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The selective hydrogenation of the biomass platform molecule furfural (FAL) to produce furfuryl alcohol (FA) is of great significance to alleviate the energy crisis. Cu-based catalysts are the most commonly used catalysts, and their catalytic performance can be optimized by changing the preparation method. This paper emphasized the effect of calcination atmosphere on the performance of a Cu/Al2O3 catalyst for the selective hydrogenation of FAL. The precursor of the Cu/Al2O3 catalyst prepared by the ammonia evaporation method was treated with different calcination atmospheres (N2 and air). On the basis of the combined results from the characterizations using in situ XRD, TEM, N2O titration, H2-TPR and XPS, the Cu/Al2O3 catalyst calcined in the N2 atmosphere was more favorable for the dispersion and reduction of Cu species and the reduction process could produce more Cu+ and Cu0 species, which facilitated the selective hydrogenation of FAL to FA. The experimental results showed that the N2 calcination atmosphere improved the FAL conversion and FA selectivity, and the FAL conversion was further increased after reduction. Cu/Al2O3-N2-R exhibited the outstanding performance, with a high yield of 99.9% of FA after 2 h at 120 °C and an H2 pressure of 1 MPa. This work provides a simple, efficient and economic method to improve the C=O hydrogenation performance of Cu-based catalysts. [ABSTRACT FROM AUTHOR]

Excessively activated microglia exhibit increased migration, resulting in tissue damage and chronic inflammation. Src was confirmed to play an important role in regulation of cell motility following lipopolysaccharide (LPS) treatment. SET8 plays an important part in multiple cellular signal pathways. In this study, we speculated that SET8 is involved in LPS-induced microglial migration via regulation of Src expression. Our study showed that LPS promoted cell migration via augmentation of Src expression in BV2 cells. Moreover, LPS treatment decreased SET8 expression and upregulated the expression of the transcription factor ETS proto-oncogene 1 (ETS1). Overexpression of both SET8 and small interfering ETS1 reversed LPS-induced Src expression and cell migration. The effects of short hairpin SET8 (shSET8) and ETS1 overexpression are the same as the effects of LPS treatment. Decrease of Src expression reversed the shSET8-induced and ETS1 overexpression-induced migration of BV2 cells. Furthermore, SET8 was observed to associate with ETS1. Chromatin immunoprecipitation assay indicated H4K20me1, a downstream target of SET8, in addition to ETS1, was enriched at the Src promoter region. Furthermore, shSET8 increased Src promoter activity and also increased the positive effect of ETS1 overexpression on Src promoter activity. This study shows that SET8 associates with ETS1 to regulate Src expression, which is involved in LPSinduced BV2 cell migration. Key words: lipopolysaccharide, BV2 cells, SET8, ETS proto-oncogene 1, cell migration. La microglie excessivement activee presente une augmentation de la migration entrainant des lesions tissulaires et de l'inflammation chronique. On a confirme que Src joue un role important dans la regulation de la motilite des cellules a la suite de l'administration de lipopolysaccharides (LPS). SET8 joue un role important dans de multiples voies de signalisation cellulaires. Dans cette etude, nous avons pose l'hypothese selon laquelle SET8 participe a la migration de la microglie provoquee par les LPS par l'intermediaire de la regulation de l'expression de Src. Notre etude a montre que les LPS favorisaient la migration des cellules par l'intermediaire de l'augmentation de l'expression de Src dans les cellules BV2. En outre, l'administration de LPS entrainait une diminution de l'expression de SET8 et une regulation a la hausse de l'expression du proto-oncogene 1 du facteur de transcription ETS (ETS1). La surexpression de SET8 comme de siETS1 permettait d'inverser l'expression de Src et la migration cellulaire engendrees par les LPS. Les effets de shSET8 et de la surexpression d'ETS1 sont les memes qu'avec l'administration de LPS. La diminution de l'expression de Src entrainait l'inversion de la migration des cellules BV2 engendree par shSET8 et et la surexpression d'ETS1. De plus, nous avons observe que SET8 est associe avec le facteur ETS1. A l'aide de l'epreuve de ChIP, nous avons montre que H4K20me1, une cible en aval de SET8, en plus du facteur ETS1, etait enrichi dans la region promotrice de Src. En outre, shSET8 entrainait une augmentation de l'activite promotrice de Src avec aussi un accroissement de l'effet positif de la surexpression d'ETS1 sur l'activite promotrice de Src. Cette etude expose que SET8 s'associe avec ETS1 dans la regulation de l'expression de Src, laquelle joue un role dans la migration des cellules BV2 provoquee par les LPS. [Traduit par la Redaction] Mots-cles: lipopolysaccharides, cellules BV2, SET8, ETS1, migration cellulaire., Introduction Microglia, macrophage-like immune cells, play a crucial role in maintaining homeostasis in the central nervous system. In response to pathological changes, microglia switch to an activated status, exhibiting wound [...]

