This thesis explores the evolution of American Western narrative after the 1893 closing of the Western Frontier. Formerly representing a seemingly limitless fuel of symbolic growth, the frontier's closing threatened further national prosperity. Without new Western lands to conquer, narratives about the West began to be romanticized in a new way, selectively omitting non-Anglo narrative elements and presenting a more palatable West in the form of celebratory conquest. Ignoring its imperial roots, this new twentieth-century mythologization of the West became an increasingly ubiquitous narrative of America's honorable origins. Despite its ties to the perpetuation of empire, the pervasiveness of contemporary Western narratives remains largely benign in resonance, resulting in a past that is wholly severed from the present. Using a New Historicist approach, this study pairs literary works with cultural artifacts, tracking the role of Western narrative in the furtherance of empire. The first chapter examines Frederick J. Turner's "The Significance of the Frontier in American History" and Owen Wister's The Virginian (1902) as representatives of the new romanticization of the West. Chapter two looks at how Willa Cather's anti-spectacle novel, Death Comes for the Archbishop (1927), responds to the spectacle of Empire at early twentieth-century World's Fairs. The final chapter pairs Japanese-American Internment during World War II with Cormac McCarthy's All the Pretty Horses (1992), as a commentary on the oppressive rhetoric of western space.

As writer, essayist, environmentalist, and westerner, Wallace Earle Stegner (1909-1993) confronted what he understood to be an imagined and literal American West constructed by myths of frontier conquest, pioneer settlement in and transformation of the western landscape, and cowboy exceptionalism that erased an historical legacy of hardship, failure, and destruction of land and people, and also a West constructed by Eastern publishers and literary critics who diminished western American literature to local color writing. In Wolf Willow: A History, a Story, and a Memory of the Last Plains Frontier (1962), Stegner uses fiction, history, and memoir to engage the mythic West's silencing of his family's failed homesteading experiences in a specific western place and the relationship of his childhood and adult selves to this place, to its history, to experiences there, and to the cultural myths that characterize his western past and present and position the West as a symbolic container of hope, opportunity, and reward for the individual and America. In an historicized western place and from childhood experiences, Stegner locates an Other western narrative and an authentic western voice that disrupts the monomythic voice and values that are out of touch not only with a modern, multicultural, urban West but also with a rural West. <br>Coming after Wolf Willow, a series of essays--"Born a Square" (1964), "On the Writing of History" (1965), and "History, Myth, and the Western Writer" (1967), reprinted in the popular The Sound of Mountain Water (1969)-- present Stegner's new theory of western American literature that re-visions the West's literary heritage and reclaims the western story, what he called "another kind of western story-telling" that engages both the present and the past Wests, acknowledges past crimes against racial others and against western lands, promotes a sense of hope for a native western art, and raises America's consciousness of the personal, environmental, and cultural costs of adhering to the metanarratives of the culturally dominant mythic West of formula fiction, Hollywood films, and television series of the 1940s through 1960s. While Stegner scholars have examined the essays independently and deem them important to Stegner's works and to the trajectory of western American literature in the 1970s forward, no study has undertaken an extended analysis of these three essays in relation to Wolf Willow to argue, as this dissertation does, that Wolf Willow contains in germinal form the foundation of Stegner's realist, place-based, and historicist theoretical construct for western American literature he advocated for in the 1960's essays. / McAnulty College and Graduate School of Liberal Arts / English / PhD / Dissertation

