Dissertations / Theses on the topic 'Damage type'
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Suwake, Natsuko. "D-type cyclins and DNA damage response." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506678.
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Lu, Kan. "Dynamics Based Damage Detection of Plate-Type Structures." University of Akron / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=akron1133818717.
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Suwaki, Natsuko. "D-type cyclins and the DNA damage response." Thesis, Imperial College London, 2008. http://hdl.handle.net/10044/1/5718.
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The cell cycle is strictly regulated to ensure the precise transmission of genetic information from one cell to its daughter cells. The DNA damage response is one of these regulatory pathways and is activated in response to both intrinsic and extrinsic genotoxic stress. Once activated, downstream signalling disrupts normal cell cycle progression, causing arrest or alternatively, cell death. One of the cell cycle proteins, cyclin D1, has been suggested to play a crucial role in integrating the cell cycle machinery and the DNA damage response. This investigation demonstrates that cyclin D1 expression responds in a dose-dependent manner to the UV-mimetic DNA damaging agent, 4-nitroquinolin 1-oxide (4NQO). Immunoblotting experiments revealed a biphasic response of cyclin D1 expression to 4NQO: cyclin D1 levels were largely unchanged following exposure of cells to low and high doses of 4NQO, whilst it was dramatically reduced after treatment with intermediate doses of 4NQO. The CDK inhibitor protein, p21, also responded in a dose-dependent manner, exhibiting elevated expression at low doses of 4NQO but was reduced or unchanged at intermediate and high doses, respectively. Exposure to IR or H2O2 triggered distinct responses by cyclin D1 and p21, indicating the likelihood that these DNA damaging agents activate distinct signalling pathways. Analyses of cellular responses by flow cytometry demonstrated that p21 expression primarily conferred resistance to damage-induced cell death whereas the level of cyclin D1 expression correlated with the mode of cell death. 4NQO-induced cyclin D1 downregulation was proteasome-dependent but was resistant to deregulation of the majority of the key damage-regulating proteins. This investigation also revealed that other members of D-type cyclin family, cyclins D2 and D3, also exhibit distinct responses to various DNA damaging agents. Preliminary observations indicated that responses of the three D-cyclins were not interdependent and they may play distinct roles in the DNA damage response.
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Bodin, Jean-Matthieu Marie Jacques Sebastien. "Buried Pipe Life Prediction in Sewage Type Environments." Thesis, Virginia Tech, 1998. http://hdl.handle.net/10919/9738.
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In this study, we develop a method of life prediction of buried pipe using the concepts of a characteristic damage state and damage accumulation. A stress analysis corresponding to the different types of load during service with environmental effects, a moisture diffusion model, and a lifetime prediction analysis combining the above models has been constructed. The model uses an elasticity solution for axial-symmetric loading in the case of pressurized pipe, and an approximate non-linear solution for transverse loading due to soil pressure in the case of buried pipe. The axial-symmetric stress analysis has been constructed taking into account the moisture content and the temperature of each ply of the laminate. The moisture diffusion model takes into account the geometry of the laminate, the different diffusivity coefficients in each ply, and also the geometric changes due to ply failure. The failure mode and material behavior of the pipe has been investigated and identified according to Owens Corning data. Thus, the code that has been developed allows one to predict the time to failure of Owens Corning industrial pipes under any time-dependent profile of environmental and loading conditions.Master of Science
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Moy, Inge. "Parameter Sensitivity of Short-term Fatigue Damage of Spar-type Wind Turbine Tower." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for marin teknikk, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-18511.
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The World’s energy demand is rapidly increasing and a good viable renewable energy source is wind power. The land-based knowledge and experience the onshore wind turbine industry possess is used to develop offshore wind turbines. With this knowledge together with the experience and knowledge of the marine industry we can design and produce a floating wind turbine. The main advantages of an offshore wind turbine are that the wind is stronger and less turbulent at sea, visual and noise annoyances can be avoided and there are large available areas at sea. In this thesis coupled time domain analyses of a floating spar-type wind turbine are performed with the intension to study parameters affecting fatigue damage at base of the tower. The software applied is SIMO/Riflex with the extension TDHmill, which gives the wind thrust force and gyro moment on the wind turbine as point loads in the tower top. Short term environment conditions are chosen from a joint distribution of simultaneous wind and waves which is based on measurements from a site in the North Sea in the period 1973 – 1999. In total 141 different environmental conditions are chosen for the sensitivity study. Mean value, standard deviation, skewness and kurtosis are calculated for axial stresses at the base of the tower. Fatigue damage is calculated from the Palmgren-Miner sum with a nominal stress SN-curve from the DNV fatigue standard. The axial stress-cycle distribution used in the Palmgren-Miner sum is found by rainflow counting. Time domain simulations are carried out for the different sea states and fatigue damage is calculated for each case. The statistical properties and fatigue damage are averaged over seven samples with different random seed number to ensure acceptable statistical uncertainty. Accumulated standard deviation shows that 5 samples of each load case are sufficient to ensure acceptable statistical uncertainty. Sensitivity study of different simulation length shows that 30 minute simulations give close to equal fatigue damage and standard deviation as 2.5 hour simulations. Sensitivity of fatigue to wave height and peak period is carried out to study the effect of varying parameters. This study suggests that the highest waves dominate the fatigue damage for the smallest peak periods. For some small wave heights the damage will be constant for a given peak period range. From this sensitivity study it is shown that if the deviation of fatigue damage between the different load cases is small, then the dominating load case of the accumulated long term fatigue damage will be dominated by the marginal probability of each load case.
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Rosales, HernaÌndez Alma L. "Mechanisms of β cell DNA damage and repair in type 1 diabetes mellitus." Thesis, University of Brighton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247817.
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Connaughton, M. D. "A study of cumulative fatigue and creep-fatigue damage in Type 316 steel." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234153.
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Peat, D. S. "The effect of herpes simplex virus type 1 on chromosomes of human cells." Thesis, University of Cambridge, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383841.
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Reiner, Joachim Christian. "Latent gate oxide damage induced by ultra-fast electrostatic discharge /." [S.l.] : [s.n.], 1995. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=11212.
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Lyraki, Rodanthi. "Molecular mechanisms underlying Retinitis pigmentosa type 2." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31254.
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The term 'Retinitis pigmentosa' (RP) represents a group of inherited, late-onset diseases characterised by progressive retinal degeneration due to photoreceptor death. Mutations in the RP2 gene are found in 7-18% of patients with X-linked RP, one of the most severe forms. The RP2 gene product is a membrane-associated protein which encompasses two distinct domains. The N-terminal domain is well characterised as possessing GTPase-activating protein (GAP) activity towards the small GTPase ARL3 and thus regulate the transport of lipid-modified proteins within the photoreceptor cell. However, it is not known if the loss of this particular function of RP2 is the sole reason that causes the disease, while the role of the protein's C-terminus remains unknown. This thesis focuses on the characterisation of two novel protein-protein interactions of RP2 with the aim to investigate novel roles of the protein. Firstly, evidence is provided that a highly-conserved cluster of RP2 residues that span both the N- and C-terminus participate in direct interaction with Osteoclast-stimulating factor 1 (OSTF1). Two hypotheses are explored about the potential role of the complex in SRC-mediated RP2 phosphorylation and the regulation of cell motility. Secondly, the catalytic subunit of DNA-dependent protein kinase (DNA PK) is identified as a novel interaction partner of RP2 in cultured cells. The two proteins are shown to co-localise in the nuclear and membrane compartments of a retinal-derived cell line and might engage in a kinase-substrate relationship. So far, no evidence was found that RP2 participates in the canonical function of DNA PK which is the regulation of DNA double-stranded breaks. Finally, the CRISPR/Cas9 genome editing method was applied on zebrafish embryos to generate a novel vertebrate animal model for the loss of RP2 function. One out of three different zebrafish lines with rp2 mutations was shown by histology to have mild late-onset thinning of the photoreceptor outer segments. The present thesis reports previously unexplored aspects of RP2's function and will, therefore, contribute to understanding the molecular mechanisms that underlie RP. Moreover, this thesis will contribute to the discussion about the usefulness of zebrafish as an RP model.
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Emam, Aly A. "Frequency response of laminated composite plates and shells with matrix cracks type of damage mode /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu148794915006947.
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Lee, Matthew L., and Jonathan M. Peterson. "CTRP3 Protects Liver Cells From Alcohol-Induced Damage, But Not Through Enhanced Akt Signaling Type." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/70.
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Alcoholic fatty liver disease (AFLD) is a significant public health concern. Excessive alcohol (ethanol) consumption causes liver cell damage and death, which results in eventual failure of the liver and death. AFLD is the number one cause of liver-related mortality in the United States. Our lab works with the novel protein C1q TNF Related Protein 3 (CTRP3), which inhibits non-alcoholic fatty liver disease, however the effects on AFLD are unknown. Therefore, the purpose of this experiment is to determine if CTRP3 prevents ethanol-induced liver cell death. The H4IIE rat hepatoma cell line was chosen for experimentation as a cell culture model of liver tissue. To determine a suitable alcohol level H4IIE cells were treated with 50, 100, and 200 mmol of ethanol for 18-24 hours. Trypan Blue was used to identify the dead/damaged cells, as only dead/damaged cells will be stained blue with this protocol. We observed that 100 mmol of ethanol consistently induced ~10% mortality rate in these cells. Next, we tested the ability of CTRP3 to reduce ethanol-induced mortality. We added purified CTRP3 protein to the cell media along with the 100 mmol ethanol treatment. The addition of CTRP3 reduced the amount of alcohol-induced cell death/damage in the H4IIE cell line by approximately 60%. Our next goal was to determine how CTRP3 reduces ethanol-induced death. The Akt signaling pathway is a well-known inhibitor of cell death. Therefore, to determine if CTRP3 attenuated ethanol-induced cell damage/death through activation of the Akt signaling pathway, another set of cells was treated with 100 mmol of ethanol and CTRP3 (with or without insulin). Western blots were used to compare the amount of active Akt (phosphorylated) in the CTRP3-treated and non-treated cells. A Western blot utilizes an electric current to separate denatured protein samples on a SDS-page gel, separating the proteins based on size. The smaller the protein the faster it migrates across the gel. The proteins are then transferred to a membrane for analysis, through exposure to commercial antigens and chemiluminescence imaging. There was no change in the amount of total or active Akt between the samples treated with or without CTRP3. We conclude that CTRP3 protects liver cells from ethanol-induced damage/death, but not through activation of the Akt pathway.
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Jones, Danielle Alice. "Adipose tissue as a mediator of inflammation and oxidative cellular damage in obesity and type 2 diabetes." Thesis, Swansea University, 2013. https://cronfa.swan.ac.uk/Record/cronfa42244.
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In the past 30 years the prevalence of obesity has almost trebled resulting in an increased incidence of type 2 diabetes mellitus (T2DM) and other co-morbidities. Visceral adipose tissue is believed to play a vital role in these conditions, but underlying mechanisms remain unclear. A close association exists between obesity, diabetes and oxidative stress, resulting in increased reactive oxygen species formation. The experiments in this thesis address this by searching for possible biochemical changes which may be specific for the onset of obesity related T2DM, as well as looking for genetic alterations at molecular and gene expression levels. This thesis also explored various techniques such as polymerase chain reaction (PCR), colorimetric assays and real-time RT-PCR. The aim was to investigate the role of adipose tissue in obesity and T2DM, focusing on markers of oxidative stress and gene expression in human visceral adipose tissue from subjects categorised as lean, obese and obese with T2DM. This cross-sectional study measured two markers of oxidative stress, two markers of DNA damage, gene expression analysis and identification of genes associated with T2DM and obesity. Specific gene sequencing was carried out on the glutathione reductase gene to determine possible gene variants. Results showed a paradoxical decrease in adipose markers of oxidative stress in subjects with obesity and T2DM. There appeared to be a protective mechanism in these subjects, displaying reduced levels of oxidative stress compared to other groups. This could be due to a significant proportion of these subjects being on ACE inhibitor and statin therapy, which may be confounding results and minimising the effects of the oxidative burden. Additionally, the same subjects showed an increased expression of the glutathione reductase gene. It is difficult to conclude if the decreased levels of oxidative stress in these subjects were a result of the increased glutathione reductase expression in the visceral adipose tissue or if there remains an unseen factor influencing the dramatic expression change seen in this group of subjects. No glutathione reductase gene variants were identified in these samples. This analysis highlighted that within this sample set, the impact of oxidative stress is in fact reversible as the antioxidant capacity in these subjects is evident, and in combination with correct drug therapy it may be possible to combat oxidative burden and reduce the subsequent damage inflicted upon the cells.
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Veinhard, Matthieu. "Endommagement surfacique de la silice avec des faisceaux laser de type LMJ." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0029.
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Chacun des 176 faisceaux du Laser MégaJoule (LMJ) délivrera une énergie de 8 kJ à 351 nm, dans le régime nanoseconde, sur une cible millimétrique. Ce flux laser est susceptible d’être absorbé par des défauts présents sous la surface des optiques et d’endommager le composant. L’optique étant affaiblie dans les zones endommagées, tir après tir, les dommages absorbent le flux laser, et leurs surfaces augmentent. Le composant optique le plus sensible de l’installation est le hublot de chambre, composant épais (34mm) exposé à de fortes valeurs de flux laser à 351 nm. Le but de cette thèse est d’étudier l’initiation et la croissance des dommages sur ce composant avec un faisceau laser dont les propriétés sont proches de celles du LMJ. Un tel faisceau est délivré par le banc d’endommagement laser MELBA, permettant d’atteindre des valeurs de flux similaires à celles du LMJ sur un profil spatial homogène circulaire dont le diamètre est de l’ordre du centimètre et avec un profil temporel accordable. Cette étude est organisée en trois axes. Premièrement, la mesure de l’amorçage des dommages sur des composants épais, en tenant compte de l’impact de l’effet Kerr. Deuxièmement, l’étude de la croissance d’une population de dommages en fonction de la fluence et de la durée d’impulsion. Troisièmement, l’étude de la croissance de très gros dommages, de tailles millimétriquesEach of the 176 beams of the Laser MégaJoule (LMJ) facility will deliver an energy of 8 kJ at 351 nm, in the nanosecond regime, on a millimeter scale target. This energy density is likely to be absorbed by sub-surface defects induced by the polishing processes. This absorption eventually leads to laser-induced damage sites. These initiated damage sites absorb the laser energy during the subsequent shots and are likely to grow in size. The thick (34mm) optical windows situated after the frequency conversion module are exposed to the highest laser energies at 351nm and are the most sensitive to these phenomena. The goal of this thesis is to study the initiation and growth of damage sites on thick optical components with a laser beam that have similar properties to those of a LMJ beam. Such a beam can be delivered by the MELBA facility which can reach similar energy densities to those that can be found on the LMJ. The beam energy is evenly distributed on a centimeter scale circular aperture and the pulse shape and duration can be defined by the user. Three main axes have been explored in this work. The measurement of damage initiation on thick fused silica optical components have firstly been studied with an accurate metrology of the energy density after the propagation through the optical component, thus taking Kerr small scale self focusing into account. The growth of a population of damage sites have secondly been studied as a function of the laser fluence and pulse duration. Finally, the growth of damage sites up to millimeter scales have been studied
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Fritsche, Stefan. "Large historical earthquakes in Switzerland : multidisciplinary studies on damage fields and site-effects /." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17710.
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Penchikala, Madhuri. "ANGIOTENSIN AT1 RECEPTOR BLOCKADE PROTECTS THE BRAIN FROM ISCHEMIC DAMAGE." Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1187382272.
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Morency, Eric. "The protein of herpes simplex virus Type 1 : from centromeres to the interphase centromere damage response." Lyon 1, 2007. http://www.theses.fr/2007LYO10317.
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Cette étude se focalise sur l'activité de la protéine ICP0 du virus Herpès Simplex de type 1. Dans le contexte de ses activités nucléaires, nous avons découvert une nouvelle réponse cellulaire suite à des dommages centromériques induits par ICP0. [. . . ]
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Soares, Bruno Marques. "Hellebrigenina, um BufodienolÃdeo com Potencial AÃÃo CompatÃvel de Inibidor CatalÃtico da Topoisomerase II." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=10367.
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CoordenaÃÃo de AperfeiÃoamento de NÃvel SuperiorOs bufodienolÃdeos sÃo esterÃides cardioativos de 24 carbonos, isolados originalmente de um extrato de pele de sapos da famÃlia Bufonidae utilizado na medicina chinesa. Os bufodienolÃdeos possuem grande variedade de atividades biolÃgicas, incluindo atividades antineoplÃsicas. Em relaÃÃo à atividade antitumoral, os bufodienolÃdeos tem demonstrado inibir o crescimento de vÃrias linhagens de cÃlulas cancerÃgenas humanas por induzir apoptose e parada do ciclo celular. O presente estudo avaliou o potencial citotÃxico e genetÃxico de seis bufodienolÃdeos em seis linhagens tumorais humanos, trÃs linhagens murinas normais e cÃlulas mononucleadas do sangue perifÃrico (CMSP) humano. Todos os seis bufodienolÃdeos foram citotÃxicos para todas as linhagens tumorais e CMSP com valores de IC50 variando entre 0,002 e 3,17 ÂM. Os bufodienolÃdeos testados nÃo apresentaram citotoxicidade para linhagens murinas normais. Desta forma, o composto hellebrigenina foi escolhido para se determinar o mecanismo de aÃÃo envolvido. Uma sequÃncia de experimentos in vitro foram realizados utilizando-se a linhagem leucÃmica HL-60. As cÃlulas foram tratadas em diferentes concentraÃÃes da amostra hellebrigenina (0,03, 0,06 e 0,12 ÂM) por 24 horas. A viabilidade das cÃlulas (nÃmero de cÃlulas viÃveis e integridade de membrana) HL-60 avaliada por citometria de fluxo, mostrou que o nÃmero de cÃlulas reduziu a partir da menor concentraÃÃo (0,03 ÂM) testada e a porcentagem de cÃlulas com membrana integra reduziu a partir da concentraÃÃo 0,06 ÂM. A anÃlise morfolÃgica por citometria de fluxo revelou aumento de cÃlulas com padrÃo apoptÃtico a partir da concentraÃÃo de 0,06 ÂM. Jà a anÃlise do conteÃdo nuclear, nos mostrou aumento de fragmentaÃÃo de DNA sub-G1 indicativo de apoptose e acÃmulo de cÃlulas na fase G2/M a partir das concentraÃÃes de 0,03 e 0,06 ÂM, respectivamente. Outros testes por citometria de fluxo revelaram que houve externalizaÃÃo da fosfatidilserina, despolarizaÃÃo mitocondrial, ativaÃÃo da caspase iniciadora 8 e consequente ativaÃÃo das caspases efetoras 3 e 7. Estes dados indicam um mecanismo citotÃxico por induÃÃo de mais de uma via apoptÃtica. Hellebrigenina nÃo foi capaz de causar danos ao DNA de HL-60 e de CMSP e nem o surgimento de aberraÃÃes cromossÃmicas em CMSP. Por meio dos estudos de docking molecular foi possÃvel predizer a ligaÃÃo entre hellebrigenina e topoisomeraseIIα humana, resultado compatÃvel com a possÃvel inibiÃÃo dessa enzima. De forma geral, os resultados apontam o potencial citotÃxico do bufodienolÃdeo hellebrigenina
Bufodienolides are cardioactive steroids of 24 carbons, originally isolated from a frogâs skin extract of the family Bufonidae used in Chinese medicine. Bufodienolides shows many biological activities, including anticancer activities. Related to antitumor activity, the bufodienolÃdeos has been shown to inhibit the growth of several human cancer cell lines by inducing apoptosis and cell cycle arrest. This study evaluated the potential cytotoxicity and genotoxicity of six bufodienolides, in six human tumor cell lines, three normal murine lineages and PBMC (peripheral blood mononuclear cells). All six bufodienolides were cytotoxic to all cell lines and tumor PBMC with IC50 values ranging from 0.002 to 3.17 ÂM. Bufodienolides showed no cytotoxicity for normal murine strains. Thus, the compound hellebrigenin was chosen to determine the action mechanism involved, a sequence of in vitro experiments were performed using HL-60 leukemia cell line. Cells were treated at different concentrations of hellebrigenin (0.03, 0.06 and 0.12 ÂM) for 24 hours. Cell viability (viable cell number and membrane integrity) HL-60 assessed by flow cytometry showed that the number of cells decreased from the lower concentration (0.03 ÂM) tested and the percentage of cells with reduced membrane integrity from 0.06 ÂM concentration. Morphological analysis by flow cytometry revealed increased apoptotic cells starting at concentrations of 0.06 ÂM. The analysis of nuclear content, showed an increase in DNA fragmentation indicative of sub-G1 apoptosis and accumulation of cells in G2 / M phase from the concentrations of 0.03 and 0.06 ÂM, respectively. Other tests by flow cytometry revealed that there was an externalization of phosphatidylserine, mitochondrial depolarization, activation of caspase 8 and initiating subsequent activation of effector caspases 3 and 7. These data indicate a cytotoxic mechanism induced by over an apoptotic pathway. Hellebrigenin was not able to cause DNA damage in HL-60 and PBMC nor the emergence of chromosomal aberrations in PBMC. Through the studies of molecular docking was possible to predict the connection between hellebrigenina and human topoisomeraseIIα, showing a result that is compatible with a possible inhibition of this enzyme. Overall, the results indicate the potential cytotoxicity of hellebrigenin
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Windt, Leon Johannes de. "Ischemia and reperfusion-induced damage of the isolated mouse heart involvement of type IIA secretory phospholipase A2 /." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=6892.
