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3. Risk of haemolytic uraemic syndrome caused by shiga-toxin-producing Escherichia coli infection in adult women in Japan

Author

Fujii, J, Mizoue, T, Kita, T, Kishimoto, H, Joh, K, Nakada, Y, Ugajin, S, Naya, Y, Nakamura, T, Tada, Y, Okabe, N, Maruyama, Y, Saitoh, K, Kurozawa, Y, Fujii, J, Mizoue, T, Kita, T, Kishimoto, H, Joh, K, Nakada, Y, Ugajin, S, Naya, Y, Nakamura, T, Tada, Y, Okabe, N, Maruyama, Y, Saitoh, K, and Kurozawa, Y

Abstract

Shiga-toxin-producing Escherichia coli (STEC) infections usually cause haemolytic uraemic syndrome (HUS) equally in male and female children. This study investigated the localization of globotriaosylceramide (Gb3) in human brain and kidney tissues removed from forensic autopsy cases in Japan. A fatal case was used as a positive control in an outbreak of diarrhoeal disease caused by STEC O157:H7 in a kindergarten in Urawa in 1990. Positive immunodetection of Gb3 was significantly more frequent in female than in male distal and collecting renal tubules. To correlate this finding with a clinical outcome, a retrospective analysis of the predictors of renal failure in the 162 patients of two outbreaks in Japan was performed: one in Tochigi in 2002 and the other in Kagawa Prefecture in 2005. This study concludes renal failure, including HUS, was significantly associated with female sex, and the odds ratio was 4·06 compared to male patients in the two outbreaks. From 2006 to 2009 in Japan, the risk factor of HUS associated with STEC infection was analysed. The number of males and females and the proportion of females who developed HUS were calculated by age and year from 2006 to 2009. In 2006, 2007 and 2009 in adults aged >20 years, adult women were significantly more at risk of developing HUS in Japan.

