Highly Efficient Spatially-Temporally Synchronized Construction of Robust Li3 PO4 -rich Solid-Electrolyte Interphases in Aqueous Li-ion Batteries.

Solid electrolyte interphase (SEI) makes the electrochemical window of aqueous electrolytes beyond the thermodynamics limitation of water. However, achieving the energetic and robust SEI is more challenging in aqueous electrolytes because the low SEI formation efficiency (SFE) only contributed from anion-reduced products, and the low SEI formation quality (SFQ) negatively impacted by the hydrogen evolution, resulting in a high Li loss to compensate for SEI formation. Herein, we propose a highly efficient strategy to construct Spatially-Temporally Synchronized (STS) robust SEI by the involvement of synergistic chemical precipitation-electrochemical reduction. In this case, a robust Li3 PO4 -rich SEI enables intelligent inherent growth at the active site of the hydrogen by the chemical capture of the OH- stemmed from the HER to trigger the ionization balance of dihydrogen phosphate (H2 PO4 - ) shift to insoluble solid Li3 PO4 . It is worth highlighting that the Li3 PO4 formation does not extra-consume lithium derived from the cathode but makes good use of the product of HER (OH- ), prompting the SEI to achieve 100 % SFE and pushing the HER potential into -1.8 V vs. Ag/AgCl. This energetic and robust SEI offers a new way to achieve anion/concentration-independent interfacial chemistry for the aqueous batteries.

LMP2 deficiency causes abnormal metabolism, oxidative stress, neuroinflammation, myelin loss and neurobehavioral dysfunctions.

BACKGROUND: Substantial evidence suggests that immunoproteasome is implicated in the various neurological diseases such as stroke, multiple sclerosis and neurodegenerative diseases. However, whether the immunoproteasome itself deficiency causes brain disease is still unclear. Therefore, the aim of this study was to explore the contribution of the immunoproteasome subunit low molecular weight protein 2 (LMP2) in neurobehavioral functions. METHODS: Male LMP2 gene completed knockout (LMP2-KO) and littermate wild type (WT) Sprague-Dawley (SD) rats aged 12-month-old were used for neurobehavioral testing and detection of proteins expression by western blotting and immunofluorescence. A battery of neurobehavioral test tools including Morris water maze (MWM), open field maze, elevated plus maze were used to evaluate the neurobehavioral changes in rats. Evans blue (EB) assay, Luxol fast blue (LFB) and Dihydroethidium (DHE) staining were applied to explore the blood-brain barrier (BBB) integrity, brain myelin damage and brain intracellular reactive oxygen species (ROS) levels, respectively. RESULTS: We firstly found that LMP2 gene deletion did not cause significantly difference in rats' daily feeding activity, growth and development as well as blood routine, but it led to metabolic abnormalities including higher levels of low-density lipoprotein cholesterol, uric acid and blood glucose in the LMP2-KO rats. Compared with the WT rats, LMP2-KO rats displayed obviously cognitive impairment and decreased exploratory activities, increased anxiety-like behavior and without strong effects on gross locomotor abilities. Furthermore, multiple myelin loss, increased BBB leakage, downregulation of tight junction proteins ZO-1, claudin-5 and occluding, and enhanced amyloid-ß protein deposition were observed in brain regions of LMP2-KO rats. In addition, LMP2 deficiency significantly enhanced oxidative stress with elevated levels of ROS, caused the reactivation of astrocytes and microglials and markedly upregulated protein expression levels of interleukin (IL)-1 receptor-associated kinase 1 (IRAK1), IL-6 and tumor necrosis factor-α (TNF-α) compared to the WT rats, respectively. CONCLUSION: These findings highlight LMP2 gene global deletion causes significant neurobehavioral dysfunctions. All these factors including metabolic abnormalities, multiple myelin loss, elevated levels of ROS, increased BBB leakage and enhanced amyloid-ß protein deposition maybe work together and eventually led to chronic oxidative stress and neuroinflammation response in the brain regions of LMP2-KO rats, which contributed to the initial and progress of cognitive impairment.

