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.
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- Creators: School of Life Sciences
Description
Students across the United States lack the necessary skills to be successful college students in Science, Technology and Math (STEM) majors and as a result post-secondary institutions are developing summer bridge programs to aid in their transition. As they develop these programs, effective theory and approach are critical to developing successful programs. Though there are a multitude of theories on successful student development, a focus on self-efficacy is critical. Summer Bridge programs across the country as well as the Bio Bridge summer program at Arizona State University were studied alone and through the lens of Cognitive Self-Efficacy Theory as mentioned in Albert Bandura's "Perceived Self-Efficacy in Cognitive Development and Functioning." Cognitive Self-Efficacy Theory provides a framework for self-efficacy development in academic settings. An analysis of fifteen bridge programs found that a large majority focused on developing academic capabilities and often overlooked development of community and social efficacy. An even larger number failed to focus on personal psychology in managing self-debilitating thought patterns based on published goals. Further, Arizona State University's Bio Bridge program could not be considered successful at developing cognitive self-efficacy or increasing retention as data was inconclusive. However, Bio Bridge was tremendously successful at developing social efficacy and community among participants and faculty. Further research and better evaluative techniques need to be developed to understand the program's effectiveness in cognitive self-efficacy development and retention.
ContributorsTummala, Sailesh Vardhan (Author) / Orchinik, Miles (Thesis director) / Brownell, Sara (Committee member) / Shortlidge, Erin (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Breast cancer affects hundreds of thousands of women a year in the United States, and kills tens of thousands. African-American women experience a lower incidence of breast cancer, yet they die at twice the rate of Caucasian women. This disparity demonstrates the ineffectiveness of mammography at decreasing mortality in women at higher risk of late stage diagnosis. In this paper I argue that the continued support of the predominating idea that the benefits of mammograms strictly outweigh their negative effects may be a factor in the continued racial disparity in breast cancer mortality between African-American and Caucasian women. In addition, I will argue that mammograms are less effective for African American women because they are predisposed to later stage diagnosis and the accompanying poorer mortality prognosis due to higher-risk environments caused by varied socio-political status. My claims are supported by studies of incidence rates, survivorship versus mortality rates, screening usage rates, late stage and early stage diagnosis rate, tumor type, and the effects of socioeconomic status on stage of diagnosis. In particular, mortality rates have not decreased parallel with increased mammogram usage, especially in African-American women. Although early stage diagnosis has drastically increased, late stage-diagnosis remains unchanged and higher in African-American women. Tumor types vary by race, and African American women tend to have tumors that are highly prolific and more likely to be metastatic. Socioeconomic factors are more of a marker for breast cancer disparities than race, however race and socio-political structures that embody racism are often intersected.
ContributorsHuper-Holmes, Chloe Lynn (Author) / Lynch, John (Thesis director) / Brian, Jennifer (Committee member) / Barrett, The Honors College (Contributor) / School of Human Evolution and Social Change (Contributor) / School of Life Sciences (Contributor)
Created2015-05
Description
Vaccine opposition is a growing problem in developed countries where dropping vaccination rates threaten general public health by laying the foundation for resurgence and reemergence of previously eradicated infectious diseases. This thesis argues that the current movement is only the most recent incarnation of opposition that has co-evolved with vaccine practices for the duration of their mutual histories. Part one provides a historical context for the current movement using the example of the development and deployment of the smallpox vaccine as a representative timeline of vaccine acceptance and opposition. Part two describes the current movement in the United States and the United Kingdom, interprets the reasons for the conclusions drawn by vaccine-concerned parents, and provides a framework for public health officials to approach the issues.
