Search

The polysulfide (PS) dissolution and low conductivity of lithium sulfides (Li2S) are generally considered the main reasons for limiting the reversible capacity of the lithium‐sulfur (Li‐S) system. However, as the inevitable intermediate between PSs and Li2S, lithium disulfide (Li2S2) evolutions are always overlooked. Herein, Li2S2 evolutions are monitored from the operando measurements on the pouch cell level. Results indicate that Li2S2 undergoes slow electrochemical reduction and chemical disproportionation simultaneously during the discharging process, leading to further PS dissolution and Li2S generation without capacity contribution. Compared with the fully oxidized Li2S, Li2S2 still residues at the end of the charging state. Therefore, instead of the considered Li2S and PSs, slow electrochemical conversions and side chemical reactions of Li2S2 are the determining factors in limiting the sulfur utilization, corresponding to the poor reversible capacity of Li‐S batteries. [ABSTRACT FROM AUTHOR]

A high‐performance all‐inorganic magnesium–lithium chloride complex (MLCC) electrolyte is synthesized by a simple room‐temperature reaction of LiCl with MgCl2 in tetrahydrofuran (THF) solvent. Molecular dynamics simulation, density functional theory calculation, Raman spectroscopy, and nuclear magnetic resonance spectroscopy reveal that the formation of [MgxLiyCl2x+y·nTHF] complex solvation structure significantly lowers the coordination number of THF in the first solvation sheath of Mg2+, which significantly enhances its de‐solvation kinetics. The MLCC electrolyte presents a stable electrochemical window up to 3.1 V (vs Mg/Mg2+) and enables reversible cycling of Mg metal deposition/stripping with an outstanding Coulombic efficiency up to 99% at current densities as high as 10 mA cm−2. Utilizing the MLCC electrolyte, a Mg/Mo6S8 full cell can be cycled for over 10 000 cycles with a superior capacity retention of 85 mA h g−1 under an ultrahigh rate of 50 C (1 C = 128.8 mA g−1). The facile synthesis of high‐performance MLCC electrolyte provides a promising solution for future practical magnesium batteries. [ABSTRACT FROM AUTHOR]

Aging‐related sarcopenia is currently the most common sarcopenia. The main manifestations are skeletal muscle atrophy, replacement of muscle fibers with fat and fibrous tissue. Excessive fibrosis can impair muscle regeneration and function. Lysyl oxidase‐like 2 (LOXL2) has previously been reported to be involved in the development of various tissue fibrosis. Here, we investigated the effects of LOXL2 inhibitor on D‐galactose (D‐gal)‐induced skeletal muscle fibroblast cells and mice. Our molecular and physiological studies show that treatment with LOXL2 inhibitor can alleviate senescence, fibrosis, and increased production of reactive oxygen species in fibroblasts caused by D‐gal. These effects are related to the inhibition of the TGF‐β1/p38 MAPK pathway. Furthermore, in vivo, mice treatment with LOXL2 inhibitor reduced D‐gal‐induced skeletal muscle fibrosis, partially enhanced skeletal muscle mass and strength and reduced redox balance disorder. Taken together, these data indicate the possibility of using LOXL2 inhibitors to prevent aging‐related sarcopenia, especially with significant fibrosis. [ABSTRACT FROM AUTHOR]

