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Left ventricular hypertrophy (LVH) is a pivotal manifestation of hypertensive organ damage associated with an increased cardiovascular risk. However, early diagnostic biomarkers for assessing LVH in patients with hypertension (HT) remain indefinite. Here, multiple bioinformatics tools combined with an experimental verification strategy were used to identify blood biomarkers for hypertensive LVH. GSE74144 mRNA expression profiles were downloaded from the Gene Expression Omnibus (GEO) database to screen candidate biomarkers, which were used to perform weighted gene co-expression network analysis (WGCNA) and establish the least absolute shrinkage and selection operator (LASSO) regression model, combined with support vector machine-recursive feature elimination (SVM-RFE) algorithms. Finally, the potential blood biomarkers were verified in an animal model. A total of 142 hub genes in peripheral blood leukocytes were identified between HT with LVH and HT without LVH, which were mainly involved in the ATP metabolic process, oxidative phosphorylation, and mitochondrial structure and function. Notably, lysosomal associated transmembrane protein 5 (LAPTM5) was identified as the potential diagnostic marker of hypertensive LVH, which showed strong correlations with diverse marker sets of reactive oxygen species (ROS) and autophagy. RT-PCR validation of blood samples and cardiac magnetic resonance imaging (CMRI) showed that the expression of LAPTM5 was significantly higher in the HT with LVH model than in normal controls, LAPTM5 demonstrated a positive association with the left ventricle wall thickness as well as electrocardiogram (ECG) parameters widths of the QRS complex and QTc interval. In conclusion, LAPTM5 may be a potential biomarker for the diagnosis of LVH in patients with HT, and it can provide new insights for future studies on the occurrence and the molecular mechanisms of hypertensive LVH.

Macrophage-mediated inflammation plays an important role in hypertensive cardiac remodeling, whereas effective pharmacological treatments targeting cardiac inflammation remain unclear. Lipoprotein-associated phospholipase A2 (Lp-PLA2) contributes to vascular inflammation-related diseases by mediating macrophage migration and activation. Darapladib, the most advanced Lp-PLA2 inhibitor, has been evaluated in phase III trials in atherosclerosis patients. However, the role of darapladib in inhibiting hypertensive cardiac fibrosis remains unknown. Using a murine angiotensin II (Ang II) infusion-induced hypertension model, we found that Pla2g7 (the gene of Lp-PLA2) was the only upregulated PLA2 gene detected in hypertensive cardiac tissue, and it was primarily localized in heart-infiltrating macrophages. As expected, darapladib significantly prevented Ang II-induced cardiac fibrosis, ventricular hypertrophy, and cardiac dysfunction, with potent abatement of macrophage infiltration and inflammatory response. RNA sequencing revealed that darapladib strongly downregulated the expression of genes and signaling pathways related to inflammation, extracellular matrix, and proliferation. Moreover, darapladib substantially reduced the Ang II infusion-induced expression of nucleotide-binding oligomerization domain-like receptor with pyrin domain 3 (NLRP3) and interleukin (IL)-1β and markedly attenuated caspase-1 activation in cardiac tissues. Furthermore, darapladib ameliorated Ang II-stimulated macrophage migration and IL-1β secretion in macrophages by blocking NLRP3 inflammasome activation. Darapladib also effectively blocked macrophage-mediated transformation of fibroblasts into myofibroblasts by inhibiting the activation of the NLRP3 inflammasome in macrophages. Overall, our study identifies a novel anti-inflammatory and anti-cardiac fibrosis role of darapladib in Lp-PLA2 inhibition, elucidating the protective effects of suppressing NLRP3 inflammasome activation. Lp-PLA2 inhibition by darapladib represents a novel therapeutic strategy for hypertensive cardiac damage treatment.

