Resolution of rupture directivity in weak events: 1-D versus 2-D source parameterizations for the 2011, M-w 4.6 and 5.2 Lorca earthquakes, Spain

Resolving robust source parameters of small-moderate magnitude earthquakes is still a challenge in seismology. We infer directivity from apparent source time functions (ASTFs) at regional distance and quantify the associated uncertainties. ASTFs are used for (i) modeling a propagating 1-D line source from the duration data and (ii) inverting the 2-D slip distribution from the full signals. Slip inversion is performed through a Popperian scheme, where random trial models are either falsified on account of large misfit, or else become members of the solution set of the inverse problem. We assess the resolution of rupture directivity representing centroid shifts from the solution set in a rose diagram. Using as example an event with well-studied rupture directivity, the 2011 Mw 5.2 Lorca (Spain) earthquake, 1-D and 2-D parameterizations yield similar estimates for direction (N213°E and N220°E, respectively) and asymmetry (67:33, 65:35) of rupture propagation, as well as rupture length (2.1 km, 2.7 km) and speed (3.5 km/s, 3.25 km/s). The high rupture velocity ≥ 90% vS may be held primarily responsible for the strong directivity effect of this earthquake. We show that inversion of apparent source durations is intrinsically unable to resolve highly asymmetric bilateral ruptures, while inversion of full ASTFs misses part of the signal's complexity, suggesting the presence of deconvolution artifacts. We extend the analysis to the Mw 4.6 foreshock of the Lorca earthquake, inferring similar directivity parameters and slip pattern as for the mainshock. The rupture toward SW of both earthquakes suggests that this direction could be inherent to the fault segment

The impact of PKR activation: from neurodegeneration to cancer

An inverse association between cancer and neurodegeneration is plausible because these biological processes share several genes and signaling pathways. Whereas uncontrolled cell proliferation and decreased apoptotic cell death governs cancer, excessive apoptosis contributes to neurodegeneration. Protein kinase R (PKR), an interferon-inducible double-stranded RNA protein kinase, is involved in both diseases. PKR activation blocks global protein synthesis through eIF2alpha phosphorylation, leading to cell death in response to a variety of cellular stresses. However, PKR also has the dual role of activating the nuclear factor kappa-B pathway, promoting cell proliferation. Whereas PKR is recognized for its negative effects on neurodegenerative diseases, in part, inducing high level of apoptosis, the role of PKR activation in cancer remains controversial. In general, PKR is considered to have a tumor suppressor function, and some clinical data show a correlation between suppressed or inactivated PKR and a poor prognosis for several cancers. However, other studies show high PKR expression and activation levels in various cancers, suggesting that PKR might contribute to neoplastic progression. Understanding the cellular factors and signals involved in the regulation of PKR in these age-related diseases is relevant and may have important clinical implications. The present review highlights the current knowledge on the role of PKR in neurodegeneration and cancer, with special emphasis on its regulation and clinical implications