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Tones, Michael Anthony. "Reoxygenation induced calcium uptake in the myocardium". Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37879.
Pełny tekst źródłaCherif, Myriam. "Hypoxia-reoxygenation injury and stress related networks in the heart". Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520611.
Pełny tekst źródłaMagagnin, Michaël Gaston Pietro. "Cellular adaptation to hypoxia and reoxygenation through gene specific mRNA translation". [Maastricht : Maastricht : Maastricht University] ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=12817.
Pełny tekst źródłaTeoh, Leok-Kheng Kristine. "Transforming growth factor-B1 and myocardial reperfusion/reoxygenation injury : in vitro studies". Thesis, University College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498511.
Pełny tekst źródłaKolamunne, Rajitha K. "Reactive oxygen and nitrogen species production in cardiomyoblasts during hypoxia and reoxygenation". Thesis, Aston University, 2010. http://publications.aston.ac.uk/10052/.
Pełny tekst źródłaViret, Muriel. "Effect of hypoxia and reoxygenation on the lower respiratory compartment of the lung /". [S.l.] : [s.n.], 2009. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000288148.
Pełny tekst źródłaEvans, Emma Louise. "The effect of hypoxia and reoxygenation on STAT3 regulation in potential cardiomyocyte models". Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/28293/.
Pełny tekst źródłaHung, T. H. "In vitro hypoxia-reoxygenation as a model for placental oxidative stress in preeclampsia". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604788.
Pełny tekst źródłaArab, Amina. "Reoxygenation of hypoxic coronary smooth muscle cells amplifies growth-retarding effects of ionizing irradiation". [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=975997874.
Pełny tekst źródłaHuang, Ying [Verfasser]. "Effects of propofol on hypoxia/reoxygenation induced neuronal cell damage in vitro. / Ying Huang". Kiel : Universitätsbibliothek Kiel, 2013. http://d-nb.info/1037109392/34.
Pełny tekst źródłaAzarbayjani, Faranak. "Common mechanism for teratogenicity of antiepileptic drugs : Drug-induced embryonic arrhythmia and hypoxia-reoxygenation damage". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5065-2/.
Pełny tekst źródłaLindblom, Emely. "Searching for the optimal radiotherapy treatment time, dose and fractionation - the role of hypoxia and reoxygenation : A modelling study". Licentiate thesis, Stockholms universitet, Fysikum, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-109348.
Pełny tekst źródłaNiklewski, Paul J. "Surrogates, In-Vitro, and Clinical Investigations into the Safety and Effectiveness of Anesthesia". University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1383644949.
Pełny tekst źródłaDonnelly, John Leo. "The effects of hypoxia and reoxygenation on the fine structure of myocardial capillaries in relation to permeability". Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243907.
Pełny tekst źródłaVohra, Hunaid Ahmed. "Apoptosis and necrosis in ischaemia/reoxygenation injury of the human myocardium : mechanism of protection by ischaemic preconditioning". Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29881.
Pełny tekst źródłaHalurkar, Manasi Suchit. "Effect of Endothelial Progenitor Cell-derived Exosomes on High Glucose and Hypoxia/ Reoxygenation-induced Injury of Astrocytes". Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1565806287371214.
Pełny tekst źródłaYerrapragada, Sri Meghana. "The Protective Effects of miR-210 Modified Endothelial Progenitor Cells Released Exosomes in Hypoxia/Reoxygenation Injured Neurons". Wright State University / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wright1629835915811575.
Pełny tekst źródłaParker, Catriona Anne. "The response of tumour cells to hypoxia and reoxygenation : roles and interactions of p53 and NF#kappa#B". Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246997.
Pełny tekst źródłaOUDOT, FABIEN. "Production d'eicosanoides par les cellules du systeme cardio-vasculaire : modulation par les acides gras polyinsatures et l'hypoxie-reoxygenation". Paris 7, 1996. http://www.theses.fr/1996PA077109.
Pełny tekst źródłaBLANC, MARIE-CELINE. "Etude des mecanismes impliques dans la survenue des lesions hepatiques d'hypoxie-reoxygenation : phenomenes de toxicite directe et indirecte". Paris 6, 1998. http://www.theses.fr/1998PA066652.
Pełny tekst źródłaThompson, Brandon. "Hypoxia/Reoxygenation Stress Modulates Atorvastatin Transport at the Blood-Brain Barrier: A Role for Organic Anion Transporting Polypeptide". Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/337292.
Pełny tekst źródłaKhawaja, Kiran [Verfasser]. "Involvement of connexin 43 in ATP release from endothelial cells during reoxygenation : Role of PKA signaling pathway / Kiran Khawaja". Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063177596/34.
Pełny tekst źródłaBarua, Anupama. "The role of neuronal nitric oxide synthase (nNOS) in ischaemia/reoxygenation-induced injury and in protection of the mammalian myocardium". Thesis, University of Leicester, 2010. http://hdl.handle.net/2381/8754.
