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ischemic brain injury
相关语句
  缺血性脑损伤
    Effect of Dynorphin A 1 ̄13 on Hypoxia Ischemic Brain Injury in Neonatal Rats
    强啡肽A_(1~13)在新生鼠缺氧、缺血性脑损伤中的作用
短句来源
    AIM: To observe influences of ischemic brain injury on proliferation and transference of endogenous neural stem cells.
    目的:观察缺血性脑损伤对内源性神经干细胞增殖、迁移的影响。
短句来源
    EXPRESSION OF LIM HOMEOBOX GENE Lhx3 AND Lhx4 AFTER THE CEREBRAL ISCHEMIC BRAIN INJURY IN ADULT RATS
    同源盒基因Lhx3和Lhx4在成年大鼠缺血性脑损伤后的表达变化
短句来源
    Heat shock protein 70 and ischemic brain injury
    热休克蛋白70与缺血性脑损伤
短句来源
    Study of mechanism of alteration of phosphoinositide system in rat hippocampus during ischemic brain injury
    缺血性脑损伤海马神经元磷酸肌醇系统的变化及其机制的探讨
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  “ischemic brain injury”译为未确定词的双语例句
    Effects of Specific COX2 Inhibitor on Ischemic Brain Injury
    选择性COX2抑制剂对脑缺血再灌注损伤的影响
短句来源
    Objectives: To study the secondary pathological changes in the central nervous system after injury and the role of dynorphin A 1 ̄13 in hypoxi ischemic brain injury in neonatal rats.
    目的:探讨强啡肽A1~13在新生鼠脑缺氧、缺血性损伤中的作用。
短句来源
    Our results suggest the differential expression of IL-1B and CD44 on astrocyte under hypoxia and reoxygenation. Our research implyed that the role of IL-16 in ischemic brain injury might be associated with the expression of some adhesion moleculars such as CD44, and the change in ECM level such as the HA might be a important factor in the inflammatory response after ischemic injury.
    我们的结果表明了在星形胶质细胞缺氧缺糖后IL-1β和CD44及其配体的差异性表达,暗示了在损伤过程中IL-1β可能会和CD44相互作用来介导缺血后损伤,此外细胞外基质的改变也可能会促进缺血损伤后炎症的发生的重要因素。
短句来源
    These results imply some specific role of c-fos and ODC after ischemic brain injury.
    上述结果提示c-fos及ODC可能在缺血型脑损伤后具有特殊作用。
短句来源
    Aim:The role of prostaglandin synthesis enzyme COX2 in mediating ischemic brain injury was investigated.
    目的 :观察脑缺血再灌注损伤中COX2的表达以及选择性COX2抑制剂SC5 812 5对脑缺血再灌注后脑梗死体积、PGE2 含量的影响。
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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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The levels of mRNAs for proto-oncogene c-fos and ornithine decarboxylase (ODC)genes were measured in rat cerebral cortex and hippocampus at various recirculation intervals after 20 minutes of ischemia. Striking increases in c-fos and ODC genes expression were observed in rat cerebral cortex 0.5-3h and 6-14h respectively after recirculation. In the meantime, delayed expression of of c-fos and ODC genes were noticed in rat hippocampus 36~72h after recirculation. In contrast to c-fos and ODC genes, c-myc gene expression...

The levels of mRNAs for proto-oncogene c-fos and ornithine decarboxylase (ODC)genes were measured in rat cerebral cortex and hippocampus at various recirculation intervals after 20 minutes of ischemia. Striking increases in c-fos and ODC genes expression were observed in rat cerebral cortex 0.5-3h and 6-14h respectively after recirculation. In the meantime, delayed expression of of c-fos and ODC genes were noticed in rat hippocampus 36~72h after recirculation. In contrast to c-fos and ODC genes, c-myc gene expression can not be induced by ischemia. These results imply some specific role of c-fos and ODC after ischemic brain injury. In this article, we analysed the mechanism that recirculation after ischemia induces c-fos and ODC genes expression, and proposed the concept - neuronal stress state to describe neuronal response to destructive stimulation.

应用大鼠椎动脉与颈内动脉结扎造成暂时性脑缺血再灌注以及RNA点杂交方法观察c-fos基因与鸟氨酸脱羧酶(ODC)基因表达的动力学过程。结果表明:大鼠大脑皮质c-fos基因在再灌后0.5至3小时表达,ODC基因在6小时至14小时表达;海马的c-fos基因则自36至72小时呈现高水平表达,ODC基因表达与之相对同步或稍延后。但是暂时性脑缺血却不能诱导c-Myc基因表达。上述结果提示c-fos及ODC可能在缺血型脑损伤后具有特殊作用。文中对缺蛋再灌引起cfos-及ODC基因表达的机制进行了分析与讨论,并提出“神经元应激状态”这一概念以描述神经元对伤害性刺激的反应历程。

Stimulation of phosphatidylinositol (PI)hydrolysis by glutamate(Glu)wasmeasured in hippocampal slices from rats receiving recovery periods of 21 day following30 min ischemic insult induced through a four- vessel occlusion model.The resultsshowed that PI hydrolysis elicited by Glu ( 500 μ)was significantly enhanced in theslices prepared from normal and ischemic rats(P<01,n=9). The effect was greater inslices from different periods(up to 21 day)after reperfusion than in slices from non- ischemic control.The hyperresponsiveness...

