[Clinical analysis of transumbilical single-incision laparoscopic cholecystectomy with totally free umbilical ring by conventional instruments].

Objective: To summarize the clinical experience of transumbilical single-port laparoscopic cholecystectomy, and evaluate its clinical utility and the feasibility of widely usage. Methods: Between April 2012 and June 2017, 500 cases who underwent transumbilical single-port laparoscopic cholecystectomy with totally free umbilical ring by conventional instruments were enrolled. The clinical data were retrospectively analyzed. Results: A total of 487 patients were successfully completed the operation. In addition, 3 cases were converted to open cholecystectomy, 10 cases were converted to multi-port laparoscopy and drainage tubes were placed in 5 cases. The mean operating time of transumbilical single-port laparoscopic cholecystectomy(from the Trocars being put to the gallbladders being removed)shortened from 72.3 min to 13.2 min. The average bleeding amount was less than 10 ml. After the operation, 3 cases had delayed bile leakage and 3 cases had transient up-regulation of bilirubin at the beginning of the technique. No patients had hemorrhage and Trocar hernia. The average hospital stay of patients was 2.1 days. The cosmetic effect was remarkable during follow-up. Conclusion: The transumbilical single-port laparoscopic cholecystectomy with totally free umbilical ring by conventional instruments should be widely carried out in hospitals at all levels because of its minimal postoperative pain, rapid recovery, hidden incision, low costs and low incidence of port-site hernia.

Defects in ZnO nanorods prepared by a hydrothermal method.

ZnO nanorod arrays were fabricated using a hydrothermal method. The nanorods were studied by scanning electron microscopy, photoluminescence (PL), time-resolved PL, X-ray photoelectron spectroscopy, and positron annihilation spectroscopy before and after annealing in different environments and at different temperatures. Annealing atmosphere and temperature had significant effects on the PL spectrum, while in all cases the positron diffusion length and PL decay times were increased. We found that, while the defect emission can be significantly reduced by annealing at 200 degrees C, the rods still have large defect concentrations as confirmed by their low positron diffusion length and short PL decay time constants.

Evaluation of an automated deformable image matching method for quantifying lung motion in respiration-correlated CT images.

We have evaluated an automated registration procedure for predicting tumor and lung deformation based on CT images of the thorax obtained at different respiration phases. The method uses a viscous fluid model of tissue deformation to map voxels from one CT dataset to another. To validate the deformable matching algorithm we used a respiration-correlated CT protocol to acquire images at different phases of the respiratory cycle for six patients with nonsmall cell lung carcinoma. The position and shape of the deformable gross tumor volumes (GTV) at the end-inhale (EI) phase predicted by the algorithm was compared to those drawn by four observers. To minimize interobserver differences, all observers used the contours drawn by a single observer at end-exhale (EE) phase as a guideline to outline GTV contours at EI. The differences between model-predicted and observer-drawn GTV surfaces at EI, as well as differences between structures delineated by observers at EI (interobserver variations) were evaluated using a contour comparison algorithm written for this purpose, which determined the distance between the two surfaces along different directions. The mean and 90% confidence interval for model-predicted versus observer-drawn GTV surface differences over all patients and all directions were 2.6 and 5.1 mm, respectively, whereas the mean and 90% confidence interval for interobserver differences were 2.1 and 3.7 mm. We have also evaluated the algorithm's ability to predict normal tissue deformations by examining the three-dimensional (3-D) vector displacement of 41 landmarks placed by each observer at bronchial and vascular branch points in the lung between the EE and EI image sets (mean and 90% confidence interval displacements of 11.7 and 25.1 mm, respectively). The mean and 90% confidence interval discrepancy between model-predicted and observer-determined landmark displacements over all patients were 2.9 and 7.3 mm, whereas interobserver discrepancies were 2.8 and 6.0 mm. Paired t tests indicate no significant statistical differences between model predicted and observer drawn structures. We conclude that the accuracy of the algorithm to map lung anatomy in CT images at different respiratory phases is comparable to the variability in manual delineation. This method has therefore the potential for predicting and quantifying respiration-induced tumor motion in the lung.

