Collectivity of neutron-rich Ti isotopes

The structure of the neutron-rich nucleus 58Ti was investigated via proton inelastic scattering in inverse kinematics at a mean energy of 42.0 MeV/nucleon. By measuring the deexcitation γ rays, three transitions with the energies of 1046(11) keV, 1376(18) keV, and 1835(27) keV were identified. The angle-integrated cross section for the 1046-keV excitation, which corresponds to the decay from the first 2+ state, was determined to be 13(7) mb. The deformation length δp,p′ was extracted from the cross section to be 0.83−0.30+0.22 fm. The energy of the first 2+ state and the δp,p′ value are comparable to the ones of 56Ti, which indicates that the collectivity of the Ti isotopes does not increase significantly with neutron number until N=36. This fact indicates that 58Ti is outside of the region of the deformation known in the neutron-rich nuclei around N=40

Low-lying Proton Intruder State in 13B

The neturon rich nucleus 13B was studied via the proton transfer reaction 4He(12Be,13B \gamma) at 50AMeV. The known 4.83-MeV excited state was strongly populated and its spin and parity were assigned to 1/2+ by comparing the angular differential cross section data with DWBA calculations. This low-lying 1/2+ state is interpreted as a proton intruder state and indicates a deformation of the nucleus.Comment: 16 pages, 3 figure

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection

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

「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

Optimization of piston for diesel engine using Kriging model

Diesel engine combustion chamber which reduces exhaust emission has been designed using CFD analysis and optimization techniques. In order to save computational time for design, the Kriging model, one of the response surface models, is adopted here. For the robust exploration, both the estimated function value of the model and its uncertainty are considered at the same time. In the present problem, the k-means method is used to limit a number of additional sample points to a reasonable level. Among the additional sample points, two combustion chamber shapes dominate the baseline configuration in terms of all objective functions. Compared with the previous optimization with the evolutionary algorithm, its computational time for design was cut by 95%. The results indicate that the present method is a practical approach for real-world applications