Glasses are promising electrolytes for use in solid-state batteries. Nevertheless, due to their amorphous structure, the mechanisms that underlie their ionic conductivity remain poorly understood. Here, ab initio molecular dynamics is used to characterize migration processes in the prototype glass, 75Li 2 S-25P 2 S 5 . Lithium migration occurs via a mechanism that combines concerted motion of lithium ions with large, quasi-permanent reorientations of PS 4 3− anions. This latter effect, known as the 'paddlewheel' mechanism, is typically observed in hightemperature crystalline polymorphs. In contrast to the behavior of crystalline materials, in the glass paddlewheel dynamics contribute to Lithium-ion mobility at room temperature. Paddlewheel contributions are confirmed by characterizing spatial, temporal, vibrational, and energetic correlations with Lithium motion. Furthermore, the dynamics in the glass differ from those in the stable crystalline analogue, γ-Li 3 PS 4 , where anion reorientations are negligible and ion mobility is reduced. These data imply that glasses containing complex anions, and in which covalent network formation is minimized, may exhibit paddlewheel dynamics at low temperature. Consequently, these systems may be fertile ground in the search for new solid electrolytes.

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Therapeutics that induce cancer cell senescence can block cell proliferation and promote immune rejection. However, the risk of tumor relapse due to senescence escape may remain high due to the long lifespan of senescent cells that are not cleared. Here we show how combining a senescence-inducing inhibitor of the mitotic kinase Aurora A (AURKA) with an MDM2 antagonist activates p53 in senescent tumors harboring wildtype 53. In the model studied, this effect is accompanied proliferation arrest, mitochondrial depolarization, apoptosis and immune clearance of cancer cells by antitumor leukocytes in a manner reliant upon CCL5, CCL1 and CXCL9. The AURKA/MDM2 combination therapy shows adequate bioavailability and low toxicity to the host. Moreover, the prominent response of patient-derived melanoma tumors to co-administered MDM2 and AURKA inhibitors offers a sound rationale for clinical evaluation. Taken together, our work provides a preclinical proof-of-concept for a combination treatment which leverages both senescence and immune surveillance to therapeutic ends.