Linked Life Data

2540344

Source:http://linkedlifedata.com/resource/pubmed/id/2540344

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1989-6-8
pubmed:abstractText
The leukotriene generation (LTB4, 20-OH-LTB4, 20-COOH-LTB4) from PMNs of severely burned patients (n = 6) was studied by reversed-phase HPLC. Granulocytes from all patients showed a decrease in leukotriene generation which only returned to normal levels when the patients recovered from their injuries. The leukotriene generation induced by different stimuli, i.e., the Ca++-ionophore A23187 (7.3 microM) or opsonized zymosan (2 mg) in the presence of exogenous arachidonic acid (60 microM) showed similar stimulation profiles. The cellular differentiation of the respective granulocyte fractions revealed that the decreased leukotriene generation was accompanied by the occurrence of immature granulocytes in the peripheral blood. Furthermore, the studies in the presence of exogenous arachidonic acid showed that the defect in leukotriene generation from granulocytes of surviving patients was due to the availability of metabolizable substrate (i.e., free arachidonic acid). Granulocytes from one nonsurviving patient showed in addition a defect in the metabolic ability of arachidonic acid to generate the respective leukotrienes. The generation of reactive oxygen species did not correlate with the observed alterations in the formation of the leukotrienes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-5282
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
435-45
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Studies on the mechanisms of granulocyte dysfunctions in severely burned patients--evidence for altered leukotriene generation.
pubmed:affiliation
Lehrstuhl für Med. Mikrobiologie und Immunologie, Arbeitsgruppe Infektabwehrmechanismen Ruhr-Universität Bochum, Federal Republic of Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't