The objective of this dissertation is to evaluate how regulatory and market factors affect title insurance charges in different states. As substantial components of home purchase closing costs, title insurance charges have been controversial for decades, and both practitioners and analysts have pointed out apparent variations in title insurance charges among states. Although existing studies have suggested a set of regulatory and market factors as explanations for these among-state variations, empirical evaluations are limited. To fill in this gap, this dissertation empirically assesses whether these factors influence title insurance charges. The research outcomes of these dissertation indicate that after taking into account market factors such as services included in title insurance charges, title-related losses, property values, state populations, home sale volumes, housing prices, and income levels, regulation styles can still partially explain the title insurance charge variations in different states. In particular, states with promulgation regulation can have a higher average title insurance charge than states allowing free competition. This dissertation also tests whether regulation affects title insurance charges by influencing competition in the market and whether regulators' characteristics are related to the effect of regulation on charges. The test results imply that appointed commissioners can be associated with a higher average title insurance charge than elected commissioners. This dissertation provides insights into the title insurance regulatory reform in different states. More broadly, one methodology (multiple model for change) used in this dissertation simultaneously assesses regulation's over-time and state-by-state effects on title insurance charges, which contributes to the development of regulation evaluation methods. The outcomes of this dissertation can also provide empirical evidence to the theoretical debate of regulation versus competition. / text

Quantitative resistance is controlled by multiple genes and has been shown to be a durable form of resistance to pathogens affecting cultivated crops including soybeans (Glycine max L. Merr). Root rot of soybean caused by Phytophthora sojae ranks among the most damaging soybean diseases. Quantitative resistance has proven durable in soybean against P. sojae, however the molecular mechanisms underlying this form of resistance are still unknown. The objective of this project is to gain insight into molecular basis of quantitative resistance in the soybean-P. sojae pathosystem. The approach was to use global transcriptional profiling based on microarray technology to identify genes that were differentially expressed in four cultivars of soybeans with varying levels of quantitative resistance at different time points during infection by P. sojae. Our results provide a better understanding of the potential regulatory factors that may contribute to quantitative resistance during early hours of P. sojae infection. / Ph. D.

Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [72]-87).

No description available.

Dissertation (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2008. / Vita. Bibliography: p. 96-110.

Thesis (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2005. / Embargoed. Vita. Bibliography: 170-172.

Made available in DSpace on 2014-06-11T19:25:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2010-02-25Bitstream added on 2014-06-13T19:32:57Z : No. of bitstreams: 1 lima_arr_me_botfm.pdf: 825853 bytes, checksum: 593e370c7aa688abb20c1b7dda04672a (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Estudos clínicos e experimentais têm sugerido que anormalidades da musculatura esquelética podem colaborar para a ocorrência precoce de dispnéia e fadiga em pacientes com insuficiência cardíaca crônica. Em músculos periféricos e respiratórios, frequentemente observa-se modificação na composição das cadeias pesadas da miosina (MyHC) na insuficiência cardíaca. Os mecanismos e vias intracelulares de sinalização responsáveis pela alteração das MyHCs ainda não estão completamente definidos. Na insuficiência cardíaca direita induzida por monocrotalina, foi verificado que a expressão dos fatores de regulação miogênica está associada a alterações no fenótipo das MyHC. Recentemente, foi verificado que o fator de necrose tumoral-alfa (TNF-α) pode modular a expressão de proteínas miofibrilares. Não identificamos estudos que avaliaram o papel dos fatores de regulação miogênica e a influência do TNF-α na composição das MyHCs no músculo diafragma durante a insuficiência cardíaca. O objetivo deste estudo é determinar se modificações nas isoformas das MyHCs são selacionadas a alterações na expressão gênica dos fatores de regulação miogênica no músculo diafragma de ratos com infarto do miocárdio, com e sem insuficiência cardíaca. Adicionalmente, verificamos se as concentrações séricas de TNF-α e de IL-6 estão relacionadas a alterações das MyHCs e da expressão gênica dos fatores de regulação miogênica. Insuficiência cardíaca foi induzida pro infarto do miocárdio. Seis meses após a cirurgia, foram constituídos três grupos de animais: Sham (n=10), IM/IC- (animais infartados com disfunção ventricular e sem insuficiência cardíaca, n=10) e IM/IC+ (animais infartados com insuficiência cardíaca, n=10). As estruturas cardíacas e a função ventricular foram avaliadas por ecocardiograma... / Several clinial and experimental studies have suggested that skeletal muscle abnormalities can contribute to early fatigue and dyspnea in heart failure patients. Changes of myosin heavy chain (MyHC) isoforms have been frequently observed in peripheral and respiratory muscles during heart failure. Pathophysiological mechanisms and intracellular signaling pathways involved on MyHCs alterations are not completely defined. In monocrotaline-induced right heart failure, it was observed that the expression of myogenic regulatory factors is associated with MyHCs phenotype changes. Tumoral necrosis factor-alpha (TNF-α) has been recently described to modulate skeletal myofibril proteins. We did not find studies evaluating the influence of myogenic regulatory factors and TNF-α serum concentration on diaphragm MyHC isoforms during heart failure. In this study we tested the hypothesis that diaphragm MyHC isoforms changes are related to myogenic regulatory factors gene expression in chronic heart failure. Additionally, we measured TNF-α and interleukin-6 serum levels to examine their correlation with both MyHC isoforms and myogenic regulatory factors gene expression. A coronary ligation nodel was employed to induce heart failure. Six months after the surgical procedure, three groups of rats were studied: Sham (n=10), infarcted rats without heart failure (MI/HF-, n=10), and infarcted rats with heart failure (MI/HF+, n=10). Cardiac structures and ventricular function were assessed by transthoracic echocardiogram. MyHC isoforms were analyzed by protein electrophoresis. Muscle fiber cross-sectional area was measured in hematoxilin-eosin stained sections and in sections submitted to NADH-TR reaction. Myogenic regulatory factors miogenin, MyoD, and MRF4 gene expression was evaluated by real time RT-PCR; TNF-α and interleukin-6 serum levels werre quantified by... (Complete abstract click electronic access below)

