The interplay between surface processes and tectonics in the actively extending central Italian Apennines

The overall objective of this project is to improve our understanding of the interplay between surface processes and tectonics in active continental rifts, based on the central part of the Italian Apennines. Three key aspects are investigated: i) The impact of dynamic mantle-induced surface uplift on normal fault activity and topographic development in active continental rifts. ii) The evolution of drainage networks in response to extensional faulting and regional uplift and the main controlling mechanisms. iii) The impact of drainage network evolution on sediment dispersal, basin stratigraphy and transient landscape evolution. These three aspects are investigated through a combined field and numerical modelling approach. This approach allows for the direct use of field data for constraining numerical models, as well the direct testing of model-based findings. Synthesised published basin stratigraphic, fault slip and geomorphic data together with new geomorphic and sedimentological fieldwork provide high quality and detailed datasets of stratigraphic and landscape evolution in the central Apennines. Regional drainage network evolution in the central Apennines is primarily controlled by the balance between the rates of filling and subsidence of normal fault-bounded basins. Basin filling occurs through the supply of sediment and water, whereas basin subsidence is mainly controlled by slip on the main basin-bounding normal fault. Drainage integration occurs when initially underfilled, endorheic basins become overfilled with sediment and water allowing basins to overspill. Because basin overspill, in turn, allows water and sediment to cascade downstream to adjacent basins where it can trigger a next drainage integration event, drainage integration predominantly follows a top-down pattern. Furthermore, drainage integration acts as a first-order control on basin stratigraphy and geomorphic development in the central Apennines, and produces a highly dynamic landscape evolution with transient conditions that can persist in the landscape for several millions of years. Two-dimensional thermo-mechanical modelling results demonstrate how the removal of mantle lithosphere leads to regional surface uplift and the localisation of extensional strain in the area of high topography. This is because the upwelling of hot buoyant sub-lithospheric mantle within the lithospheric gap causes both isostatic surface uplift and considerable weakening of the crust. Pre-defined (inherited) fault structures in this area of uplift and weakened crust become activated if the area is subject to a low rate of far-field extension. Faults interact, causing the locus of fault activity to migrate across-strike, and fault slip rates to vary markedly over 104-105 year timescales. Overall, these experiments show that mantle lithosphere removal can explain many first-order characteristics of the central Apennines, such as the correlation between fault strain rates, topography and surface uplift, enhanced surface heat fluxes, negative gravity anomalies and low P-wave velocities in the upper mantle

Immersed boundary method predictions of shear stresses for different flow topologies occuring in cerebral aneurysms

A volume-penalizing immersed boundary method is presented that facilitates the computation of incompressible fluid flow in complex flow domains. We apply this method to simulate the flow in cerebral aneurysms, and focus on the accuracy with which the flow field and the corresponding shear stress field are computed. The method is applied to laminar, incompressible flow in curved cylindrical vessels and in a model aneurysm. The time-dependent shear stress distributions over the vessel walls are visualized and interpreted in terms of the flow fields that develop. We compute shear stress levels at two different Reynolds numbers, corresponding to a steady and an unsteady flow. In the latter situation strong fluctuations in the shear stress are observed, that may be connected to raised risk-levels of aneurysm rupture

Simulation of Pulsatile Flow in Cerebral Aneurysms: From Medical Images to Flow and Forces

In this chapter we present a numerical model for the simulation of blood flow inside cerebral aneurysms. We illustrate the process of predicting flow and forces that arise in vessels and aneurysms starting from patient-specific data obtained using medical imaging techniques. Once the three-dimensional geometry is reconstructed, we discuss fluid properties of blood which allows to compute the flow. The flow of an incompressible Newtonian fluid in the human brain is simulated by using a volume penalizing immersed boundary method, in which the aneurysm geometries are represented by the so-called masking function. We impose pulsatile flow forcing, based on the direct measurement of the mean flow velocity in a vessel during a cardiac cycle and focus on effects due to changes in the flow regimes. In slow or very viscous flows the pulsatile forcing dominates the fluid dynamical response, while at faster or less viscous flows the intrinsic unsteadiness of natural incompressible flow is dominant over the pulsatile flow forcing effect. We consider a full range of physiologically relevant conditions and show high frequencies to emerge in the pulsatile response. The strong qualitative transitions in flow behavior and shear stress levels inside an aneurysm cavity at increased flow rates may contribute to the long-term risk of aneurysm rupture

Spectroscopic factors for nucleon knock-out from 16O at small missing energy.

Spectroscopic factors for one-nucleon knock-out fro

Evaluation of Vascular Control Mechanisms Utilizing Video Microscopy of Isolated Resistance Arteries of Rats

This protocol describes the use of in vitro television microscopy to evaluate vascular function in isolated cerebral resistance arteries (and other vessels), and describes techniques for evaluating tissue perfusion using Laser Doppler Flowmetry (LDF) and microvessel density utilizing fluorescently labeled Griffonia simplicifolia (GS1) lectin. Current methods for studying isolated resistance arteries at transmural pressures encountered in vivo and in the absence of parenchymal cell influences provide a critical link between in vivo studies and information gained from molecular reductionist approaches that provide limited insight into integrative responses at the whole animal level. LDF and techniques to selectively identify arterioles and capillaries with fluorescently-labeled GS1 lectin provide practical solutions to enable investigators to extend the knowledge gained from studies of isolated resistance arteries. This paper describes the application of these techniques to gain fundamental knowledge of vascular physiology and pathology in the rat as a general experimental model, and in a variety of specialized genetically engineered designer rat strains that can provide important insight into the influence of specific genes on important vascular phenotypes. Utilizing these valuable experimental approaches in rat strains developed by selective breeding strategies and new technologies for producing gene knockout models in the rat, will expand the rigor of scientific premises developed in knockout mouse models and extend that knowledge to a more relevant animal model, with a well understood physiological background and suitability for physiological studies because of its larger size

Lung Injury Pathways: Adenosine Receptor 2B Signaling Limits Development of Ischemic Bronchiolitis Obliterans Organizing Pneumonia

Purpose/Aim of the Study: Adenosine signaling was studied in bronchiolitis obliterans organizing pneumonia (BOOP) resulting from unilateral lung ischemia. Materials and Methods: Ischemia was achieved by either left main pulmonary artery or complete hilar ligation. Sprague–Dawley (SD) rats, Dahl salt sensitive (SS) rats and SS mutant rat strains containing a mutation in the A2B adenosine receptor gene (Adora2b) were studied. Adenosine concentrations were measured in bronchoalveolar lavage (BAL) by HPLC. A2A (A2AAR) and A2B adenosine receptor (A2BAR) mRNA and protein were quantified. Results: Twenty-four hours after unilateral PA ligation, BAL adenosine concentrations from ischemic lungs were increased relative to contralateral lungs in SD rats. A2BAR mRNA and protein concentrations were increased after PA ligation while miR27a, a negatively regulating microRNA, was decreased in ischemic lungs. A2AAR mRNA and protein concentrations remained unchanged following ischemia. A2BAR protein was increased in PA ligated lungs of SS rats after 7 days, and 4 h after complete hilar ligation in SD rats. SS-Adora2b mutants showed a greater extent of BOOP relative to SS rats, and greater inflammatory changes. Conclusion: Increased A2BAR and adenosine following unilateral lung ischemia as well as more BOOP in A2BAR mutant rats implicate a protective role for A2BAR signaling in countering ischemic lung injury