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12. Function after anoabdominal rectal resection and colonic J pouch-anal anastomosis

Author

Kusunoki, M., Shoji, Y., Yanagi, H., Hatada, T., Fujita, S., Sakanoue, Y., Yamamura, T., and Utsunomiya, J.

Subjects
Proctology -- Research, Colorectal cancer, Rectum, Intestines -- Physiological aspects, Health
Abstract

Surgery for cancer of the lower portion of the rectum often is able to maintain the continuity of the intestine by various procedures which removed the diseased portion of rectum and join the anus to the colon. This procedure causes patients to have increased bowel urgency, probably due to lack of fecal reservoir. To correct this problem, the surgery performed may include creation of a pouch to serve as fecal reservoir. A study was undertaken of 28 patients undergoing anoabdominal resection of the rectum with creation of a J pouch; eight other patients underwent the procedure but without creation of the reservoir. Patients were evaluated two years after surgery. The maximum capacity of the pouch was inversely correlated with frequency of defecation and fecal soiling during the day. The anal resting pressure, squeeze pressure of the anus and ability of the pouch to expand correlated with the incidence of defecation once the patient's defecation pattern was stable, at least six months after operation. The patients who had pouches created had fewer complications and needed less medication than the non-pouch group, suggesting they had a better quality of life. These findings suggest that creation of a colonic pouch decreases frequency of defecation and soiling soon after operation; there is a rapid increase in pouch capacity. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

13. Pathogenesis of acute cholecystitis after gastrectomy

Author

Takahashi, T., Yamamura, T., and Utsunomiya, J.

Subjects
Naloxone -- Evaluation, Gallbladder -- Physiological aspects, Cholecystitis -- Risk factors, Gastrectomy -- Complications, Health
Abstract

Acute acalculous cholecystitis, inflammation of the gallbladder (without gallstones), may have a more severe course than cholecystitis with gallstones; gangrene and perforation may develop earlier. Acalculous cholecystitis can occur following abdominal surgery. Of 1,096 patients who underwent gastrectomy (removal of the stomach) for stomach cancer, seven patients developed acalculous cholecystitis; these cases are reviewed. Particular attention was given to the motor function of the gallbladder both before and after stomach surgery. Patients were given egg yolk and caerulein, known to cause contraction of the gallbladder. The function of the gallbladder was evaluated by ultrasound, which was performed at intervals ranging from two weeks to six months following surgery. Enlargement of the gallbladder and the presence of sludge was noted within one month after surgery for stomach cancer. Cholecystitis commonly develops within one month of the operation when there is significantly reduced gallbladder motion. Studies performed three months following surgery showed that gallbladder contraction had returned to about preoperative levels and there was a decrease in sludge in the gallbladder. Significant improvement in gallbladder function and decreased formation of biliary sludge was observed when naloxone was given on a daily basis within the first month following gastrectomy. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

14. Association between immune-related dermatologic adverse events and efficacy of pembrolizumab in non-small cell lung cancer patients

Author

Fukuoka, T., Yamamoto, Y., Utsunomiya, J., Usami, E., Kimura, M., Yoshimura, T., Nakamura, M., and Toda, Y.

Abstract

We retrospectively evaluated the incidence of skin immune-related adverse effects (irAEs) in patients treated with pembrolizumab (PMB) and explored and the relationship between skin irAEs and PMB efficacy. Thirty-two patients with non-small cell lung cancer treated with PMB between April 2017 and May 2018 were enrolled. The patients were separated into two groups, namely, skin irAEs and no-skin irAEs group. We investigated the ratio and degree of express skin irAEs, period of skin irAEs and treatment, and the PFS between the two groups. Additionally, we evaluated the PFS between the irAE and no-irAEs groups. The median patient age was 76.5 (range 56–92) years. The European Cooperative Oncology Group Performance Status (ECOG PS) score of 26, 5, and 1 was 0–1, 2, and 3, respectively. The male/female ratio was 23/9. In terms of clinical stages, 6, 21, and 5 patients were in stages III and IV, and postoperative relapse, respectively. Skin irAEs were observed in 10 patients (31%). The progression-free survival of patients with skin irAEs (median, 390 days) was longer than that of patients without skin irAEs (median, 128.5 days). Overall, we suggested a significant association between skin irAEs and the efficacy of PMB in treating non-small cell lung cancer. As skin irAEs can be an indicator of treatment efficacy, it is important for medical staff, including pharmacists, to closely observe these adverse events.

