卒中样的

基本解释 (translations)

apoplectiform

与卒中样的相关的网络例句 [注：此内容来源于网络，仅供参考]

After comparing the clinical symptoms and physical signs between the analogous apoplexy group and apoplexy one, using American SAS statistical analysis soft ware to take logistic regression analysis on 2206 cases, combining with clinical practice, bibliography investigation and specialists experience, the main symptoms of analogous apoplexy were defined as vertigo, sensory disturbance, severe headache, visual abnormality, involuntary movement, mental aberration, epileptic attack, agnosia, alexia and agraphia, etc.

将临床上不以传统中风的突然昏仆、半身不遂、口舌歪斜、语言謇涩或不语、偏身麻木为主要临床表现的西医脑卒中统归为类中风进行研究运用类中风组与中风组临床症状体征对照的研究方法，采用美国SAS统计分析软件，对2206例调研资料进行logistic回归分析等多因素分析参考回归结果，并结合临床实际、文献调查、专家经验，从而确定了类中风的主症为眩晕，身体感觉障碍，剧烈头痛，视物异常，不随意运动，精神障碍，癫痫样发作，失认失读失写等为类中风的进一步研究奠定了基础

Methods: Retrospective study of 49 patients with confirmed primary amyloidosis and ischemic stroke.

回顾性研究已经经过确诊的原发性全身性淀粉样变性和缺血性卒中的49例病例。

Objective To analyze clinical characteristics of 3 cases of MELAS syndrome that misdiagnosed as hepers simplex virus encephalitis.

目的 分析误诊为单纯病毒性脑炎的3例线粒体脑肌病伴乳酸血症和卒中样发作的原因。

Objective To analyze clinical characteristics of 8 cases of MELAS syndrome that misdiagnosed as herpes simplex virus encephalitis.

目的分析误诊为单纯疱疹病毒性脑炎的8例线粒体脑肌病伴乳酸血症和卒中样发作综合征的临床特征。

Objective To analyze clinical characteristics of 8 cases of MELAS syndrome that misdiagnosed as herpes simplex virus encephalitis.

线粒体脑肌病伴乳酸血症和卒中样发作综合征具有线粒体脑病、高乳酸血症和卒中样发作的特征，确诊主要依赖临床表现和肌肉病理检查。

The results indicate that idebenone improves mitochondrial oxidative metabolism in the brain and suggest a therapeutic potential of idebenone for MELAS.

本结果指明艾地苯醌改善了患者大脑线粒体的氧化代谢，同时並提示艾地苯醌具有治疗MELAS（线粒体脑肌病伴高乳酸血症和卒中样发作）的潜在效应。

We report a 36-year-old man with MELAS in whom a 5-month course of high-dose oral idebenone, a derivative of coenzyme Q10, increased markedly cerebral metabolic ratio of oxygen and oxygen extraction fraction without increased cerebral blood flow with PET.

我们报告了一例36岁患MELAS（线粒体脑肌病伴高乳酸血症和卒中样发作）的患者，在口服一种辅酶Q10衍生物艾地苯醌后，显著地增加了氧气和氧提取部分的比例而同时不增加患PET症的患者的脑血流量。

After administration of L-N〓-nitro-Arginine, a specific antagonist of NOS, it was found that the basal and stimulated NO release of blood vessels (aorta, internal carotid, renal and mensenteric artery) was decreased further. The increase of coronary blood flow stimulated by Ach was also reduced further, while the platelet aggregation degree and erythrocyte aggregation index increased significantly. Pathological examination indicated that aortic endothelium was destroyed, the blood vessels in cerebral, cardiac and renal tissues were hypertrophied further and some were almost occluded. The above fin dings resulted in SHR feeded with L-NNA having high incidence of stroke rate and high degree of renal cirrhosis when compared to control SHR. The infarct and hemorrhagic focuci in cerebral tissues, infarct focuci in cardiac tissues, atrophy and hyalinedegeneration of renal glomeruli and degeneration even necrosis of renal tubuli in renal tissues were al so found. The increase ratio of brain and heart to body weight and decrease ratio of kidney to body wei ght further demonstrated that the cerebral, cardiac and renal injuries were aggravated.

在上述结果的基础上进一步给予SHR NOS特异性拮抗剂左旋亚硝基精氨酸后，血管(胸主、颈内、肾及肠系膜动脉)NO基础释放及激动剂刺激释放进一步减少，Ach刺激冠脉流量的增加和胸主动脉内膜NOS活性也进一步减少，血小板聚集程度及红细胞聚集指数显著上升，病理切片显示胸主动脉内皮细胞破坏明显，脑心肾组织内的血管进一步增厚甚至几乎阻塞，导致饲L-NNA的SHR缺血性及出血性脑卒中发生率显著高于对照SHR，脑体重比显著升高；心肌内出现明显的缺血梗塞疤痕灶，心体重比显著升高；肾小球明显萎缩、玻璃样变性，肾小管也变性甚至坏死，使肾硬化程度显著增加呈颗粒性固缩肾，肾体重比也显著减少。