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暂时性脑缺血
相关语句
  transient cerebral ischemia
     INDUCTION OF EXPRESSION OF PROTO-ONCOGENE C FOS AND ORNITHINE DECARBOXYLASE GENES BY TRANSIENT CEREBRAL ISCHEMIA
     暂时性脑缺血诱导c-fos原癌基因和鸟氨酸脱羧酶基因表达
短句来源
     Transplantation of gene-transfected neural stem cells for transient cerebral ischemia in rats
     转基因神经干细胞移植治疗暂时性脑缺血的实验研究
短句来源
     After transient cerebral ischemia, the release of cytochrome C occurs from mitochondria, preceding DNA fragmentation.
     轻中度暂时性脑缺血后细胞色素C释放至胞质 ,早于DNA片段化
短句来源
     Transient cerebral ischemia/reperfusion rat model was adopted, and the method of H&E staining, TUNEL staining (TdT-mediated dUTP Nick End Labeling) were used to observe the effect of electroacupuncture (EA) and basic fibroblast growth factor (bFGF) on neuronal death.
     采用暂时性脑缺血再灌注大鼠模型,及H&E、TUNEL细胞染色等实验技术,观察电针或碱性成纤维生长因子,以及两者合用对缺血性神经细胞死亡的影响。
短句来源
     The results showed that transient cerebral ischemia/reperfusion evidently increased the expression of NOS, as well as induced the delayed neuronal death, which included both necrosis and apoptosis.
     实验结果表明 ,暂时性脑缺血再灌注时脑内NOS表达显著增加 ,且引起延迟性细胞死亡 ,包括坏死与凋亡。
短句来源
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  transient cerebral ischemic
     Intercellular adhesion molecule 1 (ICAM 1) expression was studied with rat transient cerebral ischemic model.
     本文用暂时性脑缺血的大鼠模型对血管内皮细胞间粘附分子1(ICAM1)的表达进行了研究。
短句来源
     METHODS: Dextran was intravenously injected and quatitatively examined in the rat transient cerebral ischemic model. At the same time, endothelial glycocalyx (anionic sites) was labelled with the probe cationic gold colloid (CGC) using post-embedding technique and examined with electron microscope.
     方法 :用暂时性脑缺血的大鼠模型 ,以右旋糖酐分子为示踪剂对缺血再灌注后微血管通透性的变化进行了观察 ,同时用同一标本经K4M低温包埋 ,用阳离子胶体金包埋后标记的方法在超微结构显示缺血再灌注后内皮细胞表面糖复合物 (glycocalyx)的变化。
短句来源
  temporary cerebral ischemia
     Comparative Research on the Influences of Electroacupuncture of Adjacent and Distant Acupoints on NO Contents of Brain Tissues and Serum in Rats with Temporary Cerebral Ischemia
     电针远近部位穴位对暂时性脑缺血大鼠脑组织、血清一氧化氮含量影响的比较研究
短句来源
  “暂时性脑缺血”译为未确定词的双语例句
     Experimental Study of Neural Stem Cells Transplantation for Treatment of Cerebral Ischemia
     神经干细胞移植治疗暂时性脑缺血的实验研究
短句来源
     The incidence of angina pectoris and transient ischemic attack was different significantly when compared with control group(P<0.01 or P<0.05),but not for the other indexes between two groups(P>0.05).
     心绞痛和暂时性脑缺血发作发生率与对照组相比差异有显著性(P<0.01或P<0,05),其他各项比较差异无显著性(P>0.05)。
短句来源
     Objective To investigate neuroprotection of the prophylactic treatment of resveratrol against transient focal cerebral ischemia and its effect on matrix metalloproteinase 9 (MMP-9) in mice.
     目的探讨白藜芦醇预治疗对小鼠暂时性脑缺血的脑保护作用及其对基质金属蛋白酶-9(MMP-9)表达及活性的影响。
短句来源
     RESULTS The success rates of animal models of permanent focal cerebral ischemia in ICR and DDR mice were 96% and 70% respectively, while those of transient focal cerebral ischemia were 57% and 83% respectively.
     而暂时性脑缺血模型ICR小鼠成功率为5 7% ,DDY小鼠成功率为 83% .
短句来源
     In contrast to c-fos and ODC genes, c-myc gene expression can not be induced by ischemia.
     但是暂时性脑缺血却不能诱导c-Myc基因表达。
短句来源
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  transient cerebral ischemia
Postprandial limb-shaking: an unusual presentation of transient cerebral ischemia
      
Transient cerebral ischemia (5 min) releases unesterified fatty acids from membrane phospholipids, increasing brain concentrations of fatty acids for up to 1 h following reperfusion.
      
The effect of transient cerebral ischemia on phosphorylation of the microtubule-associated protein (MAP) τ was investigated using the rat four-vessel occlusion model.
      
These results show that cloricromene, a drug with multiple actions, improves brain injury induced by transient cerebral ischemia.
      
The 4-vessel occlusion model was used to cause transient cerebral ischemia which damages CA1 pyramidal cells in the dorsal hippocampus, but spares nonpyramidal neurons and afferents in the area.
      
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  transient cerebral ischemic
Unruptured large intracranial aneurysms in patients with transient cerebral ischemic episodes
      
This report analyzes the treatment of six patients with transient cerebral ischemic episodes in combination with large unruptured aneurysm.
      
Five patients in our series experienced transient cerebral ischemic attacks.
      
Involvement of cytokine production in pathogenesis of transient cerebral ischemic damage.
      
  temporary cerebral ischemia
Recovery without residual neurological damage after cardiac arrest with temporary cerebral ischemia is rare.
      