Immunoproteasome modulates NLRP3 inflammasome-mediated neuroinflammation under cerebral ischaemia and reperfusion conditions.

Compelling evidence showed that both nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasomes and the immunoproteasome participate in neuroinflammatory responses in cerebral ischaemia injury. Moreover, inhibition of either NLRP3 inflammasomes or the immunoproteasome attenuates both neuroinflammation and neurological deterioration during ischaemic stroke. However, the underlying mechanism between the immunoproteasome and NLRP3 inflammasomes under ischaemic stroke conditions remains to be established. In this study, using both in vitro and in vivo ischaemic models, we demonstrated that the immunoproteasome inhibition reduced the expressions of NLRP3 inflammasome-associated proteins, including NLRP3, apoptosis-associated speck-like protein (ASC), caspase-1 and mature cytokines (interleukin [IL]-1ß and IL-18). It also downregulated the levels of nuclear factor (NF)-κB and pyroptotic- and apoptotic-related proteins, and improved cell viability. In addition, inhibition of NF-κB by the small molecule inhibitor Bay-11-7082 led to lower levels of NLRP3 inflammasomes and cleaved caspase-1 proteins in BV2 cells after oxygen-glucose deprivation and reoxygenation. Together, these findings suggest that the immunoproteasome may be responsible for inducing the expression and activation of NLRP3 inflammasomes via the NF-κB pathway. Therapeutic interventions that target activation of the immunoproteasome/NF-κB/NLRP3 inflammasome pathway may provide novel prospects for the future treatment of ischaemic stroke.

Aluminum corrosion-passivation regulation prolongs aqueous batteries life.

Aluminum current collectors are widely used in nonaqueous batteries owing to their cost-effectiveness, lightweightness, and ease of fabrication. However, they are excluded from aqueous batteries due to their severe corrosion in aqueous solutions. Here, we propose hydrolyzation-type anodic additives to form a robust passivation layer to suppress corrosion. These additives dramatically lower the corrosion current density of aluminum by nearly three orders of magnitude to ~10-6 A cm-2. In addition, realizing that electrochemical corrosion accompanies anode prelithiation, we propose a prototype of self-prolonging aqueous Li-ion batteries (Al ||LiMn2O4 ||TiO2), whose capacity retention rises from 49.5% to 70.1% after 200 cycles. A sacrificial aluminum electrode where electrochemical corrosion is utilized is introduced as an electron supplement to prolong the cycling life of aqueous batteries. Our work addresses the short-life issue of aqueous batteries resulting from the corrosion of the current collector and lithium loss from side reactions.

Anion-enrichment interface enables high-voltage anode-free lithium metal batteries.

Aggressive chemistry involving Li metal anode (LMA) and high-voltage LiNi0.8Mn0.1Co0.1O2 (NCM811) cathode is deemed as a pragmatic approach to pursue the desperate 400 Wh kg-1. Yet, their implementation is plagued by low Coulombic efficiency and inferior cycling stability. Herein, we propose an optimally fluorinated linear carboxylic ester (ethyl 3,3,3-trifluoropropanoate, FEP) paired with weakly solvating fluoroethylene carbonate and dissociated lithium salts (LiBF4 and LiDFOB) to prepare a weakly solvating and dissociated electrolyte. An anion-enrichment interface prompts more anions' decomposition in the inner Helmholtz plane and higher reduction potential of anions. Consequently, the anion-derived interface chemistry contributes to the compact and columnar-structure Li deposits with a high CE of 98.7% and stable cycling of 4.6 V NCM811 and LiCoO2 cathode. Accordingly, industrial anode-free pouch cells under harsh testing conditions deliver a high energy of 442.5 Wh kg-1 with 80% capacity retention after 100 cycles.

Inhibition of the Immunoproteasome Subunit LMP7 Ameliorates Cerebral White Matter Demyelination Possibly via TGFß/Smad Signaling.

