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brain ischemic preconditioning
相关语句
  脑缺血预处理
     Changes of apoptosis and p53 protein in local-local type brain ischemic preconditioning in rats
     大鼠局灶-局灶型脑缺血预处理后细胞凋亡和p53蛋白的变化
短句来源
     Objective:To study the changes of apoptosis and p53 protein expression after local-local type brain ischemic preconditioning(IP) in rats.
     目的 :研究大鼠局灶 -局灶型脑缺血预处理 ( IP)后细胞凋亡和 p5 3蛋白表达的变化。
短句来源
     The influence of focal brain ischemic preconditioning in rat on expression of caspase-3
     大鼠局灶脑缺血预处理对caspase-3表达影响的研究
短句来源
     Methods SD adult rats were divided into 4 groups randomly:sham group,cerebral ischemia-reperfusion group,brain ischemic preconditioning group and Physcion treatment group.
     方法SD大鼠随机分为四组,分别为假手术组、脑缺血再灌注组、脑缺血预处理组和Ply治疗组。
短句来源
     ② As comparied with brain ischemic preconditioning group bax protein expression wasn't remarkable .
     ②艾灸预处理后Bax蛋白表达变化不明显,与脑缺血预处理组比较无显著差异。
短句来源
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  脑缺血预适应
     Effect of brain ischemic preconditioning on brain mitochondrial functions during the middle cerebral artery occlusion in rat
     大鼠脑缺血预适应对脑线粒体功能的影响
短句来源
     Brain ischemic preconditioning (BIP) can alleviate pathologic damages and function impairments induced by severe ischemia.
     脑缺血预适应可以减轻严重脑缺血导致的各种病理和功能损害,采用低G预适应措施后对神经元也出现了类似的保护作用。 那么,高G暴露对大鼠学习记忆功能影响作用的规律如何?
短句来源
     Astrocytes play a significant role in brain ischemic preconditioning.
     (3)Ast在脑缺血预适应中发挥重要的作用。
短句来源
  “brain ischemic preconditioning”译为未确定词的双语例句
     The present of nestin after local brain ischemic preconditioning in rat
     大鼠局灶性缺血预处理nestin表达的研究
短句来源
     Conclusion Physcion can strengthen the effect of ischemic tolerance induced by brain ischemic preconditioning and decrease the expression of IL-1β and TNF-α,they both have additive effect.
     结论Phy可增强缺血预处理诱导的脑缺血耐受作用,下调脑组织再灌注损伤时IL-1β和TNF-α的表达,二者具有叠加作用。
短句来源
     Study on alleviation of ischemic cerebral injury by transient brain ischemic preconditioning
     短暂缺血预处理减轻缺血性脑损伤的研究
短句来源
     Methods The adult SD male rats were randomly divided into five groups:group A had 40 rats for brainischemia,group B had 40 rats for brain ischemic preconditioning,group C had 40 rats for aspirin plus preconditioning,group Dhad 40 rats for Tongxinluo plus preconditioning,group E had 40 rats for beth Tongxiuluo and aspirin plus preconditioning.
     本研究采用SD 大鼠全脑—局灶脑缺血耐受模型,观察阿司匹林、通心络对再次脑缺血损伤后Bcl-2和Bax 蛋白的表达及星形胶质细胞的增生和脑源性神经营养因子表达的影响,探讨阿司匹林、通心络联合应用对脑缺血耐受的影响及其机制。 方法成年SD 雄鼠,3月龄,随机分为5组:脑缺血组即MCAO 组(n=40);
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  brain ischemic preconditioning
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.
      


Objective To investigate the role of apoptosis and apoptotic proteins p53,p21 and Bax in mechanisms of brain ischemic tolerance in rats.Methods In our study the models of focal-focal type brain ischemic preconditioning were maded by occlusion middle cerebral artery using an intraluminal filament method. Infarct sizes were measured by image analysis system.Neuronal apoptosis was identified by TUNEL staining and expressions of p53, p21 and Bax were analyzed by immunohistochemistry.Results Compared with...

