Environmental noise, especially that caused by transportation means, is viewed as a significant cause of sleep disturbances. Poor sleep causes endocrine and metabolic measurable perturbations and is associated with a number of cardiometabolic, psychiatric and social negative outcomes both in adults and children. Nocturnal environmental noise also provokes measurable biological changes in the form of a stress response, and clearly affects sleep architecture, as well as subjective sleep quality. These sleep perturbations are similar in their nature to those observed in endogenous sleep disorders. Apart from these measurable effects and the subjective feeling of disturbed sleep, people who struggle with nocturnal environmental noise often also suffer the next day from daytime sleepiness and tiredness, annoyance, mood changes as well as decreased well-being and cognitive performance. But there is also emerging evidence that these short-term effects of environmental noise, particularly when the exposure is nocturnal, may be followed by long-term adverse cardiometabolic outcomes. Nocturnal environmental noise may be the most worrying form of noise pollution in terms of its health consequences because of its synergistic direct and indirect (through sleep disturbances acting as a mediator) influence on biological systems. Duration and quality of sleep should thus be regarded as risk factors or markers significantly influenced by the environment and possibly amenable to modification through both education and counseling as well as through measures of public health. One of the means that should be proposed is avoidance at all costs of sleep disruptions caused by environmental noise.

The use of firearms is a common means of suicide. We examined the effect of a policy change in the Israeli Defense Forces reducing adolescents' access to firearms on rates of suicide. Following the policy change, suicide rates decreased significantly by 40%. Most of this decrease was due to decrease in suicide using firearms over the weekend. There were no significant changes in rates of suicide during weekdays. Decreasing access to firearms significantly decreases rates of suicide among adolescents. The results of this study illustrate the ability of a relatively simple change in policy to have a major impact on suicide rates.

No abstract

Adipose differentiation is a complex process controlled by a network of transcription factors and co-regulators. We compared the global gene expression patterns of adipogenic and nonadipogenic clones of 3T3-F442A preadipocytes and identified the transcriptional cofactor, vestigial-like 3 (Vgll3), as an inhibitor of adipogenesis. Vgll3 expression is down-regulated during terminal adipocyte differentiation in vitro and negatively correlates with weight and total fat mass in vivo. Furthermore, enforced Vgll3 expression inhibits the differentiation of preadipocytes in vitro, whereas shRNA-mediated knockdown of Vgll3 expression promotes differentiation. Expression of Vgll3 promoted the expression of genes associated with bone and chondrocyte formation, suggesting that Vgll3 participates in the decision of mesenchymal cells to proceed down the adipocyte, bone, or cartilage lineages. The elucidation of factors involved in specification of the adipocyte phenotype may aid in the identification of new strategies for the treatment of metabolic disease.

Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), are widely used for the treatment of depression and anxious disorders. The observation that depression is an independent risk factor for cardiovascular mortality and morbidity in patients with ischemic heart disease, the assessment of the central role of serotonin in pathophysiological mechanisms of depression, and reports of cases of abnormal bleeding associated with antidepressant therapy have led to investigations of the influence of antidepressants on hemostasis markers. In this review, we summarize data regarding modifications of these markers, drawn from clinical studies and case reports. We observed an association between the type of antidepressant drug and the number of abnormal bleeding case reports, with or without modifications of hemostasis markers. Drugs with the highest degree of serotonin reuptake inhibition--fluoxetine, paroxetine, and sertraline--are more frequently associated with abnormal bleeding and modifications of hemostasis markers. The most frequent hemostatic abnormalities are decreased platelet aggregability and activity, and prolongation of bleeding time. Patients with a history of coagulation disorders, especially suspected or documented thrombocytopenia or platelet disorder, should be monitored in case of prescription of any serotonin reuptake inhibitor (SRI). Platelet dysfunction, coagulation disorder, and von Willebrand disease should be sought in any case of abnormal bleeding occurring during treatment with an SRI. Also, a non-SSRI antidepressant should be favored over an SSRI or an SRI in such a context. Considering the difficulty in performing platelet aggregation tests, which are the most sensitive in SRI-associated bleeding, and the low sensitivity of hemostasis tests when performed in case of uncomplicated bleeding in the general population, establishing guidelines for the assessment of SRI-associated bleeding complications remains a challenge.

Few cerebro-renal syndromes have been described to date. Perez et al. identify a novel autosomal recessive cerebro-renal syndrome in a consanguineous Bedouin kindred, caused by a mutation in SLC30A9. The mutation disrupts the role of SLC30A9 in Zn2+ transport, leading to impaired regulation of cytosolic zinc homeostasis.

Child sexual abuse is a universal social phenomenon. Adolescents themselves can contribute to research and so help in the search for more efficient prevention and intervention strategies.

Histone modifications and their modifying enzymes are fundamentally involved in the epigenetic regulation of adipogenesis. This study aimed to define the roles of various histone modifications and their "division of labor" in fat cell differentiation. To achieve these goals, we examined the distribution patterns of eight core histone modifications at five key adipogenic regulatory genes, Pref-1, C/EBPβ, C/EBPα, PPARγ2 and aP2, during the adipogenesis of C3H 10T1/2 mouse mesenchymal stem cells (MSCs) and 3T3-L1 preadipocytes. We found that the examined histone modifications are globally stable throughout adipogenesis but show distinct and highly dynamic distribution patterns at specific genes. For example, the Pref-1 gene has lower levels of active chromatin markers and significantly higher H3 K27 tri-methylation in MSCs compared with committed preadipocytes; the C/EBPβ gene is enriched in active chromatin markers at its 3'-UTR; the C/EBPα gene is predominantly marked by H3 K27 tri-methylation in adipogenic precursor cells, and this repressive marker decreases dramatically upon induction; the PPARγ2 and aP2 genes show increased histone acetylation on both H3 and H4 tails during adipogenesis. Further functional studies revealed that the decreased level of H3 K27 tri-methylation leads to de-repression of Pref-1 gene, while the increased level of histone acetylation activates the transcription of PPARγ2 and aP2 genes. Moreover, the active histone modification-marked 3'-UTR of C/EBPβ gene was demonstrated as a strong enhancer element by luciferase assay. Our results indicate that histone modifications are gene-specific at adipogenic regulator genes, and they play distinct roles in regulating the transcriptional network during adipogenesis.