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In this work, PtCo nanoparticles (NPs) on hierarchically ordered mesoporous carbon (PtCo/OMC) are synthesized for polymer electrolyte membrane fuel cells (PEMFCs) aiming to improve the activity and durability of the Pt-based catalyst towards oxygen reduction reaction (ORR). Specifically, the OMC is prepared through a solvent evaporation-induced self-assembly (EISA) method by using a triblock copolymer PEO-PPO-PEO as the structure agent, followed by annealing in the nitrogen atmosphere to decompose the structure agent and to carbonize the carbon precursor. PtCo nanoparticles (NPs) are fabricated with an average diameter of 3.3 nm by H2 reduction and galvanic replacement in an acid solution, and then are uniformly dispersed onto the OMC via impregnation. The typical mesoporous structure of the OMC enhances the uniformly distribution and thermal stability of the small-sized PtCo NPs. The activity and the durability of the as-prepared PtCo/OMC catalyst are investigated by cyclic voltammetry (CV) and single-cell test. In the electrochemical tests, PtCo/OMC exhibits a high ECSA value of 88.56 m2g−1, and a ECSA retention of 77.5% after 5000 CV cycles. The results show that the PtCo/OMC catalyst is more active and more stable than the commercial-carbon-supported PtCo catalyst (PtCo/XC-72). PtCo nanoparticles (NPs) on hierarchically ordered mesoporous carbon (PtCo/OMC) are synthesized aiming to improve the activity and stability of the Pt-based catalyst for the oxygen reduction reaction (ORR). Due to the natural mesoporous and graphite-carbon nanostructure of the OMC, the as-prepared PtCo/OMC catalyst is more active and more stable than the PtCo NPs on the commercial Vulcan@ XC-72 support (PtCo/XC-72), showing great potential in proton exchange membrane fuel cells (PEMFCs). [ABSTRACT FROM AUTHOR]

A series of Ni-modified Mo2C catalysts with La2O3-stabilized ZrO2 supports were synthesized via template method coupled with incipient wetness impregnation and temperature-programmed carbonization. The catalyst was tested in dry reforming of methane (DRM) reaction at the temperature range from 973 to 1173 K in a fixed-bed quartz reactor under atmospheric pressure. XRD, Raman, BET, H2-TPD, SEM, EDS and TEM were conducted to characterize the phase constitution, the pore structure, the morphology and the crystal structure of the catalysts. Ni-Mo2C nanoparticles of ~ 3 nm diameter were obtained for these catalysts, and the La2O3-ZrO2 supports exhibited a cubic lattice structure with a sheet shape, which is believed to contain an abundant of oxygen vacancies. And the synergistic interaction between the oxygen vacancy in La-Zr-O solid solution and the Ni-Mo2C particles could decrease the apparent activation energy of CO2. Both of them are beneficial for accelerating DRM reaction. CH4 conversion of the best specimen catalyst reaches 94% at 1173 K, and the catalyst maintains its stability after 100-h reaction. The superior catalytic activity of NMLZ-7.5 is attributed to the improved BET surface area (33.2 m2/g), smaller crystallites, grain boundaries and oxidation-carbonization cycle of Ni-Mo2C. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the effects of cytochrome P450 2D6*10 (100C > T, rs1065852) genotype on the pharmacokinetics of dimemorfan in healthy Chinese subjects. Data were evaluated from 24 subjects in two pharmacokinetic studies who received an oral dose of 40 mg of dimemorfan syrup ( n = 12) or dimemorfan tablet ( n = 12) after providing written informed consent and being divided into three groups: subjects with CYP2D6*10 CC ( n = 5), CYP2D6*10 CT ( n = 11) and CYP2D6*10 TT ( n = 8). CC homozygotes and CT heterozygotes were defined to be C allele carriers. The CYP2D6*10 was genotyped by polymerase chain reaction-restriction fragment length polymorphism. Dimemorfan was measured by LC-MS/MS. There was significant difference in C, AUC, AUC, V, and CL values of dimemorfan observed among the three CYP2D6*10 genotype groups (GLM, P < 0.05, co-dominant model). CYP2D6*10 under the recessive model (CC + TC vs TT) was significantly associated with pharmacokinetics of dimemorfan ( P < 0.05). The C values were significantly higher in subjects with CYP2D6*10 TT (8.06 ± 4.43 ng/mL) than CYP2D6*10 CC (3.41 ± 2.79 ng/mL), CYP2D6*10 CT (3.11 ± 2.47 ng/mL), so was AUC. V/ F and CL/ F of subjects with CYP2D6*10 TT homozygotes were the lowest. We demonstrated that cytochrome P450 2D6*10 (100C > T, rs1065852) polymorphism can affect the pharmacokinetics of dimemorfan in humans, not dosage forms. [ABSTRACT FROM AUTHOR]

sensitive, specific and rapid high performance liquid chromatography-atmospheric pressure chemical ionization source-tandem mass spectrometry (LC-APCI-MS-MS) method for the determination of pilocarpine in human plasma was developed and validated. The method is based on liquid-liquid extraction, followed by a reversed-phase liquid chromatographic separation, and detected by means of tandem mass spectrometry. The linear calibration curve covered a concentration range of 2-500 μg L. The intra- and inter-day precisions for pilocarpine were <10% and the accuracies were between 90 and 110%. The method was applied successfully to a pharmacokinetic study involving 20 healthy Chinese male volunteers after oral administration of 6 mg pilocarpine. [ABSTRACT FROM AUTHOR]

Neutrophil extracellular traps (NETs) facilitate the extracellular killing of pathogens. However, excessive NETs formation and poor degradation are associated with exacerbated immune responses and tissue injury. In this study, we investigated the role of NETs in lipopolysaccharide (LPS)-mediated acute lung injury (ALI) and assessed the use of DNase I, for the treatment of ALI. Additionally, we focused on the controversial issue of whether LPS directly induces NETs release in vitro. NETs formation was detected in murine ALI tissue in vivo and was associated with increased NETs markers, citrullinated-histone H3 tissue levels and NET-DNA levels in BALF. Treatment with DNase I significantly degraded NETs and reduced citrullinated-histone H3 levels, which protected against ALI and ameliorated pulmonary oedema and total protein in BALF. In addition, DNase I significantly reduced IL-6 and TNF-α levels in plasma and BALF. In vitro, LPS-activated platelets rather than LPS alone efficiently induced NETs release. In conclusion, NETs formed during LPS-induced ALI, caused organ damage and initiated the inflammatory response. NETs degradation by DNase I promoted NET-protein clearance and protected against ALI in mice; thus, DNase I may be a new potential adjuvant for ALI therapy. Specifically, LPS induced NETs formation in an indirect manner via platelets activation. [ABSTRACT FROM AUTHOR]