This study demonstrates that the ability of a polymeric sorbent to remove organic compounds from air or water can be selectively modified by chemically altering the surface of the sorbent. Amberlite XAD-4 was grafted with functional groups of varying size including: phosphonic acid, hydroxyalkylamine, polyamine, polyethylene glycol, hydrocarbon and halogenated hydrocarbon. Grafts were selected to provide a range of polarity as characterized by dipole moment, hydrogen bonding and Hildebrand solubility parameters. Homologous graft series of varied molecular weight were included to elucidate possible steric effects on selectivity of sorption Aqueous phase, monocomponent equilibrium isotherms were determined for phenol, methyl isobutylketone, 1,2-dichloroethane, toluene and benzene with a variety of grafted XAD-4 resins. Gas phase monocomponent sorption of toluene, carbon tetrachloride, and 2-propanol vapor from dry air by XAD-4 resins was evaluated from breakthrough curves. Grafting alters the sorptive capacity of XAD-4 as a function of steric factors, graft polarities and specific chemical bonding interactions. In this study, inhibition of sorption occurred when greater than 30% of the pendant groups of the original polymer were grafted or when the graft had more than eight atoms in its longest chain. Increasing similarity of graft and sorbate polar characteristics increased sorptive capacity relative to XAD-4. Conversely, decreasing similarity decreased sorptive capacity relative to XAD-4. Enhancement of sorption by grafts that can induce dipoles, or can form electron donor-acceptor complexes with sorbates, overwhelmed inhibition resulting from adverse steric or polar factors. Similarly, hydrogen bonding of water by hydrophilic grafts competitively inhibited sorption of various sorbates / acase@tulane.edu

Located in China's far southwest, the village of Manchunman is a popular tourist destination. The village is home to some 410 people, and has, according to legend, existed as a village since the time of the Buddha (5th century BC). Long known to artists and scholars for its rich Dai culture, legendary Buddhist temple and monastery, and picturesque setting along the Mekong River, the village of Manchunman began attracting tourists in the early 1990s. In 1998, drawn by the region's natural beauty, extraordinary preservation of ethnic markers, an increase in tourism, and the village's proximity to the prefectural capital of Jinghong, a Han Chinese company and a local state farm leased land from Manchunman and four neighboring villages, built a tourism center and an entrance gate, creating the area's first large-scale tourism development, called the Xishuangbanna Dai Minority Folk Customs Park In this dissertation, based on 15 months of fieldwork in Yunnan Province of southwest China, I explore the extremely intense negotiations of ethnic identity in the Park, where Dai villagers live their lives on the 'stage' of ethnic tourism, yet the Han (majority Chinese) management company inserts themselves as the 'directors' of the cultural performance of Dai culture. I demonstrate that the Dai Park acts as a living demonstration of all three inter-related components of ethnic tourism: the search for or display of the authentic or 'Otherness', the commodification of culture, and the performance of culture. In the village of Manchunman, ethnic tourism is no longer just the Dai vs. a faceless, commercialized world or a remote discourse of authenticity. Instead, as two parties---the Dai villagers and the Han management company---endeavor to represent and display Dai culture, the essence of Dai-ness is contemplated by both sides. I argue that the resulting intense negotiations of Dai ethnicity in the Dai Park go beyond the dichotomy of Primordial/Instrumental, resulting in a triangle in which Primordialism, Instrumentalism, and Performativity are bound together and are constrained within the overarching constructionalist viewpoint of the Park authorities / acase@tulane.edu

