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The Advanced Himawari Imager (AHI) onboard Himawari-8, a next-generation geostationary meteorological satellite, provided firstly the full-disk aerosol observations every 10 min at sub-kilometer spatial resolution(5 km). This is responsible for retrieving the ground-level particulate matter of fewer than 2.5 micrometers and improving assimilation model. However, the representativeness of AHI L3 hourly Aerosol Optical Thickness (AOT) products remains unclear under different air quality conditions, Especially, over frequently polluted urban areas that feature complex surface characteristics and aerosol models. In this study, One-to-one comprehensive comparisons were conducted to evaluate the performance of three types of AHI L3 AOT products (version 3.0) based on the Aerosol Robotic NETwork (AERONET) aerosol measurements over Beijing. The overall comparisons of AHI and ground AOTs show the AHI merged AOT perform best, which the R is 0.87, RMSE is 0.25 and 52.5% of retrievals fall within the envelope of Expect Error (EE, ±(0.05 + 0.2 * AOTground)). For the different primary pollutants, the results suggested the three types AHI hourly AOT products are more suitable for the fine particulate matters (PM2.5) retrievals, especially the merged AOT with 0.87 of R, 0.29 of RMSE and 58.8% of within EE. Furthermore, when the slight and moderate pollution happened over Beijing, the AHI hourly AOT products perform well. And when the heavy pollution happened, the performance of the AHI merge AOT and L2 mean AOT is better. a case during low to high pollution suggested that AHI merged AOT can capture the similar spatial pattern to the MODIS (Deep Blue) DB or (Dark Target) DTDB merged AOT and has good consistency with ground-based air quality monitoring. These results demonstrate the AHI hourly merged AOT is a promising aerosol retrieval for air quality. [ABSTRACT FROM AUTHOR]

Pharmacokinetics and elimination of florfenicol and florfenicol amine in grouper held in sea water at 23.3 ± 0.8 °C were studied using HPLC method after they were given a single peroral dose of florfenicol at 24 mg kg−1 body weight. Florfenicol was rapidly absorbed from intestine and distributed extensively to all the tissues examined. The maximum concentrations ( Cmax, μg g−1 or μg mL−1) in plasma and tissues were observed at 2-6 h (the time to reach maximum concentration, Tmax) except for bile ( Tmax = 24 h) and were in the order of intestine (52.02 ± 25.07) > bile (49.41 ± 28.16) > gill (45.12 ± 11.10) > plasma (28.28 ± 5.43) > liver (21.97 ± 12.08) > muscle (21.63 ± 6.12) > kidney (20.88 ± 11.28) > skin (19.10 ± 5.88). The drug distribution level was higher in plasma than in extravascular tissues except for bile, based on the ratios of the area under concentration-time curve between tissue and plasma (AUCtissue/plasma). The elimination of florfenicol was rapid in fish, and the corresponding half-lives ( T1/2β) in the order of magnitude were bile (13.92 h) > muscle or liver (12.31 h) > skin (11.77 h) > plasma (11.57) > gill (11.04 h) > intestine (10.55 h) > kidney (10.05 h). The delayed Tmax, lower Cmax and longer T1/2β for florfenicol amine compared with florfenicol were measured in grouper. [ABSTRACT FROM AUTHOR]

Cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is expressed in the epithelial cells of a wide range of organs/tissues from which most cancers are derived. Although accumulating reports have indicated the association of cancer incidence with genetic variations in CFTR gene, the exact role of CFTR in cancer development and the possible underlying mechanism have not been elucidated. Here, we report that CFTR expression is significantly decreased in both prostate cancer cell lines and human prostate cancer tissue samples. Overexpression of CFTR in prostate cancer cell lines suppresses tumor progression (cell growth, adhesion and migration), whereas knockdown of CFTR leads to enhanced malignancies both in vitro and in vivo. In addition, we demonstrate that CFTR knockdown-enhanced cell proliferation, cell invasion and migration are significantly reversed by antibodies against either urokinase plasminogen activator (uPA) or uPA receptor (uPAR), which are known to be involved in various malignant traits of cancer development. More interestingly, overexpression of CFTR suppresses uPA by upregulating the recently described tumor suppressor microRNA-193b (miR-193b), and overexpression of pre-miR-193b significantly reverses CFTR knockdown-enhanced malignant phenotype and abrogates elevated uPA activity in prostate cancer cell line. Finally, we show that CFTR gene transfer results in significant tumor repression in prostate cancer xenografts in vivo. Taken together, the present study has demonstrated a previously undefined tumor-suppressing role of CFTR and its involvement in regulation of miR-193b in prostate cancer development. [ABSTRACT FROM AUTHOR]