Alloy materials such as Si and Ge are attractive as high‐capacity anodes for rechargeable batteries, but such anodes undergo severe capacity degradation during discharge–charge processes. Compared to the over‐emphasized efforts on the electrode structure design to mitigate the volume changes, understanding and engineering of the solid‐electrolyte interphase (SEI) are significantly lacking. This work demonstrates that modifying the surface of alloy‐based anode materials by building an ultraconformal layer of Sb can significantly enhance their structural and interfacial stability during cycling. Combined experimental and theoretical studies consistently reveal that the ultraconformal Sb layer is dynamically converted to Li3Sb during cycling, which can selectively adsorb and catalytically decompose electrolyte additives to form a robust, thin, and dense LiF‐dominated SEI, and simultaneously restrain the decomposition of electrolyte solvents. Hence, the Sb‐coated porous Ge electrode delivers much higher initial Coulombic efficiency of 85% and higher reversible capacity of 1046 mAh g−1 after 200 cycles at 500 mA g−1, compared to only 72% and 170 mAh g−1 for bare porous Ge. The present finding has indicated that tailoring surface structures of electrode materials is an appealing approach to construct a robust SEI and achieve long‐term cycling stability for alloy‐based anode materials.

Background: Osteoarthritis (OA) is a prevalent chronic diseases characterized by formation of osteophytes and degradation of articular cartilage. Previous evidence has identified the regulatory effects of microRNAs (miRNAs) in OA. The goal of this study is to clearly explore the biological function of miR-1207-5p in OA. Methods: MiR-1207-5p and C-X3-C motif chemokine receptor 1 (CX3CR1) expression in OA cartilages were revealed by accessing to Gene Expression Omnibus database. In vitro OA model was established by lipopolysaccharide (LPS) stimulation. Western blot and quantitative real-time polymerase chain reaction were conducted to detect the expression level of genes. Cell counting kit-8 (CCK-8) and flow cytometric experiments were performed to investigate the proliferation and apoptosis capacities of CHON-001 cells. Bioinformatics analysis was applied to predict the binding site of miR-1207-5p and CX3CR1, the connections of which were ascertained using luciferase reporter assay. Results: MiR-1207-5p expression was decreased while CX3CR1 was increased in OA cartilages. Up-regulation of miR-1207-5p alleviated the LPS-induced damage in the view of cell proliferation, apoptosis and extracellular matrix (ECM) degradation. A target of miR-1207-5p CX3CR1, its down-regulation intensified the impacts of miR-1207-5p mimic, promoted proliferation and mitigated apoptosis. LPS exposure increased the protein expression of the phosphorylated IκBα and P65, and this phenomena was reversed due to miR-1207-5p up-regulation and CX3CR1 knockdown. The treatment of Betulinic acid (BA; an activator of nuclear factor-κB pathway) reversed the miR-1207-5p mimic-induced inhibitory effect on apoptosis in LPS-treated CHON-001. Conclusion: Our results highlight that miR-1207-5p can prevent CHON-001 from LPS-stimulated injury, providing a novel biomarker for OA progression and further advancing treatment of OA.