pubmed-article:20454450 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C1335874 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0156147 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0814120 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0205214 | lld:lifeskim |
pubmed-article:20454450 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:20454450 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:20454450 | pubmed:dateCreated | 2010-5-10 | lld:pubmed |
pubmed-article:20454450 | pubmed:abstractText | Recent studies demonstrated an association of STAT4 variants with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), indicating that multiple autoimmune diseases share common susceptibility genes. We therefore investigated the influence of STAT4 variants on the susceptibility and phenotype of inflammatory bowel diseases (IBD) in a large patient and control cohort. | lld:pubmed |
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pubmed-article:20454450 | pubmed:language | eng | lld:pubmed |
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pubmed-article:20454450 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20454450 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20454450 | pubmed:issn | 1932-6203 | lld:pubmed |
pubmed-article:20454450 | pubmed:author | pubmed-author:BrandStephanS | lld:pubmed |
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pubmed-article:20454450 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20454450 | pubmed:volume | 5 | lld:pubmed |
pubmed-article:20454450 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20454450 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20454450 | pubmed:pagination | e10373 | lld:pubmed |
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