Secondary inorganic aerosol chemistry and its impact on atmospheric visibility over an ammonia-rich urban area in Central Taiwan.

This study investigated the hourly inorganic aerosol chemistry and its impact on atmospheric visibility over an urban area in Central Taiwan, by relying on measurements of aerosol light extinction, inorganic gases, and PM2.5 water-soluble ions (WSIs), and simulations from a thermodynamic equilibrium model. On average, the sulfate (SO42-), nitrate (NO3-), and ammonium (NH4+) components (SNA) contributed ∼90% of WSI concentrations, which in turn made up about 50% of the PM2.5 mass. During the entire observation period, PM2.5 and SNA concentrations, aerosol pH, aerosol liquid water content (ALWC), and sulfur and nitrogen conversion ratios all increased with decreasing visibility. In particular, the NO3- contribution to PM2.5 increased, whereas the SO42- contribution decreased, with decreasing visibility. The diurnal variations of the above parameters indicate that the interaction and likely mutual promotion between NO3- and ALWC enhanced the hygroscopicity and aqueous-phase reactions conducive for NO3- formation, thus led to severely impaired visibility. The high relative humidity (RH) at the study area (average 70.7%) was a necessary but not sole factor leading to enhanced NO3- formation, which was more directly associated with elevated ALWC and aerosol pH. Simulations from the thermodynamic model depict that the inorganic aerosol system in the study area was characterized by fully neutralized SO42- (i.e. a saturated factor in visibility reduction) and excess NH4+ amidst a NH3-rich environment. As a result, PM2.5 composition was most sensitive to gas-phase HNO3, and hence NOx, and relatively insensitive to NH3. Consequently, a reduction of NOx would result in instantaneous cuts of NO3-, PM2.5, and ALWC, and hence improved visibility. On the other hand, a substantial amount of NH3 reduction (>70%) would be required to lower the aerosol pH, driving more than 50% of the particulate phase NO3- to the gas phase, thereby making NH3 a limiting factor in shifting PM2.5 composition.

YKL-40-Induced Inhibition of miR-590-3p Promotes Interleukin-18 Expression and Angiogenesis of Endothelial Progenitor Cells.

YKL-40, also known as human cartilage glycoprotein-39 or chitinase-3-like-1, is a pro-inflammatory protein that is highly expressed in rheumatoid arthritis (RA) patients. Angiogenesis is a critical step in the pathogenesis of RA, promoting the infiltration of inflammatory cells into joints and providing oxygen and nutrients to RA pannus. In this study, we examined the effects of YKL-40 in the production of the pro-inflammatory cytokine interleukin-18 (IL-18), and the stimulation of angiogenesis and accumulation of osteoblasts. We observed that YKL-40 induces IL-18 production in osteoblasts and thereby stimulates angiogenesis of endothelial progenitor cells (EPCs). We found that this process occurs through the suppression of miR-590-3p via the focal adhesion kinase (FAK)/PI3K/Akt signaling pathway. YKL-40 inhibition reduced angiogenesis in in vivo models of angiogenesis: the chick embryo chorioallantoic membrane (CAM) and Matrigel plug models. We report that YKL-40 stimulates IL-18 expression in osteoblasts and facilitates EPC angiogenesis.