Difference between revisions of "Team:WashU StLouis/Model"
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<p style = "font-size:1vw">Because lesion formation is linearly related to UV intensity when there is no lesion repair, the number of lesions could be treated as a measure of UV intensity and the lowered rate of lesion formation could instead be considered as lowering UV intensity over time. | <p style = "font-size:1vw">Because lesion formation is linearly related to UV intensity when there is no lesion repair, the number of lesions could be treated as a measure of UV intensity and the lowered rate of lesion formation could instead be considered as lowering UV intensity over time. | ||
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| + | <p style = "font-size:1vw"> Using a differential equation model for UV bactericide, we predicted the survival of cells under a given level of UV given their DNA lesion repair rate. </p> | ||
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Revision as of 22:20, 1 November 2017
Modeling
Modeling Overview
The goal of our project is to explore radiation resistance genes to find ways to increase UV tolerance. With a changing climate, organisms grow under increasing stress of DNA damage. The overall goal of our model is to evaluate the resistance of organisms to UV and compare the growth of resistant and non-resistant cells under different levels of UV. This modeling aims to assess the commercial advantage of resistant cells compared to normal cells by predicting their growth under UV radiation. To obtain useful parameters, our models use the well-described growth and radiation death of E. coli.
Modeling Cell Death under UV
To model cell death caused by UV radiation, we made the simplifying assumption that cell death from radiation was entirely due to DNA damage. Using differential equation models for bacterial death (Kowalski et al. 2002) and DNA lesion formation and repair (Krishna et al. 2007) we could make a connection from lesion formation to cell death. The importance of this was that reducing the number of lesions by DNA repair could be linked directly to increased cell survival.
Because lesion formation is linearly related to UV intensity when there is no lesion repair, the number of lesions could be treated as a measure of UV intensity and the lowered rate of lesion formation could instead be considered as lowering UV intensity over time.
Using a differential equation model for UV bactericide, we predicted the survival of cells under a given level of UV given their DNA lesion repair rate.
