Relevant bibliographies by topics / Reoxygenation

Academic literature on the topic 'Reoxygenation'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Reoxygenation"

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Hung, Tai-Ho, Jeremy N. Skepper, D. Stephen Charnock-Jones, and Graham J. Burton. "Hypoxia-Reoxygenation." Circulation Research 90, no. 12 (June 28, 2002): 1274–81. http://dx.doi.org/10.1161/01.res.0000024411.22110.aa.

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Greene, E. L., and M. S. Paller. "Xanthine oxidase produces O2-. in posthypoxic injury of renal epithelial cells." American Journal of Physiology-Renal Physiology 263, no. 2 (August 1, 1992): F251—F255. http://dx.doi.org/10.1152/ajprenal.1992.263.2.f251.

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The hypothesis that posthypoxic renal injury is mediated by xanthine oxidase-derived oxygen free radical production was tested in an in vitro model of rat proximal tubule epithelial cells in primary culture subjected to 60 min of hypoxia and 30 min of reoxygenation. Hypoxia-reoxygenation-induced injury, measured as lactate dehydrogenase (LDH) release, was 54.0 +/- 7.1%. Inhibition of xanthine oxidase by 10(-4) M allopurinol attenuated injury (LDH release = 35.5 +/- 3.7%; P less than 0.01). Oxypurinol was similarly effective. Alternatively, cells were treated with 50 or 100 microM tungsten to inactivate xanthine oxidase. Tungsten prevented hypoxia-reoxygenation-induced superoxide radical production (basal = 97 +/- 8, hypoxia-reoxygenation = 172 +/- 12, and plus tungsten = 73 +/- 8 nmol/micrograms protein) and attenuated hypoxia-reoxygenation-induced injury (LDH release: basal = 18.8 +/- 3.0%, hypoxia-reoxygenation = 62.0 +/- 4.8%, plus 50 microM tungsten = 24.8 +/- 5.0%, and plus 100 microM tungsten = 6.0 +/- 0.7%). In addition, hypoxia and reoxygenation increased the ratio of xanthine oxidase to total activity (xanthine oxidase + xanthine dehydrogenase) from 73 to 100%. Therefore xanthine oxidase was responsible for hypoxia-reoxygenation-induced superoxide radical formation and hypoxia-reoxygenation-induced injury. Xanthine oxidase is likely to be the major source of oxygen free radicals during renal ischemia and reperfusion.
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Seiler, K. S., J. P. Kehrer, and J. W. Starnes. "Effect of perfusion pressure at reoxygenation on reflow and function in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 4 (April 1, 1992): H1029—H1035. http://dx.doi.org/10.1152/ajpheart.1992.262.4.h1029.

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The effect of coronary perfusion pressure during reoxygenation on recovery of endocardial flow, arrhythmogenesis, and mechanical function was investigated in the isolated rat heart. Hearts were subjected to 30 min of substrate-free hypoxia followed by 30 min reoxygenation at either 80 or 150 cmH2O perfusion pressure. No flow areas were quantified by 0.3% phthalocyanine blue injection after 30 min of hypoxia, 30 min reoxygenation at 80 cmH2O, or 30 min reoxygenation at 150 cmH2O. After hypoxia, 31 +/- 2% of the myocardium was unperfused. After 80 cmH2O reoxygenation, 13 +/- 4% of the heart remained unperfused. Ten of 12 (83%) 80-cmH2O hearts were in sustained fibrillation after 10 min of reoxygenation. Reoxygenation at 150 cmH2O resulted in complete reperfusion of the myocardium. Fibrillation was absent in all hearts reoxygenated at this higher pressure. Functional recovery after 30 min reoxygenation (% of normoxic heart rate x left ventricular developed pressure) was significantly (P less than 0.05) higher in 150 cmH2O vs. 80 cmH2O (60 +/- 5 vs. 42 +/- 8%). Elevating perfusion pressure upon reoxygenation appears to counter the vascular compression caused by contracture and leads to a more rapid and homogeneous restoration of coronary flow during the transition from the hypoxic to the normoxic state.
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Corno, Antonio F., and Michele Samaja. "The reoxygenation phenomenon." Journal of Thoracic and Cardiovascular Surgery 105, no. 2 (February 1993): 373. http://dx.doi.org/10.1016/s0022-5223(19)33831-0.

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DEJONG, J. "Reperfusion/reoxygenation—Introduction." Journal of Molecular and Cellular Cardiology 19 (1987): S16. http://dx.doi.org/10.1016/s0022-2828(87)80055-x.

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Hempel, S. L., D. L. Haycraft, J. C. Hoak, and A. A. Spector. "Reduced prostacyclin formation after reoxygenation of anoxic endothelium." American Journal of Physiology-Cell Physiology 259, no. 5 (November 1, 1990): C738—C745. http://dx.doi.org/10.1152/ajpcell.1990.259.5.c738.

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Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesting that cyclooxygenase activity, but not prostacyclin synthase, is affected by reoxygenation. A decrease in arachidonic acid release from cellular lipids also occurred. The reduction in cyclooxygenase activity, but not arachidonic acid release, was prevented by the presence of ibuprofen during reoxygenation. Addition of catalase or superoxide dismutase during reoxygenation increased PGI2 release but did not completely overcome the reduction relative to control cultures. These findings suggest that the increase in platelet adherence during reoxygenation may be mediated in part by a change in cyclooxygenase activity. This is only partly overcome by extracellular oxygen species scavengers but is prevented by the presence of a reversible cyclooxygenase inhibitor during reoxygenation.
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Ihnken, Kai, Kiyozo Morita, and Gerald D. Buckberg. "Delayed cardioplegic reoxygenation reduces reoxygenation injury in cyanotic immature hearts." Annals of Thoracic Surgery 66, no. 1 (July 1998): 177–82. http://dx.doi.org/10.1016/s0003-4975(98)00320-8.

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Zhang, Yanmei, Gaoyong Chen, Shuping Zhong, Fuchun Zheng, Fenfei Gao, Yicun Chen, Zhanqin Huang, et al. "N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/912310.

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N-n-butyl haloperidol iodide (F2) has been shown to antagonize myocardial ischemia/reperfusion injury by blocking calcium channels. This study explores the biological functions of ERK pathway in cardiomyocytes hypoxia/reoxygenation injury and clarifies the mechanisms by which F2ameliorates cardiomyocytes hypoxia/reoxygenation injury through the extracellular-calcium-dependent and -independent ERK1/2-related pathways. In extracellularcalcium-containing hypoxia/reoxygenation cardiomyocytes, PKCαand ERK1/2 were activated, Egr-1 protein level and cTnI leakage increased, and cell viability decreased. The ERK1/2 inhibitors suppressed extracellular-calcium-containing-hypoxia/reoxygenation-induced Egr-1 overexpression and cardiomyocytes injury. PKCαinhibitor downregulated extracellularcalcium-containing-hypoxia/reoxygenation-induced increase in p-ERK1/2 and Egr-1 expression. F2downregulated hypoxia/reoxygenation-induced elevation of p-PKCα, p-ERK1/2, and Egr-1 expression and inhibited cardiomyocytes damage. The ERK1/2 and PKCαactivators antagonized F2’s effects. In extracellular-calcium-free-hypoxia/reoxygenation cardiomyocytes, ERK1/2 was activated, LDH and cTnI leakage increased, and cell viability decreased. F2and ERK1/2 inhibitors antagonized extracellular-calcium-free-hypoxia/reoxygenation-induced ERK1/2 activation and suppressed cardiomyocytes damage. The ERK1/2 activator antagonized F2’s above effects. F2had no effect on cardiomyocyte cAMP content or PKA and Egr-1 expression. Altogether, ERK activation in extracellular-calcium-containing and extracellular-calcium-free hypoxia/reoxygenation leads to cardiomyocytes damage. F2may ameliorate cardiomyocytes hypoxia/reoxygenation injury by regulating the extracellular-calcium-dependent PKCα/ERK1/2/Egr-1 pathway and through the extracellular-calcium-independent ERK1/2 activation independently of the cAMP/PKA pathway or Egr-1 overexpression.
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Doctor, R. B., and L. J. Mandel. "Minimal role of xanthine oxidase and oxygen free radicals in rat renal tubular reoxygenation injury." Journal of the American Society of Nephrology 1, no. 7 (January 1991): 959–69. http://dx.doi.org/10.1681/asn.v17959.

