Radiation research
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Time-temperature analyses of durations of heating required to achieve isosurvival were used to compare hyperthermic cell killing of synchronous Chinese hamster ovary (CHO) cells heated in G1 or S at temperatures of 42 to 45.5 degrees C. G1 populations were obtained by incubation of mitotic cells for 90 min at 37 degrees C. S phase populations were obtained by incubation of mitotic cells for 12 h at 37 degrees C in medium supplemented with 2 micrograms/ml aphidicolin, a reversible inhibitor of DNA alpha polymerase; S phase survival was also determined in an aphidicolin-free system by using high specific activity [3H]thymidine. ⋯ Using least-squares regression of the semilog plots, the curves were analyzed either as continually bending curves or as two straight lines with a break at 43.5 degrees C. When the data were analyzed using two straight lines, no significant differences in the slopes of the time-temperature plots of G1 or S phase cells were observed. A quantitative comparison between the two methods of data analysis demonstrated that in both phases the data were better fit with a continuously curving line, rather than two straight lines.
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We performed two independent series of experiments aiming at establishing dose-response curves for lethality or oncogenic transformation in vitro following acute and protracted X-ray doses between 0.25 and 2 Gy. In the first series of experiments, we measured the survival of C3H/10T1/2 CL8 fibroblasts and their transformed counterparts (MCA TCL15) as a function of X-ray dose delivered at 0.49 Gy/min. In addition, 1- and 2-Gy doses were split into four fractions separated by 3-h intervals. ⋯ The dose-response curves for oncogenic transformation in the low-dose range between 0.25 and 2 Gy were consistent with a linear response with a positive slope 2.50 +/- 0.11 X 10(-4), 1.50 +/- 0.03 X 10(-4), or 0.87 +/- 0.05 X 10(-4) Gy-1, for acute, 1-h, or 3-h protracted exposures, respectively. Hence, relative to the acute irradiation, the 1- or 3-h protraction of the X-ray dose reduced the slopes by 0.60 +/- 0.03 or 0.35 +/- 0.03, respectively. These results indicate that in the dose range between 0.25 to 2 Gy, the dose-response curves for survival or oncogenic transformation were linear and can be modified by the temporal distribution of the X-ray dose.
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Comparative Study
Dose-rate effects in mammalian cells. IV. Repairable and nonrepairable damage in noncycling C3H 10T 1/2 cells.
Repairable and nonrepairable components of gamma-ray damage leading to cell reproductive death were determined by measuring the range over which dose rate influenced the response of non-cycling C3H 10T 1/2 mouse cells. Cell proliferation and cell cycle redistribution were eliminated as factors influencing the dose-rate effect in the system by irradiating confluent monolayers of contact inhibited cells. The radiosensitivity of the cells did not change, and no selective loss of damaged cells occurred over the extended treatment times. ⋯ Res. Q. 4, 357-397 (1968)] when the standard treatment time is changed. Comparison of our data with in vivo isoeffect curves of total dose vs dose per fraction for "early" and "late" tissue responses indicate that cell cycle redistribution should not be ignored as a factor influencing time-dose relationships in radiotherapy.
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Case Reports Comparative Study
Xeroderma Pigmentosum and medulloblastoma: chromosomal damage to lymphocytes during radiotherapy.