822 resultados para Trânsito gastrointestinal


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O campo religioso brasileiro apresenta, em sua configuração atual, uma formatação identitária extremamente diversa daquela observada em décadas anteriores. A partir dessa consideração, emerge uma problemática significativa - como compreender essas mudanças? Por que um cenário, antes extremamente resistente a transformações, agora se abre aos ventos modernizantes permitindo a recomposição de suas formas religiosas? Ora, a construção de novas identidades e a reordenação dos padrões religiosos podem ser compreendidas a partir do fenômeno do trânsito religioso, considerando ser possível iden-tificar na movimentação dos sujeitos uma dinâmica que estabelece alterações, tanto no caráter institucional e litúrgico dos grupos, bem como na vivência prática dos / das fiéis, promovendo inéditos e provisórios sistemas simbólicos. Diante da multiplicidade de oferta, os sujeitos apresentam uma mobilidade incessante num processo de ressignificação permanente, formando efêmeros mosaicos nos quais se distinguem múltiplas cores, formas, espaços, demandas, motivações, comportamentos, interesses, habitus, tradições, símbolos, disposições, estratégias, gostos e combinações. A partir dos postulados das Ciências da Religião, essa pesquisa propõe-se a analisar esse evento tendo como universo de observação a Igreja Evangélica Assembleia de Deus, Ministério São Bernardo do Campo. Objetiva demonstrar, mediante a interpretação do con-junto de dados obtidos em pesquisa de campo correlacionado com os fundamentos teóricos, a recomposição das formas religiosas institucionais e as novas identidades desenvolvidas pelos sujeitos a partir da mobilidade; estabelecer uma conexão entre os elementos indicadores da pesquisa e o fenômeno caracterizado para identificar quais são as motivações de gênero, classe, geracional e de etnia para o trânsito de homens e mulheres que circulam das mais diversas alternativas para esse grupo religioso e, considerando esse referencial, compreender como a instituição religiosa absorve esse fluxo de pessoas.

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Esta pesquisa analisa o trânsito religioso de pessoas que tiveram a sua biografia religiosa marcada pela participação/envolvimento em cultos evangélicos e que atualmente se declaram praticantes de ritos de candomblé e umbanda na região do ABCD paulista . Para a realização da mesma conduzimos entrevistas com líderes religiosos que nos ajudaram a compreender a organização dos terreiros de umbanda e candomblé na região; também aplicamos 80 questionários em oito terreiros espalhados pela região, compreendendo assim o perfil socioeconômico de seus frequentadores. Durante a análise dos questionários verificou-se a ocorrência do trânsito, de maneira ainda mais intensa entre praticantes da umbanda, e analisamos as motivações para esta movimentação religiosa, identificando ainda as motivações de gênero para esta movimentação, além das relações de trocas simbólicas estabelecidas entre os fiéis e as instituições religiosas. Verificamos os principais grupos evangélicos por onde estes sujeitos religiosos transitaram, observando possíveis semelhanças, bem como o distanciamento de suas práticas cúlticas e as práticas dos cultos afro-brasileiros.

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A proposta desta pesquisa é discutir o trânsito religioso enquanto uma ação social que só pode ser compreendida a partir de um conjunto de condições sociais e políticas que influenciam o comportamento religioso contemporâneo. O objetivo principal é analisar as motivações para a prática do trânsito religioso dos evangélicos sem religião, no contexto das igrejas evangélicas, com a finalidade de entender o surgimento de um novo sujeito da fé que escolhe romper com a fé institucional, sem ser, necessariamente, um ateu. O que motiva este sujeito a professar uma fé sem vínculo com qualquer instituição religiosa é a questão fundamental deste trabalho, que se divide em três capítulos. No primeiro, analisamos o conjunto de transformações que legitimam o comportamento de transitar entre os vários vínculos religiosos, inclusive ficar sem vínculo. No Segundo, tentamos definir quem são os sem religião e por onde transitam. E no terceiro, discutimos a questão fundamental deste trabalho. O que motiva o evangélico a se desvincular, ou seja, ser um evangélico sem igreja?

