Gotowe bibliografie tematyczne / DNA damage

Gotowa bibliografia na temat „DNA damage”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 31 lipca 2024

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Artykuły w czasopismach na temat "DNA damage"

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Chakarov, Stoyan, Rumena Petkova, George Russev i Nikolai Zhelev. "DNA damage and mutation. Types of DNA damage". BioDiscovery, nr 11 (23.02.2014): 1. http://dx.doi.org/10.7750/biodiscovery.2014.11.1.

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Yeung, ManTek, i Daniel Durocher. "Engineering a DNA damage response without DNA damage". Genome Biology 9, nr 7 (2008): 227. http://dx.doi.org/10.1186/gb-2008-9-7-227.

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Bagchi, Srilata, i Pradip Raychaudhuri. "Damaged-DNA Binding Protein-2 Drives Apoptosis Following DNA Damage". Cell Division 5, nr 1 (2010): 3. http://dx.doi.org/10.1186/1747-1028-5-3.

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Wallace, Bret D., i R. Scott Williams. "Ribonucleotide triggered DNA damage and RNA-DNA damage responses". RNA Biology 11, nr 11 (2.11.2014): 1340–46. http://dx.doi.org/10.4161/15476286.2014.992283.

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Nawy, Tal. "DNA variants or DNA damage?" Nature Methods 14, nr 4 (kwiecień 2017): 341. http://dx.doi.org/10.1038/nmeth.4254.

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Bush, Stephen P., Peter E. Hart i Eric M. Russell. "Investigating DNA Damage". American Biology Teacher 68, nr 5 (1.05.2006): 280–84. http://dx.doi.org/10.2307/4451989.

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Oksenych, Valentyn, i Denis E. Kainov. "DNA Damage Response". Biomolecules 11, nr 1 (19.01.2021): 123. http://dx.doi.org/10.3390/biom11010123.

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Bush, Stephen P., Peter E. Hart i Eric M. Russell. "Investigating DNA Damage". American Biology Teacher 68, nr 5 (2006): 280. http://dx.doi.org/10.1894/0038-4909(2006)68[280:idd]2.0.co;2.

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Skrypnyk, N. V., i O. O. Maslova. "Oxidative DNA damage". Biopolymers and Cell 23, nr 3 (20.05.2007): 202–14. http://dx.doi.org/10.7124/bc.000766.

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Giglia-Mari, G., A. Zotter i W. Vermeulen. "DNA Damage Response". Cold Spring Harbor Perspectives in Biology 3, nr 1 (27.10.2010): a000745. http://dx.doi.org/10.1101/cshperspect.a000745.

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Rozprawy doktorskie na temat "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.

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The histone H2AX has been established as a reliable biomarker of DNA damage, becoming phosphorylated rapidly following damage in discrete foci which can be correlated with DNA DSB number. In the present study, the phosphorylation of H2AX was used as a marker of DNA DSB damage to compare and contrast the damage induced by ionizing radiation, the topo II poison, etoposide, and the topo II catalytic inhibitor, ICRF-193. To examine the DNA damage numbers at time-points in the 24 hours following exposure to these damaging agents. Topo lIP null cells were used to investigate the contribution of topo II a and Pthese damage responses and the Trapped in Agarose DNA Immunostaining assay was utilised to quantify the numbers of topo II_DNA complexes formed in response to these agents. This study aimed to examine the levels of DNA damage following exposure to these damaging agents and to investigate differences in the complement of proteins associated with DNA damage-induced foci. By using both the y-H2AX and TARDIS assays and protein colocalisation techniques, the studies detailed here presents novel findings on the differing damage responses induced following these three agents.
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Fazendeiro, 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.

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RESUMO:Em 1994 a acrilamida (AA) foi classificada pela IARC como um provável cancerígeno para o homem. Para além da utilização de AA em numerosas aplicações industriais, a AA está também presente numa grande variedade de alimentos ricos em amido e processados a temperaturas elevadas. Esta exposição através da ingestão de produtos alimentares despoletou elevadas preocupações ao nível do risco para a saúde pública e poderá implicar um risco adicional para o aparecimento de cancro. A glicidamida (GA), o metabolito epóxido formado a partir da oxidação da AA provavelmente através do citocromo P450 2E1, é considerada por vários estudos, o principal responsável pela carcinogenicidade da AA. Actualmente existe uma escassez de resultados relativamente aos mecanismos de genotoxicidade da AA e GA em células de mamífero. Por este motivo, o objectivo deste estudo centra-se na avaliação das consequências genéticas da exposição à AA e GA, recorrendo-se para tal ao uso de células de mamífero como modelo. Tendo como base este objectivo avaliou-se a citotoxicidade da AA e GA, através do ensaio do MTT, e realizaram-se dois testes citogenéticos, o teste das aberrações cromossómicas (CAs) e o teste da troca de cromátides irmãs (SCEs), de modo a avaliar as lesões de DNA induzidas por estes compostos em células de hamster Chinês V79. Os resultados globalmente mostraram que a GA é mais citotóxica e clastogénica do que a AA. No âmbito deste trabalho, foi também efectuada a quantificação de aductos específicos de DNA, nomeadamente N7-(2-carbamoil-2-hidroxietil)guanina (N7-GA-Gua) e N3-(2-carbamoil-2-hidroxietil)adenina (N3-GA-Ade). Os resultados obtidos permitem afirmar que os níveis de N7-GA-Gua e a concentração de GA apresentam uma relação linear dose-resposta. Foi também identificada uma óptima correlação entre os níveis de N7-GA-Gua e a frequência de troca de cromátides irmãs. Adicionalmente, e de forma a compreender os mecanismos de toxicidade da AA, estudaram-se os mecanismos dependentes da modulação do glutationo reduzido (GSH), nomeadamente da butionina sulfoximina (BSO), um inibidor da síntese de GSH, do GSH-monoetil estér (GSH-EE), um composto permeável nas células e que é intra-celularmente hidrolisado a GSH e ainda do GSH adicionado exogenamente ao meio de cultura, em células V79. Os resultados obtidos reforçaram o papel da modulação do GSH nos efeitos de citotoxicidade e clastogenicidade da AA. Para além dos estudos efetuados com células V79, procedeu-se também à determinação da frequência de SCEs, à quantificação de aductos específicos de DNA, bem como ao ensaio do cometa alcalino em amostras de dadores saudáveis expostos à AA e GA. Tanto os resultados obtidos através do ensaio das SCE, como pela quantificação de aductos específicos de DNA, ambos efectuados em linfócitos estimulados, originaram resultados comparáveis aos obtidos anteriormente para as células V79, reforçando a ideia de que a GA é bastante mais genotóxica do que a AA. Por outro lado, os resultados obtidos pelo ensaio do cometa para exposição à AA e GA mostraram que apenas esta última aumenta o nível das lesões de DNA. Outro objectivo deste trabalho, foi a identificação de possíveis associações existentes entre as lesões de DNA, quantificadas através do ensaio das SCEs e do cometa, e biomarcadores de susceptibilidade, tendo em conta os polimorfismos genéticos individuais envolvidos na destoxificação e nas vias de reparação do DNA (BER, NER, HRR e NHEJ) em linfócitos expostos à GA. Tal permitiu identificar associações entre os níveis de lesão de DNA determinados através do ensaio das SCEs, e os polimorfismos genéticos estudados, apontando para uma possível associação entre o GSTP1 (Ile105Val) e GSTA2 (Glu210Ala) e a frequência de SCEs. Por outro lado, os resultados obtidos através do ensaio do cometa sugerem uma associação entre as lesões de DNA e polimorfismos da via BER (MUTYH Gln335His e XRCC1 Gln39Arg) e da via NER (XPC Ala499val e Lys939Gln), considerando os genes isoladamente ou combinados. Estes estudos contribuem para um melhor entendimento da genotoxicidade e carcinogenicidade da AA e GA em células de mamífero, bem como da variabilidade da susceptibilidade individual na destoxificação e reparação de lesões de DNA provocadas pela exposição a estes xenobióticos alimentares. ----------- ABSTRACT:Acrylamide (AA) has been classified as a probable human carcinogen by IARC. Besides being used in numerous industrial applications, AA is also present in a variety of starchy cooked foods. This AA exposure scenario raised concerns about risk in human health and suggests that the oral consumption of AA is an additional risk factor for cancer. A considerable number of findings strongly suggest that the reactive metabolite glycidamide (GA), an epoxide generated presumably by cytochrome P450 2E1, plays a central role in AA carcinogenesis. Until now there are a scarcity of results concerning the mechanisms of genotoxicity of AA and GA in mammalian cells. In view of that, the study described in this thesis aims to unveil the genetic consequences of AA and GA exposure using mammalian cells as a model system. With this aim we evaluated the cytotoxicity of AA and GA using the MTT assay and subsequently performed two cytogenetic end-points: chromosomal aberrations (CAs) and sister chromatid exchanges (SCEs), in order to evaluate DNA damage induced by these compounds in V79 Chinese hamster cell line. The results showed that GA was more cytotoxic and clastogenic than AA. Within the scope of this thesis the quantification of specific DNA adducts were also performed, namely N7-(2-carbamoyl-2-hydroxyethyl)guanine (N7-GA-Gua) and N3-(2-carbamoyl-2-hydroxyethyl)adenine (N3-GA-Ade). Interestingly, the GA concentration and the levels of N7-GA-Gua presented a linear dose-response relationship. Further, a very good correlation between the levels of N7-GA-Gua and the extent of SCEs were observed. In order to understand the mechanisms of AA-induced toxicity, the modulation of reduced glutathione (GSH)-dependent mechanisms were studied, namely the evaluation of the effect of buthionine sulfoximine (BSO), an effective inhibitor of GSH synthesis, of GSH-monoethyl ester (GSH-EE), a cell permeable compound that is intracellularly hydrolysed to GSH and also of GSH endogenously added to culture medium,z in V79 cell line. The overall results reinforced the role of GSH in the modulation of the cytotoxic and clastogenic effects induced by AA.Complementary to the studies performed in V79 cells, SCEs, specific DNA-adducts and alkaline comet assay in lymphocytes from healthy donors exposed to AA and GA were also evaluated. Both, the frequency of SCE and the quantification of specific GA DNA adducts, produced comparable results with those obtained in V79 cell line, reinforcing the idea that GA is far more genotoxic than AA. Further, the DNA damaging potential of AA and GA in whole blood leukocytes evaluated by the alkaline comet assay, showed that GA, but not AA, increases DNA damage. Additionally, this study aimed to identify associations between DNA damage and biomarkers of susceptibility, concerning individual genetic polymorphisms involved in detoxification and DNA repair pathways (BER, NER, HRR and NHEJ) on the GA-induced genotoxicity assessed by the SCE assay and by the alkaline comet assay. The extent of DNA damage determined by the levels of SCEs induced by GA seems to be modulated by GSTP1 (Ile105Val) and GSTA2 (Glu210Ala) genotypes. Moreover, the results obtained from the comet assay suggested associations between DNA damage and polymorphisms of BER (MUTYH Gln335His and XRCC1 Gln399Arg) and NER (XPC Ala499Val and Lys939Gln) genes, either alone or in combination. The overall results from this study contribute to a better understanding of the genotoxicity and carcinogenicity of AA and GA in mammalian cells, as well as the knowledge about the variability in individual susceptibility involved in detoxification and repair of DNA damage due to these dietary xenobiotics.
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Håkansson, 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.

