Thesis (Ph. D.)--University of Missouri--Columbia, 1997. / Typescript. Vita. Includes bibliographical references (leaves : 81-91). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2009. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May 2009" Includes bibliographical references.

Thesis (M. Phil.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 76-85).

Thesis (M.S.)--West Virginia University, 2010. / Title from document title page. Document formatted into pages; contains v, 46 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 43-46).

Thesis (Ph. D.)--Ohio State University, 2005. / Title from first page of PDF file. Includes bibliographical references (p. 137-161).

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2007. / Title from title screen (site viewed July 9, 2007). PDF text: xv, 147 p. : ill. UMI publication number: AAT 3249674. Includes bibliographical references. Also available in microfilm and microfiche formats.

Cigarette smoking (CS) represents the main causative agent underlying development and progress of COPD. Recently, involvement of CS in the pathogenesis of COPDassociated muscle abnormalities is becoming increasingly evident. Nevertheless, involved triggers and underlying mechanisms remain largely unknown. This study was conceived in order to examine effects of cigarette smoke exposure on skeletal muscle morphology, vascular supply and function. For this purpose, we have specifically designed murine COPD/emphysema model and gastrocnemius muscle was examined, while in vitro experiments were conducted using murine C2C12 skeletal muscle myocytes. In addition to the mild emphysematous changes present in the lungs of CS-exposed mice, our results demonstrated evident signs of muscle atrophy reflected by decreased fiber cross-sectional area, profound fiber size variation and reduced body mass. Furthermore, we have observed impairment in terminal myogenesis and lower number of myonuclei in skeletal muscles of CS-exposed animals despite evident activation of muscle repair process. Additionally, our results demonstrate capillary rarefaction in skeletal muscles of CS-exposed animals which was associated with deregulation of hypoxia-angiogenesis signaling, reduced levels of angiogenic factors such as HIF1-α and VEGF and enhanced expression of VHL and its partner proteins PHD2 and Ube2D1. The results of our in-vitro experiments demonstrated that VHL and its ubiquitination machinery can be synergistically regulated by TNF and hypoxia consequentially impairing angiogenic potential of skeletal muscle myocytes. Finally, we have shown that CS elicits chronic ER stress in murine skeletal muscles which is associated with activation of ERAD and apoptotic pathways as mirrored by elevated expression of Usp19, caspase 12 and caspase 3 in skeletal muscles of CSexposed animals. Moreover, molecular and morphological alterations in CS-exposed mice resulted in impairment of muscle function as reflected by their impaired exercise capacity. Taken together, from our results it is evident that cigarette smoke exposure elicits set of morphological, vascular and functional changes highly resembling those observed in COPD. Additionally, CS induces wide range of molecular alterations and signaling pathway deregulations suggesting profound effects of cigarette smoke exposure on skeletal muscle cell homeostasis.

