The hOGG1 Ser326Cys gene polymorphism and the risk of coronary ectasia in the Chinese population.

Oxidative stress (OS) is related to vascular inflammation possibly, contributing to the development of coronary ectasia (CE). Base excision repair (BER) and nucleotide excision repair are the main DNA repair pathways that can help to remove 8-hydroxydeoxyguanine (8-OHdG), a marker of OS. Human 8-oxoguanine DNA glycosylase 1 (hOGG1) is a key enzyme of the BER pathway and catalyzes the removal of 8-OHdG.

Matrix metalloproteinase-1 mitral expression and -1607 1G/2G gene promoter polymorphism in mitral chordae tendinae rupture.

Understanding the pathogenesis of mitral chordae tendinae rupture (MCTR) is essential for identification of risk factors. Mitral matrix metalloproteinase (MMP) triggers the signal cascade that instigates cardiac fibrosis, which may be a predisposing factor in MCTR. We investigated associations among MMP1 expression, MMP1 -1607 1G/2G polymorphism and mitral chordae tendinae rupture (MCTR).

The Gly460Trp polymorphism of alpha-adducin gene as a predictor of renal function decline over 4 years of follow-up in an apparently healthy Chinese population.

There were conflict data between alpha-adducin Gly460Trp genetic variant and changes of renal function. We conducted a prospective study to investigate the influence of alph-adducin Gly460Trp polymorphism on the quantitative changes of renal function. Of 1500 people screened, 112 non-diabetic normotensive elderly Chinese were recruited and received biochemistry examination at the baseline, at the second and fourth year follow-up.

The 8-oxoguanine glycosylase I (hOGG1) Ser326Cys variant affects the susceptibility to multi-vessel disease in Taiwan coronary artery disease patients.

8-hydroxydeoxyguanosine, the key lesion of oxidative DNA damage, contributes to the development of coronary artery disease (CAD). In humans, 8-hydroxydeoxyguanosine is repaired by the enzyme 8-oxoguanine glycosylase I (hOGG1). We investigated the association between the hOGG1 Ser(326)Cys polymorphism and the presence and the severity of CAD in a Taiwan population.

Functional vascular endothelial growth factor gene polymorphisms and diabetes: effect on coronary collaterals in patients with significant coronary artery disease.

Background: Vascular endothelial growth factor (VEGF) plays a pivotal role in angiogenesis. This study tested the association between functional VEGF +405 C>G (rs2010963), -2578C>A (rs699947) polymorphisms, and coronary collaterals in patients with coronary artery disease (CAD).

Method: The collateral scoring system developed by Rentrop was used to classify 393 patients according to their collaterals as either "poor" (grades 0 and 1) or "good" (grades 2 and 3).

Vascular endothelial growth factor polymorphisms and extent of coronary atherosclerosis in Chinese population with advanced coronary artery disease.

Background: Vascular endothelial growth factor (VEGF) is important in atherosclerotic development. We examined two VEGF polymorphisms, including +405 C/G (rs2010963) and -2578C/A (rs699947), to assess their relation to the extent of coronary atherosclerosis.

Methods: We recruited 398 patients with advanced coronary artery disease (CAD).

Elevated serum retinol-binding protein 4 concentrations are associated with renal dysfunction and uric acid in type 2 diabetic patients.

Background: While some studies have reported that retinol-binding protein 4 (RBP4) might induce insulin resistance, other studies have demonstrated that the presence of albuminuria in diabetic patients and increased uric acid are related to insulin resistance. Therefore, this study attempted to further investigate the relationship among serum RBP4, serum uric acid, and the severity of albuminuria in diabetic patients.

Methods: A total of 95 type 2 diabetic patients and 16 healthy subjects participated in this study.

Thiazolidinedione addition reduces the serum retinol-binding protein 4 in type 2 diabetic patients treated with metformin and sulfonylurea.

Retinol-binding protein 4 (RBP4) has been found to induce insulin resistance and to be increased in type 2 diabetes. Thiazolidinediones (TZDs) can improve insulin sensitivity through the activation of peroxisome proliferators-activated receptor-gamma (PPAR-gamma) and have been suggested as an adjunct to metformin (MF) and sulfonylurea (SU) in type 2 diabetes in a consensus statement from the ADA and EASD. Therefore, we investigated whether TZD could affect serum RBP4 level in type 2 diabetes already treated with MF and/or SU.

Decreased insulin secretion and insulin sensitivity are associated with liver function in subjects with fasting glucose between 100 and 109 mg/dL in Taiwanese population.

Objective: In 2003, the American Diabetes Association recommended that the lower limit for the diagnosis of impaired fasting glucose (IFG) should be reduced from 110 to 100 mg/dL in the analysis of the associated risk factors of IFG. It has been proposed that liver dysfunction may contribute to the development of type 2 diabetes. A primary aim was to investigate the relationship between liver enzyme and insulin resistance (IR) in IFG group.

SUMO4 M55V variant is associated with diabetic nephropathy in type 2 diabetes.

OBJECTIVE-SUMO4 mRNA was recently found to be mainly expressed in the kidney, and the methionine-to-valine substitution at codon 55 (M55V) variant of SUMO4 may induce higher nuclear factor-kappaB (NF-kappaB) activity. Because NF-kappaB is known to mediate the development of diabetic nephropathy, we examined the association between the SUMO4 M55V variant and the severity of diabetic nephropathy. RESEARCH DESIGN AND METHODS-We recruited a total of 430 patients with type 2 diabetes.

The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance.

Increased oxidative stress has been observed to contribute the development of insulin resistance. Oxidative stress is known to increase the conversion of deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OHdG). Human 8-oxoguanine glycosylase (hOGG1) is the key component responsible for the removal of 8-OHdG from oxidatively damaged DNA.