@phdthesis{Rotem2015,
  author    = {Rotem, Elam},
  title     = {Early Basso Continuo Practice: Implicit Evidence in the Music of Emilio de' Cavalieri},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-145696},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2015},
  abstract  = {In this work, Emilio de' Cavalieri's musical sources will serve as a platform in an attempt to overcome the lack of explicit original guidance and guidelines of performance practice of early basso continuo. It will offer a methodology that will allow the unraveling of implicit theory and practice hidden in the music sources themselves. The methodology of this work is based on the fact that Cavalieri's Rappresentatione di Anima e di Corpo (Rome, 1600) is printed using a unique continuo notation, which is detailed, precise, and coherent—more so than any other contemporaneous printed source. Through thorough investigation of this continuo notation, it will be possible to enrich our practical as well as theoretical knowledge of the early basso continuo. A wide range of evidences will emerge, covering a wide spectrum, from general questions of instrumentation up to the very notes that should be played. Using a special notation for illustration, I will demonstrate how Cavalieri's basso continuo figuration, when combined with the known rules of counterpoint, is at times equivalent to written-out realizations. As part of this study, different models of contrapuntal phenomena will be analyzed, mainly in the context of cadences but also in the context of other progressions that deserve to be recognized as formulas. Their theoretical structure will be uncovered as well as their actual application in music and their manner of execution. The prevalence of each phenomenon will be examined in order to distinguish common and recurrent phenomena from rarely-used formulas. In order to do this, and due to problematic historical terminology, it will be necessary to create a set of new terms inspired by Cavalieri's notation. Those terms will not be solely relevant to Cavalieri's music; the models were made flexible so that they may prove useful for future discussions or studies of early continuo in general. Out of the known early basso continuo sources, a "mini-compendium" of practical implications will be extracted in order to exhaust the practical knowledge implicit in them. This endeavor will be concluded with a list of rules and general advice drawn from the sources, but it will also reveal some problematic aspects of these sources. This endeavor will make it possible to compare the "new" implicit practical information deduced in this study with the explicit known continuo sources, and assess to what extant Cavalieri's continuo practices illuminate and complement the known knowledge from previously-studied yet opaque sources of basso continuo. The focus of this dissertation is on Cavalieri's music, but the findings proposed here will be traced so as to illuminate the broader realm of the early Baroque and the 17th century musical style at large. Finally, this new research about Cavalieri's music and continuo, along reevaluating of its place among the common continuo sources, calls for redistribution of source materials on the traditional "shelf" of early basso continuo sources.},
  language  = {en}
}
@phdthesis{Vona2014,
  author    = {Vona, Barbara C.},
  title     = {Molecular Characterization of Genes Involved in Hearing Loss},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-112170},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2014},
  abstract  = {The auditory system is an exquisitely complex sensory organ dependent upon the synchronization of numerous processes for proper function. The molecular characterization of hereditary hearing loss is complicated by extreme genetic heterogeneity, wherein hundreds of genes dispersed genome-wide play a central and irreplaceable role in normal hearing function. The present study explores this area on a genome-wide and single gene basis for the detection of genetic mutations playing critical roles in human hearing. This work initiated with a high resolution SNP array study involving 109 individuals. A 6.9 Mb heterozygous deletion on chromosome 4q35.1q35.2 was identified in a syndromic patient that was in agreement with a chromosome 4q deletion syndrome diagnosis. A 99.9 kb heterozygous deletion of exons 58-64 in USH2A was identified in one patient. Two homozygous deletions and five heterozygous deletions in STRC (DFNB16) were also detected. The homozygous deletions alone were enough to resolve the hearing impairment in the two patients. A Sanger sequencing assay was developed to exclude a pseudogene with a high percentage sequence identity to STRC from the analysis, which further solved three of the six heterozygous deletion patients with the hemizygous, in silico predicted pathogenic mutations c.2726A>T (p.H909L), c.4918C>T (p.L1640F), and c.4402C>T (p.R1468X). A single patient who was copy neutral for STRC and without pathogenic copy number