Synthesis of magnetite nanoparticles by the method of co-precipitation and study of the influence of the reaction medium on their magnetic properties

Magnetite nanoparticles were obtained using the co-precipitation method under various synthesis conditions. The phase composition was investigated using X-ray diffraction analysis. The saturation magnetization of the obtained magnetic nanoparticles was investigated using vibrating-sample magnetometer. As a result, the samples obtained in a nitrogen atmosphere reveal a higher saturation magnetization value than the ones obtained in air

Risks due to X-ray Flares during Astronaut Extravehicular Activity

Solar hard X-ray flares can expose astronauts on lunar and deep space extravehicular activities (EVAs) to dangerous acute biological doses. We combine calculations of radiative transfer through shielding materials with subsequent transfer through tissue to show that hazardous doses, taken as >= 0.1 Gy, should occur with a probability of about 10% per 100 hours of accumulated EVA inside current spacesuits. The rapid onset and short duration of X-ray flares and the lack of viable precursor events require strategies for quick retreat, in contrast to solar proton events, which usually take hours to deliver significant fluence and can often be anticipated by flares or other light-speed precursors. Our results contrast with the view that only particle radiation poses dangers for human space exploration. Heavy-element shields provide the most efficient protection from X-ray flares, since X-rays produce no significant secondary radiation. We calculate doses due to X-ray flares behind aluminum shields and estimate the required shield masses to accompany EVA rovers.Comment: 8 pages, 2 figures; to be published in Space Weathe

Time-series clustering of gene expression in irradiated and bystander fibroblasts: an application of FBPA clustering

<p>Abstract</p> <p>Background</p> <p>The radiation bystander effect is an important component of the overall biological response of tissues and organisms to ionizing radiation, but the signaling mechanisms between irradiated and non-irradiated bystander cells are not fully understood. In this study, we measured a time-series of gene expression after α-particle irradiation and applied the Feature Based Partitioning around medoids Algorithm (FBPA), a new clustering method suitable for sparse time series, to identify signaling modules that act in concert in the response to direct irradiation and bystander signaling. We compared our results with those of an alternate clustering method, Short Time series Expression Miner (STEM).</p> <p>Results</p> <p>While computational evaluations of both clustering results were similar, FBPA provided more biological insight. After irradiation, gene clusters were enriched for signal transduction, cell cycle/cell death and inflammation/immunity processes; but only FBPA separated clusters by function. In bystanders, gene clusters were enriched for cell communication/motility, signal transduction and inflammation processes; but biological functions did not separate as clearly with either clustering method as they did in irradiated samples. Network analysis confirmed p53 and NF-κB transcription factor-regulated gene clusters in irradiated and bystander cells and suggested novel regulators, such as KDM5B/JARID1B (lysine (K)-specific demethylase 5B) and HDACs (histone deacetylases), which could epigenetically coordinate gene expression after irradiation.</p> <p>Conclusions</p> <p>In this study, we have shown that a new time series clustering method, FBPA, can provide new leads to the mechanisms regulating the dynamic cellular response to radiation. The findings implicate epigenetic control of gene expression in addition to transcription factor networks.</p

Sensitivity and dose dependency of radiation-induced injury in hematopoietic stem/progenitor cells in mice

We evaluated the sensitivity and dose dependency of radiation-induced injury in hematopoietic stem/progenitor cells. Adult C57BL/6 mice were daily exposed to 0, 2, 10, 50, and 250 mGy γ-ray for 1 month in succession, respectively. The damage of hematopoietic stem/progenitor cells in bone marrow were investigated within 2 hours (acute phase) or at 3 months (chronic phase) after the last exposure. Daily exposure to over 10 mGy γ-ray significantly decreased the number and colony-forming capacity of hematopoietic stem/progenitor cells at acute phase, and did not completely recover at chronic phase with 250 mGy exposure. Interestingly, the daily exposure to 10 or 50 mGy γ-ray decreased the formation of mixed types of colonies at chronic phase, but the total number of colonies was comparable to control. Immunostaining analysis showed that the formation of 53BP1 foci in c-kit + stem/progenitor cells was significantly increased with daily exposure to 50 and 250 mGy at acute phase, and 250 mGy at chronic phase. Many genes involved in toxicity responses were up- or down-regulated with the exposures to all doses. Our data have clearly shown the sensitivity and dose dependency of radiation-induced injury in hematopoietic stem/progenitor cells of mice with daily exposures to 2 ? 250 mGy γ-ray

The Ionizing Radiation-Induced Bystander Effect: Evidence, Mechanism, and Significance

It has long been considered that the important biological effects of ionizing radiation are a direct consequence of unrepaired or misrepaired DNA damage occurring in the irradiated cells. It was presumed that no effect would occur in cells in the population that receive no direct radiation exposure. However, in vitro evidence generated over the past two decades has indicated that non-targeted cells in irradiated cell cultures also experience significant biochemical and phenotypic changes that are often similar to those observed in the targeted cells. Further, nontargeted tissues in partial body-irradiated rodents also experienced stressful effects, including oxidative and oncogenic effects. This phenomenon, termed the “bystander response,” has been postulated to impact both the estimation of health risks of exposure to low doses/low fluences of ionizing radiation and the induction of second primary cancers following radiotherapy. Several mechanisms involving secreted soluble factors, oxidative metabolism, gap-junction intercellular communication, and DNA repair, have been proposed to regulate radiation-induced bystander effects. The latter mechanisms are major mediators of the system responses to ionizing radiation exposure, and our knowledge of the biochemical and molecular events involved in these processes is reviewed in this chapter