Modeling the development of metastases from primary and locally recurrent tumors: comparison with a clinical data base for prostatic cancer.

For many types of cancer, patients who relapse locally following localized treatment such as surgery or radiation therapy are found to have a higher incidence of distant metastases than those who are locally controlled. In this study we developed a mathematical model to investigate whether the excess distant metastases arise mainly from the local recurrence or whether the primary tumors in this group of patients have an intrinsically higher metastatic potential than those of locally controlled patients of the same clinical stage. The parameters of the model were chosen to be representative of prostate cancer and the calculated results were compared with published clinical data for carcinoma of the prostate. The best agreement with the data was seen for parameters which imply somewhat more "aggressive" primary tumors for locally relapsing patients, yielding relatively high rates of micrometastatic dissemination prior to initial diagnosis. However, the model calculations indicate that more than half of the metastases in such patients originated in association with the development of a local recurrence. Therefore, achieving local control in this group of patients would be beneficial in improving long term survival.

Presence of point mutations in the N-ras gene in radiation-transformed rat embryo cells.

We study the transforming ability of X-rays in multistep carcinogenesis by irradiating primary rat cells which contain transfected c-myc oncogene. X-irradiation induces fully transformed phenotypes, including anchorage-independent growth and tumor formation in nude mice. Of seven foci examined, five exhibited an A to G conversion in codon 61 of the N-ras oncogene. Another transformed isolate has a single G to A base substitution in codon 14 in the same oncogene, while no point mutation is detected in the other focus. This is the first in vitro demonstration of the association between point mutation and X-ray-transformed cells.

Radiation-induced apoptosis: effects of cell age and dose fractionation.

The cell cycle dependence of radiation-induced apoptosis was measured using mitotically synchronized REC:myc(ch1) and Rat1:mycb cells. Cells in S and G2 phases were more susceptible; the apoptotic fraction was about 0.7-0.8 as compared to about 0.4 for G1 cells at a dose of 10 Gy. Two-dimensional cytofluorimetric analysis of cells, pulsed-labeled with bromodeoxyuridine and then irradiated with 10 Gy, showed both G1 and G2 blocks (6-8 h) for REC:myc(ch1) cells but only G2 block for Rat1:mycb cells. Consistent with these results, wild-type p53 and WAF1 (or p21), known to play a role in G1 delay, was induced by radiation in REC:myc(ch1) but not in Rat1:mycb cells. The cell cycle dependence of radiation-induced apoptosis and the absence of a G1 block for Rat1:mycb cells led to the prediction and observation of the novel "inverse split-dose effect," i.e., a radiation dose given in two equal halves separated by a few hours yielded a higher level of apoptosis relative to that resulting from the same total dose given all at once. This effect is due to cell cycle progression from G1 to the more sensitive S-G2 phase during the interval between the split doses. In contrast, the inverse split-dose effect for apoptosis is absent for REC:myc(ch1), due presumably to the radiation-induced G1 delay. Parallel split-dose experiments, but using clonogenic survival as end points, show recovery for REC:myc(ch1) cells but not for Rat1:mycb cells, reflecting the influence of split-dose, radiation-induced apoptosis.

Apoptosis induced by X-irradiation of rec-myc cells is postmitotic and not predicted by the time after irradiation or behavior of sister cells.

Rat embryo cells expressing the c-myc oncogene (rec-myc) were studied by time-lapse microscopy to determine whether radiation-induced apoptosis occurred before or after mitosis. Following X-irradiation with 9.5 Gy, cells were imaged every 3 min for 6 days. Episodes of apoptotic blebbing were very consistent from cell to cell, lasting 30-60 min, followed by cessation of movement and cell death. In contrast, the time of initiation of apoptotic blebbing was unpredictable. At least 96% of the apoptotic episodes were postmitotic, after one to four cell divisions and 2-97 h after a given division. Sister cells often behaved differently from one another, with apoptosis in one sister occurring many h or several divisions after apoptosis in the other. Thus, the onset of radiation-induced apoptosis in rec-myc cells is not strictly programmed but may result from the segregation of chromosome aberrations in the postirradiation generations.

