A family of loss-tolerant quantum coin flipping protocols

We present a family of loss-tolerant quantum strong coin flipping protocols; each protocol differing in the number of qubits employed. For a single qubit we obtain a bias of 0.4, reproducing the result of Berl\'{i}n et al. [Phys. Rev. A 80, 062321 (2009)], while for two qubits we obtain a bias of 0.3975. Numerical evidence based on semi-definite programming indicates that the bias continues to decrease as the number of qubits is increased but at a rapidly decreasing rate

Using complete measurement statistics for optimal device-independent randomness evaluation

The majority of recent works investigating the link between non-locality and randomness, e.g. in the context of device-independent cryptography, do so with respect to some specific Bell inequality, usually the CHSH inequality. However, the joint probabilities characterizing the measurement outcomes of a Bell test are richer than just the degree of violation of a single Bell inequality. In this work we show how to take this extra information into account in a systematic manner in order to optimally evaluate the randomness that can be certified from non-local correlations. We further show that taking into account the complete set of outcome probabilities is equivalent to optimizing over all possible Bell inequalities, thereby allowing us to determine the optimal Bell inequality for certifying the maximal amount of randomness from a given set of non-local correlations.Comment: 12 pages, 4 figures. v2, v3, v4: minor corrections. See also the related independent work arXiv:1309.389

Continuous input nonlocal games

We present a family of nonlocal games in which the inputs the players receive are continuous. We study three representative members of the family. For the first two a team sharing quantum correlations (entanglement) has an advantage over any team restricted to classical correlations. We conjecture that this is true for the third member of the family as well.Comment: Journal version, slight modification

What epidemiology has told us about risk factors and aetiopathogenesis in rheumatic diseases

This article will review how epidemiological studies have advanced our knowledge of both genetic and environmental risk factors for rheumatic diseases over the past decade. The major rheumatic diseases, including rheumatoid arthritis, juvenile idiopathic arthritis, psoriatic arthritis, ankylosing spondylitis, systemic lupus erythematosus, scleroderma, osteoarthritis, gout, and fibromyalgia, and chronic widespread pain, will be covered. Advances discussed will include how a number of large prospective studies have improved our knowledge of risk factors, including diet, obesity, hormones, and smoking. The change from small-scale association studies to genome-wide association studies using gene chips to reveal new genetic risk factors will also be reviewed

Why are women predisposed to autoimmune rheumatic diseases?

The majority of autoimmune diseases predominate in females. In searching for an explanation for this female excess, most attention has focused on hormonal changes - both exogenous changes (for example, oral contraceptive pill) and fluctuations in endogenous hormone levels particularly related to menstruation and pregnancy history. Other reasons include genetic differences, both direct (influence of genes on sex chromosomes) and indirect (such as microchimerism), as well as gender differences in lifestyle factors. These will all be reviewed, focusing on the major autoimmune connective tissue disorders: rheumatoid arthritis, systemic lupus erythematosus and scleroderma

Aspects of early arthritis. What determines the evolution of early undifferentiated arthritis and rheumatoid arthritis? An update from the Norfolk Arthritis Register

Over 3500 patients with recent onset inflammatory polyarthritis (IP) have been recruited by the Norfolk Arthritis Register (NOAR) since 1990. Longitudinal data from this cohort have been used to examine the prevalence and predictors of remission, functional disability, radiological outcome, cardiovascular mortality and co-morbidity and the development of non-Hodgkin's lymphoma. Rheumatoid factor titre, high baseline C-reactive protein and high baseline HAQ score are all predictors of a poor outcome. There is a strong association between possession of the shared epitope and the development of erosions. Patients who satisfy the American College of Rheumatology criteria for rheumatoid arthritis (RA) have a worse prognosis than those who do not. However, it appears that these patients are a poorly defined subset of all those with IP rather than having an entirely separate disease entity. New statistical techniques offer exciting possibilities for using longitudinal datasets such as NOAR to explore the long-term effects of treatment in IP and RA