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Life Sciences

November 19, 2020 11:22 PM
Maxwell Beers; Jace Pulsipher, Brigham Young University
November 19, 2020 10:56 PM
Courtney Smith, Brigham Young University
November 19, 2020 10:35 PM
John Capitanio; Elizabeth Wood; Alexander Baxter; Ashley Cameron, Brigham Young University
November 19, 2020 10:24 PM
Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
November 19, 2020 07:05 PM
Brooke Smyth; Moroni Lopez; Mimi Ross; Luaren Manwaring; Mathew Austin, Brigham Young University
November 19, 2020 06:59 PM
Monika Lakk; Derek Young, University of Utah
November 19, 2020 06:37 PM
Jeremy Anderson, Brigham Young University
November 19, 2020 11:01 AM
Bo Price; Kaylynn Ashby; Marianne Maughan, Utah State University Apomixis is an asexual reproductive process that omits the reducing step of meiosis (apomeiosis) thereby producing unreduced eggs that will develop into embryos without the need of gamete fusion (parthenogenesis). The lack of reduced gametes leads to progenies that have identical genomes, i.e., diversification by egg and sperm fertilization is prevented, from generation to generation. Facultative apomixis is the ability to switch from apomixis to sexual reproduction by completing the meiosis divisions to produce reduced haploid gametes. It is understood that the switch to sexual meiosis in facultative apomixis is triggered by environmental stress signals. Sexual reproduction is induced by stress to create a competitive advantage by allowing genetic diversity to increase the possibility of species adaptability and survival. Boechera is a genus of flowering angiosperms that has multiple facultative apomictic species. To understand the molecular cascade that is triggered to cause apomixis to switch to sexual reproduction, Boechera facultative apomictic ovaries were treated exogenously with hydrogen peroxide to induce oxidative stress. RNAseq is being used to identify gene expression differences between apomictic and sex-induced ovary development as a first step toward elucidating the molecular switch from apomeiosis to meiosis.
November 19, 2020 10:57 AM
Brian Jensen; Phillip Ng, Brigham Young University The purpose of this project is to invent a device capable of filtrating oil from fracking waste using a system of Carbon Infiltrated Carbon Nanotubes (CI-CNT) and its passive filtration properties. Fracking produces harmful waste material that pollutes clean water. A large-scale CI-CNT device that can filter large amounts of the microscopic oil particles from the waste will offer drilling companies a viable option to reuse the fracking mixture collected from after the fracking process instead of burying their unusable waste material underground, thereby causing less environmental damage. Pyrolytic CI-CNT’s can isolate water and oil molecules due to their superhydrophobic and oleophilic properties, unique cylindrical nanostructure, and functional groups. The CI-CNT’s will be grown on a stainless steel substrate that will give us the robustness and material properties needed to withstand the forces from fluid flow. We have designed a long channel with unique mechanical features that we anticipate will effectively separate oil from fracking waste as it interacts with it by splashing, rolling, and flowing across its surface.
November 18, 2020 08:00 PM
Dallin Hilton; Siera Theobald; Janessa Bassett, Dixie State University
November 18, 2020 07:53 PM
Brooke Smyth; Lauren Manwaring; Moroni Lopez, Brigham Young University
November 18, 2020 06:51 PM
Matt Austin; Brooke Smyth; Lauren Manwaring; Moroni Lopez, Brigham Young University
November 17, 2020 01:33 PM
Neil Duncan, Dixie State University
November 12, 2020 03:07 PM
Craig Schoenberger; Nathan Van Katwyk; Jens Griffin; Insu Kim, Brigham Young University
November 12, 2020 03:04 PM
Parker Booren; Talon Aitken; Samuel Grover; Nathan Jensen; Jackie Crabree, Brigham Young University
November 12, 2020 02:00 PM
Michelle George, Dixie State University
November 12, 2020 01:38 PM
Matthew Bradley, Brigham Young University
November 12, 2020 01:32 PM
Matt Austin; Brooke Smyth; Lauren Manwaring; Moroni Lopez, Brigham Young University
November 11, 2020 04:54 PM
Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
November 03, 2020 03:16 PM
Morgan Abbott, Utah Valley University
November 03, 2020 03:09 PM
Parker Booren; Talon Aitken; Samuel Grover; Nathan Jensen; Jackie Crabtree, Brigham Young University
November 02, 2020 10:17 AM
Matt Austin; Brooke Smyth; Lauren Manwaring; Moroni Lopez, Brigham Young University
November 02, 2020 10:01 AM
Parker Booren, Brigham Young University
October 30, 2020 10:15 AM
Parker Booren; Nathanael Jensen; Talon Aitken; Samuel Grover; Jackie Crabree, Brigham Young University
October 29, 2020 08:25 PM
Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
October 29, 2020 07:27 PM
Rosanise Odell, Westminster College
January 01, 2018 12:00 AM
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.
January 01, 2018 12:00 AM
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.
