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At least 415 records · Page 23Linked to original sources
PubMed2002

Protein kinase Cdelta overexpression enhances radiation sensitivity via extracellular regulated protein kinase 1/2 activation, abolishing the radiation-induced G(2)-M arrest.

Protein kinase C (PKC) has been widely implicated in regulation ofcell growth/cell cycle progression and apoptosis. However,the role of PKCdelta in radiosensitivity and cell cycle regulation remains unclear. Overexpression of PKCdelta increased Ca2+-independent PKC activity without altering other PKC isoforms (PKCalpha, -beta1, -epsilon, and -zeta), and extracellular regulated protein kinase (ERK) 1/2 activity was also increased in PKCdelta-specific manner. A clonogenic survival assay showed that PKCdelta-overexpressed cells had more radiosensitivity and pronounced induction of apoptosis than control cells. Flow cytometric analysis revealed that PKCdelta made the cells escape from radiation-induced G(2)-M arrest. Moreover, p53 and p21(Waf) induction by radiation were higher in PKCdelta-overexpressed cells than control cells, and PKCdelta-mediated apoptosis was reduced, when radiation-induced ERK1/2 activity was inhibited by PD98059. Furthermore, PKCdelta antisense and rottlerin, PKC inhibitor-abrogated PKCdelta-mediated radiosensitivity and reduced ERK1/2 activity to the control vector level. These results demonstrated that PKCdelta overexpression enhanced radiation-induced apoptosis and radiosensitivity via ERK1/2 activation, thereby abolishing the radiation-induced G(2)-M arrest and finally apoptosis.

3T3 Cells↗
PubMed2002

Universal and radiation-specific loci influence murine susceptibility to radiation-induced pulmonary fibrosis.

Susceptibility to radiation-induced pulmonary fibrosis is a heritable trait in mice. In a prior study of C57BL/6J (susceptible), C3Hf/Kam (resistant), and F1 and F2 mice derived from these strains, we estimated that approximately 38% of the measured phenotypic variation could be attributed to effects from a few genetic factors. In addition, we identified one genetic factor on chromosome 17 in the MHC region. To identify any additional genetic loci that might influence interstrain variability, we conducted a genome-wide linkage scan using 214 markers and the phenotypically extreme 94 (of 268) F2 mice. In regions exceeding suggestive linkage (LOD = 2.8), we followed up with additional markers. This scan revealed evidence for quantitative trait locus (QTL) on chromosomes 17 (LOD = 4.2), 1 (LOD = 4.5), and 18 (LOD = 3.9), which influence susceptibility to radiation-induced pulmonary fibrosis. An additional region containing a QTL on chromosome 6, LOD = 4.6, showed linkage in female mice only. The evidence for linkage to chromosome 18 weakened when it was analyzed jointly with other markers. These four loci are estimated to account for 70% of the genetic contribution to this trait with chromosome 17 and 1 accounting for 28 and 24%, respectively. To confirm and better define the influence of the chromosome 17-linked QTL on radiation sensitivity, we conducted studies on congenic mice in which the linked region on chromosome 17 had been transferred onto a B6.AKR or a C3.SW background. The chromosome 17-linked QTL was confirmed to influence the phenotype as the fibrotic radiation response of B6.AKR-H2(k) mice was significantly less than that of B6 mice (P = 0.0001). The QTL on chromosome 17 for radiation-induced lung fibrosis is within the same region as QTLs identified for lung damage after other insults, including bleomycin, ozone, and particle exposure, as well as for asthma, suggesting that this region of chromosome 17 may harbor a "universal" lung injury gene.

Animals↗
PubMed1991

Influence of cellular radiation sensitivity on local tumor control of human melanoma xenografts given fractionated radiation treatment.

