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Orientador: Luciana Ferreira Tatagiba Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Filosofia e Ciências Humanas Resumo: Esta pesquisa tem como tema o processo organizativo e de construção das demandas do movimento de moradores de favelas e como este movimento social foi conformando, ao longo do tempo, seu repertório de luta para afirmação da moradia digna, mediados por seu apoiador principal naquele momento, a Igreja Católica, sua relação com o governo e seu processo de aprendizagem na tentativa do atendimento de suas reivindicações. Nosso principal objetivo é descrever como se davam as interações entre moradores de favelas e poder público, na cidade de São Paulo, entre 1975 e 1982, em um momento no qual as políticas públicas para as favelas aos poucos iam se deslocando da ênfase na remoção, ainda hegemônicas, para a ideia da assistência coletiva às famílias. Para a nossa análise retomaremos, de forma mais rápida e como contraponto, a luta dos moradores dos loteamentos clandestinos, como forma de avaliarmos os diferentes padrões de resposta estatal associados à luta pela terra urbana. A pesquisa foi desenvolvida utilizando bibliografia secundária e análise de documentos do período, alguns deles produzidos pelo próprio movimento e também pela pesquisa de jornais da época Abstract: This research has as its theme the organizational process and construction of the demands of the movement of the favelas's residents and how this social movement has been conforming, over time, his repertoire of struggle for affirmation of the decent housing, mediated by its main supporter at that time, the Catholic Church, its relationship with the Government and their learning process in the attempt to support their claims. Our main goal is to describe how were the interactions between the residents of the favelas and public authorities, in the city of São Paulo, between 1975 and 1982, in a moment in which public policies for the slums would gradually moving from an emphasis on removing, still hegemonic, to the idea of collective assistance to families. For our analysis, we will quickly recapture, as a counterpoint, the struggle of the residents of illegal squatter settlements as a way of assessing the different patterns of State response associated with the struggle for urban land. The survey was developed using secondary bibliography and analysis of documents of the period, some of them produced by the movement itself and also by search of newspapers of that time Mestrado Ciência Política Mestre em Ciência Política

Three discrete regions of the African swine fever virus (ASFV) were analysed in the genomes of a wide range of isolates collected from wild and domestic pigs in Sardinia, over a 31-year period (1978-2009). The analysis was conducted by genotyping based on sequence data from three single copy ASF genes. The E183L gene encoding the structural protein p54 and part of the gene encoding the p72 protein were used to delineate genotypes, before intra-genotypic resolution of viral relationships by analysis of tetramer amino acid repeats within the hypervariable central variable region (CVR) of the B602L gene. The data revealed that these isolates did not show significant variation in their p72 and p54 sequence when compared between different isolates showing a remarkable genetic stability of these genome regions. In particular, the phylogeny revealed that all the Sardinian isolates belong to the same largest and most homogeneous p72 genotype I together with viruses from Europe, South America, the Caribbean and West Africa, and p54 genotype Ia which comprises viruses from Europe and America. The analysis of B602L gene revealed a minor difference in the number of tetramer repeats, placing the Sardinian isolates into two clusters, accordingly to their temporal distribution, namely sub-group III and sub-group X, this latter showing a deletion of 12 tetramer repeats located in the centre of the array. The genetic variation of this fragment suggests that one sub-group could be derived from the other supporting the hypothesis of a single introduction of ASFV in Sardinia. © 2011 Springer Science+Business Media, LLC.

Bone marrow contusion is a common cause of chronic joint pain in the post-traumatic knee; it is usually associated with meniscal and/or ligament damage but it may also be the only abnormal sign. In this condition MRI plays a fundamental role because it is the only imaging technique which can diagnose it and accurately assess its extent and any cortical bone and/or cartilage involvement. We investigated the diagnostic potentials of 3 MR sequences in identifying and assessing the extent of bone contusion.January, 1994, to December, 1997, we performed 539 MR examinations of the knee on 478 patients with chronic joint pain following trauma. We used T1-weighted SE, T2*-weighted GE and T1-weighted SE sequences with fat saturation (fs), paying great attention to technical parameter setting. The images were retrospectively reviewed by groups of radiologists using 2 semi-objective evaluation systems: a qualitative assessment to grade the ease of detection of the contusion with each sequence and a quantitative assessment of contusion extent and of osteochondral involvement, if any, again for each sequence.The qualitative analysis showed that GE and SE-fs sequences were superior to the conventional ones in identifying bone contusion foci; GE sequences tended to overestimate the number of poorly depictable lesions relative to SE-fs ones. The quantitative analysis showed that the conventional sequences tend to underestimate the foci extent, while GE and SE-fs sequences performed nearly the same in the assessment of high-grade lesions. The number of low-midgrade lesions was overestimated by GE sequences relative to SE-fs ones.GE and SE-fs sequences permit accurate studies of bone contusions. Diagnostic efficacy is increased by enhancing the signal from non-fatty structures within a tissue rich in fat: the quantitative reduction of the non-fatty structural component and/or its replacement with abnormal components is thus best shown. Fat-suppression sequences were more accurate in defining lesion size, which is also related to low susceptibility to the artifacts from extrinsic and especially intrinsic structural inhomogeneities. In contrast, GE sequences demonstrated high susceptibility, which caused poorer definition of the contusion borders and, consequently, overestimation of the lesion size.

