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Start Over Author "Sanada M" Publication Type Academic Journals
540 results on '"Sanada M"'

4. Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K-T, Alpermann, T, Kuo, M-C, Rostami, S, Matthews, J, Sanada, M, Liu, L-Z, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H-A, Malnassy, G, Ma, T, Garg, M, Ding, L-W, Sun, Q-Y, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, RA, Powell, BL, Lübbert, M, Chng, WJ, Tien, H-F, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, SM, Kantarjian, HM, Nowak, D, Hofmann, W-K, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L-Y, Mathews, V, and Koeffler, HP

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Oncology and Carcinogenesis, Cancer, Human Genome, Childhood Leukemia, Pediatric Cancer, Genetics, Rare Diseases, Hematology, Clinical Research, Pediatric, Cell Differentiation, DNA Mutational Analysis, DNA-Binding Proteins, Exome, Gene Expression Profiling, Humans, Leukemia, Promyelocytic, Acute, Nuclear Proteins, Recurrence, Transcription Factors, Immunology, Cardiovascular medicine and haematology, Clinical sciences, Oncology and carcinogenesis
Abstract

Acute promyelocytic leukemia (APL) is a subtype of myeloid leukemia characterized by differentiation block at the promyelocyte stage. Besides the presence of chromosomal rearrangement t(15;17), leading to the formation of PML-RARA (promyelocytic leukemia-retinoic acid receptor alpha) fusion, other genetic alterations have also been implicated in APL. Here, we performed comprehensive mutational analysis of primary and relapse APL to identify somatic alterations, which cooperate with PML-RARA in the pathogenesis of APL. We explored the mutational landscape using whole-exome (n=12) and subsequent targeted sequencing of 398 genes in 153 primary and 69 relapse APL. Both primary and relapse APL harbored an average of eight non-silent somatic mutations per exome. We observed recurrent alterations of FLT3, WT1, NRAS and KRAS in the newly diagnosed APL, whereas mutations in other genes commonly mutated in myeloid leukemia were rarely detected. The molecular signature of APL relapse was characterized by emergence of frequent mutations in PML and RARA genes. Our sequencing data also demonstrates incidence of loss-of-function mutations in previously unidentified genes, ARID1B and ARID1A, both of which encode for key components of the SWI/SNF complex. We show that knockdown of ARID1B in APL cell line, NB4, results in large-scale activation of gene expression and reduced in vitro differentiation potential.

Published
2016

5. Landscape of genetic lesions in 944 patients with myelodysplastic syndromes

Author

Haferlach, T, Nagata, Y, Grossmann, V, Okuno, Y, Bacher, U, Nagae, G, Schnittger, S, Sanada, M, Kon, A, Alpermann, T, Yoshida, K, Roller, A, Nadarajah, N, Shiraishi, Y, Shiozawa, Y, Chiba, K, Tanaka, H, Koeffler, HP, Klein, H-U, Dugas, M, Aburatani, H, Kohlmann, A, Miyano, S, Haferlach, C, Kern, W, and Ogawa, S

Subjects
Genetic Testing, Clinical Research, Rare Diseases, Human Genome, Genetics, Biotechnology, Cancer, Hematology, Adult, Aged, Aged, 80 and over, Female, Gene Frequency, Genetic Association Studies, Genetic Markers, High-Throughput Nucleotide Sequencing, Humans, Male, Middle Aged, Mutation, Mutation Rate, Myelodysplastic Syndromes, Polymorphism, Single Nucleotide, Prognosis, Proportional Hazards Models, Young Adult, next-generation sequencing, molecular markers, myelodysplastic syndromes, prognostic score, Clinical Sciences, Oncology and Carcinogenesis, Immunology
Abstract

