Source:http://linkedlifedata.com/resource/pubmed/id/18952697
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2009-3-23
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pubmed:abstractText |
Anti-neutrophil cytoplasmic antibodies (ANCA) against proteinase 3 (PR3) are postulated to injure vascular endothelium by inducing cytokine-primed neutrophils to release proteolytic enzymes and generate reactive oxygen species. Anti-PR3 induce exocytosis, and since priming is associated with upregulation of plasma membrane proteins by exocytosis of intracellular granules, we tested the hypothesis that anti-PR3 prime neutrophils in the absence of cytokines.
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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 |
Apr
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pubmed:issn |
1460-2385
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1150-7
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pubmed:meshHeading | |
pubmed:year |
2009
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pubmed:articleTitle |
Anti-proteinase 3 antibodies both stimulate and prime human neutrophils.
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pubmed:affiliation |
Department of Medicine, University of Louisville, 615 S. Preston Street, Louisville, KY 40202-1718, USA.
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pubmed:publicationType |
Journal Article
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