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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Description
Stroke is a devastating disease that affects thousands of individuals each year. Stroke, specifically cerebral ischemia, and immune responses are important areas of study and focus. Previous studies on stroke in mouse models had shown the upregulation of a specific micro-RNA: miR-1224. We hypothesized that miR-1224 was responsible for the

Stroke is a devastating disease that affects thousands of individuals each year. Stroke, specifically cerebral ischemia, and immune responses are important areas of study and focus. Previous studies on stroke in mouse models had shown the upregulation of a specific micro-RNA: miR-1224. We hypothesized that miR-1224 was responsible for the regulation of the ST2 receptor protein’s expression. We performed cellular transfection on murine splenocytes with four different miRNAs—miR-1224-mimic, miR-1224-inhibitor, miR-451-mimic, and a control. We predicted that transfection with 1224m would decrease ST2 expression, while transfection with 1224i would increase ST2 expression. Two complete trials were run, and analysis of the results included RT-PCR of both miRNA samples and mRNA samples to confirm transfection and controlled transcription. Reverse transcription and qPCR of miRNA was done in order to confirm that transfection was in fact successful. Reverse transcription and qPCR of the mRNA was done in order to confirm that ST2 mRNA was not altered; this allowed us to attribute any changes in ST2 protein levels to miRNA interactions, as the mRNA levels were consistent. Western blotting was done in order to assess relative protein content. We found that transfection with 1224m slightly decreased ST2 expression and transfection with 1224i slightly increased ST2 expression, however, after assessing the p-values through statistical analyses, neither difference was significant. As such, our hypothesis was rejected as it is not evident that miR-1224 plays a significant role on ST2 gene expression. Future studies are needed in order to analyze alternate protein targets to fully assess the role of miR-1224.
ContributorsReddy, Nihaal (Author) / Holechek, Susan (Thesis director) / Ahmad, Saif (Committee member) / Wood, Kristofer (Committee member) / School of Human Evolution and Social Change (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
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Description
Approximately 248 million people in the world are currently living with chronic Hepatitis B virus (HBV) infection. HBV and HCV infections are the primary cause of liver diseases such as cirrhosis and hepatocellular carcinomas in the world with an estimated 1.4 million deaths annually. HBV in the Republic of Peru

Approximately 248 million people in the world are currently living with chronic Hepatitis B virus (HBV) infection. HBV and HCV infections are the primary cause of liver diseases such as cirrhosis and hepatocellular carcinomas in the world with an estimated 1.4 million deaths annually. HBV in the Republic of Peru was used as a case study of an emerging and rapidly spreading disease in a developing nation. Wherein, clinical diagnosis of HBV infections in at-risk communities such the Amazon Region and the Andes Mountains are challenging due to a myriad of reasons. High prices of clinical diagnosis and limited access to treatment are alone the most significant deterrent for individuals living in at-risk communities to get the much need help. Additionally, limited testing facilities, lack of adequate testing policies or national guidelines, poor laboratory capacity, resource-limited settings, geographical isolation, and public mistrust are among the chief reasons for low HBV testing. Although, preventative vaccination programs deployed by the Peruvian health officials have reduced the number of infected individuals by year and region. To significantly reduce or eradicate HBV in hyperendemic areas and countries such as Peru, preventative clinical diagnosis and vaccination programs are an absolute necessity. Consequently, the need for a portable low-priced diagnostic platform for the detection of HBV and other diseases is substantial and urgent not only in Peru but worldwide. Some of these concerns were addressed by designing a low-cost, rapid detection platform. In that, an immunosignature technology (IMST) slide used to test for reactivity against the presence of antibodies in the serum-sample was used to test for picture resolution and clarity. IMST slides were scanned using a smartphone camera placed on top of the designed device housing a circuit of 32 LED lights at 647 nm, an optical magnifier at 15X, and a linear polarizing film sheet. Tow 9V batteries powered the scanning device LED circuit ensuring enough lighting. The resulting pictures from the first prototype showed that by lighting the device at 647 nm and using a smartphone camera, the camera could capture high-resolution images. These results conclusively indicate that with any modern smartphone camera, a small box lighted to 647 nm, and optical magnifier; a powerful and expensive laboratory scanning machine can be replaced by another that is inexpensive, portable and ready to use anywhere.
ContributorsMakimaa, Heyde (Author) / Holechek, Susan (Thesis director) / Stafford, Phillip (Committee member) / Jayasuriya, Suren (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description

A significant amount of prior research has been conducted to investigate type 2 diabetes, the most prevalent form afflicting over 90% of diabetic individuals [6]. Yet, gestational diabetes is an understudied form of diabetes that is thought to share various attributes with type 2 diabetes. It was the aim of

