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PubMedDate not supplied

Modification of radiation-induced apoptosis in radiation- or hyperthermia-adapted human lymphocytes.

We have investigated the influence of the cellular adaptive response to ionizing radiation on radiation-induced apoptosis in human cells. The adaptive response is believed to be a protective mechanism that confers resistance to the detrimental effects of ionizing radiation and that can be induced by different agents, including hyperthermia and radiation. We have used fluorescence analysis of DNA unwinding (FADU) to assay the induction of apoptosis in human peripheral blood lymphocytes by ionizing radiation. Using the FADU assay, we have observed the initial radiation-induced DNA damage, its subsequent disappearance due to enzymatic repair, and its time- and dose-dependent reappearance. We believe this reappearance of DNA damage to be indicative of the DNA fragmentation event associated with apoptosis. This interpretation has been supported at the individual cell level using an in situ terminal deoxynucleotidyl transferase (TDT) assay (Apoptag, Oncor Inc.), which detects the 3'-hydroxyl ends of fragmented DNA, and by fluorescence analysis of nuclear morphology in Hoechst 33258 stained cells. Pretreatment of cells with low-dose gamma-radiation (0.1 Gy) or mild hyperthermia (40 degrees C for 30 min) altered the extent of radiation-induced (3 Gy) apoptosis. Both pretreatments sensitized lymphocytes to become apoptotic after the 3-Gy radiation exposure. This sensitization may represent an adaptive response mechanism that reduces the risk that genetically damaged cells will proliferate. The ability to modify the probability of radiation-induced apoptosis may lower the cancer risk from a radiation exposure.

Adaptation, Physiological↗

PubMed2001

[Occurrence of BOOP outside radiation field after radiation therapy for small cell lung cancer].

We report a case of bronchiolitis obliterans organizing pneumonia (BOOP) that occurred outside the radiation field after radiation therapy for small cell lung cancer. A 74-year-old woman received chemotherapy and a total of 60 Gy of radiation therapy to the right hilum and mediastinum for small cell carcinoma of the suprahilar area of the right lung. Radiation pneumonitis developed within the radiation port 3 months after the completion of radiation therapy. She complained of cough and was admitted 7 months after completion of the radiation therapy. Chest radiography and computed tomography demonstrated peripheral alveolar opacities outside the radiation field on the side contralateral to that receiving the radiation therapy. Bronchoalveolar lavage showed that the total cell count was increased, with a markedly increased percentage of lymphocytes. Transbronchial lung biopsy revealed a histologic pattern consistent with BOOP. Treatment with corticosteroids resulted in rapid improvement of the symptoms and complete resolution of the radiographic abnormalities of the left lung. Although some cases of BOOP following radiation therapy for breast cancer have been reported, none of BOOP after radiation therapy for lung cancer have appeared in the literature.

Aged↗

PubMed1992

Radiation-induced damage to DNA in drug- and radiation-resistant sublines of a human breast cancer cell line.

An Adriamycin-resistant subline of a human breast cancer cell line, MCF-7 ADRR, has been shown to exhibit radioresistance associated with an increase in the size of the shoulder on the radiation survival curve. In the present study, damage to DNA of MCF-7 sublines WT and ADRR by 60Co gamma radiation was measured by filter elution techniques. The initial amount of DNA damage, measured by both alkaline and neutral filter elution, was lower in ADRR cells, suggesting that these cells are resistant to radiation-induced single- and double-strand DNA breaks. In the case of double-strand breaks the difference between WT and ADRR cells was significant only at the lower radiation doses studied (up to 100 Gy). In cells depleted of glutathione (GSH) by L-buthionine sulfoximine (BSO) treatment, ADRR cells were sensitized to radiation-induced DNA damage, while WT cells were unaffected. The rate of repair of single- and double-strand DNA breaks following radiation was the same for both sublines, and repair of radiation damage was not affected by BSO treatment in either cell line. The relative resistance of ADRR cells to initial DNA damage by radiation is the only difference so far detected at the molecular level which reflects radiation survival, and it is possible that other factors are involved in the resistance of ADRR cells to killing by radiation. Sensitization of ADRR cells to radiation-induced DNA damage by GSH depletion, although not likely to involve inhibition of GSH-dependent detoxification enzymes per se (irradiation was done at 4 degrees C), suggests that at the molecular level radioresponse in this subline is related to maintenance of GSH/GSSG redox equilibrium.

