神经原纤维的

Alzheimer disease: A primary degenerative cerebral disease of unknown etiology with characteristic neuropathologcal and neurochemical features, including cortical atrophy with neurofibrillary tangles and neuritic argentophilic plaques, and a marked reduction on the enzyme choline acetyltransferase, in acetylcholine itself, and in other neurotransmitters and neuromodulators.

阿尔茨海默病：一种病因未明的原发退行性大脑疾病，具有特征性的神经病理和神经生化改变，包括伴有神经原纤维缠结和神经炎性嗜银斑的皮层萎缩，胆碱乙酰转移酶、乙酰胆碱本身、以及其它神经递质和神经调质的明显减少。

Alzheimers disease is a progressive neurodegenerative disorder characterized by global cognitive decline involving memory, orientation, judgment, and reasoning, and occurs with pathological hallmarks including widespread neuronal degeneration and neuritic plaques containing amyloid-β peptide.

阿尔茨海默病(Alzheimers disease，AD)是一种以记忆、语言、认知、理解、判断及情感等智能全面低下为特征的神经退行性疾病，以神经元内大量神经原纤维缠结，神经元周围大量β淀粉样蛋白沉积为主要病理特征。

Hyperphosphorylation of tau protein composition of the original nerve fibers tangle AD is the main feature of neuropathology.

过度磷酸化的tau蛋白组成的神经原纤维缠结是AD的主要神经病理学特征之一。

BACKGROUND: One of the key neuropathological changes in Alzheimer disease is that neurofibrils over phosphorylated cytoskeletal protein composed of entwist together, and the phosphorylation of τ protein can be catalyzed by cyclin dependent kinase 5 (CDK5),however whether the phosphorylation of neurofilaments can be catalyzed by CDK5, as well as its role in the pathogenesis of Alzheimer diseases is less acknowledged.

背景：阿尔茨海默病的主要神经病理学特征之一是由过度磷酸化的细胞骨架蛋白如(o，神经细丝组成的神经原纤维缠结，细胞周期蛋白依赖性蛋白激酶5可催化蛋白的磷酸化，但神经细丝是否可被细胞周期蛋白依赖性蛋白激酶5磷酸化及其在阿尔茨海默病发病中的作用却知之甚少。

In a series of 300 brain autopsies, 18 cases were diagnosed as Alzheimer 's disease with 10 male and 8 female average age 71.2 years(61 to 86) and courses of disease 0.5 to 6 years. All of them presented some degree of intellectual impairment. The clinical symptoms Progressed gradually. Pathologically, in all cases brain atrophy (mild degree in 6 cases, moderate degree in 8 cases and severe degree in 4 cases)was observed.Microscopically large amount of senile Plaques and neurofibrillar...

在连续300例尸检脑标本中，筛选出60岁以上18例Alzheimer病，占6％；病程6个月～6年，均表现不同程度的智能障碍。18例病理检查见重度脑萎缩4例，中度8例，轻度6例；镜下于脑叶皮质和海马区见大量老年斑及神经原纤维缠结，8例海马区有颗粒空泡变性。18例脑皮质神经元均明显减少，与对照组比较差异有非常显著性（P＜0.0001）。11例AD并存有淀粉样脑血管病。

Methods OA was injected into hippocampal CA1 region of rats. We observed rat praxiology changes by Morris water maze and the senile plaques and neurobrillary tangles of hippocampus by Bielschowsky stain and the expression of β-amyloid protein and neuronal nitric oxide synthase of the rats hippocampus by immunohistochemistry.

在大鼠海马CA1区多次微量注射OA，水迷宫实验观测大鼠行为学改变；Bielschowsky染色观察海马CA1区神经原纤维缠结和老年斑等特征性病理变化；免疫组化方法观察海马CA1区Aβ1-40和nNOS的表达。

It is an important regalator for brain development, nerve location, and synaptic transmission.

过度磷酸化的tau蛋白组成的神经原纤维缠结是AD的主要神经病理学特征之一。

PART Ⅱ IMMUNOPATHOLOGICAL EVIDANCE OF SIALIC ACID STRUCTURE IN CAMPYLOBACTER JEJUNI AS THE CRITICAL ANTIGEN TO INDUCE PERIPHERAL NEUROPATHY To demonstrate the critical role of NANA structure in the pathogenesis of allergic peripheral neuropathy induced by Campylobacter jejuni and provide immunopathological evidence to confirm the supposition of molecular mimicry and cross-immunity between CJ LPS and gangliosides in nerve.

LPS免疫后第2周实验豚鼠的免疫血清中，抗LPS IgG抗体滴度均明显增高，第3周达高峰，第5周仍维持在峰水平，野生株和突变株LPS免疫血清中的抗-野生株LPS IgG抗体滴度较各自免疫前分别增高8倍和4倍，抗-突变株LPS IgG抗体滴度则较各自免疫前分别增高6.5倍和15倍；(2)全身免疫后第3周和第5周，野生株LPS免疫血清中检测到较免疫前增高6倍的抗-GM1 IgG抗体，而NANA缺失的突变株LPS免疫血清中一直未检测到抗-GM1 IgG抗体；(3)野生株LPS免疫组中有17.3％的坐骨神经原纤维发生以轴索变性为主（占65％）的免疫性损伤，与突变株LPS免疫组和对照组比较均有显著性差异。

Histologically, all tumors were composed of compacted small uniform round cells, with honycomb nests and cell-free islands of neuropil matrix within the tumor.

组织由密集的小圆形细胞组成，胞浆透明，有核周晕，呈蜂窝状结构，并有无细胞性神经原纤维岛特征。

In the negative and interrogative forms, of course, this is identical to the non-emphatic forms.

。但是，在否定句或疑问句里，这种带有"do"的方法表达的效果却没有什么强调的意思。

Go down on one's knees;kneel down

屈膝跪下。。。下跪祈祷