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At least 289 records · Page 16Linked to original sources
PubMed2004

Monocyte chemoattractant protein-1 (MCP1) promoter -2518 polymorphism may confer a susceptibility to major depressive disorder in the Korean population.

We conducted a case-control association study of the monocyte chemoattractant protein-1 (MCP1) gene -2518 polymorphism in 90 patients with major depressive disorder. Genotyping was performed by polymerase chain reaction methods. We found significant differences in genotype and allele frequencies. The present study suggests that this polymorphism may confer a susceptibility to major depressive disorder in the Korean population.

Adult↗
PubMed2001

Interleukin-10 and tumor necrosis factor gene polymorphisms and risk of coronary artery disease and myocardial infarction.

Inflammation plays an important role in the pathogenesis of atherosclerosis and acute coronary syndromes. Cytokines IL-10 and TNF-alpha exert opposite functions in inflammatory reactions, IL-10 acting predominantly as an antiinflammatory and TNF-alpha as a proinflammatory factor. Functional single nucleotide polymorphisms in the genes of IL-10, TNF-alpha, and TNF-beta are associated with gene expression and plasma levels of IL-10 and TNF-alpha. The aim of the study was to assess whether these IL-10 and TNF gene polymorphisms are related to the risk of coronary artery disease (CAD) and myocardial infarction (MI). Consecutive, angiographically examined patients with significant coronary stenoses but without symptoms or signs of old or acute MI constituted the group with CAD (n=998) and patients with old or acute MI constituted the group with MI (n=793). Subjects with neither angiographic CAD nor symptoms or signs of MI (n=340) served as controls. They were matched with the patients for age and sex. Genotyping was performed with techniques based on the polymerase chain reaction. Allele frequencies, genotype distributions, and frequencies of allele combinations for three IL-10 promoter polymorphisms, -1082G/A, -819C/T and -592C/A, were similar between CAD patients, MI patients, and matched controls. Similarly, genetic analysis did not reveal group-specific differences for the TNF-alpha promoter polymorphisms -863C/A and -308G/A, as well as for the TNF-beta intron 1 polymorphism 252G/A. In addition, no relationship was found between specific combinations of IL-10 and TNF alleles, indicative of low IL-10 and high TNF-alpha production, respectively, and CAD or MI. The lack of association persisted also after adjusting for other cardiovascular risk factors. Our findings suggest that six different and functionally relevant polymorphisms of the genes coding for IL-10, TNF-alpha, and TNF-beta are neither separately nor in cooperation associated with the risk of CAD or MI in angiographically examined patients.

Coronary Disease↗
PubMed2002

DRD4 promoter SNPs and gender effects on Extraversion in African Americans.

There is strong evidence for genetic influences on personality traits. Interest in one such gene, the dopamine D4 receptor (DRD4) grew after an exon III polymorphism was associated with Novelty Seeking and related measures of Extraversion. However, the findings were not confirmed in later studies. Recently, a -521C/T single nucleotide polymorphism (SNP) within the promoter region of the DRD4 gene was found to be related to Novelty Seeking scores in populations from Japan and Hungary. Since little is known about the role DRD4 plays in personality in other populations we evaluated if two DRD4 promoter SNPs, -521C/T and -616C/G, were related to personality traits in African Americans. Personality traits were measured by the NEO-FFI in 71 unrelated African Americans. Genotyping was performed using PCR-RFLP. Multivariate analyses of variance (MANOVA) were performed to evaluate the effects of gender and -616 and -521 genotypes on personality traits. A significant three-way interaction effect from gender, -616 genotype, and -521 genotype was observed for Extraversion scores (F(1,54) 5.86, P < 0.02). Subsequent analyses revealed that the association was mainly due to -521C/T genotype among females (P = 0.01). This study provides further evidence that genetic variation within the DRD4 promoter and gender differences contribute to variation in Novelty Seeking behaviors such as Extraversion.

Adult↗
PubMed2003

Possible association between -G308A tumour necrosis factor-alpha gene polymorphism and major depressive disorder in the Korean population.

