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[en] The full text of the publication follows. 5-Iodo-2'-deoxyuridine (IUdR) is a well known radiosensitizing agent when incorporated into cellular DNA. Attempts were made in the present work to optimize its radiosensitizing effect using low energy radiation (50 keV)  provided by the European Synchrotron Research Facility. A clonogenic assay was performed to determine the impact on cell survival upon treatment of cells containing or not IUdR with ionizing radiations of either classical high energies (Cobalt source) or using low energies (50 keV). Such low energies are expected to promote photoelectric effect on heavy atoms such as iodine . To quantify the effect, the so-called 'sensitization enhancement ratio' SER, corresponding to the ratio of the required doses to obtain 10% of survival in IUdR free cells compared to cells having incorporated IUdR, was determined for both types of radiations. A SER of 1.4 was determined for high energy radiations whereas a SER of 2 was observed for low energy radiation (50 keV). Such an increase in radiosensitivity was found to be correlated to an increase in the amount of DNA damage measured in IUdR containing cells as assessed by the comet assay. Altogether our results suggest that the concomitant use of IUdR that could be preferentially incorporated into rapidly dividing cancerous cells with low energy radiation could significantly improve radiotherapeutic treatments by reducing doses of radiation and thus side effects on normal tissues. References:  Corde, S. et al., Synchrotron radiation-based experimental determination of the optimal energy for cell radiotoxicity enhancement following photoelectric effect on stable iodinated compounds. Br J Cancer 2004; 91(3): 544-551.  Karnas, S.J., et al., Monte Carlo simulations and measurement of DNA damage from X-ray-triggered Auger cascades in iododeoxyuridine (IUdR). Radiat Environ Biophys, 2001. 40(3): 199-206. (authors)
[en] Enhanced killing of bacteria was obtained by radiation reaching the earth during total solar eclipse (February 16, 1980) than during the corresponding time of a normal day (February 26, 1980). The killing was not due to the formation of sunlight induced photoproducts of tryptophan. The damage to the bacteria exposed to sunlight could be repaired by photoreactivation. (orig.)
[en] The calculating the probability of the cell killing per hit, from radon progeny, requires the development of morphometric model of the human airway system. This study is focused on the different modeling concept. For example, several morphometric lung models have been published which differ in terms of airway structure and lung volume, there by affecting the particle deposition efficiencies. The present variety of modeling concepts suggests that the choice of specific modeling assumptions is as important for dose risk estimates as the choice of proper parameter values. The model of human lung analysed in the present study differ from those employed in the ICRP66 model, dose estimates will consequently differ from ICRP66 predictions, because its included the area of the branching the cylinders (airways tube) in the human lung. A analytical model cylinder bifurcation was created to simulate the geometry of human lung with the geometric distribution of cell nuclei in the airway wall of the tracheobronchial tree. Reported probabilities are calculated for various targets and alpha particle energies in order to show dependence of the probability of cell killing per hit from alpha particle energies and the geometry of tracheobronchial tree for the human lung, created in this study. (author)
[en] Pulmonary fibrosis is the consequence of a variety of diseases with no satisfying treatment option. Therapy induced fibrosis also limits the efficacy of chemotherapy and radiotherapy in numerous cancers. It has been proposed that fibrogenesis is not a unique pathologic process but rather, is due to an excess of the same biologic events involved in normal tissue repair. Persistent and exaggerated wound healing ultimately leads to an excess of fibroblast replication and matrix deposition. Several studies revealed that TGF-β1, collagen 1, fibronectin, various chemokine and some anti-oxidant are overexpressed in radiation induced pulmonary fibrosis. A number of studies were performed that polysaccharide extracted from Panax ginseng C.A. Meyer, ginsan, has been demonstrated to be a potent promising biological response modifier (BRM), including proliferation of lymphocytes, generation of lymphokine activated killer cells, and production of several cytokines. On the basis of several results of the ability of ginsan on modulation of redox system and cytokine balance, we examined whether ginsan directly regulates fibroblast proliferation, differentiation factors, and also investigated the mechanism of the antifibrotic effects of ginsan
[en] In the last 20 years, the field of cellular and molecular oncology has been born and has moved its first steps, with an increasingly rapid pace. Hundreds of oncogenic and oncosuppressive signaling cascades have been characterized, facilitating the development of an ever more refined and variegated arsenal of diagnostic and therapeutic weapons. Furthermore, several cancer-specific features and processes have been identified that constitute promising therapeutic targets. For instance, it has been demonstrated that microRNAs can play a critical role in oncogenesis and tumor suppression. Moreover, it turned out that tumor cells frequently exhibit an extensive metabolic rewiring, can behave in a stem cell-like fashion (and hence sustain tumor growth), often constitutively activate stress response pathways that allow them to survive, can react to therapy by engaging in non-apoptotic cell death programs, and sometimes die while eliciting a tumor-specific immune response. In this Perspective article, we discuss the main issues generated by these discoveries that will be in the limelight of molecular and cellular oncology research for the next, hopefully few years.
