Compétences attendues pour un accueil de qualité dans l’Accueil Temps Libre (ATL)

Assurer un accueil de qualité dans le périscolaire nécessite des compétences professionnelles quel que soit le statut de la personne en fonction. C’est un métier complexe, au cœur d’enjeux sociétaux essentiels. Cette conférence a pour objectif de présenter la complexité cachée de ce métier et les enjeux de formation, plus largement de professionnalisation à développer dans le court, moyen et long terme

AMPK prevents cardiac hypertrophy development by inhibiting O-GlcNAcylation

Concentric pathological cardiac hypertrophy occurs following pressure-overload. It is proposed that preventing this hypertrophy could prevent the progression towards heart failure. Our work demonstrates that AMPK activation inhibits cardiomyocyte hypertrophy independently of the previously proposed downstream targets. By contrast, we show that the anti-hypertrophic action of AMPK is caused by the inhibition of protein O-GlcNAcylation. Our study reveal that AMPK activation induces phosphorylation and inhibition of GFAT as well as decreases OGT protein expression, both enzymes being required for O-GlcNAcylation. The AMPK-mediated inhibition of protein O-GlcNAcylation and its central role in the reduction of cardiac hypertrophy bring new potential therapeutic opportunities for the treatment of this pathology.(BIFA - Sciences biomédicales et pharmaceutiques) -- UCL, 201

Cloning and expression of human brain type I inositol 1,4,5-trisphosphate 5-phosphatase: high levels of mRNA in cerebellar Purkinje cells

In brain and many other tissues, Type I inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase is the major isozyme hydrolysing the calcium-mobilizing second messenger InsP3. We recently reported the cloning and expression of dog thyroid InsP3 5-phosphatase. During the course of this cloning, screening of a human brain cDNA library allowed us to isolate a cDNA clone D1 with 91% sequence identity with the thyroid sequence. When clone D1 was expressed in Escherichia coli, the fusion protein had InsP3 5-phosphatase activity. Mr estimates of the recombinant enzyme made by unmunodetection, activity assay after SDS/PAGE or silver staining were consistent with the calculated molecular mass. In situ hybridization on human cerebellum sections localised the mRNA for this enzyme to the Purkinje cells. © 1994.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

O-GlcNAcylation, enemy or ally during cardiac hypertrophy development?

O-linked attachment of the monosaccharide β-N-acetyl-glucosamine (O-GlcNAcylation) is a post-translational modification occurring on serine and threonine residues, which is evolving as an important mechanism for the regulation of various cellular processes. The present review will, first, provide a general background on the molecular regulation of protein O-GlcNAcylation and will summarize the role of this post-translational modification in various acute cardiac pathologies including ischemia-reperfusion. Then, we will focus on research studies examining protein O-GlcNAcylation in the context of cardiac hypertrophy. A particular emphasis will be laid on the convergent but also divergent actions of O-GlcNAcylation according to the type of hypertrophy investigated, including physiological, pressure overload-induced and diabetes-linked cardiac hypertrophy. In an attempt to distinguish whether O-GlcNAcylation is detrimental or beneficial, this review will present the different O-GlcNAcylated targets involved in hypertrophy development. We will finally argue on potential interest to target O-GlcNAc processes to treat cardiac hypertrophy. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz

Studying the Role of AMPK in Cardiac Hypertrophy and Protein Synthesis.

Pathological cardiac hypertrophy, which is a compensatory mechanism established to maintain cardiac function in response to neurohormonal or mechanical stresses, becomes maladaptive with time and frequently leads to heart failure. AMP-activated protein kinase (AMPK) has been extensively described in the literature to act as a break in cardiac hypertrophy development. Its anti-hypertrophic action mostly correlates with the inhibition of several important players of cardiac hypertrophy including protein synthesis and pro-hypertrophic gene expression pathways involving the transcription factor nuclear factor of activated T cells (NFAT) and the mitogen-activated protein kinases ERK1/2. In this chapter, we describe methodologies designed to evaluate cardiomyocyte hypertrophy and its major molecular mechanisms in response to AMPK activation. Two different compounds, AICAr and the biguanide phenformin, were used to promote AMPK activation

Le Japon et le fait colonial II

Ce numéro 19 constitue le deuxième volume de notre projet éditorial « Le Japon et le fait colonial ». Il y est question du temps postcolonial au sens le plus littéral et donc chronologique de ce terme. Ce passé colonial s’entremêle avec le contexte de l’après-guerre – c’est-à-dire celui de la guerre froide –, et des conflits « chauds », contexte qui complique lourdement la question du règlement du passé. Les numéros 18 et 19 développent une thèse forte : il est impossible de restituer une sorte de grande mécanique générale qui caractériserait tout ce qui est origine et conséquence de la colonisation japonaise. La colonisation n’est pas un bloc monolithique, mais un phénomène dynamique et protéiforme, qui se développe tantôt en adéquation avec son terrain d’élection (ce que démontrent les politiques, au pluriel, de développement), tantôt contre ses propres intérêts à moyen ou long terme (ce que virent, fort tôt, certains critiques et commentateurs japonais). Notre objet était d’illustrer la complexité, parfois aussi les ambiguïtés, de la situation et des discours tant du colonisateur que du colonisé, tant de l’ancien colonisateur que de l’ancien colonisé

Noninvasive monitoring of fibre fermentation in healthy volunteers by analyzing breath volatile metabolites: lessons from the FiberTAG intervention study.