Pełny tekst źródłaAlpuerto, Jasper Benedict Battad. "Physiological, Metabolic, and Transcriptional Analysis of Submergence Tolerance in Rice and Nitrogen Use Efficiency in Wheat". Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/92003.
Pełny tekst źródłaPHD
Bhogal, Ricky Harminder. "The role of oxidative stress and CD154-mediated reactive oxygen species in regulating hepatocyte cell death during hypoxia and hypoxia-reoxygenation". Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/3857/.
Pełny tekst źródłaIbbotson, Kathryn, Joshua Yell i Patrick T. Ronaldson. "Nrf2 signaling increases expression of ATP-binding cassette subfamily C mRNA transcripts at the blood–brain barrier following hypoxia-reoxygenation stress". BIOMED CENTRAL LTD, 2017. http://hdl.handle.net/10150/623277.
Pełny tekst źródłaGonçalves, Julio Cesar de Souza Inácio. "Avaliação de metodologias para a determinação indireta do coeficiente de reoxigenação superficial (K2)". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/18/18138/tde-26102017-155547/.
Pełny tekst źródłaThe surface reoxygenation coefficient (K2) is the most important parameter in the water quality mathematical modelling in streams. It indirectly measures the ability of a water mass recover quality after a release of wastewater. Predictive techniques have been produced for estimating K2, but they achieved only partial success; some are inaccurate and others are expensive. This work includes contributions from experimental and theoretical studies about methods for the indirect determination of the surface reoxygenation coefficient. Studies were carried out in a jet-agitated vessel and were planned to assess the correlations between surface reoxygenation and physical phenomena, which are related to the new methods for the prediction of K2. The cooling of a solid metal, total dissolved solids (TDS) concentration decay, vertical component velocity near the free surface were the physical phenomena investigated. Mathematical models have been produced using linear regression analysis between K2 and thermal transfer coefficient (Kt), associated with the solid metal cooling; K2 vs. H (depth of the water in the vessel) and mass transfer coefficient by convection (hm), associated with the TDS concentration decay; and K2 and turbulence kinetic energy dissipation rate (ε), associated with the vertical component velocity near the free surface. Results revealed that there is a strong correlation between K2 and the physical parameters here investigated, statistically confirmed by correlation coefficients above 0,9. The applicability of the approach used here is limited to hydrodynamic conditions in which the tests were performed, once there is no theoretical basis, or experimental, indicating that the relations between the physical parameters are constant and independent of the turbulence level. It is suggested that field tests with the development of specific methods are a next step for future research, rendering useful the methods studied here.
Vanderlelie, Jessica, i n/a. "Placental Oxidative Stress in Preeclampsia". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060918.161726.
Pełny tekst źródłaAbujamara, Laís Donini. "Efeitos da pré-exposição ao cobre sobre respostas bioquímicas da anêmona-do-mar Bunodosoma cangicum a hipóxiae reoxigenação". reponame:Repositório Institucional da FURG, 2012. http://repositorio.furg.br/handle/1/4039.
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Os organismos bentônicos intermareais enfrentam oscilações periódicas nos níveis de oxigênio na água associadas ao ciclo de marés. Durante o recuo da maré, eles ficam expostos ao ar e sujeitos a hipóxia, favorecendo uma redução nas espécies reativas de oxigênio (ERO) e nas defesas antioxidantes. Porém, na reoxigenação há um aumento acentuado na geração de ERO. Para minimizar os prejuízos desse processo, existem mecanismos antecipatórios, tal como o aumento das defesas antioxidantes durante a hipóxia. Por sua vez, o estresse causado por poluentes químicos, como o cobre, pode alterar o padrão destas respostas. Neste estudo foram avaliadas respostas de biomarcadores associados ao estresse oxidativo e metabolismo (capacidade antioxidante total contra radicais peroxil - ACAP, atividade da superóxido dismutase - SOD, concentração de glutationa reduzida - GSH, peroxidação lipídica - LPO e concentração de ATP) na anêmona Bunodosoma cangicum pré-exposta (96 h) ao cobre (6,1 ± 2.7 μg.L-1) e submetida a hipóxia (6 h a 0.5 mgO2.L-1) seguida da reoxigenação (6 h a 7.5 mg O2.L-1). Nas anêmonas controle não foram observadas variações na ACAP, GSH, LPO e ATP. Entretanto, a atividade da SOD aumentou durante a hipóxia. Nas anêmonas pré-expostas ao cobre, a ACAP foi reduzida na hipóxia e reoxigenação. A atividade da SOD não se alterou e a concentração de GSH aumentou no início do experimento, na hipóxia e na reoxigenação. A concentração de ATP diminuiu na reoxigenação, porém a LPO não se alterou em todas as condições experimentais. Estes resultados indicam a existência de mecanismos antecipatórios para prevenção dos efeitos negativos da reoxigenação em B. cangicum e que a exposição ao cobre em concentração ambientalmente relevante afeta negativamente estes mecanismos.