Published
2021

19. Tolvaptan in Patients with Autosomal Dominant Polycystic Kidney Disease

Author

Torres VE, Chapman AB, Devuyst O, Gansevoort RT, Grantham JJ, Higashihara E, Perrone RD, Krasa HB, Ouyang J, Czerwiec FS, Tempo team, Gross P, Schulze B, Bichet D, Chauveau D, Peeters P, Voiculescu M, Manunta P, Tuazon J, Watnick T, Goral S, Horie S, Nutahara K, Torres V, Chapman A, Gansevoort R, Perrone R, Czerwiec F, Goldstein S, Cowley B, Fukagawa M, Torra R, Wei LJ, Cook T, Toto R, Agarwal R, August P, Bakris G, Beddhu S, Corwin H, Ruilope L, Rosa-Diez G, De La Fuente J, Martin R, Massari P, Novoa P, Rial M, Wasserman A, Faull R, Fraser I, Johnson D, Pedagagos E, Lian M, Pollock C, Cooper B, Rangan G, Russ G, McDonald S, Thomas M, Khoo D, Walker R, Pirson Y, Laecke V, Van der Niepen P, Sennesael J, Barre P, Alam A, Soroka S, Dieperink H, Strandgaard S, Petersen L, Berthoux F, Canaud B, Gontiers-Picard A, Huart A, Combe C, Delmas Y, Dussol B, Laville M, Guebre-Egziabher F, Mignon F, Michel C, Rieu P, Noel N, Ryckelynck J, Lobbedez T, Dellanna F, Kleophas W, Feldkamp T, Witzke O, Nurnberger J, Zeltner R, Walz G, Zeier M, Sommerer C, Bianchi S, Capasso G, Miranda N, Magistroni R, Bracale M, Remuzzi G, Rota S, Villa G, Tilocca P, Asahi K, Kato T, Endo M, Umezono T, Fujigaki Y, Kato A, Fukatsu A, Hasegawa H, Tayama Y, Hasegawa M, Hosoya T, Hanaoka K, Iehara N, Iino Y, Tsuruoka S, Imai E, Isaka Y, Ishimura E, Ito S, Sato H, Kamata K, Sakamoto H, Kamura K, Kusano E, Muto S, Kuwahara M, Matsubara A, Yorioka N, Mochizuki T, Narita I, Naya Y, Nihei N, Yukio N, Nishio S, Nitta K, Tsuchiya K, Okamura M, Sasaki S, Rai T, Seta K, Sugawara A, Shibazaki S, Sugiyama S, Tabei K, Takaichi K, Tomita K, Kitamura K, Tsukamoto Y, Tsuruya K, Nakano T, Ubara Y, Watanabe T, Yamamoto T, Yoshida K, Ishii D, Yuzawa Y, Meijer E, Vervloet M, Ciechanowski K, Wisniewska M, Gutowska-Jablonska M, Marcinkowska-Królewicz M, Klatko W, Wiśniewski T, Klinger M, Krajewska M, Ksiazek A, Orłowska G, Malecki R, Gontarek-Kacprzak J, Nowicki M, Makówka A, Rutkowski B, Wołyniec W, Rydzewski A, Sulowicz W, Jasik P, Covic A, Volovat C, Mircescu G, Petrescu L, Bobeica R, Barbarash O, Chesnokova L, Borovoy S, Demina L, Shostka G, Idovu M, Tkalich L, Geynits O, Tomilina N, Foggensteiner L, Holt S, Kingswood J, Lambie S, Peel R, MacDougall I, Tucker B, MacPhee I, Maxwell A, Brown H, Mikhail A, Bastin L, Turner N, Neary J, Wheeler D, Maxwell P, Wilkie M, Ong A, Zehnder D, Aldridge N, Adler S, Klein M, Battle D, Bennett W, Berger B, Dell K, Blumenfeld J, Donahue S, Bolin P, Browder R, Perry A, Oskoui F, Culpepper M, Dahl N, Edelstein C, Clegg L, Fischer D, Kaplan M, Kaveh K, Pankhaniya R, Koren M, Mansur K, Lafayette R, Lamar W, Lee J, Mahnensmith R, Nachman P, Mottl A, Miskulin D, Petersen J, Radhakrishnan J, Roppolo M, Basireddy M, Rosner M, Bolton W, Schulman G, Steed L, Steinman T, Hogan M, Venuto R, Turban S, Winklhofer F., Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Torres, Ve, Chapman, Ab, Devuyst, O, Gansevoort, Rt, Grantham, Jj, Higashihara, E, Perrone, Rd, Krasa, Hb, Ouyang, J, Czerwiec, F, Tempo, Team, Gross, P, Schulze, B, Bichet, D, Chauveau, D, Peeters, P, Voiculescu, M, Manunta, P, Tuazon, J, Watnick, T, Goral, S, Horie, S, Nutahara, K, Torres, V, Chapman, A, Gansevoort, R, Perrone, R, Goldstein, S, Cowley, B, Fukagawa, M, Torra, R, Wei, Lj, Cook, T, Toto, R, Agarwal, R, August, P, Bakris, G, Beddhu, S, Corwin, H, Ruilope, L, Rosa-Diez, G, De La Fuente, J, Martin, R, Massari, P, Novoa, P, Rial, M, Wasserman, A, Faull, R, Fraser, I, Johnson, D, Pedagagos, E, Lian, M, Pollock, C, Cooper, B, Rangan, G, Russ, G, Mcdonald, S, Thomas, M, Khoo, D, Walker, R, Pirson, Y, Laecke, V, Van der Niepen, P, Sennesael, J, Barre, P, Alam, A, Soroka, S, Dieperink, H, Strandgaard, S, Petersen, L, Berthoux, F, Canaud, B, Gontiers-Picard, A, Huart, A, Combe, C, Delmas, Y, Dussol, B, Laville, M, Guebre-Egziabher, F, Mignon, F, Michel, C, Rieu, P, Noel, N, Ryckelynck, J, Lobbedez, T, Dellanna, F, Kleophas, W, Feldkamp, T, Witzke, O, Nurnberger, J, Zeltner, R, Walz, G, Zeier, M, Sommerer, C, Bianchi, S, Capasso, G, Miranda, N, Magistroni, R, Bracale, M, Remuzzi, G, Rota, S, Villa, G, Tilocca, P, Asahi, K, Kato, T, Endo, M, Umezono, T, Fujigaki, Y, Kato, A, Fukatsu, A, Hasegawa, H, Tayama, Y, Hasegawa, M, Hosoya, T, Hanaoka, K, Iehara, N, Iino, Y, Tsuruoka, S, Imai, E, Isaka, Y, Ishimura, E, Ito, S, Sato, H, Kamata, K, Sakamoto, H, Kamura, K, Kusano, E, Muto, S, Kuwahara, M, Matsubara, A, Yorioka, N, Mochizuki, T, Narita, I, Naya, Y, Nihei, N, Yukio, N, Nishio, S, Nitta, K, Tsuchiya, K, Okamura, M, Sasaki, S, Rai, T, Seta, K, Sugawara, A, Shibazaki, S, Sugiyama, S, Tabei, K, Takaichi, K, Tomita, K, Kitamura, K, Tsukamoto, Y, Tsuruya, K, Nakano, T, Ubara, Y, Watanabe, T, Yamamoto, T, Yoshida, K, Ishii, D, Yuzawa, Y, Meijer, E, Vervloet, M, Ciechanowski, K, Wisniewska, M, Gutowska-Jablonska, M, Marcinkowska-Królewicz, M, Klatko, W, Wiśniewski, T, Klinger, M, Krajewska, M, Ksiazek, A, Orłowska, G, Malecki, R, Gontarek-Kacprzak, J, Nowicki, M, Makówka, A, Rutkowski, B, Wołyniec, W, Rydzewski, A, Sulowicz, W, Jasik, P, Covic, A, Volovat, C, Mircescu, G, Petrescu, L, Bobeica, R, Barbarash, O, Chesnokova, L, Borovoy, S, Demina, L, Shostka, G, Idovu, M, Tkalich, L, Geynits, O, Tomilina, N, Foggensteiner, L, Holt, S, Kingswood, J, Lambie, S, Peel, R, Macdougall, I, Tucker, B, Macphee, I, Maxwell, A, Brown, H, Mikhail, A, Bastin, L, Turner, N, Neary, J, Wheeler, D, Maxwell, P, Wilkie, M, Ong, A, Zehnder, D, Aldridge, N, Adler, S, Klein, M, Battle, D, Bennett, W, Berger, B, Dell, K, Blumenfeld, J, Donahue, S, Bolin, P, Browder, R, Perry, A, Oskoui, F, Culpepper, M, Dahl, N, Edelstein, C, Clegg, L, Fischer, D, Kaplan, M, Kaveh, K, Pankhaniya, R, Koren, M, Mansur, K, Lafayette, R, Lamar, W, Lee, J, Mahnensmith, R, Nachman, P, Mottl, A, Miskulin, D, Petersen, J, Radhakrishnan, J, Roppolo, M, Basireddy, M, Rosner, M, Bolton, W, Schulman, G, Steed, L, Steinman, T, Hogan, M, Venuto, R, Turban, S, Winklhofer, F., University of Zurich, Torres, Vicente E, Feldkamp, Thorsten (Beitragende*r), and Witzke, Oliver (Beitragende*r)

