236 research outputs found

    B^F Theory and Flat Spacetimes

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    We propose a reduced constrained Hamiltonian formalism for the exactly soluble BFB \wedge F theory of flat connections and closed two-forms over manifolds with topology Σ3×(0,1)\Sigma^3 \times (0,1). The reduced phase space variables are the holonomies of a flat connection for loops which form a basis of the first homotopy group π1(Σ3)\pi_1(\Sigma^3), and elements of the second cohomology group of Σ3\Sigma^3 with value in the Lie algebra L(G)L(G). When G=SO(3,1)G=SO(3,1), and if the two-form can be expressed as B=eeB= e\wedge e, for some vierbein field ee, then the variables represent a flat spacetime. This is not always possible: We show that the solutions of the theory generally represent spacetimes with ``global torsion''. We describe the dynamical evolution of spacetimes with and without global torsion, and classify the flat spacetimes which admit a locally homogeneous foliation, following Thurston's classification of geometric structures.Comment: 21 pp., Mexico Preprint ICN-UNAM-93-1

    Effect of leisure activities on inflammation and cognitive function in an aging sample

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    Cardiovascular disease risk factors (CVDRFs) increase the risk of dementia. The purpose of this study was to examine whether leisure activities (mental, physical, and social activities) modified the effect of CVDRFs on inflammatory markers and cognitive function in middle and old age. A secondary-data analysis study was conducted using data from 405 middle-age participants (40-59 years) and 342 old-age participants (60-84 years) who participated in the Survey of Midlife Development in the United States (MIDUS). CVDRFs were obtained from a combination of self-report medical history and blood-based biomarkers. Three CVDRF groups (≤1, 2, and ≥3 CVDRFs) were identified. More CVDRFs were significantly associated with higher levels of inflammatory markers in both age groups, and associated with lower levels of executive function (EF) in the old age group. CVDRFs were not related to the frequency of leisure activities in either age group. After controlling for covariates, higher levels of physical activities were significantly associated with lower levels of inflammatory markers, and higher levels of mental activities were associated with higher levels of cognitive function. In the old age group, physical activities also moderated the effect of CVDRFs on episodic memory (EM), and mental activities moderated the effect of CVDRFs on interleukin-6 (IL-6). Multiple CVDRFs may be associated with poorer cognitive function and higher inflammatory markers, but middle-age and older adults with CVDRFs may not engage in frequent physical and cognitive activities that may be protective. It is important to develop strategies to facilitate engagement in these activities from midlife

    Robust Inference of Trees

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    This paper is concerned with the reliable inference of optimal tree-approximations to the dependency structure of an unknown distribution generating data. The traditional approach to the problem measures the dependency strength between random variables by the index called mutual information. In this paper reliability is achieved by Walley's imprecise Dirichlet model, which generalizes Bayesian learning with Dirichlet priors. Adopting the imprecise Dirichlet model results in posterior interval expectation for mutual information, and in a set of plausible trees consistent with the data. Reliable inference about the actual tree is achieved by focusing on the substructure common to all the plausible trees. We develop an exact algorithm that infers the substructure in time O(m^4), m being the number of random variables. The new algorithm is applied to a set of data sampled from a known distribution. The method is shown to reliably infer edges of the actual tree even when the data are very scarce, unlike the traditional approach. Finally, we provide lower and upper credibility limits for mutual information under the imprecise Dirichlet model. These enable the previous developments to be extended to a full inferential method for trees.Comment: 26 pages, 7 figure

    Missing values: sparse inverse covariance estimation and an extension to sparse regression

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    We propose an l1-regularized likelihood method for estimating the inverse covariance matrix in the high-dimensional multivariate normal model in presence of missing data. Our method is based on the assumption that the data are missing at random (MAR) which entails also the completely missing at random case. The implementation of the method is non-trivial as the observed negative log-likelihood generally is a complicated and non-convex function. We propose an efficient EM algorithm for optimization with provable numerical convergence properties. Furthermore, we extend the methodology to handle missing values in a sparse regression context. We demonstrate both methods on simulated and real data.Comment: The final publication is available at http://www.springerlink.co

    Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts

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    BACKGROUND: The magnitude of the association between Helicobacter pylori and incidence of gastric cancer is unclear. H pylori infection and the circulating antibody response can be lost with development of cancer; thus retrospective studies are subject to bias resulting from classifi- cation of cases as H pylori negative when they were infected in the past. AIMS: To combine data from all case control studies nested within prospective cohorts to assess more reliably the relative risk of gastric cancer associated with H pylori infection.To investigate variation in relative risk by age, sex, cancer type and subsite, and interval between blood sampling and cancer diagnosis. METHODS: Studies were eligible if blood samples for H pylori serology were collected before diagnosis of gastric cancer in cases. Identified published studies and two unpublished studies were included. Individual subject data were obtained for each. Matched odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated for the association between H pylori and gastric cancer. RESULTS: Twelve studies with 1228 gastric cancer cases were considered. The association with H pylori was restricted to noncardia cancers (OR 3.0; 95% CI 2.3–3.8) and was stronger when blood samples for H pylori serology were collected 10+ years before cancer diagnosis (5.9; 3.4–10.3). H pylori infection was not associated with an altered overall risk of cardia cancer (1.0; 0.7–1.4). CONCLUSIONS: These results suggest that 5.9 is the best estimate of the relative risk of non-cardia cancer associated with H pylori infection and that H pylori does not increase the risk of cardia cancer. They also support the idea that when H pylori status is assessed close to cancer diagnosis, the magnitude of the non-cardia association may be underestimated

    Tensor-scalar gravity and binary-pulsar experiments

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    Some recently discovered nonperturbative strong-field effects in tensor-scalar theories of gravitation are interpreted as a scalar analog of ferromagnetism: "spontaneous scalarization". This phenomenon leads to very significant deviations from general relativity in conditions involving strong gravitational fields, notably binary-pulsar experiments. Contrary to solar-system experiments, these deviations do not necessarily vanish when the weak-field scalar coupling tends to zero. We compute the scalar "form factors" measuring these deviations, and notably a parameter entering the pulsar timing observable gamma through scalar-field-induced variations of the inertia moment of the pulsar. An exploratory investigation of the confrontation between tensor-scalar theories and binary-pulsar experiments shows that nonperturbative scalar field effects are already very tightly constrained by published data on three binary-pulsar systems. We contrast the probing power of pulsar experiments with that of solar-system ones by plotting the regions they exclude in a generic two-dimensional plane of tensor-scalar theories.Comment: 35 pages, REVTeX 3.0, uses epsf.tex to include 9 Postscript figure

    Model-independent measurement of t\boldsymbol{t}-channel single top quark production in ppˉ\boldsymbol{p\bar{p}} collisions at s=1.96\boldsymbol{\sqrt{s}=1.96} TeV

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    We present a model-independent measurement of tt-channel electroweak production of single top quarks in \ppbar collisions at s=1.96  TeV\sqrt{s}=1.96\;\rm TeV. Using 5.4  fb15.4\;\rm fb^{-1} of integrated luminosity collected by the D0 detector at the Fermilab Tevatron Collider, and selecting events containing an isolated electron or muon, missing transverse energy and one or two jets originating from the fragmentation of bb quarks, we measure a cross section \sigma({\ppbar}{\rargap}tqb+X) = 2.90 \pm 0.59\;\rm (stat+syst)\; pb for a top quark mass of 172.5  GeV172.5\;\rm GeV. The probability of the background to fluctuate and produce a signal as large as the one observed is 1.6×1081.6\times10^{-8}, corresponding to a significance of 5.5 standard deviations.Comment: 8 pages, 4 figures, submitted to Phys. Lett.

    Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980�2015: a systematic analysis for the Global Burden of Disease Study 2015