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Essa pesquisa estabelece uma relação entre gênero, religião e modernidade, demonstrando quais as implicações deste fenômeno para a religiosidade contemporânea. Nosso objetivo principal é o de compreender o fenômeno do trânsito religioso de homens no contexto da Universidade Metodista de São Paulo, para isso a pesquisa está desdobrada em três momentos: na compreensão das principais características da modernidade e sua influência na constituição da religiosidade dos sujeitos; na análise da representação social da masculinidade e seu processo de constituição das identidades de gênero; e na verificação da ocorrência do trânsito religioso entre homens e mulheres por intermédio da pesquisa quantitativa, e as principais motivações sócio-religiosas para a ocorrência deste fenômeno entre os homens

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Esta dissertação tem por objetivo investigar a existência demotivações de gênero para o trânsito religioso de pentecostais para a Igreja Metodista. Para tanto, o primeiro passo é demonstrar a incidência deste fluxo migratório. Em seguida levantar e analisar as motivações paraa migração deste grupo para uma igreja protestante história. Neste sentido, o primeiro capítulo aborda assuntos correlatos ao tema como a religião, a modernidade e o campo religioso brasileiro, porque é no mundo que os papéis de gênero são remodelados e emerge a transitoriedade humana em um contexto de pluralidade e sincretismo religioso ao qual pertecem o protestantismo histórico e o pentecostalismo. O segundo capítulo descreve as origens domovimento metodista, sua entrada no Brasil e na cidade de São Paulo,as bases doutrinárias e costumes, bem como delimita o campo de pesquisa nela inserido, encerra com caracterização do trânsito religioso,destaca dados estatísticos, dinâmicas, razões e consequências sobre este fenômeno,cruzando-os com dados da pesquisa de campo realizada na Igreja Metodista do Distrito Grande ABC. Por fim, o terceiro capítulo, traz a tona à discussão sobre a questão de gênero, apresenta conceitos, caracterização e sua relevância na religião e no trânsito religioso, encerra com a análise das motivações deste fluxo migratório de pentecostais para a Igreja Metodista sob a perspectiva de gênero.

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This study concerns the nature of nitric oxide synthase (NOS) and the role of nitric oxide (NO) in the rat gastrointestinal tract. The major objectives were (i) to characterise NOS isoforms in the gastric glandular mucosa, (ii) to localise NOS isoforms in the rat gastric glandular mucosa, (iii) to investigate the role of NO in carbachol-stimulated gastric mucus secretion, (iv) to investigate the nature of NOS and small intestine. Immunoblotting was performed using polyclonal antisera raised against two peptides found in the rat brain NOS sequence and commercial monoclonal antibodies directed against neuronal and endothelial isoforms of NOS. A160kDa band was detected in brain and gastric mucosal samples with antibodies and antisera directed against neuronal NOS sequences, and a 140kDa band was detected in gastric mucosal samples using an anti-endothelial NOS antibody. An intense 160kDa neuronal NOS band was detected in a high-density fraction of gastric mucosal cells separated on a Percoll gradient. Detection of neuronal NOS by a carboxyl-terminal antiserum in samples of brain, but not of gastric mucosa, could be blocked by the peptide (20g/ml) against which the antibody was raised. After affinity purification, recognition of gastric mucosal NOS was blocked by peptide. Particulate neuronal NOS was found in the brain by immunoblotting while 94% of gastric mucosal enzyme was soluble. Gastric mucosal endothelial NOS was 95% particulate. 95% of NOS activity in the gastric mucosa was due to neuronal NOS. Paraformaldehyde- and acetone-fixed gastric mucosal sections were subject to immunocytochemistry using the above antibodies. Neuronal NOS was localised to the surface mucosal epithelial cells while endothelial NOS was associated with microvessels at the base of the mucosa and to larger vessels in the submucosa. Intragastric administration of carbachol or 16, 16-dimethyl prostaglandin E2 increased the thickness of the rat gastric mucus layer. The NOS inhibitor NG-nitro-L-arginine methyl ester dose-dependently, and selectively, prevented the stimulatory effect of carbachol. Ca2+-independent NOS activity in rat ileal, jejunal and colonic muscle was increased after LPS induction. Ca2+-dependent activity was not affected. Distribution of inducible NOS protein paralleled Ca2+ -independent activity. LPS treatment did not affect the content of neuronal NOS in colonic muscle.

