Shedding Light on the Compton-thick Active Galactic Nucleus in the Ultra-luminous Infrared Galaxy UGC 5101 with Broadband X-ray Spectroscopy

We report the broadband X-ray spectra of the ultra-luminous infrared galaxy (ULIRG) UGC 5101 in the 0.25-100 keV band observed with Swift/Burst Alert Telescope (BAT), NuSTAR, Suzaku, XMM-Newton, and Chandra. A Compton-thick AGN obscured with a hydrogen column density of $\approx 1.3\times10^{24}$ cm$^{-2}$ is detected above 10 keV. A spectral fit with a numerical torus model favors a large half opening angle of the torus, $>41$ degrees, suggesting that the covering fraction of material heavily obscuring the X-ray source is moderate. The intrinsic 2-10 keV luminosity is determined to be $\approx 1.4\times 10^{43}$ erg s$^{-1}$, which is $\approx$2.5 times larger than the previous estimate using only data below 10 keV with a simple spectral model. We find that UGC 5101 shows the ratio between the [O IV] 26 $\mu$m line and 2-10 keV luminosities similar to those of normal Seyfert galaxies, along with other ULIRGs observed with NuSTAR, indicating that a significant portion of local ULIRGs are not really "X-ray faint" with respect to the flux of forbidden lines originating from the narrow line region (NLR). We propose a possible scenario that (1) the AGN in UGC 5101 is surrounded not only by Compton-thick matter located close to the equatorial plane but also by Compton-thin ($N_\mathrm{H} \sim 10^{21}$ cm$^{-2}$) matter in the torus-hole region and (2) it is accreting at a high Eddington rate with a steep UV to X-ray spectral energy distribution. Nevertheless, we argue that AGNs in many ULIRGs do not look extraordinary (i.e., extremely X-ray faint), as suggested by recent works, compared with normal Seyferts.Comment: 11 pages, 7 figures, accepted for publication in Ap

Broadband X-ray Spectral Analysis of the Double-Nucleus Luminous Infrared Galaxy Mrk 463

We present a broadband (0.4–70 keV) X-ray spectral analysis of the luminous infrared galaxy (LIRG) system Mrk 463 observed with Nuclear Spectroscopic Telescope Array (NuSTAR), Chandra, and XMM-Newton, which contains double active galactic nuclei (AGNs; Mrk 463E and Mrk 463W) with a separation of ~3.8 kpc. Detecting their transmitted hard X-ray >10 keV continua with NuSTAR, we confirm that Mrk 463E and Mrk 463W have AGNs with intrinsic luminosities of (1.6–2.2) × 10^(43) and (0.5–0.6) × 10^(43) erg s^(−1) (2–10 keV) obscured by hydrogen column densities of 8 × 10^(23) and 3 × 10^(23) cm^(−2), respectively. Both nuclei show strong reflection components from cold matter. The luminosity ratio between X-ray (2–10 keV) and [O IV] 25.89 μm of Mrk 463E is ~5 times smaller than those of normal Seyfert galaxies, suggesting that the intrinsic SED is X-ray weak relative to the UV luminosity. In fact, the bolometric AGN luminosity of Mrk 463E estimated from L'-band (3.8 μm), [O IV] 25.89 μm, and [Ne V] 14.32 μm lines indicate a large bolometric-to-X-ray luminosity ratio, κ_(2–10 keV) ≈ 110–410, and a high Eddington ratio, λ_(Edd) ~ 0.4–0.8. We suggest that the merger triggered a rapid growth of the black hole in Mrk 463E, which is not yet deeply "buried" by circumnuclear dust. By contrast, the L'-band luminosity of Mrk 463W is unusually small relative to the X-ray luminosity, suggesting that the Eddington ratio is low (<10^(−3)) and it might be still in an early phase of merger-driven AGN activity

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