Polyphenol oxidase/gold nanoparticles/mesoporous carbon-modified electrode as an electrochemical sensing platform for rutin in dark teas.

In the communication, by virtue of the excellent conductivity and great surface area of mesoporous carbon (FDU-15), the enhanced conductivity of Au NPs, and the good electrochemical response of polyphenol oxidase (PPO) to rutin, a PPO/AuNPs/FDU-15-modified electrode was used as a candidate for the determination of rutin in dark teas with satisfactory results.

Sn-doped hematite modified by CaMn2O4 nanowire with high donor density and enhanced conductivity for photocatalytic water oxidation.

Herein, we report a novel nanocomposite consisting of n-type Sn-doped hematite and p-type CaMn2O4 nanowire (CaMn2O4/α-Fe2O3). The nanocomposite was characterized by X-ray diffraction (XRD), high resolution transmission electron microscopy (HRTEM), ultraviolet-visible absorption spectroscopy, X-ray photoelectron spectroscopy (XPS), which showed that nanospindle-like Sn-doped hematite and CaMn2O4 nanowire contact intimately in the nanocomposite, resulting in efficient charge transfer and separation. Photoelectrochemical results reveal that the nanocomposite possesses higher donor density, enhanced conductivity and lower overpotential for dioxygen evolution. In addition, the nanocomposite demonstrates high photocatalytic activity for water oxidation to produce oxygen in a photoelectrochemical cell. The amount of O2 evolved from the optimized photoanode of the photoelectrochemical cell was 1.98 µmol in 2 h of simulated sunlight irradiation. This work demonstrates a facile synthesis of a novel nanocomposite as anode material for photocatalytic water oxidation to produce O2.

Genipin attenuates hyperoxia-induced lung injury and pulmonary hypertension via targeting glycogen synthase kinase-3 ß in neonatal rats.

OBJECTIVES: Bronchopulmonary dysplasia is the most common chronic lung disease of infancy and is associated with pulmonary hypertension (PH). Inhibition of glycogen synthase kinase (GSK)-3 ß has been shown to attenuate lung injury and PH in hyperoxia-exposed newborn rats. Genipin has been widely used for the treatment of inflammatory diseases. The aim of this study was to show that genipin decreased the expression of GSK-3 ß in lung tissues of hyperoxia-exposed rat pups. METHODS: We established models of hyperoxia-exposed rat pups, evaluated lung injury and pulmonary hypertension and detected the mRNA and protein expression of key molecules. RESULTS: Hyperoxia resulted in the reduction of survival rate and histologic injury of lung tissues; an increase of the messenger RNA (mRNA) expression of transforming growth factor-ß1, extracellular matrix proteins collagen-I and fibronectin, and α-smooth muscle actin; an increase of right ventricular (RV) systolic pressure and the weight ratio of RV to left ventriclar (LV) plus septum (S) (RV/LV + S) were inhibited by genipin. Genipin also decreased the levels of tumor necrosis factor-α, interleukin-1 ß, and interleukin-6 in both bronchoalveolar lavage fluid and lung tissues after hyperoxia exposure. In addition, genipin inhibited p65 nuclear factor-κB nuclear translocation and matrix metalloproteinase-2 and -9 expression. Moreover, hyperoxia resulted in an increase of methane dicarboxylic aldehyde content and a decrease of superoxide dismutase activity, catalytic subunit of glutamate-cysteine ligase, modified subunit of glutamate-cysteine ligase, and nuclear factor erythroid 2-related factor 2 expression were inhibited by genipin. All these effects induced by genipin were blocked by upregulation of GSK-3 ß. Genipin downregulated GSK-3 ß expression, decreased nuclear factor-κB translocation, increased nuclear factor erythroid 2-related factor 2 expression, attenuated inflammation and oxidative stress, leading to amelioration of lung injury and PH in hyperoxia-exposed rat pups. CONCLUSION: Overall, genipin may provide a novel therapeutic option for preventing and treating infants with bronchopulmonary dysplasia.

Identification of core pathways based on attractor and crosstalk in ischemic stroke.

Ischemic stroke is a leading cause of mortality and disability around the world. It is an important task to identify dysregulated pathways which infer molecular and functional insights existing in high-throughput experimental data. Gene expression profile of E-GEOD-16561 was collected. Pathways were obtained from the database of Kyoto Encyclopedia of Genes and Genomes and Retrieval of Interacting Genes was used to download protein-protein interaction sets. Attractor and crosstalk approaches were applied to screen dysregulated pathways. A total of 20 differentially expressed genes were identified in ischemic stroke. Thirty-nine significant differential pathways were identified according to P<0.01 and 28 pathways were identified with RP<0.01 and 17 pathways were identified with impact factor >250. On the basis of the three criteria, 11 significant dysfunctional pathways were identified. Among them, Epstein-Barr virus infection was the most significant differential pathway. In conclusion, with the method based on attractor and crosstalk, significantly dysfunctional pathways were identified. These pathways are expected to provide molecular mechanism of ischemic stroke and represents a novel potential therapeutic target for ischemic stroke treatment.

