Thesis (M.S.)--West Virginia University, 2002. / Title from document title page. Document formatted into pages; contains xv, 142 p. : ill., maps (some col.). Vita. Includes abstract. Includes bibliographical references.

Thesis (M.S.)--West Virginia University, 2002. / Title from document title page. Document formatted into pages; contains xv, 155 p. : ill. (some col.), maps (some col.). Includes abstract. Includes bibliographical references.

Thesis (Ph. D.)--Auburn University, 2009. / Abstract. Vita. Includes bibliographical references (p. 109-117).

Thesis (M. Phil.)--University of Hong Kong, 1975. / Typescript.

Awakening Days at Dead River traces the history of a remote public park in north Hillsborough County that was once a privately-owned riverside enclave with modest cabins, and home to a popular fish camp on the Hillsborough River. The timeframe focuses on the mid-twentieth century to present, with a contextual background of earlier history in the immediate area. The story recounts the adventures and challenges of a select group of homeowners and visitors who experienced life on the Hillsborough and Dead Rivers during that timeframe. It also shows how the area evolved into a public property when regional flood control trumped private landownership, in some cases through eminent domain. Finally, the story shows how this event altered Dead River's course from Florida developed, to Florida reclaimed, the clues of the former often hidden by the growth of the woods. Research entails: interviews with former Dead River homeowners and their families (some shared photographs), and people who frequented the fish camp; a journal with text and photographs by Dead River homeowner Arthur Yates; interviews with two year-round live-in rangers who have overseen Dead River since it became a park; studying records of the Southwest Florida Water Management District (SWFWMD or Swiftmud), the state-run agency that acquired the property to manage regional flooding , including detailed appraisals, maps and correspondence; interviews with Swiftmud officials associated with Dead River; and keeping a first-hand journal of observances walking the woods at Dead River and paddling its waters. As offered above, Dead River Park has many intriguing themes worth studying. That several of its former residents and weekenders are still living, are still Floridians, and have distinct memories of their "Old Florida" fun, makes it a timely study, as well. Finally, since Dead River Park is a public entity, it is worth knowing its history; park-goers might embrace its legacy as theirs.

Rematerializing the Art Object examines Eleanor Antin's The Eight Temptations and Carving: A Traditional Sculpture. Temptations re-presents Antin's diet for Carving in a formal language of camp, mocking the dominant avant-garde culture and inspiring a less idea-based interpretation. Section one contextualizes Carving's formal qualities within a broader aesthetic history of photography and sculpture. Section two focuses on how Antin creates an amalgam of Renaissance and Baroque imagery in Temptations. Section three argues that Antin constructs a camp adaptation of the diet reducing the impact of an overly emotional woman and the seriousness of conceptualism to a cliché. Throughout, the thesis centers on the formal and aesthetic manifestations of Antin's humor. A performance within a performance, Temptations's parodic art history denounces pragmatic photography and empowers Antin as an artist and as a woman. / text

Traumatic neuronal injury inevitably causes plasmalemmal damage, and sometimes leads to axonal severance. For any eukaryotic cell to survive following traumatic injury, the plasmalemma must be repaired (sealed). Plasmalemmal sealing occurs via a Ca²⁺-dependent accumulation of vesicles or other membranous structures that form a plug at the damage site. Using uniquely identified and damaged rat hippocampal B104 cells that extend neurites with axonal properties, or rat sciatic nerves, plasmalemmal sealing is assessed by exclusion of an extracellular dye from each damaged B104 cell, or sciatic nerves ex vivo. B104 cells with neurites transected nearer (<50 [micrometres]) to the soma seal at a lower frequency and slower rate compared to cells with neurites transected farther (>50 [micrometres]) from the soma. Sealing in B104 cells is enhanced by 1) increased [cAMP], 2) increased PKA activity, 3) increased Epac activity, 4) H₂O₂ and 5) Poly-ethylene glycol (PEG). Sealing is decreased by 1) PKA inhibition, 2), Botulinum toxins A, B, E, 3) Tetanus toxin 4), NEM, 5) Brefeldin A, 6) nPKC inhibition, 7) DTT, 8) Melatonin and 9) Methylene Blue. Substances (NEM, Bref A, PKI, db-cAMP, PEG) that affect plasmalemmal sealing in B104 cells in vitro have similar effects on plasmalemmal sealing in rat sciatic nerves ex vivo. Based on data from co-application of enhancers and inhibitors of sealing, I propose a plasmalemmal sealing model having four partly redundant, parallel pathways mediated by 1) PKA, 2) Epac, 3) cytosolic oxidation and 4) nPKCs. The identification and confirmation of these pathways may provide novel clinical targets for repairing and/or recovery from traumatic injury. The fusogenic compound PEG rapidly repairs axonal continuity of severed axons, potentially by rejoining severed proximal and distal axons. PEG-fusion is influenced by plasmalemmal sealing, since unsealed axons are easier to PEG fuse. I demonstrate that PEG restores morphological continuity, and improves behavioral recovery following crush-severance to sciatic nerves in rats in vivo. Co-application of Mel or MB prior to PEG application further improves PEG fusion (as measured by electrophysiology) and behavioral recovery following crush-severance in vivo. These PEG data may provide novel clinical techniques for rapidly repairing axonal severance. / text

