Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:15878341rdf:typepubmed:Citationlld:pubmed
pubmed-article:15878341lifeskim:mentionsumls-concept:C0007634lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0006434lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0034693lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0028128lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0039194lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0162638lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0079395lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0007586lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0441889lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0237477lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0205263lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C1879547lld:lifeskim
pubmed-article:15878341lifeskim:mentionsumls-concept:C0205227lld:lifeskim
pubmed-article:15878341pubmed:issue1lld:pubmed
pubmed-article:15878341pubmed:dateCreated2005-5-9lld:pubmed
pubmed-article:15878341pubmed:abstractTextMajor physical traumas provoke a systemic inflammatory response and immune dysfunction. In a model of thermal injury in rats, we previously showed that an overproduction of nitric oxide (NO) was responsible for the collapse of lymphoproliferative responses. In the present work, we performed a time-course analysis of cell proliferation and cell death parameters in order to establish the sequence of events triggered by the high NO output in Wistar/Han rat splenocytes activated with Con A, 10 days after burn injury. We demonstrate that activated T cells from burned rats never divided whereas normal T cells underwent four division cycles. However, T cells from both burned and normal rat entered the G1 phase as shown by increase of cell size, mitochondria hyperpolarization, and expression of cyclin D1. Burned rat T cells progressed to the late G1 phase as shown by expression of the nuclear Ki-67 antigen, but they never entered the S phase. They underwent apoptosis as shown by morphological parameters, disruption of transmembrane mitochondrial potential, and DNA fragmentation. Persistent accumulation of the p53 protein accompanied these phenomena. NO synthase inhibitors antagonize alterations of cell proliferation and cell death parameters in burned rat T cells and accelerated p53 turnover.lld:pubmed
pubmed-article:15878341pubmed:languageenglld:pubmed
pubmed-article:15878341pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:citationSubsetIMlld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:15878341pubmed:statusMEDLINElld:pubmed
pubmed-article:15878341pubmed:monthMaylld:pubmed
pubmed-article:15878341pubmed:issn0014-4827lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:MathieuJacque...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:ChancerelleYv...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:LevacherMarys...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:De...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:Dinh-XuanAnh...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:FlorentinIrèn...lld:pubmed
pubmed-article:15878341pubmed:authorpubmed-author:ValentiLionel...lld:pubmed
pubmed-article:15878341pubmed:issnTypePrintlld:pubmed
pubmed-article:15878341pubmed:day15lld:pubmed
pubmed-article:15878341pubmed:volume306lld:pubmed
pubmed-article:15878341pubmed:ownerNLMlld:pubmed
pubmed-article:15878341pubmed:authorsCompleteYlld:pubmed
pubmed-article:15878341pubmed:pagination150-67lld:pubmed
pubmed-article:15878341pubmed:dateRevised2006-11-15lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:meshHeadingpubmed-meshheading:15878341...lld:pubmed
pubmed-article:15878341pubmed:year2005lld:pubmed
pubmed-article:15878341pubmed:articleTitleHigh levels of endogenous nitric oxide produced after burn injury in rats arrest activated T lymphocytes in the first G1 phase of the cell cycle and then induce their apoptosis.lld:pubmed
pubmed-article:15878341pubmed:affiliationLaboratoire de Physiologie Respiratoire, Faculté de Médecine Cochin/Port-Royal, Université Paris V, 24 rue du Faubourg Saint Jacques, 75014 Paris, France. valentilio@yahoo.frlld:pubmed
pubmed-article:15878341pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:15878341pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed