Готові списки джерел за темами / Repair Assisted Damage Detection

Добірка наукової літератури з теми "Repair Assisted Damage Detection"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 29 січня 2023

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Статті в журналах з теми "Repair Assisted Damage Detection"

Holton, Nathaniel W., Yuval Ebenstein, and Natalie R. Gassman. "Broad spectrum detection of DNA damage by Repair Assisted Damage Detection (RADD)." DNA Repair 66-67 (June 2018): 42–49. http://dx.doi.org/10.1016/j.dnarep.2018.04.007.

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Lee, Kevin J., Elise Mann, Luciana Madeira da Silva, Jennifer Scalici, and Natalie R. Gassman. "DNA damage measurements within tissue samples with Repair Assisted Damage Detection (RADD)." Current Research in Biotechnology 1 (November 2019): 78–86. http://dx.doi.org/10.1016/j.crbiot.2019.11.001.

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Gilat, Noa, Dmitry Torchinsky, Sapir Margalit, Yael Michaeli, Sigal Avraham, Hila Sharim, Nadav Elkoshi, Carmit Levy, Shahar Zirkin, and Yuval Ebenstein. "Rapid Quantification of Oxidation and UV Induced DNA Damage by Repair Assisted Damage Detection-(Rapid RADD)." Analytical Chemistry 92, no. 14 (June 24, 2020): 9887–94. http://dx.doi.org/10.1021/acs.analchem.0c01393.

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Krieger, Kimiko L., Jie H. Gohlke, Kevin J. Lee, Danthasinghe Waduge Badrajee Piyarathna, Patricia D. Castro, Jeffrey A. Jones, Michael M. Ittmann, Natalie R. Gassman, and Arun Sreekumar. "Repair-Assisted Damage Detection Reveals Biological Disparities in Prostate Cancer between African Americans and European Americans." Cancers 14, no. 4 (February 17, 2022): 1012. http://dx.doi.org/10.3390/cancers14041012.

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African Americans (AA) are two times more likely to be diagnosed with and succumb to prostate cancer (PCa) compared to European Americans (EA). There is mounting evidence that biological differences in these tumors contribute to disparities in patient outcomes. Our goal was to examine the differences in DNA damage in AA and EA prostate tissues. Tissue microarrays with matched tumor-benign adjacent pairs from 77 AA and EA PCa patients were analyzed for abasic sites, oxidative lesions, crosslinks, and uracil content using the Repair Assisted Damage Detection (RADD) assay. Our analysis revealed that AA PCa, overall, have more DNA damage than EA PCa. Increased uracil and pyrimidine lesions occurred in AA tumors, while EA tumors had more oxidative lesions. AA PCa have higher levels of UMP and folate cycle metabolites than their EA counterparts. AA PCa showed higher levels of UNG, the uracil-specific glycosylase, than EA, despite uracil lesions being retained within the genome. AA patients also had lower levels of the base excision repair protein XRCC1. These results indicate dysfunction in the base excision repair pathway in AA tumors. Further, these findings reveal how metabolic rewiring in AA PCa drives biological disparities and identifies a targetable axis for cancer therapeutics.

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Mann, Elise K., Kevin J. Lee, Dongquan Chen, Luciana Madeira da Silva, Valeria L. Dal Zotto, Jennifer Scalici, and Natalie R. Gassman. "Associations between DNA Damage and PD-L1 Expression in Ovarian Cancer, a Potential Biomarker for Clinical Response." Biology 10, no. 5 (April 29, 2021): 385. http://dx.doi.org/10.3390/biology10050385.

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Programmed death ligand-1 (PD-L1) inhibitors are currently under investigation as a potential treatment option for ovarian cancer. Although this therapy has shown promise, its efficacy is highly variable among patients. Evidence suggests that genomic instability influences the expression of PD-L1, but little is known about this relationship in ovarian cancer. To examine the relationship between PD-L1 expression and genomic instability, we measured DNA damage using Repair Assisted Damage Detection (RADD). We then correlated the presence of persistent DNA damage in the ovarian tumor with protein expression of PD-L1 using immunohistochemistry. Ovarian tumors showed a high prevalence of oxidative DNA damage. As the level of oxidative DNA damage increased, we saw a significant correlation with PD-L1 expression. The highest correlation between DNA damage and PD-L1 expression was observed for mucinous ovarian tumors (r = 0.82), but a strong correlation was also observed for high grade serous and endometrioid tumors (r = 0.67 and 0.69, respectively). These findings link genomic instability to PD-L1 protein expression in ovarian cancer and suggest that persistent DNA damage can be used as a potential biomarker for patient selection for immunotherapy treatment.

