T-Dualities and Courant Algebroid Relations

We develop a new approach to T-duality based on Courant algebroid relations which subsumes the usual T-duality as well as its various generalisations. Starting from a relational description for the reduction of exact Courant algebroids over foliated manifolds, we introduce a weakened notion of generalised isometries that captures the generalised geometry counterpart of Riemannian submersions when applied to transverse generalised metrics. This is used to construct T-dual backgrounds as generalised metrics on reduced Courant algebroids which are related by a generalised isometry. We prove an existence and uniqueness result for generalised isometric exact Courant algebroids coming from reductions. We demonstrate that our construction reproduces standard T-duality relations based on correspondence spaces. We also describe how it applies to generalised T-duality transformations of almost para-Hermitian manifolds.Comment: 68 page

Activation of the JAK/STAT pathway leads to proliferation of ST14A central nervous system progenitor cells

We were interested in whether central nervous system progenitor cells possess the signal transduction machinery necessary to mediate cytokine functions and whether this machinery can become activated upon stable expression of a particular cytokine receptor. For this purpose we utilized a previously obtained conditionally immortalized striatum-derived nestin-positive cell line (ST14A). We found that ST14A cells express Jak2, but not Jak1 or Tyk2. An identical pattern of expression was found in embryonic striatal tissue. To evaluate the susceptibility of these cytokine specific cytoplasmic transducers to activation, ST14A cells were stably transfected with the alpha and beta (AIC2A) chains of the murine interleukin-3 receptor. Four independent lines expressing both the alpha and beta receptor subunits were obtained. We found that cells from each of these lines were induced to proliferate upon exposure to interleukin-3. Dose response curve, antibody blocking experiments and binding studies revealed that the response was mediated by the reconstituted high affinity interleukin-3 receptor. Immunoprecipitation studies on these cells showed that Jak2 and Stat5 were being phosphorylated after stimulation of the reconstituted receptor. These results indicate that members of the JAK/STAT family of proteins are expressed in central nervous system progenitor cells and are susceptible to activation through stimulation of an exogenously expressed cytokine receptor, ultimately leading to cell proliferation

Wild-type huntingtin protects from apoptosis upstream of caspase-3

Expansion of a polyglutamine sequence in the N terminus of huntingtin is the gain-of-function event that causes Huntington's disease. This mutation affects primarily the medium-size spiny neurons of the striatum. Huntingtin is expressed in many neuronal and non-neuronal cell types, implying a more general function for the wild-type protein. Here we report that wild-type huntingtin acts by protecting CNS cells from a variety of apoptotic stimuli, including serum withdrawal, death receptors, and pro-apoptotic Bcl-2 homologs. This protection may take place at the level of caspase-9 activation. The full-length protein also modulates the toxicity of the poly-Q expansion. Cells expressing full-length mutant protein are susceptible to fewer death stimuli than cells expressing truncated mutant huntingtin

Wild-type huntingtin protects from apoptosis upstream of caspase-3

Expansion of a polyglutamine sequence in the N terminus of huntingtin is the gain-of-function event that causes Huntington's disease. This mutation affects primarily the medium-size spiny neurons of the striatum. Huntingtin is expressed in many neuronal and non-neuronal cell types, implying a more general function for the wild-type protein. Here we report that wild-type huntingtin acts by protecting CNS cells from a variety of apoptotic stimuli, including serum withdrawal, death receptors, and pro-apoptotic Bcl-2 homologs. This protection may take place at the level of caspase-9 activation. The full-length protein also modulates the toxicity of the poly-Q expansion. Cells expressing full-length mutant protein are susceptible to fewer death stimuli than cells expressing truncated mutant huntingtin

Product market competition with differentiated goods and social welfare in the presence of an industry-wide union

Mainstream locus communis indicates that a more competitive product market leads to higher social welfare levels. Using a Conjectural Variation (CV) model, this research note analyzes the effects on welfare of different degrees of product market competition in a duopoly with differentiated goods. Bargaining between the firms and the industry-wide union occurs under the Efficient Bargaining (EB) model. The work indicates that, with close substitute goods, social welfare is maximized for the inter- mediate levels of market competition, whereas more independent goods lead to the standard result of a high welfare level under competitive markets.info:eu-repo/semantics/publishedVersio

Reverse discrimination and efficiency in education

This article shows that reverse discrimination policies can find a justification purely on efficiency grounds. We study the optimal provision of education when households belong to different groups, differing in the distribution of the potential to benefit from education among individuals, which is private information. The main result is that high-potential individuals from groups with relatively few high-potential individuals should receive more education than otherwise identical individuals from groups with a more favorable distribution of these benefits

Privatization in the presence of foreign competition and strategic policies

Recent evidence shows that developing and transition economies are increasingly privatizing their public firms and also experiencing rapid growth of inward foreign direct investment (FDI). In an international mixed oligopoly with strategic tax/subsidy policies, we analyze the interaction between privatization and FDI. We find that the incentive for FDI increases with privatization. However, the possibility of FDI reduces the degree of privatization. Our paper shows that FDI policies reducing the fixed-cost of undertaking FDI may need to complement the privatization policies to attract FDI and to improve domestic welfare