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brain ischemic tolerance
相关语句
  脑缺血耐受
     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
     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
短句来源
     The mechanism of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP) involves cascades of events including release of neurotransmitter, activation of receptors and gene expression.
     脑缺血预处理(cerebral ischemic preconditioning,CIP)诱导的脑缺血耐受(brain ischemic tolerance,BIT)的产生涉及神经介质、受体及基因的表达等一系列过程。
短句来源
     Objective: To investigate the expression of Hypoxia inducible factor-1a (HIF-1a ) and its target gene Erythropoietin (EPO) in the model of brain ischemic tolerance induced by ischemic preconditioning through twice occlusion of middle cerebral artery in rats.
     目的 建立大鼠大脑中动脉局灶性缺血再灌注模型,通过先后两次线栓阻塞大脑中动脉,观察脑缺血预处理诱导脑缺血耐受形成中缺氧诱导因子-1α(Hypoxia inducible factor-1α,HIF-1α)及其靶基因促红细胞生成素(Erythropoietin,EPO)表达的变化,探讨其在脑缺血耐受机制中的作用。
短句来源
     The Experimental Study of the Expression of HIF-1a and Its Target Gene EPO in the Rat Model of Brain Ischemic Tolerance
     HIF-1α及其靶基因EPO在大鼠脑缺血耐受中表达的实验研究
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  “brain ischemic tolerance”译为未确定词的双语例句
     EFFECTS OF THE METABOTROPIC GLUTAMATE RECEPTOR LIGAND(s)-4C3HPG ON THE INDUCTION OF BRAIN ISCHEMIC TOLERANCE IN THE RAT
     代谢性谷氨酸受体配体(s)-4C3HPG对大鼠脑缺血耐受性诱导的影响
短句来源
     Conclusion LIP could induce the increase in HSP70 expression in the hippocampus CA1,suggesting that HSP70 might play a role in the induction of brain ischemic tolerance induced by LIP.
     结论损伤性脑缺血前给予LIP,可明显增加CA1区HSP70的阳性表达,诱导CA1区锥体细胞耐受缺血损伤。
短句来源
     Brain Ischemic Tolerance Induced by Spreading Depression in Rats in Vivo
     扩散性抑制诱导大鼠皮层缺血耐受的在体研究
短句来源
     The adenosine (ADO) mechanism is an important explaining for the protective effects of cerebral ischemic preconditioning (CIP) on neurons. The protective effects are usually referred to as brain ischemic tolerance (BIT). CIP lead to increases in synthesis and release of adenosine.
     腺苷机制是解释脑预缺血(cerebral ischemic preconditioning,CIP)神经保护作用的一个重要学说,即CIP引起脑细胞合成和释放腺苷(adenosine,ADO)增加,后者与其特异性受体结合发挥对神经元的保护作用。
短句来源
     2. To investigate the effects of electroacupuncture with various frequencies on the degree of induced brain ischemic tolerance in rats with focal cerebral ischemia.
     2.比较不同频率电针灸(2/5Hz、2/15Hz、2/100Hz)重复刺激“百会第四军医大学硕士学位论文穴”的预处理脑保护效果,寻找理想的电针灸频率:
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  相似匹配句对
     Ischemia and Ischemic Tolerance in the Brain an Overview
     脑缺血与缺血耐受
短句来源
     Experimental study on the acupuncture induced brain ischemic tolerance
     针刺诱导脑缺血耐受的实验研究
短句来源
     Brain-derived erythropoietin and its effects on brain ischemic tolerance
     脑源性EPO及其脑缺血耐受作用
短句来源
     The Role of Nitric Oxide in the Induction of Brain Ischemic Tolerance
     一氧化氮在脑缺血耐受诱导中的作用
短句来源
     Progress in the study on the mechanisms underlying brain ischemic tolerance
     脑缺血耐受机制的研究进展
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  brain ischemic tolerance
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.
      


