http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Koo, Bon-Chul,McKee, Christopher F.,Suh, Kyung-Won,Moon, Dae-Sik,Onaka, Takashi,Burton, Michael G.,Hiramatsu, Masaaki,Bessell, Michael S.,Gaensler, B. M.,Kim, Hyun-Jeong,Lee, Jae-Joon,Jeong, Woong-Seo IOP Publishing 2011 The Astrophysical journal Vol.732 No.1
<P>We report new mid-infrared (MIR) observations of the remarkable object IRAS 15099-5856 using the space telescopes AKARI and Spitzer, which demonstrate the presence of prominent crystalline silicate emission in this bright source. IRAS 15099-5856 has a complex morphology with a bright central compact source (IRS1) surrounded by knots, spurs, and several extended (similar to 4') arc-like filaments. The source is seen only at >= 10 mu m. The Spitzer mid-infrared spectrum of IRS1 shows prominent emission features from Mg-rich crystalline silicates, strong [Ne II] 12.81 mu m, and several other faint ionic lines. We model the MIR spectrum as thermal emission from dust and compare with the Herbig Be star HD 100546 and the luminous blue variable R71, which show very similar MIR spectra. Molecular line observations reveal two molecular clouds around the source, but no associated dense molecular cores. We suggest that IRS1 is heated by UV radiation from the adjacent O star Muzzio 10 and that its crystalline silicates most likely originated in a mass outflow from the progenitor of the supernova remnant (SNR) MSH 15-52. IRS1, which is embedded in the SNR, could have been shielded from the SN blast wave if the progenitor was in a close binary system with Muzzio 10. If MSH 15-52 is a remnant of Type Ib/c supernova (SN Ib/c), as has been previously proposed, this would confirm the binary model for SN Ib/c. IRS1 and the associated structures may be the relics of massive star death, as shaped by the supernova explosion, the pulsar wind, and the intense ionizing radiation of the embedded O star.</P>
M. SHINO,H. YOSHITAKE,M. HIRAMATSU,T. SUNDA,M. KAMATA 한국자동차공학회 2014 International journal of automotive technology Vol.15 No.5
The objective of this study is to propose the indices which detect the deviated state of drivers while driving byconsidering drivers’ judgment process and using road environment and naturalistic driving behavior database. To realize thisobjective, drivers’ speed choice behavior around curve situations was focused and the speed choice process was formulated. Moreover, a deviated state detection method considering the formulated speed choice process around curve situations wasproposed and the validity of the method was examined.
Toyoshima, R.,Hiramatsu, N.,Yoshida, M.,Amemiya, K.,Mase, K.,Mun, B.,Kondoh, H. Royal Society of Chemistry 2017 Chemical communications Vol.53 No.94
<P>Catalytic CO oxidation over Pd(111) and Pd70Au30(111) surfaces was investigated by in situ spectroscopic observations to understand the alloying effect. The reaction behaviour on Pd70Au30(111) is greatly different from that on Pd(111). Pd monomer and dimer ensembles can act as active centers, whereas triangular-shaped trimers and larger ensembles are inactive.</P>
RUNX1–Survivin Axis Is a Novel Therapeutic Target for Malignant Rhabdoid Tumors
Masamitsu Mikami,Tatsuya Masuda,Takuya Kanatani,Katsutsugu Umeda,Hidefumi Hiramatsu,Hirohito Kubota,Tomoo Daifu,Atsushi Iwai,Etsuko Yamamoto Hattori,Kana Furuichi,Saho Takasaki,Sunao Tanaka,Yasuzumi M 한국분자세포생물학회 2022 Molecules and cells Vol.45 No.12
Malignant rhabdoid tumor (MRT) is a highly aggressive pediatric malignancy with no effective therapy. Therefore, it is necessary to identify a target for the development ofnovel molecule-targeting therapeutic agents. In this study, we report the importance of the runt-related transcription factor 1 (RUNX1) and RUNX1–Baculoviral IAP (inhibitor of apoptosis) Repeat-Containing 5 (BIRC5/survivin) axis in the proliferation of MRT cells, as it can be used as an ideal target for anti-tumor strategies. The mechanism of this reaction can be explained by the interaction of RUNX1 with the RUNX1-binding DNA sequence located in the survivin promoter and its positive regulation. Specific knockdown of RUNX1 led to decreased expression of survivin, which subsequently suppressed the proliferation of MRT cells in vitro and in vivo. We also found that our novel RUNX inhibitor, Chb-M, which switches off RUNX1 using alkylating agent-conjugated pyrrole-imidazole polyamides designed to specifically bind to consensus RUNX-binding sequences (5′-TGTGGT-3′), inhibited survivin expression in vivo. Taken together, we identified a novel interaction between RUNX1 and survivin in MRT. Therefore the negative regulation of RUNX1 activity may be a novel strategy for MRT treatment
