (+/-) rats, and experimental epilepsy did not impair any aspects of learning and memory in either wild-type or Tsc2 (+/-) rats. In contrast, rearing in the open field, novel object exploration and social exploration was reduced in na < ve Tsc2 (+/-) rats. Seizures induced anxiety and social evade, and reduced social exploration and social contact behavior in wild-type and Tsc2 (+/-) rats. Our study shows that Tsc2 haploinsufficiency and developmental status epilepticus in wild-type and Tsc2 (+/-) rats independently lead to autistic-like social deficit behaviors. The results suggest that the gene mutation may be sufficient to lead to some social deficits, and that seizures have a direct and additive effect to increase the likelihood and range of autistic-like behaviors. C1 [Waltereit, Robert; Japs, Birte; Bartsch, Dusan] Cent Inst Mental Hlth, Dept Mol Biol, D-68159 Mannheim, Germany. [Waltereit, Robert; Japs, Birte; Schneider, Miriam; Bartsch, Dusan] Univ Heidelberg, Mannheim Med Fac, D-68159 Mannheim, Germany. [Waltereit, Robert] Cent Inst Mental Hlth, Dept Psychiat & Psychotherapy, D-68159 Mannheim, Germany. [Schneider, Miriam] Cent Inst Mental Hlth, Dept Psychopharmacol, D-68159 Mannheim, Germany. [de Vries, Petrus J.] Cambridgeshire & Peterborough NHS Fdn Trust, Cambridge, England. [de Vries, Petrus J.] Univ Cambridge, Dev Psychiat Sect, Cambridge, England. RP Waltereit, R (reprint author), Cent Inst Mental Hlth, Dept Mol Biol, J 5, D-68159 Mannheim, Germany. EM robert.waltereit@zi-mannheim.de FU Tuberose Sklerose Deutschland; Deutsche Forschungsgemeinschaft [SFB 636] FX This work was supported by research grants from Tuberose Sklerose Deutschland to R. W. and Deutsche Forschungsgemeinschaft SFB 636 to D. B. The authors would like to thank Lena Wendler for excellent technical support and Dr. Mathias Zink for help with an initial experiment. 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O., 2006, UNDERSTANDING AUTISM Moy SS, 2007, BEHAV BRAIN RES, V176, P4, DOI 10.1016/j.bbr.2006.07.030 O'Callaghan FJK, 2004, ARCH DIS CHILD, V89, P530, DOI 10.1136/adc.2003.026815 Rennebeck G, 1998, P NATL ACAD SCI USA, V95, P15629, DOI 10.1073/pnas.95.26.15629 Sayin U, 2004, EPILEPSIA, V45, P1539, DOI 10.1111/j.0013-9580.2004.54903.x Schneider M, 2008, ADDICT BIOL, V13, P345, DOI 10.1111/j.1369-1600.2008.00117.x Smalley SL, 1998, J AUTISM DEV DISORD, V28, P407, DOI 10.1023/A:1026052421693 Spence SJ, 2009, PEDIATR RES, V65, P599, DOI 10.1203/PDR.0b013e31819e7168 Tordjman S, 2007, BEHAV GENET, V37, P61, DOI 10.1007/s10519-006-9120-5 Turk J, 2009, ACTA PAEDIATR, V98, P675, DOI 10.1111/j.1651-2227.2008.01184.x Viding E, 2007, BEHAV GENET, V37, P51, DOI 10.1007/s10519-006-9105-4 Waltereit R, 2006, J NEUROCHEM, V96, P407, DOI 10.1111/j.1471-4159.2005.03538.x Waltereit R, 2008, LEARN MEMORY, V15, P348, DOI 10.1101/lm.808608 NR 31 TC 18 Z9 18 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD MAY PY 2011 VL 41 IS 3 SI SI BP 364 EP 372 DI 10.1007/s10519-010-9399-0 PG 9 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 769RH UT WOS:000291035400004 PM 20927644 ER PT J AU Fisch, GS Davis, R Youngblom, J Gregg, J AF Fisch, Gene S. Davis, Ryan Youngblom, Janey Gregg, Jeff TI Genotype-Phenotype Association Studies of Chromosome 8p Inverted Duplication Deletion Syndrome SO BEHAVIOR GENETICS LA English DT Article DE Subtelomeric deletion; Inverted duplication deletion 8p21-23; Intellectual disability; Autism; CGH microarray ID AUTISM SPECTRUM DISORDERS; WOLF-HIRSCHHORN-SYNDROME; MENTAL-RETARDATION; SHORT ARM; SUBTELOMERIC REARRANGEMENTS; BEHAVIORAL-PROBLEMS AB Individuals diagnosed with chromosome 8p inverted duplication deletion (invdupdel(8p)) manifest a wide range of clinical features and cognitive impairment. The purpose of this study is to employ array CGH technology to define more precisely the cytogenetic breakpoints and regions of copy number variation found in several individuals with invdupdel(8p), and compare these results with their neuropsychological characteristics. We examined the cognitive-behavioral features of two male and two female children, ages 3-15 years, with invdupdel(8p). We noted cognitive deficits that ranged from mild to severe, and adaptive behavior composites that ranged from significantly to substantially lower than adequate levels. CARS scores, a measure of autistic behavior, identified three children with autism or autistic-like features. Three of the four children exhibited attention deficits and hyperactivity consistent with a DSM-IV-TR diagnosis of ADHD. One child showed extreme emotional lability. Interestingly, intellectual disability was not correlated with deletion size, nor was the deletion location associated with the autistic phenotype. On the other hand, the duplication length in 8p21.1/8p22 was associated with cognitive deficit. In addition, a small locus of over-expression in 8p21.3 was common for all three participants diagnosed as autistic. A limitation of the study is its small sample size. Further analyses of the deleted and over-expressed regions are needed to ascertain the genes involved in cognitive function and, possibly, autism. C1 [Fisch, Gene S.] NYU, Dept Epidemiol & Hlth Promot, Coll Dent, New York, NY 10003 USA. [Fisch, Gene S.] NYU, Dept Epidemiol & Hlth Promot, Coll Nursing, New York, NY 10003 USA. [Davis, Ryan; Gregg, Jeff] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. [Youngblom, Janey] Calif State Univ, Dept Biol Sci, Stanislaus, CA USA. RP Fisch, GS (reprint author), NYU, Dept Epidemiol & Hlth Promot, Coll Dent, New York, NY 10003 USA. 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Genet. PD MAY PY 2011 VL 41 IS 3 SI SI BP 373 EP 380 DI 10.1007/s10519-011-9447-4 PG 8 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 769RH UT WOS:000291035400005 PM 21259039 ER PT J AU Huijbregts, SCJ de Sonneville, LMJ AF Huijbregts, Stephan C. J. de Sonneville, Leo M. J. TI Does Cognitive Impairment Explain Behavioral and Social Problems of Children with Neurofibromatosis Type 1? SO BEHAVIOR GENETICS LA English DT Article DE Neurofibromatosis Type 1; Social functioning; Behavior problems; Information processing speed; Cognitive control; Social information processing ID TUBEROUS SCLEROSIS COMPLEX; AUTISM; ADOLESCENTS; NF1; DISORDERS; BRAIN; ATTENTION; DEFICITS; MATTER; ADHD AB Thirty NF1-patients (mean age 11.7 years, SD = 3.3) and 30 healthy controls (mean age 12.5 years, SD = 3.1) were assessed on social skills, autistic traits, hyperactivity-inattention, emotional problems, conduct problems, and peer problems. Cognitive control, information processing speed, and social information processing were measured using 5 computer tasks. GLM analyses of variance showed significant group differences, to the disadvantage of NF1-patients, on all measures of behavior, social functioning and cognition. General cognitive ability (a composite score of processing speed, social information processing, and cognitive control) accounted for group differences in emotional problems, whereas social information processing accounted for group differences in conduct problems. Although reductions were observed for group differences in other aspects of behavior and social functioning after control for (specific) cognitive abilities, group differences remained evident. Training of cognitive abilities may help reducing certain social and behavioral problems of children with NF1, but further refinement regarding associations between specific aspects of cognition and specific social and behavioral outcomes is required. C1 [Huijbregts, Stephan C. J.; de Sonneville, Leo M. J.] Leiden Univ, Dept Educ & Child Studies Clin Child & Adolescent, Leiden Inst Brain & Cognit, NL-2300 RB Leiden, Netherlands. RP Huijbregts, SCJ (reprint author), Leiden Univ, Dept Educ & Child Studies Clin Child & Adolescent, Leiden Inst Brain & Cognit, NL-2300 RB Leiden, Netherlands. EM shuijbregts@fsw.leidenuniv.nl FU Dutch Neurofibromatosis Society (NFVN) FX The authors are grateful to Dutch Neurofibromatosis Society (NFVN), which provided an unconditional financial donation to SH in order to facilitate NF1-related research and helped with recruitment of study participants. A further "thank you" goes out to the NF1-patients and their families and friends for participation in this study. 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Genet. PD MAY PY 2011 VL 41 IS 3 SI SI BP 430 EP 436 DI 10.1007/s10519-010-9430-5 PG 7 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 769RH UT WOS:000291035400011 PM 21184163 ER PT J AU Ploog, BO AF Ploog, Bertram O. TI Selective attention to visual compound stimuli in squirrel monkeys (Saimiri sciureus) SO BEHAVIOURAL PROCESSES LA English DT Article; Proceedings Paper CT 33rd Annual Meeting of the Society-for-the-Quantitative-Analyses-of-Behavior CY MAY 27-29, 2010 CL San Antonio, TX SP Soc Quantitat Anal Behav DE Discrimination learning; Attention; Excitatory and inhibitory control; Autism; Stimulus overselectivity; Impulsivity ID AUTISTIC-CHILDREN; PARTIAL-REINFORCEMENT; OVER-SELECTIVITY; DISCRIMINATION; OVERSELECTIVITY; COLOR; FORM; CUES; IMPULSIVITY; PERFORMANCE AB Five squirrel monkeys served under a simultaneous discrimination paradigm with visual compound stimuli that allowed measurement of excitatory and inhibitory control exerted by individual stimulus components (form and luminance/"color"), which could not be presented in isolation (i.e., form could not be presented without color). After performance exceeded a criterion of 75% correct during training, unreinforced test trials with stimuli comprising recombined training stimulus components were interspersed while the overall reinforcement rate remained constant for training and testing. The training-testing series was then repeated with reversed reinforcement contingencies. The findings were that color acquired greater excitatory control than form under the original condition, that no such difference was found for the reversal condition or for inhibitory control under either condition, and that overall inhibitory control was less pronounced than excitatory control. The remarkably accurate performance throughout suggested that a forced 4-s delay between the stimulus presentation and the opportunity to respond was effective in reducing "impulsive" responding, which has implications for suppressing impulsive responding in children with autism and with attention deficit disorder. (C) 2011 Elsevier B.V. All rights reserved. C1 [Ploog, Bertram O.] CUNY Coll Staten Isl, Dept Psychol, Staten Isl, NY 10314 USA. [Ploog, Bertram O.] CUNY Grad Sch & Univ Ctr, New York, NY USA. RP Ploog, BO (reprint author), CUNY Coll Staten Isl, Dept Psychol, 4S-105,2800 Victory Blvd, Staten Isl, NY 10314 USA. 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Processes PD MAY PY 2011 VL 87 IS 1 SI SI BP 115 EP 124 DI 10.1016/j.beproc.2010.12.015 PG 10 WC Psychology, Biological; Behavioral Sciences; Zoology SC Psychology; Behavioral Sciences; Zoology GA 767VL UT WOS:000290886400016 PM 21215303 ER PT J AU Carretto, E Betalli, P Salvador, R Zanatta, L Morbin, T Nicoletti, L Guariso, G Galeazzi, F Gamba, PG Costantini, M AF Carretto, Elena Betalli, Pietro Salvador, Renato Zanatta, Lisa Morbin, Tiziana Nicoletti, Loredana Guariso, Graziella Galeazzi, Francesca Gamba, Pier Giorgio Costantini, Mario TI Autism and Esophageal Achalasia in Childhood: A Possible Correlation? Report on Two Cases SO GASTROENTEROLOGY LA English DT Meeting Abstract CT Conference on Digestive Disease Week 2011 CY MAY 07-10, 2011 CL Chicago, IL NR 0 TC 0 Z9 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAY PY 2011 VL 140 IS 5 SU 1 BP S234 EP S234 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 758LW UT WOS:000290167300947 ER PT J AU Peeters, B Benninga, MA Loots, CM van der Pol, RJ Burgers, R Philips, E Wepster, B Tabbers, M Noens, I AF Peeters, Babette Benninga, Marc A. Loots, Clara M. van der Pol, Rachel J. Burgers, Rosa Philips, Elise Wepster, Bente Tabbers, Merit Noens, Ilse TI Autism Spectrum Disorders and Autism Spectrum Symptoms in Children With Functional Defecation Disorders SO GASTROENTEROLOGY LA English DT Meeting Abstract CT Conference on Digestive Disease Week 2011 CY MAY 07-10, 2011 CL Chicago, IL NR 0 TC 0 Z9 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAY PY 2011 VL 140 IS 5 SU 1 BP S742 EP S743 PG 2 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 758LW UT WOS:000290167303314 ER PT J AU Freed, J Adams, C Lockton, E AF Freed, Jenny Adams, Catherine Lockton, Elaine TI Literacy skills in primary school-aged children with pragmatic language impairment: a comparison with children with specific language impairment SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE pragmatic language impairment; specific language impairment; literacy; reading; writing ID READING-COMPREHENSION; WRITTEN LANGUAGE; COMMUNICATION CHECKLIST; DISORDERS; AUTISM; DEFICITS; ABILITY AB Background: Children with pragmatic language impairment (CwPLI) are characterized by difficulties with the interpersonal use of language in social contexts and they possess a range of language difficulties that affect their educational attainment. Since literacy skills are central to this attainment, one way of identifying appropriate support needs for CwPLI would be to profile their reading and writing skills as a group. Aims: To investigate the word reading, non-word reading, reading comprehension, and written expression skills of CwPLI and a comparison group of children with specific language impairment (CwSLI). CwSLI were recruited in order to examine any overlaps in literacy impairments for the two groups. Methods & Procedures: Primary school-aged CwPLI (n = 59) and CwSLI (n = 12) were recruited from speech and language therapists. Children completed standardized assessments of literacy skills. The level of impairment for each component literacy skill was examined for CwPLI and CwSLI. Outcomes & Results: For the CwPLI, group mean scores on each of the literacy skills were at the lower end of the normal range compared with population norms. The range of individual scores was large, with some children scoring near floor level and others scoring up to 2 SDs (standard deviations) above the mean, illustrating the heterogeneity of literacy skills within the group. For the CwSLI, group mean scores on each of the literacy skills were between 1 SD and 2 SDs below the population mean. CwSLI were significantly more impaired on all of the literacy measures compared with CwPLI. This difference remained even when receptive language ability and non-verbal intelligence were controlled for. Conclusions & Implications: The results demonstrate that there is a high level of literacy impairment within CwPLI and CwSLI, providing evidence that individualized literacy skill intervention is important for the long-term academic outcome of these children. C1 [Freed, Jenny; Adams, Catherine; Lockton, Elaine] Univ Manchester, Manchester M13 9PL, Lancs, England. RP Freed, J (reprint author), Univ Manchester, Oxford Rd, Manchester M13 9PL, Lancs, England. EM jenny.freed@manchester.ac.uk CR ADAMS C, SOCIAL COMMUNICATION Adams C, 2006, INT J LANG COMM DIS, V41, P41, DOI 10.1080/13693780500179793 Adams C, 2001, ASSESSMENT COMPREHEN, P6 Adams C, 2009, INT J LANG COMM DIS, V44, P301, DOI 10.1080/13682820802051788 Bishop D., 2000, SPEECH LANGUAGE IMPA, P99 Bishop D. V. M., 2003, CHILDRENS COMMUNICAT Bishop D. V. 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J. Lang. Commun. Disord. PD MAY-JUN PY 2011 VL 46 IS 3 BP 334 EP 347 DI 10.3109/13682822.2010.500316 PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 764KA UT WOS:000290627200008 PM 21575074 ER PT J AU Jaber, MA AF Jaber, Mohamed Abdullah TI Dental caries experience, oral health status and treatment needs of dental patients with autism SO JOURNAL OF APPLIED ORAL SCIENCE LA English DT Article DE Autism; Autistic disorder; Dental caries; Dental care for disabled; Dental care for children; Oral health ID SPECTRUM DISORDERS; EPIDEMIOLOGY; DIAGNOSIS; CHILDREN; CARE AB Objectives: Autism is a lifelong neurodevelopmental disorder. The aims of this study were to investigate whether children with autism have higher caries prevalence, higher periodontal problems, or more treatment needs than children of a control group of non-autistic patients, and to provide baseline data to enable comparison and future planning of dental services to autistic children. Material and Methods: 61 patients with autism aged 6-16 years (45 males and 16 females) attending Dubai and Sharjah Autism Centers were selected for the study. The control group consisted of 61 non-autistic patients chosen from relatives or friends of autistic patients in an attempt to have matched age, sex and socioeconomic status. Each patient received a complete oral and periodontal examination, assessment of caries prevalence, and caries severity. Other conditions assessed were dental plaque, gingivitis, restorations and treatment needs. Chi-square and Fisher's exact test of significance were used to compare groups. Results: The autism group had a male-to-female ratio of 2.8:1. Compared to controls, children with autism had significantly higher decayed, missing or filled teeth than unaffected patients and significantly needed more restorative dental treatment. The restorative index (RI) and Met Need Index (MNI) for the autistic children were 0.02 and 0.3, respectively. The majority of the autistic children either having poor 59.0% (36/61) or fair 37.8% (23/61) oral hygiene compared with healthy control subjects. Likewise, 97.0% (59/61) of the autistic children had gingivitis. Conclusions: Children with autism exhibited a higher caries prevalence, poor oral hygiene and extensive unmet needs for dental treatment than non-autistic healthy control group. Thus oral health program that emphasizes prevention should be considered of particular importance for children and young people with autism. C1 Ajman Univ Sci & Technol, Coll Dent, Dept Surg Sci, Sch Dent, Ajman, U Arab Emirates. RP Jaber, MA (reprint author), Ajman Univ Sci & Technol, Coll Dent, Dept Surg Sci, Sch Dent, Al Jurf Campus,POB 346, Ajman, U Arab Emirates. 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Appl. Oral Sci. PD MAY-JUN PY 2011 VL 19 IS 3 BP 212 EP 217 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 769YU UT WOS:000291055000006 PM 21625735 ER PT J AU Rommelse, NNJ Geurts, HM Franke, B Buitelaar, JK Hartman, CA AF Rommelse, Nanda N. J. Geurts, Hilde M. Franke, Barbara Buitelaar, Jan K. Hartman, Catharina A. TI A review on cognitive and brain endophenotypes that may be common in autism spectrum disorder and attention-deficit/hyperactivity disorder and facilitate the search for pleiotropic genes SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE Autism spectrum disorder; Attention-deficit/hyperactivity disorder; Phenotype; Endophenotype; Genetics; Neuropsychology; Cognition; MRI; DTI; EEG ID DEFICIT-HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDER; HIGH-FUNCTIONING AUTISM; INFORMATION-PROCESSING SPEED; CORTICAL THICKNESS ANALYSIS; FIGURES TASK-PERFORMANCE; VOXEL-BASED MORPHOMETRY; CARD SORTING TEST; AND/OR PDD-NOS; RESPONSE-INHIBITION AB We propose to bring together the hitherto rather separate research fields of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), and argue that by contrasting and combining findings of the endophenotypes of ASD and ADHD new insights can be gained into the etiology and pathophysiology of these two disorders. Given the highly heritable nature of both disorders, studies of the genes explaining the shared origins of the two neurodevelopmental disorders seem particularly called for. Instead of the clinical diagnosis, using neurocognitive measures as (endo)phenotypes that index genetic liability appears a powerful tool in gene finding. We, therefore, extensively reviewed the literature and not only included research wherein ASD and ADHD were compared within a single study, but extended our search also to the separate lines of cognitive neuroscience research. We discuss which cognitive and brain measures will be useful in future genetic studies targeting pleiotropic genes for ASD and ADHD. By specifying the most promising endophenotypic measures we chart the future course for endophenotypic research in ASD and ADHD. We also discuss the various models that may explain the frequent co-occurrence of ASD and ADHD. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Rommelse, Nanda N. J.; Franke, Barbara] Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Psychiat, NL-6525 ED Nijmegen, Netherlands. [Rommelse, Nanda N. J.; Buitelaar, Jan K.] Child & Adolescent Psychiat Univ Ctr Nijmegen, Karakter, Nijmegen, Netherlands. [Geurts, Hilde M.] Univ Amsterdam, Dept Psychon, Amsterdam, Netherlands. [Geurts, Hilde M.] Dr Leo Kannerhuis Amsterdam Clin, Amsterdam, Netherlands. [Franke, Barbara] Radboud Univ Nijmegen, Med Ctr, Dept Human Genet, NL-6525 ED Nijmegen, Netherlands. [Buitelaar, Jan K.] Radboud Univ Nijmegen, Med Ctr, Donders Inst Brain Cognit & Behav, Dept Cognit Neurosci, NL-6525 ED Nijmegen, Netherlands. [Hartman, Catharina A.] Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, Interdisciplinary Ctr Psychiat Epidemiol Er Res, Sch Behav & Cognit Neurosci, NL-9713 AV Groningen, Netherlands. RP Rommelse, NNJ (reprint author), Radboud Univ Nijmegen Med Ctr, Dept Psychiat, Reinier Postlaan 12, Nijmegen, Netherlands. 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Biobehav. Rev. PD MAY PY 2011 VL 35 IS 6 BP 1363 EP 1396 DI 10.1016/j.neubiorev.2011.02.015 PG 34 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 768YS UT WOS:000290976600005 PM 21382410 ER PT J AU Press, C AF Press, Clare TI Action observation and robotic agents: Learning and anthropomorphism SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE Action observation network; Mirror neuron; Associative learning; Theory of mind ID MIRROR-NEURON SYSTEM; AUTISM SPECTRUM DISORDERS; AUTOMATIC IMITATION; PREMOTOR CORTEX; MOVEMENT INTERFERENCE; IMPOSSIBLE MOVEMENTS; NEWBORN-INFANTS; EEG EVIDENCE; TOP-DOWN; PERCEPTION AB The 'action observation network' (AON), which is thought to translate observed actions into motor codes required for their execution, is biologically tuned: it responds more to observation of human, than non-human, movement. This biological specificity has been taken to support the hypothesis that the AON underlies various social functions, such as theory of mind and action understanding, and that, when it is active during observation of non-human agents like humanoid robots, it is a sign of ascription of human mental states to these agents. This review will outline evidence for biological tuning in the AON, examining the features which generate it, and concluding that there is evidence for tuning to both the form and kinematic profile of observed movements, and little evidence for tuning to belief about stimulus identity. It will propose that a likely reason for biological tuning is that human actions, relative to non-biological movements, have been observed more frequently while executing corresponding actions. If the associative hypothesis of the AON is correct, and the network indeed supports social functioning, sensorimotor experience with non-human agents may help us to predict, and therefore interpret, their movements. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Press, Clare] Univ Reading, Sch Psychol & Clin Language Sci, Reading RG6 6AL, Berks, England. [Press, Clare] UCL, Inst Neurol, Wellcome Trust Ctr Neuroimaging, London WC1N 3BG, England. RP Press, C (reprint author), Univ Reading, Sch Psychol & Clin Language Sci, Reading RG6 6AL, Berks, England. EM c.m.press@reading.ac.uk FU Medical Research Council; Economic and Social Research Council FX CP was supported by an interdisciplinary postdoctoral fellowship awarded jointly by the Medical Research Council and the Economic and Social Research Council. I am grateful to Geoffrey Bird, Cecilia Heyes and James Kilner for comments on an earlier version of the manuscript. 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Remarkably, even though this study uses data from two different rodent species (due to the data limitations), we still find that the connectivity of the majority of brain regions is highly predictable from their gene expression levels-the outgoing (incoming) connectivity is successfully predicted for 73% (56%) of brain regions, with an overall fairly marked accuracy level of 0.79 (0.83). Many genes are found to play a part in predicting both the incoming and outgoing connectivity (241 out of the 500 top selected genes, p-value<1e-5). Reassuringly, the genes previously known from the literature to be involved in axon guidance do carry significant information about regional brain connectivity. Surveying the genes known to be associated with the pathogenesis of several brain disorders, we find that those associated with schizophrenia, autism and attention deficit disorder are the most highly enriched in the connectivity-related genes identified here. Finally, we find that the profile of functional annotation groups that are associated with regional connectivity in the rodent is significantly correlated with the annotation profile of genes previously found to determine neural connectivity in C. elegans (Pearson correlation of 0.24, p<1e-6 for the outgoing connections and 0.27, p<1e-5 for the incoming). Overall, the association between connectivity and gene expression in a specific extant rodent species' brain is likely to be even stronger than found here, given the limitations of current data. C1 [Wolf, Lior; Goldberg, Chen; Manor, Nathan; Sharan, Roded; Ruppin, Eytan] Tel Aviv Univ, Blavatnik Sch Comp Sci, IL-69978 Tel Aviv, Israel. [Ruppin, Eytan] Tel Aviv Univ, Sch Med, IL-69978 Tel Aviv, Israel. RP Wolf, L (reprint author), Tel Aviv Univ, Blavatnik Sch Comp Sci, IL-69978 Tel Aviv, Israel. EM wolf@cs.tau.ac.il; ruppin@post.tau.ac.il FU Israel Science Foundation FX RS and ER thank the Israel Science Foundation (http://www.isf.org.il/) for support from the Bikura research grants. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. 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SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE microdeletion; distal 16p11.2; obesity; autism; developmental delay; epilepsy ID URINARY-TRACT CAKUT; CONGENITAL-ANOMALIES; MENTAL-RETARDATION; DEVELOPMENTAL DELAY; CHROMOSOME 16P11.2; AUTISM; OBESITY; GENES; INDIVIDUALS; PHENOTYPE AB One of the recently recognized microdeletion syndromes is the 16p11.2 deletion syndrome (593 kb; similar to 29.5Mb to similar to 30.1 Mb), associated with developmental delay, autism spectrum disorder, epilepsy, and obesity. Less frequently reported is a smaller 220 kb deletion, adjacent and distal to this 16p11.2 deletion, which has been referred to as the atypical 16p11.2 deletion (220 kb; similar to 28.74Mb to similar to 28.95 Mb). 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TI Deletion of the Immunoglobulin Domain of IL1RAPL1 Results in Nonsyndromic X-Linked Intellectual Disability Associated With Behavioral Problems and Mild Dysmorphism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE IL1RAPL1; non-syndromic XLID; deletion; behavior problems ID IDIOPATHIC MENTAL-RETARDATION; ACCESSORY PROTEIN-LIKE; ADRENAL HYPOPLASIA; GENE; FAMILY; CHROMOSOME; INACTIVATION; MUTATIONS; INVERSION; AUTISM AB X-Linked intellectual disability accounts for a significant fraction of males with cognitive impairment. Many of these males present with a non-syndromic phenotype and presently mutations in 17 X-linked genes are associated with these patients. Mutations in IL1RAPL1 have been found in multiple families with non-syndromic X-linked intellectual disability. All of the published mutations predict loss of function of the protein. We have identified an additional two families with deletions of a portion of the gene that give rise to cognitive impairment, as well as some behavioral problems and mild dysmorphism. Our clinical findings better delineate the phenotypic spectrum associated with IL1RAPL1 mutations. (C) 2011 Wiley-Liss, Inc. C1 [Franek, Karl J.; Butler, Julia; Simensen, Richard; Friez, Michael J.; Bartel, Frank; Moss, Tonya; DuPont, Barbara; Skinner, Cindy; Stevenson, Roger E.; Schwartz, Charles E.] Greenwood Genet Ctr, JC Self Res Inst Human Genet, Ctr Mol Studies, Greenwood, SC 29646 USA. [Johnson, John; Berry, Katherine] Shodair Childrens Hosp, Dept Med Genet, Helena, MT USA. [Bauman, Margaret] Harvard Univ, Massachusetts Gen Hosp, Boston, MA 02115 USA. RP Schwartz, CE (reprint author), Greenwood Genet Ctr, JC Self Res Inst Human Genet, Ctr Mol Studies, 113 Gregor Mendel Circle, Greenwood, SC 29646 USA. EM ceschwartz@ggc.org FU NICHD [R01HD26208]; South Carolina Department of Disabilities and Special Needs (SCDDSN) FX We thank the members of the families for their participation in this study. This work was supported by a NICHD grant (R01HD26208) to C.E.S. and in part by a grant from the South Carolina Department of Disabilities and Special Needs (SCDDSN). This article is dedicated to the memory of Ethan Francis Schwartz 1996-1998. 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The adult carriers are phenotypicaly normal and fertile; the boy shows macrocephaly, psychomotor retardation, and atypical autism. The FISH on cultured lymphocytes confirmed that the redundant Yq heterochromatin was attached to the 4p-subtelomeric region maintained on the der(4). Sperm FISH analysis performed in a normospermic der(4) carrier showed a significant distortion of the expected 1:1 ratio of the X-and Y-bearing spermatozoa in favor of the X chromosome and significant lack of Y, der(4) spermatozoa. The overall lack of Y spermatozoa was not balanced even by a relative excess of Y, 4 sperm. The analysis of X, Y, 7, 8, 18, and 21 sperm disomy and diploidy did not indicate any inter-chromosomal effect. The chromosome 4 disomy was significantly increased but still very low to be of considerable reproductive significance. The neurodevelomental phenotype of the boy was probably caused by a gene mutation. 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We used the frameworks of the International Classification of Functioning, Disability and Health (ICF) and Positive Youth Development (PYD) to explore occupational therapy research progress toward the goals of the Centennial Vision. We organized 46 research articles by research type and classified them within these two frameworks. Most reviewed published research investigated variables representing constructs falling within the ICF domains of Body Functioning and Activity. The effect of occupational therapy interventions on PYD resided primarily in building competence. To meet the tenets of the Centennial Vision, occupational therapists must document changes in children's engagement in everyday life situations and build the evidence of occupational therapist's efficacy in facilitating participation. C1 [Bendixen, Roxanna M.; Kreider, Consuelo M.] Univ Florida, Dept Occupat Therapy, Gainesville, FL 32610 USA. 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PD MAY PY 2011 VL 73 IS 5 BP 485 EP 497 PG 13 WC Literature SC Literature GA 764DE UT WOS:000290607800001 ER PT J AU McLennan, Y Polussa, J Tassone, F Hagerman, R AF McLennan, Yingratana Polussa, Jonathan Tassone, Flora Hagerman, Randi TI Fragile X Syndrome SO CURRENT GENOMICS LA English DT Article DE Fragile X; trinucleotide repeat; Prader-Willi phenotype; obesity; mGluR antagonists ID MENTAL-RETARDATION PROTEIN; PRADER-WILLI-SYNDROME; KNOCKOUT MICE; MOUSE MODEL; MESSENGER-RNA; MITOCHONDRIAL DYSFUNCTION; TREMOR/ATAXIA SYNDROME; OXIDATIVE STRESS; OUTCOME MEASURES; DENDRITIC SPINE AB Recent data from a national survey highlighted a significant difference in obesity rates in young fragile X males (31%) compared to age matched controls (18%). Fragile X syndrome (FXS) is the most common cause of intellectual disability in males and the most common single gene cause of autism. This X-linked disorder is caused by an expansion of a trinucleotide CGG repeat (> 200) on the promotor region of the fragile X mental retardation 1 gene (FMR1). As a result, the promotor region often becomes methylated which leads to a deficiency or absence of the FMR1 protein (FMRP). Common characteristics of FXS include mild to severe cognitive impairments in males but less severe cognitive impairment in females. Physical features of FXS include an elongated face, prominent ears, and post-pubertal macroorchidism. Severe obesity in full mutation males is often associated with the Prader-Willi phenotype (PWP) which includes hyperphagia, lack of satiation after meals, and hypogonadism or delayed puberty; however, there is no deletion at 15q11-q13 nor uniparental maternal disomy. Herein, we discuss the molecular mechanisms leading to FXS and the Prader-Willi phenotype with an emphasis on mouse FMR1 knockout studies that have shown the reversal of weight increase through mGluR antagonists. Finally, we review the current medications used in treatment of FXS including the atypical antipsychotics that can lead to weight gain and the research regarding the use of targeted treatments in FXS that will hopefully have a significantly beneficial effect on cognition and behavior without weight gain. C1 [Hagerman, Randi] Univ Calif Davis Hlth Syst, MIND Inst, UCHSC, Sacramento, CA 95817 USA. [Tassone, Flora] Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA. [Hagerman, Randi] Univ Calif Davis Hlth Syst, Dept Pediat, Sacramento, CA 95817 USA. RP Hagerman, R (reprint author), Univ Calif Davis Hlth Syst, MIND Inst, UCHSC, 2825 50th St, Sacramento, CA 95817 USA. EM Randi.hagerman@ucdmc.ucdavis.edu FU National Institute of Health [HD036071, HD02274]; Neurotherapeutic Research Institute (NTRI) [DE019583, NIA RL1 AG032119, NINDS RL1 NS062412, NIDA TL1 DA024854, DA024854]; National Institute on Aging [AG032119, AG032115]; National Center for Research Resources [UL1 RR024146]; Health and Human Services Administration of Developmental Disabilities [90DD05969] FX This work was supported by National Institute of Health grants HD036071 and HD02274; Neurotherapeutic Research Institute (NTRI) grants DE019583, NIA RL1 AG032119, NINDS RL1 NS062412, NIDA TL1 DA024854, and DA024854; National Institute on Aging grants AG032119 and AG032115; National Center for Research Resources UL1 RR024146; support from the Health and Human Services Administration of Developmental Disabilities grant 90DD05969. 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Subjects: Forty infants (16 males) were followed between the ages of 2 days and 21 months for durations ranging from 4 to 21 months (2616 measurements). Study design: Longitudinal anthropometric measurements were assessed weekly (n = 12), semi-weekly (n = 24) and daily (n = 4) during home visits. Individual head circumference growth was investigated for the presence of saltatory patterns. Coincident analysis tested the null hypothesis that head growth was randomly coupled to length growth. Results: Head circumference growth during infancy is saltatory (p<0.05), characterized by median increments of 0.20 cm (95% confidence interval, 0.10-0.30 cm) in 24-h, separated by intervals of no growth ranging from 1 to 21 days. Daily assessments identified that head growth saltations were coupled to length growth saltations within a median time frame of 2 days (interquartile 0-4, range 1-8 days). Assessed at semi-weekly and weekly intervals, an average 82% (SD 0.13) of head growth saltations was non-randomly concordant with length growth (p <= 0.006). Conclusions: Normal infant head circumference grows by intermittent, episodic saltations that are temporally coupled to growth in total body length by a process of integrated physiology that remains to be described. (C) 2011 Elsevier Ireland Ltd. All rights reserved. C1 [Lampl, Michelle] Emory Univ, Dept Anthropol, Atlanta, GA 30322 USA. [Johnson, Michael L.] Univ Virginia Hlth Syst, Dept Pharmacol, Charlottesville, VA 22908 USA. [Johnson, Michael L.] Univ Virginia Hlth Syst, Dept Med, Charlottesville, VA 22908 USA. RP Lampl, M (reprint author), Emory Univ, Dept Anthropol, 1557 Dickey Dr, Atlanta, GA 30322 USA. EM mlampl@emory.edu RI Lampl, Michelle/B-1619-2013 FU Wenner-Gren Foundation; Developmental Psychobiology Research Group; Grant Foundation; NIH [R01 RR019991] FX Data collection was supported by the Wenner-Gren Foundation, the Developmental Psychobiology Research Group and the Grant Foundation (ML). The analytic work was supported in part by NIH grant R01 RR019991 (MLJ). No study sponsors participated in any manner in the preparation of the manuscript. 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PD MAY PY 2011 VL 87 IS 5 BP 361 EP 368 DI 10.1016/j.earlhumdev.2011.02.001 PG 8 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA 767BX UT WOS:000290831400007 PM 21419585 ER PT J AU Michelson, M Eden, A Vinkler, C Leshinsky-Silver, E Kremer, U Lerman-Sagie, T Lev, D AF Michelson, Marina Eden, Avi Vinkler, Chana Leshinsky-Silver, Esther Kremer, Uri Lerman-Sagie, Tally Lev, Dorit TI Familial partial trisomy 15q11-13 presenting as intractable epilepsy in the child and schizophrenia in the mother SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY LA English DT Article DE 15q11-q13; Epilepsy; Schizophrenia; Supernumerary marker chromosome ID GENOTYPE-PHENOTYPE CORRELATION; DUP(15) SUPERNUMERARY MARKER; INV DUP(15); DUPLICATION; CHROMOSOME; TRIPLICATIONS; MECHANISM; 15Q13.3; AUTISM AB Various rearrangements involve the proximal long arm of chromosome 15, including deletions, duplications, translocations, inversions and supernumerary marker chromosome of an inverted duplication. The large marker 15, that contains the Prader-Willi syndrome (PWS)/Angelman syndrome (AS) chromosome region, is usually associated with an abnormal phenotype of moderate to severe mental retardation, seizures, poor motor coordination, early-onset central hypotonia, autism and autistic-like behavior, schizophrenia and mild dysmorphic features. We report a ten year-old girl with normal intelligence prior to the onset of seizures, who developed severe intractable epilepsy at the age of seven years. Family history was significant for a mother with recurrent episodes of acute psychosis. The patient's and mother's karyotype revealed 47,XX+m. Array comparative genomic hybridization (A-CGH) identified a gain of 13 BAC clones from 15q11.2 through 15q13.1, which was then confirmed by FISH to be part of the marker chromosome. This duplicated region contains the SNRPN/UBE3A locus. This case demonstrates that a duplication of 15q11-13 can present differently in the same family either as intractable epilepsy or as a psychiatric illness and that intelligence can be preserved. We suggest that CGH microarray should be performed in cases with intractable epilepsy or schizophrenia, with or without mental retardation. (C) 2010 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved. C1 [Michelson, Marina; Vinkler, Chana; Lev, Dorit] Wolfson Med Ctr, Inst Med Genet, IL-58100 Holon, Israel. [Michelson, Marina; Eden, Avi; Vinkler, Chana; Leshinsky-Silver, Esther; Lerman-Sagie, Tally; Lev, Dorit] Wolfson Med Ctr, Metab Neurogenet Clin, IL-58100 Holon, Israel. [Eden, Avi; Lerman-Sagie, Tally] Wolfson Med Ctr, Pediat Neurol Unit, IL-58100 Holon, Israel. [Leshinsky-Silver, Esther] Wolfson Med Ctr, Mol Genet Lab, IL-58100 Holon, Israel. 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J. Paediatr. Neurol. PD MAY PY 2011 VL 15 IS 3 BP 230 EP 233 DI 10.1016/j.ejpn.2010.11.001 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 767GA UT WOS:000290842100007 PM 21145272 ER PT J AU Delbroek, H Steyaert, J Legius, E AF Delbroek, Hanne Steyaert, Jean Legius, Eric TI An 8.9 year old girl with autism and Gorlin syndrome SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY LA English DT Article DE Gorlin syndrome; Nevoid basal cell carcinoma syndrome; PTCH1 gene; Autism ID BASAL-CELL CARCINOMA; SONIC-HEDGEHOG; HEAD CIRCUMFERENCE; PATHWAY; PROLIFERATION; TUMORIGENESIS; DISORDERS; GROWTH AB We present an 8.9 year old girl diagnosed with autism and macrocrania. Because of macrocrania, hypertelorism and epidermal punctiform lesions in the palm of the hand, Gorlin syndrome was clinically suspected and molecularly confirmed by finding a deletion of 22 base pairs in the PTCH1 gene. The possibility of an association between autism and Gorlin syndrome is discussed. (C) 2010 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved. C1 [Legius, Eric] Catholic Univ Louvain, Dept Human Genet, B-3000 Louvain, Belgium. [Delbroek, Hanne; Steyaert, Jean] Catholic Univ Louvain, Dept Child & Adolescent Psychiat, B-3000 Louvain, Belgium. [Steyaert, Jean] Univ Maastricht, Dept Clin Genet, Maastricht, Netherlands. RP Legius, E (reprint author), Catholic Univ Louvain, Dept Human Genet, Herestr 49, B-3000 Louvain, Belgium. EM Eric.Legius@uzleuven.be RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 FU Fonds voor Wetenschappelijk Onderzoek Vlaanderen FX We thank the Fonds voor Wetenschappelijk Onderzoek Vlaanderen for financial support to EL (G.0469.10N). 