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At least 613 records · Page 34Linked to original sources
PubMed2004

Radiation exposure of personnel during intraoperative radiotherapy (IORT): radiation protection aspects.

Intraoperative radiotherapy (IORT) is a multidisciplinary procedure which combines two conventional methods of cancer treatment surgery and radiation therapy. The purpose is to deliver a large single dose to the surgically exposed tumor bed while minimizing doses to normal tissues. Intraoperative radiation therapy (IORT) is a technique which allows irradiating the patient directly after the surgical operation using a linear accelerator that can be situated in the operating room. For medical accelerators with energy over 10MeV the need to characterize the neutron spectra for this particular situation arises from the fact that, when neutron spectra is not fully known, it becomes necessary to be more cautious introducing a weight factor wR of 20 (maximum value). This leads to overesteem the equivalent dose due to neutrons and it indicates to introduce additional (mobile) shields for photon and neutrons radiation not easily achievable in an operating room.

Combined Modality Therapy↗
PubMedDate not supplied

[The influence of the water with decreased content of heavy stable hydrogen and oxygen (18O) isotope on development of radiation injuries at gamma-radiation in low dose].

The investigations of the water with decreased content of heavy stable hydrogen and of oxygen (18O) isotope received by the method of rectification were conducted on development of radiation injuries in organisms of the experimental animals. The objects of the investigation were male mice of Balb/c line. The animals were irradiated at the unit PX-gamma-30 with the gamma-radiation source 60Co in the dose of 25 sGy. It was observed that the water with decreased content of heavy stable hydrogen and of oxygen (18O) isotope influences positively the processes of restoration. It was manifested in decrease of the degree of gravity of radiation injuries in immune system organs (thymus and spleen), peripheral blood and marrow cells.

Animals↗
PubMedDate not supplied

[Electromagnetic radiation in the radiofrequency range: radiation safety].

Existing safety standards for electromagnetic radiation in the radio frequency range, including microwave radiation, adopted in the USSR, Great Britain, Poland, Czechoslovakia, USA, Canada, FRG and recommended by IRPA/INIRC are described. It is proposed to use the value 0.4 W/kg as the basic value of an absorbed dose rate which corresponds to the energy flux density 100 W/m2 for frequencies over 2 GHz. The concepts of an effective dose rate and effective dose are discussed. Various questions of how to provide safety of those working with electromagnetic radiations are considered.

Canada↗
PubMed1986

Radiation-induced taste aversion: effects of radiation exposure level and the exposure-taste interval.

Radiation-induced taste aversion has been suggested to possibly play a role in the dietary difficulties observed in some radiotherapy patients. In rats, these aversions can still be formed even when the radiation exposure precedes the taste experience by several hours. This study was conducted to examine whether increasing the radiation exposure level could extend the range of the exposure-taste interval that would still support the formation of a taste aversion. Separate groups of rats received either a 100 or 300 R gamma-ray exposure followed 1, 3, 6, or 24 h later by a 10-min saccharin (0.1% w/v) presentation. A control group received a sham exposure followed 1 h later by a 10-min saccharin presentation. Twenty-four hours following the saccharin presentation all rats received a series of twelve 23-h two-bottle preference tests between saccharin and water. The results indicated that the duration of the exposure-taste interval plays an increasingly more important role in determining the initial extent of the aversion as the dose decreases. The course of recovery from taste aversion seems more affected by dose than by the temporal parameters of the conditioning trial.

Animals↗
PubMed1984

An oxygen effect for gamma-radiation induction of radiation resistance in yeast.

