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- 저자 : Masato Uchino (검색결과 4 건)
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Development of International Standardization Using Debris Environment Models for Spacecraft Design
Masato Uchino,Yasuhiro Akahoshi,Yukihito Kitazawa,Tekeo Goka,Hiroto Nagai 한국항공우주학회 2008 한국항공우주학회 학술발표회 논문집 Vol.- No.-
Accurate estimations of impact flux of debris, relative impact velocity, and impact angle of space debris on an orbit are necessary for reliable design of spacecrafts. Space agencies of some countries have their space debris environment models which can estimate debris flux as a function of the size, relative impact velocity, and impact angle in a spacecraft orbit. However. it is known that the calculation results of models have not been always consistent with each other. In the present. since an estimation result of debris impact depends on the choice of debris environment model, no unified estimation exists in design of spacecrafts. Therefore, international standardization of estimation using the debris environment model is required and the proposal of the international standard is being prepared in Japan. In this paper, as the first step of the international standardization of estimation of debris environment model, we compare the estimation results of debris impact flux in the low earth orbit calculated by three available debris environment models: ORDEM2000 of NASA, MASTER2001 of NASA, and MASTER2005 that is the an upgrade version of MASTER2001. In addition, we suggest a reasonable method using the three debris environment models for the international standardization of spacecraft design.
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( Iwao Saiki ),( Miki Yara ),( Tsuyoshi Yamanaka ),( Hiroyuki Uchino ),( Masato Inazu ) 한국응용약물학회 2020 Biomolecules & Therapeutics(구 응용약물학회지) Vol.28 No.2
Prostate cancer is one of the most common cancers in men. Choline PET or PET/CT has been used to visualize prostate cancer, and high levels of choline accumulation have been observed in tumors. However, the uptake system for choline and the functional expression of choline transporters in prostate cancer are not completely understood. In this study, the molecular and functional aspects of choline uptake were investigated in the LNCaP prostate cancer cell line along with the correlations between choline uptake and cell viability in drug-treated cells. Choline transporter-like protein 1 (CTL1) and CTL2 mRNA were highly expressed in LNCaP cells. CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. [<sup>3</sup>H]Choline uptake was mediated by a single Na+-independent, intermediate-affinity transport system in the LNCaP cells. The anticancer drugs, flutamide and bicalutamide, inhibited cell viability and [3H]choline uptake in a concentration-dependent manner. The correlations between the effects of these drugs on cell viability and [3H]choline uptake were significant. Caspase-3/7 activity was significantly increased by both flutamide and bicalutamide. Furthermore, these drugs decreased CTL1 expression in the prostate cancer cell line. These results suggest that CTL1 is functionally expressed in prostate cancer cells and are also involved in abnormal proliferation. Identification of this CTL1-mediated choline transport system in prostate cancer cells provides a potential new therapeutic target for the treatment of this disease.
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Nagashima, Fumiaki,Nishiyama, Ryohta,Iwao, Beniko,Kawai, Yuiko,Ishii, Chikanao,Yamanaka, Tsuyoshi,Uchino, Hiroyuki,Inazu, Masato The Korean Society of Applied Pharmacology 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.4
In this study, we examined the molecular and functional characterization of choline uptake in the human esophageal cancer cells. In addition, we examined the influence of various drugs on the transport of [$^3H$]choline, and explored the possible correlation between the inhibition of choline uptake and apoptotic cell death. We found that both choline transporter-like protein 1 (CTL1) and CTL2 mRNAs and proteins were highly expressed in esophageal cancer cell lines (KYSE series). CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. Choline uptake was saturable and mediated by a single transport system, which is both $Na^+$-independent and pH-dependent. Choline uptake and cell viability were inhibited by various cationic drugs. Furthermore, a correlation analysis of the potencies of 47 drugs for the inhibition of choline uptake and cell viability showed a strong correlation. Choline uptake inhibitors and choline deficiency each inhibited cell viability and increased caspase-3/7 activity. We conclude that extracellular choline is mainly transported via a CTL1. The functional inhibition of CTL1 by cationic drugs could promote apoptotic cell death. Furthermore, CTL2 may be involved in choline uptake in mitochondria, which is the rate-limiting step in S-adenosylmethionine (SAM) synthesis and DNA methylation. Identification of this CTL1- and CTL2-mediated choline transport system provides a potential new target for esophageal cancer therapy.
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Fumiaki Nagashima,Ryohta Nishiyama,Beniko Iwao,Yuiko Kawai,Chikanao Ishii,Tsuyoshi Yamanaka,Hiroyuki Uchino,Masato Inazu 한국응용약물학회 2018 Biomolecules & Therapeutics(구 응용약물학회지) Vol.26 No.4
In this study, we examined the molecular and functional characterization of choline uptake in the human esophageal cancer cells. In addition, we examined the influence of various drugs on the transport of [3H]choline, and explored the possible correlation between the inhibition of choline uptake and apoptotic cell death. We found that both choline transporter-like protein 1 (CTL1) and CTL2 mRNAs and proteins were highly expressed in esophageal cancer cell lines (KYSE series). CTL1 and CTL2 were located in the plasma membrane and mitochondria, respectively. Choline uptake was saturable and mediated by a single transport system, which is both Na+-independent and pH-dependent. Choline uptake and cell viability were inhibited by various cationic drugs. Furthermore, a correlation analysis of the potencies of 47 drugs for the inhibition of choline uptake and cell viability showed a strong correlation. Choline uptake inhibitors and choline deficiency each inhibited cell viability and increased caspase-3/7 activity. We conclude that extracellular choline is mainly transported via a CTL1. The functional inhibition of CTL1 by cationic drugs could promote apoptotic cell death. Furthermore, CTL2 may be involved in choline uptake in mitochondria, which is the rate-limiting step in S-adenosylmethionine (SAM) synthesis and DNA methylation. Identification of this CTL1- and CTL2-mediated choline transport system provides a potential new target for esophageal cancer therapy.
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