Dissertations / Theses on the topic 'Glial cells'
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Förster, Bettina Ulrike. "Talin in glial cells." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612772.
Full textNazareth, Lynn. "Determining Cellular and Molecular Mechanisms Behind Glial Cell Phagocytosis." Thesis, Griffith University, 2021. http://hdl.handle.net/10072/408099.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Pharmacy & Med Sci
Griffith Health
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Schuliga, Michael, and michael schuliga@deakin edu au. "Steroidogenesis in cultured mammalian glial cells." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20061207.154152.
Full textMellor, Robert. "Neurochemical studies on cultured glial cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300038.
Full textStuckey, Crystal Elaine. "Oxidative Stress and Cell Death in Osmotically Swollen Glial Cells." Wright State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=wright1208492663.
Full textRabah, Yasmine. "Satellite glial cell-proprioceptor interactions in dorsal root ganglia Characterization of transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia Satellite glial cells modulate proprioceptive neuron function." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB208.
Full textProprioceptive neurons (one’s own neurons) are necessary for controlling motor control and locomotion. They arise from muscle spindles and tendons and synapse onto ventral horn motoneurons to deliver information about the length and contraction of muscles. Proprioceptor somata reside within the dorsal root ganglia (DRG) and are tightly enwrapped in a thin sheath of GFAP-expressing glial cells, called satellite glial cells (SGCs). Interestingly, SGCs express a number of Gq protein- coupled receptors (Gq GPCRs), which can be activated by neurotransmitters released by sensory neuron somata. Sensory neuron somata also express a number of receptors and transmitters. Both the expression of receptors and the close contact between SGCs and sensory neurons led to the hypothesis that these two cell types communicate. There is emerging evidence that SGCs and nociceptive sensory neuron (pain-sensing neurons) somata can communicate. Furthermore, to date, there is no study conducted on SGC-proprioceptor interaction. We hypothesized that SGC Gq GPCR signaling induces the release of neuroactive molecules from SGCs, leading to the modulation of proprioceptor activity. The main goal of this project has been to test this hypothesis using complementary technical approaches (2-photon Ca2+ imaging, immunohistochemistry, biochemistry and behavior) combined with a powerful chemogenetic DREADD-based tool to activate SGC Gq GPCR activity. We have demonstrated ex vivo that SGCs modulate proprioceptive neuron activity through a purinergic pathway. In order to test the physiological relevance of this discovery in vivo, we performed sensorimotor behavioral experiments and have shown that activating GFAP-expressing glial cells induces sensorimotor deficits. Determining whether SGC-induced proprioceptor activity has profound implications in the understanding of sensorimotor functions in health and diseases
Nutt, Catherine L. "Mechanisms of drug resistance in glial cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq28512.pdf.
Full textGao, Yuanqing. "Hypothalamic Glial Cells in Diet Induced Obesity." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1447071648.
Full textNieweg, Katja. "Cholesterol biosynthesis in neurons and glial cells." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/NIEWEG_Katja_2007.pdf.
Full textNieweg, Katja Pfrieger Frank. "Cholesterol biosynthesis in neurons and glial cells." Strasbourg : Université de Strasbourg, 2009. http://eprints-scd-ulp.u-strasbg.fr:8080/1048/01/NIEWEG_Katja_2007.pdf.
Full textKRISHNA, CHANDRAN ADWAID MANU. "MÜLLER GLIAL CELLS IN EPIRETINAL MEMBRANE FORMATION." Doctoral thesis, Università degli studi di Brescia, 2022. http://hdl.handle.net/11379/551759.
