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cerebral ischemic preconditioning     
相关语句
  脑预缺血
     Increase in amount and affinity of adenosine receptor in rat hippocampal cellular membranes induced by cerebral ischemic preconditioning and its protective effects on the neurons
     脑预缺血引起大鼠海马细胞膜腺苷受体数量和亲和力升高及其对神经元的保护作用
短句来源
     The adenosine (ADO) mechanism is an important explaining for the protective effects of cerebral ischemic preconditioning (CIP) on neurons. The protective effects are usually referred to as brain ischemic tolerance (BIT). CIP lead to increases in synthesis and release of adenosine.
     腺苷机制是解释脑预缺血(cerebral ischemic preconditioning,CIP)神经保护作用的一个重要学说,即CIP引起脑细胞合成和释放腺苷(adenosine,ADO)增加,后者与其特异性受体结合发挥对神经元的保护作用。
短句来源
  脑缺血预适应
     Method:114 healthy male Wistar rats were randomly divided into 7 groups,i. e.  false operation control (FO)group, cerebral ischemic preconditioning (CIPC) group, ischemic reperfusion (IR) group, NNK 1 group, NNK 2 group, ASP 1 group and ASP 2 group.
     方法 :健康雄性成年Wistar大鼠 114只 ,随机分为假手术组 (FO )、脑缺血预适应 (CIPC)模型组、缺血再灌注 (is chemicreperfusion ,IR)模型组、NNK 1组、NNK 2组、ASP(阿司匹林 ) 1组、ASP 2组。
短句来源
     Objective To explore initially the role of extracellular signal-regulated kinase (ERK1/2) in cerebral ischemic preconditioning.
     目的初步探讨细胞外信号调节激酶(ERK1/2)在大鼠脑缺血预适应中(IPC)的作用。
短句来源
     Objective:To research the influence of Naoningkang (NNK) on endothelin 1 (ET 1) and nitric oxide (NO) level in the model rats of cerebral ischemic preconditioning (CIPC), and observe the protective effects of herbs on ischemic cerebral tissue.
     目的 :研究中药脑宁康 (NNK)对脑缺血预适应 (cerebralischemicpreconditioning ,CIPC)模型大鼠不同时刻ET 1、NO含量的影响 ,以观察中药对缺血脑组织的保护作用。
短句来源
     (2) Except sham operation group, groups a-mong cerebral ischemic preconditioning models showed less changes in CD62P level than those among cerebral ischemia-reperfusion model.
     ②脑缺血预适应模型中除假手术组外,各组CD 62P值均较脑缺血再灌注模型变化幅度小。
短句来源
     CONCLUSION: NNK has positive effect on CD62P expression in both cerebral ischemic preconditioning and cerebral ischemia-reperfusion models, and the effect of NNK group is a little superior to that of aspirin group, this suggests that NNK can inhibit its aggregation, improve local mierocir-culation of brain through interfering in activation of platelet so as to protect cerebral neurons.
     结论:脑宁康颗粒对脑缺血再灌注和脑缺血预适应状态下的CD 62P表达均有良性效应,其强度略高于阿司匹林,说明脑宁康颗粒通过干扰血小板活化,抑制其聚集、改善脑局部微循环,从而保护脑神经元。
短句来源
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  脑缺血预处理
     The expression of apoptosis related genes Bcl-2 and Bax after cerebral ischemic preconditioning in hippocampal CA1 area and its significance
     脑缺血预处理后凋亡相关基因Bcl-2、Bax在海马CA1区的表达及意义
短句来源
     Expression and significance of GAP-43 in hippocampal CA1 region after cerebral ischemic preconditioning in neonatal rats
     新生鼠脑缺血预处理后海马CA1区GAP-43的表达
短句来源
     The mechanism of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP) involves cascades of events including release of neurotransmitter, activation of receptors and gene expression.
     脑缺血预处理(cerebral ischemic preconditioning,CIP)诱导的脑缺血耐受(brain ischemic tolerance,BIT)的产生涉及神经介质、受体及基因的表达等一系列过程。
短句来源
     Objective We observed effects of cerebral ischemic preconditioning (CIP) on apoptosis induced by lethal ischemic insult,and influence of α-methyl-(4-tetrazolyl-phenyl) glycine(MTPG),the antagonist of metabotropic glutamate receptor 2/3 (mGluR2/3),on the effect of the CIP.
     目的观察组代谢型谷氨酸受体阻断剂α-methyl-(4-tetrazolyl-phenyl)glycine(MTPG)对脑缺血预处理(cerebralischemicpreconditioning,CIP)抗损伤性缺血所致海马神经元凋亡作用的影响。
短句来源
     Expressions of synaptophysin and heat shock protein 70 in hippocampus CA1 region after cerebral ischemic preconditioning in newborn rats
     脑缺血预处理对新生鼠海马CA1区突触素及热休克蛋白70的影响
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  “cerebral ischemic preconditioning”译为未确定词的双语例句
     Cerebral ischemic preconditioning test group(IP): 2 min cerebral ischemia and 24 h reperfusion followed by cerebral ischemia 10 min;
     IP组:预处理缺血组,予2 min脑缺血,再灌注24 h后,再次脑缺血10 min;
短句来源
     Expressions of apoptosis-associated genes Bcl-2,Bcl-xl and Bax mRNAs in rat cerebral ischemic preconditioning
     凋亡相关基因Bcl-2、Bcl-xl和Bax mRNA在大鼠缺血预处理脑组织中的表达
短句来源
     cerebral ischemic preconditioning group (group C, n = 5): 3 min cerebral ischemia and 24 h reperfusion followed by cerebral ischemia 10 min;
     C组,预处理缺血组( n=5),予3min全脑缺血,再灌24h后,再次全脑缺血10min;
短句来源
     Cerebral ischemic preconditioning control group(IC): 2 min cerebral ischemia only;
     IC组:预处理对照组,予2 min脑缺血后未再次缺血;
短句来源
     cerebral ischemic preconditioning control group (group B, n = 5 ): 3 min cerebral ischemia only;
     B组,预处理对照组( n= 5),予 3min全脑缺血后未再次缺血;
短句来源
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Objective To determine influence of the cerebral ischemia preconditioning on the neural apoptosis. Methods The whole cerebral ischemia was induced with four-blood vessel occlusion. Twentyone Wistar rats were randomly divided into four groups, sham--operation control group (group A, n = 5 ): without cerebral ischemia; cerebral ischemic preconditioning control group (group B, n = 5 ): 3 min cerebral ischemia only; cerebral ischemic preconditioning group (group C, n = 5): 3 min cerebral...

