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6. Blood Pressure Level and Variability During Long-Term Prasugrel or Clopidogrel Medication After Stroke

Author

Toyoda, Kazunori, primary, Yamagami, Hiroshi, additional, Kitagawa, Kazuo, additional, Kitazono, Takanari, additional, Nagao, Takehiko, additional, Minematsu, Kazuo, additional, Uchiyama, Shinichiro, additional, Tanahashi, Norio, additional, Matsumoto, Masayasu, additional, Nagata, Izumi, additional, Nishikawa, Masakatsu, additional, Nanto, Shinsuke, additional, Shirai, Toshiaki, additional, Abe, Kenji, additional, Ikeda, Yasuo, additional, Ogawa, Akira, additional, Ozaki, Yukio, additional, Go, Yoshinori, additional, Gi, Hidefuku, additional, Furui, Eisuke, additional, Kosaka, Satoru, additional, Uenohara, Hiroshi, additional, Fukuyama, Kozo, additional, Maruki, Chikashi, additional, Takenaka, Katsunobu, additional, Ogiichi, Tsuneaki, additional, Matsushima, Kazushi, additional, Osaki, Masato, additional, Nakagawa, Hidemitsu, additional, Aoki, Michio, additional, Sakai, Nobuyuki, additional, Kuroki, Kazuhiko, additional, Mori, Takahisa, additional, Uno, Eiichi, additional, Terasaki, Tadashi, additional, Metoki, Norifumi, additional, Naka, Takashi, additional, Ohnishi, Hideyuki, additional, Koyama, Hideki, additional, Ogihara, Kotaro, additional, Kiriyama, Hideki, additional, Oki, Shuuichi, additional, Murao, Kei, additional, Matsumoto, Masahiro, additional, Suzuki, Kazunari, additional, Saito, Shinjiro, additional, Suda, Sumio, additional, Sadatomo, Takashi, additional, Miyake, Hiroji, additional, Itamoto, Kouji, additional, Fujita, Keishi, additional, Ohashi, Toshihiko, additional, Ito, Hiroki, additional, Ito, Yasuhiro, additional, Dehara, Makoto, additional, Hitotsumatsu, Tsutomu, additional, Hirose, Makoto, additional, Nakagaki, Yusuke, additional, Takemura, Sunao, additional, Tomimitsu, Hiroyuki, additional, Izuta, Makoto, additional, Mekaru, Susumu, additional, Kin, Shigenari, additional, Akaike, Yuji, additional, Miyatake, Masaki, additional, Wada, Naomichi, additional, Shibata, Norio, additional, Koyama, Kazuo, additional, Ichikawa, Yasumitsu, additional, Torii, Tsuyoshi, additional, Nakane, Hiroshi, additional, Kobayashi, Yasushi, additional, Kida, Shinya, additional, Nishino, Shigeki, additional, Tabata, Hitoshi, additional, Sano, Motoki, additional, Fuｊigasaki, Hiroto, additional, Nagatsuka, Kazuyuki, additional, Koga, Masatoshi, additional, Fujita, Hitoshi, additional, Yasaka, Masahiro, additional, Nakahara, Kimihiro, additional, Tomiyama, Masahiko, additional, Fujita, Tsuneo, additional, Hoshi, Seiichiro, additional, Ota, Takahiro, additional, Orimo, Satoshi, additional, Momose, Yoshio, additional, Yamashita, Katsuhiro, additional, Shingaki, Tatsuya, additional, Kaku, Yasuhiko, additional, Terasawa, Hideo, additional, Kawamoto, Yukihiko, additional, Tokunaga, Yoshiharu, additional, Chiba, Kei, additional, Okada, Yoshio, additional, Yanai, Yoshimi, additional, Sato, Atsushi, additional, Miake, Hirotomo, additional, Imai, Shu, additional, Morimoto, Masanori, additional, Nunomura, Mitsuru, additional, Irie, Shinsuke, additional, Konno, Shu, additional, Kanzawa, Takao, additional, Hayase, Makoto, additional, Yoshino, Kimihiro, additional, Izumidani, Tomohiko, additional, Kanda, Masutaro, additional, Kurokawa, Shinichiro, additional, Kawada, Sanami, additional, Takase, Keiichiro, additional, Takashima, Hiroshi, additional, Haraguchi, Koichi, additional, Murai, Hiroshi, additional, Suzuki, Mikio, additional, Shimohata, Mitsuteru, additional, Takeuchi, Shigekazu, additional, Asakura, Ken, additional, Seguchi, Tatsuya, additional, Toba, Yasuyuki, additional, Nitta, Eishun, additional, Moriki, Akihito, additional, Koan, Yoko, additional, Kaneko, Yoshiro, additional, Suzuki, Hisahiko, additional, Yoshida, Yasumasa, additional, Naka, Yutaka, additional, Katayama, Shinji, additional, Imamura, Eiji, additional, Kazekawa, Kiyoshi, additional, Yu, Iwae, additional, Satoh, Akira, additional, Maruyama, Junichi, additional, Takahashi, Akira, additional, Arimoto, Hirohiko, additional, Hasegawa, Yasuhiro, additional, Fukazawa, Seiji, additional, Nishimura, Yasuaki, additional, Yamada, Tomonori, additional, Tsuji, Tetsuro, additional, Wakayama, Akatsuki, additional, Murao, Kenichi, additional, Tominaga, Atsushi, additional, Takaba, Hitonori, additional, Shimazaki, Mitsunori, additional, Ishibashi, Yasuhiro, additional, Oguni, Eiichi, additional, Kuroyanagi, Takayuki, additional, Tanno, Hirokazu, additional, Kawada, Norikazu, additional, Hondo, Hideki, additional, Matsuoka, Hideki, additional, Umemura, Toshitaka, additional, Hazama, Takanori, additional, Nishio, Masami, additional, Kawaba, Tomoyuki, additional, Wada, Hirochiyo, additional, Kamitsukasa, Ikuo, additional, Endo, Sumio, additional, Ueda, Toshihiro, additional, Narumi, Osamu, additional, Ino, Tadashi, additional, Yamada, Takeshi, additional, Urabe, Takao, additional, Ota, Koichi, additional, Kato, Tokunori, additional, Nomura, Kyoichi, additional, Ieda, Toshiaki, additional, Kagawa, Masahiro, additional, Mizota, Takamitsu, additional, Sueyoshi, Kenji, additional, Nakajima, Yoshikazu, additional, Fujita, Toshiaki, additional, Teramoto, Yoshifumi, additional, Mori, Katsuharu, additional, Takaya, Satoru, additional, Uemura, Kazuya, additional, Inukai, Akira, additional, Kubo, Michiya, additional, Takahashi, Ryoichi, additional, Takahashi, Tsutomu, additional, Kawauchi, Masamitsu, additional, Hirahara, Kazuho, additional, Matsumoto, Sadayuki, additional, Masuo, Osamu, additional, Nishi, Shinsuke, additional, Niwa, Jun, additional, Kubo, Naohiko, additional, Yamamoto, Kanji, additional, Watanabe, Sadayoshi, additional, Okuda, Satoshi, additional, Okamoto, Kensho, additional, Masago, Atsuo, additional, Ohuchi, Masafumi, additional, Harada, Kunihiko, additional, Hashimoto, Yoichiro, additional, Hayashi, Kentaro, additional, Fujita, Nobuya, additional, Mori, Shuichi, additional, Sakaguchi, Manabu, additional, Noda, Kosumo, additional, Aoki, Takeshi, additional, Nakase, Taizen, additional, Shibuya, Satoshi, additional, Kamei, Satoshi, additional, Kanbayashi, Chisaku, additional, Hattori, Naoyuki, additional, Takashima, Shutaro, additional, Manabe, Yasuhiro, additional, Kobayashi, Nobuaki, additional, Takano, Katsunobu, additional, Ajiki, Minoru, additional, Kondo, Yoshiyuki, additional, Hashikawa, Kazuo, additional, Ikezoe, Koji, additional, Morita, Mitsuya, additional, Sakai, Keiichi, additional, Toi, Sono, additional, Iwamura, Makoto, additional, Takeuchi, Juji, additional, Suenaga, Toshihiko, additional, Takao, Masaki, additional, Kimura, Takashi, additional, Ozaki, Akihiko, additional, Kadekaru, Tsutomu, additional, Kato, Tsutomu, additional, Yamashita, Kosuke, additional, Ago, Tetsuro, additional, Tamaru, Shinichi, additional, Sekijima, Yoshiki, additional, Ito, Hisashi, additional, Yamasaki, Masahiro, additional, Kawai, Hiromichi, additional, Imai, Keisuke, additional, Sekine, Tomoyuki, additional, Inoya, Hiroshi, additional, Sawada, Motoshi, additional, Mano, Kazuo, additional, Sonoo, Masahiro, additional, and Ikeda, Masaki, additional

