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brain ischemic
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  脑缺血
     AIM: To investigate the difference of electroacupuncture with various frequencies(2/5Hz, 2/15Hz, 2/100Hz) on the degree of induced brain ischemic tolerance in rats.
     目的:探讨不同频率电针预处理(2/5Hz,2/15Hz,2/100Hz)对诱导脑缺血耐受程度是否有差别。
短句来源
     In CIP+brain ischemic insu lt group, no obvious neuronal damage was found in 3min-3d-6min(CIP for 3 min w as followed by a brain ischemic insult for 6 min at an interval of 3 d, the same as the following) and 3 min-3 d-10 min groups, indicating that CIP effect ively protected neurons of the CA1 hippocampus against DND normally induced by i schemic insult for 6 or 10 min.
     CIP+损伤性脑缺血组中,3min-3d-6min(3min CIP后间隔三天给予6min损伤性脑缺血,下同)和3min-3d-10min组DND不明显,提示CIP可有效地保护海马CA1区神经元,防止6min或10min损伤性脑缺血诱导的DND。
短句来源
     ① Comparison of neuron-specific enolase density: It was significantly higher in transient brain ischemic attack group than in control group (23.53±12.35) vs (14.29±6.83) μg/L, t=2.678, P < 0.01.
     ①神经元特异性烯醇酶浓度的比较:短暂性脑缺血发作组明显高于对照组[(23.53±12.35,14.29±6.83)μg/L,t=2.678,P<0.01]。
短句来源
     Experimental Study of Moxibustion Preconditioning Effect on Bcl-2 and Bax Protein Expression of Hippocampal CA_1 Section after Rat's Full Brain Ischemic
     艾灸预处理对全脑缺血大鼠海马CA_1区Bcl-2和Bax蛋白表达影响的实验研究
短句来源
     The experimental study on relationship between the brain ischemic tolerance and neuronal apoptosis and expression of p53,p21 and Bax
     脑缺血耐受与细胞凋亡及p53、p21、Bax表达关系的实验研究
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  缺血脑
     Effect of Electro-acupuncture on Proliferation, Migration of Neural Stem Cell after Brain Ischemic Injury in Rats
     电针对缺血脑损伤大鼠神经干细胞增殖迁移的影响
短句来源
     Methods:The objective of this present study is to make animal brain ischemic model with middle cerebral artery occlusion(MCAO)by nylon thread,then measure the numbers and anatomic distribution of nerve cells apoptosis, assay the SOD and LPO content in same ischemic tissue.
     故测定缺血脑区出现DNA片断化的凋亡细胞数量变化及在缺血脑区的分布状况,以了解脑缺血的病理生理及寻求防治措施。 方法:利用线栓法制成大脑中动脉缺血动物模型,测定脑组织SOD、LPO含量变化及凋亡细胞的密度变化;
短句来源
     Objective By studying the changes of O-free radical, NO and NOS when rats of acute brain ischemic were dealed with sub-temperature, to discuss the protection mechanism of sub-temperature to brain tissue.
     目的研究亚低温状态下,大鼠急性脑缺血时氧自由基超氧化物歧化酶(SOD)和一氧化氮(NO)、一氧化氮合酶(NOS)的改变,探讨亚低温对缺血脑组织的保护机制。
短句来源
  “brain ischemic”译为未确定词的双语例句
     RESULTS: Compared with EAAC1 sense group, the volume of brain ischemic infarction [(105.67±8.70) mm~3] was reduced after brain microinjection of EAAC1 antisense.
     结果:注射EAAC1反义寡核苷酸组大鼠梗塞体积[(105.67±8.70)mm3]显著小于正义组。
短句来源
     Objective To discuss the feasibility of treating the brain ischemic stroke by the co-transplantation of the neural stem cells(NSCs) and the endothelial progenitor cells(EPCs).
     目的探讨神经干细胞(neural stem cells,NSCs)与血管内皮祖细胞(endothelial progenitor cells,EPCs)共移植治疗缺血性脑卒中应用的可能。
短句来源
     Alleviation of brain ischemic edema in rats by LY367385, a selective antagonist of metabotropic glutamate receptor 1
     代谢型谷氨酸受体1亚型选择性拮抗剂LY367385对抗大鼠缺血性脑水肿
短句来源
     ResultsThe average intra-operative brain ischemic time was (20±6)min vs (4.2±0.7)min in the early and recent cases separately, P<0.01.No mortality and stroke occurred during 30 days after operation.
     结果 早期手术组颈动脉平均阻断时间 (2 0± 6 )min ,近期手术组颈动脉平均缺血时间 (4 2± 0 7)min ,P <0 0 1。 术后 30d内无死亡和脑卒中。
短句来源
     AIM: To investigate the changes of expression of Nogo-A at different time points in brain ischemic infarct rats.
     目的:研究神经生长抑制因子Nogo-A mRNA在大鼠缺血性脑梗塞脑内不同时点表达的变化与功能恢复的关系,探讨Nogo-A基因在缺血性脑梗塞中神经再生的作用。
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  brain ischemic
The results suggested that phosphorylation of ERK1/2, rather than synthesis of ERK1/2 proteins, was promoted in brain ischemic preconditioning, and that the promotion was partly mediated by NO signal pathway.
      
