Lack of accurate data for epidemiological studies of low dose radiation effects necessitates development of dosimetric models allowing prediction of cancer risks for different organs. The objective of this work is to develop a model of the radiation response of human bronchiolar tissue with single cell resolution. The computer model describes epithelial tissue as an ensemble of individual cells, with the geometry of a human bronchiole and the properties of different cell types are taken into account. The model simulates the tissue kinetics and radiation exposure in four dimensions: three spatial dimensions and a temporal dimension. The bronchiole is modeled as a regular hollow cylinder with the epithelial cells of three different types (basal, secretory, and ciliated) lining its interior. For the purposes of assessment of radiation damage to the cells only the nuclei of the cells have been modeled. Subroutines describing cellular kinetics have been developed to simulate cell turnover in a normal epithelial tissue. Monte Carlo subroutines have been developed to simulate exposure to alpha particles; the GEANT4 toolkit has been used to simulate exposure to low LET radiation. Each hit cell is provided with a record of energy deposition, and this record is passed to the progeny if the cell survives. The model output provides data on the number of basal progenitor cells in different phases of a cell life-cycle and secretory to ciliated cell ratio after several generations of cell proliferation. The model calculates labeling and mitotic indices and estimates the average cell turnover time for the bronchiolar tissue. Microdosimetric calculations are performed for cells traversed by ionizing particles. The model will be used to assess the accumulation of damage in cells due to protracted low level radiation exposure. The model output may provide directions for the future experimental design.

Background: Prenatal ethanol exposure (PNEE) causes irreversible intellectual and behavioral disabilities, clinically known as fetal alcohol spectrum disorder. Few neuropathologic studies of human brain exist. Hypotheses: First, markers of oxidative stress persist following PNEE. Second, PNEE is associated with inhibitory and excitatory neuron changes. Methods: Human brain autopsies (153) with known PNEE were reviewed; 18 cases (fetus to adult) and controls were selected. Oxidative stress and neuronal differentiation markers were used for immunohistochemistry. Results: There were no obvious differences between control and PNEE brains using oxidative stress markers. In human PNEE brains, glutamatergic neurons were reduced 15.96 % and 18.03% in dentate gyrus and temporal cortex, respectively. GABAergic neurons reactive for parvalbumin were reduced in all hippocampal regions (CA1= 57.86%, CA3= 65.15%, and DG= 53.39%) and temporal cortex (44.13%) in all age groups. Conclusion: GABAergic neuron reduction in human following PNEE could explain motor and behavior distractibility in FASD individuals.

Recent investigations have suggested that the use of emotion-avoidance or emotion- suppression strategies to cope with anxiety contributes to the development and maintenance of anxiety disorders, and that substituting these strategies with emotional acceptance can lead to effective symptom reduction. We wished to consider whether attempts to suppress the negative emotions associated with exposure therapy would serve to impede emotional processing and symptom reduction, and conversely, whether acceptance of these emotions would augment treatment efficacy. Fifty-nine participants displaying marked claustrophobic fear were assigned to receive 30 minutes of exposure (enclosure in a small chamber) while receiving, A) instructions to accept and allow the experience of unpleasant emotions (ACC), B) instructions to control and suppress the experience of unpleasant emotions (SUP), or C) no instructions regarding emotion regulation (exposure only; EO). Outcome assessments were conducted prior to treatment, immediately following treatment, and at one-month follow-up, and included fear and heart rate reactivity in response to a behavioral approach test. We predicted that ACC participants would display greater reductions in claustrophobic fear than EO participants, and that EO participants would in turn display greater reductions in claustrophobic fear than SUP participants. These hypotheses were not supported. In addition, a detailed analysis of treatment process data was conducted. Peak fear ratings, claustrophobic threat expectancies, self-efficacy, and acceptance of anxiety were collected over the course of the treatment session, and hierarchical linear modeling (HLM) was used to produce individual growth curves for these variables. Three hypotheses were formulated: 1) ACC participants would display a more rapid improvement in these measures than SUP and EO participants, 2) threat expectancies, self-efficacy and anxiety would mediate reductions in fear over the course of treatment, and 3) mediational pathways would be moderated by treatment condition. Though no support was found for our first process hypothesis, treatment specific mediation was found. Among ACC participants, self-efficacy and suffocation expectancies mediated the session-fear relationship, and among EO participants, entrapment expectancies mediated this relationship. Among SUP participants, no significant mediators were identified. / text

