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PubMed2000

Interleukin 6, tumour necrosis factor alpha, interleukin 1beta and interleukin 1 receptor antagonist promoter or coding gene polymorphisms in multiple myeloma.

Proinflammatory cytokines such as interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-alpha) and IL-1beta are considered to be involved in the pathogenesis of multiple myeloma (MM). In the present study, we examined a G/C polymorphism at position -174 in the promoter region of IL-6, a biallelic polymorphism at position -308 in the promoter region of TNF-alpha, the TaqI restriction fragment length polymorphism in exon 5 of IL-1beta and a variable number of identical tandem repeat polymorphisms in intron 2 of IL-1 receptor antagonist (IL-1Ra) genes. The alleles of these loci are known to influence the level of production of the cytokines and the IL-1Ra. Seventy-three patients with MM, 27 with monoclonal gammopathy of undetermined significance (MGUS) and 129 healthy individuals were included. No difference was found between patients and healthy controls or between MM and MGUS patients in the distributions of genotypes and frequencies of alleles of the IL-6 (-174), TNF-alpha (-308), IL-1beta TaqI and IL-1Ra gene polymorphisms. No associations between the polymorphisms at the loci under study and clinical factors such as age, sex, clinical stage at onset and M-protein type were observed. Our results indicate that the cytokine (IL-6, TNF-alpha and IL-1beta) and IL-Ra gene polymorphisms do not confer susceptibility to the development of MM.

Adult↗
PubMed2005

Renin-angiotensin system gene polymorphisms: relationship with blood pressure and microalbuminuria in telmisartan-treated hypertensive patients.

This study analyzed the relationship between four renin-angiotensin system (RAS) gene polymorphisms and the response to blood pressure lowering and development of microalbuminuria in 206 patients with essential hypertension treated once daily for 12 months with telmisartan 80 mg. Seated cuff blood pressure and urinary albumin excretion (UAE) were measured throughout the study. Patients were screened for the presence of the A-6G variant of the angiotensinogen gene, angiotensin-converting enzyme insertion/deletion polymorphism, and the A1166C and C573T polymorphisms of the angiotensin II type 1 receptor gene. No significant association was found between the presence of any gene polymorphism and the reduction of blood or UAE following telmisartan treatment. The results indicate that these RAS gene polymorphisms do not affect the antihypertensive activity and renoprotection in mild-to-moderate hypertensive patients treated with telmisartan.

Aged↗
PubMed2004

Renin angiotensin aldosterone system and ACE I/D gene polymorphism in high-altitude pulmonary edema.

INTRODUCTION: People who visit high altitude are exposed to a stressful environment, and many of them suffer from altitude-induced conditions, including high altitude pulmonary edema (HAPE). We investigated the renin angiotensin aldosterone system (RAAS) and the possible association of angiotensin converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism in the development of HAPE in Indian men. METHODS: Subjects were all low-altitude natives: 19 men who developed HAPE within 1-3 d of arrival at 3000 to 3800 m (patients); and 20 age-matched men who did not develop HAPE during a period of a month or more at > or = 3500 m (controls). We recorded the arterial oxygen saturation (Sao2), heart rate (HR), and blood pressure (BP) of both groups and measured their levels of plasma renin activity (PRA), ACE, aldosterone, and serum electrolytes. Polymerase chain reaction was used to investigate a 287 base pair alu repeat sequence I/D polymorphism in the ACE gene. RESULTS: Compared with controls, patients showed a significantly lower Sao2 and a higher HR. They also had significantly higher plasma PRA, aldosterone, ACE, and serum sodium (Na+) and potassium (K+). No significant difference was observed in ACE I/D allele frequencies. DISCUSSION: The results suggested that RAAS is involved in the development of HAPE in low-altitude natives, but there is no association of ACE I/D gene polymorphism with HAPE.

Adult↗
PubMed2004

Influence of the interleukin-6 -174 G/C gene polymorphism on exercise training-induced changes in glucose tolerance indexes.

