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The Global ETD Search service is a free service for researchers
to find electronic theses and dissertations. This service is
provided by the
Networked Digital Library of Theses and Dissertations.
Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
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Showing 11 to 20 of 1094 (0.066 seconds)Spelling suggestions: "subject:"cultiple atherosclerosis"" "subject:"bmultiple atherosclerosis""
| 11 |
Iron and multiple sclerosis /Bloem, Liezl. January 2007 (has links)
Thesis (MSc)--University of Stellenbosch, 2007. / Bibliography. Also available via the Internet.
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| 12 |
Dietary assessment and self-perceived impact of food in persons with multiple sclerosisKilborn, Sally J. January 2008 (has links)
No description available.
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| 13 |
Investigations into the mechanism of improvement of disability after alemtuzumab treatment of relapsing-remitting multiple sclerosisMosely, Suzanne Isabelle Sylvie January 2014 (has links)
No description available.
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| 14 |
Maximum likelihood methods for the detection of genetic linkage and association using affected sibling pairsHolmans, Peter Alan January 1994 (has links)
No description available.
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| 15 |
An investigation into the effects of lymphocyte derived soluble factors on mixed glial cell cultures from cerebra of 1-2 day old neonatal CFHB rat pupsRoitt, S. M. January 1988 (has links)
No description available.
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| 16 |
An investigation of the viral enhancement of EAEClark, Brendan January 1988 (has links)
No description available.
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| 17 |
Receptor mediated phagocytosis of myelin by macrophages and microgliaMoseley, Karen Lorraine January 1998 (has links)
No description available.
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| 18 |
The cellular biology of the oligodendrocyte-type 2 astrocyte (O-2A) lineage : implications for demyelination and remyelinationWren, Damian Richard January 1988 (has links)
No description available.
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| 19 |
Influence of focal brain damage on autoimmune disease of the central nervous systemSun, Dong January 1999 (has links)
No description available.
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| 20 |
Investigating the role of auto-immune responses to transient axonal glycoprotein-1 (TAG-1) in experimental autoimmune encephalomyelitis (EAE)Parikh, Khyati January 2009 (has links)
To examine the pathophysiological consequences of autoimmunity to TAG-1, CD4<sup>+</sup> T cells and autoantibodies specific for TAG-1 were generated and their potential to induce EAE was investigated in a rat model. An adoptive transfer of T cells specific for the first two immunoglobulin domains of TAG-1 initiates an intense inflammatory response in both the cortex and spinal cord in the Dark Agouti and Lewis rats. This is particularly interesting as conventional models of EAE are of little help in investigating the pathomechanisms responsible for cortical tissue damage, as the cortex is only rarely targeted by myelin-specific autoimmune responses in this animal model of Multiple Sclerosis (MS). Moreover, when a demyelinating antibody like Z2 (anti-MOG) antibody was co-transferred with TAG-1-specific T cells it resulted in demyelination not only in the spinal cord white matter but also the grey matter and triggered demyelination coupled with macrophage infiltration in the perivascular areas of the cortex. This new model of cortical demyelination is exciting as it bears some resemblance with chronic progressive MS. However, two different monoclonal antibodies (4D7/TAG1) and 3.1C12) specific to TAG-1, when co-transferred with TAG-1 specific T cells, failed to mediate tissue damage in the CNS. Although the role of TAG-1-specific antibodies in EAE remained inconclusive from the preliminary experiments, this study clearly demonstrates TAG-1-specific T cells as a new tool to mediate EAE highlighting cortical pathology which can be exploited further to investigate the factors that control regional differences in the pathogenesis of inflammatory demyelinating lesions in the CNS. This new model might provide novel insights into the development of cortical pathology in MS patients and will ultimately guide to design therapeutic approaches in MS.
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