Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-3-17
pubmed:abstractText
Myocardial function is severely compromised during sepsis. Several underlying mechanisms have been proposed. The innate immune system, i.e. toll-like receptor (TLR) 2 and 4, significantly contributes to cardiac dysfunction. Little is known regarding TLR9 and its pathogenic ligand bacterial DNA in the myocardium. We therefore studied the role of TLR9 in myocardial inflammation and cardiac contractility.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CPG-oligonucleotide, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/DNA, Bacterial, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1beta, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6, http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Oligodeoxyribonucleotides, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Tlr9 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 9, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0008-6363
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
26-35
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:18194990-Animals, pubmed-meshheading:18194990-Cells, Cultured, pubmed-meshheading:18194990-Cytokines, pubmed-meshheading:18194990-DNA, Bacterial, pubmed-meshheading:18194990-Disease Models, Animal, pubmed-meshheading:18194990-Immunity, Innate, pubmed-meshheading:18194990-Interleukin-1beta, pubmed-meshheading:18194990-Interleukin-6, pubmed-meshheading:18194990-Mice, pubmed-meshheading:18194990-Mice, Inbred C57BL, pubmed-meshheading:18194990-Mice, Knockout, pubmed-meshheading:18194990-Myocardial Contraction, pubmed-meshheading:18194990-Myocarditis, pubmed-meshheading:18194990-Myocardium, pubmed-meshheading:18194990-NF-kappa B, pubmed-meshheading:18194990-Nitric Oxide Synthase Type II, pubmed-meshheading:18194990-Oligodeoxyribonucleotides, pubmed-meshheading:18194990-RNA, Messenger, pubmed-meshheading:18194990-Sarcomeres, pubmed-meshheading:18194990-Sepsis, pubmed-meshheading:18194990-Time Factors, pubmed-meshheading:18194990-Toll-Like Receptor 9, pubmed-meshheading:18194990-Tumor Necrosis Factor-alpha
pubmed:year
2008
pubmed:articleTitle
Bacterial DNA induces myocardial inflammation and reduces cardiomyocyte contractility: role of toll-like receptor 9.
pubmed:affiliation
Department for Anesthesiology and Intensive Care Medicine, University Hospital Bonn, Sigmund-Freud-Strasse 25, Bonn 53105, Germany. pascal.knuefermann@ukb.uni-bonn.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't