Preformed Pt nanoparticles supported on nanoshaped CeO2 for total propane oxidation

Pt-based catalysts have been widely used for the removal of short-chain volatile organic compounds (VOCs), such as propane. In this study, we synthesized Pt nanoparticles with a size of ca. 2.4 nm and loaded them on various fine-shaped CeO2 with different facets to investigate the effect of CeO2 morphology on the complete oxidation of propane. The Pt/CeO2-o catalyst with {111} facets exhibited superior catalytic activity compared to the Pt/CeO2-r catalyst with {110} and {100} facets. Specifically, the turnover frequency (TOF) value of Pt/CeO2-o was 1.8 times higher than that of Pt/CeO2-r. Moreover, Pt/CeO2-o showed outstanding long-term stability during 50 h. X-ray photoelectron spectroscopy (XPS) and diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) revealed that the excellent performance of Pt/CeO2-o is due to the prevalence of metallic Pt species, which promotes C–C bond cleavage and facilitates the rapid removal of surface formate species. In contrast, a stronger metal–support interaction in Pt/CeO2-r leads to easier oxidation of Pt species and the accumulation of intermediates, which is detrimental to the catalytic activity. Our work provides insight into the oxidation of propane on different nanoshaped Pt/CeO2 catalysts.Peer ReviewedPostprint (published version

[2-(2-Chloro­phen­yl)-2-hy­droxy­eth­yl](isoprop­yl)ammonium 4-hy­droxy­benzoate

The title molecular salt, C11H17ClNO+·C7H5O3 −, was obtained by the reaction of racemic clorprenaline and 4-hy­droxy­benzoic acid. In the crystal, the components are connected by O—H⋯O and N—H⋯O hydrogen bonds, resulting in a two-dimensional hydrogen-bonded network

RAB31 Targeted by MiR-30c-2-3p Regulates the GLI1 Signaling Pathway, Affecting Gastric Cancer Cell Proliferation and Apoptosis

Background: Gastric cancer (GC), one of the most common cancers worldwide, is highly malignant and fatal. Ras-related protein in brain 31 (RAB31), a member of the RAB family of oncogenes, participates in the process of carcinogenesis and cancer development; however, its role in GC progression is unknown.Methods: In our study, 90 pairs of tissue microarrays were used to measure the levels of RAB31 protein by immunochemistry, and 22 pairs of fresh tissue were used to measure the levels of RAB31 mRNA by quantitative PCR. We also investigated the effects of RAB31 on tumor growth both in vitro and in vivo.Results: RAB31 was overexpressed in GC tissues, and its overexpression predicted poor survival in patients. In a nude mouse model, depletion of RAB31 inhibited tumor growth. In vitro, silencing of RAB31 suppressed cell viability, promoted cell cycle arrest, enhanced apoptosis, and affected the expression of cell cycle and apoptotic proteins; these effects were mediated by glioma-associated oncogene homolog 1 (GLI1). Co-immunoprecipitation and immunofluorescence assays confirmed that RAB31 interacted with GLI1. In addition, luciferase reporter assays and Western blotting showed that microRNA-30c-2-3p modulated the RAB31/GLI1 pathway by targeting the 3′-untranslated region of RAB31.Conclusions: Collectively, these data show that RAB31 is regulated by microRNA-30c-2-3p, and functions as an oncogene in GC tumorigenesis and development by interacting with GLI1. Therefore, targeting the miR-30c-2-3p/RAB31/GLI1 axis may be a therapeutic intervention for gastric cancer

Inhibition of UGT1A1 by natural and synthetic flavonoids

Flavonoids are widely distributed phytochemicals in vegetables, fruits and medicinal plants. Recent studies demonstrate that some natural flavonoids are potent inhibitors of the human UDP-glucuronosyltransferase 1A1 (UGT1A1), a key enzyme in detoxification of endogenous harmful compounds such as bilirubin. In this study, the inhibitory effects of 56 natural and synthetic flavonoids on UGT1A1 were assayed, while the structure–inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated. The results demonstrated that the C-3 and C-7 hydroxyl groups on the flavone skeleton would enhance UGT1A1 inhibition, while flavonoid glycosides displayed weaker inhibitory effects than their corresponding aglycones. Further investigation on inhibition kinetics of two strong flavonoid-type UGT1A1 inhibitors, acacetin and kaempferol, yielded interesting results. Both flavonoids were competitive inhibitors against UGT1A1-mediated NHPN-O-glucuronidation, but were mixed and competitive inhibitors toward UGT1A1-mediated NCHN-O-glucuronidation, respectively. Furthermore, docking simulations showed that the binding areas of NHPN, kaempferol and acacetin on UGT1A1 were highly overlapping, and convergence with the binding area of bilirubin within UGT1A1. In summary, detailed structure-inhibition relationships of flavonoids as UGT1A1 inhibitors were investigated carefully and the findings shed new light on the interactions between flavonoids and UGT1A1, and will contribute considerably to the development of flavonoid-type drugs without strong UGT1A1 inhibition.Peer reviewe