A polymorphism in the IL-6 gene, a G-to-C substitution 176 bp upstream of the ATG translation initiation site, has been associated with diabetes prevalence and insulin resistance. Interventions including exercise training are frequently used to modify cardiovascular disease risk factors. Consequently, this project examined associations between the IL-6 -174 genotype and oral glucose tolerance test outcomes in 50- to 75-yr-old sedentary men and postmenopausal women before and after aerobic exercise training. Among the 87 individuals who started the study, 56 were retested after 6 mo of aerobic exercise training. Subject characteristics at baseline did not differ between the IL-6 genotype groups with the exception of fasting glucose, which was higher (P = 0.02, covariates age, gender, and ethnicity) in the CC genotype group. The training-induced change in glucose area under the curve during the oral glucose tolerance test varied between the IL-6 -174 genotype groups (P = 0.05, covariates age, gender, ethnicity, baseline glucose area under the curve, and percent body fat change) with a significant decrease occurring only in the GG genotype group. Insulin outcomes did not differ among the groups at baseline or after training. Training-induced changes in weight, percent body fat, maximal oxygen consumption, fasting glucose, and an insulin sensitivity index also changed similarly among the genotype groups. In conclusion, fasting glucose and the extent to which glucose tolerance changes with exercise training may be influenced by the IL-6 -174 gene polymorphism.

Age Factors↗
PubMed2003

Mannose binding lectin gene polymorphism in patients with type I diabetes.

Our purpose was to investigate a possible relationship between occurrence of type I diabetes and polymorphism of the mannose binding lectin gene. Polymorphism of codon 54 of the mannose binding lectin (MBL) gene, whose presence of the minority allele leads to significant reduction of serum MBL concentration, was investigated in 128 Japanese patients with type I diabetes and 78 healthy volunteers by restriction fragment length polymorphism method. Frequencies of the minority allele were compared between the patient group and the control group. Frequency of the minority allele was 24.2% in the patient group and 19.9% in the control group. The probability of being heterozygous or homozygous for the minority allele was 41.4% in the patient group and 33.3% in the control group. Patients with DRB1*0405-DQB1*0401 and/or DRB1*0901-DQB1*0303 haplotypes, the two major type I diabetes-prone human leukocyte antigen haplotypes, showed a slightly higher probability of being heterozygous or homozygous for allele B of the MBL gene. Possession of the minority allele of the MBL gene may be a minor risk factor for having type I diabetes.

Age of Onset↗
PubMed2003

Estrogen receptor alpha gene polymorphisms and peak bone density in Chinese nuclear families.

PBD is an important determinant of osteoporotic fractures. Few studies were performed to search for genes underlying PBD variation in Chinese populations. We tested linkage and/or association of the estrogen receptor alpha gene polymorphism with PBD in 401 Chinese nuclear families. This study suggests the ER-alpha gene may have some minor effects on PBM variation in the Chinese population. Low peak bone density (PBD) in adulthood is an important determinant of osteoporotic fractures in the elderly. PBD variation is mainly regulated by genetic factors. Extensive molecular genetics studies have been performed to search for genes underlying PBD variation, largely in whites. Few studies were performed in Chinese populations. In this study, we simultaneously test linkage and/or association of the estrogen receptor alpha (ER-alpha) gene polymorphism with PBD in 401 Chinese nuclear families (both parents plus their female children) of 1260 subjects, with the 458 children generally between 20 and 40 years of age. All the subjects were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) at polymorphic PvuII and XbaI sites inside the ER-alpha gene. Bone mineral density was measured at the lumbar spine (L1-L4) and hip (femoral neck, trochanter, and intertrochanteric region). Raw bone mineral density values were adjusted by age, height, and weight as covariates. We detected marginally significant results for within-family association (transmission disequilibrium; p = 0.054) between the spine bone mineral density variation and the ER-alpha XbaI genotypes. For the hip bone mineral density variation, significant (p < 0.05) linkage results were generally found for the two intragenic markers. Analyses of the haplotypes defined by the two markers confer further evidence for linkage of the ER-alpha with the hip PBD variation. In conclusion, this study suggests that the ER-alpha gene may have minor effects on PBD variation in our Chinese population.

Asian People↗
PubMed2005

Lack of association between the CYP11B2 gene polymorphism and preeclampsia, eclampsia, and the HELLP syndrome in Turkish women.