Made available in DSpace on 2014-06-11T19:23:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-08-26Bitstream added on 2014-06-13T19:28:57Z : No. of bitstreams: 1 pinheiro_cm_me_arafcf.pdf: 768209 bytes, checksum: cba436e655065dfd90d0f20696a3bc21 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Universidade Estadual Paulista (UNESP) / O Diabetes mellitus é um dos mais importantes problemas de saúde pública, ocasionando complicações crônicas como a atrofia muscular e perda da qualidade de vida do paciente. Quando ocorre uma lesão articular, o músculo responde com um processo de atrofia onde é gerada uma modificação no tecido muscular funcionalmente relacionado com essa articulação. Contudo, estudos experimentais que contribuam ao esclarecimento da relação entre inflamação articular e as modificações histológicas e da expressão gênica do músculo de animais diabéticos não têm sido desenvolvidos. Outro parâmetro importante que deve ser estudado é a atividade da enzima creatina cinase (CK) uma vez que sua atividade pode ser alterada em função de várias causas como na injúria, distrofia, inflamação ou necrose da musculatura esquelética ou cardíaca. O presente projeto teve por objetivo estudar o efeito da inflamação aguda do tornozelo sobre os músculos Sóleo (SO) e Tibial Anterior (TA), investigando a presença de alterações histológicas, alterações na expressão gênica dos atrogenes atrogina-1e MuRF-1 e na atividade da creatina cinase em músculos de ratos não-diabéticos e diabéticos com e sem tratamento insulínico. Foram estudados 54 ratos Wistar (150g). A indução do diabetes foi por via intrapenitoneal com 50mg de estreptozotocina (STZ) por Kg de peso corporal, dissolvida em tampão citrato pH 4,5. Para a inflamação a articulação do tornozelo foi mantida em 90° localizando a fossa distal e posterior ao maléolo lateral, introduzindo nesta zona uma agulha de diâmetro 26 com 0.03ml carragenina a 3%. Os grupos de animais diabéticos com terapia insulínica foram tratados duas vezes ao dia (as 8h e 17h) com 2,5 U de insulina NPH durante 13 dias, totalizando 5U/dia A insulina foi administrada por via subcutânea... / Diabetes mellitus is one of the most serious public health problems, which diminishes the quality of life of the patient and leads to many chronic complications, one of which is muscle atrophy. When a joint is injured, the muscle responds with a process of atrophy in which a change occurs in the muscle tissue functionally related to the joint. However, no experimental studies have been carried out to clarify the relationship between joint inflammation and changes in the histology and gene expression of muscles in diabetic animals. Another important variable that should be studied is the activity of the enzyme creatine kinase (CK), since it can be altered under various conditions, such as injury, muscular dystrophy, inflammation or necrosis of skeletal or heart muscle. The aim of this project was to study the effect of acute inflammation of the ankle on the soleus (SO) and tibialis anterior (TA) muscles, by noting the histological changes, changes in the expression of the atrophy-related genes (atrogenes) atrogin-1 and MuRF-1 and activity of CK in muscles of non-diabetic and diabetic rats, treated and untreated with insulin. We studied 54 Wistar rats (150g). Diabetes was induced by intraperitoneal injection of 50mg streptozotocin (STZ) per kg body weight, dissolved in citrate buffer (pH 4.5). To induce inflammation, the ankle joint was held at 90°, with the fossa located distal and posterior to the lateral malleolus, and inserting a 26-gauge needle into this region, with 0.03mL of 3% carrageenan. The groups of insulin-treated diabetic animals were treated twice a day (at 8 am and 5 pm) by subcutaneous injection with... (Complete abstract click electronic access below)

Orientador: Iguatemy Lourenço Brunetti / Coorientador: Tania de Fatima Salvani / Banca: Thiago Luiz de Russo / Banca: Amanda Martins Baviera / Resumo: O Diabetes mellitus é um dos mais importantes problemas de saúde pública, ocasionando complicações crônicas como a atrofia muscular e perda da qualidade de vida do paciente. Quando ocorre uma lesão articular, o músculo responde com um processo de atrofia onde é gerada uma modificação no tecido muscular funcionalmente relacionado com essa articulação. Contudo, estudos experimentais que contribuam ao esclarecimento da relação entre inflamação articular e as modificações histológicas e da expressão gênica do músculo de animais diabéticos não têm sido desenvolvidos. Outro parâmetro importante que deve ser estudado é a atividade da enzima creatina cinase (CK) uma vez que sua atividade pode ser alterada em função de várias causas como na injúria, distrofia, inflamação ou necrose da musculatura esquelética ou cardíaca. O presente projeto teve por objetivo estudar o efeito da inflamação aguda do tornozelo sobre os músculos Sóleo (SO) e Tibial Anterior (TA), investigando a presença de alterações histológicas, alterações na expressão gênica dos atrogenes atrogina-1e MuRF-1 e na atividade da creatina cinase em músculos de ratos não-diabéticos e diabéticos com e sem tratamento insulínico. Foram estudados 54 ratos Wistar (150g). A indução do diabetes foi por via intrapenitoneal com 50mg de estreptozotocina (STZ) por Kg de peso corporal, dissolvida em tampão citrato pH 4,5. Para a inflamação a articulação do tornozelo foi mantida em 90° localizando a fossa distal e posterior ao maléolo lateral, introduzindo nesta zona uma agulha de diâmetro 26 com 0.03ml carragenina a 3%. Os grupos de animais diabéticos com terapia insulínica foram tratados duas vezes ao dia (as 8h e 17h) com 2,5 U de insulina NPH durante 13 dias, totalizando 5U/dia A insulina foi administrada por via subcutânea... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Diabetes mellitus is one of the most serious public health problems, which diminishes the quality of life of the patient and leads to many chronic complications, one of which is muscle atrophy. When a joint is injured, the muscle responds with a process of atrophy in which a change occurs in the muscle tissue functionally related to the joint. However, no experimental studies have been carried out to clarify the relationship between joint inflammation and changes in the histology and gene expression of muscles in diabetic animals. Another important variable that should be studied is the activity of the enzyme creatine kinase (CK), since it can be altered under various conditions, such as injury, muscular dystrophy, inflammation or necrosis of skeletal or heart muscle. The aim of this project was to study the effect of acute inflammation of the ankle on the soleus (SO) and tibialis anterior (TA) muscles, by noting the histological changes, changes in the expression of the atrophy-related genes (atrogenes) atrogin-1 and MuRF-1 and activity of CK in muscles of non-diabetic and diabetic rats, treated and untreated with insulin. We studied 54 Wistar rats (150g). Diabetes was induced by intraperitoneal injection of 50mg streptozotocin (STZ) per kg body weight, dissolved in citrate buffer (pH 4.5). To induce inflammation, the ankle joint was held at 90°, with the fossa located distal and posterior to the lateral malleolus, and inserting a 26-gauge needle into this region, with 0.03mL of 3% carrageenan. The groups of insulin-treated diabetic animals were treated twice a day (at 8 am and 5 pm) by subcutaneous injection with... (Complete abstract click electronic access below) / Mestre

