Institution
University of Bordeaux
Education•Bordeaux, France•
About: University of Bordeaux is a education organization based out in Bordeaux, France. It is known for research contribution in the topics: Population & Laser. The organization has 28811 authors who have published 55536 publications receiving 1619635 citations. The organization is also known as: UB.
Topics: Population, Laser, Raman spectroscopy, Polymerization, Crystal structure
Papers published on a yearly basis
Papers
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TL;DR: In this article, the authors present a dynamic model exploiting action settings, observation settings and debate-of-idea settings for the ultimate goal of conshucting strategic and tactical knowledge in team sports.
Abstract: In team sports, playing well means choosing the right course of action at the right moment and performing that course of action efficiently and consistently throughout the match. Research on decision making in sports indicates that although experts make more accurate decisions based on earlier occurring information, they tend to have speed, rather than accuracy, context-specific advantage in decision making. In light of the key notion of configuration of play, elements underlying its perception and interpretation and the ensuing anticipation and decision making are discussed. In connection with teachinglearning settings, observation and verbalization are presented as key strategies for eliciting critical thinking and the development of strategic and tactical knowledge. Finally, the authors present a dynamic model exploiting (a) action settings. (b) observation settings, and (c) debate-of-idea settings for the ultimate goal of conshucting strategic and tactical knowledge in team sports.
255 citations
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TL;DR: In this paper, the authors compare calculated (pH and TA) and measured (equilibra- tor and headspace) water pCO2 in a large array of temperate and tropical freshwaters.
Abstract: Inland waters have been recognized as a signifi- cant source of carbon dioxide (CO2) to the atmosphere at the global scale. Fluxes of CO2 between aquatic systems and the atmosphere are calculated from the gas transfer velocity and the water-air gradient of the partial pressure of CO2 (pCO2). Currently, direct measurements of waterpCO2 remain scarce in freshwaters, and most published pCO2 data are calculated from temperature, pH and total alkalinity (TA). Here, we compare calculated (pH and TA) and measured (equilibra- tor and headspace) water pCO2 in a large array of temperate and tropical freshwaters. The 761 data points cover a wide range of values for TA (0 to 14 200 µmol L 1 ), pH (3.94 to 9.17), measured pCO2 (36 to 23 000 ppmv), and dissolved organic carbon (DOC) (29 to 3970 µmol L 1 ). Calculated pCO2 were > 10 % higher than measured pCO2 in 60 % of the samples (with a median overestimation of calculated pCO2 compared to measured pCO2 of 2560 ppmv) and were > 100 % higher in the 25 % most organic-rich and acidic samples (with a median overestimation of 9080 ppmv). We suggest these large overestimations of calculated pCO2 with respect to measured pCO2 are due to the combination of two cumulative effects: (1) a more significant contribution of or- ganic acids anions to TA in waters with low carbonate alka- linity and high DOC concentrations; (2) a lower buffering ca- pacity of the carbonate system at low pH, which increases the sensitivity of calculated pCO2 to TA in acidic and organic- rich waters. No empirical relationship could be derived from our data set in order to correct calculated pCO2 for this bias. Owing to the widespread distribution of acidic, organic-rich freshwaters, we conclude that regional and global estimates of CO2 outgassing from freshwaters based on pH and TA data only are most likely overestimated, although the magni- tude of the overestimation needs further quantitative analysis. Direct measurements of pCO2 are recommended in inland waters in general, and in particular in acidic, poorly buffered freshwaters.
255 citations
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TL;DR: Therapeutic strategies aimed at preserving and/or restoring the integrity of the endothelial glycocalyx, reversing the procoagulant and pro-inflammatory phenotype of injured endothelial cells and slowing renal fibrosis hold promise for the treatment of renal disease.