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J. Paediatr. Neurol. PD MAY PY 2011 VL 15 IS 3 BP 268 EP 270 DI 10.1016/j.ejpn.2010.12.001 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 767GA UT WOS:000290842100014 PM 21190878 ER PT J AU Lehnhardt, FG Gawronski, A Volpert, K Schilbach, L Tepest, R Huff, W Vogeley, K AF Lehnhardt, F. -G. Gawronski, A. Volpert, K. Schilbach, L. Tepest, R. Huff, W. Vogeley, K. TI Autism Spectrum Disorders in Adulthood: Clinical and Neuropsychological Findings of Aspergers Syndrome Diagnosed Late in Life SO FORTSCHRITTE DER NEUROLOGIE PSYCHIATRIE LA German DT Article DE Asperger syndrome; high-functioning autism; neuropsychological profile; diagnosis late in life; autism spectrum quotient; theory of mind ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; EXECUTIVE FUNCTIONS; CENTRAL COHERENCE; SOCIAL COGNITION; REVISED VERSION; QUOTIENT AQ; MIND; CHILDREN; DEPRESSION AB Introduction: High-functioning autism (HFA) and Aspergers syndrome (AS) are autism spectrum disorders (ASD) characterised by disturbances in social interaction, both verbal and non-verbal communication and repetitive and/or restrictive behaviour since early childhood. Symptoms appear generally during early childhood and adolescence. The increasing need to clarify diagnostic queries in advanced age led to the constitution of specialised outpatient clinics for adults involving a growing amount of HFA/AS subjects diagnosed late in life. However, thus far neuropsychological data about this group are scarce. Methods: We present a subgroup of 39 patients with HFA/AS (mean age at diagnosis 31.1 +/- 8.9 years) who were consecutively diagnosed at the autism outpatient clinic at the Department of Psychiatry at the University Hospital Cologne. Autistic symptoms (autism spectrum quotient; AQ), depressive symptoms (Beck depression inventory; BDI), general intelligence (HAWIE-R), social cognition ("theory of mind", ToM) and executive functioning (COWAT) were systematically studied in comparison to a control group matched for age, education, gender and intelligence (n = 39). Results: HFA/AS subjects presented higher AQ scores (40.4 +/- 5.2) as opposed to the healthy controls (13.5 +/- 4.8). Neuropsychologically, patients showed deficits in social cognition, executive functions and in subtests of HAWIE-R related to verbal comprehension and perceptual organisation as opposed to the healthy control group. Discussion: The diagnosis of autistic disorders in adulthood basically relies on the clinical assessment of autistic core symptoms which were corroborated by high AQ values. The self-rating instrument AQ was found to be highly discriminative between the HFA/AS group and the healthy control group. The neuropsychological profile of adult HFA/AS patients diagnosed late in life is compatible with that of previously investigated HFA/AS populations. These findings show that such basic autism-associated deficits persist until adulthood, although patients are able to learn social rules. C1 [Lehnhardt, F. -G.; Gawronski, A.; Volpert, K.; Schilbach, L.; Tepest, R.; Huff, W.; Vogeley, K.] Uniklin Koln, Klin & Poliklin Psychiat & Psychotherapie, D-50937 Cologne, Germany. 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Psychiatr. PD MAY PY 2011 VL 79 IS 5 BP 290 EP 297 DI 10.1055/s-0031-1273233 PG 8 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 767TP UT WOS:000290880000005 PM 21544761 ER PT J AU Trasande, L Liu, YH AF Trasande, Leonardo Liu, Yinghua TI Reducing The Staggering Costs Of Environmental Disease In Children, Estimated At $76.6 Billion In 2008 SO HEALTH AFFAIRS LA English DT Article ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT-HYPERACTIVITY DISORDER; NATIONAL CHILDRENS; UNITED-STATES; CHILDHOOD OBESITY; AMERICAN CHILDREN; DEVELOPING BRAIN; PUBLIC-HEALTH; AIR-POLLUTION; US CHILDREN AB A 2002 analysis documented $54.9 billion in annual costs of environmentally mediated diseases in US children. However, few important changes in federal policy have been implemented to prevent exposures to toxic chemicals. We therefore updated and expanded the previous analysis and found that the costs of lead poisoning, prenatal methylmercury exposure, childhood cancer, asthma, intellectual disability, autism, and attention deficit hyperactivity disorder were $76.6 billion in 2008. To prevent further increases in these costs, efforts are needed to institute premarket testing of new chemicals; conduct toxicity testing on chemicals already in use; reduce lead-based paint hazards; and curb mercury emissions from coal-fired power plants. C1 [Trasande, Leonardo] Mt Sinai Sch Med, New York, NY USA. [Liu, Yinghua] Natl Childrens Study New York No New Jersey Ctr, New York, NY USA. RP Trasande, L (reprint author), Mt Sinai Sch Med, New York, NY USA. 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PD MAY PY 2011 VL 30 IS 5 BP 863 EP 870 DI 10.1377/hlthaff.2010.1239 PG 8 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 761WD UT WOS:000290430800009 PM 21543421 ER PT J AU Hart, JE Whalon, KJ AF Hart, Juliet E. Whalon, Kelly J. TI Creating Social Opportunities for Students With Autism Spectrum Disorder in Inclusive Settings SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Article DE autism spectrum disorder; social/behavioral strategies; inclusion ID HIGH-FUNCTIONING CHILDREN; SCRIPT-FADING PROCEDURE; MODELING INTERVENTIONS; SPECIAL-EDUCATION; METAANALYSIS; INDIVIDUALS; SKILLS AB Increasing numbers of students with autism spectrum disorder (ASD) are being included in general education settings. Learners with ASD can benefit from the general education curriculum, with some achieving at a high academic level. Yet, social communication and behavioral difficulties can present challenges to their successful inclusion. Instructional priorities for children with ASD include social communication interventions that teach children how to spontaneously initiate functional communication in academic and social contexts. This article describes evidence-based strategies that will help educators create opportunities for social interaction for students with ASD in the context of naturally occurring classroom activities and routines. C1 [Hart, Juliet E.] Arizona State Univ, Mary Lou Fulton Teachers Coll, Phoenix, AZ 85069 USA. [Whalon, Kelly J.] Coll William & Mary, Williamsburg, VA USA. RP Hart, JE (reprint author), Arizona State Univ, Mary Lou Fulton Teachers Coll, POB 37100,Mail Code 3151, Phoenix, AZ 85069 USA. EM Juliet.Hart@asu.edu CR [Anonymous], 1994, QUICK REF DIAGN CRIT Bauminger N, 2008, J AUTISM DEV DISORD, V38, P1211, DOI 10.1007/s10803-007-0501-2 Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BELLINI S, 2010, BEYOND BEHAV, V19, P26 Bellini S, 2007, EXCEPT CHILDREN, V73, P264 Bellini S, 2007, REM SPEC EDUC, V28, P153, DOI 10.1177/07419325070280030401 Cook BG, 2008, INTERV SCH CLIN, V44, P69, DOI 10.1177/1053451208321452 Delano ME, 2007, REM SPEC EDUC, V28, P33, DOI 10.1177/07419325070280010401 DUNLAP G, 1999, AUTISM AUTISM SPECTR Eaves LC, 1997, J DEV PHYS DISABIL, V9, P277, DOI 10.1023/A:1024944226971 Freedeen RM, 2006, PIVOTAL RESPONSE TRE, P165 Gersten R, 2005, EXCEPT CHILDREN, V71, P149 GREENWOOD CR, 1997, WE CAN CLASSWIDE PEE Harrower JK, 2001, BEHAV MODIF, V25, P762, DOI 10.1177/0145445501255006 Hart JE, 2008, INTERV SCH CLIN, V44, P116, DOI 10.1177/1053451207310346 HORNER RH, 2005, EXCEPT CHILDREN, V71, P161 Johnson D., 1994, COOPERATIVE LEARNING Klin A., 2005, HDB AUTISM PERVASIVE, P88 KOEGEL RL, 1995, TEACHING CHILDREN AU, P66 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 Leekam S, 2007, CHILDRENS COMPREHENS, P104 Loveland K. 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Seltzer, Marsha Mailick Taylor, Julie Lounds TI Change in Maternal Criticism and Behavior Problems in Adolescents and Adults With Autism Across a 7-Year Period SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Article DE parenting; autism; expressed emotion; criticism; behavior problems ID CHILD-RELATIONSHIP QUALITY; EXPRESSED EMOTION; YOUNG-ADULTS; ANTISOCIAL-BEHAVIOR; SPECTRUM DISORDERS; BIPOLAR DISORDER; PARENTING STRESS; FAMILIES; SCHIZOPHRENIA; SYMPTOMS AB In a previous study, high levels of maternal criticism predicted increased behavior problems in adolescents and adults with autism spectrum disorders (ASD) over an 18-month period (Greenberg, Seltzer, Hong, & Orsmond, 2006). The current investigation followed these families over a period of 7 years to examine the longitudinal course of criticism and behavior problems, to assess the association between their trajectories, and to determine the degree to which change in each of these factors predicted levels of criticism and behavior problems at the end of the study period. A sample of 118 mothers coresiding with their adolescent and adult children with ASD provided open-ended narratives about their children and reported on the children's behavior problems at 4 waves. Maternal criticism was derived from expressed emotion ratings of the narratives. Criticism exhibited low but significant stability over the 7-year period, and behavior problems exhibited high stability. Through latent growth curve modeling, (a) criticism was found to have increased over time, but only for the group of families in which the sons or daughters transitioned from high school services during the study period; (b) individual changes in criticism and behavior problems were positively correlated over the 7-year period; and (c) changes in criticism predicted levels of behavior problems at the conclusion of the study. Changes in behavior problems were not predictive of end levels of criticism. Implications for intervention and prevention efforts are discussed. C1 [Baker, Jason K.; Smith, Leann E.; Greenberg, Jan S.; Seltzer, Marsha Mailick] Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. [Taylor, Julie Lounds] Vanderbilt Univ, Kennedy Ctr, Nashville, TN 37235 USA. RP Baker, JK (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave,Room 533, Madison, WI 53705 USA. 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TI Autism spectrum disorders SO NERVENARZT LA German DT Editorial Material ID CIRCUITRY; CHILDREN; HUMANS C1 [Meyer-Lindenberg, A.] Zent Inst Seel Gesundheit, Klin Psychiat & Psychotherapie, D-68159 Mannheim, Germany. RP Meyer-Lindenberg, A (reprint author), Zent Inst Seel Gesundheit, Klin Psychiat & Psychotherapie J5, D-68159 Mannheim, Germany. 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M. Poustka, L. Chiocchetti, A. TI Genetics and animal modeling of autism spectrum disorders SO NERVENARZT LA German DT Article DE Autism spectrum disorders; Genetics; Copy number variation; Synaptogenesis; Animal model ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOME-WIDE LINKAGE; SCAN AB Autism spectrum disorders (ASD) are pervasive developmental disorders with a complex phenotype in respect to communication, verbal development, and social behavior. Manifold molecular genetic analyses point towards a multifactorial genetic predisposition. For the identification of central key mechanisms large consortia have performed linkage analysis, genome-wide association, and copy number variation (CNV) studies, which led to the characterization of risk factors for ASD like CNV and single nucleotide polymorphisms but also single rare mutations. 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Koehne, S. TI Brain imaging in autism spectrum disorders SO NERVENARZT LA German DT Article DE Autism; Functional imaging; Connectivity; Theory of mind; Executive functions ID HIGH-FUNCTIONING AUTISM; SENTENCE COMPREHENSION; COGNITIVE NEUROSCIENCE; EXECUTIVE FUNCTION; FIXATION PATTERNS; ASPERGER-SYNDROME; WHITE-MATTER; UNDERCONNECTIVITY; CONNECTIVITY; FMRI AB In the past two decades, an increasing number of functional and structural brain imaging studies has provided insights into the neurobiological basis of autism spectrum disorders (ASD). This article summarizes pertinent functional brain imaging studies addressing the neuronal underpinnings of ASD symptomatology (impairments in social interaction and communication, repetitive and restrictive behavior) and associated neuropsychological deficits (theory of mind, executive functions, central coherence), complemented by relevant structural imaging findings. 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Poustka, L. Holtmann, M. TI Autism and ADHD across the life span Differential diagnoses or comorbidity? SO NERVENARZT LA German DT Article DE Autism; Attention deficit hyperactivity disorder; Comorbidity; Aetiology; Stimulants ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; GENOME-WIDE ASSOCIATION; SPECTRUM DISORDERS; SOCIAL COMMUNICATION; GENETIC INFLUENCES; FAMILIAL TRAIT; TWIN SAMPLE; CHILDREN AB Exclusion criteria of the DSM-IV-TR and ICD-10 do prevent dual diagnoses of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASD). However, inattention, impulsivity and hyperactivity are amongst the most frequent associated symptoms of ASD. Psychopathological, neuropsychological, brain imaging and genetic studies suggest possible pathophysiological links between ASD and ADHD. 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Banaschewski, T. Poustka, F. TI Psychopharmacology of autism spectrum disorders SO NERVENARZT LA German DT Article DE Autism; Comorbidity; Aggression; Psychopharmacology; Atypical antipsychotic agents ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED CROSSOVER; CONTROLLED-RELEASE MELATONIN; DOUBLE-BLIND; CONTROLLED-TRIAL; PHARMACOLOGICAL-TREATMENT; REPETITIVE BEHAVIORS; CHILDREN; RISPERIDONE; OXYTOCIN AB Autism spectrum disorders (ASD) are persistent, heterogeneous conditions that display many comorbid problems. Especially maladaptive behaviours like increased irritability, aggression, impulsivity and self-injurious behaviours are perceived as enormously stressful and can interfere with interventions targeting social and communication deficits. Medication treatments focussing on troubling comorbid problems in ASD can be fundamentally ameliorative, although core features of the disorder itself cannot be sufficiently treated. 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TI Psychobiosocial interventions for autism SO NERVENARZT LA German DT Article DE Psychiatry; Autism spectrum disorders; Neurodevelopmental disorder; Behavior therapy; Neuropsychotherapy ID FACIAL AFFECT; SPECTRUM DISORDERS; CHILDREN; RECOGNITION; PREVALENCE; PREDICTORS; SAMPLE; ADULTS AB A multitude of interventions is offered for the treatment of autism spectrum disorders (ASD). However, only few have demonstrated scientific evidence, and even the evaluated methods need further examination of their mechanisms and scope. This article provides a brief summary of the premises and principles of successful psychobiosocial ASD intervention. ABA, TEACCH, PECS, social skills and cognitive training are described as examples for established approaches to ASD. Training of mu-suppression using neurofeedback and reanimation of the fusiform gyrus and amygdala using computer-aided facial affect recognition training are introduced as neurobiologically based ASD interventions. 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Michel, T. M. TI Genetic and brain structure anomalies in autism spectrum disorders. Towards an understanding of the aetiopathogenesis SO NERVENARZT LA German DT Review DE Autism spectrum disorders; Genes; MRI; Brain structure ID GROWTH FACTOR/SCATTER FACTOR; QUANTITATIVE TRAIT LOCUS; RECEPTOR SUBUNIT GENES; ANGELMAN-SYNDROME; REELIN GENE; LINKAGE-DISEQUILIBRIUM; HEAD CIRCUMFERENCE; INFANTILE-AUTISM; POSTERIOR-FOSSA; YOUNG-CHILDREN AB Autism spectrum disorders (ASD) are pervasive development disorders with high heritability and an as yet unclear aetiology. So far molecular genetic research was able to identify several candidate genes for the disorder which are functionally linked to neurotransmission and neuronal migration, cortical organisation and synaptic plasticity. MRI studies repeatedly showed a higher total brain volume for ASD patients. The volume increase was most pronounced for the frontal and the temporal lobes and peaked in early childhood. 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Lichtblau, A. Peters, J. Biscaldi-Schaefer, M. Ebert, D. van Elst, L. T. TI Psychotherapy of Asperger syndrome in adults SO NERVENARZT LA German DT Review DE Asperger syndrome; Social skills; Group therapy; Adults; Freiburger Aspergerspezifische Therapie fur Erwachsene ID SOCIAL-SKILLS INTERVENTIONS; HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; MIND; CLASSIFICATION; INDIVIDUALS; CHILDREN AB There is an increase in awareness in professionals that the Asperger syndrome (AS) in adulthood is associated with specific problems and burdens which may well differ from those in childhood and adolescence. The core symptoms of AS generally persist into adulthood, however in contrast to childhood and adolescence there is no specific support system for adults in Germany. Also the environment of the afflicted patient changes thus producing different challenges and problems. In addition a subgroup of patients with high functioning AS primarily presents in adulthood generally due to secondary psychosocial problems, depression or anxiety. Difficulties in social interaction, problems with modified daily routines and unforeseen situations cause severe frustration for the majority of the patients. While several therapy programs have been developed and implemented for children and adolescents, for adults there are none. Also there is a lack of comprehensive concepts addressing the specific needs of adult patients with AS. From an economic perspective this is particularly unfortunate since affected people often have good or excellent partial abilities and might be very valuable employees. In this article existing therapeutic concepts for AS are summarized and a newly designed group therapy program for adult patients with Asperger syndrome in Freiburg is introduced (Freiburg Asperger-spezifische Therapie fur Erwachsene, FASTER) which specifically addresses the needs and problems of adult patients with AS. C1 [Fangmeier, T.; Lichtblau, A.; Peters, J.; Ebert, D.; van Elst, L. T.] Univ Freiburg Klinikum, Abt Psychiat & Psychotherapie, D-79104 Freiburg, Germany. [Fangmeier, T.] Inst Informat & Gesell, Abt Kognit Wissensch, Freiburg, Germany. [Biscaldi-Schaefer, M.] Univ Freiburg Klinikum, Abt Psychiat & Psychotherapie Kindes & Jugendalte, D-79104 Freiburg, Germany. RP Fangmeier, T (reprint author), Univ Freiburg Klinikum, Abt Psychiat & Psychotherapie, Hauptstr 5, D-79104 Freiburg, Germany. 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Pourre, F. Maffre, T. Raynaud, J-P TI Social skills training groups for children and adolescents with Asperger syndrome: A review SO ARCHIVES DE PEDIATRIE LA French DT Review ID AUTISM SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; INTERVENTION; PROGRAM; INDIVIDUALS; CHILDHOOD; MODEL AB Background. First described in 1944 by Hans Asperger, Asperger syndrome (AS) is now considered in international diagnostic classifications as one of the pervasive developmental disorders (PDD) or autism spectrum disorders (ASD). The main symptoms of AS are severe impairment in social interaction and communication, and restricted interests, without significant delay in cognitive and language development. Its prevalence is not clearly established but might be around 0.26 per 1000. Symptoms of high-functioning autism (H FA), which is not an official diagnostic category, are quite similar. Children and adolescents with AS or HFA mostly have a social skills deficit, in connection with a lack of understanding concerning the rules governing social interactions. This deficit often leads to social isolation and peer rejection, which can alter their quality of life. Their lack of social skills can also have effects on success at school or work, integration among peers and mental health. According to recent guidelines of the French national authority for health (Haute autorite de sante, HAS) about the special needs of persons with PDD, professionals have to develop evidence-based interventions, emphasizing social interactions and participation, as described by the international classification of functioning, disability and health (ICF): social and professional participation as well as participation in leisure activities, clubs and societies, etc. Objectives. To explore the studies that give evidence of the value of these social skills training groups, to review the methods and programs worked out in these groups, and to highlight the best general operating principles to be adopted and combined. Methods. Systematic searches of electronic databases, journals, and reference lists identified 12 studies published since 1984, involving social competence group interventions, led by psychotherapists who were trained in cognitive behavioral therapies (CBT), for children and adolescents from 6 to 18 years old with a diagnosis of AS or HFA. Results. According to these 12 studies, these interventions are useful and significantly effective. Adaptation of their contents and educational means to how children and adolescents with AS function is necessary to facilitate learning and decrease anxiety. Concerning the groups' setting, most of these studies insist on the value of working with a small number of participants and creating a friendly, predictable and structured environment (even the progress of the sessions itself has to be structured). The programs' contents should ally didactic teaching and training exercises, which should be diverse and adapted to the objectives. The techniques usually applied in CBT (role plays, modeling, problem-solving strategies, etc.), must be completed with strategies known to be appropriate for children and adolescents with ASD, such as social scenarios. Conclusions. Although new studies are necessary to assess the generalization and long-term efficacy of such approaches, this review confirms the advantages of the main methods of social skills training groups for children and adolescents with AS. It opens up perspectives to developing new programs of social skills training groups, integrating various approaches, dimensions and objectives, working on a long-term basis. (C) 2011 Elsevier Masson SAS. All rights reserved. C1 [Andanson, J.; Pourre, F.; Maffre, T.; Raynaud, J-P] CHU Toulouse, Hop La Grave, Serv Univ Psychiat Enfant & Adolescent, TSA 60033, F-31059 Toulouse 9, France. [Maffre, T.] Hop La Grave, Ctr Ressources Autisme Midi Pyrenees, TSA 60033, F-31059 Toulouse 9, France. [Raynaud, J-P] Univ Toulouse 3, INSERM, U1027, F-31062 Toulouse, France. RP Raynaud, JP (reprint author), CHU Toulouse, Hop La Grave, Serv Univ Psychiat Enfant & Adolescent, TSA 60033, F-31059 Toulouse 9, France. EM raynaud.jph@chu-toulouse.fr CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Attwood T., 2008, COMPLETE GUIDE ASPER Baker J. 