14 results on '"Takashi, Tamiya"'
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2. The Influence of Age on the Outcomes of Traumatic Brain Injury: Findings from a Japanese Nationwide Survey (J-ASPECT Study-Traumatic Brain Injury)
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Yamagami, Keitaro, primary, Kurogi, Ryota, additional, Kurogi, Ai, additional, Nishimura, Kunihiro, additional, Onozuka, Daisuke, additional, Ren, Nice, additional, Kada, Akiko, additional, Nishimura, Ataru, additional, Arimura, Koichi, additional, Ido, Keisuke, additional, Mizoguchi, Masahiro, additional, Sakamoto, Tetsuya, additional, Kayama, Takamasa, additional, Suzuki, Michiyasu, additional, Arai, Hajime, additional, Hagihara, Akihito, additional, Iihara, Koji, additional, Takigami, Masayoshi, additional, Kamiyama, Kenji, additional, Houkin, Kiyohiro, additional, Nishi, Shougo, additional, Yoshimoto, Tetsuyuki, additional, Kaneko, Sadao, additional, Oka, Koji, additional, Ooyama, Hiroshi, additional, Kamada, Kyousuke, additional, Makino, Kenichi, additional, Tokumitsu, Naoki, additional, Sako, Kazuhiro, additional, Suzuki, Susumu, additional, Suzuki, Nozomi, additional, Izumi, Naoto, additional, Nitta, Kazumi, additional, Ootaki, Masahumi, additional, Isobe, Masanori, additional, Nishiya, Mikio, additional, Yamazaki, Takaaki, additional, Mabuchi, Syouji, additional, Ogasawara, Kuniaki, additional, Kubo, Naohiko, additional, Shimizu, Yukihiko, additional, Saito, Keiichi, additional, Yamanome, Tatumi, additional, Yoshino, Atsuo, additional, Fujitsuka, Mitsuyuki, additional, Takami, Masaaki, additional, Ohtaka, Hirotoshi, additional, Hirano, Teruyuki, additional, Shiokawa, Yosiaki, additional, Okada, Takaharu, additional, Suzuki, Ichiro, additional, Kohno, Michihiro, additional, Haraoka, Jou, additional, Arai, Yoshinori, additional, Kawamura, Noriyoshi, additional, Isoshima, Akira, additional, Yasue, Masaharu, additional, Takayoshi Kobayashi, Mitsuhiko Hokari, additional, Kawai, Kensuke, additional, Maehara, Taketoshi, additional, Noguchi, Makoto, additional, Hoshino, Haruhiko, additional, Hiyama, Hirofumi, additional, Yoshida, Kensaku, additional, Utsugi, Osamu, additional, Takeda, Yasuaki, additional, Tamaki, Kouichi, additional, Karasudani, Hirohide, additional, Urabe, Takao, additional, Kobayashi, Shiro, additional, Nakamura, Michio, additional, Koguchi, Yorio, additional, Ono, Junichi, additional, Suda, Sumio, additional, Hadeishi, Hiromu, additional, Fukutake, Toshio, additional, Wakui, Kenji, additional, Tanno, Hirokazu, additional, Ishige, Naoki, additional, Ohasi, Takashi, additional, Sakai, Hideki, additional, Nishimura, Yasuaki, additional, Watanabe, Takayuki, additional, Matsumoto, Takashi, additional, Koketsu, Naoki, additional, Hirose, Yuichi, additional, Doyu, Manabu, additional, Hasegawa, Toshinori, additional, Kuwayama, Naoto, additional, Terao, Shinichi, additional, Mizutani, Nobuhiko, additional, Suzaki, Noriyuki, additional, Okuda, Satoshi, additional, Yasui, Keizo, additional, Seki, Yukio, additional, Hasegawa, Yasuhiro, additional, Ikeda, Akira, additional, Takeuchi, Youtarou, additional, Ohara, Sigeki, additional, Araki, Yoshio, additional, Wakabayashi, Toshihiko, additional, Tanaka, Hisashi, additional, Yoshimoto, Junpei, additional, Sugiura, Makoto, additional, Koichiro, Ogura, additional, Kobayashi, Nozomu, additional, Yamada, Tomonori, additional, Kato, Amami, additional, Toshiho, Ohtsuki, additional, Wakayama, Akatsuki, additional, Takahashi, Jun, additional, Kataoka, Hiroharu, additional, Yoshimine, Toshiki, additional, Nakajima, Yoshikazu, additional, Gi, Hidehuku, additional, Uranishi, Ryunosuke, additional, Nakamura, Yusaku, additional, Yamanaka, Kazunori, additional, Ohmori, Kazumi, additional, Matsumoto, Hiroyuki, additional, Oiwa, Yoshitugu, additional, Uemura, Yosihiko, additional, Fujiwara, Hiroaki, additional, Iwai, Yoshiyasu, additional, Morikawa, Masashi, additional, Tane, Kazuyuki, additional, Hashikawa, Kazuo, additional, Fujinaka, Toshiyuki, additional, Yoneda, Shunichi, additional, Yamashita, Kohsuke, additional, Kitano, Masahiko, additional, Tominaga, Shinsuke, additional, Nakamura, Kazuhito, additional, Kono, Katsuhiko, additional, Ohata, Kenji, additional, Taniguchi, Hirokatsu, additional, Hazama, Takanori, additional, Kuroiwa, Toshihiko, additional, Tamura, Yoji, additional, Maeno, Kazusige, additional, Arai, Motohiro, additional, Iwase, Masaaki, additional, Hashimoto, Kenji, additional, Yamada, Keisuke, additional, Turuno, Takashi, additional, Ichinose, Tsutomu, additional, Kurokawa, Shinichiro, additional, Matsuyama, Takeshi, additional, Fujita, Toshiaki, additional, Yuguchi, Takamichi, additional, Teramoto, Yoshihumi, additional, Kakita, Hiroto, additional, Matsuo, Takayuki, additional, Izumo, Tsuyoshi, additional, Ryu, Nobutoshi, additional, Naoki