2,830 research outputs found

    On Representational Redundancy, Surplus Structure, and the Hole Argument

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    We address a recent proposal concerning 'surplus structure' due to Nguyen et al. ['Why Surplus Structure is Not Superfluous.' Br. J. Phi. Sci. Forthcoming.] We argue that the sense of 'surplus structure' captured by their formal criterion is importantly different from---and in a sense, opposite to---another sense of 'surplus structure' used by philosophers. We argue that minimizing structure in one sense is generally incompatible with minimizing structure in the other sense. We then show how these distinctions bear on Nguyen et al.'s arguments about Yang-Mills theory and on the hole argument

    On Representational Redundancy, Surplus Structure, and the Hole Argument

    Get PDF
    We address a recent proposal concerning 'surplus structure' due to Nguyen et al. ['Why Surplus Structure is Not Superfluous.' Br. J. Phi. Sci. Forthcoming.] We argue that the sense of 'surplus structure' captured by their formal criterion is importantly different from---and in a sense, opposite to---another sense of 'surplus structure' used by philosophers. We argue that minimizing structure in one sense is generally incompatible with minimizing structure in the other sense. We then show how these distinctions bear on Nguyen et al.'s arguments about Yang-Mills theory and on the hole argument

    The neural basis of external responsiveness in prolonged disorders of consciousness

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    Objective: To investigate the structural integrity of fibre tracts underlying overt motor behaviour in PDOC. Methods: This cross-sectional study examined 15 PDOC patients and 22 healthy participants. Eight PDOC patients met the criteria for the vegetative state, 5 met the criteria for the minimally conscious state and 2 met the criteria for emerging from the minimally conscious state. We used fibre tractography to reconstruct the white matter fibres known to be involved in voluntary motor execution (i.e., those connecting thalamus with M1, M1 with cerebellum, and cerebellum with thalamus) and used fractional anisotropy (FA) as a measure of their integrity. Results: PDOC patients showed significantly reduced FA relative to controls on the fibres connecting thalamus and M1. This went above and beyond a widespread injury to the white matter and correlated with clinical severity. In a subset of patients, we also identified a similar pattern of injury in the fibres connecting M1 and cerebellum but a relative preservation of those connecting cerebellum and thalamus. Conclusions: Our results suggest that structural damage to motor fibres may lead to reduced responsiveness in PDOC patients across all diagnostic sub-categories, and therefore behavioural assessments may underestimate the level of retained cognitive function and awareness across the PDOC spectrum

    On Representational Redundancy, Surplus Structure, and the Hole Argument

    Get PDF
    We address a recent proposal concerning 'surplus structure' due to Nguyen et al. ['Why Surplus Structure is Not Superfluous.' Br. J. Phi. Sci. Forthcoming.] We argue that the sense of 'surplus structure' captured by their formal criterion is importantly different from---and in a sense, opposite to---another sense of 'surplus structure' used by philosophers. We argue that minimizing structure in one sense is generally incompatible with minimizing structure in the other sense. We then show how these distinctions bear on Nguyen et al.'s arguments about Yang-Mills theory and on the hole argument

    Mathematical Responses to the Hole Argument: Then and Now

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    We argue that several apparently distinct responses to the hole argument, all invoking formal or mathematical considerations, should be viewed as a unified "mathematical response". We then consider and rebut two prominent critiques of the mathematical response before reflecting on what is ultimately at issue in this literature

    Teleost Growth Factor Independence (Gfi) Genes Differentially Regulate Successive Waves of Hematopoiesis

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    Growth Factor Independence (Gfi) transcription factors play essential roles in hematopoiesis, differentially activating and repressing transcriptional programs required for hematopoietic stem/progenitor cell (HSPC) development and lineage specification. In mammals, Gfi1a regulates hematopoietic stem cells (HSC), myeloid and lymphoid populations, while its paralog, Gfi1b, regulates HSC, megakaryocyte and erythroid development. In zebrafish, gfi1aa is essential for primitive hematopoiesis; however, little is known about the role of gfi1aa in definitive hematopoiesis or about additional gfi factors in zebrafish. Here, we report the isolation and characterization of an additional hematopoietic gfi factor, gfi1b. We show that gfi1aa and gfi1b are expressed in the primitive and definitive sites of hematopoiesis in zebrafish. Our functional analyses demonstrate that gfi1aa and gfi1b have distinct roles in regulating primitive and definitive hematopoietic progenitors, respectively. Loss of gfi1aa silences markers of early primitive progenitors, scl and gata1. Conversely, loss of gfi1b silences runx-1, c-myb, ikaros and cd41, indicating that gfi1b is required for definitive hematopoiesis. We determine the epistatic relationships between the gfi factors and key hematopoietic transcription factors, demonstrating that gfi1aa and gfi1b join lmo2, scl, runx-1 and c-myb as critical regulators of teleost HSPC. Our studies establish a comparative paradigm for the regulation of hematopoietic lineages by gfi transcription factors.Stem Cell and Regenerative Biolog
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