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A prerequisite for a multicellular organism to survive is the ability to correctly replicate and repair DNA while minimizing the number of heritable mutations. To achieve this, cells need a balanced supply of deoxyribonucleoside triphosphates (dNTPs), the precursors for DNA synthesis. The rate-limiting step in de novo biosynthesis of dNTPs is catalyzed by the enzyme ribonucleotide reductase (RNR). The classic eukaryotic RNR enzyme consists of a large and a small subunit. Together, these subunits form a heterotetrameric RNR complex. The larger subunit harbours active sites whereas the smaller subunit contains a stable tyrosyl free radical. Both subunits are required for RNR activity. Since failure to correctly regulate de novo dNTP biosynthesis can lead to misincorporation of nucleotides into DNA, genetic abnormalities and cell death, RNR activity is tightly regulated. The regulation of RNR activity involves cell cycle-specific expression and degradation of the RNR proteins, as well as binding of allosteric effectors to the large RNR subunit. In this thesis, in vitro assays based on purified recombinant RNR proteins, in combination with in vivo assays, have been used successfully to study the regulation of RNR activity in response to DNA damage. I present new findings regarding the function of an alternative mammalian RNR small subunit, and on the role of a small RNR inhibitor protein of fission yeast, during normal growth and after DNA damage. I also show conclusively that there are fundamental differences in the regulation of dNTP biosynthesis between the cells of higher and lower eukaryotes after DNA damage.
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Håkansson, Pelle. "Ribonucleotide reductase and DNA damage /". Umeå : Medicinsk biokemi och biofysik, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-706.