Resumo: Estudos clínicos e experimentais têm sugerido que anormalidades da musculatura esquelética podem colaborar para a ocorrência precoce de dispnéia e fadiga em pacientes com insuficiência cardíaca crônica. Em músculos periféricos e respiratórios, frequentemente observa-se modificação na composição das cadeias pesadas da miosina (MyHC) na insuficiência cardíaca. Os mecanismos e vias intracelulares de sinalização responsáveis pela alteração das MyHCs ainda não estão completamente definidos. Na insuficiência cardíaca direita induzida por monocrotalina, foi verificado que a expressão dos fatores de regulação miogênica está associada a alterações no fenótipo das MyHC. Recentemente, foi verificado que o fator de necrose tumoral-alfa (TNF-α) pode modular a expressão de proteínas miofibrilares. Não identificamos estudos que avaliaram o papel dos fatores de regulação miogênica e a influência do TNF-α na composição das MyHCs no músculo diafragma durante a insuficiência cardíaca. O objetivo deste estudo é determinar se modificações nas isoformas das MyHCs são selacionadas a alterações na expressão gênica dos fatores de regulação miogênica no músculo diafragma de ratos com infarto do miocárdio, com e sem insuficiência cardíaca. Adicionalmente, verificamos se as concentrações séricas de TNF-α e de IL-6 estão relacionadas a alterações das MyHCs e da expressão gênica dos fatores de regulação miogênica. Insuficiência cardíaca foi induzida pro infarto do miocárdio. Seis meses após a cirurgia, foram constituídos três grupos de animais: Sham (n=10), IM/IC- (animais infartados com disfunção ventricular e sem insuficiência cardíaca, n=10) e IM/IC+ (animais infartados com insuficiência cardíaca, n=10). As estruturas cardíacas e a função ventricular foram avaliadas por ecocardiograma... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Several clinial and experimental studies have suggested that skeletal muscle abnormalities can contribute to early fatigue and dyspnea in heart failure patients. Changes of myosin heavy chain (MyHC) isoforms have been frequently observed in peripheral and respiratory muscles during heart failure. Pathophysiological mechanisms and intracellular signaling pathways involved on MyHCs alterations are not completely defined. In monocrotaline-induced right heart failure, it was observed that the expression of myogenic regulatory factors is associated with MyHCs phenotype changes. Tumoral necrosis factor-alpha (TNF-α) has been recently described to modulate skeletal myofibril proteins. We did not find studies evaluating the influence of myogenic regulatory factors and TNF-α serum concentration on diaphragm MyHC isoforms during heart failure. In this study we tested the hypothesis that diaphragm MyHC isoforms changes are related to myogenic regulatory factors gene expression in chronic heart failure. Additionally, we measured TNF-α and interleukin-6 serum levels to examine their correlation with both MyHC isoforms and myogenic regulatory factors gene expression. A coronary ligation nodel was employed to induce heart failure. Six months after the surgical procedure, three groups of rats were studied: Sham (n=10), infarcted rats without heart failure (MI/HF-, n=10), and infarcted rats with heart failure (MI/HF+, n=10). Cardiac structures and ventricular function were assessed by transthoracic echocardiogram. MyHC isoforms were analyzed by protein electrophoresis. Muscle fiber cross-sectional area was measured in hematoxilin-eosin stained sections and in sections submitted to NADH-TR reaction. Myogenic regulatory factors miogenin, MyoD, and MRF4 gene expression was evaluated by real time RT-PCR; TNF-α and interleukin-6 serum levels werre quantified by... (Complete abstract click electronic access below) / Orientador: Marina Politi Okoshi / Coorientador: Katashi Okoshi / Banca: Márcia Koike / Banca: Paula Schmidt Azevedo Gaiolla / Mestre