Intertidal benthic organisms are subjected to changes in oxygen availability during the tidal cycle. A hypoxic condition may occur during air exposure, thus favoring a decreased level of oxygen reactive species (ROS) and antioxidant defenses. However, during re-oxygenation a ROS overproduction may occur. Anticipatory mechanisms such as a buildup of antioxidant defenses under hypoxia could be present to avoid a possible oxidative damage occurring during these processes. In turn, chemical stress induced pollutants such as copper may affect the response of these mechanisms. In the present study, the response of biomarkers associated with oxidative stress and energy (total antioxidant capacity against peroxyl radicals - ACAP, superoxide dismutase activity - SOD, lipid peroxidation - LPO, reduced glutathione - GSH, and ATP concentration) were evaluated in the sea anemone Bunadosoma cangicum pre-exposed (96 h) to copper (6.1 ± 2.7 μg.L-1) and submitted to hypoxia (6 h at 5 mg O2.L-1) followed by re-oxygenation (6 h at 7.5 mg O2.L-1). In sea anemones kept under control conditions, ACAP, GSH concentration, LPO and ATP concentration did not change over the experimental time. However, SOD activity was increased under hypoxia. In sea anemones pre-exposed to copper, ACAP was reduced under hypoxia and re-oxygenation. GSH concentration was increased during hypoxia and reoxygenation, while ATP concentration was reduced during re-oxygenation. These findings indicate that B. cangicum shows anticipatory mechanisms to avoid the oxidative stress during re-oxygenation and that pre-exposure to an environmentally relevant concentration of copper affects these mechanisms.
Vanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Caligtan, Marc J. "Ischemic Preconditioning Protects Adult Rat Cardiomyocytes Against Necrosis but not Apoptosis, via Activation of PKG". VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1442.
Pełny tekst źródłaMatsubayashi, Keiko. "Contribution of cytochrome P450 3A pathway to bromocriptine metabolism and effects of ferrous iron and hypoxia-reoxygenation on its elimination in the perfused rat liver". Kyoto University, 1997. http://hdl.handle.net/2433/202219.
Pełny tekst źródłaKanji, Hussein D. "Differential roles for sarcK¦A¦T¦P and mitoK¦A¦T¦P channels in hypoxia and reoxygenation injury, a study of cell viability and ion channel pharmacology". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ64965.pdf.
Pełny tekst źródłaCosta, Daniel Jadyr Leite. "Estudo da influência de macro-rugosidades do leito de um canal hidráulico sobre o coeficiente de reoxigenação superficial". Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/18/18138/tde-11052011-085142/.
Pełny tekst źródłaThe parameter that determines the process of oxygen transfer through the air-water interface in flows with free surface is the superficial reaeration coefficient, \'K IND.2\'. There are a large quantity of equations in the cientific literature that perform the prevision of the reaeration coefficient; however, most of them consider only some of the hydraulic characteristics of water body; for example, the velocity and the depth. Most of these equations have empirical origin and are adequate just for a specific water body. In addition to these two parameters (velocity and depth of flow), there are another twelve important parameters in reoxygenation studies in superficial waters. In this context, the aim of this work was to study the influence of bed roughness of a channel on the superficial reaeration coefficient, under laboratory conditions. Besides the roughness, the conditions of mean velocity of the flow and depth of water were varied. The variation of roughness was done with implementation of obstacles with known geometry, arranged transversely to the flow direction, and called macro-roughness. The results have shown evidences that the surface reaeration coefficient is controlled significantly by the roughness of the channel bed. Two mathematical models of semi-empirical origin for the \'K IND.2\' prevision were developed, which incorporate hydrodynamic and geometric variables considered relevant in the process of mass transfer in air-water interface.
Silveira, Alexandre. "Influência da umidade atmosférica sobre o mecanismo de transferência de gases através da interface água-atmosfera". Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/18/18138/tde-29082016-091551/.
Pełny tekst źródłaThe influence of the atmospheric humidity on the process of absorption of oxygen by a water body through its free surface is presented herein. Laboratory experiments were run for the reoxygenation of a water mass kept in a cylindrical vessel under mechanical agitation. The quality of the atmospheric air transferring oxygen to water is controlled and the tests are run with several levels of air humidity, what renders different rates of evaporation. The corresponding coefficients of reaeration K2 (h-1) are determined for each experiment. The correlation between these two latter parameters is investigated. The process of reoxygenation is analyzed initially using a classical methodology based on traditional mathematical models (possibly inadequate). An original model for the same analysis is proposed in this work.
Wagner, Kay-Dietrich. "Effekte von Hypoxie und Reoxygenierung auf die kontraktile Funktion von Vorhoftrabekeln und Rattenpapillarmuskeln - Möglichkeiten der Protektion". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 1998. http://dx.doi.org/10.18452/14401.
Pełny tekst źródłaThis study characterizes the contractile function of human atrial trabeculae and rat left ventricular papillary muscles during hypoxia / reoxygenation as the major components of ischemia / reperfusion. Further characteristics of ischemia were simulated by increased extracellular K+ concentration and acidosis during hypoxia. Insights into the cellular Ca2+ regulation were obtained from action potential recordings, from measurements of sarcoplasmic reticulum (SR) Ca2+ transport, and from force-interval relations. We examined changes in SR calcium transport, creatine kinase (CK) system, the antioxidant enzymes glutathionperoxidase (GSH-Px) and superoxiddismutase (SOD) 6 wks. after infarction (MI) due to coronary ligation in rats. Phenotypic modifications vs. sham operation (SHAM) were related to the contractile response of hypertrophied papillary muscle to hypoxia / reoxygenation. The oxygen radical scavengers histidine and butylhydroxytoluene were applied during hypoxia and rapid reoxygenation to protect the myocardium against oxygen radical damage. Generally, human atrial trabeculae were less sensitive to reduced oxygen supply and reoxygenation when compared to rat papillary muscles. In human atrial trabeculae, isometric peak force development recovered better after simulated ischemia than after hypoxia but the regulation of contractile function was clearly disturbed. In rat papillary muscles, rapid reoxygenation caused a better recovery of contractile function after hypoxia. Application of the oxygen radical scavengers histidine, butylhydroxytoluene, and especially their combination during hypoxia / reoxygenation had additional cardioprotective effects. In MI vs. SHAM we observed under aerobic control conditions: decreses in isometric contraction and relaxation rate, a reduced Vmax-equivalent of sarcomeric shortening, a faster twitch-to- twitch decay of post-rest potentiation (PRC) which correlated closely to the decrease in SR Ca2+ uptake (-25%), a decrease in CK activity (-20%), reduced CK-MI and CK-MM, increased CK-MB and CK-BB, and enhanced activities of SOD (+40%) and GSH-Px (+50%). During hypoxia, an initial increase in peak force (PF) was followed by a slower PF decline in MI vs. SHAM. During reoxygenation, rates of contraction and relaxation recovered better in MI. In SHAM but not MI, twitch-to-twitch decay of PRC was accelerated after reoxygenation vs. aerobic control. The results suggest that adaptive changes in SR Ca2+ handling, CK isoenzymes, and antioxidant enzymes may contribute to higher resistance against reduced O2 supply and reoxygenation in hypertrophy due to MI.
Chen, Hongjiang. "Studies on Cell Injury Induced by Hypoxia-Reoxygenation and Oxidized Low Density Lipoprotein : With Special Reference to the Protectiove Effect of Mixed Tocopherols, Omega-3 Fatty Acids and Transforming Growth Factor-beta1". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3769.
Pełny tekst źródłaBravo, Daniela Manzoli [UNIFESP]. "Avaliação das cinéticas do consumo de oxigênio e da reoxigenação muscular esquelética na recuperação do exercício de alta intensidade em pacientes com miopatia mitocondrial: implicações sobre os mecanismos de intolerância ao exercício". Universidade Federal de São Paulo (UNIFESP), 2011. http://repositorio.unifesp.br/handle/11600/9055.
Pełny tekst źródłaFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Introdução: Os pacientes com Miopatia Mitocondrial (MM) e Oftalmoplegia Externa Progressiva (OEP) apresentam disfunção na cadeia respiratória com incapacidade de aumentar a extração de oxigênio muscular e sintetizar ATP aerobicamente, levando à intolerância ao esforço e lentificação da cinética do O2. Quando a extração de oxigênio é comprometida, na tentativa de se manter o consumo de oxigênio muscular, uma hipótese é que estes pacientes poderiam aumentar compensatoriamente a oferta de oxigênio, apresentando, assim, uma resposta hipercinética cardiovascular e ventilatória. Por outro lado, alguns indícios de menor oferta de oxigênio foram encontrados em pacientes com MM, como um menor fluxo sanguíneo muscular no antebraço e uma maior capacidade de produção de ATP após a suplementação de oxigênio. A cinética do O2 na fase de recuperação (REC) nos fornece, assim, subsídios quanto ao pagamento do débito de oxigênio tecidual e ao reabastecimento do estoque de oxigênio sanguíneo após o exercício. Ao nosso conhecimento, a cinética do O2 REC nunca foi avaliada nos pacientes com MM, assim como a integração desta variável com as respostas não-invasivas cardiovasculares e de extração de oxigênio muscular. Objetivo: contrastar as dinâmicas da oferta e da utilização de oxigênio na recuperação do exercício em pacientes com MM; e identificar os principais mecanismos fisiopatológicos da intolerância ao esforço nestes indivíduos. Métodos: Foram avaliadas em 12 pacientes com MM e 12 controles saudáveis, as cinéticas de recuperação: (i) do O2 pulmonar, (ii) da variação na concentração da deoxiemoglobina ([HHb], mensurada pela espectroscopia de raios quasi infravermelhos - NIRS) no vasto lateral, (iii) do débito cardíaco (DC) por bioimpedância transtorácica, após um teste de carga constante de alta intensidade (70% da carga máxima atingida em teste incremental prévio) até o limite da tolerância em cicloergômetro. Resultados: Foram observadas cinéticas mais lentas de reoxigenação da [HHb], ([HHb] = 43,7 ± 21,2 vs 27,5 ± 6,7) e do O2 ( O2 = 58,1 ± 25,1 vs 38,8 ± 7,6) nos pacientes com MM em relação aos controles, respectivamente. Estas respostas foram associadas a uma cinética de DC mais rápida em relação ao O2, nos pacientes comparados aos controles (T½DC * 1,44 / O2 = 1,3 ± 0,4 vs 1,7 ± 0,6). Conclusão: Os pacientes com MM na forma OEP apresentam, na recuperação do exercício de alta intensidade, um pagamento elevado do débito de oxigênio contraído no exercício e reoxigenação mais lenta da [HHb]. Estas respostas, associadas à cinética mais rápida do DC em relação ao O2 são indícios de que possa haver um déficit no transporte de oxigênio microvascular, além do comprometimento mitocondrial característico desta doença.
