Matching Items (18)
Filtering by
- All Subjects: Mathematical Modeling
- Creators: School of Mathematical and Statistical Sciences
- Creators: Kostelich, Eric
- Creators: Kang, Yun
- Member of: Theses and Dissertations
- Status: Published
Description
A functioning food web is the basis of a functioning community and ecosystem. Thus, it is important to understand the dynamics that control species behaviors and interactions. Alterations to the fundamental dynamics can prove detrimental to the future success of our environment. Research and analysis focus on the global dynamics involved in intraguild predation (IGP), a three species subsystem involving both competition and predation. A mathematical model is derived using differential equations based on pre-existing models to accurately predict species behavior. Analyses provide sufficient conditions for species persistence and extinction that can be used to explain global dynamics. Dynamics are compared for two separate models, one involving a specialist predator and the second involving a generalist predator, where systems involving a specialist predator are prone to unstable dynamics. Analyses have implications in biological conservation tactics including various methods of prevention and preservation. Simulations are used to compare dynamics between models involving continuous time and those involving discrete time. Furthermore, we derive a semi-discrete model that utilizes both continuous and discrete time series dynamics. Simulations imply that Holling's Type III functional response controls the potential for three species persistence. Complicated dynamics govern the IGP subsystem involving the white-footed mouse, gypsy moth, and oak, and they ultimately cause the synchronized defoliation of forests across the Northeastern United States. Acorn mast seasons occur every 4-5 years, and they occur simultaneously across a vast geographic region due to universal cues. Research confirms that synchronization can be transferred across trophic levels to explain how this IGP system ultimately leads to gypsy moth outbreaks. Geographically referenced data is used to track and slow the spread of gypsy moths further into the United States. Geographic Information Systems (GIS) are used to create visual, readily accessible, displays of trap records, defoliation frequency, and susceptible forest stands. Mathematical models can be used to explain both changes in population densities and geographic movement. Analyses utilizing GIS softwares offer a different, but promising, way of approaching the vast topic of conservation biology. Simulations and maps are produced that can predict the effects of conservation efforts.
ContributorsWedekin, Lauren (Author) / Kang, Yun (Thesis advisor) / Green, Douglas (Committee member) / Miller, William (Committee member) / Arizona State University (Publisher)
Created2012
Description
Predicting resistant prostate cancer is critical for lowering medical costs and improving the quality of life of advanced prostate cancer patients. I formulate, compare, and analyze two mathematical models that aim to forecast future levels of prostate-specific antigen (PSA). I accomplish these tasks by employing clinical data of locally advanced prostate cancer patients undergoing androgen deprivation therapy (ADT). I demonstrate that the inverse problem of parameter estimation might be too complicated and simply relying on data fitting can give incorrect conclusions, since there is a large error in parameter values estimated and parameters might be unidentifiable. I provide confidence intervals to give estimate forecasts using data assimilation via an ensemble Kalman Filter. Using the ensemble Kalman Filter, I perform dual estimation of parameters and state variables to test the prediction accuracy of the models. Finally, I present a novel model with time delay and a delay-dependent parameter. I provide a geometric stability result to study the behavior of this model and show that the inclusion of time delay may improve the accuracy of predictions. Also, I demonstrate with clinical data that the inclusion of the delay-dependent parameter facilitates the identification and estimation of parameters.