[en] In studying the cell death mechanism by radioactivity, people discovered that apoptosis is a kind of form in the died cell induced by radioactivity. Meanwhile, apoptosis is closely related with radioactivity. In the recently years, there are more and more article about apoptosis induced by radioactivity. The article review the phenomenon about apoptosis induced by radioactivity and the newest research about improving tumor control by radioactivity inducing apoptosis. (authors)
[en] It is inevitable for living objects to expose themselves to multiple factors present in the environment. The combined effect of multi-factors is hard to estimate and predict in advance. Especially factors harmful to organisms can synergistically interact with each other. When the effect of the combined action is greater than expected additivity, it is called synergism or supra-additivity. Ionizing radiation can cause cell death, mainly due to its ability to produce reactive oxygen species in cells. Mercury is one of widespread environmental pollutants which is known to have toxic effects on organisms. There are many reports indicating its genotoxic potential in a variety of aquatic species. Synergistic effects of radiation and mercury on human cells was previously reported. Aerobically growing organisms suffer from exposure to oxidative stress, caused by partially reduced forms of molecular oxygen, known as reactive oxygen species. These are highly reactive and capable of damaging cellular constituents such as DNA, lipids and proteins. Consequently, cells from many different organisms have evolved mechanisms to protect their components against reactive oxygen species. Reactive oxygen species can also be formed by exposure of cells either to ionizing radiation or redox cycling chemicals present in the environment like heavy metals. PLHC-1 hepatoma cell line derived from top minnow (Poeciliopsis lucida) is the most commonly used cell line in toxicology. The PLHC-1 cells are easy to cultivate, and can be used for screening the toxicity of chemicals. The present study was done to evaluate the combined effects of radiation with mercury chloride on the PLHC-1 cells
[en] Purpose: To determine the impact of prolonged fraction delivery times (FDTs) simulating intensity-modulated radiotherapy (IMRT) on cultured nasopharyngeal carcinoma (NPC) cell killing. Methods and Material: Cultured NPC cell lines CNE1 and CNE2 were used in this study. The biological effectiveness of fractionated irradiation protocols simulating conventional external beam radiotherapy and IMRT (FDT of 15, 36, and 50 minutes) was estimated with standard colony assay, and the differences in cell surviving fractions after irradiation with different protocols were tested by use of the paired t test. The impact degree of prolonged FDTs (from 8 to 50 minutes) on cell killing was also assessed by the dose-modifying factors, which were estimated by comparing the effectiveness of intermittently delivered 2 Gy with that of continuously delivered 1.5 to 2 Gy. Results: The cell surviving fractions of both CNE1 and CNE2 after fractionated irradiation simulating IMRT were higher than those simulating conventional external beam radiotherapy (p < 0.05). The dose-modifying factors for a fraction dose of 2 Gy increased from 1.05 to 1.18 for CNE1 and from 1.05 to 1.11 for CNE2 with the FDT being prolonged from 15 to 50 minutes. Conclusions: This study showed that the prolonged FDTs simulating IMRT significantly decreased the cell killing in both CNE1 and CNE2 cell lines, and these negative effects increased with the FDT being prolonged from 15 to 50 minutes. These effects, if confirmed by in vivo and clinical studies, need to be considered in designing IMRT treatments for NPC.