Philosophical Aspects of Quantum Information Theory

Quantum information theory represents a rich subject of discussion for those interested in the philosphical and foundational issues surrounding quantum mechanics for a simple reason: one can cast its central concerns in terms of a long-familiar question: How does the quantum world differ from the classical one? Moreover, deployment of the concepts of information and computation in novel contexts hints at new (or better) means of understanding quantum mechanics, and perhaps even invites re-assessment of traditional material conceptions of the basic nature of the physical world. In this paper I review some of these philosophical aspects of quantum information theory, begining with an elementary survey of the theory, seeking to highlight some of the principles and heuristics involved. We move on to a discussion of the nature and definition of quantum information and deploy the findings in discussing the puzzles surrounding teleportation. The final two sections discuss, respectively, what one might learn from the development of quantum computation (both about the nature of quantum systems and about the nature of computation) and consider the impact of quantum information theory on the traditional foundational questions of quantum mechanics (treating of the views of Zeilinger, Bub and Fuchs, amongst others).Comment: LaTeX; 55pp; 3 figs. Forthcoming in Rickles (ed.) The Ashgate Companion to the New Philosophy of Physic

Quantum Mechanics on Spacetime I: Spacetime State Realism

What ontology does realism about the quantum state suggest? The main extant view in contemporary philosophy of physics is wave-function realism. We elaborate the sense in which wave-function realism does provide an ontological picture; and defend it from certain objections that have been raised against it. However, there are good reasons to be dissatisfied with wave-function realism, as we go on to elaborate. This motivates the development of an opposing picture: what we call spacetime state realism; a view which takes the states associated to spacetime regions as fundamental. This approach enjoys a number of beneficial features, although, unlike wave-function realism, it involves non-separability at the level of fundamental ontology. We investigate the pros and cons of this non-separability, arguing that it is a quite acceptable feature; even one which proves fruitful in the context of relativistic covariance. A companion paper discusses the prospects for combining a spacetime-based ontology with separability, along lines suggested by Deutsch and HaydenComment: LaTeX; 29 pages, 1 Fig. Forthcoming in the British Journal for the Philosophy of Scienc

Proper and Improper Separability

The distinction between proper and improper mixtures is a staple of the discussion of foundational questions in quantum mechanics. Here we note an analogous distinction in the context of the theory of entanglement. The terminology of `proper' versus `improper' separability is proposed to mark the distinction.Comment: 10 pages, LaTex, uses amsmath, 2 .eps figures. v2 additional figure; and reference and footnote to Seevinck and Uffink (2001). To appear in International Journal of Quantum Informatio

Why special relativity should not be a template for a fundamental reformulation of quantum mechanics

In a comparison of the principles of special relativity and of quantum mechanics, the former theory is marked by its relative economy and apparent explanatory simplicity. A number of theorists have thus been led to search for a small number of postulates - essentially information theoretic in nature - that would play the role in quantum mechanics that the relativity principle and the light postulate jointly play in Einstein's 1905 special relativity theory. The purpose of the present paper is to resist this idea, at least in so far as it is supposed to reveal the fundamental form of the theory. It is argued that the methodology of Einstein's 1905 theory represents a victory of pragmatism over explanatory depth; and that its adoption only made sense in the context of the chaotic state state of physics at the start of the 20th century - as Einstein well knew

Non-locality and gauge freedom in Deutsch and Hayden's formulation of quantum mechanics

Deutsch and Hayden have proposed an alternative formulation of quantum mechanics which is completely local. We argue that their proposal must be understood as having a form of `gauge freedom' according to which mathematically distinct states are physically equivalent. Once this gauge freedom is taken into account, their formulation is no longer local.Comment: 3 page

Epigenetic regulation of F2RL3 associates with myocardial infarction and platelet function

DNA hypomethylation at the F2RL3 (F2R like thrombin or trypsin receptor 3) locus has been associated with both smoking and atherosclerotic cardiovascular disease; whether these smoking-related associations form a pathway to disease is unknown. F2RL3 encodes protease-activated receptor 4, a potent thrombin receptor expressed on platelets. Given the role of thrombin in platelet activation and the role of thrombus formation in myocardial infarction, alterations to this biological pathway could be important for ischemic cardiovascular disease. METHODS: We conducted multiple independent experiments to assess whether DNA hypomethylation at F2RL3 in response to smoking is associated with risk of myocardial infarction via changes to platelet reactivity. Using cohort data (N=3205), we explored the relationship between smoking, DNA hypomethylation at F2RL3, and myocardial infarction. We compared platelet reactivity in individuals with low versus high DNA methylation at F2RL3 (N=41). We used an in vitro model to explore the biological response of F2RL3 to cigarette smoke extract. Finally, a series of reporter constructs were used to investigate how differential methylation could impact F2RL3 gene expression. RESULTS: Observationally, DNA methylation at F2RL3 mediated an estimated 34% of the smoking effect on increased risk of myocardial infarction. An association between methylation group (low/high) and platelet reactivity was observed in response to PAR4 (protease-activated receptor 4) stimulation. In cells, cigarette smoke extract exposure was associated with a 4.9% to 9.3% reduction in DNA methylation at F2RL3 and a corresponding 1.7-(95% CI, 1.2–2.4, P=0.04) fold increase in F2RL3 mRNA. Results from reporter assays suggest the exon 2 region of F2RL3 may help control gene expression. CONCLUSIONS: Smoking-induced epigenetic DNA hypomethylation at F2RL3 appears to increase PAR4 expression with potential downstream consequences for platelet reactivity. Combined evidence here not only identifies F2RL3 DNA methylation as a possible contributory pathway from smoking to cardiovascular disease risk but from any feature potentially influencing F2RL3 regulation in a similar manner

Localization of type 1 diabetes susceptibility to the MHC class I genes HLA-B and HLA-A

The major histocompatibility complex (MHC) on chromosome 6 is associated with susceptibility to more common diseases than any other region of the human genome, including almost all disorders classified as autoimmune. In type 1 diabetes the major genetic susceptibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1 (refs 1-3), but these genes cannot completely explain the association between type 1 diabetes and the MHC region. Owing to the region's extreme gene density, the multiplicity of disease-associated alleles, strong associations between alleles, limited genotyping capability, and inadequate statistical approaches and sample sizes, which, and how many, loci within the MHC determine susceptibility remains unclear. Here, in several large type 1 diabetes data sets, we analyse a combined total of 1,729 polymorphisms, and apply statistical methods - recursive partitioning and regression - to pinpoint disease susceptibility to the MHC class I genes HLA-B and HLA-A (risk ratios >1.5; Pcombined = 2.01 × 10-19 and 2.35 × 10-13, respectively) in addition to the established associations of the MHC class II genes. Other loci with smaller and/or rarer effects might also be involved, but to find these, future searches must take into account both the HLA class II and class I genes and use even larger samples. Taken together with previous studies, we conclude that MHC-class-I-mediated events, principally involving HLA-B*39, contribute to the aetiology of type 1 diabetes. ©2007 Nature Publishing Group