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such changes were observed in HPCs. Furthermore, irradiated HSCs and their progeny exhibited a
significant impairment in clonogenic function revealed by the cobblestone area-forming cell and colony
forming cellassays, respectively. These long-term effects of proton radiation on HSCs may be attributable
to the induction of chronic oxidative stress in HSCs, because HSCs from irradiated mice exhibited a
significant increase in ROS production. In addition, the increased production of ROS in HSCs was associated
with a significant reduction in HSC quiescence and an increase in DNA damage measured by the γ-H2AX
foci assay. These findings suggest that exposure to proton radiation can lead to long-term HSC injury.



(PS1-11) DNA damage induction in bovine lymphocytes after the Fukushima nuclear accident. Asako J.
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Nakamura ; Masatoshi Suzuki ; Christophe E. Redon ; Yoshikazu Kuwahara ; William M. Bonner ; and
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Manabu Fukumoto, Ibraki University, Mito, Ibaraki, Japan ; Tohoku University, Sendai, Miyagi, Japan ;
and National Institutes of Health, Bethesda, MD
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The Fukushima Daiichi Nuclear Power Plant (FNPP) accident was one of the worst nuclear
disasters in human history and resulted in widespread radiation contamination over large habitable areas.
Several studies have documented the distribution of radionuclides in soil samples and animal organs
throughout the contaminated region. However, assessing how such contamination affects the health of
living organisms requires different techniques. One key consequence of ionizing radiation is the induction
of DNA damage. One type of DNA damage, the double-strand break (DSB) can be sensitively quantitated
utilizing the induced phosphorylation of histone H2AX at DSB sites. The creation of a DNA DSB in
eukaryotic cells is generally accompanied by the formation of hundreds of phosphorylated H2AX (γ-H2AX)
molecules in the chromatin flanking the DSB site. Antibodies to γ-H2AX allow the visualization of a "focus"
at the DSB site. These foci form the basis of many biodosimetry assays used in both basic and clinical
research to quantify radiation-induced DSBs. One of these assays utilizes lymphocytes in blood samples
taken non-invasively by phlebotomy. Here, we evaluate the biological effects of the radiation fallout in
the region surrounding the FNPP by quantifying DSBs in blood lymphocytes taken from cattle grazing in
the exclusion zone. Our finding reveal that a greater than two-fold increase in fraction of damaged
lymphocytes is observed in all cohorts within the 20 km exclusion zone in Fukushima. While levels of DNA
damage slightly decrease over 700-days period of sample collection, the extent of damage appeared to
be independent of the distance from the accident site within the exclusion zone. This study is the first to
evaluate the biological impact of the accident utilizing the γ-H2AX assay.



(PS1-12) The effect of low dose medical radiation exposures on inflammation and fibrosis in the heart.
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Stephanie Puukila ; Jennifer Lemon ; Douglas Boreham ; and Neelam Khaper, Lakehead University,
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Thunder Bay, Canada ; McMaster University, Hamilton, Canada ; and Laurentian University, Sudbury,
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Canada
It is well known that high dose radiation exposure can cause deleterious biological consequences
such as cell death, mutation, cancer, inflammation, and immune suppression. However, low dose
radiation may have a beneficial effect in radiation induced damage, where a prior, adapting, low dose
exposure can ameliorate the damage induced by the high radiation dose. The aim of this study was to test
the hypothesis that low doses of diagnostic radiation from Computed Tomography (CT) and Positron
Emission Tomography (PET) scans can induce an adaptive response and protect cardiac tissue from high





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