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A three-dimensional finite element code to analyze coupled thermomechanical deformations of composites has been developed. It incorporates geometric nonlinearities, delamination between adjoining layers, and damage due to fiber breakage, fiber/matrix debonding, and matrix cracking. The three damage modes are modeled using the theory of internal variables and the delamination by postulating a failure envelope in terms of the transverse stresses; the damage degrades elastic moduli. The delamination of adjoining layers is simulated by the nodal release technique. Coupled nonlinear partial differential equations governing deformations of a composite, and the pertinent initial and boundary conditions are first reduced to coupled ordinary differential equations (ODEs) by the Galerkin method. These are integrated with respect to time with the Livermore solver for ODEs. After each time step, the damage in an element is computed, and material properties modified. The code has been used to analyze several static and transient problems; computed results have been found to compare well with the corresponding test results. The effect of various factors such as the fiber orientation, ply stacking sequence, and laminate thickness on composite's resistance to shock loads induced by underwater explosions has been delineated. / Ph. D.

Traumatic brain injury (TBI) is a major medical concern that has demonstrated to be particularly challenging to treat because of the disparity amongst injury modes and severities. Increased use of explosive devices during combat has caused blast TBI (bTBI) to become a widespread consequence in military and Veteran populations, and impact-related trauma from contact-related sports or motor vehicle accidents has made mild impact-induced TBIs (concussion) a major health problem. There is a high risk for those who have sustained a TBI to develop behavioral and cognitive disorders following injury, and these symptoms can present as delayed onset, causing diagnosis to be a major feat when planning for treatment and long-term healthcare. Both preclinical and clinical studies report the neuropathological changes following TBI, yet investigating the distinct mechanistic changes in blast and impact trauma that contribute to pathological disparities has yet to be elucidated. Microglia dynamics play a key role in initiating the inflammatory response after injury, as microglia become activated by undergoing morphological changes that influence their function in the injured brain, and unique signaling pathways influence their functional inflammatory states. While previous literature report on the unique responses of microglia, their mediated-inflammatory responses are still not well defined. This work aimed to investigate the acute and subacute responses of microglia to injury through their diverse activation states following blast and impact trauma. The work herein employed rodent models to investigate these changes, finding that microglia activation was spatially and temporally heterogeneous within and across injury paradigms. Three days following bTBI, activated microglia in the cortex displayed morphologies similar to microglia that are known to increase their interactions with dysfunctional synapses, while dystrophic microglia were prevalent in the hippocampus seven days following injury. Moreover, transhemispheric changes in microglia activation were noted following impact TBI, with stressed/primed microglia responding to immune challenges of the cortex at three days, whereas a unique morphological state that was markedly different from those traditionally reported in CNS injury and disease was present within the hippocampus three- and seven-days following injury. State-of-the-art cell sorting techniques were used for in vivo analysis of microglia, which also exhibited that functional changes of microglia vary between injury paradigms, providing insight into how differences in primary insult may elicit distinct signaling pathways involved in microglia-mediated inflammatory responses. These in vivo studies were then crucial in understanding the malleable responses of microglia to complex injuries such as "blast plus impact" TBI, indicating that phenotypic changes in microglia following this injury are also unique and spatially heterogeneous. To date, therapeutic efforts for TBI are limited due to the lack of understanding the underlying mechanisms that influence TBI pathology. This work also investigated novel therapeutic targets, noting that administration of polyester nanoparticles restored microglia to baseline levels following impact. The fundamental research presented in this study is innovative and advantageous as it can provide essential data into targeted and personalized treatments that can improve long-term healthcare and ultimately, the quality of life for those suffering from a TBI. / Doctor of Philosophy / Traumatic brain injury (TBI) is a major medical concern that has demonstrated to be particularly challenging to treat because of the differences in injury modes and severities. Increased use of explosive devices during combat has caused blast TBI (bTBI) to become a widespread result in military and Veteran populations, and impact-related trauma from contact sports or motor vehicle accidents has made mild impact-induced TBIs (concussion) a major health problem. There is a high risk for those who have sustained a TBI to develop behavioral and cognitive disorders following injury, and these symptoms can present later on, causing diagnosis to be a major feat when planning for treatment and long-term healthcare. Microglia play a key role in inducing the inflammatory response after injury, as they change shape and size, which then influences their function in the injured brain. Although prior research reports on the unique responses of microglia, their effects on inflammation following TBI are still not well defined. This work aimed to investigate the early responses of microglia to injury through their diverse activation states following blast and impact trauma. The experiments in this study used animal models, finding that microglia activation can be distinct across time and brain regions, which may be injury-type-specific. To date, therapeutic efforts of TBI are limited due to the lack of understanding the underlying mechanisms that influence TBI pathology. This work also investigated beneficial treatments for TBI, noting that administration of nanoparticles helped restore microglia to levels similar to the control group. The fundamental research presented in this study is innovative and important as it can provide essential data into targeted and personalized treatments that can improve long-term healthcare and ultimately the quality of life for those suffering from a TBI.

