糖尿病大鼠脑GSK-3与PP-2A失调诱导tau蛋白过度磷酸化

探讨胰岛素缺乏的糖尿病大鼠皮层糖原合酶激酶-3(GSK-3)及蛋白磷酯酶-2A(PP-2A)变化及其对tau蛋白磷酸化的作用.用链脲佐菌素(streptozotocin,STZ)建立胰岛素缺乏的糖尿病大鼠模型,用放射性配体结合实验检测了GSK-3和PP-2A的活性,蛋白质印迹检测了tau蛋白的磷酸化水平及PP-2A的表达.结果提示:在糖尿病大鼠皮层,GSK-3活性升高,PP-2A活性及表达降低,tau蛋白在Ser198/Ser199/Ser202和Ser396/Ser404位点磷酸化.应用GSK-3的选择性抑制剂Li2CO3后,GSK-3活性降低,PP-2A活性及表达恢复,tau蛋白在Ser198/Ser199/Ser202和Ser396/Ser404位点磷酸化水平降低.研究提示:糖尿病大鼠皮层GSK-3升高可能抑制PP-2A的活性,升高的GSK-3和降低的PP-2A协同促进tau蛋白的磷酸化.     

建立海南黎族永生细胞库

采用EB病毒转化外周血B淋巴细胞加环胞霉素A法,建立了含54株海南黎族永生细胞库(男性56%,女性44%),有亲缘关系者占13%。供血者身体健康,三代无与其他民族或支系通婚史。 Abstract:　An immortalized cell bank of the Li Nationality in Hainan Province was successfully established using of cyclosporin A in establishing Epstein-Barr virus transformed human lymphoblastoid cell lines(LCL). This cell bank contains 54 continuous LCL of the RUN LI. All the blood donors are healthy, without intermarriage with other nationalities or different nationality branches for three generations. Moreover male and female make up 56% and 44% of the total donors respectively. 13% of the donors have blood relation.     

Pseudomonas sp.引起欧洲鳗Li烂鳃病的初步研究

欧洲鳗鲡［Ａｎｇｕｉｌｌａ 　ａｎｇｕｉｌｌａ（Ｌ．）］养殖过程中,细菌性疾病危害严重,其中烂鳃病周年发生且发病率高。欧洲鳗烂鳃病常与寄生虫病、真菌病并发,因而给治疗带来了困难。鳗鲡烂鳃病病原主要有柱状屈桡杆菌、噬纤维菌等［１－３］。本文报告由 Ｐｓｅｕｄｏｍｏｎａｓ　ｓｐ．引起的欧洲鳗鲡烂鳃病。１材料与方法１．１病原菌分离取无寄生虫与真菌感染,鳃丝溃烂的濒死病鳗,用无菌生理盐水冲洗体表三遍,解剖取出鳃,经无菌生理盐水充分冲洗后,捣烂鳃丝,接种环取样于普通平板培养基划线,３０℃培养２４ｈ后,挑取形…     

In memory of Prof. C. C. Li

Professor Ching Chun Li (C. C. Li), one of the greatest geneticists in the world and a pioneer of genetics in China, passed away fifteen years ago (Fig. 1). Let us remember him together.**Do you know who the greatest, world-renown Chinese geneticist is?" The answer,**C. C. Li, of course!” would puzzle most, if not all, of us;many in our generation don't know Who is Who (Atte ntion! Li, not Lee, the latter of which was gen erally used as the general spelli ng of that gen eration)(Fig. 2).