Rozprawy doktorskie: „Central nervous system”

1

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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2

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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3

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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4

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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5

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.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 133-153).
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.
by Kristin Briana Bernick.
Ph.D.

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6

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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7

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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8

Radke, James Melvin. "Studies involving somatostatin systems in the rodent central nervous system". Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26518.

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Somatostatin is a neuropeptide found throughout the brain. Several studies have established its anatomical distribution as being quite heterogenous with relatively high concentrations appearing in the limbic and striatal systems. Presently, very little is known about the functions of somatostatin systems in the brain and how they interact with other transmitter systems. The following report is a summary of experiments undertaken to assess the functional and chemical interactions of somatostatin with other neurotransmitter systems. Previous studies have established that the dopaminergic inputs to the basal ganglia are important for locomotor activity and reward. These systems have also been implicated in several mental and neural diseases such as schizophrenia, depression, and Parkinson’s disease. In the first experiment, interactions between dopamine and somatostatin systems were examined using paradigms involving behavioural responses to dopamine agonists. Depletion of somatostatin levels by the drug cysteamine was found to attenuate amphetamine- and apomorphine-mediated motor behaviours but not the reinforcing aspects of amphetamine. The second experiment attempted to further characterize the nature of the dopamine-somatostatin interaction by examining the effects of haloperidol, a dopamine antagonist, on central somatostatin levels. Short term treatment with haloperidol decreased striatal somatostatin levels. Long term treatment (8 months) with haloperidol failed to alter somatostatin levels in the caudate-putamen. Since somatostatin levels appear to be normal in Parkinsonian brains, the effects of MPTP poisoning in mice on central somatostatin levels was also studied to examine the accuracy of this animal model of Parkinson's disease and examine the effects of dopaminergic lesions on somatostatin levels. The results of this experiment indicate that MPTP causes a dose dependent increase in nigral somatostatin levels without altering striatal or cortical levels. These results are in partial disagreement with results obtained from both post-mortem Parkinsonian brains and primates given MPTP, thereby questioning the accuracy of this mouse model of Parkinson's disease. The final experiment examined the effects of the anticonvulsant-antidepressant carbamazepine on central somatostatin levels in the rat. Although the chemical mechanisms responsible for the therapeutic effects of carbamazepine are unknown, previous studies have suggested that its efficacy in the treatment of both manic-depression and epilepsy may be associated with the ability of this drug to reduce the abnormal somatostatin levels observed in these diseases. In this experiment, neither acute, chronic, nor withdrawal from chronic treatment with carbamazepine were found to alter the levels of somatostatin in rats. The lack of effects of carbamazepine on basal somatostatin levels may indicate somatostatin cells are susceptible to carbamazepine only under pathological situations. Together, these results are discussed in the context of recent observations of abnormal somatostatin levels in several diseases of the central nervous system and provide some insight into the interactions and functions of somatostatin systems in the normal and abnormal brain.
Medicine, Faculty of
Graduate

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9

Lothian, Carina. "Nestin regulation in the embryonic and adult CNS /". Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-057-1/.

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10

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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11

Roche, Anie Kavita. "Evaluation of modifications in the central nervous system during inflammation /". Diss., ON-CAMPUS Access For University of Minnesota, Twin Cities Click on "Connect to Digital Dissertations", 1998. http://www.lib.umn.edu/articles/proquest.phtml.

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12

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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13

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.
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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14

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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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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29

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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30

Smorodska, O., I. Shandyba, P. Bileckiy, Роман Андрійович Москаленко, Роман Андреевич Москаленко, Roman Andriiovych Moskalenko, Андрій Миколайович Лобода i in. "Affection of central nervous system in MELAS syndrome". Thesis, Karger Publishers, 2017. http://essuir.sumdu.edu.ua/handle/123456789/65352.

