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    Establishment of the Transgenic Model of Alzheimer's Disease and the Study of Pathogenesis
    阿尔茨海默病转基因动物模型的建立与发病机理研究
    Objective To establish a transient expression system of mouse DVL-lcDNA recombinant plasmid in cultured wild-type mouse Neuroblastoma 2a (N2a), for the further use in studying the role of Wnt signaling in Alzheimer disease pathogenesis.
    目的将鼠dishevelled-1(DVL-1)cDNA重组质粒转染到培养的鼠成神经瘤细胞N2a,建立瞬时表达系统,为研究Wnt信号途径在阿尔茨海默病(AD)发病中的作用提供实验基础。
    Set up Alzheimer's Disease Cell Apoptosis Model with PC-12 Cell Induced by Aβ_(25-35)
    Aβ诱导PC-12细胞凋亡建立阿尔茨海默病细胞模型(英文)
    Examination of Alzheimer's disease model with spatial reference memory and spatial working memory
    空间参考记忆和空间工作记忆检测阿尔茨海默病模型的研究
    Establishment of novel animal model with Alzheimer′s disease
    一种新型阿尔茨海默病动物模型的建立
    The experimental study on an animal model of Alzheimer′s disease by intraventricular injection of the immunotoxin 192-IgG-saporin
    免疫毒素192-IgG-saporin侧脑室注射建立阿尔茨海默病动物模型的实验研究
    A Study of Animal Model with Alzheimer's Disease
    阿尔茨海默病动物模型制备方法的研究
    Epidemiological studies have established that the epsilon 4 allele of the apolipoprotein (apo) E gene (APOE) constitutes an important risk factor for Alzheimer's disease (AD).
    流行病学调查显示,载脂蛋白E基因(apolipoprotein E gene,APOE)的ε4等位基因是阿尔茨海默病(Alzheimer's disease,AD)的重要危险因素。
    ObjectiveThe deposition of 3 -amyloid protein(Aβ) in the brain is believed to be one of the causes of Alzheimer's disease(AD),and Aβ is the proteolytic product of amyloid precursor protein(APP).
    阿尔茨海默病(Alzheimer's disease,AD)的病因之一是脑内淀粉样蛋白(β-amyloid protein,Aβ)的产生和分泌,β来自脑内淀粉样前体蛋白(Amyloid precursor protein,APP)。
    Many researches indicate that Mints are the important material which regulate APP metablism and Aβ production.
    许多研究表明Mints是调节APP代谢和Aβ产生的重要物质,被认为在阿尔茨海默病的病因、病理过程中发挥着极为重要的作用。
    Alzheimer's disease (AD) is a common neurodegenerative disease, which is characterized clinically by a progressive loss of memory and cognitive impairment.
    阿尔茨海默病(Alzheimer's disease,AD)是一种常见的中枢神经系统退行性变性疾病,其主要临床表现为进行性记忆减退和认知障碍。
    Study indicated that over-expression and activation of complement accompany with the whole pathogenesis in Alzheimer's disease, the lesions mediated by complement is one of the important links of action mechanism of Aβtoxicity.
    研究资料显示,补体系统的活化伴随着阿尔茨海默病(Alzheimer’s disease,AD)的整个病理过程,补体系统介导的损害是Aβ细胞毒性作用机制中的重要环节之一。
 

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