A novel approach to data-driven modeling of damage-induced elastic wave propagation

Current research into the simulation of elastic stress wave propagation utilizes user-imposed energy functions to drive the required energy changes for the production of elastic waves that propagate through the continuum model. This thesis proposes a novel approach to theoretically investigate the creation and propagation of elastic stress waves in a computational model by linking "experimental data-driven" quasi-static crack growth simulations with dynamic simulations for transient elastic wave propagation. The quasi-static simulations are used to determine both the displacement, strain and stress fields associated with crack initiation and the rate at which the crack will grow. As these elastic fields change over time as a function of crack growth increments, the dynamic model is used to capture the changes in the stored energy that lead to new equilibrium states for a developing crack, as well as the transient path followed to achieve this structural evolution. Within this energy balance lies the production and propagation of elastic stress waves associated with energy released by the crack growth. In the computational models, specific locations are selected for monitoring in- and out-of-plane displacement, velocity and acceleration. Such data generated by the model and captured by numerical sensors are analyzed in both time and frequency domains and are compared to related experimental measurements. The computationally generated transient elastic stress waves that propagate through the model produce the equivalent of what is known as Acoustic Emissions, providing in this way an innovative approach to directly link fracture mechanics with theory related to nondestructive testing. The research findings in this thesis are expected to contribute towards the design of more efficient strategies for the fundamental understanding of the fracture process, as well as for the reliable damage monitoring in structural health monitoring applications.M.S., Mechanical Engineering -- Drexel University, 201

Can we learn from the pathogenetic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae?

The purpose of this review-hypothesis is to discuss the literature which had proposed the concept that the mechanisms by which infectious and inflammatory processes induce cell and tissue injury, in vivo, might paradoxically involve a deleterious synergistic ‘cross-talk’, among microbial- and host-derived pro-inflammatory agonists. This argument is based on studies of the mechanisms of tissue damage caused by catalase-negative group A hemolytic streptococci and also on a large body of evidence describing synergistic interactions among a multiplicity of agonists leading to cell and tissue damage in inflammatory and infectious processes. A very rapid cell damage (necrosis), accompanied by the release of large amounts of arachidonic acid and metabolites, could be induced when subtoxic amounts of oxidants (superoxide, oxidants generated by xanthine-xanthine oxidase, HOCl, NO), synergized with subtoxic amounts of a large series of membrane-perforating agents (streptococcal and other bacterial-derived hemolysins, phospholipases A 2 and C, lysophosphatides, cationic proteins, fatty acids, xenobiotics, the attack complex of complement and certain cytokines). Subtoxic amounts of proteinases (elastase, cathepsin G, plasmin, trypsin) very dramatically further enhanced cell damage induced by combinations between oxidants and the membrane perforators. Thus, irrespective of the source of agonists, whether derived from microorganisms or from the hosts, a triad comprised of an oxidant, a membrane perforator, and a proteinase constitutes a potent cytolytic cocktail the activity of which may be further enhanced by certain cytokines. The role played by non-biodegradable microbial cell wall components (lipopolysaccharide, lipoteichoic acid, peptidoglycan) released following polycation- and antibiotic-induced bacteriolysis in the activation of macrophages to release oxidants, cytolytic cytokines and NO is also discussed in relation to the pathophysiology of granulomatous inflammation and sepsis. The recent failures to prevent septic shock by the administration of only single antagonists is disconcerting. It suggests, however, that since tissue damage in post-infectious syndromes is caused by synergistic interactions among a multiplicity of agents, only cocktails of appropriate antagonists, if administered at the early phase of infection and to patients at high risk, might prevent the development of post-infectious syndromes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72535/1/j.1574-695X.1999.tb01357.x.pd