ABSTRACT
A total of 1 685 school-age children selected from Hangzhou received lung function testing to evaluate the short-term effects of air pollution on their lung function. The results showed that in every 10 μg/m3 increase of average concentration of PM2.5 and PM10 on the day of the test and the day before the test,peak expiratory flow (PEF) decreased 0.039 (95%CI: 0.012-0.067) L/s and 0.031 (95% CI:0.011-0.051) L/s,respectively. When the average concentration of SO2 increased 10 μg/m3 on the day of test and the day prior to the test, PEF and 75% of the forced vital capacity that has not been exhaled (MEF75) decreased 0.437 (95%CI: 0.217-0.658) L/s and 0.396 (95%CI: 0.180-0.613) L/s. After being adjusted for NO2,with every 10 μg/m3 increase of average concentration of PM2.5 and PM10 on the day of the test and the day before the test,PEF and MEF75 decreased 0.056 (95%CI: 0.028-0.085), 0.053(95%CI: 0.027-0.081) and 0.047 (95%CI: 0.026-0.068) L/s,0.044 (95%CI: 0.023-0.065) L/s on the day before the test, respectively. The results indicate that air pollution have short-term and lag effects on lung function of school-age children in Hangzhou.
ABSTRACT
OBJECTIVE To examine the synergistic inhibiory effect of combination of mammalian target of sirolimus (Rapamycin) (mTOR) inhibitor everolimus and AKT inhibitor MK-2206 on hepatocar-cinoma cell proliferation. METHODS HepG2 and BEL-7402 cells were treated with sirolimus and evero-limus alone for 0, 1, 3, 6, 12 and 24 h or in combination with insulin-like growth factor 1 receptor (IGF-1R) inhibitor NVP-AEW541 or AKT inhibitor MK2206 for 24 h. p70S6K and AKT kinase activityies were detected by Western blotting. Plate clone formation assay and CCK8 assay were used to detect the growth and proliferation of hepatocarcinoma cells treated with everolimus and MK2206 alone or in combi-nation. RESULTS Sirolimus and everolimus inhibited p70S6K activity while causing feedback activa-tion of AKT kinase activity at different time points (P<0.01). NVP-AEW541 and MK-2206 could inhibit AKT kinase feedback activation by everolimus (P<0.05). Colony formation of hepatocarcinoma cells treated with everolimus and MK-2206 in combination was significantly inhibited compared with everolimus or MK-2206 alone (P<0.01). Everolimus and MK-2206 in combination inhibited the proliferation rate of two types of hepatocarcinoma cancer cells by more than 45％ compared with everolimus used alone (P<0.01). CONCLUSION The resistance of sirolimus and its derivatives in hepatocellular carcinoma cells may be achieved throngh the feedback-activated PI3K/AKT pathway, and the combination therapy can synergistically inhibit the growth and proliferation of hepatocarcinoma cells.