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Auteur Rui LUO |
Documents disponibles écrits par cet auteur (2)
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Interparental conflict and depressive symptoms among Chinese adolescents: A longitudinal moderated mediation model / Rui LUO in Development and Psychopathology, 35-2 (May 2023)
[article]
Titre : Interparental conflict and depressive symptoms among Chinese adolescents: A longitudinal moderated mediation model Type de document : Texte imprimé et/ou numérique Auteurs : Rui LUO, Auteur ; Fumei CHEN, Auteur ; Li KE, Auteur ; Yun WANG, Auteur ; Yunyan ZHAO, Auteur ; Yuhan LUO, Auteur Article en page(s) : p.972-981 Langues : Anglais (eng) Mots-clés : interparental conflict adolescent depressive symptoms family functioning cultural beliefs about adversity Index. décimale : PER Périodiques Résumé : While the detrimental effect of interparental conflict on adolescent depression is well-established, the underlying mechanisms linking the two continue to be inadequately understood. This study investigated the mediating role of family functioning and the moderating role of cultural beliefs about adversity in the association between interparental conflict and adolescent depression. The samples included 651 Chinese adolescents (mean age at Time 1 = 13.27 years; 56.5% girls) from a two-wave longitudinal study with data spanning 1 year. The findings from path modeling analyses provided evidence for the mediating role of family functioning; these findings indicated that interparental conflict can damage family functioning, which in turn exacerbates the risk of adolescent depression. The moderating role of cultural beliefs about adversity was also demonstrated by interactions between interparental conflict and cultural beliefs about adversity, as well as, family functioning and cultural beliefs about adversity. The results indicated a buffering role of cultural beliefs about adversity on the deleterious effect of interparental conflict on adolescent depression. They also suggested that lower levels of family functioning was associated with increased depression among adolescents were lower in cultural beliefs about adversity. En ligne : http://dx.doi.org/10.1017/S0954579422000190 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=504
in Development and Psychopathology > 35-2 (May 2023) . - p.972-981[article] Interparental conflict and depressive symptoms among Chinese adolescents: A longitudinal moderated mediation model [Texte imprimé et/ou numérique] / Rui LUO, Auteur ; Fumei CHEN, Auteur ; Li KE, Auteur ; Yun WANG, Auteur ; Yunyan ZHAO, Auteur ; Yuhan LUO, Auteur . - p.972-981.
Langues : Anglais (eng)
in Development and Psychopathology > 35-2 (May 2023) . - p.972-981
Mots-clés : interparental conflict adolescent depressive symptoms family functioning cultural beliefs about adversity Index. décimale : PER Périodiques Résumé : While the detrimental effect of interparental conflict on adolescent depression is well-established, the underlying mechanisms linking the two continue to be inadequately understood. This study investigated the mediating role of family functioning and the moderating role of cultural beliefs about adversity in the association between interparental conflict and adolescent depression. The samples included 651 Chinese adolescents (mean age at Time 1 = 13.27 years; 56.5% girls) from a two-wave longitudinal study with data spanning 1 year. The findings from path modeling analyses provided evidence for the mediating role of family functioning; these findings indicated that interparental conflict can damage family functioning, which in turn exacerbates the risk of adolescent depression. The moderating role of cultural beliefs about adversity was also demonstrated by interactions between interparental conflict and cultural beliefs about adversity, as well as, family functioning and cultural beliefs about adversity. The results indicated a buffering role of cultural beliefs about adversity on the deleterious effect of interparental conflict on adolescent depression. They also suggested that lower levels of family functioning was associated with increased depression among adolescents were lower in cultural beliefs about adversity. En ligne : http://dx.doi.org/10.1017/S0954579422000190 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=504 Replication of linkage at chromosome 20p13 and identification of suggestive sex-differential risk loci for autism spectrum disorder / Donna WERLING in Molecular Autism, (February 2014)
[article]
