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receptor (RAR) and vitamin D receptor (VDR). The RXR/RAR dimer is activated by ligand all
trans retinoic acid (ATRA), which culminates in gut-specific effector T cell migration. Similarly,
the VDR/RXR dimer binds 1,25(OH)2D3 to cause skin-specific effector T cell migration.
Targeted migration is a potent addition to current vaccines, as it would induce activated T cell
trafficking to appropriate areas of the immune system and ensure optimal stimulation (40).
ATRA, while in use clinically, is limited by toxicity and chemical instability. Rexinoids
are stable, synthetically developed ligands specific for the RXR. We have previously shown that
select rexinoids can enhance upregulation of gut tropic CCR9 receptors on effector T cells.
However, it is important to establish whether these cells can actually migrate, to show the
potential of rexinoids as vaccine adjuvants that can cause gut specific T cell migration.
Additionally, since the RXR is a major contributor to VDR-mediated transcription and
epidermotropism (15), it is worth investigating whether these compounds can also function as
adjuvants that promote migration by increasing expression of skin tropic CCR10 receptors on T
cells.
Prior experiments have demonstrated that select rexinoids can induce gut tropic migration
of CD8+ T cells in an in vitro assay and are comparable in effectiveness to ATRA (7). The effect
of rexinoids on CD4+ T cells is unknown however, so the aim of this project was to determine if
rexinoids can cause gut tropic migration in CD4+ T cells to a similar extent. A secondary aim
was to investigate whether varying concentrations in 1,25-Dihydroxyvitamin D3 can be linked to
increasing CCR10 upregulation on Jurkat CD4+ T cells, with the future aim to combine 1,25
Dihydroxyvitamin D3 with rexinoids.
These hypotheses were tested using murine splenocytes for the migration experiment, and
human Jurkat CD4+ T cells for the vitamin D experiment. Migration was assessed using a
Transwell chemotaxis assay. Our findings support the potential of rexinoids as compounds
capable of causing gut-tropic migration in murine CD4+ T cells in vitro, like ATRA. We did not
observe conclusive evidence that vitamin D3 causes upregulated CCR10 expression, but this
experiment must be repeated with a human primary T cell line.
This project explores modern healthcare related disparities in Phoenix, Arizona, as well as the overarching historical structures that have influenced public health within the city. Historical and systemic racism, harmful housing policies, barriers preventing upwards economic mobility, and purposeful measures put in place by business leaders and city officials are all explored as factors impacting current disparities in access to care. In order to fully analyze the gaps in care, different areas, both high and low-income, are analyzed throughout history in order to understand shifting demographics and policies. The project concludes with an in-depth look at current public health efforts within Maricopa County, as well as with future policy recommendations.
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.