依达拉奉治疗急性脑梗死的临床分析

研究表明,自由基在脑梗死后继发性脑损伤中起重要作用,依达拉奉(化学名3-甲基-1-苯基-2-吡唑啉-5-酮)为自由基清除剂,对脑细胞有保护作用,近年开始应用临床,2007-01~2008-06使用依达拉奉治疗急性脑梗死30例,取得较好疗效,现报道如下.     

Animal Models of Neurodevelopmental Disorders published

正Animal Models of Neurodevelopmental Disorders(ISBN:978-1-4939-2708-1,e Book ISBN:978-1-4939-2709-8)was published by Humana Press in September 2015.The editor of this book is Jerome Yager,Division of Pediatric Neurology,     

The Molecular Basis of Autism published

正The Molecular Basis of Autism(ISBN:978-1-4939-2189-8,e Book ISBN:978-1-4939-2190-4)was published by Springer-Verlag New York in 2015.The editor of this book is S.Hossein Fatemi,Department of Neuroscience and Pharmacology,     

Systems Biology of Alzheimer's Disease published

正Systems Biology of Alzheimer's Disease(ISBN:978-1-4939-2626-8,e Book ISBN:978-1-4939-2627-5)will be published byHumana Press in 2016.The editors of this book are Juan I.Castrillo and Stephen G.Oliver,Department of BiochemistryCambridge Systems Biology Centre,University of Cambridge,UK.     

14-3-3和CLIC4蛋白在U251细胞自噬中的相互作用

目的通过饥饿诱导神经胶质瘤U251细胞发生自噬,探讨细胞CLIC4和14-3-3蛋白在饥饿条件下诱导自噬过程中的相互作用。方法通过Hoechst、14-3-3 epsilon、CLIC4染色于共聚焦显微镜下观察抑制CLIC4表达对于饥饿条件下,14-3-3 epsilon蛋白与CLIC4共定位的影响。通过Western Blot技术检测Beclin 1及14-3-3蛋白表达。免疫共沉淀技术检测14-3-3 epsilon蛋白与CLIC4蛋白的结合水平。结果共聚焦显微镜观察14-3-3 epsilon和CLIC4荧光染色结果显示,饥饿条件下,14-3-3 epsilon蛋白与CLIC4共定位显著增加,并广泛分布于胞浆及细胞核中。同时Western Blot结果表明抑制CLIC4表达能够引起14-3-3蛋白以及自噬相关蛋白Beclin1表达增加。饥饿条件下,14-3-3 epsilon蛋白与CLIC4共沉淀增强,而抑制CLIC4表达能够降低两者结合水平。结论 14-3-3epsilon蛋白与CLIC4的相互作用由于RNA干扰而减弱,促进了14-3-3蛋白水平上调,进而增强了14-3-3蛋白对Beclin1信号通路的调节,引起Beclin1表达增加,进一步激活饥饿条件下U251细胞自噬过程。     

Cellular Therapy for Stroke and CNS Injuries published

正Cellular Therapy for Stroke and CNS Injuries(ISBN:978-3-319-11480-4,e Book ISBN:978-3-319-11481-1)was publishedby Springer International Publishing in 2015.The editors of this book are Li-Ru Zhao(Department of Neurosurgery,State     

脑微出血对认知功能影响的meta分析

目的探讨脑微出血对认知功能的影响。方法检索中国知网、万方、中国生物医学数据库;Medline、Cochrane Library、Embase英文数据库。使用Rev Man 5.3计算出加权均数差(WMD)和评价发表偏倚。结果该研究共纳入7篇文献,包括366例脑微出血患者和424例未检测出脑微出血的患者。Mo CA总分的WMD是-6.27,95%CI[-7.63,-4.91](P0.01),视空间执行功能的WMD是-1.63,95%CI[-2.06,-1.20](P0.01),命名功能的WMD是-0.42,95%CI[-0.55,-0.29](P0.01),记忆功能的WMD是-1.48,95%CI[-2.32,-0.64](P0.01),注意力的WMD是-0.75,95%CI[-1.13,-0.37](P0.01),语言功能的WMD是-0.43,95%CI[-0.58,-0.28](P0.01),抽象思维的WMD是-0.65,95%CI[-0.98,-0.32](P0.01),定向力的WMD是-0.06,95%CI[-0.11,-0.01](P=0.010.05)。通过剔出每一篇文献进行敏感性分析,结果变化不大。结论该研究显示了脑微出血与认知功能的所有方面均有相关性。但是该结果仍需要大规模的循证医学证据去验证。     

