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The tantalum oxide film was fabricated using an anodization process in a 0.5M H 2 SO 4 electrolyte. The evolution and corrosion resistance mechanism of anodized film on the Ta surface has been investigated by experiments and theoretical calculations. The results indicate that the sample with an anodic oxidation voltage of 20V and an anodic oxidation time of 60 min (Ta 20-60) exhibits the thickest oxidation film, measuring 360.00 nm and comprising an outer porous layer and an inner dense layer. Ta 20-60 demonstrates the highest E corr value of 0.009 V and the lowest I corr value of 0.879 μA cm−2, with a minimal density of point defects at 1.24 × 1019 cm−3, which imparts superior corrosion resistance. The calculation result shows that the growth rate of Ta anodic oxidation film is controlled by the diffusion and migration of vacancy defects. The O atom passes through one bridge site from the tetrahedral gap to another tetrahedral gap (Path 1) on the complete (110) surface has a low diffusion barrier of 0.470 eV and the shortest diffusion path of 2.04 Å, which is the most favorable path for the diffusion of O atoms. This paper offers a fresh perspective on the corrosion resistance of tantalum while furnishing guidance for improving Ta oxide film performance. [ABSTRACT FROM AUTHOR]

Background: Cayratia albifolia C.L.Li (CAC) is a traditional Chinese herbal medicine used to treat inflammatory diseases. Our laboratory has firstly reported that the water extract from CAC relieved lipopolysaccharide (LPS)-induced inflammation, however stronger evidence is still needed to prove its anti-inflammatory effects and the mechanisms involved are also ambiguous.Purpose: This study sought to provide more evidence for the application of CAC in alleviating infectious inflammation and disclose novel pharmacological mechanisms.Methods: Mice were injected with zymA into their paws or peritoneal cavities, and then treated with CAC. ELISA, immunofluorescence and flow cytometry were performed to detect the cytokines (IL-1β, IL-6, TNF-α and IL-10) generation, the cell infiltration, and the CD86 or CD206 expression of macrophages. Then in vitro assays were performed on bone marrow-derived macrophages (BMDMs) and peritoneal macrophages (PMs) to detect their expression of iNOS, arg-1 and the cytokines above. On mechanisms, western blotting (WB), electrophoretic mobility shift assay (EMSA) and flow cytometry were carried out to measure NF-κB transcriptional activity, mitochondrial bioactivity and the mTORC1 activation when BMDMs were stimulated by zymA and treated with CAC. Finally, the chemical components consisted in the extract were analyzed by LC-MS.Results: 200 mg/kg CAC clearly inhibited zymA induced mouse paw edema and reduced the contents of IL-1β, IL-6 and TNF-α rather than IL-10 in local tissues. CAC also reduced CD86 but not CD206 in macrophages in situ. Through in vitro experiments, it was discovered that CAC reduced the protein and mRNA levels of IL-1β, IL-6 and TNF-α, and also inhibited iNOS expression, but showed no influence on IL-10 and arg-1 in macrophages. We found CAC reduced NF-κB transcriptional activity, down-regulated mitochondrial membrane potential and ROS levels, and inhibited mTORC1 activity. Finally, we identified 15 major compounds in the extract, among which 4-guanidinobutyric acid and kynurenic acid were the most abundant.Conclusion: This study provides further evidence that CAC significantly reduces zymA induced infectious inflammation. In addition, this novel data revealed that CAC restrained M1 rather than promoting M2 macrophages polarization via multi-target inhibitory effects, based on its potentially active components. [ABSTRACT FROM AUTHOR]