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Second round of Launch Pad selections includes eight newcomers
The National Reactor Innovation Center at Idaho National Laboratory has announced 13 project selections across 12 companies for the Nuclear Energy Launch Pad, a Department of Energy–led program that integrates reactor and fuel facility authorization, testing, and deployment support for private nuclear developers.
The Launch Pad emerged from the Reactor Pilot Program and Fuel Line Pilot Program.
According to INL, projects selected include reactor development and nuclear fuel cycle advancements, including fabrication, enrichment, and conversion technologies.
Toshiyuki Umata, Toshiyuki Norimura
Fusion Science and Technology | Volume 60 | Number 3 | October 2011 | Pages 1193-1196
Biology | Proceedings of the Ninth International Conference on Tritium Science and Technology | doi.org/10.13182/FST11-A12629
Articles are hosted by Taylor and Francis Online.
A large amount of tritium is required as the fuel source for the nuclear fusion reaction. As a result, during the routine operation or in case of accidents, one of the major issues is the assessment of the biological effects of tritium released from nuclear fusion power plants. In this study, the mutagenic effects of tritiated water (HTO) were compared to those of 137Cs irradiation on spleen T lymphocytes of wild (p53+/+) mice and p53-deficient (p53-/-) mice. In both mice, TCR variant fractions induced by HTO was higher than those by simulation-irradiation of 137Cs rays. When compared on the basis of the induced TCR variant fractions in p53-/- mice at 3 Gy, tritium rays appear to be 1.7 times more mutagenic than rays. On the other hand, in p53+/+ mice, HTO injection increased induced TCR variant fractions significantly, whereas simulation-irradiation did not increase those at all. In order to elucidate the reason responsible for this difference in p53+/+ mice, we investigated the apoptotic ability of spleen T lymphocytes. As a result, the apoptotic ability of spleen T lymphocytes from p53+/+ mice exposed to HTO was reduced significantly compared to that from p53+/+ mice not exposed.