Published
2021
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15. A clinical overview of familial adenomatous polyposis derived from the database of the Polyposis Registry of Japan

Author

Takehira Yamamura, Koichi Koizumi, Hirotoshi Hasegawa, Kazuo Shirouzu, Rectum, Kazuo Tamura, Tetsuichiro Muto, Takayuki Morita, Takeo Iwama, Takashi Hirai, Kenichi Sugihara, and Utsunomiya J

Subjects
Adenoma, Adult, Male, Oncology, congenital, hereditary, and neonatal diseases and abnormalities, medicine.medical_specialty, Early cancer, Adolescent, Colorectal cancer, Population, Rectum, Familial adenomatous polyposis, Sex Factors, Japan, Surgical oncology, Internal medicine, medicine, Humans, Registries, Stage (cooking), Child, education, Aged, Neoplasm Staging, Aged, 80 and over, education.field_of_study, business.industry, Age Factors, Infant, Newborn, Infant, Cancer, Hematology, General Medicine, Middle Aged, medicine.disease, digestive system diseases, medicine.anatomical_structure, Adenomatous Polyposis Coli, Databases as Topic, Child, Preschool, Female, Surgery, Colorectal Neoplasms, business
Abstract

The clinical situation of familial adenomatous polyposis (FAP) in Japan has changed in the period since the last analysis of data of the Japanese Polyposis Center. To reevaluate our data and elucidate the changes we analyzed the records of the 1390 FAP patients in 900 families registered with the Polyposis Committee of the Japanese Society for Cancer of the Colon and Rectum. In the 13-year period 1990-2003, clinical differences between men and women with FAP diminished. The postoperative prognosis was substantially better in patients without advanced colorectal cancer (stageor = T2) than in those with early cancer or no cancer. Mean age at death improved from 42.5 years in the period before 1990 to 46.0 years, and it was a result of a decreased proportion of deaths from colorectal cancer. The distribution of colorectal cancer in FAP patients was similar to that in the general population. Desmoid tumors accounted for about 10% of deaths in the recent 13 years (1990-2003). The cumulative risk of rectal cancer in the preserved rectum was 12% at 10 years and 23% at 15 years. The registry system in Japan revealed a new clinical situation in FAP patients, and the findings of this study will be useful to improve the prognosis of patients with FAP.

Published
2004
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16. General lectures (II)