Tubb4b (tubulin beta-4b chain) is essential for spermatogonia cell growth and development as a microtubule network protein, and its regulatory mechanism remains to be studied. To deeply understand the role of Tubb4b in spermatogonia cell proliferation and the cell cycle, we studied the role of spermatogonia in the control and TUBB4B-KO groups in different cell cycle phases by flow cytometry. We detected the crucial protein CDK2 in each stage by qRT–PCR and Western blotting. The results showed that under the induction of serum starvation, thymidine, and nocodazole under different conditions, mouse spermatogonia remained in the G0-G1 phase, S phase, and G2-M phase, respectively, and the change in the spermatogonia cycle in the Tubb4b-KO group was slower than that in the control group. In the study of cycle synchronization, it was found that the mRNA level of Cdk2 in the G2-M phase increased significantly (P Tubb4b-KO group, the mRNA level of Cdk2 increased significantly in the G0-G1 phase (P

Semaphorin 4C (SEMA4C), is an important regulator of axonal guidance and aggravates tumor development. However, the roles and prognostic value of SEMA4C in colorectal cancer (CRC) remain unclear. Here, bioinformatics analyses of transcriptome data from multiple CRC patient datasets and immunohistochemical staining of a CRC tissue microarray (TMA) (n=83) showed that SEMA4C mRNA and protein expression were higher in CRC tissues than normal colorectal tissues. SEMA4C mRNA and protein expression correlated with pathologic stage and metastasis in CRC patients. Higher SEMA4C expression was associated with shorter overall survival, consensus molecular subtype 4 (CMS4), and DNA hypomethylation of SEMA4C in CRC patients. Multivariate Cox regression analyses revealed that SEMA4C expression was an independent prognostic predictor in CRC patients. Gene set expression analysis (GSEA) illustrated that SEMA4C expression had remarkable correlations with epithelial-mesenchymal transition (EMT) as well as hedgehog, Wnt/β-catenin, TGF-β, and Notch signaling pathways. Receiver operating characteristic (ROC) curve analysis demonstrated that SEMA4C expression accurately distinguished between the CMS4 and CMS1-3 subtypes of CRC patients. By inhibiting EMT, SEMA4C silencing reduced in vitro proliferation, migration, and invasion by CRC cells. These findings suggest that SEMA4C is a CMS4-associated gene that enhances CRC progression by inducing EMT.

To explore the role of jasmonic acid in seed germination of rice under Cd stress, the growth indices of JJ818 and NJ9108 under the bud stage were measured for identifying study the molecular mechanism of variety difference in cadmium tolerance. The tolerant variety JJ818 and the sensitive variety NJ9108 were treated under 150 µmol·L− 1 Cd concentration, methyl jasmonate (MeJA), and Ibuprofen (IBU) alone or in combination. The germination rate, root length, bud length, soluble protein content, soluble sugar content, and sugar components, α-amylase activity, and its related gene expression were measured. The results showed that the root length of the two rice materials were significantly inhibited during germination under the Cd treatment, however, the germination rate and shoot length had little affected. MeJA decreased the germination rate, root length and shoot length, and the contents of soluble sugar and sugar components and α-amylase activity as well. However, IBU treatment showed the opposite trend. Cd treatment also decreased the expression of the αAmy and RL1, and the accompanying changes of up-regulated the gene expression of JIOsPR10, OsLOX1, and OsLOX4 related to synthesizing jasmonic acid(JA). The results showed that JA negatively regulates the cadmium of rice and the genes related to the synthesis and response of JA were related to the variety difference in cadmium tolerance at the bud stage. Compared with the NJ9108, JJ818 was insensitive to jasmonic acid.