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Johnstone, 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.

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Aldosari, 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/.

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Acute myeloid leukaemia (AML) is a heterogeneous myeloid malignancy characterized by clonal expansion of abnormal/immature hematopoietic precursor cells in the bone marrow. A side compartment in the BM niche consists of abnormal, quiescent cells, which are called dormant leukemic initiating cells (DLICs). Patients with AML tend to respond well to remission induction chemotherapy, but relapse is common because current therapies cannot completely eradicate leukemic cells. It is widely accepted that CD34+CD38− DLICs are more resistant to chemotherapy and that they contribute to drug resistance and relapse of AML to a greater extent than progenitor CD34+CD38+ cells. DLICs have been extensively characterised, but they remain a critical area of investigation for clinical research because of the low prevalence of DLICs and similarity to normal HSCs. A model of dormancy in vitro that shows most of the features of DLICs had previously been established in the Nottingham Haematology Group. This study used this model and aimed to investigate whether the response to DNA damage was different in dormancy-enriched cells compared to cycling leukemic cells following chemotherapy. The amount of DNA damage was assessed up to 24 hours pre- and post- drug treatment using the neutral Comet assay. Lower levels of damage were observed in dormancy-enriched cells following etoposide (ETO) treatment at 4 hours (p = 0.04), although this switched at the 24 hour time point where accumulated DNA double-stranded breaks (DSBs), in dormancy-enriched KG1a cells were associated with a higher percentage of viable cells. DNA damage response cascade markers in both dormancy-enriched and cycling cells showed phosphorylation by flow cytometry (phospho-H2AX139, pATM-S1981, H2AX142, and pChk-Thr68) in response to conventional AML chemotherapy. Significantly lower levels of cleaved PARP-Asp214 and active caspase 3 were observed in dormancy-enriched cells treated with ara-c (p = 0.0001) or ETO (p = 0.0001) at 24 hours, strongly indicating that survival responses are activated in dormancy-enriched cells. Induction of 53BP1 foci, the hallmark of non-homologous end joining (NHEJ) was observed following treatment with ara-c (p = 0.038) and ETO (p = 0.049) in dormancy-enriched cells, indicating the NHEJ repair pathway is the preferred mechanism for DSB repair. At the molecular level, BTG2 expression was involved in the DNA damage response. Significant induction of BTG2 was detected in cycling treated cells with ETO for 24 hours. In conclusion, this study provides evidence that phosphorylation of H2AX139 and H2AX142 is a key response marker that may explain the mechanism underlying the drug resistance of DLICs and induction of repair. Therefore, results of this study may help in devising novel treatment strategies for AML that target H2AX142 of DLICs to permanently eradicate all leukemic cells and improve overall survival.
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Yu, 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.

