Browsing by Author "Lukic, Ruzica (55773200300)"
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Publication Increased systemic sST2 in patients with end stage renal disease contributes to milder liver damage during HCV infection(2020) ;Lukic, Ruzica (55773200300) ;Cupic, Majа (15730255400) ;Gajovic, Nevena (56698359000) ;Jurisevic, Milena (55696341000) ;Mijailovic, Zeljko (6506982098) ;Davidovic, Bojana (56315878600) ;Kujundžic, Bojan (56568315000) ;Joksimovic, Bojan (56955484200) ;Arsenijevic, Nebojša (6507926547)Jovanovic, Ivan (55044296300)Introduction: Hepatitis C Virus (HCV) is the leading cause of chronic liver disease and is a serious global health problem. Hepatitis C infection is highly prevalent in patients with end stage renal disease (ESRD), due to frequent exposure to blood and blood products, nosocomial transmission of HCV, and prolong hemodialysis duration. The aim of the study was to evaluate the influence of IL-33/ST2 signaling pathway on severity of the liver disease in ESRD HCV+ patients. Methodology: Blood samples from patients with end stage renal disease (ESRD) and hepatitis C infection (HCV), 20 patients with HCV infection, 20 patients with ESRD and 20 healthy control donor patients were taken for the examination of biochemical parameters, for the determination of the serum cytokine concentration, and for the molecular diagnostics of HCV. Results: Systemic sST2 positively correlated with serum level of urea and creatinine, respectively. Serum sST2 was significantly increased in ESRD HCV+ patients in comparison to HCV+ group. sST2/IL-1, sST2/IL-4 and sST2/IL-23 ratios were significantly increased in serum of ESRD HCV+ patients in comparison to HCV+ patients. Significantly higher systemic level of sST2 and sST2/IL-1 and sST2/IL-4 ratios were measured in ESRD patients compared to non-ESRD patients. Conclusion: These results suggested that elevated level sST2, as the consequence of renal failure, causes less destruction of liver in HCV infection. Copyright © 2020 Lukic et al. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. - Some of the metrics are blocked by yourconsent settings
Publication Increased systemic sST2 in patients with end stage renal disease contributes to milder liver damage during HCV infection(2020) ;Lukic, Ruzica (55773200300) ;Cupic, Majа (15730255400) ;Gajovic, Nevena (56698359000) ;Jurisevic, Milena (55696341000) ;Mijailovic, Zeljko (6506982098) ;Davidovic, Bojana (56315878600) ;Kujundžic, Bojan (56568315000) ;Joksimovic, Bojan (56955484200) ;Arsenijevic, Nebojša (6507926547)Jovanovic, Ivan (55044296300)Introduction: Hepatitis C Virus (HCV) is the leading cause of chronic liver disease and is a serious global health problem. Hepatitis C infection is highly prevalent in patients with end stage renal disease (ESRD), due to frequent exposure to blood and blood products, nosocomial transmission of HCV, and prolong hemodialysis duration. The aim of the study was to evaluate the influence of IL-33/ST2 signaling pathway on severity of the liver disease in ESRD HCV+ patients. Methodology: Blood samples from patients with end stage renal disease (ESRD) and hepatitis C infection (HCV), 20 patients with HCV infection, 20 patients with ESRD and 20 healthy control donor patients were taken for the examination of biochemical parameters, for the determination of the serum cytokine concentration, and for the molecular diagnostics of HCV. Results: Systemic sST2 positively correlated with serum level of urea and creatinine, respectively. Serum sST2 was significantly increased in ESRD HCV+ patients in comparison to HCV+ group. sST2/IL-1, sST2/IL-4 and sST2/IL-23 ratios were significantly increased in serum of ESRD HCV+ patients in comparison to HCV+ patients. Significantly higher systemic level of sST2 and sST2/IL-1 and sST2/IL-4 ratios were measured in ESRD patients compared to non-ESRD patients. Conclusion: These results suggested that elevated level sST2, as the consequence of renal failure, causes less destruction of liver in HCV infection. Copyright © 2020 Lukic et al. This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. - Some of the metrics are blocked by yourconsent settings
Publication Mechanisms of intracellular chlamydiae survival; [Mehanizmi intracelularnog preživljavanja hlamidija](2016) ;Lukic, Ruzica (55773200300) ;Lukovic, Bojana (57189443662) ;Gajovic, Nevena (56698359000) ;Prljic, Slava (57189444454)Djukic, Slobodanka (6603568490)Chlamydiae are Gram-negative, non-motile, obligate intracellular, and spherically shaped bacteria with a diameter of 0.2-1.5 μm. Chlamydiae are present in several different morphological forms: the elementary body, the reticular body, and in the last several years, there has been the observation of a third form known as the persistent or atypical form. The intracellular localization of Chlamydia provides a unique replication cycle that occurs inside a membrane-surrounded vacuole in the host cell cytoplasm and is significantly different from the method of multiplication of other microorganisms. Chlamydiae are capable of manipulating different signalling pathways inside the infected cell, thus avoiding the host immune response. This ensures intracellular multiplication, survival, and long-term persistence of Chlamydiae. There are two basic means of achieving this persistence: inhibition of apoptosis and manipulation of NF-κB (nuclear factor kappa B)-mediated signals in the host. © 2016, University of Kragujevac, Faculty of Science, All rights reserved.