稳定整合靶向性14—3—3ζ基因RNA干涉载体的胶质瘤细胞系建立

目的构建针对细胞凋亡抑制蛋白14-3-3ζ基因的特异性RNA干涉载体,并建立稳定转染该干涉载体的人胶质瘤细胞系。方法根据14-3-3ζ编码序列,设计并合成针对14-3-3ζ基因的特异性RNA干涉片断,并将其克隆入pSilencer3．1．H1neo干涉载体中,构建14-3-3ζ基因shRNA真核表达载体pSilencer-14-3-3ζ。重组载体pSilencer-14-3-3ζ和pSilencer3．1-Hlneo阴性对照载体pSilencer3．1-HlneoNegative经脂质体LipofectamineTM2000介导法转染胶质瘤细胞株U251;转染细胞经过G418筛选,采用Westernblot方法分别在蛋白水平检测、筛选G418抗性的克隆细胞。结果酶切鉴定和核苷酸序列分析证实,成功构建了14-3-3ζ基因shRNA真核表达载体pSilencer-14-3-3ζ,经酶切、测序鉴定证实克隆正确。获得了稳定转染pSilencer-14-3-3ζ载体的胶质瘤细胞株。结论14-3-3ζ基因特异性RNA干涉载体能够显著抑制14-3-3ζ基因在U251细胞中的表达,这为进一步研究14-3-3ζ在胶质瘤细胞系U251中的生物学功能和作用机制奠定了实验基础。     

The Molecular Basis of Autism published

<正>The Molecular Basis of Autism(ISBN:978-1-4939-2189-8,eBook ISBN:978-1-4939-2190-4)was published by Springer-Verlag New York in 2015.The editor of this book is S.Hossein Fatemi,Department of Neuroscience and Pharmacology,University of Minnesota School of Medicine.     

Encyclopedia of Computational Neuroscience published

正Encyclopedia of Computational Neuroscience(ISBN:978-1-4614-6674-1,e Book ISBN:978-1-4614-6676-5)was published by Springer-Verlag New York in 2015.The editors of this book are Dieter Jaeger(Department of Biology,Emory University)and Ranu Jung(Department of Biomedical Engineering,Florida International University).     

Systems Biology of Alzheimer's Disease published

正Systems Biology of Alzheimer's Disease(ISBN:978-1-4939-2626-8,e Book ISBN:978-1-4939-2627-5)will be published by Humana Press in 2016.The editors of this book are Juan I.Castrillo and Stephen G.Oliver,Department of Biochemistry Cambridge Systems Biology Centre,University of Cambridge.     

Animal Models of Neurodevelopmental Disorders published

正Animal Models of Neurodevelopmental Disorders(ISBN:978-1-4939-2708-1,e Book ISBN:978-1-4939-2709-8)was published by Humana Press in September 2015.The editor of this book is Jerome Yager,Division of Pediatric Neurology,University of Alberta.Providing a spectrum of models that is reflective of the various species that can be utilized in experimentation on     

Epigenetic Methods in Neuroscience Research published

<正>Epigenetic Methods in Neuroscience Research (ISBN:978-1-4939-2753-1,eBook ISBN:978-1-4939-2754-8)was published by Springer in 2016.The editor of this book is Nina N.Karpova,Neuroscience Center,University of Helsinki.This volume presents state-of-the-art methods for reliable detection of epigenetic changes in the nervous system.Epigenetic     

