24 research outputs found

    Artificial cilia : a physical model for ciliary propulsion

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    Most microorganisms use cilia or flagella as a means of propulsion. These low Reynolds number swimming mechanisms have been studied theoretically and experimentally on living organisms. However, so far very few physical experimental models have been realised. We describe here the fabrication of microscopic artificial cilia, actuated by a magnetic field. These artificial cilia share with real cilia a large aspect ratio, great flexibility, and the actuation by a magnetic torque distributed along thier full lenght. We studied the planar and three-dimensional beatings of these magnetic cilia. We also characterized the forces and flows induced in the surrounding fluid.De nombreux micro-organismes vivants se propulsent en utilisant des cils ou des flagelles. Cette nage à petit nombre de Reynolds a fait l'objet de nombreuses études théoriques et expérimentales sur les organismes vivants. Toutefois il existe très peu de modèles physiques expérimentaux. Nous décrivons ici la construction des cils artificiels microscopiques actionnés par un champ magnétique. Ces cils artificiels ont en commun avec les cils réels un très grand allongement, une grande flexibilité et un mode d'actuation par couple réparti. Nous avons étudié les dynamiques de battement (planaire et tridimensionnel) de ces cils magnétiques. Nous avons également caractérisé les forces et les écoulements qu'ils induisent dans le fluide environnant

    Cils artificiels (modèle physique pour la propulsion ciliée)

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    PARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

    Tethered fleximags as artificial cilia

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    Flexible superparamagnetic filaments ('fleximags') are very slender elastic filaments, which can be driven by distributed magnetic torques to mimic closely the behaviour of biological flagella. Previously, fleximags have been used as a basis for artificial micro-swimmers capable of transporting small cargos Dreyfus et al. (Nature, vol. 437, 2005, p. 862). Here, we demonstrate how these filaments can be anchored to a wall to make carpets of artificial micro-magnetic cilia with tunable densities. We analyse the dynamics of an artificial cilium under both planar and three-dimensional beating patterns. We show that the dynamics are controlled by a single characteristic length scale varying with the inverse square root of the driving frequency, providing a mechanism to break the fore and aft symmetry and to generate net fluxes and forces. However, we show that an effective geometrical reciprocity in the filament dynamics creates intrinsic limitations upon the ability of the artificial flagellum to pump fluid when driven in two dimensions

    Pericyte mechanics and mechanobiology

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    International audiencePericytes are mural cells of the microvasculature, recognized by their thin processes and protruding cell body. Pericytes wrap around endothelial cells and play a central role in regulating various endothelial functions, including angiogenesis and inflammation. They also serve as a vascular support and regulate blood flow by contraction. Prior reviews have examined pericyte biological functions and biochemical signaling pathways. In this Review, we focus on the role of mechanics and mechanobiology in regulating pericyte function. After an overview of the morphology and structure of pericytes, we describe their interactions with both the basement membrane and endothelial cells. We then turn our attention to biophysical considerations, and describe contractile forces generated by pericytes, mechanical forces exerted on pericytes, and pericyte responses to these forces. Finally, we discuss 2D and 3D engineered in vitro models for studying pericyte mechano-responsiveness and underscore the need for more evolved models that provide improved understanding of pericyte function and dysfunction

    Luminal Flow Actuation Generates Coupled Shear and Strain in a Microvessel-on-Chip

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    Abstract In the microvasculature, blood flow-derived forces are key regulators of vascular structure and function. Consequently, the development of hydrogel-based microvessel-on-chip systems that strive to mimic the in vivo cellular organization and mechanical environment has received great attention in recent years. However, despite intensive efforts, current microvessel- on-chip systems suffer from several limitations, most notably failure to produce physiologically relevant wall strain levels. In this study, a novel microvessel-on-chip based on the templating technique and using luminal flow actuation to generate physiologically relevant levels of wall shear stress and circumferential stretch is presented. Normal forces induced by the luminal pressure compress the surrounding soft collagen hydrogel, dilate the channel, and create large circumferential strain. The fluid pressure gradient in the system drives flow forward and generates realistic pulsatile wall shear stresses. Rigorous characterization of the system reveals the crucial role played by the poroelastic behavior of the hydrogel in determining the magnitudes of the wall shear stress and strain. The experimental measurements are combined with an analytical model of flow in both the lumen and the porous hydrogel to provide an exceptionally versatile user manual for an application-based choice of parameters in microvessels-on-chip. This unique strategy of flow actuation adds a dimension to the capabilities of microvessel-on-chip systems and provides a more general framework for improving hydrogel-based in vitro engineered platforms. Abstract Figur