Qishen granule (QSG) is a frequently prescribed traditional Chinese medicine formula, which improves heart function in patients with heart failure (HF). However, the cardioprotective mechanisms of QSG have not been fully understood. The current study aimed to elucidate whether the effect of QSG is mediated by ameliorating cytoplasmic calcium (Ca2+) overload in cardiomyocytes. The HF rat model was induced by left anterior descending (LAD) artery ligation surgery. Rats were randomly divided into sham, model, QSG-low dosage (QSG-L) treatment, QSG-high dosage (QSG-H) treatment, and positive drug (diltiazem) treatment groups. 28 days after surgery, cardiac functions were assessed by echocardiography. Levels of norepinephrine (NE) and angiotensin II (AngII) in the plasma were evaluated. Expressions of critical proteins in the calcium signaling pathway, including cell membrane calcium channel CaV1.2, sarcoendoplasmic reticulum ATPase 2a (SERCA2a), calcium/calmodulin-dependent protein kinase type II (CaMKII), and protein phosphatase calcineurin (CaN), were measured by Western blotting (WB) and immunohistochemistry (IHC). Echocardiography showed that left ventricular ejection fraction (EF) and fractional shortening (FS) value significantly decreased in the model group compared to the sham group, and illustrating heart function was severely impaired. Furthermore, levels of NE and AngII in the plasma were dramatically increased. Expressions of CaV1.2, CaMKII, and CaN in the cardiomyocytes were upregulated, and expressions of SERCA2a were downregulated in the model group. After treatment with QSG, both EF and FS values were increased. QSG significantly reduced levels of NE and AngII in the plasma. In particular, QSG prevented cytoplasmic Ca2+ overload by downregulating expression of CaV1.2 and upregulating expression of SERCA2a. Meanwhile, expressions of CaMKII and CaN were inhibited by QSG treatment. In conclusion, QSG could effectively promote heart function in HF rats by restoring cardiac Ca2+ homeostasis. These findings revealed novel therapeutic mechanisms of QSG and provided potential targets in the treatment of HF.

Petal-like Ni(OH) 2 −MnO x nanosheets were fabricated by electrochemical cathodic co-deposition on carbon fiber paper from Mn 2+ /Ni 2+ solutions. For the nanosheet electrode incorporating 25% nickel, the specific capacitance of 344 F g −1 at a current density of 0.5 A g −1 with a cycling stability of 92.5% after 10,000 cycles was obtained in 0.5 M Na 2 SO 4 electrolyte. A symmetric supercapacitor device assembled from this as-fabricated electrode demonstrated the energy density of 17.36 Wh kg −1 at the power density of 249 W kg −1 and 1.8 Wh kg −1 at 5.01 kW kg −1 , respectively. It showed an excellent cycling stability with a loss of only 3.3% after 10,000 cycles at the current density of 5 A g −1 . These remarkable electrochemical performances are attributed to that the nickel enhanced the robustness of the porous structure and the conductivity of the pristine MnO x , which facilitates the charge transfer and ion diffusion during the long time cycling. Our results suggest a great potential in developing energy storage devices from manganese oxide based electrodes by incorporating nickel in the lattice.

Flower-like cobalt-nickel binary oxide was prepared as electrode materials for supercapacitors via cathodic electrodeposition. The deposition experiments were performed at the constant potential of −1 V on Ni foam substrate without any surfactant and template. Scanning electron microscopy (SEM) images indicate that the flower-like Co3O4 nano-sheet layers are homogeneously distributed on NiO layer with length of about 200 nm. The as-prepared Co3O4-NiO exhibits a specific capacitance of 687.5 F g−1 at the current density of 0.5 A g−1 (vs. Ag/AgCl). Meanwhile, they show excellent rate performance (94% retained from 0.5 A g−1 to 10 A g−1) and outstanding cycle life (92% retained after 2500 cycles). These results indicate that the flower-like cobalt-nickel binary oxide electrode deposited on Ni foam can be considered as a promising candidate for the supercapacitor electrode materials.

