16859660

Source:http://linkedlifedata.com/resource/pubmed/id/16859660

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0003069, umls-concept:C0038952, umls-concept:C0277785, umls-concept:C0332161, umls-concept:C0600519, umls-concept:C1549649, umls-concept:C1879547, umls-concept:C2349209
pubmed:issue	4
pubmed:dateCreated	2006-8-14
pubmed:abstractText	Myocardial contractility is enhanced in transgenic (TG) mice with cardiac-restricted overexpression of the alpha1A-adrenergic receptors (alpha1A-AR). We tested the hypothesis that this enhanced inotropy protects against dysfunction and remodeling after myocardial infarction (MI).
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/0077427
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Actins, http://linkedlifedata.com/resource/pubmed/chemical/Adra1a protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor, http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/Fibronectins, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxyproline, http://linkedlifedata.com/resource/pubmed/chemical/Myosin Heavy Chains, http://linkedlifedata.com/resource/pubmed/chemical/Nonmuscle Myosin Type IIB, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-1, http://linkedlifedata.com/resource/pubmed/chemical/nonmuscle myosin type IIB heavy...
pubmed:status	MEDLINE
pubmed:month	Sep
pubmed:issn	0008-6363
pubmed:author	pubmed-author:DartAnthony MAM, pubmed-author:DuXiao-JunXJ, pubmed-author:FinchAngela MAM, pubmed-author:GaoXiao-MingXM, pubmed-author:GrahamRobert MRM, pubmed-author:HannanRoss ARA, pubmed-author:KiriazisHelenH, pubmed-author:MingZiqiuZ, pubmed-author:MooreXiao-LeiXL, pubmed-author:SuYidanY
pubmed:issnType	Print
pubmed:day	1
pubmed:volume	71
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	735-43
pubmed:dateRevised	2010-11-18
pubmed:meshHeading	pubmed-meshheading:16859660-Actins, pubmed-meshheading:16859660-Aging, pubmed-meshheading:16859660-Animals, pubmed-meshheading:16859660-Atrial Natriuretic Factor, pubmed-meshheading:16859660-Collagen, pubmed-meshheading:16859660-Echocardiography, pubmed-meshheading:16859660-Female, pubmed-meshheading:16859660-Fibronectins, pubmed-meshheading:16859660-Heart Failure, pubmed-meshheading:16859660-Hydroxyproline, pubmed-meshheading:16859660-Male, pubmed-meshheading:16859660-Mice, pubmed-meshheading:16859660-Mice, Transgenic, pubmed-meshheading:16859660-Myocardial Infarction, pubmed-meshheading:16859660-Myocardium, pubmed-meshheading:16859660-Myosin Heavy Chains, pubmed-meshheading:16859660-Nonmuscle Myosin Type IIB, pubmed-meshheading:16859660-Random Allocation, pubmed-meshheading:16859660-Receptors, Adrenergic, alpha-1, pubmed-meshheading:16859660-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16859660-Time Factors, pubmed-meshheading:16859660-Ventricular Dysfunction, Left, pubmed-meshheading:16859660-Ventricular Remodeling
pubmed:year	2006
pubmed:articleTitle	Transgenic alpha1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival.
pubmed:affiliation	Experimental Cardiology Laboratory, Baker Heart Research Institute, and Alfred Heart Centre, Alfred Hospital, Melbourne, Australia. xiaojun.du@baker.edu.au
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't