Observations of [C II] 158 micron Line and Far-infrared Continuum Emission toward the High-latitude Molecular Clouds in Ursa Major

We report the results of a rocket-borne observation of [C II] 158\micron line and far-infrared continuum emission at 152.5\micron toward the high latitude molecular clouds in Ursa Major. We also present the results of a follow-up observation of the millimeter ^{12}CO J=1-0 line over a selected region observed by the rocket-borne experiment. We have discovered three small CO cloudlets from the follow-up ^{12}CO observations. We show that these molecular cloudlets, as well as the MBM clouds(MBM 27/28/29/30), are not gravitationally bound. Magnetic pressure and turbulent pressure dominate the dynamic balance of the clouds. After removing the HI-correlated and background contributions, we find that the [C II] emission peak is displaced from the 152.5\micron and CO peaks, while the 152.5\micron continuum emission is spatially correlated with the CO emission. We interpret this behavior by attributing the origin of [C II] emission to the photodissociation regions around the molecular clouds illuminated by the local UV radiation field. We also find that the ratio of the molecular hydrogen column density to velocity-integrated CO intensity is 1.19+-0.29x10^{20} cm^{-2} (K kms^{-1})^{-1} from the FIR continuum and the CO data. The average [C II] /FIR intensity ratio over the MBM clouds is 0.0071, which is close to the all sky average of 0.0082 reported by the FIRAS on the COBE satellite. The average [C II]/CO ratio over the same regions is 420, which is significantly lower than that of molecular clouds in the Galactic plane.Comment: 15 pages, LaTeX (aaspp4.sty) + 2 tables(apjpt4.sty) + 6 postscript figures; accepted for publication in the Astrophysical Journal; Astrophys. J. in press (Vol. 490, December 1, 1997 issue

関節リウマチ(RA)患者のNSAIDs長期投与における胃粘膜障害発生因子ならびにファモチジンの治療効果に関する検討

The objective of this study was to investigate the prevalence of gastric mucosal injury induced by nonsteroidal anti-inflammatory drugs (NSAIDs) in patients with rheumatoid arthritis (RA). Upper gastrointestinal endoscopy was performed on 100 RA patients treated with NSAIDs. Patient factors potentially contributing to the development of NSAID-induced gastric mucosal injury were identified by logistic regression analysis; gastric mucosal injury and ulcers were used as objective variables. Gastric mucosal injury was detected in 62 of 100 patients, and eight of these patients had ulcers. Previous history of ulcers, lifestyle, NSAID dosage, and body mass index were associated with the development of gastric mucosal injury, and the use of diclofenac and steroid dose were associated with the development of ulcers. Disease-modifying antirheumatic drugs (DMARDs) did not appear to influence the risk of NSAID-induced gastric mucosal injury. RA patients treated for long periods with NSAIDs for RA symptoms should be controlled with DMARDs, without consideration of increased doses of steroids, in terms of risk for NSAID-induced gastric mucosal injury. Simultaneously, concomitant use of histamine-2 receptor antagonists (H2RA) such as famotidine should be considered.博士（医学）・乙第1354号・平成27年3月16日© Japan College of Rheumatology 2009© Springer International Publishing AG, Part of Springer Science+Business Medi

Signature of hidden order and evidence for periodicity modification in URu₂Si₂

The detail of electronic structures near the Fermi level in URu2Si2 has been investigated employing state-of-art laser angle-resolved photoemission spectroscopy. The observation of a narrow dispersive band near the Fermi level in the ordered state as well as its absence in a Rh-substituted sample strongly suggest that the emergence of the narrow band is a clear signature of the hidden-order transition. The temperature dependence of the narrow band, which appears at the onset of the hidden-order transition, invokes the occurrence of periodicity modification in the ordered state, which is shown for the first time by any spectroscopic probe. We compare our data to other previous studies and discuss possible implications

The Second Survey of the Molecular Clouds in the Large Magellanic Cloud by NANTEN I: Catalog of Molecular Clouds

The second survey of the molecular clouds in 12CO (J = 1-0) was carried out in the Large Magellanic Cloud by NANTEN. The sensitivity of this survey is twice as high as that of the previous NANTEN survey, leading to a detection of molecular clouds with M_CO > 2 x 10^4 M_sun. We identified 272 molecular clouds, 230 of which are detected at three or more observed positions. We derived the physical properties, such as size, line width, virial mass, of the 164 GMCs which have an extent more than the beam size of NANTEN in both the major and minor axes. The CO luminosity and virial mass of the clouds show a good correlation of M_VIR propto L_CO^{1.1 +- 0.1} with a Spearman rank correlation of 0.8 suggesting that the clouds are in nearly virial equilibrium. Assuming the clouds are in virial equilibrium, we derived an X_CO-factor to be ~ 7 x 10^20 cm^-2 (K km s^-1)^-1. The mass spectrum of the clouds is fitted well by a power law of N_cloud(>M_CO) proportional to M_CO^{-0.75 +- 0.06} above the completeness limit of 5 x 10^4 M_sun. The slope of the mass spectrum becomes steeper if we fit only the massive clouds; e.g., N_cloud (>M_CO) is proportional to M_CO^{-1.2 +- 0.2} for M_CO > 3 x 10^5 M_sun.Comment: 54 pages in total, 18 figures (21 files) and 4 tables, to appear in Astrophysical Journal Supplement Series. A full color version with higher resolution figures is available at http://www.a.phys.nagoya-u.ac.jp/~kawamura/research/NANTEN_LMC_1_preprint_highres.pd

