Human amniotic mesenchymal stem cells-derived conditioned medium and exosomes alleviate oxidative stress-induced retinal degeneration by activating PI3K/Akt/FoxO3 pathway.

Age-related macular degeneration (AMD) is the leading cause of vision loss among the elderly, which is primarily attributed to oxidative stress-induced damage to the retinal pigment epithelium (RPE). Human amniotic mesenchymal stem cells (hAMSC) were considered to be one of the most promising stem cells for clinical application due to their low immunogenicity, tissue repair ability, pluripotent potential and potent paracrine effects. The conditional medium (hAMSC-CM) and exosomes (hAMSC-exo) derived from hAMSC, as mediators of intercellular communication, play an important role in the treatment of retinal diseases, but their effect and mechanism on oxidative stress-induced retinal degeneration are not explored. Here, we reported that hAMSC-CM alleviated H2O2-induced ARPE-19 cell death through inhibiting mitochondrial-mediated apoptosis pathway in vitro. The overproduction of reactive oxygen species (ROS), alteration in mitochondrial morphology, loss of mitochondrial membrane potential and elevation of Bax/Bcl2 ratio in ARPE-19 cells under oxidative stress were efficiently reversed by hAMSC-CM. Moreover, it was found that hAMSC-CM protected cells against oxidative injury via PI3K/Akt/FoxO3 signaling. Intriguingly, exosome inhibitor GW4869 alleviated the inhibitory effect of hAMSC-CM on H2O2-induced decrease in cell viability of ARPE-19 cells. We further demonstrated that hAMSC-exo exerted the similar protective effect on ARPE-19 cells against oxidative damage as hAMSC-CM. Additionally, both hAMSC-CM and hAMSC-exo ameliorated sodium iodate-induced deterioration of RPE and retinal damage in vivo. These results first indicate that hAMSC-CM and hAMSC-exo protect RPE cells from oxidative damage by regulating PI3K/Akt/FoxO3 pathway, suggesting hAMSC-CM and hAMSC-exo will be a promising cell-free therapy for the treatment of AMD in the future.

CD38 deficiency promotes skeletal muscle and brown adipose tissue energy expenditure through activating NAD+-Sirt1-PGC1α signaling pathway.

Obesity is a metabolic syndrome characterized by abnormal lipid deposition and energy imbalance. CD38 is a single-chain transmembrane glycoprotein widely expressed in a variety of cell types. The roles of skeletal muscle and brown fat in CD38 deficiency under HFD-induced obesity remain unknown. In this study, we established obesity model with HFD and examined the changes in metabolites with metabonomics. Our results showed that CD38 expression was increased in muscle and brown fat after HFD treatment. Moreover, the results of metabonomics showed that CD38 deficiency significantly altered the metabolites in energy metabolism, cofactor generation, and redox homeostasis. Furthermore, CD38 deficiency reduced the expressions of NADPH oxidase 2 and FASN in mRNA level. We found that the expressions of Sirt1, Sirt3, and PGC1α were upregulated in CD38-deficient muscle tissue. In brown fat, the Sirt1-3, cell death inducing DFFA-like effector A, ELOVL3, and Dio2 expressions were increased in CD38-deficient mice. Our results showed the uncoupling protein 1 expression was upregulated. And NAD+ supplementation increased the expression of Sirt1 and PGC1α after palmitic acid treatment. Taken together, our results demonstrated that the protection of CD38 deficiency on HFD-induced obesity was related to the inhibition of oxidative stress and increasing energy expenditure via activating NAD+/Sirtuins signaling pathways in muscle and brown fat.

CD38 Deficiency Alleviates Diabetic Cardiomyopathy by Coordinately Inhibiting Pyroptosis and Apoptosis.

