Frictional and lithological controls on shallow slow slip at the Northern Hikurangi Margin

Slow slip events (SSEs) have been identified at subduction zones globally as an important link in the continuum between elastodynamic ruptures and stable creep. The northern Hikurangi margin is home to shallow SSEs which propagate to within 2 km of the seafloor and possibly to the trench, providing insights into the physical conditions conducive to SSE behavior. We report on a suite of friction experiments performed on protolith material entering the SSE source region at the Hikurangi margin, collected during the International Ocean Discovery Program Expedition 375. We performed velocity stepping and slide-hold-slide experiments over a range of fault slip rates, from plate rate (5 cm/yr or 1.6 × 10−9 m/s) to ∼1 mm/s (10−3 m/s) and quantified the frictional velocity dependence and healing rates for a range of lithologies atdifferent stresses. The frictional velocity dependence (a-b) and critical slip distance DC increase with fault slip rate in our experiments. We observe atransition from velocity weakening to strengthening at slip rates of ∼0.3 µm/s. This velocity dependence of DC could be due to a combination of dilatant strengthening and a widening of the active shear zone at higher slip rates. We document low healing rates in the clay-rich volcaniclastic conglomerates, which lie above the incoming plate basement at least locally, and relatively higher healing rates in the chalk lithology. Finally, our experimental constraints on healing rates in different input lithologies extrapolated to timescales of 1–10 years are consistent with the geodetically inferred low stress drops and healing rates characteristic of the Hikurangi SSEs

Application of constitutive friction laws to glacier seismicity

While analysis of glacial seismicity continues to be a widely used method for interpreting glacial processes, the underlying mechanics controlling glacial stick-slip seismicity remain speculative. Here, we report on laboratory shear experiments of debris-laden ice slid over a bedrock asperity under carefully controlled conditions. By modifying the elastic loading stiffness, we generated the first laboratory icequakes. Our work represents the first comprehensive lab observations of unstable ice-slip events and replicates several seismological field observations of glacier slip, such as slip velocity, stress drop, and the relationship between stress drop and recurrence interval. We also observe that stick-slips initiate above a critical driving velocity and that stress drop magnitude decreases with further increases in velocity, consistent with friction theory and rock-on-rock friction laboratory experiments. Our results demonstrate that glacier slip behavior can be accurately predicted by the constitutive rate-and-state friction laws that were developed for rock friction

Frictional Behavior of Input Sediments to the Hikurangi Trench, New Zealand

AbstractThe Hikurangi subduction zone hosts shallow slow‐slip events, possibly extending to the seafloor. The mechanisms allowing for this behavior are poorly understood but are likely a function of the frictional properties of the downgoing seafloor sediments. We conducted friction experiments at a large range of effective stresses, temperatures, and velocities on incoming sediment to the Hikurangi subduction zone to explore the possible connection of frictional properties to slow‐slip events. These experiments were conducted on multiple apparatuses, allowing us to access a wider range of deformation conditions than is available on any one machine. We find that the material frictionally weakens and becomes less velocity strengthening with increasing effective stress, whereas temperature has only a small effect on both friction and frictional stability. When driven at the plate convergence rate, the sediment exhibits velocity‐weakening behavior. These results imply that the frictional properties of the sediment package subducting at Hikurangi could promote slow‐slip events at the pressures, temperatures, and strain rates expected along the plate boundary thrust up to 10‐km depth without requiring elevated pore fluid pressures. The transition to velocity‐strengthening behavior at faster slip rates could provide a mechanism for limiting unstable slip to slow‐sliding velocities, rather than accommodating deformation through ordinary earthquakes

Study of the plutino object (208996) 2003 AZ84 from stellar occultations: size, shape and topographic features

