Role of V-V dimerization on electronic and magnetic properties of ilmenite-type CoVO3.

Structural, electronic and magnetic properties of ilmenite-type CoVO3have been explored via the generalized gradient approximation + effective HubbardUeffcorrection, in the framework of density functional theory. Our results indicate that high temperature rhombohedralR3-phase is metallic with oxidation states and electronic configurations Co2+(t2g↑3eg↑2t2g↓2eg↓0), V4+(t2g↑1eg↑0t2g↓0eg↓0), respectively, while low temperature triclinicP1-phase, induced from spin-Peierls transition in the V-V dimerization manner, is insulating, maintaining charge and electronic states unchanged. Furthermore, the A-type antiferromagnetic ordering, where the ferromagnetic honeycomb layers are anti-aligned along the stacking axis, is identified to be the magnetic ground state for the low temperature phase, in nice agreement with experimental findings, analogous to CoTiO3. The unexpected intralayer ferromagnetic couplings can be attributed to the intraorbitalt2g-t2gexchange coupling, which was assumed to be small earlier and ignored, but actually large in honeycomb cobaltates with 3d7electronic configuration. In addition, the computed magnetic moment on Co2+ion ranges from 2.5 to 2.7µB, HubbardUeffdependent, close to idealS= 3/2 state, rather than the anticipatedJeff= 1/2 state. Furthermore, the supplemental calculations, taking spin-orbit coupling (SOC) into account, uncover faint orbital moments of 0.21-0.27µBat the Co site, illustrating the insignificance of SOC. Except for the inevitable trigonal distortions, the excessive structural distortion triggered by the formation V-V dimerization, i.e. the breaking of trigonal symmetry around Co2+, further lifts the degeneracy oft2gorbitals and increases crystal field splitting, driving it away from potential candidates for realizing Kitaev model physics.

Salidroside Inhibits Ganglion Cell Apoptosis by Suppressing the Müller Cell Inflammatory Response in Diabetic Retinopathy.

PURPOSE: This study aimed to investigate the role of salidroside (SAL) in the cellular communication between Müller cells and retinal ganglion cells in diabetic mice. METHODS: The diabetes mellitus (DM) animal models were established by the intraperitoneal injection of streptozotocin and treatment with SAL via gavage or by the injection of IL-22BP into the vitreous cavity. Immunohistochemistry was used to measure the expression of the glial fibrillary acidic protein in Müller cells. The expression of IL-22 and IL-22Rα1 in retinal tissues was assessed by immunofluorescence. Western blotting was used to measure the expression of inflammatory and apoptosis-related proteins. Hematoxylin-eosin staining, TUNEL staining, and flow cytometry were used to analyze the apoptosis of retinal ganglion cells. The effect of cellular interactions was explored by Transwell assays. RESULTS: Western blotting showed that glial fibrillary acidic protein, IL-22 protein expression was significantly upregulated in the DM animal models compared with the control mice. Immunofluorescence showed that IL-22 was highly expressed in Müller cells and IL-22Rα1 was expressed in ganglion cells in the retina of DM mice. Hematoxylin-eosin and TUNEL staining results showed an increase in the number of ganglion cells apoptotic in DM. However, SAL reversed these phenomena. Meanwhile, after coculture with Müller cells, Western blotting suggested that ganglion cells secreted p-STAT3, and c-caspase3 protein expression was increased. More interestingly, the treatment of IL-22BP and SAL inhibited the expression of the p-STAT3 and c-caspase3 proteins. Flow cytometry indicates that compared with the control group, the apoptosis rate of ganglion cells was increased in the high glucose group, while the apoptosis rate of cells in the recombinant IL-22 protein group was significantly increased, while the SAL inhibited ganglion cells apoptosis. CONCLUSION: SAL inhibits the apoptosis of retinal ganglion cells via the IL-22/STAT3 pathway in Müller cells.

Relationship between IL-22 and IL-22BP in diabetic cognitive dysfunction.

