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Dissertations / Theses on the topic 'Adenoviral; Nervous system; Central'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

Regardsoe, Emma Louise. "An investigation into the role of Fas ligand as a potential immunomodulatory molecule for CNS gene therapy." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365794.

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2

Zheng, Luyu. "The role of Coxsackie and Adenovirus receptor in the central nervous system." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86782.

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The Coxsackie and adenovirus receptor (CAR), a newly described regulator of neurite outgrowth in the developing central nervous system (CNS), is an adhesion molecule of the immunoglobulin superfamily. CAR is highly expressed in the developing brain, but its level is down-regulated in adult nervous system. Recently, CAR has been demonstrated to mediate homophilic cell-cell adhesion in tumor cell-lines and to be a transmembrane component of the tight junction in epithelial cells. We observed that neurons grown in the presence of soluble CAR have longer neurites compared to BSA control. Furthermore, the presence of soluble CAR was able to overcome the inhibitory effect of cytokines (TNFα) and restore the neurite length to control level. In addition, using hippocampal neuron cultures prepared from CAR embryos in which exon 2 of CAR is flanked by LoxP sites ("CAR-flox"), and infected with the adenovirus AdV-CRE-GFP or control vector (AdV-BFP), we demonstrated that both neuron survival and neurite length were affected by knockown of CAR expression. It has been shown that general knockout of CAR results in embryonic lethality; by breeding CAR-floxed mice (a generous gift of Jeffrey Bergelson, U. Pennsylvania) to synapsin-1-Cre transgenic mice we have developed conditional knockout mice in which CAR is deleted specifically in the nervous system. Here, we report some morphological alterations observed in animals lacking CAR in the CNS. The results of this study will further our understanding of the role CAR plays in developmental processes in the brain.<br>Le récepteur du coxsackievirus et de l'adénovirus (CAR) est une molécule d'adhérence de la famille immunoglobuline. CAR est exprimée dans le cerveau avant la naissance, mais le niveau est réduit dans le cerveau adulte. Récemment, il a été montré que CAR est nécéssaire pour l'adhérence entre les cellules tumorales, et qu'il est aussi un composant de la jonction transmembranaire des cellules épithéliales. Nous avons observé que les neurones mis en culture en présence d'une forme soluble de CAR dévelopent des prologements cellulaires plus longs comparés aux neurones qui sont en présence de BSA. En outre, la présence de la forme soluble de CAR neutralise l'effet inhibiteur du cytokine TNFα. En utilisant des neurones hippocampiques préparé à partir d'embryons CAR dans lequel l'exon 2 de CAR est flanqué de sites loxP (CARFLOX), et infecté par l'adénovirus AdV-CRE-GFP ou vecteur contrôle (AdV-BFP), nous avons démontré que la survie des neurones et la longueur des neurites ont été affectés par la diminution de l'expresssion de CAR. Nouse avons aussi croisé les CARFLOX avec des souris transgéniques exprimant la recombinase Cre sous le contrôle du promoteur de la synapsine I afin de produire des souris dans lesquelles l'expression de CAR serait en baisse spécifiquement dans le système nerveux central. Nous rapportons ici quelques altérations morphologiques observées chez ces animaux. Les résultats de cette étude permettra d'approfondir notre compréhension du rôle que CAR joue dans les processus de développement du cerveau.

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3

Gonzalez, Sarah Charlotte. "An investigation into retrograde transport of adenovirus vectors in the central nervous system." Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398162.

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4

Hornsey, Mark Alan. "Adenovirus-mediated delivery of transgenes to both the central nervous system and peripheral targets : potential and problems." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393405.

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5

Nunes, Rafaella Almeida Lima. "Aplicação de técnicas moleculares no diagnóstico laboratorial complementar das infecções virais do sistema nervoso central no Hospital Universitário da USP." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-19032014-160513/.