Qishenkeli (QSKL) is one of the Chinese medicine formulae for treating heart failure and has been shown to have an antifibrotic effect. However, the mechanism of its therapeutic effects remains unclear. In this study, we aimed to explore whether QSKL could exert an antifibrotic effect by attenuating ras homolog family member A (RhoA) and mitogen activated protein kinase (MAPK) pathways. Rats were randomly divided into sham group, model group, QSKL group, and positive control group. Heart failure was induced by ligation of the left ventricle anterior descending artery. Cardiac functions were measured by echocardiography and collagen deposition was assessed by Masson staining. Expressions of the key molecules involved in the RhoA and MAPK pathways were also measured. Twenty-one days after surgery, cardiac functions were severely impaired and collagen deposition was remarkable, while QSKL treatment could improve heart functions and alleviate collagen deposition. Further results demonstrated that the effects may be mediated by suppressing expressions of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). Moreover, expressions of RhoA, Rho-associated protein kinase 1/2 (ROCK1/2), and phosphorylated myosin light chain (p-MLC) were also downregulated by QSKL compared with the model group. The cardioprotective mechanism of QSKL on heart failure is probably mediated by regulating both the MAPK and RhoA signaling pathways.

Nanocrystalline LaOx/NiO composite electrodes were synthesized via two types of facile cathodic electrodeposition methods onto nickel foam followed by thermal annealing without any binders. Scanning electron microscopy and transmission electron microscopy investigation revealed that LaOx nanocrystalline particles with an average diameter of 50 nm are uniformly distributed in the NiO layer or alternately deposited with the NiO layer onto the substrate. It is speculated that LaOx particles can participate in the faradaic reaction directly and offer more redox sites. Besides this, the unique Ni/La layered structure facilitates the diffusion of ions and retards the electrode polarization, thus leading to a better rate capability and cycling stability of NiO. As a result, the obtained electrodes display very competitive electrochemical performance (a specific capacitance of 1238 F g−1 at a current density of 0.5 A g−1, excellent rate capability of 86% of the original capacitance at 10 A g−1 and excellent cycling stability of 93% capacitance after 10 000 cycles). In addition, asymmetric coin devices were assembled using LaOx/NiO as the positive electrode and active carbon as the negative electrode. The assembled asymmetric devices demonstrate a high energy density of 13.12 W h kg−1 at a power density of 90.72 W kg−1.

NiO/LaNiO3 (NiO/LNO) film electrode was prepared by spin-coating technique on Pt/Ti/SiO2/Si(100) substrates. The crystal structure and surface morphology were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM), respectively. Cyclic voltammetry (CV), galvanostatic charge/discharge, electrochemical impedance spectroscopy (EIS) and cyclic charge-discharge measurements were employed to evaluate the electrochemical performance of the electrode. The effect of LNO layer on the performance of the NiO/LNO electrode was also investigated. The NiO/LNO electrode with appropriate LNO content possesses high specific capacitance (2030 F/g at 0.5 A/g) and good cyclability (specific capacitance retention of 83% after 1000 cycles). The present study suggests that NiO/LNO film is a promising electrode material for supercapacitor.

Si-Miao-Yong-An decoction (SMYAD), a Chinese herbal formula, has been used in treating ischemic cardiovascular diseases. However, the cardioprotective mechanism of SMYAD treating heart failure (HF) remains unclear. Herein we investigated the effect of SMYAD on isoprenaline (ISO)-induced HF in C57BL/6 mice. Cardiac function and pathological changes in myocardial tissue were evaluated as well as A-type natriuretic peptide (ANP) and brain natriuretic peptide (BNP) expression. The underlying mechanism of SMYAD was deciphered using UHPLC MS/MS coupled with bioinformatics and was verified. SMYAD treatment significantly ameliorated cardiac function, reduced collagen deposition and cardiomyocyte apoptosis, reversed cardiac hypertrophy and down-regulated the expression levels of ANP and BNP mRNA compared with those in HF mice. Decipherment analyses based on 138 ingredients prompted that anti-oxidation was the key mechanism of SMYAD treating HF. In vitro and in vivo, SMYAD showed antioxidant activity, significantly up-regulated superoxide dismutase (SOD)-1 and SOD-2 mRNA expression levels and reduced NADP/NADPH ratio. Moreover, the increased expression levels of NADPH oxidase 2 (NOX2), p47phox and Rac family small GTPase 1 (Rac1) were obviously ameliorated after SMYAD treatment. Together, this study reveals that SMYAD can apparently improve heart function of ISO-induced HF mice by inhibiting the myocardial oxidative stress through restoring the equilibrium of SOD and NOX2.

