by Chan, Ting Wah Victor. / Bibliography: leaves 131-149 / Thesis (M.Phil.) -- Chinese University of Hong Kong, 1983

by Lam Wai Pui. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 146-170.

by Choy Wing Yiu. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 115-121). / DESCRIPTIVE NOTE --- p.iii / ACKNOWLEDGEMENTS --- p.v / Chapter CHAPTER ONE: --- BRIEF REVIEW OF THE WATR-CPMG AND OTHER SOLVENT SUPPRESSION METHODS --- p.1 / Chapter 1.0 --- Introduction --- p.1 / Chapter 1.1 --- Some Common Solvent Suppression Techniques --- p.2 / Chapter 1.1.1 --- Brief Summary of Some Common Solvent Suppression Techniques --- p.2 / Chapter 1.1.2 --- Criteria for the Evaluation of Solvent Suppression Methods --- p.8 / Chapter 1.2 --- Application of the WATR-CPMG Method in Solvent Suppression --- p.10 / Chapter 1.2.1 --- The CPMG Pulse Sequence --- p.10 / Chapter 1.2.2 --- The Theory of Solvent Suppression by WATR Method --- p.12 / Chapter 1.3 --- Scope of this Thesis --- p.15 / Chapter CHAPTER TWO: --- OPTIMIZATION OF WATR-CPMG PARAMETERS FOR QUANTITATIVE ANALYSIS IN DILUTE AQUEOUS SOLUTION --- p.19 / Chapter 2.1 --- Investigation of the WATR-CPMG Parameters --- p.19 / Chapter 2.1.1 --- Use of Ammonium Chloride as Proton Exchange Reagent --- p.19 / Chapter 2.1.2 --- The pH Dependence of the Proton Exchange Process --- p.21 / Chapter 2.1.3 --- Relaxation Delay Time --- p.27 / Chapter 2.1.4 --- Measurement of T1 of Protons In Aqueous Solution --- p.31 / Chapter 2.1.5 --- The position of the Carrier Frequency --- p.41 / Chapter 2.1.6 --- Modelling of the Off-Resonance Effect --- p.46 / Chapter 2.1.7 --- The Tau Value Used in the WATR-CPMG Method --- p.51 / Chapter 2.2 --- The Setting of Acquisition Parameters and Data Processing --- p.57 / Chapter 2.2.1 --- Digital Resolution and Spectral Width --- p.57 / Chapter 2.2.2 --- The Setting of Receiver Gain --- p.60 / Chapter 2.3 --- Summary --- p.61 / Chapter CHAPTER THREE: --- APPLICATION OF THE WATR-CPMG METHOD TO THE QUANTITATIVE ANALYSIS OF GLUCOSE IN BLOOD PLASMA AND DILUTE AQUEOUS SOLUTION --- p.62 / Chapter 3.0 --- Introduction --- p.62 / Chapter 3.1 --- Experimental Section --- p.62 / Chapter 3.1.1 --- Characterization of the Metabolites in Blood Plasma --- p.62 / Chapter 3.1.2 --- Reagents --- p.66 / Chapter 3.1.3 --- Solution Preparations --- p.66 / Chapter 3.1.4 --- Measurement of Plasma Glucose by Glucose Oxidase Method --- p.67 / Chapter 3.1.5 --- NMR Measurement --- p.68 / Chapter 3.1.6 --- HPLC Measurement --- p.78 / Chapter 3.2 --- Results and Discussion --- p.79 / Chapter 3.2.1 --- Analysis of Results --- p.79 / Chapter 3.2.2 --- Discussion --- p.84 / Chapter 3.2.3 --- Conclusion --- p.85 / Chapter CHAPTER FOUR: --- HOMODECOUPLED WATR-CPMG METHOD --- p.86 / Chapter 4.0 --- Introduction --- p.86 / Chapter 4.1 --- Application of Combined Time Sharing Homodecoupling WATR-CPMG Method for Quantitative Analysis in Aqueous Solution --- p.87 / Chapter 4.1.1 --- The Time Sharing Homonuclear Decoupling and Average Hamiltonian Theory --- p.87 / Chapter 4.1.2 --- Homodecoupling in Aqueous Solution --- p.89 / Chapter 4.2 --- Experimental --- p.90 / Chapter 4.2.1 --- The Preliminary Investigation --- p.90 / Chapter 4.2.2 --- Homodecoupl ing in 30%D20/70%D20 Solution --- p.97 / Chapter 4.2.3 --- Homodecoupling-CPMG (HDCPMG) in Quantitative Analysis --- p.102 / Chapter 4.3 --- Conclusion --- p.110 / Chapter CHAPTER FIVE: --- CONCLUSION --- p.113 / BIBLIOGRAPHY --- p.115 / APPENDIX I The Computer Simulation of the Off-Resonance Effect on the Water Signal Suppression --- p.122 / APPENDIX II The Computer Simulation Program --- p.125 / APPENDIX III The Simulation Data --- p.129

