29 research outputs found

    The West African Monsoon Onset: a concise comparison of definitions

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    The onset of the West African Monsoon (WAM) marks a vital time for local and regional stakeholders. Whilst the seasonal progression of monsoon winds and the related migration of precipitation from the Guinea Coast towards the Soudan/Sahel is apparent, there exist contrasting man-made definitions of what the WAM onset means. Broadly speaking, onset can be analyzed regionally, locally or over a designated intermediate scale. There are at least eighteen distinct definitions of the WAM onset in publication with little work done on comparing observed onset from different definitions or comparing onset realizations across different datasets and resolutions. Here, nine definitions have been calculated using multiple datasets of different metrics at different resolution. It is found that mean regional onset dates are consistent across multiple datasets and different definitions. There is low inter-annual variability in regional onset suggesting that regional seasonal forecasting of the onset provides few benefits over climatology. In contrast, local onsets show high spatial, inter-annual and inter-definition variability. Furthermore it is found that there is little correlation between local onset dates and regional onset dates across West Africa implying a disharmony between regional measures of onset and the experience on a local scale. The results of this study show that evaluation of seasonal monsoon onset forecasts is far from straightforward. Given a seasonal forecasting model, it is possible to simultaneously have a good and bad prediction of monsoon onset simply through selection of onset definition and observational dataset used for comparison

    Identification of mediators involved in the Follistatin actions on skeletal muscle : proteomic and transcriptomic approaches

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    Follistatin has been shown to induce a marked increase in muscle mass. In addition, it impacts on muscle contractility and energy metabolism. However, the molecular mechanisms responsible for these phenotypic changes remain unclear. The aim of this thesis was to characterize the skeletal muscle proteome, transcriptome and secretome of mice overexpressing Follistatin in order to identify new mediators in the Follistatin actions on skeletal muscle. Our work provides molecular-level insights to explain the observed muscle phenotypic changes in both fast and slow muscles, including modifications in energy metabolism, fiber type, insulin and calcium signalings, as well as membrane repair and regeneration. Furthermore, we demonstrate that IGF-I and PAK1 are dispensable for the hypertrophic effect of Follistatin, in contrast to insulin. From a metabolic point of view, we show that Follistatin increases GLUT4 vesicles translocation independently of the PAK1 activity kinase. Finally, we provide the first putative secretome of skeletal muscle overexpressing Follistatin.(BIFA - Sciences biomédicales et pharmaceutiques) -- UCL, 201

    Une science de la rencontre. L’écologie scientifique au service de formations interdisciplinaires

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    International audienceLooking back at the essence of scientific ecology is at the core of this article in which we try to show how this discipline can enrich, in many aspects, interdisciplinary trainings. Ecology has long been ignoring the integration of human beings into its field of study. However, in view of the crises we are currently experiencing, the ecological perspective has taken a turn towards more transversal approaches. We will see how this science of encounter (encounter of disciplines, schools of thought, values, rationalities) and of knowledge of the sensible allows a paradigm shift through key concepts such as (socio)-ecosystems, complexity, dynamics, interrelationships or uncertainties. Questions and knowledge that scientific ecology raises are therefore intended to promote a better general understanding of the functioning of human societies nested within living systems.Dans cet article, nous revenons sur ce qui constitue le cœur de l’écologie scientifique, et montrons comment cette discipline peut enrichir les formations interdisciplinaires à plusieurs égards. L’écologie a longtemps eu tendance à laisser l’être humain en dehors de son champ d’étude. Or, au regard des crises que nous vivons actuellement, la perspective écologique a pris un tournant pour s’orienter vers des approches plus transversales. Nous verrons comment cette science de la rencontre (rencontre des disciplines, des courants de pensée, des valeurs, des rationalités…) et de la connaissance du sensible permet un changement de paradigme au travers de concepts clés, tels que les (socio-écosystèmes, la complexité, la dynamique, les interrelations ou encore les incertitudes. Les questionnements et savoirs issus de l’écologie scientifique ont donc vocation à favoriser une meilleure compréhension générale des fonctionnements des sociétés humaines imbriquées au sein des systèmes vivants

