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.
Papers published on a yearly basis
Papers
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TL;DR: A novel approach for solving the cell-formation problem based on implementation of a GA, called modified genetic algorithm (MGA), based on Emergent Synthesis idea, of top-down problem decomposition and emerging solution from bottom-up feedback is presented.
39 citations
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University of Warsaw1, Chungbuk National University2, Osaka University3, Tel Aviv University4, Ohio State University5, University of Rijeka6, Las Cumbres Observatory Global Telescope Network7, University of Copenhagen8, University of Notre Dame9, Istituto Nazionale di Fisica Nucleare10, University of Concepción11, University of Cambridge12, Nagoya University13, Massey University14, University of Auckland15, Konan University16, University of British Columbia17, College of Industrial Technology18, Victoria University of Wellington19, Texas A&M University20, Korea Astronomy and Space Science Institute21, Auckland University of Technology22, Harvard University23, University of Canterbury24, University of Toulouse25, Institut d'Astrophysique de Paris26, European Southern Observatory27, University of Tasmania28, University of Vienna29, Space Telescope Science Institute30, NASA Exoplanet Science Institute31, Heidelberg University32, Qatar Foundation33, University of St Andrews34, Max Planck Society35, Liverpool John Moores University36, University of Salerno37, University of Göttingen38, Chinese Academy of Sciences39, University of Manchester40, Aarhus University41, Perimeter Institute for Theoretical Physics42, National Autonomous University of Mexico43, Keele University44, University of Liège45, Ames Research Center46
TL;DR: The OGLE-2011-BLG-0265 microlensing system as discussed by the authors was the first to detect a Jupiter-mass planet orbiting an M-dwarf star.
Abstract: We report the discovery of a Jupiter-mass planet orbiting an M-dwarf star that gave rise to the microlensing event OGLE-2011-BLG-0265. Such a system is very rare among known planetary systems and thus the discovery is important for theoretical studies of planetary formation and evolution. High-cadence temporal coverage of the planetary signal, combined with extended observations throughout the event, allows us to accurately model the observed light curve. However, the final microlensing solution remains degenerate, yielding two possible configurations of the planet and the host star. In the case of the preferred solution, the mass of the planet is M-p = 0.9 +/- 0.3 M-J, and the planet is orbiting a star with a mass M = 0.22 +/- 0.06 M-circle dot. The second possible configuration (2 sigma away) consists of a planet with M-p = 0.6 +/- 0.3M(J) and host star with M = 0.14 +/- 0.06M(circle dot). The system is located in the Galactic disk 3-4 kpc toward the Galactic bulge. In both cases, with an orbit size of 1.5-2.0 AU, the planet is a "cold Jupiter"-located well beyond the "snow line" of the host star. Currently available data make the secure selection of the correct solution difficult, but there are prospects for lifting the degeneracy with additional follow-up observations in the future, when the lens and source star separate.
38 citations
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TL;DR: The results show that a primed type I IFN subnetwork contributes to an immediate-early antiviral state induced by type II IFN activation of macrophages, with a potential further amplification loop contributed by transient induction of IFN-β.
Abstract: Activated macrophages play a central role in controlling inflammatory responses to infection and are tightly regulated to rapidly mount responses to infectious challenge. Type I interferon (alpha/beta interferon [IFN-α/β]) and type II interferon (IFN-γ) play a crucial role in activating macrophages and subsequently restricting viral infections. Both types of IFNs signal through related but distinct signaling pathways, inducing a vast number of interferon-stimulated genes that are overlapping but distinguishable. The exact mechanism by which IFNs, particularly IFN-γ, inhibit DNA viruses such as cytomegalovirus (CMV) is still not fully understood. Here, we investigate the antiviral state developed in macrophages upon reversible inhibition of murine CMV by IFN-γ. On the basis of molecular profiling of the reversible inhibition, we identify a significant contribution of a restricted type I IFN subnetwork linked with IFN-γ activation. Genetic knockout of the type I-signaling pathway, in the context of IFN-γ stimulation, revealed an essential requirement for a primed type I-signaling process in developing a full refractory state in macrophages. A minimal transient induction of IFN-β upon macrophage activation with IFN-γ is also detectable. In dose and kinetic viral replication inhibition experiments with IFN-γ, the establishment of an antiviral effect is demonstrated to occur within the first hours of infection. We show that the inhibitory mechanisms at these very early times involve a blockade of the viral major immediate-early promoter activity. Altogether our results show that a primed type I IFN subnetwork contributes to an immediate-early antiviral state induced by type II IFN activation of macrophages, with a potential further amplification loop contributed by transient induction of IFN-β.
38 citations
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TL;DR: The results of this study indicate that the list of priority pollutants usually determined in the attempt to evaluate the risk of adverse effects to marine wildlife should be reconsidered.
38 citations
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TL;DR: Special emphasis will be given on increased susceptibility to infections due to obesity-related low-grade chronic inflammation, higher expression of angiotensin converting enzyme-2 and pathway-associated components, as well as decreased vitamin D bioavailability, since all of them provide easier ways for the virus to enter into host cells, replicate and stunt adequate immune responses.
38 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 |