Morphometric and physical characteristics distinguishing adult Patagonian lamprey, Geotria macrostoma from the pouched lamprey, Geotria australis

The pouched lamprey, Geotria australis Gray, 1851, has long been considered monotypic in the Geotriidae family with a wide southern temperate distribution across Australasia and South America. Recent studies have provided molecular and morphological evidence for a second Geotria species in South America; Geotria macrostoma (Burmeister, 1868). The aim of this study was to determine morphometric and physical characteristics of adult G. macrostoma that further differentiate this re-instated species of Geotriidae from G. australis. The diagnostic features discriminating immature adult G. macrostoma from G. australis when entering fresh water, are distinct differences in dentition, oral papillae and fimbriae counts and differences in coloration. In addition, G. macrostoma display greater growth of the prebranchial region and oral disc and has a deeper body depth and higher condition fac tor. All current ecological knowledge of the genus Geotria is based on Australasian popula tions, which may not be applicable to G. macrostoma. To ensure the conservation and protection of the Patagonian lamprey as a re-identified species, further investigations are needed to understand its life history, biology and ecology throughout its range.Fil: Baker, Cindy F.. National Institute of Water and Atmospheric Research; Nueva ZelandaFil: Riva Rossi, Carla Marcela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Centro Nacional Patagónico. Instituto de Diversidad y Evolución Austral; ArgentinaFil: Quiroga, Analía Pamela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Centro Nacional Patagónico. Instituto de Diversidad y Evolución Austral; ArgentinaFil: White, Emily. National Institute of Water and Atmospheric Research; Nueva ZelandaFil: Williams, Peter. National Institute of Water and Atmospheric Research; Nueva ZelandaFil: Kitson, Jane. Kitson Consulting; Nueva ZelandaFil: Bice, Christopher M.. South Australian Research And Development Institute; Australia. University of Adelaide; AustraliaFil: Renaud, Claude B.. Canadian Museum Of Nature; CanadáFil: Potter, Ian. Murdoch University; AustraliaFil: Neira, Francisco J.. Neira Marine Sciences Consulting; AustraliaFil: Baigún, Claudio. Universidad Nacional de San Martín. Instituto de Investigación en Ingeniería Ambiental; Argentin

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

Archived - General Information (DO NOT USE)

DO NOT USE - The goal of this component was to document the data collection process of the Silent Cities Dataset. This component is just left for archive