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The Pultruded Rod Stitched Efficient Unitized Structure (PRSEUS) concept is characterized by through-thickness VectranTM stitching of warp-knit carbonabric prior to resin infusion. A series of novel lightning strike tests were performed on a PRSEUS panel. The panel’s lightning damage resistance was characterized as a function of peak current (50-200 kA) and strike location (mid-bay, stringer, frame). Both visual inspections and through-transmission-ultrasonic C-scans were used to investigate the damage resistance at the strike locations and to assess various damage mechanisms and morphologies. The size and severity of the damaged area depend strongly on the fiber orientation in the outermost ply, the amount of current injected into the panel, and the strike location relative to stitching lines. Increasing the current magnitude drastically increases the damaged area. Also, the presence of VectranTM structural stitches profoundly reduced the size and severity of lighting damage relative to similar strikes performed in panel regions without stitching.

Lightning damage resistance of unstitched carbon/epoxy laminates and a Pultruded Rod Stitched Efficient Unitized Structure (PRSEUS) panel were characterized by laboratory-scale lightning strike tests and multiphysics-based lightning strike finite element (FE) models. This dissertation combines three related research topics: (1) a three-dimensional (3D) heat transfer problem, (2) lightning damage resistance assessments of carbon/epoxy laminates, and (3) lightning damage resistance of PRSEUS panel. The first project deals with a 3D analytical heat transfer problem as a solid foundation for understanding the steady-state temperature distribution in an anisotropic composite heat spreader. The second project characterizes lightning damage to unprotected carbon/epoxy laminates and laminates with either copper mesh (CM) or pitch carbon fiber paper (PCFP) protection layers subjected to standard impulse current waveforms, consistent with actual lightning waveforms, with 50, 125, and 200 kA nominal peak currents. Multiphysics-based FE models were developed to predict matrix thermal decomposition (a primary form of lightning damage) in unprotected, CM-protected, and PCFP-protected carbon/epoxy laminates. The predicted matrix decomposition domains in the damaged laminates showed good agreement with experimental results available in the literature. Both the CM and the PCFP lightning protection layers successfully mitigated lightning damage development in the underlying composites. The third project includes lightning damage characterization of a PRSEUS panel. Laboratory-scale lightning strike tests with nominal 50, 125, and 200 kA peak currents were performed at the mid-bay, stringer, frame, and frame/stringer intersection locations of the PRSEUS panel. The elliptical regions of intense local damage were elongated along the outermost lamina’s carbon fiber direction, consistent with observations from the unstitched carbon/epoxy laminates. However, the damaged PRSEUS panel exhibited unique damage features due to use of warp-knitted fabrics and through-thickness VectranTM stitches. The polyester threads used to weave the warp-knitted laminates locally confined small-scale fiber damage. This resulted in somewhat periodic and scattered small tufts of carbon fibers near the lightning attachments. Through-thickness VectranTM stitches also confined intense local damage development at the stringer and frame locations. The polyester warp-knit fabric skins and through-thickness VectranTMstitches have a significant beneficial effect on lightning damage development on a PRSEUS panel.

A multiscale continuum model for fragmentation in ductile metals was developed, motivated by structure-property relationships obtained from lower length scale and numerical simulations. Fragmentation occurs during high strain rate deformation as the result of widespread internal damage in the form of void or crack nucleation, growth, and coalescence. The connection between internal damage structures and fragmentation was determined through Molecular Dynamics (MD) simulations of high rate deformation in copper, iron, and iron-carbon alloys. The fragmentation metric of interest in this study is the fragment size, which is represented in MD simulations by the fragment length scale, or the solid volume per surface area ratio. Three deformation modes of varying stress triaxialities, plane strain tension, equibiaxial expansion, and isotropic expansion, provide a range of damage growth behavior allowing the fragment length scale to be correlated to damage structures under different conditions. Modified Embedded Atom Method (MEAM) potentials for the materials enable the representation of damage (and newly created free surfaces) under the extreme conditions. Continuum, nonhomogeneous percolation simulations establish a criterion for fragmentation based on internal damage structure. The continuum percolation simulations are motivated by void size and shape information taken from experimental fracture surfaces of an aluminum 7085 alloy. The combination of the percolation based fragmentation criterion and MD motivated fragmentation model yields a framework for the multiscale modeling of fragmentation.

