827 resultados para pedagogy of resistance for social transformation


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La presente tesis doctoral aborda el estudio del proyecto de vivienda colectiva social desde la noción de norma, entendida desde la sistematización o normalización de los instrumentos del proyecto arquitectónico de vivienda protegida. Esto es, desde una idea de tipificación taxonómica en cuanto ajuste a un conjunto de reglas comunes productoras de sistemas normativos. La hipótesis de partida se basa en la consideración de la vivienda pública como un laboratorio de estudio histórico de los ideales de confort y calidad de vida. Este campo de pruebas ha constituido una sólida base que ha servido como punto de encuentro muy particular entre proyecto y normativa desde las primeras vanguardias europeas hasta la actualidad. El principal objetivo de la investigación es la revalorización de una normativa de vivienda que ha producido ejemplos de innegable calidad en el contexto nacional e internacional, así como un intento de actualización de su codificación. La investigación se sirve de los instrumentos específicos de la disciplina arquitectónica para explicar una disociación detectada desde la segunda mitad del siglo pasado entre la utopía del proyecto social de vivienda y el pragmatismo de la norma que lo regula, más allá de los aspectos sociales y culturales asociados a las nuevas composiciones familiares, las tecnologías cambiantes, los ritos domésticos contemporáneos o el valor creciente del tiempo libre. La propuesta de una nueva terminología que aborde nuevas relaciones en el acercamiento al proyecto de vivienda desde la normativa española deriva en un conjunto de estrategias de proyecto desde las que proponer sistemas normativos. Dichas estrategias se basan principalmente en mecanismos de cualificación espacial que permitan un nuevo acercamiento entre dichas normas y las formas de habitar actuales. ABSTRACT This doctoral thesis deals with the study of the project of social collective housing from the notion of rule, understanding it from the systematization or standardization of the instruments of architectural project for social housing. Thus, it deals with an idea of taxonomic typification as an adjustment to a set of common rules which produce regulation systems. The initial hypothesis is based on the consideration of public housing as a laboratory for studying the historical ideals of comfort and quality of life. This testing ground has been a solid base that has served as a very specific meeting point between project and regulations from the first European avant‐garde to nowadays. The main objective of this research is the revaluation of housing regulations, which have produced examples of undeniable quality in the national and international stage, as well as an attempt to update their codification. The research assumes the specific tools of the discipline of architecture for explaining a dissociation detected between the utopia of the project for social housing and the pragmatism of the regulations from the second half of last century, beyond social and cultural aspects associated to the new family arrangements, the changing technologies, the contemporary domestic rituals or the rising value of leisure time. The proposal of a new terminology that tackles new relations in the approach to housing project from the Spanish legislation results in a set of strategies to propose regulation systems. Those strategies are mainly based on mechanisms for spatial qualification which allow a new approach between these rules and the current ways of living.

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Artículo de crítica de la arquitectura y la aplicación de ésta a la docencia de proyectos arquitectónicos.

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Los medios sociales han revolucionado la manera en la que los consumidores se relacionan entre sí y con las marcas. Las opiniones publicadas en dichos medios tienen un poder de influencia en las decisiones de compra tan importante como las campañas de publicidad. En consecuencia, los profesionales del marketing cada vez dedican mayores esfuerzos e inversión a la obtención de indicadores que permitan medir el estado de salud de las marcas a partir de los contenidos digitales generados por sus consumidores. Dada la naturaleza no estructurada de los contenidos publicados en los medios sociales, la tecnología usada para procesar dichos contenidos ha menudo implementa técnicas de Inteligencia Artificial, tales como algoritmos de procesamiento de lenguaje natural, aprendizaje automático y análisis semántico. Esta tesis, contribuye al estado de la cuestión, con un modelo que permite estructurar e integrar la información publicada en medios sociales, y una serie de técnicas cuyos objetivos son la identificación de consumidores, así como la segmentación psicográfica y sociodemográfica de los mismos. La técnica de identificación de consumidores se basa en la huella digital de los dispositivos que utilizan para navegar por la Web y es tolerante a los cambios que se producen con frecuencia en dicha huella digital. Las técnicas de segmentación psicográfica descritas obtienen la posición en el embudo de compra de los consumidores y permiten clasificar las opiniones en función de una serie de atributos de marketing. Finalmente, las técnicas de segmentación sociodemográfica permiten obtener el lugar de residencia y el género de los consumidores. ABSTRACT Social media has revolutionised the way in which consumers relate to each other and with brands. The opinions published in social media have a power of influencing purchase decisions as important as advertising campaigns. Consequently, marketers are increasing efforts and investments for obtaining indicators to measure brand health from the digital content generated by consumers. Given the unstructured nature of social media contents, the technology used for processing such contents often implements Artificial Intelligence techniques, such as natural language processing, machine learning and semantic analysis algorithms. This thesis contributes to the State of the Art, with a model for structuring and integrating the information posted on social media, and a number of techniques whose objectives are the identification of consumers, as well as their socio-demographic and psychographic segmentation. The consumer identification technique is based on the fingerprint of the devices they use to surf the Web and is tolerant to the changes that occur frequently in such fingerprint. The psychographic profiling techniques described infer the position of consumer in the purchase funnel, and allow to classify the opinions based on a series of marketing attributes. Finally, the socio-demographic profiling techniques allow to obtain the residence and gender of consumers.

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Inorganic arsenic, a human carcinogen, is enzymatically methylated for detoxication, consuming S-adenosyl-methionine (SAM) in the process. The fact that DNA methyltransferases (MeTases) require this same methyl donor suggests a role for methylation in arsenic carcinogenesis. Here we test the hypothesis that arsenic-induced initiation results from DNA hypomethylation caused by continuous methyl depletion. The hypothesis was tested by first inducing transformation in a rat liver epithelial cell line by chronic exposure to low levels of arsenic, as confirmed by the development of highly aggressive, malignant tumors after inoculation of cells into Nude mice. Global DNA hypomethylation occurred concurrently with malignant transformation and in the presence of depressed levels of S-adenosyl-methionine. Arsenic-induced DNA hypomethylation was a function of dose and exposure duration, and remained constant even after withdrawal of arsenic. Hyperexpressibility of the MT gene, a gene for which expression is clearly controlled by DNA methylation, was also detected in transformed cells. Acute arsenic or arsenic at nontransforming levels did not induce global hypomethylation of DNA. Whereas transcription of DNA MeTase was elevated, the MeTase enzymatic activity was reduced with arsenic transformation. Taken together, these results indicate arsenic can act as a carcinogen by inducing DNA hypomethylation, which in turn facilitates aberrant gene expression, and they constitute a tenable theory of mechanism in arsenic carcinogenesis.

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Inflammatory destruction of insulin-producing β cells in the pancreatic islets is the hallmark of insulin-dependent diabetes mellitus, a spontaneous autoimmune disease of non-obese diabetic mice resembling human juvenile (type I) diabetes. Histochemical analysis of diabetic pancreata revealed that mononuclear cells infiltrating the islets and causing autoimmune insulitis, as well as local islet cells, express the CD44 receptor; hyaluronic acid, the principal ligand of CD44, is detected in the islet periphery and islet endothelium. Injection of anti-CD44 mAb 1 hr before cell transfer of diabetogenic splenocytes and subsequently on alternate days for 4 weeks induced considerable resistance to diabetes in recipient mice, reflected by reduced insulitis. Contact sensitivity to oxazolone was not influenced by this treatment. A similar antidiabetic effect was observed even when the anti-CD44 mAb administration was initiated at the time of disease onset: i.e., 4–7 weeks after cell transfer. Administration of the enzyme hyaluronidase also induced appreciable resistance to insulin-dependent diabetes mellitus, suggesting that the CD44–hyaluronic acid interaction is involved in the development of the disease. These findings demonstrate that CD44-positive inflammatory cells may be a potential therapeutic target in insulin-dependent diabetes.

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Over 2 billion people are estimated to be infected with virulent Mycobacterium tuberculosis, yet fewer than 10% progress to clinical tuberculosis within their lifetime. Twin studies and variations in the outcome of tuberculosis infection after exposure to similar environmental risks suggest genetic heterogeneity among individuals in their susceptibility to disease. In a mouse model of tuberculosis, we have established that resistance and susceptibility to virulent M. tuberculosis is a complex genetic trait. A new locus with a major effect on tuberculosis susceptibility, designated sst1 (susceptibility to tuberculosis 1), was mapped to a 9-centimorgan (cM) interval on mouse chromosome 1. It is located 10–19 cM distal to a previously identified gene, Nramp1, that controls the innate resistance of mice to the attenuated bacillus Calmette–Guérin vaccine strain. The phenotypic expression of the newly identified locus is distinct from that of Nramp1 in that sst1 controls progression of tuberculosis infection in a lung-specific manner. Mice segregating at the sst1 locus exhibit marked differences in the growth rates of virulent tubercle bacilli in the lungs. Lung lesions in congenic sst1-susceptible mice are characterized by extensive necrosis and unrestricted extracellular multiplication of virulent mycobacteria, whereas sst1-resistant mice develop interstitial granulomas and effectively control multiplication of the bacilli. The resistant allele of sst1, although powerful in controlling infection, is not sufficient to confer full protection against virulent M. tuberculosis, indicating that other genes located outside of the sst1 locus are likely also to be important for controlling tuberculosis infection.

