41 research outputs found

    Structures en grands déplacements couplées à des fluides en mouvement

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    Projet M3NLe calcul en configuration Eulérienne d'écoulements visqueux dans des structures fortement défor­mables (écoulements dans des tuyaux collabables, amortisseurs hydrauliques) pose des problÚmes difficiles de compatibilité cinématique et d'actualisation de géo­mé­trie. Pour surmonter ces difficultés, on propose de traiter la structure et le fluide comme un milieu continu unique et d'en rapporter le mouvement à la configuration de calcul délimitée par la structure au repos. Le problÚme obtenu est ensuite séparé en une partie fluide et une partie solide par décomposition de l'espace des vitesses cinématiquement admissibles. Cette séparation conduit ainsi à une modélisation purement lagrangienne de la structure couplée à une formulation ALE du problÚme fluide. Cette stratégie a trois avantages qui sont développés dans l'article~: - - - elle permet d'introduire des schémas de discrétisation en temps et des algorithmes de couplage simples qui respectent la compatibilité cinématique à l'interface et qui ont les bonnes propriétés énergétiques~; - - - elle autorise l'emploi d'éléments finis indépendants sur la structure et sur le domaine fluide~; - - - elle permet d'utiliser directement les modÚles récents de coques hyperélastiques en grands déplacements, et de garantir ainsi la cohérence mathématique et l'objectivité du modÚle de structure choisi. Cette méthodologie a été intégrée dans un code de calcul industriel et a été validée sur des problÚmes industriels de calcul d'amortisseurs hydrauliques présentés en fin d'article

    Finite Element Approximation of a Geometrically Exact Shell Model

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    Projet MENUSIN, Projet MODULEFThe purpose of this work is to develop finite element models for geometrically exact nonlinear shells. The originality of our approach is to work in a fixed cartesian basis. After a brief introduction of the shell model, the paper presents two finite elements approximations specially developed for this problem. The first uses conforming Argyris triangles, the second develops nonlinear DKT triangles. Both models are validated by several numerical tests

    Different Transport Mechanisms in Plant and Human AMT/Rh-type Ammonium Transporters

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    The conserved family of AMT/Rh proteins facilitates ammonium transport across animal, plant, and microbial membranes. A bacterial homologue, AmtB, forms a channel-like structure and appears to function as an NH3 gas channel. To evaluate the function of eukaryotic homologues, the human RhCG glycoprotein and the tomato plant ammonium transporter LeAMT1;2 were expressed and compared in Xenopus oocytes and yeast. RhCG mediated the electroneutral transport of methylammonium (MeA), which saturated with Km = 3.8 mM at pHo 7.5. Uptake was strongly favored by increasing the pHo and was inhibited by ammonium. Ammonium induced rapid cytosolic alkalinization in RhCG-expressing oocytes. Additionally, RhCG expression was associated with an alkali-cation conductance, which was not significantly permeable to NH4+ and was apparently uncoupled from the ammonium transport. In contrast, expression of the homologous LeAMT1;2 induced pHo-independent MeA+ uptake and specific NH4+ and MeA+ currents that were distinct from endogenous currents. The different mechanisms of transport, including the RhCG-associated alkali-cation conductance, were verified by heterologous expression in appropriate yeast strains. Thus, homologous AMT/Rh-type proteins function in a distinct manner; while LeAMT1;2 carries specifically NH4+, or cotransports NH3/H+, RhCG mediates electroneutral NH3 transport

    Identification of Genetic Factors that Modify Clinical Onset of Huntington’s Disease

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    SummaryAs a Mendelian neurodegenerative disorder, the genetic risk of Huntington’s disease (HD) is conferred entirely by an HTT CAG repeat expansion whose length is the primary determinant of the rate of pathogenesis leading to disease onset. To investigate the pathogenic process that precedes disease, we used genome-wide association (GWA) analysis to identify loci harboring genetic variations that alter the age at neurological onset of HD. A chromosome 15 locus displays two independent effects that accelerate or delay onset by 6.1 years and 1.4 years, respectively, whereas a chromosome 8 locus hastens onset by 1.6 years. Association at MLH1 and pathway analysis of the full GWA results support a role for DNA handling and repair mechanisms in altering the course of HD. Our findings demonstrate that HD disease modification in humans occurs in nature and offer a genetic route to identifying in-human validated therapeutic targets in this and other Mendelian disorders.PaperCli