The fermentation of dietary fibre (DF) leads to the production of bioactive metabolites, the most volatile ones being excreted in the breath. The aim of this study was to analyze the profile of exhaled breath volatile metabolites (BVM) and gastrointestinal symptoms in healthy volunteers after a single ingestion of maltodextrin (placebo) versus chitin-glucan (CG), an insoluble DF previously shown to be fermented into short-chain fatty acids (SCFA) by the human microbiota in vitro. Maltodextrin (4.5 g at day 0) or CG (4.5 g at day 2) were added to a standardized breakfast in fasting healthy volunteers (n = 15). BVM were measured using selected ion flow tube mass spectrometry (SIFT-MS) throughout the day. A single ingestion of 4.5 g CG did not induce significant gastrointestinal discomfort. Untargeted metabolomics analysis of breath highlighted that 13 MS-fragments (among 408 obtained from ionizations of breath) discriminated CG versus maltodextrin acute intake in the posprandial state. The targeted analysis revealed that CG increased exhaled butyrate and 5 other BVM - including the microbial metabolites 2,3-butanedione and 3-hydroxybutanone - with a peak observed 6 h after CG intake. Correlation analyses with fecal microbiota (Illumina 16S rRNA sequencing) spotlighted as a potential genus responsible for the presence of butyric acid, triethylamine and 3-hydroxybutanone in the breath. In conclusion, measuring BMV in the breath reveals the microbial signature of the fermentation of DF after a single ingestion. This protocol allows to analyze the time-course of released bioactive metabolites that could be proposed as new biomarkers of DF fermentation, potentially linked to their biological properties. Trial registration: Clinical Trials NCT03494491. Registered 11 April 2018 - Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT03494491

AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation

AMPK activation inhibits cardiac hypertrophy. Here the authors show that this occurs independently of previously proposed mechanisms and that AMPK controls the phosphorylation of the aminotransferase GFAT, thereby preventing cardiac hypertrophy through the reduction of protein O-GlcNAcylation

Isoprenylated human brain type I inositol 1,4,5-trisphosphate 5-phosphatase controls Ca2+ oscillations induced by ATP in Chinese hamster ovary cells.

D-myo-Inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase and 3-kinase are thought to be critical regulatory enzymes in the control of InsP3 and Ca2+ signaling. In brain and many other cells, type I InsP3 5-phosphatase is the major phosphatase that dephosphorylates InsP3 and D-myo-inositol 1,3,4,5-tetrakisphosphate. The type I 5-phosphatase appears to be associated with the particulate fraction of cell homogenates. Molecular cloning of the human brain enzyme identifies a C-terminal farnesylation site CVVQ. Post-translational modification of this enzyme promotes membrane interactions and changes in specific activity. We have now compared the cytosolic Ca2+ ([Ca2+]i) responses induced by ATP, thapsigargin, and ionomycin in Chinese hamster ovary (CHO-K1) cells transfected with the intact InsP3 5-phosphatase and with a mutant in which the C-terminal cysteine cannot be farnesylated. [Ca2+]i was also measured in cells transfected with an InsP3 3-kinase construct encoding the A isoform. The Ca2+ oscillations detected in the presence of 1 microM ATP in control cells were totally lost in 87.5% of intact (farnesylated) InsP3 5-phosphatase-transfected cells, while such a loss occurred in only 1.1% of the mutant InsP3 5-phosphatase-transfected cells. All cells overexpressing the InsP3 3-kinase also responded with an oscillatory pattern. However, in contrast to control cells, the [Ca2+]i returned to base-line levels in between a couple of oscillations. The [Ca2+]i responses to thapsigargin and ionomycin were identical for all cells. The four cell clones compared in this study also behaved similarly with respect to capacitative Ca2+ entry. In permeabilized cells, no differences in extent of InsP3-induced Ca2+ release nor in the threshold for InsP3 action were observed among the four clones and no differences in the expression levels of the various InsP3 receptor isoforms could be shown between the clones. Our data support the contention that the ATP-induced increase in InsP3 concentration in transfected CHO-K1 cells is essentially restricted to the site of its production near the plasma membrane, where it can be metabolized by the type I InsP3 5-phosphatase. This enzyme directly controls the [Ca2+]i response and the Ca2+ oscillations in intact cells.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe