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As vitaminas do complexo B e o ferro estão presentes em farinhas de cereais, alimentos amplamente consumidos pela população brasileira. O teor natural desses compostos em farinhas de cereais pode ser significativo no cálculo de uma dieta bem balanceada e o consumo de produtos industrializados enriquecidos com vitaminas do complexo B e ferro ajuda a contribuir na ingestão diária recomendada desses micronutrientes. Tabelas Mundiais de Composição de Alimentos apresentam dados incompletos das vitaminas do complexo B e do ferro em farinhas de cereais. No Brasil, a adição de ácido fólico e ferro em farinhas de milho e trigo produzidas para fins industriais é obrigatória desde 2002. Deste modo, para a adequação dos teores de rotulagem de produtos enriquecidos com vitaminas e ferro se fazem necessários o desenvolvimento e a validação de metodologias analíticas confiáveis e sensíveis para análise de vitaminas do complexo B e ferro em alimentos que apresentam tais micronutrientes em quantidades baixas, porém significativas, que correspondem aos teores naturalmente presentes. O objetivo do presente trabalho é a avaliação dos teores de sete vitaminas do complexo B (B1, B2, B6, ácido pantotênico, ácido fólico, niacina e biotina) e ferro em cinco farinhas de cereais (aveia, arroz, cevada, milho e trigo) utilizadas como matéria prima de produtos enriquecidos na indústria alimentícia, utilizando métodos validados. / Complex B vitamins and iron are present in some cereal foods, a kind of food largely consumed by Brazilian people. The total of these micronutrients can be significant at the dairy ingestion portion and in the consume of industrialized products enriched with complex B vitamins and iron contribute in the recommended dietary intake of these micronutrients. Table of food composition do not report complete data of complex B vitamins and iron in cereal flours. In Brazil, since 2002 the addition of folic acid and iron in com and wheat flours is compulsory. Therefore, to adapt the label of some products enriched with vitamins and iron, there is necessary the development and validation of analytical methods. These methods must be reliable and with enough sensitivity to analyse complex B vitamins and iron, in low concentration, wich are natural content in food. The purpose of this work is the evaluation, with validated methods, of the content of seven complex B vitamíns (B1, B2, B6, niacin, folic acid, pantothenic acid and biotin) and iron in five kinds of cereal flours (oat, rice, barley, com and wheat). These raw materiais are used in food industry in order to enrich the industrialized products.

