Thesis (M.S.)--University of Massachusetts Amherst, 2008. / Includes bibliographical references (p. 33-40).

published_or_final_version / Zoology / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Medicine / Master / Master of Philosophy

published_or_final_version / abstract / Orthopaedics and Traumatology / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Pathology / Master / Master of Philosophy

published_or_final_version / abstract / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / Surgery / Doctoral / Doctor of Philosophy

Addenda page on inside back cover. Bibliography: leaves 153-176. Mucopolysaccharideosis type IIIA (MPS IIIA, Sanfilippo A syndrome) is an autosomal recessive lysosomal storage disease, with a prevalence in Australia of 1 in 114,000. MPS IIIA is caused by a deficiency of the lysosomal enzyme sulphamidase which is needed together with other exohydrolases and a N-acetyltransferase to break down the glycosaminoglycan heparan sulphate to sulphate and monosaccharides. Patients are characterised by severe central nervous systems degeneration together with mild somatic involvement; this disproportionate correlation is unique amongst the mucopolysaccharidoses. Features include severe behavioural disturbances, such as hyperactivity and aggressiveness, coarse hair and mild hepatosplenomegaly. Death is usually in the mid- to late-teenage years. Enzyme replacement therapy by intravenous administration of recombinant human NS (rhNS) has been proposed as a potential therapy for MPS IIIA. This thesis suggests that rhNS, entering the brain in the first few weeks of life, is able to retard the behaviour and learning difficulties in MPS IIIA mice.

Copies of author's previously published articles inserted inside back cover. / Bibliography: leaves 137-179. / x, 179, [26] leaves, [28] leaves of plates : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / The aims of this study are to determine whether latent HSV genomes are a result of viral DNA amplification in the PNS during the establishment phase and to investigate the relationship between HSV DNA copy number and viral transcriptional activity during latent infection of the PNS. In order to map the distribution of viral nucleic acid sequences in latently infected sensory ganglia, experiments are undertaken using a mouse model that makes novel use of the segmental sensory innervation of flank skin. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1995?

Addenda page on inside back cover. / Bibliography: leaves 153-176. / xiii, 176 leaves ; ill. (some col.) ; 30 cm / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Mucopolysaccharideosis type IIIA (MPS IIIA, Sanfilippo A syndrome) is an autosomal recessive lysosomal storage disease, with a prevalence in Australia of 1 in 114,000. MPS IIIA is caused by a deficiency of the lysosomal enzyme sulphamidase which is needed together with other exohydrolases and a N-acetyltransferase to break down the glycosaminoglycan heparan sulphate to sulphate and monosaccharides. Patients are characterised by severe central nervous systems degeneration together with mild somatic involvement; this disproportionate correlation is unique amongst the mucopolysaccharidoses. Features include severe behavioural disturbances, such as hyperactivity and aggressiveness, coarse hair and mild hepatosplenomegaly. Death is usually in the mid- to late-teenage years. Enzyme replacement therapy by intravenous administration of recombinant human NS (rhNS) has been proposed as a potential therapy for MPS IIIA. This thesis suggests that rhNS, entering the brain in the first few weeks of life, is able to retard the behaviour and learning difficulties in MPS IIIA mice. / Thesis (Ph.D.)--University of Adelaide, Dept. of Paediatrics, 2003