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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017526,
umls-concept:C0018787,
umls-concept:C0033085,
umls-concept:C0185117,
umls-concept:C0205307,
umls-concept:C0439799,
umls-concept:C0457405,
umls-concept:C0521324,
umls-concept:C0597298,
umls-concept:C0597484,
umls-concept:C2911684
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pubmed:issue |
3
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pubmed:dateCreated |
2009-1-27
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pubmed:abstractText |
Reentrant arrhythmias often develop in the setting of myocardial infarction and ensuing slow propagation. Increased Na(+) channel expression could prevent or disrupt reentrant circuits by speeding conduction if channel availability is not limited by membrane depolarization within the diseased myocardium. We therefore asked if, in the setting of membrane depolarization, action potential (AP) upstroke and normal conduction can be better preserved by the expression of a Na(+) channel isoform with altered biophysical properties compared to the native cardiac Na(+) channel isoform, namely having a positively shifted, voltage-dependent inactivation.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-10484414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-10501828,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-10533567,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-11156892,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-11440985,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-11761415,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-1352987,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-1375397,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-15042347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-15105172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-15309249,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-16043776,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-16194689,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-16203911,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-16330086,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-16399841,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-1717173,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-17916158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-17993321,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-18160685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-18363088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-559096,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-6251234,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-6833648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-7131569,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-7836935,
http://linkedlifedata.com/resource/pubmed/commentcorrection/18977767-9054762
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1755-3245
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pubmed:author |
pubmed-author:BucchiAnnalisaA,
pubmed-author:ChenMingM,
pubmed-author:CohenIra SIS,
pubmed-author:DunWenW,
pubmed-author:EntchevaEmiliaE,
pubmed-author:JiaZhihengZ,
pubmed-author:KumariSindhuS,
pubmed-author:LuJiaJ,
pubmed-author:ProtasLevL,
pubmed-author:RobinsonRichard BRB,
pubmed-author:RosenMichael RMR
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
81
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
528-35
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pubmed:dateRevised |
2011-7-22
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pubmed:meshHeading |
pubmed-meshheading:18977767-Action Potentials,
pubmed-meshheading:18977767-Animals,
pubmed-meshheading:18977767-Animals, Newborn,
pubmed-meshheading:18977767-Arrhythmias, Cardiac,
pubmed-meshheading:18977767-Cells, Cultured,
pubmed-meshheading:18977767-Gene Therapy,
pubmed-meshheading:18977767-Gene Transfer Techniques,
pubmed-meshheading:18977767-Heart Ventricles,
pubmed-meshheading:18977767-Humans,
pubmed-meshheading:18977767-Muscle, Skeletal,
pubmed-meshheading:18977767-Muscle Proteins,
pubmed-meshheading:18977767-Mutagenesis, Site-Directed,
pubmed-meshheading:18977767-Myocytes, Cardiac,
pubmed-meshheading:18977767-Point Mutation,
pubmed-meshheading:18977767-Potassium,
pubmed-meshheading:18977767-Rats,
pubmed-meshheading:18977767-Sodium Channel Blockers,
pubmed-meshheading:18977767-Sodium Channels,
pubmed-meshheading:18977767-Tetrodotoxin,
pubmed-meshheading:18977767-Time Factors
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pubmed:year |
2009
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pubmed:articleTitle |
Expression of skeletal but not cardiac Na+ channel isoform preserves normal conduction in a depolarized cardiac syncytium.
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pubmed:affiliation |
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, 630 West 168 Street, Room PH7West-318, New York, NY 10032, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study
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