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Hu, Shuting, and 胡舒婷. "Resorcinol-type phenolic compounds from natural sources inhibut α-MSH induced melanogenesis and UVA-induced DNA damage." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/207207.
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Sunlight exposure is inevitable to all humans and UV radiation in the sunlight usually causes damages to the skin. Tanning, first appearing when UV injures occur, is a pigmentation process which can be considered as a natural defense mechanism of the organism. Melanin plays an important role in the prevention of the skin from harmful environmental factors such as UV radiation. However, the excess accumulation of melanin causes hyperpigmentation, which is associated with a number of unhealthy conditions including solar lentigines, melasma, freckles and post-inflammatory hyperpigmentation. Therefore, the development of safe and effective hypopigmenting agents is of great importance.
The depigmenting effects of oxyresveratrol and trans-dihydromorin, as well as moracenin D, sanggenon T, mulberrofuran G and kuwanon O, were investigated in murine b16f10 melanoma cell line and its synergetic non-tumor melanocyte melan-a cells. All these six resorcinol type phenolic compounds (RTPs) were found to reveal significant hypopigmenting effects in murine b16f10 melanoma cell line. Oxyresveratrol and Kuwanon O presented the greatest inhibition on melanin synthesis at low concentration with the suppression on tyrosinase activity. However, in melan-a cells, only oxyresveratrol, trans-dihydromorin, kuwanon O and sanggenon T decreased melanin content significantly. The subsequent mechanisms studies explained the difference. In b16 cells, all of these RTPs induced post-transcriptional degradations of MITF without suppressing its mRNA expression, leading to significant decreases of TRP-1 and TRP-2 production, while in melan-a cells, the levels of tyrosinase, as well as TRP-1and TRP-2 were suppressed by MITF downregulation at both transcription and translation level. Among these RTPs, kuwanon O induced the greatest suppression on the tyrosinase families via MITF down-regulation. Sanggenon T, trans-dihydromorin and oxyresveratrol also exhibited same action of mechanism with weaker activities than kuwanon O. Further evaluations in artificial skin model demonstrated the outstanding depigmenting effects of kuwanon O, sanggenon T and trans-dihydromorin. The inhibitory effect by oxyresveratrol is negligible. It can be therefore inferred that a non-tumor melanocytes system might be more suitable for screening depigmenting agents applied to normal skin cells. Hypopigmenting agents effective in b16 melanoma system may not be so effective on normal melanocytes. Meanwhile, according to the structure-activity relationships studies of theses RTPs, to screen or synthesize resorcinol flavonone derivatives with an isoprenyl group in the Diels-Alder substituent might be a novel approach for the search of potent hypopigmenting agents.
The photoprotective effects of these RTPs were also investigated, as UV radiation not only dominants the skin tanning level, but also induces genetic damage and mutations in the epidermal basal layer of human skin. Oxyresveratrol and kuwanon O were found to reveal photoprotective effects on human primary epidermal keratinocytes by enhancement of DNA repair after 4.32 J/cm2 UVA radiation. They exhibited suppressions on cellular ROS induced by UVA and H2O2. Nitrotyrosine levels enhanced by UVA irradiation were also suppressed by them. Moreover, oxyresveratrol even increased cell viability after 4.32 J/cm2 UVA radiation. The possibility of oxyresveratrol and kuwanon O for prevention of photocarcinogenesis in humans is a potential avenue for investigation.
In summary, the research contributed to the knowledge of depigmenting and photoprotective effects of resorcinol type phenolic compounds from natural sources. The findings support natural polyphenols as cosmetic ingredients or pharmaceutical composition in purpose of skin lightening or clinic therapy.published_or_final_version
Biological Sciences
Doctoral
Doctor of Philosophy
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Holtzapple, Emilee R. "RelA as a Potential Regulator of Inflammation and Tissue Damage in Streptozotocin-Induced Diabetic STAT5 Knockout Mice." Ohio University Honors Tutorial College / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1461342848.
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Martinez-Flores, Rene. "DAMAGE ASSESSMENT POTENTIAL OF A NOVEL SYSTEM IDENTIFICATION TECHNIQUE - EXPERIMENTAL VERIFICATION." Diss., Tucson, Arizona : University of Arizona, 2005. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1028%5F1%5Fm.pdf&type=application/pdf.
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BOTTRELL, John Robert, and John Bottrell@dsl-riotinto com au. "ACCIDENT DENOMINATORS RELATIVE TO AGE GROUPS IN HEAVY INDUSTRIES OF THE PORT HEDLAND REGION OF WESTERN AUSTRALIA." Edith Cowan University. Computing, Health And Science: School Of Exercise, Biomedical & Health Science, 2007. http://adt.ecu.edu.au/adt-public/adt-ECU2007.0045.html.
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The aim of this research is to investigate characteristics of accident denominators across age groups in mining and associated process industries in the Port Hedland region of Western Australia. Emphasis has been focussed on comparing young, inexperienced groups with older, more experienced groups. A literature review revealed some key contributors to accidents among younger workers, in particular, those who had only recently entered the workforce. The review also revealed contributors impacting accidents regarding other age groups over a wide range of industry types. From these findings an accident construct model and questionnaire were designed to identify contributing and mitigating denominators which input to accidents occurring across the defined age groups.
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Gibbs-Seymour, Ian David. "The multiple roles of A-type lamins in cellular aging, cell cycle progression and the DNA damage response." Thesis, Durham University, 2011. http://etheses.dur.ac.uk/3491/.
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A-type lamins are a group of type V intermediate filaments whose main members are lamin A and C. Lamins A/C are components of the nuclear lamina and are encoded by the LMNA gene. Lamins A/C have a variety of cellular functions, including maintaining the structural integrity of the nucleus and the regulation of signal transduction pathways, transcription factors and DNA replication. Mutations in LMNA give rise to a diverse spectrum of diseases, termed laminopathies, which include premature aging syndromes. In Chapter 3, I sought to understand the role of wild type lamin A in normal cellular aging. Lamin A C-terminal cysteine residues were irreversibly oxidized during the in vitro aging of human dermal fibroblasts (HDFs), which impaired the ability of lamin A to form disulfide bonds, causing loss of function. Furthermore, loss of these cysteine residues induced premature senescence, suggesting that these cysteine residues are important for lamin A function during cellular aging. In Chapter 4, I extended previous findings implicating A-type lamins in the control of cell cycle progression. Loss of A-type lamins or its nucleoplasmic binding partner, LAP2α, caused delayed G1/S-phase progression, reduced cellular proliferation and cell cycle exit. Proliferative defects could not be rescued via treatment with anti-oxidants. In Chapters 5 and 6, I addressed the role of wild type mature lamin A/C in the DNA damage response (DDR). A-type lamins interact with the DDR mediator protein 53BP1 via its Tudor domain. Loss of LMNA caused endogenous DNA damage and loss of 53BP1 protein levels. Furthermore, loss of LMNA resulted in defective DNA repair that ultimately led to increased sensitivity to DNA damage. Together, the data presented here extends previous findings implicating A-type lamins in cell cycle progression and provides novel insights into the cellular roles of A-type lamins in cellular aging and the DNA damage response.
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Віхрова, Ірина Олександрівна, Ирина Александровна Вихрова, Iryna Oleksandrivna Vikhrova, Андрій Миколайович Лобода, Андрей Николаевич Лобода, and Andrii Mykolaiovych Loboda. "Significance of urinary Aminopeptidase N in early diagnosis of kidney damage in children with type 1 diabetes mellitus." Thesis, Lithuanian University of Health Sciences, 2021. https://essuir.sumdu.edu.ua/handle/123456789/83663.
Full textAbstract:
Мета. Метою цього дослідження було вивчити особливості рівнів амінопептидази N (ANPEP) в сечі у дітей залежно від тривалості діабету.
