Fly ash consists of various metal oxides which can remove SO2 gas by the catalyst effect. When fly ash is added in the preparation process of pitch-based activated carbon, the pitch particles aggregate and fly ash is embedded in the activated carbon. To increase SO2 gas removal performance, activated carbon was prepared by surface-treated fly ash and petroleum-based pitch. Carboxyl groups were introduced into the fly ash by malic acid treatment. The introduced carboxyl groups acted as an activation agent to create micropore around the fly ash, and created micropores were exposed to the fly ash outside of the activated carbon. The exposed fly ash increased removal amount of SO2 gas by a catalytic effect of the metal oxides. The SO2 gas removal performance improved by 34% because of the catalyst effect of the exposed fly ash and improvement in the micropore structure in the activated carbon.

Here, the stability of stainless steel 316 (SS-316) was investigated to identify its applicability in the oxide reduction process, as a component in related equipment, to produce a complicated gas mixture composed of O2 and Cl2 under an argon (Ar) atmosphere. The effects of the mixed gas composition were investigated at flow rates of 30 mL/min O2, 20 mL/min O2 + 10 mL/min Cl2, 10 mL/min O2 + 20 mL/ min Cl2, and 30 mL/min Cl2, each at 600℃, during a constant argon flow rate of 170 mL/min. It was found that the corrosion of SS-316 by the chlorine gas was suppressed by the presence of oxygen, while the reaction proceeded linearly with the reaction time regardless of gas composition. Surface observation results revealed an uneven surface with circular pits in the samples that were fed mixed gases. Thermodynamic calculations proposed the combination of Fe and Ni chlorination reactions as an explanation for this pit formation phenomenon. An exponential increase in the corrosion rate was observed with an increase in the reaction temperature in a range of 300 ~ 600℃ under a flow of 30 mL/min Cl2 + 170 mL/min Ar.

Equine follicle stimulating hormone receptor (eFSHR) has a large extracellular domain and an intracellular domain containing approximately 10 phosphorylation sites within the G protein-coupled receptor. This study was conducted to analyze the function of phosphorylation sties at the eFSHR C-terminal region. We constructed a mutant of eFSHR, in which the C-terminal cytoplasmic tail was truncated at residue 641 (eFSHR-t641). This removed 10 potential phosphorylation sites from the C-terminal region of the intracellular loop. The eFSHR-wild type (eFSHR-wt) and eFSHR-t641 cDNAs were subcloned into the pCMV-ARMS1-PK2 expression vector. These plasmids were transfected into PathHunter CHO-K1 Parental cells expressing β-arrestin 2 enzyme acceptor fusion protein and analyzed for agonist-induced cAMP response. The cAMP response in cells expressing eFSHR-t641 was lower than the response in cells expressing eFSHR-wt. EC50 values of eFSHR-wt and eFSHR-t641 were 1079 ng/mL and 1834 ng/mL, respectively. eFSHR-t641 was approximately 0.58-fold compared with that of eFSHR-wt. The maximal response in eFSHR-wt and eFSHR-t641 was 24.7 nM and 16.7 nM, respectively. The Rmax value of phosphorylation sites in eFSHR-t641 was also decreased to approximately 68.4% of that in eFSHR-wt. The collective data implicate that the phosphorylation sites in the eFSHR C-terminal region have a pivotal role in signal transduction in PathHunter CHO-K1 cells, and indicate that β-arrestin is involved in coupling the activated receptors to the internalization system.

Hepatic stellate cells (HSCs) play essential roles in normal and pathophysiological function in liver. In steady state, HSCs contribute to retinoid storage, immune tolerance, and extracellular matrix (ECM) homeostasis. Upon liver injury, they become activated and lead to morphological and functional changes. Studies have demonstrated that activation of HSCs by various stimuli such as toxins, microbial infection, or metabolic overload can promote the fibrotic changes in liver by production of ECM. Herein, we provide current knowledge about the basic characteristics of HSCs and the mechanism by which they are activated.