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Rashki Ghaleno, Leila, AliReza Alizadeh, Joël R. Drevet, Abdolhossein Shahverdi, and Mojtaba Rezazadeh Valojerdi. "Oxidation of Sperm DNA and Male Infertility." Antioxidants 10, no. 1 (January 12, 2021): 97. http://dx.doi.org/10.3390/antiox10010097.

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One important reason for male infertility is oxidative stress and its destructive effects on sperm structures and functions. The particular composition of the sperm membrane, rich in polyunsaturated fatty acids, and the easy access of sperm DNA to oxidative damage due to sperm cell specific cytologic and metabolic features (no cytoplasm left and cells unable to mount stress responses) make it the cell type in metazoans most susceptible to oxidative damage. In particular, oxidative damage to the spermatozoa genome is an important issue and a cause of male infertility, usually associated with single- or double-strand paternal DNA breaks. Various methods of detecting sperm DNA fragmentation have become important diagnostic tools in the prognosis of male infertility and such assays are available in research laboratories and andrology clinics. However, to date, there is not a clear consensus in the community as to their respective prognostic value. Nevertheless, it is important to understand that the effects of oxidative stress on the sperm genome go well beyond DNA fragmentation alone. Oxidation of paternal DNA bases, particularly guanine and adenosine residues, the most sensitive residues to oxidative alteration, is the starting point for DNA damage in spermatozoa but is also a danger for the integrity of the embryo genetic material independently of sperm DNA fragmentation. Due to the lack of a spermatozoa DNA repair system and, if the egg is unable to correct the sperm oxidized bases, the risk of de novo mutation transmission to the embryo exists. These will be carried on to every cell of the future individual and its progeny. Thus, in addition to affecting the viability of the pregnancy itself, oxidation of the DNA bases in sperm could be associated with the development of conditions in young and future adults. Despite these important issues, sperm DNA base oxidation has not attracted much interest among clinicians due to the lack of simple, reliable, rapid and consensual methods of assessing this type of damage to the paternal genome. In addition to these technical issues, another reason explaining why the measurement of sperm DNA oxidation is not included in male fertility is likely to be due to the lack of strong evidence for its role in pregnancy outcome. It is, however, becoming clear that the assessment of DNA base oxidation could improve the efficiency of assisted reproductive technologies and provide important information on embryonic developmental failures and pathologies encountered in the offspring. The objective of this work is to review relevant research that has been carried out in the field of sperm DNA base oxidation and its associated genetic and epigenetic consequences.

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Huston, Dryver, David Hurley, Kenneth Gollins, Anthony Gervais, and Tim Ziegler. "Damage Detection and Autonomous Repair System Coordination." Advances in Structural Engineering 14, no. 1 (February 2011): 41–45. http://dx.doi.org/10.1260/1369-4332.14.1.41.

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Cooke, Marcus S., Ian D. Podmore, Nalini Mistry, Mark D. Evans, Karl E. Herbert, Helen R. Griffiths, and Joseph Lunec. "Immunochemical detection of UV-induced DNA damage and repair." Journal of Immunological Methods 280, no. 1-2 (September 2003): 125–33. http://dx.doi.org/10.1016/s0022-1759(03)00269-2.

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Helleday, Thomas, Fredrik Johansson, and Dag Jenssen. "The DRAG Test: An Assay for Detection of Genotoxic Damage." Alternatives to Laboratory Animals 29, no. 3 (May 2001): 233–41. http://dx.doi.org/10.1177/026119290102900309.

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A high throughput assay (the DRAG test) is described, which could be a useful tool for the detection of repairable DNA adducts, and which is based on the inhibition of the growth of DNA repair-deficient Chinese hamster ovary (CHO) cells. The cytotoxicity of a test substance towards DNA repair-deficient CHO cell lines is compared with the corresponding cytotoxicity in the parental wild-type CHO cell line (AA8). A more pronounced toxicity toward a DNA repair-deficient cell line is interpreted as being the consequence of its inability to repair the DNA adduct induced by the compound. (+)-7β,8α-Dihydroxy-9α,10α-epoxy-7,8,9,10-tetrahydrobenzo[ a]pyrene, camptothecin, ethyl methanesulphonate and mitomycin C were used as reference substances, and the overall results indicate that the DRAG test could be useful in the screening of compounds for the production of repairable DNA adducts. The main advantages with the DRAG test are that it provides a relevant endpoint, it is rapid, it requires small amounts of the test item, and it permits a large number of compounds to be tested.

