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The Arizona Child Acoustic Database consists of longitudinal audio recordings from a group of children over a critical period of growth and development (ages 2-7 years). The goal of this database is to 1) document acoustic changes in speech production that may be related to physical growth 2) inform development of a model of speech production for child talkers. This work was funded by NSF BSC-1145011 awarded to Kate Bunton, Ph.D. and Brad Story, Ph.D, Principal Investigators. This database contains longitudinal audio recordings of 55 American English speaking children between the ages of 2-7 at 3-month intervals. Since children began the study at different ages, some children have fewer recording sessions than others. The database can also be used to provide cross-sectional data for children of a specific age. Please refer to the subject data table for information on specific sessions available here http://arizona.openrepository.com/arizona/handle/10150/316065. All children were recorded using the same protocol; therefore, task numbers are consistent across children and sessions. A calibration tone is included as Record 1 for all sessions. The speech protocol focused on production of English monopthong and diphthong vowels in isolation, sVd, hVd, and monosyllabic real words. In addition, the protocol includes several nonsense vowel-to-vowel transitions. Speakers were prompted either verbally by investigators or by graphical prompts. Details of the protocol with reference to task numbers can be found in the protocol spreadsheet available here http://arizona.openrepository.com/arizona/handle/10150/316065. Details on data recording: All samples were recorded digitally using an AKG SE 300B microphone with a mouth to mic distance of approximately 10 inches. Signals were recorded digitally using a Marantz PMD671, 16 bit PCM (uncompressed) at 44.1KHz. Recordings are made available in .wav format. Individual zip files contain all recordings from a single session.

The Arizona Child Acoustic Database consists of longitudinal audio recordings from a group of children over a critical period of growth and development (ages 2-7 years). The goal of this database is to 1) document acoustic changes in speech production that may be related to physical growth 2) inform development of a model of speech production for child talkers. This work was funded by NSF BSC-1145011 awarded to Kate Bunton, Ph.D. and Brad Story, Ph.D, Principal Investigators. This database contains longitudinal audio recordings of 55 American English speaking children between the ages of 2-7 at 3-month intervals. Since children began the study at different ages, some children have fewer recording sessions than others. The database can also be used to provide cross-sectional data for children of a specific age. Please refer to the subject data table for information on specific sessions available here http://arizona.openrepository.com/arizona/handle/10150/316065. All children were recorded using the same protocol; therefore, task numbers are consistent across children and sessions. A calibration tone is included as Record 1 for all sessions. The speech protocol focused on production of English monopthong and diphthong vowels in isolation, sVd, hVd, and monosyllabic real words. In addition, the protocol includes several nonsense vowel-to-vowel transitions. Speakers were prompted either verbally by investigators or by graphical prompts. Details of the protocol with reference to task numbers can be found in the protocol spreadsheet available here http://arizona.openrepository.com/arizona/handle/10150/316065. Details on data recording: All samples were recorded digitally using an AKG SE 300B microphone with a mouth to mic distance of approximately 10 inches. Signals were recorded digitally using a Marantz PMD671, 16 bit PCM (uncompressed) at 44.1KHz. Recordings are made available in .wav format. Individual zip files contain all recordings from a single session.

The Arizona Child Acoustic Database consists of longitudinal audio recordings from a group of children over a critical period of growth and development (ages 2-7 years). The goal of this database is to 1) document acoustic changes in speech production that may be related to physical growth 2) inform development of a model of speech production for child talkers. This work was funded by NSF BSC-1145011 awarded to Kate Bunton, Ph.D. and Brad Story, Ph.D, Principal Investigators. This database contains longitudinal audio recordings of 55 American English speaking children between the ages of 2-7 at 3-month intervals. Since children began the study at different ages, some children have fewer recording sessions than others. The database can also be used to provide cross-sectional data for children of a specific age. Please refer to the subject data table for information on specific sessions available here http://arizona.openrepository.com/arizona/handle/10150/316065. All children were recorded using the same protocol; therefore, task numbers are consistent across children and sessions. A calibration tone is included as Record 1 for all sessions. The speech protocol focused on production of English monopthong and diphthong vowels in isolation, sVd, hVd, and monosyllabic real words. In addition, the protocol includes several nonsense vowel-to-vowel transitions. Speakers were prompted either verbally by investigators or by graphical prompts. Details of the protocol with reference to task numbers can be found in the protocol spreadsheet available here http://arizona.openrepository.com/arizona/handle/10150/316065. Details on data recording: All samples were recorded digitally using an AKG SE 300B microphone with a mouth to mic distance of approximately 10 inches. Signals were recorded digitally using a Marantz PMD671, 16 bit PCM (uncompressed) at 44.1KHz. Recordings are made available in .wav format. Individual zip files contain all recordings from a single session.