Thermal response of oncogene-transfected rat cells.

Rat embryo cells or Rat-1 fibroblasts were transfected with either an activated c-myc or a c-Ha-ras from the T24/EJ bladder carcinoma, or they were cotransfected with both. A gene conferring neomycin or hygromycin resistance was also cotransfected so that independent cell lines could be selected by growth in medium containing the antibiotic. Certain isolates from cells transfected with only one type of oncogene were further transformed by exposure to 600 cGy of 250-kVp X-rays. Successful transfection and transformation were characterized by altered morphology, increased plating efficiency, shorter doubling time, longer life span, foci formation, anchorage-independent growth, and Southern and Northern hybridization analysis. The thermal response of these cells at different stages of oncogenic transformation was examined by exposing exponentially growing cells to 45 degrees C for 0 to 45 min and measuring cellular survivals using colony formation assay. We found that cells transfected with myc oncogene, singly or in combination with ras, were more sensitive to thermal stress. Aside from that, the cells' thermal sensitivity was not affected by the degree or the nature of transformation.

Using computerized video time lapse for quantifying cell death of X-irradiated rat embryo cells transfected with c-myc or c-Ha-ras.

Rat embryo fibroblasts that had been transfected with the c-myc or c-Ha-ras oncogene were X-irradiated, after which individual cells and their progeny were followed in multiple fields for 5-6 days by computerized video time lapse microscopy to quantify the lethal events that resulted in loss of clonogenic survival. The loss of clonogenic survival of X-irradiated (9.5 or 2.5 Gy) REC:myc cells was attributed almost entirely to the cells dying by apoptosis, with almost all of the apoptosis occurring after the progeny had divided from one to four times. In contrast, the loss of clonogenic survival of X-irradiated REC:ras cells was attributed to two processes. After 9.5 Gy, approximately approximately 60% of the nonclonogenic cells died by apoptosis (with a very small amount of necrosis), and the other 40% underwent a senescent-type process in which some of the cells and their progeny stopped dividing but remained as viable cells throughout 140 h of observation. Both processes usually occurred after the cells had divided and continued to occur in the cells' progeny for up to five divisions after irradiation. Furthermore, the duration of the apoptotic process was shorter for REC:myc cells (0.5-1 h) than for REC:ras cells (4-5 h). By using computerized video time lapse to follow individual cells, we were able to determine the mode of cell death. This cannot be determined by conventional clonogenic survival experiments. Also, only by following the individual cells and their progeny can the true amount of apoptosis be determined. The cumulative percentage of apoptosis scored in whole populations, without distinguishing between the progeny of individually irradiated cells, does not reflect the true amount of apoptosis that occurs in cells that undergo postmitotic apoptosis after irradiation. Scoring cell death in whole populations of cells gives erroneous results because both clonogenic and nonclonogenic cells are dividing as nonclonogenic cells are apoptosing or senescing over a period of many days. For example, after 9.5 Gy, which causes reproductive cell death in 99% of both types of cells, the cumulative percentage of the cells scored as dead in the whole population at 60- 80 h after irradiation, when the maximum amount of cumulative apoptosis occurred, was approximately 60% for REC:myc cells, compared with only approximately 40% for REC:ras cells.

Synergistic effect of the v-myc oncogene with H-ras on radioresistance.