Objective To determine influence of the cerebral ischemia preconditioning on the neural apoptosis. Methods The whole cerebral ischemia was induced with four-blood vessel occlusion. Twentyone Wistar rats were randomly divided into four groups, sham--operation control group (group A, n = 5 ): without cerebral ischemia; cerebral ischemic preconditioning control group (group B, n = 5 ): 3 min cerebral ischemia only; cerebral ischemic preconditioning group (group C, n = 5): 3 min cerebral ischemia and 24 h reperfusion followed by cerebral ischemia 10 min; and cerebral ischemia group(group D, n = 6): cerebral ischemia 10 min. The apoptotic neural cells were detected by flow cytometry in the rat neocortex. Results The apoptotic cells percentages of group A, B, C and D were (0. 2680 ±0. 2035 ) %, (0. 2780 ±0. 1780) %, (0. 3500 ±0 .0744) % and (0. 6280 ±0 .2181 ) %, respectively. Without significant differeces between group A, B and C (P > 0 .05 ), but the apoptotic cells percentages were markedly in group A, B and C lower than in group D (P < 0.05 ) .Conclusions Cerebral ischemic preconditioning can suppress the apoptosis of neural cells following ischemia.

目的探讨缺血预处理对神经细胞凋亡的影响。方法采用四动脉阻断法大鼠全脑缺血模型,21只Wistar大鼠,腹腔注射戊巴比妥钠麻醉。大鼠分四组:A组,假手术对照组(n=5),未予脑缺血处理; B组,预处理对照组( n= 5),予 3min全脑缺血后未再次缺血; C组,预处理缺血组( n=5),予3min全脑缺血,再灌24h后,再次全脑缺血10min;D组,脑缺血组,予全脑缺血10min。各组动物均在再灌72h后断头取脑。采用流式细胞计数仪检测大鼠前脑皮质凋亡细胞的百分数。结果A组的凋亡细胞百分数是(0.2680 ± 0.2035)%, B组(0.2780±0. 1780)%, C组(0.3500±0.0744)%, D组(0.6280±0.2181)%,A、B及C组间无显著性差异(P<0.05),D组凋亡细胞百分数显著高于A、B及 C组( P< 0. 05)。结论脑缺血预处理可抑制缺血诱导的神经细胞凋亡。

Objective To determine the expressions of apoptosis-regulated genes Bcl-2,Bcl-xl and Bax in rat cerebral ischemic preconditioning.Methods Forty-eight Wistar rats were randomly divided into four groups:sham-operation control group(SHC group),cerebral ischemic preconditioning control group(CIPC group),ischemic preconditioning-cerebral ischemia group(IPCI group)and cerebral ischemic group(CI group).The rats were reperfused in 24h,48h or 72h in each group following ischemia.Semi-quantity...