High-throughput DNA sequencing significantly contributed to diagnosis and prognostication in patients with myelodysplastic syndromes (MDS). We determined the biological and prognostic significance of genetic aberrations in MDS. In total, 944 patients with various MDS subtypes were screened for known/putative mutations/deletions in 104 genes using targeted deep sequencing and array-based genomic hybridization. In total, 845/944 patients (89.5%) harbored at least one mutation (median, 3 per patient; range, 0-12). Forty-seven genes were significantly mutated with TET2, SF3B1, ASXL1, SRSF2, DNMT3A, and RUNX1 mutated in >10% of cases. Many mutations were associated with higher risk groups and/or blast elevation. Survival was investigated in 875 patients. By univariate analysis, 25/48 genes (resulting from 47 genes tested significantly plus PRPF8) affected survival (P

Published
2014

9. P037 - Topic: AS04-MDS Biology and Pathogenesis/AS04a-Normal, MDS, and leukemic stem cells: DER(1;7)(Q10;P10) DEFINES A DISTINCT SUBTYPE OF MYELODYSPLASIA

Author

Okuda, R., Ochi, Y., Saiki, R., Chonabayashi, K., Hiramoto, N., Sanada, M., Handa, H., Kasahara, S., Sato, S., Kanemura, N., Kitano, T., Watanabe, M., Kern, W., Creignou, M., Shiraishi, Y., Usuki, K., Imashuku, S., Hellstrom-Lindberg, E., Haferlach, T., Chiba, S., Sezaki, N., Shih, L.-Y., Miyazaki, Y., Yoshida, Y., Ishikawa, T., Ohyashiki, K., Atsuta, Y., Shiozawa, Y., Miyano, S., Makishima, H., Nannya, Y., and Ogawa, S.

Published
2023
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10. Somatic PHF6 mutations in 1760 cases with various myeloid neoplasms

Author

Mori, T, Nagata, Y, Makishima, H, Sanada, M, Shiozawa, Y, Kon, A, Yoshizato, T, Sato-Otsubo, A, Kataoka, K, Shiraishi, Y, Chiba, K, Tanaka, H, Ishiyama, K, Miyawaki, S, Mori, H, Nakamaki, T, Kihara, R, Kiyoi, H, Koeffler, H P, Shih, L-Y, Miyano, S, Naoe, T, Haferlach, C, Kern, W, Haferlach, T, Ogawa, S, and Yoshida, K

Published
2016
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14. O09 - Topic: AS04-MDS Biology and Pathogenesis/AS04b-Clonal diversity & evolution: MYELOID NEOPLASMS WITH GERMLINE AND SOMATIC DDX41 MUTATIONS

Author

Makishima, H., Nannya, Y., Momozawa, Y., Gurnari, C., Kulasekararaj, A., Yoshizato, T., Takeda, J., Atsuta, Y., Shiozawa, Y., Iijima-Yamashita, Y., Saiki, R., Yoshida, K., Shiraishi, Y., Nagata, Y., Onizuka, M., Nakagawa, M., Itonaga, H., Kanda, Y., Miyazaki, Y., Sanada, M., Tsurumi, H., Kasahara, S., Kondo-Takaori, A., Ohyashiki, K., Kiguchi, T., Matsuda, F., Jansen, J., Papaemmanuil, E., Creignou, M., Tobiasson, M., Hellström-Lindberg, E., Polprasert, C., Malcovati, L., Cazzola, M., Haferlach, T., Maciejewski, J., Kamatani, Y., Miyano, S., and Ogawa, S.

Published
2021
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27. Erratum: Comprehensive mutational analysis of primary and relapse acute promyelocytic leukemia

