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hypoxic ischemic brain damage
相关语句
  缺氧缺血性脑损伤
     Expression of NgR mRNA and NgR Protein in Brain Tissues of Newborn Rats with Hypoxic Ischemic Brain Damage
     新生鼠缺氧缺血性脑损伤脑组织NgR mRNA和NgR蛋白表达及意义
短句来源
     AIM: To study the expression of HSP70 and pathologic damage in hippocampal CA 1 after hypoxic ischemic brain damage(HIBD)in neonatal rats and the effect of monosialotetrahexosylganglioside(GM 1)on it .
     目的 :研究新生大鼠缺氧缺血性脑损伤 (HIBD)后海马CA1区 70ku热休克蛋白 (HSP70 )表达、病理学损伤变化和外源性单唾液酸四已唐神经节苷脂 (GM1)对HSP70表达及病理学损伤的影响 .
短句来源
     A Dynamic Observation on Interleukin 1 β Gene Transcription in Neonate Rats with Hypoxic Ischemic Brain Damage
     新生大鼠缺氧缺血性脑损伤后白细胞介素-1β基因转录的动态观察
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     Caspase and hypoxic ischemic brain damage
     半胱天冬酶与缺氧缺血性脑损伤
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     Objective To study the protective effects of polyclonal antibody to tumor necrosis factor(TNF)α on hypoxic ischemic brain damage (HIBD) of neonatal rats.
     目的研究肿瘤坏死因子(TNF)α多克隆抗体对新生大鼠缺氧缺血性脑损伤(HIBD)后大脑的保护效应。
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  缺血缺氧性脑损伤
     ALM To study the effects of ginkgo biloba extract (GbE) on expressions of neuron specific enolase (NSE) and S 100 protein(S 100) mRNA in newborn rat brain after hypoxic ischemic brain damage (HIBD) and the mechanism of GbE against HIBD.
     目的 研究银杏叶提取物 (GbE)对新生鼠缺血缺氧性脑损伤 (HIBD)后脑组织神经元特异性烯醇化酶 (NSE)、S 10 0蛋白 (S 10 0 )mRNA表达的影响 ,以探讨GbE抗脑缺血缺氧的药理作用机制。
短句来源
     Protection of Mild Hypothermia on the Hypoxic ischemic Brain Damage in Rats
     亚低温对缺血缺氧性脑损伤保护作用的若干生化指标的研究
短句来源
     The Expression of bc1-2 Gene in Hippocampus of Hypoxic Ischemic Brain Damage
     新生大鼠缺血缺氧性脑损伤与bcl-2基因表达的关系
短句来源
     Objective To investigate the changes of cerebral superoxide dismutase(SOD), malondialdehyde(MDA)and nitric oxide(NO) after intrauterine fetal distress in rats in order to defermine whether hypoxic ischemic brain damage(HIBD) occurred in uterus.
     目的 观察胎鼠宫内窘迫后脑组织超氧化物歧化酶 (SOD)、丙二醛 (MDA)、以及一氧化氮 (N O)的变化 ,以探讨新生儿期的缺血缺氧性脑损伤 (HIBD)是否在宫内已经开始发生。
短句来源
     In recent years, studies have demonstrated that TGF β 1 level enhances in hypoxic ischemic brain damage(HIBD), TGF β 1 can accelerate renovation of the nerve cells injured by hypoxia and ischemia through many approaches.
     转化生长因子β1可以通过多种途径促进缺血缺氧性脑损伤所引起的神经细胞的康复。
短句来源
  脑缺氧缺血
     Conclusion The animal model can be used for the study of the neonatal hypoxic ischemic brain damage. \;
     结论 采用小鼠做急性脑缺氧缺血的动物模型 ,脑缺氧缺血效果明显 ,本模型的建立 ,可用于人的急性脑缺氧缺血的病理学、生理学及其药物治疗等诸多方面的类比实验研究
短句来源
  “hypoxic ischemic brain damage”译为未确定词的双语例句
     The expression of bc1-2 gene in hippocampus area of neonatal rats with hypoxic ischemic brain damage
     新生大鼠脑缺血时海马区bc1-2基因的表达
短句来源
     【Methods】 80 seven-day-old Wistar rats were divided into 10 groups(8 for each) randomly as below: normal control group,fake surgery group and hypoxic ischemic brain damage(HIBD) model group-1,3,7,10,12,24,48,72 h.
     【方法】将80只新生7日龄Wistar大鼠随机分为10组(即正常对照组、假手术组和HIBD模型组-1、3、7、10、12、24、48、72 h),每组8只。
短句来源
     Objective To study the effects of 17β estradiol (17β E 2) on extracellular glutamate(Glu) level post hypoxic ischemic brain damage(HIBD) in neonatal rats and to explore whether 17β E 2 has some protective effects on HIBD.
     目的 研究 17β 雌二醇 (17β E2 )对新生大鼠缺氧缺血脑损伤 (HIBD)后谷氨酸 (Glu)释放的影响 ,探讨 17β E2 是否对HIBD有保护作用。
短句来源
     Methods Seven day old Sprague Dawley (SD) rats were randomly divided into 3 groups:sham operated group ( n = 12), hypoxic ischemic brain damage (HIBD) group ( n = 15), BC group ( n = 13).
     方法 新生 7日龄SD大鼠随机分为假手术组 (n =12 )、缺氧缺血组 (HIBD组 ,n =15 )、黄芩苷治疗组 (BC组 ,n =13 )。
短句来源
     Effect of MK 801 on calcium overload of cerebral cortex nerve cells with hypoxic ischemic brain damage
     MK-801对缺氧缺血性大脑皮质神经细胞钙超载影响的研究
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  hypoxic ischemic brain damage
A neuropathological study of 41 forensic autopsy cases of hypoxic/ischemic brain damage has been undertaken, using immunohistochemical staining to detect the 70-kDa heat shock protein (hsp70) and the status of the glial cells.
      


