789 resultados para Davidson


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OBJETIVO: Estimar a prevalência do tabagismo em estudantes e os fatores associados.MÉTODOS: Foram utilizados dados secundários, provenientes do inquérito Vigescola realizado em Curitiba (PR), Florianópolis (SC) e Porto Alegre (RS) em 2002 e 2004. A amostra compreendeu 3.690 escolares de 13 a 15 anos, cursando as sétima e oitava séries do ensino fundamental e primeira do ensino médio, em escolas públicas e privadas. Para a análise dos resultados foram estimadas proporções ponderadas, odds ratio (OR), e utilizada a técnica de regressão logística múltipla.RESULTADOS: As taxas de prevalência de tabagismo corresponderam a 10,7 por cento (IC 95 por cento: 10,2;11,3) em Florianópolis, 12,6 por cento (IC 95 por cento: 12,4;12,9) em Curitiba e 17,7 por cento (IC 95 por cento: 17,4;18,0) em Porto Alegre. Os fatores associados ao tabagismo em escolares em Curitiba foram: sexo feminino (OR=1,49), pai fumante (OR=1,59), amigos fumantes (OR=3,46), exposição à fumaça do tabaco fora de casa (OR=3,26) e possuir algum objeto com logotipo de marca de cigarro (OR=3,29). Em Florianópolis, as variáveis associadas ao tabagismo foram escolares do sexo feminino (OR=1,26), ter amigos fumantes (OR=9,31), exposição à fumaça do tabaco em casa (OR=2,03) e fora de casa (OR=1,45) e ter visto propaganda em cartazes (OR=1,82). Em Porto Alegre, as variáveis que estiveram associadas com o uso de tabaco pelos escolares foram sexo feminino (OR=1,57), idade entre 14 anos (OR=1,77) e 15 anos (OR=2,89), amigos fumantes (OR=9,12), exposição à fumaça do tabaco em casa (OR=1,87) e fora de casa (OR=1,77) e possuir algo com logotipo de marca de cigarro (OR=2,83).CONCLUSÕES: Há elevada prevalência de tabagismo entre escolares de 13 a 15 anos, cujos fatores significativamente associados comuns às três capitais são: ter amigos fumantes e estar exposto à fumaça ambiental fora de casa

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O envelhecimento populacional é um fato marcante da transição demográfica. O estudo das causas básicas em idosos permite visualizar seu perfil epidemiológico, embora possa ser prejudicado pela alta proporção de causas mal definidas. O objetivo deste trabalho é descrever a mortalidade dos idosos por essas causas no Brasil. A fonte dos dados foi o Sistema de Informações sobre Mortalidade do Ministério da Saúde.Entre as variáveis, a principal modalidade foi a causa básica mal definida [ Capítulo XVIII da Classificação Estatística Internacional de Doenças e Problemas Relacionados à Saúde-Décima Revisão (CID-10)]. O decréscimo desses óbitos em idosos foi de 35 por cento entre 1996 e 2005.Considerando os óbitos de 60 a 69 anos e os de 80 e mais anos, as proporções de mal definidos aumentaram em 9,9 por cento e 14,8 por cento, respectivamente, no ano de 2005. Métodos visando a sua diminuição são sugeridos, salientando-se que o fato mais importante é o de os médicos preencherem adequadamente as declarações de óbito- com as reais causas básicas, conseqüênciais e terminais-, objetivo maior dos estudiosos

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Ao mensurar-se mortalidade materna, é necessário distinguir ' mortes por causas maternas' e 'mortes maternas' Para a Organização Mundial da Saúde-OMS-,mortes maternas são as que ocorrem na gestação, no parto e até 42 dias após o parto; e mortes por causas maternas englobam as causas classificadas no Capítulo XV da Classificação Estatística Internacional de Doenças e Problemas Relacionados à Saúde, Décima Revisão (CID-10), incluindo as ocorridas quando passados 42 dias do parto. Apresentam-se resultados da investigação de mortes femininas em idade fértil-10 a 49 anos- nas capitais de Estados e no Distrito Federal do Brasil, em 2002. Adotou-se a metodologia RAMOS, comparando-se as causas básicas das declarações de óbito originais com as das declarações preenchidas após o resgate de informações, obtidas em entrevistas domiciliares e prontuários. Entre as mortes por causas maternas originais, 15,9 por cento não eram mortes maternas, de acordo com a definição da OMS. Houve, concomitantemente, subenumeração de mortes maternas. Sugestões são feitas para melhorar o preenchimento das declarações de óbito e inclusão de novas categorias na CID-10, visando melhorar a informação das causas maternas

