Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity. - Wikidata - awgldk - TriplyDB

Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity.

Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity.

http://www.wikidata.org/entity/Q43587199

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Modeling anterior development in mice: diet as modulator of risk for neural tube defects Maternal diabetes alters transcriptional programs in the developing embryo.Maternal dietary glycemic intake and the risk of neural tube defects Gene-environment interactions, folate metabolism and the embryonic nervous system.Protein kinase Cβ2 inhibition reduces hyperglycemia-induced neural tube defects through suppression of a caspase 8-triggered apoptotic pathway.Diabetic embryopathy: a role for the epigenome?Decoding the oxidative stress hypothesis in diabetic embryopathy through proapoptotic kinase signaling.The essential role of protein kinase Cδ in diabetes-induced neural tube defects Diabetic embryopathy: studies using a rat embryo culture system and an animal model.Advances in understanding the molecular causes of diabetes-induced birth defects.Experimental mechanisms of diabetic embryopathy and strategies for developing therapeutic interventions.New concepts in diabetic embryopathy The status of diabetic embryopathy.Acephalous lamb from an in vitro-produced sheep embryo.Alterations in methylation and expression levels of imprinted genes H19 and Igf2 in the fetuses of diabetic mice Responses of the embryonic epigenome to maternal diabetes Diabetic uterus environment may play a key role in alterations of DNA methylation of several imprinted genes at mid-gestation in mice.The "Other" Inositols and Their Phosphates: Synthesis, Biology, and Medicine (with Recent Advances in myo-Inositol Chemistry).Management of Type 2 diabetes and pregnancy.Genetic basis of susceptibility to teratogen induced birth defects.Intrauterine growth retardation in experimental diabetes: possible role of the placenta.Cardiac malformations are associated with altered expression of vascular endothelial growth factor and endothelial nitric oxide synthase genes in embryos of diabetic mice.Nitroxide radicals protect cultured rat embryos and yolk sacs from diabetic-induced damage.

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P2860

Induction of embryonic dysmorphogenesis by high glucose concentration, disturbed inositol metabolism, and inhibited protein kinase C activity.

http://www.wikidata.org/entity/Q43587199

description

2001 nî lūn-bûn

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2001年の論文

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2001年学术文章

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2001年学术文章

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2001年学术文章

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2001年学术文章

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2001年学术文章

@zh-my

2001年学术文章

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2001年學術文章

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2001年學術文章

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name

Induction of embryonic dysmorp ...... ted protein kinase C activity.

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Induction of embryonic dysmorp ...... ted protein kinase C activity.

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type

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Induction of embryonic dysmorp ...... ted protein kinase C activity.

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Induction of embryonic dysmorp ...... ted protein kinase C activity.

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Induction of embryonic dysmorp ...... ted protein kinase C activity.

@en

Induction of embryonic dysmorp ...... ted protein kinase C activity.

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Birth Defects Research Part A: Clinical and Molecular Teratology

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Induction of embryonic dysmorp ...... ted protein kinase C activity.

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P2093

C R Wentzel

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M B Gäreskog

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P Wentzel

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U J Eriksson

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P2860

Pathogenesis of diabetes-induced congenital malformations.

Outcomes of pregnancy in insulin dependent diabetic women: results of a five year population cohort study.

Hyperglycemia-induced teratogenesis is mediated by a functional deficiency of arachidonic acid.

Whole-embryo culture and the study of mammalian embryos during organogenesis.

PGE2 prevents anomalies induced by hyperglycemia or diabetic serum in mouse embryos.

Effects of hyperglycaemia on sorbitol and myo-inositol contents of cultured embryos: treatment with aldose reductase inhibitor and myo-inositol supplementation.

Patterns of congenital anomalies and relationship to initial maternal fasting glucose levels in pregnancies complicated by type 2 and gestational diabetes.

Beta-hydroxybutyrate increases reactive oxygen species in late but not in early postimplantation embryonic cells in vitro.

Induction of endothelin-1 expression by glucose: an effect of protein kinase C activation.

Insulin regulated PKC isoform mRNA in rat adipocytes.

P304

193-201

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scholarly article

P356

10.1002/TERA.1034

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5

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63

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2001-05-01T00:00:00Z

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11320530

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