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Article: Paraoxonase 1 gene Q192R polymorphism affects stroke and myocardial infarction risk

TitleParaoxonase 1 gene Q192R polymorphism affects stroke and myocardial infarction risk
Authors
KeywordsIschemic stroke
Paraoxonase
Polymorphism
Myocardial infarction
Issue Date2006
Citation
Clinical Biochemistry, 2006, v. 39, n. 3, p. 191-195 How to Cite?
AbstractObjectives: Paraoxonase (PON1), an enzyme associated with high-density lipoprotein (HDL) particles, inhibits oxidation and atherogenesis. We sought to investigate the association of the PON1 Q192R polymorphism with stroke and heart disease. Design and methods: In a case control study, we genotyped 242 ischemic stroke, 231 myocardial infarction (MI), and 310 healthy control subjects, all Chinese. Results: R-containing genotypes (R+) were associated with vascular disease, OR = 1.5, P = 0.03. RR was increased in MI patients who were either smokers (OR = 3.1, P = 0.01), male, or younger than 60. R+ but not RR genotypes were increased in stroke patients, particularly large artery type (OR = 2.6 and P = 0.02 for R+, OR =1.0 for RR) or among smokers. The relative dearth of RR in stroke might be due to earlier MI or death in at-risk people, such as smokers. R+ genotypes were increased with stroke in hypertensive (OR = 2.1, P = 0.02) but not normotensive (OR = 1.0) subjects. Conclusions: PON1 192R+ genotypes were associated with stroke and MI, particularly in subsets of patients, in patterns suggesting a possible survivor effect. © 2006 The Canadian Society of Clinical Chemists. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/292573
ISSN
2023 Impact Factor: 2.5
2023 SCImago Journal Rankings: 0.703
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBaum, Larry-
dc.contributor.authorNg, Ho Keung-
dc.contributor.authorWoo, Kam Sang-
dc.contributor.authorTomlinson, Brian-
dc.contributor.authorRainer, Timothy Hudson-
dc.contributor.authorChen, Xiangyan-
dc.contributor.authorCheung, Wing Sze-
dc.contributor.authorYin Chan, Daniel Kam-
dc.contributor.authorThomas, G. Neil-
dc.contributor.authorWai Tong, Cindy See-
dc.contributor.authorWong, Ka Sing-
dc.date.accessioned2020-11-17T14:56:46Z-
dc.date.available2020-11-17T14:56:46Z-
dc.date.issued2006-
dc.identifier.citationClinical Biochemistry, 2006, v. 39, n. 3, p. 191-195-
dc.identifier.issn0009-9120-
dc.identifier.urihttp://hdl.handle.net/10722/292573-
dc.description.abstractObjectives: Paraoxonase (PON1), an enzyme associated with high-density lipoprotein (HDL) particles, inhibits oxidation and atherogenesis. We sought to investigate the association of the PON1 Q192R polymorphism with stroke and heart disease. Design and methods: In a case control study, we genotyped 242 ischemic stroke, 231 myocardial infarction (MI), and 310 healthy control subjects, all Chinese. Results: R-containing genotypes (R+) were associated with vascular disease, OR = 1.5, P = 0.03. RR was increased in MI patients who were either smokers (OR = 3.1, P = 0.01), male, or younger than 60. R+ but not RR genotypes were increased in stroke patients, particularly large artery type (OR = 2.6 and P = 0.02 for R+, OR =1.0 for RR) or among smokers. The relative dearth of RR in stroke might be due to earlier MI or death in at-risk people, such as smokers. R+ genotypes were increased with stroke in hypertensive (OR = 2.1, P = 0.02) but not normotensive (OR = 1.0) subjects. Conclusions: PON1 192R+ genotypes were associated with stroke and MI, particularly in subsets of patients, in patterns suggesting a possible survivor effect. © 2006 The Canadian Society of Clinical Chemists. All rights reserved.-
dc.languageeng-
dc.relation.ispartofClinical Biochemistry-
dc.subjectIschemic stroke-
dc.subjectParaoxonase-
dc.subjectPolymorphism-
dc.subjectMyocardial infarction-
dc.titleParaoxonase 1 gene Q192R polymorphism affects stroke and myocardial infarction risk-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.clinbiochem.2006.01.010-
dc.identifier.pmid16472799-
dc.identifier.scopuseid_2-s2.0-33644936372-
dc.identifier.volume39-
dc.identifier.issue3-
dc.identifier.spage191-
dc.identifier.epage195-
dc.identifier.isiWOS:000236568300002-
dc.identifier.issnl0009-9120-

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