ContributorsKost, Stephanie Michelle (Author) / Lynch, John (Thesis director) / Hurlbut, Ben (Committee member) / Robert, Jason (Committee member) / Barrett, The Honors College (Contributor) / Department of Psychology (Contributor) / School of Life Sciences (Contributor)
Created2013-12
Description
The organic cation transporter 3 (OCT3) is a polyspecific monoamine transporter
found in the human and rat brain. In Rats, OCT3 is the only known monoamine transporter inhibited by physiological concentrations of corticosteroids. We hypothesized that CORT- mediated inhibition of OCT3 blocks the clearance of serotonin (5-HT) leading to an increase 5-HT receptor-mediated signaling. In experiment 1, due to conflicting reports on the location of OCT3 mRNA in the rat brain, in situ hybridization was performed on brain tissue sections. RNA was extracted from rat brain tissue, reverse transcribed into cDNA, and then polymerase chain reaction (PCR) was performed to generate riboprobe templates. The riboprobe templates were then used for in vitro transcription of digoxigenin (DIG)-labeled riboprobes complementary to OCT3. In experiment 2, 12 rats from an identical cohort were exposed to a chronic restraint stress paradigm (two hours/day for seven days, STRESS group), while the other 12 remained in their home cages (CTRL group). Twenty-four hours after the last stressor, all animals were euthanized and their brains immediately removed and frozen. Bilateral tissue punches were collected from 300μm coronal sections from the CA1 region of the dorsal hippocampus, basolateral amygdala (BLA), and dorsomedial hypothalamus (DMH). The relative OCT2, OCT3, and 5HT2a mRNA levels from each tissue punch were determined via quantitative real-time polymerase chain reaction (qPCR). The results of experiment 1 confirmed the presence of OCT3 mRNA in the CA1, amygdala, and the DMH. The results of experiment 2 show that chronic restraint stress did not alter gene expression for 5-HT2A, OCT2, and OCT3. These data may help reveal new information involving OCT3’s role in the hippocampus, amygdala and DMH in regards to localization and mRNA expression levels after exposure to a stressor.
found in the human and rat brain. In Rats, OCT3 is the only known monoamine transporter inhibited by physiological concentrations of corticosteroids. We hypothesized that CORT- mediated inhibition of OCT3 blocks the clearance of serotonin (5-HT) leading to an increase 5-HT receptor-mediated signaling. In experiment 1, due to conflicting reports on the location of OCT3 mRNA in the rat brain, in situ hybridization was performed on brain tissue sections. RNA was extracted from rat brain tissue, reverse transcribed into cDNA, and then polymerase chain reaction (PCR) was performed to generate riboprobe templates. The riboprobe templates were then used for in vitro transcription of digoxigenin (DIG)-labeled riboprobes complementary to OCT3. In experiment 2, 12 rats from an identical cohort were exposed to a chronic restraint stress paradigm (two hours/day for seven days, STRESS group), while the other 12 remained in their home cages (CTRL group). Twenty-four hours after the last stressor, all animals were euthanized and their brains immediately removed and frozen. Bilateral tissue punches were collected from 300μm coronal sections from the CA1 region of the dorsal hippocampus, basolateral amygdala (BLA), and dorsomedial hypothalamus (DMH). The relative OCT2, OCT3, and 5HT2a mRNA levels from each tissue punch were determined via quantitative real-time polymerase chain reaction (qPCR). The results of experiment 1 confirmed the presence of OCT3 mRNA in the CA1, amygdala, and the DMH. The results of experiment 2 show that chronic restraint stress did not alter gene expression for 5-HT2A, OCT2, and OCT3. These data may help reveal new information involving OCT3’s role in the hippocampus, amygdala and DMH in regards to localization and mRNA expression levels after exposure to a stressor.
ContributorsTompkins, Heather Camila (Author) / Orchinik, Miles (Thesis director) / Neisewander, Janet (Committee member) / Talboom, Joshua (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2013-05
Description
There is a higher incidence of asthma, worse outcomes, and a higher burden of disease in Black Americans compared to white Americans. This thesis aims to understand asthma disparities in the Black population by analyzing a variety of social determinants of health and genetic factors that may contribute to these racial health disparities. Based on the evidence collected, a variety of interventions are discussed that explore potential solutions to address the critical issue.
ContributorsHaldorsen, Kamilla (Author) / Lynch, John (Thesis director) / Hendrickson, Kirstin (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
Description
There are many parallels between human and equine sports medicine, including the roots of athletics, the development of specialized medicine, and injuries to the athletes. The most remarkable similarities are seen in tendinopathies. Because of the similarities between human and equine tendons, equine athletes serve as one of the best animal models to study tendon physiology and tendon injuries for application to human medicine. Because of this, many therapies have already successfully crossed from one realm of sports medicine to the other, the most notable of which are stem cell therapy, Interleukin-1 Receptor Antagonist (IRAP), and platelet rich plasma (PRP) therapies. There are also several therapies on the horizon that are very promising to potentially be successful in both human and equine athletes. However, some of these novel therapies are raising ethical questions. There are many regulations in place to protect against or address potential ethical conflicts in human medicine. The same trend is not seen in equine medicine. While there are rules enforced by many equestrian federations regarding ethical concerns and veterinary medicine, the information is not nearly as complete as it should be. Because they lack the autonomy that typical human patient possesses, equine athletes require significantly more advocacy from their veterinarians than human athletes do from their physicians. Additionally, there is a lack of large animal model studies secondary to cost and overall value of equine athletes to their owners, riders, and trainers. Ultimately it becomes an issue of veterinary ethics whether to pursue a novel or conventional treatment for an equine athlete. With biotechnology advancing as quickly as it is, new studies must be done and new regulations must be written in order to keep all fields of sports medicine operating safely and ethically for all athletes involved, regardless of species.
