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

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

status: publishe

Preface

edition: 1stestatus: publishe

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

Data from: Degree of glutathione deficiency and redox imbalance depend on subtype of mitochondrial disease and clinical status

Mitochondrial disorders are associated with decreased energy production and redox imbalance. Glutathione plays a central role in redox signaling and protecting cells from oxidative damage. In order to understand the consequences of mitochondrial dysfunction on in vivo redox status, and to determine how this varies by mitochondrial disease subtype and clinical severity, we used a sensitive tandem mass spectrometry assay to precisely quantify whole blood reduced (GSH) and oxidized (GSSG) glutathione levels in a large cohort of mitochondrial disorder patients. Glutathione redox potential was calculated using the Nernst equation. Compared to healthy controls (n = 59), mitochondrial disease patients (n = 58) as a group showed significant redox imbalance (redox potential −251 mV±9.7, p<0.0001) with an increased level of oxidation by ~9 mV compared to controls (−260 mV±6.4). Underlying this abnormality were significantly lower whole blood GSH levels (p = 0.0008) and GSH/GSSG ratio (p = 0.0002), and significantly higher GSSG levels (p<0.0001) in mitochondrial disease patients compared to controls. Redox potential was significantly more oxidized in all mitochondrial disease subgroups including Leigh syndrome (n = 15), electron transport chain abnormalities (n = 10), mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (n = 8), mtDNA deletion syndrome (n = 7), mtDNA depletion syndrome (n = 7), and miscellaneous other mitochondrial disorders (n = 11). Patients hospitalized in metabolic crisis (n = 7) showed the greatest degree of redox imbalance at −242 mV±7. Peripheral whole blood GSH and GSSG levels are promising biomarkers of mitochondrial dysfunction, and may give insights into the contribution of oxidative stress to the pathophysiology of the various mitochondrial disorders. In particular, evaluation of redox potential may be useful in monitoring of clinical status or response to redox-modulating therapies in clinical trials

Scientific Rationale for a Greatly Densified Permanent Seismic Network in the Central Plains Untilizing USArray

The Central Plains (CP) area of the conterminous U.S. is characterized by a diverse amalgamation of tectonic features developed over the past 2 billion years. Boundaries between three major Precambrian terranes and one of the largest continental rift systems on Earth (the Midcontinent Rift) are located in this area. Preliminary geophysical studies suggest that the mantle transition between the Cenozoic Cordilleran and the \u27stable\u27 North American craton lies within the western part of this area. In addition, some of the greatest historical earthquakes in the conterminous United States have occurred in the New Madrid Seismic Zone in the southeastern CP. Therefore, detailed geoscientific studies of the CP will significantly improve our understanding of: (1) the growth, modification, and destruction of continental lithosphere; (2) the nature of the active-to-stable transitional area in the mantle; and (3) the formation mechanism of intra-continent earthquakes. However, the understanding of basement structure in the CP is rudimentary because it is obscured by sedimentary cover, and is thus greatly dependent on a state of the art permanent broadband seismic network. The lack of damaging historic earthquakes in most of the CP has resulted in fewer seismological research efforts relative to the western US. Over the past several decades, seismology has evolved into a much broader branch of geoscience that examines not only earthquakes, but also the structure and dynamics of the Earth\u27s deep interior using data from permanent stations collected over decades. The detectability of the current sparse seismic network in the area can be greatly improved by converting some of the USArray stations into permanent ones. The greatly-densified permanent seismic network will dramatically improve our capability for studying the velocity, anisotropy, and layered structures of the Earth\u27s crust, mantle and core, detecting small earthquakes, assessing seismic risks, and providing effective education and outreach to the general public. To facilitate such an effort, CPEP (Central Plains Earthscope Partnership) was established in 2007. Currently CPEP involves about 60 geoscientists from four CP states (NE, IA, KS, MO)

Degree of Glutathione Deficiency and Redox Imbalance Depend on Subtype of Mitochondrial Disease and Clinical Status

<div><p>Mitochondrial disorders are associated with decreased energy production and redox imbalance. Glutathione plays a central role in redox signaling and protecting cells from oxidative damage. In order to understand the consequences of mitochondrial dysfunction on <i>in vivo</i> redox status, and to determine how this varies by mitochondrial disease subtype and clinical severity, we used a sensitive tandem mass spectrometry assay to precisely quantify whole blood reduced (GSH) and oxidized (GSSG) glutathione levels in a large cohort of mitochondrial disorder patients. Glutathione redox potential was calculated using the Nernst equation. Compared to healthy controls (n = 59), mitochondrial disease patients (n = 58) as a group showed significant redox imbalance (redox potential −251 mV±9.7, p<0.0001) with an increased level of oxidation by ∼9 mV compared to controls (−260 mV±6.4). Underlying this abnormality were significantly lower whole blood GSH levels (p = 0.0008) and GSH/GSSG ratio (p = 0.0002), and significantly higher GSSG levels (p<0.0001) in mitochondrial disease patients compared to controls. Redox potential was significantly more oxidized in all mitochondrial disease subgroups including Leigh syndrome (n = 15), electron transport chain abnormalities (n = 10), mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (n = 8), mtDNA deletion syndrome (n = 7), mtDNA depletion syndrome (n = 7), and miscellaneous other mitochondrial disorders (n = 11). Patients hospitalized in metabolic crisis (n = 7) showed the greatest degree of redox imbalance at −242 mV±7. Peripheral whole blood GSH and GSSG levels are promising biomarkers of mitochondrial dysfunction, and may give insights into the contribution of oxidative stress to the pathophysiology of the various mitochondrial disorders. In particular, evaluation of redox potential may be useful in monitoring of clinical status or response to redox-modulating therapies in clinical trials.</p></div

GSH_project_MasterList

Excel file containing oxidized and reduced glutathione data in patients and controls