Subjects
Male, Tolvaptan, Medizin, 2700 General Medicine, SIROLIMUS, Kidney, V2 RECEPTOR ANTAGONIST, 10052 Institute of Physiology, Aquaretic, VASOPRESSIN V-2-RECEPTOR ANTAGONIST, Polycystic Kidney, 10035 Clinic for Nephrology, Medicine (all), General Medicine, Organ Size, Middle Aged, Adolescent, Adult, Benzazepines, Double-Blind Method, Female, Glomerular Filtration Rate, Humans, Polycystic Kidney, Autosomal Dominant, Sodium, Young Adult, Antidiuretic Hormone Receptor Antagonists, LONG-ACTING SOMATOSTATIN, Autosomal Dominant, 10076 Center for Integrative Human Physiology, OPC-41061, medicine.symptom, medicine.drug, medicine.medical_specialty, RENAL-FUNCTION, CYST GROWTH, Autosomal dominant polycystic kidney disease, Urology, Renal function, Kidney Volume, 610 Medicine & health, Placebo, Article, VOLUME PROGRESSION, Cystic kidney disease, Internal medicine, medicine, HYPONATREMIA, business.industry, urogenital system, ORAL TOLVAPTAN, medicine.disease, Endocrinology, Albuminuria, 570 Life sciences, biology, business
Abstract

BACKGROUND: The course of autosomal dominant polycystic kidney disease (ADPKD) is often associated with pain, hypertension, and kidney failure. Preclinical studies indicated that vasopressin V 2 -receptor antagonists inhibit cyst growth and slow the decline of kidney function. METHODS: In this phase 3, multicenter, double-blind, placebo-controlled, 3-year trial, we randomly assigned 1445 patients, 18 to 50 years of age, who had ADPKD with a total kidney volume of 750 ml or more and an estimated creatinine clearance of 60 ml per minute or more, in a 2:1 ratio to receive tolvaptan, a V 2 -receptor antagonist, at the highest of three twice-daily dose regimens that the patient found tolerable, or placebo. The primary outcome was the annual rate of change in the total kidney volume. Sequential secondary end points included a composite of time to clinical progression (defined as worsening kidney function, kidney pain, hypertension, and albuminuria) and rate of kidney-function decline. RESULTS: Over a 3-year period, the increase in total kidney volume in the tolvaptan group was 2.8% per year (95% confidence interval [CI], 2.5 to 3.1), versus 5.5% per year in the placebo group (95% CI, 5.1 to 6.0; P