Resistance of tumors to irradiation or chemotherapeutic agents is thought to be one of the reasons why patients who present with early malignancies may not be cured. Much is now known about the molecular mechanisms that underlie drug resistance, but until recently little was known about genetic contributions to radiation resistance. Some evidence now links oncogenes, particularly the ras family of oncogenes, to radiation resistance but heterogeneity between tumors and cell lines has complicated this analysis. Primary rat embryo cells have been chosen as a model system in which the effects on radiation resistance of the H-ras oncogene could be studied on a uniform genetic background. These cells offer several useful advantages. The cells prior to transformation are diploid, and because they have been in culture only for a few passages prior to transformation with the oncogene it is unlikely that any preexisting mutation affecting radiation response could be present. Additionally, the use of rat embryo cells permitted the study of the effects of a second oncogene on the appearance of the radioresistant phenotype. The results show that the activated H-ras oncogene is associated with radiation resistance in primary rat cells after transformation but that the effect of the oncogene by itself is small. However, the oncogene v-myc, which has no effect on radiation resistance by itself, has a synergistic effect on radiation resistance with H-ras. There appear to be differences in the phenotype of radiation resistance associated with these two forms of transfectants. Thus, radiation resistance seen with H-ras by itself is characterized by a change in the slope of the radiation survival curve at high radiation doses but little or no change within the should region of the radiation survival curve. Radiation resistance seen in H-ras plus v-myc transformants is also characterized by an increase in the slope of the curve at high doses but there is also a large effect within the shoulder region of the radiation survival curve. These studies led to the following conclusions: (a) the radioresistant phenotype is not due to preexisting genetic heterogeneity in the cells prior to transfection; (b) the radiation resistant phenotype of cells transformed by H-ras is seen to a greater degree in cells which also contain the v-myc oncogene; (c) the v-myc oncogene may play an important role in the phenotype of radiation resistance at low doses that is within the range most critical for clinical practice.

Down-regulation of gadd153 by c-myc in rat fibroblasts and its effect on cell growth and radiation-induced apoptosis.

Using differential display reverse transcription PCR (DDRT - PCR), we found that a 360 bp cDNA fragment was absent in several c-myc transfected rat fibroblasts: REC:myc, REC:myc + ras and rat1-myc. These cells also showed enhanced sensitivity to gamma ray-induced apoptosis. This cDNA fragment was present in the parental REC (Rat Embryo Cells) and rat1 cells, and in c-Ha-ras transfected REC (REC:ras), all of which were relatively resistant to gamma ray-induced apoptosis. The cDNA fragment was subsequently cloned and used as a probe to screen a rat1 cDNA library, and identified as one of the growth arrest and DNA damaging-inducible genes, gadd153. In addition to the down-regulation of rat gadd153 in all the c-myc transfectants, methyl methanesulfonate (MMS)-induced transcription of the gadd153 was attenuated. The rat1-myc cells, when successfully transfected with and stably expressing the rat gadd153, showed a significantly longer doubling time compared to the parental cells. However, overexpression of gadd153 in rat1-myc cells did not affect gamma ray-induced apoptosis. Thus, the suppression of gadd153 appears to be inversely correlated with that of myc, but not involved in the myc-dependent apoptotic pathway.

Predictors of improved outcome for patients with localized prostate cancer treated with neoadjuvant androgen ablation therapy and three-dimensional conformal radiotherapy.

