rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
5
|
pubmed:dateCreated |
2009-4-6
|
pubmed:abstractText |
Maternal diabetes during pregnancy increases the risk of congenital malformations such as neural tube defects (NTDs). Although the mechanism of this effect is uncertain, it is known that levels of nitric oxide synthase (NOS) and nitric oxide are elevated in embryos of a mouse model of diabetes. We postulated that overproduction of nitric oxide causes diabetes-induced congenital malformations and that inhibition of inducible NOS (iNOS) might prevent diabetic embryopathy.
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
1432-0428
|
pubmed:author |
pubmed-author:HayasakaSS,
pubmed-author:HayashiYY,
pubmed-author:KaneCC,
pubmed-author:MuraseTT,
pubmed-author:MurataYY,
pubmed-author:OisoYY,
pubmed-author:OyamaKK,
pubmed-author:SatoNN,
pubmed-author:SugimuraYY,
pubmed-author:TakagishiYY,
pubmed-author:UchidaAA
|
pubmed:issnType |
Electronic
|
pubmed:volume |
52
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
962-71
|
pubmed:meshHeading |
pubmed-meshheading:19283362-Amidines,
pubmed-meshheading:19283362-Animals,
pubmed-meshheading:19283362-Body Weight,
pubmed-meshheading:19283362-Crosses, Genetic,
pubmed-meshheading:19283362-Diabetes Mellitus, Experimental,
pubmed-meshheading:19283362-Disease Models, Animal,
pubmed-meshheading:19283362-Female,
pubmed-meshheading:19283362-Fetal Resorption,
pubmed-meshheading:19283362-Fetus,
pubmed-meshheading:19283362-Heterocyclic Compounds, 2-Ring,
pubmed-meshheading:19283362-Litter Size,
pubmed-meshheading:19283362-Mice,
pubmed-meshheading:19283362-Mice, Inbred ICR,
pubmed-meshheading:19283362-Mice, Knockout,
pubmed-meshheading:19283362-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:19283362-Neural Tube Defects,
pubmed-meshheading:19283362-Nitric Oxide Synthase Type II,
pubmed-meshheading:19283362-Pregnancy
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pubmed:year |
2009
|
pubmed:articleTitle |
Prevention of neural tube defects by loss of function of inducible nitric oxide synthase in fetuses of a mouse model of streptozotocin-induced diabetes.
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pubmed:affiliation |
Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Chikusa-ku, Nagoya, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|