7 research outputs found
Detections of [C II] 158 m and [O III] 88 m in a Local Lyman Continuum Emitter, Mrk 54, and its Implications to High-redshift ALMA Studies
We present integral field, far-infrared (FIR) spectroscopy of Mrk 54, a local
Lyman Continuum Emitter (LCE), obtained with FIFI-LS on the Stratospheric
Observatory for Infrared Astronomy. This is only the second time, after Haro
11, that [C II] 158 m and [O III] 88 m spectroscopy of the known LCEs
have been obtained. We find that Mrk 54 has a strong [C II] emission that
accounts for % of the total FIR luminosity, whereas it has only moderate
[O III] emission, resulting in the low [O III]/[C II] luminosity ratio of
. In order to investigate whether [O III]/[C II] is a useful
tracer of (LyC escape fraction), we examine the correlations of
[O III]/[C II] and (i) the optical line ratio of [O III]
5007 \AA/[O II] 3727 \AA, (ii) specific star formation rate, (iii) [O III] 88
m/[O I] 63 m ratio, (iv) gas phase metallicity, and (v) dust
temperature based on a combined sample of Mrk 54 and the literature data from
the Herschel Dwarf Galaxy Survey and the LITTLE THINGS Survey. We find that
galaxies with high [O III]/[C II] luminosity ratios could be the result of high
ionization (traced by ), bursty star formation, high
ionized-to-neutral gas volume filling factors (traced by [O III] 88 m/[O
I] 63 m), and low gas-phase metallicities, which is in agreement with
theoretical predictions. We present an empirical relation between the [O
III]/[C II] ratio and based on the combination of the [O III]/[C
II] and correlation, and the known relation between
and . The relation implies that high-redshift galaxies with high
[O III]/[C II] ratios revealed by ALMA may have ,
significantly contributing to the cosmic reionization.Comment: 14 pages, 5 figures, Accepted for publication in Ap
Recommended from our members
Gas conditions of a star-formation selected sample in the first billion years
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
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