[Research progress of hepatic non-parenchymal cells in nonalcoholic steatohepatitis].

Non-alcoholic steatohepatitis (NASH) is an important link for the progression of metabolic-related fatty liver disease to end-stage liver disease such as cirrhosis and hepatocellular carcinoma, which seriously endangers human health. NASH pathogenesis is complex, and involves the interaction between hepatic parenchymal and non-parenchymal cells (NPCs), sinusoidal endothelial cells, Kupffer cells, hepatic stellate cells, and so on. Herein, the relevant research progress of NPCs in the pathogenesis of NASH is reviewed in order to further understand the role of NPCs in NASH.

Promoted diffusion mechanism of Fe2.7wt.%Si-Fe10wt.%Si couples under magnetic field by atomic-scale observations.

Diffusion behavior of newly designed Fe2.7wt.%Si-Fe10wt.%Si couples at 1100 °C for up to 12 h has been investigated under the 0, 0.8 and 3 T magnetic fields. Diffusion thickness of solid solution layer and weight percent of Si on Fe2.7wt.%Si side increase significantly under a magnetic field. Application of a magnetic field promotes the diffusion of solid solution layer through the possible diffusion of vacancies mainly due to the appearance of defects, which has been demonstrated by the increased dislocation density and broadening of the typical XRD peaks. Replacement of Si sits by Fe atoms in the crystal structure leads to the appearance of Fe diffraction peaks, which has been confirmed by the increased interplanar spacings under a magnetic field. The magnetic field benefits the depinning of dislocations and leads to higher dislocation density because of the magnetoplastic effect which has been confirmed by the significantly reduced thickness of Fe2.7wt.%Si. Nano-sized Fe3Si particles precipitate in the matrix with an orientation relationship on Fe10wt.%Si side as {220}Fe3Si || {220}matrix & < 1-10 >Fe3Si || < 1-10 >matrix. Fe3Si particles pin dislocation moving and lead to higher dislocation density.