Liquefaction Potential Evaluation Along Active Faults at the Head of the Gulf of Aqaba, Jordan

The city of Aqaba, Jordan lies within a major seismic region along the active plate boundary of the Dead Sea Transform. A NE-trending, strike-slip fault that originates in the Gulf of Aqaba apparently terminates under the city along four NW-trending normal- to oblique-slip faults. These normal faults accommodate active tectonic subsidence at the head of the Gulf of Aqaba. Paleoearthquake data from five trench excavations across these faults were collected to characterize the closest seismic source to the city. Ground rupture from an earthquake produced a fault scarp sometime before A.D. 1045-1278. A minimum estimate for the magnitude of the earthquake is M 6, the minimum threshold for surface ground rupture. Several multiple event scarps suggests that a minimum of seven earthquakes have occurred since 5 to 6 ka. This yields a minimum recurrence of earthquakes on the Aqaba fault seismic source of approximately 700-850 years. Subsurface exploration of boreholes and trench exposures indicates that the stratigraphic sequence is composed of liquefaction susceptible sediments. Shallow subsurface deposits consist of aeolian and beach sand interbedded with alluvial silt, sand, and gravel in the upper parts of the Quaternary fan deposits. We evaluated the liquefaction potential using Seed’s cyclic stress ratio approach. This method is based on the corrected field blow count of the Standard Penetration Test to an energy of 60% and effective overburden pressure of 100 kPa with corresponding attenuated peak ground acceleration of 0.1,0.2g, and 0.3g. Preliminary results of the liquefaction mapping indicate that the coastal areas have a high potential to liquefy and could experience severe damage as a result of earthquake shaking. Our analyses suggest that the eastern parts of the city lie predominantly within a nonliquefaction susceptibility zone

Rationale for a Permanent Seismic Network in the U.S. Central Plains Utilizing USArray

The eastern two thirds of the coterminous United States (from the Rocky Mountain Front to the east coast) are sparsely equipped with seismic monitoring instruments, with the number of permanent broadband seismic stations per unit area of the order of 5–10% of that in the western U.S. orogenic zone. In this Forum, we use the Central Plains area (CP)—defined here as the fourstate area including Nebraska, Kansas, Iowa, and Missouri—as an example to argue that a greatly densified permanent seismic network in the stable part of the United States could significantly improve our understanding of the processes that led to the formation and four-dimensional structure of the continental lithosphere. The network would also serve as an excellent facility for longterm earthquake monitoring and for public education and outreach. This issue is timely because a state-of-the-art, uniform network could be established by simply converting a small portion of the portable stations in the ongoing USArray project into permanent ones without affecting the overall progress of the USArray

International Geoscience Programme IGCP567 Earhtquake Archaeology. Archaeoseismology along the Alpine-Himalayan seismic zone

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Archaeoseismology: Past, Present and Future

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Earthquake Archaeology - Just a Good Story?

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International Geoscience Programme IGCP567 Earthquake Archaeology. Archaeoseismology along the Alpine-Himalayan seismic zone

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A summary of the IGCP 567 Archaeoseismology along the Alpine-Himalayan Seismic Zone Project

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Preface

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Evidence of redox imbalance in a patient with succinic semialdehyde dehydrogenase deficiency

The pathophysiology of succinic semialdehyde dehydrogenase (SSADH) deficiency is not completely understood. Oxidative stress, mitochondrial pathology, and low reduced glutathione levels have been demonstrated in mice, but no studies have been reported in humans. We report on a patient with SSADH deficiency in whom we found low levels of blood reduced glutathione (GSH), and elevations of dicarboxylic acids in urine, suggestive of possible redox imbalance and/or mitochondrial dysfunction. Thus, targeting the oxidative stress axis may be a potential therapeutic approach if our findings are confirmed in other patients