OBJECTIVES: Chronic cerebral hypoperfusion induces white matter ischemic injury and cognitive impairment, whereas the mechanism remains unclear. Immunoproteasomes have been implicated in the pathogenesis of acute ischemia stroke and multiple sclerosis. However, the expression and role of immunoproteasomes in the brain of chronic cerebral hypoperfusion remain to be clarified. METHODS: Chronic white matter ischemic injury mice models were induced by bilateral carotid artery stenosis (BCAS). A selective immunoproteasome subunit low-molecular-mass peptide-7 (LMP7) inhibitor PR957 was administered to mice. Cognitive function, white matter integrity, and potential pathways were assessed after BCAS. RESULTS: The present study found that chronic cerebral hypoperfusion following BCAS induced cerebral white matter demyelination and cognitive impairment, accompanied with elevated expression of the immunoproteasomes LMP2 and LMP7, activation of astrocytes and microglia, and increased production of inflammatory cytokines (e.g., interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), IL-10, transforming growth factor-ß1 (TGFß1), and insulin-like growth factor-1 (IGF-1)). However, inhibition of LMP7 with the specific proteasome inhibitor PR957 significantly mitigated the histological damage of the white matter, suppressed inflammatory response, and paralleled by an improvement of cognitive function. Furthermore, treatment of PR957 significantly upregulated the level of TGFß1, the total expression level, and the phosphorylation level of Smad2/3 and promoted brain remyelination. Surprisingly, PR957 alone had no effects on the neuroinflammation response and the activation of TGFß/Smad signaling in the sham-operated (BCAS-nonoperated) mice. CONCLUSIONS: The possible mechanism underlying this was attributed to that the immunoproteasome regulates TGFß/Smad signaling-mediated neuroinflammation and oligodendrocyte remyelination.

Electronic Conductive Inorganic Cathodes Promising High-Energy Organic Batteries.

The electrochemical utilization of organic electrode materials (OEMs) is highly dependent on an excess amount of inactive carbon at the expense of low packing density and energy density. In this work, the challenges by substituting inactive carbon with electronic conductive inorganic cathode (ECIC) materials, which are endowed with high electronic conductivity to transport electrons for redox reactions of the whole electrodes, high ion-storage capacity to act as secondary active materials, and strong affinity with OEMs to inhibit their dissolution, are addressed. Combining representative ECICs (TiS2 and Mo6 S8 ) with organic electrode materials (perylene-3,4,9,10-tetracarboxylic dianhydride (PTCDA) and hexaazatrinaphthalene (HATN)) simultaneously achieves high capacity, low porosity, lean electrolyte, and thus high energy density. High gravimetric and volumetric energy densities of 153 Wh kg-1 and 200 Wh L-1 are delivered with superior cycling stability in a 30 mA h-level Li/PTCDA-TiS2 pouch cell. The proof-of-concept of organic-ECIC electrodes is also successfully demonstrated in monovalent Na, divalent Mg, and trivalent Al batteries, indicating their feasibility and generalizability. With the discovery of more ECIC materials and OEMs, it is anticipated that the proposed organic-ECIC system can result in further improvements at cell level to compete with transition metal-based Li-ion batteries.

Inhibition of the immunoproteasome LMP2 ameliorates ischemia/hypoxia-induced blood-brain barrier injury through the Wnt/ß-catenin signalling pathway.

