20 research outputs found

    El Terremoto de Tocopilla de Mw=7.7 (Norte de Chile) del 14 de Noviembre de 2007: Resultados preliminares de la geodesia especial (InSAR)

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    A Mw 7.7 subduction earthquake occurred on November 14, 2007 in Tocopilla (northern Chile). This region (between 16.5ºS and 23.5ºS) had been identified as major seismic gap (~1000 km length) since the South Peru (Mw= 9.1, 16 August 1868) and the Iquique (Mw=9.0, 10 May 1877) megathrust earthquakes. This gap was reduced to 500 km after the Arequipa (Mw = 8.3, 23 June 2001) and the Antofagasta (Mw = 8.1, 30 July 1995) earthquakes. We compute interferograms using Envisat ASAR images acquired before and after the Tocopilla earthquake to infer the location, geometry and slip of the rupture. Elastic modeling of this data allows us to infer that the 2007 main rupture extended over an area of ~150 x 60 km2, between 35 and 55 km depth, with a mean displacement of ~ 1.3 m. That means that the Tocopilla earthquake ruptured the deeper part of the seismogenic interface, probably within the transition zone. This earthquake released a little portion of the slip deficit accumulated in the seismic gap during the last 130 years (~ 10m). Hence the Tocopilla event may constitute a precursor of a future large thrust event in the current 500 km seismic gap that continues accumulating elastic strain from 1877.Un terremoto de subducción de Mw 7.7 tuvo lugar el 14 de Noviembre de 2007 en Tocopilla (norte de Chile). Esta región (entre 16.5ºS y 23.5º S) había sido identificada como una gran laguna sísmica (de ~ 1000 km de longitud) desde los terremotos del Sur de Perú (Mw = 9.1, 16 de Agosto de 1868) y de Iquique (Mw = 9.0, 10 de Mayo de 1877). La extensión de la laguna se redujo después de los terremotos de Arequipa (Mw = 8.3, 23 de Junio de 2001) y de Antofagasta (Mw=8.1, 30 de Julio de 1995). Hemos calculado interferogramas a partir de imágenes ASAR Envisat adquiridas antes y después del terremoto de Tocopilla para deducir la localización, geometría y deslizamiento asociados a la rotura. La modelización elástica de estos datos indica que la ruptura principal de 2007 se propagó sobre un área de ~150 x 60 km2, entre 35 y 55 km de profundidad, con un deslizamiento medio de ~1.3 m. Esto significa que el terremoto de Tocopilla rompió la parte profunda de la interfase sismogéncia, probablemente dentro de la zona de transición. Este terremoto relajó una porción muy pequeña del déficit de deslizamiento acumulado en la laguna sísmica durante los últimos 130 años (~10 m). Por lo tanto, el evento de Tocopilla podría constituir un precursor de un gran terremoto de subducción en la laguna sísmica actual de 500 km que continua acumulando deformación elástica desde 1877.Depto. de Geodinámica, Estratigrafía y PaleontologíaFac. de Ciencias GeológicasTRUEFrench National Research Agencypu

    On a coupled PDE model for image restoration

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    In this paper, we consider a new coupled PDE model for image restoration. Both the image and the edge variables are incorporated by coupling them into two different PDEs. It is shown that the initial-boundary value problem has global in time dissipative solutions (in a sense going back to P.-L. Lions), and several properties of these solutions are established. This is a rough draft, and the final version of the paper will contain a modelling part and numerical experiments

    Repositioning of the global epicentre of non-optimal cholesterol

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    High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol—which is a marker of cardiovascular risk—changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95% credible interval 3.7 million–4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world.</p

    Repositioning of the global epicentre of non-optimal cholesterol

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    High blood cholesterol is typically considered a feature of wealthy western countries1,2. However, dietary and behavioural determinants of blood cholesterol are changing rapidly throughout the world3 and countries are using lipid-lowering medications at varying rates. These changes can have distinct effects on the levels of high-density lipoprotein (HDL) cholesterol and non-HDL cholesterol, which have different effects on human health4,5. However, the trends of HDL and non-HDL cholesterol levels over time have not been previously reported in a global analysis. Here we pooled 1,127 population-based studies that measured blood lipids in 102.6 million individuals aged 18 years and older to estimate trends from 1980 to 2018 in mean total, non-HDL and HDL cholesterol levels for 200 countries. Globally, there was little change in total or non-HDL cholesterol from 1980 to 2018. This was a net effect of increases in low- and middle-income countries, especially in east and southeast Asia, and decreases in high-income western countries, especially those in northwestern Europe, and in central and eastern Europe. As a result, countries with the highest level of non-HDL cholesterol�which is a marker of cardiovascular risk�changed from those in western Europe such as Belgium, Finland, Greenland, Iceland, Norway, Sweden, Switzerland and Malta in 1980 to those in Asia and the Pacific, such as Tokelau, Malaysia, The Philippines and Thailand. In 2017, high non-HDL cholesterol was responsible for an estimated 3.9 million (95 credible interval 3.7 million�4.2 million) worldwide deaths, half of which occurred in east, southeast and south Asia. The global repositioning of lipid-related risk, with non-optimal cholesterol shifting from a distinct feature of high-income countries in northwestern Europe, north America and Australasia to one that affects countries in east and southeast Asia and Oceania should motivate the use of population-based policies and personal interventions to improve nutrition and enhance access to treatment throughout the world. © 2020, The Author(s), under exclusive licence to Springer Nature Limited

    Spontaneous, immune-mediated gastric inflammation in SAMP1/YitFc mice, a model of Crohn&apos;s-like gastritis

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    Background & Aims: Crohn's disease (CD) can develop in any region of the gastrointestinal tract, including the stomach. The etiology and pathogenesis of Crohn's gastritis are poorly understood, treatment approaches are limited, and there are not many suitable animal models for study. We characterized the features and mechanisms of chronic gastritis in SAMP1/YitFc (SAMP) mice, a spontaneous model of CD-like ileitis, along with possible therapeutic approaches. Methods: Stomachs from specific pathogen-free and germ-free SAMP and AKR mice (controls) were evaluated histologically; the presence of Helicobacter spp was tested in fecal pellets by polymerase chain reaction analysis. In vivo gastric permeability was quantified by fractional excretion of sucrose, and epithelial tight junction protein expression was measured by quantitative reverse-transcription polymerase chain reaction analysis. The effects of a proton pump inhibitor (PPI) or corticosteroids were measured, and the ability of pathogenic immune cells to mediate gastritis was assessed in adoptive transfer experiments. Results: SAMP mice developed Helicobacter-negative gastritis, characterized by aggregates of mononuclear cells, diffuse accumulation of neutrophils, and disruption of epithelial architecture; SAMP mice also had increased gastric permeability compared with controls, without alterations in expression of tight junction proteins. The gastritis and associated permeability defect observed in SAMP mice were independent of bacterial colonization and reduced by administration of corticosteroids but not a PPI. CD4 + T cells isolated from draining mesenteric lymph nodes of SAMP mice were sufficient to induce gastritis in recipient SCID mice. Conclusions: In SAMP mice, gastritis develops spontaneously and has many features of CD-like ileitis. These mice are a useful model to study Helicobacter-negative, immune-mediated Crohn's gastritis
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