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Rouse, J. "Interfaces Between the Detection, Signaling, and Repair of DNA Damage." Science 297, no. 5581 (July 26, 2002): 547–51. http://dx.doi.org/10.1126/science.1074740.

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Більше джерел

Дисертації з теми "Repair Assisted Damage Detection"

Haines, Nia. "Damage detection during transcription coupled DNA repair in Escherichia coli." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.690774.

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Transcription coupled DNA repair (TCR) is a sub-pathway of nucleotide excision repair (NER), which enhances the repair of damage on the template strand of active genes. In E. coli, this is initiated by stalling of the transcribing RNA polymerase (RNAP) at the lesion. This results in recruitment of the Mfd helicase which displaces RNAP, allowing repair to be carried out by Uvr proteins through the NER pathway. In this work, in order to better understand damage recognition in this pathway, single lesion-containing plasmid templates were created and analysed for repair. In these experiments the RNAP stalling step was separated from damage recognition by artificially stalling the RNAP upstream of the lesion. The results demonstrated that RNAP does not need to be stalled directly at a lesion in order to stimulate enhanced repair of a downstream lesion on the transcribed strand. This occurs both for the classical cyclopyrimidine dimer TCR substrate and the non-RNAP-stalling biotin and abasic site lesions. The TCR pathway was also shown to be inherently strand specific, as even lesions far downstream of the stalled RNAP were only repaired by TCR if they were on the transcribed strand. Introduction of a backtracking OpS transcriptional pause instead of a complete RNAP stall was also shown to induce an increase in downstream repair ofnon-RNAPstalling lesions. This downstream repair ability is likely facilitated by the observed translocation ability of the Mfd protein after RNAP displacement, and suggests that Mfd is part of a translocating damage search complex which is able to detect damage away from the initial RNAP stall site. The possible role of UvrD in backtracking RNAP to facilitate an Mfd-independent TCR pathway was investigated, however no evidence for this proposed ability of UvrD was observed. To try and understand the complexity of TCR and the possibly overlapping pathways, the initial steps in developing a high throughput genome wide in vivo assay for TCR were carried out.

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Kannappan, Laxmikant Aerospace Civil &amp Mechanical Engineering Australian Defence Force Academy UNSW. "Damage detection in structures using natural frequency measurements." Awarded by:University of New South Wales - Australian Defence Force Academy. Aerospace, Civil & Mechanical Engineering, 2009. http://handle.unsw.edu.au/1959.4/44852.

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In the last two decades, the emphasis in aircraft maintenance has been on developing online structural health monitoring systems to replace conventional non destructive inspection techniques which require considerable down-time, human effort and cost. Vibration based damage detection is one of the most promising techniques for implementation in Structural Health Monitoring (SHM). In vibration based methods, the presence of damage is detected by monitoring changes in one of the dynamic parameters of the structure, resonant frequencies, modeshapes or damping characteristics. Compared to modeshape based methods, frequency based methods have the advantage that measurements need to be taken only at a single location. Previous developments on frequency based techniques have relied on Finite Element Model updating; analytical techniques have hitherto been restricted to beams due to the complexity in developing equations for cracked two dimensional structures. In this thesis the analytical approach using an energy formulation is extended to plates with through-thickness cracks, where modeshapes from either numerical modelling or experimental measurements can be employed to determine the energy of vibration. It is demonstrated that by using a hybrid approach, incorporating experimentally measured modeshapes along with measured changes in frequencies, the damage parameters can be estimated without resorting to theoretical modelling or numerical analysis. The inverse problem of finding the crack location, size and orientation from measured changes in frequencies is addressed using minimisation techniques. The forward problem and the inverse algorithm is first validated using numerical simulation and experimental testing of beams with edge cracks and centre cracks. The application of the methodology to the two dimensional case is then validated by numerical simulation and experimental modal analysis of plates with through thickness cracks. A statistical procedure is developed for determination of the 90/95 probability of crack detection and the minimum detectable crack size in both cases. It is demonstrated that the measurement of frequency changes can be successfully employed to detect and assess the location and size of cracks in beams and plates, using modeshapes from theory, Finite Element Analysis.