In this investigation a method is suggested for determining the dynamic, elastic response of a thin hemispherical shell subjected to a head-on attack by the initial shock wave of an underwater explosion. The shell which is fastened to the end of a fixed, semi-infinite tube of the same radius is surrounded by a high density fluid similar to water, and the internal cavity of the shell is filled with a low density fluid similar to air. The initial shock wave moves through the high density fluid. In the neighborhood of the obstacle, the shock front propagates in the direction of the axis of the semi-infinite tube and makes initial contact with the obstruction at the tip of the hemisphere at time equal to 0+. The following basic assumptions are used to define the mathematical model for the physical problem. The shock wave is considered to be a plane pressure pulse with exponential decay, the surrounding fluid is treated as if it were an acoustic medium, and the low density fluid is assumed to exert a constant pressure over the interior surface of the shell. The thin, hemispherical shell is regarded as being constructed of an isotropic, homogeneous, Hookean material of constant thickness. This shell experiences only small displacements. Moreover, in this model, the hemispherical shell is attached to a rigid, semi-infinite tube in such a way that the normal and in-plane displacements of the middle surface of the shell and the slope of the middle surface of the shell in the longitudinal direction are all zero at the shell-tube connection. The investigation for the solution to this axisymmetric problem, in which the mathematical formulations on the displacements of the shell and the velocity potential of the fluid are coupled, is begun with the separation of the displacements of the middle surface of the shell into two parts, ( )_M and ( )_B displacements. These are then shown to be analogous to the "membrane" and "pure bending" displacements familiar in the theory of static shells. The governing equations and the determinative conditions for the ( )_M displacements are found to be independent of the ( )_B displacements, while in the ( )_B formulation the ( )_M displacements are found to appear only in the determinative conditions. An approximate solution which is valid for small time and in which Poisson's ratio and the in-plane inertia term are assumed to be zero is obtained for the ( )_M displacements. A complementary solution for the ( )_B displacements which is valid in the neighborhood of the shell-tube connection is determined by using geometric and kinematic approximations in the ( )_B formulation. Approximate solutions for the displacements of the middle surface of the shell are then formulated by combining the ( )_M and ( )_B expressions above with the assumptions (valid only for the stated small time range) that the ( )_B contribution to the in-plane displacement is negligible over the entire shell and that the ( )_B contribution to the normal displacement is negligible except in the region near the shell-tube connection. Numerical results are calculated for a steel shell immersed in sea water and these results are presented in the form of tables and plots. / Ph. D.

