Tailoring vanadium oxide crystal orientation for high-performance aqueous zinc-ion batteries.

Due to the increasing demand for higher security and low-cost energy storage systems, the main research focus has been developing a suitable substitute for lithium-ion batteries. Aqueous zinc ion batteries (AZIBs) are considered the best alternative to lithium-ion batteries in large-scale energy storage devices. Owing to its high capacity, vanadate is a promising cathode material for AZIBs. The crystallographic orientation of cathode materials dramatically influences the rate performance and cycling life. Here, Mg0.57V5O12·2.3H2O (MgVO) with favorable (001) crystal orientation and significantly improved electrochemical performance is prepared by a simple stirring method. The crystal growth orientations of MgVO are altered by adjusting the aging time of the reactant solution. The (001)-orientated grain growth of MgVO delivers a 232.5 mA h g-1 capacity at 5 A g-1 with a 94% capacity retention rate after 1400 cycles. The zinc ion storage performance of MgVO demonstrates that the orientation-controlled method can design effective cathode materials for high-performance ZIBs.

Low-current-density stability of vanadium-based cathodes for aqueous zinc-ion batteries.

Vanadium-based cathodes have received widespread attention in the field of aqueous zinc-ion batteries, presenting a promising prospect for stationary energy storage applications. However, the rapid capacity decay at low current densities has hampered their development. In particular, capacity stability at low current densities is a requisite in numerous practical applications, typically encompassing peak load regulation of the electricity grid, household energy storage systems, and uninterrupted power supplies. Despite possessing notably high specific capacities, vanadium-based materials exhibit severe instability at low current densities. Moreover, the issue of stabilizing electrode reactions at these densities for vanadium-based materials has been explored insufficiently in existing research. This review aims to investigate the matter of stability in vanadium-based materials at low current densities by concentrating on the mechanisms of capacity fading and optimization strategies. It proposes a comprehensive approach that includes electrolyte optimization, electrode modulation, and electrochemical operational conditions. Finally, we presented several crucial prospects for advancing the practical development of vanadium-based aqueous zinc-ion batteries.

Reconstructing interfacial manganese deposition for durable aqueous zinc-manganese batteries.

Low-cost, high-safety, and broad-prospect aqueous zinc-manganese batteries (ZMBs) are limited by complex interfacial reactions. The solid-liquid interfacial state of the cathode dominates the Mn dissolution/deposition process of aqueous ZMBs, especially the important influence on the mass and charge transfer behavior of Zn2+ and Mn2+. We proposed a quasi-eutectic electrolyte (QEE) that would stabilize the reversible behavior of interfacial deposition and favorable interfacial reaction kinetic of manganese-based cathodes in a long cycle process by optimizing mass and charge transfer. We emphasize that the initial interfacial reaction energy barrier is not the main factor affecting cycling performance, and the good reaction kinetics induced by interfacial deposition during the cycling process is more conducive to the stable cycling of the battery, which has been confirmed by theoretical analysis, quartz crystal microbalance with dissipation monitoring, depth etching X-ray photon-electron spectroscopy, etc. As a result, the QEE electrolyte maintained a stable specific capacity of 250 mAh g-1 at 0.5 A g-1 after 350 cycles in zinc-manganese batteries. The energy density retention rate of the ZMB with QEE increased by 174% compared to that of conventional aqueous electrolyte. Furthermore, the multi-stacked soft-pack battery with a cathodic mass load of 54.4 mg maintained a stable specific capacity of 200 mAh g-1 for 100 cycles, demonstrating its commercial potential. This work proves the feasibility of adapting lean-water QEE to the stable aqueous ZMBs.

In/Ce Co-doped Li3VO4 and Nitrogen-modified Carbon Nanofiber Composites as Advanced Anode Materials for Lithium-ion Batteries.