To determine the role of adenosine (ADO) receptor in the induction of brain ischemic tolerance, changes in amount and affinity of ADO receptor in rat hippocampal cellular membranes after transient ischemia were investigated using radioligand binding method. Ischemia for 6 min resulted in an apparent delayed neuron death (DND) in the hippocampus, while ischemia for 3 min did not cause DND. Preconditioning ischemia for 3 min could apparently decrease DND caused by ischemia for 6 min after the preconditioning...

To determine the role of adenosine (ADO) receptor in the induction of brain ischemic tolerance, changes in amount and affinity of ADO receptor in rat hippocampal cellular membranes after transient ischemia were investigated using radioligand binding method. Ischemia for 6 min resulted in an apparent delayed neuron death (DND) in the hippocampus, while ischemia for 3 min did not cause DND. Preconditioning ischemia for 3 min could apparently decrease DND caused by ischemia for 6 min after the preconditioning at an interval of 1 d reperfusion. In correspondence with the histological changes, ischemia for 3 min caused an increase in amount and affinity of ADO receptor at 1 or 3 days after reperfusion ( P <0 05 vs sham), while ischemia for 6 min caused a decrease in the amount and an increase in the affinity ( P <0 05 vs sham). Compared with the rats suffering from ischemia for 6 min followed by reperfusion for 4 h and 1 or 3 d, the amount and affinity of ADO receptor increased in rats with preconditioning ischemia (3 min) 1 d before the ischemia for 6 min The above results showed that cerebral ischemic preconditioning increased the amount and affinity of ADO receptor in hippocampal cellular membranes, and resisted the down regulating of ADO receptor caused by severe ischemia, suggesting an important role of the increase in amount and affinity of ADO receptor in the induction of brain ischemic tolerance.

采用放射性配基结合法 ,测定大鼠全脑缺血后海马细胞膜腺苷 (adenosine,ADO)受体数量及亲和力的变化 ,以探讨其与脑缺血耐受形成之间的关系。发现缺血 6min即可导致海马组织明显的神经元延迟性死亡 (de layedneurondeath ,DND) ,缺血 3min不足以引起海马组织明显的DND ;而经过 3min预缺血处理 ,可明显减轻间隔1d后 6min缺血引起的海马DND (P <0 0 1)。与此相对应 ,缺血 3min再灌 1和 3d时 ,ADO受体数量及亲和力明显高于sham组 (P <0 0 5 ) ,而缺血 6min再灌 1和 3d时 ,ADO受体数量明显低于sham组 (P <0 0 5 ) ,但亲和力高于sham组 (P <0 0 5 )。与单纯 6min缺血再灌 4h、1和 3d时相比 ,3min预缺血 + 6min缺血 (间隔 1d)再灌后 ,ADO受体数量及亲和力均显著升高 (P <0 0 5 )。这些结果表明 ,脑预缺血处理可使大鼠海马细胞膜ADO受体数量增多 ,亲和力增强 ,并能对抗损伤性缺血引起的ADO受体数量减少 ,提示腺苷受体数量及亲和力的变化在脑缺血...

采用放射性配基结合法 ,测定大鼠全脑缺血后海马细胞膜腺苷 (adenosine,ADO)受体数量及亲和力的变化 ,以探讨其与脑缺血耐受形成之间的关系。发现缺血 6min即可导致海马组织明显的神经元延迟性死亡 (de layedneurondeath ,DND) ,缺血 3min不足以引起海马组织明显的DND ;而经过 3min预缺血处理 ,可明显减轻间隔1d后 6min缺血引起的海马DND (P <0 0 1)。与此相对应 ,缺血 3min再灌 1和 3d时 ,ADO受体数量及亲和力明显高于sham组 (P <0 0 5 ) ,而缺血 6min再灌 1和 3d时 ,ADO受体数量明显低于sham组 (P <0 0 5 ) ,但亲和力高于sham组 (P <0 0 5 )。与单纯 6min缺血再灌 4h、1和 3d时相比 ,3min预缺血 + 6min缺血 (间隔 1d)再灌后 ,ADO受体数量及亲和力均显著升高 (P <0 0 5 )。这些结果表明 ,脑预缺血处理可使大鼠海马细胞膜ADO受体数量增多 ,亲和力增强 ,并能对抗损伤性缺血引起的ADO受体数量减少 ,提示腺苷受体数量及亲和力的变化在脑缺血耐受形成过程中发挥了重要的作用。

