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5. Proof-of-principle Experiment of 4He Excimer Cluster Generation via Neutron-3He Absorption Reaction for Visualization of Velocity Fields in Superfluid 4He

Author

Matsushita, T., primary, Sonnenschein, V., additional, Iguchi, T., additional, Ito, D., additional, Kitaguchi, M., additional, Kiyanagi, Y., additional, Guo, W., additional, Saito, Y., additional, Shinohara, T., additional, Shimizu, H.M., additional, Suzuki, S., additional, Tsuji, Y., additional, Tomita, H., additional, Hayashida, H., additional, Hishida, M., additional, Hiroi, K., additional, Hirota, K., additional, Maruyama, T., additional, Waki, S., additional, and Wada, N., additional

Published
2020
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6. Manipulator system for constructing overhead distribution lines

Author

Ohnishi, H., Tsuchihashi, H., Waki, S., Mochizuki, K., Yamamoto, T., Watanabe, H., and Furukawa, H.

Subjects
Power lines -- Installation, Manipulators -- Design and construction, Electric power systems -- Maintenance and repair, Business, Computers, Electronics, Electronics and electrical industries
Abstract

This paper describes the manipulator for live-line construction of high-voltage overhead power transmission lines (line voltage 6.6 kV) that is being jointly developed by Tokyo Electric Power and other companies. It describes this system's development concept, makeup, functions, and design, as well as operability tests using actual-scale transmission line poles. In this research, development began in 1984. As the first step, a prototype model of a ground-mounted twin-arm manipulator was trial-manufactured in 1985. As the second step, in 1988 a truck-mounted system was developed in which the twin-arm manipulator was mounted on a 'cherrypicker' vehicle. As the third step, a practical system was developed based on these results. In the development of this system, the task of development of the individual items of equipment was shared as follows. Project leader, Conceptual design, Utility evaluation: The Tokyo Electric Power (Company, Inc.) Development of manipulator system: The Furukawa Electric (Co., Ltd.), Fuji Electric (Co., Ltd.) System mounting vehicles: Aichi Sharyo (Co., Ltd.) Operability testing, development of construction methods: Kandenko (Co., Ltd.)

Published
1993

8. Development of appropriate fatty acid formulations to raise the contractility of constructed myocardial tissues

Author

Azumi Yoshida, Waki Sekine, Jun Homma, Hidekazu Sekine, Yu Yamasaki Itoyama, Daisuke Sasaki, Katsuhisa Matsuura, Eiji Kobayashi, and Tatsuya Shimizu

Subjects
Energy production, Fatty acid, β-oxidation, Culture medium, Cardiomyocyte, Medicine (General), R5-920, Cytology, QH573-671
Abstract

Introduction: Heart disease is a major cause of mortality worldwide, and the annual number of deaths due to heart disease has increased in recent years. Although heart failure is usually managed with medicines, the ultimate treatment for end-stage disease is heart transplantation or an artificial heart. However, the use of these surgical strategies is limited by issues such as thrombosis, rejection and donor shortages. Regenerative therapies, such as the transplantation of cultured cells and tissues constructed using tissue engineering techniques, are receiving great attention as possible alternative treatments for heart failure. Research is ongoing into the potential clinical use of cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs). However, the energy-producing capacity of cardiomyocytes maintained under previous culture conditions is lower than that of adult primary cardiomyocytes due to immaturity and a reliance on glucose metabolism. Therefore, the aims of this study were to compare the types of fatty acids metabolized between cardiomyocytes in culture and heart cells in vivo and investigate whether the addition of fatty acids to the culture medium affected energy production by cardiomyocytes. Methods: A fatty acid-containing medium was developed based on an analysis of fatty acid consumption by rat primary cardiomyocytes (rat-CMs), and the effects of this medium on adenosine triphosphate (ATP) production were investigated through bioluminescence imaging of luciferase-expressing rat-CMs. Next, the fatty acid content of the medium was further adjusted based on analyses of fatty acid utilization by porcine hearts and hiPSC-CMs. Oxygen consumption analyses were performed to explore whether the fatty acid-containing medium induced hiPSC-CMs to switch from anaerobic metabolism to aerobic metabolism. Furthermore, the effects of the medium on contractile force generated by hiPSC-CM-derived tissue were evaluated. Results: Rat serum, human serum and porcine plasma contained similar types of fatty acid (oleic acid, stearic acid, linoleic acid, palmitic acid and arachidonic acid). The types of fatty acid consumed were also similar between rat-CMs, hiPSC-CMs and porcine heart. The addition of fatty acids to the culture medium increased the bioluminescence of luciferase-expressing rat-CMs (an indirect measure of ATP level), oxygen consumption by hiPSC-CMs, and contractile force generated by cardiac tissues constructed from hiPSC-CMs. Conclusions: hiPSC-CMs metabolize similar types of fatty acid to those consumed by rat-CMs and porcine hearts. Furthermore, the addition of these fatty acids to the culture medium increased energy production by rat-CMs and hiPSC-CMs and enhanced the contractility of myocardial tissue generated from hiPSC-CMs. These findings suggest that the addition of fatty acids to the culture medium stimulates aerobic energy production by cardiomyocytes through β-oxidation. Since cardiomyocytes cultured in standard media rely primarily on anaerobic glucose metabolism and remain in an immature state, further research is merited to establish whether the addition of fatty acids to the culture medium would improve the energy-producing capacity and maturity of hiPSC-CMs and cardiac tissue constructed from these cells. It is possible that optimizing the metabolism of cultured cardiomyocytes, which require high energy production to sustain their contractile function, will improve the properties of hiPSC-CM-derived tissue, allowing it to be better utilized for disease modeling, drug screening and regenerative therapies for heart failure.

