The roles of women, animals, and nature in traditional Japanese and Western folk tales continue to be parallel to the roles of women, animals, and nature in modern Japanese and Western Culture. This is a result of the values and morals that are encapsulated within these folk tales.

Bibliography : leaves 85-115

This thesis examines the struggle between the camps of narratology and ludology over video game narrative and what that struggle means for the existence of emergent narratives in video games. It argues that emergent narratives are clear and present in current video games but too stringent definitions can complicate their recognition. Emergent narratives are not flights of fancy but definable and repeatable narrative structures. / Video games can sustain a range of narrative structural possibilities, both unconventional and traditional, but perhaps the most interesting of these possibilities is an emergent narrative. Narrative emergence encompasses narrative structures where a player's choices drive and shape the events of the particular game's storyline. Video games support such narratives as the result of an interactive exchange between the computer game and its player. This thesis analyzes these interactive narrative exchanges as they occur in Tale of Tales' The Path, Bioware's Dragon Age: Origins, and other recent game titles in contrast with choices and structures from more traditional games. / Furthermore, this thesis discusses, with help from Psychoanalytic theory, why players seek out and play through emergent narratives. This structure's entrancing power embodies the strengths of narratives from mediums over. Players play to satisfy their own curiosity for knowing the end and feeling out death. When gamers play through emergent narratives, they play for a narrative and a final conclusion of their own making.

Freshwater mussels are in decline, with over 70% of North American species categorized as endangered, threatened or of special concern. In an effort to create a nonlethal protocol for health evaluation of freshwater mussels we conducted a series of investigations on wild and captive populations of Elliptio complanata. We tested a method for nonlethal hemolymph collection and found no growth or survival effects in 30 sampled animals relative to 30 controls. We surveyed unionid populations from 19 different stream reaches from a rural region of North Carolina to provide a set of baseline ranges for hemolymph composition in healthy populations. These parameters included hemolymph calcium, magnesium, phosphorus, cell count, glucose, aspartate aminotransferase (AST), ammonia and protein. We tested these parameters in a captive population held under relatively uniform conditions and found most stable over time. Delta 15N declined substantially over time in captivity, likely in response to a large change in environmental _15N signatures. We tested health parameters in three groups of Elliptio complanata after three months under low, moderate or high feed conditions. The treatment groups varied in hemolymph glycogen, magnesium, calcium and phosphorus concentrations and in foot tissue _15N and _13C, providing possible indicators of subtle change in nutritional condition. We also transplanted Elliptio complanata from a stream enriched in _15N-N03 to a relatively depleted stream and evaluated the lag time required for mussel nitrogen isotope signatures to reflect new environmental signatures. We found a slow turnover time but relatively little variability compared to water signatures, suggesting that bivalves may be useful indicators of chronic nutrient loading in rivers and streams. We conclude that, with further research, hemolymph can be a valuable and safe tool for assessment of freshwater mussel population and habitat health.

