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Search Results: 1 - 10 of 401662 matches for " Winfried M?rz "
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Effect of the rs2259816 polymorphism in the HNF1A gene on circulating levels of c-reactive protein and coronary artery disease (the ludwigshafen risk and cardiovascular health study)
Marcus E Kleber, Tanja B Grammer, Wilfried Renner, Winfried Mrz
BMC Medical Genetics , 2010, DOI: 10.1186/1471-2350-11-157
Abstract: We investigated the association of the rs2259816 polymorphism in the HNF1A gene with the circulating level of C-reactive protein and the hazard of coronary artery disease in the LURIC Study cohort.Compared to CC homozygotes, the level of C-reactive protein was decreased in carriers of at least one A-allele. Each A-allele decreased CRP by approximately 15%. The odds ratio for coronary artery disease was only very slightly increased in carriers of the A-allele and this association did not reach statistical significance.In the LURIC Study cohort the A-allele of rs2259816 is associated with decreased CRP but not with coronary artery disease.C-reactive protein (CRP) is a well established biochemical marker of inflammation and has been used to predict future cardiovascular disease [1-3]. As its level is increased in patients suffering from coronary artery disease (CAD) the idea has been put forward that it might play an active role in the development of the disease. Although numerous studies have been conducted, this issue has not been finally settled yet [4-6]. Most of these studies didn't find an association between CRP and CAD [7-13] whereas a few did present some evidence in favor of this idea [14-16].A recent meta-analysis has shown that associations of CRP with ischemic vascular disease depend considerably on conventional risk factors and other markers of inflammation making a causal role of CRP in the development of CAD also unlikely [17].Genetic factors have been estimated to have a great influence on the variance in plasma CRP level [18-20]. A number of polymorphisms of the CRP gene (MIM 123260) or its promoter that act in this way have been described so far [8-11,14-16,21-32] but they only account for a minor part of the assumed heritability.Recently, polymorphisms in the HNF1A gene (also known asTCF1, MIM 142410) have been linked to the levels of C-reactive protein and coronary artery disease [33-36]. This gene encodes the transcription factor hepatocyte nuclea
Genetic variants of the promoter of the heme oxygenase-1 gene and their influence on cardiovascular disease (The Ludwigshafen Risk and Cardiovascular Health Study)
Nicola Lüblinghoff, Karl Winkler, Bernhard R Winkelmann, Ursula Seelhorst, Britta Wellnitz, Bernhard O Boehm, Winfried Mrz, Michael M Hoffmann
BMC Medical Genetics , 2009, DOI: 10.1186/1471-2350-10-36
Abstract: We included 3219 subjects in the current analysis, 2526 with CAD including a subgroup of CAD and MI (n = 1339) and 693 controls. Coronary status was determined by coronary angiography. Risk factors and biochemical parameters (bilirubin, iron, LDL-C, HDL-C, and triglycerides) were determined by standard procedures. The dinucleotide repeat was analysed by PCR and subsequent sizing by capillary electrophoresis, the -413A>T polymorphism by PCR and RFLP.In the LURIC study the allele frequency for the -413A>T polymorphism is A = 0,589 and T = 0,411. The (GT)n repeats spread between 14 and 39 repeats with 22 (19.9%) and 29 (47.1%) as the two most common alleles. We found neither an association of the genotypes or allelic frequencies with any of the biochemical parameters nor with CAD or previous MI.Although an association of these polymorphisms with the appearance of CAD and MI have been published before, our results strongly argue against a relevant role of the (GT)n repeat or the -413A>T SNP in the HMOX1 promoter in CAD or MI.Low-grade inflammation and oxidation are important mechanisms involved in the complex pathological process of atherogenesis [1]. Several cardiovascular risk factors, such as smoking, type 2 diabetes, hypertension, and dyslipidemia, increase the production of reactive oxygen species (ROS) in the arterial wall. In response to oxidative stress the expression of endogenous stress proteins including heme oxygenase (HO) is increased. HO is a rate-limiting enzyme in the degradation of heme to biliverdin releasing equimolar quantities of free iron and carbon monoxide, a potent anti-apoptotic and proliferation promoting compound [2]. The reduction of biliverdin by biliverdin reductase leads to the generation of bilirubin, a potent endogenous antioxidant [3,4]. Recently, it could be shown that bilirubin has an antiproliferative effect on vascular smooth muscle cells, too [5].In humans two isoforms of heme oxygenase, HO-1 and HO-2, have been described. HO-1 is