The radiocurability of human melanoma xenografts was studied by treating tumors with multiple fractions of 2.0 Gy and using local tumor control at 180 days as end point. Three melanoma lines (E. F., G. E., M. F.) that are only weakly immunogenic in athymic nude mice (BALB/c-nu/nu/BOM) were selected for the study. The tumor radiocurability was found to differ considerably among the lines; the radiation doses required to achieve local control of 50% of the tumors irradiated (TCD50s; mean +/- SE) were 85.0 +/- 4.7 Gy (E.F.), 60.3 +/- 5.4 Gy (G.E.), and 99.3 +/- 5.7 Gy (M. F.). The radiation sensitivity in vitro of cells isolated directly from tumors also differed significantly among the lines. The TCD50 showed positive correlations with the surviving fraction after 2.0 Gy in vitro, the surviving fraction after two doses of 2.0 Gy (4-h interval) in vitro, and the surviving fraction after 4.0 Gy at a low dose rate (1.25 cGy/min) in vitro. Thus, the differences in tumor radiocurability among the lines were mainly a consequence of cellular differences in the capacity to repair radiation damage. Comparisons of measured TCD50s with theoretical TCD50s, calculated from cell-surviving fractions measured in vitro after radiation treatment in vitro or in vivo, suggested that other tumor parameters, e.g., rate of population between radiation fractions, also had a significant impact on the TCD50. However, this study strongly supports the assumptions that the surviving fraction at 2.0 Gy in vitro is a useful parameter for prediction of clinical tumor radiocurability.

Animals↗
PubMed1991

Interaction between radiation and drug damage in mammalian cells. V. DNA damage and repair induced in LZ cells by adriamycin and/or radiation.

A multi-drug-resistant cell line selected in increasing concentrations of Adriamycin and designated LZ (J. A. Belli, Radiat. Res. 119, 88-100, 1989) is shown to exhibit a survival response characterized by radiation sensitivity and Adriamycin resistance. To determine if this response is due to alterations in either the initial levels of damage induced or the repair of DNA damage, LZ cells and the parental V79 cells were exposed to either radiation or Adriamycin and the damage and repair were measured with alkaline or nondenaturing filter elution. After exposure to radiation, induction and repair of both single-strand and double-strand breaks were equivalent. LZ cells exposed to 100 micrograms/ml Adriamycin for 1 h contained no measurable damage while the same treatment induced breaks and crosslinks in V79 cells. Pretreatment of LZ cells for 1 h with Adriamycin before irradiation did not alter either the initial levels of induced damage or the repair of strand breakage. These results suggest that (1) mechanisms other than differential induction and repair of strand breaks are responsible for the increased radiation sensitivity in LZ, and (2) the lack of Adriamycin-induced DNA damage in LZ is at least partially responsible for the increased cell survival after treatment.

Animals↗
PubMed1990

[Injuries of the sigmoid colon following radiation therapy of carcinoma of the uterine cervix--a method of estimating the radiation dose to the sigmoid colon].

Grade 2 or 3 injuries of the sigmoid colon were observed in 4 out of 42 patients with carcinoma of the uterine cervix who were treated by radiation therapy. The irradiation was planned as the combination of the external irradiation (whole pelvic 30 Gy and 20 Gy with central shielding by 25 fractions, 5 weeks) and the intracavitary irradiation (RALS, 19 Gy at point A by 3 fractions). To analyze the causes of the radiation sigmoiditis, we have investigated the following factors: age, dose at point A, dose at point C, grade of tandem dislocation, uterine angle, obesity score, evidence of previous surgery to the pelvic cavity and hypertension. The dose at point C and the grade of tandem dislocation were determined from the confirming X-Ps at RALS therapy and external irradiation. The superimposition of these films was performed with corrections for the angle between the projection direction of the X-Ps and the vertical magnification factor of the central shielding area. Point C was defined as a point 2 cm anterior to the intersection of the tandem axis and a curvilinear line 1 cm outside from the margin of central shield on the X-Ps. Grades of tandem disclocation were decided as the number of tandem tips which were outside of the central shielding area on X-Ps. As the results, the doses at point C showed very high statistical significance (p less than 0.001) with the evidence of radiation sigmoiditis. All the cases with radiation sigmoiditis were received over 1290cGy at point C. Age had also some significance (p less than 0.05) with radiation sigmoiditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1989

[Delayed radiation necrosis of the temporal lobe following radiation therapy of maxillary carcinoma].

A case of delayed radiation necrosis following radiation therapy for maxillary carcinoma was reported. The diagnosis of this case for the radiation necrosis was clinically suggestive and established by the pathological findings of autopsy. This 66 year-old man had been treated by the partial resection for the right maxillary carcinoma with chemotherapy (pepleomycin 110 mg, adriamycin 20 mg). Pre- and postoperatively total dose of 5040 rads were irradiated with cobalt therapy during 42 days at a dose of 180 rads and 5 times in a week through two ports at 8 x 8 cm field including right orbital region. Three years 7 months after radiation therapy he complained of disorientation, recent memory disturbance and slight left hemiparesis. On enhanced CT irregular ring enhanced mass lesion was seen in left temporal lobe inside the radiation field with extensive low density over temporal lobe on plain CT. MR imaging demonstrated that T 1-weighted spin echo images with a 50-msec repetition time (TR) and 22-msec echo time (TE) had irregular low signal intensity and extensive high signal intensity combined with partially low intensity in the central area on T2 weighted spin echo images with 2300 msec TR and 100 msec TR. There were not appeared vascular obstruction and stenosis on right carotid angiogram. He improved remarkably on clinical symptoms and CT by treating of dexamethasone and osmotic diuretics, but died of pneumonia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Radiation myelopathy of the mouse spinal cord--isoeffect correlations after fractionated radiation.