Fluorescence detection of glutathione and oxidized glutathione in blood with a NIR-excitable cyanine probe.

Cyanine has been widely utilized as a near infrared (NIR) fluorophore for detection of glutathione (GSH). However, the excitation of most of the reported cyanine-based probes was less than 800 nm, which inevitably induce biological background absorption and lower the sensitivity, limiting their use for detection of GSH in blood samples. To address this issue, here, a heptamethine cyanine probe (DNIR), with a NIR excitation wavelength at 804 nm and a NIR emission wavelength at 832 nm, is employed for the detection of GSH and its oxidized form (GSSG) in blood. The probe displays excellent selectivity for GSH over GSSG and other amino acids, and rapid response to GSH, in particular a good property for indirect detection of GSSG in the presence of enzyme glutathione reductase and the reducing agent nicotinamideadenine dinucleotide phosphate, without further separation prior to fluorescent measurement. To the best of our knowledge, this is the first attempt to explore NIR fluorescent approach for the simultaneous assay of GSH and GSSG in blood. As such, we expect that our fluorescence sensors with both NIR excitation and NIR emission make this strategy suitable for the application in complex physiological systems.

Mesoporous tungsten oxide modified by nanolayered manganese-calcium oxide as robust photoanode for solar water splitting.

Described herein is the synthesis, characterization and photoelectrochemical behavior of a novel composite consisting of nanolayered manganese-calcium oxide (MCO) and mesoporous tungsten trioxide (WO3). The samples were characterized by transmission electron microscopy (TEM), and X-ray diffraction (XRD). The results demonstrated that superior interfacial contacts had been formed between WO3 and MCO. UV-vis diffuse reflectance spectroscopy (DRS), photoelectrochemical characterization, and incident photon-to-current efficiency (IPCE) revealed an enhanced light harvesting and effective electron-hole separation. A photoelectrochemical (PEC) cell composed of the n-type MCO/WO3 as a photoanode and platinum sheet as a counter electrode was assembled to estimate the feasibility for overall water splitting under a solar simulator illumination. The photocatalytic hydrogen and oxygen production from the photochemical cell with optimized photocatalyst (MCO/WO3-9) under 2 h simulated solar light irradiation was 1.9 µmol and 0.7 µmol, respectively, at low extra bias (0.90 V vs. RHE). Our investigation suggests that coupling MCO with n-type semiconductor WO3 as photoanode is a promising method to improve the activity of overall water splitting to generate oxygen and hydrogen.

Long Sleep Duration Is an Independent Risk Factor for Incident Atrial Fibrillation in a Chinese Population: A Prospective Cohort Study.

There is limited information on the relation between sleep duration and incident atrial fibrillation. We aimed to investigate this association in a Chinese population using cohort data from a study in Kailuan. The analysis included 87,693 participants (age range, 18-98 years) free of atrial fibrillation at the baseline survey. Participants were divided into three categories according to self-reported sleep duration: ≤6.0 hours, 7 hours (ref), ≥8.0 hours. Atrial fibrillation diagnosis was made on a standard 12-lead electrocardiogram and via self-reported history. Cox proportional hazards models were used to calculate hazard ratio (HR) and confidence interval (CI) for atrial fibrillation, according to sleep duration. During median follow-up of 7.89 (range, 6.36-8.57) years, 322 cases of atrial fibrillation had occurred. Using 7 hours of sleep as the reference group, multivariable adjusted HRs (95% CI) for atrial fibrillation were 1.07 (0.75-1.53), 1.0 (ref), and 1.50 (1.07-2.10), from lowest to highest category of sleep duration. Secondary analysis showed no evidence of interactions between sleep duration and sex and snoring on the risk of incident atrial fibrillation (p = 0.75/0.25). We conclude long sleep duration may be a potential predictor/marker for incident atrial fibrillation.

A method for measurement of free cadmium species in waters using diffusive gradients in thin films technique with an ion-imprinted sorbent.

A diffusive gradients in thin films (DGT) device for the analysis of free Cd(II) species, based on Cd(II) ion-imprinted sorbent (IIS) as the binding agents and commercial polyethersulfone membrane (PES) as diffusion layer, was developed (PES/IIS-DGT). DGT time-series experiments showed that the mass of free Cd(II) species accumulated by PES/IIS-DGT was linear vs. time (R(2) = 0.9953) and the concentration of free Cd(II) species by PES/IIS-DGT was in good agreement with the total dissolved concentrations of free Cd(II) species in simple synthetic solutions where free ionic species dominated. PES/IIS-DGT performance was independent in the range of pH 4.5-7.5 and ionic strength range from 1.0 × 10(-3) to 0.7 mol L(-1). The measurement of free Cd(II) species in synthetic solution containing different concentrations of ligands by PES/IIS-DGT showed an excellent agreement with the value measured by Cd(II) ion selective electrodes (Cd-ISE), indicating that PES/IIS-DGT method is more suitable than Cd-ISE for the measurement of low concentration of free Cd(II) species due to the enrichment of IIS for the analytes.