OBJECTIVE: The present study was aimed at examining the association between the -G308A tumour necrosis factor-alpha gene polymorphism and major depressive disorder (MDD) in the Korean population. METHODS: One hundred and eight in-patients with MDD and 125 healthy controls participated in this study. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: Genotype and allele distributions in patients with MDD (P=0.024 and P=0.0125, respectively), were significantly different from those of the controls. In particular, subjects with MDD had an increased frequency of the TNF2 (A) allele. CONCLUSION: The present study suggests that the -G308A tumour necrosis factor-alpha gene polymorphism may have a potential role for susceptibility to MDD in the Korean population.

Asian People↗
PubMed2006

Quantification of the power of Hardy-Weinberg equilibrium testing to detect genotyping error.

Deviation from Hardy-Weinberg equilibrium has become an accepted test for genotyping error. While it is generally considered that testing departures from Hardy-Weinberg equilibrium to detect genotyping error is not sensitive, little has been done to quantify this sensitivity. Therefore, we have examined various models of genotyping error, including error caused by neighboring SNPs that degrade the performance of genotyping assays. We then calculated the power of chi-square goodness-of-fit tests for deviation from Hardy-Weinberg equilibrium to detect such error. We have also examined the affects of neighboring SNPs on risk estimates in the setting of case-control association studies. We modeled the power of departure from Hardy-Weinberg equilibrium as a test to detect genotyping error and quantified the effect of genotyping error on disease risk estimates. Generally, genotyping error does not generate sufficient deviation from Hardy-Weinberg equilibrium to be detected. As expected, genotyping error due to neighboring SNPs attenuates risk estimates, often drastically. For the moment, the most widely accepted method of detecting genotyping error is to confirm genotypes by sequencing and/or genotyping via a separate method. While these methods are fairly reliable, they are also costly and time consuming.

Alleles↗
PubMed1999

DNA from urine sediment or buccal cells can be used for blood group molecular genotyping.

Accurate blood group antigen typing of red blood cells with a positive direct antiglobulin test or from a recently transfused patient has been a long-standing problem. To overcome this problem, we evaluated the feasibility of using somatic cells as a source of DNA for molecular genotyping. Two sources of cells that could be obtained by noninvasive procedures were chosen for analysis: urine samples, which were already available in the clinical laboratory, and buccal epithelial cells collected with cotton wool swabs. DNA, prepared using a commercial kit, was subjected to polymerase chain reaction amplification and followed by digestion with the appropriate restriction enzyme. Genotyping was performed for three alleles encoded by polymorphic genes on three different chromosomes, namely KEL1/KEL2, JKA/JKB, and FYA/FYB. Genotyping results were compared to the results of typing performed on red blood cells using standard hemagglutination techniques. Results given by samples freshly collected from volunteer donors were concordant. Although results obtained with samples collected from hospital patients were initially not in agreement with the phenotyping results, adjustments to the test protocol resulted in concordance. DNA from blood, urine sediment, or buccal cells can be used for blood group molecular genotyping.

Journal Article↗
PubMed1998

Genotypic characterization of seven strains of Mycoplasma fermentans isolated from synovial fluids of patients with arthritis.

We performed a genotypic characterization of seven strains of Mycoplasma fermentans which have been isolated from the synovial fluid of patients with rheumatoid arthritis (n = 2), spondyloarthropathy (n = 1), and unclassified arthritis (n = 4). We compared them to three reference strains (strains PG18 and K7 and incognitus strain) and to a clinical isolate from the urethra of a patient with nongonococcal urethritis. The characterization methods included electrophoresis of native DNA, arbitrarily primed PCR, and restriction fragment length polymorphism analysis following conventional and pulsed-field gel electrophoresis. Southern blot analysis with a probe internal to an insertion sequence was performed with the restriction products produced by the last two techniques. No extrachromosomal DNA sequences were detected. The M. fermentans strains identified by these methods did not present a unique profile, but they could be separated into two main categories: four articular isolates were genetically related to PG18 and the three other isolates, the urethral isolate, and the incognitus strain were related to K7. We also looked for the presence of the bacteriophage MAV1 (associated with the arthritogenic property of Mycoplasma arthritidis in rodents) in the M. fermentans strains. MAV1 DNA was not detected in either the clinical isolates or the reference strains of M. fermentans.

Adult↗
PubMed2002

Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy.