Breast Neoplasms↗

PubMed2004

Use of a sterile, disposable, radiation-absorbing shield reduces occupational exposure to scatter radiation during pectoral device implantation.

The aim of this study was to demonstrate the effectiveness of a radiation-absorbing shield in reducing physicians' occupational radiation exposure during pectoral device implantation. A sterile, disposable, lead-free radiation-absorbing surgical drape containing x-ray attenuation material was evaluated. Twenty procedures used the radiation absorbing drape, and 20 were performed without the shielding. Radiation exposure was measured using thermoluminescent dosimetry collar badges. Use of the protective shield was associated with a time adjusted 80% reduction in radiation dose (0.009 mrem/s with shielding vs 0.047 mrem/s without shielding, P < 0.05) to the physician performing the procedures. The radiation-absorbing surgical drape did not interfere with technical performance nor add procedural time, and all procedures were successfully completed. This study demonstrates that a sterile, disposable, radiation-absorbing drape provides a convenient means of augmenting conventional radiation shielding. Use of this protective shielding greatly reduces operators' occupational exposure to scatter radiation during pectoral device implantation without compromising sterility or procedural technique.

Bismuth↗

PubMedDate not supplied

Combined radiation therapy and surgery in the management of advanced head and neck cancer: final report of study 73-03 of the Radiation Therapy Oncology Group.

Between March 1973 and June 1979, patients with advanced operable squamous cell carcinoma of the supraglottic larynx or hypopharynx were randomly allocated to receive either preoperative radiation therapy (5,000 rad) or postoperative radiation therapy (6,000 rad). Patients with oral cavity or oropharynx lesions were randomly assigned either preoperative radiation, postoperative radiation, or definitive radiation therapy (6,500-7,000 rad), with surgery reserved for salvage if residual disease was present 6 weeks after completion of irradiation. Three hundred twenty patients were evaluable with a median follow-up of 60 months. Based on results in 277 patients across all four regions combined, locoregional control was significantly better for patients assigned to receive postoperative radiation therapy (65%) compared with those assigned to receive preoperative radiation therapy (48%, P = 0.04). This was due to a higher rate of both persistent and recurrent local and regional disease in the preoperative group. Survival also showed a trend to be better in the postoperative group (38%) compared with the preoperative group (33%, P = 0.10). Rates of severe surgical and radiation therapy complications were similar overall. Forty-three patients were evaluable for each of the three treatment regimens assigned to patients with oral cavity or oropharynx lesions. Due to the small number of patients available for this portion of the trial, the observed differences for overall survival (4-year percentage 33% overall; 30% preoperative, 36% postoperative, 33% definitive radiation therapy) and for locoregional control (45% overall; 43% preoperative, 52% postoperative, 38% definitive radiation therapy) were not statistically significant. The use of definitive radiation therapy with surgical rescue as an ethically justified alternative treatment for these tumors remains a question for further research.

Carcinoma, Squamous Cell↗

PubMed2002

Radiation exposure to the corporeal bodies during 3-dimensional conformal radiation therapy for prostate cancer.

PURPOSE: Radiation therapy for prostate cancer is associated with the development of post-treatment erectile dysfunction. Use of 3-dimensional (D) conformal delivery techniques has reduced delivery of radiation to periprostatic tissues. However, the exact magnitude of radiation that the corporeal bodies are exposed to using this delivery technique is currently unknown. This study was undertaken to calculate the radiation dose delivered to the corporeal bodies during 3-D conformal radiotherapy. MATERIALS AND METHODS: Ten patients with proven prostate adenocarcinoma who underwent pre-therapy computerized tomography simulation and radiation delivery planning had the proximal corporeal bodies outlined on axial computerized tomography. The dose to the proximal penile tissues was then calculated using computer modeling. RESULTS: The total dose of radiation administered to the prostate and seminal vesicles was 73.8 Gy. Mean radiation delivered to the most proximal 2 cm. of the corporeal bodies was 31 +/- 12.8 Gy., equating to 43% of the total dose of radiation delivered to the prostate and seminal vesicles. CONCLUSIONS: These data indicate that large doses of radiation are being delivered to erectile tissue in the proximal penis despite careful pretreatment planning for 3-D conformal radiation therapy for prostate cancer. These data should encourage the development of radiation delivery strategies that minimize corporeal tissue exposure.

