Matching Items (393)
Description
The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding in 1871 of the Société Nationale de Musique by Camille Saint-Saëns (1835-1921) and Romain Bussine (1830-1899) made possible the promotion of contemporary French composers. The founding of the Société des Instruments à Vent by Paul Taffanel (1844-1908) in 1879 also invigorated a new era of chamber music for wind instruments. Within this groundbreaking environment, Mélanie Hélène Bonis (pen name Mel Bonis) entered the Paris Conservatory in 1876, under the tutelage of César Franck (1822-1890). Many flutists are dismayed by the scarcity of repertoire for the instrument in the Romantic and post-Romantic traditions; they make up for this absence by borrowing the violin sonatas of Gabriel Fauré (1845-1924) and Franck. The flute and piano works of Mel Bonis help to fill this void with music composed originally for flute. Bonis was a prolific composer with over 300 works to her credit, but her works for flute and piano have not been researched or professionally recorded in the United States before the present study. Although virtually unknown today in the American flute community, Bonis's music received much acclaim from her contemporaries and deserves a prominent place in the flutist's repertoire. After a brief biographical introduction, this document examines Mel Bonis's musical style and describes in detail her six works for flute and piano while also offering performance suggestions.
ContributorsDaum, Jenna Elyse (Author) / Buck, Elizabeth (Thesis advisor) / Holbrook, Amy (Committee member) / Micklich, Albie (Committee member) / Schuring, Martin (Committee member) / Norton, Kay (Committee member) / Arizona State University (Publisher)
Created2013
ContributorsMatthews, Eyona (Performer) / Yoo, Katie Jihye (Performer) / Roubison, Ryan (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-25
ContributorsHoeckley, Stephanie (Performer) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-24
Description
The NLR family, pyrin domain-containing 3 (NLRP3) inflammasome is essential for the innate immune response to danger signals. Importantly, the NLRP3 inflammasome responds to structurally and functionally dissimilar stimuli. It is currently unknown how the NLRP3 inflammasome responds to such diverse triggers. This dissertation investigates the role of ion flux in regulating the NLRP3 inflammasome. Project 1 explores the relationship between potassium efflux and Syk tyrosine kinase. The results reveal that Syk activity is upstream of mitochondrial oxidative signaling and is crucial for inflammasome assembly, pro-inflammatory cytokine processing, and caspase-1-dependent pyroptotic cell death. Dynamic potassium imaging and molecular analysis revealed that Syk is downstream of, and regulated by, potassium efflux. Project 1 reveals the first identified intermediate regulator of inflammasome activity regulated by potassium efflux. Project 2 focuses on P2X7 purinergic receptor-dependent ion flux in regulating the inflammasome. Dynamic potassium imaging revealed an ATP dose-dependent efflux of potassium driven by P2X7. Surprisingly, ATP induced mitochondrial potassium mobilization, suggesting a mitochondrial detection of purinergic ion flux. ATP-induced potassium and calcium flux was found to regulate mitochondrial oxidative signaling upstream of inflammasome assembly. First-ever multiplexed imaging of potassium and calcium dynamics revealed that potassium efflux is necessary for calcium influx. These results suggest that ATP-induced potassium efflux regulates the inflammasome by calcium influx-dependent mitochondrial oxidative signaling. Project 2 defines a coordinated cation flux dependent on the efflux of potassium and upstream of mitochondrial oxidative signaling in inflammasome regulation. Lastly, this dissertation contributes two methods that will be useful for investigating inflammasome biology: an optimized pipeline for single cell transcriptional analysis, and a mouse macrophage cell line expressing a genetically encoded intracellular ATP sensor. This dissertation contributes to understanding the fundamental role of ion flux in regulation of the NLRP3 inflammasome and identifies potassium flux and Syk as potential targets to modulate inflammation.