Published
2022
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11. General lectures (II)

Author

Segawa, K., Nakazawa, S., Koide, N., Imai, K., Matsuo, N., Yamamoto, Y., Shiobara, M., Shimada, H., Kawai, K., Machida, K., Okabe, N., Hoshi, Y., Koizumi, Y., Watanuki, T., Hiroshima, Y., Matsusaka, Y., Katase, K., Sakuma, Y., Matoba, N., Murata, N., Toyama, Y., Murai, S., Nukaga, A., Ishimatsu, N., Watanabe, Y., Abe, M., Ono, Y., Hirai, K., Iwabuchi, S., Suzuki, K., Aoki, T., Masamura, K., Yoshida, K., Ikeuchi, J., Nagao, F., Kobayashi, A., Toriie, S., Nakajima, M., Kohli, M., Ida, K., Kawai, K., Masuda, M., Hattori, T., Fujita, S., Tamada, T., Inoue, K., Usui, T., Yamaya, S., Ohtsuka, K., Shiraki, Y., Fujishima, S., Tochikubo, O., Miyamoto, S., Ueda, A., Asano, K., Kunisada, M., Miyake, H., Fujii, Y., Yoshimoto, S., Hiramatsu, K., Nakano, S., Takeda, T., Kitamura, K., Horiguchi, Y., Okada, K., Okada, M., Kuwabara, T., Tanaka, M., Konno, K., Hattori, T., Isobe, K., Iwasaki, A., Unoura, T., Matsumoto, M., Yoshida, T., Takahashi, I., Abe, M., Maeda, H., Hayashi, T., Koizumi, H., Iwasaki, M., Takahashi, K., Honda, T., Ariga, K., Mohri, S., Suga, Y., Ono, T., Kobayashi, K., Mizuno, T., Sameshima, Y., Shiozaki, Y., Sasakawa, M., Hiramatsu, A., Ikehara, K., Nagata, T., Tatsumi, K., Abe, M., Aoki, M., Iwasaki, S., Aizawa, T., Kajiwara, K., Sata, K., Omata, S., Imamura, K., Kondo, K., Sajima, H., Sato, Y., Kiryu, H., Mimoto, S., Masuoka, T., Kira, K., Mizumoto, R., Kuratsuka, H., Honjo, I., Hojo, Y., Nakajima, H., Tosaka, T., Arai, O., Kobayashi, N., Obata, N., Ito, S., Takaoka, T., Uragami, Y., Kitamura, Y., Kishi, S., Fujii, S., Okuda, H., Hirano, K., Kano, H., Ogino, M., Ueda, Y., Nishiwaki, K., Iwamura, N., Aoki, T., Hiramatsu, K., Kamada, T., Suematsu, T., Fusamoto, H., Okuda, H., Abe, H., Katayama, S., Yamaguchi, K., Fukuda, M., Ishii, T., Kaito, I., Sato, S., Sasaki, H., Onodera, H., Yamanaka, M., Akagi, K., Miyazaki, S., Okumura, M., Omae, T., Nakamura, Y., Wada, M., Nakai, Y., Inoue, S., Arima, T., Yamasaki, S., Takano, T., Katsuta, Y., Yano, T., Isoda, K., Aramaki, T., Fukuda, N., Ichikawa, T., Okumura, H., Adachi, Y., Inoue, R., Iwasaki, Y., Tanaka, S., Yamamoto, T., Wakisaka, G., Nakaya, H., Takase, S., Ikegami, F., Takada, A., Kobayashi, K., Takeuchi, J., Kato, Y., Funayama, A., Kakumu, S., Ito, S., Okuyama, S., Taoka, Y., Endo, T., Chizuka, R., Yanagida, T., Chizuka, S., Usui, H., Ando, T., Takai, T., Wakahara, T., Kojima, M., Fukazawa, T., Takahashi, Y., Miyamura, S., Urakawa, T., Shima, T., Miyaji, K., Okazaki, T., Kashimura, S., Koyama, K., Yamauchi, H., Matsuo, Y., Takagi, Y., Muto, I., Owada, Y., Otowa, T., Sato, T., Naito, C., Okada, K., Sugawara, K., Nokiba, T., Fujii, Y., Kido, H., Sasaki, M., Sugai, Y., Nishimura, G., Nanbu, H., Kamiyama, Y., Yamada, T., Yamaoka, Y., Takeda, H., Ohsawa, T., Kamano, T., Mizukami, T., Kitamura, O., Ozawa, K., Takasan, H., Honjo, I., Miyasaki, R., Katayama, T., Amakawa, T., Hirose, K., Furukawa, Y., Noguchi, M., Okamoto, M., Maezawa, H., Tanaka, N., Yamada, S., Hisata, T., Hata, C., Sawa, J., Kato, Y., Mituda, Y., Oohira, S., Hayasaka, A., Okuyama, T., Fukui, S., Takeda, T., Furuichi, T., Yamamitsu, S., Yamauchi, K., Konishi, Y., Maeda, S., Setoyama, S., Otsuji, S., Ibata, T., Niu, H., Ogawa, A., Tujioka, E., Maeda, T., Takewa, M., Matumoto, T., Tamada, K., Maeda, A., Sumita, H., Iseki, Y., Yukawa, S., Nitta, Y., Isida, K., Nomoto, H., Setoyama, S., Maeda, S., Otsuji, S., Sato, R., Sato, G., Toyokawa, S., Yamamoto, G., Ohtomi, S., Haga, M., Ueno, Y., Fukuda, M., Endo, R., Yokota, T., Ohsawa, J., Kohno, A., Ohtoshi, E., Yasugi, H., Ichikawa, H., Mizumoto, R., Honjo, I., Ando, K., Suzuki, H., Nishiwaki, T., Kishimoto, T., Miki, T., Takeshige, K., Sawada, M., Hidemura, R., Yamamoto, S., Itoh, S., Kashiwagi, T., Kishida, M., Imamura, O., Suematus, T., Kamada, T., Sakoda, K., Kawada, T., Arima, Y., Kamimura, T., Takesue, M., Katsuki, T., Akita, H., Yakeishi, Y., Takehisa, I., Miyasato, K., Yoshida, H., Hidemura, R., Kubota, K., Aoki, S., Suzuki, S., Kishimoto, T., Miyahara, T., Ando, K., Nishiwaki, T., Miki, T., Takeshige, K., Sawada, M., Itoh, S., Yamamoto, S., Fujiwara, K., Sakai, T., Oda, T., Igarashi, S., Fukuhara, M., Tsujii, T., Tamura, T., Matsuoka, Y., Takahashi, H., Sakamoto, T., Fukuda, S., Oku, M., Matsui, T., Morita, T., Oyazato, Y., Kimura, K., Moriya, W., Fukui, S., Suzuki, K., Morimoto, S., Tsuiki, S., Shoji, K., Nakai, Y., Hata, M., Kubo, J., Yoshizawa, K., Nagayama, K., Ozawa, Y., Yoshida, M., Horiguchi, M., Machii, A., Nitta, Y., Aiso, Y., Kitahara, N., Kitazawa, E., Fukuda, K., Saiti, N., Murakami, Y., Nao, Y., Okazaki, I., Funatsu, K., Maruyama, K., Takagi, B., Yasuraoka, S., Ishii, K., Matsuzaki, S., Takahashi, H., Ishii, H., Kamegaya, K., Sambe, K., Ishikawa, H., Tajima, Y., Kuroda, A., Ishihara, Y., Sato, N., Ishikawa, I., Noro, T., Kakumoto, Y., Mekjian, H. S., Thomford, N. R., Yokomura, T., Adachi, S., Yamamoto, A., Saito, I., Kawamura, A., Miyata, M., Kasai, S., Kawanishi, N., Tamaki, A., Mito, M., Kasai, Y., Hasumi, A., Uchiyama, T., Tachikawa, Y., Takanashi, T., Kanke, T., Matsuda, K., Takanashi, T., Kanke, T., Matsuda, K., Hamana, G., Sakuma, M., Sugita, T., Tomita, K., Yamasaki, S., Tsuzuki, T., Uekusa, M., Matsuzaki, M., Takagi, B., Tsuchiya, M., Uchimura, M., Murohisa, T., Muto, Y., Ishigaki, J., Waki, S., Tsuchiya, R., Sho, M., Furukawa, M., Suzuki, N., Nagashima, H., Matsushiro, T., Saitoh, T., Nakamura, N., Hatanaka, T., Kobayashi, N., Nakamura, Y., Sato, T., Tooi, K., Tanaka, Y., Kadokura, N., Okada, Y., Yanakgi, I., Tanaka, N., Sekiya, V. M., Adachi, K., Miyashita, M., Moriyama, Y., Onda, M., Yoshioka, M., Teraoka, T., Shimizu, Y., Fujishima, G., Ookawa, K., Miki, M., Shirota, A., Aihara, K., Shiga, T., Sano, H., Hayashi, S., Hori, M., Sato, H., Chuman, Y., Tsukase, S., Nakahara, N., Ehira, S., Setoyama, S., Nishimata, H., Irisa, T., Tokutome, K., Nakashima, Y., Koga, H., Yokoyama, H., Otsuji, T., Chujo, Y., Yamamoto, T., Gotoda, S., Uchiyama, S., Kosaki, G., Ohkura, H., Mukojima, T., Hattori, N., Sasaki, O., Soejima, K., Inokuchi, K., Utsunomiya, J., Maki, T., Iwama, T., Matsunaga, Y., Shimomura, T., Nakajima, T., Ichikawa, S., Miyanaga, T., Sengoku, K., Hamaguchi, E., Aoki, N., Nomura, T., Matsuoka, A., Suzuki, N., Nagahama, A., Kazumi, T., Miyawaki, H., Sakamoto, T., Miyasaki, K., Kato, K., Miyazaki, Y., Harada, N., Yamada, K., Tashiro, S., Sakai, K., Ho, N., Murayama, H., Yada, M., Sakabe, T., Shimizu, H., Kuroki, M., Nishida, S., Kato, K., Ishiyama, S., Yukawa, K., Hayashi, M., Soh, K., Doi, K., Fukuda, M., Nakagawa, A., Yukawa, E., Uematsu, Y., Nara, K., Hattori, H., Watanabe, M., Yoshida, H., Sato, K., Okuse, S., Sato, K., Murotani, T., Takasu, S., Konta, M., Uchiya, T., Fujimaki, N., Yoshida, K., Yoshikawa, K., Uchida, M., Nakamura, N., Nagao, F., Kawana, S., Tamura, K., Hashimoto, T., Kobayashi, K., Hara, T., Nosaka, J., Fukui, O., Inaba, E., Otsukasa, S., Sanada, K., Hiraide, H., Senyo, G., Ootani, A., Nakayama, T., Takei, S., Miki, H., Tanaka, M., Minota, S., Nakayama, K., Nakagawa, K., Shiraishi, T., Kawauchi, H., Nagaya, H., Mizushima, K., Tachimi, Y., Namiki, M., Masuda, K., Mitsutani, N., Mukuta, T., Koizumi, T., Takeuchi, T., Nemoto, T., Takabayashi, H., Takagi, M., Hongo, Y., Kojima, H., Nishimura, M., Hino, S., Hirayama, J., Nakamura, M., Irisa, T., Koga, S., Hirayama, C., Kikuch, S., Ito, M., Hidano, S., Ooya, T., Banno, H., Tomura, A., Kato, K., Koyama, T., Takei, T., Tomimura, T., Yamauchi, M., Kobayashi, K., Nakaya, Y., Takase, S., Kato, Y., Takeuchi, J., Ikegami, F., Matsuda, Y., Takada, A., Udo, K., Kojima, M., Hukuda, N., Kametani, M., Miyagawa, T., Wakahara, T., Takahashi, Y., Imaeda, T., Senda, K., Fujita, S., Okubo, H., Kanoda, K., Miyashita, B., Ishizuka, H., Goto, T., Oto, K., Kaneda, H., Hase, M., Matsuda, J., Kawai, T., Ikehara, H., Baba, S., Ishii, M., Tozawa, T., Inoue, E., Mizuno, N., Saeki, S., Nakaji, T., Narabayashi, T., Okuno, T., Yamada, H., Tanno, M., Chiba, K., Iio, M., Shibata, K., Furuhashi, F., Mizuochi, K., Ohashi, S., Kato, K., Nakano, M., Otsuka, S., Irie, M., Akima, M., Maruyama, Y., Oyamada, F., Nagata, E., Kubo, Y., Arishima, T., Otsuyama, Y., Kaneto, A., Shimogawa, Y., Tanigawa, K., Okabe, N., Nakajima, K., Onishi, S., Kasahara, A., Shimizu, T., Ikehara, Y., Tajima, H., Okamoto, A., Komibuchi, T., Negoro, T., Nihonsugi, A., Ishii, M., Tozawa, T., Ogawa, Y., Otani, H., Ishida, M., Yashima, H., Shoji, K., Tsuiki, S., Morimoto, S., Nakai, Y., Ryo, M., Ozawa, Y., Tanaka, T., Horiguchi, M., Taketa, K., Watanabe, A., Yumoto, Y., Tanaka, A., Takesue, A., Aoe, H., Ueda, M., Shimamura, J., Kosaka, K., Kashiwara, E., Orita, K., Konaga, E., Suzuki, K., Tanaka, S., Kaneda, S., Ogawa, K., Tamura, H., Okanishi, S., Ueda, T., Horie, H., Kamachi, M., Asihara, T., Daido, R., Izumi, T., Kurihara, M., Sumida, M., Haraikawa, M., Hayakawa, H., Shirakabe, H., Yasui, A., Noguchi, M., Okamoto, M., Furukawa, Y., Miyasaki, R., Hirose, K., Katayama, T., and Maezawa, H.

