An Ionic Liquid Electrolyte Additive for High-Performance Lithium-Sulfur Batteries.

With the development of mobile electronic devices, there are more and more requirements for high-energy storage equipment. Traditional lithium-ion batteries, like lithium-iron phosphate batteries, are limited by their theoretical specific capacities and might not meet the requirements for high energy density in the future. Lithium-sulfur batteries (LSBs) might be ideal next-generation energy storage devices because they have nearly 10 times the theoretical specific capacities of lithium-ion batteries. However, the severe capacity decay of LSBs limits their application, especially at high currents. In this study, an ionic liquid (IL) electrolyte additive, TDA+TFSI, was reported. When 5% of the TDA+TFSI additive was added to a traditional ether-based organic electrolyte, the cycling performance of the LSBs was significantly improved compared with that of the LSBs with the pure traditional organic electrolyte. At a rate of 0.5 C, the discharge specific capacity in the first cycle of the LSBs with the 5% TDA+TFSI electrolyte additive was 1167 mAh g-1; the residual specific capacities after 100 cycles and 300 cycles were 579 mAh g-1 and 523 mAh g-1, respectively; and the average capacity decay rate per cycle was only 0.18% in 300 cycles. Moreover, the electrolyte with the TDA+TFSI additive had more obvious advantages than the pure organic ether-based electrolyte at high charge and discharge currents of 1.0 C. The residual discharge specific capacities were 428 mAh g-1 after 100 cycles and 399 mAh g-1 after 250 cycles, which were 13% higher than those of the LSBs without the TDA+TFSI additive. At the same time, the Coulombic efficiencies of the LSBs using the TDA+TFSI electrolyte additive were more stable than those of the LSBs using the traditional organic ether-based electrolyte. The results showed that the LSBs with the TDA+TFSI electrolyte additive formed a denser and more uniform solid electrolyte interface (SEI) film during cycling, which improved the stability of the electrochemical reaction.

miR-146a Maintains Immune Tolerance of Kupffer Cells and Facilitates Hepatitis B Virus Persistence in Mice.

Kupffer cells (KCs), the largest tissue-resident macrophage population in the body, play a central role in maintaining a delicate balance between immune tolerance and immunity in the liver. However, the underlying molecular mechanism remains elusive. In this study, we show that KCs express high levels of miR-146a, which is under control of the PU.1 transcription factor. miR-146a deficiency promoted KCs differentiation toward a proinflammatory phenotype; conversely, miR-146a overexpression suppressed this phenotypic differentiation. We found that hepatitis B virus (HBV) persistence or HBV surface Ag treatment significantly upregulated miR-146a expression and thereby impaired polarization of KCs toward a proinflammatory phenotype. Furthermore, in an HBV carrier mouse model, KCs depletion by clodronate liposomes dramatically promoted HBV clearance and enhanced an HBV-specific hepatic CD8+ T cell and CD4+ T cell response. Consistent with this finding, miR-146a knockout mice cleared HBV faster and elicited a stronger adaptive antiviral immunity than wild-type mice. In vivo IL-12 blockade promoted HBV persistence and tempered the HBV-specific CTL response in the liver of miR-146a knockout mice. Taken together, our results identified miR-146a as a critical intrinsic regulator of an immunosuppressive phenotype in KCs under inflammatory stimuli, which may be beneficial in maintenance of liver homeostasis under physiological condition. Meanwhile, during HBV infection, miR-146a contributed to viral persistence by inhibiting KCs proinflammatory polarization, highlighting its potential as a therapeutic target in HBV infection.

A Non-Flammable Zwitterionic Ionic Liquid/Ethylene Carbonate Mixed Electrolyte for Lithium-Ion Battery with Enhanced Safety.

Today, the requirement for clean, highly efficient, and safe energy seems to be higher and higher due to non-renewable energy and pollution of the environment. At this moment, lithium-ion batteries (LIBs) look like a reliable solution for this dilemma since they have huge energy density. However, the flammability of the conventional electrolyte used in the LIBs is one of critical disadvantages of LIBs, which compromises the safety issue of LIBs. Herein, we reported a non-flammable zwitterionic ionic liquid-based electrolyte named TLPEC, which was fabricated by simply mixing a novel zwitterionic ionic liquid TLP (93 wt%) and ethylene carbonate (EC, 7 wt%). The TLPEC electrolyte exhibited a wide electrochemical potential window of 1.65-5.10 V and a robust ionic conductivity of 1.0 × 10-3 S cm-1 at 20 °C, which renders TLPEC to be a suitable electrolyte for LIBs with enhanced safety performance. The LIBs, with TLPEC as the electrolyte, exhibited an excellent performance in terms of excellent rate capability, cycling stability, and high specific capacity at 25 and 60 °C, which were attributed to the stability and high ionic conductivity of TLPEC electrolyte during cycling as well as the excellent interface compatibility of TLPEC electrolyte with lithium anode.

Extracellular gp96 is a crucial mediator for driving immune hyperactivation and liver damage.

Liver failure leads to the massive necrosis of hepatocytes, releasing large amounts of intracellular components including damage-associated molecular patterns (DAMPs). We found that extracellular gp96 levels in serum were elevated in patients with chronic hepatitis B infection (CHB) and acute-on-chronic liver failure (ACLF). Meanwhile, the gp96 level positively correlated with hepatic necroinflammation. We employed two mouse liver damage and liver failure models induced by lipopolysaccharide (LPS) plus D-galactosamine (D-Galn), and concanavalin A (ConA) to identify the function of extracellular gp96. As a result, the inhibition of extracellular gp96 by a specific peptide efficiently mitigated both LPS/D-Galn- and ConA-induced liver injury and immune hyperactivation, whereas exogenous gp96 aggravated the symptoms of hepatic injury in mice but not in Kupffer cells-ablated mice. The exposure of Kupffer cells to gp96 induced the secretion of pro-inflammatory cytokines. Collectively, our data demonstrate that gp96 released from necrotic hepatocytes aggravates immune hyperactivation and promotes liver damage and possibly the development of liver failure mainly by activating Kupffer cells.