Kitagawa, Wataru Haraguchi, additional, Kaminogo, Makio, additional, Sakamoto, Seisaburo, additional, Tokunaga, Yosiharu, additional, Urasaki, Ei-Ichirou, additional, Kuratsu, Junichi, additional, Takada, Akira, additional, Terasaki, Tadashi, additional, Hisami Oosima, Isao Fuwa, additional, Yamashiro, Shigeo, additional, Hiromasa Tsuiki, Makoto Yoshikawa, additional, Koga, Kazunari, additional, Egami, Hiroshi, additional, Kawamura, Tadao, additional, Mitsuo, Kunihiko, additional, Masaki Morisige, Takamitu Hikawa, additional, Takeda, Yuu, additional, Yamaguchi, Yutaka, additional, Shunro Uchinokura, Shiro Miyata, additional, Goya, Tomokazu, additional, Takeshima, Hideo, additional, Yatsushiro, Kazutaka, additional, Ohta, Hajime, additional, Nagadou, Tatsui, additional, Hirahara, Kazuho, additional, Obara, Souichi, additional, Seto, Hiroshi, additional, Moroki, Koiti, additional, Arita, Kazunori, additional, Ishiuchi, Shogo, additional, Uchihara, Toshimitsu, additional, Mekaru, Susumu, additional, Nagamine, Tomoaki, additional, Jin Momoji, Naoki Tomiyama, additional, Atusi Kimoto, Kouzi Idomari, additional, Kadekaru, Tsutomu, additional, Syamoto, Hirosi, additional, Sasaki, Osamu, additional, Minagawa, Makoto, additional, Takahashi, Hideaki, additional, Hiroyuki Arai, Kiyoshi Onda, additional, Takeuchi, Shigekazu, additional, Abe, Hiroshi, additional, Fukuda, Osamu, additional, Kouno, Mitsuo, additional, Tamura, Tetsuro, additional, Michiya Kubo, Yukio Horie, additional, Hondo, Hiroaki, additional, Takada, Hisashi, additional, Masuoka, Toru, additional, Shirasaki, Naoki, additional, Nitta, Hisashi, additional, Yasuo Katsuki, Makoto Kimura, additional, Hisato Minamide, Yutaka Hayashi, additional, Munemoto, Shigeru, additional, Ikeda, Kiyonobu, additional, Yutaka Hayashi, Mitsutoshi Nakada, additional, Sato, Syuji, additional, Hatano, Taketo, additional, Yamamura, Osamu, additional, Kabuto, Masanori, additional, Jyunya Hayashi, Takahiro Sakuma, additional, Kinouchi, Hiroyuki, additional, Koizumi, Hidehito, additional, Imae, Syougo, additional, Fujita, Manabu, additional, Suga, Masakazu, additional, Kanehisa Kohno, Shinji Iwata, additional, Zenke, Kiichiro, additional, Fujisawa, Mutsuo, additional, Mizobuchi, Hikaru, additional, Hayashi, Satoru, additional, Morimoto, Masanori, additional, Ueba, Tetsuya, additional, Nishimura, Hiroyuki, additional, Ikawa, Naoki, additional, Matsumoto, Yuzo, additional, Kannuki, Seiji, additional, Kagawa, Masahiro, additional, Hayashi, Naoki, additional, Atsushi Shindo, Takashi Tamiya, additional, Yoshino, Kimihiro, additional, Masaoka, Tetsuya, additional, Nakahara, Ichiro, additional, Satoshi Suzuki, Akira Nakamizo, additional, Okamoto, Yuji, additional, Takahashi, Haruki, additional, Hirakawa, Katsuyuki, additional, Nagata, Shinji, additional, Ookura, Akio, additional, Yoshiro Kaneko, Hidenori Yoshida, additional, Nakane, Hiroshi, additional, Inoue, Isao, additional, Hitotsumatsu, Tsutomu, additional, Kouichi Kuramoto, Terukazu Kuramoto, additional, Hiromichi Ooishi, Yoshihisa Matumoto, additional, Masani Nonaka, Tooru Inoue, additional, Morioka, Motohiro, additional, Shuji Sakata, Hiroshi Sugimori, additional, Takashima, Hiroshi, additional, Ishihara, Shin-Ichiro, additional, Suzuyama, Kenji, additional, Miyazono, Masayuki, additional, Itaro Hattori, Masafumi Morimoto, additional, Ozaki, Satoshi, additional, Hirota, Nobuo, additional, Yasuhiko Mochimatsu, Yasunori Takemoto, additional, Takagi, Makoto, additional, Kenji Nakayama, Isao Yamamoto, additional, Hiroshi Tanaka, Yoshinori Uchida, additional, Sakata, Katsumi, additional, Nobutaka, Kawahara, additional, Nomura, Motohiro, additional, Ozawa, Hitoshi, additional, Tsumura, Kotaro, additional, Michiyuki Maruyama, Makoto Inaba, additional, Mori, Tatsuro, additional, Mori, Takahisa, additional, Sugitani, Masato, additional, Tanaka, Yuichiro, additional, Yamada, Masaru, additional, Matsumae, Mitsunori, additional, Onitsuka, Keiichirou, additional, Tatsuya Takahashi, Kosuke Miyahara, additional, Endou, Sumio, additional, Takahashi, Hidekazu, additional, Kaidu, Hiroyuki, additional, Chikashi Maruki, Akira Tsunoda, additional, Fujimaki, Takamitsu, additional, Ooigawa, Hidetoshi, additional, Masatsugu Uchida, Masahiko Tanaka, additional, Kouiti Katoh, Hiroshi