Методи. Ми проаналізували 3 групи дітей з цукровим діабетом 1 типу та групу порівняння дітей без діабету з Обласної дитячої клінічної лікарні м Суми. ANPEP вимірювали за допомогою імуноферментного аналізу з використанням набору антитіл до біомаркерів нирок людини (R&D Systems, Міннеаполіс, Міннесота, США). Результати були отримані за допомогою BioRad ChemiDoc Touch. Масиви аналізували напівкількісно з використанням програмного забезпечення BioRad Image Lab.
Результати. У дослідження були включені 47 дітей з діабетом і 8 дітей без діабету. Рівень ANPEP в сечі збільшився в 2,6 рази у дітей з тривалістю діабету менше одного року порівняно з контрольною групою. Рівні ANPEP були підвищені в 3,2 рази у дітей з тривалістю діабету від одного до п'яти років. У дітей з тривалістю діабету понад 5 років маркер збільшився в 2,7 рази.
Висновок. Підвищення рівня ANPEP в сечі спостерігалося в перший рік діабету у дітей. Вимірювання рівня ANPEP в сечі може бути корисним для діагностики діабетичної нефропатії.Цель. Целью настоящего исследования было изучить особенности уровней Аминопептидазы N (ANPEP) в моче у детей в зависимости от продолжительности диабета. Методы. Мы проанализировали 3 группы детей с сахарным диабетом 1 типа и группу сравнения детей без диабета из Областной детской клинической больницы г. Сумы. ANPEP измеряли с помощью иммуноферментного анализа с использованием набора антител к биомаркерам почек человека (R&D Systems, Миннеаполис, Миннесота, США). Результаты были получены с помощью BioRad ChemiDoc Touch. Массивы анализировали полуколичественно с использованием программного обеспечения BioRad Image Lab. Результаты. В исследование были включены 47 детей с диабетом и 8 детей без диабета. Уровень ANPEP в моче увеличился в 2,6 раза у детей с длительностью диабета менее одного года по сравнению с контрольной группой. Уровни ANPEP были повышены в 3,2 раза у детей с длительностью диабета от одного до пяти лет. У детей с длительностью диабета более 5 лет маркер увеличился в 2,7 раза. Заключение. Повышение уровня ANPEP в моче наблюдалось в первый год диабета у детей. Измерение уровня ANPEP в моче может быть полезно для диагностики диабетической нефропатии.
Aim. The aim of the current study was to investigate the features ANPEP levels in urine of children depending on the duration of diabetes. Methods. We analysed 3 groups of children with type 1 diabetes mellitus and comparison group of children without diabetes from Regional Children’s Clinical Hospital in Sumy. ANPEP was measured by ELISA using a Proteome Profiler Human Kidney Biomarker Antibody Array (R&D Systems, Minneapolis, MN, USA). Results were detected with BioRad ChemiDoc Touch. The arrays were analysed semiquantitatively, using BioRad Image Lab Software. Results. The study included 47 children with diabetes and 8 children without diabetes. The level of ANPEP in urine increased 2.6-fold in children with the duration of diabetes below one year compared to the control group. ANPEP levels were elevated 3.2-fold in children with duration of diabetes from one to five years. In children with duration of diabetes duration, the marker increased 2.7 times. Conclusion. Increase urinary ANPEP was observed in the first year of diabetes in children. Measuring the level of ANPEP in urine may be useful for the diagnosis of diabetic nephropathy.
26
Datta, Antara. "Human T Lymphotropic Virus Type 1 (HTLV-1) Accessory Protein p30 Modulates Cell Cycle and DNA Damage Signaling." The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1184007936.
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Chitnis, Meenali M. "Type 1 insulin-like growth factor receptor inhibition as treatment for urological cancer." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:21282ce9-ce6b-4d26-b262-a3fca6d9c9fc.
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The type 1 insulin-like growth factor receptor (IGF-1R) is a receptor tyrosine kinase that mediates diverse cellular functions including growth, differentiation, migration and apoptosis protection. IGF-1R signalling has been implicated in tumorigenesis in a variety of cancers, and IGF-1R inhibitory drugs are currently undergoing clinical evaluation. Previous work in our laboratory has shown IGF-1R over-expression in urological cancers at both the mRNA and protein level, thus making it a potential therapeutic target. The first aim of this project was to develop a protocol for IGF-1R immunohistochemistry, investigate the expression and cellular distribution of the IGF-1R receptor in clear cell renal cell carcinomas (ccRCC), and assess correlation with clinical parameters. In tissue microarray analysis, IGF-1R was detected in ~90% of 195 ccRCCs, with signal in the plasma membrane, cytoplasm and also in the nucleus. The presence of nuclear IGF-1R in up to 50% of ccRCCs and its association with adverse prognosis was a novel finding, and suggests that nuclear IGF-1R may influence ccRCC biology. Further investigations will clarify its role in the nucleus and its potential as a prognostic biomarker. The second aim was to investigate effects of IGF-1R inhibition on radiosensitivity and DNA repair, following previous work in our laboratory showing that IGF-1R depletion enhances chemo- and radio-sensitivity, delays double strand break (DSB) resolution, and may play a role in the homologous recombination (HR) pathway of DNA DSB repair. However, the repair defect seen in these early experiments was larger than could be entirely explained by a defect in HR. The current project used a small molecule IGF-1R tyrosine kinase inhibitor AZ12253801 (AstraZeneca), which blocked IGF-1 induced IGF-1R activation and inhibited cell survival. AZ12253801 enhanced the radiosensitivity of prostate cancer cells, which appeared to be independent of effects of IGF-1R inhibition on cell cycle distribution and apoptosis induction. IGF-1R inhibition delayed the resolution of γH2AX foci, supporting a potential role for the IGF-1R in DSB repair. This delay in focus resolution was apparent at early time-points (less than 4 hr), and was epistatic with DNA dependent protein kinase (DNAPK) inhibition in prostate cancer cells and DNAPK deficiency in glioblastoma cells. These results suggest a role for the IGF-1R in the non-homologous end-joining (NHEJ) pathway of DNA DSB repair. A cell-based reporter assay in HEK-293 cells confirmed that IGF-1R inhibition suppressed DSB repair by NHEJ, helping to explain the radiosensitization demonstrated upon IGF-1R inhibition. There was lack of support for a transcriptional effect, with no significant change observed in gene expression on microarray analysis. Although the mechanism of this effect remains unclear, the observed inhibition of NHEJ has implications for the use of IGF-1R inhibitors in combination with DNA damaging agents in cancer treatment.
28
Dumas, Karine. "Implication de la protéine REDD1 dans les maladies métaboliques associées à l’obésité : REDD1 = Regulated in Development and DNA damage responses 1." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2019. http://www.theses.fr/2019AZUR4045.
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L’obésité est définie comme une accumulation excessive de graisse pouvant conduire à des problèmes de santé et sa prévalence mondiale ne cesse d’augmenter. L’obésité s’accompagne de désordres métaboliques comme la résistance à l’insuline, la stéatose hépatique et le diabète de type 2. REDD1 (Regulated in Development DNA damages responses 1) régule de nombreuses voies de signalisation impliquées dans la modulation de la balance énergétique cellulaire. Dans mon laboratoire d’accueil, nous avons montré que REDD1 est impliqué dans la voie de signalisation de l’insuline. L’objectif de ma thèse est d’étudier l’implication de REDD1 dans les complications métaboliques induites par l’obésité. L’expression de REDD1 est augmentée dans le tissu adipeux épididymaire et le foie de souris contrôles (WT) nourries avec un régime obésogène (HFD). De plus, son expression est augmentée dans le foie de patients obèses atteints de stéatose hépatique et est corrélée avec le degré de la pathologie et la résistance à l’insuline des patients. Afin d’identifier le rôle de REDD1 dans le développement des pathologies induites par l’obésité, nous avons caractérisé le phénotype de souris invalidées pour REDD1 (KO) soumises à un régime HFD. Lors d’un régime HFD, les souris REDD1-KO développent une obésité et une résistance à l’insuline identique aux souris WT. Cependant, les souris REDD1-KO sont protégées du développement de la stéatose hépatique. Aucune modification de l’expression des protéines impliquées dans l’import et l’export hépatiques des acides gras n’a été mise en évidence. Dans le foie des souris REDD1- KO, l’expression des protéines impliquées dans la lipogenèse est diminuée alors que l’expression des protéines qui régulent la β-oxydation des acides gras est augmentée. Dans le foie des souris WT, le développement de la stéatose hépatique s’accompagne d’une augmentation de la taille des mitochondries. Par contre, dans le foie des souris REDD1-KO, le régime HFD n’induit pas d’augmentation de la taille des mitochondries et l’expression des protéines impliquées dans la régulation de la mitophagie est augmentée. Ces résultats suggèrent que lors d’un stress métabolique comme un régime obésogène, le foie des souris invalidées pour REDD1 pourrait être protégé d’un dysfonctionnement mitochondrial grâce à une exacerbation de l’autophagie. Dans la seconde partie de ma thèse, nous avons étudié le phénotype des souris hétérozygotes pour REDD1 (REDD1-He) soumises à un régime HFD. La diminution partielle de REDD1 n’affecte pas le développement de l’obésité par rapport aux souris WT, ni le développement de la stéatose hépatique. Cependant, sous régime HFD, l’intolérance au glucose et la résistance à l’insuline des souris REDD1-He sont augmentées par rapport aux souris WT-HFD. Les souris REDD1-He semblent oxyder difficilement les lipides en période de jeûne et ont une répartition des tissus adipeux différente que les souris WT. En conclusion, mes travaux de thèse ont permis de montrer pour la première fois l’implication de REDD1 dans le développement de la stéatose hépatique lors de l’obésitéObesity is defined as an abnormal fat accumulation which could lead to health disorders and its prevalence is in constant increase worldwide. Obesity is associated with insulin resistance, hepatic steatosis and type 2 diabetes. REDD1 (Regulated in Development DNA damages responses 1) regulates most of signaling pathways implicated in cell energetic balance. In my host lab, we have demonstrated that REDD1 is implicated in insulin signaling pathway. The goal of my thesis was to study the REDD1 implication in obesity associated metabolic diseases. We observed that REDD1 expression was increased in epidydimal adipose tissue and in liver of control high fat diet (HFD) fed-mice (WT). Furthermore, REDD1 expression was increased in liver biopsies from obese patients with hepatic steatosis and its expression was correlated with the severity of the pathology and insulin resistance. To identify the role of REDD1 in the development of obesity-induced diseases, we have characterized the phenotype of REDD1 knockout mice (REDD1-KO) fed with HFD. Under HFD, the REDD1-KO mice showed a similar weight gain and insulin resistance compared to WT mice. Interestingly, REDD1-KO mice were protected from hepatic steatosis under HFD. In liver of REDD1-KO mice, no modification of protein expression implicated in hepatic lipid flux was observed. In REDD1-KO mice liver, we observed a decrease of protein expression implicated in lipogenesis pathways associated to an increase of the expression of proteins involved in β-oxydation. In WT mice, hepatic steatosis is correlated with an increase of mitochondrial size. In REDD1-KO mice, HFD did not induce an enlargement of mitochondria. Moreover, the expression pattern of proteins involved in autophagy and mitophagy is increased in HFD REDD1-KO livers. Our results suggest that in HFD conditions, liver of REDD1- KO mice could be protected from mitochondrial dysfunction because of an increase of mitophagy. In a second part of my thesis, we have studied the effect of partial decrease of REDD1 expression on obesity-induced complications using REDD1 heterozygous mice (REDD1-He). Partial decrease of REDD1 did not influence weight gain and hepatic steatosis development under HFD compared to WT mice. However, REDD1-He mice have developed an important glucose and insulin resistance under HFD compared to WT mice. This is associated with an impairment of the use of lipid as substrate during fasting. To conclude, my thesis research project allows us to show for the first time that REDD1 is implicated in hepatic steatosis under obesity
29
Yu, Yanan. "NF1 Patient Missense Variants Predict a Role for ATM in Modifying Neurofibroma Initiation." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1592395217393569.
