666 resultados para Disappeared


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A presente tese procura demonstrar como a Igreja Católica, a partir de Leão XIII, despertou para a questão social, particularmente a dos trabalhadores, fornecendo uma intelectualidade que influenciaria muitas gerações de católicos que aí encontrariam o substrato e o contraponto das concepções marxistas. Com o avanço das correntes progressistas dentro da Igreja, estes se reorientaram e tentaram fazer o cruzamento entre o marxismo e o cristianismo, que culminaria com a Teologia da Libertação. Este foi o momento do encontro também com o movimento sindical, por meio de seus militantes e das Comunidades Eclesiais de Base. Essa intersecção forneceu a base moral que norteou o movimento sindical no final dos anos 70, dando origem ao chamado novo sindicalismo . Os militantes acreditavam que a classe trabalhadora estava engajada e comprometida com as mudanças sociais, quando, na verdade, esta pensava em suas questões mais particulares. Com o tempo, a Igreja, por meio de sua hierarquia, fragmentou a rede de apoio ao movimento sindical e a utopia se desvaneceu.(AU)

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A presente tese procura demonstrar como a Igreja Católica, a partir de Leão XIII, despertou para a questão social, particularmente a dos trabalhadores, fornecendo uma intelectualidade que influenciaria muitas gerações de católicos que aí encontrariam o substrato e o contraponto das concepções marxistas. Com o avanço das correntes progressistas dentro da Igreja, estes se reorientaram e tentaram fazer o cruzamento entre o marxismo e o cristianismo, que culminaria com a Teologia da Libertação. Este foi o momento do encontro também com o movimento sindical, por meio de seus militantes e das Comunidades Eclesiais de Base. Essa intersecção forneceu a base moral que norteou o movimento sindical no final dos anos 70, dando origem ao chamado novo sindicalismo . Os militantes acreditavam que a classe trabalhadora estava engajada e comprometida com as mudanças sociais, quando, na verdade, esta pensava em suas questões mais particulares. Com o tempo, a Igreja, por meio de sua hierarquia, fragmentou a rede de apoio ao movimento sindical e a utopia se desvaneceu.(AU)

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O jornal Expositor Cristão, órgão oficial da Igreja Metodista no Brasil, nasceu em 1886, com uma proposta que se poderia chamar de ecumênica: seu primeiro nome, Methodista Catholico, revela o desejo de universalidade, confirmado pelo editorial de estréia. Seu criador, o missionário norte-americano John James Ransom, pretendia um veículo de orientação doutrinária que não fosse sectário, em consonância com a tradição wesleyana. Mas o Metodista Católico teve vida curta: em pouco mais de um ano passou a se chamar Expositor Cristão. O campo religioso brasileiro vivia, então, o período da controvérsia apologética, com a inserção do protestantismo de missão, de origem anglo-saxã, em contraposição ao catolicismo romano. O nome do recém-nascido jornal foi mais uma vítima dos embates. Este trabalho se dispôs a avaliar como o jornal tratou a questão do ecumenismo desde esse período até a entrada da Igreja Metodista no CONIC, Conselho Nacional de Igrejas Cristãs, no início da década de 1980. A pesquisa constatou que o anticatolicismo arraigado no metodismo brasileiro em seus primórdios jamais desapareceu por completo. Notou também que o metodismo não esteve imune aos conflitos interdenominacionais existentes no próprio meio evangélico. Em que pese o reconhecido pioneirismo da Igreja Metodista na criação de organismos ecumênicos brasileiros, o ecumenismo sempre enfrentou barreiras internas, mais ou menos explícitas. E o jornal Expositor Cristão, criado para ser um veículo de informação e formação doutrinária, nem sempre comunicou com a necessária clareza qual o significado que a Igreja Metodista confere à palavra ecumenismo e como ela o pratica. Em alguns momentos, a coexistência entre ecumenismo e antiecumenismo no interior do campo metodista não foi trazida à luz dos debates pelo jornal, mas permaneceu oculta por omissões e ambivalências. É o que este trabalho pôde constatar a partir de uma avaliação qualitativa do conteúdo do jornal.(AU)