Diabetic cardiomyopathy is one of the diabetes mellitus-induced cardiovascular complications that can result in heart failure in severe cases, which is characterized by cardiomyocyte apoptosis, local inflammation, oxidative stress, and myocardial fibrosis. CD38, a main hydrolase of NAD+ in mammals, plays an important role in various cardiovascular diseases, according to our previous studies. However, the role of CD38 in diabetes-induced cardiomyopathy is still unknown. Here, we report that global deletion of the CD38 gene significantly prevented diabetic cardiomyopathy induced by high-fat diet plus streptozotocin (STZ) injection in CD38 knockout (CD38-KO) mice. We observed that CD38 expression was up-regulated, whereas the expression of Sirt3 was down-regulated in the hearts of diabetic mice. CD38 deficiency significantly promoted glucose metabolism and improved cardiac functions, exemplified by increased left ventricular ejection fraction and fractional shortening. In addition, we observed that CD38 deficiency markedly decreased diabetes or high glucose and palmitic acid (HG + PA)-induced pyroptosis and apoptosis in CD38 knockout hearts or cardiomyocytes, respectively. Furthermore, we found that the expression levels of Sirt3, mainly located in mitochondria, and its target gene FOXO3a were increased in CD38-deficient hearts and cardiomyocytes with CD38 knockdown under diabetic induction conditions. In conclusion, we demonstrated that CD38 deficiency protected mice from diabetes-induced diabetic cardiomyopathy by reducing pyroptosis and apoptosis via activating NAD+/Sirt3/FOXO3a signaling pathways.

Electrocardiographic localization of peripherally inserted central catheter tip position in critically ill patients with advanced cancer: An application study.

BACKGROUND: We compared the methods of electrocardiogram (ECG) and X-ray localization of the peripherally inserted central catheter (PICC) tip position, in order to find a more convenient, practical, and safe method. OBJECTIVE: To investigate the value of applying electrocardiographic localization of the PICC tip position in critically ill patients with advanced cancer in Hebei Province, China. METHOD: Enrolled 137 advanced cancers requiring PICC placement. The position of the catheter tip was localized with the bedside electrocardiogram in real time. Then, the localization was performed using a chest X-ray (the gold standard). The accuracy of electrocardiographic location was checked. RESULTS: Specific P waves were observed in 130 patients. No change in the P waves was observed for the remaining seven patients. The age of the latter group of patients was more advanced (87.29 [5.15] years), a significant difference to that of the 130 patients with specific P waves (71.58 [14.84] years) (t = -6.704, p < .001). Specific P waves not only involve ascendance in P waves but also ascendance in QRS waves. CONCLUSIONS: The use of an ECG to localize the PICC tip in critically ill patients with advanced cancer may replace the unnecessary use of chest X-rays. Specific P waves not only involve an increase in P waves but also an increase in QRS waves. If there is no change in the P wave, a chest X-ray film must be obtained. In elderly patients, because there is a possibility of catheter tip malposition, a comprehensive evaluation should be performed before surgery.

Effect of Mn2+ on the phosphorus removal and bioflocculation under anoxic condition.

Manganese ion (Mn2+) generated from metallurgical, steel making and chemical industries enters sewage treatment plants and affects the sludge activity and flocculation. The effect of Mn2+ on the removal of chemical oxygen demand (COD) and total phosphorus (TP) and sludge activity were investigated in anoxic zone of an anaerobic/anoxic/oxic (A2O) process. The compositions and structures of extracellular polymeric substances (EPS) were characterized using three-dimensional excitation emission matrix fluorescence spectroscopy (3D-EEM), X-ray photoelectron spectroscopy (XPS) and Fourier transform infrared spectroscopy (FTIR) to reveal the relationship among Mn2+, EPS and sludge flocculation. The results showed that low concentration of Mn2+ (<5 mg/L) improved removal efficiencies of COD and TP and increased the activity of alkaline phosphatase, acid phosphatase and dehydrogenase. Meanwhile, the addition of Mn2+ increased total EPS, sludge contact angle, Zeta potential and sludge particle size, and thus enhanced sludge flocculation. However, high concentration of Mn2+ (>10 mg/L) hindered microbial flocculation and reduced removal efficiencies of the pollutants. When Mn2+was 5 mg/L, removal efficiencies of COD and TP reached 65% and 90%, respectively. Sludge flocculation was the best and SVI was 70.56 mL/g. The changes of Mn2+ concentration caused deviation of groups' compositions in LB-EPS and TB-EPS, where the main components were always protein (PN) and polysaccharide (PS). The addition of Mn2+ resulted in the degradation of humic acids. However, it did not give rise to significant morphology changes of EPS.

