33 research outputs found

    Relativistic mean field description for the shears band mechanism in 84^{84}Rb

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    For the first time, the Relativistic Mean Field (RMF) model is applied to the shears band recently observed in 3784_{37}^{84}Rb. Signals of the appearance of the shears mechanism, such as smooth decreases of the shears angle and of the BB(M1)/BB(E2) ratio with keeping the nearly constant tilt angle, are well reproduced. Thus it is shown that the microscopic RMF model can nicely describe the shears band in this nucleus.Comment: 5 pages, 6 eps figures included, uses REVTeX and epsf.sty, to appear in Phys. Rev.

    On the nature of nuclear dissipation, as a hallmark for collective dynamics at finite excitation

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    We study slow collective motion of isoscalar type at finite excitation. The collective variable is parameterized as a shape degree of freedom and the mean field is approximated by a deformed shell model potential. We concentrate on situations of slow motion, as guaranteed, for instance, by the presence of a strong friction force, which allows us to apply linear response theory. The prediction for nuclear dissipation of some models of internal motion are contrasted. They encompass such opposing cases as that of pure independent particle motion and the one of "collisional dominance". For the former the wall formula appears as the macroscopic limit, which is here simulated through Strutinsky smoothing procedures. It is argued that this limit hardly applies to the actual nuclear situation. The reason is found in large collisional damping present for nucleonic dynamics at finite temperature TT. The level structure of the mean field as well as the TT-dependence of collisional damping determine the TT-dependence of friction. Two contributions are isolated, one coming from real transitions, the other being associated to what for infinite matter is called the "heat pole". The importance of the latter depends strongly on the level spectrum of internal motion, and thus is very different for "adiabatic" and "diabatic" situations, both belonging to different degrees of "ergodicity".Comment: 50 pages plus 10 figures, uuencoded postscript file

    DOCK2 is involved in the host genetics and biology of severe COVID-19

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    「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target

    Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome : Insights from the LUNG SAFE study

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    Publisher Copyright: © 2020 The Author(s). Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Background: Concerns exist regarding the prevalence and impact of unnecessary oxygen use in patients with acute respiratory distress syndrome (ARDS). We examined this issue in patients with ARDS enrolled in the Large observational study to UNderstand the Global impact of Severe Acute respiratory FailurE (LUNG SAFE) study. Methods: In this secondary analysis of the LUNG SAFE study, we wished to determine the prevalence and the outcomes associated with hyperoxemia on day 1, sustained hyperoxemia, and excessive oxygen use in patients with early ARDS. Patients who fulfilled criteria of ARDS on day 1 and day 2 of acute hypoxemic respiratory failure were categorized based on the presence of hyperoxemia (PaO2 > 100 mmHg) on day 1, sustained (i.e., present on day 1 and day 2) hyperoxemia, or excessive oxygen use (FIO2 ≥ 0.60 during hyperoxemia). Results: Of 2005 patients that met the inclusion criteria, 131 (6.5%) were hypoxemic (PaO2 < 55 mmHg), 607 (30%) had hyperoxemia on day 1, and 250 (12%) had sustained hyperoxemia. Excess FIO2 use occurred in 400 (66%) out of 607 patients with hyperoxemia. Excess FIO2 use decreased from day 1 to day 2 of ARDS, with most hyperoxemic patients on day 2 receiving relatively low FIO2. Multivariate analyses found no independent relationship between day 1 hyperoxemia, sustained hyperoxemia, or excess FIO2 use and adverse clinical outcomes. Mortality was 42% in patients with excess FIO2 use, compared to 39% in a propensity-matched sample of normoxemic (PaO2 55-100 mmHg) patients (P = 0.47). Conclusions: Hyperoxemia and excess oxygen use are both prevalent in early ARDS but are most often non-sustained. No relationship was found between hyperoxemia or excessive oxygen use and patient outcome in this cohort. Trial registration: LUNG-SAFE is registered with ClinicalTrials.gov, NCT02010073publishersversionPeer reviewe
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