Damage to motor areas of the brain, caused by stroke, can produce devastating motor deficits, including aberrant control of force. After stroke, reorganization of the brain’s motor system has been identified as one of the fundamental mechanisms involved in recovery of motor control after stroke. Yet, few studies have investigated how force production and modulation are encoded in the brain after stroke and how this relates to motor outcome. Thus, the purpose of this study was to (1) understand how past neuroimaging literature has contributed to establishing common patterns of brain reorganization during both relative and absolute force production after stroke, (2) examine how brain function is reorganized during force production and modulation in individuals with stroke, and (3) relate this task-related reorganization of brain function to the amount of paretic arm use after stroke. In the second chapter, we systematically reviewed all relevant literature examining brain activation during force production after stroke. The following chapters (chapters 3 and 4) applied functional magnetic resonance imaging (fMRI) to examine the neural correlates of force production and modulation after stroke. Chapter 2 supports differences in task-related brain activation dependent on features of stroke, such as severity and chronicity, as well as influence of rehabilitation. In addition, results suggest that activation of common motor areas of the brain during force production can be identified in relation to functional outcome after stroke. Results from the subsequent two chapters (3 and 4), demonstrate that brain function reorganizes in terms of absolute, and not relative force production after stroke. Specifically, stroke participants exhibit greater activation of motor areas than healthy controls when matched for absolute force production. Moreover, there is a relationship between paretic arm usage and brain activation, where stroke participants having less paretic arm use, as measured using wrist accelerometers, exhibit higher brain activation. Results of this thesis suggest that during absolute force production, brain activation may approach near maximal levels in stroke participants at lower forces than healthy controls. Furthermore, this effect may be amplified even further in subjects with less paretic arm usage, as increased activation in motor areas occurs in participants with less arm use after stroke. Ultimately, the results from this thesis will contribute to research relevant to brain reorganization in individuals with stroke and may lead to the development of new, beneficial therapeutic interventions that optimize brain reorganization and improve functional recovery after stroke.

A new crystal plasticity scheme for explicit time integration codes is developed based on a forward Euler algorithm in the first part of this paper. The new numerical model is incorporated in the UMAT subroutine for implementing rate dependent crystal plasticity model in LS-DYNA/Explicit. The material is modeled as a Face centered cubic (FCC) polycrystalline aggregate, and a finite element analysis based on rate-dependent crystal plasticity is developed to simulate large strain behaviour. Accordingly, an element or a number of elements of the finite element mesh is considered to represent a single crystal within the polycrystal aggregate and the constitutive response at a material point is given by the single crystal constitutive model. The second part of this thesis presents two applications of the crystal plasticity scheme used in conjunction with numerical modeling of three-dimensional (3D) real microstructures. First, finite element meshes containing both particle and texture data are created with solid elements. Particle size, location and orientation are represented by 3D ellipsoids and the elements within these ellipsoids are given rigid properties. Simulations of in-plane plane strain with different combinations of texture and particle location are performed. The effect on texture development, strain magnitudes, and strain localizations is investigated. Second, the three dimensional (3D) polycrystalline microstructure of the aluminum alloy AA5754 is modeled and subjected to three different strain rates for each strain path. The effect of strain paths, strain rates and thermal softening on the formation of localized deformation is investigated. Simulations show that strain path is the most dominant factor in localized deformation and texture evolution.

A new crystal plasticity scheme for explicit time integration codes is developed based on a forward Euler algorithm in the first part of this paper. The new numerical model is incorporated in the UMAT subroutine for implementing rate dependent crystal plasticity model in LS-DYNA/Explicit. The material is modeled as a Face centered cubic (FCC) polycrystalline aggregate, and a finite element analysis based on rate-dependent crystal plasticity is developed to simulate large strain behaviour. Accordingly, an element or a number of elements of the finite element mesh is considered to represent a single crystal within the polycrystal aggregate and the constitutive response at a material point is given by the single crystal constitutive model. The second part of this thesis presents two applications of the crystal plasticity scheme used in conjunction with numerical modeling of three-dimensional (3D) real microstructures. First, finite element meshes containing both particle and texture data are created with solid elements. Particle size, location and orientation are represented by 3D ellipsoids and the elements within these ellipsoids are given rigid properties. Simulations of in-plane plane strain with different combinations of texture and particle location are performed. The effect on texture development, strain magnitudes, and strain localizations is investigated. Second, the three dimensional (3D) polycrystalline microstructure of the aluminum alloy AA5754 is modeled and subjected to three different strain rates for each strain path. The effect of strain paths, strain rates and thermal softening on the formation of localized deformation is investigated. Simulations show that strain path is the most dominant factor in localized deformation and texture evolution.

