Thesis (Ph. D.)--Illinois State University, 1985. / Title from title page screen, viewed June 7, 2005. Dissertation Committee: David F. Weber (chair), Herman Brockman, Tsan Iang Chuang, Alan Katz, Derek McCracken. Includes bibliographical references (leaves 118-142) and abstract. Also available in print.

Thesis (Ph. D.)--Lehigh University, 2005. / Includes bibliographical references (leaves 98-112).

A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg, for the degree of Master of Science (Medicine). / Objective: To determine the relationship between asbestos exposure and chromosome damage, as depicted by sister chromatid exchange frequency. Design: Descriptive, cross-sectional study. Setting: Asbestos-products factory Subjects: 31 asbestos-exposed subjects and 21 unexposed subjects Main outcome measure: Mean sister chromatid exchange (SCE) frequency per metaphase cell. Results: The control group had a slightly higher mean SCE frequency per cell than the exposed group (3.4%) but this difference was not statistically significant (p = 0.5935). Smoking contributed significantly to SCE frequencies in both the exposed and unexposed groups. The mean SCE frequencies per cell in the exposed group were 10.49 for smokers and 8.59 for non-smokers (p = 0.0078). The frequencies for smokers and non-smokers in the unexposed group were 10.83 and 8.58, respectively (p = 0.0257). Conclusions: The failure to observe an increase in SCE frequency does not rule out asbestos exposure as a genotoxic agent. Rather, it may help to resolve the limitations of this method for detecting genetic damage. Alternatively, the fibre levels to which this group was exposed may have been too low to cause chromosome damage. / WHSLYP2016

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Thesis (Ph.D.) - University of Glasgow, 2008. / Ph.D. thesis submitted to the Division of Biochemistry and Molecular Biology, Biomedical and Life Sciences (IBLS), University of Glasgow, 2008. Includes bibliographical references. Print version also available.

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In the present study DNA damage was measured in peripheral blood lymphocytes from polyposis coli and colorectal cancer patients, treated with different dietary and environmental compounds and compared with lymphocytes from healthy individuals. In addition, confounding factors such as age, gender, alcohol intake and smoking habits were taken into consideration. The assays used in this study included the Comet assay, the Micronucleus assay, the Micronucleus-FISH assay and the sister chromatid exchange assay. The food mutagens, PhIP and IQ, as well as titanium dioxide nanoparticles (TiO2 NPs) induced a dose dependent increase in the DNA damage and chromosomal abnormalities in all tested groups regardless of confounding factors. Prior to experiments physicochemical characterisation of nanoparticles was conducted. In the presence of the flavonoids, quercetin and rutin that were acting in an antioxidant manner, the DNA damage resulting from the highest doses of food mutagens was significantly reduced. Thus, dietary supplementation with flavonoid-rich vegetables and fruits may prove very effective in protection against oxidative stress. The polyposis coli and colon cancer patients were more susceptible to food mutagens, PhIP and IQ, as well as TiO2 NPs, and in the majority of cases had a higher level of DNA damage in the Comet assay and higher cytogenetic damage in the Micronucleus assay. In the final project, twelve frequently encountered (NewGeneris) chemical compounds were evaluated to establish their damaging potential in lymphocytes and spermatozoa from healthy donors. The highest damage was produced by DNA reactive aldehydes, food mutagens and benzo[a]pyrene when assessed with the neutral and alkaline Comet assay with and without metabolic activation.

Le complexe cohésine maintient associées les chromatides sœurs depuis la réplication jusqu’à leur ségrégation en mitose. Une question majeure est de comprendre comment la cohésion est établie lors de la phase S. Chez les mammifères et S. pombe, les cohésines sont associées de manière labile aux chromosomes pré-réplicatifs et l’établissement de la cohésion en phase S s’accompagne de la stabilisation de l’association des cohésines aux chromosomes. L’objectif de ce travail est de comprendre comment la dynamique des cohésines est régulée et comment son inhibition créée la cohésion.En G1 les cohésines associées aux chromosomes s’échangent avec le pool soluble et leur dissociation dépend de Pds5 et Wapl. La première partie de ce travail présente les résultats d’un crible génétique visant à identifier de nouveaux régulateurs de la dynamique des cohésines.L’établissement de la cohésion nécessite l’acétyltransférase Eso1 mais pas en contexte Δwpl1, indiquant que la seule mais essentielle fonction d’Eso1 est de s’opposer à celle de Wapl. L’acétylation de Smc3 par Eso1 contribue mais n’est pas suffisante pour contrecarrer Wapl, suggérant l’existence d’un autre événement dépendant d’Eso1. En G1, Pds5 agit avec Wapl pour dissocier les cohésines des chromosomes mais après la phase S, Pds5 est requise pour leur maintien sur les chromosomes et pour la cohésion à long terme. Pds5 co-localise avec la fraction stable de cohésines mais pas Wapl. Nous suggérons un modèle dans lequel la cohésion est créée par deux événements d’acétylation couplés à la progression de la fourche de réplication conduisant à l’éviction de Wapl des cohésines destinées à produire la cohésion. / Following DNA replication, sister chromatids are connected by cohesin to ensure their correct segregation during mitosis. How cohesion is created is still enigmatic. The cohesin subunit Smc3 becomes acetylated by ECO1, a conserved acetyl-transferase, and this change is required for cohesion. As in mammals, fission yeast cohesin is not stably bound to G1 chromosomes but a fraction becomes stable when cohesion is made. The aim of this work was to understand how cohesin dynamics is regulated and how the change in cohesin dynamics creates cohesion.In G1 chromatin bound cohesin exchange with the soluble pool and the unloading reaction relies in part on Wapl. The first part of this study reports on the identification of G1/S factors as new candidate regulators of cohesin dynamics.Following S phase a stable cohesin fraction is made. The acetyl-transferase Eso1 is not required for this reaction when the wpl1 gene is deleted. Yet, it is in wild-type cells, showing that the sole but essential Eso1 function is counteracting Wapl. Eso1 acetylates the cohesin sub-unit Smc3. This renders cohesin less sensitive to Wapl but does not confer the stable binding mode, suggesting the existence of a second Eso1-dependent event. The cohesin sub-unit Pds5 act together with Wapl to promote cohesin removal from G1 chromosomes but after S phase Pds5 is essential for cohesin retention on chromosomes and long term cohesion. Pds5 co-localizes with the stable cohesin fraction whereas Wapl does not. We suggest a model in which cohesion establishment is made by two acetylation events coupled to fork progression leading to Wapl eviction while keeping Pds5 on cohesin complexes intended to make cohesion.