Life Sciences

Mark Albrecht; Brock Orme; Mary Jo Tufte, Southern Utah University

Grace Hoffmann; Monika Lakk, University of Utah

Tyler Johnson, Utah Valley University

Aaron Wallace; Brad Hauck; Michelle White; Michele Hansen, University of Utah

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

Hal Jones; Dan Schindler; Brynne Anderson; Mary Rosbach; Chandler Warr, Brigham Young University

Matt Austin, Brooke Smyth, Lauren Manwaring, Moroni Lopez, Brigham Young University Type 2 diabetes is characterized by the inability of pancreatic ë_-cells, which secrete insulin, to regulate blood glucose levels. The glucose-regulating mechanisms of these dysfunctional ë_-cells exhibit a gradual insensitivity to insulin, caused by prolonged hyperglycemia. Treatment for individuals suffering from Type 2 diabetes is limited to supplementary insulin injections. However, recent studies have revealed that powerful anti-oxidants called flavanols, which are found in cocoa, affect insulin secretion and glucose tolerance of ë_-cells. We isolated three fractions from the whole cocoa extract: monomeric catechin-rich, oligomeric procyandin-rich and polymeric procyandin-rich flavanols. Because cellular respiration is closely related to insulin secretion, we hypothesize that these fractions may exert their anti-diabetic effects by enhancing cellular respiration. To determine the effects of cocoa flavanols on ë_-cell respiration, we performed respiration assays on INS-1 ë_-cell lines incubated with increasing concentrations of whole cocoa extract, monomeric, polymeric and oligomeric catechin fractions or a control. We present data demonstrating the effect of these compounds on ë_-cell respiration. Advancements based on our research could provide an innovative therapeutic alternative to current diabetes treatment and new insight into the respiratory pathways of ë_-cells, affording new targets for a multitude of potential gene therapies.

Kirk Harter; Spencer Drennan; Liza Jarman; Weon Kim; Gregory Boatwright, Brigham Young University

Teya Mathews; Andrea Monzon, Brigham Young University

Diana Villicana; Kaitlin Veylupek, Southern Utah University

Ellison Goodrich, Salt Lake Community College

Ashton Omdahl; Shun Sambongi; Megan Major; Emily LeBaron; Dallas Larsen; Daniel Lewis, Brigham Young University

Chloe Jensen; Thomas Jarman, Brigham Young University

John Hancock; Benjamin Bickman; Kyle Kener; Kevin Garland; Claudia M Tellez Freitas; Scott Weber; Chad Hancock, 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.

Erin Kinnally; Jefferson Hunter; John Capitanio; Erika Jones; Elizabeth Wood, Brigham Young University

Li Szhen Teh; Preston Larsen; Ian Sudbury; McKay Christensen; Ranae Zauner, Utah Valley University

Stephen Smith, Southern Utah University

Angel Guerra; Curtis Hoffmann, Utah Valley University

Agueda Rodriguez; Michael Hope, Southern Utah University

Dominique Pablito, University of Utah

Kyson McBride, Southern Utah University

Bess Bauer, Weber State University

Hal Jones, Brigham Young University

Joselyn Rodriguez, University of Utah

Jacob Delano, Utah Valley University

Sydney Stephens, University of Utah

CaBri Montano, Utah Valley University

Sophie Overbeck, Weber State University

Kyleigh Tyler, Utah State University

Erin Kinnally; John Capitanio; Elizabeth Wood; Angus Bennion; Ryno Kruger; Christina Barr; Stephen Lindell; Stephen Suomi, Brigham Young University

Jacob Shaner, Brigham Young University

Riannon Smith; Melena Garrett, Utah State University

Courtney Smith, Brigham Young University

Spencer Bagley, Brigham Young University

Ireland Green, Weber State University

Yolancee Nguyen; Mark Silvis; David Kircher; Sean Strain, University of Utah

Jace Buxton, Dixie State University

Jaimi Butler; Ashley Kijowski; Claire Prasad, Westminster College

Paola Garrison-Tovar; Jazmine James; Denton Shepherd, Southern Utah University

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

Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University

Karaleen Anderson; Mariel Hatch, Utah Valley University

Jordan Parker, Southern Utah University

Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University

Aaron Leifer, Jasmine Banner, Collin Christensen, Trevor Lloyd, Kenneth Call, Brigham Young University Approximately 9.4 percent of the United States is affected by type 1 or type 2 diabetes. Diabetes results from the body’s inability to maintain healthy blood glucose levels due to the loss of pancreatic ë_-cells (insulin secreting cells) or from the body’s insulin sensitive cells becoming insulin resistant. Both type 1 and type 2 diabetes results in a loss of functional ë_-cells. The current treatments for diabetes are insulin injections or transplants, many times requiring up to three donors per transplant. Neither option is an optimal cure: insulin injections do not cure the disease, and transplants are not available to the majority of people. We propose that being able to replicate ë_-cells in-vivo would allow us to provide a cure to diabetes. ë_-cells stop reproducing (proliferating) soon after birth except in a few occasions such as obesity and pregnancy, leading us to believe that there are key gene(s) that induce cell proliferation when activated. Finding these gene(s) would present a viable cure, being able to grow ë_-cells in-vivo for transplantation or even injection. The gene MafA is present in mature ë_-cells and previous research has revealed its vital role in the pancreas. MafA is turned on around embryonic day 15.5 and steadily increases expression up until the cell becomes a mature ë_-cell. The time period when MafA is turned on corresponds with when a ë_-cell is proliferating and developing leading us to believe that MafA is crucial to finding a cure. Here we show the effect of MafA overexpression on INS1 832/13 ë_-cell proliferation, survival, and insulin secretion.

Sydney Cahoon, University of Utah

Colton Smith, Dixie State University

Weston Elison, Brigham Young University

Tason Turek, Dixie State University