Full textAn epiretinal membrane (ERM) is a thin layer of fibrous tissue that can form on the surface of the retina macular area and cause vision problems. Müller glial cells appear to play a pivotal role in the pathogenesis of ERM, where various cytokines and growth factors may act as autocrine and paracrine modulators by triggering Müller cell proliferation, migration, collagen contraction, transdifferentiation, and increased expression of gliosis markers. Vitreous humor may represent a reservoir of pathological mediators that accumulate during the progression of retinal diseases. Here, the vitreous fluid obtained from iERM and PDR patients was used as a tool to investigate the activation that occurs in Müller cells in disease progression. During the first part of my Ph.D. thesis work, I participated in a research project in which we showed that surgically removed iERMs are characterized by a different pattern of expression of a series of the cell population, extracellular matrix, and cytokine/growth factor biomarkers relevant to the pathogenesis of the disease. Further, the hierarchical clustering of the gene expression data identified two molecular clusters of iERM membranes associated with distinct clinical and SD-OCT features (named iERM-A and iERM-B). iERM-A patients are characterized by less severe clinical features and a more "quiescent" iERM gene expression profile when compared to iERM-B patients. Further, I focused on understanding the role of Müller glial cells in the pathogenesis of iERM. During the progression of iERM, Müller glial cells undergo a glial-to-mesenchymal transition (GMT), a transdifferentiation process characterized by the downregulation of Müller cell markers paralleled by the upregulation of pro-fibrotic myofibroblast markers. The present study demonstrated that the vitreous fluid obtained from the iERM patients induces proliferation, migration, and GMT in MIO-M1 Müller cells, a phenotype consistent with Müller cell behaviour during iERM progression. However, even though the vitreous fluid obtained from iERM-A patients could induce a complete GMT in MIO-M1 cells, iERM-B samples caused only a partial GMT, characterized by the downregulation of Müller cell markers in the absence of upregulation of pro-fibrotic myofibroblast markers. For the final part of my thesis work, the vitreous fluid obtained from PDR patients was used as a tool to investigate the activation that occurs in Müller cells during PDR. The results show that PDR vitreous induces the acquisition of an activated phenotype in Müller cells, characterized by an increase in cell proliferation and migration, intracellular signalling activation, and proinflammatory cytokine/chemokine expression. Surprisingly, we found that the acquisition of this phenotype is not related to VEGF stimulation, whereas treatment of Müller cells with basic fibroblast growth factor (FGF2) induces a significant increase in the expression of various cytokines/chemokines in MIO-M1 cells. Accordingly, the anti-VEGF drug ranibizumab does not affect Müller cell activation mediated by PDR vitreous whereas treatment with the FGF receptor (FGFR) tyrosine kinase inhibitor BGJ398, the pan-FGF trap NSC12, the multi-target heparin-binding protein antagonist N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe Boc2, or the anti-inflammatory drug hydrocortisone inhibits, at least in part,the activity of PDR vitreous samples. Together, the results indicate that a relationship may exist among the ability of iERM vitreous to modulate GMT in Müller cells, the molecular profile of the corresponding iERMs, and the clinical features of iERM patients. Also, these data point to a role for various mediators besides VEGF in the response elicited by PDR vitreous in Müller cells.
BENCIVENNI, SERENA. "Glial cells and neuroinflammation: the adenosinergic contribution." Doctoral thesis, Università degli studi di Ferrara, 2018. http://hdl.handle.net/11392/2478763.
Full textThe hallmark of neuroinflammation is the activation of microglia, the immunocompetent cells of the CNS, releasing a number of pro-inflammatory mediators implicated in the pathogenesis of several neurological diseases such as AD, PD, MS and ischemic stroke. The innate immune TLR4, localized on the surface of microglia, is a first-line host defense receptor against invading microorganisms and LPS, a component of the cell wall of gram-negative bacteria, was first identified as the TLR ligand. ARs interacting with TLR4 influence on many immune properties of microglia and are implicated in numerous physiological and pathophysiological states in CNS. Indeed, Ado, a ubiquitous nucleoside with important immunomodulatory functions, has been found to take part in the principal microglial activation processes spanning from proliferation, process extension, retraction, migration and cytokine production. On this background, the aim of this study was to investigate the adenosinergic contribution to glial cell mediated-neuroinflammation by analyzing the expression of ARs and the signalling pathways, transcription factors and cytokines activated by them in different pathophysiological conditions linked to hypoxic and inflammatory conditions. The aim of studies reported in chapter 1 was to investigate whether Ado may affect microglia functions by acting on HIF-1α modulation, the main transcription factor of hypoxia-inducible genes, involved in the immune response, being regulated in normoxia by inflammatory mediators. Primary murine microglia were activated with LPS with or without Ado, Ado receptor agonists and antagonists and HIF-1α accumulation and downstream genes regulation were determined. Ado increased LPS-induced HIF-1α accumulation leading to an increase in HIF-1α target genes involved in cell metabolism and pathogens killing but did not induce HIF-1α dependent genes related to angiogenesis