We present results derived from four stellar occultations by the plutino object (208996) 2003~AZ$_{84}$, detected at January 8, 2011 (single-chord event), February 3, 2012 (multi-chord), December 2, 2013 (single-chord) and November 15, 2014 (multi-chord). Our observations rule out an oblate spheroid solution for 2003~AZ$_{84}$'s shape. Instead, assuming hydrostatic equilibrium, we find that a Jacobi triaxial solution with semi axes $(470 \pm 20) \times (383 \pm 10) \times (245 \pm 8)$~km % axis ratios $b/a= 0.82 \pm 0.05$ and $c/a= 0.52 \pm 0.02$, can better account for all our occultation observations. Combining these dimensions with the rotation period of the body (6.75~h) and the amplitude of its rotation light curve, we derive a density $\rho=0.87 \pm 0.01$~g~cm$^{-3}$ a geometric albedo $p_V= 0.097 \pm 0.009$. A grazing chord observed during the 2014 occultation reveals a topographic feature along 2003~AZ$_{84}$'s limb, that can be interpreted as an abrupt chasm of width $\sim 23$~km and depth $> 8$~km or a smooth depression of width $\sim 80$~km and depth $\sim 13$~km (or an intermediate feature between those two extremes)

Genome-Wide Association Study and Gene Expression Analysis Identifies CD84 as a Predictor of Response to Etanercept Therapy in Rheumatoid Arthritis

Anti-tumor necrosis factor alpha (anti-TNF) biologic therapy is a widely used treatment for rheumatoid arthritis (RA). It is unknown why some RA patients fail to respond adequately to anti-TNF therapy, which limits the development of clinical biomarkers to predict response or new drugs to target refractory cases. To understand the biological basis of response to anti-TNF therapy, we conducted a genome-wide association study (GWAS) meta-analysis of more than 2 million common variants in 2,706 RA patients from 13 different collections. Patients were treated with one of three anti-TNF medications: etanercept (n = 733), infliximab (n = 894), or adalimumab (n = 1,071). We identified a SNP (rs6427528) at the 1q23 locus that was associated with change in disease activity score (ΔDAS) in the etanercept subset of patients (P = 8×10-8), but not in the infliximab or adalimumab subsets (P>0.05). The SNP is predicted to disrupt transcription factor binding site motifs in the 3′ UTR of an immune-related gene, CD84, and the allele associated with better response to etanercept was associated with higher CD84 gene expression in peripheral blood mononuclear cells (P = 1×10-11 in 228 non-RA patients and P = 0.004 in 132 RA patients). Consistent with the genetic findings, higher CD84 gene expression correlated with lower cross-sectional DAS (P = 0.02, n = 210) and showed a non-significant trend for better ΔDAS in a subset of RA patients with gene expression data (n = 31, etanercept-treated). A small, multi-ethnic replication showed a non-significant trend towards an association among etanercept-treated RA patients of Portuguese ancestry (n = 139, P = 0.4), but no association among patients of Japanese ancestry (n = 151, P = 0.8). Our study demonstrates that an allele associated with response to etanercept therapy is also associated with CD84 gene expression, and further that CD84 expression correlates with disease activity. These findings support a model in which CD84 genotypes and/or expression may serve as a useful biomarker for response to etanercept treatment in RA patients of European ancestry. © 2013 Cui et al

Shear behavior of DFDP-1 borehole samples from the Alpine Fault, New Zealand, under a wide range of experimental conditions

The Alpine Fault is a major plate-boundary fault zone that poses a major seismic hazard in southern New Zealand. The initial stage of the Deep Fault Drilling Project has provided sample material from the major lithological constituents of the Alpine Fault from two pilot boreholes. We use laboratory shearing experiments to show that the friction coefficient µ of fault-related rocks and their precursors varies between 0.38 and 0.80 depending on the lithology, presence of pore fluid, effective normal stress, and temperature. Under conditions appropriate for several kilometers depth on the Alpine Fault (100 MPa, 160 °C, fluid-saturated), a gouge sample located very near to the principal slip zone exhibits µ = 0.67, which is high compared with other major fault zones targeted by scientific drilling, and suggests the capacity for large shear stresses at depth. A consistent observation is that every major lithological unit tested exhibits positive and negative values of friction velocity dependence. Critical nucleation patch lengths estimated using representative values of the friction velocity-dependent parameter a−b and the critical slip distance D c , combined with previously documented elastic properties of the wall rock, may be as low as ~3 m. This small value, consistent with a seismic moment M o = ~4 × 1010 for an M w = ~1 earthquake, suggests that events of this size or larger are expected to occur as ordinary earthquakes and that slow or transient slip events are unlikely in the approximate depth range of 3–7 km

