Tesis sobre el tema "DNA damage"
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Sunter, Nicola. "DNA Damage Responses". Thesis, University of Newcastle Upon Tyne, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.489314.
Texto completoFazendeiro, Marta Sofia Pereira Pingarilho. "DNA damage induced by acrylamide: roe of genetic polymorphisms in DNA damage levels". Doctoral thesis, Faculdade de Ciências Médicas. UNL, 2013. http://hdl.handle.net/10362/10000.
Texto completoHåkansson, Pelle. "Ribonucleotide reductase and DNA damage". Doctoral thesis, Umeå universitet, Institutionen för medicinsk kemi och biofysik, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-706.
Texto completoHåkansson, Pelle. "Ribonucleotide reductase and DNA damage /". Umeå : Medicinsk biokemi och biofysik, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-706.
Texto completoJohnstone, Elaine Claire. "Ifosfamide metabolism and DNA damage". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264417.
Texto completoAldosari, Sahar. "Assessment of DNA damage and DNA damage response and repair in dormancy-enriched leukemia cells". Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/47257/.
Texto completoYu, Emma Pei Kuen. "Mitochondrial DNA damage, dysfunction and atherosclerosis". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648537.
Texto completoFarooq, Sabya. "Free radical induced oxidative DNA damage". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30749.
Texto completoBykov, Vladimir J. "UV-induced DNA damage in humans /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3345-6/.
Texto completoLampus, Daniele Jacopo. "Towards IR Probes of DNA Damage". Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518828.
Texto completoJansson, Martin D. "Regulation of the DNA damage response". Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.504493.
Texto completoKuimova, Marina K. "Designing infrared probes of DNA damage". Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416394.
Texto completoAlhebshi, H. "Molecular pathways controlling DNA damage response". Thesis, University of Salford, 2018. http://usir.salford.ac.uk/48475/.
Texto completoParkes, Eileen. "The immune response to DNA damage". Thesis, Queen's University Belfast, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709693.
Texto completoNdlebe, Thabisile S. "Oxidative Damage in DNA: an Exploration of Various DNA Structures". Diss., Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-05112006-154326/.
Texto completoDonald F. Doyle, Committee Member ; Bridgette Anne Barry, Committee Member ; Dr. Gary B. Schuster, Committee Chair ; Nicholas V. Hud, Committee Member ; Roger M. Wartell, Committee Member.
Krusong, Kuakarun. "Recognition and repair of DNA damage by uracil DNA glycosylase". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417133.
Texto completoCooley, Nicola. "Quantitative associations betweenn DNA damage, DNA repair and celluar outcomes". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499845.
Texto completoKaliyaperumal, Saravanan. "hMSH6 Protein Phosphorylation: DNA Mismatch Repair or DNA Damage Signaling?" Connect to full text in OhioLINK ETD Center, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=mco1242933021.
Texto completo"In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Sciences." Title from title page of PDF document. Bibliography: p. 174-180, p. 201-238.
Mikhed, Yuliya [Verfasser]. "The role of DNA damage in the pathogenesis of nitrate tolerance - nitrosative versus oxidative DNA damage / Yuliya Mikhed". Mainz : Universitätsbibliothek Mainz, 2015. http://d-nb.info/1080187529/34.
Texto completoVonarx, Edward J. y mikewood@deakin edu au. "The repair and tolerance of DNA damage in higher plants". Deakin University. School of Biological and Chemical Sciences, 2000. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20051110.135641.
Texto completoKarakoula, Aikaterini. "Studies on UV-induced DNA damage and repair to human DNA". Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29692.
Texto completoAtwal, Mandeep. "Myeloperoxidase enhances DNA damage induced by drugs targeting DNA topoisomerase II". Thesis, University of Newcastle upon Tyne, 2017. http://hdl.handle.net/10443/3956.
Texto completoMENTEGARI, ELISA. "DNA damage tolerance by specialized DNA polymerases in humans and plants". Doctoral thesis, Università degli studi di Pavia, 2018. http://hdl.handle.net/11571/1243288.
