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brain ischemic reperfusion
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  脑缺血再灌注
     ② Count of survival neurons in layer V of area I in parietal cortex: One day after reperfusion, survival nerve density of the brain ischemic reperfusion model group [(338.8±31.2) /mm2] was significantly lower than that of blank control group [(753.4±60.8)/mm2] (F=129.36, P < 0.05);
     ②脑顶皮质Ⅰ区Ⅴ层幸存神经元计数:再灌注1d,脑缺血再灌注对照组幸存神经元密度较空白对照组显著降低犤(338.8±31.2),(753.4±60.8)个/mm2,F=129.36,P<0.05犦;
短句来源
     ObjectiveTo observe the effects of ginsenoside Rg_2 on the space learning and memory and the expression of Glu,NMDA receptor subunits NR_1 and NR_(2B) of hippocampus neuron in rats with whole brain ischemic reperfusion.
     目的观察全脑缺血再灌注对大鼠空间学习记忆和海马神经元Glu、N-甲基-D-天冬氨酸受体(NMDAR)亚单位NR1、NR2B表达的影响,探讨人参皂苷Rg2的干预作用。
短句来源
     There was no significant difference between the saline control group, normal brain tissue extract group and brain ischemic reperfusion model group at different time points (F=1.76, P > 0.05).
     各时间段生理盐水对照组、正常脑组织提取液对照组与脑缺血再灌注对照组间的正常及针刺预处理脑组织提取液差异不显著(F=1.76,P>0.05)。
短句来源
     The Experimental Study of Erythropoietin Protection Against Brain Ischemic Reperfusion Oxidation Injury
     促红细胞生成素对脑缺血再灌注氧化损伤的实验研究
短句来源
     Objective To investigate the effects of endotoxin preconditioning on endogenous IL-1Rα in rat hippocampus after global brain ischemic reperfusion.
     目的 探讨内毒素预处理对大鼠全脑缺血 再灌注后海马内生性白细胞介素 1受体拮抗剂 (IL 1Rα)的影响及意义。
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  “brain ischemic reperfusion”译为未确定词的双语例句
     Brain ischemic procondition (BIP) or BIT refers to that the brain could produce marked tolerance to lately the more time ischemic brain harm after one or multiple times transient brain ischemic reperfusion.
     脑缺血预适应(brain ischemic procondition,BIP),或称脑缺血耐受(brainischemic tolerance,BIT)是指脑组织一次或多次短暂性缺血再灌注后,大脑对以后较长时间的缺血性损伤产生显著的耐受性,表现为脑神经细胞死亡明显减少,脑梗死体积显著缩小,神经功能缺损明显减轻等。
短句来源
     Conclusions Aspirin,even at low dose,inhibits the acute inflammation in brain ischemic reperfusion injury,which is related to inhibition of the activity of NF-κB and the expression of TNF-α and IL-1β.
     其机制可能与抑制NF-κB的激活和IL-1β、TNF-α表达有关。
短句来源
     CHANGES OF CYTOKINES IN RATS PLASMA AFTER FOCAL BRAIN ISCHEMIC REPERFUSION AND EFFECTS OF NIMODIPING
     局灶性脑缺血鼠血浆细胞因子变化及尼莫地平的治疗效果
短句来源
     Aspirin inhibits the inflammation in brain ischemic reperfusion
     阿司匹林对脑缺血炎症反应的抑制作用
短句来源
     at the 4th week and the 2nd month,it was decreased in each region Conclusions The hippocampal NMDA receptor is related to the cognitive impairment of VD rat model In the early phase of the brain ischemic reperfusion injury,the expression of NMDAR mRNA increase,which mediate the exitotoxicity,but it decrease in the anaphase,which might be correlated to the learning and memory impairment of VD Therefore it supply the foundation to use antagonist or agonist of EAAs receptor in the VD therapy
     结论 大鼠海马区NMDAR与学习记忆有关 ,在脑缺血的早期表达增高介导了兴奋毒性作用 ; 但在缺血后期 ,NMDARmRNA表达减低可能与学习记忆损害有关 ,为进一步进行NMDAR拮抗剂和激动剂治疗VD的研究提供了实验依据。
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     Aspirin inhibits the inflammation in brain ischemic reperfusion
     阿司匹林对脑缺血炎症反应的抑制作用
短句来源
     Extremity Ischemic Reperfusion
     肢体缺血再灌注损伤
短句来源
     Change of erythropoietin expression in rat brain of ischemic reperfusion
     缺血再灌注大鼠脑内促红细胞生成素表达的变化
短句来源
     (3) Expression of brain tissue N F - K B P65 in ischemic reperfusion increased.
     ③缺血再灌注脑组织 NF-K B P65表达增高。
短句来源
     Protective effect of constant magnetic field on ischemic-reperfusion brain
     恒定磁场对缺血再灌注脑组织的保护作用(英文)
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The brain ischemic reperfusion model was set up by rat 4VO method.Then the mitochondria and microsome fractions were purified respectivly by the same procedure. Their main phospholipids in normal group,ischemia 15 min group,reperfusion 1hr, 1 day and 3 days groups were tested. It revealed that the phospholipid metatolism changed more during reperfusion than during ischemia,and the phospholipid metabolisms of mitochondria and microsome were different. It suggested that neuron damage might be...

