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Spinel LiMn2O4 (LMO) with a three-dimensional structure has become one of the cathode materials that has gained the most interest due to its safety, low price and abundant resources. However, the lithium ion transmission is limited by large particle size and particle agglomeration of LMO. Thus, reducing the particle size and agglomeration of LMO can effectively improve its lithium ion transmission. Here, we synthesized a LMO cathode material with a nanoscale crystal size using the flexible expanded graphite (EG) soft template and Pichini method. EG-controlled particle size and particle agglomeration of LMO is conducive to charge transfer and diffusion of lithium ions between LMO and the electrolyte, meanwhile, there are more redox sites on the nanosized LMO particles, which makes the redox reaction of LMO more thorough during the charge and discharge process, resulting in high capacitance performance. In order to obtain the considerably required lithium-ion capacitors (LICs) with high energy density and power density, we assembled aqueous LMO//activated carbon (AC) LICs with 5 M LiNO3 as the aqueous electrolytes, which are environmentally friendly, safe, low cost and have higher electrical conductivity than organic electrolytes. The optimal LIC has an energy density of 32.63 W h kg−1 at a power density of 500 W kg−1 and an energy density of 8.06 W h kg−1 at a power density of 10 000 W kg−1, which is higher than most of the LMO-based LICs in previous reports. After 2000 cycles, the specific capacitance retention rate was 75.9% at a current density of 3 A g−1. Therefore, our aqueous LMO//AC LICs synthesized by the soft template/Pichini method have wide prospects and are suitable for low-cost, high-safety and high-power applications.

It is reported that olivine-type lithium iron phosphate (LFP) for Li-ion batteries is one of the most widely utilized cathode materials, but its high-power applications are limited due to its intrinsically poor ion transfer rate and conductivity. Therefore, it is highly desired to fabricate LFP Li-ion capacitors (LICs) with high power performance and excellent cyclic reversibility, especially in safe, low cost and environmentally friendly aqueous electrolytes. Here, we fabricate LFP/expanded graphite (EG) nanocomposites by a one-step process, in which polyethylene glycol (PEG) is used as the particle growth inhibitor combined with vacuum infiltration of the LFP precursor into EG as a conductive sub-phase, and further investigate their high-power performance in aqueous LICs. Embedding spherical LFP nanoparticles with well-controlled size and agglomeration into the pores of EG and wrapping LFP nanoparticles by EG films contribute to the rapid electron and ion diffusion in LFP/EG composites, resulting in excellent cyclic reversibility and rate performance of LFP/EG composites. The aqueous LFP/EG//active carbon (AC) LICs were assembled in LiNO3 electrolytes with LFP/EG composites and AC as the positive and negative electrodes, respectively. The optimal LIC shows a power density of 2367.9 W kg−1 at an energy density of 6.5 W h kg−1, dramatically favorable rate characteristics and excellent cycle life with 82.1% capacitance retention of its primary capacitance at 2 A g−1 after 6000 cycles, markedly higher than those of the commercial LFP LIC. The presented aqueous LFP/EG//AC LICs with excellent electrochemical performance are expected to have broad high-power appliances that are cost-sensitive and highly secure.

Olivine-type LiFePO4 (LFP) is one of the most widely utilized cathode materials for high power Li-ion batteries (LIBs). In spite of rapidly growing popularity of LIBs, the rate performance of the highest power LFP cells is still insufficiently high for some high-power applications. In this work we demonstrate that vacuum-infiltration of LFP precursors into pores of low-cost expanded graphite (EG), an in-situ sol-gel process, followed by calcination, allows formation of LFP/EG nanocomposites that demonstrate remarkable performance in higher power Li-ion capacitor (LIC) applications. Such composites comprise spherical LFP particles embedded into EG pores and additionally wrapped by EG films, forming a highly efficient and stable conducting network. Such a morphology greatly accelerates Li-ion diffusion and improves Li-ion exchange between LFP and electrolyte. As a result, compared to commercial LFP particles of comparable size, the optimized LFP/EG nanocomposite shows significantly higher rate performance, dramatically better stability and higher specific capacitance of up to about 1200 F g−1. The use of environmentally friendly, safe and low-cost aqueous electrolyte is particularly advantageous for LIC applications that are cost-sensitive and require enhanced safety. Our results demonstrate a great promise of our approach, which is additionally applicable for a broad range of other intercalation chemistries.

