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

Seismic imaging of the shallow crust beneath the Krafla central volcano, NE Iceland

We studied the seismic velocity structure beneath the Krafla central volcano, NE Iceland, by performing 3-D tomographic inversions of 1453 earthquakes recorded by a temporary local seismic network between 2009 and 2012. The seismicity is concentrated primarily around the Leirhnjúkur geothermal field near the center of the Krafla caldera. To obtain robust velocity models, we incorporated active seismic data from previous surveys. The Krafla central volcano has a relatively complex velocity structure with higher P wave velocities (V_p) underneath regions of higher topographic relief and two distinct low-V_p anomalies beneath the Leirhnjúkur geothermal field. The latter match well with two attenuating bodies inferred from S wave shadows during the Krafla rifting episode of 1974–1985. Within the Leirhnjúkur geothermalreservoir, we resolved a shallow (−0.5 to 0.5 km below sea level; bsl) region with low-V_p/V_s values and a deeper (0.5–1.5 km bsl) high-V_p/V_s zone. We interpret the difference in the velocity ratios of the two zones to be caused by higher rock porosities and crack densities in the shallow region and lower porosities and crack densities in the deeper region. A strong low-V_p/V_s anomaly underlies these zones, where a superheated steam zone within felsic rock overlies rhyolitic melt

Estrogen- and Progesterone (P4)-Mediated Epigenetic Modifications of Endometrial Stromal Cells (EnSCs) and/or Mesenchymal Stem/Stromal Cells (MSCs) in the Etiopathogenesis of Endometriosis

Endometriosis is a common chronic inflammatory condition in which endometrial tissue appears outside the uterine cavity. Because ectopic endometriosis cells express both estrogen and progesterone (P4) receptors, they grow and undergo cyclic proliferation and breakdown similar to the endometrium. This debilitating gynecological disease affects up to 15% of reproductive aged women. Despite many years of research, the etiopathogenesis of endometrial lesions remains unclear. Retrograde transport of the viable menstrual endometrial cells with retained ability for attachment within the pelvic cavity, proliferation, differentiation and subsequent invasion into the surrounding tissue constitutes the rationale for widely accepted implantation theory. Accordingly, the most abundant cells in the endometrium are endometrial stromal cells (EnSCs). These cells constitute a particular population with clonogenic activity that resembles properties of mesenchymal stem/stromal cells (MSCs). Thus, a significant role of stem cell-based dysfunction in formation of the initial endometrial lesions is suspected. There is increasing evidence that the role of epigenetic mechanisms and processes in endometriosis have been underestimated. The importance of excess estrogen exposure and P4 resistance in epigenetic homeostasis failure in the endometrial/endometriotic tissue are crucial. Epigenetic alterations regarding transcription factors of estrogen and P4 signaling pathways in MSCs are robust in endometriotic tissue. Thus, perspectives for the future may include MSCs and EnSCs as the targets of epigenetic therapies in the prevention and treatment of endometriosis. Here, we reviewed the current known changes in the epigenetic background of EnSCs and MSCs due to estrogen/P4 imbalances in the context of etiopathogenesis of endometriosis