and inflammation. The stimulatory effect of Ado on HIF-1α and its target genes was essentially exerted by activation of A2A through ERK1/2 (or p44/42) and A2B subtypes via p38 MAPKs and Akt phosphorylation. Furthermore, the nucleoside raised VEGF and decreased TNF-α levels, by activating A2B subtypes. Our results show that Ado increases GLUT-1 and iNOS gene expression in a HIF-1α-dependent way, through A2A and A2B ARs, suggesting their role in the regulation of microglial cells function following injury. However, inhibition of TNF-α adds an important anti-inflammatory effect only for the A2B subtype. The aim of studies reported in chapter 2 was to indagate the potential role of ARs in the modulation of IL-6 secretion and cell proliferation in primary microglial cells. The A2B AR agonist BAY 60-6583 stimulated IL-6 increase under normoxia and hypoxia, in a dose- and time-dependent way. In cells incubated with the blockers of PLC, PKC-ε and PKC-delta the IL-6 increase due to A2B AR activation was strongly reduced, whilst it was not affected by the inhibitor of AC. Investigation of cellular signalling involved in the A2B AR effect revealed that only the inhibitor of p38 MAPK was able to block the agonist effect on IL-6 secretion, whilst inhibitors of ERK1/2, JNK1/2 MAPKs and Akt were not. Stimulation of p38 by BAY 60-6583 was A2B AR dependent, through PLC, PKC-ɛ and PKC-delta but not AC pathway, in both normoxia and hypoxia. Finally, BAY 60-6583 increased microglial cell proliferation involving A2B AR, PLC, PKC-ε PKC-delta and p38 signalling. Our results show for the first time that Ado by activating A2B ARs increases IL-6 protein levels and cell proliferation through a pathway dependent on PLC, PKC-ε, PKC-delta, and p38 signalling. These findings add new molecular pathways activated by Ado in microglia to give a reduction of genes and cytokines involved in inflammation and hypoxic injury that may cohexist in stroke, ischemia and other CNS disorders.
BOZZO, MATTEO. "Glial cells of the developing amphioxus: a molecular study." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1043680.
Full textDe, Pascalis Chiara. "Role of intermediate filaments in collective cell migration of glial cells." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066026.
Full textDuring morphogenesis, tissue repair and cancer, cells can migrate in a mesenchymal and collective manner. The cytoskeleton is essential for migration, but whereas actin and microtubules have been extensively studied, the role of intermediate filaments (IFs) is still largely unknown. IF depletion generally decreases migration speed and IF proteins are frequently found upregulated in invasive tumours. Because of IF properties, we hypothesise that they may be key players in cell mechanics during migration. To study the role of IFs in collective migration we used astrocytes, the main glial cells of the central nervous system. Astrocytes migrate collectively during development and astrogliosis in response to pathological or traumatic signals. Astrocytes express three main cytoplasmic IFs: nestin, GFAP (Glial Fibrillary Acidic Protein) and vimentin, which form a dense network. IF proteins are upregulated during astrogliosis and glioblastomas, highly invasive and lethal brain tumours. Whether upregulation of IFs is responsible for glioblastoma invasion is still unknown. During wound-induced collective migration, IFs control nuclear positioning, polarisation and migration. We found that IFs regulate collective directed migration in a stiffness-dependent manner. They act in concert with the cytolinker protein plectin to control focal adhesions and adherens junctions. IFs control actin dynamics and organisation and regulate the distribution of cell tractions and stresses across the migrating cell monolayer. These results demonstrate the crucial role of IFs in the mechanical properties of migrating cells
De, Pascalis Chiara. "Role of intermediate filaments in collective cell migration of glial cells." Electronic Thesis or Diss., Paris 6, 2017. http://www.theses.fr/2017PA066026.
Full textDuring morphogenesis, tissue repair and cancer, cells can migrate in a mesenchymal and collective manner. The cytoskeleton is essential for migration, but whereas actin and microtubules have been extensively studied, the role of intermediate filaments (IFs) is still largely unknown. IF depletion generally decreases migration speed and IF proteins are frequently found upregulated in invasive tumours. Because of IF properties, we hypothesise that they may be key players in cell mechanics during migration. To study the role of IFs in collective migration we used astrocytes, the main glial cells of the central nervous system. Astrocytes migrate collectively during development and astrogliosis in response to pathological or traumatic signals. Astrocytes express three main cytoplasmic IFs: nestin, GFAP (Glial Fibrillary Acidic Protein) and vimentin, which form a dense network. IF proteins are upregulated during astrogliosis and glioblastomas, highly invasive and lethal brain tumours. Whether upregulation of IFs is responsible for glioblastoma invasion is still unknown. During wound-induced collective migration, IFs control nuclear positioning, polarisation and migration. We found that IFs regulate collective directed migration in a stiffness-dependent manner. They act in concert with the cytolinker protein plectin to control focal adhesions and adherens junctions. IFs control actin dynamics and organisation and regulate the distribution of cell tractions and stresses across the migrating cell monolayer. These results demonstrate the crucial role of IFs in the mechanical properties of migrating cells
Gale, Zoe. "Glial cell line-derived neurotrophic factor effects on dental pulp cells and osteoblast-like cells." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3268/.