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Nitric oxide is a free-radical gas which can exert both protective and damaging effects. The objectives of the thesis were: (i) to investigate arginine metabolism in isolated rat gastric mucosal cells, (ii) to investigate the role of NO in the induction of ornithine decarboxylase in the rat gastric mucosa damaged by hypertonic saline in vivo, (iii) to expose primary cultures of guinea-pig gastric mucosal cells to oxidative challenge and an NO donor, and to investigate the response in terms of heat shock protein 72 (HSP 72) induction, and (iv) to investigate the induction of iNOS and the role of potential modulators of activity in gastric cell lines. Isolated rat gastric mucosal cells converted exogenous arginine to ornithine and citrulline. This metabolism of arginine was not affected by a range of NO synthase inhibitors, but was reduced by the arginase inhibitors NG-hydroxy-L-arginine and L-ornithine. Thus, the predominant pathway of arginine metabolism involves arginase and ornithine transcarbamoylase, not NO synthase. Pretreatment of rats with NG-nitro-L-arginine promoted activation of ornithine decarboxylase after intragastric hypertonic saline, but did not increase acid phosphatase release (damage). NO may therefore restrict activation of ornithine decarboxylase in response to damage. Exposure of primary cultures of guinea-pig gastric mucosal cells to S-nitroso-N-acetyl-penicillamine (SNAP) caused a concentration dependent induction of HSP 72, which was inhibited by an NO scavenger and blockade of transcription. The effect of SNAP was enhanced by decreasing the intracellular reduced thiol content with diethyl maleate, which itself also induced HSP 72 formation. Substantial amounts of NO may induce defensive responses in cells. Induction of iNOS was not detected in HGT-1 or AGS cells exposed to cytokines. Conclusions An arginase pathway may restrict availability of arginine for NO synthase in gastric mucosa or may be present to supply ornithine for polyamine synthesis. NO may modulate the response to damage of the stomach epithelium in vivo. Exogenous NO may induce a defensive response in gastric mucosal cells.

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This study was undertaken to increase knowledge of the mechanisms of inter- and intracellular signalling in the gastrointestinal tract. Specific aims were: to use cell lines to elucidate factors affecting growth of gastric cells, to investigate the distribution and aspects of function of isoforms of protein kinase C in a gastric cell line and in the rat gastrointestinal tract and to determine the presence and regulation of nitric oxide synthase in gastrointestinal tissues from the rat and in cell lines. The gastric cancer cell line HGT-1 was used to investigate control of growth. Increases in cell number were found to be dependent on the seeding density of the cells. In cells plated at low density insulin, epidermal growth factor and gastrin all increased cell number. Gastrin produced a bell-shaped dose response curve with a maximum activity at 5nM. No effect of gastrin was apparent in cells plated at high density. α and β isoforms of protein kinase C were found, by immunoblotting procedures, to be widespread in the gastrointestinal tract of the rat, but protein kinase Cε was confined to the gastric mucosa and gastrointestinal smooth muscle. HGT-1 cells contained protein kinase C α and ε but β or γ were not detected. Preincubation of HGT-1 cells for 24h with 1μM phorbol-12,13-dibutyrate down-regulated protein kinase C α but not ε. The inhibition by the activator of protein kinase C, 12-O-tetradecanoylphorbol 13-acetate (TPA) of the histamine-stimulated increase in cAMP in HGT-1 cells was down regulated by phorbol-12,13-dibutyrate. Inhibition of histamine-stimulation of adenylate cyclase by TPA was Ca2+-dependent and inhibited by the addition of an antibody to protein kinase C α. A role for protein kinase C α in modulating the effect of histamine on adenylate cyclase in HGT-1 cells is suggested. No nitric oxide synthase activity was detected in the gastrointestinal cell lines HGT-l, MKN-45 or CaCo-2. Ca2+-dependent nitric oxide synthase activity was observed in the gastric mucosa and the gastrointestinal smooth muscle from stomach to colon. The gastric: mucosal enzyme was soluble and showed half-maximal activity at 400nM Ca2+. Pretreatment of rats with endotoxin (3mg/kg body weight) induced nitric oxide synthase activity in both jejunal, ileal and colonic mucosa and muscle. A major portion of the induced activity in ileal and colonic mucosa was Ca2+-independent. Nitric oxide synthase activity in a high-density fraction of gastric mucosal cells was inhibited in a dose-dependent fashion by L-nitroarginine, NG-monomethyl-L-arginine, trifluoperazine and L-canavanine (in descending order of potency). Preincubation with okadaic acid and addition of ATPlMg2+ to the homogenisation buffer inhibited enzyme activity, which implies that phosphorylation inhibits gastric mucosal nitric oxide synthase.