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Jones, Kristi L. "Saccharomyces Cerevisiae as a Model Organism to Delineate Initial Lesion Detection Events in Chromatin Repair: A Focus On Ddb2-Mediated GG-NER." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/584.

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DNA damage repair is an essential and complex cellular process. Although the basic mechanisms of nucleotide excision repair (NER) have been studied for decades, some mechanistic details remain elusive. The lesion detection step remains one of the most elusive in the process of NER in the contest of chromatin. The work described herein addresses the initial events in the lesion detection step of chromatin repair, also referred to as global genome repair (GG-NER). Both the role of post-translational modifications of lesion identification proteins, and the initial sequence of events in recruitment of repair and remodeling factors are investigated. First, the controversial role of ubiquitination of DDB2 (a human lesion detection protein) is investigated. Due to documented DDB2 function in alternative physiological processes, its direct role in GG-NER is hard to study in human cells. To overcome this obstacle, we established the budding yeast, Saccharomyces cerevisiae as an alternative, simplified model organism to study DDB2-mediated GG-NER. Using this system, we show that inconsistent with the widely accepted model, rapid degradation of DDB2 post-UV irradiation is not an absolute requirement for progression of GG-NER. However, interestingly, our data suggest a role for ubiquitination in the release of DDB2 from chromatin. In both UV and mock treated samples, ubiquitin deficient cells had significantly higher amounts of DDB2 remaining bound to the chromatin compared to the isogenic parent cells. The discussion focuses on the possible physiological relevance of these observations. Additionally, the recruitment of the SWI/SNF chromatin remodeling complex to the silent HML (Hidden MAT Left) locus was also investigated. SWI/SNF is known to require recruitment for its role in transcription; therefore we investigate this requirement in GG-NER. Based on previously published data that indicate an UV-stimulated association of SWI/SNF and Rad4 (a lesion detection protein), we hypothesized that Rad4 is involved in recruitment of SWI/SNF to damaged DNA. Interestingly, our data suggest that Rad4 is not an absolute requirement for recruitment of Snf6 to the HML locus following UV irradiation. However, Rad16 appears to be. These data present an interesting insight into the lesion detection step in GG-NER and this will be discussed.

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Rabieifaradonbeh, Mohammad. "Investigation of the molecular pathogenesis of newly emerged Newcastle disease virus in Indonesia." Thesis, 2021. https://hdl.handle.net/2440/133088.

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Newcastle Disease Virus (NDV) has caused significant outbreaks in South-East Asia, particularly in Indonesia. Australia is currently free from virulent strains of NDV. However, the introduction of virulent NDV strains is a severe risk for the Australian poultry industry. Indonesia is the closest country to Australia and spillover might occur through migratory birds. Two viral strains from recent outbreaks have been isolated and analyses by full genome sequencing and phylogenetic assays. This study was conducted to determine the pathogenesis, candidate genes, biological pathways and tissue tropism of recently emerged genotype VII of NDV (NDV-GVII) viral strains. Chickens were experimentally infected with live NDV-GVII virus. Tissue samples were collected after euthanasia of birds. A transcriptomic analysis based on RNA sequencing (RNA-Seq) of spleen was performed in chickens challenged with NDV-GVII and a control group. Repair Assisted Damage Detection (RADD), and immunohistochemistry staining of Viral HN, caspase-3 and MLKL antigens were employed to analyse DNA damage levels, viral load, apoptosis and necroptosis markers, respectively. Phylogenetic study results revealed that these two strains were identical and belong to genotype VII.1, class II cluster of avian paramyxoviruses, and have significant differences in amino acid identities with La Sota strain. In total, 6361 genes were differentially expressed that included 3506 up-regulated genes and 2855 down-regulated genes. Real-time PCR of ten selected differentially expressed genes (DEGs) from the RNA-Seq results showed agreement between the two technologies in detecting DEGs as the correlation between them is 0.98. Functional and network analysis of DEGs showed down regulation of ElF2 signalling, mTOR signalling, the proliferation of lymphatic system cells, signalling by Rho family GTPases and synaptogenesis signalling in spleen. We have also identified increased expression of IFIT5, PI3K, AGT and PLP1 genes in NDV-GVII infected chickens. Bursal atrophy was associated with profound expression of MLKL and only patchy distribution of viral antigen, providing evidence that the mechanism of lymphoid depletion involved a non-apoptotic pathway of programmed cell death termed necroptosis. RADD and oxididative RADD analysis of bursa showed a DNA damage pattern consistent with the programmed cell death rather than necrosis, consistent with MLKL stain results. MLKL expression in the spleen was less pronounced and largely restricted to the central portion of periarteriolar lymphoid sheaths, while other regions of white pulp expressed neither MLKL nor caspase-3. A shift in tissue tropism from neurologic and gastrointestinal to the immune system compared to previously reported NDV-GVII strains was also observed in this strain. Significant differences in amino acid identities of circulation viruses and La Sota strain as the most common vaccine strain used in Indonesia shed more light on the probable reason for vaccine failure against these NDV strains and highlights the urgent need for updated vaccine development strategies in South-East Asia. Our findings in activation of autophagy-mediated cell death, lymphotropic and synaptogenesis signalling pathways provide new insights into the molecular pathogenesis of this newly emerged NDV-GVII. This study is the first report of using RADD assay for DNA damage analysis in NDV infection and revealed the persistence of oxidative lesion in the genome after viral challenge. Together with observations of karyorhexis, fibrinous inflammation, and RADD analyses, we conclude that necrosis was responsible for the majority of lymphoid depletion in the spleen. Therefore, we speculate that the progression of NDV infection may deplete various subsets of lymphocytes by different mechanisms.
Thesis (Ph.D.) -- University of Adelaide, School of Animal and Veterinary Sciences, 2021