ContributorsBaez, Javier (Author) / Kuang, Yang (Thesis advisor) / Kostelich, Eric (Committee member) / Crook, Sharon (Committee member) / Gardner, Carl (Committee member) / Nagy, John (Committee member) / Arizona State University (Publisher)
Created2017
Description
Glioblastoma multiforme (GBM) is a malignant, aggressive and infiltrative cancer of the central nervous system with a median survival of 14.6 months with standard care. Diagnosis of GBM is made using medical imaging such as magnetic resonance imaging (MRI) or computed tomography (CT). Treatment is informed by medical images and includes chemotherapy, radiation therapy, and surgical removal if the tumor is surgically accessible. Treatment seldom results in a significant increase in longevity, partly due to the lack of precise information regarding tumor size and location. This lack of information arises from the physical limitations of MR and CT imaging coupled with the diffusive nature of glioblastoma tumors. GBM tumor cells can migrate far beyond the visible boundaries of the tumor and will result in a recurring tumor if not killed or removed. Since medical images are the only readily available information about the tumor, we aim to improve mathematical models of tumor growth to better estimate the missing information. Particularly, we investigate the effect of random variation in tumor cell behavior (anisotropy) using stochastic parameterizations of an established proliferation-diffusion model of tumor growth. To evaluate the performance of our mathematical model, we use MR images from an animal model consisting of Murine GL261 tumors implanted in immunocompetent mice, which provides consistency in tumor initiation and location, immune response, genetic variation, and treatment. Compared to non-stochastic simulations, stochastic simulations showed improved volume accuracy when proliferation variability was high, but diffusion variability was found to only marginally affect tumor volume estimates. Neither proliferation nor diffusion variability significantly affected the spatial distribution accuracy of the simulations. While certain cases of stochastic parameterizations improved volume accuracy, they failed to significantly improve simulation accuracy overall. Both the non-stochastic and stochastic simulations failed to achieve over 75% spatial distribution accuracy, suggesting that the underlying structure of the model fails to capture one or more biological processes that affect tumor growth. Two biological features that are candidates for further investigation are angiogenesis and anisotropy resulting from differences between white and gray matter. Time-dependent proliferation and diffusion terms could be introduced to model angiogenesis, and diffusion weighed imaging (DTI) could be used to differentiate between white and gray matter, which might allow for improved estimates brain anisotropy.
ContributorsAnderies, Barrett James (Author) / Kostelich, Eric (Thesis director) / Kuang, Yang (Committee member) / Stepien, Tracy (Committee member) / Harrington Bioengineering Program (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
Description
Currently in synthetic biology only the Las, Lux, and Rhl quorum sensing pathways have been adapted for broad engineering use. Quorum sensing allows a means of cell to cell communication in which a designated sender cell produces quorum sensing molecules that modify gene expression of a designated receiver cell. While useful, these three quorum sensing pathways exhibit a nontrivial level of crosstalk, hindering robust engineering and leading to unexpected effects in a given design. To address the lack of orthogonality among these three quorum sensing pathways, previous scientists have attempted to perform directed evolution on components of the quorum sensing pathway. While a powerful tool, directed evolution is limited by the subspace that is defined by the protein. For this reason, we take an evolutionary biology approach to identify new orthogonal quorum sensing networks and test these networks for cross-talk with currently-used networks. By charting characteristics of acyl homoserine lactone (AHL) molecules used across quorum sensing pathways in nature, we have identified favorable candidate pathways likely to display orthogonality. These include Aub, Bja, Bra, Cer, Esa, Las, Lux, Rhl, Rpa, and Sin, which we have begun constructing and testing. Our synthetic circuits express GFP in response to a quorum sensing molecule, allowing quantitative measurement of orthogonality between pairs. By determining orthogonal quorum sensing pairs, we hope to identify and adapt novel quorum sensing pathways for robust use in higher-order genetic circuits.
ContributorsMuller, Ryan (Author) / Haynes, Karmella (Thesis director) / Wang, Xiao (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Department of Chemistry and Biochemistry (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Glioblastoma Multiforme (GBM) is an aggressive and deadly form of brain cancer with a median survival time of about a year with treatment. Due to the aggressive nature of these tumors and the tendency of gliomas to follow white matter tracks in the brain, each tumor mass has a unique growth pattern. Consequently it is difficult for neurosurgeons to anticipate where the tumor will spread in the brain, making treatment planning difficult. Archival patient data including MRI scans depicting the progress of tumors have been helpful in developing a model to predict Glioblastoma proliferation, but limited scans per patient make the tumor growth rate difficult to determine. Furthermore, patient treatment between scan points can significantly compound the challenge of accurately predicting the tumor growth. A partnership with Barrow Neurological Institute has allowed murine studies to be conducted in order to closely observe tumor growth and potentially improve the current model to more closely resemble intermittent stages of GBM growth without treatment effects.
