| pubmed-article:11753206 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11753206 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:11753206 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:11753206 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
| pubmed-article:11753206 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:11753206 | lifeskim:mentions | umls-concept:C2697585 | lld:lifeskim |
| pubmed-article:11753206 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11753206 | pubmed:dateCreated | 2001-12-25 | lld:pubmed |
| pubmed-article:11753206 | pubmed:abstractText | Lipopolysaccharide and D-galactosamine induced lethality and apoptotic liver injury is dependent upon endogenously produced TNF-alpha. Unlike the response to high dose lipopolysaccharide alone, death in this model is a direct result of hepatocyte apoptosis. In a series of recent studies, we have demonstrated that mortality and hepatic injury following lipopolysaccharide administration in D-galactosamine-sensitized mice is dependent upon secreted 17 kDa TNF-alpha acting primarily through the p55 TNF receptor. Transgenic mice expressing null forms of TNF-alpha, the p55 receptor, or expressing only a cell-associated form of TNF-alpha exhibited no mortality and only modest liver injury when challenged with 8 mg of D-galactosamine and 100 ng of lipopolysaccharide. Although Fas ligand expression is increased in the liver, it appeared to play no significant role in outcome, since mice expressing a mutant form of Fas ligand are still sensitive to LPS- and D-galactosamine-induced lethality. Finally, we have seen significant variation in LPS- and D-galactosamine-mediated lethality among different strains of mice. The non-obese diabetic or NOD mouse is highly resistant to LPS-and D-galactosamine-induced lethality, and this appears to be secondary to a post-receptor defect in p55 TNF receptor signaling. The studies confirm an essential role for TNF-alpha and p55 TNF receptor signaling in the hepatocyte apoptosis and lethality associated with lipopolysaccharide and D-galactosamine administration. | lld:pubmed |
| pubmed-article:11753206 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11753206 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11753206 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11753206 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11753206 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11753206 | pubmed:issn | 0968-0519 | lld:pubmed |
| pubmed-article:11753206 | pubmed:author | pubmed-author:MoldawerL LLL | lld:pubmed |
| pubmed-article:11753206 | pubmed:author | pubmed-author:OberholzerAA | lld:pubmed |
| pubmed-article:11753206 | pubmed:author | pubmed-author:EdwardsC... | lld:pubmed |
| pubmed-article:11753206 | pubmed:author | pubmed-author:BahjatF RFR | lld:pubmed |
| pubmed-article:11753206 | pubmed:author | pubmed-author:OberholzerCC | lld:pubmed |
| pubmed-article:11753206 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11753206 | pubmed:volume | 7 | lld:pubmed |
| pubmed-article:11753206 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11753206 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11753206 | pubmed:pagination | 375-80 | lld:pubmed |
| pubmed-article:11753206 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:11753206 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11753206 | pubmed:articleTitle | Genetic determinants of lipopolysaccharide and D-galactosamine-mediated hepatocellular apoptosis and lethality. | lld:pubmed |
| pubmed-article:11753206 | pubmed:affiliation | Department of Surgery, University of Florida College of Medicine Gainesville, Florida 32610, USA. | lld:pubmed |
| pubmed-article:11753206 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11753206 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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