[Simulation of air pollution characteristics and estimates of environmental capacity in Zibo City].

To develop a new pattern of air pollution control that is based on the integration of "concentration control, total amount control, and quality control", and in the context of developing national (2011-2015 air pollution control plan for key areas) and (Environmental protection plan of Zibo municipality for the "12th Five-Year Plan" period), a simulation of atmospheric dispersion of air pollutants in Zibo City and its peripheral areas is carried out by employing CALPUFF model, and the atmospheric environmental capacity of SO2, NO(x) and PM10 is estimated based on the results of model simulation and using multi-objective linear programming optimization. The results indicates that the air pollution in Zibo City is significantly related to the pollution sources outside of Zibo City, which contributes to the annual average concentration of SO2, NO2 and PM10 in Zibo City by 26.34%, 21.23%, and 14.58% respectively. There is a notable interaction between districts and counties of Zibo municipality, in which the contribution of SO2, NO(x) and PM10 emissions in surrounding counties and districts to the annual average concentrations of SO2, NO2 and PM10 in downtown area are 35.96%, 43.17%, and 17.69% respectively. There is a great variation in spatial sensitivity of air pollutant emission, and the environmental impact of unit pollutant emissions from Zhoucun, Huantai, Zhangdian and Zichuan is greater than that released from other districts/counties. To meet the requirement of (Ambient air quality standard) (GB 3095-2012), the environmental capacities of SO2, NO(x) and PM10 of Zibo City are only 8.03 x 10(4) t, 19.16 x 10(4) t and 3.21 x 10(4) t, respectively. Therefore, it is imperative to implement regional air pollution joint control in Shandong peninsula in order to ensure the achievement of air quality standard in Zibo City.

Cathepsin L expression and regulation in human abdominal aortic aneurysm, atherosclerosis, and vascular cells.

The cysteine protease cathepsin L is one of the most potent mammalian elastases and collagenases, widely expressed at basal levels in most tested tissues and cell types, and regulated by pro-inflammatory stimuli. The inflammatory arterial diseases abdominal aortic aneurysm (AAA) and atherosclerosis involve extensive vascular remodeling that requires elastolysis and collagenolysis. This study examined the hypothesis that cathepsin L is over-expressed in human AAA and atherosclerotic lesions and its expression in vascular cell types found in these lesions is regulated by pro-inflammatory cytokines. Immunohistochemical and tissue extract immunoblot analysis demonstrated increased expression of cathepsin L in human AAA and atheromata and localized its expression to lesional smooth muscle cells (SMC), endothelial cells (EC), and macrophages. In primary cultured human SMC, EC, and monocyte-derived macrophages, pro-inflammatory cytokines or growth factors induced the expression of cathepsin L and its activity against extracellular collagen and elastin. Patients with coronary artery stenosis (n=65) had higher serum cathepsin L levels than those without lesions detectable by quantitative coronary angiography (n=30) (1.47+/-0.33 ng/ml versus 0.60+/-0.06 ng/ml, p<0.02). A strong correlation between the percent of stenosis of left anterior descending coronary artery and serum cathepsin L levels in patients with stenosis (R=0.542, p<0.0001), also suggests involvement of cathepsin L in these vascular diseases.