Selenomethionine, an organic derivative of selenium, has been found to be the predominate selenium component of the dietary cancer chemopreventive agent selenized yeast that has been shown to decrease the incidence and mortality rate of lung, colon, and prostate cancers. Another organic selenium derivative found in the selenized yeast is Se-methylselenocysteine. However, the mechanism of action of the anti-cancer effects of these selenium compounds has yet to be identified. To evaluate the effects of these compounds on growth of the cancer cell types mentioned earlier, various cancer cell lines were treated with either compound. Both selenium compounds were able to induce growth inhibition and alterations in the cell cycle, with selenomethionine being the most potent. Previously, our laboratory has shown that treating cancer cells with selenomethionine depleted polyamines. Polyamines are cations that are needed for various roles in growth and proliferation. To extend these findings to an in vivo model, we gave selenomethionine in the diet (1ppm and 2ppm) for 16 weeks to male F344 rats in the azoxymethane (AOM) rat colon carcinogenesis model. The results showed no significant changes in colonic polyamine levels, however, there were significant changes in the development of microadenomas between control and treated groups. Selenomethionine was able to decrease the promotional effects of colon carcinogenesis through a polyamine-independent mechanism. Next, we tested the hypothesis that selenomethionine might affect cell growth by mechanisms involving cyclooxygenases, specifically the inducible isoform COX-2. Cyclooxygenases (COX-1 and COX-2) are enzymes that metabolize arachidonic acid to various prostaglandins. The human adenocarcinoma cell lines HT-29 and HCA-7, that express variable levels of COX-2, were treated for up to 6 days with selenomethionine. Selenomethionine induced growth inhibition in both cell lines and decreased COX-2 protein expression in the treated groups. Also, prostaglandin (PG) E2 levels were decreased in both treated groups at the latter timepoints. The HCA-7 cell line had a dose and time-dependent decrease in RNA levels treated with selenomethionine, whereas, no effects were observed on RNA expression of the HT-29 cell line. In summary, selenomethionine has chemopreventive effects in colon carcinogenesis by potentially modulating COX-2 proteins in cancer cells.

This study was designed to compare pain intensity during a clinical event (fingerstick) in children with Sickle Cell Disease (SCD) who have experienced recurrent episodic pain, against those children without SCD who have not experienced recurrent pain. A convenience sample of sixty-six 7--12 year old children was obtained, 33 with SCD from the sickle cell clinic and a matched (age, sex, ethnic origin) group of 33 children without SCD from the community. Pain intensity using the Coloured Analogue Scale (McGrath et al., 1996) and, medical fears using the Child Medical Fears Scale (Broome & Hellier, 1987) were measured following the fingerstick. The number of hospitalisations and the number of experiences with needles were examined for their relationship to pain intensity or medical fears. Multivariate analysis of variance revealed no significant differences in either pain intensity or medical fears between the two groups. There was a moderate, significant correlation between pain intensity and medical fears for the entire sample (r = .269, p < .03). Among children with SCD, those who had more than the median number of hospitalisations (6), reported lower medical fear scores (p < .01). This finding suggests adaptation on the part of these children to their chronic illness and to hospitalisations.

The object of this study was to investigate the scope of cognitive control over vestibulo-ocular reflex (VOR) performance during rotational vestibular stimulation. Human subjects, with head fixed to the body, were rotated in the dark through 20$ sp circ$ at 40$ sp circ$/s while trying to "look" at an earth-fixed target which was viewed straight ahead just before extinguishing the lights. During this rotation an apparent error of performance was systematically introduced by displacing this target at constant velocity through 12$ sp circ$, either in the same direction as the subject (Diminishing paradigm), or in the opposite direction (Augmenting paradigm). After cessation of rotation the target was re-illuminated and the subject allowed to see the final positional "error" of his/her oculomotor performance. During each trial they were asked either to try and CORRECT or NOT to CORRECT for the extrinsically induced "errors". In a subsequent, series of experiments, 2 hrs of synchronous rotation of the subject and the surrounding visual scene was used to produce adaptive attenuation of the VOR ($ approx$26%). The central component of the second experimental series was performance of the gaze stabilization test described above, conducted on the adapted subjects. (Abstract shortened by UMI.)

<p> The temporomandibular joint (TMJ) complex consists of the condyle, articular eminence, and articular disc. This disc divides the intracapsular components of the joint into upper and lower joint spaces. Magnetic resonance imaging (MRI) is considered the reference standard for soft tissue diagnosis of the TMJ. One aim of the study was to identify if an association exists between arthralgia of the TMJ and MRI identified joint effusion.</p><p> The clinical significance of identifying the presence of TMJ effusion on MRI lies in its potential association with inflammation, clinically assessed as pain at the lateral TMJ pole or around the pole area. Unfortunately the literature has been divided in asserting whether pain in the joint area is associated with the presence of MRI assessed effusion. A systematic review of the literature was unable to provide conclusive evidence for or against an association between TMJ pain and effusion.</p><p> Materials and methods: Clinical and imaging findings from 336 joints were obtained from a historical cohort involving individuals with temporomandibular disorders. Two by two tables of association were used to determine if clinical signs associated with arthralgia were associated with the presence of ipsilateral effusion in the TMJ. These clinical signs included pain on range of motion (maximum unassisted and assisted opening as well as excursive movements), TMJ manipulation (compression and translation), and palpation of the lateral pole of the TMJ and around the TMJ pole. In addition, a total pain score (range 0-7) was created which represented the sum of positive responses to pain on any of the clinical range of motion tests. Statistical testing included the T-test to test for possible association of joint effusion with any pain to these clinical measures.</p><p> Results: Statistical tests of association between joint effusion and range of motion, excursions, protrusion, joint manipulation and palpation all had p values > .05.</p><p> Conclusion: The results suggest that there is no statistically significant association between an MRI diagnosis of joint effusion and TMJ arthralgia. </p>

