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W Renner

Publications and source records attributed to W Renner.

At least 37 records · Page 2Linked to original sources
PubMed2001

Vascular dysfunction in hyperhomocyst(e)inemia. Implications for atherothrombotic disease.

Elevated plasma homocyst(e)ine is currently accepted as a major, independent risk factor for atherosclerosis and venous thrombosis. Even moderate hyperhomocyst(e)inemia is prospectively associated with increased risk of mortality in patients with cardiovascular disease. However, the underlying mechanisms resulting in vascular damage are not clearly defined. The endothelium exerts fundamental control on the vascular tone, coagulation and fibrinolysis. Injury to the endothelium followed by dysfunction is an early key event preceding manifestation of vessel pathology. Acute and chronic exposure of endothelium to homocyst(e)ine induces impairment of endothelial function associated with altered homeostasis and morphologic changes of the vessel wall. Investigations of the role of homocyst(e)ine in the endothelium-dependent function in healthy subjects and cardiovascular patients have recently added important clinical insight with implications for the treatment of cardiovascular disease. Importantly, the damaging effects of hyperhomocyst(e)inemia on endothelial function are, at least in part, reversible in patients with established vascular disease, supporting further the hypothesis that homocyst(e)ine-lowering through vitamin supplementation may have vasoprotective effects.

Endothelium, Vascular↗
PubMed2001

The PlA1/A2 polymorphism of platelet glycoprotein IIIa is not associated with deep venous thrombosis.

BACKGROUND: Platelet glycoprotein (GP) IIb/IIIa, a fibrinogen and von Willebrand factor binding membrane receptor, has an important role in platelet aggregation. A common leucine33-proline polymorphism (PlA1/A2) of the gene encoding the GP IIIa subunit is associated with platelet reactivity and has been proposed as a risk factor for atherothrombotic disease. The aim of this study was to investigate the role of this polymorphism for deep venous thrombosis (DVT). METHODS: We performed a case-control study including 206 patients with documented DVT and a sex- and age-matched group of 310 control subjects. GP IIIa genotypes were determined by restriction fragment analysis of amplimers containing the polymorphic site. RESULTS: A1/A1, A1/A2 and A2/A2 genotypes were found in 67.0, 31.6 and 1.5 percent of patients and 72.3, 25.8 and 1.9 percent of controls (p=0.35), PlA2 allele frequencies were 0.17 in patients and 0.15 in controls (p=0.92). Odds ratio of the PlA2 allele for DVT was 1.21 (95 percent CI 0.85-1.71, p=0.29) and remained insignificant after adjustment for factor V Leiden and prothrombin 20210A genotypes (1.22, 95 percent CI 0.86-1.75, p=0.27). CONCLUSIONS: Our data suggest that the PlA1/A2 polymorphism of GP IIIa is not associated with DVT.

Adult↗
PubMed2000

Prothrombin G20210A, factor V Leiden, and factor XIII Val34Leu: common mutations of blood coagulation factors and deep vein thrombosis in Austria.

Mutations in the gene for prothrombin (F2 20210A) and factor V (F5 1691A, factor V Leiden) are established risk factors for deep venous thrombosis (DVT). Recently, a mutation in the gene for factor XIII (F13 100T) leading to a Valine-Leucine exchange at amino acid position 34 has been reported to be protective against DVT. To analyze the role of these mutations for DVT in Austria, we analyzed their prevalence in 154 patients with documented DVT and 308 sex- and age-matched control subjects. Allele frequencies of F2 20210A, F5 1691A, and F13 100T were 0.018, 0.039, and 0.274 among controls, and 0.045, 0.120, and 0.211 among patients, respectively. Odds ratios for DVT associated with F2 20210A, F5 1691A, and F13 100T alleles were 2.5 (95% CI: 1.1-5.7), 3.4 (95% CI: 1.9-5.8), and 0.7 (95% CI: 0.5-1.0). We conclude that F2 20210A, F5 1691A, and F13 100T are common mutations in the Austrian population. F2 20210A and F5 1691 increase the risk for DVT, whereas F13 100T is associated with a decreased risk for DVT. Routinely, analysis of these mutations may help to analyze the individual risk for DVT.

Adolescent↗
PubMed2000

Venturesomeness and extraversion as correlates of juvenile drivers' traffic violations.

Ninety-eight juvenile traffic offenders, 81 men and 17 women, were examined regarding the personality traits of extraversion, neuroticism, psychoticism, impulsiveness and venturesomeness and compared with a control group of 149 applicants for driving licences, 82 male and 67 female. The participants of the study were administered German translations of the Eysenck personality questionnaire (EPQ-R) and the impulsiveness/venturesomeness/empathy questionnaire (IVE). Traffic offenders had significantly higher scores on the venturesomeness dimension as compared to the control group, and male offenders scored significantly higher on extraversion than did male controls. Hypotheses regarding a relationship between traffic offences and psychoticism and impulsiveness were not confirmed, however. It is concluded that traffic violations in juveniles should primarily be viewed within the scope of normal behaviour and do not necessarily imply serious personality disorder.

