Na-ion batteries (SIBs) require novel anode materials which have high ion storage capability and low working voltage to make SIBs competitive compared to Li-ion batteries (LIBs). From this perspective, we present the origin of improved electrochemical performances of phosphate doped hard carbon (P-HC) which can meet the two requirements mentioned above through combining experiment with the calculations of atomic/electronic structures. We disclosed that the capacity enhancement is accompanied by the changed voltage profile, which results from the introduced phosphate functional groups. The emerged redox peak turned out to be generated by the electrochemical reaction of Na ions near the phosphate-carbon environment. First-principles calculations elaborated that the phosphate introduction here generates electron holes near the Fermi level that is generally considered as evidence of p-type semiconductors to improve electronic conductivity. This expectation has been proven by comparatively measuring the electrical conductivities of pristine hard carbon and P-HC. A close investigation into charge distribution indicated that the electron hole is generated mainly by the higher reducibility of the doped phosphate than the surrounding carbon atoms in P-HC. This discovery well explains the underlying principles for the enhanced electrochemical performance of P-HC, thereby showing a way to design highly functional hard carbon structures toward higher capacity with Na ions.

Recent evidence in adipocytes points to a role for synuclein-γ in metabolism and lipid droplet dynamics, but interestingly this factor is also robustly expressed in peripheral neurons. Specific regulation of the synuclein-γ gene (Sncg) by PPARγ requires further evaluation, especially in peripheral neurons, prompting us to test if Sncg is a bona fide PPARγ target in murine adipocytes and peripheral somatosensory neurons derived from the dorsal root ganglia (DRG). Sncg mRNA was decreased in 3T3-L1 adipocytes (~68%) by rosiglitazone, and this effect was diminished by the PPARγ antagonist T0070907. Chromatin immunoprecipitation experiments confirmed PPARγ protein binding at two promoter sequences of Sncg during 3T3-L1 adipogenesis. Rosiglitazone did not affect Sncg mRNA expression in murine cultured DRG neurons. In subcutaneous human WAT samples from two cohorts treated with pioglitazone (>11 wks), SNCG mRNA expression was reduced, albeit highly variable and most evident in type 2 diabetes. Leptin (Lep) expression, thought to be coordinately-regulated with Sncg based on correlations in human adipose tissue, was also reduced in 3T3-L1 adipocytes by rosiglitazone. However, Lep was unaffected by PPARγ antagonist, and the LXR agonist T0901317 significantly reduced Lep expression (~64%) while not impacting Sncg. The results support the concept that synuclein-γ shares some, but not all, gene regulators with leptin and is a PPARγ target in adipocytes but not DRG neurons. Regulation of synuclein-γ by cues such as PPARγ agonism in adipocytes is logical based on recent evidence for an important role for synuclein-γ in the maintenance and dynamics of adipocyte lipid droplets.