14 research outputs found

    The Stationary Distribution of Competitive Lotka-Volterra Population Systems with Jumps

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    Dynamics of Lotka-Volterra population with jumps (LVWJ) have recently been established (see Bao et al., 2011, and Bao and Yuan, 2012). They provided some useful criteria on the existence of stationary distribution and some asymptotic properties for LVWJ. However, the uniqueness of stationary distribution for nā‰„2 and asymptotic pathwise estimation limtā†’+āˆžā”(1/t)āˆ«0tā€|X(s)|pdsā€‰(p>0) are still unknown for LVWJ. One of our aims in this paper is to show the uniqueness of stationary distribution and asymptotic pathwise estimation for LVWJ. Moreover, some characterizations for stationary distribution are provided

    Spectral Element Numerical Investigation of Flow between Three Cylinders in an Equilateral-Triangular Arrangement with Different Spacing Distances

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    Two-dimensional incompressible Navier-Stokes equations are numerically solved using the high resolution spectral element method at Reynolds number 200. The flow between three cylinders in an equilateral-triangular arrangement is investigated. The center-to-center spacing distance ratio between two circular cylinders is varied from 1.5 to 12. Present numerical results show that the flow patterns and force characteristics are the result of the combined effects of Reynolds number, spacing distance, configuration arrangement, and incident angle. For the small spacing distance ratio of 1.5, the well-known biased flow phenomenon in the gap of downstream cylinders is found. And the biased flow is bistable in our study but not monostable. A small spacing distance means lower Strouhal number, drag, and root-mean-square lift coefficients. In the medium spacing distance ratio of 4.0, the suppressed effect of vortex shedding for the presence of the side-by-side downstream cylinders disappeared. Mean drag coefficients of downstream cylinders are basically identical to the value of flow past around a single circular cylinder. For the large spacing distance ratio of 8.0, the effects between three cylinders basically disappeared. The mean drag and lift coefficients, root-mean-square lift coefficients, and Strouhal number of three cylinders are essentially equivalent to those values of a single circular cylinder

    DataSheet_1_Hypoxia-inducible factor-2Ī± promotes fibrosis in non-alcoholic fatty liver disease by enhancing glutamine catabolism and inhibiting yes-associated protein phosphorylation in hepatic stellate cells.pdf

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    Non-alcoholic fatty liver disease (NAFLD) has a high global prevalence and affects approximately one-third of adults, owing to high-fat dietary habits and a sedentary lifestyle. The role of hypoxia-inducible factor 2Ī± (HIF-2Ī±) in NAFLD progression remains unknown. This study aimed to investigate the effects of chronic hypoxia on NAFLD progression by examining the role of hypoxia-inducible factor 2Ī± (HIF-2Ī±) activation and that of hepatic stellate cell (HSC)-derived myofibroblasts through glutaminolysis. We hypothesised that hypoxia exacerbates NAFLD by promoting HIF-2Ī± upregulation and inhibiting phosphorylated yes-associated protein (YAP), and that increasing YAP expression enhances HSC-derived myofibroblasts. We studied patients with NAFLD living at high altitudes, as well as animal models and cultured cells. The results revealed significant increases in HSC-derived myofibroblasts and collagen accumulation caused by HIF-2Ī± and YAP upregulation, both in patients and in a mouse model for hypoxia and NAFLD. HIF-2Ī± and HIF-2Ī±-dependent YAP downregulation reduced HSC activation and myofibroblast levels in persistent chronic hypoxia. Furthermore, hypoxia-induced HIF-2Ī± upregulation promoted YAP and inhibited YAP phosphorylation, leading to glutaminase 1 (GLS1), SLC38A1, Ī±-SMA, and Collagen-1 overexpression. Additionally, hypoxia restored mitochondrial adenosine triphosphate production and reactive oxygen species (ROS) overproduction. Thus, chronic hypoxia-induced HIF-2Ī± activation enhances fibrosis and NAFLD progression by restoring mitochondrial ROS production and glutaminase-1-induced glutaminolysis, which is mediated through the inhibition of YAP phosphorylation and increased YAP nuclear translocation. In summary, HIF-2Ī± plays a pivotal role in NAFLD progression during chronic hypoxia.</p

    DataSheet_1_Hypoxia-inducible factor-2Ī± promotes fibrosis in non-alcoholic fatty liver disease by enhancing glutamine catabolism and inhibiting yes-associated protein phosphorylation in hepatic stellate cells.pdf

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    Non-alcoholic fatty liver disease (NAFLD) has a high global prevalence and affects approximately one-third of adults, owing to high-fat dietary habits and a sedentary lifestyle. The role of hypoxia-inducible factor 2Ī± (HIF-2Ī±) in NAFLD progression remains unknown. This study aimed to investigate the effects of chronic hypoxia on NAFLD progression by examining the role of hypoxia-inducible factor 2Ī± (HIF-2Ī±) activation and that of hepatic stellate cell (HSC)-derived myofibroblasts through glutaminolysis. We hypothesised that hypoxia exacerbates NAFLD by promoting HIF-2Ī± upregulation and inhibiting phosphorylated yes-associated protein (YAP), and that increasing YAP expression enhances HSC-derived myofibroblasts. We studied patients with NAFLD living at high altitudes, as well as animal models and cultured cells. The results revealed significant increases in HSC-derived myofibroblasts and collagen accumulation caused by HIF-2Ī± and YAP upregulation, both in patients and in a mouse model for hypoxia and NAFLD. HIF-2Ī± and HIF-2Ī±-dependent YAP downregulation reduced HSC activation and myofibroblast levels in persistent chronic hypoxia. Furthermore, hypoxia-induced HIF-2Ī± upregulation promoted YAP and inhibited YAP phosphorylation, leading to glutaminase 1 (GLS1), SLC38A1, Ī±-SMA, and Collagen-1 overexpression. Additionally, hypoxia restored mitochondrial adenosine triphosphate production and reactive oxygen species (ROS) overproduction. Thus, chronic hypoxia-induced HIF-2Ī± activation enhances fibrosis and NAFLD progression by restoring mitochondrial ROS production and glutaminase-1-induced glutaminolysis, which is mediated through the inhibition of YAP phosphorylation and increased YAP nuclear translocation. In summary, HIF-2Ī± plays a pivotal role in NAFLD progression during chronic hypoxia.</p

    Robust Anisotropic Composite Particles with Tunable Janus Balance

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    We report a general emulsion approach to protrude a lobe by swelling the polymer core from a coreā€“shell structure, achieving anisotropic Janus composite particles with tunable chemistry, shape, size, and size ratio of the two parts thus Janus balance. Oil-in-water emulsion is employed to swell a polymer core through the crack open hole within the shell, and the core protrusion is restricted in the particle/oil confined compartments enveloped with surfactant. When monomers are used as the oil solvents, cross-linking can strengthen the polymer lobe to tolerate against organic solvents. By tuning polymerization time and monomer/particle weight ratio, the size ratio of the polymer/inorganic parts thus Janus balance of the composite particles is continuously tunable across from more hydrophilic to more lipophilic. The robust anisotropic particles with tunable Janus balance can be further used as solid surfactants to tune microstructure of emulsions
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