Orientador: Miguel Arcanjo Areas / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-15T14:53:44Z (GMT). No. of bitstreams: 1 Ramos_LuizAlbertoFerreira_M.pdf: 1275435 bytes, checksum: f06c87a51cddb170d7e8f43b748231ce (MD5) Previous issue date: 2010 / Resumo: A Hipertensão Arterial Pulmonar (HAP) é uma patologia caracterizada pelo aumento da resistência dos vasos pulmonares, aumento na pressão Arterial pulmonar e hipertrofia do ventrículo direito, prejudicando as trocas gasosas alveolares e a função cardíaca. Por outro lado, a melatonina (N-Acetil-5- metoxitriptamina), o principal hormônio produzido pela glândula pineal, pode reduzir o tônus do músculo liso vascular promovendo redução da resistência periférica e, consequentemente, diminuição da pressão arterial em ratos hipertensos. O objetivo deste trabalho foi avaliar o efeito da melatonina sobre parâmetros cardiovasculares de ratos portadores de HAP induzida por monocrotalina. Ratos Wistar adultos pesando com 250g foram distribuídos em quatro grupos experimentais (n=5): CO (controle); CML (controle melatonina); MT (monocrotalina); MTML (monocrotalina+melatonina). A HAP foi induzida pela administração de dose única de monocrotalina (60 mg/kg i.p.) no primeiro dia de experimento. Melatonina (15 mg/kg i.p.) foi administrada diariamente, durante os 28 dias do período experimental. Os animais foram anestesiados (ketamina 100 mg/kg + xilazina 7 mg/kg de peso corpóreo i.m.) para a obtenção de parâmetros eletrocardiográficos e avaliação da pressão arterial e, posteriormente foram submetidos à eutanásia por aprofundamento anestésico, para o estudo da reatividade vascular e para análise histológica do coração e pulmões. Os resultados mostraram que melatonina reduziu significativamente a resposta contrátil da artéria pulmonar em relação aos ratos controles e portadores de HAP para resposta mínima da reatividade vascular à noradrenalina. A análise histológica mostrou que a melatonina aumentou significativamente a área do lúmen das artérias pré-acinares pulmonares e a área alveolar do grupo MTML, em relação ao grupo MT, o qual apresentou valores significativamente reduzidos, em relação ao grupo CO. Além disso, a melatonina proporcionou nos animais tratados com monocrotalina menor desvio do eixo elétrico para a direita em consequência, provavelmente, do menor grau de hipertrofia ventricular direita o que acarretou em redução do intervalo QT e, consequentemente, na prevenção do risco de morte súbita decorrente das alterações cardíacas desencadeadas pela hipertensão arterial pulmonar. Melatonina, também, preveniu a redução da pressão arterial média nos animais cuja oxigenação tecidual encontrava-se, provavelmente, prejudicada pelas alterações pulmonares e cardíacas induzidas pela monocrotalina. Concluindo, melatonina atenuou os efeitos deletérios da monocrotalina sobre parâmetros cardiovasculares e pulmonares neste modelo de hipertensão arterial pulmonar / Abstract: Pulmonary arterial hypertension (PAH) is a disease characterized by increased pulmonary vascular resistance, increased pulmonary arterial pressure and right ventricular hypertrophy and impairs alveolar gas exchange and cardiac function. Moreover, melatonin (N-acetyl-5-metoxytryptamine), the main hormone produced by the pineal gland can reduce the tone of vascular smooth muscle was a reduction in peripheral resistance and thus lowering blood pressure in hypertensive rats. The objective of this study was to evaluate the effect of melatonin on cardiovascular parameters of rats with monocrotaline-induced PAH. Male Wistar rats weighing 250g were divided into four experimental groups (n = 5): CO (control), CML (control melatonin), MT (monocrotaline), MTML (monocrotaline + melatonin). PAH was induced by administration of single dose of monocrotaline (60 mg / kg ip) on the first day of the experiment. Melatonin (15 mg / kg ip) was administered daily for 28 days trial period. The animals were anesthetized (Ketamine 100 mg / kg + xylazine 7 mg / kg body weight im) to obtain electrocardiographic parameters and blood pressure evaluation and later euthanized by deep anesthesia, to study the vascular reactivity and for histological analysis of the heart and lungs. The results showed that melatonin significantly reduced the contractile response of pulmonary artery and control rats with PAH for maximum response of vascular reactivity to norepinephrine. Histological analysis showed that melatonin significantly increased the lumen area of the pre-acinar pulmonary alveolar area and the group's HTML, for the TM group, which had significantly reduced compared to the CO group. Moreover, melatonin delivered