Angiotensin-converting enzyme (ACE) I/D polymorphism has been implicated as a genetic marker for progression of glomerular disease. Studies of ACE genotypes in adults with IgA nephropathy (IgAN) have yielded conflicting results. We performed ACE genotyping on 79 patients with IgAN diagnosed prior to age 18 years who had either progressed to end-stage renal disease (ESRD) or are now more than 5 years post biopsy. Mean follow-up was 14.8 years for those with normal renal function. Forty-three (54.4%) subjects had normal renal function and a normal urinalysis at last evaluation. Sixteen (20%) progressed to ESRD and 1 has chronic renal insufficiency. Kaplan-Meier survival curves for progression to ESRD did not differ significantly for the ACE DD, ID, and II genotype groups (P=0.095, log-rank test). By univariate analysis, presence of hypertension and degree of proteinuria at diagnosis, and unfavorable histology but not ACE genotype, was significantly associated with progression to ESRD. In the Cox proportional hazards model that included grade of proteinuria, the ACE D allele was a significant independent predictor of outcome with a hazard ratio of 2.37 (P=0.031). Our data, while inconclusive, suggest that the ACE D allele may associate with poor outcome in pediatric IgAN.

Adolescent↗
PubMed2003

Polymorphisms in the vitamin D receptor gene and the risk of calcium nephrolithiasis in children.

OBJECTIVE: Polymorphism in the Vitamin D Receptor (VDR) gene has recently been reported to be associated with calcium metabolism disorders. This study was conducted to investigate the association of VDR gene polymorphism with the risk of calcium nephrolithiasis. METHODS: We investigated the VDR ApaI, BsmI and TaqI polymorphisms, in relation to serum calcium, phosphate, intact parathyroid hormone and 1.25(OH)(2)D(3) in 64 hypercalciuric stone-forming children and 90 healthy children. DNA was isolated from peripheral blood, and genotyping was performed with PCR-based methods. RESULTS: The frequency of ApaI AA genotype was significantly higher in the children with calcium nephrolithiasis than the controls (chi(2)=9.5; p=0.008). The distribution of BsmI and TaqI genotypes in stone-forming patients was similar to those in the control group. There was a significant association between TaqI TT genotype and the strength of the family history. The patients with TT genotype were observed to have a 8 times more risk than patients with Tt/tt genotype for recurrent stone episodes (OR 8, 95%CI 1.61-39.6). CONCLUSION: VDR genotype determination may provide a tool to identify individuals who are at a risk for calcium nephrolithiasis.

Adolescent↗
PubMed1998

Plucked hair samples as a source of DNA: reliability of dinucleotide microsatellite genotyping.

To test whether plucked hairs are a reliable source of DNA for genotyping microsatellite loci, we carried out experiments using one, three, or 10 hairs per extract for 50 alpine marmots. For each extract, seven independent genotypings were performed for the same locus (multiple-tubes approach). Two types of genotyping errors were recorded: a false homozygote defined as the detection of only one allele of a true heterozygote, and a false allele defined as a PCR-generated allele that was not one of the alleles of the true genotype. Using DNA extracted from one, three, or 10 hairs the overall error rate was 14.00%, 4.86%, and 0.29%, respectively. Based on our results, we conclude that 10 hairs should be used to obtain consistently reliable genotypings using the single-tube approach, and that a single plucked hair could represent a reliable source of DNA if the multiple-tubes approach is used. For future studies of dinucleotide repeat diversity using DNA extracted from one to three shed or plucked hairs, we strongly recommend initiating an appropriate pilot study to quantify the error rate and to determine the reliability of the single-tube approach.

Alleles↗
PubMed1999

Adhesion molecule polymorphisms in chronic renal allograft failure.

