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Search Results: 1 - 10 of 297557 matches for " J. Silman "
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Quantum dice rolling
N. Aharon,J. Silman
Physics , 2009,
Abstract: A coin is just a two sided dice. Recently, Mochon proved that quantum weak coin flipping with an arbitrarily small bias is possible. However, the use of quantum resources to allow N remote distrustful parties to roll an N-sided dice has yet to be addressed. In this paper we show that contrary to the classical case, N-sided dice rolling with arbitrarily small bias is possible for any N. In addition, we present a six-round three-sided dice rolling protocol, achieving a bias of 0.181, which incorporates weak imbalanced coin flipping.
Many-region vacuum entanglement: Distilling a W state
J. Silman,B. Reznik
Physics , 2005, DOI: 10.1103/PhysRevA.71.054301
Abstract: We investigate the correlations between any number of arbitrarily far-apart regions of the vacuum of the free Klein-Gordon field by means of its finite duration coupling to an equal number of localized detectors. We show that the correlations between any N such regions enable us to distill an N-partite W state, and therefore exhibit true $N$-fold entanglement. Furthermore, we show that for N=3, the correlations cannot be reproduced by a hybrid local-nonlocal hidden-variable model. For N >= 4 the issue remains open.
Quantum dice rolling: A multi-outcome generalization of quantum coin flipping
N. Aharon,J. Silman
Physics , 2009, DOI: 10.1088/1367-2630/12/3/033027
Abstract: We generalize the problem of coin flipping to more than two outcomes and parties. We term this problem dice rolling, and study both its weak and strong variants. We prove by construction that in quantum settings (i) weak N-sided dice rolling admits an arbitrarily small bias for any value of N, and (ii) two-party strong N-sided dice rolling saturates the corresponding generalization of Kitaev's bound for any value of N. In addition, we make use of this last result to introduce a family of optimal 2m-party strong n^m-sided dice rolling protocols for any value of m and n.
Long-range entanglement in the Dirac vacuum
J. Silman,B. Reznik
Physics , 2006, DOI: 10.1103/PhysRevA.75.052307
Abstract: Recently, there have been a number of works investigating the entanglement properties of distinct noncomplementary parts of discrete and continuous Bosonic systems in ground and thermal states. The Fermionic case, however, has yet to be expressly addressed. In this paper we investigate the entanglement between a pair of far-apart regions of the 3+1 dimensional massless Dirac vacuum via a previously introduced distillation protocol [B. Reznik et al., Phys. Rev. A 71, 042104 (2005)]. We show that entanglement persists over arbitrary distances, and that as a function of L/R, where L is the distance between the regions and R is their typical scale, it decays no faster than exp(-(L/R)^2). We discuss the similarities and differences with analogous results obtained for the massless Klein-Gordon vacuum.
Three-region vacuum nonlocality
J. Silman,B. Reznik
Physics , 2005,
Abstract: The correlations between three arbitrarily far-apart regions of the vacuum state of the free Klein-Gordon field are investigated by means of its finite duration coupling to three localized detectors. It is shown that these correlations cannot be reproduced in terms of a hybrid local-nonlocal hidden-variable model, i.e., the correlations between three arbitrarily separated regions of the vacuum are fully nonlocal.
Psychological stress and fibromyalgia: a review of the evidence suggesting a neuroendocrine link
Anindya Gupta, Alan J Silman
Arthritis Research & Therapy , 2004, DOI: 10.1186/ar1176
Abstract: Fibromyalgia is the second most common diagnosis made in rheumatology clinics [1], yet its aetiology remains a source of controversy. It has been suggested that fibromyalgia is a functional/psychological disorder and that the symptoms of fibromyalgia are simply due to somatisation of distress [2]. In support of this construct, there is definite evidence from population-based studies that psychological distress, particularly early-life trauma such as parental loss and abuse, can predict the future development of chronic widespread pain and fibromyalgia [3,4]. However, such observations leave unanswered the question of exactly how psychological factors translate into chronic physical pain.The alternative hypothesis is that fibromyalgia has an organic basis [5]. The possible neuroendocrine origins of fibromyalgia have been extensively investigated, based on the specific hypothesis that abnormalities of various endocrine axes, and certain neurotransmitters, might be responsible for the development of the fibromyalgia syndrome [6-8].The present review attempts to reconcile the conflict between psychological factors and physiological factors as a basis for fibromyalgia, by determining whether there are cogent neuroendocrine pathways that explain how psychological stress could lead to the symptoms of the fibromyalgia syndrome. Although these systems are clearly interconnected, the review will consider separately the potential role of the hypothalamic–pituitary–adrenal (HPA) axis, the role of the growth hormone axis, the role of sex steroids (both androgens and oestrogens), and the role of the neurotransmitters serotonin and substance P. Schematic representations of these systems are shown in Figs 1 and 2.The HPA axis, along with the sympatho-adrenal system, is the principal stress-response system in the human body. Acute stress causes the hypothalamus to release corticotrophin-releasing hormone (CRH) into the hypothalamic–hypophysial portal system. CRH releases adrenocorti
What epidemiology has told us about risk factors and aetiopathogenesis in rheumatic diseases
Jacqueline E Oliver, Alan J Silman
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2585