in animals treated with monocrotaline minor electrical axis deviation to the right as a result, probably the lowest degree of right ventricular hypertrophy which resulted in a reduction of the QT interval and thus to prevent the risk of sudden death due of cardiac abnormalities triggered by pulmonary arterial hypertension. Melatonin also prevented the reduction in mean arterial pressure in animals in which tissue oxygenation was, probably affected by changes in pulmonary and cardiac changes induced by monocrotaline. In conclusion, melatonin attenuated the deleterious effects of monocrotaline on cardiovascular parameters in this model of pulmonary arterial hypertension / Mestrado / Fisiologia / Mestre em Biologia Funcional e Molecular

Orientador: Miguel Arcanjo Areas / Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-25T17:57:02Z (GMT). No. of bitstreams: 1 Ramos_LuizAlbertoFerreira_D.pdf: 4150802 bytes, checksum: 044f485e191cccd920c14229719c65ce (MD5) Previous issue date: 2014 / Resumo: A Hipertensão Arterial Pulmonar (HAP) é uma patologia caracterizada pelo aumento da resistência dos vasos pulmonares, aumento da pressão arterial pulmonar e hipertrofia do ventrículo direito do coração, prejudicando as trocas gasosas alveolares e a função cardíaca. Por outro lado, a melatonina (N-Acetil-5-metoxitriptamina), hormônio produzido principalmente pela glândula pineal, diminui o tônus do músculo liso vascular promovendo redução da resistência periférica, assim como efeito cardioprotetor devido a sua ação antioxidante. O objetivo deste trabalho foi avaliar o provável efeito cardioprotetor da melatonina em ratos portadores de HAP. A HAP foi induzida pela administração de dose única de monocrotalina (60mg/kg ip) no primeiro dia do período experimental. Após os primeiros 15 dias, tempo necessário à instalação da HAP, melatonina (10mg/kg ip) foi administrada diariamente, durante 13 dias. Os animais foram distribuídos em quatro grupos experimentais (n=5): CO (controle); MEL (controle melatonina); MCT (monocrotalina); MCT+MEL (monocrotalina+melatonina). Ao final do período experimental de 28 dias, os animais foram anestesiados (ketamina 100mg/kg + xilazina 7mg/kg de peso i.m) para a determinação de parâmetros eletrocardiográficos e da Variabilidade da Frequência Cardíaca (VFC). Posteriormente, foram submetidos à eutanásia, por aprofundamento anestésico, obtendo-se o coração para a determinação de biomarcadores cardíacos, enzimas antioxidantes do tecido cardíaco, parâmetros hemodinâmicos e análise histológica das artérias coronárias do ventrículo direito. Os resultados do ECG mostraram que a melatonina, nos animais portadores de HAP, minimizou as alterações na frequência cardíaca, na despolarização atrial e ventricular, assim como nos parâmetros indicativos de risco de morte súbita. Além disso, melatonina reduziu a hipertrofia ventricular direita, preveniu o aumento da espessura da camada média das artérias coronárias e aumentou a atividade das enzimas antioxidantes do coração dos animais portadores de HAP, o que pode ter contribuído para a ausência dos eventos do ECG indicativos de isquemia miocárdica, como observados no grupo MCT. Quanto aos aspectos hemodinâmicos, melatonina preveniu a redução da pressão arterial média, da pressão sistólica e do índice de relaxamento ventricular melhorando, assim, a função sistólica e diastólica dos animais estudados. Em conclusão, melatonina exerceu efeito protetor contra as alterações cardíacas decorrentes da hipertensão arterial pulmonar induzida pela monocrotalina / Abstract: Pulmonary Arterial Hypertension (PAH) is a disease characterized by increased pulmonary vascular resistance, higher pulmonary artery pressure and right ventricular hypertrophy of the heart and impairs alveolar gas exchange and cardiac function. Furthermore, melatonin (N-acetyl-5-methoxytryptamine) is a hormone produced primarily by the pineal gland, which decreases the tone of vascular smooth muscle promoting a reduction in peripheral resistance, as well as cardioprotective effect due to its antioxidant action. The objective of this study was to evaluate the probable cardioprotective effect of melatonin in rats with PAH. PAH was induced by administration of a single dose of monocrotaline (60mg/kg ip) on the 1st day of the experimental period. After 15 days, the time needed to install the HAP melatonin (10mg/kg i.p.) was administered daily further 13 days. The animals were divided into four experimental groups (n = 5): CO (control); MEL (control melatonin); MCT (monocrotaline); MCT + MEL (monocrotaline + melatonin). At the end of the experimental period (28 days), the animals were anesthetized (100mg/kg ketamine + xylazine 7mg/kg weight i.m.) to determine the ECG parameters and Heart Rate Variability (HRV). The animals were subsequently euthanized by deep anesthesia, give the hearts were resected to determine the cardiac biomarkers, antioxidant enzymes in cardiac tissue, hemodynamic parameters and the histological analysis of the coronary arteries were from the right ventricle. The ECG results showed that melatonin, in PAH rats, reduced changes in heart rate, atrial and ventricular depolarization, as well as in parameters indicative of risk of sudden death. Moreover, melatonin reduced the right ventricular hypertrophy, prevented the increase in medial thickness of the coronary arteries, increasing the activity of antioxidant enzymes in the heart of PAH animals, which may have contributed to the absence of ECG events indicative of myocardial ischemia, as observed in the MCT group. Regarding hemodynamic aspects melatonin prevented the reduction in mean arterial pressure, systolic pressure and left ventricular relaxation rate, thereby improving systolic and diastolic function in the animals studied. In conclusion, melatonin exerted a protective effect against heart changes resulted from monocrotaline-induced pulmonary hypertension / Doutorado / Fisiologia / Doutor em Biologia Funcional e Molecular

Thesis (M.A.)--University of Montana, 2007. / Title from title screen. Description based on contents viewed Oct. 5, 2007. Includes bibliographical references (p. 61-64).

Orientadores: Denise Vaz de Macedo, Dagmar Ruth Stach-Machado / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-15T21:15:50Z (GMT). No. of bitstreams: 1 Ferrucci_DaniloLopes_M.pdf: 1810214 bytes, checksum: 4728c1ea4c33f76583148c1588199a23 (MD5) Previous issue date: 2018-08-15T18:15:37Z / Resumo: Os músculos esqueléticos são constituídos por fibras musculares e pela matriz extracelular. Em resposta ao exercício, o músculo apresenta a habilidade de transformar o estresse mecânico da contração muscular em adaptações de cunho biológico, a esse processo deu-se o nome de mecanotransdução. Embora pouco se saiba sobre a importância da matriz extracelular como mecanoreceptor, trabalhos anteriores mostram que o exercício pode causar alterações na expressão e atividade das metaloproteinases, que podem resultar em modificações na matriz extracelular. Nesse contexto, as MMPs são vistas como pivôs centrais e, através da degradação da matriz extracelular podem gerar fragmentos protéicos com funções distintas das proteínas integras, liberando ainda citocinas e fatores de crescimento associados à matriz, que em interação com receptores celulares fornecem informações à célula sobre o microambiente extracelular, regulando o comportamento e adaptação do tecido. O objetivo do presente estudo foi avaliar o efeito de três sessões diárias de exercício exaustivo, realizados com diferentes pausas recuperativas entre as sessões, grupo E1(1h) e grupo E2 (3h), durante 6 dias consecutivos, na expressão das MMPs 2 e 9 e dos TIMPs 1 e 2; e nas concentrações e atividade biológica das MMPs nas porções vermelha (GV) e branca (GB) do músculo Gastrocnêmio de ratos Wistar. Os animais foram sacrificados após 1°, 3° e 6° dias de exercício e os fragmentos coletados do músculo gastrocnêmio foram analisados via ELISA, zimografia e qRT-PCR. Como controle (C) do protocolo experimental utilizou-se ratos sedentários. Os animais exercitados (E) mostraram aumento de desempenho a partir do 4° dia. Não houve diferença significativa na perfomance dos grupos E1 e E2. Os genes analisados mostraram-se igualmente expressos em resposta ao exercício em ambas as porções do músculo gastrocnêmio, contudo, o grupo E1 apresentou alterações mais acentuadas do que E2 para todos os biomarcadores analisados. O grupo E1 mostrou aumento na expressão das MMPs 2 e 9 no 3° dia de exercício, em ambas as regiões do músculo gastrocnêmio. Com relação aos TIMPs 1 e 2, os dados obtidos demonstram o aumento na expressão no GV e GB em resposta ao exercício (E1 e E2), em todos os tempos experimentais analisados. Todavia esse aumento foi mais acentuado para o grupo E1. A concentração total de MMP-2 nos grupos e E1 e E2 mostrou-se diminuída em todos os períodos analisados, para GV e GB. A atividade das isoformas latente e intermediária da MMP-2 apresentou-se