BACKGROUND: CD4 + T helper (Th)22 cells play a regulatory role in autoimmune diseases such as type 1 diabetes mellitus. The Th22-related cytokine interleukin (IL)-22, the expression of which is increased in diabetes mellitus (DM), can act as a neurotrophic factor to protect neurons from apoptosis. Paradoxically, neuronal apoptosis and learning and memory decline occur in DM. In this study, we investigated the relationship between IL-22 and its receptors IL-22Rα1 and IL-22 binding protein (IL-22BP, a soluble inhibitor of IL-22) in diabetic encephalopathy (DE) and the effects of IL-22 on hippocampal neurons, learning and memory. METHODS: A C57BL/6 mouse model of diabetes was constructed by intraperitoneal injection of streptozotocin. The mice were randomly divided into 4 groups: the control group, diabetes group, diabetes + recombinantIL-22 (rIL-22) group and diabetes + IL-22BP group. The Morris water maze test was used to evaluate learning and memory, the expression of IL-22 was measured by ELISA, and Evans Blue staining was used to evaluate blood-brain barrier permeability. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was used to measure the mRNA expression of IL-22 and IL-22Rα1 in the hippocampus. The morphology and number of hippocampal neurons were assessed by Nissl staining, and TUNEL staining was used to detect hippocampal neuronal apoptosis. Immunofluorescence was used to analyze IL-22Rα1 expression and localization in hippocampus, and Western blotting was used to evaluate the expression of IL-22, IL-22Rα1, IL-22BP, and the apoptosis related proteins Caspase-3 and C-caspase-3. RESULTS: Compared with those in the control group, mice in the diabetes group showed cognitive decline; apoptosis of hippocampal neurons; increased expression of hippocampal Caspase-3, C-Caspase-3, IL-22, IL-22Rα1, and IL-22BP; and a decreased IL-22/IL-22BP ratio. Learning and memory were improved, neuronal apoptosis was attenuated, IL-22Rα1 expression and the IL-22/IL-22BP ratio were increased, and caspase-3 and C-caspase-3 expression was decreased in the rIL-22-treated group compared with the diabetes group. IL-22BP treatment aggravated diabetic cognitive dysfunction and pathological alterations in the hippocampus, decreased the IL-22/IL-22BP ratio, and increased the expression of caspase-3 and C-caspase-3 in mice with diabetes. CONCLUSION: A decrease in the IL-22/IL-22BP ratio plays an important role in diabetic cognitive dysfunction, and rIL-22 can effectively alleviate DE. Herein, we shed light on the interaction between IL-22 and IL-22BP as therapeutic targets for DM.

Salidroside Alleviates Diabetic Cognitive Dysfunction Via B3galt2/F3/Contactin Signaling Pathway in Mice.

Diabetes is frequently accompanied by cognitive impairment with insidious onset, and progressive cognitive and behavioral changes. ß-1, 3-galactosyltransferase 2 (B3galt2) contributes to glycosylation, showing a clue for neuronal apoptosis, proliferation and differentiation. However, the role of B3galt2 in diabetic cognitive dysfunction (DCD) has not been investigated. In the present study, we aimed to explore the role of B3galt2 in DCD. Additionally, the potential therapeutic effects of salidroside on DCD was also explored. Diabetic C57BL/6J mice showed cognitive dysfunction together with down-regulated B3galt2. Overexpression of B3galt2 reversed the cognitive decline of diabetic C57BL/6J. Moreover, cognitive impairment was aggravated in B3galt2+/- diabetic mice compared with C57BL/6J diabetic mice. Immunohistochemistry fluorescence indicated that B3galt2 and F3/Contactin were co-localized in the hippocampal regions. Importantly, the expression of F3/Contactin can be regulated by the manipulation of B3galt2, overexpression of which assuaged hippocampal neuronal damage, protected the synapsin, and reduced neuronal apoptosis in diabetic mice. Interestingly, SAL alleviated DCD and reversed the expression of B3galt2 in diabetic C57BL/6J mice. These findings indicate that inhibition of B3galt2/F3/Contactin pathway contributes to DCD, and participates in SAL reversed DCD.

Astragaloside IV Alleviates Brain Injury Induced by Hypoxia via the Calpain-1 Signaling Pathway.

