Despite progress in solid-state battery engineering, our understanding of the chemo-mechanical phenomena that govern electrochemical behavior and stability at solid-solid interfaces remains limited compared to solid-liquid interfaces. Here, we use operando synchrotron X-ray computed microtomography to investigate the evolution of lithium/solid-state electrolyte interfaces during battery cycling, revealing how the complex interplay between void formation, interphase growth, and volumetric changes determines cell behavior. Void formation during lithium stripping is directly visualized in symmetric cells, and the loss of contact at the interface between lithium and the solid-state electrolyte (Li 10 SnP 2 S 12) is found to be the primary cause of cell failure. Reductive interphase formation within the solid-state electrolyte is simultaneously observed, and image segmentation reveals that the interphase is redox-active upon charge. At the cell level, we postulate that global volume changes and loss of stack pressure occur due to partial molar volume mismatches at either electrode. These results provide new insight into how chemo-mechanical phenomena can impact cell performance, which is necessary to understand for the development of solid-state batteries. File list (2) download file view on ChemRxiv Manuscript Updated.pdf (1.08 MiB) download file view on ChemRxiv Supplementary Information.pdf (1.02 MiB)

As the scale of transistors and capacitors in electronics is reduced to less than a few nanometers, leakage currents pose a serious problem to the device's reliability. To overcome this dilemma, high-κ materials that exhibit a larger permittivity and band gap are introduced as gate dielectrics to enhance both the capacitance and block leakage simultaneously. Currently, HfO 2 is widely used as a high-κ dielectric; however, a higher-κ material remains desired for further enhancement. To find new high-κ materials, we conduct a high-throughput ab initio calculation for band gap and permittivity. The accurate and efficient calculation is enabled by newly developed automation codes that fully automate a series of delicate methods in a highly optimized manner. We can, thus, calculate 41800 structures of binary and ternary oxides from the Inorganic Crystal Structure Database and obtain a total property map. We confirm that the inverse correlation relationship between the band gap and permittivity is roughly valid for most oxides. However, new candidate materials exhibit interesting properties, such as large permittivity, despite their large band gaps. Analyzing these materials, we discuss the origin of large κ values and suggest design rules to find new high-κ materials that have not yet been discovered.

No abstract

The prM protein of Japanese encephalitis virus (JEV) contains a single potential N-linked glycosylation site, N 15 -X 16 -T 17 , which is highly conserved among JEV strains and closely related flaviviruses. To investigate the role of this site in JEV replication and pathogenesis, we manipulated the RNA genome by using infectious JEV cDNA to generate three prM mutants (N15A, T17A, and N15A/T17A) with alanine substiting for N 15 and/or T 17 and one mutant with silent point mutations introduced into the nucleotide sequences corresponding to all three residues in the glycosylation site. An analysis of these mutants in the presence or absence of endoglycosidases confirmed the addition of oligosaccharides to this potential glycosylation site. The loss of prM N glycosylation, without significantly altering the intracellular levels of viral RNA and proteins, led to an Ϸ20-fold reduction in the production of extracellular virions, which had protein compositions and infectivities nearly identical to those of wild-type virions; this reduction occurred at the stage of virus release, rather than assembly. This release defect was correlated with small-plaque morphology and an N-glycosylation-dependent delay in viral growth. A more conservative mutation, N15Q, had the same effect as N15A. One of the four prM mutants, N15A/T17A, showed an additional defect in virus growth in mosquito C6/36 cells but not human neuroblastoma SH-SY5Y or hamster BHK-21 cells. This cell type dependence was attributed to abnormal N-glycosylationindependent biogenesis of prM. In mice, the elimination of prM N glycosylation resulted in a drastic decrease in virulence after peripheral inoculation. Overall, our findings indicate that this highly conserved N-glycosylation motif in prM is crucial for multiple stages of JEV biology: prM biogenesis, virus release, and pathogenesis.Japanese encephalitis virus (JEV) is a member of the genus Flavivirus, which consists of Ϸ80 enveloped RNA viruses in the family Flaviviridae (5,22,36). The flaviviruses include many other clinically important human pathogens, such as dengue virus (DENV), yellow fever virus, West Nile virus (WNV), St. Louis encephalitis virus, Murray Valley encephalitis virus, and tick-borne encephalitis virus (TBEV). JEV is transmitted in an enzoonotic cycle between mosquito vectors and vertebrate hosts, with pigs and ardeid birds as the primary viremia-amplifying hosts and reservoirs, respectively, and with humans as incidental hosts (4). JEV is the most important cause of epidemic encephalitis in many Asian countries, leading to permanent neuropsychiatric sequelae and even death in children and young adults (13,60,64,66). Over the past two decades, JEV has spread throughout the Indonesian archipelago (9, 75) to the Australian territories (41,42,65), attracting increasing attention in the arena of international public health.JEV contains a single-stranded, positive-sense RNA genome of Ϸ11,000 nucleotides. The RNA genome has a cap structure at the 5Ј end and lacks a poly(A) tail at the 3Ј end (37)...