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Abstract Direct stock purchase plans offer low trading costs. However, some plans batch orders and execute trades once per week. If prices spike during batch buying, or plummet during batch [...]

Abstract Retail certificates of deposit provide financial institutions with funds and depositors with income. Because interest rates and terms on deposits vary, understanding the reasons for the variation should help [...]

Chlamydiae are obligate intracellular pathogens that can exhibit a broad host range in infection tropism despite maintaining near genomic identity. Here, we have investigated the molecular basis for this unique host--pathogen relationship. We show that human and murine chlamydial infection tropism is linked to unique host and pathogen genes that have coevolved in response to host immunity. This intimate host--pathogen niche revolves around a restricted repertoire of host species-specific IFN-[gamma]-mediated effector responses and chlamydial virulence factors capable of inhibiting these effector mechanisms. In human epithelial cells, IFN-[gamma] induces indoleamine 2,3-dioxygenase expression that inhibits chlamydial growth by depleting host tryptophan pools. Human chlamydial strains, but not the mouse strain, avoid this response by the production of tryptophan synthase that rescues them from tryptophan starvation. Conversely, in murine epithelial cells IFN-[gamma] induces expression of p47 GTPases, but not indoleamine 2,3-dioxygenase. One of these p47 GTPases (ligp1) was shown by small interfering RNA silencing experiments to specifically inhibit human strains, but not the mouse strain. Like human strains and their host cells, the murine strain has coevolved with its murine host by producing a large toxin possessing YopT homology, possibly to circumvent host GTPases. Collectively, our findings show chlamydial host infection tropism is determined by IFN-[gamma]-mediated immunity. immunity | virulence factors | pathogenesis | defense | coevolution

BackgroundThe T-cell response to chlamydia genital tract infections in humans and mice is unusual because the majority of antigen-specific CD8 T cells are not class I restricted (referred to here as “unrestricted” or “atypical”). We previously reported that a subset of unrestricted murine chlamydia-specific CD8 T cells had a cytokine polarization pattern that included interferon (IFN)-γ and interleukin (IL)-13.MethodsIn this study, we investigated the transcriptome of CD8γ13 T cells, comparing them to Tc1 clones using microarray analysis. That study revealed that CD8γ13 polarization included IL-5 in addition to IFN-γ and IL-13. Adoptive transfer studies were performed with Tc1 clones and a CD8γ13 T-cell clone to determine whether either influenced bacterial clearance or immunopathology during Chlamydia muridarum genital tract infections. ResultsTo our surprise, an adoptively transferred CD8γ13 T-cell clone was remarkably proficient at preventing chlamydia immunopathology, whereas the multifunctional Tc1 clone did not enhance clearance or significantly alter immunopathology. Mapping studies with major histocompatibility complex (MHC) class I- and class II-deficient splenocytes showed our previously published chlamydia-specific CD8 T-cell clones are MHC class II restricted.ConclusionsThe MHC class II-restricted CD8 T cells may play an important role in protection from intracellular pathogens that limit class I antigen presentation or diminish CD4 T-cell numbers or impair their function. [ABSTRACT FROM AUTHOR]

Background: Chlamydia trachomatis and Chlamydia muridarum are intracellular bacterial pathogens of mucosal epithelial cells. CD4 T cells and major histocompatibility complex (MHC) class II molecules are essential for protective immunity against them. Antigens presented by dendritic cells (DCs) expand naive pathogen-specific T cells (inductive phase), whereas antigens presented by epithelial cells identify infected epithelial cells as targets during the effector phase. We previously showed that DCs infected by C trachomatis or C muridarum present epitopes from a limited spectrum of chlamydial proteins recognized by Chlamydia-specific CD4 T cells from immune mice.Methods: We hypothesized that Chlamydia-infected DCs and epithelial cells present overlapping sets of Chlamydia-MHC class II epitopes to link inductive and effector phases to generate protective immunity. We tested that hypothesis by infecting an oviductal epithelial cell line with C muridarum, followed by immunoaffinity isolation and sequencing of MHC class I- and II-bound peptides.Results: We identified 26 class I-bound and 4 class II-bound Chlamydia-derived peptides from infected epithelial cells. We were surprised to find that none of the epithelial cell class I- and class II-bound chlamydial peptides overlapped with peptides presented by DCs.Conclusions: We suggest the discordance between the DC and epithelial cell immunoproteomes has implications for delayed clearance of Chlamydia and design of a Chlamydia vaccine. [ABSTRACT FROM AUTHOR]

Say on Pay is a corporate governance mechanism required by the Dodd-Frank Wall Street Reform and Consumer Protection Act of 2010. The mechanism gave hope for control of an agency and managerial power problem. The problem focused on executive pay that appeared to be higher than necessary for efficient business operations in companies where agency problems caused a residual loss exacerbated by managerial power. The problem was addressed by requiring public companies to give their stockholders the opportunity to review and comment on executive pay with non-binding votes called Say on Pay. The objective of this study is to look for evidence that Say on Pay reduced the impact of agency and managerial power problems by reducing executive pay. A search for reductions in executive pay was done in large U.S. companies by comparing levels of executive pay before and after Say on Pay. Levels of executive pay are examined as ratios of pay to size, pay to earnings, and pay to overhead expense. The results are consistent with agency and managerial power theories because most pay ratios fell after the implementation of Say on Pay voting. Pay ratios fell the most in companies whose pay ratios were the highest before the implementation of Say on Pay. [ABSTRACT FROM AUTHOR]

The objectives of this paper are threefold: to evaluate a number of probability distributions with respect to their ability to accurately describe selected financial data; use the estimated parameters of the "best fitting" distribution to estimate the value at risk (VaR), and expected shortfall, and illustrate the need for analysts, risk managers, and traders to discover the distribution that provides the best fit for the specific data set under consideration. It is widely known, but infrequently accepted, that many assumptions underlying many probability distributions, including the normal distribution, do not provide appropriate descriptions of many financial data. In such instances, they provide an inadequate basis for measuring risk exposures and estimates of the adequate amount of economic capital to be held to be held against the existing risk exposures. Recent financial events and financial reversals have renewed interest in the discovery, measurement, analysis, and management of the risk exposures faced by financial institutions and other business firms. This renewed interest has causes analysts to reexamine past practices and explore new approaches to the measurement and management of risk exposure faced by their institutions in particular and the practice of risk management in general. Given this climate a worthy venture would be to evaluate a number of probability distributions, many of which are esoteric to risk analysis, and some that even exist at the periphery of statistical analysis. Frequently risk managers routinely try to fit probability distributions they have used in the past without trying new distributions in order to see if they can provide a better fit for their new data sample. The analyst should be open to the selection of the most appropriate probability distribution because of the bearing it has on the determination of the appropriate amount of economic capital to be held against the probable losses. This study applies sixty five distributions to a sample of the daily Euro/Dollar exchange rate data in order to ascertain the probability distribution that provides the best "goodness of fit" for the sample period. The coefficients derived from this distribution are then used in the estimation of the value at risk and expected shortfall faced by a trading floor given this scenario. [ABSTRACT FROM AUTHOR]