Le diabète de type 1 (DT1) est une maladie auto-immune caractérisée par la destruction des cellules β pancréatiques par les cellules immunitaires, ce qui entraîne une insuffisance en insuline. L’étude des souris Non-Obese Diabetic (NOD), qui développent spontanément le diabète auto-immun, a permis l'identification de plusieurs loci de susceptibilité associés au diabète, appelés Idds. D’ailleurs, Idd1 est lié au locus du CMH. L’utilisation de souris congéniques NOD.B6-Idd1 et B6.NOD-Idd1 a démontré qu’Idd1 est nécessaire mais insuffisant pour la progression du diabète auto-immun. Précédemment, nous avons démontré que les allèles de résistance au locus Idd2 offrent une protection significative contre l’apparition du diabète auto-immun, semblable à Idd1. Pour identifier les facteurs génétiques minimaux requis pour l'apparition du DT1, nous avons introduit les loci NOD Idd1 et Idd2 chez des souris B6, générant des souris doubles congéniques B6.Idd1.Idd2. Bien que la combinaison de Idd1 et Idd2 n’est pas suffisante pour induire l’apparition du diabète, nous avons observé une infiltration immunitaire dans le pancréas exocrine des souches congéniques B6 Idd2. De plus, nous avons observé d'importantes différences phénotypiques dans les sous-populations de lymphocytes T chez les souris B6.Idd1.Idd2 par rapport aux souris simple congéniques, suggérant une interaction épistatique entre Idd1 et Idd2 dans la modulation des fonctions des lymphocytes T. De plus, des augmentations de neutrophiles et de la fibrose spécifiques à Idd2 ont été découvertes, suggérant qu’Idd2 est impliqué dans le processus cellulaire inflammatoire du diabète auto-immun. Dans l’ensemble, ces données montrent que la combinaison des allèles de susceptibilité Idd1 et Idd2 ne mène pas à la progression du diabète auto-immun. Des facteurs génétiques ou environnementaux supplémentaires sont donc nécessaires pour provoquer le diabète auto-immun chez la souris. Néanmoins, nous constatons que les allèles NOD au niveau des locus Idd2 coopèrent pour induire une inflammation et une infiltration immunitaire dans le pancréas. / Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β cells by immune cells, leading to an insulin deficiency. Non-Obese Diabetic (NOD) mice, which spontaneously develop autoimmune diabetes, have enabled the identification of several loci associated with diabetes susceptibility, termed Idds. Notably, Idd1 is linked to the MHC locus and resistance alleles at this locus provide full protection from diabetes onset. Conversely, C57BL/6 (B6) mice bearing NOD Idd1 alleles exhibit immune infiltration in the pancreas without causing overt diabetes. These results show that NOD Idd1 alleles are necessary but not sufficient for autoimmune diabetes progression. In a previous study, we demonstrated that diabetes resistance alleles at the Idd2 locus provide significant protection from autoimmune diabetes onset, second to Idd1. To identify the minimal genetic factors required for T1D onset, we introduced the NOD Idd1 and Idd2 loci in B6 mice, generating B6.Idd1.Idd2 double congenic mice. Although the introduction of susceptibility alleles at both Idd1 and Idd2 was not sufficient to induce diabetes onset, we observed immune infiltration in the exocrine pancreas of B6 Idd2 congenic strains. In addition, we observed important phenotypic differences in T cell subsets in B6.Idd1.Idd2 mice relative to single congenic mice, suggesting epistatic interaction between Idd1 and Idd2 in modulating T cell functions. Moreover, Idd2-specific increases in neutrophils and fibrosis were discovered, suggesting that Idd2 is involved in the inflammatory cellular process of autoimmune diabetes. Altogether, these data show that susceptibility alleles at Idd1 and Idd2 together are not sufficient to autoimmune diabetes progression. Additional genetic factors or environmental triggers are therefore required to cause autoimmune diabetes in mice. Still, we find that NOD alleles at the Idd2 loci cooperate to induce inflammation and immune infiltration in the pancreas.

Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Architecture, 2000. / Includes bibliographical references (p. 183-225). / This thesis will analyze the architect William Ralph Emerson's (1833-1917) Boston Art Club building (1881-82) and its station within Boston and New York's art culture. Even though there has been considerable research on the Gilded Age in general and certain art clubs specifically, this club remains a neglected element in art's social history. During the rising development of art culture, a small group of artists founded the Boston Art Club (1854-1950) as a vehicle for production, education and promotion of the arts. To assert their club's presence within patrons' circles, the members commissioned a flagship clubhouse adjacent to Art Square (now known as Copley Square). Emerson, primarily a residential architect and the first Shingle Style architect, won the competition with a unique amalgamation of Queen Anne and Richardson Romanesque styles, an alliance with the nearby Museum of Fine Arts and the Ruskin and the English Pre-Raphaelites. The resultant clubhouse was a declaration of the club's presence amid America's established art culture. Through this building design the Club asserted its status for the thirty years that the arts prevailed on Boston's Art Square. The Art Club's reign, along with the building's prominence, ended when the Museum deemed their building's architectural style out of date, among other reasons. That faithful decision to abandon Art Square and the revival Ruskinian Gothic style would take with it the reverence for the Art Club's building and, eventually, the club itself. Within forty years and through several other struggles the Art Club closed its doors, ending a chapter that began with the need for art in Boston, thrived within the culture of the Gilded Age and sank from the changing trends in architecture. / by Michelle Leah Hoeffler. / S.M.