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The role of xanthine oxidase and oxygen free radicals in postischemic reperfusion injury in the rat kidney remains controversial. Proximal tubules, the focal segment affected by ischemic renal injury, were isolated in bulk, assayed for xanthine oxidase activity, and subjected to 60 min of anoxia or hypoxia and 60 min of reoxygenation to evaluate the participation of xanthine oxidase and oxygen radicals in proximal tubule reoxygenation injury. The total xanthine oxidase in isolated rat proximal tubules was 1.1 mU/mg of protein, approximately 30% to 40% of the activity found in rat intestine and liver. Lactate dehydrogenase release, an indicator of irreversible cell damage, increased substantially during anoxia (39.8 +/- 2.3 versus 9.8 +/- 1.8% in controls) with an additional 8 to 12% release during reoxygenation. Addition of 0.2 mM allopurinol, a potent xanthine oxidase inhibitor, and dimethylthiourea, a hydroxyl radical scavenger, failed to protect against the reoxygenation lactate dehydrogenase release. Analysis of xanthine oxidase substrate levels after anoxia and flux rates during reoxygenation indicates that hypoxanthine and xanthine concentrations are in a 15-fold excess over the enzyme Km and 0.3 mU/mg of protein of xanthine oxidase activity exists during reoxygenation. Hypoxic tubule suspensions had a minimal lactate dehydrogenase release during hypoxia and failed to demonstrate accelerated injury upon reoxygenation. In conclusion, although xanthine oxidase is present and active during reoxygenation in isolated rat proximal tubules, oxygen radicals did not mediate reoxygenation injury.
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Agulló, Luis, David García-Dorado, Javier Inserte, Amaya Paniagua, Pasi Pyrhonen, Joan Llevadot, and Jordi Soler-Soler. "l-Arginine limits myocardial cell death secondary to hypoxia-reoxygenation by a cGMP-dependent mechanism." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 5 (May 1, 1999): H1574—H1580. http://dx.doi.org/10.1152/ajpheart.1999.276.5.h1574.

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The objective of this study was to investigate the effect ofl-arginine supplementation on myocardial cell death secondary to hypoxia-reoxygenation. Isolated rat hearts ( n = 51) subjected to 40 min of hypoxia and 90 min of reoxygenation received 3 mMl-arginine and/or 1 μM 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ; a selective inhibitor of soluble guanylyl cyclase) throughout the experiment or during the equilibration, hypoxia, or reoxygenation periods. The incorporation ofl-[3H]arginine into myocytes during energy deprivation was investigated in isolated adult rat myocytes. The addition ofl-arginine to the perfusate throughout the experiment resulted in higher cGMP release ( P < 0.05), reduced lactate dehydrogenase release ( P < 0.05), and increased pressure-rate product ( P < 0.05) during reoxygenation. These effects were reproduced whenl-arginine was added only during equilibration, but addition ofl-arginine during hypoxia or reoxygenation had no effect. Addition of ODQ either throughout the experiment or only during reoxygenation reversed the beneficial effects of l-arginine.l-[3H]arginine was not significantly incorporated into isolated myocytes subjected to energy deprivation. We conclude thatl-arginine supplementation protects the myocardium against reoxygenation injury by cGMP-mediated actions. To be effective during reoxygenation,l-arginine must be added before anoxia.
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Dissertations / Theses on the topic "Reoxygenation"

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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.

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Cherif, 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.

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Magagnin, 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.

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Teoh, 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.

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Kolamunne, Rajitha K. "Reactive oxygen and nitrogen species production in cardiomyoblasts during hypoxia and reoxygenation." Thesis, Aston University, 2010. http://publications.aston.ac.uk/10052/.

