2018 Abstracts

Taylor Clement, Southern Utah University

Mariah Richins; Jefferson Last, Dixie State University

Jacob Delano, Utah Valley University

Kyson McBride, Southern Utah University

Spencer Bagley, Brigham Young University

Mariah Clayson; Maverik Shumway; Brian Anderson, Southern Utah University

Chloe Jensen; Thomas Jarman, Brigham Young University

Michael Lange; Don Rodriguez; Elijah Bingham, Brigham Young University

Karaleen Anderson, Mariel Hatch, Caeleb Harris, Anastasiia Matkovska, Kendrick Kiggins, Levi Neely, Utah Valley University Mucormycosis is a life-threatening disease that occurs in immunocompromised individuals, such as burn, cancer and diabetic patients. Amphotericin B is the current line of treatment for the disease, however it is known to have many adverse side effects including cell toxicity. Due to the high mortality and morbidity associated with the disease even when treated with Amphotericin B, it is vital that new combination therapeutic techniques be investigated in order to more effectively treat the disease. Mucromycosis is most often caused by a filamentous, opportunistic fungi called Rhizopus oryzae. This species causes up to 80% of infections and is the most common species isolated from confirmed Mucormycosis sites. Origanum vulgare (oregano) oil has been shown to have broad anti-microbial properties in various studies. This study investigates the ability of oregano oil to lower the concentration of Amphotericin B needed to successfully inhibit R. oryzae biofilms. Various concentrations of oregano oil and Amphotericin B are tested to determine the optimal concentration ratio that maximizes biofilm inhibition. Synergistic activity of oregano oil and Amp B could be used to decrease the amount of Amphotericin B needed to treat Mucormycosis infections while still utilizing the antifungal properties of Oregano oil.

Karaleen Anderson; Li Szhen Teh; Mariel Hatch; Caeleb Harris; Hannah; Stephanie Pare, Utah Valley University

Jordan Parker, Southern Utah University

Kaden Jordan, Dixie State University

Joshua Wilkerson; Seung-Ook Yang; Parker J. Funk; Steven K. Stanley, Brigham Young University

Jaimi Butler; Ashley Kijowski; Claire Prasad, Westminster College

Karaleen Anderson; Mariel Hatch, Utah Valley University

Ashley Wiltsie, University of Utah

Trevor Lloyd; Mason Poffenbarger; Austin Ricks; Andrew Barlow; Zoey Fishburn, Brigham Young University

Aaron Leifer, Jasmine Banner, Collin Christensen, Trevor Lloyd, Kenneth Call, Brigham Young University Diabetes Mellitus has become a worldwide epidemic affecting over 400 million people. Both type 1 and type 2 diabetes result from the body’s inability to produce or respond to insulin in order to regulate blood sugar. In both cases, the insulin secreting ë_-cells in the pancreatic Islets of Langerhans have become endangered and in many cases non-functional. The function of these ë_-cells is defined by their ability to multiply and maintain a steady number, to defend against induced cell death and ultimately to secrete insulin. Since ë_-cell production reaches its peak during fetal development, this would suggest that diabetics have an inactive pathway to produce functional ë_-cells. However, recent studies have identified key transcription factors that aid pancreatic progenitors in becoming functional ë_-cells. Pdx1 is a transcription factor that is active throughout the ë_-cell pathway and found in mature ë_-cells. Research has identified Pdx1 as a key component in helping both ë±-cells and ë_-cells proliferate and even in reprogramming ë±-cells to become functional ë_-cells. Additionally, Pdx1 has been identified to help ë_-cells effectively secrete insulin. We present data demonstrating the effect of Pdx1 adenoviral over-expression on three independent markers of functional ë_-cell mass: 1) cell proliferation, 2) cell survival, and 3) insulin content and secretion. Defining the effect of Pdx1 on each of these parameters will provide further data to explore therapeutic interventions for diabetic patients.

Kayleigh Ingersoll, Brigham Young University

Nayla Rhein, Southern Utah University

Parker Booren, Nathanael Jensen, Talon Aitken, Samuel Grover, Jackie Crabree, Brigham Young University Diabetes continues to grow at a rapid rate, affecting the lives of both young and old. Both Type 1 and Type 2 diabetes lead to eventual ë_ cell depletion (and subsequent decrease in insulin secretion). This can be treated through ë_ cell transplantation from the pancreata of cadavers. Currently, collecting sufficient ë_ cells for one diabetic patient requires pancreata from multiple cadavers. If proliferation can be induced in a donor’s aged ë_ cells, transplantation would become more effective as one donor now becomes sufficient to serve one or two patients. Nkx6.1 is a transcription factor that increases insulin secretion and induces proliferation of young rat ë_ cells (5 weeks) through the upregulation of its target genes: VGF, Nr4a1 and Nr4a3. Aged rat ë_ cells (5+ months) fail to proliferate after overexpression of Nkx6.1. We have also shown that upregulation of Nkx6.1’s target genes is disrupted in these aged ë_ cells. This may be due to changes in expression of a binding partner necessary for Nkx6.1’s upregulation of these target genes or to changes in Nkx6.1 posttranslational modifications that impede binding partner interactions in aged ë_ cells. We present data from co-immunoprecipitation and mass spectrometry experiments that reveal the presence or absence of Nkx6.1’s binding partner in young and aged ë_ cells. Furthermore, we present mass spectrometry results of Nkx6.1 posttranslational modification from young and old ë_ cells. This data will increase understanding on the ability of Nkx6.1 to upregulate its target genes in an aged ë_ cell.

Aleksei Ananin, Southern Utah University

Andrew Piskadlo; Adele Reynolds; Anna Robert; Gaurav Pandey, Westminster College

Jared Blanchard, Brigham Young University

Kate Hendricks, Brigham Young University

Lauren Nickell, Southern Utah University

Brigham Pope; Daniel Joaquin; Jacob Hickey, Brigham Young University

Andrew Kennedy, University of Utah

Jonathan Shumway; Scott George, Brigham Young University

Michael Maynard; Alex Mitchell, Dixie State University

Katie Varela, Brigham Young University

Jace Howell, Dixie State University

Ryker Haddock, Brigham Young University

Jacob Delano; Nicholas Brian, Utah Valley University

Anastasiia Matkovska; Austin Bettridge; Jeff Keller, Utah Valley University

Landon Graham, Utah State University

Allyson Berri, University of Utah

Candy Roland, Dixie State University

Trevor Tonks, Utah Valley University

Jodi Shegrud, Weber State University

Spencer Waters, Brigham Young University

Jayce Davis, Southern Utah University

Brayden Ross, Southern Utah University

Luke Tuttle, University of Utah

Tessa Brunnenmeyer, Southern Utah University

Kevin Toney, Brigham Young University

Emily Demke, Utah Valley University

Aubrey Keeler, Brigham Young University

Venice Jardine, Brigham Young University

Alexandria DeGrauw, University of Utah