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- All Subjects: Violin and piano music
ContributorsChang, Ruihong (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-29
Description
Four Souvenirs for Violin and Piano was composed by Paul Schoenfeld (b.1947) in 1990 as a showpiece, spotlighting the virtuosity of both the violin and piano in equal measure. Each movement is a modern interpretation of a folk or popular genre, re- envisioned over intricate jazz harmonies and rhythms. The work was commissioned by violinist Lev Polyakin, who specifically requested some short pieces that could be performed in a local jazz establishment named Night Town in Cleveland, Ohio. The result is a work that is approximately fifteen minutes in length. Schoenfeld is a respected composer in the contemporary classical music community, whose Café Music (1986) for piano trio has recently become a staple of the standard chamber music repertoire. Many of his other works, however, remain in relative obscurity. It is the focus of this document to shed light on at least one other notable composition; Four Souvenirs for Violin and Piano. Among the topics to be discussed regarding this piece are a brief history behind the genesis of this composition, a structural summary of the entire work and each of its movements, and an appended practice guide based on interview and coaching sessions with the composer himself. With this project, I hope to provide a better understanding and appreciation of this work.
ContributorsJanczyk, Kristie Annette (Author) / Ryan, Russell (Thesis advisor) / Campbell, Andrew (Committee member) / Norton, Kay (Committee member) / Arizona State University (Publisher)
Created2015
ContributorsWhite, Aaron (Performer) / Kim, Olga (Performer) / Hammond, Marinne (Performer) / Shaner, Hayden (Performer) / Yoo, Katie (Performer) / Shoemake, Crista (Performer) / Gebe, Vladimir, 1987- (Performer) / Wills, Grace (Performer) / McKinch, Riley (Performer) / Freshmen Four (Performer) / ASU Library. Music Library (Publisher)
Created2018-04-27
ContributorsRosenfeld, Albor (Performer) / Pagano, Caio, 1940- (Performer) / ASU Library. Music Library (Publisher)
Created2018-10-03
Neuroinflammation Following Experimental Diffuse Brain Injury in Pre-pubertal and Peri-pubertal Rats
Description
Traumatic brain injury is the leading cause of mortality and morbidity in children and adolescents. Adolescence is a critical time in development where the body and brain undergoes puberty, which not only includes reproductive maturation, but also adult social and cognitive development. Brain-injury-induced disruptions can cause secondary inflammation processes and as a result, pediatric TBI can lead to significant life-long and debilitating morbidities that continue long after initial injury. In this study, neuroinflammation following diffuse brain injury was explored in prepubertal and peripubertal rats using an adapted method of midline fluid percussion injury (mFPI) for juvenile rats to further understand the relationship between pediatric TBI and puberty disruption due to endocrine dysfunction. We expect the adapted mFPI model to be effective in producing diffuse, moderate brain injury in juvenile rats and hypothesize that pre-pubertal rats (PND35) will have increased neuroinflammation compared to peri-pubertal rats (PND17) and shams because of the potential neuroprotective nature of sex steroids. Male Sprague-Dawley rats (n=90) were subjected to either a diffuse midline fluid percussion injury (mFPI) or sham injury at post-natal day (PND) 17 (pre-puberty) or PND35 (peri-puberty). Animals were sacrificed at different time points defined as days post injury (DPI) including 1DPI, 7DPI and 25DPI to represent both acute and chronic time points, allowing for comparisons within groups (injury vs. sham) and across groups (PND17 vs PND35). Body weight of the rats was measured postoperatively at various time points throughout the study to follow recovery. Tissue was collected and subjected to Heamatoxylin and Eosin (H&E) stain to visualize histology and evaluate the application of diffuse mFPI to juvenile rats. In addition, tissue underwent immunohistochemical analysis using 3,3'-diaminobenzidine (DAB) to stain for ionized calcium binding proteins (Iba1) in order to assess injury-related neuroinflammation in the form of microglia activation. Diffuse brain injury using the mFPI model did not affect rat body weight or cause overt cell death, suggesting adaption of the adult mFPI model for juvenile rats is representative of moderate diffuse brain injury. In addition, diffuse TBI lead to morphological changes in microglia suggesting there is an increased inflammatory response following initial insult, which may directly contribute to improper activation of pubertal timing and progression in adolescent children affected. Since there is little literature on the full effects of puberty dysfunction following TBI in the pediatric population, there is a significant need to further assess this area in order to develop improved interventions and potential therapies for this affected population.
