27 research outputs found

    Circum-Arctic lithosphere-basin evolution : An overview

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    Acknowledgements The Special Issue editors thank the contributors for their hard work and dedication in the preparation of the papers presented here, and also Victoria Pease for her active support throughout the process and in particular in co-convening the conference session giving rise to this Special Issue. In particular, we thank the Editor-in-chief, Dr. Rob Govers for his patience, guidance and valued advice throughout the process. Also, we appreciate the work of the Tectonophysics editorial and production teams for bringing the Special Issue to print. R. Ernst, G. Oakey and an anonymous reviewer provided a multitude of helpful suggestions to improve the manuscript. This Special Issue is a contribution to the Geological Survey of Canada's Geomapping for Energy and Minerals (GEM2) Program, Canada's Extended Continental Shelf Program, and the Circum-Arctic Lithosphere Evolution (CALE) network. ESS Contribution No. 20160152.Peer reviewedPostprin

    Vp/Vs ratios in the Parnaíba Basin from joint active-passive seismic analysis – Implications for continental amalgamation and basin formation

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    Acknowledgements The authors thank Jordi Julià and two anonymous reviewers for valuable comments on an earlier version of the manuscript. Thanks to the PBAP program for the availability of WARR, DSR and teleseismic three-component data (Project 5547: BP ENERGY/FUB/FINATEC— PARNAÍBA BASIN REFRACTION EXPERIMENT). RAF thanks CNPq and INCT Estudos Tectînicos (CNPq, CAPES, FAP-DF) for research fellowship and funds. *The data that support the findings of this study may be available from the authors upon reasonable request.Peer reviewedPublisher 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 hospitalization2–4 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

    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

    Geological features of the northeastern Canadian Arctic margin revealed from analysis of potential field data

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    Acknowledgements We thank Dr. Richard W. Saltus (U. S. Geological Survey, Colorado USA) for providing the new Circum-Arctic magnetic anomaly grid (CAMP-M) compilation dataset and the Geophysical Data Centre of the Geological Survey of Canada Ottawa for the gravity data used in this study. The first author (GKA) has been supported by the Nigerian Government scholarship through the academic staff training scheme of the Tertiary Education Trust Fund (TETFund) and the Management of the Nasarawa State University, Keffi Nigeria; hence, they are hereby gratefully acknowledged. We are grateful to the two anonymous reviewers, Dr. Larry Lane (Guest Editor) and Prof. Rob Govers (Editor-in-Chief) for their constructive comments and suggestions which greatly improved the manuscript. This study is part of the Circum-Arctic Lithosphere Evolution (CALE) ProjectPeer reviewedPostprin

    Jurassic–Cretaceous low paleolatitudes from the circum-Black Sea region Crimea and Pontides) due to True Polar Wander

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    In a recent study, paleomagnetic and paleoenvironmental data from Adria (as part of the African plate) suggest a trend toward much lower (~15°) latitudes from Early Jurassic to Earliest Cretaceous at the position of Adria than suggested by the apparent polar wander (APW) paths. The smoothing of existing (APW) paths has most likely caused this low-latitude episode to be overlooked. In this study, we test if the low paleolatitudes in the Jurassic to Early Cretaceous can also be found in Eurasia, i.e. Crimea (Ukraine) and the Pontides (Turkey) that are situated in the present-day Black Sea region. Our Eurasian data suggest the same low Late Jurassic to Early Cretaceous paleolatitudes as shown for Africa. The Jurassic to Lower Cretaceous time span is characterized by Tethys subduction between the African and Eurasian continents and these subduction zones likely functioned as an anchor in the mantle. Therefore, we regard it unlikely that both the African and Eurasian plates moved by > 1500 km south and subsequently north with respect to the mantle, as suggested by the paleomagnetic results. True polar wander (TPW) provides a mechanism that rotates the Earth's crust and mantle with respect to its core, and it was recently quantified. The period from 195-135. Ma (Early Jurassic to Earliest Cretaceous) is subject to clockwise TPW, which could well explain our results. We conclude that TPW rather than plate tectonics is the cause of low Late Jurassic to Early Cretaceous African and Eurasian paleolatitudes in the eastern Mediterranean area. © 2010 Elsevier B.V
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