ABSTRACT
To realize the development of rechargeable sodium batteries, new positive electrode materials without less abundant elements are explored. Enrichment of sodium contents in host structures is required to increase the theoretical capacity as electrode materials, and therefore Na-excess compounds are systematically examined in a binary system of Na2 TiO3 -NaMnO2 . After several trials, synthesis of Na-excess compounds with a cation disordered rocksalt structure is successful by adapting a mechanical milling method. Among the tested electrode materials, Na1.14 Mn0.57 Ti0.29 O2 in this binary system delivers a large reversible capacity of ≈200 mA h g-1 , originating from reversible redox reactions of cationic Mn3+ /Mn4+ and anionic O2- /On - redox confirmed by X-ray absorption spectroscopy. Holes in oxygen 2p orbitals, which are formed by electrochemical oxidation, are energetically stabilized by electron donation from Mn ions. Moreover, reversibility of anionic redox is significantly improved compared with a former study on a binary system of Na3 NbO3 -NaMnO2 tested as model electrode materials.
ABSTRACT
Bone is a highly metabolic organ that undergoes continuous remodeling to maintain its structural integrity. During development, bones, in particular osteoblasts, rely on glucose uptake. However, the role of glucose metabolism in osteocytes is unknown. Osteocytes are terminally differentiated osteoblasts orchestrating bone modeling and remodeling. In these cells, parathyroid hormone (PTH) suppresses Sost/sclerostin expression (a potent inhibitor of bone formation) by promoting nuclear translocation of class IIa histone deacetylase (HDAC) 4 and 5 and the repression of myocyte enhancer factor 2 (MEF2) type C. Recently, Scriptaid, an HDAC complex co-repressor inhibitor, has been shown to induce MEF2 activation and exercise-like adaptation in mice. In muscles, Scriptaid disrupts the HDAC4/5 co-repressor complex, increases MEF2C function, and promotes cell respiration. We hypothesized that Scriptaid, by affecting HDAC4/5 localization and MEF2C activation, might affect osteocyte functions. Treatment of the osteocytic Ocy454-12H cells with Scriptaid increased metabolic gene expression, cell respiration, and glucose uptake. Similar effects were also seen upon treatment with PTH, suggesting that both Scriptaid and PTH can promote osteocyte metabolism. Similar to PTH, Scriptaid potently suppressed Sost expression. Silencing of HDAC5 in Ocy454-12H cells abolished Sost suppression but not glucose transporter type 4 (Glut4) up-regulation induced by Scriptaid. These results demonstrate that Scriptaid increases osteocyte respiration and glucose uptake by mechanisms independent of HDAC complex inhibition. In osteocytes, Scriptaid, similar to PTH, increases binding of HDAC5 to Mef2c with suppression of Sost but only partially increases receptor activator of NF-κB ligand (Rankl) expression, suggesting a potential bone anabolic effect.
