東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Genetic polymorphisms and interactio...

Winston, Carla Antonia.

FindBook

Google Book

Amazon

博客來

Genetic polymorphisms and interactions associated with myocardial infarction.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Genetic polymorphisms and interactions associated with myocardial infarction./
作者:	Winston, Carla Antonia.
面頁冊數:	191 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0531.
Contained By:	Dissertation Abstracts International64-02B.
標題:	Biology, Genetics. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080375

Genetic polymorphisms and interactions associated with myocardial infarction.
Winston, Carla Antonia.

Genetic polymorphisms and interactions associated with myocardial infarction. - 191 p.

Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0531.

Thesis (Ph.D.)--Emory University, 2003.

Myocardial infarction (MI) is characterized by arterial occlusion and thrombosis. Genes involved in vasoconstriction, smooth muscle cell proliferation, fibrinolysis, and oxidative stress may contribute to MI. Polymorphisms in angiotensin I converting enzyme (ACE), angiotensin II type I receptor (AT1R), plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (TPA), and endothelial cell nitric oxide synthase (ecNOS) were examined for association with MI in a study of 245 incident MI cases and 202 controls with no history of thrombosis. Objectives were to estimate marginal effects of gene polymorphisms, to assess gene-gene and gene-environment interactions, and to compare case-control versus case-only genetic interaction results. AT1R transversion from adenine (A) to cytosine (C) at nucleotide position 1166 was associated with MI. Threefold association between AT1R CC genotype and MI observed in Whites (odds ratio (OR) = 3.10) was attenuated when Blacks were included (race-adjusted OR = 2.64). The C allele is rare in Blacks. After controlling for self-reported race, there was no association among controls between genotypes and potential confounding factors including age, gender, education, income, body mass index, and comorbid medical conditions. Interactions were assessed for genes in the renin-angiotensin system (ACE, AT1R), the fibrinolytic system (TPA, PAI-1), and endothelial cell nitric oxide synthase (ecNOS). Gene-gene interactions within each molecular pathway were not significant. We assessed interaction of genetic effects by demographic (age, race, gender) and medical (hypertension, diabetes, obesity, smoking) factors. Gender interaction with PAI-1 genotype was significant in case-control (p = 0.03) and case-only analyses (p = 0.003), though there was no overall association between PAI-1 genotype and MI. We observed no effect modification by other medical or demographic factors. Further studies of AT1R and PAI-1 genes may yield insight into the complex etiology of MI.Subjects--Topical Terms:

1017730
Biology, Genetics.

Genetic polymorphisms and interactions associated with myocardial infarction.
LDR:02876nmm 2200265 4500 001 1861859
005 20041215074114.5
008 130614s2003 eng d
035 $a (UnM)AAI3080375
035 $a AAI3080375
040 $a UnM $c UnM
100 1 $a Winston, Carla Antonia. $3 1949439
245 1 0 $a Genetic polymorphisms and interactions associated with myocardial infarction.
300 $a 191 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0531.
500 $a Adviser: Harland Austin.
502 $a Thesis (Ph.D.)--Emory University, 2003.
520 $a Myocardial infarction (MI) is characterized by arterial occlusion and thrombosis. Genes involved in vasoconstriction, smooth muscle cell proliferation, fibrinolysis, and oxidative stress may contribute to MI. Polymorphisms in angiotensin I converting enzyme (ACE), angiotensin II type I receptor (AT1R), plasminogen activator inhibitor 1 (PAI-1), tissue plasminogen activator (TPA), and endothelial cell nitric oxide synthase (ecNOS) were examined for association with MI in a study of 245 incident MI cases and 202 controls with no history of thrombosis. Objectives were to estimate marginal effects of gene polymorphisms, to assess gene-gene and gene-environment interactions, and to compare case-control versus case-only genetic interaction results. AT1R transversion from adenine (A) to cytosine (C) at nucleotide position 1166 was associated with MI. Threefold association between AT1R CC genotype and MI observed in Whites (odds ratio (OR) = 3.10) was attenuated when Blacks were included (race-adjusted OR = 2.64). The C allele is rare in Blacks. After controlling for self-reported race, there was no association among controls between genotypes and potential confounding factors including age, gender, education, income, body mass index, and comorbid medical conditions. Interactions were assessed for genes in the renin-angiotensin system (ACE, AT1R), the fibrinolytic system (TPA, PAI-1), and endothelial cell nitric oxide synthase (ecNOS). Gene-gene interactions within each molecular pathway were not significant. We assessed interaction of genetic effects by demographic (age, race, gender) and medical (hypertension, diabetes, obesity, smoking) factors. Gender interaction with PAI-1 genotype was significant in case-control (p = 0.03) and case-only analyses (p = 0.003), though there was no overall association between PAI-1 genotype and MI. We observed no effect modification by other medical or demographic factors. Further studies of AT1R and PAI-1 genes may yield insight into the complex etiology of MI.
590 $a School code: 0665.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Health Sciences, Public Health. $3 1017659
690 $a 0369
690 $a 0573
710 2 0 $a Emory University. $3 1017429
773 0 $t Dissertation Abstracts International $g 64-02B.
790 1 0 $a Austin, Harland, $e advisor
790 $a 0665
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080375