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
CD4+CD25+ FOXP3+ cells are recognized as the most reliable regulatory T cell subset. However, the intracellular nature of the FOXP3 transcription factor limits its use for the isolation or selection of viable regulatory T cells for adoptive immunotherapy. Nuclear localization of FOXP3 has been more strongly associated with induced regulatory

CD4+CD25+ FOXP3+ cells are recognized as the most reliable regulatory T cell subset. However, the intracellular nature of the FOXP3 transcription factor limits its use for the isolation or selection of viable regulatory T cells for adoptive immunotherapy. Nuclear localization of FOXP3 has been more strongly associated with induced regulatory T cell (Treg) function than increased expression of FOXP3 alone. Several different cell culture methods and T cell activation techniques can induce increased expression of FOXP3 in a variety of T cell models, but Rapamycin (an mTOR inhibitor) was recently shown to differentially induce nuclear localization of FOXP3 when compared with IL-10 and TGFβ. Feline Tregs have been well characterized and share many of the phenotypic and functional characteristics of murine and human Tregs. We cultured feline Mya-1 T cells in conditions that would differentially promote effector or regulatory phenotypes and correlated nuclear localization of FOXP3 with other quantitative morphologic features using imaging flow cytometry. We compared the morphologic features of cells with high intra-nuclear concentrations of FOXP3 cultured without IL-2, with IL-2, and with IL-2 and Rapamycin before and after non-specific antigenic stimulation with Concanavalin-A. This analysis may help identify a population of pure regulatory T cells that would be more likely to maintain regulatory function following in-vitro expansion and activation. Furthermore, the feline T cell model could help elucidate important differences between murine and human Treg cells that would further translational efforts in adoptive immunotherapy. Now, we ask if nuclear localization of FOXP3 could be used to identify other morphologic differences between activated effector and regulatory T cells using a feline T cell line.
ContributorsRojas, Arturo Nikolas (Author) / Sweazea, Karen (Thesis director) / Mexas, Angela (Committee member) / Murphy, Andrea (Committee member) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
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Description
High fat diets (HFD) are known to cause hepatic non-alcoholic steatosis in rats in as few as four weeks. Accumulation of triglycerides in liver and skeletal muscle is associated with insulin resistance and obesity. However, studies of fat accumulation in cardiac muscle are not as prevalent. Therefore, the first hypothesis

High fat diets (HFD) are known to cause hepatic non-alcoholic steatosis in rats in as few as four weeks. Accumulation of triglycerides in liver and skeletal muscle is associated with insulin resistance and obesity. However, studies of fat accumulation in cardiac muscle are not as prevalent. Therefore, the first hypothesis of this study was that HFD would lead to hepatic steatosis as well as lipid accumulation in pectoralis and cardiac muscles, tissues responsible for the majority of postprandial glucose disposal. Prior studies also indicated that HFD leads to increased inflammation and oxidative stress within the vasculature resulting in impaired endothelium-dependent vasodilation, however biomarkers of immune system reactivity were not assessed. Therefore, the second aim of this study was to explore additional pathways of immune system reactivity and stress (natural antibodies; heat shock protein 60 (HSP60)) in rats fed either a control (chow) or high fat (HFD) diet. HSP60 has also recently been recognized as an early marker of vascular dysfunction in humans. The hypothesis was that immune system reactivity and early vascular dysfunction would be heightened in rats fed a HFD compared to chow-fed controls. Young male Sprague-Dawley rats (140-160g) were maintained on a chow diet (5% fat, 57.33% carbohydrate, 3.4kcal/g) or HFD (60% fat, 20% carbohydrate, 5.24 kcal/g) for 6 weeks. HFD rats developed hepatic steatosis with significantly elevated liver triglyceride concentrations compared to chow-fed controls (20.73±2.09 vs.9.75±0.52 mg triglycerides/g tissue, respectively; p=0.001). While lipid accumulation appeared to be evident in the pectoralis muscle from HFD rats, triglyceride concentrations were not significantly different from controls. Likewise, there was no evidence of lipid infiltration in cardiac muscles of HFD rats. Lipid accumulation in the liver of overweight HFD rats may contribute to the observed insulin resistance in these animals. Contrary to the second hypothesis, there were no significant differences in plasma HSP60 expression between HFD and chow rats (p>0.05). Likewise, hemagglutination and hemolysis responses were similar between HFD and chow-fed rats (p>0.05). These findings suggest that immune system responses may not be affected by 6 weeks of high fat intake and that HSP60 is not an early marker of vascular dysfunction in this rodent model.
ContributorsLiss, Tyler Jessee (Author) / Sweazea, Karen (Thesis director) / Shaibi, Gabriel (Committee member) / Johnston, Carol (Committee member) / Barrett, The Honors College (Contributor) / School of Nutrition and Health Promotion (Contributor) / School of Historical, Philosophical and Religious Studies (Contributor)
Created2013-05
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Description
Background: To determine the effect of sumac on vasodilation and oxidative stress in vascular tissue. This study hypothesized that sumac would increase vasodilation and reduce vascular damage in vascular tissue taken from rats to improve symptoms and risk of vascular dementia.
Methods: Male Sprague-Dawley rats were fed a chow diet

Background: To determine the effect of sumac on vasodilation and oxidative stress in vascular tissue. This study hypothesized that sumac would increase vasodilation and reduce vascular damage in vascular tissue taken from rats to improve symptoms and risk of vascular dementia.
Methods: Male Sprague-Dawley rats were fed a chow diet or a high fat diet (HFD) for ten weeks. Endothelium-dependent vasodilation was measured in isolated mesenteric arterioles that were treated with or without 80 µg/ml sumac in the superfusate throughout the experiment.
Results: Sumac did not improve vasodilation or in ex vivo arteries from rats fed a high fat diet. There were trends of improved vasodilation in sumac treated vessels from high fat diet rats, but sumac did not significantly improve vasodilation. In rats fed a chow diet, sumac prevented phenylephrine (PE) constriction in the vascular tissue. The most likely cause for this is the presence of Gallic acid in sumac. Another possible explanation is the presence of nitrates in sumac which may have prevented PE vasoconstriction.
Conclusions: Sumac did not significantly improve vasodilation in isolated arteries from rats fed a high fat diet. The results are inconclusive for the improvement of symptoms or risk of vascular dementia. In vivo treatment with sumac should be tested as results may differ.
ContributorsLambries, Lorne Flores (Co-author) / Sweazea, Karen (Co-author, Thesis director) / Gonzales, Rayna (Co-author, Committee member) / Basile, Anthony (Co-author, Committee member) / Barbares, Julia (Co-author) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05