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As estatísticas de mortalidade são usadas em epidemiologia e saúde pública como indicador de nível de saúde, em avaliações de programas de saúde e em estudos populacionais visando a comparar tendências temporais e diferenças geográficas. Uma das variáveis utilizadas nesse tipo de análise é a causa básica da morte. Entretanto, existem críticas quanto à qualidade das estatísticas baseadas nas causas de morte declaradas pelos médicos nos atestados de óbito. O objetivo deste artigo é refletir sobre a fidedignidade das causas de morte declaradas pelos médicos nos atestados de óbito, com base em estudos realizados segundo diferentes metodologias, e comenta a validade das estatísticas de mortalidade segundo causas

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O objetivo foi comparar as mortes maternas existentes no Sistema de Informações sobre Mortalidade (SIM/MS) com as do "Estudo da mortalidade de mulheres em idade fértil" e estimar novos fatores de correção. Analisaram-se 7.332 declarações de óbito feminino (DO) de dez a 49 anos, de residentes nas capitais brasileiras, no 1o semestre de 2002. Realizou-se pareamento dos conjuntos de DO (as originalmente preenchidas pelos médicos e aquelas obtidas com o resgate de dados) com as DO do SIM/MS. A subenumeração das mortes por causas maternas, no SIM/MS, foi de 21,4 por cento e, das mortes maternas, 16 por cento . Os novos fatores de ajuste para as mortes maternas nas regiões brasileiras foram: 0,93 (Norte), 1,17 (Nordeste), 1,28 (Sudeste), 1,10 (Sul) e 1,47 (Centro-oeste); para o pa's, foi igual a 1,19. Os Comitês de Morte Materna investigam os óbitos femininos em idade fértil, mas, ainda, restam imprecisões que podem inviabilizar condutas preventivas eficientes

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Biogeochemistry is hosting this special thematic issue devoted to studies of land-water interactions, as part of the Large-scale Biosphere-Atmosphere Experiment in Amaznia (LBA). This compilation of papers covers a broad range of topics with a common theme of coupling land and water processes, across pristine and impacted systems. Findings highlighted that hydrologic flowpaths are clearly important across basin size and structure in determining how water and solutes reach streams. Land-use changes have pronounced impacts on flowpaths, and subsequently, on stream chemistry, from small streams to large rivers. Carbon is produced and transformed across a broad array of fluvial environments and wetlands. Surface waters are not only driven by, but provide feedback to, the atmosphere.

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Recent research has focused on the N-methyl-D-aspartate receptor system as a major site of ethanol action in the brain and specifically on compensatory changes in the expression of the polyamine-sensitive NR2B subunit. Therefore, we examined the effects of chronic ethanol treatment on polyamine homeostasis in the rat brain. Wistar rats were made dependent by ethanol vapor inhalation. This caused a rise in hippocampal ornithine decarboxylase (ODC) activity that was correlated with the appearance of physiological dependence. ODC activity returned to control levels within 3 days of ethanol withdrawal. Enzyme activity also increased in the cerebral cortex, striatum, and cerebellum of the ethanol-dependent rats. The concentration of the polyamines (putrescine, spermidine, and spermine) in the hippocampus was increased in ethanol-dependent rats. Injection of the ODC inhibitor, gamma-difluoromethylornithine (500 mg/kg) at the onset of withdrawal resulted in a significant reduction in the severity of withdrawal behaviors. The level of ODC activity and the severity of withdrawal behaviors were positively correlated. Perturbed polyamine homeostasis may represent an important molecular component in the initiation of ethanol withdrawal behaviors in the ethanol-dependent rat.