The transient response of various plate structures subject to blast loads is analyzed. In particular, simply supported isotropic and laminated composite plates are modeled using the commercial finite element code NASTRAN and the method of modal superposition. Both analysis procedures are used to quantify the linear transient response of such plates subject to uniform and patch blast loads. Furthermore, NASTRAN is used to study the nonlinear response of plates subject to close proximity explosions. Also considered here is the case for which a blast loaded plate impacts another closely neighboring plate. The NASTRAN solution used here accounts for nonlinearities due to large plate deflections, plasticity, and plate-to-plate contact. Many studies are currently available in which the blast load is considered to be spatially uniform across the plate; with a temporal distribution described by step, N-pulse, or Friedlander equations. The novel aspect considered here is the case for which the blast pressure is due to a close proximity explosion, and it is therefore taken to be both spatially and temporally varying. A FORTRAN program is described which automates the application of an arbitrary blast load to a generic finite element mesh. The results presented here are a collection of analyses performed for a variety of parameters important to the dynamic response of blast loaded contacting plates. Conclusions are drawn concerning the influence of the various parameters on the nature of the plate response and the quality of the solution. / Master of Science

Modeling and simulation have played an essential role in understanding the effects of blast waves. However, a broad area of engineering problems, such as vehicle structures, buildings, bridges, or even the human body, can benefit by accurately predicting the response to blasts with little need for test or event data. This thesis reviews fundamental concepts of blast waves and explosives and discusses research in blast scaling. Blast scaling is a method that reduces the computational costs associated with modeling blasts by using empirical data and numerically calculating blast field parameters over time for various types and sizes of explosives. This computational efficiency is critical in studying blast waves' near and far-field effects. This thesis also reviews research to differentiate between free-air blasts and gun muzzle blasts and the progress of modeling the muzzle blast-structure interaction. The main focus of this thesis covers an investigation of different numerical and analytical solutions to a simple aerospace structure subjected to blast pressure. The thesis finally presents a tool that creates finite element loads utilizing muzzle blast scaling methods. This tool reduces modeling complexity and the need for multiple domains such as coupled computational fluid dynamics and finite element models by coupling blast scaling methods to a finite element model. / Master of Science / {Numerical integration methods have helped solve many complex problems in engineering and science due to their ability to solve non-linear equations that describe many phenomena. These methods are beneficial because of how well they lend to programming into a computer, and their impact has grown with the increases in computing power. In this thesis, ``modeling and simulation" refers to the characterization and prediction of an event's outcome through the use of computers and numerical techniques. Modeling and simulation play important roles in studying the effects of blast waves in many areas of engineering research such as aerospace, biomedical, naval, and civil. Their capability to predict the outcome of the interaction of a blast wave to vehicle structures, buildings, bridges, or even the human body while requiring limited experimental data has the chance to benefit a wide area of engineering problems. This thesis reviews fundamental concepts of blast waves, explosives, and research that has applied blast loading in modeling and simulation. This thesis describes the complexity of modeling an axially symmetric blast wave interaction by comparing the numerical and theoretical response blast loaded structure.

Corrosion of reinforcing steel embedded in concrete due to the presence of moisture, aggressive chemicals, inadequate cover, and other factors can lead to deterioration that substantially reduces the strength and serviceability of the affected structure. Accounting for corrosion degradation is critical for evaluation and assessment of the load carrying capacity of existing reinforced concrete (RC) structures. However, little is known about the relationship between high strain rate blast loading and the degradation effects that govern corrosion damaged structures such as concrete cover cracking, reduction in reinforcement areas, and deterioration of bond between concrete and steel. Ten identical RC beams were constructed and tested, half under blast loading conditions