Origin of the Co-Seismic Variations of Elastic Properties in the Crust: Insight From the Laboratory.

Seismological observations highlighted that earthquakes are often followed by changes in elastic properties around the fault zone. Here, we studied the origin of these variations using stick-slip experiments on saw-cut granite samples presenting different degrees of bulk damage (i.e., microcracks). Stick-slip events were induced under triaxial compression configuration with continuous active ultrasonic measurements at confining pressures representative of upper crustal conditions (15-120 MPa). Both the P-wave velocity ( V P ) and amplitude ( A P ) showed drops, concurrently with stress drops, and had a non-monotonic dependence toward the fault's stress state. Our experimental results suggest that co-seismic changes in V P were mostly controlled by the elastic re-opening of microcracks in the bulk, rather than by co-seismic damage or the formation of fault gouge. Co-seismic changes in A P were controlled by a combination of elastic re-opening of microcracks in the bulk and inelastic processes (i.e., co-seismic damage and gouge formation and dilation).

Glucose-6-phosphate dehydrogenase plays a crucial role in protection from redox-stress-induced apoptosis.

Glucose-6-phosphate dehydrogenase-deleted embryonic stem (ES) cells (G6pd Delta) proliferate in vitro without special requirements, but when challenged with oxidants fail to sustain glutathione disulphide reconversion to reduced glutathione (GSH), entering a condition of oxidative stress. Here, we investigate the signalling events downstream of GSH oxidation in G6pd Delta and wild-type (wt) ES cells. We found that G6pd Delta ES cells are very sensitive to oxidants, activating an apoptotic pathway at oxidant concentrations otherwise sublethal for wt ES cells. We show that the apoptotic pathway activated by low oxidant concentrations is accompanied by mitochondria dysfunction, and it is therefore blocked by the overexpression of Bcl-X(L). Bcl-X(L) does not inhibit the decrease in cellular GSH and reactive oxygen species formation following oxidant treatment. We also found that oxidant treatment in ES cells is followed by the activation of the MEK/extracellular signal-regulated kinase (ERK) pathway. Interestingly, ERK activation has opposite outcomes in G6pd Delta ES cells compared to wt, which has a proapoptotic function in the first and a prosurvival function in the latter. We show that this phenomenon can be regulated by the cellular GSH level.