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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0018809,
umls-concept:C0031671,
umls-concept:C0185117,
umls-concept:C0332161,
umls-concept:C0332453,
umls-concept:C0376618,
umls-concept:C0542341,
umls-concept:C0599946,
umls-concept:C1456820,
umls-concept:C1522564,
umls-concept:C1710082,
umls-concept:C2911684
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pubmed:issue |
1
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pubmed:dateCreated |
2008-3-17
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pubmed:abstractText |
Lipopolysaccharide (LPS) induces tumor necrosis factor-alpha (TNF-alpha) expression in cardiomyocytes, which contributes to myocardial dysfunction during sepsis. The purpose of this study was to investigate the role of phosphatidylinositol (PI) phospholipase Cgamma1 (PLCgamma1) in cardiac TNF-alpha expression, and myocardial dysfunction during endotoxemia.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/1-(6-((3-methoxyestra-1,3,5(10)-trie...,
http://linkedlifedata.com/resource/pubmed/chemical/Diglycerides,
http://linkedlifedata.com/resource/pubmed/chemical/Estrenes,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphodiesterase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipase C gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Plcg1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidinones,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0008-6363
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
90-7
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pubmed:meshHeading |
pubmed-meshheading:18079103-Animals,
pubmed-meshheading:18079103-Animals, Newborn,
pubmed-meshheading:18079103-Cardiomyopathies,
pubmed-meshheading:18079103-Cells, Cultured,
pubmed-meshheading:18079103-Diglycerides,
pubmed-meshheading:18079103-Disease Models, Animal,
pubmed-meshheading:18079103-Endotoxemia,
pubmed-meshheading:18079103-Estrenes,
pubmed-meshheading:18079103-Inositol 1,4,5-Trisphosphate,
pubmed-meshheading:18079103-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:18079103-Lipopolysaccharides,
pubmed-meshheading:18079103-Mice,
pubmed-meshheading:18079103-Mice, Inbred C57BL,
pubmed-meshheading:18079103-Mice, Knockout,
pubmed-meshheading:18079103-Myocardial Contraction,
pubmed-meshheading:18079103-Myocytes, Cardiac,
pubmed-meshheading:18079103-Phosphodiesterase Inhibitors,
pubmed-meshheading:18079103-Phospholipase C gamma,
pubmed-meshheading:18079103-Phosphorylation,
pubmed-meshheading:18079103-Pyrrolidinones,
pubmed-meshheading:18079103-RNA Interference,
pubmed-meshheading:18079103-Signal Transduction,
pubmed-meshheading:18079103-Transfection,
pubmed-meshheading:18079103-Tumor Necrosis Factor-alpha
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pubmed:year |
2008
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pubmed:articleTitle |
Disruption of phospholipase Cgamma1 signalling attenuates cardiac tumor necrosis factor-alpha expression and improves myocardial function during endotoxemia.
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pubmed:affiliation |
Center for Critical Illness Research, Lawson Health Research Institute, VRL 6th Floor, 800 Commissioners Road, London, Ontario, Canada N6A 4G5. tpeng2@uwo.ca
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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