variations had compound heterozygous mutations [c. 2303_2313+1del12 (p.G768Vfs*77) and c.5125A>G (p.T1709A)] in STRC. It has been shown that STRC has been previously underestimated as a hearing loss gene. One additional patient is described who does not have pathogenic copy number variation but is the only affected member of his family having hearing loss with a paternally segregating translocation t(10;15)(q26.13;q21.1). Twenty-four patients without chromosomal aberrations and the above described patient with an USH2A heterozygous deletion were subjected to a targeted hearing loss gene next generation sequencing panel consisting of either 80 or 129 hearing-relevant genes. The patient having the USH2A heterozygous deletion also disclosed a second mutation in this gene [c.2276G>T (p.C759F)]. This compound heterozygous mutation is the most likely cause of hearing loss in this patient. Nine mutations in genes conferring autosomal dominant hearing loss [ACTG1 (DFNA20/26); CCDC50 (DFNA44); EYA4 (DFNA10); GRHL2 (DFNA28); MYH14 (DFNA4A); MYO6 (DFNA22); TCF21 and twice in MYO1A (DFNA48)] and four genes causing autosomal recessive hearing loss were detected [GJB2 (DFNB1A); MYO7A (DFNB2); MYO15A (DFNB3), and USH2A]. Nine normal hearing controls were also included. Statistical significance was achieved comparing controls and patients that revealed an excess of mutations in the hearing loss patients compared to the control group. The family with the GRHL2 c.1258-1G>A mutation is only the second family published worldwide with a mutation described in this gene to date, supporting the initial claim of this gene causing DFNA28 hearing loss. Audiogram analysis of five affected family members uncovered the progressive nature of DFNA28 hearing impairment. Regression analysis predicted the annual threshold deterioration in each of the five family members with multiple audiograms available over a number of years.},
  subject      = {Molekularbiologie},
  language  = {en}
}
@phdthesis{Solanki2013,
  author    = {Solanki, Narendra},
  title     = {Novelty choice in Drosophila melanogaster},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-103219},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {This study explores novelty choice, a behavioral paradigm for the investigation of visual pattern recognition and learning of the fly Drosophila melanogaster in the flight simulator. Pattern recognition in novelty choice differs significantly from pattern recognition studied by heat conditioning, although both paradigms use the same test. Out of the four pattern parameters that the flies can learn in heat conditioning, novelty choice can be shown for height (horizontal bars differing in height), size and vertical compactness but not for oblique bars oriented at +/- 45°. Upright and inverted Ts [differing in their centers of gravity (CsOG) by 13°] that have been extensively used for heat conditioning experiments, do not elicit novelty choice. In contrast, horizontal bars differing in their CsOG by 13° do elicit novelty choice; so do the Ts after increasing their CsOG difference from 13° to 23°. This indicates that in the Ts the heights of the CsOG are not the only pattern parameters that matter for the novelty choice behavior. The novelty choice and heat conditioning paradigms are further differentiated using the gene rutabaga (rut) coding for a type 1 adenylyl cyclase. This protein had been shown to be involved in memory formation in the heat conditioning paradigm. Novelty choice is not affected by mutations in the rut gene. This is in line with the finding that dopamine, which in olfactory learning is known to regulate Rutabaga via the dopamine receptor Dumb in the mushroom bodies, is dispensable for novelty choice. It is concluded that in novelty choice the Rut cAMP pathway is not involved. Novelty choice requires short term working memory, as has been described in spatial orientation during locomotion. The protein S6KII that has been shown to be involved in visual orientation memory in walking flies is found here to be also required for novelty choice. As in heat conditioning the central complex plays a major role in novelty choice. The S6KII mutant phenotype for height can be rescued in some subsets of the ring neurons of the ellipsoid body. In addition the finding that the ellipsoid body mutants ebo678 and eboKS263 also show a mutant phenotype for height confirm the importance of ellipsoid body for height novelty choice. Interestingly some neurons in the F1 layer of the fan-shaped body are necessary for height novelty choice. Furthermore, different novelty choice phenotypes for different pattern parameters are found with and without mushroom bodies. Mushroom bodies are required in novelty choice for size but they are dispensable for height and vertical compactness. This special circuit requirement for the size parameter in novelty choice is found using various means of interference with mushroom body function during development or adulthood.},
  subject      = {Taufliege},
  language  = {en}
}