Adenocarcinoma↗

PubMed2002

The utility of external beam radiation and intracystic 32P radiation in the treatment of craniopharyngiomas.

BACKGROUND: The management of craniopharyngiomas has historically been controversial in terms of the extent of initial surgical resection and the use of additional treatments. Various options include radical excision versus a more conservative surgical approach followed by external beam radiation; most recently, intracystic 32P radiation has been used in selected patients. METHODS: We reviewed our experience with 25 patients with craniopharyngiomas treated between 1984 and 1999 to assess the effectiveness of external beam radiation and intracystic 32P radiation therapy in preventing progression and recurrence of local disease. RESULTS: All patients underwent surgery as a component of initial therapy for their histologically-proven craniopharyngiomas. Fifteen patients additionally received external beam radiation. Forty-five percent of patients who underwent incomplete resections followed by external beam radiation required additional therapy. In contrast, 80% of patients who had incomplete resections without post-operative external beam radiation required further treatment. Seven patients had intracystic 32P colloid injections. Neither of the two patients receiving 32P intracystic radiation as part of their initial therapy needed further treatment. Only one of the five patients receiving 32P intracavitary radiation for disease progression following initial therapy required further intervention. Of the remaining four patients, three enjoyed responses to treatment and one had stable disease. CONCLUSIONS: Our observations support the use of external beam radiation for prevention of tumor progression in adults unable to receive a complete surgical resection. Our results additionally suggest that intracystic 32P radiation results in control of cystic components of craniopharyngiomas in the majority of cases.

Adolescent↗

PubMed1989

Mutation and sister chromatid exchange induction in Chinese hamster ovary (CHO) cells by pulsed excimer laser radiation at 193 nm and 308 nm and continuous UV radiation at 254 nm.

We compared mutagenesis and sister chromatid exchange (SCE) induction by 193 nm and 308 nm pulsed excimer laser radiation with 254 nm low intensity continuous wave UV light in Chinese hamster ovary (CHO) cells in culture. The 254 nm radiation was most mutagenic of the radiations, in accordance with expectation, and also was most effective in increasing the level of SCEs. The 193 nm radiation was mutagenic at the ouabain resistance locus, but not at the HGPRT locus. However, 193 nm radiation was also strongly cytotoxic at energies producing measurable mutations. This radiation also caused a dose-related increase in SCEs. Pulsed excimer radiation at 308 nm was mutagenic at both loci, and also increased the incidence of SCEs. Comparison of the ratio of mutants/surviving cells at the D37 after radiation showed similar values for 254 nm and 308 nm at the HGPRT locus, but at the ouabain resistance locus, the ratio for the 308 nm radiation was about 5 times that for 254 nm radiation. These results indicate that some risk for mutagenesis may accompany the use of excimer radiation in the UVA region in therapeutic applications.

Animals↗

PubMed1991

Inhibition of epidermal Langerhans cell function by low dose ultraviolet B radiation. Ultraviolet B radiation selectively modulates ICAM-1 (CD54) expression by murine Langerhans cells.

