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Kraków, Poland

Guzik B.,Jagiellonian University | Chwala M.,St. John Grande Hospital | Matusik P.,Jagiellonian University | Ludew D.,Jagiellonian University | And 8 more authors.
Polskie Archiwum Medycyny Wewnetrznej | Year: 2011

INTRODUCTION: Varicose vein disease is one of the most common morbidities in the developed countries. Recent studies have shown that oxidative stress is increased in varicose veins (VV) and venous insufficiency. However, the exact mechanisms of oxidative stress in VV remain unknown. OBJECTIVES: The aim of the study was to measure superoxide anion production and analyze its enzymatic sources in VV in comparison with control human saphenous veins (HSV). Superoxide production was also compared between the proximal and distal segments of the veins. PATIENTS AND METHODS: Proximal and distal segments of varicose veins (14 patients, aged 52 ±3.5 years) and control veins (15 patients, aged 56 ±4 years) were obtained during VV removal or elective coronary artery bypass graft surgery, respectively. Subjects were matched for age, sex, and the major risk factors for atherosclerosis. Superoxide was measured by lucigenin-enhanced chemiluminescence (5 μmol/l) in the presence and absence of oxidase inhibitors. RESUTS: Superoxide production was increased in VV compared with control HSV. This increase was particularly evident in the distal segments of VV. There was a significant correlation between superoxide production in the proximal and distal segments of HSV but not of VV. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and uncoupled nitric oxide synthase (NOS) were the major sources of superoxide in VV, because their inhibitors greatly attenuated superoxide production in VV. CONCLUSIONS: NADPH oxidases and NOS could represent valuable drug targets for pharmacological treatment and prevention of varicose vein disease. Oxidative stress may provide a link between endothelial dysfunction, inflammation, and immune activation and the development of chronic venous dysfunction. Copyright by Medycyna Praktyczna, 2011. Source

Kozka M.A.,Jagiellonian University | Bijak P.,Jagiellonian University | Chwala M.,St. John Grande Hospital | Mrowiecki T.,St. John Grande Hospital | And 5 more authors.
Annals of Vascular Surgery | Year: 2014

Background: Several studies have documented that weather factors, seasons of the year, time of the day, and even changes in moon phases have an impact on the occurrence of rupture of an abdominal aortic aneurysm (RAAA); however, the available data are confounding. The objective of this study was to determine the impact of these factors on the prevalence and mortality rate of RAAA. Methods: This is a retrospective analysis of medical records of patients treated for RAAA over a 10-year period. Weather data (i.e., atmospheric pressure, air temperature, humidity, visibility, and wind speed) and weather events (i.e., rain, snow, and storms, etc) were obtained from the local meteorologic weather station and analyzed for a correlation with RAAA. Results: Five hundred thirty patients with RAAA were identified, and these patients presented on 478 days during the 10-year study period (3,652 days), with the overall in-hospital mortality rate of 48.7%. The RAAA mortality was higher during weekends and national holidays, when compared to weekdays (59% vs 45%; P = 0.006) and in patients admitted between 3-7 am when compared to work day hours (65.5% vs 44.1%; P = 0.035). Season changes had no influence on the frequency of RAAA; however, summer seemed to be associated with an increase in mortality as opposed to autumn (54.4% vs 42.5%; P = 0.047). Mean atmospheric pressure (and fluctuations thereof) and other weather factors, including phases and parts of the moon, did not correlate with RAAA occurrence or its mortality. Conclusions: Patients with RAAA who were admitted on weekends, national holidays and in late night hours had lower survival rates. Weather factors (including atmospheric pressure) do not influence the prevalence and mortality of RAAA. © 2014 Elsevier Inc. All rights reserved. Source

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