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583 results on '"Nawroth PP"'

1. Transient hyperthyroidism after surgery for secondary hyperparathyroidism: a common problem

Author

Rudofsky G, Tsioga M, Reismann P, Leowardi C, Kopf S, Grafe IA, Nawroth PP, and Isermann B

Subjects
hyperthyroidism, secondary hyperparathyroidism, palpation thyroiditis, parathyroidectomy, thyroglobulin, Medicine
Abstract

Abstract Background Postoperative hyperthyroidism occurs in approximately one third of patients following parathyroidectomy due to primary hyperparathyroidism (PHP), but has only rarely been described in secondary hyperparathyroidism (SHP). The frequency, course, and laboratory markers of postoperative hyperthyroidism in SHP remain unknown. Our purpose was to evaluate the frequency and the clinical course of postoperative hypcrthyroidism following surgery of SHP and to determine the diagnostic value of thyroglobulin in this setting. Material and Methods A total of 40 patients undergoing parathyroidectomy because of SHP were included in this study. Thyroid stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fl4), and thyroglobulin (Tg) were determined one day before and on day 1, 3, 5, 10, and 40 after surgery. At each of these visits patients were clinically evaluated for signs or symptoms of hyperthyroidism. Results Biochemical evidence of hyperthyroidism was evident in 77% of patients postoperatively despite of preoperatively normal serum levels. TSH dropped from 1.18 ± 0.06mU/L to 0.15 ± 0.07mU/L (p = 0.0015). Free triiodothyronine (fT3) and fT4 levels increased from 2.86 ± 0.02ng/L and 10.32 ± 0.13ng/L, respectively, to their maximum of 4.83 ± 0.17ng/L and 19.35 ± 0.58ng/L, respectively. Thyroglobulin levels rose from 3.8 ± 0.8ng/mL to 111.8 ± 45.3ng/mL (p < 0.001). At day 40 all thyroid related laboratory values were within normal range. Correlation analysis of postoperative values revealed significant correlations for lowest TSH (r = -0.32; p = 0.038), and highest fT3 (r = 0.55; p < 0.001) and fT4 levels (r = 0.67; p < 0.001) with Tg. Conclusion Transient hyperthyroidism is frequent after parathyroidectomy for SHP with Tg being a suitable marker. Awareness of this self-limiting disorder is important to avoid inappropriate and potentially harmful treatment.

Published
2011
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7. Unravelling the methylglyoxal effect on the angiogenic process

Author

NIGRO, CECILIA, LEONE, ALESSIA, FIORY, FRANCESCA, MIRRA, PAOLA, PROCOPIO, TERESA, BEGUINOT, FRANCESCO, MIELE, CLAUDIA, Prevenzano, I, Fleming, Th, Nawroth, Pp, Volpe, A, Falco, R, Nigro, Cecilia, Leone, Alessia, Fiory, Francesca, Mirra, Paola, Prevenzano, I, Fleming, Th, Nawroth, Pp, Procopio, Teresa, Volpe, A, Falco, R, Beguinot, Francesco, and Miele, Claudia

Published
2015

10. Methylglyoxal impairs endothelial insulin sensitivity both in vitro and in vivo

Author

Nigro C, RACITI GA, Leone A, Fleming TH, Longo M, Prevenzano I, Fiory F, Mirra P, D'Esposito V, Ulianich L, Nawroth PP, Formisano P, Beguinot F, Miele C., FIORY, FRANCESCA, Nigro, C, Raciti, Ga, Leone, A, Fleming, Th, Longo, M, Prevenzano, I, Fiory, F, Mirra, P, D'Esposito, V, Ulianich, L, Nawroth, Pp, Formisano, P, Beguinot, F, Miele, C., and Fiory, Francesca

Subjects
medicine.medical_specialty, Nitric Oxide Synthase Type III, Endothelium, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, Nitric Oxide, Nitric oxide, Mice, chemistry.chemical_compound, Insulin resistance, Enos, Internal medicine, Internal Medicine, medicine, Animals, Insulin, Phosphorylation, Endothelial dysfunction, Protein kinase B, biology, Endothelial Cells, Pyruvaldehyde, medicine.disease, biology.organism_classification, Glutathione, IRS1, medicine.anatomical_structure, Endocrinology, chemistry, Insulin Receptor Substrate Proteins, Insulin Resistance, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

