Siloxane coatings for surfaces are essential in many scientific and industrial applications. We describe a straightforward gas-phase evaporation technique in inert atmosphere and introduce a practical and reliable silanization protocol adaptable to different silane types. The primary aim of depositing ultrathin siloxane films on surfaces is to enable a reproducible and homogenous surface functionalization without agglomeration effects during the layer formation. To realize high-quality and large-area coatings, it is fundamental to understand the reaction conditions of the silanes, the process of the siloxane layer formation, and the possible influence of the substrate morphology. We used three typical silane types to exemplify the potential and versatility of our process: aminopropyltriethoxysilane, glycidoxypropyltrimethoxysilane, and 1 H,1 H,2 H,2 H-perfluorooctyl-trichlorosilane. The ultrathin siloxane layers, which are generally difficult to characterize, were precisely investigated with high-resolution surface-characterization methods to verify our concept in terms of reproducibility and coating quality. Our results show that this gas-phase evaporation protocol is easily adaptable to all three, widely used silane types also enabling a large-area upscale.

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Clinical studies demonstrated that nonalcoholic steatohepatitis is associated with liver-related outcomes in chronic hepatitis B. Furthermore, primary biliary fibrosis and biliary atresia occurred in patients with HBV infection. Interestingly, hepatitis B virus surface protein (HBs) transgenic mice spontaneously develop hepatic steatosis. Our aim is to investigate the effect of Abcb4 knockout-induced cholestasis on liver steatosis in HBs transgenic mice. Hybrids of HBs transgenic and Abcb4−/− mice were bred on the BALB/c genetic background. Lipid synthesis, storage, and catabolism as well as proteins and genes that control lipid metabolism were analyzed using HPTLC, qPCR, western blot, electrophoretic mobility shift assay (EMSA), lipid staining, and immunohistochemistry. Hepatic neutral lipid depots were increased in HBs transgenic mice and remarkably reduced in Abcb4−/− and HBs/Abcb4−/− mice. Similarly, HPTLC-based quantification analyses of total hepatic lipid extracts revealed a significant reduction in the amount of triacylglycerols (TAG), while the amount of free fatty acids (FFA) was increased in Abcb4−/− and HBs/Abcb4−/− in comparison to wild-type and HBs mice. PLIN2, a lipid droplet-associated protein, was less expressed in Abcb4−/− and HBs/Abcb4−/−. The expression of genes-encoding proteins involved in TAG synthesis and de novo lipogenesis (Agpat1, Gpat1, Mgat1, Dgat1, Dgat2, Fasn, Hmgcs1, Acc1, Srebp1-c, and Pparγ) was suppressed, and AMPK and CREB were activated in Abcb4−/− and HBs/Abcb4−/− compared to wild-type and HBs mice. Simulating cholestatic conditions in cell culture resulted in AMPK and CREB activation while FASN and PLIN2 were reduced. A concurrent inhibition of AMPK signaling revealed normal expression level of FASN and PLIN2, suggesting that activation of AMPK–CREB signaling regulates hepatic lipid metabolism, i.e. synthesis and storage, under cholestatic condition. In conclusions, in vivo and mechanistic in vitro data suggest that cholestasis reduces hepatic lipid storage via AMPK and CREB signaling. The results of the current study could be the basis for novel therapeutic strategies as NASH is a crucial factor that can aggravate chronic liver diseases.