Non‐alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle, while exercise is beneficial for NAFLD. Dysregulated microRNAs (miRs) control the pathogenesis of NAFLD. However, whether exercise could prevent NAFLD via targeting microRNA is unknown. In this study, normal or high‐fat diet (HF) mice were either subjected to a 16‐week running program or kept sedentary. Exercise attenuated liver steatosis in HF mice. MicroRNA array and qRT‐PCR demonstrated that miR‐212 was overexpressed in HF liver, while reduced by exercise. Next, we investigated the role of miR‐212 in lipogenesis using HepG2 cells with/without long‐chain fatty acid treatment (±FFA). FFA increased miR‐212 in HepG2 cells. Moreover, miR‐212 promoted lipogenesis in HepG2 cells (±FFA). Fibroblast growth factor (FGF)‐21, a key regulator for lipid metabolism, was negatively regulated by miR‐212 at protein level in HepG2 cells. Meanwhile, FFA downregulated FGF‐21 both at mRNA and protein levels in HepG2 cells. Also, FGF‐21 protein level was reduced in HF liver, while reversed by exercise in vivo. Furthermore, siRNA‐FGF‐21 abolished the lipogenesis‐reducing effect of miR‐212 inhibitor in HepG2 cells (±FFA), validating FGF‐21 as a target gene of miR‐212. These data link the benefit of exercise and miR‐212 downregulation in preventing NAFLD via targeting FGF‐21.

Purpose: The purpose of this study was to construct a multi-center cross-sectional study to predict self-regulated learning (SRL) levels of Chinese medical undergraduates. Methods: We selected medical undergraduates by random sampling from five universities in mainland China. The classical regression methods (logistic regression and Lasso regression) and machine learning model were combined to identify the most significant predictors of SRL levels. Nomograms were built based on multivariable models. The accuracy, discrimination, and generalization of our nomograms were evaluated by the receiver operating characteristic curves (ROC) and the calibration curves and a high quality external validation. Results: There were 2052 medical undergraduates from five universities in mainland China initially. The nomograms constructed based on the non-overfitting multivariable models were verified by internal validation (C-index: learning motivation: 0.736; learning strategy: 0.744) and external validation (C-index: learning motivation: 0.986; learning strategy: 1.000), showing decent prediction accuracy, discrimination, and generalization. Conclusion: Comprehensive nomograms constructed in this study were useful and convenient tools to evaluate the SRL levels of undergraduate medical students in China.

Hepatic ischemia‑reperfusion injury (HIRI) often occurs following surgical procedures such as liver resection and transplantation. However, despite its clinical prominence, to the best of our knowledge, there remain no effective strategies to treat HIRI. Therefore, the aim of present study was to identify therapeutic agents that can exert beneficial effects against HIRI. The present study found that following hepatic IR modeling in mice, gastrodin (Gas) pretreatment improved the IR outcomes in terms of the serum biochemical indexes (alanine transaminase and aspartate transaminase), tissue biochemical indexes (superoxide dismutase, malondialdehyde and reduced glutathione content) and tissue pathology (H&E staining). In addition, compared with those in the IR + vehicle group, the IR + Gas group showed upregulated expression levels of nuclear erythroid 2‑related factor 2, heme oxygenase 1 and Bcl‑2 as detected by western blotting and reverse transcription‑quantitative PCR. The mRNA and protein expression levels of Bax and caspase‑3 were downregulated in the IR + Gas group compared with the IR + vehicle group. Concurrently, no significant differences were observed in the parameters between the Sham + vehicle and the Sham + Gas groups, indicating that Gas pretreatment may not cause liver damage. In conclusion, the findings of the present study revealed that Gas pretreatment exerted a protective effect in HIRI through both antioxidant and anti‑apoptotic mechanisms.

Background: Taspase 1 (TASP1) is a highly conserved protease involved in site-specific proteolysis. Existing researches have revealed a link between TASP1 expression and carcinogenesis. However, limited data are available regarding the prognosis and functions of TASP1 in hepatocellular carcinoma (HCC). Methods: Western Blotting and qRT-PCR were employed to evaluate the level of TASP1 in HCC cell lines and clinical specimens. TASP1 expression was further calculated in clinical specimens by immunohistochemistry and the mRNA level of TASP1 in HCC was analyzed using Oncomine and UALCAN databases. The TASP1 promoter methylation modification was shown via MEXPRESS and UALCAN. The association between TASP1 expression and postoperative prognosis was evaluated using Kaplan–Meier and Cox regression analysis in clinical patients. The effect of TASP1 on HCC prognosis was analyzed via Kaplan-Meier plotter, GEPIA and UALCAN. Additionally, the regulators, kinases, miRNA and transcription factor targets of TASP1 were identified using LinkedOmics. Moreover, cBioPortal was used to detect the genetic alteration of TASP1. Finally, TIMER was utilized to assess the relation between TASP1 and the immune cell infiltration, whereas the correlation of TASP1 with three immune factors was detected through TISIDB. Results: TASP1 expression was increased in HCC cell lines and HCC tissues. CNV and DNA methylation of TASP1 were changed. Survival analysis revealed that high TASP1 expression was correlated with overall survival (OS). Functional network analysis about TASP1 in HCC showed that the double-strand break repair, peptidyl-threonine modification, spindle organization, peptidyl-lysine modification and microtubule-based movement were modulated. Furthermore, TASP1 expression revealed puissant relation to the infiltration of immune cells and three immune factors in HCC. Conclusion: These data indicate that TASP1 may act as a potential prognostic marker in HCC and regulate HCC via multiple mechanisms.