Previous studies by Stoker et al., (1999b) and Shyr et al., (1986) examined the role of the rat dam's prolactin (Prl) during lactation on subsequent development on the offspring. Shyr identified a critical role for milk-derived Prl in postnatal development of tuberoinfundibular dopamanergic neurons (TIDA) by dosing lactating dams with bromocriptine, a dopamine (DA) agonist, on postnatal day (PND) 2-5, and PND 9-12 to block the release of maternal Prl in the milk. Offspring deprived of milk Prl from PND 2-5 showed a decrease in DA concentration and turnover rate in the median eminence on PND 33-35, demonstrating the importance of Prl to normal TIDA development. Furthermore, this decrease in DA was associated with hyperprolactinemia in male offspring when serum concentrations were measured on PND 30-32. However, no disruption of the TIDA development was observed in dams dosed from PND 9-12, suggesting that PND 2-5 was a sensitive time point for normal development of TIDA neurons. Stoker et al., (1999b) found that exposure of the dam to atrazine during the first 4 days of lactation suppressed maternal suckling-induced prolactin release. Interestingly, this treatment also led to an increased incidence of lateral prostate inflammation in adult offspring. However, prostate inflammation was absent in the male offspring when the atrazine-treated dam was co-treated with ovine prolactin. These observations have led to the hypothesis that decreased maternal prolactin (following atrazine or bromocriptine exposure) will lead to impaired TIDA development and elevated levels of prolactin in the juvenile male offspring (as shown by Shyr et al., 1986 and Stoker et al., 1999b). The two basic assumptions of this hypothesis have yet to be examined and are the focus of this study. First, can an increase in the concentration of serum Prl be determined in male offspring of dams treated with atrazine during early lactation; and second, is there evidence of a decrease in TIDA neuronal activity (DA concentration and turnover) following atrazine exposure? The potential of this herbicide to affect hormones normally present in milk and transiently alter development of the human offspring may be of concern to human health. Lactating females were dosed from PND 1-9, twice a day with 12.5, 25, or 50 mg/kg atrazine or 0.209 mg/kg bromocritine (PND 1-5). Male pups were selected and killed two hours before lights were turned off (14:10 light cycle). Serum Prl and TIDA neuronal development results supported both basic assumptions. An increase in serum Prl in male offspring of both atrazine 12.5 mg/kg and bromocriptine-treated dams were identified on PND 12 and 35, which was also consistent with prior reports by Shyr et al. (1986). The increase in serum Prl also coincided with decreased TIDA neuronal activity on PND 35. However, a non-linear dose response was observed following atrazine exposure to the dam in both brain aminergic and serum Prl concentrations in the offspring. Also, both compounds caused significant changes in the developmental profiles of dopamine and dopaminergic activity in all three brain areas tested. Although the atrazine data revealed a non-linear dose response in the offspring, the fact that the lowest dose of this herbicide produced changes that were similar to the positive control suggests that indeed this complex mode of action is affected by atrazine-treatment. Due to the complexity of the maternal-neonatal unit, subsequent studies examining the offspring at a later age will be required.

Di(n-butyl) phthalate (DBP) is an antiandrogen with known human exposure. The objectives of this thesis were to investigate the development of male reproductive tract malformations secondary to in utero DBP exposure from the fetus to the adult, to characterize the effects of DBP on fetal testicular gene expression for the steroidogenic enzymes, and to further explore DBP?s potential for inducing Leydig cell adenomas following gestational exposure. In utero DBP exposure led to a characteristic set of fetal testicular lesions including large aggregates of fetal Leydig cells, multinucleated gonocytes, and increased numbers of gonocytes. In addition to the testicular effects, DBP also caused maldevelopment of the epididymides. During the early postnatal period the fetal testicular lesions became less apparent while decreased numbers of spermatocytes were observed. Underdeveloped epididymides noted in fetuses remained small or failed to fully develop resulting in epididymides with missing components. Malformed epididymides were fully manifest in the adult with absent portions observed both unilaterally and bilaterally. Testicular atrophy with loss of spermatocytes became more severe as gestationally exposed animals matured. Gene expression for the steroidogenic enzymes was examined in testes exposed to DBP in utero. Gene expression was decreased for P450 side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase, and P450c17; while mRNA expression for 17beta-hydroxysteroid dehydrogenase, which catalyzes the final step in testosterone biosynthesis, was not altered. In utero exposure to DBP failed to induce an increased incidence of classical Leydig cell adenomas. However, a dysgenetic lesion composed of numerous poorly differentiated Leydig cells surrounding immature seminiferous tubules was identified. Testicular dysgenesis was observed with a similar incidence between age groups in mature rats, which supports in utero induction by DBP rather than development over time. Together these data provide insight into the molecular mechanisms underlying the induction of DBP-initiated male reproductive tract malformations.

