Search

A series of V-xCe/Ti catalysts was prepared by a step impregnation method with gradual increased Ce amount. Compared to the commercial V–W/Ti catalysts, the V-xCe/Ti catalysts exhibited considerably higher CO x selectivity during the oxidation of naphthalene (Nap), and less intermediates or by-products were detected both in gas phase and on the surface of the catalysts. Through a series of characterizations, it was found that abundance of weak basic sites in the form of OH was introduced by Ce, as well as the oxygen vacancies caused by the redox cycle of V4++Ce4+↔V5++Ce3+. The weak basic sites introduced by Ce could greatly enhance the Nap adsorption, and the Nap adsorbed was quickly converted to naphthol on Ce–OH. Furthermore, V existed at a high valence with the interaction of V and Ce, and the oxygen vacancies also increased the O ads and O OH. It improved the redox ability and the regeneration of Ce–OH on V-xCe/Ti catalysts. The intermediates could be further oxidized, and the Ce–OH consumed in the reaction could recover quickly. Therefore, almost 100% Nap conversion and a high CO x selectivity was observed in the V-xCe/Ti catalysts system. [Display omitted] • Ce introduced a lot of weak basic sites in the form of Ce–OH. • More naphthalene could adsorb and convert to naphthol on the weak basic sites. • V was kept at high valence and oxygen vacancies were produce through the interaction of Ce and V. • The intermediates during the naphthalene oxidation were further oxidized to enhance the CO x selectivity. [ABSTRACT FROM AUTHOR]

Arsenic trioxide (ATO) has a long history and it is recognized as both poison and drug for more than two thousand years. Since the establishment of ATO as a frontline therapeutic agent for acute promyelocytic leukemia (APL), the survival of APL patients have been greatly improved and APL is turned from highly fatal to highly curable disease. Mechanistically, ATO can induce PML/RARα fusion protein degradation, causing APL cell differentiation and apoptosis. On the other hand, the side effects such as differentiation syndrome, cardiac conduction abnormalities and liver toxicity are often observed during the ATO treatment of APL in clinic. It is likely that the therapeutic and adverse effects of ATO is probably associated with its distinct pattern of metabolism and direct or indirect effects on different organs. In this review, we provided a comprehensive and in-depth elaboration of the cytotoxic mechanisms of ATO and its methylated metabolites based on in vivo or in vitro studies, trying to clarify the importance of achieving balance between the toxicity and anti-leukemic activity of ATO in APL treatment. • ATO is the most successful metallodrug for different diseases treatment. • ATO has turned the APL from highly fatal disease into highly curable one. • Metabolic pattern of ATO is associated with its therapeutic and adverse effects. • ATO plus ATRA is better tolerated than ATRA plus chemotherapy. [ABSTRACT FROM AUTHOR]

Early growth response factor 1 (Egr-1) is a zinc finger transcription factor which responses rapidly to a variety of extracellular stimuli. Previous studies have suggested that Egr-1 exerts pathological functions in chronic obstructive pulmonary disease (COPD) by regulation of cigarette smoking-induced autophagy, cell death, and inflammation. However, little is known about the role of Egr-1 in regulation of mucus production in airway epithelium. In this study, we observed that cigarette smoke extract (CSE) induced a successive expression of Egr-1 and MUC5AC in human bronchial epithelial (HBE) cells. Knockdown of Egr-1 markedly attenuated CSE-induced MUC5AC production, and chromatin immunoprecipitation revealed that Egr-1 transcriptionally bound to MUC5AC promoter upon CSE stimulation. Concurrently, CSE increased the expression of c-Jun and c-Fos, two subunits of activator protein 1 (AP-1) which also critically regulates CSE-induced MUC5AC in HBE cells. CSE also induced a physical interaction of Egr-1 and AP-1, and knockdown of Egr-1 significantly decreased CSE-induced expression of c-Fos and c-Jun. Furthermore, knockdown of c-Fos remarkably attenuated the CSE-induced Egr-1 binding to MUC5AC promoter. These data taken together demonstrate that Egr-1 is essential for CSE-induced MUC5AC production in HBE cells likely through interaction with and modulation of AP-1, and re-emphasize targeting Egr-1 as a novel therapeutic strategy for COPD. [ABSTRACT FROM AUTHOR]

• Lipid metabolism is involved in asthma progression. • The functions of various cells in asthma are regulated by lipid metabolism. • Lipid metabolism may serve as a promising candidate in asthma therapy. Asthma is a chronic inflammatory disease of the lungs that poses a considerable health and socioeconomic burden. Several risk factors work synergistically to affect the progression of asthma. Lipid metabolism, especially in distinct cells such as T cells, macrophages, granulocytes, and non-immune cells, plays an essential role in the pathogenesis of asthma, as lipids are potent signaling molecules that regulate a multitude of cellular response. In this review, we focused on the metabolic pathways of lipid molecules, especially fatty acids and their derivatives, and summarized their roles in various cells during the pathogenesis of asthma along with the current pharmacological agents targeting lipid metabolism. [ABSTRACT FROM AUTHOR]