Texto completoJansson, Kristina. "Oxidative damage and the DNA glycosylase MutYH /". Göteborg : Department of Cell and Molecular Biology, University of Gothenburg, 2010. http://hdl.handle.net/2077/22092.
Texto completoSuwake, Natsuko. "D-type cyclins and DNA damage response". Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506678.
Texto completoWoollons, Arjida. "DNA damage induced by sunbeds and sunlight". Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251706.
Texto completoCooke, Marcus S. "Immunochemical investigation of UV-induced DNA damage". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30738.
Texto completoKotturi, Gopaul. "Correlating and measuring DNA damage and mutations". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0009/NQ52763.pdf.
Texto completoJiranusornkul, Supat. "Molecular modelling studies of DNA damage recognition". Thesis, University of Nottingham, 2008. http://eprints.nottingham.ac.uk/11303/.
Texto completoSoman, Sony. "OXIDATIVE DAMAGE TO DNA IN ALZHEIMER'S DISEASE". UKnowledge, 2013. http://uknowledge.uky.edu/chemistry_etds/28.
Texto completoGordon, Anthony T. "Persistence of carcinogen damage in nuclear DNA". Thesis, University of Nottingham, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318312.
Texto completoThomas, Nicola Alison. "RecA expression and DNA damage in mycobacteria". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299376.
Texto completoCatterall, Helen. "Mechanisms of free radical damage to DNA". Thesis, University of York, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359256.
Texto completoMittal, Sukant. "Micropatterned cell arrays for detecting DNA damage". Thesis, Massachusetts Institute of Technology, 2008. http://hdl.handle.net/1721.1/44734.
Texto completoIncludes bibliographical references (leaves 66-72).
Numerous agents are capable of interacting with DNA and damaging it. Permanent changes in the DNA structure can be both mutagenic and cytotoxic; therefore, methods to measure the susceptibility of cells to mutations are important for risk assessment and identifying therapeutic interventions. One classical method for assessing DNA damage at a global level is the COMET assay, based on electrophoretic extension of the nuclear DNA in single cells embedded in agarose. In this assay, the size and shape of the extended 'comet tail' can be correlated to breaks in the DNA. This assay was first developed in the mid 1980s for non adherent cells such as lymphocytes; however, it has been plagued by technical difficulties, low throughput, and lab-to lab variation. These challenges have been exacerbated in adhesion-dependent cells as DNA damage accrues variably over time as they are enzymatically detached from their microenvironment. This thesis explores whether the COMET assay can be improved by micropatterning adherent cells prior to agarose embedding. Hepatocytes were chosen as a model cell type and x-ray radiation was chosen as a model DNA damaging agent. In order to establish the feasibility of measuring x-ray induced damage on hepatocyte DNA, standard curves were first generated for hepatocytes suspended in agarose. These experiments revealed a minimum detectable threshold of 1 Gy and displayed a monotonic increase in DNA damage in response to exposures up to 10 Gy. In comparison, adherent hepatocytes overlaid with agarose and irradiated in situ displayed similar levels of mean damage but lower levels of variability than suspended cells. We hypothesize that the decreased variability could be due to a reduction in programmed cell death incurred by detachment of adherent cells.
(cont.) Finally, we explored the feasibility of performing the comet assay by in situ irradiation of a micropatterned array of adherent cells. Single cell hepatocyte patterning was achieved by photolithographic patterning of collagen I on glass and optimization of seeding conditions. Gradiations of x-ray exposure were achieved by employing localized domains of lead shielding between the cells and the source. As a proof of principle, we obtained two domains of differential x-ray exposure and the resulting DNA damage was similar in the micropatterned format to the randomly-organized adherent format. Several challenges emerged from these experiments including potential interactions of DNA with the glass surface leading to 'streaking' artifacts. Nonetheless, with increased resolution of x-ray exposure, and further technical improvements, this assay has the potential to offer both reduced variability for adherent cells as well as assay multiplexing due to spatial encoding of x-ray dosage.
by Sukant Mittal.