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Farooq, Sabya. "Free radical induced oxidative DNA damage". Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/30749.

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Oxidative DNA damage has been implicated in processes such as carcinogenesis, mutagenesis, ageing and cell death. Reactive oxygen species (ROS) such as superoxide (O2), hydrogen peroxide (H2O 2) and hydroxyl radical (OH*) are produced in mammalian cells as a result of aerobic metabolism. However excess generation of these species by endogenous or exogenous sources can result in damage to DNA, producing a large number of sugar and base lesions. In order to understand the biological consequences of such free radical induced damage it is essential to characterise and quantitate this damage. This study describes the establishment of sensitive and specific techniques to chemically characterise and quantitate three markers of oxidative DNA damage, namely: cis-thymine glycol (Tg), 5-hydroxymethyluracil (5-OHMeU) and 8-hydroxyguanine (8-OHG). Techniques using gas chromatography/mass spectrometry (GC/MS) were established for Tg and 5-OHMeU, following their derivatisation with N-methyl-N-(tert-butyldimethylsilyl) trifluoroacetamide (MTBSTFA). Standards of Tg and 5-OHMeU were synthesised, and stable isotopically labelled analogues were prepared as internal standards. Analysis of the DNA was carried out at the base level and therefore required acidic hydrolysis of the DNA in order to release the modified and intact bases. For the quantitation of 8-OHG a novel procedure using high performance liquid chromatography (HPLC) - electrochemical detection (ECD) with guanase incubation of DNA hydrolysates was established. The established assays were used to quantitate DNA lesions in vitro and in vivo. In vitro dose response curves were established for the three markers upon gamma-irradiation of DNA. In vivo results of an animal inhalation study indicated there was not a significant increase in oxidative damage upon exposure to crocidolite. An antioxidant supplementation study in humans placental DNA also did not show a significant reduction in levels of the three markers upon supplementation. Comparable background levels of Tg and 5-OHMeU were observed in human and calf thymus DNA, while 8-OHG levels were found to be significantly higher.
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Bykov, Vladimir J. "UV-induced DNA damage in humans /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3345-6/.

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Lampus, Daniele Jacopo. "Towards IR Probes of DNA Damage". Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518828.

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Książki na temat "DNA damage"

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Mosammaparast, Nima, red. DNA Damage Responses. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2063-2.

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Wolfram, Siede, Kow Yoke Wah i Doetsch Paul W, red. DNA damage recognition. New York: Taylor & Francis, 2006.

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Dizdaroglu, Miral, i R. Stephen Lloyd, red. DNA Damage, DNA Repair and Disease. Cambridge: Royal Society of Chemistry, 2020. http://dx.doi.org/10.1039/9781839160769.

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Dizdaroglu, Miral, i R. Stephen Lloyd, red. DNA Damage, DNA Repair and Disease. Cambridge: Royal Society of Chemistry, 2020. http://dx.doi.org/10.1039/9781839162541.

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Laboratory, Cold Spring Harbor, red. Biological responses to DNA damage. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory Press, 2000.

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International Congress on DNA Damage and Repair (1st 1987 Rome, Italy). DNA damage and repair. New York: Plenum Press, 1989.

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Nickoloff, Jac A., i Merl F. Hoekstra. DNA Damage and Repair. New Jersey: Humana Press, 1998. http://dx.doi.org/10.1385/0896033562.

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Nickoloff, Jac A., i Merl F. Hoekstra. DNA Damage and Repair. New Jersey: Humana Press, 1998. http://dx.doi.org/10.1385/089603500x.

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Nickoloff, Jac A., i Merl F. Hoekstra. DNA Damage and Repair. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592590950.

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Nickoloff, Jac A., i Merl F. Hoekstra, red. DNA Damage and Repair. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-455-9.

