42 research outputs found

    A different view of wind in X-ray binaries: the accretion disc corona source 2S 0921-630

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    Accretion disc coronae (ADC) sources are very high inclination neutron star or black hole binaries, where the outer accretion flow blocks a direct view of the central source. The weak observed X-ray emission is instead produced mainly by scattering of the intrinsic radiation from highly ionized gas surrounding the source, the ADC. However, the origin of this scattering material is still under debate. We use the ADC source 2S 0921-630 (V395 Car) to test whether it is consistent with a thermal-radiative wind produced by the central X-ray source illuminating and puffing up the outer disc. This wind is clearly visible in blueshifted absorption lines in less highly inclined systems, where the source is seen directly through this material. Using the phenomenological photoionized plasma model, we first characterize the parameter that drives emission lines observed in 2S0921 in XMM–Newton and Chandra data. Following this, we run the Monte Carlo radiation transfer simulation to get scattered/reprocessed emissions in the wind, with the density and velocity structure obtained from the previous work. Our model agrees with all the wind emission lines in the Chandra high and medium energy grating spectra for an intrinsic source luminosity of L > 0.2 LEdd. This result strongly favours thermal-radiative winds as the origin of the ADC. We also show how high-resolution spectra via microcalorimeters can provide a definitive test by detecting blueshifted absorption lines

    Orbital- and spin-phase variability in the X-ray emission from the accreting pulsar Cen X-3

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    We analyzed 39 ks NuSTAR observation data of the high mass X-ray binary Cen X-3 in order to investigate the orbital- and spin-phase spectral variability. The observation covers the orbital phase of Φ=0.199\Phi=0.199-0.4140.414 of the source, where Φ=0\Phi=0 corresponds to the mid-eclipse. The orbital-phase-resolved spectroscopy revealed that low energy photons are more dominant for the spectral fluctuation, and a large part of the variability can be explained in terms of absorption by clumps of stellar wind. The spin-phase-resolved spectroscopy together with energy-resolved pulse profiles, on the other hand, presented large flux variations in high energy bands, which suggests that the origin of the variability is the different efficiency of Comptonization inside the accretion column. The energy band which includes Fe emission lines or cyclotron resonance scattering feature (CRSF) shows distinct variability compared to the nearby bands. The Fe lines show low variability along the spin phase, which indicates that the emission regions are apart from the neutron star. The central energy and strength of the CRSF are both positively correlated with the spin-phase-resolved flux, which suggests that the emitted photons face stronger magnetic fields and deeper absorption when they come from high-flux regions. We also examined the independence of the orbital- and spin-phase variability. They showed no correlation with each other and were highly independent, which implies the accretion stream is stable during the observation.Comment: 20 pages, 12 figures, accepted for publication in Ap

    Circumnuclear Multi-phase Gas in the Circinus Galaxy. V. The Origin of the X-Ray Polarization in the Circinus Galaxy

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    The Imaging X-ray Polarimetry Explorer (IXPE) detected X-ray polarization in the nearest Seyfert 2 galaxy, the Circinus galaxy, for the first time. To reproduce the IXPE results, we computed the degree of polarization based on two types of radiative hydrodynamic simulations: a parsec-scale three-dimensional model and a sub-parsec-scale axisymmetric model with a higher spatial resolution. In a series of papers, we confirmed that these models naturally explain the multi-wavelength observations of the Circinus galaxy from radio to X-rays. We used a Monte Carlo Simulation for Astrophysics and Cosmology code to compute the linear polarization of continuum emission. We found that the degree of polarization based on the parsec-scale radiation-driven fountain model was smaller than that observed with the IXPE. The degree of polarization based on the sub-parsec-scale model depends on the hydrogen number density of the disk (dd), and the degree of polarization obtained from our simulation is consistent with that observed with the IXPE in the case of logd/cm313\log d/\mathrm{cm}^{-3} \geq 13. We investigate where the photons are Compton scattered and imply that the origin of the X-ray polarization in the Circinus galaxy is the outflow inside 0.01 pc0.01 \ \mathrm{pc}. In this case, the degree of polarization may change over a timescale of approximately ten years.Comment: 11 pages, 8 figures, accepted for publication in Ap

