32 research outputs found
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 < 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