Thesis (MSc)--University of Stellenbosch, 2005. / Bibliography. Also available via the Internet.

Thesis--University of California, Berkeley, 1962. / "UC-4 Chemistry" -t.p. "TID-4500 (17th Ed.)" -t.p. Errata sheet at end. Includes bibliographical references (p. 255-263).

Introduction: Cardiac hypertrophy is an adaptive response to increased myocardial workload that becomes maladaptive when hypertrophied hearts are exposed to an acute metabolic stress, such as ischemia/reperfusion. Acceleration of glycolysis occurs as part of the hypertrophic response and may be maladaptive because it enhances glycolytic metabolite accumulation and proton production. Activation of AMP-activated protein kinase (AMPK), a kinase involved in the regulation of energy metabolism, is proposed as a mechanism for the acceleration of glycolysis in hypertrophied hearts. However, this concept has not yet been proven conclusively. Additionally, several studies suggest that AMPK is involved in hypertrophic remodeling of the heart by influencing cardiac myocyte growth, a suggestion that remains controversial. Hypothesis: AMPK mediates hypertrophic remodeling in response to pressure overload. Specifically, AMPK activation is a cellular signal responsible for accelerated rates of glycolysis in hypertrophied hearts. Additionally, AMPK influences myocardial structural remodeling and gene expression by limiting hypertrophic growth. Experimental Approach: To test this hypothesis, H9c2 cells, derived from embryonic rat hearts, were treated with (1 µM) arginine vasopressin (AVP) to induce hypertrophy. Substrate utilization was measured and the effects of AMPK inhibition by either Compound C or by adenovirus-mediated transfer of dominant negative AMPK were determined. Subsequently, adenovirus-mediated transfer of constitutively active form of AMPK (CA-AMPK) was expressed in H9c2 to specifically increase AMPK activity and, thereby, further characterize the role of AMPK in hypertrophic remodeling. Results: AVP induced a metabolic profile in hypertrophied H9c2 cells similar to that in intact hypertrophied hearts. Glycolysis was accelerated and palmitate oxidation was reduced with no significant alteration in glucose oxidation. These changes were associated with AMPK activation, and inhibition of AMPK ameliorated but did not normalize the hypertrophy-associated increase in glycolysis. CA-AMPK stimulated both glycolysis and fatty acid oxidation, and also increased protein synthesis and content. Howver, CA-AMPK did not induce a pathological hypertrophic phenotype as assessed by atrial natriuretic peptide expression. Conclusion: Acceleration of glycolysis in AVP-treated hypertrophied heart muscle cells is partially dependent on AMPK. AMPK is a positive regulator of cell growth in these cells, but does not induce pathological hypertrophy when acting alone. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate

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Consumers associate meat color with quality. In some cases, especially in fresh and cured hams, the surface of a ham, whole, boneless or sectioned and formed displays a color gradient, which is unsightly and generally is considered of lower quality and must be discounted or processed different where color is less critical to the ultimate value of the resulting product. This disparity in color uniformity across fresh and cured products is sometimes known as two-toning and is most often found in the semimembranosus (SM) and associated muscles of fresh hams and is exacerbated with curing. The underlying color of fresh meat may be a function of postmortem metabolism or the underlying characteristics of those muscles involved. Therefore, the objective of this study is to determine the changes in underlying muscle type and postmortem metabolism in those muscles responsible for fresh ham color variation. Semimembranosus (SM) muscles of 15 mixed bred pigs were collected at 30 min and 1440 min postmortem, and muscle color was determined and muscles were collected and snap frozen for various energy metabolism analyses. Differences in color (L*, a* and b*) were noted across the face of the muscle by zone and time (P < 0.0001) but no differences were detected in pH and lactate, glucose, glucose-6-phosphate, and glycogen metabolisms. Glycolytic potential was also measured on a lactate basis and showed no differences across zone (P = 0.0746) but increased over time (P < 0.006). Lactate and pH were plotted and showed a linear relationship linear relationship (R2 = 0.928337) at 30 min (P < 0.0001) and at 1440 min (R2 = 0.161412; P < 0.0015). Muscle type characteristics showed no difference between zones and time. Buffering capacity showed a significant difference at pH 6 (P < 0.0359) and with time across all pH measured (P < 0.0001). These data suggest inherent differences, such as location and function, in the semimembranosus muscle may be more critical in developing fresh color than aberrations in postmortem metabolism. / Master of Science

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No description available.

Thesis (M.S.)--Brigham Young University. Dept. of Physiology and Developmental Biology, 2006. / Includes bibliographical references (p. 37-44).

Thesis (Ph. D.)--University of Washington, 2002. / Vita. Includes bibliographical references (leaves 115-132).

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