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The problem of acute cerebrovascular accident (ACVA) has enormous socio-economic importance due to its significant prevalence. Since the ACVA have clinical and pathogenetic polymorphism, problem of differential diagnosis of diseases that mimic their clinic raised up. This problem was illustrated by the clinical case we present.Difficulty of differential diagnostic illustrated by case with patient who initially hospitalized with a diagnosis of ACVA, but later during dynamic monitoring and additional examinations diagnosis of MELAS syndrome was found. Aim: differential diagnosis of rare mitochondrial disease and acute cerebrovascular accident. Patients & Methods. Women, 54 years, come to the emergency room in hospital with stroke-like episode. Due to the local protocol she was examined with laboratory analysis, MRI of cerebri with vessels, CT and MRI of spine, EEG, consultation of ophthalmologist. Also were made analysis for cuprum, cerruloplasmine,homocysteine, transferrine, ferrum, lactate and biopsy of muscular tissues. Results: During neurological examination symptoms of ACAV were not found. MRI of the basal nuclei (mostly in globi pallidi) of the brain were found irregular symmetrical focuses (size 14x18 mm) without clear contours, with slightly increased intensity in T1 mode and low signal intensity on T2 mode. Bilateral in subcortical areas of white matter were found sites of gliosis (size 3x3,2 mm) in both frontal-parietal areas. In the vessels of the brain changes were not found. In analysys of blood serum were found normal levels of copper, ceruloplasmin, homocysteine and ferrum. However, moderate increase in lactate levels were observed. Within EEG epileptic activity was not found. A biopsy of muscle tissue revealed the phenomenon of "ragged red fibers" (severity score of 3-4), a sharp decrease in glycogen during the PAS-reaction. According to the results of examination of the patient were excluded ACVA (hemorrhagic and embolic), Wilson's disease, migraine and epilepsy. Biopsy showed the presence of muscle mitochondrial disease. Conclusion. Increased levels of lactate in the blood serum, the presence of the phenomenon of "ragged red muscle fibers" and found neurological symptoms indicate a reasonable suspicion about the presence of the MELAS syndrome. This case is also valuable because of the late manifestation of the MELAS syndrome (at the age of 54), that creates additional complexity of diagnosis.

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31

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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32

Ebrahimkhani, Saeideh. "Exosomal MicroRNA Signatures in Central Nervous System Diseases". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20208.

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During the last decade there has been a growing interest in studying extracellular vesicles, in particular exosomes and their miRNA contents. Exosomes are released by almost all cell types. They are packed with specific information, stable against degradation processes, are small and flexible enough to cross the blood-brain barrier (BBB), and are readily found in biological fluids including blood. MicroRNAs (miRNAs) are involved in nearly every cellular process and play a regulatory role in central nervous system (CNS) associated diseases. Accordingly, exosomal miRNAs could be ideal biomarkers to measure CNS disease activity and treatment response. In this thesis, the aim was to establish a robust protocol to investigate whether the differential expression of serum exosomal miRNA can be used as a biomarker for the accurate diagnosis of the CNS diseases multiple sclerosis (MS) and glioblastoma multiforme (GBM), as well as for the monitoring of disease progression and treatment response. Exosomes were purified from serum and their RNA contents profiled using highthroughput sequencing. In my first study, I profiled exosome–associated miRNAs in serum samples from MS patients and identified distinct biomarkers for the diagnosis of MS and identification of the disease subtype. In my second study, I investigated the effect of treatment in MS patients. I hypothesised that the deregulation of serum exosomal miRNAs is associated with the efficacy of therapy and is predictive of MS activity phases. Finally, I studied serum exosomal miRNA profiles to discover diagnostic biomarkers for GBM, and to demonstrate the applicability of my protocol to other neurological diseases. Taken together, my results demonstrate the exceptional utility of serum exosomal miRNA profiles as a blood-based biomarker to diagnose the CNS associated diseases, using a robust and easily reproducible protocol.

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33

周韋基 i Wai-kei Dominic Chau. "A morphometric study of axon-glial interactions". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31212141.

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Chau, Wai-kei Dominic. "A morphometric study of axon-glial interactions /". [Hong Kong] : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14801486.

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35

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.
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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36

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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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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Stumpf, da Silva Taisa Regina. "Delivery Systems to Enhance Neural Regeneration in the Central Nervous System". Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39391.

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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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Kopp, Jutta Maria. "Expression, regulation and functional aspects of the NPY Y1 receptors in rat /". Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4776-7/.

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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.
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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42

Zhang, Fan. "Modulation of genomic expression in the central nervous system". Doctoral thesis, Universite Libre de Bruxelles, 1997. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212219.

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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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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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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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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.
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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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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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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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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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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