This study addressed the location of the breathing movement and its relationship to stress levels. Sixty-three Ball State students voluntarily participated by completing the A-State and A-Trait forms of the State-Trait Anxiety Inventory (STAI). Under the pretense that they would be questioned about music later, each participant also listened to preselected music for about 4 minutes in both seated and reclining positions. The participants were unaware that their breathing was being observed. During the listening portion of the study from behind a one-way mirror, 3 trained observers rated each breath as either thoracic or non-thoracic. The percentage of total breaths that were thoracic was calculated for each subject in both positions. Interrater reliability was determined inadequate for data of participants in the reclining position. The scores on the STAI and the percentage of thoracic breaths were the variables analyzed. A Pearson R correlation was then used to test the hypotheses. Null hypothesis 1, that there is no relationship between percentage of total breaths that are thoracic in a seated position and scores for AState, was upheld. Also, no relationship was found between percentage of total breaths that are thoracic in a seated position and scores for A-Trait, therefore, null hypothesis 2 was also upheld. This study also found that 71% of the participants breathing style is primarily thoracic. These findings and procedural effects on the outcome as well as implications for further research were discussed. / Fisher Institute for Wellness

vi, 508 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Psychiatry, 1974

Thesis (Ph.D.)--Pacific Graduate School of Psychology, 1995. / Source: Dissertation Abstracts International, Volume: 56-10, Section: B, page: 5768. Chair: Dolores Gallagher-Thompson.

Thesis (Ph.D.)--The University of Alabama at Birmingham, 2006. / (UMI)AAI3226737. Adviser: Mary M. Boggiano. Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 4147.

Thesis (Ph.D.)--Fairleigh Dickinson University, 2005. / Source: Dissertation Abstracts International, Volume: 65-11, Section: B, page: 6086. Chair: Christopher A. Capuano. Available also in print.

<p> Basal forebrain corticopetal cholinergic neurons are critical for contextual and cued fear memory in the conditioned suppression paradigm, but neural mechanisms that alter these neurons in fear memory remain unknown. Interestingly, basal forebrain cholinergic lesions have no effect on behavioral performance in commonly-studied fear conditioning paradigms like Pavlovian conditioned freezing or fear-potentiated startle, yet impair fear memory in the conditioned suppression paradigm. Many studies conducted have experimented with lesions of cell bodies of corticopetal cholinergic neurons in the nucleus basalis magnocellularis (NBM), but there is a void in the literature defining which specific projections may be responsible for their discrepant role in different fear memory paradigms. The basal forebrain projects to the anterior cingulate cortex (ACC), a subregion of the medial prefrontal cortex. The ACC is a well-established portion of the fear circuit across all fear conditioning paradigms and has a clear role in decision-making in the conditioned suppression paradigm. Given the role in choice conflict that the ACC plays in operant tasks involved in the conditioned suppression paradigm, it is plausible that it may be a region that allows basal forebrain cholinergic neurons to alter a fear memory in the conditioned suppression paradigm. The goal of this study is to examine the specific roles that basal forebrain cholinergic projections to the ACC play in fear memory, specifically in the conditioned suppression paradigm. These lesions may target specific cholinergic input to the ACC from the NBM in the basal forebrain and this may isolate a specific fear circuit involved in fear memory in the conditioned suppression paradigm. Data have suggested that ACC lesioned animals demonstrate less fear-conditioned suppression over sham animals, but further experiments and cohorts of animals are required. If ACC cholinergic lesions are shown to produce deficits in fear memory in the conditioned suppression paradigm, it may suggest that the presence of the appetitive task, which only occurs in the conditioned suppression paradigm and not in any of the other commonly studied fear paradigms, may be able to elicit changes in functional connectivity to incorporate this projection from the NBM to the ACC to the fear circuit. Discrepancies in fear memory between fear conditioning paradigms demand to be addressed because assumptions about functional connectivity across different paradigms are assumed to be similar in the literature. If the notion of paradigmdependent functional connectivity presented here is true, deductions about this functional connectivity may only be made in the context of one fear paradigm and may not necessarily be applicable across paradigms. In other words, to say that Pavlovian fear conditioning and fear-potentiated startle are indicative of the broad neurobiology of fear memory would only be looking at a fraction of the reality behind how fear circuitry operates. In order to further the literature to propose holistic circuits, molecular processes and constructs that apply to all fear memory regardless of protocol or paradigm, it is necessary to investigate neural involvement across alternative fear paradigms, like conditioned suppression. This study supports the novel idea that neural circuitry that supports fear can expand with new learning tasks or events and therefore, may be more susceptible to change than previously considered, but future studies are required</p><p>