Endurance ou force dans le réentrainement à l'effort chez des patients atteints d'artériopathie oblitérante des membres inférieurs: revue de la littérature : travail de Bachelor

Introduction : Les modalités d’un réentrainement à l’effort chez les patients atteints d’artériopathie oblitérante des membres inférieurs (AOMI) sont décrites de façon précises et structurées concernant la marche, mais restent controversées pour le renforcement. L’objectif de cette revue de la littérature est de comparer un entrainement de force et d’endurance chez les patients atteints d’AOMI au stade d’ischémie d’effort symptomatique ou non sur la distance totale de marche. Méthode : Nous avons effectué nos recherches sur les bases de données Medline, PEDro, Cochrane, CINHAL, embase BDSP et Kinédoc. Nos mots clés regroupaient 3 catégories ; les patients atteints d’AOMI au stade d’ischémie d’effort, l’entrainement de force et celui d’endurance. L’outcome étudié était centré sur la distance totale de marche. L’évaluation de la qualité des articles s’est faite avec l’échelle PEDro. Résultats : Une de nos trois études a montré une amélioration cliniquement significative de la distance totale de marche (DTM) en faveur d’un entrainement de force à haute intensité progressive comparé à un entrainement de marche. Les deux autres études ont démontré une amélioration similaire de la DTM évaluée sur tapis quelles que soient les modalités d’entrainement (marche ou force). Conclusion : Les études montrent que les bénéfices d’un entrainement de marche et d’un renforcement sont similaires. Cependant, une étude récente a montré qu’un entrainement de force à haute intensité permettrait d’améliorer aussi la DTM. Ce type d’entrainement apporte un intérêt supplémentaire puisqu’il ne déclenche pas de douleur de claudication par rapport à l’entrainement de marche. De futures études apporteront sûrement une réponse définitive quant aux bénéfices du renforcement

Nesprins are mechanotransducers that discriminate epithelial-mesenchymal transition programs

© 2020 Déjardin et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).LINC complexes are transmembrane protein assemblies that physically connect the nucleoskeleton and cytoskeleton through the nuclear envelope. Dysfunctions of LINC complexes are associated with pathologies such as cancer and muscular disorders. The mechanical roles of LINC complexes are poorly understood. To address this, we used genetically encoded FRET biosensors of molecular tension in a nesprin protein of the LINC complex of fibroblastic and epithelial cells in culture. We exposed cells to mechanical, genetic, and pharmacological perturbations, mimicking a range of physiological and pathological situations. We show that nesprin experiences tension generated by the cytoskeleton and acts as a mechanical sensor of cell packing. Moreover, nesprin discriminates between inductions of partial and complete epithelial-mesenchymal transitions. We identify the implicated mechanisms, which involve α-catenin capture at the nuclear envelope by nesprin upon its relaxation, thereby regulating β-catenin transcription. Our data thus implicate LINC complex proteins as mechanotransducers that fine-tune β-catenin signaling in a manner dependent on the epithelial-mesenchymal transition program.This material is based on work supported by the Centre national de la recherche scientifique (CNRS), Agence nationale de la recherche (ANR; grants ANR-13-JSV5-0007 and ANR-14-CE09-0006), France BioImaging (ANR-10-INBS-04), la Ligue contre le Cancer (REMX17751 to P.M. Davidson), and the Fondation ARC pour la Recherche sur le Cancer (PDF20161205227 to P.M. Davidson). P.S. Carollo has received funding from the European Union’s Horizon 2020 Framework Programme for Research and Innovation (Marie Skłodowska-Curie grant agreement 665850-INSPIRE) and acknowledges the Ecole Doctorale Frontières de l'Innovation en Recherche et Éducation (FIRE) Programme Bettencourt. E.R. Gomes was supported by a European Research Council consolidator grant (617676).info:eu-repo/semantics/publishedVersio

Spontaneous migration of cellular aggregates from giant keratocytes to running spheroids

Despite extensive knowledge on the mechanisms that drive singlecell migration, those governing the migration of cell clusters, as occurring during embryonic development and cancer metastasis,remain poorly understood. Here, we investigate the collective migration of cell on adhesive gels with variable rigidity, using 3D cellular aggregates as a model system. After initial adhesion to the substrate, aggregates spread by expanding outward a cell monolayer, whose dynamics is optimal in a narrowrange of rigidities. Fast expansion gives rise to the accumulation of mechanical tension that leads to the rupture of cell–cell contacts and the nucleation of holes within the monolayer, which becomes unstable and undergoes dewetting like a liquid film. This leads to a symmetry breaking and causes the entire aggregate to move as a single entity. Varying the substrate rigidity modulates the extent of dewetting and induces different modes of aggregate motion: “giant keratocytes,” where the lamellipodium is a cell monolayer that expands at the front and retracts at the back; “penguins,” characterized by bipedal locomotion; and “running spheroids,” for nonspreading aggregates. We characterize these diverse modes of collectivemigration by quantifying the flows and forces that drive them, andwe unveil the fundamental physical principles that govern these behaviors, which underscore the biological predisposition of living material to migrate, independent of length scale

Adhésion cellulaire et tubes de membrane : Quelques aspects dynamiques, mécaniques et rhéologiques

