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You searched for +publisher:"Georgia Tech" +contributor:("Michelle C. LaPlaca"). Showing records 1 – 3 of 3 total matches.

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Georgia Tech

1. Zhong, Yinghui. Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes.

Degree: PhD, Biomedical Engineering, 2006, Georgia Tech

Stable single-unit recordings from the nervous system using microelectrode arrays can have significant implications for the treatment of a wide variety of sensory and movement disorders. However, the long-term performance of the implanted neural electrodes is compromised by the formation of glial scar around these devices, which is a typical consequence of the inflammatory tissue reaction to implantation-induced injury in the CNS. The glial scar is inhibitory to neurons and forms a barrier between the electrode and neurons in the surrounding brain tissue. Therefore, to maintain long-term recording stability, reactive gliosis and other inflammatory processes around the electrode need to be minimized. This work has succeeded in the development of neural electrode coatings that are capable of sustained release of anti-inflammatory agents while not adversely affecting the electrical performance of the electrodes. The effects of coating methods, initial drug loadings on release kinetics were investigated to optimize the coatings. The physical properties of the coatings and the bioactivity of released anti-inflammatory agents were characterized. The effect of the coatings on the electrical property of the electrodes was tested. Two candidate anti-inflammatory agents were screened by evaluating their anti-inflammatory potency in vitro. Finally, neural electrodes coated with the anti-inflammatory coatings were implanted into rat brains to assess the anti-inflammatory potential of the coatings in vivo. This work represents a promising approach to attenuate astroglial scar around the implanted silicon neural electrodes, and may provide a promising strategy to improve the long-term recording stability of silicon neural electrodes. Advisors/Committee Members: Ravi V. Bellamkonda (Committee Chair), Julia E. Babensee (Committee Member), Michelle C. LaPlaca (Committee Member), Robert J. McKeon (Committee Member), Todd C. McDevitt (Committee Member).

Subjects/Keywords: Neural implant; Drug delivery; Coatings; Inflammation; Glial scar; Nervous system; Electrodes; Implants, Artificial; Foreign-body reaction; Wound healing; Neuroglia; Coatings; Controlled release preparations; Anti-inflammatory agents

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APA (6th Edition):

Zhong, Y. (2006). Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/19760

Chicago Manual of Style (16th Edition):

Zhong, Yinghui. “Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes.” 2006. Doctoral Dissertation, Georgia Tech. Accessed September 18, 2020. http://hdl.handle.net/1853/19760.

MLA Handbook (7th Edition):

Zhong, Yinghui. “Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes.” 2006. Web. 18 Sep 2020.

Vancouver:

Zhong Y. Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes. [Internet] [Doctoral dissertation]. Georgia Tech; 2006. [cited 2020 Sep 18]. Available from: http://hdl.handle.net/1853/19760.

Council of Science Editors:

Zhong Y. Development and Characterization of Anti-Inflammatory Coatings for Implanted Neural Probes. [Doctoral Dissertation]. Georgia Tech; 2006. Available from: http://hdl.handle.net/1853/19760


Georgia Tech

2. Lessing, Marcus Christian. The acute cellular and behavioral response to mechanical neuronal injury.

Degree: PhD, Biomedical Engineering, 2008, Georgia Tech

Traumatic brain injury (TBI) is a major health and socioeconomic concern in the United States and across the globe. Experimental models of TBI are used to study the mechanisms underlying cell dysfunction and death that result from injury, the functional deficits that result from injury, and the potential of various therapies to treat injury. This thesis explores the fundamental mechanical damage associated with brain trauma, investigating the effects of mechanical deformation on neurons at the molecular, cellular, tissue, and animal levels. First, a novel hydrogel system was developed to support 3-D neuronal cultures, and the cultures were studied in an in vitro model of neuronal injury. The dependence of cell viability on hydrogel stiffness and extracellular matrix ligand concentration revealed a role for molecular interactions in the cellular response to injury. Subsequently, in a rat model of TBI neuronal plasma membrane damage was observed coincidentally with cell death within the hippocampus; however not all permeable cells died, suggesting a complex role for plasma membrane damage in neuronal degeneration. The spatial profile of permeable cells in the hippocampus reveals further heterogeneity of neuronal plasma membrane damage, with populations of cells in certain hippocampal subregions exhibiting an increased vulnerability to plasma membrane damage. These observations support recent finite element model predictions of strains in the brain during injury. Finally a system for measuring locomotor disturbances is used for the first time following brain injury. Continued investigation of how neurons deform and fail mechanically will contribute to the understanding of the pathophysiology of brain injury and may help identify potential therapeutic targets. Advisors/Committee Members: Michelle C. LaPlaca, Ph.D. (Committee Chair), Andres J. Garcia, Ph.D. (Committee Member), Edward H. Pettus (Committee Member), Marc E. Levenston, Ph.D. (Committee Member), Suzanne G. Eskin, Ph.D. (Committee Member).

