Full-waveform inversion of triplicated data using a normalized-correlation-coefficient-based misfit function

In seismic full-waveform inversion (FWI), the choice of misfit function determines what information in data is used and ultimately affects the resolution of the inverted images of the Earth's structure. Misfit functions based on traveltime have been successfully applied in global and regional tomographic studies. However, wave propagation through the upper mantle results in multiple phases arriving at a given receiver in a narrow time interval resulting in complicated waveforms that evolve with distance. To extract waveform information as well as traveltime, we use a misfit function based on the normalized correlation coefficient (CC). This misfit function is able to capture the waveform complexities in both phase and relative amplitude within the measurement window. It is also insensitive to absolute amplitude differences between modeled and recorded data, which avoids problems due to uncertainties in source magnitude, radiation pattern, receiver site effects or even miscalibrated instruments. These features make the misfit function based on normalized CC a good candidate to achieve high-resolution images of complex geological structures when interfering phases coexist in the measurement window, such as triplication waveforms. From synthetic tests, we show the advantages of this misfit function over the cross-correlation traveltime misfit function. Preliminary inversion of data from an earthquake in Northeast China images a sharper and stronger amplitude slab stagnant in the middle of the transition zone than FWI of cross-correlation traveltime

Low-velocity zone atop the 410-km seismic discontinuity in the northwestern United States

The seismic discontinuity at 410 km depth in the Earth's mantle is generally attributed to the phase transition of (Mg,Fe)_2SiO_4 from the olivine to wadsleyite structure. Variation in the depth of this discontinuity is often taken as a proxy for mantle temperature owing to its response to thermal perturbations. For example, a cold anomaly would elevate the 410-km discontinuity, because of its positive Clapeyron slope, whereas a warm anomaly would depress the discontinuity. But trade-offs between seismic wave-speed heterogeneity and discontinuity topography often inhibit detailed analysis of these discontinuities, and structure often appears very complicated. Here we simultaneously model seismic refracted waves and scattered waves from the 410-km discontinuity in the western United States to constrain structure in the region. We find a low-velocity zone, with a shear-wave velocity drop of 5%, on top of the 410-km discontinuity beneath the northwestern United States, extending from southwestern Oregon to the northern Basin and Range province. This low-velocity zone has a thickness that varies from 20 to 90 km with rapid lateral variations. Its spatial extent coincides with both an anomalous composition of overlying volcanism and seismic 'receiver-function' observations observed above the region. We interpret the low-velocity zone as a compositional anomaly, possibly due to a dense partial-melt layer, which may be linked to prior subduction of the Farallon plate and back-arc extension. The existence of such a layer could be indicative of high water content in the Earth's transition zone

Shear-Wave Splitting and Mantle Flow Beneath the Colorado Plateau and its Boundary with the Great Basin

Shear-wave splitting measurements from SKS and SKKS phases show fast polarization azimuths that are subparallel to North American absolute plate motion within the central Rio Grande Rift (RGR) and Colorado Plateau (CP) through to the western rim of the CP, with anisotropy beneath the CP and central RGR showing a remarkably consistent pattern with a mean fast azimuth of 4 degrees +/- degrees 6 E of N. Approaching the rim from the southeast, fast anisotropic directions become north-northeast-south-southwest (NNE-SSW), rotate counter clockwise to north-south in the CP-GB transition, and then to NNW-SSE in the western Great Basin ( GB). This change is coincident with uppermost mantle S-wave velocity perturbations that vary from +4% beneath the western CP and the eastern edge of the Marysvale volcanic field to about -8% beneath the GB. Corresponding delay times average 1.5 sec beneath the central CP, decrease to approximately 0.8 sec near the CP-GB transition, and increase to about 1.2 sec beneath the GB. For the central CP, we suggest anisotropy predominantly controlled by North American plate motion above the asthenosphere. The observed pattern of westward-rotating anisotropy from the western CP through the CP-GB transition may be influenced to asthenospheric flow around a CP lithospheric keel and/or by vertical flow arising from edge-driven small-scale convection. The anisotropic transition from the CP to the GB thus marks a first-order change from absolute plate motion dominated lithosphere-asthenosphere shear to a new regime controlled by regional flow processes. The NNW-SSE anisotropic fast directions of split SKS waves in the eastern GB area are part of a broad circular pattern of seismic anisotropic fast direction in the central GB that has recently been hypothesized to be due to toroidal flow around the sinking Juan de Fuca-Gorda slab.National Science Foundation EAR 9706094, 9707188, 9707190, 0207812Los Alamos National Laboratory Institute of Geophysics and Planetary PhysicsNational Science Foundation Cooperative EAR-000430Department of Energy National Nuclear Security AdministrationGeological Science