A one cm long segment of the lower thoracic upper lumbar spinal cord of mice was irradiated using one, two, three, five, seven, ten, 15, 20 and 25 daily fractions. The animals were checked for paraparesis of the hind legs over their entire life span up to two years. The ED 50-values for radiation myelopathy for intervals of 250 up to 550 days were calculated. The resulting isoeffect curves follow an upward bending course being flat for one to five fractions and then getting steeper up to 25 fractions with a slope of 0.27 to 0.30. For intervals between 250 and 550 days the isoeffect curves run a parallel course. Only ED 50-values for intervals of 550 days post radiation omitting data above 6 Gy/fraction fit the linear quadratic cell survival (LQ) model with an alpha/beta value of 6.5 Gy which is relatively high compared to alpha/beta-values for late damage of normal tissues. Incomplete repair between fractions or overlapping effects of the cell systems responsible for radiation myelopathy (oligodendrocytes and endothelial cells) might account for failure of the other isoeffect data to fit the LQ-model. There are important differences of the isoeffect correlations of rat and mouse radiation myelopathy probably due to different repair characteristics and kinetics between the involved cells. On the other hand similarities of isoeffect correlations of man, rat and mouse are observed. Therefore the model of mouse radiation myelopathy presented in this paper might be used to test new treatment strategies.

Animals↗
PubMed1994

[The assessment of combined exposure to radiation and chemical factors based on the study of the morbidity of personnel in radiation-chemical manufacture].

The study analyzed the work conditions of personnel engaged into production of plastic modified by radiation. The analysis revealed that the staffers exposed to combined action of radiation and chemical factors face 6 times more intensive harm from radiation resulting in more cardiovascular diseases. All that should be considered in setting the norms for annual radiation doses at workplaces. Real production demands maximal allowable dose to equal 1 rem/year, if the personnel is exposed to chemicals (ozone, nitrogen oxides, ethylene, formaldehyde, acrolein). The scientist elaborated a method to evaluate combined action of chemicals and radiation, which is based on dependence of morbidity on personnel's age. During the further calculation of summarized factor all previous parameters are added, given their enhance.

Absenteeism↗
PubMed1993

Oncogene- transformed NIH 3T3 cells display radiation resistance levels indicative of a signal transduction pathway leading to the radiation-resistant phenotype.

Oncogenes and their normal counterparts, proto-oncogenes, are functionally important cellular genes which interact with one another as components of signal transduction pathways leading to cell growth and differentiation. Numerous reports in the literature have also begun to link these genes to the phenomenon of cellular radiation resistance. In this report we examine the radiation resistance level of NIH 3T3 cells transformed by various oncogenes in an attempt to define the intracellular pathway to the radiation-resistant phenotype. The results demonstrate that an analogous signaling pathway is apparently involved in acquisition of radiation resistance. Serine/threonine protein kinase oncogenes such as raf, mos, and PKC play a central role in the pathway. Moreover, specific oncogenes upstream (sis, HER-2, met, trk, and ras) and downstream (ets and myc) of these important signaling mediators can also influence the radiation resistance level of the cells.

3T3 Cells↗
PubMed1999

The influence of ionizing radiation on the CLARION 1.2 cochlear implant during radiation therapy.

