[en] The purpose of this study is to investigate the effect of developed product on skin and reproductive system of animal due to irradiation via in vivo test, and finally acquire fundamental data for evaluation of protective materials on degenerative damages. <1st year> - Evaluate the effect of candidate materials on UV-induced skin damages · Test the effect of candidate materials to protect the skin from photodamage, the gross and microscopic changes in the skin of hairless mice and materials-treated mice exposed chronically to UV <2nd year> - Evaluate the effect of developed product (HemoHIM) on radiation-induced reproductive system (female) damages - Evaluate the effect of developed product (HemoHIM) on chemical-induced reproductive system (female) damages <3rd year> - Evaluate the effect of developed product (HemoHIM) on radiation-induced reproductive system (male) damages - Evaluate the effect of developed product (HemoHIM) on chemical-induced reproductive system (male) damages

[en] The degree and distribution of damage to buildings subjected to earthquakes is a concern of the Chinese Government and the public. Seismic damage data indicates that seismic capacities of different types of building structures in various regions throughout mainland China are different. Furthermore, the seismic capacities of the same type of structure in different regions may vary. The contributions of this research are summarized as follows: 1) Vulnerability matrices and earthquake damage matrices of masonry structures in mainland China were chosen as research samples. The aim was to analyze the differences in seismic capacities of sample matrices and to present general rules for categorizing seismic resistance. 2) Curves relating the percentage of damaged masonry structures with different seismic resistances subjected to seismic demand in different regions of seismic intensity (VI to X) have been developed. 3) A method has been proposed to build vulnerability matrices of masonry structures. The damage ratio for masonry structures under high-intensity events such as the Ms 6.1 Panzhihua earthquake in Sichuan province on 30 August 2008, was calculated to verify the applicability of this method. This research offers a significant theoretical basis for predicting seismic damage and direct loss assessment of groups of buildings, as well as for earthquake disaster insurance.

[en] Pseudo-excitation (PE) method is a recently developed damage identification method for flexible structures containing components like beams, plates and shells. Characterized by the high-order spatial derivatives, the approach has been shown to feature a high sensitivity to local damage. However, two major issues, i.e. susceptibility to measurement noise and unknown material/structural properties, hamper its practical applications. To tackle these problems, an adaptive damage localization method is proposed for plate-type structures, which combines the PE method with hierarchical clustering. In the proposed method, a general dynamic equilibrium model, involving unknown material/structural properties, is statistically identified and further used for damage localization. Moreover, noise-induced effects are quantified by using a hierarchical clustering for performance assessment of damage localization and process optimization of spatial derivative estimation to achieve more accurate damage localization. Meanwhile, a data fusion scheme is developed to avoid blind inspection zones, thus enhancing the capability of damage localization. Both numerical and experimental studies of cantilever plates containing two damage zones are conducted to validate the feasibility and the effectiveness of the proposed adaptive damage localization method. Results demonstrate that the proposed method outperforms the traditional PE method in terms of detection accuracy and robustness. (paper)

[en] The pathogenesis of sulfur mustard (SM) toxicity is not fully understood, although it is related to reactive oxygen and nitrogen species, oxidative stress, DNA damage, poly (ADP-ribose) polymerase activation within the affected cell. We, therefore, made an attempt whether epigenetic aberrations may contribute to pathogenesis of SM poisoning in rats' lung. A total of 40 male SD rats were divided into 4 groups. Group 1 served as control and given 2 ml saline, three groups received single dose of mechlorethamine (MEC) (3.5 mg/kg subcutaneously) with the same time intervals. Group 2 received MEC only; group 3 received histone deacetylase (HDAC) inhibitor (Trichostatine A) (1 mg/kg) and group 4 received DNA methyl transferase (DNMT) inhibitor (5-Azacytidine) (0.02 mg/kg), intraperitoneally. MEC injection resulted in severe lung toxicity with strong interstitial and alveolar edema, hemorrhage, emphysematous changes as well as mild inflammatory cell infiltration and septal thickening. In group 3, the HDAC inhibitor significantly reduced interstitial and alveolar edema, hemorrhage and inflammatory cell infiltration. On the other hand, we have observed severe lung damage by using DNMT inhibitor (group 4). In HDAC inhibitor group, the results were close to sham group. In DNMT inhibitor group, however, lungs were worse than MEC group results. These preliminary results revealed that, SM itself and/or its intracellular metabolites may perturb the epigenetic environment of the affected cell in lung tissue. Hypothetically, MEC may cause HDAC induction leading to a variety of gene silencing. Trichostatine A can reduce the active enzyme level and can reactivate the already silenced genes. Further studies are needed to clarify the involvement of epigenetic perturbations in the pathogenesis of mustard toxicity.(author)

[en] The neutron detector G.A.M.I.N. developed in the CEN Saclay delivers a measuring signal proportional to the number of radiation damage reactions in graphite. After testing and calibration in the reactors ISIS and OSIRIS in Saclay, the detector has been applied in an irradiation programme extended over the more important types of research reactors. The aim of this programme was studying of the effect of different reactor irradiation positions upon the radiation damage. The irradiation of those detectors in the D₂O reactor FRJ-2 and their measurement is reported here. The result is in agreement with that from other D₂O reactors, displaying a graphite damage function about 10% larger than the average result in the core of H₂O reactors, related to the same number of Ni58(n,p)Co58 reactions. Differences in the fuel burn-up or in the irradiation position (height) within the surrounding fuel element have no influence upon the result. (orig.)

