Magnesium, the second most abundant cation in the cell, is involved in a diverse range of biochemical activities. This project focuses on the mechanism of magnesium import into the cell through the action of Alr1p. Alr1p resides in the plasma membrane of yeast and belongs to the CorA-Alr1p-Mrs2p family of magnesium channels. Potential regulators of CorA were found through genetic screening and yeast two-hybrid screens have pulled out interactors of Alr1p. Interactors that influence Alr1p and its conformation will, with very high probability, also change the channel’s ability for magnesium import. Membrane proteins are not easily amenable to traditional yeast two-hybrid screens due to their hydrophobic nature. The goal of this thesis is to identify interactors of Alr1p using iMYTH, a modified yeast two-hybrid method. Of the eighteen Alr1p interactors identified, Vma3p and Vma11p, which are both subunits of the V-ATPase, showed the most promise for further Alr1p interaction characterizations.

国立情報学研究所で電子化したコンテンツを使用している。

Typescript. / Thesis (Ph. D.)--University of Hawaii at Manoa, 1979. / Bibliography: leaves 91-97. / Microfiche. / xii, 97 leaves ill. (some col.) 29 cm

Ultra Wideband (UWB) communication systems occupy large bandwidths with very low power spectral densities. This feature makes UWB channels highly rich in multipaths. To exploit the temporal diversity, a UWB receiver usually incorporates Rake reception. Each multipath in the channel carries just a fraction of the signal energy. This phenomenon dictates a Rake receiver with a large number of fingers to achieve good energy capture and output signal to noise ratio (SNR). Eventually, the Rake structure becomes very complex from analysis and design perspectives and incurs higher manufacturing cost. The first contribution of this thesis is to propose channel shortening or time domain equalization as a technique to reduce the complexity of the UWB Rake receiver. It is analyzed that most of the existing channel shortening equalizer (CSE) designs are either system specific or optimize a parameter not critical or even available in UWB systems. The CSE designs which are more generic and use commonly critical cost functions may perform poorly due to particular UWB channel profiles and related statistical properties. Consequently, the main contribution of the thesis is to propose several CSE designs to address the specific needs of UWB systems. These CSE designs not only exploit some general but also some UWB specific features to perform the task more efficiently. The comparative analysis of the proposed CSEs, some existing designs and the conventional Rake structures leads towards the conclusion. It is finally shown that the use of CSE at the receiver front end greatly simplifies the Rake structure and the associated signal processing.

Thesis (M.S.)--Auburn University, 2008. / Abstract. Vita. Includes bibliographical references.

Thesis (Ph. D.)--Johns Hopkins University, 1892. / Life. Reprinted from the Publications of the Modern Language Association of America, vol. X, no. 1. Bibliography: p. 12-16.

Master-Arbeit Universiẗat St. Gallen, 2009.

Thesis (Ph. D.)--University of Washington, 2005. / Vita. Includes bibliographical references (leaves 84-89).

Master-Arbeit Univ. St. Gallen, 2006.

In coordination with the New York City Medical Examiner's Office, we received the sequence of a mutated SCN5A gene that was found in a five-week-old girl who died in her sleep. SCN5A codes for the voltage-gated cardiac sodium channel alpha subunit (Nav1.5) and is responsible for the fast depolarization in phase zero of the cardiac action potential. The mutations that were present in the girl's SCN5A gene were a missense mutation, Q1832E, and a truncation mutation, R1944X. In order to gain an understanding of the conditions that led to the patient's death, we carried out a functional analysis on the mutant channels and measured how their properties differed from wild type Nav1.5 properties. For our functional analysis we carried out mutagenesis reactions to produce three experimental constructs in order to examine independent effects of Q1832E or R1944X, and to examine their interaction (mutant Nav1.5 that contains both Q1832E or R1944X; as was found in the genetic screen). These constructs were transfected into HEK 293 cells and studied using the patch clamp analysis using the whole cell configuration. Experiments were carried out to test the Nav1.5 current voltage relationships, the recovery from inactivation properties, and steady state inactivation properties. The data demonstrated that each of the three constructs resulted in a significantly reduced current density when compared to wild type Nav1.5 currents. The gating properties of the mutant channels were similar to those of wild type Nav1.5, though Nav1.5-R1944X did show a statistically significant slower recovery from inactivation than the wild type channel. Though more experimentation is needed to determine the mechanism behind the reduced current in the mutant channels, our data shows that each of the mutations is sufficient to produce a severely dysfunctional channel and this is likely the cause of the patient's death.