Workplace Social Capital and Mental Health among Chinese Employees: A Multi-Level, Cross-Sectional Study

Background: Whereas the majority of previous research on social capital and health has been on residential neighborhoods and communities, the evidence remains sparse on workplace social capital. To address this gap in the literature, we examined the association between workplace social capital and health status among Chinese employees in a large, multilevel, cross-sectional study. Methods: By employing a two-stage stratified random sampling procedure, 2,796 employees were identified from 35 workplaces in Shanghai during March to November 2012. Workplace social capital was assessed using a validated and psychometrically tested eight-item measure, and the Chinese language version of the WHO-Five Well-Being Index (WHO-5) was used to assess mental health. Control variables included sex, age, marital status, education level, occupation status, smoking status, physical activity, and job stress. Multilevel logistic regression analysis was conducted to explore whether individual- and workplace-level social capital was associated with mental health status. Results: In total, 34.9% of workers reported poor mental health (WHO-5,13). After controlling for individual-level sociodemographic and lifestyle variables, compared to workers with the highest quartile of personal social capital, workers with the third, second, and lowest quartiles exhibited 1.39 to 3.54 times greater odds of poor mental health, 1.39 (95% CI: 1.10– 1.75), 1.85 (95% CI: 1.38–2.46) and 3.54 (95% CI: 2.73–4.59), respectively. Corresponding odds ratios for workplace-level social capital were 0.95 (95% CI: 0.61–1.49), 1.14 (95% CI: 0.72–1.81) and 1.63 (95% CI: 1.05–2.53) for the third, second, and lowest quartiles, respectively. Conclusions: Higher workplace social capital is associated with lower odds of poor mental health among Chinese employees. Promoting social capital at the workplace may contribute to enhancing employees’ mental health in China

IRE1β Inhibits Chylomicron Production by Selectively Degrading MTP mRNA

SummaryMicrosomal triglyceride transfer protein (MTP) is needed to assemble chylomicrons in the endoplasmic reticulum (ER) of enterocytes. We explored the role of an ER stress protein, inositol-requiring enzyme 1β (IRE1β), in regulating this process. High-cholesterol and high-fat diets decreased intestinal IRE1β mRNA in wild-type mice. Ire1b−/− mice fed high-cholesterol and high-fat diets developed more pronounced hyperlipidemia because these mice secreted more chylomicrons and expressed more intestinal MTP, though not hepatic MTP, than wild-type mice did. Chylomicron secretion and MTP expression also were increased in primary enterocytes isolated from cholesterol-fed Ire1b−/− mice. There was no correlation between ER stress and MTP expression. Instead, cell culture studies revealed that IRE1β, but not its ubiquitous homolog IRE1α, decreased MTP mRNA through increased posttranscriptional degradation. Conversely, knockdown of IRE1β enhanced MTP expression. These studies show that IRE1β plays a role in regulating MTP and in chylomicron production

Endothelial progenitor cells display clonal restriction in multiple myeloma

BACKGROUND: In multiple myeloma (MM), increased neoangiogenesis contributes to tumor growth and disease progression. Increased levels of endothelial progenitor cells (EPCs) contribute to neoangiogenesis in MM, and, importantly, covary with disease activity and response to treatment. In order to understand the mechanisms responsible for increased EPC levels and neoangiogenic function in MM, we investigated whether these cells were clonal by determining X-chromosome inactivation (XCI) patterns in female patients by a human androgen receptor assay (HUMARA). In addition, EPCs and bone marrow cells were studied for the presence of clonotypic immunoglobulin heavy-chain (IGH) gene rearrangement, which indicates clonality in B cells; thus, its presence in EPCs would indicate a close genetic link between tumor cells in MM and endothelial cells that provide tumor neovascularization. METHODS: A total of twenty-three consecutive patients who had not received chemotherapy were studied. Screening in 18 patients found that 11 displayed allelic AR in peripheral blood mononuclear cells, and these patients were further studied for XCI patterns in EPCs and hair root cells by HUMARA. In 2 patients whose EPCs were clonal by HUMARA, and in an additional 5 new patients, EPCs were studied for IGH gene rearrangement using PCR with family-specific primers for IGH variable genes (V(H)). RESULTS: In 11 patients, analysis of EPCs by HUMARA revealed significant skewing (≥ 77% expression of a single allele) in 64% (n = 7). In 4 of these patients, XCI skewing was extreme (≥ 90% expression of a single allele). In contrast, XCI in hair root cells was random. Furthermore, PCR amplification with V(H )primers resulted in amplification of the same product in EPCs and bone marrow cells in 71% (n = 5) of 7 patients, while no IGH rearrangement was found in EPCs from healthy controls. In addition, in patients with XCI skewing in EPCs, advanced age was associated with poorer clinical status, unlike patients whose EPCs had random XCI. CONCLUSION: Our results suggest that EPCs in at least a substantial subpopulation of MM patients are related to the neoplastic clone and that this is an important mechanism for upregulation of tumor neovascularization in MM

