小鼠胚胎中12三体与维生素A诱导的无脑畸形及相关畸形的比较。 - Suppr

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超能文献

A comparison between trisomy 12 and vitamin A induced exencephaly and associated malformations in the mouse embryo.

作者信息

Putz B, Krause G, Garde T, Gropp A

出版信息

Virchows Arch A Pathol Anat Histol. 1980;386(1):65-80. doi: 10.1007/BF00432645.

DOI:10.1007/BF00432645

PMID:6773238

Abstract

摘要

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A comparison between trisomy 12 and vitamin A induced exencephaly and associated malformations in the mouse embryo.小鼠胚胎中12三体与维生素A诱导的无脑畸形及相关畸形的比较。

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引用本文的文献

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本文引用的文献

The teratogenic effects of hypervitaminosis A upon the face and mouth of inbred mice.维生素A过多症对近交系小鼠面部和口腔的致畸作用。

Ann N Y Acad Sci. 1960 Mar 29;85:42-55. doi: 10.1111/j.1749-6632.1960.tb49947.x.

Morphogenesis of malformation due to excessive vitamin. A. V. Embryological studies on the inner ear malformation of rats due to excessive vitamin A.过量维生素所致畸形的形态发生。A.V. 关于过量维生素A导致大鼠内耳畸形的胚胎学研究。

Osaka City Med J. 1962;11:105-19.

[Teratogenic action of hypervitaminosis A in the mouse as a function of th embryonic stage].[小鼠维生素A过多症的致畸作用与胚胎发育阶段的关系]

C R Seances Soc Biol Fil. 1960;154:1353-5.

Influence of the neural tube on the differentiation of the inner ear in the mammalian embryo.神经管对哺乳动物胚胎内耳分化的影响。

Nature. 1966 Jan 8;209(5019):219-20. doi: 10.1038/209219a0.

Exencephaly in the syndrome of trisomy no. 12 of the foetal mouse.

Nature. 1974 May 10;249(453):145-7. doi: 10.1038/249145a0.

Skullbase malformations in rat fetuses with hypervitaminosis A-induced exencephaly.维生素A过多症诱导无脑儿的大鼠胎儿的颅底畸形。

Teratology. 1973 Feb;7(1):49-55. doi: 10.1002/tera.1420070108.

Robertsonian chromosomal variation and identification of metacentric chromosomes in feral mice.野生小鼠中罗伯逊染色体变异及中着丝粒染色体的鉴定

Chromosoma. 1972;39(3):265-88. doi: 10.1007/BF00290787.

Systematic approach to the study of trisomy in the mouse. II.

Cytogenet Cell Genet. 1975;14(1):42-62. doi: 10.1159/000130318.

Autosomal monosomy and trisomy causing developmental failure.常染色体单体性和三体性导致发育衰竭。

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The pathogenesis of the Treacher Collins syndrome (mandibulofacial dysostosis).下颌面骨发育不全综合征（又称特雷彻·柯林斯综合征）的发病机制。

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