Objective To investigate the role of apoptosis and apoptotic proteins p53,p21 and Bax in mechanisms of brain ischemic tolerance in rats.Methods In our study the models of focal-focal type brain ischemic preconditioning were maded by occlusion middle cerebral artery using an intraluminal filament method. Infarct sizes were measured by image analysis system.Neuronal apoptosis was identified by TUNEL staining and expressions of p53, p21 and Bax were analyzed by immunohistochemistry.Results Compared with the lethal ischemic group, the volume of infarct was greatly reduced when MCAO 20 minutes was performed as ischemic preconditioning( P< 0.05). Both numbers of TUNEL positive cells and p53 protein positive cells decreased ( P< 0.05),but no difference of p21 and Bax expression was found in ischemic penumbra in the ischemic preconditioning group.Conclusion Our data suggest that ischemic tolerance is induced by inhibiting p53 expression which may alleviate neuronal apoptosis after severe cerebral ischemia. Expression of p21 and Bax may not be mandatory to the acquisition of ischemic tolerance in rats.

目的 探讨大鼠局灶性缺血预处理的脑保护作用与细胞凋亡及凋亡相关因子p5 3、p2 1和Bax的关系。方法 采用线栓法阻塞大鼠大脑中动脉造成脑缺血预处理和致死性缺血模型 ,图像分析测算相对梗死体积 ,使用TUNEL染色标记神经细胞凋亡 ,免疫组化染色观察p5 3、p2 1和Bax蛋白表达。结果 与致死缺血组比较 ,缺血预处理组梗死体积减少 4 6 % (P <0 0 5 ) ,半暗区TUNEL阳性细胞数和p5 3阳性细胞数均明显降低 (均P <0 0 5 ) ,p2 1和Bax阳性细胞数无显著变化 (均P >0 0 5 )。结论 缺血预处理可能通过抑制严重缺血后p5 3表达 ,减轻神经细胞凋亡 ,发挥脑保护作用。p2 1和Bax在脑缺血耐受形成中可能不起重要作用。

Objective:To study the changes of apoptosis and p53 protein expression after local-local type brain ischemic preconditioning(IP) in rats.Methods:We made the middle cerebral artery occlusion(MCAO) of rats using an intraluminal monofilament, 20 minutes MCAO was used as IP,72 hours after reperfusion,a 2 hours MCAO was used and 24 hours after that, we performed brain sections and histology analysis, and used TUNEL staining to label the neuronal apoptosis and immunohistochemistry to detect the expression...

Objective:To study the changes of apoptosis and p53 protein expression after local-local type brain ischemic preconditioning(IP) in rats.Methods:We made the middle cerebral artery occlusion(MCAO) of rats using an intraluminal monofilament, 20 minutes MCAO was used as IP,72 hours after reperfusion,a 2 hours MCAO was used and 24 hours after that, we performed brain sections and histology analysis, and used TUNEL staining to label the neuronal apoptosis and immunohistochemistry to detect the expression of p53 protein. Results:Compared with the 2 hours MCAO group,the volume of the brain infarction in IP group reduced to 46%(P<0.05). The number of TUNEL positive cells(P<0.05),decreased greatly in IP group too.The number of p53 protein positive cortical cells increased considerably after 2 hours MCAO with 24 hours reperfusion,IP group this increase is less significant(P<0.05).Conclusion:Brain IP may protect neural tissues through anti-apoptosis and p53 may play a role in the development of the ischemic tolerance.

