Domain decomposition based on the spectral element method for frequency-domain computational elastodynamics

We propose a domain decomposition method based on the spectral element method(DDM-SEM)for elastic wave computation in frequency domain.It combines the high accuracy of the spectral element method and the high degree of parallelism of a domain decomposition technique,which makes this method suitable for accurate and efficient simulations of large scale problems in elastodynamics.In the DDM-SEM,the original large-scale problem is divided into a number of well designed subdomains.We use the spectral element method independently for each subdomain,and the neighboring subdomains are connected by a frequency-domain version of Riemann transmission condition(RTC)for elastic waves.For the proposed method,we can employ the non-conforming meshes and different interpolation orders in different subdomains to maximize the efficiency.By separating the internal and boundary unknowns of each subdomain,an efficient and naturally parallelizable block LDU direct solver is developed to solve the final system matrix.Numerical experiments verify its accuracy and efficiency,and show that the proposed DDM-SEM can be a promising numerical tool for accurately and effectively solving large and multi-scale problems of elastic waves.It is potentially valuable for the frequency domain seismic inversion where multiple source illuminations are required.

Histones of Neutrophil Extracellular Traps Induce CD11b Expression in Brain Pericytes Via Dectin-1 after Traumatic Brain Injury

The brain pericyte is a unique and indispensable part of the blood-brain barrier(BBB),and contributes to several pathological processes in traumatic brain injury(TBI).However,the cellular and molecular mechanisms by which pericytes are regulated in the damaged brain are largely unknown.Here,we show that the formation of neutrophil extracellular traps(NETs)induces the appearance of CD11b^(+)pericytes after TBI.These CD11b^(+)pericyte subsets are characterized by increased permeability and pro-inflammatory profiles compared to CD11b-pericytes.Moreover,histones from NETs by Dectin-1 facilitate CD11b induction in brain pericytes in PKC-c-Jun dependent manner,resulting in neuroinflammation and BBB dysfunction after TBI.These data indicate that neutrophil-NET-pericyte and histone-Dectin-1-CD11b are possible mechanisms for the activation and dysfunction of pericytes.Targeting NETs formation and Dectin-1 are promising means of treating TBI.