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Your search keyword '"Takayama, Chihiro"' showing total 7 results
Start Over Author "Takayama, Chihiro" Publication Type Academic Journals
7 results on '"Takayama, Chihiro"'

1. Japanese Clinical Practice Guidelines for Rehabilitation in Critically Ill Patients 2023 (J-ReCIP 2023)

Author

Unoki, Takeshi, Hayashida, Kei, Kawai, Yusuke, Taito, Shunsuke, Ando, Morihide, Iida, Yuki, Kasai, Fumihito, Kawasaki, Tatsuya, Kozu, Ryo, Kondo, Yutaka, Saitoh, Masakazu, Sakuramoto, Hideaki, Sasaki, Nobuyuki, Saura, Ryuichi, Nakamura, Kensuke, Ouchi, Akira, Okamoto, Saiko, Okamura, Masatsugu, Kuribara, Tomoki, Kuriyama, Akira, Matsuishi, Yujiro, Yamamoto, Norimasa, Yoshihiro, Shodai, Yasaka, Taisuke, Abe, Ryo, Iitsuka, Takahito, Inoue, Hiroyasu, Uchiyama, Yuki, Endo, Satoshi, Okura, Kazuki, Ota, Kohei, Otsuka, Takahisa, Okada, Daisuke, Obata, Kengo, Katayama, Yukiko, Kaneda, Naoki, Kitayama, Mio, Kina, Shunsuke, Kusaba, Ryuichi, Kuwabara, Masanari, Sasanuma, Naoki, Takahashi, Masahiro, Takayama, Chihiro, Tashiro, Naonori, Tatsuno, Junko, Tamura, Takahiko, Tamoto, Mitsuhiro, Tsuchiya, Asuka, Tsutsumi, Yusuke, Nagato, Tadashi, Narita, Chihiro, Nawa, Tomohiro, Nonoyama, Tadayoshi, Hanada, Masatoshi, Hirakawa, Kotaro, Makino, Akiko, Masaki, Hirotaka, Matsuki, Ryosuke, Matsushima, Shinya, Matsuda, Wataru, Miyagishima, Saori, Moromizato, Masaru, Yanagi, Naoya, Yamauchi, Kota, Yamashita, Yuhei, Yamamoto, Natsuhiro, Liu, Keibun, Wakabayashi, Yuki, Watanabe, Shinichi, Yonekura, Hiroshi, Nakanishi, Nobuto, Takahashi, Tetsuya, and Nishida, Osamu

Published
2023
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2. ARDS clinical practice guideline 2021

Author

Nakashima, Takuro, Masunaga, Aiko, Tanaka, Aiko, Inoue, Akihiko, Higashi, Akiko, Tanikawa, Atsushi, Ujiro, Atsushi, Takayama, Chihiro, Kasugai, Daisuke, Kawakami, Daisuke, Ueno, Daisuke, Satoh, Daizoh, Kai, Shinichi, Ota, Kohei, Hagiwara, Yoshihiro, Hamaguchi, Jun, Fujii, Ryo, Hongo, Takashi, Kishihara, Yuki, Masunaga, Naohisa, Yamamoto, Ryohei, Okazaki, Satoru Robert, Uchimido, Ryo, Terayama, Tetsuro, Hokari, Satoshi, Sakamoto, Hitoshi, Dongli, Nakataki, Emiko, Tabata, Erina, Okazawa, Seisuke, Kotajima, Futoshi, Ishimaru, Go, Hoshino, Haruhiko, Yoshida, Hideki, Iwai, Hidetaka, Nakagawa, Hiroaki, Sugimura, Hiroko, Narumiya, Hiromichi, Okano, Hiromu, Nakamura, Hiroshi, Sugimoto, Hiroshi, Hashimoto, Hiroyuki, Ito, Hiroyuki, Dote, Hisashi, Imahase, Hisashi, Sato, Hitoshi, Katsurada, Masahiro, Osawa, Ichiro, Kamei, Jun, Maki, Jun, Sugihara, Jun, Takeshita, Jun, Fujimoto, Junichi, Ishikawa, Junichi, Kosaka, Junko, Shibata, Junpei, Hashimoto, Katsuhiko, Nakano, Yasushi, Kikuyama, Kazuki, Shimizu, Kazushige, Okada, Kazuya, Kawano, Keishi, Anan, Keisuke, Ota, Keisuke, Kano, Ken-ichi, Asano, Kengo, Hondo, Kenichi, Ishii, Kenji, Fujita, Kensuke, Ogawa, Kenta, Ito, Kentaro, Tokunaga, Kentaro, Ishii, Kenzo, Kusumoto, Kohei, Takimoto, Kohei, Yamada, Kohei, Naito, Koichi, Yamashita, Koichi, Yoshinaga, Koichi, Yamauchi, Kota, Murata, Maki, Konda, Makiko, Hamamoto, Manabu, Aga, Masaharu, Kashiura, Masahiro, Ishikawa, Masami, Ozaki, Masayuki, Kono, Michihiko, Kyo, Michihito, Hayashi, Minoru, Abe, Mitsuhiro, Sato, Mitsunori, Sakai, Mizu, Kainuma, Motoshi, Tominaga, Naoki, Iguchi, Naoya, Nakagawa, Natsuki, Aoki, Nobumasa, Nishioka, Norihiro, Miyashita, Norihisa, Seki, Nozomu, Ikebe, Ryo, Imai, Ryosuke, Tate, Ryota, Sato, Ryuhei, Miyakawa, Sachiko, Kazuma, Satoshi, Nakano, Satoshi, Tetsumoto, Satoshi, Yoshimura, Satoshi, Yoshitake, Shigenori, Hoshi, Shin-etsu, Ohki, Shingo, Sato, Shintaro, Yoshihiro, Shodai, Ihara, Shoichi, Yamamoto, Shota, Koide, Shunichi, Kimata, Shunsuke, Saito, Shunsuke, Yasuo, Shunsuke, Sekine, Shusuke, Mimuro, Soichiro, Wada, Soichiro, Sugimura, Sosuke, Ishihara, Tadashi, Kaneko, Tadashi, Nagato, Tadashi, Maruhashi, Takaaki, Tamura, Takahiro, Ohno, Takanori, Ichiyama, Takashi, Niwa, Takashi, Ueji, Takashi, Ogura, Takayuki, Kawasaki, Takeshi, Tanaka, Takeshi, Umegaki, Takeshi, Furukawa, Taku, Omura, Taku, Nagao, Takumi, Mayumi, Takuya, Taniguchi, Takuya, Yoshida, Takuya, Shimatani, Tatsutoshi, Murata, Teppei, Sato, Tetsuya, Sawamoto, Tohru, Koukei, Yoshifumi, Takehara, Tomohiro, Ueda, Tomomi, Katsuta, Tomoya, Nishino, Tomoya, Yokoyama, Toshiki, Higashijima, Ushio, Iwanaga, Wataru, Inoue, Yasushi, Iwashita, Yoshiaki, Yamada, Yoshie, Kubota, Yoshifumi, Suido, Yoshihiro, Tomioka, Yoshihiro, Fujimoto, Yoshihisa, Fujita, Yoshihito, Yamaguchi, Yoshikazu, Nakamura, Yoshimi, Abe, Yoshinobu, Eguchi, Yoshitomo, Oshima, Yoshiyasu, Fukuda, Yosuke, Iwasaki, Yudai, Yasufuku, Yuichi, Shono, Yuji, Nakatani, Yuka, Nakamori, Yuki, Ito, Yukie, Tanabe, Yuko, Nagamine, Yusuke, Nakamura, Yuta, Kurihara, Yutaro, Tasaka, Sadatomo, Ohshimo, Shinichiro, Takeuchi, Muneyuki, Yasuda, Hideto, Ichikado, Kazuya, Tsushima, Kenji, Egi, Moritoki, Hashimoto, Satoru, Shime, Nobuaki, Saito, Osamu, Matsumoto, Shotaro, Nango, Eishu, Okada, Yohei, Hayashi, Kenichiro, Sakuraya, Masaaki, Nakajima, Mikio, Okamori, Satoshi, Miura, Shinya, Fukuda, Tatsuma, Kamo, Tetsuro, Yatabe, Tomoaki, Norisue, Yasuhiro, Aoki, Yoshitaka, Iizuka, Yusuke, Kondo, Yutaka, Narita, Chihiro, Taito, Shunsuke, Hayashi, Takuya, Terayama, Takero, Kataoka, Jun, Nishimura, Tetsuro, Yonekura, Hiroshi, Ando, Koichi, Yoshida, Takuo, Masuyama, Tomoyuki, and Sanui, Masamitsu

Published
2022
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3. Involvement of the mitochondrial retrograde pathway in dihydrosphingosine-induced cytotoxicity in budding yeast.

Author

Takayama, Chihiro, Koga, Ayano, Sakamoto, Risa, Arita, Nobuaki, and Tani, Motohiro

Subjects
*MITOCHONDRIA, *SUPPRESSOR mutation, *YEAST, *CELLULAR signal transduction, *SPHINGOLIPIDS
Abstract

Sphingoid long-chain bases are essential intermediates of ceramides and complex sphingolipids, and function in the regulation of various signal transduction systems. Previously, we found that, in budding yeast, intracellularly accumulated dihydrosphingosine (DHS) causes mitochondrial reactive-oxygen species (ROS)-mediated cytotoxicity, which is much stronger than phytosphingosine. In this study, we screened for suppressor mutations that confer resistance to DHS, and identified RTG2 , which encodes upregulation of the mitochondrial retrograde signaling pathway (RTG pathway). Deletion of RTG3 encoding transcriptional factor for the RTG pathway suppressed the cytotoxicity of DHS, whereas deletion of MKS1 or point mutation of LST8 , both of which cause increased activity of the RTG pathway, enhanced the cytotoxicity. Moreover, the deletion of RTG3 also suppressed the DHS-induced increases in ROS levels. Finally, it was found that the RTG pathway is activated on DHS treatment. These results suggested that the cytotoxicity of DHS is partially mediated through activation of the RTG pathway. [Display omitted] • Three yeast mutants exhibiting resistance to dihydrosphingosine (DHS) were isolated. • Activation of the RTG pathway causes enhancement of the cytotoxic activity of DHS. • Loss of the RTG pathway suppresses the DHS cytotoxicity. • DHS causes activation of the RTG pathway. [ABSTRACT FROM AUTHOR]

Published
2022
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4. ROS-mediated synthetic growth defect caused by impaired metabolism of sphingolipids and phosphatidylserine in budding yeast.

Author

Toda, Takumi, Urita, Atsuya, Koga, Ayano, Takayama, Chihiro, and Tani, Motohiro

Subjects
GENETIC mutation, YEAST, CELL growth, REACTIVE oxygen species, METABOLISM
Abstract

Previously, we found that yeast exhibits a strong growth defect with the combination of a lack of gene involved in structural modification of sphingolipids and repression of the phosphatidylserine synthase gene. Here we found that the double gene mutation causes reactive oxygen species-mediated cell growth defect, which is suppressed by deletion of LEM3 encoding the subunit of phospholipid flippase. [ABSTRACT FROM AUTHOR]

Published
2020
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6. Loss of tolerance to multiple environmental stresses due to limitation of structural diversity of complex sphingolipids.

Author

Koga A, Takayama C, Ishibashi Y, Kono Y, Matsuzaki M, and Tani M

Subjects
Cell Membrane metabolism, DNA-Binding Proteins metabolism, Saccharomyces cerevisiae metabolism, Stress, Physiological, Transcription Factors metabolism, Saccharomyces cerevisiae Proteins metabolism, Sphingolipids metabolism
Abstract

Structural diversity of complex sphingolipids is important for maintenance of various cellular functions; however, the overall picture of the significance of this structural diversity remains largely unknown. To investigate the physiological importance of the structural diversity of complex sphingolipids, we here constructed a complex sphingolipid structural diversity disruption library in budding yeast, which comprises 11 mutants including with combinations of deletions of sphingolipid-metabolizing enzyme genes. The sensitivity of the mutants to various environmental stresses revealed that the more the structural variation of complex sphingolipids is limited, the more stress sensitivity tends to increase. Moreover, it was found that in mutant cells with only one subtype of complex sphingolipid, Slt2 MAP kinase and Msn2/4 transcriptional factors are essential for maintenance of a normal growth and compensation for reduced tolerance of multiple stresses caused by loss of complex sphingolipid diversity. Slt2 and Msn2/4 are involved in compensation for impaired integrity of cell walls and plasma membranes caused by loss of complex sphingolipid diversity, respectively. From these findings, it was suggested that loss of structural diversity of complex sphingolipids affects the environment of the cell surface, including both plasma membranes and cell walls, which could cause multiple environmental stress hypersensitivity.

Published
2022
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7. Efficacy of Higher Positive End-Expiratory Pressure Ventilation Strategy in Patients With Acute Respiratory Distress Syndrome: A Systematic Review and Meta-Analysis.

Author

Yamamoto R, Sugimura S, Kikuyama K, Takayama C, Fujimoto J, Yamashita K, Norisue Y, and Narita C

Abstract

Previous systematic reviews and meta-analyses assessing the pooled effects of higher positive end-expiratory pressure (PEEP) failed to show significantly reduced mortality in patients with acute respiratory distress syndrome (ARDS). Some new randomized controlled trials (RCTs) have been reported and an updated systematic review is needed to evaluate the use of higher PEEP in patients with ARDS. We searched MEDLINE, Cochrane Central Register of Controlled Trials (CENTRAL), EMBASE, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Igaku-Chuo-Zasshi, ICTRP, the National Institute of Health Clinical Trials Register, and the reference list of recent guidelines. We included RCTs to compare the higher PEEP ventilation strategy with the lower strategy in patients with ARDS. Two authors independently assessed the eligibility of the studies and extracted the data. The primary outcomes were 28-day mortality. The GRADE (Grading of Recommendations, Assessment, Development, and Evaluations) methodology was used to evaluate the certainty of the evidence. Among the 6530 screened records, 16 randomized trials involving 4150 patients were included in our meta-analysis. When comparing higher PEEP versus lower PEEP, the pooled risk ratio (RR) for 28-day mortality was 0.85 (15 studies, n=4108, 95% CI 0.72 to 1.00, I 2 =58%, low certainty of evidence). Subgroup analysis by study participants with a low tidal volume (LTV) strategy showed an interaction (P for interaction, 0.001). Our study showed that in patients with ARDS, the use of higher PEEP did not significantly reduce 28-day mortality compared to the use of lower PEEP., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2022, Yamamoto et al.)

Published
2022
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