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The classification and development of cadmium-induced limb defects in mice.

作者信息

Messerle K, Webster W S

出版信息

Teratology. 1982 Feb;25(1):61-70. doi: 10.1002/tera.1420250109.

DOI:10.1002/tera.1420250109
PMID:7064112
Abstract
摘要

相似文献

1
The classification and development of cadmium-induced limb defects in mice.镉诱导小鼠肢体缺陷的分类与发展
Teratology. 1982 Feb;25(1):61-70. doi: 10.1002/tera.1420250109.
2
Cadmium induced limb defects in mice: strain associated differences in sensitivity.镉诱导小鼠肢体缺陷：品系间敏感性差异
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3
Histological changes induced in developing limb buds of C57BL mouse embryos submitted in utero to the combined influence of acetazolamide and cadmium sulphate.
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4
Proteomic analysis to characterize differential mouse strain sensitivity to cadmium-induced forelimb teratogenesis.蛋白质组学分析以表征不同小鼠品系对镉诱导的前肢致畸作用的敏感性差异。
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5
Potentiation of acetazolamide induced ectrodactyly in SWV and C57BL/6J mice by cadmium sulfate.硫酸镉对SWV和C57BL/6J小鼠乙酰唑胺诱导的缺指（趾）畸形的增强作用。
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6
Exacerbation of limb malformations in legless (lgl) homozygotes by retinoic acid (RA).
Prog Clin Biol Res. 1993;383B:735-8.
7
Protection against cadmium-induced limb malformations by pretreatment with cadmium or mercury.通过镉或汞预处理预防镉诱导的肢体畸形。
Teratology. 1980 Jun;21(3):357-60. doi: 10.1002/tera.1420210312.
8
Differential effects of 4-hydroperoxycyclophosphamide on limb development in vitro.4-氢过氧环磷酰胺对体外肢体发育的不同影响。
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Differential sensitivity of the SWV and C57BL/6 mouse strains to the teratogenic action of single administrations of cadmium given throughout the period of anterior neuropore closure.SWV和C57BL/6小鼠品系在前神经孔关闭期间单次给予镉的致畸作用的差异敏感性。
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10
Genetic and pathologic aspects of retinoic acid-induced limb malformations in the mouse.视黄酸诱导的小鼠肢体畸形的遗传和病理方面
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Gestational Cd Exposure in the CD-1 Mouse Induces Sex-Specific Hepatic Insulin Insensitivity, Obesity, and Metabolic Syndrome in Adult Female Offspring.妊娠镉暴露致 CD-1 小鼠成年雌性子代肝胰岛素敏感性降低、肥胖和代谢综合征，且具有性别特异性。
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Delayed vasculogenesis and impaired angiogenesis due to altered Ang-2 and VE-cadherin levels in the chick embryo model following exposure to cadmium.在镉暴露后的鸡胚模型中，由于血管生成素-2（Ang-2）和血管内皮钙黏蛋白（VE-cadherin）水平改变导致血管生成延迟和血管生成受损。
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Altered PITX2 and LEF1 gene expression in the cadmium-induced omphalocele in the chick model.鸡模型中镉诱导的脐膨出中PITX2和LEF1基因表达的改变
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Pre-treatment with N-acetylcysteine upregulates superoxide dismutase 2 and catalase genes in cadmium-induced oxidative stress in the chick omphalocele model.在鸡卵黄囊疝模型中，N-乙酰半胱氨酸预处理可上调镉诱导的氧化应激中的超氧化物歧化酶2和过氧化氢酶基因。
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HoxB2, HoxB4 and Alx4 genes are downregulated in the cadmium-induced omphalocele in the chick model.在鸡模型中，镉诱导的脐膨出中HoxB2、HoxB4和Alx4基因表达下调。
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Disruption of calreticulin-mediated cellular adhesion signaling in the cadmium-induced omphalocele in the chick model.在鸡模型中，镉诱导的脐膨出中钙网蛋白介导的细胞黏附信号的破坏。
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Cadmium induces retinoic acid signaling by regulating retinoic acid metabolic gene expression.镉通过调节视黄酸代谢基因表达来诱导视黄酸信号传导。
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Downregulation of ROCK-I and ROCK-II gene expression in the cadmium-induced ventral body wall defect chick model.镉诱导的鸡胚腹侧体壁缺损模型中ROCK-I和ROCK-II基因表达的下调
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Interactive effects of cadmium and retinoic acid on mouse limb bud development in vitro.镉与视黄酸对体外培养小鼠肢芽发育的交互作用。
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