Thesis (Ph. D.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.

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published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

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This study compared the effect of various immunosuppressive therapies on the development of lupus nephritis using a murine model of SLE, the MRL lpr/lpr mouse. The agents investigated were cyclosporin A (CsA), FK506, rapamycin and mycophenolate mofetil (MM). Female MRL lpr/lpr mice at 12 weeks old were treated with CsA (40mg/kg/day p.o.), FK506 (2.5mg/kg/3 times/week or/day s.c.), rapamycin (1.5mg/kg.day s.c.), MM (50mg/kg/2 times daily p.o.) or vehicle controls. These groups were compared with untreated MRL lpr/lpr and also untreated MRL +/+ mice which do not develop this autoimmune disease. Disease progression was assessed using various markers for SLE and glomerular dysfunction. The results obtained showed CsA and rapamycin to both inhibit glomerular proliferation and reduce glomerular macrophage infiltrate. In addition, rapamycin also reduced chronic inflammatory cell infiltrate, lymphadenopathy and splenomegaly. Rapamycin treated animals did not develop skin lesions and alopecia which became apparent on mice from other groups. In contrast neither low or high dose FK506 treatments prevented the development of the autoimmune pathological features, including renal disease. Likewise, mycophenolate mofetil had no beneficial effects in disease prevention. In conclusion, it appears that both rapamycin and CsA but not FK506 or mycophenolate mofetil reduce macrophage infiltration, glomerular proliferation and, in the case of rapamycin chronic inflammatory cell infiltrate and lymphadenopathy, in the MRL lpr/lpr mouse.

Thesis (M.A.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / The gene Myh9 encodes non-muscle myosin heavy chain I lA, an essential podocyte cytoskeleton structural protein. Abnormalities in the MYH9 gene are associated with chronic kidney disease (common in people of African ancestry) and rare hereditary autosomal dominant syndromes. In the current study, preexisting heterozygous Myh9 knockout mice aged 9 and 17 months were investigated to assess the biological role of the gene Myh9 product, non-muscle myosin IIA, in kidney structure and function. The objective was to determine the effects of potentially decreased expression of Myh9 genetic alteration and the role of Myh9 in the pathogenesis of chronic kidney disease (especially focal segmental glomerulosclerosis), and to develop a model to further study Myh9- related kidney disorders. Our results demonstrated that deletion of one allele of Myh9 in 129/Sv mice had no effect on the kidney structure compared with wildtype mice despite a significant decrease in expression of Myh9 in the heterozygous mice. / 2031-01-01

212 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (M.D.)--University of Adelaide, Dept. of Medicine, 1973

No description available.

Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 148-170).

Thesis (Ph. D.)--University of Hong Kong, 2009. / Includes bibliographical references (leaves 286-318). Also available in print.