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hypoxic ischemic brain damaged
相关语句
  脑缺氧缺血
     The Replication of Acute Hypoxic Ischemic Brain Damaged Animal Model in Baby Mice
     新生小鼠急性脑缺氧缺血动物模型的建立
短句来源
     Objective To replicate the acute hypoxic ischemic brain damaged animal model.
     目的 建立急性脑缺氧缺血的动物模型。
短句来源
  “hypoxic ischemic brain damaged”译为未确定词的双语例句
     Protective Effect of Nerve Growth Factor by Periphery in Neonate Rats with Hypoxic Ischemic Brain Damaged
     外周应用NGF对新生大鼠缺氧缺血性脑损伤的保护作用
短句来源
  相似匹配句对
     Brain hypoxic and ischemic proconditioning
     脑缺血缺氧预处理
短句来源
     Hypoxic Ischemic Encephalopathy and Apoptosis
     缺氧缺血型脑病与细胞凋亡
短句来源
     Ultrasonography in the Diagnosis of Hypoxic Ischemic Encephalopathy
     新生儿缺氧缺血性脑病的超声诊断
短句来源
     Caspase and hypoxic ischemic brain damage
     半胱天冬酶与缺氧缺血性脑损伤
短句来源
     Erythropoietinand Hypoxic-ischemic Brain Damage
     促红细胞生成素与缺氧缺血性脑损伤
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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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