OBJECTIVES: It is possible that altered control of aldosterone synthase gene (CYP11B2) expression or translation may be responsible for hypertension. Hypertension is one of the major components of preeclampsia. We present here a study investigating the association between the CYP11B2 gene polymorphism in the promoter region at the position of -344 and preeclampsia. STUDY DESIGN: We analyzed a group of Turkish women for preeclampsia (n=143), eclampsia (n=36), and the HELLP syndrome (n=55) and compared them with controls (n=147). Genotypes for CYP11B2 were determined by polymerase chain reaction followed by digestion with BsuRI restriction enzyme. RESULTS: The -344T/T, -344C/T, and -344C/C genotypes were found at comparable frequencies among the study groups, between the study and control groups, and between the study groups combined and the control group (p>0.05). We combined the genotypes of TC and CC (polymorphic) and compared them with the TT (wild-type) genotype. There was no significant difference in the frequency of the TC plus CC genotypes among the study groups, between the study and control groups, and between the study groups combined and the control group (p>0.05). There was no association of the CYP11B2 polymorphism among the preeclampsia, eclampsia, and HELLP groups and controls. CONCLUSIONS: The CYP11B2 gene polymorphism is not directly associated with preeclampsia, eclampsia, and the HELLP syndrome in women with these conditions. Therefore, this polymorphism may not be a risk factor for these disorders, at least not in the Turkish population.

Adolescent↗
PubMed2002

ecNOS gene polymorphism is associated with endothelium-dependent vasodilation in Type 2 diabetes.

The association between endothelial constitutive nitric oxide synthase (ecNOS) gene polymorphism and vascular endothelial function has not been clarified. We investigated the impact of ecNOS gene polymorphism on endothelial function in 95 patients with Type 2 diabetes (ecNOS genotype: 4b/b, n = 62; 4b/a, n = 30; 4a/a, n = 3). Flow-mediated (endothelium dependent, FMD) and nitroglycerin-induced (endothelium independent, NTG) vasodilations of the right brachial artery were studied using a phase-locked echotracking system. There were no significant differences in clinical characteristics among the ecNOS genotypes. The FMD was significantly lower in the patients with ecNOS4a allele than in those without ecNOS4a allele (P < 0.05). Multiple regression analysis showed that ecNOS4a allele and mean blood pressure were significant independent determinants for reduced FMD in all patients (R(2) = 0.122, P = 0.0025). The ecNOS4a allele was an independent determinant for reduced FMD in smokers but not in nonsmokers. These results suggest that ecNOS4a allele is a genetic risk factor for endothelial dysfunction in diabetic patients, especially in smokers.

Aged↗
PubMed2003

Cytochrome P450 and manganese superoxide dismutase genes polymorphisms in systemic lupus erythematosus.

OBJECTIVES: To investigate the role of cytochrome P450 1A1 (CYP1A1) and manganese superoxide dismutase (Mn SOD) genes polymorphisms in the pathogenesis of systemic lupus erythematosus (SLE) in Taiwan. METHODS: CYP1A1 and Mn SOD genes polymorphisms were determined by the polymerase chain reaction/restriction fragment length polymorphism (RFLP) method in 90 patients with SLE and 94 healthy controls. RESULTS: The genotype frequency of CYP1A1 4887C/A was significantly higher in patients with SLE than in controls. The allele and phenotype frequencies of CYP1A1 4887A were also significantly increased in SLE patients. In contrast, there were no significant differences in the genotype, allele and phenotype frequencies of Mn SOD C1183T polymorphisms between patients with SLE and controls. We also found that SLE patients with CYP1A1 4887A had a trend of increasing prevalence of renal involvement, while Mn SOD C1183T polymorphisms were not associated with the renal involvement in SLE. CONCLUSIONS: CYP1A1 4887A may be a precipitating factor for the development of SLE. It also tended to be associated with the occurrence of renal involvement in SLE patients. A synergistic effect was found between CYP1A1 4887C/A and Mn SOD 1183T/T on the susceptibility to SLE.

Adult↗
PubMed2003

Cholecystokinin, cholecystokinin-A receptor and cholecystokinin-B receptor gene polymorphisms in Parkinson's disease.