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Pediatr. PD MAY PY 2011 VL 18 IS 5 BP 589 EP 596 DI 10.1016/j.arcped.2011.02.019 PG 8 WC Pediatrics SC Pediatrics GA 764BU UT WOS:000290604200021 PM 21458972 ER PT J AU Vivanti, G McCormick, C Young, GS Abucayan, F Hatt, N Nadig, A Ozonoff, S Rogers, SJ AF Vivanti, Giacomo McCormick, Carolyn Young, Gregory S. Abucayan, Floridette Hatt, Naomi Nadig, Aparna Ozonoff, Sally Rogers, Sally J. TI Intact and Impaired Mechanisms of Action Understanding in Autism SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article DE action understanding; autism; emotions; theory of mind; social cognition; eye tracking ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; SOCIAL COGNITION; JOINT ATTENTION; YOUNG-CHILDREN; EYE CONTACT; EMOTION RECOGNITION; GOAL ATTRIBUTION; DIRECTED ACTION; MENTAL STATES AB Typically developing children understand and predict others' behavior by extracting and processing relevant information such as the logic of their actions within the situational constraints and the intentions conveyed by their gaze direction and emotional expressions. Children with autism have difficulties understanding and predicting others' actions. With the use of eye tracking and behavioral measures, we investigated action understanding mechanisms used by 18 children with autism and a well-matched group of 18 typically developing children. Results showed that children with autism (a) consider situational constraints in order to understand the logic of an agent's action and (b) show typical usage of the agent's emotional expressions to infer his or her intentions. We found (c) subtle atypicalities in the way children with autism respond to an agent's direct gaze and (d) marked impairments in their ability to attend to and interpret referential cues such as a head turn for understanding an agent's intentions. C1 [Vivanti, Giacomo] La Trobe Univ, Olga Tennison Autism Res Ctr, Sch Psychol Sci, Bundoora, Vic 3086, Australia. [McCormick, Carolyn; Young, Gregory S.; Abucayan, Floridette; Ozonoff, Sally; Rogers, Sally J.] Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. [Hatt, Naomi] Univ Calif Davis, Dept Psychol, Davis, CA 95616 USA. [Nadig, Aparna] McGill Univ, Sch Commun Sci & Disorders, Montreal, PQ, Canada. 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Psychol. PD MAY PY 2011 VL 47 IS 3 BP 841 EP 856 DI 10.1037/a0023105 PG 16 WC Psychology, Developmental SC Psychology GA 757KI UT WOS:000290083500019 PM 21401220 ER PT J AU Kramer, RSS King, JE Ward, R AF Kramer, Robin S. S. King, James E. Ward, Robert TI Identifying personality from the static, nonexpressive face in humans and chimpanzees: evidence of a shared system for signaling personality SO EVOLUTION AND HUMAN BEHAVIOR LA English DT Article DE Signaling; Faces; Personality; Chimpanzees ID PAN-TROGLODYTES; FACIAL CUES; BEHAVIOR; DIMENSIONS; DOMINANCE; AUTISM; IMAGES AB Many aspects of personality are honestly signaled on the human face, as shown by accurate identification of personality traits from static images of unknown faces with neutral expressions. Here, we examined the evolutionary history of this signal system. In four studies, we found that untrained human observers reliably discriminated characteristics related to extraversion solely from nonexpressive facial images of chimpanzees (Pan troglodytes). In chimpanzees, as in humans, there is therefore information in the static, nonexpressive face that signals aspects of an individual's personality. We suggest that this performance is best explained by shared personality structure and signaling in the two species. (C) 2011 Elsevier Inc. All rights reserved. C1 [Ward, Robert] Bangor Univ, Sch Psychol, Wolfson Ctr Clin & Cognit Neurosci, Bangor LL57 2AS, Gwynedd, Wales. [King, James E.] Univ Arizona, Tucson, AZ USA. RP Ward, R (reprint author), Bangor Univ, Sch Psychol, Wolfson Ctr Clin & Cognit Neurosci, Bangor LL57 2AS, Gwynedd, Wales. 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Highly penetrant microdeletions and microduplications of 16p11.2 contribute to the pathogenesis of autism spectrum disorder, but the extent to which these variants account for the total burden of idiopathic autism spectrum disorders has not been systematically investigated. Methods: A systematic literature review and meta-analysis were performed to determine the prevalence of these variants among individuals diagnosed with autism spectrum disorders. A planned subgroup analysis was conducted to assess prevalence differences between sporadic and familial autism spectrum disorder cases. Results: In the combined analysis of 3613 idiopathic autism spectrum disorder cases from seven studies, the meta-analytic prevalence of these microdeletions and microduplications was 0.76% (95% CI, 0.51-1.12%). When stratified by copy number variant-type, the prevalence of microdeletions was 0.50% (95% CI, 0.31-0.82%) and the prevalence of microduplications was 0.28% (95% CI, 0.14-0.56%). Sporadic autism spectrum disorder cases showed only a slightly higher prevalence than familial cases. Conclusion: The number needed to test to identify one such variant is 132 patients (95% CI, 89-198). Such information, especially as it pertains to diagnostic yield in genetic testing, should prove useful to clinicians considering chromosomal microarray analysis in subjects with autism spectrum disorders. Genet Med 2011: 13(5): 377-384. C1 [Walsh, Kyle M.; Bracken, Michael B.] Yale Univ, Ctr Perinatal Pediat & Environm Epidemiol, Sch Publ Hlth, New Haven, CT USA. RP Walsh, KM (reprint author), 1 Church St,6th Floor, New Haven, CT 06510 USA. 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Med. PD MAY PY 2011 VL 13 IS 5 BP 377 EP 384 DI 10.1097/GIM.0b013e3182076c0c PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 761XO UT WOS:000290435700002 PM 21289514 ER PT J AU Parellada, M AF Parellada, Mara TI Textbook of Autism Spectrum Disorders SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Book Review CR HOLLANDER E, 2011, TXB AUTISM SPECTRUM, DOI DOI 10.1176/APPI.AJP.2010.09091328 NR 1 TC 0 Z9 0 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 MAY PY 2011 VL 168 IS 5 BP 554 EP 555 DI 10.1176/appi.ajp.2011.11010046 PG 2 WC Psychiatry SC Psychiatry GA 757MG UT WOS:000290089000023 ER PT J AU Brugha, TS McManus, S Bankart, J Scott, F Purdon, S Smith, J Bebbington, P Jenkins, R Meltzer, H AF Brugha, Traolach S. McManus, Sally Bankart, John Scott, Fiona Purdon, Susan Smith, Jane Bebbington, Paul Jenkins, Rachel Meltzer, Howard TI Epidemiology of Autism Spectrum Disorders in Adults in the Community in England SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; QUOTIENT AQ; PREVALENCE; CHILDREN; SERVICE; UPDATE AB Context: To our knowledge, there is no published information on the epidemiology of autism spectrum disorders (ASDs) in adults. If the prevalence of autism is increasing, rates in older adults would be expected to be lower than rates among younger adults. Objective: To estimate the prevalence and characteristics of adults with ASD living in the community in England. Design: A stratified, multiphase random sample was used in the third national survey of psychiatric morbidity in adults in England in 2007. Survey data were weighted to take account of study design and nonresponse so that the results were representative of the household population. Setting: General community (ie, private households) in England. Participants: Adults (people 16 years or older). Main Outcome Measures: Autism Diagnostic Observation Schedule, Module 4 in phase 2 validated against the Autism Diagnostic Interview-Revised and Diagnostic Interview for Social and Communication Disorders in phase 3. A 20-item subset of the Autism-Spectrum Quotient self-completion questionnaire was used in phase 1 to select respondents for phase 2. Respondents also provided information on sociodemographics and their use of mental health services. Results: Of 7461 adult participants who provided a complete phase 1 interview, 618 completed phase 2 diagnostic assessments. The weighted prevalence of ASD in adults was estimated to be 9.8 per 1000 (95% confidence interval, 3.0-16.5). Prevalence was not related to the respondent's age. Rates were higher in men, those without educational qualifications, and those living in rented social (government-financed) housing. There was no evidence of increased use of services for mental health problems. Conclusions: Conducting epidemiologic research on ASD in adults is feasible. The prevalence of ASD in this population is similar to that found in children. The lack of an association with age is consistent with there having been no increase in prevalence and with its causes being temporally constant. Adults with ASD living in the community are socially disadvantaged and tend to be unrecognized. C1 [Brugha, Traolach S.; Bankart, John; Smith, Jane; Meltzer, Howard] Univ Leicester, Dept Hlth Sci, Leicester LE5 4PW, Leics, England. [McManus, Sally; Purdon, Susan] Natl Ctr Social Res, London, England. [Scott, Fiona] Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. [Bebbington, Paul] UCL, Dept Mental Hlth Sci, London, England. [Jenkins, Rachel] Kings Coll London, Inst Psychiat, London WC2R 2LS, England. RP Brugha, TS (reprint author), Univ Leicester, Leicester Gen Hosp, Dept Hlth Sci, Gwendolen Rd, Leicester LE5 4PW, Leics, England. EM tsb@le.ac.uk RI Bebbington, Paul/C-1939-2008; Jenkins, Rachel/E-4287-2010 OI Bebbington, Paul/0000-0002-6030-7456; Jenkins, Rachel/0000-0002-2958-0331 FU National Health Service Information Centre for Health and Social Care and Department of Health; National Institute for Health Research and Department of Health FX This study was supported by the National Health Service Information Centre for Health and Social Care and Department of Health; autism follow-up was supported by the National Institute for Health Research and Department of Health Policy Research Programme. 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Gen. Psychiatry PD MAY PY 2011 VL 68 IS 5 BP 459 EP 466 PG 8 WC Psychiatry SC Psychiatry GA 757UY UT WOS:000290114500005 PM 21536975 ER PT J AU Hazlett, HC Poe, MD Gerig, G Styner, M Chappell, C Smith, RG Vachet, C Piven, J AF Hazlett, Heather Cody Poe, Michele D. Gerig, Guido Styner, Martin Chappell, Chad Smith, Rachel Gimpel Vachet, Clement Piven, Joseph TI Early Brain Overgrowth in Autism Associated With an Increase in Cortical Surface Area Before Age 2 Years SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; SPECTRUM DISORDER; NEURODEVELOPMENTAL DISORDERS; ABNORMALITIES; CHILDHOOD; CHILDREN; DISEASE; SIZE; MRI AB Context: Brain enlargement has been observed in 2-year-old children with autism, but the underlying mechanisms are unknown. Objective: To investigate early growth trajectories in brain volume and cortical thickness. Design: Longitudinal magnetic resonance imaging study. Setting: Academic medical centers. Participants: Fifty-nine children with autism spectrum disorder (ASD) and 38 control children. Intervention: Children were examined at approximately 2 years of age. Magnetic resonance imaging was repeated approximately 24 months later (when aged 4-5 years; 38 children with ASD; 21 controls). Main Outcome Measures: Cerebral gray and white matter volumes and cortical thickness. Results: We observed generalized cerebral cortical enlargement in individuals with ASD at both 2 and 4 to 5 years of age. Rate of cerebral cortical growth across multiple brain regions and tissue compartments in children with ASD was parallel to that seen in the controls, indicating that there was no increase in rate of cerebral cortical growth during this interval. No cerebellar differences were observed in children with ASD. After controlling for total brain volume, a disproportionate enlargement in temporal lobe white matter was observed in the ASD group. We found no significant differences in cortical thickness but observed an increase in an estimate of surface area in the ASD group compared with controls for all cortical regions measured (temporal, frontal, and parieto-occipital lobes). Conclusions: Our longitudinal magnetic resonance imaging study found generalized cerebral cortical enlargement in children with ASD, with a disproportionate enlargement in temporal lobe white matter. There was no significant difference from controls in the rate of brain growth for this age interval, indicating that brain enlargement in ASD results from an increased rate of brain growth before age 2 years. The presence of increased cortical volume, but not cortical thickness, suggests that early brain enlargement may be associated with increased cortical surface area. Cortical surface area overgrowth in ASD may underlie brain enlargement and implicates a distinct set of pathogenic mechanisms. C1 [Hazlett, Heather Cody] Univ N Carolina, Carolina Inst Dev Disabil, Dept Psychiat, Chapel Hill, NC 27599 USA. [Poe, Michele D.] Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC 27599 USA. [Styner, Martin] Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. [Gerig, Guido] Univ Utah, Sci Comp & Imaging Inst, Salt Lake City, UT USA. RP Hazlett, HC (reprint author), Univ N Carolina, Carolina Inst Dev Disabil, Dept Psychiat, CD-B 3367, Chapel Hill, NC 27599 USA. EM hcody@med.unc.edu RI Poe, Michele/K-6615-2012 OI Poe, Michele/0000-0001-9693-3638 FU National Institutes of Health [MH61696, MH64580, P30 HD03110]; National Alliance for Medical Image Computing [PHS-NIH EB005149-04] FX This work was supported by National Institutes of Health grants MH61696, MH64580, and P30 HD03110 (principal investigator, Dr Piven) and PHS-NIH EB005149-04 (principal investigator, Ron Kikinis, MD) from the National Alliance for Medical Image Computing. 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Gen. Psychiatry PD MAY PY 2011 VL 68 IS 5 BP 467 EP 476 PG 10 WC Psychiatry SC Psychiatry GA 757UY UT WOS:000290114500007 PM 21536976 ER PT J AU Mouridsen, SE Rich, B Isager, T AF Mouridsen, Svend Erik Rich, Bente Isager, Torben TI A longitudinal study of epilepsy and other central nervous system diseases in individuals with and without a history of infantile autism SO BRAIN & DEVELOPMENT LA English DT Article DE Infantile autism; Epilepsy; Central nervous system diseases ID NATIONAL-HOSPITAL-REGISTER; SPECTRUM DISORDERS; INTELLECTUAL DISABILITY; CHILDREN; POPULATION; PREVALENCE; CHILDHOOD; COHORT AB Objective: To compare the prevalence and types of epilepsy and other central nervous system (CNS) diseases in a clinical sample of 118 individuals diagnosed as children with infantile autism (IA) with 336 matched controls from the general population. Methods: All participants were screened through the nationwide Danish National Hospital Register (DNHR). The average observation time was 30.3 years (range 27-30 years), and mean age at follow-up was 42.7 years (range 27-57 years). Results: 01 the 118 individuals with IA, 29 (24.6%) were registered with at least one epilepsy diagnosis against 5 (1.5%) in the comparison group (p < 0.0001; OR = 21.6; 95% CI 8.1-57.3). Other CNS diseases occurred with low frequency in both groups and only cerebral palsy, unspecified (p = 0.02) was significantly more frequent among participants with a history of IA. Conclusions: Our study lends further support to the notion that epilepsy, but not other CNS diseases, is a common comorbid condition in IA. Low intelligence, but not gender, was a risk factor for epilepsy in IA. (C) 2010 The Japanese Society of Child Neurology. Published by Elsevier B.V. All rights reserved. C1 [Mouridsen, Svend Erik] Bispebjerg Hosp, Ctr Child & Adolescent Psychiat, Copenhagen, Denmark. [Rich, Bente] Int Rehabil Council Torture Victims, Copenhagen, Denmark. [Isager, Torben] Glostrup Univ Hosp, Ctr Child & Adolescent Psychiat, Glostrup, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Ctr Child & Adolescent Psychiat, Copenhagen, Denmark. 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PD MAY PY 2011 VL 33 IS 5 BP 361 EP 366 DI 10.1016/j.braindev.2010.07.002 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 761AI UT WOS:000290366400001 PM 20655678 ER PT J AU Esposito, G Venuti, P Apicella, F Muratori, F AF Esposito, Gianluca Venuti, Paola Apicella, Fabio Muratori, Filippo TI Analysis of unsupported gait in toddlers with autism SO BRAIN & DEVELOPMENT LA English DT Article DE Autistic disorder; Motor development; Unsupported gait; Symmetry; Movement ID HIGH-FUNCTIONING AUTISM; MOTOR STEREOTYPIES; ASPERGERS-SYNDROME; CHILDREN; DISORDER; CEREBELLAR; LOCOMOTION; DIAGNOSIS; INFANCY; AGE AB Aims: A number of studies have suggested the importance of motor development in autism. Motor development has been considered a possible bio-marker of autism since it does not depend on either social or linguistic development. In this study, using retrospective video analysis we investigated the first unsupported gait in toddlers with autism. Methods: Fifty-five toddlers, belonging to three groups were recruited: toddlers with autistic disorder (AD, n = 20, age 14.2 mo, sd 1.4 mo) and as comparison groups: typically developing toddlers (TD, n = 20, age 12.9 mo, sd 1.1 mo) and toddlers with non-autistic developmental delays of mixed aetiology (DD, n = 15, age 13.1 mo, sd 0.8 mo). The Walking Observation Scale (WOS) and the Positional Pattern for Symmetry during Walking (PPSW) were used to gather data on the first unsupported gait. The WOS includes 11 items that analyze gait through three axes: foot movements; arm movements; general movements while the PPSW analyses static and dynamical symmetry during gait. Results: Our results have identified significant differences in gait patterns among the group of toddlers with AD as opposed to the control groups. Significant differences between AD and the two control groups were found for both WOS (p < .001) and PPSW (p < .001). 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EM gianluca.esposito@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 CR Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 ESHKOL N, 2001, ESHKOLWACHEMAN MOV 1 Esposito G, 2008, PERCEPT MOTOR SKILL, V106, P259, DOI 10.2466/PMS.106.1.259-269 Esposito G, 2009, BRAIN DEV-JPN, V31, P131, DOI 10.1016/j.braindev.2008.04.005 Gillberg C, 1999, DEV PSYCHOPATHOL, V11, P567, DOI 10.1017/S0954579499002217 Goldman S, 2009, DEV MED CHILD NEUROL, V51, P30, DOI 10.1111/j.1469-8749.2008.03178.x Hadders-Algra M, 2008, EARLY HUM DEV, V84, P787, DOI 10.1016/j.earlhumdev.2008.09.002 HALLETT M, 1993, ARCH NEUROL-CHICAGO, V50, P1304 Harris KM, 2008, PEDIATR NEUROL, V38, P267, DOI 10.1016/j.pediatrneurol.2007.12.008 Iverson M.J., 2007, J AUTISM DEV DISORD, V37, P158 Jansiewicz EM, 2006, J AUTISM DEV DISORD, V36, P613, DOI 10.1007/s10803-006-0109-y Loh A, 2007, J AUTISM DEV DISORD, V37, P25, DOI 10.1007/s10803-006-0333-5 Mandelbaum DE, 2006, DEV MED CHILD NEUROL, V48, P33, DOI 10.1017/S0012162206000089 McCleery JP, 2009, BIOL PSYCHIAT, V66, P950, DOI 10.1016/j.biopsych.2009.07.031 Mink JW, 1996, PROG NEUROBIOL, V50, P381, DOI 10.1016/S0301-0082(96)00042-1 Minshew NJ, 2004, NEUROLOGY, V63, P2056 Morton SM, 2004, NEUROSCIENTIST, V10, P247, DOI 10.1177/1073858404263517 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Ozonoff S, 2008, J AUTISM DEV DISORD, V38, P644, DOI 10.1007/s10803-007-0430-0 Provost B, 2007, J AUTISM DEV DISORD, V37, P321, DOI 10.1007/s10803-006-0170-6 Rinehart NJ, 2006, DEV MED CHILD NEUROL, V48, P272, DOI 10.1017/S0012162206000594 Rinehart NJ, 2006, DEV MED CHILD NEUROL, V48, P819, DOI 10.1017/S0012162206001769 Teitelbaum O, 2004, P NATL ACAD SCI USA, V101, P11909, DOI 10.1073/pnas.0403919101 Teitelbaum P, 1998, P NATL ACAD SCI USA, V95, P13982, DOI 10.1073/pnas.95.23.13982 Welsh JP, 2002, ADV NEUROL, V89, P331 NR 26 TC 15 Z9 15 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 MAY PY 2011 VL 33 IS 5 BP 367 EP 373 DI 10.1016/j.braindev.2010.07.006 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA 761AI UT WOS:000290366400002 PM 20708861 ER PT J AU Stein, T Senju, A Peelen, MV Sterzer, P AF Stein, Timo Senju, Atsushi Peelen, Marius V. Sterzer, Philipp TI Eye contact facilitates awareness of faces during interocular suppression SO COGNITION LA English DT Article DE Eye contact; Gaze processing; Binocular rivalry; Interocular suppression; Unconscious processing ID CONTINUOUS FLASH SUPPRESSION; GAZE-DIRECTION; BINOCULAR SUPPRESSION; INVISIBLE FACES; CHILDREN; RESPONSES; FEARFUL; AUTISM; EXPRESSIONS; INFORMATION AB Eye contact captures attention and receives prioritized visual processing. Here we asked whether eye contact might be processed outside conscious awareness. Faces with direct and averted gaze were rendered invisible using interocular suppression. In two experiments we found that faces with direct gaze overcame such suppression more rapidly than faces with averted gaze. Control experiments ruled out the influence of low-level stimulus differences and differential response criteria. These results indicate an enhanced unconscious representation of direct gaze, enabling the automatic and rapid detection of other individuals making eye contact with the observer. (C) 2011 Elsevier B.V. All rights reserved. C1 [Stein, Timo; Sterzer, Philipp] Charite Campus Mitte, Dept Psychiat, D-10117 Berlin, Germany. [Stein, Timo; Sterzer, Philipp] Berlin Sch Mind & Brain, Berlin, Germany. [Senju, Atsushi] Univ London, Ctr Brain & Cognit Dev, London, England. [Peelen, Marius V.] Univ Trent, CIMeC, Ctr Mind Brain Sci, Rovereto, Italy. [Sterzer, Philipp] Bernstein Ctr Computat Neurosci, Berlin, Germany. RP Stein, T (reprint author), Charite Campus Mitte, Dept Psychiat, Charitepl 1, D-10117 Berlin, Germany. 