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Enterovírus (HEV), herpesvírus 1 e 2 (HHV-1 e HHV-2) e adenovírus (HAdV) são importantes agentes de infecções do SNC. Neste trabalho, técnicas moleculares foram aplicadas para a detecção destes vírus em quadros de infecção do SNC. Amostras de líquor foram colhidas de pacientes atendidos no HU-USP entre agosto e novembro/2010 e fevereiro/2012 a janeiro/2013. Através da Nested-PCR HEV foram detectados em 9,8% das amostras, HAdV em 2,5% e HHV-1 e 2 em 1,1%, além de 3 casos de coinfecção, 2 entre HEV e HHV, e 1 entre HEV e HAdV. O material genético viral foi extraído através dos métodos Qiaamp DNA Blood (Qiagen®) e MagMAXTM Viral RNA Isolation (Ambiom), e este último pareceu mais adequado à aplicação na rotina clínica. A análise quimiocitológica do líquor mostrou-se importante no direcionamento da conduta clínica, mas a detecção do vírus é fundamental para a conclusão do diagnóstico. A PCR em tempo real, cuja padronização foi iniciada neste trabalho, consiste em importante ferramenta para a utilização futura no diagnóstico complementar das infecções virais do SNC.<br>Enteroviruses (HEV), herpesviruses 1 and 2 (HHV-1 and HHV-2) and adenoviruses (HAdV) are important causative agents of infections of the CNS. In this study, molecular techniques were applied to the detection of these viruses. CSF samples were collected from patients treated at the University Hospital of USP, between August and November, 2010, and February 2012 and January 2013. By the Nested-PCR reaction, HEV were detected in 9.8% of the samples, HAdV in 2.5% and HHV-1 and 2 in 1.1%. There were 3 cases of coinfection: 2 with HEV and HHV and other with HEV and HAdV. The viral genetic materials were extracted by QIAamp DNA Blood kit (Qiagen®) and MagMAXTM Viral RNA Isolation (Ambiom), and the second one showed to be more suitable for the application in clinical diagnosis. The CSF chemocytologic analysis proved to be important in directing the clinical conduct, but the detection of viruses is essential for the diagnosis. The real time PCR, which standardization was initiated in this work, will be an important tool for complementary diagnosis of viral infections of the CNS.

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6

Solomon, Thomas. "Central nervous system infections in Vietnam." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340736.

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7

Zhang, Hui. "Remyelination in the central nervous system." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/8095.

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Multiple Sclerosis (MS) is an inflammatory disease which causes areas of demyelination in the Central Nervous System (CNS) and affects only humans. Current therapies for MS are focused on anti-inflammatory treatment, which reduce the occurrence and clinical relapses of the disease. However, progressive disability of the disease is related to axonal degeneration. After demyelination, remyelination occurs, which helps repair the demyelinated lesions and protects axons from degeneration. However, this endogenous remyelination is inefficient, and currently there are no therapies available to enhance remyelination. The aim of this thesis was to first characterize a fast and reliable model to study CNS remyelination in vitro, and second to investigate the role of semaphorin 3a (Sema3A) and semaphorin 3f (Sema3F) signaling in CNS remyelination. Various in vivo models have been developed to investigate the pathology of multiple sclerosis, and can be used to test remyelination therapies. However, in vivo models are expensive, animal- and time- consuming. Until now, there has been no well-characterized and robust in vitro model for remyelination study. In this thesis, an ex vivo slice culture system with mouse brain and spinal cord was developed, and characterized by immunofluorescent microscopy and transmission electron microscopy, for CNS remyelination study. Automated (re)myelinating quantification by image pro plus software was developed and validated to provide a fast and reliable way for testing factors that change remyelination efficiency. Two such factors are Sema3A and 3F, which were initially identified as axon guidance cues during development. Sema3A (repulsive) and 3F (attractive) were proved to play a role in oligodendrocyte precursor cell (OPC) migration during development, and hypothesized to be important in remyelination. In this thesis, I investigated the effects and mechanisms for this by adding recombinant SEMA3A or SEMA3F or by knockdown their obligatory receptors Neuropilin (Nrp) 1 and 2, using lentivirus induced miRNAi. Slice culture and primary OPC culture were used to determine the effect on OPC survival, migration, proliferation, differentiation and myelination.

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8

Poland, Stephen D. "Central nervous system infection with human cytomegalovirus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq21311.pdf.

