Existence of global strong solutions to a beam-fluid interaction system

We study an unsteady non linear fluid-structure interaction problem which is a simplified model to describe blood flow through viscoleastic arteries. We consider a Newtonian incompressible two-dimensional flow described by the Navier-Stokes equations set in an unknown domain depending on the displacement of a structure, which itself satisfies a linear viscoelastic beam equation. The fluid and the structure are fully coupled via interface conditions prescribing the continuity of the velocities at the fluid-structure interface and the action-reaction principle. We prove that strong solutions to this problem are global-in-time. We obtain in particular that contact between the viscoleastic wall and the bottom of the fluid cavity does not occur in finite time. To our knowledge, this is the first occurrence of a no-contact result, but also of existence of strong solutions globally in time, in the frame of interactions between a viscous fluid and a deformable structure

Detailed Anatomical and Electrophysiological Models of Human Atria and Torso for the Simulation of Atrial Activation

Atrial arrhythmias, and specifically atrial fibrillation (AF), induce rapid and irregular activation patterns that appear on the torso surface as abnormal P-waves in electrocardiograms and body surface potential maps (BSPM). In recent years both P-waves and the BSPM have been used to identify the mechanisms underlying AF, such as localizing ectopic foci or high-frequency rotors. However, the relationship between the activation of the different areas of the atria and the characteristics of the BSPM and P-wave signals are still far from being completely understood. In this work we developed a multi-scale framework, which combines a highly-detailed 3D atrial model and a torso model to study the relationship between atrial activation and surface signals in sinus rhythm. Using this multi scale model, it was revealed that the best places for recording P-waves are the frontal upper right and the frontal and rear left quadrants of the torso. Our results also suggest that only nine regions (of the twenty-one structures in which the atrial surface was divided) make a significant contribution to the BSPM and determine the main P-wave characteristics.This work was partially supported by the "VI Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion Tecnologica" from the Ministerio de Economia y Competitividad of Spain and the European Commission (European Regional Development Funds - ERDF - FEDER), Award Number: TIN2012-37546-C03-01 (Recipient: Ana Ferrer); the "Programa Estatal de Investigacion, Desarrollo e Innovacion Orientado a los Retos de la Sociedad" from the Ministerio de Economia y Competitividad and the European Commission (European Regional Development Funds - ERDF - FEDER), Award Number: TIN2014-59932-JIN (Recipient: Rafael Sebastion); and the "Programa Prometeo" from the Generalitat Valenciana, Award Number: 2012/030 (Recipient: Laura Martinez).Ferrer Albero, A.; Sebastián Aguilar, R.; Sánchez Quintana, D.; Rodriguez, JF.; Godoy, EJ.; Martinez, L.; Saiz Rodríguez, FJ. (2015). Detailed Anatomical and Electrophysiological Models of Human Atria and Torso for the Simulation of Atrial Activation. PLoS ONE. 10(11):1-29. https://doi.org/10.1371/journal.pone.0141573S129101

Nerve electrophysiological changes in rats with early induced diabetes

In rats with diabetes induced at weaning, pathological examinations have shown that the reduction of myelin thickness occurs earlier than axon size reduction. The aim of this study was to provide a detailed description of neurophysiological changes during nerve growth and maturation in rats with streptozotocin-induced diabetes in prepubertal stage. Five-day male Wistar rats received an injection of streptozotocin. Motor and sensory conduction velocities increased until 6.5 months in diabetic and control rats and at this age it became lower in diabetic rats. In diabetic rats, the amplitudes of the compound motor action potentials (CMAP) were lower by the 3 months and did not increase later. The amplitudes and areas of sensory action potentials (SNAP) increased until 9 months in both groups. SNAP duration decreased with ageing. Sensory peak 1 and peak 2 latencies became longer from 6.5 to 9 months in diabetic rats, with a longer latency difference between the 2 sensory peaks by 4 months. At 3 and 4 months of age, peak 1 and peak 2 latencies correlated with SNAP amplitude and duration in control rats but not in diabetic rats. In conclusion, in rats with early induced diabetes, the earliest electrophysiological impairments consist of lower CMAP amplitudes, and longer difference between latencies of sensory peaks 1 and 2. These sequential neurophysiological changes should be considered when testing new therapeutic approaches in diabetic neuropathy