Synergistic effect of porous carbon shell confinement and catalytic conversion of nickel nanoparticle cores for improved lithium-sulfur batteries.

Lithium-sulfur batteries (LSBs) are some of the most promising energy storage systems to break the ceiling of Li-ion batteries. However, the notorious shuttle effect and slow redox kinetics give rise to low sulfur utilization and discharge capacity, poor rate performance, and fast capacity decay. It is proved that the reasonable design of the electrocatalyst is one of the important ways to improve the electrochemical performance of LSBs. Here, a core-shell structure with gradient adsorption capacity for reactants and sulfur products was designed. The Ni nanoparticles core coated with graphite carbon shell was prepared by one-step pyrolysis of Ni-MOF precursors. The design takes advantage of the principle that the adsorption capacity decreases from the core to the shell, and the Ni core with strong adsorption capacity is easy to attract and capture soluble lithium polysulfide (LiPS) during the discharge/charging process. This trapping mechanism prevents the diffusion of LiPSs to the outer shell and effectively inhibits the shuttle effect. In addition, the Ni nanoparticles within the porous carbon, as the active center, expose most of the inherent active sites to the surface area, thus achieving a rapid transformation of LiPSs, significantly reducing the reaction polarization, and improving the cyclic stability and reaction kinetics of LSB. Therefore, the S/Ni@PC composites exhibited excellent cycle stability (a capacity of 417.4 mA h g-1 for 500 cycles at 1C with a fading rate of 0.11%) and outstanding rate performance (1014.6 mA h g-1 at 2C). This study provides a promising design solution of Ni nanoparticles embedded in porous carbon for high-performance, safe and reliable LSB.

Discovery by Virtual Screening of an Inhibitor of CDK5-Mediated PPARγ Phosphorylation.

Thiazolidinedione PPARγ agonists such as rosiglitazone and pioglitazone are effective antidiabetic drugs, but side effects have limited their use. It has been posited that their positive antidiabetic effects are mainly mediated by the inhibition of the CDK5-mediated Ser273 phosphorylation of PPARγ, whereas the side effects are linked to classical PPARγ agonism. Thus compounds that inhibit PPARγ Ser273 phosphorylation but lack classical PPARγ agonism have been sought as safer antidiabetic therapies. Herein we report the discovery by virtual screening of 10, which is a potent PPARγ binder and in vitro inhibitor of the CDK5-mediated phosphorylation of PPARγ Ser273 and displays negligible PPARγ agonism in a reporter gene assay. The pharmacokinetic properties of 10 are compatible with oral dosing, enabling preclinical in vivo testing, and a 7 day treatment demonstrated an improvement in insulin sensitivity in the ob/ob diabetic mouse model.