Publications by authors named "A Dziedziczko"

Smoking tobacco can induce formation of inflammable state in respiratory tract and cause lungs damage. Experimental investigations affirm, that the exposure to tobacco smoke causes growth of penetrability of blood-vessels, which favors the enlarged migration of inflammable cells. The growth of exposure to reactive forms of oxygen and concentration changes of cellular antioxidants enzymes, leads to disorders in balance of proteinases and antiproteinases and oxidative stress.

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An increasing amount of basic scientific data indicates that adhesion molecules may be involved in the pathogenesis of vessel re-narrowing in patients undergoing coronary angioplasty. Furthermore, inflammation is suggested to be a pivotal mechanism linking atherosclerosis and restenosis. The aim of this study was to assess if periprocedural evaluation of soluble P-selectin (sP-selectin) and E-selectin (sE-selectin) possesses any additive value in the restenosis prediction to C-reactive protein (CRP) measurement.

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Alternations in airway wall architecture, particularly increased smooth muscle mass are associated with pathogenesis of asthma. Muscle fiber hyperplasia and hypertrophy is a major contributor to the increase in smooth muscle mass. Airway smooth muscle was traditionally considered to have only contractile and proliferative functions and has little attention with regard to its ability to express and release inflammatory mediators.

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Chronic inflammation is recognized as a primary factor in the development of asthma, and its role in the induction of the remodeling of the airways has recently been emphasized. Changes in airway structure such as thickening of the airway wall are common findings in cases of asthma. Thickening of the epithelial reticular basement membrane has been reported to show a positive correlation with airway hyperresponsiveness, the frequency of asthma attacks, and the numbers of fibroblasts and myofibroblasts that lie external and adjacent to it.

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Objective And Design: It is believed that the magnitude of the systemic inflammatory response induced by percutaneous coronary intervention (PCI) impacts on the long-term outcomes in patients with stable angina (SA) and unstable angina (UA). We aimed to determine whether an inflammatory response appears in in-stent restenosis (ISR) patients undergoing balloon angioplasty and to assess its pattern and magnitude in relation to SA and UA subjects.

Subjects: 80 patients (59 with SA, 10 with UA, 11 with ISR) were enrolled into the prospective study.

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