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Hypoxia is a stress condition in which tissues are deprived of an adequate O2 supply; this may trigger cell death with pathological consequences in cardiovascular or neurodegenerative disease. Reperfusion is the restoration of an oxygenated blood supply to hypoxic tissue and can cause more cell injury. The kinetics and consequences of reactive oxygen and nitrogen species (ROS/RNS) production in cardiomyoblasts are poorly understood. The present study describes the systematic characterization of the kinetics of ROS/RNS production and their roles in cell survival and associated protection during hypoxia and hypoxia/reperfusion. H9C2 cells showed a significant loss of viability under 2% O2 for 30min hypoxia and cell death; associated with an increase in protein oxidation. After 4h, apoptosis induction under 2% O2 and 10% O2 was dependent on the production of mitochondrial superoxide (O2-•) and nitric oxide (•NO), partly from nitric oxide synthase (NOS). Both apoptotic and necrotic cell death during 2% O2 for 4h could be rescued by the mitochondrial complex I inhibitor; rotenone and NOS inhibitor; L-NAME. Both L-NAME and the NOX (NADPH oxidase) inhibitor; apocynin reduced apoptosis under 10% O2 for 4h hypoxia. The mitochondrial uncoupler; FCCP significantly reduced cell death via a O2-• dependent mechanism during 2% O2, 30min hypoxia. During hypoxia (2% O2, 4h)/ reperfusion (21% O2, 2h), metabolic activity was significantly reduced with increased production of O2-• and •NO, during hypoxia but, partially restored during reperfusion. O2-• generation during hypoxia/reperfusion was mitochondrial and NOX- dependent, whereas •NO generation depended on both NOS and non-enzymatic sources. Inhibition of NOS worsened metabolic activity during reperfusion, but did not effect this during sustained hypoxia. Nrf2 activation during 2% O2, a sustained hypoxia and reperfusion was O2-•/•NO dependent. Inhibition of NF-?B activation aggravated metabolic activity during 2% O2, 4h hypoxia. In conclusion, mitochondrial O2-•, but, not ATP depletion is the major cause of apoptotic and necrotic cell death in cardiomyoblasts under 2% O2, 4h hypoxia, whereas apoptotic cell death under 10% O2, 4h, is due to NOS-dependent •NO. The management of ROS/RNS rather than ATP is required for improved survival during hypoxia. O2-• production from mitochondria and NOS is cardiotoxic during hypoxia/reperfusion. NF-?B activation during hypoxia and NOS activation during reperfusion is cardiomyoblast protective.
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Viret, 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.

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Evans, 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/.

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Cardiomyocyte apoptosis is an important contributory factor towards the progression of ischaemic heart disease. Signal Transducer and Activator of Transcription 3 (STAT3) is a transcription factor has that been implicated in normal heart development and function. Most interestingly, STAT3 also appears to play a role in cardioprotection, including hypoxic preconditioning. In this thesis the levels and activities of ST A T3 were measured in response to hypoxic insult in primary rat cardiomyocytes (RCMs) and two cardiomyocyte cell lines (H9c2 and P19CL6 cells). P19CL6 cells were extremely sensitive to hypoxia-induced apoptosis whereas RCMs and H9c2 cells were highly resistant. Apoptosis in P19CL6 cells correlated with loss of STAT3 DNA binding, which was preceded by serine phosphorylation and followed by loss of tyrosine phosphorylation. Treatment with LIF partially protected P19CL6 cells from hypoxia-induced apoptosis, as did exogenous expression of STAT3 but not a redox-insensitive ST AT3 mutant (STAT3C3s ). Moreover, STAT3 expression rescued mitochondrial ATP production during hypoxia whereas the redox-insensitive mutant did not. These data indicate that the contribution of STAT3 to cardiomyocyte survival under hypoxic stress involves the maintenance of mitochondrial function by a redox-dependent mechanism. Understanding how STAT3 is regulated in cardiomyocytes will be important for the development of therapeutic approaches for ischaemic heart disease in the future.
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Hung, 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.

