ObjectivesWorkplace violence is relatively frequent among medical professionals who work in otorhinolaryngology units. This phenomenon reduces the quality of provided medical care and increases the incidence of depressive symptoms among physicians and nurses, seriously affecting their job satisfaction and work efficiency with a negative attitude towards providing treatment. Few existing studies have assessed workplace-violence-related factors associated with depressive symptoms among otorhinolaryngology physicians and nurses.MethodsWe conducted a cross-sectional study in grade A tertiary hospitals of Heilongjiang province in Northern China, to evaluate the occurrence and level of depressive symptoms among otorhinolaryngology physicians and nurses and to analyse the relationship between them and workplace-violence-related risk factors and demographic variables.ResultsOf all our participating professionals, (379 otorhinolaryngologists and 273 nurses), 57.2% were found to have depressive symptoms, whereas, of the respondents who had suffered from physical violence, 71.25% had depressive symptoms. Professionals with less than 1 year of experience, as well as professionals who more frequently worked alone, were more likely to suffer from depressive symptoms than their colleagues.ConclusionsThis research addresses an emerging issue of clinical practice, and its results differ from those of previous studies; specifically, it indicates that the frequency of depressive symptoms among otorhinolaryngology physicians and nurses may be influenced by physical violence, the number of coworkers they have for more than half of their working hours and other workplace-violence-related factors. To reduce the depressive symptoms caused by workplace violence and improve the quality of medical services, medical institutions should implement effective measures to prevent the occurrence of physical violence, strengthen team cooperation ability and increase peer support.
Background/Aims: Alcohol consumption has been shown to cause neuroinflammation and increase a variety of immune-related signaling processes. Microglia are a crucial part of alcohol-induced neuroinflammation and undergo apoptosis. Even though the importance of these inflammatory processes in the effects of alcohol-related neurodegeneration have been established, the mechanism of alcohol-induced microglia apoptosis is unknown. In prior research, we discovered that alcohol increases expression of salt-inducible kinase 1 (SIK1) in rodent brain tissue. In this study, we sought to determine what role SIK1 expression plays in alcohol-induced neuroinflammation as well as whether and by what mechanism it regulates microglia apoptosis. Methods: Adult C57BL/6 mice were divided into four groups and for 3 weeks treated with either 0%, 5%, 10%, or 15% alcohol during 3 hour periods. The mice were sacrificed and their brains excised for analysis. Additionally, primary microglia were isolated from neonatal mice. SIK1 expression in alcohol-treated brain tissue and microglia was analyzed via RT-PCR and western blotting. TUNEL staining, caspase-3, and caspase-9 activity assays were performed to evaluate microglial apoptosis. Cell fluorescence staining and NF-κB luciferase activity assays were used to evaluate the effects of SIK1 expression on the NF-κB signaling pathway. Results: SIK1 expression was increased in the brains of mice that consumed alcohol, and this effect was seen in mouse primary microglia. SIK1 knockdown in microglia increased alcohol-induced apoptosis in these cells. Furthermore, SIK1 reduced NF-κB signaling pathway factors, and SIK1 knockdown in microglia promoted alcohol-induced NF-κB activity. TUNEL staining, caspase-3, and caspase-9 activity assays consistently revealed that alcohol-induced microglial apoptosis was inhibited by depletion of p65. Finally, we determined that NF-κB signaling is required for alcohol-induced, SIK1-mediated apoptosis in microglia. Conclusion: This study establishes for the first time not only that SIK1 is crucial to regulating alcohol-induced microglial apoptosis, but also that the NF-κB signaling pathway is required for its activity. Overall, our results help elucidate mechanisms of alcohol-induced neuroinflammation.
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