RESUMEN
Radioactive nuclides are induced in irradiation devices and patients during high-energy photon and ion beam radiotherapies. These nuclides potentially become sources of exposure to radiation workers. Radiological technologists (RTs) are often required to enter an irradiation room and approach activated devices and patients. In this study, annual doses to RTs working in a carbon ion radiotherapy facility were estimated based on measurements with the Si-semiconductor personal dosemeter. In addition, the time decay of dose around a patient couch after irradiation was obtained by phantom experiments. The annual Hp(10) values for passive and scanned beams were estimated to be 61 and 2 µSv, respectively, when assuming the number of treatments in 2013. These are much lower than the ICRP recommended dose limit for radiation workers. The time-series data of dose to RTs during their work and the time decay of the dose should be helpful for reducing their dose further.
Asunto(s)
Carbono/química , Radioterapia de Iones Pesados/métodos , Exposición Profesional/análisis , Radioisótopos/análisis , Radiometría/instrumentación , Tecnología Radiológica/métodos , Humanos , Iones , Exposición Profesional/prevención & control , Fantasmas de Imagen , Dosis de Radiación , Radiometría/métodos , Dosificación Radioterapéutica , Semiconductores , Silicio/química , Tecnología Radiológica/instrumentación , Factores de Tiempo , Recursos HumanosRESUMEN
A large number of indolyl-4-azaindolyl thiazoles, nortopsentin analogues, were conveniently synthesized. The antiproliferative activity of the new derivatives was examined against four human tumor cell lines with different histologic origin. Seven derivatives consistently reduced the growth of the experimental models independently of TP53 gene status and exhibited the highest activity against the malignant peritoneal mesothelioma (STO) cell line. The most active compound of this series acts as a CDK1 inhibitor, and was found to cause cell cycle arrest at G2/M phase, to induce apoptosis by preventing the phosphorylation of survivin in Thr(34) and to increase the cytotoxic activity of paclitaxel in STO cells.