It is highly desired to introduce active nitrogen atoms and abundant pore structures for enhanced electrochemical performances of carbon materials for supercapacitors. Hence a facile one-step carbonization/activation method was adopted to treat different mass ratios of polyvinylpyrrolidone/melamine formaldehyde resin (PVP/MF) and ammonium carbonate in order to obtain porous N-doped carbon (PNC). Symmetric supercapacitors with PNC as electrodes were assembled using KOH aqueous electrolyte. It is clearly demonstrated that due to the introduction of ammonium carbonate the resulting PNC displays increased specific surface areas, enriched pore structures and increased active nitrogen concentration. The ratio-optimized PNC with 7 wt% ammonium carbonate exhibits the highest proportion of negatively charged N-6 and N-5 with the pseudocapacitance and the highest micropore volume with the electrical double-layer capacitance, which also lead to the decrease of charge transfer resistance and the increase of transfer rate of electrolyte ions in the pores, and these are beneficial effects for the improvement of the overall capacitive performances. The ratio-optimized PNC displays an enhanced specific capacitance, which is about 32% higher than that of the PNC prepared without ammonium carbonate. And the symmetric supercapacitor assembled with the ratio-optimized PNC shows superior cycling performance and its capacitance retention is 94.43% after 1500 cycles at 20 mA cm−2.

Background & Aims Immune checkpoint inhibitors have some efficacy in the treatment of hepatocellular carcinoma (HCC). Programmed cell death 1 ligand 1 (PD-L1), expressed on some cancer cells, binds to the receptor programmed cell death 1 (PDCD1, also called PD1) on T cells to prevent their proliferation and reduce the antigen-tumor immune response. Immune cells that infiltrate some types of HCCs secrete interferon gamma (IFNG). Some HCC cells express myocyte enhancer factor 2D (MEF2D), which has been associated with shorter survival times of patients. We studied whether HCC cell expression of MEF2D regulates expression of PD-L1 in response to IFNG. Methods We analyzed immune cells from 20 fresh HCC tissues by flow cytometry. We analyzed 225 fixed HCC tissues (from 2 cohorts) from patients in China by immunohistochemistry and obtained survival data. We created mice with liver-specific knockout of MEF2D (MEF2DLPC-KO mice). We knocked out or knocked down MEF2D, E1A binding protein p300 (p300), or sirtuin 7 (SIRT7) in SMMC-7721, Huh7, H22, and Hepa1-6 HCC cell lines, some incubated with IFNG. We analyzed liver tissues from mice and cell lines by RNA sequencing, immunoblot, dual luciferase reporter, and chromatin precipitation assays. MEF2D protein acetylation and proteins that interact with MEF2D were identified by coimmunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls), were transplanted into BALB/c mice, and some mice were given antibodies to deplete T cells. Mice bearing orthotopic tumors grown from HCC cells, with or without knockout of SIRT7, were given injections of an antibody against PD1. Growth of tumors was measured, and tumors were analyzed by immunohistochemistry and flow cytometry. Results In human HCC specimens, we found an inverse correlation between level of MEF2D and numbers of CD4+ and CD8+ T cells; level of MEF2D correlated with percentages of PD1-positive or TIM3-positive CD8+ T cells. Knockout of MEF2D from H22 cells reduced their growth as allograft tumors in immune-competent mice but not in immune-deficient mice or mice with depletion of CD8+ T cells. When MEF2D-knockout cells were injected into immune-competent mice, they formed smaller tumors that had increased infiltration and activation of T cells compared with control HCC cells. In human and mouse HCC cells, MEF2D knockdown or knockout reduced expression of PD-L1. MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. Overexpression of p300 in HCC cells, or knockout of SIRT7, promoted acetylation of MEF2D and increased its binding, along with acetylated histones, to the promoter region of CD274. Exposure of HCC cells to IFNG induced expression of p300 and its binding MEF2D, which reduced the interaction between MEF2D and SIRT7. MEF2D-induced expression of PD-L1 upon IFNG exposure was independent of interferon-regulatory factors 1 or 9. In HCC cells not exposed to IFNG, SIRT7 formed a complex with MEF2D that attenuated expression of PD-L1. Knockout of SIRT7 reduced proliferation of HCC cells and growth of tumors in immune-deficient mice. Compared with allograft tumors grown from control HCC cells, in immune-competent mice, tumors grown from SIRT7-knockout HCC cells expressed higher levels of PD-L1 and had reduced infiltration and activation of T cells. In immune-competent mice given antibodies to PD1, allograft tumors grew more slowly from SIRT7-knockout HCC cells than from control HCC cells. Conclusions Expression of MEF2D by HCC cells increases their expression of PD-L1, which prevents CD8+ T-cell–mediated antitumor immunity. When HCC cells are exposed to IFNG, p300 acetylates MEF2D, causing it to bind the CD274 gene promoter and up-regulate PD-L1 expression. In addition to promoting HCC cell proliferation, SIRT7 reduced acetylation of MEF2D and expression of PD-L1 in HCC cells not exposed to IFNG. Strategies to manipulate this pathway might increase the efficacy of immune therapies for HCC.