diminuída em ambos os grupos exercitados no GB e apenas no grupo E1 para o GV. A atividade e concentração da MMP-9 não foram detectadas neste estudo. O protocolo agudo utilizado nesse estudo induziu um aumento significativo no desempenho dos animais, independente do tempo de pausa entre as sessões. O efeito adaptativo observado nas MMPs 2 e 9 em GV e GB foi de diminuição quantitativa e qualitativa. Possivelmente o aumento significativo na expressão gênica tanto das MMPs quanto TIMPs no grupo E1, permitiu um remodelamento acelerado na matriz extracelular do tecido, que possibilitou a melhora significativa no desempenho a partir do 3° dia. Considerando que ambos os tempo de pausa foram igualmente eficientes para aumentar a performance, seria melhor utilizar uma pausa de 3h entre as sessões, pois o processo de sinalização de síntese protéica demanda grande quantidade de energia, e depende da oferta de nutrientes em quantidade e qualidade adequada para a resposta / Abstract: Skeletal muscles are composed by muscle fibers and extracellular matrix. In response to exercise, muscles have the ability to transform mechanical stress from their contraction in biological adaptations, and, this process was called echanotransduction. Although little is known about the importance of the extracellular matrix acting as mechanoreceptors in this process, previous studies have shown that exercise can cause changes in the MMPs genetic expression and activity on the extracellular matrix. In this context, MMPs play the central role, once that the extracellular matrix degradation can generate fragments that are bioactive compounds and can interact with cell receptors to provide information regarding to extracellular microenvironment to the cells. Therefore, MMPs can regulate the behavior and adaptation of the muscle. The aims of this study were to evaluate the effect of three daily sessions of exhaustive exercise (performed with different recuperative breaks between sessions for six consecutive days) on the MMP-2, MMP-9 and tissue inhibitors of metalloproteinases 1 and 2 (TIMPs) gene expression, as well as, MMP's concentration and biological activities on the rat gastrocnemius muscle red (RG) and white (WG) portions. The animals were sacrificed on exercise-days 1, 3 and 6 and muscle fragments were collected and stored for later analysis through zymography, ELISA and qRT-PCR. Sedentary rats were used as controls. The exercised animals (E) showed an increased performance from the 4th day (p <0.05). There was no statistical difference between the performance of E1 and E2 groups. The genes examined were similarly expressed in response to exercise on the analyzed muscle regions, however, the group E1 have more pronounced changes than E2 when these biomarkers was analyzed. The E1 showed an increased expression of MMP-2 and -9 on the 3rd day of exercise comparing to the control group for RG e WG. Regarding TIMPs 1 and 2, our data showed an increase on their expression in RG and WG responsive to exercise (E1 and E2) during all time experimental points, but this increase was more pronounced in group E1. Furthermore, total concentration of MMP-2 in both groups was significantly reduced when compared to sedentary animals for all time points and muscle regions. The activity of latent and intermediate MMP-2 isoforms were significantly reduced in both exercised groups in the WG and, only, in the E1 to the RG. MMP-9 concentration and activities were not detected in this study. The acute protocol designed for this study induced an increase in the animal performances, regardless of the pauses employed between sessions. The adaptive effect observed in MMP-2 and 9 in the RG and WG was reduced quantitatively and qualitatively, due to the increased expression of both MMPs and TIMPs in group E1 leading to an accelerated remodeling the gastrocnemius extracellular matrix, allowing a significant improvement on performance since the third day onwards. Considering that both rest periods were equally effective to improve physical performance, rest periods of 3 hours between sessions are more adequate due to processes of protein synthesis, once that demands a great amount of energy and depends on the supply of nutrients in quantity and quality suitable for the positive response / Mestrado / Bioquimica / Mestre em Biologia Funcional e Molecular

Thesis (Ph. D.)--Ohio State University, 2006. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2009 Jun 15

No description available.