Quantum Gravity Phenomenology, Lorentz Invariance and Discreteness

Contrary to what is often stated, a fundamental spacetime discreteness need not contradict Lorentz invariance. A causal set's discreteness is in fact locally Lorentz invariant, and we recall the reasons why. For illustration, we introduce a phenomenological model of massive particles propagating in a Minkowski spacetime which arises from an underlying causal set. The particles undergo a Lorentz invariant diffusion in phase space, and we speculate on whether this could have any bearing on the origin of high energy cosmic rays.Comment: 13 pages. Replaced version with corrected fundamental solution, missing m's (mass) and c's (speed of light) added and reference on diffusion on the three sphere changed. Note with additional references added and addresses updated, as in published versio

Discreteness and the transmission of light from distant sources

We model the classical transmission of a massless scalar field from a source to a detector on a background causal set. The predictions do not differ significantly from those of the continuum. Thus, introducing an intrinsic inexactitude to lengths and durations - or more specifically, replacing the Lorentzian manifold with an underlying discrete structure - need not disrupt the usual dynamics of propagation.Comment: 16 pages, 1 figure. Version 2: reference adde

A histories perspective on characterizing quantum non-locality

We introduce a framework for studying non-locality and contextuality inspired by the path integral formulation of quantum theory. We prove that the existence of a strongly positive joint quantum measure -- the quantum analogue of a joint probability measure -- on a set of experimental probabilities implies the Navascues-Pironio-Acin (NPA) condition $Q^1$ and is implied by the stronger NPA condition $Q^{1+AB}$. A related condition is shown to be equivalent to $Q^{1+AB}$.Comment: 28 page

A Bell Inequality Analog in Quantum Measure Theory

One obtains Bell's inequalities if one posits a hypothetical joint probability distribution, or {\it measure}, whose marginals yield the probabilities produced by the spin measurements in question. The existence of a joint measure is in turn equivalent to a certain causality condition known as ``screening off''. We show that if one assumes, more generally, a joint {\it quantal measure}, or ``decoherence functional'', one obtains instead an analogous inequality weaker by a factor of $\sqrt{2}$. The proof of this ``Tsirel'son inequality'' is geometrical and rests on the possibility of associating a Hilbert space to any strongly positive quantal measure. These results lead both to a {\it question}: ``Does a joint measure follow from some quantal analog of `screening off'?'', and to the {\it observation} that non-contextual hidden variables are viable in histories-based quantum mechanics, even if they are excluded classically.Comment: 38 pages, TeX. Several changes and added comments to bring out the meaning more clearly. Minor rewording and extra acknowledgements, now closer to published versio

Murray Valley encephalitis virus surveillance and control initiatives in Australia.

Mechanisms for monitoring Murray Valley encephalitis (MVE) virus activity include surveillance of human cases, surveillance for activity in sentinel animals, monitoring of mosquito vectors and monitoring of weather conditions. The monitoring of human cases is only one possible trigger for public health action and the additional surveillance systems are used in concert to signal the risk of human disease, often before the appearance of human cases. Mosquito vector surveillance includes mosquito trapping for speciation and enumeration of mosquitoes to monitor population sizes and relative composition. Virus isolation from mosquitoes can also be undertaken. Monitoring of weather conditions and vector surveillance determines whether there is a potential for MVE activity to occur. Virus isolation from trapped mosquitoes is necessary to define whether MVE is actually present, but is difficult to deliver in a timely fashion in some jurisdictions. Monitoring of sentinel animals indicates whether MVE transmission to vertebrates is actually occurring. Meteorological surveillance can assist in the prediction of potential MVE virus activity by signalling conditions that have been associated with outbreaks of Murray Valley encephalitis in humans in the past. Predictive models of MVE virus activity for south-eastern Australia have been developed, but due to the infrequency of outbreaks, are yet to be demonstrated as useful for the forecasting of major outbreaks. Surveillance mechanisms vary across the jurisdictions. Surveillance of human disease occurs in all States and Territories by reporting of cases to health authorities. Sentinel flocks of chickens are maintained in 4 jurisdictions (Western Australia, the Northern Territory, Victoria and New South Wales) with collaborations between Western Australia and the Northern Territory. Mosquito monitoring complements the surveillance of sentinel animals in these jurisdictions. In addition, other mosquito monitoring programs exist in other States (including South Australia and Queensland). Public health control measures may include advice to the general public and mosquito management programs to reduce the numbers of both mosquito larvae and adult vectors. Strategic plans for public health action in the event of MVE virus activity are currently developed or being developed in New South Wales, the Northern Territory, South Australia, Western Australia and Victoria. A southern tri-State agreement exists between health departments of New South Wales, Victoria and South Australia and the Commonwealth Department of Health and Aged Care. All partners have agreed to co-operate and provide assistance in predicting and combatting outbreaks of mosquito-borne disease in south-eastern Australia. The newly formed National Arbovirus Advisory Committee is a working party providing advice to the Communicable Diseases Network Australia on arbovirus surveillance and control. Recommendations for further enhancement of national surveillance for Murray Valley encephalitis are described