Previous evidence in a lower eukaryote indicated the lack of an oxygen effect for ionizing radiation induction of radioresistance [P. E. Bryant, Nature (London) 261, 588-590 (1976)], suggesting that the signal for induction may be different from that in prokaryotes, where DNA damage by a variety of agents has been shown to induce SOS. type repair and radioresistance. We show here that prior exposure to a sublethal dose of gamma radiation caused induction of radioresistance in Saccharomyces cerevisiae, and that the rate of induction was proportional to the initial dose. Irradiation in oxygen produced a higher rate of increase in resistance, per unit dose, than irradiation in nitrogen, with an oxygen enhancement ratio of 2.8. The maximum level of resistance reached in response to saturating doses was the same regardless of the presence or absence of O2 during the initial irradiation. At less than saturating doses, however, the maximum increase in resistance was higher, per unit dose, following irradiation in the presence of O2 than in its absence. Oxic doses which gave the maximum possible in increase the level of resistance were considerably less than those required to produce the maximum rate of increase in resistance. These results suggest a difference in the level at which DNA damage saturates these processes. These results also indicate that the use of DNA damage as a signal for induction of radiation resistance has probably been conserved during the evolution of prokaryotes to lower eukaryotes.

Cell Survival↗
PubMed1978

[Quantitative description of the process of cellular radiation inactivation. IX. Remarks on the relative biological effectiveness of ionizing radiations in the reproductive death of diploid and polyploid cells].

The relative biological effectiveness (RBE) has been considered for three kinds of cell radiation damages: subdamages (sublethals), one-track, and two-track lethal damages. In contrast to the "dual theory", which postulates the square relation between the lethal damage yield and the specific energy, it is assumed that the one-track lethal yield is linearly related to the specific energy per cell nucleus. As a result, the identical dependence has been obtained of both one-track lethals and subdamages on specific energy and absorbed dose. It is established that RBE for all three kinds of damages does not depend on the radiation dose. It is shown that RBE for subdamages and one-track lethals depends on LET of radiation only, and involves molecular parameters of sensitive cell structures. Within the limits of this assumption, the relations are general for all the types of eukaryotic cells. These can be used for a further development of the RBE theory, with spectra of LET, the track structure of charged particles, the contribution of delta-electrons etc being taken into consideration.

Cell Division↗
PubMed1997

Apoptosis and response to radiation: implications for radiation therapy.

Apoptosis is a mode of cell death that is currently of intense research interest in developmental and cancer biology. For more than 40 years, radiobiologists have been aware of cells in irradiated specimens that display the features of apoptosis. Despite this knowledge, however, it has proved difficult to elucidate the role of apoptosis in end points important in radiation therapy and to distinguish its role from that of other modes of cell death, namely, reproductive cell death. In this article, the evidence relevant to this question will be critically reviewed. Conclusions that have significant implications for radiation therapy will be drawn to suggest that tumor cells with apoptotic propensity are more sensitive to radiation. If this hypothesis is confirmed, strategies can be envisioned that may restore apoptotic propensity to radioresistant tumor cells for therapeutic benefit.

Adenocarcinoma↗
PubMed1997

Nonmonotonic behavior of the dose dependence of the radiation effect on cells in vitro exposed to pulsed laser radiation at lambda = 820 nm.

BACKGROUND AND OBJECTIVE: In recent years, clinical low-intensity laser therapy practice has used pulsed radiation, mainly from semiconductor lasers. Experimental works devoted to the study of relationships between biological and clinical effects and parameters of pulsed radiation are practically absent. STUDY DESIGN/MATERIALS AND METHODS: The radiation source was a laser diode emitting at 820 nm (292 and 700 Hz, duty factor 80%; doses from 7 J/m2 to 5 x 10(5) J/m2; intensities 4, 12, 51, 152, 633, and 1,900 W/m2; irradiation time from 1 to 30 s). Four biological models were used: nucleated cells of murine spleen (splenocytes) and bone marrow (karyocytes), murine blood, and HeLa cells cultivated in vitro. The intensity of luminol-amplified chemiluminescence (in case of murine models) and the adhesion of HeLa cell membranes were measured as a function of the irradiation dose. RESULTS: Within the wide exposure dose range used we obtained seven maxima in the dose vs. biological effect curves: at fluences near 20, 1 x 10(2), 3 x 10(2), 8 x 10(2), 3 x 10(3), 1 x 10(4), and 3 x 10(4) J/m2. The peaks coincided for all four models. CONCLUSION: The dose curves obtained with different cellular systems are of the same type and are characterized by seven peaks in the dose interval studied (7 J/m2 to 5 x 10(5) J/m2).