Alcohol dependence (alcoholism) is a complex disease influenced by both environmental factors and genetic predisposition. Mouse models have been used to study many alcohol dependence-related traits and the genetics that underlie them. Two of the most commonly used mice in alcohol research are the C57BL/6J (B6) and DBA/2J (D2) inbred strains, which diverge on several alcohol-related traits including the development of acute physical dependence. Here we utilized the B6 and D2 mice as a genetic model of acute physical dependence, coupled with mRNA Differential Display (DD) and cDNA microarray analysis, to uncover the transcriptional response of the brain to an acute dose of alcohol as a function of time. About 150 genetically divergent and alcohol-responsive genes were identified between the whole brains of B6 and D2 mice using DD and were added as additional targets to the mouse microarrays. Microarray analysis of the prefrontal cortex of B6 and D2 mice revealed strain-specific, acute alcohol-responsive transcriptome remodeling manifested as temporal patterns of gene expression. Distinct expression patterns were identified for physiologically relevant alcohol-related consequences including intoxication, withdrawal and neuroadaptation. In silico characterization of the differentially expressed genes showed genotype dependent and independent transcriptional regulation and functional classification. In addition, categorization of differentially expressed genes by their cellular profiles revealed that some of the genes were known to be more highly expressed in either excitatory or inhibitory neuronal cell types. Our results indicate that the B6 and D2 prefrontal cortices have very different cellular and molecular responses to acute alcohol exposure. The specific roles that the genes identified in this study may play in mediating the divergent alcohol-related behavior between the strains warrant further study. / text

This study characterizes B vitamin supplement use prior to and during pregnancy, changes in dietary one-carbon nutrient intakes (folate, vitamin B12, vitamin B6, choline, betaine and methionine) and most significant dietary sources. In Canadian women (Toronto, Ontario) supplemental (n=364) and dietary intakes (using a food frequency questionnaire) (n=290) were assessed during early and late pregnancy. Majority reported using a B vitamin-containing supplement prior (60%) to and during early (93%) and late (89%) pregnancy. Median supplemental intakes of folic acid, B12 and B6 were 1000 µg/d, 2.6 µg/d and 1.9 mg/d, respectively. Dietary one-carbon nutrient intakes did not change appreciably between early and late pregnancy. Most significant sources of folate and B6 were fruits and vegetables, of folic acid were cereals and grains and of B12 were dairy and egg products. Overall, this study provides novel information about one-carbon nutrient intakes in pregnancy which are crucial in maternal and child health.

This study characterizes B vitamin supplement use prior to and during pregnancy, changes in dietary one-carbon nutrient intakes (folate, vitamin B12, vitamin B6, choline, betaine and methionine) and most significant dietary sources. In Canadian women (Toronto, Ontario) supplemental (n=364) and dietary intakes (using a food frequency questionnaire) (n=290) were assessed during early and late pregnancy. Majority reported using a B vitamin-containing supplement prior (60%) to and during early (93%) and late (89%) pregnancy. Median supplemental intakes of folic acid, B12 and B6 were 1000 µg/d, 2.6 µg/d and 1.9 mg/d, respectively. Dietary one-carbon nutrient intakes did not change appreciably between early and late pregnancy. Most significant sources of folate and B6 were fruits and vegetables, of folic acid were cereals and grains and of B12 were dairy and egg products. Overall, this study provides novel information about one-carbon nutrient intakes in pregnancy which are crucial in maternal and child health.

Elevated plasma total homocysteine (ptHcy) or hyperhomocysteinemia (hHcy) independently predicts cardiovascular disease in predialysis chronic kidney disease (pCKD). Folate status is one of the known nutritional determinants of ptHcy. In the era of folic acid food fortification, this cross-sectional study aimed to describe in pCKD subjects (n=48): 1) Prevalence of hHcy. 2) Intake and status of nutrients involved in homocysteine metabolism. 3) Determinants of ptHcy. The prevalence of hHcy was 93.8% (95% CI: 81.8 to 98.4). Median (25th, 75th percentile) total folate intake from food and supplements was 389 (282,640) µg DFE/d. No subject was folate deficient (red blood cell < 317 nmol/L). Red blood cell folate (r = - 0.406, p=0.004) and energy-protein undernutrition (r = 0.357, p=0.013) independently predicted ptHcy. To conclude, total folate intake among subjects with pCKD was sufficient to prevent folate deficiency but not able to prevent a high prevalence of hHcy.