Published
2012

20. Aberrant expression of microRNAs and the miR-1/MET pathway in canine hepatocellular carcinoma

Author

Lai, Y.-C., primary, Ushio, N., additional, Rahman, M. M., additional, Katanoda, Y., additional, Ogihara, K., additional, Naya, Y., additional, Moriyama, A., additional, Iwanaga, T., additional, Saitoh, Y., additional, Sogawa, T., additional, Sunaga, T., additional, Momoi, Y., additional, Izumi, H., additional, Miyoshi, N., additional, Endo, Y., additional, Fujiki, M., additional, Kawaguchi, H., additional, and Miura, N., additional

Published
2018
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22. Risk of haemolytic uraemic syndrome caused by shiga-toxin-producing Escherichia coli infection in adult women in Japan

Author

Fujii, J, Mizoue, T, Kita, T, Kishimoto, H, Joh, K, Nakada, Y, Ugajin, S, Naya, Y, Nakamura, T, Tada, Y, Okabe, N, Maruyama, Y, Saitoh, K, Kurozawa, Y, Fujii, J, Mizoue, T, Kita, T, Kishimoto, H, Joh, K, Nakada, Y, Ugajin, S, Naya, Y, Nakamura, T, Tada, Y, Okabe, N, Maruyama, Y, Saitoh, K, and Kurozawa, Y

Abstract

Shiga-toxin-producing Escherichia coli (STEC) infections usually cause haemolytic uraemic syndrome (HUS) equally in male and female children. This study investigated the localization of globotriaosylceramide (Gb3) in human brain and kidney tissues removed from forensic autopsy cases in Japan. A fatal case was used as a positive control in an outbreak of diarrhoeal disease caused by STEC O157:H7 in a kindergarten in Urawa in 1990. Positive immunodetection of Gb3 was significantly more frequent in female than in male distal and collecting renal tubules. To correlate this finding with a clinical outcome, a retrospective analysis of the predictors of renal failure in the 162 patients of two outbreaks in Japan was performed: one in Tochigi in 2002 and the other in Kagawa Prefecture in 2005. This study concludes renal failure, including HUS, was significantly associated with female sex, and the odds ratio was 4·06 compared to male patients in the two outbreaks. From 2006 to 2009 in Japan, the risk factor of HUS associated with STEC infection was analysed. The number of males and females and the proportion of females who developed HUS were calculated by age and year from 2006 to 2009. In 2006, 2007 and 2009 in adults aged >20 years, adult women were significantly more at risk of developing HUS in Japan., identifier:https://www.cambridge.org/core/journals/epidemiology-and-infection/article/risk-of-haemolytic-uraemic-syndrome-caused-by-shigatoxinproducing-escherichia-coli-infection-in-adult-women-in-japan/8CB4982B3F447BC66E9A5430B9FDF367

Published
2016

24. 210 Randomized study of intravesical chemotherapy using pirarubicin in low- and intermediate risk non-muscle-invasive bladder cancer in Japan - comparison one immediate postoperative intravesical chemotherapy with short-term adjuvant intravesical chemotherapy after TURBT

Author

Naya, Y., primary, Shiraishi, T., additional, Oishi, M., additional, Ueda, T., additional, Nakanishi, H., additional, Nakamura, T., additional, Hongo, F., additional, Iwata, T., additional, Kanazawa, M., additional, Mikami, K., additional, Kamoi, K., additional, Okihara, K., additional, and Ukimura, O., additional

Published
2016
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25. Risk of haemolytic uraemic syndrome caused by shiga-toxin-producingEscherichia coliinfection in adult women in Japan

Author

FUJII, J., primary, MIZOUE, T., additional, KITA, T., additional, KISHIMOTO, H., additional, JOH, K., additional, NAKADA, Y., additional, UGAJIN, S., additional, NAYA, Y., additional, NAKAMURA, T., additional, TADA, Y., additional, OKABE, N., additional, MARUYAMA, Y., additional, SAITOH, K., additional, and KUROZAWA, Y., additional

