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: It is shown that developmentally impaired human embryos elicit an endoplasmic stress response in human decidual cells, and that trypsin, a serine protease released by pre-implantation embryos, elicits Ca2+ signaling in endometrial epithelial cells.
Abstract: Human embryos frequently harbor large-scale complex chromosomal errors that impede normal development. Affected embryos may fail to implant although many first breach the endometrial epithelium and embed in the decidualizing stroma before being rejected via mechanisms that are poorly understood. Here we show that developmentally impaired human embryos elicit an endoplasmic stress response in human decidual cells. A stress response was also evident upon in vivo exposure of mouse uteri to culture medium conditioned by low-quality human embryos. By contrast, signals emanating from developmentally competent embryos activated a focused gene network enriched in metabolic enzymes and implantation factors. We further show that trypsin, a serine protease released by pre-implantation embryos, elicits Ca2+ signaling in endometrial epithelial cells. Competent human embryos triggered short-lived oscillatory Ca2+ fluxes whereas low-quality embryos caused a heightened and prolonged Ca2+ response. Thus, distinct positive and negative mechanisms contribute to active selection of human embryos at implantation.
232 citations
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TL;DR: In this paper, the susceptibility of certain inbred mouse strains to murine cytomegalovirus (MCMV) is related to their inability to generate a strong natural killer (NK) cell response.
Abstract: The susceptibility of certain inbred mouse strains to murine cytomegalovirus (MCMV) is related to their inability to generate a strong natural killer (NK) cell response. We addressed here whether the MCMV susceptibility of the BALB/c strain is due to viral functions that control NK cell activation in a strain-specific manner. MCMV expresses two proteins, gp48 and gp40, that are encoded by the genes m06 and m152, respectively; they down-regulate major histocompatibility complex (MHC) class I expression at the plasma membrane. Using MCMV deletion mutants and revertants, we found that gp40 but not gp48 controls NK cell activation. Absence of gp40 improved antiviral NK cell control in BALB/c, but not C57BL/6, mice. Down-regulation of H-60, the high-affinity ligand for the NKG2D receptor, was the mechanism by which gp40 modulates NK cell activation. Thus, a single herpesvirus protein has a dual function in inhibiting both the adaptive as well as the innate immune response.
220 citations
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TL;DR: The molecular network involving phosphatidylinositol 3 kinase (PI3K)/PTEN-PDK1 signaling in oocytes that controls the survival, loss and activation of primordial follicles, which together determine reproductive aging and the length of reproductive life in females are pinpointed.
Abstract: The molecular mechanisms that control reproductive aging and menopausal age in females are poorly understood. Here, we provide genetic evidence that 3-phosphoinositide-dependent protein kinase-1 (P ...
217 citations
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TL;DR: In this article, the authors investigated relations among strengths of character in 881 students from Croatian universities and examined links between strengths and various well-being indices, finding that vitality (with zest, hope, curiosity, gratitude, and optimism/hope) emerged with the strongest associations with elevated life satisfaction, subjective vitality, satisfaction of autonomy, relatedness, and competence needs, and a pleasurable, engaging, and meaningful existence.
216 citations
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TL;DR: It is shown that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection, and this results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy.
Abstract: Immune cells, including natural killer (NK) cells, recognize transformed cells and eliminate them in a process termed immunosurveillance. It is thought that tumor cells evade immunosurveillance by shedding membrane ligands that bind to the NKG2D-activating receptor on NK cells and/or T cells, and desensitize these cells. In contrast, we show that in mice, a shed form of MULT1, a high-affinity NKG2D ligand, causes NK cell activation and tumor rejection. Recombinant soluble MULT1 stimulated tumor rejection in mice. Soluble MULT1 functions, at least in part, by competitively reversing a global desensitization of NK cells imposed by engagement of membrane NKG2D ligands on tumor-associated cells, such as myeloid cells. The results overturn conventional wisdom that soluble ligands are always inhibitory and suggest a new approach for cancer immunotherapy.
215 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 |