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甲状腺素注射不会导致sg/sg小鼠过早诱导胸苷激酶。

Thyroxine injections do not cause premature induction of thymidine kinase in sg/sg mice.

作者信息

Messer A

机构信息

Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201.

出版信息

J Neurochem. 1988 Sep;51(3):888-91. doi: 10.1111/j.1471-4159.1988.tb01825.x.

Abstract

Severe hyperthyroidism from the time of birth causes a premature induction and termination of thymidine kinase activity in the cerebella of wild-type mice. This leads to elevated enzyme levels at postnatal days 5 and 6, with significantly lower levels by postnatal day 7 (which is actually the time of peak activity in normal animals). In this study, neonatal hyperthyroidism does not have significant effects on postnatal day 5, 6, or 7 enzyme levels in the neurological mutant staggerer. This is consistent with the hypothesis that thyroid hormone exerts its effects via the Purkinje cells, which are reduced in number and grossly stunted in the mutant.

摘要

从出生起就患有严重甲状腺功能亢进症会导致野生型小鼠小脑内胸苷激酶活性过早诱导和终止。这会导致出生后第5天和第6天酶水平升高,而到出生后第7天(实际上是正常动物活性峰值时间)水平则显著降低。在本研究中,新生儿甲状腺功能亢进症对神经学突变体蹒跚小鼠出生后第5天、第6天或第7天的酶水平没有显著影响。这与甲状腺激素通过浦肯野细胞发挥作用的假设一致,在突变体中浦肯野细胞数量减少且严重发育不良。

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