970 resultados para D-GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE
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The biosynthesis of (2S)-2-methyl-2-(4'-methyl-3-pentenyl)-8-(3-methyl-2-butenyl)-2H-1-benzopyran-6-carboxylic acid (gaudichaudianic acid), the major metabolite in leaves and roots of Piper gaudichaudianum Kunth (Piperaceae), has been investigated employing [1(-13) C]-D-glucose as precursor. The labelling pattern in the isolated gaudichaudianic acid was determined by quantitative 13 C NMR spectroscopy analysis and was consistent with involvement of both mevalonic acid and 2-C-methyl-D-erythritol-4-phosphate pathways in the formation of the dimethylallyl- and geranyl-derived moieties. The results confirmed that both plastidic and cytoplasmic pathways are able to provide isopentenyl diphosphate units for prenylation of p-hydroxybenzoic acid. (c) 2007 Elsevier Ltd. All rights reserved.
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Statement of problem. There are few studies on titanium casting shrinkage, and phosphate-bonded investments for titanium casting have not produced appropriate marginal fit.Purpose. The purpose of this study was to determine the thermal shrinkage of titanium and the setting and thermal expansion of 3 phosphate-bonded investments.Material and methods. The thermal shrinkage between the melting temperature and room temperature was calculated using a titanium thermal expansion coefficient. The thermal and setting expansion were measured for 3 phosphate bonded investments: Rematitan Plus (RP) specific for titanium, Rema Exakt (RE), and Castorit Super C (CA), using different special liquid concentrations (100%, 75%, and 50%). Setting expansion was measured for cylindrical specimens 50 mm long x 8 mm in diameter with a transducer. The heating and cooling curves were obtained with a dilatometer (DIL 402 PC). The total expansion curve was drawn using software, and temperatures to obtain expansion equivalent to titanium casting shrinkage were determined (n=5). In addition, the total expansion of the control group (RP at 430 degrees C) was measured, as well as the temperatures at which the other groups achieved equivalent total expansion (n=5). Data were analyzed by 1-way ANOVA and the Tukey HSD test (alpha=.05).Results. Titanium casting shrinkage was estimated as 1.55%. RP did not achieve this expansion. RE achieved expansion of 1.55% only with a special liquid concentration of 100% at 594 degrees C. CA with all special liquid concentrations attained this expansion (351 degrees C to 572 degrees C). Total expansion of the control group was 0.86%, and the other groups reached that expansion within the range of 70 degrees C to 360 degrees C.Conclusions. Only RE and CA demonstrated sufficient expansion to compensate for titanium casting shrinkage. All groups reached total expansion equivalent to that of the control group at significantly lower temperatures.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Metabolic studies involving the incorporation of [1-13C]-D- glucose into intact leaves of Piper aduncum (Piperaceae) have indicated that both the mevalonate (MVA) and the pyruvate-triose (MEP) non-mevalonate pathways are implicated in the biosynthesis of isoprene moieties present in methyl 2,2-dimethyl-2H-1-chromene-6-carboxylate (1) and methyl 2,2-dimethyl-8- (3′-methyl-2′-butenyl)-2H-1-chromene-6-carboxylate (2). The pattern of incorporation of label from [1-13C]-D-glucose into these chromenes was determined by quantitative 13C NMR spectroscopy. The results confirmed that biosynthetic compartment of 1 and 2 could either be the plastid and/ or the cytosol or, possibly, an additional compartment such as the plastid inter-membrane space. ©2007 Sociedade Brasileira de Química.
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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an enzymopathy in which reduced NADPH concentrations are not maintained, resulting in oxidative damage. We evaluated G6PD activity, oxidative stress levels and Trolox equivalent antioxidant capacity in individuals with the A-(202G>A) mutation for G6PD deficiency. Five hundred and forty-four peripheral blood samples were screened for G6PD deficiency; we also analyzed lipid peroxidation products measured as thiobarbituric acid reactive species and Trolox equivalent antioxidant capacity. Men with the A-(202G>A) mutation had lower G6PD activity than women with the same mutation. Individuals with the A-(202G>A) mutation also differed in mean Trolox equivalent antioxidant capacity values but not for thiobarbituric acid reactive species values. We concluded that A-(202G>A) mutation is associated with reduced G6PD activity and increased Trolox equivalent antioxidant capacity. ©FUNPEC-RP.
