Thesis (M.Med.Sc.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 16-19). Also available in print.

Thesis (M.Med.Sc.)--University of Hong Kong, 2003. / Includes bibliographical references (leaves 42-57). Also available in print.

Thesis (M.S.)--Missouri State University, 2009. / "May 2009." Includes bibliographical references (leaves 83-86). Also available online.

Thesis (Ph. D.)--West Virginia University, 2005. / Title from document title page. Document formatted into pages; contains v, 76 p. : ill. Includes abstract. Includes bibliographical references (p. 71-76).

Thesis (Ph.D.) - University of St Andrews, November 2007.

Universiẗat, Diss., 2003--Frankfurt (Main).

Thesis (M.S.)--Brigham Young University. Dept. of Plant and Animal Sciences, 2005. / Includes bibliographical references (p. 40-41).

Much evidence now exists to show that unbalanced DNA precursor pools cause DNA replicational infidelity in vitro. However, there are relatively few data with in vivo systems. Experiments were performed therefore, to determine if unbalanced precursor pools could be induced in vivo and if so, what affect this would have on various genetic markers. The nucleoside thymidine was shown to be completely non-toxic to the rat when administered orally, negative in the dominant lethal assay and was only marginally clastogenic in the micronucleus test. Treatment of human lymphocyte chromosomes with the essential amino acid arginine, arrested cell division possibly due to a predominance of arginine-rich histones limiting the chromatin-condensation during mitosis. Thymidine administered i. p. to mice induced marked increases in the proportions of abnormal sperm and the same effect, to a lesser extent, was seen in rats. The affected germ-cell stages were the mid - to late pachytene spermatocytes. These affects were probably due to base-misincorporation occuring during unscheduled DNA synthesis. The purine nucleoside adenine caused dose-related increases in the frequency of abnormal sperm in mice. In rats, a proportion of animals given 150mg/kg adenine showed high levels of abnormal sperm whilst others were unaffected. Examination of mice in the generation revealed that the damage to the germ-cells was transmissible. The simultaneous administration of deoxycytidine with excess thymidine to mice partly inhibited the effects on sperm morphology indicating that those effects were due to precursor pool imbalance. In addition, an analytical technique was developed to measure nucleosides and bases in the testes using HPLC. The method proved to be rapid, reproducible and quantitative and showed that 1hr following i. p. injection, thymidine levels in the testes increased markedly and thereafter quickly return to control levels. Finally, experiments were initiated to investigate the mechanisms underlying the formation of morphogically abnormal sperm. Polyacrylamide gel electrophoresis was used to identify membrane proteins in sperm from both control and treated animals.

TGF-beta1 plays an important role in the pathogenesis of experimental and clinical glomerulosclerosis and tubufointerstitial fibrosis. Associations have been described between polymorphisms of cytokine and growth factor genes and susceptibility to, or progression of, an increasing number of diseases. In this study, single nucleotide polymorphisms (SNPs) in the TGFbeta1 gene were investigated as possible markers for the progression of chronic renal failure (CRF). One hundred and forty two Caucasian patients with CRF were screened for four TGFB1 SNPs: T-509C in the promoter region; Arg25Pro and Leu10Pro in exon 1 and Thr263Ile in exon 5. There were significant differences between CRF patients and controls in allele frequencies of two of the SNPs (Leu10Pro and C-509T), indicating an association with susceptibility to CRF, We also observed a significant association between rate of progression of CRF (the slope of the reciprocal of serum creatinine v time) and genotype, both at codon 25 (odds ratio 3.77, 95% confidence interval, 2.2 - 6, p < 0.001) and at the -509 promoter site (odds ratio 1.67, 95% confidence interval 1.1-2.5), p < 0.005) in patients with primary nephropathy (excluding PKD). Genotype at codon 25 was also associated with severity of proteinuria (p= 0.038), plasma TGF-B1 protein levels (p = 0,01), and the severity of glomerulosclerosis (p < 0.05). Genotype at C-509T was associated with the level of renal tubular TGF-B1 immunostmning (p = 0.0006) and with renal interstitial inflammatory cellular infiltration (p=0,015). There was a highly significant correlation between the degree of cellular infiltration in renal tissues and tubular TGF-beta1 immunostaining.

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