The computation of the radiative transfer equation is expensive mainly due to two stiff terms:the transport term and the collision *** stiffness in the former comes from the fact that particles(such as photons)travel ...
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The computation of the radiative transfer equation is expensive mainly due to two stiff terms:the transport term and the collision *** stiffness in the former comes from the fact that particles(such as photons)travel at the speed of light,while that in the latter is due to the strong scattering in the optically thick *** study the fully implicit scheme for this equation to account for the *** main challenge in the implicit treatment is the coupling between the spacial and angular coordinates that requires the large size of the to-be-inverted matrix,which is also ill-conditioned and not necessarily *** main idea is to utilize the spectral structure of the ill-conditioned matrix to construct a pre-conditioner,which,along with an exquisite split of the spatial and angular dependence,significantly improve the condition number and allows a matrix-free *** also design a fast solver to compute this pre-conditioner explicitly in *** method is shown to be efficient in both diffusive and free streaming limit,and the computational cost is comparable to the state-of-the-art *** examples including anisotropic scattering and two-dimensional problems are provided to validate the effectiveness of our method.
Gene expression at the individual cell-level resolution, as quantified by single-cell RNA-sequencing (scRNA-seq), can provide unique insights into the pathology and cellular origin of diseases and complex traits. Here...
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Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes and molecular mechanisms that are often specific to cell type. Here, to characterize the genetic contribution...
Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes and molecular mechanisms that are often specific to cell type. 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) 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 scores 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.
Reproducibility of computational studies is a hallmark of scientific methodology. It enables researchers to build with confidence on the methods and findings of others, reuse and extend computational pipelines, and th...
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