Integrated case teaching based on clinical competency in Nanjing Medical University / 中华医学教育探索杂志

Curriculum integration and problem based learning (PBL) is the development trend of medical education all over the world,and it is an effective mode to train high-quality medical talents to meet the needs of the times and national medical and health services.However,PBL is difficult to popularize in an all-round way at present due to the large enrollment of clinical medicine major in medical colleges and universities in China.Aiming at integrating knowledge and focusing on ability,Nanjing Medical University implemented a problem-based two-way integrated case teaching after top-level design,careful trial and steady promotion and has achieved initial results and improved the clinical competency of medical students.

Effects of methamphetamine acute exposure on neural damage / 中华急诊医学杂志

Objective To explore the neural damage induced by acute exposure to methamphetamine (METH).Methods The mice were administrated with METH,then the stereotyped behavior of mice was evaluated,and spatial recognition memory was analyzed by Y-maze test.In addition,nitric oxide synthase (NOS) activity was detected by kit,and the apoptotic proteins including Bax,Bcl-2,Caspase-3 were assayed by using Western blot.The DNA injury induced by METH was observed by using the comet assay.Moreover,mitochondrial membrane potential was detected to assess the toxic effects of METH on mitochondria by JC-1.With the Western blot assay,the phosphorylation of MAPK signaling pathways were also investigated.Results Acute METH exposure significantly increased the stereotyped behavior in mice,and spatial recognition ability of mice was obviously decreased.On the molecular level,total nitric oxide synthase (TNOS) and induced nitric oxide synthase (iNOS) were increased,and the apoptotic proteins,such as Bax and cleaved caspase-3 were markedly enhanced.With the comet assay,it showed that METH exposure resulted in DNA damage.In parallel,mitochondrial membrane was damaged which manifested as mitochondrial membrane potential decreased.With the western blot,It was further found that METH enhanced the activation of MAPKs.However,p38 MAPK signahng pathway was demonstrated to be the only one factor involved in METH-induced neural damage.Conclusion METH induced neural damage,and MAPK signaling pathways might be involved in this process,since inhibition of p38 MAPK signaling pathway significantly ameliorated METH-induced neural damage.