脑损伤

Ourresults demonstrate that the expression of mouse BACE 1 is transcriptionally regulatedby HIF-1 and provide a molecular mechanism for increased incidence of ADfollowing cerebral ischemic and stroke injuries.

以上结果说明BACE1基因的表达受转录因子HIF-1的调控，并为脑缺血和中风损伤增加AD发生率的现象提供了分子机制。

The main results and conclusions are as follows: 1. Culrured neurons were damaged by simulated cerebral ischemia and reperfusion in vitro: Results:(1) The activity of the darnaged neurons was decreased, the survival rate was descent.(2) The transudation rate of LDH in cultured medium increased obviously.

体外模拟脑缺血再灌注造成了培养神经元的损伤：表现为：(1)受损神经元的活性降低，细胞存活率下降；(2)细胞培养液LDH的漏出率明显提高；(3)细胞死亡率显著上升；(4)NOS染色强阳性细胞数在缺血期和再灌注早期明显增多。

Cytomorphology changes occurred obviously in cultured neurons such as cell edema, cell atrophy, etc."Jiu Nao Ning"Injection could improve the activity, decrease the transudation rate of LDH and the apoptotic rate. It could also increase the contents of DNA, RNA and improve the pathologic changes in cultured neurons.

救脑宁注射液高、中、低剂量组，在各时间点表现出不同程度地提高细胞代谢率、降低LDH漏出率和凋亡率的作用，与模型组比较p＜0.05；同时也显示出改善细胞形态学异常变化、增加细胞内DNA、RNA含量，保护神经细胞功能与结构免遭损伤等作用，以中剂量效果最好，其与清开灵的药效作用相比，要么相似要么更佳。

objective to observe the protection of typha angustifolial l extract against rats cerebral ischemia reperfusion injury. methods cerebral ischemia reperfusion models of rats were used, 40 rats were divided into 4 groups randomly to observe the activity of brain tissue lactic dehydrogenase and superoxide dismutase and content of malondial dehyde.

目的 观察蒲黄提取物对脑缺血再灌注损伤的保护作用；方法采用大鼠脑缺血再灌注模型；取sd大鼠40只，随机分为4组，给药组分别给予蒲黄提取物0.2g/kg，0.4g/kg灌胃15 d；另设对照组及假手术组；观察脑组织乳酸脱氢酶和超氧化物歧化酶活性及丙二醛含量变化。

These results suggest that nimodipine in addition to its cerebral vasodilating effect may protect brain from ischemic neuronal damage through modifying iNOS expression in the infarct area, and imply that 〓 may be involved in the iNOS expression in ischemic brain tissue which contributes to the recruitment of penumbra into infarction after transient focal cerebral ischemia.

上述结果表明，除了扩张脑血管外，尼莫地平可能还通过抑制iNOS在缺血性脑组织的表达阻止NO过量产生而起到脑缺血损伤的保护作用。鉴于尼莫地平是典型的钙拮抗剂，本结果还提示〓可能涉及缺血脑组织的iNOS表达，从而介入半暗区向梗死区转变的病理过程。

Some related specilist point out ,the modernists dependent upon mobile phone more and more , the mobile phone is not the same as the common ionization radiation ,the wavelength of electronmagnetic wave emanated by the mobile phone is 900MHz to 1800MHz. Although, the DNA has not been damaged by it to certain degree yet , but this microwave can radiate to the depth of encephalic 4 to 6cm . stimulate the water molecules and cells moving ,result in the temperature of corresponding tissue raising 0.1c, induce the fever reflection such as the headache,disfunction of blood supply in brain, cauterized feeling on the skin of face ,ear as well as the skin around the ear etc .also induce the non-fever reflection such as the changing of sleeping style ,raising blood pressureand and disfunction of recognization etc.

0有关专家指出，现代人越来越离不开手机，但不同于普通的电离辐射，手机发射的电磁波波长为900MHz--1800MHz，虽然尚没有达到损伤DNA的程度，但此种微波可以辐射深度达颅内4--6cm，刺激水分子和细胞发生运动，导致相应组织温度上升0.1c，引发如头痛，脑供血障碍，面部皮肤烧灼感及耳部及耳周皮肤烧灼感等热反应，而且可以引起诸如睡眠方式的改变，血压升高，认知功能障碍等非热反应。

Kanic acid was injected into guinea pigs' cochleae and the excitotoxicity model was established. After a week the recombinant plasmid was transferred into SGCs of guinea pigs' cochlea treated with HAT. The following week the expression of NT-3 was examined by the immunohistochemical method, and the morphology of SGNs was observed under the electronic microscope after 4 weeks, in the mean time the changes of auditory brain-stein response were examined.

通过耳蜗灌注海人酸(kainic acid， KA)建立豚鼠耳蜗兴奋性损伤模型，在给KA 1周后利用HAT携带重组质粒进行耳蜗灌注以转染耳蜗螺旋神经节细胞，免疫组化法观察转染后1周NT-3的表达及4周后电镜下螺旋神经节细胞形态学变化，同时观察对听觉脑干诱发电位(auditory brain-stem response， ABR)的影响。

The machanism may be that 7-NI inhibits activation of nNOS and decreases the number of overproducing neuronal NO in hippocampal during anoxia,so the ability of hippicampal slices against anoxic injury is increased and neurotoxic role of neuronal NO during anoxia is definite.

作用机理可能是7-NI抑制nNOS活性降低缺氧后海马神经原性NO的过多形成，从而提高海马脑片抗缺氧损伤的能力，更加明确了缺氧早期神经原性NO的神经毒性作用。

The cerebral mitochondrial impairment model provides a new method to investigate the pathologies and medicines of AD.

NaN3造成的脑线粒体损伤模型为AD机理和治疗药物的研究提供了新的途径。

The effects of gastrodine on the expression of glial fibrillary acidic protein, the transuding amount of lactic dehydrogenase, and the activity of nitric oxide synthase in cultured astrocytes of young rats with lesions caused by simulated cerebral ischemia and reperfusion, were determined in this experiment.

观察天麻素对脑缺血再灌注损伤星形胶质细胞胶原纤维酸性蛋白表达、乳酸脱氢酶漏出量以及一氧化氮合成酶活性的影响。结果：天麻素大、小剂量组GFAP纤维样改变减轻，强阳性反应细胞数减少；LDH漏出量下降；NOS活性减弱。

John Robbins lives with his family in Santa Cruz, California.

约翰罗宾和家人居住在加利福尼亚州的圣克鲁斯县。

The international background is mainly the economic ties among different nations tented to be widen and deepen at the peace and development times.

国际背景主要是和平与发展时代条件下的世界各国经济贸易联系的日益加深。