Chromosomal Damage and Repair
The primary cause of radiation induced cell death is thought to be damage to the nuclear material caused by local secondary electron production. Protons deposit energy at higher linear energy transfer (LET) than electromagnetic radiation. Exploration of the repair mechanisms induced by the two types of radiation damage may elucidate genes involved in various types of repair.
The examination of fungal radiation repair mutants, in which specific genes have been disabled, is revealing repeatable differences in the rate, efficiency and pattern of repair caused by loss of specific gene functions.
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Macromolecular Structure and Function
Subatomic particles are valuable for visualizing sub-microscopic structure and function via methods both destructive and
non-destructive. Just as electrons have been utilized to visualize structure by both transmission and scanning electron microscopy,
proton radiography can be used to visualize different qualities of structure on the same scale. The Small Angle Neutron Scatterer
(SANS) associated with the Low Energy Neutron Source (LENS) will be used to visualize molecular structures
within thick samples when that project is completed.
The structure of the tRNA processing ribozyme RNaseP is being examined using the RERS platform to fragment the ribozyme and examine the
remaining functionality. It has been discovered that the rybozyme, folded into its active form is relatively radiation damage
resistant. However, if the structure is denatured, the rybozyme cannot resume its functional form. This process reveals significant
damage at low levels of radiation that does not prohibit function.
Radiation Biology of the Myocardium
Much damage has been done to patients' cardiovascular systems during radiation therapy, and the body of literature concerning myocardial radiation damage is based largely upon this anecdotal evidence. However, because the vascular tissue, specifically the endothelium, is sensitive to low levels of radiation, most of the damage documented is actually due to anoxia. When the vessels that supply blood to the heart muscle are damaged, the muscle suffers from loss of oxygen, often resulting in heart failure. Proton radiation can be delivered to narrow channels of myocardium, about 2 mm in diameter. The radiation effects to the muscle itself can then be studied, separate from the anoxic effect of damaged endothelium. In addition, the radiation has been demonstrated to cause a neovascularization surrounding the irradiated channel. This myocardial revascularization may be beneficial for re-oxygenating anoxic myocardial tissue.
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Radiation Biology of Choroidal Neovascular Membrane
Because vascular endothelium is sensitive to radiation damage, it may be possible to affect the development of these membranes by the application of radiation. A neonatal mouse model has been developed to study the growth of retinal vasculature following irradiation. Fluorescent antibodies have been used to visualize the developing membranes. A series of experiments will be conducted to determine the most effective way to deliver radiation to damage the vascular development without damaging the healthy eye and optic nerve.
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Clinical Trial of Proton Therapy for AMD
The radiation biophysicists at IUCF collaborate with the clinicians at the Midwest Proton Radiotherapy Institute (MPRI) to develop clinical trials. In 1997, a clinical trial to investigate the efficacy of proton radiation for reversing or arresting the development of choroidal neovascular membrane associated with Age-Related Macular Degeneration. For this study, IUCF personnel designed and built the first proton therapy facility at IUCF.
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