ObjectiveTo conduct an overview of systematic reviews on the impact of evidence-based learning (EBL) method on medical education. MethodsThe CNKI, WanFang Data, VIP, CBM, PubMed, Embase, Cochrane Library, and Web of Science databases were electronically searched to collect the relevant systematic reviews or meta-analyses of the application of EBL method in medical education from inception to May, 2024. Two researchers conducted the literature screening and data extraction independently. The AMSTAR 2, ROBIS tool, PRISMA 2020, and GRADE system were separately used to evaluate the methodological quality, the risk of bias, the quality of reporting, and the quality of evidence of included studies. ResultsA total of 16 systematic reviews/meta-analyses were included. The methodological quality evaluation by AMSTAR 2 showed that the quality level of 16 studies was very low. The results of ROBIS tool showed that 1 study was low risk of bias and 15 studies were high risk of bias. The GRADE evaluation of the evidence quality for 36 outcome indicators in the included studies revealed that 6 were of moderate quality, 12 were of low quality, and the rest were of very low quality. ConclusionEBL method has demonstrated significant effects in improving theoretical performance, practical skills, and critical thinking abilities among medical students. However, the methodological and evidence quality of the current systematic reviews/meta-analyses are low.
ObjectiveTo investigate the role of the adenosine monophosphate-activated protein kinase (AMPK)-ULK1-mediated autophagy pathway in cigarette smoke (CS)-induced skeletal muscle atrophy. Methods C57BL/6 mice were used as subjects and divided into control group and cigarette smoke exposure group (CS group). The model of pulmonary emphysema was established by exposing C57BL/6 mice to CS for 24 weeks. Hematoxylin-eosin (HE) staining was used to observe the morphological changes in the alveoli and gastrocnemius muscle. The number of autophagosomes in the muscle tissue was quantified by transmission electron microscopy. The expression of autophagy-related proteins was detected using immunofluorescence and western blotting. A skeletal muscle atrophy model was established by treating C2C12 myoblasts with cigarette smoke extract (CSE) and divided into a control group and a CSE group. Additionally, C2C12 cell lines with AMPK overexpression were constructed using lentivirus. Further interventions were performed using the autophagy inhibitor 3-Methyladenine (3-MA), the AMPK activator AICAR, and the AMPK inhibitor Dorsomorphin (Compound C). Western blot was applied to detect the expression levels of autophagy-related proteins (LC3B, p62, Beclin1) and key proteins of the AMPK/ULK1 pathway (phosphorylated AMPK and phosphorylated ULK1). Autophagosomes in cells were detected using mCherry-GFP-LC3B-labeled adenovirus. Changes in the diameter of C2C12 myotubes were examined by immunofluorescence. Results CS exposure induced skeletal muscle atrophy in mice, accompanied by enhanced autophagy mediated by the AMPK-ULK1 pathway. In vitro, compared with the control group, the CSE group exhibited AMPK pathway activation and significantly increased expression of autophagy-related proteins LC3B, p62, and Beclin1, along with decreased myotube diameter. The AMPK activator AICAR and AMPK overexpression also promoted skeletal muscle autophagy and induced myotube atrophy, while the AMPK inhibitor Compound C effectively alleviated CSE-induced skeletal muscle autophagy and myotube atrophy. ConclusionCS can induce skeletal muscle atrophy by activating the AMPK-ULK1 signaling pathway and enhancing the subsequent autophagic process.