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The purpose of this study was to determine the relationship between ornithine decarboxylase activity (ODC; a marker for perturbed cell development), the blood alcohol level, and alcohol-induced microencephaly in the developing rat brain after binge treatment with ethanol vapour. By manipulating ethanol flow we were able to adjust vapour concentrations (24-65 mg ethanol/l air) such that an acute exposure of ethanol vapour for 3 h resulted in a range of blood alcohol levels (2.3-5.5 mg/ml). Acute studies showed that ethanol dose-dependently inhibited rat hippocampal and cerebellar ODC activity at PND4-PND10. There was a significant correlation between the blood alcohol level and degree of inhibition at all ages tested. Chronic treatment from PND4 to PND9 caused a significant decrease in both brain to body weight ratio and in hippocampal and cerebellar ODC activities at PND10. These results indicate that ethanol-induced disruption in ODC could play a significant role in ethanol's teratogenic effects during early postnatal development. (C) 1998 Elsevier Science Inc.

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Giles and Goss (1980) have suggested that, if a futures market provides a forward pricing function, then it is an efficient market. In this article a simple test for whether the Australian Wool Futures market is efficient is proposed. The test is based on applying cointegration techniques to test the Law of One Price over a three, six, nine, and twelve month spread of futures prices. We found that the futures market is efficient for up to a six-month spread, but no further into the future. Because futures market prices can be used to predict spot prices up to six months in advance, woolgrowers can use the futures price to assess when they market their clip, but not for longer-term production planning decisions. (C) 1999 John Wiley & Sons, Inc.

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Administration of polyamines into the central nervous system results in tissue damage, possibly through the excitotoxic actions of the NMDA receptor. Direct injection of 100 nmol of spermine into the rat striatum produced a lesion equivalent to approximately 50% of the striatum. Analysis of the DNA in this region revealed the distinct ladder-like pattern of degradation often associated with apoptosis. This DNA fragmentation was confirmed in vivo using terminal deoxynucleotidyl-transferase-mediated biotinylated deoxyuridine triphosphate nick end labelling (TUNEL). The morphology of the TUNEL-positive cells showed marked differences at the needle tract when compared with cells in damaged areas away from the needle tract, suggesting a differential mechanism of cell death in these two regions. The patterns of p53, c-Fos and c-Jun protein expression were determined using immunohistochemistry. The number of p53-immunoreactive cells increased up to 14 h and returned to basal levels by 24 h. c-Fos protein expression transiently increased, peaking at 8 h after injection, c-Jun exhibited a protracted pattern of expression, remaining elevated up to 24 h. p53 protein expression was colocalised with TUNEL staining in areas away from the needle tract, but not in cells at the needle tract, suggesting once again a differential mechanism of cell death. At 14 h, c-Fos and c-Jun were not colocalised with TUNEL staining, suggesting that they are either not involved with the cell death process or that the time course of protein expression and the onset of DNA fragmentation do not overlap. This work represents the first characterisation of processes associated with cell death induced by spermine in vivo.

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Glutamate-mediated neurotransmission may be involved in the range of adaptive changes in brain which occur after ethanol administration in laboratory animals, and in chronic alcoholism in human cases. Excitatory amino acid transmission is modulated by a complex system of receptors and other effecters, the efficacy of which can be profoundly affected by altered gene or protein expression. Local variations in receptor composition may underlie intrinsic regional variations in susceptibility to pathological change. Equally, ethanol use and abuse may bring about alterations in receptor subunit expression as the essence of the adaptive response. Such considerations may underlie the regional localization characteristic of the pathogenesis of alcoholic brain damage, or they may form part of the homeostatic change that constitutes the neural substrate for alcohol dependence. (C) 2000 Elsevier Science Ltd. All rights reserved.

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Two small RNAs regulate the timing of Caenorhabditis elegans development(1,2). Transition from the first to the second larval stage fates requires the 22-nucleotide lin-4 RNA(1,3,4), and transition from late larval to adult cell fates requires the 21-nucleotide let-7 RNA 2. The lin-4 and let-7 RNA genes are not homologous to each other, but are each complementary to sequences in the 3' untranslated regions of a set of protein-coding target genes that are normally negatively regulated by the RNAs1,2,5,6. Here we have detected let-7 RNAs of similar to 21 nucleotides in samples from a wide range of animal species, including vertebrate, ascidian, hemichordate, mollusc, annelid and arthropod, but not in RNAs from several cnidarian and poriferan species, Saccharomyces cerevisiae, Escherichia coli or Arabidopsis. We did not detect lin-4 RNA in these species. We found that let-7 temporal regulation is also conserved: let-7 RNA expression is first detected at late larval stages in C. elegans and Drosophila, at 48 hours after fertilization in zebrafish, and in adult stages of annelids and molluscs. The let-7 regulatory RNA may control late temporal transitions during development across animal phylogeny.

