Institution
Pompeu Fabra University
Education•Barcelona, Spain•
About: Pompeu Fabra University is a education organization based out in Barcelona, Spain. It is known for research contribution in the topics: Population & Context (language use). The organization has 8093 authors who have published 23570 publications receiving 858431 citations. The organization is also known as: Universitat Pompeu Fabra & UPF.
Topics: Population, Context (language use), Gene, Computer science, Politics
Papers published on a yearly basis
Papers
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TL;DR: A primary and beneficial role is uncovered for the senescence-associated secretory phenotype in promoting cell plasticity and tissue regeneration and the concept that transient therapeutic delivery of senescent cells could be harnessed to drive tissue regeneration is introduced.
Abstract: Senescence is a form of cell cycle arrest induced by stress such as DNA damage and oncogenes. However, while arrested, senescent cells secrete a variety of proteins collectively known as the senescence-associated secretory phenotype (SASP), which can reinforce the arrest and induce senescence in a paracrine manner. However, the SASP has also been shown to favor embryonic development, wound healing, and even tumor growth, suggesting more complex physiological roles than currently understood. Here we uncover timely new functions of the SASP in promoting a proregenerative response through the induction of cell plasticity and stemness. We show that primary mouse keratinocytes transiently exposed to the SASP exhibit increased expression of stem cell markers and regenerative capacity in vivo. However, prolonged exposure to the SASP causes a subsequent cell-intrinsic senescence arrest to counter the continued regenerative stimuli. Finally, by inducing senescence in single cells in vivo in the liver, we demonstrate that this activates tissue-specific expression of stem cell markers. Together, this work uncovers a primary and beneficial role for the SASP in promoting cell plasticity and tissue regeneration and introduces the concept that transient therapeutic delivery of senescent cells could be harnessed to drive tissue regeneration.
398 citations
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TL;DR: This article reviews the mechanisms of resistance, epidemiology, and clinical impact and current and upcoming therapeutic options of Pseudomonas aeruginosa, and describes future options, such as use of vaccines, antibodies, bacteriocins, anti-quorum sensing, and bacteriophages.
Abstract: In recent years, the worldwide spread of the so-called high-risk clones of multidrug-resistant or extensively drug-resistant (MDR/XDR) Pseudomonas aeruginosa has become a public health threat. This article reviews their mechanisms of resistance, epidemiology, and clinical impact and current and upcoming therapeutic options. In vitro and in vivo treatment studies and pharmacokinetic and pharmacodynamic (PK/PD) models are discussed. Polymyxins are reviewed as an important therapeutic option, outlining dosage, pharmacokinetics and pharmacodynamics, and their clinical efficacy against MDR/XDR P. aeruginosa infections. Their narrow therapeutic window and potential for combination therapy are also discussed. Other "old" antimicrobials, such as certain β-lactams, aminoglycosides, and fosfomycin, are reviewed here. New antipseudomonals, as well as those in the pipeline, are also reviewed. Ceftolozane-tazobactam has clinical activity against a significant percentage of MDR/XDR P. aeruginosa strains, and its microbiological and clinical data, as well as recommendations for improving its use against these bacteria, are described, as are those for ceftazidime-avibactam, which has better activity against MDR/XDR P. aeruginosa, especially strains with certain specific mechanisms of resistance. A section is devoted to reviewing upcoming active drugs such as imipenem-relebactam, cefepime-zidebactam, cefiderocol, and murepavadin. Finally, other therapeutic strategies, such as use of vaccines, antibodies, bacteriocins, anti-quorum sensing, and bacteriophages, are described as future options.
395 citations
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VU University Amsterdam1, Erasmus University Rotterdam2, University of Zurich3, Harvard University4, Cornell University5, Hospital for Special Surgery6, University of Amsterdam7, University of Toronto8, Statens Serum Institut9, University of Copenhagen10, University of Queensland11, University of Essex12, ETH Zurich13, Broad Institute14, University of Oxford15, German Institute for Economic Research16, Max Planck Society17, Pompeu Fabra University18, University of Edinburgh19, University of Oulu20, University of California, San Diego21, University of Lübeck22, Institut Pere Mata23, University of Colorado Boulder24, University of Konstanz25, University of North Carolina at Chapel Hill26, University of Fribourg27, Karolinska Institutet28, St. Joseph's Healthcare Hamilton29, University of Guelph30, Ludwig Maximilian University of Munich31, University of Cologne32, University of Innsbruck33, University College London34, University of Chicago35, Imperial College London36, University of Tartu37, Stockholm School of Economics38, Geisinger Health System39, Catalan Institution for Research and Advanced Studies40, University of Mainz41, University of Southern California42, Uniformed Services University of the Health Sciences43, Western General Hospital44, Translational Research Institute45, University of Minnesota46, New York University47, National Bureau of Economic Research48
TL;DR: This paper found evidence of substantial shared genetic influences across risk tolerance and the risky behaviors: 46 of the 99 general risk tolerance loci contain a lead SNP for at least one of their other GWAS, and general risk-tolerance is genetically correlated with a range of risky behaviors.
Abstract: Humans vary substantially in their willingness to take risks. In a combined sample of over 1 million individuals, we conducted genome-wide association studies (GWAS) of general risk tolerance, adventurousness, and risky behaviors in the driving, drinking, smoking, and sexual domains. Across all GWAS, we identified hundreds of associated loci, including 99 loci associated with general risk tolerance. We report evidence of substantial shared genetic influences across risk tolerance and the risky behaviors: 46 of the 99 general risk tolerance loci contain a lead SNP for at least one of our other GWAS, and general risk tolerance is genetically correlated ([Formula: see text] ~ 0.25 to 0.50) with a range of risky behaviors. Bioinformatics analyses imply that genes near SNPs associated with general risk tolerance are highly expressed in brain tissues and point to a role for glutamatergic and GABAergic neurotransmission. We found no evidence of enrichment for genes previously hypothesized to relate to risk tolerance.
395 citations
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TL;DR: The data support that the interaction of CD94/NKG2C with HCMV-infected fibroblasts, concomitant to the inhibition of human leukocyte antigen (HLA) class I expression, promotes an outgrowth of CD 94/NKg2C(+) NK cells.
395 citations
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22 Jan 2009TL;DR: The Iraq debate in British parliament as discussed by the authors was a seminal moment in the history of the UK's political debate on the Iraq war. But it was not a watershed moment in British political life.
Abstract: 1. Introduction 2. Context and social cognition 3. Context and society 4. Context and culture 5. Context and politics: the Iraq debate in British parliament 6. Conclusions.
394 citations
Authors
Showing all 8248 results
Name | H-index | Papers | Citations |
---|---|---|---|
Andrei Shleifer | 171 | 514 | 271880 |
Paul Elliott | 153 | 773 | 103839 |
Bert Brunekreef | 124 | 806 | 81938 |
Philippe Aghion | 122 | 507 | 73438 |
Anjana Rao | 118 | 337 | 61395 |
Jordi Sunyer | 115 | 798 | 57211 |
Kenneth J. Arrow | 113 | 411 | 111221 |
Xavier Estivill | 110 | 673 | 59568 |
Roderic Guigó | 108 | 304 | 106914 |
Mark J. Nieuwenhuijsen | 107 | 647 | 49080 |
Jordi Alonso | 107 | 523 | 64058 |
Alfonso Valencia | 106 | 542 | 55192 |
Luis Serrano | 105 | 452 | 42515 |
Vadim N. Gladyshev | 102 | 490 | 34148 |
Josep M. Antó | 100 | 493 | 38663 |