Barrett, The Honors College Thesis/Creative Project Collection
Barrett, The Honors College at Arizona State University proudly showcases the work of undergraduate honors students by sharing this collection exclusively with the ASU community.
Barrett accepts high performing, academically engaged undergraduate students and works with them in collaboration with all of the other academic units at Arizona State University. All Barrett students complete a thesis or creative project which is an opportunity to explore an intellectual interest and produce an original piece of scholarly research. The thesis or creative project is supervised and defended in front of a faculty committee. Students are able to engage with professors who are nationally recognized in their fields and committed to working with honors students. Completing a Barrett thesis or creative project is an opportunity for undergraduate honors students to contribute to the ASU academic community in a meaningful way.
This paper will serve as a review of relevant scleractinian coral biology and genetics, discuss the ecological and biological impacts of growth anomalies in scleractinians, discuss the importance of studying this phenomena in terms of conservation, outline and discuss the processes undertaken to elucidate possible genetic markers of the growth anomalies, as well as discuss growth anomalies within the context of other coral disease and the anthropocene to add clarity no the subject to the oncological discussion taking place around such anomalies.
Cooperative cellular phenotypes are universal across multicellular life. Division of labor, regulated proliferation, and controlled cell death are essential in the maintenance of a multicellular body. Breakdowns in these cooperative phenotypes are foundational in understanding the initiation and progression of neoplastic diseases, such as cancer. Cooperative cellular phenotypes are straightforward to characterize in extant species but the selective pressures that drove their emergence at the transition(s) to multicellularity have yet to be fully characterized. Here we seek to understand how a dynamic environment shaped the emergence of two mechanisms of regulated cell survival: apoptosis and senescence. We developed an agent-based model to test the time to extinction or stability in each of these phenotypes across three levels of stochastic environments.
Public education and involvement with evolutionary theory has long been limited by both the complexity of the subject and societal pushback. Furthermore, effective and engaging evolution education has become an elusive feat that often fails to reflect the types of questions that evolution research attempts to address. Here, we explore the best methods to present scientific research using interactive educational models to facilitate the learning experience of the audience most effectively. By creating artistic and game-play oriented models, it becomes possible to simplify the multifaceted aspects of evolution research such that it enables a larger, more inclusive, audience to better comprehend these complexities. In allowing the public to engage with highly interactive education materials, the full spectrum of the scientific process, from hypothesis construction to experimental testing, can be experienced and understood. Providing information about current cancer evolution research in a way that is easy to access and understand and accompanying it with an interactive model that reflects this information and reinforces learning shows that research platforms can be translated into interactive teaching tools that make understanding evolutionary theory more accessible.
Age is the most significant risk factor for cancer development in humans. The somatic mutation theory postulates that the accumulation of genomic mutations over time results in cellular function degradation which plays an important role in understanding aging and cancer development. Specifically, degradation of the mechanisms that underlie somatic maintenance can occur due to decreased immune cell function and genomic responses to DNA damage. Research has shown that this degradation can lead to the accumulation of mutations that can cause cancer in humans. Despite recent advances in our understanding of cancer in non-human species, how this risk factor translates across species is poorly characterized. Here, we analyze a veterinarian cancer dataset of 4,178 animals to investigate if age related cancer prevalence is similar in non-human animals. We intend for this work to be used as a primary step towards understanding the potential overlap and/or uniqueness between human and non-human cancer risk factors. This study can be used to better understand cancer development and how evolutionary processes have shaped somatic maintenance across species.
Cancers of the reproductive tissues make up a significant portion of the cancer burden and mortality experienced by humans. Humans experience several proximal causative carcinogens that explain a portion of cancer risk, but an evolutionary viewpoint can provide a unique lens into the ultimate causes of reproductive cancer vulnerabilities. A life history framework allows us to make predictions on cancer prevalence based on a species’ tempo of reproduction. Moreover, certain variations in the susceptibility and prevalence of cancer may emerge due to evolutionary trade-offs between reproduction and somatic maintenance. For example, such trade-offs could involve the demand for rapid proliferation of cells in reproductive tissues that arises with reproductive events. In this study, I compiled reproductive cancer prevalence for 158 mammalian species and modeled the predictive power of 13 life history traits on the patterns of cancer prevalence we observed, such as Peto’s Paradox or slow-fast life history strategies. We predicted that fast-life history strategists will exhibit higher neoplasia prevalence risk due to reproductive trade-offs. Furthering this analytical framework can aid in predicting cancer rates and stratifying cancer risk across the tree of life.
