Soil moisture modelling of a SMOS pixel: interest of using the PERSIANN database over the Valencia Anchor Station

In the framework of Soil Moisture and Ocean Salinity (SMOS) Calibration/Validation (Cal/Val) activities, this study addresses the use of the PERSIANN-CCS<sup>1</sup>database in hydrological applications to accurately simulate a whole SMOS pixel by representing the spatial and temporal heterogeneity of the soil moisture fields over a wide area (50×50 km<sup>2</sup>). The study focuses on the Valencia Anchor Station (VAS) experimental site, in Spain, which is one of the main SMOS Cal/Val sites in Europe. <br><br> A faithful representation of the soil moisture distribution at SMOS pixel scale (50×50 km<sup>2</sup>) requires an accurate estimation of the amount and temporal/spatial distribution of precipitation. To quantify the gain of using the comprehensive PERSIANN database instead of sparsely distributed rain gauge measurements, comparisons between in situ observations and satellite rainfall data are done both at point and areal scale. An overestimation of the satellite rainfall amounts is observed in most of the cases (about 66%) but the precipitation occurrences are in general retrieved (about 67%). <br><br> To simulate the high variability in space and time of surface soil moisture, a Soil Vegetation Atmosphere Transfer (SVAT) model – ISBA (Interactions between Soil Biosphere Atmosphere) is used. The interest of using satellite rainfall estimates as well as the influence that the precipitation events can induce on the modelling of the water content in the soil is depicted by a comparison between different soil moisture data. Point-like and spatialized simulated data using rain gauge observations or PERSIANN – CCS database as well as ground measurements are used. It is shown that a good adequacy is reached in most part of the year, the precipitation differences having less impact upon the simulated soil moisture. The behaviour of simulated surface soil moisture at SMOS scale is verified by the use of remote sensing data from the Advanced Microwave Scanning Radiometer on Earth observing System (AMSR-E). We show that the PERSIANN database provides useful information at temporal and spatial scales in the context of soil moisture retrieval. <br><br> <br><br> <sup>1</sup>Precipitation Estimation from Remotely Sensed Information using Artificial Neural Networks-Cloud Classification System – <a href="http://chrs.web.uci.edu/persiann"target="_blank">http://chrs.web.uci.edu/persiann</a&gt

Aerodynamic Shape Optimization of a Blended-Wing-Body Aircraft

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/106465/1/AIAA2013-283.pd

E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer

Human papillomaviruses (HPV) are a major cause of malignancy worldwide, contributing to ~5% of all human cancers including almost all cases of cervical cancer and a growing number of ano-genital and oral cancers. HPV-induced malignancy is primarily driven by the viral oncogenes, E6 and E7, which manipulate host cellular pathways to increase cell proliferation and enhance cell survival, ultimately predisposing infected cells to malignant transformation. Consequently, a more detailed understanding of viral-host interactions in HPV-associated disease offers the potential to identify novel therapeutic targets. Here, we identify that the c-Jun N-terminal kinase (JNK) signalling pathway is activated in cervical disease and in cervical cancer. The HPV E6 oncogene induces JNK1/2 phosphorylation in a manner that requires the E6 PDZ binding motif. We show that blockade of JNK1/2 signalling using small molecule inhibitors, or knockdown of the canonical JNK substrate c-Jun, reduces cell proliferation and induces apoptosis in cervical cancer cells. We further demonstrate that this phenotype is at least partially driven by JNK-dependent activation of EGFR signalling via increased expression of EGFR and the EGFR ligands EGF and HB-EGF. JNK/c-Jun signalling promoted the invasive potential of cervical cancer cells and was required for the expression of the epithelial to mesenchymal transition (EMT)-associated transcription factor Slug and the mesenchymal marker Vimentin. Furthermore, JNK/c-Jun signalling is required for the constitutive expression of HPV E6 and E7, which are essential for cervical cancer cell growth and survival. Together, these data demonstrate a positive feedback loop between the EGFR signalling pathway and HPV E6/E7 expression, identifying a regulatory mechanism in which HPV drives EGFR signalling to promote proliferation, survival and EMT. Thus, our study has identified a novel therapeutic target that may be beneficial for the treatment of cervical cancer