RESUMO
A novel traceable point-like 68Ge/68Ga source was developed for calibration of positron emission tomography (PET) scanners. The source was equipped with a spherically symmetric acrylic positron absorber. The physical characteristics of photons emitted from the point-like source were evaluated by Monte Carlo simulation, considering possible geometrical uncertainties. The calibration factor of a clinical PET/CT scanner was evaluated using four manufactured point-like sources as a practical application of the point-like source. The results were consistent with that determined by the conventional cross-calibration method. The traceable point-like 68Ge/68Ga source is expected to be a simple and practical tool for determining the calibration factor and evaluating the physical characteristics of PET scanners.
Assuntos
Radioisótopos de Gálio , Germânio , Tomografia por Emissão de Pósitrons combinada à Tomografia Computadorizada/instrumentação , Radioisótopos , Calibragem , Método de Monte CarloRESUMO
Cancer development often involves mutagenic replication of damaged DNA by the error-prone translesion synthesis (TLS) pathway. Aberrant activation of this pathway plays a role in tumorigenesis by promoting genetic mutations. Rev1 controls the function of the TLS pathway, and Rev1 expression levels are associated with DNA damage induced cytotoxicity and mutagenicity. However, it remains unclear whether deregulated Rev1 expression triggers or promotes tumorigenesis in vivo. In this study, we generated a novel Rev1-overexpressing transgenic (Tg) mouse and characterized its susceptibility to tumorigenesis. Using a small intestinal tumor model induced by N-methyl-N-nitrosourea (MNU), we found that transgenic expression of Rev1 accelerated intestinal adenoma development in proportion to the Rev1 expression level; however, overexpression of Rev1 alone did not cause spontaneous development of intestinal adenomas. In Rev1 Tg mice, MNU-induced mutagenesis was elevated, whereas apoptosis was suppressed. The effects of hREV1 expression levels on the cytotoxicity and mutagenicity of MNU were confirmed in the human cancer cell line HT1080. These data indicate that dysregulation of cellular Rev1 levels leads to the accumulation of mutations and suppression of cell death, which accelerates the tumorigenic activities of DNA-damaging agents.
Assuntos
Adenoma/etiologia , Apoptose/genética , Carcinógenos/toxicidade , Expressão Gênica , Neoplasias Intestinais/etiologia , Nucleotidiltransferases/genética , Mutação Puntual , Adenoma/patologia , Alelos , Animais , Linhagem Celular Tumoral , Transformação Celular Neoplásica/induzido quimicamente , Transformação Celular Neoplásica/genética , Dano ao DNA , DNA Polimerase Dirigida por DNA , Modelos Animais de Doenças , Progressão da Doença , Frequência do Gene , Genótipo , Neoplasias Intestinais/mortalidade , Neoplasias Intestinais/patologia , Masculino , Camundongos , Camundongos Transgênicos , Carga TumoralRESUMO
Sealed radioactive sources which have small activity were employed for the determination of response and tests for non-linearity and energy dependence of detector responses. Close source-to-detector geometry (at 0.3 m or less) was employed to practical tests for portable dose meters to accumulate statistically sufficient ionizing currents. Difference between response in the present experimentally studied field and in the reference field complied with ISO 4037 due to non-uniformity of radiation fluence at close geometry was corrected by use of Monte Carlo simulation. As a consequence, corrected results were consistent with the results obtained in the ISO 4037 reference field within their uncertainties.
Assuntos
Dosímetros de Radiação , Monitoramento de Radiação/instrumentação , Algoritmos , Calibragem , Césio/análise , Simulação por Computador , Acidente Nuclear de Fukushima , Humanos , Japão , Método de Monte Carlo , Dinâmica não Linear , Fótons , Monitoramento de Radiação/métodos , Radiação Ionizante , Liberação Nociva de Radioativos , Valores de ReferênciaRESUMO
PURPOSE: Previous studies using mouse osteoblast derived MC3T3-E1 and mouse myoblast derived C2C12 cells have not completely explained the mechanisms responsible for osteoradionecrosis. Thus, the aim of this study was to advance the in vitro experimental approaches for investigations of osteoradionecrosis. MATERIALS AND METHODS: The pluripotent stem cell line, mouse embryo derived C3H10T1/2, was treated with all-trans-retinoic acid after irradiation (1, 3 and 6 Gy), and cell growth, cell cycle distribution, apoptosis, and alkaline phosphatase (ALP) activity were assessed. RESULTS: We demonstrated that ionising radiation inhibited the growth and decreased ALP activity in C3H10T1/2 cells. The decrease in cell growth was not due to apoptosis but was due to cell cycle delay. The decrease in ALP activity persisted in cells that were induced to an osteoblastic lineage 24 h after irradiation. CONCLUSIONS: Our results suggested that C3H10T1/2 cells are suitable for investigating the effects of ionising irradiation on osteoblast precursor cells.