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The transition from proliferating neuroepithelial precursor cells to neuronal lineages is accompanied by rapid global changes in gene expression in coordination with epigenetic modifications at the level of the chromatin structure. A number of genetic studies have begun to reveal how epigenetic deregulation results in neurodevelopmental disorders such as mental retardation, autism, Rubinstein-Taybi syndrome and Rett syndrome. In this review we focus on the role of the methyl-CpG binding protein 2 (MeCP2) during development of the central nervous system and its involvement in Rett syndrome. First, we present recent findings that indicate a previously unconsidered role of glial cells in the development of Rett syndrome. Next, we discuss evidence of how MeCP2 deficiency or loss of function results in aberrant gene expression leading to Rett syndrome. We also discuss MeCP2's function as a repressor and activator of gene expression and the role of its different target genes, including microRNAs, during neuronal development. Finally, we address different signaling pathways that regulate MeCP2 expression at both the post-transcriptional and post-translational level, and discuss how mutations in MeCP2 may result in lack of responsiveness to environmental signals. C1 [Diaz de Leon-Guerrero, Sol; Pedraza-Alva, Gustavo; Perez-Martinez, Leonor] Univ Nacl Autonoma Mexico, Inst Biotecnol, Dept Med Mol & Bioproc, Lab Neuroinmunobiol, Cuernavaca 62271, Morelos, Mexico. RP de Leon-Guerrero, SD (reprint author), Univ Nacl Autonoma Mexico, Inst Biotecnol, Dept Med Mol & Bioproc, Lab Neuroinmunobiol, AP 510-3, Cuernavaca 62271, Morelos, Mexico. EM leonor@ibt.unam.mx FU DGAPA; CONACYT FX We are grateful to Dr Felix Recillas-Targa (Instituto de Fisiologia Celular, UNAM) for insightful scientific discussions and to Oswaldo Lopez and Virginia Barajas for technical support. This work was supported by DGAPA and CONACYT. The authors declare no conflict of interest. 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EM leehk@postech.ac.kr; dsl@snu.ac.kr; hkang211@snu.ac.kr; kbn1@snu.ac.kr; mkchung@wisc.edu RI Kim, Boong Nyun/J-5397-2012 FU MEST [R31-2008-000-10103-0]; NRF; Ministry of Science and Technology [M103KV010016-08K2201-01610]; Government of Korea FX Manuscript received February 06, 2011; revised March 31, 2011; accepted April 01, 2011. Date of publication April 07, 2011; date of current version May 04, 2011. This work was supported by Grant R31-2008-000-10103-0 from the WCU project of the MEST and the NRF and by a grant (M103KV010016-08K2201-01610) from Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology. The work of M. K. Chung was supported by the WCU Grant from the Government of Korea. Asterisk indicates corresponding author. 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TI Three phases of DiGeorge/22q11 deletion syndrome pathogenesis during brain development: Patterning, proliferation, and mitochondrial functions of 22q11 genes SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE Schizophrenia; Autism; ADHD; Development ID CARDIO-FACIAL SYNDROME; SYNDROME CANDIDATE GENE; MOUSE MODEL; VELOCARDIOFACIAL/DIGEORGE-SYNDROME; TBX1 HAPLOINSUFFICIENCY; CORTICAL THICKNESS; PREFRONTAL CORTEX; FRONTAL-CORTEX; RETINOIC ACID; ADULT BRAIN AB DiGeorge. or 22q11 deletion syndrome (22q11DS), the most common survivable human genetic deletion disorder, is caused by deletion of a minimum of 32 contiguous genes on human chromosome 22, and presumably results from diminished dosage of one, some, or all of these genes particularly during development. Nevertheless, the normal functions of 22q11 genes in the embryo or neonate, and their contribution to developmental pathogenesis that must underlie 22q11DS are not well understood. Our data suggests that a substantial number of 22q11 genes act specifically and in concert to mediate early morphogenetic interactions and subsequent cellular differentiation at phenotypically compromised sites the limbs, heart, face and forebrain. When dosage of a broad set of these genes is diminished, early morphogenesis is altered, and initial 22q11DS phenotypes are established. Thereafter, functionally similar subsets of 22q11 genes especially those that influence the cell cycle or mitochondrial function remain expressed, particularly in the developing cerebral cortex, to regulate neurogenesis and synaptic development. When dosage of these genes is diminished, numbers, placement and connectivity of neurons and circuits essential for normal behavior may be disrupted. Such disruptions likely contribute to vulnerability for schizophrenia, autism, or attention deficit/hyperactivity disorder seen in most 22q11DS patients. (C) 2010 ISDN. Published by Elsevier Ltd. All rights reserved. C1 [LaMantia, A. -S.] George Washington Univ, Sch Med & Hlth Sci, Dept Physiol & Pharmacol, Washington, DC 20052 USA. George Washington Univ, Sch Med & Hlth Sci, GW Inst Neurosci, Washington, DC 20052 USA. RP LaMantia, AS (reprint author), George Washington Univ, Sch Med & Hlth Sci, Dept Physiol & Pharmacol, 2300 Eye St NW, Washington, DC 20052 USA. EM phmasl@gwumc.edu RI Maynard, Thomas/I-9039-2012 OI Maynard, Thomas/0000-0001-6976-3936 FU NARSAD; NICHD [HD42182]; NIMH [MH64065] FX We thank Amanda Peters for assistance with various phases of the work done in our laboratory. DWM and TMM are recipients of NARSAD Young Investigator Awards. NICHD (HD42182 to A.-S.L.), NIMH Silvio M. Conte Grant (MH64065), and NARSAD Independent Investigator Awards (ASL) have provided support. Confocal microscopy and RNA expression analysis utilized UNC Neuroscience Center core facilities (NS031768). 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Akbarian, Schahram TI White matter neuron alterations in schizophrenia and related disorders SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Review DE Interstitial white matter neurons; Subplate; Interneurons; Radial glia; Ventricular zone; Subventricular zone; Cerebral cortex; Neurodevelopmental disorder; Microglia; Inflammation ID DORSOLATERAL PREFRONTAL CORTEX; HUMAN CEREBRAL-CORTEX; POSITIVE STRIATAL INTERNEURONS; DENDRITIC SPINE DENSITY; ENTORHINAL CORTEX; BIPOLAR DISORDER; SUBPLATE NEURONS; CORTICAL DEVELOPMENT; GABAERGIC INTERNEURONS; POSTNATAL-DEVELOPMENT AB Increased density and altered spatial distribution of subcortical white matter neurons (WMNs) represents one of the more well replicated cellular alterations found in schizophrenia and related disease. In many of the affected cases, the underlying genetic risk architecture for these WMN abnormalities remains unknown. Increased density of neurons immunoreactive for Microtubule-Associated Protein 2 (MAP2) and Neuronal Nuclear Antigen (NeuN) have been reported by independent studies, though there are negative reports as well; additionally, group differences in some of the studies appear to be driven by a small subset of cases. Alterations in markers for inhibitory (GABAergic) neurons have also been described. For example, downregulation of neuropeptide Y (NPY) and nitric oxide synthase (NOS1) in inhibitory WMN positioned at the gray/white matter border, as well as altered spatial distribution, have been reported. While increased density of WMN has been suggested to reflect disturbance of neurodevelopmental processes, including neuronal migration, neurogenesis, and cell death, alternative hypotheses such as an adaptive response to microglial activation in mature CNS, as has been described in multiple sclerosis-should also be considered. We argue that larger scale studies involving hundreds of postmortem specimens will be necessary in order to clearly establish the subset of subjects affected. Additionally, these larger cohorts could make it feasible to connect the cellular pathology to environmental and genetic factors implicated in schizophrenia, bipolar disorder, and autism. These could include the 22q11 deletion (Velocardiofacial/DiGeorge) syndrome, which in some cases is associated with neuronal ectopias in white matter. (C) 2010 ISDN. Published by Elsevier Ltd. All rights reserved. C1 [Connor, Caroline M.; Crawford, Benjamin C.; Akbarian, Schahram] Univ Massachusetts, Brudnick Neuropsychiat Res Inst, Dept Psychiat, Sch Med, Worcester, MA 01604 USA. RP Akbarian, S (reprint author), Univ Massachusetts, Brudnick Neuropsychiat Res Inst, Dept Psychiat, Sch Med, Worcester, MA 01604 USA. 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J. Dev. Neurosci. PD MAY PY 2011 VL 29 IS 3 SI SI BP 325 EP 334 DI 10.1016/j.ijdevneu.2010.07.236 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 758BQ UT WOS:000290135200014 PM 20691252 ER PT J AU Liptak, GS Kennedy, JA Dosa, NP AF Liptak, Gregory S. Kennedy, Jenny A. Dosa, Nienke P. TI Social Participation in a Nationally Representative Sample of Older Youth and Young Adults With Autism SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; transition; outcome assessment; International Classification of Diseases ID FOLLOW-UP; CHILDREN; DISORDERS; SPECTRUM; HEALTH; INDIVIDUALS; ADOLESCENTS; POPULATION; PREDICTORS; CHILDHOOD AB Objective: To describe social participation and identify factors that affect it in a nationally representative sample of adolescents and young adults with autism. Methods: Longitudinal cohort study using data from the National Longitudinal Transition Study-2. The World Health Organization International Classification of Functioning, Disability, and Health model was used with participation as the dependent category. Results: A nationally representative sample of 725 youth with autism representing a weighted sample of 21,010 individuals was followed up for 4 years. The mean age at first interview was 15.4 years and 19.2 years at follow-up. More than half the youth at follow-up had not gotten together with friends in the previous year and 64% had not talked on the phone with a friend. Being employed or in secondary education was associated with the following factors (odds ratios): problems conversing (0.67), being teased (0.17), mental retardation (0.06), being above the poverty level (4.17), not using prescription medicine (4.11), general health status (2.30), and parental involvement with school (1.69) (all p < .001). Conclusions: Many adolescents and young adults with autism become increasingly isolated. Although each aspect of social participation had its own distinct pattern of factors related to it, the ability to communicate effectively, less severe autism, coming from an environment that was not impoverished and having parents who advocated were associated with more positive outcomes. These data provide insights into the factors that affect the participation of youth with autism during their transition years and should ultimately lead to interventions that could improve those transitions. C1 [Liptak, Gregory S.; Kennedy, Jenny A.; Dosa, Nienke P.] SUNY Upstate Med Ctr, Golisano Childrens Hosp, Dept Pediat, Syracuse, NY 13210 USA. RP Liptak, GS (reprint author), SUNY Upstate Med Ctr, Golisano Childrens Hosp, Dept Pediat, 750 E Adams St, Syracuse, NY 13210 USA. 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Dev. Behav. Pediatr. PD MAY PY 2011 VL 32 IS 4 BP 332 EP 340 DI 10.1097/DBP.0b013e318213f56c PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 755YD UT WOS:000289976100009 PM 21502871 ER PT J AU Marcus, SC Durkin, M AF Marcus, Steven C. Durkin, Michael TI Stimulant Adherence and Academic Performance in Urban Youth With Attention-Deficit/Hyperactivity Disorder SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE stimulant; adherence; academic performance; school; ADHD ID DEFICIT HYPERACTIVITY DISORDER; TERM SCHOOL OUTCOMES; AFRICAN-AMERICAN; CHILDREN; ADHD; METHYLPHENIDATE; MEDICATION; ADOLESCENTS; ACHIEVEMENT; CHILDHOOD AB Objective: This analysis assessed whether stimulant adherence was associated with improvement in academic grade point average (GPA) among children diagnosed with and treated for attention-deficit/hyperactivity disorder (ADHD). Method: Medicaid claims were merged with academic records from Philadelphia public schools of Medicaid-eligible children in first through eighth grades who were diagnosed with ADHD and who had filled one or more stimulant prescription. Students diagnosed with mental retardation, autism, or speech, hearing, visual, or language impairments were excluded. Marking periods were scored for GPA (range: 0-4.0) based on English, mathematics, social studies, and science grades and for stimulant adherence (medication possession ratio >= 0.70). Random and fixed-effects models estimated the effects of stimulant adherence on GPA, between all adherent and nonadherent marking periods in aggregate and within individual student's marking periods, respectively. Results: A total of 3,543 students contributed 29,992 marking periods, of which 18.6% were adherent. Mean GPA was significantly higher during stimulant-adherent (2.18) than stimulant-nonadherent (1.99) marking periods in aggregate (p < .0001). The regression coefficient representing within-student association between stimulant adherence and GPA over time was 0.108 (p < .0001), indicating that adherence was associated with a 0.108 increase in GPA. In stratified analyses, analogous coefficients were 0.106 for boys, 0.111 for girls, 0.078 for elementary students, and 0.118 for middle school students (all p < .0001). The association was stronger among students with (0.139) than without (0.088) comorbid disruptive behavior disorders (both p < .0001). Conclusions: Stimulant adherence, although found to be low among urban elementary and middle school students diagnosed with ADHD, was associated with a marginal improvement in GPA. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(5):480-489. C1 [Marcus, Steven C.] Univ Penn, Sch Social Policy & Practice, Philadelphia, PA 19103 USA. [Marcus, Steven C.] Philadelphia Vet Affairs Med Ctr, Ctr Hlth Equ Res & Promot, Philadelphia, PA USA. [Durkin, Michael] Ortho McNeil Janssen Sci Affairs LLC, Titusville, NJ USA. RP Marcus, SC (reprint author), Univ Penn, Sch Social Policy & Practice, 3701 Locust Walk, Philadelphia, PA 19103 USA. EM marcuss@sp2.upenn.edu FU Ortho-McNeil Janssen Scientific Affairs, LLC; Eli Lilly and Co., Bristol-Myers Squibb; Johnson and Johnson FX This project was funded by Ortho-McNeil Janssen Scientific Affairs, LLC.Dr. Marcus has received grant support from Ortho-McNeil Janssen, and has served as a consultant to Eli Lilly and Co., Bristol-Myers Squibb, and AstraZeneca. Mr. Durkin holds stock in Johnson and Johnson. 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Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2011 VL 50 IS 5 BP 480 EP 489 DI 10.1016/j.jaac.2011.02.007 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 757GH UT WOS:000290073000009 PM 21515197 ER PT J AU Marrus, N Faughn, C Shuman, J Petersen, SE Constantino, JN Povinelli, DJ Pruett, JR AF Marrus, Natasha Faughn, Carley Shuman, Jeremy Petersen, Steve E. Constantino, John N. Povinelli, Daniel J. Pruett, John R., Jr. TI Initial Description of a Quantitative, Cross-Species (Chimpanzee-Human) Social Responsiveness Measure SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE comparative cognition; autism; Social Responsiveness Scale; chimpanzee; nonhuman primate ID PERVASIVE DEVELOPMENTAL DISORDERS; PAN-TROGLODYTES; AUTISTIC TRAITS; DIAGNOSTIC INTERVIEW; GENERAL-POPULATION; PERSONALITY; MIND; RECIPROCITY; BEHAVIOR; DOMINANCE AB Objective: Comparative studies of social responsiveness, an ability that is impaired in autism spectrum disorders, can inform our understanding of both autism and the cognitive architecture of social behavior. Because there is no existing quantitative measure of social responsiveness in chimpanzees, we generated a quantitative, cross-species (human chimpanzee) social responsiveness measure. Method: We translated the Social Responsiveness Scale (SRS), an instrument that quantifies human social responsiveness, into an analogous instrument for chimpanzees. We then retranslated this "Chimpanzee SRS" into a human "Cross-Species SRS" (XSRS). We evaluated three groups of chimpanzees (n = 29) with the Chimpanzee SRS and typical and human children with autism spectrum disorder (ASD; n = 20) with the XSRS. Results: The Chimpanzee SRS demonstrated strong interrater reliability at the three sites (ranges for individual ICCs: 0.534 to 0.866; mean ICCs: 0.851 to 0.970). As has been observed in human beings, exploratory principal components analysis of Chimpanzee SRS scores supports a single factor underlying chimpanzee social responsiveness. Human subjects' XSRS scores were fully concordant with their SRS scores (r = 0.976, p = .001) and distinguished appropriately between typical and ASD subjects. One chimpanzee known for inappropriate social behavior displayed a significantly higher score than all other chimpanzees at its site, demonstrating the scale's ability to detect impaired social responsiveness in chimpanzees. Conclusion: Our initial cross-species social responsiveness scale proved reliable and discriminated differences in social responsiveness across (in a relative sense) and within (in a more objectively quantifiable manner) human beings and chimpanzees. J. Am. Acad. Child Adolesc. Psychiatry, 2011;50(5):508-518. C1 [Marrus, Natasha] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. [Faughn, Carley; Povinelli, Daniel J.] Univ Louisiana, Lafayette, LA USA. [Shuman, Jeremy] Indiana State Univ, Terre Haute, IN 47809 USA. RP Marrus, N (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid,Box 8134, St Louis, MO 63110 USA. EM marrusn@psychiatry.wustl.edu FU James S. McDonnell Foundation [K12 EY16336] FX This research was supported by a James S. McDonnell Foundation Centennial Fellowship (D.P.) and K12 EY16336 (J.P.). 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Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2011 VL 50 IS 5 BP 508 EP 518 DI 10.1016/j.jaac.2011.01.009 PG 11 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 757GH UT WOS:000290073000012 PM 21515200 ER PT J AU Miller, JS Gabrielsen, T Villalobos, M Alleman, R Wahmhoff, N Carbone, PS Segura, B AF Miller, Judith S. Gabrielsen, Terisa Villalobos, Michele Alleman, Rebecca Wahmhoff, Natalie Carbone, Paul S. Segura, Brandon TI The Each Child Study: Systematic Screening for Autism Spectrum Disorders in a Pediatric Setting SO PEDIATRICS LA English DT Article DE autism; screening-early childhood; community pediatrics; early intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; TRAITS QUESTIONNAIRE ESAT; MODIFIED CHECKLIST; TODDLERS; SURVEILLANCE; POPULATION AB OBJECTIVE: The goal of this study was to investigate the feasibility and outcome of a systematic autism screening process for all toddlers (aged 14-30 months) in a large, community-based pediatric practice. METHODS: All toddlers who presented to the clinic during the 6-month screening period were eligible. We used 2 screening questionnaires and allowed physicians to refer directly to capture as many children as possible. Receptionists and medical assistants distributed and collected screening questionnaires; research staff did all scoring and follow-up, either by telephone or in person when indicated. RESULTS: We obtained a high rate of screening (80% of eligible children). Of the 796 children screened, 3 had already been diagnosed with an autism spectrum disorder (ASD); an additional 10 children who showed signs of early ASD that warranted further evaluation or intervention were identified. Formal screening measures identified more children with ASD than did clinical judgment or caregiver concerns; however, no single method (ie, questionnaire, caregiver concerns, provider concerns) identified all children with signs of early ASD. We had excellent participation from racially and ethnically diverse families, including Spanish-speaking families. Thirty-two percent of the children who were screened did not present for a well-child visit during the study period and were screened at a sick visit, follow-up visit, or injection appointment. CONCLUSIONS: A partnership between pediatricians and autism specialists resulted in effective, systematic autism screening. Future studies should examine how to create effective systems of care. Pediatrics 2011;127:866-871 C1 [Miller, Judith S.; Gabrielsen, Terisa; Villalobos, Michele; Alleman, Rebecca; Wahmhoff, Natalie] Univ Utah, Dept Psychiat, Salt Lake City, UT USA. [Carbone, Paul S.; Segura, Brandon] Univ Utah, Dept Pediat, Salt Lake City, UT USA. RP Miller, JS (reprint author), Childrens Hosp Philadelphia, Ctr Autism Res, 3535 Market St,8th Floor,Suite 860, Philadelphia, PA 19104 USA. EM millerj3@email.chop.edu FU Centers for Disease Control and Prevention [U01DD000068-01]; Department of Pediatrics at the University of Utah; Utah Department of Health (Health Resources and Services Administration Maternal and Child Health Bureau) [BC B04MC000321-02] FX This study was supported by grants to Dr Miller from the Centers for Disease Control and Prevention (U01DD000068-01), the Department of Pediatrics at the University of Utah, and the Utah Department of Health (Health Resources and Services Administration Maternal and Child Health Bureau BC B04MC000321-02). 