Deletion of DOCK2, a regulator of the actin cytoskeleton in lymphocytes, suppresses cardiac allograft rejection

Allograft rejection is induced by graft tissue infiltration of alloreactive T cells that are activated mainly in secondary lymphoid organs of the host. DOCK2 plays a critical role in lymphocyte homing and immunological synapse formation by regulating the actin cytoskeleton, yet its role in the in vivo immune response remains unknown. We show here that DOCK2 deficiency enables long-term survival of cardiac allografts across a complete mismatch of the major histocompatibility complex molecules. In DOCK2-deficient mice, alloreactivity and allocytotoxicity were suppressed significantly even after in vivo priming with alloantigens, which resulted in reduced intragraft expression of effector molecules, such as interferon-γ, granzyme B, and perforin. This is mediated, at least in part, by preventing potentially alloreactive T cells from recruiting into secondary lymphoid organs. In addition, we found that DOCK2 is critical for CD28-mediated Rac activation and is required for the full activation of alloreactive T cells. Although DOCK2-deficient, alloreactive T cells were activated in vitro in the presence of exogenous interleukin-2, these T cells, when transferred adoptively, failed to infiltrate into the allografts that were transplanted into RAG1-deficient mice. Thus, DOCK2 deficiency attenuates allograft rejection by simultaneously suppressing multiple and key processes. We propose that DOCK2 could be a novel molecular target for controlling transplant rejection

High-Mass Cloud Cores in the eta Carinae Giant Molecular Cloud

We carried out an unbiased survey for massive dense cores in the giant molecular cloud associated with eta Carinae with the NANTEN telescope in 12CO, 13CO, and C18O 1-0 emission lines. We identified 15 C18O cores. Two of the 15 cores are associated with IRAS point sources whose luminosities are larger than 10^4 Lo, which indicates that massive star formation is occuring within these cores. Five cores including the two with IRAS sources are associated with MSX point sources. We detected H13CO+ (1-0) emission toward 4 C18O cores, one of which is associated with neither IRAS nor MSX point sources. This core shows the presence of a bipolar molecular outflow in 12CO (2-1), which indicates that star formation is also occuring in the core. In total, six C18O cores out of 15 are experienced star formation, and at least 2 of 15 are massive-star forming cores in the eta Car GMC. We found that massive star formation occurs preferentially in cores with larger column density, mass, number density, and smaller ratio of virial mass to LTE mass Mvir/M. We also found that the cores in the eta Car GMC are characterized by large line width and Mvir/M on average compared to the cores in other GMCs. We investigated the origin of a large amount of turbulence in the eta Car GMC. We propose the possibility that the large turbulence was pre-existing when the GMC was formed, and is now dissipating. Mechanisms such as multiple supernova explosions in the Carina flare supershell may have contributed to form a GMC with a large amount of turbulence.Comment: 41 pages, including 11 fugures and 9 tables. Accepted by ApJ. Author changed. Paper with high resolution figures is available at http://astrol.cias.osakafu-u.ac.jp/~yonekura/work/paper/etaCar

DOCK2 is a Rac activator that regulates motility and polarity during neutrophil chemotaxis

Neutrophils are highly motile leukocytes, and they play important roles in the innate immune response to invading pathogens. Neutrophil chemotaxis requires Rac activation, yet the Rac activators functioning downstream of chemoattractant receptors remain to be determined. We show that DOCK2, which is a mammalian homologue of Caenorhabditis elegans CED-5 and Drosophila melanogaster Myoblast City, regulates motility and polarity during neutrophil chemotaxis. Although DOCK2-deficient neutrophils moved toward the chemoattractant source, they exhibited abnormal migratory behavior with a marked reduction in translocation speed. In DOCK2-deficient neutrophils, chemoattractant-induced activation of both Rac1 and Rac2 were severely impaired, resulting in the loss of polarized accumulation of F-actin and phosphatidylinositol 3,4,5-triphosphate (PIP3) at the leading edge. On the other hand, we found that DOCK2 associates with PIP3 and translocates to the leading edge of chemotaxing neutrophils in a phosphatidylinositol 3-kinase (PI3K)–dependent manner. These results indicate that during neutrophil chemotaxis DOCK2 regulates leading edge formation through PIP3-dependent membrane translocation and Rac activation