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bilateral hippocampus
相关语句
  双侧海马
    Effects of bilateral hippocampus infusion with neuropeptide Y 3-36 on learning and its memory and mechanism in rats
    双侧海马注射神经肽Y3-36对大鼠学习记忆的影响
短句来源
    METHODS:Intrahippocampal administration of antisense and missense oligodeoxynu cleotides(ODN) against neuropeptide Y2 receptor mRNA or saline was performed to the bilateral hippocampus of rats.
    方法:双侧海马插管注射Y2受体的反义、错义寡核苷酸或生理盐水,应用RT-PCR和免疫组化方法检测大鼠海马中c-fos基因在跳台法训练后的表达水平变化。
短句来源
    Results :(1)The level of BDNFmRNA in the bilateral hippocampus was increased after cerebral ischemia and reperfusion.
    结果 :( 1 )脑缺血及缺血再灌注均能诱导双侧海马神经元BDNFm RNA水平增高 ;
短句来源
    Within1d,NOS neuronal degeneration was seen in bilateral hippocampus,ipsilateral diencephalons and mesen-cephalon.
    1d后双侧海马和伤侧间脑等部位的NOS神经元溃变;
短句来源
    Methods NPY Y2 receptor specific agonist NPY 3-36 was infused into the bilateral hippocampus of adult rats. Control group were infused with saline. And the effect of learning and memory in rats was examined by the step down test.
    方法 建立学习记忆障碍模型 ,双侧海马插管注射Y2特异性激动剂NPY 3 36 ,观察其对大鼠学习记忆的影响 ,并利用免疫组化方法 ,检测与学习记忆密切相关的即刻早期基因c -fos表达情况。
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  “bilateral hippocampus”译为未确定词的双语例句
    Objective To find out the profile of perception of emotion in patients with lesions in bilateral cingulate gyrus, bilateral hippocampus and prefrontal cortex, and to test which of these areas are involved in the special network of fear processing.
    目的探讨扣带回、海马以及额叶损伤患者的情绪认知特征,验证这些脑结构参与情绪加工以及恐惧的特异性神经机制的假说。
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  bilateral hippocampus
This study was performed to evaluate the effect of seizures on the bilateral hippocampus in mesial temporal lobe epilepsy (mTLE) and neocortical epilepsy by single voxel proton magnetic resonance spectroscopy (MRS).
      
The volume of the bilateral hippocampus was significantly smaller in the major depression group than that in control group.
      


Objective: To study the change of brain derived neurotrophic factor mRNA (BDNFmRNA)in hippocampus and the effect of BDNF on the hippocampus neurons after focal cerebral ischemia and reperfusion in rats.Methods:The level of BDNFmRNA was measured in the rat hippocampus using in situ hybridization.Results :(1)The level of BDNFmRNA in the bilateral hippocampus was increased after cerebral ischemia and reperfusion.(2)The lower level of BDNFmRNA in the hippocampus with serious ischemia was found than...

Objective: To study the change of brain derived neurotrophic factor mRNA (BDNFmRNA)in hippocampus and the effect of BDNF on the hippocampus neurons after focal cerebral ischemia and reperfusion in rats.Methods:The level of BDNFmRNA was measured in the rat hippocampus using in situ hybridization.Results :(1)The level of BDNFmRNA in the bilateral hippocampus was increased after cerebral ischemia and reperfusion.(2)The lower level of BDNFmRNA in the hippocampus with serious ischemia was found than that with slight ischemia.(3)The level of BDNFmRNA following the reperfusion was increased continuously.It was the highest at 12 hours and recovered basal level at 72 hours after the reperfusion.Conclusion: The regional basal BDNFmRNA level showed here positively correlated with cellular resistance to ischemic damage,and it was consistent with the hypothesis of a neuroprotective role of BDNF.

目的 :探讨脑缺血再灌注损伤后脑内脑源性神经营养因子 ( BDNF) m RNA水平的变化规律 ,推测BDNF对损伤病理的影响。方法 :线栓法制作大鼠脑缺血再灌注模型 ,原位杂交检测大鼠海马神经元内BDNFm RNA,图象分析间接定量 BDNFm RNA水平。结果 :( 1 )脑缺血及缺血再灌注均能诱导双侧海马神经元BDNFm RNA水平增高 ;( 2 )缺血损伤过重后海马神经元 BDNFm RNA水平增高的程度反而小 ;( 3 )再灌注后BDNFm RNA的水平继续升高 ,高峰值出现在 1 2小时 ,至 72小时降至对照组水平 ;两侧海马的变化趋势类似。结论 :海马神经元在脑缺血及再灌注损伤后将升高 BDNFm RNA的表达以保护神经元 ,海马各区 BDNFm RNA基础水平与海马神经元病理改变程度呈负相关。

Purpose To study the expression of heme oxygenase protein during early focal ischemia in rats. Methods The expression of heme oxygenase(HO) 1 protein during early focal cerebral ischemia was investigated by using immunohistochemistry and computer image analysis in middle cerebral artery occlusion in rats. Results HO??1 expression was observed in the neurons and gliacytes of the ipsilateral cerebral cortex infarction area and hippocampus at 30 miniute after occlusion.With time going on ,the expression ...