PURPOSE: To identify prognostic variables that predict for improved biochemical and local control outcome in patients with localized prostatic cancer treated with neoadjuvant androgen deprivation (NAAD) and three-dimensional conformal radiotherapy (3D-CRT). MATERIALS AND METHODS: Between 1989 and 1995, 213 patients with localized prostate cancer were treated with a 3-month course of NAAD that consisted of leuprolide acetate and flutamide before 3D-CRT. The purpose of NAAD in these patients was to reduce the preradiotherapy target volume so as to decrease the dose delivered to adjacent normal tissues and thereby minimize the risk of morbidity from high-dose radiotherapy. The median pretreatment prostate-specific antigen (PSA) level was 15.3 ng/mL (range, 1 to 560 ng/mL). The median 3D-CRT dose was 75.6 Gy (range, 64.8 to 81 Gy), and the median follow-up time was 3 years (range, 1 to 7 years). RESULTS: The significant predictors for improved outcome as identified in a multivariate analysis included pretreatment PSA level < or = 10.0 ng/mL(P < .00), NAAD-induced preradiotherapy PSA nadir < or = 0.5 ng/mL (P < .001), and clinical stage < or = T2c (P < .04). The 5-year PSA relapse-free survival rates were 93%, 60%, and 40% for patients with pretreatment PSA levels < or = 10 ng/mL, 10 to 20 ng/mL, and greater than 20 ng/mL, respectively (P < .001). Patients with preradiotherapy nadir levels < or = 0.5 ng/mL after 3 months of NAAD experienced a 5-year PSA relapse-free survival rate of 74%, as compared with 40% for patients with higher nadir levels (P < .001). The incidence of a positive biopsy among 34 patients pretreated with androgen ablation was 12%, as compared with 39% for 117 patients treated with 3D-CRT alone who underwent a biopsy (P < .001). CONCLUSION: For patients treated with NAAD and high-dose 3D-CRT, pretreatment PSA, preradiotherapy PSA nadir response, and clinical stage are important predictors of biochemical outcome. Patients with NAAD-induced PSA nadir levels greater than 0.5 ng/mL before radiotherapy are more likely to develop biochemical failure and may benefit from more aggressive therapies.

Comparison of the 5-year outcome and morbidity of three-dimensional conformal radiotherapy versus transperineal permanent iodine-125 implantation for early-stage prostatic cancer.

PURPOSE: To compare the prostate-specific antigen (PSA) relapse-free survival outcome and incidence of late toxicity for patients with early-stage prostate cancer treated at a single institution with either three-dimensional conformal radiotherapy (3D-CRT) or transperineal permanent implantation (TPI) with iodine-125 seeds. MATERIALS AND METHODS: Patients with favorable-risk prostate cancer, defined as a pretreatment PSA of less than or equal to 10.0 ng/mL, Gleason score of 6 or lower, and stage less than or equal to T2b, were selected for this analysis. Between 1989 and 1996, 137 such patients were treated with 3D-CRT and 145 with TPI. The median ages of the 3D-CRT and TPI groups were 68 years and 64 years, respectively. The median dose of 3D-CRT was 70.2 Gy, and the median implant dose was 150 Gy. Prostate-specific antigen relapse was defined according to the American Society of Therapeutic Radiation Oncology Consensus Statement, and toxicity was graded according to the Radiation Therapy Oncology Group morbidity scoring scale. The median follow-up times for the 3D-CRT and TPI groups were 36 and 24 months, respectively. RESULTS: Eleven patients (8%) in the 3D-CRT group and 12 patients (8%) in the TPI group developed a biochemical relapse. The 5-year PSA relapse-free survival rates for the 3D-CRT and the TPI groups were 88% and 82%, respectively (P = .09). Protracted grade 2 urinary symptoms were more prevalent among patients treated with TPI compared with 3D-CRT. Grade 2 urinary toxicity, which was manifest after the implant and persisted for more than 1 year after this procedure, was observed in 45 patients (31%) in the TPI group. In these 45 patients, the median duration of grade 2 urinary symptoms was 23 months (range, 12 to 70 months). On the other hand, acute grade 2 urinary symptoms resolved within 4 to 6 weeks after completion of 3D-CRT, and the 5-year actuarial likelihood of late grade 2 urinary toxicity for the 3D-CRT group was only 8%. The 5-year actuarial likelihood of developing a urethral stricture (grade 3 urinary toxicity) for the 3D-CRT and TPI groups was 2% and 12%, respectively (P<.0002). Of 45 patients who developed grade 2 or higher urinary toxicity after TPI, the likelihood of resolution or significant improvement of these symptoms at 36 months from onset was 59%. The 5-year likelihood of grade 2 late rectal toxicity for the 3D-CRT and TPI patients was similar (6% and 11%, respectively; P = .97). No patient in either group developed grade 3 or higher late rectal toxicity. The 5-year likelihood of posttreatment erectile dysfunction among patients who were initially potent before therapy was 43% for the 3D-CRT group and 53% for the TPI group (P = .52). CONCLUSION: Both 3D-CRT and TPI are associated with an excellent PSA outcome for patients with early-stage prostate cancer. Urinary toxicities are more prevalent for the TPI group and subsequently resolve or improve in most patients. In addition to evaluating long-term follow-up, future comparisons will require detailed quality-of-life assessments to further determine the impact of these toxicities on the overall well-being and quality of life of the individual patient.

