BackgroundUneven distribution of health resources is higher in Tibet than in other regions. The development of core professional capability for general practitioners (GPs) is the main goal of continuing medical education (CME) training programs.AimThis study aimed to explore the needs of CME for GPs and provide advice for the development of policy, practice, and CME curriculums.MethodsWe conducted a cross-sectional online survey among GPs in Tibet Autonomous Region, China. We designed an online questionnaire including the demographic section, training contents, and training formats about CME.ResultsA total of 108 questionnaires were included in this study. Notably, 79 (73.15%) were women and 56 participants (51.85%) were working in primary care settings. We developed a curriculum priority: first-choice, major alternatives, and secondary considerations. The topics identified as first-choice for CME were related to “cardiovascular disease” (85.19%), “respiratory disease” (81.48%), and “digestive disease” (80.56%). Major alternatives included two essential knowledge and eight clinical skill items. We rated 10 items as secondary considerations. Only 39.81% ranked mental health as an essential priority; bedside teaching (51.85%) was the first choice.ConclusionWe presented priority areas identified in this study to focus on CME for GPs in Tibet. The 23 topics may reflect the features of general practice, which increasingly require common disease management skills, while a demand-oriented curriculum and staged training plans should be adopted. CME programs should be adapted dynamically to respond to evolving needs.
Propofol is a widely used intravenous anesthetic shown to exert a cardioprotective role against oxidative stress and ischemia/reperfusion injury in rat cardiac H9c2 cells. However, the regulatory mechanisms and functions of propofol in human cardiomyocytes remain unknown. The present study chemically induced hypoxia with cobalt chloride (CoCl 2 ) to mimic cardiomyocyte ischemic injury in human cardiac AC16 and HCM cells. To investigate its underlying mechanisms, propofol was added to the cells before the chemical hypoxia phase. The present results suggested that, in response to hypoxia, mitochondrial membrane potential was lost, and cardiomyocyte viability and superoxide dismutase levels decreased. However, the present results showed that reactive oxygen species and malondialdehyde levels increased. The present results suggested that these effects were significantly reversed following propofol treatment. Additionally, the present results suggested that the protective effect of propofol against CoCl 2 -induced injury may be inhibited by the activation of the JNK signaling pathways. The present results indicated that propofol pre-treatment inhibited CoCl 2 -induced myocardial injury by preventing mitochondrial dysfunction, which may be partially due to the activation of the JNK signaling pathways. Therefore, propofol may exert anti-oxidative effects in human cardiac cells. The present results suggested that propofol may be used as a treatment for oxidative stress-related cardiac disorders.
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