Great Canadian Lagerstätten 3. Late Ordovician Konservat-Lagerstätten in Manitoba

Konservat-Lagerstätten, deposits in which soft-bodied or lightly sclerotized fossils are preserved, are very rare in Ordovician strata. Three significant sites are known from Upper Ordovician rocks in Manitoba: at Cat Head – McBeth Point, William Lake, and Airport Cove. These sites are in two distinct sedimentary basins: the former two are in the Williston Basin, while the latter is in the Hudson Bay Basin. All three sites contain marine fossils, but each has a different assemblage that contributes a distinct piece of the diversity picture. Important groups represented at one or more of the sites include seaweeds (algae), sponges, cnidarian medusae (jellyfish), conulariids, trilobites, eurypterids, xiphosurids (horseshoe crabs), and pycnogonids (‘sea spiders’). The different biotas reflect depositional conditions at each site. Many of the fossils are unknown elsewhere in the Ordovician at the family level or higher. The province of Manitoba therefore makes a significant contribution to knowledge of Late Ordovician biodiversity.SOMMAIRELes lagerstätten de conservation, ces sédiments contenant des fossiles d’organismes à corps mou ou légèrement sclérotisés particulièrement bien conservés, sont très rares dans les strates ordoviciennes.  Trois sites d’importance sont connus dans des roches de l'Ordovicien supérieur à Cat Head, Manitoba, soit McBeth Point, William Lake et  Airport Cove.  Ces sites sont situés dans deux bassins sédimentaires distincts : les deux premiers sont situés dans le bassin de Williston, tandis que le second est situé dans le bassin de la baie d'Hudson.  Les trois sites contiennent des fossiles marins, mais chacun présente un assemblage différent, chacun montrant une composante distincte de la diversité biologique d’alors.  Les groupes les plus importants représentés, dans un ou plusieurs de ces sites, sont les algues, les éponges, les cnidarian medusae (méduses), les conularides, les trilobites, les euryptérides, xiphosurides (limules) et pycnogonides.  Les différents biotopes reflètent les conditions de dépôt de chaque site.  Nombre de ces fossiles sont inconnus ailleurs dans l'Ordovicien, au niveau de la famille ou du taxon supérieur de la classification.  Ainsi, la province du Manitoba offre-t-elle une contribution importante à la connaissance de la biodiversité de l'Ordovicien supérieur

Spectroscopic and photometric analysis of HS 1136+6646: A hot young DAO+K7V post-common- envelope, pre-cataclysmic variable binary

Copyright © 2004 IOP Publishing / American Astronomical SocietyExtensive photometric and spectroscopic observations have been obtained for HS 1136+6646. The observations reveal a newly formed post–common-envelope binary system containing a hot ~DAO.5 primary and a highly irradiated secondary. HS 1136+6646 is the most extreme example yet of a class of short-period hot H-rich white dwarfs with K–M companion systems such as V471 Tau and Feige 24. HS 1136+6646 is a double-line spectroscopic binary showing emission lines of H I, He II, C II, Ca II, and Mg II, due in part to irradiation of the K7 V secondary by the hot white dwarf. Echelle spectra reveal the hydrogen emission lines to be double-peaked with widths of ~200 km s-1, raising the possibility that emission from an optically thin disk may also contribute. The emission lines are observed to disappear near the inferior conjunction. An orbital period of 0.83607 ± 0.00003 days has been determined through the phasing of radial velocities, emission-line equivalent widths, and photometric measurements spanning a range of 24 months. Radial velocity measurements yield an amplitude of KWD = 69 ± 2 km s-1 for the white dwarf and KK7V = 115 ± 1 km s-1 for the secondary star. In addition to orbital variations, photometric measurements have also revealed a low-amplitude modulation with a period of 113.13 minutes and a semiamplitude of 0.0093 mag. These short-period modulations are possibly associated with the rotation of the white dwarf. From fits of the Balmer line profiles, the white dwarf is estimated to have an effective temperature and gravity of ~70,000 K and log g ~ 7.75, respectively. However, this optically derived temperature is difficult to reconcile with the far-UV spectrum of the Lyman line region. Far Ultraviolet Spectroscopic Explorer spectra show the presence of O VI absorption lines and a spectral energy distribution whose slope persists nearly to the Lyman limit. The extremely high temperature of the white dwarf, from both optical and UV measurements, indicates that the binary system is one of the earliest post–common-envelope objects known, having an age around 7.7 × 105 yr. Although the spectrum of the secondary star is best represented by a K7 V star, indications are that the star may be overly luminous for its mass.NASAParticle and Astronomy Research Council, UKNS

Can Oxygen Set Thermal Limits in an Insect and Drive Gigantism?

Contains fulltext : 111575.pdf (publisher's version ) (Open Access

A haemagglutination test for rapid detection of antibodies to SARS-CoV-2

Serological detection of antibodies to SARS-CoV-2 is essential for establishing rates of seroconversion in populations, and for seeking evidence for a level of antibody that may be protective against COVID-19 disease. Several high-performance commercial tests have been described, but these require centralised laboratory facilities that are comparatively expensive, and therefore not available universally. Red cell agglutination tests do not require special equipment, are read by eye, have short development times, low cost and can be applied at the Point of Care. Here we describe a quantitative Haemagglutination test (HAT) for the detection of antibodies to the receptor binding domain of the SARS-CoV-2 spike protein. The HAT has a sensitivity of 90% and specificity of 99% for detection of antibodies after a PCR diagnosed infection. We will supply aliquots of the test reagent sufficient for ten thousand test wells free of charge to qualified research groups anywhere in the world

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

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

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

A first update on mapping the human genetic architecture of COVID-19

peer reviewe