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| 1 | 脓毒症的发病机制和治疗新进展显示文摘本文介绍了脓毒血症的发病机制和临床治疗策略。在发病机制中细胞因子网络的作用,以及脓毒血症与补体系统和凝血系统的相互影响是目前研究的热点和进展,治疗中靶向细胞凋亡的治疗是脓毒血症治疗新策略。 | 邓小明 | 2010 | 中国继续医学教育2010，2，4： | 4 |
| 2 | 急性心肌梗死患者细胞凋亡水平影响因素的分析显示文摘目的探讨急性心肌梗死(AMI)时可能影响细胞凋亡水平的因素。方法73例AMI患者分别根据发病到入院的时间、患者年龄、病变部位和冠状动脉病变支数进行分组,检测血清细胞凋亡信号分子sFas水平。结果不同的缺血时间组之间血清sFas浓度差异具有显著性(P<0.05),而不同年龄组、不同冠状动脉病变程度组、不同心肌梗死部位组之间血清sFas浓度差异无显著性(P>0.05)。结论细胞凋亡水平随缺血时间的延长而增加,提示我们在AMI治疗中应及时而有效地恢复心肌细胞的血液供应,从而改善AMI患者的预后。 | 张磊 张麟 | 2006 | 中国医药2006，1，6： | 3 |
| 3 | Responses of CDKs and p53 in Delayed Ischemic Neuronal Death显示文摘Stroke is a debilitating disease that affects millions each year. While in many cases cerebral ischemic injury can be limited by effective resuscitation or thrombolytic treatment, the injured neurons wither in a process known as delayed neuronal death (DND). Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered. Of particular interest are two groups of signal proteins that participate in apoptosis cyclin dependent kinases (CDKs) and p53 among a myriad of signaling events after an ischemic insult. Recent investigations have shown that CDKs, a family of enzymes initially known for their role in cell cycle regulation, are activated in injured neurons in DND. As for p53, new reports suggest that its up regulation may represent a failed attempt to rescue injured neurons, although its up regulation was previously considered an indication of apoptosis. These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage. In this review, the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre clinical data to explore CDK inhibition as a potential neuroprotective target. Finally, using CDK inhibition as an example, this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic injury. | 王伏虎 | 2002 | Journal of Nanjing Medical University2002，16，2： | 0 |
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