Cracked pavement slabs lead to uncomfortable and eventual unsafe driving conditions for motorists. Replacement of cracked pavement slabs can interrupt traffic flow in the form of lane closures. In Florida, the traffic demands are high and pavement repairs need to be carried out swiftly typically using concrete with high cement contents and accelerators to create rapid setting and strength gain. The concrete used in these pavement replacements is usually accompanied by a high temperature rise, making the replaced slabs susceptible to cracking. Cracking is a result of developed tensile stresses in the concrete, which exceed the concrete's tensile strength capacity. This research is being conducted to determine the risk of cracking for pavement slabs with varying dosages of chloride based accelerator used to promote high early strength. To analyze the effect of the accelerator, five different concrete mixtures including a control were assessed in a series of tests with varying accelerator dosages. Experiments included: mortar cube testing, concrete cylinder testing, autogenous deformation measured with a free-shrinkage frame, and restrained stress analysis using a rigid cracking frame. The findings indicate that accelerators are necessary to meet the strength requirements, and that the higher the accelerator dose, the higher the early shrinkage in the first 24 hours determined from the free shrinkage frame. Accidental overdose of the chloride-based accelerator results in the highest cracking potential and the highest shrinkage when tested under field generated temperature profiles.

Thesis (doctoral)--Universiẗat Frankfurt (Main), 2005. / Includes bibliographical references (p. ix-xxv).

Thesis (doctoral)--Universiẗat Köln, 2005. / Includes bibliographical references (p. 243-263).

Multiple sclerosis (MS) is an immune-mediated prevalent chronic demyelinating and neurodegenerative disease of the central nervous system that begins with an abrupt onset during early adulthood. MS is idiopathic, but many factors are thought to influence the pathogenesis of the disease, which include genetic, gender and environmental factors. To date, there is much evidence that suggest that both the onset and progression of MS is facilitated by both viral infections and stress. Theiler’s murine encephalomyelitis virus (TMEV) is a picornavirus that upon inoculation into susceptible strains of mice (i.e. SJL and CBA) causes a persistent infection which, in turn, results in an early acute encephalomyelitis followed by a late chronic immune-mediated demyelinating and neurodegenerative disease that pathologically resembles MS. In contrast, resistant mice (i.e C57BL/6 and BALB/c) are able to clear the virus from the CNS, and consequently do not develop chronic demyelination. Previous studies indicated that stress during early infection of susceptible mice can increase CNS viral titers and alter dissemination of TMEV, decrease early cytokine and chemokine expression in the spleen and CNS, and result in an exacerbated late demyelinating disease. The studies herein, focused on the hypothesis that chronic stress during early infection with TMEV infection would lead to drastic immunosuppression of both innate and adaptive arms of immunity, and that this immunosuppression may overcome the genetically controlled resistance of C57BL/6 mice to Theiler’s virus-induced demyelination. In these series of studies, we were able to show that stress, regardless of mouse strain susceptibility, decreases NK cell activity, and increased viral titers at day 1 p.i. Furthermore, after seven days of stress, susceptible mice demonstrated decreased virus specific T-cell effector function in both the CNS and spleens as indicated by a globalized reduction in type 1 and type 2 cytokines, as well as transcription factors. Importantly, these decreased responses were, in part, attributable to the actions of glucocorticoids. However, stress during early infection of C57BL/6 mice did not alter resistance to demyelination. These results begin to shed light on how stress, infection, and genetics can influence the onset of human MS.