produced using the Virginia Tech Shock Tube Research Facility and the other half under quasi-static loading. The blast tests were conducted to investigate how increasing blast pressure and impulse affect the global displacement response and damage modes of beams subjected to blast loads. The quasi-static tests were performed to establish fundamental data on the load-deflection characteristics of corroded RC beams. One beam from each testing group served as a control specimen and was not corroded while the remaining beams were subjected to varying levels of corrosion (5%, 10%, 15%, and 20%) of the longitudinal reinforcement along the midspan region. The specimens were corroded using an accelerated corrosion technique in a tank of 3% sodium chloride solution and a constant electrical current, creating a controlled environment for varying levels of corrosion. An analytical model was also created using a single degree of freedom (SDOF) approach which predicted the performance of corroded RC beams under blast loading. The results of the quasi-static tests revealed that as corrosion levels increased, the load to cause yielding decreased, the yield displacements decreased, and failure occurred earlier for all specimens. This was accompanied by increased damage to the concrete cover and the addition of longitudinal corrosion induced cracking. For the blast loaded specimens, the results demonstrated that the maximum displacements and residual displacements increased beyond the expected response limits for corrosion levels greater than 5%, but at corrosion levels less than 5% there was no significant change in displacements. Damage levels increased by one or more categories with the introduction of even small levels of corrosion of less than 5%. At corrosion levels greater than 5%, before loading was applied, the specimens exhibited moderate damage due to the introduction of corrosion induced cracking. After loading, the specimens sustained hazardous damage at progressively lower blast volumes. The failure mode changed from ductile to sudden and brittle failure at corrosion levels greater than 5% but remained ductile with flexural failures at low corrosion levels below 5%. The experimental results could be predicted with a high level of accuracy using the SDOF approach, provided that the degraded strength of corroded concrete cover, degraded mechanical properties of corroded steel, length of the corroded region, and determination of either uniform or pitting corrosion are accounted for. Overall, the introduction of corrosion to an RC beam subjected to blast loading resulted in decreased strength and ductility across all specimens but with most disastrous effects occurring at corrosion levels of 5% or greater. A recommendation is made to adjust the response limits in ASCE/SEI 59 to account for corrosion in RC beams. / Master of Science / The threat of blast loads, resulting from either terrorist attacks or accidental explosions, poses a significant threat to the structural integrity of buildings, life safety of occupants, and the functionality of the structure. Corrosion of reinforcing steel embedded in concrete, due to the presence of moisture, aggressive chemicals, and other factors, can lead to deterioration that substantially weakens the affected structure. Accounting for corrosion degradation is critical for evaluation and assessment of the strength of existing reinforced concrete structures. However, little is known about the effects of blast loading on the adverse nature that governs corrosion damaged structures. Ten identical reinforced concrete beams were constructed and tested, half under blast loading and the other half under quasi-static loading. The blast loaded beams were subjected to a series of increasing blast volumes until failure was reached. Five identical beams were tested under quasi-static loading to provide a baseline comparison against the blast loaded beams. One beam from each testing group served as a control specimen and was not corroded while the remaining beams were subjected to varying levels of corrosion of the steel reinforcement. An analytical model was also created to predict the performance of corroded reinforced concrete beams under blast loading. The results of the study showed that as corrosion levels increased, the displacements increased beyond the expected response limits. Damage levels became increasingly more severe with the introduction of corrosion at all levels. The behavior changed from ductile to brittle at corrosion levels greater than 5% but remained ductile with flexural failures at corrosion levels below 5%. Overall, the introduction of corrosion to a concrete beam subjected to blast loading resulted in decreased strength and ductility across all specimens but with most disastrous effects occurring at corrosion levels of 5% or greater. A recommendation is made to adjust the response the limits in the code to account for corrosion in reinforced concrete beams.

