The use of neural networks in the field of development geology is in its infancy. In this study, a neural network will be used to identify flow units in Happy Spraberry Field, Garza County, Texas. A flow unit is the mappable portion of the total reservoir within which geological and petrophysical properties that affect the flow of fluids are consistent and predictably different from the properties of other reservoir rock volumes (Ebanks, 1987). Ahr and Hammel (1999) further state a highly "ranked" flow unit (i.e. a good flow unit) would have the highest combined values of porosity and permeability with the least resistance to fluid flow. A flow unit may also include nonreservoir features such as shales and cemented layers where combined porosity-permeability values are lower and resistance to fluid flow much higher (i.e. a poor flow unit) (Ebanks, 1987). Production from Happy Spraberry Field primarily comes from a 100 foot interval of grainstones and packstones, Leonardian in age, at an average depth of 4,900 feet. Happy Spraberry Field is unlike most fields in that the majority of the wells have been cored in the zone of interest. This fact more easily lends the Happy Spraberry Field to a study involving neural networks. A neural network model was developed using a data set of 409 points where X and Y location, depth, gamma ray, deep resistivity, density porosity, neutron porosity, lab porosity, lab permeability and electrofacies were known throughout Happy Spraberry Field. The model contained a training data set of 205 cases, a verification data set of 102 cases and a testing data set of 102 cases. Ultimately two neural network models were created to identify electrofacies and reservoir quality (i.e. flow units). The neural networks were able to outperform linear methods and have a correct classification rate of 0.87 for electrofacies identification and 0.75 for reservoir quality identification.

Thesis (Ph. D.)--University of Washington, 2001. / Vita. Includes bibliographical references (leaves 59-63).

Thesis (Ph.D.)--York University, 2008. Graduate Programme in Applied Mathematics. / Typescript. Includes bibliographical references (leaves 225-239). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:NR46003

Thesis (Ph. D.)--University of Washington, 2003. / Vita. Includes bibliographical references (leaves 76-80).

Neural stem cells (NSCs) are defined as multipotent stem cells. They are able to self-renew and differentiate into mature cells, such as neurons, oligodendrocytes and astrocytes. Neurotoxicity of lead (Pb2+) has been extensively investigated by many previous studies. These studies proved that lead is a potent toxin that affects nervous system, especially children’s brain. However, most of these studies focused on the negative effects of lead on the differentiated or mature cell types in the brains instead of NSCs. The aim of this study was to reveal the effects of Pb2+ on viability, proliferation and differentiation of NSCs derived from the hippocampus of newborn rats aged 7 days and adult rats aged 90 days in vitro. NSCs harvested from the rat hippocampus were cultured in proliferation medium. After 6-8 days, free-floating neurospheres formed. The neurospheres were dissociated and plated onto poly-L-lysine coated 96-well plate and coverslips. Some dissociated cells were characterized by being stained with anti-nestin to show the presence of NSCs. This project was divided into three parts. In the first part, the Passage 2 (P2) cells plated onto 96-well plate were cultured in the proliferation medium with different concentrations of lead acetate (0-200μM) for 48 hours, followed by 3- (4,5-cimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to detect the effects of Pb2+ on the cell viability. In the second part, P2-NSCs plated onto coverslips in wells were cultured in the proliferation medium with different concentrations of lead acetate (0-200μM). Then, 10 μM bromodeoxyuridine (BrdU) was added into the culture medium for additional 24 hours, followed by immunocytochemistry staining with anti-BrdU. In the last part, the dissociated P2-NSCs plated onto coverslips were allowed to grow in the differentiation medium of neurons, astrocytes or oligodendrocytes with different concentrations of lead acetate (0-200μM). After 6 days, immunocytochemistry staining with anti-microtubule-associated protein 2 (anti-MAP2), anti-glial fibrillary acidic protein (anti-GFAP) or anti-RIP was used to detect the differentiation commitment of affected NSCs. Low level of Pb2+ (1-10μM) had no effect on the viability of adult hippocampal neural stem cells (hNSCs). However, Pb2+ exposure at the concentration of 10μM could lead to significant cell death of newborn hNSCs. High level of Pb2+ (50-200μM) caused significant cell death of both newborn and adult hNSCs. Newborn hNSCs were sensitive to Pb2+ toxicity in proliferation assay. Even a low concentration (1μM) of lead could lead to significant inhibition of cell proliferation. High level of Pb2+ (50-200μM) suppressed proliferation of both newborn and adult hNSCs significantly. Moderate to high levels of Pb2+ exposure (50-200μM) significant decreased the percentage of mature neurons cultured from both newborn and adult hNSCs. Furthermore, 10μM or more Pb2+could significantly inhibited the oligodendrocyte differentiation of both newborn and adult hNSCs. However, Pb2+ could also stimulate the astrocyte differentiation of hNSCs. Lead concentrations higher than 10μM and 50μM could respectively lead to a significant increase in the percentage of mature astrocytes differentiated from newborn and adult hNSCs. The data showed that Pb2+ inhibited not only the viability and proliferation of rat hNSCs but also the neuronal and oligodendrocyte differentiation in vitro; moreover activated astrocyte differentiation of the hNSCs of both newborn and adult rats were observed with high concentration of Pb2+ in vitro. Also, it was revealed that the hNSCs of newborn rats were more sensitive than those from adult rats to Pb2+ cytoxicity. / published_or_final_version / Anatomy / Master / Master of Medical Sciences

