Knockout of AKAP150 improves impaired BK channel-mediated vascular dysfunction through the Akt/GSK3ß signalling pathway in diabetes mellitus.

Vascular dysfunction resulting from diabetes is an important factor in arteriosclerosis. Previous studies have shown that during hyperglycaemia and diabetes, AKAP150 promotes vascular tone enhancement by intensifying the remodelling of the BK channel. However, the interaction between AKAP150 and the BK channel remains open to discussion. In this study, we investigated the regulation of impaired BK channel-mediated vascular dysfunction in diabetes mellitus. Using AKAP150 null mice (AKAP150-/- ) and wild-type (WT) control mice (C57BL/6J), diabetes was induced by intraperitoneal injection of streptozotocin. We found that knockout of AKAP150 reversed vascular remodelling and fibrosis in mice with diabetes and in AKAP150-/- diabetic mice. Impaired Akt/GSK3ß signalling contributed to decreased BK-ß1 expression in aortas from diabetic mice, and the silencing of AKAP150 increased Akt phosphorylation and BK-ß1 expression in MOVAS cells treated with HG medium. The inhibition of Akt activity caused a decrease in BK-ß1 expression, and treatment with AKAP150 siRNA suppressed GSK3ß expression in the nuclei of MOVAS cells treated with HG. Knockout of AKAP150 reverses impaired BK channel-mediated vascular dysfunction through the Akt/GSK3ß signalling pathway in diabetes mellitus.

PVT1 induces NSCLC cell migration and invasion by regulating IL-6 via sponging miR-760.

Non-small-cell lung carcinoma (NSCLC) accounts for approximately 80% of lung cancers with a high metastatic potential. Elucidating the mechanism of NSCLC metastasis will provide new promising targets for NSCLC therapy and benefit its prognosis. Plasmacytoma variant translocation 1 (PVT1) has been proven to be overexpressed in NSCLC. Although the oncogenic role of PVT1 in NSCLC has been reported, its mechanism remains unclear. Here, we verified that the knockdown of PVT1 inhibited NSCLC cell migration and invasion, and that its inhibitory role on A549 cells and H1299 cells was antagonized by interleukin-6 (IL-6) treatment. The results revealed that PVT1 regulates IL-6 by sponging miR-760 and identified the binding site of miR-760 in the 3'-UTR of IL-6. In conclusion, a new mechanism was revealed, wherein PVT1 regulates NSCLC cell migration and invasion via miR-760/IL-6, suggesting PVT1/miR-760/IL-6 as promising prognostic biomarkers and therapeutic targets for NSCLC metastasis.

Cardiac function modulation depends on the A-kinase anchoring protein complex.

The A-kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP-associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm.

Comparative physiological, metabolomic, and transcriptomic analyses reveal developmental stage-dependent effects of cluster bagging on phenolic metabolism in Cabernet Sauvignon grape berries.

BACKGROUND: Light conditions significantly influence grape berry ripening and the accumulation of phenolic compounds, but the underlying molecular basis remains partially understood. Here, we applied integrated transcriptomics and pathway-level metabolomics analyses to investigate the effect of cluster bagging during various developmental stages on phenolic metabolism in Cabernet Sauvignon grapes. RESULTS: Bagging treatments had limited effects on berry quality attributes at harvest and did not consistently affect phenolic acid biosynthesis between seasons. Significantly elevated flavan-3-ol and flavonol contents were detected in re-exposed berries after bagging during early-developmental stages, while bagging after véraison markedly inhibited skin anthocyanin accumulation. Several anthocyanin derivatives and flavonol glycosides were identified as marker phenolic metabolites for distinguishing bagged and non-bagged grapes. Coordinated transcriptional changes in the light signaling components CRY2 and HY5/HYHs, transcription regulator MYBA1, and enzymes LAR, ANR, UFGT and FLS4, coincided well with light-responsive biosynthesis of the corresponding flavonoids. The activation of multiple hormone signaling pathways after both light exclusion and re-exposure treatments was inconsistent with the changes in phenolic accumulation, indicating a limited role of plant hormones in mediating light/darkness-regulated phenolic biosynthesis processes. Furthermore, gene-gene and gene-metabolite network analyses discovered that the light-responsive expression of genes encoding bHLH, MYB, WRKY, NAC, and MADS-box transcription factors, and proteins involved in genetic information processing and epigenetic regulation such as nucleosome assembly and histone acetylation, showed a high positive correlation with grape berry phenolic accumulation in response to different light regimes. CONCLUSIONS: Altogether, our findings provide novel insights into the understanding of berry phenolic biosynthesis under light/darkness and practical guidance for improving grape features.

