34 research outputs found

    The impact of inflation risk on forward trading and production

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    This paper examines the behavior of a competitive firm that faces joint price and inflation risk. Given that the price risk is negatively correlated with the inflation risk in the sense of expectation dependence, we show that the firm optimally opts for an over-hedge (under-hedge) if the firm’s coefficient of relative risk aversion is everywhere no greater (no smaller) than unity. We show further that banning the firm from forward trading may induce the firm to produce more or less, depending on whether the price risk premium is positive or negative, respectively. While the price risk premium is unambiguously negative in the absence of the inflation risk, it is not the case when the inflation risk prevails. In contrast to the conventional wisdom, forward hedging needs not always promote production should firms take inflation seriously.info:eu-repo/semantics/publishedVersio

    On the Schoenberg Transformations in Data Analysis: Theory and Illustrations

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    The class of Schoenberg transformations, embedding Euclidean distances into higher dimensional Euclidean spaces, is presented, and derived from theorems on positive definite and conditionally negative definite matrices. Original results on the arc lengths, angles and curvature of the transformations are proposed, and visualized on artificial data sets by classical multidimensional scaling. A simple distance-based discriminant algorithm illustrates the theory, intimately connected to the Gaussian kernels of Machine Learning

    Rotavirus NSP1 Inhibits NFÎșB Activation by Inducing Proteasome-Dependent Degradation of ÎČ-TrCP: A Novel Mechanism of IFN Antagonism

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    Mechanisms by which viruses counter innate host defense responses generally involve inhibition of one or more components of the interferon (IFN) system. Multiple steps in the induction and amplification of IFN signaling are targeted for inhibition by viral proteins, and many of the IFN antagonists have direct or indirect effects on activation of latent cytoplasmic transcription factors. Rotavirus nonstructural protein NSP1 blocks transcription of type I IFNα/ÎČ by inducing proteasome-dependent degradation of IFN-regulatory factors 3 (IRF3), IRF5, and IRF7. In this study, we show that rotavirus NSP1 also inhibits activation of NFÎșB and does so by a novel mechanism. Proteasome-mediated degradation of inhibitor of ÎșB (IÎșBα) is required for NFÎșB activation. Phosphorylated IÎșBα is a substrate for polyubiquitination by a multisubunit E3 ubiquitin ligase complex, Skp1/Cul1/F-box, in which the F-box substrate recognition protein is ÎČ-transducin repeat containing protein (ÎČ-TrCP). The data presented show that phosphorylated IÎșBα is stable in rotavirus-infected cells because infection induces proteasome-dependent degradation of ÎČ-TrCP. NSP1 expressed in isolation in transiently transfected cells is sufficient to induce this effect. Targeted degradation of an F-box protein of an E3 ligase complex with a prominent role in modulation of innate immune signaling and cell proliferation pathways is a unique mechanism of IFN antagonism and defines a second strategy of immune evasion used by rotaviruses

    Some general results for moments in bivariate distributions

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    Integration by parts formula in n variables, Integration by parts in two variables, Bivariate survival function, Covariance between two functions, Generalized Gamma function,
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