Stimulation of phosphatidylinositol (PI)hydrolysis by glutamate(Glu)wasmeasured in hippocampal slices from rats receiving recovery periods of 21 day following30 min ischemic insult induced through a four- vessel occlusion model.The resultsshowed that PI hydrolysis elicited by Glu ( 500 μ)was significantly enhanced in theslices prepared from normal and ischemic rats(P<01,n=9). The effect was greater inslices from different periods(up to 21 day)after reperfusion than in slices from non- ischemic control.The hyperresponsiveness to Glu was always accompanied by an increasein AIF_4 ̄- -stimulated formation of ̄3H-inositol phosphates.In addition,the availability ofan increased number or higher affinity of Glu receptors and the stimulation of PI hydro-lysis by carbachol or norepinephrine in the injured slices were not observed.These resu- lts suggested that the enhanced PI turnover responsiveness to Glu is the result,at least inpart,of functional changes at the G- protein level and may contribute to the pathophy-siology of ischemic brain injury or to the regenerative phenomena that accompany theischemic damage.

采用四动脉闭塞全脑缺血模型,观察大鼠缺血30min再灌注21d不同时间中,外源性谷氨酸(Glu)对海马脑片磷脂酰肌醇(PI)代谢的影响和偶联该系统的G蛋白功能变化。结果显示,Glu(500μmol/L)对正常和缺血再灌注海马脑片肌醇磷酸(IP)生成均具明显的促进作用(P<0.01,n=9),其中以缺血再灌注后IP的升高为显著,并且这种Glu刺激的IP堆积效应随缺血再灌注时间的延长在21d中持续存在。与此同时,还观察到缺血再灌注24h至7d中,海马神经元Glu受体密度(Bmax)显著下降(P<0.01,n=8),亲和力(Kd)无显著变化。提示脑缺血再灌注后Glu刺激的PI代谢增强是由于Glu受体与磷脂酶C(PLC)间产生高反应所致。应用四氟化铝(AlF_4 ̄-)可得到与上述Glu刺激IP生成相同的结果,而氨甲酰胆碱(Cah)和去甲肾上腺素(NE)对IP水平的作用不受脑缺血和再灌注的影响。表明缺血状态下的这种Glu与PLC间的高反应可能是特异的,并通过偶联该系统的G蛋白功能变化介导。

Objectives: To study the secondary pathological changes in the central nervous system after injury and the role of dynorphin A 1 ̄13 in hypoxi ischemic brain injury in neonatal rats. Methods: Changes of concentrations of dynorphin A 1 ̄13 immunoreactives in some brain areas at different times after brain injury and the effect of injecting 8 μl dynorphin A 1 ̄13 anti serum into the medulla pool on pathological process of brain injury were observed in perinatal...

Objectives: To study the secondary pathological changes in the central nervous system after injury and the role of dynorphin A 1 ̄13 in hypoxi ischemic brain injury in neonatal rats. Methods: Changes of concentrations of dynorphin A 1 ̄13 immunoreactives in some brain areas at different times after brain injury and the effect of injecting 8 μl dynorphin A 1 ̄13 anti serum into the medulla pool on pathological process of brain injury were observed in perinatal cerebral hypoxia ischemic rat models prepared by permanent ligation of right common carotid artery combined with a temporary systematic hypoxia at 37℃ in 7 day old Wistar rats. Results: Concentrations of dynorphin A 1 ̄13 in cortex, hypothalamus and hippocampus increased significantly after the injury. Microinjection of anti dynorphin A 1 ̄13 serum into the medulla pool 1h preinjury might markedly reduce brain edema and improve the physiological condition. Conclusions: Dynorphin A 1 ̄13 plays a role in the pathophysiological process of brain hypoxia ischemia and excessive amount of dynorphin A 1 ̄13 had some detrimental effect on the process.

目的:探讨强啡肽A1~13在新生鼠脑缺氧、缺血性损伤中的作用。方法:将7日龄新生鼠右侧颈总动脉结扎并在低氧环境下制成半球性脑缺氧、缺血模型,观察脑损伤后不同时间、不同脑区强啡肽A1~13免疫活性物质含量的改变,和小脑延髓池注射强啡肽A1~13抗血清对脑损伤病理过程的影响。结果:新生鼠脑组织缺氧、缺血后不同时间,强啡肽A1~13含量在皮层、下丘脑和海马回均显著升高,以大脑皮层含量升高最为明显;小脑延髓池注射8μl强啡肽A1~13抗血清,可明显减轻损伤后脑水肿,改善新生鼠的一般状况。结论:强啡肽A1~13参与脑缺氧、缺血的病理过程,过量的强啡肽A1~13有加重脑缺氧、缺血后病理改变的作用。

 
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