Although employing solid polymer electrolyte (SPE) in all‐solid‐state lithium/sulfur (ASSLS) batteries is a promising approach to obtain a power source with both high energy density and safety, the actual performance of SPE‐ASSLS batteries still lag behind conventional lithium/sulfur batteries with liquid ether electrolyte. In this work, combining characterization methods of X‐ray photoelectron spectroscopy, in situ optical microscopy, and three‐electrode measurement, a direct comparison between these two battery systems is made to reveal the mechanism behind their performance differences. In addition to polysulfides, it is found that the initial elemental sulfur can also dissolve into and diffuse through the SPE to reach the anode. Different from the shuttle effect that causes uniform corrosion on the anode in a liquid electrolyte, dissolved sulfur species in SPE unevenly passivate the anode surface and lead to the inhomogeneous Li+ plating/stripping at the anode/SPE solid‐solid interface. Such inhomogeneity eventually causes void formation at the interface, which leads to the failure of SPE‐ASSLS batteries. Based on this understanding, a protection interlayer is designed to inhibit the shuttling of sulfur species, and the modified SPE‐ASSLS batteries show much‐improved performance in cycle life. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a metabolic disorder that can lead to cognitive dysfunction. The hippocampus plays an important role in the cognitive function. Research has identified correlations between hippocampal impairment and diabetes, yet their intermediate remains unclear. Soluble epoxide hydrolase (sEH) is an enzyme that degrades epoxyeicosatrienoic acids (EETs), which have multiple protective effects by suppressing inflammation, apoptosis and oxidative stress. In this study, under diabetic conditions both hippocampal injury and cognitive decline are accompanied by upregulation of sEH. Moreover, the sEH inhibitor trans‐4‐[4‐(3‐adamantan‐1‐y1‐ureido)‐cyclohexyloxy]‐benzoic acid (t‐AUCB) prevents cognitive dysfunction and decreased ROS accumulation and apoptosis in the diabetic hippocampus. t‐AUCB treatment restored neuronal synaptic plasticity by restoring the expression of the postsynaptic proteins Postsynaptic density protein‐95 (PSD95) and N‐methyl‐d‐aspartate receptor subunit 2B (NR2B), the levels of which were positively correlated with Proline‐rich tyrosine kinase 2 (Pyk2) levels under diabetic conditions. Thus, we suggest that hippocampal protection via sEH inhibition might be a potential therapeutic approach to attenuate the progression of cognitive decline in diabetes. [ABSTRACT FROM AUTHOR]

Non‐nucleophilic electrolytes that can reversibly plate/strip Mg are essential for realizing high‐performance rechargeable Mg/S batteries. In contrast to organometallic electrolytes, all‐inorganic electrolytes based on MgCl2‐AlCl3 complexes are more cost‐effective and hold better stability to air and moisture. A recently developed electrolyte that contains tetrahydrofuran solvated divalent Mg cation, [Mg·6THF][AlCl4]2, has exhibited decent compatibility with the sulfur cathode. However, it suffers a large overpotential and short cycle life, which hinders its applications in Mg/S batteries. Here, an efficient plating/stripping of Mg is realized successfully by using LiCl to dissolve MgCl2 from the electrolyte/electrode interface. As a result, the overpotential of Mg plating/stripping is remarkably reduced to 140/140 mV at a current density of 500 µA cm−2. Both experiments and density functional theory (DFT) calculations reveal that the LiCl‐assisted solubilization of MgCl2 facilitates the exposure of fresh surface on the Mg anode. Utilizing such an LiCl‐activation strategy, Mg/S full batteries with a significantly extended cycle life of over 500 cycles, as well as coulombic efficiency close to 100%, are achieved successfully. This work demonstrates the role of LiCl‐assisted interface activation on extending the cycle‐life Mg/S batteries with all‐inorganic electrolytes. [ABSTRACT FROM AUTHOR]

Diabetes is considered as a risk for cognitive decline, which is characterized by neurodegenerative alteration and innate immunity activation. Recently, complement 3 (C3), the critical central component of complement system, has been reported to play a key role in neurodegenerative alterations under pathological condition. Receptor for advanced glycation end products (RAGE) activation is confirmed to mediate several inflammatory cytokines production. However, whether C3 activation participates in the diabetic neuropathology and whether this process is regulated by RAGE activation remains unknown. The present study aimed to investigate the role of C3 in streptozotocin‐induced diabetic mice and high glucose‐induced primary astrocytes and the underlying modulatory mechanisms. The decreased synaptophysin density and increased C3 deposition at synapses were observed in the diabetic brain compared to the control brain. Furthermore, the elevated C3 was co‐localized with GFAP‐positive astrocytes in the diabetic brain slice in vivo and high glucose‐induced astrocytes culture in vitro. Diabetes/high glucose‐induced up‐regulation of C3 expression at gene, protein and secretion levels, which were attenuated by pre‐treatment with RAGE, p38MAPK and NF‐κB inhibitors separately. These results demonstrate that high glucose induces C3 up‐regulation via RAGE‐ p38MAPK‐NF‐κB signalling in vivo and in vitro, which might be associated with synaptic protein loss. [ABSTRACT FROM AUTHOR]

