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2,069 results on '"Arai, Ken"'

201. Proceedings from the Albert Charitable Trust Inaugural Workshop on white matter and cognition in aging

Author

Sorond, Farzaneh A., primary, Whitehead, Shawn, additional, Arai, Ken, additional, Arnold, Douglas, additional, Carmichael, S. Thomas, additional, De Carli, Charles, additional, Duering, Marco, additional, Fornage, Myriam, additional, Flores-Obando, Rafael E., additional, Graff-Radford, Jonathan, additional, Hamel, Edith, additional, Hess, David C., additional, Ihara, Massafumi, additional, Jensen, Majken K., additional, Markus, Hugh S., additional, Montagne, Axel, additional, Rosenberg, Gary, additional, Shih, Andy Y., additional, Smith, Eric E., additional, Thiel, Alex, additional, Tse, Kai Hei, additional, Wilcock, Donna, additional, and Barone, Frank, additional

Published
2019
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218. Frpo: a novel single-stranded DNA promoter for transcription and for primer RNA synthesis of DNA replication

Author

Masai, Hisao and Arai, Ken-ichi

Subjects
DNA, RNA -- Synthesis, Biological sciences
Abstract

A new single-stranded DNA promoter functions effectively for E.coli RNA polymerase. Through the stimulation of SSB, the new single stranded DNA promoter (Frpo sequence) instructs the RNA polymerase to begin transcription at a definite site within Frpo. Transcription at Frpo also functions for preparing DNA replication since RNAs synthesized on SSB-coated single-stranded Frpo are practically elongated into DNA chains by DNA polymerase III holoenzyme.

Published
1997

223. Role of Perivascular Oligodendrocyte Precursor Cells in Angiogenesis After Brain Ischemia

Author

Kishida, Natsue, Maki, Takakuni, Takagi, Yasushi, Yasuda, Ken, Kinoshita, Hisanori, Ayaki, Takashi, Noro, Takayuki, Kinoshita, Yusuke, Ono, Yuichi, Kataoka, Hiroharu, Yoshida, Kazumichi, Lo, Eng H., Arai, Ken, Miyamoto, Susumu, Takahashi, Ryosuke, Kishida, Natsue, Maki, Takakuni, Takagi, Yasushi, Yasuda, Ken, Kinoshita, Hisanori, Ayaki, Takashi, Noro, Takayuki, Kinoshita, Yusuke, Ono, Yuichi, Kataoka, Hiroharu, Yoshida, Kazumichi, Lo, Eng H., Arai, Ken, Miyamoto, Susumu, and Takahashi, Ryosuke

Abstract

Background－Oligodendrocyte precursor cells (OPCs) regulate neuronal, glial, and vascular systems in diverse ways and display phenotypic heterogeneity beyond their established role as a reservoir for mature oligodendrocytes. However, the detailed phenotypic changes of OPCs after cerebral ischemia remain largely unknown. Here, we aimed to investigate the roles of reactive OPCs in the ischemic brain. Methods and Results－The behavior of OPCs was evaluated in a mouse model of ischemic stroke produced by transient middle cerebral artery occlusion in vivo. For in vitro experiments, the phenotypic change of OPCs after oxygen glucose derivation was examined using a primary rat OPC culture. Furthermore, the therapeutic potential of hypoxic OPCs was evaluated in a mouse model of middle cerebral artery occlusion in vivo. Perivascular OPCs in the cerebral cortex were increased alongside poststroke angiogenesis in a mouse model of middle cerebral artery occlusion. In vitro RNA‐seq analysis revealed that primary cultured OPCs increased the gene expression of numerous pro‐angiogenic factors after oxygen glucose derivation. Hypoxic OPCs secreted a greater amount of pro‐angiogenic factors, such as vascular endothelial growth factor and angiopoietin‐1, compared with normoxic OPCs. Hypoxic OPC‐derived conditioned media increased the viability and tube formation of endothelial cells. In vivo studies also demonstrated that 5 consecutive daily treatments with hypoxic OPC‐conditioned media, beginning 2 days after middle cerebral artery occlusion, facilitated poststroke angiogenesis, alleviated infarct volume, and improved functional disabilities. Conclusions－Following cerebral ischemia, the phenotype of OPCs in the cerebral cortex shifts from the parenchymal subtype to the perivascular subtype, which can promote angiogenesis. The optimal use of hypoxic OPCs secretome would provide a novel therapeutic option for stroke.