Published
2021
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10. An NEFHfounder mutation causes broad phenotypic spectrum in multiple Japanese families

Author

Ando, Masahiro, Higuchi, Yujiro, Okamoto, Yuji, Yuan, Junhui, Yoshimura, Akiko, Takei, Jun, Taniguchi, Takaki, Hiramatsu, Yu, Sakiyama, Yusuke, Hashiguchi, Akihiro, Matsuura, Eiji, Nakagawa, Hiroto, Sonoda, Ken, Yamashita, Toru, Tamura, Akiko, Terasawa, Hideo, Mitsui, Jun, Ishiura, Hiroyuki, Tsuji, Shoji, and Takashima, Hiroshi

Abstract

Background and aims: Mutations in neurofilament genes have been linked to several neuromuscular disorders. The neurofilament heavy (NEFH) gene was identified as the causative gene of Charcot–Marie–Tooth disease type 2CC (CMT2CC) in 2016, with a toxic gain of function mechanism caused by the translation and aggregation of cryptic amyloidogenic element (CAE) in the 3′ untranslated region (UTR). But the NEFH-related clinical and genetic spectrums are still unclear in Japan. Methods: We analyzed all variants in the NEFHgene from our in-house whole-exome sequencing data, established from Japanese nationwide patients with neuromuscular disorders, including Charcot–Marie–Tooth (CMT) disease and spinal muscular atrophy (SMA). Results: We identified a c.3017dup (p.Pro1007Alafs*56) variant in NEFHfrom three families clinically diagnosed with CMT, and one family with SMA. In addition to the patients presented with typical peripheral neuropathies, pyramidal signs were observed from one CMT patient. Whereas the SMA patients showed severe characteristic weakness of triceps brachii and quadriceps femoris. All of these four families reside in Kagoshima Prefecture of Japan, and a following haplotype analysis strongly suggests a founder effect. Interpretation: This is the original report referring to a founder mutation in NEFH. The clinical diversity in our study, comprising CMT, with or without pyramidal signs, and SMA, suggest an extensive involvement of peripheral nerve, anterior horn cells, or both. Our findings broaden the phenotypic spectrum of NEFH-related disorders.

Published
2022
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16. A homozygous mutation of VWA3B causes cerebellar ataxia with intellectual disability.

Author

Toshitaka Kawarai, Atsushi Tajima, Yukiko Kuroda, Naoki Saji, Orlacchio, Antonio, Hideo Terasawa, Hirotaka Shimizu, Yasushi Kita, Yuishin Izumi, Takao Mitsui, Issei Imoto, Ryuji Kaji, Kawarai, Toshitaka, Tajima, Atsushi, Kuroda, Yukiko, Saji, Naoki, Terasawa, Hideo, Shimizu, Hirotaka, Kita, Yasushi, and Izumi, Yuishin

Subjects
CEREBELLAR ataxia, NEURODEGENERATION, CELL survival, VON Willebrand factor, AMINO acids, BLOOD coagulation factors, CEREBELLUM, CONSANGUINITY, GENEALOGY, GENETIC techniques, MAGNETIC resonance imaging, PEOPLE with intellectual disabilities, NEUROLOGIC examination, PROTEINS, ATROPHY, SEQUENCE analysis, GENOTYPES
Abstract

Background: Hereditary cerebellar ataxia constitutes a heterogeneous group of neurodegenerative disorders, occasionally accompanied by other neurological features. Genetic defects remain to be elucidated in approximately 40% of hereditary cerebellar ataxia cases in Japan. We attempted to identify the gene responsible for autosomal recessive cerebellar ataxia with intellectual disability.Methods: The present study involved three patients in a consanguineous Japanese family. Neurological examination and gene analyses were performed in all family members. We performed genome-wide linkage analysis including single nucleotide polymorphism arrays, copy-number variation analysis and whole exome sequencing. To clarify the functional alteration resulting from the identified mutation, we performed cell viability assay of cultured cells expressing mutant protein.Results: One homozygous region shared among the three patients on chromosomes 2p16.1-2q12.3 was identified. Using whole exome sequencing, six homozygous variants in genes in the region were detected. Only one variant, VWA3B c.A1865C, results in a change of a highly conserved amino acid (p.K622T) and was not present in control samples. VWA3B encodes a von Willebrand Factor A Domain-Containing Protein 3B with ubiquitous expression, including the cerebellum. The viability of cultured cells expressing the specific K622T mutation was proved to decrease through the activation of apoptotic pathway.Conclusions: Mutated VWA3B was found to be likely associated with cerebellar degeneration with intellectual disability. Although a rare cause of cerebellar degeneration, these findings indicate a critical role for VWA3B in the apoptosis pathway in neuronal tissues. [ABSTRACT FROM AUTHOR]

Published
2016
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22. [Cerebral peduncle infarction with pure dysarthria--case report].

Author

Kataoka S, Terasawa H, and Touji H

Subjects
Aged, 80 and over, Cerebral Infarction diagnosis, Diffusion Magnetic Resonance Imaging, Glossopharyngeal Nerve, Humans, Male, Posterior Cerebral Artery, Pyramidal Tracts, Vagus Nerve, Cerebral Infarction complications, Dysarthria etiology, Mesencephalon
Abstract

A 82 year-old male having a long history of hypertension was admitted for dysarthria. Neurological examination revealed dysarthria with mild disturbance of left-sided soft palate elevation. No lingual palsy nor facial weakness were noted. No motor weakness in the upper and lower extremities was noted. Diffusion-weighted image and T2 weighted image revealed a small high signal lesion localized in the medial one-third of the left cerebral peduncle. There were bilateral stenotic lesions of the posterior cerebral artery at P1 portion in intracranial magnetic resonance angiography. Pure dysarthria can be caused by disruption of the supranuclear fiber of glossopharyngeal and vagal nerve nucleus in the corticobulbar tract, which can be localized in the medial portion of the cerebral peduncle.

Published
2007

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