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739 results on '"Willeit J."'

152. Functional recovery after ischemic stroke — /INS;A matter of age. Results from/INS; the Austrian stroke unit registry

Author

Knoflach, M., primary, Matosevic, B., additional, Rücker, M., additional, Furtner, M., additional, Mair, A., additional, Wille, G., additional, Zangerle, A., additional, Werner, P., additional, Ferrari, J., additional, Schmidauer, C., additional, Seyfang, L., additional, Kiechl, S., additional, and Willeit, J., additional

Published
2013
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155. T-cell reactivity against HSP60 is a risk factor for early atherosclerosis.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep Infectieziekten Immunologie, Knoflach, M., Kiechl, S., Mayrl, B., Kind, M., Gaston, J.H., van der Zee, R., Faggionato, A., Mayr, A., Poewe, W., Willeit, J., Wick, G., Risk Assessment of Toxic and Immunomodulatory Agents, Dep Infectieziekten Immunologie, Knoflach, M., Kiechl, S., Mayrl, B., Kind, M., Gaston, J.H., van der Zee, R., Faggionato, A., Mayr, A., Poewe, W., Willeit, J., and Wick, G.

Published
2007

156. Identification of atherosclerosis-associated conformational heat shock protein 60 epitopes by phage display and structural alignment.

Author

Risk Assessment of Toxic and Immunomodulatory Agents, Dep Infectieziekten Immunologie, Perschinka, H., Wellenzohn, B., Parson, W., van der Zee, R., Willeit, J., Kiechl, S., Wick, G., Risk Assessment of Toxic and Immunomodulatory Agents, Dep Infectieziekten Immunologie, Perschinka, H., Wellenzohn, B., Parson, W., van der Zee, R., Willeit, J., Kiechl, S., and Wick, G.

Published
2007

160. W48 GENETIC VARIATION WITHIN ADIPONUTRIN IS ASSOCIATED WITH LIPOPROTEIN METABOLISM AND LIVER FUNCTION

Author

Kollerits, B., primary, Coassin, S., additional, Beckmann, N.D., additional, Teumer, A., additional, Kiechl, S., additional, Döring, A., additional, Kavousi, M., additional, Hunt, S.C., additional, Lamina, C., additional, Paulweber, B., additional, Kutalik, Z., additional, Nauck, M., additional, van Duijn, C.M., additional, Heid, I.M., additional, Willeit, J., additional, Brandstätter, A., additional, Adams, T.D., additional, Mooser, V., additional, Aulchenko, Y.S., additional, Völzke, H., additional, and Kronenberg, F., additional

Published
2010
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163. Raising the bar on telomere epidemiology

Author

Ehrlenbach, S., primary, Willeit, P., additional, Kiechl, S., additional, Willeit, J., additional, Reindl, M., additional, Schanda, K., additional, Kronenberg, F., additional, and Brandstatter, A., additional

Published
2010
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164. Immunology of atherosclerosis. Demonstration of heat shock protein 60 expression and T lymphocytes bearing alpha/beta or gamma/delta receptor in human atherosclerotic lesions

Author

Kleindienst, R., Xu, Q., Willeit, J., Waldenberger, F. R., Weimann, S., and Wick, G.

Subjects
Adult, Aged, 80 and over, Male, Arteriosclerosis, Receptors, Antigen, T-Cell, alpha-beta, T-Lymphocytes, Antibodies, Monoclonal, Fluorescent Antibody Technique, Enzyme-Linked Immunosorbent Assay, Receptors, Antigen, T-Cell, gamma-delta, Chaperonin 60, Middle Aged, Immunohistochemistry, Muscle, Smooth, Vascular, Carotid Arteries, Phenotype, Humans, Female, Endothelium, Vascular, Tunica Intima, Aorta, Heat-Shock Proteins, Research Article, Aged
Abstract

Our previous work revealed the presence of a great number of activated T lymphocytes in early human atherosclerotic lesions, and we were able to induce atherosclerosis in normocholesterolemic rabbits by immunization with Mycobacterium tuberculosis heat-shock protein (HSP) 65. We hypothesized this latter phenomenon to arise from cross-reactivity of mycobacterial HSP 65 with the endogenously expressed homologous 60-kd form of this stress protein. To study HSP 60 expression and the phenotype of intima infiltrating T lymphocytes relative to the T cell receptor (TCR) in human atherosclerotic lesions, specimens of aorta, carotid arteries, and internal mammary arteries and veins, as well as saphenous veins and vena cava from 27 subjects, aged 23 to 80 years, were examined using immunohistochemical and immunofluorescence techniques on serial frozen tissue sections. HSP 60 was detected on endothelium, smooth muscle cells, and/or mononuclear cells of all carotid and aortic specimens, whereas vessels of smaller diameter, serving as reference specimens for normal intima without atherosclerotic lesions and mononuclear infiltration, showed no detectable expression of this stress protein. Furthermore, although the majority of CD3+ cells within the mononuclear cell infiltrates of atherosclerotic lesions bear the alpha/beta TCR, a considerable portion also consisted of gamma/delta TCR+ cells. Thus, 9.7% of T cells in the transition zone between normal intima and fatty streaks carry the gamma/delta TCR, a proportion that decreases to 6.6% and 4.3% in fatty streaks and atherosclerotic plaques, respectively. We conclude that the intensity of HSP 60 expression correlates positively with the atherosclerotic severity and that most lymphocytes participating in atherogenesis bear the alpha/beta TCR, although gamma/delta TCR+ cells are also enriched in atherosclerotic lesions. Expression of HSP 60 by intimal cells, caused, eg, by hemodynamic shear forces, may be responsible for recruitment of HSP-sensitized T cells, thus leading to the induction of an initiating inflammatory process in atherosclerosis. Other risk factors, such as high serum cholesterol levels, contribute to the final outcome of the disease.

