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cerebral ischemic pretreatment
相关语句
  脑缺血预处理
     Expression and Cellular Localization of a Novel Cerebral Ischemic Pretreatment Related Gene Mipu1 and Identification of Mouse Mipu1 Gene Homology
     脑缺血预处理相关新基因Mipu1的表达,亚细胞定位及其小鼠同源基因的克隆
短句来源
     Expression of Mip1 gene in rat brain after cerebral ischemic pretreatment
     大鼠全脑缺血预处理后脑Mip1基因表达
短句来源
     Expression of c-fos Protooncogene Protein (FOS) in the Rat Brain After Cerebral Ischemic Pretreatment
     大鼠脑缺血预处理后脑内c-fos基因FOS表达及意义
短句来源
     The third group was divided into 2 subgroups: the experimental subgroup and the false operation control subgroup. The expression of Mip1 gene in hippocampus and cortex of rat brain was detected by the technique of Northern hybridization after cerebral ischemic pretreatment.
     第3组分为实验组(缺血预处理组)、假手术组,采用Northern杂交法检测Mip1在大鼠海马和前皮质在全脑缺血预处理后的表达情况。
短句来源
     Conclusion Global cerebral ischemic pretreatment in rat can induce protective effects on ischemia/reperfusion injuries 24 hours after the pretreatment.
     结论:大鼠全脑缺血预处理对其后24h的损伤性全脑缺血-再灌注有保护作用。
短句来源
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  “cerebral ischemic pretreatment”译为未确定词的双语例句
     Methods SD rats were divided into 3 groups randomly,among which two groups were examined by brain water detection or histological observation to prove the successful establishment of the cerebral ischemic pretreatment and cerebral ischemia/reperfusion model.
     方法SD大鼠随机分成3组,建立大鼠全脑预缺血及缺血再灌注模型,其中2组通过脑水含量测定和组织学改变观察证实模型复制成功。
短句来源
     Results The expression of Mip1 in the 12 h,24 h experimental groups, following 3 minutes cerebral ischemic pretreatment,was higher than that of false operation control group.
     结果实验鼠全脑缺血3 min(预处理)后12 h组、24 h组海马和前皮质Mip1表达均高于假手术组。
短句来源
     Effect of focal cerebral ischemic pretreatment on expression of brain-derived neurotrophic factors in rats with cerebral ischemic tolerance
     局灶性缺血预处理对脑缺血耐受大鼠神经营养因子表达的影响
短句来源
     The experimental group was treated with cerebral ischemic pretreatment for 3 minutes to compare with sham-operated control.
     实验组大鼠行全脑3min缺血预处理,假手术组给予假手术。
短句来源
     Objective To observe the protective effects of cerebral ischemic pretreatment on the following cerebral ischemic reperfusion injuries.
     目的 观察缺血预处理对脑缺血再灌注损伤的保护作用。
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  相似匹配句对
     Cerebral ischemia, pretreatment of ischemia and ischemic tolerance
     脑缺血与缺血预处理及缺血耐受
短句来源
     Conclusion BS pretreatment has protective effect on ischemic cerebral injury.
     结论 双侧颈总动脉夹闭并生理盐水右侧颈内动脉灌注对脑再次缺血有明显的保护作用。
短句来源
     Cerebral ischemic injury and Akt
     脑缺血损伤与Akt研究的进展
短句来源
     Pathogenesis of Ischemic Cerebral Apoplexy
     缺血性脑中风的发病机理探讨
短句来源
     Effect of focal cerebral ischemic pretreatment on the expressions of 15-Lipoxygenase in rats
     15-脂氧化酶及其m RNA在局灶性脑缺血预处理大鼠中作用机制的探讨
短句来源
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Objective To observe the protective effects of cerebral ischemic pretreatment on the following cerebral ischemic reperfusion injuries. Methods Cerebral ischemic pretreatment followed by the cerebral ischemic reperfusion of alternative intervals was performed in the grouped wistar rats by obstructing four blood vessels. The hippocampus neuron damage was measured semiqantitively. Results The hippocampus neuron damage after 3 minutes vessels clipped in the experimental groups...