    Glucocorticoid-induced skeletal muscle atrophy

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    Many pathological states characterized by muscle atrophy (e.g., sepsis, cachexia, starvation, metabolic acidosis and severe insulinopenia) are associated with an increase in circulating glucocorticoids (GC) levels, suggesting that GC could trigger the muscle atrophy observed in these conditions. GC-induced muscle atrophy is characterized by fast-twitch, glycolytic muscles atrophy illustrated by decreased fiber cross-sectional area and reduced myofibrillar protein content. GC-induced muscle atrophy results from increased protein breakdown and decreased protein synthesis. Increased muscle proteolysis, in particular through the activation of the ubiquitin proteasome and the lysosomal systems, is considered to play a major role in the catabolic action of GC. The stimulation by GC of these two proteolytic systems is mediated through the increased expression of several Atrogenes ("genes involved in atrophy"), such as FOXO, Atrogin-1, and MuRF-1. The inhibitory effect of GC on muscle protein synthesis is thought to result mainly from the inhibition of the mTOR/S6 kinase 1 pathway. These changes in muscle protein turnover could be explained by changes in the muscle production of two growth factors, namely Insulin-like Growth Factor (IGF)-I, a muscle anabolic growth factor and Myostatin, a muscle catabolic growth factor. This review will discuss the recent progress made in the understanding of the mechanisms involved in GC-induced muscle atrophy and consider the implications of these advancements in the development of new therapeutic approaches for treating GC-induced myopathy. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting

    Comparative Proteomic and Transcriptomic Analysis of Follistatin-Induced Skeletal Muscle Hypertrophy.

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    Skeletal muscle, the most abundant body tissue, plays vital roles in locomotion and metabolism. Myostatin is a negative regulator of skeletal muscle mass. In addition to increasing muscle mass, Myostatin inhibition impacts muscle contractility and energy metabolism. To decipher the mechanisms of action of the Myostatin inhibitors, we used proteomic and transcriptomic approaches to investigate the changes induced in skeletal muscles of transgenic mice overexpressing Follistatin, a physiological Myostatin inhibitor. Our proteomic workflow included a fractionation step to identify weakly expressed proteins and a comparison of fast versus slow muscles. Functional annotation of altered proteins supports the phenotypic changes induced by Myostatin inhibition, including modifications in energy metabolism, fiber type, insulin and calcium signaling, as well as membrane repair and regeneration. Less than 10% of the differentially expressed proteins were found to be also regulated at the mRNA level but the Biological Process annotation, and the KEGG pathways analysis of transcriptomic results shows a great concordance with the proteomic data. Thus this study describes the most extensive omics analysis of muscle overexpressing Follistatin, providing molecular-level insights to explain the observed muscle phenotypic changes

    Incarner l'Ă©cologie : s'ouvrir aux mondes vivants

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    L’écologie est une science jeune qui s’est construite comme une nouvelle discipline scientifique dès la fin du XIX siècle, mais qui tire ses origines d’une accumulation de connaissances remontant à plusieurs siècles. Sa raison d’être est l’étude du monde vivant non-humain et de ses multiples interactions complexes et dynamiques. Cette science, qui ne cesse d’évoluer, nous offre de nombreux enseignements qu’il est nécessaire de mobiliser pour comprendre et agir dans un monde incertain. Elle est une grande source d’inspiration pour faire face aux profondes crises écologiques et sociales qui bousculent nos sociétés. C’est pourquoi nous mobilisons à la fois théorie et pratique, réflexion et action, science et conscience. Dans ce livre, nous tenterons de naviguer à travers la diversité des débats, des concepts et des évolutions scientifiques de l’écologie. Nous invitons les lecteurs à plonger au cœur d’une science transformative et en transformation, et à cheminer dans les méandres d’une écologie « incarnée » faisant prendre conscience de notre enracinement existentiel dans un habitat unique : la Terre. Laissez-vous guider dans cette extraordinaire aventure pédagogique et réflexive !Raccorder l’enseignement supérieur aux enjeux écologiques et sociaux de notre époque : telle est l’ambition du collectif d’enseignants-chercheurs FORTES qui a réfléchi et écrit le volume de la collection des Petits manuels de la Grande transition que vous tenez entre les mains

    Toll-Like Receptor 4 Knockout Mice Are Protected against Endoplasmic Reticulum Stress Induced by a High-Fat Diet.