Wanihuti, additional, Hyodo, Akio, additional, Asakura, Ken, additional, Nakajima, Shigeyoshi, additional, Kanzawa, Takao, additional, Kurihara, Hideyuki, additional, Ohmori, Sigehiro, additional, Hiroshi Kusunoki, Mitsugi Yoshinao, additional, Magarisawa, Satoshi, additional, Okabe, Shinichi, additional, Kujiraoka, Yuuji, additional, Tsuruoka, Shin, additional, Takeshita, Mikihiko, additional, Akira Matsumura, Tetsuya Yamamoto, additional, Uemura, Kazuya, additional, Tabata, Hitoshi, additional, Sonobe, Makoto, additional, Ryoji Yoshida, Masashi Nakatsukasa, additional, Shimoeda, Norifumi, additional, Kunimine, Hideo, additional, Ishihara, Masayuki, additional, Murai, Nozomu, additional, Murakami, Nobukuni, additional, Kidooka, Minoru, additional, Iwamoto, Yoshihiro, additional, Tenjin, Hiroshi, additional, Masahiko Takamasu, Kouji Shiga, additional, Mori, Nobuhito, additional, Kose, Shigeru, additional, Kohmura, Eiji, additional, Matsumoto, Keigo, additional, Sakaki, Takayuki, additional, Miyake, Hiroji, additional, Mabuchi, Eiichiro, additional, Yokota, Masayuki, additional, Yosihiro Kuga, Hideyuki Ohnishi, additional, Kimura, Mitsuru, additional, Masaaki Saiki, Osamu Narumi, additional, Nakajima, Norio, additional, Asahi, Minoru, additional, Koyama, Junji, additional, Noda, Shinya, additional, Iida, Junichi, additional, Fujita, Toyohisa, additional, Nakase, Hiroyuki, additional, Toru Hoshida, Hidehiro Hirabayashi, additional, Fujimoto, Takayoshi, additional, Nakao, Naoyuki, additional, Tanaka, Yoshiyuki, additional, Ozaki, Fuminori, additional, Nakamura, Yoshinari, additional, Miki, Kazuhito, additional, Watanabe, Takashi, additional, Hasegawa, Seiko, additional, Konno, Hiromu, additional, Takemura, Atsuhito, additional, Okubo, Atsuya, additional, Saito, Hitoshi, additional, Taizen Nakase, Tatsuya Ishikawa, additional, Toshio Sasajima, Hiroaki Shimizu, additional, Sasou, Masayuki, additional, Watanabe, Yoichi, additional, Kiyoshi Saito, Taku Sato, additional, Masahiro Satoh, Satoshi Taira, additional, Koizumi, Takayuki, additional, Shoji Mashiyama, Yasuhiro Suzuki, additional, Oikawa, Tomoyoshi, additional, Sonoda, Yukihiko, additional, Shinjiro Saito, Rei Kondo, additional, Shinoda, Atsuo, additional, Kamatsuka, Eiichiro, additional, So, Keiten, additional, Kinjo, Toshihiko, additional, Kennji Itou, Tooru Sasaki, additional, Hiroaki Shimizu, Hidenori Endo, additional, Karibe, Hirosi, additional, Takahashi, Kou, additional, Nakajima, Masayuki, additional, Watanabe, Kazuyoshi, additional, Takayama, Motohiro, additional, Komuro, Taro, additional, Fumio Suzuki, Hisao Hirai, additional, Suzuki, Hidenori, additional, Murata, Hiroto, additional, Miya, Fumitaka, additional, Kanamaru, Kenji, additional, Tamura, Akira, additional, Harada, Kiyoshi, additional, Fukazawa, Seiji, additional, Takehara, Seiya, additional, Watanabe, Yoshihiko, additional, Nakayama, Teiji, additional, Hiroshi Nagura, Haruhiko Sato, additional, Chiharu Tanoi, Shinji Amano, additional, Kuroda, Katsuhiro, additional, Morooka, Satoru, additional, Masashi Kitagawa, Takafumi Wataya, additional, Koide, Kazuo, additional, Tanigawara, Tetsuya, additional, Iwama, Toru, additional, Ito, Junki, additional, Noda, Shinji, additional, Kouno, Kazuyuki, additional, Kitazawa, Kazuo, additional, Toshiki Takemae, Yoshikazu Kusano, additional, Hokama, Masanobu, additional, Yoshihisa Nishiyama, Hiroki Sato, additional, Seguchi, Tatsuya, additional, Yoshihiko Inui, Sumio Kobayashi, additional, Oohigashi, Youji, additional, Muraoka, Shinsuke, additional, Miyatake, Masaki, additional, Nakagawa Shinichi, Kensuke Hayashida, additional, Inoue, Atsushi, additional, Sakai, Keiichi, additional, Yamaguchi, Shuhei, additional, Fusao Ikawa, Tatsuya Mizoue, additional, Hideki Irie, Gen Ishida, additional, Kagawa, Takato, additional, Namba, Yoichiro, additional, Nakashima, Hiroyuki, additional, Koji Abe, Isao Date, additional, Uno, Masaaki, additional, Sen Yamagata, Masaki Chin, additional, Soitiro Takao, Hidemiti Sasayama, additional, Kouji Muneda, Hideyuki Yoshida, additional, Watanebe, Akira, additional, Katou, Syouichi, additional, Hamada, Yasuhiro, additional, Nishizaki, Takafumi, additional, Yamashita, Katsuhiro, additional, Ryuji Nakamura, Takaharu Nakamura, additional, Wakabayashi, Shinichi, additional, Okazaki, Takahito, additional, Kurisu, Kaoru, additional, Matsumoto, Masayasu, additional, Katsuzo Kiya, Atsushi Tominaga, additional, Syuichi Oki, Masaaki Shibukawa, additional, Nakahara, Toshinori, additional, Okita, Shinji, additional, Torii, Tuyosi, additional, Kenjirou Fujiwara, Minoru