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Metal anodes represent as a prime choice for the coming generation rechargeable batteries with high energy density. However, daunting challenges including electrode volume variation and inevitable side reactions preclude them from becoming a viable technology. Here, a facile replacement reaction was employed to fabricate a three-dimensional (3D) interdigitated metal/solid electrolyte composite electrode, which not only provides a stable host structure for buffering the volume change within the composite but also prevents side reactions by avoiding the direct contact between active metal and liquid electrolyte. As a proof-of-concept demonstration, a 3D interdigitated zinc (Zn) metal/solid electrolyte architecture was fabricated via a galvanic replacement reaction between Zn metal foil and indium (In) chloride solution followed by electrochemical activation, featuring the interdigitation between metallic Zn and amorphous indium hydroxide sulfate (IHS) with high Zn 2+ conductivity (56.9 ± 1.8 mS cm −1 ), large Zn 2+ transference number (0.55), and high electronic resistivity [(2.08 ± 0.01) × 10 3 Ω cm]. The as-designed Zn/IHS electrode sustained stable electrochemical Zn plating/stripping over 700 cycles with a record-low overpotential of 8 mV at 1 mA cm −2 and 0.5 mAh cm −2 . More impressively, it displayed cycle-stable performance with low overpotential of 10 mV under ultrahigh current density and areal capacity (20 mA cm −2 , 20 mAh cm −2 ), which outperformed all the reported Zn metal electrodes in mild aqueous electrolyte. The fabrication of interdigitated metal/solid electrolyte was generalized to other metal pairs, including Zn/Sn and Zn/Co, which provide inspiration for next-generation Zn metal batteries with high energy density and reversibility.

Metallic Zn is a preferred anode material for rechargeable aqueous batteries towards a smart grid and renewable energy storage. Understanding how the metal nucleates and grows at the aqueous Zn anode is a critical and challenging step to achieve full reversibility of Zn battery chemistry, especially under fast-charging conditions. Here, by combining in situ optical imaging and theoretical modeling, we uncover the critical parameters governing the electrodeposition stability of the metallic Zn electrode, that is, the competition among crystallographic thermodynamics, kinetics, and Zn 2 + -ion diffusion. Moreover, steady-state Zn metal plating/ stripping with Coulombic efficiency above 99 % is achieved at 10-100 mA cm À 2 in a reasonably high concentration (3 M) ZnSO 4 electrolyte. Significantly, a long-term cycling-stable Zn metal electrode is realized with a depth of discharge of 66.7 % under 50 mA cm À 2 in both Zn j j Zn symmetrical cells and MnO 2 j j Zn full cells.

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Accumulated evidence demonstrates that Japanese encephalitis virus (JEV) infection triggers endoplasmic reticulum (ER) stress and neuron apoptosis. ER stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) has been reported to induce apoptosis under acute or prolonged ER stress. However, the precise role of PERK in JEV-induced apoptosis and encephalitis remains unknown. Here, we report that JEV infection activates the PERK-ATF4-CHOP apoptosis pathway both in vitro and in vivo. PERK activation also promotes the formation of stress granule, which in turn represses JEV-induced apoptosis. However, PERK inhibitor reduces apoptosis, indicating that JEV-activated PERK predominantly induces apoptosis via the PERK-ATF4-CHOP apoptosis pathway. Among JEV proteins that have been reported to induce ER stress, only JEV NS4B can induce PERK activation. PERK has been reported to form an active molecule by dimerization. The coimmunoprecipitation assay shows that NS4B interacts with PERK. Moreover, glycerol gradient centrifugation shows that NS4B induces PERK dimerization. Both the LIG-FHA and the LIG-WD40 domains within NS4B are required to induce PERK dimerization, suggesting that JEV NS4B pulls two PERK molecules together by simultaneously interacting with them via different motifs. PERK deactivation reduces brain cell damage and encephalitis during JEV infection. Furthermore, expression of JEV NS4B is sufficient to induce encephalitis via PERK in mice, indicating that JEV activates PERK primarily via its NS4B to cause encephalitis. Taken together, our findings provide a novel insight into JEV-caused encephalitis. IMPORTANCE Japanese encephalitis virus (JEV) infection triggers endoplasmic reticulum (ER) stress and neuron apoptosis. ER stress sensor protein kinase R-like endoplasmic reticulum kinase (PERK) has been reported to induce apoptosis under acute or prolonged ER stress. However, whether the PERK pathway of ER stress response plays important roles in JEV-induced apoptosis and encephalitis remains unknown. Here, we found that JEV infection activates ER stress sensor PERK in neuronal cells and mouse brains. PERK activation induces apoptosis via the PERK-ATF4-CHOP apoptosis pathway upon JEV infection. Among the JEV proteins prM, E, NS1, NS2A, NS2B, and NS4B, only NS4B activates PERK. Moreover, activated PERK participates in apoptosis and encephalitis induced by JEV and NS4B. These findings provide a novel therapeutic approach for JEV-caused encephalitis.