Single nucleotide polymorphisms at the TRAF1/C5 locus are associated with rheumatoid arthritis in a Han Chinese population

<p>Abstract</p> <p>Background</p> <p>Genetic variants in <it>TRAF1C5 </it>and <it>PTPN22 </it>genes have been shown to be significantly associated with arthritis rheumatoid in Caucasian populations. This study investigated the association between single nucleotide polymorphisms (SNPs) in <it>TRAF1/C5 </it>and <it>PTPN22 </it>genes and rheumatoid arthritis (RA) in a Han Chinese population. We genotyped SNPs rs3761847 and rs7021206 at the <it>TRAF1/C5 </it>locus and rs2476601 SNP in the <it>PTPN22 </it>gene in a Han Chinese cohort composed of 576 patients with RA and 689 controls. The concentrations of anti-cyclic citrullinated peptide antibodies (CCP) and rheumatoid factor (RF) were determined for all affected patients. The difference between the cases and the controls was compared using <it>χ</it>²analysis.</p> <p>Results</p> <p>Significant differences in SNPs rs3761847 and rs7021206 at <it>TRAF1/C5 </it>were observed between the case and control groups in this cohort; the allelic p-value was 0.0018 with an odds ratio of 1.28 for rs3761847 and 0.005 with an odds ratio of 1.27 for rs7021206. This significant association between rs3761847 and RA was independent of the concentrations of anti-CCP and RF. No polymorphism of rs2476601 was observed in this cohort.</p> <p>Conclusions</p> <p>We first demonstrated that genetic variants at the <it>TRAF1/C5 </it>locus are significantly associated with RA in Han Chinese, suggesting that <it>TRAF1/C5 </it>may play a role in the development of RA in this population, which expands the pathogenesis role of <it>TRAF1/C5 </it>in a different ethnicity.</p

Anti-PAD4 autoantibodies in rheumatoid arthritis: levels in serum over time and impact on PAD4 activity as measured with a small synthetic substrate

Isoform 4 of the human peptidylarginine deiminase (hPAD4) enzyme may be responsible for the citrullination of antigens in rheumatoid arthritis (RA) and has been shown to be itself the target of disease-specific autoantibodies. Here, we have tested whether the level of serum anti-hPAD4 antibodies in RA patients is stable over a period of 10 years and whether the antibodies influence hPAD4-mediated deimination of the small substrate N-α-Benzoyl-l-arginine ethyl ester. RA sera (n = 128) obtained at baseline and after 10 years were assessed for anti-hPAD4 antibodies by a specific immunoassay. For 118 RA patients, serum anti-hPAD4 IgG levels were stable over 10 years. Seven patients who were negative for anti-PAD4 IgG at baseline had become positive after 10 years. Further, total IgG from selected RA patients and controls were purified, and a fraction was depleted for anti-hPAD4 antibodies. Kinetic deimination assays were performed with total IgG and depleted fractions. The kcat and Km values of hPAD4-mediated deimination of N-α-Benzoyl-l-arginine ethyl ester were not affected by the depletion of the anti-hPAD4 antibodies from the total IgG pool. In conclusion, RA patients remain positive for anti-hPAD4 antibodies over time and some patients who are initially anti-hPAD4 negative become positive later in the disease course. The anti-hPAD4 antibodies did not affect the enzymatic activity of hPAD4 when the small substrate N-α-Benzoyl-l-arginine ethyl ester was used. However, this finding may not exclude an effect of these autoantibodies on citrullination of protein substrates in RA