Immunosuppressive effects of low levels of ultraviolet B (UVB) radiation on cutaneous immune responses have been attributed to deleterious effects of UVB radiation on epidermal Langerhans cells (LC). To determine how UVB radiation modulates LC function we examined the effect of in vitro UVB exposure on LC accessory cell activity and surface phenotype. Exposure of BALB/c murine epidermal cells to low dose (less than or equal to 200 J/m2) UVB radiation in vitro inhibited their ability to support the mitogenic response of unstimulated, accessory cell-depleted splenic T cells to anti-CD3 mAb. LC accessory cell activity was also inhibited when LC were exposed to UVB radiation in situ, although several-fold higher doses of UVB radiation were required to achieve complete inhibition of LC function. This dose-dependent inhibition was mediated through a direct effect on LC that could not be reversed by IL-1 or IL-6 alone or in combination, or granulocyte-macrophage-CSF. TNF-alpha did not inhibit LC accessory cell function in this assay and anti-TNF-alpha neutralizing antibodies did not reverse the inhibitory effects of UVB radiation. UVB irradiated LC failed to participate in the anti-CD3-dependent clustering that normally occurs between T cells and LC during the proliferative response of murine T cells to anti-CD3 mAb, suggesting that UV radiation may interfere with accessory cell function by preventing intercellular adhesion. Two-color flow cytometric studies revealed low levels of the ICAM-1 on freshly isolated LC and some keratinocytes. ICAM-1 expression on LC increased 15 to 20-fold within the first 24 h in vitro and continued to increase during a 72-h culture period. The integrin LFA-1 was not identified on freshly isolated or cultured LC but was detected on responding T cells. Prior exposure of LC to UVB radiation (50 or 100 J/m2) inhibited the increase in ICAM-1 expression that normally occurs in vitro by up to 70% whereas surface levels of class II MHC Ag, CD45 and Fc-gamma receptors were not affected. Blocking studies revealed that anti-CD3 induced T cell proliferation and T cell-LC cluster formation was inhibited by both anti-LFA-1 and anti-ICAM-1 mAb suggesting that ICAM-1 expressed on LC must bind to LFA-1 on T cells to facilitate proliferative responses of T cells to anti-CD3 mAb. We conclude that the in vitro inhibitory effects of low dose UVB radiation on LC accessory function may result because UVB radiation prevents upregulation of ICAM-1 expression by LC in culture.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2005

Effects of N1, N13-diethylnorspermine (DENSPM) and X-radiation treatment on human colorectal tumor clones with varying X-radiation and drug responses.

This study was designed to examine the effects of treatment with N1, N13-diethylnorspermine (DENSPM), a spermine analog, and X radiation on survival and on the polyamine and spermidine/spermine N1-acetyltransferase (SSAT) levels in closely related human colorectal tumor (HCT116) clones exhibiting a wide range of X-radiation and drug responses. After treatment with DENSPM and X radiation, clonogenic cell survival was measured. SSAT protein levels were measured by Western blot analysis and SSAT enzymatic activities by the conversion of [1-14C]acetyl-CoA into [1-14C]acetylspermidine. Polyamine [i.e. putrescine (PUT), spermine (SPM) and spermidine (SPD)] levels were measured with high-performance liquid chromatography. DENSPM enhanced the efficacy of radiation treatment in HCT116, HCT116-Clone2 (a radiation-resistant clone) and HCT116-Clone10 (a clone with similar X-radiation response as the parental HCT116 cells) but not in HCT116-CloneK (an X-radiation-sensitive but relatively drug-resistant clone). Treatment with DENSPM without X radiation caused the most significant increase in SSAT activity (approximately 22-fold) and an almost complete depletion of SPD levels in HCT116-CloneK. Our results suggest that (a) the lack of sensitization of X-radiation treatment by DENSPM in HCT116-CloneK was likely due to the prior depletion of SPD levels by DENSPM alone, (b) natural polyamine contents and/or inducibility of SSAT may be important factors influencing cellular response to combined X-radiation and DENSPM treatments, and (c) more importantly, there may be a potentially novel role for combining polyamine analogs such as DENSPM with X rays.

Antineoplastic Agents↗

PubMed1985

X-ray and UV-radiation sensitivity of circulating lymphocytes in multiple epidermal cancer in relation to previous radiation exposure.

