Australian residents are tax-advantaged, relative to American investors, in their access to imputation tax credits on Australian stocks. This paper provides evidence consistent with a difference in dividend valuations between Australian stocks and their American Depositary Receipts (ADRs). The ex-dividend drop-off ratio is lower for ADRs relative to their underlying Australian stocks and this difference is most pronounced for stocks that have imputation tax credits and high dividend yields. Consistent with dividend capture trading in the Australian market, the difference in drop-off ratios is driven by both temporarily higher Australian cum-prices and temporarily lower Australian ex-prices. Abnormal trading volume about the ex-day is present in both markets and in the Australian market the abnormal volume is greater for dividends with imputation tax credits. Dividend-related trading leads to price differences across the markets on the ex-dividend day. Price differences are also observed when the stock and the ADR trade with different dividend entitlements due to different ex-dividend dates.
Multiple Sclerosis (MS) is a disease characterized by immune-mediated destruction of central nervous system (CNS) myelin. Current MS therapies aim to block peripheral immune cells from entering the CNS. While these treatments limit new inflammatory activity in the CNS, no treatment effectively prevents long-term disease progression and disability accumulation in MS patients. One explanation for this paradox is that current therapies are ineffective at targeting immune responses already present in the CNS. To this end, we sought to understand the metabolic properties of T cells that mediate ongoing inflammation in the demyelinating CNS. Using experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice, a well-studied model of MS, we showed that the CD4+ and CD8+ T cells that invade the EAE CNS are highly glycolytic. This elevation of glycolysis is mediated by upregulated expression of the glycolytic machinery, and is essential for inflammatory responses to myelin. Surprisingly, we found that an inhibitor of glyceraldehyde-3 phosphate (GAPDH), 3-bromopyruvic acid (3-BrPa), blocks IFN-γ but not IL-17A production in immune cells isolated from the EAE CNS. Indeed, in vitro studies confirmed that the production of IFN-γ by differentiated Th1 cells is more sensitive to 3-BrPa than the production of IL-17A by Th17 cells. Finally, in transfer models of EAE, 3-BrPa robustly attenuates the encephalitogenic potential of EAE-driving immune cells. These data are one of the first to demonstrate the metabolic properties of T cells in the demyelinating CNS in vivo.
Reviews previous research on predicting financial distress and the effects of US Chapter 11 bankruptcy (C11B); and explains how survival analysis and Cox’s (1972) proportional hazards model can be used to estimate the financial outcome for the shareholders of C11B. Reduces a previous data set (Russel et al 1999) of 154 companies entering C11B between 1984 and 1993 to 59 (54 of which gave no value to shareholders) and estimates two models to predict this: one based on firm‐specific covariates only and the other adding market‐wide covariates. Explains the methodology, presents the results and uses receiver operating characteristic curves to compare the predictive accuracy of the two. Finds little difference between the and suggests using the simpler model. Briefly summarizes the variables which are most useful in predicting the value outcomes of C11B for shareholders and recognizes the limitations of the study.
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