Mean BTC for different factors and CON results.

<p>(a) Mean BTC under three different IFOV conditions. (b) Mean BTC for different genders. (c) Mean BTC for different CON results.</p

Descriptive statistical results and ANOVA analysis results for NG in different AOIs.

<p>Descriptive statistical results and ANOVA analysis results for NG in different AOIs.</p

Descriptive statistical results and ANOVA analysis results for GD in different AOIs.

<p>Descriptive statistical results and ANOVA analysis results for GD in different AOIs.</p

Mean AGD in different AOIs for different factors and CON results.

<p>(a) Mean AGD in different AOIs under different IFOV conditions. (b) Mean AGD in different AOIs for different genders. (c) Mean AGD in different AOIs for different CON results.</p

Descriptive statistics and ANOVA results for BTC.

<p>Descriptive statistics and ANOVA results for BTC.</p

Mean NG in different AOIs for different factors and CON results.

<p>(a) Mean NG in different AOIs under three different IFOV conditions. (b) Mean NG in different AOIs for different genders. (c) Mean NG in different AOIs for different CON results.</p

Descriptive statistical results and logistic regression results for COR.

<p>Descriptive statistical results and logistic regression results for COR.</p

Classification of AOIs.

<p>a) Right AOI. (b) Left AOI. (c) Forward roadway AOI. (d) Collision vehicle AOI.</p

The Multiple Role of Bromide Ion in PPCPs Degradation under UV/Chlorine Treatment

This study investigated the role of bromide ions in the degradation of nine pharmaceuticals and personal care products (PPCPs) during the UV/chlorine treatment of simulated drinking water containing 2.5 mgC L⁻¹ natural organic matter (NOM). The kinetics of contributions from UV irradiation and from oxidation by free chlorine, free bromine, hydroxyl radical and reactive halogen species were evaluated. The observed loss rate constants of PPCPs in the presence of 10 μM bromide were 1.6–23 times of those observed in the absence of bromide (except for iopromide and ibuprofen). Bromide was shown to play multiple roles in PPCP degradation. It reacts rapidly with free chlorine to produce a trace amount of free bromine, which then contributes to up to 55% of the degradation of some PPCPs during 15 min of UV/chlorine treatment. Bromide was also shown to reduce the level of HO^• and to change the reactive chlorine species to bromine-containing species, which resulted in decreases in ibuprofen degradation and enhancement in carbamazepine and caffeine degradation, respectively. Reactive halogen species contributed to between 37 and 96% of the degradation of the studied PPCPs except ibuprofen in the presence of 10 μM bromide ion. The effect of bromide is non-negligible during the UV/chlorine treatment

Table2_A Novel N-Arylpyridone Compound Alleviates the Inflammatory and Fibrotic Reaction of Silicosis by Inhibiting the ASK1-p38 Pathway and Regulating Macrophage Polarization.docx

Silicosis is one of the potentially fatal occupational diseases characterized by respiratory dysfunction, chronic interstitial inflammation, and fibrosis, for which treatment options are limited. Previous studies showed that a novel N-arylpyridone compound named AKEX0011 exhibited anti-inflammatory and anti-fibrotic effects in bleomycin-induced pulmonary fibrosis; however, it is unknown whether it could also be effective against silicosis. Therefore, we sought to investigate the preventive and therapeutic roles of AKEX0011 in a silicosis rodent model and in a silica-stimulated macrophage cell line. In vivo, our results showed that AKEX0011 ameliorated silica-induced imaging lung damages, respiratory dysfunction, reduced the secretion of inflammatory and fibrotic factors (TNF-α, IL-1β, IL-6, TGF-β, IL-4, and IL-10), and the deposition of fibrosis-related proteins (collagen I, fibronectin, and α-SMA), regardless of early or advanced therapy. Specifically, we found that AKEX0011 attenuated silicosis by inhibiting apoptosis, blocking the ASK1-p38 MAPK signaling pathway, and regulating polarization of macrophages. In vitro, AKEX0011 inhibited macrophages from secreting inflammatory cytokines and inhibited apoptosis of macrophages in pre-treated and post-treated models, concurrent with blocking the ASK1-p38 pathway and inhibiting M1 polarization. Collectively, AKEX0011, as a novel N-arylpyridone compound, exerted protective effects for silica-induced pulmonary inflammation and fibrosis both in vivo and in vitro, and hence, it could be a strong drug candidate for the treatment of silicosis.</p