The cellular sensitivity to X rays (200 kV, 16 mA) and UV radiation (254 nm) was examined in lymphocytes from three groups of patients with multiple epidermal malignant tumors, selected by their clinical history of carcinogenesis. Eight patients previously exposed to low energy ionizing radiation (less than or equal to 12 kV) had an increased cellular sensitivity to UV radiation as well as X rays compared with 24 age and sex matched controls. This indicates the existence of a cellular cross-sensitivity to UV radiation and ionizing radiation not previously established for human cells. In contrast six patients previously exposed to high energy ionizing radiation (between 25 and 170 kV) had normal cellular response to both UV radiation and X rays, indicating a different biologic effect of low and high energy ionizing radiation. In the third group of patients, previously exposed to therapeutic UV radiation/excess sunlight, the lymphocytes had a normal response to X rays, but an increased sensitivity to UV radiation. The possibility of evaluating the individual risk at radiation exposure is suggested.

Adult↗

PubMed2005

Genetic and epigenetic features in radiation sensitivity. Part II: implications for clinical practice and radiation protection.

Recent progress especially in the field of gene identification and expression has attracted greater attention to the genetic and epigenetic susceptibility to cancer, possibly enhanced by ionising radiation. This issue is especially important for radiation therapists since hypersensitive patients may suffer from adverse effects in normal tissues following standard radiation therapy, while normally sensitive patients could receive higher doses of radiation, offering a better likelihood of cure for malignant tumours. Although only a small percentage of individuals are "hypersensitive" to radiation effects, all medical specialists using ionising radiation should be aware of the aforementioned progress in medical knowledge. The present paper, the second of two parts, reviews human disorders known or strongly suspected to be associated with hypersensitivity to ionising radiation. The main tests capable of detecting such pathologies in advance are analysed, and ethical issues regarding genetic testing are considered. The implications for radiation protection of possible hypersensitivity to radiation in a part of the population are discussed, and some guidelines for nuclear medicine professionals are proposed.

Epigenesis, Genetic↗

PubMed2026

Radiation-resistant and desiccation-tolerant bacteria from the Chavara-Neendakara high background radiation area, india: phenotypic characterisation and genomic insights.

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.

India↗

PubMed2004

Radiation protection by diethyldithiocarbamate: protection of membrane and DNA in vitro and in vivo against gamma-radiation.

Diethyldithiocarbamate (DDTC) is studied for its antioxidant and radioprotective abilities. DDTC at a concentration of 0.5 mM reduced DPPH radical. DDTC reduced the damage to deoxyribose resulting from hydroxyl radicals generated by Fenton reaction, indicating that the radioprotective abilities of this compound could be due to the free radical scavenging. DDTC protected rat liver microsomal membranes in vitro from peroxidative damage in lipids (measured as TBARS) resulting from 50 Gy gamma-radiation. It also protected plasmid pBR322 DNA from radiation-induced strand breaks. An oral administration of DDTC to mice before whole body gamma-radiation exposure (4 Gy) resulted in a reduction of radiation-induced lipid peroxides in the liver homogenates. An administration of DDTC to mice before gamma-radiation reduced the radiation-induced DNA damage as studied by single cell gel-electrophoresis (comet assay). The comet parameters such as tail length, tail moment, and percent of DNA in tail were found to increase in the blood leukocytes of mice exposed to 4 Gy gamma-radiation. When DDTC was administered to mice before the radiation exposure, the increase in the comet parameters as a result of radiation was prevented, indicating a protection of cellular DNA. The present study has implication for the potential use of DDTC as a radioprotector.

Administration, Oral↗

PubMed1979

Mutagenicity of cross-links and monoadducts of furocoumarins (psoralen and angelicin) induced by 360-nm radiation in excision-repair-defective and radiation-insensitive strains of Saccharomyces cerevisiae.

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.

DNA Repair↗

PubMed1986

Stage II invasive adenocarcinoma of the ovary: results of treatment by whole abdominal radiation plus pelvic boost versus pelvic radiation plus oral melphalan chemotherapy.