S.M.
Haleux, Pauline. "DNA damage responses in plant stem cells". Thesis, University of East Anglia, 2014. https://ueaeprints.uea.ac.uk/52055/.
Texto completoMcAllister, Maeve. "Computational modelling of radiation damage to DNA". Thesis, Queen's University Belfast, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707538.
Texto completoLittle, Elizabeth J. "DNA damage sensors in the checkpoint response". Diss., The University of Arizona, 2003. http://hdl.handle.net/10150/289950.
Texto completoZheng, Zhi-Ying 1957. "Bile acid-induced DNA damage in bacteria". Thesis, The University of Arizona, 1990. http://hdl.handle.net/10150/291421.
Texto completoMiller, Olivia. "Reactive Intermediates in Hypoxia-Selective DNA Damage". Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/honors/73.
Texto completoDogo, Federico. "MODELS OF DNA DAMAGE, REPAIR, AND MISREPAIR". Doctoral thesis, Università degli studi di Trieste, 2015. http://hdl.handle.net/10077/10889.
Texto completoWithin the range of the Virtual Biophysics Lab tumour growth numerical simulator, this work aims to develop a mathematical model able to describe the cell cycle desynchronization observed in the cell populations and the effects of DNA damage and repair due to ionizing radiation. Following a review of the already available models, some other original ones are proposed; one of these has been also tested on tumour cells by means of cytometry: the results of the related data analysis are not yet conclusive.
Nell'ambito del simulatore numerico di crescita tumorale Virtual Biophysics Lab, questo lavoro mira a sviluppare un modello matematico adatto a descrivere la desincronizzazione cellulare osservata nelle popolazioni cellulari e gli effetti del danno e riparazione del DNA indotti da radiazioni ionizzanti. A seguito di una recensione dei modelli già esistenti, ne vengono proposti alcuni altri originali; uno di questi è stato anche testato su cellule tumorali attraverso la citofluorimetria: i risultati della relativa analisi dati non sono ancora decisivi.
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Fisher, Mark. "Intra and extracellular responses to DNA damage". Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/214106/1/Mark_Fisher_Thesis.pdf.
Texto completoLangerak, Petra. "@DNA damage tolerance from error free UV-damage bypass to mutagenesis of immunoglobulin genes /". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/.
Texto completoNajeeb, Hishyar Azo. "Redox modulation of oxidatively induced DNA damage by ascorbate enhances melanoma cancer cell DNA damage formation & cell killing". Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/36021.
Texto completoJumpathong, Watthanachai. "The dynamic interplay between DNA damage and metabolism : the metabolic fate and transport of DNA lesions and novel DNA damage derived from intermediary metabolism". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/93772.
Texto completoThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references.
The work presented in this thesis explores two novel and complementary facets of endogenous DNA damage: the development of biomarkers of inflammation based on metabolites of DNA damage products and the formation of DNA adducts by electrophilic products of intermediary metabolism. From the first perspective, endogenous DNA damage generated by reactive oxygen and nitrogen species from inflammation and oxidative stress has shown strong mechanistic links to the pathophysiology of cancer and other human diseases, with the damage products reflecting all types of damage chemistries including oxidation, deamination, halogenation, nitration and alkylation. However, the use of DNA damage products as biomarkers has been limited by poor understanding of the damage actually arising in tissues and a lack of appreciation of the fate of DNA damage products from the moment of formation at the site of damage to release from cells to final excretion from the body. The goal of the work presented in the first part of this thesis was to investigate the metabolic fates of the base propenal products arising from 4'-oxidation of 2'-deoxyribose in DNA, one of the most common products of DNA oxidation, and to define