The quinoa at the time of COVID-19: new coordination between Andean producers. (Agriculture et syst..mes alimentaires face .. la Covid-19.) [French]

Quinoa has been cultivated for millennia in the Andes since its domestication on the shores of Lake Titicaca, between Peru and Bolivia. As a rustic crop of the Andean highlands, it has conquered the international market for less than thirty years. Today, Peru has become the world's leading producer and the majority of its production is exported. Produced locally by small-scale farmers and consumed globally, quinoa reflects the context of the globalization of agriculture and food. The COVID-19 crisis has also affected Peru and it raises questions about the robustness and resilience of export food chains. This opinion article looks back at debates organized in May-June 2020 in Peru. After recalling the general context of the cultivation of quinoa and the link between COVID-19, agriculture and biodiversity, we highlight the links between health crisis, agricultural crisis and food crisis. This global pandemic offers us the opportunity to question the current agricultural models to draw lessons to build the future. The projection of new solidarities through a collective trademark appears to carry a transnational territorial project at Andean level. Accompanying the actors to make it an inclusive development model requires adapted participatory tools.

Increased von willebrand factor (VWF) and factor VIII (FVIII) levels in severe acute respiratory syndrome SARS-CoV2-positive pneumonia compared with severe acute respiratory syndrome SARS-CoV2-negative: A case-control study

Background : The SARS-COV-2 direct interaction with Angiotensin-Converting-Enzyme-2 (ACE2) membrane receptor on pulmonary epithelial and endothelial cells, impairs angiotensin 1-7 production and its vasculoprotective role, promoting an upregulation of the ACE/angiotensinII/angiotensinII receptor type-1 pathway. The consequent endothelial activation and increasing secretion of VWF and FVIII levels contributes to complement activation and leukocyte extravasation, leading to local microcirculation damage. Aims : Our case-control study is aimed to investigate the characteristics of thrombotic microangiopathies (TMA)-like syndromes in COVID-19 evaluating VWF, FVIII and ADAMTS-13 levels, because the complement-mediated TMA and multiorgan microvascular lesions, observed in COVID-19 patients, seem not attributable to typical TMA. Methods : Ten COVID-19 cases presenting fever, cough and sore throat, admitted to the Fondazione Policlinico Gemelli IRCCS, Rome, and diagnosed by RT-PCR, were compared to ten control patients with non-SARS-CoV-2 interstitial pneumonia, diagnosed by chest Xray/computerized tomography;notably no patient needed mechanical ventilation. ADAMTS-13 activity was measured by a FRET-based assay;FVIII levels by a two-stage clotting assay, while VWF:antigen and VWF:activity were evaluated by chemiluminescence assays. Platelet count, schistocytes, D-dimer, C-reactive protein were centrally measured. Results : COVID-19 pneumonia patients compared with controls showed a marked elevation of both VWF:Ag (median values: 324.1 Vs 139.5%, P < 0.0001) and VWF:act levels (median values: 341.5 Vs 133%, P < 0.001), as well as FVIII levels (median values: 202.5 Vs 123%, P < 0.0001), consistent with the presence of a thrombophilic condition;without significant differences in ADAMTS-13 activity (median values: 69 Vs 76%, P = 0.473). In both groups, D-dimer and C-reactive protein levels were elevated, but not statistically different, platelet counts were normal, and schistocytes, a typical TMAs hallmark, were not observed Conclusions : The increased VWF/FVIII levels in COVID-19 pneumonia cases compared with non-COVID-19 controls cannot be fully explained by the inflammatory state alone and was likely caused by SARS-CoV-2-mediated downregulation of the ACE2 axis, resulting in damage to the local microcirculation and increased leukocyte extravasation.

COVID-19 Patient Outcome Prediction Using Selected Features from Emergency Department Data and Feed-Forward Neural Networks

The severity of COVID-19 varies dramatically, ranging from asymptomatic infection to severe respiratory failure and death. Currently, few prognostic markers for disease outcomes exist, impairing patient triaging and treatment. Here, we train feed-forward neural networks on electronic health records of 819 confirmed SARS-CoV-2 positive patients admitted to a two-site NHS Trust hospital in London, England. To allow early risk assessment, the models ingest data collected in the emergency department (ED) to predict subsequent admission to intensive care, need for mechanical ventilation and in-hospital mortality. We apply univariate selection and recursive feature elimination to find the minimal subset of clinical variables needed for accurate prediction. Our models achieve AUC-ROC scores of 0.78 to 0.87, outperforming standard clinical risk scores. This accuracy is reached with as few as 13% of clinical variables routinely collected within the ED, which increases the practical applicability of such algorithms. Hence, state-of-the-art neural networks can predict severe COVID-19 accurately and early from a small subset of clinical variables. © 2021, ICST Institute for Computer Sciences, Social Informatics and Telecommunications Engineering.

From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from COVID-19.

We concisely review clinical, autopsy, experimental and molecular data of 2019 coronavirus disease (COVID-19). Angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy emerge as distinctive features. Briefly, entry of the virus into microvessels can profoundly disrupt the local renin-angiotensin system, cause endothelial injury, activate the complement cascade and induce powerful thromboinflammatory reactions, involving, in particular, von Willebrand factor, that, if widespread, may lead to microvascular plugging, ischemia and, ultimately, organ failure. We believe the current COVID-19 data consolidate a widely unrecognised paradigm of potentially fatal thromboinflammatory microvascular disease.