Institution
University of Seville
Education•Seville, Andalucía, Spain•
About: University of Seville is a education organization based out in Seville, Andalucía, Spain. It is known for research contribution in the topics: Population & Model predictive control. The organization has 20098 authors who have published 47317 publications receiving 947007 citations. The organization is also known as: Universidad de Sevilla.
Topics: Population, Model predictive control, Control theory, Nonlinear system, Context (language use)
Papers published on a yearly basis
Papers
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University of Milan1, Spanish National Research Council2, University of Parma3, University of Bern4, University of Helsinki5, University of Düsseldorf6, Bangor University7, University of Kiel8, University of Natural Resources and Life Sciences, Vienna9, National University of Ireland, Galway10, University of Florence11, University College Dublin12, University of Milano-Bicocca13, Utrecht University14, Joseph Fourier University15, University of Seville16, University of Leeds17, Maynooth University18, Claude Bernard University Lyon 119, Université de Namur20, Wageningen University and Research Centre21, King Abdulaziz University22, University of Grenoble23
TL;DR: By interfering with pathogen adhesion, such glycocompounds including glycopolymers, glycoclusters, glycodendrimers and glyconanoparticles have the potential to improve or replace antibiotic treatments that are now subverted by resistance.
Abstract: Multivalency plays a major role in biological processes and particularly in the relationship between pathogenic microorganisms and their host that involves protein-glycan recognition. These interactions occur during the first steps of infection, for specific recognition between host and bacteria, but also at different stages of the immune response. The search for high-affinity ligands for studying such interactions involves the combination of carbohydrate head groups with different scaffolds and linkers generating multivalent glycocompounds with controlled spatial and topology parameters. By interfering with pathogen adhesion, such glycocompounds including glycopolymers, glycoclusters, glycodendrimers and glyconanoparticles have the potential to improve or replace antibiotic treatments that are now subverted by resistance. Multivalent glycoconjugates have also been used for stimulating the innate and adaptive immune systems, for example with carbohydrate-based vaccines. Bacteria present on their surfaces natural multivalent glycoconjugates such as lipopolysaccharides and S-layers that can also be exploited or targeted in anti-infectious strategies.
449 citations
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TL;DR: Although there is overwhelming information demonstrating the immunoenhancing properties of melatonin, many questions related to the cytokines involved and the mechanisms of action of the indoleamine require answers.
Abstract: In this paper we review the historical milestones that first highlighted the existence of a relationship between melatonin and the immune system and we summarize data from experiments which correlate the rhythmic production of melatonin with the rhythmic activity of the immune system. The effects of pinealectomy and in vivo administration of melatonin on a variety of immune parameters, including specific and non-specific immunity are considered and we also present contradictory data concerning the effect of melatonin in cultured immunocompetent cells and a possible scheme of how melatonin regulates the production of a number of cytokines. Finally, the mechanism of action of melatonin in the immune system is discussed. Many data suggest the existence of both nuclear and membrane receptors for melatonin in the immune system. Both of these appear to be clearly identified but their specific physiological role is still under discussion. In summary, although there is overwhelming information demonstrating the immunoenhancing properties of melatonin, many questions related to the cytokines involved and the mechanisms of action of the indoleamine require answers.
446 citations
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TL;DR: This review discusses recent advances in the understanding of the ways in which different organs detect and respond to acute changes in oxygen tension.
Abstract: This review discusses recent advances in the understanding of the ways in which different organs detect and respond to acute changes in oxygen tension. A group of specialized tissues constitutes an oxygen-sensing system that responds rapidly to even minor changes in oxygen tension.
445 citations
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TL;DR: A novel model predictive control for constrained (non-square) linear systems to track piecewise constant references is presented, which ensures constraint satisfaction and asymptotic evolution of the system to any target which is an admissible steady-state.
444 citations
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TL;DR: The results demonstrated that the autophagic flux is impaired in the liver from both NAFLD patients and murine models ofNAFLD, as well as in lipid-overloaded human hepatocytes, and it could be due to elevated ER stress leading to apoptosis.
Abstract: The pathogenic mechanisms underlying the progression of non-alcoholic fatty liver disease (NAFLD) are not fully understood. In this study, we aimed to assess the relationship between endoplasmic reticulum (ER) stress and autophagy in human and mouse hepatocytes during NAFLD. ER stress and autophagy markers were analyzed in livers from patients with biopsy-proven non-alcoholic steatosis (NAS) or non-alcoholic steatohepatitis (NASH) compared with livers from subjects with histologically normal liver, in livers from mice fed with chow diet (CHD) compared with mice fed with high fat diet (HFD) or methionine-choline-deficient (MCD) diet and in primary and Huh7 human hepatocytes loaded with palmitic acid (PA). In NASH patients, significant increases in hepatic messenger RNA levels of markers of ER stress (activating transcription factor 4 (ATF4), glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP)) and autophagy (BCN1) were found compared with NAS patients. Likewise, protein levels of GRP78, CHOP and p62/SQSTM1 (p62) autophagic substrate were significantly elevated in NASH compared with NAS patients. In livers from mice fed with HFD or MCD, ER stress-mediated signaling was parallel to the blockade of the autophagic flux assessed by increases in p62, microtubule-associated protein 2 light chain 3 (LC3-II)/LC3-I ratio and accumulation of autophagosomes compared with CHD fed mice. In Huh7 hepatic cells, treatment with PA for 8 h triggered activation of both unfolding protein response and the autophagic flux. Conversely, prolonged treatment with PA (24 h) induced ER stress and cell death together with a blockade of the autophagic flux. Under these conditions, cotreatment with rapamycin or CHOP silencing ameliorated these effects and decreased apoptosis. Our results demonstrated that the autophagic flux is impaired in the liver from both NAFLD patients and murine models of NAFLD, as well as in lipid-overloaded human hepatocytes, and it could be due to elevated ER stress leading to apoptosis. Consequently, therapies aimed to restore the autophagic flux might attenuate or prevent the progression of NAFLD.
438 citations
Authors
Showing all 20465 results
Name | H-index | Papers | Citations |
---|---|---|---|
Russel J. Reiter | 169 | 1646 | 121010 |
Aaron Dominguez | 147 | 1968 | 113224 |
Jose M. Ordovas | 123 | 1024 | 70978 |
Detlef Lohse | 104 | 1075 | 42787 |
Miroslav Krstic | 95 | 955 | 42886 |
María Vallet-Regí | 95 | 711 | 41641 |
John S. Sperry | 93 | 160 | 35602 |
Jose Rodriguez | 93 | 803 | 58176 |
Shun-ichi Amari | 90 | 495 | 40383 |
Michael Ortiz | 87 | 467 | 31582 |
Bruce J. Paster | 84 | 261 | 28661 |
Floyd E. Dewhirst | 81 | 229 | 42613 |
Joan Montaner | 80 | 489 | 22413 |
Francisco B. Ortega | 79 | 503 | 26069 |
Luis Paz-Ares | 77 | 592 | 31496 |