Linked Life Data

18316490

Source:http://linkedlifedata.com/resource/pubmed/id/18316490

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2008-3-18
pubmed:abstractText
Cardiac dyssynchrony in the failing heart worsens global function and efficiency and generates regional loading disparities that may exacerbate stress-response molecular signaling and worsen cell survival. We hypothesized that cardiac resynchronization (CRT) from biventricular stimulation reverses such molecular abnormalities at the regional and global levels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/14-3-3 Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent..., http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Glycogen Synthase Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha, http://linkedlifedata.com/resource/pubmed/chemical/bcl-Associated Death Protein, http://linkedlifedata.com/resource/pubmed/chemical/glycogen synthase kinase 3 beta, http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1524-4539
pubmed:author
pubmed:issnType
Electronic
pubmed:day
18
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1369-77
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:18316490-14-3-3 Proteins, pubmed-meshheading:18316490-Animals, pubmed-meshheading:18316490-Apoptosis, pubmed-meshheading:18316490-Bundle-Branch Block, pubmed-meshheading:18316490-Calcium-Calmodulin-Dependent Protein Kinases, pubmed-meshheading:18316490-Cardiac Pacing, Artificial, pubmed-meshheading:18316490-Dogs, pubmed-meshheading:18316490-Enzyme Activation, pubmed-meshheading:18316490-Forkhead Transcription Factors, pubmed-meshheading:18316490-Glycogen Synthase Kinase 3, pubmed-meshheading:18316490-Heart Failure, pubmed-meshheading:18316490-Phosphorylation, pubmed-meshheading:18316490-Protein Processing, Post-Translational, pubmed-meshheading:18316490-Proto-Oncogene Proteins c-akt, pubmed-meshheading:18316490-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:18316490-Random Allocation, pubmed-meshheading:18316490-Stroke Volume, pubmed-meshheading:18316490-Tachycardia, Ectopic Atrial, pubmed-meshheading:18316490-Tachycardia, Ventricular, pubmed-meshheading:18316490-Tumor Necrosis Factor-alpha, pubmed-meshheading:18316490-bcl-Associated Death Protein, pubmed-meshheading:18316490-p38 Mitogen-Activated Protein Kinases
pubmed:year
2008
pubmed:articleTitle
Reversal of global apoptosis and regional stress kinase activation by cardiac resynchronization.
pubmed:affiliation
Division of Cardiology, School of Medicine, Department of Biomedical Engineering, Johns Hopkins University Medical Institutions, Baltimore, MD 21205, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Evaluation Studies, Research Support, N.I.H., Extramural