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缺血性脑损伤的
    Conclusion The expressions of STAT3 increased might indicate the transmission course in ischemic nerve cell signal,and play a key role in neuron apoptosis of ischemic brain injury.
    结论STAT3蛋白表达增强可能介导缺血性脑损伤的信号转导过程,其在脑缺血损伤神经元凋亡过程中起关键作用。
    Protective effects of the MK801 on the hypoxic ischemic brain injury
    MK801对缺氧缺血性脑损伤的保护作用
    Objective To study the influence of electroacupuncture on the expression of Nestin in neural stem cells after focal cerebral ischemia in rats and to explore the mechanism of electroacupuncture in treating ischemic brain injury.
    目的研究电针治疗对成年大鼠脑缺血后缺血侧神经干细胞巢蛋白(nestin)表达的影响,探讨电针治疗缺血性脑损伤的作用机制。
    AIM To investigate effects of piracetam on calcium activated potassium channels of hippocampal neurons in hypoxic rats so as to reveal the electrophysiological mechanism about the anti-effect of piracetam on ischemic brain injury.
    目的:研究吡拉西坦对缺氧大鼠海马神经元钙激活钾通道的作用,以揭示吡拉西坦抗缺血性脑损伤的电生理途径。
    The Protect Effect of K~+ Channel Openers (KCOS) on Ischemic Brain Injury in Rat
    钾通道开放剂对大鼠缺血性脑损伤的保护作用
    Nursing Care of Neonates With Hypoxic Ischemic Brain Injury Accepted Sub-hypothermia Therapy
    亚低温治疗新生儿缺氧缺血性脑损伤的护理
    Anti-oxidation mechanism of tetramethylpyrazine against ischemic brain injury
    川芎嗪的抗氧化机制对缺血性脑损伤的保护作用
    Reactive ability of nerve stem cell to ischemic brain injury
    神经干细胞对缺血性脑损伤的反应能力(英文)
    The present study chosen two kinds of Huoxue Huayu drugs, Angelica sinensis and Erigeron Breviscapus, investigated the protective effect of the Huoxue Huayu drugs for the ischemic brain injury in following six aspects, for the hippocampal neurons in hypoxia lesion, as well as potential effect for the neural regeneration, aims to elucidates the mechanisms of Huoxue Huayu drugs.
    本文选择两种活血化瘀药当归和灯盏花,从6个方面研究药物对缺血性脑损伤的保护作用,对神经元缺氧损伤的直接保护作用,及可能的神经再生作用,旨在阐明活血化瘀药的作用机制。
    Inflammatory reactions of central nerve system play an essential role in the pathophysiologic process of ischemic brain injury, especially during the enlargement of damage and the secondary damage after ischemia.
    中枢神经系统的炎症反应,在缺血性脑损伤的病理生理过程中发挥着重要的作用,尤其是在缺血后的继发性损伤及损伤的扩大的过程中扮演重要角色。
    At present, the study of molecular mechanism of ischemic brain injury has been becoming a hotspot, and people advanced a lot of theories on it, but till now we still do not understand the mechanism exactly.
    近年来,缺血性脑损伤的分子机制已成为国内外学者研究的热点课题之一,提出了许多假说,但其详细机制仍然不很清楚。
    Conclusion: NOS> NO probably involved in ischemic brain injury of ICH, an excess of NO do damage to brain tissue.
    结果提示:NOS、NO可能参与了脑出血后缺血性脑损伤的过程,过量的NO对脑组织具有损害作用。
    With the progress of molecular biology, recently it is found that the ischemic cascade reaction, called“ischemic cascade”, including ischemic-hypoxic energy metabolic dysfuntion,release of excitatory neuromediator, calcium over inflow, free radical reaction, cell apoptosis and so on, makes the central part of ischemic brain injury.
    随着分子生物学的发展,近年发现缺血、缺氧造成的能量代谢障碍—兴奋性神经介质释放—钙过量内流—自由基反应—细胞死亡等一系列缺血性连锁反应是导致缺血性脑损伤的中心环节,称之为缺血瀑布。 围绕这一理论,通过药物或其他手段干预阻断瀑布反应链中不同机制、不同环节的生化和代谢紊乱被称为神经保护治疗。
    Although there have been a large number of studies involved in many aspects of ischemic brain injury, the biological mechanisms of post-stroke depression are still in the dark.
    尽管已有大量文献涉及缺血性脑损伤的诸多方面,但脑卒中后抑郁的生物学机制尚不甚明了。
    This suggests that intensifying the synthesis and release of ET may be one of the mechanisms for the involvement of monocytes in the pathologic process of ischemic brain injury during acute cerebral infarction. DXM can improve this process by inhibition of producing monocyte-derived ET. 
    提示:急性脑梗塞时,单核细胞增加ET的合成与释放可能是其参与缺血性脑损伤过程的机制之一,而DXM则抑制其合成与释放,具有改善缺血性脑损伤的作用
    CONCLUSION:ET may be deleterious to cerebral infarction and the protective action of EGb761 in ischemic brain injury may be related to its action in lowering ET concentration.
    结论:EGb761对缺血性脑损伤的保护作用可能与其抑制脑缺血急性期ET的生成有关
    Conclusions The TNF α may be a pathogenic factor in senile cerebral infarction and an important factor in the worsening of ischemic brain injury.
    结论  TNF α是老年脑梗塞的致病因子和加重缺血性脑损伤的重要因素
    Aim:To investigate the effects of K + channel openers in ischemic brain injury.
    目的 :探讨K+ 通道开放剂对于缺血性脑损伤的保护作用。
    Neural stem cells and differentiated cells were identified by immunocytochemistry. Newborn rats were sustained hypoxic ischemic brain injury. One week later, animals received neural stem cells transplants(operated group=16) or PBS transplants(control group=8).
    用出生 7天的SD大鼠的新生鼠制作缺氧缺血性脑损伤的动物模型 ,7天后接受神经干细胞移植 (移植组 ,n =16只 ) ,同时设置对照组 ,只注射磷酸缓冲液 (对照组 ,n=8只 )。
    Objective To investigate the roles of peripheral blood mononuclear cells (PBMC) in the pathogenesis of ischemic brain injury.
    目的 探讨单个核细胞参与缺血性脑损伤的机制。
 

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