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Pós-graduação em Alimentos e Nutrição - FCFAR
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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A primaquina pode acarretar sérios eventos adversos, com destaque para a toxicidade ao sangue. O objetivo deste trabalho é determinar a metemoglobinemia de 20 pacientes com malária por Plasmodium vivax tratados com primaquina, comparando-os segundo o sexo e a expressão da glicose-6-fosfato desidrogenase. Métodos: Quantificação da metemoglobina por espectrofotometria visível e avaliação qualitativa da glicose-6-fosfato desidrogenase. Resultados: A metemoglobinemia variou de 2,85 a 5,45% nos pacientes do sexo masculino e de 3,77 a 7,34% no feminino. Conclusões: A instituição da terapia aumentou de maneira significativa os teores de metemoglobina, sem manifestação clínica evidente e independente do sexo e da atividade enzimática.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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O efeito adverso da primaquina na dose de 0,50mg/kg/dia foi investigado em onze pacientes com malária vivax (três com deficiência de glicose-6-fosfato desidrogenase). Alterações clínicas e laboratoriais indicaram hemólise aguda apenas nos enzimopênicos, o que fez com que o tratamento fosse interrompido. Nossos resultados sugerem a necessidade do emprego de um teste de triagem para a deficiência de G6PD em áreas endêmicas de malária vivax a fim de se evitar complicações causadas pelo uso da primaquina.
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A malária vivax é uma doença que a cerca de 40% da população mundial, utiliza-se no tratamento desta, cloroquina (150 mg) e primaquina (15 mg). Esta é uma 8- aminoquinolina com ação esquizonticida tecidual. Dentre seus efeitos adversos se destaca a capacidade de oxidar a hemoglobina, de maneira dose dependente, que é agravada nos indivíduos com deficiência da glicose-6-fosfato desidrogenase. Ao se considerar a ausência de estudos referentes aos teores de metemoglobina e sua correlação com as concentrações plasmáticas de primaquina nos pacientes com malária vivax, justifica-se a realização deste estudo empregando-se como ferramentas a monitorização das concentrações sanguíneas de primaquina e sua correlação com os teores de metemoglobina. Neste sentido, foi realizado seguimento clínico-laboratorial de 20 pacientes com malária vivax antes (D0) e após três (D3), sete (D7) e quatorze (D14) dias iniciado o tratamento, bem como a validação do método para determinação de primaquina por cromatografia líquida de alta eficiência (CLAE). A metemoglobinemia foi avaliada pela técnica de Hegesh et al. (1970) e a glicose-6-fosfato desidrogenase pelo teste colorimétrico de Brewer et al. (1962). A metodologia validada demonstrou parâmetros aplicáveis à determinação de primaquina, cujos teores médios em D3, D7 e D14 foram de 227±106 ng/mL, 191±97 ng/mL e 160±128ng/mL. Não foram obervadas diferenças significativas nas concentrações do fármaco quanto ao sexo dos pacientes participantes e nos diversos dias do estudo. Os teores médios de metemoglobina em D0, D3, D7 e D14 foram de 1,15±0,9%, 4,1±2%, 5,7±2% e 3±1,4%, respectivamente. Foi observado aumento no teor de metemoglobina após administração do fármaco, sem diferença quanto ao sexo. Não foi observada correlação significativa entre os teores de metemoglobina e as concentrações plasmáticas de primaquina em ambos os sexos. Os coeficientes de correlação de Pearson para os sexos masculino e feminino foram 0.8296 e 0.8137, respectivamente. Foi observada deficiência da expressão da enzima glicose-6- fosfato desidrogenase em seis pacientes do sexo masculino sem diferenças entre os teores de metemoglobina e das concentrações plasmáticas de Primaquina, quando comparados com pacientes com expressão normal da enzima.