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Hemmings, K. E., Kirsten Riches-Suman, M. A. Bailey, D. J. O'Regan, N. A. Turner, and K. E. Porter. "Role of microRNA-145 in DNA damage signalling and senescence in vascular smooth muscle cells of Type 2 diabetic patients." MDPI, 2021. http://hdl.handle.net/10454/18477.
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YesIncreased cardiovascular morbidity and mortality in individuals with type 2 diabetes (T2DM) is a significant clinical problem. Despite advancements in achieving good glycaemic control, this patient population remains susceptible to macrovascular complications. We previously discovered that vascular smooth muscle cells (SMC) cultured from T2DM patients exhibit persistent phenotypic aberrancies distinct from those of individuals without a diagnosis of T2DM. Notably, persistently elevated expression levels of microRNA-145 co-exist with characteristics consistent with aging, DNA damage and senescence. We hypothesised that increased expression of microRNA-145 plays a functional role in DNA damage signalling and subsequent cellular senescence specifically in SMC cultured from the vasculature of T2DM patients. In this study, markers of DNA damage and senescence were unambiguously and permanently elevated in native T2DM versus non-diabetic (ND)-SMC. Exposure of ND cells to the DNA-damaging agent etoposide inflicted a senescent phenotype, increased expression of apical kinases of the DNA damage pathway and elevated expression levels of microRNA-145. Overexpression of microRNA-145 in ND-SMC revealed evidence of functional links between them; notably increased secretion of senescence-associated cytokines and chronic activation of stress-activated intracellular signalling pathways, particularly the mitogen-activated protein kinase, p38a. Exposure to conditioned media from microRNA-145 overexpressing cells resulted in chronic p38a signalling in naïve cells, evidencing a paracrine induction and reinforcement of cell senescence. We conclude that targeting of microRNA-145 may provide a route to novel interventions to eliminate DNA-damaged and senescent cells in the vasculature and to this end further detailed studies are warranted.
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Danga, Helga Tariro. "Investigation of electron-beam deposition and related damage in p-Si by means of Laplace and conventional deep-level transient spectroscopy." Thesis, University of Pretoria, 2019. http://hdl.handle.net/2263/77896.
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The study of defects in semiconductors has been on-going for over 50 years. During this time, researchers have been studying the origins and identity of process induced defects, a task which has proved to be very demanding. While defects in silicon, the most widely used semiconductor, have been widely studied, there is more literature on n-type silicon than on p-type silicon. Compared to n-type silicon, p-type silicon is challenging to work with when it comes to making good Schottky diodes. A good rectifying device is essential for the performing of electrical characterisation techniques such as deep-level transient spectroscopy. In spite of this challenge p-silicon cannot be ignored. Many of the electronic devices are a combination of both n- and p-silicon therefore the need to understand the electronic properties of both materials.
In this thesis, defects introduced in p-Si by electron beam deposition (EBD) were investigated. In order to understand these defects better, defects introduced by conditions of electron beam deposition (EBD) without metal deposition, were investigated. This process will be referred to as electron beam exposure (EBE). Finally, the defects were compared to defects induced by alpha-particle irradiation.
EBD defects, introduced during electron beam deposition (EBD) of titanium (Ti) contacts on p-Si were investigated. The Schottky contacts were annealed within a temperature range of 200–400 oC. Current-voltage (I-V) measurements were conducted to monitor the change in electrical characteristics with every annealing step. Deep-level transient spectroscopy (DLTS) and Laplace-DLTS techniques were employed to identify the defects introduced after EBD and isochronal annealing of the Ti Schottky contacts. DLTS revealed that the main defects introduced during metallisation were hole traps with activation energy of 0.05 eV, 0.23 eV and 0.38 eV. Depth profiles of these defects showed that the formed close to the interface within a depth of 0.4 μm.
Defects induced by EBE were studied by exposing samples for 50 minutes after which nickel (Ni) Schottky contacts were fabricated using resistive deposition. Only one defect with an activation energy of 0.55 eV was observed. This activation energy is similar to that of the I-defect. DLTS depth profiling revealed that the defect could be detected up to a depth of 0.8μm below the junction, which is significantly deeper than EBD defects.
Defects induced when p-Si was irradiated by alpha particles from a 5.4 MeV americium (Am) 241 foil radioactive source with a fluence rate of 7×106 cm−2 s−1 at room temperature were investigated. After exposure at a fluence of 5.1×1010 cm−2, hole traps with the following activation energies were observed: 0.10 eV, identified as a tri-vacancy related defect, 0.33 eV, the interstitial carbon (Ci), 0.52 eV, a B-related defect and 0.16 eV. Low temperature irradiation experiments were also carried out using alpha- particles with the same fluence rate. Measurements were taken between 35 K and 120 K. The defect levels were at 0.10 eV, 0.14 eV and 0.18 eV. These levels were attributed to the boron-substitutional vacancy complex, the mono-vacancy and a vacancy-related defect, respectively. We conclude that EBD and EBE induced more complex defects than those induced by alpha-particle irradiation.Thesis (PhD)--University of Pretoria, 2019.
Physics
PhD
Unrestricted
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Afsar, Nilufer. "Effect Of Cold Stress On Antioxidant Mechanism Of Winter And Spring Type Barley ( Hordeum Vulgare L.) Cultivars." Master's thesis, METU, 2007. http://etd.lib.metu.edu.tr/upload/3/12608514/index.pdf.
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In this study, effect of cold stress on physiology and biochemistry of two Turkish barley cultivars, winter type Tarm-92 and spring type Zafer-160, was studied. For chilling stress treatment, cultivars were exposed to +4 ºC for 1, 3 and 7 days, and for freezing stress application acclimated cultivars (+4 º
C for 3 days) were treated with -3 º
C and -7 º
C. After freezing stress treatment, a recovery period was applied for 4 days at 4 º
C. Following analyses were performed on leaf and root tissues: growth parameters (length, wet-dry weights), malondialdehyde (MDA) content, proline content, hydrogen peroxide content (H2O2) electrolyte leakage, PS II fluorescence (Fv/Fm), antioxidant enzyme activities such as catalase (CAT: EC 1.11.1.6), ascorbate peroxidase (APX: EC 1.11.1.11) and glutathione reductase (GR: EC 1.6.4.2). It was observed that effect of cold was more at freezing temperatures than chilling temperature. Cold dependent damage was more obvious as the duration of chilling temperature increased. Growth retardation, membrane damage, leaf catalase deactivation were more apparent and leaf glutathione reductase activity increase was less in spring type cultivar Zafer than in winter type Tarm. These results indicated that winter type barley cultivar is more cold tolerant than spring type barley.
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Fiskin, Gokce. "A Case Study On The Stability Of Berm Type Coastal Defense Structures." Master's thesis, METU, 2004. http://etd.lib.metu.edu.tr/upload/12605604/index.pdf.
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Coastal defense structures have primary importance from obtainabilty of resources and benefits served by the coastal regions point of view. However, the construction of coastal defense structures demand a high amount of investment. Therefore, in order to reduce the risk of collapse of these structures, model studies should be carried during the design process.
In this study, model investigations were carried out on Eastern Black Sea Highway Project regarding the serviceability and damage thus stability parameters. 5 different models were constructed as berm type rubble-mound breakwaters using Van Der Meer&rsquos approach and berm design guidelines, with a scale of 1/31.08 and they were tested both for breaking and non-breaking waves. The experiments took place in the Coastal and Harbor Engineering Laboratory of the Middle East Technical University, Civil Engineering Department. The models were constructed and tested with different berm widths and armor stone sizes forming the back armor layer in order to examine the effect of these design parameters on the stability and serviceability of the coastal defense structure to obtain the optimum alternative cross-section. Cumulative damage was minimum for the cross-section constructed with berm width 15 m assigning the width of the prototype. Water spray and run-up values were also not significant. The test results were confirming with Van Der Meer design approach.