Coronary artery disease (CAD) is one of the leading causes of deaths worldwide. Energy metabolism disorders, including a reduction in fatty acids oxidation and upregulation of glycolysis pathway, are involved in the process of CAD. Therapeutic angiogenesis has become a promising treatment for CAD. Traditional Chinese medicines, such as Danqi Pill (DQP), have been proven to be effective in treating CAD in China for many years. However, the pro-angiogenic effects of DQP based on fatty acids oxidation are still unknown and the mechanism is worthy of investigation. In this study, left anterior descending (LAD) coronary artery was ligated to induce the CAD models in vivo, and cardiac functions were examined using echocardiography. Human umbilical vein endothelial cells (HUVEC) were subjected to H2O2-induced oxidative stress in vitro. The effects of DQP on CAD rat models and in vitro HUVEC were detected. Our results showed that DQP had cardio-protective effects in rat model. The intensity of capillaries in the marginal area of infarction of the rat heart was increased remarkably in DQP group, and the expression of PPARα and VEGF-2 were increased. The key enzymes involved in the transportation and intake of fatty acids, including CPT1A and CD36, both increased. In H2O2-induced endothelial cells injury models, DQP also showed protective roles and promoted capillary-like tube formation. DQP up-regulated key enzymes in fatty acids oxidation in H2O2-treated HUVEC. In addition, inhibition of CPT1A compromised the pro-angiogenic effects of DQP. In conclusion, fatty acids oxidation axis PPARα-CD36-CPT1A was involved in the pro-angiogenic roles of DQP against CAD. Cardiac CPT1A may serve as a target in therapeutic angiogenesis in clinics.

BACKGROUND: Coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been characterized as a pandemic around the world. Cardiac complications can occur in patients with COVID-19 and can be fatal in severe cases. Recently, it was reported that SARS-CoV-2 used the angiotensin-converting enzyme 2 (ACE2) as a cellular receptor to gain entry into the host cell. However, whether SARS-CoV-2 can directly infect heart tissues and the potential mechanism of cardiac injury in COVID-19 have not been determined. METHODS: To investigate the expression of ACE2 in heart tissues, we performed a bioinformatic analysis from public databases involving mRNA and protein expression. The correlation between ACE2 expression and virus-related genes was analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database. Gene ontology (GO) and protein-protein interaction (PPI) analyses were performed to explore the roles of ACE2. RESULTS: ACE2 expression in the heart was significantly higher than that in the lung. Compared with the other coronavirus receptors, such as aminopeptidase N (ANPEP) or dipeptidyl peptidase 4 (DPP4), the mRNA and protein expression of ACE2 was increased in the heart. Moreover, the mRNA expression of ACE2 was substantially upregulated in patients with dilated cardiomyopathy. Importantly, the expression of ACE2 was positively correlated with genes that regulate viral reproduction and transmission. The GO and PPI analyses showed that the functions of proteins interacting with ACE2 were significantly enriched in the regulation of the viral process and inflammatory response. CONCLUSIONS: Our study provided bioinformatics evidence that the interaction between SARS-CoV-2 and ACE2 in the heart could contribute to COVID-19-mediated myocardial damage via the virus-induced cytopathic effect, triggering a cardiac inflammatory storm. Therefore, the close monitoring of cardiac function and early clinical intervention may be pivotal to preventing cardiac injury-related mortality in patients with COVID-19.