Author

Segawa, K., Nakazawa, S., Koide, N., Imai, K., Matsuo, N., Yamamoto, Y., Shiobara, M., Shimada, H., Kawai, K., Machida, K., Okabe, N., Hoshi, Y., Koizumi, Y., Watanuki, T., Hiroshima, Y., Matsusaka, Y., Katase, K., Sakuma, Y., Matoba, N., Murata, N., Toyama, Y., Murai, S., Nukaga, A., Ishimatsu, N., Watanabe, Y., Abe, M., Ono, Y., Hirai, K., Iwabuchi, S., Suzuki, K., Aoki, T., Masamura, K., Yoshida, K., Ikeuchi, J., Nagao, F., Kobayashi, A., Toriie, S., Nakajima, M., Kohli, M., Ida, K., Kawai, K., Masuda, M., Hattori, T., Fujita, S., Tamada, T., Inoue, K., Usui, T., Yamaya, S., Ohtsuka, K., Shiraki, Y., Fujishima, S., Tochikubo, O., Miyamoto, S., Ueda, A., Asano, K., Kunisada, M., Miyake, H., Fujii, Y., Yoshimoto, S., Hiramatsu, K., Nakano, S., Takeda, T., Kitamura, K., Horiguchi, Y., Okada, K., Okada, M., Kuwabara, T., Tanaka, M., Konno, K., Hattori, T., Isobe, K., Iwasaki, A., Unoura, T., Matsumoto, M., Yoshida, T., Takahashi, I., Abe, M., Maeda, H., Hayashi, T., Koizumi, H., Iwasaki, M., Takahashi, K., Honda, T., Ariga, K., Mohri, S., Suga, Y., Ono, T., Kobayashi, K., Mizuno, T., Sameshima, Y., Shiozaki, Y., Sasakawa, M., Hiramatsu, A., Ikehara, K., Nagata, T., Tatsumi, K., Abe, M., Aoki, M., Iwasaki, S., Aizawa, T., Kajiwara, K., Sata, K., Omata, S., Imamura, K., Kondo, K., Sajima, H., Sato, Y., Kiryu, H., Mimoto, S., Masuoka, T., Kira, K., Mizumoto, R., Kuratsuka, H., Honjo, I., Hojo, Y., Nakajima, H., Tosaka, T., Arai, O., Kobayashi, N., Obata, N., Ito, S., Takaoka, T., Uragami, Y., Kitamura, Y., Kishi, S., Fujii, S., Okuda, H., Hirano, K., Kano, H., Ogino, M., Ueda, Y., Nishiwaki, K., Iwamura, N., Aoki, T., Hiramatsu, K., Kamada, T., Suematsu, T., Fusamoto, H., Okuda, H., Abe, H., Katayama, S., Yamaguchi, K., Fukuda, M., Ishii, T., Kaito, I., Sato, S., Sasaki, H., Onodera, H., Yamanaka, M., Akagi, K., Miyazaki, S., Okumura, M., Omae, T., Nakamura, Y., Wada, M., Nakai, Y., Inoue, S., Arima, T., Yamasaki, S., Takano, T., Katsuta, Y., Yano, T., Isoda, K., Aramaki, T., Fukuda, N., Ichikawa, T., Okumura, H., Adachi, Y., Inoue, R., Iwasaki, Y., Tanaka, S., Yamamoto, T., Wakisaka, G., Nakaya, H., Takase, S., Ikegami, F., Takada, A., Kobayashi, K., Takeuchi, J., Kato, Y., Funayama, A., Kakumu, S., Ito, S., Okuyama, S., Taoka, Y., Endo, T., Chizuka, R., Yanagida, T., Chizuka, S., Usui, H., Ando, T., Takai, T., Wakahara, T., Kojima, M., Fukazawa, T., Takahashi, Y., Miyamura, S., Urakawa, T., Shima, T., Miyaji, K., Okazaki, T., Kashimura, S., Koyama, K., Yamauchi, H., Matsuo, Y., Takagi, Y., Muto, I., Owada, Y., Otowa, T., Sato, T., Naito, C., Okada, K., Sugawara, K., Nokiba, T., Fujii, Y., Kido, H., Sasaki, M., Sugai, Y., Nishimura, G., Nanbu, H., Kamiyama, Y., Yamada, T., Yamaoka, Y., Takeda, H., Ohsawa, T., Kamano, T., Mizukami, T., Kitamura, O., Ozawa, K., Takasan, H., Honjo, I., Miyasaki, R., Katayama, T., Amakawa, T., Hirose, K., Furukawa, Y., Noguchi, M., Okamoto, M., Maezawa, H., Tanaka, N., Yamada, S., Hisata, T., Hata, C., Sawa, J., Kato, Y., Mituda, Y., Oohira, S., Hayasaka, A., Okuyama, T., Fukui, S., Takeda, T., Furuichi, T., Yamamitsu, S., Yamauchi, K., Konishi, Y., Maeda, S., Setoyama, S., Otsuji, S., Ibata, T., Niu, H., Ogawa, A., Tujioka, E., Maeda, T., Takewa, M., Matumoto, T., Tamada, K., Maeda, A., Sumita, H., Iseki, Y., Yukawa, S., Nitta, Y., Isida, K., Nomoto, H., Setoyama, S., Maeda, S., Otsuji, S., Sato, R., Sato, G., Toyokawa, S., Yamamoto, G., Ohtomi, S., Haga, M., Ueno, Y., Fukuda, M., Endo, R., Yokota, T., Ohsawa, J., Kohno, A., Ohtoshi, E., Yasugi, H., Ichikawa, H., Mizumoto, R., Honjo, I., Ando, K., Suzuki, H., Nishiwaki, T., Kishimoto, T., Miki, T., Takeshige, K., Sawada, M., Hidemura, R., Yamamoto, S., Itoh, S., Kashiwagi, T., Kishida, M., Imamura, O., Suematus, T., Kamada, T., Sakoda, K., Kawada, T., Arima, Y., Kamimura, T., Takesue, M., Katsuki, T., Akita, H., Yakeishi, Y., Takehisa, I., Miyasato, K., Yoshida, H., Hidemura, R., Kubota, K., Aoki, S., Suzuki, S., Kishimoto, T., Miyahara, T., Ando, K., Nishiwaki, T., Miki, T., Takeshige, K., Sawada, M., Itoh, S., Yamamoto, S., Fujiwara, K., Sakai, T., Oda, T., Igarashi, S., Fukuhara, M., Tsujii, T., Tamura, T., Matsuoka, Y., Takahashi, H., Sakamoto, T., Fukuda, S., Oku, M., Matsui, T., Morita, T., Oyazato, Y., Kimura, K., Moriya, W., Fukui, S., Suzuki, K., Morimoto, S., Tsuiki, S., Shoji, K., Nakai, Y., Hata, M., Kubo, J., Yoshizawa, K., Nagayama, K., Ozawa, Y., Yoshida, M., Horiguchi, M., Machii, A., Nitta, Y., Aiso, Y., Kitahara, N., Kitazawa, E., Fukuda, K., Saiti, N., Murakami, Y., Nao, Y., Okazaki, I., Funatsu, K., Maruyama, K., Takagi, B., Yasuraoka, S., Ishii, K., Matsuzaki, S., Takahashi, H., Ishii, H., Kamegaya, K., Sambe, K., Ishikawa, H., Tajima, Y., Kuroda, A., Ishihara, Y., Sato, N., Ishikawa, I., Noro, T., Kakumoto, Y., Mekjian, H. S., Thomford, N. R., Yokomura, T., Adachi, S., Yamamoto, A., Saito, I., Kawamura, A., Miyata, M., Kasai, S., Kawanishi, N., Tamaki, A., Mito, M., Kasai, Y., Hasumi, A., Uchiyama, T., Tachikawa, Y., Takanashi, T., Kanke, T., Matsuda, K., Takanashi, T., Kanke, T., Matsuda, K., Hamana, G., Sakuma, M., Sugita, T., Tomita, K., Yamasaki, S., Tsuzuki, T., Uekusa, M., Matsuzaki, M., Takagi, B., Tsuchiya, M., Uchimura, M., Murohisa, T., Muto, Y., Ishigaki, J., Waki, S., Tsuchiya, R., Sho, M., Furukawa, M., Suzuki, N., Nagashima, H., Matsushiro, T., Saitoh, T., Nakamura, N., Hatanaka, T., Kobayashi, N., Nakamura, Y., Sato, T., Tooi, K., Tanaka, Y., Kadokura, N., Okada, Y., Yanakgi, I., Tanaka, N., Sekiya, V. M., Adachi, K., Miyashita, M., Moriyama, Y., Onda, M., Yoshioka, M., Teraoka, T., Shimizu, Y., Fujishima, G., Ookawa, K., Miki, M., Shirota, A., Aihara, K., Shiga, T., Sano, H., Hayashi, S., Hori, M., Sato, H., Chuman, Y., Tsukase, S., Nakahara, N., Ehira, S., Setoyama, S., Nishimata, H., Irisa, T., Tokutome, K., Nakashima, Y., Koga, H., Yokoyama, H., Otsuji, T., Chujo, Y., Yamamoto, T., Gotoda, S., Uchiyama, S., Kosaki, G., Ohkura, H., Mukojima, T., Hattori, N., Sasaki, O., Soejima, K., Inokuchi, K., Utsunomiya, J., Maki, T., Iwama, T., Matsunaga, Y., Shimomura, T., Nakajima, T., Ichikawa, S., Miyanaga, T., Sengoku, K., Hamaguchi, E., Aoki, N., Nomura, T., Matsuoka, A., Suzuki, N., Nagahama, A., Kazumi, T., Miyawaki, H., Sakamoto, T., Miyasaki, K., Kato, K., Miyazaki, Y., Harada, N., Yamada, K., Tashiro, S., Sakai, K., Ho, N., Murayama, H., Yada, M., Sakabe, T., Shimizu, H., Kuroki, M., Nishida, S., Kato, K., Ishiyama, S., Yukawa, K., Hayashi, M., Soh, K., Doi, K., Fukuda, M., Nakagawa, A., Yukawa, E., Uematsu, Y., Nara, K., Hattori, H., Watanabe, M., Yoshida, H., Sato, K., Okuse, S., Sato, K., Murotani, T., Takasu, S., Konta, M., Uchiya, T., Fujimaki, N., Yoshida, K., Yoshikawa, K., Uchida, M., Nakamura, N., Nagao, F., Kawana, S., Tamura, K., Hashimoto, T., Kobayashi, K., Hara, T., Nosaka, J., Fukui, O., Inaba, E., Otsukasa, S., Sanada, K., Hiraide, H., Senyo, G., Ootani, A., Nakayama, T., Takei, S., Miki, H., Tanaka, M., Minota, S., Nakayama, K., Nakagawa, K., Shiraishi, T., Kawauchi, H., Nagaya, H., Mizushima, K., Tachimi, Y., Namiki, M., Masuda, K., Mitsutani, N., Mukuta, T., Koizumi, T., Takeuchi, T., Nemoto, T., Takabayashi, H., Takagi, M., Hongo, Y., Kojima, H., Nishimura, M., Hino, S., Hirayama, J., Nakamura, M., Irisa, T., Koga, S., Hirayama, C., Kikuch, S., Ito, M., Hidano, S., Ooya, T., Banno, H., Tomura, A., Kato, K., Koyama, T., Takei, T., Tomimura, T., Yamauchi, M., Kobayashi, K., Nakaya, Y., Takase, S., Kato, Y., Takeuchi, J., Ikegami, F., Matsuda, Y., Takada, A., Udo, K., Kojima, M., Hukuda, N., Kametani, M., Miyagawa, T., Wakahara, T., Takahashi, Y., Imaeda, T., Senda, K., Fujita, S., Okubo, H., Kanoda, K., Miyashita, B., Ishizuka, H., Goto, T., Oto, K., Kaneda, H., Hase, M., Matsuda, J., Kawai, T., Ikehara, H., Baba, S., Ishii, M., Tozawa, T., Inoue, E., Mizuno, N., Saeki, S., Nakaji, T., Narabayashi, T., Okuno, T., Yamada, H., Tanno, M., Chiba, K., Iio, M., Shibata, K., Furuhashi, F., Mizuochi, K., Ohashi, S., Kato, K., Nakano, M., Otsuka, S., Irie, M., Akima, M., Maruyama, Y., Oyamada, F., Nagata, E., Kubo, Y., Arishima, T., Otsuyama, Y., Kaneto, A., Shimogawa, Y., Tanigawa, K., Okabe, N., Nakajima, K., Onishi, S., Kasahara, A., Shimizu, T., Ikehara, Y., Tajima, H., Okamoto, A., Komibuchi, T., Negoro, T., Nihonsugi, A., Ishii, M., Tozawa, T., Ogawa, Y., Otani, H., Ishida, M., Yashima, H., Shoji, K., Tsuiki, S., Morimoto, S., Nakai, Y., Ryo, M., Ozawa, Y., Tanaka, T., Horiguchi, M., Taketa, K., Watanabe, A., Yumoto, Y., Tanaka, A., Takesue, A., Aoe, H., Ueda, M., Shimamura, J., Kosaka, K., Kashiwara, E., Orita, K., Konaga, E., Suzuki, K., Tanaka, S., Kaneda, S., Ogawa, K., Tamura, H., Okanishi, S., Ueda, T., Horie, H., Kamachi, M., Asihara, T., Daido, R., Izumi, T., Kurihara, M., Sumida, M., Haraikawa, M., Hayakawa, H., Shirakabe, H., Yasui, A., Noguchi, M., Okamoto, M., Furukawa, Y., Miyasaki, R., Hirose, K., Katayama, T., and Maezawa, H.

