ASU Electronic Theses and Dissertations
This collection includes most of the ASU Theses and Dissertations from 2011 to present. ASU Theses and Dissertations are available in downloadable PDF format; however, a small percentage of items are under embargo. Information about the dissertations/theses includes degree information, committee members, an abstract, supporting data or media.
In addition to the electronic theses found in the ASU Digital Repository, ASU Theses and Dissertations can be found in the ASU Library Catalog.
Dissertations and Theses granted by Arizona State University are archived and made available through a joint effort of the ASU Graduate College and the ASU Libraries. For more information or questions about this collection contact or visit the Digital Repository ETD Library Guide or contact the ASU Graduate College at gradformat@asu.edu.
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A mathematical model is developed for the spread of rabies in a spatially distributed fox population to model the spread of the rabies epizootic through middle Europe that occurred in the second half of the 20th century. The model considers both territorial and wandering rabid foxes and includes a latent period for the infection. Since the model assumes these two kinds of rabid foxes, it is a system of both partial differential and integral equations (with integration
over space and, occasionally, also over time). To study the spreading speeds of the rabies epidemic, the model is reduced to a scalar Volterra-Hammerstein integral equation, and space-time Laplace transform of the integral equation is used to derive implicit formulas for the spreading speed. The spreading speeds are discussed and implicit formulas are given for latent periods of fixed length, exponentially distributed length, Gamma distributed length, and log-normally distributed length. A number of analytic and numerical results are shown pertaining to the spreading speeds.
Further, a numerical algorithm is described for the simulation
of the spread of rabies in a spatially distributed fox population on a bounded domain with Dirichlet boundary conditions. I propose the following methods for the numerical approximation of solutions. The partial differential and integral equations are discretized in the space variable by central differences of second order and by
the composite trapezoidal rule. Next, the ordinary or delay differential equations that are obtained this way are discretized in time by explicit
continuous Runge-Kutta methods of fourth order for ordinary and delay differential systems. My particular interest
is in how the partition of rabid foxes into
territorial and diffusing rabid foxes influences
the spreading speed, a question that can be answered by purely analytic means only for small basic reproduction numbers. I will restrict the numerical analysis
to latent periods of fixed length and to exponentially
distributed latent periods.
The results of the numerical calculations
are compared for latent periods
of fixed and exponentially distributed length
and for various proportions of territorial
and wandering rabid foxes.
The speeds of spread observed in the
simulations are compared
to spreading speeds obtained by numerically solving the analytic formulas
and to observed speeds of epizootic frontlines
in the European rabies outbreak 1940 to 1980.
prostate cancer is most commonly treated with hormonal therapy. The idea behind
hormonal therapy is to reduce androgen production, which prostate cancer cells
require for growth. Recently, the exploration of the synergistic effects of the drugs
used in hormonal therapy has begun. The aim was to build off of these recent
advancements and further refine the synergistic drug model. The advancements I
implement come by addressing biological shortcomings and improving the model’s
internal mechanistic structure. The drug families being modeled, anti-androgens,
and gonadotropin-releasing hormone analogs, interact with androgen production in a
way that is not completely understood in the scientific community. Thus the models
representing the drugs show progress through their ability to capture their effect
on serum androgen. Prostate-specific antigen is the primary biomarker for prostate
cancer and is generally how population models on the subject are validated. Fitting
the model to clinical data and comparing it to other clinical models through the
ability to fit and forecast prostate-specific antigen and serum androgen is how this
improved model achieves validation. The improved model results further suggest that
the drugs’ dynamics should be considered in adaptive therapy for prostate cancer.
changes in the diffusion, growth, and death parameters was performed, in order to find a set of parameter values that accurately model observed tumor growth for a given patient. Additional changes were made to the diffusion parameters to account for the arrangement of nerve tracts in the brain, resulting in varying rates of diffusion. In general, small changes in the growth rates had a large impact on the outcome of the simulations, and for each patient there exists a set of parameters that allow the model to simulate a tumor that matches observed tumor growth in the patient over a period of two or three months. Furthermore, these results are more accurate with anisotropic diffusion, rather than isotropic diffusion. However, these parameters lead to inaccurate results for patients with tumors that undergo no observable growth over the given time interval. While it is possible to simulate long-term tumor growth, the simulation requires multiple comparisons to available MRI scans in order to find a set of parameters that provide an accurate prognosis.