Functional protection against cardiac diseases depends on ATP-sensitive potassium channels.

ATP-sensitive potassium channels (KATP) channels are widely distributed in various tissues, including pancreatic beta cells, muscle tissue and brain tissue. KATP channels play an important role in cardioprotection in physiological/pathological situations. KATP channels are inhibited by an increase in the intracellular ATP concentration and are stimulated by an increase in the intracellular MgADP concentration. Activation of KATP channels decreases ischaemia/reperfusion injury, protects cardiomyocytes from heart failure, and reduces the occurrence of arrhythmias. KATP channels are involved in various signalling pathways, and their participation in protective processes is regulated by endogenous signalling molecules, such as nitric oxide and hydrogen sulphide. KATP channels may act as a new drug target to fight against cardiovascular disease in the development of related drugs in the future. This review highlights the potential mechanisms correlated with the protective role of KATP channels and their therapeutic value in cardiovascular diseases.

Exogenous hydrogen sulfide attenuates the development of diabetic cardiomyopathy via the FoxO1 pathway.

BACKGROUND: Previous studies have suggested that exogenous hydrogen sulfide can alleviate the development of diabetic cardiomyopathy (DCM) by inhibiting oxidative stress, inflammation, and apoptosis. However, the underlying mechanism is not fully understood. Nuclear expression and function of the transcription factor Forkhead box protein O (FoxO1) have been associated with cardiovascular diseases, and thus, the importance of FoxO1 in DCM has gained increasing attention. This study was designed to investigate the interactions between hydrogen sulfide (H2 S) and nuclear FoxO1 in DCM. METHODS: Diabetes was induced in adult male C57BL/6J mice by intraperitoneal injection of streptozotocin and was treated with H2 S donor sodium hydrosulfide for 12 weeks. The H9C2 cardiomyoblast cell line and neonatal rat cardiomyocytes (NRCMs) were treated with the slow-releasing H2 S donor GYY4137 before high-glucose (HG) exposure with or without pretreatment with the Akt inhibitor MK-2206 2HCl. Changes in FoxO1 protein phosphorylation and subcellular localization were determined in H9C2 cells, NRCMs, and cardiac tissues from normal and diabetic mice. Cardiac structure and function in the diabetic mice were evaluated by echocardiography and histological analysis and compared with those in control animals. RESULTS: The echocardiographic and histopathological data indicated that exogenous H2 S improved cardiac function and attenuated cardiac hypertrophy and myocardial fibrosis in diabetic mice. H2 S also improved HG-induced oxidative stress and apoptosis in cardiac tissue and NRCMs. In addition, H2 S induced FoxO1 phosphorylation and nuclear exclusion in vitro and in vivo, and this function was not inhibited by MK-2206 2HCl. Alanine substitution mutation of three sites in FoxO1-enhanced FoxO1 transcriptional activity, and subsequent treatment with exogenous H2 S could not prevent HG-induced nuclear retention. CONCLUSIONS: Our data indicate that H2 S is a novel regulator of FoxO1 in cardiac cells and provide evidence supporting the potential of H2 S in inhibiting the progression of DCM.

Safflor yellow A protects neonatal rat cardiomyocytes against anoxia/reoxygenation injury in vitro.