Published
2019

224. Promoting neuro-supportive properties of astrocytes with epidermal growth factor hydrogels

Author

Chan, Su Jing, Niu, Wanting, Hayakawa, Kazuhide, Hamanaka, Gen, Wang, Xiaoying, Cheah, Pike See, Guo, Shuzhen, Yu, Zhangyang, Arai, Ken, Selim, Magdy H., Kurisawa, Motoichi, Spector, Myron, Lo, Eng H., Chan, Su Jing, Niu, Wanting, Hayakawa, Kazuhide, Hamanaka, Gen, Wang, Xiaoying, Cheah, Pike See, Guo, Shuzhen, Yu, Zhangyang, Arai, Ken, Selim, Magdy H., Kurisawa, Motoichi, Spector, Myron, and Lo, Eng H.

Abstract

Biomaterials provide novel platforms to deliver stem cell and growth factor therapies for central nervous system (CNS) repair. The majority of these approaches have focused on the promotion of neural progenitor cells and neurogenesis. However, it is now increasingly recognized that glial responses are critical for recovery in the entire neurovascular unit. In this study, we investigated the cellular effects of epidermal growth factor (EGF) containing hydrogels on primary astrocyte cultures. Both EGF alone and EGF‐hydrogel equally promoted astrocyte proliferation, but EGF‐hydrogels further enhanced astrocyte activation, as evidenced by a significantly elevated Glial fibrillary acidic protein (GFAP) gene expression. Thereafter, conditioned media from astrocytes activated by EGF‐hydrogel protected neurons against injury and promoted synaptic plasticity after oxygen–glucose deprivation. Taken together, these findings suggest that EGF‐hydrogels can shift astrocytes into neuro‐supportive phenotypes. Consistent with this idea, quantitative‐polymerase chain reaction (qPCR) demonstrated that EGF‐hydrogels shifted astrocytes in part by downregulating potentially negative A1‐like genes (Fbln5 and Rt1‐S3) and upregulating potentially beneficial A2‐like genes (Clcf1, Tgm1, and Ptgs2). Further studies are warranted to explore the idea of using biomaterials to modify astrocyte behavior and thus indirectly augment neuroprotection and neuroplasticity in the context of stem cell and growth factor therapies for the CNS. Stem Cells Translational Medicine 2019 Biomaterials provide novel platforms to deliver stem cell and growth factor therapies for central nervous system repair. Our data suggest that epidermal growth factor‐containing hydrogels can shift astrocytes into potentially beneficial A2‐like phenotypes that may augment neuroprotection and neuroplasticity during the recovery phase after brain injury.

Published
2019

233. Abstracts of selected papers presented at the 30th Annual Meeting of the Japanese Society of Gastroenterology October 20–22, 1988 — Kagoshima, Japan