Published
1974
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15. General Lectures-(II)

Author

Toriie, S., Nakajima, M., Kohli, Y., Takebayashi, M., Misaki, F., Kobayashi, A., Hashimoto, Y., Mitsuyoshi, Y., Ida, K., Kawai, K., Fujita, R., Kumura, F., Takahashi, M., Ohsawa, H., Hasegawa, Y., Kidokoro, T., Jojima, Y., Miyoshi, H., Okumura, Y., Yokouchi, A., Asano, H., Uehara, A., Oka, S., Saito, H., Yaginuma, M., Yamamoto, T., Asano, A., Nakamura, M., Okada, Y., Tomioka, T., Tamesue, N., Ikeda, S., Kunisaki, T., Emura, T., Yasumoto, M., Someya, N., Goto, A., Morokuma, K., Sakamoto, H., Kasaki, Y., Imamura, K., Amano, I., Iwanaga, K., Okugawa, N., Ninomiya, K., Yoshida, S., Okabe, N., Shimogawa, Y., Nakajima M., Ida, K., Akasaka, Y., Shimamoto, K., Misaki, F., Toriie, S., Tada, M., Sugawara, K., Chikayasu, I., Takeda, H., Kawai, K., Shibue, T., Yamaguchi, A., Osame, T., Shimada, K., Hori, M., Irisa, T., Miura, Y., Hanamure, B., Chuman, Y., Sato, H., Kizu, M., Kasugai, T., Kuno, N., Aoki, I., Nitta, Y., Machii, A., Murakami, Y., Aiso, Y., Kitahara, N., Yoshizawa, Y., Hishinuma, Y., Nao, Y., Ishiyama, K., Watanabe, M., Kimura, T., Hara, T., Sakaue, S., Shinoda, T., Ito, R., Hayashi, K., Sugie, H., Sekizawa, H., Nakamura, S., Kondo, J., Tanaka, E., Taniguchi, T., Kanayama, M., Koizumi, S., Watabiki, S., Ikeda, S., Tamura, K., Okada, Y., Arai, T., Saito, T., Tojo, S., Furuya, M., Hanaue, H., Ogoshi, K., Murohisa, B., Uchimura, M., Ishigaki, J., Waki, S., Nakafuji, H., Iida, F., Aratake, K., Nakano, T., Ono, N., Hara, I., Sassa, T., Takahashi, T., Inoue, J., Maruyama, Y., Mori, Y., Kawamura, T., Imai, F., Yorita, S., Saegusa, M., Ishihara, F., Asukata, I., Matsuda, M., Wakabayashi, K., Mitani, S., Sugahara, K., Ishikawa, K., Nakayoshi, A., Nakamoto, M., Kono, A., Oda, T., Sato, Y., Takahashi, T., Nagao, F., Nagano, M., Furusawa, T., Nakama, T., Itoh, H., Nishimura, M., Tsutsumi, K., Saito, H., Yoshida, K., Ito, H., Yoshimura, M., Yoshioka, K., Shimizu, T., Kuroda, C., Uchida, H., Ishida, O., Inoue, T., Hasegawa, S., Mitsusada, K., Kajiyama, Y., Matsuzawa, Y., Yokota, K., Hayashida, Y., Ikegudhi, S., Shida, S., Tsurumi, K., Ito, K., Kamiya, K., Takada, H., Ueno, S., Onda, M., Kojima, G., Shoji, E., Miyaji, M., Goto, K., Nitta, Y., Yazaki, Y., Ito, M., Kozuka, M., Tanabe, A., Murate, H., Takeuchi, T., Koshikawa, M., Kato, N., Maeda, K., Hayashi, K., Tsuru, T., Ooyama, I., Kukimoto, H., Nakashima, Y., Katsuki, T., Ueda, N., Kanno, T., Noda, A., Toda, Y., Hayakawa, T., Nakajima, S., Morishita, R., Furukawa, K., Ikeda, F., Fujii, M., Yamamoto, T., Wakisaka, G., Matasumoto, Y., Ono, H., Hirose, S., Kobayashi, K., Sawabu, N., Takeuchi, J., Kajikawa, K., Takada, A., Hirai, Y., Ohki, I., Sato, K., Tasaka, S., Sato, A., Aono, G., Kidokoro, T., Takezoe, K., Jojima, Y., Ohara, T., Soma, S., Ukawa, S., Yamaguchi, S., Shirahama, T., Sugiyama, K., Koyama, H., Haga, M., Arikawa, H., Toyokawa, H., Sato, R., Ueno, Y., Karasawa, Y., Onuma, H., Suzuki, H., Murakami, T., Yasui, A., Ichinose, Y., Hirase, Y., Okazaki, T., Takai, T., Watanabe, K., Kato, M., Yamada, M., Tsuji, T., Kunito, Y., Kobayashi, S., Udo, K., Iriyama, K., Sugiura, Y., Takahashi, Y., Kawamura, O., Ando, S., Hayashi, K., Tsuji, K., Yukawa, Y., Saito, N., Miyazawa, M., Imai, K., Tabayashi, T., Ito, H., Umehara, S., Watanabe, Y., Murai, S., Nukaga, A., Ishimatsu, N., Sotoyama, S., Abe, M., Hirai, K., Yoshida, K., Aoki, T., Nagao, F., Aoki, Y., Taniguchi, K., Wada, N., Tabuse, K., Yanagi, I., Tsuhada, K., Katsumi, M., Nakamura, K., Takemoto, K., Yamaura, Y., Karibe, N., Yamada, G., Ichikawa, H., Ogiwara, M., Matsushita, M., Kobayashi, I., Kusano, M., Yasuna, O., Hayashi, S., Yoshizumi, M., Kojima, Y., Matsubayashi, K., Yamamoto, T., Nishimura, R., Koga, M., Tachibana, M., Kurata, M., Suto, H., Ichinose, I., Ishizuka, K., Shimoda, M., Onai, M., Akiyama, T., Sekiguchi, T., Kobayashi, S., Matsuyoshi, M., Yonezawa, N., Kasamatsu, M., Yokota, Y., Toyoda, T., Uchimoto, I., Kanamoto, M., Fukai, Y., Sugawara, K., Katoh, M., Takebayashi, M., Mitsuyoshi, Y., Shimamoto, K., Nakamura, I., Tamura, M., Nishio, M., Mukaide, Y., Kuzumoto, Y., Ota, K., Yoshida, T., Sakamoto, A., Akiyama, T., Kaneko, S., Yanagida, M., Kishimoto, S., Miyaji, K., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Yasutake, K., Irie, K., Ijiri, Y., Sato, H., Nishijima, H., Ogino, K., Okuno, T., Date, H., Yao, T., Koga, Y., Tomioka, T., Fuyuno, S., Okabe, H., Mitsui, H., Tamechika, Y., Masuda, N., Fujiwara, T., Sakimura, M., Okada, Y., Takamura, Y., Kono, T., Kurihara, M., Sumida, M., Izumi, T., Haraikawa, M., Hayakawa, H., Shirakabe, H., Yasui, A., Ushio, K., Okamoto, M., Noguchi, M., Kinoshita, A., Yamada, T., Ichikawa, H., Shimotori, K., Kudo, T., Mukaida, I., Ishikawa, H., Sato, K., Shirane, T., Kano, A., Suzuki, T., Tanaka, M., Iwanaga, T., Taniguchi, H., Inawashiro, M., Endo, N., Kawamura, T., Suzuki, Sh., Suzuki, H., Maki, T., Hayakawa, K., Ikezawa, H., Jao, C. C., Yamada, K., Nakamura, M., Tanaka, M., Maruyama, M., Nagasako, K., Oi, I., Kozu, T., Yamashita, K., Yokoyama, I., Endo, M., Takemoto, T., Nakayama, K., Hayakawa, R., Ishiguro, M., Nakano, H., Nakazawa, S., Tsuboi, Y., Yamase, H., Yamashita, T., Fujita, T., Ishikawa, Y., Ito, N., Mitsuno, T., Kanazawa, K., Yamashiro, M., Kubo, T., Iizuka, H., Watanabe, T., Sanada, M., Satoh, H., Shimada, H., Kusama, S., Ishikawa, K., Ikeda, K., Naramoto, J., Koga, M., Okazaki, Y., Nakamura, K., Kawamura, S., Fujimoto, S., Urayama, S., Matsuura, H., Sekitani, T., Sasayama, T., Nakagawa, K., Toyama, K., Nakagawa, S., Takada, T., Kusaka, K., Takaba, S., Satomura, A., Suzuki, T., Kawakami, Y., Watanabe, Y., Suzuki, H., Koike, T., Joh, S., Hara, T., Tamura, K., Kobayagawa, K., Hashimoto, T., Uemura, F., Fukui, O., Takahashi, M., Takasato, Y., Shirakawa, K., Hisamatsu, M., Saito, T., Ashizawa, S., Sakurane, Y., Miyamura, K., Sasaki, H., Katsumi, M., Ura, S., Emoto, M., Tatsumi, Y., Totsuka, Y., Chiba, N., Ozeki, M., Nakazawa, M., Takamura, S., Iida, F., Sawano, Y., Sugita, T., Funabiki, T., Watanabe, S., Moriya, T., Tomita, N., Nishida, K., Todo, A., Miyake, T., Suzaki, Y., Yamamoto, Y., Ariyoshi, J., Hajiro, K., Oishi, M., Yanagihara, K., Nakamura, A., Kuramata, H., Soeda, S., Kondo, N., Akashi, M., Hemmi, T., Kadono, H., Ito, T., Tsuchiya, R., Ikeda, Y., Futatsuki, K., Nomoto, S., Kino, I., Arai, M., Shimazu, H., Kobori, O., Ishikawa, K., Hiroshima, Y., Matsusaka, Y., Katase, K., Sakuma, Y., Murata, N., Komura, K., Ando, H., Ohara, K., Hayashi, A., Suzuki, M., Watanuki, T., Asano, T., Koide, N., Shiobara, M., Matsuo, N., Imai, K., Segawa, K., Nakazawa, S., Okabe, N., Kawai, K., Matsumoto, K., Shimada, H., Machida, K., Koizumi, Y., Hoshi, Y., Oi, M., Watanuki, T., Seki, H., Matsumura, M., Kimura, M., Yoshimura, M., Ishikawa, I., Kishi, S., Kondo, Y., Uchida, Y., Harada, H., Mandai, M., Kikuchi, T., Mishima, K., Yamagata, Y., Suyama, T., Kawagoe, K., Inagawa, T., Kishimoto, S., Sugiya, T., Kai, T., Miyoshi, A., Fukumoto, S., Watanabe, K., Kojo, H., Turuhara, I., Miyoshi, Y., Okamoto, K., Inata, H., Okamoto, H., Sakurai, S., Sugiyama, M., Sasaki, H., Miura, K., Kurihara, T., Sakumoto, K., Okita, E., Tanaka, H., Ishihara, K., Okawa, M., Okumura, Y., Watanabe, Y., Nishizaki, N., Murakami, T., Saito, K., Aoyagi, K., Hamaguchi, E., Kitamura, T., Matsuo, Y., Seki, A., Mori, H., Ishikawa, T., Nakajima, T., Shimomura, T., Sengoku, K., Aoyagi, K., Hamaguchi, E., Uchiya, Y., Yabana, T., Konta, M., Kamijo, K., Yachi, A., Okuse, S., Ohara, H., Sato, K., Wada, T., Kurata, M., Furuta, K., Nishii, M., Yamawaki, T., Nishii, K., Umeda, K., Yoshida, H., Ito, H., Okabayashi, T., Kato, Y., Yatsuji, Y., Suzuki, Y., Nomura, K., Matsumoto, K., Kamisaka, K., Motoki, T., Kamii, K., Kameda, H., Imamura, H., Uchiya, T., Ishizawa, M., Nishizaki, H., Murakami, T., Orimo, H., Yoshida, A., Yoshida, A., Orimo, H., Fujita, T., Oda, T., Itoh, Z., Honda, R., Takeuchi, S., Fukushima, T., Suda, T., Shinonaga, M., Ishiguro, N., Fujisawa, S., Nishiyama, K., and Ohkubo, T.