High mortality rates from cardiovascular disease underscore the need for improved therapies. Thus, it is important to further our understanding of factors and mechanisms promoting cardiac protection and repair. Fibroblast growth factor-2 (FGF-2), administered to the heart before or during injury exerts beneficial effects such as cytoprotection and angiogenesis. However, the effects of a chronic elevation in endogenous FGF-2 on recovery/remodeling after ischemic injury are not known. My hypothesis was that chronic elevation in endogenous FGF-2 expression (in FGF-2 overexpressing transgenic mice) exerts beneficial effects such as improved function after isoproterenol-induced injury in vivo. The first study showed that treatment with the β-adrenergic agonist isoproterenol resulted in exaggerated levels of cellular infiltration and myocardial disarray in transgenic FGF-2 versus non-transgenic mouse myocardium. This was suggestive of increased cardiac injury in transgenic FGF-2 mice. Inhibition of T cells using the immunosuppressants cyclosporine A or antibodies against CD3ε attenuated cellular infiltration in transgenic FGF-2 mice, to levels comparable to those of non-transgenic mice, suggesting a T lymphocyte-mediated effect. Overall morphological data suggested that chronic FGF-2 elevation might have created an adverse outcome after cardiac injury. In a follow-up study the effect of chronic FGF-2 elevation on cardiac function was examined, as measured by tissue Doppler imaging (TDI), after isoproterenol administration. FGF-2 overexpressing mice displayed improved cardiac function compared to controls, after isoproterenol, both acutely (24 h) and in a sustained fashion (2-4 weeks). The FGF-2 associated functional improvement at 2-4 weeks was attenuated following immunosuppression with cyclosporine A, but not treatment with anti-CD3ε antibodies. The FGF-2–associated functional improvement may be partially attributed to a cyclosporine A-sensitive (but anti-CD3-insensitive) infiltrating cell population. Thus cellular infiltration, in response to elevated FGF-2, may have a net beneficial effect. In a third study, non-transgenic mice were put through a brief swimming protocol (exercise) prior to isoproterenol. This acute bout of exercise resulted in significant improvement in TDI function, compared to control groups, measured at 24 hours up to 4 weeks post-isoproterenol. In conclusion, increased endogenous cardiac FGF-2 expression, or an acute bout of exercise, exert sustained beneficial effects against isoproterenol-induced cardiac injury.

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The development of algorithms to efficiently determine an optimal path through a complex environment is a continuing area of research within Computer Science. When such environments can be represented as a graph, established graph search algorithms, such as Dijkstra’s shortest path and A*, can be used. However, many environments are constructed from a set of regions that do not conform to a discrete graph. The Weighted Region Problem was proposed to address the problem of finding the shortest path through a set of such regions, weighted with values representing the cost of traversing the region. Robust solutions to this problem are computationally expensive since finding shortest paths across a region requires expensive minimisation. Sampling approaches construct graphs by introducing extra points on region edges and connecting them with edges criss-crossing the region. Dijkstra or A* are then applied to compute shortest paths. The connectivity of these graphs is high and such techniques are thus not particularly well suited to environments where the weights and representation frequently change. The Field D* algorithm, by contrast, computes the shortest path across a grid of weighted square cells and has replanning capabilites that cater for environmental changes. However, representing an environment as a weighted grid (an image) is not space-efficient since high resolution is required to produce accurate paths through areas containing features sensitive to noise. In this work, we extend Field D* to weighted simplicial complexes – specifically – triangulations in 2D and tetrahedral meshes in 3D. Such representations offer benefits in terms of space over a weighted grid, since fewer triangles can represent polygonal objects with greater accuracy than a large number of grid cells. By exploiting these savings, we show that Triangulated Field D* can produce an equivalent path cost to grid-based Multi-resolution Field D*, using up to an order of magnitude fewer triangles over grid cells and visiting an order of magnitude fewer nodes. Finally, as a practical demonstration of the utility of our formulation, we show how Field D* can be used to approximate a distance field on the nodes of a simplicial complex, and how this distance field can be used to weight the simplicial complex to produce contour-following behaviour by shortest paths computed with Field D*.

GLP-2 is a potent intestinotrophic peptide that can increase mucosal growth, intestinal blood flow, and nutrient absorption when administered exogenously. We aimed to delineate the effects of endogenous GLP-2R signalling in conditions of nutrient deprivation and excess. Using a mouse with a targeted genetic deletion of the Glp2r gene (Glp2r-/-), we addressed the hypothesis that the known GLP-2R is required for intestinal adaptation to nutrient deprivation and excess. In Chapter 2, we demonstrate that Glp2r−/− mice fasted for 24 hours and re-fed for 24 hours failed to increase intestinal growth and jejunal crypt cell proliferation compared to littermate Glp2r+/+ mice. Administration of EGF to Glp2r−/− during the re-feeding period rescued this re-feeding defect. Wildtype mice re-fed for 30, 90, and 180 minutes following a 24 hour fast displayed increased jejunal mRNA levels of the ErbB ligands amphiregulin, epiregulin and HB-EGF. Treatment with the pan ErbB inhibitor CI-1033 inhibited induction of these ErbB ligands in jejunum of mice in association with prevention of crypt cell proliferation. Re-feeding also caused an increase in jejunal p-Akt levels and treatment with CI-1033 prevented increased p-Akt levels. Moreover, re-fed Glp2r−/− mice failed to increase ErbB ligands or p-Akt levels 90 minutes following re-feeding when compared to Glp2r+/+ littermates. Therefore, the GLP-2R is essential for re-feeding induced intestinal adaptation by activating the ErbB network and p-Akt to increase crypt cell proliferation. In Chapter 3, we show that the known GLP-2R is not required for intestinal adaptation to a perceived nutrient deprivation challenge (STZ-induced diabetes) or chronic nutrient excess (high-fat diet induced glucose intolerance). Although exogenous GLP-2 administration has been previously shown to stimulate glucagon secretion, glucose homeostasis was normal in STZ-diabetic and high fat fed Glp2r−/− mice. We also developed a third model of diabetes and glucose intolerance: ob/ob: Glp2r−/−. In the absence of GLP-2R signalling, ob/ob mice display improved oral but impaired intraperitoneal glucose tolerance, elevated fed and fasted glucose levels, increased circulating glucagon, decreased beta cell and increased alpha cell mass. Taken together, these results suggest that endogenous GLP-2R signalling is essential for intestinal and islet adaptation to conditions of nutrient deprivation and excess.