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氨基酸毒性
相关语句
  amino acid toxicity
     Excitatory Amino Acid Toxicity and Ischemic Brain Injury
     兴奋性氨基酸毒性与缺血性脑损伤
短句来源
     External bFGF can promote neuron survival and antagonice excitatory amino acid toxicity in vitro.
     应用外源性bFGF可促进神经元的存活和突起生长,拮抗兴奋性氨基酸毒性
短句来源
     3.Estrogen can resist the excitability amino acid toxicity and stable the solubility of calcium ion in cells.
     3、雌激素能拮抗兴奋性氨基酸毒性,稳定细胞内钙离子溶度。
短句来源
  “氨基酸毒性”译为未确定词的双语例句
     The Effect of GM-1 to Impaired SH-SY5Y Cultured in vitro by Excitatory Amino Acids
     神经节苷脂(GM-1)对体外培养SH-SY5Y细胞兴奋性氨基酸毒性损伤的作用
短句来源
     The Effect of Modified rhaFGF to SH-SY5Y Impaired by Excitatory Amino Acids
     rhaFGF改构体对SH-SY5Y细胞兴奋性氨基酸毒性损伤的作用
短句来源
     Objective Investigate the protective effect of GM-1 to impaired SH-SY5Y cultured in vitro by (excitatory) amino acids.
     目的探讨神经节苷脂(GM1)对体外培养SH SY5Y细胞兴奋性氨基酸毒性损伤的保护作用。
短句来源
     ② After cerebral ischemia and reperfusion, GM1 is use to neurodamage from Excitatory Amino Acids.
     ②早期使用GM1治疗对脑缺血再灌注损伤有明确的保护作用 ,其机制与抗兴奋性氨基酸毒性有关。
短句来源
     The therapeutic advance in amyotrophic lateral sclerosis are reviewed including anti-glutamatergic treatment, immunotherapy, gene therapy and neuroprotection.
     本文就肌萎缩侧索硬化的治疗进展,包括抗兴奋性氨基酸毒性治疗、免疫治疗、基因治疗及神经保护治疗的现状和进展作介绍。
短句来源
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  相似匹配句对
     Research and Production of Composite Amino Acid Used as Medicine
     药用复合氨基酸的研制及毒性试验
短句来源
     Toxicity of Ionic Liquids
     离子液体的毒性
短句来源
     CHEMICAL SYNTHESIS OF AMINO ACIDS
     氨基酸的化学合成
短句来源
     Effect of Amino Acids on Tobacco Alternaria alternata Phytotoxin Virulence
     氨基酸对烟草赤星病菌毒素毒性的影响
短句来源
     (SDS-PAGE analysis, HPLC analysis, amino acid composition analysis and bioidentity assay.)
     HPLC、氨基酸
短句来源
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  amino acid toxicity
However, no clinical data indicating specific amino acid toxicity in formula-fed children without errors in metabolism are known.
      


Objective:To observe the protective effect of Huanshaodan(HSD) in mouse brain in a steady ischemia-reperfusion model. Methods: Step-through experiment, receptor binding test and choline acetyl-transferase (CAT) activity detemination was performed. Results: After HSD treatment, mice made much less mistakes in step-through experiment than sham grouPS. Meanwhile the 3H-MK801 binding of cerebral cortex and hippocampus tissues was significantly decreased. CAT activity Of cerebral cortex and hippocampus tissue were...

Objective:To observe the protective effect of Huanshaodan(HSD) in mouse brain in a steady ischemia-reperfusion model. Methods: Step-through experiment, receptor binding test and choline acetyl-transferase (CAT) activity detemination was performed. Results: After HSD treatment, mice made much less mistakes in step-through experiment than sham grouPS. Meanwhile the 3H-MK801 binding of cerebral cortex and hippocampus tissues was significantly decreased. CAT activity Of cerebral cortex and hippocampus tissue were increased respectively. COnclusion: HSD might antagonize ischemia injury of brain through modulating excessive activation of glutamate N-methyl-D-Aspartic acid receptors.