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    The purpose of this study was to investigate whether toll-like receptor 4 (TLR4) is implicated in the development of endoplasmic reticulum stress (ER stress) observed after a high-fat diet (HFD) in liver, skeletal muscle and adipose tissue. TLR4(-/-) and C57BL/6J wild-type mice (WT) were fed with chow or HFD (45% calories from fat) during 18 weeks. An oral glucose tolerance-test was performed. The animals were sacrificed in a fasted state and the tissues were removed. TLR4 deletion protected from body weight gain and glucose intolerance induced by HFD whereas energy intake was higher in transgenic mice suggesting larger energy expenditure. HFD induced an ER stress in skeletal muscle, liver and adipose tissue of WT mice as assessed by BiP, CHOP, spliced and unspliced XBP1 and phospho-eIF2α. TLR4(-/-) mice were protected against HFD-induced ER stress. Then, we investigated the main signaling downstream of TLR4 namely the NF-κB pathway, expecting to identify the mechanism by which TLR4 is able to activate ER stress. The mRNA levels of cytokines regulated by NF-κB namely TNFα, IL-1β and IL-6, were not changed after HFD and phospho-IκB-α (ser 32) was not changed. Our results indicate that TLR4 is essential for the development of ER stress related to HFD. Nevertheless, the NFκ-B pathway does not seem to be directly implicated. The reduced fat storage in TLR4(-/-) mice could explain the absence of an ER stress after HFD

    Activation of ER stress by hydrogen peroxide in C2C12 myotubes

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    The purpose of this study was to examine the link between oxidative stress and endoplasmic reticulum (ER) stress in myogenic cells. C2C12 myotubes were incubated with hydrogen peroxide (H2O2, 200 μM) and harvested 4h or 17 h after the induction of this oxidative stress. A massive upregulation of binding immunoglobulin protein (BiP) was found, indicating the presence of ER stress. Nevertheless, the three branches of the unfolded protein response (UPR) were not activated to the same extent. The double-stranded RNA-dependent protein kinase (PKR)-like ER kinase (PERK) branch was the most activated as shown by the increase of phospho-eukaryotic translation-initiation factor 2α (eIF2α, Ser51) and the mRNA levels of activating transcription factor 4 (ATF4), C/EBP homologous (CHOP) and tribbles homolog 3 (TRB3). The slight increase in the spliced form of X-box binding protein 1 (XBP1s) together with the decrease of the unspliced form (XBP1u) indicated a higher endoribonuclease activity of inositol-requiring 1α (IRE1α). The transcriptional activity of activating transcription factor 6 (ATF6) remained unchanged after incubation with H2O2. The mechanisms by which the three branches of UPR can be specifically regulated by oxidative stress are currently unresolved and need further investigations.status: publishe

    Activation of ER stress by hydrogen peroxide in C2C12 myotubes.

    No full text
    The purpose of this study was to examine the link between oxidative stress and endoplasmic reticulum (ER) stress in myogenic cells. C2C12 myotubes were incubated with hydrogen peroxide (H2O2, 200μM) and harvested 4h or 17h after the induction of this oxidative stress. A massive upregulation of binding immunoglobulin protein (BiP) was found, indicating the presence of ER stress. Nevertheless, the three branches of the unfolded protein response (UPR) were not activated to the same extent. The double-stranded RNA-dependent protein kinase (PKR)-like ER kinase (PERK) branch was the most activated as shown by the increase of phospho-eukaryotic translation-initiation factor 2α (eIF2α, Ser51) and the mRNA levels of activating transcription factor 4 (ATF4), C/EBP homologous (CHOP) and tribbles homolog 3 (TRB3). The slight increase in the spliced form of X-box binding protein 1 (XBP1s) together with the decrease of the unspliced form (XBP1u) indicated a higher endoribonuclease activity of inositol-requiring 1α (IRE1α). The transcriptional activity of activating transcription factor 6 (ATF6) remained unchanged after incubation with H2O2. The mechanisms by which the three branches of UPR can be specifically regulated by oxidative stress are currently unresolved and need further investigations
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