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Strategies for delaying pest resistance to genetically modified crops that produce Bacillus thuringiensis (Bt) toxins are based primarily on theoretical models. One key assumption of such models is that genes conferring resistance are rare. Previous estimates for lepidopteran pests targeted by Bt crops seem to meet this assumption. We report here that the estimated frequency of a recessive allele conferring resistance to Bt toxin Cry1Ac was 0.16 (95% confidence interval = 0.05–0.26) in strains of pink bollworm (Pectinophora gossypiella) derived from 10 Arizona cotton fields during 1997. Unexpectedly, the estimated resistance allele frequency did not increase from 1997 to 1999 and Bt cotton remained extremely effective against pink bollworm. These results demonstrate that the assumptions and predictions of resistance management models must be reexamined.

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Dynamic behaviors of liposomes caused by interactions between liposomal membranes and surfactant were studied by direct real-time observation by using high-intensity dark-field microscopy. Solubilization of liposomes by surfactants is thought to be a catastrophic event akin to the explosion of soap bubbles in the air; however, the actual process has not been clarified. We studied this process experimentally and found that liposomes exposed to various surfactants exhibited unusual behavior, namely continuous shrinkage accompanied by intermittent quakes, release of encapsulated liposomes, opening up, and inside–out topological inversion.

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GD25 cells lacking β1 integrins or expressing β1A with mutations of conserved cytoplasmic tyrosines (Y783, Y795) to phenylalanine have poor directed migration to platelet-derived growth factor or lysophosphatidic acid when compared with GD25 cells expressing wild-type β1A. We studied the effects of v-src on these cells. Transformation with v-src caused tyrosine and serine phosphorylation of wild-type β1A but not of Y783/795F doubly mutated β1A. v-src-transformed cells had rounded and/or fusiform morphology and poor assembly of fibronectin matrix. Adhesion to fibronectin or laminin and coupling of focal contacts to actin-containing cytoskeleton were preserved in transformed Y783/795F cells but lost on transformation when β1A was wild type. Transformed Y783/795F cells also retained ability, albeit limited, to migrate across filters, whereas transformed cells with wild-type β1A were unable to transverse filters. Studies of single tyrosine mutants showed that the more important tyrosine for retaining ability to adhere, assemble focal contacts, and migrate is Y783. These results suggest that overactive phosphorylation of cytoplasmic residues of β1A, particularly Y783, accounts in part for the phenotype of v-src-transformed cells.

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Jaagsiekte sheep retrovirus (JSRV) can induce rapid, multifocal lung cancer, but JSRV is a simple retrovirus having no known oncogenes. Here we show that the envelope (env) gene of JSRV has the unusual property that it can induce transformation in rat fibroblasts, and thus is likely to be responsible for oncogenesis in animals. Retrovirus entry into cells is mediated by Env interaction with particular cell-surface receptors, and we have used phenotypic screening of radiation hybrid cell lines to identify the candidate lung cancer tumor suppressor HYAL2/LUCA2 as the receptor for JSRV. HYAL2 was previously described as a lysosomal hyaluronidase, but we show that HYAL2 is actually a glycosylphosphatidylinositol (GPI)-anchored cell-surface protein. Furthermore, we could not detect hyaluronidase activity associated with or secreted by cells expressing HYAL2, whereas we could easily detect such activity from cells expressing the related serum hyaluronidase HYAL1. Although the function of HYAL2 is currently unknown, other GPI-anchored proteins are involved in signal transduction, and some mediate mitogenic responses, suggesting a potential role of HYAL2 in JSRV Env-mediated oncogenesis. Lung cancer induced by JSRV closely resembles human bronchiolo-alveolar carcinoma, a disease that is increasing in frequency and now accounts for ≈25% of all lung cancer. The finding that JSRV env is oncogenic and the identification of HYAL2 as the JSRV receptor provide tools for further investigation of the mechanism of JSRV oncogenesis and its relationship to human bronchiolo-alveolar carcinoma.

