168 research outputs found

    On the timeliness of price discovery

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    Price discovery is the process whereby value-relevant, private information becomes impounded or reflected in a stock's publicly-observable market price. The timeliness of price discovery refers to how quickly that process takes effect. There is no reason to believe either that all private information is discovered equally quickly or that price discovery is equally speedy for all firms. The latter observation suggests it would be worthwhile knowing why the timeliness of price discovery differs across firms, even the more so in an environment where all listed companies by law must disclose most material price-sensitive information as soon as they become aware of it. The other observation, that not all private information is discovered equally quickly, implies we should focus on a material, periodic event when we compare timeliness across firms. A good candidate is the announcement of the company's annual results, since for many years is has been known that annual earnings alone captures at least half the value-relevant information released by the average firm over the 12 months leading up to this date. We use various approaches to explore measures of timeliness and what they can tell us. We review a number of studies that have considered various aspects of timeliness in different countries and extend and contrast their findings. We also examine the relationship between the timeliness of price discovery and analogous measures based upon firms' formal disclosures to the share market and upon analysts' consensus earnings forecasts. Finally, we report on an issue of major concern to regulators and market operators, namely the influence of corporate governance on the timeliness of price discovery

    The role of credibility in the relation between management forecasts and analyst forecasts in Japan

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    We explore the relation between management forecasts and analyst forecasts to determine whether a moderating role exists for credibility. Two types of credibility are examined: management credibility and analyst credibility. Management credibility is evaluated by management\u27s forecasting ability (based upon prior forecast outcomes) and the firm\u27s underlying Corporate Governance (CG) structure. Analyst credibility is assessed by their forecasting ability only, based upon prior forecast outcomes. Two questions are addressed by this study: (1) does management credibility moderate the relation between management\u27s initial forecasts and initial analyst forecasts? and, (2) is the relation between analyst forecasts and subsequent management forecast revisions moderated by analyst credibility

    On the statistical mechanics of prion diseases

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    We simulate a two-dimensional, lattice based, protein-level statistical mechanical model for prion diseases (e.g., Mad Cow disease) with concommitant prion protein misfolding and aggregation. Our simulations lead us to the hypothesis that the observed broad incubation time distribution in epidemiological data reflect fluctuation dominated growth seeded by a few nanometer scale aggregates, while much narrower incubation time distributions for innoculated lab animals arise from statistical self averaging. We model `species barriers' to prion infection and assess a related treatment protocol.Comment: 5 Pages, 3 eps figures (submitted to Physical Review Letters

    All clinically-relevant blood components transmit prion disease following a single blood transfusion: a sheep model of vCJD

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    Variant CJD (vCJD) is an incurable, infectious human disease, likely arising from the consumption of BSE-contaminated meat products. Whilst the epidemic appears to be waning, there is much concern that vCJD infection may be perpetuated in humans by the transfusion of contaminated blood products. Since 2004, several cases of transfusion-associated vCJD transmission have been reported and linked to blood collected from pre-clinically affected donors. Using an animal model in which the disease manifested resembles that of humans affected with vCJD, we examined which blood components used in human medicine are likely to pose the greatest risk of transmitting vCJD via transfusion. We collected two full units of blood from BSE-infected donor animals during the pre-clinical phase of infection. Using methods employed by transfusion services we prepared red cell concentrates, plasma and platelets units (including leucoreduced equivalents). Following transfusion, we showed that all components contain sufficient levels of infectivity to cause disease following only a single transfusion and also that leucoreduction did not prevent disease transmission. These data suggest that all blood components are vectors for prion disease transmission, and highlight the importance of multiple control measures to minimise the risk of human to human transmission of vCJD by blood transfusion

    Foodborne transmission of bovine spongiform encephalopathy to nonhuman primates

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    Risk for human exposure to bovine spongiform encephalopathy (BSE)-inducing agent was estimated in a nonhuman primate model. To determine attack rates, incubation times, and molecular signatures, we orally exposed 18 macaques to 1 high dose of brain material from cattle with BSE. Several macaques were euthanized at regular intervals starting at 1 year postinoculation, and others were observed until clinical signs developed. Among those who received >5 g BSE-inducing agent, attack rates were 100% and prions could be detected in peripheral tissues from 1 year postinoculation onward. The overall median incubation time was 4.6 years (3.7-5.3). However, for 3 macaques orally exposed on multiple occasions, incubation periods were at least 7-10 years. Before clinical signs were noted, we detected a non-type 2B signature, indicating the existence of atypical prion protein during the incubation period. This finding could affect diagnosis of variant Creutzfeldt-Jakob disease in humans and might be relevant for retrospective studies of positive tonsillectomy or appendectomy specimens because time of infection is unknown

    The syntax of ‘-cā’ (*-kwe) in Ahunavaiti Gāthā

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    This paper seeks to provide a full description of the syntactic behaviour of the enclitic co-ordinate conjunction -cā in the earliest stage of the Avestan language. By studying the occurrences of the particle in Ahunavaiti Gāthā, a distributive analysis is provided together with an interpretative hypothesis of its distributive dynamics. Two syntactic levels, phrase and sentence, are taken into consideration. Finally, a syntactic domain-based variation is argued and two clitic functional variants are identified as synchronically operating conjunction strategies

    Biochemical Properties of Highly Neuroinvasive Prion Strains

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    Infectious prions propagate from peripheral entry sites into the central nervous system (CNS), where they cause progressive neurodegeneration that ultimately leads to death. Yet the pathogenesis of prion disease can vary dramatically depending on the strain, or conformational variant of the aberrantly folded and aggregated protein, PrPSc. Although most prion strains invade the CNS, some prion strains cannot gain entry and do not cause clinical signs of disease. The conformational basis for this remarkable variation in the pathogenesis among strains is unclear. Using mouse-adapted prion strains, here we show that highly neuroinvasive prion strains primarily form diffuse aggregates in brain and are noncongophilic, conformationally unstable in denaturing conditions, and lead to rapidly lethal disease. These neuroinvasive strains efficiently generate PrPSc over short incubation periods. In contrast, the weakly neuroinvasive prion strains form large fibrillary plaques and are stable, congophilic, and inefficiently generate PrPSc over long incubation periods. Overall, these results indicate that the most neuroinvasive prion strains are also the least stable, and support the concept that the efficient replication and unstable nature of the most rapidly converting prions may be a feature linked to their efficient spread into the CNS
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