Titre : Replication of linkage at chromosome 20p13 and identification of suggestive sex-differential risk loci for autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : Donna WERLING, Auteur ; Jennifer K. LOWE, Auteur ; Rui LUO, Auteur ; Rita M. CANTOR, Auteur ; Daniel GESCHWIND, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASDs) are male-biased and genetically heterogeneous. While sequencing of sporadic cases has identified de novo risk variants, the heritable genetic contribution and mechanisms driving the male bias are less understood. Here, we aimed to identify familial and sex-differential risk loci in the largest available, uniformly ascertained, densely genotyped sample of multiplex ASD families from the Autism Genetics Resource Exchange (AGRE), and to compare results with earlier findings from AGRE. From a total sample of 1,008 multiplex families, we performed genome-wide, non-parametric linkage analysis in a discovery sample of 847 families, and separately on subsets of families with only male, affected children (male-only, MO) or with at least one female, affected child (female-containing, FC). Loci showing evidence for suggestive linkage (logarithm of odds =2.2) in this discovery sample, or in previous AGRE samples, were re-evaluated in an extension study utilizing all 1,008 available families. For regions with genome-wide significant linkage signal in the discovery stage, those families not included in the corresponding discovery sample were then evaluated for independent replication of linkage. Association testing of common single nucleotide polymorphisms (SNPs) was also performed within suggestive linkage regions. We observed an independent replication of previously observed linkage at chromosome 20p13 (P 0.01), while loci at 6q27 and 8q13.2 showed suggestive linkage in our extended sample. Suggestive sex-differential linkage was observed at 1p31.3 (MO), 8p21.2 (FC), and 8p12 (FC) in our discovery sample, and the MO signal at 1p31.3 was supported in our expanded sample. No sex-differential signals met replication criteria, and no common SNPs were significantly associated with ASD within any identified linkage regions. With few exceptions, analyses of subsets of families from the AGRE cohort identify different risk loci, consistent with extreme locus heterogeneity in ASD. Large samples appear to yield more consistent results, and sex-stratified analyses facilitate the identification of sex-differential risk loci, suggesting that linkage analyses in large cohorts are useful for identifying heritable risk loci. Additional work, such as targeted re-sequencing, is needed to identify the specific variants within these loci that are responsible for increasing ASD risk. En ligne : http://dx.doi.org/10.1186/2040-2392-5-13 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227
in Molecular Autism > (February 2014)[article] Replication of linkage at chromosome 20p13 and identification of suggestive sex-differential risk loci for autism spectrum disorder [Texte imprimé et/ou numérique] / Donna WERLING, Auteur ; Jennifer K. LOWE, Auteur ; Rui LUO, Auteur ; Rita M. CANTOR, Auteur ; Daniel GESCHWIND, Auteur.
Langues : Anglais (eng)
in Molecular Autism > (February 2014)
Index. décimale : PER Périodiques Résumé : Autism spectrum disorders (ASDs) are male-biased and genetically heterogeneous. While sequencing of sporadic cases has identified de novo risk variants, the heritable genetic contribution and mechanisms driving the male bias are less understood. Here, we aimed to identify familial and sex-differential risk loci in the largest available, uniformly ascertained, densely genotyped sample of multiplex ASD families from the Autism Genetics Resource Exchange (AGRE), and to compare results with earlier findings from AGRE. From a total sample of 1,008 multiplex families, we performed genome-wide, non-parametric linkage analysis in a discovery sample of 847 families, and separately on subsets of families with only male, affected children (male-only, MO) or with at least one female, affected child (female-containing, FC). Loci showing evidence for suggestive linkage (logarithm of odds =2.2) in this discovery sample, or in previous AGRE samples, were re-evaluated in an extension study utilizing all 1,008 available families. For regions with genome-wide significant linkage signal in the discovery stage, those families not included in the corresponding discovery sample were then evaluated for independent replication of linkage. Association testing of common single nucleotide polymorphisms (SNPs) was also performed within suggestive linkage regions. We observed an independent replication of previously observed linkage at chromosome 20p13 (P 0.01), while loci at 6q27 and 8q13.2 showed suggestive linkage in our extended sample. Suggestive sex-differential linkage was observed at 1p31.3 (MO), 8p21.2 (FC), and 8p12 (FC) in our discovery sample, and the MO signal at 1p31.3 was supported in our expanded sample. No sex-differential signals met replication criteria, and no common SNPs were significantly associated with ASD within any identified linkage regions. With few exceptions, analyses of subsets of families from the AGRE cohort identify different risk loci, consistent with extreme locus heterogeneity in ASD. Large samples appear to yield more consistent results, and sex-stratified analyses facilitate the identification of sex-differential risk loci, suggesting that linkage analyses in large cohorts are useful for identifying heritable risk loci. Additional work, such as targeted re-sequencing, is needed to identify the specific variants within these loci that are responsible for increasing ASD risk. En ligne : http://dx.doi.org/10.1186/2040-2392-5-13 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227