Kinematics and dynamics of the east pacific rise linked to a stable, deep-mantle upwelling

Earth’s tectonic plates are generally considered to be driven largely by negative buoyancy associated with subduction of oceanic lithosphere. In this context, mid-ocean ridges (MORs) are passive plate boundaries whose divergence accommodates flow driven by subduction of oceanic slabs at trenches. We show that over the past 80 million years (My), the East Pacific Rise (EPR), Earth’s dominant MOR, has been characterized by limited ridge-perpendicular migration and persistent, asymmetric ridge accretion that are anomalous relative to other MORs. We reconstruct the subduction-related buoyancy fluxes of plates on either side of the EPR. The general expectation is that greater slab pull should correlate with faster plate motion and faster spreading at the EPR. Moreover, asymmetry in slab pull on either side of the EPR should correlate with either ridge migration or enhanced plate velocity in the direction of greater slab pull. Based on our analysis, none of the expected correlations are evident. This implies that other forces significantly contribute to EPR behavior. We explain these observations using mantle flow calculations based on globally integrated buoyancy distributions that require core-mantle boundary heat flux of up to 20 TW. The time-dependent mantle flow predictions yield a long-lived deep-seated upwelling that has its highest radial velocity under the EPR and is inferred to control its observed kinematics. The mantle-wide upwelling beneath the EPR drives horizontal components of asthenospheric flows beneath the plates that are similarly asymmetric but faster than the overlying surface plates, thereby contributing to plate motions through viscous tractions in the Pacific region

Economics of education research: a review and future prospects

In this paper we offer an appraisal of the economics of education research area, charting its history as a field and discussing the ways in which economists have contributed both to education research and to education policy-making. In particular, we highlight the theoretical and methodological contributions that economists have made to the field of education during the last 50 years. Despite the success of the economics of education as a field of inquiry, we argue that some of the contributions made by economists could be limited if the economics of education is seen as quite distinct from the other disciplines working in the field of education. In these areas of common interest, economists need to work side by side with the other major disciplines in the field of education if their contribution to the field is to be maximised, particularly in terms of applying improved methodology. We conclude that the study of education acquisition and its economic and social impact in the economics of education research area is very likely to remain a fertile research ground. Acknowledgement

Constraints on the interpretation of S-to-P receiver functions

We present results from forward modelling to study the feasibility of using S-to-P converted phases to image the seismic discontinuity structure of the crust and upper mantle. We show that a significant level of P-wave energy arriving before the direct S-wave arrival can interfere with the S-to-P converted phases of interest and may result in Sp receiver function phases that do not represent true earth structure. The source of this P-wave energy is attributable to a number of phases, including those that have undergone multiple reflections off the Earth's surface. For deep focus earthquakes (300–600 km deep), a significant amount of P-wave energy is observed from pPPP, pPPPP and sPPPP phases, and arrives within the same time window as predicted for S-to-P converted phases from the direct S phase arrival. Furthermore, for earthquakes at all depths, interfering P-wave energy arrives within the same time window as predicted for S-to-P converted phases from the SKS phase arrival, limiting the usefulness of SKSp receiver functions for upper mantle imaging. To isolate true Sp receiver function phases from contamination due to other P-wave phases, we find it necessary to stack receiver functions from a range of epicentral distances and depths in order to aid the suppression of noise and other unwanted phases. We provide constraints on the noise levels to be expected as a function of epicentral distance and earthquake depth. We find that the lowest noise levels are achievable by restricting epicentral distance to less than 75 degrees and the depth of earthquakes used to less than 300 km