Author

Madan, V, Shyamsunder, P, Han, L, Mayakonda, A, Nagata, Y, Sundaresan, J, Kanojia, D, Yoshida, K, Ganesan, S, Hattori, N, Fulton, N, Tan, K T, Alpermann, T, Kuo, M C, Rostami, S, Matthews, J, Sanada, M, Liu, L-Z, Shiraishi, Y, Miyano, S, Chendamarai, E, Hou, H A, Malnassy, G, Ma, T, Garg, M, Ding, L W, Sun, Q Y, Chien, W, Ikezoe, T, Lill, M, Biondi, A, Larson, R A, Powell, B L, Lübbert, M, Chng, W J, Tien, H F, Heuser, M, Ganser, A, Koren-Michowitz, M, Kornblau, S M, Kantarjian, H M, Nowak, D, Hofmann, W K, Yang, H, Stock, W, Ghavamzadeh, A, Alimoghaddam, K, Haferlach, T, Ogawa, S, Shih, L Y, Mathews, V, and Koeffler, H P

Published
2016
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34. General Lectures-(II)

Author

Toriie, S., Nakajima, M., Kohli, Y., Takebayashi, M., Misaki, F., Kobayashi, A., Hashimoto, Y., Mitsuyoshi, Y., Ida, K., Kawai, K., Fujita, R., Kumura, F., Takahashi, M., Ohsawa, H., Hasegawa, Y., Kidokoro, T., Jojima, Y., Miyoshi, H., Okumura, Y., Yokouchi, A., Asano, H., Uehara, A., Oka, S., Saito, H., Yaginuma, M., Yamamoto, T., Asano, A., Nakamura, M., Okada, Y., Tomioka, T., Tamesue, N., Ikeda, S., Kunisaki, T., Emura, T., Yasumoto, M., Someya, N., Goto, A., Morokuma, K., Sakamoto, H., Kasaki, Y., Imamura, K., Amano, I., Iwanaga, K., Okugawa, N., Ninomiya, K., Yoshida, S., Okabe, N., Shimogawa, Y., Nakajima M., Ida, K., Akasaka, Y., Shimamoto, K., Misaki, F., Toriie, S., Tada, M., Sugawara, K., Chikayasu, I., Takeda, H., Kawai, K., Shibue, T., Yamaguchi, A., Osame, T., Shimada, K., Hori, M., Irisa, T., Miura, Y., Hanamure, B., Chuman, Y., Sato, H., Kizu, M., Kasugai, T., Kuno, N., Aoki, I., Nitta, Y., Machii, A., Murakami, Y., Aiso, Y., Kitahara, N., Yoshizawa, Y., Hishinuma, Y., Nao, Y., Ishiyama, K., Watanabe, M., Kimura, T., Hara, T., Sakaue, S., Shinoda, T., Ito, R., Hayashi, K., Sugie, H., Sekizawa, H., Nakamura, S., Kondo, J., Tanaka, E., Taniguchi, T., Kanayama, M., Koizumi, S., Watabiki, S., Ikeda, S., Tamura, K., Okada, Y., Arai, T., Saito, T., Tojo, S., Furuya, M., Hanaue, H., Ogoshi, K., Murohisa, B., Uchimura, M., Ishigaki, J., Waki, S., Nakafuji, H., Iida, F., Aratake, K., Nakano, T., Ono, N., Hara, I., Sassa, T., Takahashi, T., Inoue, J., Maruyama, Y., Mori, Y., Kawamura, T., Imai, F., Yorita, S., Saegusa, M., Ishihara, F., Asukata, I., Matsuda, M., Wakabayashi, K., Mitani, S., Sugahara, K., Ishikawa, K., Nakayoshi, A., Nakamoto, M., Kono, A., Oda, T., Sato, Y., Takahashi, T., Nagao, F., Nagano, M., Furusawa, T., Nakama, T., Itoh, H., Nishimura, M., Tsutsumi, K., Saito, H., Yoshida, K., Ito, H., Yoshimura, M., Yoshioka, K., Shimizu, T., Kuroda, C., Uchida, H., Ishida, O., Inoue, T., Hasegawa, S., Mitsusada, K., Kajiyama, Y., Matsuzawa, Y., Yokota, K., Hayashida, Y., Ikegudhi, S., Shida, S., Tsurumi, K., Ito, K., Kamiya, K., Takada, H., Ueno, S., Onda, M., Kojima, G., Shoji, E., Miyaji, M., Goto, K., Nitta, Y., Yazaki, Y., Ito, M., Kozuka, M., Tanabe, A., Murate, H., Takeuchi, T., Koshikawa, M., Kato, N., Maeda, K., Hayashi, K., Tsuru, T., Ooyama, I., Kukimoto, H., Nakashima, Y., Katsuki, T., Ueda, N., Kanno, T., Noda, A., Toda, Y., Hayakawa, T., Nakajima, S., Morishita, R., Furukawa, K., Ikeda, F., Fujii, M., Yamamoto, T., Wakisaka, G., Matasumoto, Y., Ono, H., Hirose, S., Kobayashi, K., Sawabu, N., Takeuchi, J., Kajikawa, K., Takada, A., Hirai, Y., Ohki, I., Sato, K., Tasaka, S., Sato, A., Aono, G., Kidokoro, T., Takezoe, K., Jojima, Y., Ohara, T., Soma, S., Ukawa, S., Yamaguchi, S., Shirahama, T., Sugiyama, K., Koyama, H., Haga, M., Arikawa, H., Toyokawa, H., Sato, R., Ueno, Y., Karasawa, Y., Onuma, H., Suzuki, H., Murakami, T., Yasui, A., Ichinose, Y., Hirase, Y., Okazaki, T., Takai, T., Watanabe, K., Kato, M., Yamada, M., Tsuji, T., Kunito, Y., Kobayashi, S., Udo, K., Iriyama, K., Sugiura, Y., Takahashi, Y., Kawamura, O., Ando, S., Hayashi, K., Tsuji, K., Yukawa, Y., Saito, N., Miyazawa, M., Imai, K., Tabayashi, T., Ito, H., Umehara, S., Watanabe, Y., Murai, S., Nukaga, A., Ishimatsu, N., Sotoyama, S., Abe, M., Hirai, K., Yoshida, K., Aoki, T., Nagao, F., Aoki, Y., Taniguchi, K., Wada, N., Tabuse, K., Yanagi, I., Tsuhada, K., Katsumi, M., Nakamura, K., Takemoto, K., Yamaura, Y., Karibe, N., Yamada, G., Ichikawa, H., Ogiwara, M., Matsushita, M., Kobayashi, I., Kusano, M., Yasuna, O., Hayashi, S., Yoshizumi, M., Kojima, Y., Matsubayashi, K., Yamamoto, T., Nishimura, R., Koga, M., Tachibana, M., Kurata, M., Suto, H., Ichinose, I., Ishizuka, K., Shimoda, M., Onai, M., Akiyama, T., Sekiguchi, T., Kobayashi, S., Matsuyoshi, M., Yonezawa, N., Kasamatsu, M., Yokota, Y., Toyoda, T., Uchimoto, I., Kanamoto, M., Fukai, Y., Sugawara, K., Katoh, M., Takebayashi, M., Mitsuyoshi, Y., Shimamoto, K., Nakamura, I., Tamura, M., Nishio, M., Mukaide, Y., Kuzumoto, Y., Ota, K., Yoshida, T., Sakamoto, A., Akiyama, T., Kaneko, S., Yanagida, M., Kishimoto, S., Miyaji, K., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Shiraki, Y., Inoue, K., Tamada, T., Usui, T., Ohtsuka, K., Yamada, S., Fujishima, S., Tamiya, A., Saji, K., Ueda, A., Yasutake, K., Irie, K., Ijiri, Y., Sato, H., Nishijima, H., Ogino, K., Okuno, T., Date, H., Yao, T., Koga, Y., Tomioka, T., Fuyuno, S., Okabe, H., Mitsui, H., Tamechika, Y., Masuda, N., Fujiwara, T., Sakimura, M., Okada, Y., Takamura, Y., Kono, T., Kurihara, M., Sumida, M., Izumi, T., Haraikawa, M., Hayakawa, H., Shirakabe, H., Yasui, A., Ushio, K., Okamoto, M., Noguchi, M., Kinoshita, A., Yamada, T., Ichikawa, H., Shimotori, K., Kudo, T., Mukaida, I., Ishikawa, H., Sato, K., Shirane, T., Kano, A., Suzuki, T., Tanaka, M., Iwanaga, T., Taniguchi, H., Inawashiro, M., Endo, N., Kawamura, T., Suzuki, Sh., Suzuki, H., Maki, T., Hayakawa, K., Ikezawa, H., Jao, C. C., Yamada, K., Nakamura, M., Tanaka, M., Maruyama, M., Nagasako, K., Oi, I., Kozu, T., Yamashita, K., Yokoyama, I., Endo, M., Takemoto, T