AIMS/HYPOTHESIS: Insulin exerts a direct action on vascular cells, thereby affecting the outcome and progression of diabetic vascular complications. However, the mechanism through which insulin signalling is impaired in the endothelium of diabetic individuals remains unclear. In this work, we have evaluated the role of the AGE precursor methylglyoxal (MGO) in generating endothelial insulin resistance both in cells and in animal models. METHODS: Time course experiments were performed on mouse aortic endothelial cells (MAECs) incubated with 500 μmol/l MGO. The glyoxalase-1 inhibitor S-p-bromobenzylglutathione-cyclopentyl-diester (SpBrBzGSHCp2) was used to increase the endogenous levels of MGO. For the in vivo study, an MGO solution was administrated i.p. to C57BL/6 mice for 7 weeks. RESULTS: MGO prevented the insulin-dependent activation of the IRS1/protein kinase Akt/endothelial nitric oxide synthase (eNOS) pathway, thereby blunting nitric oxide (NO) production, while extracellular signal-regulated kinase (ERK1/2) activation and endothelin-1 (ET-1) release were increased by MGO in MAECs. Similar results were obtained in MAECs treated with SpBrBzGSHCp2. In MGO- and SpBrBzGSHCp2-exposed cells, inhibition of ERK1/2 decreased IRS1 phosphorylation on S616 and rescued insulin-dependent Akt activation and NO generation, indicating that MGO inhibition of the IRS1/Akt/eNOS pathway is mediated, at least in part, by ERK1/2. Chronic administration of MGO to C57BL/6 mice impaired whole-body insulin sensitivity and induced endothelial insulin resistance. CONCLUSIONS/INTERPRETATION: MGO impairs the action of insulin on the endothelium both in vitro and in vivo, at least in part through an ERK1/2-mediated mechanism. These findings may be instrumental in developing novel strategies for preserving endothelial function in diabetes.

Published
2014

15. Cation channels of the TRPC family contribute to development of nephropathy and retinopathy in the STZ model

Author

Schumacher, D, primary, Matka, C, additional, Sachdeva, R, additional, Dietrich, N, additional, Schlotterer, A, additional, Mathar, I, additional, Homberg, S, additional, Kriebs, U, additional, Stettner, P, additional, Nawroth, PP, additional, Gröne, HJ, additional, Hammes, HP, additional, Fleming, T, additional, and Freichel, M, additional

Published
2016
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43. Receptor for advanced glycation end products (RAGE) deficiency attenuates the development of atherosclerosis in diabetes

Author

Soro-Paavonen, A, Watson, AMD, Li, J, Paavonen, K, Koitka, A, Calkin, AC, Barit, D, Coughlan, MT, Drew, BG, Lancaster, GI, Thomas, M, Forbes, JM, Nawroth, PP, Bierhaus, A, Cooper, ME, Jandeleit-Dahm, KA, Soro-Paavonen, A, Watson, AMD, Li, J, Paavonen, K, Koitka, A, Calkin, AC, Barit, D, Coughlan, MT, Drew, BG, Lancaster, GI, Thomas, M, Forbes, JM, Nawroth, PP, Bierhaus, A, Cooper, ME, and Jandeleit-Dahm, KA

Abstract

OBJECTIVE: Activation of the receptor for advanced glycation end products (RAGE) in diabetic vasculature is considered to be a key mediator of atherogenesis. This study examines the effects of deletion of RAGE on the development of atherosclerosis in the diabetic apoE(-/-) model of accelerated atherosclerosis. RESEARCH DESIGN AND METHODS: ApoE(-/-) and RAGE(-/-)/apoE(-/-) double knockout mice were rendered diabetic with streptozotocin and followed for 20 weeks, at which time plaque accumulation was assessed by en face analysis. RESULTS: Although diabetic apoE(-/-) mice showed increased plaque accumulation (14.9 +/- 1.7%), diabetic RAGE(-/-)/apoE(-/-) mice had significantly reduced atherosclerotic plaque area (4.9 +/- 0.4%) to levels not significantly different from control apoE(-/-) mice (4.3 +/- 0.4%). These beneficial effects on the vasculature were associated with attenuation of leukocyte recruitment; decreased expression of proinflammatory mediators, including the nuclear factor-kappaB subunit p65, VCAM-1, and MCP-1; and reduced oxidative stress, as reflected by staining for nitrotyrosine and reduced expression of various NADPH oxidase subunits, gp91phox, p47phox, and rac-1. Both RAGE and RAGE ligands, including S100A8/A9, high mobility group box 1 (HMGB1), and the advanced glycation end product (AGE) carboxymethyllysine were increased in plaques from diabetic apoE(-/-) mice. Furthermore, the accumulation of AGEs and other ligands to RAGE was reduced in diabetic RAGE(-/-)/apoE(-/-) mice. CONCLUSIONS: This study provides evidence for RAGE playing a central role in the development of accelerated atherosclerosis associated with diabetes. These findings emphasize the potential utility of strategies targeting RAGE activation in the prevention and treatment of diabetic macrovascular complications.

Published
2008

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