Li3VO4 (LVO) is considered as a novel alternative anode material for lithium-ion batteries (LIBs) due to its high capacity and good safety. However, the inferior electronic conductivity impedes its further application. Here, nanofibers (nLICVO/NC) with In/Ce co-doped Li3VO4 strengthened by nitrogen-modified carbon are prepared. Density functional theory calculations demonstrate that In/Ce co-doping can substantially reduce the LVO band gap and achieve orders of magnitude increase (from 2.79 × 10-4 to 1.38 × 10-2 S cm-1) in the electronic conductivity of LVO. Moreover, the carbon-based nanofibers incorporated with 5LICVO nanoparticles can not only buffer the structural strain but also form a good framework for electron transport. This 5LICVO/NC material delivers high reversible capacities of 386.3 and 277.9 mA h g-1 at 0.1 and 5 A g-1, respectively. Furthermore, high discharge capacities of 335 and 259.5 mA h g-1 can be retained after 1200 and 4000 cycles at 0.5 and 1.6 A g-1, respectively (with the corresponding capacity retention of 98.4 and 78.7%, respectively). When the 5LICVO/NC anode assembles with commercial LiNi1/3Co1/3Mn1/3O2 (NCM111) into a full cell, a high discharge capacity of 191.9 mA h g-1 can be retained after 600 cycles at 1 A g-1, implying an inspiring potential for practical application in high-efficiency LIBs.

A Comparison of Amplitude-and Time-Dependent Cyclic Deformation Behavior for Fully-Austenite Stainless Steel 316L and Duplex Stainless Steel 2205.

Austenite and duplex stainless steels are widely used in engineering, and the latter exhibits a more excellent combination of mechanical properties and corrosion resistance due to the coexistence of austenite and ferrite and higher nitrogen. However, fatigue failure still threatens their structural integrity. A comprehensive comparison of their cyclic deformation behavior is a major foundation to understand the role of duplex-phase microstructure and nitrogen in the safety assessment of engineering components. Thus, in this paper, the cyclic deformation behavior of fully-austenitic stainless steel 316L and duplex stainless steel 2205 was studied by a series of low cycle fatigue tests with various strain amplitudes, loading rates and tensile holding. A theoretical mechanism diagram of the interaction between nitrogen and dislocation movements during cyclic loads was proposed. Results show that the cyclic stress response of 2205 was the primary cyclic hardening, followed by a long-term cyclic softening regardless of strain amplitudes and rates, while an additional secondary hardening was observed for 316L at greater strain amplitudes. Cyclic softening of 2205 was restrained under slower strain rates or tensile holding due to the interaction between nitrogen and dislocations. The cyclic plasticity of 2205 started within the austenite, and gradually translated into the ferrite with the elevation of the cyclic amplitude, which lead to a decreased hardening ratio with the increase in amplitude and a shorter fatigue life for a given smaller plastic strain amplitude.

Experimental and Analytical Analysis of Mechanical Properties for Large-Size Lattice Truss Panel Structure Including Role of Connected Structure.

The large-size lattice truss panel structure (LTPS) is continually increasing for higher upsizing, but the roles of its connected structures on the mechanical properties are always ignored during the previous structural integrity assessment. Thus, in this paper, a series of mechanical tests, including the fabricating of panel-to-panel LTPSs, monotonous tensile, and three- and four-point bending tests, were performed to comprehensively understand the mechanical behavior. Furthermore, a theoretical model including the role of connected structures was developed to predict both the elastic and plastic deformation behavior of panel-to-panel LTPS. Results show that the connected structure has a very significant effect on the mechanical properties of panel-to-panel LTPS during the three-bending tests, and I-beam element depresses its carrying capacity. The developed theoretical model was proved to accurately predict the experimental results, and the maximum error was limited within 20%. Finally, the dimensional effects of the connection components on mechanical properties were also analyzed by the theoretical model, and indicated that the panel-to-panel LTPS will present better mechanical performance than the intact structure when the width of I-beam element exceeds 12.2 mm or the its length downgrades to 39.1 mm, which provide a comprehensive guidance for the engineering design of large-size LTPS.

In Situ Defect Induction in Close-Packed Lattice Plane for the Efficient Zinc Ion Storage.