., Nakayama, K., Hayakawa, R., Ishiguro, M., Nakano, H., Nakazawa, S., Tsuboi, Y., Yamase, H., Yamashita, T., Fujita, T., Ishikawa, Y., Ito, N., Mitsuno, T., Kanazawa, K., Yamashiro, M., Kubo, T., Iizuka, H., Watanabe, T., Sanada, M., Satoh, H., Shimada, H., Kusama, S., Ishikawa, K., Ikeda, K., Naramoto, J., Koga, M., Okazaki, Y., Nakamura, K., Kawamura, S., Fujimoto, S., Urayama, S., Matsuura, H., Sekitani, T., Sasayama, T., Nakagawa, K., Toyama, K., Nakagawa, S., Takada, T., Kusaka, K., Takaba, S., Satomura, A., Suzuki, T., Kawakami, Y., Watanabe, Y., Suzuki, H., Koike, T., Joh, S., Hara, T., Tamura, K., Kobayagawa, K., Hashimoto, T., Uemura, F., Fukui, O., Takahashi, M., Takasato, Y., Shirakawa, K., Hisamatsu, M., Saito, T., Ashizawa, S., Sakurane, Y., Miyamura, K., Sasaki, H., Katsumi, M., Ura, S., Emoto, M., Tatsumi, Y., Totsuka, Y., Chiba, N., Ozeki, M., Nakazawa, M., Takamura, S., Iida, F., Sawano, Y., Sugita, T., Funabiki, T., Watanabe, S., Moriya, T., Tomita, N., Nishida, K., Todo, A., Miyake, T., Suzaki, Y., Yamamoto, Y., Ariyoshi, J., Hajiro, K., Oishi, M., Yanagihara, K., Nakamura, A., Kuramata, H., Soeda, S., Kondo, N., Akashi, M., Hemmi, T., Kadono, H., Ito, T., Tsuchiya, R., Ikeda, Y., Futatsuki, K., Nomoto, S., Kino, I., Arai, M., Shimazu, H., Kobori, O., Ishikawa, K., Hiroshima, Y., Matsusaka, Y., Katase, K., Sakuma, Y., Murata, N., Komura, K., Ando, H., Ohara, K., Hayashi, A., Suzuki, M., Watanuki, T., Asano, T., Koide, N., Shiobara, M., Matsuo, N., Imai, K., Segawa, K., Nakazawa, S., Okabe, N., Kawai, K., Matsumoto, K., Shimada, H., Machida, K., Koizumi, Y., Hoshi, Y., Oi, M., Watanuki, T., Seki, H., Matsumura, M., Kimura, M., Yoshimura, M., Ishikawa, I., Kishi, S., Kondo, Y., Uchida, Y., Harada, H., Mandai, M., Kikuchi, T., Mishima, K., Yamagata, Y., Suyama, T., Kawagoe, K., Inagawa, T., Kishimoto, S., Sugiya, T., Kai, T., Miyoshi, A., Fukumoto, S., Watanabe, K., Kojo, H., Turuhara, I., Miyoshi, Y., Okamoto, K., Inata, H., Okamoto, H., Sakurai, S., Sugiyama, M., Sasaki, H., Miura, K., Kurihara, T., Sakumoto, K., Okita, E., Tanaka, H., Ishihara, K., Okawa, M., Okumura, Y., Watanabe, Y., Nishizaki, N., Murakami, T., Saito, K., Aoyagi, K., Hamaguchi, E., Kitamura, T., Matsuo, Y., Seki, A., Mori, H., Ishikawa, T., Nakajima, T., Shimomura, T., Sengoku, K., Aoyagi, K., Hamaguchi, E., Uchiya, Y., Yabana, T., Konta, M., Kamijo, K., Yachi, A., Okuse, S., Ohara, H., Sato, K., Wada, T., Kurata, M., Furuta, K., Nishii, M., Yamawaki, T., Nishii, K., Umeda, K., Yoshida, H., Ito, H., Okabayashi, T., Kato, Y., Yatsuji, Y., Suzuki, Y., Nomura, K., Matsumoto, K., Kamisaka, K., Motoki, T., Kamii, K., Kameda, H., Imamura, H., Uchiya, T., Ishizawa, M., Nishizaki, H., Murakami, T., Orimo, H., Yoshida, A., Yoshida, A., Orimo, H., Fujita, T., Oda, T., Itoh, Z., Honda, R., Takeuchi, S., Fukushima, T., Suda, T., Shinonaga, M., Ishiguro, N., Fujisawa, S., Nishiyama, K., and Ohkubo, T.

