Electrolyte design or functional development is very effective at promoting the performance of sodium-ion batteries, which are attractive for electrochemical energy storage devices due to abundant sodium resources and low cost. The roadmap of the sodium ion batteries based on electrolyte materials was drawn firstly and shows that the electrolyte type decides the electrochemical window and energy density.

In operando XRD and TXM‐XANES approaches demonstrate that structure evolution in NaNi1/3Fe1/3Mn1/3O2 during cycling follows a continuous change, and the formation of a nonequilibrium solid solution phase in the existence of two phases. An O3′ and P3′ monoclinic phase occur, and redox couples of Ni3+/Ni4+ and Fe3+/Fe4+ are mainly responsible in the charge voltage range from 4.0 to 4.3 V.

MYH9 has dual functions in tumors. However, its role in inducing tumor stemness in hepatocellular carcinoma (HCC) is not yet determined. Here, we found that MYH9 is an effective promoter of tumor stemness that facilitates hepatocellular carcinoma pathogenesis. Importantly, targeting MYH9 remarkably improved the survival of hepatocellular carcinoma-bearing mice and promoted sorafenib sensitivity of hepatocellular carcinoma cells in vivo. Mechanistic analysis suggested that MYH9 interacted with GSK3β and reduced its protein expression by ubiquitin-mediated degradation, which therefore dysregulated the β-catenin destruction complex and induced the downstream tumor stemness phenotype, epithelial-mesenchymal transition, and c-Jun signaling in HCC. C-Jun transcriptionally stimulated MYH9 expression and formed an MYH9/GSK3β/β-catenin/c-Jun feedback loop. X protein is a hepatitis B virus (HBV)-encoded key oncogenic protein that promotes HCC pathogenesis. Interestingly, we observed that HBV X protein (HBX) interacted with MYH9 and induced its expression by modulating GSK3β/β-catenin/c-Jun signaling. Targeting MYH9 blocked HBX-induced GSK3β ubiquitination to activate the β-catenin destruction complex and suppressed cancer stemness and EMT. Based on TCGA database analysis, MYH9 was found to be elevated and conferred poor prognosis for hepatocellular carcinoma patients. In clinical samples, high MYH9 expression levels predicted poor prognosis of hepatocellular carcinoma patients. These findings identify the suppression of MYH9 as an alternative approach for the effective eradication of CSC properties to inhibit cancer migration, invasion, growth, and sorafenib resistance in HCC patients. Our study demonstrated that MYH9 is a crucial therapeutic target in HCC.

Background/Aims: Increased production of multiple pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6, plays an essential pathogenic role in the progression of systemic lupus erythematosus (SLE). Recent studies have characterized itaconate as a novel and potent nuclear-factor-E2-related factor 2 (Nrf2) activator that activates Nrf2 signaling by alkylating cysteine residues on Keap1 (Kelch-like ECH-associated protein 1). Methods: THP-1 human macrophages and peripheral blood mononuclear cells (PBMCs) of SLE patients were treated with 4-octyl itaconate (OI). Nrf2 signaling activation was tested by qPCR assay and western blotting. mRNA expression and the production of multiple pro-inflammatory cytokines were tested by qPCR and enzyme-linked immunosorbent assays, respectively. Nuclear factor (NF)-κB activation was tested by the p65 DNA-binding assay. Results: We demonstrated that OI, the cell-permeable derivative of itaconate, induced Keap1-Nrf2 dissociation, Nrf2 protein accumulation, and nuclear translocation, which enabled the transcription and expression of multiple Nrf2-dependentantioxidant enzymes (heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1, and glutamate-cysteine ligase modifier subunit) in THP-1 human macrophages. OI also induced significant Nrf2 activation in SLE patient-derived PBMCs. OI pretreatment inhibited mRNA expression and the production of multiple pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in SLE patient-derived PBMCs and lipopolysaccharide (LPS)-activated THP-1 cells. OI potently inhibited NF-κB activation in SLE patient-derived PBMCs and LPS-activated THP-1 cells. Importantly, Nrf2 silencing (by targeted short hairpin RNA) or knockout (by CRISPR/Cas9 gene-editing method) almost abolished OI-induced anti-oxidant and anti-inflammatory actions in SLE patient-derived PBMCs and LPS-activated THP-1 cells. Conclusion: OI activates Nrf2 signaling to inhibit the production of pro-inflammatory cytokines in human macrophages and SLE patient-derived PBMCs. OI and itaconate could have important therapeutic value for the treatment of SLE.