Brain ischemic preconditioning was performed with four-vessel occlusion for 3 min.
      
Nitric Oxide Participates in the Induction of Brain Ischemic Tolerance via Activating ERK1/2 Signaling Pathways
      
The purpose of this study was to investigate the role of superoxide dismutase (SOD) and catalase (CAT) in brain ischemic tolerance induced by ischemic preconditioning.
      
We report a case of a 61-year-old man who was admitted to our hospital for transient brain ischemic attack.
      
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Using a modified method of Pulsinelli's induction of brain ischemic damage in wistar rat by 4-vessel occlusion, calcium content in hippocampus was found significantly higher in ischemic group. Nimodipine (1 mg/kg) was injected intraperitoneally following brain ischemia, the calcium content in hippocampus had no significant difference between Nimodipine treated group and ischemic group.

本文将51只雄性Wistar大鼠随机分成假手术对照组、缺血组、缺血-尼莫地平组。采用改良Pulsinelli法建立鼠脑缺血模型,并经脑电图监测及组织病理学检查证实缺血模型是成功的。缺血-尼莫地平组的大鼠在夹闭颈总动脉造成鼠脑暂时性缺血的同时於腹腔内注射尼莫地平。比较对照组及暂时性缺血再灌注72小时后海马组织钙含量,用原子吸收分光光度计测定发现缺血组海马组织钙含量增高,但缺血-尼莫地平组海马组织钙含量与缺血组差异无显著性。

Abstract In the model of ischemia and reperfusion on Gerbil brains,it was found that energy metabolism was inhibited after 50 min of ischemia which was resuming after 30 min of reperfusion,but which went into secondary deterioration after 120 min of reperfusion.Pyritinol could markedly improve energy metabolism after 50 min of ischemia,and also suppress the development of secondary deterioration in energy metabolism after 120 min of reperfusion.The protective effect of pyritinol on brain ischemic injury...

Abstract In the model of ischemia and reperfusion on Gerbil brains,it was found that energy metabolism was inhibited after 50 min of ischemia which was resuming after 30 min of reperfusion,but which went into secondary deterioration after 120 min of reperfusion.Pyritinol could markedly improve energy metabolism after 50 min of ischemia,and also suppress the development of secondary deterioration in energy metabolism after 120 min of reperfusion.The protective effect of pyritinol on brain ischemic injury and its mechanisms was discussed.

用沙土鼠制成缺血及再灌注模型,观察到在缺血50min时脑能量代谢明显障碍,再灌注3Omin时有所改善,而在再灌注120min时发生迟发性能量代谢恶化。吡硫醇(脑复新)可明显改善缺血50min时的能量代谢,并能纠正再灌注120min时的迟发性能量代谢恶化。本文讨论吡硫醇对脑损伤保护作用的机制。

The effects of nimodipine,verapamil,and diltiazem at the dose of 10 μg/kg boluses and 0.5μg/kg. min given within 5h on the brain calcium accumulation,and the sodium,potassium ions and water shifts after middle cerebral artery occlusion in rabbits were studied. Nimodipine significantly reduced the calcium accumulation by 64%,and the sodium, potassium ions and water shifts by 64%, 67%, and 40% respectively. Verapamil decreased the items mentioned above by 39%,48%,45%,and 39%,respectively,and its effect of reducing...

The effects of nimodipine,verapamil,and diltiazem at the dose of 10 μg/kg boluses and 0.5μg/kg. min given within 5h on the brain calcium accumulation,and the sodium,potassium ions and water shifts after middle cerebral artery occlusion in rabbits were studied. Nimodipine significantly reduced the calcium accumulation by 64%,and the sodium, potassium ions and water shifts by 64%, 67%, and 40% respectively. Verapamil decreased the items mentioned above by 39%,48%,45%,and 39%,respectively,and its effect of reducing the calcium accumulation was lower than that of nimodipine. There was no significant improvment in the ions and water shifts due to diltiazem. The results demonstrate that calcium antagonists can protect brain ischemia by reducing calcium ion enteririg ischemic cells,and indirectly reducing the sodium,potassium and water shifts in brain ischemic cells.

尼莫地平治疗兔右大脑中动脉闭塞5h,明显降低脑钙积累64%,降低脑Na、K、H2O转移分别为64%、67%、40%;维拉帕米的上述作用分别为39%、48%、45%、39%,其降钙作用明显弱于尼莫地平;硫氮卓酮对离子和水的异常转移无明显改善。提示钙拮抗剂可能通过阻滞钙内流降低钙积累,并间接抑制离子和水异常转移,减轻离子性脑水肿。

 
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