Systems Biology of Alzheimer's Disease published

正Systems Biology of Alzheimer's Disease(ISBN:978-1-4939-2626-8,e Book ISBN:978-1-4939-2627-5)will be published byHumana Press in 2016.The editors of this book are Juan I.Castrillo and Stephen G.Oliver,Department of BiochemistryCambridge Systems Biology Centre,University of Cambridge,UK.Alzheimer's disease(AD)and many other neurodegenerative disorders are multifactorial in nature,involving a combination of     

Epigenetic Methods in Neuroscience Research published

正Epigenetic Methods in Neuroscience Research(ISBN:978-1-4939-2753-1,e Book ISBN:978-1-4939-2754-8)will bepublished by Springer in 2016.The editor of this book is Nina N.Karpova,Neuroscience Center,University of Helsinki,Finland.This volume presents state-of-the-art methods for reliable detection of epigenetic changes in the nervous system.Epigenetic     

新型抗精神病药一奎的平

奎的平(Quetiapine),商品名思瑞康(Seroguel)、启维(湖南洞庭药业股份有限公司产),是一种二苯二氮炎衍生物,化学名:2-[2-(4-二苯[b,5][1,4]硫噻平-11-Y1-1呱嗪)乙氧]-乙醇-(E)-2-富马酸盐,结构类似于氯氟平和奥兰扎平,是继利培酮、奥兰扎平之后第三个新型非典型抗精神病药。     

帕金森病模型中热休克蛋白mRNA的表达

热休克蛋白（heat shock proteins, Hsp）在多种神经变性疾病模型中表达增加,并对细胞产生保护作用,因此我们用1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）和它的脑内活性代谢物1-甲基-4-苯基-吡啶离子（MPP＋）制备帕金森病（Parkinson disease, PD）动物和细胞模型,观察Hsp70和Hsp40的人类同源物HDJ-1 mRNA的动态变化和表达部位。     

Systems Biology of Alzheimer's Disease published

正Systems Biology of Alzheimer's Disease(ISBN:978-1-4939-2626-8,e Book ISBN:978-1-4939-2627-5)will be published by Humana Press in 2016.The editors of this book are Juan I.Castrillo and Stephen G.Oliver,Department of Biochemistry and Cambridge Systems Biology Centre,University of Cambridge.Alzheimer's disease(AD)and many other neurodegenerative disorders are multifactorial in nature,involving a combination of     

β-catenin/Tcf-4转录调控AKT2基因表达促进人脑胶质瘤细胞恶性转化的研究

目的 探究胶质瘤中β- catenin/Tcf -4转录调控AKT2基因以促进其恶性表型转化的机制.方法 CHIP - PCR及荧光素酶实验确立AKT2启动子区的Tcf -4结合位点及活性.阿司匹林( ASA)阻断β- catenin/Tcf -4转录复合物活性及恢复AKT2基因的表达后,流式细胞术检测细胞周期,Annexin V检测凋亡及Transwell实验检测侵袭能力.结果 CHIP - PCR表明,AKT2基因启动子区存在两个Tcf -4结合位点- 349/- 343 bp(位点1)和- 3491/- 3497 bp(位点2).荧光素酶实验结果显示位点2的活性比位点1的强.抑制β - catenin/Tcf -4转录活性后,细胞周期阻滞于G0/G1期,侵袭能力下降;恢复AKT2的表达后,细胞S期比例增加,侵袭能力增强.结论 β- catenin/Tcf -4可以直接转录调控AKT2来促进胶质瘤细胞的增殖和侵袭.     

Animal Models of Neurodevelopmental Disorders published

正Animal Models of Neurodevelopmental Disorders(ISBN:978-1-4939-2708-1,e Book ISBN:978-1-4939-2709-8)was published by Humana Press in September 2015.The editor of this book is Jerome Yager,Division of Pediatric Neurology,University of Alberta.Providing a spectrum of models that is reflective of the various species that can be utilized in experimentation on disorders