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You searched for +publisher:"Virginia Tech" +contributor:("Rzigalinski, Beverly Anne"). Showing records 1 – 3 of 3 total matches.

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Virginia Tech

1. Cotrone, Thomas Steven. Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD.

Degree: PhD, Biomedical and Veterinary Sciences, 2017, Virginia Tech

Post-traumatic stress disorder (PTSD) is a psychological disorder that can cause great social/economic hardship. Progress towards treating PTSD has been slow due to a lack of understanding of its pathogenesis. This dissertation aimed to address this issue by investigating the involvement of the astrocytic glutamate reuptake transporter, GLT-1, and regional differences in expression of NMDA receptor subtypes in the development of a rat model of PTSD. We hypothesized that impaired astrocytic glutamate reuptake inhibits long-term memory processes, and that concurrent presence of glucocorticoids (GCs) during situational trauma selectively inhibits fear extinction memory processes in the prefrontal cortex, but not of conditioned fear memory processes in the amygdala, due to differences between these brain regions in expression of NMDA receptor subtypes. The effect of GLT-1 manipulation was studied in vivo. Utilizing the Single Prolonged Stress (SPS) model of PTSD, rats were either exposed to SPS or not. Within these groups, rats were administered a saline sham, a GLT-1 facilitator (ceftriaxone (CEF)), or a GLT-1 inhibitor (dihydrokainic acid (DHK)). Using Classical Fear Conditioning (CFC) and Fear Extinction (EXT) paradigms, retention of fear extinction memories was measured to determine the effect of GLT-1 manipulation on SPS-induced behavior (i.e., impaired fear extinction retention). From the brain of each rat, the amygdala, hippocampus, and prefrontal cortex (PFC) were collected and expression of GLT-1, p-CREB (a molecular indicator of long-term memory), and glucocorticoid receptor (GR, a molecular indicator of a PTSD-like state) were quantified. Analysis of the behavioral data showed that SPS exposure alone reduced the retention of extinction memories, but CEF and DHK both eliminated this effect. Analysis of the brain tissues revealed that SPS induced an increase in GR expression in the hippocampus. SPS also increased GLT-1 expression, but not p-CREB, in the PFC and amygdala. To evaluate the involvement of regional differences in NMDA receptor subtype expression ex vivo, tissue sections of amygdala, hippocampus, and PFC were taken from SPS and non-SPS exposed rats. Synaptic transmission was stimulated in these tissues using bicuculline in the presence of glucocorticoids, NVP-AA077 (a NR2A NMDA receptor subtype inhibitor), or Ro-25 (a NR2B NMDA receptor subtype inhibitor). P-CREB was measured in the tissues treated with GCs to determine if GCs exert greater inhibition of long-term memory in the PFC (a region reported to express high NR2A) than in the amygdala (a region reported to express high NR2B). P-CREB was also measured in the tissues treated with NVP or Ro-25 to determine if these reported receptor profile differences could be demonstrated, and if they changed following SPS exposure. Contrary to the stated hypothesis, analysis of non-SPS exposed rats revealed that GCs, NVP, and Ro-25 decreased p-CREB in all three regions with no differences between regions. However, in the SPS exposed group, p-CREB was not… Advisors/Committee Members: Klein, Bradley G. (committeechair), Ehrich, Marion F. (committeechair), Rzigalinski, Beverly Anne (committee member), MacPhail, Robert (committee member), Jortner, Bernard S. (committee member).

Subjects/Keywords: PTSD; astrocyte; GLT-1; NR2A; NR2B; glutamate reuptake

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Cotrone, T. S. (2017). Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD. (Doctoral Dissertation). Virginia Tech. Retrieved from http://hdl.handle.net/10919/86415

Chicago Manual of Style (16th Edition):

Cotrone, Thomas Steven. “Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD.” 2017. Doctoral Dissertation, Virginia Tech. Accessed December 05, 2020. http://hdl.handle.net/10919/86415.

MLA Handbook (7th Edition):

Cotrone, Thomas Steven. “Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD.” 2017. Web. 05 Dec 2020.

Vancouver:

Cotrone TS. Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD. [Internet] [Doctoral dissertation]. Virginia Tech; 2017. [cited 2020 Dec 05]. Available from: http://hdl.handle.net/10919/86415.