Nicaraven inhibits TNFα-induced endothelial activation and inflammation through suppression of NF-κB signaling pathway.

Inflammation-induced activation and dysfunction of endothelial cells play an important role in the pathology of multiple vascular diseases. Nicaraven, a potent hydroxyl radical scavenger, has recently been found to have anti-inflammatory roles; however, the mechanism of its action is not fully understood. Here we investigated the effects of Nicaraven on tumor necrosis factor α (TNFα) - induced inflammatory response in human umbilical vein endothelial cells and we explore the underlying mechanisms related to the nuclear factor-κB (NF-κB) signaling pathway. Our results showed that Nicaraven significantly reduced the reactive oxygen species production after TNFα stimulation. Nicaraven suppressed TNFα-induced mRNA expression of multiple adhesion molecules and pro-inflammatory cytokines, including vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin, MCP-1, TNFα, interleukin-1ß (IL-1ß), IL-6, and IL-8. In addition, Nicaraven inhibited monocyte adhesion and reduced the protein levels of VCAM-1 and ICAM-1. Mechanistically, Nicaraven prevented TNFα-induced activation of NF-κB signaling pathway by suppressing the phosphorylation of NF-κB p65, IκBα, and IκB kinase (IKK)α/ß, stabilizing IκBα, and inhibiting the translocation of p65 from cytosol to nucleus. Finally, we showed that Nicaraven improved the functions of endothelial cells, seen as the upregulation of endothelial nitric oxide synthase and increased nitric oxide levels. Our findings indicated that Nicaraven effectively inhibits TNFα-induced endothelial activation and inflammatory response at least partly through inhibiting NF-κB signaling pathway.

Effects of Al3+ on the microstructure and bioflocculation of anoxic sludge.

The aluminum ions generated from mining aluminum, electrolytic aluminum and the industrial production of aluminum-based coagulants (such as AlCl3 and Al2(SO4)3) enter sewage treatment plants and interact with activated sludges. An anaerobic/anoxic/oxic (A2O) process was used to reveal the effects of Al3+ on the pollutant removal efficiencies, bioflocculation and the microstructure of sludge. The results showed that a low concentration of Al3+ improved the pollutant removal efficiencies and increased the sludge particle size. However, a high concentration of Al3+ hindered microbial flocculation and reduced the pollutant removal efficiencies. With a 10 mg/L Al3+ addition, the chemical oxygen demand (COD), total nitrogen (TN) and NH4+-N increased by 3%, 16% and 27%, and reached as high as 68%, 60% and 87%, respectively. At the same time, the dehydrogenase activity, flocculation ability (FA) and contact angle of the sludge reached their maximum levels at 41.3 mg/L/hr, 45% and 79.63°, respectively. The specific surface area of the sludge decreased to 7.084 m2/g and the sludge pore size distribution shifted to concentrate in the mesoporous range. Most of Al3+ was adsorbed on the surface of sludge, changing the physicochemical properties and physical structure of the sludge.

FKBP12.6 protects heart from AngII-induced hypertrophy through inhibiting Ca2+ /calmodulin-mediated signalling pathways in vivo and in vitro.

