The Threads of Biosystems Engineering

The core concepts, or threads, of Biosystems Engineering (BSEN) are variously understood by those within the discipline, but have never been unequivocally defined due to its early stage of development. This makes communication and teaching difficult compared to other well established engineering subjects. Biosystems Engineering is a field of Engineering which int egrates engineering science and design with applied biological, environmental and agricultural sciences. It represents an evolution of the Agricultural Engineering discipline applied to all living organisms not including biomedical applications. The basic key element for the emerging EU Biosystems Engineering program of studies is to ensure that it offers essential minimum fundamental engine ering knowledge and competences . A core curriculum developed by Erasmus Thematic Networks is used as benchmark for Agr icultural and Biosystems Engineering studies in Europe. The common basis of the core curriculum for the discipline across the Atlantic , including a minimum of competences comprising the Biosystems Engineering core competencies, has been defined by an Atlan tis project , but this needs to be taken further by defining the threads linking courses together. This paper presents a structured approach to define the Threads of BSEN . The definition of the mid-level competences and the associated learning outcomes has been one of the objectives of the Atlantis programme TABE.NET. The mid-level competences and learning outcomes for each of six specializations of BSEN are defined while the domain-specific knowledge to be acquired for each outcome is proposed. Once the proposed definitions are adopted, these threads will be available for global development of the BSEN

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease