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2. List of participants

Author

M. Abe, M. Abo, T. Abukawa, J. Adachi, A. Agui, O. Aita, Y. Aiura, J. Ajello, O. Akaki, H. Akazawa, H. Aksela, S. Aksela, J. Allen, Z. Altun, K. Amemiya, M. Amusia, K. An, J. Andersen, S. Aoki, I. Arakawa, T. Araki, U. Arp, M. Asensio, Y. Awaya, K. Awazu, H. Azuma, Y. Azuma, Y. Baba, H. Bando, Z. Bao, U. Becker, P. Bengtsson, S. Bobashev, A. Bocquet, J. Breton, Y. Cai, C. Caldwell, C. Cauletti, A. Chainani, J. Che, C. Chen, L. Chen, X. Chen, N. Cherepkov, T. Cho, C. Christou, J. Chung, M. Couprie, S. Cramer, L. Da Silva, H. Daimon, K. Deguchi, D. Dessau, V. Dhanak, V. Dolmatov, W. Drube, S. Echigo, A. Ehresmann, S. Eisebitt, T. Ejima, A. Ejiri, O. Endo, J. England, Y. Enta, C. Fadley, J. Feldhaus, E. Filatova, M. Finazzi, M. Finkenthal, D. Fischer, U. Flechsig, K. Franzén, L. Frasinski, T. Fujikawa, A. Fujimori, S. Fujimori, M. Fujisawa, K. Fujita, M. Fujita, K. Fukui, H. Fukutani, J. Ghijsen, E. Gluskin, Q. Guo, P. Guyon, C. Hague, R. Hall, H. Hamamatsu, Z. Han, J. Hansen, T. Hanyu, N. Happo, T. Hara, I. Harada, Y. Harada, M. Hasegawa, S. Hasegawa, T. Hatano, P. Hatherly, T. Hattori, T. Hayaishi, T. Hayasi, C. Heck, U. Heinzmann, K. Hieda, K. Higashiyama, Y. Hirai, A. Hiraya, T. Hirayama, S. Hirose, A. Hishikawa, A. Hopkirk, Y. Horikawa, N. Hosaka, K. Huber, W. Huff, Z. Hussain, C. Hwang, K. Ibrahim, T. Ibuki, K. Ichikawa, M. Ichikawa, J. Igarashi, Y. Iguchi, K. Iimura, D. Iinuma, Y. Iketaki, H. Ikeura, S. Imada, Y. Imaizumi, A. Imanishi, H. Inokuchi, I. Inoue, M. Ishigame, E. Ishiguro, H. Ishii, T. Ishii, H. Ishijima, I. Ishizue, G. Isoyama, K. Ito, M. Itoh, Y. Itoh, M. Iwami, K. Iwano, K. Iwasaki, S. Iwata, C. Jacobsen, T. Jikimoto, T. Jo, L. Johansson, U. Johansson, K. Jouda, C. Jung, N. Kabachnik, G. Kaindl, A. Kakizaki, M. Kamada, A. Kamata, I. Kamenskikh, K. Kameta, K. Kamiya, Y. Kamiya, K. Kan'no, T. Kanomata, M. Kasaya, T. Kashiwakura, R. Kato, Y. Kato, R. Katoh, T. Kaurila, J. Kawai, T. Kawamura, Y. Kayanuma, K. Kaznacheyev, E. Kennedy, M. Kiguchi, H. Kihara, Y. Kimpara, A. Kimura, H. Kimura, K. Kimura, S. Kimura, T. Kinoshita, M. Kirm, E. Kisker, T. Kitade, M. Kitajima, Y. Kitajima, H. Kitamura, M. Kitaura, K. Kobayashi, M. Kobayashi, T. Koda, J. Kohagura, T. Koide, F. Koike, M. Koike, T. Koike, T. Koizumi, T. Kojima, K. Kondo, Y. Kondo, M. Kono, S. Kono, R. Korde, T. Koseki, N. Kosugi, A. Kotani, M. Kotani, N. Kouchi, M. Kowalski, M. Koyama, I. Koyano, M. Krause, J. Krupa, H. Kumigashira, T. Kuninobu, S. Kurita, M. Kusaka, G. Kutluk, P. Lablanquie, F. Lama, F. Larkins, C. Latimer, T. Lebrun, D. Lee, K. Lee, T. Lee, F. Legrand, B. Lewis, D. Li, I. Lindau, F. Liu, G. Lodha, E. Lu, A. Lushchik, I. Lyakhovskaya, N. Mårtensson, Y. Ma, S. Machida, F. Maeda, S. Maeyama, H. Maezawa, N. Manakov, G. Margaritondo, S. Masui, T. Masuoka, F. Matsui, T. Matsukawa, M. Matsumoto, S. Matsumoto, T. Matsushita, M. Matsuzawa, G. Mattogno, A. Messina, V. Mikhailin, K. Mimura, T. Minami, A. Misu, T. Mitsuishi, K. Mitsuke, R. Mitsumoto, T. Miyahara, T. Miyamae, N. Miyamoto, H. Miyauchi, T. Mizokawa, H. Morgan, I. Mori, T. Mori, P. Morin, Y. Morioka, J. Mosnier, I. Munro, E. Murakami, T. Murata, Y. Murata, T. Muro, I. Nagakura, S. Nagaoka, T. Nagata, L. Nahon, K. Nakagawa, I. Nakai, S. Nakai, Y. Nakai, H. Nakaishi, N. Nakajima, H. Nakamura, M. Nakamura, M. Nakatake, M. Nakazawa, H. Namatame, T. Namioka, T. Nanba, S. Naoe, K. Nasu, M. Neeb, I. Nenner, Y. Nishihara, H. Nishioka, M. Niwano, J. Nordgren, D. Norman, C. Nowak, R. Nyholm, H. Nylén, H. Ogasawara, T. Ogata, S. Oh, J. Ohara, H. Ohashi, T. Ohchi, K. Ohmori, A. Ohnishi, N. Ohno, T. Ohta, H. Oji, K. Okada, T. Okajima, T. Okane, T. Okuda, M. Okunishi, M. Okusawa, C. Olson, M. Onellion, I. Ono, K. Ono, J. Onsgaard, H. Onuki, M. Oshima, I. Ouchi, Y. Ouchi, M. Oura, C. Park, S. Park, R. Perera, Y. Petroff, E. Poliakoff, W. Pong, K. Prabhakaran, R. Pratt, M. Qvarford, O. Rader, S. Rahn, K. Randall, R. Reininger, R. Rosenberg, J. Rubensson, P. Sainctavit, N. Saito, T. Saito, T. Saitoh, Y. Saitoh, K. Sakamoto, M. Sakano, Y. Sakisaka, J. Samson, D. Sarma, T. Sasaki, T. Sasano, H. Sato, N. Sato, S. Sato, Y. Sato, E. Savchenko, W. Schattke, F. Schlachter, V. Schmidt, N. Schwentner, K. Seki, T. Sekiguchi, T. Sekitani, A. Sekiyama, H. Seno, M. Shafi, T. Sham, L. Sheng, C. Shi, T. Shidara, E. Shigemasa, H. Shimada, K. Shimada, I. Shimamura, Y. Shimizu, I. Shimoyama, S. Shin, H. Shiraga, M. Shirai, T. Shishidou, L. Shmaenok, K. Shobatake, M. Simon, N. Smith, K. Soda, A. Solov'yov, B. Sonntag, D. Spanke, V. Stankevitch, I. Steinberger, P. Steiner, S. Suga, H. Sugawara, D. Sutherland, I. Suzuki, M. Suzuki, N. Suzuki, S. Suzuki, T. Suzuki, Y. Taguchi, N. Takahashi, T. Takahashi, Y. Takakuwa, Y. Takata, K. Takatsuchi, A. Takeichi, H. Takenaka, Y. Takizawa, A. Tanaka, K. Tanaka, M. Tanaka, S. Tanaka, T. Tanaka, J. Tang, K. Tani, M. Taniguchi, T. Tayu, S. Terada, L. Terminello, H. Tezuka, Y. Tezuka, R. Thissen, M. Tinone, I. Tokue, B. Tonner, E. Toyota, P. Troussel, K. Ueda, Y. Ueda, N. Ueno, R. Uhrberg, M. Ukai, T. Umehara, T. Uozumi, T. Urisu, P. Vaeterlein, G. Van der Laan, M. Van Hove, P. Viane, J. Voss, X. Wang, M. Watanabe, N. Watanabe, Y. Watanabe, J. Weaver, J. West, E. van Wezenbeek, S. Whitfield, D. Woodruff, L. Wu, R. Wu, P. Xu, W. Xu, K. Yagi, S. Yagi, A. Yagishita, T. Yamada, T. Yamakawa, H. Yamamoto, M. Yamamoto, Y. Yamamoto, T. Yamanaka, K. Yamanouchi, K. Yamashita, M. Yanagihara, S. Yang, Y. Yang, H. Yeom, M. Yimagawa, R. Ynzunza, T. Yokoya, T. Yokoyama, A. Yoshida, H. Yoshida, K. Yoshi, D. Yoshimura, M. Yuri, T. Zama, P. Zeitoun, X. Zhang, Y. Zhang, G. Zimmerer, and R. Zimmermann

Published
1996
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5. LIST OF CONTRIBUTERS

Author

S. Abe, K. Adachi, K. Aoki, K. Bessho, D. Bloch, S. Chikazumi, M. Date, F.R. de Boer, P.F. de Châtel, P. de Groot, L.J. de Jongh, G. De Vos, V.V. Eremenko, P. Feldmann, S. Foner, J.J.M. Franse, P.H. Frings, S. Fujiwara, K. Fukamichi, Y. Fukushima, H. Fukutani, R.J. Gambino, R. Gersdorf, M. Guillot, K.G. Gurtovoj, K. Hanzawa, I. Harada, T. Harada, Z. Henkie, F. Herlach, K. Higashi, H. Hirabayashi, H. Hiroyoshi, M. Honda, H. Hori, A. Hoshi, H. Ido, M. Ikebe, A. Isihara, Y. Isikawa, Y. Iwasa, V. Jaccarino, P. Janssen, Y. Kakudate, T. Kaneko, T. Kasuya, K. Katagiri, K. Katsumata, G. Kiko, A.R. King, M. Kobayashi, T. Komatsubara, A. Kotani, N. Kunitomi, N. Kuroda, K. Kurosawa, M. Kusakabe, A.S. Lagutin, Z.-H. Lee, M.J. Leupold, Zhi-Yi Liu, A. Marchand, P.J. Markowski, H. Maruyama, T. Mashimo, M. Matsui, W.C.M. Mattens, T.R. McGuire, A. Menovsky, A. Misu, N. Miura, S. Miura, H. Miyajima, T. Miyazaki, H. Mollymoto, K. Motizuki, M. Motokawa, F.A. Muller, Y. Muto, K. Nagayama, Y. Nakagawa, K. Nakamura, K. Nakao, N. Niitsuma, Y. Nishina, S. Noguchi, K. Noto, K. Okuda, F. Ono, R. Orbach, V.I. Ozhogin, Shiao-Thur Pan, R. Pauthenet, J.C. Picoche, L.W. Roeland, P. Rub, L.G. Rubin, S. Saito, T. Sakakibara, K. Sato, T. Satoh, H.J. Schneider-Muntau, Bao-Gen Shen, T. Shintomi, Y. Shiwa, H. Suematsu, K. Sugiyama, N. Suzuki, T. Suzuki, Y. Takada, S. Takagi, K. Takegahara, K. Tanaka, T. Tsuda, S. Tsuge, J. Tuchendler, J.C. Vallier, J. Voiron, M. Wake, Yi-Zhong Wang, K. Watanabe, R.J. Weggel, J.E.C. Williams, J. Witters, E.P. Wohlfarth, J.C. Wolfrat, Yong-Sheng Wu, O. Yamada, S. Yamada, A. Yamagishi, H. Yamauchi, A. Yanase, Fu-Min Yang, H. Yashima, H. Yasuoka, M. Yoshida, T. Yosida, and Xi-Chao Zhao

Published
1983
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6. Final 3-year Results of the Dasatinib Discontinuation Trial in Patients With Chronic Myeloid Leukemia Who Received Dasatinib as a Second-line Treatment.

Author

Okada M, Imagawa J, Tanaka H, Nakamae H, Hino M, Murai K, Ishida Y, Kumagai T, Sato S, Ohashi K, Sakamaki H, Wakita H, Uoshima N, Nakagawa Y, Minami Y, Ogasawara M, Takeoka T, Akasaka H, Utsumi T, Uike N, Sato T, Ando S, Usuki K, Mizuta S, Hashino S, Nomura T, Shikami M, Fukutani H, Ohe Y, Kosugi H, Shibayama H, Maeda Y, Fukushima T, Yamazaki H, Tsubaki K, Kukita T, Adachi Y, Nataduka T, Sakoda H, Yokoyama H, Okamoto T, Shirasugi Y, Onishi Y, Nohgawa M, Yoshihara S, Morita S, Sakamoto J, and Kimura S

Subjects
Female, Follow-Up Studies, Fusion Proteins, bcr-abl genetics, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive blood, Leukemia, Myelogenous, Chronic, BCR-ABL Positive genetics, Male, Middle Aged, Recurrence, Remission Induction, Risk Factors, Treatment Outcome, Antineoplastic Agents therapeutic use, Dasatinib therapeutic use, Deprescriptions, Leukemia, Myelogenous, Chronic, BCR-ABL Positive drug therapy, Protein Kinase Inhibitors therapeutic use
Abstract

Introduction: We previously reported an interim analysis of the DADI (dasatinib discontinuation) trial. The results showed that 48% of patients with chronic myeloid leukemia in the chronic phase who maintained a deep molecular response (DMR) for ≥ 1 year could discontinue second- or subsequent-line dasatinib treatment safely at a median follow-up of 20 months. However, the results from longer follow-up periods would be much more useful from a clinical perspective., Patients and Methods: The DADI trial was a prospective, multicenter trial conducted in Japan. After confirming a stable DMR for ≥ 1 year, dasatinib treatment subsequent to imatinib or nilotinib was discontinued. After discontinuation, the loss of DMR (even of 1 point) was defined as stringent molecular relapse, thereby triggering therapy resumption. The predictive factors of treatment-free remission (TFR) were analyzed., Results: The median follow-up period was 44.0 months (interquartile range, 40.5-48.0 months). The estimated overall TFR rate at 36 months was 44.4% (95% confidence interval, 32.0%-56.2%). Only 2 patients developed a molecular relapse after the 1-year cutoff point. The presence of imatinib resistance was a significant risk factor for molecular relapse. Moreover, high natural killer cell and low γδ + T-cell and CD4 + regulatory T-cell (CD25 + CD127 low ) counts before discontinuation correlated significantly with successful therapy discontinuation., Conclusion: These findings suggest that discontinuation of second- or subsequent-line dasatinib after a sustained DMR of ≥ 1 year is feasible, especially for patients with no history of imatinib resistance. In addition, the natural killer cell count was associated with the TFR., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2018
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7. Different T-cell receptor repertoires between lesions and peripheral blood in acute graft-versus-host disease after allogeneic bone marrow transplantation.

Author

Kubo K, Yamanaka K, Kiyoi H, Fukutani H, Ito M, Hayakawa R, Ohno R, and Naoe T

Subjects
Acute Disease, Amino Acid Sequence, Base Sequence, Female, Graft vs Host Disease blood, Graft vs Host Disease genetics, Humans, Middle Aged, Molecular Sequence Data, Receptors, Antigen, T-Cell immunology, Transplantation, Homologous, Bone Marrow Transplantation adverse effects, Graft vs Host Disease immunology, Receptors, Antigen, T-Cell genetics
Abstract

From the viewpoint of T-cell receptor (TCR) repertoire, we studied the role of T cells in acute graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation (allo-BMT) from an HLA-identical sibling. By means of inverse polymerase chain reaction method and DNA sequencing, we analyzed TCR-alpha and -beta transcripts from GVHD lesions and peripheral blood (PB) in a patient with typical GVHD together with PB from donor. At the initial onset of GVHD, V alpha-7 and -19 subfamilies were oligoclonally expanded in the PB compared with those in the oral mucosal lesions. At the second onset, V alpha-2, and V beta-6 subfamilies were more frequently detected in the cutaneous lesion than in the PB. Some TCR transcripts were recurrently found either in the mucosal or cutaneous lesions (or in both) and not in the PB. Furthermore, some of recurrent TCR transcripts in the lesions shared V gene segments and common motifs of complementarity determining region-3. These findings suggested that T cells infiltrating the GVHD lesions recognized a limited kind of antigens presented by patient's tissues with GVHD, and that T-cell repertoire in the GVHD lesions was different from that in the PB.

Published
1996

8. Bernard-Soulier syndrome Kagoshima: Ser 444-->stop mutation of glycoprotein (GP) Ib alpha resulting in circulating truncated GPIb alpha and surface expression of GPIb beta and GPIX.

Author

Kunishima S, Miura H, Fukutani H, Yoshida H, Osumi K, Kobayashi S, Ohno R, and Naoe T

Subjects
Adult, Amino Acid Sequence, Antibodies, Antibodies, Monoclonal, Blood Platelets metabolism, DNA blood, DNA isolation & purification, DNA Primers, Female, Humans, Lymphocytes metabolism, Male, Molecular Sequence Data, Nuclear Family, Peptides immunology, Platelet Membrane Glycoproteins analysis, Platelet Membrane Glycoproteins biosynthesis, Polymerase Chain Reaction, Reference Values, Bernard-Soulier Syndrome blood, Bernard-Soulier Syndrome genetics, Platelet Membrane Glycoproteins genetics, Point Mutation, Serine
Abstract

The platelet membrane glycoprotein (GP)Ib/IX complex is composed of three polypeptides, GPIb alpha, GPIb beta, and GPIX, and functions as a platelet receptor for von Willebrand factor. All three subunits are reported to be requisite for efficient surface expression of the complex. The absence of the GPIb/IX complex on platelet membrane is the hallmark of a congenital qualitative platelet disorder, termed the Bernard-Soulier syndrome (BSS). We describe here the molecular basis of a novel variant phenotype of BSS in a female patient, designated as BSS Kagoshima. Her platelets completely lacked the surface expression of GPIb alpha, but expressed a residual amount of GPIb beta and GPIX. Unexpectedly, her platelets and plasma contained a truncated GPIb alpha polypeptide with an apparent molecular weight of 116 kD (under nonreducing conditions). The amounts of truncated protein were 23% and 60% of the normal values in platelets and plasma, respectively. The abnormal protein contained a normal amount of sialic acid as demonstrated by digestion with neuraminidase. DNA sequencing analysis showed a homozygous single nucleotide substitution from the serine codon (TCA) to a nonsense codon (TAA) at residue 444 in the GPIb alpha gene. The mutant gene generated a truncated GPIb alpha molecule lacking the transmembrane region and cytoplasmic tail. Her parents were heterozygotes for the mutation. These findings suggest that this type of truncated GPIb alpha was produced, normally glycosylated, and subsequently secreted into the plasma. Furthermore, the truncated GPIb alpha might be associated with the process of the surface expression of incomplete GPIb/IX complex, GPIb beta and GPIX.

Published
1994

9. Haemolytic uraemic syndrome during FK506 therapy.

Author

Ichihashi T, Naoe T, Yoshida H, Kiyoi H, Fukutani H, Kubo K, Yamauchi T, Saito H, and Ohno R

Subjects
Adult, Female, Humans, Bone Marrow Transplantation, Graft vs Host Disease drug therapy, Hemolytic-Uremic Syndrome chemically induced, Tacrolimus adverse effects
Published
1992
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