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G I Rice

Publications and source records attributed to G I Rice.

8 recordsLinked to original sources
PubMed2001

Human endothelial cell-derived nuclear proteins that recognise polymorphic DNA elements in the von Willebrand factor gene promoter include YY1.

Four common base-change polymorphisms have been found in the von Willebrand factor gene promoter: (-1793 C/G, -1234 T/C, -1185 G/A and -1051 A/G). All four polymorphisms are in strong linkage disequilibrium and recent reports have indicated these polymorphisms are associated with plasma vWF:Ag levels suggesting that one or more of these elements influence regulation of the vWF gene. We report that human endothelial cell-derived trans-acting factors display allelic preferences in binding activity to each polymorphic site. The common A allele variant of the -1051 polymorphism and the rarer A allele variant of the -1185 polymorphism provided specific binding of nuclear proteins. The G allele counterpart of these two variants did not produce any complex formation indicating that the nucleotide substitution at these positions alters the DNA binding ability of nuclear factors. The two alleles of the -1234 polymorphism produced two complexes with a similar migration pattern however stronger binding was found to the common T variant of this allele. Two specific complexes associated with the rarer G allele of the -1793 polymorphism, but only one associated with the C allele. Supershift experiments revealed that the trans-acting factor YYI recognised the slower migrating complex formed on the -1234 T/C and the -1051 A polymorphic sites with a strong binding preference for the -1234 T allele variant. The identification of YY1 as a component of the factors that recognise these elements suggests that this ubiquitous nuclear protein may play a role in the regulation of the vWF promoter.

Base Sequence↗
PubMed1999

Angiotensin converting enzyme and angiotensin II type 1-receptor gene polymorphisms and risk of ischaemic heart disease.

OBJECTIVE: Polymorphisms in several genes of the renin-angiotensin system have been implicated as risk factors for myocardial infarction and ischaemic heart disease. In particular, it has been suggested that the angiotensin converting enzyme insertion/deletion (I/D) polymorphism and the angiotensin II type 1 receptor A1166C polymorphisms might act synergistically to increase the risk of myocardial infarction. The aim of this study was to investigate associations between the angiotensin converting enzyme I/D polymorphism and angiotensin II type 1 receptor polymorphisms and ischaemic heart disease. METHODS: We screened 331 white European patients who were recruited for routine angiographic investigation of chest pain, and 287 healthy white European controls for the angiotensin converting enzyme I/D and angiotensin II type 1 receptor A1166C polymorphisms, and related the genotype frequencies to angiotensin converting enzyme levels and the clinical phenotypes of atheroma and history of myocardial infarction. RESULTS: Angiotensin converting enzyme levels were related to I/D polymorphism but not to angiotensin II type 1 receptor polymorphism genotypes. I/D polymorphism and angiotensin II type 1 receptor genotypes did not relate individually to risk of myocardial infarction or atheroma in univariate or multivariate analysis. However, evidence of a synergistic relationship between the AC/II and CC/DD genotypes and coronary stenosis in the major arteries was found. No evidence of any relationship between these polymorphisms and history of myocardial infarction by World Health organisation (WHO) criteria was detected. CONCLUSION: These findings suggest that there is a weak relationship between the angiotensin converting enzyme I/D and angiotensin II type 1 receptor A1166C polymorphisms and coronary atheroma, but no evidence of a relationship with history of myocardial infarction.

Aged↗
PubMed1998

FVIII coagulant activity and antigen in subjects with ischaemic heart disease.

Raised factor VIII coagulant activity has been associated with Ischaemic Heart Disease and Myocardial Infarction (MI). We measured FVIII:C and FVIII:Ag levels in 288 white European patients characterised for extent of atheroma by coronary angiography and for a history of MI by WHO criteria, and 313 white European healthy controls. FVIII:Ag levels were higher in patients than controls after adjustment for confounding variables (1.17 IU/ml patients, 1.03 IU/ml controls [p <0.0005]), whereas FVIII:C levels were lower in patients (1.26 IU/ml patients, 1.45 IU/ml controls [p<0.0005]). FVIII:Ag levels were higher in patients with MI and with angiographic evidence of atheroma than controls. FVIII:Ag levels but not FVIII:C levels were a significant independent risk factor for MI in multivariate analysis (Odds Ratio 2.40[1.35-4.27] [p = 0.003]). No association of FVIII:Ag or FVIII:C levels and presence or extent of atheroma was found in multivariate analysis. In conclusion, this study found an independent association of FVIII:Ag but not FVIII:C with MI.

Aged↗
PubMed1997

Angiotensin-converting enzyme (ACE) gene polymorphisms in patients characterised by coronary angiography.

The angiotensin converting enzyme (ACE) gene is implicated as a risk factor for coronary artery disease and myocardial infarction (MI). An insertion/deletion (I/D) polymorphism is believed to be in linkage disequilibrium with a functional site elsewhere. Ten polymorphisms have recently been identified in the ACE gene. We screened patients undergoing coronary angiography (n = 258) for six of these polymorphisms (T-5491C, T-93C, A-240T, T1237C, D/I and 4656(CT)2/3), and identified a further two rare polymorphisms. ACE levels were associated with genotype for all polymorphisms analysed individually by one way ANOVA (P < 0.0005). The polymorphisms occurring in the 5' region were in negative linkage disequilibrium with the exonic and 3' region polymorphisms. The A-240T polymorphism had the greatest association with ACE levels (R2 = 14%); none of the others were significantly associated with levels when adjustment was made for A-240T. None of the polymorphisms were associated with the extent of coronary atheroma. Two of the promoter polymorphisms (A-240T and T-93C) were weakly related to the occurrence of MI (P = 0.03 and P = 0.05, respectively, by chi 2 analysis). The TT genotype of A-240T appeared to be protective against MI with an odds ratio of 0.31 (95% confidence interval, 0.12, 0.83). These findings indicate that polymorphisms in the ACE gene promoter region may have a stronger association with disease than the I/D polymorphism.

Adult↗
PubMedDate not supplied

The paraoxonase Gln-Arg 192 polymorphism in subjects with ischaemic heart disease.

BACKGROUND: Human serum paraoxonase activity is related to the paraoxonase Gln-Arg 192 polymorphism genotype. The purpose of this study was to investigate the association between the Gln-Arg 192 polymorphism of paraoxonase and ischaemic heart disease (IHD). METHODS: Four hundred and forty patients with a history suggestive of IHD, and characterized by coronary angiography, and 527 healthy controls were studied. Patients were grouped according to paraoxonase genotype, presence or absence of diseased coronary arteries (on the basis of 50% stenosis), and history of myocardial infarction as judged by World Health Organization criteria. Patients were genotyped for the paraoxonase Gln-Arg 192 polymorphism by polymerase chain reaction. RESULTS: No significant relationship was found between paraoxonase genotype and age, sex, body mass index, smoking, triglycerides or hypertension. However, by oneway analysis of variance, cholesterol was found to be significantly associated with paraoxonase genotype in male patients [AA 5.9 (5.8-6.1), AB 6.2 (6.0-6.4), BB 5.7 (5.4-6.1); P = 0.04]. The Gln-Arg 192 polymorphism was found to have no significant effect on the number of patients having diseased coronary arteries, or having myocardial infarction (P = 0.97 for both). In logistic regression models, paraoxonase genotype did not remain a significant independent predictor of stenosis or myocardial infarction. CONCLUSION: This study failed to show an association between the Gln-Arg 192 polymorphism of paraoxonase and the clinical phenotypes of coronary atheroma and acute myocardial infarction.

Aged↗