Orientador: Maeli Dal Pai Silva / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-05T10:23:42Z (GMT). No. of bitstreams: 1 Lopes_FrancisdaSilva_M.pdf: 7866898 bytes, checksum: ade20c607baab16a33f7564ca3630b10 (MD5) Previous issue date: 2005 / Resumo: A insuficiência cardíaca (IC) é caracterizada pela intolerância ao exercício físico, devido à fadiga precoce e à dispnéia. Entre as alterações que podem contribuir para a dispnéia nesta síndrome, tem sido descrita a miopatia diafragmática com atrofia e mudanças na miosina de cadeia pesada (MHC) do tipo II "rápida" para a do tipo I "lenta". Entretanto, os mecanismos regulatórios músculos específicos que alteram a expressão das isoformas de miosinas no diafragma durante a IC não são conhecidos. O objetivo do presente trabalho foi determinar, no músculo diafragma (DIA) de ratos Wistar com IC induzida por monocrotalina, se a transição da expressão protéica das MHCs está associada com alterações na expressão do RNAm dos fatores de regulação miogênicos (MRF). A região costal do diafragma de ratos Wistar machos (3-4 semanas de idade; 80-100g) dos grupos IC (n= 09) e Controle (CT; n= 06) foi estudada quando os sinais de IC estavam evidentes, aproximadamente 22 dias após a administração da monocrotalina nos animais IC. A expressão de MyoD e miogenina foi determinada através da técnica de RT-PCR enquanto que a expressão das MHCs foi estudada através de eletroforese por gel de poliacrilamida. Os animais com IC apresentaram diminuição tanto na expressão protéica da MHC Ila/llx quanto na expressão gênica de MyoD, sem alterar a expressão das MHCs I e IIb e da miogenina. Em conclusão, na IC, a alteração na expressão do RNAm da MyoD pode, em parte, explicar a alteração na expressão protéica da MHC Ilalllx / Abstract: Heart failure (HF) is characterized bya reduced tolerance to exercise due to early fatigue and dyspnea. Alterations that may contribute to dyspnea in this syndrome are diaphragmatic myopathy with atrophy and shift from type 11 "fast" to type I "slow" myosin heavy chain (MHC). However, the skeletal muscle-specific molecular regulatory mechanisms that alter MHC expression in the diaphragm during heart failure have not been defined. The purpose of this investigation was to determine whether myosin heavy chain expression during heart failure is associated with changes in myogenic regulatory factors (MRFs) mRNA expression in Wistar rat diaphragm with heart failure (HF) induced by monocrotaline. Costal diaphragm (DIA) muscle from HF (n=09) and control (n=06) 3-4 week old, 80-100g male Wistar rats was studied when overt HF had developed in the HF animais 22 days after monocrotaline administration. MyoD and myogenin expression were determined by RT-PCR, MHC isoform expression was determined by polyacrylamide gel electrophoresis. HF animais presented decreased myosin heavy chain lIa/llx protein isoform and MyoD gene expression content, without altering MHC I & IIb and myogenin expression. In summary, our results show that in HF, alterations in MyoD mRNA expression may, in part, explain alterations in MHC lIalllx content / Mestrado / Biologia Celular / Mestre em Biologia Celular e Estrutural

The general poor service delivery in municipalities raised the question of whether the incorporation of an intrapreneurship spirit might contribute in enhancing the effectiveness of service delivery in municipalities. The study aimed to examine whether intrapreneurship, if implemented within the O.R. Tambo District Municipality, can improve service delivery. The primary objective was to explore the intrapreneurship practices that can improve service delivery within the municipalities. A qualitative approach was used in the study. Twelve in-depth, semi-structured interviews were conducted with middle and top managers of the district municipalities. Intrapreneurship was then established to be a positive culture that could be adopted by municipalities to foster innovation and enable efficient and effective service delivery. The results of the study showed that, while there is a general appreciation for intrapreneurship, there are many factors that are working against the success of intrapreneurship in the municipality. These factors need to be addressed if an innovation and intrapreneurial culture is to be fostered in municipalities. The findings were used to develop a framework illustrating the municipality’s internal environment and intrapreneurship. / Business Management / M. Com. (Business Management)