MITSuME--Multicolor Imaging Telescopes for Survey and Monstrous Explosions

Development of MITSuME is reported. Two 50-cm optical telescopes have been built at Akeno in Yamanashi prefecture and at Okayama Astrophysical Observatory (OAO) in Okayama prefecture. Three CCD cameras for simultaneous g'RcIc photometry are to be mounted on each focal plane, covering a wide FOV of about 30" x 30". The limiting magnitude at V is fainter than 18. In addition to these two optical telescopes, a 91-cm IR telescope with a 1 deg x 1 deg field of view is being built at OAO, which performs photometry in YJHK bands. These robotic telescopes can start the observation of counterparts of a GRB within a minute from an alert. We aim to obtain photometric redshifts exceeding 10 with these telescopes. The performance and the current construction status of the telescopes are presented.Comment: 4 pages, 3 figures, 4th Workshop on Gamma-Ray Burst in the Afterglow Era, Roma, October 18-22, 200

Gauged Nambu-Jona-Lasinio model with extra dimensions

We investigate phase structure of the D (> 4)-dimensional gauged Nambu-Jona-Lasinio (NJL) model with $\delta(=D-4)$ extra dimensions compactified on TeV scale, based on the improved ladder Schwinger-Dyson (SD) equation in the bulk. We assume that the bulk running gauge coupling in the SD equation for the SU(N_c) gauge theory with N_f massless flavors is given by the truncated Kaluza-Klein effective theory and hence has a nontrivial ultraviolet fixed point (UVFP). We find the critical line in the parameter space of two couplings, the gauge coupling and the four-fermion coupling, which is similar to that of the gauged NJL model with fixed (walking) gauge coupling in four dimensions. It is shown that in the presence of such walking gauge interactions the four-fermion interactions become ``nontrivial'' even in higher dimensions, similarly to the four-dimensional gauged NJL model. Such a nontriviality holds only in the restricted region of the critical line (``nontrivial window'') with the gauge coupling larger than a non-vanishing value (``marginal triviality (MT)'' point), in contrast to the four-dimensional case where such a nontriviality holds for all regions of the critical line except for the pure NJL point. In the nontrivial window the renormalized effective potential yields a nontrivial interaction which is conformal invariant. The exisitence of the nontrivial window implies ``cutoff insensitivity'' of the physics prediction in spite of the ultraviolet dominance of the dynamics. In the formal limit D -> 4, the nontrivial window coincides with the known condition of the nontriviality of the four-dimensional gauged NJL model, $9/(2N_c) < N_f - N_c < 9/2 N_c$.Comment: 34 pages, 6 figures, references added, to appear in Phys.Rev.D. The title is changed in PR

Swift and Suzaku Observations of the X-Ray Afterglow from the GRB 060105

Results are presented of early X-ray afterglow observations of GRB 060105 by Swift and Suzaku. The bright, long gamma-ray burst GRB 060105 triggered the Swift Burst Alert Telescope (BAT) at 06:49:28 on 5 January 2006. The Suzaku team commenced a pre-planned target of opportunity observation at 19 ks (5.3 hr) after the Swift trigger. Following the prompt emission and successive very steep decay, a shallow decay was observed from T_0+187 s to T_0+1287 s. After an observation gap during T_0 +(1.5-3) ks, an extremely early steep decay was observed in T_0+(4-30) ks. The lightcurve flattened again at T_0+30 ks, and another steep decay followed from T_0+50 ks to the end of observations. Both steep decays exhibited decay indices of 2.3 - 2.4. This very early break, if it is a jet break, is the earliest case among X-ray afterglow observations, suggesting a very narrow jet whose opening angle is well below 1 degree. The unique Suzaku/XIS data allow us to set very tight upper limits on line emission or absorption in this GRB. For the reported pseudo-redshift of z=4.0+/-1.3 the upper limit on the iron line equivalent width is 50 eV.Comment: 8 pages, 5 figures, Accepted for publication in PASJ Suzaku Special Issue (vol. 58

Measurement of Inclusive Production of Neutral Pions from Upsilon(4S) Decays

Using the Belle detector operating at the KEKB e+e- storage ring, we have measured the mean multiplicity and the momentum spectrum of neutral pions from the decays of the Upsilon(4S) resonance. We measure a mean of 4.70 +/- 0.04 +/- 0.22 neutral pions per Upsilon(4S) decay.Comment: 15 pages, 4 figs. Submitted to Phys.Rev.