Genetic variation in Fcγ receptor IIa and risk of coronary heart disease: negative results from two large independent populations
Mahir Karakas, Michael M Hoffmann, Caren Vollmert, Dietrich Rothenbacher, Christa Meisinger, Bernhard Winkelmann, Natalie Khuseyinova, Bernhard O B?hm, Thomas Illig, Winfried Mrz, Wolfgang Koenig
BMC Medical Genetics , 2009, DOI: 10.1186/1471-2350-10-46
Abstract: FcγRIIa-R/H131 polymorphisms were determined in a population of 527 patients with a history of myocardial infarction and 527 age and gender matched controls drawn from a population-based MONICA- Augsburg survey. In the LURIC population, 2227 patients with angiographically proven CHD, defined as having at least one stenosis ≥ 50%, were compared with 1032 individuals with stenosis <50%.In both populations genotype frequencies of the FcγRIIa gene did not show a significant departure from the Hardy-Weinberg equilibrium. FcγRIIa R(-131) → H genotype was not independently associated with lower risk of CHD after multivariable adjustments, neither in the MONICA population (odds ratio (OR) 1.08; 95% confidence interval (CI) 0.81 to 1.44), nor in LURIC (OR 0.96; 95% CI 0.81 to 1.14).Our results do not confirm an independent relationship between FcγRIIa genotypes and risk of CHD in these populations.Fcγ receptors (FcγR) bind the Fc portion of immunoglobulin (Ig) and thereby link antigen recognition by antibodies with cell-based effector mechanisms [1-4]. Although FcγRIIa (or CD32) [GenBank: BC019931] is expressed on various cells involved in atherogenesis like monocytes, macrophages, platelets and neutrophils, and though it has been detected immunocytochemically in human atherosclerotic lesions, its potential active role in atherosclerosis is still a matter of controversy [5,6]. Calverley et al. showed FcγRIIa expression to be increased in platelets of patients experiencing an acute atherothrombotic event or who were clinically healthy but had two or more atherosclerosis risk factors; by contrast, Pfeiffer et al. reported decreased expression of FcγRIIa on peripheral blood monocytes in patients with severe atherosclerosis [7,8].A specific genetic polymorphism affecting its function has been described in the FcγRIIa, causing an amino acid exchange from arginine (R) to histidine (H) at position 131. H131 is the only FcγR that recognizes IgG2 efficiently. The codominantly express
Homoarginine and Progression of Chronic Kidney Disease: Results from the Mild to Moderate Kidney Disease Study
Christiane Drechsler, Barbara Kollerits, Andreas Meinitzer, Winfried Mrz, Eberhard Ritz, Paul K?nig, Ulrich Neyer, Stefan Pilz, Christoph Wanner, Florian Kronenberg, for the MMKD Study Group
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063560
Abstract: Background Homoarginine is an amino acid derivative mainly synthesized in the kidney. It is suggested to increase nitric oxide availability, enhance endothelial function and to protect against cardiovascular diseases. We aimed to investigate the relation between homoarginine, kidney function and progression of chronic kidney disease (CKD). Methods We measured plasma homoarginine concentrations in baseline samples of the Mild to Moderate Kidney Disease (MMKD) Study, a prospective cohort study of 227 patients with CKD in Europe. Homoarginine concentrations were available in 182 of the baseline samples and in 139 of the prospectively-followed patients. We correlated homoarginine concentrations to parameters of kidney function. The association between homoarginine and progression of CKD was assessed during a follow-up of up to seven years (median 4.45 years, interquartile range 2.54–5.19) using Cox regression analysis. Progression of CKD was defined as doubling of baseline serum creatinine and/or end-stage renal disease. Results Study participants were at baseline on average 47±13 years old and 65% were male. Mean±standard deviation of homoarginine concentrations were 2.5±1.1 μmol/L and concentrations were incrementally lower at lower levels of GFR with mean concentrations of 2.90±1.02 μmol/L (GFR>90 ml/min), 2.64±1.06 μmol/L (GFR 60–90 ml/min), 2.52±1.24 μmol/L (GFR 30–60 ml/min) and 2.05±0.78 μmol/L (GFR<30 ml/min), respectively (p = 0.002). The age- and sex-adjusted risk to reach the renal endpoint was significantly higher by 62% with each decrease by one standard deviation (1.1 μmol/L) of homoarginine (HR 1.62, 95% CI 1.16–2.27, p = 0.005). This association was independent of proteinuria (HR 1.56, 95% CI 1.11–2.20, p = 0.01), and was slightly attenuated when adjusting for GFR (HR 1.40 (95% CI 0.98–1.98, p = 0.06). Conclusions Homoarginine concentrations are directly correlated with kidney function and are significantly associated with the progression of CKD. Low homoarginine concentrations might be an early indicator of kidney failure and a potential target for the prevention of disease progression which needs further investigations.