The levels of mRNAs for proto-oncogene c-fos and ornithine decarboxylase (ODC)genes were measured in rat cerebral cortex and hippocampus at various recirculation intervals after 20 minutes of ischemia. Striking increases in c-fos and ODC genes expression were observed in rat cerebral cortex 0.5-3h and 6-14h respectively after recirculation. In the meantime, delayed expression of of c-fos and ODC genes were noticed in rat hippocampus 36~72h after recirculation. In contrast to c-fos and ODC genes, c-myc gene expression...

The levels of mRNAs for proto-oncogene c-fos and ornithine decarboxylase (ODC)genes were measured in rat cerebral cortex and hippocampus at various recirculation intervals after 20 minutes of ischemia. Striking increases in c-fos and ODC genes expression were observed in rat cerebral cortex 0.5-3h and 6-14h respectively after recirculation. In the meantime, delayed expression of of c-fos and ODC genes were noticed in rat hippocampus 36~72h after recirculation. In contrast to c-fos and ODC genes, c-myc gene expression can not be induced by ischemia. These results imply some specific role of c-fos and ODC after ischemic brain injury. In this article, we analysed the mechanism that recirculation after ischemia induces c-fos and ODC genes expression, and proposed the concept - neuronal stress state to describe neuronal response to destructive stimulation.

应用大鼠椎动脉与颈内动脉结扎造成暂时性脑缺血再灌注以及RNA点杂交方法观察c-fos基因与鸟氨酸脱羧酶(ODC)基因表达的动力学过程。结果表明:大鼠大脑皮质c-fos基因在再灌后0.5至3小时表达,ODC基因在6小时至14小时表达;海马的c-fos基因则自36至72小时呈现高水平表达,ODC基因表达与之相对同步或稍延后。但是暂时性脑缺血却不能诱导c-Myc基因表达。上述结果提示c-fos及ODC可能在缺血型脑损伤后具有特殊作用。文中对缺蛋再灌引起cfos-及ODC基因表达的机制进行了分析与讨论,并提出“神经元应激状态”这一概念以描述神经元对伤害性刺激的反应历程。

In the present study we examined the ischemic neuronal damage of hippocampus following transient ischemia in the rat model of four-vessel occlusion.By LM three different type of heteroge- nous changes were observed as previous paper described.Ultrastructural examination revealed the pyramidal cell with neuronal somata swollen and axon terminals dilated and edematous.The ER cisterane were distended and fragmented.In addition we used a modification of the oxalate-pyroan- timonate technigue to demonstrate the specific...

In the present study we examined the ischemic neuronal damage of hippocampus following transient ischemia in the rat model of four-vessel occlusion.By LM three different type of heteroge- nous changes were observed as previous paper described.Ultrastructural examination revealed the pyramidal cell with neuronal somata swollen and axon terminals dilated and edematous.The ER cisterane were distended and fragmented.In addition we used a modification of the oxalate-pyroan- timonate technigue to demonstrate the specific subeellular compartmentalization of Ca~(++)pyroanti- monate precipitates.EM examination indicated swollen mitochondria in the soma of pyramidal neu- ron and in the myelinated fibers contained different degree of calcium.The microvacuoles were in- dentified as swollen mitochondria,swollen axon terminal and dilated ER cisterane by EM.Owing to the Ca~(++)pyroantimonate precipitate found in the microvacuolation neurons it should be consid- ered as an irreverisible change and suggested Ca~(++)overload playing a critical role in the pathologi- cal process.

阻断4条血管诱发大鼠暂时性脑缺血后,海马结构内神经元呈损伤性改变。光镜下见3种不同类型神经元损伤,以 CA1区锥体细胞的迟发性神经元死亡变化最显著;超微结构见受损锥体细胞主要累及线粒体和内质网;超微结构组织化学显示受损的线粒体及有髓神经纤维的轴索鞘内含有不等量的钙沉积。电镜观察表明,肿胀的线粒体、轴突终末及扩张的内质网即为光镜下所见的微空泡,从而证实神经元微空泡变为不可逆损伤,Ca~(++)超载进一步导致细胞死亡。对细胞内钙增加在发病机制中的重要作用进行了分析和讨论。

Activated neutrophils contribute to tissue injury after organic ischemia and reperfusion. Increased expression of cellular adhesion molecules are prerequiste for leukocytes adhesion to vascular endothelial cells and migration into surrounding tissues. We therefore used rat transient cerebral ischemic model to investigate the expression of intercellular adhesion molecule 1 (ICAM 1) and found that the up regulation of ICAM 1 on cerebral microvessels was time depedent and markedly increased after 1 h ischemia...

Activated neutrophils contribute to tissue injury after organic ischemia and reperfusion. Increased expression of cellular adhesion molecules are prerequiste for leukocytes adhesion to vascular endothelial cells and migration into surrounding tissues. We therefore used rat transient cerebral ischemic model to investigate the expression of intercellular adhesion molecule 1 (ICAM 1) and found that the up regulation of ICAM 1 on cerebral microvessels was time depedent and markedly increased after 1 h ischemia following 6h reperfusion. While leukocytes highly adhered to vessel walls and infiltrated into injury tissue after 9 h reperfusion. Our data indicate that ICAM 1 may mediate the pathologic process of ischemia reperfusion injury.

本文用暂时性脑缺血的大鼠模型,对细胞间粘附分子-1(ICAM-1)的表达进行了研究。免疫组化结果显示ICAM-1在正常大鼠脑血管内皮有微量表达,经缺血1h,再灌3h、6h、9h、12h后其表达量呈时间依赖性增加,于再灌6h后达到高峰。病理切片见再灌9h后缺血区白细胞渗出明显并见局灶变性坏死的神经细胞。结果说明ICAM-1表达量的增加与脑缺血-再灌注损伤的病理过程密切相关。

 
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