Cholecystokinin modulates the release of dopamine and dopamine-related behaviours in the mesolimbic pathway, where cholecystokinin and dopamine coexist in dopaminergic neurones. Because cholecystokinin and its receptors (A and B) have a functional interaction with dopaminergic neurotransmission, alterations in them may constitute a predisposition for Parkinson's disease. We performed a case-control study to investigate the association between the cholecystokinin system and Parkinson's disease using genetic markers for three genes: cholecystokinin and its two receptors (A and B). One hundred and sixty patients with Parkinson's disease and 160 controls, matched for age, gender, ethnic origin and area of residence, were recruited. Cholecystokinin -45C>T, cholecystokinin-A receptor 779T>C and cholecystokinin-B receptor 1550G>A gene polymorphisms were studied using polymerase chain reaction-restriction fragment length polymorphism analyses. These three gene polymorphisms showed no correlation with risk of Parkinson's disease; however, the cholecystokinin CT/TT genotype was associated with a 4.429-fold increased risk for visual hallucinations in Parkinson's disease. Cholecystokinin-A receptor and B receptor polymorphisms, considered alone, showed no correlation with hallucinations in Parkinson's disease; however, a combined effect was found in patients with hallucinations harboring both the cholecystokinin CT/TT and cholecystokinin-A receptor TC/CC genotypes. Parkinson's disease patients harboring this genotype have a 5.922-fold increased risk for developing visual hallucinations. These results suggest that, in Chinese, visual hallucinations in Parkinson's disease are associated with cholecystokinin -45C>T polymorphism, and this association was still observed in the presence of the cholecystokinin-A receptor TC/CC genotype, indicating a possible interaction of these two genes in the visual hallucinogenesis in Parkinson's disease.

Case-Control Studies↗
PubMed1997

The angiotensin II type 1 receptor gene polymorphism is associated with coronary artery vasoconstriction.

OBJECTIVES: This study sought to assess the potential association of the angiotensin-converting enzyme (ACE) and angiotensin II type 1 (AT1) receptor gene polymorphisms on coronary vasomotion in humans. BACKGROUND: Abnormal coronary vasomotion plays a role in the clinical expression of coronary atherosclerosis. The components of the renin-angiotensin system are important determinants of vasomotor tone. Furthermore, epidemiologic evidence suggests that these components are involved in the pathogenesis of coronary artery disease. Indeed, two genetic polymorphisms of the ACE and AT1 receptor genes were synergistically associated with the occurrence of myocardial infarction. The influence of these genetic polymorphisms on the risk of myocardial infarction may be related, at least in part, to a deleterious effect on coronary vasomotion. METHODS: We studied the response of angiographically normal human coronary arteries after intravenous injection of methylergonovine maleate, a potent vasoconstrictor whose effects have been previously explored in various aspects of coronary artery disease. We characterized the ACE and AT1 receptor genotypes in a consecutive series of 140 patients with normal coronary arteries. Coronary vasomotion was assessed with quantitative coronary angiography. RESULTS: No effect of the ACE gene polymorphism was detected. Conversely, the patients carrying the AT1 receptor CC genotype (n = 13) had significantly greater vasoconstriction in distal coronary vessels (p < 0.009). CONCLUSIONS: The AT1 receptor gene polymorphism is associated with coronary vasomotion in humans.

Adult↗
PubMed1998

[Association between ACE gene polymorphism and therapeutic responsiveness of ACEI in diabetic nephropathy].

OBJECTIVE: [corrected] To clarify the association between ACE gene polymorphism and therapeutic responsiveness of ACEI in diabetic nephropathy. METHOD: With the polymerase chain reaction technique, the angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism was studied in 31 NIDDM patients, 58 NIDDM patients with nephropathy, and 50 normal controls. RESULTS: There was no significant difference in the frequency of ACE genotypes among those NIDDM patients, NIDDM patients with nephropathy and nomal controls. Among 40 patients of DN group treated with ACE inhibitor(ACE-I), there was significant difference in genotype distribution between 19 efficacious cases and 21 nonefficacious cases: 8/2/9 vs 1/3/17 had DD/DI/II genotypes responsively (P < 0.01), DD genotype was best and II genotype was worst in therapeutic efficacy of ACE-I in NIDDM patients with nephropathy. CONCLUSION: The examination of ACE gene polymorphism is helpful for the diagnosis of the therapeutic efficacy of ACE-I in NIDDM with nephropathy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

The renin-angiotensin system and endothelial nitric oxide synthase gene polymorphisms and cyclosporine toxicity in renal transplant patients.