Ebola Zaire Virus Blocks Type I Interferon Production by Exploiting the Host SUMO Modification Machinery

Ebola Zaire virus is highly pathogenic for humans, with case fatality rates approaching 90% in large outbreaks in Africa. The virus replicates in macrophages and dendritic cells (DCs), suppressing production of type I interferons (IFNs) while inducing the release of large quantities of proinflammatory cytokines. Although the viral VP35 protein has been shown to inhibit IFN responses, the mechanism by which it blocks IFN production has not been fully elucidated. We expressed VP35 from a mouse-adapted variant of Ebola Zaire virus in murine DCs by retroviral gene transfer, and tested for IFN transcription upon Newcastle Disease virus (NDV) infection and toll-like receptor signaling. We found that VP35 inhibited IFN transcription in DCs following these stimuli by disabling the activity of IRF7, a transcription factor required for IFN transcription. By yeast two-hybrid screens and coimmunoprecipitation assays, we found that VP35 interacted with IRF7, Ubc9 and PIAS1. The latter two are the host SUMO E2 enzyme and E3 ligase, respectively. VP35, while not itself a SUMO ligase, increased PIAS1-mediated SUMOylation of IRF7, and repressed Ifn transcription. In contrast, VP35 did not interfere with the activation of NF-κB, which is required for induction of many proinflammatory cytokines. Our findings indicate that Ebola Zaire virus exploits the cellular SUMOylation machinery for its advantage and help to explain how the virus overcomes host innate defenses, causing rapidly overwhelming infection to produce a syndrome resembling fulminant septic shock

The Yeast Tor Signaling Pathway Is Involved in G2/M Transition via Polo-Kinase

The target of rapamycin (Tor) protein plays central roles in cell growth. Rapamycin inhibits cell growth and promotes cell cycle arrest at G1 (G0). However, little is known about whether Tor is involved in other stages of the cell division cycle. Here we report that the rapamycin-sensitive Tor complex 1 (TORC1) is involved in G2/M transition in S. cerevisiae. Strains carrying a temperature-sensitive allele of KOG1 (kog1-105) encoding an essential component of TORC1, as well as yeast cell treated with rapamycin show mitotic delay with prolonged G2. Overexpression of Cdc5, the yeast polo-like kinase, rescues the growth defect of kog1-105, and in turn, Cdc5 activity is attenuated in kog1-105 cells. The TORC1-Type2A phosphatase pathway mediates nucleocytoplasmic transport of Cdc5, which is prerequisite for its proper localization and function. The C-terminal polo-box domain of Cdc5 has an inhibitory role in nuclear translocation. Taken together, our results indicate a novel function of Tor in the regulation of cell cycle and proliferation

Recruitment of Histone Deacetylase 3 to the Interferon-A Gene Promoters Attenuates Interferon Expression

Induction of Type I Interferon (IFN) genes constitutes an essential step leading to innate immune responses during virus infection. Sendai virus (SeV) infection of B lymphoid Namalwa cells transiently induces the transcriptional expression of multiple IFN-A genes. Although transcriptional activation of IFN-A genes has been extensively studied, the mechanism responsible for the attenuation of their expression remains to be determined.In this study, we demonstrate that virus infection of Namalwa cells induces transient recruitment of HDAC3 (histone deacetylase 3) to IFN-A promoters. Analysis of chromatin-protein association by Chip-QPCR demonstrated that recruitment of interferon regulatory factor (IRF)3 and IRF7, as well as TBP correlated with enhanced histone H3K9 and H3K14 acetylation, whereas recruitment of HDAC3 correlated with inhibition of histone H3K9/K14 acetylation, removal of IRF7 and TATA-binding protein (TBP) from IFN-A promoters and inhibition of virus-induced IFN-A gene transcription. Additionally, HDAC3 overexpression reduced, and HDAC3 depletion by siRNA enhanced IFN-A gene expression. Furthermore, activation of IRF7 enhanced histone H3K9/K14 acetylation and IFN-A gene expression, whereas activation of both IRF7 and IRF3 led to recruitment of HDAC3 to the IFN-A gene promoters, resulting in impaired histone H3K9 acetylation and attenuation of IFN-A gene transcription.Altogether these data indicate that reversal of histone H3K9/K14 acetylation by HDAC3 is required for attenuation of IFN-A gene transcription during viral infection