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the erythrogenin theory states that the kidney, in response to hypoxia , produces a substance that enzymatically converts a circulating a-globulin to active Ep.The renal erythropoietic factor is called erythrogenin and the plasma substrate , which is thought to be of hepatic origin ,is called erythropoietinogen.such a factor has been extracted from the light mitochondrial fraction of kidneys and is capable of generating Ep when incubated with palsma from normal animals . this factor has litte direct effect on erythropoiesis in plethoric mice , this work has been reproduced in some laboratories , but not in others. According to the proerythropoietin theory , the kidneys produce an inactive molecule which contains intact Ep.Evidence for this consists of the following :Incubation of a light mitochondrial fraction from hypoxic rat kidneys with serum from normal rabbits results in active Ep which is immunologically rat in origin .Antibody to Ep labeled with fluorescein binds to renal glomeruli, which indicates the presence of Ep in the kidneys. The inhibitor theory suggests that complete Ep is produced by the kidney, but it may be inactivated by a lipid-soluble inhibitor during the extraction process. Contact with normal serum neutralizes the inhibitor and allows extraction of biologically active Ep.Further support for this ,and also the pro-Ep theory, comes from the observation that when hourly Ep production in an intact hypoxic medium almost completely free of serum, production of Ep continued , which indicates that the kidneys were capable of producing the hormone without need for much serum protein. A consensus does not yet exist on how Ep is made by the kidney .Much more work is necessary to determine which of the above hypotheses might be correct. however, it seems clear that the kidney is the principal site regulating production of the hormone .

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wjmsicuan(金币+20, 翻译EPI+1): 翻译的有些生硬,希望继续努力!!!谢谢 2011-03-05 10:52:11
erythrogenin理论认为肾对缺氧的反应产生一种物质,转换酶循环的A -球蛋白到Ep。肾脏红细胞生成因子称为erythrogenin和血浆基质,这被认为是肝源性的,被称为erythropoietinogen。有一种从肾脏轻线粒体的一小部分提取的因子,与正常动物孵化是能产生内啡肽。这一因子对多血症小鼠杂乱红细胞有直接的影响,这项工作已在一些实验室被重复,但有些则没有。据proerythropoietin理论,肾脏产生一个无效的分子包含完整Ep。证据由以下内容组成:一轻缺氧大鼠肾脏线粒体片段与正常兔血清培养,结果在免疫鼠原位产生活化Ep。抗体荧光标记Ep与肾小球结合,这表明了EP在肾脏的存在。该抑制剂理论认为,完整的Ep是由肾脏产生,但它可能是在提取过程中由脂溶性抑制剂灭活。与正常血清接触能中和抑制剂,并允许提取有生物活性的Ep。进一步支持,也是亲Ep的理论,从观察来,在完全缺氧情况下每小时内啡肽的生产几乎完全不需血清,而内啡肽继续产生,这表明肾脏不需要许多血清蛋白就能生产很多激素。Ep如何由肾脏产生还没有达成共识。确定上述假设哪些可能是正确的还有许多工作要做。但是,有一点看似很清楚,肾脏是产生调节性激素的主要位点。
2楼2011-03-04 08:04:19
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wjmsicuan(金币+50): 相比前面,要好些,希望继续努力!!谢谢 2011-03-05 10:54:36
红细胞生成素理论认为,肾对缺氧产生应激时,在酶的作用下将循环中的α-球蛋白转换为Ep。肾脏红细胞生成因子称为红细胞生成素,被认为是肝源性的血浆基质被称为促红细胞生成素原。这样一种因子已经从肾脏线粒体轻质部分提取,与正常动物血浆一起孵育是能产生Ep。这一因子对多血症小鼠红细胞生成没有直接的影响,这项工作已在一些实验室被再现,但在其它实验室则无法重复。据促红细胞生成素理论,肾脏产生一个无活性的分子包含完整的Ep。证据由以下内容组成:缺氧大鼠肾脏线粒体轻质部分与正常兔血清培养,结果产生有活性的免疫鼠原性Ep。荧光标记的Ep抗体与肾小球结合,这表明了EP在肾脏的存在。抑制剂理论认为,完整的Ep是由肾脏产生,但它可能是被脂溶性抑制剂在提取过程中灭活。与正常血清接触能中和抑制剂,从而有可能提取到有生物活性的Ep。进一步支持,也来源于促红细胞生成素理论,曾经观察到,在几乎没有血清、完全缺氧情况下,以小时计的Ep生成不仅发生,而且能继续产生,这表明肾脏不需要许多血清蛋白就能生成激素。Ep如何由肾脏生成尚无共识达成。确定上述假设哪些可能正确,还有许多工作必须要做。但有一点似乎是清楚的,那就是:肾脏是调节激素生成的主要位点。
3楼2011-03-04 09:10:15
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