In situ electrochemical activation brings unexpected electrochemical performance improvements to electrode materials, but the mechanism behind it still needs further study. Herein, an electrochemically in situ defect induction in close-packed lattice plane of vanadium nitride oxide (VNx Oy ) in aqueous zinc-ion battery is reported. It is verified by theoretical calculation and experiment that the original compact structure is not suitable for the insert of Zn2+ ion, while a highly active one after the initial electrochemical activization accompanied by the in situ defect induction in close-packed lattice plane of VNx Oy exhibits efficient zinc ion storage. As expected, activated VNx Oy can achieve very high reversible capacity of 231.4 mA h g-1 at 1 A g-1 and cycle stability upto 6000 cycles at 10 A g-1 with a capacity retention of 94.3%. This work proposes a new insight for understanding the electrochemically in situ transformation to obtain highly active cathode materials for the aqueous zinc-ion batteries.

Increasing Accessible Subsurface to Improving Rate Capability and Cycling Stability of Sodium-Ion Batteries.

Numerous studies have reported that the enhancement of rate capability of carbonaceous anode by heteroatom doping is due to the increased diffusion-controlled capacity induced by expanding interlayer spacing. However, percentage of diffusion-controlled capacity is less than 30% as scan rate is larger than 1 mV s-1 , suggesting there is inaccuracy in recognizing principle of improving rate capability of carbonaceous anode. In this paper, it is found that the heteroatom doping has little impact on interlayer spacing of carbon in bulk phase, meaning that diffusion-controlled capacity is hard to be enhanced by doping. After synergizing with tensile stress, however, the interlayer spacing in subsurface region is obviously expanded to 0.40 nm, which will increase the thickness of accessible subsurface region at high current density. So SRNDC-700 electrodes display a high specific capacity of 160.6 and 69.5 mAh g-1 at 20 and 50 A g-1 , respectively. Additionally, the high reversibility of carbon structure insures ultralong cycling stability and hence attenuation of SRNDC-700 is only 0.0025% per cycle even at 10 A g-1 for 6000 cycles. This report sheds new insight into mechanism of improving electrochemical performance of carbonaceous anode by doping and provides a novel design concept for doping carbon.

Bimetallic organic framework derivation of three-dimensional and heterogeneous metal selenides/carbon composites as advanced anodes for lithium-ion batteries.

Heterogeneous structures have been attracting increasing attention in energy storage and conversion applications due to the phase interface and synergistic effect of multiple components. Herein, bimetal organic framework analogues were introduced to construct a Zn/Co bimetallic selenide heterostructure within a 3D-porous N-doped carbon matrix by a NaCl template-assisted lyophilization and annealing process. The cross-linked 3D network can enhance the transport kinetics for both lithium ions and electrons. The stress resulting from the cycling process can be released by interconnected channels in the composite. ZnSe and CoSe2 experience electrochemical reactions at different potentials, which can buffer volume changes mutually to effectively increase structural stability. Meanwhile, abundant active sites due to the heterostructure enhance pseudocapacitive performance and reaction kinetics, resulting in high specific capacity and good rate performance. As anode materials for lithium-ion batteries, the three-dimensional ZnSe/CoSe2-C composite exhibits a high reversible capacity of 700 mA h g-1 after 500 cycles at 1 A g-1.

Retracted Article: Long noncoding RNA ANRIL knockdown increases sensitivity of non-small cell lung cancer to cisplatin by regulating the miR-656-3p/SOX4 axis.