Objective To determine the expressions of apoptosis-regulated genes Bcl-2,Bcl-xl and Bax in rat cerebral ischemic preconditioning.Methods Forty-eight Wistar rats were randomly divided into four groups:sham-operation control group(SHC group),cerebral ischemic preconditioning control group(CIPC group),ischemic preconditioning-cerebral ischemia group(IPCI group)and cerebral ischemic group(CI group).The rats were reperfused in 24h,48h or 72h in each group following ischemia.Semi-quantity RT-PCR and in situ hybridization were adopted to investigate Bcl-2,Bcl-xl and Bax mRNAs expressions.Results Using semi-quantity RT-PCR,compared with those in SHC group,Bcl-2 mRNA expression increased greatly after 24h and 48h reperfusions in CIPC group and after 24h reperfusion in IPCI,guoup(P<)005),and Bcl-xl mRNA expression rose obviously after 24h reperfusion in CIPC and IPCI groups,while Bax mRNA expression were not significantly different among four groups(WTBX]P>005)P>005).Using in situ hybridization,Bcl-2 and Bcl-xl mRNA expressions increased after 24h reperfusion in CIPC and IPCI group(P<005), without significant difference in Bax mRNA expression among four groups (P>005).Conclusions The expressions of Bcl-2 and Bcl-xl mRNAs increase following cerebral ischemic preconditioning,suggesting that anti-apoptosis genes play important roles in the maintenance of cellular viability after ischemia.

目的 检测脑缺血预处理大鼠脑组织中凋亡调控基因Bcl 2、Bcl xl和Bax的表达。方法 假手术对照组、预处理对照组、预处理缺血组和缺血组Wistar大鼠分别再灌 2 4h ,48h和 72h ,采用半定量逆转录聚合酶链反应 (RT PCR)和原位分子杂交 (ISH)方法对脑组织Bcl 2、Bcl xl和BaxmRNA的表达进行检测。结果 半定量RT PCR显示 :与假手术对照组相比 ,预处理对照组大鼠再灌 2 4h、48h和预处理缺血组大鼠再灌 2 4h脑组织Bcl 2mRNA的表达增高 ;预处理对照组和预处理缺血组大鼠再灌 2 4h脑组织Bcl xlmRNA的表达增高 (P <0 0 5 )。而四组大鼠BaxmRNA的表达无显著性差异 (P >0 0 5 )。ISH方法显示与假手术对照组及缺血组相比 ,预处理对照组和预处理缺血组大鼠再灌 2 4h脑组织Bcl 2、Bcl xlmRNA的表达增高 (P <0 0 5 ) ,各组大鼠BaxmRNA的表达无显著性差异 (P >0 0 5 )。结论 脑缺血预处理后Bcl 2、Bcl xlmRNA的表达增高 ,可能是脑缺血预处理内源性抗损伤的机制之一。

Objective To study the expression of apoptosis regulated genes bcl 2 and bax nocoprotein expression and its significance in rat cerebral ischemic preconditioning. Methods With immunohistochemical assay, bcl 2 and baxexpression were studied in rat brains which were divided into four groups: the sham-operation control group, the cerebral ischemic group and the cerebral ischemic preconditioning group. Results Bcl 2 oncoprotein was induced in cerebral ischemic preconditioning...

Objective To study the expression of apoptosis regulated genes bcl 2 and bax nocoprotein expression and its significance in rat cerebral ischemic preconditioning. Methods With immunohistochemical assay, bcl 2 and baxexpression were studied in rat brains which were divided into four groups: the sham-operation control group, the cerebral ischemic group and the cerebral ischemic preconditioning group. Results Bcl 2 oncoprotein was induced in cerebral ischemic preconditioning control group. Bax oncoprotein expression had no obviously difference in four groups. Conclusions The expression of bcl 2 and bax oncoprotein after sublethal ischemic preconditioning might be associated with the preconditioning protection against neuronal damage following subsequent lethal ischemia.

目的 :探讨凋亡相关基因bcl 2和bax蛋白在脑缺血预处理过程中的表达及意义。方法 :用免疫组织化学SP法分别对假手术对照组、缺血预处理对照组、缺血组和缺血预处理组大鼠前脑组织冰冻切片进行检测。结果 :缺血预处理对照组bcl 2蛋白的表达高于其他 3组 ,而各组bax蛋白表达差异不显著。结论 :缺血预处理对bcl 2蛋白表达的诱导可能是缺血预处理产生抗损伤保护性机制的原因之一

 
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