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Auteur Catherine E. KING |
Documents disponibles écrits par cet auteur (1)
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Lack of Evidence for Genomic Instability in Autistic Children as Measured by the Cytokinesis-Block Micronucleus Cytome Assay / Penelope A. E. MAIN in Autism Research, 8-1 (February 2015)
[article]
Titre : Lack of Evidence for Genomic Instability in Autistic Children as Measured by the Cytokinesis-Block Micronucleus Cytome Assay Type de document : Texte imprimé et/ou numérique Auteurs : Penelope A. E. MAIN, Auteur ; Philip THOMAS, Auteur ; Manya T. ANGLEY, Auteur ; Robyn L. YOUNG, Auteur ; Adrian ESTERMAN, Auteur ; Catherine E. KING, Auteur ; Michael F. FENECH, Auteur Article en page(s) : p.94-104 Langues : Anglais (eng) Mots-clés : autism genomic instability DNA damage B vitamins behaviour riboflavin Index. décimale : PER Périodiques Résumé : Autism spectrum disorders are a set of neurodevelopmental disorders that are highly hereditable. Increased genomic instability has been observed in other heritable paediatric neurobiological disorders; therefore, the aim of our study was to test the hypothesis that DNA damage is increased in children with autism and that B vitamin status may explain variations in genome integrity between autistic and normal children. We compared 35 children with autism, 27 of their siblings without autism and 25 age- and gender-matched community controls for genomic stability using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay, B vitamins and homocysteine, as well as autism-related behaviours. It was found that there were no differences in CBMN-cyt biomarkers between the three groups. Vitamin B2 was significantly raised in children with autism and their siblings compared with controls (P?=?0.027 and P?=?0.016 respectively) but there was no difference in other B vitamins or homocysteine. In conclusion, although replication using a larger cohort is needed, it appears unlikely that genomic instability is a feature of the aetiology of autism. We cannot rule out in utero effects or other types of DNA damage not measured by the CBMN-cyt assay. En ligne : http://dx.doi.org/10.1002/aur.1428 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=256
in Autism Research > 8-1 (February 2015) . - p.94-104[article] Lack of Evidence for Genomic Instability in Autistic Children as Measured by the Cytokinesis-Block Micronucleus Cytome Assay [Texte imprimé et/ou numérique] / Penelope A. E. MAIN, Auteur ; Philip THOMAS, Auteur ; Manya T. ANGLEY, Auteur ; Robyn L. YOUNG, Auteur ; Adrian ESTERMAN, Auteur ; Catherine E. KING, Auteur ; Michael F. FENECH, Auteur . - p.94-104.
Langues : Anglais (eng)
in Autism Research > 8-1 (February 2015) . - p.94-104
Mots-clés : autism genomic instability DNA damage B vitamins behaviour riboflavin Index. décimale : PER Périodiques Résumé : Autism spectrum disorders are a set of neurodevelopmental disorders that are highly hereditable. Increased genomic instability has been observed in other heritable paediatric neurobiological disorders; therefore, the aim of our study was to test the hypothesis that DNA damage is increased in children with autism and that B vitamin status may explain variations in genome integrity between autistic and normal children. We compared 35 children with autism, 27 of their siblings without autism and 25 age- and gender-matched community controls for genomic stability using the cytokinesis-block micronucleus cytome (CBMN-cyt) assay, B vitamins and homocysteine, as well as autism-related behaviours. It was found that there were no differences in CBMN-cyt biomarkers between the three groups. Vitamin B2 was significantly raised in children with autism and their siblings compared with controls (P?=?0.027 and P?=?0.016 respectively) but there was no difference in other B vitamins or homocysteine. In conclusion, although replication using a larger cohort is needed, it appears unlikely that genomic instability is a feature of the aetiology of autism. We cannot rule out in utero effects or other types of DNA damage not measured by the CBMN-cyt assay. En ligne : http://dx.doi.org/10.1002/aur.1428 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=256