Published
1973
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35. The role of T cells in pathogenesis and protective immunity to murine malaria.

Author

Waki, S., Uehara, S., Kanbe, K., Ono, K., Suzuki, M., and Nariuchi, H.

Subjects
*T cells, *ANTIGEN presenting cells, *IMMUNITY, *ANTIGENS, *TUMOR necrosis factors, *CYTOKINES
Abstract

T-cell-mediated immunity to a virulent strain of Plasmodium berghei NK65 (Pb NK65) and to an attenuated derivative (Pb XAT) of the strain were examined in CBA mice by the administration of monoclonal antibodies against T-cell subsets or interferon-gamma (IFN-γ). The injection of anti- CD8+ or anti-IFN-γ delayed the mortality of mice infected with Pb NK65, although it did not affect the parasitaemia. In the late stage of PB NK65 infection, T cells, especially CD8+ T cells, were increased in number in the liver at the expense of splenic CD8+ T cells. These CD8+ T cells released IFN-γ in culture without antigen stimulation and were thought to induce tumour necrosis factor- alpha (TN F-α) production by the cells in the liver. In mice infected with Pb XAT, or mice primed with Pb XAT and then challenged with Pb NK65, CD4+ T cells had a crucial role in preventing parasite growth and in protective immunity. IFN-γ was again the key molecule in protective immunity. These results suggest that T cells stimulated with malaria antigen play important roles both in protective immunity and pathogenesis depending upon their subsets; CD8+ T cells in pathogenesis, and CD4+ T cells in protective immunity. These apparently contradictory responses may be mediated by the same cytokine, IFN-γ. [ABSTRACT FROM AUTHOR]

Published
1992

36. Severe muscle damage induced by high carbohydrate intake from elemental diet in a patient with Crohn's disease.

Author

Waki, Shinya, Kawanami, Chiharu, Kanda, Fumio, Uenoyama, Yoshito, Maekawa, Toru, Fukui, Hirokazu, Okada, Akihiko, Matsushima, Yumi, Kishi, Kiyohiko, Kinoshita, Yoshikazu, Chiba, Tsutomu, Waki, S, Kawanami, C, Kanda, F, Uenoyama, Y, Maekawa, T, Fukui, H, Okada, A, Matsushima, Y, and Kishi, K

Subjects
CROHN'S disease, CREATINE kinase, MUSCLE diseases, SKELETAL muscle injuries, ELEMENTAL diet, NUTRITION disorders, SKELETAL muscle, DISEASE complications
Abstract

Crohn's disease is associated with complications in multiple organs. However, there are very few reported cases of patients with Crohn's disease with muscle symptoms and/or high serum creatine phospho-kinase (CPK) levels. We report here a patient with Crohn's disease who experienced skeletal muscle damage with extremely high serum CPK level during treatment with an elemental diet. The non-parenteral administration of large amounts of carbohydrate and limited glycogen degradation capability may be a possible causative mechanism for this elemental diet-induced muscle damage. [ABSTRACT FROM AUTHOR]

Published
1998
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37. X-ray sensitivity and DNA synthesis in synchronous culture of Plasmodium falciparum.

Author

Waki, S., Yonome, I., and Suzuki, M.

Abstract

The relationship between parasite development and sensitivity to irradiation with X-rays was investigated during a single synchronous cycle of Plasmodium falciparum in culture. The sensitivity of the parasites to irradiation was closely correlated with the phases of DNA synthesis. Their sensitivity was greatest at the ring stage in development, but decreased at the trophozoite stage when DNA synthesis begins. Lowest sensitivity was found when DNA synthesis was most rapid as the parasites were transforming from late trophozoite to schizont forms. These findings suggest that DNA is the target of the lethal radiation damage in the parasites. [ABSTRACT FROM AUTHOR]

Published
1985
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38. Acquirement of protective immunity in mice through infection with an attenuated isolate and its failure in parent virulent Plasmodium berghei.

Author

Waki, S., Takagi, T., and Suzuki, M.

Abstract

In virulent Plasmodium berghei infection, mice showed suppressive responses to sheep red blood cells SRBC (PFC) as well as the parasite antigen (DTH) and developed autoantibodies against homologous lymphocytes. On the other hand, mice infected with an attenuated variant derived from P. berghei did not show these responses but developed solid protective immunity against parent parasite infection accompanied by high antibody titre. When such an immune serum was transferred into mice, attenuated parasite infection was completely eliminated. These results show that an attenuated variant stimulates antibody production, which contributes to protection against the parasites. In contrast, in virulent P. berghei infections harmful immunopathological responses against the host are more prominent than protective immune responses against the parasites. [ABSTRACT FROM AUTHOR]

Published
1989
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41. Roles of CD4(+) T cells and gamma interferon in protective immunity against Babesia microti infection in mice.

Author

Igarashi, I, Suzuki, R, Waki, S, Tagawa, Y, Seng, S, Tum, S, Omata, Y, Saito, A, Nagasawa, H, Iwakura, Y, Suzuki, N, Mikami, T, and Toyoda, Y

Abstract

Babesia microti produces a self-limiting infection in mice, and recovered mice are resistant to reinfection. In the present study, the role of T cells in protective immunity against challenge infection was examined. BALB/c mice which recovered from primary infection showed strong protective immunity against challenge infection. In contrast, nude mice which failed to control the primary infection and were cured with an antibabesial drug did not show protection against challenge infection. Treatment of immune mice with anti-CD4 monoclonal antibody (MAb) diminished the protective immunity against challenge infection, but treatment with anti-CD8 MAb had no effect on the protection. Transfer of CD4(+) T-cell-depleted spleen cells resulted in higher parasitemia than transfer of CD8(+) T-cell-depleted spleen cells. A high level of gamma interferon (IFN-gamma), which was produced by CD4(+) T cells, was observed for the culture supernatant of spleen cells from immune mice, and treatment of immune mice with anti-IFN-gamma MAb partially reduced the protection. Moreover, no protection against challenge infection was found in IFN-gamma-deficient mice. On the other hand, treatment of immune mice with MAbs against interleukin-2 (IL-2), IL-4, or tumor necrosis factor alpha did not affect protective immunity. These results suggest essential requirements for CD4(+) T cells and IFN-gamma in protective immunity against challenge infection with B. microti.

