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Older nursing home residents who took medications for dementia and incontinence at the same time had a 50 percent faster decline in function than those who were being treated only for dementia, according to a study from researchers at Wake Forest University School of Medicine and colleagues.

老年人的护理之家的居民谁了药物的老年痴呆症和性尿失禁在同一时间内有一个50 %的速度下降,功能比那些谁被处理,不仅对老年痴呆症,根据一项研究,从研究后,森林大学医学院的和他的同事。

In 55 % of cases the paraphrenic syndrome has the course of mixed and fantastic confabulatory paraphrenia.

在 55%的持续性进行性患者中,存在混合型与幻想虚构的妄想痴呆症状;而相对较少的,在 45%的患者中,有较为系统的与扩张性的妄想痴呆症状。

objective to study gastrodia elata blume to effect tau protein,sod,mda expression in gyrus hippocampi and cerebral cortex of experimental mice.methods to inject okadaic acid to mice ventriculus lateralis and to measure tau protein level,sod activity and lipid superoxide mda content of sod control group,oa injection group,oa and gastiodia elata injection solution group.results tau protein of experimental group(p<0.05/p>0.05),sod was lower than model group(p<0.001) and was higher than control group(p<0.05).conclusion gastrodia elata blume can increase sod activity and reduce tau protein expression and superoxide lipid forming in brain tissue of experimental dementia mice caused by oa.it can prevent and treat ad.

目的 观察天麻对痴呆模型大鼠海马、皮质神经元微管相关蛋白、超氧化物歧化酶和脂质过氧化物丙二醛表达的影响,探讨其治疗阿尔茨海默病(alzheimer disease,ad)的作用机制。方法用冈田酸(okadaic acid,oa)注射大鼠侧脑室造模,测定模型组、实验组、对照组海马和皮质tau蛋白、sod、mda的含量。结果实验组tau蛋白低于模型组(p<0.001),高于对照组(p<0.05);sod高于模型组(p<0.001)和对照组(p<0.05);mda低于模型组(p<0.001),高于对照组(p<0.05)。结论天麻可增强oa致实验性痴呆大鼠脑组织sod活性,降低mda蓄积和tau蛋白生成,具有防治阿尔茨海默病的作用。

The method uses radiative immunity analysis, determine 43 senile domentia and 33 hemal sexes are gawkish (the β in VD) patient and plasma of 58 healthy old people - the content; analysis of amylaceous appearance albumen and β of observation AD patient - the variable relation of the content of amylaceous appearance albumen and GDS process is reached and treat from beginning to end.

方法应用放射免疫分析,测定43例老年性痴呆和33例血管性痴呆患者及58例健康老年人血浆中的β-淀粉样蛋白的含量;分析和观察AD患者β-淀粉样蛋白的含量和GDS进程的变量关系及和治疗前后β-淀粉样蛋白含量的变化。

Objective To examine the value of Edaravone in the treatment of vascular dementia through ethologic and pathologic changes induced by chronic cerebral ischemiaMethods Wistar rats were randomly divided into sham operated group,model group,edaravone group and duxil groupThe chronic cerebral hypoperfusion models were made by permanent bilateral occlusion of both common carotid arteriesThe memory ability and ultramicrostructure of brain tissue were observedResults The escape latencies in model group were more significantly prolonged than that in the other groups (P<005)But there was no significant difference between edaravone and duxil groupAnd pathologic changes observed by electron microscope in nerve cell of edaravone group and duxil group and model group were fairly light than that in sham operated groupEdaravone group had increased mitochondrium and frontal membranous synaptic vesicle and more productive metabolic activityConclusions Edaravone can lessen injures of hippocampal neurons loss to improve the spatial learning and memory abilitiesAnd it is proved further that edaravone can treat VD

目的 观察依达拉奉对慢性缺血致血管性痴呆大鼠行为学及形态学的影响,探讨依达拉奉在治疗VD中的应用价值。方法实验分假手术组、模型组及都可喜对照组及依达拉奉治疗组,应用双侧颈总动脉结扎方法制备慢性脑缺血大鼠痴呆模型,观察各组大鼠的记忆功能及脑组织超微结构改变。结果缺血组水迷宫表现同对照组、都可喜组及依达拉奉组相比有显著差异(P<005),依达拉奉组与都可喜组相比未见显著差异。同时电镜观察结果也发现依达拉奉组及都可喜组与模型组及假手术组相比神经细胞病理改变较轻,且依达拉奉组线粒体及前膜突触小泡增多,代谢活动较都可喜组旺盛。结论依达拉奉可能通过减轻海马神经元的损伤来改善慢性脑缺血大鼠空间学习记忆障碍,证明依达拉奉对慢性缺血致VD大鼠具有治疗作用。

Vascular dementia is a dementia syndrome due to impairment of brain tissue resulting from a series of cerebrovascular factors, which leads to dysfunction of memorizing, cognition, etc.. It is a common and frequently encountered disease in middle-aged and geratic population.

血管性痴呆(Vascular Dementia,VD)是由一系列脑血管因素导致脑组织损害引起的痴呆综合征,造成患者在记忆、认知等方面的功能障碍,是中老年人群的多发病、常见病。

The purpose of this research is to discuss the probable mechanism of acupuncture treatment combined with pharmacotherapy regulating glutamatergic function and anti-free radical effect on the dementia rats due to hippocampal CA, lesions induced by quinolinic acid. So that the author can provide the clinical application of acupuncture treatment combined with pharmacotherapy with experimental evidences in treating Alzheimers disease.

本文的研究目的是探讨针药结合对喹啉酸(Quinolinic Acid,QA)损毁海马CA_1区所致痴呆大鼠模型的中枢兴奋性神经递质谷氨酸(glutamate,Glu)和抗氧化指标的影响及其对提高痴呆大鼠学习记忆能力的可能机理,为临床针药结合治疗阿尔茨海默氏病(Alzheimers disease,AD)提供实验依据。

Objective: The research of Mild Cognitive Impairment is the hot issue for its high risk for AD, redounding to identify the high risk individual and to find out the methods of prevention.

目的:轻度认知功能障碍因为其高度的AD危险性已成痴呆研究领域的的热点课题,研究MCI有助于识别痴呆高危个体并对探索有效干预途径有重要作用。

Dementia of the Alzheimer type is the leading cause of dementias for the elders.It is a progressively neurodegenerative disorder characterized by global cognitive decline.

阿尔茨海默类痴呆是老年痴呆中最常见的一种,它以渐进性的神经功能退化并伴随着整体认知能力的下降为特征。

If the same results can be obtained from human trials of TMS, this procedure could become an important tool for treating memory-related diseases like Alzheimer's, which result from neuron loss in the hippocampus.

如果对人体尝试颅磁刺激可以得到相同的结果,那么这项研究就能成为治疗像老年痴呆这样与记忆相关疾病的重要方法,老年痴呆症是由大脑海马体结构神经元缺失而导致的。

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