OBJECTIVE: This study aimed to determine the maximum dose of radiation the CLARION 1.2 cochlear implant can withstand safely. INTRODUCTION: Cochlear implants restore functional hearing to patients with sensorineural deafness. Because some patients may need radiation therapy, it is important to investigate the influence of ionizing radiation on cochlear implant function. METHODS: This study tested the function of four CLARION 1.2 implants (Advanced Bionics, Sylmar, CA, U.S.A.) after varying radiation treatments with gamma rays. The first implant received a cumulative dosage of 69 Gy over nine treatments (single doses between 0.1-30 Gy). The second was irradiated with a total of 90 Gy, receiving three treatments of 30 Gy each. The third and fourth received doses more typical of patient therapy (i.e., 2 Gy) approximately 30 times, for a cumulative dosage of approximately 60 Gy. Implant function was tested after every treatment; the CLARION implant incorporates a back-telemetry system, allowing impedance and current output testing. RESULTS: Despite the type of treatment, the results were quite consistent: difficulties in function occurred when the cumulative dosage inside the implant was approximately 60 Gy. The first implant recovered completely and the second recovered partially. DISCUSSION: The CLARION 1.2 cochlear implant seems to safely withstand approximately 60 Gy of radiation before experiencing functional difficulties. In a clinical situation, the implant would not likely be in the target volume irradiated, and thus the patient's therapeutic cumulative dosage might be higher.

Cochlear Implants↗
PubMed2002

Significant reduction of radiation exposure to operator and staff during cardiac interventions by analysis of radiation leakage and improved lead shielding.

The objectives of this study were to disclose and to reduce occupational radiation leakage in invasive cardiology. Prospectively, we analyzed various dose parameters for 330 coronary procedures. We used a Rando phantom to measure scatter entrance skin air kerma to the operator (S-ESAK-O) during fluoroscopy for all standard tube angulations, and to plot isodose lines for 0 degrees /0 degrees -posterior anterior angulation. The patient's measured dose area product due to diagnostic catheterization and elective percutaneous transluminal coronary angioplasty was 6.2 and 10.4 Gycm(2), which represents 11% and 13% of currently typical values, respectively. With use of 0.5- and 1.0-mm overcouch and undercouch shielding, it was possible to reduce the mean of 4,686 nSv/Gycm(2) to 677 and 277 nSv/Gycm(2), respectively. Closure of radiation leakage up to 897 microSv/hour at the operator's gonadal height (80 to 105 cm), not heretofore described, was achieved by an additional 1.0-mm, lead-equivalent undercouch-top and overcouch-flap adjacent to the table, down to a S-ESAK-O/dose area product level of 47.5 nSv/Gycm(2). With use of a 0.5-mm lead apron, collar, glasses, foot-switch shield and 1.0-mm lead cover around the patient's thighs, the operator received a mean S-ESAK-O of 8.5, while his forehead, eyes, thyroid, chest, gonads, and hands were exposed to 68.2, 1.2, 1.2, 1.2, 0.8, and 58.2 nSv/Gycm(2), respectively. In conclusion, radiation-attenuating intervention techniques and improved lead protection can effectively contribute to a new state of the art in invasive cardiology, with reduction of operator radiation exposure to 0.8% of typical S-ESAK-O levels in advanced catheterization laboratories.

Aged↗
PubMed1998

Radiation-induced instability and its relation to radiation carcinogenesis.

PURPOSE: A model that identifies radiation-induced genetic instability as the earliest cellular event in the multi-step sequence leading to radiation-induced cancer was previously proposed. In this paper ongoing experiments are discussed which are designed to test this model and its predictions in mouse mammary epithelial cells. RESULTS: Several lines of evidence are presented that appear to support this model: first, the development of delayed mutations in p53 following irradiation in altered growth variants; secondly, the high frequencies for the induction of both instability and transformation following irradiation in mammary epithelial cells; and finally, the demonstration that susceptibility to the induction of cytogenetic instability is a heritable trait that correlates with susceptibility to transformation and radiation-induced mammary cancer. Mice resistant to transformation and mammary cancer development are also resistant to the development of instability after irradiation. In contrast, mice sensitive to transformation and cancer are also sensitive to the development of cytogenetic instability. CONCLUSIONS: Data from this laboratory and from the studies cited above suggest a specific, and perhaps unique, role for radiation-induced instability as a critical early event associated with initiation of the carcinogenic process.

Animals↗
PubMed1975

An approach to the surveying of radiation environments for radiation protection purposes.

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.

Gamma Rays↗
PubMed2004

Upper dose thresholds for radiation-induced adaptive response against cancer in high-dose-exposed, cancer-prone, radiation-sensitive Trp53 heterozygous mice.

