|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
4
|
|
pubmed:dateCreated |
2003-2-20
|
|
pubmed:abstractText |
Delayed apoptosis of primed neutrophils (PMNs) may facilitate PMN-mediated tissue injury leading to multiple organ failure (MOF). We previously reported delayed apoptosis and priming of PMNs in severely injured patients at risk for MOF. Our in vitro and in vivo data have implicated phospholipids in PMN cytotoxicity following trauma and shock. The phospholipid signaling pathway remains to be elucidated, but may involve protein kinase C (PKC). We hypothesized that circulating platelet-activating factor (PAF) and PAF-like proinflammatory phospholipids mediate delayed postinjury PMN apoptosis and that PKC is integral to the signaling pathway.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Azepines,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Indoles,
http://linkedlifedata.com/resource/pubmed/chemical/Maleimides,
http://linkedlifedata.com/resource/pubmed/chemical/Phospholipids,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet Activating Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet Aggregation Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Triazoles,
http://linkedlifedata.com/resource/pubmed/chemical/bepafant,
http://linkedlifedata.com/resource/pubmed/chemical/bisindolylmaleimide I
|
|
pubmed:status |
MEDLINE
|
|
pubmed:issn |
1096-2964
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
2
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
289-93; discussion 294-5
|
|
pubmed:dateRevised |
2007-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:12593704-Adolescent,
pubmed-meshheading:12593704-Adult,
pubmed-meshheading:12593704-Aged,
pubmed-meshheading:12593704-Apoptosis,
pubmed-meshheading:12593704-Azepines,
pubmed-meshheading:12593704-Enzyme Inhibitors,
pubmed-meshheading:12593704-Humans,
pubmed-meshheading:12593704-Indoles,
pubmed-meshheading:12593704-Injury Severity Score,
pubmed-meshheading:12593704-Maleimides,
pubmed-meshheading:12593704-Middle Aged,
pubmed-meshheading:12593704-Neutrophils,
pubmed-meshheading:12593704-Phospholipids,
pubmed-meshheading:12593704-Plasma,
pubmed-meshheading:12593704-Platelet Activating Factor,
pubmed-meshheading:12593704-Platelet Aggregation Inhibitors,
pubmed-meshheading:12593704-Protein Kinase C,
pubmed-meshheading:12593704-Signal Transduction,
pubmed-meshheading:12593704-Time Factors,
pubmed-meshheading:12593704-Triazoles,
pubmed-meshheading:12593704-Wounds and Injuries
|
|
pubmed:year |
2001
|
|
pubmed:articleTitle |
Neutrophil apoptosis is delayed by trauma patients' plasma via a mechanism involving proinflammatory phospholipids and protein kinase C.
|
|
pubmed:affiliation |
Department of Surgery, Denver Health Medical Center and University of Colorado Health Sciences Center, Denver, CO, USA. wlbiffl@usasurg.org
|
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