January 01, 2018 12:00 AM
Christian Kodele, Lian Li, Jane Yang, University of Utah Non-Hodgkin lymphoma (NHL) is an immune disease mostly of B-cell origin (eighty-five percent of the time) as well as the ninth leading cause of cancer death in the United States. Although treatments for NHLs greatly improved following the FDA approval of Rituximab (RTX), refractive malignancies still occur that are nonresponsive and/or resistance to current therapies in at least a third of all patients. This has been attributed both to the inability of immune effector cells (eg., macrophages, natural killer cells) to hypercrosslink ligated monoclonal antibodies (mAbs), and to Fc receptor (FcR)-mediated endocytosis or ‰ÛÏtrogocytosis‰Û of CD20 antigens. In order to address these clinical obstacles, we designed a novel paradigm in macromolecular therapeutics that can specifically kill cancer cells without a drug. This paradigm is based on the use of anti-CD20 Fab’ fragments in a multivalent system. Crosslinking of CD20 receptors leads to receptor clustering, transfer to lipid rafts, opening of a calcium channel, and ultimately apoptosis. Additionally, the removal of the Fc fragment resulted enticingly in both the rendering of the system to be immune dependent and in decreasing the numerous adverse effects. In this study, we have used human serum albumin (HSA) as the multivalent carrier of RTX based Fab’ fragments. We have covalently attached multiple Fab’ fragments to HSA, characterized the nanoconjugate’s physiochemical properties, and evaluated its efficacy to induce apoptosis of Raji B cells in vitro. The efficacy of the nanoconjugate to induce apoptosis was determined with Annexin V assay and flow cytometry. The interaction of the nanoconstruct with Raji cells was characterized using confocal microscopy of Cy5 labeled conjugates. As predicted, the HSA-(Fab’)x conjugate was able to induce cell death in vitro. The results of the Annexin V apoptosis assay showed that 38.9 percent of the cell population treated with the conjugate became apoptotic, while 13.6 and 15.7 percent of the cell populations untreated and treated with whole RTX mAb became apoptotic respectively. Furthermore, images recorded by use of confocal microscopy suggest that the attachment of HSA-(Fab’)x conjugate to the cell membrane is CD20 specific. While not conclusive, the combination of these results suggest that the mechanism of action involves cross-linking of the CD20 receptor, which subsequently induces apoptosis. We believe these results warrant further investigation of the mechanism of action of HSA-(Fab’)x, as well as the treatment potential of this nanoconjugate.
January 01, 2018 12:00 AM
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.
January 01, 2018 12:00 AM
Diabetes affects over 30 million Americans and 185,000 Utahn’s. Type 1 and Type 2 diabetes are characterized by decreased functional β-cell mass and insulin production. Diabetes also results in increased circulating glucose and fatty acid levels, which damage and destroy β-cells over time. Our study will shed further light on the effects of palmitate, the most commonly made fatty acid in the liver, on hyperlipidemia. In this study we test the specific effects of chronic palmitate exposure on various cell lines acclimated to 0.15 mM, 0.3 mM, and 0.5 mM concentrations of palmitate. We demonstrate the effects of progressive long-term exposure to palmitate on β-cell proliferation and resistance to apoptosis. We demonstrate mechanistic changes that result in the observed phenotypes. Our goal in this study is to explore how β-cells adapt to exposure to hyperlipidemia, and to define interventions to protect β-cells from the harmful effects of hyperlipidemia.
January 01, 2018 12:00 AM
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.
January 01, 2018 12:00 AM
Courtney Smith, Brigham Young University
January 01, 2018 12:00 AM
Weston Elison, Brigham Young University
January 01, 2018 12:00 AM
Jace Buxton, Dixie State University
January 01, 2018 12:00 AM
Joshua Wilkerson; Seung-Ook Yang; Parker J. Funk; Steven K. Stanley, Brigham Young University
January 01, 2018 12:00 AM
Sydney Cahoon, University of Utah
January 01, 2018 12:00 AM
Karaleen Anderson; Li Szhen Teh; Mariel Hatch; Caeleb Harris; Hannah; Stephanie Pare, Utah Valley University
January 01, 2018 12:00 AM
Jordan Parker, Southern Utah University
January 01, 2018 12:00 AM
Li Szhen Teh; Preston Larsen; Ian Sudbury; McKay Christensen; Ranae Zauner, Utah Valley University
January 01, 2018 12:00 AM
Erin Kinnally; Jefferson Hunter; John Capitanio; Erika Jones; Elizabeth Wood, Brigham Young University
January 01, 2018 12:00 AM
Paola Garrison-Tovar; Jazmine James; Denton Shepherd, Southern Utah University
January 01, 2018 12:00 AM
Aaron Leifer; Jasmine Banner; Collin Christensen; Trevor Lloyd; Kenneth Call, Brigham Young University
January 01, 2018 12:00 AM
Yolancee Nguyen; Mark Silvis; David Kircher; Sean Strain, University of Utah