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首页> 外文期刊>Human Reproduction >INVITED SESSION, SESSION 01: KEYNOTE LECTURES, Monday 4 July 2011 08:30 - 09:30
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INVITED SESSION, SESSION 01: KEYNOTE LECTURES, Monday 4 July 2011 08:30 - 09:30

机译:会议,会议01:主题演讲,2011年7月4日,星期一08:30-09:30

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With the advent of the human genome project in the 1990s, DNA markers became available, allowing us to determine the parent and meiotic stage of origin of human aneuploid conditions. This approach has been extensively used to study the origin of trisomies, with one over-arching conclusion: the vast majority of clinically recognized trisomies derive from errors in the development of the egg and, in particular, from nondisjunction occurring in the first maternal meiotic division (MI). However, against this general background, it has also become apparent that there is considerable chromosome-to-chromosome variation, indicating that individual chromosomes behave differently with respect to mechanisms of meiotic nondisjunction.
机译:随着1990年代人类基因组计划的到来,DNA标记变得可用,使我们能够确定人类非整倍体状况的起源和减数分裂阶段。这种方法已被广泛用于研究三体性的起源,并得出一个总体结论:绝大多数临床上公认的三体性来源于卵子发育的错误,尤其是源于第一次母系减数分裂中的非分离现象。 (MI)。但是,在这种总体背景下,也已经很明显,染色体之间存在相当大的变异,表明各个染色体在减数分裂非分离机制方面的行为有所不同。

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