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生殖细胞缺陷(gcd)小鼠作为卵巢早衰的模型。

Germ cell deficient (gcd) mouse as a model of premature ovarian failure.

作者信息

Duncan M, Cummings L, Chada K

机构信息

Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, Piscataway 08854.

出版信息

Biol Reprod. 1993 Aug;49(2):221-7. doi: 10.1095/biolreprod49.2.221.

Abstract

Premature ovarian failure (POF) in women is characterized as menopause commencing before age 35. Although some cases of POF appear to be inherited, no experimental animal models of familial POF are available. Recently a mouse mutation has been identified that results in infertility due to a lack of primordial germ cells arising in early embryonic development. It was observed that shortly after puberty, females homozygous for this mutation entered reproductive senescence as defined by high levels of circulating gonadotropins, inability to respond either hormonally or functionally to superovulation, and a disrupted estrous cycle. Also, the ovaries completely lacked developing follicles and the endometrium was inactive. However, these mice had undergone complete sexual development as determined by age of vaginal opening, mammary gland histology, and sexual behavior. Thus, these animals closely mimic familial premature ovarian failure and may be useful models for study of the pathogenesis and treatment of this condition.

摘要

女性的卵巢早衰(POF)的特征是在35岁之前开始出现绝经。尽管某些POF病例似乎是遗传性的,但目前尚无家族性POF的实验动物模型。最近发现了一种小鼠突变,该突变由于早期胚胎发育中缺乏原始生殖细胞而导致不育。据观察,青春期后不久,该突变的纯合雌性小鼠进入生殖衰老状态,其特征为循环促性腺激素水平升高、对超排卵无激素或功能反应以及发情周期紊乱。此外,卵巢完全缺乏发育中的卵泡,子宫内膜无活性。然而,根据阴道口开放年龄、乳腺组织学和性行为确定,这些小鼠已经历了完全的性发育。因此,这些动物紧密模拟家族性卵巢早衰,可能是研究这种疾病发病机制和治疗方法的有用模型。

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