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发布者:鑫达医学翻译 发布时间:2013-02-27 8:50:52 阅读:

原文:
Keeping in mind that most mitochondrial proteins are encoded by the nuclear genome, mitochondria contain many copies of their own mitochondrial Dna (mtDna). human mtDna is a 16,569 bp circular molecule containing 37 mitochondrial genes that encode 13 polypeptide mrc components, in addition to two ribosomal rnas (rrnas) and 22 transfer rnas (trnas) that support protein synthesis within the mitochondrion using its own genetic code. Because mtDna is only inherited maternally, many mtDna single nucleotide polymorphisms (snPs) have accumulated in sequence along maternal lineages. In fact, a number of stable snPs in mtDna coding regions have been used to define related groups of mtDna haplogroups. Interestingly, 95% of the european population fall into one of nine mtDna haplo groups: h, i, J, K, t, u, v, w and X. 
The accumulation of mtDna deletions and point mutations correlates with a decline in mitochondrial function, which is thought to contribute to pathologies such as alzheimer disease and Parkinson disease, and aging.40 Point mutations at specific sites in the mtDna control region accumulate at high levels in certain tissues; for example, mutations occur at high frequency at t414G in cultured fibroblasts, a189G and t408a in muscle, and c150t in white blood cells.  mutations at c150t in the mtDna of chondrocytes have also been described (F. J. Blanco, unpublished data). somatic mtDna mutations induced by mutagens such as ros or no also contribute to the decline in mitochondrial acti vity that occurs in oa chondrocytes. indeed, results from a 2009 study indicate that there is decreased mtDna integrity and higher accumulation of mtDna damage in chondrocytes from oa patients compared to those from normal individuals. A reduced capacity of oa chondrocytes to repair mtDna damage is reportedly associated with apoptosis. in a study examining the accumulation of the mtDna4977 deletion (which is associated with aging) in knee cartilage, its frequency was found to increase in aging cartilage, so this mutation may have a role in the development of oa.
 

译文:
多数线粒体蛋白为核基因组编码,线粒体自身含有多个拷贝的线粒体DNA(mtDNA)。人mtDNA为环状,碱基数量为16569bp,含37个线粒体基因可编码13种参与线粒体呼吸链的成分,2种核糖体RNA,以及22种tRNA(参与线粒体内部蛋白合成)。鉴于线粒体为母系遗传,因此多种mtDNA单核苷酸多样性(SNP)也随母系积累。大量稳定的mtDNA单核苷酸多样性(SNP)编码区已被用以判定相关的mtDNA单倍型类群。目前共识别出9种单倍型类型(H, I, J, K, T, U, V, W及X),95%的欧洲群体属于同一类mtDNA单倍型类群。 
mtDNA缺失与点突变累积至一定程度时,可引发线粒体功能降低,将有可能导致病变,如老年性痴呆、帕金森及衰老等。40特定组织内mtDNA调控区特定点突变出现较高水平的累积,如培养的成纤维细胞出现高频率的T414G突变,肌肉细胞内存在大量A189G及T408A突变,白细胞内存在大量C150T突变。既往已经报道软骨细胞mtDNA存在C150T突变(F. J. Blanco未发表数据)。诱变剂(如活性氧或一氧化氮)诱导的体细胞mtDNA突变也可导致软骨细胞内线粒体活性降低。2009年开展的一项研究表明,与常人相比,骨关节炎患者软骨细胞内mtDNA存在大量损伤,且mtDNA结构完整性降低。骨关节炎患者软骨细胞线粒体损伤修复活性降低与细胞凋亡相关。一项旨在测定膝关节软骨mtDNA4977缺失(与衰老相关)的研究表明,老化软骨内缺失频率升高,因此推断该种突变可能在诱发骨关节炎过程中有一定作用。


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