Thesis (M.S.)--Florida State University, 2004. / Advisor: Dr. Jeanne Flannery, Florida State University, School of Nursing, Dept. of Graduate Studies. Title and description from dissertation home page (viewed Sept. 29, 2004). Includes bibliographical references.

Thesis (Ph. D.)--University of Canterbury, 2009. / Typescript (photocopy). "6 July 2009." Includes bibliographical references (p. [205]-224). Also available via the World Wide Web.

Thesis (M. Phil.)--University of Hong Kong, 2006. / Restricted as requested by author. Restricted access for 1 year 2007--03--28 ; approval pending. Also available online.

Thesis (M. Phil.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.

Thesis (Ph. D.)--Dept. of Exercise and Sport Science, University of Utah, 2006. / Includes bibliographical references (leaves [58]-68).

Thesis (Ph. D.)--University of Utah, 2006. / Includes bibliographical references (leaves [58]-68). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Orientador: Pedro Thadeu Galvão Vianna / Banca: Norma Sueli Pinheiro Módolo / Banca: Geraldo Rolim Rodrigues Junior / Banca: João Abrão / Banca: Eneida Maria Vieira / Resumo: A isquemia/reperfusão (I/R) provoca lesão nas células renais, que pode ser potencializada pela ocorrência de hiperglicemia, em ratos anestesiados com isoflurano. Sabe-se que a melatonina apresenta efeito protetor em órgãos, atuando nos produtos do estresse oxidativo. Os objetivos foram avaliar se a melatonina oferece proteção renal na I/R associada à hiperglicemia transitória e se potencializa a ação protetora do isoflurano. Foram estudados 36 ratos Wistar machos distribuídos, aleatoriamente, em seis Grupos: MH - Melatonina e Hiperglicemia; M - Melatonina; H - Hiperglicemia; I - Isoflurano SH - Sham e Hiperglicemia e S - Sham. Todos os ratos foram anestesiados com isoflurano em concentrações entre 1 a 3%. A pressão arterial média (PAM), a temperatura e saturação de oxigênio foram aferidas ao longo do experimento. Hiperglicemia foi induzida com 2,5 g.kg-1 de solução de glicose a 50% e a melatonina utilizada na dose de 20 mg.kg-1, ambas por via intraperitoneal. Todos os animais foram submetidos à nefrectomia direita. Nos grupos SH e S não houve isquemia. Os valores da glicemia (mg.dL-1) e da creatinina (mg.dL-1) foram obtidos através de coleta de sangue na artéria carótida em três momentos: após finalizada a dissecção da artéria carótida esquerda (M1), imediatamente antes da retirada do "clamp" da artéria renal esquerda (M2) e 24 horas após, imediatamente após a nefrectomia esquerda (M3), quando os animais retornaram ao laboratório foram anestesiados com a mesma técnica para coleta da última amostra sanguínea. O rim retirado foi preparado e enviado para análise histológica, realizada através da escala para avaliação da necrose tubular (0 a 5 = lesão máxima). Houve tratamento estatístico para os valores: peso, temperatura, saturação de oxigênio, PAM, glicose, creatinina e escore de lesão histológica. Não houve diferença entre o peso... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Ischemia/reperfusion (I/R) cause renal cell injury that may be worsened by hyperglycemia in rats anesthetized with isoflurane. N-acetyl-5- methoxytryptamine (melatonin) is known to have a protective effect on multiple organs by acting on the products of oxidative stress. The objectives of this study were to determine whether melatonin provides renal protection during I/R associated with transient hyperglycemia, and whether it enhances isoflurane protective action. Thirty-six Wistar male rats were randomly allocated into six groups: MH - hyperglycemia and melatonin; M - melatonin; H - hyperglycemia; I - isoflurane, SH - sham and hyperglycemia, and S - sham. All rats were anesthetized with isoflurane at concentrations of 1 to 3%. Mean arterial pressure (MAP), temperature and oxygen saturation were measured throughout the experiment. Hyperglycemia was induced by intraperitoneal 2.5 g.kg-1 of glucose solution at 50%, and 20 mg.kg-1 of melatonin. All animals underwent right side nephrectomy. There was no ischemia in groups SH and S. Glycemia (mg.dL-1) and creatinine (mg.dL-1) values were obtained through the collection of blood from the carotid artery at three time points: following anesthesia and dissection of the left carotid artery (M1), immediately before left renal artery declamping (M2), and 24 hours after the end of the experiment, immediately following left nephrectomy (M3), when the animals returned to the laboratory and were anesthetized by the same technique for the last blood collection. The kidney was removed for histologic analysis, which was performed using the tubular necrosis score system (0 to 5 = maximum lesion). Weight, temperature, oxygen saturation, MAP, glucose, creatinine and histologic lesion score values were statistically treated. No difference in weight, temperature and oxygen saturation were observed. MAP parameters showed statistically significant... (Complete abstract click electronic access below) / Doutor

