Radiation research. Supplement最新文献

{"title":"Preparatory clinical studies of Pi-mesons at TRIUMF.","authors":"G B Goodman,&nbsp;P Dixon,&nbsp;G K Lam,&nbsp;R Harrison,&nbsp;R O Kornelsen,&nbsp;C M Ludgate,&nbsp;A D Flores","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Eighty patients have been treated with Pi-mesons (pions) at TRIUMF between 1979-1984. The patients had tumors rarely curable by standard methods and had no prior radiotherapy. The distribution by site included skin, metastatic nodules (13), brain, glioblastoma multiforme (32), pelvis, rectosigmoid (15), prostate (12), bladder (7), and ovary (1). The studies involve serial escalations of pion dose until maximum tissue tolerance is reached, monitoring the response at each dose increment. Sites were chosen for study where lack of local control is a significant cause of treatment failure with conventional radiation therapy. The low dose rate and the available beam access at TRIUMF limit the number of patients treated and the volume treatable. A 3-D treatment planning program is in use, and a 3-D display of the dose distribution delivered in brain tumor treatments has been developed using the PET scanner. In practice, new methods introduced for measurement of tissue response include tumor growth delay curves, fine-needle biopsy mapping, and PET scanning of brain tumors. The use of endoscopic assessment of the rectosigmoid region is emphasized. Treatment results of glioblastoma multiforme show that the median survival for patients treated to 125 pion cGy/fx is in the range of 187-198 days; for patients receiving 170 cGy per dose/fraction (fx) the range is 290-315 days, and for those receiving 200-220 cGy/fx the median survival is in excess of 290 days. For pelvic malignancies the local control obtained with doses of 2500 cGy or less was 50% in 12 assessable patients; it was 75% in 20 patients who had 3000 cGy or more.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 ","pages":"S279-84"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14137026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Complication probability as assessed from dose-volume histograms.","authors":"J T Lyman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Optimization of a treatment plan for radiation therapy will produce a plan with the highest probability for tumor control without exceeding an acceptable complication rate. To achieve this goal it is necessary to have a means to estimate probabilities of local control and normal tissue complication. In general, good treatment plans deliver a high uniform dose to the target volume and lower doses to the surrounding normal tissues. The tolerance dose values available for various normal tissues are usually assumed to apply to partial or full volumes of the tissue which have been uniformly irradiated. These values are the best guidelines for estimating complication probabilities in tissues that receive a uniform dose to a fraction of the tissue and no dose to the remainder. Dose-volume histograms are one means of evaluating the uniformity of the irradiation on the tissues. Frequently the normal tissues are not uniformly irradiated as is demonstrated by dose-volume histograms for different treatment plans. A recursive algorithm which uses these tolerance dose data has been written and can be applied to arbitrary dose-volume histograms to estimate the complication probability.</p>","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 ","pages":"S13-9"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14984024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell-cycle-dependent recovery from heavy-ion damage in G1-phase cells.","authors":"E A Blakely,&nbsp;P Y Chang,&nbsp;L Lommel","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The cell-cycle-dependent capacity of synchronized G1-phase human T-1 cells to repair damage from either 425 MeV/u Bragg peak neon ions or 225 kVp X rays has been compared. The dose-survival response to each radiation was measured at early (1.5 h), mid (3.0 h), and late (4.5 h) times after mitotic selection. In addition the age response was characterized by irradiating cell populations at seven ages between 1.5 and 6.0 h after mitosis with single doses of either radiation. Repair of potentially lethal damage (PLDR) was evaluated in both the dose-survival and age-response experiments by holding irradiated cultures at 37 degrees C for 6 h in PBS or PBS containing 60 microM of the DNA polymerase inhibitor 1-beta-D-arabinofuranosyladenine (beta-araA) before trypsinization and plating. Delayed plating showed significant PLDR at all ages irradiated with X rays, with up to 10-fold increases of survival depending on the dose and the cell age at irradiation. There was negligible PLDR after neon-ion exposures to early and mid G1-phase cells; only late G1-phase cells repaired neon damage. The beta-araA treatment after X rays reduced the shoulder of the survival curves at all G1 ages studied, and in early and mid G1 reduced survival below the immediately plated control. beta-araA similarly reduced repair of PLD where it was measurable after neon ions. Differences between low- and high-LET radiation damage and repair are discussed.