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药物机制
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  drug mechanism
     Objective To discuss the drug mechanism in improving absorption of rales of children pneumonia treated with 654-2 and mannitol.
     目的 探讨 6 5 4- 2与甘露醇促使小儿肺炎口罗音吸收的药物机制
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  “药物机制”译为未确定词的双语例句
     Mechanism of plasmid-mediated quinolone resistance of Klebsiella
     质粒介导的克雷伯菌耐喹诺酮类药物机制研究
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     Objective To discuss the clinical application effect and its mechanism of rabeprazole.
     目的 探讨雷贝拉唑的临床应用效果及药物机制
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     Study on Medicinal Mechanism of Anti-Fibrosis
     抗肝纤维化药物机制研究
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     Study on the Antimicrobial Resistance in Shigella spp.and Its Mechanism of Quinolones Resistance
     志贺菌属细菌耐药性及其耐喹诺酮类药物机制的研究
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     Application Study of Non-drug Mechanism Primary Initiative on Reducing the Post-Operative Aches
     非药物机制原发主动消减术后疼痛应用研究
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     P and mechanism of increased INa.
     P 的机制
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     An overview on mechanisms of antiobese medicines
     药物减肥机制研究概述
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     Search for the Antimalarial Mechanism of Artemisinin
     青蒿素类药物作用机制的探讨
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     Developing Mechanism
     发展机制
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     Drug Addiction
     药物成瘾性
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  drug mechanism
This is of relevance to drug mechanism studies, as ceramide is a known messenger of apoptosis.
      
We find that depending on the model and on the drug mechanism function, Tmax may increase, decrease, decrease and then increase, or stay the same, as the drug dose is increased.
      
This type of question test several concepts emphasized in class from drug mechanism to understanding an ECG.
      


Calmodulin is a low-molecular weight, high affinity calcium-binding protein which mediates many of the intercellular effects of calcium in eukaryotic cells. Calmodulin has been shown to activate or modulate intercellularly a large series of protein in a calcium-dependent manner, including the Ca2++ Mg2+-ATPase. Many drugs from the therapeutic classes mentioned inhibit calmodulin-actiated functions. The studies of calmodulin are of importance to Physiology, Biochemistry, and Pharmacology.In this Paper, We present...

Calmodulin is a low-molecular weight, high affinity calcium-binding protein which mediates many of the intercellular effects of calcium in eukaryotic cells. Calmodulin has been shown to activate or modulate intercellularly a large series of protein in a calcium-dependent manner, including the Ca2++ Mg2+-ATPase. Many drugs from the therapeutic classes mentioned inhibit calmodulin-actiated functions. The studies of calmodulin are of importance to Physiology, Biochemistry, and Pharmacology.In this Paper, We present a method to prepare enhancement of Ca2+ + Mg2+-ATP are activity on erythrocyte membrane by high(39000×g) or low (1800×g) speed centrifugation with homolysis in isosmotic imidazole buffer.

本文介绍用等渗咪唑缓冲液溶血,并用低温高速或常速离心机制备出一种带钙调节蛋白(简称CaM)的红细胞膜。它具有与膜稳定结合的CaM,在钙离子存在下可以激活膜上的靶酶——Ca~(2+)+Mg~(2+)-ATP酶活性,为研究CaM功能及有关药物机制提供一种简便而理想的材料。

The model system with human fetsl hepatocytes injured by CCl4 fof observation of the protective effect of drugs against hepatitis was established and its application was reported in this article.The fetal hepatocytes were obtained from the human fetus aged between 5 and 7 monthes by enzyme digestion with 1% collagenase type I.The hepatocytes in primary culture pretreated with medicines for treatment of hepatitis for 16 hours and then exposed to CCl4 for 4hours were investigated under scanning electron microscope...

The model system with human fetsl hepatocytes injured by CCl4 fof observation of the protective effect of drugs against hepatitis was established and its application was reported in this article.The fetal hepatocytes were obtained from the human fetus aged between 5 and 7 monthes by enzyme digestion with 1% collagenase type I.The hepatocytes in primary culture pretreated with medicines for treatment of hepatitis for 16 hours and then exposed to CCl4 for 4hours were investigated under scanning electron microscope and transmission electron microscope.The results showed that the effect of the medicines on human fetal hepatocytes could be well observed with this model system and the mechanisms could be further studied by changes of structure of hepatocytes and transaminase and SOD in the culture medium.The results are also confirmed by applying two medicines with the model.It is suggested that this model can be used for sieving the substances Protecting hepatocytes. The prospects of further application were also discussed.

通过人胎肝细胞体外培养,建立四氰化碳(CCl4)中毒模型。在扫描电镜及透射电镜下观察药物对肝细胞的保护作用及药物对肝细胞的毒性作用。通过对甘草甜素和水飞蓟宾的研究,证明了该方法简单、结果稳定可靠。它不仅有助于保肝药物的机制研究,还能对多种药物保肝作用作对比研究。

AIM To establish a stable cellular model and obtain a relatively homogenous cell population for our studies of ischemia through a simple and effective episode. METHOD To investigate the molecular mechanism of neuronal ischemia, PC12 and NG108 15 cell lines were now popular in neuroscience research use. RESULT After 20 min exposed in a glucose free and hypoxia medium executed by Na 2S 2O 4(1,2,4 or 8 mmol·L -1 ), the MK801 binding or PC and NG cells was significantly higher than that in the control...

AIM To establish a stable cellular model and obtain a relatively homogenous cell population for our studies of ischemia through a simple and effective episode. METHOD To investigate the molecular mechanism of neuronal ischemia, PC12 and NG108 15 cell lines were now popular in neuroscience research use. RESULT After 20 min exposed in a glucose free and hypoxia medium executed by Na 2S 2O 4(1,2,4 or 8 mmol·L -1 ), the MK801 binding or PC and NG cells was significantly higher than that in the control groups, while the binding activities of m , n cholinergic receptors in the same cells decreased as compared to the control. Morphologic changes also showed cells dysfunction. Futhermore, pretreatment of APV markedly lowered the NMDA receptor activities in the ischemic cells and the cells seemed better survival. CONCLUSION Ischemic model using Na 2S 2O 4 and glucose free medium may well build up the excessive activation of glutamate NMDA receptors and cholinergic dysfunction in cells.

目的利用稳定的细胞模型进行药物机制研究,对探讨药物等对缺血的影响十分重要。方法结合形态学和受体功能研究方法,利用连二亚硫酸钠消除培养基中的氧合并培养基质缺糖导致拟缺血细胞,并对其细胞功能和缺血机制进行了探讨。结果这种拟缺血模型造成了体外培养细胞上类似与体内细胞缺血的变化,细胞肿胀变性甚至坏死,细胞膜上兴奋性氨基酸(EAA)的N甲基D天冬氨酸(NMDA)受体活性增强,伴随其他功能性受体如胆碱能(M、N)受体活性降低。经NMDA受体特异性拮抗剂———2氨基膦酸基戊酸(APV)作用后,NMDA受体激活明显被抑制,细胞所受缺血损伤也有减轻。同时将NG细胞与PC细胞的胆碱能受体活性变化进行了比较,发现NG活性变化与连二亚硫酸钠剂量变化关系更为稳定。结论提示利用连二亚硫酸钠可模拟体内缺血机制,其主要机制与NMDA受体激活有关

 
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