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Détail de l'auteur
Auteur Jiebiao WANG |
Documents disponibles écrits par cet auteur (2)
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Brief Report: Health Expenditures for Children with Autism and Family Financial Well-Being in China / Ling ZHOU in Journal of Autism and Developmental Disorders, 52-8 (August 2022)
[article]
Titre : Brief Report: Health Expenditures for Children with Autism and Family Financial Well-Being in China Type de document : Texte imprimé et/ou numérique Auteurs : Ling ZHOU, Auteur ; Jiebiao WANG, Auteur ; Jin HUANG, Auteur Article en page(s) : p.3712-3717 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder Autistic Disorder Child China Cost of Illness Health Expenditures Humans Autism Financial well-being Health expenditure Quality of life Index. décimale : PER Périodiques Résumé : Little is known on the financial well-being of families raising children with autism spectrum disorders (ASD). Family financial well-being has important impacts on the development of children with ASD. The study uses a 2019 survey collected from Chinese families raising a child with ASD (N=3064) to examine their financial well-being and its association with health expenditures for children. Extensive control variables (i.e., demographic and socioeconomic characteristics of children, respondents, and their families) are adjusted in analyses. Findings suggest that the amount of health expenditures is negatively associated with respondents' perception of their financial status. The significance of health expenditures disappears after household material hardship is adjusted. Health expenditures affect financial well-being mainly through resource competitions against family needs. En ligne : http://dx.doi.org/10.1007/s10803-021-05214-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=485
in Journal of Autism and Developmental Disorders > 52-8 (August 2022) . - p.3712-3717[article] Brief Report: Health Expenditures for Children with Autism and Family Financial Well-Being in China [Texte imprimé et/ou numérique] / Ling ZHOU, Auteur ; Jiebiao WANG, Auteur ; Jin HUANG, Auteur . - p.3712-3717.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 52-8 (August 2022) . - p.3712-3717
Mots-clés : Autism Spectrum Disorder Autistic Disorder Child China Cost of Illness Health Expenditures Humans Autism Financial well-being Health expenditure Quality of life Index. décimale : PER Périodiques Résumé : Little is known on the financial well-being of families raising children with autism spectrum disorders (ASD). Family financial well-being has important impacts on the development of children with ASD. The study uses a 2019 survey collected from Chinese families raising a child with ASD (N=3064) to examine their financial well-being and its association with health expenditures for children. Extensive control variables (i.e., demographic and socioeconomic characteristics of children, respondents, and their families) are adjusted in analyses. Findings suggest that the amount of health expenditures is negatively associated with respondents' perception of their financial status. The significance of health expenditures disappears after household material hardship is adjusted. Health expenditures affect financial well-being mainly through resource competitions against family needs. En ligne : http://dx.doi.org/10.1007/s10803-021-05214-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=485 De novo missense variants disrupting protein-protein interactions affect risk for autism through gene co-expression and protein networks in neuronal cell types / Siwei CHEN in Molecular Autism, 11 (2020)
[article]
Titre : De novo missense variants disrupting protein-protein interactions affect risk for autism through gene co-expression and protein networks in neuronal cell types Type de document : Texte imprimé et/ou numérique Auteurs : Siwei CHEN, Auteur ; Jiebiao WANG, Auteur ; Ercument CICEK, Auteur ; Kathryn ROEDER, Auteur ; Haiyuan YU, Auteur ; Bernie DEVLIN, Auteur Article en page(s) : 76 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Cell-type-specific transcriptome De novo missense variation Protein–protein interaction Index. décimale : PER Périodiques Résumé : BACKGROUND: Whole-exome sequencing studies have been useful for identifying genes that, when mutated, affect risk for autism spectrum disorder (ASD). Nonetheless, the association signal primarily arises from de novo protein-truncating variants, as opposed to the more common missense variants. Despite their commonness in humans, determining which missense variants affect phenotypes and how remains a challenge. We investigate the functional relevance of de novo missense variants, specifically whether they are likely to disrupt protein interactions, and nominate novel genes in risk for ASD through integrated genomic, transcriptomic, and proteomic analyses. METHODS: Utilizing our previous interactome perturbation predictor, we identify a set of missense variants that are likely disruptive to protein-protein interactions. For genes encoding the disrupted