Thesis (Ph.D.)--University of Wisconsin--Madison, 2007. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (p. 143-152).

Thesis (Ph.D.)--University of Wisconsin--Madison, 2007. / Includes bibliographical references (p. 143-152). Also available on the Internet.

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Chan Kin Fai. / "April 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 151-157). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

"July 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

The synthesis of several dihydrofurans of type 179 was accomplished by the flash vacuum pyrolysis of vinyloxiranes of type 178 obtained from the addition of the dienolate of ethyl-2-bromocrotonate (177) to various aldehydes (176). Thus, dihydrofurans were prepared from aldehydes in an overall intermolecular [2+3] dihydrofuran annulation. / Master of Science

The interactions of a model synthetic liquid fuel reactant (furan) with a model hydrodeoxygenation catalyst (clean and sulfided single crystal molybdenum) were investigated using the following UHV tools: Auger electron spectroscopy (AES), low energy electron diffraction (LEED), and temperature programed reaction spectroscopy (TPRS). In addition to furan, the reactions of hydrogen, carbon monoxide, ethylene, and propene on clean and sulfided Mo(110) were also examined. All adsorbates exposed to the extremely reactive clean or sulfided Mo(110) surface decomposed, yielding gaseous H��� and surface C. In addition, furan TPRS caused the production of gaseous CO. The presence of background hydrogen caused no major changes in the TPRS of furan or the other adsorbates. Sulfur pre-adsorption caused the chemical shifting of H��� TPRS peaks. Both sulfur and carbon pre-adsorption resulted in the Van der Waal's radius blocking of adsorption sites for all adsorbates studied. / Graduation date: 1997

The aryl hydrocarbon receptor (AHR) mediates the toxic effects of halogenated aromatic hydrocarbons (HAHs), including 2,3,7,8-tetrachlorodibenzo-p-dioxin, 2,3,4,7,8-pentachlorodibenzofuran and 2,3,7,8-tetrachlorodibenzofuran. Y322 is believed to play a role in binding-independent activation of AHR by atypical inducers, such as omeprazole. I examined AHR-mediated regulation of and coactivator recruitment to CYP1A1, CYP1B1, HES1 and TiPARP in T-47D and HuH7 cells. All compounds induced expression of each gene in both cell lines, with some temporal differences between the HAHs and omeprazole. Chromatin immunoprecipitation assays demonstrated activator-, cell line- and gene-selectivity in AHR coactivator recruitment. Omeprazole induced AHR degradation which was prevented by MG-132 pre-treatment. Y322 was found to be important for maximal AHR activation by 2,3,7,8-TCDD and 2,3,4,7,8-PeCDF, but required for 2,3,7,8-TCDF and Omp in an AHR-deficient MCF-7 cells. My findings provide further evidence for cell-, gene- and ligand-dependent differences in AHR-mediated gene expression and coactivator recruitment, and a role for Y322 in AHR activation.

The aryl hydrocarbon receptor (AHR) mediates the toxic effects of halogenated aromatic hydrocarbons (HAHs), including 2,3,7,8-tetrachlorodibenzo-p-dioxin, 2,3,4,7,8-pentachlorodibenzofuran and 2,3,7,8-tetrachlorodibenzofuran. Y322 is believed to play a role in binding-independent activation of AHR by atypical inducers, such as omeprazole. I examined AHR-mediated regulation of and coactivator recruitment to CYP1A1, CYP1B1, HES1 and TiPARP in T-47D and HuH7 cells. All compounds induced expression of each gene in both cell lines, with some temporal differences between the HAHs and omeprazole. Chromatin immunoprecipitation assays demonstrated activator-, cell line- and gene-selectivity in AHR coactivator recruitment. Omeprazole induced AHR degradation which was prevented by MG-132 pre-treatment. Y322 was found to be important for maximal AHR activation by 2,3,7,8-TCDD and 2,3,4,7,8-PeCDF, but required for 2,3,7,8-TCDF and Omp in an AHR-deficient MCF-7 cells. My findings provide further evidence for cell-, gene- and ligand-dependent differences in AHR-mediated gene expression and coactivator recruitment, and a role for Y322 in AHR activation.