Backward magnetostatic surface spin waves in exchange coupled Co/FeNi bilayers

Propagation of backward magnetostatic surface spin waves (SWs) in exchange coupled Co/FeNi bilayers are studied by using Brillouin light scattering (BLS) technique. Two types of SWs modes were identified in our BLS measurements. They are magnetostatic surface waves (MSSWs) mode and perpendicular standing spin waves (PSSWs) mode. The dispersion relations of MSSWs obtained from the Stokes and Anti-Stokes measurements display respectively positive and negative group velocities. The Anti-Stokes branch with positive phase velocities and negative group velocities, known as backward magnetostatic surface mode originates from the magnetostatic interaction of the bilayer. The experimental data are in good agreement with the theoretical calculations. Our results are useful for understanding the SWs propagation and miniaturizing SWs storage devices

Nonreciprocal ultrastrong magnon-photon coupling in the bandgap of photonic crystals

We observe a nonreciprocal ultrastrong magnon-photon coupling in the bandgap of photonic crystals by introducing a single crystal YIG cylinder into copper photonic crystals cavity as a point defect. The coupling strength reaches up to 1.18 GHz, which constitutes about 10.9% of the photon energy compared to the photon frequency around 10.8 GHz. It is fascinating that the coupling achieves unidirectional signal transmission in the whole bandgap. This study demonstrates the possibility of controlling nonreciprocal magnon-photon coupling by manipulating the structure of photonic crystals, providing new methods to investigate the influence of magnetic point defects on microwave signal transmission.Comment: 6 pages, 5 figure

Genetic Drivers of Heterogeneity in Type 2 Diabetes Pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P \u3c 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care

Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes1,2 and molecular mechanisms that are often specific to cell type3,4. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P &lt; 5 × 10-8) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores5 in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.</p