Rapid prototyping as a faculty-wide activity: An innovative approach to the redesign of courses and instructional medthods at the University of Twente

At the Faculty of Educational Science and Technology (Toegepaste Onderwijskunde, T.O.) of the University of Twente a revolutionary process of institutional change is occurring. Under the banner of C@MPUS+, we have made a commitment to blend the best of our old values of good teaching and an attractive campus life with new didactics and advanced technologies so that we can extend our already unique curriculum and instructional practice over distance and time, as well as enrich it

An On-Going Journey: Technology as a Learning Workbench

Reflection document by Prof. dr. B.A. Collis and Prof. dr. J.C.M.M. Moonen on the occasion of their retirement as professors in the Faculty of Behavioral Sciences of the University of Twente on Thursday 15 September 200

Portability and networked learning environments

Abstract The portability of educational software is defined as the likelihood of software usage, with or without adaptation, in an educational environment different from that for which it was originally designed and produced. Barriers and research relevant to the portability of electronic learning resources are discussed and organised into a portability-limiting factors model. With the increase in number and scope of networked learning environments, portability issues take on a new dimension. Using electronic (study) books as an example, the portability problem space of networked learning environments is explored

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