3,121 research outputs found

    How to play fair in international environmental agreements? - Bridging psychological and economic methods

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    Global public good provision (e.g. environmental quality) confronts us with problems demanding both national and international co-operation. However among sovereign nations reaching agreement on mutual public good provision is difficult. Slowing down global warming is just one example. Due to the diffusion of greenhouse gases in the earth's atmosphere it is attractive for each individual state that other countries commit themselves to climate protection, whereas one's own state using the free-rider-strategy benefits from the protective measures of the others without making any costly national contribution. On the other hand such a strategic behaviour clashes with moral values, especially concerning motives of justice within society. Should free-riding be preferred from the strategic point of view or rather, out of consideration to justice, national commitments to contribute to climate protection? Therefore, an analysis of how appraisals of justice and strategic considerations interact is a challenge to international (environmental) policy. Taking a game-theoretic point of view, we analyse three psychological-empirical conceptions of justice: need, equality and equity, and point out how these principles are able to determine the type of game nations are expected to play. --

    The Basics of Display Calculi

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    The aim of this paper is to introduce and explain display calculi for a variety of logics. We provide a survey of key results concerning such calculi, though we focus mainly on the global cut elimination theorem. Propositional, first-order, and modal display calculi are considered and their properties detailed

    How to play fair in international environmental agreements? - Bridging psychological and economic methods

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    Global public good provision (e.g. environmental quality) confronts us with problems demanding both national and international co-operation. However among sovereign nations reaching agreement on mutual public good provision is difficult. Slowing down global warming is just one example. Due to the diffusion of greenhouse gases in the earth's atmosphere it is attractive for each individual state that other countries commit themselves to climate protection, whereas one's own state using the free-rider-strategy benefits from the protective measures of the others without making any costly national contribution. On the other hand such a strategic behaviour clashes with moral values, especially concerning motives of justice within society. Should free-riding be preferred from the strategic point of view or rather, out of consideration to justice, national commitments to contribute to climate protection? Therefore, an analysis of how appraisals of justice and strategic considerations interact is a challenge to international (environmental) policy. Taking a game-theoretic point of view, we analyse three psychological-empirical conceptions of justice: need, equality and equity, and point out how these principles are able to determine the type of game nations are expected to play

    MicroRNA networks surrounding APP and amyloid-β metabolism - implications for Alzheimer's disease

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    MicroRNAs (miRNAs) are small non-coding RNA regulators of protein synthesis that function as "fine-tuning" tools of gene expression in development and tissue homeostasis. Their profiles are significantly altered in neurodegenerative diseases such as Alzheimer's disease (AD) that is characterized by both amyloid-β (Aβ) and tau deposition in brain. A key challenge remains in determining how changes in miRNA profiles translate into biological function in a physiological and pathological context. The key lies in identifying specific target genes for deregulated miRNAs and understanding which pathogenic factors trigger their deregulation. Here we review the literature about the intricate network of miRNAs surrounding the regulation of the amyloid precursor protein (APP) from which Aβ is derived by proteolytic cleavage. Normal brain function is highly sensitive to any changes in APP metabolism and miRNAs function at several steps to ensure that the correct APP end product is produced and in the right form and abundance. Disruptions in this miRNA regulatory network may therefore alter Aβ production, which in turn can affect miRNA expression

    Neuronal network disintegration: common pathways linking neurodegenerative diseases

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    Neurodegeneration refers to a heterogeneous group of brain disorders that progressively evolve. It has been increasingly appreciated that many neurodegenerative conditions overlap at multiple levels and therefore traditional clinicopathological correlation approaches to better classify a disease have met with limited success. Neuronal network disintegration is fundamental to neurodegeneration, and concepts based around such a concept may better explain the overlap between their clinical and pathological phenotypes. In this Review, promoters of overlap in neurodegeneration incorporating behavioural, cognitive, metabolic, motor, and extrapyramidal presentations will be critically appraised. In addition, evidence that may support the existence of large-scale networks that might be contributing to phenotypic differentiation will be considered across a neurodegenerative spectrum. Disintegration of neuronal networks through different pathological processes, such as prion-like spread, may provide a better paradigm of disease and thereby facilitate the identification of novel therapies for neurodegeneration

    Dendritic TAU-telidge

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    info:eu-repo/semantics/publishedVersio

    Performance measures of net-enabled hypercompetitive industries: the case of tourism

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    This paper investigates the theory and practise of e-metrics. It examines the tourism sector as one of the most successful sectors on-line and identifies best practice in the industry. Qualitative research with top e-Marketing executives demonstrates the usage and satisfaction levels from current e-metrics deployment, selection of e-metrics for ROI calculation as well as intention of new e-metrics implementation and future trends and developments. This paper concludes that tourism organizations gradually realise the value of e-measurement and are willing to implement e-metrics to enable them evaluate the effectiveness of their planning processes and assess their results against their short and the long term objectives

    Nigrostriatal pathology with reduced astrocytes in LRRK2 S910/S935 phosphorylation deficient knockin mice

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    Leucine-rich repeat kinase 2 (LRRK2) is genetically implicated in both familial and sporadic Parkinson's disease (PD). Moreover, LRRK2 has emerged as a compelling therapeutic target for the treatment of PD. Consequently, there is much interest in understanding LRRK2 and its role in PD pathogenesis. LRRK2 is constitutively phosphorylated on two serines, S910 and S935, that are required for interaction of LRRK2 with members of the 14-3-3 family of scaffolding proteins. Pathogenic LRRK2 missense mutations impair the phosphorylation of LRRK2 at these sites, but whether this contributes to PD pathology is unclear. To better understand how loss of LRRK2 phosphorylation relates to PD pathology, we have studied double knockin mice in which Lrrk2's serine 910 and 935 have both been mutated to alanine and can therefore no longer be phosphorylated. Nigrostriatal PD pathology was assessed in adult mice, aged mice, and mice inoculated with α-synuclein fibrils. Under all paradigms there was evidence of early PD pathology in the striatum of the knockin mice, namely alterations in dopamine regulating proteins and accumulation of α-synuclein. Striatal pathology was accompanied by a significant decrease in the number of astrocytes in the knockin mice. Despite striatal pathology, there was no degeneration of dopamine neurons in the substantia nigra and no evidence of a PD motor phenotype in the knockin mice. Our results suggest that modulation of LRRK2 serine 910 and 935 phosphorylation sites may have implications for dopamine turnover and astrocyte function, but loss of phosphorylation at these residues is not sufficient to induce PD neurodegeneration.</p
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