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Книги з теми "Repair Assisted Damage Detection"

Chen, Suren. Feasibility study of mobile scanning technology for fast damage detection of rural bridge using wireless sensors. Fargo, N.D.]: Mountain-Plains Consortium, 2010.

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Loh. Monitoring, Identification and Damage Detection of Structures, Ch. Taylor & Francis Group, 2010.

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Morassi, Antonino, and Fabrizio Vestroni. Dynamic Methods for Damage Detection in Structures. Springer London, Limited, 2008.

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Antonino, Morassi, Vestroni F, and International Centre for Mechanical Sciences., eds. Dynamic methods for damage detection in structures. Wien: Springer, 2008.

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Dynamic Methods for Damage Detection in Structures CISM International Centre for Mechanical Sciences. Springer, 2010.

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(US), National Research Council. Detection and Repair of Fatigue Damage in Welded Highway Bridges (Report - National Cooperative Highway Research Program ; 206). Transportation Research Board, 1991.

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Частини книг з теми "Repair Assisted Damage Detection"

den Engelse, L., J. S. Ploem, C. P. Wild, and E. Scherer. "Visualization and Computer-Assisted Quantification of DNA Modifications in Individual Cells." In DNA Damage and Repair, 251–62. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4757-5016-4_26.

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Gallina, Alberto, Paweł Paćko, and Łukasz Ambroziński. "Model Assisted Probability of Detection in Structural Health Monitoring." In Advanced Structural Damage Detection, 57–72. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118536148.ch3.

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Biswas, M., A. K. Pandey, and M. M. Samman. "Modal Technology for Damage Detection of Bridges." In Bridge Evaluation, Repair and Rehabilitation, 161–74. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-2153-5_12.

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Weston, Ainsley, Elise D. Bowman, David K. Manchester, and Curtis C. Harris. "Fluorescence Detection of Lesions in DNA." In DNA Damage and Repair in Human Tissues, 63–81. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0637-5_5.

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Shaposhnikov, Sergey, and Andrew Collins. "Twelve-Gel Comet Assay Format for Quick Examination of DNA Damage and Repair." In Fast Detection of DNA Damage, 181–86. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7187-9_16.

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Lyapin, A. A., and Y. Y. Shatilov. "Vibration-Based Damage Detection of Steel Pipeline Systems." In Non-destructive Testing and Repair of Pipelines, 63–72. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56579-8_5.

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Randerath, Kurt, and Erika Randerath. "Detection of Human DNA Adducts by 32P-Postlabeling." In DNA Damage and Repair in Human Tissues, 13–32. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0637-5_2.

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Bohr, Vilhelm A. "Methods to Measure the Repair of Genes." In Technologies for Detection of DNA Damage and Mutations, 131–38. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-0301-3_10.

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Patenge, Nadja. "Quantification of DNA Damage and Repair in Mitochondrial, Nuclear, and Bacterial Genomes by Real-Time PCR." In Fast Detection of DNA Damage, 159–66. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7187-9_14.

