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In the radiotherapy of malignant tumors of the oral cavity, the exact distribution of radiation dosage in the neighborhood of metallic dental replacement has been uncertain so far. Many authors therefore asked that crowns and bridges be removed before radiotherapy. By means of lithium fluoride thermo-luminescence dosimetry, punctate measurements of doses are possible for the first time. In view of the dose values obtained, removal of metallic dental replacement before the beginning of radiotherapy as a prophylactic measure to prevent radioosteomyelitis appears not to be necessary.
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Radiation-resistant microorganisms that survive high doses of ionising radiation serve as valuable models for understanding stress adaptation; however, the genomic determinants underlying extreme radiation tolerance in bacteria from natural environments with high background radiation remain insufficiently characterised. Bacterial isolates from the Chavara-Neendakara HBRA (Kerala, India) were evaluated for desiccation tolerance, and the desiccation-resistant isolates were subsequently exposed to gamma irradiation (1-10 kGy) using a 60Co source. Isolates were identified through 16S rRNA sequencing, morphologically characterised by FE-SEM, and screened for antibiotic susceptibility. The highly radiation-resistant strain underwent whole-genome sequencing via Oxford Nanopore Technology, with De novo assembly, polishing, and genome annotation. Four bacterial isolates (Micrococcaceae and Paenibacillaceae) exhibited D10 values of 1-7 kGy, including one multidrug-resistant strain; no endospores were observed in the Paenibacillus isolate under the tested conditions. Paenibacillus sp. HBRA004 survived 10 kGy gamma radiation, exceeding all previously reported HBRA isolates by over fourfold. Its 5.0 Mbp genome (GC = 48.27%, ≥ 99% completeness) encodes five mechanistically independent DNA repair pathways; homologous recombination (recA, recN, radA), base excision repair (mutM, mutY, mutT), mismatch repair (mutL, mutS), nucleotide excision repair (uvrA, uvrB, uvrD), and non-homologous end joining (ku, ligD), alongside a redundant antioxidant network comprising triple-copy Fe/Mn-family superoxide dismutases and ahpC peroxiredoxin. A thioredoxin system (trxA, trxB, msrA) and manganese uptake via mntH may contribute to further layers of ROS defence. Their specific contribution to the HBRA004 phenotype remains to be experimentally and comparatively validated. These findings represent the first genomically characterised 10 kGy-resistant bacterial isolate from the Chavara-Neendakara HBRA, establishing a new benchmark for radiation tolerance within this ecologically significant environment. Pathway depth, gene copy amplification, and Mn/Fe homeostasis appear to be candidate mechanisms contributing to high-level radiation tolerance, consistent with patterns in other radiation-resistant taxa, though their contribution requires functional validation.
The furocoumarin psoralen can form both monoadducts and cross-links with DNA when combined with 360-nm radiation, whereas the analog angelicin can form monoadducts only. Psoralen plus 360-nm radiation causes mutation induction with a slope of 2 (log-log plot) for a radiation-insensitive strain, whereas angelicin action with 360-nm radiation displays a slope of unity. For a radiation-sensitive mutant defective in the excision-repair pathway, the actions of both angelicin and psoralen plus 360-nm radiation exhibit one-target kinetics, but at higher exposures psoralen plus 360-nm radiation assumes a slope of 2. The excision-repair-defective strain is considerably more sensitive to the furocoumarins plus 360-nm radiation than is the radiation-insensitive strain, both for killing and mutation induction. The simplest explanation for the data is that both cross-links and monoadducts, formed by furocoumarins with DNA when exposed to 360-nm radiation, are capable of inducing mutations, and that monoadducts are repaired 20 times more efficiently than cross-links by the excision-repair pathway.
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The main body of this document consists of four major sections: A) An introduction describing the scope of Committee operations and providing a brief exposition of the concepts of radiation protection; B) A survey of experimental and theoretical data on cosmic radiations that have been obtained in individual research projects with emphasis on investigations that were performed under the sponsorship of the Committee. The studies evaluate galactic and solar radiation as a function of altitude and magnetic latitude; C) Best current estimates of cosmic radiation levels in the atmosphere; and D) Radiation protection recommendations dealing with maximum permissible doses and operational aspects covering satellite warning systems, on-board instrumentation, and forecasting. Nine annexes submitted by individual authors cover various of these subjects in greater detail.
Radiation toxicology is the quantification of radiation pathophysiology. It is based upon the development of more precise and accurate radiation dose response data in humans. Such information is particularly important because of the development of combined radiation therapy and chemotherapy. The search for models which will predict radiation injury is presented along with innovative approaches to the 3-dimensional reconstruction of isodose curves in autopsy material, and ultrastructural studies.
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ICRF 159 has been shown to increase the X-radiation sensitivity of exponentially growing EMT6 mouse tumour cells in vitro. This was found only with ICRF 159 exposure times longer than 10 h and only when the drug was given before irradiation. The increase in radiation sensitivity was expressed as a reduction of the shoulder of the radiation survival curve. As ICRF 159 was shown to have no effect on the repair of sub-lethal radiation damage, it was concluded that the drug reduced the capacity to accumulate such damage. ICRF 159 was also shown to have no effect on the repair of potentially lethal radiation damage in late plateau cells.
