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Abstract. Serpentinite has been proposed as a cause of both low strength and aseismic creep of fault zones. To test these hypotheses, we have measured the strength of chrysotile-, lizardite-, and antigorite-rich serpentinite gouges under hydrothermal conditions, with emphasis on chrysotile, which has thus far received little attention. At 25øC, the coefficient of friction, g, of chrysotile gouge is roughly 0.2, whereas the lizardite-and antigorite-rich gouges are at least twice as strong. The very low room temperature strength of chrysotile is a consequence of its unusually high adsorbed water content. When the adsorbed water is removed, chrysotile is as strong as pure antigorite gouge at room temperature. Heating to -200øC causes the frictional strengths of all three gouges to increase. Limited data suggest that different polytypes of a given serpentine mineral have similar strengths; thus deformation-induced changes in polytype should not affect fault strength. At 25øC, the chrysotile gouge has a transition from velocity strengthening at low velocities to velocity weakening at high velocities, consistent with previous studies. At temperatures up to -200øC, however, chrysotile strength is essentially independent of velocity at low velocities. Overall, chrysotile has a restricted range of velocity-strengthening behavior that migrates to higher velocities with increasing temperature. Less information on velocity dependence is available for the lizardite and antigorite gouges, but their behavior is consistent with that outlined for chrysotile. The marked changes in velocity dependence and strength of chrysotile with heating underscore the hazards of using room temperature data to predict fault behavior at depth. The velocity behavior at elevated temperatures does not rule out serpentinite as a cause of aseismic slip, but in the presence of a hydrostatic fluid pressure gradient, all varieties of serpentine are too strong to explain the apparent weakness of faults such as the San Andreas.

Coronary artery disease (CAD) is a leading cause of death, yet its genetic determinants are not fully elucidated. We report a multi-ethnic genome-wide association study of CAD involving nearly a quarter of a million cases, incorporating the largest cohorts to date of Whites, Blacks, and Hispanics from the Million Veteran Program with existing studies including CARDIoGRAMplusC4D, UK Biobank, and Biobank Japan. We verify substantial and nearly equivalent heritability of CAD across multiple ancestral groups, discover 107 novel loci including the first nine on the X-chromosome, identify the first eight genome-wide significant loci among Blacks and Hispanics, and demonstrate that two common haplotypes are largely responsible for the risk stratification at the well-known 9p21 locus in most populations except those of African origin where both haplotypes are virtually absent. We identify 15 loci for angiographically derived burden of coronary atherosclerosis, which robustly overlap with the strongest and earliest loci reported to date for clinical CAD. Phenome-wide association analyses of novel loci and externally validated polygenic risk scores (PRS) augment signals from the insulin resistance cluster of risk factors and consequences, extend previously established pleiotropic associations of loci with traditional risk factors to include smoking and family history, and confirm a substantially reduced transferability of existing PRS to Blacks. Downstream integrative genomic analyses reinforce the critical role of endothelial, fibroblast, and smooth muscle cells within the coronary vessel wall in CAD susceptibility. Our study highlights the value of a multi-ethnic design in efficiently characterizing the genetic architecture of CAD across all human populations.

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