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Santella, Regina M., Xiao Yen Yang, Ling Ling Hsieh, Tie Lan Young, Xiao Qing Lu, Marina Stefanidis, and Frederica P. Perera. "Immunologic Methods for the Detection of Carcinogen Adducts in Humans." In DNA Damage and Repair in Human Tissues, 33–44. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-0637-5_3.

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Тези доповідей конференцій з теми "Repair Assisted Damage Detection"

Richter, G. "Damage detection and repair measures regarding medium-voltage latticed towers." In 14th International Conference and Exhibition on Electricity Distribution (CIRED 1997 - Distributing Power for the Millennium). IEE, 1997. http://dx.doi.org/10.1049/cp:19970531.

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Myers, Oliver J., and Sourav Banerjee. "Coupled Damage Precursor Detection." In ASME 2015 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/smasis2015-8950.

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This conceptual research focuses on identifying damage precursors in carbon fiber reinforced polymer laminates. By coupling integrated in situ sensing elements (magnetostrictive particles) and multi-scale ultrasonic inspection (Quantitative Ultrasonic Imaging) with minimum hardware the authors are able to capture and gain an understanding of damage precursors. Preliminary damage precursors can be identified and quantified and correlated to a particular failure mode(s) and/or fabrication process accelerating the need for a sensing/repair strategy that could be implemented to capture the specific precursor prior to the onset of cracks. Capturing and mitigating damage precursors ahead of micro-crack formulation will slow the evolution of the damage precursors to micro-cracks, mitigate adverse loading environment, and develop techniques to reduce stress and loading below the endurance limit to keep it from being fatigued.

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Mills, Wilbur K., Antonio M. C. Reis, and Lurdes Queimado. "Abstract 2546: A novel DNA damage detection assay reveals a critical role ofXPFin the repair of endogenous damage." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2546.

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Bode, Michel D., Justin Newcomer, and Stephanie Fitchett. "Transfer function model-assisted probability of detection for lap joint multi site damage detection." In REVIEW OF PROGRESS IN QUANTITATIVE NONDESTRUCTIVE EVALUATION: Volume 31. AIP, 2012. http://dx.doi.org/10.1063/1.4716423.

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Synaszko, Piotr, Michal Salacinski, and Patryk Ciezak. "The An Approach to Damage Detection in Metal Sandwich Structures with Composite-Metal Patch Bonded Repair." In AeroTech Congress & Exhibition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2017. http://dx.doi.org/10.4271/2017-01-2050.

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MORIOT, JÉRÉMY, NICOLAS QUAEGEBEUR, ALAIN LE DUFF, and PATRICE MASSON. "Model-assisted Assessment of Damage Detection and Localization using Guided Wave-based Imaging Techniques." In Structural Health Monitoring 2017. Lancaster, PA: DEStech Publications, Inc., 2017. http://dx.doi.org/10.12783/shm2017/13892.

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"An Artificial Intelligence Approach to Objective Health Monitoring and Damage Detection in Concrete Bridge Girders." In "SP-298: Advanced Materials and Sensors Towards Smart Concrete Bridges: Concept, Performance, Evaluation, and Repair". American Concrete Institute, 2014. http://dx.doi.org/10.14359/51687081.

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"Performance of Bridge Decks in a Cold Region and a High-fidelity Sensing System for Damage Detection." In "SP-298: Advanced Materials and Sensors Towards Smart Concrete Bridges: Concept, Performance, Evaluation, and Repair". American Concrete Institute, 2014. http://dx.doi.org/10.14359/51687087.

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KOO, BONSUNG, RYAN GUNCKEL, ADITI CHATTOPADHYAY, and LENORE DAI. "Molecular Dynamics Study for Self-Sensing/Self-Healing Materials to Simulate Damage Detection and Repair in Thermoset Polymer Matrix." In American Society for Composites 2018. Lancaster, PA: DEStech Publications, Inc., 2018. http://dx.doi.org/10.12783/asc33/25941.

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Takagi, Kiyoshi, Hiroshi Sato, and Muneharu Saigo. "Damage detection and gain-scheduled control of CFRP smart board mounting the metal core assisted piezoelectric fiber." In Smart Structures and Materials, edited by Ralph C. Smith. SPIE, 2005. http://dx.doi.org/10.1117/12.598419.

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