Background: Burnout is a stress-induced syndrome considered to be closely related to work. Although social support could relief burnout syndrome, its effect on learning burnout in medical students remains unclear. The objectives of the study are to evaluate the association between learning burnout and social support in Chinese medical students.Methods: A cross-sectional online survey was distributed to students who participated in online learning in a medical college in Wuhan during the COVID-19 epidemic. We used the Lian version of the Maslach Burnout Inventory (MBI) to assess learning burnout and the Social Support Rating Scale (SSRS) to assess social support. Chi-square tests were used to analyze factors associated with burnout. Independent t-test and multiple logistic regression were explored to analyze the relationship between social support and burnout.Results: A total of 684 students have completed the survey (response rate: 30.9%), of which 315 (46.12%) met standard criteria for learning burnout. Multiple logistic regression analysis has revealed that seniors, low family income and low social support were significant predictors of learning burnout (χ² = 41.983, p < 0.001). After adjusting for the grade and family income, there was a significant and relevant association between social support and learning burnout (OR = 0.937; 95% CI: 0.905–0.970; p < 0.001).Conclusions: Learning burnout was highly prevalent in medical students at our college. Senior students and low family income might be risk factors for learning burnout. Social support, especially subjective support and utilization of support might play a protective role in reducing the risk of learning burnout.

Non-alcoholic fatty liver disease (NAFLD) encompasses hepatic steatosis, non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma. It is the primary cause of chronic liver disorders, with a high prevalence but no approved treatment. Therefore, it is indispensable to find a trustworthy therapy for NAFLD. Recently, mounting evidence illustrates that Sirtuin 1 (SIRT1) is strongly associated with NAFLD. SIRT1 activation or overexpression attenuate NAFLD, while SIRT1 deficiency aggravates NAFLD. Besides, an array of therapeutic agents, including natural compounds, synthetic compounds, traditional Chinese medicine formula, and stem cell transplantation, alleviates NALFD via SIRT1 activation or upregulation. Mechanically, SIRT1 alleviates NAFLD by reestablishing autophagy, enhancing mitochondrial function, suppressing oxidative stress, and coordinating lipid metabolism, as well as reducing hepatocyte apoptosis and inflammation. In this review, we introduced the structure and function of SIRT1 briefly, and summarized the effect of SIRT1 on NAFLD and its mechanism, along with the application of SIRT1 agonists in treating NAFLD.

Forkhead box transcription factor M1 (FOXM1) is a proliferation‐associated transcription factor involved in tumorigenesis through transcriptional regulation of its target genes in various cells, including dendritic cells (DCs). Although previous work has shown that FOXM1 enhances DC maturation in response to house dust mite allergens, it is not known whether FOXM1 affects DC maturation in the context of tumor‐specific immunity. In this study, we examined the central role of FOXM1 in regulating bone marrow‐derived dendritic cell (BMDC) maturation phenotypes and function in pancreatic cancer and colon cancer. FOXM1 retarded maturation phenotypes of BMDCs, inhibited promotion of T‐cell proliferation, and decreased interleukin‐12 (IL‐12) p70 in tumor‐bearing mice (TBM). Notably, FOXM1 expression was epigenetically regulated by dimethylation on H3 lysine 79 (H3K79me2), a modification present in both tumor cells and BMDCs. Increased H3K79me2 enrichment was observed at the FOXM1 promoter in both BMDCs from TBM, and in BMDCs from wild‐type mice cultured with tumor‐conditioned medium that mimics the tumor microenvironment (TME). Furthermore, inhibition of the H3K79 methyltransferase DOT1L not only decreased enrichment of H3K79me2, but also downregulated expression of FOXM1 and partially reversed its immunosuppressive effects on BMDCs. Furthermore, we found that FOXM1 upregulated transcription of Wnt family number 5A (Wnt5a) in BMDCs in vitro; we also observed that exogenous Wnt5a expression abrogated BMDC maturation phenotypes by inhibiting FOXM1 and H3K79me2 modification. Therefore, our results reveal that upregulation of FOXM1 by H3K79me2 in pancreatic cancer and colon cancer significantly inhibits maturation phenotypes and function of BMDCs through the Wnt5a signaling pathway, and thus provide novel insights into FOXM1‐based antitumor immunotherapy.