Nakagawa, additional, Syuuhei Nishimura, Takashi Matsuoka, additional, Naoyuki Isobe, Osamu Hamasaki, additional, Shinji Nagahiro, Junichiro Satomi, additional, Agawa, Masahito, additional, Oka, Hirofumi, additional, Yoshimura, Kunikazu, additional, Kato, Tsutomu, additional, Satoshi Minoshima, Nobuaki Kobayasi, additional, Mikuni, Nobuhiro, additional, Tanikawa, Rokuya, additional, Sasaki, Jyunkou, additional, Otawara, Yasunari, additional, Tominaga, Teiji, additional, Sasaki, Tatsuya, additional, Takemura, Sunao, additional, Kawakami, Masahisa, additional, Ihara, Satoshi, additional, Shibata, Yasushi, additional, Saegusa, Takashi, additional, Iuchi, Toshihiko, additional, Ito, Chiaki, additional, Okuda, Osamu, additional, Yoshida, Kazunari, additional, Masateru Katayama, Sadao Suga, additional, Akihiro, Oikawa, additional, Miura, Naohisa, additional, Ota, Takahiro, additional, Kumabe, Toshihiro, additional, Suzuki, Sachio, additional, Kumagai, Takashi, additional, Nishimaki, Keiichi, additional, Hongo, Kazuhiro, additional, Shigeta, Hiroaki, additional, Hattori, Kazuyoshi, additional, Uozumi, Yoichi, additional, Nakahara, Norimoto, additional, Hashimoto, Nobukazu, additional, Shu Imai, Shinichi Shirakami, additional, Okumura, Yoshinari, additional, Kazuhiro Yokoyama, Ryo Tamaki, additional, Miyamoto, Susumu, additional, Yamamoto, Kazuo, additional, Ichioka, Tsugumichi, additional, Inoue, Tsuyoshi, additional, Kinoshita, Manabu, additional, Saitoh, Minoru, additional, Aihara, Hideo, additional, Miyake, Hajimu, additional, Tukasa Nishiura, Kotaro Ogihara, additional, Nishino, Shigeki, additional, Miyoshi, Yasuyuki, additional, Arisawa, Tadashi, additional, Shoji Tsuchimoto, Shigeru Daido, additional, Kinoshita, Kimihisa, additional, Keisuke Migita, Kiyoshi Yuki, additional, Akatsuka, Keiichi, additional, Fujisawa, Hirosuke, additional, Shono, Tadahisa, additional, Tsugu, Hitoshi, additional, Hayashi, Shuji, additional, Toshio Matsushima, Tatsuya Abe, additional, Nakashima, Susumu, additional, Tuji, Takehisa, additional, Kaga, Akihiko, additional, Kanemaru, Reizou, additional, Takasaki, Koji, additional, Imamura, Junichi, additional, Noha, Masahiro, additional, Watanabe, Saburo, additional, Sakai, Nobuyuki, additional, Hiroaki Minami, Yasuhisa Yoshida, additional, Okumura, Tomoyoshi, additional, Nishimura, Shinjitsu, additional, Numazawa, Shinichi, additional, Masanori Tsutsumi, Kiyoshi Kazekawa, additional, Fukuyama, Kouzou, additional, and Fujimoto, Yasuhiro, additional
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- 2019
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3. The effects of d-allose on transient ischemic neuronal death and analysis of its mechanism
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Richard F. Keep, Tetsuhiko Toyoshima, Yanan Liu, Takashi Tamiya, Aya Shinomiya, Toshifumi Itano, Masaaki Tokuda, and Takehiro Nakamura
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Male ,medicine.medical_specialty ,Time Factors ,Microdialysis ,Ischemia ,Glutamic Acid ,Hippocampus ,Brain damage ,Gerbil ,medicine.disease_cause ,Neuroprotection ,Drug Administration Schedule ,Internal medicine ,medicine ,Animals ,Lactic Acid ,Cerebral Cortex ,Neurons ,Analysis of Variance ,Movement Disorders ,business.industry ,General Neuroscience ,Glutamate receptor ,Deoxyguanosine ,medicine.disease ,Oxygen ,Disease Models, Animal ,Glucose ,Endocrinology ,8-Hydroxy-2'-Deoxyguanosine ,Ischemic Attack, Transient ,Anesthesia ,medicine.symptom ,Gerbillinae ,business ,Reperfusion injury ,Oxidative stress ,DNA Damage - Abstract
The present study investigates the neuroprotective effects of d-allose, a rare sugar, against ischemia/reperfusion injury in a gerbil model. Transient forebrain ischemia was induced by occlusion of the bilateral common carotid arteries for 5 min. D-Allose was intravenously injected before and after ischemia (200 mg/kg). Extracellular glutamate and lactate release from the gerbil brain, and PO₂ profiles were monitored during ischemia and reperfusion. We also examined neuronal death and oxidative damage in the hippocampus one week after ischemia reperfusion, and investigated functional outcome. D-Allose administration suppressed glutamate and lactate release compared to vehicle controls. Brain damage, 8-OHdG levels (a marker of oxidative stress) and locomotor activities were significantly decreased by D-allose treatment. The present results suggest that d-allose reduces delayed neuronal death and behavioral deficits after transient ischemia by changing cerebral metabolism and inhibiting oxidative stress.
