Institution
University of Rijeka
Education•Rijeka, Croatia•
About: University of Rijeka is a education organization based out in Rijeka, Croatia. It is known for research contribution in the topics: Population & Tourism. The organization has 3471 authors who have published 7993 publications receiving 110386 citations. The organization is also known as: Rijeka University & Sveučilište u Rijeci.
Topics: Population, Tourism, European union, Immune system, Cytotoxic T cell
Papers published on a yearly basis
Papers
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TL;DR: The epidemiological study was carried out on 1,324 examinees, 530 males and 794 females, employed in 5 highly represented groups of professional activities in Rijeka, and suggested that standing in the workplace, weight handling while working, and working indoors were risk factors for varicose veins.
Abstract: This research aims to establish the effect of working conditions on the appearance of varicose veins. The epidemiological study was carried out on 1,324 examinees, 530 males and 794 females, employed in 5 highly represented groups of professional activities in Rijeka (catering, trade, light industry, heavy industry and finances). The data were collected by survey and clinical examination. Varicose veins were more prevalent in the trade than in the office workers (odds ratio (OR) = 2.08; 95% confidence interval (CI) = 1.31-3.31), and more prevalent in catering industries than in the office workers (OR = 1.56; 95% CI = 1.001-2.43). chi 2-testing suggested that standing in the workplace (OR = 1.35; 95% CI = 0.95-1.92), weight handling while working (OR = 1.29; 95% CI = 1.01-1.64) and working indoors (OR = 1.61; 95% CI = 1.02-2.53) were risk factors for varicose veins. By multiple logistic regression, the following risk factors were isolated in the total population: female sex (OR = 1.92; 95% CI = 1.37-2.67), workplace (OR = 0.89; 95% CI = 0.78-0.99), age (OR = 1.05; 95% CI = 1.03-1.07), body mass index (OR = 1.04; 95% CI = 1.01-1.07) and family history of the disease (OR = 1.99; 95% CI = 1.55-2.57).
48 citations
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TL;DR: This paper condenses the extensive experience of the European Monoclonal Antibody Network to help researchers identify antibodies specific for their target antigen, enabling both time and cost effective generation of high quality antibody-based data fit for publication.
Abstract: Antibodies are widely exploited as research/diagnostic tools and therapeutics. Despite providing exciting research opportunities, the multitude of available antibodies also offers a bewildering array of choice. Importantly, not all companies comply with the highest standards, and thus many reagents fail basic validation tests. The responsibility for antibodies being fit for purpose rests, surprisingly, with their user. This paper condenses the extensive experience of the European Monoclonal Antibody Network to help researchers identify antibodies specific for their target antigen. A stepwise strategy is provided for prioritising antibodies and making informed decisions regarding further essential validation requirements. Web-based antibody validation guides provide practical approaches for testing antibody activity and specificity. We aim to enable researchers with little or no prior experience of antibody characterization to understand how to determine the suitability of their antibody for its intended purpose, enabling both time and cost effective generation of high quality antibody-based data fit for publication.
47 citations
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TL;DR: It is considered that the Th1/Th2 paradigm, as useful as it has been, is now no longer adequate and is obsolete, with a key feature being the link between uterine cytokine dysregulation and abnormal uterine vascular scores.
47 citations
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TL;DR: It is found that single nucleotide polymorphism in TLR10 (rs11096957) is associated with risk for TB, and SNPs in the proinflammatory IL17A and IL17F genes were not significantly associated with tuberculosis in the Croatian population.
Abstract: Proinflammatory conditions leading to activation of macrophages via interferon-γ bear an important role in host defence against intracellular bacteria such as Mycobacterium tuberculosis (Mt). Interleukin-17 plays a similar role, as it appears to be also an activator of macrophages. Recently, the TLR-10 was identified as an anti-inflammatory factor that exerts its action via association with the TLR-2 chain at the cell surface of macrophages, the latter being an Mt-binding protein. We have previously found that gene polymorphisms that either inactivate the TLR2 gene product or have a dominant-negative role are associated with tuberculosis (TB) in Croatian population. We have now extended our survey and found that single nucleotide polymorphism (SNP) in TLR10 (rs11096957) is associated with risk for TB. Homozygotes carrying the A allele are associated with predisposition to disease as analysed by the dominant model of inheritance. In contrast, SNPs in the proinflammatory IL17A and IL17F genes (rs2275913 and rs763780, respectively), found previously to correlate with the disease occurrence in Chinese population, were not significantly associated with tuberculosis in the Croatian population.
47 citations
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TL;DR: It is shown that the induction of eIF2α phosphorylation during infection with an m142- and m143-deficient MCMV is specifically mediated by PKR, not by the related eIF1α kinases PERK or GCN2, and is responsible for the essentiality of m142 and m 143.
Abstract: Double-stranded RNA (dsRNA) produced during viral infection activates several cellular antiviral responses. Among the best characterized is the shutoff of protein synthesis mediated by the dsRNA-dependent protein kinase (PKR) and the oligoadenylate synthetase (OAS)/RNase L system. As viral replication depends on protein synthesis, many viruses have evolved mechanisms for counteracting the PKR and OAS/RNase L pathways. The murine cytomegalovirus (MCMV) proteins m142 and m143 have been characterized as dsRNA binding proteins that inhibit PKR activation, phosphorylation of the translation initiation factor eIF2α, and a subsequent protein synthesis shutoff. In the present study we analyzed the contribution of the PKR- and the OAS-dependent pathways to the control of MCMV replication in the absence or presence of m142 and m143. We show that the induction of eIF2α phosphorylation during infection with an m142- and m143-deficient MCMV is specifically mediated by PKR, not by the related eIF2α kinases PERK or GCN2. PKR antagonists of vaccinia virus (E3L) or herpes simplex virus (γ34.5) rescued the replication defect of an MCMV strain with deletions of both m142 and m143. Moreover, m142 and m143 bound to each other and interacted with PKR. By contrast, an activation of the OAS/RNase L pathway by MCMV was not detected in the presence or absence of m142 and m143, suggesting that these viral proteins have little or no influence on this pathway. Consistently, an m142- and m143-deficient MCMV strain replicated to high titers in fibroblasts lacking PKR but did not replicate in cells lacking RNase L. Hence, the PKR-mediated antiviral response is responsible for the essentiality of m142 and m143.
47 citations
Authors
Showing all 3537 results
Name | H-index | Papers | Citations |
---|---|---|---|
Igor Rudan | 142 | 658 | 103659 |
Nikola Godinovic | 138 | 1469 | 100018 |
Ivica Puljak | 134 | 1436 | 97548 |
Damir Lelas | 133 | 1354 | 93354 |
D. Mekterovic | 110 | 449 | 46779 |
Ulrich H. Koszinowski | 96 | 281 | 27709 |
Michele Doro | 79 | 437 | 20090 |
Robert Zivadinov | 73 | 522 | 18636 |
D. Dominis Prester | 70 | 363 | 16701 |
Daniel Ferenc | 70 | 225 | 16145 |
Vladimir Parpura | 64 | 226 | 18050 |
Stipan Jonjić | 62 | 227 | 19363 |
Dario Hrupec | 60 | 288 | 13345 |
Alessandro Laviano | 59 | 298 | 14609 |
Tomislav Terzić | 58 | 271 | 10699 |