AIM: To investigate the effects of safflor yellow A (SYA), a flavonoid extracted from Carthamus tinctorius L, on cultured rat cardiomyocytes exposed to anoxia/reoxygenation (A/R). METHODS: Primary cultured neonatal rat cardiomyocytes were exposed to anoxia for 3 h followed by reoxygenation for 6 h. The cell viability was measured using MTT assay. The releases of lactate dehydrogenase (LDH) and creatine kinase (CK), level of malondialdehyde (MDA), and activities of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were analyzed. Hoechst 33258 staining and changes in Bcl-2/Bax ratio and caspase 3 activity were used to examine A/R-induced apoptosis. RESULTS: The A/R exposure markedly decreased the viability of cardiomyocytes, suppressed the activities of SOD, GSH, CAT and GSH-Px, and Bcl-2 protein expression. Meanwhile, the A/R exposure markedly increased the release of LDH and CK, and MDA production in the cardiomyocytes, and increased the rate of apoptosis, caspase 3 activity, Bax protein expression. Pretreatment with SYA (40, 60 and 80 nmol/L) concentration-dependently blocked the A/R-induced changes in the cardiomyocytes. Pretreatment of the cardiomyocytes with the antioxidant N-acetylcysteine (NAC, 200 µmol/L) produced protective effects that were comparable to those caused by SYA (80 nmol/L). CONCLUSION: SYA protects cultured rat cardiomyocytes against A/R injury, maybe via inhibiting cellular oxidative stress and apoptosis.

Mume Fructus (Prunus mume Sieb. et Zucc.) extract accelerates colonic mucosal healing of mice with colitis induced by dextran sulfate sodium through potentiation of cPLA2-mediated lysophosphatidylcholine synthesis.

BACKGROUND: Mume Fructus (MF) is the fruit of Prunus mume Sieb. et Zucc, a plant of Rosaceae family. Previous studies demonstrated that MF was capable of ameliorating ulcerative colitis (UC) in mice, its action mechanism needs to be clarified. PURPOSE: This study deciphered whether and how MF extract accelerates colonic mucosal healing, the therapeutic endpoint of UC. METHODS: Biochemical, histopathological and qRT-PCR analyses were utilized to define the therapeutic efficacy of MF on dextran sulfate sodium (DSS)-induced colitis in mice. UHPLC-QTOF-MS/MS-based metabolomics technique was adopted to explore the changes of endogenous metabolites associated with UC and responses to MF intervention. qRT-PCR analysis was performed to confirm the molecular pathway in vivo. The effects of MF and lysophosphatidylcholine (LPC) on cell viability, wound healing, proliferation, and migration were examined through a series of in vitro experiments. Moreover, the effects of different subtypes of phospholipase A2 (PLA2) inhibitors on MF-treated colonic epithelial cells were detected by wound healing test and transwell assay. RESULTS: Orally administered MF could alleviate colitis in mice mainly by accelerating the healing of colonic mucosa. Guided by an unbiased metabolomics screen, we identified LPC synthesis as a major modifying pathway in colitis mice after MF treatment. Notably, MF facilitated the synthesis of LPC by enhancing the expression of PLA2 in colitis mice. Mechanistically, MF and LPC accelerated wound closure by promoting cell migration. Moreover, the promotion of MF on wound healing and migration of colonic epithelial cells was blunted by a cytosolic phospholipase A2 (cPLA2) inhibitor. CONCLUSION: MF can facilitate colonic mucosal healing of mice with colitis through cPLA2-mediated intestinal LPC synthesis, which may become a novel therapeutic agent of UC.

Rational construction of graphitic carbon nitride composited Li-rich Mn-based oxide cathode materials toward high-performance Li-ion battery.

Li-rich Mn-based oxides (LRMOs) are considered as one of the most-promising cathode materials for next generation Li-ion batteries (LIBs) because of their high energy density. Nevertheless, the intrinsic shortcomings, such as the low first coulomb efficiency, severe capacity/voltage fade, and poor rate performance seriously limit its commercial application in the future. In this work, we construct successfully g-C3N4 coating layer to modify Li1.2Mn0.54Ni0.13Co0.13O2 (LMNC) via a facile solution. The g-C3N4 layer can alleviate the side-reaction between electrolyte and LMNC materials, and improve electronic conduction of LMNC. In addition, the g-C3N4 layer can suppress the collapse of structure and improve cyclic stability of LMNC materials. Consequently, g-C3N4 (4 wt%)-coated LMNC sample shows the highest initial coulomb efficiency (78.5%), the highest capacity retention ratio (78.8%) and the slightest voltage decay (0.48 V) after 300 loops. Besides, it also can provide high reversible capacity of about 300 and 93 mAh g-1 at 0.1 and 10C, respectively. This work proposes a novel approach to achieve next-generation high-energy density cathode materials, and g-C3N4 (4 wt%)-coated LMNC shows an enormous potential as the cathode materials for next generation LIBs with excellent performance.

