Source:http://linkedlifedata.com/resource/pubmed/id/10657008
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2000-3-27
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pubmed:abstractText |
Inflammatory mediators play a key role in acute pancreatitis and the resultant multiple organ dysfunction syndrome, which is the primary cause of death in this condition. Recent studies have confirmed the critical role played by inflammatory mediators such as TNF-alpha, IL-1beta, IL-6, IL-8, PAF, IL-10, C5a, ICAM-1, and substance P. The systemic effects of acute pancreatitis have many similarities to those of other conditions such as septicaemia, severe burns, and trauma. The delay between the onset of inflammation in the pancreas and the development of the systemic response makes acute pancreatitis an ideal experimental and clinical model with which to study the role of inflammatory mediators and to test novel therapies. Elucidation of the key mediators involved in the pathogenesis of acute pancreatitis will facilitate the development of clinically effective anti-inflammatory therapy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-3417
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 John Wiley & Sons, Ltd.
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pubmed:issnType |
Print
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pubmed:volume |
190
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
117-25
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
2000
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pubmed:articleTitle |
Inflammatory mediators in acute pancreatitis.
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pubmed:affiliation |
Department of Surgery, Royal Liverpool University Hospital, University of Liverpool, Liverpool, L69 3GA, UK.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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