Institution
University of Geneva
Education•Geneva, Switzerland•
About: University of Geneva is a education organization based out in Geneva, Switzerland. It is known for research contribution in the topics: Population & Galaxy. The organization has 26887 authors who have published 65265 publications receiving 2931373 citations. The organization is also known as: Geneva University & Universite de Geneve.
Topics: Population, Galaxy, Planet, Stars, Context (language use)
Papers published on a yearly basis
Papers
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TL;DR: The roles of mitochondria in the generation of ROS-derived anti-microbial effectors, the interplay of mitochondia and ROS with autophagy and the formation of DNA extracellular traps, and activation of the NLRP3 inflammasome by ROS and mitochondria are discussed.
Abstract: Reactive oxygen species (ROS) are integral components of multiple cellular pathways even though excessive or inappropriately localized ROS damage cells. ROS function as anti-microbial effector molecules and as signaling molecules that regulate such processes as NF-kB transcriptional activity, the production of DNA-based neutrophil extracellular traps (NETs), and autophagy. The main sources of cellular ROS are mitochondria and NADPH oxidases (NOXs). In contrast to NOX-generated ROS, ROS produced in the mitochondria (mtROS) were initially considered to be unwanted by-products of oxidative metabolism. Increasing evidence indicates that mtROS have been incorporated into signaling pathways including those regulating immune responses and autophagy. As metabolic hubs, mitochondria facilitate crosstalk between the metabolic state of the cell with these pathways. Mitochondria and ROS are thus a nexus of multiple pathways that determine the response of cells to disruptions in cellular homeostasis such as infection, sterile damage, and metabolic imbalance. In this review, we discuss the roles of mitochondria in the generation of ROS-derived anti-microbial effectors, the interplay of mitochondria and ROS with autophagy and the formation of DNA extracellular traps, and activation of the NLRP3 inflammasome by ROS and mitochondria.
612 citations
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TL;DR: It is demonstrated that Shh is required for cell proliferation in the mouse forebrain's subventricular zone (SVZ) stem cell niche and for the production of new olfactory interneurons in vivo, and the role of Shh signaling in the regulation of stem cell lineages in the adult mammalian brain is demonstrated.
Abstract: Sonic hedgehog (Shh) signaling controls many aspects of ontogeny, orchestrating congruent growth and patterning. During brain development, Shh regulates early ventral patterning while later on it is critical for the regulation of precursor proliferation in the dorsal brain, namely in the neocortex, tectum and cerebellum. We have recently shown that Shh also controls the behavior of cells with stem cell properties in the mouse embryonic neocortex, and additional studies have implicated it in the control of cell proliferation in the adult ventral forebrain and in the hippocampus. However, it remains unclear whether it regulates adult stem cell lineages in an equivalent manner. Similarly, it is not known which cells respond to Shh signaling in stem cell niches. Here we demonstrate that Shh is required for cell proliferation in the mouse forebrain's subventricular zone (SVZ) stem cell niche and for the production of new olfactory interneurons in vivo. We identify two populations of Gli1+ Shh signaling responding cells: GFAP+ SVZ stem cells and GFAP- precursors. Consistently, we show that Shh regulates the self-renewal of neurosphere-forming stem cells and that it modulates proliferation of SVZ lineages by acting as a mitogen in cooperation with epidermal growth factor (EGF). Together, our data demonstrate a critical and conserved role of Shh signaling in the regulation of stem cell lineages in the adult mammalian brain, highlight the subventricular stem cell astrocytes and their more abundant derived precursors as in vivo targets of Shh signaling, and demonstrate the requirement for Shh signaling in postnatal and adult neurogenesis.
612 citations
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TL;DR: A review of the cerebral substrates of the central executive component of the working memory model is presented in this article, where it is shown that different executive functions (manipulating and updating of information, dual-task coordination, inhibition and shifting processes) not only recruit various frontal areas but also depend upon posterior (mainly parietal) regions.
612 citations
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Istituto Giannina Gaslini1, Cincinnati Children's Hospital Medical Center2, University of Paris3, Semmelweis University4, Rambam Health Care Campus5, National Health Service6, Istanbul University7, University of Toronto8, Turkish Ministry of Health9, University of Geneva10, Charité11, Federal University of Rio de Janeiro12, University College London13, Katholieke Universiteit Leuven14, Rikshospitalet–Radiumhospitalet15, University of Paris-Sud16, Karolinska Institutet17, Hacettepe University18, Rio de Janeiro State University19, Novartis20, University of Genoa21
TL;DR: These two phase 3 studies show the efficacy and safety of canakinumab in systemic JIA with active systemic features, and among the 100 patients who underwent randomization in the withdrawal phase, the risk of flare was lower among patients who continued to receive canakinUMab than among those who were switched to placebo.
Abstract: A B S T R AC T BACKGROUND Interleukin-1 is pivotal in the pathogenesis of systemic juvenile idiopathic arthritis (JIA). We assessed the efficacy and safety of canakinumab, a selective, fully human, anti–interleukin-1β monoclonal antibody, in two trials. METHODS In trial 1, we randomly assigned patients, 2 to 19 years of age, with systemic JIA and active systemic features (fever; ≥2 active joints; C-reactive protein, >30 mg per liter; and glucocorticoid dose, ≤1.0 mg per kilogram of body weight per day), in a double-blind fashion, to a single subcutaneous dose of canakinumab (4 mg per kilo gram) or placebo. The primary outcome, termed adapted JIA ACR 30 response, was defined as improvement of 30% or more in at least three of the six core criteria for JIA, worsening of more than 30% in no more than one of the criteria, and resolution of fever. In trial 2, after 32 weeks of open-label treatment with canakinumab, pa tients who had a response and underwent glucocorticoid tapering were randomly assigned to continued treatment with canakinumab or to placebo. The primary outcome was time to flare of systemic JIA. RESULTS At day 15 in trial 1, more patients in the canakinumab group had an adapted JIA ACR 30 response (36 of 43 [84%], vs. 4 of 41 [10%] in the placebo group; P<0.001). In trial 2, among the 100 patients (of 177 in the open-label phase) who underwent randomization in the withdrawal phase, the risk of flare was lower among patients who continued to receive canakinumab than among those who were switched to pla cebo (74% of patients in the canakinumab group had no flare, vs. 25% in the pla
611 citations
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TL;DR: This paper studied the interplay between the child's action sequences and his implicit theories which the observer infers from the sequences rather than from his verbal comments, focusing on the role of counterexamples and on shifts in attention from goal to means.
609 citations
Authors
Showing all 27203 results
Name | H-index | Papers | Citations |
---|---|---|---|
JoAnn E. Manson | 270 | 1819 | 258509 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Kari Stefansson | 206 | 794 | 174819 |
David Baltimore | 203 | 876 | 162955 |
Mark I. McCarthy | 200 | 1028 | 187898 |
Michael S. Brown | 185 | 422 | 123723 |
Yang Gao | 168 | 2047 | 146301 |
Napoleone Ferrara | 167 | 494 | 140647 |
Marc Weber | 167 | 2716 | 153502 |
Alessandro Melchiorri | 151 | 674 | 116384 |
Andrew D. Hamilton | 151 | 1334 | 105439 |
David P. Strachan | 143 | 472 | 105256 |
Andrew Beretvas | 141 | 1985 | 110059 |
Rainer Wallny | 141 | 1661 | 105387 |
Josh Moss | 139 | 1019 | 89255 |