A Variant In the Abo Gene Explains the Variation in Soluble E-Selectin Levels—Results from Dense Genotyping in Two Independent Populations
Mahir Karakas, Jens Baumert, Marcus E. Kleber, Barbara Thorand, Dhayana Dallmeier, Günther Silbernagel, Tanja B. Grammer, Wolfgang Rottbauer, Christa Meisinger, Thomas Illig, Winfried Mrz, Wolfgang Koenig
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051441
Abstract: Background Elevated soluble (s) E-selectin levels have been associated with various cardiovascular diseases. Recently, genetic variants in the ABO blood group have been related to E-selectin levels in a small cohort of patients with type 1 diabetes. We evaluated whether this association is reproducible in two large samples of Caucasians. Methodology/ Principal Findings Data of the present study was drawn from the population-based MONICA/KORA Augsburg study (n = 1,482) and the patients-based LURIC study (n = 1,546). A high-density genotyping array (50K IBC Chip) containing single-nucleotide polymorphisms (SNPs) from E-selectin candidate genes selected on known biology of E-selectin metabolism, mouse genetic studies, and human genetic association studies, was used for genotyping. Linear regression analyses with adjustment for age and sex (and survey in KORA) were applied to assess associations between gene variants and sE-selectin concentrations. A number of 12 SNPs (in KORA) and 13 SNPs (in LURIC), all from the ABO blood group gene, were significantly associated with the log-transformed concentration of E-selectin. The strongest association was observed for rs651007 with a change of log-transformed sE-selectin per one copy of the minor allele of ?0.37 ng/ml (p = 1.87×10?103) in KORA and ?0.35 ng/ml (p = 5.11×10?84) in LURIC. Inclusion of rs651007 increased the explained sE-selectin variance by 0.256 in KORA and 0.213 in LURIC. All SNPs had minor allele frequencies above 20% showing a substantial gene variation. Conclusions/ Significance Our findings in two independent samples indicate that the genetic variants at the ABO locus affect sE-selectin levels. Since distinct genome-wide association studies linked the ABO gene with myocardial infarction (MI) in the presence of coronary atherosclerosis and with coronary artery disease, these findings may not only enhance our understanding of adhesion molecule biology, but may also provide a focus for several novel research avenues.
The MHC2TA -168A>G gene polymorphism is not associated with rheumatoid arthritis in Austrian patients
Babak Yazdani-Biuki, Kerstin Brickmann, Klaus Wohlfahrt, Thomas Mueller, Winfried Mrz, Wilfried Renner, Manuela Gutjahr, Uwe Langsenlehner, Peter Krippl, Thomas C Wascher, Bernhard Paulweber, Winfried Graninger, Hans-Peter Brezinschek
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar1974
Abstract: Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune disease characterized by inflammation of the synovium and subsequent joint destruction [1]. It is a complex disease, with genetic and environmental factors contributing to its etiology. The prevalence of RA in Europe ranges from 0.3% to 1.6%, with higher prevalence in the north of Europe [2]. Studies in twins suggest that the genetic component of RA accounts for approximately 60% of disease susceptibility [3].The concept of a strong genetic component to susceptibility to RA is well established, and the HLA-DRB1 locus is estimated to account for approximately 30% [4]. Several HLA-DRB1 alleles encoding the 'shared epitope' are recognized as disease-risk alleles or disease-severity alleles [5-7]. In addition, a strong association between RA-specific autoantibodies and PTPN22 has been reported [8,9]. Several genome-wide linkage studies and numerous association studies involving positional and/or functional candidate genes have tried to identify further RA susceptibility loci, with controversial results in different populations [10,11].Swanberg and colleagues recently reported an association of a common -168A>G polymorphism in the MHC2TA gene with differential major histocompatibility complex (MHC) II molecule expression and susceptibility to diseases with inflammatory components, such as multiple sclerosis or RA [12]. Although the results of that study were convincing and biologically plausible, the need for replication of this association has been raised [13].The aim of this study was therefore to validate and extend the reported association of the MHC2TA -168A>G polymorphism with RA in a group of 373 Austrian Caucasian RA cases and 373 healthy Austrian Caucasian controls.A total of 362 RA patients and 351 healthy controls, all Caucasians, were included in the study after informed consent and approval by the local ethics committee were obtained. All patients fulfilled the American College of Rheumatology (
