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ischemic brain injury
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  缺血性脑损伤
    CONCLUSION: Through upregulating the expression of apurinic/apyrimidinic endonuclease, MCI186 can improve the repair ability of brain tissue in the course of ischemic injury, decrease the infarct area, so as to protect ischemic brain injury.
    结论:MCI-186可通过上调缺血脑组织中脱嘌呤/脱嘧啶核酸内切酶的表达水平,增强脑组织对缺血引起的氧自由基损伤的修复能力,缩小梗死范围,因而对缺血性脑损伤具有保护作用。
短句来源
    The results indicated that CXT could improve brainABSTRACTedema and ischemic brain injury.
    以上结果表明CXT可以改善脑水肿,保护受损神经元,改善缺血性脑损伤
短句来源
    All experimental results above showed that the anti-cerebral ischemia effects of CXT. The mechanism maybe involved in decreasing brain energy exhaust, inhibiting platelet aggregation ,ABSTRACTreducing oxygen free radicals (OFR) by increasing the action of SOD and decreasing contents of MDA, improving ischemic brain injury and improving blood rheology.
    初步药效学实验研究表明,CXT有防治脑缺血作用,其作用机制可能与降低脑耗能,抑制血小板聚集,改善血液流变学,并通过升高SOD活力、降低MDA含量减少氧自由基,改善缺血性脑损伤等作用有关。
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    Propofol can reduce cerebral blood flow, decrease intracranial pressure (ICP), and decrease cerebral metabolic requirement for oxygen (CMRO2),and produce the neuropeotective effects in ischemic brain injury,but the study on the influence of propofol on traumatic brain injury is little so far.
    而异丙酚作为一种新的静脉全麻药可减少脑血流量、降低颅内压及脑氧代谢,对缺血性脑损伤有保护作用。 但有关异丙酚对创伤性脑损伤的作用效应研究还较少。
短句来源
    ATP-sensitive K + channels are iatreusiologic targets for many diseases such as hypertension, angina pectoris, diabetes mellitus and ischemic brain injury.
    ATP敏感性钾通道是高血压、心绞痛、糖尿病及缺血性脑损伤等多种疾病的治疗靶点之一。
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  “ischemic brain injury”译为未确定词的双语例句
    Protection of naoyi an granule in ischemic brain injury secondary to intracerebral hemorrhage in rats
    脑溢安对实验性大鼠脑出血继发性脑缺血损伤的保护作用
短句来源
    Inhibitory effects of chiral 3-n-butylphthalide on inflammation following focal ischemic brain injury in rats~1
    手性丁基苯酞对大鼠局灶性脑缺血后炎症的抑制作用(英文)
短句来源
    Also, we have found that ONO-1078 is protective against ischemic brain injury in focal cerebral ischemia.
    在脑缺血研究中,本实验室已建立了大鼠和小鼠的局灶性脑缺血模型,并发现白三烯受体拮抗剂ONO-1078对大鼠和小鼠的浙江大学博士学位论文局灶性脑缺血具有保护作用。
短句来源
    Conclusion Hyperglycemia could exacerbate ischemic brain injury after thrombolysis through leukocytes infiltration.
    结论高血糖通过增加白细胞浸润加重溶栓治疗后脑组织损伤 ;
短句来源
    Conclusion Melatonin obviously attenuated ischemic brain injury by MCAO,elevated the activity of NOS and content of NO in primitive ischemia and inhibited them in the second time,indicating that the protective effect of melatonin was associated with the debasement of NO-content and NOS-activity and the antagonism to peroxyl radical.
    与模型组比较 ,缺血 30分钟 ,褪黑素使NO含量及NOS活性升高 ,6小时、2 4小时降低。 结论褪黑素对大鼠局灶脑缺血有一定的保护作用 ,其机制可能与降低脑组织中NO含量和NOS活性 ,减轻脑组织自由基的损伤有关
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  ischemic brain injury
Inhibition of neurotransmitter release may, in part, be responsible for the protective effect of pentobarbital in ischemic brain injury.
      
This study demonstrated that bradykinin postconditioning induces protection against ischemic brain injury and promotes neuronal survival.
      
Plasticity of Neurons and Glia Following Neonatal Hypoxic-Ischemic Brain Injury in Rats
      
We propose the monitoring of serine, asparagine, and threonine, together with excitatory amino acids, as an index of the degree of ischemic brain injury.
      
Research on ischemic brain injury has established a central role of mitochondria in neuron death (1-3).
      
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Aim: To explore the protective effect and its mechanism of the traditional Chinese medicine complex, naoyi an granule(NYAG), on intracerebral hemorrhage(ICH) in rats. Methods: Collagenase induced ICH rats were used. Inducible nitric oxide synthase(iNOS) activity of ischemic cerebral cortex surrounding the intracerebral hematoma was assayed by monitoring the conversion of L 3H arginine to L 3H citrulline. Pathologic changes in the same area were observed with transmission electron microscope...

Aim: To explore the protective effect and its mechanism of the traditional Chinese medicine complex, naoyi an granule(NYAG), on intracerebral hemorrhage(ICH) in rats. Methods: Collagenase induced ICH rats were used. Inducible nitric oxide synthase(iNOS) activity of ischemic cerebral cortex surrounding the intracerebral hematoma was assayed by monitoring the conversion of L 3H arginine to L 3H citrulline. Pathologic changes in the same area were observed with transmission electron microscope on the 2nd day, the 4th day and the 7th day after ICH. Results: The iNOS activities of NYA treated group decreased remarkably(P<0.01) compared with those of the saline treated group. Ultrastructural observation also indicated that NYAG ameliorated the brain edema, cell degeneration and necrosis. Conclusions: The inhibitory effect of NYAG on iNOS activity may be related to its protection against ischemic brain injury secondary to ICH.

