2,325 research outputs found

    Vortex shedding from tapered, triangular plates: taper and aspect ratio effects

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    Further experiments on features of the vortex shedding from tapered flat plates normal to an airstream are described. The work extends that of Castro and Rogers (2002) and concentrates on the study of the effects of varying the spanwise aspect ratio for a fixed shape plate, by appropriate adjustment of end-plates, and of the nature of the shedding as the degree of taper becomes very large, so that the body is more like a triangular plate—e.g. an isosceles triangle—than a slightly tapered plate. With the taper ratio TR defined as the ratio of plate length to average cross-stream width, the paper concentrates on the range 0.58<TR<60. Reynolds numbers, based on the average plate width, exceed 104. It is confirmed that for a small enough taper ratio the geometrical three-dimensionality is sufficiently strong that all signs of periodic vortex shedding cease. For all other cases, however, the flow at different locations along the span can vary substantially, depending on taper. There appear to be at least four different regimes, each appropriate for a different range of taper ratio. These various regimes are described

    Building hyperbolic metrics suited to closed curves and applications to lifting simply

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    Let γ\gamma be an essential closed curve with at most kk self-intersections on a surface S\mathcal{S} with negative Euler characteristic. In this paper, we construct a hyperbolic metric ρ\rho for which γ\gamma has length at most MkM \cdot \sqrt{k}, where MM is a constant depending only on the topology of S\mathcal{S}. Moreover, the injectivity radius of ρ\rho is at least 1/(2k)1/(2\sqrt{k}). This yields linear upper bounds in terms of self-intersection number on the minimum degree of a cover to which γ\gamma lifts as a simple closed curve (i.e. lifts simply). We also show that if γ\gamma is a closed curve with length at most LL on a cusped hyperbolic surface S\mathcal{S}, then there exists a cover of S\mathcal{S} of degree at most NLeL/2N \cdot L \cdot e^{L/2} to which γ\gamma lifts simply, for NN depending only on the topology of S\mathcal{S}.Comment: 18 pages, 7 figures. Comments welcome

    FA1 Induces Pro-Inflammatory and Anti-Adipogenic Pathways/Markers in Human Myotubes Established from Lean, Obese, and Type 2 Diabetic Subjects but Not Insulin Resistance

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    Aims: Delta like 1/fetal antigen 1 (Dlk1/FA1) is a protein secreted by hormone producing cells in adult human and mice that is known to inhibit adipogenesis. Recent studies demonstrated the role of Dlk1/FA1 in inducing insulin resistance in mice. To investigate the involvement of circulating Dlk1/FA1 in insulin resistance and type 2 diabetes in human subjects, we studied the effects of chronic FA1 on the intermediary metabolism in myotubes established from lean, obese, and type 2 diabetic (T2D) subjects. Methods: Myotube cultures were established from lean and obese control subjects, and obese T2D subjects and treated with soluble FA1 for 4 days supplemented with/without palmitate (PA). Lipid- and glucose metabolism were studied with labeled precursors while quantitative expression of genes was analyzed using real-time PCR. Results: Diabetic myotubes express significantly reduced insulin stimulated glucose metabolism compared to lean myotubes and a significantly decreased basal PA oxidation. Chronic FA1 exposure did not affect the intermediary metabolism in myotubes. Insulin sensitivity of glucose and lipid metabolism was not affected by chronic FA1 exposure in myotubes established from lean, obese, and T2D subjects. Instead, chronic FA1 exposure induced pro-inflammatory cytokines expression (IL-6 and CCL2) in association with reducing adipogenic markers (ADD1, AP2, CD36, and PPARg2) in myotubes. Consistent with this observation, addition of FA1 to cultured myotubes was show to significantly inhibit their differentiation into adipocyte. Conclusion: Our results exclude direct effects of FA1 on glucose and lipid metabolism in cultured myotubes established from lean, obese, and T2D subjects. Therefore, the pathogenesis of FA1-induced IR might mainly be mediated via the FA1-induced stimulation of pro-inflammatory cytokines, which on turn inhibit adipogenesis in human myotubes
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