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Upon the loss of glucose as the main carbon source cells have developed different mechanisms in order to adapt to this stress and promote survival. In Saccharomyces cerevisiae one such mechanism is acetylation, a post-translational modification performed by a lysine acetyltransferase (KAT) complex, such as NuA4, which has been previously shown to regulate different glucose metabolic pathways. Despite its known role upon glucose starvation, it is not currently understood how NuA4 itself is regulated in response to acute glucose deprivation (GD). I determine here that NuA4 complex protein levels (including catalytic protein Esa1), structure, activity, and localization are not impacted by acute GD. Despite GD showing no impact to NuA4 itself, it does result in the remodelling of both the interactome and acetylome of the complex where 160 proteins were identified to change interaction with Esa1-TAP and 93 acetylation sites were identified. As well GD results in a shift in localization of interacting proteins from nuclear upon standard growth to cytoplasmic. As well the changing interactome shows enrichment for proteins related to regulation of transcription and translation, metabolic pathways like glycolysis and gluconeogenesis, and others related to the cellular stress response. From the interactome three sets of proteins, Pab1, Eaf5/7/3, and Fas1 and Fas2, were studied further to greater characterize their interaction with NuA4 as they change interaction upon GD. Eaf7 protein levels were shown to decrease upon GD and both Fas1 and Fas2 levels were shown to increase in response to NuA4 deletion mutants. Together this work provides a greater understanding of the cellular response to acute GD stress, and how NuA4 plays a role in response to that stress in order to promote cell survival.

No description available.

Graduation date: 1995

Graduation date: 1995

Thesis (M.S.)--Oregon State University, 2007. / Printout. Includes bibliographical references (leaves 111-114). Also available on the World Wide Web.

Horses with high energy requirements are generally fed two large concentrate meals per day, either in the form of grain or pellets. The postprandial elevation of blood glucose resulting from this type of feeding has the potential to alter production of hormones such as leptin. Leptin is an adipose-derived protein that promotes satiety in normal animals. The objective of this study was to determine if feeding large amounts of concentrate twice each day would alter serum leptin concentration. Nine horses were placed into three groups (A, B, and C) and each group was rotated through three feeding schedules (2x, 3x, and 4x) in a 3 x 3 Latin square design. Horses were fed twice per day on the 2x schedule, three times per day on the 3x schedule, and four times per day on the 4x schedule. Horses were fed the same total amount of concentrate per day throughout the study, although meal size varied with the number of times the horse was fed per day. Horses were weighed and scored for body condition on the first day of each period. Each treatment period lasted for 11 days. Blood was drawn on days one, four, and seven of each period and leptin concentration was determined by radioimmunoassay. On the afternoon of the tenth day of each period, horses were fitted with jugular catheters and blood was drawn every two hours for 24-hours to determine the circadian rhythm of leptin secretion. Additionally, blood was taken 30 minutes prior to and every 30 minutes after the morning meal to determine postprandial plasma glucose concentrations. Mean and peak glucose values were higher on the 2x schedule than the 3x or 4x schedules (P < 0.05). Leptin concentration was highest in horses on the 3x schedule, although when these data were normalized to baseline (day one) values, leptin was highest on the 2x schedule (P < 0.05). Serum leptin concentration was highly correlated with body condition score (P < 0.01), but not gender (P = 0.82), and leptin increased throughout the study (P < 0.05). Data from the 24-hour collection showed that serum leptin concentration varied with time in horses on the 2x but not the 4x schedule (P < 0.05). Linear regression of data from the 2x schedule indicates that the pattern of change may be modeled by a quadratic equation (P < 0.05). This study demonstrates that feeding horses large carbohydrate meals twice per day disrupts the normal pattern of leptin in the horse, possibly affecting appetite and other physiological processes.