base propenal metabolites as potential biomarkers of oxidative stress. This project was approached with systematic metabolite profiling, starting with prediction of potential base propenal metabolites based on a priori knowledge of its chemical reactivity as an [alpha],[beta]-unsaturated aldehyde toward glutathione (GSH) in non-enzymatic reactions and in rat liver cell extracts. Of 15 potential candidates predicted and identified from these in vitro studies, analysis of urine samples from rats given intravenous doses (IV) of thymine propenal revealed three major metabolites: thymine propenoic acid and two mercapturic acid derivatives, which accounted for ~6% of the injected dose. An additional four metabolites, including conjugates with GSH, cysteinylglycine and cysteine, were observed in bile and accounted for ~22% of the dose. One of the major metabolites detected in urine and bile, a bis-mercapturic acid adduct of reduced thymine propenal was detected as a background excretory product in saline-treated rats and was significantly elevated after oxidative stress caused by treatment with bleomycin and CCl₄. Our observations suggest that metabolism and disposition of damaged biomolecules should be considered as crucial factors in the development of biomarkers relevant to inflammation and oxidative stress. The second part of this thesis addresses the complementary hypothesis that electrophilic metabolites generated endogenously from intermediary metabolism can react with DNA to form adducts. This concept is illustrated here with glyoxylate from the glyoxylate metabolic cycle, whicvh plays a key role as an alternative to the TCA cycle in plants, bacteria, protists and fungi under changing conditions of environmental nutrients. The goal of this project was to characterize DNA adducts caused by glyoxylate in the mycobacterium M. smegmatis, with the studies motivated by the higher-than-expected mutation rate of mycobacteria during dormancy induced by nutrient deprivation and a shift to utilization of the glyoxylate cycle. Initially, in vitro reactions of 2'-deoxyguanosine (dG) with glyoxylate yielded N²-carboxyhydroxymethyl dG (N²-CHMdG) as the only adduct. However, the adduct proved to be unstable, so a reduction-based analytical method was developed to yield the stable amine derivative, N2-carboxymethyl dG (N²-CMdG). This stable adduct was used to develop an isotope-dilution chromatography-coupled tandem mass spectrometry method to quantify N²-CHMdG as N²-CMdG in calf thymus DNA treated with glyoxylate in vitro. This analytical method was then applied to quantify and compare the level N2-CMdG in (1) wild-type M. smegmatis grown in rich medium (7H9) or in minimal M9 medium supplemented with acetate, the latter inducing a switch from the TCA cycle to the glyoxylate cycle; and (2) the isocitrate dehydrogenase (ICD)-deficient mutant of M. smegmatis. Mycobacteria grown in the acetate medium experienced a 2-fold increase in the adduct compared to those grown in 7H9. Similarly, the adduct increased 2-fold in the ICD mutant compared to wild-type M. smegmatis grown in 7H9. The results support the idea that shifts in intermediary metabolism can lead to DNA damage that may cause mutations associated with nutrient deprivation in mycobacteria, with implications for the genetic toxicology of other metabolism-derived electrophiles.
by Watthanachai Jumpathong.
Ph. D.
Wiltshire, Timothy D. "DNA damage response activated by anti-cancer agent, irofulven". Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5390.
Texto completoTitle from document title page. Document formatted into pages; contains ix, 227 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
Xu, Meng. "Oxidative DNA Damage Modulates Trinucleotide Repeat Instability Via DNA Base Excision Repair". FIU Digital Commons, 2014. http://digitalcommons.fiu.edu/etd/1576.
Texto completoPhillips, Lara Gayle. "The role of DNA polymerase delta and WRN in DNA damage tolerance". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608621.
Texto completoRoos, Wynand Paul. "The influence of DNA damage, DNA repair and chromatin structure on radiosensitivity". Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52540.
