146 research outputs found

    AKARI/FIS Mapping of the ISM-Wind Bow Shock around Alpha Ori

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    We present 10' x 50' scan maps around an M supergiant Alpha Ori at 65, 90, 140 and 160 microns obtained with the AKARI Infrared Astronomy Satellite. Higher spatial resolution data with the exact analytic solution permit us to fit the de-projected shape of the stellar wind bow shock around Alpha Ori to have the stand-off distance of 4.8', position angle of 55 degrees and inclination angle of 56 degrees. The shape of the bow shock suggests that the peculiar velocity of Alpha Ori with respect to the local medium is v_* = 40 (n_H)^(-1/2), where n_H is the hydrogen nucleus density at Alpha Ori. We find that the local medium is of n_H = 1.5 to 1.9 cm^(-3) and the velocity of the local flow is at 11 km s^(-1) by using the most recent astrometric solutions for Alpha Ori under the assumption that the local medium is moving away from the Orion OB 1 association. AKARI images may also reveal a vortex ring due to instabilities on the surface of the bow shock as demonstrated by numerical models. This research exemplifies the potential of AKARI All-Sky data as well as follow-up observations with Herschel Space Telescope and Stratospheric Observatory for Infrared Astronomy for this avenue of research in revealing the nature of interaction between the stellar wind and interstellar medium.Comment: 8 pages, 2 figures, to be published in PASJ Vol. 60 Special Issue on Recent Results from AKAR

    Oxidation behaviour of lattice oxygen in Li-rich manganese-based layered oxide studied by hard X-ray photoelectron spectroscopy

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    The oxidation/reduction behaviours of lattice oxygen and transition metals in a Li-rich manganese-based layered oxide Li[Li0.25Ni0.20Mn0.55]O1.93 are investigated by using hard X-ray photoelectron spectroscopy (HAX-PES). By making use of its deeper probing depth rather than in-house XPS analyses, we clearly confirm the formation of O- ions as bulk oxygen species in the active material. They are formed on the 1st charging process as a charge compensation mechanism for delithiation and decrease on discharging. In particular, the cation-anion dual charge compensation involving Ni and O ions is suggested during the voltage slope region of the charging process. The Ni ions in the material are considered to increase the capacity delivered by a reversible anion redox reaction with the suppression of O2 gas release. On the other hand, we found structural deterioration in the cycled material. The O- species are still observed but are electrochemically inactive during the 5th charge-discharge cycle. Also, the oxidation state of Ni ions is divalent and inactive, although that of Mn ions changes reversibly. We believe that this is associated with the structural rearrangement occurring after the activation process during the 1st charging, leading to the formation of spinel- or rocksalt-like domains over the sub-surface region of the particles

    Liganded Thyroid Hormone Receptor Inhibits Phorbol 12-O-Tetradecanoate-13-Acetate-Induced Enhancer Activity via Firefly Luciferase cDNA

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    Thyroid hormone receptor (TR) belongs to the nuclear hormone receptor (NHR) superfamily and regulates the transcription of its target genes in a thyroid hormone (T3)-dependent manner. While the detail of transcriptional activation by T3 (positive regulation) has been clarified, the mechanism of T3-dependent repression (negative regulation) remains to be determined. In addition to naturally occurring negative regulations typically found for the thyrotropin β gene, T3-bound TR (T3/TR) is known to cause artificial negative regulation in reporter assays with cultured cells. For example, T3/TR inhibits the transcriptional activity of the reporter plasmids harboring AP-1 site derived from pUC/pBR322-related plasmid (pUC/AP-1). Artificial negative regulation has also been suggested in the reporter assay with firefly luciferase (FFL) gene. However, identification of the DNA sequence of the FFL gene using deletion analysis was not performed because negative regulation was evaluated by measuring the enzymatic activity of FFL protein. Thus, there remains the possibility that the inhibition by T3 is mediated via a DNA sequence other than FFL cDNA, for instance, pUC/AP-1 site in plasmid backbone. To investigate the function of FFL cDNA as a transcriptional regulatory sequence, we generated pBL-FFL-CAT5 by ligating FFL cDNA in the 5' upstream region to heterologous thymidine kinase promoter in pBL-CAT5, a chloramphenicol acetyl transferase (CAT)-based reporter gene, which lacks pUC/AP-1 site. In kidney-derived CV1 and choriocarcinoma-derived JEG3 cells, pBL-FFL-CAT5, but not pBL-CAT5, was strongly activated by a protein kinase C activator, phorbol 12-O-tetradecanoate-13-acetate (TPA). TPA-induced activity of pBL-FFL-CAT5 was negatively regulated by T3/TR. Mutation of nt. 626/640 in FFL cDNA attenuated the TPA-induced activation and concomitantly abolished the T3-dependent repression. Our data demonstrate that FFL cDNA sequence mediates the TPA-induced transcriptional activity, which is inhibited by T3/TR

