Replacing organic liquid electrolyte with inorganic solid electrolytes (SE) can potentially address the inherent safety problems in conventional rechargeable batteries. However, solid-state batteries (SSBs) have been plagued by the relatively low ionic conductivity of SEs and large charge-transfer resistance between electrode and SE. Here, a new design strategy is reported for improving the ionic conductivity of SE by self-forming a composite material. An optimized Na + ion conducting composite electrolyte derived from the Na 1+n Zr 2 Si n P 3−n O 12 NASICON (Na Super Ionic Conductor) structure is successfully synthesized, yielding ultrahigh ionic conductivity of 3.4 mS cm −1 at 25 °C and 14 mS cm −1 at 80 °C. On the other hand, in order to enhance the charge-transfer rate at the electrode/electrolyte interface, an interface modification strategy is demonstrated by utilization of a small amount of nonflammable and nonvolatile ionic liquid (IL) at the cathode side in SSBs. The IL acts as a wetting agent, enabling a favorable interface kinetic in SSBs. The Na 3 V 2 (PO 4 ) 3 /IL/SE/Na SSB exhibits excellent cycle performance and rate capability. A specific capacity of ≈90 mA h g −1 is maintained after 10 000 cycles without capacity decay under 10 C rate at room temperature. This provides a new perspective to design fast ion conductors and fabricate long life SSBs.

A solvent-free ceramic/polymer composite solid electrolyte has been proposed and demonstrated well in solid-state Na batteries for the first time.

Two cyclodepsipeptides and a known cyclodepsipeptide valinomycin were isolated from a culture of the marine actinomycete Streptomyces sp. P11-23B. Their structures were established based on NMR, HRESIMS, and MS-MS spectroscopic interpretation as well as by chemical degradation. Both streptodepsipeptides P11A and P11B inhibited proliferation of different glioma cell lines, with IC values ranging from 0.1 μM to 1.4 μM. Streptodepsipeptide P11A was found to block the cell cycle at the G/G phase and induce apoptosis in glioma cells. Further investigation demonstrated that streptodepsipeptide P11A downregulated expression of HK2, PFKFB3, PKM2, GLS, and FASN, important tumor metabolic enzymes. Data from this study suggested that targeting multiple tumor metabolic regulators might be one anti-glioma mechanism of streptodepsipeptide P11A. A possible mechanism for this class of streptodepsipeptides is reported herein.