Zn-ion batteries (ZIBs) have a broad application prospect because of their advantages of high power, large capacity, and high energy density. However, the development of high-capacity, long-lifespan ZIBs is challenging because of the faster dendrite growth and the occurrence of the hydrogen evolution reaction. Laser-induced graphene (LIG) is a material with many defects and heteroatoms. Because of these characteristics, it plays an important role in improving nucleation. A simple and effective method for preparing LIG was proposed in this paper, and the LIG was covered on the surface of Zn foil to form a composite structure. This structure substantially reduces the nucleation overpotential of Zn and slows down the dendrite growth of Zn by improving the nucleation behavior of Zn2+. Simultaneously, the three-dimensional porous structure increases the specific surface area of the electrode, so the battery has a larger specific capacity. Compared with the bare Zn electrode, the composite electrode possesses lower overpotential and longer cycle life. In addition, the full battery using activated carbon as the active material exhibits great rate and cycle performance. This facile and scalable approach may solve the problem of Zn dendrite growth, which is crucial for the large-scale application of ZIBs.
Osteoarthritis (OA) is one of the most common forms of arthritis. However, the pathogenesis of OA remains unclear. Previous studies suggested that stromal-cell-derived factor (SDF)-1 was associated with some characteristic changes in cartilage. The aim of this study is, therefore, to explore the mechanism of SDF-1 promotes chondrocyte mineralization in OA. The effect of SDF-1 was analyzed with human C-28/I2 chondrocytes. The chondrocytes were transfected with pEX-4-ANKH or siRNA and treated with related inhibitor. The chondrocytes were subjected to Alizarin red S staining, PiPer phosphate assay kit, Alkaline phosphatase staining , RT-PCR and Western blot analysis. In vitro, SDF-1 markedly promoted the mineralization of chondrocytes and suppressed the expression of ANKH, the endogenous mineralization inhibitor. ANKH overexpressed in the chondrocytes significantly decreased the levels of the mineralization in response to SDF-1 treatment. Moreover, SDF-1 promoted an increase in the expression of p-TAK1 and p-IKKβ、p-IkB、p-NF-kB p65. Furthermore, SDF-1 induced decrease in ANKH expression was blocked by IKKβVI (IkB kinase inhibitor). To conclude, SDF-1 suppresses the expression of ANKH via activating NF-kB pathway to aggravate human chondrocytes calcification, suggesting blockade of SDF-1 might be a novel therapy for treatment of OA patients.
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