Workplace bullying and violence as risk factors for type 2 diabetes: a multicohort study and meta-analysis

Aims/hypothesis

The aim of this multicohort study was to examine whether employees exposed to social stressors at work, such as workplace bullying and violence, have an increased risk of type 2 diabetes.

Methods

The study included 45,905 men and women (40–65 years of age and free of diabetes at baseline) from four studies in Sweden, Denmark and Finland. Workplace bullying and violence were self-reported at baseline. Incident diabetes was ascertained through national health and medication records and death registers. Marginal structural Cox models adjusted for age, sex, country of birth, marital status and educational level were used for the analyses.

Results

Nine per cent of the population reported being bullied at work and 12% were exposed to workplace violence or threats of violence. Bullied participants had a 1.46 (95% CI 1.23, 1.74) times higher risk of developing diabetes compared with non-bullied participants. Exposure to violence or threats of violence was also associated with a higher risk of diabetes (HR 1.26 [95% CI 1.02, 1.56]). The risk estimates attenuated slightly when taking BMI into account, especially for bullying. The results were similar for men and women, and were consistent across cohorts.

Conclusions/interpretation

We found a higher risk of incident type 2 diabetes among employees exposed to bullying or violence in the workplace. Further research is needed to determine whether policies to reduce bullying and violence at work may reduce the incidence of type 2 diabetes in working populations. Research on the mechanisms is also highly warranted.

     

C-reactive protein (CRP) and serum phospholipase A2 in the assessment of the severity of acute pancreatitis.

The present study examines the value of C-reactive protein (CRP) determinations in the assessment of the severity of acute pancreatitis and the correlation of CRP with serum phospholipase A2 activity and the clinical status. Fifty three patients with acute pancreatitis were studied; 17 with haemorrhagic pancreatitis and 36 with a mild form of the disease. S-phospholipase A2 activity increased significantly (p less than 0.05) in patients with fatal pancreatitis but not in those with mild disease. Phospholipase A2 concentrations were below 10 nmol FFA/ml min in mild, while they rose to 20-40 nmol FFA/ml min in haemorrhagic pancreatitis. In fatal cases very high (up to 50-60 nmol FFA/ml min) serum phospholipase A2 concentrations were recorded. The increase in CRP was greater in the patients with severe pancreatitis. One day after admission mean CRP was 280 mg/l in patients with haemorrhagic and 45 mg/l in those with the mild pancreatitis (p less than 0.001). High CRP values also correlated with the prognostic signs indicative of severe pancreatitis. CRP and S-phospholipase A2 determinations are valuable in the early assessment of the severity of acute pancreatitis, but the CRP assay is much easier to include in hospital routine.     

Predicting the risk of extinction from shared ecological characteristics

Understanding the ultimate causes of population declines and extinction is vital in our quest to stop the currently rampant biodiversity loss. Comparison of ecological characteristics between threatened and nonthreatened species may reveal these ultimate causes. Here, we report an analysis of ecological characteristics of 23 threatened and 72 nonthreatened butterfly species. Our analysis reveals that threatened butterflies are characterized by narrow niche breadth, restricted resource distribution, poor dispersal ability, and short flight period. Based on the characteristics, we constructed an ecological extinction risk rank and predicted which of the currently nonthreatened species are at the highest risk of extinction. Our analysis reveals that two species currently classified as nonthreatened are, in fact, at high risk of extinction, and that the status of a further five species should be reconsidered.     

Platelet membrane collagen receptor glycoprotein VI polymorphism is associated with coronary thrombosis and fatal myocardial infarction in middle-aged men

Glycoprotein VI is a platelet collagen receptor binding to subendothelial collagen after a rupture of an atherosclerotic plaque. The GPVI gene is polymorphic with several SNPs and the T13254C polymorphism predicting amino acid substitution (serine to proline) has been associated with the risk of MI in a preliminary study. We studied the association of the GPVI T13254C with fatal myocardial infarction (MI) and coronary artery disease among the 300 men of the Helsinki Sudden Death Study (HSDS). Genotype frequencies were 77.9% for TT, 20.7% for CT and 1.4% for CC. We found a significant association (P = 0.02) between the C-allele carriers (CT or CC) and coronary thrombosis (OR 2.5, 95% CI: 1.05-6.2). There was also a tendency (P = 0.07) for an association between the C-allele and acute myocardial infarction (AMI) (OR 2.2). The average area of complicated coronary lesions was also significantly (P = 0.01) larger in carriers compared to non-carriers of the C-allele. Our findings support previous results on the role of this GPVI polymorphism, or another linked polymorphism, as a possible predictor of the risk of coronary thrombosis.     

Sleep duration and sleep disturbances partly explain the association between depressive symptoms and cardiovascular mortality: the Whitehall II cohort study

Depressive symptoms are associated with an increased risk of death, but most of this association remains unexplained. Our aim was to explore the contribution of sleep duration and disturbances to the association between depressive symptoms, all‐cause and cardiovascular disease mortality. A total of 5813 (4220 men and 1593 women) aged 50–74 years at baseline, participants of the British Whitehall II prospective cohort study, were included. Depressive symptoms, sleep duration and disturbances were assessed in 2003–04. Mortality was ascertained through linkage to the national mortality register until August 2012, with a mean follow‐up of 8.8 years. Depressive symptoms were associated with an increased risk of mortality from all causes [hazard ratio (HR) = 1.51; 95% confidence interval (CI): 1.16–1.97)] and cardiovascular diseases (HR = 1.63; 95% CI: 1.01–2.64) after adjustment for sociodemographic characteristics. Further adjustment for sleep duration and disturbances reduced the association between depressive symptoms and cardiovascular mortality by 21% (HR = 1.53; 95% CI: 0.91–2.57). Sleep seems to have a role, as a mediator or confounder, in explaining the association between depressive symptoms and cardiovascular mortality. These findings need replication in larger studies with longer follow‐up.     

Enterovirus-induced gene expression profile is critical for human pancreatic islet destruction

Aims/hypothesis

Virally induced inflammatory responses, beta cell destruction and release of beta cell autoantigens may lead to autoimmune reactions culminating in type 1 diabetes. Therefore, viral capability to induce beta cell death and the nature of virus-induced immune responses are among key determinants of diabetogenic viruses. We hypothesised that enterovirus infection induces a specific gene expression pattern that results in islet destruction and that such a host response pattern is not shared among all enterovirus infections but varies between virus strains.

Methods

The changes in global gene expression and secreted cytokine profiles induced by lytic or benign enterovirus infections were studied in primary human pancreatic islet using DNA microarrays and viral strains either isolated at the clinical onset of type 1 diabetes or capable of causing a diabetes-like condition in mice.

Results

The expression of pro-inflammatory cytokine genes (IL-1-α, IL-1-β and TNF-α) that also mediate cytokine-induced beta cell dysfunction correlated with the lytic potential of a virus. Temporally increasing gene expression levels of double-stranded RNA recognition receptors, antiviral molecules, cytokines and chemokines were detected for all studied virus strains. Lytic coxsackievirus B5 (CBV-5)-DS infection also downregulated genes involved in glycolysis and insulin secretion.

Conclusions/interpretation

The results suggest a distinct, virus-strain-specific, gene expression pattern leading to pancreatic islet destruction and pro-inflammatory effects after enterovirus infection. However, neither viral replication nor cytotoxic cytokine production alone are sufficient to induce necrotic cell death. More likely the combined effect of these and possibly cellular energy depletion lie behind the enterovirus-induced necrosis of islets.