in recent years,the results of many experiments show that excitatory amino acids such as glutamate and aspartate mediate hypoxic-ischemic brain damage by its receptors,and excitatory amino acid antagonists can prevent hypoxic-ischemic brain damage.This experiment studied the hypoxia model in murine cortical cell culture,the neuronal injury caused by hypoxia and excitatory amino acid agonist NMDA,and the preventive effect of NMDA antagonists CPP,Ket and non-NMDA...

in recent years,the results of many experiments show that excitatory amino acids such as glutamate and aspartate mediate hypoxic-ischemic brain damage by its receptors,and excitatory amino acid antagonists can prevent hypoxic-ischemic brain damage.This experiment studied the hypoxia model in murine cortical cell culture,the neuronal injury caused by hypoxia and excitatory amino acid agonist NMDA,and the preventive effect of NMDA antagonists CPP,Ket and non-NMDA antagonist NBQX.The result indicated that (1)the NMDA receptor of excitatory amino acids mediated hypoxia neuronal damage;(2)both NMDA antagonists CPP,Ket and non-NMDA antagonist NBQX prevented neurons from hypoxia injury. Our study suggests that excitatory amino acid antagonists will be the new clinical therapeutic passway of brain ischemia.

近年来,许多研究的结果显示,兴奋性氨基酸谷氨酸、天冬氨酸等通过其受体介导了缺氧、缺血性脑损伤,同时兴奋性氨基酸受体拮抗剂对缺氧、缺血性脑损伤有一定的保护作用。本文研究了离体培养的小鼠皮层神经细胞的缺氧模型,并观察缺氧和兴奋性氨基酸受体激动剂N-甲基-D-天冬氨酸(NMDA)对神经细胞的损伤作用,同时应用兴奋性氨基酸NMDA受体拮抗剂CPP、Ket,及非NMDA受体拮抗剂NBQX观察其对缺氧及NMDA毒性损伤的保护作用。结果表明:(1)兴奋性氨基酸NMDA受体参与介导了缺氧引起的神经元损伤,(2)NMDA受体拮抗剂CPP、Ket和非NMDA拮抗剂NBQX对缺氧引起的神经元损伤均有良好的保护作用。研究结果提示,兴奋性氨基酸受体拮抗剂有望成为临床脑缺血治疗的一个很有价值的途径。

