9,468 research outputs found

    Corruption, Seigniorage and Growth: Theory and Evidence

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    This paper presents an analysis of the effect of bureaucratic corruption on economic growth through a public finance transmission channel. At the theoretical level, we develop a simple dynamic general equilibrium model in which financial intermediaries make portfolio decisions on behalf of agents, and bureaucrats collect tax revenues on behalf of the government. Corruption takes the form of the embezzlement of public funds, the effect of which is to increase the government’s reliance on seigniorage finance. This leads to an increase in inflation which, in turn, reduces capital accumulation and growth. At the empirical level, we use data on 82 countries over a 20-year period to test the predictions of our model. Taking proper account of the government’s budget constraint, we find strong evidence to support these predictions under different estimation strategies. Our results are robust to a wide range of sensitivity tests.corruption, seigniorage, inflation, growth

    Exploring the fragile antiferromagnetic superconducting phase in CeCoIn5

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    CeCoIn5 is a heavy fermion Type-II superconductor which exhibits clear indications of Pauli-limited superconductivity. A variety of measurements give evidence for a transition at high magnetic fields inside the superconducting state, when the field is applied either parallel to or perpendicular to the c axis. When the field is perpendicular to the c axis, antiferromagnetic order is observed on the high-field side of the transition, with a magnetic wavevector of (q q 0.5), where q = 0.44 reciprocal lattice units. We show that this order remains as the magnetic field is rotated out of the basal plane, but the associated moment eventually disappears above 17 degrees, indicating that the anomalies seen with the field parallel to the c axis are not related to this magnetic order. We discuss the implications of this finding.Comment: Accepted Physical Review Letters, September 2010. 4 pages, 4 figure

    Preclinical characterization of drug like glucocorticoid induced leucine zipper peptide analogs

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    poster abstractMany intermolecular interactions in a eukaryotic cell are mediated through protein-peptide interactions. For efficient interaction, the peptide scans the protein surface for a large enough pocket into which it anchors through a small number of residues/core motif that contribute maximally to the free energy of binding. Of special significance is the preponderance of proline rich sequences that preferentially adopt the left-handed polyproline type II (PPII) helical conformation in the interface peptides. Availability of both side chain and backbone carbonyls for interaction makes PPII helix an excellent recognition motif. Glucocorticoid induced leucine zipper (GILZ), is a glucocorticoid responsive protein that has been shown to suppress immuno-inflammatory responses by preventing the nuclear translocation of the p65 subunit of the transcription factor nuclear factor-kappa B (NF-ÎşB). Mutational and binding studies localized the sites of interaction to the proline rich region at the carboxy terminus of GILZ and the transactivation domain of p65. Similar to most intermolecular interactions mediated by proline rich motifs the strength of interaction between the GILZ and the p65 proteins is in the micromolar concentration suggesting weak binding kinetics. A widely used strategy in the discovery of peptide drugs involves exploitation of the complementary surfaces of the naturally occurring binding partners. We observed that a synthetic peptide (GILZ-P) derived from the proline rich region of GILZ suppressed immune mediated inflammatory responses in mice. Here we characterize GILZ-P structurally and evaluate its toxicity and efficacy in mature human macrophage like THP-1 cells. We show that the GILZ-P adopts an extended polyproline type II helical conformation. Functionally GILZ-P is non-toxic, suppresses NF B activation on by activated macrophages suggesting a therapeutic potential in pathologies wherein persistent inflammation plays critical role in the disease initiation and/or progression
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