Thesis (M.Ag.Sci.)--University of Adelaide, Dept. of Animal Physiology,1980.

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In recent years, great advances have been made in the field of stem cell differentiation. Seminal insights in the area of developmental biology and tissue regeneration have made ex vivo differentiated cells a realistic alternative for transplantation applications. The recent application of these murine-based insights to human systems has paved new paths in autoimmune disease, chemotherapy, and immuno-deficiency research. Such strides would eliminate the hurdles associated with adoptive transfer including limited availability of transplantable cells, site morbidity, difficulties in cell isolation and expansion lag time. Current approaches in ex vivo hematopoiesis and T cell differentiation have begun to explore the effects of biomaterials on differentiation efficiency. These approaches, however, have not fully studied the quantitative effects of biomaterials and their properties on hematopoietic and T cell differentiation generation. Our goal was to design biomaterials whose properties could be tailored to improve differentiation efficiencies in T cell differentiation. Our work is dedicated to fabricating and characterizing Notch ligand functionalized microbeads for T cell differentiation applications. Our work has shown stable functionalization of Notch ligands on microbeads that can be quantitatively varied to achieve optimal Notch signaling. We have also demonstrated limited cellular toxicity and effective Notch signaling upon exposure to Notch ligand functionalized beads. Finally, we have successfully differentiated T cell progenitors from hematopoietic stem cells using the functionalized microbeads. As a side study, we have fabricated and characterized polymeric PLA scaffolds that were systematically varied and studied for their effects on hematopoietic differentiation efficiency. Insights gained from these studies should provide a better understanding of the microenvironmental signals in hematopoiesis and aid in the development of efficient technologies for the production of hematopoietic progenitors and T cells for therapeutic applications.

Thesis (Ph. D.)--University of Texas at Austin, 2007. / Vita. Includes bibliographical references.

Thesis (M.D.)--University of Adelaide, 1985. / Includes bibliographical references (leaves 1-14 of section Reference).

Thesis (Ph. D. in Biochemistry)--Vanderbilt University, Aug. 2008. / Title from title screen. Includes bibliographical references.

Thesis (Ph. D.)--Illinois State University, 1996. / Title from title page screen, viewed May 30, 2006. Dissertation Committee: H. Tak Cheung (chair), Herman E. Brockman, Alan J. Katz, Marjorie A. Jones, Brian J. Wilkinson. Includes bibliographical references (leaves 97-105) and abstract. Also available in print.

Bone circulation in Hemorrhagic Shock was studied in 35 male mongrel dogs. The term hemorrhagic shock is defined in this thesis as persistent profound hypotensive syndrome, due to acute hemorrhage of more than one third of blood volume. The method of induction of shock consisted of removal of one third of estimated blood volume (8% of body weight) at a rate of 25 - 50 ml/min, and subsequently dropping the systemic blood pressure in a stepwise manner until the maintaining level of 30 - 35 mmHg is reached. The central venous pressure, pulse and respiratory rates were also recorded. Bone circulation was studied by (1) recording the blood flow through a cannula inserted into the tibial nutrient vein or artery and (2) recording the intramedullary pressure of tibia. When one third of estimated blood volume was removed, the bone blood flow through the nutrient vessel decreased to 22.5 ± 3.4% of control level. The decreased bone blood flow persisted as long as the hemorrhagic shock was maintained for 4-18 hours. The decreased bone blood flow was also evidenced by a profound and persistent fall of the intramedullary pressure of bone. Reinfusion into the animal of lost blood within fifteen minutes to six hours after hemorrhage resulted in a complete or partial recovery of the control systemic blood pressure as well as the control rate of bone blood flow and the control level of intramedullary pressure of bone. The curve showing relationship between the changes in bone blood flow and the systemic blood pressure is an exponential one with concavity towards the flow axis. This indicates that bone has a vasomotor control mechanism of increasing peripheral resistance during hemorrhagic shock. This was substantiated by the following observations: (1) The severity of decrease in bone blood flow on the side of lumbar sympathectomy was much milder (16% less) compared to the side of the intact sympathetic nerve; (2) Dibenzyline (phenoxybenzamine) a sympatholytic drug or alpha-receptor blocking agent alters the pressure-flow curve of bone circulation in chock to a linear pattern which indicates that the drug blocks the bone vasoconstricting mechanism(s). It is concluded that bone blood flow decreases in hemorrhagic shock and is not merely due to a decrease in circulatory blood volume, but also due to sympathetic and catecholamine hormonal vasoconstrictor mechanisms. / Surgery, Department of / Medicine, Faculty of / Graduate

Thesis (Ph. D.)--University of Chicago, Dept. of Neurobiology, Pharmacology and Physiology, December 1999. / Includes bibliographical references. Also available on the Internet.

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