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Gaborit, Pierre. "Unification des modèles d’endommagement de type Lemaitre, pour la fatigue LCF/HCF, multiaxiale et aléatoire." Thesis, Cachan, Ecole normale supérieure, 2015. http://www.theses.fr/2015DENS0041.
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Les travaux présentés concernent le développement d'un modèle de prévision de durée de vie unifié pour traiter les problématiques de fatigue à faible et grand nombre de cycles. Le modèle est basé sur une approche à deux échelles et un endommagement de type Lemaitre. Le caractère "en vitesse" de la loi d'endommagement permet de traiter des chargements complexes, non proportionnels et aléatoires. Une campagne expérimentale de fatigue sur 12 éprouvettes cruciformes en alliage TA6V pour application aérospatiale est présentée. Elle comporte des essais biaxiaux proportionnels et non proportionnels ainsi que des cas de chargement pseudo-aléatoires. L'utilisation de la corrélation d'images numériques prises dans la zone utile permet d'évaluer les déformations locales en réponse aux sollicitations appliquées. Les cas de chargements sont simulés afin de confronter les déformations de surface et les durées de vie obtenues par calcul, aux résultats expérimentaux. Parmi les contributions théoriques présentées dans le manuscrit, sont à noter : - La proposition d'une nouvelle loi d'évolution pour écrouissage cinématique adaptée au comportement élastoplastique du TA6V sous chargement cyclique; - L'utilisation d'une correction élastoplastique locale permettant d'évaluer les déformations plastiques en surface à partir de calculs de structures linéaires; - L'amélioration d'un critère de micro-plasticité pour la prise en compte des effets de contrainte moyenne et de triaxialité en fatigue à grand nombre de cycles; - L'unification de deux lois d'endommagement afin d'étendre le domaine de validité du modèle initial vers les durées de vie à faible nombre de cycles. La démarche s'appuyant sur le cadre thermodynamique de la mécanique des milieux continus, de nombreuses perspectives d'amélioration du modèle sont discutéesThis work presents the proposal of a unifying predictive model to deal with LCF and HCF problems. It is based on a two-scale approach initially developed by Lemaitre. As the damage evolution law is rate written, complexity due to non proportional and random loadings may also be treated. An experimental fatigue campaign of 12 cross shaped samples made of TA6V alloy for aerospace applications is presented. It includes not only proportional and non proportional biaxial tests but also pseudo random loadings. Digital Image Correlation is used to evaluate the local strains from pictures taken in the zone of interest. Loadings are the simulated and both strains and lifetimes are compared to experimental observations. Among the theoretical contributions presented in this work, the main are: - A new kinematic hardening evolution law for the modeling of elasto-plasticity of TA6V alloy under cyclic loadings; - Use of local elastoplastic correction from linear Finite Element Calculation to estimate plastic strains in the structure zone of interests; - Improvements of the micro-plastic yield function to take into account mean stress effect and triaxiality effects in the lifetime prediction in HCF domain; - A unifying method of two damage variables in order to extend the validity domain of the initial model to shorter lifetimes (LCF). As the model is based on a thermodunamical framework for continuum mechanics, several extension are mentioned as future propects
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Sweetman, Sandra Frances. "An investigation of bleomycin induced DNA damage and repair in wild-type and thymidine kinase deficient human and murine cell lines." Thesis, University of Ulster, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242069.
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Sánchez, Peña Enric. "Estudi DMAGE: Diabetes Mellitus and damage caused by Advanced Glycation End-products." Doctoral thesis, Universitat de Lleida, 2018. http://hdl.handle.net/10803/663150.
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Els productes avançats de glicació avançada (AGEs) constitueixen un grup complex de compostos formats per la lenta glicació no enzimàtica de proteïnes, lípids i àcids nucleics, dels quals s'han dilucidat aproximadament 20 fins el present. No existeix evidència de si la magnitud de la deposició d'AGEs en el teixit subcutani està relacionada amb la malaltia ateromatosa, les primeres etapes de la malaltia renal crònica, la funció pulmonar i l'obesitat. Aquests són els primers estudis en què l'autofluorescència cutània (SAF) s'ha avaluat en una cohort asimptomàtica de mitjana edat sense esdeveniments cardiovasculars coneguts que mostren una estreta relació entre la SAF i la càrrega de plaques ateromatoses així com amb la disfunció renal i pulmonar. També hi ha una SAF augmentada en pacients amb obesitat mòrbida i síndrome metabòlica principalment a expenses de la presència de diabetis mellitus tipus 2. Durant els primers 5 anys després de la cirurgia bariàtrica, no es va observar una disminució de la SAF.Los productos finales de glicación avanzada (AGEs) constituyen un grupo complejo de compuestos formados por la lenta glicación no enzimática de proteínas, lípidos y ácidos nucleicos, de los que se han dilucidado aproximadamente 20 hasta el presente. No existe evidencia de si la magnitud de la deposición de AGEs en el tejido subcutáneo está relacionada con la enfermedad ateromatosa, las primeras etapas de la enfermedad renal crónica, la función pulmonar y la obesidad. Estos son los primeros estudios en que la autofluorescencia cutánea (SAF) se ha evaluado en una cohorte asintomática de mediana edad sin eventos cardiovasculares conocidos que muestran una estrecha relación entre la SAF y la carga de placas ateromatosas así como con la disfunción renal y pulmonar. También hay una SAF aumentada en pacientes con obesidad mórbida y síndrome metabólico principalmente a expensas de la presencia de diabetes mellitus tipo 2. Durante los primeros 5 años después de la cirugía bariátrica, no se observó una disminución de la SAF.
The advanced glycation end-productsAGEs constitute a complex group of compounds formed by the slow non-enzymatic glycation of proteins, lipids, and nucleic acids, of which about 20 have been elucidated to date. No evidence exists whether the magnitude of the AGEs deposition in subcutaneous tissue are related with the atheromatous disease, the first stages of chronic kidney disease, the pulmonary function as well as obesity. These are the first studies in which skin autofluorescence (SAF) has been evaluated in a middle-aged asymptomatic cohort without known cardiovascular events displaying a close relationship between SAF and atheromatous plaque burden as well as kidney and pulmonary dysfuncion. There is also an increased SAF in patients with morbid obesity and metabolic syndrome mainly at the expense with the presence of type 2 diabetes. During the first 5 years after bariatric surgery, are not associated with a decrease in SAF.
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Ozler, Basar. "A Case Study On The Submerged Berm Type Coastal Defense Structures." Master's thesis, METU, 2004. http://etd.lib.metu.edu.tr/upload/12605605/index.pdf.
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Coastal defense structures are built in order to protect valuable coastal regions from the destructive effects of the waves. Due to the cost of coastal defense structures and the economical potential of the coastal regions, failure of such structures could cause loss of high amounts of investment. Therefore in the design and construction of coastal structures, it is of vital importance to achieve an optimum design which is not neither underdesigned nor overdesigned.
In this study, Submerged Berm type coastal defense structures with several different cross-sections were tested for stability under storm conditions. Damage analyses of the different models were carried out to compare the structure characteristics under storm conditions and to obtain the most economical and stable cross-section.
For the model studies, 5 different models were constructed by using Van der Meer&rsquos approach and berm design guidelines. Models were constructed with a model scale of 1:31.08 in the wave flume in the Coastal and Harbor Engineering Laboratory, Civil Engineering Department, METU. The newly designed and optimized berm type structure was proved to be successful and economical.
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Bottrell, John R. "Accident denominators relative to age groups in heavy industries of the Port Hedland region of Western Australia." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2007. https://ro.ecu.edu.au/theses/8.
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The aim of this research is to investigate characteristics of accident denominators across age groups in mining and associated process industries in the Port Hedland region of Western Australia. Emphasis has been focussed on comparing young, inexperienced groups with older, more experienced groups. A literature review revealed some key contributors to accidents among younger workers, in particular, those who had only recently entered the workforce. The review also revealed contributors impacting accidents regarding other age groups over a wide range of industry types. From these findings an accident construct model and questionnaire were designed to identify contributing and mitigating denominators which input to accidents occurring across the defined age groups.
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Guillaud, Nicolas. "Tolérance aux dommages générés par impact de structures composites épaisses. Application aux réservoirs composites hyperbares." Thesis, Paris, ENSAM, 2015. http://www.theses.fr/2015ENAM0040/document.
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Cette thèse s'est déroulée dans le cadre du projet TOLEDO (Tolérance aux dommages par impact des réservoirs hyperbares) piloté par Air Liquide en partenariat avec le CEA Le Ripault et l'institut PPRIME.L'hydrogène est stocké au sein de réservoirs de type IV à une pression de service de 700 bar.Ces structures composites présentent comme particularités d'être épaisses (> 30 mm), d'avoir une forte courbure et d'être préchargées en pression lors d'un éventuel impact.Notre travail a montré que ces particularités modifient le type, la quantité et la localisation des différents endommagements couramment observés (rupture de fibres, délaminage et fissuration matricielle).Les endommagements ont pu être quantifiés par le biais de méthodes simples et originales.L'influence des particularités sur le comportement à l'impact a pu être déterminée par l'utilisation de deux dispositifs expérimentaux conçus et réalisés au cours de cette thèse.Le premier permet de précontraindre en tension uniaxiale des plaques composites épaisses.Le second permet de précharger en état de membrane un tube composite ce qui a permis de montrer que le cas d'impact le plus critique vis-à-vis des réservoirs est lorsque ces derniers sont vides.Cette étude a permis de mettre en évidence la criticité des ruptures de fibres sur les pertes de performance au sein des réservoirs hyperbares.Un modèle numérique prenant en compte la dispersion des contraintes à rupture et des différents types d'endommagements a été développé.Il permet d'introduire un endommagement initial et a confirmé certains résultats expérimentauxThis thesis took place within the framework of the project TOLEDO (Tolerance in the damage by impact of the hyperbaric reservoirs) managed by Air Liquide in partnership with the CEA Le Ripault and PPRIME institute.The hydrogen is stored within the type IV vessel at a servive pressure of 700 bar.These composite structures present as peculiarities to be thick (> 30 mm), to have a strong curvature and to be precharged in pressure during a possible impact.Our work showed that these peculiarities modify the type, the quantity and the localization of the various usually observed damages (fiber breakage, délamination and matrix cracking).The damages were able to be quantified by means of simple and original methods.The influence of the peculiarities on the behavior in the impact was able to be determined by the use of two experimental devices designed and realized during this thesis.The first one allows to preload a thick composite plates in uniaxial tension thick composite plates.The second allows to preload in state of membrane a composite pipe and allowed to show that the most critical impact towards reservoirs is when they are empty.This study allowed to highlight the criticality of the fiber breakage on the loss of performance within the hyperbaric reservoirs.A digital model taking into account the dispersal of the failure stress and various types of damages was developed.It also allows to introduce an initial damage and confirm some experimental results
40
Keller, Seitz Monika U. "The role of recombination in aflatoxin B₁-induced DNA damage in Saccharomyces cerevisiae and the Seg1 protein of Saccharomyces cerevisiae is a membrane-associated multidrugtransporter /." Zürich, 2001. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=14321.
