中文摘要：

背景：在麻醉实践的批评事件的分析在改进耐心的安全强调非技术的技巧(NTS ) 的重要角色。因此，关于 NTS 询问被加到医药管理(公里) 模拟器训练改进麻醉学者的尖锐危机才能。这研究的目的是在经历训练的不同类型以后在一个模仿的麻醉危机比较 NTS 和二组麻醉学者的公里性能。方法：42 个麻醉学者随机被分到二个不同训练组，与参予训练会议的二模拟的每个组一起。(NTS+MMG ) 一个组正在训练 NTS 的包括的广泛的询问(资源管理，计划，领导和通讯) 并且公里，当另外的组(MMG ) 收到了更简单的询问时，那完全集中于公里。NTS 的质量和公里性能的质量被考察情形的录象带评估。结果：NTS+MMG 没比 MMG 证明优异关于行为并且公里标记。NTS 表演的质量显著地相关(P【0.01 ) 在两个组随 MM 行动(P【0.01 ) 显著地与 NTS 示范的数量，并且也相关。结论：当时，包括 NTS 和公里询问训练的一次单个会话没改进麻醉学者的 NTS 表演与麻醉学者相比仅仅收到了公里训练。这可能显示经常的更多或训练的个人被需要改进参加者的 NTS 表演。

英文摘要：

AIM： To investigate the signaling pathways implicated in phosphatidylethanolamine （PE）-induced apoptosis of human hepatoma HepG2 cells. METHODS： Inhibitory effects of PE on human hepatoma HepG2 cells were detected by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay. Cell cycle, apoptosis and mitochondrial transmembrane potential （△ψm） were analyzed by flow cytometry. Immunocytochemical assay and Western blotting were used to examine Bcl-2, Bax and caspase-3 protein levels in HepG2 cells treated with PE. RESULTS： PE inhibited the growth of HepG2 cells in a dose- and time- dependent manner. It did not affect the cell cycle, but induced apoptosis. PE significantly decreased △ψm at 0.25, 0.5 and 1 mmol/L, respectively, suggesting that PE induces cell apoptosis by decreasing the mitochondrial transmembrane potential. The Bcl-2 expression level induced by different concentrations of PE was lower than that in control groups. However, the Bax expression level induced by PE was higher than that in the control group. Meanwhile, PE increased the caspase-3 expression in a dose- and time-dependent manner. CONCLUSION： Exogenous PE induces apoptosis of human hepatoma HepG2 cells via the bcl-2/bax pathway.