Published
2015
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30. Genome-wide association study identified SNP on 15q24 associated with bladder cancer risk in Japanese population

Author

Matsuda, K., primary, Takahashi, A., additional, Middlebrooks, C. D., additional, Obara, W., additional, Nasu, Y., additional, Inoue, K., additional, Tamura, K., additional, Yamasaki, I., additional, Naya, Y., additional, Tanikawa, C., additional, Cui, R., additional, Figueroa, J. D., additional, Silverman, D. T., additional, Rothman, N., additional, Namiki, M., additional, Tomita, Y., additional, Nishiyama, H., additional, Kohri, K., additional, Deguchi, T., additional, Nakagawa, M., additional, Yokoyama, M., additional, Miki, T., additional, Kumon, H., additional, Fujioka, T., additional, Prokunina-Olsson, L., additional, Kubo, M., additional, Nakamura, Y., additional, and Shuin, T., additional

Published
2014
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35. Tumour suppressors miR-1 and miR-133a target the oncogenic function of purine nucleoside phosphorylase (PNP) in prostate cancer.

Author

Kojima S, Chiyomaru T, Kawakami K, Yoshino H, Enokida H, Nohata N, Fuse M, Ichikawa T, Naya Y, Nakagawa M, Seki N, Kojima, S, Chiyomaru, T, Kawakami, K, Yoshino, H, Enokida, H, Nohata, N, Fuse, M, Ichikawa, T, and Naya, Y

Abstract

Background: Our recent analyses of miRNA expression signatures showed that miR-1 and miR-133a were significantly reduced in several types of cancer. Interestingly, miR-1 and miR-133a are located on the same chromosomal locus in the human genome. We examined the functional significance of miR-1 and miR-133a in prostate cancer (PCa) cells and identified the novel molecular targets regulated by both miR-1 and miR-133a.Methods and Results: The expression levels of miR-1 and miR-133a were significantly downregulated in PCa compared with non-PCa tissues. Restoration of miR-1 or miR-133a in PC3 and DU145 cells revealed significant inhibition of proliferation, migration, and invasion. Molecular target identification by genome-wide gene expression analysis and luciferase reporter assay showed that purine nucleoside phosphorylase (PNP) was directly regulated by both miRNAs. Silencing of the PNP gene inhibited proliferation, migration, and invasion in both PC3 and DU145 cells. Immunohistochemistry detected positive staining of PNP in PCa specimens.Conclusions: Downregulation of miR-1 and miR-133a was a frequent event in PCa and both function as tumour suppressors. The PNP is a novel target gene of both miRNAs and potentially functions as an oncogene. Therefore, identification of novel molecular networks regulated by miRNAs may provide new insights into the underlying causes of PCa oncogenesis. [ABSTRACT FROM AUTHOR]

Published
2012
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38. Radioresistance of cancer stem-like cell derived from canine tumours.

Author

Tanabe, A., Deguchi, T., Sato, T., Nemoto, Y., Maruo, T., Madarame, H., Shida, T., Naya, Y., Ogihara, K., and Sahara, H.

Subjects
LUNG cancer treatment, CANIDAE, CANCER radiotherapy, CANCER stem cells, DRUG resistance in cancer cells, DISEASES
Abstract

Cancer stem-like cells ( CSCs)/cancer-initiating cells ( CICs) are a small subpopulation of cancer cells that are responsible for the initiation, recurrence and metastasis of cancer. We previously demonstrated that, using the Hoechst 33342 dye-based side population technique, CSCs/ CICs in canine lung adenocarcinoma cell line exist. In this study, as CSCs/ CICs are known to form spheres in anchorage-independent environment in vitro, we evaluated the stemness of spheroid cells derived from canine lung adenocarcinoma and osteosarcoma cells by expression of stemness markers, and investigated radioresistance. Spheroid cells showed greater expression of stemness markers Oct-4 and CD133 gene than those of adherent-cultured cells. In nude mouse xenograft models, spheroid cells showed higher tumourigenic ability than adherent-cultured cells. In addition, spheroid cells showed significantly resistant against radioactivity as compared with adherent-cultured cells. These results suggest that spheroid cells could possess stemness and provide a CSCs/ CICs research tool to investigate CSCs/ CICs of canine tumour cells. [ABSTRACT FROM AUTHOR]

Published
2016
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