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Prairie voles (Microtus ochrogaster) are monogamous rodents that form pair bonds characterized by a preference for a familiar social partner. In male prairie voles, exposure to either the stress of swimming or exogenous injections of corticosterone facilitate the development of a social preference for a female with which the male was paired after injection or swimming. Conversely, adrenalectomy inhibits partner preference formation in males and the behavioral effects of adrenalectomy are reversed by corticosterone replacement. In female prairie voles, swim stress interferes with the development of social preferences and corticosterone treatments inhibit the formation of partner preferences, while adrenalectomized females form preferences more quickly than adrenally intact controls. Because sex differences in both behavior and physiology are typically reduced in monogamous species, we initially predicted that male and female prairie voles would exhibit similar behavioral responses to corticosterone. However, our findings suggest an unanticipated sexual dimorphism in the physiological processes modulating social preferences. This dimorphic involvement of stress hormones in pair bonding provides a proximate mechanism for regulating social organization, while permitting males and females to adapt their reproductive strategies in response to environmental challenges.

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The observed in vitro and in vivo benefit of combination treatment with anti-human immunodeficiency virus (HIV) agents prompted us to examine the potential of resistance development when two protease inhibitors are used concurrently. Recombinant HIV-1 (NL4-3) proteases containing combined resistance mutations associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme activity. Subsequent construction of HIV-1 (NL4-3) proviral clones containing the same mutations yielded viruses that were severely impaired in growth or nonviable, confirming that combination therapy may be advantageous. However, passage of BMS-186318-resistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug treatment, produced viable viruses resistant to both BMS-186318 and the second compound. The predominant breakthrough virus contained the G48V/A71T/V82A protease mutations. The clone-purified RF (G48V/A71T/V82A) virus, unlike the corresponding defective NL4-3 triple mutant, grew well and displayed cross-resistance to four distinct protease inhibitors. Chimeric virus and in vitro mutagenesis studies indicated that the RF-specific protease sequence, specifically the Ile at residue 10, enabled the NL4-3 strain with the triple mutant to grow. Our results clearly indicate that viral genetic background will play a key role in determining whether cross-resistance variants will arise.

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Poverty increases children's exposure to stress, elevating their risk for developing patterns of heightened sympathetic and parasympathetic stress reactivity. Repeated patterns of high sympathetic activation and parasympathetic withdrawal place children at risk for anxiety disorders. This study evaluated whether providing social support to preschool-age children during mildly stressful situations helps reduce reactivity, and whether this effect partly depends on children's previously assessed baseline reactivity patterns. The Biological Sensitivity to Context (BSC) theory proposes that highly reactive children may be more sensitive than less reactive children to all environmental influences, including social support. In contrast, conventional physiological reactivity (CPR) theory contends that highly reactive children are more vulnerable to the impact of stress but are less receptive to the potential benefits present within their social environments. In this study, baseline autonomic reactivity patterns were measured. Children were then randomly assigned to a high-support or neutral control condition, and the effect of social support on autonomic response patterns was assessed. Results revealed an interaction between baseline reactivity profiles and experimental condition. Children with patterns of high-reactivity reaped more benefits from the social support in the experimental condition than did their less reactive peers. Highly reactive children experienced relatively less reactivity reduction in the neutral condition while experiencing relatively greater reactivity reduction in the support condition. Despite their demonstrated stability over time, reactivity patterns are also quite susceptible to change at this age; therefore understanding how social support ameliorates reactivity will further efforts to avert stable patterns of high-reactivity among children with high levels of stress, ultimately reducing risk for anxiety disorders.

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Con la intención de experimentar con nuevas formas de aprendizaje a través de la Educomunicación y de los MOOCs sociales o sMOOC, creamos una experiencia de aprendizaje colaborativo y de empoderamiento individual y social, a través de nuestra propuesta “Road sMOOC: Un viaje Eduktransformador”, llevado a cabo en la Plataforma ECOLearning. La finalidad de este sMOOC ha sido emprender un viaje de descubrimiento personal y de alfabetización digital crítica, motivando a los participantes a que dejen aflorar su potencial transformador y que participen activamente en las redes sociales, generando así un aprendizaje colectivo y aumentando el impacto social de nuestras acciones. Se reflexiona sobre los autores que nos inspiraron, sobre lo que entendemos por Educomunicación transformadora y las posibilidades que ofrecen los sMOOC. Finalmente resumimos los objetivos, recursos creados, aprendizajes compartidos y conclusiones que surgen al co-crear una identidad colectiva y un espíritu de trabajo en comunidad como “Eduktransformers”.