Between January 1969 and February 1975, 344 patients with carcinoma of the esophagus were managed primarily at the Princess Margaret Hospital, Toronto. One hundred sixty-eight (168) of the patients were treated palliatively and 176 of the patients were treated by radical doses of radiation, surgical resection or both. Survival of the radical treatment group was biphasic, the steeper component being identical to the survival of the palliative treatment group, thereby representing a group of patients that did not respond to radical treatment. Analysis of pretreatment assessment parameters indicated that all patients with T1 lesions (length less than or equal to 5 cm, circumference incomplete) and all patients with Stage I disease responded to treatment. Patients who were female, age greater than or equal to 70 years, N0 or had well differentiated squamous cell histology, responded to treatment in at least 80% of cases. No patient with extralymphatic distant metastases responded to treatment. The presence of other major disease did not affect response to treatment. Thirty patients had surgical resections and their survival was not significantly greater than the 146 patients who had radical radiation alone. Survival analysis revealed an optimum range of nominal standard dose (NSD) of 1602--1714 rets (median 1679 rets) for patients treated by radiation alone. An optimum port size (area) of 100--140 cm2 was observed for patients receiving 5000 rads and supervoltage irradiation gave a significantly improved survival in comparison with megavoltage irradiation. Sixty-seven percent (67%) of patients treated by radical doses or radiation developed esophageal strictures postradiation and on the basis of radiological, endoscopic or histological evidence 75% of these strictures were considered to be associated with the persistence of malignancy. On the basis of postmortem examinations (32) and death certificates there was overall an 80% failure to control the disease locally and 95% of strictures were associated with persistence of malignancy in the esophagus. Thirty-one of the 146 patients receiving radical radiation alone had palliation for esophageal obstruction following radiotherapy. The construction of a physiological bypass (e.g., colon) resulted in a mean survival of 215 days which was much longer than the survival observed with rigid esophageal tubes (35 days) or gastrostomy tubes (58 days).
One hundred and eighty-eight patients with inoperable or unresectable bronchogenic carcinoma were stratified by cell type, TNM staging, and prior surgery and then randomized into two treatment groups: continuous radiation therapy and split-course radiation therapy. There was no difference in clinical or objective improvement in the two groups. Survival rates for cases of squamous cell carcinoma, small cell carcinoma, and adrenocarcinoma were the same after both regimens of therapy. Split-course therapy resulted in a significantly better survival rate in cases of large cell carcinoma but the number of cases was small. We doubt that the difference is clinically significant. Objective roentgenographic response was accompanied by improved survival in squamous cell carcinoma, but not in the other three cell types. Split-course radiation therapy is superior to continuous radiation therapy because it is better tolerated by the patient and because re-examination of the patient prior to the second half of split-course therapy permits the detection of new metastatic disease that has become manifest during the rest period and spares the patient the futile second half of radiation therapy.
Many of the inadequacies of the system presently used for surveying environments containing penetrating radiation stem from the impossibility of defining a radiation parameter which is additive, measurable and closely related to peak dose equivalent in the body. Many of the present conceptual difficulties would be eliminated if surveys were made in terms of a quantity 'dose equivalent ceiling' defined as the sum of the peak dose equivalents generated by all the components of the field if each were incident normally to the front face of an anthropomorphic phantom. 'Dose equivalent ceiling' is close to the quantity measured by existing instruments, is both additive and measurable, and can be rigorously related to primary radiation field quantities. It is always greater than peak dose equivalent in the body, and would be used to define an exposure period during which a given dose equivalent could not be exceeded. The dose to specific parts of the person's body would then be estimated by personal dosimetry. Fields of low penetrating radiation could continue to be surveyed in terms of dose to specific superficial organs. Dose equivalent ceiling, which corresponds to the instrumental measurement, exceeds dose equivalent index, an indication of peak dose equivalent in the body, by a factor which can be as large as six.
Measurements of radiation in 54 patients and examiners during endoscopic-retrograde cholangiopancreaticography (ERCP) were analyzed. The values of radiation were relatively low and were compared favorably with those of gastroenterologic x-ray diagnostics. With greater experience it can be lowered further. Dangerous exposition to radiation was not found in patient or in examiner. The values obtained are far below the maximum dose permitted by radiation legislation. The question of a danger from repeated examination is not important, on the contrary, due to minimal exposition, the frequency of ERCP can be increased.
A young woman, successfully treated for Hodgkin's disease with radiation and MOPP chemotherapy, incurred a devastating stroke months after radiation therapy to the neck and other areas. There was no premonitory clinical history of cerebrovascular attacks. Autopsy showed unilateral thrombotic occlusion of the internal carotid artery unassociated with neoplastic or fibrotic annular constriction of the vessel. There was medial thickening and fibroblastic proliferation within the carotid artery. Areas of focal elastic membrane degeneration involved the cervical portions of the carotid. Thrombus was organized to the damaged vessel wall and was propagated into the intracranial vessels. Aneurysm formation and arterial hemorrhages were absent. These vascular changes occurred in an area of extensive radiation (7200 rads). Pathoanatomical studies in this patient indicate that radiation-induced vascular changes were associated with a "delayed" stroke.