Trp53 heterozygous mice are radiation-sensitive and cancer-prone. Groups of 7-8-week-old female Trp53 heterozygous mice were exposed to 4 Gy of 60Co gamma radiation at high (0.5 Gy/min) or low (0.5 mGy/min) dose rate. Other groups received 10 or 100 mGy at low dose rate 24 h prior to the 4-Gy dose. Tumor frequency and latency were measured over the animals' life span. Exposure to 10 mGy prior to 4 Gy resulted in a small (approximately 5%) but significant life-span regain and increased latency (approximately 9%) for all malignant tumors taken together, but 100 mGy further reduced life span slightly (approximately 7%). Latency responses were tumor type-specific. The prior 10-mGy exposure resulted in a small (approximately 7%) regain in latency for lymphomas but no change in latency for spinal osteosarcomas. Increasing the adapting dose to 100 mGy eliminated the increase in lymphoma latency and further reduced life span (approximately 8%). A 10-mGy dose prior to 4 Gy at low dose rate had no effects. Adapting exposures had no significant effect on tumor frequency. We conclude that a single low dose induced a small protective response in vivo in Trp53+/- mice, reducing the carcinogenic effects of a subsequent large, high-dose-rate exposure by increasing tumor latency. The upper dose threshold at which low-dose protective effects gave way to detrimental effects was tumor type-specific, as found previously for spontaneous tumors in these same cancer-prone mice (Radiat. Res. 159, 320-327, 2003). However, the upper dose thresholds appear to be lower (below 100 mGy) for radiation-induced tumors than for the same tumors appearing spontaneously.

Adaptation, Physiological↗
PubMedDate not supplied

[Quantitative characteristics of radiation injury of the spermatogenic epithelium and the rate of its recovery after exposure to fast neutrons and gamma-radiation].

The paper submits the results of studies on the kinetics of spermatogenous epithelium cell number after exposure to fast neutrons (60-300 cGy) and gamma-radiation (200-600 cGy). It was shown that a relative decrease in the quantity of spermatocytes is determined by an exponential dose-response curve with D0 of 35 and 120 cGy for neutrons and gamma-radiation respectively. For spermatides and spermatozoa a single D0 value of 20 and 55 cGy was obtained for neutrons and gamma-radiation respectively. As the radiation dose increases the recovery process in the epithelium is substantially decelerated. The equation T1/2 = T1/2(0)e0.0009D well describes the dependence of the half-recovery period T1/2 upon the equivalent dose.

Animals↗
PubMedDate not supplied

Epidemiological studies on radiation carcinogenesis in human populations following acute exposure: nuclear explosions and medical radiation.

The present review provides an understanding of our current knowledge of the carcinogenic effect of low-dose radiation in man, and surveys the epidemiological studies of human populations exposed to nuclear explosions and medical radiation. Discussion centers on the contributions of quantitative epidemiology to present knowledge, the reliability of the dose-incidence data, and those relevant epidemiological studies that provide the most useful information for risk estimation of cancer induction in man. Reference is made to dose-incidence relationships from laboratory animal experiments where they may obtain, for problems and difficulties in extrapolation from data obtained at high doses to low doses, and from animal data to the human situation. The paper describes the methods of application of such epidemiological data for estimation of excess risk of radiation-induced cancer in exposed human populations and discusses the strengths and limitations of epidemiology in guiding radiation protection philosophy and public health policy.

Adolescent↗
PubMed1976

[Radiation load of patients and radiation-exposed personnel in the endoscopic retrograde cholangio-pancreaticography].

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.

Body Burden↗
PubMed1989

Selective internal radiation therapy: distribution of radiation in the liver.

Selective internal radiation therapy for primary and secondary liver cancer involves the intra-hepatic arterial injection of microspheres containing yttrium-90. The microspheres become entrapped primarily in, and thus preferentially irradiate, tumour tissue. During a clinical trial with this therapy it has been possible to take tumour and normal liver tissue samples, after microsphere injection, and measure their specific activity. Absorbed tissue radiation doses were then calculated for tumour and normal tissue samples from a total of nine patients. The mean tumour to normal tissue ratio for radiation dose for the nine patients was approximately 6:1 with a range of 0.4:1-45:1. Injection of similar amounts of activity in different patients resulted in markedly differing tissue doses depending on liver size and tumour burden. Normal liver tissue doses of between 9 and 75 Gy were measured while corresponding tumour tissue doses ranged from 34 to 147 Gy. Selective internal radiation therapy, combined with the blood flow changes resulting from angiotensin II administration, can provide preferentially high radiation doses to tumour tissue within the liver whilst relatively sparing the surrounding normal liver tissue.

Adenocarcinoma↗