The LandSense Innovation Challenge

The LandSense project aims to build an innovative citizen observatory for Land Use & Land Cover (LULC) monitoring, by connecting citizens with Earth Observation (EO) data to transform current approaches to environmental decision making. Through EO-driven mobile and web applications, LandSense promotes citizens to not only play a key role in environmental monitoring, but also to be directly involved in the co-creation of such applications. Currently within the EU’s EO monitoring framework, especially in the domain of LULC dynamics, there is a need for low-cost methods for acquiring high quality in-situ data to create timely, accurate and well-validated data products. LandSense aims to disrupt the EO data economy by creating marketable solutions that can provide a step-change in LULC monitoring activities both within and beyond Europe. In order to promote and stimulate the fast adoption of the project outcomes, the consortium proposes organization of the LandSense Innovation Challenge: Finals at the ECSA Conference 2020. This interactive session would facilitate collaboration and innovation among stakeholders within the value chain related to land mapping and citizen science. As such, the LandSense Innovation Challenge targets individuals, web-entrepreneurs, start-ups and SMEs coming from all participating Horizon 2020 countries, to present innovative IT solutions addressing one of the three LandSense domains: Urban Landscape Dynamics, Agricultural Land Use, and Forest & Habitat Monitoring. The challenge focuses on exploiting data streams coming from the LandSense Citizen Observatory, which consist of a diverse set of data including land cover change detection, threats to natural habitats, greenspace monitoring, etc., to design novel LULC solutions targeted at the citizen science community. In addition, participants will be encouraged to access data from the Sentinel Hub Service or other relevant EO data sources as well as the LandSense Quality Assurance Service in their solution. The process for the LandSense Innovation Challenge will be divided into two stages. First, there will be public call for ideas (Feb/March 2020) to which teams can submit proposals. After a review of the applications, a select number of shortlisted teams (5 to 10) will be invited to join the finals in Trieste to pitch their ideas to a jury of experts. Teams attending the finals will have the opportunity to discover more about LandSense, get coaching/mentoring to improve their pitches and network with the vibrant EO and citizen science communities. The winning team will not only receive a grand prize but also continue collaboration with the LandSense consortium to further advance their solution

Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants

Coronavirus disease 2019 (COVID-19) spawned a global health crisis in late 2019 and is caused by the novel coronavirus SARS-CoV-2. SARS-CoV-2 infection can lead to elevated markers of endothelial dysfunction associated with higher risk of mortality. It is unclear whether endothelial dysfunction is caused by direct infection of endothelial cells or is mainly secondary to inflammation. Here, we investigate whether different types of endothelial cells are susceptible to SARS-CoV-2. Human endothelial cells from different vascular beds including umbilical vein endothelial cells, coronary artery endothelial cells (HCAEC), cardiac and lung microvascular endothelial cells, or pulmonary arterial cells were inoculated in vitro with SARS-CoV-2. Viral spike protein was only detected in HCAECs after SARS-CoV-2 infection but not in the other endothelial cells tested. Consistently, only HCAEC expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2), required for virus infection. Infection with the SARS-CoV-2 variants B.1.1.7, B.1.351, and P.2 resulted in significantly higher levels of viral spike protein. Despite this, no intracellular double-stranded viral RNA was detected and the supernatant did not contain infectious virus. Analysis of the cellular distribution of the spike protein revealed that it co-localized with endosomal calnexin. SARS-CoV-2 infection did induce the ER stress gene EDEM1, which is responsible for clearance of misfolded proteins from the ER. Whereas the wild type of SARS-CoV-2 did not induce cytotoxic or pro-inflammatory effects, the variant B.1.1.7 reduced the HCAEC cell number. Of the different tested endothelial cells, HCAECs showed highest viral uptake but did not promote virus replication. Effects on cell number were only observed after infection with the variant B.1.1.7, suggesting that endothelial protection may be particularly important in patients infected with this variant