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Featured researches published by Nobuyoshi Tamagawa.
Pediatric Diabetes | 2012
Tohru Yorifuji; Rika Fujimaru; Yuki Hosokawa; Nobuyoshi Tamagawa; Momoko Shiozaki; Katsuya Aizu; Kazuhiko Jinno; Yoshihiro Maruo; Hironori Nagasaka; Toshihiro Tajima; Koji Kobayashi; Tatsuhiko Urakami
Yorifuji T, Fujimaru R, Hosokawa Y, Tamagawa N, Shiozaki M, Aizu K, Jinno K, Maruo Y, Nagasaka H, Tajima T, Kobayashi K, Urakami T. Comprehensive molecular analysis of Japanese patients with pediatric‐onset MODY‐type diabetes mellitus.
Journal of Medical Genetics | 2012
Tohru Yorifuji; Rie Kawakita; Yuki Hosokawa; Rika Fujimaru; Emi Yamaguchi; Nobuyoshi Tamagawa
GATA6 haploinsufficiency has recently been reported as the most frequent cause of neonatal diabetes with pancreatic agenesis. Although all previously reported cases represented a de novo mutation with complete agenesis or pronounced hypoplasia of the pancreas, in this study we identified a family with a dominantly inherited mutation. Unlike previously reported cases, the degree of pancreatic hypoplasia and the severity of diabetes varied among members of the family, ranging from neonatally lethal diabetes with only a remnant of pancreatic tissue to adult-onset diabetes associated with dorsal agenesis of the pancreas. These observations further broaden the clinical spectrum of diabetes associated with GATA6 haploinsufficiency.
Diabetic Medicine | 2014
R. Kawakita; Yuki Hosokawa; Rika Fujimaru; Nobuyoshi Tamagawa; Tatsuhiko Urakami; K. Takasawa; K. Moriya; H. Mizuno; Yoshihiro Maruo; M. Takuwa; Hironori Nagasaka; Y. Nishi; Yukiyo Yamamoto; Katsuya Aizu; Tohru Yorifuji
To investigate the molecular and clinical characteristics of the largest series of Japanese patients with glucokinase maturity‐onset diabetes of the young (GCK‐MODY), and to find any features specific to Asian people.
Pediatric Diabetes | 2014
Tohru Yorifuji; Yukiko Hashimoto; Rie Kawakita; Yuki Hosokawa; Rika Fujimaru; Kazue Hatake; Nobuyoshi Tamagawa; Hisakazu Nakajima; Masayo Fujii
The most common form of transient neonatal diabetes mellitus (TNDM) is 6q24‐related TNDM. Patients are treated with insulin during the neonatal period until spontaneous remission. However, diabetes often recurs in adolescence, and there is no standard therapy for patients with a relapse. A paternal duplication at the 6q24 critical region spanning the pleiomorphic adenoma gene‐like 1 PLAGL1 gene was found in a Japanese patient with TNDM relapse. The patient was treated with a dipeptidyl peptidase‐4 (DPP4) inhibitor, alogliptin, at a dose of 25 mg per day. Immediately after treatment initiation, his hemoglobin A1c (HbA1c) levels dropped from 7.0–7.5% (52–58 mmol/mol) to 6.0–6.5% (41–47 mmol/mol) and remained stable for over a year. We reported the successful treatment of relapsed 6q24‐related TNDM with a DPP4 inhibitor. Although insulin has been the conventional treatment for such patients, treatments targeting the GLP1 pathway can be a useful alternative because these patients retain the β cell mass and responsiveness through G protein‐coupled pathways.
Diabetic Medicine | 2015
Tohru Yorifuji; Keiko Matsubara; Azumi Sakakibara; Yukiko Hashimoto; Rie Kawakita; Yuki Hosokawa; Rika Fujimaru; Akiko Murakami; Nobuyoshi Tamagawa; Kazue Hatake; Hironori Nagasaka; Junichi Suzuki; Tatsuhiko Urakami; M. Izawa; Masayo Kagami
Abnormalities in the imprinted locus on chromosome 6q24 are the most common causes of transient neonatal diabetes mellitus (6q24‐related transient neonatal diabetes). 6q24‐Related transient neonatal diabetes is characterized by the patient being small‐for‐gestational age, diabetes mellitus at birth, spontaneous remission within the first few months and frequent recurrence of diabetes after childhood. However, it is not clear whether individuals with 6q24 abnormalities invariably develop transient neonatal diabetes. This study explored the possibility that 6q24 abnormalities might cause early‐onset, non‐autoimmune diabetes without transient neonatal diabetes.
