68 research outputs found
A Spectral Study of the Black Hole Candidate XTE J1752-223 in the High/Soft State with MAXI, Suzaku and Swift
We report on the X-ray spectral analysis of the black hole candidate XTE\
J1752--223 in the 2009--2010 outburst, utilizing data obtained with the
MAXI/Gas Slit Camera (GSC), the Swift/XRT, and Suzaku, which work
complementarily. As already reported by Nakahira et al. (2010) MAXI monitored
the source continuously throughout the entire outburst for about eight months.
All the MAXI/GSC energy spectra in the high/soft state lasting for 2 months are
well represented by a multi-color disk plus power-law model. The innermost disk
temperature changed from 0.7 keV to 0.4 keV and the disk flux
decreased by an order of magnitude. Nevertheless, the innermost radius is
constant at 41 km, where is the
source distance in units of 3.5 kpc and the inclination. The multi-color
disk parameters obtained with the MAXI/GSC are consistent with those with the
Swift/XRT and Suzaku. The Suzaku data also suggests a possibility that the disk
emission is slightly Comptonized, which could account for broad iron-K features
reported previously. Assuming that the obtained innermost radius represents the
innermost stable circular orbit for a non-rotating black hole, we estimate the
mass of the black hole to be 5.510.28 , where the correction for the stress-free inner boundary condition
and color hardening factor of 1.7 are taken into account. If the inclination is
less than 49 as suggested from the radio monitoring of transient jets
and the soft-to-hard transition in 2010 April occurred at 1--4% of Eddignton
luminosity, the fitting of the Suzaku spectra with a relativistic
accretion-disk model derives constraints on the mass and the distance to be
3.1--55 and 2.3--22 {\rm kpc}, respectively. This confirms that the
compact object in XTE J1752--223 is a black hole.Comment: 12 pages including 7 figures and 4 tables, accepted for publication
in PAS
A Shock-Induced Pair of Superbubbles in the High-Redshift Powerful Radio Galaxy MRC 0406-244
We present new optical spectroscopy of the high-redshift powerful radio
galaxy MRC 0406244 at redshift of 2.429. We find that the two extensions
toward NW and SE probed in the rest-frame ultraviolet image are heated mainly
by the nonthermal continuum of the active galactic nucleus. However, each
extension shows a shell-like morphology, suggesting that they are a pair of
superbubbles induced by the superwind activity rather than by the interaction
between the radio jet and the ambient gas clouds. If this is the case, the
intense starburst responsible for the formation of superbubbles could occur
yr ago. On the other hand, the age of the radio jets may
be of the order of yr, being much shorter than the starburst age.
Therefore, the two events, i.e., the starburst and the radio-jet activities,
are independent phenomena. However, their directions of the expanding motions
could be governed by the rotational motion of the gaseous component in the host
galaxy. This idea appears to explain the alignment effect of MRC 0406244.Comment: 4 pages (emulateapj.sty), Fig. 1 (jpeg) + Fig.2 (eps). Accepted for
publications in ApJ (Letters
MiR-33a is a therapeutic target in SPG4-related hereditary spastic paraplegia human neurons
Recent reports, including ours, have indicated that microRNA (miR)-33 located within the intron of sterol regulatory element binding protein (SREBP) 2 controls cholesterol homeostasis and can be a potential therapeutic target for the treatment of atherosclerosis. Here, we show that SPAST, which encodes a microtubule-severing protein called SPASTIN, was a novel target gene of miR-33 in human. Actually, the miR-33 binding site in the SPAST 3′-UTR is conserved not in mice but in mid to large mammals, and it is impossible to clarify the role of miR-33 on SPAST in mice. We demonstrated that inhibition of miR-33a, a major form of miR-33 in human neurons, via locked nucleic acid (LNA)-anti-miR ameliorated the pathological phenotype in hereditary spastic paraplegia (HSP)-SPG4 patient induced pluripotent stem cell (iPSC)-derived cortical neurons. Thus, miR-33a can be a potential therapeutic target for the treatment of HSP-SPG4
Recipient mucosal-associated invariant T cells control GVHD within the colon
Mucosal-associated invariant T (MAIT) cells are a unique innate-like T cell subset that responds to a wide array of bacteria and yeast through recognition of riboflavin metabolites presented by the MHC class I–like molecule MR1. Here, we demonstrate using MR1 tetramers that recipient MAIT cells are present in small but definable numbers in graft-versus-host disease (GVHD) target organs and protect from acute GVHD in the colon following bone marrow transplantation (BMT). Consistent with their preferential juxtaposition to microbial signals in the colon, recipient MAIT cells generate large amounts of IL-17A, promote gastrointestinal tract integrity, and limit the donor alloantigen presentation that in turn drives donor Th1 and Th17 expansion specifically in the colon after BMT. Allogeneic BMT recipients deficient in IL-17A also develop accelerated GVHD, suggesting MAIT cells likely regulate GVHD, at least in part, by the generation of this cytokine. Indeed, analysis of stool microbiota and colon tissue from IL-17A–/– and MR1–/– mice identified analogous shifts in microbiome operational taxonomic units (OTU) and mediators of barrier integrity that appear to represent pathways controlled by similar, IL-17A–dependent mechanisms. Thus, MAIT cells act to control barrier function to attenuate pathogenic T cell responses in the colon and, given their very high frequency in humans, likely represent an important population in clinical BMT
The Wnt agonist R-spondin1 regulates systemic graft-versus-host disease by protecting intestinal stem cells
R-spondin1 stimulates the proliferation of intestinal stem cells through the Wnt signaling pathway and protects against graft-versus-host disease
CSF-1–dependant donor-derived macrophages mediate chronic graft-versus-host disease
Chronic GVHD (cGVHD) is the major cause of late, nonrelapse death following stem cell transplantation and characteristically develops in organs such as skin and lung. Here, we used multiple murine models of cGVHD to investigate the contribution of macrophage populations in the development of cGVHD. Using an established IL-17–dependent sclerodermatous cGVHD model, we confirmed that macrophages infiltrating the skin are derived from donor bone marrow (F4/80+CSF-1R+CD206+iNOS–). Cutaneous cGVHD developed in a CSF-1/CSF-1R–dependent manner, as treatment of recipients after transplantation with CSF-1 exacerbated macrophage infiltration and cutaneous pathology. Additionally, recipients of grafts from Csf1r–/– mice had substantially less macrophage infiltration and cutaneous pathology as compared with those receiving wild-type grafts. Neither CCL2/CCR2 nor GM-CSF/GM-CSFR signaling pathways were required for macrophage infiltration or development of cGVHD. In a different cGVHD model, in which bronchiolitis obliterans is a prominent manifestation, F4/80+ macrophage infiltration was similarly noted in the lungs of recipients after transplantation, and lung cGVHD was also IL-17 and CSF-1/CSF-1R dependent. Importantly, depletion of macrophages using an anti–CSF-1R mAb markedly reduced cutaneous and pulmonary cGVHD. Taken together, these data indicate that donor macrophages mediate the development of cGVHD and suggest that targeting CSF-1 signaling after transplantation may prevent and treat cGVHD
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