Removal of Elemental Mercury from Flue Gas by Thermally Activated Ammonium Persulfate in A Bubble Column Reactor

In this article, a novel technique on removal of elemental mercury (Hg⁰) from flue gas by thermally activated ammonium persulfate ((NH₄)₂S₂O₈) has been developed for the first time. Some experiments were carried out in a bubble column reactor to evaluate the effects of process parameters on Hg⁰ removal. The mechanism and kinetics of Hg⁰ removal are also studied. The results show that the parameters, (NH₄)₂S₂O₈ concentration, activation temperature and solution pH, have significant impacts on Hg⁰ removal. The parameters, Hg⁰, SO₂ and NO concentration, only have small effects on Hg⁰ removal. Hg⁰ is removed by oxidations of (NH₄)₂S₂O₈, sulfate and hydroxyl free radicals. When (NH₄)₂S₂O₈ concentration is more than 0.1 mol/L and solution pH is lower than 9.71, Hg⁰ removal by thermally activated (NH₄)₂S₂O₈ meets a pseudo-first-order fast reaction with respect to Hg⁰. However, when (NH₄)₂S₂O₈ concentration is less than 0.1 mol/L or solution pH is higher than 9.71, the removal process meets a moderate speed reaction with respect to Hg⁰. The above results indicate that this technique is a feasible method for emission control of Hg⁰ from flue gas

Oxidation Removal of Nitric Oxide from Flue Gas Using an Ultraviolet Light and Heat Coactivated Oxone System

The oxidation removal process of nitric oxide (NO) from flue gas using an ultraviolet (UV) light and heat coactivated oxone (potassium peroxymonosulfate, 2KHSO₅·KHSO₄·K₂SO₄) system in an UV (254 nm)-impinging stream reactor was studied. The main process parameters (e.g., light intensity, oxone concentration, solution temperature, solution pH, flue gas composition, and flow rate of flue gas and solution), products, mechanism, and kinetics of NO removal were studied. The results show that UV and oxone have a significant synergistic effect for promoting free radical production and improving NO removal. NO removal was improved via increasing the light intensity, oxone concentration, or solution flow rate and was inhibited with increasing the NO concentration, SO₂ concentration, or flue gas flow rate. Solution temperature and pH have double impacts on NO removal. UV light activation for oxone is the main source of SO₄^– ^• and ^•OH. Heat activation for oxone is the complementary source of SO₄^– ^• and ^•OH. SO₄^– ^• and ^•OH are the key oxidizing agents and play an important role in NO removal. Oxone plays a complementary role in NO removal. The NO removal process is a fast reaction and meets a total 1.44 order reaction (i.e., 1.0 order for NO and 0.44 order for oxone). The key kinetic parameters of NO removal were also determined

5-hydroxytryptamine Receptor (5-HT\u3csub\u3e1D\u3c/sub\u3eR) Promotes Colorectal Cancer Metastasis by Regulating Axin1/β-catenin/MMP-7 Signaling Pathway

Overexpression of 5-hydroxytryptamine (5-HT) in human cancer contributes to tumor metastasis, but the role of 5-HT receptor family in cancer has not been thoroughly explored. Here, we report overexpression of 5-HT1D receptor (5-HT1DR) was associated with Wnt signaling pathway and advanced tumor stage. The underlying mechanism of 5-HT1DR-promoted tumor invasion was through its activation on the Axin1/β-catenin/MMP-7 pathway. In an orthotopic colorectal cancer mouse model, we demonstrated that a 5-HT1DR antagonist (GR127935) effectively inhibited tumor metastasis through targeting Axin1. Furthermore, in intestinal epithelium cells, we observed that 5-HT1DR played an important role in cell invasion via Axin1/β-catenin/MMP-7 pathway. Together, our findings reveal an essential role of the physiologic level of 5-HT1DR in pulmonary metastasis of colorectal cancer

5-hydroxytryptamine Receptor (5-HT\u3csub\u3e1D\u3c/sub\u3eR) Promotes Colorectal Cancer Metastasis by Regulating Axin1/β-catenin/MMP-7 Signaling Pathway

Overexpression of 5-hydroxytryptamine (5-HT) in human cancer contributes to tumor metastasis, but the role of 5-HT receptor family in cancer has not been thoroughly explored. Here, we report overexpression of 5-HT1D receptor (5-HT1DR) was associated with Wnt signaling pathway and advanced tumor stage. The underlying mechanism of 5-HT1DR-promoted tumor invasion was through its activation on the Axin1/β-catenin/MMP-7 pathway. In an orthotopic colorectal cancer mouse model, we demonstrated that a 5-HT1DR antagonist (GR127935) effectively inhibited tumor metastasis through targeting Axin1. Furthermore, in intestinal epithelium cells, we observed that 5-HT1DR played an important role in cell invasion via Axin1/β-catenin/MMP-7 pathway. Together, our findings reveal an essential role of the physiologic level of 5-HT1DR in pulmonary metastasis of colorectal cancer