A further investigation to mechanism of the electrorheological effect of waxy oils:Behaviors of charged particles under electric field

Exposing waxy oils to an electric field may significantly improve their cold flowability.Our previous study has shown that interfacial polarization,i.e.,charged particle accumulation on the wax particle surface,is the primary mechanism of the electrorheological behavior of waxy oils.However,the way that charged particles interact with wax particles under an electric field remains unknown.In this study,we found no viscosity and impedance change for two waxy crude oils after their exposure to a high-voltage electric field.However,the yield stresses were reduced obviously.We thus proposed that the collision of colloidal particles such as resins and asphaltenes with the wax particles could be an essential mechanism that the wax particle structure was weakened.To verify this hypothesis,a series of ad hoc experiments were carried out,i.e.,by performing electrorheological tests on model waxy oils containing additives removable under an electric field,including electrically-neutral colloidal particles(Fe3O4),charged colloidal particles(resins),and oil-soluble electrolyte(C22H14CoO4),respectively,and demonstrated that upon application of a high-voltage electric field,charged particles in a waxy oil may move and thus collide with wax particles,and consequently adhere to the wax particle surface.The particle collision results in damage to the wax particle network,and the electrostatic repulsion arising from the adhesion of the charged particle on the wax particle diminishes attraction between wax particles.This study clarifies the process of interfacial polarization.

Protection of plasma transfusion against lipopolysaccharide/D-galactosamine-induced fulminant hepatic failure through inhibiting apoptosis of hepatic cells in mice

Fulminant hepatic failure is a severe clinical condition associated with extremely poor outcomes and high mortality. A number of studies have demonstrated the ability of plasma transfusion to successfully treat fulminant hepatic failure, but the underlying mechanisms are not well understood. The aim of the present study is to define the mechanisms of plasma transfusion treatment in lipopolysaccharide/D-galactosamine(LPS/D-Gal N)-induced mice. LPS/D-Gal N treatment in mice causes significant hepatic failure, including increasing serum aspartate aminotransferase(AST) and alanine aminotransferase(ALT) levels, histopathological changes in centrilobular necrosis and inflammatory cells, and the up-regulation of inflammation(tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6)). When LPS/D-Ga IN-induced mice were treated with plasma, these changes were halted. Results showed that plasma transfusion significantly reduced mortality, and decreased the levels of AST, ALT, and inflammation factors such as TNF-α and IL-6. The expression levels of cleaved Caspase-3, BAX, and p53 were down-regulated and Bcl-2 was up-regulated, suggesting that plasma can reduce LPS/D-Gal N-induced apoptosis. The protective mechanism of plasma against LPS/D-Gal N-induced fulminant hepatic failure is related to the inhibition of the inflammatory response and the reduction in apoptosis through the down-regulation of the p53-induced apoptotic pathway.