Bibliography: leaves 318-347. / ix, 347 [24] leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / A major problem in the production of agricultural crops including wheat, is the damage caused by destructive plant parasitic nematodes, among these the root lesion nematode (Pratylenchus spp.) The association of P. neglectus with fungi in ceraeal root disease has been reported. Infection is associated with leaf yellowing, which reduces plant photosynthesis and grain yield. In nematode infested soil, well fertilized crops are usually less affected. / Thesis (Ph.D.)--University of Adelaide, Dept. of Plant Science, 1996?

Bibliography: leaves 121-141. / viii, 151 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Plant Science, 1996?

Erratum pasted onto front end-paper. / Copies of author's previously published article inserted. / Bibliography: leaves 167-180. / 180 leaves, [51] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Reanalyses the effects of the absence of CreA in the cell, raises antibodies for the detection of CreA and identifies new loci involved in carbon catabolite repression by using different genetic selection methods. / Thesis (Ph.D.)--University of Adelaide, Dept. of Genetics, 1999?

Includes bibliographical references (leaves 265-296). / vi, 296 leaves, [14] leaves of plates : ill. (some col.), maps ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Pathogens associated with root damage were investigated in the Murray Mallee region of South Australia over the 1987-1989 growing seasons. Occurence of fungal species and the root lesion nematode (Pratylenchus neglectus) was assessed, and related to the appearance and severity of symptoms on the roots. Field experiments were supplemented with innoculation tests in the glasshouse and laboratory. / Thesis (Ph.D.)--University of Adelaide, Depts. of Plant Science and Crop Protection, 1991

Includes bibliography / vii, 161, [208] leaves : ill ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1985

Bibliography: leaves 116-124 / [10], 124, [64] leaves : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1985

Bibliography: leaves 118-130 / v, 130 leaves, [23] leaves of plates : ill ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Biochemistry, 1984

Uroplakin 1B (UPKIB) is an integral structural protein interacting with uroplakins 1A, 2 and 3 to form hexameric plaques along the bladder lumen in the asymmetric unit membrane of urothelial umbrella cells in humans and other mammals. UPKIB mRNA expression is deregulated in transitional cell carcinomas (TCCs), however the mechanisms of regulation of UPKIB have not been established. Using genome databases, a Xenopus UPKIB homologue was identified. Maximum Parsimony and BAMBE (Bayesian Analysis in Molecular Biology and Evolution) data support a close evolutionary relationship between mammalian and amphibian UPKIB mRNA. Using Unigene, UPKIB human expressed sequence tags were identified in tissues including brain, skeletal muscle and liver, suggesting the relatively widespread distribution of this membrane protein. The UPKIB genomic structure was also deduced using genome databases. Contig AC083800, identified in a high throughput genomic sequence database, spanned UPKIB and 9 exons and 8 introns were defined. A 67bp 5' untranslated region was identified using 5' rapid amplification of cDNA ends. This product was sequenced and a putative UPKIB promoter and transcription start site was deduced. Contig AC083800 spanned the transcription start site and putative promoter. Transcription factor binding motif prediction programs detected no TATA box, but did predict a CCAAT box and several binding motifs including 4 Sp-1 sites and a NFKB site. A weak CpG island was identified within a 0.5kb region including the putative promoter, exon 1 and intron 1, which was 54% GC rich with CpG:GpC ratio of 0.46, containing 15 CpG dinucleotides. Seven TCC cell lines and five peripheral blood lymphocyte samples were analysed for UPKIB expression using RT-PCR and two cell lines expressed UPKIB transcripts. Eleven CpG sites in the putative promoter were investigated for methylation using bisulfite modification analysis in normal PBL, TCC cell lines and patient TCC samples. An inverse correlation was established in TCC cell lines between UPKIB mRNA expression and degree of methylation. 5-Aza-2'deoxycytidine induced UPKIB mRNA expression in T24 cells, previously observed not to express UPKIB. Sequence analysis of patient samples revealed more complex CpG methylation patterns, reflecting tumour heterogeneity. In summary, the uroplakin 1B gene has been characterised and one mechanism of regulation of gene expression involves methylation. / Thesis (Ph.D.)--Dept of Surgery, 2003.