Thesis (MTech (Biomedical Technology))--Cape Peninsula University of Technology, 2016. / Type 2 diabetes mellitus (T2DM) is a metabolic disorder which is characterised by insulin resistance, defective insulin secretion or both. The chronic state of hyperglycemia in diabetes is associated with microvascular complications and macrovascular complications which account for an estimated 80% of deaths as a result of cardiovascular complications. Type 2 diabetes mellitus is an inflammatory disease and pro- inflammatory stimuli in the form of activated endothelial cells, render the vascular endothelial surface attractive for both platelets and leukocytes. Activated platelets bind to the exposed extracellular matrix (ECM) and also to each other in both physiological haemostasis and pathological thrombosis. They can also adhere to leukocytes. Platelet leukocyte interactions are divided into 3 stages; these include the initiation of the interaction, stabilization of the aggregates and amplification of leukocyte activation. This study attempts to contribute to the current knowledge of T2DM by investigating the percentage of monocytes and neutrophils forming aggregates with platelets in pre-diabetes and diabetes and comparing this to non- diabetes individuals as well as the up regulation of pro-thrombotic and activation antigens on the surface of monocytes and neutrophils (Tissue Factor and CD69). Levels of platelet activation and function will be determined by both plate monocyte aggregates (PMA) and platelet neutrophil aggregates (PNA). A total of 124 individuals were recruited from Bellville South, Cape Town, South Africa. This comprised of diabetes (DM) (n=15), pre-diabetes (pre-T2DM) (n=25) and controls (n=84). All individuals were screened for diabetes using the oral glucose tolerance test (OGTT). Platelet leukocyte measurements were performed using the Navios 8-colour flow cytometer. The median percentage of circulating platelets bound to monocytes (%PMAs) was significantly increased in the T2DM 49.04[36.78-62] and the Pre-T2DM 48.96[36.72-61.2],groups, compared to the control group 7.2[5.4-9], p<0.0001. The median %PNAs, which show interactions between neutrophils and platelets, were significantly increased in the T2DM group 13.56[10.17-16.95] compared to the control group 6.01[4.51-7.51] p<0.0001. Platelet monocyte aggregates (PMAs) were higher in both the pre-T2DM and T2DM groups when compared to the control group indicating increased interactions between platelets and monocytes. In addition to forming aggregates with leukocytes, the platelets were able to initiate activation and phenotypic change to the leukocytes by increasing the expression of CD69 and TF (CD142). This finding provides further evidence that there is a link between the inflammatory process and the prothrombotic activity evident in diabetes and pre-diabetes individuals. Furthermore, we describe elevated levels of circulating activated neutrophils which directly correlate with increased PNA formation in both the pre-T2DM and T2DM group. / South African Medical Research Council

Orientador: Débora Cristina Damasceno / Resumo: Early embryos recovered from diabetic rats show increased number of blastomeres undergoing apoptosis and decreased total number of blastomeres, suggesting impaired litter size and newborn weight. This might increase the chances of metabolic disorders in adulthood of these animals. Since diabetes-induced hyperglycemia impairs the redox balance, the aim was to evaluate the embryonic oxidative stress status before the implantation in order to identify whether there are differences in levels of oxidative stress in early embryos from diabetic dams. Thus, we hypothesized the decreased cell number found in early embryos recovered from diabetic rats is due to the low embryonic ability to maintain their own redox balance. Our study shows that rats with streptozotocin-induced mild and severe diabetes present impaired redox status in early pregnancy. This maternal unbalance directly influences the embryonic redox status, reflecting the increased reactive oxygen species in the morula stage. We also showed that regardless of hyperglycemic level the embryos trigger defense mechanisms involved in the excessive free radical scavenging as an attempt to survive. Nevertheless, the success of this defense mechanism seems to depend on maternal hyperglycemia, highlighting the importance of the programmed pregnancy as well as appropriate medical care starting in early stages of human diabetic pregnancy. / Doutor

The prevailing paradigm is that cardiac ANG II is synthesized in the extracellular space from components of the circulating and/or local renin-angiotensin system. The recent discovery of intracrine effects of ANG II led us to determine whether ANG II is synthesized intracellularly in neonatal rat ventricular myocytes (NRVM). NRVM, incubated in serum-free medium, were exposed to isoproterenol or high glucose in the absence or presence of candesartan, which was used to prevent angiotensin type 1 (AT1) receptor-mediated internalization of ANG II. ANG II was measured in cell lysates and the culture medium, which represented intra- and extracellularly synthesized ANG II, respectively. Isoproterenol increased ANG II concentration in cell lysates and medium of NRVM in the absence or presence of candesartan. High glucose markedly increased ANG II synthesis only in cell lysates in the absence and presence of candesartan. Western analysis showed increased intracellular levels of angiotensinogen, renin, and chymase in high-glucose-exposed cells. Confocal immunofluorocytometry confirmed the presence of ANG II in the cytoplasm and nucleus of high-glucose-exposed NRVM and along the actin filaments in isoproterenol-exposed cells. ANG II synthesis was dependent on renin and chymase in high-glucose-exposed cells and on renin and angiotensin-converting enzyme in isoproterenol-exposed cells. In summary, the site of ANG II synthesis, intracellular localization, and the synthetic pathway in NRVM are stimulus dependent. Significantly, NRVM synthesized and retained ANG II intracellularly, which redistributed to the nucleus under high-glucose conditions, suggesting a role for an intracrine mechanism in diabetic conditions.