Solid electrolytes possessing sufficient ionic conductivity and electrochemical stability are urgently needed for the fabrication of all-solid-state Li-ion batteries (LIBs). In this study, we focus on a solid-state oxide electrolyte LiZr 2 (PO 4 ) 3 (LZP), which has NASICON structure and electrochemically stable Zr 4+ ions. Using density functional theory (DFT) to calculate the electrochemical window of LZP, we find that it is unstable against Li metal, in accordance with our experimental results. The Li-ion transport is investigated using first-principles molecular dynamics (FPMD) simulations. The calculated Li-ion conductivity at room temperature (5.0 × 10 −6 S/cm) and the activation energy for Li-ion diffusion (0.43 eV) are in fair agreement with experimental results. The mechanism of Li-ion conduction in LZP is revealed by analyzing the Li-ion trajectories in the FPMD simulations. It is found that each Li ion migrates between 6b sites as it is pushed out or repelled by other Li ions around these 6b sites. Hence, the high Li-ion conductivity is attributed to a migration mechanism driven by Frenkel-like defect.

PARP enzyme plays a key role in the cellular machinery responsible for DNA damage repair. PTEN is a tumorsuppressor gene deactivating PI3K downstream of EGFR signaling. We hypothesize that PTEN-deficient lung cancer cells suppressed DNA damage signaling and that the absence of PTEN can sensitize these cells to a concurrent treatment of a DNA-damaging agent (cisplatin) and a PARP inhibitor (olaparib). To investigate the effect of olaparib and cisplatin on PTEN-deficient lung tumors, two EGFR-mutant (deletion in exon19) non-small cell lung cancer (NSCLC) cell lines, PC-9 (PTEN wild-type) and H1650 (PTEN loss), were used. We transfected intact PTEN gene into H1650 cells (H1650 PTENþ ) and knocked down PTEN expression in the PC-9 cells (PC-9 PTENÀ ) using short hairpin RNA (shRNA). Combination of cisplatin with olaparib showed a synergistic effect in vitro according to the combination index in H1650 cells. Restoration of PTEN in the H1650 cells decreased sensitivity to the combination. Ablation of PTEN in PC-9 cells increased sensitivity to olaparib and cisplatin. We also examined the effectiveness of cisplatin and olaparib in a xenograft model using H1650 and PC-9 PTENÀ cells. The combination of cisplatin with olaparib was more effective than each agent individually. This effect was not observed in a xenograft model using H1650 PTENþ and PC-9 cells. Mechanistic investigations revealed that PTEN deficiency caused reductions in nuclear RAD51 and RPA focus formation and phosphorylated Chk1 and Mre11.