Animals↗
PubMed1975

Unilateral hypoglossal nerve atrophy as a late complication of radiation therapy ofhead and neck carcinoma: a report of four cases and a review of the literature on peripheral and cranial nerve damages after radiation therapy.

The case histories of four patients who developed hemiatrophy of the tongue from 3 to9 years after a course of curative radiation therapy for carcinomas of the head and neck are presented. These patients subsequently followed for from 1 1/2 to 6 years withoutlocal recurrence of the tumor, distant metastasis, or involvement of other cranial nerves, indicative of only a unilateral hypoglossal nerve atrophy. A review of the literatureshowed that peripheral and cranial nerve damages after radiation therapy have been reported for the optic nerve, hypoglossal nerve, oculomotor nerve, abducens nerve, recurrent laryngeal nerve, brachial plexus nerves and peripheral nerves of the extremeties. Reviewof clinical and experimental data indicated that in most cases, the damages were probably caused by extensive connective tissue fibrosis around and infiltrating the nerve trunks. Three possible types of peripheral and cranial nerve damages after radiation therapy are identified.

Cranial Nerves↗
PubMed1976

Interaction between radiation and drug damage in mammalian cells. II. The effect of actinomycin-D on the repair of the sublethal radiation damage in plateau phase cells.

The effect of actinomycin-D (AMD) on radiation damage repair was studied in plateau phase V79 Chinese hamster cells. Sublethal radiation damage repair, as demonstrated by survival fluctuations following two x-ray exposures separted by time, was observed in our plateau phase cells. Plateau phase cells exposed to 0.01-0.04 mug/ml AMD (a nontoxic regimen to 8 hours) between x-ray exposures were less able to repair sublethal damage. If plateau phase cells were plated at low dilutions into fresh medium (conditions for resuming exponential growth) immediately after the first x-ray dose, and exposed to 0.01--0.04 mug/ml AMD until the second dose, inhibition of sublethal damage repair and additional cell killing were observed particularly at 0.04 mug/ml AMD. It is suggested that radiation-drug damage interactions should be studied in plateau phase cells and in cells resuming exponential growth after plateau phase (possibly analogous to "recruitment"), as well as in exponential phase cultures.

Animals↗
PubMed1977

Effect of thymosin in vitro on T cell levels during radiation therapy: correlations with radiation portal and initial T cell levels.

The effect of thymosin in vitro on percent T cells was determined in 388 blood specimens from patients with head and neck, mediastinal, and pelvic malignancies during radiation therapy, in 94 untreated patients with these malignancies, and 277 normal adults. Changes in percent T cell levels after incubation of lymphocytes with thymosin did not correlate with tumor histology or cumulative radiation dose, but in all groups correlated with radiation portal and initial T cell levels. T cell levels increased by a similar increment in normals and in the untreated patients. During irradiation, the mean levels after incubation with thymosin did not change in patients with head and neck and pelvic malignancies, but in patients with mediastinal malignancies the levels increased significantly more than in normals. For a given T cell level, the increase in patients with mediastinal malignancies was greater than in patients with pelvic malignancies, and as a group was greater than in patients with head and neck malignancies. The results can be explained by an increase in circulating thymosin-responsive lymphocytes during mediastinal irradiation due to suppression of a function of the thymus important for maturation of these cells, and a decrease in these cells during pelvic irradiation due to a deleterious effect on precursors in pelvic bone marrow. The results thus provide a rationale for clinical trials to assess the efficacy of thymosin in averting declines of T cell levels in patients receiving mediastinal irradiation.

Adolescent↗
PubMed1992

A randomized trial of accelerated hyperfractionated radiation therapy and bis-chloroethyl nitrosourea for malignant glioma. A preliminary report of Radiation Therapy Oncology Group 83-02.

