[Satellite retrieval of a heavy pollution process in January 2013 in China].

By simulating vertical stratification data of PM2.5 with the third-generation air quality model CMAQ and high resolution relative humidity data with mesoscale meteorological model WRF, MODIS AOD data were revised by vertical and humidity correcting method, respectively. A linear regression model between revised AOD and PM2.5 was built, and the linear correlation coefficient was r = 0.77 (n = 57, P < 0.01). Based on this model, the average monthly concentrations of PM2.5 in 10 km resolution in January 2013 were firstly retrieved in the country, and the population exposure level was analyzed. The results showed that the areas where average monthly concentrations of PM2.5 was greater than 100 µg x m(-3) and 200 µg x m(-3) in January 2013 were 10.99% and 1.34% of the national terrestrial area, respectively, and the ratios of exposed population were as high as 45.01% and 6.31%, respectively.

[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.

Chronic application of nonylphenol-induced apoptosis via suppression of bcl-2 transcription and up-regulation of active caspase-3 in mouse brain.

Nonylphenol (NP) is an endocrine disruptor, which has been reported to have adverse effects on reproductive and immune systems. However, the influence of NP on the central nervous system (CNS) has not been extensively explored. The present study was performed to investigate the effects of chronic administration of NP on the apoptosis-related protein expression in mouse brain by in situ hybridization, RT-PCR and immunoblotting assays. The expression of bcl-2 mRNA was down-regulated by NP at the doses of 100 and 200mg/(kg day) (p<0.05), whereas the expression of bax mRNA was not affected in NP treated mice (p>0.05). Furthermore, as the main executor of apoptosis, the expression of active caspase-3 was up-regulated by 100 and 200mg/(kg day) NP (p<0.01), which is in accord with the results of terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) (p<0.05). These results suggest that chronic application of NP could sensitize the mice brain to apoptosis.

Elevation of inducible nitric oxide synthase and cyclooxygenase-2 expression in the mouse brain after chronic nonylphenol exposure.

The present study was performed to investigate the effects of chronic administration of nonylphenol (NP) on the expression of inflammation-related genes in the brains of mice. NP was given orally by gavages at 0, 50, 100, and 200 mg/kg/d. The expression of inflammatory enzymes, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), was evaluated by immunohistochemistry and immunoblotting assays. The nitric oxide (NO) level and nitric oxide synthase (NOS) activity were also measured by biochemical analyses. The results showed that NP at a high dose (200 mg/kg/d) significantly increased the expression of iNOS and COX-2 in both the hippocampus and cortex. In parallel with the increase in iNOS expression, the NO level was significantly greater at the dose of 200 mg/kg/d, compared to the control. The activity of NOS was also increased in the brain of mice at the dose of 100 and 200 mg/kg/d. These findings demonstrate that NP may have the potential to induce the chronic inflammation or cause neurotoxicity in the mouse brain.

The anti-apoptosis effects of daidzein in the brain of D-galactose treated mice.

The purpose of this study was to explore the neuroprotective effects of daidzein on the apoptotic pathway in the hippocampus and cortex of D-galactose treated mice. For this purpose we have examined the expression of bcl-2 mRNA, bax mRNA and caspase-3 in the hippocampus and cortex of D-galactose-treated mice after fed with 10 or 5 mg/kg of daidzein. The results of in situ hybridization experiments indicate that daidzein could help increase the transcriptions of bcl-2 and decrease the transcriptions of bax in those brain regions of D-galactose-treated mice. Furthermore, immunohistochemical studies showed that daidzein could reduce the expression of caspase-3 in both brain regions. These results suggest that daidzein in soybean can inhibit the D-gal induced apoptosis via Bcl-2/Bax apoptotic pathway and be a potential medical candidate for neurodegeneration therapy.