Probing transport in quantum many-fermion simulations via quantum loop topography

Quantum many-fermion systems give rise to diverse states of matter that often reveal themselves in distinctive transport properties. While some of these states can be captured by microscopic models accessible to numerical exact quantum Monte Carlo simulations, it nevertheless remains challenging to numerically access their transport properties. Here we demonstrate that quantum loop topography (QLT) can be used to directly probe transport by machine learning current-current correlations in imaginary time. We showcase this approach by studying the emergence of superconducting fluctuations in the negative-U Hubbard model and a spin-fermion model for a metallic quantum critical point. For both sign-free models, we find that the QLT approach detects a change in transport in very good agreement with their established phase diagrams. These proof-of-principle calculations combined with the numerical efficiency of the QLT approach point a way to identify hitherto elusive transport phenomena such as non-Fermi liquids using machine learning algorithms.Comment: 7 pages, 5 figure

Topological gravity on the lattice

In this paper we show that a particular twist of $\mathcal{N}=4$ super Yang-Mills in three dimensions with gauge group SU(2) possesses a set of classical vacua corresponding to the space of flat connections of the {\it complexified} gauge group $SL(2,C)$. The theory also contains a set of topological observables corresponding to Wilson loops wrapping non-trivial cycles of the base manifold. This moduli space and set of topological observables is shared with the Chern Simons formulation of three dimensional gravity and we hence conjecture that the Yang-Mills theory gives an equivalent description of the gravitational theory. Unlike the Chern Simons formulation the twisted Yang-Mills theory possesses a supersymmetric and gauge invariant lattice construction which then provides a possible non-perturbative definition of three dimensional gravity.Comment: 10 page

zDALY: An adjusted indicator to estimate the burden of zoonotic diseases

The burden of human diseases in populations, or for an individual, is frequently estimated in terms of one of a number of Health Adjusted Life Years (HALYs). The Disability Adjusted Life Year (DALY) is a widely accepted HALY metric and is used by the World Health Organization and the Global Burden of Disease studies. Many human diseases are of animal origin and often cause ill health and production losses in domestic animals. The economic losses due to disease in animals are usually estimated in monetary terms. The monetary impact on animal health is not compatible with HALY approaches used to measure the impact on human health. To estimate the societal burden of zoonotic diseases that have substantial human and animal disease burden we propose methodology which can be accommodated within the DALY framework. Monetary losses due to the animal disease component of a zoonotic disease can be converted to an equivalent metric using a local gross national income per capita deflator. This essentially gives animal production losses a time trade-off for human life years. This is the time required to earn the income needed to replace that financial loss. This can then be assigned a DALY equivalent, termed animal loss equivalents (ALE), and added to the DALY associated with human ill health to give a modified DALY. This is referred to as the “zDALY”. ALEs could also be estimated using willingness-to-pay for animal health or survey tools to estimate the replacement time value for animals with high societal or emotional value (for example pets) that cannot be calculated directly using monetary worth. Thus the zDALY estimates the impact of a zoonotic disease to animal and human health. The losses due to the animal disease component of the modified DALY are straightforward to calculate. A number of worked examples such as echinococcosis, brucellosis, Q fever and cysticercosis from a diverse spectrum of countries with different levels of economic development illustrate the use of the zDALY indicator

Taurolidine-citrate lock solution (TauroLock) significantly reduces CVAD-associated grampositive infections in pediatric cancer patients

