hypoxia-ischemia 中文意思是什麼
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Effects of androgen on superoxide dismutase activity and malonaldehyde content in brain tissues of newborn rats after hypoxia and ischemia
雄激素干預后缺氧缺血新生大鼠腦組織超氧化物歧化酶活性及丙二醛含量的變化 -
Szaflarski, j, burtmm d, silverstein fs. cerebral hypoxia - ischemia stimulates cytokine gene expression in perinaltal rats. stroke, 1995, 26 : 1093
李崗，屠永華，趙光東.腫瘤壞死因子在局部腦缺血/再灌流中的表達.卒中與神經疾病， 1999 ， 6 : 236 237 -
It is well known that paf, a membrane lipid derivative molecule, is increased duing ischemia and hypoxia, which stimulates the further release of glutamate at presynaptic endings. ginkgolide b, one of the component of ginkgo biloba leaves, is a potent paf receptor antagonist
研究者們在篩選和尋找防治缺血缺氧性腦損傷的過程中，已經確實證明了天然銀杏葉的組分之一ginkgolideb是一種強有力的高特異性天然paf受體拮抗劑，可與位於突觸前膜的特異性paf受體結合。 -
Effects of the extract of bulbus allii macrostemi on hypoxia and myocardial ischemia and reperfusion
人工蟲草提取物抗心律失常作用的研究 -
Change of orphanin content in hypothalamus and peripheral blood of fetal rats with ischemia and hypoxia
缺血缺氧胎鼠下丘腦及外周血孤啡肽含量的變化 -
Interventional effects of adenosine triphosphate - magnesium chloride in newborn rats with cerebral injury due to hypoxia - ischemia
氯化鎂對新生大鼠缺氧缺血性腦損傷的干預作用 -
To make clear the hypothesis, a middle cerebral artery occlusion ( mcao ) and hypoxia and glucose - deprivation ( hgd ) ischemic models were used in in vivo and in vitro study, respectively. we first studied the cellular localization of kvl. 2 and the co - localization of kvl. 2 protein and vegf receptors flk - 1 and flt - 1, observed the effect of mcao on kvl. 2 expression and phosphrylation in the rat brain in vivo, then investigated the effect of vegf on ischemia / hypoxia cell damage and tyrosine phosphorylation of kvl. 2 in sh - sy5y cells. finally, in order to further elucidate the relationship between vegf ' s neuroprotection and its regulation on kvl. 2 phosphorylation, we used a specific antisense oligodeoxynucleotide ( odn ) to knockdown the expression of endogenous vegf to observe its role in ischemia / hypoxia cell damage and regulation of kvl. 2 phosphorylation
為了驗證上述假設，本文分別在整體和離體水平，採用大腦中動脈缺血（ middlecerebralarteryocclusion ， mcao ）和體外氧?糖剝奪（ hypoxiaandglucose - deprivation ， hgd ）缺血模型，首先了解了kv1 . 2蛋白的細胞定位及與vegf受體flk - 1和flt - 1的共存情況，觀察了整體mcao后缺血再灌不同時間大鼠腦內kv1 . 2蛋白的磷酸化水平變化，然後通過外源性給予vegf蛋白，在sh - sy5y細胞株上觀察其對缺血細胞存活率及kv1 . 2蛋白磷酸化水平的影響，最後利用vegf反義脫氧寡核苷酸（ oligodeoxynucleotide ， odn ）特異阻斷內源性vegf蛋白的表達，觀察內源性vegf蛋白在缺血細胞損傷及調節kv1 . 2蛋白磷酸化中的作用，以進一步明確vegf缺血保護效應與其調節kv1 . 2蛋白磷酸化之間的關系。
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