Genes with high penetrance for syndromic and non-syndromic autism typically function within the nucleus and regulate gene expression.

BACKGROUND: Intellectual disability (ID), autism, and epilepsy share frequent yet variable comorbidities with one another. In order to better understand potential genetic divergence underlying this variable risk, we studied genes responsible for monogenic IDs, grouped according to their autism and epilepsy comorbidities. METHODS: Utilizing 465 different forms of ID with known molecular origins, we accessed available genetic databases in conjunction with gene ontology (GO) to determine whether the genetics underlying ID diverge according to its comorbidities with autism and epilepsy and if genes highly penetrant for autism or epilepsy share distinctive features that set them apart from genes that confer comparatively variable or no apparent risk. RESULTS: The genetics of ID with autism are relatively enriched in terms associated with nervous system-specific processes and structural morphogenesis. In contrast, we find that ID with highly comorbid epilepsy (HCE) is modestly associated with lipid metabolic processes while ID without autism or epilepsy comorbidity (ID only) is enriched at the Golgi membrane. Highly comorbid autism (HCA) genes, on the other hand, are strongly enriched within the nucleus, are typically involved in regulation of gene expression, and, along with IDs with more variable autism, share strong ties with a core protein-protein interaction (PPI) network integral to basic patterning of the CNS. CONCLUSIONS: According to GO terminology, autism-related gene products are integral to neural development. While it is difficult to draw firm conclusions regarding IDs unassociated with autism, it is clear that the majority of HCA genes are tightly linked with general dysregulation of gene expression, suggesting that disturbances to the chronology of neural maturation and patterning may be key in conferring susceptibility to autism spectrum conditions.

Consequences of intimate partner violence against women on under-five child mortality in Bangladesh.

It is well established that intimate partner violence (IPV) against women adversely affects maternal morbidity and mortality. But a limited number of studies were found in the literature regarding the association between IPV and under-five child mortality. In this article, using Bangladesh Demographic and Health Survey (BDHS) 2007 data, we examined the effect of IPV on under-five child mortality. A product-limit approach was used for bivariate survival analysis, and Cox proportional hazard multiple regression models were used to investigate the effect of IPV controlling potential confounders. In bivariate analysis, the variables exposure to IPV, mother's age at birth, mother's education, residence type, division, number of children, wealth index, occupation, access to media, and decision autonomy were found to be potential risk factors for child mortality. Results indicated that women exposed to IPV were more likely to experience under-five child mortality compared with women not exposed. The unadjusted hazard ratio for IPV was 1.21 (95% confidence interval [CI] = [1.09, 1.35]) with p value < .01, whereas it was 1.16 (95% CI = [1.04, 1.29]) with p value < .01 and 1.13 (95% CI = [1.01, 1.26]) with p value < .05 in two adjusted models. These results implied that IPV against women is a problem not only for women but also for their children's survival.