Accidents, Traffic↗
PubMed2000

C242T polymorphism of the p22 phox gene is not associated with peripheral arterial occlusive disease.

Formation of reactive oxygen metabolites is vital for the microbicidal activity of phagocytes. As an unwanted side effect, these metabolites may contribute to oxidative stress in the vasculature and thus lead to arteriosclerosis. p22 phox, a component of the NADH/NADPH oxidase in phagocytes and vascular smooth muscle cells, is essential for production of reactive oxygen metabolites. Recently, a C/T polymorphism at position 242 of the p22 phox gene has been associated with coronary artery disease (CAD), suggesting a protective effect of the 242 T allele on the vasculature. In the present study, we analysed the relation of this polymorphism to peripheral arterial occlusive disease (PAOD). C242T polymorphism was determined by restriction fragment polymorphism (RFLP) analysis in 324 patients with documented PAOD and 295 control subjects without any known arterial disease. p22 phox 242 T allele frequencies and genotype distributions were not significantly different between patients and controls; the adjusted relative risk associated with the 242 T allele was 1.14 (95% CI 0.84-1.54, P=0.39), assuming an additive effect of the T allele. C242T polymorphism was not associated with the age of patients at the onset of the disease. Our data indicate that C242T polymorphism of the p22 phox gene is not associated with PAOD.

Aged↗
PubMed2000

Association of the vitamin D receptor genotype BB with low bone density in hyperthyroidism.

Bone mineral density (BMD) is modulated by genetic and environmental factors or certain diseases. In several conditions such as low calcium intake, an influence of vitamin D receptor (VDR) polymorphisms on BMD has been suggested. In the present study, we investigated the relationship of Bsm I and Fok I polymorphisms of the VDR gene and BMD in patients with hyperthyroidism, a disease that often results in low BMD. Bsm I and Fok I genotypes were determined in 76 postmenopausal hyperthyroid patients and 62 healthy postmenopausal women as controls. Patients and controls were matched for age, time since menopause, and lifestyle factors and were free of estrogen medication. BMD evaluation included axial dual X-ray absorptiometry (DXA) and peripheral quantitative computed tomography (PQCT). Low BMD was defined as -2.5 STD below the young adult mean value. Biochemical parameters investigated were thyroid hormones, osteocalcin, and 25-(OH)-vitamin D3 as well as routine laboratory data. Low BMD was found in 61% of hyperthyroid patients and in only 23% of euthyroid controls. In the group of hyperthyroid patients with low bone density, the BB genotype (VDR Bsm I polymorphisms) was significantly more frequent (39%) than in controls (13%; p = 0.003) and hyperthyroid patients with normal BMD (6%; p = 0.013). The odds ratio (OR) for low BMD in patients with BB genotype was 5.7 (95% CI, 1.7-19.1; p < 0.005) as compared with the Bb and bb genotypes and 5.5 (95% CI, 2.3-13.2; p < 0.0001) for hyperthyroidism alone. The cumulative risk for low BMD in patients with hyperthyroidism and BB genotype was 31.4 (95% CI, 3.9-256; p < 0.0003). VDR Fok I genotypes showed no significant relationship with BMD or other general or bone-specific parameters. Thus, hyperthyroidism and the genetic background of a BB genotype may promote synergistically the development of low BMD in hyperthyroid patients. Screening for the BB genotype in these patients therefore could help to identify those with particularly high risk for the development of low BMD and allow early treatment.

Absorptiometry, Photon↗
PubMed2000

Factor II G20210A and factor V G1691A gene mutations and peripheral arterial occlusive disease.

BACKGROUND: G to A mutations at positions 20210 of the prothrombin gene (F2) and 1691 of the factor V gene (F5) are established risk factors for venous thrombosis. Several factors associated with coagulation and/or fibrinolysis have been associated with arterial occlusive disease, but the role of F2 20210A and F5 1691A for arterial occlusive disease remains unclear. OBJECTIVE: To investigate if F2 20210A and F5 1691A are associated with peripheral arterial occlusive disease (PAOD). METHODS AND RESULTS: We analyzed the prevalence of F2 20210A and F5 1691A alleles in 336 patients with documented PAOD at Fontaine stage II-IV and 300 controls without vascular disease. Allele frequencies in patients and controls were 0.013 and 0.022 for F2 20210A, and 0.042 and 0.045 for F5 1691, respectively, both differences being not statistically significant. CONCLUSION: Our data suggest that mutations F2 G20210A and F5 G1691A are not associated with PAOD.

Aged↗
PubMed1998

Apoptosis induced by filarial parasitic sheath protein in HEp 2 cell lines blocked by ectopic expression of bcl 2.