Background: Mitochondrial Myopathy patients (MM) and Progressive External Ophthalmoplegia (PEO) present with respiratory chain dysfunction and inability to increase muscle oxygen extraction and aerobic ATP synthesis, leading to exercise intolerance and slower O2 kinetics. When oxygen extraction is impaired, in an attempt to maintain muscle oxygen uptake, these patients could increase oxygen delivery, thus exhibiting a hyperkinetic cardiovascular and ventilatory response. On the other hand, some evidence of oxygen delivery impairment was found in MM patients, such as a decrease in muscle blood flow in the forearm and a greater capacity for ATP production after oxygen supplementation. Recovery O2 kinetics provides information on tissue oxygen debt repayment and oxygen blood store replenishment after exercise. To our knowledge, recovery O2 kinetics has never been evaluated in MM patients, as well as its integration with the non-invasive cardiovascular and muscle reoxygenation responses. Objective: to contrast oxygen delivery and utilization dynamics on exercise recovery of MM patients and to identify the main pathophysiologic mechanisms of exercise intolerance in these subjects. Methods: Were evaluated in 12 MM patients and 12 healthy controls, the recovery kinetics of: (i) O2 (ii) deoxyhemoglobin variation ([HHb], measured by near-infrared spectroscopy - NIRS) in vastus lateralis, (iii) cardiac output (CO) by transthoracic bioimpedance, after a high-intensity constant work rate test (70% of maximal workload in a previous incremental test) to the limit of tolerance in a cycle ergometer. Results: We detected slower kinetics for [HHb] ([HHb] = 43.7 ± 21.2 vs. 27.5 ± 6.7) and for O2 ( O2 = 58.1 ± 25.1 vs. 38.8 ± 7.6) in MM patients compared to controls, respectively. Additionally, these responses were associated with a faster recovery CO kinetics in relation to O2 kinetics in MM patients compared to controls (T½DC*1,44 / O2 = 1,3 ± 0,4 vs. 1,7 ± 0,6). Conclusion: Patients with MM and PEO present with a higher oxygen debt and slower reoxygenation kinetics in the recovery of a high-intensity exercise test. Those responses were associated with a faster CO recovery in relation to O2 kinetics, indicating a microvascular oxygen transport deficit, besides the characteristic mitochondrial impairment observed in these patients.
TEDE
BV UNIFESP: Teses e dissertações
Maia, Guilherme Del Nero. "Análise dos parâmetros cinéticos no fenômeno da reoxigenação e desoxigenação da água". Universidade de São Paulo, 2003. http://www.teses.usp.br/teses/disponiveis/18/18138/tde-17102016-154830/.
Pełny tekst źródłaThe reoxygenation in wastewater is seen in the technical literature in an analogous way as the reoxygenation of clean water. The effects of the oxygen consumed by active bacteria population are quantified with the introduction of the parameters alpha and beta. Alpha corrects for the volumetric mass transfer coefficient and beta corrects for the dissolved oxygen saturation concentration. The present research intends to make explicit the kinetic of the process, in order to supply conceptual support to a better understanding of the phenomenon. The research is done through experimental work, followed by conceptual, mathematical modeling. Stripping with nitrogen is used as an oxygen sink instead of microorganisms. Thus, a physical process replaces the biochemical process. The proposed mathematical model fitted well to the experimental data, and its validation could be obtained through the statistical analyses done.
Aubert, Vivien. "Lésions d'ischémie-reperfusion rénale en transplantation : modélisation par agents des effets de l’oxygénation sur la dynamique cellulaire-tissulaire de l'inflammation et de la fibrose". Thesis, Poitiers, 2015. http://www.theses.fr/2015POIT1405/document.
