Structure and classification of zoophytes. By James D. Dana.

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Financial structure choice in owner-managed firms : entrepreneurial characteristics, utility of control, and the competitive context

Magdeburg, Univ., Fak. für Wirtschaftswiss., Diss., 2011

Duke Activity Status Index em Doenças Cardiovasculares: Validação de Tradução em Português

Fundamentos: O Duke Activity Status Index (DASI) avalia a capacidade funcional de pacientes com doença cardiovascular (DCV), mas não há versão validada em português para doenças cardiovasculares. Objetivos: Traduzir e adaptar culturalmente o DASI para o idioma português do Brasil, e verificar suas propriedades psicométricas na avaliação da capacidade funcional de pacientes com doenças cardiovasculares. Métodos: O DASI foi traduzido para o português, verificado pela retrotradução para o inglês e avaliado por um comitê de especialistas. A versão pré-teste foi avaliada pela primeira vez em 30 indivíduos. As propriedades psicométricas e a correlação com o teste de esforço foram verificadas em um segundo grupo de 67 indivíduos. Uma análise fatorial exploratória foi realizada em todos os 97 pacientes para verificar a validade de construto do DASI. Resultados: O coeficiente de correlação intraclasse para a confiabilidade teste-reteste foi de 0,87 e para a confiabilidade entre avaliadores foi de 0,84. O alfa de Cronbach para consistência interna foi de 0,93. A validade concorrente foi verificada por correlações positivas significativas de pontuações do DASI com o VO2 max (r = 0,51, p < 0,001). A análise fatorial mostrou dois fatores que explicaram 54% da variância total, com o fator 1 responsável por 40 % da variância. A aplicação do DASI requer entre um e três minutos e meio por paciente. Conclusão: A versão brasileira do DASI parece ser um instrumento válido, confiável, rápido e fácil de administrar para avaliar a capacidade funcional em pacientes com doenças cardiovasculares.

Obesity does not Lead to Imbalance Between Myocardial Phospholamban Phosphorylation and Dephosphorylation

Background: The activation of the beta-adrenergic system promotes G protein stimulation that, via cyclic adenosine monophosphate (cAMP), alters the structure of protein kinase A (PKA) and leads to phospholamban (PLB) phosphorylation. This protein participates in the system that controls intracellular calcium in muscle cells, and it is the primary regulator of sarcoplasmic reticulum calcium pump activity. In obesity, the beta-adrenergic system is activated by the influence of increased leptin, therefore, resulting in higher myocardial phospholamban phosphorylation via cAMP-PKA. Objective: To investigate the involvement of proteins which regulate the degree of PLB phosphorylation due to beta-adrenergic activation in obesity. In the present study, we hypothesized that there is an imbalance between phospholamban phosphorylation and dephosphorylation, with prevalence of protein phosphorylation. Methods: Male Wistar rats were randomly distributed into two groups: control (n = 14), fed with normocaloric diet; and obese (n = 13), fed with a cycle of four unsaturated high-fat diets. Obesity was determined by the adiposity index, and protein expressions of phosphatase 1 (PP-1), PKA, PLB, phosphorylated phospholamban at serine16 (PPLB-Ser16) were assessed by Western blot. Results: Obesity caused glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hyperleptinemia and did not alter the protein expression of PKA, PP-1, PLB, PPLB-Ser16. Conclusion: Obesity does not promote an imbalance between myocardial PLB phosphorylation and dephosphorylation via beta-adrenergic system.

Lipoprotein (a): Structure, Pathophysiology and Clinical Implications

The chemical structure of lipoprotein (a) is similar to that of LDL, from which it differs due to the presence of apolipoprotein (a) bound to apo B100 via one disulfide bridge. Lipoprotein (a) is synthesized in the liver and its plasma concentration, which can be determined by use of monoclonal antibody-based methods, ranges from < 1 mg to > 1,000 mg/dL. Lipoprotein (a) levels over 20-30 mg/dL are associated with a two-fold risk of developing coronary artery disease. Usually, black subjects have higher lipoprotein (a) levels that, differently from Caucasians and Orientals, are not related to coronary artery disease. However, the risk of black subjects must be considered. Sex and age have little influence on lipoprotein (a) levels. Lipoprotein (a) homology with plasminogen might lead to interference with the fibrinolytic cascade, accounting for an atherogenic mechanism of that lipoprotein. Nevertheless, direct deposition of lipoprotein (a) on arterial wall is also a possible mechanism, lipoprotein (a) being more prone to oxidation than LDL. Most prospective studies have confirmed lipoprotein (a) as a predisposing factor to atherosclerosis. Statin treatment does not lower lipoprotein (a) levels, differently from niacin and ezetimibe, which tend to reduce lipoprotein (a), although confirmation of ezetimibe effects is pending. The reduction in lipoprotein (a) concentrations has not been demonstrated to reduce the risk for coronary artery disease. Whenever higher lipoprotein (a) concentrations are found, and in the absence of more effective and well-tolerated drugs, a more strict and vigorous control of the other coronary artery disease risk factors should be sought.

Entwurf, Entwicklung und Optimierung von kompakten HF-Mikrostreifen-Filtern mittels "Defected Ground Structure"-Technik (DGS)

Magdeburg, Univ., Fak. für Elektrotechnik und Informationstechnik, Diss., 2010

Left Atrial Volume Index and Prediction of Events in Acute Coronary Syndrome: Solar Registry

Background: According to some international studies, patients with acute coronary syndrome (ACS) and increased left atrial volume index (LAVI) have worse long-term prognosis. However, national Brazilian studies confirming this prediction are still lacking. Objective: To evaluate LAVI as a predictor of major cardiovascular events (MCE) in patients with ACS during a 365-day follow-up. Methods: Prospective cohort of 171 patients diagnosed with ACS whose LAVI was calculated within 48 hours after hospital admission. According to LAVI, two groups were categorized: normal LAVI (≤ 32 mL/m2) and increased LAVI (> 32 mL/m2). Both groups were compared regarding clinical and echocardiographic characteristics, in- and out-of-hospital outcomes, and occurrence of ECM in up to 365 days. Results: Increased LAVI was observed in 78 patients (45%), and was associated with older age, higher body mass index, hypertension, history of myocardial infarction and previous angioplasty, and lower creatinine clearance and ejection fraction. During hospitalization, acute pulmonary edema was more frequent in patients with increased LAVI (14.1% vs. 4.3%, p = 0.024). After discharge, the occurrence of combined outcome for MCE was higher (p = 0.001) in the group with increased LAVI (26%) as compared to the normal LAVI group (7%) [RR (95% CI) = 3.46 (1.54-7.73) vs. 0.80 (0.69-0.92)]. After Cox regression, increased LAVI increased the probability of MCE (HR = 3.08, 95% CI = 1.28-7.40, p = 0.012). Conclusion: Increased LAVI is an important predictor of MCE in a one-year follow-up.

Isothermal drying of pore networks : influence of pore structure on drying kinetics

Drying of porous media, pore network, pore structure, capillary forces, viscous forces, drying kinetics