The effect of staggered administration of zinc sulfate on the pharmacokinetics of oral cephalexin.

AIMS: To investigate the effect of zinc sulfate on pharmacokinetics of cephalexin when administered concurrently or at strategically spaced dosing times designed to avoid the potential interaction in healthy volunteers. METHODS: In this study, all subjects (n= 12) were randomized to receive the following four treatments, separated by a wash-out period of 7 days: cephalexin 500mg alone, concomitantly with zinc 250mg, 3h after zinc 250mg or 3h before zinc 250mg. RESULTS: All subjects completed the study safely. Zinc supplements administered concurrently with cephalexin significantly decreased the peak serum concentration (C(max) ), area under the plasma concentration-time curve from zero to infinity (AUC(0-∞) ) and the time for which the plasma concentration of the drug remained above the minimal inhibitory concentration of the pathogenic organism (T > MIC) of cephalexin [mean percentage decrease (95% confidence intervals) of 31.05% (22.09-40.01%), 27.40% (18.33-36.47%) and 22.33% (12.51-32.16%), respectively; P < 0.05] compared with administration of cephalexin alone. Also, administration of zinc 3h before cephalexin decreased the C(max) , AUC(0-∞) and T > MIC of the drug compared with administration of cephalexin alone [mean percentage decrease (95% confidence intervals) of 11.48% (3.40-19.55%), 18.12% (9.63-26.60%) and 23.75% (14.30-33.20%), respectively; P < 0.05]. In contrast, the pharmacokinetics of cephalexin was not notably altered by administration of zinc 3h after cephalexin dosing (P > 0.05). CONCLUSIONS: The significant interaction between zinc and cephalexin might affect the clinical outcome of cephalexin therapy. The dosing recommendation is that zinc sulfate can be safely administered 3h after a cephalexin dose.

Targeting the KCa3.1 channel suppresses diabetes-associated atherosclerosis via the STAT3/CD36 axis.

BACKGROUND: In diet-induced arterial atherosclerosis, increased KCa3.1 channel was associated with atherosclerotic plaque progression and instability. Macrophages are involved in the formation of atherosclerotic plaques, and the release of inflammatory cytokines and oxygen free radicals promotes plaque progression. However, whether the macrophage KCa3.1 channel facilitates diabetes-accelerated atherosclerosis is still unclear. This study investigated atherosclerotic plaque in ApoE-/- mice regulated by the KCa3.1 channel. METHODS AND RESULTS: In vivo, blocking KCa3.1channel inhibit the development of the atherosclerotic lesion in diabetic ApoE-/- mice fed with a high-fat diet. In vitro, upregulation of KCa3.1 channel level occurred in RAW264.7 cells treated with HG plus ox-LDL in a time-dependent manner. Blocking KCa3.1 significantly reduced the uptake of ox-LDL in mice peritoneal macrophages. Further studies indicated the KCa3.1 siRNA and TRAM-34 (KCa3.1 inhibitor) attenuated the scavenger receptor CD36 expression via inhibiting STAT3 phosphorylation. CONCLUSION: Blockade of macrophage KCa3.1 channel inhibit cellular oxidized low-density lipoprotein accumulation and decrease proinflammation factors expression via STAT3/CD36 axis. This study provided a novel therapeutic target to reduce the risk of atherosclerosis development in diabetic patients.

Construction of Carbon-Coated LiMn0.5Fe0.5PO4@Li0.33La0.56TiO3 Nanorod Composites for High-Performance Li-Ion Batteries.