Pełny tekst źródłaIn renal preservation-transplantation, ischemia-reperfusion (IR) causes graft inflammation and fibrosis, dysfunction and loss. Events involved in IR injury grow identified, but their intricacy hampers prediction and therapeutics. Based on a detailed bibliographical analysis, we propose an Agent-Based Model of renal response to IR injury at cell and tissue levels, created with the modeling tool NetLogo.First, we develop and validate a dynamic model of the oxygenation of the renal cortex, featuring blood perfusion, oxygen diffusion, and oxygen consumption (driven by sodium filtered load and transport). We then adapt this model to oxygen steady-state, and PO2 level is coupled to energetic status (ATP) in epithelial and endothelial cells (aerobic and anaerobic pathways). Cell viability is coupled to ATP level, leading to a semi-phenomenological representation of repair/survival versus apoptosis/necrosis. Finally, we explore (and verify) cell and tissue fate during simulated IR sequences, with the gradual addition of key elements of inflammation (leukocytes infiltration, injury signals, phagocytosis) and fibrosis (fibroblasts, collagen). Model evolution toward the resolution of inflammation/tissue regeneration or toward tissue fibrosis is observed along imposed conditions (duration/intensity, ischemia vs hypoxemia). Results are compared to experiments from our laboratory.This construction is the first model of the effects of oxygenation on cell-tissue dynamics during renal inflammation-fibrosis response to IR. Ultimately, it will allow to address clinical and therapeutic aspects of renal transplantation and conservation
Jan, Budour H. 1984. "The Role of Kindlin-2 in the progression of renal fibrosis". Doctoral thesis, Universitat Pompeu Fabra, 2017. http://hdl.handle.net/10803/543848.
Pełny tekst źródłaLa enfermedad renal crónica (ERC) se caracteriza habitualmente por lesiones histológicas relacionadas con la glomeruloesclerosis y la fibrosis tubulointersticial (FTI). La progresión de la FTI se induce por múltiples mecanismos moleculares como factores de transcripción, toxinas metabólicas y moléculas de estrés. Uno de los mediadores clave en esta progresión es TGF-1 que induce respuestas en gran variedad de tipos celulares. En las células tubulares renales, la activación del TGF-1 requiere la unión de Kindlin-2 al receptor de TGF-1. La expresión de Kindlin-2 se testó en tres condiciones de lesión distintas y se encontró su correlación con la progresión del proceso fibrótico renal. Después de 48 horas, 7 días y 45 días tras una lesión isquémica, el tejido renal de ratón expresó Kindlin-2 de una forma similar durante la evolución del proceso fibrótico. En las biopsias humanas con características compatibles con la necrosis tubular aguda (NTA), Kindlin-2 se detectó en varias zonas del tejido renal. Se describió una alta expresión en túbulos y en células de músculo liso de las arterias se encontró disminuido. Este perfil fue opuesto en las biopsias sin características histológicas de NTA. Kindlin-2 está activado en los procesos más inmediatos en la lesión y se mantiene a lo largo de la progresión, asumiendo un papel necesario en este proceso.
Assaly, Rana. "Protection du myocarde ischémique et pore géant mitochondrial : applications pharmacologiques". Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00734466.
Pełny tekst źródłaPomper, Jörn K. "Interaktion zwischen Sauerstoffspannung und epileptiformer Aktivität und deren Einfluss auf Zellschäden in juvenilen organotypischen hippokampalen Schnittkulturen der Ratte". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2006. http://dx.doi.org/10.18452/15416.
Pełny tekst źródłaHippocampal damage during infancy is thought to play an important role in the pathogenesis of temporal lobe epilepsy. Epileptic seizures and perinatal asphyxia are two frequent causes of these damages. Sustained epileptiform activity induced in the low Mg2+-model of epileptic seizures leads to cell damage in organotypic hippocampal slice cultures (OHSC) of the rat, which are used as a surrogate for the infantile hippocampus. During a previous study utilising this model the suspicion arose that increased oxygen tension could have an additional damaging effect. My first series of experiments proved that increased oxygen tension (60 %, 95 %) lead to reversible and irreversible cell damage in OHSC compared to 20%-oxygen tension. Cell damage was determined by alterations of evoked field potentials, i.e. decrement of amplitude, increment of latency and paired pulse index, as well as by propidium iodide fluorescence. The second series of experiments showed that increased oxygen tension applied after an hypoxic period (hyperoxic reoxygenation) result in augmented cell damage compared to normoxic reoxygenation. With the third series of experiments it could be excluded that increased oxygen tension is an essential condition for the occurrence of cell damage due to sustained epileptiform activity. In order to elucidate the damaging role of spreading depressions (SD), which emerge during epileptiform activity, a method was established in the fourth series of experiments that allowed the reliable induction of SD-like events in normoxic OHSC. Repetitive SD-like events induced by this method led to cell damage, assessed by alterations of electrophysiological characteristics of SD-like events, decrement of evoked field potential amplitude and propidium iodide fluorescence.
Le, Pape Sylvain. "Rôle de la réponse au mauvais repliement protéique dans l'endothélium vasculaire au cours de l'hypoxie-réoxygénation". Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT1411.
