80 research outputs found

    Kawasaki-type Dynamics: Diffusion in the kinetic Gaussian model

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    In this article, we retain the basic idea and at the same time generalize Kawasaki's dynamics, spin-pair exchange mechanism, to spin-pair redistribution mechanism, and present a normalized redistribution probability. This serves to unite various order-parameter-conserved processes in microscopic, place them under the control of a universal mechanism and provide the basis for further treatment. As an example of the applications, we treated the kinetic Gaussian model and obtained exact diffusion equation. We observed critical slowing down near the critical point and found that, the critical dynamic exponent z=1/nu=2 is independent of space dimensionality and the assumed mechanism, whether Glauber-type or Kawasaki-type.Comment: accepted for publication in PR

    The effect of scaling building configuration blast experiments on positive phase blast wave parameters

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    Explosions in an urban setting can have a significant negative impact. There is a need to further understand the loading effects caused by the blast’s interaction with structures. In conjunction with this, the effects of scaling and understanding the limitations of laboratory experiments are equally important given the cost incurred for full-scale experiments. The aim of this study was to determine the scaling effects on blast wave parameters found for reduced-scale urban blast scenario laboratory experiments. This paper presents the results of numerical modelling and physical experiments on detonating cuboidal PE-4 charges and measuring the pressure in direct line of sight and at three distinct positions around the corner of a small-scale “building” parallel to the rear wall. Two scales were used, namely 75% and 100%. Inter-scaling between 75% and 100% worked fairly well for positions shielded by the corner of the wall. Additionally, the lab-scale results were compared to similar (but not identical) field trials at an equivalent scale of 250%. The comparison between lab-scale idealised testing and the larger-scale field trials published by Gajewksi and Sielicki in 2020, indicated sensitivity to factors such as detonator positioning, explosive material, charge confinement/mounting, building surface roughness, and environment

    Exploratory Behavior, Trap Models and Glass Transitions

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    A random walk is performed on a disordered landscape composed of NN sites randomly and uniformly distributed inside a dd-dimensional hypercube. The walker hops from one site to another with probability proportional to exp[βE(D)]\exp [- \beta E(D)], where β=1/T\beta = 1/T is the inverse of a formal temperature and E(D)E(D) is an arbitrary cost function which depends on the hop distance DD. Analytic results indicate that, if E(D)=DdE(D) = D^{d} and NN \to \infty, there exists a glass transition at βd=πd/2/Γ(d/2+1)\beta_d = \pi^{d/2}/\Gamma(d/2 + 1). Below TdT_d, the average trapping time diverges and the system falls into an out-of-equilibrium regime with aging phenomena. A L\'evy flight scenario and applications to exploratory behavior are considered.Comment: 4 pages, 1 figure, new versio

    Relationship between dynamical heterogeneities and stretched exponential relaxation

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    We identify the dynamical heterogeneities as an essential prerequisite for stretched exponential relaxation in dynamically frustrated systems. This heterogeneity takes the form of ordered domains of finite but diverging lifetime for particles in atomic or molecular systems, or spin states in magnetic materials. At the onset of the dynamical heterogeneity, the distribution of time intervals spent in such domains or traps becomes stretched exponential at long time. We rigorously show that once this is the case, the autocorrelation function of the renewal process formed by these time intervals is also stretched exponential at long time.Comment: 8 pages, 4 figures, submitted to PR

    Meta-analysis of type 2 Diabetes in African Americans Consortium

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    Type 2 diabetes (T2D) is more prevalent in African Americans than in Europeans. However, little is known about the genetic risk in African Americans despite the recent identification of more than 70 T2D loci primarily by genome-wide association studies (GWAS) in individuals of European ancestry. In order to investigate the genetic architecture of T2D in African Americans, the MEta-analysis of type 2 DIabetes in African Americans (MEDIA) Consortium examined 17 GWAS on T2D comprising 8,284 cases and 15,543 controls in African Americans in stage 1 analysis. Single nucleotide polymorphisms (SNPs) association analysis was conducted in each study under the additive model after adjustment for age, sex, study site, and principal components. Meta-analysis of approximately 2.6 million genotyped and imputed SNPs in all studies was conducted using an inverse variance-weighted fixed effect model. Replications were performed to follow up 21 loci in up to 6,061 cases and 5,483 controls in African Americans, and 8,130 cases and 38,987 controls of European ancestry. We identified three known loci (TCF7L2, HMGA2 and KCNQ1) and two novel loci (HLA-B and INS-IGF2) at genome-wide significance (4.15 × 10(-94)<P<5 × 10(-8), odds ratio (OR)  = 1.09 to 1.36). Fine-mapping revealed that 88 of 158 previously identified T2D or glucose homeostasis loci demonstrated nominal to highly significant association (2.2 × 10(-23) < locus-wide P<0.05). These novel and previously identified loci yielded a sibling relative risk of 1.19, explaining 17.5% of the phenotypic variance of T2D on the liability scale in African Americans. Overall, this study identified two novel susceptibility loci for T2D in African Americans. A substantial number of previously reported loci are transferable to African Americans after accounting for linkage disequilibrium, enabling fine mapping of causal variants in trans-ethnic meta-analysis studies.Peer reviewe