INTRODUCTION: Expansive masses arising from periskeletal soft tissues are a frequent challenge for the imaging specialist. Lesion diagnosis and characterization, and the assessment of benign/malignant nature are very important factors for treatment planning. We investigated MR capabilities in distinguishing benign from malignant masses and for histopathologic lesion characterization, also in the light of the latest most authoritative literature reports. MATERIAL AND METHODS: February 1995 to November 1997, we examined 237 patients with known space-occupying lesions arising from periskeletal soft tissues. T1- and PD/T2-weighted SE images were acquired on the most suitable planes. The findings were independently evaluated by two groups of radiologists who were asked a benignity/malignancy judgment based on specific morphological criteria and then a presumptive histopathologic characterization. The results were then compared with pathologic findings. RESULTS: We had high agreement rates for benignity/malignancy judgements, with only < or = 3.8% error rates. In contrast, rates were quite variable for histopathologic characterization and differed greatly by lesion type. The lesions, defined as malignant, could not be characterized histologically in approximately 18% of cases by both groups. DISCUSSION AND CONCLUSIONS: Our results, which are in substantial agreement with the recent authoritative literature, confirm MRI as an extremely reliable tool for distinguishing benign from malignant expansive masses arising from periskeletal soft tissues. On the contrary, MRI exhibits good specificity in histopathologic characterization only for the masses with such development as to permit identification of the anatomical compartment of origin, which are usually benign, as well as the masses with typical or pathognomonic tissue signal.

International Thermonuclear Experimental Reactor-Fusion Energy Advanced Tokamak (ITER-FEAT) Breeding Blanket (BB) will be different from the design defined by the released version named ‘ITER-98’ from the size as well as the neutron wall loading (NWL) point of view. In fact global dimensions and output power of ITER-FEAT have been approximately reduced by a factor of 3. The BB under study corresponds to the main solutions of ITER-98 project [1] [2] , that is: breeder in tube, consisting of pellets of a Lithium compound; neutron multiplier made of a pebble bed of Beryllium; cooling plates (using pressurized water as coolant) as basic cell boundaries; stainless steel as structural material. This paper deals with the neutronic as well as the thermal mechanical analyses of the envisaged BB in order to assess its performances in terms of Tritium production and thermal mechanical resistance. The code MCNP version 4B [3] has been used for the neutronic analyses while the thermal-mechanical analyses have been performed by means of the FEM codes MARC and ANSYS . The preliminary analyses demonstrated that the proposed BB verifies the temperature constraints for the Breeder (temperature contained in the ‘thermal window’) as well as for the multiplier (Be temperature lower than 500 °C), but the configuration of the breeder and multiplier in the basic cell have to be modified in order to obtain a Tritium Breeder Ratio larger than 1.

We have previously reported that the cytokines IFN-gamma and TNF-alpha each upregulate the expression of class I MHC proteins and, in combination, induce the expression of class II MHC proteins on pancreatic islet cells. IFN-gamma and TNF-alpha are therefore implicated in the immunologic destruction of beta-cells in insulin-dependent diabetes mellitus. The objective of the present study was to define the effects of IFN-gamma and TNF-alpha on the function and viability of murine pancreatic islet beta-cells in vitro. Exposure of islets for 3 days to 200 U/ml of either IFN-gamma or TNF-alpha did not affect glucose-stimulated insulin release, but at higher concentrations (2000 U/ml) of either cytokine there was significant inhibition of glucose-stimulated insulin release. In combination, IFN-gamma and TNF-alpha each at 200 U/ml caused significant inhibition of glucose-stimulated insulin release; at 2000 U/ml glucose-stimulated insulin release was abolished. In time-course experiments, glucose-stimulated insulin release from islets exposed to IFN-gamma and TNF-alpha each at 1000 U/ml was significantly increased at 4-h (twofold increase compared with control islets), decreased back to control levels at 18 h, significantly inhibited by 24 h (threefold decrease compared with control islets), and completely abolished by 48 h. The progressive impairment of beta-cell function mediated by IFN-gamma plus TNF-alpha was associated with morphologic derangement of the islets that were almost totally disintegrated by day 6 of exposure to the cytokines. At day 6, insulin content of the islets was significantly reduced by exposure to TNF-alpha but not IFN-gamma. The combination of IFN-gamma and TNF-alpha resulted in a further dose-dependent depletion in insulin content compared with TNF-alpha alone. The synergistic functional and cytotoxic effects of IFN-gamma and TNF-alpha are consistent with a direct role for these cytokines in the destruction of beta-cells in insulin-dependent diabetes.

A very rare case of isolated juvenile osteochondroses of epiphyseal metacarpal head nuclei is reported (Mauclaire's disease).

A derivative of ammonia caramel colour (AC) is known to induce a selective lymphopenia in rats. Accordingly, the haematological effects were studied in mice of oral administration in drinking water of 2-acetyl-4(5)-tetrahydroxybutylimidazole (THI), the component of AC responsible for lymphopenia. Initially five groups of BALB/c mice (five mice per group) were given doses of THI ranging from 0 to 200 parts/10(6) and bled weekly. Doses of THI from 5 to 100 parts/10(6) had no effect on circulating leucocytes over 6 weeks, but lymphopenia occurred with 200 parts/10(6). An increase in the concentration of THI to 400 parts/10(6) in the group on the lowest dose resulted in lymphopenia. An increase in dosage in two groups of mice, to 1000 and 2000 parts/10(6), resulted in marked lymphopenia. The number of neutrophils, eosinophils and monocytes remained unchanged throughout the experiment. Measurement of the proportions of CD4(L3T4)+ and CD8(Ly2)+ lymphocytes in lymph nodes from mice on high doses of THI did not show a selective depression of either subset, although both were increased relative to non-T cells. THI causes a selective lymphopenia in mice, as in rats, but at relatively higher doses, and merits investigation in mice as an experimental treatment for states of lymphocyte excess or overactivity.