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Browsing by Author "Gajovic, Nevena (56698359000)"

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    Antimelanoma Effects of Alchemilla vulgaris: A Comprehensive In Vitro and In Vivo Study
    (2024)
    Jelača, Sanja (57211914032)
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    Jovanovic, Ivan (55044296300)
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    Bovan, Dijana (58848251800)
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    Pavlovic, Sladjana (35747071500)
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    Gajovic, Nevena (56698359000)
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    Dunđerović, Duško (56515503700)
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    Dajić-Stevanović, Zora (13613292900)
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    Acović, Aleksandar (57992303600)
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    Mijatović, Sanja (6508347659)
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    Maksimović-Ivanić, Danijela (6507584634)
    Due to the rich ethnobotanical and growing evidence-based medicine records, the Alchemillae herba, i.e., the upper parts of the Lady’s mantle (Alchemilla vulgaris L.), was used for the assessment of antimelanoma activity. The ethanolic extract of A. vulgaris strongly suppressed the viability of B16F1, B16F10, 518A2, and Fem-X cell lines. In contrast to the in vitro study, where the B16F1 cells were more sensitive to the treatment than the more aggressive counterpart B16F10, the results obtained in vivo using the corresponding syngeneic murine model were quite the opposite. The higher sensitivity of B16F10 tumors in vivo may be attributed to a more complex response to the extract compared to one triggered in vitro. In addition, the strong immunosuppressive microenvironment in the B16F1 model is impaired by the treatment, as evidenced by enhanced antigen-presenting potential of dendritic cells, influx and activity of CD4+ T and CD8+ T lymphocytes, decreased presence of T regulatory lymphocytes, and attenuation of anti-inflammatory cytokine production. All these effects are supported by the absence of systemic toxicity. A. vulgaris extract treatment results in a sustained and enhanced ability to reduce melanoma growth, followed by the restoration of innate and adopted antitumor immunity without affecting the overall physiology of the host. © 2024 by the authors.
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    Increased systemic sST2 in patients with end stage renal disease contributes to milder liver damage during HCV infection
    (2020)
    Lukic, Ruzica (55773200300)
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    Cupic, Majа (15730255400)
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    Gajovic, Nevena (56698359000)
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    Jurisevic, Milena (55696341000)
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    Mijailovic, Zeljko (6506982098)
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    Davidovic, Bojana (56315878600)
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    Kujundžic, Bojan (56568315000)
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    Joksimovic, Bojan (56955484200)
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    Arsenijevic, Nebojša (6507926547)
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    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.
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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)
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    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.
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    Mechanisms of intracellular chlamydiae survival; [Mehanizmi intracelularnog preživljavanja hlamidija]
    (2016)
    Lukic, Ruzica (55773200300)
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    Lukovic, Bojana (57189443662)
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    Gajovic, Nevena (56698359000)
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    Prljic, Slava (57189444454)
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    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.

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