Perfectionism is implicated in the onset, course, and remission of disordered eating (Bastiani, Rao, Weltzin, & Kaye, 1995; Bruch, 1979; Cockell et al., 2002; Stice, 2002; Tozzi, et al., 2005; Vohs, Bardone, Joiner, & Abramson, 1999; references are contained in Appendix F on p. 271). Building on the above research tradition, this dissertation proposed and evaluated a model relating perfectionism to binge eating. This new model is termed the Perfectionism Model of Binge Eating (PMOBE). According to the PMOBE, perfectionism confers vulnerability to binge eating by generating encounters with and by magnifying responses to specific triggers of binge eating: namely, perceived discrepancies, low self-esteem, depressive affect, and dietary restraint. <p>A multi-site, 7-day, web-based structured daily diary study was conducted to test the PMOBE. Overall, 566 female university students participated, and these individuals provided 3509 useable diary responses. A data analytic strategy involving structural equation modeling and multilevel modeling generally supported the PMOBE. For example, a structural model relating socially prescribed perfectionism (i.e., perceiving that others are demanding perfection of oneself) to binge eating through the aforementioned binge eating triggers demonstrated acceptable fit. Multilevel mediation also indicated that the influence of self-oriented perfectionism (i.e., demanding perfection of oneself) and socially prescribed perfectionism on binge eating operated through the abovementioned binge eating triggers (excepting dietary restraint). Support for multilevel moderation was limited, but suggested that the relationship between self-oriented perfectionism and binge eating was conditional upon dietary restraint. <p>This study is, to my knowledge, the first to examine the perfectionism-disordered eating connection using a structured daily diary methodology. Thus, this study offered a unique perspective apart from the usual cross-sectional and nomothetic research on perfectionism and eating pathology. In particular, this study suggested that, in their day-to-day lives, perfectionistic individuals (especially socially prescribed perfectionists) inhabit a world permeated with putative triggers of binge eating. Although perfectionism appeared to generate exposure to binge eating triggers, by and large, it did not seem to magnify responses to these same triggers (Bolger & Zuckerman, 1995, p. 890). A somewhat qualified version of the PMOBE was thus supported, with socially prescribed perfectionism assuming greater importance than self-oriented perfectionism and with perfectionism conferring vulnerability to binge eating by generating environments with, but not magnifying responses to, binge triggers. Overall, this dissertation contributed new knowledge to our understanding of the precipitants and the correlates of binge eating and highlighted the idea that perfectionism may play an important part in binge eating.

Perfectionism is implicated in the onset, course, and remission of disordered eating (Bastiani, Rao, Weltzin, & Kaye, 1995; Bruch, 1979; Cockell et al., 2002; Stice, 2002; Tozzi, et al., 2005; Vohs, Bardone, Joiner, & Abramson, 1999; references are contained in Appendix F on p. 271). Building on the above research tradition, this dissertation proposed and evaluated a model relating perfectionism to binge eating. This new model is termed the Perfectionism Model of Binge Eating (PMOBE). According to the PMOBE, perfectionism confers vulnerability to binge eating by generating encounters with and by magnifying responses to specific triggers of binge eating: namely, perceived discrepancies, low self-esteem, depressive affect, and dietary restraint. <p>A multi-site, 7-day, web-based structured daily diary study was conducted to test the PMOBE. Overall, 566 female university students participated, and these individuals provided 3509 useable diary responses. A data analytic strategy involving structural equation modeling and multilevel modeling generally supported the PMOBE. For example, a structural model relating socially prescribed perfectionism (i.e., perceiving that others are demanding perfection of oneself) to binge eating through the aforementioned binge eating triggers demonstrated acceptable fit. Multilevel mediation also indicated that the influence of self-oriented perfectionism (i.e., demanding perfection of oneself) and socially prescribed perfectionism on binge eating operated through the abovementioned binge eating triggers (excepting dietary restraint). Support for multilevel moderation was limited, but suggested that the relationship between self-oriented perfectionism and binge eating was conditional upon dietary restraint. <p>This study is, to my knowledge, the first to examine the perfectionism-disordered eating connection using a structured daily diary methodology. Thus, this study offered a unique perspective apart from the usual cross-sectional and nomothetic research on perfectionism and eating pathology. In particular, this study suggested that, in their day-to-day lives, perfectionistic individuals (especially socially prescribed perfectionists) inhabit a world permeated with putative triggers of binge eating. Although perfectionism appeared to generate exposure to binge eating triggers, by and large, it did not seem to magnify responses to these same triggers (Bolger & Zuckerman, 1995, p. 890). A somewhat qualified version of the PMOBE was thus supported, with socially prescribed perfectionism assuming greater importance than self-oriented perfectionism and with perfectionism conferring vulnerability to binge eating by generating environments with, but not magnifying responses to, binge triggers. Overall, this dissertation contributed new knowledge to our understanding of the precipitants and the correlates of binge eating and highlighted the idea that perfectionism may play an important part in binge eating.