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AlSi7Mg0.35 alloy was cast into permanent moulds using different pouring temperatures (725 to 625degreesC). As the pouring temperature decreased, the as-cast microstructure changed from a coarse dendritic structure, through fine equiaxed grains to fine rosette-like grains. The as-cast materials were then partially remelted and isothermally held at 580degreesC prior to semisolid casting into a stepped die. The feedstock material cast from a high temperature filled only half the die, with severe segregation and other defects. The low-temperature-poured material completely filled the die with negligible porosity. The quality of semisolid castings is significantly affected by the microstructure of the semisolid feedstock material that arises from a combination of as-cast and subsequent thermal treatment conditions. The paper describes (a) the influence of pouring temperature on the microstructure of feedstock; (b) microstructure evolution through remelting and (c) the quality of semisolid castings produced with this material. For A17Si0.35Mg alloy, low temperature pouring in the range of 625-650degreesC followed by suitable isothermal holding treatment can result in good quality semisolid casting.

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Aldehyde dehydrogenases (ALDHs) catabolize toxic aldehydes and process the vitamin A-derived retinaldehyde into retinoic acid (RA), a small diffusible molecule and a pivotal chordate morphogen. In this study, we combine phylogenetic, structural, genomic, and developmental gene expression analyses to examine the evolutionary origins of ALDH substrate preference. Structural modeling reveals that processing of small aldehydes, such as acetaldehyde, by ALDH2, versus large aldehydes, including retinaldehyde, by ALDH1A is associated with small versus large substrate entry channels (SECs), respectively. Moreover, we show that metazoan ALDH1s and ALDH2s are members of a single ALDH1/2 clade and that during evolution, eukaryote ALDH1/2s often switched between large and small SECs after gene duplication, transforming constricted channels into wide opened ones and vice versa. Ancestral sequence reconstructions suggest that during the evolutionary emergence of RA signaling, the ancestral, narrow-channeled metazoan ALDH1/2 gave rise to large ALDH1 channels capable of accommodating bulky aldehydes, such as retinaldehyde, supporting the view that retinoid-dependent signaling arose from ancestral cellular detoxification mechanisms. Our analyses also indicate that, on a more restricted evolutionary scale, ALDH1 duplicates from invertebrate chordates (amphioxus and ascidian tunicates) underwent switches to smaller and narrower SECs. When combined with alterations in gene expression, these switches led to neofunctionalization from ALDH1-like roles in embryonic patterning to systemic, ALDH2-like roles, suggesting functional shifts from signaling to detoxification.

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Systemic injection of kainic acid (KA) results in characteristic behaviors and programmed cell death in some regions of the rat brain. We used KA followed by recovery at 4 degrees C to restrict damage to limbic structures and compared patterns of immediate early gene (IEG) expression and associated DNA binding activity in these damaged areas with that in spared brain regions. Male Wistar rats were injected with BA (12 mg/kg, ip) and kept at 4 degrees C for 5 h. This treatment reduced the severity of behaviors and restricted damage (observed by Nissl staining) to the CA1 and CA3 regions of the hippocampus and an area including the entorhinal cortex. DNA laddering, characteristic of apoptosis, was first evident in the hippocampus and the entorhinal cortex 18 and 22 h after RA, respectively. The pattern of IEG mRNA induction fell into three classes: IEGs that were induced in both damaged and spared areas (c-fos, fos B, jun B, and egr-1), IEGs that were induced specifically in the damaged areas (fra-2 and c-jun), and an IEG that was significantly induced by saline injection and/or the cold treatment (jun D). The pattern of immunoreactivity closely followed that of mRNA expression. Binding to the AP-1 and EGR DNA consensus sequences increased in all three regions studied. This study describes a unique modification of the animal model of ICA-induced neurotoxicity which may prove a useful tool for dissecting the molecular cascade that ultimately results in programmed cell death. (C) 1997 Academic Press.