Orientadores: Athanase Billis, Luciana Rodrigues de Meirelles / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas / Made available in DSpace on 2018-08-16T20:47:04Z (GMT). No. of bitstreams: 1 Brasil_AntonioAugustoAzevedoVital_M.pdf: 4698841 bytes, checksum: 5d8edbe0e4ce7ce977504d4197f2f985 (MD5) Previous issue date: 2010 / Resumo: A relação entre a atrofia inflamatória com a neoplasia intraepitelial alto grau e o carcinoma, é controversa. Tem sido sugerida uma relação topográfica e que o epitélio proliferativo da atrofia inflamatória possa progredir para neoplasia intraepitelial prostática alto grau (NIPAG) e/ou carcinoma (CA). O propósito do nosso estudo foi analisar em espécimes de prostatectomia radical uma possível relação topográfica entre estas lesões. Um total de 3186 quadrantes pertencentes a 100 prostatectomias radicais completamente representadas, foi analisado. Determinou-se a frequência de quadrantes mostrando: somente atrofia inflamatória (AI), AI+CA, AI+NIPAG, ou AI+NIPAG+CA. A extensão e a distância entre as lesões foram avaliadas através de um método semiquantitativo de contagem de pontos previamente descrito. Também foram analisados focos de atrofia completa ou parcial sem inflamação. Os métodos estatísticos empregados foram os testes de Kruskal-Wallis e Mann-Whitney, e o coeficiente de correlação de Spearman. A média dos quadrantes exibindo somente AI, AI+CA, AI+NIPAG, e AI+NIPAG+CA foi 3.29, 2.51, 0.77, e 0.44; e a amplitude (0-21), (0-11), (0-6), (0-4), respectivamente (p<0.01). A maioria dos focos de AI estavam a uma distância >5mm dos focos de NIPAG e CA. Não houve correlação significativa entre a extensão da AI (p= 0.64, r= 0.05) com a extensão da NIPAG. Houve uma significativa correlação negativa entre a extensão da AI (p=0.01, r=-0.27) com a extensão do CA. Resultados similares foram encontrados considerando focos de atrofia com ou sem inflamação. Focos de atrofia parcial não evidenciaram inflamação crônica inespecífica. Nosso estudo não evidenciou associação topográfica significativa entre AI, NIPAG e/ou CA / Abstract: It is controversial whether there is any relationship of proliferative inflammatory atrophy (PIA) to high-grade prostatic intraepithelial neoplasia (HGPIN) and cancer (CA). It has been suggested a topographic relation and a potential of the proliferative epithelium in PIA to progress to HGPIN and/or CA. The aim of this study was to analyze in radical prostatectomies a possible topographic relation of the lesions. A total of 3186 quadrants from 100 whole-mount consecutive surgical specimens was examined. The frequency of quadrants showing: only PIA, PIA+CA, PIA+HGPIN, or PIA+HGPIN+CA was determined. Extent and distance between the lesions were evaluated by a semiquantitative point-count method previously described. We also studied foci with partial or complete atrophy without inflammation. The statistical methods included the Kruskal-Wallis and the Mann-Whitney tests and the Spearman correlation coefficient. The mean (range) of quadrants showing only PIA, PIA+CA, PIA+HGPIN, and PIA+HGPIN+CA was 3.29 (0-21), 2.51 (0-11), 0.77 (0-6), and 0.44 (0-4), respectively (p<0.01). Most of the foci of PIA were significantly located in a distance >5mm than <5mm from HGPIN or CA. There was no significant correlation between extent of PIA (p=0.64, r=0.05) with extent of HGPIN. There was a significant negative correlation of extent of PIA (p=0.01, r=-0.27) with extent of CA. Similar results were found considering foci either with or without inflammation. Chronic inespecific inflammation was not seen in foci of partial atrophy. A topographic relation of PIA to HGPIN and/or CA was not supported by our study / Mestrado / Anatomia Patologica / Mestre em Ciências Médicas