This study examined Hurricane Katrina damage in southeast Mississippi to identify stand and site characteristics that may contribute to wind-related damage. Aggregated forest plot-level biometrics were coupled with storm meteorology, topographical features, and soil attributes using GIS techniques to produce damage maps for specific tree species. Regression Tree Analysis was utilized to explore the relationship between damage type and distance variables (distance to coast/storm track). Results indicated that the total damage class had the greatest relationship with distance variables; individual damage classes (shear and blowdown) displayed a better relationship with stand-level variables (Quadratic Mean Diameter, Lorey’s Mean Height, Trees Per Hectare). Logistic regressions identified a negative relationship between damage and height variation, elevation, slope, and aspect and a positive relationship with TPH. For plots/stands nearest to the coast and storm track height variation, TPH, QMD, and LMH consistently predicted damage levels for most species examined.

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The thesis presents a method of evaluation for blade damage in Combustion Turbine Compressor Section. This method involves use of multiple domains within a single Finite Element Model to predict the effect of damage on the blade properties. This approach offers significant time and effort savings when compared to traditional evaluation methods of similar problems. It is demonstrated via examples that the multi-domain modeling approach yields acceptable accuracy results. The economical implications of described method are readily applicable to both the industrial and the aerospace Combustion Turbine fields. It is economically impractical to replace the blade at each damage occurrence. However, the evaluation time involved in making associated decisions can be extensive if traditional methods of evaluation are used. The specific contributions of this study are twofold: 1. Time savings during evaluation 2. Compressor Blades may be returned to service which are otherwise replaced

During the course of normal DNA replication, replication forks are constantly encountering "housekeeping" types of routine damage to the DNA template that may cause the forks to stall or collapse. One product of this fork collapse is the induction of the SOS response, a coordinated global response to help pause the growth and replication of a cell while DNA damage is addressed and repaired. In E. coli, this response is activated by the formation of ssDNA, to which the RecA protein binds and forms a nucleoprotein filament, which acts as the activator for autocleavage of the LexA transcriptional repressor, which normally represses expression of SOS genes. Damage responses are crucial to maintaining genomic integrity, and are therefore essential to all forms of life, and this type of regulatory system is highly conserved. However, cells have mechanisms for tightly regulating induction of these responses, and can often repair routine damage to their chromosomes without the need to induce SOS. This is chiefly evidenced by the observation that more than 20% of cells in a population have RecA filaments, but less than 1% are induced for SOS. How cells make this decision to induce SOS is the subject of this work. This dissertation describes three projects aimed at examining molecular mechanisms by which cells regulate RecA filaments, and therefore the decision to induce the SOS response. The first examines the disparity between the formation of RecA filaments, as evidenced by RecA-GFP foci, and the induction of SOS in the absence of damage, using a psulA-gfp reporter system. It is shown that there are three independent factors that repress SOS expression in undamaged E. coli cells. These are radA, the amount of recA in the cell, and in some circumstances recX. The first two limit SOS in wild type cells in the absence of external damage, while the third is an additional factor required in xthA mutants, likely due to the fact there are more RecA loading events in these mutants. These factors are thought to change the character and reduce the half-life and persistence of RecA filaments in the cell. The second project shows that suppression of SOS through the use of recA4162 and uvrD303 mutants is substrate and situation-specific. This specificity is demonstrated by the fact that, while both recA4162 and uvrD303 can suppress SOS in the SOS constitutive mutant recA730, recA4162 can only suppress SOS when the signal occurs at replication forks and not at any other place on the chromosome, while uvrD303 appears to suppress SOS with less specificity, and can suppress after UV (shown previously), at induced DSBs, and other places not directly at the replication fork. Here mutants of different replication factors are used that uncouple the replisome and induce SOS to a high degree. The third project determines the factors necessary for loading RecA filaments at the replication fork versus other locations on the chromosome when SOS is induced in the absence of damage, and helps elucidate further mechanisms for induction of SOS at these substrates. It is shown that the sbcB and recJ exonucleases assist in inappropriate RecA filament formation by substrate processing exclusively at replication forks, but not other substrates, likely through mechanisms that are reliant on the activities of the RecA loading factors RecBCD and RecFOR.

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