Pulmonary fibrosis is typically accompanied by inflammation, which is thought to play a role in its pathogenesis, and occurs with occupational exposure to particulates and metals, such as asbestos and vanadium pentoxide (V2O5). Lipopolysaccharide (LPS), a model of acute lung injury and inflammation, chronic bronchitis, and pulmonary fibrosis, upregulates platelet-derived growth factor receptor (PDGF-Rα) in rat lung fibroblasts (RLF). PDGF, a potent mitogen and chemoattractant for mesenchymal cells, is an important mediator in fibrotic lung diseases. This dissertation examines the effects of pre-existing inflammation, induced by LPS, on carbon nanotube (CNT)- and V2O5-induced pulmonary fibrosis in rats and the involvement of PDGF signaling. Rats were pretreated with 2.5 mg/kg LPS by intranasal aspiration, followed 24 hr later by 4 mg /kg CNT, carbon black (CB), or V2O5 administered by intratracheal instillation. Total and differential cell counts, lactate dehydrogenase (LDH), total protein, and PDGF and transforming growth factor-β (TGF-β) protein levels (by ELISA) were examined in bronchoalveolar lavage (BAL) fluid of control and CB- and MWCNT âexposed rats. Lungs from all animals were collected for histopathological analysis, immunohistochemistry, and qPCR of the Pdgf-a, Pdgf-c, Pdgf-rα, and Tgf-β genes. Pdgf-a, Pdgf-c, Pdgf-rα, Tgf-β, and Col1a2 gene expression was also measured in vitro in RLF and NR8383 rat alveolar macrophages in response to CNT or CB with and without LPS. In vivo, CNT and CB caused fibroproliferative, granulomatous lesions, which were located primarily in the alveolar ducts and alveoli. Pretreatment with LPS significantly increased collagen deposition associated with these lesions. In the BAL fluid, LPS pretreatment lead to increases in LDH, total protein, and PDGF-AA protein in rats exposed to MWCNT, and an increase in inflammatory cells in CB-exposed rats compared to controls. In vitro, LPS stimulated Pdgf-rα gene expression in RLF, and LPS and nanoparticles synergistically increased Pdgf-a expression in NR8383 cells. Combined LPS/V2O5 exposure augmented V2O5-induced pulmonary inflammation, airway epithelial necrosis, and fibrosis and amplified in vivo collagen gene expression. The airway lesions were of particular interest because LPS pretreatment increased the incidence of bronchiolitis obliterans-like lesions, including subepithelial fibrosis and intraluminal fibrotic polyps. These data confirm that LPS pretreatment augments the fibrotic effects of CNT and V2O5 in rats, which likely involves enhanced PDGF signaling. This dissertation provides evidence that pre-existing pulmonary inflammation, as occurs with chronic obstructive pulmonary diseases or cigarette smoking, can enhance pulmonary fibrotic responses to environmental agents. Furthermore, exposure to environmental LPS may play a role in the pathogenesis of some fibrotic lung diseases.

Extensive predator control programs and habitat alterations reduced red wolves, once native to the southeastern United States, to a remnant population found in only a small portion of their historic range by the late 1960?s. Coyotes expanded their range into territories previously occupied by red wolves. As wolves became scarce, they began to breed with the more prevalent coyote. Introgression threatened the continued existence of the genetic integrity of the red wolf. The U.S. Fish and Wildlife Service, following a planned extirpation and institution of a captive breeding program, reintroduced red wolves to northeastern North Carolina in 1987. Though surveys had shown no evidence of coyotes in the reintroduction area, coyotes expanded their range eastward and a small red wolf population again interfaced with an increasing coyote population. The movement of introgression within the red wolf population is akin to the movement of an infectious disease. Identification of ?infected? and ?non-infected? individuals is accomplished at an early age in this population through pup assessments in the den. Intervention is accomplished through the use of sterilized coyotes and coyote-wolf hybrids to prevent the spread of the ?disease? to ?susceptible? individuals. Understanding how the ?disease? moves through the population by describing movement rates and the potential for contact between ?infected? and ?susceptible? individuals is accomplished through the analysis of telemetry locations of radiocollared individuals. The model for this ?disease? is also presented and evaluated to determine the effectiveness of intervention strategies in controlling the spread of this ?disease?.