Published
1973
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41. A novel protein, MAPO1, that functions in apoptosis triggered by O6-methylguanine mispair in DNA.

Author

Komori, K., Takagi, Y., Sanada, M., Lim, T.-H., Nakatsu, Y., Tsuzuki, T., Sekiguchi, M., and Hidaka, M.

Subjects
PROTEINS, APOPTOSIS, MUTAGENESIS, DNA replication, METHYL methanesulfonate, GENETIC mutation, PHOSPHORYLATION
Abstract

O6-Methylguanine produced in DNA induces mutation due to its ambiguous base-pairing properties during DNA replication. To suppress such an outcome, organisms possess a mechanism to eliminate cells carrying O6-methylguanine by inducing apoptosis that requires the function of mismatch repair proteins. To identify other factors involved in this apoptotic process, we performed retrovirus-mediated gene-trap mutagenesis and isolated a mutant that acquired resistance to a simple alkylating agent, N-methyl-N-nitrosourea (MNU). However, it was still sensitive to methyl methanesulfonate, 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea, etoposide and ultraviolet irradiation. Moreover, the mutant exhibited an increased mutant frequency after exposure to MNU. The gene responsible was identified and designated Mapo1 (O6-methylguanine-induced apoptosis 1). When the expression of the gene was inhibited by small interfering RNA, MNU-induced apoptosis was significantly suppressed. In the Mapo1-defective mutant cells treated with MNU, the mitochondrial membrane depolarization and caspase-3 activation were severely suppressed, although phosphorylation of p53, CHK1 and histone H2AX was observed. The orthologs of the Mapo1 gene are present in various organisms from nematode to humans. Both mouse and human MAPO1 proteins expressed in cells localize in the cytoplasm. We therefore propose that MAPO1 may play a role in the signal-transduction pathway of apoptosis induced by O6-methylguanine-mispaired lesions.Oncogene (2009) 28, 1142–1150; doi:10.1038/onc.2008.462; published online 12 January 2009 [ABSTRACT FROM AUTHOR]

Published
2009
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43. A computer-aided diagnosis system to screen for osteoporosis using dental panoramic radiographs.

Author

Nakamoto, T., Taguchi, A., Ohtsuka, M., Suei, Y., Fujita, M., Tsuda, M., Sanada, M., Kudo, Y., Asano, A., and Tanimoto, K.

