Thesis (Ph. D.)--School of Pharmacy and Dept. of Chemistry. University of Missouri--Kansas City, 2005. / "A dissertation in pharmaceutical sciences and chemistry." Advisor: Steven H. Neau and Thomas P. Johnston. Typescript. Vita. Description based on contents viewed Mar. 12, 2007; title from "catalog record" of the print edition. Includes bibliographical references (leaves 97-108). Online version of the print edition.

Propranolol (PROP) is a β-blocker prescribed mainly to treat human cardiac diseases but with its wide usage it often makes its way into the aquatic environment. This study examined whether PROP alters developmental patterns and catecholamine (CA)-regulated processes in the zebrafish (Danio rerio) and if exposure during early life alters the stress response and behaviors of adults. The 48 h LC50 was 21.6 mg/L, well above environmental levels (0.00059 mg/L). Embryos/larvae continuously PROP-exposed had decreased and increased transcript levels of the β1-adrenoceptor at 1 dpf and 5 dpf, respectively. Stressed, PROP-exposed zebrafish had reduced testosterone and estradiol levels and exhibited less anxiety behaviours than control fish. Furthermore, adults previously PROP-exposed as embryos/larvae had decreased growth in terms of body length (0.0006 mg/L PROP) and mass (20 mg/L PROP). Changes in cholesterol and testosterone levels occurred in PROP-exposed fish. Thus PROP-exposure alters developmental patterns and CA-regulated process that are essential for normal behaviours and responses to stress, and at least some of these changes persist in the adult zebrafish.

Diamagnetic measurements of poloidal beta have been performed in the STOR-M tokamak by a flux loop placed exterior to the vacuum chamber. Poloidal beta is defined as the ratio of plasma kinetic pressure to poloidal magentic field pressure. Compensation for the vacuum toroidal field has been performed using a non-enclosing co-planar coil, and vibrational compensation from auxiliary coils. It was found that in STOR-M conditions (20\% toroidal magnetic field decay over discharge) there is significant influence on the diamagnetic flux measurements from strong residual signals, presumably from image currents being induced by the toroidal field coils, requiring further compensation. A blank (non-plasma) shot is used specifically to eliminate the residual component which is not proportional to the toroidal magnetic field. Data from normal ohmic discharge operation is presented and calculations of poloidal beta from coil data ($eta_ heta simeq 0.5$) is found to be in reasonable agreement with the values of poloidal beta obtained from measurements of electron density and Spitzer temperature with neoclassical corrections for trapped electrons. Contributions present in the blank shot (residual) signal and the limitations of this method are discussed. A pulse with Compact Toroid Injection was examined and compared to a normal ohmic discharge, and one where the Compact Toroid Injector was used to supply the tokamak with neutral gas. Soft X-Ray (SXR) measurements were taken and compared. There is a strong agreement between the profiles of the poloidal beta and the SXR measurements. The bulk plasma thermal energy was measured and found to increase by 5.6 J following the injection of a CT. The diamagnetic measurements appear to be affected by image currents induced in the chamber walls by the plasma current, and also by plasma position fluctuations. Future work outlining the possibilty of compensating these currents and improving the measurements is presented.

Diamagnetic measurements of poloidal beta have been performed in the STOR-M tokamak by a flux loop placed exterior to the vacuum chamber. Poloidal beta is defined as the ratio of plasma kinetic pressure to poloidal magentic field pressure. Compensation for the vacuum toroidal field has been performed using a non-enclosing co-planar coil, and vibrational compensation from auxiliary coils. It was found that in STOR-M conditions (20\% toroidal magnetic field decay over discharge) there is significant influence on the diamagnetic flux measurements from strong residual signals, presumably from image currents being induced by the toroidal field coils, requiring further compensation. A blank (non-plasma) shot is used specifically to eliminate the residual component which is not proportional to the toroidal magnetic field. Data from normal ohmic discharge operation is presented and calculations of poloidal beta from coil data ($eta_ heta simeq 0.5$) is found to be in reasonable agreement with the values of poloidal beta obtained from measurements of electron density and Spitzer temperature with neoclassical corrections for trapped electrons. Contributions present in the blank shot (residual) signal and the limitations of this method are discussed. A pulse with Compact Toroid Injection was examined and compared to a normal ohmic discharge, and one where the Compact Toroid Injector was used to supply the tokamak with neutral gas. Soft X-Ray (SXR) measurements were taken and compared. There is a strong agreement between the profiles of the poloidal beta and the SXR measurements. The bulk plasma thermal energy was measured and found to increase by 5.6 J following the injection of a CT. The diamagnetic measurements appear to be affected by image currents induced in the chamber walls by the plasma current, and also by plasma position fluctuations. Future work outlining the possibilty of compensating these currents and improving the measurements is presented.