Resilient and exposure-resilient functions are functions whose output appears random even if some portion of their input is either revealed or fixed. We explore an alternative way of characterizing these objects that ties them explicitly to the theory of randomness extractors and simplifies current proofs of basic results. We also describe the inclusions and separations governing the various classes of resilient and exposure-resilient functions. Using this knowledge, we explore the possibility of improving existing constructions of these functions and prove that one specific method of doing so is impossible.

Many children and adolescents in South Africa are being exposed as witnesses or are direct victims of violence in today's society. The purpose of this study is to explore what violent exposure adolescents have experienced and to develop a programme that includes coping skills, expression of emotion and communication. The research formed part of the FLAGH study. The research was done in the form of action research where the adolescents took part in the whole process of developing the programme. The study was done in four phases. In the first phase a random sample of 36 adolescents from Fikadibeng School in the North West Province were selected. They completed the Coping Responses Inventory-Youth Form, the Survey of exposure to community violence, Things I have seen and heard questionnaire and the Self-expression and control scales. In the second phase the programme was developed using the results of the pre-testing and a literature study on the effects of the exposure of violence on children. During the third phase the developed programme was pilot tested on a randomly selected group of the children and the post-testing took place in order to evaluate and adjust the programme according to the results found. Suggestion for the adjustment of the programme was done during the fourth phase of the study. Adolescents were largely exposed to community violence. They also displayed tendencies to internalize anger and used looking for guidance and cognitive avoidance as part of their coping repertoire. The programme proved to benefit the children in their coping with violence. It is recommended that for the future, larger groups of adolescents should be evaluated and programmes should be presented to a larger community in order to assist adolescent in their use of coping skills. / Thesis (M.A. (Clinical Psychology))--North-West University, Potchefstroom Campus, 2005.

No description available.

Maternal consumption of alcohol during pregnancy is associated with alterations in fetal development that negatively impact the offspring causing neurochemical and neurobehavioural dysfunction termed fetal alcohol spectrum disorders; the most severe outcome is fetal alcohol syndrome. Changes in maternal and fetal hypothalamic-pituitary-adrenal (HPA) axis activation, induction of cytochrome P450 2E1 (CYP2E1) enzyme activity and alterations in micronutrient status, including folate, following chronic ethanol exposure (CEE) are key contributors to the neuroendocrine and neurobehavioural effects observed in offspring. This study tested the following hypotheses: Maternal consumption of ethanol throughout pregnancy can: alter maternal and fetal HPA axis function and induce CYP2E1 enzyme activity in the third-trimester-equivalent; decrease folate status in the maternal-fetal unit, which can be mitigated by folic acid supplementation; and cause neurobehavioural deficits in offspring at low-moderate dose of maternal ethanol consumption. These hypotheses were tested in the guinea pig, a well established model of ethanol neurobehavioural teratogenicity. CEE had no effect on maternal HPA axis function at any gestational day (GD). Fetal cortisol was unaffected by CEE, but did increase with gestational age in both CEE and control. CEE increased maternal and GD 65 fetal liver CYP2E1 enzyme activity. Maternal supplementation with folic acid did not mitigate CEE fetal growth restriction, but did increase maternal red blood cell (RBC) folate at term. At term, maternal supplementation prevented the CEE-induced decrease in fetal liver folate, did not affect fetal RBC folate, and did not mitigate the nutritional-deficit-induced decrease in fetal hippocampal folate. Maternal consumption of 5% (v/v) ethanol decreased offspring birth weight, increased spontaneous locomotor activity, increased preference for ethanol, and delayed learning on day two of Morris water maze testing in young adult offspring. These data indicate that, in the guinea pig: there is a threshold blood ethanol concentration for HPA axis activation; CEE can induce CYP2E1 in the GD 65 fetus; folic acid supplementation is not protective in this model of CEE; and low-moderate CEE can cause neurobehavioural perturbations in offspring. / Thesis (Ph.D, Pharmacology & Toxicology) -- Queen's University, 2012-05-31 14:38:44.391

