J NEUROSCI:脑科学研究院脑缺血后星形胶质细胞的神经保护机制研究取得新进展

2017-03-11 佚名 复旦大学脑科学研究院

脑卒中、心搏骤停、大型心脏手术等都会引起脑缺血,从而引起脑内神经元的损伤、死亡以及脑功能障碍。寻找降低神经损伤、促进神经保护的有效途径,是脑缺血临床治疗研究的首要目的。星形胶质细胞是脑内含量最多的一类细胞,在脑缺血后具有神经保护和加重神经损伤的双重潜能。因此,探索脑缺血后星形胶质细胞的变化及其规律,对于寻找有效途径,调动星形胶质细胞的神经保护作用、抑制其对神经元的损伤非常重要。陈献华副教授带领她的

卒中、心搏骤停、大型心脏手术等都会引起脑缺血,从而引起脑内神经元的损伤、死亡以及脑功能障碍。寻找降低神经损伤、促进神经保护的有效途径,是脑缺血临床治疗研究的首要目的。星形胶质细胞是脑内含量最多的一类细胞,在脑缺血后具有神经保护和加重神经损伤的双重潜能。因此,探索脑缺血后星形胶质细胞的变化及其规律,对于寻找有效途径,调动星形胶质细胞的神经保护作用、抑制其对神经元的损伤非常重要。陈献华副教授带领她的研究生经过5年多的探索,在星形胶质细胞的神经保护机制的研究方面取得重要突破,发现了cpg15蛋白,一种在生理状态下不表达在星形胶质细胞中的神经营养因子,在脑缺血后的海马星形胶质细胞中大量表达,并可以分泌到细胞外,作用于海马神经元,降低其损伤,或促进其修复。该研究成果已于近日发表在国际神经科学著名期刊《神经科学杂志》(Journal of Neuroscience)上。


该研究是在脑缺血小鼠模型和培养的细胞模拟缺血模型上,利用基因敲除等分子生物学的手段进行的。该研究还进一步对脑缺血后调控星形胶质细胞中cpg15基因表达的途径进行了探索,找到了参与调控的相关信号通路。该研究为将星形胶质细胞作为脑缺血疾病临床治疗的干预靶点提供了重要依据。

这一研究成果由博士生赵晶晶,硕士生胡捷先在导师陈献华副教授的指导下完成。该课题获得了国家自然科学基金重点和面上项目、上海市重点学科建设项目的资助。

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    2017-03-12 lsndxfj
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目的:评估辛辛那提院前卒中量表(CPSS)和急诊室卒中识别(ROSIER)工具对急诊科(ED)儿童脑发作的症状的区分情况。方法:回顾性的应用ROSIER和CPSS工具评估2003到2010间的101个卒中儿童,并且从2009到2010年,前瞻性的应用于279例对照组儿童。CPSS阳性为≥1阳性体征(面/不对称的肢体无力、言语障碍),ROSIER阳性为得分≥1。评估这两种工具和患者真实状态之间的准确

Stroke:脑缺血后进行的miRNAs全基因组揭示再灌注相关的miRNA簇有哪些?

循环中改变的miRNA组与脑缺血/再灌注相关,但与脑出血无关,意味着可以作为急性期再灌注的一个潜在生物学标志物。再灌注诱导的位于X染色体内血清素受体HTR2C内含子中的miR-1264/1298/448集群的病理生理作用需要进一步研究调查。

J Hypertens:通过血管事件分析验证急性卒中降压治疗的效果

目的:急性脑出血和缺血性脑卒中早期降血压治疗似乎都是有益的。研究者在斯堪的那维亚坎地沙坦急性卒中试验中,应用新型分析血管事件的方法,观察这种效应是否取决于治疗的时间。方法:斯堪的那维亚坎地沙坦急性卒中试验是一项随机、对照试验,缺血性或出血性卒中30 h内安慰剂和坎地沙坦对照。在前6个月,2029例患者中231(11.4%)有血管事件(血管性死亡、非致死性卒中或非致死性心肌梗死)。血管事件后应用改良

Neurology:年轻脑缺血患者,发生心血管事件的风险较高

目的:为了研究年轻卒中患者复发性心脏、动脉和静脉事件的长期风险,以及不同病因亚组间,这些风险的不同。方法:研究人群包括来自赫尔辛基卒中登记记录(HYSR)的15-49岁缺血性脑卒中(1994-2007年)患者970例。研究者从芬兰护理登记和统计记录中获得直到2012年的随访数据。应用生命表分析累积15年的风险,Cox回归分析得出基于HR的相对风险(RR)和相应的置信区间(CI)。结果:在中位数为1