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Armentrout, Erin I. "Sensing of Host Cell Contact by the Pseudomonas aeruginosa Type III Secretion System." Case Western Reserve University School of Graduate Studies / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=case1499965816504161.
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Laribi, Mohamed Amine. "Caractérisation et Modélisation du comportement micromécanique des matériaux composites SMC sous chargement thermomécanique de type quasi-statique et fatigue." Thesis, Paris, ENSAM, 2018. http://www.theses.fr/2018ENAM0062/document.
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L’utilisation des matières composites est fortement conditionnée par la capacité du constructeur ou du sous-traitant à dimensionner les structures automobiles sous divers types de chargements complexes tel que la fatigue. Le présent travail de thèse a pour objectif de développer un outil de modélisation par transition d’échelles couplée à une approche phénoménologique afin d’apporter une réponse à un besoin de maîtrise du dimensionnement de pièce de structure en composite SMC (polyester chargé en fibres de verre) soumis à des sollicitations de type fatigue sous différents niveaux de température 23°C, 80°C et -30°C. Pour ce faire, le travail a été mené selon deux axes principaux. En premier lieu, une investigation expérimentale sous chargement monotone et fatigue. Les résultats de l’analyse expérimentale de l’endommagement du matériau a permis d’accéder aux données nécessaires à la construction d’un modèle micromécanique constituant la base des approches prédictives de la durée de vie des SMC sous chargements cycliques constituant la seconde phase de travail. Ainsi, deux approches de modélisations hybrides phénoménologiques/micromécaniques ont été proposées. Elles sont toutes les deux basées sur une modélisation micromécanique qui permet de traduire le comportement mécanique du matériau d’étude sous chargement monotone avec prise en compte de la microstructure et de l’endommagement. Ces deux approches prédictives ne nécessitent qu’un nombre limité d’essais et d’investigations expérimentales mais restent bien fiables et pertinentes dans leurs capacités de prédire la durée de vie d’un matériau composite SMC sous chargement en fatigue. L’approche est validée dans le cas de chargements thermomécaniques séquentiels à température ou amplitude variableThe composite materials are strongly conditioned by the ability of the company to design the automotive structures under various complexes loadings such as fatigue. The aim of this thesis is to develop a multi-scale modeling coupled to a phenomenological approach in order to provide a response to the dimensioning need of structural parts subjected to cyclic loading at different temperatures of 23°C, 80°C and -30°C. By this way, the work was conducted along two main lines; firstly, an experimental investigation under monotonic and fatigue loadings. The results of this experimental study provide the necessary data for the construction of a micromechanical model which constitute the basis of the second part of this work; the predictive approaches of the fatigue lifetime for SMC composite. Thus, two hybrid, phenomenological/micromechanical, modeling approaches have been proposed. Both are based on a micromechanical modeling that allows describing the mechanical behavior of our material under monotonic loading, taking into account the microstructure and the damage phenomenon. These two predictive models require only a limited number of experimental tests and investigations but remain very reliable in their capacity to predict the lifetime of an SMC composite material under fatigue loading. The approach is validated in the case of thermomechanical sequential loadings at variable temperatures or amplitudes
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Doolittle, Lauren May. "The Impact of Alveolar Type II Cell Mitochondrial Damage and Altered Energy Production on Acute Respiratory Distress Syndrome Development During Influenza A Virus Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu159224389333959.
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Shirinbayan, Mohammadali. "Étude du comportement mécanique et de l’endommagement de divers matériaux composites smc soumis à des chargements de type dynamique, fatigue et dynamique post-fatigue." Thesis, Paris, ENSAM, 2017. http://www.theses.fr/2017ENAM0013/document.
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Le dimensionnement au crash des structures automobiles en matériaux composites à renforts discontinus tels que les SMC est généralement réalisé sur la base de données expérimentales recueillies sur des matériaux vierges n’ayant subi aucun chargement depuis leur mise en œuvre. Or, les accidents proviennent après quelques années de mise en service durant lesquelles la structure composite est soumise généralement à des sollicitations de type fatigue à plus ou moins grande amplitude. La prise en compte d’un pré-endommagement éventuel en fatigue devient alors essentielle si l’on veut rester réaliste. Par ailleurs, de nouvelles formulations de matériaux composites SMC ont été récemment développées. Leur comportement en fatigue et sous sollicitation rapide étaient jusqu’à lors inexplorés. Cette étude à caractère fortement expérimentale a donc pour but d’apporter la connaissance nécessaire au dimensionnement de structures en matériaux SMC de diverses formulations, notamment le A-SMC et le LD-SMC. Le premier correspond à une matrice vinylester fortement renforcée de mèches de fibres de verre (50%). Le second correspond à une formulation proche de celle d’un SMC standard dans laquelle on a rajouté un fort taux de billes de verre creuse afin de réduire la densité. Une analyse multi-échelle permet de mettre en évidence l’influence de la microstructure sur les phénomènes d’endommagement sous sollicitation quasi-statique, dynamique et fatigue. Des méthodes originales d’analyse expérimentale sont développées afin de corréler ces mécanismes aux comportements macroscopiques observés. Les essais dynamiques rapides optimisés sont réalisés jusqu’à des vitesses de déformation de l’ordre de 80 s-1 et mettent en évidence un comportement visco-endommageable pour les deux matériaux SMC étudiés. Le décalage du seuil d’endommagement et la baisse de la cinétique d’endommagement observés à l’échelle macroscopique sont directement corrélés au seuil et cinétique des mécanismes d’endommagement observés à l’échelle locale telles que la rupture à l’interface fibre-matrice ou bille-matrice, la microfissuration de la matrice et le pseudo-délaminage entre les mèches de fibres de verre. Par ailleurs, une analyse multi-échelle du même type est également réalisée sous sollicitation de type fatigue dans laquelle les fréquences varient de 10 à 100 Hz. Une étude de l’influence des phénomènes d’auto-échauffement sur l’endommagement et le comportement du A-SMC est proposée. Enfin, une analyse originale des propriétés résiduelles sous sollicitation rapide d’échantillons préalablement fatigués à différents niveaux de fraction de durée de vie met en évidence une forte influence de l’histoire du chargement sur la sensibilité du A-SMC à la vitesse de sollicitation. L’ensemble des résultats de cette étude, de par son apport de compréhension des phénomènes mis en jeu, constitue la base expérimentale nécessaire à la construction d’outils de dimensionnement adaptés aux structures SMC sous sollicitations cycliques et dynamiquesClassically, crash design of automotive composite structures made of discontinuous reinforcements such as SMC is usually based on experimental data obtained from virgin materials without any history of loading. However, crash events always occur after a few years of use during which composite structure is generally subjected to more or less important fatigue loading. Taking into account of a potential pre-damage in fatigue becomes essential if we want to stay realistic. Moreover, new formulations of SMC composites have been developed recently. Up to now, their fatigue and dynamic behavior were never being explored. This study, of a mostly experimental nature, aims to provide the knowledge necessary for design of structures made of various SMC formulations including A-SMC and LD-SMC. The first one is a vinylester matrix reinforced with a high content of glass fibers (50%). The second corresponds to a standard SMC formulation in which we added a high content of hollow glass micro-sphere in order to reduce density. A systematic multi-scale analysis allows to highlight the influence of the microstructure on damage phenomena under quasi-static, dynamic and fatigue loading. Original experimental methods are developed to correlate these mechanisms to the observed macroscopic behavior. Optimized dynamic tests are performed at strain rate up to 80 s-1 and highlight a visco-damageable behavior for the two SMC materials in study. Damage threshold delay and reduction of damage kinetics observed at the macroscopic scale are directly correlated to the threshold and kinetic of damage development observed at the local scale such as fiber-matrix or matrix-microsphere interfaces, matrix micro-cracking and pseudo-delamination between the bundles of glass fiber. Moreover, a similar multi-scale analysis is also performed under fatigue loading in which the frequency ranges from 10 to 100 Hz. A study of the influence of the self-heating phenomenon on the fatigue damage behavior of A-SMC is proposed. Finally, an original analysis of the remaining dynamic properties of samples which were previously submitted to fatigue loading until different levels of lifetime highlights a strong influence of the history of the loading on the strain rate sensitivity of the A-SMC. Considering the high contribution of this study in term of comprehension of the phenomena involved in the mechanical response of SMC materials, all of the experimental findings of this study provide the physical background crucial to build structural design tools for SMC subjected to cyclic and dynamic loading
45
Dompierre, Benoît. "Fiabilité mécanique des assemblages électroniques utilisant des alliages du type SnAgCu." Phd thesis, Ecole Centrale de Lille, 2011. http://tel.archives-ouvertes.fr/tel-00604954.
