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Immiscibility in the Nickel Ferrite-Zinc Ferrite Spinel Binary
Immiscibility in the trevorite (NiFe{sub 2}O{sub 4}) - franklinite (ZnFe{sub 2}O{sub 4}) spinel binary is investigated by reacting 1:1:2 molar ratio mixtures of NiO, ZnO and Fe{sub 2}O{sub 3} in a molten salt solvent at temperatures in the range 400-1000 C. Single phase stability is demonstrated down to about 730 C (the estimated consolute solution temperature, T{sub cs}). A miscibility gap/solvus exists below Tcs. The solvus becomes increasingly asymmetric at lower temperatures and extrapolates to n - values = 0.15, 0.8 at 300 C. A thermodynamic analysis, which accounts for changes in configurational and magnetic ordering entropies during cation mixing, predicts solvus phase compositions at room temperature in reasonable agreement with those determined by extrapolation of experimental results. The delay between disappearance of magnetic ordering above T{sub C} = 590 C (for NiFe{sub 2}O{sub 4}) and disappearance of a miscibility gap at T{sub cs} is explained by the persistence of long-range ordering correlations in a quasi-paramagnetic region above T{sub C}
Dual and selective lipid inhibitors of cyclooxygenases and lipoxygenase: a molecular docking study
Surface and grain-boundary energies as well as surface mass transport in polycrystalline yttrium oxide
Meiotic Development Features Relevant to Prophase Specific Chromosomal Characteristics in Saccharomyces cerevisiae
Potential Role of Leptin, Adiponectin and Three Novel AdipokinesâVisfatin, Chemerin and Vaspinâin Chronic Hepatitis
Chronic hepatitis C (CHC) is generally a slowly progressive disease, but some factors associated with rapid progression have been identified. Steatosis, independently of its metabolic or viral origin, leads to liver injury and fibrosis. It is suggested that hepatitis C virus may contribute to a wide spectrum of metabolic disturbancesânamely, steatosis, insulin resistance, increased prevalence of impaired glucose tolerance, type 2 diabetes mellitus and lipid metabolism abnormalities. Adipokines, which are produced mainly by adipose tissue, may influence the inflammatory response and insulin sensitivity and contribute to the development of metabolic abnormalities in CHC and also regulate fibrogenesis and angiogenesis. Visfatin was described as an adipokine with immunomodulating and proinflammatory properties that promotes B-cell maturation and enhances activation of leukocytes, synthesis of adhesion molecules and production of proinflammatory cytokines. Visfatin exerts insulin-mimetic effects, decreases plasma glucose levels and regulates cell energy balance. Chemerin stimulates chemotaxis of dendritic cells, macrophages and natural killer (NK) cells toward the site of inflammation. On the other hand, it inhibits synthesis of proinflammatory mediators and enhances adiponectin production, influences adipocyte differentiation and maturation and regulates glucose uptake in adipocytes. Vaspin expression in human adipose tissue seems to be a compensatory mechanism associated with obesity and insulin resistance. Vaspin suppresses leptin, tumor necrosis factor (TNF)-α and resistin expression. Leptin protects against liver steatosis but accelerates fibrosis progression and exacerbates the inflammatory process. In contrast, adiponectin exerts a hepatoprotective effect. In this report, data indicating a possible role of these adipokines in the pathogenesis of chronic hepatitis are summarized