45 research outputs found

    Monte Carlo approach of the islanding of polycrystalline thin films

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    We computed by a Monte Carlo method derived from the Solid on Solid model, the evolution of a polycrystalline thin film deposited on a substrate during thermal treatment. Two types of substrates have been studied: a single crystalline substrate with no defects and a single crystalline substrate with defects. We obtain islands which are either flat (i.e. with a height which does not overcome a given value) or grow in height like narrow towers. A good agreement was found regarding the morphology of numerical nanoislands at equilibrium, deduced from our model, and experimental nanoislands resulting from the fragmentation of YSZ thin films after thermal treatment.Comment: 20 pages, 7 figure

    Morphological instabilities of a thin film on a Penrose lattice: a Monte Carlo study

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    We computed by a Monte Carlo method the thermal relaxation of a polycrystalline thin film deposited on a Penrose lattice. The thin film was modelled by a 2 dimensional array of elementary domains, which have each a given height. During the Monte Carlo process, the height of each of these elementary domains is allowed to change as well as their crystallographic orientation. After equilibrium is reached at a given numerical temperature, all elementary domains have changed their orientation into the same one and small islands appear, preferentially on the domains of the Penrose lattice located in the center of heptagons. This method is a new numerical approach to study the influence of the substrate and its defects on the islanding process of polycrystalline films.Comment: 9 pages,5 figure

    Nuclear reaction rates and energy in stellar plasmas : The effect of highly damped modes

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    The effects of the highly damped modes in the energy and reaction rates in a plasma are discussed. These modes, with wavenumbers kkDk \gg k_{D}, even being only weakly excited, with less than kBTk_{B}T per mode, make a significant contribution to the energy and screening in a plasma. When the de Broglie wavelength is much less than the distance of closest approach of thermal electrons, a classical analysis of the plasma canComment: 42nd Annual Meeting of the APS Division of Plasma Physics, invited tal

    Deficiency in type 1 insulin-like growth factor receptor in mice protects against oxygen-induced lung injury

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    BACKGROUND: Cellular responses to aging and oxidative stress are regulated by type 1 insulin-like growth factor receptor (IGF-1R). Oxidant injury, which is implicated in the pathophysiology of a number of respiratory diseases, acutely upregulates IGF-1R expression in the lung. This led us to suspect that reduction of IGF-1R levels in lung tissue could prevent deleterious effects of oxygen exposure. METHODS: Since IGF-1R null mutant mice die at birth from respiratory failure, we generated compound heterozygous mice harboring a hypomorphic (Igf-1r(neo)) and a knockout (Igf-1r(-)) receptor allele. These IGF-1R(neo/- )mice, strongly deficient in IGF-1R, were subjected to hyperoxia and analyzed for survival time, ventilatory control, pulmonary histopathology, morphometry, lung edema and vascular permeability. RESULTS: Strikingly, after 72 h of exposure to 90% O(2), IGF-1R(neo/- )mice had a significantly better survival rate during recovery than IGF-1R(+/+ )mice (77% versus 53%, P < 0.05). The pulmonary injury was consistently, and significantly, milder in IGF-1R(neo/- )mice which developed conspicuously less edema and vascular extravasation than controls. Also, hyperoxia-induced abnormal pattern of breathing which precipitated respiratory failure was elicited less frequently in the IGF-1R(neo/- )mice. CONCLUSION: Together, these data demonstrate that a decrease in IGF-1R signaling in mice protects against oxidant-induced lung injury

    Loss of ATF2 Function Leads to Cranial Motoneuron Degeneration during Embryonic Mouse Development

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    The AP-1 family transcription factor ATF2 is essential for development and tissue maintenance in mammals. In particular, ATF2 is highly expressed and activated in the brain and previous studies using mouse knockouts have confirmed its requirement in the cerebellum as well as in vestibular sense organs. Here we present the analysis of the requirement for ATF2 in CNS development in mouse embryos, specifically in the brainstem. We discovered that neuron-specific inactivation of ATF2 leads to significant loss of motoneurons of the hypoglossal, abducens and facial nuclei. While the generation of ATF2 mutant motoneurons appears normal during early development, they undergo caspase-dependent and independent cell death during later embryonic and foetal stages. The loss of these motoneurons correlates with increased levels of stress activated MAP kinases, JNK and p38, as well as aberrant accumulation of phosphorylated neurofilament proteins, NF-H and NF-M, known substrates for these kinases. This, together with other neuropathological phenotypes, including aberrant vacuolisation and lipid accumulation, indicates that deficiency in ATF2 leads to neurodegeneration of subsets of somatic and visceral motoneurons of the brainstem. It also confirms that ATF2 has a critical role in limiting the activities of stress kinases JNK and p38 which are potent inducers of cell death in the CNS

    Increased 30-Day Mortality in Very Old ICU Patients with COVID-19 Compared to Patients with Respiratory Failure without COVID-19

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    Purpose: The number of patients ≥ 80 years admitted into critical care is increasing. Coronavirus disease 2019 (COVID-19) added another challenge for clinical decisions for both admission and limitation of life-sustaining treatments (LLST). We aimed to compare the characteristics and mortality of very old critically ill patients with or without COVID-19 with a focus on LLST. Methods: Patients 80 years or older with acute respiratory failure were recruited from the VIP2 and COVIP studies. Baseline patient characteristics, interventions in intensive care unit (ICU) and outcomes (30-day survival) were recorded. COVID patients were matched to non-COVID patients based on the following factors: age (± 2 years), Sequential Organ Failure Assessment (SOFA) score (± 2 points), clinical frailty scale (± 1 point), gender and region on a 1:2 ratio. Specific ICU procedures and LLST were compared between the cohorts by means of cumulative incidence curves taking into account the competing risk of discharge and death. Results: 693 COVID patients were compared to 1393 non-COVID patients. COVID patients were younger, less frail, less severely ill with lower SOFA score, but were treated more often with invasive mechanical ventilation (MV) and had a lower 30-day survival. 404 COVID patients could be matched to 666 non-COVID patients. For COVID patients, withholding and withdrawing of LST were more frequent than for non-COVID and the 30-day survival was almost half compared to non-COVID patients. Conclusion: Very old COVID patients have a different trajectory than non-COVID patients. Whether this finding is due to a decision policy with more active treatment limitation or to an inherent higher risk of death due to COVID-19 is unclear.info:eu-repo/semantics/publishedVersio

    Autoantibodies against type I IFNs in patients with life-threatening COVID-19

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    Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-w (IFN-w) (13 patients), against the 13 types of IFN-a (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men
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