M.Sc. / The current study sought to investigate the relationship between stress and illness, while examining the effects of daily stressors, depression, hardiness, social support and coping skills on this relationship. The information gathered was then used to design a time and cost effective questionnaire to predict people prone to stress-related illness. This questionnaire has been called the Stress Fitness Scale. The subjects (n = 44) were split into three groups (healthy, ill, and neither ill nor healthy) according to their scores on Gurin's Psychosomatic Symptom List for non-parametric statistical analysis. Scores on the Hardiness Scale, Perceived Social Support Friends and Family, Beck Depression Inventory, COPE, Hassles and Uplifts Scale and Life Experiences were analysed and significant differences were found between the ill and healthy groups in all five areas using a Mann-Whitney U test. An intercorrelation matrix was performed and significant correlation was found between Stress Fitness and the other scales, although not for all the sub-scales. Many of these correlations corresponded with the differences found between the two groups using the Mann-Whitney U test. Item analysis was performed on the Stress Fitness Scale. Significant inter correlation was found for all the items of the Prone sub-scale, and all but three items of the Protect sub-scale. Although further research is necessary, from this limited study the Stress Fitness Scale appears to provide a time and cost effective way of predicting people prone to stress-related illness.

Previous findings showed that mild chronic restraint stress causes motor impairments in rats. These behavioural impairments might be related to molecular changes in brain areas that regulate motor functions, such as the cerebellum. Little is known about the role of the cerebellum in stress-induced behavioural alteration. We hypothesized that alteration in animal behaviour after chronic restraint stress is due to brain-specific changes in miRNA and proteins encoding gene expression. Our results revealed that expression of three miRNAs and 39 mRNAs was changed significantly after two weeks of stress. Furthermore, we verified one putative target for one of the changed miRNAs and expression of four randomly selected genes. Changes in gene expression disappeared after two weeks of recovery from stress. These findings provide a novel insight into stress-related mechanisms of gene expression underlying altered behavioural performance. The observations bear implications for the prevention and treatment of stress-related disorders and disease. / xii, 109 leaves. : ill. ; 29 cm

Stress has been shown to exacerbate cell death and cognitive deficits after ischemic injury in rodents, however, little is known of the effects of stress on motor recovery. The objective of this present thesis is to examine the effects of chronic stress on skilled motor recovery after devascularization lesion in rats. It was found that pre-lesion stress induced the most behavioural impairments, while post-lesion stress exacerbated infarct volume. The effects of chronic multiple stress on skilled motor recovery after lesion was also examined. Chronic multiple stress did not modulate skilled motor recovery nor did it have any influence on infarct volume. Additionally, stress had effect on edema after devascularization lesion. The present thesis suggests that the time of exposure to chronic stress in respect to the ischemic lesion, in addition to the type of stress, will differentially affect recovery and compensation in rats. / xii, 122 leaves : ill. ; 29 cm.

M.A. / Die doel van hierdie studie was tweeledig van aard. Die eerste doelstelling was om 'n behoeftebepaling te doen ten einde vas te stel wat die pasiente se algemene behoeftes is ten opsigte van narkose. Die tweede doelstelling was om 'n streshanteringsprogram te ontwikkel, toe te pas op toepaslike proefpersone, en te evalueer aan die hand van vier afhanklike veranderlikes, naamlik angsvlak, pynvlak, irrasionele kognisies en lokus van kontrole. Hierdie streshanteringsprogram is ontwikkel om prakties uitvoerbaar en pasi ntvriendelik gerig te wees sodat die effektiwiteit. vir toekomstige volgehoue gebruik getoets kon word.

Stress-related cognitive changes are still a matter of debate. In some particular neuropathological conditions such as focal ischemia, cognitive functions have been shown to be significantly impaired. These conditions, however, may be improved by some factors such as steroid hormones. The purpose of the current thesis was to assess the structural and functional effects of corticosterone-related experiences on the hippocampus before and after endothelin-1 (ET-1)-induced stroke. We found corticosterone-related experiences enhance the hippocampal recovery, and improve its function in both wet and dryland tasks after ET-1-induced focal stroke. Structural and functional effects of such experiences prior to the focal ischemia in the hippocampus, however, showed that stress, not corticosterone is a strong inhibitor for hippocampal recovery. / xii, 252 leaves : ill. ; 29 cm. --

