Objective To introduce a new way to solve the problem of field-field junction in the traditional radiotherapy of the nasopharyngeal carcinoma better.Methods Using the 3-dimentional planning system,the dose distribution of traditional radiotherapy and the electronic beam irradiation technology of L shape field for nasopharyngeal carcinoma in 2D-or 3D-CRT could be gotten.Results The dose coverage of V95 of the gross tumor volume(GTV)satisfied the clinical requirements.The highest dose in the electronic beam irradiation of L shape field was 7200 cGy,while it was 8900 cGy in the traditional way.The volume of dose that over 6500 cGy of throat was 19.64 ％ in the former,the latter was 31.95 ％.Conclusion The electronic beam irradiation technology of L shape field is better than the traditional radiotherapy in field-field junction and in dose distribution.Since that,the electronic beam irradiation technology of L shape field is worth of application for the treatment of nasopharyngeal carcinoma.

Purpose: Simulating calculation the dose distribution of the total body irradiation (TBI) with three dimension treatment planning system(3D-TPS ). Materials and Methods: For TBI, the source skin distance(SSD) is 380 cm, field size is 40 cm × 40cm, and collimator angle is 45°. The percent dose depth (PDD) and onset axis ratio (OAR) of the linac accelerator is measured with the big water phantom self-made. In the same radiation condition, the PDD and OAR of water which is simulated calculation with the 3D-TPS is compared with the measurement results to confirm whether the 3D-TPS can calculate the TBI dose distribution. The dose distribution of the human phantom is calculated with 3D-TPS, which is compared and confirmed with the film and TLD measurements. Results: The maximum error of PDD and OAR in the water phantom between the measurements and calculations of 3D-TPS are 3% and 6%. The calculation results of the 3D-TPS is according with the measurement results of the film and TLD approximately. Conclusions: 3D-TPS could simulate calculation the dose distribution for TBI accurately. It is possible to improve more uniform dose for TBI with corresponding compensator for specific patient.

Objective: This study was to investigate the effects of MEHP on isolated rat heart and explore its mechanism. Methods: The experiments were performed with Langendorff-perfused rat heart with a Langendorff apparatus. 35 SD rats were used in the experiment and there were 5 rats per group. MEHP at doses of 3.125, 6.250, 12.500 and 25.000 μmol/L were given to the hearts for 25 minutes. Effects of NAC at concentration of 5 mmol/L were evaluated by co-treatment with 12.500 or 25.000 μmol/L MEHP. Data was collected per 5 minutes for 25 minutes. The heart rate, LVDP, LVEDP, dp/dtmax, and dp/dtmin were measured and analyzed using a PL3508 Data Acquisition and Analysis System. 200 waves at least were required each time. LDH contents in heart lavage fluid were determined by photometric assays using the automated biochemical analyzer. A section of the heart tissue was used for histopathological examination. DCFH-DA method was used to detect the levels of reactive oxygen species in different groups of heart tissues. Results: There was a concentration dependent decrease of heart rate (P<0.05) . At concentrations of 6.250, 12.500 and 25.000 μmol/L, MEHP significantly decreased the LVDP, dp/dtmax and dp/dtmin (P<0.05) , and this decrease is more pronounced with perfusion time. As the MEHP was given up to 6.250, 12.500 and 25.000 μmol/L, a statistical significance was found in the increase of LVEDP (P<0.05) . For dp/dtmin, a significant increase was observed at the concentration of 3.125 μmol/L when perfused with 10 and 15 min (P<0.05) , but this increase disappeared over time. LDH in cardiac perfusate increased as the MEHP given a higher concentration (P<0.05) . Compared with the control group, Histopathological analysis showed edema of myocardial tissue and cells, and inflammatory cells infiltration and myocardial cells necrosis were obvious in the MEHP perfusion groups. Myocardial ROS levels of the four MEHP treatment groups were all significantly higher than that of control group (P<0.05) . These heart damage induced by MEHP could be attenuated by NAC in different degrees. Conclusion MEHP can induce damage to myocardial tissue of isolated rat heart and one possible mechanism is the oxidative stress