BACKGROUND: Disruption of the blood-brain barrier (BBB) after a stroke can lead to brain injury and neurological impairment. Previous work confirmed the involvement of the immunoproteasome subunit of low molecular mass peptide 2 (LMP2) in the pathophysiology of ischemia stroke. However, the relationship between the immunoproteasome LMP2 and the BBB remains unclear. METHODS: Adult male Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion/reperfusion (MCAO/R). Three days before MCAO, the rats were treated with lentivirus-mediated LMP2 shRNA preparations by stereotactical injection into the ipsilateral hemispheric region. The rat brain microvascular endothelial cell (RBMVEC) line was exposed to oxygen-glucose deprivation/reperfusion (OGD/R) to mimic ischemic conditions in vitro. The RNA interference-mediated knockdown of LMP2 or ß-catenin was analysed in vivo and in vitro. Analysis of the quantity of extravasated Evans blue (EB) and cerebral fluorescent angiography were performed to evaluate the integrity of the BBB. Immunofluorescence and Western blotting were employed to detect the expression of target proteins. Cell migration was evaluated using a scratch migration assay. The results of immunofluorescence, Western blotting and cell migration were quantified using the software ImageJ (Version 1.53m). Parametric data from different groups were compared using one-way ANOVA followed by the least significant difference (LSD) test. RESULTS: Cerebral ischemia led to lower levels of structural components of the BBB such as tight junction proteins (occludin, claudin-1 and ZO-1) in the MCAO/R group compared with the sham group (P < 0.001). However, inhibition of the immunoproteasome LMP2 restored the expression of these proteins, resulting in higher levels of occludin, claudin-1 and ZO-1 in the LMP2-shRNA group compared with the control-shRNA group (P < 0.001). In addition, inhibition of the immunoproteasome LMP2 contributed to higher microvascular density and decreased BBB permeability [e.g., the quantity of extravasated EB: LMP2-shRNA group (58.54 ± 7.37) µg/g vs. control-shRNA group (103.74 ± 4.32) µg/g, P < 0.001], and promoted the upregulation of Wnt-3a and ß-catenin proteins in rats following MCAO/R. In vitro experiments, OGD/R induced marked upregulation of LMP2, proapoptotic protein Bax and cleaved caspase-3, and downregulation of occludin, claudin-1, ZO-1 and Bcl-2, as well as inhibition of the Wnt/ß-catenin pathway Wnt-3a and ß-catenin proteins in RBMVECs, compared with the control group under normal culture conditions (P < 0.001). However, silencing of LMP2 gene expression reversed these protein changes and promoted proliferation and migration of RBMVECs following OGD/R. Silencing of ß-catenin by transfection of RBMVECs with ß-catenin-siRNA aggravated the downregulation of tight junction proteins, and reduced the proliferation and migration of RBMVECs following OGD/R, compared with the control-siRNA group (P < 0.001). LMP2-siRNA and ß-catenin-siRNA co-transfection partly counteracted the beneficial effects of silencing LMP2-siRNA on the levels of tight junction proteins in RBMVECs exposed to OGD/R. CONCLUSION: This study suggests that inhibition of the immunoproteasome LMP2 ameliorates ischemia/hypoxia-induced BBB injury, and that the molecular mechanism involves the immunoproteasome-regulated activation of the Wnt/ß-catenin signalling pathway under ischemic conditions.

Amorphous Redox-Rich Polysulfides for Mg Cathodes.

The lack of appropriate cathodes is restraining the advances of Mg batteries. Crystalline cathode materials suffer from sluggish reaction kinetics and low-capacity delivery. The finite type of crystalline structure further confines the rational design of cathode materials. Herein, we proposed amorphization and anion enrichment as a brand-new strategy to not only enhance the solid-state ion diffusion and provide more ion-storage sites in amorphous structure but also contribute to the local transfer of multiple electrons through the additional anionic redox centers. Accordingly, a series of amorphous titanium polysulfides (a-TiS x , x = 2, 3, and 4) were designed, which significantly outperformed their crystalline counterparts and achieved a highly competitive energy density of ∼260 Wh/kg. The unique Mg2+ storage mechanism involves the dissociation/formation of S-S bonds and changes in the coordination number of Ti, namely, a mixture of conversion and intercalation reaction, accompanied by the joint cationic (Ti) and anionic (S) redox-rich chemistry. Our proposed amorphous and redox-rich design philosophy might provide an innovative direction for developing high-performance cathode materials for multivalent-ion batteries.

Amorphous anion-rich titanium polysulfides for aluminum-ion batteries.