ContributorsNewbold, Kelsey Bevier (Author) / Newbern, Jason (Thesis director) / Rowe, Rachel (Committee member) / Ortiz, J. Bryce (Committee member) / School of Mathematical and Natural Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Tumor associated microglia-and-macrophages (TAMS) may constitute up to 30% of the composition of glioblastoma. Through mechanisms not well understood, TAMS are thought to aid the progression and invasiveness of glioblastoma. In an effort to investigate properties of TAMS in the context of glioblastoma, I utilized data from a PDGF-driven rat model of glioma that highly resembles human glioblastoma. Data was collected from time-lapse microscopy of slice cultures that differentially labels glioma cells and also microglia cells within and outside the tumor microenvironment. Here I show that microglia localize in the tumor and move with greater speed and migration than microglia outside the tumor environment. Following previous studies that show microglia can be characterized by certain movement distributions based on environmental influences, in this study, the majority of microglia movement was characterized by a power law distribution with a characteristic power law exponent lower than outside the tumor region. This indicates that microglia travel at greater distances within the tumor region than outside of it.
ContributorsJuliano, Joseph Dominic (Author) / Kostelich, Eric (Thesis director) / Nagy, John (Committee member) / Swanson, Kristin (Committee member) / Barrett, The Honors College (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Department of Chemistry and Biochemistry (Contributor)
Created2013-12
ContributorsCao, Yuchen (Performer) / Chen, Sicong (Performer) / Soberano, Chino (Performer) / Nam, Michelle (Performer) / Collins, Clarice (Performer) / Witt, Juliana (Performer) / Liu, Jingting (Performer) / Chen, Neilson (Performer) / Zhang, Aihua (Performer) / Jiang, Zhou (Performer) / ASU Library. Music Library (Publisher)
Created2018-04-25
Description
Neuroinflammation is an important secondary injury response occurring after traumatic brain injury (TBI). Anxiety-like disorders are commonly exacerbated after TBI and are mediated through the amygdala; however, the amygdala remains understudied despite its important contribution in processing emotional and stressful stimuli. Therefore, we wanted to study neuroinflammation after experimental TBI using midline fluid percussion in rodent models. We assessed microglia morphology over time post-injury in two circuit related nuclei of the amygdala, the basolateral amygdala (BLA) and central amygdala of the nucleus (CeA), using skeletal analysis. We also looked at silver staining and glial fibrillary acidic protein (GFAP) to evaluate the role of neuropathology and astrocytosis to evaluate for neuroinflammation in the amygdala. We hypothesized that experimental diffuse TBI leads to microglial activation in the BLA-CeA circuitry over time post-injury due to changes in microglial morphology and increased astrocytosis in the absence of neuropathology. Microglial cell count was found to decrease in the BLA at 1 DPI before returning to sham levels by 28 DPI. No change was found in the CeA. Microglial ramification (process length/cell and endpoints/cell) was found to decrease at 1DPI compared to sham in the CeA, but not in the BLA. Silver staining and GFAP immunoreactivity did not find any evidence of neurodegeneration or activated astrocytes in the respectively. Together, these data indicate that diffuse TBI does not necessarily lead to the same microglial response in the amygdala nuclei, although an alternative mechanism for a neuroinflammatory response in the CeA likely contributes to the widespread neuronal and circuit dysfunction that occurs after TBI.
ContributorsHur, Yerin (Author) / Newbern, Jason (Thesis director) / Thomas, Theresa Currier (Committee member) / Beitchman, Joshua (Committee member) / School of Molecular Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05