The brain ischemic reperfusion model was set up by rat 4VO method.Then the mitochondria and microsome fractions were purified respectivly by the same procedure. Their main phospholipids in normal group,ischemia 15 min group,reperfusion 1hr, 1 day and 3 days groups were tested. It revealed that the phospholipid metatolism changed more during reperfusion than during ischemia,and the phospholipid metabolisms of mitochondria and microsome were different. It suggested that neuron damage might be due to biomembrane dysfunction that resulted from the abnormality of phospholipid metabolism.

本文利用大白鼠4血管结扎法建立脑缺血再灌流模型,同时制备脑组织线粒体和微粒体组分,检测假手术组,缺血15min,再灌lh、ld和3d各组生物膜主要磷脂的含量变化,发现再灌流时磷脂代谢变化比缺血期幅度大,并且线粒体主要组成磷脂和微粒体主要组成磷脂代谢变化规律并不一致,证明磷脂代谢异常导致了生物膜功能丧失,造成了神经元的损伤。

Objective: To study the effect of Erigeron injection (EI) on cerebral ischemic injury. Methods: Animal model of brain ischemic/reperfusion was established in male Wistar rats and the effect of EI on proteinkinase C (PKC) activity, intraneuronal free calcium and regional cortex blood flow (rCBF) were observed. Results: EI could prevent the activation of PKC, calcium overload and decrease of RCBF induced by cerebral ischemia/reperfusion. Conclusion: EI could prevent neuronal ischemic...

Objective: To study the effect of Erigeron injection (EI) on cerebral ischemic injury. Methods: Animal model of brain ischemic/reperfusion was established in male Wistar rats and the effect of EI on proteinkinase C (PKC) activity, intraneuronal free calcium and regional cortex blood flow (rCBF) were observed. Results: EI could prevent the activation of PKC, calcium overload and decrease of RCBF induced by cerebral ischemia/reperfusion. Conclusion: EI could prevent neuronal ischemic injury by inhibiting activation of PKC.

目的 :研究灯盏花注射液对神经元缺血损伤的作用。方法 :采用大鼠全脑缺血 /再灌流模型 ,观察了灯盏花注射液对蛋白激酶C活性、神经元内游离钙浓度及皮层局部脑血流的影响。结果 :发现灯盏花注射液可以防止脑缺血 /再灌流诱发的蛋白激酶C的激活、钙超载及皮层局部血流的降低。结论 :灯盏花注射液可以抑制蛋白激酶C的激活 ,防治神经元缺血性损伤。

Objective Inflammatory cytokines and endothline play an important role in brain injury during ischemic reperfusion.In this study,inflammatory cytokines were investigated to determine the changes of TNFα and IL-1β after brain ischemic reperfusion and interferential effect of nimodiping on TNFαand IL-1β.Methods The animal models of the focal middle cerebral arterial ischemic reperfusion were established in Wistar rats.Nimodiping was administered by introvenous drip.The plasma levels of TNFα、IL-1βwere...

Objective Inflammatory cytokines and endothline play an important role in brain injury during ischemic reperfusion.In this study,inflammatory cytokines were investigated to determine the changes of TNFα and IL-1β after brain ischemic reperfusion and interferential effect of nimodiping on TNFαand IL-1β.Methods The animal models of the focal middle cerebral arterial ischemic reperfusion were established in Wistar rats.Nimodiping was administered by introvenous drip.The plasma levels of TNFα、IL-1βwere measured by radioimmunoassay.Rusults The levels of TNFαand IL-1βin plasma were elevated after 1h brain ischemia and 1h reperfusion in rats.Nimodiping can significantly reduce the content of TNFαand IL-1β in plasma.Conclusion The results indicate that TNFαand IL-1β participate in cerebral ischemia reperfusion lesion,which can be reduced by nimodiping,and nimodiping can protect nerve cells from injurg through inhibiting TNFαand IL-1β production.

目的 探讨脑缺血再灌注后血浆TNFα、IL - 1β变化及尼莫地平对其含量的影响。 方法 采用线栓法制备大鼠局灶性脑缺血再灌注模型 ,用放射免疫方法检测脑缺血再灌注后血浆TNFα、IL - 1β变化 ,以及尼莫地平对TNFα、IL - 1β的拮抗作用。 结果 缺血再灌组与假手术组相比 ,血浆TNFα、IL - 1β含量明显增加 ,应用尼莫地平组TNFα、IL - 1β水平均降低。 结论 TNFα、IL - 1β参与了局灶性脑缺血再灌注损伤的病理过程 ,尼莫地平通过降低TNFα、IL - 1β的含量发挥一定的脑保护作用。

 
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