The carbon-coated LiMn0.5Fe0.5PO4@Li0.33La0.56TiO3 nanorod composites (denoted as C/LMFP@LLTO) have been successfully obtained according to a common hydrothermal synthesis following a post-calcination treatment. The morphology and particle size of LiMn0.5Fe0.5PO4 (denoted as LMFP) are not changed by the coating. All electrode materials exhibit nanorod morphology; they are 100-200 nm in length and 50-100 nm in width. The Li0.33La0.56TiO3 (denoted as LLTO) coating can facilitate the charge transfer to enhance lithiation/delithiation kinetics, leading to an excellent rate performance and cycle stability of an as-obtained C/LMFP@LLTO electrode material. The reversible discharge capacities of C/LMFP@LLTO (3 wt %) at 0.05 and 5 C are 146 and 131.3 mA h g-1, respectively. After 100 cycles, C/LMFP@LLTO (3 wt %) exhibits an outstanding capacity of 106.4 mA h g-1 with an 81% capacity retention rate at 5 C, indicating an excellent reversible capacity and good cycle capacity. Therefore, it can be considered that LLTO coating is a prospective pathway to exploit the electrochemical performances of C/LMFP.

Comprehensive analysis of the ceRNA network in coronary artery disease.

With the rapid aging of the population, coronary artery disease (CAD) has become one of the most fatal chronic diseases. However, the genetic mechanism of CAD is still unclear. The purpose of this study is to construct the lncRNA-miRNA-mRNA regulatory network for CAD diseases and systematically identify differentially expressed genes in patients with coronary heart disease. In this study, two lncRNA datasets (GSE69587 and GSE113079) and a microRNA dataset (GSE105449) which contained 393 and 38 CAD samples were selected. In addition, two mRNA datasets which named GSE113079 (98 CAD samples) and GSE9820 (8 CAD samples) were selected to search the differentially expressed genes (DEGs). By comparing the expression data between CAD and control samples, a total of 1111 lncRNAs, 2595 mRNAs and 22 miRNAs were identified. Based on the DEGs, a lncRNA-miRNA-mRNA ceRNA network was constructed to explore the hub nodes in CAD. In the ceRNA network, the lncRNAs KCNQ1OT1 and H19 showed high connectivity with the nine miRNAs. GO and KEGG results showed that genes in ceRNA networks were mainly involved in nitrogen compound metabolic process, PI3K-Akt signaling pathway and retrograde endocannabinoid signaling. These findings will improve the understanding of the occurrence and development mechanism of CAD.

Boosting the lithium storage performance of Na2Li2Ti6O14 anodes by g-C3N4 modification.

Na2Li2Ti6O14 particles were prepared by a simple solid-state process, and then g-C3N4-coated Na2Li2Ti6O14 composites were constructed by a facile solution route for the first time. The g-C3N4-coated Na2Li2Ti6O14 multicomponent composites because of their unique architecture as negative materials for Li-ion batteries can be expected to exhibit a significantly improved cycling stability and reversible capacity even at high rates. g-C3N4 (5 wt%)-coated Na2Li2Ti6O14 shows a discharge (charge) capacity of 184.4 (184.3) mA h g-1 at 500 mA g-1 after 100 cycles, which is larger than that of pristine Na2Li2Ti6O14 with a discharge (charge) capacity of 122.8 (122.0) mA h g-1. The use of g-C3N4 with a carbon framework containing abundant nitrogen provides more active sites and surface defects for redox reactions and Li-ion transport. The g-C3N4 coating decreases the impedance between the electrolyte and Na2Li2Ti6O14 and enhances the charge transfer, ionic conductivity and diffusion ability of Li ions of Na2Li2Ti6O14. This work offers an efficient way to design high-performance Na2Li2Ti6O14-based materials for advanced lithium ion battery, and g-C3N4 (5 wt%)-coated Na2Li2Ti6O14 shows an enormous potential as a negative material for next generation Li-ion batteries with excellent performance.

Effect of BIN1 on cardiac dysfunction and malignant arrhythmias.

Heart failure (HF) is the end-stage syndrome for most cardiac diseases, and the 5-year morbidity and mortality of HF remain high. Malignant arrhythmia is the main cause of sudden death in the progression of HF. Recently, bridging integrator 1 (BIN1) was discovered as a regulator of transverse tubule function and calcium signalling in cardiomyocytes. BIN1 downregulation is linked to abnormal cardiac contraction, and it increases the possibility of malignant arrhythmias preceding HF. Because of the detectability of cardiac BIN1 in peripheral blood, BIN1 may serve as a predictor of HF and may be useful in therapy development. However, the mechanism of BIN1 downregulation in HF and how BIN1 regulates normal cardiac function under physiological conditions remain unclear. In this review, recent progress in the biological studies of BIN1-related cardiomyocytes and the effect of cardiac dysfunction and malignant arrhythmia will be discussed.