目的 :研究大鼠局灶 -局灶型脑缺血预处理 ( IP)后细胞凋亡和 p5 3蛋白表达的变化。方法 :采用线栓法建立大鼠大脑中动脉闭塞 ( MCAO)模型 ,以 MCAO2 0 m in作为 IP,再灌注 72 h行 MCAO2 h,再灌注 2 4 h后取脑切片作组织学分析 ,用 TUNEL和免疫组织化学法分别观测细胞凋亡和 p5 3蛋白表达的变化。结果 :与 MCAO 2 h组比较 ,IP组脑梗死体积减少 4 6 % ( P<0 .0 5 ) ;IP组 TU NEL 阳性细胞数明显少于对照组 ( P<0 .0 5 ) ;MCAO2 h再灌注2 4 h后 ,皮层 p5 3阳性细胞数明显增多 ,IP组减轻这种增多 ( P<0 .0 5 )。结论 :脑 IP可能通过抗凋亡机制对神经组织起保护作用 ,而 p5 3可能在脑缺血耐受形成中发挥一定作用。

Objective To investigate the influence of astrocyte-conditioned medium (ACM), ACM treated with Kangdai-1, and ACM plus Kangdai-1 on the neurons damaged by simulated cerebral ischemia/reperfusion in vitro.Method First, the isolation, purification and cultivation of rat cortical astrocytes and neurons, and establishment of the model of stimulated cerebral damage by ischemia/reperfusion were carried out. Then, the ACM, ACM treated with Kangdai-1, and ACM plus Kangdai-1 collected 18 hours after ischemia/reperfusion,...

Objective To investigate the influence of astrocyte-conditioned medium (ACM), ACM treated with Kangdai-1, and ACM plus Kangdai-1 on the neurons damaged by simulated cerebral ischemia/reperfusion in vitro.Method First, the isolation, purification and cultivation of rat cortical astrocytes and neurons, and establishment of the model of stimulated cerebral damage by ischemia/reperfusion were carried out. Then, the ACM, ACM treated with Kangdai-1, and ACM plus Kangdai-1 collected 18 hours after ischemia/reperfusion, were used to culture the damaged neurons in a concentration of 1∶5. Last, the activity, survival rate and death rate of the cultured neurons, the culture fluid leakage rate of LDH, and the expressed amount of NOS-intense positive cells, were detected. Results All ACM, ACM treated with Kangdai-1, and ACM plus Kangdai-1 could markedly increase the activity and survival rate of the damaged neurons, and markedly decrease the death rate of the damaged neurons, the culture fluid leakage rate of LDH, and the expression of NOS-intense positive cells, with a sequence of potency as: ACM treated with Kangdai-1>ACM plus Kangdai-1>ACM. Conclusion (1) The neurons damaged by simulated cerebral ischemia/reperfusion in vitro showe a phasic change of damage-compensation-redamage-restoration; (2) ACM showes significant protective and repairing effects on damaged neurons; (3) Astrocytes play an important role in the process of brain ischemic preconditioning; (4) Kandai-1 may indirectly protect and repair damaged neurons through astrocytes.

目的 探讨体外模拟脑缺血再灌注损伤条件下星形胶质细胞条件培养液(ACM)、经抗呆Ⅰ号作用的星形胶质细胞条件培养液(ACMK)及ACM与抗呆Ⅰ号联合应用(ACM+K)对损伤神经元的影响。方法 先分别进行大鼠大脑皮质星形胶质细胞(Ast)和神经元的分离纯化培养及体外模拟脑缺血再灌注损伤模型的建立,然后用再灌18 h后收集的ACM、ACMK和ACM+K以1∶5的浓度来培养损伤后的神经元,最后测定其神经元的活性、存活率、死亡率、培养液乳酸脱氢酶(LDH)的漏出率和NOS强阳性细胞的表达量。结果 ACM、ACMK和ACM+K均能使脑缺血再灌注损伤后神经元的活性和存活率明显提高,使死亡率、细胞培养液LDH的漏出率和NOS强阳性细胞的表达量显著降低,其作用 ACMK>ACM+K>ACM。结论 ①经体外模拟脑缺血再灌注损伤的神经元呈损伤→代偿→再损伤→恢复的时相变化;②ACM对受损的神经元具有重要的保护和修复作用;③Ast在脑缺血预适应(BIP)中发挥重要的作用;④抗呆Ⅰ号可通过Ast间接地保护和修复受损的神经元。

 
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