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Części książek na temat "DNA damage"

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Speer, Tod W., Christin A. Knowlton, Michelle Kolton Mackay, Charlie Ma, Lu Wang, Larry C. Daugherty, Brandon J. Fisher i in. "DNA Damage". W Encyclopedia of Radiation Oncology, 158. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_607.

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Durant, Stephen T. "DNA Damage". W Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1669-7.

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Durant, Stephen T. "DNA Damage". W Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-642-27841-9_1669-8.

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Douki, Thierry, i Jean Cadet. "DNA Damage". W Encyclopedia of Astrobiology, 667–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-44185-5_451.

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Cadet, Jean, i Thierry Douki. "DNA Damage". W Encyclopedia of Astrobiology, 447–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-11274-4_451.

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Plevani, Paolo. "DNA Damage". W Encyclopedia of Systems Biology, 607. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_724.

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Durant, Stephen T. "DNA Damage". W Encyclopedia of Cancer, 1382–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-46875-3_1669.

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Durant, Stephen T. "DNA Damage". W Encyclopedia of Cancer, 1129–33. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1669.

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Sharma, Bechan, i Nitika Singh. "DNA damage". W Environmental Damage to DNA and the Protective Effects of Phytochemicals, 113–20. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9780429342059-10.

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Douki, Thierry, i Jean Cadet. "DNA Damage". W Encyclopedia of Astrobiology, 1–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2021. http://dx.doi.org/10.1007/978-3-642-27833-4_451-4.

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Streszczenia konferencji na temat "DNA damage"

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Prevenslik, Thomas. "DNA Damage by Nanoparticles". W ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13198.

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Nanoparticles (NPs) have provided significant technological advancements including bactericidal agents in food processing, and treatment of cancer tumors. However, there is a darkside. Over the past decade, experiments [1,2] have shown NPs to be a health risk by inducing DNA damage that can lead to cancer.
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Becher, R., JA Holme, A. Solhaug, KE Rakkestad, VE Ansteinsson, JT Samuelsen, HJ Dahlman, PE Schwarze i I. Skaar. "DNA Damage and DNA Damage Response Induced by Mould Spores and Mycotoxins." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3174.

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Rogers, Kim R., A. Apostol i J. Cembrano. "Optical detection of DNA damage". W Photonics East (ISAM, VVDC, IEMB), redaktorzy Tuan Vo-Dinh i Robert L. Spellicy. SPIE, 1999. http://dx.doi.org/10.1117/12.338987.

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Guo, Changhong, Yuwei Cao, Rui Li, Liang Si, Jun Ma i Zening Yuan. "Nitrobenzene Induces DNA Damage in Tobacco". W 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE 2010). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5516350.

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Dordevic, Milos, Konstantinos Chatzipapas, Ngoc Hoang Tran, Dousatsu Sakata, Ivan Petrovic, Aleksandra Ristic-Fira, Sara Zein i in. "Simulation of DNA damage using the “molecularDNA” example application of Geant4-DNA". W 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.144d.

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The scientific community has a large interest in the studies of DNA damage and response after exposure to ionizing radiation. Several in-silico methods have been proposed so far to model and study the mechanisms of DNA damage using Monte Carlo simulations. The “molecularDNA” example is one of the most recent applications to simulate the irradiation of human cancer cells and bacteria using Geant4-DNA. This example enables the simulation of the physical, physico-chemical and chemical stages of liquid water irradiation, including radiolytic processes following the particle irradiation of the pre-defined human cell geometries and it can be used to calculate the early direct and non-direct DNA damage such as single (SSB) and double strand breaks (DSB) as well as DNA fragment distribution. The application is user friendly and can be used following simple macro commands. The results of the Monte Carlo simulation are compared to experimental data of DSB yields, as well as with previously published simulation data.
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Head, Pamelasara E., Hui Zhang i David S. Yu. "Abstract A114: SIRT2 directs DNA-PKcs in the DNA damage response". W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; October 26-30, 2017; Philadelphia, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1535-7163.targ-17-a114.