ContributorsSnyder, Lena Haley (Author) / Kostelich, Eric (Thesis director) / Frakes, David (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Harrington Bioengineering Program (Contributor)
Created2014-05
Description
Mortality of 1918 influenza virus was high, partly due to bacteria coinfections. We characterize pandemic mortality in Arizona, which had high prevalence of tuberculosis. We applied regressions to over 35,000 data points to estimate the basic reproduction number and excess mortality. Age-specific mortality curves show elevated mortality for all age groups, especially the young, and senior sparing effects. The low value for reproduction number indicates that transmissibility was moderately low.
ContributorsJenner, Melinda Eva (Author) / Chowell-Puente, Gerardo (Thesis director) / Kostelich, Eric (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Pogonomyrmex californicus (a species of harvester ant) colonies typically have anywhere from one to five queens. A queen can control the ratio of female to male offspring she produces, field research indicating that this ratio is genetically hardwired and does not change over time relative to other queens. Further, a queen has an individual reproductive advantage if she has a small reproductive ratio. A colony, however, has a reproductive advantage if it has queens with large ratios, as these queens produce many female workers to further colony success. We have developed an agent-based model to analyze the "cheating" phenotype observed in field research, in which queens extend their lifespans by producing disproportionately many male offspring. The model generates phenotypes and simulates years of reproductive cycles. The results allow us to examine the surviving phenotypes and determine conditions under which a cheating phenotype has an evolutionary advantage. Conditions generating a bimodal steady state solution would indicate a cheating phenotype's ability to invade a cooperative population.
ContributorsEngel, Lauren Marie Agnes (Author) / Armbruster, Dieter (Thesis director) / Fewell, Jennifer (Committee member) / School of Mathematical and Statistical Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
The increased number of novel pathogens that potentially threaten the human population has motivated the development of mathematical and computational modeling approaches for forecasting epidemic impact and understanding key environmental characteristics that influence the spread of diseases. Yet, in the case that substantial uncertainty surrounds the transmission process during a rapidly developing infectious disease outbreak, complex mechanistic models may be too difficult to be calibrated quick enough for policy makers to make informed decisions. Simple phenomenological models that rely on a small number of parameters can provide an initial platform for assessing the epidemic trajectory, estimating the reproduction number and quantifying the disease burden from the early epidemic phase.
Chapter 1 provides background information and motivation for infectious disease forecasting and outlines the rest of the thesis.
In chapter 2, logistic patch models are used to assess and forecast the 2013-2015 West Africa Zaire ebolavirus epidemic. In particular, this chapter is concerned with comparing and contrasting the effects that spatial heterogeneity has on the forecasting performance of the cumulative infected case counts reported during the epidemic.
In chapter 3, two simple phenomenological models inspired from population biology are used to assess the Research and Policy for Infectious Disease Dynamics (RAPIDD) Ebola Challenge; a simulated epidemic that generated 4 infectious disease scenarios. Because of the nature of the synthetically generated data, model predictions are compared to exact epidemiological quantities used in the simulation.
In chapter 4, these models are applied to the 1904 Plague epidemic that occurred in Bombay. This chapter provides evidence that these simple models may be applicable to infectious diseases no matter the disease transmission mechanism.
Chapter 5, uses the patch models from chapter 2 to explore how migration in the 1904 Plague epidemic changes the final epidemic size.
The final chapter is an interdisciplinary project concerning within-host dynamics of cereal yellow dwarf virus-RPV, a plant pathogen from a virus group that infects over 150 grass species. Motivated by environmental nutrient enrichment due to anthropological activities, mathematical models are employed to investigate the relevance of resource competition to pathogen and host dynamics.
Chapter 1 provides background information and motivation for infectious disease forecasting and outlines the rest of the thesis.
In chapter 2, logistic patch models are used to assess and forecast the 2013-2015 West Africa Zaire ebolavirus epidemic. In particular, this chapter is concerned with comparing and contrasting the effects that spatial heterogeneity has on the forecasting performance of the cumulative infected case counts reported during the epidemic.