BACKGROUND: The third and final randomization of Radiation Therapy Oncology Group (RTOG) 83-02 was performed to identify the maximal tolerated dose and potential efficacy of accelerated hyperfractionated radiation therapy (AHRT) in 1.6 Gy twice-daily fractions for adult malignant glioma. METHODS: From December 1987 to July 1989, 304 patients with malignant glioma were stratified by age, performance status, and histologic findings and randomized to receive total AHRT doses of 48.0 or 54.4 Gy, with 80 mg/m2 of bis-chloroethyl nitrosourea (BCNU) for 3 days every 8 weeks. Distribution of other prognostic factors, including neurologic function, extent of surgery, tumor size, and sex, was comparable in each treatment arm. RESULTS: One Grade 5 radiation therapy (RT)-related toxic effect was reported (in the 54.4-Gy treatment arm), and the incidence of late Grade 3-5 RT-related toxic effects at 18 months was 1% at 48.0 Gy and 4% at 54.4 Gy. The median survival times (MST) for the 48.0 Gy and 54.4 Gy treatment arms were 11.7 and 10.8 months, respectively, comparable to the MST in prior RTOG trials with a similar proportion of patients with glioblastoma multiforme (79%). For the 123 patients who were 60 years of age or older, the MST for the 48.0 Gy and 54.4 Gy treatment arms were 8.9 and 10.4 months, respectively, and compare favorably with the MST of 6.0 months reported with standard RT and BCNU treatment used for 101 patients who were 60 years of age or older in two prior RTOG malignant glioma trials (74-01 and 79-18). Although these results differ significantly (P = 0.0015), this contrast is not significant when adjusted by performance status. CONCLUSIONS: The maximum tolerated dose of AHRT has yet to be identified, and pursuit of this information may most benefit patients with malignant glioma who are 60 years of age or older.

Carmustine↗
PubMed1993

Improved survival duration in patients with unresected solitary brain metastasis using accelerated hyperfractionated radiation therapy at total doses of 54.4 gray and greater. Results of Radiation Therapy Oncology Group 85-28.

BACKGROUND: Although there have been occasional reports of improved response with greater doses of irradiation for unresected brain metastases, dose escalation has not been systematically studied in a cohort of patients with solitary brain metastasis. The current study examines this group of patients to evaluate dose escalation using accelerated hyperfractionated radiation therapy (XRT) with regard to survival, patterns of failure, and toxicity. METHOD: Radiation Therapy Oncology Group (RTOG) 85-28, a Phase I/II randomized trial of accelerated hyperfractionated XRT for patients with unresected supratentorial brain metastases, enrolled 153 patients with solitary brain metastasis. Whole brain dose was 32 Gray (Gy) administered in 1.6 Gy fractions twice a day with an interfraction interval of 4-8 hours. Boost dose was escalated to total doses of 48.0, 54.4, 64.0, and 70.4 Gy. RESULTS: Acute and late toxicities were acceptable. The median survival time and 1-year survival rates were 4.9 months and 20% at 48 Gy; 5.4 months and 33% at 54.4 Gy; 7.2 months and 28% at 64 Gy; and 8.2 months and 37% at 70.4 Gy, respectively. Comparison of the upper three dose treatment arms to the 48 Gy treatment arm revealed a superior survival time with doses of 54.4 Gy and greater (P = 0.05). Improvement in neurologic function appeared to increase with dose escalation, with 25% of patients experiencing improvement at doses of 48 Gy, 38% at 54.4 Gy, 50% at 64 Gy, and 63% at 70.4 Gy (P = not significant). CONCLUSION: A radiation dose response for survival time appears to exist with the use of accelerated hyperfractionated XRT for patients with unresected solitary brain metastasis.

Adenocarcinoma↗
PubMed1991

Murine radiation myeloid leukaemogenesis: a possible role for radiation-sensitive sites on chromosome 2.

There is a paucity of informative data on the potentially important role of specific sites of chromosomal instability in oncogenic processes. Chromosome 2 deletions and rearrangements are known to characterise radiation-induced acute myeloid leukaemia in the mouse. Here we statistically establish a concordance between chromosome 2 breakpoint clusters in these leukaemias and chromosome 2 rearrangements carried at a high in vivo frequency by progeny of irradiated haemopoietic cells. Mechanisms of radiation myeloid leukaemogenesis are discussed with respect to multiple radiation-sensitive sites encoded on chromosome 2 and the possible influence of genomic imprinting on inductive processes.