BACKGROUND: Chronic allograft failure (CAF) is a major cause of late graft loss in renal transplantation. Up-regulation of adhesion molecules has been demonstrated in renal allograft biopsies during both acute and chronic rejection, and these molecules are known to regulate leukocyte migration into the graft. METHODS: A single-center retrospective study was performed between 1985 and 1996 on renal transplant recipients who developed CAF. Genotyping was performed for five polymorphisms in intercellular adhesion molecule-1 (ICAM-1), E-selectin, and L-selectin. Frequency data for the polymorphisms in the CAF group (N = 62) and their matched donors, where available (N = 33), were compared with a group of recipients with graft survival of more than 10 years (N = 110) and a group of United Kingdom (UK) controls (N = 101). RESULTS: A variant allele in exon 4 of ICAM-1 (R241) was more common in the CAF recipients compared with both long-term survivors and UK controls (19.4 vs. 10.0 and 9.4%, P = 0.015 and 0.025). In addition, stratification by time to graft failure caused by CAF revealed more rapid failure in the presence of another ICAM-1 variant in the recipient (E469) in exon 6 (P = 0.033). CONCLUSIONS: ICAM-1 polymorphisms may represent a predetermined genetic risk factor for CAF. The polymorphism in exon 4 is in the Mac-1 binding site, and that in exon 6 is in the fifth immunoglobulin-like domain. Potential mechanisms of action of ICAM-1 variants in CAF include an alteration of activity as an adhesion molecule, altered costimulation, or a minor histocompatibility antigen.

Alleles↗
PubMed2004

Glutathione S-transferase M1 polymorphism may contribute to schizophrenia in the Korean population.

The association between Glutathione S-Transferase M1 gene (GSTM1) polymorphism and schizophrenia was examined. One hundred and eleven in-patients with schizophrenia and 130 healthy controls were enrolled in this study. Genotyping was performed using a polymerase chain reaction-based method. The GSTM1 null genotype was significantly more frequent in the schizophrenia patients than in the controls (P=0.014, odds ratio=1.93, 95% confidence interval=1.115-3.351). On the other hand, the GSTM1 genotype variants were not associated with tardive dyskinesia or total abnormal involuntary movement scale scores. This study suggests that, at least in the Korean population, the GSTM1 polymorphism may confer susceptibility to the development of schizophrenia but not to tardive dyskinesia.

Adult↗
PubMed2003

Genotyping patients with recent blood transfusions.

BACKGROUND: Many studies have used polymerase chain reaction amplification (PCR) to genotype for common polymorphisms in intensive-care units (ICUs) where blood transfusions are common. Evidence that donor leukocytes in transfused blood can be detected by PCR of the recipient blood suggests that this minor population of donor white cells (microchimerism) can interfere with genotyping of allelic polymorphisms in critically ill transfused patients. To investigate this possibility, we assayed DNA extracted from the blood and buccal cells of ICU patients for 2 common polymorphisms in the TNF-beta gene and the surfactant protein-B (SP-B) gene. METHODS: Study subjects were ICU patients from the Massachusetts General Hospital (Boston, MA) enrolled into a study on the molecular epidemiology of acute respiratory distress syndrome between January 1999 and October 2000. Blood and buccal cells were collected and DNA was extracted from 145 patients. Genotyping was performed by enzyme digestion and pyrosequencing. RESULTS: The Kappa statistics comparing the genotype results from blood and buccal cells were 0.98 (95% confidence interval [CI] = 0.94-1.01) for TNFB and 0.95 (CI = 0.87-1.02) for SP-B. When the analysis was restricted only to the 107 patients who were transfused, the Kappa statistic remained high at 0.97 (CI = 0.93-1.01) for TNFB and 0.93 (CI = 0.84-1.03) for SP-B. CONCLUSION: We conclude that microchimerism from allogeneic blood transfusion is unlikely to have major effects on the genotype results of common polymorphisms in large molecular epidemiology studies conducted in the critical care setting if DNA is collected within a day after transfusions.

Alleles↗
PubMed2005

Neutrophil glutamine deficiency in relation to genotype in children with cystic fibrosis.

Pulmonary disease in cystic fibrosis (CF) is characterized by a chronic neutrophil-dominated inflammation of lung tissue. Inasmuch as some amino acids (AA) play a pivotal role in various aspects of neutrophil metabolism, the aim of this study was to investigate a possible alteration of neutrophil AA metabolism and to evaluate its relation (if any) with the genotype. We performed plasma and neutrophil AA analysis in 26 CF patients with known genotype, 10 patients with non-CF bronchiectasis, and 20 normal subjects. The CF group showed a significant decrease of free intracellular neutrophil glutamine (Gln) content compared with controls and the non-CF bronchiectasis group. In the latter group, levels of neutrophil Gln were significantly lower compared with the controls. Amino acid plasma concentration in non-CF bronchiectasis showed a decrease of Gln and taurine compared with controls. Neutrophil Gln content showed values significantly lower in CF patients with severe mutations (class I, II, and III mutations) compared with mild mutations (class IV and V mutations). Results of our study add further evidence for intrinsic neutrophil alterations that could play an important role in the pathogenesis of chronic pulmonary disease in CF patients.