Background: Trimethylamine N-oxide, a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients, has been associated with a poor prognosis for patients with cardiovascular disease. However, the role and underlying mechanisms of trimethylamine N-oxide in the cardiac function of patients with heart failure with preserved ejection fraction (HFpEF) have not been elucidated.Methods and Results: C57BL/6 mice were fed a normal diet, high-choline (1.2%) diet, and/or 3-dimethyl-1-butanol diet 3 weeks before the operation (uninephrectomy followed by a continuous saline or aldosterone infusion). Mice were assessed for 4 weeks after the operation. Echocardiographic and hemodynamic measurements were performed. Blood samples were evaluated for choline, trimethylamine N-oxide, and inflammatory factor levels. Left ventricular tissues were collected to assess myocardial fibrosis and inflammation. Left ventricular hypertrophy, pulmonary congestion, and diastolic dysfunction were markedly exacerbated in HFpEF mice fed high-choline diets compared with mice fed the control diet. Myocardial fibrosis and inflammation were markedly increased in HFpEF mice fed high-choline diets compared with animals fed the control diet. Additionally, 3,3-dimethyl-1-butanol DMB markedly ameliorated cardiac diastolic dysfunction, myocardial fibrosis and inflammation in the choline-fed HFpEF mice.Conclusions: A high-choline diet exacerbates cardiac dysfunction, myocardial fibrosis, and inflammation in HFpEF mice, and 3,3-dimethyl-1-butanol ameliorates the high-choline diet-induced cardiac remodeling. [ABSTRACT FROM AUTHOR]

The conformational conversion of the cellular prion protein (PrPC) into its β-sheet-rich scrapie isoform (PrPSc) causes fatal prion diseases, which are also called transmissible spongiform encephalopathies (TSEs). Recent studies suggest that the expression of PrPC by the PRNP gene is crucial for the development of TSEs. Therefore, the identification of the exogenous and endogenous stimulating factors that regulate PRNP expression would help to understand the pathogenesis of TSEs. Here, we demonstrate that forkhead box O3a (FOXO3a) negatively regulates PRNP expression by binding to the PRNP promoter, which is negatively regulated by insulin-like growth factor 1 (IGF-1). Our results show that the IGF-1-induced enhancement of PRNP mRNA and protein levels is due to the activation of the PI3K-Akt signaling pathway. The activation of Akt then induces the phosphorylation of FOXO3a, leading to its translocation from the nucleus to the cytoplasm and preventing its binding to the PRNP promoter. Treatment with the PI3K-Akt inhibitor LY294002 induces the nuclear retention of FOXO3a, which leads to a decrease in PRNP expression. We present a new IGF-1-PI3K-Akt-FOXO3a pathway, which influences PRNP expression. The results of this work are vital for understanding the function of PrPC and for future therapeutic approaches to human TSEs. [ABSTRACT FROM AUTHOR]