We examined the prevalence of emotional and behavioral problems and associated risk and protective factors among children and adolescents ages 6 to 18 years reared in orphanages in Turkey ( = 461, 87.9% of all eligible subjects) compared with a nationally representative community sample of similarly-aged youngsters brought up by their own families ( = 2280). Using the 90th percentile as the cut-off criterion, it was found that the Teacher's Report Form (TRF) score was higher for children and adolescents in orphanage care than in the community (23.2%, orphanage v. 11%, community). Multiple regression models explained 73% of the total variance of TRF Total Problems score for children and adolescents in orphanages. Regular contact with parents or relatives, between classroom teachers and orphanage staff, appropriate task involvement, perceived social support and competency were significant protective factors against emotional and behavioral problems. Younger age at first admission, being small for age, and feelings of stigmatization were associated with higher TRF Problem Scores (<.05). Parental psychiatric disorder was unrelated to emotional and behavioral problems in children reflecting that psychosocial adversity and parenting problems in of themselves lead to institutionalization, irrespective of identifiable parental mental disorder. The findings are interpreted in the light of an urgent need for development of early intervention programs that promote community care of children by preventing separation from families, provision of support services for families in need, and development of counseling programs to prevent abandonment, abuse and neglect. Finding ways for child welfare professionals to collaborate more closely with early intervention programs would also increase the viable opportunities and rights of children and adolescents currently cared for in the system. Finally, alternative cost-effective care models need to be promoted including foster care or adoption systems and family based homes in the community.
The aim of this study was to investigate the relationship between autism spectrum disorders development and exposure to mono-(2-ethylhexyl)-phthalate (MEHP), di-(2-ethylhexyl)-phthalate (DEHP), and bisphenol A (BPA), 1 of the endocrine disruptors, among phthalates. The study included 48 children with autism spectrum disorder (27 boys, 21 girls) and 41 healthy subjects (24 boys, 17 girls) as controls. Serum MEHP, DEHP, and BPA levels were measured by using high-performance liquid chromatography. Children with autism spectrum disorder had significantly increased serum MEHP, DEHP, and BPA concentrations (0.47 ± 0.14 µg/ml, 2.70 ± 0.90 µg/ml, 1.25 ± 0.30 ng/ml) compared to healthy control subjects (0.29 ± 0.05 µg/ml, 1.62 ± 0.56 µg/ml, 0.88 ± 0.18 ng/ml) respectively (P = .000). The fact that higher serum MEHP, DEHP, and BPA were found levels in the autism spectrum disorder group compared to healthy controls suggests that endocrine disruptors may have a role in the pathogenesis of autism spectrum disorders.
Autism spectrum disorder (ASD) is a group of developmental pathologies that impair social communication and cause repetitive behaviors. The suggested roles of noncoding RNAs in pathology led us to perform a comparative analysis of the microRNAs expressed in the serum of human ASD patients. The analysis of a cohort of 45 children with ASD revealed that six microRNAs (miR-19a-3p, miR-361-5p, miR-3613-3p, miR-150-5p, miR-126-3p, and miR-499a-5p) were expressed at low to very low levels compared to those in healthy controls. A similar but less pronounced decrease was registered in the clinically unaffected parents of the sick children and in their siblings but never in any genetically unrelated control. Results consistent with these observations were obtained in the blood, hypothalamus and sperm of two of the established mouse models of ASD: valproic acid-treated animals and Cc2d1a +/− heterozygotes. In both instances, the same characteristic miRNA profile was evidenced in the affected individuals and inherited together with disease symptoms in the progeny of crosses with healthy animals. The consistent association of these genetic regulatory changes with the disease provides a starting point for evaluating the changes in the activity of the target genes and, thus, the underlying mechanism(s). From the applied societal and medical perspectives, once properly confirmed in large cohorts, these observations provide tools for the very early identification of affected children and progenitors. Autism spectrum disorders (ASDs) encompass a range of disorders characterized by impaired social interactions and communications, together with repetitive stereotypic behaviors (refs. 1-5 for recent reviews). The genetic architecture underlying the range of ASD symptoms has been investigated (reviewed by Iakoucheva et al. 1). Mutations in more than 100 genes involved in brain development and neural activity have been identified in patients and are thought to confer a risk for ASD 2,3 , but a constant association that would suggest a causal relationship has not been observed. The same conclusion was recently reached from a large-scale exon sequencing analysis 4. Hence, mouse models that reproduce characteristic elements of the disease have been developed 5. As in other instances, attention has recently been focused on a peculiar class of regulatory alterations that modifies noncoding (nc) RNAs 6 with putative regulatory functions in the synthesis of proteins. One class of these alterations comprises the genes encoding 22 nt-long RNA (often abbreviated miRNAs) that regulate the expression of homologous target genes by blocking translation and inducing the degradation of the mRNAs 7. Among the miRNA genes in the mammalian genome (several hundred in the human genome), a large subset is expressed in the brain 8 , and dysfunctions of particular miRNAs have been tentatively associated with neuropathological conditions, including ASD 9,10 , with however diverging patterns of expression. They may reflect still unknown complexities of the dis...
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