Published
1999

42. Gamma interferon production is critical for protective immunity to infection with blood-stage Plasmodium berghei XAT but neither NO production nor NK cell activation is critical.

Author

Yoneto, T, Yoshimoto, T, Wang, C R, Takahama, Y, Tsuji, M, Waki, S, and Nariuchi, H

Abstract

We have examined the roles of gamma interferon (IFN-gamma), nitric oxide (NO), and natural killer (NK) cells in the host resistance to infection with the blood-stage malarial parasite Plasmodium berghei XAT, an irradiation-induced attenuated variant of the lethal strain P. berghei NK65. Although the infection with P. berghei XAT enhanced NK cell lytic activity of splenocytes, depletion of NK1.1(+) cells caused by the treatment of mice with anti-NK1.1 antibody affected neither parasitemia nor IFN-gamma production by their splenocytes. The P. berghei XAT infection induced a large amount of NO production by splenocytes during the first peak of parasitemia, while P. berghei NK65 infection induced a small amount. Unexpectedly, however, mice deficient in inducible nitric oxide synthase (iNOS-/-) cleared P. berghei XAT after two peaks of parasitemia were observed, as occurred for wild-type control mice. Although the infected iNOS-/- mouse splenocytes did not produce a detectable level of NO, they produced an amount of IFN-gamma comparable to that produced by wild-type control mouse splenocytes, and treatment of these mice with neutralizing anti-IFN-gamma antibody led to the progression of parasitemia and fatal outcome. CD4(-/-) mice infected with P. berghei XAT could not clear the parasite, and all these mice died with apparently reduced IFN-gamma production. Furthermore, treatment with carrageenan increased the susceptibility of mice to P. berghei XAT infection. These results suggest that neither NO production nor NK cell activation is critical for the resistance to P. berghei XAT infection and that IFN-gamma plays an important role in the elimination of malarial parasites, possibly by the enhancement of phagocytic activity of macrophages.

Published
1999

45. Dirofilaria immitis:Immunohistochemical Localization of Acid Proteinase in the Adult Worm

Author

Sato, K., Yamaguchi, H., Waki, S., Suzuki, M., and Nagai, Y.

Abstract

The distribution of Dirofilaria immitisacid proteinase in adult worm tissue was examined biochemically and immunohistochemically. About 45% of the total proteinase activity of 700gsupernatant, which was obtained from the 0.25 Msucrose homogenate of live adult worms, was found in the 100,000gsupernatant by subcellular centrifugation analysis. The distribution pattern of the proteinase activity observed by Percoll density gradient centrifugation coincided with that of glucose-6-phosphatase, a marker cytosolic enzyme, suggesting that the acid proteinase was present in vivoin a membrane-free form, possibly in the cytosol or secretory fluid. Immunostaining for the proteinase in the parasite tissue using the IgG1 (κ-type) monoclonal antibody, H-1, revealed immunoreactive enzyme primarily inside the cell as small grains, but not on the cell surface, and immunoreactivity was distributed widely in worm tissues such as lateral cords, dorsal and ventral median cords, the anterior end of the parasite, and intestinal epithelial cells in granular form. In the male reproductive system, the testicular wall and germ cells were labeled with the antibody, and in the female, uterine walls, fertilized eggs, and developing eggs as well as microfilaria were labeled. In conclusion, D. immitisacid proteinase is widely distributed in the adult parasite tissue, possibly functioning not only in nutrition metabolism but also in production of sperm and microfilariae, etc.

Published
1995
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49. Reduced T helper 1 responses in IL-12 p40 transgenic mice

Author

Takayuki Yoshimoto, Wang, C. -R, Yoneto, T., Waki, S., Sunaga, S., Komagata, Y., Mitsuyama, M., Miyazaki, J. -I, and Nariuchi, H.

Subjects
Cytotoxicity, Immunologic, Male, Plasmodium berghei, Immunology, Mice, Transgenic, Th1 Cells, Interleukin-12, Recombinant Proteins, Malaria, Killer Cells, Natural, Mice, Inbred C57BL, Mice, Immune Tolerance, Animals, Cytokines, Immunology and Allergy, Female, Disease Susceptibility, Transgenes, Injections, Intraperitoneal
Abstract

To investigate the antagonistic effect of IL-12 p40 on IL-12 activity in vivo, we generated transgenic (Tg) mice in which p40 gene was regulated by a liver-specific promoter. Three Tg mouse lines were generated, and they expressed the p40 transgene predominantly in liver. Serum p40 level was extremely high, and it consisted of mainly monomer and homodimer and also of higher m.w. complexes. These Tg mice did not show any apparent phenotypic difference from control littermates in lymphoid cells. Enhancement of NK cell lytic activity in spleen by administration of rIL-12 to these mice was greatly diminished. Ag-induced cytokine production was impaired: decreased production of IFN-γ and increased production of IL-4 and IL-10. Delayed-type hypersensitivity response was also significantly reduced. Moreover, these Tg mice showed increased susceptibility to the infection with an intracellular pathogen, blood-stage Plasmodium berghei XAT, which is an irradiation-induced attenuated substrain of P. berghei NK65, presumably due to the decreased IFN-γ production. These results suggest that p40 functions as an IL-12 antagonist in vivo, and that Th1 responses in p40 Tg mice are significantly reduced. Thus, these Tg mice could be a useful model to evaluate the inhibitory effect of p40 on IL-12-mediated various immune responses in vivo.

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