In chapter 3, two simple phenomenological models inspired from population biology are used to assess the Research and Policy for Infectious Disease Dynamics (RAPIDD) Ebola Challenge; a simulated epidemic that generated 4 infectious disease scenarios. Because of the nature of the synthetically generated data, model predictions are compared to exact epidemiological quantities used in the simulation.
In chapter 4, these models are applied to the 1904 Plague epidemic that occurred in Bombay. This chapter provides evidence that these simple models may be applicable to infectious diseases no matter the disease transmission mechanism.
Chapter 5, uses the patch models from chapter 2 to explore how migration in the 1904 Plague epidemic changes the final epidemic size.
The final chapter is an interdisciplinary project concerning within-host dynamics of cereal yellow dwarf virus-RPV, a plant pathogen from a virus group that infects over 150 grass species. Motivated by environmental nutrient enrichment due to anthropological activities, mathematical models are employed to investigate the relevance of resource competition to pathogen and host dynamics.
ContributorsPell, Bruce (Author) / Kuang, Yang (Thesis advisor) / Chowell-Puente, Gerardo (Committee member) / Nagy, John (Committee member) / Kostelich, Eric (Committee member) / Gardner, Carl (Committee member) / Arizona State University (Publisher)
Created2016
Description
Studying the effects of viruses and toxins on honey bees is important in order to understand the danger these important pollinators are exposed to. Hives exist in various environments, and different colonies are exposed to varying environmental conditions and dangers. To properly study the changes and effects of seasonality and pesticides on the population dynamics of honey bees, the presence of each of these threats must be considered. This study aims to analyze how infected colonies grapple more deeply with changing, seasonal environments, and how toxins in pesticides affect population dynamics. Thus, it addresses the following questions: How do viruses within a colony affect honey bee population dynamics when the environment is seasonal? How can the effects of pesticides be modeled to better understand the spread of toxins? This project is a continuation of my own undergraduate work in a previous class, MAT 350: Techniques and Applications of Applied Mathematics, with Dr. Yun Kang, and also utilizes previous research conducted by graduate students. Original research focused on the population dynamics of honey bee disease interactions (without considering seasonality), and a mathematical modeling approach to analyze the effects of pesticides on honey bees. In order to pursue answers to the main research questions, the model for honey bee virus interaction was adapted to account for seasonality. The adaptation of this model allowed the new model to account for the effects of seasonality on infected colony population dynamics. After adapting the model, simulations with arbitrary data were run using RStudio in order to gain insight into the specific ways in which seasonality affected the interaction between a honey bee colony and viruses. The second portion of this project examines a system of ordinary differential equations that represent the effect of pesticides on honey bee population dynamics, and explores the process of this model’s formulation. Both systems of equations used as the basis for each model’s research question are from previous research reports. This project aims to further that research, and explore the applications of applied mathematics to biological issues.
ContributorsReveles, Anika (Author) / Kang, Yun (Thesis director) / Nishimura, Joel (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Natural Sciences (Contributor) / School of Earth and Space Exploration (Contributor)
Created2023-05
Description
In this project we focus on COVID-19 in a university setting. Arizona State University has a very large population on the Tempe Campus. With the emergence of diseases such as COVID-19, it is very important to track how such a disease spreads within that type of community. This is vital for containment measures and the safety of everyone involved. We found in the literature several epidemiology models that utilize differential equations for tracking a spread of a disease. However, our goal is to provide a granular look at how disease may spread through contact in a classroom. This thesis models a single ASU classroom and tracks the spread of a disease. It is important to note that our variables and declarations are not aligned with COVID-19 or any other specific disease but are chosen to exemplify the impact of some key parameters on the epidemic size. We found that a smaller transmissibility alongside a more spread-out classroom of agents resulted in fewer infections overall. There are many extensions to this model that are needed in order to take what we have demonstrated and align those ideas with COVID-19 and it’s spread at ASU. However, this model successfully demonstrates a spread of disease through single-classroom interaction, which is the key component for any university campus disease transmission model.
ContributorsJoseph, Mariam (Author) / Bartko, Ezri (Co-author) / Sabuwala, Sana (Co-author) / Milner, Fabio (Thesis director) / O'Keefe, Kelly (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Division of Teacher Preparation (Contributor)
Created2022-12