Pełny tekst źródłaIschemia-reperfusion injury (IRI) is a syndrome combining the cessation of blood flow followed by its reestablishment in the organ. IRI is encountered in various pathologies including acute coronary syndrome, vascular surgery but also solid organ transplantation at the time of organ preservation. Ischemia induces numerous metabolic disorders resulting in cellular stress among which the mitochondria and the endoplasmic reticulum (ER) are the most injured organelles.Our research project aimed at understanding the impact of ER stress and its response, the Unfolded Protein Response (UPR), during IRI. We investigated the activation kinetics and the specific role of each UPR pathway – IRE1α–XBP1, PERK-eIF2α-ATF4 and ATF6 – on the survival of human arterial endothelial cells subjected to different durations of IR. We observed a successive activation of PERK-eIF2α-ATF4, ATF6 and IRE1α-XBP1 pathways proportionally to the duration of cold ischemia. We employed bioinformatics methods, pharmacological agents and post-transcriptional gene silencing techniques (siRNA) and we observed that ATF6 pathway was detrimental, that PERK-eIF2α-ATF4 was protective only when pharmacologically over-activated, and that IRE1α-XBP1 pathway has a dual role.By extrapolating these to the clinics, our results support the UPR as a therapeutic target to improve graft survival and the quality of life of the transplanted patients but also they indicate a possible use of UPR mediators as biomarkers of organ quality during transplantation
Bensaid, Samir. "Mise en place de contre-mesures pour limiter la perte protéique de cellules musculaires squelettiques consécutive à l’hypoxie cellulaire". Thesis, Lille 2, 2019. http://www.theses.fr/2019LIL2S021.
Pełny tekst źródłaBackground and aims : Chronic exposure to severe hypoxia has deleterious effects on the muscular system, in particular on skeletal muscle mass. Hypoxia leads to imbalance of protein homeostasis, decreasing protein synthesis (mainly regulated through PI3K-Akt-mTOR pathway) while increasing protein degradation (mainly through autophagy and proteasomal degradation). In contrast, mechanical stimuli and nutrients, particularly the branched-chain amino acids (BCAA), induce activation of the mTOR pathway in human and rat skeletal muscle as well as and in cultured muscle cells, and decrease protein catabolism. In a model of skeletal muscle cell culture, we attempt to determine whether the combination of mechanical stimulation, nutritional supplementation and reoxygenation could reverse the deleterious effects of hypoxia on protein homeostasis.Experimental methodsWe induced a hypoxic stress on skeletal muscle murine cells differentiated into myotubes C2C12: four days after differentiation, the C2C12 myotubes were placed into a hypoxic chamber at 4% O2 for 24h. Electrical stimulation was applied to the cells using a pulse generator to provide electric pulses. Following the ES treatment, myotubes were firstly supplemented with branched-chain amino acids (BCAA: mixture of leucine, isoleucine and valine added to culture media) while placed to normoxia during 2 hours (corresponding so to a reoxygenation protocol).ResultsAfter 24 hours of hypoxia, the morphological analysis of myotubes shows a significant decrease in their diameter, translating the activation of protein degradation pathways at the expense of protein synthesis pathways. When applied separately, each treatment has little effect on the mTOR pathway and morphology of myotubes. However, the combination of electrical stimulation, supplementation BCAA and reoxygenation lead to an increase of the phosphorylation of key proteins involved in protein synthesis pathway (Akt and p70S6 kinase), thus reflecting their activation state. In addition, morphological analysis shows a significant increase in myotube diameter and fusion index (reflecting the state of differentiation), a sign of the presence of muscle hypertrophy.ConclusionOur preliminary results suggested that mTOR pathway responds to a combination of electrostimulation, nutrient supplementation and reoxygenation by phosphorylation of key regulators of protein synthesis, and could reverse the protein loss induced by hypoxia
Feliu, Catherine. "Implication des récepteurs P1 et P2 dans la protection des cellules endothéliales au cours de l’hypoxie-reoxygenation Complementary Role of P2 and adenosine receptors in ATP induced-anti-apoptotic effects against hypoxic injury of HUVECs Current knowledge on the role of P2Y receptors in cardioprotection against ischemia-reperfusion Intra-extracellular quantification of nucleotides and adenosine using UHPLCHRMS: improvement of robustness by the use of ascorbic acid in mobile phase Description of the novel cytoprotective action pathways of ticagrelor against hypoxic lesions at the endothelium". Thesis, Reims, 2019. http://www.theses.fr/2019REIMM202.
