| pubmed-article:12427787 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0682610 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0670896 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0243127 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:12427787 | lifeskim:mentions | umls-concept:C0443331 | lld:lifeskim |
| pubmed-article:12427787 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:12427787 | pubmed:dateCreated | 2002-11-12 | lld:pubmed |
| pubmed-article:12427787 | pubmed:abstractText | Circulating levels of endotoxin (or lipopolysaccharide (LPS)) and anti-endotoxin antibodies are increased in patients with inflammatory bowel disease, supporting the hypothesis of a role for endogenous bacterial products in the pathogenesis of these disorders. | lld:pubmed |
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| pubmed-article:12427787 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12427787 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12427787 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:12427787 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12427787 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:12427787 | pubmed:issn | 0017-5749 | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:LevyEE | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:BeaulieuJ FJF | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:Cerf-Bensussa... | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:LentzeM JMJ | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:SeidmanE GEG | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:DionneSS | lld:pubmed |
| pubmed-article:12427787 | pubmed:author | pubmed-author:RuemmeleF MFM | lld:pubmed |
| pubmed-article:12427787 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12427787 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:12427787 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12427787 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12427787 | pubmed:pagination | 842-8 | lld:pubmed |
| pubmed-article:12427787 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12427787 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12427787 | pubmed:articleTitle | Lipopolysaccharide modulation of normal enterocyte turnover by toll-like receptors is mediated by endogenously produced tumour necrosis factor alpha. | lld:pubmed |