A significant amount of prior research has been conducted to investigate type 2 diabetes, the most prevalent form afflicting over 90% of diabetic individuals [6]. Yet, gestational diabetes is an understudied form of diabetes that is thought to share various attributes with type 2 diabetes. It was the aim of this project to investigate a proposed mechanism of the disease, the contra-insulin effect, through a cell-culture experiment. To address the question of whether glycemic and hormonal conditions of cell-culture media affect Hs 795.Pl morphology, cellular growth, and glucose uptake, immunocytochemistry (ICC) and a glucose uptake assay was performed. It was hypothesized that higher the presence of hormones, specifically lactogen, in cell culture media will exacerbate the contra-insulin effect, decreasing the glucose uptake of the Hs 795.Pl cells and inducing abhorrent cell morphology. Qualitatively, estradiol and cortisol had a severe impact on cellular morphology indicative of stress and death. As for glucose uptake, it was decreased when the hormones were isolated compared to all together with estradiol thought to be majorly inhibitory to insulin’s proper functioning. It was concluded that cell morphology, growth, and glucose uptake were detrimentally impacted by the gestational hormones, especially those of cortisol and estrogen.

ContributorsPickett, Sydney (Author) / Gilchrist, Alex (Co-author) / Holechek, Susan (Thesis director) / Clarke, Richard (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2023-05
Description

A significant amount of prior research has been conducted to investigate type 2 diabetes, the most prevalent form afflicting over 90% of diabetic individuals [6]. Yet, gestational diabetes is an understudied form of diabetes that is thought to share various attributes with type 2 diabetes. It was the aim of

A significant amount of prior research has been conducted to investigate type 2 diabetes, the most prevalent form afflicting over 90% of diabetic individuals [6]. Yet, gestational diabetes is an understudied form of diabetes that is thought to share various attributes with type 2 diabetes. It was the aim of this project to investigate a proposed mechanism of the disease, the contra-insulin effect, through a cell-culture experiment. To address the question of whether glycemic and hormonal conditions of cell-culture media affect Hs 795.Pl morphology, cellular growth, and glucose uptake, immunocytochemistry (ICC) and a glucose uptake assay was performed. It was hypothesized that higher the presence of hormones, specifically lactogen, in cell culture media will exacerbate the contra-insulin effect, decreasing the glucose uptake of the Hs 795.Pl cells and inducing abhorrent cell morphology. Qualitatively, estradiol and cortisol had a severe impact on cellular morphology indicative of stress and death. As for glucose uptake, it was decreased when the hormones were isolated compared to all together with estradiol thought to be majorly inhibitory to insulin’s proper functioning. It was concluded that cell morphology, growth, and glucose uptake were detrimentally impacted by the gestational hormones, especially those of cortisol and estrogen.

ContributorsGilchrist, Alex (Author) / Pickett, Sydney (Co-author) / Holechek, Susan (Thesis director) / Clarke, Richard (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / Historical, Philosophical & Religious Studies, Sch (Contributor)
Created2023-05
Description

The burden of dementia and its primary cause, Alzheimer’s disease, continue to devastate many with no available cure although present research has delivered methods for risk calculation and models of disease development that promote preventative strategies. Presently Alzheimer’s disease affects 1 in 9 people aged 65 and older amounting to

The burden of dementia and its primary cause, Alzheimer’s disease, continue to devastate many with no available cure although present research has delivered methods for risk calculation and models of disease development that promote preventative strategies. Presently Alzheimer’s disease affects 1 in 9 people aged 65 and older amounting to a total annual healthcare cost in 2023 in the United States of $345 billion between Alzheimer’s disease and other dementias making dementia one of the costliest conditions to society (“2023 Alzheimer’s Disease Facts and Figures,” 2023). This substantial cost can be dramatically lowered in addition to a reduction in the overall burden of dementia through the help of risk prediction models, but there is still a need for models to deliver an individual’s predicted time of onset that supplements risk prediction in hopes of improving preventative care. The aim of this study is to develop a model used to predict the age of onset for all-cause dementias and Alzheimer’s disease using demographic, comorbidity, and genetic data from a cohort sample. This study creates multiple regression models with methods of ordinary least squares (OLS) and least absolute shrinkage and selection operator (LASSO) regression methods to understand the capacity of predictor variables that estimate age of onset for all-cause dementia and Alzheimer’s disease. This study is unique in its use of a diverse cohort containing 346 participants to create a predictive model that originates from the All of Us Research Program database and seeks to represent an accurate sampling of the United States population. The regression models generated had no predictive capacity for the age of onset but outline a simplified approach for integrating public health data into a predictive model. The results from the generated models suggest a need for continued research linking risk factors that estimate time of onset.