    Application of X-Ray Clumpy Torus Model (XCLUMPY) to 10 Obscured Active Galactic Nuclei Observed with Suzaku and NuSTAR

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    We apply XCLUMPY, an X-ray spectral model from a clumpy torus in an active galactic nucleus (AGN), to the broadband X-ray spectra of 10 obscured AGNs observed with both Suzaku and NuSTAR. The infrared spectra of these AGNs were analyzed with the CLUMPY code. Since XCLUMPY adopts the same clump distribution as that in the CLUMPY, we can directly compare the torus parameters obtained from the X-ray spectra and those from the infrared ones. The torus angular widths determined from the infrared spectra (σIR\sigma_{\mathrm{IR}}) are systematically larger than those from the X-ray data (σX\sigma_{\mathrm{X}}); the difference (σIRσX\sigma_{\mathrm{IR}}-\sigma_{\mathrm{X}}) correlates with the inclination angle determined from the X-ray spectrum. These results can be explained by the contribution from dusty polar outflows to the observed infrared flux, which becomes more significant at higher inclinations (more edge-on views). The ratio of the hydrogen column density and V-band extinction in the line of sight absorber shows large scatter (\simeq1 dex) around the Galactic value, suggesting that a significant fraction of AGNs have dust-rich circumnuclear environments.Comment: 17 pages, 3 figures, accepted for publication in Ap

    RANKLが誘導する破骨細胞分化におけるROSの役割と、Febuxostatによる破骨細胞分化抑制効果

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    Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox’s anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage

    AXL confers intrinsic resistance to osimertinib and advances the emergence of tolerant cells

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    A novel EGFR-tyrosine kinase inhibitor (TKI), osimertinib, has marked efficacy in patients with EGFR-mutated lung cancer. However, some patients show intrinsic resistance and an insufficient response to osimertinib. This study showed that osimertinib stimulated AXL by inhibiting a negative feedback loop. Activated AXL was associated with EGFR and HER3 in maintaining cell survival and inducing the emergence of cells tolerant to osimertinib. AXL inhibition reduced the viability of EGFR-mutated lung cancer cells overexpressing AXL that were exposed to osimertinib. The addition of an AXL inhibitor during either the initial or tolerant phases reduced tumor size and delayed tumor re-growth compared to osimertinib alone. AXL was highly expressed in clinical specimens of EGFR-mutated lung cancers and its high expression was associated with a low response rate to EGFR-TKI. These results indicated pivotal roles for AXL and its inhibition in the intrinsic resistance to osimertinib and the emergence of osimertinib-tolerant cells

    Transient IGF-1R inhibition combined with osimertinib eradicates AXL-low expressing EGFR mutated lung cancer

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    Drug tolerance is the basis for acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) including osimertinib, through mechanisms that still remain unclear. Here, we show that while AXL-low expressing EGFR mutated lung cancer (EGFRmut-LC) cells are more sensitive to osimertinib than AXL-high expressing EGFRmut-LC cells, a small population emerge osimertinib tolerance. The tolerance is mediated by the increased expression and phosphorylation of insulin-like growth factor-1 receptor (IGF-1R), caused by the induction of its transcription factor FOXA1. IGF-1R maintains association with EGFR and adaptor proteins, including Gab1 and IRS1, in the presence of osimertinib and restores the survival signal. In AXL-low-expressing EGFRmut-LC cell-derived xenograft and patient-derived xenograft models, transient IGF-1R inhibition combined with continuous osimertinib treatment could eradicate tumors and prevent regrowth even after the cessation of osimertinib. These results indicate that optimal inhibition of tolerant signals combined with osimertinib may dramatically improve the outcome of EGFRmut-LC
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