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Force-extension of the Amylose Polysaccharide
Myasthenia gravis (MG) is an autoimmune disorder in which auto-antibodies directed at the acetylcholine receptors (AChR) of the neuromuscular junction (NMJ) block, alter or destroy their targets. The anti-AChR antibodies cause activation of the classical complement pathway leading to inflammatory in...
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| Format: | Thesis |
| Language: | English |
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Department of Computer Science
2014
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| _version_ | 1867614339067805696 |
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| access_status_str | Open Access |
| author | van den Berg, Rudolf |
| author_browse | van den Berg, Rudolf |
| author_facet | van den Berg, Rudolf |
| author_sort | van den Berg, Rudolf |
| collection | Thesis |
| description | Myasthenia gravis (MG) is an autoimmune disorder in which auto-antibodies directed at the acetylcholine receptors (AChR) of the neuromuscular junction (NMJ) block, alter or destroy their targets. The anti-AChR antibodies cause activation of the classical complement pathway leading to inflammatory injury at the NMJ. Decay Accelerating Factor (DAF), a member of complement regulatory proteins, prevents activation of autologous components of complement pathways. The absence of DAF, in knock-out mouse models, has been shown to significantly increase the susceptibility to experimental autoimmune MG. A previous study showed that a high proportion of South African MG patients of African genetic ancestry develop immunosuppressive therapy-resistant extraocular muscle (EOM) dysfunction. We hypothesized that these patients have deficient DAF expression in their EOMs resulting in less protection from complement injury. Sequence analysis of relevant regions of the DAF gene revealed a single nucleotide polymorphism (SNP), c.-198C>G, in the promoter region in MG patients of African genetic ancestry with severe EOM MG involvement (MG n=101; Control n= 132; Odds ratio= 6.6; p=0.009). DAF-luciferase reporter assays, using 3 different cell lines (COS-7, HT1080 and C2C12) revealed that the c.-198C>G SNP (Mut-DAF) led to an increase in DAF promoter activity ( |
| format | Thesis |
| id | oai:open.uct.ac.za:11427/6372 |
| institution | University of Cape Town (South Africa) |
| language | eng |
| last_indexed | 2026-06-10T12:50:28.121Z |
| license_str | Not specified — see source repository |
| provenance_str_mv | Harvested via OAI-PMH from UCTD — University of Cape Town Open Access Repository |
| publishDate | 2014 |
| publishDateRange | 2014 |
| publishDateSort | 2014 |
| publisher | Department of Computer Science |
| publisherStr | Department of Computer Science |
| record_format | dspace |
| source_str | UCTD — University of Cape Town Open Access Repository |
| spelling | oai:open.uct.ac.za:11427/6372 Force-extension of the Amylose Polysaccharide van den Berg, Rudolf Information Technology Myasthenia gravis (MG) is an autoimmune disorder in which auto-antibodies directed at the acetylcholine receptors (AChR) of the neuromuscular junction (NMJ) block, alter or destroy their targets. The anti-AChR antibodies cause activation of the classical complement pathway leading to inflammatory injury at the NMJ. Decay Accelerating Factor (DAF), a member of complement regulatory proteins, prevents activation of autologous components of complement pathways. The absence of DAF, in knock-out mouse models, has been shown to significantly increase the susceptibility to experimental autoimmune MG. A previous study showed that a high proportion of South African MG patients of African genetic ancestry develop immunosuppressive therapy-resistant extraocular muscle (EOM) dysfunction. We hypothesized that these patients have deficient DAF expression in their EOMs resulting in less protection from complement injury. Sequence analysis of relevant regions of the DAF gene revealed a single nucleotide polymorphism (SNP), c.-198C>G, in the promoter region in MG patients of African genetic ancestry with severe EOM MG involvement (MG n=101; Control n= 132; Odds ratio= 6.6; p=0.009). DAF-luciferase reporter assays, using 3 different cell lines (COS-7, HT1080 and C2C12) revealed that the c.-198C>G SNP (Mut-DAF) led to an increase in DAF promoter activity ( 2014-08-13T19:25:47Z 2014-08-13T19:25:47Z 2009 Master Thesis Masters MSc http://hdl.handle.net/11427/6372 eng application/pdf Department of Computer Science Faculty of Science University of Cape Town |
| spellingShingle | Information Technology van den Berg, Rudolf Force-extension of the Amylose Polysaccharide |
| thesis_degree_str | Master's |
| title | Force-extension of the Amylose Polysaccharide |
| title_full | Force-extension of the Amylose Polysaccharide |
| title_fullStr | Force-extension of the Amylose Polysaccharide |
| title_full_unstemmed | Force-extension of the Amylose Polysaccharide |
| title_short | Force-extension of the Amylose Polysaccharide |
| title_sort | force extension of the amylose polysaccharide |
| topic | Information Technology |
| url | http://hdl.handle.net/11427/6372 |
| work_keys_str_mv | AT vandenbergrudolf forceextensionoftheamylosepolysaccharide |