Author

Oda, Ichiro, Ogawa, Kaoru, Okada, Shuichi, Ueno, Keiichi, Itoh, Tohru, Horiguchi, Yuji, Kijima, Hiroshi, Inui, Kazuo, Koga, Akitoshi, Hamamoto, Tetsuro, Tsukada, Hideaki, Tamada, Takashi, Nakamura, Takahiko, Okanoue, T., Koike, Daisuke, Abe, Hirohiko, Miura, Tsutomu, Hashimoto, Shuji, Oda, M., Azuma, T., Nagata, Shigeyuki, Ishii, Hiromasa, Kawada, Norifumi, Mizoguchi, Yasuhiro, Yoshikawa, Yuji, Oka, Hiroshi, Ichida, Takafumi, Ichida, Fumihiro, Ueno, Takato, Tanikawa, Kyuichi, Kokudo, Norihiro, Kawasaki, Seiji, Onji, Morikazu, Miyaoka, Hiroaki, Yokosuka, Osamu, Omata, Masao, Ikeda, Hiroshi, Tsuji, Takao, Hayashi, Shigeki, Fujiwara, Kenji, Yasunaga, Mitsuru, Okita, Kiwamu, Takase, Koujirou, Tameda, Yukihiko, Ohnishi, Hiroo, Sugihara, Jun-ichi, Kojima, Hideo, Kamimura, Tomoteru, Tanaka, Eiji, Yoda, Hidetoshi, Kanno, Atsushi, Ohtsuki, Masao, Miyata, Yasuji, Koga, Shunichi, Unoura, Masashi, Tanaka, Nobuyoshi, Kodama, Takahiro, Nishimura, Hideo, Suzuki, Kazuyuki, Madarame, Takeo, Komatsu, Masafumi, Ookubo, Shunji, Nishiyama, Masataka, Saito, Shozo, Kumashiro, Ryukichi, Tanikawa, Kyuichi, Ikeda, Kenji, Kumada, Hiromitsu, Nishiguchi, Shuhei, Kuroki, Tetsuo, Yoshiba, Makoto, Takeuchi, Yukari, Morito, Takao, Kasukawa, Reiji, Takeda, Isao, Nakano, Satoshi, Matsumura, Kenzo, Imanari, Tomohiro, Lee, Shigeki, Fujita, Naotaka, Mine, Tetsuya, Sato, Eiichi, Suyama, Masafumi, Ariyama, Jo, Takahashi, Toshihisa, Hirano, Masanori, Hirai, Atsushi, Yamakawa, Tatsuo, Kamiya, Junichi, Nimura, Yuji, Yoshimoto, Hideo, Ikeda, Seiyo, Yamasuji, Tadashi, Saeki, Keizo, Itoh, Masaki, Kajiyama, Goro, Seki, Hideichi, Kimura, Ken, Nakamura, Hiroshi, Tsuchiya, Yukihiro, Omura, Ryosuke, Tanaka, Shinya, Shimakura, Katsuhide, Matsuda, Yoshiaki, Wakabayashi, Tokio, Morimoto, Hideo, Kamiya, Yasutaka, Okayama, Yasutaka, Kobayashl, Masao, Fujimoto, Sotaro, Yamaguchi, Atsumasa, Shibue, Tadashi, Akashi, Ryukichi, Hattori, Masahiro, Takehira, Yasunori, Tsugane, Yasutoshi, Tashiro, Yoshinori, Kuwayama, Hajime, Kon, Yoichi, Higuchi, Tsugio, Hirata, Nobuto, Kano, Tomoyuki, Kurimoto, Kumiko, Kubota, Y., Seki, T., Kamura, Yoshimine, Nakayama, Toshimichi, Yoshimura, Hitoshi, Yoshioka, Tetsuya, Akimoto, Kimihiko, Mine, Tetsuya, Sato, Eiichi, Ohnishi, Hirohide, Ogata, Etsuro, Igarashi, Atsushi, Kadowaki, Atsushi, Yaoita, Tsutomu, Sato, Naoki, Monma, Kimitsune, Kogure, Hiroaki, Tajima, Yoshio, Takanashi, Hideki, Tsuchiya, Yukihiro, Haniya, Kazuo, Ohto, Masao, Murata, Ikuo, Tanaka, Takashi, Sakabe, Takashi, Kato, Takashi, Koike, Tadashi, Watanabe, Tetsuya, Nakamura, Tetsuo, Kato, H., Ikai, I., Nishimura, N., Kobayashi, N., Ozawa, K., Ono, Katsuyuki, Sata, Michio, Abe, Hirohiko, Tanikawa, Kyuichi, Kadowaki, Ken, Ikoma, Jiro, Kojima, Yuji, Murata, Tetsuya, Kakehashi, Ryuichi, Ibe, Toshio, Kano, Uichiro, Ito, Tetsuo, Tanaka, Takeshi, Watanabe, Shozo, Suzuki, Shiro, Nakazawa, Osamu, Kohda, Kyuhei, Ohyama, Kohzo, Terada, Shoki, Sazaki, Katsuhiko, Kure, Teikichi, Morita, Koetsu, Shida, Osamu, Muramatsu, Hiroshi, Niitsu, Yoshiro, Tozuka, Shinichi, Sakai, Yoshinori, Ikeda, Takaaki, Koyama, Wataru, Sakamoto, Shigemi, Kanayama, Masaaki, Tanaka, Naohide, Arakawa, Yasuyuki, Matsuo, Yutaka, Takaguchi, Kouichi, Yamada, Gotaro, Matsuura, Kazuharu, Ikeda, Hirosi, Iwasaki, Yoshiaki, Nouso, Kazuhiro, Matsueda, Kazuhiro, Sawahara, Masahiko, Fujiki, Shigeatsu, Mizuno, Motowo, Yama, Shingo Kino, Tsuji, Takao, Nadano, Seijin, Horiike, Norio, Michitaka, Kojiro, Kumon, Izumi, Ogawa, Yasushi, Yamaguchi, Shuji, Onji, Morikazu, Ohta, Yasuyuki, Nishi, Masaaki, Matsuzaki, Yasushi, Tanaka, Naomi, Matsumoto, Hisashi, Chuganji, Yoshimichi, Osuga, Toshiaki, Shoji, S., Kurata, M., Wakashima, M., Itoh, Y., Hagiri, M., Kondou, T., Katayama, M., Nishizawa, K., Takikawa, H., Ohsawa, H., Miyake, M., Yamanaka, M., Ooka, Teruji, Akita, Masahiko, Kim, Hogen, Kato, Michio, Masuzawa, Manabu, Okuyama, Takumasa, Akiyama, Masahiko, Ishigami, Yoshitaka, Tamura, Kazuya, Fukui, Osamu, Abe, Hiroshi, Kamada, Takenobu, Arai, Ken, Shindo, Michiko, Okuno, Tadao, Matsumoto, Masayuki, Takeda, Makoto, Takino, Tatsuro, Sokawa, Yoshihiro, Omata, M., Yokosuka, O., Ito, Y., Hosoda, K., Ohto, M., Fuse, Yoshinobu, Kodama, Tadashi, Sugiyama, Kenji, Nakajo, Shinobu, Ajitsu, Shin, Takahashi, Tsuneo, Kuroe, K., Murata, Y., Ikeda, Hideo, and Tanikawa, Kyuichi

