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.
Displaying 1 - 8 of 8
Filtering by
- Creators: School of Life Sciences
Description
Monoamine neurotransmitters (e.g., serotonin, norepinephrine, and dopamine) are powerful modulators of mood and cognitive function in health and disease. We have been investigating the modulation of monoamine clearance in select brain regions via organic cation transporters (OCTs), a family of nonselective monoamine transporters. OCTs are thought to complement the actions of selective monoamine transporters in the brain by helping to clear monoamines from the extracellular space; thus, assisting to terminate the monoamine signal. Of particular interest, stress hormones (corticosterone; CORT) inhibit OCT3-mediated transport of monoamine, to putatively lead to prolonged monoamine signaling. It has been demonstrated that stress levels of CORT block OCT3 transport in the rat hypothalamus, an effect that likely underlies the rapid, stress-induced increase in local monoamines. We examined the effect of chronic variable stress (CVS) on the development of mood disorders and OCT3 expression in limbic and hypothalamic regions of the rat brain. Animals subjected to CVS (14-days with random stressor exposure two times/day) showed reduced body weight gain, indicating that CVS was perceived as stressful. However, behavioral tests of anxiety and depressive-like behaviors in rats showed no group differences. Although there were no behavioral effects of stress, molecular analysis revealed that there were stress-related changes in OCT3 protein expression. In situ hybridization data confirmed that OCT3 mRNA is expressed in the hippocampus, amygdala, and hypothalamus. Analysis of Western blot data by two-way ANOVA revealed a significant treatment effect on OCT3 protein levels, with a significant decrease in OCT3 protein in the amygdala and hippocampus in CVS rats, compared to controls. These data suggest an important role for CORT sensitive OCT3 in the reduction of monoamine clearance during stress.
ContributorsBoyll, Piper Savannah (Author) / Orchinik, Miles (Thesis director) / Conrad, Cheryl (Committee member) / Talboom, Joshua (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
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
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
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
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
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
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
Arizona State University and Banner Thunderbird Hospital have partnered to provide pre-med students with an internship at a local emergency department. Students entering into this program will have access to each patient's vital signs, medical imaging, lab tests, and medications. This access presents students with an opportunity to learn about a variety of tools used in the assessment and treatment of emergency room patients. In order to enhance the amount of knowledge students take away from the program, I created a handbook summarizing a variety of diagnostic tests and medications. The first section of the handbook (assessment) is spilt up into the three following categories: vital signs, medical imaging, and lab tests. The second section (treatment) consists of one category, medications. Each section was written with emphasis on basic physiology, and is intended to provide pre-med students with a foundation for building further medical knowledge. Although this handbook was tailored to the information students are most likely to encounter working in Banner Thunderbird Hospital's emergency department, it is still appropriate for any student interested in learning about emergency medicine.
ContributorsBecker, Bryson (Author) / Orchinik, Miles (Thesis director) / Washo-Krupps, Delon (Committee member) / School of Life Sciences (Contributor) / W.P. Carey School of Business (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05