Cauliflower-like NiCo2S4 nanoparticles (NPs) for use as battery-type materials have been synthesized via a simple one-step route solvothermal method with thioacetamide (TAA) as the sulfur source. The synthesis of the Ni–Co precursors and the S2− anion exchange reactions occur at the same time, which is time-effective and cost-effective compared to other methods. The obtained NiCo2S4 NPs display very competitive electrochemical performance (a specific capacitance of 2480 F g−1 is achieved at a current density of 0.5 A g−1, excellent rate capability with 68% of the original capacitance remained at 10 A g−1 and ideal cycle stability with 80% capacitance remained after 3000 cycles) with high mass-loading (5 mg cm−2). In addition, low-cost activated balsam pear pulp (ABPP) is developed as a capacitor-type carbon material for supercapacitors with ideal electrochemical performances. The asymmetric hybrid capacitors (AHCs) are further assembled into pouch cells using battery-type NiCo2S4 NPs as the positive electrode, capacitor-type ABPP as the negative electrode and flexible carbon papers as the current collector. The AHCs demonstrate high power density (3.52 kW kg−1 at an energy density of 3.72 Wh kg−1) and cycle stability (72.4% after 9000 cycles).

Background Uterine corpus endometrial carcinoma (UCEC) is a clinically heterogeneous disease, and this heterogeneity is associated with tumor development, clinical characteristics, and prognostic outcomes. Mutant-allele tumor heterogeneity (MATH) is a novel, non-biased, quantitative measure to assess intra-tumor heterogeneity based on next-generation sequencing data. We aimed to explore the use of MATH as a measure for tumor heterogeneity and its prognostic role in UCEC patients. Methods We calculated MATH scores from the available data of 560 UCEC patients from The Cancer Genome Atlas (TCGA) and investigated their correlations with clinical characteristics, genetic alterations, and overall survival. Predictive accuracy was quantified using the area under the receiver operating characteristic curve (AUC) and the index of concordance (C-index). Results In total, 242 MATH scores were obtained from the UCEC cohort. MATH scores were significantly related to age, race, cancer type, clinical stage, histological grade, molecular type, targeted molecular therapy, and hormonal therapy. Furthermore, the genomic pattern on the basis of MATH scores showed that mutation rates of TP53 (tumor protein p53) and ARID1A (AT-rich interaction domain 1A) were independently associated with MATH scores. Correlation analysis revealed a significantly positive association of MATH scores with the fraction of somatic copy number alteration (SCNA). Importantly, a high MATH score was significantly associated with shorter overall survival [hazard ratio (HR), 2.342; 95% confidence interval (CI), 1.110-4.942]. Multivariate Cox regression combined with stratified analysis revealed that the MATH score is an independent prognostic factor in UCEC patients under 60 years old, and predictive quantification showed the MATH score had an AUC of 0.756 and a C-index of 0.845. Conclusions Our results suggest that MATH, a practical and useful way to measure intra-tumor heterogeneity, may serve as a significant biomarker for the prognosis of patients with UCEC, enabling more accurate prediction of clinical outcomes.