Long-term hypoxia can induce oxidative stress and apoptosis in hippocampal neurons that can lead to brain injury diseases. Astragaloside IV (AS-IV) is widely used in the antiapoptotic therapy of brain injury diseases. However, its mechanism of action is still not fully understood. In this study, we investigated the effect of AS-IV on hypoxia-induced oxidative stress and apoptosis in hippocampal neurons and explored its possible mechanism. In vivo, mice were placed in a hypoxic circulatory device containing 10% O2 and gavaged with AS-IV (60 and 120 mg/kg/d) for 4 weeks. In vitro, mouse hippocampal neuronal cells (HT22) were treated with hypoxia (1% O2) for 24 hours in the presence or absence of AS-IV, MDL-28170 (calpain-1 inhibitor), or YC-1 (HIF-1α inhibitor). The protective effect of AS-IV on brain injury was further explored by examining calpain-1 knockout mice. The results showed that hypoxia induced damage to hippocampal neurons, impaired spatial learning and memory abilities, and increased oxidative stress and apoptosis. Treatment with AS-IV or calpain-1 knockout improved the damage to hippocampal neurons and spatial learning and memory, attenuated oxidative stress and inhibited cell apoptosis. These changes were verified in HT22 cells. Overexpression of calpain-1 abolished the improvement of AS-IV on apoptosis and oxidative stress. In addition, the effects of AS-IV were accompanied by decreased calpain-1 and HIF-1α expression, and YC-1 showed a similar effect as AS-IV on calpain-1 and caspase-3 expression. In conclusion, this study demonstrates that AS-IV can downregulate the calpain-1/HIF-1α/caspase-3 pathway and inhibit oxidative stress and apoptosis of hippocampal neurons induced by hypoxia, which provides new ideas for studying the antiapoptotic activity of AS-IV.

Th22 cells induce Müller cell activation via the Act1/TRAF6 pathway in diabetic retinopathy.

T helper 22 (Th22) cells have been implicated in diabetic retinopathy (DR), but it remains unclear whether Th22 cells involve in the pathogenesis of DR. To investigate the role of Th22 cells in DR mice, the animal models were established by intraperitoneal injection of STZ and confirmed by fundus fluorescein angiography and retinal haematoxylin-eosin staining. IL-22BP was administered by intravitreal injection. IL-22 level was measured by ELISA in vivo and in vitro. The expression of IL-22Rα1 in the retina was assessed by immunofluorescence. We assessed GFAP, VEGF, ICAM-1, inflammatory-associated factors and the integrity of blood-retinal barrier in control, DR, IL-22BP, and sham group. Müller cells were co-cultured with Th22 cells, and the expression of the above proteins was measured by immunoblotting. Plasmid transfection technique was used to silence Act1 gene in Müller cells. Results in vivo and in vitro indicated that Th22 cells infiltrated into the DR retinal and IL-22Rα1 expressed in Müller cells. Th22 cells promoted Müller cells activation and inflammatory factor secretion by secreting IL-22 compared with high-glucose stimulation alone. In addition, IL-22BP ameliorated the pathological alterations of the retina in DR. Inhibition of the inflammatory signalling cascade through Act1 knockdown alleviated DR-like pathology. All in all, the results suggested that Th22 cells infiltrated into the retina and secreted IL-22 in DR, and then IL-22 binding with IL-22Rα1 activated the Act1/TRAF6 signal pathway, and promoted the inflammatory of Müller cells and involved the pathogenesis of DR.

Ni(HCO3)2 nanosheet/nickel tetraphosphate (Ni(P4O11)) nanowire composite as a high-performance electrode material for asymmetric supercapacitors.