Although cyclosporine has improved graft survival, the toxicity of the drug frequently causes problem for renal transplant patients. Cyclosporine displays deleterious effects due to direct toxicity to the nephrons and vasoconstriction of afferent arterioles, effects that may be due to increased angiotensin II and decreased nitric oxide activity. We sought to examine the relation between cyclosporine toxicity and the RAS (angiotensin-converting enzyme, angiotesinogen, angiotensin 1 and 2 receptors, and ecNOS) gene polymorphisms in 111 renal transplant patients. Retrospectively, we correlated the results of graft biopsies from these 111 patients, with the cumulative drug doses (mg), mean blood levels (mg/mL), mean daily doses (mg), and mean doses (mg/kg/d) of cyclosporine. Overall 125 patients (38 women, 87 men) were enrolled in the study. Their mean age was 34.47 +/- 11.04 years. Twenty patients displayed cyclosporine toxicity on graft biopsy; 91 showed no evidence of the disorder. We could not find any relation between cyclosporine toxicity and gene polymorphisms (P >.05), although the mean mg/kg/d dose was significantly high among cyclosporine toxicity group (P =.028, RR = 1.42). In recent studies angiotensin II and nitric oxide have been suggested to be related to cyclosporine toxicity; however, our results failed to reveal an association between cyclosporine toxicity and angiotensin II or nitric oxide-related gene polymorphisms.

Angiotensinogen↗
PubMed2002

Preproendothelin-1 gene polymorphism is related to a change in vascular reactivity in the human mammary artery in vitro.

A gene polymorphism of preproendothelin-1 (a G-to-T transversion that predicts a Lys/Asn change at codon 198) associated with an increased risk of hypertension has been recently described in patients carrying the T allele. No study has yet determined the impact of this polymorphism on vascular reactivity, although a functional role for endothelin-1 in the pathophysiology of hypertension has been clarified. At subthreshold concentrations, endothelin-1 and angiotensin II induce a potentiation of alpha-adrenergic-dependent vascular tone caused by an increased sensitivity of the contractile apparatus to calcium. We investigated phenylephrine-induced tone and its amplification by endothelin-1 and angiotensin II in human mammary artery rings in vitro. Contractions to phenylephrine (0.1 to 100 micromol) and endothelin-1 (0.1 to 300 nmol) were not significantly different in rings from GT/TT (n=27) and GG (n=21) patients. A subthreshold concentration of endothelin-1 (10 pmol) potentiated a phenylephrine-induced contraction (eg, 44 +/- 12% increase in tone with phenylephrine 1 micromol/L, P<0.001) that was significantly higher in the GT/TT group than in the GG group (eg, 44 +/- 12% versus 82 +/- 11%, P<0.01). A similar effect on response to phenylephrine was observed with a subthreshold concentration of angiotensin II. We also found a higher response to calcium in arteries from GT/TT patients. Endothelium-dependent or -independent relaxations were unaffected by the genotype. These data suggest that the preproendothelin-1 gene polymorphism is associated with a higher potentiating effect of endothelin-1 and angiotensin II, probably in relation with higher calcium sensitivity. These changes in vascular reactivity might help to understand the relations between this polymorphism and cardiovascular disorders.

Acetylcholine↗
PubMed2000

Aging affects the association between endothelial nitric oxide synthase gene polymorphism and acute myocardial infarction in the Korean male population.

OBJECTIVES: The aging process affects responsiveness and other functions of endothelium and vascular smooth muscle cells, predisposing the old vessels to the development of atherosclerotic lesions. Endothelial nitric oxide synthase (ecNOS) gene polymorphisms were shown to affect the occurrence of acute myocardial infarction (AMI). We hypothesized that aging may affect the association between the ecNOS gene polymorphism and AMI. METHODS: We investigated the age-related distribution of the ecNOS gene a/b polymorphism in 121 male AMI patients and 206 age-matched healthy male controls. RESULTS: The aa, ab and bb genotypes were found in 1, 49 and 156 cases among the control subjects and 5, 23 and 93 cases among the AMI patients, respectively. There was a significant correlation between the ecNOS polymorphism and AMI (p = 0.045). When the correlation was analyzed by age, the significance remained only in the group below the age of 51 (p = 0.009). The proportion of smokers was increased in the young patients when compared to the old patients (p = 0.033), indicating that smoking also has greater effect on the younger population. The incidences of hypertension and diabetes mellitus, however, were similar in both populations. CONCLUSION: Our work provides the first evidence that links ecNOS polymorphism to the risk of AMI in relation to age. Young persons who smoke or have ecNOSaa genotype may have an increased risk of developing AMI. The functional as well as structural changes associated with aging in the vascular endothelium may mask the effect of the ecNOS polymorphism in the development of AMI in old persons.