published_or_final_version / Chinese Medicine / Doctoral / Doctor of Philosophy

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

Neural stem cells (NSCs) exist in both embryonic and adult neural tissues and are characterized by their self-renewal capacity and multipotency that contribute to the generation of three major cell types in the vertebrate central nervous system (CNS):neurons, oligodendrocytes and astrocytes. The tremendous therapeutic potential of NSCs to treat the neurodegenerative diseases and repair brain injuries has provoked intensive study in the molecular regulation of their induction, maintenance and differentiation. Previous study reported that Sox9, a member of high-mobility-group(HMG) containing SoxE transcription factors family, plays important roles in regulating the formation and maintenance of NSCs in both mouse and chick CNS, as well as the cell fate switch between neuronal and glial. Whether it plays similar roles in human NSCs (hNSCs)is still unknown. My RT-qPCR analysis showed that SOX9is expressed at a basal level in human embryonic stem cells (hESCs) and up-regulated upon commitment into neural lineage and maintained at a high level in hESCs-derived hNSCs. I therefore hypothesized that SOX9 might also be involved in the induction, maintenance and differentiation of hNSCs. To test this, two stable hESC lines(HES2)were generated with each constitutively expressing short hairpin RNA (shRNA) against SOX9andGL2 Luciferase (Luc, as control) respectively. Upon neural induction, SOX9-knock-down(KD) hESCs were able to commit neural lineage and differentiate into NSCs/neurospheres (NSPs), however, these NSCs exhibited reduced multipotency and glial marker (GALC, CD44) expressions but enhanced self-renewal compared to the shLuc NSCs. Hence, SOX9 is required for both the induction and maintenance of multipotent hNSCs. Strikingly, extensive TUJ1+ neurites and advance groupings of these neurites into bundles were observed in SOX9-KD NSPs after three days and seven days neuronal differentiation respectively, suggesting premature neurogenesis as a result of SOX9 ablation. In addition, RT-qPCR analysis revealed down-regulated expression of NSC marker HES1but induced proneural basic helix-loop-helix transcription factor MASH1in shSOX9-1208 NSCs. The inhibitory role of HES1 on the expression and functions of MASH1 has been reported to be essential for the timely generation of neurons. Hence, ablation of SOX9 is likely to relieve the inhibition on MASH1activity via down-regulated HES1expression and leads to early neuronal differentiation. Expression of the potent neurite blocker NG2 was also found to be reduced in SOX9-KD NSCs which may explain the extensive neurite network observed. Altogether, similar to previous studies in mouse NSCs, SOX9 is also required for the induction and maintenance of hNSCs. However, this study further reveals a putative novel role of SOX9 in preventing premature neuronal differentiation by regulating the expressions of HES1 to counteract MASH1 function and NG2 to control neurite outgrowth. / published_or_final_version / Biochemistry / Master / Master of Philosophy

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Our sensory experiences are encoded in the patterns of activity of the neurons in our brain. While we know we are capable of sensing and responding to a constantly changing sensory environment, we often study neural activity by repeatedly presenting the same stimulus and analyzing the average neural response. It is not understood how the average neural response represents the dynamic neural activity that produces our perceptions. In this work, we use functional imaging of the rodent primary somatosensory cortex, specifically the whisker representations, and apply classic signal-detection methods to test the predictive power of the average neural response. Stimulus features such as intensity are thought to be perceptually separable from the average representation; however, we show that stimulus intensity cannot be reliably decoded from neural activity from only a single experience. Instead, stimulus intensity was encoded only across many experiences. We observed this probabilistic neural code in multiple classic sensory paradigms including complex temporal stimuli (pairs of whisker deflections) and multi-whisker stimuli. These data suggest a novel framework for the encoding of stimulus features in the presence of high-neural variability. Specifically we suggest that our brains can compensate for unreliability by encoding information redundantly across cortical space. This thesis predicts that a somatosensory stimulus is not encoded identically each time it is experienced; instead, our brains use multiple redundant pathways to create a reliable sensory percept.