Nickel compounds, especially Ni(HCO3)2 (here denoted as NiC), have been widely combined with other materials to obtain composites with a more favorable structure that exhibit excellent electrochemical performance as supercapacitors. Unfortunately, the complicated processes for preparing such composites directly restrict their further application. Herein, we prepared a NiC/nickel tetraphosphate (Ni(P4O11)) nanocomposite (NiC/NiP) by introducing [Formula: see text] ions into the NiC reaction system; this composite can be applied in high-performance supercapacitors. The micromorphology of NiC/NiP material displayed an appropriate combination of NiP nanowires and thin NiC nanosheets, which provide sufficient active sites, short ion diffusion paths and fast ion diffusion speeds. NiC/NiP material exhibited an excellent rate performance of 70.2% retained capacity, although the current was increased by 15 times (1196 F g-1 at 2.0 A g-1 and 840 F g-1 at 30 A g-1). The energy density of a NiC/NiP//active carbon (AC) asymmetric supercapacitor fabricated in 6 M KOH was as much as 39.02 W h kg-1 and 26.67 W h kg-1 under corresponding power densities of 160 W kg-1 and 8000 W kg-1, respectively. The asymmetric supercapacitor delivered a stable cyclic performance of 78% capacitive retention after 5000 continuous charge/discharge cycles. More importantly, a 2.5 V light-emitting diode was lit successfully by two NiC/NiP//AC asymmetric supercapacitors in series. These results confirm that NiC/NiP nanocomposite has great potential in practical applications of electrochemical energy storage devices.

A flexible copper sulfide @ multi-walled carbon nanotubes cathode for advanced magnesium-lithium-ion batteries.

The hybrid magnesium-lithium-ion batteries (MLIBs) are promising alternatives in large-scale energy storage field owing to low cost and high safety of magnesium batteries and fast diffusion rate of Li-ion in the electrode. Herein, a free-standing and binder-free copper sulfide/Multi-walled carbon nanotubes film cathode (F-CuS-CNT), along with Mg-Li dual-salt electrolyte and dendrite-free Mg anode, is employed to construct the MLIBs. At room temperature (25 °C), the F-CuS-CNT electrode with a CuS content up to 70% exhibits a high initial specific capacity of 479 mAh g-1 (∼85.5% of the theoretical capacity) and a considerable cycling stability (165 mAh g-1 even after 100 cycles at the current density of 30 mA g-1), which far surpasses those of conventional CuS electrode. The excellent electrochemical performances of the F-CuS-CNTs electrode can be attributed to its excellent flexible network architecture as well as abundant pores, which provide more stable conductive buffering layers for CuS particles and higher Li+ diffusion dynamics during the charging/discharging process. This work demonstrates that constructing a flexible and free-standing film electrode could improve the electrochemical performances of MLIBs and may be an appropriate select of preparing flexible MLIBs.

Charge ordering and magnetic frustration in CsFe2F6.

The structural, electronic and magnetic properties of a charge-ordered iron fluoride material CsFe2+Fe3+F6 have been explored by density functional theory calculations based on the generalized gradient approximation + U approach, which was implemented in the VASP code. The material exhibits a 3D pyrochlore-related structure which consists of corner-shared Fe2+F6 and Fe3+F6 octahedra. Our results confirm that CsFe2F6 is a Mott-Hubbard insulator, and bears a magnetically frustrated ground state in which the localized 3d electrons are antiferromagnetically coupled between the homogeneous Fe ions (Fe3+-Fe3+ along the b axis, and Fe2+-Fe2+ along the a axis), while interactions between the heterogeneous Fe ions (Fe3+-Fe2+ along the c axis) are frustrated, consistent with Goodenough-Kanamori superexchange interactions. Although the disproportionation of the total 3d charge is extremely low, explicit evidence is provided on the charge ordering by an order parameter, which is defined as the difference in minority d yz orbital (in the local coordinates) occupations between the Fe3+ and Fe2+ cations. In addition, spin ordering and the spin-orbit coupling effect play an insignificant role in the charge ordering and the preferential occupation of the d yz orbital scenario in CsFe2F6.

Field emission of carbon quantum dots synthesized from a single organic solvent.

In this paper, a facile synthesis of carbon quantum dots (CQDs) and its field emission performance are reported. The CQDs are prepared from a single N, N-dimethylformamide acting as carbon and nitrogen-doping sources simultaneously. The CQDs are investigated by photoluminescence, transmission electron microscopy and x-ray photoelectron spectroscopy. The CQDs have an average size of 3 nm and are doped with N atoms. CQD dispersion shows strong fluorescence under UV illumination. For the first time, the field emission behavior of CQDs coated on Si substrate is studied. As a candidate of cold cathode, the CQDs display good field emission performance. The CQD emitter reaches the current density of 1.1 mA cm(-2) at 7.0 V µm(-1) and exhibits good long-term emission stability, suggesting promising application in field emission devices.