Pełny tekst źródłaDuring cardiac ischemia, the lesion is triggered in the endothelium and progresses to the surrounding cardiomyocytes. Purinergic signalling plays an important role during ischemia/reperfusion (I/R) events. Many studies have been carried out to study the mechanisms of protection of nucleotides and nucleosides, without studying their specific roles on the endothelium. In this work, we report an increase in extracellular concentrations of ATP and adenosine from the endothelium exposed to hypoxia. We report a protective effect of extracellular ATP and a complementary role of the P2 and P1 receptors. P2 receptors protective effects involve the PI3K, ERK1/2, mKATP channel signalling and also involve NOS. The protection mediated by the P1 receptors involves the MEK/ERK1/2, PKA and NOS. In a second step, we describe a new cytoprotective mechanism of ticagrelor, independent of the blood element and its antiplatelet anti-aggregating effect. This mechanism is initiated by the increased of extracellular adenosine bioavailability, which triggers protective effects via its A3 and A2A receptors. This may explain, in part, the reported cardioprotective effects of the ticagrelor in clinical studies. Together, our data support the protective role of ATP and adenosine against deleterious effects ofendothelium hypoxia and suggest a beneficial role for these mediators in different ischemia, including cardiac, renal or cerebral ischemia
Lai, Mei-Hsiu, i 賴美秀. "Hypoxia and Reoxygenation Induced Arrhythmogenesis on Pulmonary Vein and Atrium". Thesis, 2010. http://ndltd.ncl.edu.tw/handle/53403595875130821697.
Pełny tekst źródła國防醫學院
生理學研究所
98
Introduction Atrial fibrillation (AF) is the most important clinical arrhythmia which induces cardiac dysfunction and increase mortality and morbidity. Ischemia -reperfusion injury is a common condition after heart transplantation. Studies on hypoxia/reoxygenation-induced AF is associated with significant morbidities. Pulmonary veins (PVs) were known to be important sources of ectopic beats with the initiation of paroxysmal atrial fibrillation and the foci of ectopic atrial tachycardia. Aim The purpose of this study is to examine the effects of hypoxia and reoxygenation in the electrophysiological characteristics of pulmonary vein (PV), left atrium (LA) and right atrium (RA) and to investigate the role of ATP sensitive potassium channel (KATP) and oxidative stress in the genesis of ischemia/reperfusion induced atrial fibrillation. Methods and Methods Conventional microelectrodes were used to record action potential (AP) and a transducer to record contractile force after superfusion of hypoxia (95% N2+5% CO2) and reoxygenation (97% O2+3% CO2) application in isolated right superior PV, LA and RA tissue samples obtained from rabbits. Acute exposed to glibenclamide 100μM (a K+ATP channel blockers) or pinacidil 30μM (a K+ATP channel openers) in the presence of hypoxia on PV and LA. Acute exposed to N-mercaptopropionyl-glycine 5mM (N-MPG, free radical •OH scavenger) and chloramphenicol 300μM (CA, an antibiotics) in the presence of reoxygenation on PV. Results (1) Hypoxia decreased the PV spontaneous rates from 1.75±0.14 Hz to 0.83±0.11 Hz and after reoxygenation PV spontaneous rates was recovered but not to control level. Hypoxia and reoxygenation easily induced early afterdepolarizations (EAD)、delayed afterdepolarizations (DAD) and burst firings in PV. (2) Hypoxia shortened APD90 in PV and LA. After reoxygenation on PV, APD90 was recovered but not in LA. In addition, hypoxia and reoxygenation had no significant effects on APD90 in RA. However hypoxia caused to decrease in contractile force in both LA and RA, and recovered partially after reoxygenation. (3) Hypoxia-induced pacemaker activity decreasing was eliminated by exposure to glibenclamide (100μM) on PV. In addition, pinacidil (30μM) administration could significantly decrease spontaneous rates. Simultaneous exposure to both glibenclamide (100μM) and hypoxia abolished the reduction in APD90 of hypoxia alone on PV and LA. (4) N-MPG (5mM) administration in the presence of reoxygenation on PV could decrease incidence of burst firing induced by reoxygenation. (5) Pre-treatment with chloramphenicol (300μM) in the presence of reoxygenation, spontaneous rates was significantly recovered and decreased incidence of burst firing induced by reoxygenation. (6) Pre-treatment with chloramphenicol (300μM) in the presence of reoxygenation compared with reoxygenation alone, ROS was significantly decreased. Conclusions The present experiments show that hypoxia and reoxygenation significantly increases PV arrhythmogenesis mainly through an generation of ROS. Hypoxia /reoxygenation-induced arrhythmia were suppressed by the administration of chloramphenicol through an inhibition of ROS. In addition, K+ATP channel played a role of protection. It could protect against Hypoxia-induced arrhythmia.
Shin, Eyun-Jung. "Leptin protects rat cardiomyocytes from H2O2-and hypoxia/reoxygenation-induced Apoptosis /". 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR51626.
Pełny tekst źródłaTypescript. Includes bibliographical references (leaves 77-94). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR51626
Dixon, Ian M. C. "Altered sarcolemmal Na+-C2+ exchange in hearts subjected to hypoxia-reoxygenation". 1987. http://hdl.handle.net/1993/24437.
Pełny tekst źródłaFang, Chih-Wen, i 方治文. "Biological effects of reoxygenation on hypoxia-treated clear cell renal cell carcinoma". Thesis, 2013. http://ndltd.ncl.edu.tw/handle/72645935398026289024.
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