9,796 research outputs found

    MacIntyre and Kovesi on the Nature of Moral Concepts

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    Julius Kovesi was a moral philosopher contemporary with Alasdair MacIntyre, and dealing with many of the same questions as MacIntyre. In our view, Kovesi’s moral philosophy is rich in ideas and worth revisiting. MacIntyre agrees: Kovesi’s Moral Notions, he has said, is ‘a minor classic in moral philosophy that has not yet received its due’. Kovesi was not a thinker whose work fits readily into any one tradition. Unlike the later MacIntyre, he was not a Thomistic Aristotelian, nor even an Aristotelian. He saw his viewpoint as Platonic, or perhaps more accurately as Socratic. His writings, unlike MacIntyre’s, have little to say about justice. However, Kovesi did offfer a theory of practical reason. His main contention was that all human social life embodies a set of concepts that govern and guide that life, concepts without which that life would be impossible. These include our moral concepts. For Kovesi, moral concepts are not external to, but constitutive of social life in any of its possible forms. But in the course of his argument he also developed a way of thinking about how concepts work, which we term ‘conceptual functionalism’, and which we will elucidate

    Moral Notions, with Three Papers on Plato

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    Morality is often thought of as non-rational or sub-rational. In Moral Notions, first published in 1967, Julius Kovesi argues that the rationality of morality is built into the way we construct moral concepts. In showing this he also resolves the old Humean conundrum of the relation between 'facts' and 'values'. And he puts forward a method of reasoning that might make 'applied ethics' (at present largely a hodge-podge of opinions) into a constructive discipline. Kovesi's general theory of concepts - important in its own right - is indebted to his interpretation of Plato, and his three papers on Plato, first published here, explain this debt. This new edition of Moral Notions also includes a foreward by Philippa Foot, a biography of the author, and a substantial afterword in which the editors, Robert Ewin and Alan Tapper, explain the signficance of Kovesi's work

    The Air-temperature Response to Green/blue-infrastructure Evaluation Tool (TARGET v1.0) : an efficient and user-friendly model of city cooling

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    The adverse impacts of urban heat and global climate change are leading policymakers to consider green and blue infrastructure (GBI) for heat mitigation benefits. Though many models exist to evaluate the cooling impacts of GBI, their complexity and computational demand leaves most of them largely inaccessible to those without specialist expertise and computing facilities. Here a new model called The Air-temperature Response to Green/blue-infrastructure Evaluation Tool (TARGET) is presented. TARGET is designed to be efficient and easy to use, with fewer user-defined parameters and less model input data required than other urban climate models. TARGET can be used to model average street-level air temperature at canyon-to-block scales (e.g. 100 m resolution), meaning it can be used to assess temperature impacts of suburb-to-city-scale GBI proposals. The model aims to balance realistic representation of physical processes and computation efficiency. An evaluation against two different datasets shows that TARGET can reproduce the magnitude and patterns of both air temperature and surface temperature within suburban environments. To demonstrate the utility of the model for planners and policymakers, the results from two precinct-scale heat mitigation scenarios are presented. TARGET is available to the public, and ongoing development, including a graphical user interface, is planned for future work

    VISTA Milky Way public survey

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    We propose a public IR variability survey, named \Vista Variables in the Vía Láctea" (V V V ), of the Milky Way bulge and an adjacent section of the mid-plane where star formation activity is high. This would take 1920 hours, covering ~ 109 point sources within an area of 520 sq deg, including 33 known globular clusters and ~ 350 open clusters. The final products will be a deep IR atlas in 5 passbands and a catalogue of ~ 106 variable point sources. These will produce a 3-D map of the surveyed region (unlike single-epoch surveys that only give 2-D maps) using well-understood primary distance indicators such as RR Lyrae stars. It will yield important information on the ages of the populations. The observations will be combined with data from MACHO, OGLE, EROS, VST, SPITZER, HST, CHANDRA, INTEGRAL, and ALMA for a complete understanding of the variable sources in the inner Milky Way. Several important implications for the history of the Milky Way, for globular cluster evolution, for the population census of the bulge and center, and for pulsation theory would follow from this survey

    Genetic variation at MECOM, TERT, JAK2 and HBS1L-MYB predisposes to myeloproliferative neoplasms

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    Clonal proliferation in myeloproliferative neoplasms (MPN) is driven by somatic mutations in JAK2, CALR or MPL, but the contribution of inherited factors is poorly characterized. Using a three-stage genome-wide association study of 3,437 MPN cases and 10,083 controls, we identify two SNPs with genome-wide significance in JAK2V617F-negative MPN: rs12339666 (JAK2; meta-analysis P=1.27 × 10−10) and rs2201862 (MECOM; meta-analysis P=1.96 × 10−9). Two additional SNPs, rs2736100 (TERT) and rs9376092 (HBS1L/MYB), achieve genome-wide significance when including JAK2V617F-positive cases. rs9376092 has a stronger effect in JAK2V617F-negative cases with CALR and/or MPL mutations (Breslow–Day P=4.5 × 10−7), whereas in JAK2V617F-positive cases rs9376092 associates with essential thrombocythemia (ET) rather than polycythemia vera (allelic χ2 P=7.3 × 10−7). Reduced MYB expression, previously linked to development of an ET-like disease in model systems, associates with rs9376092 in normal myeloid cells. These findings demonstrate that multiple germline variants predispose to MPN and link constitutional differences in MYB expression to disease phenotype
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