We previously observed that disruption of FK506-binding protein 12.6 (FKBP12.6) gene resulted in cardiac hypertrophy in male mice. Studies showed that overexpression of FKBP12.6 attenuated thoracic aortic constriction (TAC)-induced cardiac hypertrophy in mice, whereas the adenovirus-mediated overexpression of FKBP12.6 induced hypertrophy and apoptosis in cultured neonatal cardiomyocytes, indicating that the role of FKBP12.6 in cardiac hypertrophy is still controversial. In this study, we aimed to investigate the roles and mechanisms of FKBP12.6 in angiotensin II (AngII)-induced cardiac hypertrophy using various transgenic mouse models in vivo and in vitro. FKBP12.6 knockout (FKBP12.6-/- ) mice and cardiac-specific FKBP12.6 overexpressing (FKBP12.6 TG) mice were infused with AngII (1500 ng/kg/min) for 14 days subcutaneously by implantation of an osmotic mini-pump. The results showed that FKBP12.6 deficiency aggravated AngII-induced cardiac hypertrophy, while cardiac-specific overexpression of FKBP12.6 prevented hearts from the hypertrophic response to AngII stimulation in mice. Consistent with the results in vivo, overexpression of FKBP12.6 in H9c2 cells significantly repressed the AngII-induced cardiomyocyte hypertrophy, seen as reductions in the cell sizes and the expressions of hypertrophic genes. Furthermore, we demonstrated that the protection of FKBP12.6 on AngII-induced cardiac hypertrophy was involved in reducing the concentration of intracellular Ca2+ ([Ca2+ ]i), in which the protein significantly inhibited the key Ca2+ /calmodulin-dependent signalling pathways such as calcineurin/cardiac form of nuclear factor of activated T cells 4 (NFATc4), calmodulin kinaseII (CaMKII)/MEF-2, AKT/Glycogen synthase kinase 3ß (GSK3ß)/NFATc4 and AKT/mTOR signalling pathways. Our study demonstrated that FKBP12.6 protects heart from AngII-induced cardiac hypertrophy through inhibiting Ca2+ /calmodulin-mediated signalling pathways.

CD38 Deficiency Protects Heart from High Fat Diet-Induced Oxidative Stress Via Activating Sirt3/FOXO3 Pathway.

BACKGROUND/AIMS: Previous studies showed that CD38 deficiency protected heart from ischemia/reperfusion injury and high fat diet (HFD)-induced obesity in mice. However, the role of CD38 in HFD-induced heart injury remains unclear. In the present study, we have investigated the effects and mechanisms of CD38 deficiency on HFD-induced heart injury. METHODS: The metabolites in heart from wild type (WT) and CD38 knockout (CD38-/-) mice were examined using metabolomics analysis. Cell viability, lactate hydrogenase (LDH) release, super oxide dismutase (SOD) activity, reactive oxygen species (ROS) production, triglyceride concentration and gene expression were examined by biochemical analysis and QPCR. RESULTS: Our results revealed that CD38 deficiency significantly elevated the intracellular glutathione (GSH) concentration and GSH/GSSG ratio, decreased the contents of free fatty acids and increased intracellular NAD+ level in heart from CD38-/- mice fed with HFD. In addition, in vitro knockdown of CD38 significantly attenuated OA-induced cellular injury, ROS production and lipid synthesis. Furthermore, the expression of mitochondrial deacetylase Sirt3 as well as its target genes FOXO3 and SOD2 were markedly upregulated in the H9C2 cell lines after OA stimulation. In contrast, the expressions of NOX2 and NOX4 were significantly decreased in the cells after OA stimulation. CONCLUSION: Our results demonstrated that CD38 deficiency protected heart from HFD-induced oxidative stress via activating Sirt3/FOXO3-mediated anti-oxidative stress pathway.

Simultaneous determination of glaucocalyxin A and glaucocalyxin B in rat plasma by LC-MS/MS and its application to a pharmacokinetic study after oral administration of Rabdosia japonica extract.

A specific and sensitive liquid chromatography tandem mass spectrometry (LC-MS/MS) method was developed and validated for the analysis of glaucocalyxin A and glaucocalyxin B in rat plasma using praeruptorin A as an internal standard. Separation was performed on a Hypurity C18 column (2.1 × 50 mm, 5 µm) with isocratic elution using 0.2% formic acid in water-acetonitrile (20:80, v/v). Mass spectrometric detection was conducted using selected reaction monitoring via an electrospray ionization source. Both analytes exhibited good linearity within their concentration ranges (r2 > 0.9932). The lower limit of quantitation of glaucocalyxin A and glaucocalyxin B was 1.10 ng/mL. Intra- and inter-day precision exhibited an RSD within 14.5%, and the accuracy (RE) ranged from -12.1 to 15.0% at the lower limit of quantitation and three quality control levels. The developed assay was successfully applied to a pharmacokinetic study of glaucocalyxin A and glaucocalyxin B in rats after oral administration of Rabdosia japonica extract.

CD38 promotes angiotensin II-induced cardiac hypertrophy.

Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2 O2 -induced injury and hypoxia/reoxygenation-induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored. Here, we investigated the roles and mechanisms of CD38 in angiotensin II (Ang-II)-induced cardiac hypertrophy. Following 14 days of Ang-II infusion with osmotic mini-pumps, a comparable hypertension was generated in both of CD38 knockout and wild-type mice. However, the cardiac hypertrophy and fibrosis were much more severe in wild-type mice compared with CD38 knockout mice. Consistently, RNAi-induced knockdown of CD38 decreased the gene expressions of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and reactive oxygen species generation in Ang-II-stimulated H9c2 cells. In addition, the expression of SIRT3 was elevated in CD38 knockdown H9c2 cells, in which SIRT3 may further activate the FOXO3 antioxidant pathway. The intracellular Ca2+ release induced by Ang-II markedly decreased in CD38 knockdown H9c2 cells, which might be associated with the decrease of nuclear translocation of NFATc4 and inhibition of ERK/AKT phosphorylation. We concluded that CD38 plays an essential role in cardiac hypertrophy probably via inhibition of SIRT3 expression and activation of Ca2+ -NFAT signalling pathway. Thus, CD38 may be a novel target for treating cardiac hypertrophy.

Inhibition of NAMPT aggravates high fat diet-induced hepatic steatosis in mice through regulating Sirt1/AMPKα/SREBP1 signaling pathway.

BACKGROUND: Nonalcoholic fatty liver disease is one of the most common liver diseases in the world and is a typical hepatic manifestation of metabolic syndrome which is characterized with lipid accumulation in liver. Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals. The aim of this study was to investigate the effects of NAMPT on high fat diet-induced hepatic steatosis. METHODS: Hepatic steatosis model was induced by high fat diet (HFD) in C57BL/6 mice in vivo. HepG2 and Hep1-6 hepatocytes were transfected with NAMPT vector plasmid or treated with NAMPT inhibitor FK866 and then incubated with oleic acid. Lipids accumulation was examined by HE staining or oil red staining. Quantitative RT-PCR and Western blot were used to measure expressions of the genes involved in lipogenic synthesis. RESULTS: FK866 significantly promoted liver steatosis in the mice fed with HFD and hepatic lipid accumulation in vitro, accompanied by the increases of the expressions of lipogenic genes such as sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FASN). Nicotinamide mononucleotide (NMN) and NAD+ significantly rescued the actions of FK866 in vitro. In contrast, overexpression of NAMPT in HepG2 and Hep1-6 hepatocytes ameliorated hepatic lipid accumulation. In addition, FK866 decreased the protein levels of Sirt1 and phospho-AMPKα in liver of the HFD fed mice. Furthermore, Resveratrol, a Sirt1 activator, significantly reduced lipogenic gene expressions, while EX-527, a Sirt1 specific inhibitor, had the opposite effects. CONCLUSION: Our results demonstrated that inhibition of NAMPT aggravated the HFD- or oleic acid-induced hepatic steatosis through suppressing Sirt1-mediated signaling pathway. On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC. On the other hand, the reduced Sirt1 activity alleviated the activation of AMPKα to further enhance SREBP1 activities.

Yeast Surface Display of Escherichia coli Enterotoxin and Its Effects of Intestinal Microflora and Mucosal Immunity.

Enterotoxigenic Escherichia coli (ETEC) is a significant cause of infectious diarrhea in animals. In this study, yeast surface display technology was employed to investigate the effects of ETEC enterotoxin fusion protein on the intestinal flora and mucosal immunity of rats. ETEC estA, estB, and eltAB (heat-labile and heat-stable toxins) were expressed on the surface of yeast. Rats were divided into normal saline, yeast and display yeast groups. Fecal and jejunal content samples were collected on the 7th, 14th, and 21st days. Rats were then fed ETEC for 3 days before again collecting these samples. Levels of SIgA, IL-2, IL-4, IFN-γ, and microbial population density and diversity were documented by ELISA, T-RFLP and real-time PCR. The results demonstrated that estA, estB, and eltAB fusion proteins were expressed on the surface of yeast. Following ETEC challenge, levels of SIgA, IL-2, IL-4, IFN-γ, and, the numbers and variety of intestinal microbes were significantly increased in rats receiving display yeast and yeast. These factors were significantly decreased in rats given normal saline and yeast. Our results indicate that display yeast and yeast can increase the number and diversity of intestinal microbes in rats and improve intestinal immune function. After ETEC challenge, the display yeast can better maintain the balance of intestinal bacteria and mucosal immunity.

miR-223 Regulates Adipogenic and Osteogenic Differentiation of Mesenchymal Stem Cells Through a C/EBPs/miR-223/FGFR2 Regulatory Feedback Loop.