Cellular Mechanism Underlying Hydrogen Sulfide Mediated Epithelial K+ Secretion in Rat Epididymis

As a novel gasotransmitter, hydrogen sulfide (H2S) elicits various physiological actions including smooth muscle relaxation and promotion of transepithelial ion transport. However, the pro-secretory function of H2S in the male reproductive system remains largely unclear. The aim of this study is to elucidate the possible roles of H2S in modulating rat epididymal intraluminal ionic microenvironment essential for sperm storage. The results revealed that endogenous H2S-generating enzymes cystathionine β-synthetase (CBS) and cystathionine γ-lyase (CSE) were both expressed in rat epididymis. CBS located predominantly in epithelial cells whilst CSE expressed primarily in smooth muscle cells. The relative expression level of CBS and CSE escalated from caput to cauda regions of epididymis, which was paralleled to the progressively increasing production of endogenous H2S. The effect of H2S on epididymal epithelial ion transportation was investigated using short-circuit current (ISC), measurement of intracellular ion concentration and in vivo rat epididymal microperfusion. Our data showed that H2S induced transepithelial K+ secretion via adenosine triphosphate-sensitive K+ (KATP) channel and large conductance Ca2+-activated K+ (BKCa) channel. Transient receptor potential vanilloid 4 (TRPV4) channel-mediated Ca2+ influx was implicated in the activation of BKCa channel. In vivo studies further demonstrated that H2S promoted K+ secretion in rat epididymal epithelium. Inhibition of endogenous H2S synthesis caused a significant decrease in K+ concentration of cauda epididymal intraluminal fluid. Moreover, our data demonstrated that high extracellular K+ concentration actively depressed the motility of cauda epididymal sperm in a pH-independent manner. Collectively, the present study demonstrated that H2S was vital to the formation of high K+ concentration in epididymal intraluminal fluid by promoting the transepithelial K+ secretion, which might contribute to the maintenance of the cauda epididymal sperm in quiescent dormant state before ejaculation

Measurement of the Bottom-Strange Meson Mixing Phase in the Full CDF Data Set

We report a measurement of the bottom-strange meson mixing phase \beta_s using the time evolution of B0_s -> J/\psi (->\mu+\mu-) \phi (-> K+ K-) decays in which the quark-flavor content of the bottom-strange meson is identified at production. This measurement uses the full data set of proton-antiproton collisions at sqrt(s)= 1.96 TeV collected by the Collider Detector experiment at the Fermilab Tevatron, corresponding to 9.6 fb-1 of integrated luminosity. We report confidence regions in the two-dimensional space of \beta_s and the B0_s decay-width difference \Delta\Gamma_s, and measure \beta_s in [-\pi/2, -1.51] U [-0.06, 0.30] U [1.26, \pi/2] at the 68% confidence level, in agreement with the standard model expectation. Assuming the standard model value of \beta_s, we also determine \Delta\Gamma_s = 0.068 +- 0.026 (stat) +- 0.009 (syst) ps-1 and the mean B0_s lifetime, \tau_s = 1.528 +- 0.019 (stat) +- 0.009 (syst) ps, which are consistent and competitive with determinations by other experiments.Comment: 8 pages, 2 figures, Phys. Rev. Lett 109, 171802 (2012

Degradation aspects of water formation and transport in Proton Exchange Membrane Fuel Cell: A review

This review paper summarises the key aspects of Proton Exchange Membrane Fuel Cell (PEMFC) degradation that are associated with water formation, retention, accumulation, and transport mechanisms within the cell. Issues related to loss of active surface area of the catalyst, ionomer dissolution, membrane swelling, ice formation, corrosion, and contamination are also addressed and discussed. The impact of each of these water mechanisms on cell performance and durability was found to be different and to vary according to the design of the cell and its operating conditions. For example, the presence of liquid water within Membrane Electrode Assembly (MEA), as a result of water accumulation, can be detrimental if the operating temperature of the cell drops to sub-freezing. The volume expansion of liquid water due to ice formation can damage the morphology of different parts of the cell and may shorten its life-time. This can be more serious, for example, during the water transport mechanism where migration of Pt particles from the catalyst may take place after detachment from the carbon support. Furthermore, the effect of transport mechanism could be augmented if humid reactant gases containing impurities poison the membrane, leading to the same outcome as water retention or accumulation. Overall, the impact of water mechanisms can be classified as aging or catastrophic. Aging has a long-term impact over the duration of the PEMFC life-time whereas in the catastrophic mechanism the impact is immediate. The conversion of cell residual water into ice at sub-freezing temperatures by the water retention/ accumulation mechanism and the access of poisoning contaminants through the water transport mechanism are considered to fall into the catastrophic category. The effect of water mechanisms on PEMFC degradation can be reduced or even eliminated by (a) using advanced materials for improving the electrical, chemical and mechanical stability of the cell components against deterioration, and (b) implementing effective strategies for water management in the cell