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Saul, Robert A. Saal, Howard M. Braddock, Stephen R. Enns, Gregory M. Gruen, Jeffrey R. Perrin, James M. Tarini, Beth Anne Hanson, James W. Lloyd-Puryear, Michele Ann Musci, Thomas J. Rasmussen, Sonja Ann Spire, Paul TI Clinical Report-Health Supervision for Children With Fragile X Syndrome SO PEDIATRICS LA English DT Article DE fragile X syndrome; FMR1-related conditions; mental retardation; health guidelines ID PREMATURE OVARIAN FAILURE; TREMOR/ATAXIA SYNDROME; FMR1 PREMUTATION; AUTISM; EXPERIENCES; POPULATION; DISORDERS; ATTITUDES; FXTAS AB Fragile X syndrome (an FMR1-related disorder) is the most commonly inherited form of mental retardation. Early physical recognition is difficult, so boys with developmental delay should be strongly considered for molecular testing. The characteristic adult phenotype usually does not develop until the second decade of life. Girls can also be affected with developmental delay. Because multiple family members can be affected with mental retardation and other conditions (premature ovarian failure and tremor/ataxia), family history information is of critical importance for the diagnosis and management of affected patients and their families. This report summarizes issues for fragile X syndrome regarding clinical diagnosis, laboratory diagnosis, genetic counseling, related health problems, behavior management, and age-related health supervision guidelines. The diagnosis of fragile X syndrome not only involves the affected children but also potentially has significant health consequences for multiple generations in each family. Pediatrics 2011; 127: 994-1006 C1 [Lloyd-Puryear, Michele Ann] US Hlth Resources & Serv Adm, Rockville, MD 20857 USA. [Rasmussen, Sonja Ann] Ctr Dis Control & Prevent, Atlanta, GA USA. 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Veenstra-VanderWeele, Jeremy TI A Systematic Review of Secretin for Children With Autism Spectrum Disorders SO PEDIATRICS LA English DT Review DE autism spectrum disorders; secretin ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; SYNTHETIC SECRETIN; PORCINE SECRETIN; RAT AB CONTEXT: As many as 1 in every 110 children in the United States has an autism spectrum disorder (ASD). Secretin is 1 of many medical treatments studied for treating the symptoms of ASDs, but there is currently no consensus regarding which interventions are most effective. OBJECTIVE: To systematically review evidence regarding the use of secretin in children with ASDs who are aged 12 years and younger. METHODS: We searched the Medline, PsycINFO, and ERIC (Education Resources Information Center) databases from 2000 to May 2010 and reference lists of included articles. Two reviewers independently assessed each study against predetermined inclusion/exclusion criteria. Two reviewers 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: Evidence from 7 randomized controlled trials supports a lack of effectiveness of secretin for the treatment of ASD symptoms including language and communication impairment, symptom severity, and cognitive and social skill deficits. No studies have resulted in significantly greater improvements in measures of language, cognition, or autistic symptoms when compared with placebo; study authors who reported improvement over time did so equally for both the intervention and placebo groups. CONCLUSIONS: Secretin has been studied extensively in multiple randomized controlled trials, and there is clear evidence that it lacks benefit. The studies of secretin included in this review uniformly point to a lack of significant impact of secretin in the treatment of ASD symptoms. Given the high strength of evidence for a lack of effectiveness, secretin as a treatment approach for ASDs warrants no further study. Pediatrics 2011;127:e1322-e1325 C1 [Krishnaswami, Shanthi; McPheeters, Melissa L.] Vanderbilt Univ, Inst Med & Publ Hlth, Vanderbilt Evidence Based Practice Ctr, Nashville, TN USA. [McPheeters, Melissa L.] Vanderbilt Univ, Vanderbilt Med Ctr, Dept Obstet & Gynecol, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Psychiat, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pediat, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Treatment & Res Inst Autism Spectrum Disorders, Vanderbilt Kennedy Ctr, Nashville, TN USA. RP McPheeters, ML (reprint author), 2525 W End Ave,Suite 600,6th Floor, Nashville, TN 37203 USA. EM melissa.mcpheeters@vanderbilt.edu FU Autism Speaks; American Academy of Child and Adolescent Psychiatry; NARSAD; Seaside Therapeutics; Roche Pharmaceuticals; Novartis; Agency for Healthcare Research and Quality [HHSA 290 2007 10065 I]; National Institute of Mental Health; Eunice Kennedy Shriver National Institute of Child Health and Human Development FX Dr Veenstra-VanderWeele has received research support from Autism Speaks, the American Academy of Child and Adolescent Psychiatry, NARSAD, Seaside Therapeutics, Roche Pharmaceuticals, and Novartis. The other authors have indicated they have no financial relationships relevant to this article to disclose.This project was supported by the Agency for Healthcare Research and Quality (contract number HHSA 290 2007 10065 I). Dr Veenstra-VanderWeele has received research support from the National Institute of Mental Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the Agency for Healthcare Research and Quality. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT CHARLTON CG, 1983, PEPTIDES, V4, P739, DOI 10.1016/0196-9781(83)90029-3 Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 Coniglio SJ, 2001, J PEDIATR-US, V138, P649, DOI 10.1067/mpd.2001.112474 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 FREMEAU RT, 1983, J NEUROSCI, V3, P1620 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Levy SE, 2003, ARCH DIS CHILD, V88, P731, DOI 10.1136/adc.88.8.731 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Molloy CA, 2002, J AUTISM DEV DISORD, V32, P545, DOI 10.1023/A:1021202930206 Owens DK, 2010, J CLIN EPIDEMIOL, V63, P513, DOI 10.1016/j.jclinepi.2009.03.009 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 Roberts W, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.5.e71 TULASSAY Z, 1992, DIGESTION, V51, P211 Unis AS, 2002, J AM ACAD CHILD PSY, V41, P1315, DOI 10.1097/01.CHI.0000024858.60748.4C Warren Z., 2011, AHRQ PUBLICATION, V11-EHC029-EF WATANABE Y, 1991, GASTROENTEROL JPN, V26, P86 Williams KW, 2005, COCHRANE DB SYST REV, V3 NR 19 TC 9 Z9 9 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 MAY PY 2011 VL 127 IS 5 BP E1322 EP E1325 DI 10.1542/peds.2011-0428 PG 4 WC Pediatrics SC Pediatrics GA 757OO UT WOS:000290097800028 PM 21464196 ER PT J AU McPheeters, ML Warren, Z Sathe, N Bruzek, JL Krishnaswami, S Jerome, RN Veenstra-VanderWeele, J AF McPheeters, Melissa L. Warren, Zachary Sathe, Nila Bruzek, Jennifer L. Krishnaswami, Shanthi Jerome, Rebecca N. Veenstra-VanderWeele, Jeremy TI A Systematic Review of Medical Treatments for Children With Autism Spectrum Disorders SO PEDIATRICS LA English DT Review DE autism spectrum disorders; antipsychotics; risperidone; aripiprazole; serotonin-reuptake inhibitors; citalopram; fluoxetine; psychostimulants ID PERVASIVE DEVELOPMENTAL DISORDERS; COGNITIVE-BEHAVIORAL THERAPY; RANDOMIZED CONTROLLED-TRIAL; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; RETROSPECTIVE ANALYSIS; RISPERIDONE TREATMENT; CROSSOVER TRIAL; ADOLESCENTS; HYPERACTIVITY AB CONTEXT: As many as 1 in every 110 children in the United States has an autism spectrum disorder (ASD). Many medical treatments for ASDs have been proposed and studied, but there is currently no consensus regarding which interventions are most effective. OBJECTIVE: To systematically review evidence regarding medical treatments for children aged 12 years and younger with ASDs. METHODS: We searched the Medline, PsycInfo, and ERIC (Education Resources Information Center) databases from 2000 to May 2010, regulatory data for approved medications, and reference lists of included articles. Two reviewers independently assessed each study against predetermined inclusion/exclusion criteria. Studies of secretin were not included in this review. Two reviewers 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: Evidence supports the benefit of risperidone and aripiprazole for challenging and repetitive behaviors in children with ASDs. Evidence also supports significant adverse effects of these medications. Insufficient strength of evidence is present to evaluate the benefits or adverse effects for any other medical treatments for ASDs, including serotonin-reuptake inhibitors and stimulant medications. CONCLUSIONS: Although many children with ASDs are currently treated with medical interventions, strikingly little evidence exists to support benefit for most treatments. Risperidone and aripiprazole have shown benefit for challenging and repetitive behaviors, but associated adverse effects limit their use to patients with severe impairment or risk of injury. Pediatrics 2011;127:e1312-e1321 C1 [McPheeters, Melissa L.; Sathe, Nila; Bruzek, Jennifer L.; Krishnaswami, Shanthi] Vanderbilt Univ, Inst Med & Publ Hlth, Vanderbilt Evidence Based Practice Ctr, Med Ctr, Nashville, TN USA. [McPheeters, Melissa L.] Vanderbilt Univ, Med Ctr, Dept Obstet & Gynecol, Nashville, TN 37232 USA. [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Psychiat, Nashville, TN USA. [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pediat, Nashville, TN USA. [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Vanderbilt Kennedy Ctr, Treatment & Res Inst Autism Spectrum Disorders, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN USA. [Jerome, Rebecca N.] Vanderbilt Univ, Dept Biomed Informat, Nashville, TN USA. [Jerome, Rebecca N.] Vanderbilt Univ, Eskind Biomed Lib, Nashville, TN USA. RP Veenstra-VanderWeele, J (reprint author), 465 21st Ave S,7158 Med Res Bldg 3, Nashville, TN 37232 USA. EM j.vvw@vanderbilt.edu FU Marino Autism Research Institute; Autism Speaks; Simons Foundation; American Academy of Child and Adolescent Psychiatry; NARSAD; Seaside Therapeutics; Roche Pharmaceuticals; Novartis; Agency for Healthcare Research and Quality [HHSA 290 2007 10065 I]; National Institute of Mental Health; Eunice Kennedy Shriver National Institute of Child Health and Human Development; Maternal and Child Health Bureau; National Science Foundation FX Dr Warren has received research support from the Marino Autism Research Institute, Autism Speaks, and the Simons Foundation; and Dr Veenstra-VanderWeele has received research support from Autism Speaks, the American Academy of Child and Adolescent Psychiatry, NARSAD, Seaside Therapeutics, Roche Pharmaceuticals, and Novartis. The other authors have indicated they have no financial relationships relevant to this article to disclose.This project was supported by the Agency for Healthcare Research and Quality (contract number: HHSA 290 2007 10065 I). 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 Maternal and Child Health Bureau, the National Science Foundation, and the Agency for Healthcare Research and Quality; and Dr Veenstra-VanderWeele has received research support from the National Institute of Mental Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the Agency for Healthcare Research and Quality. 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Sathe, Nila Foss-Feig, Jennifer H. Glasser, Allison Veenstra-VanderWeele, Jeremy TI A Systematic Review of Early Intensive Intervention for Autism Spectrum Disorders SO PEDIATRICS LA English DT Review DE autism spectrum disorders; early intervention; behavioral intervention ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; COMMUNICATION; PREDICTORS; PARENTS; TRIAL; OUTCOMES; PROGRAM; SCHOOL AB CONTEXT: Early intensive behavioral and developmental interventions for young children with autism spectrum disorders (ASDs) may enhance developmental outcomes. OBJECTIVE: To systematically review evidence regarding such interventions for children aged 12 and younger with ASDs. METHODS: We searched Medline, PsycINFO, and ERIC (Education Resources Information Center) from 2000 to May 2010. Two reviewers independently assessed studies against predetermined inclusion/exclusion criteria. Two reviewers independently extracted data regarding participant and intervention characteristics, assessment techniques, and outcomes and assigned overall quality and strength-of-evidence ratings using predetermined criteria. RESULTS: Thirty-four unique studies met inclusion criteria. Seventeen studies were case series; 2 were randomized controlled trials. We rated 1 study as good quality, 10 as fair quality, and 23 as poor quality. The strength of the evidence overall ranged from insufficient to low. Studies of University of California Los Angeles/Lovaas-based interventions and variants reported clinically significant gains in language and cognitive skills in some children, as did 1 randomized controlled trial of an early intensive developmental intervention approach (the Early Start Denver Model). Specific parent-training approaches yielded gains in short-term language function and some challenging behaviors. Data suggest that subgroups of children displayed more prominent gains across studies, but participant characteristics associated with greater gains are not well understood. CONCLUSIONS: Studies of Lovaas-based approaches and early intensive behavioral intervention variants and the Early Start Denver Model resulted in some improvements in cognitive performance, language skills, and adaptive behavior skills in some young children with ASDs, although the literature is limited by methodologic concerns. Pediatrics 2011;127:e1303-e1311 C1 [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Psychiat, Nashville, TN 37203 USA. [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pediat, Nashville, TN 37203 USA. [Warren, Zachary; Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Treatment & Res Inst Autism Spectrum Disorders, Vanderbilt Kennedy Ctr, Nashville, TN 37203 USA. [McPheeters, Melissa L.; Sathe, Nila; Glasser, Allison] Vanderbilt Univ, Inst Med & Publ Hlth, Vanderbilt Evidence Based Practice Ctr, Nashville, TN 37203 USA. [McPheeters, Melissa L.] Vanderbilt Univ, Vanderbilt Med Ctr, Dept Obstet & Gynecol, Nashville, TN 37203 USA. [Foss-Feig, Jennifer H.] Vanderbilt Univ, Dept Psychol & Human Dev, Nashville, TN 37203 USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37203 USA. [Veenstra-VanderWeele, Jeremy] Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN 37203 USA. RP Warren, Z (reprint author), Vanderbilt Univ, Dept Psychiat, 230 Appleton Pl,PMB 74, Nashville, TN 37203 USA. EM zachary.warren@vanderbilt.edu FU Marino Autism Research Institute; Autism Speaks; Simons Foundation; American Academy of Child and Adolescent Psychiatry; NARSAD; Seaside Therapeutics; Roche Pharmaceuticals; Novartis; AHRQ [HHSA 290 2007 10065 I]; National Institute of Mental Health; Eunice Kennedy Shriver National Institute of Child Health and Human Development; Maternal and Child Health Bureau; National Science Foundation FX Dr Warren has received research support from the Marino Autism Research Institute, Autism Speaks, and the Simons Foundation; and Dr Veenstra-VanderWeele has received research support from Autism Speaks, the American Academy of Child and Adolescent Psychiatry, NARSAD, Seaside Therapeutics, Roche Pharmaceuticals, and Novartis. The other authors have indicated they have no financial relationships relevant to this article to disclose.This project was supported by the AHRQ (contract number HHSA 290 2007 10065 I). 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 Maternal and Child Health Bureau, the National Science Foundation, and the AHRQ; and Dr Veenstra-VanderWeele has received research support from the National Institute of Mental Health, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the AHRQ. CR Aldred C, 2004, J CHILD PSYCHOL PSYC, V45, P1420, DOI 10.1111/j1469-7610.2004.00338.x American Psychiatric Association, 2000, DIAGN STAT MAN MENT Anan RM, 2008, BEHAV INTERVENT, V23, P165, DOI 10.1002/bin.262 Arick J. 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TI Children With Autism Spectrum Disorder and Literacy Instruction: An Exploratory Study of Elementary Inclusive Settings SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article DE autism spectrum disorder; autism; Asperger syndrome; reading; reading instruction ID INDIVIDUALS; ABILITY AB Little is known about how children with autism spectrum disorder (ASD) experience reading instruction in the context of a natural learning environment. This qualitative study centered on three students with ASD who received reading instruction primarily in the general education classroom setting. Observation, interview, and archival data were collected and analyzed to learn how students with ASD engaged in reading instruction and responded to teacher strategies employed to facilitate learning. Findings describe the strengths shown and challenges experienced by children with ASD during literacy instruction. Limited exposure to systematic comprehension instruction hindered the literacy acquisition of learners ASD. Implications for general and special educators are described. C1 [Whalon, Kelly J.] Coll William & Mary, Williamsburg, VA 23187 USA. [Hart, Juliet E.] Arizona State Univ, Phoenix, AZ USA. RP Whalon, KJ (reprint author), Coll William & Mary, POB 8795, Williamsburg, VA 23187 USA. EM kjwhal@wm.edu CR Calhoon JA, 2001, J AUTISM DEV DISORD, V31, P491, DOI 10.1023/A:1012268909286 Chiang H., 2007, FOCUS AUTISM OTHER D, V22, P259, DOI DOI 10.1177/10883576070220040801 Corbin Juliet, 2007, BASICS QUALITATIVE R, Vthird GRISWOLD E, 2002, FOCUS AUTISM OTHER D, V17, P94 Hart JE, 2008, INTERV SCH CLIN, V44, P116, DOI 10.1177/1053451207310346 Mayes S. 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PD MAY-JUN PY 2011 VL 32 IS 3 BP 243 EP 255 DI 10.1177/0741932510362174 PG 13 WC Education, Special SC Education & Educational Research GA 754LN UT WOS:000289856200006 ER PT J AU Campolo, D Taffoni, F Formica, D Schiavone, G Keller, F Guglielmelli, E AF Campolo, Domenico Taffoni, Fabrizio Formica, Domenico Schiavone, Giuseppina Keller, Flavio Guglielmelli, Eugenio TI Inertial-Magnetic Sensors for Assessing Spatial Cognition in Infants SO IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING LA English DT Article DE Ecological assessment; instrumented toys; infield calibration; neurodevelopmental engineering ID EARLY-DIAGNOSIS; ACCELEROMETERS; CALIBRATION; MOVEMENT; AUTISM AB This letter describes a novel approach to the assessment of spatial cognition in children. In particular, we present a wireless instrumented toy embedding magneto-inertial sensors for orientation tracking, specifically developed to assess the ability to insert objects into holes. To be used in naturalistic environments (e. g., day cares), we also describe an in-field calibration procedure based on a sequence of manual rotations, not relying on accurate motions or sophisticated equipment. The final accuracy of the proposed system, after the mentioned calibration procedure, is derived by direct comparison with a gold-standard motion tracking device. In particular, both systems are subjected to a sequence of ten single-axis rotations (approximately 90 degrees, back and forth), about three different axes. The rms of the angular error between the two measurements (gold-standard versus proposed systems) was evaluated for each trial. In particular, the average rms error is under 2.. This study indicates that a technological approach to ecological assessment of spatial cognition in infants is indeed feasible. As a consequence, prevention through screening of large number of infants is at reach. C1 [Campolo, Domenico] Nanyang Technol Univ, Sch Mech & Aerosp Engn, Singapore 639798, Singapore. [Taffoni, Fabrizio; Formica, Domenico; Guglielmelli, Eugenio] Univ Campus Biomed, Biomed Robot & Biomicrosyst Lab, I-00128 Rome, Italy. [Schiavone, Giuseppina] European Space Agcy, Adv Concepts Team, NL-2200 AG Noordwijk, Netherlands. [Keller, Flavio] Univ Campus Biomed, Lab Dev Neurosci, I-00128 Rome, Italy. RP Campolo, D (reprint author), Nanyang Technol Univ, Sch Mech & Aerosp Engn, Singapore 639798, Singapore. EM d.campolo@ntu.edu.sg; f.taffoni@unicampus.it; D.Formica@unicampus.it; G.Schiavone@unicampus.it; F.Keller@unicampus.it; e.guglielmelli@unicampus.it RI Formica, Domenico/G-9403-2011; Campolo, Domenico/G-5648-2010 FU European Union [FP6-NEST/ADVENTURE, 015636, ICT-2007.3.2-231722-IM-CLeVeR]; Academic Research Fund (AcRF) [Tier1 (RG 40/09)]; Ministry of Education, Singapore FX Manuscript received October 10, 2010; revised December 7, 2010; accepted December 15, 2010. Date of publication January 13, 2011; date of current version April 20, 2011. This work was supported in part by the European Union, FP6-NEST/ADVENTURE program, under Contract 015636, in part by the FP7ICT project under Grant ICT-2007.3.2-231722-IM-CLeVeR, and in part by the Academic Research Fund (AcRF) Tier1 (RG 40/09), Ministry of Education, Singapore. Asterisk indicates corresponding author. 