ContributorsWaslewski, Samantha Paige (Author) / Lynch, John (Thesis director) / Foley, James (Committee member) / School of Life Sciences (Contributor) / Dean, W.P. Carey School of Business (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
Description
The goal of my study is to test the overarching hypothesis that art therapy is effective because it targets emotional dysregulation that often accompanies significant health stressors. By reducing the salience of illness-related stressors, art therapy may improve overall mood and recovery, particularly in patients with cancer. After consulting the primary literature and review papers to develop psychological and neural mechanisms at work in art therapy, I created a hypothetical experimental procedure to test these hypotheses to explain why art therapy is helpful to patients with chronic illness. Studies found that art therapy stimulates activity of multiple brain regions involved in memory retrieval and the arousal of emotions. I hypothesize that patients with chronic illness have a reduced capacity for emotion regulation, or difficulty recognizing, expressing or altering illness-related emotions (Gross & Barrett, 2011). Further I hypothesize that art therapy improves mood and therapeutic outcomes by acting on the emotion-processing regions of the limbic system, and thereby facilitating the healthy expression of emotion, emotional processing, and reappraisal. More mechanistically, I propose art therapy reduces the perception or salience of stressors by reducing amygdala activity leading to decreased activation of the hypothalamic-pituitary-adrenal (HPA) axis. The art therapy literature and my hypothesis about its mechanisms of action became the basis of my proposed study. To assess the effectiveness of art therapy in alleviating symptoms of chronic disease, I am specifically targeting patients with cancer who exhibit a lack of emotional regulation. Saliva is collected 3 times a week on the day of intervention: morning after waking, afternoon, and evening. Stress levels are tested using one-hour art therapy sessions over the course of 3 months. The Perceived Stress Scale (PSS) assesses an individual's perceived stress and feelings in past and present situations, for the control and intervention group. To measure improvement in overall mood, 10 one-hour art sessions are performed on patients over 10 weeks. A one-hour discussion analyzing the participants' artwork follows each art session. The Spielberger State-Trait Anxiety Inventory (STAI) assesses overall mood for the intervention and control groups. I created rationale and predictions based on the intended results of each experiment.
ContributorsAluri, Bineetha C. (Author) / Orchinik, Miles (Thesis director) / Davis, Mary (Committee member) / Essary, Alison (Committee member) / School of Life Sciences (Contributor) / School for the Science of Health Care Delivery (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Schizophrenia is a debilitating psychiatric disorder with poorly understood genetic and environmental factors. An allelic variant of complement component 4 (C4), a protein first identified in innate immune response is strongly associated with schizophrenia. In the brain, activity of C4 leads to dendritic pruning, a process that may be causal in disease progression. Environmental factors, such as early life exposure to significant stressors also associate with increased risk of schizophrenia in later life. My hypothesis is that these factors do not act independently, but rather in tandem to influence disease etiology.
This hypothesis is supported by previous studies demonstrating that stress-induced elevation of glucocorticoids increases the transcription of C4. I propose that activated glucocorticoid receptors directly increase C4 protein expression as a transcription factor activator. Additionally, I propose that activated glucocorticoid receptors inhibit the expression of the transcription factor nuclear factor-light-chain-enhancer of activated B cells (NF-κB), thereby leading to decreased expression of the C4 inhibitor CUB and Sushi multiple domains 1 (CSMD1).
Glucocorticoid receptors and C4 are richly expressed in the hippocampus, a region critical in memory consolidation, spatial, and declarative memory. I propose that stress-induced upregulation of C4 activity in the hippocampus promotes excessive synaptic pruning, contributing to specific deficits and hippocampal shrinkage seen in schizophrenia. Stress exposure during fetal development and adolescence likely acts through the proposed mechanisms to increase hippocampal C4 activity and subsequent schizophrenia risk. These mechanisms may reveal novel interactions between environmental and genetic risk factors in the etiology of schizophrenia through complement activation.