Background Cardiac fibrosis is a common pathological progress of cardiovascular disease resulting from the excessive accumulation of extracellular matrix (ECM). Transforming growth factor (TGF)-β/SMADs pathway is a canonical signaling pathway which directly induces expressions of ECM related genes. Qishen Granule (QSG), a traditional Chinese formula developed from Zhen-Wu Decoration for heart failure (HF), has been proven to have definite therapeutic effects on cardiac fibrosis. However, its underlying mechanisms remain unclear. Purpose To investigate the effects of QSG on TGF-β pathway and the downstream mediators including Smad3 and Glycogen synthase kinase (GSK)-3β. Methods HF model was induced by ligation of left coronary artery on male Sprague-Dawley (SD) rats. Rat were randomly divided into four groups including sham group, model group, QSG group and Fosinopril control group. Rats in each group were treated for 28 days, and 2D echocardiography was adopted to evaluate the heart function. The degree of cardiac fibrosis was assessed by Hematoxylin-Eosin (HE), Masson's trichrome and Picrosirius red (PSR) staining. Contents of collagen Ⅰ and Ⅲ were assessed by immunohistochemical method. Expressions of genes and proteins in TGF-β/SMADs and PI3K-GSK-3 signaling pathways were detected by Real-time Fluorescence Quantitative PCR (RT-qPCR) and Western blot respectively. TGF-β1-treated cardiac fibroblasts of neonatal SD rats were adopted for in vitro studies. Results 28 days after the surgery, cardiac ejection fraction (EF) and fractional shortening (FS) values in the model group showed a remarkable decrease, indicating the induction of HF model. QSG and Fosinopril elevated the EF and FS values, demonstrating cardio-protective effects. Pathological staining and immunohistochemistry showed that the contents of collagen I and III dramatically increased in the cardiac tissue of the model group compared with the sham group while QSG treatment reduced collagen contents. Furthermore, expressions of TGF-β1, p-Smad3 and p-GSK-3β were significantly decreased in the QSG treatment group compared with the model group, suggesting that the QSG may attenuate cardiac fibrosis through regulating TGF-β/Smad3 pathway. In vitro study further showed that the productions of type Ⅰ and Ⅲ collagen and α-smooth muscle actin (α-SMA) of cardiac fibroblasts were significantly increased by incubation with TGF-β1. QSG could markedly reduce the secretion of collagen Ⅰ and Ⅲ and α-SMA expression. Protein expressions of p-Smad3, PI3K, p-Akt and p-GSK-3β were significantly up-regulated by stimulation of TGF-β1. Treatment with QSG could suppress the activity of Smad3 and PI3K-GSK-3β signaling pathway in cardiac fibroblasts. Conclusion QSG improves cardiac function through inhibiting cardiac fibrosis. The anti-fibrotic effects are potentially mediated by the inhibition of the TGF-β/Smad3 pathway and the phosphorylation of GSK-3β.

Nanocrystalline LaO

Ag-doped manganese oxide was deposited on carbon fiber via a cathodic reduction method, then the deposits were dehydrogenized and oxidised by heat treatment at 350 °C for 4 h. Scanning electron microscopy, X-ray diffraction and X-ray photoelectron spectroscopy were utilized to characterize the structure and state of the deposits. The results show that manganese oxide presents an amorphous fibrous structure and is a mixture of tetravalent and trivalent. The cyclic voltammetry curves measured with three-electrode methods in 0.5 M Na2SO4 electrolyte reveal that the specific capacitance of manganese oxide without and with Ag is about 450 and 825 F g−1 at the scan rate of 5 mV s−1, respectively. Hence, Ag doping improves the pseudo-capacitor behavior. The MnOx-based supercapacitors fabricated with 0.5 M Na2SO4 as electrolyte are characterized by cyclic voltammetry and galvanostatic charge–discharge to investigate the electrochemical properties. In order to study the cycle life of the devices the galvanostatic charge–discharge process is cycled 3000 times and the specific capacitance shows almost no change after 3000 cycles.

Nanostructured Mn–Cu binary oxides (MCO) were prepared by thermal decomposition of the precursor obtained by ball milling of Mn and Cu salts. Tailoring the material characteristics and thus the electrochemical performance of the oxide is attempted by component changing (Cu content from 0 mol% to 50 mol%). The crystal structure and surface morphology were characterized by X-ray diffraction (XRD) and scanning electron microscopy (SEM), respectively. Cyclic voltammetry, impedance and galvanostatic charge–discharge measurements were employed to investigate the electrochemical performance of the composite electrodes. When the molar ratio of Mn and Cu in composite material is 90:10, the specific capacitance of MCO calculated from the cyclic voltammetry curves is 422 F g−1, however, that of pure Mn2O3 is 92 F g−1 in 6 M KOH electrolyte and at scan rate of 5 mV s−1, respectively. The specific capacitance of MCO electrode is much larger than that of pure Mn2O3. Moreover, the composite electrodes show high power density.

The dielectric constant and electrical conductivity of a composite of two insulators, poly(1,1-difluoroethylene) (yellow) and K(2)CO(3) (white), increased dramatically near the percolation threshold f(c) (f=concentration of K(2)CO(3)). This intriguing phenomenon can be interpreted in terms of interface percolation caused by the formation of chemically activated interfaces.