pubmed-article:19590623 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C0012655 | lld:lifeskim |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C0001339 | lld:lifeskim |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C0017431 | lld:lifeskim |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C0521117 | lld:lifeskim |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
pubmed-article:19590623 | lifeskim:mentions | umls-concept:C1333402 | lld:lifeskim |
pubmed-article:19590623 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:19590623 | pubmed:dateCreated | 2009-7-10 | lld:pubmed |
pubmed-article:19590623 | pubmed:abstractText | The renin-angiotensin system (RAS) has been implied in the pathogenesis of various diseases including acute and chronic pancreatitis. Angiotensin-converting enzyme (ACE) is the key enzyme in activating the RAS. Deletion (D)-type polymorphism in the 16th intron of the ACE gene has been associated with higher serum levels of the enzyme. Inhibition of ACE was found to ameliorate acute pancreatitis in animal models suggesting that ACE plays a role in pathogenesis and progression of acute pancreatitis. Objectives were to investigate the occurrence of the ACE insertion/deletion (I/D) polymorphism in acute pancreatitis patients and its association with the severity of the disease. | lld:pubmed |
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pubmed-article:19590623 | pubmed:language | eng | lld:pubmed |
pubmed-article:19590623 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19590623 | pubmed:status | PubMed-not-MEDLINE | lld:pubmed |
pubmed-article:19590623 | pubmed:month | Feb | lld:pubmed |
pubmed-article:19590623 | pubmed:issn | 1365-182X | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:WhitcombDavid... | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:SlivkaAdamA | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:OrucNevinN | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:PapachristouG... | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:LambJanetteJ | lld:pubmed |
pubmed-article:19590623 | pubmed:author | pubmed-author:AvulaHarithaH | lld:pubmed |
pubmed-article:19590623 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:19590623 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:19590623 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19590623 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19590623 | pubmed:pagination | 45-9 | lld:pubmed |
pubmed-article:19590623 | pubmed:dateRevised | 2010-6-10 | lld:pubmed |
pubmed-article:19590623 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19590623 | pubmed:articleTitle | Angiotensin-converting enzyme gene DD genotype neither increases susceptibility to acute pancreatitis nor influences disease severity. | lld:pubmed |
pubmed-article:19590623 | pubmed:affiliation | Department of Medicine, Division of Gastroenterology, University of Pittsburgh, PA, USA. | lld:pubmed |
pubmed-article:19590623 | pubmed:publicationType | Journal Article | lld:pubmed |
entrez-gene:1636 | entrezgene:pubmed | pubmed-article:19590623 | lld:entrezgene |
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