The morphological phenotypic characters involving sexual selection but with highly individual variability are likely to challenge the prezygotic isolating mechanism driven by differentiation of mechanical structures. This kind of characters may also puzzle species identification and taxonomy. Therefore clarifying the correlation between the phenotypic variability and biological/non-biological factors becomes necessary in order to understand the role of this phenomenon under natural selection and sexual selection. The Syntomini represents one of the few lepidopterous groups that exhibit highly individual variability in both wing pattern and reproductive structures. The evolutionary and taxonomic significance of this phenomenon, however, has never been studied using modern methods although it has been documented for long. In order to test several hypotheses relevant to phenotypic variability, the present study focuses the phylogenetic relationship of Amata wilemani Rothschild, 1914, a subalpine moth species with extremely high variability in wing coloration and genitalia. The phylogenetic relationship between the three color morphs of A. wilemani and 38 Syntomini species plus 2 Lithosiinae outgroups was reconstructed using fragments of COI, EF1a and 28S. All color morphs of A. wilemani were recovered to form a monophyletic group under all data partitioning strategies with Amata formosensis (Wileman, 1928) or its closely related species in China as the potential sister group. The result of gene network analysis suggests low divergence between haplotypes of A. wilemani. Because no correlation between color morphs, phenology, geographical distribution, altitudinal gradient, and genitalic morphlogy was detected, it is concluded that A. wilemani should be regarded as a single species with high phenotypic variability, and this may suggest existence of intraspecific competition. The present study also found that Amata karapinensis (Strand, 1915), which was synonymized with A. wilemani by previous authors, should be revived. The incongruence between the phylogenetic relationships based on morphological and molecular characters shows a need of a comprehensive phylogenetic study of this highly diverse group.

Although neural plasticity has traditionally been studied within the brain, evidence indicates that the spinal cord is quite plastic as well. Spinal neurons can even support a simple form of instrumental learning (Grau et al., 1998), as indicated by spinally transected rats’ ability to exhibit an increase in hind limb flexion duration when limb extension is associated with shock (controllable shock). If limb extension is not associated with shock (uncontrollable shock), a learning deficit develops. Recent research indicates that other forms of plasticity, such as long-term potentiation and central sensitization, do not depend on neural activity alone, but also on glial cells. I examined whether glial cells are also necessary in spinal instrumental learning and the learning deficit. Therefore, two glial inhibitors were selected: minocycline and fluorocitrate. To examine the role of glial cells in spinal instrumental learning, rats received intrathecal minocycline, fluorocitrate, or saline prior to testing with 30-minutes of controllable leg-shock. Results indicate that both drugs dose-dependently reduced acquisition, with higher doses resulting in shorter response durations. Once the response was acquired, fluorocitrate did not alter response maintenance. This suggests that glial cells are involved in the acquisition, but not the maintenance, of spinal learning. To examine the role of glial cells in the spinal learning deficit rats were given intrathecal minocycline, fluorocitrate, or saline prior to testing with 6-minutes of uncontrollable tail shock or no shock. Twenty-four hours later all rats were tested with 30-minutes of controllable leg-shock. Results indicated the learning deficit induced by uncontrollable shock was prevented by prior administration of fluorocitrate. Minocycline did not prevent the deficit; moreover, it appears that even in the absence of shock, minocycline caused a learning deficit. Overall, this data indicate that glial cells are necessary for the acquisition of spinal instrumental learning and the learning deficit. Furthermore, it provides further evidence for the role of glial cells in plasticity.