In the "adhesion" section, we have shown that the dynamics of vesicleadhesion induced by specific stickers was either governed by the diffusion of ligandsin the membrane or by the reaction time between immobilized receptors and ligands,depending on the chemical preparation of the decorated substrate. In contrast, theearly stages of living cell adhesion seem to be controlled by the viscous dissipationinside the cell.In the "tubes" section, we have studied the formation and the elongation ofmembrane tethers. First, by pulling long tubes from firmly adhered vesicles, wedemonstrated that the resulting unusual force-extension trace was the signature ofan elastic stretching of the lipid membrane. Second, by analyzing both experimentallyand theoretically the interaction and coalescence of two tethers, we proposed a novelmethod to determine the bending rigidity of phospholipid vesicles. Third, we haverevisited the mechanical and rheological description of tethers extracted from redblood cells and we evidenced a shear-thinning behavior of the membrane during theelongation, which indicates the significant influence of the underlying spectrinnetwork.Dans la partie "adhésion", nous avons montré que la dynamique d'adhésionde vésicules induite par des ligands spécifiques était gouvernée soit par la diffusionde ligands dans la membrane, soit par le temps de réaction entre le ligand et lerécepteur, dépendant de la préparation chimique des surfaces. Au contraire, lespremières étapes de l'adhésion de cellules semblent être contrôlées par ladissipation visqueuse à l'intérieur de la cellule.Dans la partie "tubes de membrane", nous avons étudié la formation etl'élongation de tubes de membrane. Tout d'abord, en formant des tubes à partir devésicules adhérées, nous avons montré que l'élongation des tubes s'accompagned'un étirement élastique de la membrane. Ensuite, en analysant expérimentalementet théoriquement l'interaction et la coalescence de deux tubes membranaires, nousavons proposé une méthode pour déterminer la rigidité de courbure de vésiculeslipidiques. Enfin, nous avons revisité la description mécanique de tubes extraits deglobules rouges et nous avons mis en évidence un comportement rhéofluidifiant dela membrane durant l'élongation, indiquant l'influence du squelette de spectrine

Adhésion cellulaire et tubes de membrane (quelques aspects dynamiques, mécaniques et rhéologiques)

PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Bilayer curling and winding in a viscous fluid

International audienceInduced spontaneous curvature is a new mechanism of microcapsules bursting by nucleation and growth of a hole surrounded by a curling rim. Here we study the dynamics of curling on a macroscopic scale induced by the elastic curvature of a bilayer of tracing paper and tape after soaking by water. The ribbon which is fully stretched at time t = 0 is immersed in a viscous oil. We observe the winding from the free end and find two regimes: rolling at constant velocity at short times, and a slowdown at long times. We interpret these two regimes by a balance of the elastic driving force and the friction force on the roll

Detachment and fracture of cellular aggregates

International audienceThe dynamics of cellular adhesion and deadhesion, which play key roles in many cellular processes, have most often been studied at the scale of single bonds or single cells. However, multicellular adhesion and deadhesion are also central processes in tissue mechanics, morphogenesis, and pathophysiology, where collective tissue phenomena may introduce additional effects that are absent at the single-cell level. In this paper we present experiments on the adhesion of cellular aggregates and a laboratory model system to study tissue mechanics. We introduce a technique to measure the forces and energies involved in the detachment of an aggregate from a substrate (which can be viewed as a cellular tack assay) and in the fracture between two partially fused aggregates, as a function of the adhesion time, the pulling speed, and the cadherin density at the cell surface. We develop a model based on polymer physics to interpret the observations. We identify a significant contribution to the adhesion energy of viscous dissipation mechanisms present at the tissue scale that are absent at the single-cell level, as well as a significant effect of the speed at which the separation force is applied

Curling instability induced by swelling

We study the spontaneous curving observed when a strip of tracing paper is deposited on a water surface. The differential swelling across the ribbon thickness leads to a curling of the sheet, with the curvature increasing to a maximum and then relaxing as the sheet becomes completely wet. We develop a theoretical model, in good agreement with our experimental observations and relevant to the understanding of curling instabilities induced by asymmetric swelling of natural or synthetic shells. © 2011 The Royal Society of Chemistry

Actin Stress Fibers Response and Adaptation under Stretch

One of the many effects of soft tissues under mechanical solicitation in the cellular damage produced by highly localized strain. Here, we study the response of peripheral stress fibers (SFs) to external stretch in mammalian cells, plated onto deformable micropatterned substrates. A local fluorescence analysis reveals that an adaptation response is observed at the vicinity of the focal adhesion sites (FAs) due to its mechanosensor function. The response depends on the type of mechanical stress, from a Maxwell-type material in compression to a complex scenario in extension, where a mechanotransduction and a self-healing process takes place in order to prevent the induced severing of the SF. A model is proposed to take into account the effect of the applied stretch on the mechanics of the SF, from which relevant parameters of the healing process are obtained. In contrast, the repair of the actin bundle occurs at the weak point of the SF and depends on the amount of applied strain. As a result, the SFs display strain-softening features due to the incorporation of new actin material into the bundle. In contrast, the response under compression shows a reorganization with a constant actin material suggesting a gliding process of the SFs by the myosin II motors