Published
1990
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236. Sharing of the interleukin-2 (IL-2) receptor gamma chain between receptors for IL-2 and IL-4

Author

Kondo, Motonari, Takeshita, Toshikazu, Ishii, Naoto, Nakamura, Masataka, Watanabe, Sumiko, Arai, Ken-ichi, and Sugamura, Kazuo

Subjects
Interleukin-2 -- Research, Cellular signal transduction -- Research, Drug receptors -- Research, Science and technology, Research
Abstract

The γ chain of the interleukin-2 (IL-2) receptor is an indispensable subunit for IL-2 binding and intracellular signal transduction. A monoclonal antibody to the γ chain, TUGm2, inhibited IL-2 binding to the functional IL-2 receptors and also inhibited IL-4--induced cell growth and the high-affinity binding of IL-4 to the CTLL-2 mouse T cell line. Another monoclonal antibody, TUGm3, which reacted with the γ chain cross-linked with IL-2, also immunoprecipitated the γ chain when cross-linked with IL-4. These results suggest that the IL-2 receptor γ chain is functionally involved in the IL-4 receptor complex., Functional high-affinity receptors for cytokines are generally complexes consisting of binding subunits (α chains) with low affinities to ligands and effector subunits (β chains) to transduce signals, both of which [...]

Published
1993

244. Effects of O-GlcNAcylation on functional mitochondrial transfer from astrocytes.

Author

Park, Ji-Hyun, Nakamura, Yoshihiko, Li, Wenlu, Hamanaka, Gen, Arai, Ken, Lo, Eng H, and Hayakawa, Kazuhide