ContributorsGoeringer, Cayden (Author) / Holechek, Susan (Thesis director) / Sellner, Erin (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / School of Music, Dance and Theatre (Contributor)
Created2023-05
Description

Memory CD8+ T cells protect against secondary viral infections. They develop and maintain exclusively in circulation (e.g. central memory - Tcm) or are excluded from re-circulation (resident memory - Trm). The extracellular ATP receptor P2RX7 promotes both Tcm and Trm generation. High (P2RX7hi) P2RX7-expressing early effector cells show survival, memory

Memory CD8+ T cells protect against secondary viral infections. They develop and maintain exclusively in circulation (e.g. central memory - Tcm) or are excluded from re-circulation (resident memory - Trm). The extracellular ATP receptor P2RX7 promotes both Tcm and Trm generation. High (P2RX7hi) P2RX7-expressing early effector cells show survival, memory and pluripotency genes. Conversely, many terminal effector (TE) and apoptosis genes are upregulated in low (P2RX7lo) P2RX7-expressing cells. Among these genes is the zinc-finger transcriptional repressor Zeb2, which promotes TE differentiation at the expense of the memory cell pool. Given that Zeb2 was higher in P2RX7lo early effector cells, we postulated that Zeb2 ablation would allow P2RX7-deficient CD8+ T cells to skew towards memory subsets. To test this, we used RNP-based CRISPR-Cas9 to knockout Zeb2 in wild type or P2RX7-deficient P14 cells. At the memory timepoint, Zeb2 ablation led to a rescue of the ability of P2RX7-deficient cells to differentiate into the CD62L+ Tcm and CD69hiCD103hi Trm subsets, as well as increase the population of each. Our data suggest that P2RX7 imprints a pro-memory signature that is, to some extent, dependent on the negative regulation of Zeb2.

ContributorsVan Dijk, Sarah (Author) / Holechek, Susan (Thesis director) / Borges da Silvs, Henrique (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / School of Molecular Sciences (Contributor) / School of International Letters and Cultures (Contributor)
Created2021-12
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ContributorsVan Dijk, Sarah (Author) / Holechek, Susan (Thesis director) / Borges da Silvs, Henrique (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2021-12
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ContributorsVan Dijk, Sarah (Author) / Holechek, Susan (Thesis director) / Borges da Silvs, Henrique (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2021-12
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Description
This research project investigated known and novel differential genetic variants and their associated molecular pathways involved in Type II diabetes mellitus for the purpose of improving diagnosis and treatment methods. The goal of this investigation was to 1) identify the genetic variants and SNPs in Type II diabetes to develo

This research project investigated known and novel differential genetic variants and their associated molecular pathways involved in Type II diabetes mellitus for the purpose of improving diagnosis and treatment methods. The goal of this investigation was to 1) identify the genetic variants and SNPs in Type II diabetes to develop a gene regulatory pathway, and 2) utilize this pathway to determine suitable drug therapeutics for prevention and treatment. Using a Gene Set Enrichment Analysis (GSEA), a set of 1000 gene identifiers from a Mayo Clinic database was analyzed to determine the most significant genetic variants related to insulin signaling pathways involved in Type II Diabetes. The following genes were identified: NRAS, KRAS, PIK3CA, PDE3B, TSC1, AKT3, SOS1, NEU1, PRKAA2, AMPK, and ACC. In an extensive literature review and cross-analysis with Kegg and Reactome pathway databases, novel SNPs located on these gene variants were identified and used to determine suitable drug therapeutics for treatment. Overall, understanding how genetic mutations affect target gene function related to Type II Diabetes disease pathology is crucial to the development of effective diagnosis and treatment. This project provides new insight into the molecular basis of the Type II Diabetes, serving to help untangle the regulatory complexity of the disease and aid in the advancement of diagnosis and treatment. Keywords: Type II Diabetes mellitus, Gene Set Enrichment Analysis, genetic variants, KEGG Insulin Pathway, gene-regulatory pathway
ContributorsBucklin, Lindsay (Co-author) / Davis, Vanessa (Co-author) / Holechek, Susan (Thesis director) / Wang, Junwen (Committee member) / Nyarige, Verah (Committee member) / School of Human Evolution & Social Change (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
Description

This project uses All of Us Data to analyze how well of a predictor APOE ε4 is in the Latinx community, a high grandparent care community. APOE is used as a predictor for Alzheimer’s disease, but it is unknown, due to the lack of studies, how strong of a predictor

This project uses All of Us Data to analyze how well of a predictor APOE ε4 is in the Latinx community, a high grandparent care community. APOE is used as a predictor for Alzheimer’s disease, but it is unknown, due to the lack of studies, how strong of a predictor it will be for Latinx individuals. This project aims to understand if the increased risk of Alzheimer’s disease among Hispanics is associated with a different level of ε4 gene frequency.

ContributorsPerez, Julianna (Author) / Holechek, Susan (Thesis director) / Lopez, Gilberto (Committee member) / Barrett, The Honors College (Contributor) / Computer Science and Engineering Program (Contributor) / School of Life Sciences (Contributor)
Created2023-05