Adult↗
PubMed2003

Lack of association of catechol-O-methyltransferase gene polymorphism in obsessive-compulsive disorder.

The COMT gene has been implicated to be involved in the pathogenesis of obsessive-compulsive disorder (OCD) and various other psychiatric disorders. COMT enzyme activity is governed by a common genetic polymorphism at codon 158 that results in substantial 3- to 4-fold variation in enzymatic activity [a high-activity COMT variant (H) and a low activity variant (L)]. This study evaluates the association between OCD and the COMT gene polymorphism. Fifty-nine OCD patients that were diagnosed according to DSM-IV criteria and 114 healthy control subjects were included in the study. PCR technique was used for molecular analysis. The genotypic pattern of distribution of the COMT gene (H/H, H/L, and L/L genotypes) was not different between the OCD patients and controls. There were no significant differences among the patients with positive family history for OCD, those with negative family history for OCD, and the controls with respect to allele frequencies of the COMT gene polymorphisms. Patients that were homozygous or heterozygous for the L allele had significantly higher insight scores (i.e., poorer insight) on Y-BOCS compared to those homozygous for the H allele. We did not find an association between OCD, family history for OCD, and the COMT gene polymorphism. This study suggests that the COMT gene polymorphism is not directly associated with OCD in our patient group.

Adolescent↗
PubMed2004

Analysis of interleukin-1 receptor antagonist gene polymorphism in Chinese patients with Alzheimer's disease.

OBJECTIVE: To identify an interaction between the interleukin-1 receptor antagonist gene polymorphism and risk of Alzheimer's disease. METHODS: The study included 117 healthy controls, 85 patients with Alzheimer's disease in a Northeastern Chinese population of Han nationality. Genotypes were determined by a polymerase chain reaction amplification of the intron 2 fragment, harbouring a variable number of short tandem nucleotide sequences. Amplification products were separated on a 2% agarose gel. RESULTS: The allele 2 frequency was 27% in healthy controls, and 21% in patients with Alzheimer's disease. Thus for allele 2 as well as for all other alleles, genotypes, or carriage rates, no significant differences compared with controls. CONCLUSIONS: No association of interleukin-1 receptor antagonist gene polymorphism with Alzheimer's disease was identified in this population. It is also possible that the increased risk and disease modifying effects are caused by linkage disequilibrium with other genomic variants in other nearby genes.

Aged↗
PubMed2002

[Frequency of donor TNF-alpha gene polymorphism in patients with graft versus host disease following hematopoietic stem cell transplantation].

To study the effect of donor TNF-alpha gene polymorphism on severe acute and extensive chronic graft versus host disease (GVHD), TNF-alpha gene polymorphism was analyzed by denaturing high performance liquid chromatography (DHPLC) and DNA sequencing in twenty-one patients with III/IV degree acute GVHD and twenty-seven patients with extensive chronic GVHD. The results showed that the frequency of TNF-alpha-308 (G/A) significantly increased in patients with III/IV degree acute GVHD compared to 0/I degree aGVHD patients (8/21 vs 1/28) (P < 0.01) and the frequency of TNF-alpha-308 (G/A) is significantly higher in patients with extensive chronic GVHD than in patients without chronic GVHD (7/23 vs 1/17) (P < 0.05). However, the frequency of TNF-alpha-238 (G/A) does not significantly changed in patients with III/IV degree acute GVHD and extensive chronic GVHD. In conclusion, the TNF-alpha-308 (G/A) is likely to contribute to high risk for III/IV degree acute GVHD and extensive chronic GVHD.

Base Sequence↗