Yoshiki Ban
Yamaguchi University
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Publication
Featured researches published by Yoshiki Ban.
Reproductive Toxicology | 2002
Yoshiki Ban; Takahiro Sato; Toshio Nakatsuka; Masayuki Kemi; Keiji Samura; Hiroyoshi Matsumoto; Mark A. Cukierski; Matthew J. van Zwieten
Male rats were treated with a muscarinic receptor antagonist at 3, 10, and 100mg/kg/day for 4 weeks prior to mating with untreated females and their reproductive status was determined on gestation days (GD) 15-17. Treatment-related decreases in the pregnancy rate were observed at 100mg/kg/day without any effects on mating performance. Impairment of male fertility by this compound was also observed after treatment for 1 week, but there were no effects after a 1-week withdrawal period suggesting reversibility of the effect. There were no treatment-related effects on sperm production or motility, or testicular histopathology in any group. In order to determine whether the reduced fertility was a class effect of muscarinic receptor antagonists, atropine was examined. Males received atropine for 1 week at 62.5 and 125 mg/kg/day and were mated with untreated females. A low pregnancy rate associated with a decrease in the number of implantations was observed at 125 mg/kg/day. The effect on implantation was also observed at 62.5mg/kg/day. These findings suggest that the impairment of fertility in male rats induced by muscarinic receptor antagonists is a class effect, and has a relatively short onset of effect and is quickly reversible.
Toxicological Sciences | 1996
Yoshiki Ban; Toshio Nakatsuka; Hiroyoshi Matsumoto; Fumihiko Ikemoto; Takashi Makita
Previous study revealed that calcium channel blockers (CCBs) reduced embryonic heart rates (HRs) and produced morphological abnormalities when Gestational Day (GD) 11.5 rat embryos were cultured for 20 hr. The present study was to investigate whether a calcium channel agonist, Bay K 8644 (BAY), prevented CCB-induced embryotoxicity in vitro. GD 11.5 embryos were exposed to nifedipine (NIF), diltiazem (DIL), and verapamil (VER) either alone or in combination with BAY at 0.1, 1.0, and 10 micrograms/ml. These doses of BAY alone had no effect on gross morphology. Embryonic HRs were increased at 10 micrograms/ml of BAY, but were within control levels at 0.1 and 1.0 microgram/ml. The doses of NIF, DIL, and VER were 40, 6.0, and 2.0 micrograms/ml, respectively, and were the minimum concentrations to produce a 100% effect on morphological abnormalities. Embryonic HRs were reduced to 22, 31, and 34% below control levels in the NIF, DIL, and VER groups, respectively. The negative chronotropic effects of CCBs were inhibited by coadministration with BAY, depending on its concentration. When embryos exposed to each CCB were supplemented with BAY at 1.0 or 10 micrograms/ml, embryonic HRs were comparable to those of controls. Combined exposures of each CCB and 10 micrograms/ml BAY did not cause any morphological abnormalities. These results suggested that mechanisms of CCB embryotoxicity were directly related to pharmacological consequences of calcium channel blockage in developing rats.
Congenital Anomalies | 2018
Yuka Kirihata; Yoshiki Ban; Chiaki Nakamori; Hironori Takagi; Tomonori Hashimoto; Shunsuke Tsutsumi
The present study aimed at examining postnatal repairability of sodium valproate‐induced skeletal alterations in rats. Sodium valproate (400 mg/kg) or the vehicle (distilled water) was orally administrated to pregnant Sprague‐Dawley rats from gestation days 9 to 11. Fetuses and pups were obtained on gestation day 21 and postnatal day 11, respectively, and their skeletons were stained with Alizarin red S and Alcian blue and examined. Sodium valproate‐induced costal and vertebral alterations in the fetuses included discontinued rib cartilage, fused rib, full or short supernumerary rib, bipart ossification of thoracic centrum, supernumerary lumbar vertebrae, and lumbarization. In pups, however, discontinued rib cartilage was not observed, and the incidence of a short supernumerary rib was significantly lower than that in the fetuses, suggesting that these alterations are postnatally repairable.
Journal of Toxicological Sciences | 2009
Shigeharu Tsujioka; Yoshiki Ban; L. David Wise; Takayuki Tsuchiya; Takahiro Sato; Kenta Matsue; Takanori Ikeda; Minoru Sasaki; Masaru Nishikibe
Journal of Toxicological Sciences | 1999
Yoshiki Ban; Urumi Asanabe; Satoru Inagaki; Minoru Sasaki; Toshio Nakatsuka; Hiroyoshi Matsumoto
Journal of Toxicological Sciences | 2005
Takahiro Sato; Yoshiki Ban; Miki Uchida; Eri Gondo; Masakatsu Yamamoto; Yoshiko Sekiguchi; Akiko Sakaue; Masayuki Kemi; Toshio Nakatsuka
Journal of Toxicological Sciences | 2001
Yoshiki Ban; Masato Naya; Tatsuya Nishimura; Masako Kaneto; Kurajiro Kishi; Tadahiro Inoue; Hiroshi Yoshizaki; Yojiro Ooshima
Journal of Toxicological Sciences | 2002
Shunsuke Tsutsumi; Yoshimasa Hamada; Masashi Kato; Toshihiko Kumazawa; Atsushi Yokoyama; Toshiaki Numa; Yoshihiko Endo; Yoshiki Ban; Takeshi Morita
Congenital Anomalies | 2003
E. Gondo; Yoshiki Ban; M. Uchida; T. Sato; M. Yamamoto; Y. Sekiguchi; Toshio Nakatsuka; M. Kemi
Congenital Anomalies | 1999
Yoshiki Ban; U. Asanabe; S. Inagaki; M. Sasaki; Toshio Nakatsuka; H. Matsumoto
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National Institute of Advanced Industrial Science and Technology
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