采用胶原酶诱导大鼠脑出血模型,以3H精氨酸转化测定法检测血肿周围缺血脑组织诱导型一氧化氮合酶(iNOS) 活性,并用电镜观察其病理改变,以探讨脑溢安颗粒( 简称脑溢安) 治疗脑出血的作用机制。结果显示:脑溢安明显抑制脑组织iNOS活性( P < 0 .01) ,改善脑组织水肿、细胞变性和坏死等神经病理改变。提示脑溢安对脑出血继发性脑缺血损伤具有保护作用,其机制可能与其抑制iNOS活性有关

AIM: To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and box. following brain ischemia. METHODS: Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method. RESULTS: Melatonin decreased the infarct area and prevented the neuronal death after...

AIM: To study the protective effect of melatonin against neuronal injury and the possible roles of alteration in the expression of bcl-2 and box. following brain ischemia. METHODS: Brain ischemia was induced by left middle cerebral artery occlusion (MCAO) for 60 min in rats. Brain damage was evaluated by the infarct area and the neuronal cell counting. The expression of bcl-2 and bax was analyzed by immunohistochemical method. RESULTS: Melatonin decreased the infarct area and prevented the neuronal death after 24-h reperfusion following 1-h MCAO. Melatonin given before the ischemia enhanced the expression of bcl-2 in the penumbra area and had no significant effect on the expression of bax. CONCLUSION: Melatonin effectively attenuated ischemic brain injury and increased the expression of neuronal bcl-2 in the ischemic brain, indicating that the protective effect of melatonin was associated with up-regulation of bcl-2 in ischemia-induced neuronal death.

目的:研究褪黑激素对受损伤脑神经元的保护作用和对脑缺血后bcl-2,bax表达的影响,方法:用大鼠大脑中动脉梗死再灌注脑缺血模型,以脑梗死面积和存活细胞百分率作为脑损伤指标,用免疫组化的方法分析bcl-2,bax的表达,结果:缺血再灌后24 h褪黑激素呈剂量依赖性的减少脑梗死面积,减少缺血周边区细胞死亡,并显著增加该区bcl-2的表达,而对bar的表达则无明显影响,结论:褪黑激素具有明显减少缺血性神经细胞死亡的作用,该作用机制可能与神经细胞上bcl-2的表达有关。

Objective To evaluate the relationship between hyperglycemia and leukocytes infiltration and the effects of dextran sulfate on thrombolytic therapy in the hyperglycemic rat embolic stroke.Methods Dextran sulfate or saline was intravenously administered after 0.5h ischemia in thromboembolic model of hyperglycemic rat,which produced by intraperitioneally injection of 50% dextrose 30 minutes before ischemia.All rats were received urokinase injection after 2h ours ischemia.leukocytes infiltration and infarct size...

Objective To evaluate the relationship between hyperglycemia and leukocytes infiltration and the effects of dextran sulfate on thrombolytic therapy in the hyperglycemic rat embolic stroke.Methods Dextran sulfate or saline was intravenously administered after 0.5h ischemia in thromboembolic model of hyperglycemic rat,which produced by intraperitioneally injection of 50% dextrose 30 minutes before ischemia.All rats were received urokinase injection after 2h ours ischemia.leukocytes infiltration and infarct size were evaluated at 24h ours after ischemia.Results Treated with urokinase alone,the number of leukocytes infiltration and infarct size in hyperglycemic rat were increased compared with those in normoglycemic rat ( P <0 01, P <0 05).In hyperglycemic rats,treated with combination of urokinase and dextran sulfate,number of leukocytes infiltration and infarct size were decreased compared with those in treated with urokinase alone ( P <0 01, P <0 05).Conclusion Hyperglycemia could exacerbate ischemic brain injury after thrombolysis through leukocytes infiltration.Combination of dextran sulfate and urokinase could inhibit leukocytes infiltration and reduce infarct volume in hyperglycemic rat.

目的探讨高血糖与溶栓治疗后白细胞浸润的关系 ,以及糖酐酯对高血糖大鼠溶栓治疗的影响。方法通过复制高血糖大鼠模型 ,自体血栓栓塞大脑中动脉 ,缺血 30分钟静脉予以糖酐酯或生理盐水 ,缺血 2小时经颈外动脉注入尿激酶溶栓 ,观察缺血 2 4小时浸润白细胞数及梗死灶大小。结果缺血 2 4小时 ,高血糖大鼠溶栓组与正常血糖大鼠溶栓组比较 ,缺血周边区浸润白细胞数明显增多 (P <0 0 1) ,梗死灶增大 (P <0 0 5 )。高血糖大鼠联合糖酐酯溶栓组较高血糖大鼠溶栓组浸润白细胞数减少 (P <0 0 1) ,梗死灶减小 (P <0 0 5 ) ;与正常血糖大鼠溶栓组比较 ,白细胞数减少 (P <0 0 5 ) ,梗死灶虽有减小的趋势 ,但差异无显著意义。结论高血糖通过增加白细胞浸润加重溶栓治疗后脑组织损伤 ;糖酐酯可以抑制高血糖大鼠溶栓治疗后白细胞的浸润 ,减小梗死灶。

 
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