Aqueous rechargeable zinc (Zn) metal batteries show great application prospects in grid-scale energy storage devices due to their good safety, low cost, and considerable energy density. However, the electrical and topographical inhomogeneity caused by the native passivation layer of metallic Zn foil leads to inhomogeneous electrochemical plating and stripping of metallic Zn, and the limited accessible area to the electrolyte of the regular foil electrode causes the poor rate capability, which together hinder the practical application of the Zn metal electrode in rechargeable aqueous batteries. In this work, we show that the native passivation layer on the Zn foil electrode can be removed by a simple chemical polishing strategy, associated with the formation of a three-dimensional ridge-like structure of metallic Zn (r-Zn) on the surface of the Zn foil electrode due to the selective etching of weak crystallographic planes and grain boundary of metallic Zn. The clean and uniform surface of the metallic Zn electrode enables homogeneous plating and stripping of metallic Zn, and the ridge-like structure of r-Zn increases the accessible surface area to the electrolyte and reduces the local current density, which elevates the electrochemical performance of the Zn metal anode with regard to the cycling stability and rate capability. It is demonstrated that a r-Zn anode cycles stably for over 200 h at 1 mA cm −2 and 0.5 mA h cm −2 with a low overpotential of 20 mV, which far outperforms 39 h of cycling with an overpotential of 72 mV for its pristine metallic Zn counterpart.

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Objective: Cervical spondylotic myelopathy is regarded as a chronic, special incomplete spinal cord injury, so the sensory components transmitted to thalamus decreased after distal spinal cord injury, which lead the disturbance of thalamus-cortex circuits, which might explain the alterations of clinical function of cervical spondylotic myelopathy patients. However, for lack of effective methods to evaluate the disturbance circuits and how the relative mechanism adapt to the recovery of cervical spondylotic myelopathy patients after decompression. Therefore, this study aim to explore how the possible mechanism of thalamus-cortex circuits reorganization adapt to the recovery of clinical function. Methods: Regard thalamus as the interest area, we evaluate the brain functional connectivity within 43 pre-operative cervical spondylotic myelopathy patients, 21 post-operative (after 3 months) cervical spondylotic myelopathy patients and 43 healthy controls. Functional connectivity difference between pre-/post-operative cervical spondylotic myelopathy group and healthy controls group were obtained by two independent samples t-test, and difference between pre-operative cervical spondylotic myelopathy and post-operative cervical spondylotic myelopathy group were obtained by paired t-test. Clinical function was measured via Neck Disability Index and Japanese Orthopaedic Association scores. Furthermore, Pearson correlation were used to analyse the correlation between functional connectivity values and clinical scores. Results: Compared with healthy controls group, pre-operative cervical spondylotic myelopathy group showed increased functional connectivity between left thalamus and bilateral lingual gyrus/cuneus/right cerebellum posterior lobe (Voxel P-value <0.01, Cluster P-value <0.05, GRF corrected); post-operative cervical spondylotic myelopathy group manifested decreased functional connectivity between right thalamus and bilateral paracentral lobe/precentral gyrus but significantly increased between right thalamus and pons/superior temporal gyrus. In comparison with pre-operative cervical spondylotic myelopathy group, post-operative cervical spondylotic myelopathy group showed increased functional connectivity between bilateral thalamus and posterior cingulate lobe, angular gyrus, medial prefrontal, but significantly decreased functional connectivity between bilateral thalamus and paracentral lobe/precentral gyrus. The functional connectivity between left thalamus and bilateral lingual gyrus/cuneus/right cerebellum posterior lobe in pre-operative cervical spondylotic myelopathy group have a significantly positive correlation with sensory Japanese Orthopaedic Association scores (r = 0.568, P < 0.001). The functional connectivity between thalamus and paracentral lobe/precentral gyrus in post-operative cervical spondylotic myelopathy group have a significantly positive correlation with upper limb movement Japanese Orthopaedic Association scores (r = 0.448, P = 0.042). Conclusion: Pre- or post-operative cervical spondylotic myelopathy patients showed functional connectivity alteration between thalamus and cortex, which suggest adaptive changes may favor the preservation of cortical sensorimotor networks before and after cervical cord decompression, and supply the improvement of clinical function.