Synthesis of Capsule-like Porous Hollow Nanonickel Cobalt Sulfides via Cation Exchange Based on the Kirkendall Effect for High-Performance Supercapacitors.

To construct a suitable three-dimensional structure for ionic transport on the surface of the active materials for a supercapacitor, porous hollow nickel cobalt sulfides are successfully synthesized via a facile and efficient cation-exchange reaction in a hydrothermal process involving the Kirkendall effect with γ-MnS nanorods as a sacrificial template. The formation mechanism of the hollow nickel cobalt sulfides is carefully illustrated via the tuning reaction time and reaction temperature during the cation-exchange process. Due to the ingenious porous hollow structure that offers a high surface area for electrochemical reaction and suitable paths for ionic transport, porous hollow nickel cobalt sulfide electrodes exhibit high electrochemical performance. The Ni(1.77)Co(1.23)S4 electrode delivers a high specific capacity of 224.5 mAh g(-1) at a current density of 0.25 A g(-1) and a high capacity retention of 87.0% at 10 A g(-1). An all-solid-state asymmetric supercapacitor, assembled with a Ni(1.77)Co(1.23)S4 electrode as the positive electrode and a homemade activated carbon electrode as the negative electrode (denoted as NCS//HMC), exhibits a high energy density of 42.7 Wh kg(-1) at a power density of 190.8 W kg(-1) and even 29.4 Wh kg(-1) at 3.6 kW kg(-1). The fully charged as-prepared asymmetric supercapacitor can light up a light emitting diode (LED) indicator for more than 1 h, indicating promising practical applications of the hollow nickel cobalt sulfides and the NCS//HMC asymmetric supercapacitor.

All-solid-state high performance asymmetric supercapacitors based on novel MnS nanocrystal and activated carbon materials.

All-solid-state high-performance asymmetric supercapacitors (ASCs) are fabricated using γ-MnS as positive electrode and porous eggplant derived activated carbon (EDAC) as negative electrode with saturated potassium hydroxide agar gel as the solid electrolyte. The laminar wurtzite nanostructure of γ-MnS facilitates the insertion of hydroxyl ions into the interlayer space, and the manganese sulfide nanowire offers electronic transportation channels. The size-uniform porous nanostructure of EDAC provides a continuous electron pathway as well as facilitates short ionic transportation pathways. Due to these special nanostructures of both the MnS and the EDAC, they exhibited a specific capacitance of 573.9 and 396 F g(-1) at 0.5 A g(-1), respectively. The optimized MnS//EDAC asymmetric supercapacitor shows a superior performance with specific capacitance of 110.4 F g(-1) and 89.87% capacitance retention after 5000 cycles, a high energy density of 37.6 Wh kg(-1) at a power density of 181.2 W kg(-1) and remains 24.9 Wh kg(-1) even at 5976 W kg(-1). Impressively, such two assembled all-solid-state cells in series can light up a red LED indicator for 15 minutes after fully charged. These impressive results make these pollution-free materials promising for practical applications in solid aqueous electrolyte-based ASCs.

Morphology controlled synthesis of monodispersed manganese sulfide nanocrystals and their primary application in supercapacitors with high performances.

Monodispersed hollow spindle-like nanosphere (HS-NS) and tetrapod nanorod (TP-NR) MnS nanocrystals are obtained via a facile template-free hydrothermal process. The MnS nanocrystals are used as supercapacitor materials and they exhibit high performances. The TP-NR nanocrystals show a higher specific capacitance of 704.5 F g(-1) compared to the HS-NS nanocrystals, and both show higher values compared to manganese oxide.

Atorvastatin prevents amyloid-ß peptide oligomer-induced synaptotoxicity and memory dysfunction in rats through a p38 MAPK-dependent pathway.