AIM: To investigate the acupoint specificity of brain ischemic tolerance induced by preconditioning with repeated electroacupuncture at "Baihui" acupoint in rats with transient focal cerebral ischemia. METHODS: 40 SD male rats were randomly divided into 4 groups ( n =10 each): Animals in control group received no pretreatment, animals in PB group were intraperitoneally injected with pentobarbital sodium 40 mg/kg a day for 5 days, animals in EA1 group received electroacupuncture at the "Baihui" acupiont...

AIM: To investigate the acupoint specificity of brain ischemic tolerance induced by preconditioning with repeated electroacupuncture at "Baihui" acupoint in rats with transient focal cerebral ischemia. METHODS: 40 SD male rats were randomly divided into 4 groups ( n =10 each): Animals in control group received no pretreatment, animals in PB group were intraperitoneally injected with pentobarbital sodium 40 mg/kg a day for 5 days, animals in EA1 group received electroacupuncture at the "Baihui" acupiont 30 min a day for 5 days under pentobarbital sodium anesthesia and animals in EA2 group received electroacupuncture at the point 1.0 cm right from "Baihui" acupoint 30 min a day for 5 days under pentobarbital sodium anesthesia. 24h after the last treatment, the right middle cerebral artery occlusion model (MCAO) was induced for 120 min in all animals. The neurological deficit scores (NDS) were evaluated at 24h after reperfusion and then rats were sacrificed under deep anesthesia. The brain was cut into 6 2 mm-thick coronal sections and infarct volumes were determined by TTC staining. RESULTS: ① EA1 group showed lower NDS than that in control and PB groups ( P <0.05). There was no significant difference of NDS among the other groups. ② The infarct volume of EA1 group was smaller than that in any other groups ( P <0.01). The infarct volume of EA2 group was smaller compared with that in control or PB groups ( P < 0.01). No significant difference was observed between control and PB groups ( P >0.05). CONCLUSION: The ischemic tolerance induced by preconditioning with repeated electroacupuncture at preconditioning in rats with focal cerebral ischemia has acupoint specificity.

目的 :观察电针刺激对大鼠局灶性缺血 /再灌注损伤的预处理效应的穴位特异性 .方法 :SD雄性大鼠 4 0只随机分为 4组 (n =10 ) ,即空白对照组 (Control)、戊巴比妥对照组(PB)、针刺百会穴组 (EA1)和针刺穴位旁开组 (EA2 ) .Control组未行任何处理 ;PB组腹腔注射戊巴比妥钠 4 0mg·kg-1·d-1,连续 5d;针刺EA1组和EA2组在戊巴比妥钠麻醉下分别用重复电针刺激 (30min·d-1× 5d)百会穴和百会穴右旁开 1.0cm处 .最后一次处理的 2 4h后 ,所有动物在异氟醚麻醉下用颈内动脉线栓法致右侧大脑中动脉栓塞 12 0min .再灌注 2 4h后 ,行神经功能障碍评分 ,并取大脑行TTC染色以测量脑梗死容积 .结果 :①神经功能障碍评分EA1组的评分优于Control组和PB组 (P <0 .0 5 ) ,与EA2组比较无差异 .EA2组、Control组和PB组的评分无显著差异 ;②脑梗死容积EA1组的脑梗死容积较其他 3组显著减少 (P <0 .0 1) .EA2组的梗死容积较Control组和PB组显著减小 (P <0 .0 1) .Cont...