Subjects
PANORAMIC radiography, MEDICAL radiography, DIAGNOSTIC imaging, COMPUTER systems, OSTEOPOROSIS in women, MEDICAL research
Abstract

Objectives: An eroded inferior cortex of the mandible detected on dental panoramic radiographs is useful for identifying post-menopausal women with low skeletal bone mineral density (BMD) or osteoporosis. The purposes of this study were to develop a computer-aided diagnosis (CAD) system that automatically determines cortical erosion of the mandible on dental panoramic radiographs and to assess the validation of this CAD system. Methods: A CAD system was developed based on mathematical morphology for identifying post-menopausal women with low skeletal BMD or osteoporosis, based on World Health Organization criteria, by identifying whether the endosteal margin of mandibular cortical bone was eroded. The sensitivity, specificity, predictive value, accuracy and likelihood for a positive risk result were calculated using dichotomous 2 × 2 tables using 100 panoramic radiographs. Results: For identifying women with low skeletal BMD, the sensitivity and specificity were 76.8% and 61.1%, respectively, the positive and negative predictive values were 90.0% and 36.7%, accuracy was 74.0% and the likelihood for positive risk was 1.96. The respective values for identifying women with osteoporosis were 94.4% and 43.8%, the positive and negative predictive values were 48.6% and 93.3%, respectively, the accuracy was 62.0% and the likelihood for positive risk was 1.68. Conclusion: Our results suggest that a CAD system applied to dental panoramic radiographs may be useful for identifying post-menopausal women with low skeletal BMD or osteoporosis. [ABSTRACT FROM AUTHOR]

Published
2008
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44. ERCC5 is a novel biomarker of ovarian cancer prognosis.

Author

Walsh CS, Ogawa S, Karahashi H, Scoles DR, Pavelka JC, Tran H, Miller CW, Kawamata N, Ginther C, Dering J, Sanada M, Nannya Y, Slamon DJ, Koeffler HP, Karlan BY, Walsh, Christine S, Ogawa, Seishi, Karahashi, Hisae, Scoles, Daniel R, and Pavelka, James C

Published
2008
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48. Iron loss prediction considering the rotational field and flux density harmonics in IPMSM and SynRM.

Author

Ma, L., Sanada, M., Morimoto, S., and Takeda, Y.

Subjects
*ELECTRIC displacement, *ELECTRICAL harmonics, *FINITE element method, *IRON, *ELECTRONICS, *ELECTRICAL engineering
Abstract

Examines the influence of the rational field as well as flux density harmonics on the iron loss calculation based on finite element method. Revision of the conventional method to account for the effect of additional iron losses due to the appearance of rational flux density vector and harmonics; Verification that the improved precision of iron loss calculation can be achieved by using the proposed method.

Published
2003
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49. Detection of Vascular Disease Risk in Women by Panoramic Radiography.

Author

Taguchi, A., Suei, Y., Sanada, M., Higashi, Y., Ohtsuka, M., Nakamoto, T., Tsuda, M., Ohama, K., and Tanimoto, K.

Subjects
VASCULAR disease diagnosis, PANORAMIC radiography, MENOPAUSE, WOMEN, VASCULAR diseases, BONE density
Abstract

Low bone mineral density and rapid bone loss of the skeleton are associated with mortality risk from vascular diseases in post-menopausal women. Panoramic radiographic measurements are considered as indicators of skeletal bone mineral density or bone turnover. We hypothesize that such measurements may be associated with vascular disease risk in post-menopausal women. Associations of mandibular cortical shape and width on panoramic radiographs with skeletal bone mineral density and risk factors related to vascular diseases were investigated in 87 post-menopausal women. Cortical shape was associated with skeletal bone mineral density, low-density lipoprotein cholesterol, apolipoprotein B, resting heart rate, and endothelial dysfunction. Cortical width was associated with skeletal bone mineral density, low-density lipoprotein cholesterol, and apolipoprotein A1. Dentists may be able to refer women with increased risk of vascular diseases, as well as low bone mineral density, to medical professionals for further examination by panoramic findings. [ABSTRACT FROM AUTHOR]

Published
2003
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