Mesenchymal stem cells (MSCs) are widely used in cartilage tissue engineering to repair articular cartilage defects. However, hypertrophy of chondrocytes derived from MSCs might hinder the stabilization of hyaline cartilage. Thus, it is very important to find a suitable way to maintain the chondrogenic phenotype of chondrocytes. It has been reported that cordycepin has anti-inflammatory and anti-tumor functions. However, the role of cordycepin in chondrocyte hypertrophy remains unclear. Therefore, the objective of this study was to determine the effect of cordycepin on chondrogenesis and chondrocyte hypertrophy in MSCs and ATDC5 cells. Cordycepin upregulated chondrogenic markers including Sox9 and collagen type II while down-regulated hypertrophic markers including Runx2 and collagen type X. Further exploration showed that cordycepin promoted chondrogenesis through inhibiting Nrf2 while activating BMP signaling. Besides, cordycepin suppressed chondrocyte hypertrophy through PI3K/Bapx1 pathway and Notch signaling. Our results indicated cordycepin had the potential to maintain chondrocyte phenotype and reconstruct engineered cartilage. [BMB Reports 2016; 49(10): 548-553].

Bone homeostasis is maintained by the balance between osteoblastic bone formation and osteoclastic bone resorption. Osteoclasts are multinucleated cells derived from hematopoietic stem cells (HSCs) or monocyte/macrophage progenitor cells and formed by osteoclasts precursors (OCPs) fusion. Cyanidin is an anthocyanin widely distributed in food diet with novel antioxidant activity. However, the effect of cyanidin on osteoclasts is still unknown. We investigated the effect of cyanidin on RANKL-induced osteoclasts differentiation and cell fusion. The results showed that cyanidin had a dual effect on RANKL-induced osteoclastogenesis. Lower dosage of cyanidin ( 10 µg/ml) has an inhibitory effect. Fusogenic genes like CD9, ATP6v0d2, DC-STAMP, OC-STAMP, and osteoclasts related genes like NFATc1, mitf, and c-fos were all regulated by cyanidin consistent to its dual effect. Further exploration showed that low concentration of cyanidin could increase osteoclasts fusion whereas higher dosage of cyanidin lead to the increase of LXR-β expression and activation which is suppressive to osteoclasts differentiaton. All these results showed that cyanidin exhibits therapeutic potential in prevention of osteoclasts related bone disorders.