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|Type of Document
||Microsomal epoxide hydrolase and Glutathione-S- transferase Gene Polymorphism in man with Chronic Obstructive Pulmonary Disease|
|Date of Defense
microsomal epoxide hydrolase
restriction fragment length polymorphism
chronic obstructive pulmonary disease
||Genetic association studies have implicated a variety of gene in COPD pathogenesis, such as GST (Glutathione-S-transferase) and mEPH (microsomal epoxide hydrolase) for COPD patients in Taiwan. The current problem in studies of genetic polymorphism of GST and mEPH in COPD is the different results from various studies. These may occur because of the phenotype definitions, sex or ethnic difference. The aim of this study is to confirm and advance our knowledge of the role of this genetic variation in COPD. |
The genotypes of 149 patients with COPD and 125 control subjects were evaluated by polymerase chain reaction and followed by restriction fragment length polymorphism analysis of the mEPH and GST (GST-P1 and M1) genes. All subjects were men over 40 years-old who smoked.
The mEPH 113 (His113/His113) mutant homozygote had a strong association with COPD (OR 1.84, 95%CI: 1.03-3.27), patients with the His113 mutant homozygote was increased in COPD patients as compared with the control group (43.6% [65/149] vs. 30.4% [38/125]; p= 0.024). No significant difference of GST genetic variation between COPD and control group was noted.
mEPH 113 mutant homozygote but not GST gene polymorphism was a significant risk factor in susceptibility to COPD in male smokers.
||Ching-Mei Hsu - chair|
Chiung-Zuei Chen - co-chair
Ming-Hong Tai - advisor
Indicate in-campus at 0 year and off-campus access at 1 year.|
|Date of Submission