<p>Abstract</p> <p>Background</p> <p>Taurolidin/Citrate (TauroLock™), a lock solution with broad spectrum antimicrobial activity, may prevent bloodstream infection (BSI) due to coagulase-negative staphylococci (CoNS or 'MRSE' in case of methicillin-resistant isolates) in pediatric cancer patients with a long term central venous access device (CVAD, Port- or/Broviac-/Hickman-catheter type).</p> <p>Methods</p> <p>In a single center prospective 48-months cohort study we compared all patients receiving anticancer chemotherapy from April 2003 to March 2005 (group 1, heparin lock with 200 IU/ml sterile normal saline 0.9%; Canusal^®Wockhardt UK Ltd, Wrexham, Wales) and all patients from April 2005 to March 2007 (group 2; taurolidine 1.35%/Sodium Citrate 4%; TauroLock™, Tauropharm, Waldbüttelbrunn, Germany).</p> <p>Results</p> <p>In group 1 (heparin), 90 patients had 98 CVAD in use during the surveillance period. 14 of 30 (47%) BSI were 'primary Gram positive BSI due to CoNS (n = 4) or MRSE (n = 10)' [incidence density (ID); 2.30 per 1000 inpatient CVAD-utilization days].</p> <p>In group 2 (TauroLock™), 89 patients had 95 CVAD in use during the surveillance period. 3 of 25 (12%) BSI were caused by CoNS. (ID, 0.45). The difference in the ID between the two groups was statistically significant (P = 0.004).</p> <p>Conclusion</p> <p>The use of Taurolidin/Citrate (TauroLock™) significantly reduced the number and incidence density of primary catheter-associated BSI due to CoNS and MRSE in pediatric cancer patients.</p

The promoter polymorphism -232C/G of the PCK1 gene is associated with type 2 diabetes in a UK-resident South Asian population

Background: The PCK1 gene, encoding cytosolic phosphoenolpyruvate carboxykinase (PEPCK-C), has previously been implicated as a candidate gene for type 2 diabetes (T2D) susceptibility. Rodent models demonstrate that over-expression of Pck1 can result in T2D development and a single nucleotide polymorphism (SNP) in the promoter region of human PCK1 (-232C/G) has exhibited significant association with the disease in several cohorts. Within the UK-resident South Asian population, T2D is 4 to 6 times more common than in indigenous white Caucasians. Despite this, few studies have reported on the genetic susceptibility to T2D in this ethnic group and none of these has investigated the possible effect of PCK1 variants. We therefore aimed to investigate the association between common variants of the PCK1 gene and T2D in a UK-resident South Asian population of Punjabi ancestry, originating predominantly from the Mirpur area of Azad Kashmir, Pakistan. \ud \ud Methods: We used TaqMan assays to genotype five tagSNPs covering the PCK1 gene, including the -232C/G variant, in 903 subjects with T2D and 471 normoglycaemic controls. \ud \ud Results: Of the variants studied, only the minor allele (G) of the -232C/G SNP demonstrated a significant association with T2D, displaying an OR of 1.21 (95% CI: 1.03 - 1.42, p = 0.019). \ud \ud Conclusion: This study is the first to investigate the association between variants of the PCK1 gene and T2D in South Asians. Our results suggest that the -232C/G promoter polymorphism confers susceptibility to T2D in this ethnic group. \ud \ud Trial registration: UKADS Trial Registration: ISRCTN38297969

Increasing dominance of large lianas in Amazonian forests

Ecological orthodoxy suggests that old-growth forests should be close to dynamic equilibrium, but this view has been challenged by recent findings that neotropical forests are accumulating carbon and biomass, possibly in response to the increasing atmospheric concentrations of carbon dioxide. However, it is unclear whether the recent increase in tree biomass has been accompanied by a shift in community composition. Such changes could reduce or enhance the carbon storage potential of old-growth forests in the long term. Here we show that non-fragmented Amazon forests are experiencing a concerted increase in the density, basal area and mean size of woody climbing plants (lianas). Over the last two decades of the twentieth century the dominance of large lianas relative to trees has increased by 1.7–4.6% a year. Lianas enhance tree mortality and suppress tree growth, so their rapid increase implies that the tropical terrestrial carbon sink may shut down sooner than current models suggest. Predictions of future tropical carbon fluxes will need to account for the changing composition and dynamics of supposedly undisturbed forests