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- 2014
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4. Ameliorative effects of yokukansan on behavioral deficits in a gerbil model of global cerebral ischemia
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Kazunori Sumitani, Toshifumi Itano, Feng Lu, Takehiro Nakamura, Tetsuhiko Toyoshima, Tohru Yamamoto, Richad F. Keep, Aya Shinomiya, Takashi Tamiya, and Yanan Liu
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Male ,Kampo ,Yokukansan ,Ischemia ,Motor Activity ,Pharmacology ,medicine.disease_cause ,Gerbil ,Neuroprotection ,Brain Ischemia ,Brain ischemia ,In Situ Nick-End Labeling ,Animals ,Medicine ,Maze Learning ,Molecular Biology ,Analysis of Variance ,Cell Death ,Dose-Response Relationship, Drug ,business.industry ,Mental Disorders ,General Neuroscience ,Apoptosis Inducing Factor ,medicine.disease ,Disease Models, Animal ,Anesthesia ,Neurology (clinical) ,Gerbillinae ,business ,Reperfusion injury ,Oxidative stress ,DNA Damage ,Drugs, Chinese Herbal ,Developmental Biology - Abstract
The aim of this study was to investigate the neuroprotective effects of yokukansan, a traditional Kampo medicine, on the behavioral dysfunction induced by cerebral ischemia/reperfusion injury in gerbils. Gerbils were treated with yokukasan by oral gavage for 30 days, once per day, until the day before induction of ischemia, which was induced by occluding the bilateral common carotid artery for 5 min. The effects of yokukansan (50, 100 and 300 mg/kg) were examined by measuring neuronal damage and behavioral deficits (locomotor activity, 8-arm radial maze task). The anti-inflammatory and anti-oxidant properties of yokukansan were also examined. Administration of yokukansan at 300 mg/kg significantly reduced hippocampal neuronal death after brain ischemia, inhibited the ischemia-induced inflammatory response and DNA oxidative damage. Yokukansan also reduced ischemia-induced locomotor hyperactivity and improved memory impairment. These findings suggest that yokukansan can inhibit the inflammatory response, oxidative damage and subsequent neuronal death induced by cerebral ischemia/reperfusion injury, and also can contribute to improvement in neurological deficits following such injury.
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- 2014
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5. Hyper-glucose metabolism in the cervical spinal cord of ALS patients
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Nozomi Hishikawa, Takashi Tamiya, Kota Sato, Yusuke Fukui, Tetsuhiro Hatakeyama, Toru Yamashita, Yoshihiro Nishiyama, Yasuyuki Ohta, Koji Abe, and Nobuyuki Kawai
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medicine.medical_specialty ,medicine.anatomical_structure ,Endocrinology ,Neurology ,business.industry ,Internal medicine ,medicine ,Neurology (clinical) ,Carbohydrate metabolism ,Spinal cord ,business - Published
- 2017
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6. Aldosterone induces myofibroblastic transdifferentiation and collagen gene expression through the Rho-kinase dependent signaling pathway in rat mesangial cells
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Akira Nishiyama, Hirofumi Hitomi, Guo-Xing Zhang, Suwarni Diah, Mas R.W. Abdul Hamid, Yukiko Nagai, Shoji Kimura, Takashi Tamiya, Wei Zhang, and Liu Gang
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medicine.medical_specialty ,Pyridines ,Spironolactone ,Biology ,Muscle Development ,Muscle hypertrophy ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Mineralocorticoid receptor ,Internal medicine ,Myosin ,medicine ,Animals ,Aldosterone ,Rho-associated protein kinase ,Mineralocorticoid Receptor Antagonists ,rho-Associated Kinases ,Mesangial cell ,Transdifferentiation ,Hypertrophy ,Cell Biology ,Amides ,Eplerenone ,Rats ,Receptors, Mineralocorticoid ,Endocrinology ,Gene Expression Regulation ,chemistry ,Cell Transdifferentiation ,Mesangial Cells ,Collagen ,Signal transduction ,Signal Transduction - Abstract
There is accumulating evidence indicating the role of aldosterone in the pathogenesis of hypertension and renal injury. In this study, we investigated the role of the Rho-kinase dependent signaling pathway in aldosterone-induced myofibroblastic transdifferentiation and collagen gene expression in rat mesangial cells (RMCs). Stimulation with aldosterone (1 nmol/L) significantly increased phosphorylation of myosin phosphatase target subunit-1 (MYPT-1), a marker of Rho-kinase activity, with a peak at 20 min in RMCs. Pre-incubation with a selective mineralocorticoid receptor antagonist, eplerenone (10 micromol/L), or a specific Rho-kinase inhibitor, Y27632 (10 micromol/L), attenuated the aldosterone-induced increase in MYPT-1 phosphorylation. Aldosterone also induced hypertrophy in RMCs, accompanied by an increase in actin polymerization and expression of alpha-smooth muscle actin (alpha-SMA), a myofibroblastic transdifferentiation marker. Collagen type I, III and IV mRNA levels were also increased with aldosterone stimulation. Pre-treatment with eplerenone or Y27632 prevented the aldosterone-induced cell hypertrophy, actin polymerization, the increase in alpha-SMA expression and the increases of collagen type I, III, IV mRNA levels in RMCs. These results suggest that aldosterone-induced mesangial cell hypertrophy is associated with cell transformation, leading to an increase in collagen gene expression via the Rho-kinase dependent signaling pathway.