</p>","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 ","pages":"S145-57"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14984025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-LET radiation carcinogenesis.","authors":"R J Fry,&nbsp;P Powers-Risius,&nbsp;E L Alpen,&nbsp;E J Ainsworth","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The dose-response curves for the induction of tumors by high-LET radiation are complex and are insufficiently understood. There is no model or formulation to describe the dose-response relationship over a range 0-100 rad. Evidence suggests that at doses below 20 rad the response is linear, at least for life shortening and some tumor systems. Thus limiting values of RBEs for the induction of cancer in various tissues can be determined, but it will require sufficient data obtained at low single doses or with small fractions. The results obtained from experiments with heavy ions indicate an initial linear response with a plateauing of the curve at a tumor incidence level that is dependent on the type of tissue. The RBE values for the heavy ions using 60Co gamma rays as the reference radiation increase with the estimated LET from 4 or 4H to about 27 for 56Fe and 40Ar. The dose responses and RBEs for 56Fe and 40Ar are similar to those for fission neutrons. These findings suggest the possibility that the effectiveness for tumor induction reaches a maximum.</p>","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 ","pages":"S188-95"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14984028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Saturable repair models of radiation action in mammalian cells.","authors":"D. Goodhead","doi":"10.2307/3576633","DOIUrl":"https://doi.org/10.2307/3576633","url":null,"abstract":"Most quantitative models of radiation action in mammalian cells make the implicit assumption that all relevant repair processes proceed in a dose-independent manner. Thus it is implicitly assumed that the repair processes (1) follow totally unsaturated kinetics, (2) are not themselves inactivated by the radiation, and (3) are not enhanced by the presence of radiation damage. Contradiction of any of these three assumptions could have important theoretical and practical implications. The possible relevance of (1) and (2) in mammalian cells is discussed by considering a selection of saturable repair (and related) models. Repair inactivation is improbable, but repair saturation provides a ready explanation of common radiobiological phenomena without the need for the existence of \"sublethal\" damage. Furthermore, such models can \"explain\" additional phenomena which appear as contradictions to some sublethal damage models. Recent experiments by Wheeler and Wierowski have demonstrated the existence of dose-dependent repair of DNA damage in mammalian cells.","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"83 9 1","pages":"S58-67"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83225733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Charged particle cytogenetics: effects of LET, fluence, and particle separation on chromosome aberrations.","authors":"C. Geard","doi":"10.2307/3576638","DOIUrl":"https://doi.org/10.2307/3576638","url":null,"abstract":"Induced rearrangements of chromosomes, disrupting the orderly sequence and/or separation of the genetic material, are responsible for a significant proportion of cellular lethality, genetic mutation, and, as has become increasingly apparent in recent years, human cancer. The quantitative observation of chromosomal aberrations induced by ionizing radiations led early to the realization that as linear energy transfer (LET) increased, curvilinear dose responses became increasingly linear. Those few studies that examined aberrations as a function of LET found that the optimally effective LET was about 100 keV per micrometer, results consistent with those observed for other end points. The majority of chromosomal aberrations originate from molecular interaction between pairs of lesions (misrepair), with differences in sensitivity to aberration induction through the cell cycle. In Chinese hamster V-79 cells for all LET values studied, aberrations are most frequent in G2, then G1, then S phase of the cell cycle. The variation in sensitivity through the cell cycle changes from a factor of about 5 for 10 keV/micron particles to about 3 for 80 keV/micron particles. In the G2 phase a curvilinear dose response (G1 and S being linear) is found for all LETs occurring at fluences where there are substantial distances (greater than or equal to 3 micron) between particles. It is possible that for this one phase of the cell cycle a saturation of repair capabilities occurs as a function of both fluence and LET. When cells were irradiated with associated charged particles (molecular ions) it was found that even when two particles were separated by distances of less than 100 nm their effect was much less than one particle of twice the LET (the equivalent of 0 distance separation). This implies that the vast majority of molecular interactions which result in chromosomal aberrations occur as a consequence of interaction between damaged sites formed only a few nanometers from each other. It is clear that an analysis of chromosomal aberrations produced by charged particles can provide considerable insight into basic radiobiological mechanisms and into the organization of the mammalian genome.","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"1 1","pages":"S112-21"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87361568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lethal, potentially lethal, and nonlethal damage induction by heavy ions in cultured human cells.","authors":"P. Todd, J. Wood, J. Walker, S. Weiss","doi":"10.2307/3583505","DOIUrl":"https://doi.org/10.2307/3583505","url":null,"abstract":"In the fields of high-LET radiotherapy and space radiation safety it is important to know the relative probabilities with which a cell whose nucleus is struck by a heavy ion will be damaged or killed. Experiments were performed in