Full textCotterill, Claire Louise. "Semliki Forest virus-induced apoptosis in glial cells." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29712.
Full textBianco, F. "The role of P2X7 receptor in glial cells." Doctoral thesis, Università degli Studi di Milano, 2007. http://hdl.handle.net/2434/63133.
Full textGöritz, Christian. "Influence of glial cells on postnatal differentiation of rat retinal ganglion cells." [S.l. : s.n.], 2005. http://www.diss.fu-berlin.de/2005/65/index.html.
Full textGöritz, Christian. "Influence of glial cells on postnatal differentiation of rat retinal ganglion cells." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. https://publication-theses.unistra.fr/public/theses_doctorat/2005/GORITZ_Christian_2005.pdf.
Full textJacques, Cécile. "Etude du rôle et du mécanisme d'action des facteurs de transcription glial cell deficient/glial cells missing au cours du développement." Université Louis Pasteur (Strasbourg) (1971-2008), 2007. https://publication-theses.unistra.fr/public/theses_doctorat/2007/JACQUES_Cecile_2007.pdf.
Full textGcm-Gcm2 transcription factors are known for their role in glial and plasmatocytes differentiation in Drosophila embryo. During my PhD, I have shown that gcm-gcm2 genes are required for terminal differentiation of a subpopulation of tendon cells. Thereafter, we showed that the chicken c-GCM1 orthologue is required during embryogenesis for the differentiation of spinal cord neural precursors into neurons. We have also shown that gcm genes are expressed and required in post-embryonic neural brain lineages of Drosophila. All these studies show that the specific role of Gcm transcription factors depends on the cellular context in which they are expressed. A two hybrid screen enabled me to identify the cofactor dpias and its study has allowed me to show the implication of Gcm in larval hematopoiesis
Jacques, Cécile Giangrande Angela. "Étude du rôle et du mécanisme d'action des facteurs de transcription Glial cell deficient/Glial cells missing au cours du développement." Strasbourg : Université de Strasbourg, 2009. http://eprints-scd-ulp.u-strasbg.fr:8080/1139/01/JACQUES_Cecile_2007.pdf.
Full textBlackburn, Daniel J. "The role of glial cells in motor neuron disease." Thesis, University of Sheffield, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.531123.
Full textActon, David. "Regulation of mammalian spinal locomotor networks by glial cells." Thesis, University of St Andrews, 2017. http://hdl.handle.net/10023/10133.
Full textTESTA, FRANCESCA. "EVALUATION OF rHIgM22 EFFECT ON MIXED GLIAL CELLS CULTURE." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/543913.
Full textMallick, Ali Sameer. "Stem cell therapies for sensorineural hearing loss : understanding the role of glial cells." Thesis, University of Sheffield, 2017. http://etheses.whiterose.ac.uk/19788/.
Full textDelbaz, Seyed Ali. "Multi-nucleated glial cells and the implication for neural health." Thesis, Griffith University, 2017. http://hdl.handle.net/10072/379570.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Environment and Sc
Science, Environment, Engineering and Technology
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Downing, Trevor. "THE RELATIONSHIP BETWEEN LACTIC ACID, REACTIVE OXYGEN SPECIES AND THE HYPOXIA-INDUCED ACIDIFICATION SEEN IN CHEMOSENSITIVE NEURONS OF THE NUCLEUS TRACTUS SOLITARIUS (NTS)." Wright State University / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=wright1158455199.
Full textTIBERI, ALEXIA. "A glial side to the neurotrophin field: studying the effects of neurotrophins on glial cells in the CNS." Doctoral thesis, Scuola Normale Superiore, 2020. http://hdl.handle.net/11384/94548.
Full textSinclair, Michael S. "Modulation of Peripheral Taste Function by Glial-like Taste Cells." Scholarly Repository, 2012. http://scholarlyrepository.miami.edu/oa_dissertations/715.
Full textKöritzer, Julia. "Biophysical effects of cold atmopheric plasma on glial tumor cells." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-162120.
Full textKeen, Leigh John. "The growth and pharmacology of insect glial cells in vitro." Thesis, Oxford Brookes University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359837.
