1. Benson PR. {{Network Characteristics, Perceived Social Support, and Psychological Adjustment in Mothers of Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2012 (Apr 7)
This study examined the characteristics of the support networks of 106 mothers of children with ASD and their relationship to perceived social support, depressed mood, and subjective well-being. Using structural equation modeling, two competing sets of hypotheses were assessed: (1) that network characteristics would impact psychological adjustment directly, and (2) that network effects on adjustment would be indirect, mediated by perceived social support. Results primarily lent support to the latter hypotheses, with measures of network structure (network size) and function (proportion of network members providing emotional support) predicting increased levels of perceived social support which, in turn, predicted decreased depressed mood and increased well-being. Results also indicated that increased interpersonal strain in the maternal network was directly and indirectly associated with increased maternal depression, while being indirectly linked to reduced well-being. Study limitations and implications are discussed.
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2. Celestino-Soper PB, Skinner C, Schroer R, Eng P, Shenai J, Nowaczyk MM, Terespolsky D, Cushing D, Patel GS, Immken L, Willis A, Wiszniewska J, Matalon R, Rosenfeld JA, Stevenson RE, Kang SH, Cheung SW, Beaudet AL, Stankiewicz P. {{Deletions in chromosome 6p22.3-p24.3, including ATXN1, are associated with developmental delay and autism spectrum disorders}}. {Mol Cytogenet};2012 (Apr 5);5(1):17.
ABSTRACT: Interstitial deletions of the short arm of chromosome 6 are rare and have been associated with developmental delay, hypotonia, congenital anomalies, and dysmorphic features. We used array comparative genomic hybridization in a South Carolina Autism Project (SCAP) cohort of 97 subjects with autism spectrum disorders (ASDs) and identified an ~ 5.4 Mb deletion on chromosome 6p22.3-p23 in a 15-year-old patient with intellectual disability and ASDs. Subsequent database queries revealed five additional individuals with overlapping submicroscopic deletions and presenting with developmental and speech delay, seizures, behavioral abnormalities, heart defects, and dysmorphic features. The deletion found in the SCAP patient harbors ATXN1, DTNBP1, JARID2, and NHLRC1 that we propose may be responsible for ASDs and developmental delay.
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3. Gilgenkrantz S. {{[Autism, the untraceable gene: from science to business]}}. {Med Sci (Paris)};2012 (Mar);28(3):329-330.
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4. Lopez M, Schulz EG, Baroud T, Hudson A, Wilson M. {{The Arkansas Autism Developmental Disabilities Monitoring (AR ADDM) project: statewide autism surveillance in a rural state}}. {J Ark Med Soc};2012 (Mar);108(10):220, 222-224.
In 2002, the Arkansas Autism and Developmental Disabilities Monitoring (AR ADDM) project collected data on the number and characteristics of resident children aged 8 years using a retrospective record review standardized methodology. This paper provides a first-look epidemiology of ASDs among 8 year old Arkansas children using data from the 2002 study year. Overall prevalence estimates, demographic distribution and a temporal lag from concerns identified to diagnosis of ASDs among 8 year olds in Arkansas were similar to that in other sites. Dissemination of information that promotes timely resolution of developmental concerns and improving educational services will benefit children with autism in Arkansas.
5. Macari SL, Campbell D, Gengoux GW, Saulnier CA, Klin AJ, Chawarska K. {{Predicting Developmental Status from 12 to 24 Months in Infants at Risk for Autism Spectrum Disorder: A Preliminary Report}}. {J Autism Dev Disord};2012 (Apr 7)
The study examined whether performance profiles on individual items of the Toddler Module of the Autism Diagnostic Observation Schedule at 12 months are associated with developmental status at 24 months in infants at high and low risk for developing Autism Spectrum Disorder (ASD). A nonparametric decision-tree learning algorithm identified sets of 12-month predictors of developmental status at 24 months. Results suggest that identification of infants who are likely to exhibit symptoms of ASD at 24 months is complicated by variable patterns of symptom emergence. Fine-grained analyses linking specific profiles of strengths and deficits with specific patterns of symptom emergence will be necessary for further refinement of screening and diagnostic instruments for ASD in infancy.
