X-ray standing wave and reflectometric characterization of multilayer structures

Microstructural characterization of synthetic periodic multilayers by x-ray standing waves have been presented. It has been shown that the analysis of multilayers by combined x-ray reflectometry (XRR) and x-ray standing wave (XSW) techniques can overcome the deficiencies of the individual techniques in microstructural analysis. While interface roughnesses are more accurately determined by the XRR technique, layer composition is more accurately determined by the XSW technique where an element is directly identified by its characteristic emission. These aspects have been explained with an example of a 20 period Pt/C multilayer. The composition of the C-layers due to Pt dissolution in the C-layers, Pt$_{x}$C$_{1-x}$, has been determined by the XSW technique. In the XSW analysis when the whole amount of Pt present in the C-layers is assumed to be within the broadened interface, it l eads to larger interface roughness values, inconsistent with those determined by the XRR technique. Constraining the interface roughness values to those determined by the XRR technique, requires an additional amount of dissolved Pt in the C-layers to expl ain the Pt fluorescence yield excited by the standing wave field. This analysis provides the average composition Pt$_{x}$C$_{1-x}$ of the C-layers .Comment: 12 pages RevTex, 10 eps figures embedde

Gaussian Tunneling Model of c-Axis Twist Josephson Junctions

We calculate the critical current density $J^J_c$ for c-axis Josephson tunneling between identical high temperature superconductors twisted an angle $\phi_0$ about the c-axis. We model the tunneling matrix element squared as a Gaussian in the change of wavevector q parallel to the junction, $<|t({\bf q})|^2>\propto\exp(-{\bf q}^2a^2/2\pi^2\sigma^2)$. The $J^J_c(\phi_0)/J^J_c(0)$ obtained for the s- and extended-s-wave order parameters (OP's) are consistent with the Bi$_2$Sr$_2$CaCu$_2$O$_{8+\delta}$ data of Li {\it et al.}, but only for strongly incoherent tunneling, $\sigma^2\ge0.25$. A $d_{x^2-y^2}$-wave OP is always inconsistent with the data. In addition, we show that the apparent conventional sum rule violation observed by Basov et al. might be understandable in terms of incoherent c-axis tunneling, provided that the OP is not $d_{x^2-y^2}$-wave.Comment: 6 pages, 6 figure

Electron Dynamics in Nd1.85_{1.85}Ce.15_{.15}CuO4+δ_{4+\delta}: Evidence for the Pseudogap State and Unconventional c-axis Response

Infrared reflectance measurements were made with light polarized along the a- and c-axis of both superconducting and antiferromagnetic phases of electron doped Nd$_{1.85}$Ce$_{.15}$CuO$_{4+\delta}$. The results are compared to characteristic features of the electromagnetic response in hole doped cuprates. Within the CuO$_2$ planes the frequency dependent scattering rate, 1/$\tau(\omega)$, is depressed below $\sim$ 650 cm$^{-1}$; this behavior is a hallmark of the pseudogap state. While in several hole doped compounds the energy scales associated with the pseudogap and superconducting states are quite close, we are able to show that in Nd$_{1.85}$Ce$_{.15}$CuO$_{4+\delta}$ the two scales differ by more than one order of magnitude. Another feature of the in-plane charge response is a peak in the real part of the conductivity, $\sigma_1(\omega)$, at 50-110 cm$^{-1}$ which is in sharp contrast with the Drude-like response where $\sigma_1(\omega)$ is centered at $\omega=0$. This latter effect is similar to what is found in disordered hole doped cuprates and is discussed in the context of carrier localization. Examination of the c-axis conductivity gives evidence for an anomalously broad frequency range from which the interlayer superfluid is accumulated. Compelling evidence for the pseudogap state as well as other characteristics of the charge dynamics in Nd$_{1.85}$Ce$_{.15}$CuO$_{4+\delta}$ signal global similarities of the cuprate phase diagram with respect to electron and hole doping.Comment: Submitted to PR

Multilevel Monte Carlo methods

The author's presentation of multilevel Monte Carlo path simulation at the MCQMC 2006 conference stimulated a lot of research into multilevel Monte Carlo methods. This paper reviews the progress since then, emphasising the simplicity, flexibility and generality of the multilevel Monte Carlo approach. It also offers a few original ideas and suggests areas for future research

Identification of multiple risk loci and regulatory mechanisms influencing susceptibility to multiple myeloma

Genome-wide association studies (GWAS) have transformed our understanding of susceptibility to multiple myeloma (MM), but much of the heritability remains unexplained. We report a new GWAS, a meta-analysis with previous GWAS and a replication series, totalling 9974 MM cases and 247,556 controls of European ancestry. Collectively, these data provide evidence for six new MM risk loci, bringing the total number to 23. Integration of information from gene expression, epigenetic profiling and in situ Hi-C data for the 23 risk loci implicate disruption of developmental transcriptional regulators as a basis of MM susceptibility, compatible with altered B-cell differentiation as a key mechanism. Dysregulation of autophagy/apoptosis and cell cycle signalling feature as recurrently perturbed pathways. Our findings provide further insight

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

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