Is burnout a mediating factor between sharps injury and workrelated factors or musculoskeletal pain?

BACKGROUND Burnout,musculoskeletal pain,and sharps injuries(SIs)affect medical workers.AIM To establish a model between SIs,burnout,and the risk factors to assess the extent to which burnout affects SIs.METHODS This questionnaire was used for an observational and cross-sectional study,which was based on members at a hospital affiliated with a medical university in Taichung,Taiwan,in 2020.The valid responses constituted 68.5%(1734 of 2531).The items were drawn from the Nordic Musculoskeletal Questionnaire and Copenhagen burnout inventory and concerned work experience,occupational category,presence of chronic diseases,sleep duration,overtime work,and work schedule.Factor analysis,chi-square test,Fisher exact test,Multiple linear,logistic regression and Sobel test were conducted.The present analyses were performed using SAS Enterprise Guide 6.1 software(SAS Institute Inc.,Cary,NC,United States),and significance was set at P<0.05.RESULTS Personal and work-related burnout ranks, sex, work experience ranks, occupationalgroups, drinking in the past month, sleep duration per day, presence ofchronic diseases, overtime work ranks, and work schedule were associated withSIs. Frequent upper limb and lower limb pain (pain occurring every day or once aweek) determined to be related to SIs. High personal burnout (> Q3) and highwork-related burnout (> Q3) mediated the relationship between SIs and frequentlower limb pain. Similarly, frequent lower limb pain mediated the relationship ofSIs with high personal and high work-related burnout. High personal and highwork-related burnout mediated the relationships of SIs with overtime work andirregular shift work. The mediating model provides strong evidence of anassociation between mental health and SIs.CONCLUSIONBurnout was determined to contribute to SIs occurrence;specifically, it mediatedthe relationships of SIs with frequent musculoskeletal pain, overtime work, andirregular shift work.

Transcriptional Factor Snail Mediates Epithelial-Mesenchymal Transition in Human Bronchial Epithelial Cells Induced by Silica

Epithelial-mesenchymal transition （EMT） plays an important role in fibrotic diseases. We have previously showed that silica induces EMT in human bronchial epithelial cells （BECs）; however, the underlying mechanism of silica-induced EMT is poorly understood. In the present study, we investigated the role of Snail in silica-induced EMT in human BECs in vitro. Human BECs were treated with silica at various concentrations and incubation times. Then MTr assay, western blot, electrophoretic mobility shift assay （EMSA）, and small interfering RNA （siRNA） transfection were performed. We found that silica increased the expression and DNA binding activity of Snail in human BECs. SNAI silica-induced expression siRNA upregulated the siRNA inhibited the of Snail. Moreover, SNAI expression of epithelial marker E-cadherin, but attenuated the expression of mesenchymal marker a-smooth muscle actin and vimentin in silica-stimulated cells. These results suggest that Snail mediates the silica-induced EMT in human BECs.

Activation of epidermal growth factor receptor mediates myocardial ischemia/reperfusion arrhythmias in anaesthetized rats

Objectives Epidermal growth factor receptor （EGFR）is a receptor protein tyrosine kinase and plays a critical role in the development and function of the heart.Previous studies have demonstrated that EGFR is involved in regulating electrical excitability of the heart.The present study was designed to investigate whether EGFR activation would mediate myocardial arrhythmias induced by ischemia/reperfu- sion in anaesthetized rats.Methods and results Myocardial ischemia/reperfusion arrhythmias were induced by 10 min ligation of the left anterior descending coronary artery,followed by a 30 min reperfusion in anaesthetized rats.Incidence and severity of cardiac arrhythmias were significantly reduced by pretreatment with the EGFR kinase inhibitor AG556.Phosphorylation level of myocardial EGFR was increased during ischemia and at early reperfusion.Intramyocardial transfection of EGFR siRNA reduced EGFR mRNA and protein,and decreased the incidence of ventricular fibrillation induced by reperfusion.Interestingly,tyrosine phosphorylation levels of cardiac Na+ channel(INa) and L-type Ca2+ channel(ICa.l) were significantly increased at corresponding time points to the alteration of phosphorylated EGFR level during reperfusion.AG556 pretreatment countered the increased tyrosine phosphorylation level of Na+ and L-type Ca2+ channels induced by reperfusion.No significant alteration was observed in tyrosine phosphorylation levels of cardiac Kv4.2 and Kir2.1 channels during the cardiac ischemia/reperfusion. Conclusions These results demonstrate for the first time that EGFR plays an important role in the genesis of myocardial ischemia/reperfusion arrhythmias,which is likely mediated at least in part by enhancing tyrosine phosphorylation of cardiac Na+ and L-type Ca2+ channels.