Learning about forest futures under climate change through transdisciplinary collaboration across traditional and western knowledge systems

We provide an overview of a transdisciplinary project about sustainable forest management under climate change. Our project is a partnership with members of the Menominee Nation, a Tribal Nation located in northern Wisconsin, United States. We use immersive virtual experiences, translated from ecosystem model outcomes, to elicit human values about future forest conditions under alternative scenarios. Our project combines expertise across the sciences and humanities as well as across cultures and knowledge systems. Our management structure, governance, and leadership behaviors have both fostered and constrained our work and must be continuously responsive to changing group dynamics. Our project presents opportunities for substantial contributions to society, including insights and knowledge about complementary ways of knowing, skills training, and professional development, and opportunities for reflexive learning about effective transdisciplinary, translational, and transformative scientific processes

The development of British accountancy in the nineteenth century: A technological determinist approach

This article argues that some of the most popular treatments of the development of accountancy in Britain do not accord with the historical evidence. This is true of the functionalist's altruistic view of the profession and of the predominant paradigm�-�the Weberian 'professional project'. There is no evidence in the early history of British accountancy to support the concepts of, for example: monopolistic closure, credentialism, or the social construction of skill. Instead, using a model based on technological determinism, the article reasserts the importance of the industrialisation process in forming the accountancy profession, and sees the formation of the chartered societies as largely set up to brand the accountants' training and thereby preserve the value of their human capital.Professions, Accounting History, Chartered Accountancy, Technological Determinism,

Author Correction: The mutational constraint spectrum quantified from variation in 141,456 humans (Nature, (2020), 581, 7809, (434-443), 10.1038/s41586-020-2308-7)

10.1038/s41586-020-03174-8Nature590784

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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