Abstract: Acute heart failure due to myocarditis is not common in Takayasu arteritis, let alone in combination with thrombosis affecting both ventricles and pulmonary arteries. The concomitant infection of non‐tuberculosis mycobacterium further complicates the clinical scenario and poses challenges for implementation of tailored treatments. This case report describes a teenage girl with a history of intermittent claudication and Erythema Nodosum who developed acute heart failure. Detailed clinical investigations and imaging techniques confirmed the diagnosis. [ABSTRACT FROM AUTHOR]

Type 1 diabetes results from destruction of pancreatic beta cells by autoreactive T cells. Both CD4+ and CD8+ T cells have been shown to mediate beta-cell killing. While CD8+ T cells can directly recognize MHC class I on beta cells, the interaction between CD4+ T cells and beta cells remains unclear. Genetic association studies have strongly implicated HLA-DQ alleles in human type 1 diabetes. Here we studied MHC class II expression on beta cells in nonobese diabetic mice that were induced to develop diabetes by diabetogenic CD4+ T cells with T-cell receptors that recognize beta-cell antigens. Acute infiltration of CD4+ T cells in islets occurred with rapid onset of diabetes. Beta cells from islets with immune infiltration expressed MHC class II mRNA and protein. Exposure of beta cells to IFN-γ increased MHC class II gene expression, and blocking IFN-γ signaling in beta cells inhibited MHC class II upregulation. IFN-γ also increased HLA-DR expression in human islets. MHC class II+ beta cells stimulated the proliferation of beta-cell-specific CD4+ T cells. Our study indicates that MHC class II molecules may play an important role in beta-cell interaction with CD4+ T cells in the development of type 1 diabetes. [ABSTRACT FROM AUTHOR]

CD8+ T cells kill pancreatic β-cells in a cell-cell contact-dependent mechanism in the non-obese diabetic mouse. CD4+ T lymphocytes are also able to kill pancreatic β-cells, but they do not directly contact β-cells and may use another cell type as the actual cytotoxic cell. Natural killer (NK) cells could have this role but it is uncertain whether they are cytotoxic towards β-cells. Therefore, the requirement for NK cells in β-cell destruction in the CD4-dependent T-cell antigen receptor transgenic NOD4.1 mice was examined. NK cells failed to kill β-cells in vitro, even in the absence of major histocompatibility complex class I. We observed only 9.7±1.1% of islet infiltrating NK cells from NOD4.1 mice expressing the degranulation marker CD107a. Diabetogenic CD4+ T cells transferred disease to NODscid.IL2Rγ−/− mice lacking NK cells, indicating that NK cells do not contribute to β-cell death in vitro or in vivo. However, depletion of NK cells reduced diabetes incidence in NOD4.1 mice, suggesting that NK cells may help to maintain the right environment for cytotoxicity of effector cells. [ABSTRACT FROM AUTHOR]

Rechargeable magnesium/sulfur (Mg/S) batteries are widely regarded as one of the alternatives to lithium‐ion batteries. However, a key factor restricting their application is the lack of suitable electrolyte. Herein, an electrolyte additive that can reduce the polarization voltage is developed and 98.7% coulombic efficiency is realized. The as‐prepared Mg‐ion electrolyte exhibits excellent Mg plating/stripping performance with a low overpotential of 0.11 V for plating process, and high anodic stability up to 3.0 V (vs Mg/Mg2+). When it is coupled with magnesium polysulfide, which has high reactivity and is homogeneously distributed on carbon matrix, the Mg/S cells deliver a good cycling stability with a high discharge capacity over 1000 mAh g−1 for more than 50 cycles. A Y‐based Mg‐ion electrolyte that can greatly improve the performance of the Mg/S cells is reported. The new Y‐based electrolyte exhibits unprecedented properties in comparison with conventional Al‐based electrolytes. When it is coupled with the magnesium polysulfide cathode, a Mg/S cell with an ultrahigh capacity of 1000 mA h g−1 with an excellent cycling performance over 50 cycles is achieved. [ABSTRACT FROM AUTHOR]