Alkam, T.,Mamiya, T.,Kimura, N.,Yoshida, A.,Kihara, D.,Tsunoda, Y.,Aoyama, Y.,Hiramatsu, M.,Kim, H. C.,Nabeshima, T. Springer Science + Business Media 2017 Psychophamacology Vol.234 No.12
<P>Increased risk of attention-deficit/hyperactivity disorder (AD/HD) is partly associated with the early developmental exposure to nicotine in tobacco smoke. Emerging reports link tobacco smoke exposure or prenatal nicotine exposure (PNE) with AD/HD-like behaviors in rodent models. We have previously reported that PNE induces cognitive behavioral deficits in offspring and decreases the contents of dopamine (DA) and its turnover in the prefrontal cortex (PFC) of offspring It is well known that the dysfunction of DAergic system in the brain is one of the core factors in the pathophysiology of AD/HD. Therefore, we examined whether the effects of PNE on the DAergic system underlie the AD/HD-related behavioral changes in mouse offspring. PNE reduced the release of DA in the medial PFC (mPFC) in mouse offspring. PNE reduced the number of tyrosine hydroxylase (TH)-positive varicosities in the mPFC and in the core as well as the shell of nucleus accumbens, but not in the striatum. PNE also induced behavioral deficits in cliff avoidance, object-based attention, and sensorimotor gating in offspring. These behavioral deficits were attenuated by acute treatment with atomoxetine (3 mg/kg, s.c.) or partially attenuated by acute treatment with MPH (1 mg/kg, s.c.). Taken together, our findings support the notion that PNE induces neurobehavioral abnormalities in mouse offspring by disrupting the DAergic system and improve our understanding about the incidence of AD/HD in children whose mothers were exposed to nicotine during their pregnancy.</P>
Inhibitory receptor paired Ig-like receptor B is exploited by Staphylococcus aureus for virulence.
Nakayama, Masafumi,Kurokawa, Kenji,Nakamura, Kyohei,Lee, Bok Luel,Sekimizu, Kazuhisa,Kubagawa, Hiromi,Hiramatsu, Keiichi,Yagita, Hideo,Okumura, Ko,Takai, Toshiyuki,Underhill, David M,Aderem, Alan,Ogas American Association of Immunologists 2012 Journal of Immunology Vol. No.
<P>The innate immune system has developed to acquire a wide variety of pattern-recognition receptors (PRRs) to identify potential pathogens, whereas pathogens have also developed to escape host innate immune responses. ITIM-bearing receptors are attractive targets for pathogens to attenuate immune responses against them; however, the in vivo role of the inhibitory PRRs in host-bacteria interactions remains unknown. We demonstrate in this article that Staphylococcus aureus, a major Gram-positive bacteria, exploits inhibitory PRR paired Ig-like receptor (PIR)-B on macrophages to suppress ERK1/2 and inflammasome activation, and subsequent IL-6 and IL-1β secretion. Consequently, Pirb(-/-) mice infected with S. aureus showed enhanced inflammation and more effective bacterial clearance, resulting in resistance to the sepsis. Screening of S. aureus mutants identified lipoteichoic acid (LTA) as an essential bacterial cell wall component required for binding to PIR-B and modulating inflammatory responses. In vivo, however, an LTA-deficient S. aureus mutant was highly virulent and poorly recognized by macrophages in both wild-type and Pirb(-/-) mice, demonstrating that LTA recognition by PRRs other than PIR-B mediates effective bacterial elimination. These results provide direct evidence that bacteria exploit the inhibitory receptor for virulence, and host immune system counterbalances the infection.</P>