This study examined the effects of slowing down presentation of facial expressions and their corresponding vocal sounds on facial expression recognition and facial and/or vocal imitation in children with autism. Twelve autistic children and twenty-four normal control children were presented with emotional and non-emotional facial expressions on CD-Rom, under audio or silent conditions, and under dynamic visual conditions (slowly, very slowly, at normal speed) plus a static control. Overall, children with autism showed lower performance in expression recognition and more induced facial-vocal imitation than controls. In the autistic group, facial expression recognition and induced facial-vocal imitation were significantly enhanced in slow conditions. Findings may give new perspectives for understanding and intervention for verbal and emotional perceptive and communicative impairments in autistic populations.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s10803-006-0223-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Nr4a1 and Nr4a3 redundantly control clonal deletion and contribute to an anergy-like transcriptome in auto-reactive thymocytes to impose tolerance in mice.
Nat Commun
January 2025
Division of Rheumatology, Rosalind Russell and Ephraim P. Engleman Arthritis Research Center, Department of Medicine, University of California, San Francisco, CA, 94143, USA.
The Nr4a nuclear hormone receptors are transcriptionally upregulated in response to antigen recognition by the T cell receptor (TCR) in the thymus and are implicated in clonal deletion, but the mechanisms by which they operate are not clear. Moreover, their role in central tolerance is obscured by redundancy among the Nr4a family members and by their reported functions in Treg generation and maintenance. Here we take advantage of competitive bone marrow chimeras and the OT-II/RIPmOVA model to show that Nr4a1 and Nr4a3 are essential for the upregulation of Bcl2l11/BIM and thymic clonal deletion by self-antigen.
View Article and Find Full Text PDFOral administration of LEAP2 enhances immunity against Edwardsiella tarda through regulation of gut bacterial community and metabolite in mudskipper.
Fish Shellfish Immunol
January 2025
State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-Products, School of Marine Sciences, Ningbo University, Ningbo 315211, P.R. China; Laboratory of Biochemistry and Molecular Biology, School of Marine Sciences, Meishan Campus, Ningbo University, Ningbo 315832, China; Key Laboratory of Aquacultural Biotechnology of Ministry of Education, Ningbo University, Ningbo 315211, P.R. China. Electronic address:
The liver-expressed antimicrobial peptide 2 (LEAP2) is gaining recognition for its immune regulatory functions beyond direct antimicrobial activity. In this study, we investigated the role of mudskipper (Boleophthalmus pectinirostris) LEAP2 (BpLEAP2) in enhancing the survival, gut health, and immune resilience against Edwardsiella tarda infection. Pre-oral delivery of BpLEAP2 significantly improved survival rates and mitigated infection-induced damage to the gut, as evidenced by preserved villus length and goblet cell count.
View Article and Find Full Text PDFToll-like receptor 2/6-stimulated HMC-1 mast cells promote keratinocyte migration in wound healing.
PLoS One
January 2025
Departments of Microbiology, College of Medicine, Ewha Womans University, Seoul, Korea.
Mast cells, immune sentinels that respond to various stimuli in barrier organs, provide defense by expressing pattern recognition receptors, such as Toll-like receptors (TLRs). They may affect inflammatory responses and wound healing. Here, we investigated the effect of TLR2/6-stimulated mast cells on wound healing in keratinocytes.
View Article and Find Full Text PDFTail Anchored protein insertion mediated by CAML and TRC40 links to neuromuscular function in mice.
PLoS Genet
January 2025
Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 1st St. SW, Rochester, Minnesota 55905, United States of America.
Motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) and progressive bulbar palsy, involve loss of muscle control resulting from death of motor neurons. Although the exact pathogenesis of these syndromes remains elusive, many are caused by genetically inherited mutations. Thus, it is valuable to identify additional genes that can impact motor neuron survival and function.
View Article and Find Full Text PDFPlasticity of cell death pathways ensures GSDMD activation during Yersinia pseudotuberculosis infection.
Cell Rep
January 2025
Immunology Translational Research Programme, Life Sciences Institute, National University of Singapore, Singapore 117456, Singapore; Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117545, Singapore. Electronic address:
Macrophages express pattern recognition and cytokine receptors that mediate proinflammatory signal transduction pathways to combat microbial infection. To retaliate against such responses, pathogenic microorganisms have evolved multiple strategies to impede innate immune signaling. Recent studies demonstrated that YopJ suppression of TAK1 signaling during Yersinia pseudotuberculosis infection promotes the assembly of a RIPK1-dependent death-inducing complex that enables caspase-8 to directly cleave and activate gasdermin D (GSDMD).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!