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9

Hüppi, Petra Susan. "Serum antibodies to central nervous system antigens /." [S.l : s.n.], 1986. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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10

Bernick, Kristin Briana. "Cell biomechanics of the central nervous system." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/67202.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2011.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 133-153).<br>Traumatic brain injury (TBI) is a significant cause of death and morbidity in both the civilian and military populations. The major causes of TBI, such as motor vehicle accidents, falls, sports concussions, and ballistic and explosive blast threats for military personnel, are well established and extensively characterized; however, there remains much to be learned about the specific mechanisms of damage leading to brain injury, especially at the cellular level. In order to understand how cells of the central nervous system (CNS) respond to mechanical insults and stimuli, a combined modeling/experimental approach was adopted. A computational framework was developed to accurately model how cells deform under various macroscopically imposed loading conditions. In addition, in vitro (cell culture) models were established to investigate damage responses to biologically relevant mechanical insults. In order to develop computational models of cell response to mechanical loading, it is essential to have accurate material properties for all cells of interest. In this work, the mechanical responses of neurons and astrocytes were quantified using atomic force microscopy (AFM) at three different loading rates and under relaxation to enable characterization of both the elastic and viscous components of the cell response. AFM data were used to calibrate an eight-parameter rheological model implemented in the framework of a commercial finite element package (Abaqus). Model parameters fit to the measured responses of neurons and astrocytes provide a quantitative measure of homogenized nonlinear viscoelastic properties for each cell type. In order to ensure that the measured responses could be considered representative of cell populations in their physiological environment, cells were also grown and tested on substrates of various stiffness, with the softest substrate mimicking the stiffness of brain tissue. Results of this study showed both the morphology and measured force response of astrocytes to be significantly affected by the stiffness of their substrate, with cells becoming increasingly rounded on soft substrates. Results of simulations suggested that changes in cell morphology were able to account for the observed changes in AFM force response, without significant changes to the cell material properties. In contrast, no significant changes in cell morphology were observed for neurons. These results highlight the importance of growing cells in a biologically relevant environment when studying mechanically mediated responses, such as TBI. To address this requirement, we developed two model systems with CNS cells grown in soft, 3D gels to investigate damage arising from dynamic compressive loading and from a shock pressure wave. These damage protocols, coupled with the single cell computational models, provide a new tool set for characterizing damage mechanisms in CNS cells and for studying TBI in highly controllable in vitro conditions.<br>by Kristin Briana Bernick.<br>Ph.D.

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11

Coutinho, Maria Ester Freitas Barbosa Pereira. "Central nervous system autoimmunity in neuropsychiatric disorders." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:389fb830-4b4e-4201-9965-19acb2c63ff3.

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The recent history of autoimmune neurology is marked by the discovery of many central nervous system (CNS) antibody-mediated diseases. These disorders are caused by antibodies that target important proteins expressed in the neuronal surface, which are believed to be directly pathogenic. These antibodies are immunoglobulin G (IgG) isotype and, as such, have the potential to cross the placenta during gestation. Foetal exposure to CNS-targeting antibodies could alter developing neuronal circuits, leading to disease. However, the consequences of exposure to these antibodies during neurodevelopment has hardly been considered. To study the relationship between maternal antibodies towards neuronal surface proteins and neurodevelopmental disorders in the foetus a dual approach was undertaken. First, pregnancy serum samples from mothers of children later diagnosed with a neurodevelopmental disorder and from mothers of children with typical development were screened for the presence of neuronal surface antibodies. Next, the effects of pathogenic neuronal surface antibodies in the offspring were assessed in a maternal-to-foetal transfer mouse model. Antibodies to neuronal surface proteins in the gestational serum, particularly CASPR2 antibodies, were found to associate with an increased risk of mental retardation and disorders of psychological development in the progeny. The animal model showed that mice exposed in utero to CASPR2 antibodies have long term behavioural sequelae and histological findings suggestive of abnormalities in brain development. These findings support a model in which maternal antibodies towards foetal neuronal proteins cause long-term behavioural deficits and permanent abnormalities at the cellular and synaptic level in a subset of children with neurodevelopmental disorders.

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12

Suzumura, Akio. "Microglia : Immunoregulatory cells in the central nervous system." Nagoya University School of Medicine, 2002. http://hdl.handle.net/2237/5375.

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13

Piani, Daniela. "Immune-mediated cytotoxicity in the central nervous system /." [S.l.] : [s.n.], 1993. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10423.