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Depuis la restriction de l'utilisation du plomb dans l'électronique, les alliages de brasure de type SnPb ont été remplacés majoritairement par des alliages de type SnAgCu (SAC). Des travaux précédents ont révélé un phénomène de vieillissement de ces alliages, caractérisé par une forte variation des propriétés mécaniques et se stabilisant après plusieurs années à température ambiante. L'objectif de ce travail est d'étudier l'influence du vieillissement thermique sur l'endommagement des assemblages électroniques utilisant l'alliage SAC305 sous chargements mécaniques.L'étude s'est d'abord concentrée sur le comportement mécanique du SAC305, puis sur l'endommagement des joints brasés.L'impact du vieillissement sur le comportement mécanique a été évalué à l'échelle massive ainsi qu'à l'échelle d'un joint brasé. L'évolution de la dureté et du comportement mécanique cyclique à température ambiante a été reliée à un phénomène de grossissement de grain. Des essais de compression sur billes en SAC305, représentatives de la structure réelle, ont montré les mêmes évolutions. Deux modèles de comportement viscoplastique ont été développés à l'échelle d'un joint brasé pour l'alliage dans l'état initial et dans l'état vieilli. Des simulations numériques réalisées à l'aide de ces modèles, ont permis de valider cette approche.L'influence du vieillissement sur l'endommagement des joints brasés en SAC305 a été évaluée à l'aide d'essais de torsion cycliques sur cartes assemblées. Les résultats montrent que le vieillissement induit une diminution du nombre de cycles à la défaillance en fatigue oligocyclique, élément très important pour la gestion du risque dans les équipements électroniques
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Rytter, Elisabet. "Effect of Dietary Antioxidants on Oxidative Stress, Inflammation and Metabolic Factors : Studies in Subjects with Overweight and with Type 2 Diabetes." Doctoral thesis, Uppsala universitet, Oxidativ stress och inflammation, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-134938.
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Observational studies have indicated that fruit and vegetables, and dietary antioxidants may play an important role in reducing the risk of chronic diseases, potentially by affecting pathogenic mechanisms such as oxidative stress and inflammation. Clinical trials investigating the effects of supplementation with single or a few antioxidants in high doses have, however, shown inconsistent results and thus have not been able to support the observational findings. It was therefore hypothesised that a supplement, containing a combination of antioxidants mainly extracted from fruit and vegetables, and supplied at moderate doses, might act more beneficially than single antioxidants given at pharmacological doses. The effects of such a supplement were investigated in two interventional studies described in this thesis. The effects on antioxidant status, metabolic control, oxidative stress and inflammation were investigated in overweight men and in patients with type 2 diabetes, subjects that could be expected to have elevated levels of oxidative stress and inflammatory activity. The results of the studies did not support the hypothesis that supplementation with antioxidants from fruit and vegetables may have beneficial effects by counteracting oxidative stress and inflammation, despite markedly increased plasma antioxidant concentrations. However, interesting associations were observed in diabetes patients at baseline between intake of antioxidant rich food as well as levels of antioxidants in plasma, and markers of oxidative stress and inflammation. These associations are compatible with the hypothesis that a high intake of fruit and vegetables and dietary antioxidants decrease oxidative stress levels, have anti-inflammatory effects and a beneficial influence on glycaemic control. The results also indicated that glycaemic control may affect the level of oxidative stress. The absence of beneficial effects from antioxidants might to some extent be explained by the initial levels of oxidative stress and inflammation and by the antioxidative status in the subjects included in the studies. Since the levels generally were comparable with those observed in healthy subjects, this might have decreased the ability to observe any beneficial effects of supplementation with additional antioxidants. Continued investigations are needed to characterise the individuals who potentially might benefit from antioxidant supplementation. In view of apparent positive effects from a high intake of fruit and vegetables found in observational studies and until more knowledge is available from interventional trials about possible benefits and potential risks of antioxidant supplementation it still seems reasonable to recommend a diet rich in fruit and vegetables.
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Åsgård, Rikard. "Effects of Antioxidants and Pro-oxidants on Oxidative Stress and DNA Damage using the Comet Assay : Studies on Blood Cells from Type 2 Diabetes Subjects and Mouse Lymphoma Cells." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-217886.
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Diet and oral supplements comprise two distinct sources of antioxidants known to prevent oxidative stress. Beneficial effects from antioxidants have been seen for patients at risk for type 2 diabetes. The aim of this thesis was to evaluate the positive effects of antioxidants against oxidative stress and DNA damage in type 2 diabetes subjects. We also used antioxidants as tools to determine the mechanisms behind genotoxicity induced by mutagenic pro-oxidative agents in mouse lymphoma cells. Several techniques were used to measure oxidative stress and DNA damage, but the main technique used was alkaline comet assay. The results showed that the fruit and vegetable intake was inversely related to oxidative stress in type 2 diabetes subjects. However, oral supplementary intake of 20 antioxidants did not decrease oxidative stress biomarkers. In studies on mouse lymphoma cells, using the alkaline comet assay, DNA damage was induced by catechol and o-phenylenediamine (OPD), while 4-nitro-o-phenylenediamine (4-NOPD) induced only oxidative damage, showing different mechanisms of action behind the mutagenicity of the compounds. Also, oxidative stress was induced by catechol and 4-NOPD, whereas imbalances in the nucleotide pool were seen after exposure to OPD or 4-NOPD. Addition of antioxidants together with these pro-oxidants showed that β-carotene was able to reduce DNA damage at low concentrations of catechol, but increased DNA damage at high concentration. In comparison, addition of α-tocopherol slightly decreased catechol-induced DNA damage at all concentrations of catechol. However, no effect of α-tocopherol was seen on OPD-or 4-NOPD-induced DNA damage. In conclusion, antioxidants from fruits and vegetables, but not from oral supplements, reduced oxidative stress in type 2 diabetes patients, suggesting fruits and vegetables being a healthier source for antioxidant-intake, as compared to oral supplements. Different mechanisms of action for mutagenic pro-oxidants were shown in mouse lymphoma cells, introducing the nucleotide pool as an interesting target for oxidative stress. Reduction of catechol-induced DNA damage by β-carotene or α-tocopherol was shown, with a pro-oxidative action of β-carotene at high concentration of catechol, Interestingly, α-tocopherol was not able to decrease OPD- or 4-NOPD-induced DNA damage, supporting different mechanisms of action behind the genotoxicity from the three pro-oxidants.
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Lautrou, Nicolas. "Amorçage de fissure de fatigue dans un joint soudé de type naval : étude expérimentale et numérique." Université de Bretagne occidentale, 2007. http://www.theses.fr/2007BRES2051.
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Ce travail porte sur l'étude du comportement en fatigue d'assemblages soudés en acier S355NL, représentatifs d'éléments de structures navales. L'objectif est de développer une méthodologie pour estimer la durée de vie à l'amorçage d'une fissure de fatigue pour ce type de structures. L'approche proposée se décompose en deux étapes. Premièrement, un calcul de structure par éléments finis permet d'obtenir les cycles contraintedéformation stabilisés en tout point de l'assemblage soudé pour un chargement d'amplitude constante ou variable. Ce calcul prend en compte le comportement élastoplastique du métal de base, une variation de la limite d'élasticité dans la soudure basée sur des mesures de dureté, la géométrie locale du pied de cordon mesurée sur des photos de profil des éprouvettes, et éventuellement la présence de contraintes résiduelles. Deuxièmement, dans le cas où une adaptation élastique rapide se produit, un post-traitement permet de calculer la durée de vie à l'amorçage d'une fissure de fatigue, par l'utilisation d'un modèle d'endommagement à deux échelles basé sur les travaux de Lemaitre et al. . Les paramètres matériaux de ce modèle ont été identifiés à partir de courbes d'endurance établies pour le métal de base. Pour valider l'approche proposée, des essais de fatigue en flexion quatre points ont été réalisés sur des éprouvettes soudées réalisées par DCNS. Pour compléter l'analyse, des mesures de contraintes résiduelles présentes dans les éprouvettes soudées ont été réalisées par diffraction de rayons X. Les comparaisons entre les durées de vie expérimentales et les durées de vie calculées sont encourageantes pour la campagne d'essais réalisée.
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May, Abdelghani. "Etude du comportement cyclique et de l'endommagement par fatigue d'un alliage d'aluminium anisotrope du type 2017A." Phd thesis, INSA de Rouen, 2013. http://tel.archives-ouvertes.fr/tel-00925413.
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Cette thèse s'ajoute aux différents travaux de recherche qui traitent des alliages d'aluminium fortement utilisés dans l'industrie aéronautique et contribue fortement à comprendre le comportement élastoplastique en chargement cyclique à contrainte imposée du 2017A. L'apport essentiel de ce travail est l'étude de l'anisotropie propre du matériau utilisé à travers le suivi de l'évolution des différents paramètres caractérisant la plasticité cyclique de notre matériau. En effet, nous avons caractérisé cette anisotropie en comparant le comportement du matériau en traction-compression avec celui de la torsion alternée selon l'évolution cyclique de la réponse contrainte-déformation, l'évolution de l'état stabilisé, l'évolution des variables d'écrouissages cinématique et isotrope ainsi que l'anisotropie selon le comportement en fatigue et endommagement. Pour mieux affiner la partie expérimentale de ce travail, des investigations microstructurales des faciès de rupture de toutes les éprouvettes utilisées ont été effectuées afin de mieux comprendre les mécanismes d'endommagement cyclique dans notre matériau. Dans la partie numérique de cette thèse, nous avons réalisé des simulations numériques en utilisant la dernière version du modèle multimécanismes qui tient compte de l'anisotropie du matériau. Les résultats de ces simulations, réalisées en considérant les mêmes conditions de nos essais expérimentaux, confirment les capacités de cette nouvelle version à estimer le comportement élastoplastique d'un matériau anisotrope.
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Nakov, Philipp [Verfasser], and Felix [Akademischer Betreuer] Bischof. "The role of C-C motif chemokine ligand 7, C-C motif chemokine ligand 11 and interleukin-9 in T helper type 9 cell mediated neuronal damage / Philipp Nakov ; Betreuer: Felix Bischof." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/1204879877/34.
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