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In nature, non-covalent interactions are as important and dynamic as they are elusive. As such, the study of non-covalent interactions both in vivo and in vitro has proven to be challenging. Given the potential benefits of elucidating protein-protein, ligand-receptor, and other biologically relevant interactions, the development of methodologies for the study of non-covalent interactions is an attractive goal.Biologically encoded protein and peptide libraries that connect the genotypic information with the expressed phenotype have emerged in recent years as powerful methods for studying non-covalent interactions. One of the quintessential platforms for the creation of such libraries is phage display. In phage display, the connection between genetic information and the corresponding protein allows for the iterative isolation and amplification of library members that possess a desired function. Hence, an in vitro selection can be used to isolate epitopes that bind to desired targets or display specific attributes.We have sought to develop novel phage display methodologies that have the potential to expand the scope of this in vitro selection platform. Specifically, we developed a method for the non-covalent attachment of a small molecule ligand to a cyclic peptide library. This system localizes the phage display library to the ligand binding site, thus allowing for the translation of the selected cyclic peptides to a covalently tethered bivalent inhibitor.The first class of biological molecules that we chose to target with our methodology is the biologically and therapeutically important class of enzymes called protein kinases. In the first demonstration of this strategy, we were able to isolate cyclic peptide ligands for the model kinase PKA (cAMP-dependent protein kinase), which were subsequently translated to a bivalent inhibitor. This inhibitor showed both increased affinity and selectivity for PKA in relation to other protein kinases.In a separate project, we sought to develop a method for the isolation of small molecule-responsive mutants of a well-characterized protein scaffold from a phage display library. During these investigations, we discovered interesting homologous single-point mutations of the protein that resulted in large spherical oligomers that may mimic species relevant to the study of protein misfolding diseases such as Alzheimer's.

During the development of atherosclerosis, contractile vascular smooth muscle cells (VSMCs) change to cells capable of migrating and proliferating to mediate repair, where the responses may be adaptive or mal-adaptive in effect. Cyclic adenosine monophosphate (cAMP)-elevating agents have been shown to inhibit migration of VSMC. cAMP activity within the cell is known to be ubiquitous and dynamic, requiring control through signal termination mechanisms for cellular homeostasis. Phosphodiesterase (PDE) enzymes are central to this critical regulatory process catalyzing the hydrolysis of cAMP. A great deal of insight into the role of PDEs in defining compartmentalization of cAMP signaling has arisen predominately from recent studies on the cAMP-specific PDE4 family. Compartmentalization of PDE4 is mediated by their unique N-terminal domains, which have been proposed to provide the “postcodes/zipcodes” for cellular localization. PDE4D isoforms vary widely, yet their conservation over evolutionary time suggests important non-redundant roles in distinct cellular processes. To study the potential role of individual PDE4D isoforms we seek to utilize the unique N-terminal targeting domains that are proposed to be responsible for their protein-protein interactions and site-directed localization. Herein, we report on the expression, targeting and localization of five “long” PDE4D isoforms and the impact on cell morphology of certain amino-terminal domains of individual PDE4D constructs expressing green fluorescent protein (NT-PDE4D/GFP) in human aortic smooth muscle cells (HASMCs). Through the development of engineered NT-PDE4D/GFP expression plasmids, we were able to study the cell biological impacts associated with the overexpression of individual PDE4D amino-terminal variants in HASMCs. We show that NT-PDE4D5/GFP and NT-PDE4D7/GFP expressing cells exhibited an elongated cell morphology, where this effect was much more marked in NT-PDE4D7/GFP expressing cells, exhibiting multiple leading edge structures and highly elongated “tails”. We identify a potential role for PDE4D7 targeting in the regulation of cell polarity and migration. Our results suggest the novel idea that PDE4D7, rather than the four other long PDE4D isoforms (PDE4D3, PDE4D5, PDE4D8, or PDE4D9), represents the dominant PDE4D variant involved in controlling cAMP-mediated effects on cell tail retraction dynamics. / Thesis (Master, Pathology & Molecular Medicine) -- Queen's University, 2014-03-13 13:00:31.684 / Video I: Time-lapse video of GFP-expressing cell migration in HASMC. GFP expressing cells did not differ in cell migration or morphology compared to non-injected control cells. HASMCs were microinjected with GFP construct. Representative images of micoinjected GFP cells were taken 24 h post-injection overnight at 30min intervals using a Zeiss Axiovert S100 microscope and processed as described in Materials & Methods. (10X) / Video II: Time-lapse video of NT-PDE4D7/GFP-expressing cell migration in HASMC. NT-PDE4D7/GFP expressing cells exhibit elongated tail and decrease in cell migration compared to non-injected control cells. HASMCs were microinjected with NT-PDE4D7/GFP construct. Particle tracking of NT-PDE4D7 cells showed cleaving and full detachment of elongated tail. Representative images of micoinjected NT-PDE4D7 cells were taken 24 h post-injection overnight at 30min intervals using a Zeiss Axiovert S100 microscope and processed as described in Materials & Methods. (10X)