From Big Data to Big Displays: High-Performance Visualization at Blue Brain

Blue Brain has pushed high-performance visualization (HPV) to complement its HPC strategy since its inception in 2007. In 2011, this strategy has been accelerated to develop innovative visualization solutions through increased funding and strategic partnerships with other research institutions. We present the key elements of this HPV ecosystem, which integrates C++ visualization applications with novel collaborative display systems. We motivate how our strategy of transforming visualization engines into services enables a variety of use cases, not only for the integration with high-fidelity displays, but also to build service oriented architectures, to link into web applications and to provide remote services to Python applications.Comment: ISC 2017 Visualization at Scale worksho

BlueBrain/Brayns: 3.2.2 Release

Visualizer for large-scale and interactive ray-tracing of neuron

BlueBrain/MorphIO: Allow to throw warnings instead of writing them to stderr/stdout

remove -j2 from cpp_test.sh - not an option for cmake (#269) Adding C++ tests (#263) Fix for compat with recent HighFive (#268) Minimal solution to raising of warning instead of writing them (#266) apply ignoring logic to raised warnings as well (#271) Consider custom section types from 5 up to 10 (#274) fix broken links and include README to readthedocs (#276) narrow conditions when WARNING_NEUROMORPHO_SOMA_NON_CONFORM is thrown (#275

A Machine-Generated View of the Role of Blood Glucose Levels in the Severity of COVID-19

SARS-CoV-2 started spreading toward the end of 2019 causing COVID-19, a disease that reached pandemic proportions among the human population within months. The reasons for the spectrum of differences in the severity of the disease across the population, and in particular why the disease affects more severely the aging population and those with specific preconditions are unclear. We developed machine learning models to mine 240,000 scientific articles openly accessible in the CORD-19 database, and constructed knowledge graphs to synthesize the extracted information and navigate the collective knowledge in an attempt to search for a potential common underlying reason for disease severity. The machine-driven framework we developed repeatedly pointed to elevated blood glucose as a key facilitator in the progression of COVID-19. Indeed, when we systematically retraced the steps of the SARS-CoV-2 infection, we found evidence linking elevated glucose to each major step of the life-cycle of the virus, progression of the disease, and presentation of symptoms. Specifically, elevations of glucose provide ideal conditions for the virus to evade and weaken the first level of the immune defense system in the lungs, gain access to deep alveolar cells, bind to the ACE2 receptor and enter the pulmonary cells, accelerate replication of the virus within cells increasing cell death and inducing an pulmonary inflammatory response, which overwhelms an already weakened innate immune system to trigger an avalanche of systemic infections, inflammation and cell damage, a cytokine storm and thrombotic events. We tested the feasibility of the hypothesis by manually reviewing the literature referenced by the machine-generated synthesis, reconstructing atomistically the virus at the surface of the pulmonary airways, and performing quantitative computational modeling of the effects of glucose levels on the infection process. We conclude that elevation in glucose levels can facilitate the progression of the disease through multiple mechanisms and can explain much of the differences in disease severity seen across the population. The study provides diagnostic considerations, new areas of research and potential treatments, and cautions on treatment strategies and critical care conditions that induce elevations in blood glucose levels