    Luminal flow actuation generates coupled shear and strain in a microvessel-on-chip

    No full text
    International audienceIn the microvasculature, blood flow-derived forces are key regulators of vascular structure and function. Consequently, the development of hydrogel-based microvessel-on-chip systems that strive to mimic the in vivo cellular organization and mechanical environment has received great attention in recent years. However, despite intensive efforts, current microvessel-on-chip systems suffer from several limitations, most notably failure to produce physiologically relevant wall strain levels. In this study, a novel microvessel-on-chip based on the templating technique and using luminal flow actuation to generate physiologically relevant levels of wall shear stress and circumferential stretch is presented. Normal forces induced by the luminal pressure compress the surrounding soft collagen hydrogel, dilate the channel, and create large circumferential strain. The fluid pressure gradient in the system drives flow forward and generates realistic pulsatile wall shear stresses. Rigorous characterization of the system reveals the crucial role played by the poroelastic behavior of the hydrogel in determining the magnitudes of the wall shear stress and strain. The experimental measurements are combined with an analytical model of flow in both the lumen and the porous hydrogel to provide an exceptionally versatile user manual for an application-based choice of parameters in microvessels-on-chip. This unique strategy of flow actuation adds a dimension to the capabilities of microvessel-on-chip systems and provides a more general framework for improving hydrogel-based in vitro engineered platforms

    Ultrasound internal tattooing

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    Micropipette Force Probe to quantify single-cell force generation: application to T cell activation

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    International audienceIn response to engagement of surface molecules, cells generate active forces that regulate many cellular processes. Developing tools that permit gathering mechanical and morphological information on these forces is of the utmost importance. Here we describe a new technique, the micropipette force probe, that uses a micropipette as a flexible cantilever that can aspirate at its tip a bead that is coated with molecules of interest and is brought in contact with the cell. This technique simultaneously allows tracking the resulting changes in cell morphology and mechanics as well as measuring the forces generated by the cell. To illustrate the power of this technique, we applied it to the study of human primary T lymphocytes (T-cells). It allowed the fine monitoring of pushing and pulling forces generated by T-cells in response to various activating antibodies and bending stiffness of the micropipette. We further dissected the sequence of mechanical and morphological events occurring during T-cell activation to model force generation and to reveal heterogeneity in the cell population studied. We also report the first measurement of the changes in Young’s modulus of T-cells during their activation, showing that T-cells stiffen within the first minutes of the activation process

    Distinct timing of neutrophil spreading and stiffening during phagocytosis

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    International audiencePhagocytic cells form the first line of defense in an organism, engulfing microbial pathogens. Phagocytosis involves cell mechanical changes that are not yet well understood. Understanding these mechanical modifications promises to shed light on the immune processes that trigger pathological complications. Previous studies showed that phagocytes undergo a sequence of spreading events around their target followed by an increase in cell tension. Seemingly in contradiction, other studies observed an increase in cell tension concomitant with membrane expansion. Even though phagocytes are viscoelastic, few studies have quantified viscous changes during phagocytosis. It is also unclear whether cell lines behave mechanically similarly to primary neutrophils. We addressed the question of simultaneous versus sequential spreading and mechanical changes during phagocytosis by using immunoglobulin-G-coated 8-and 20-mm-diameter beads as targets. We used a micropipettebased single-cell rheometer to monitor viscoelastic properties during phagocytosis by both neutrophil-like PLB cells and primary human neutrophils. We show that the faster expansion of PLB cells on larger beads is a geometrical effect reflecting a constant advancing speed of the phagocytic cup. Cells become stiffer on 20-than on 8-mm beads, and the relative timing of spreading and stiffening of PLB cells depends on target size: on larger beads, stiffening starts before maximal spreading area is reached but ends after reaching maximal area. On smaller beads, the stiffness begins to increase after cells have engulfed the bead. Similar to PLB cells, primary cells become stiffer on larger beads but start spreading and stiffen faster, and the stiffening begins before the end of spreading on both bead sizes. Our results show that mechanical changes in phagocytes are not a direct consequence of cell spreading and that models of phagocytosis should be amended to account for causes of cell stiffening other than membrane expansion
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