Objective To observe the protective effects of cerebral ischemic pretreatment on the following cerebral ischemic reperfusion injuries. Methods Cerebral ischemic pretreatment followed by the cerebral ischemic reperfusion of alternative intervals was performed in the grouped wistar rats by obstructing four blood vessels. The hippocampus neuron damage was measured semiqantitively. Results The hippocampus neuron damage after 3 minutes vessels clipped in the experimental groups was no significant difference compared with which in the blank comparative group. While this damage in the groups of 3 days interval following 6 min ischemic reperfusion was diminished significantly compare with non pretreatment comparative groups and other experimental groups. Conclusion The protective effects of the ischemic pretreatment on the following cerebral ischemic reperfusion injuries are associated with the ischemic pretreatment time, the following ischemic damage time and the interval between the above 2 ischemia.

目的 观察缺血预处理对脑缺血再灌注损伤的保护作用。方法 采用四血管阻断法对实验鼠分组进行全脑缺血预处理及缺血后再灌注, 半定量法观察海马区神经元受损情况。结果 实验组四血管阻断3 分钟( 预处理) 后海马区神经元受损与对照组无显著差异;3 天间隔6 分钟全脑缺血再灌注组神经元受损较其他组明显减轻。结论 缺血预处理对脑缺血再灌注损伤保护作用与全脑缺血预处理时间, 后续全脑缺血再灌注损伤时间及两者间的时间间隔有关。

Objective To investigate the FOS expression changes in rat brain after ischemic pretreatment and the relationship between FOS and ischemic tolerance.Method The cerebral ischemia model of the wister rats was established by occluding four blood vessels.The FOS experssion in the hippocampus neurons was determined by using SABC immunocytochemical technique with against c-fos protooncogene antibody of rabbit.Results The FOS expression in the 30',12h,24h and 72h four experimental groups following cerebral ischemic...

Objective To investigate the FOS expression changes in rat brain after ischemic pretreatment and the relationship between FOS and ischemic tolerance.Method The cerebral ischemia model of the wister rats was established by occluding four blood vessels.The FOS experssion in the hippocampus neurons was determined by using SABC immunocytochemical technique with against c-fos protooncogene antibody of rabbit.Results The FOS expression in the 30',12h,24h and 72h four experimental groups following cerebral ischemic pretreatment were obviously higher than that of false operafion control group (all P<0 01),especially 72h group,its expression levels was significantly higher than that of other three expeimental groups(P<0 01).Conclusion After transient 3 minutes non-injury cerebral ischemia,FOS expression in rat brain was significantly increased following reperfusion 72 hours,which indicate that the FOS expression in brain might be one of the important factors inducing cerebral ischemic tolerance mechanism.

目的 探讨脑缺血预处理后脑组织原癌基因c-fos基因表达蛋白FOS变化及其与脑缺血耐受产生之间的关系。方法 通过建立大鼠全脑缺血模型 ,采用兔抗c -fos原癌基因抗体SABC免疫组化技术对脑缺血再灌注后的海马神经元进行检测FOS表达。结果 实验鼠四血管阻断 (预处理 ) 3min后 ,12h组、2 4h组及 72h组FOS表达均显著高于对照组 (假手术组 ) ,P值均 <0 0 1,72h组最为显著。结论 大鼠短暂非损伤性 3min缺血再灌注 72h后脑内海马神经元中FOS表达显著增高。FOS表达增高是脑缺血耐受保护机制的一部分

AIM:To study the effect of focal ischemic pretreatment on the expression of brain derived neurotrophic factors(BDNF) and investigate the relationship between BDNF and ischemic tolerance in rat and its function in endogenetic protective mechanism. METHODS:Thirty SD rats were randomly divided into 3 groups:experiment group,sham operation group and control group,ten rats for each group. The models with focal cerebral ischemic tolerance were obtained with thread blocking.The rats in experiment group received 2...