Several miRNAs have recently been identified to regulate adipocyte or osteoblast differentiation or both. In this study, miR-223 was found to be involved in the reciprocal regulation of adipocyte and osteoblast differentiation. miR-223 was induced in primary cultured mouse marrow stromal cell, mesenchymal line C3H10T1/2 and stromal line ST2 after adipogenic treatment. Conversely, it was reduced in preosteoblast MC3T3-E1 after osteogenic treatment. Supplementing miR-223 levels using synthetic miR-223 mimics significantly suppressed the growth of the C3H10T1/2 and ST2 cells and induced the progenitor cells to fully differentiate into adipocytes, along with induction of adipocyte-specific transcription factors peroxisome proliferator-activated receptor γ, CCAAT/enhancer binding protein-α (C/EBPα), and marker genes aP2 and adipsin. By contrast, depletion of the endogenous miR-223 using synthetic miR-223 inhibitor repressed the progenitor cells to differentiate. The effects of miR-223 on adipocyte formation from ST2 cells were also demonstrated by using lentivirus that overexpresses miR-223. Conversely, supplementing miR-223 blocked ST2 to differentiate into osteoblasts. Fibroblast growth factor receptor 2 (Fgfr2), a critical regulator of osteoblast, was shown to be a direct target of miR-223 by using dual luciferase reporter assay. Knockdown of Fgfr2 in C3H10T1/2 downregulated phosphorylation of ERK1/2 and upregulated expression of C/EBPα and dramatically enhanced the differentiation of the cells into adipocytes. Further investigation of mechanisms that control miR-223 expression demonstrated that C/EBPs induced miR-223 expression through binding to the promoter regions of the miR-223. Taken together, our study provides evidences that miR-223 regulates adipocyte and osteoblast differentiation through a novel C/EBPs/miR-223/FGFR2 regulatory feedback loop.

Simultaneous determination of cucurbitacin IIa and cucurbitacin IIb of Hemsleya amabilis by HPLC-MS/MS and their pharmacokinetic study in normal and indomethacin-induced rats.

A selective and sensitive HPLC-MS/MS method was developed for the simultaneous determination of cucurbitacin IIa (cuIIa) and cucurbitacin IIb (cuIIb), the major bioactive cucurbitacins of Hemsleya amabilis, in rat plasma using euphadienol as internal standard (IS). After liquid-liquid extraction with dichloromethane, separation was achieved on a Syncronis HPLC C18 column (150 mm × 4.6 mm, 5 µm) using an isocratic mobile phase system consisting of acetonitrile-water (85:15, v/v) at a flow rate of 0.6 mL/min with a split ratio of 1:2. Detection was performed on a TSQ Quantum Ultra mass spectrometer equipped with an positive-ion electrospray ionization source. The lower limits of quantification (LLOQs) were 0.25 and 0.15 ng/mL for cuIIa and cuIIb, respectively. The intra- and inter-day precision was <11.5% for the LLOQs and each quality control level of the analytes, and accuracy was between -9.1 and 7.6%. The extraction recoveries of the analytes and IS from rat plasma were all >87.1%. The method was fully validated and applied to compare the pharmacokinetic profiles of the two cucurbitacins in rat plasma after oral administration of H. amabilis extract between normal and indomethacin-induced rats. Copyright © 2016 John Wiley & Sons, Ltd.

Controlled establishment of advanced local high-entropy NiCoMnFe-based layered double hydroxide for zinc batteries and low-temperature supercapacitors.

