1,586 research outputs found
On Vague Computers
Vagueness is something everyone is familiar with. In fact, most people think
that vagueness is closely related to language and exists only there. However,
vagueness is a property of the physical world. Quantum computers harness
superposition and entanglement to perform their computational tasks. Both
superposition and entanglement are vague processes. Thus quantum computers,
which process exact data without "exploiting" vagueness, are actually vague
computers
Empirically-Informed Modal Rationalism
In this chapter, it is suggested that our epistemic access to metaphysical modality generally involves rationalist, a priori elements. However, these a priori elements are much more subtle than ‘traditional’ modal rationalism assumes. In fact, some might even question the ‘apriority’ of these elements, but I should stress that I consider a priori and a posteriori elements especially in our modal inquiry to be so deeply intertwined that it is not easy to tell them apart. Supposed metaphysically necessary identity statements involving natural kind terms are a good example: the fact that empirical input is crucial in establishing their necessity has clouded the role and content of the a priori input, as I have previously argued (Tahko forthcoming). For instance, the supposed metaphysically necessary identity statement involving water and its microstructure can only be established with the help of a controversial a priori principle concerning the determination of chemical properties by microstructure. The Kripke-Putnam framework of modal epistemology fails precisely because it is unclear whether the required a priori element is present. My positive proposal builds on E. J. Lowe’s work. Lowe holds that our knowledge of metaphysical modality is based on our knowledge of essence. Lowe’s account strives to offer a uniform picture of modal epistemology: essence is the basis of all our modal knowledge. This is the basis of Lowe’s modal rationalism. I believe that Lowe’s proposal is on the right lines in the case of abstract objects, but I doubt that it can be successfully applied to the case of natural kinds. Accordingly, the case of natural kinds will be my main focus and I will suggest that modal rationalism, at least as it is traditionally understood, falls short of explaining modal knowledge concerning natural kinds. Yet, I think that Lowe has identified something of crucial importance for modal epistemology, namely the essentialist, a priori elements present in our modal inquiry. The upshot is that rather than moving all the way from modal rationalism to modal empiricism, a type of hybrid approach, ‘empirically-informed modal rationalism’, can be developed.Peer reviewe
Ontological dependence in a spacetime-world
Priority Monism (hereafter, ‘Monism’), as defined by Jonathan Schaffer (Philos Rev 119:131–176, 2010), has a number of components. It is the view that: the cosmos exists; the cosmos is a maximal actual concrete object, of which all actual concrete objects are parts; the cosmos is basic—there is no object upon which the cosmos depends, ontologically; ontological dependence is a primitive and unanalysable relation. In a recent attack, Lowe (Spinoza on monism. Palgave Macmillan, London, pp 92–122, 2012) has offered a series of arguments to show that Monism fails. He offers up four tranches of argument, with different focuses. These focal points are: (1) being a concrete object; (2) aggregation and dependence; (3) analyses of ontological dependence; (4) Schaffer’s no-overlap principle. These are all technical notions, but each figures at the heart of a cluster of arguments that Lowe puts forward. To respond, I work through each tranche of argument in turn. Before that, in the first section, I offer a cursory statement of Monism, as Schaffer presents it in his 2010 paper, Monism: The Priority of the Whole. I then respond to each of Lowe’s criticisms in turn, deploying material from Schaffer’s 2009 paper Spacetime: the One Substance, as well as various pieces of conceptual machinery from Lowe’s own works (The possibility of metaphysics. Clarendon, Oxford, 1998, 2010) to deflect Lowe’s (Spinoza on monism. Palgave Macmillan, London, pp 92–122, 2012) attacks. In the process of defending Monism from Lowe (Spinoza on monism. Palgave Macmillan, London, pp 92–122, 2012), I end up offering some subtle refinements to Schaffer’s (Philos Rev 119:131–176, 2010) view and explain how the resulting ‘hybrid’ view fares in the wider dialectic
What Angles Can Tell Us About What Holes Are Not
In this paper I argue that holes are not objects, but should instead be construed as properties or relations. The argument proceeds by first establishing a claim about angles: that angles are not objects, but properties or relations. It is then argued that holes and angles belong to the same category, on the grounds that they share distinctive existence and identity conditions. This provides an argument in favour of categorizing holes as one categorizes angles. I then argue that a commitment to the existence of properties to be identified with holes provides sufficient resources to account for true claims about holes. © 2011 Springer Science+Business Media B.V
Counterfactual reasoning and knowledge of possibilities
Williamson has argued against scepticism concerning our metaphysically modal knowledge, by arguing that standard patterns of suppositional reasoning to counterfactual conclusions provide reliable sources of correct ascriptions of possibility and necessity. The paper argues that, while Williamson’s claims relating to necessity may well be right, he has not provided adequate reasons for thinking that the familiar modes of counterfactual reasoning to which he points generalise to provide a decent route to ascriptions of possibility. The paper also explores another path to ascriptions of possibility that may be extracted from Williamson’s ideas, before briefly considering the general status of counterfactual reasoning in relation to our knowledge of possibilities
Early growth response 2 (EGR2) is a novel regulator of the senescence programme.
