| pubmed-article:15521016 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0525033 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0014597 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0009368 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0018850 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C1514526 | lld:lifeskim |
| pubmed-article:15521016 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15521016 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:15521016 | pubmed:dateCreated | 2004-11-2 | lld:pubmed |
| pubmed-article:15521016 | pubmed:abstractText | The extent and severity of mucosal injury in inflammatory bowel diseases are determined by the disequilibrium between 2 opposing processes: reparative and cytoprotective mechanisms vs. inflammation-induced injury. Probiotics may provide clinical benefit by ameliorating colitis; however, their mechanisms of action remain largely unknown. Our objective was to investigate microbial-epithelial interactions that could explain the beneficial therapeutic effects of probiotics. | lld:pubmed |
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| pubmed-article:15521016 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15521016 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:15521016 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15521016 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:15521016 | pubmed:issn | 0016-5085 | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:PetrofElaine... | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:KojimaKeishiK | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:De... | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:MuschMark WMW | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:ChangEugene... | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:RopeleskiMark... | lld:pubmed |
| pubmed-article:15521016 | pubmed:author | pubmed-author:TaoYunY | lld:pubmed |
| pubmed-article:15521016 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15521016 | pubmed:volume | 127 | lld:pubmed |
| pubmed-article:15521016 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15521016 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15521016 | pubmed:pagination | 1474-87 | lld:pubmed |
| pubmed-article:15521016 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15521016 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15521016 | pubmed:articleTitle | Probiotics inhibit nuclear factor-kappaB and induce heat shock proteins in colonic epithelial cells through proteasome inhibition. | lld:pubmed |
| pubmed-article:15521016 | pubmed:affiliation | Department of Medicine, University of Chicago, Chicago, IL 60637, USA. | lld:pubmed |
| pubmed-article:15521016 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15521016 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15521016 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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