Chronic filarial patients exhibit an occult manifestation, Tropical Pulmonary Eosinophilia, (TPE), caused by an exaggerated immune response to shed and circulating filarial antigens, leading to extensive lung damage. We have attempted to examine the disease in vitro using the human epithelial cell line, HEp2. Filarial sheath proteins induce apoptosis in HEp2 cells characterized by chromatin condensation, internucleosomal DNA cleavage, positive staining for TUNEL assay and shows a sub-G1 peak on FACS analysis. In order to understand subcellular events and to analyse the protective role of bcl2, we engineered HEp2 to overexpress Bcl2 protein. HEp2 bcl2 cells do not undergo apoptosis on exposure to filarial sheath protein, indicating that filarial protein-induced apoptosis in epithelial cells proceeds via a pathway, inhibitable by overexpression of bcl 2.

Animals↗
PubMed1997

TraM of plasmid R1 controls transfer gene expression as an integrated control element in a complex regulatory network.

Site-directed mutagenesis was used to investigate the functions of the traM gene in plasmid R1-mediated bacterial conjugation. Three mutant alleles, a null mutation, a sense mutation and a stop mutation, were recombined back into the R1-16 plasmid, a transfer-derepressed (finO-) variant of plasmid R1. The frequency of conjugative transfer of the traM null mutant derivative of R1-16 was 10(7)-fold lower than that of the isogenic parent plasmid, showing the absolute requirement for this gene in conjugative transfer of plasmid R1. Measurements of the abundance of plasmid specified traJ, traA and traM mRNAs, TraM protein levels, and complementation studies indicated that the traM gene of plasmid R1 has at least two functions in conjugation: (i) positive control of transfer gene expression; and (ii) a function in a process distinct from gene expression. Since expression of the negatively autoregulated traM gene is itself affected positively by the expression of the transfer operon genes, this gene constitutes a decisive element within a regulatory circuit that co-ordinates expression of the genes necessary for horizontal DNA transfer. Based on our studies, we present a novel model for the regulation of the transfer genes of plasmid R1 that might also be applicable to other IncF plasmids.

Alleles↗
PubMed1995

Expression of genes kdsA and kdsB involved in 3-deoxy-D-manno-octulosonic acid metabolism and biosynthesis of enterobacterial lipopolysaccharide is growth phase regulated primarily at the transcriptional level in Escherichia coli K-12.

We have cloned and sequenced a cluster of six open reading frames containing gene kdsA from Escherichia coli K-12. The gene encodes 3-deoxy-D-manno-octulosonate 8-phosphate synthetase (KDO-8-phosphate synthetase), which catalyzes formation of 3-deoxy-D-manno-octulosonic acid (KDO), an essential component of enterobacterial lipopolysaccharide. We have also identified two other genes, hemA and prfA, at the beginning of the cluster. Deletion analysis shows that kdsA, the terminal gene of this putative operon, is transcribed from its own promoter located within the cluster rather than from two promoters preceding this group of six open reading frames. Northern (RNA) blot analysis as well as lacZ operon fusion experiments reveal that the expression of gene kdsA occurs maximally in the early log phase and falls to a low level in the late log and stationary phases. Hence, this gene is subjected to growth phase-dependent regulation at the transcriptional level. Similarly, we show that expression of gene kdsB, which codes for the CTP:CMP-3-deoxy-D-manno-octulosonate cytidyltransferase (CMP-KDO-synthetase), is also growth regulated. This enzyme catalyzes the activation of KDO via formation of CMP-KDO, which is necessary for the incorporation of KDO into lipid A. We have identified the promoter of gene kdsB, whose expression is growth regulated in the same way as that of kdsA. Despite the fact that transcription of genes kdsA and kdsB is shut off as cells enter stationary phase, KDO-8-phosphate synthetase as well as CMP-KDO-synthetase activities are still present at various levels during stationary-phase growth of an E. coli K-12 culture.

Aldehyde-Lyases↗
PubMed1989

[Clinical significance of intrinsic sympathomimetic activity of the beta blocker carteolol. II: Comparative studies of carteolol and pindolol in patients with bradycardia].

Completing previous studies in patients with sinus bradycardia (Med. Klin. 82 [1987], 647-650) we compared metoprolol with carteolol and pindolol, pindolol with carteolol, no treatment with carteolol (in two groups) in five series of the paired comparisons of Holter-ECG each. With change from metoprolol to carteolol or pindolol (dose ratio 10:1) lowest heart rate on Holter-ECG increased by 28 or 29% without change of exercise heart rate. Direct comparison of pindolol and carteolol revealed a very similar heart rate profile, indicating equipotent beta blockade and ISA. In patients with previous beta blocker induced bradycardia, carteolol did not change a normal resting heart rate off treatment. However, in patients with spontaneous sinus bradycardia carteolol increased lowest heart rate (+14%, due to overriding ISA) and lowered exercise heart rate (-15%, due to overriding beta blockade). A beta blocker induced sinus bradycardia consistently improved with change of treatment to carteolol and pindolol. With caution carteolol and pindolol may also be used despite spontaneous sinus bradycardia.

Adult↗