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14

Lamvik, Kate K. "Central Nervous System Associations in Neurofibromatosis Type 1." Cincinnati, Ohio : University of Cincinnati, 2007. http://rave.ohiolink.edu/etdc/view.cgi?acc_num=ucin1179426618.

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Thesis (M.S.)--University of Cincinnati, 2007.<br>Advisor: Dr. Elizabeth K. Schorry. Title from electronic thesis title page (viewed June 30, 2010). Includes abstract. Keywords: Neurofibromatosis type 1 (NF1); optic pathway glioma (OPG); central nervous system (CNS). Includes bibliographical references.

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15

Lee, Yong Beom. "Cytokine network in the human central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0022/NQ38925.pdf.

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16

Weber, Wilhelm Evert Jacob. "Cellular auto-immunity in central nervous system disease." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1988. http://arno.unimaas.nl/show.cgi?fid=5594.

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17

Jackson, Johanna Sara. "Stem cell tracking in the central nervous system." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.446551.

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18

Bell, Michael David. "Factors regulating inflammation in the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308694.

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19

Smith, Imogen. "Cannabinoid receptor signalling in the central nervous system." Thesis, University of Reading, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.553656.

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The GPCRs CB1R and CB2R are targets for endocannabinoids, exogenous synthetic agents and phytocannabinoids derived from Cannabis plants. However, the pharmacological properties of many phytocannabinoids remain to be elucidated. The present work focused on activity of cannabinoids at CB1R, and potentially other targets, in brain membrane preparations and a cell culture model of epileptiform activity. The synthetic cannabinoids WIN55,212-2 (CB1/2R agonist) and AM251 (CB1R antagonist), and the phytocannabinoids fl9_THCV, CBO and CBG were investigated using radioligand binding and [35SjGTPyS assays to assess pharmacological actions, and patch-clamp electrophysiology to study functional effects. Radioligand competition binding assays using the CB1R antagonist [3HjSR141716A demonstrated high affinity binding of AM251 and WIN55,212-2, moderate affinity of fl9_ THCV, and weak affinity of CBO and CBG. [35SjGTPyS binding assays were used to construct concentration response curves for all compounds, and showed potent efficacious agonism by WIN55,212-2, whilst fl9_THCV, CBO, and CBG showed no agonist activity. AM251 and fl9_ THCV were used in Schild analyses, and demonstrated potent antagonism of CB1R at submicromolar concentrations. At higher concentrations, AM251 and fl9_THCV caused depression of [35SjGTPyS binding. For AM251, but not fl9_THCV, further investigations demonstrated an adenosine Al receptor component of this depression. To enable functional studies, a novel cell culture model of Mg2+-free pre-treatment induced epileptiform activity in mouse cortical neurones was successfully developed. In electrophysiological investigations WIN55,212-2 and fl9 -THCV reduced action potential firing in epileptiform neurones. The effects of WIN55,212 were blocked by AM251, suggesting a CB1R-mediated mechanism. fl9_THCV, CBG and AM251 reduced peak action potential amplitude, potentially via a non-CBR mechanism. Further investigations showed fl9_THCV and CBG reduced peak Na+ conductance suggesting functional, potentially therapeutic, effects via voltage-gated Na+ channels. These data demonstrate novel forms of cannabinoid signalling in the CNS, show that phytocannabinoids have a range of CBR affinities, and may have additional targets in the CNS.

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20

Sussman, Jonathan David. "Glial lineages in the adult central nervous system." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625026.

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21

McQuaid, Stephen. "Measles virus infection of the central nervous system." Thesis, Queen's University Belfast, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287361.

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22

Davies, M. "5-hydroxytryptamine receptors in the central nervous system." Thesis, Bucks New University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382505.

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23

Panni, Moeen. "Neuron-target interactions in the central nervous system." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337889.

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24

Staley, Kristina. "Targeting gene expression to the central nervous system." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319537.

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25

Galtrey, Clare Margaret. "Central nervous system plasticity and peripheral nerve repair." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614254.

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26

Roberts, Malcolm Ian. "Death receptor 3 in the central nervous system." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.615645.