Published
1974
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19. Effect of aspirin on the induction of apoptosis in colorectal adenocarcinoma cell-lines

Author

Tomoko Hashimoto, Ji Furuyama, Shigetoshi Ichii, Utsunomiya J, and R Yoshikawa

Subjects
Cancer Research, Aspirin, Cell, Cancer, General Medicine, Biology, Cell cycle, medicine.disease_cause, medicine.disease, medicine.anatomical_structure, Oncology, Apoptosis, Cell culture, Cancer research, medicine, DNA fragmentation, Carcinogenesis, medicine.drug
Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit experimental carcinogenesis and their use in humans has been related epidemiologically to a reduced risk of colorectal polyps and cancer, although the mechanism involved is not known. We found that aspirin triggered the death of SW948 human colorectal adenocarcinoma cells through activation of an apoptotic pathway. Exposure of SW480 and SW948 cells to 25 mu M aspirin for 5 h resulted in the detatchment of cells from the monolayer culture at 48 h. SW948 cells with continuous exposure to 25 mu M aspirin exhibited various morphological and biochemical characteristics of apoptosis, including compact patches of condensed nuclear chromatin, and DNA fragmentation. These in vitro data suggest that apoptosis may play a role in the antitumor effect of aspirin and other NSAIDs and that the induction of apoptosis may provide an attractive therapeutic target in colorectal carcinogenesis.

Published
2011

20. Mechanism of carcinogenesis in familial tumors

Author

Takehira Yamamura, Tetsuya Takagawa, Yoshihiro Fukuda, Takashi Nishigami, Kazuo Tamura, Ken Sagayama, Kazuhiko Nakagawa, Jun-ichi Furuyama, Utsunomiya J, Kiyoshi Kusuhara, Naohisa Takeda, Takayuki Matsumoto, and Takeo Iwama

Subjects
Genetics, DNA Repair, Colorectal cancer, Microsatellite instability, Caretaker gene, Hematology, General Medicine, Cell cycle, Biology, medicine.disease, medicine.disease_cause, Germline mutation, Cell Transformation, Neoplastic, Oncology, Neoplasms, Proto-Oncogenes, medicine, Humans, Surgery, DNA mismatch repair, Genes, Tumor Suppressor, Genetic Predisposition to Disease, Carcinogenesis, Gene
Abstract

It is thought that malignant tumors occur through interactions of multiple environmental factors and a personal genetic factor. A normal somatic cell having an intrinsic function is able to acquire the characteristics of a malignant cell under the influence of many factors. A small percentage of all tumors have obvious familial aggregation. These entities are called familial cancer. The familial cancer syndrome is well defined for colorectal cancer, breast cancer, endocrine neoplasia, and so on. Traits of familial tumors are sequentially inherited by offspring through gametes in a Mendelian fashion, most commonly in an autosomal-dominant manner. Carcinogenesis requires multiple genetic events. A patient with a familial tumor is ahead of an individual without any germline mutation in the carcinogenesis process. In such a situation, patients frequently suffer from multiple malignant tumors at a young age. It is well known that three major genes are closely related to the cell cycle and tumorigenesis. These gene types are protooncogenes, tumor suppressor genes, and DNA mismatch repair genes. Proto-oncogenes function to accelerate cells during the G1 or growth phase of the cell cycle. Tumor suppressor genes act as blocks against cell growth and proliferation. Inactivation of tumor suppressor genes requires alterations in both alleles. These phenomena are known as Knudson's two-hits theory. However, DNA mismatch repair genes are known as caretaker genes and correct mismatch pair generation during DNA replication. Germline mutation of DNA mismatch repair genes causes hereditary nonpolyposis colorectal cancer. The tumor phenotype from patients with hereditary nonpolyposis colorectal cancer is demonstrated to be microsatellite instability positive.

