Tsunami earthquakes possibly widespread manifestations of frictional conditional stability

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/94799/1/grl15921.pd

Effects of subducted seamounts on megathrust earthquake nucleation and rupture propagation

Author Posting. © American Geophysical Union, 2012. This article is posted here by permission of American Geophysical Union for personal use, not for redistribution. The definitive version was published in Geophysical Research Letters 39 (2012): L24302, doi:10.1029/2012GL053892.Subducted seamounts have been linked to interplate earthquakes, but their specific effects on earthquake mechanism remain controversial. A key question is under what conditions a subducted seamount will generate or stop megathrust earthquakes. Here we show results from numerical experiments in the framework of rate- and state-dependent friction law in which a seamount is characterized as a patch of elevated effective normal stress on the thrust interface. We find that whether subducted seamounts generate or impede megathrust earthquakes depends critically on their relative locations to the earthquake nucleation zone defined by depth-variable friction parameters. A seamount may act as a rupture barrier and such barrier effect is most prominent when the seamount sits at an intermediate range of the seamount-to-trench distances (20–100% of the nucleation-zone-to-trench distance). Moreover, we observe that seamount-induced barriers can turn into asperities on which megathrust earthquakes can nucleate at shallow depths and rupture the entire seismogenic zone. These results suggest that a strong barrier patch may not necessarily reduce the maximum size of earthquakes. Instead, the barrier could experience large coseismic slip when it is ruptured.This work is supported by the NSF Grant EAR-1015221 and WHOI Deep Ocean Exploration Institute awards 27071150 and 25051162.2013-06-1

Analysis of the 23 June 2001 M w = 8.4 Peru underthrusting earthquake and its aftershocks

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95298/1/grl16079.pd

Radiated seismic energy and earthquake source duration variations from teleseismic source time functions for shallow subduction zone thrust earthquakes

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95490/1/jgrb14117.pd

Seismogenic zone structure of the southern Middle America Trench, Costa Rica

The shallow seismogenic portion of subduction zones generates damaging large and great earthquakes. This study provides structural constraints on the seismogenic zone of the Middle America Trench offshore central Costa Rica and insights into the physical and mechanical characteristics controlling seismogenesis. We have located ~300 events that occurred following the MW 6.9, 20 August 1999, Quepos, Costa Rica, underthrusting earthquake using a three-dimensional velocity model and arrival time data recorded by a temporary local network of land and ocean bottom seismometers. We use aftershock locations to define the geometry and characteristics of the seismogenic zone in this region. These events define a plane dipping at 19° that marks the interface between the Cocos Plate and the Panama Block. The majority of aftershocks occur below 10 km and above 30 km depth below sea level, corresponding to 30–35 km and 95 km from the trench axis, respectively. Relative event relocation produces a seismicity pattern similar to that obtained using absolute locations, increasing confidence in the geometry of the seismogenic zone. The aftershock locations spatially correlate with the downdip extension of the oceanic Quepos Plateau and reflect the structure of the main shock rupture asperity. This strengthens an earlier argument that the 1999 Quepos earthquake ruptured specific bathymetric highs on the downgoing plate. We believe that subduction of this highly disrupted seafloor has established a set of conditions which presently limit the seismogenic zone to be between 10 and 35 km below sea level

Multidimensional analyses reveal modulation of adaptive and innate immune subsets by tuberculosis vaccines

We characterize the breadth, function and phenotype of innate and adaptive cellular responses in a prevention of Mycobacterium tuberculosis infection trial. Responses are measured by whole blood intracellular cytokine staining at baseline and 70 days after vaccination with H4:IC31 (subunit vaccine containing Ag85B and TB10.4), Bacille Calmette-Guerin (BCG, a live attenuated vaccine) or placebo (n = ~30 per group). H4:IC31 vaccination induces Ag85B and TB10.4-specific CD4 T cells, and an unexpected NKTlike subset, that expresses IFN-γ, TNF and/or IL-2. BCG revaccination increases frequencies of CD4 T cell subsets that either express Th1 cytokines or IL-22, and modestly increases IFNγ-producing NK cells. In vitro BCG re-stimulation also triggers responses by donor-unrestricted T cells, which may contribute to host responses against mycobacteria. BCG, which demonstrated efficacy against sustained Mycobacterium tuberculosis infection, modulates multiple immune cell subsets, in particular conventional Th1 and Th22 cells, which should be investigated in discovery studies of correlates of protection

Beyond the marrow:insights from comprehensive next-generation sequencing of extramedullary multiple myeloma tumors

Extramedullary multiple myeloma (EMM) is an aggressive form of multiple myeloma (MM). This study represents the most comprehensive next-generation sequencing analysis of EMM tumors (N = 14) to date, uncovering key molecular features and describing the tumor microenvironment. We observed the co-occurrence of 1q21 gain/amplification and MAPK pathway mutations in 79% of EMM samples, suggesting that these are crucial mutational events in EMM development. We also demonstrated that patients with mutated KRAS and 1q21 gain/amplification at the time of diagnosis have a significantly higher risk of EMM development (HR = 2.4, p = 0.011) using data from a large CoMMpass dataset. We identified downregulation of CXCR4 and enhanced cell proliferation, along with reduced expression of therapeutic targets (CD38, SLAMF7, GPRC5D, FCRH5), potentially explaining diminished efficacy of immunotherapy. Conversely, we identified significantly upregulated EZH2 and CD70 as potential future therapeutic options. For the first time, we report on the tumor microenvironment of EMM, revealing CD8+ T cells and NK cells as predominant immune effector cells using single-cell sequencing. Finally, this is the first longitudinal study in EMM revealing the molecular changes from the time of diagnosis to EMM relapse.</p