Blast-induced neurotrauma (BINT) is a prevalent brain injury within both military and civilian populations due to current engagement in overseas conflict and ongoing terrorist events worldwide. In the early 2000s, 78% of injuries were attributable to an explosive mechanism during overseas conflicts, which has led to increased incidences of BINT [1a]. Clinical manifestations of BINT include long-term psychological impairments, which are driven by the underlying cellular and molecular sequelae of the injury. Development of effective treatment strategies is limited by the lack of understanding on the cellular and molecular level [2a]. The overall hypothesis of this work is that epigenetic regulatory mechanisms contribute to the progression of the BINT pathology and neurological impairments. Epigenetic mechanisms, including DNA methylation and histone acetylation, are important processes by which cells coordinate neurological and cellular response to environmental stimuli. To date, the role of epigenetics in BINT remains largely unknown. To test this hypothesis, an established rodent model of BINT was employed [3a]. Analysis of DNA methylation, which is involved in memory processes, showed decreased levels one week following injury, which was accompanied by decreased expression of the enzyme responsible for facilitating the addition of methyl groups to DNA. The one week time point also showed dramatic decreases in histone acetylation which correlated to decline in memory. This change was observed in astrocytes and may provide a mechanistic understanding for a hallmark characteristic of the injury. Treatment with a specific enzyme inhibitor was able to mitigate some of the histone acetylation changes. This corresponded with reduced astrocyte activation and an altered behavioral phenotype, which was characterized by high response to novelty. The diagnostic efficacy of epigenetic changes following blast was elucidated by the accumulation of cell-free nucleic acids in cerebrospinal fluid one month after injury. Concentrations of these molecules shows promise in discriminating between injured and non-injured individuals. To date, the diagnostic and therapeutic efforts of BINT have been limited by the lack of a mechanistic understanding of the injury. This work provides novel diagnostic and therapeutic targets. The clinical potential impact on diagnosis and therapeutic intervention has been demonstrated. / Ph. D. / Blast-induced neurotrauma (BINT) is a prevalent brain injury within both military and civilian populations due to current engagement in overseas conflict and ongoing terrorist events worldwide. In the early 2000s, 78% of injuries were attributable to an explosive mechanism during overseas conflicts which has led to increased incidences of BINT [1a]. Clinical manifestations of BINT include long-term psychological impairments which are driven by the underlying cellular and molecular sequelae of the injury. To date, the development of effective treatment strategies has been unsuccessful. The work described herein seeks to evaluate the specific cellular mechanisms that contribute to the progression of the BINT pathology and neurological impairments. Epigenetic mechanisms are regulatory mechanisms that coordinate DNA modifications and DNA storage to facilitate altered cellular phenotypes. DNA modifications often involves DNA methylation, which is the addition of methyl groups to the DNA backbone. DNA storage is regulated by specific modifications to histone proteins. Histone acetylation is a well-studied modification process that is capable inciting either chromatin relaxation or compaction. Both DNA methylation and histone acetylation are important processes by which cells coordinate neurological and cellular response to environmental stimuli. To date, the role of epigenetics in BINT remains largely unknown. An established rodent model of BINT was employed [3a]. Analysis of DNA methylation, which is involved in memory processes, showed decreased levels one week following injury which was accompanied by decreased expression of one of the enzymes responsible for facilitating the addition of methyl groups to DNA. The one week time point also showed dramatic decreases in histone acetylation which correlated to memory impairment. This change was observed in astrocytes which are support cells in the brain and are particularly vulnerable to blast-induced aberrations. Drug administration, targeting the histone acetylation equilibrium, successfully mitigated astrocyte activation and altered the behavioral phenotype. Diagnosis of BINT remains clinically challenging. An accumulation of cell-free nucleic acids was observed the in cerebrospinal fluid one month after injury. Concentrations of these molecules shows promise in discriminating between injured and non-injured individuals. These nucleic acids are susceptible to DNA methylation and may provide a platform for studying epigenetic biomarkers. To date, the diagnostic and therapeutic efforts of BINT have been limited by the lack of a mechanistic understanding of the injury. This work provides novel diagnostic and therapeutic targets. The potential clinical impact on diagnosis and therapeutic intervention has been demonstrated.

The blast loading on a structure is a function of the incident blast wave characteristics, that is, overpressure and dynamic pressure. But the most damaging effect to the guy cable from a nuclear explosion would be the dynamic pressure caused by the high winds which follow the chock front. This dynamic pressure reaches its maximum value very rapidly, almost zero time after the passage of the shock front, and then decays exponentially as shown by equation (17). The work of this thesis has been the investigation of a guy cable under blast loading by correcting the tension during each small time interval. The results from this procedure are considerably smaller than those in the analytical work of Mr. D. A. Ball. From this point of view, we know that the tension of the cable in such a problem can not be considered as constant. / Master of Science