Published
2004

21. Planning the human variome project: the Spain report.

Author

Kaput, J., Cotton, R.G., Hardman, L., Watson, M., Aqeel, A.I. Al, Al-Aama, J.Y., Al-Mulla, F., Alonso, S., Aretz, S., Auerbach, A.D., Bapat, B., Bernstein, I.T., Bhak, J., Bleoo, S.L., Blocker, H., Brenner, S.E., Burn, J., Bustamante, M., Calzone, R., Cambon-Thomsen, A., Cargill, M., Carrera, P., Cavedon, L., Cho, Y.S., Chung, Y.J., Claustres, M., Cutting, G., Dalgleish, R., Dunnen, J.T. den, Diaz, C., Dobrowolski, S., Santos, M.R. dos, Ekong, R., Flanagan, S.B., Flicek, P., Furukawa, Y., Genuardi, M., Ghang, H., Golubenko, M.V., Greenblatt, M.S., Hamosh, A., Hancock, J.M., Hardison, R., Harrison, T.M., Hoffmann, R., Horaitis, R., Howard, H.J., Barash, C.I., Izagirre, N., Jung, J., Kojima, T., Laradi, S., Lee, Y.S., Lee, J.Y., Gil-da-Silva-Lopes, V.L., Macrae, F.A., Maglott, D., Marafie, M.J., Marsh, S.G., Matsubara, Y., Messiaen, L.M., Moslein, G., Netea, M.G., Norton, M.L., Oefner, P.J., Oetting, W.S., O'Leary, J.C., Ramirez, A.M. de, Paalman, M.H., Parboosingh, J., Patrinos, G.P., Perozzi, G., Phillips, I.R., Povey, S., Prasad, S., Qi, M., Quin, D.J., Ramesar, R.S., Richards, C.S., Savige, J., Scheible, D.G., Scott, R.J., Seminara, D., Shephard, E.A., Sijmons, R.H., Smith, T.D., Sobrido, M.J., Tanaka, T., Tavtigian, S.V., Taylor, G.R., Teague, J., Topel, T., Ullman-Cullere, M., Utsunomiya, J., Kranen, H.J. van, Vihinen, M., Webb, E., Weber, T.K., Yeager, M., Kaput, J., Cotton, R.G., Hardman, L., Watson, M., Aqeel, A.I. Al, Al-Aama, J.Y., Al-Mulla, F., Alonso, S., Aretz, S., Auerbach, A.D., Bapat, B., Bernstein, I.T., Bhak, J., Bleoo, S.L., Blocker, H., Brenner, S.E., Burn, J., Bustamante, M., Calzone, R., Cambon-Thomsen, A., Cargill, M., Carrera, P., Cavedon, L., Cho, Y.S., Chung, Y.J., Claustres, M., Cutting, G., Dalgleish, R., Dunnen, J.T. den, Diaz, C., Dobrowolski, S., Santos, M.R. dos, Ekong, R., Flanagan, S.B., Flicek, P., Furukawa, Y., Genuardi, M., Ghang, H., Golubenko, M.V., Greenblatt, M.S., Hamosh, A., Hancock, J.M., Hardison, R., Harrison, T.M., Hoffmann, R., Horaitis, R., Howard, H.J., Barash, C.I., Izagirre, N., Jung, J., Kojima, T., Laradi, S., Lee, Y.S., Lee, J.Y., Gil-da-Silva-Lopes, V.L., Macrae, F.A., Maglott, D., Marafie, M.J., Marsh, S.G., Matsubara, Y., Messiaen, L.M., Moslein, G., Netea, M.G., Norton, M.L., Oefner, P.J., Oetting, W.S., O'Leary, J.C., Ramirez, A.M. de, Paalman, M.H., Parboosingh, J., Patrinos, G.P., Perozzi, G., Phillips, I.R., Povey, S., Prasad, S., Qi, M., Quin, D.J., Ramesar, R.S., Richards, C.S., Savige, J., Scheible, D.G., Scott, R.J., Seminara, D., Shephard, E.A., Sijmons, R.H., Smith, T.D., Sobrido, M.J., Tanaka, T., Tavtigian, S.V., Taylor, G.R., Teague, J., Topel, T., Ullman-Cullere, M., Utsunomiya, J., Kranen, H.J. van, Vihinen, M., Webb, E., Weber, T.K., and Yeager, M.

Abstract

Contains fulltext : 81952.pdf (publisher's version ) (Closed access), The remarkable progress in characterizing the human genome sequence, exemplified by the Human Genome Project and the HapMap Consortium, has led to the perception that knowledge and the tools (e.g., microarrays) are sufficient for many if not most biomedical research efforts. A large amount of data from diverse studies proves this perception inaccurate at best, and at worst, an impediment for further efforts to characterize the variation in the human genome. Because variation in genotype and environment are the fundamental basis to understand phenotypic variability and heritability at the population level, identifying the range of human genetic variation is crucial to the development of personalized nutrition and medicine. The Human Variome Project (HVP; http://www.humanvariomeproject.org/) was proposed initially to systematically collect mutations that cause human disease and create a cyber infrastructure to link locus specific databases (LSDB). We report here the discussions and recommendations from the 2008 HVP planning meeting held in San Feliu de Guixols, Spain, in May 2008.