This hypothesis is supported by previous studies demonstrating that stress-induced elevation of glucocorticoids increases the transcription of C4. I propose that activated glucocorticoid receptors directly increase C4 protein expression as a transcription factor activator. Additionally, I propose that activated glucocorticoid receptors inhibit the expression of the transcription factor nuclear factor-light-chain-enhancer of activated B cells (NF-κB), thereby leading to decreased expression of the C4 inhibitor CUB and Sushi multiple domains 1 (CSMD1).
Glucocorticoid receptors and C4 are richly expressed in the hippocampus, a region critical in memory consolidation, spatial, and declarative memory. I propose that stress-induced upregulation of C4 activity in the hippocampus promotes excessive synaptic pruning, contributing to specific deficits and hippocampal shrinkage seen in schizophrenia. Stress exposure during fetal development and adolescence likely acts through the proposed mechanisms to increase hippocampal C4 activity and subsequent schizophrenia risk. These mechanisms may reveal novel interactions between environmental and genetic risk factors in the etiology of schizophrenia through complement activation.
ContributorsHoegh, Emily Marie (Author) / Orchinik, Miles (Thesis director) / Newbern, Jason (Committee member) / Talboom, Joshua (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
Type-two diabetes represents a pathological state of insulin resistance due to systemic, complex interactions between numerous identified and linked metabolic genes. According to current medical literature, the genetic predisposition to type-two diabetes, coupled with environmental risk-factors, such as poverty and poor dietary habits, further exacerbate the risk of developing the disease. My research investigated the hypothesis that government poverty programs are associated with the surge in type-two diabetes among people of low socioeconomic status. My research suggests that government subsidies for the Commodity Supplemental Food Program, Women Infants and Children, Supplemental Nutrition Assistance Program, National School Lunch Program, and corn production influence individual dietary choices that lead to consumption of excessive amounts of refined sugars and fats and a surge in the prevalence of obesity, known risk-factors for developing type-two diabetes. These policies and programs may directly or indirectly promote and incentivize diets with excessive refined sugars and fats. As such, current programs paradoxically contradict current medical literature and direct individual choices that have increased the known risk-factors for developing type-two diabetes. Future efforts should reassess poverty and agricultural subsidy programs in relation to medical recommendations for diabetes prevention. The enormous societal and economic burden associated with type-two diabetes calls for further research to assess the efficacy of current public policy and the allocation of government funds.
ContributorsCarabajal, Christian James (Author) / Orchinik, Miles (Thesis director) / Maienschein, Jane (Committee member) / Opat, Melissa (Committee member) / College of Integrative Sciences and Arts (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
The stress response facilitates our ability to deal effectively with threatening situations, but exposure to severe or chronic stressors can lead to undesirable neural, physiological, and behavioral outcomes. Chronic stress is associated with structural changes in the rat hippocampus, with corresponding deficits in learning and memory. Recent studies have uncovered an inherent neuroplasticity that allows the hippocampus to recover from these stress-induced neural changes. Underlying mechanisms likely involve several different cellular and molecular pathways. In order to gain a more comprehensive understanding of these pathways, we investigated differences in protein expression throughout the timeline of chronic stress and recovery. Male Sprague-Dawley rats were randomly assigned to chronic restraint stress for 6hr/d/10d or 6hr/d/21d, stress for 6hr/d/21d followed by a recovery period of no stress for 10 or 21 days, or a control group. The proteome from the hippocampus of these rats was sequenced using liquid chromatography tandem mass spectrometry (LC-MS/MS) and analyzed. We hypothesized that chronic stress alters interneuronal signaling in the hippocampus by enhancing or attenuating the expression of proteins responsible for synaptic plasticity (functional) and neuronal structure (morphology). So far we have found that structural proteins, such as alpha-internexin, homer protein homolog 3, neurofilament light, and vimentin were significantly altered by chronic stress and recovery. In contrast, proteins necessary for or associated with myelination such as 2',3'-cyclic-nucleotide 3'-phosphodiesterase, myelin-associated glycoprotein, myelin basic protein S, and myelin proteolipid protein were significantly downregulated by chronic stress. Collectively, these results will provide a resource for further investigations into the mechanisms of the brain's recovery from chronic stress.
ContributorsKachemov, Marketta Marilyn (Author) / Orchinik, Miles (Thesis director) / Pirrotte, Patrick (Committee member) / Conrad, Cheryl (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05