Abstract: This article will review epidemiological studies that have advanced the knowledge of both genetic and environmental risk factors for the rheumatic diseases, outlining the major advances that have been achieved over the past decade (Table 1). It will focus on the following diseases: rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), systemic lupus erythematosus (SLE), scleroderma (Scl), osteoarthritis (OA), gout, and fibromyalgia (FM) and chronic widespread pain (CWP).A number of large prospective studies have improved our knowledge of risk factors: the Framingham Study [1] and the Chingford 1000 Women Study [2] for OA, the Nurses' Health Study cohort for RA [3] and SLE [4], the European Prospective Investigation of Cancer in Norfolk (EPIC-Norfolk) for inflammatory polyarthritis [5], and the Health Professionals Follow-up Study for gout [6]. These types of studies provide valuable and robust information. Unfortunately, epidemiological data often are obtained from retrospective studies and underpowered case-control studies, resulting in contradictory findings (for example, studies on the role of caffeine in RA). Although some of the studies have found significant associations with novel risk factors, these studies often suffer from poor design. Meta-analyses have also been performed in an attempt to form conclusions from the available epidemiological data and these are also discussed.Over the past decade, genetic research has moved from the approach of small-scale association studies, to test for candidate genes in case-control studies, to whole-genome scans of linkage based on sibling pairs which proved to be limited in the small numbers of both pairs and markers (both in the hundreds). The more recent and exciting approach has been genome-wide association studies using gene chips which have allowed hundreds of thousands of single-nucleotide polymorphisms (SNPs) to be investigated as exemplified by
Aspects of early arthritis. What determines the evolution of early undifferentiated arthritis and rheumatoid arthritis? An update from the Norfolk Arthritis Register
Deborah PM Symmons, Alan J Silman
Arthritis Research & Therapy , 2006, DOI: 10.1186/ar1979
Abstract: The Norfolk Arthritis Register (NOAR) was established during 1989. By the beginning of 1990, all the general practitioners in what was then the Norwich Health Authority had been visited and asked to participate. From 1 January 1990, the general practitioners and local rheumatologists referred to NOAR all adults (aged ≥16) whom they saw with two or more swollen joints, lasting for 4 weeks or more, with an onset of symptoms after 1 January 1989.After receiving a notification, NOAR sends one of its team of metrologists (research nurses) to the patient's home to take a standardised history and to examine the joints for tenderness, swelling and deformity/damage [1]. In addition, a blood sample is taken for rheumatoid factor (RF) measurement and for DNA extraction. Serum is also stored. The patient completes a Health Assessment Questionnaire (HAQ) [2] adapted for British use [3].Over 3,500 patients have now been recruited by NOAR. Although the 15 years since NOAR was established have seen dramatic changes in the range of disease-modifying antirheumatic drugs (DMARDS) that are available and the way in which they are used, one of the fundamental questions that NOAR was set up to address remains highly pertinent. This is the question of whether it is possible to predict, early in the course of the disease, a patient's natural history.This question becomes ever more relevant as it is now well accepted that patients who are destined to have persistent disabling arthritis should start DMARD therapy as soon as possible (preferably within the first 12 weeks of disease). Patients who fail to respond to DMARD therapy should be moved on to a biologic agent. Set against this is the fact that many patients with recent-onset arthritis do well. In some patients, the arthritis resolves completely and many patients never develop any significant disability or radiological erosions. It would be exposing these patients to unnecessary risk to give them intensive DMARD therapy or even biologic
Why are women predisposed to autoimmune rheumatic diseases?
Jacqueline E Oliver, Alan J Silman
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2825
Abstract: Autoimmune diseases of all organ sites and systems affect approximately 8% of the population, around 78% of whom are women [1]. The diseases are estimated as being the fourth leading cause of disability in women. There is a consistent female excess for the major connective tissue autoimmune diseases (Table 1); this excess varies between 2:1 and 9:1. Recent evidence has highlighted gender differences in disease activity as well as incidence, with women with rheumatoid arthritis (RA) having worse disease activity than men with RA [2]; it is unclear, however, whether this relates to the measures of disease activity used rather than to the disease activity itself.Interestingly, the peak female:male ratio for all three major autoimmune connective tissue disorders (RA, systemic lupus erythematosus (SLE) and scleroderma (Scl)) is generally observed in the late teens to the forties, coinciding with the greatest changes in hormone levels. RA affects around 0.8% of the UK adult population and is around three times more common in women than in men, with a peak age of onset in the fifth decade of life. In later years, the incidence-gender ratio reduces to around 2:1 in 55 to 64 year olds, shifting to a male excess in those over 75 years old [3]. The gender ratio for Scl has been reported to vary between 1:1 and 14:1 [4]. The ratio varies between age groups with slightly higher ratios (3.4:1) in the childbearing years (aged 15 to 44 years) and lower ratios (2.4:1) in the postmenopausal years, with the female:male ratio averaging 3:1 [5]. SLE has an earlier disease onset than both RA and Scl, peaking in the childbearing years (late teens to early forties) with a female:male ratio of around 9:1 [6].Autoimmune diseases are known to vary by both ethnicity and geographical location. RA shows a wide variation in its incidence and prevalence worldwide. Southern European countries have a lower occurrence compared with north European and North American countries, and the disease also has
On the relation between Bell inequalities and nonlocal games
J. Silman,S. Machnes,N. Aharon
Physics , 2007, DOI: 10.1016/j.physleta.2008.03.001
Abstract: We investigate the relation between Bell inequalities and nonlocal games by presenting a systematic method for their bilateral conversion. In particular, we show that while to any nonlocal game there naturally corresponds a unique Bell inequality, the converse is not true. As an illustration of the method we present a number of nonlocal games that admit better odds when played using quantum resources
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