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    Background Improving survival and extending the longevity of life for all populations requires timely, robust evidence on local mortality levels and trends. The Global Burden of Disease 2015 Study (GBD 2015) provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015. These results informed an in-depth investigation of observed and expected mortality patterns based on sociodemographic measures. Methods We estimated all-cause mortality by age, sex, geography, and year using an improved analytical approach originally developed for GBD 2013 and GBD 2010. Improvements included refinements to the estimation of child and adult mortality and corresponding uncertainty, parameter selection for under-5 mortality synthesis by spatiotemporal Gaussian process regression, and sibling history data processing. We also expanded the database of vital registration, survey, and census data to 14�294 geography�year datapoints. For GBD 2015, eight causes, including Ebola virus disease, were added to the previous GBD cause list for mortality. We used six modelling approaches to assess cause-specific mortality, with the Cause of Death Ensemble Model (CODEm) generating estimates for most causes. We used a series of novel analyses to systematically quantify the drivers of trends in mortality across geographies. First, we assessed observed and expected levels and trends of cause-specific mortality as they relate to the Socio-demographic Index (SDI), a summary indicator derived from measures of income per capita, educational attainment, and fertility. Second, we examined factors affecting total mortality patterns through a series of counterfactual scenarios, testing the magnitude by which population growth, population age structures, and epidemiological changes contributed to shifts in mortality. Finally, we attributed changes in life expectancy to changes in cause of death. We documented each step of the GBD 2015 estimation processes, as well as data sources, in accordance with Guidelines for Accurate and Transparent Health Estimates Reporting (GATHER). Findings Globally, life expectancy from birth increased from 61·7 years (95 uncertainty interval 61·4�61·9) in 1980 to 71·8 years (71·5�72·2) in 2015. Several countries in sub-Saharan Africa had very large gains in life expectancy from 2005 to 2015, rebounding from an era of exceedingly high loss of life due to HIV/AIDS. At the same time, many geographies saw life expectancy stagnate or decline, particularly for men and in countries with rising mortality from war or interpersonal violence. From 2005 to 2015, male life expectancy in Syria dropped by 11·3 years (3·7�17·4), to 62·6 years (56·5�70·2). Total deaths increased by 4·1 (2·6�5·6) from 2005 to 2015, rising to 55·8 million (54·9 million to 56·6 million) in 2015, but age-standardised death rates fell by 17·0 (15·8�18·1) during this time, underscoring changes in population growth and shifts in global age structures. The result was similar for non-communicable diseases (NCDs), with total deaths from these causes increasing by 14·1 (12·6�16·0) to 39·8 million (39·2 million to 40·5 million) in 2015, whereas age-standardised rates decreased by 13·1 (11·9�14·3). Globally, this mortality pattern emerged for several NCDs, including several types of cancer, ischaemic heart disease, cirrhosis, and Alzheimer's disease and other dementias. By contrast, both total deaths and age-standardised death rates due to communicable, maternal, neonatal, and nutritional conditions significantly declined from 2005 to 2015, gains largely attributable to decreases in mortality rates due to HIV/AIDS (42·1, 39·1�44·6), malaria (43·1, 34·7�51·8), neonatal preterm birth complications (29·8, 24·8�34·9), and maternal disorders (29·1, 19·3�37·1). Progress was slower for several causes, such as lower respiratory infections and nutritional deficiencies, whereas deaths increased for others, including dengue and drug use disorders. Age-standardised death rates due to injuries significantly declined from 2005 to 2015, yet interpersonal violence and war claimed increasingly more lives in some regions, particularly in the Middle East. In 2015, rotaviral enteritis (rotavirus) was the leading cause of under-5 deaths due to diarrhoea (146�000 deaths, 118�000�183�000) and pneumococcal pneumonia was the leading cause of under-5 deaths due to lower respiratory infections (393�000 deaths, 228�000�532�000), although pathogen-specific mortality varied by region. Globally, the effects of population growth, ageing, and changes in age-standardised death rates substantially differed by cause. Our analyses on the expected associations between cause-specific mortality and SDI show the regular shifts in cause of death composition and population age structure with rising SDI. Country patterns of premature mortality (measured as years of life lost YLLs) and how they differ from the level expected on the basis of SDI alone revealed distinct but highly heterogeneous patterns by region and country or territory. Ischaemic heart disease, stroke, and diabetes were among the leading causes of YLLs in most regions, but in many cases, intraregional results sharply diverged for ratios of observed and expected YLLs based on SDI. Communicable, maternal, neonatal, and nutritional diseases caused the most YLLs throughout sub-Saharan Africa, with observed YLLs far exceeding expected YLLs for countries in which malaria or HIV/AIDS remained the leading causes of early death. Interpretation At the global scale, age-specific mortality has steadily improved over the past 35 years; this pattern of general progress continued in the past decade. Progress has been faster in most countries than expected on the basis of development measured by the SDI. Against this background of progress, some countries have seen falls in life expectancy, and age-standardised death rates for some causes are increasing. Despite progress in reducing age-standardised death rates, population growth and ageing mean that the number of deaths from most non-communicable causes are increasing in most countries, putting increased demands on health systems. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens

    Search for the lepton-flavour violating decay D0e±μD^0 \to e^\pm\mu^\mp

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    A search for the lepton-flavour violating decay D0e±μD^0 \to e^\pm \mu^\mp is made with a dataset corresponding to an integrated luminosity of 3.03.0 fb1^{-1} of proton-proton collisions at centre-of-mass energies of 77 TeV and 88 TeV, collected by the LHCb experiment. Candidate D0D^0 mesons are selected using the decay D+D0π+D^{*+} \to D^0 \pi^+ and the D0e±μD^0 \to e^\pm \mu^\mp branching fraction is measured using the decay mode D0Kπ+D^0 \to K^- \pi^+ as a normalisation channel. No significant excess of D0e±μD^0 \to e^\pm \mu^\mp candidates over the expected background is seen, and a limit is set on the branching fraction, B(D0e±μ)<1.3×108\mathcal{B}(D^0 \to e^\pm \mu^\mp) < 1.3 \times 10^{-8}, at 90 % confidence level. This is an order of magnitude lower than the previous limit and it further constrains the parameter space in some leptoquark models and in supersymmetric models with R-parity violation.A search for the lepton-flavour violating decay D0→e±μ∓ is made with a dataset corresponding to an integrated luminosity of 3.0fb−1 of proton–proton collisions at centre-of-mass energies of 7 TeV and 8 TeV , collected by the LHCb experiment. Candidate D0 mesons are selected using the decay D⁎+→D0π+ and the D0→e±μ∓ branching fraction is measured using the decay mode D0→K−π+ as a normalization channel. No significant excess of D0→e±μ∓ candidates over the expected background is seen, and a limit is set on the branching fraction, B(D0→e±μ∓)<1.3×10−8 , at 90% confidence level. This is an order of magnitude lower than the previous limit and it further constrains the parameter space in some leptoquark models and in supersymmetric models with R-parity violation.A search for the lepton-flavour violating decay D0e±μD^0 \to e^\pm \mu^\mp is made with a dataset corresponding to an integrated luminosity of 3.0 fb1^{-1} of proton-proton collisions at centre-of-mass energies of 77 TeV and 88 TeV, collected by the LHCb experiment. Candidate D0D^0 mesons are selected using the decay D+D0π+D^{*+} \to D^0 \pi^+ and the D0e±μD^0 \to e^\pm \mu^\mp branching fraction is measured using the decay mode D0Kπ+D^0 \to K^-\pi^+ as a normalisation channel. No significant excess of D0e±μD^0 \to e^\pm \mu^\mp candidates over the expected background is seen, and a limit is set on the branching fraction, B(D0e±μ)<1.3×108\mathcal{B}(D^0 \to e^\pm \mu^\mp) < 1.3 \times 10^{-8}, at 90 % confidence level. This is an order of magnitude lower than the previous limit and it further constrains the parameter space in some leptoquark models and in supersymmetric models with R-parity violation

    Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990�2015: a systematic analysis for the Global Burden of Disease Study 2015

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    Background Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. Methods We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. Findings Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs offset by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs. Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined. Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies. From 2005 to 2015, HALE at birth increased by an average of 2·9 years (95 uncertainty interval 2·9�3·0) for men and 3·5 years (3·4�3·7) for women, while HALE at age 65 years improved by 0·85 years (0·78�0·92) and 1·2 years (1·1�1·3), respectively. Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability. Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI. At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violence, and various NCDs. Interpretation Health is improving globally, but this means more populations are spending more time with functional health loss, an absolute expansion of morbidity. The proportion of life spent in ill health decreases somewhat with increasing SDI, a relative compression of morbidity, which supports continued efforts to elevate personal income, improve education, and limit fertility. Our analysis of DALYs and HALE and their relationship to SDI represents a robust framework on which to benchmark geography-specific health performance and SDG progress. Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform financial and research investments, prevention efforts, health policies, and health system improvement initiatives for all countries along the development continuum. Funding Bill & Melinda Gates Foundation. © 2016 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY licens
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