which synchronous cultured human T-1 cells (presumptive HeLa) were irradiated with natural alpha particles of energy approximately 3.5 MeV at various times after mitotic selection up to the middle of S phase. Nuclear-area histograms were determined as a function of time after mitosis under conditions identical to those used for irradiation. The efficiency with which one particle passing through the nucleus killed a cell was found to be 0.14-0.20. This value was extrapolated to experimental cell survival data obtained when asynchronous cultured human cells were irradiated with He, Li, B, C, N, O, Ne, Ar ions of energy 6.58 or 5.5 MeV/amu, and the cell killing efficiency was found to be in the broad range of 0.5-1.0 under single-hit conditions. Similarly irradiated cells were examined for colony-size distribution by an image analysis technique, and it was found that the loss of large colonies was dose and LET-dependent in a systematic way. Dose-response data suggest two predominant subpopulations, resistant and sensitive cells, and it appears that the sensitive population is affected by single-hit kinetics. The single-hit coefficient for the induction of inherited slow growth varied with LET in a similar way to that for survival. The action cross section for this form of heritable damage appears to be comparable to the geometric cross section of the cell nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"9 1","pages":"S5-12"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80047420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biochemistry of DNA lesions.","authors":"J. Ward","doi":"10.2307/3576637","DOIUrl":"https://doi.org/10.2307/3576637","url":null,"abstract":"Ionizing radiation produces a range of damage types in cellular DNA. All damage types do not have the same biological significance. Here arguments are presented supporting the view that lesions in which damage is present on both strands in a local region of the DNA (locally multiply damaged sites--LMDS) will present problems for cellular repair processes. We have previously shown that lesions produced in DNA by individual OH radicals, i.e., single OH species acting alone, are ineffective in mammalian cell killing [J.F. Ward, W.F. Blakely, and E.I. Joner, Radiat. Res. 103, 383-392 (1985)]. We have similar evidence in mutagenesis studies (Ward and Calabro-Jones, unpublished data). Thus the formation of such damage by individual OH radicals formed by ionizing radiation would be similarly ineffectual. Earlier [J.F. Ward, Radiat. Res. 86, 185-195 (1981)] we suggested that OH-radical scavenging studies were consistent with the scavenging of OH radicals in volumes of high radical density, spurs, etc., i.e., in volumes which, when they overlap the DNA, will cause the production of LMDS. The individual constituent lesions of LMDS will be formed as a result of direct ionization or as a result of an OH-radical attack. Both mechanisms can lead to base damage or strand breakage. It is clear that damage in both bases of a deoxyribonucleotide pair leads to loss of base sequence information and can be repaired correctly only by accident or in a recombinational process.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"82 1","pages":"S103-11"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77527142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An alternative to absorbed dose, quality, and RBE at low exposures.","authors":"V P Bond,&nbsp;M N Varma,&nbsp;C A Sondhaus,&nbsp;L E Feinendegen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The microdosimetric distribution of event sizes, especially for small exposures and high-LET radiation, represents both a fractional involvement of the exposed cell population and variable amounts of energy transferred to the \"hit\" cells. To determine the fraction of cells that will respond quantally (be transformed) after receiving a hit of a given size, a hit size effectiveness function (HSEF) which appears to have a threshold has been derived from experimental data for pink mutations in Tradescantia. The value of the HSEF at each event size, multiplied by the fractional number of cells hit at that event size, and summed over all event sizes, yields a single value representing the fractional number of quantally responding cells and thus the population impairment for a given exposure. The HSEF can be obtained by unfolding (deconvoluting) several sets of biological and microdosimetric data obtained with radiation of overlapping event size distributions.</p>","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 ","pages":"S52-7"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14985208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heavy-ion effects on mammalian cells: inactivation measurements with different cell lines.","authors":"H. Wulf, W. Kraft-Weyrather, H. Miltenburger, E. Blakely, C. Tobias, G. Kraft","doi":"10.2307/3576639","DOIUrl":"https://doi.org/10.2307/3576639","url":null,"abstract":"In track segment experiments, the inactivation of different mammalian cells by heavy charged particles between helium and uranium in the energy range between 1 and 1000 MeV/u has been measured at the heavy ion accelerator Unilac, Darmstadt, the Tandem Van de Graaf, Heidelberg, and the Bevalac, Berkeley. The inactivation cross sections calculated from the final slope of the dose-effect curves are given as a function of the particle energy and the linear energy transfer.","PeriodicalId":77888,"journal":{"name":"Radiation research. Supplement","volume":"8 1","pages":"S122-34"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88841520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}