O3-type NaNi Fe Mn O (NaNFM) is well investigated as a promising cathode material for sodium-ion batteries (SIBs), but the cycling stability of NaNFM still needs to be improved by using novel electrolytes or optimizing their structure with the substitution of different elements sites. To enlarge the alkali-layer distance inside the layer structure of NaNFM may benefit Na diffusion. Herein, the effect of Ca-substitution is reported in Na sites on the structural and electrochemical properties of Na Ca NFM (x = 0, 0.05, 0.1). X-ray diffraction (XRD) patterns of the prepared Na Ca NFM samples show single α-NaFeO type phase with slightly increased alkali-layer distance as Ca content increases. The cycling stabilities of Ca-substituted samples are remarkably improved. The Na Ca Ni Fe Mn O (Na Ca NFM) cathode delivers a capacity of 116.3 mAh g with capacity retention of 92% after 200 cycles at 1C rate. In operando XRD indicates a reversible structural evolution through an O3-P3-P3-O3 sequence of Na Ca NFM cathode during cycling. Compared to NaNMF, the Na Ca NFM cathode shows a wider voltage range in pure P3 phase state during the charge/discharge process and exhibits better structure recoverability after cycling. The superior cycling stability of Na Ca NFM makes it a promising material for practical applications in sodium-ion batteries.

P2-structured Na 0.67 Ni 0.33 Mn 0.67 O 2 (PNNMO) is a promising Na-ion battery cathode material, but its rapid capacity decay during cycling remains a hurdle. Li doping in layered transition-metal oxide (TMO) cathode materials is known to enhance their electrochemical properties. Nevertheless, the influence of Li at different locations in the structure has not been investigated. Here, the crystallographic role and electrochemical impact of lithium on different sites in PNNMO is investigated in Li x Na 0.67– y Ni 0.33 Mn 0.67 O 2+δ (0.00 ≤ x ≤ 0.2, y = 0, 0.1). Lithium occupancy on prismatic Na sites is promoted in Na-deficient (Na < 0.67) PNNMO, evidenced by ex situ and operando synchrotron X-ray diffraction, X-ray absorption spectroscopy, and 7 Li solid-state nuclear magnetic resonance. Partial substitution of Na with Li leads to enhanced stability and slightly increased specific capacity compared to PNNMO. In contrast, when lithium is located primarily on octahedral TM sites, capacity is increased but at the cost of stability.

Background: Post-translational modification is involved in regulating IRE1 signaling. Results: CHIP ubiquitinated IRE1 and regulated the IRE1/TRAF2/JNK pathway. Conclusion: Ubiquitination is a post-translational modification that is required for IRE1 signal transduction. Significance: This study may provide the first evidence that the IRE1/TRAF2/JNK pathway is regulated by ubiquitination.

Because of the low cost and high abundance of sodium, room-temperature sodium-ion batteries have recently been considered as an alternative power source to lithium-ion batteries. In contrast to the electrochemical performance of the batteries, safety has been paid much less attention, but safety is a critical consideration because sodium-ion batteries are intended for large-scale electrochemical energy storage applications. Herein, we have reported a NaNi 1/3 Fe 1/3 Mn 1/3 O 2 /hard carbon full cell with a good cycling performance and high Coulombic efficiency. The energy density of this pouch cell is close to 95 Wh/kg, and the capacity retention of the NFM full cell attained at 92.6% after 100 cycle numbers. Moreover, we have further used accelerating rate calorimetry, scanning electron microscopy, and operando synchrotron high-energy X-ray diffraction to investigate the thermal/chemical stability of charged Na x Ni 1/3 Fe 1/3 Mn 1/3 O 2 cathode material at both cell and component level. It is found that the thermal decomposition of desodiated Na x Ni 1/3 Fe 1/3 Mn 1/3 O 2 is a redox reaction that can be facilitated with the presence of either a reductive environment, such as electrolytes, or a strong oxidative environment that can result from a higher degree of desodiation. The findings presented in this work can guide future development of advanced sodium-ion batteries for practical application.