Abstract: The kidney harbours different types of endothelia, each with specific structural and functional characteristics. The glomerular endothelium, which is highly fenestrated and covered by a rich glycocalyx, participates in the sieving properties of the glomerular filtration barrier and in the maintenance of podocyte structure. The microvascular endothelium in peritubular capillaries, which is also fenestrated, transports reabsorbed components and participates in epithelial cell function. The endothelium of large and small vessels supports the renal vasculature. These renal endothelia are protected by regulators of thrombosis, inflammation and complement, but endothelial injury (for example, induced by toxins, antibodies, immune cells or inflammatory cytokines) or defects in factors that provide endothelial protection (for example, regulators of complement or angiogenesis) can lead to acute or chronic renal injury. Moreover, renal endothelial cells can transition towards a mesenchymal phenotype, favouring renal fibrosis and the development of chronic kidney disease. Thus, the renal endothelium is both a target and a driver of kidney and systemic cardiovascular complications. Emerging therapeutic strategies that target the renal endothelium may lead to improved outcomes for both rare and common renal diseases.
255 citations
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TL;DR: The central actors of mitochondrial fusion and fission are presented and the role of mitochondrial dynamics in neuronal physiology and pathophysiology is reviewed and particular emphasis is placed on DRP1,MFN1-2, and OPA1 as well as on GDAP1, a protein of the mitochondrial outer membrane preferentially expressed in neurons.
254 citations
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TL;DR: A unique combination of high-resolution nanoparticle and bulk live imaging approaches are used to demonstrate that anti-N-methyl-d-aspartate receptor autoantibodies from patients with encephalitis strongly alter, in a time-dependent manner, the surface content and trafficking of GluN2-NMDA receptor subtypes.
Abstract: Autoimmune synaptic encephalitides are recently described human brain diseases leading to psychiatric and neurological syndromes through inappropriate brain-autoantibody interactions. The most frequent synaptic autoimmune encephalitis is associated with autoantibodies against extracellular domains of the glutamatergic N-methyl-d-aspartate receptor, with patients developing psychotic and neurological symptoms in an autoantibody titre-dependent manner. Although N-methyl-d-aspartate receptors are the primary target of these antibodies, the cellular and molecular pathway(s) that rapidly lead to N-methyl-d-aspartate receptor dysfunction remain poorly understood. In this report, we used a unique combination of high-resolution nanoparticle and bulk live imaging approaches to demonstrate that anti-N-methyl-d-aspartate receptor autoantibodies from patients with encephalitis strongly alter, in a time-dependent manner, the surface content and trafficking of GluN2-NMDA receptor subtypes. Autoantibodies laterally displaced surface GluN2A-NMDA receptors out of synapses and completely blocked synaptic plasticity. This loss of extrasynaptic and synaptic N-methyl-d-aspartate receptor is prevented both in vitro and in vivo, by the activation of EPHB2 receptors. Indeed, the anti-N-methyl-d-aspartate receptor autoantibodies weaken the interaction between the extracellular domains of the N-methyl-d-aspartate and Ephrin-B2 receptors. Together, we demonstrate that the anti-N-methyl-d-aspartate receptor autoantibodies from patients with encephalitis alter the dynamic retention of synaptic N-methyl-d-aspartate receptor through extracellular domain-dependent mechanism(s), shedding new light on the pathology of the neurological and psychiatric disorders observed in these patients and opening possible new therapeutic strategies.
254 citations
Authors
Showing all 28995 results
Name | H-index | Papers | Citations |
---|---|---|---|
Nicholas G. Martin | 192 | 1770 | 161952 |
George F. Koob | 171 | 935 | 112521 |
Daniel J. Jacob | 162 | 656 | 76530 |
Arthur W. Toga | 159 | 1184 | 109343 |
James M. Tour | 143 | 859 | 91364 |
Floyd E. Bloom | 139 | 616 | 72641 |
Herbert Y. Meltzer | 137 | 1148 | 81371 |
Jean-Marie Tarascon | 136 | 853 | 137673 |
Stanley Nattel | 132 | 778 | 65700 |
Michel Haïssaguerre | 117 | 757 | 62284 |
Liquan Chen | 111 | 689 | 44229 |
Marion Leboyer | 110 | 773 | 50767 |
Jean-François Dartigues | 106 | 631 | 46682 |
Alexa S. Beiser | 106 | 366 | 47457 |
Robert Dantzer | 105 | 497 | 46554 |