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O jornal Expositor Cristão, órgão oficial da Igreja Metodista no Brasil, nasceu em 1886, com uma proposta que se poderia chamar de ecumênica: seu primeiro nome, Methodista Catholico, revela o desejo de universalidade, confirmado pelo editorial de estréia. Seu criador, o missionário norte-americano John James Ransom, pretendia um veículo de orientação doutrinária que não fosse sectário, em consonância com a tradição wesleyana. Mas o Metodista Católico teve vida curta: em pouco mais de um ano passou a se chamar Expositor Cristão. O campo religioso brasileiro vivia, então, o período da controvérsia apologética, com a inserção do protestantismo de missão, de origem anglo-saxã, em contraposição ao catolicismo romano. O nome do recém-nascido jornal foi mais uma vítima dos embates. Este trabalho se dispôs a avaliar como o jornal tratou a questão do ecumenismo desde esse período até a entrada da Igreja Metodista no CONIC, Conselho Nacional de Igrejas Cristãs, no início da década de 1980. A pesquisa constatou que o anticatolicismo arraigado no metodismo brasileiro em seus primórdios jamais desapareceu por completo. Notou também que o metodismo não esteve imune aos conflitos interdenominacionais existentes no próprio meio evangélico. Em que pese o reconhecido pioneirismo da Igreja Metodista na criação de organismos ecumênicos brasileiros, o ecumenismo sempre enfrentou barreiras internas, mais ou menos explícitas. E o jornal Expositor Cristão, criado para ser um veículo de informação e formação doutrinária, nem sempre comunicou com a necessária clareza qual o significado que a Igreja Metodista confere à palavra ecumenismo e como ela o pratica. Em alguns momentos, a coexistência entre ecumenismo e antiecumenismo no interior do campo metodista não foi trazida à luz dos debates pelo jornal, mas permaneceu oculta por omissões e ambivalências. É o que este trabalho pôde constatar a partir de uma avaliação qualitativa do conteúdo do jornal.(AU)

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The ability of Neisseria meningitidis (MC) to interact with cellular barriers is essential to its pathogenesis. With epithelial cells, this process has been modeled in two steps. The initial stage of localized adherence is mediated by bacterial pili. After this phase, MC disperse and lose piliation, thus leading to a diffuse adherence. At this stage, microvilli have disappeared, and MC interact intimately with cells and are, in places, located on pedestals of actin, thus realizing attaching and effacing (AE) lesions. The bacterial attributes responsible for these latter phenotypes remain unidentified. Considering that bacteria are nonpiliated at this stage, pili cannot be directly responsible for this effect. However, the initial phase of pilus-mediated localized adherence is required for the occurrence of diffuse adherence, loss of microvilli, and intimate attachment, because nonpiliated bacteria are not capable of such a cellular interaction. In this work, we engineered a mutation in the cytoplasmic nucleotide-binding protein PilT and showed that this mutation increased piliation and abolished the dispersal phase of bacterial clumps as well as the loss of piliation. Furthermore, no intimate attachment nor AE lesions were observed. On the other hand, PilT− MC remained adherent as piliated clumps at all times. Taken together these data demonstrate that the induction of diffuse adherence, intimate attachment, and AE lesions after pilus-mediated adhesion requires the cytoplasmic PilT protein.

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We demonstrate performance-related changes in cortical and cerebellar activity. The largest learning-dependent changes were observed in the anterior lateral cerebellum, where the extent and intensity of activation correlated inversely with psychophysical performance. After learning had occurred (a few minutes), the cerebellar activation almost disappeared; however, it was restored when the subjects were presented with a novel, untrained direction of motion for which psychophysical performance also reverted to chance level. Similar reductions in the extent and intensity of brain activations in relation to learning occurred in the superior colliculus, anterior cingulate, and parts of the extrastriate cortex. The motion direction-sensitive middle temporal visual complex was a notable exception, where there was an expansion of the cortical territory activated by the trained stimulus. Together, these results indicate that the learning and representation of visual motion discrimination are mediated by different, but probably interacting, neuronal subsystems.

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Down-regulation of the initial burst of viremia during primary HIV infection is thought to be mediated predominantly by HIV-specific cytotoxic T lymphocytes, and the appearance of this response is associated with major perturbations of the T cell receptor repertoire. Changes in the T cell receptor repertoire of virus-specific cytotoxic T lymphocytes were analyzed in patients with primary infection to understand the failure of the cellular immune response to control viral spread and replication. This analysis demonstrated that a significant number of HIV-specific T cell clones involved in the primary immune response rapidly disappeared. The disappearance was not the result of mutations in the virus epitopes recognized by these clones. Evidence is provided that phenomena such as high-dose tolerance or clonal exhaustion might be involved in the disappearance of these monoclonally expanded HIV-specific cytotoxic T cell clones. These findings should provide insights into how HIV, and possibly other viruses, elude the host immune response during primary infection.

