8 research outputs found

    MOFs-Derived Mn<sub><i>x</i></sub>O<sub><i>y</i></sub>C<sub><i>z</i></sub> Supported Bimetallic Au–Pt Catalyst for the Catalytic Oxidation of Glycerol to Glyceric Acid

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    The specific structure of the support and the interactions between the catalyst components can lead to electron transfer, which in turn could affect the catalytic performance in heterogeneous catalytic reactions. In this paper, we have successfully prepared MnxOyCz composite materials from the calcination of the Mn-organic framework. Then bimetallic Au–Pt nanoparticles (NPs) were supported onto MnxOyCz via the colloidal-deposition method. These catalysts were tested in the selective oxidation of glycerol to glyceric acid under basic conditions. The results demonstrated that the catalytic activity of the bimetallic Au–Pt/MnxOyCz catalyst is considerably superior to those of the monometallic (Au and Pt) supported catalysts. Under the optimized conditions, 100% of glycerol can convert with 57.3% selectivity of glyceric acid. Multicharacterizations showed that the strong interaction between Au and Pt in the Au–Pt/MnxOyCz catalyst can enhance the dispersion of Au–Pt alloy NPs, promoting the electronic coupling effect on the metal surface. At the same time, the rich oxygen vacancies in this catalyst can facilitate the activation of oxygen, which causes the Au–Pt/MnxOyCz catalyst to show better catalytic activity. Specifically, the interaction between Au and Pt not only decreases the particle size of the Au–Pt alloy NPs but also promotes the reduction of Mn-based oxides and the mobility of oxygen. The absence of Au leads to a decrease in Pt 4f7/2 binding energy, resulting in an enrichment of electrons at the Pt active site and enhancing the oxidation ability of the primary hydroxyl group. In addition, the Au–Pt/MnxOyCz catalyst showed excellent stability without substantial loss of activity after being recycled five times. The insights and methodology may provide some new guidance for the reasonable design of bimetallic catalysts for the catalytic oxidation of biopolyols under mild conditions

    Association of the <i>FCN2</i> Gene Single Nucleotide Polymorphisms with Susceptibility to Pulmonary Tuberculosis

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    <div><p>Ficolin-2 (FCN2) is an innate immune pattern recognition molecule that can activate the complement pathway, opsonophagocytosis, and elimination of the pathogens. The present study aimed to investigate the association of the <i>FCN2</i> gene single nucleotide polymorphisms (SNPs) with susceptibility to pulmonary tuberculosis (TB). A total of seven SNPs in exon 8 (+6359 C>T and +6424 G>T) and in the promoter region (-986 G>A, -602 G>A, -557 A>G, -64 A>C and -4 A>G) of the <i>FCN2</i> gene were genotyped using the PCR amplification and DNA sequencing methods in the healthy controls group (n = 254) and the pulmonary TB group (n = 282). The correlation between SNPs and pulmonary TB was analyzed using the logistic regression method. The results showed that there were no significant differences in the distribution of allelic frequencies of seven SNPs between the pulmonary TB group and the healthy controls group. However, the frequency of the variant homozygous genotype (<i>P</i> = 0.037, -557 A>G; <i>P</i> = 0.038, -64 A>C; <i>P</i> = 0.024, +6424 G>T) in the TB group was significantly lower than the control group. After adjustment for age and gender, these variant homozygous genotypes were found to be recessive models in association with pulmonary TB. In addition, -64 A>C (<i>P</i> = 0.047) and +6424 G>T (<i>P</i> = 0.03) were found to be codominant models in association with pulmonary TB. There was strong linkage disequilibrium (r<sup>2</sup> > 0.80, <i>P</i> < 0.0001) between 7 SNPs except the -602 G>A site. Therefore, -557 A>G, -64 A>C and +6424 G>T SNPs of the <i>FCN2</i> gene were correlated with pulmonary TB, and may be protective factors for TB. This study provides a novel idea for the prevention and control of TB transmission from a genetics perspective.</p></div

    Haplotype frequencies of polymorphisms variants of the -986 G>A, -602 G>A, +6359 C>T and +6424 G>T SNPs in patients with pulmonary TB and healthy controls.

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    <p><sup>a</sup> Adjusted for age and sex.</p><p>Freq: frequency of haplotype; OR: odds ratios; 95% CI: 95% confidence intervals.</p><p>Haplotype frequencies of polymorphisms variants of the -986 G>A, -602 G>A, +6359 C>T and +6424 G>T SNPs in patients with pulmonary TB and healthy controls.</p

    Distribution of the <i>FCN2</i> SNP allele frequencies and genotype frequencies in the pulmonary TB group (n = 282) and the control group (n = 254).

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    <p>SNP: single nucleotide polymorphism; HWE: Hardy-Weinberg Equilibrium; N: numbers; Freq: frequency; OR: odds ratios; 95% CI: 95% confidence intervals; <i>P</i> value and odd ratio were obtained by Chi-square test.</p><p>Distribution of the <i>FCN2</i> SNP allele frequencies and genotype frequencies in the pulmonary TB group (n = 282) and the control group (n = 254).</p

    Haploview plot illustrating the linkage disequilibrium (LD) of the FCN2 variants.

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    <p><b>A</b>: Linkage disequilibrium of 7 functional <i>FCN2</i> single nucleotide polymorphism (SNPs) in the healthy controls. Block 1 represent the 2 SNPs (−557A>G and −64 A>C) completely linked. <b>B</b>: Linkage disequilibrium of 7 functional <i>FCN2</i> SNPs in the pulmonary TB group. Block 1 represent the 3 SNPs (−557A>G, −64 A>C and +6424 G>T) completely linked. Open squares indicate a high degree of LD (LD coefficient D′ = 1) between pairs of markers. Numbers indicate the r<sup>2</sup> value.</p
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