Abstract

Mitochondria may be transferred from cell to cell in the central nervous system and this process may help defend neurons against injury and disease. But how mitochondria maintain their functionality during the process of release into extracellular space remains unknown. Here, we report that mitochondrial protein O-GlcNAcylation is a critical process to support extracellular mitochondrial functionality. Activation of CD38-cADPR signaling in astrocytes robustly induced protein O-GlcNAcylation in mitochondria, while oxygen-glucose deprivation and reoxygenation showed transient and mild protein modification. Blocking the endoplasmic reticulum – Golgi trafficking with Brefeldin A or slc35B4 siRNA reduced O-GlcNAcylation, and resulted in the secretion of mitochondria with decreased membrane potential and mtDNA. Finally, loss-of-function studies verified that O-GlcNAc-modified mitochondria demonstrated higher levels of neuroprotection after astrocyte-to-neuron mitochondrial transfer. Collectively, these findings suggest that post-translational modification by O-GlcNAc may be required for supporting the functionality and neuroprotective properties of mitochondria released from astrocytes. [ABSTRACT FROM AUTHOR]

Published
2021
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247. Contributors

Author

Adams, Harold P., Jr., Adeoye, Opeolu, Albers, Gregory W., Alexandrov, Andrei V., Amin-Hanjani, Sepideh, An, Hongyu, Anderson, Craig S., Anrather, Josef, Aparicio, Hugo J., Arai, Ken, Aronowski, Jaroslaw, Atchaneeyasakul, Kunakorn, Audebert, Heinrich, Auer, Roland N., Awad, Issam A., Ay, Hakan, Baltan, Selva, Balu, Ramani, Behbahani, Mandana, Benavente, Oscar R., Bershad, Eric M., Berthaud, Jimmy V., Blackburn, Spiros L., Bonati, Leo H., Bösel, Julian, Bousser, Marie Germaine, Broderick, Joseph P., Brown, Martin M., Brown, Wendy, Brust, John C.M., Bushnell, Cheryl, Canhão, Patrícia, Caplan, Louis R., Carrión-Penagos, Julián, Castellanos, Mar, Caunca, Michelle R., Chabriat, Hugues, Chamorro, Angel, Chen, Jieli, Chen, Jun, Chopp, Michael, Christorforids, Greg, Connolly, E. Sander, Jr., Cramer, Steven C., Cucchiara, Brett L., Czap, Alexandra L., Dannenbaum, Mark J., Davis, Patricia H., Dawson, Ted M., Dawson, Valina L., Day, Arthur L., De Silva, T. Michael, de Sousa, Diana Aguiar, Del Brutto, Victor J., del Zoppo, Gregory J., Derdeyn, Colin P., Di Tullio, Marco R., Diener, Hans Christoph, Diringer, Michael N., Dobkin, Bruce H., Dzialowski, Imanuel, Elkind, Mitchell S.V., Elm, Jordan, Feigin, Valery L., Ferro, José Manuel, Field, Thalia S., Fischer, Marlene, Fornage, Myriam, Furie, Karen L., Garcia-Bonilla, Lidia, Giannotta, Steven L., Gobin, Y. Pierre, Goldberg, Mark P., Goldstein, Larry B., Gonzales, Nicole R., Greer, David M., Grotta, James C., Guo, Ruiming, Gutierrez, Jose, Harmel, Peter, Howard, George, Howard, Virginia J., Hwang, Jee-Yeon, Iadecola, Costantino, Jahan, Reza, Jickling, Glen C., Joutel, Anne, Kasner, Scott E., Katan, Mira, Kellner, Christopher P., Khan, Muhib, Kidwell, Chelsea S., Kim, Helen, Kim, Jong S., Kircher, Charles E., Krings, Timo, Krishnamurthi, Rita V., Kurth, Tobias, Lansberg, Maarten G., Levy, Elad I., Liebeskind, David S., Liew, Sook-Lei, Lin, David J., Lisle, Benjamin, Lo, Eng H., Lyden, Patrick D., Maki, Takakuni, Maragkos, Georgios A., Marosfoi, Miklos, McCullough, Louise D., Meckler, Jason M., Meschia, James Frederick, Messé, Steven R., Mocco, J, Mokin, Maxim, Mooney, Michael A., Morgenstern, Lewis B., Moskowitz, Michael A., Mullen, Michael T., Nägel, Steffen, Nedergaard, Maiken, Neira, Justin A., Newman, Sarah, Nicholson, Patrick J., Norrving, Bo, O’Donnell, Martin, Ofengeim, Dimitry, Ogata, Jun, Ogilvy, Christopher S., Orrù, Emanuele, Ortega-Gutiérrez, Santiago, Padrick, Matthew Maximillian, Parsha, Kaushik, Parsons, Mark, Patel, Neil V., Patel, Virendra I., Pawlikowska, Ludmila, Pérez, Adriana, Perez-Pinzon, Miguel A., Picard, John M., Polster, Sean P., Powers, William J., Puetz, Volker, Putaala, Jukka, Rabinovich, Margarita, Ransom, Bruce R., Roa, Jorge A., Rosenberg, Gary A., Rossitto, Christina P., Rundek, Tatjana, Russin, Jonathan J., Sacco, Ralph L., Safouris, Apostolos, Samaniego, Edgar A., Sansing, Lauren H., Satani, Nikunj, Sattenberg, Ronald J., Saver, Jeffrey L., Savitz, Sean I., Schmidt, Christian, Seshadri, Sudha, Sharma, Vijay K., Sharp, Frank R., Sheth, Kevin N., Siddiqi, Omar K., Singhal, Aneesh B., Sobey, Christopher G., Sommer, Clemens J., Spetzler, Robert F., Stapleton, Christopher J., Strickland, Ben A., Su, Hua, Suarez, José I., Takayama, Hiroo, Tarsia, Joseph, Tatlisumak, Turgut, Thomas, Ajith J., Thompson, John W., Tsivgoulis, Georgios, Tournier-Lasserve, Elizabeth, Vidal, Gabriel, Wakhloo, Ajay K., Weksler, Babette B., Willey, Joshua Z., Wintermark, Max, Wong, Lawrence K.S., Xi, Guohua, Xu, Jinchong, Yaghi, Shadi, Yamaguchi, Takenori, Yang, Tuo, Yasaka, Masahiro, Zahuranec, Darin B., Zhang, Feng, Zhang, John H., Zheng, Zhitong, Zukin, R. Suzanne, and Zweifler, Richard M.