Previous work has shown that the spinal cord is capable of supporting a simple form of instrumental learning. Subjects that receive controllable shock to an extended hind limb will increase the duration of limb flexion over time in order to reduce net shock exposure. Exposure to as little as 6 minutes of uncontrollable stimulation prior to instrumental testing can elicit a long-lasting learning deficit. Prior work has suggested that this deficit may reflect an overexcitation of spinal neurons akin to central sensitization, and that learning is inhibited by the saturation of plasticity. The experiments in this dissertation were designed to test the role of the cytokine tumor necrosis factor alpha (TNFa) in the induction and expression of the deficit. It is believed that the inflammatory properties of TNFa may mediate the excitatory processes that lead to maladaptive spinal functioning. Experiments 1 and 2 tested the necessity of endogenous TNFa in the deficit produced by uncontrollable shock. These experiments showed that the inhibition of endogenous TNFa blocks both the induction and expression of the shock-induced deficit, suggesting a necessary role for TNFa in mediating the inhibition of spinal learning. Conversely, Experiment 3 was designed to test the sufficiency for TNFa in producing a learning deficit. I found that treatment with exogenous TNFa undermined spinal learning in a dose-dependent fashion, whether given immediately, or 24 hours prior to testing. Experiment 4 demonstrated that the long-term TNFa-induced deficit is mediated by TNFa receptor activity, as a TNF inhibitor given prior to testing blocked the expression of this deficit. As TNFa has been shown to be predominantly of glial origin, I next assessed the role that glia play in the TNFa-induced deficit. Experiment 5 showed that inhibiting glial metabolism prior to TNFa treatment blocked the capacity for TNFa to produce a long-term deficit. Experiment 6 assessed the potential for TNFa inhibition to block the deficit induced by lipopolysaccharide (LPS), an agent known to induce TNFa. TNFa has also been shown to drive neural excitation by increasing the trafficking of calciumpermeable AMPA receptors to the active zone of the post-synaptic bouton. Experiment 7 showed that selectively antagonizing these receptors prior to testing blocked the TNFa- induced deficit, suggesting a possible post-synaptic mechanism by which TNFa exerts its effects. Finally, histological evidence was sought to reinforce the previous behavioral findings. Experiment 8 used quantitative RT-PCR to assess the differential expression of TNFa mRNA in uncontrollably shocked subjects as compared to those receiving controllable shock and no shock. To determine concentrations of TNFa protein, an ELISA was run in Experiment 9 comparing uncontrollably shocked subjects to unshocked controls.

The neural mechanisms underlying vocal motor control are poorly understood in mammalian systems. Particularly lacking are details pertaining to the mechanisms and neuroanatomical basis of sensory-motor integration and vocal plasticity, both of which are thought to be essential for evolutionarily advanced vocal behaviors like birdsong or human speech. Based on clinical evidence and imaging studies in humans, as well as its known significance for motor control in general, the basal ganglia (BG) have been hypothesized as a key site for audio-vocal integration, but direct evidence of this is lacking. In this dissertation, I will fill this gap by providing experimental evidence that the basal ganglia are an important component of the forebrain vocal motor pathway. First, I present two examples of vocal plasticity in Tadarida brasiliensis that can serve as powerful behavioral assays of audio-vocal integration. Secondly I provide evidence of BG functions in audio-vocal integration by knocking down striatal dopamine levels with the neurotoxin 1-methyl-4-phenyl-1,2,3,6 tetrahydropyrridine (MPTP). Finally, I will utilize the D1-type receptor specific agonist SKF82958 and antagonist SCH23390 to examine how the direct pathway of the BG regulates vocal production and sensorymotor integration. The behavioral results of these experiments indicate that the bats have a complex and context depended vocal response to noise stimuli that can be used to examine the neurological control of vocal plasticity. Further, the pharmacological evidence demonstrated that the BG was necessary for maintaining and modulating normal muscle force during vocal production. Finally, the mechanism of action in the basal ganglia was found to depend at least partly on activity at D1-type dopamine receptors. The results of this dissertation support the hypothesis that the BG is a critical structure in the modulation of vocal commands in the forebrain vocal-motor pathway. Pathological or pharmacological disruption of dopamine signaling severely degraded the bats abilities to produce natural sounding calls or make adaptive changes to the acoustic environment. These results have implications for research into the treatment of basal ganglia disorders such as Parkinson’s disease, providing an animal model for the study of hypokinetic dysarthria.