The development of high-performance electrodes is essential for improving the charge storage performance of rechargeable devices. In this study, local high-entropy C, N co-doped NiCoMnFe-based layered double hydroxide (C/N-NiCoMnFe-LDH, C/N-NCMF) were designed using a novel method. Multi-component synergistic effects can dramatically modulate the surface electron density, crystalline structure, and band-gap of the electrode. Thus, the electrical conductivity, electron transfer, and affinity for the electrolyte can be optimized. Additionally, the C/N-NCMF yielded a high specific capacitance (1454F·g-1) at 1 A·g-1. The electrode also exhibited excellent cycling stability, with 62 % capacitance retention after 5000 cycles. Moreover, the assembled Zn||C/N-NCMF battery and the C/N-NCMF//AC hybrid supercapacitor yielded excellent energy densities of 63.1 and 35.4 Wh·kg-1 at power densities of 1000 and 825 W·kg-1, and superior cycling performance with 69 % and 88.7 % capacitance retention after 1000 and 30,000 cycles, respectively. Furthermore, the electrode maintained high electrochemical activity and stability and ensured high energy density, power density, and cycling stability of the rechargeable devices even at a low temperature (-20 °C). This study paves a new pathway for regulating the electrochemical performance of LDH-based electrodes.

Designed Synthesis and Electrochemical Performance Regulation of the Hierarchical Hollow Structure Cu2S/Cu7S4/NC Anode for Hybrid Supercapacitors.

Copper-based compounds have attracted increasing attention as electrode materials for rechargeable devices, but their poor conductivity and insufficient stability inhibit their further development. Herein, an effective method has been proposed to improve the electrochemical properties of the copper-based electrodes by coating carbon materials and generating unique micro/nanostructures. The prepared Cu2S/Cu7S4/NC with hierarchical hollow structure possesses excellent electrochemical performance, attributing to the composition and structure optimization. The superior charge storage performance has been assessed by theoretical and experimental research. Specifically, the Cu2S/Cu7S4/NC exhibits remarkably higher electrical conductivity and lower adsorption-free energy for O* and OH* than those of Cu2O. Moreover, the Cu2S/Cu7S4/NC delivers a high specific capacitance of 1261.3 F·g-1 at the current density of 1 A·g-1 and also has great rate performance at higher current densities, which are much better than those of the Cu2O nanocubes. In addition, the assembled hybrid supercapacitor using Cu2S/Cu7S4/NC as the anode exhibits great energy density, power density, and cycling stability. This study has proposed a novel and feasible method for the synthesis of high-performance copper-based electrodes and their electrochemical performance regulation, which is of great significance for the advancement of high-quality electrode materials and rechargeable devices.

Human amniotic MSCs-mediated anti-inflammation of CD206hiIL-10hi macrophages alleviates isoproterenol-induced ventricular remodeling in mice.

BACKGROUND: Human amniotic mesenchymal stem cells (hAMSCs) derived from amniotic membrane have multilineage differentiation, immunosuppressive, and anti-inflammation which makes them suitable for the treatment of various diseases. OBJECTIVE: This study aimed to explore the therapeutic effect and molecular mechanism of hAMSCs in ventricular remodeling (VR). METHODS: hAMSCs were characterized by a series of experiments such as flow cytometric analysis, immunofluorescence, differentiative induction and tumorigenicity. Mouse VR model was induced by isoproterenol (ISO) peritoneally, and the therapeutic effects and the potential mechanisms of hAMSCs transplantation were evaluated by echocardiography, carboxy fluorescein diacetate succinimidyl ester (CFSE) labeled cell tracing, histochemistry, qRT-PCR and western blot analysis. The co-culturing experiments were carried out for further exploring the mechanisms of hAMSCs-derived conditioned medium (CM) on macrophage polarization and fibroblast fibrosis in vitro. RESULTS: hAMSCs transplantation significantly alleviated ISO-induced VR including cardiac hypertrophy and fibrosis with the improvements of cardiac functions. CFSE labeled hAMSCs kept an undifferentiated state in heart, indicating that hAMSCs-mediated the improvement of ISO-induced VR might be related to their paracrine effects. hAMSCs markedly inhibited ISO-induced inflammation and fibrosis, seen as the increase of M2 macrophage infiltration and the expressions of CD206 and IL-10, and the decreases of CD86, iNOS, COL3 and αSMA expressions in heart, suggesting that hAMSCs transplantation promoted the polarization of M2 macrophages and inhibited the polarization of M1 macrophages. Mechanically, hAMSCs-derived CM significantly increased the expressions of CD206, IL-10, Arg-1 and reduced the expressions of iNOS and IL-6 in RAW264.7 macrophages in vitro. Interestingly, RAW264.7-CM remarkably promoted the expressions of anti-inflammatory factors such as IL-10, IDO, and COX2 in hAMSCs. Furthermore, the CM derived from hAMSCs pretreated with RAW264.7-CM markedly inhibited the expressions of fibrogenesis genes such as αSMA and COL3 in 3T3 cells. CONCLUSION: Our results demonstrated that hAMSCs effectively alleviated ISO-induced cardiac hypertrophy and fibrosis, and improved the cardiac functions in mice, and the underlying mechanisms might be related to inhibiting the inflammation and fibrosis during the ventricular remodeling through promoting the polarization of CD206hiIL-10hi macrophages in heart tissues. Our study strongly suggested that by taking the advantages of the potent immunosuppressive and anti-inflammatory effects, hAMSCs may provide an alternative therapeutic approach for prevention and treatment of VR clinically.

