Performance of transition metal-carbon multilayer mirrors from 80 to 350 eV

We report measurements and theoretical calculations of the reflectivity and resolving power of multilayer mirrors made of alternate layers of a transition metal (Co, Fe, V, and Cr) and carbon (2d approx. = 140 A) from 80 to 350 eV

Time evolution of stimulated Raman scattering and two-plasmon decay at laser intensities relevant for shock ignition in a hot plasma

Laser–plasma interaction (LPI) at intensities 1015–1016 W cm2 is dominated by parametric instabilities which can be responsible for a significant amount of non-collisional absorption and generate large fluxes of high-energy nonthermal electrons. Such a regime is of paramount importance for inertial confinement fusion (ICF) and in particular for the shock ignition scheme. In this paper we report on an experiment carried out at the Prague Asterix Laser System (PALS) facility to investigate the extent and time history of stimulated Raman scattering (SRS) and two-plasmon decay (TPD) instabilities, driven by the interaction of an infrared laser pulse at an intensity 1:2 1016 W cm2 with a 100 mm scalelength plasma produced from irradiation of a flat plastic target. The laser pulse duration (300 ps) and the high value of plasma temperature (4 keV) expected from hydrodynamic simulations make these results interesting for a deeper understanding of LPI in shock ignition conditions. Experimental results show that absolute TPD/SRS, driven at a quarter of the critical density, and convective SRS, driven at lower plasma densities, are well separated in time, with absolute instabilities driven at early times of interaction and convective backward SRS emerging at the laser peak and persisting all over the tail of the pulse. Side-scattering SRS, driven at low plasma densities, is also clearly observed. Experimental results are compared to fully kinetic large-scale, two-dimensional simulations. Particle-in-cell results, beyond reproducing the framework delineated by the experimental measurements, reveal the importance of filamentation instability in ruling the onset of SRS and stimulated Brillouin scattering instabilities and confirm the crucial role of collisionless absorption in the LPI energy balance

HRS white paper on clinical utilization of digital health technology.

This collaborative statement from the Digital Health Committee of the Heart Rhythm Society provides everyday clinical scenarios in which wearables may be utilized by patients for cardiovascular health and arrhythmia management. We describe herein the spectrum of wearables that are commercially available for patients, and their benefits, shortcomings and areas for technological improvement. Although wearables for rhythm diagnosis and management have not been examined in large randomized clinical trials, undoubtedly the usage of wearables has quickly escalated in clinical practice. This document is the first of a planned series in which we will update information on wearables as they are revised and released to consumers

Ectodysplasin target gene Fgf20 regulates mammary bud growth and ductal invasion and branching during puberty

Mammary gland development begins with the appearance of epithelial placodes that invaginate, sprout, and branch to form small arborized trees by birth. The second phase of ductal growth and branching is driven by the highly invasive structures called terminal end buds (TEBs) that form at ductal tips at the onset of puberty. Ectodysplasin (Eda), a tumor necrosis factor-like ligand, is essential for the development of skin appendages including the breast. In mice, Eda regulates mammary placode formation and branching morphogenesis, but the underlying molecular mechanisms are poorly understood. Fibroblast growth factor (Fgf) receptors have a recognized role in mammary ductal development and stem cell maintenance, but the ligands involved are ill-defined. Here we report that Fgf20 is expressed in embryonic mammary glands and is regulated by the Eda pathway. Fgf20 deficiency does not impede mammary gland induction, but compromises mammary bud growth, as well as TEB formation, ductal outgrowth and branching during puberty. We further show that loss of Fgf20 delays formation of Eda-induced supernumerary mammary buds and normalizes the embryonic and postnatal hyperbranching phenotype of Eda overexpressing mice. These findings identify a hitherto unknown function for Fgf20 in mammary budding and branching morphogenesis

Personalized estimation of one-year mortality risk after elective hip or knee arthroplasty for osteoarthritis

Aims To develop and validate patient-centred algorithms that estimate individual risk of death over the first year after elective joint arthroplasty surgery for osteoarthritis. Methods A total of 763,213 hip and knee joint arthroplasty episodes recorded in the National Joint Registry for England and Wales (NJR) and 105,407 episodes from the Norwegian Arthroplasty Register were used to model individual mortality risk over the first year after surgery using flexible parametric survival regression. Results The one-year mortality rates in the NJR were 10.8 and 8.9 per 1,000 patient-years after hip and knee arthroplasty, respectively. The Norwegian mortality rates were 9.1 and 6.0 per 1,000 patient-years, respectively. The strongest predictors of death in the final models were age, sex, body mass index, and American Society of Anesthesiologists grade. Exposure variables related to the intervention, with the exception of knee arthroplasty type, did not add discrimination over patient factors alone. Discrimination was good in both cohorts, with c-indices above 0.76 for the hip and above 0.70 for the knee. Time-dependent Brier scores indicated appropriate estimation of the mortality rate (≤ 0.01, all models). Conclusion Simple demographic and clinical information may be used to calculate an individualized estimation for one-year mortality risk after hip or knee arthroplasty (https://jointcalc.shef.ac.uk). These models may be used to provide patients with an estimate of the risk of mortality after joint arthroplasty