Long noncoding RNAs (lncRNAs) are implicated in the development of chemoresistance in many cancers. However, the effect and mechanism of lncRNA antisense noncoding RNA in the INK4 locus (ANRIL) on cisplatin (CDDP) resistance in non-small cell lung cancer (NSCLC) remain unclear. The levels of ANRIL, microRNA (miR)-656-3p and sex-determining region Y-related high-mobility group box 4 (SOX4) in NSCLC tissues and cells were detected by quantitative real-time polymerase chain reaction or western blotting. Cell viability, apoptosis, migration and epithelial-to-mesenchymal transition (EMT) were assessed by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT assay), flow cytometry, trans-well assays and western blotting, respectively. The xenograft model was established using CDDP-resistant NSCLC cells. The target association between miR-656-3p and ANRIL or SOX4 was validated by luciferase reporter assay and RNA immunoprecipitation. ANRIL expression was increased in CDDP-resistant NSCLC tissues and cells. Knockdown of ANRIL decreased cell viability, migration and EMT but induced apoptosis in CDDP-resistant NSCLC cells. Moreover, silencing of ANRIL reduced xenograft tumor growth in vivo. miR-656-3p was targeted by ANRIL and its exhaustion attenuated the suppressive role of ANRIL knockdown in CDDP resistance in NSCLC cells. SOX4 acted as a target of miR-656-3p and was positively regulated by ANRIL. Collectively, interference of ANRIL repressed CDDP resistance through promoting apoptosis and inhibiting cell viability, migration and EMT by up-regulating miR-656-3p and down-regulating SOX4, indicating a new target to improve the chemotherapeutic efficacy in NSCLC.

APOL1-G1 in Nephrocytes Induces Hypertrophy and Accelerates Cell Death.

People of African ancestry carrying certain APOL1 mutant alleles are at elevated risk of developing renal diseases. However, the mechanisms underlying APOL1-associated renal diseases are unknown. Because the APOL1 gene is unique to humans and some primates, new animal models are needed to understand the function of APOL1 in vivo We generated transgenic Drosophila fly lines expressing the human APOL1 wild type allele (G0) or the predominant APOL1 risk allele (G1) in different tissues. Ubiquitous expression of APOL1 G0 or G1 in Drosophila induced lethal phenotypes, and G1 was more toxic than was G0. Selective expression of the APOL1 G0 or G1 transgene in nephrocytes, fly cells homologous to mammalian podocytes, induced increased endocytic activity and accumulation of hemolymph proteins, dextran particles, and silver nitrate. As transgenic flies with either allele aged, nephrocyte function declined, cell size increased, and nephrocytes died prematurely. Compared with G0-expressing cells, however, G1-expressing cells showed more dramatic phenotypes, resembling those observed in cultured mammalian podocytes overexpressing APOL1-G1. Expressing the G0 or G1 APOL1 transgene in nephrocytes also impaired the acidification of organelles. We conclude that expression of an APOL1 transgene initially enhances nephrocyte function, causing hypertrophy and subsequent cell death. This new Drosophila model uncovers a novel mechanism by which upregulated expression of APOL1-G1 could precipitate renal disease in humans. Furthermore, this model may facilitate the identification of APOL1-interacting molecules that could serve as new drug targets to treat APOL1-associated renal diseases.

[Effects of Different Shading Treatment and Planting Patterns on Several Main Characters and Yield of Elephantopus scaber].

OBJECTIVE: To study the growth and yield of Elephantopus scaber under different light conditions. METHODS: Several main characters and yield performances were studied under six shading treatment as well as two planting patterns. RESULTS: The plant height, leaf number, root length and root-shoot ratio were increased under moderate shading. With the increase of shading ratio, the process of Elephantopus scaber vegetative growth to reproductive growth were shortened, seed yield, dry biomass and root yield decreased as well. Among different shading treatments, dry seed-yield showed 8. 46 ~31. 10 kg/667 m2 dry biomass showed 327. 28 ~ 800. 95 kg/ 667 m2 and dry root yield showed 30. 65 ~ 70. 72 kg/667 m2. CONCLUSION: Elephantopus scaber is a light-demanding but shade-tolerant plant. The patterns of hole seeding were suggested in planting, and not more than 60% shade density may be good under plantations.

The basic domain of HIV-tat transactivating protein is essential for its targeting to lipid rafts and regulating fibroblast growth factor-2 signaling in podocytes isolated from children with HIV-1-associated nephropathy.