interactions, we evaluate their expression patterns across developing brains and within specific cell types, using both bulk and inferred cell-type-specific brain transcriptomes. Connecting all disrupted pairs of proteins, we construct an "ASD disrupted network." Finally, we integrate protein interactions and cell-type-specific co-expression networks together with published association data to implicate novel genes in ASD risk in a cell-type-specific manner. RESULTS: Extending earlier work, we show that de novo missense variants that disrupt protein interactions are enriched in individuals with ASD, often affecting hub proteins and disrupting hub interactions. Genes encoding disrupted complementary interactors tend to be risk genes, and an interaction network built from these proteins is enriched for ASD proteins. Consistent with other studies, genes identified by disrupted protein interactions are expressed early in development and in excitatory and inhibitory neuronal lineages. Using inferred gene co-expression for three neuronal cell types-excitatory, inhibitory, and neural progenitor-we implicate several hundred genes in risk (FDR?[Formula: see text]0.05),?~?60% novel, with characteristics of genuine ASD genes. Across cell types, these genes affect neuronal morphogenesis and neuronal communication, while neural progenitor cells show strong enrichment for development of the limbic system. LIMITATIONS: Some analyses use the imperfect guilt-by-association principle; results are statistical, not functional. CONCLUSIONS: Disrupted protein interactions identify gene sets involved in risk for ASD. Their gene expression during brain development and within cell types highlights how they relate to ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00386-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=433
in Molecular Autism > 11 (2020) . - 76 p.[article] De novo missense variants disrupting protein-protein interactions affect risk for autism through gene co-expression and protein networks in neuronal cell types [Texte imprimé et/ou numérique] / Siwei CHEN, Auteur ; Jiebiao WANG, Auteur ; Ercument CICEK, Auteur ; Kathryn ROEDER, Auteur ; Haiyuan YU, Auteur ; Bernie DEVLIN, Auteur . - 76 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 76 p.
Mots-clés : Autism spectrum disorder Cell-type-specific transcriptome De novo missense variation Protein–protein interaction Index. décimale : PER Périodiques Résumé : BACKGROUND: Whole-exome sequencing studies have been useful for identifying genes that, when mutated, affect risk for autism spectrum disorder (ASD). Nonetheless, the association signal primarily arises from de novo protein-truncating variants, as opposed to the more common missense variants. Despite their commonness in humans, determining which missense variants affect phenotypes and how remains a challenge. We investigate the functional relevance of de novo missense variants, specifically whether they are likely to disrupt protein interactions, and nominate novel genes in risk for ASD through integrated genomic, transcriptomic, and proteomic analyses. METHODS: Utilizing our previous interactome perturbation predictor, we identify a set of missense variants that are likely disruptive to protein-protein interactions. For genes encoding the disrupted interactions, we evaluate their expression patterns across developing brains and within specific cell types, using both bulk and inferred cell-type-specific brain transcriptomes. Connecting all disrupted pairs of proteins, we construct an "ASD disrupted network." Finally, we integrate protein interactions and cell-type-specific co-expression networks together with published association data to implicate novel genes in ASD risk in a cell-type-specific manner. RESULTS: Extending earlier work, we show that de novo missense variants that disrupt protein interactions are enriched in individuals with ASD, often affecting hub proteins and disrupting hub interactions. Genes encoding disrupted complementary interactors tend to be risk genes, and an interaction network built from these proteins is enriched for ASD proteins. Consistent with other studies, genes identified by disrupted protein interactions are expressed early in development and in excitatory and inhibitory neuronal lineages. Using inferred gene co-expression for three neuronal cell types-excitatory, inhibitory, and neural progenitor-we implicate several hundred genes in risk (FDR?[Formula: see text]0.05),?~?60% novel, with characteristics of genuine ASD genes. Across cell types, these genes affect neuronal morphogenesis and neuronal communication, while neural progenitor cells show strong enrichment for development of the limbic system. LIMITATIONS: Some analyses use the imperfect guilt-by-association principle; results are statistical, not functional. CONCLUSIONS: Disrupted protein interactions identify gene sets involved in risk for ASD. Their gene expression during brain development and within cell types highlights how they relate to ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00386-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=433