AIM: To investigate whether atorvastatin treatment could prevent Aß1-42 oligomer (AßO)-induced synaptotoxicity and memory dysfunction in rats, and to elucidate the mechanisms involved in the neuroprotective actions of atorvastatin. METHODS: SD rats were injected with AßOs (5 nmol, icv). The rats were administrated with atorvastatin (10 mg·kg(-1)·d(-1), po) for 2 consecutive weeks (the first dose was given 5 d before AßOs injection). The memory impairments were evaluated with Morris water maze task. The expression of inflammatory cytokines in the hippocampus was determined using ELISA assays. The levels of PSD-95 and p38MAPK proteins in rat hippocampus were evaluated using Western blot analysis. For in vitro experiments, cultured rat hippocampal neurons were treated with AßOs (50 nmol/L) for 48 h. The expression of MAP-2 and synaptophysin in the neurons was detected with immunofluorescence. RESULTS: The AßO-treated rats displayed severe memory impairments in Morris water maze tests, and markedly reduced levels of synaptic proteins synaptophysin and PSD-95, increased levels of inflammatory cytokines (IL-1ß, IL-6 and TNF-α) and p38MAPK activation in the hippocampus. All these effects were prevented or substantially attenuated by atorvastatin administration. Pretreatment of cultured hippocampal neurons with atorvastatin (1 and 5 µmol/L) concentration-dependently attenuated the AßO-induced synaptotoxicity, including the loss of dendritic marker MAP-2, and synaptic proteins synaptophysin and PSD-95. Pretreatment of the cultured hippocampal neurons with the p38MAPK inhibitor SB203580 (5 µmol/L) blocked the AßO-induced loss of synaptophysin and PSD-95. CONCLUSION: Atorvastatin prevents AßO-induced synaptotoxicity and memory dysfunction through a p38MAPK-dependent pathway.

Atorvastatin enhances neurite outgrowth in cortical neurons in vitro via up-regulating the Akt/mTOR and Akt/GSK-3ß signaling pathways.

AIM: To investigate whether atorvastatin can promote formation of neurites in cultured cortical neurons and the signaling mechanisms responsible for this effect. METHODS: Cultured rat cerebral cortical neurons were incubated with atorvastatin (0.05-10 µmol/L) for various lengths of time. For pharmacological experiments, inhibitors were added 30 min prior to addition of atorvastatin. Control cultures received a similar amount of DMSO. Following the treatment period, phase-contrast digital images were taken. Digital images of neurons were analyzed for total neurite branch length (TNBL), neurite number, terminal branch number, and soma area by SPOT Advanced Imaging software. After incubation with atorvastatin for 48 h, the levels of phosphorylated 3-phosphoinoside-dependent protein kinase-1 (PDK1), phospho-Akt, phosphorylated mammalian target of rapamycin (mTOR), phosphorylated 4E-binding protein 1 (4E-BP1), p70S6 kinase (p70S6K), and glycogen synthase kinase-3ß (GSK-3ß) in the cortical neurons were evaluated using Western blotting analyses. RESULTS: Atorvastatin (0.05-10 µmol/L) resulted in dose-dependent increase in neurite number and length in these neurons. Pretreatment of the cortical neurons with phosphatidylinositol 3-kinase (PI3K) inhibitors LY294002 (30 µmol/L) and wortmannin (5 µmol/L), Akt inhibitor tricribine (1 µmol/L) or mTOR inhibitor rapamycin (100 nmol/L) blocked the atorvastatin-induced increase in neurite outgrowth, suggesting that atorvastatin promoted neurite outgrowth via activating the PI3K/Akt/mTOR signaling pathway. Atorvastatin (10 µmol/L) significantly increased the levels of phosphorylated PDK1, Akt and mTOR in the cortical neurons, which were prevented by LY294002 (30 µmol/L). Moreover, atorvastatin (10 µmol/L) stimulated the phosphorylation of 4E-BP1 and p70S6K, the substrates of mTOR, in the cortical neurons. In addition, atorvastatin (10 µmol/L) significantly increased the phosphorylated GSK-3ß level in the cortical neurons, which was prevented by both LY294002 and tricribine. CONCLUSION: These results suggest that activation of both the PI3K/Akt/mTOR and Akt/GSK-3ß signaling pathways is responsible for the atorvastatin-induced neurite outgrowth in cultured cortical neurons.