Adolescent↗
PubMed2002

CYP2C19 genotype and S-mephenytoin 4'-hydroxylation phenotype in a Chinese Dai population.

AIMS: To investigate the incidence of the CYP2C19 polymorphism in the Chinese Dai population. METHODS: One hundred and ninety-three healthy Chinese Dai volunteers were identified with respect to CYP2C19 by genotype and phenotype analyses. A polymerase chain reaction-restriction fragment length polymorphism method was performed for genotyping procedures. The 4'-hydroxymephenytoin (4'-OH-MP) and S/R-mephenytoin ( S/R-MP) excreted in the urine were determined by high-performance liquid chromatography and gas chromatography, respectively. RESULTS: Eighteen subjects were identified as poor metabolisers (PMs). The frequency of PMs in the Chinese Dai subjects was 9.3% (95% confidence interval 5.2, 13.4), which is lower than that in the Chinese Han population ( P<0.05). Chinese Dai subjects had a higher frequency of the mutant CYP2C19*2 allele (0.303) and a lower frequency of the mutant CYP2C19*3 allele (0.034). These two mutant alleles could explain all deficiencies of CYP2C19 activity in the Chinese Dai subjects. The frequency of the CYP2C19*3 allele is significantly lower than that in the Chinese Han population ( P<0.05). The mean S/R ratio was lower in the homozygous extensive metabolisers (EMs) compared with that in heterozygous EMs ( P<0.01), and the latter was lower than that in the PMs ( P<0.01). Furthermore, the mean S/R ratio in CYP2C19*3/ CYP2C19*2 heterozygous PMs was possibly lower than that in the CYP2C19*2/ CYP2C19*2 homozygous PMs ( P<0.05). CONCLUSION: The frequencies of PMs and CYP2C19*3 allele in the Chinese Dai population are significantly lower than those in the Han population. The CYP2C19 genotype analysis is largely consistent with the mephenytoin phenotype analysis. The variability of S/R ratios in EMs and PMs shows a gene-dosage effect.

Adolescent↗
PubMed2003

Diet-dependent obesity and hypercholesterolemia in the New Zealand obese mouse: identification of a quantitative trait locus for elevated serum cholesterol on the distal mouse chromosome 5.

AIMS: New Zealand obese (NZO) mice exhibit a polygenic syndrome of obesity, insulin resistance, and hypercholesterolemia that resembles the human metabolic syndrome. This study was performed in order to locate genes responsible for elevated serum cholesterol and to compare their effects under a standard and high fat diet. METHODS: A backcross population of NZO with SJL mice (NZO x F1(SJL x NZO)) was generated. Mice were raised on a normal or high fat diet and were monitored for 22 weeks (body weight, serum cholesterol, and blood glucose). A genome-wide scan was performed by genotyping of approximately 200 polymorphic microsatellite markers by PCR and linkage analysis was performed with the MAPMAKER program. RESULTS: In the genome-wide scan, a single susceptibility locus for hypercholesterolemia (Chol1/NZO, maximum LOD score 14.5 in a combined population of 523 backcross mice) was identified on chromosome 5. Cholesterol levels were significantly elevated in both male and female homozygous carriers of the Chol1/NZO allele. The locus maps 40cM distal of the previously described obesity locus Nob1 in the vicinity of the marker D5Mit244 and in the vicinity of hypercholesterolemia QTL previously identified in the NZB, CAST, and C57BL/6J strains. Chol1/NZO was not associated with elevated body weight, serum insulin, or hyperglycemia. The high fat diet significantly increased serum cholesterol levels, but the fat content of the diet did not alter the absolute effect of Chol1/NZO. CONCLUSIONS: Chol1/NZO is a major susceptibility locus on the distal mouse chromosome 5, which produces gender-independent hypercholesterolemia in NZO mice. The effect of Chol1/NZO was independent of the dietary fat content and was not associated with the other traits of the metabolic syndrome. Thus, it is suggested that the responsible gene might be involved in cholesterol metabolism.

