Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
附件 1:征文要求 1、摘要内容跟会议主题相关,分为模型创建、疾病机理、新药评价和基因 功能 4 个专题,投稿时请注明所属专题。摘要论点明确、叙述清楚、文字精炼, 限 800 字以内,包括题目、作者及单位、E-Mail 地址。要求使用英文撰写,所有 字体为 Times New Roman;标题为四号字加粗,署名小四号字,单位小五号字, 正文五号字单倍行距(详见下面范例)。 2、请尽量提交近年来尚未发表的学术论文摘要。 3、请提供能反映您成就的个人资料(不超过 500 字)及近期照片。 4、本次会议采用邮件投稿,请将稿件统一发送至会务组邮箱: [email protected]。投稿截止日期:2014 年 10 月 31 日。 摘要范例 Decreased mitochondrial DNA copy number in the hippocampus and peripheral blood during opiate addiction is mediated by autophagy and can be salvaged by melatonin Yue-Mei Feng,1,2 Yun-Fang Jia,1,2 Ling-Yan Su,1,2 Dong Wang,1,2 Li Lv,1,2 Lin Xu1,* Yong-Gang Yao1,* 1Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province; Kunming Institute of Zoology; Kunming, Yunnan China; 2University of Chinese Academy of Sciences; Beijing, China Abstract:Drug addiction is a chronic brain disease that is a serious social problem and causes enormous financial burden. Because mitochondrial abnormalities have been associated with opiate addiction, we examined the effect of morphine on mtDNA levels in rat and mouse models of addiction and in cultured cells. We found that mtDNA copy number was significantly reduced in the hippocampus and peripheral blood of morphine-addicted rats and mice compared with control animals. Concordantly, decreased mtDNA copy number and elevated mtDNA damage were observed in the peripheral blood from opiate-addicted patients, indicating detrimental effects of drug abuse and stress. In cultured rat pheochromocytoma (PC12) cells and mouse neurons, morphine treatment caused many mitochondrial defects, including a reduction in mtDNA copy number that was mediated by autophagy. Knockdown of the Atg7 gene was able to counteract the loss of mtDNA copy number induced by morphine. The mitochondria-targeted antioxidant melatonin restored mtDNA content and neuronal outgrowth and prevented the increase in autophagy upon morphine treatment. In mice, coadministration of melatonin with morphine ameliorated morphine-induced behavioral sensitization, analgesic tolerance and mtDNA content reduction. During drug withdrawal in opiate-addicted patients and improvement of protracted abstinence syndrome, we observed an increase of serum melatonin level. Taken together, our study indicates that opioid addiction is associated with mtDNA copy number reduction and neurostructural remodeling. These effects appear to be mediated by autophagy and can be salvaged by melatonin. Keywords: addiction, morphine, mitochondrial dysfunction, autophagy, melatonin * Corresponding Author, E-mail: [email protected] or [email protected] 个人简介范例 Prof. Lin Xu, Principle Investigator and Director, Key Lab of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences. The research is mainly focused on the fundamental basis of neuronal information encoding, storage and retrieval and the underlying cellular and molecular mechanisms; building animal models to investigate the pathogenesis of a series of psychiatry disorders including drug addiction, depression, autism, Schizophrenia and AD; utilizing the natural plant recourses to develop novel drugs for the treatment of anti-psychiatry disorders. More than 60 papers were published in these high-ranked journals such as Nature, PNAS, Neuron, Cell and Biol Psychiatry. Won rewards including “Tan-jiazheng life scientific innovation prize”, “973 special advanced individual” etc. and applied a number of domestic and foreign patents. More than 30 postgraduated students got MSc or PhD.