Purpose To study the expression of heme oxygenase protein during early focal ischemia in rats. Methods The expression of heme oxygenase(HO) 1 protein during early focal cerebral ischemia was investigated by using immunohistochemistry and computer image analysis in middle cerebral artery occlusion in rats. Results HO??1 expression was observed in the neurons and gliacytes of the ipsilateral cerebral cortex infarction area and hippocampus at 30 miniute after occlusion.With time going on ,the expression of HO?? 1 increased,HO??1 expression was observed in the ipsilateral infarction border area,frontal and cingulated cortex,thalamus,hypothalamus and bilateral hippocampus. Conclusions Strong and long lasting expression of HO??1 protein is evidently significant physiological consequences in the recovery of neuronal tissue from ischemic injury in focal cerebral ischemia.

目的 研究局灶性脑缺血血红素氧合酶 (HO)在脑内的表达。方法 采用大鼠大脑中动脉栓塞致脑缺血 ,对缺血早期不同时间点进行HO 1免疫组化及病理学研究 ,并应用计算机图像分析技术计算HO 1表达的强弱。结果 栓塞后 3 0min皮质及海马即有HO 1阳性神经元和胶质细胞 ,且随着时间推移 ,HO 1的表达逐渐增强 ,HO 1主要分布在灶周皮质、梗死皮质区、梨状皮质内的神经元及胶质细胞 ,丘脑、下丘脑、海马齿状回的神经元及对测海马也出现HO 1的表达。结论 脑缺血时脑内HO 1迅速而强烈的表达可能是脑组织对自身损伤的恢复机制

Objective:To research the relationship between diaschisis and nitric oxide synthase(NOS)neuron loss,vasoconstriction subsequent to excitotoxin lesion.Methods:Local microinjection of kainic acid into parietal cortex of rats and stained withβ-NADPH histochemistry and EA50histological staining.Results:1h post-lesion,there was degeneration of NOS neurons and some of non-NOS neurons in bilateral cortex,hippocampus and cerebellar cortex.By4h post-lesion,there was a32%~39%reduction in diameter of mi-crovasculature...

Objective:To research the relationship between diaschisis and nitric oxide synthase(NOS)neuron loss,vasoconstriction subsequent to excitotoxin lesion.Methods:Local microinjection of kainic acid into parietal cortex of rats and stained withβ-NADPH histochemistry and EA50histological staining.Results:1h post-lesion,there was degeneration of NOS neurons and some of non-NOS neurons in bilateral cortex,hippocampus and cerebellar cortex.By4h post-lesion,there was a32%~39%reduction in diameter of mi-crovasculature that was strictly confined to the areas of NOS neuronal degeneration.By8h,the NOS nerve terminals become dust-like and lose of nerve fiber density was seen throughout the ipsilateral cortex.Within1d,NOS neuronal degeneration was seen in bilateral hippocampus,ipsilateral diencephalons and mesen-cephalon.2~5d post-lesion,concomitant with the NOS containing neurons-degeneration,induced NOS activity was faintly visible in neurons of cerebral cortex and hippocampus,and large number of neurons were lost in CA3and CA4subfieds of hippocampus in7d post-lesion.Conclusion:These findings suggested that diaschi-sis is related to excitotoxic death of NOS and non-NOS neurons.The loss of NO contributes to vasoconstric-tion which is responsible for the reduced blood flow and metabolism in affected regions.

目的研究局部皮质注射海仁酸导致NOS神经元损伤及血管收缩与神经功能联系障碍的关系。方法将微量海仁酸注射到大鼠顶叶,β-NADPH组织化学及EA50组织学染色。结果注射后1h双侧大脑皮质、海马和小脑皮质均可见NOS神经元和一些非NOS神经元溃变; 4 h后NOS阳性神经元损伤区域微血管的直径缩小了32%~39%; 8 h后NOS阳性神经末梢溃变呈细颗粒状;1d后双侧海马和伤侧间脑等部位的NOS神经元溃变; 2~5 d后皮质、海马等部位的部分神经元诱导表达NOS活性;7 d后双侧海马CA3和CA4大量神经元丢失。结论神经功能联系障碍与兴奋性神经毒所致的跨突触NOS神经元和非NOS神经元损伤有关,NOS神经元损伤所致的NO减少导致血管收缩,引起受损区域的脑血流减少及代谢功能障碍。

 
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