855 resultados para Competitive Exclusion Principle


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The society wrestles with mass social change congruent with economic globalization and the communications revolution. This change creates new challenges for the social work profession in the areas of social and economic justice. This article analyzes the terminology of the new global era, words that signify a paradigm shift in outlook, most of them a reaction to the new authoritarianism of the age. Globalization, oppression, social exclusion, human rights, harm reduction, and restorative justice are the representative terms chosen.

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Addressing the situation of marginalised youth has been central to policy initiatives directed at tackling poverty and social exclusion in the UK in recent years. The period since 1997 has therefore witnessed a renewed emphasis upon the development of a coherent framework for youth policy in the UK with the goal of promoting youth inclusion and participation. Nevertheless, understanding the nature and prospects for policies designed to tackle youth exclusion involves a deeper interrogation of the concept of ‘social exclusion’ and its applications within UK policy debates. Here, it is argued that whilst considerable progress has been made in the promotion of a coherent and integrated strategy for youth inclusion in the UK such policies are unlikely to be effective without a re-conceptualisation of the nature of social exclusion, its causes and consequences. In particular, a more holistic understanding is called for which extends beyond an emphasis on labour market activation policies as a response to the circumstances facing marginalised youth in the UK and elsewhere, and one which interrogates exclusionary processes and institutional practices rather than addressing only the symptoms of disadvantage.

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A great share of literature on social exclusion has been based mainly on the analysis of official survey data. Whereas these efforts have provided insights into the characteristics and conditions of those people living at the margins of mainstream social relations, they have however failed to encompass those who live beyond these very margins. Meanwhile, research on these hidden subpopulations, such as homeless and other vulnerable groups, remains generally less abundant and is significantly detached from the theoretical core of the debate on social exclusion. The concern about these shortcomings lies at the heart of our research. We seek to bring some light to the area by using data made available by an organization that provides services to people experiencing homelessness in Barcelona (Spain). The data sample contains clients in early stages of exclusion and others in chronic situations. Thus, we attempt to identify some of the variables that operate in preventing the "chronification" of those individuals in situation of social exclusion. Our findings suggest that certain variables such as educational level, income and housing type, which are considered to be central predictors in the analysis of poverty, behave differently when analyzing differences between stages of social exclusion. Although these results cannot be extrapolated to the whole Spanish or European reality, they could provide useful insight for future investigations on this topic.

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The receptor tyrosine kinase MET is a prime target in clinical oncology due to its aberrant activation and involvement in the pathogenesis of a broad spectrum of malignancies. Similar to other targeted kinases, primary and secondary mutations seem to represent an important resistance mechanism to MET inhibitors. Here, we report the biologic activity of a novel MET inhibitor, EMD1214063, on cells that ectopically express the mutated MET variants M1268T, Y1248H, H1112Y, L1213V, H1112L, V1110I, V1206L, and V1238I. Our results demonstrate a dose-dependent decrease in MET autophosphorylation in response to EMD1214063 in five out of the eight cell lines (IC50 2-43nM). Blockade of MET by EMD1214063 was accompanied by a reduced activation of downstream effectors in cells expressing EMD1214063-sensitive mutants. In all sensitive mutant-expressing lines, EMD1214063 altered cell cycle distribution, primarily with an increase in G1 phase. EMD1214063 strongly influenced MET-driven biological functions, such as cellular morphology, MET-dependent cell motility and anchorage-independent growth. To assess the in vivo efficacy of EMD1214063, we used a xenograft tumor model in immunocompromised mice bearing NIH3T3 cells expressing sensitive and resistant MET mutated variants. Animals were randomized for the treatment with EMD1214063 (50mg/kg/day) or vehicle only. Remarkably, five days of EMD1214063 treatment resulted in a complete regression of the sensitive H1112L-derived tumors, while tumor growth remained unaffected in mice with L1213V tumors and in vehicle-treated animals. Collectively, the current data identifies EMD1214063 as a potent MET small molecule inhibitor with selective activity towards mutated MET variants.