[en] The Service des Piles de Saclay is now testing a miniaturized tungsten damage detector. Tests now being carried out should give the limits of operating conditions (may be up to 500-600 deg C). The response of the detector, based on the variation in electrical conductivity, is fairly near that of metals in general. This experimental tool could give flow measurements of damage doses in various materials. Spectrum calculations using the APOLLO code, help fit the response of the detector to various currently used damage models

[en] While it is well known that ionizing radiation (IR) can damage nuclei, its underlying mechanism has been poorly characterized. Given that IR can elevate cellular levels of reactive oxygen species (ROS) and also that ROS can induce DNA damage, ROS may be involved in the IR-induced nuclear damage. However, this possibility has not been directly addressed. The mechanism whereby IR induces ROS generation is unclear. In the case of other types of stimuli, such as growth factors, cytokines, and chemokines, NADPH oxidase, a plasma membrane enzyme that can generate superoxide dismutase, was shown to be stimulated. Therefore, this study investigated the possible role of NADPH oxidase in IR-induced nuclear damage

[en] As ¹³¹I therapy, used to achieve ablation of thyroid gland remnant, can cause chromosome damage in cultured peripheral lymphocytes especially, we investigated whether administration of radioiodine may induce early genome damage in peripheral T lymphocytes of adolescents with differentiated thyroid carcinoma (DTC). We studied 11 patients, aged 14.8 ± 3.1 years, who assumed ¹³¹I (range: 1.11-4.44 GBq) to ablate thyroid remnant. A blood sample for micronucleus assay and for evaluating expression of some genes involved in the DNA repair or the apoptosis pathways was obtained from each patient 1 h before (T₀) and 24 (T₁) and 48 h (T₂) post-radioiodine administration. Compared to T₀, we did not find any difference in the number of micronucleated cells at both T₁ and T₂ in any subject. Nine out of 11 patients had altered expression levels in a majority of the DNA repair and apoptosis genes at T₁, which decreased at T₂. We demonstrated for the first time that peripheral cells of DTC children and adolescents who received ¹³¹I at a mean dosage of 3.50 ± 0.37 GBq did not show chromosome damage within 48 h from the end of radiometabolic therapy. This may be due to a prompt activation of the cell machinery that maintains the integrity of the genome to prevent harmful double-strand breaks from progressing to chromosome mutations, either by repairing the lesions or by eliminating the most seriously damaged cells via apoptosis. (orig.)

[en] Purpose: To explore whether interactions between normal epithelial and mesenchymal cells can modulate the extent of radiation-induced DNA damage in one or both types of cells. Methods and Materials: Human primary thyrocytes (PT), diploid fibroblasts BJ, MRC-5, and WI-38, normal human mammary epithelial cells (HMEC), and endothelial human umbilical cord vein endothelial cells (HUV-EC-C), cultured either individually or in co-cultures or after conditioned medium transfer, were irradiated with 0.25 to 5 Gy of γ-rays and assayed for the extent of DNA damage. Results: The number of γ-H2AX foci in co-cultures of PT and BJ fibroblasts was approximately 25% lower than in individual cultures at 1 Gy in both types of cells. Reciprocal conditioned medium transfer to individual cultures before irradiation resulted in approximately a 35% reduction of the number γ-H2AX foci at 1 Gy in both types of cells, demonstrating the role of paracrine soluble factors. The DNA-protected state of cells was achieved within 15 min after conditioned medium transfer; it was reproducible and reciprocal in several lines of epithelial cells and fibroblasts, fibroblasts, and endothelial cells but not in epithelial and endothelial cells. Unlike normal cells, human epithelial cancer cells failed to establish DNA-protected states in fibroblasts and vice versa. Conclusions: The results imply the existence of a network of reciprocal interactions between normal epithelial and some types of mesenchymal cells mediated by soluble factors that act in a paracrine manner to protect DNA from genotoxic stress

[en] Values for the damage exposure parameters fluence > 1.0 MeV, fluence > 0.1 MeV, and dpa were determined for all locations of metallurgical specimens in the test assembly of the ORR-PSF irradiation experiment. Determination is based on dosimetry measurements by HEDL and the fluence calculations by R.E. Maerker and B.A. Worley at ORNL. The LSL-M2 adjustment procedure was used. The space dependency of the damage parameter values can be presented as a cosine-exponential function. Uncertainties are between 5 and 10%