Full textSmith, Peter Michael. "Investigations into the myelinating capability of transplanted porcine glial cells." Thesis, University of Cambridge, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624554.
Full textNg, Wai Yee. "Ginsenosides on the growth and proliferation of glial tumor cells." HKBU Institutional Repository, 2008. http://repository.hkbu.edu.hk/etd_ra/998.
Full textDe, Simone Francesca Isabella. "Neuroimmune regulation of JCV by immune mediators in glial cells." Doctoral thesis, Universita degli studi di Salerno, 2015. http://hdl.handle.net/10556/2045.
Full textThe human polyomavirus JC (JCV) is a small DNA virus responsible for the initiation of progressive multifocal leukoencephalopathy (PML), an often lethal disease of the brain characterized by lytic infection of oligodendrocytes in the central nervous system (CNS). Patients undergoing immune modulatory therapies for the treatment of autoimmune diseases such as multiple sclerosis, and individuals with an impaired-immune system, most notably AIDS patients, are in the high risk group of developing PML. Previous studies suggested that soluble immune mediators secreted from PBMCs inhibited viral genomic replication. However little is known regarding the molecular mechanism of this regulation. Here we investigated the impact of conditioned media (CM) from activated PBMCs on viral replication and gene expression by molecular virology techniques. Our data showed that viral gene expression as well as viral replication was suppressed by the CM. Further studies revealed that soluble immune mediators from PBMCs possessed a dual control on T-antigen expression at transcription and post-transcription level. These observations demonstrate a novel role of immune mediators in regulation of JCV gene expression, and provide a new avenue of research to understand molecular mechanism of viral reactivation in patients who are at risk of developing PML. [edited by author]
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Tassoni, Alessia. "Retinal glial responses to mesenchymal stem cell transplantation." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709042.
Full textDean, Charlotte Hannah. "The transcription factors dHAND and eHAND and the growth factor HGF are involved in peripheral nervous system development." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367740.
Full textDavis, Hedvika. "Glial differentiation of human umbilical stem cells in 2D and 3D environments." Doctoral diss., University of Central Florida, 2011. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/4931.
Full textID: 029808916; System requirements: World Wide Web browser and PDF reader.; Mode of access: World Wide Web.; Thesis (Ph.D.)--University of Central Florida, 2011.; Includes bibliographical references (p. 77-86).
Ph.D.
Doctorate
Burnett School of Biomedical Sciences
Medicine
Biomedical Sciences
Franceschini, Isabelle A. "Cellular and molecular studies on olfactory bulb ensheathing cells." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301803.
Full textWahl, Vincent. "Wirkung von Osteopontin auf die osmotische Volumenregulation von Müller- und Bipolarzellen der Rattennetzhaut." Doctoral thesis, Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-198550.
Full textChen, Mo. "Natural products and glial cell therapy for repairing the nervous system." Thesis, Griffith University, 2019. http://hdl.handle.net/10072/389731.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Environment and Sc
Science, Environment, Engineering and Technology
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Vrotsos, Emmanuel George. "MCP-1 and APP involvement in glial differentiation and migration of neuroprogenitor cells." Orlando, Fla. : University of Central Florida, 2009. http://purl.fcla.edu/fcla/etd/CFE0002517.
Full text李勝修 and Shengxiu Li. "The role of glial cells in the survival and axonal regeneration of retinal ganglion cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238932.
Full textLi, Shengxiu. "The role of glial cells in the survival and axonal regeneration of retinal ganglion cells /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20897650.
Full textTeare, Katrina Anne. "Designing a delivery system for glial cells for spinal cord repair." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.428927.
Full textLawton, Michelle. "The effect of heavy metals on differentiated neuronal and glial cells." Thesis, Nottingham Trent University, 2007. http://irep.ntu.ac.uk/id/eprint/219/.
Full textCoulibaly, Aminata P. "Changes in Sympathetic Preganglionic Neurons and Associated Glial Cells following Injury." Miami University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=miami1281032308.
Full textEduafo, Augusta K. "Mechanisms of Hyperglycemia-Induced ROS Production in Osmotically Swollen Glial Cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1433185840.
Full textMouzannar, Raymond. "Higher order chromatin degradation induced by hydrogen peroxide in glial cells." Morgantown, W. Va. : [West Virginia University Libraries], 2001. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=2098.
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Donohue, Carolyn Elizabeth. "EXPRESSION OF Npcl IN GLIAL CELLS CORRECTS STERILITY IN Npcl-/- MICE." Thesis, The University of Arizona, 2009. http://hdl.handle.net/10150/192331.
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