Podocyte injury has a critical role in the pathogenesis of HIV-associated nephropathy (HIVAN). The HIV-1 transactivator of transcription (Tat), combined with fibroblast growth factor-2 (FGF-2), can induce the dedifferentiation and proliferation of cultured human podocytes. Cellular internalization of Tat requires interactions with heparan sulfate proteoglycans and cholesterol-enriched lipid rafts (LRs). However, the specific distribution of Tat in human podocytes and its ability to associate with LRs have not been documented. Here, we found that Tat is preferentially recruited to LRs in podocytes isolated from children with HIVAN. Furthermore, we identified arginines in the basic domain (RKKRRQRRR) of Tat as essential for (1) targeting Tat to LRs, (2) Tat-mediated increases in the expression of Rho-A and matrix metalloproteinase-9 in LRs, and (3) Tat-mediated enhancement of FGF-2 signaling in human podocytes and HIV-transgenic mouse kidneys and the exacerbation of renal lesions in these mice. Tat carrying alanine substitutions in the basic domain (AKKAAQAAA) remained localized in the cytosol and did not associate with LRs or enhance FGF-2 signaling in cultured podocytes. These results show the specific association of Tat with LRs in podocytes isolated from children with HIVAN, confirm Tat as a regulator of FGF-2 signaling in LRs, and identify the key domain of Tat responsible for promoting these effects and aggravating renal injury in HIV-transgenic mice. Moreover, these results provide a molecular framework for developing novel therapies to improve the clinical outcome of children with HIVAN.

Self MHC class I-licensed NK cells enhance adaptive CD8 T-cell viral immunity.

MHC class I (MHC I) is essential to NK- and T-cell effector and surveillance functions. However, it is unknown whether MHC I polymorphism influences adaptive immunity through NK cells. Previously, we found that MHC I D(k), a cognate ligand for the Ly49G2 inhibitory receptor, was essential to NK control of murine (M)CMV infection. Here we assessed the significance of NK inhibitory receptor recognition of MCMV on CD8 T cells in genetically defined MHC I D(k) disparate mice. We observed that D(k)-licensed Ly49G2⁺ NK cells stabilized and then enhanced conventional dendritic cells (cDCs) recovery after infection. Furthermore, licensed NK support of cDC recovery was essential to enhance the tempo, magnitude, and effector activity of virus-specific CD8 T cells. Minimal cDC and CD8 T-cell number differences after low-dose MCMV in D(k) disparate animals further implied that licensed NK recognition of MCMV imparted qualitative cDC changes to enhance CD8 T-cell priming.

MHC class I D(k) expression in hematopoietic and nonhematopoietic cells confers natural killer cell resistance to murine cytomegalovirus.

NK cell-mediated murine cytomegalovirus (MCMV) resistance (Cmv(r)) is under H-2(k) control in MA/My mice, but the underlying gene(s) is unclear. Prior genetic analysis mapped Cmv(r) to the MHC class I (MHC-I) D(k) gene interval. Because NK cell receptors are licensed by and responsive to MHC class I molecules, D(k) itself is a candidate gene. A 10-kb genomic D(k) fragment was subcloned and microinjected into MCMV-susceptible (Cmv(s)) (MA/My.L-H2(b) x C57L)F(1) or (B6 x DBA/2)F(2) embryos. Transgenic founders, which are competent for D(k) expression and germline transgene transmission, were identified and further backcrossed to MA/My.L-H2(b) or C57L mice. Remarkably, D(k) expression delivered NK-mediated resistance in either genetic background. Further, NK cells with cognate inhibitory Ly49G receptors for self-MHC-I D(k) were licensed and critical in protection against MCMV infection. In radiation bone marrow chimeras, NK resistance was significantly diminished when MHC-I D(k) expression was restricted to only hematopoietic or nonhematopoietic cells. Thus, MHC-I D(k) is the H-2(k)-linked Cmv(r) locus; these findings suggest a role for NK cell interaction with D(k)-bearing hematopoietic and nonhematopoietic cells to shape NK-mediated virus immunity.

MHC class I Dk locus and Ly49G2+ NK cells confer H-2k resistance to murine cytomegalovirus.

