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Phase Transition in C4H12NI·I2
H. Ishigami,M. Shiro,M. Sumita,S. Sato,T. Hori,Y. Tsunashima 한국물리학회 2003 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.42 No.IV
The title compound C4H12NII2 was prepared addition of iodine to a tetramethylammonium iodide. The crystal showed anomalies at 218 K, 238 K and 308 K on dierential scanning calorimetry (DSC) measurement, whereas the crystal of tetramethylammonium iodide showed no anomaly. Crystal was grown by slow evaporation from an ethanol solution at 298 K. The crystal structure of orthorhombic C4H12NII2 of room temperature determined by use of a Imaging Plate diractometer is space group Pnnm, a = 14.115(1) A, b = 10.0997(7) A, c = 8.3019(5) A, V = 1183.5(3) A3, Z = 4. The present work reports the details of the crystal structure and phase transition of C4H12NII2.
Search for the H Dibaryon in (K-, K+) Reactions
Bahk,S. Y.,Chung,K. S,Chung,S. H.,Funahashi,H.,Hahn,C. H.,Hara,T.,Hirata,S.,Hoshino,K.,Ieiri,M.,Iijima,T.,Imai,K.,Ishigami,T.,Itow,Y.,Kazuno,M.,Kikuchi,K.,Kim,C. O.,Kim,D. C.,Kim,J. Y.,Kobayashi,M.,Ko 國立昌原大學校 基礎科學硏究所 1992 基礎科學硏究所論文集 Vol.3 No.-
We have studied(??) reactions from an emulsion target. The S--2H dibaryon has been searched for by the analysis of the ??? momentum spectrum together with emulsion data. No evidence of H production was observed in the mass range of 1.90-2.16 GeV/c². Upper limits for the production cross section of the H are (0.2-0.6)% of that for the quasifree ??? production at the 90% confidence level.
Jang, B.,Jeon, Y. C.,Shin, H. Y.,Lee, Y. J.,Kim, H.,Kondo, Y.,Ishigami, A.,Kim, Y. S.,Choi, E. K. HUMANA PRESS INC 2018 Molecular Neurobiology Vol.55 No.4
<P>Myelin basic protein (MBP) citrullination by peptidylarginine deiminase (PAD) enzymes leads to incomplete protein-lipid bilayer interactions and vulnerability to proteolytic enzymes, resulting in disorganization of the myelin sheath in the central nervous system. Therefore, citrullinated MBP (citMBP) has been suggested as a hallmark of demyelination, but how citMBP is implicated in prion diseases remains unknown. For the first time, we developed mouse monoclonal anti-citMBP IgG1 (clones 1B8, 1H1, and 3C6) and IgM (clone 3G5) antibodies that recognize human citMBP at its R25, R122, and R130 residues and at its C-terminal region (or the corresponding sites in mouse MBP), respectively. Using a biochemical, immunohistochemical, and immunogold-silver staining for electron microscopy techniques, we found that MBP residue R23 (corresponding to human R25) was specifically citrullinated, was stained as intense punctae in the corpus callosum, the striatum, and the cerebellar white matter, and was predominantly localized in disorganized myelin in the brains of scrapie-infected mice. In the brains of Creutzfeldt-Jakob disease (CJD) patients, MBP residues R25, R122, and R130 were markedly citrullinated and were stained as fibrils and punctae. In particular, white matter regions, such as the midbrain and the medulla, exhibited high levels of citMBP compared to other regions. However, the high levels of citMBP were not correlated with PAD2 expression. The clone 3G5 recognized significantly increased expression of the 18.5 kDa and/or 21.5 kDa variants of MBP in prion disease. Our findings suggest that significantly increased levels of citMBP may reflect demyelinating neuropathology, and that these newly developed antibodies may be useful for identifying demyelination.</P>
Evidence of Weak Decay of Heavy Double Hypernuclei
Aoki, S.,Bahk, S. Y.,Chung, K. S.,Chung, S. H.,Funahashi, H.,Hahn, C. H.,Hara, T.,Hirata, S.,Hoshino, K.,Ieiri, M.,Iijima, T.,Imai, K.,Ishigami, T.,Itow, Y.,Kazuno, M.,Kikuchi, K.,Kim, C. O.,Kim, D. C 國立昌原大學校 基礎科學硏究所 1992 基礎科學硏究所論文集 Vol.3 No.-
We have studied 80 events of candidates for ??? capture star at rest in nuclear emulsion, where ??? hyperons are produced in (??????) reactions identified by a ?? spectrometer. The weak decay of heavy double hypernuclei is confirmed, studying the distribution of visible energy-release and the probability of emission of two fast protons, in comparison with those for single hypernuclei.
