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In Beijing, capital of China, decreasing visibility has become a serious problem on people's life, thus a hot environmental concern. An urban roadside site in Beijing was chosen to collect 24-h TSP, PM10 and PM2.5 samples for one month each season from June 2009 to March 2010. The PM mass concentrations, and the concentrations of ions, EC, OC and metals in PM10 and PM2.5 were measured, and their correlation with visibility, as well as the influence of weather factors on visibility were studied. The results showed that daily mean concentrations of TSP, PM10 and PM2.5 were 75-1350 μg/m^3 (mean 275.8), 29-448 μg/m^3 (mean 187) and up to 300 μg/m^3 (mean 92.6), with the number of days exceeding the secondary standard (GB3095-2012) representing 33.3%, 59.8% and 51.0%, respectively. All PM concentrations were higher in spring than in other seasons. Obvious seasonal variations were observed for certain ions, OC, EC and metal concentrations in PM10 and PM2.5. Average mean visibility was low (5.64 km), showing better visibility in summer than in other seasons. PM10 and PM2.5 showed stronger negative correlation with visibility giving coefficients of -0.52 and -0.50. Almost all significant correlations were negative and occurred in autumn for visibility with TSP, PM10 and PM2.5, and with ions, EC and OC in both PM10 and PM2.5. The only positive and significant correlation was found between fine OC and visibility. Negative and significant correlations were also observed for visibility with humidity in autumn and winter, and with minimum temperature in all seasons but summer.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is effective in reducing axonal damage associated with traumatic brain injury (TBI), and has immunomodulatory properties. Toll-like receptor 4 (TLR4) is an important mediator of the innate immune response. It significantly contributes to neuroinflammation induced by brain injury. However, it remains unknown whether exogenous PACAP can modulate TBI through the TLR4/adapter protein myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway. In this study, we investigated the potential neuroprotective mechanisms of PACAP pretreatment in a weight-drop model of TBI. PACAP38 was microinjected intracerebroventricularly before TBI. Brain samples were extracted from the pericontusional area in the cortex and hippocampus. We found that TBI induced significant upregulation of TLR4, with peak expression occurring 24 h post-trauma, and that pretreatment with PACAP significantly improved motor and cognitive dysfunction, attenuated neuronal apoptosis, and decreased brain edema. Pretreatment with PACAP inhibited upregulation of TLR4 and its downstream signaling molecules MyD88, p-IκB, and NF-κB, and suppressed increases in the levels of the downstream inflammatory agents interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), in the brain tissue around the injured cortex and in the hippocampus. Administration of PACAP both in vitro and in vivo attenuated the ability of the TLR4 agonist lipopolysaccharide (LPS) to increase TLR4 protein levels. Therefore, PACAP exerts a neuroprotective effect in this rat model of TBI, by inhibiting a secondary inflammatory response mediated by the TLR4/MyD88/NF-κB signaling pathway in microglia and neurons, thereby reducing neuronal death and improving the outcome following TBI.