Afterslip and viscoelastic relaxation following the 2011 Tohoku-oki earthquake (Mw9.0) inferred from inland GPS and seafloor GPS/Acoustic data

We simultaneously estimate 2.5 years of afterslip and viscoelastic relaxation, as well as coseismic slip, for the 2011 Tohoku-oki earthquake. Displacements at inland GPS and seafloor GPS/Acoustic stations are inverted using viscoelastic Green's functions for a model with an upper elastic layer and lower viscoelastic substrate. The result shows that afterslip is isolated from the rupture area and possibly asperities of historical earthquakes and has almost decayed by 10 September 2013, 2.5 years after the main shock. The inversion result also suggests that observed landward postseismic displacements at the seafloor GPS/Acoustic stations are caused by the viscoelastic relaxation, whereas trenchward displacements at inland stations are mainly an elastic response to afterslip

Spatial and temporal evolution of stress and slip rate during the 2000 Tokai slow earthquake

Author Posting. © American Geophysical Union, 2006. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Journal of Geophysical Research 111 (2006): B03409, doi:10.1029/2004JB003426.We investigate an ongoing silent thrust event in the Tokai seismic gap along the Suruga-Nankai Trough, central Japan. Prior to the event, continuous GPS data from April 1996 to the end of 1999 show that this region displaced ∼2 cm/yr to the northwest relative to the landward plate. The GPS time series show an abrupt change in rate in mid-June 2000 that continues as of mid-2005. We model this transient deformation, which we refer to as the Tokai slow thrust slip event, as caused by slip on the interface between the Philippine Sea and Amurian plates. The spatial and temporal distribution of slip rate is estimated with Kalman filter based inversion methods. Our inversions reveal two slow subevents. The first initiated in late June 2000 slightly before the Miyake-jima eruption. The locus of slip then propagated southeast in the second half of 2000, with maximum slip rates of about 15 cm/yr through 2001. A second locus of slip initiated to the northeast in early 2001. The depth of the slip zone is about 25 km, which may correspond to the transition zone from a seismogenic to a freely sliding zone. The cumulative moment magnitude of the slow slip event up to November 2002 is M w ∼ 6.8. We calculate shear stress changes on the plate interface from the slip histories. Stress change as a function of slip rate shows trajectories similar to that inferred for high-speed ruptures; however, the maximum velocity is 8 orders of magnitude less than in normal earthquakes.Part of this study is supported by JSPS Postdoctral Fellowships for Research Abroad

Residual laminin-binding activity and enhanced dystroglycan glycosylation by LARGE in novel model mice to dystroglycanopathy

Hypoglycosylation and reduced laminin-binding activity of α-dystroglycan are common characteristics of dystroglycanopathy, which is a group of congenital and limb-girdle muscular dystrophies. Fukuyama-type congenital muscular dystrophy (FCMD), caused by a mutation in the fukutin gene, is a severe form of dystroglycanopathy. A retrotransposal insertion in fukutin is seen in almost all cases of FCMD. To better understand the molecular pathogenesis of dystroglycanopathies and to explore therapeutic strategies, we generated knock-in mice carrying the retrotransposal insertion in the mouse fukutin ortholog. Knock-in mice exhibited hypoglycosylated α-dystroglycan; however, no signs of muscular dystrophy were observed. More sensitive methods detected minor levels of intact α-dystroglycan, and solid-phase assays determined laminin binding levels to be ∼50% of normal. In contrast, intact α-dystroglycan is undetectable in the dystrophic Largemyd mouse, and laminin-binding activity is markedly reduced. These data indicate that a small amount of intact α-dystroglycan is sufficient to maintain muscle cell integrity in knock-in mice, suggesting that the treatment of dystroglycanopathies might not require the full recovery of glycosylation. To examine whether glycosylation defects can be restored in vivo, we performed mouse gene transfer experiments. Transfer of fukutin into knock-in mice restored glycosylation of α-dystroglycan. In addition, transfer of LARGE produced laminin-binding forms of α-dystroglycan in both knock-in mice and the POMGnT1 mutant mouse, which is another model of dystroglycanopathy. Overall, these data suggest that even partial restoration of α-dystroglycan glycosylation and laminin-binding activity by replacing or augmenting glycosylation-related genes might effectively deter dystroglycanopathy progression and thus provide therapeutic benefits

A Forecasting Procedure for Plate Boundary Earthquakes Based on Sequential Data Assimilation

A forecasting procedure is proposed for plate boundary earthquakes in subduction zones. It is based on spatio-temporal variation in slip velocity on the plate interface, which causes interplate earthquakes. Model outputs are not only information about the occurrence of great earthquakes (time, place, and magnitude) but also information about the physical state evolution that causes earthquakes. To overcome the difficulty in forecasting earthquake generation resulting from uncertainty both in the physical model and in the observation data, we introduce a type of sequential data assimilation. In this method, we compare observed crustal deformation data to simulations of several great interplate earthquake generation cycles. We are currently constructing a prototype, applying this forecasting procedure to the Nankai Trough, Southwest Japan, where great interplate earthquakes have occurred and are anticipated