Subjects/Keywords: In vivo; In vitro; Traumatic brain injury; Brain Wounds and injuries; Cell membranes; Brain damage

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

APA (6th Edition):

Lessing, M. C. (2008). The acute cellular and behavioral response to mechanical neuronal injury. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/31808

Chicago Manual of Style (16th Edition):

Lessing, Marcus Christian. “The acute cellular and behavioral response to mechanical neuronal injury.” 2008. Doctoral Dissertation, Georgia Tech. Accessed September 18, 2020. http://hdl.handle.net/1853/31808.

MLA Handbook (7th Edition):

Lessing, Marcus Christian. “The acute cellular and behavioral response to mechanical neuronal injury.” 2008. Web. 18 Sep 2020.

Vancouver:

Lessing MC. The acute cellular and behavioral response to mechanical neuronal injury. [Internet] [Doctoral dissertation]. Georgia Tech; 2008. [cited 2020 Sep 18]. Available from: http://hdl.handle.net/1853/31808.

Council of Science Editors:

Lessing MC. The acute cellular and behavioral response to mechanical neuronal injury. [Doctoral Dissertation]. Georgia Tech; 2008. Available from: http://hdl.handle.net/1853/31808


Georgia Tech

3. Prado, Gustavo R. Neuronal Plasma Membrane Disruption in Traumatic Brain Injury.

Degree: PhD, Biomedical Engineering, 2004, Georgia Tech

During a traumatic insult to the brain, tissue is subjected to large stresses at high rates which often surpass cellular thresholds leading to cell dysfunction or death. Cellular events that occur at the time of and immediately after an insult are poorly understood. Immediately following traumatic brain injury (TBI), the neuronal plasma membrane may become disrupted and potentiate detrimental pathways by allowing extracellular contents to gain access to the cytosol. In the current study, neuronal plasma membrane disruption was assessed in vivo following moderate unilateral controlled cortical impact in rats using a normally cell-impermeant fluorescent compound as a plasma membrane permeability marker. This fluorescent dye was injected into the cerebrospinal fluid and was allowed to diffuse into the brain. TBI caused a widespread acute disruption of neuronal membranes which was significantly different compared to uninjured brains. Affected cells were present in cortex and hippocampal regions. These findings were complemented by an in vitro model of TBI where membrane disruption was quantified and its mechanisms elucidated. Permeability marker(s) were added to neuronal cultures before the insult as indicators for increases in plasma membrane permeability. The percentage of cells containing the permeability marker was dependent on the molecular mass, as smaller molecules gained access to a higher percentage of cells than larger ones. Permeability increases were also positively correlated with the rate of insult. Membrane disruption was transient, evidenced by a robust resealing within the first minute after the insult. In addition, membrane resealing was found to be dependent on extracellular Ca2+, as chelation of the ion abolished a significant amount of resealing. We have also investigated the effects of mechanically-induced plasma membrane disruptions on neuronal network electrical activity. We have developed a multielectrode array system that allows the study of electrical activity before, during, and after a traumatic insult to neurons. Endogenous electrical activity of neuronal cultures presented a heterogeneous response following mechanical insult. Moreover, spontaneous firing dysfunction induced by injury outlasted the presence of membrane disruptions. This study provides a multi-faceted approach to elucidate the role of neuronal plasma membrane disruptions in TBI and its functional consequences. Advisors/Committee Members: Dr. Michelle C. LaPlaca (Committee Chair), Dr. Edward Pettus (Committee Member), Dr. Mark R. Prausnitz (Committee Member), Dr. Stephen P. DeWeerth (Committee Member), Dr. Steven M. Potter (Committee Member).

Subjects/Keywords: Multielectrode array; Neurons; Rat; Electrophysiology; Calcium; Resealing; Neurons; Membranes (Biology) Electric properties; Cell membranes Wounds and injuries; Cell membranes Permeability; Brain Wounds and injuries

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

APA (6th Edition):

Prado, G. R. (2004). Neuronal Plasma Membrane Disruption in Traumatic Brain Injury. (Doctoral Dissertation). Georgia Tech. Retrieved from http://hdl.handle.net/1853/7260

Chicago Manual of Style (16th Edition):

Prado, Gustavo R. “Neuronal Plasma Membrane Disruption in Traumatic Brain Injury.” 2004. Doctoral Dissertation, Georgia Tech. Accessed September 18, 2020. http://hdl.handle.net/1853/7260.

MLA Handbook (7th Edition):

Prado, Gustavo R. “Neuronal Plasma Membrane Disruption in Traumatic Brain Injury.” 2004. Web. 18 Sep 2020.

Vancouver:

Prado GR. Neuronal Plasma Membrane Disruption in Traumatic Brain Injury. [Internet] [Doctoral dissertation]. Georgia Tech; 2004. [cited 2020 Sep 18]. Available from: http://hdl.handle.net/1853/7260.

Council of Science Editors:

Prado GR. Neuronal Plasma Membrane Disruption in Traumatic Brain Injury. [Doctoral Dissertation]. Georgia Tech; 2004. Available from: http://hdl.handle.net/1853/7260

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