Developments in megavoltage cone beam CT with an amorphous silicon EPID: reduction of exposure and synchronization with respiratory gating.

We have studied the feasibility of a low-dose megavoltage cone beam computed tomography (MV CBCT) system for visualizing the gross tumor volume in respiratory gated radiation treatments of nonsmall-cell lung cancer. The system consists of a commercially available linear accelerator (LINAC), an amorphous silicon electronic portal imaging device, and a respiratory gating system. The gantry movement and beam delivery are controlled using dynamic beam delivery toolbox, a commercial software package for executing scripts to control the LINAC. A specially designed interface box synchronizes the LINAC, image acquisition electronics, and the respiratory gating system. Images are preprocessed to remove artifacts due to detector sag and LINAC output fluctuations. We report on the output, flatness, and symmetry of the images acquired using different imaging parameters. We also examine the quality of three-dimensional (3D) tomographic reconstruction with projection images of anthropomorphic thorax, contrast detail, and motion phantoms. The results show that, with the proper choice of imaging parameters, the flatness and symmetry are reasonably good with as low as three beam pulses per projection image. Resolution of 5% electron density differences is possible in a contrast detail phantom using 100 projections and 30 MU. Synchronization of image acquisition with simulated respiration also eliminated motion artifacts in a moving phantom, demonstrating the system's capability for imaging patients undergoing gated radiation therapy. The acquisition time is limited by the patient's respiration (only one image per breathing cycle) and is under 10 min for a scan of 100 projections. In conclusion, we have developed a MV CBCT system using commercially available components to produce 3D reconstructions, with sufficient contrast resolution for localizing a simulated lung tumor, using a dose comparable to portal imaging.

Developments in nuclear magnetic resonance imaging and spectroscopy: application to radiation oncology.

Nuclear magnetic resonance techniques have advanced to the point where functional, physiologic, and biochemical information may be obtained from patients. Magnetic resonance imaging of tissue water can be used to measure perfusion and diffusion with submillimeter resolution. Magnetic resonance spectroscopy may be applied to the assessment of tissue metabolites that contain protons, phosphorus, fluorine, or other nuclei. The combination of imaging and spectroscopy technologies has lead to spectroscopic imaging techniques that are capable of mapping proton metabolites at resolutions as small as 0.25 cm(3) within the time constraints of a clinical imaging study. This article provides a brief review of magnetic resonance techniques for imaging of tissue physiological function and addresses possible applications in the realm of radiation oncology.

Studies with cytotoxic agents suggest that apoptosis is not a major determinant of clonogenic death in neuroblastoma cells.

We have previously reported the selection of a radioresistant human neuroblastoma cell line, Clone F, from IMR32 cells. We have shown that clonogenic radioresistance in these cells is accompanied by a reduced level of radiation-induced apoptosis [Cancer Res 55 (1995) 4915]. Here, we measured the response of these lines to several cytotoxic agents, in terms of clonogenicity and apoptosis. In the clonogenic assay, the radioresistant line was also resistant to cisplatin, melphalan and doxorubicin, but not to perillyl alcohol. However, all these agents produced less apoptosis in the Clone F cells, except cisplatin, which failed to induce any apoptosis in either cell line. Reduced apoptosis cannot be the cause of the Clone F cells' resistance to cisplatin. By extension, the Clone F cells' resistance to radiation and other agents cannot be due to diminished apoptosis either. Based on these results, apoptosis may not be a useful surrogate for clonogenic outcome.

