An artificial intelligence tool for heterogeneous team formation in the classroom

Nowadays, there is increasing interest in the development of teamwork skills in the educational context. This growing interest is motivated by its pedagogical effectiveness and the fact that, in labour contexts, enterprises organize their employees in teams to carry out complex projects. Despite its crucial importance in the classroom and industry, there is a lack of support for the team formation process. Not only do many factors influence team performance, but the problem becomes exponentially costly if teams are to be optimized. In this article, we propose a tool whose aim it is to cover such a gap. It combines artificial intelligence techniques such as coalition structure generation, Bayesian learning, and Belbin's role theory to facilitate the generation of working groups in an educational context. This tool improves current state of the art proposals in three ways: i) it takes into account the feedback of other teammates in order to establish the most predominant role of a student instead of self-perception questionnaires; ii) it handles uncertainty with regard to each student's predominant team role; iii) it is iterative since it considers information from several interactions in order to improve the estimation of role assignments. We tested the performance of the proposed tool in an experiment involving students that took part in three different team activities. The experiments suggest that the proposed tool is able to improve different teamwork aspects such as team dynamics and student satisfaction

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 hospitalization2–4 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

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

Management Teams

Meredith Belbin's work on teams has become part of everyday language in organizations all over the world. All kinds of teams and team behaviours are covered. At the end of the book is a self-perception inventory so that readers can match their own personalities to particular team roles. Management Teams is required reading for managers concerned with achieving results by getting the best from their key personnel

Tim Manajemen : Bagaimana Membentuk dan Mengefektifkan

XV + 220 hlm .; 23 c