Introduction to the Special Issue on the 2004 Sumatra–Andaman Earthquake and the Indian Ocean Tsunami

The great Sumatra–Andaman earthquake of 26 December 2004 (UTC 00:58:53) was a momentous event, whether measured by scientific or human standards. Sadly, what is currently regarded as the third largest earthquake in recorded history led to the worst tsunami disaster in recorded history, with the loss of more than 200,000 lives and devastation throughout the Bay of Bengal. About three months later, on 28 March 2005, the Nias–Simeulue earthquake, near the southern end of the 2004 rupture, shocked the region again. Fortunately, this M_w 8.7 earthquake, the second largest earthquake in the past decade, was less destructive. These earthquakes and resulting tsunamis have been a sobering reminder to many in the community of earthquake scientists that the subject of our professional lives can have enormous impact on humanity. Hopefully, the legacy of the science presented in this volume will be a greater understanding of earthquake and tsunami processes that will be useful in advancing the resilience of our communities to Nature’s violence

The Great Sumatra-Andaman Earthquake of 26 December 2004

The two largest earthquakes of the past 40 years ruptured a 1600-kilometer-long portion of the fault boundary between the Indo-Australian and southeastern Eurasian plates on 26 December 2004 [seismic moment magnitude (M_w) = 9.1 to 9.3] and 28 March 2005 (M_w = 8.6). The first event generated a tsunami that caused more than 283,000 deaths. Fault slip of up to 15 meters occurred near Banda Aceh, Sumatra, but to the north, along the Nicobar and Andaman Islands, rapid slip was much smaller. Tsunami and geodetic observations indicate that additional slow slip occurred in the north over a time scale of 50 minutes or longer

The Enterovirus 71 A-particle Forms a Gateway to Allow Genome Release: A CryoEM Study of Picornavirus Uncoating

Since its discovery in 1969, enterovirus 71 (EV71) has emerged as a serious worldwide health threat. This human pathogen of the picornavirus family causes hand, foot, and mouth disease, and also has the capacity to invade the central nervous system to cause severe disease and death. Upon binding to a host receptor on the cell surface, the virus begins a two-step uncoating process, first forming an expanded, altered "A-particle", which is primed for genome release. In a second step after endocytosis, an unknown trigger leads to RNA expulsion, generating an intact, empty capsid. Cryo-electron microscopy reconstructions of these two capsid states provide insight into the mechanics of genome release. The EV71 A-particle capsid interacts with the genome near the icosahedral two-fold axis of symmetry, which opens to the external environment via a channel ~10 Å in diameter that is lined with patches of negatively charged residues. After the EV71 genome has been released, the two-fold channel shrinks, though the overall capsid dimensions are conserved. These structural characteristics identify the two-fold channel as the site where a gateway forms and regulates the process of genome release. © 2013 Shingler et al

Exploring the Potential Linkages Between Oil-Field Brine Reinjection, Crystalline Basement Permeability, and Triggered Seismicity for the Dagger Draw Oil Field, Southeastern New Mexico, USA, Using Hydrologic Modeling

We used hydrologic models to explore the potential linkages between oil-field brine reinjection and increases in earthquake frequency (up to Md 3.26) in southeastern New Mexico and to assess different injection management scenarios aimed at reducing the risk of triggered seismicity. Our analysis focuses on saline water reinjection into the basal Ellenburger Group beneath the Dagger Draw Oil field, Permian Basin. Increased seismic frequency (\u3eMd 2) began in 2001, 5 years after peak injection, at an average depth of 11 km within the basement 15 km to the west of the reinjection wells. We considered several scenarios including assigning an effective or bulk permeability value to the crystalline basement, including a conductive fault zone surrounded by tighter crystalline basement rocks, and allowing permeability to decay with depth. We initially adopted a 7 m (0.07 MPa) head increase as the threshold for triggered seismicity. Only two scenarios produced excess heads of 7m five years after peak injection. In the first, a hydraulic diffusivity of 0.1 m2s-1 was assigned to the crystalline basement. In the second, a hydraulic diffusivity of 0.3 m2s-1 was assigned to a conductive fault zone. If we had considered a wider range of threshold excess heads to be between 1 and 60m, then the range of acceptable hydraulic diffusivities would have increased (between 0.1-0.01 m2s-1 and 1-0.1 m2s-1 for the bulk and fault zone scenarios, respectively). A permeability–depth decay model would have also satisfied the 5-year time lag criterion. We also tested several injection management scenarios including redistributing injection volumes between various wells and lowering the total volume of injected fluids. Scenarios that reduced computed excess heads by over 50% within the crystalline basement resulted from reducing the total volume of reinjected fluids by a factor of 2 or more

Slab pull, slab weakening, and their relation to deep intra‐slab seismicity

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/96237/1/grl19851.pd