Tonic immobility, TI, is an innate fear response in many vertebrate animals, induced by brief physical restraint. It is a widespread theory that chickens (Gallus gallus) reared under stressful conditions react stronger in tonic immobility tests, i.e. stay still and lay still for a longer period of time, than individuals reared under more stress-free conditions. In our study we attempted to see if stressful conditions early in life (temporary isolation from the flock on a daily basis) had any effect on how the individuals handled the stressful and fear-evoking experience of tonic immobility tests. A total of 77 chickens of the HyLine strain of White Leghorn were used. Three sets of tests were performed; first at the hatchery facility at Linköpings universitet; second after a stressful experience – the moving to the Wood-Gush facility at Vreta jordbruksgymnasium; and a random sample with about half of the birds the third time, also at Vreta. The results were inconclusive, but pointed more in the direction of the early-in-life stress having no effect on TI tests rather than the other way around.

Multiple sclerosis (MS) is an immune-mediated prevalent chronic demyelinating and neurodegenerative disease of the central nervous system that begins with an abrupt onset during early adulthood. MS is idiopathic, but many factors are thought to influence the pathogenesis of the disease, which include genetic, gender and environmental factors. To date, there is much evidence that suggest that both the onset and progression of MS is facilitated by both viral infections and stress. Theiler’s murine encephalomyelitis virus (TMEV) is a picornavirus that upon inoculation into susceptible strains of mice (i.e. SJL and CBA) causes a persistent infection which, in turn, results in an early acute encephalomyelitis followed by a late chronic immune-mediated demyelinating and neurodegenerative disease that pathologically resembles MS. In contrast, resistant mice (i.e C57BL/6 and BALB/c) are able to clear the virus from the CNS, and consequently do not develop chronic demyelination. Previous studies indicated that stress during early infection of susceptible mice can increase CNS viral titers and alter dissemination of TMEV, decrease early cytokine and chemokine expression in the spleen and CNS, and result in an exacerbated late demyelinating disease. The studies herein, focused on the hypothesis that chronic stress during early infection with TMEV infection would lead to drastic immunosuppression of both innate and adaptive arms of immunity, and that this immunosuppression may overcome the genetically controlled resistance of C57BL/6 mice to Theiler’s virus-induced demyelination. In these series of studies, we were able to show that stress, regardless of mouse strain susceptibility, decreases NK cell activity, and increased viral titers at day 1 p.i. Furthermore, after seven days of stress, susceptible mice demonstrated decreased virus specific T-cell effector function in both the CNS and spleens as indicated by a globalized reduction in type 1 and type 2 cytokines, as well as transcription factors. Importantly, these decreased responses were, in part, attributable to the actions of glucocorticoids. However, stress during early infection of C57BL/6 mice did not alter resistance to demyelination. These results begin to shed light on how stress, infection, and genetics can influence the onset of human MS.

Thesis (doctoral)--Universität Witten/Herdecke, 2005. / Includes bibliographical references (p. 13-33).

The experience of stress may contribute to increased food consumption and selection of unhealthy food options. Resource depletion theory suggests stress temporarily depletes resources needed to regulate behavior. Depletions of self-control may result in subsequent failure to regulate eating behaviors, which is particularly salient in restrained eaters. Restraint theory posits people high in dietary restraint require significant effort to control eating. Emotional eating theory further suggests palatable foods may be used to regulate emotional stress reactions. Relaxation exercises to mitigate stress reactions are recommended in eating and weight management programs, but lack quality scientific support. The current study examined the efficacy of a brief relaxation intervention on stress-related eating in a sample of at-risk women. Self-regulatory resources and affect were tested as mechanisms of action. A sample of 139 women high in dietary restraint completed a stress-task and were subsequently randomized to a relaxation intervention or control group. Participants were presented with foods varied on taste and fat content. Affect, subjective relaxation, and self-regulatory resources were measured at baseline, pre-, and post-intervention. Participation in a relaxation intervention resulted in significantly less food consumption (p < .05), with a trend toward lower consumption of sweet food (p = .05), compared to controls. Multiple mediator models examining proposed indirect effects of group on eating outcomes were not supported, with the exception of change in subjective relaxation as a significant indirect effect for high-fat food consumption. This study is the first to provide experimental evidence of the efficacy of relaxation in mitigating the effects of stress on eating. Limitations, implications, and future research directions are discussed.