Published
2022
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248. Cloning of an interleukin-3 receptor gene: a member of a distinct receptor gene family

Author

Itoh, Naoto, Yonehara, Shin, Schreurs, Jolanda, Gorman, Daniel M., Maruyama, Kazuo, Ishii, Ai, Yahara, Ichiro, and Arai, Ken-Ichi

Subjects
Tyrosine -- Genetic aspects -- Research, Interleukin-3 -- Genetic aspects -- Research, Immunological adjuvants -- Genetic aspects -- Research, Interleukins -- Research, Cloning -- Research -- Genetic aspects, Science and technology, Genetic aspects, Research
Abstract

Cloning of an Interleukin-3 Receptor Gene: A Member of a Distinct Receptor Gene Family INTERLEUKIN-3, PRIMARILY PROduced by activated T cells, stimulates colony formation of multiple lineages (multi-CSF), maintains spleen [...]

Published
1990

249. Wireless magnetic motion capture system--compensatory tracking of positional error caused by mutual inductance

Author

Hashi, Shuichiro, Toyoda, Masaharu, Yabukami, Shin, Ishiyama, Kazushi, Okazaki, Yasuo, and Arai, Ken Ichi

Subjects
Motion detectors -- Design and construction, Magnetic devices -- Design and construction, Business, Electronics, Electronics and electrical industries
Abstract

A wireless magnetic motion capture system using an LC resonant magnetic marker was developed and has been studied. The positional error of the system caused by mutual inductance between the exciting coil and the LC marker was examined. It has been found that the impedance change of the exciting coil due to a resonance of the LC marker perturbs the strength of the magnetic field which is used for marker excitation. The more a marker approaches the exciting coil, the larger it becomes. This fluctuation induces an error in the marker signal which is measured by the pickup coils and is necessary for positional calculation. Then, the compensatory process in consideration of the mutual inductance has been employed for positional calculation in order to improve the positional accuracy. From the compensation, the absolute positional accuracy is less than 2 mm within 140 mm of the pickup coil array. Index Terms--Compensatory tracking, LC resonant magnetic marker, positional error, wireless motion capture system.

Published
2007

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