Temporal and spatial evolution of a waxing then waning catastrophic density current revealed by chemical mapping

We reconstruct the behavior of a catastrophic sustained radial pyroclastic density current as it waxed then waned during its brief lifespan. By subdividing the deposit into 8 time slices using a chemical tracer, we show that the sustained current initially was topographically restricted, but that its leading edge advanced in all directions, encroaching upon and gradually ascending hills. During peak flow the current reached its maximum extent and overtopped all topographic highs. After this, and while the current direction from source was maintained, the leading edge gradually retreated sourceward. High-resolution analysis of the depositional architecture reveals how the flow dynamics evolved and runout distance of the sustained density current rapidly increased then decreased, reflecting the dominant influence of changing mass flux, as demonstrated in numerical models but not previously distinguished in a natural deposit

The Dialectics of Identity of the Modern and Postmodern Art

Ako pojam identiteta shvatimo u hegelijanskom smislu kao iskustvo što ga svijest stječe o sebi, onda se taj pojam nameće kao ključan u razmatranju (vizualne) umjetnosti XX. stoljeća. Prema Hegelu, moderna umjetnost transcendira mogućnost adekvatnog izražavanja svoga duhovnog sadržaja pukom osjetilnom reprezentacijom (koja je kao takvu određuje) te stoga zahtijeva pojmovnu refleksiju. Budući da je umjetnost uvijek i dio stvarnosti i o stvarnosti, propitivanje njezina vlastita pojma ide ruku pod ruku s ontološkom problematikom. Epistemološke promjene koje konstituiraju i modernu i postmodernu odražavaju se tako u dijalektici pojma moderne i postmoderne umjetnosti. Prema nekim autorima ta je dijalektika određena značajnim promjenama u teoriji subjekta, kulturalnim razlikama i tehnologiji.If the notion of identity is considered in the Hegelian sense as the experience of the consciousness about itself, then this notion becomes of key importance in reflecting upon the 20th-century (visual) art. Modern art, in Hegel’s view, transcends the possibility of an adequate expression of its spiritual content by its merely sensuous representation (that defines it as such) and hence calls for a reflection on its notion. Since art has always been both part of and about reality, the questioning of its own notion goes hand in hand with the ontological problematics. The epistemological changes that constitute both Modernism and Postmodernism thus reflect themselves in the dialectics of the notion of modern and postmodern art. According to some authors, such dialectics is determined by important changes which took place in the theory of the subject, in cultural differences as well as in technology

Discovery of two new super-eruptions from the Yellowstone hotspot track (USA): is the Yellowstone hotspot waning?

Super-eruptions are amongst the most extreme events to affect Earth’s surface, but too few examples are known to assess their global role in crustal processes and environmental impact. We demonstrate a robust approach to recognize them at one of the best-preserved intraplate large igneous provinces, leading to the discovery of two new super-eruptions. Each generated huge and unusually hot pyroclastic density currents that sterilized extensive tracts of Idaho and Nevada in the United States. The ca. 8.99 Ma McMullen Creek eruption was magnitude 8.6, larger than the last two major eruptions at Yellowstone (Wyoming). Its volume exceeds 1700 km3, covering ≥12,000 km2. The ca. 8.72 Ma Grey’s Landing eruption was even larger, at magnitude of 8.8 and volume of ≥2800 km3. It covers ≥23,000 km2 and is the largest and hottest documented eruption from the Yellowstone hotspot. The discoveries show the effectiveness of distinguishing and tracing vast deposit sheets by combining trace-element chemistry and mineral compositions with field and paleomagnetic characterization. This approach should lead to more discoveries and size estimates, here and at other provinces. It has increased the number of known super-eruptions from the Yellowstone hotspot, shows that the temporal framework of the magmatic province needs revision, and suggests that the hotspot may be waning

The RESET project: constructing a European tephra lattice for refined synchronisation of environmental and archaeological events during the last c. 100 ka

This paper introduces the aims and scope of the RESET project (. RESponse of humans to abrupt Environmental Transitions), a programme of research funded by the Natural Environment Research Council (UK) between 2008 and 2013; it also provides the context and rationale for papers included in a special volume of Quaternary Science Reviews that report some of the project's findings. RESET examined the chronological and correlation methods employed to establish causal links between the timing of abrupt environmental transitions (AETs) on the one hand, and of human dispersal and development on the other, with a focus on the Middle and Upper Palaeolithic periods. The period of interest is the Last Glacial cycle and the early Holocene (c. 100-8 ka), during which time a number of pronounced AETs occurred. A long-running topic of debate is the degree to which human history in Europe and the Mediterranean region during the Palaeolithic was shaped by these AETs, but this has proved difficult to assess because of poor dating control. In an attempt to move the science forward, RESET examined the potential that tephra isochrons, and in particular non-visible ash layers (cryptotephras), might offer for synchronising palaeo-records with a greater degree of finesse. New tephrostratigraphical data generated by the project augment previously-established tephra frameworks for the region, and underpin a more evolved tephra 'lattice' that links palaeo-records between Greenland, the European mainland, sub-marine sequences in the Mediterranean and North Africa. The paper also outlines the significance of other contributions to this special volume: collectively, these illustrate how the lattice was constructed, how it links with cognate tephra research in Europe and elsewhere, and how the evidence of tephra isochrons is beginning to challenge long-held views about the impacts of environmental change on humans during the Palaeolithic. © 2015 Elsevier Ltd.RESET was funded through Consortium Grants awarded by the Natural Environment Research Council, UK, to a collaborating team drawn from four institutions: Royal Holloway University of London (grant reference NE/E015905/1), the Natural History Museum, London (NE/E015913/1), Oxford University (NE/E015670/1) and the University of Southampton, including the National Oceanography Centre (NE/01531X/1). The authors also wish to record their deep gratitude to four members of the scientific community who formed a consultative advisory panel during the lifetime of the RESET project: Professor Barbara Wohlfarth (Stockholm University), Professor Jørgen Peder Steffensen (Niels Bohr Institute, Copenhagen), Dr. Martin Street (Romisch-Germanisches Zentralmuseum, Neuwied) and Professor Clive Oppenheimer (Cambridge University). They provided excellent advice at key stages of the work, which we greatly valued. We also thank Jenny Kynaston (Geography Department, Royal Holloway) for construction of several of the figures in this paper, and Debbie Barrett (Elsevier) and Colin Murray Wallace (Editor-in-Chief, QSR) for their considerable assistance in the production of this special volume.Peer Reviewe

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

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

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