Does the frequency of reminders matter for their effectiveness? A randomized controlled trial

We assess the impact of reminder frequency on the probability of paying overdue property taxes in a randomized controlled trial in China. One reminder a week (sent as a text message) considerably increases the probability of tax compliance and results in tangible fiscal gains compared to a one-off reminder. However, increasing the frequency of reminders to two text messages a week diminishes their effectiveness. The takeaway of our study is that frequent reminders are an important trigger for human behavior, nonetheless, beyond a certain frequency the effectiveness of additional reminders seems to decline

The BCL6 RD2 Domain Governs Commitment of Activated B Cells to Form Germinal Centers

To understand how the Bcl6 transcriptional repressor functions in the immune system, we disrupted its RD2 repression domain in mice. Bcl6RD2MUT mice exhibit a complete loss of germinal center (GC) formation but retain normal extrafollicular responses. Bcl6RD2MUT antigen-engaged B cells migrate to the interfollicular zone and interact with cognate T helper cells. However, these cells fail to complete early GC-commitment differentiation and coalesce as nascent GC aggregates. Bcl6 directly binds and represses trafficking receptors S1pr1 and Gpr183 by recruiting Hdac2 through the RD2 domain. Deregulation of these genes impairs B cell migration and may contribute to GC failure in Bcl6RD2MUT mice. The development of functional GC-TFH cells was partially impaired in Bcl6RD2MUT mice. In contrast to Bcl6−/− mice, Bcl6RD2MUT animals experience no inflammatory disease or macrophage deregulation. These results reveal an essential role for RD2 repression in early GC commitment and striking biochemical specificity in Bcl6 control of humoral and innate immune-cell phenotypes

Model fit, odds ratios, and 95% confidence intervals for multilevel regression models of workplace social capital and mental health.

<p>Model fit, odds ratios, and 95% confidence intervals for multilevel regression models of workplace social capital and mental health.</p

Developmental neurotoxicity of reserpine exposure in zebrafish larvae (Danio rerio)

Reserpine is widely used for treatment of hypertension and schizophrenia. As a specific inhibitor of monoamine transporters, reserpine is known to deplete monoamine neurotransmitters and cause decreased movement symptoms. However, how zebrafish larvae respond to reserpine treatment is not well studied. Here we show that swimming distance and average velocity are significantly reduced after reserpine exposure under various stimulatory conditions. Using liquid chromatograph mass spectrometer analysis, decreased levels of monoamines (e.g. dopamine, noradrenaline, and serotonin) were detected in reserpine-treated larvae. Moreover, reserpine treatment significantly reduced the number of dopaminergic neurons, which was identified with th (Tyrosine Hydroxylase) in situ hybridization in the preoptic area. Interestingly, dopaminergic neuron development-associated genes, such as otpa, otpb, wnt1, wnt3, wnt5 and manf; were downregulated in reserpine treated larvae. Our data indicates that 2 mg/L reserpine exposure induces dopaminergic neuron damage in the brain, demonstrating a chemical induced depression-like model in zebrafish larvae for future drug development.</p