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27

Rist, Julia Maria. "Rejuvenating remyelination in the ageing central nervous system." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608517.

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28

Almeida, Rafael. "Axon-glia interactions during central nervous system myelination." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21038.

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Myelination drastically speeds up action potential propagation along axons, which is fundamental for the correct function of neuronal circuits. However, axon-oligodendrocyte interactions regulating the onset of myelin formation remain unclear. I sought to determine how reticulospinal axons control myelination, as they are the first myelinated in the zebrafish spinal cord. I genetically manipulated zebrafish in order to either remove such axons from a region of the spinal cord, or to increase their number, and characterized oligodendrocyte-lineage cells following this axonal loss- or gain-of-function. In kinesin-binding protein (kbp) mutants, reticulospinal hindbrain neurons start axonogenesis but axons fail to grow along the entire spinal cord as in wildtype, providing an axon-deficient posterior spinal cord and an intact anterior region. I found that early stages of oligodendrocyte development, such as the specification of oligodendrocyte precursors, their distribution and migration were not affected in the posterior spinal cord of these mutants. However, both the proliferation and the survival of late precursors were impaired, resulting in a significant reduction of mature oligodendrocytes in the posterior region of mutants at the onset of myelination. Since the anterior spinal cord of mutants is indistinguishable from wildtype, these results demonstrate that reticulospinal axons provide a mitogenic and a survival signal to a subset of developing OPCs, enabling their differentiation and lineage progression. I then found that the absence of reticulospinal axons did not affect the timing of oligodendrocyte differentiation, which matured on time, suggesting that this follows an intrinsic timer, as previous studies suggested. Oligodendrocytes also did not myelinate incorrect axonal targets, but instead adapted to the reduced axonal surface by elaborating fewer myelin sheaths. Additionally, oligodendrocytes made shorter sheaths, and also incorrectly ensheathed neuron somas in the mutant spinal cord, suggesting that either kbp function or a precise amount of axonal surface are required to prevent ectopic myelination of somas and to promote the longitudinal growth of myelin sheaths. In wildtype animals, the two reticulospinal Mauthner axons are the very first myelinated in the spinal cord. In animals where Notch1a function is temporarily abrogated or hoxb1 genes are temporarily upregulated, supernumerary Mauthner neurons are generated. I found that these extra axons are robustly myelinated, with no impairment of myelination of adjacent axons. Surprisingly, the number of oligodendrocytes was not altered, but I found that each individual oligodendrocyte elaborated more myelin sheaths, whose total length was also longer than in wildtypes. Additionally, dorsal oligodendrocytes, which normally myelinate only small-calibre dorsal axons, readily extended processes ventrally to myelinate the supernumerary large-calibre Mauthner axons, in addition to small-calibre axons. These results suggest that oligodendrocytes are plastic and are not destined to myelinate a particular type of axon, and conversely, that axonal signals that induce myelination are similar for different axons. The long-standing observation that oligodendrocytes tend to myelinate either few large axons or many small axons thus reflects local interactions of oligodendrocyte processes with the nearby axons, rather than different subtypes of oligodendrocytes specified by an intrinsic programme of differentiation. Collectively, this work shows that axons extensively influence both oligodendrocyte lineage progression and oligodendrocyte myelinating potential in vivo.

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Gifford, Andrew Neal. "Catecholaminergic neurotransmission in the insect central nervous system." Thesis, University of St Andrews, 1989. http://hdl.handle.net/10023/15042.

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Wheeler, Natalie A. "Autotaxin in Central Nervous System Development and Disease." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4104.