acase@tulane.edu

acase@tulane.edu

acase@tulane.edu

acase@tulane.edu

Zinc plays a major role in ethanol metabolism and a deficiency of this metal is a consistent finding in chronic alcohol abusers. The mechanism by which zinc deficiency would impart its deleterious effects was the thesis of this research In vivo ethanol metabolic rate is significantly decreased in zinc deficient animals. An adaptive increase in ethanol metabolic rate is observed in rats on chronic alcohol consumption; however, decreased ethanol metabolic rate is observed in zinc deficient alcoholic rats. This decrease in ethanol clearance is due to a decrease in the activity of a zinc metalloenzyme, hepatic alcohol dehydrogenase. Alcohol dehydrogenase (ADH) reversibly catalyzes the oxidation of ethanol to acetaldehyde. The optimum activity of the low Km mitochondrial aldehyde dehydrogenase is dependent on mitochondrial membrane integrity. Loss of membranous structure results in decreased acetaldehyde metabolism. Mitochondrial enzyme studies do indicate that mitochondrial structure may be compromised in zinc deficient alcoholic rats resulting in decreased in vivo aldehyde dehydrogenase activity. Impaired acetaldehyde metabolism would result in increased intracellular levels of acetaldehyde which in turn would inhibit ADH. Since ADH reversibly catalyzes oxidation of alcohol to acetaldehyde, an increase in in vivo acetaldehyde concentrations would also have an inhibitory effect on the enzyme's activity and contribute towards decreased alcohol metabolism The deleterious effects of alcohol abuse are believed to be due to lipid peroxidation mediated by free radicals. Mitochondrial and microsomal lipid peroxidation was not increased in zinc deficiency or chronic ethanol consumption but was significantly increased if the two factors were combined, i.e. in zinc deficient alcoholic rats. Activity of enzymes associated with mitochondrial and microsomal membranes were also decreased in zinc deficient alcoholic animals. This suggests that the membrane integrity of these subcellular fractions is impaired. An imbalance in free radical metabolism has been postulated as the underlying mechanism of lipid peroxidation. Microsomal mixed function oxidases are increased and antioxidant enzyme activities are decreased suggesting that there may be an increase in the free radicals, resulting in increased lipid peroxidation. Secondly, acetaldehyde is being increasingly suggested as a hepatotoxin. Increased concentrations of acetaldehyde in vivo in alcohol consuming zinc deficient animals may also contribute to ethanol induced toxicity by reacting with functional groups of various enzymes and rendering them inactive. (Abstract shortened with permission of author.) / acase@tulane.edu

acase@tulane.edu

Purpose. The purpose of this dissertation is to determine the efficacy of a novel aggressive method, which employs four basic theories of social work, for recruiting subjects to clinical trials Methods. Breast and prostate cancer patients were recruited in waves at 13 cancer centers for participation in a clinical trial. Each wave was randomly assigned to recruitment by the aggressive method (N = 85 breast cancer patients; N = 192 prostate cancer patients) or the passive control (N = 389 breast cancer patients; N = 443 prostate cancer patients) Results. The accrual for breast cancer patients recruited by the aggressive method was 48% compared to 26% for the passive method (p < .0001) The accrual for prostate cancer patients recruited by the aggressive method was 31% compared to 15% for the passive method (p < .0001) Discussion. The results demonstrate a highly significant advantage to employing the basic principles of social work in aggressive attempts to recruit subjects to clinical trials / acase@tulane.edu

Promoter recruitment to genes representing different paradigms of ERalpha promoter interaction was assessed to test the hypothesis that gene specific transcription by ERalpha is regulated by receptor phosphorylation that will, in turn, direct recruitment of specific coregulator proteins needed for gene expression. Using chromatin immunoprecipitation (ChIP), it was determined that there is a gene-specific and ligand-dependent recruitment of coregulators to ERalpha target genes. Increased recruitment of AIB-1 and NCoR was detected only at the c-myc AP-1 in response to 17beta-estradiol and at the pS2 ERE in response to 4-hydroxytamoxifen respectively. In addition, GRIP-1 recruitment was increased to cyclin D1 CRE only in response to 4-hydroxytamoxifen, but to the c-myc AP-1 in response to both 17beta-estradiol and 4-hydroxytamoxifen. Furthermore, siRNA-mediated down regulation of SRC-1, GRIP-1 and AIB-1, revealed the importance of these transcriptional coactivators in 4-hydroxytamoxifen-mediated transcriptional repression. For example, incubation of MCF-7 cells with 4-hydroxytamoxifen results in a significant decrease in gene expression. Downregulation of GRIP-1 by siRNA results in an increase in cyclin D1 gene expression levels in response to tamoxifen similar to that of cells incubated with vehicle Novel ERalpha phospho-specific antibodies and ERalpha phosphorylation site mutants were used to determine the impact of 17beta-estradiol and 4-hydroxytamoxifen on several aspects of ERalpha function. In response to 17beta-estradiol, increased phosphorylation at ERalpha Ser 118 and 305 and decreased phosphorylation of Ser 167 were detected. In response to 4-hydroxytamoxifen, increased ERalpha Ser 118, 167 and 236 phosphorylation was detected. An examination of ERalpha recruitment to target genes revealed that phosphorylation of the sites in the absence of ligand were retained in ligand-dependent ERalpha recruitment to target genes. For example in the absence of ligand and in the presence of 17beta-estradiol and 4-hydroxytamoxifen, ERalpha recruited to c-myc AP-1 is phosphorylated at Ser 167 and 305. The addition of 17beta-estradiol and 4-hydroxytamoxifen, however, resulted in the ligand-specific phosphorylation of additional sites. Importantly, effects of individual phosphorylation sites on ER(+) breast cancer cell proliferation were detected using transient transfection of single phosphorylation site mutants despite the fact that phosphoproteins, such as ERalpha, are often phosphorylated at multiple sites at the same time. Taken together, these results suggest that ERalpha phosphorylation directs a gene-specific recruitment of ERalpha and transcriptional coregulators to ERalpha target gene promoters / acase@tulane.edu