Indiana University-Purdue University Indianapolis (IUPUI) / Type 2 diabetes manifests from peripheral insulin resistance and a loss of functional beta cell mass due to decreased beta cell function, survival, and/or proliferation. Beta cell stressors impair each of these factors by activating stress response mechanisms, including endoplasmic reticulum (ER) stress. The glucolipotoxic environment of the diabetic milieu also activates a stress response in beta cells, resulting in death and decreased survival. Whereas the cell cycle machinery (comprised of cyclins, kinases, and inhibitors) regulates proliferation, its involvement during beta cell stress in the development of diabetes is not well understood. Interestingly, in a screen of multiple cell cycle inhibitors, p21 was dramatically upregulated in INS-1-derived 832/13 cells and rodent islets by two independent pharmacologic inducers of beta cell stress - dexamethasone and thapsigargin. In addition, glucolipotoxic stress mimicking the diabetic milieu also induced p21. To further investigate p21’s role in the beta cell, p21 was adenovirally overexpressed in 832/13 cells and rat islets. As expected given p21’s role as a cell cycle inhibitor, p21 overexpression decreased [3H]-thymidine incorporation and blocked the G1/S and G2/M transitions as quantified by flow cytometry. Interestingly, p21 overexpression activated apoptosis, demonstrated by increased annexin- and propidium iodide-double-positive cells and cleaved caspase-3 protein. p21-mediated caspase-3 cleavage was inhibited by either overexpression of the anti-apoptotic mitochondrial protein Bcl-2 or siRNA-mediated suppression of the pro-apoptotic proteins Bax and Bak. Therefore, the intrinsic apoptotic pathway is central for p21-mediated cell death. Like glucolipotoxicity, p21 overexpression inhibited the insulin cell survival signaling pathway while also impairing glucose-stimulated insulin secretion, an index of beta cell function. Under both conditions, phosphorylation of insulin receptor substrate-1, Akt, and Forkhead box protein-O1 was reduced. p21 overexpression increased Bim and c-Jun N-terminal Kinase, however, siRNA-mediated reduction or inhibition of either protein, respectively, did not alter p21-mediated cell death. Importantly, islets of p21-knockout mice treated with the ER stress inducer thapsigargin displayed a blunted apoptotic response. In summary, our findings indicate that p21 decreases proliferation, activates apoptosis, and impairs beta cell function, thus being a potential target to inhibit for the protection of functional beta cell mass.

Indiana University-Purdue University Indianapolis (IUPUI) / Diabetes mellitus affects an estimated 285 million people worldwide, and a central component of diabetes pathophysiology is diminished pancreatic islet beta cell function resulting in the inability to manage blood glucose effectively. The beta cell is a highly specialized metabolic factory that possesses a number of specialized characteristics, chief among these a highly developed endoplasmic reticulum (ER). The sarco endoplasmic reticulum Ca2+ ATPase 2b (SERCA2b) pump maintains a steep Ca2+ gradient between the cytosol and ER lumen, and while the Pancreatic and duodenal homeobox 1 (Pdx-1) transcription factor is known to play an indispensable role in beta cell development and function, recent data also implicate Pdx-1 in the maintenance of ER health. Our data demonstrates that a decrease of beta cell Pdx-1 occurs in parallel with decreased SERCA2b expression in models of diabetes, while in silico analysis of the SERCA2b promoter reveals multiple putative Pdx-1 binding sites. We hypothesized that Pdx-1 loss under inflammatory and diabetic conditions leads to decreased SERCA2b with concomitant alterations in ER health. To test this, siRNA-mediated knockdown of Pdx-1 was performed in INS-1 cells. Results revealed reduced SERCA2b expression and decreased ER Ca2+, which was measured using an ER-targeted D4ER adenovirus and fluorescence lifetime imaging microscopy. Co-transfection of human Pdx-1 with a reporter fused to the human SERCA2 promoter increased luciferase activity three-fold relative to the empty vector control, and direct binding of Pdx-1 to the proximal SERCA2 promoter was confirmed by chromatin immunoprecipitation. To determine whether restoration of SERCA2b could rescue ER stress induced by Pdx-1 loss, Pdx1+/- mice were fed high fat diet for 8 weeks. Isolated islets from these mice demonstrated increased expression of spliced Xbp1, signifying ER stress, while subsequent SERCA2b overexpression in isolated islets reduced spliced Xbp1 levels to that of wild-type controls. These results identify SERCA2b as a direct transcriptional target of Pdx-1 and define a novel role for altered ER Ca2+ regulation in Pdx-1 deficient states.

Sport and dance injuries have increased despite improvements in coaching techniques and medical care. Other factors, including psychological ones, were therefore thought to play a role in injury vulnerability. Most of the attempts to explain how psychological variables can affect an athlete's predisposition to injury have been based on anxiety or stress concepts. In this survey type study an interactive approach to stress has been adopted with the goal of finding a relationship between stress and injury in a group of professional ballet dancers. No simple direct relationship was found. Multiple regression analysis was performed and a more complicated relationship between stress indicators and injury was found. When an attempt was made to investigate the significant interaction, no significant correlations were found. However, the correlations were found to be large and negative. This could indicate that if the sample size had been larger significant correlations may have been found. / Psychology / M.A. (Psychology)

Sport and dance injuries have increased despite improvements in coaching techniques and medical care. Other factors, including psychological ones, were therefore thought to play a role in injury vulnerability. Most of the attempts to explain how psychological variables can affect an athlete's predisposition to injury have been based on anxiety or stress concepts. In this survey type study an interactive approach to stress has been adopted with the goal of finding a relationship between stress and injury in a group of professional ballet dancers. No simple direct relationship was found. Multiple regression analysis was performed and a more complicated relationship between stress indicators and injury was found. When an attempt was made to investigate the significant interaction, no significant correlations were found. However, the correlations were found to be large and negative. This could indicate that if the sample size had been larger significant correlations may have been found. / Psychology / M.A. (Psychology)