Delicate Design of ZnS@In2S3 Core-Shell Structures with Modulated Photocatalytic Performance under Simulated Sunlight Irradiation.

ZnS@In2S3 core-shell structures with high photocatalytic activity have been delicately designed and synthesized. The unique structure and synergistic effects of the composites have an important influence on the improvement of photocatalytic activity. The photocatalytic activity has been studied by photodegrading individual eosin B (EB) and the mixture solution consisting of eosin B and rhodamine B (EB-RhB) in the presence of hydrogen peroxide (H2O2) under simulated sunlight irradiation. The results show that all of the photocatalysts with different contents of In2S3 exhibit enhanced catalytic activity compared to pure ZnS for the degradation of EB and EB-RhB solution. When the theoretical molar ratio of ZnS to In2S3 was 1:0.5, the composite presents the highest photocatalytic efficiency, which could eliminate more than 98% of EB and 94% of EB-RhB. At the same time, after five cycles of photocatalytic tests, the photocatalytic efficiency could be about 96% for the degradation of the EB solution, and relatively high photocatalytic activity could also be obtained for the degradation of the EB-RhB mixed solution. This work has proposed a facile synthetic process to realize the controlled preparation of core-shell ZnS@In2S3 composites with effectively modulated structures and compositions, and the composites have also proved to be high-efficiency photocatalysts for the disposal of complicated pollutants.

Electrochemical Performance of Corn Waste Derived Carbon Electrodes Based on the Intrinsic Biomass Properties.

The exploration of cost-effective and sustainable biomass-derived carbon materials as electrodes for energy conversion and storage has gained extensive attention in recent research studies. However, the selection of the biomass and the electrochemical performance regulation of the derived biochar, as well as their interrelationship still remain challenging for practical application. Herein, corn wastes with high carbon content (>40%), corn cob and corn silk, were selected as precursors for the preparation of high value-added and high yield carbon materials via a modified synthetic process. Uniquely, this work put emphasis on the theoretical and experimental investigations of how the biomass properties influence the composition and nanostructure regulation, the electrolyte ion adsorption free energy, and the electrical conductivity of the derived carbon materials as well as their electrochemical performance optimization. Owing to the favorable specific surface area, the hierarchical porous structure, and the diverse elemental distribution, corn cob and corn silk derived carbon materials (CBC and SBC) present great potential as promising electrodes for alkaline aqueous zinc batteries and supercapacitors. The assembled CBC//Zn and SBC//Zn zinc batteries deliver high energy densities of 63.0 Wh kg-1 and 39.1 Wh kg-1 at a power density of 575 W kg-1, with excellent cycling performance of 91.1% and 84.3% capacitance retention after 10,000 cycles. As for the assembled symmetric supercapacitors, high energy densities of 14.9 Wh kg-1 and 13.6 Wh kg-1, and superior long-term cycling stability of 99.3% and 96.6% capacitance retention after 20,000 cycles could be achieved. This study highlights the advantages of utilizing corn cob and corn silk as carbon sources on the designed synthesis of carbon electrodes, and presents a meaningful perspective in the investigation of biomass-derived carbon materials and their potential applications in rechargeable devices.