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Um dos métodos clássicos da geofísica de exploração é o Método de Eletrorresistividade, estabelecido há um século pelos irmãos Schlumberger e desde então amplamente empregado em prospecção mineral, estudos ambientais e hidrogeologia e em pesquisa de fontes geotermais. Conceitualmente o método consiste de injeção de corrente elétrica na subsuperfície e de medida de diferença de potencial elétrico, resultante da interação da corrente com o meio. As localizações dessas fontes e receptores são determinadas pelo arranjo escolhido para o levantamento. Após o processamento, obtém-se pseudo-seções de resistividade aparente que indicam a distribuição de condutividade em subsuperfície. Devido à simplicidade dos fundamentos físicos de sua formulação, o método apresenta fácil implementação computacional quando comparado aos métodos eletromagnéticos de fonte controlada. Na literatura há inúmeros trabalhos de modelagem computacional, onde se calcula a resposta para problemas 2-D e 3-D. Nestes trabalhos, as pseudo-seções são obtidas a partir do cálculo do potencial elétrico total. Neste trabalho, apresentaremos a resposta da modelagem de eletroresistividade 2-D com o arranjo dipolo-dipolo, obtida a partir do potencial elétrico secundário. A solução é calculada através do método de elementos finitos usando malhas não estruturadas. Para efeito de validação, os resultados são comparados com a resposta 2-D obtida a partir dos potencias totais.
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The most important role played by the enzyme Glucose- 6-Phosphate Dehydrogenase (G6PD) in erythrocyte metabolism is in generating energy and reducing power used to protect the cell against oxidative attack. G6PD deficiency is the erythroenzymopathy that most frequently causes hemolytic anemia, and more than 130 molecular variants have already been identified. The aim of this study was to analyze the genetic mutations in the G6PD-deficient adult males in the population of the region of Araraquara, São Paulo State. Out of 5087 male blood donors, 89 were deficient for G6PD, as confirmed by assaying the enzyme activity and electrophoresis on cellulose acetate. Thus, a frequency of 1.75% of G6PD-deficient patients was found, this value being similar to other investigations in São Paulo state. Molecular analysis was performed by amplification of genomic DNA with specific primers and digestion with restriction enzymes. In 96.6% of the patients, the G6PD A¯ variant was observed, with mutations at residues 376(A→G) and 202(G→A). Mean G6PD specific activity among the patients was 1.31 IU.g Hb-1.min-1 at 37ºC, that is 10.8% of the normal activity of the G6PD B enzyme. The variant forms G6PD A¯ 680(G→T) and 968(T→C) were not found. In 3.4% of the deficient individuals, the G6PD Mediterranean variant was found, with a mutation at 563(C→T). In these cases, mean enzymatic activity was 0.25 IU.g Hb-1.min-1 at 37ºC, or 2.1% of the enzymatic activity of G6PD B. The use of traditional techniques, allied to the identification of the different molecular variants, is important for the understanding of the structural and functional properties and hemolytic behavior of the red blood cells of the patient.
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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
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Background: Although iron deficiency is considered to be the main cause of anemia in children worldwide, other contributors to childhood anemia remain little studied in developing countries. We estimated the relative contributions of different factors to anemia in a population-based, cross-sectional survey. Methodology: We obtained venous blood samples from 1111 children aged 6 months to 10 years living in the frontier town of Acrelandia, northwest Brazil, to estimate the prevalence of anemia and iron deficiency by measuring hemoglobin, erythrocyte indices, ferritin, soluble transferrin receptor, and C-reactive protein concentrations. Children were simultaneously screened for vitamin A, vitamin B-12, and folate deficiencies; intestinal parasite infections; glucose-6-phosphate dehydrogenase deficiency; and sickle cell trait carriage. Multiple Poisson regression and adjusted prevalence ratios (aPR) were used to describe associations between anemia and the independent variables. Principal Findings: The prevalence of anemia, iron deficiency, and iron-deficiency anemia were 13.6%, 45.4%, and 10.3%, respectively. Children whose families were in the highest income quartile, compared with the lowest, had a lower risk of anemia (aPR, 0.60; 95% CI, 0.37-0.98). Child age (<24 months, 2.90; 2.01-4.20) and maternal parity (>2 pregnancies, 2.01; 1.40-2.87) were positively associated with anemia. Other associated correlates were iron deficiency (2.1; 1.4-3.0), vitamin B-12 (1.4; 1.0-2.2), and folate (2.0; 1.3-3.1) deficiencies, and C-reactive protein concentrations (>5 mg/L, 1.5; 1.1-2.2). Conclusions: Addressing morbidities and multiple nutritional deficiencies in children and mothers and improving the purchasing power of poorer families are potentially important interventions to reduce the burden of anemia.