Published
1993

166. Genetic evidence for a role of adiponutrin in the metabolism of apolipoprotein B-containing lipoproteins

Author

Kollerits, B., primary, Coassin, S., additional, Beckmann, N. D., additional, Teumer, A., additional, Kiechl, S., additional, Doring, A., additional, Kavousi, M., additional, Hunt, S. C., additional, Lamina, C., additional, Paulweber, B., additional, Kutalik, Z., additional, Nauck, M., additional, van Duijn, C. M., additional, Heid, I. M., additional, Willeit, J., additional, Brandstatter, A., additional, Adams, T. D., additional, Mooser, V., additional, Aulchenko, Y. S., additional, Volzke, H., additional, and Kronenberg, F., additional

Published
2009
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175. Reply

Author

Werner, P., primary, Kiechl, S., additional, Loscher, W., additional, Poewe, W., additional, and Willeit, J., additional

Published
2004
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176. Prevalence of insulin resistance in metabolic disorders: the Bruneck Study.

Author

Bonora E, Kiechl S, Willeit J, Oberhollenzer F, Egger G, Targher G, Alberiche M, Bonadonna RC, Muggeo M, Bonora, E, Kiechl, S, Willeit, J, Oberhollenzer, F, Egger, G, Targher, G, Alberiche, M, Bonadonna, R C, and Muggeo, M

Abstract

The prevalence of insulin resistance in the most common metabolic disorders is still an undefined issue. We assessed the prevalence rates of insulin resistance in subjects with impaired glucose tolerance (IGT), NIDDM, dyslipidemia, hyperuricemia, and hypertension as identified within the frame of the Bruneck Study. The study comprised an age- and sex-stratified random sample of the general population (n = 888; aged 40-79 years). Insulin resistance was estimated by homeostasis model assessment (HOMA(IR)), preliminarily validated against a euglycemic-hyperinsulinemic clamp in 85 subjects. The lower limit of the top quintile of HOMA(IR) distribution (i.e., 2.77) in nonobese subjects with no metabolic disorders (n = 225) was chosen as the threshold for insulin resistance. The prevalence of insulin resistance was 65.9% in IGT subjects, 83.9% in NIDDM subjects, 53.5% in hypercholesterolemia subjects, 84.2% in hypertriglyceridemia subjects, 88.1% in subjects with low HDL cholesterol, 62.8% in hyperuricemia subjects, and 58.0% in hypertension subjects. The prevalence of insulin resistance in subjects with the combination of glucose intolerance (IGT or NIDDM), dyslipidemia (hypercholesterolemia and/or hypertriglyceridemia and/or low HDL cholesterol), hyperuricemia, and hypertension (n = 21) was 95.2%. In isolated hypercholesterolemia, hypertension, or hyperuricemia, prevalence rates of insulin resistance were not higher than that in nonobese normal subjects. An appreciable number of subjects (n = 85, 9.6% of the whole population) was insulin resistant but free of IGT, NIDDM, dyslipidemia, hyperuricemia, and hypertension. These results from a population-based study documented that 1) in hypertriglyceridemia and a low HDL cholesterol state, insulin resistance is as common as in NIDDM, whereas it is less frequent in hypercholesterolemia, hyperuricemia, and hypertension; 2) the vast majority of subjects with multiple metabolic disorders are insulin resistant; 3) in isolated hypercholesterolemia, hyperuricemia, or hypertension, insulin resistance is not more frequent than can be expected by chance alone; and 4) in the general population, insulin resistance can be found even in the absence of any major metabolic disorders. [ABSTRACT FROM AUTHOR]

Published
1998
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180. Reply

Author

Wiedermann, C.J, primary, Kiechl, S, additional, Dunzendorfer, S, additional, Schratzberger, P, additional, and Willeit, J, additional

Published
2000
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193. Diabetes is an independent predictor for severe osteoarthritis: results from a longitudinal cohort study.

Author

Schett G, Kleyer A, Perricone C, Sahinbegovic E, Iagnocco A, Zwerina J, Lorenzini R, Aschenbrenner F, Berenbaum F, D'Agostino MA, Willeit J, Kiechl S, Schett, Georg, Kleyer, Arndt, Perricone, Carlo, Sahinbegovic, Enijad, Iagnocco, Annamaria, Zwerina, Jochen, Lorenzini, Rolando, and Aschenbrenner, Franz

Abstract

Objective: To evaluate if type 2 diabetes is an independent risk predictor for severe osteoarthritis (OA).Research Design and Methods: Population-based cohort study with an age- and sex-stratified random sample of 927 men and women aged 40-80 years and followed over 20 years (1990-2010).Results: Rates of arthroplasty (95% CI) were 17.7 (9.4-30.2) per 1,000 person-years in patients with type 2 diabetes and 5.3 (4.1-6.6) per 1,000 person-years in those without (P < 0.001). Type 2 diabetes emerged as an independent risk predictor for arthroplasty: hazard ratios (95% CI), 3.8 (2.1-6.8) (P < 0.001) in an unadjusted analysis and 2.1 (1.1-3.8) (P = 0.023) after adjustment for age, BMI, and other risk factors for OA. The probability of arthroplasty increased with disease duration of type 2 diabetes and applied to men and women, as well as subgroups according to age and BMI. Our findings were corroborated in cross-sectional evaluation by more severe clinical symptoms of OA and structural joint changes in subjects with type 2 diabetes compared with those without type 2 diabetes.Conclusions: Type 2 diabetes predicts the development of severe OA independent of age and BMI. Our findings strengthen the concept of a strong metabolic component in the pathogenesis of OA. [ABSTRACT FROM AUTHOR]

Published
2013
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