Ichthyobodo necator is a member of the Order Kinetoplastida and an important fish ectoparasite with a broad host and ecological range. When Ichthyobodo were exposed to the anesthetic tricaine, buffered with sodium bicarbonate, parasites remained attached to the skin of fish. When parasites were exposed to unbuffered tricaine, they detached almost completely from the skin. This finding indicated that tricaine should always be buffered when fish are to be clinically evaluated to prevent a reduction or complete loss in parasite load. Unbuffered tricaine was used to collect large numbers of parasites from the skin and gills of hybrid striped bass (Morone saxatilis male x M. chrysops female) for DNA isolation and analysis. A method for obtaining samples for DNA isolation without use of tricaine was also determined. Four preservation methods (Utermohl?s solution, ethanol, formalin, freezing) and two DNA isolation methods (DNA isolation kit, crude lysate) were examined. It was concluded that ethanol-fixation was the best preservation method for DNA isolation and PCR amplification of Ichthyobodo DNA. Using these methods, genomic DNA was isolated from Ichthyobodo trophonts collected from five freshwater and one marine fish. The 18S ribosomal RNA (rRNA) gene from each isolate was PCR amplified, cloned and sequenced. The 18S rRNA gene suggested that rather than being a single species, Ichthyobodo represented a complex of at least four different species, each of which occupied a distinct geographical region. The 18S rRNA gene was also amplified and cloned for related kinetoplastid speceis. Phylogenetic relationships within the Order Kinetoplastida (suborders Bodonina and Trypanosomatina) were determined. The suborder Bodonina appeared to contain at least 3 major lineages, none of which correlated with currently recognized families. Ichthyobodo had the most divergent sequence within the Bodonina, indicating it was the most genetically distinct bodonid currently known. The study of Ichthyobodo has contributed to a new understanding of phylogenetics and systematics for the Order Kinetoplastida, as well as insight into the potential for the spread of this parasite locally, nationally and internationally.

Airway remodeling observed in chronic inflammatory diseases of the respiratory system is characterized by mucous cell hyperplasia, smooth muscle cell proliferation and subepithelial fibrosis. Interleukin (IL)-13 is a central mediator in the pathogenesis of inflammatory airway diseases playing a significant role in epithelial remodeling. In this study, we examined mechanisms through which IL-13 induces proliferation of normal human bronchial epithelial (NHBE) cells maintained in air/liquid interface culture in vitro, a model that allows for the maintenance of differentiated structure and function. It was found that IL-13-induced proliferation of NHBE cells is mediated by the autocrine/paracrine action of transforming growth factor-a (TGFa) that is produced by the epithelial cells and subsequently binds to the epidermal growth factor receptor (EGFR) on these cells. IL-13-induced release of TGFa involves the rapid mobilization of intracellular stores of TGFa to the apical cell surface, where membrane bound TGFa is cleaved by tumor necrosis factor-a converting enzyme (TACE), resulting in released growth factor. Both neutralizing anti-TGFa antibodies and the EGFR tyrosine kinase inhibitor AG1478 block IL-13-induced proliferation in concentration-dependent manners. Additionally, IL-13 induces the activation of the mitogen activated (MAP) kinase pathway and the phosphatidylinositol 3-kinase (PI3K) pathway, both of which are required for IL-13-induced proliferation. However, activation of the MAP kinase pathway by IL-13 does not appear to be TGFa mediated, as neutralizing anti-TGFa antibodies and EGFR tyrosine kinase inhibitors have little effect on IL-13-induced MAP kinase. PI3K was found to be involved in IL-13-induced release of TGFa as the specific inhibitor of PI3K, LY294002, blocks release of the growth factor. In summary, IL-13-induced proliferation of NHBE cells involves the intracellular redistribution and subsequent TACE-mediated release of TGFa, an event mediated by PI3K. This proliferation then involves the interaction of TGFa with the EGFR and requires activation of both the MAP kinase and the PI3K signaling cascades. These data establish a mechanistic framework for further study into the effects of IL-13 on bronchial epithelial cells as well as additional cell types that may interact with IL-13, or growth factors induced by this cytokine, in an in vivo setting.