Elevated plasma total homocysteine (ptHcy) or hyperhomocysteinemia (hHcy) independently predicts cardiovascular disease in predialysis chronic kidney disease (pCKD). Folate status is one of the known nutritional determinants of ptHcy. In the era of folic acid food fortification, this cross-sectional study aimed to describe in pCKD subjects (n=48): 1) Prevalence of hHcy. 2) Intake and status of nutrients involved in homocysteine metabolism. 3) Determinants of ptHcy. The prevalence of hHcy was 93.8% (95% CI: 81.8 to 98.4). Median (25th, 75th percentile) total folate intake from food and supplements was 389 (282,640) µg DFE/d. No subject was folate deficient (red blood cell < 317 nmol/L). Red blood cell folate (r = - 0.406, p=0.004) and energy-protein undernutrition (r = 0.357, p=0.013) independently predicted ptHcy. To conclude, total folate intake among subjects with pCKD was sufficient to prevent folate deficiency but not able to prevent a high prevalence of hHcy.

Tese de Doutorado apresentada ao Programa de Pós-Graduação em Ciências da Saúde para obtenção do título de Doutora em Ciências da Saúde. / A meningite pneumocócica é umas das mais complexas e graves infecções do sistema nervoso central (SNC) associada com distúrbios neurológicos e neuropsicológicos. Os compostos bacterianos são mediadores pró-inflamatórios que induzem a resposta imune e a degradação do triptofano através da via da quinurenina e podem contribuir para lesão do SNC associada com meningite bacteriana. A falta de uniformidade nos danos gera dificuldade para avaliar a severidade e o grau dos prejuízos neuronais, criando obstáculos para novas terapias no tratamento. A vitamina B6 atua como co-fator de enzimas que catalisam um grande número de reações envolvidas no metabolismo do triptofano, impedindo o acúmulo de intermediários neurotóxicos, podendo prevenir danos ao hospedeiro. A vitamina B9 desempenha um papel importante na neuroplasticidade e preservação da integridade neuronal e tem sido postulada como anti-depressiva, anti-maníaca e neuroprotetora. No presente estudo, foram avaliados os efeitos da vitamina B6 e B9 sobre a memória, parâmetros de estresse oxidativo, níveis do fator neurotrófico derivado do cérebro (BDNF) e integridade da barreira hematoencefálica (BHE) no hipocampo e córtex de ratos Wistar adultos submetidos à meningite pneumocócica. Os animais receberam injeção na cisterna magna de 10 μL de suspensão de Streptococcus pneumoniae ou líquido cefalorraquidiano (LCR) artificial para o grupo controle. Grupos experimentais vitamina B6: controle/salina; controle/B6; meningite/salina e meningite/B6 e receberam 360 μL de vitamina B6 (600 mg/kg) ou salina estéril por via subcutânea em 0 e 18 horas após a indução da meningite. Grupos experimentais vitamina B9: controle/salina; controle/B9 10 mg/Kg; controle/B9 50 mg/Kg; meningite/salina, meningite/B9 10 mg/Kg e meningite/B9 50 mg/Kg. A vitamina B9 foi dissolvida em água e administrada via oral por gavagem iniciando o tratamento 18 horas após a indução e seguindo por 7 dias, 1 vez ao dia. Os parâmetros de estresse oxidativo foram avaliados em 24 horas e 10 dias após a indução da meningite. A integridade da BHE foi avaliada em 12, 18 e 24 horas após a indução. Os parâmetros comportamentais foram avaliados em 10 dias após a indução da meningite pelos testes de habituação ao campo aberto, esquiva inibitória e reconhecimento de objetos. Após, os animais foram mortos por decapitação para avaliação dos níveis de BDNF. Em 24 horas após a indução da meningite houve um aumento dos níveis de TBARS, carbonilação de proteínas, nitrito/nitrato e atividade da MPO no hipocampo e córtex pré-frontal; a atividade da SOD foi diminuída no hipocampo e aumentada no córtex pré-frontal e não houve diferença na atividade da CAT no hipocampo, enquanto que no córtex pré-frontal foi diminuída no grupo meningite/salina. Dez dias após a indução, os parâmetros de estresse oxidativo se mantiveram aumentados. Houve quebra da BHE em todos os tempos avaliados e o tratamento com ambas as vitaminas preveniu essa disfunção. Nos animais submetidos à meningite o tratamento com vitamina B6 e B9 preveniu o comprometimento cognitivo e aumentou os níveis de BDNF no hipocampo. O tratamento com vitamina B6 e B9 foi capaz de prevenir estresse oxidativo, quebra da BHE, aumentar os níveis de BDNF e prevenir danos cognitivos em ratos Wistar submetidos à meningite por S. pneumoniae.