Taxation and Corporate Pension Policy

Section I introduces the material in the context of existing research. In Section II the effects of the tax structure on the desirability of having pension plans and on the funding and investment policies of such plans is discussed. Section III discusses the discrepancies between the prescriptions presented above and current practice. The Appendix contains a detailed analysis of each of the two tax provisions that apply to corporate pension plans.

Treatment Recommendations for Locally Advanced, Non-Small-Cell Lung Cancer: The Influence of Physician and Patient Factors

To determine the impact of patient age, comorbidity, and physician factors on treatment recommendations for locally-advanced, unresectable non-small cell lung cancer (NSCLC)

Pseudo-acetylation of multiple sites on human Tau proteins alters Tau phosphorylation and microtubule binding, and ameliorates amyloid beta toxicity

Tau is a microtubule-associated protein that is highly soluble and natively unfolded. Its dysfunction is involved in the pathogenesis of several neurodegenerative disorders including Alzheimer's disease (AD), where it aggregates within neurons. Deciphering the physiological and pathogenic roles of human Tau (hTau) is crucial to further understand the mechanisms leading to its dysfunction in vivo. We have used a knock-out/knock-in strategy in Drosophila to generate a strain with hTau inserted into the endogenous fly tau locus and expressed under the control of the endogenous fly tau promoter, thus avoiding potential toxicity due to genetic over-expression. hTau knock-in (KI) proteins were expressed at normal, endogenous levels, bound to fly microtubules and were post-translationally modified, hence displaying physiological properties. We used this new model to investigate the effects of acetylation on hTau toxicity in vivo. The simultaneous pseudo-acetylation of hTau at lysines 163, 280, 281 and 369 drastically decreased hTau phosphorylation and significantly reduced its binding to microtubules in vivo. These molecular alterations were associated with ameliorated amyloid beta toxicity. Our results indicate acetylation of hTau on multiple sites regulates its biology and ameliorates amyloid beta toxicity in vivo

When Feedback Interventions Backfire: Why Higher Performance Feedback May Result in Lower Self-Perceived Competence and Satisfaction with Performance

In relative performance evaluation systems, appraisers may choose to adopt stricter or laxer evaluation criteria. When laxer (vs. stricter) criteria are used, higher absolute performance evaluations become easier (vs. harder) to achieve. Thus, each appraisee's absolute performance feedback and the mean of the distribution of absolute performance feedback are shifted upward (vs. downward). Yet, relative performance remains constant. When evaluation outcomes depend solely on relative performance, can the adoption of laxer (vs. stricter) criteria-leading to higher absolute performance feedback but no change in relative performance-influence appraisees' satisfaction with performance? Despite the ubiquity of such systems in organizations, research has not addressed this question. This article points to an important gap between practitioners' beliefs and research findings. We show that while most appraisers believe that higher absolute performance feedback will automatically result in more satisfaction with performance, the opposite may also happen. Specifically, we find that appraisees with a stronger (vs. weaker) chronic or contextual need to engage in social comparison are more satisfied with lower (vs. higher) absolute performance feedback. Overall, we demonstrate why and how feedback interventions in relative performance evaluation systems may backfire, and suggest a set of practical guidelines for maximizing appraisees' satisfaction with performance in such systems

Tau filament self-assembly and structure: tau as a therapeutic target

Tau plays an important pathological role in a group of neurodegenerative diseases called tauopathies, including Alzheimer's disease, Pick's disease, chronic traumatic encephalopathy and corticobasal degeneration. In each disease, tau self-assembles abnormally to form filaments that deposit in the brain. Tau is a natively unfolded protein that can adopt distinct structures in different pathological disorders. Cryo-electron microscopy has recently provided a series of structures for the core of the filaments purified from brain tissue from patients with different tauopathies and revealed that they share a common core region, while differing in their specific conformation. This structurally resolvable part of the core is contained within a proteolytically stable core region from the repeat domain initially isolated from AD tau filaments. Tau has recently become an important target for therapy. Recent work has suggested that the prevention of tau self-assembly may be effective in slowing the progression of Alzheimer's disease and other tauopathies. Here we review the work that explores the importance of tau filament structures and tau self-assembly mechanisms, as well as examining model systems that permit the exploration of the mode of action of potential inhibitors