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The “crisis of the social issue” in the EU has led to a certain consensus in the need to renew the organizational and institutional model of public administration. The core of the reform implies important administrative changes in most of the European welfare states. Those changes are inspired on theories such as the new public management, management by objectives or partnership. Such changes involve both semantic (“sharing responsibilities”, “effective costs”, or the substitution of “citizen under an administration” by “consumer”) and political (predominance of scattered forms of power and the individualization of responsibilities) transformations which operate in the framework of individuals and State relations. The paradigms of activation and flexicurity have been central in this public administration modernization project. This commitment with new forms of governance of social issues has important consequences for the political and moral foundations of social cohesion, and the Spanish case is not an exception. This paper aims at looking at those representations of “modernization” (as they appear in debates about the employment services restructuring policies) in detail as well as providing references to the trajectory of such reforms of public services since the early eighties to the beginning of the crisis.

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Type III galactosaemia is a hereditary disease caused by reduced activity in the Leloir pathway enzyme, UDP-galactose 4'-epimerase (GALE). Traditionally, the condition has been divided into two forms-a mild, or peripheral, form and a severe, or generalized, form. Recently it has become apparent that there are disease states which are intermediate between these two extremes. Three mutations associated with this intermediate form (S81R, T150M and P293L) were analysed for their kinetic and structural properties in vitro and their effects on galactose-sensitivity of Saccharomyces cerevisiae cells that were deleted for the yeast GALE homologue Gal10p. All three mutations result in impairment of the kinetic parameters (principally the turnover number, k(cat)) compared with the wild-type enzyme. However, the degree of impairment was mild compared with that seen with the mutation (V94M) associated with the generalized form of epimerase deficiency galactosaemia. None of the three mutations tested affected the ability of the protein to dimerize in solution or its susceptibility to limited proteolysis in vitro. Finally, in the yeast model, each of the mutated patient alleles was able to complement the galactose-sensitivity of gal10 Delta cells as fully as was the wild-type human allele. Furthermore, there was no difference from control in metabolite profile following galactose exposure for any of these strains. Thus we conclude that the subtle biochemical and metabolic abnormalities detected in patients expressing these GALE alleles likely reflect, at least in part, the reduced enzymatic activity of the encoded GALE proteins.

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