Alpha Particles↗
PubMed1983

Radiation induced osteosarcoma of the sacrum following radiation of an undiagnosed bone lesion.

Years ago a 20-year-old patient presented with low back pain. Radiologically a cystic lesion of the sacrum was found and interpreted as malignant tumor. Without biopsy and histological diagnosis the patient was given radiation therapy with 21 000 rad. One year later a similar lesion was radiated in the left femoral neck. A pathological fracture ensued recessitating several operations. Twenty years after initial radiation therapy the patient developed a rapidly growing tumor of the sacrum, metastasizing to the lungs. One year later he died.

Adult↗
PubMed1999

Energy loss due to radiation in postmortem cooling. Part B: Energy balance with respect to radiation.

With the help of the law of Stefan and Boltzmann and a model for the cooling of exposed skin derived from the data of Lyle and Cleveland, the radiation energy loss ER can be calculated according to the following formula: [formula in text] where epsilon represents the emissivity of the skin (0.98), sigma the Stefan-Boltzmann constant, AR the radiating surface area, TS(0) the skin temperature at death, TE the environmental temperature and Z' = 0.1017 the gradient of the skin temperature curve. Additionally, an energy loss due to conduction and convection EC has to be taken into account. Comparing the energy losses due to radiation, conduction and convection with the decrease ET of the thermal energy in the body, calculated from mean heat capacity (3.45 kJ/(kg degrees K)), body mass and decrease of mean body temperature, there is a surplus of energy in the very early postmortem period, which can be explained only by an internal source of energy EI. Alltogether the following balance equation can be formulated: ET + EI = ER + EC Since the body temperature decreases in the early postmortem period, EI can be estimated by: EI(t) > or = max (ER(t) - ET(t), 0). The values obtained range up to 500 kJ for a medium sized (175 cm), medium weight (75 kg) body at an environmental temperature of 5 degrees C and are compatible with estimations of Lundquist for supravital energy production by breakdown of glycogen.

Body Mass Index↗
PubMed2006

Ototoxicity of cisplatin plus standard radiation therapy vs. accelerated radiation therapy in glioblastoma patients.

PURPOSE: To assess the effect of cisplatin (CDDP) plus concurrent radiation therapy on hearing loss. METHODS: 451 patients with glioblastoma multiforme (GBM) were randomly assigned after surgery to: Arm A: Carmustine (BCNU) + standard radiation therapy (SRT); Arm B: BCNU + accelerated radiation therapy (ART: 160 cGy twice daily for 15 days); Arm C: CDDP + BCNU + SRT; or Arm D: CDDP + BCNU + ART. Patients on arms C and D received audiograms at baseline, and prior to the start of RT, and prior to cycles 3 and 6. Otologic toxicities were recorded at each visit. RESULTS: 56% of patients had hearing loss at baseline. 13% and 50% of patients experienced worsening ototoxicity after 1 year of treatment in arms A and B vs. C and D, respectively, with 13% of those on arms C and D experiencing significant ototoxicity (>or= grade 3) at 6 months. Increasing age was associated with an increased risk of ototoxicity. CONCLUSIONS: Increased exposure to CDDP increases the risk of ototoxicity over time. Older patients are more susceptible to hearing loss with CDDP. The low proportion of patients with clinically significant ototoxicity suggests that baseline screening is unnecessary in GBM patients.

Adult↗
PubMed1986

A study of heat and radiation response of a malignant, melanin-producing cell line derived from C3H 10T1/2 cells transformed in culture by radiation.

The mouse C3H 10T1/2 cell line was transformed to the malignant state using ionizing radiation. One of the transformed lines (R25) that was isolated, displayed some properties similar to malignant melanoma cells. The cells became dark and pigmented after prolonged time in culture and this cell line produced tumors in C3H mice. The radiation survival curve of R25 had a large shoulder which was also observed for human melanoma cell lines. R25 was more resistant to heating at 45.0 degrees C than the normal cell line. Heating at 45.0 degrees C before irradiation resulted in a reduction of the survival curve shoulder. The heat and radiation sensitivity of R25 did not appear to be related to the melanin content of these cells.

Animals↗