Published
2009

22. Planning the Human Variome Project: The Spain Report

Author

Kaput, J, Cotton, RGH, Hardman, L, Watson, M, Al Aqeel, AI, Al-Aama, JY, Al-Mulla, F, Alonso, S, Aretz, S, Auerbach, AD, Bapat, B, Bernstein, IT, Bhak, J, Bleoo, SL, Bloecker, H, Brenner, SE, Burn, J, Bustamante, M, Calone, R, Cambon-Thomsen, A, Cargill, M, Carrera, P, Cavedon, L, Cho, YS, Chung, Y-J, Claustres, M, Cutting, G, Dalgleish, R, den Dunnen, JT, Diaz, C, Dobrowolski, S, dos Santos, MRN, Ekong, R, Flanagan, SB, Flicek, P, Furukawa, Y, Genuardi, M, Ghang, H, Golubenko, MV, Greenblatt, MS, Hamosh, A, Hancock, JM, Hardison, R, Harrison, TM, Hoffmann, R, Horaitis, R, Howard, HJ, Barash, CI, Izagirre, N, Jung, J, Kojima, T, Laradi, S, Lee, Y-S, Lee, J-Y, Gil-da-Silva-Lopes, VL, Macrae, FA, Maglott, D, Marafie, MJ, Marsh, SGE, Matsubara, Y, Messiaen, LM, Moeslein, G, Netea, MG, Norton, ML, Oefner, PJ, Oetting, WS, O'Leary, JC, Oller de Ramirez, AM, Paalman, MH, Parboosingh, J, Patrinos, GP, Perozzi, G, Phillips, IR, Povey, S, Prasad, S, Qi, M, Quin, DJ, Ramesar, RS, Richards, CS, Savige, J, Scheible, DG, Scott, RJ, Seminara, D, Shephard, EA, Sijmons, RH, Smith, TD, Sobrido, M-J, Tanaka, T, Tavtigian, SV, Taylor, GR, Teague, J, Toepel, T, Ullman-Cullere, M, Utsunomiya, J, van Kranen, HJ, Vihinen, M, Webb, E, Weber, TK, Yeager, M, Yeom, YI, Yim, S-H, Yoo, H-S, Kaput, J, Cotton, RGH, Hardman, L, Watson, M, Al Aqeel, AI, Al-Aama, JY, Al-Mulla, F, Alonso, S, Aretz, S, Auerbach, AD, Bapat, B, Bernstein, IT, Bhak, J, Bleoo, SL, Bloecker, H, Brenner, SE, Burn, J, Bustamante, M, Calone, R, Cambon-Thomsen, A, Cargill, M, Carrera, P, Cavedon, L, Cho, YS, Chung, Y-J, Claustres, M, Cutting, G, Dalgleish, R, den Dunnen, JT, Diaz, C, Dobrowolski, S, dos Santos, MRN, Ekong, R, Flanagan, SB, Flicek, P, Furukawa, Y, Genuardi, M, Ghang, H, Golubenko, MV, Greenblatt, MS, Hamosh, A, Hancock, JM, Hardison, R, Harrison, TM, Hoffmann, R, Horaitis, R, Howard, HJ, Barash, CI, Izagirre, N, Jung, J, Kojima, T, Laradi, S, Lee, Y-S, Lee, J-Y, Gil-da-Silva-Lopes, VL, Macrae, FA, Maglott, D, Marafie, MJ, Marsh, SGE, Matsubara, Y, Messiaen, LM, Moeslein, G, Netea, MG, Norton, ML, Oefner, PJ, Oetting, WS, O'Leary, JC, Oller de Ramirez, AM, Paalman, MH, Parboosingh, J, Patrinos, GP, Perozzi, G, Phillips, IR, Povey, S, Prasad, S, Qi, M, Quin, DJ, Ramesar, RS, Richards, CS, Savige, J, Scheible, DG, Scott, RJ, Seminara, D, Shephard, EA, Sijmons, RH, Smith, TD, Sobrido, M-J, Tanaka, T, Tavtigian, SV, Taylor, GR, Teague, J, Toepel, T, Ullman-Cullere, M, Utsunomiya, J, van Kranen, HJ, Vihinen, M, Webb, E, Weber, TK, Yeager, M, Yeom, YI, Yim, S-H, and Yoo, H-S

Abstract

The remarkable progress in characterizing the human genome sequence, exemplified by the Human Genome Project and the HapMap Consortium, has led to the perception that knowledge and the tools (e.g., microarrays) are sufficient for many if not most biomedical research efforts. A large amount of data from diverse studies proves this perception inaccurate at best, and at worst, an impediment for further efforts to characterize the variation in the human genome. Because variation in genotype and environment are the fundamental basis to understand phenotypic variability and heritability at the population level, identifying the range of human genetic variation is crucial to the development of personalized nutrition and medicine. The Human Variome Project (HVP; http://www.humanvariomeproject.org/) was proposed initially to systematically collect mutations that cause human disease and create a cyber infrastructure to link locus specific databases (LSDB). We report here the discussions and recommendations from the 2008 HVP planning meeting held in San Feliu de Guixols, Spain, in May 2008.

Published
2009

23. Effects of neuropeptides on smooth muscle contraction after small bowel transplantation

Author

Hiromitsu Ishii, Masato Kusunoki, Utsunomiya J, and T. Yamamura

Subjects
medicine.medical_specialty, Contraction (grammar), Neuropeptide, Substance P, Biology, In Vitro Techniques, digestive system, Sincalide, chemistry.chemical_compound, Internal medicine, Intestine, Small, medicine, Animals, Guanethidine, Neurotensin, digestive, oral, and skin physiology, Neuropeptides, Osmolar Concentration, Muscle, Smooth, Smooth muscle contraction, Organ Transplantation, Small intestine, Rats, Transplantation, medicine.anatomical_structure, Endocrinology, chemistry, Rats, Inbred Lew, Surgery, Gastrointestinal Motility, hormones, hormone substitutes, and hormone antagonists, medicine.drug
Abstract