The strong electrostatic interaction between Al3+ and close-packed crystalline structures, and the single-electron transfer ability of traditional cationic redox cathodes, pose challenged for the development of high-performance rechargeable aluminum batteries. Here, to break the confinement of fixed lattice spacing on the diffusion and storage of Al-ion, we developed a previously unexplored family of amorphous anion-rich titanium polysulfides (a-TiS x , x = 2, 3, and 4) (AATPs) with a high concentration of defects and a large number of anionic redox centers. The AATP cathodes, especially a-TiS4, achieved a high reversible capacity of 206 mAh/g with a long duration of 1000 cycles. Further, the spectroscopy and molecular dynamics simulations revealed that sulfur anions in the AATP cathodes act as the main redox centers to reach local electroneutrality. Simultaneously, titanium cations serve as the supporting frameworks, undergoing the evolution of coordination numbers in the local structure.

Iodine Vapor Transport-Triggered Preferential Growth of Chevrel Mo6S8 Nanosheets for Advanced Multivalent Batteries.

Owing to its unique structure, Chevrel phase (CP) is a promising candidate for applications in rechargeable multivalent (Mg and Al) batteries. However, its wide applications are severely limited by time-consuming and complex synthesis processes, accompanied by uncontrollable growth and large particle sizes, which will magnify the charge trapping effect and lower the electrochemical performance. Here, an iodine vapor transport reaction (IVT) is proposed to obtain large-scale and highly pure Mo6S8 nanosheets, in which iodine helps to regulate the growth kinetics and induce the preferential growth of Mo6S8, as a typical three-dimensional material, to form nanosheets. When applied in rechargeable multivalent (Mg and Al) batteries, Mo6S8 nanosheets show very fast kinetics owing to the short diffusion distance, thereby exhibiting lower polarization, higher capacities, and better low-temperature performance (up to -40 °C) compared to that of microparticles obtained via the conventional method. It is anticipated that Mo6S8 nanosheets would boost the application of Chevrel phase, especially in areas of energy storage and catalysis, and the IVT reaction would be generalized to a wide range of inorganic compound nanosheets.

Water-in-Salt Electrolyte Promotes High-Capacity FeFe(CN)6 Cathode for Aqueous Al-Ion Battery.

Prussian blue analogues (PBAs) are considered to be ideal multivalent cation host materials due to their unique open-framework structure. In aqueous solution, however, the PBAs' cathodes have a low reversible capacity limited by the single electrochemical group Fe(CN)63- and high crystal water content. They also suffer from fast cycle fading, resulting from significant oxygen/hydrogen evolution and cathode dissolution. In this work, a high-capacity PBA-type FeFe(CN)6 cathode with double transition metal redox sites is successfully demonstrated in 5 m Al(CF3SO3)3 Water-in-Salt electrolyte (Al-WISE). Due to Al-WISE having a wide electrochemical window (2.65 V) and low dissolution of the cathode, our PBA cathode exhibits a high discharge capacity of 116 mAh/g and the superior cycle stability >100 cycles with capacity fading of 0.39% per cycle.

Self-Assembly of Silicon@Oxidized Mesocarbon Microbeads Encapsulated in Carbon as Anode Material for Lithium-Ion Batteries.

The utilization of silicon/carbon composites as anode materials to replace the commercial graphite is hampered by their tendency to huge volumetric expansion, costly raw materials, and complex synthesis processes in lithium-ion batteries. Herein, self-assembly method is successfully applied to prepare hierarchical silicon nanoparticles@oxidized mesocarbon microbeads/carbon (Si@O-MCMB/C) composites for the first time, in which O-MCMB core and low-cost sucrose-derived carbon shell not only effectively enhance the electrical conductivity of the anode, but also mediate the dramatic volume change of silicon during cycles. At the same time, the carbon can act as "adhesive", which is crucial in enhancing the adhesive force between Si and O-MCMB in the composites. The as-obtained Si@O-MCMB/C delivers an initial reversible capacity of 560 mAh g-1 at 0.1 A g-1, an outstanding cyclic retention of 92.8% after 200 cycles, and respectable rate capability. Furthermore, the synthetic route presented here is efficient, less expensive, simple, and easy to scale up for high-performance composites.