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- 2008
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7. Effect of Delayed Mild Brain Hypothermia on Edema Formation After Intracerebral Hemorrhage in Rats
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Masahiko Kawanishi, Seigo Nagao, Nobuyuki Kawai, Takashi Tamiya, Chengyi Luo, and Takehiro Nakamura
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Male ,medicine.medical_specialty ,Time Factors ,Neutrophils ,Lameness, Animal ,Brain Edema ,medicine.disease_cause ,Neuroprotection ,Rats, Sprague-Dawley ,Lesion ,Brain ischemia ,chemistry.chemical_compound ,Hypothermia, Induced ,Internal medicine ,Edema ,medicine ,Animals ,Coloring Agents ,Gait Disorders, Neurologic ,Cerebral Hemorrhage ,Peroxidase ,Respiratory Burst ,Evans Blue ,Intracerebral hemorrhage ,business.industry ,Rehabilitation ,Brain ,Deoxyguanosine ,Recovery of Function ,Hypothermia ,medicine.disease ,Rats ,Oxidative Stress ,Endocrinology ,chemistry ,8-Hydroxy-2'-Deoxyguanosine ,Blood-Brain Barrier ,Anesthesia ,Surgery ,Neurology (clinical) ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,business ,Oxidative stress ,DNA Damage - Abstract
Secondary consequences of intracerebral hemorrhage (ICH) including inflammation, edema, and oxidative damage all contribute to cell death after ICH. Brain hypothermia (BH) has been used as an effective neuroprotective treatment in experimental brain ischemia and traumatic brain injury. In this study, we first attempted to evaluate the effect of delayed mild BH (35 degrees C) on brain edema formation 48 hours after ICH. BH was started 3, 6, 12, and 24 hours after the induction of 100 muL of autologous blood into the basal ganglia (hypothermic [HT]; HT3: n = 4, HT6: n = 6, HT12: n = 11, HT24: n = 6) in rats. To examine the protective mechanism of BH, blood-brain barrier (BBB) permeability to Evans blue, accumulation of polymorphonuclear leukocyte, and oxidative DNA damage in the lesion were compared between normothermic (NT) (37 degrees C) and HT6 rats 48 hours after ICH. Finally, neurologic recovery was assessed using behavioral tests in NT and HT6 rats 48 hours after ICH. Brain water content in the ispilateral basal ganglia was significantly reduced with delayed BT compared with NT (n = 7, 81.8 +/- 0.7% v HT3: 78.9 +/- 0.8%, P < .01; HT6: 78.7 +/- 0.6%, P < .01; HT12: 79.4 +/- 1.1%, P < .01; HT24: 80.3 +/- 0.6%, P < .01). The BBB disruption to Evans blue was significantly reduced with BH (HT6: n = 6) compared with NT (n = 6) rats in the ipsilateral basal ganglia (23.0 +/- 5.2 v 42.3 +/- 4.0 ng/g wet tissue, P < .05). HT6 treatment (n = 6) significantly inhibited the accumulation of polymorphonuclear leukocyte compared with NT treatment (n = 6) (0.43 +/- 0.22 v 1.49 +/- 0.61 DeltaAbs/mg tissue, P < .05). HT6 treatment (n = 3) also significantly reduced oxidative DNA damage determined with 8-hydroxyl-2'-deoxyguanosine compared with NT treatment (n = 3) (92 +/- 18 v 40 +/- 7 pg 8-hydroxyl-2'-deoxyguanosine/mug DNA, P < .05). Furthermore, HT6 treatment (n = 5) significantly improved neurologic recovery assessed with forelimb placing score compared with NT treatment (42.0 +/- 5.8 v 12.0 +/- 3.7, P < .05). In conclusion, mild BH significantly reduces the brain edema formation after ICH, even when the BH is applied 24 hours after hematoma induction in rats. Several neuroprotective mechanisms, including reduced BBB disruption, inflammation and oxidative damage, are suggested in this study.
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- 2008
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8. Chiari I malformation accompanied by assimilation of the atlas, Klippel-Feil syndrome, and syringomyelia: case report
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Takahiro Jinnai, Nobuyuki Kawai, Yoshihito Matsumoto, Katsuzo Kunishio, Takashi Tamiya, Seigo Nagao, and Masahiro Kagawa
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Klippel–Feil syndrome ,Humans ,Medicine ,Foramen Magnum ,Cervical Atlas ,Foramen magnum ,medicine.diagnostic_test ,business.industry ,Occipital bone ,Magnetic resonance imaging ,Anatomy ,Middle Aged ,Decompression, Surgical ,medicine.disease ,Spinal cord ,Magnetic Resonance Imaging ,Spinal column ,Syringomyelia ,Arnold-Chiari Malformation ,medicine.anatomical_structure ,Klippel-Feil Syndrome ,Female ,Surgery ,Neurology (clinical) ,Tomography, X-Ray Computed ,business ,Vertebral column - Abstract
Background Chiari I malformation, accompanied by superposed bony anomaly of the craniovertebral junction, is comparatively rare. We report a case of Chiari I malformation accompanied by assimilation of the atlas, Klippel-Feil syndrome, and syringomyelia. Case Description The patient was a 61-year-old woman demonstrating numbness of the extremities, sensory impairment, muscular weakness, and tendon hyper-reflexia. X-ray images and CT scans demonstrated assimilation of the atlas to the occipital bone, C2 and C3 fusion, abnormal passage of the vertebral arteries, and an anomalous bony mass on the right lateral mass of the atlas protruding into the spinal column. The odontoid process was also deviated to the left. Magnetic resonance images demonstrated bilateral descent of the cerebellar tonsils and syringomyelia extending from C6 to T8. Computed tomographic scans with the head rotated to the right demonstrated increased narrowing of the vertebral column caused by the right lateral mass of the atlas, and MR images confirmed exaggerated deformation of the spinal cord at the same region. This deformation manifested no neurologic symptoms, and we therefore performed foramen magnum decompression and duraplasty using Gore-Tex (W.L. Gore & Associates, Inc., Flagstaff, AZ). In the early postoperative period, neurologic symptoms improved. Conclusion We believe it is important that a treatment plan for Chiari I malformation accompanied by bony anomaly of the craniovertebral junction be determined based on morphologic investigation of the region supplemented by dynamic imaging–based evaluation of instability, or a careful inspection for atypical passage of the vertebral arteries, a frequent site of complication.