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During development, oligodendrocytes (OLGs), the myelinating cells of the central nervous system (CNS), undergo a stepwise progression during which OLG progenitors, specified from neural stem/progenitor cells, differentiate into fully mature myelinating OLGs. This progression along the OLG lineage is characterized by well-synchronized changes in morphology and gene expression patterns. The studies presented in this dissertation identified the extracellular factor Autotaxin (ATX) as a novel upstream signal modulating HDAC1/2 activity and gene expression in cells of the OLG lineage. Using the zebrafish as an in vivo model system, as well as rodent primary OLG cultures, this functional property of ATX was found to be mediated by its lysoPLD activity, which has been well-characterized to generate the lipid signaling molecule lysophosphatidic acid (LPA). LPA binds to Gprotein-coupled LPA receptors (LPARs) on the surface of OLGs to initiate downstream signaling events. ATX’s lysoPLD activity was found to modulate HDAC1/2 regulated gene expression during a time window coinciding with the transition from OLG progenitor to early differentiating OLG. When looking further downstream of the ATX-LPA axis, down-regulation of LPA receptor 6 (LPA6) was found to reduce the expression of OLG differentiation genes as well as the overall process network area of OLGs. Thus, LPA6 plays a role in both the gene expression and morphology changes seen in OLG differentiation. These findings prove useful for future therapeutic targets needed for demyelinating diseases of the CNS such as Multiple Sclerosis (MS), in which OLGs fail to differentiate into mature OLGs, needed for remyelination. Additionally, white matter injury has been frequently reported in HIV+ patients. Previous studies showed that HIV-1 Tat (transactivator of transcription), a viral protein that is produced and secreted by HIV-infected cells, is a toxic factor to OLGs. We show here that Tat treatment reduces the expression of OLG differentiation genes and the overall process network area of OLGs. Additionally, Tat-treated OLGs have reduced ATX lysoPLD activity and there is a physical interaction between Tat and ATX. Together, these data strongly suggest functional implications of Tat blocking ATX’s lysoPLD activities and thus the ATX-LPA signaling axis proves to play a significant role in the development of OLGs.

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31

Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.

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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.

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32

Foster, Michelle Tranace. "Central nervous system regulation of fat cell lipid mobilization the role of the sympathetic nervous system /." restricted, 2005. http://etd.gsu.edu/theses/available/etd-11162005-154631/.

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Thesis (Ph. D.)--Georgia State University, 2005.<br>Timothy Bartness, committee chair; Elliott Albers, Ruth Harris , Sarah Pallas, committee members. Electronic text (181 p. : ill.)) : digital, PDF file. Description based on contents viewed July 17, 2007. Includes bibliographical references (p. 148-181).

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33

Tep-Cullison, Chhavy R. "Distinct roles of p75 regulation on myelination in the peripheral nervous system and central nervous system." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1299179635.

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34

Eckert, Bodil. "Hypoglycaemia studies on central and peripheral nerve function /." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/57426099.html.

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35

Zhang, Xiaochun. "Involvement of neuroinflammation in models of neurodegeneration." Laramie, Wyo. : University of Wyoming, 2008. http://proquest.umi.com/pqdweb?did=1663059561&sid=3&Fmt=2&clientId=18949&RQT=309&VName=PQD.

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36

Fundytus, Marian Elaine. "Central nervous system and peripheral signs of opioid abstinence." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=56639.

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It was hypothesized that a metabolite of morphine, morphine-3-glucuronide (M3G), contributes to the expression of symptoms seen during withdrawal from morphine. To test this hypothesis, the behaviors observed during precipitated withdrawal from morphine and sufentanil were compared. Sufentanil was chosen because, like morphine, it acts primarily at the mu opioid receptor, but has different metabolites. Differences in the abstinence syndromes produced by the two drugs may therefore be attributable to the actions of metabolites, rather than the primary opioid actions of morphine and sufentanil. Although there were some differences in the occurrence of symptoms, morphine and sufentanil withdrawal were very similar. Therefore, the evidence was inconclusive as to the contribution of metabolites during withdrawal.<br>Systemic administration of M3G alone and in combination with morphine produced no withdrawal-like behaviors. However, when these drugs were given centrally, withdrawal-like behaviors were observed in conjunction with seizures. The seizures were not attenuated by naloxone (but were alleviated by an anti-convulsant), indicating that they were not mediated by opioid receptors. The behaviors resembled those seen by previous investigators following high doses of morphine. The results suggest that M3G may play a role in the toxic effects of high doses of morphine.

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37

Goudreau, Guy. "Transgenic models of retrovirus-mediated central nervous system diseases." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=39908.

