14 research outputs found

    Electron acceleration with improved Stochastic Differential Equation method: cutoff shape of electron distribution in test-particle limit

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    We develop a method of stochastic differential equation to simulate electron acceleration at astrophysical shocks. Our method is based on It\^{o}'s stochastic differential equations coupled with a particle splitting, employing a skew Brownian motion where an asymmetric shock crossing probability is considered. Using this code, we perform simulations of electron acceleration at stationary plane parallel shock with various parameter sets, and studied how the cutoff shape, which is characterized by cutoff shape parameter aa, changes with the momentum dependence of the diffusion coefficient β\beta. In the age-limited cases, we reproduce previous results of other authors, a2βa\approx2\beta. In the cooling-limited cases, the analytical expectation aβ+1a\approx\beta+1 is roughly reproduced although we recognize deviations to some extent. In the case of escape-limited acceleration, numerical result fits analytical stationary solution well, but deviates from the previous asymptotic analytical formula aβa\approx\beta.Comment: corrected typos, 10 pages, 4 figures, 2 tables, JHEAp in pres

    Numerical studies on the structure of the cosmic ray electron halo in starburst galaxies

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    The structure of the cosmic ray electron halo of a starburst galaxy depends strongly on the nature of galactic wind and the configuration of the magnetic field. We have investigated these dependencies by solving numerically the propagation of electrons originating in starburst galaxies, most likely in supernova remnants. The calculations are made for several models for the galactic winds and for the configuration of the magnetic fields for comparison with observations. Our simulation of a quasi-radio halo reproduces both the extended structure of ~ 9 kpc and the subtle hollow structure near the polar region of the radio halo that are observed in the starburst galaxy NGC 253. These findings suggest the existence of strong galactic wind in NGC 253.Comment: 4 pages, 6 figures, to appear in Proceeding of the conference "The multi messenger approach to high energy gamma ray sources", Barcelona, July 200

    胸部外科手術後のPeak cough flow とMaximum phonation time の関係

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    研究論文Original Articles 手術後の肺活量(VC)が咳嗽力(PCF)に影響を及ぼすことは明らかだが,最大発声持続時間(MPT)で評価される声門閉鎖機能低下がPCF に及ぼす影響は明らかとなっていない.本研究では呼吸器外科手術後の患者28 例においてMPT とPCF の関係を明らかにすることを目的とし,手術後1 日目〜5 日目にPCF,MPT,VC を測定した.手術後5 日目までPCF およびMPT は,手術前と比較し有意に低下した(p <0.05). またPCF とMPT の回復率には手術後1 日目のみに相関関係を認めた(r= 0.53,p <0.05).PCF とVC の回復率は手術後1 日目〜5 日目まで相関を認めた(r = 0.41-0.27,p <0.05).手術後の声門閉鎖機能低下が咳嗽力に及ぼす影響は,人工呼吸器離脱後1日目までで,その後はVC の影響を強く受けると考えられた. The vital capacity( VC) after thoracic surgery affects peak cough flow( PCF). However, the influence of glottic closure deterioration evaluated by maximum phonation time (MPT) on PCF is not clear. We clarified the relationship between coughing and vocal cord function in 28 patients after thoracic surgery. We measured the PCF, MPT, and VC on postoperative days 1 to 5. On postoperative day 1, the mean PCF decreased to 58.0% and the mean MPT decreased to 62.5%. The mean PCFs and MPTs on postoperative days 1 to 5 were significantly lower than the preoperative PCF and MPT, respectively (p < 0.05). There was a positive correlation between the rates of change in the PCF and MPT only on postoperative day 1 (r = 0.53, p < 0.05). There was also a positive correlation between the rates of change in the PCF and VC on postoperative days 1 to 5 (r = 0.41–0.27, p < 0.05). Cough intensity was affected by the vocal cord function on postoperative day 1. However, after postoperative day 2, the cough intensity was not influenced by the vocal cord function. Declining glottal closure function( vocal cord function) immediately after surgery affects the cough intensity and vocal function. The influence of reduction in glottic closure function after surgery on coughing decline was observed up to 1 day after the withdrawal of ventilatory support. After the secondpostoperative day, the PCF was strongly influenced by the VC

    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

    Cosmic-Ray Lithium Production in the Nova Ejecta

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