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- 2006
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9. A Case of Solitary Subependymal Giant Cell Astrocytoma
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Shigeru Daido, Takashi Tamiya, Tomotsugu Ichikawa, Isao Date, Yo Niida, Akiko Wakisaka, Shoichi Koizumi, and Soichiro Takao
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Genetics ,congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Subependymal giant cell astrocytoma ,Somatic cell ,Brain tumor ,Astrocytoma ,Biology ,medicine.disease ,nervous system diseases ,Pathology and Forensic Medicine ,Loss of heterozygosity ,Tuberous sclerosis ,medicine ,Molecular Medicine ,Missense mutation ,TSC2 - Abstract
Subependymal giant cell astrocytoma (SEGA) is a unique brain tumor arising in tuberous sclerosis complex (TSC), an autosomal dominant inherited phacomatosis. There are several case reports of solitary SEGA without any other manifestations of TSC. Usually these cases are thought to be forme fruste of TSC due to somatic mosaicism. However, no previous reports have used molecular methodology to fully investigate mutations in TSC genes or the possibility of somatic mosaicism. Here, we report a 20-year-old woman with a brain tumor. Pathological diagnosis was consistent with SEGA, but comprehensive clinical screening found no other lesions indicative of TSC. Molecular analysis of the tumor revealed loss of heterozygosity and allelic mutation (5228G>A, R1743Q) of TSC2. To detect the small fraction of mosaic mutation in somatic cells, we developed a highly sensitive new method: triple-nested polymerase chain reaction-restriction fragment length polymorphism. The identical TSC2 missense mutation was not detected in any other tissues from the same patient, including peripheral blood, buccal mucosa, urinary sediment, nail, and hair. According to these results, this patient should be considered as having SEGA that developed from two somatic hit mutations in TSC2, rather than being a TSC2 patient with a very small fraction of somatic mosaicism.
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- 2005
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10. Mesenchymal stem cells that produce neurotrophic factors reduce ischemic damage in the rat middle cerebral artery occlusion model
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Kazunori Kato, Osamu Honmou, Hirofumi Hamada, Sachie Hirai, Masayoshi Kobune, Katsunori Sasaki, Isao Date, Yoshinori Ito, Kazuhiko Kurozumi, Kiminori Nakamura, Yutaka Kawano, Takashi Tamiya, Hiroaki Uchida, Keiji Ishii, and Kiyohiro Houkin
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Male ,medicine.medical_specialty ,medicine.medical_treatment ,Tetrazolium Salts ,Ciliary neurotrophic factor ,Brain Ischemia ,Cell therapy ,Neurotrophic factors ,Internal medicine ,Drug Discovery ,Genetics ,Glial cell line-derived neurotrophic factor ,Animals ,Humans ,Medicine ,Nerve Growth Factors ,Rats, Wistar ,Hematoxylin ,Molecular Biology ,Stroke ,Cells, Cultured ,Pharmacology ,Staining and Labeling ,biology ,business.industry ,Cerebral infarction ,Mesenchymal stem cell ,Infarction, Middle Cerebral Artery ,Mesenchymal Stem Cells ,Genetic Therapy ,medicine.disease ,Rats ,Disease Models, Animal ,Endocrinology ,Cytokine ,nervous system ,biology.protein ,Eosine Yellowish-(YS) ,Molecular Medicine ,business - Abstract
Mesenchymal stem cells (MSC) were reported to ameliorate functional deficits after stroke in rats, with some of this improvement possibly resulting from the action of cytokines secreted by these cells. To enhance such cytokine effects, we previously transfected the telomerized human MSC with the BDNF gene using a fiber-mutant adenovirus vector and reported that such treatment contributed to improved ischemic recovery in a rat transient middle cerebral artery occlusion (MCAO) model. In the present study, we investigated whether other cytokines in addition to BDNF, i.e., GDNF, CNTF, or NT3, might have a similar or greater effect in this model. Rats that received MSC-BDNF (P < 0.05) or MSC-GDNF (P < 0.05) showed significantly more functional recovery as demonstrated by improved behavioral test results and reduced ischemic damage on MRI than did control rats 7 and 14 days following MCAO. On the other hand, rats that received MSC-CNTF or MSC-NT3 showed neither functional recovery nor ischemic damage reduction compared to control rats. Thus, MSC transfected with the BDNF or GDNF gene resulted in improved function and reduced ischemic damage in a rat model of MCAO. These data suggest that gene-modified cell therapy may be a useful approach for the treatment of stroke.
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- 2005
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11. BDNF Gene-Modified Mesenchymal Stem Cells Promote Functional Recovery and Reduce Infarct Size in the Rat Middle Cerebral Artery Occlusion Model
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Osamu Honmou, Kazunori Kato, Takashi Tamiya, Katsunori Sasaki, Hiroaki Uchida, Masayoshi Kobune, Kiminori Nakamura, Yutaka Kawano, Isao Date, Kiyohiro Houkin, Yoshinori Ito, Hirofumi Hamada, Sachie Hirai, and Kazuhiko Kurozumi
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Stromal cell ,medicine.medical_treatment ,Genetic enhancement ,Genetic Vectors ,Ischemia ,DNA Fragmentation ,Pharmacology ,Mesenchymal Stem Cell Transplantation ,Adenoviridae ,Drug Discovery ,Genetics ,Animals ,Humans ,Medicine ,Molecular Biology ,business.industry ,Cerebral infarction ,Brain-Derived Neurotrophic Factor ,Mesenchymal stem cell ,Infarction, Middle Cerebral Artery ,Mesenchymal Stem Cells ,Genetic Therapy ,Anatomy ,Transfection ,medicine.disease ,Magnetic Resonance Imaging ,Rats ,Disease Models, Animal ,Phenotype ,Cytokine ,medicine.anatomical_structure ,Molecular Medicine ,Bone marrow ,business - Abstract
Examination of the clinical therapeutic efficacy of using bone marrow stromal cells, including mesenchymal stem cells (MSC), has recently been the focus of much investigation. MSC were reported to ameliorate functional deficits after stroke in rats, with some of this improvement possibly resulting from the action of cytokines secreted by these cells. To enhance such cytokine effects, we transfected telomerized human MSC with the BDNF gene using a fiber-mutant F/RGD adenovirus vector and investigated whether these cells contributed to improved functional recovery in a rat transient middle cerebral artery occlusion (MCAO) model. BDNF production by MSC-BDNF cells was 23-fold greater than that seen in uninfected MSC. Rats that received MSC-BDNF showed significantly more functional recovery than did control rats following MCAO. Specifically, MRI analysis revealed that the rats in the MSC-BDNF group exhibited more significant recovery from ischemia after 7 and 14 days. The number of TUNEL-positive cells in the ischemic boundary zone was significantly smaller in animals treated with MSC-BDNF compared to animals in the control group. These data suggest that MSC transfected with the BDNF gene may be useful in the treatment of cerebral ischemia and may represent a new strategy for the treatment of stroke.