Thirty-one patients with histologically confirmed FIGO Stage II adenocarcinoma of the ovary were prospectively treated in two sequential studies: 3000 rad of whole abdominal radiation therapy over 6 weeks by an open field technique followed by 2000 rad pelvic boost over 2 weeks (group 1, 16 patients, 1972-1974) or 5000 rad of pelvic radiation therapy over 5 weeks followed by a year of melphalan chemotherapy at a dose of 0.2 mg/kg/day for 5 days every 4 weeks (group 2, 15 patients, 1975-1982). Abdominal radiation included the entire peritoneal cavity and both diaphragms; the liver was not shielded. Only 2 patients had residual disease greater than 2 cm. No group 1 patients underwent pretherapy restaging laparoscopy prior to radiation or second look laparotomy after treatment. Eighty percent of group 2 patients underwent restaging laparoscopy (10) or staging laparotomy (2) prior to radiation. All group 2 patients underwent second look procedures if no evidence of disease. No patient developed intestinal complications secondary to radiation requiring surgery. Eighty-one percent of group 1 patients and to date 40% of group 2 patients developed recurrences. Size of residual disease prior to radiation, histologic grade, and substage (IIA, B, or C) did not correlate with recurrences. Five-year estimated survival was 40 and 50% for groups 1 and 2, respectively. Three thousand rad of wole abdominal radiation plus 2000 rad pelvic boost or 5000 rad pelvic radiation plus melphalan did not appear to improve survival over surgery alone. The role of radiation therapy in Stage II ovarian cancer remains unclear.

Adenocarcinoma↗

PubMed2006

Computational evaluation of changes in ionizing radiation dose distribution in tissues caused by EM applicators when external radiation and hyperthermia act simultaneously.

PURPOSE: The presented theoretical study investigates the influence of CFMA-like electromagnetic microstrip applicators (MAs) on ionizing radiation intensity and depth radiation dose distribution (DRDD) in irradiated tissues which are tightly covered with a MA. METHODS: It is shown that at relatively low photon energy (<200 keV) the MA does not affect noticeable the profile of the DRDD curve and does not lead to skin overdosing. Nevertheless, it significantly (up to 20-35%) decreases the low energy ionizing radiation intensity. For high energy photons (>1 MeV), on the contrary, the decrease of radiation intensity, caused by the MA, is small (3-10%), but the profile of the DRDD curve, calculated by means of the Monte-Carlo method, is significantly affected. RESULTS: The radiation dose maximum is shifted to the skin, resulting in possible skin overdosing. Radiation absorption characteristics of MA are calculated and compared with published parameters of EM horn and US applicators now in use for external simultaneous radiation and hyperthermia (ESRH) procedures. The MA provides the minor ionizing radiation absorption. Due to it and owing to their conformability with the tissue surface the MAs would not require any additional means or devices to be used for ESRH treatment procedures with any common ionizing radiation equipment. CONCLUSIONS: The necessity of development means for decreasing the time of radiation equipment occupation during ESRH procedures is pointed out.

Absorption↗

PubMed2003

Repeat intracoronary radiation for recurrent in-stent restenosis in patients who failed intracoronary radiation.

BACKGROUND: Intracoronary radiation therapy (IRT) is the only proven treatment for in-stent restenosis (ISR). It is, however, associated with a significant failure rate. The present study evaluated the outcomes of patients who underwent repeat intracoronary radiation for recurrent ISR. METHODS AND RESULTS: Fifty-one consecutive patients who failed a previous radiation treatment, presented with angina and angiographic evidence of ISR, and were treated with percutaneous coronary intervention (PCI) and repeat radiation to the same segment were studied. Twenty-five patients were treated with gamma radiation in a dose of 15 Gy, and 26 were treated with beta radiation doses of 18.3 to 23 Gy. The mean cumulative dose for this cohort was 39.5+/-11.9 Gy (range, 29 to 75.6 Gy). The outcomes of those patients were compared with outcomes of 299 patients who also failed initial radiation but were treated with repeat conventional PCI to a previously irradiated segment without repeat radiation. At 9 months after treatment, the repeat-IRT group had lower rates of target lesion revascularization (23.5% versus 54.6%; P<0.001) and major adverse cardiac events, including target vessel revascularization (29.4% versus 61.3%; P<0.001). At 9 months, patients with repeat IRT were free of angiographic and clinical events related to the radiation therapy. CONCLUSIONS: Repeat gamma or beta radiation to treat failed IRT for ISR after conventional PCI is safe and effective at 9 months and should be considered as a therapeutic option for this difficult patient subset.

Angina Pectoris↗