Basically, my dissertation focuses on License Auctions. Four chapters of my dissertation are theoretical analysis of license auctions. Broadly speaking, I analyze the effects of different auction rules on revenue, efficiency and social welfare. The first chapter studies the flaw in the design of the 2000 Turkish GSM auction. In this auction, the Turkish government wants to raise as much revenue as possible and to increase competition in the cell-phone market by selling two licenses to new firms via a sequential auction, but it ends up with only one license sold. I identify this auction design failure. And I also show that if the auction were designed as a “simultaneous auction”, the government would sell two licenses and receive more revenue. In the second chapter, I show that if the cost asymmetry between the bidding firms is large enough, then having fewer firms in the market will surprisingly result in higher social welfare. This result is contrast to the common or general case in which “social welfare” will be higher if there are more firms competing in the market. In the third chapter, I characterize the optimal bidding strategies of local and global bidders for two heterogeneous licenses in a multi-unit simultaneous ascending auction with synergies. I determine the optimal bidding strategies in the presence of an exposure problem and show that global bidders may accept a loss even when they win all licenses and moreover, if a “bid-withdrawal” rule is introduced to the auction, the exposure problem disappears, and the simulation results show that revenue will be higher. In the last chapter, I study the Canadian AWS auction in which 40 percent spectrum are set aside for new firms. I characterize the effect of spectrum set-aside auctions on seller's revenue, consumer surplus and social welfare. I show that a spectrum set aside may not only encourage new entry and increase competition in the downstream market, but also under some circumstance, decreases the seller's revenue and consumer surplus. But a spectrum set aside results in inefficient allocation, and this inefficient entry further reduces social welfare.

Environmental xenoestrogens (EEs) are chemicals that when they enter the body, the body responds to them as it would to endogenous estrogens. Humans are exposed to these chemicals on a daily basis via natural components, additives and contaminants in food and water, through the use of pharmaceuticals and personal care products such as sunscreens, lotions and toothpaste. Exposure to EEs is thought to result in adverse effects on humans such as decreased fertility, increased susceptibility to hormone-sensitive cancers, deformities of the male genitalia and precocious puberty in females. The critical window of exposure is thought to be early fetal development, when tissues are rapidly differentiating under the control of endogenous estrogens. However, there is limited data in the literature on human fetal exposure to EEs. The first objective of this study was to assess human fetal exposure to a suite of 35 EEs by analysis of paired samples of amniotic fluid and maternal urine were collected from 32 New Zealand women between 14 and 20 weeks gestation. The analytical chemistry methods required for this study were developed and validated. The results demonstrate that fetal exposure is highly correlated with maternal exposure. This study is the first to report maternal urine levels of two UV filters and amniotic fluid levels of parabens, UV filters and triclosan. A model based on simple additivity of effect was developed that combined the measured concentrations with literature data on relative estrogenic potency to assess the magnitude of the estrogen signal that may be attributed to the EEs. This model suggests that the fetus may experience an estrogen signal due to the measured EEs that could be as large as the endogenous estrogen signal. A second objective was to use computational docking to study the interactions of the EEs with the human estrogen receptor (hER) protein. The docking studies show that the rigid endogenous ligand, 17β-estradiol (E2) interacts with the hER to produce a single, well-defined complex with the receptor and the flexible EEs produce multiple, distinct energy-equivalent complexes. EEs are not able to interact with the binding cavity to stabilise the rigid hER-E2-like topology of the complex. As a result, the hER-EE complexes can be thought of as more pliable or ‘floppy’ and thus able to respond to the cell context in multiple ways, leading to variations in gene expression in different target tissues. These multiple pathways may explain the range of physiological responses attributed to exposure that depend on the timing of exposure and the sex of the individual exposed.

This thesis addresses the much needed quantitative assessment of the physiological effects the magnetic fields used in MRI. MRI has a well-earned reputation for being a safe, non-ionising alternative imaging modality for both the patient and MR practioner alike. Although the operating environment can prove hazardous for inexperienced and untrained personnel, appropriate training and adoption of safe working practices can prevent adverse incidents.