Thesis (Ph. D.)--Ohio State University, 2002. / Title from first page of PDF file. Document formatted into pages; contains xiii, 177 p.; also includes graphics (some col.). Includes bibliographical references (p. 160-177). Available online via OhioLINK's ETD Center

Thesis (Ph. D.)--University of Hong Kong, 1996. / Includes bibliographical references (leaf 72-104).

Thesis (M.S.)--Rutgers University, 2007. / "Graduate Program in Biomedical Engineering." Includes bibliographical references (p. 36-38).

Thesis (Ed. D.)--Columbia University. / Includes bibliographical references (leaves 182-192).

Thesis supervisor: Joshua A. Weiner. Includes bibliographic references (p. 105-121).

Thesis (Ph. D.)--Virginia Commonwealth University, 2006. / Prepared for: School of Nursing. Bibliography: leaves 165-183. Also available online via the Internet.

1] Spinal cords from mouse embryos were successfully prepared and maintained in primary dissociated cell culture, for periods in excess of 10 weeks. 2] Stable intracellular recordings were made from spinal neurones which had been sustained in these cultures. 3] Experiments were made on these spinal neurones using various amino acids and peptides. Solutions of these compounds were discretely applied by pressure ejection. 4] L-Glutamate, GABA and glycine evoked responses which appeared the same as those documented previously. 5] Ethylene-diamine did not evoke a response from the spinal neurones tested. 6] Only a small percentage of the spinal neurones responded to met5- and leu5 - enkephalin, FMRFamide, neurotensin and glycyl L-glutamine. Supplementing the cultures with tissue from other organs did not increase the percentage of spinal neurones which were capable of responding to peptide. 7] Met5 -enkephalin and leu5 -enkephalin each evoked responses from the spinal neurones. 8] The enkephalin-evoked depolarizations accompanied by an increased input resistance were apparently voltage dependent. These responses were abolished at potentials more negative than -90mV and did not invert under normal recording conditions. 9] The enkephalin-evoked depolarizations associated with a decreased input resistance had extrapolated inversion potentials of -20mV. No voltage dependence was seen. 10] Enkephalins also evoked responses which had an inversion potential close to the resting membrane potential. These were accompanied by a decreased input resistance and were not desensitized by prolonged application of peptide. 11] None of these responses showed obvious desensitization with prolonged application, however, they were all attenuated by naloxone. 12] Met5 -enkephalin was apparently more potent than leu5 -enkephalin on a small number of neurones. Furthermore, met5 -enkephalin application, during the weaker response from those neurones to leu5 -enkephalin, evoked a attenuated response. 13] FMRFamide evoked two responses from these spinal neurones. These responses were seen separately and mixed. In the latter case they were referred to as biphasic responses. 14] The depolarizing response to FMRFamide was accompanied by an increase in input resistance. Potassium had some involvement in these responses. 15] The FMRFamide responses which were accompanied by a decreased input resistance showed a great variety of inversion potentials between neurones. These actions were dependent upon sodium and chloride ions. 16] Enkephalin and FMRFamide, when applied separately to the same spinal neurone, did not evoke the same response. 17] Responses evoked by neurotensin were hyperpolarizations associated with a decreased input resistance. These responses were dependent upon potassium and independent of chloride ions. 18] Glycyl L-glutamine evoked two types of hyperpolarizing response from the spinal neurones. These could appear separately or combined. 19] The faster responses to glycyl L-glutamine were apparently dependent on potassium ions. 20] The slower responses to glycyl L-glutamine were apparently insensitive to changes in extracellular potassium or chloride. However, these responses were sensitive to intracellular injection of chloride ions. 21] At concentrations of peptide which evoked a response from other spinal neurones, none of the peptides produced any measurable modulation of amino acid-evoked responses.

The question of how a single cell can grow, divide, and ultimately acquire a distinct function within an adult animal is central to the field of developmental biology. An elegant way to address this question is by studying the specification of a specific cell type, for example, vertebrate motoneurons. For an animal to be able to move and behave appropriately, individual motoneurons (MNs) must correctly innervate specific muscles. For this to happen, MNs must first be specified and then must differentiate into distinct subtypes, each of which is classified in part by the muscle it innervates. MN subtype specification is dependent on both the acquisition of MN-specific characteristics as well as the failure to acquire characteristics specific to interneurons, cells that only innervate other neurons. The entire process of specification is initiated in progenitor cells and relies on the correct spatial and temporal expression of specific genes. Previous work in various vertebrate models has identified some of the key genes involved in MN specification, most notably transcription factors such as olig2, nkx6s, lhxs, mnxs, and islet1. In this dissertation, I use the zebrafish model to demonstrate novel roles in MN specification for two of these families of transcription factors - the lhxs and the mnxs. I provide evidence that both lhx3 and lhx4 are necessary for normal MN and ventral interneuron (IN) development and work by preventing MNs from expressing IN-specific characteristics. I also show that mnx1, mnx2a, and mnx2b are necessary in MNs both to promote the acquisition of some MN subtype-specific characteristics and to prevent the acquisition of some IN-specific characteristics and appear to be working in part through interactions with islet1. Finally, I identify an intermediate filament gene, inab, as being expressed in a subset of zebrafish MNs and a ventral IN and as having a potential role in the axon outgrowth of a specific MN subtype. Together, this work provides evidence for a mechanism of MN specification dependent on the expression of genes that both promote aspects of MN fate and inhibit aspects of IN fate. This dissertation includes previously unpublished co-authored material.

No description available.

M.A. / The power of positive thinking to promote and maintain well-being has enjoyed widespread popular appeal. Spurred largely by the development of the Life Orientation Test (LOT) (Scheier & Carver, 1985), mounting evidence now attests to the apparent benefits conferred by an optimistic life outlook. Optimism, the inclination to expect favourable outcomes, has been linked to both psychological and physical well-being (Taylor, et al., 1992; Cheng & Hamid, 1997; Marshall, Wortman, Kusalas, Hervig, & Vickers, 1992; Scheier, Carver & Bridges, 1994; Scheier et al., 1989; Segerstrom, Taylor, Kemeny, & Fahey, 1998). Optimists and pessimists have been shown to differ in the manner in which they cope with the challenges in their lives. They differ in their stable coping tendencies and in the kinds of coping responses that they spontaneously generate when given hypothetical coping situations (Scheier, Weintraub, & Carver, 1986). Optimists also differ from pessimists in the manner in which they cope with serious disease and with concerns about specific health threats (Friedman, et al., 1992), and these coping mechanisms in optimists in turn have been linked to improved physical and psychological functioning. There is also a clear biological link between optimism and physical well-being and this has been noted in such areas as immune functioning (Peterson & Bossio, 2002). The current study examines these apparent benefits of optimism on health and explores the medical bases for this connection. The study also examines whether these benefits may be of use in the treatment and recovery from the unique secondary medical complications experienced by those who are spinal cord injured.