Animals↗
PubMed2006

Association of the PTPN22 R620W polymorphism with anti-topoisomerase I- and anticentromere antibody-positive systemic sclerosis.

OBJECTIVE: To determine any associations of the PTPN22 R620W single-nucleotide polymorphism (SNP) with systemic sclerosis (SSc) or with anticentromere antibody (ACA)-positive or anti-topoisomerase I (anti-topo I) antibody-positive SSc, in a case-control study of US white, black, Hispanic, and Choctaw Indian individuals. METHODS: A total of 850 white, 130 black, 120 Hispanic, and 20 Choctaw Indian patients with SSc were compared with 430 white, 164 black, 146 Hispanic, and 76 Choctaw Indian control subjects, respectively. All subjects were living in the US. PTPN22 SNP (rs2476601) genotyping was performed by TaqMan 5' allelic discrimination assay and pyrosequencing. RESULTS: The PTPN22 CT/TT genotype showed significant association with anti-topo I antibody-positive SSc in white patients (odds ratio [OR] 2.21, 95% confidence interval [95% CI] 1.3-3.7) and with ACA-positive white patients with SSc (OR 1.70, 95% CI 1.1-2.7). Frequency of the PTPN22*T allele also showed significant association with anti-topo I antibody-positive SSc in white patients (OR 2.03, 95% CI 1.3-3.2). When data for patients in the 3 ethnic groups (black, white, and Hispanic) were combined, a significant association with both genotype and allele frequencies was observed, suggesting a trend toward association in ACA-positive and anti-topo I antibody-positive SSc. Stepwise logistic regression analysis (controlled for the confounding effects of sex and race) showed that the PTPN22 CT/TT genotype was associated with a significantly higher risk of SSc compared with the CC genotype (for patients with SSc, OR 1.64, 95% CI 1.2-2.2; for ACA-positive patients with SSc, OR 1.63, 95% CI 1.0-2.6; for anti-topo I antibody-positive SSc, OR 2.33, 95% CI 1.5-3.7). CONCLUSION: Our results indicate that the PTPN22 R620W polymorphism is associated with ACA-positive and anti-topo I antibody-positive subsets of SSc and represents a risk factor in both white patients and black patients. The association of subsets of SSc with the PTPN22 R620W polymorphism further strengthens the classification of SSc within the spectrum of autoimmune diseases and strongly suggests the involvement of common susceptibility genes and similarly disordered immunoregulatory pathways.

Autoantibodies↗
PubMed2004

Association between TNF-alpha and TGF-beta genotypes in infants and parental history of allergic rhinitis and asthma.

The development and expression of allergic rhinitis and asthma may be influenced by the elaboration of specific cytokines. Cytokine genotypes moderate illness severity in a variety of inflammatory disorders. Cytokine genotyping was performed on 124 infants (85% white, 57% male) to determine whether specific cytokine genotypes are associated with a parental history of allergic rhinitis and/or asthma. DNA was extracted from buccal brushings and assayed for tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), interleukin (IL)-6, IL-10, and transforming growth factor (TGF)-beta1 genotypes using polymerase chain reaction-sequence specific primer technology. Outcomes consisted of parental history of allergy and asthma, and results were evaluated by logistic regression. TNF-alpha and TGF-beta genotypes were related to maternal and/or paternal history of allergic rhinitis and asthma, respectively. The frequencies of the genotype associated with high production of TNF-alpha were 41% versus 18% in infants with and without a parental history of allergic rhinitis, respectively (p < 0.01). The frequencies of the genotype associated with low production of TGF-beta1 were 14% versus 1% in infants with and without a parental history of asthma, respectively (p < 0.01). There were no associations between IFN-gamma, IL-6, and IL-10 genotypes and any of the outcome parameters. These results suggest a role for TNF-alpha and TGF-beta1 genotypes in the pathogenesis of allergic rhinitis and asthma, respectively. If confirmed by future studies, cytokine genotyping may be a useful tool for identifying at-risk infants who may benefit from the selective use of preventative and/or early intervention treatments for these disorders.

Asthma↗