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dc.contributor.authorLatkovskis, Gustavs
dc.contributor.authorLicis, Normunds
dc.contributor.authorKrivmane, Baiba
dc.contributor.authorErglis, Andrejs
dc.date.accessioned2015-12-02T20:08:06Z
dc.date.available2015-12-02T20:08:06Z
dc.date.issued2011
dc.identifier.urihttps://dspace.lu.lv/dspace/handle/7/31265
dc.description.abstractCyclooxigenase (COX)-1, formally known as prostanglandin endoperoxideH synthetase-1,mediates synthesis of prostaglandin H2,which is subsequently converted to various biologically active metabolites including thromboxane (TX) A2 [1]. TXA2 is synthesized and released by activated platelets and strongly reinforces thrombus formation, a critical pathway in the pathogenesis of myocardial infarction (MI). Inhibition of COX-1-derived TXA2 in platelets by low-dose aspirin administration reduces incidence of MI [2]. Hypothetically, MI-risk could also be modified by genetic variants that affect activity or expression of COX-1. Many single nucleotide polymorphisms (SNP) in the gene encoding COX-1 (PTGS1) have been described; including functional alterations in both coding and non-coding regions [3,4].We have evaluated if two of such variations are related to the risk ofMI in a historic cohort of patients with coronary artery disease (CAD).en_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.relation.ispartofseriesThrombosis Research;Vol. 125, No. 6
dc.rightsinfo:eu-repo/semantics/restrictedAccessen_US
dc.subjectResearch Subject Categories::MEDICINEen_US
dc.titleA common promoter variant of the gene encoding cyclooxygenase-1 (PTGS1) is related to decreased incidence ofmyocardial infarction in patients with coronary artery diseaseen_US
dc.title.alternativeLetter to the Editors-in-Chief
dc.typeinfo:eu-repo/semantics/otheren_US
dc.identifier.doi10.1016/j.thromres.2010.12.019


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