Clinical Medical Research Center

Tokyo, Japan

Clinical Medical Research Center

Tokyo, Japan
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Soen S.,Kinki University | Fukunaga M.,Kawasaki Medical School | Sugimoto T.,The University of Shimane | Sone T.,Kawasaki Medical School | And 8 more authors.
Journal of Bone and Mineral Metabolism | Year: 2013

In 1995, the Japanese Society for Bone and Mineral Metabolism (now the Japanese Society for Bone and Mineral Research) established the Osteoporosis Diagnostic Criteria Review Committee. Following discussion held at the 13th scientific meeting of the Society in 1996, the Committee, with the consensus of its members, proposed diagnostic criteria for primary osteoporosis. The Committee revised those criteria in 1998 and again in 2000. The Japanese Society for Bone and Mineral Research and Japan Osteoporosis Society Joint Review Committee for the Revision of the Diagnostic Criteria for Primary Osteoporosis aimed at obtaining international consistency and made a revised edition based on the new findings in 2012. © 2013 The Japanese Society for Bone and Mineral Research and Springer Japan.


Orimo H.,Japan Osteoporosis Foundation | Nakamura T.,University of Occupational and Environmental Health Japan | Hosoi T.,National Center for Geriatrics and Gerontology | Iki M.,Kinki University | And 10 more authors.
Archives of Osteoporosis | Year: 2012

Introduction: In 1998, the first Japanese practice guidelines on osteoporosis was published. It has been updated several times, with the most recent being the full-scale 2011 edition and its abridged edition. The present guidelines provide information for the managements of primary osteoporosis in postmenopausal women and men over 50 years old, a summary of the evidence for the treatment of secondary osteoporosis, and a summary of the evidence for the prevention of osteoporosis in younger people. Method: The present Executive Summary is primarily based on the content of the 2011 Japanese abridged edition. One of the key changes is revision of the criteria for initiation of pharmacological treatment, along with an introduction of the fracture risk factors used in FRAX®. Key figures and tables were selected from the Japanese abridged edition and a reference list was added. Result and conclusions: The essential points of the Japanese practice guidelines on osteoporosis were translated into English for the first time. It is hoped that the content of the guidelines becomes known throughout the world. © 2012 The Author(s).


Shang W.-B.,Clinical Medical Research Center | Luo Z.-K.,Nanjing University | Li X.-H.,Changzhou Fourth Peoples Hospital | Liu L.,Changzhou Fourth Peoples Hospital | And 5 more authors.
Chinese Journal of Pharmacology and Toxicology | Year: 2014

OBJECTIVE To explore the effect and underlying mechanism of promethazine (PMZ) on proarrhythmia in guinea pigs. METHODS (1) In vivo ECG recordings were made to analyze effects of jugular intravenous (iv) injection of PMZ on ECG in guinea pigs. PMZ was injected in this order: 3.83虠 7.67虠15.33虠38.33 mg·kg-1 cumulatively. (2) In vitro ECG recordings were made to analyze effects of PMZ on ECG in isolated hearts of guinea pigs. PMZ was perfused in such order: 0.1虠1虠10虠 50 μmol·L-1. (3) L-type Ca2+ currents from ventricular myocytes in guinea pigs were recorded to investigate the PMZ's blocking effect. PMZ was perfused in such order: 0.1虠1虠10虠50 μmol·L-1 虠washout. (4) hNav1.5 and hERG currents were recorded to investigate the PMZ's blocking effects. PMZ-perfused in such order: 1虠3虠10虠30 μmol·L-1 for hNav1.5 current analysis, and 0.3虠1虠3虠10 μmol·L-1 for hERG current analysis. RESULTS (1) PMZ (15.33 mg·kg-1) significantly prolonged QRS intervals in guinea pigs in vivo ECG (P<0.05). PMZ (38.33 mg·kg-1) prolonged QRS, QTc, and P-R intervals but reduced the heart rate (P<0.05). PMZ (10 μmol·L-1) reduced the heart rate of isolated guinea pig hearts. PMZ 50 μmol-L-1 prolonged QRS and QTc intervals and further reduced the heart rate (P<0.05). (3) PMZ inhibited the L-type Ca2+ current from ventricular myocytes in guinea pigs in a concentration-dependent manner with the IC50 of (8.9±1.0) μmol·L-1. (4) PMZ inhibited the hNav1.5 and hERG currents in a concentration-dependent manner with the IC50 of 6.1±1.5 and (1.6±0.2) μmol·L-1, respectively. CONCLUSION PMZ might cause arrhythmia at overdoses and incombination with other drugs which have potential blocking effect on INa, Ca2+ and Ikr currents. The proarrhythmic effect of PMZ might be mediated by the blocking effect on INa, Ca2+ and Ikr currents.

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