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Child Neurol. PD MAY PY 2011 VL 26 IS 5 BP 540 EP 547 DI 10.1177/0883073810384869 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 756YX UT WOS:000290051800001 PM 21421903 ER PT J AU Xi, CY Lu, Y Tan, YH Hua, TY Zhao, YJ Liu, XM Gao, H AF Xi, Chun-Yan Lu, Yao Tan, Ying-Hua Hua, Tian-Yi Zhao, Yun-Jing Liu, Xiao-Mei Gao, Hong TI Analysis of MECP2 Gene Copy Number in Boys With Autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE autism; MECP2 gene; duplication ID CPG-BINDING PROTEIN-2; RETT-SYNDROME; DUPLICATION SYNDROME; MENTAL-RETARDATION; DEVELOPMENTAL REGRESSION; RECURRENT INFECTIONS; SPECTRUM DISORDERS; QUANTITATIVE PCR; MUTATIONS; REGION AB Autism is a severe neurodevelopmental disorder with a strong genetic basis. The methyl-CpG binding protein 2 gene (MECP2) is a dosage-sensitive gene in brain development and has been implicated as a candidate gene for autism. 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[Liu, Xiao-Mei; Gao, Hong] China Med Univ, Shengjing Hosp, Cent Lab, Shenyang, Peoples R China. RP Xi, CY (reprint author), China Med Univ, Shengjing Hosp, Dept Dev Pediat, 36 Sanhao St, Shenyang 110004, Peoples R China. EM xichy2006@yahoo.com.cn FU National Natural Science Foundation of China [30872802]; Educational Foundation of Liaoning Province, China [2008816] 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 National Natural Science Foundation of China (Grant number: 30872802) and Educational Foundation of Liaoning Province, China (Grant number: 2008816). 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We evaluated the prevalence of an abnormal head circumference in children with autism in Israel and compared it with the head circumferences of children with developmental language disorder and children with normal development. We did not find a higher prevalence of macrocephaly among Israeli children with autism spectrum disorder (4.4%). Although children with autism spectrum disorder had a significantly higher rate of a head circumference above the 75th percentile compared with children with developmental language disorder, it was not significantly different compared with normal controls. We conclude that there is no increased prevalence of macrocephaly in Israeli children with autism; this can be attributed to a different genetic background. C1 [Davidovitch, Michael; Golan, Dafna; Vardi, Orna] Child Dev Ctr, Jerusalem, Israel. [Lev, Dorit] Wolfson Med Ctr, Genet Inst, Holon, Israel. [Lerman-Sagie, Tally] Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. 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Child Neurol. PD MAY PY 2011 VL 26 IS 5 BP 580 EP 585 DI 10.1177/0883073810387666 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 756YX UT WOS:000290051800007 PM 21464237 ER PT J AU Barrow, WJ Jaworski, M Accardo, PJ AF Barrow, William J. Jaworski, Margie Accardo, Pasquale J. TI Persistent Toe Walking in Autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE autism; toe walking; language disorders; communication disorders; Asperger syndrome AB The records of 954 ambulatory children presenting for initial evaluation to a university developmental pediatrician were reviewed for the prevalence of persistent toe walking and associated tight heel cords. The incidence of persistent toe walking (20.1%) and tight heel cords (12.0%) were found to be higher in 324 children with an autistic spectrum disorder but lower (10.0%/3.0%) in 30 children with Asperger syndrome. These results confirm the previously reported high incidence of toe walking in children with autism and with language disorders and also raise the possibility of a secondary orthopedic deformity that can complicate long-term management of these patients. C1 [Accardo, Pasquale J.] Virginia Commonwealth Univ, Child Dev Clin, Richmond, VA USA. RP Accardo, PJ (reprint author), Virginia Commonwealth Univ, Child Dev Clin, 3600 W Broadway, Richmond, VA USA. 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PD MAY PY 2011 VL 26 IS 5 BP 619 EP 621 DI 10.1177/0883073810385344 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 756YX UT WOS:000290051800012 PM 21285033 ER PT J AU Marks, H Goldenthal, M Valencia, I Legido, A Ezugha, H Anderson, CE AF Marks, Harold Goldenthal, Michael Valencia, Ignacio Legido, Agustin Ezugha, Herbert Anderson, Carol E. TI Response to Correspondence on "5q14.3 Deletion Manifesting as Mitochondrial Disease and Autism: Case Report" SO JOURNAL OF CHILD NEUROLOGY LA English DT Letter C1 [Marks, Harold; Goldenthal, Michael; Valencia, Ignacio; Legido, Agustin; Ezugha, Herbert] St Christophers Hosp Children, Neurol Sect, Philadelphia, PA 19133 USA. [Anderson, Carol E.] St Christophers Hosp Children, Dept Pediat, Philadelphia, PA 19133 USA. RP Marks, H (reprint author), St Christophers Hosp Children, Neurol Sect, Philadelphia, PA 19133 USA. CR Castro-Gago M, 2006, PEDIATR NEUROL, V34, P204, DOI 10.1016/j.pediatrneurol.2005.07.011 Ezugha H, 2010, J CHILD NEUROL, V25, P1232, DOI 10.1177/0883073809361165 Filipek PA, 2003, ANN NEUROL, V53, P801, DOI 10.1002/ana.10596 NR 3 TC 0 Z9 0 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 MAY PY 2011 VL 26 IS 5 BP 660 EP 661 DI 10.1177/0883073811404069 PG 2 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 756YX UT WOS:000290051800026 ER PT J AU Frankel, FD Gorospe, CM Chang, YC Sugar, CA AF Frankel, Frederick D. Gorospe, Clarissa M. Chang, Ya-Chih Sugar, Catherine A. TI Mothers' reports of play dates and observation of school playground behavior of children having high-functioning autism spectrum disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Social skills; autism; Asperger's disorder; friendship ID COMPETENCE; PEER; FRIENDSHIP; RATINGS; ADOLESCENCE; INITIATIONS; PARENTS; TEACHER AB Background: Children with high-functioning autism spectrum disorders (ASD) are generally included with typically developing peers at school. They have difficulties interacting with peers on the school playground. Previous literature suggests that having play dates in the home may be related to better peer acceptance at school. Methods: This study examines the relationship between mother-reported play date frequency and amount of conflict, and peer interaction observed on the school playground for a sample of 27 boys and 4 girls meeting structured interview and observation criteria for ASD. Measures of intellectual functioning, adaptive behavior, and social skills were included in a stepwise regression analysis to account for their impact on relationships between maternal play date reports, general peer acceptance at school (as rated by the child's teacher) and observations of school playground behavior. Results: Results revealed that children with autism spectrum disorders who had more play dates in their home tended to spend a greater amount of time engaged in behaviors such as mutual offering of objects, conversing and other turn-taking activities with peers on the school playground. They also received more positive responses to their overtures from peers. These relationships remained highly significant even after accounting for other demographic, general social, and cognitive variables. Conclusions: The present results suggest that play date frequency is strongly related to school playground behavior. Owing to the design of this study, future research must assess whether play dates in the home promote better peer relationships on the playground or the reverse. In either case, the assessment of play dates, as well as observation of spontaneous unsupervised social interactions, are important outcome measures to consider in social skills interventions for children with high-functioning ASD. C1 [Frankel, Frederick D.; Gorospe, Clarissa M.; Chang, Ya-Chih; Sugar, Catherine A.] Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Los Angeles, CA USA. RP Frankel, FD (reprint author), 300 UCLA Med Plaza, Los Angeles, CA 90095 USA. EM ffrankel@ucla.edu FU National Institute of Mental Health [U54 MH68172]; NICHD; NIDCD; NINDS; Marian Sigman; STAART Center FX This research was supported by NIH Research Grant U54 MH68172 funded by the National Institute of Mental Health, NICHD, NIDCD and NINDS, Marian Sigman, STAART Center Program Principal Investigator and Fred Frankel, Project Principal Investigator. The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the NIH. The authors gratefully acknowledge the invaluable assistance of Pegeen Cronin, Ph.D. and staff of the UCLA Center for Autism Research and Treatment evaluation core. The authors are also indebted to Connie Kasari, Ph.D. and her staff for training study observers on the playground behavior codes. CR Baker J. E., 2003, SOCIAL SKILLS TRAINI Bauminger N, 2008, J AUTISM DEV DISORD, V38, P1211, DOI 10.1007/s10803-007-0501-2 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Baxter A., 1997, J DEV DISABILITIES, V5, P112 BUHRMESTER D, 1990, CHILD DEV, V61, P1101, DOI 10.1111/j.1467-8624.1990.tb02844.x BURACK JA, 1997, AUTISM PERVASIVE DEV, P796 CAPPS L, 1995, DEV PSYCHOPATHOL, V7, P137 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 FRANKEL F, 2010, FRIENDS FOREVER PARE Frankel F, 2010, MEASURING QUAL UNPUB Frankel F., 2003, CHILDRENS FRIENDSHIP FRANKEL F, 2010, J AUTISM DE IN PRESS GOTTMAN JM, 1983, MONOGRAPH SOC RES CH, V48 Gresham F. M., 1990, SOCIAL SKILLS RATING Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hollingshead A. A., 1975, 4 FACTOR INDEX UNPUB KASARI C, 2010, PLAYGROUND OBS UNPUB Koegel RL, 2005, RES PRACT PERS SEV D, V30, P93, DOI 10.2511/rpsd.30.2.93 LAGRECA AM, 1981, J ABNORM CHILD PSYCH, V9, P167 Ladd G. 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TI TPH2 G/T polymorphism is associated with hyperphagia, IQ, and internalizing problems in Prader-Willi syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Behavior problems; genetics; intelligence; internalizing disorder; neurochemistry; Prader-Willi syndrome ID TRYPTOPHAN HYDROXYLASE-2 GENE; TRANSMISSION DISEQUILIBRIUM; SLEEP DISTURBANCE; STROOP TASK; DISORDER; VARIANTS; CHILDREN; AUTISM; EPIDEMIOLOGY; DEPRESSION AB Background: Prader-Willi syndrome (PWS) is a genetic, neurodevelopmental disorder characterized by intellectual disabilities, growth hormone dysregulation, hyperphagia, increased risks of morbid obesity, compulsive behaviors, and irritability. As aberrant serotonergic functioning is strongly implicated in PWS, we examined associations between the PWS phenotype and polymorphisms in tryptophan hydroxylase 2 (TPH2), the rate-limiting enzyme in the biosynthesis of serotonin in the brain. Methods: Ninety-two individuals with PWS aged 4 to 50 years (M = 21.97) were genotyped for the TPH2 G703-T polymorphism. IQ testing was conducted in offspring, and parents completed questionnaires that tapped their child's compulsivity, hyperphagia, and other behavior problems. Results: As expected, the frequency of G/T or T/T polymorphisms in participants with PWS (39%) was similar to rates found in the general population (38%). Compared to those with a homozygous (G/G) genotype, individuals with a T allele had significantly higher hyperphagic behavior, drive, and severity scores, and they also had a younger age of onset of hyperphagia. Those with a T allele also had higher IQ scores than their counterparts. Females with a T allele had significantly higher internalizing symptoms, primarily anxiety and depression, than all others. Conclusions: TPH2 G/T polymorphisms, and presumed loss of enzyme function, were associated with specific aspects of the PWS phenotype. Aberrant serotonergic functioning is strongly implicated in hyperphagia in PWS, and females with TPH2 T alleles may be at higher risk for affective or mood disorders. Findings hold promise for examining other serotonin-altering genes in PWS, and for future serotonin-altering treatment trials. C1 [Dykens, Elisabeth M.; Roof, Elizabeth] Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, Dept Psychol & Human Dev, Nashville, TN 37203 USA. [Dykens, Elisabeth M.] Vanderbilt Univ, Dept Psychiat, Nashville, TN 37203 USA. [Dykens, Elisabeth M.; Roof, Elizabeth] Vanderbilt Univ, Dept Pediat, Nashville, TN 37203 USA. [Bittel, Douglas] Childrens Mercy Hosp, Kansas City, MO 64108 USA. [Bittel, Douglas] Univ Missouri, Kansas City Sch Med, Dept Pediat, Kansas City, MO 64110 USA. [Butler, Merlin G.] Univ Kansas, Med Ctr, Dept Psychiat & Behav Sci, Kansas City, KS 66103 USA. [Butler, Merlin G.] Univ Kansas, Med Ctr, Dept Pediat, Kansas City, KS 66103 USA. RP Dykens, EM (reprint author), Vanderbilt Univ, Vanderbilt Kennedy Ctr, 230 Appleton Pl,Peabody Box 40, Nashville, TN 37203 USA. EM elisabeth.dykens@vanderbilt.edu FU NICHD Rare Disease Consortium [U54 HD061222]; Prader-Willi Syndrome Associations (USA); Vanderbilt CTSA (Vanderbilt Institute for Clinical and Translational Research); NICHD [R01HD035684, P30HD015052] FX The authors are grateful to the families and individuals with Prader-Willi syndrome who participated in the study. This work was supported by NICHD Rare Disease Consortium Grant U54 HD061222 (Dykens and Butler), the Prader-Willi Syndrome Associations (USA) (Dykens and Butler), the Vanderbilt CTSA (Vanderbilt Institute for Clinical and Translational Research), and NICHD Grants R01HD035684 (Dykens) and P30HD015052 (Dykens). 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Child Psychol. Psychiatry PD MAY PY 2011 VL 52 IS 5 BP 580 EP 587 DI 10.1111/j.1469-7610.2011.02365.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 751PZ UT WOS:000289631400010 PM 21418060 ER PT J AU Paul, R Fuerst, Y Ramsay, G Chawarska, K Klin, A AF Paul, Rhea Fuerst, Yael Ramsay, Gordon Chawarska, Kasia Klin, Ami TI Out of the mouths of babes: vocal production in infant siblings of children with ASD SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Autism; speech; vocalization; infant siblings ID AUTISM SPECTRUM DISORDERS; PERVASIVE DEVELOPMENTAL DISORDERS; EARLY LEXICAL ACQUISITION; PHONOLOGICAL DEVELOPMENT; 2ND YEAR; INDIVIDUAL-DIFFERENCES; FAMILIAL AGGREGATION; BROADER PHENOTYPE; FOLLOW-UP; LANGUAGE AB Background: Younger siblings of children with autism spectrum disorders (ASD) are at higher risk for acquiring these disorders than the general population. Language development is usually delayed in children with ASD. The present study examines the development of pre-speech vocal behavior in infants at risk for ASD due to the presence of an older sibling with the disorder. Methods: Infants at high risk (HR) for ASD and those at low risk, without a diagnosed sibling (LR), were seen at 6, 9, and 12 months as part of a larger prospective study of risk for ASD in infant siblings. Standard clinical assessments were administered, and vocalization samples were collected during play with mother and a standard set of toys. Infant vocal behavior was recorded and analyzed for consonant inventory, presence of canonical syllables, and of non-speech vocalizations, in a cross-sectional design. Children were seen again at 24 months for provisional diagnosis. Results: Differences were seen between risk groups for certain vocal behaviors. Differences in vocal production in the first year of life were associated with outcomes in terms of autistic symptomotology in the second year. Conclusions: Early vocal behavior is a sensitive indicator of heightened risk for autistic symptoms in infants with a family history of ASD. C1 [Paul, Rhea] Yale Child Study Ctr, Commun Disorders Sect, New Haven, CT 06510 USA. [Fuerst, Yael] So Connecticut State Univ, New Haven, CT 06515 USA. [Ramsay, Gordon] Haskins Labs Inc, New Haven, CT 06511 USA. RP Paul, R (reprint author), Yale Child Study Ctr, Commun Disorders Sect, 40 Temple St 6B, New Haven, CT 06510 USA. EM rhea.paul@yale.edu FU NIMH Autism Center of Excellence [P50 MH81756]; National Institute of Mental Health (NIMH) [P01-03008]; NIDCD [K24 HD045576]; Simons Foundation FX Preparation of this paper was supported by NIMH Autism Center of Excellence grant P50 MH81756; Research Grant P01-03008 funded by the National Institute of Mental Health (NIMH); MidCareer Development Award K24 HD045576 funded by NIDCD to Rhea Paul; as well as by the Simons Foundation. We wish to thank the families who participated in this research. 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Child Psychol. Psychiatry PD MAY PY 2011 VL 52 IS 5 BP 588 EP 598 DI 10.1111/j.1469-7610.2010.02332.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 751PZ UT WOS:000289631400011 PM 21039489 ER PT J AU Zhu, HP Sun, YR Zeng, JH Sun, HY AF Zhu, Huaping Sun, Yaoru Zeng, Jinhua Sun, Hongyu TI Mirror neural training induced by virtual reality in brain-computer interfaces may provide a promising approach for the autism therapy SO MEDICAL HYPOTHESES LA English DT Article ID SPECTRUM DISORDERS; SYSTEM; INTENTIONS; CHILDREN AB Previous studies have suggested that the dysfunction of the human mirror neuron system (hMNS) plays an important role in the autism spectrum disorder (ASD). In this work, we propose a novel training program from our interdisciplinary research to improve mirror neuron functions of autistic individuals by using a BCI system with virtual reality technology. It is a promising approach for the autism to learn and develop social communications in a VR environment. A test method for this hypothesis is also provided. (C) 2011 Elsevier Ltd. All rights reserved. C1 [Zhu, Huaping; Sun, Yaoru; Zeng, Jinhua; Sun, Hongyu] Tongji Univ, Dept Comp Sci & Technol, Shanghai 200092, Peoples R China. RP Sun, YR (reprint author), Tongji Univ, Dept Comp Sci & Technol, CaoAn Rd 4800, Shanghai 200092, Peoples R China. EM 8zhuhuaping@tongji.edu.cn; yaoru@tongji.edu.cn; Omrzeng@tongji.edu.cn; 6hongyusun@tongji.edu.cn FU National Natural Science Foundation of China [60775019, 60970062]; Shanghai Pujiang Program [09PJ1410200]; Science and Technology Commission of Shanghai Municipality [09511502500] FX This work was supported by the Grants from the National Natural Science Foundation of China (60775019 and 60970062); the Shanghai Pujiang Program (09PJ1410200) and the Science and Technology Commission of Shanghai Municipality (09511502500). 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Hypotheses PD MAY PY 2011 VL 76 IS 5 BP 646 EP 647 DI 10.1016/j.mehy.2011.01.022 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 757KT UT WOS:000290084600010 PM 21300442 ER PT J AU King, CR AF King, Chiara R. TI A novel embryological theory of autism causation involving endogenous biochemicals capable of initiating cellular gene transcription: A possible link between twelve autism risk factors and the autism 'epidemic' SO MEDICAL HYPOTHESES LA English DT Article ID NEURAL-TUBE DEFECTS; PERICONCEPTIONAL VITAMIN SUPPLEMENTATION; PERVASIVE DEVELOPMENTAL DISORDERS; CENTRAL-NERVOUS-SYSTEM; HERPES-SIMPLEX-VIRUS; ALPHA-FETOPROTEIN; RETINOIC ACID; SPECTRUM DISORDERS; VALPROIC ACID; FOLIC-ACID AB Human alpha-fetoprotein is a pregnancy-associated protein with an undetermined physiological role. As human alpha-fetoprotein binds retinoids and inhibits estrogen-dependent cancer cell proliferation, and because retinoic acid (a retinol metabolite) and estradiol (an estrogen) can both initiate cellular gene transcription, it is hypothesized here that alpha-fetoprotein functions during critical gestational periods to prevent retinoic acid and maternal estradiol from inappropriately stimulating gene expression in developing brain regions which are sensitive to these chemicals. Prenatal/maternal factors linked to increased autism risk include valproic acid, thalidomide, alcohol, rubella, cytomegalovirus, depression, schizophrenia, obsessive-compulsive disorder, autoimmune disease, stress, allergic reaction, and hypothyroidism. It will be shown how each of these risk factors may initiate expression of genes which are sensitive to retinoic acid and/or estradiol - whether by direct promotion or by reducing production of alpha-fetoprotein. It is thus hypothesized here that autism is not a genetic disorder, but is rather an epigenetic disruption in brain development caused by gestational exposure to chemicals and/or conditions which either inhibit alpha-fetoprotein production or directly promote retinoic acid-sensitive or estradiol-sensitive gene expression. This causation model leads to potential chemical explanations for autistic brain morphology, the distinct symptomatology of Asperger's syndrome, and the differences between high-functioning and low-functioning autisms with regard to mental retardation, physical malformation, and sex ratio. It will be discussed how folic acid may cause autism under the retinoic acid/estradiol model, and the history of prenatal folic acid supplementation will be shown to coincide with the history of what is popularly known as the autism epidemic. It is thus hypothesized here that prenatal folic acid supplementation has contributed to the post-1980 increase in US autism diagnoses. 