Capital Assets Pricing Model (CAPM) proposed by Sharpe (1964) is the most popular model for evaluation of expected returns. Based on CAPM, beta is the only cause for the expected return. However, Banz (1981) and Reinganum (1981) argue that firm size is also influential for asset returns even beta is controlled. The size effect is called an anomaly for the pricing model based on CAPM. Besides size, Fama and French (1992) show that the Book-to-Market ratio is also significant for the stock returns. Basically, the size and Book-to-Market challenge the role of beta in evaluating the expected returns of assets. Nevertheless, Kothari, Shanken and Sloan (1995) show that beta is the only cause of asset returns if longer holding returns are conducted in the tests of the pricing model. This thesis employs two kinds of length of holding return to examine the effects of size and beta in the asset returns. For shorter holding beta, we use the weekly data while we use monthly beta for longer holding return. We find that beta and size are both positively related to asset returns. No matter which length of holding return is applied. However, the positive relation between size and expected return in Taiwan needs further investigation.

Alzheimer¡¦s disease (AD), one of the most common dementia, is characterized by the formation two types of aggregation in the brain: senile plaques and neurofibrillary tangles (NFTs). NFTs are composed of hyperphosphorylated Tau. Tau protein mainly expressed in brain and was identified as one of the microtubule-associated proteins (MAPs). Hyperphophorylation on Tau affects its binding to tubulin and capacity to promote microtubule assembly. A number of proline-directed kinase capable of phosphorylating PHF-Tau have been identified, including Glycogen Synthase Kinase-3£] (GSK-3£]). Here we demonstrated that GSK3£] can co-purify with PHFs and can co-localize with Tau in vitro in N18 cells. To examine the phosphorylation mechanism of Tau by GSK-3£], N-terminal, C-terminal, T231A, T231E, 154~441, S396A, S400A, S404A, S413A and S396A S400A mutants of Tau were used, respectively. We were able to demonstrate that phosphorylation on Thr231 and Ser404 in Tau may play important roles for GSK3£] phosphorylation and its functional regulation. Most importantly, we have proved that T231P motif is necessary and critical for Tau phosphorylation by GSK3£]. Moreover, we used T231E, S396E and S400E mutants of Tau to understand the functional regulation of Tau by GSK3£] phosphorylation by tubulin assembly assay. Surprisingly, we observed all of these Tau mutants can promote tubulin assembly and form tubulin bundles in N18 cells. It has been proved that Pin1 WW domain can bind to Cdc2-phosphorylated Thr-231-Pro motif of Tau and restore the ability of Tau to promote tubulin assembly. In this study, we also studied whether Pin1 can regulate GSK3£]- phosphorylated Tau. The results show that Pin1 WW domain can bind to phosphorylated Thr-231 of Tau by GSK3£] and restore the ability of Tau to promote tubulin assembly.

Thesis (Ph.D.)--York University, 2008. Graduate Programme in Biology. / Typescript. Includes bibliographical references. Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR46006

Thesis (M. Sc.)--York University, 1999. Graduate Programme in Biological Science. / Typescript. Includes bibliographical references (leaves 71-85). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ39215.

Thesis (doctoral)--Universität, Hohenheim, 2001.

published_or_final_version / Medicine / Master / Master of Medical Sciences