Training future generations to deliver evidence-based conservation and ecosystem management

1. To be effective, the next generation of conservation practitioners and managers need to be critical thinkers with a deep understanding of how to make evidence-based decisions and of the value of evidence synthesis. 2. If, as educators, we do not make these priorities a core part of what we teach, we are failing to prepare our students to make an effective contribution to conservation practice. 3. To help overcome this problem we have created open access online teaching materials in multiple languages that are stored in Applied Ecology Resources. So far, 117 educators from 23 countries have acknowledged the importance of this and are already teaching or about to teach skills in appraising or using evidence in conservation decision-making. This includes 145 undergraduate, postgraduate or professional development courses. 4. We call for wider teaching of the tools and skills that facilitate evidence-based conservation and also suggest that providing online teaching materials in multiple languages could be beneficial for improving global understanding of other subject areas.Peer reviewe

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

Short-term water quality variability in two tropical estuaries, central Sumatra

Estuaries261156-165ESTU

Compartmentalisation of beachface sediments along the southwestern coast of Australia

10.1016/S0025-3227(99)00046-8Marine Geology1621145-164MAGE

Morphological variation in the polyps of the scleractinian coral Favia speciosa (Dana) around Singapore

10.1023/A:1017570100029Hydrobiologia444227-235HYDR

Linkage and evolution of conjugate strike-slip fault zones in limestones of Somerset and Northumbria

Conjugate strike-slip fault zones that cover metre-scale areas at Beadnell, Northumbria, and Kilve, Somerset, were initiated as conjugate vein arrays. Early conjugate faults are linked by the propagation of one fault that eventually by-passes the other fault. A model for the development of strike-slip faults is presented, using fault and vein geometries and the position of damage zones with respect to the master faults as an indication of the propagation direction. This model includes the evolution of networks from (1) the initial random development of vein arrays, to (2) the isolated development of several unconnected conjugate fault segments that pass into vein arrays, through (3) the intersection of a conjugate set of master faults and linkage with minor antithetic faults, and the formation of new vein arrays with extensional geometries after a linked network of faults is established, to (4) breaching of intersection points by dominant faults, and finally (5) the propagation towards oversteps that are breached to form a through-going fault. The geometry of the active structures simplifies with time, as strain is localised along the master fault, but the complexities are preserved in the fault walls

Photographic technique for the study of coral morphometrics

Raffles Bulletin of Zoology492191-19