目的 :观察电针刺激对大鼠局灶性缺血 /再灌注损伤的预处理效应的穴位特异性 .方法 :SD雄性大鼠 4 0只随机分为 4组 (n =10 ) ,即空白对照组 (Control)、戊巴比妥对照组(PB)、针刺百会穴组 (EA1)和针刺穴位旁开组 (EA2 ) .Control组未行任何处理 ;PB组腹腔注射戊巴比妥钠 4 0mg·kg-1·d-1,连续 5d;针刺EA1组和EA2组在戊巴比妥钠麻醉下分别用重复电针刺激 (30min·d-1× 5d)百会穴和百会穴右旁开 1.0cm处 .最后一次处理的 2 4h后 ,所有动物在异氟醚麻醉下用颈内动脉线栓法致右侧大脑中动脉栓塞 12 0min .再灌注 2 4h后 ,行神经功能障碍评分 ,并取大脑行TTC染色以测量脑梗死容积 .结果 :①神经功能障碍评分EA1组的评分优于Control组和PB组 (P <0 .0 5 ) ,与EA2组比较无差异 .EA2组、Control组和PB组的评分无显著差异 ;②脑梗死容积EA1组的脑梗死容积较其他 3组显著减少 (P <0 .0 1) .EA2组的梗死容积较Control组和PB组显著减小 (P <0 .0 1) .Control和PB组间的梗死容积无差异 (P >0 .0 5 ) .结论 :重复电针刺激预处理对大鼠局灶性脑缺血 /再灌注损伤的预处理效应有穴位特异性 .

AIM: To investigate whether oncogene c fos is involved in the regulation of the brain ischemic tolerance induced by oxygen inhaling preconditioning. METHODS: SD rats were randomly divided into 2 groups: oxygen inhaling preconditioning group and control group ( n =6 each). The rats in oxygen inhaling preconditioning group inhaled Pure oxyen for 24 h, while the control animals inhaled 210 mL·L -1 Pure oxgen for 24 h. 24 h after the treatment, all the rats were perfused transcardially and...

AIM: To investigate whether oncogene c fos is involved in the regulation of the brain ischemic tolerance induced by oxygen inhaling preconditioning. METHODS: SD rats were randomly divided into 2 groups: oxygen inhaling preconditioning group and control group ( n =6 each). The rats in oxygen inhaling preconditioning group inhaled Pure oxyen for 24 h, while the control animals inhaled 210 mL·L -1 Pure oxgen for 24 h. 24 h after the treatment, all the rats were perfused transcardially and the brains were moved out. The Fos expression in rat brain was detected by using ABC immunohistochemistry method and the difference between the two groups was studied. RESULTS: There was a wide spread expression of Fos like reactivity production and the distribution patterns in the two groups were similar. However, the Fos expression increased in oxygen inhaling preconditioning rats in the following brain areas: solitary tract nucleus, area postrema, lateral parabranchial nucleus, caudal part of spinal nucleus of 5th nerve, ventrol tegmental nucleus, periaqueductal nucleus, supramammillary nucleus, supraoptic nucleus, hippocampus, subiculum, posterolateral cortical amygdaloid nucleus, anterior cortical amygdaloid nucleus, lateral septal nucleus, bed nucleus of stria terminalis, globus pallidus, Calleja island, occipital cortex, retrosplenial cortex, parietal cortex, forelimb and hindlimb area of cortex, and frontal cortex. CONCLUSION: Some nuclei can be activated by oxygen inhaling preconditioning. Oncogene c fos is involved in the regulation of the brain ischemic tolerance induced by oxygen inhaling preconditioning.

目的 :观察原癌基因c fos是否参与了对吸氧预处理诱导脑缺血耐受的产生 .方法 :随机将大鼠分为 2组 :吸氧预处理组和对照组 (每组n =6) .吸氧组大鼠吸纯氧 2 4h ,对照组大鼠吸 2 10mL·L-1O2 2 4h .2 4h后经心灌流、取脑 ;用免疫组化法观察Fos蛋白在大鼠脑内的表达 ,比较两组大鼠的表达差异 .结果 :Fos样免疫反应阳性神经元在脑内分布广泛 ,两组动物脑内的Fos阳性细胞的分布模式非常相似 .但吸氧预处理的大鼠脑内许多脑区Fos表达明显增多、增强 .结论 :吸氧预处理可激活脑内的一些核团 ;原癌基因c fos参与了对吸氧预处理诱导脑缺血耐受的调节

 
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