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- 2004
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12. Angioplasty and coiling of ruptured aneurysm with symptomatic vasospasm: technical case report
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Takashi Ohmoto, Takashi Tamiya, Atsushi Katsumata, Kenji Sugiu, and Yasuhiro Ono
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Adult ,Male ,medicine.medical_specialty ,Percutaneous ,medicine.medical_treatment ,Aneurysm, Ruptured ,Aneurysm ,Angioplasty ,Occlusion ,medicine ,Humans ,Vasospasm, Intracranial ,cardiovascular diseases ,Embolization ,medicine.diagnostic_test ,Vascular disease ,business.industry ,Intracranial Aneurysm ,Vasospasm ,medicine.disease ,Embolization, Therapeutic ,Cerebral Angiography ,Surgery ,Treatment Outcome ,cardiovascular system ,Neurology (clinical) ,Radiology ,business ,Cerebral angiography - Abstract
BACKGROUND Treating a ruptured cerebral aneurysm during symptomatic vasospasm is very difficult. We describe the successful endovascular treatment of such a case and discuss its efficacy. CASE PRESENTATION A 34-year-old man had a sudden onset of severe headache. One week later, he was referred to our institute with gradually progressing right hemiparesis and global aphasia. Cerebral angiography demonstrated severe vasospasm of the left internal carotid artery system and an anterior communicating artery aneurysm. With the patient under general anesthesia, 90% occlusion of the aneurysm was achieved with detachable coils after successful dilatation of the spastic vessels. The patient had an uneventful postoperative course and his neurologic symptoms were improved. Seven months after the endovascular treatment, the enlarged neck remnant of the aneurysm was successfully clipped without difficulty. CONCLUSION The simultaneous treatment of a ruptured aneurysm and vasospasm with percutaneous transluminal angioplasty and coils can produce a better outcome for the patient.
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- 2003
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13. Quantitative analysis of growth-related factors in human pituitary adenomas
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Toshio Ogura, Fumio Otsuka, Takayoshi Yamauchi, Takashi Ohmoto, Hirofumi Makino, and Takashi Tamiya
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medicine.medical_specialty ,Adenoma ,Physiology ,Growth factor ,medicine.medical_treatment ,Clinical Biochemistry ,Basic fibroblast growth factor ,Biology ,medicine.disease ,Biochemistry ,Cellular and Molecular Neuroscience ,chemistry.chemical_compound ,Insulin-like growth factor ,Endocrinology ,medicine.anatomical_structure ,Anterior pituitary ,chemistry ,Epidermal growth factor ,Pituitary adenoma ,Internal medicine ,Acromegaly ,medicine - Abstract
To elucidate the contribution of growth factors to the development, growth and behavior of human pituitary adenomas, the authors used competitive reverse transcription-polymerase chain reactions to quantify expression of mRNAs for growth factors extracted from pituitary adenomas. As previously diagnosed by endocrinologic evaluation, the pituitary adenomas in this study consisted of six prolactin-producing, six growth hormone (GH)-producing, four follicle-stimulating hormone producing and six nonfunctioning adenomas. The mRNAs examined included those for platelet-derived growth factor (PDGF) B-chain, transforming growth factor (TGF)-β1, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF)-I and -II; proliferating cell nuclear antigen (PCNA) as an indicator of cell proliferation; and pituitary-specific transcription factor-1 (Pit-1) which is a nuclear transcription factor expressed in the anterior pituitary. All factors except the last were expressed in all adenomas, and expression of PDGF B-chain, TGF-β1, EGF, bFGF and IGF-II did not differ between the four adenoma varieties. Pit-1 was expressed only in GH- and prolactin-producing adenomas. PCNA expression also showed no differences. However, IGF-I mRNA in GH-producing adenomas was significantly lower than in prolactin-producing and nonfunctioning adenomas despite high serum IGF-I levels (1121±253 ng/ml). The analysis on IGF-I receptor mRNA was significantly lowered in GH-producing adenoma compared with the other types of adenoma. These findings suggest that the attenuation of negative feedback through the pituitary GH–IGF-I axis may be involved in development of GH-producing adenoma.
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- 1999
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14. Erratum to 'BDNF gene-modified mesenchymal stem cells promote functional recovery and reduce infarct size in the rat middle cerebral artery occlusion model' [Molecular Therapy 9: 189–197 (2004), doi:10.1016/j.ymthe.2003.10.012]
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Hirofumi Hamada, Sachie Hirai, Katsunori Sasaki, Kazuhiko Kurozumi, Osamu Honmou, Yoshinori Ito, Takashi Tamiya, Isao Date, Kazunori Kato, Kiyohiro Houkin, Kiminori Nakamura, Yutaka Kawano, Masayoshi Kobune, and Hiroaki Uchida
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Pharmacology ,Pathology ,medicine.medical_specialty ,business.industry ,Mesenchymal stem cell ,Infarct size ,Functional recovery ,Molecular therapy ,Bdnf gene ,Drug Discovery ,Genetics ,Molecular Medicine ,Medicine ,Middle cerebral artery occlusion ,business ,Molecular Biology - Abstract
The publisher regrets that several corrections requested by the authors were not completed.
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- 2004
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