Rabbits with vancomycin-loaded in MAO scaffolds showed the inhibition of bone infection and enhancement of osteogenesis, resulting in better outcomes than in the other groups. Overall, these findings demonstrated the potential of this 3D printed porous Ti6Al4V, with good osteogenesis and sustained vancomycin release properties, for application in the treatment of complex bone infections.Interactions between atoms and light in optical cavities provide a means of investigating collective (many-body) quantum physics in controlled environments. Such ensembles of atoms in cavities have been proposed for studying collective quantum spin models, where the atomic internal levels mimic a spin degree of freedom and interact through long-range interactions tunable by changing the cavity parameters1-4. Non-classical steady-state phases arising from the interplay between atom-light interactions and dissipation of light from the cavity have previously been investigated5-11. These systems also offer the opportunity to study dynamical phases of matter that are precluded from existence at equilibrium but can be stabilized by driving a system out of equilibrium12-16, as demonstrated by recent experiments17-22. These phases can also display universal behaviours akin to standard equilibrium phase transitions8,23,24. Here, we use an ensemble of about a million strontium-88 atoms in an optical cavity to simulate a collective Lipkin-Meshkov-Glick model25,26, an iconic model in quantum magnetism, and report the observation of distinct dynamical phases of matter in this system. Our system allows us to probe the dependence of dynamical phase transitions on system size, initial state and other parameters. These observations can be linked to similar dynamical phases in related systems, including the Josephson effect in superfluid helium27, or coupled atomic28 and solid-state polariton29 condensates. The system itself offers potential for generation of metrologically useful entangled states in optical transitions, which could permit quantum enhancement in state-of-the-art atomic clocks30,31.Epitaxial heterostructures based on oxide perovskites and III-V, II-VI and transition metal dichalcogenide semiconductors form the foundation of modern electronics and optoelectronics1-7. Halide perovskites-an emerging family of tunable semiconductors with desirable properties-are attractive for applications such as solution-processed solar cells, light-emitting diodes, detectors and lasers8-15. Their inherently soft crystal lattice allows greater tolerance to lattice mismatch, making them promising for heterostructure formation and semiconductor integration16,17. Atomically sharp epitaxial interfaces are necessary to improve performance and for device miniaturization. However, epitaxial growth of atomically sharp heterostructures of halide perovskites has not yet been achieved, owing to their high intrinsic ion mobility, which leads to interdiffusion and large junction widths18-21, and owing to their poor chemical stability, which leads to decomposition of prior layers during the fabrication of subsequent layers. Therefore, understanding the origins of this instability and identifying effective approaches to suppress ion diffusion are of great importance22-26. Here we report an effective strategy to substantially inhibit in-plane ion diffusion in two-dimensional halide perovskites by incorporating rigid π-conjugated organic ligands. We demonstrate highly stable and tunable lateral epitaxial heterostructures, multiheterostructures and superlattices. Near-atomically sharp interfaces and epitaxial growth are revealed by low-dose aberration-corrected high-resolution transmission electron microscopy. Molecular dynamics simulations confirm the reduced heterostructure disorder and larger vacancy formation energies of the two-dimensional perovskites in the presence of conjugated ligands. These findings provide insights into the immobilization and stabilization of halide perovskite semiconductors and demonstrate a materials platform for complex and molecularly thin superlattices, devices and integrated circuits.Megathrust earthquakes are responsible for some of the most devastating natural disasters1. To better understand the physical mechanisms of earthquake generation, subduction zones worldwide are continuously monitored with geophysical instrumentation. One key strategy is to install stations that record signals from Global Navigation Satellite Systems2,3 (GNSS), enabling us to track the non-steady surface motion of the subducting and overriding plates before, during and after the largest events4-6. https://www.selleckchem.com/products/prt062607-p505-15-hcl.html Here we use a recently developed trajectory modelling approach7 that is designed to isolate secular tectonic motions from the daily GNSS time series to show that the 2010 Maule, Chile (moment magnitude 8.8) and 2011 Tohoku-oki, Japan (moment magnitude 9.0) earthquakes were preceded by reversals of 4-8 millimetres in surface displacement that lasted several months and spanned thousands of kilometres. Modelling of the surface displacement reversal that occurred before the Tohoku-oki earthquake suggests an initial slow slip followed by a sudden pulldown of the Philippine Sea slab so rapid that it caused a viscoelastic rebound across the whole of Japan. Therefore, to understand better when large earthquakes are imminent, we must consider not only the evolution of plate interface frictional processes but also the dynamic boundary conditions from deeper subduction processes, such as sudden densification of metastable slab.All normal somatic cells are thought to acquire mutations, but understanding of the rates, patterns, causes and consequences of somatic mutations in normal cells is limited. The uterine endometrium adopts multiple physiological states over a lifetime and is lined by a gland-forming epithelium1,2. Here, using whole-genome sequencing, we show that normal human endometrial glands are clonal cell populations with total mutation burdens that increase at about 29 base substitutions per year and that are many-fold lower than those of endometrial cancers. Normal endometrial glands frequently carry 'driver' mutations in cancer genes, the burden of which increases with age and decreases with parity. Cell clones with drivers often originate during the first decades of life and subsequently progressively colonize the epithelial lining of the endometrium. Our results show that mutational landscapes differ markedly between normal tissues-perhaps shaped by differences in their structure and physiology-and indicate that the procession of neoplastic change that leads to endometrial cancer is initiated early in life.