Cerebral small vessel disease genomics and its implications across the lifespan

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. Here, we identify 27 genome-wide loci for WMH-volume in a cohort of 50,970 older individuals, accounting for modification/confounding by hypertension. Aggregated WMH risk variants were associated with altered white matter integrity (p = 2.5×10-7) in brain images from 1,738 young healthy adults, providing insight into the lifetime impact of SVD genetic risk. Mendelian randomization suggested causal association of increasing WMH-volume with stroke, Alzheimer-type dementia, and of increasing blood pressure (BP) with larger WMH-volume, notably also in persons without clinical hypertension. Transcriptome-wide colocalization analyses showed association of WMH-volume with expression of 39 genes, of which four encode known drug targets. Finally, we provide insight into BP-independent biological pathways underlying SVD and suggest potential for genetic stratification of high-risk individuals and for genetically-informed prioritization of drug targets for prevention trials.Peer reviewe

Cerebral small vessel disease genomics and its implications across the lifespan

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. Here, we identify 27 genome-wide loci for WMH-volume in a cohort of 50,970 older individuals, accounting for modification/confounding by hypertension. Aggregated WMH risk variants were associated with altered white matter integrity (p = 2.5×10-7) in brain images from 1,738 young healthy adults, providing insight into the lifetime impact of SVD genetic risk. Mendelian randomization suggested causal association of increasing WMH-volume with stroke, Alzheimer-type dementia, and of increasing blood pressure (BP) with larger WMH-volume, notably also in persons without clinical hypertension. Transcriptome-wide colocalization analyses showed association of WMH-volume with expression of 39 genes, of which four encode known drug targets. Finally, we provide insight into BP-independent biological pathways underlying SVD and suggest potential for genetic stratification of high-risk individuals and for genetically-informed prioritization of drug targets for prevention trials.</p

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke - the second leading cause of death worldwide - were conducted predominantly in populations of European ancestry(1,2). Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis(3), and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach(4), we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry(5). Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries.</p

Stroke genetics informs drug discovery and risk prediction across ancestries

Previous genome-wide association studies (GWASs) of stroke — the second leading cause of death worldwide — were conducted predominantly in populations of European ancestry1,2. Here, in cross-ancestry GWAS meta-analyses of 110,182 patients who have had a stroke (five ancestries, 33% non-European) and 1,503,898 control individuals, we identify association signals for stroke and its subtypes at 89 (61 new) independent loci: 60 in primary inverse-variance-weighted analyses and 29 in secondary meta-regression and multitrait analyses. On the basis of internal cross-ancestry validation and an independent follow-up in 89,084 additional cases of stroke (30% non-European) and 1,013,843 control individuals, 87% of the primary stroke risk loci and 60% of the secondary stroke risk loci were replicated (P < 0.05). Effect sizes were highly correlated across ancestries. Cross-ancestry fine-mapping, in silico mutagenesis analysis3, and transcriptome-wide and proteome-wide association analyses revealed putative causal genes (such as SH3PXD2A and FURIN) and variants (such as at GRK5 and NOS3). Using a three-pronged approach4, we provide genetic evidence for putative drug effects, highlighting F11, KLKB1, PROC, GP1BA, LAMC2 and VCAM1 as possible targets, with drugs already under investigation for stroke for F11 and PROC. A polygenic score integrating cross-ancestry and ancestry-specific stroke GWASs with vascular-risk factor GWASs (integrative polygenic scores) strongly predicted ischaemic stroke in populations of European, East Asian and African ancestry5. Stroke genetic risk scores were predictive of ischaemic stroke independent of clinical risk factors in 52,600 clinical-trial participants with cardiometabolic disease. Our results provide insights to inform biology, reveal potential drug targets and derive genetic risk prediction tools across ancestries