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Genotype-by-smoking interaction and ...

Avery, Christy L.

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Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae./
作者:	Avery, Christy L.
面頁冊數:	251 p.
附註:	Adviser: Kari E. North.
Contained By:	Dissertation Abstracts International68-11B.
標題:	Health Sciences, Epidemiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288983
ISBN:	9780549322016

Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae.
Avery, Christy L.

Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae. - 251 p.

Adviser: Kari E. North.

Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2007.

Although the association between cigarette smoking and atherosclerosis is well established, the mechanisms by which smoking initiates vascular disease remain poorly understood. As heritable differences in DNA repair ability can influence the effect of environmental exposures such as cigarette smoke, we evaluated how 36 DNA repair variants from five genes (XRCC1, APEX1, hOgg1, XPD, and XRCC3) modified the association between ever-smoking and two atherosclerosis outcomes in Atherosclerosis Risk in Communities (ARIC) Study participants: intimal-medial thickness (IMT) and incident coronary heart disease (CHD).

ISBN: 9780549322016Subjects--Topical Terms:

1019544
Health Sciences, Epidemiology.

Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae.
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245 1 0 $a Genotype-by-smoking interaction and the risk of atherosclerosis and its clinical sequelae.
300 $a 251 p.
500 $a Adviser: Kari E. North.
500 $a Source: Dissertation Abstracts International, Volume: 68-11, Section: B, page: 7221.
502 $a Thesis (Ph.D.)--The University of North Carolina at Chapel Hill, 2007.
520 $a Although the association between cigarette smoking and atherosclerosis is well established, the mechanisms by which smoking initiates vascular disease remain poorly understood. As heritable differences in DNA repair ability can influence the effect of environmental exposures such as cigarette smoke, we evaluated how 36 DNA repair variants from five genes (XRCC1, APEX1, hOgg1, XPD, and XRCC3) modified the association between ever-smoking and two atherosclerosis outcomes in Atherosclerosis Risk in Communities (ARIC) Study participants: intimal-medial thickness (IMT) and incident coronary heart disease (CHD).
520 $a The incident CHD analysis was conducted using all cases 1987-1998 (N=1,086) and a random sample (N=1,065) selected from the entire ARIC cohort at baseline (cohort random sample, CRS). Incidence rate ratios were estimated by piecewise constant models and departures from additivity were measured with interaction contrast ratios. When priors for genetic and environmental effects were added to the first-stage model, tagSNPs rs3213282 (XRCC1), rs50871 (XPD), and rs3212024 (XRCC3) were associated with an increase in the estimated effect of ever-smoking on incident CHD while tagSNPs rs1799782 (XRCC1) and rs861531 (XRCC3) were associated with a decrease.
520 $a We also evaluated the association between DNA repair variants, cigarette smoking, and baseline mean IMT using linear regression models in ARIC participants selected into the CRS. When priors for genetic and environmental effects were added to the first-stage linear regression model, tagSNPs rs3213282 ( XRCC1), rs3213245 (XRCC1), rs3212024 (XRCC3 ), and rs3136814 (APEX1) were associated with increases in the estimated effect of ever-smoking on baseline mean IMT while tagSNPs rs3136817 (APEX1) and rs1799794 (XRCC3) were associated with decreases.
520 $a Few population-based studies examining the relationship between DNA repair variants, cigarette smoking and atherosclerosis have been published. Our results can stimulate inquiries into potential mechanisms linking cigarette smoke exposure and atherosclerotic diseases and help bridge the gap between observed trends and CHD biology. Future studies in different populations will undoubtedly be required to validate our results and improve our understanding of the complex relationships between DNA repair variants, cigarette smoking, and atherothrombotic disease.
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650 4 $a Health Sciences, Epidemiology. $3 1019544
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710 2 $a The University of North Carolina at Chapel Hill. $b Epidemiology. $3 1269376
773 0 $t Dissertation Abstracts International $g 68-11B.
790 $a 0153
790 1 0 $a Heiss, Gerardo $e committee member
790 1 0 $a Lange, Ethan M. $e committee member
790 1 0 $a North, Kari E., $e advisor
790 1 0 $a Olshan, Andrew F. $e committee member
790 1 0 $a Poole, Charles $e committee member
791 $a Ph.D.
792 $a 2007
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3288983