目的:为探讨中药古成方“还少丹”的脑保护机制,观察了该药对脑兴奋性损伤模型的预防及治疗作用。方法:利用小鼠双侧颈总动脉结扎及反复再灌的手术造成小鼠智力下降(避暗实验次数增多)的脑损伤模型,从行为学方面观察了还少丹对脑损伤小鼠学习记忆能力的改善作用,并进一步利用受体研究方法考察了该药的脑保护机制。结果:还少丹可明显减少术后小鼠避暗实验的错误次数(模型组为2.00±0.34次/5min,单纯治疗组为0.75±0.25次/5min,P<0.01;预防加治疗组为0.38±0.18次/5min,P<0.01)。受体结合实验表明,还少丹明显抑制小鼠脑损伤后引起的大脑皮层、海马两部位N-甲基-D-天冬氨酸(即NMDA)受体的激活,与模型组比较,有明显差异(P均<0.01);同时发现用药后胆碱乙酸化转移酶(CAT)的活性明显提高(P<0.01)。结论:揭示该药具有对抗兴奋性氨基酸毒性的作用。还少丹还可明显增强脑损伤模型的皮层、海马部位的CAT活性。

Levels of excitatory and inhibitory amino acids in different brain regions and effect of acupuncture on metabolism of excitatory amino acids in the mouse of rapidly aging and dementia(SAM P/8)were observed Results indicated that synthesis and degradation of excitatory amino acids in the hippocampus,cortex and striatum in P/8 rats were at hyperfunctional state and inhibitory amino acids changed to a certain extent as compared with the normally ...

Levels of excitatory and inhibitory amino acids in different brain regions and effect of acupuncture on metabolism of excitatory amino acids in the mouse of rapidly aging and dementia(SAM P/8)were observed Results indicated that synthesis and degradation of excitatory amino acids in the hippocampus,cortex and striatum in P/8 rats were at hyperfunctional state and inhibitory amino acids changed to a certain extent as compared with the normally aging rats(SAM R/1);acupuncture could decrease obviously the abnormal increase of glutamic acid,glutamine and asparagine It is suggested that acupuncture has regulative action on metabolism of excitatory amino acids,and toxicity of excitatory amino acids play an important role in pathologic mechanisms of aging and dementia,and regulative action of acupuncture on excitatory amino acids may be one of important mechanisms treating aging and dementia

在观察快速老化痴呆模型小鼠 ( SAM-P/ 8)不同脑区 EAAS和 IAAS水平的基础上 ,重点研究了针刺对 EAAS代谢的影响。结果表明 ,与正常老化 SAM-R/ 1鼠比较 ,P/ 8海马、皮层及纹状体的 EAAS合成及降解均处于亢进状态 ,IAAS亦存在一定程度的改变。针刺可以明显降低异常升高的 Glu及 Gln、Asn水平 ,提示针刺具有调整 EAAS代谢的作用。研究表明兴奋性氨基酸毒性在老化痴呆的发病机制中起重要作用 ,针刺对 EAAS代谢的调整作用可能是其治疗老化痴呆的重要机制之一

The effects of different consistency of glial cell linederived neurotrophic factor(GDNF)on the excitatory amino acid and resumption cerebellar cortical neurons in injured cultured neonatal rat in vivo were observed.The findings were as follows:GDNF in cultures may considerably decreasd the degeneration and death of neurons with quantity-effect relationship.High density GDNF may resist the neurotoxicity of excited amino-acid and defense neurons to accelerate recovery and functioral survival.

取新生大鼠小脑皮质进行体外神经细胞培养 ,用兴奋性氨基酸建立神经元变性损害模型 ,并在培养液中加入不同浓度胶质细胞衍生性神经营养因子 (GDNF) ,观察其对兴奋性氨基酸毒性的影响及受损神经元的恢复。结果表明 :在培养液中加入 GDNF可明显减轻小脑皮质神经元变性、死亡 ,并呈正量效关系。提示 GDNF可拮抗兴奋性氨基酸神经毒性 ,对小脑皮质神经元有保护、促进其存活和功能恢复作用

 
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