    Global, regional, and national incidence, prevalence, and years lived with disability for 328 diseases and injuries for 195 countries, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

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    As mortality rates decline, life expectancy increases, and populations age, non-fatal outcomes of diseases and injuries are becoming a larger component of the global burden of disease. The Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) provides a comprehensive assessment of prevalence, incidence, and years lived with disability (YLDs) for 328 causes in 195 countries and territories from 1990 to 2016

    Global, regional, and national under-5 mortality, adult mortality, age-specific mortality, and life expectancy, 1970–2016: a systematic analysis for the Global Burden of Disease Study 2016

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    BACKGROUND: Detailed assessments of mortality patterns, particularly age-specific mortality, represent a crucial input that enables health systems to target interventions to specific populations. Understanding how all-cause mortality has changed with respect to development status can identify exemplars for best practice. To accomplish this, the Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) estimated age-specific and sex-specific all-cause mortality between 1970 and 2016 for 195 countries and territories and at the subnational level for the five countries with a population greater than 200 million in 2016. METHODS: We have evaluated how well civil registration systems captured deaths using a set of demographic methods called death distribution methods for adults and from consideration of survey and census data for children younger than 5 years. We generated an overall assessment of completeness of registration of deaths by dividing registered deaths in each location-year by our estimate of all-age deaths generated from our overall estimation process. For 163 locations, including subnational units in countries with a population greater than 200 million with complete vital registration (VR) systems, our estimates were largely driven by the observed data, with corrections for small fluctuations in numbers and estimation for recent years where there were lags in data reporting (lags were variable by location, generally between 1 year and 6 years). For other locations, we took advantage of different data sources available to measure under-5 mortality rates (U5MR) using complete birth histories, summary birth histories, and incomplete VR with adjustments; we measured adult mortality rate (the probability of death in individuals aged 15-60 years) using adjusted incomplete VR, sibling histories, and household death recall. We used the U5MR and adult mortality rate, together with crude death rate due to HIV in the GBD model life table system, to estimate age-specific and sex-specific death rates for each location-year. Using various international databases, we identified fatal discontinuities, which we defined as increases in the death rate of more than one death per million, resulting from conflict and terrorism, natural disasters, major transport or technological accidents, and a subset of epidemic infectious diseases; these were added to estimates in the relevant years. In 47 countries with an identified peak adult prevalence for HIV/AIDS of more than 0·5% and where VR systems were less than 65% complete, we informed our estimates of age-sex-specific mortality using the Estimation and Projection Package (EPP)-Spectrum model fitted to national HIV/AIDS prevalence surveys and antenatal clinic serosurveillance systems. We estimated stillbirths, early neonatal, late neonatal, and childhood mortality using both survey and VR data in spatiotemporal Gaussian process regression models. We estimated abridged life tables for all location-years using age-specific death rates. We grouped locations into development quintiles based on the Socio-demographic Index (SDI) and analysed mortality trends by quintile. Using spline regression, we estimated the expected mortality rate for each age-sex group as a function of SDI. We identified countries with higher life expectancy than expected by comparing observed life expectancy to anticipated life expectancy on the basis of development status alone. FINDINGS: Completeness in the registration of deaths increased from 28% in 1970 to a peak of 45% in 2013; completeness was lower after 2013 because of lags in reporting. Total deaths in children younger than 5 years decreased from 1970 to 2016, and slower decreases occurred at ages 5-24 years. By contrast, numbers of adult deaths increased in each 5-year age bracket above the age of 25 years. The distribution of annualised rates of change in age-specific mortality rate differed over the period 2000 to 2016 compared with earlier decades: increasing annualised rates of change were less frequent, although rising annualised rates of change still occurred in some locations, particularly for adolescent and younger adult age groups. Rates of stillbirths and under-5 mortality both decreased globally from 1970. Evidence for global convergence of death rates was mixed; although the absolute difference between age-standardised death rates narrowed between countries at the lowest and highest levels of SDI, the ratio of these death rates-a measure of relative inequality-increased slightly. There was a strong shift between 1970 and 2016 toward higher life expectancy, most noticeably at higher levels of SDI. Among countries with populations greater than 1 million in 2016, life expectancy at birth was highest for women in Japan, at 86·9 years (95% UI 86·7-87·2), and for men in Singapore, at 81·3 years (78·8-83·7) in 2016. Male life expectancy was generally lower than female life expectancy between 1970 and 2016, an
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