上海市药理学会第十六届学术年会通知（第一轮）
上海市药理学会第十六届学术年会即将召开，欢迎各位会员及相关专业人员积极参加，会议免收注册费。
会议时间：2015年12月11日 星期五13:00-18:00
会议地点：第二军医大学药学院报告厅。
地址：杨浦区国和路325号。
1. 资格要求：投稿者为第一作者（不含并列第一），必须为本会会员，年龄≤35岁（附身份证复印件）。
2. 评审：投稿论文经学会安排评议，并选出一、二、三等奖各若干名，获奖论文将做大会报告。
3. 发表时间要求：大会只接收在2015.1.1—2015.12.11之间正式发表的文章。2014年底发表，去年未及参评的文章可参评，之前已经评过的文章不再重复评奖。
4. 稿件要求：
(1) 稿件正文用英文书写，包括以下内容：
① 题目、作者、单位；
② 刊登的杂志、年份、卷(期)号、起止页码，并在括号内标出该杂志2013年度的影响因子；
③ 摘要：包括目的、方法、结果、结论。必要时对原文摘要的格式进行改写。
④ 范例见后，严格按照范例格式书写。
(2) 提供发表文章的PDF原文。
(3) 提供联系方式：姓名(中文)，手机号码，email地址。
5. 截止日期：2015年11月31日。
6. 递交方式：论文摘要、PDF文章，身份证复印件、会议回执可通过e-mail发送至：aifangquan@sina.com。联系电话：全爱芳021-65493951。
上海市药理学会(盖章)
2015年 10月 26日
摘要范例
The association of autophagy with polyethylenimine-induced cytotoxity in nephritic and hepatic cell lines
Biomaterials, 2011; 32: 8613-8625 (IF 7.882)
Xiao-Ling Gao, Lei Yao, Qing-Xiang Song, Liang Zhu, Zheng Xia, Hong-Zhuan Chen
Department of Pharmacology, Institute of Medical Sciences, Shanghai Jiaotong University School of Medicine, 280 South Chongqing Road, Shanghai, 200025, PR China
Abstract
Aim: Polyethylenimine (PEI) is one of the most effective and widely used cationic macromolecules in experimental gene transfer/therapy protocols. However, the further clinical application of PEI is largely impeded by its cytotoxicity. Here we performed a fundamental investigation on the mechanism of PEI-induced cytotoxicity in both hepatic and nephritic cell lines.
Methods: Cell viability following PEI treatment was measured by CCK-8 assay; The effects of PEI on various cellular organelles were evaluated by high content screening assay; Fluorescence-activated cell sorting analysis was applied to characterize cellular apoptosis; Transmission electron microscopy, confocal microscopy and western blotting techniques were applied to characterize cellular autophagy; Role of autophagy in PEI-induced cytotoxicity was determined following the incorporation of autophagy inducer or inhibitor; Endocytosis pathway of PEI and its role in PEI-induced autophagy were also evaluated by transfecting the cells with GFP-Rabs or following the involvement of endocytosis inhibitors.
Results: It was demonstrated that besides necrosis and apoptosis, autophagy was apparently associated with PEI-induced cytotoxicity and contributed to aggravated cell damage. Specifically, at the early stage (3 h) of PEI-induced cytotoxicity, autophagy was mainly correlated with lysosome damage, but in the later phase (after a 24-h recovery), autophagy was mainly related with mitochondrial injury. Modulation of Rab5, Rab7 expression and inhibition of clathrin-mediated endocytosis pathway significantly affected the formation of autophagosome, which suggested that the endolysosome transport pathway especially the clathrin-mediated endocytosis at least partly facilitated PEI-induced autophagy.
Conclusion: As PEI-induced autophagy played a causative role in its cytotoxicity, it’s highly recommended to design PEI-based gene-carriers that could avoid the endolysosome transport pathway.
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第一作者姓名：XXX；通讯作者姓名：XXX；单位：XXX
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