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By using AlCrTiZrNb alloy target and Si targets, the (AlCrTiZrNb) N/Si3N4 nano-multilayer films with different Si3N4 thicknesses were prepared by multi-target magnetron sputtering system on the single crystal silicon substrate. The microstructure and mechanical properties of the samples were analyzed by X-ray diffraction (XRD), high-resolution transmission electron microscopy (HRTEM), scanning electron microscopy (SEM) and nano-indentation techniques. The results showed that, as the thickness of Si3N4 layer increases, the crystallinity and mechanical properties of the sample first increase and then decrease? a cubic-structured phase appears in the XRD patterns. When the Si3N4 layer thickness is 0.5 run, the XRD pattern presents the largest (111) peak intensity, indicating the strongest crystallinity, and the hardness and elastic modulus reach the highest values, which are 30.6 and 298 GPa, respectively. The HRTEM observations show the columnar crystal growth of the nano-multilayer films when the Si3N4 layer thickness is 0.5 nm. Under the template of (AlCrTiZrNb) N layer, the Si3N4 layer changes from amorphous to cubic phase and grow epitaxially with (AlCrTiZrNb) N layers. The strengthening of the nano-multilayer films can he attributed to the coherent interface between (AlCrTiZrNb)N and Si3N4 layers. [ABSTRACT FROM AUTHOR]

The pathogenesis and progression of nonalcoholic fatty liver disease (NAFLD) are closely associated with the activation of the innate immune system. This article reviews how various types of immune cells, Toll-like receptors, and their downstream signaling pathways are involved in insulin resistance and mediate oxidative stress, inflammation, and fibrosis in the liver. Reduction or elimination of dendritic cells delays inflammatory responses and fibrosis in the liver. A decrease in natural killer T cells induces lipid accumulation at the stage of simple steatosis, but alleviates fibrosis at the inflammation stage. The mTOR signaling pathways for insulin and amino acids suppresses autophagy through short-term or long-term regulation, which leads to endoplasmic reticulum stress and altered insulin resistance, thereby modulating the development and progression of NAFLD. The research on the mechanisms by which traditional Chinese medicine offers therapeutic benefits for NAFLD increasingly focuses on the potential role of immunity. [ABSTRACT FROM AUTHOR]