Texto completoENGLISH ABSTRACT: The factors which control radiosensitivity are of vital importance for the understanding of cell inactivation and for cancer therapy. Cell cycle blocks, total induced DNA damage, DNA repair, apoptosis and chromatin structure are likely to playa role in the responses leading to cell death. I have examined aspects of irradiation-induced G2/M blocks in DNA damage and repair. In HT29, L132 and ATs4 cells the total amount of induced DNA damage by isodoses of 4.5 Gy, 5 Gy and 2 Gy was found to be 14 %, 14 % and 12 % respectively. Most of the DNA repair was completed before the G2/M maximum and only 3 % of DNA damage remains to be restored in the G2/M block. The radiosensitivity in eleven cell lines was found to range from SF2 of 0.02 to 0.61. By FADU assay the undamaged DNA at 5 Gy was found to range from 56% to 93%. The initial DNA damage and radiosensitivity were highly correlated (r2=0. 81). After 5 Gy irradiation and 12 hours repair two groups of cell lines emerged. The group 1 cell lines restored undamaged DNA to a level ranging from 94 % to 98 %. The group 2 cell lines restored the undamaged DNA to a level ranging from 77 % to 82 %. No correlation was seen between residual DNA damage remaining after 12 hours repair and radiosensitivity. In CHO-K1 cells chromatin condensation induced by Nocodazole was found to marginally increase the radiosensitivity as shown by the change of the mean inactivation dose (D) from 4.446 to 4.376 Gy. Nocodazole also increased the initial DNA damage, induced by 5 Gy, from 7 % to 13 %. In xrs1 cells these conditions increased the radiosensitivity from D of 1.209 to 0.7836 Gy and the initial DNA damage from 43 % to 57 %. Disruption of chromatin structure with a hypertonic medium was found to increase radiosensitivity in CHO-K1 cells from D of 4.446 to 3.092 Gy and the initial DNA damage from 7 % to 15 %. In xrs1 cells these conditions caused radiosensitivity to decrease from D of 1.209 to 1.609 Gy and the initial DNA damage from 43 % to 36 %. Repair inhibition by Wortmannin increased the radiosensitivity in CHO-K1 from a D of 5.914 Gy in DMSO controls to a D 3.043 Gy. In xrs1 cells repair inhibition had no effect on radiosensitivity. Significant inhibition of repair was seen in CHO-K1 at 2 hours (p<0.0001) and at 20 hours (p=0.0095). No inhibition of repair was seen in xrs1 cells at 2 hours (p=0.6082) or 20 hours (p=0.6069). While DNA repair must be allocated to the post-irradiation period, the G2/M block seen in p53 mutants reaches a maximum only 12 hours post-irradiation when most of the repair is completed. As the G2/M block resolves and cells reenter cycle 28 hours after the G2 maximum it appears that repair processes cannot be the only reason for the G2IM cell cycle arrest. At low doses of irradiation initial DNA damage correlates with radiosensitivity. This suggests that the initial DNA damage is a determinant for radiosensitivity. Repair of DNA double-strand breaks by the non-homologous end joining (NHEJ) mechanism, identified by inhibition with Wortmannin, was shown to influence residual DNA damage and cell survival. Both the initial DNA damage and DNA repair were found to be influenced by chromatin structure. Chromatin structure was modulated by high salt and by Nocodazole, and has heen identified as a parameter which influences radiosensitivity.