Essential NK cell-mediated murine CMV (MCMV) resistance is under histocompatibility-2(k) (H-2(k)) control in MA/My mice. We generated a panel of intra-H2(k) recombinant strains from congenic C57L.M-H2(k/b) (MCMV resistant) mice for precise genetic mapping of the critical interval. Recombination breakpoint sites were precisely mapped and MCMV resistance/susceptibility traits were determined for each of the new lines to identify the MHC locus. Strains C57L.M-H2(k)(R7) (MCMV resistant) and C57L.M-H2(k)(R2) (MCMV susceptible) are especially informative; we found that allelic variation in a 0.3-megabase interval in the class I D locus confers substantial difference in MCMV control phenotypes. When NK cell subsets responding to MCMV were examined, we found that Ly49G2(+) NK cells rapidly expand and selectively acquire an enhanced capacity for cytolytic functions only in C57L.M-H2(k)(R7). We further show that depletion of Ly49G2(+) NK cells before infection abrogated MCMV resistance in C57L.M-H2(k)(R7). We conclude that the MHC class I D locus prompts expansion and activation of Ly49G2(+) NK cells that are needed in H-2(k) MCMV resistance.

Deficient major histocompatibility complex-linked innate murine cytomegalovirus immunity in MA/My.L-H2b mice and viral downregulation of H-2k class I proteins.

NK cells are key effectors of innate immunity and host survival during cytomegalovirus (CMV) infection. Innate murine CMV (MCMV) resistance in MA/My mice requires Ly49H/m157-independent H-2k-linked NK cell control. Here we show that replacement of MA/My H-2k with C57L H-2b susceptibility genes led to a remarkable loss of innate virus immunity, though NK gamma interferon was induced in H-2b and H-2k strains shortly after infection. Thus, H-2b genes expressed in C57L or MA/My.L-H2b are sufficient in alerting NK cells to intrusion but fail to support NK restraint of viral infection. In addition, novel H-2 recombinant strains were produced and utilized in a further refinement of a critical genetic interval controlling innate H-2k-linked MCMV resistance. Importantly, this analysis excluded the gene interval from Kk class I through class II. The responsible gene(s) therefore resides in an interval spanning Dk class Ia and more-distal major histocompatibility complex (MHC) nonclassical class Ib genes. Recently, the NK activation receptor Ly49P and MHC class I Dk proteins were genetically implicated in MCMV resistance, in part because Ly49P-expressing reporter T cells could specifically bind Dk molecules on MCMV-infected mouse embryonic fibroblasts (MEFs). However, as we found that H-2k innate resistance differs in the C57L or MA/My backgrounds and because MCMV very efficiently downregulates H-2k class I proteins in L929 cells and primary MEFs shortly after infection, a Ly49P/Dk model should not fully explain H-2k-linked MCMV resistance.

Requisite H2k role in NK cell-mediated resistance in acute murine cytomegalovirus-infected MA/My mice.

Human CMV infections are a major health risk in patients with dysfunctional or compromised immunity, especially in patients with NK cell deficiencies, as these are frequently associated with high morbidity and mortality. In experimental murine CMV (MCMV) infections, Ly49H activation receptors on C57BL/6 (B6) NK cells engage m157 viral ligands on MCMV-infected cells and initiate dominant virus control. In this study, we report that MCMV resistance in MA/My relies on Ly49H-independent NK cell-mediated control of MCMV infection as NK cells in these mice do not bind anti-Ly49H mAb or soluble m157 viral ligands. We genetically compared MA/My resistance with MCMV susceptibility in genealogically and NK gene complex-Ly49 haplotype-related C57L mice. We found that MCMV resistance strongly associated with polymorphic H2k-linked genes, including MHC and non-MHC locations by analysis of backcross and intercross progeny. The H2b haplotype most frequently, but not absolutely, correlated with MCMV susceptibility, thus confirming a role for non-MHC genes in MCMV control. We also demonstrate a definite role for NK cells in H2k-type MCMV resistance because their removal from C57L.M-H2k mice before MCMV infection diminished immunity. NK gene complex-linked polymorphisms, however, did not significantly influence MCMV control. Taken together, effective NK cell-mediated MCMV control in this genetic system required polymorphic H2k genes without need of Ly49H-m157 interactions.