Source:http://linkedlifedata.com/resource/pubmed/id/11371409
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2001-5-23
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| pubmed:abstractText |
Recent studies have suggested that two polymorphisms of the beta(2)-adrenergic receptor (beta(2)AR) gene at codons 16 (arginine to glycine) and 27 (glutamine to glutamate) affect an individual's airway responsiveness, or response to acute or chronic beta(2)-agonist therapy but are not risk factors for asthma. We hypothesize that there is an interaction effect on asthma between the beta(2)AR gene polymorphisms and cigarette smoking. A case-control study was conducted in 128 asthma cases and 136 control individuals identified from 10,014 studied subjects in rural Anqing, China. Allele-specific polymerase chain reaction (PCR) was used to genotype beta(2)AR gene polymorphisms. Multiple logistic regression was used to adjust for potential confounding factors. We found a marginally significant interaction between cigarette smoking and beta(2)AR-16 genotype after adjusting for important confounding factors (p = 0.06). Specifically, we found that compared with never-smoking Gly-16 homozygotes, those ever-smokers who are Arg-16 homozygotes had a significantly increased risk of asthma (odds ratio [OR] = 7.81; 95% confidence interval [CI]: 2.07 to 29.5). This association showed a clear dose-response relationship with the number of cigarettes smoked. However, there was no significant association of asthma with polymorphisms of the beta(2)AR at position 27 (OR = 1.38; 95% CI: 0.69 to 2.73). Our study suggests a gene-environment interaction between the Arg-16 genotype and ever cigarette smoking with respect to the susceptibility of an individual to asthma.
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| pubmed:grant | |
| pubmed:commentsCorrections | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
1073-449X
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
163
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1404-9
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11371409-Adult,
pubmed-meshheading:11371409-Asthma,
pubmed-meshheading:11371409-Case-Control Studies,
pubmed-meshheading:11371409-China,
pubmed-meshheading:11371409-Confounding Factors (Epidemiology),
pubmed-meshheading:11371409-Female,
pubmed-meshheading:11371409-Forced Expiratory Volume,
pubmed-meshheading:11371409-Genetic Predisposition to Disease,
pubmed-meshheading:11371409-Genotype,
pubmed-meshheading:11371409-Homozygote,
pubmed-meshheading:11371409-Humans,
pubmed-meshheading:11371409-Logistic Models,
pubmed-meshheading:11371409-Male,
pubmed-meshheading:11371409-Middle Aged,
pubmed-meshheading:11371409-Polymerase Chain Reaction,
pubmed-meshheading:11371409-Polymorphism, Genetic,
pubmed-meshheading:11371409-Prevalence,
pubmed-meshheading:11371409-Questionnaires,
pubmed-meshheading:11371409-Receptors, Adrenergic, beta-2,
pubmed-meshheading:11371409-Risk Factors,
pubmed-meshheading:11371409-Sex Distribution,
pubmed-meshheading:11371409-Smoking
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| pubmed:year |
2001
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| pubmed:articleTitle |
Association of asthma with beta(2)-adrenergic receptor gene polymorphism and cigarette smoking.
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| pubmed:affiliation |
Program for Population Genetics, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|