To search for the changes of serum neurospecific enolase (NSE) concentration and cranial CT sean in the neonatal hypoxic ischemic encephalopathy (HIE).Methods Twenty neonates of HIE were examined.The concentration of serum NSE was measured by enzyme-linked immunosorbent assay (ELISA) of 3 days and 7 days of life.The cranial CT sean was examined in the first week of life.Results The concentrations of serum NSE at 3 days of life increased in 20 HIE neonates, especilly in moderate and heavy ones, and...

To search for the changes of serum neurospecific enolase (NSE) concentration and cranial CT sean in the neonatal hypoxic ischemic encephalopathy (HIE).Methods Twenty neonates of HIE were examined.The concentration of serum NSE was measured by enzyme-linked immunosorbent assay (ELISA) of 3 days and 7 days of life.The cranial CT sean was examined in the first week of life.Results The concentrations of serum NSE at 3 days of life increased in 20 HIE neonates, especilly in moderate and heavy ones, and they were identical with the clinical manifestation.The cramal CT scan showed no differences with the clinical manifestation in them in the light and moderate ones.Conclusions NSE is a reliable marker for early diagnosis of HIE and estimate of hypoxic-ischemic brain damage. The cranial CT saan together with serum NSf are much help for the diagnosis and cure of HIE.

目的探讨血清神经元特异性烯醇化酶(NSE)和头颅CT在新生儿缺氧缺血性脑病(HIE)诊断中的作用。方法HIR患儿20例,用酶联免疫法测定生后8天、7天血清NSE浓度。生后1周内行头颅CT检查。结果HIE患儿血清NSE在生后3天均升高,尤以中、重度明显,与临床分度一致。重度HIE患儿头颅CT分度与临床一致,轻、中度头颅CT分度与临床不平行。结论血清NSE测定是早期诊断HIE及判断脑损伤的有效指标,头颅CT检查结合血清NSE测定可更为准确地帮助HIE的诊断和治疗。

Objective: To observe and quantitatively analyse morphologic changes of pyramidal neuronicmitochondria in hippocampal CA1 in newborn rats with hypoxic-ischemic brain damage (HIBD). Methotls: Newborn-rat HIBD model was set, observed and measured, for morphology of mitochondria byelectron microscope and by biogenetic stereology. Results: Mitochondria were swollen,and cristae weredissolved. broken down and disappeared. Mitochondrial average circumference and average area increased, while...

Objective: To observe and quantitatively analyse morphologic changes of pyramidal neuronicmitochondria in hippocampal CA1 in newborn rats with hypoxic-ischemic brain damage (HIBD). Methotls: Newborn-rat HIBD model was set, observed and measured, for morphology of mitochondria byelectron microscope and by biogenetic stereology. Results: Mitochondria were swollen,and cristae weredissolved. broken down and disappeared. Mitochondrial average circumference and average area increased, while specific surface, the cristal membrane density and average cristal length decreased. Conclusiou: The result suggests that HIBD can result in the changes of mitochondrial morphology. Biogenetic stereology quantitative analysis shows exactly mitochondrial morphologic changes, especially mitochondrial functional area. Intracellular energy metabolism obstruction is an important factor causingbrain damage.

目的:观察及定量分析新生鼠缺氧缺血性脑损伤时脑选择性易损区海马CA1区锥体细胞线粒体形态改变。方法:制备新生鼠缺氧缺血性脑损伤模型,电镜观察、生物体视学测量线粒体形态。结果:缺氧缺血性脑损伤时线粒体肿胀,嵴溶解、断裂和消失。线粒体平均截面周长和平均截面积增加;比表面、嵴膜密度及嵴平均截线长减少。结论:缺氧缺血性脑损伤时线粒体形态发生显著变化。生物体视学定量分析准确反应了线粒体形态,尤其是功能区的改变。细胞内能量代谢障碍是脑损伤的重要环节。

 
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