    Trk-fused gene (TFG) regulates pancreatic beta cell mass and insulin secretory activity

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    The Trk-fused gene (TFG) is reportedly involved in the process of COPII-mediated vesicle transport and missense mutations in TFG cause several neurodegenerative diseases including hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P). The high coincidence ratio between HMSN-P and diabetes mellitus suggests TFG to have an important role(s) in glucose homeostasis. To examine this possibility, β-cell specific TFG knockout mice (βTFG KO) were generated. Interestingly, βTFG KO displayed marked glucose intolerance with reduced insulin secretion. Immunohistochemical analysis revealed smaller β-cell masses in βTFG KO than in controls, likely attributable to diminished β-cell proliferation. Consistently, β-cell expansion in response to a high-fat, high-sucrose (HFHS) diet was significantly impaired in βTFG KO. Furthermore, glucose-induced insulin secretion was also markedly impaired in islets isolated from βTFG KO. Electron microscopic observation revealed endoplasmic reticulum (ER) dilatation, suggestive of ER stress, and smaller insulin crystal diameters in β-cells of βTFG KO. Microarray gene expression analysis indicated downregulation of NF-E2 related factor 2 (Nrf2) and its downstream genes in TFG depleted islets. Collectively, TFG in pancreatic β-cells plays a vital role in maintaining both the mass and function of β-cells, and its dysfunction increases the tendency to develop glucose intolerance.This study was partly supported by a Grant-in-Aid for Research Activity Start-up (JSPS KAKENHI Grant Number JP15H06427) (to T.Y.) from the Ministry of Education, Science, Sports and Culture, Japan, and grants from Mitsubishi Tanabe Pharma (to T.Y.), Novartis Pharma (to T.Y.), Takeda Science Foundation (to Y.N.), Asahi Life Foundation (to Y.N.) and The Uehara Memorial Foundation (to Y.N.)

    Measurement of low-energy antiproton detection efficiency in BESS below 1 GeV

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    An accelerator experiment was performed using a low-energy antiproton beam to measure antiproton detection efficiency of BESS, a balloon-borne spectrometer with a superconducting solenoid. Measured efficiencies showed good agreement with calculated ones derived from the BESS Monte Carlo simulation based on GEANT/GHEISHA. With detailed verification of the BESS simulation, the relative systematic error of detection efficiency derived from the BESS simulation has been determined to be ±\pm5%, compared with the previous estimation of ±\pm15% which was the dominant uncertainty for measurements of cosmic-ray antiproton flux.Comment: 13 pages, 7 figure

    GATA2 Mediates Thyrotropin-Releasing Hormone-Induced Transcriptional Activation of the Thyrotropin β Gene

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    Thyrotropin-releasing hormone (TRH) activates not only the secretion of thyrotropin (TSH) but also the transcription of TSHβ and α-glycoprotein (αGSU) subunit genes. TSHβ expression is maintained by two transcription factors, Pit1 and GATA2, and is negatively regulated by thyroid hormone (T3). Our prior studies suggest that the main activator of the TSHβ gene is GATA2, not Pit1 or unliganded T3 receptor (TR). In previous studies on the mechanism of TRH-induced activation of the TSHβ gene, the involvements of Pit1 and TR have been investigated, but the role of GATA2 has not been clarified. Using kidney-derived CV1 cells and pituitary-derived GH3 and TαT1 cells, we demonstrate here that TRH signaling enhances GATA2-dependent activation of the TSHβ promoter and that TRH-induced activity is abolished by amino acid substitution in the GATA2-Zn finger domain or mutation of GATA-responsive element in the TSHβ gene. In CV1 cells transfected with TRH receptor expression plasmid, GATA2-dependent transactivation of αGSU and endothelin-1 promoters was enhanced by TRH. In the gel shift assay, TRH signal potentiated the DNA-binding capacity of GATA2. While inhibition by T3 is dominant over TRH-induced activation, unliganded TR or the putative negative T3-responsive element are not required for TRH-induced stimulation. Studies using GH3 cells showed that TRH-induced activity of the TSHβ promoter depends on protein kinase C but not the mitogen-activated protein kinase, suggesting that the signaling pathway is different from that in the prolactin gene. These results indicate that GATA2 is the principal mediator of the TRH signaling pathway in TSHβ expression

    Measurements of Cosmic-ray Low-energy Antiproton and Proton Spectra in a Transient Period of the Solar Field Reversal

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    The energy spectra of cosmic-ray low-energy antiprotons and protons have been measured by BESS in 1999 and 2000, during a period covering the solar magnetic field reversal. Based on these measurements, a sudden increase of the antiproton to proton flux ratio following the solar magnetic field reversal was observed, and it generally agrees with a drift model of the solar modulation.Comment: 4 pages, 4 figures, revised version accepted for publication in Phys. Rev. Let
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