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The gene for the maturation protein of the single-stranded RNA coliphage MS2 is preceded by an untranslated leader of 130 nt, which folds into a cloverleaf, i.e., three stem–loop structures enclosed by a long distance interaction (LDI). This LDI prevents translation because its 3′ moiety contains the Shine–Dalgarno sequence of the maturation gene. Previously, several observations suggested that folding of the cloverleaf is kinetically delayed, providing a time window for ribosomes to access the RNA. Here we present direct evidence for this model. In vitro experiments show that ribosome binding to the maturation gene is faster than refolding of the denatured cloverleaf. This folding delay appears related to special properties of the leader sequence. We have replaced the three stem–loop structures by a single five nt loop. This change does not affect the equilibrium structure of the LDI. Nevertheless, in this construct, the folding delay has virtually disappeared, suggesting that now the RNA folds faster than ribosomes can bind. Perturbation of the cloverleaf by an insertion makes the maturation start permanently accessible. A pseudorevertant that evolved from an infectious clone carrying the insertion had overcome this defect. It showed a wild-type folding delay before closing down the maturation gene. This experiment reveals the biological significance of retarded cloverleaf formation.

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IAPs comprise a family of inhibitors of apoptosis found in viruses and animals. In vivo binding studies demonstrated that both baculovirus and Drosophila IAPs physically interact with an apoptosis-inducing protein of Drosophila, Reaper (RPR), through their baculovirus IAP repeat (BIR) region. Expression of IAPs blocked RPR-induced apoptosis and resulted in the accumulation of RPR in punctate perinuclear locations which coincided with IAP localization. When expressed alone, RPR rapidly disappeared from the cells undergoing RPR-induced apoptosis. Expression of P35, a caspase inhibitor, also blocked RPR-induced apoptosis and delayed RPR decline, but RPR remained cytoplasmic in its location. Mutational analysis of RPR demonstrated that caspases were not directly responsible for RPR disappearance. The physical interaction of IAPs with RPR provides a molecular mechanism for IAP inhibition of RPR’s apoptotic activity.

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Widespread species- and genus-level extinctions of mammals in North America and Europe occurred during the last deglaciation [16,000–9,000 yr B.P. (by 14C)], a period of rapid and often abrupt climatic and vegetational change. These extinctions are variously ascribed to environmental change and overkill by human hunters. By contrast, plant extinctions since the Middle Pleistocene are undocumented, suggesting that plant species have been able to respond to environmental changes of the past several glacial/interglacial cycles by migration. We provide evidence from morphological studies of fossil cones and anatomical studies of fossil needles that a now-extinct species of spruce (Picea critchfieldii sp. nov.) was widespread in eastern North America during the Last Glacial Maximum. P. critchfieldii was dominant in vegetation of the Lower Mississippi Valley, and extended at least as far east as western Georgia. P. critchfieldii disappeared during the last deglaciation, and its extinction is not directly attributable to human activities. Similarly widespread plant species may be at risk of extinction in the face of future climate change.

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Photoreceptor proteins of the phytochrome family mediate light-induced inhibition of stem (hypocotyl) elongation during the development of photoautotrophy in seedlings. Analyses of overt mutant phenotypes have established the importance of phytochromes A and B (phyA and phyB) in this developmental process, but kinetic information that would augment emerging molecular models of phytochrome signal transduction is absent. We have addressed this deficiency by genetically dissecting phytochrome-response kinetics, after having solved the technical issues that previously limited growth studies of small Arabidopsis seedlings. We show here, with resolution on the order of minutes, that phyA initiated hypocotyl growth inhibition upon the onset of continuous red light. This primary contribution of phyA began to decrease after 3 hr of irradiation, the same time at which immunochemically detectable phyA disappeared and an exclusively phyB-dependent phase of inhibition began. The sequential and coordinated actions of phyA and phyB in red light were not observed in far-red light, which inhibited growth persistently through an exclusively phyA-mediated pathway.