AFRIKAANSE OPSOMMING: Die faktore wat betrokke is in die meganisme van stralings-sensitisering is van hoogs belang vir die begrip van sel inaktiveering en kanker terapie. Sel siklus blokke, totale geïnduseerde DNS skade, DNS herstel, apoptose en chromatien struktuur is moontlike rol vertolkers in die sellulêre response wat ly tot seldood. Ek het die aspekte van stralings-geïnduseerde G2/M blokke in DNS skade en DNS herstelondersoek. Die hoeveelheid geïnduseerde DNS skade, deur ooreenstemmende stralings-dosisse, in HT29, L132 en ATs4 selle is 14 %, 14 % en 12 %. Meeste van die DNS herstel is klaar voordat die G2/M maksimum beryk word en net 3 % DNS skade blyoor om herstel te word in die G2/M blok. Die stralings-sensitiwiteit in elf sel lyne varieer tussen 'n SF2 van 0.02 en 0.61. Deur die gebruik van die FADU metode is gevind dat die onbeskadigde DNS na 5 Gy bestraling varieer tussen 56 % en 93 %. Die totale geïnduseerde DNS skade en stralings-sensitiwiteit was hoogs gekorreleer (r2=0.81). Na 5 Gy bestraling en 12 ure herstel kan die sel lyne in twee groepe gegroepeer word. Die groep 1 sellyne herstel die onbeskadigde DNS terug na 'n vlak wat varieer tussen 94 % en 98 %. Die groep 2 sel lyne herstel die onbeskadigde DNS terug tot op 'n vlak wat varieer tussen 77 % en 82 %. Geen korrelasie is gesien tussen oorblywende DNS skade en stralings-sensitiwiteit na 12 ure herstel nie. In die CHO-K1 sel lyn, chromatien kompaksie geïnduseer deur Nocodazole, vererger die stralings- sensitiwiteit soos gesien deur die gemiddelde inaktiveerings dosis (D) wat verlaag het van 4.446 tot 4.376. Nocodazole het ook die totale DNS skade verhoog van 7 % tot 13 %. Onder dieselfde kondisies, in die xrs1 sel lyn, is 'n verergering van stralings-sensitiwiteit (D) gesien van 1.209 tot 0.7836 en verhoog ONS skade van 43 % tot 57 %. Die ontwrigting van die chromatien struktuur deur die gebruik van hipertoniese medium het die stralings-sensitiwiteit (D) vererger in CHO-K1 selle van 4.446 tot 3.092. Die totale ONS skade is verhoog van 7 % tot 15 %. Onder dieselfde kondisies, in die xrs1 sellyn, verbeter die stralings-sensitiwiteit (D) van 1.209 tot 1.609 en die totale ONS skade verminder van 43 % tot 36 %. ONS herstel inaktiveering in die teenwoordigheid van Wortmannin het die stralings-sensitiwiteit (D) in CHO-K1 selle vererger van 5.914 in DMSO verwysings kondisies tot 3.043. Die ONS herstel inaktiveering in xrs1 selle het geen uitwerking gehaat op stralingssensitiwiteit nie. Noemenswaardige inaktiveering van ONS herstel is gesien in CHO-K1 selle na 2 ure (p<0.0001) en na 20 ure (p=0.0095). Geen inaktiveering is gesien in xrs1 selle na 2 ure (p=0.6082) of na 20 ure (p=0.6069) nie. TerwylONS herstel moet plaasvind na die bestralings periode, beryk die G2/M blok in p53 gemuteerde selle sy maksimum 12 ure na bestraling terwyl meeste van die ONS herstel alreeds voltooi is. Aangesien die G2/M blok eers 28 ure later begin sirkuleer moet die G2/M blok nog 'n funksie vervul anders as ONS herstel. By lae dosisse van bestraling korreleer die totale geïnduseerde ONS skade met stralings-sensitiwiteit. Dit dui daarop dat die totale ONS skade 'n bepalende faktor moet wees in stralings-sensitiwiteit. Die herstel van ONS skade deur die nie-homoloë eindpunt samevoeging (NHES) meganisme, geïdentifiseer deur inaktiveering deur Wortmann in, het 'n invloed op oorblywende ONS skade en sellulêre oorlewing. Beide die totale ONS skade en ONS herstel was beïnvloed deur die chromatien struktuur. Chromatien struktuur was gemoduleer deur hoë sout konsentrasies en deur Nocodazole, en is geïdentifiseer as a belangrike parameter wat stralings-sensitiwiteit beïnvloed.
Brockmann, William G. Eick J. David. "An investigation of a rapid fluorescence microtiter plate methodology for measuring chemically-induced DNA damage, suitable for use in development of a primary DNA damage database". Diss., UMK access, 2004.
Buscar texto completo"A dissertation in oral biology and pharmacology." Advisor: J. David Eick. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed Feb. 22, 2006. Includes bibliographical references (leaves 176-189). Online version of the print edition.
Bowden, Gemma M. "Assay of DNA photoproducts". Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318877.
Texto completo