Porous spherical NiO@NiMoO4@PPy nanoarchitectures as advanced electrochemical pseudocapacitor materials.

In this work, a rational design and construction of porous spherical NiO@NiMoO4 wrapped with PPy was reported for the application of high-performance supercapacitor (SC). The results show that the NiMoO4 modification changes the morphology of NiO, and the hollow internal morphology combined with porous outer shell of NiO@NiMoO4 and NiO@NiMoO4@PPy hybrids shows an increased specific surface area (SSA), and then promotes the transfer of ions and electrons. The shell of NiMoO4 and PPy with high electronic conductivity decreases the charge-transfer reaction resistance of NiO, and then improves the electrochemical kinetics of NiO. At 20Ag-1, the initial capacitances of NiO, NiMoO4, NiO@NiMoO4 and NiO@NiMoO4@PPy are 456.0, 803.2, 764.4 and 941.6Fg-1, respectively. After 10,000 cycles, the corresponding capacitances are 346.8, 510.8, 641.2 and 904.8Fg-1, respectively. Especially, the initial capacitance of NiO@NiMoO4@PPy is 850.2Fg-1, and remains 655.2Fg-1 with a high retention of 77.1% at 30Ag-1 even after 30,000 cycles. The calculation result based on density function theory shows that the much stronger Mo-O bonds are crucial for stabilizing the NiO@NiMoO4 composite, resulting in a good cycling stability of these materials.

Critical regulation of atherosclerosis by the KCa3.1 channel and the retargeting of this therapeutic target in in-stent neoatherosclerosis.

Coronary heart disease is a serious cardiovascular illness. Percutaneous coronary artery stent implantation has become a routine way to treat coronary heart disease. Although studies have shown how a drug-eluting stent could improve the efficacy of clinical treatment, 10~20% of in-stent restenosis is still an important outcome that restricts the clinical efficacy of drug-eluting stent implantations and causes cardiovascular events such as angina pectoris, acute myocardial infarction, and sudden death. The KCa3.1 channel plays an important role in neoatherosclerosis of in-stent restenosis by regulating macrophage function. Recent studies have shown that the KCa3.1 channel, which belongs to the family of calcium-activated potassium channels, plays an important role in the occurrence and development of various inflammatory diseases by regulating cell membrane potentials and calcium signaling in the processes of macrophage migration and mitogen-stimulated vascular smooth muscle cell and fibroblast proliferation. The KCa3.1 channel is activated by elevated intracellular calcium levels. Inhibition of the KCa3.1 channel can effectively slow the progression of arterial plaque rupture and reduce the degree of vascular restenosis, and so substances that can carry out this inhibition are expected to become targeted drugs for the treatment of in-stent neoatherosclerosis. This article reviews the pathological and physiological roles of the KCa3.1 channel and its roles in the disease prognosis of in-stent neoatherosclerosis.

Enhanced electrochemical property of FePO4-coated LiNi0.5Mn1.5O4 as cathode materials for Li-ion battery.

Pristine LiNi0.5Mn1.5O4 and FePO4-coated one with Fd-3m space groups were prepared by a sol-gel method. The structure and performance were studied by X-ray diffraction (XRD) rietveld refinement, scanning electron microscopy (SEM), high resolution transmission electron microscopy (HRTEM), energy dispersive spectrometer (EDS) mapping, electrochemical impedance spectroscopy (EIS) and charge-discharge tests, respectively. The lattice parameters of all samples almost remain the same from the Rietveld refinement, revealing that the crystallographic structure has no obvious difference between pristine LiNi0.5Mn1.5O4 and FePO4-coated one. All materials show similar morphologies with uniform particle distribution with small particle size, and FePO4 coating does not affect the morphology of LiNi0.5Mn1.5O4 material. EDS mapping and HRTEM show that FePO4 may be successfully wrapped around the surfaces of LiNi0.5Mn1.5O4 particles, and provides an effective coating layer between the electrolyte and the surface of LiNi0.5Mn1.5O4 particles. FePO4 (1wt%)-coated LiNi0.5Mn1.5O4 cathode shows the highest discharge capacity at high rate (2C) among all samples. After 80 cycles, the reversible discharge capacity of FePO4 (1wt%) coated LiNi0.5Mn1.5O4 is 117mAhg-1, but the pristine one only has 50mAhg-1. FePO4 coating is an effective and controllable way to stabilize the LiNi0.5Mn1.5O4/electrolyte interface, and avoids the direct contact between LiNi0.5Mn1.5O4 powders and electrolyte, then suppresses the side reactions and enhances the electrochemical performance of the LiNi0.5Mn1.5O4.

