SMOS L1C and L2 Validation in Australia

Extensive airborne field campaigns (Australian Airborne Cal/val Experiments for SMOS - AACES) were undertaken during the 2010 summer and winter seasons of the southern hemisphere. The purpose of those campaigns was the validation of the Level 1c (brightness temperature) and Level 2 (soil moisture) products of the ESA-led Soil Moisture and Ocean Salinity (SMOS) mission. As SMOS is the first satellite to globally map L-band (1.4GHz) emissions from the Earth?s surface, and the first 2-dimensional interferometric microwave radiometer used for Earth observation, large scale and long-term validation campaigns have been conducted world-wide, of which AACES is the most extensive. AACES combined large scale medium-resolution airborne L-band and spectral observations, along with high-resolution in-situ measurements of soil moisture across a 50,000km2 area of the Murrumbidgee River catchment, located in south-eastern Australia. This paper presents a qualitative assessment of the SMOS brightness temperature and soil moisture products

Global-scale comparison of passive (SMOS) and active (ASCAT) satellite based microwave soil moisture retrievals with soil moisture simulations (MERRA-Land)

AbstractGlobal surface soil moisture (SSM) datasets are being produced based on active and passive microwave satellite observations and simulations from land surface models (LSM). This study investigates the consistency of two global satellite-based SSM datasets based on microwave remote sensing observations from the passive Soil Moisture and Ocean Salinity (SMOS; SMOSL3 version 2.5) and the active Advanced Scatterometer (ASCAT; version TU-Wien-WARP 5.5) with respect to LSM SSM from the MERRA-Land data product. The relationship between the global-scale SSM products was studied during the 2010–2012 period using (1) a time series statistics (considering both original SSM data and anomalies), (2) a space–time analysis using Hovmöller diagrams, and (3) a triple collocation error model. The SMOSL3 and ASCAT retrievals are consistent with the temporal dynamics of modeled SSM (correlation R>0.70 for original SSM) in the transition zones between wet and dry climates, including the Sahel, the Indian subcontinent, the Great Plains of North America, eastern Australia, and south-eastern Brazil. Over relatively dense vegetation covers, a better consistency with MERRA-Land was obtained with ASCAT than with SMOSL3. However, it was found that ASCAT retrievals exhibit negative correlation versus MERRA-Land in some arid regions (e.g., the Sahara and the Arabian Peninsula). In terms of anomalies, SMOSL3 better captures the short term SSM variability of the reference dataset (MERRA-Land) than ASCAT over regions with limited radio frequency interference (RFI) effects (e.g., North America, South America, and Australia). The seasonal and latitudinal variations of SSM are relatively similar for the three products, although the MERRA-Land SSM values are generally higher and their seasonal amplitude is much lower than for SMOSL3 and ASCAT. Both SMOSL3 and ASCAT have relatively comparable triple collocation errors with similar spatial error patterns: (i) lowest errors in arid regions (e.g., Sahara and Arabian Peninsula), due to the very low natural variability of soil moisture in these areas, and Central America, and (ii) highest errors over most of the vegetated regions (e.g., northern Australia, India, central Asia, and South America). However, the ASCAT SSM product is prone to larger random errors in some regions (e.g., north-western Africa, Iran, and southern South Africa). Vegetation density was found to be a key factor to interpret the consistency with MERRA-Land between the two remotely sensed products (SMOSL3 and ASCAT) which provides complementary information on SSM. This study shows that both SMOS and ASCAT have thus a potential for data fusion into long-term data records

Bringing the commercial determinants of health out of the shadows : a review of how the commercial determinants are represented in conceptual frameworks

BACKGROUND: The term 'commercial determinants of health' (CDOH) is increasingly focussing attention upon the role of tobacco, alcohol and food and beverage companies and others-as important drivers of non-communicable diseases (NCDs). However, the CDOH do not seem to be clearly represented in the most common social determinants of health (SDOH) frameworks. We review a wide range of existing frameworks of the determinants of health to determine whether and how commercial determinants are incorporated into current SDOH thinking. METHODS: We searched for papers and non-academic reports published in English since 2000 describing influences on population health outcomes. We included documents with a formal conceptual framework or diagram, showing the integration of the different determinants. RESULTS: Forty-eight framework documents were identified. Only one explicitly included the CDOH in a conceptual diagram. Ten papers discussed the commercial determinants in some form in the text only and fourteen described negative impacts of commercial determinants in the text. Twelve discussed positive roles for the private sector in producing harmful commodities. Overall, descriptions of commercial determinants are frequently understated, not made explicit, or simply missing. The role of commercial actors as vectors of NCDs is largely absent or invisible in many of the most influential conceptual diagrams. CONCLUSIONS: Our current public health models may risk framing public health problems and solutions in ways that obscure the role that the private sector, in particular large transnational companies, play in shaping the broader environment and individual behaviours, and thus population health outcomes

Public-private partnerships and the politics of alcohol policy in England : the Coalition Government's Public Health 'Responsibility Deal'

BACKGROUND: The 2010-2015 Conservative-led Coalition Government launched their flagship Public Health Responsibility Deal (PHRD) for England in 2011; a year before their alcohol strategy. This co-regulatory regime placed alcohol industry actors at the heart of policy-making, but was viewed with scepticism by public health actors. This article examines the ways in which the PHRD structured the alcohol policy environment throughout this period, which included the rejection of evidence-based policies such as minimum unit pricing. METHODS: This article draws on 26 semi-structured interviews with policy actors (parliamentarians, civil servants, civil society actors and academics) in 2018. Respondents were identified and recruited using purposive sampling. Interviews were recorded, transcribed and analysed using thematic coding. RESULTS: The PHRD shaped the context of alcohol policy development at Westminster throughout this period. It circumscribed the policy space by taking evidence-based measures not amenable to industry partnership off the agenda. While the PHRD created important opportunities for industry engagement with policy-makers, it undermined public health actors' access to government, particularly following their withdrawal from the process. Moreover, the PHRD demonstrates the enduring appeal of partnership as a policy idea for governments, despite a lack of evidence of their effectiveness. CONCLUSIONS: This study of the PHRD demonstrates the ways in which industry actors are able to influence policy through long-term relationship building and partnership working on policy decision-making. Whilst such partnership approaches may appear to have the potential to mitigate some of alcohol harms, they create fundamental conflicts of interest, and may undermine the very causes they seek to further

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