Senescence, a state of stable growth arrest, plays an important role in ageing and age-related diseases in vivo. Although the INK4/ARF locus is known to be essential for senescence programmes, the key regulators driving p16 and ARF transcription remain largely underexplored. Using siRNA screening for modulators of the p16/pRB and ARF/p53/p21 pathways in deeply senescent human mammary epithelial cells (DS HMECs) and fibroblasts (DS HMFs), we identified EGR2 as a novel regulator of senescence. EGR2 expression is up-regulated during senescence, and its ablation by siRNA in DS HMECs and HMFs transiently reverses the senescent phenotype. We demonstrate that EGR2 activates the ARF and p16 promoters and directly binds to both the ARF and p16 promoters. Loss of EGR2 down-regulates p16 levels and increases the pool of p16- p21- 'reversed' cells in the population. Moreover, EGR2 overexpression is sufficient to induce senescence. Our data suggest that EGR2 is a direct transcriptional activator of the p16/pRB and ARF/p53/p21 pathways in senescence and a novel marker of senescence
Biomarkers of subclinical inflammation and increases in glycaemia, insulin resistance and beta-cell function in non-diabetic individuals: the Whitehall II study
Objective: Higher systemic levels of pro-inflammatory biomarkers and low adiponectin are associated with increased risk of type 2 diabetes, but their associations with changes in glycaemic deterioration before onset of diabetes are poorly understood. We aimed to study whether inflammation-related biomarkers are associated with 5-year changes in glucose and insulin, HbA1c, insulin sensitivity and beta-cell function before the diagnosis of type 2 diabetes and whether these associations may be bidirectional.
Design and methods: We used multiple repeat measures (17 891 person-examinations from 7683 non-diabetic participants) from the Whitehall II study to assess whether circulating high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL6), IL1 receptor antagonist (IL1Ra) and adiponectin are associated with subsequent changes in glycaemia, insulin, insulin resistance and beta-cell function (based on oral glucose tolerance tests). We examined bidirectionality by testing if parameters of glucose metabolism at baseline are associated with changes in inflammation-related biomarkers.
Results: Higher hsCRP and IL6 were associated with increases in fasting insulin, insulin resistance and, for IL6, with beta-cell function after adjustment for confounders. Higher adiponectin was associated with decreases in fasting glucose, HbA1c, fasting insulin, insulin resistance and beta-cell function. The reverse approach showed that 2-h glucose and insulin sensitivity were associated with changes in IL1Ra. Fasting insulin and insulin resistance showed inverse associations with changes in adiponectin.
Conclusions: Subclinical inflammation is associated with development of increased glycaemia, insulin resistance and beta-cell function in non-diabetic individuals. These findings are consistent with the hypothesis that inflammation-related processes may increase insulin resistance and lead to a compensatory upregulation of beta-cell function
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