AIM:To study the effect of focal ischemic pretreatment on the expression of brain derived neurotrophic factors(BDNF) and investigate the relationship between BDNF and ischemic tolerance in rat and its function in endogenetic protective mechanism. METHODS:Thirty SD rats were randomly divided into 3 groups:experiment group,sham operation group and control group,ten rats for each group. The models with focal cerebral ischemic tolerance were obtained with thread blocking.The rats in experiment group received 2 hour ischemia with pretreatment of 10 minute ischemia 3 days later and they were killed after 22 hour reperfusion. Sham operation group exposed anatomic structure for 10 minutes and other treatment followed experiment group.The control group received twice sham operation.The determination of infarct volume rate,histopathological changes,immunohistochemistry staining and image analysis methods were used to compare the changes of BDNF expression in each group. RESULTS:There was significant difference in infarct volum between sham operation group[(126.0±22.4) mm3] and ischemia group[(102.0±24.2) mm3] (P< 0.05).Compared with the other groups,the cerebral pathological changes in sham operation group were the most obvious.The pathological change in experiment group was not as obvious as sham operation group.Although the dissolved neurons in the cortex and basal ganglion,nucleus shrinkage in experiment group were detected,the structure of neuron array in cerebral cortex was normal.The positive expression of BDNF was identified with brown yellow in cytoplasm.Significant differences in the mean absorbance(A) of positive cells were found between the sham operation group and control group as well as between the experimental group and the groups of sham operation and control(P< 0.01). CONCLUSION:Focal cerebral ischemic pretreatment can provide obviously protective function for the followed cerebral infarction and induce ischemic tolerance.The possible mechanism may be the up regulation of the expression of BDNF.

目的:观察局灶性缺血预处理对脑源性神经营养因子(brain-derivedneurotrophicfactor,BDNF)的表达影响,探讨神经营养因子与缺血耐受的关系及其在内源性保护机制中的作用。方法:实验选用30只SD大鼠,随机将30只大鼠分为实验组、假手术组、对照组,每组10只。利用线栓法建立局灶性脑缺血耐受的动物模型。实验组预缺血10min,3d后给于缺血2h,再灌注22h处死。假手术组暴露解剖结构10min,3d后同实验组;对照组两次均为假手术。运用对脑梗死体积的测定、光镜下组织病理改变及免疫组织化学染色和图像分析比较各组BDNF的表达变化。结果:假手术组梗死体积犤(126.0±22.4)mm3犦与预缺血组犤(102.0±24.2)mm3犦比较,差异有显著性意义(P<0.05)。假手术组病理改变最为明显,实验组病理改变明显轻于假手术组,仍可见皮质和基底核神经细胞溶解,核皱缩,但可见尚存的大脑皮质的正常神经元排列结构。对照组未见明显的病理改变。本实验中BDNF蛋白阳性细胞表达定位于胞浆呈棕黄色。假手术组阳性细胞的平均吸光度(A值)与对照组比较,差异有显著性意义(P<0.05)。实验组阳性细胞的平均A值与...

目的:观察局灶性缺血预处理对脑源性神经营养因子(brain-derivedneurotrophicfactor,BDNF)的表达影响,探讨神经营养因子与缺血耐受的关系及其在内源性保护机制中的作用。方法:实验选用30只SD大鼠,随机将30只大鼠分为实验组、假手术组、对照组,每组10只。利用线栓法建立局灶性脑缺血耐受的动物模型。实验组预缺血10min,3d后给于缺血2h,再灌注22h处死。假手术组暴露解剖结构10min,3d后同实验组;对照组两次均为假手术。运用对脑梗死体积的测定、光镜下组织病理改变及免疫组织化学染色和图像分析比较各组BDNF的表达变化。结果:假手术组梗死体积犤(126.0±22.4)mm3犦与预缺血组犤(102.0±24.2)mm3犦比较,差异有显著性意义(P<0.05)。假手术组病理改变最为明显,实验组病理改变明显轻于假手术组,仍可见皮质和基底核神经细胞溶解,核皱缩,但可见尚存的大脑皮质的正常神经元排列结构。对照组未见明显的病理改变。本实验中BDNF蛋白阳性细胞表达定位于胞浆呈棕黄色。假手术组阳性细胞的平均吸光度(A值)与对照组比较,差异有显著性意义(P<0.05)。实验组阳性细胞的平均A值与假手术组、对照组比较,差异有显著性意义(P<0.01)。结论:局灶性缺血预处理对随后的脑梗死有明显的保护作用,能够诱导缺血耐受的产生,其可能的机制是

 
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