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Ueno, Yuya, Shota Yamazaki, Hiromichi Hoshina i Masahiko Harata. "THz irradiation reduces the DNA damage marker γH2AX in human cells: THz wave enhances DNA damage repair?" W 2022 47th International Conference on Infrared, Millimeter and Terahertz Waves (IRMMW-THz). IEEE, 2022. http://dx.doi.org/10.1109/irmmw-thz50927.2022.9895933.

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Asadi, Mahmoud, Tyler Blair, Ben Kuiper, Bruce Cunningham, Tim Shamburger, Brendan Looyenga i Rogelio Morales. "DNA Tracer Technology Applications in Hydraulic Fracturing Flowback Analyses". W SPE International Conference and Exhibition on Formation Damage Control. SPE, 2022. http://dx.doi.org/10.2118/208865-ms.

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Abstract A new and robust tracer technology, based on Nano-sized encapsulated silica DNA sequences is presented. This cutting-edge technology enables a bond of each DNA sequence to a magnetic core particle and encapsulates it with silica. Therefore, one can have infinite sequences of DNA tracers. Each DNA tracer, with its identity signature, can be easily identified and characterized with no interferences. Unique chemistry makes these DNA tracers, either water-wet or oil-wet. The water-wet tracers can be used in hydraulic fracturing to precisely and accurately analyze flowback, both qualitatively and quantitatively. The oil-wet tracers can be used in evaluating the source and quantity of oil production in hydraulic fracturing. In-depth laboratory testing indicates that these tracers, unlike current industry used chemical tracers, are stable at high temperature, do not react with formation mineralogy to form reservoir rock plating, do not partition, and do not disintegrate over time. These tracers are injected in the liquid-laden slurry at very low concentrations and can be detected at parts per trillion.
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Pilzecker, B., OA Buoninfante, JY Song, C. Pritchard, IJ Huijbers, J. Vivié, S. Philipsen, PCM Van den Berk i H. Jacobs. "PO-397 DNA damage tolerance is essential for the DNA damage response network and hematopoietic stem cell maintenance". W Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.423.

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Jarvis, Ian W., Kristian Dreij i Ulla Stenius. "Abstract 5359: TGFβ promotes the DNA damage response and repair of DNA damage induced by benzo[a]pyrene". W Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5359.

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Raporty organizacyjne na temat "DNA damage"

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Kisby, Glen. DNA Damage Induced Neuronal Death. Fort Belvoir, VA: Defense Technical Information Center, październik 1999. http://dx.doi.org/10.21236/ada375640.

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Phoebe L. Stewart. Cryo-EM Imaging of DNA-PK DNA Damage Repair Complexes. Office of Scientific and Technical Information (OSTI), czerwiec 2005. http://dx.doi.org/10.2172/841088.

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Sevilla, M. D. Mechanisms for radiation damage in DNA. Office of Scientific and Technical Information (OSTI), grudzień 1992. http://dx.doi.org/10.2172/7176057.

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Sevilla, M. D. Mechanisms for radiation damage in DNA. Office of Scientific and Technical Information (OSTI), styczeń 1990. http://dx.doi.org/10.2172/5018151.

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Green, Brian M. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-Replication. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2005. http://dx.doi.org/10.21236/ada436928.

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Green, Brian M., i Joachim J. Li. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2007. http://dx.doi.org/10.21236/ada467931.

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Green, Brian. DNA Damage and Genomic Instability Induced by Inappropriate DNA Re-replication. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2006. http://dx.doi.org/10.21236/ada482750.

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Scott, Kenneth L., i Sharon E. Plon. Alternative DNA Damage Checkpoint Pathways in Eukaryotes. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2001. http://dx.doi.org/10.21236/ada396714.

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Wilson, David. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2001. http://dx.doi.org/10.21236/ada396847.

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Thompson, Lawrence H. Repair Machinery for Radiation-Induced DNA Damage. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2002. http://dx.doi.org/10.21236/ada407373.

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