14517168

Source:http://linkedlifedata.com/resource/pubmed/id/14517168

Download in:

Switch to

Custom View

Named Graph Language Inference

Statements in which the resource exists as a subject.
Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0008013, umls-concept:C0017296, umls-concept:C0027051, umls-concept:C0231174, umls-concept:C0599946, umls-concept:C0600520, umls-concept:C1517004
pubmed:issue	17
pubmed:dateCreated	2003-10-28
pubmed:abstractText	Increased expression of monocyte chemoattractant protein-1 (MCP-1) has recently been described in clinical and experimental failing heart. However, its pathophysiological significance in heart failure remains obscure. We thus determined whether MCP-1 is increased in post-myocardial infarction (MI) hearts and its blockade can attenuate the development of left ventricular (LV) remodeling and failure.
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/0147763
pubmed:citationSubset	AIM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/Matrix Metalloproteinases, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status	MEDLINE
pubmed:month	Oct
pubmed:issn	1524-4539
pubmed:author	pubmed-author:EgashiraKensukeK, pubmed-author:HayashidaniShunjiS, pubmed-author:HoghPP, pubmed-author:IkeuchiMasakiM, pubmed-author:MatsusakaHidenoriH, pubmed-author:ShiomiTetsuyaT, pubmed-author:SuematsuNobuhiroN, pubmed-author:TakeshitaAkiraA, pubmed-author:TsutsuiHiroyukiH
pubmed:issnType	Electronic
pubmed:day	28
pubmed:volume	108
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	2134-40
pubmed:dateRevised	2007-11-15
pubmed:meshHeading	pubmed-meshheading:14517168-Angiotensin II, pubmed-meshheading:14517168-Animals, pubmed-meshheading:14517168-Chemokine CCL2, pubmed-meshheading:14517168-Cytokines, pubmed-meshheading:14517168-Disease Models, Animal, pubmed-meshheading:14517168-Disease Progression, pubmed-meshheading:14517168-Gene Expression Regulation, pubmed-meshheading:14517168-Gene Therapy, pubmed-meshheading:14517168-Heart Failure, pubmed-meshheading:14517168-Humans, pubmed-meshheading:14517168-Immunohistochemistry, pubmed-meshheading:14517168-Male, pubmed-meshheading:14517168-Matrix Metalloproteinases, pubmed-meshheading:14517168-Mice, pubmed-meshheading:14517168-Muscle, Skeletal, pubmed-meshheading:14517168-Myocardial Infarction, pubmed-meshheading:14517168-Myocardium, pubmed-meshheading:14517168-Sequence Deletion, pubmed-meshheading:14517168-Survival Rate, pubmed-meshheading:14517168-Tumor Necrosis Factor-alpha, pubmed-meshheading:14517168-Ventricular Dysfunction, Left, pubmed-meshheading:14517168-Ventricular Remodeling
pubmed:year	2003
pubmed:articleTitle	Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction.
pubmed:affiliation	Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't