Direct Observation of Sequential Weak Decay of a Double Hypernucleus
AOKI, S.,BAHK, S. Y.,CHUNG, K. S.,CHUNG, S. H.,FUNAHASHI, H.,HAHN, C. H.,HARA, T.,HIRATA, S.,HOSHINO, K.,IEIRI, M.,IIJIMA, T.,IMAI, K.,ISHIGAMI, T.,ITOW, Y.,KAZUNO, M.,KIKUCHI, K.,KIM, C. O.,KIM, D. C 國立昌原大學校 基礎科學硏究所 1992 基礎科學硏究所論文集 Vol.3 No.-
We have studied stars in nuclear emulsion due to the capture at rest of the ??? hyperons produced in the(???) reaction. The sequential weak decay of a double hypernucleus(nucleus with S= -2) has been directly observed. The double hypernucleus is assigned as either ???? or ????. This assignment excludes the existence of the H dibaryon lighter than 2203.7±0.7 MeV/c².
Jung, K. J.,Lee, E. K.,Kim, S. J.,Song, C. W.,Maruyama, N.,Ishigami, A.,Kim, N. D.,Im, D. S.,Yu, B. P.,Chung, H. Y. Springer Science + Business Media 2015 Journal of molecular medicine Vol.93 No.3
<P>Recent studies on senescence marker protein-30 (SMP30) have shown that it has an important functional role in the aging process, but its precise participation in cellular works has not been fully determined. We hypothesize that SMP30 plays crucial roles in signaling processes by modulating the balance of protein tyrosine kinase (PTK)/protein tyrosine phosphatase (PTP) and in activating proinflammatory NF-kappa B. An experimental paradigm of gain and loss of SMP30 function was established using SMP30-overexpressed YPEN-1 cells (herein referred to as 'SMP30(+) cells') and SMP30 (Y/-) knockout mouse kidneys. The resulting data show that SMP30 expression suppressed oxidative stress-induced PTK/PTP dysregulation and PP1/2A inactivation in SMP30(+) cells, leading to the suppression of NF-kappa B activation. In the kidneys of SMP30 (Y/-) mice, SMP30 deficiency was found to induce NF-kappa B activation via the upstream signaling of NIK/IKK and MAPKs and to upregulate downstream NF-kappa B-responsive gene expression. In this study, we also demonstrate for the first time that SMP30 deficiency induced PTK activity in SMP30 (Y/-) kidneys, thereby significantly increasing the tyrosine phosphorylation of a catalytic subunit of PP2A (PP2Ac-Tyr307). Based on these findings, we propose that SMP30 involves NF-kappa B regulation through the PTK/PTP balance and that the age-related decrease of SMP30 causes NF-kappa B activation, which contributes to an exacerbation of the inflammatory process during aging. Key message SMP30-deficient mice induced a shorter lifespan and redox changes. Overexpression of SMP30 prevented oxidative stress insults. The depletion of SMP30 increased redox-related PTK/PTP imbalance and PP1/PP2A inactivation. The depletion of SMP30 caused an elevation of NF-kappa B-responsive inflammatory markers. SMP30 may be a potent inhibitory protein against oxidative stress and chronic inflammation.</P>
Protective effects of KI against on the acute hepatic Liver injury of SMP30 knock-out mice
( Moon Jung Goo ),( Hye Rim Lee ),( Mi Ran Ki ),( Hae Young Chung ),( Akihito Ishigami ),( Kyu Shik Jeong ),( Jin Kyu Park ),( Da Hee Jeong ),( Ho Yong Park ),( Kwang Hee Son ),( Dong Ha Sin ),( Sun H 한국수의병리학회 2006 학술대회 Vol.10 No.-