We utilize a simple instrumental (response-outcome) learning task to measure spinal plasticity in the isolated spinal cord. Peripheral uncontrollable nociceptive input has been shown to disrupt spinal instrumental learning and induce enhance tactile reactivity. In contrast, 1.5mA of continuous shock has been found to induce antinociception and protect spinal plasticity from the detrimental consequences of uncontrollable stimulation. The experiments of this dissertation examined the link between the beneficial effects of continuous stimulation and antinociception. The results replicated previous work examining the protective and antinociceptive effect of 1.5mA of continuous shock (Experiments 1-2). Novel to this research was the inclusion of a lower (0.5mA) intensity continuous stimulation. Results revealed that 0.5mA of continuous shock induced a comparable antinociception to that seen with 1.5mA of continuous shock (Experiment 1). At this lower intensity, however, continuous shock was unable to protect the isolated spinal cord from the detrimental effect of intermittent stimulation (Experiment 2). Further examination revealed that co-administration of intermittent and continuous shock did not affect continuous shockinduced antinociception. This was true at both the higher (1.5mA) and lower (0.5mA) intensities of continuous shock (Experiment 3). When 0.5mA of continuous shock was administered prior to intermittent shock, this intensity of continuous shock was better able to immunize the spinal cord from the induction of the learning deficit than 1.5mA (Experiment 4). Further analysis called into question the link between antinociception and the protective effect of continuous shock, as the beneficial effect of continuous shock outlasted the expression of antinociception (Experiment 5). Moreover, 0.5mA of continuous shock was found to reverse the expression of the learning deficit, when continuous stimulation was given after intermittent shock treatment (Experiment 6). While blocking the induction of antinociception was not sufficient to prevent the immunizing effect of continuous shock, data suggest that the mu opioid receptor is implicated in the beneficial impact of continuous stimulation (Experiments 7 and 8). Endogenous brain derived neurotrophic factor (BDNF) release was also found to play a role (Experiment 9). Moreover, continuous shock was found to down-regulate the expression of early genes implicated in the development of central sensitization, c-fos and c-jun. Finally, we found that while continuous stimulation was detrimental to locomotor recovery after spinal cord injury, the combined treatment of continuous and intermittent shock did not negatively affect recovery (Experiments 11 and 12).

This study presents a method for predicting the undrained behavior of plate anchors, including out-of-plane loading of simple plates and performance of suction embedded plate anchors (SEPLA). Three dimensional finite element models are used to investigate the behavior of square and rectangular plate anchors under normal loading with eccentricity in any direction. Upper bound analyses are performed for parallel loading and torsion loading. A simple model is then fit to the FE and upper bound solutions to determine required fitting parameters for both square and rectangular plates. The simple models can, in turn, be used both to predict anchor capacity and as yield surfaces for conducting plastic limit analyses, a method capable of predicting post yield anchor trajectory. The model predictions are shown in reasonable good agreement with the experimental results. For SEPLA, a theoretical model of plastic limit analysis is developed to predict the trajectory during the “keying” process and the ultimate capacity after the “keying” is complete. The predicted results are consistent with relevant known solutions.

The user programmable features (UPF) of the finite element code ANSYS® are used to generate a customized ANSYS-executable including a more general creep behaviour of materials and a damage module. The numerical approach for the creep behaviour is not restricted to a single creep law (e.g. strain hardening model) with parameters evaluated from a limited stress and temperature range. Instead of this strain rate - strain relations can be read from external creep data files for different temperature and stress levels. The damage module accumulates a damage measure based on the creep strain increment and plastic strain increment of the load step and the current fracture strains for creep and plasticity (depending on temperature and stress level). If the damage measure of an element exceeds a critical value this element is deactivated. Examples are given for illustration and verification of the new program modules.