We have previously shown that increased intestinal contraction after small bowel transplantation was associated with marked enhancement in the nonadrenergic, noncholinergic (NANC) intrinsic neural component. In the present study, we examined the effect of three NANC neurotransmitters (substance P, neurotensin, and cholecystokinin-octapeptide, CCK-OP) on jejunal longitudinal muscle strips after syngeneic total small bowel transplantation in rats. Fourteen rats were divided into a normal control group (n = 7) and a group tested 4 weeks after transplantation (n = 7). A superfusion system was used to evaluate the in vitro effects of the three neuropeptides in the presence of atropine and guanethidine. In the control group, maximum contractile response to substance P, neurotensin, and CCK-OP was 5.16 +/- 0.30, 1.46 +/- 0.15, and 1.13 +/- 0.17 mg tension/mg wet weight, respectively, while the values for the transplanted group were 5.71 +/- 0.29, 2.52 +/- 0.17, and 1.20 +/- 0.18 mg tension/mg wet weight. These results show that neurotensin-induced contraction increased significantly after transplantation, but substance P appeared to be the dominant NANC neurotransmitter in both normal and transplanted small bowel.

Published
1997

25. Allele Loss and Kras Mutation Involved in the Development of Colorectal Tumors in Patients with Familial Adenomatous Polyposis

Author

Akiyoshi Yamanaka, Chieko Sato, Utsunomiya J, Kiyoko Tanaka, Takeo Mori, Madoka Seki, Michiko Miyaki, Mieko Okamoto, Takeo Iwama, and Morio Koike

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Pathology, medicine.medical_specialty, business.industry, Chromosome, medicine.disease, medicine.disease_cause, digestive system diseases, Familial adenomatous polyposis, Loss of heterozygosity, Dysplasia, Cancer research, Medicine, KRAS, Allele, Mutation frequency, business, neoplasms, Gene
Abstract

To investigate the mechanism of colon carcinogenesis, the loss of heterozygosity and Kras mutation were analyzed in 24 advanced FAP carcinomas, 20 advanced non-FAP carcinomas, and 111 FAP polyps with distinct histopathological dysplasia. Allele loss was observed in advanced FAP carcinomas most frequently on chromosome 5q (38%), 17p(57%), 18(36%) and 22q(35%). Non-FAP carcinomas exhibited allele losses similar to those in the FAP carcinomas. The frequency of allele loss in polyps from FAP patients was low, but it was higher in more advanced polyps; the loss was observed on chromosome 5q (24%) in severe adenomas, and on chromosome 5q (25%) and 17p(30%) in intramucosal early carcinomas. Kras mutations were detected in 50% of the advanced FAP carcinomas. The mutation frequency in polyps was lower than that in advanced carcinomas, the frequency increasing with polyp size. The present results suggest, in addition to the FAP gene on chromosome 5q, a significant role of cumulative changes in multiple tumor suppressor genes and the Kras gene during the development of colon tumors.

Published
1990
Full Text
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26. An Attempt for Identification of Hereditary Nonpolyposis Colorectal Cancer in Japan

Author

Masato Kusunoki, Y. Sakanoue, Utsunomiya J, Yoshio Miki, and Tooru Sakiyama

Subjects
Oncology, Pathology, medicine.medical_specialty, Colorectal cancer, business.industry, Incidence (epidemiology), Cancer, Primary cancer, medicine.disease, digestive system diseases, Internal medicine, medicine, Cancer Family, Proximal colon, Multiple tumors, Family history, business, neoplasms
Abstract

In order to identify hereditary non-polyposis colorectal cancer (HNPCC) in Japan, we analyzed clinical characteristics of 10 families of colorectal cancer (CRC) with two or more affected relatives in our department (the personal series) and of 39 families reported as familial CRC or cancer family syndrome in Japanese literatures (the reported series). The characteristics of CRC in the reported series in comparison with general CRC were earlier onset, higher incidence of multiple tumor, predominance in the proximal colon, and excess of multiple primary cancer in the other organs. They were similar to those of USA and Finland except for more frequent association with gastric cancer in the reported series. Gastric cancer patient with onset in age of 60 or younger in family history of CRC may be regarded as a clinical marker suggestive for HNPCC. The reason for failure to demonstrate the characteristics of HNPCC in the personal series is to be further clarified by study with our data based on larger scale.

Published
1990
Full Text
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33. Molecular nature of colon tumors in hereditary nonpolyposis colon cancer, familial polyposis, and sporadic colon cancer

Author

Konishi, M, primary, Kikuchi-Yanoshita, R, additional, Tanaka, K, additional, Muraoka, M, additional, Onda, A, additional, Okumura, Y, additional, Kishi, N, additional, Iwama, T, additional, Mori, T, additional, Koike, M, additional, Ushio, K, additional, Chiba, M, additional, Nomizu, S, additional, Konishi, F, additional, Utsunomiya, J, additional, and Miyaki, M, additional

Published
1996
Full Text
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35. Surgical Management of Familial Adenomatous Polyposis.

Author

Utsunomiya, J. and Gondo, N.

Abstract

Focuses on the clinical approaches to familial adenomatous polyposis (FAP) involving patients as well their family members. Data on the disease; Preoperative diagnosis; Surgical techniques for the disease.

Published
1999

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