A possible observational evidence for θ−2\theta^{-2} angular distribution of opening half-angle of GRB jets

We propose a method to estimate the pseudo jet opening half-angle of GRBs using the spectral peak energy (\Ep)--peak luminosity relation (so called Yonetoku relation) as well as the \Ep--collimation-corrected $\gamma$-ray energy relation (so called Ghirlanda relation). For bursts with known jet break times and redshifts, we compared the pseudo jet opening half-angle with the standard one and found that the differences are within a factor 2. We apply the method to 689 long GRBS. We found that the distribution function of the pseudo jet opening half-angle obeys $f(\theta_j)\propto\theta_j^{-2.2 \pm 0.2}$ with possible cutoffs for $\theta_j 0.3$ although the log-normal fit is also possible. $\theta^{-2}$ distribution is compatible with the structured jet model. From the distribution function we found that the beaming correction for the rate of GRBs is $\sim 340$, which means $\sim 10^{-5}$ yr$^{-1}$ galaxy$^{-1}$ or only one in $10^2$ type Ib/c supernovae. We also found the evolution of the distribution function as a function of the redshift.Comment: 5 pages, 5 figures, submitted to MNRA

A Four-Step Model for the IL-6 Amplifier, a Regulator of Chronic Inflammations in Tissue-Specific MHC Class II-Associated Autoimmune Diseases

It is commonly thought that autoimmune diseases are caused by the breakdown of self-tolerance, which suggests the recognition of specific antigens by autoreactive CD4+ T cells contribute to the specificity of autoimmune diseases (Marrack et al., 2001; Mathis and Benoist, 2004). In several cases, however, even for diseases associated with class II major histocompatibility complex (MHC) alleles, the causative tissue-specific antigens recognized by memory/activated CD4+ T cells have not been established (Mocci et al., 2000; Skapenko et al., 2005). Rheumatoid arthritis (RA) and arthritis in F759 knock-in mice (F759 mice) are such examples (Atsumi et al., 2002; Brennan et al., 2002; Falgarone et al., 2009). These include associations with class II MHC and CD4 molecules; increased numbers of memory/activated CD4+ T cells; and improved outcomes in response to suppressions and/or deficiencies in class II MHC molecules, CD4+ T cells, and the T cell survival cytokine IL-7. Regarding the development of arthritis in F759 mice, it is not only the immune system, but also non-immune tissue that are involved, indicating that the importance of their interactions (Sawa et al., 2006, 2009; Ogura et al., 2008; Hirano, 2010; Murakami et al., 2011). Furthermore, we have shown that local events such as microbleeding together with an accumulation of activated CD4+ T cells in a manner independent of tissue antigen-recognitions induces arthritis in the joints of F759 mice (Murakami et al., 2011). For example, local microbleeding-mediated CCL20 expression induce such an accumulation, causing arthritis development via chronic activation of an IL-17A-dependent IL-6 signaling amplification loop in type 1 collagen+ cells that is triggered by CD4+ T cell-derived cytokine(s) such as IL-17A, which leads to the synergistic activation of STAT3 and NFκB in non-hematopoietic cells in the joint (Murakami et al., 2011). We named this loop the IL-6-mediated inflammation amplifier, or IL-6 amplifier for short (Ogura et al., 2008; Hirano, 2010; Murakami et al., 2011). Thus, certain class II MHC-associated, tissue-specific autoimmune diseases, including some RA subtypes, may be induced by local events that cause an antigen-independent accumulation of effector CD4+ T cells followed by the induction of the IL-6 amplifier in the affected tissue. In other words, in certain cases, the target tissue itself may determine the specificity of the autoimmune disease via activation of the IL-6 amplifier. To explain this hypothesis, we have proposed a four-step model for MHC class II-associated autoimmune diseases (Murakami et al., 2011): (1) T cell activation regardless of antigen specificity; (2) local events inducing a tissue-specific accumulation of activated T cells; (3) transient activation of the IL-6 amplifier; and (4) enhanced sensitivity to cytokines in the target tissue. The interaction of these events results in chronic activation of the IL-6 amplifier and subsequent manifestation of autoimmune diseases. Thus, the IL-6 amplifier, which is chronically activated by these four events, is a critical regulator of chronic inflammations in tissue-specific MHC class II-associated autoimmune diseases

Redshift Dependent Lag-Luminosity Relation in 565 BASTE Gamma Ray Bursts

We compared redshifts $z_Y$ from Yonetoku relation and $z_{lag}$ from the lag-luminosity relation for 565 BASTE GRBs and were surprised to find that the correlation is very low. Assuming that the luminosity is a function of both $z_Y$ and the intrinsic spectral lag $\tau_{lag}$, we found a new redshift dependent lag-luminosity relation as $L=7.5\times 10^{50}{\rm erg/s}(1+z)^{2.53}\tau_{lag}^{-0.282}$ with the correlation coefficient of 0.77 and the chance probability of $7.9\times 10^{-75}$. To check the validity of this method, we examined the other luminosity indicator, Amati relation, using $z_Y$ and the observed fluence and found the correlation coefficient of 0.92 and the chance probability of $5.2\times 10^{-106}$. Although the spectral lag is computed from two channels of BATSE, our new lag-luminosity relation suggests that a possible lag-luminosity relation in the \swift era should also depend on redshift

Non-Equilibrium Ionization States of GRB Environments

Iron spectral features are thought to be the best tracer of a progenitor of gamma-ray bursts (GRBs). The detections of spectral features such as an iron line and/or a Radiative Recombination edge and Continuum (RRC) were reported in four X-ray afterglows of GRBs. However their properties were different each other burst by burst. For example, Chandra observation of GRB 991216 reported both the strong H-like iron line together with its RRC. On the contrary, Yoshida et al. (2001) report only a detection of the strong RRC in GRB 970828 with ASCA. Since it is difficult to produce the strong RRC, we have to consider special condition for the line and/or the RRC forming region. In this paper, we point out a possibility of a ``non-equilibrium ionization state'' for the line and the RRC forming region.Comment: 10pages, 2figures. Accepted for ApJL. This is a companion paper by A.Yoshida et. a

Flight Performance of the AKARI Cryogenic System

We describe the flight performance of the cryogenic system of the infrared astronomical satellite AKARI, which was successfully launched on 2006 February 21 (UT). AKARI carries a 68.5 cm telescope together with two focal plane instruments, Infrared Cameras (IRC) and Far Infrared Surveyor (FIS), all of which are cooled down to cryogenic temperature to achieve superior sensitivity. The AKARI cryogenic system is a unique hybrid system, which consists of cryogen (liquid helium) and mechanical coolers (2-stage Stirling coolers). With the help of the mechanical coolers, 179 L (26.0 kg) of super-fluid liquid helium can keep the instruments cryogenically cooled for more than 500 days. The on-orbit performance of the AKARI cryogenics is consistent with the design and pre-flight test, and the boil-off gas flow rate is as small as 0.32 mg/s. We observed the increase of the major axis of the AKARI orbit, which can be explained by the thrust due to thermal pressure of vented helium gas.Comment: 19 pages, 10 figures, and 6 tables. Accepted for publication in the AKARI special issue of the Publications of the Astronomical Society of Japa