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ischemic neuronal damage     
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  缺血性神经元损害
     Recent studies indicated that nitric oxide(NO) play an important role in disease of central neurological system and take part in ischemic neuronal damage.
     近年来发现一氧化氮(nitric oxide,NO)在神经系统损害中起重要作用,并且参与了缺血性神经元损害
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  神经元缺血性损伤
     Conclusion: ①The synaptic vesicle Zn 2+ released and then translocated into postsynaptic neurons after forebrain ischemia/reperfusion and played a role in ischemic neuronal damage.
     结论 :①前脑缺血 /再灌注后 ,海马神经元突触前末梢游离Zn2 + 的释放和扩散增加 ,Zn2 + 移位至突触后神经元并参与神经元缺血性损伤 ;
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     APPROACH TO THE RELATIONSHIP BETWEEN THE CHANGES OF THE CONTENT OF FREE ZINC IN HIPPOCAMPUS AND ISCHEMIC NEURONAL DAMAGE
     海马结构游离锌变化与神经元缺血性损伤关系的探讨
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  神经原缺血性损伤
     EA also substantially reduced the ischemic neuronal damage after 10 min of cerebral ischemia and 24 h of reperfusion.
     同时电针能明显减轻缺血10min后再灌注24小时的神经原缺血性损伤
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  缺血性神经细胞损伤的
     Objective To explore the expression of singal transducers and activators of transcription(STAT 3) during focal cerebral ischemic reperfusive injury in rats and the relationship between ischemic neuronal damage and it.
     目的 探讨信号转导和转录激活子 (STAT) 3在大鼠局灶性脑缺血再灌注损伤中的表达及其与缺血性神经细胞损伤的关系。
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      ischemic neuronal damage
    The exact role played by the differential increase in the levels of 5-HT to the other catecholamines in the pathogenesis of ischemic neuronal damage remains unclear and warrants further study.
          
    The present results may offer clues to elucidate the mechanisms of ischemic neuronal damage.
          
    The possible significance of these changes in the pathogenesis of ischemic neuronal damage is discussed.
          
    Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage.
          
    Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage.
          
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    The CA1 subfield hippocampus of 43 Mongolia gerbils divided into three groups (normal, ischemial and reperfusive) was observed by electron microscopy. All the animals were subjected to bilateral carotid occlusion for 7 min and trans-cardiac perfusion fixation was performed 0, 30, 90min and 3, 6, 12 h or 1, 2, and 4 days afterwards except that 4 gerbils of the normal group were subjected to perfusive fixation only. The result showed that pyramidal cells in CA1 subfield presented a series of changes after ischemia...

    The CA1 subfield hippocampus of 43 Mongolia gerbils divided into three groups (normal, ischemial and reperfusive) was observed by electron microscopy. All the animals were subjected to bilateral carotid occlusion for 7 min and trans-cardiac perfusion fixation was performed 0, 30, 90min and 3, 6, 12 h or 1, 2, and 4 days afterwards except that 4 gerbils of the normal group were subjected to perfusive fixation only. The result showed that pyramidal cells in CA1 subfield presented a series of changes after ischemia and during reperfusion, From 0 min to 3 h following occlusion, there were no serious lesions, only a light loss was produced, such as "reactive change" and "ischemic cells change". 6 h later, pyramidal cells showed an accumulation of ER. 1 to 4 days later ischemia, the lamellar alignment of proliferated cisterus of the ER and "delayed neuronal death" were the most conspicuous findings in these cells.The result again indicated that the damage of CA1 pyramidal cells is slow and may differ from those which are thought to be typical of ischemic neuronal damage.

    本文迭用蒙古沙土鼠复制急性脑缺血再灌流模型,并动态观察海马CA,区锥体细胞在不同再灌流时间内超微结构的演变。发现再灌流损伤不同于传统的缺血病变,其形态改变至少需要6小时才开始出现,作者认为脑缺血病变与再灌流损伤同属细胞内氧的利用异常,但由于机制的不同,故病变各有特征。高氧性细胞内用氧异常致使超氧化物阴离子自由基(0_2~-)产生增多的理论能解释再灌流病变的实质。

    Ligation of right MCA was performed in a serles of experimental animal of divided into 4 groups. Group A was treated with perflourotripropylamine FTPA, 20% mannitol, dexamethasone;Group B was treated with FTPA,20% mannitol, dexamethasone and the blood vessel was reconstructed 4 hours later.Group C was control;Group D:of the blood vessels only 4 has later.All of this dogs were sacrificed After 24 hours.There were ischemic neuronal damage in different degree in all specimens under microscope. The results...

    Ligation of right MCA was performed in a serles of experimental animal of divided into 4 groups. Group A was treated with perflourotripropylamine FTPA, 20% mannitol, dexamethasone;Group B was treated with FTPA,20% mannitol, dexamethasone and the blood vessel was reconstructed 4 hours later.Group C was control;Group D:of the blood vessels only 4 has later.All of this dogs were sacrificed After 24 hours.There were ischemic neuronal damage in different degree in all specimens under microscope. The results of this experlmental therapeutic research was that the clinical findings of Group A and B were better than Group C and D,and the perceatage of the cerebral ischemic area and volume of ischea(?)ia (%, HAI and %, HVI) were less than Group C and D. There was a statistically significant difference between Group A,B and Group C,D (p<0.05). The combined treatment with FTPS, 20% mannitol and dexamethasone may reduce the degree of cerebral edema, delay the formation of cerebral infarction and provide an opportunity for 2-4 hrs. to reconstruction of the blood supply.

    利用大脑中动脉区实验性脑梗塞模型狗32只,随机分为药物治疗组(甲);药物治疗加4小时重建术组(乙);对照组(丙);单纯4小时重建术组(丁)。对实验动物进行临床观察和24小时处死后脑病理学的研究,结果甲、乙组的临床和神经元缺血损害较丙、丁组轻微,尤以乙组更为显著,经统计学处理差异有显著性(P<0.01)。认为对急性脑缺血早期采用适当剂量的脑保护剂,可有效地减轻脑缺血缺氧状态,降低脑水肿程度,延缓脑梗塞灶形成,为2~4小时脑血管重建术创造有利条件。

    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...

    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。

     
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