The aim of this thesis was to investigate the possibility of using buccal cells derived from a multi layered epithelial tissue from the oral mucosa as a model to identify potential biomarkers of genomic instability in relation to normal ageing and premature ageing syndromes such as AD and DS. A buccal micronucleus cytome assay was developed and used to investigate biomarkers for DNA damage, cell proliferation and cell death in healthy young, healthy old and young Down’s syndrome cohorts. Cells with micronuclei, karyorrhectic cells, condensed chromatin cells and basal cells increased significantly with normal ageing (P<0.0001). Cells with micronuclei and binucleated cells increased (P<0.0001) and condensed chromatin, karyorrhectic, karyolytic and pyknotic cells decreased (P<0.002) significantly in Down’s syndrome relative to young controls. The buccal micronucleus cytome assay was used to measure ratios of buccal cell populations and micronuclei in clinically diagnosed Alzheimer’s patients compared to age and gender matched controls. Frequencies of basal cells (P<0.0001), condensed chromatin cells (P<0.0001) and karyorrhectic cells (P<0.0001) were found to be significantly lower in Alzheimer’s patients, possibly reflecting changes in the cellular kinetics or structural profile of the buccal mucosa. Changes in telomere length were investigated using a quantitative RTm-PCR method to measure absolute telomere length (in Kb per diploid genome) and show agerelated changes in white blood cells and buccal cell telomere length (in kb per diploid genome) in normal healthy individuals and Alzheimer’s patients. We observed a significantly lower telomere length in white blood cells (P<0.0001) and buccal cells (P<0.01) in Alzheimer’s patients relative to healthy age-matched controls (31.4% and 32.3% respectively). However, there was a significantly greater telomere length in hippocampus cells of Alzheimer’s brains (P=0.01) compared to control samples (49.0). Buccal cells were also used to investigate chromosome 17 and 21 aneuploidy. A 1.5 fold increase in trisomy 21 (P<0.001) and a 1.2 fold increase in trisomy 17 (P<0.001) was observed in buccal cells of Alzheimer’s patients compared to age and gender matched controls. Chromosome 17 and chromosome 21 monosomy and trisomy increase significantly with age (P<0.001). Down’s syndrome, which exhibits similar neuropathological features to those observed in Alzheimer’s disease also showed a strong increase in chromosome 17 monosomy and trisomy compared to matched controls (P<0.001). However, aneuploidy rate for chromosome 17 and 21 in the nuclei of hippocampus cells of brains from Alzheimer’s patients and controls were not significantly different. Observations that AD individuals have altered plasma folate, B12 and Hcy levels compared to age-matched controls who have not been clinically diagnosed with AD were investigated. Genotyping studies were undertaken to determine whether polymorphisms within particular genes of the folate methionine pathway contributed to AD pathogenesis. Correlations between folate, B12 and Hcy status with previously determined buccal micronucleus assay cytome biomarkers for DNA damage, cell proliferation and cell death markers was investigated. Lastly, the potential protective effects of phytonutrient polyphenols on genomic instability events in a transgenic mouse model for AD were investigated. We determined the effects of curcumin and GSE polyphenols on DNA damage by testing the mice over a 9 month period utilizing a buccal micronucleus cytome assay, an erythrocyte micronucleus assay and measuring telomere length in both buccal cells and olfactory lobe brain tissue. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1313395 / Thesis (Ph.D.) -- The University of Adelaide, School of Molecular and Biomedical Science, 2008

Hereditary Motor and Sensory Neuropathy-Russe (HMSNR) is a rare recessive form of Charcot-Marie-Tooth disease (CMT) that has been identified in the European Gypsy (Roma) population. Clinically, HMSNR manifests with typical CMT symptoms, while no associated features have been detected. Distinct neuropathological features of HMSNR include the presence of numerous clusters of thinly myelinated fibres originating from regenerative activity. HMSNR has been previously mapped to chromosome 10q using a large Bulgarian Gypsy kindred. Subsequent identification of related chromosome 10q haplotypes in Spanish and Romanian Gypsy families suggested a founder mutation in the Gypsy population as the cause of HMSNR. This thesis describes the refined mapping of the HMSNR gene by generating a high-density physical-genetic map of the HMSNR region containing 20 microsatellite markers and 229 SNPs and insertion/deletions which allowed meticulous mapping of recombination breakpoints resulting in a reduction of the HMSNR gene region from 1 Mb to just 63.8 kb. Analysis of positional candidates by direct sequencing included 14 known genes, 7 predicted genes and 42 expressed sequence tags (ESTs) nonoverlapping with the genes. 78 putative HMSNR mutations were identified, two of which exhibit complete segregation with the HMSNR phenotype. Both are located in the so-called testis-specific part of unexpected candidate gene hexokinase 1 (HK1), in a rare alternative untranslated 5’ exon of HK1 and in the adjacent downstream intron. Expression analysis of transcripts containing the alternative exon suggests that the exon is not confined to testis but may be expressed in the nervous system. It remains to be speculated how a gene that functions in the fundamental process of energy generation might be involved in a neuropathy. Further investigations are likely to expand the knowledge about the importance of HK1 in the peripheral nervous system and may elucidate new roles of HK1