Council of Science Editors:

Cotrone TS. Evaluation of the Role of Astrocyte Glutamate Transport and of Synaptic NMDA Receptor Subtype Representation in the Pathogenesis of PTSD. [Doctoral Dissertation]. Virginia Tech; 2017. Available from: http://hdl.handle.net/10919/86415


Virginia Tech

2. Zhang, Wen. Mechanism of genistein in the regulation of pancreatic beta-cell proliferation.

Degree: MS, Human Nutrition, Foods, and Exercise, 2007, Virginia Tech

This study was designed to examine the effect of genistein, a botanical derived primarily from legumes, on pancreatic β-cell proliferation and the related molecular mechanisms. Diabetes mellitus is a major and growing public health problem worldwide. Both in type 1 (T1D) and type 2 diabetes (T2D), the deterioration of glycemic control over time is primarily caused by an inadequate mass and progressive dysfunction of β-cells. Therefore, the search for novel, safe and cost-effective agents that can enhance islet β-cell proliferation, thereby preserving β-cell mass, could be one of the essential strategies to prevent diabetes, given that β-cells have the potential to regenerate by proliferation of pre-existing b-cells in both physiological condition and after onset of diabetes. Genistein has various biological actions. However, studies on whether genistein has an effect on pancreatic β-cell function are very limited. Our laboratory recently found that genistein activates cAMP/protein kinase A (PKA) signaling in both clonal β-cells and mouse islets. Here I present evidence that genistein induced cellular proliferation of clonal rat pancreatic β-cells (INS1) and human islets following 24 h of incubation. This effect was dose-dependent with 5 µM genistein inducing a maximal 41% increase. The effect of genistein on cell proliferation was not dependent on estrogen receptors because this effect was not blocked by the estrogen receptor inhibitor ICI182,780. In addition, the genistein effect on β-cell proliferation was not shared by 17-β-estradiol or a host of structurally related flavonoid compounds, suggesting that this genistein action is structure-specific. Pharmacological or molecular intervention of PKA or MEK1/2, the upstream kinase of p42/44 mitogen activated protein kinases (ERK1/2), completely abolished the genistein-stimulated proliferation of INS1 cells and human islets, suggesting that both molecules are essential for genistein action. Consistent with its effect on cell proliferation, genistein increased intracellular cAMP and subsequently activated PKA in human islets. Genistein also caused a rapid and sustained phosphorylation of ERK1/2 with a maximal increase of 185% at 5 µM genistein. The genistein-induced ERK1/2 activation was completely ablated by inhibition of PKA in INS1 cells and human islets. Furthermore, I found that genistein induced protein expression of cyclin D1, a nuclear target of PKA and ERK1/2 activation and a major cell-cycle regulator essential for ï ¢-cell growth. These findings demonstrated that genistein may be a plant-derived growth factor for pancreatic β-cells involving induction of cyclin D1 via activation of the cAMP/PKA-dependent ERK1/2 signaling pathway, thereby providing a novel role for genistein in the regulation of pancreatic β-cell function. Advisors/Committee Members: Liu, Dongmin (committeechair), Houston, Michael E. (committee member), Rzigalinski, Beverly Anne (committee member).

Subjects/Keywords: ERK1/2; protein kinase A; islets; cAMP; cell proliferation; pancreatic β-cell; Genistein

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Zhang, W. (2007). Mechanism of genistein in the regulation of pancreatic beta-cell proliferation. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/35772

Chicago Manual of Style (16th Edition):

Zhang, Wen. “Mechanism of genistein in the regulation of pancreatic beta-cell proliferation.” 2007. Masters Thesis, Virginia Tech. Accessed December 05, 2020. http://hdl.handle.net/10919/35772.

MLA Handbook (7th Edition):

Zhang, Wen. “Mechanism of genistein in the regulation of pancreatic beta-cell proliferation.” 2007. Web. 05 Dec 2020.

Vancouver:

Zhang W. Mechanism of genistein in the regulation of pancreatic beta-cell proliferation. [Internet] [Masters thesis]. Virginia Tech; 2007. [cited 2020 Dec 05]. Available from: http://hdl.handle.net/10919/35772.