ContributorsYaron, Jordan Robin (Author) / Meldrum, Deirdre R (Thesis advisor) / Blattman, Joseph N (Committee member) / Glenn, Honor L (Committee member) / Arizona State University (Publisher)
Created2015
ContributorsMcClain, Katelyn (Performer) / Buringrud, Deanna (Contributor) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-31
Description
Most drugs work by binding to receptors on the cell surface. These receptors can then carry the message into the cell and have a wide array of results. However, studying how fast the binding is can be difficult. Current methods involve extracting the receptor and labeling them, but both these steps have issues. Previous works found that binding on the cell surface is accompanied with a small change in cell size, generally an increase. They have also developed an algorithm that can track these small changes without a label using a simple bright field microscope. Here, this relationship is further explored by comparing edge tracking results to a more widely used method, surface plasmon resonance. The kinetic constants found from the two methods are in agreement. No corrections or manipulations were needed to create agreement. The Bland-Altman plots shows that the error between the two methods is about 0.009 s-1. This is about the same error between cells, making it a non-dominant source of error.
ContributorsHunt, Ashley (Author) / Tao, Nongjian (Thesis advisor) / Ros, Alexandra (Committee member) / Borges, Chad (Committee member) / Arizona State University (Publisher)
Created2018
ContributorsHur, Jiyoun (Performer) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-01
Description
Vaccinia virus (VV) is a prototype virus of the Orthopox viruses. The large dsDNA virus composed of 200kbp genome contains approximately 200 genes and replicates entirely in the cytosol. Since its use as a live vaccine against smallpox that leads to the successful eradication of smallpox, Vaccinia has been intensely studied as a vaccine vector since the large genome allows for the insertion of multiple genes. It is also studied as a molecular tool for gene therapy and gene functional study. Despite its success as a live vaccine, the vaccination causes some mild to serious bur rare adverse events in vaccinees such as generalized Vaccinia and encepharitis. Therefore, identification of virulence genes and removal of these genes to create a safer vaccine remain an important tasks. In this study, the author seeks to elucidate the possible relationship between immune evading proteins E3 and B19. VV did not allow double deletions of E3 and B19, indicating the existence of a relationship between the two genes.
ContributorsBarclay, Shizuka (Author) / Jacobs, Bertram (Thesis director) / Ugarova, Tatiana (Committee member) / Kibler, Karen (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-05
Description
Phosphoinositol-Dependent Kinase 1 (PDK1) acts in conjunction with phosphorylated lipids such as Phosphoinositol-3,4,5-triphosphate (PIP3) to activate a variety of proteins that regulate mechanisms ranging from cell growth and survival to cytoskeletal rearrangement. In this investigation PDK1 was examined in the context of cellular division. The techniques of immunocytochemistry and live cell imaging were used to visualize the effects of the inhibition of PDK1 on division in HeLa cells. Division was impaired at metaphase of mitosis. The inhibited cells were unable to initiate anaphase cell-elongation ultimately leading to the flattening of spherical, metaphase cells. Preliminary studies with imunocytochemistry and live cell imaging suggested that insulin treatment reversed PDK1 inhibition, but the results were not statistically significant. Therefore, the recovery of PDK1 inhibition by insulin treatment could not be confirmed. Based on these observations a possible reason for the inability of the treated cells to complete cytokinesis could be the role of PDK1 in the Rho-kinase pathway that is required for the processes cell-elongation necessary for anaphase of mitosis.
ContributorsMasserano, Benjamin Max (Author) / Capco, David (Thesis director) / Baluch, Debra (Committee member) / Chandler, Douglas (Committee member) / Barrett, The Honors College (Contributor) / School of International Letters and Cultures (Contributor) / School of Life Sciences (Contributor)
Created2014-05
ContributorsZaleski, Kimberly (Contributor) / Kazarian, Trevor (Performer) / Ryan, Russell (Performer) / IN2ATIVE (Performer) / ASU Library. Music Library (Publisher)
Created2018-09-28