医学英文文献阅读 高殿帅

文献(学术论文)阅读 医学学术论文 综述

徐州医学院生物学教研室

高殿帅

综 述 发展的轨迹(线索) 现状的总结(归纳) 指出存在的问题 提出解决问题的策略

不是今天要的内容！有机会再讲。

医学学术论文学术论文是某一学术课题在实验性、理论性或观 测性上具有新的科学研究成果或创新见解的知识 和科学记录；或是某种已知原理应用于实际中取 得新进展的科学总结，用以提供学术会议上宣读、 交流或讨论；或在学术刊物上发表；或作其他用 途的书面文件。 学术论文具有四大特点：①学术性 ②科学性 ③ 创造性 ④理论性

学术论文(科研文章) 学术论文的形态结构(格式)

传递学术论文信息的语言单位 理解学术论文的三层境界

学术论文的形态结构(格式) 题名 作者 摘要 关键词 引言 材料与方法 结果 讨论 致谢 参考文献

How to write a scientific article 如何写科学文章The structure of an article 文章的结构 Ensures the article is correctly identified in Provides supplementary data abstracting and indexing services for the expert reader Ensures previously published work is recognized Keywords 关键词 Main text 正文 Introduction 引言 Methods 方法 Results 结果 Discussion 讨论 Acknowledgments 致谢 References Supplementary material 参考文献 补充资料

Title 题目

Authors 作者

Abstract 摘要

Clearly describes contents Explains the hypothesis Describes succinctly what was done Ensures recognition for the writer/s Explains how the data were collected Describes what was discovered Discusses the implications of the findings Ensures those who helped in the

research are recognized

题 名 题名是以最恰当、最简洁的词语反映学术论文中最重要的 特定内容的逻辑组合。

题名应该具有吸引力。

题名举例 Neural stem and progenitor cells retain their potential for proliferation and differentiation into functional neurons despite lower number in aged brain. Radial glia-like cells persist in the adult rat brain. Noggin expands neural stem cells in the adult hippocampus. Upregulation of chemokine receptor expression by IL-10/IL-4 in adult neural stem cells.

题 名 注意句法结构：完整的句子？ 特定的词组？ 注意内容结构：处理因素 实验对象 实验效应(观察指标)

题名分析Death receptors and caspases but not mitochondria are activated in the GDNF- or BDNF-deprived dopaminergic neurons

摘 要 20世纪60年代国外首先提出科技论文应附摘要，《中华医 学杂志》英文版1972年也提出要求附摘要。

20世纪80年代加拿大温哥华一个研究小组进一步提出结构 式摘要，即要求摘要写法分成四部分，分别冠以标题

,使 读者无需查阅正文即可基本了解实质性内容。

摘 要 摘要具有独立性和自含性，即不阅读全文，就能获得必要 的信息。

摘要一般应说明研究工作目的、材料与方法、结果、结论 等，而重点是结果和结论。

Death Receptors and Caspases But Not Mitochondria Are Activated in the GDNF- or BDNF-Deprived Dopaminergic Neurons

Neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF), promote survival of midbrain dopaminergic neurons, but the death pathways activated in the dopaminergic neurons by deprivation of these factors are poorly studied. We show here that deprivation of GDNF or BDNF triggers a novel mitochondria-independent death pathway in the cultured embryonic dopaminergic neurons: cytochrome c was not released from the mitochondria to cytosol, proapoptotic protein Bax was not activated, and overexpressed Bcl-xL did not block the death. Caspases were critically required, because the death was completely blocked by caspase inhibitor BAF [boc-aspartyl(OMe)-fluoromethylketone] and overexpression of dominantnegative mutants of caspase-9, -3, and -7 significantly blocked the death. Also, the death receptor pathway was involved, because blockage of caspase-8 or FADD (Fas-associated protein with death domain), an adapter required for caspase-8 activation, inhibited death induced by GDNF or BDNF deprivation. Ligation of Fas by agonistic anti-Fas antibody induced apoptosis in the GDNF- or BDNFmaintained neurons, and inhibition of Fas by Fas-Fc chimera blocked the death of GDNF- or BDNF-deprived neurons, whereas FAIML (long isoform of Fas apoptosis inhibitorymolecule) could control the activity of Fas in the dopaminergic neurons.

请翻译！Neurotrophic factors, including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF), promote survival of midbrain dopaminergic neurons, but the death pathways activated in the dopaminergic neurons by deprivation of these factors are poorly studied.包括GDNF和BDNF在内的神经营养因子能促进中脑 DA能神经元的存活，但很少有人研究，在这些DA 能神经元内，由于剥夺这些营养因子而激活的细胞 死亡信号通路是什么。

We show here that deprivation of GDNF or BDNF triggers a novel mitochondriaindependent death pathway in the cultured embryonic dopaminergic neurons: cytochrome c was not released from the mitochondria to cytosol, proapoptotic protein Bax was not activated, and overexpressed Bcl-xL did not block the death.

这里，我们的结果显示：在体外培养的胚胎源DA能神经细胞，剥夺GDNF或 BDNF,激活了这些细胞内一条新的非线粒体依赖性死亡信号通路。因为，没有 细胞色素C从线粒体释放到胞浆、前凋亡蛋白Bax也没有被激活，且过表达Bcl-xL 也不能阻止细胞的死亡。

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