Leukemia & Lymphoma | 2015
Masahiro Yoshida; Nobuyoshi Tamagawa; Takafumi Nakao; Hiroshi Kanashima; Hideya Ueda; Akiko Murakami; Toru Yorifuji; Takahisa Yamane
DISCLAIMER: The ideas and opinions expressed in the journal’s Just Accepted articles do not necessarily reflect those of Informa Healthcare (the Publisher), the Editors or the journal. The Publisher does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of the material contained in these articles. The reader is advised to check the appropriate medical literature and the product information currently provided by the manufacturer of each drug to be administered to verify the dosages, the method and duration of administration, and contraindications. It is the responsibility of the treating physician or other health care professional, relying on his or her independent experience and knowledge of the patient, to determine drug dosages and the best treatment for the patient. Just Accepted articles have undergone full scientific review but none of the additional editorial preparation, such as copyediting, typesetting, and proofreading, as have articles published in the traditional manner. There may, therefore, be errors in Just Accepted articles that will be corrected in the final print and final online version of the article. Any use of the Just Accepted articles is subject to the express understanding that the papers have not yet gone through the full quality control process prior to publication. Just Accepted by Leukemia & Lymphoma
Pediatric Diabetes | 2018
Tohru Yorifuji; Shinji Higuchi; Rie Kawakita; Yuki Hosokawa; Takane Aoyama; Akiko Murakami; Yoshiko Kawae; Kazue Hatake; Hironori Nagasaka; Nobuyoshi Tamagawa
Causative mutations cannot be identified in the majority of Asian patients with suspected maturity‐onset diabetes of the young (MODY).
Global pediatric health | 2017
Yoshiko Nakano; Kai Yamasaki; Yasunori Otsuka; Atsushi Ujiro; Rie Kawakita; Nobuyoshi Tamagawa; Keiko Okada; Hiroyuki Fujisaki; Tohru Yorifuji; Junichi Hara
Creative Commons Non Commercial CC-BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits noncommercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). Brief Report
International Journal of Pediatric Endocrinology | 2015
Yukiko Hashimoto; Azumi Sakakibara; Rie Kawakita; Yuki Hosokawa; Rika Fujimaru; Tetsuro Nakamura; Hiroko Fukushima; Aiko Igarashi; Michiya Masue; Hironori Nishibori; Nobuyoshi Tamagawa; Akiko Murakami; Kazue Hatake; Tohru Yorifuji
The focal form of congenital hyperinsulinism (CHI) is characterized by a cluster of abnormal insulin-oversecreting β cells within a restricted area of the pancreas. Although identification of the focal lesion is very important in the management of CHI, it has been reported that imaging studies, including computed tomography (CT), magnetic resonance imaging (MRI) scans, or angiography, are not helpful in identifying the focal lesion. Currently, fluorine-18-L-dihydroxyphenylalanine positron emission tomography (18F-DOPA PET) is believed to be the only imaging modality that can identify the focal lesions. In this report, however, we present a case of a 7-month-old girl with the focal form of CHI, caused by a loss-of-function mutation in the ABCC8 gene, whose lesion was clearly visible as a hyperenhancing nodule on contrast-enhanced CT and dynamic MRI imaging.
Journal of Pediatric Hematology Oncology | 2017
Shin-ichi Tsujimoto; Yoshiko Nakano; Tomoo Osumi; Keiko Okada; Meri Ouchi-Uchiyama; Keisuke Kataoka; Yoichi Fujii; Kentaro Ohki; Masafumi Seki; Nobuyoshi Tamagawa; Junko Takita; Seishi Ogawa; Nobutaka Kiyokawa; Junichi Hara; Motohiro Kato