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This thesis concerns the mechanism through which enteral delivery of glucose results in a larger insulin response than an equivalent parenteral glucose load. Preliminary studies in which mice received a glucose solution either intragastrically or intraperitoneally confirmed this phenomenon. An important regulatory system in this respect is the entero-insular axis, through which insulin secretion is influenced by neural and endocrine communication between the gastrointestinal tract and the pancreatic islets of Langerhans. Using an in vitro system involving static incubation of isolated (by collagenase digestion) islets of Langerhans, the effect of a variety of gastrointestinal peptides on the secretion of the four main islet hormones, namely insulin, glucagon, somatostatin and pancreatic polypeptide, was studied. The gastrointestinal peptides investigated in this study were the secretin family, comprising secretin, glucagon, gastric inhibitory polypeptide (GIP), vasoactive intestinal polypeptide (VIP), peptide histidine isoleucine (PHI) and growth hormone releasing factor (GRF). Gastrin releasing peptide (GRP) was also studied. The results showed that insulin release was stimulated by all peptides studied except PHI, glucagon release was stimulated by all peptides tested, except GRF which suppressed glucagon release, somatostatin release was stimulated by GIP and GRF but suppressed by VIP, PHI, glucagon and secretin, and PP release was stimulated by GIP and GRF, but suppressed by PHI. The insulinotropic effect of GRP was investigated further. A perifusion system was used to examine the time-course of insulin release from isolated islets after stimulation with GRP. GRP was shown to be insulinotropic only in the presence of physiologically elevated glucose concentrations and both first and second phases of insulin release were augmented. There was no effect at substimulatory or very high glucose concentrations. Studies using a cultured insulin-secreting islet cell line, the RINm5F cell line, were undertaken to elucidate the intracellular mechanism of action of GRP. This peptide did not enhance insulin release via an augmentation of glucose metabolism, or via the adenylate cyclase/cyclic AMP secondary messenger system. The pattern of changes of cytosolic free calcium in response to GRP, which involved both mobilization of intracellular stores and an influx of extracellular calcium, suggested the involvement of phosphatidylinositol bisphosphate breakdown as a mediator of the effect of GRP on insulin secretion.

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Metformin is an effective agent with a good safety profile that is widely used as a first-line treatment for type 2 diabetes, yet its mechanisms of action and variability in terms of efficacy and side effects remain poorly understood. Although the liver is recognised as a major site of metformin pharmacodynamics, recent evidence also implicates the gut as an important site of action. Metformin has a number of actions within the gut. It increases intestinal glucose uptake and lactate production, increases GLP-1 concentrations and the bile acid pool within the intestine, and alters the microbiome. A novel delayed-release preparation of metformin has recently been shown to improve glycaemic control to a similar extent to immediate-release metformin, but with less systemic exposure. We believe that metformin response and tolerance is intrinsically linked with the gut. This review examines the passage of metformin through the gut, and how this can affect the efficacy of metformin treatment in the individual, and contribute to the side effects associated with metformin intolerance.

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