Single Nucleotide Variants in the Protein C Pathway and Mortality in Dialysis Patients
Gürbey Ocak, Christiane Drechsler, Carla Y. Vossen, Hans L. Vos, Frits R. Rosendaal, Pieter H. Reitsma, Michael M. Hoffmann, Winfried Mrz, Willem H. Ouwehand, Raymond T. Krediet, Elisabeth W. Boeschoten, Friedo W. Dekker, Christoph Wanner, Marion Verduijn
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097251
Abstract: Background The protein C pathway plays an important role in the maintenance of endothelial barrier function and in the inflammatory and coagulant processes that are characteristic of patients on dialysis. We investigated whether common single nucleotide variants (SNV) in genes encoding protein C pathway components were associated with all-cause 5 years mortality risk in dialysis patients. Methods Single nucleotides variants in the factor V gene (F5 rs6025; factor V Leiden), the thrombomodulin gene (THBD rs1042580), the protein C gene (PROC rs1799808 and 1799809) and the endothelial protein C receptor gene (PROCR rs867186, rs2069951, and rs2069952) were genotyped in 1070 dialysis patients from the NEtherlands COoperative Study on the Adequacy of Dialysis (NECOSAD) cohort) and in 1243 dialysis patients from the German 4D cohort. Results Factor V Leiden was associated with a 1.5-fold (95% CI 1.1–1.9) increased 5-year all-cause mortality risk and carriers of the AG/GG genotypes of the PROC rs1799809 had a 1.2-fold (95% CI 1.0–1.4) increased 5-year all-cause mortality risk. The other SNVs in THBD, PROC, and PROCR were not associated with 5-years mortality. Conclusion Our study suggests that factor V Leiden and PROC rs1799809 contributes to an increased mortality risk in dialysis patients.
Changes in the Prevalence, Treatment and Control of Hypertension in Germany? A Clinical-Epidemiological Study of 50.000 Primary Care Patients
Alexander Michael Labeit, Jens Klotsche, Lars Pieper, David Pittrow, Franziska Einsle, Günter Karl Stalla, Hendrik Lehnert, Sigmund Silber, Andreas Michael Zeiher, Winfried Mrz, Martin Wehling, Hans-Ulrich Wittchen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0052229
Abstract: Introduction Medical societies have developed guidelines for the detection, treatment and control of hypertension (HTN). Our analysis assessed the extent to which such guidelines were implemented in Germany in 2003 and 2001. Methods Using standardized clinical diagnostic and treatment appraisal forms, blood pressure levels and patient questionnaires for 55,518 participants from the cross-sectional Targets and Essential Data for Commitment of Treatment (DETECT) study (2003) were analyzed. Physician’s diagnosis of hypertension (HTNdoc) was defined as coding hypertension in the clinical appraisal questionnaire. Alternative definitions used were physician’s diagnosis or the patient’s self-reported diagnosis of hypertension (HTNdoc,pat), physician’s or patient’s self-reported diagnosis or a BP measurement with a systolic BP≥140 mmHg and/or a diastolic BP≥90 (HTNdoc,pat,bp) and diagnosis according to the National Health and Nutrition Examination Survey (HTNNHANES). The results were compared with the similar German HYDRA study to examine whether changes had occurred in diagnosis, treatment and adequate blood pressure control (BP below 140/90 mmHg) since 2001. Factors associated with pharmacotherapy and control were determined. Results The overall prevalence rate for hypertension was 35.5% according to HTNdoc and 56.0% according to NHANES criteria. Among those defined by NHANES criteria, treatment and control rates were 56.0% and 20.3% in 2003, and these rates had improved from 55.3% and 18.0% in 2001. Significant predictors of receiving antihypertensive medication were: increasing age, female sex, obesity, previous myocardial infarction and the prevalence of comorbid conditions such as coronary heart disease (CHD), hyperlipidemia and diabetes mellitus (DM). Significant positive predictors of adequate blood pressure control were CHD and antihypertensive medication. Inadequate control was associated with increasing age, male sex and obesity. Conclusions Rates of treated and controlled hypertension according to NHANES criteria in DETECT remained low between 2001 and 2003, although there was some minor improvement.
Be Prepared - Teaching Students what they need to know []
Mrz, Richard
GMS Zeitschrift für Medizinische Ausbildung , 2007,
Abstract:
Gesellschaftsmitteilungen
Mrz R
Zeitschrift für Gef??medizin , 2005,
Abstract:
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