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Lyme disease is a common tick-borne illness caused by the Gram-negative bacterium Borrelia burgdorferi. An outer membrane protein of Borrelia burgdorferi, P66, has been suggested as a possible target for Lyme disease treatments. However, a lack of structural information available for P66 has hindered attempts to design medications to target the protein. Therefore, this study attempted to find methods for expressing and purifying P66 in quantities that can be used for structural studies. It was found that by using the PelB signal sequence, His-tagged P66 could be directed to the outer membrane of Escherichia coli, as confirmed by an anti-His Western blot. Further attempts to optimize P66 expression in the outer membrane were made, pending verification via Western blotting. The ability to direct P66 to the outer membrane using the PelB signal sequence is a promising first step in determining the overall structure of P66, but further work is needed before P66 is ready for large-scale purification for structural studies.
The field of biomedical research relies on the knowledge of binding interactions between various proteins of interest to create novel molecular targets for therapeutic purposes. While many of these interactions remain a mystery, knowledge of these properties and interactions could have significant medical applications in terms of understanding cell signaling and immunological defenses. Furthermore, there is evidence that machine learning and peptide microarrays can be used to make reliable predictions of where proteins could interact with each other without the definitive knowledge of the interactions. In this case, a neural network was used to predict the unknown binding interactions of TNFR2 onto LT-ɑ and TRAF2, and PD-L1 onto CD80, based off of the binding data from a sampling of protein-peptide interactions on a microarray. The accuracy and reliability of these predictions would rely on future research to confirm the interactions of these proteins, but the knowledge from these methods and predictions could have a future impact with regards to rational and structure-based drug design.
Arguably the most noteworthy result was its flourishing musical community. Composers and performers who had worked together in Prague prior to the war were able to continue to do so freely in ways that Jewish people were not allowed anywhere else in occupied Europe. They kept the musicians in Theresienstadt—delaying their deportations to Auschwitz—longer than almost anyone else in the camp, until the threat of Soviet liberation was imminent. This thesis aims to explore the lives and works of four Theresienstadt composers: Viktor Ullmann, Pavel Haas, Gideon Klein, and Hans Krása. All four of these artists were successful prior to the war, spent time in Theresienstadt, and were sent to Auschwitz on the same transport on October 16, 1944. Three of the four died in the gas chambers of Auschwitz, and Klein was sent on to the Fürstengrube concentration camp, where he was shot and killed in January 1945. These composers and their music should be remembered, studied, and performed, not only for historical and moral reasons, but also for artistic ones. Their works represent some of the finest music in the German tradition written during this period. In conjunction with this paper, I have arranged Gideon Klein’s String Trio—one of the pieces profiled here—for saxophone quartet. Members of the Arizona State University saxophone studio will perform it twice in April. I hope that the performances will help make audiences aware of the strength of the music that came out of Theresienstadt, and reinforce the fact that it remains highly relevant. In this thesis, the composers’ careers before and during their time in Theresienstadt will be traced, as well as the measures they took to preserve their music, their interactions with each other, and their efforts to use hidden messages in their music. It is hoped that this document will help fill an important gap in the history of European music in the twentieth century.
Apolipoprotein (ApoE) plays an important role in the transport of lipids in the brain for normal functioning. There are three different isoforms of ApoE which are coded for by three alleles (E2, E3, E4). Patients carrying at least one copy of ApoE E4 are known to be at higher risk for developing Alzheimer’s disease (AD) and earlier onset of symptoms. This is due to the buildup of amyloid plaques and neurofibrillary tangles of the brain from the accumulation of tau proteins, which are associated with the progression of Alzheimer’s disease. However, findings on ApoE E2 have shown that it may be a protective allele since it is linked to a decreased risk of formation of amyloid plaques and neurofibrillary tangles. To study this phenomenon within the context of a local population group, polymerase chain reaction and gel electrophoresis were conducted on extracted DNA samples. The principal goal in this research study was to genotype ApoE variants using single nucleotide polymorphism (SNP) specific primers, and polymerase chain reaction to analyze the frequency in the Tempe population to determine future healthcare needs.
