A desirable catalyst for efficiently controlling NO x emissions often demands excellent SO2 poisoning resistance. Here, we introduced Ce to modify birnessite-MnO2 to obtain a Ce-MnO2 catalyst with excellent activity (T 90 = 85 °C) for the selective catalytic reduction of NO with NH3 (NH3-SCR) at low temperatures. Compared with the MnO2 catalyst that was severely deactivated after poisoning, the Ce-MnO2 catalyst showed a significant improvement in SO2 resistance with the NO conversion slightly decreasing from 100 to 95% at 150 °C. Physicochemical characterizations combined with density functional theory calculations indicated that the sulfates formed on Mn species and Ce species played different roles in the SCR reaction. The SO3 2– adsorbed on the surface of the MnO2 catalyst can react with NH3 to form ammonium sulfites, leading to the deactivation of the catalyst. However, the SO4 2– from Ce2(SO4)3 on the sulfated Ce-MnO2 catalyst existed as new adsorption sites of NH4 +, thus providing this catalyst with more acid sites. In addition, SO2 was preferentially adsorbed and oxidized on Ce species, thereby protecting the Mn active centers from sulfation and deactivation. This work reveals the mechanism of Ce in promoting SO2 resistance over birnessite-MnO2 from the perspective of sulfates.
BackgroundThe morbidity and mortality of cancer increase remarkably every year. It's a heavy burden for family and society. The detection of prognostic biomarkers can help to improve the theraputic effect and prolong the lifetime of patients. microRNAs have an influential role in cancer prognosis. The results of articles discussing the relationship between microRNA polymorphisms and cancer prognosis are inconsistent.MethodsWe conduct a meta-analysis of 19 publications concerning the association of four common polymorphisms, mir-146a rs2910164, mir-149 rs2292832, mir-196a2 rs11614913 and mir-499 rs3746444, with cancer prognosis. Pooled Hazard Ratios with 95% Confidence Intervals for the relationship between four genetic polymorphisms and Overall Survival, Recurrence-free Survival, Disease-free survival, recurrence are calculated. Subgroup analysis by population and type of tumor are conducted.ResultsGG genotype of mir-146a may be the protective factor for overall survival, especially in Caucasian population. C-containing genotypes of mir-196a2 act as a risk role for overall survival. The same result exists in Asian population, in Non-Small Cell Lung Cancer and digestive cancer. The patients with C allele of mir-149 have a better overall survival, especially in Non-Small Cell Lung Cancer. No significant results are obtained for mir-499 polymorphisms.ConclusionsGenetic polymorphisms in mir-146a, mir-196a2 and mir-149 may be associated with overall survival. This effect varies with different types of cancer. Genetic polymorphism in mir-499 may have nothing to do with cancer prognosis.
MicroRNA biosynthesis genes can affect the regulatory effect of global microRNAs to target mRNA and hence influence the genesis and development of human cancer. Here, we selected five single nucleotide polymorphisms (SNPs) (rs7813, rs2740349, rs2291778, rs910924, rs595961) in two key microRNA biosynthesis genes (GEMIN4 and AGO1) and systematically evaluated the association between these SNPs, the gene-environment interaction and lung cancer risk. To control the impact of cigarette smoking on lung cancer, we recruited Chinese female non-smokers for the study. The total number of lung cancer cases and cancer-free controls were 473 and 395 in the case-control study. Four SNPs showed statistically significant associations with lung cancer risk. After Bonferroni correction, rs7813 and rs595961 were evidently still associated with lung cancer risk. In the stratified analysis, our results revealed that all five SNPs were associated with the risk of lung adenocarcinoma; after Bonferroni correction, significant association was maintained for rs7813, rs910924 and rs595961. Haplotype analysis showed GEMIN4 haplotype C-A-G-T was a protective haplotype for lung cancer. In the combined unfavorable genotype analysis, with the increasing number of unfavorable genotypes, a progressively increased gene-dose effect was observed in lung adenocarcinoma. We also found that individuals exposed to cooking oil fumes showed a relatively high risk of lung cancer, but no interactions were found between cooking oil fume exposure or passive smoking exposure with these SNPs, either on an additive scale or a multiplicative scale. Overall, this is the first study showing that rs7813 and rs595961 could be meaningful as genetic markers for lung cancer risk.
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