Robust Strategy for Crafting Li5Cr7Ti6O25@CeO2 Composites as High-Performance Anode Material for Lithium-Ion Battery.

A facile strategy was developed to prepare Li5Cr7Ti6O25@CeO2 composites as a high-performance anode material. X-ray diffraction (XRD) and Rietveld refinement results show that the CeO2 coating does not alter the structure of Li5Cr7Ti6O25 but increases the lattice parameter. Scanning electron microscopy (SEM) indicates that all samples have similar morphologies with a homogeneous particle distribution in the range of 100-500 nm. Energy-dispersive spectroscopy (EDS) mapping and high-resolution transmission electron microscopy (HRTEM) prove that CeO2 layer successfully formed a coating layer on a surface of Li5Cr7Ti6O25 particles and supplied a good conductive connection between the Li5Cr7Ti6O25 particles. The electrochemical characterization reveals that Li5Cr7Ti6O25@CeO2 (3 wt %) electrode shows the highest reversibility of the insertion and deinsertion behavior of Li ion, the smallest electrochemical polarization, the best lithium-ion mobility among all electrodes, and a better electrochemical activity than the pristine one. Therefore, Li5Cr7Ti6O25@CeO2 (3 wt %) electrode indicates the highest delithiation and lithiation capacities at each rate. At 5 C charge-discharge rate, the pristine Li5Cr7Ti6O25 only delivers an initial delithiation capacity of ∼94.7 mAh g-1, and the delithiation capacity merely achieves 87.4 mAh g-1 even after 100 cycles. However, Li5Cr7Ti6O25@CeO2 (3 wt %) delivers an initial delithiation capacity of 107.5 mAh·g-1, and the delithiation capacity also reaches 100.5 mAh g-1 even after 100 cycles. The cerium dioxide modification is a direct and efficient approach to improve the delithiation and lithiation capacities and cycle property of Li5Cr7Ti6O25 at large current densities.

Light-induced Variation in Phenolic Compounds in Cabernet Sauvignon Grapes (Vitis vinifera L.) Involves Extensive Transcriptome Reprogramming of Biosynthetic Enzymes, Transcription Factors, and Phytohormonal Regulators.

Light environments have long been known to influence grape (Vitis vinifera L.) berry development and biosynthesis of phenolic compounds, and ultimately affect wine quality. Here, the accumulation and compositional changes of hydroxycinnamic acids (HCAs) and flavonoids, as well as global gene expression were analyzed in Cabernet Sauvignon grape berries under sunlight exposure treatments at different phenological stages. Sunlight exposure did not consistently affect the accumulation of berry skin flavan-3-ol or anthocyanin among different seasons due to climatic variations, but increased HCA content significantly at véraison and harvest, and enhanced flavonol accumulation dramatically with its timing and severity degree trend. As in sunlight exposed berries, a highly significant correlation was observed between the expression of genes coding phenylalanine ammonia-lyase, 4-coumarate: CoA ligase, flavanone 3-hydroxylase and flavonol synthase family members and corresponding metabolite accumulation in the phenolic biosynthesis pathway, which may positively or negatively be regulated by MYB, bHLH, WRKY, AP2/EREBP, C2C2, NAC, and C2H2 transcription factors (TFs). Furthermore, some candidate genes required for auxin, ethylene and abscisic acid signal transductions were also identified which are probably involved in berry development and flavonoid biosynthesis in response to enhanced sunlight irradiation. Taken together, this study provides a valuable overview of the light-induced phenolic metabolism and transcriptome changes, especially the dynamic responses of TFs and signaling components of phytohormones, and contributes to the further understanding of sunlight-responsive phenolic biosynthesis regulation in grape berries.