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Neurological diseases are a common consequence of retroviral infections. The pathogenesis of these diseases however remains undetermined. In an attempt to elucidate the mechanisms involved in certain of these disorders, we have used an experimental approach involving transgenic mice. Transgenic animals provide an important tool in the study of retroviral diseases, since they allow us to circumvent the complex process of retroviral infection. In addition, when retroviral sequences are expressed under the regulation of a CNS-specific promoter, transgenic experiments allow us to evaluate the effects of expressing viral gene products in a given CNS cell population. Specific aspects of the neurological disorders caused by HIV-1, HTLV-1, and Cas-Br-E MuLV were evaluated. Transgenic mice experiments were generated in order to study the pathogenesis of the CNS white matter diseases caused by human retroviruses HIV-1 and by HTLV-1, and to evaluate the function of astroglial cells in mediating the CNS disease associated with Cas-Br-E MuLV infection. On the basis of our experimental results, we propose novel pathogenic mechanisms which may contribute to our understanding of the CNS diseases caused by these retroviruses.

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Akers, Stephen Matthew. "Modeling central nervous system involvement in acute lymphoblastic leukemia." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11227.

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Thesis (Ph. D.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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39

Mabon, Joy. "Strategies to reduce inflammation in the central nervous system." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ39851.pdf.

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40

Lyng, Eric E. Bottiglieri Teodoro. "Gamma Hydroxybutyrate (GHB) : mechanisms of central nervous system toxicity /." Waco, Tex. : Baylor University, 2006. http://hdl.handle.net/2104/4211.

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41

Stromnes, Ingunn Margarete. "T cell determinants of central nervous system autoimmune disease /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8333.

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42

Vidyadaran, Sharmili. "Neuroprotective properties of HSP27 in the central nervous system." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424392.

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43

Matyszak, M. K. "Immune mediated inflammatory responses in the central nervous system." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334846.

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44

Tran, Thi Hong Chau. "Clinical and pathological aspects of central nervous system infection." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578010.

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Central nervous system (CNS) infection remains a major cause of mortality and morbidity worlwide. This thesis focuses on the causes, prognostic markers, and pathogenesis of meningitis in adults in Viet Nam and explores the pharmacokinetic properties of fluoroquinolones in the treatment of tuberculous meningitis (TBM). Chapter One provides an introduction to infections of the CNS in Viet Nam. Chapter Two describes the clinical studies of CNS infections at the Hospital for Tropical Diseases in Viet Nam which underpin this thesis. Mycobacterium tuberculosis is the most common cause of CNS infections with the three commonest causes of acute pyogenic meningitis Streptococcus suis, Streptococcus pneumoniae and Neisseria meningitidis. In Chapter Three, I report on a study of the pathogenesis of meningitis and encephalitis in particular the role for Metalloproteinase/Tissue Inhibitor of Metalloproteinase. One of the most challenging situations is to distinguish partially treated pyogenic meningitis from TBM and viral meningitis and encephalitis. I identified two major clinical factors that can help distinguish TBM from pyogenic meningitis- gingivo-herpes and deafness are very much more common in pyogenic meningitis than in TBM (Odds Ratio 32). In Chapter Four, I develop a clinical aligorithm and in Chapter Five, a prognostic system to determine which variables can be used to predict the clinical outcome.TBM remains very difficult to treat. In Chapter Six, I report the results of a pharmacokinetic study aimed to identify the optimal fluoroquinolone to be used for the treatment of TBM. My results demonstrate levofloxacin has a better pharmacokinetic profile than ciprofloxacin or gatifloxacin for the treatment of TBM.

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Ives, N. K. "Bilirubin transport and toxicity in the central nervous system." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604974.

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46

Ruddick, Jon Paul. "Characterisation of ABCG transporters in the central nervous system." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289547.

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47

Chen, Vivian Susan Matsushima Glenn K. "Immune mediators of central nervous system demyelination and remyelination." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1844.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Doctorate of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.

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48

Zhou, Qiao Bronner-Fraser Marianne. "Glial cell development in the vertebrate central nervous system /." Diss., Pasadena, Calif. : California Institute of Technology, 2003. http://resolver.caltech.edu/CaltechETD:etd-04092003-155305.

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Rhodes, Katherine Emily. "Oligodendrocyte precursor cells in the injured central nervous system." Thesis, University of Cambridge, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620605.

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50

Christ, Andreas Fridolin. "High resolution mechanical mapping of central nervous system tissue." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609861.

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