Council of Science Editors:

Zhang W. Mechanism of genistein in the regulation of pancreatic beta-cell proliferation. [Masters Thesis]. Virginia Tech; 2007. Available from: http://hdl.handle.net/10919/35772


Virginia Tech

3. Ikuma, Kaoru. The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies.

Degree: MS, Environmental Sciences and Engineering, 2007, Virginia Tech

Oxidative stress-inducing chemical contamination in the environment is a significant concern for public health. The depletion of antioxidants by these chemicals results in oxidative stress which may cause detrimental effects in many cell types. For example, multiple stress responses may be activated in bacteria and several disorders including neurodegenerative disorders may occur in mammalian organisms. Oxidative chemicals also have negative effects on engineered water systems as an oxidative stress response in bacteria has been implicated to cause process failure in wastewater treatment facilities. Therefore, it is essential to monitor oxidative chemical contamination in water environments to provide early warning of potential negative effects. Whole-cell biosensors that indicate bacterial stress responses to oxidative toxic agents can be powerful tools in environmental monitoring. An oxidative stress response found in many Gram-negative heterotrophic bacteria called the glutathione-gated potassium efflux (GGKE) mechanism is a good biological indicator to be used in a biosensor designed to detect the presence of oxidative chemicals in water. The authors of this study propose the development of a GGKE biosensor using an environmental strain of Pseudomonas aeruginosa. The abundance of the global antioxidant glutathione, the gating compound in GGKE, in various cell types suggests that there may be connections between the responses of the different cell types to oxidative stress. In this study, specific oxidative stress responses in two distantly related cell types were studied: the GGKE mechanism in Gram-negative heterotrophic bacteria, and mitochondrial dysfunction in rat brain cells. Furthermore, the use of an octanol-based emulsification method for the immobilization of P. aeruginosa in calcium alginate microbeads was evaluated for long-term mechanical stability, viability, and GGKE response of the immobilized cells. The immobilization of cells is an important factor in the design of a whole-cell biosensor, and must yield viable and active cells over time. This study showed that the dose-dependent responses of GGKE in Pseudomonas aeruginosa cells and of mitochondrial dysfunction in a mixed culture of rat brain cells to a model oxidative electrophilic chemical, N-ethylmaleimide, correspond well to each other. We also showed that both responses are accompanied by the depletion of intracellular glutathione, which precedes the GGKE response in P. aeruginosa as well as mitochondrial damage in rat brain cells. Thus, this study suggests that bacterial responses to oxidative stress involving glutathione, such as GGKE, could potentially be used as an early warning to predict the presence of bioavailable oxidative chemicals that can induce oxidative stress in eukaryotic systems. Although further research is needed, this suggests that bacterial stress response biosensors may be used to predict oxidative stress responses in mammalian brain cells. The octanol-based emulsification method produced P.… Advisors/Committee Members: Love, Nancy G. (committeechair), Little, John C. (committee member), Love, Brian J. (committee member), Rzigalinski, Beverly Anne (committee member).

Subjects/Keywords: glutathione-gated potassium efflux; biosensor; alginate; oxidative stress; Pseudomonas aeruginosa

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Ikuma, K. (2007). The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/34423

Chicago Manual of Style (16th Edition):

Ikuma, Kaoru. “The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies.” 2007. Masters Thesis, Virginia Tech. Accessed December 05, 2020. http://hdl.handle.net/10919/34423.

MLA Handbook (7th Edition):

Ikuma, Kaoru. “The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies.” 2007. Web. 05 Dec 2020.

Vancouver:

Ikuma K. The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies. [Internet] [Masters thesis]. Virginia Tech; 2007. [cited 2020 Dec 05]. Available from: http://hdl.handle.net/10919/34423.

Council of Science Editors:

Ikuma K. The Development of a Bacterial Biosensor Designed to Detect Oxidative Chemicals in Water: Correlating Sensor Relevance to Mammalian Brain Cells and Assessing Bacterial Cell Immobilization Strategies. [Masters Thesis]. Virginia Tech; 2007. Available from: http://hdl.handle.net/10919/34423

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