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The role of channel inactivation in the molecular mechanism of calcium (Ca2+) channel block by phenylalkylamines (PAA) was analyzed by designing mutant Ca2+ channels that carry the high affinity determinants of the PAA receptor site [Hockerman, G. H., Johnson, B. D., Scheuer, T., and Catterall, W. A. (1995) J. Biol. Chem. 270, 22119–22122] but inactivate at different rates. Use-dependent block by PAAs was studied after expressing the mutant Ca2+ channels in Xenopus oocytes. Substitution of single putative pore-orientated amino acids in segment IIIS6 by alanine (F-1499-A, F-1500-A, F-1510-A, I-1514-A, and F-1515-A) gradually slowed channel inactivation and simultaneously reduced inhibition of barium currents (IBa) by (−)D600 upon depolarization by 100 ms steps at 0.1 Hz. This apparent reduction in drug sensitivity was only evident if test pulses were applied at a low frequency of 0.1 Hz and almost disappeared at the frequency of 1 Hz. (−)D600 slowed IBa recovery after maintained membrane depolarization (1–3 sec) to a comparable extent in all channel constructs. A drug-induced delay in the onset of IBa recovery from inactivation suggests that PAAs promote the transition to a deep inactivated channel conformation. These findings indicate that apparent PAA sensitivity of Ca2+ channels is not only defined by drug interaction with its receptor site but also crucially dependent on intrinsic gating properties of the channel molecule. A molecular model for PAA-Ca2+ channel interaction that accounts for the relationship between drug induced inactivation and channel block by PAA is proposed.

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We optically imaged a visual masking illusion in primary visual cortex (area V-1) of rhesus monkeys to ask whether activity in the early visual system more closely reflects the physical stimulus or the generated percept. Visual illusions can be a powerful way to address this question because they have the benefit of dissociating the stimulus from perception. We used an illusion in which a flickering target (a bar oriented in visual space) is rendered invisible by two counter-phase flickering bars, called masks, which flank and abut the target. The target and masks, when shown separately, each generated correlated activity on the surface of the cortex. During the illusory condition, however, optical signals generated in the cortex by the target disappeared although the image of the masks persisted. The optical image thus was correlated with perception but not with the physical stimulus.

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Lipoproteins are emulsion particles that consist of lipids and apolipoproteins. Their natural function is to transport lipids and/or cholesterol to different tissues. We have taken advantage of the hydrophobic interior of these natural emulsions to solubilize DNA. Negatively charged DNA was first complexed with cationic lipids containing a quaternary amine head group. The resulting hydrophobic complex was extracted by chloroform and then incorporated into reconstituted chylomicron remnant particles (≈100 nm in diameter) with an efficiency ≈65%. When injected into the portal vein of mice, there were ≈5 ng of a transgene product (luciferase) produced per mg of liver protein per 100 μg injected DNA. This level of transgene expression was ≈100-fold higher than that of mice injected with naked DNA. However, such a high expression was not found after tail vein injection. Histochemical examination revealed that a large number of parenchymal cells and other types of cells in the liver expressed the transgene. Gene expression in the liver increased with increasing injected dose, and was nearly saturated with 50 μg DNA. At this dose, the expression was kept at high level in the liver for 2 days and then gradually reduced and almost disappeared by 7 days. However, by additional injection at day 7, gene expression in the liver was completely restored. By injection of plasmid DNA encoding human α1-antitrypsin, significant concentrations of hAAT were detected in the serum of injected animals. This is the first nonviral vector that resembles a natural lipoprotein carrier.

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Trypanosoma cruzi is a protozoan parasite that belongs to an early branch in evolution. Although it lacks several features of the pathway of protein N-glycosylation and oligosaccharide processing present in the endoplasmic reticulum of higher eukaryotes, it displays UDP-Glc:glycoprotein glucosyltransferase and glucosidase II activities. It is herewith reported that this protozoan also expresses a calreticulin-like molecule, the third component of the quality control of glycoprotein folding. No calnexin-encoding gene was detected. Recombinant T. cruzi calreticulin specifically recognized free monoglucosylated high-mannose-type oligosaccharides. Addition of anti-calreticulin serum to extracts obtained from cells pulse–chased with [35S]Met plus [35S]Cys immunoprecipitated two proteins that were identified as calreticulin and the lysosomal proteinase cruzipain (a major soluble glycoprotein). The latter but not the former protein disappeared from immunoprecipitates upon chasing cells. Contrary to what happens in mammalian cells, addition of the glucosidase II inhibitor 1-deoxynojirimycin promoted calreticulin–cruzipain interaction. This result is consistent with the known pathway of protein N-glycosylation and oligosaccharide processing occurring in T. cruzi. A treatment of the calreticulin-cruzipain complexes with endo-β-N-acetylglucosaminidase H either before or after addition of anti-calreticulin serum completely disrupted calreticulin–cruzipain interaction. In addition, mature monoglucosylated but not unglucosylated cruzipain isolated from lysosomes was found to interact with recombinant calreticulin. It was concluded that the quality control of glycoprotein folding appeared early in evolution, and that T. cruzi calreticulin binds monoglucosylated oligosaccharides but not the protein moiety of cruzipain. Furthermore, evidence is presented indicating that glucosyltransferase glucosylated cruzipain at its last folding stages.