60 research outputs found

    Population dynamics of the Devils Hole pupfish

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    A model is constructed to simulate fluctuations in monthly population sizes of the Devils Hole pupfish between January 1973 and August 1976. A variety of biological parameters is estimated, and adult mortality is partitioned into natural and environmentally-dependent components. The simulations capture the seasonal fluctuations in population size, and only seven predicted population sizes differ from those observed by 20% or more. The model is used to make testable predictions about the life history of this species and interactions of the parameters are discussed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/42634/1/10641_2004_Article_BF00002582.pd

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

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    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

    Galactic plane IPHAS-POSSI proper motion survey

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    The IPHAS-POSS-I proper motion survey combines data from the INT Photometric Hα survey (Drew et al., 2005MNRAS.362..753D 2005MNRAS.362..753D) with SuperCOSMOS scans of POSS-I plates (Hambly et al., 2001MNRAS.326.1279H 2001MNRAS.326.1279H). The sample covers roughly 1400deg2 of the IPHAS survey area and contains 103058 objects with significant proper motions below 150mas/yr in the magnitude range 13.5<r'< 19. Once the final IPHAS survey is completed the catalogue will be updated

    Galactic plane IPHAS-POSSI proper motion survey

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    Item does not contain fulltextThe IPHAS-POSS-I proper motion survey combines data from the INT Photometric Hα survey (Drew et al., 2005MNRAS.362..753D 2005MNRAS.362..753D) with SuperCOSMOS scans of POSS-I plates (Hambly et al., 2001MNRAS.326.1279H 2001MNRAS.326.1279H). The sample covers roughly 1400deg2 of the IPHAS survey area and contains 103058 objects with significant proper motions below 150mas/yr in the magnitude range 13.5<r'< 19. Once the final IPHAS survey is completed the catalogue will be updated.nul
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