<p>The Maghrebian tectonic domain in North Africa is here examined in the light of the recent GPS and seismotectonic results. The region includes the plate boundary in the western Mediterranean previously characterized by transpression and block rotation. The crustal deformation is documented along the Atlas Mountains in terms of the displacement field, with strain partitioning largely controlled by plate motions. The tectonic and seismotectonic analysis is based on our published data on shortening directions of Quaternary faulting and folding compared with present-day seismotectonic characteristics (earthquake moment tensors) of significant seismic events that allow an estimate of local and regional deformation rates in North Africa. Shortening directions oriented NE-SW to NW-SE for the Pliocene and Quaternary, respectively, and the S shape of the Quaternary anticline axes are in agreement with the 2°/Myr to 4°/Myr clockwise rotation obtained from paleomagnetic results on small tectonic blocks in the Tell Atlas. The continuous GPS data and results are obtained from the network in Morocco operative 1999 to 2006, the REGAT network in Algeria since 2007, and the network in Tunisia with data collected from 2014 to 2018. In addition, we add the most recent GPS results in southern Spain and southern Italy. The NW-SE to NNW-SSE 5 ±1.5 mm/yr convergence velocity and strain distribution of the Maghrebian tectonic domain is controlled by crustal block tectonics driven by E-W trending right-lateral faulting and NE-SW thrust-related folding. The correlation between the active transpression tectonic structures and velocity field shows a geodynamic framework consistent with the oblique plate convergence of Africa towards Eurasia. </p>

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

No abstract

No abstract

The rapid increase in the population of many of the older major cities within the countries of the Saharan-Arabian Desert is steering vast and disorganized urban expansion and in many cases introducing adverse environmental impacts such as soil erosion, rise in groundwater levels, and contamination of shallow aquifers, as well as development of deformational features including land subsidence. Using the rapidly growing city of Riyadh (1992: 467 km2; 2018: 980 km2), the capital of the Kingdom of Saudi Arabia as a test site, we utilized Small Baseline Subset (SBAS) interferometric analyses of 2016 to 2018 Sentinel-1 images together with multi-temporal high-resolution images viewable on Google Earth, GPS, field, land use land cover (LULC), and geological data to assess the distribution and rates of land subsidence and their causal effects. Three main causes of subsidence were identified and assessed: (1) discharge of wastewater effluents from septic systems in newly urbanized areas that lead to an increase in soil moisture, rise in groundwater levels, waterlogging, and wetting and hydrocompaction of dry alluvium loose sediments causing land subsidence (up to −20 mm/y) in wadis and lowlands; (2) the subsurface dissolution of karst formation by wastewater effluents and the collapse of voids and cavities at depth under stresses introduced by heavy construction machinery, causing sagging and land subsidence (up to −5 mm/y); and (3) leveling, compaction, and degradation of municipal and building waste materials in organized landfills and disorganized dump sites that resulted in significant land subsidence (up to −21 mm/y) and differential settling that could jeopardize the stability of structures erected over these sites. Our findings highlight the potential use of the advocated integrated approach to assess the nature and extent of land deformation associated with rapid urban growth in arid lands, and to identify areas most impacted for the purpose of directing and prioritizing remediation efforts.

No abstract

No abstract

No abstract