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Hypotheses PD MAY PY 2011 VL 76 IS 5 BP 653 EP 660 DI 10.1016/j.mehy.2011.01.024 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 757KT UT WOS:000290084600012 PM 21388746 ER PT J AU Nickl-Jockschat, T Michel, TM AF Nickl-Jockschat, T. Michel, T. M. TI The role of neurotrophic factors in autism SO MOLECULAR PSYCHIATRY LA English DT Review DE autism; autism spectrum disorders; BDNF; genes; neurotrophic factors; NT-3 ID NERVE-GROWTH-FACTOR; HIGH-FUNCTIONING AUTISM; BDNF VAL66MET POLYMORPHISM; COMT VAL(158)MET GENOTYPE; LONG-TERM POTENTIATION; DECREASED SERUM-LEVELS; 1ST 3 YEARS; SPECTRUM DISORDER; RETT-SYNDROME; INFANTILE-AUTISM AB Autism spectrum disorders (ASDs) are pervasive developmental disorders that frequently involve a triad of deficits in social skills, communication and language. For the underlying neurobiology of these symptoms, disturbances in neuronal development and synaptic plasticity have been discussed. The physiological development, regulation and survival of specific neuronal populations shaping neuronal plasticity require the so-called 'neurotrophic factors' (NTFs). These regulate cellular proliferation, migration, differentiation and integrity, which are also affected in ASD. Therefore, NTFs have gained increasing attention in ASD research. This review provides an overview and explores the key role of NTFs in the aetiology of ASD. We have also included evidence derived from neurochemical investigations, gene association studies and animal models. By focussing on the role of NTFs in ASD, we intend to further elucidate the puzzling aetiology of these conditions. Molecular Psychiatry (2011) 16, 478-490; doi: 10.1038/mp.2010.103; published online 12 October 2010 C1 [Nickl-Jockschat, T.; Michel, T. M.] Rhein Westfal TH Aachen, Dept Psychiat & Psychotherapy, D-52074 Aachen, Germany. 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Psychiatr. PD MAY PY 2011 VL 16 IS 5 BP 478 EP 490 DI 10.1038/mp.2010.103 PG 13 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 754UY UT WOS:000289884400004 PM 20938434 ER PT J AU Gressens, P Ferriero, DM AF Gressens, Pierre Ferriero, Donna M. TI 21st Century Research in Pediatric Psychiatry INTRODUCTION SO PEDIATRIC RESEARCH LA English DT Editorial Material ID DISORDERS; AUTISM; CHILD C1 [Gressens, Pierre] Hop Robert Debre, INSERM, U676, F-75019 Paris, France. [Gressens, Pierre] Univ London Imperial Coll Sci Technol & Med, Inst Reprod & Dev Biol, London W12 0NN, England. [Ferriero, Donna M.] Univ Calif San Francisco, Sch Med, Dept Pediat, San Francisco, CA 94143 USA. [Ferriero, Donna M.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. RP Gressens, P (reprint author), Hop Robert Debre, INSERM, U676, F-75019 Paris, France. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 1R EP 2R PN 2 PG 2 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100001 PM 21471777 ER PT J AU Johnson, S Marlow, N AF Johnson, Samantha Marlow, Neil TI Preterm Birth and Childhood Psychiatric Disorders SO PEDIATRIC RESEARCH LA English DT Article ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM SPECTRUM DISORDERS; PERINATAL RISK-FACTORS; CHILDREN BORN; WEIGHT INFANTS; BEHAVIORAL-PROBLEMS; SCHOOL-AGE; GESTATIONAL-AGE; FOLLOW-UP AB Epidemiologic studies have, for many years, identified preterm birth as a significant risk factor for psychiatric disorders. There has been a recent resurgence of interest in neurobehavioral outcomes after preterm birth. In this article, we review clinical cohort studies of the prevalence, etiology, and risk factors for psychiatric sequelae in ex-preterm children. Studies using diagnostic psychiatric evaluations are few in number but typically report a 3- to 4-fold increased risk for disorders in middle childhood. Our review of studies reveals a "preterm behavioral phenotype" characterized by an increased risk for symptoms and disorders associated with inattention, anxiety, and social difficulties. The most contemporary studies have also reported a markedly increased prevalence of autism spectrum disorders (ASD) in preterm populations. Our examination of the correlates and comorbidities of psychiatric disorders is indicative of a different causative pathway that may be associated with altered brain development after pretem birth. Despite the low population attributable risk, the frequency of these symptoms and disorders means that psychiatric screening is likely to be beneficial in this vulnerable population. (Pediatr Res 69: 11R-18R, 2011) C1 [Johnson, Samantha] Univ Leicester, Dept Hlth Sci, Leicester LE1 6TP, Leics, England. [Marlow, Neil] UCL, Inst Womens Hlth, London WC1E 6AU, England. RP Johnson, S (reprint author), Univ Leicester, Dept Hlth Sci, 22-28 Princess Rd W, Leicester LE1 6TP, Leics, England. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 11R EP 18R DI 10.1203/PDR.0b013e318212faa0 PN 2 PG 8 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100003 PM 21289534 ER PT J AU Frye, RE Rossignol, DA AF Frye, Richard E. Rossignol, Daniel A. TI Mitochondrial Dysfunction Can Connect the Diverse Medical Symptoms Associated With Autism Spectrum Disorders SO PEDIATRIC RESEARCH LA English DT Article ID NECROSIS-FACTOR-ALPHA; OXIDATIVE STRESS; PROPIONIC-ACID; RETT-SYNDROME; CYTOCHROME-C; MOUSE MODEL; CHILDREN; DISEASE; GLUTATHIONE; ABNORMALITIES AB Autism spectrum disorder (ASD) is a devastating neurodevelopmental disorder. Over the past decade, evidence has emerged that some children with ASD suffer from undiagnosed comorbid medical conditions. One of the medical disorders that has been consistently associated with ASD is mitochondrial dysfunction. Individuals with mitochondrial disorders without concomitant ASD manifest dysfunction in multiple high-energy organ systems, such as the central nervous, muscular, and gastrointestinal (GI) systems. Interestingly, these are the identical organ systems affected in a significant number of children with ASD. This finding increases the possibility that mitochondrial dysfunction may be one of the keys that explains the many diverse symptoms observed in some children with ASD. This article will review the importance of mitochondria in human health and disease, the evidence for mitochondrial dysfunction in ASD, the potential role of mitochondrial dysfunction in the comorbid medical conditions associated with ASD, and how mitochondrial dysfunction can bridge the gap for understanding how these seemingly disparate medical conditions are related. We also review the limitations of this evidence and other possible explanations for these findings. This new understanding of ASD should provide researchers a pathway for understanding the etiopathogenesis of ASD and clinicians the potential to develop medical therapies. (Pediatr Res 69: 41R-47R, 2011) C1 [Frye, Richard E.] Univ Texas Hlth Sci Ctr Houston, Childrens Learning Inst, Dept Pediat, Houston, TX 77030 USA. [Rossignol, Daniel A.] Int Child Dev Resource Ctr, Melbourne, FL 32934 USA. RP Frye, RE (reprint author), 7000 Fannin,UCT 2478, Houston, TX 77030 USA. EM richard.e.frye@uth.tmc.edu FU National Institute of Neurological Disorders and Stroke (NINDS) [K23NS046565]; Jane Botsford Johnson Foundation FX Supported, in part, by the National Institute of Neurological Disorders and Stroke (NINDS), Grant K23NS046565, and the Jane Botsford Johnson Foundation. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 41R EP 47R DI 10.1203/PDR.0b013e318212f16b PN 2 PG 7 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100007 PM 21289536 ER PT J AU Marco, EJ Hinkley, LBN Hill, SS Nagarajan, SS AF Marco, Elysa J. Hinkley, Leighton B. N. Hill, Susanna S. Nagarajan, Srikantan S. TI Sensory Processing in Autism: A Review of Neurophysiologic Findings SO PEDIATRIC RESEARCH LA English DT Review ID EVENT-RELATED POTENTIALS; BRAIN-STEM RESPONSES; NON-SPEECH SOUNDS; SPECTRUM DISORDERS; MULTISENSORY INTEGRATION; CONTRAST SENSITIVITY; SELECTIVE ATTENTION; MISMATCH NEGATIVITY; TACTILE SENSITIVITY; TYPICAL DEVELOPMENT AB Atypical sensory-based behaviors are a ubiquitous feature of autism spectrum disorders (ASDs). In this article, we review the neural underpinnings of sensory processing in autism by reviewing the literature on neurophysiological responses to auditory, tactile, and visual stimuli in autistic individuals. We review studies of unimodal sensory processing and multisensory integration that use a variety of neuroimaging techniques, including electroencephalography (EEG), magnetoencephalography (MEG), and functional MRI. We then explore the impact of covert and overt attention on sensory processing. With additional characterization, neurophysiologic profiles of sensory processing in ASD may serve as valuable biomarkers for diagnosis and monitoring of therapeutic interventions for autism and reveal potential strategies and target brain regions for therapeutic interventions. (Pediatr Res 69: 48R-54R, 2011) C1 [Marco, Elysa J.; Hill, Susanna S.] Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. [Marco, Elysa J.] Univ Calif San Francisco, Dept Psychiat, San Francisco, CA 94143 USA. [Marco, Elysa J.] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. [Hinkley, Leighton B. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 48R EP 54R DI 10.1203/PDR.0b013e3182130c54 PN 2 PG 7 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100008 PM 21289533 ER PT J AU Constantino, JN AF Constantino, John N. TI The Quantitative Nature of Autistic Social Impairment SO PEDIATRIC RESEARCH LA English DT Article ID SPECTRUM DISORDERS; LANGUAGE IMPAIRMENT; GENERAL-POPULATION; RECURRENT REARRANGEMENTS; HIRSCHSPRUNG DISEASE; MULTIPLE-INCIDENCE; CHILDREN; TRAITS; PHENOTYPE; FAMILIES AB Autism, like intellectual disability, represents the severe end of a continuous distribution of developmental impairments that occur in nature, that are highly inherited, and that are orthogonally related to other parameters of development. A paradigm shift in understanding the core social abnormality of autism as a quantitative trait rather than as a categorically defined condition has key implications for diagnostic classification, the measurement of change over time, the search for underlying genetic and neurobiologic mechanisms, and public health efforts to identify and support affected children. Here, a recent body of research in genetics and epidemiology is presented to examine a dimensional reconceptualization of autistic social impairment as manifested in clinical autistic syndromes, the broader autism phenotype, and normal variation in the general population. It illustrates how traditional categorical approaches to diagnosis may lead to misclassification of subjects (especially girls and mildly affected boys in multiple-incidence autism families), which can be particularly damaging to biological studies and proposes continued efforts to derive a standardized quantitative system by which to characterize this family of conditions. (Pediatr Res 69: 55R-62R, 2011) C1 [Constantino, John N.] Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. [Constantino, John N.] Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid Ave,CB 8134, St Louis, MO 63110 USA. EM constantino@wustl.edu FU National Institute of Child Health and Human Development [HD42541] FX Supported by a Grant from the National Institute of Child Health and Human Development (HD42541) [J.N.C.]. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 55R EP 62R DI 10.1203/PDR.0b013e318212ec6e PN 2 PG 8 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100009 PM 21289537 ER PT J AU Chen, R Jiao, Y Herskovits, EH AF Chen, Rong Jiao, Yun Herskovits, Edward H. TI Structural MRI in Autism Spectrum Disorder SO PEDIATRIC RESEARCH LA English DT Article ID VOXEL-BASED MORPHOMETRY; HIGH-FUNCTIONING AUTISM; CORPUS-CALLOSUM; WHITE-MATTER; CORTICAL THICKNESS; PRESCHOOL-CHILDREN; ASPERGERS-SYNDROME; BRAIN STRUCTURE; DIFFUSION; ABNORMALITIES AB Magnetic resonance (MR) examination provides a powerful tool for investigating brain structural changes in children with autism spectrum disorder (ASD). We review recent advances in the understanding of structural MR correlates of ASD. We summarize findings from studies based on voxel-based morphometry, surface-based morphometry, tensor-based morphometry, and diffusion-tensor imaging. Finally, we discuss diagnostic models of ASD based on MR-derived features. (Pediatr Res 69: 63R-68R, 2011) C1 [Chen, Rong] Univ Penn, Dept Radiol, Ctr Sci, Philadelphia, PA 19104 USA. RP Chen, R (reprint author), Univ Penn, Dept Radiol, Ctr Sci, 3600 Market St, Philadelphia, PA 19104 USA. EM rong.chen@uphs.upenn.edu FU National Institute of Aging [R01 AG13743]; National Institute of Mental Health; National Cancer Institute; NIH [R03 EB009310]; University of Pennsylvania; China Scholarship Council [2008101370]; National Natural Science foundation of China [30570655]; Scientific Research Foundation of Graduate School of Southeast University [YBJJ1011] FX R.C. and E.H.H. are supported by National Institutes of Health Grant R01 AG13743, which is funded by the National Institute of Aging. the National Institute of Mental Health, and the National Cancer Institute. They are also supported by NIH R03 EB009310. R.C. is supported by Institute for the Translational Medicine and Therapeutics fellowship of University of Pennsylvania. Y.J. is supported by the China Scholarship Council (Project number 2008101370), the National Natural Science foundation of China (Project number 30570655). and the Scientific Research Foundation of Graduate School of Southeast University (YBJJ1011). 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The processes of social cognition are also supported by reward circuitry, underpinned by the dopaminergic neurotransmitter system. Reward processes build social relationships, in parenting and pair-bonding, and influence social interactions that require trust, or display altruism. The impact of emotional regulation upon social behavior, including mood and anxiety, is also mediated through the serotonergic system. Variation in activity of serotonergic networks in the brain influences emotional responsivity, including subjective feelings, physiological responses, emotional expressions, and the tendency to become engaged in action as a consequence of a feeling state. Genetic variation in the receptors associated with OT. AVP, dopamine, and serotonin has been intensively studied in humans and animal models. Recent findings are building an increasingly coherent picture of regulatory mechanisms. (Pediatr Res 69: 85R-91R, 2011) C1 [Skuse, David H.] UCL, Inst Child Hlth, Dept Behav & Brain Sci, London WC1N 1EH, England. [Gallagher, Louise] St James Hosp, Trinity Coll Dublin, Trinity Ctr Hlth Sci, Dublin 8, Ireland. RP Skuse, DH (reprint author), UCL, Inst Child Hlth, Dept Behav & Brain Sci, London WC1N 1EH, England. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 85R EP 91R DI 10.1203/PDR.0b013e318212f562 PN 2 PG 7 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100013 PM 21289535 ER PT J AU Zahir, FR Brown, CJ AF Zahir, Farah R. Brown, Carolyn J. TI Epigenetic Impacts on Neurodevelopment: Pathophysiological Mechanisms and Genetic Modes of Action SO PEDIATRIC RESEARCH LA English DT Article ID RUBINSTEIN-TAYBI-SYNDROME; DNA METHYLATION; MENTAL-RETARDATION; HEAD CIRCUMFERENCE; MOLECULAR CHARACTERIZATION; HISTONE MODIFICATIONS; DEVELOPMENTAL DELAY; EMBRYONIC LETHALITY; CHROMOSOME 16P13.3; NERVOUS-SYSTEM AB Disruptions of genes that are involved in epigenetic functions are known to be causative for several mental retardation/intellectual disability (MR/ID) syndromes. Recent work has highlighted genes with epigenetic functions as being implicated in autism spectrum disorders (ASDs) and schizophrenia. (SCZ). The gene-environment interaction is an important factor of pathogenicity for these complex disorders. Epigenetic modifications offer a mechanism by which we can explain how the environment interacts with, and is able to dynamically regulate, the genome. This review aims to provide an overview of the role of epigenetic deregulation in the etiopathology for neurodevelopment disease. (Pediatr Res 69: 92R-100R, 2011) C1 [Zahir, Farah R.; Brown, Carolyn J.] Univ British Columbia, Dept Med Genet, Vancouver, BC V6H 3N1, Canada. RP Zahir, FR (reprint author), Univ British Columbia, Med Genet Res Unit, Womens & Childrens Hosp, Box 153,4500 Oak St, Vancouver, BC V6H 3N1, Canada. EM farahz@interchange.ubc.ca RI feng, jian/G-9313-2011; Brown, Carolyn/A-5159-2014 OI Brown, Carolyn/0000-0002-8959-0101 FU Child and Family Research Institute, Vancouver, Canada FX F.R.Z. is supported by a fellowship from the Child and Family Research Institute, Vancouver, Canada. 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Res. PD MAY PY 2011 VL 69 IS 5 BP 92R EP 100R DI 10.1203/PDR.0b013e318213565e PN 2 PG 9 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100014 PM 21293311 ER PT J AU Korkmaz, B AF Korkmaz, Bars TI Theory of Mind and Neurodevelopmental Disorders of Childhood SO PEDIATRIC RESEARCH LA English DT Article ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDER; SOCIAL COGNITIVE NEUROSCIENCE; EXECUTIVE FUNCTION; EMPATHIC ACCURACY; MENTAL STATES; INDIVIDUAL-DIFFERENCES; CONGENITAL BLINDNESS; ASPERGER-SYNDROME; YOUNG-CHILDREN AB To a large extent, the human infant is socialized through the acquisition of a specific cognitive mechanism known as theory of mind (ToM), a term which is currently used to explain a related set of intellectual abilities that enable us to understand that others have beliefs, desires, plans, hopes, information, and intentions that may differ from our own. Various neurodevelopmental disorders, such as autism spectrum disorders, attention deficit hyperactivity disorder, developmental language disorders, and schizophrenia, as well as acquired disorders of the right brain (and traumatic brain injury) impair ToM. ToM is a composite function, which involves memory, joint attention, complex perceptual recognition (such as face and gaze processing), language, executive functions (such as tracking of intentions and goals and moral reasoning), emotion processing-recognition, empathy, and imitation. Hence, ToM development is dependent on the maturation of several brain systems and is shaped by parenting, social relations, training, and education; thus, it is an example of the dense interaction that occurs between brain development and (social) environment. (Pediatr Res 69: 101R-108R, 2011) C1 Istanbul Univ, Cerrahpasa Med Fac, Dept Neurol, Div Child Neurol, TR-34301 Istanbul, Turkey. RP Korkmaz, B (reprint author), Istanbul Univ, Cerrahpasa Med Fac, Dept Neurol, Div Child Neurol, TR-34301 Istanbul, Turkey. 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PD MAY PY 2011 VL 69 IS 5 BP 101R EP 108R DI 10.1203/PDR.0b013e318212c177 PN 2 PG 8 WC Pediatrics SC Pediatrics GA 753WO UT WOS:000289811100015 PM 21289541 ER PT J AU Moskowitz, A Heim, G AF Moskowitz, Andrew Heim, Gerhard TI Eugen Bleuler's Dementia Praecox or the Group of Schizophrenias (1911): A Centenary Appreciation and Reconsideration SO SCHIZOPHRENIA BULLETIN LA English DT Article DE schizophrenia; Bleuler; dissociation ID PSYCHOTIC DISORDER; DIAGNOSIS; SYMPTOMS; DELUSIONS; MODEL AB On the 100th anniversary of the publication of Eugen Bleuler's Dementia Praecox or the Group of Schizophrenias, his teachings on schizophrenia from that seminal book are reviewed and reassessed, and implications for the current revision of the category of schizophrenia, with its emphasis on psychotic symptoms, drawn. Bleuler's methods are contrasted with Kraepelin's, and 4 myths about his concept of schizophrenia addressed. We demonstrate that (1) Bleuler's concept of schizophrenia has close ties to historical and contemporary concepts of dissociation and as such the public interpretation of schizophrenia as split personality has some historical basis; (2) Bleuler's concept of loosening of associations does not refer narrowly to a disorder of thought but broadly to a core organically based psychological deficit which underlies the other symptoms of schizophrenia; (3) the "4 A's," for association, affect, ambivalence, and autism, do not adequately summarize Bleuler's teachings on schizophrenia and marginalize the central role of splitting in his conception; and (4) Bleuler's ideas were more powerfully influenced by Pierre Janet, particularly with regard to his diagnostic category Psychasthenia, than by Sigmund Freud. We conclude that Bleuler's ideas on schizophrenia warrant reexamination in the light of current criticism of the emphasis on psychotic symptoms in the schizophrenia diagnosis and argue for the recognition of the dissociative roots of this most important psychiatric category. C1 [Moskowitz, Andrew] Aarhus Univ, Dept Psychol, Aarhus, Denmark. RP Moskowitz, A (reprint author), Aarhus Univ, Dept Psychol, Aarhus, Denmark. 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