上海市药理学会第十八届学术年会

暨上海市药学会药理学专委会年度工作会议

（第二轮通知）

上海市药理学会第十八届学术年会暨上海市药学会药理学专委会年度工作会议即将召开，欢迎各位会员及相关专业人士积极参加。

上海市药理学会与中国药理学会、中国卒中学会、中国药理学会心血管药理专业委员会、上海市药学会、以及全国各高校和科研院所、各大医院的著名专家教授、海外学者有着极其广泛的联系和学术交流。多次成功地举办/协办全国性和国际性学术会议。

上海市药理学会第十八届学术年会和上海市药学会药理学专业委员会年度工作会议以药理学和药学最新的研究与进展为主要内容，采用大会报告、专题报告、青年优秀论文报告等多种形式，将邀请来自全国以及上海市各著名高校、研究院和各大医院著名专家教授参会、会议期间还将举行青年优秀论文评奖活动。

一、大会组织机构

主办单位：上海市药理学会 上海市药学会药理学专业委员会

承办单位：中科院上海药物所

主要参加单位：复旦大学，交通大学，同济大学，第二军医大学，中科院上海药物所，国家新药安全评价中心，上海计划生育研究所，上海中医药大学，上海第一人民医院，上海第十人民医院，长海医院，长征医院，徐汇区中心医院

二、大会组织委员会和学术委员会

大会主席：左建平

名誉主席：王永铭 苏定冯 丁健 陈红专

副 主 席：缪朝玉 马璟 黄志力

秘 书 长：刘霞

副秘书长；唐玮

会务主任：全爱芳

三、委 员：(以汉语拼音为序)

曹永兵 毛士龙 王逸平 王永祥 邓中平 叶德全 刘景根 刘皋林 朱依谆 朱 焰 朱 亮 李 佳 陈 红 曲卫敏 沈甫明 侍 茹 张雪梅 姜远英 胡晋红 俞 强 陶 霞 耿美玉 徐宏喜 程能能 楼丽广

四、大会时间和地点

大会将于 2017 年 12月 15日在上海中科院药物研究所举办。

五、   会议免收注册费

六、   论文投稿截止日期： 2017 年 11 月 30 日

七、   会务组联系方式

会务组 e-mail：aifangquan@sina.com。联系电话：全爱芳 021-65493951

参展、赞助联系人：杨磊

电话：15510093885、18500177492

邮箱： yaolixuehui@163.com

八、 论文投稿

即日起开展“青年优秀论文”评选工作，欢迎投稿，有关要求通知如下：

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 2017.1.1—2017.12.30 之间正式发表（含 online）的文章。 2016 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影响因子；

③ 摘要：包括目的、方法、结果、结论四部分。 也可以是发表格式。

④ 范例见后， 除摘要以外，其他信息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： 2017 年 11 月 30 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。

7. 注：无论投稿与否，均欢迎参会。

上海市药理学会(盖章)

2017 年 11 月 15 日

摘要范例

GM1-modified lipoprotein-like nanoparticle: multifunctional nanoplatform for the combination therapy of Alzheimer's Disease
ACS Nano. 2015;9:10801-16. (IF:13.334)
Huang M1#, Hu M1#, Song Q1, Song H1, Huang J1, Gu X1, Wang X1, Chen J2, Kang T2, Feng X2, Jiang D2, Zheng G3, Chen H1*, Gao X1*.
1Department of Pharmacology, Institute of Medical Sciences, Shanghai Jiao Tong
University School of Medicine , 280 South Chongqing Road, Shanghai, 200025, People's
Republic of China.
2Department of Pharmaceutics, Key Laboratory of Smart Drug Delivery, Ministry of
Education & PLA, School of Pharmacy, Fudan University , 826 Zhangheng Road,
Shanghai 201203, People's Republic of China.
3Department of Medical Biophysics and Ontario Cancer Institute, University of Toronto ,
Toronto, Ontario M5G 1L7, Canada.
#The authors contributed equally to this work
* Corresponding authors
Abstract
Aim: Alzheimer’s disease (AD) exerts a heavy health burden for modern society and has a complicated pathological background. The accumulation of extracellular β-amyloid (Aβ) is crucial in AD pathogenesis, and Aβ-initiated secondary pathological processes could independently lead to neuronal degeneration and pathogenesis in AD. Thus, the development of combination therapeutics that can not only accelerate Aβ clearance but also simultaneously protect neurons or inhibit other subsequent pathological cascade represents a promising strategy for AD intervention.
Methods: The particle size distributions and zeta potential of all the nanoformulations were measured via a Zetasizer Nano-ZS90 system; The morphology and size of GM1-rHDL and αNAP-GM1-rHDL were observed under a Hitachi H-7650 transmission electron microscope ; The soluble forms of Aβ, both monomer and oligomer were used to characterize the Aβ-binding affinity of GM1-rHDL via a surface plasmon resonance (SPR) analysis; The cellular uptake of FAM-Aβ1–42 was quantitatively analyzed using an HCS instruments; The remaining intracellular Aβ1–42 levels were quantified with an ELISA kit and normalized to total protein of the lysates. Confocal microscopy was applied to characterize the cellular distribution of DIO-GM1-rHDL; In order to evaluate the brain transport efficiency of GM1-rHDL following intranasal administration, GM1-rHDL and rHDL were separately 125I labeled using the Bolton–Hunter procedureand their radioactivities in different brain sections and in the peripheral organs after nasal dosing were determined with a γ-counter and expressed as percentage of the injected dose per gram of tissue (% ID/g); The neuronal cell viability, mean neurite length, and mean branch point counts quantified via the Neuronal Profiling Bioapplication software. Morphology of the primary neurons was imaged with HCS; ICR mice were intrahippocampally co-injected with Aβ1–42 and IBO to serve as the AD animal model with mice injected with artificial CSF applied as the normal control (sham); The Morris water maze (MWM) test was used to assess the spatial learning and memory of the animals ; The neuroprotective effects of αNAP-GM1-rHDL were evaluated morphologically following Nissl and HE staining. Immunohistochemical analysis was also performed to evaluate the ability of αNAP-GM1-rHDL in reducing Aβ deposition.
Results: We designed a nanostructure, monosialotetrahexosylganglioside (GM1)-modified reconstituted high density lipoprotein (GM1-rHDL), that possesses antibody-like high binding affinity to Aβ, facilitates Aβ degradation by microglia, and Aβ efflux across the blood–brain barrier (BBB), displays high brain biodistribution efficiency following intranasal administration, and simultaneously allows the efficient loading of a neuroprotective peptide, NAP, as a nanoparticulate drug delivery system for the combination therapy of AD. The resulting multifunctional nanostructure, αNAP-GM1-rHDL, was found to be able to protect neurons from Aβ1–42 oligomer/glutamic acid-induced cell toxicity better than GM1-rHDL in vitro and reduced Aβ deposition, ameliorated neurologic changes, and rescued memory loss more efficiently than both αNAP solution and GM1-rHDL in AD model mice following intranasal administration with no observable cytotoxicity noted.
Conclusion: Our work presented the therapeutic potential of GM1-rHDL, not only in accelerating Aβ clearance but also in inhibiting the subsequent pathological cascades, as a promising multifunctional nanoplatform for the combination therapy of AD.

以下信息请提供中文：
联系人姓名：XXX；手机号码：XXXX； email地址：XXXX
第一作者姓名：XXX；通讯作者姓名：XXX；单位：XXX