@misc{oai:repo.qst.go.jp:00069061,
 author = {Bing, Wang and Tanaka, Kaoru and Shang, Yi and Vares, Guillaume and Morimoto, Yasuko and Nakajima, Tetsuo and Nenoi, Mitsuru and Hayata, Isamu and 王 冰 and 田中 薫 and 尚 奕 and Ｇｕｉｌｌａｕｍｅ Ｖａｒｅｓ and 森本 泰子 and 中島 徹夫 and 根井 充 and 早田 勇},
 month = {Jul},
 note = {A radiation-induced adaptive response, which was judged as reduction of both fetal death and digital malformation, was demonstrated in fetal mice by priming low-dose radiation on E11 prior to a high-dose irradiation on E12. Suppression of the digital defects was correlated to the inhibition of radiation-induced apoptosis. The priming dose was mouse strain-related. Both Trp53 alleles were essential for induction of the adaptive response. Furthermore, existence of the dose-rate effect was verified for delivery of the priming dose. There was a high postnatal mortality in the offspring that survived from prenatal death. Postnatal retardation, alteration in adult behavior, and life span shortening were observed in the survivals. In addition, a significantly increased radiosensitivity to the killing effect was also observed in the postnatal survivals. These results indicate that radiation-induced adaptive response in fetal mice is due to a complex interplay between dose, dose rate and animal factors such as the strain, developmental stage, and gene background. Though the priming dose could rescue some mice from high dose irradiation, the survivals are not healthy as alterations in development, behavior and radiosensitivity were observed. This work was supported in part by the Budget for New Nuclear Crossover Research from the Ministry of education, Culture, Sports, Sciences and Technology, Japan., 13th International Congress of Radiation Research},
 title = {Study on radiation-induced adaptive response in fetal mice.},
 year = {2007}
}