Effect of oxytocin on the behavioral activity in the behavioral despair depression rat model.

Oxytocin (OXT), a nonapeptide posterior hormone of the pituitary, is mainly synthesized and secreted in the hypothalamic paraventricular nucleus (PVN) and supraoptic nucleus (SON). The present study was to investigate in which level, brain or periphery, OXT effecting on the behavioral activity in the behavioral despair depression rat model. The results showed that (1) either the forced swimming or the tail suspension significantly increased OXT concentration in the brain (PVN, SON, frontal cortex, hippocampus, amygdala, lumbar spinal cord) and in the periphery (posterior pituitary and serum); (2) intraventricular injection (icv) of OXT decreased the animal immobility time, whereas OXT receptor antagonist-desGly-NH2, d(CH2)5[D-Tyr2, Thr-sup-4]OV (icv) increased the animal immobility time in a dose-dependent manner in forced swimming test (FST) and in tail suspension test (TST); (3) neither OXT nor OXT receptor antagonist (intravenous injection) influenced the animal immobility time in FST and in TST. OXT levels were increased in several areas of the brain and in the periphery following the behavioral despair, one stressor, yet pre-treatment with OXT appeared to be beneficial in term of reducing immobility time. The data suggested that behavioral despair could enhance OXT synthesis and secretion not only in the brain but also in the periphery, and OXT in the brain rather than the periphery played a role in the behavioral despair depression.

Efficient bioconversion of echinocandin B to its nucleus by overexpression of deacylase genes in different host strains.

Anidulafungin, which noncompetitively inhibits ß-(1,3)-D-glucan synthase in fungal cell wall biosynthesis, is the newest antifungal drug to be developed. Echinocandin B deacylase from Actinoplanes utahensis NRRL 12052 catalyzes the cleavage of the linoleoyl group of echinocandin B, a key step in the process of manufacturing anidulafungin. Unfortunately, the natural yield of echinocandin B nucleus is low. In our study, the echinocandin B deacylase gene was systematically overexpressed by genetic engineering in its original producer, A. utahensis, and in the heterologous hosts Streptomyces lividans TK24 and Streptomyces albus. The introduction of additional copies of the gene, under the control of PermE* or its native promoter, into hosts showed significant increases in its transcription level and in the efficiency of the bioconversion of echinocandin B to its nucleus. The conditions for the cultivation and bioconversion of A. utahensis have been optimized further to improve production. As a result, while the wild-type strain initially produced 0.36 g/liter, a concentration of 4.21 g/liter was obtained after the generation of a strain with additional copies of the gene and further optimization of the reaction conditions. These results are useful for enhancing echinocandin B nucleus production in A. utahensis. Our study could enable the engineering of commercially useful echinocandin B nucleus-overproducing stains.

Single nucleotide polymorphism in DNMT3B promoter and the risk for idiopathic thrombocytopenic purpura in Chinese population.

OBJECTIVE: Epigenetic changes in gene expression, including DNA methylation and histone modifications, might contribute to autoimmunity. DNA methylation is mediated by a family of DNA methyltransferases. Polymorphisms of the DNA methyltransferase 3B (DNMT3B) gene may influence DNMT3B activity on DNA methylation, thereby modulating the susceptibility to some diseases. The purpose of this study was to investigate the association between the single nucleotide polymorphism (SNP) in promoter of the DNMT3B gene and the risk for development of idiopathic thrombocytopenic purpura (ITP). METHODS: In this hospital-based case-control study, the DNMT3B SNP was genotyped in 201 patients with ITP and 136 healthy controls by polymerase chain reaction-restriction fragment length polymorphism. RESULTS: The C/C genotype was not detected in both the patients with ITP and the controls. In the controls, the frequencies of T/T and C/T genotypes and T and C alleles were 97.8%, 2.2%, 98.9%, and 1.1%, respectively. There was no significant difference in genotype and allele distribution between the patients with ITP and the controls (P = 0.745 and 0.747, respectively). No significant difference was observed in genotype and allele distribution between the two groups when stratified by the age. The similar results were shown among the four groups of patients with ITP: acute childhood, chronic childhood, acute adult, and chronic adult. CONCLUSION: This polymorphism was distributed similarly between the patients with ITP and the controls. It demonstrated that it may not be used as a stratification marker to predict the susceptibility to ITP, at least in the population of North China.