Global priorities for reduction of cetacean bycatch. Scientific Committee document SC/56/BC2, International Whaling Commission, July 2004, Sorrento, Italy

Progress at reducing the scale and conservation impact of cetacean bycatch has been slow, sporadic and limited to a few specific fisheries or circumstances. As a result bycatch remains perhaps the greatest immediate and well-documented threat to cetacean populations globally. Having recognized the critical importance of reducing bycatch levels to prevent the depletion, and in some cases extinction, of cetacean populations, World Wildlife Fund-US launched a global bycatch initiative early in 2002. Their strategy calls on governmental and non-governmental bodies to move quickly, cooperatively and thoughtfully to achieve bycatch reduction. As a supportive step a working group was established to identify priorities and provide guidance on how financial and other resources should be invested to address bycatch issues. The group will conduct a global survey of cetacean bycatch problems, classify and rank those problems according to an agreed set of criteria and provide a clear rationale for each problem assigned high priority for funding and intervention. The working group will emphasise: (1) situations that are especially critical (e.g. a species’ or population’s survival is immediately at risk from bycatch) and are not being addressed adequately; (2) circumstances where rapid progress could be made with a modest investment of resources; (3) situations in which bycatch is believed to pose a threat to cetaceans but a quantitative assessment is needed to verify the risk; and (4) fisheries in which a currently available solution (technical, socioeconomic or a combination) appears feasible. The report of the working group will be directed at governmental decision makers, aid agencies, nongovernmental organizations and related audiences

Global priorities for reduction of cetacean bycatch

Progress at reducing the scale and conservation impact of cetacean bycatch has been slow, sporadic, and limited to a few specific fisheries or circumstances. As a result, bycatch remains perhaps the greatest immediate and well-documented threat to cetacean populations globally. Having recognized the critical importance of reducing bycatch levels to prevent the depletion, and in some cases extinction, of cetacean populations, World Wildlife Fund-US launched a global bycatch initiative early in 2002. Their strategy calls on governmental and non-governmental bodies to move quickly, cooperatively, and thoughtfully to achieve bycatch reduction. As a supportive step, a working group was established to identify priorities and provide guidance on how financial and other resources should be invested to address bycatch issues. The group conducted a global survey of cetacean bycatch problems and identified a series of specific problems that should be addressed as priorities, with emphasis on: (1) situations that are especially critical (e.g. a species’ or population’s survival is immediately at risk from bycatch) and are not being addressed adequately; (2) circumstances where rapid progress could be made with a modest investment of resources; (3) situations in which bycatch is believed to pose a threat to cetaceans but a quantitative assessment is needed to verify the risk; and (4) fisheries in which a currently available solution (technical, socio-economic, or a combination) appears feasible

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

Knickpoints and crescentic bedform interactions in submarine channels

Submarine channels deliver globally important volumes of sediments, nutrients, contaminants and organic carbon into the deep sea. Knickpoints are significant topographic features found within numerous submarine channels, which most likely play an important role in channel evolution and the behaviour of the submarine sediment-laden flows (turbidity currents) that traverse them. Although prior research has linked supercritical turbidity currents to the formation of both knickpoints and smaller crescentic bedforms, the relationship between flows and the dynamics of these seafloor features remains poorly constrained at field-scale. This study investigates the distribution, variation and interaction of knickpoints and crescentic bedforms along the 44km long submarine channel system in Bute Inlet, British Columbia. Wavelet analyses on a series of repeated bathymetric surveys reveal that the floor of the submarine channel is composed of a series of knickpoints that have superimposed, higher-frequency, crescentic bedforms. Individual knickpoints are separated by hundreds to thousands of metres, with the smaller superimposed crescentic bedforms varying in wavelengths from ca 16m to ca 128m through the channel system. Knickpoint migration is driven by the passage of frequent turbidity currents, and acts to redistribute and reorganize the crescentic bedforms. Direct measurements of turbidity currents indicate the seafloor reorganization caused by knickpoint migration can modify the flow field and, in turn, control the location and morphometry of crescentic bedforms. A transect of sediment cores obtained across one of the knickpoints show sand–mud laminations of deposits with higher aggradation rates in regions just downstream of the knickpoint. The interactions between flows, knickpoints and bedforms that are documented here are important because they likely dominate the character of preserved submarine channel-bed deposits

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