Technology in Parkinson's disease:challenges and opportunities

The miniaturization, sophistication, proliferation, and accessibility of technologies are enabling the capture of more and previously inaccessible phenomena in Parkinson's disease (PD). However, more information has not translated into a greater understanding of disease complexity to satisfy diagnostic and therapeutic needs. Challenges include noncompatible technology platforms, the need for wide-scale and long-term deployment of sensor technology (among vulnerable elderly patients in particular), and the gap between the "big data" acquired with sensitive measurement technologies and their limited clinical application. Major opportunities could be realized if new technologies are developed as part of open-source and/or open-hardware platforms that enable multichannel data capture sensitive to the broad range of motor and nonmotor problems that characterize PD and are adaptable into self-adjusting, individualized treatment delivery systems. The International Parkinson and Movement Disorders Society Task Force on Technology is entrusted to convene engineers, clinicians, researchers, and patients to promote the development of integrated measurement and closed-loop therapeutic systems with high patient adherence that also serve to (1) encourage the adoption of clinico-pathophysiologic phenotyping and early detection of critical disease milestones, (2) enhance the tailoring of symptomatic therapy, (3) improve subgroup targeting of patients for future testing of disease-modifying treatments, and (4) identify objective biomarkers to improve the longitudinal tracking of impairments in clinical care and research. This article summarizes the work carried out by the task force toward identifying challenges and opportunities in the development of technologies with potential for improving the clinical management and the quality of life of individuals with PD. © 2016 International Parkinson and Movement Disorder Society

Inherited variation in immune genes and pathways and glioblastoma risk

To determine whether inherited variations in immune function single-nucleotide polymorphisms (SNPs), genes or pathways affect glioblastoma risk, we analyzed data from recent genome-wide association studies in conjunction with predefined immune function genes and pathways. Gene and pathway analyses were conducted on two independent data sets using 6629 SNPs in 911 genes on 17 immune pathways from 525 glioblastoma cases and 602 controls from the University of California, San Francisco (UCSF) and a subset of 6029 SNPs in 893 genes from 531 cases and 1782 controls from MD Anderson (MDA). To further assess consistency of SNP-level associations, we also compared data from the UK (266 cases and 2482 controls) and the Mayo Clinic (114 cases and 111 controls). Although three correlated epidermal growth factor receptor (EGFR) SNPs were consistently associated with glioblastoma in all four data sets (Mantel–Haenzel P values = 1 × 10−5 to 4 × 10−3), independent replication is required as genome-wide significance was not attained. In gene-level analyses, eight immune function genes were significantly (minP < 0.05) associated with glioblastoma; the IL-2RA (CD25) cytokine gene had the smallest minP values in both UCSF (minP = 0.01) and MDA (minP = 0.001) data sets. The IL-2RA receptor is found on the surface of regulatory T cells potentially contributing to immunosuppression characteristic of the glioblastoma microenvironment. In pathway correlation analyses, cytokine signaling and adhesion–extravasation–migration pathways showed similar associations with glioblastoma risk in both MDA and UCSF data sets. Our findings represent the first systematic description of immune genes and pathways that characterize glioblastoma risk

A Centennial Retrospective on Charles Williams

Edited transcript of a panel discussion (including audience contributions) at the 17th Mythopoeic Society Conference