Conformal radiation treatment: a critical appraisal.

Significant technical advances have improved the precision of radiation treatment of human malignancies and permitted dose-escalation studies. However, a number of challenges remain, particularly in the clinical and radiobiological aspects of radiotherapy. Even with these deficiencies, it is likely that improved overall treatment results will be forthcoming with 3DCRT. Nevertheless, the cost-effectiveness of this approach needs to be assessed, based on the magnitude of the improvement in the treatment of various disease sites.

Permanent implants using Au-198, Pd-103 and I-125: radiobiological considerations based on the linear quadratic model.

Based on the linear-quadratic model, we perform calculations to compare the possible radiobiologic results achieved with permanent implants using Au-198, Pd-103, and I-125. We examine the influence of the radiobiophysical parameters (i.e. alpha, beta, SLD repair kinetics, tumor doubling time (Tp), tumor growth delay, and prescribed dose) on the calculated radiobiologic indices or endpoints. The radiobiologic indices or endpoints include the effective treatment time (Teff) (beyond which the additional dose delivered is wasted), the biologically effective dose (BED), and cell surviving fractions. Within the range of reported values of the various parameters, Tp is the most significant in affecting Teff, BED, and the degree of cell inactivation. The effect of Tp and Teff and BED is larger for isotopes with longer half-lives, for which the rate of tumor regrowth is more important. For Tp of 5 to 30 days, the Teff are 14 to 21 days for Au-198, 58 to 102 days for Pd-103, and 120 to 275 days for I-125. For this range of Tp, the wasted doses are less than 5% for Au-198, 15 to 3% for Pd-103, and 30 to 5% for I-125. For reference prescription doses of 60, 120, and 160 Gy for implants using Au-198, Pd-103, and I-125, respectively, the BED and the associated cell-kill is the lowest for Au-198, whereas Pd-103 and I-125 implants are more effective for fast-growth (Tp less than 10 days) and slow-growth (Tp greater than 10 days) tumors, respectively.

Repair of radiation induced damage--dependence on oxygen and energy status.

Repair of radiation-induced sublethal damage by Chinese hamster V-79 cells is studied under conditions of different pO2 (15 ppm to 21%) and cellular energy status. Cellular ATP content and energy charge are drastically reduced when cells are deprived of both oxygen and nutrient. Both indices are within normal range when cells are provided with nutrients or trace levels of oxygen (300 ppm). When deprived of nutrient, hypoxic (15 ppm O2) cells do not repair SLD, while cells in 300 ppm O2 do. Thus, cellular SLD repair appears to be dependent on cellular energy status which in turn is sensitive to oxygen concentration. Relatedly, nutrient deprived hypoxic cells are sensitized to radiation with storage under 23 degrees C, a phenomenon which may stem from a decrease of endogenous glutathione content.

The relative biological effectiveness of I-125 and Pd-103.

PURPOSE: To determine the relative biological effectiveness (RBE) of I-125 and Pd-103 relative to Co-60. METHODS AND MATERIALS: A cell line REC:ras, derived from rat embryo cells, was used. Cells in exponential or plateau phase were irradiated at dose rates of about 0.07 Gy/h and 0.14 Gy/h. To circumvent the interface effect, cells were grown and irradiated on membranes made of cellulose acetate, which has an effective Z of 7.5. I-125 and Pd-103 seeds were placed in a custom designed template that yielded a homogeneous dose distribution in the plane of the cell culture. The dose rates of irradiation were measured by calibrated thermoluminescence dosimetry (TLD) chips. RESULTS AND CONCLUSIONS: Our measurements yielded an RBE of about 1.4 for I-125 at dose rates of about 0.07 Gy/h, and an RBE of about 1.9 for Pd-103 at dose rates of about 0.07 Gy/h and 0.14 Gy/h. The RBE of I-125 is similar to those measured by other investigators, the RBE for Pd-103 is being reported for the first time.