    CAG repeat not polyglutamine length determines timing of Huntington’s disease onset

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    Variable, glutamine-encoding, CAA interruptions indicate that a property of the uninterrupted HTT CAG repeat sequence, distinct from the length of huntingtin’s polyglutamine segment, dictates the rate at which Huntington’s disease (HD) develops. The timing of onset shows no significant association with HTT cis-eQTLs but is influenced, sometimes in a sex-specific manner, by polymorphic variation at multiple DNA maintenance genes, suggesting that the special onset-determining property of the uninterrupted CAG repeat is a propensity for length instability that leads to its somatic expansion. Additional naturally occurring genetic modifier loci, defined by GWAS, may influence HD pathogenesis through other mechanisms. These findings have profound implications for the pathogenesis of HD and other repeat diseases and question the fundamental premise that polyglutamine length determines the rate of pathogenesis in the “polyglutamine disorders.

    Crack propagation from a pre-existing flaw at a notch root. II: Detailed form of the stress intensity factors at the initial crack tip and conclusion

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    This paper pursues the study of crack kinking from a pre-existing crack emanating from some notch root. It was shown in Part I that the stress intensity factors at the tip of the small initial crack are given by universal (that is, applicable in all situations, whatever the geometry of the body and the loading) formulae; they depend only on the `stress intensity factor of the notch' (the multiplicative coefficient of the singular stress field near the apex of the notch in the absence of the crack), the length of the crack, the aperture angle of the notch and the angle between its bisecting line and the direction of the crack. Here we identify the universal functions of the two angles just mentioned which appear in these formulae, by considering the model problem of an infinite body endowed with a notch with straight boundaries and a straight crack of unit length. The treatment uses Muskhelishvili's complex potentials formalism combined with some conformal mapping. The solution is expressed in the form of an infinite series involving an integral operator, which is evaluated numerically. Application of Goldstein and Salganik's principle of local symmetry then leads to prediction of the kink angle of the crack extension. It is found that although the direction of the crack is closer to that of the bisecting line of the notch after kinking than before it, the kink angle is not large enough for the crack tip to get closer to this line after kinking, except perhaps in some special situations

    Crack propagation from a pre-existing flaw at a notch root. I. Introduction and general form of the stress intensity factors at the initial crack tip

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    This paper and its companion are devoted to the study of crack kinking from some small pre-existing crack originating from a notch root (the notch root radius being zero). Both the notch boundaries and the initial crack are allowed to be curved; also, the geometry of the body and the loading are totally arbitrary. The ingredients required are knowledge of the stress intensity factors at the initial crack tip and use of a suitable mixed mode propagation criterion. This paper is devoted to the first point, and more specifically to establishing the general (that is, not yet fully explicit) form of the formulae giving these stress intensity factors. The method used is based on changes of scale (homogeneity properties of the equations of elasticity) on the one hand, and on continuity of the displacement and stresses at a given, fixed point with respect to the crack length on the other hand. The formulae derived for the stress intensity factors at the tip of the small crack are of universal value: they apply to any situation, whatever the geometry of the body, the notch and the crack and whatever the loading, the stress intensity factors depending always only upon the `stress intensity factor of the notch' (the multiplicative coefficient of the singular stress field near the notch root in the absence of the crack), the length of the crack, the aperture angle of the notch and the angle between its bisecting line and the direction of the crack

    Analyse d'une filiÚre de prise en charge des accidents vasculaires cérébraux (mise en place d'une unité neuro-vasculaire)

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    LILLE2-BU Santé-Recherche (593502101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF
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