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Oxidative stress of the placenta is considered a key intermediary step in the pathogenesis of preeclampsia, but the cause for the stress remains unknown. Ischaemia-reperfusion injury, as a result of intermittent placental perfusion secondary to deficient trophoblast invasion of the endometrial arteries, is a possible mechanism. This thesis therefore tests whether hypoxia-reoxygenation (H/R) in vitro can induce placental oxidative stress, and cause increased apoptosis and production of tumour necrosis factor-α as seen in the preeclamptic placenta. The first aim was to examine the oxidative status of human placental tissues during periods of hypoxia and reoxygenation in vitro. Rapid generation of reactive oxygen species (ROS) was detected using a fluorescent marker when hypoxic villous samples were reoxygenated. The expression of oxidative stress markers including nitrotyrosine residues, 4-hydroxy-2-nonenal adducts, and inducible heat shock protein 72 was greatly increased in villous samples subjected to H/R compared to the controls maintained under constant hypoxia. Furthermore, preloading villous samples with ROS scavengers such as desferrioxamine and α-phenyl-N-tert-butylnitrone significantly reduced the levels of oxidative stress in H/R. Having demonstrated that in vitro H/R is capable of inducing oxidative stress in a reproducible and manipulable manner, investigations were next carried out to study the effects of resultant oxidative stress on apoptosis within the trophoblast. Compared to hypoxic and normoxic controls, there was a significant increase in the release of cytochrome c from mitochondria, activation of caspase , and cleavage of poly (ADP-ribose) polymerase in villous samples subjected to H/R. These events were associated with an increased number of syncytiotrophoblastic nuclei displaying apoptotic changes and increased lactate dehydrogenase release into the medium. The causal relationship between the generation of ROS and these apoptotic changes was revealed by the fact that pre-administration of desferrioxamine attenuated the insult.
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Arab, 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.

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Huang, 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.

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Books on the topic "Reoxygenation"

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Lucchesi, Benedict R. Myocardial reoxygenation injury (Current concepts). The Upjohn Company, 1990.

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Schiller, Erich. Free Radicals and Inhalation Pathology: Respiratory System, Mononuclear Phagocyte System - Hypoxia and Reoxygenation - Pneumoconioses and other Granulomatoses - Cancer. Springer, 2004.

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Schiller, Erich, H. Bartsch, and W. Kriz. Free Radicals and Inhalation Pathology: Respiratory System, Mononuclear Phagocyte System Hypoxia and Reoxygenation Pneumoconioses and Other Granulomatoses Cancer. Springer, 2013.

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Schiller, Erich, H. Bartsch, and W. Kriz. Free Radicals and Inhalation Pathology: Respiratory System, Mononuclear Phagocyte System Hypoxia and Reoxygenation Pneumoconioses and Other Granulomatoses Cancer. Springer London, Limited, 2013.

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Azarbayjani, Faranak. Common Mechanism for Teratogenicity of Antiepileptic Drugs: Drug-Induced Embryonic Arrhythmia and Hypoxia-Reoxygenation Damage (Comprehensive Summaries ... from the Faculty of Pharmacy, 253). Uppsala Universitet, 2001.

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Book chapters on the topic "Reoxygenation"

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Schmierer, Bernhard. "Reoxygenation." In Encyclopedia of Systems Biology, 1846. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_773.

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Caraceni, Paolo, Antonio Gasbarrini, Franco Trevisani, Marco Domenicali, Giovanni Gasbarrini, David H. Van Thiel, and Mauro Bernardi. "Reoxygenation Injury in Isolated Rat Hepatocytes." In New Trends in Hepatology, 104–12. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0357-9_12.

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Henderson, A. H. "Ischemic/Hypoxic and Reperfusion/Reoxygenation Contractures: Mechanisms." In Diastolic Relaxation of the Heart, 73–82. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4615-6832-2_9.

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Piper, H. M., S. Buderus, A. KrÜtzfeldt, T. Noll, S. Mertens, and R. Spahr. "Sensitivity of the endothelium to hypoxia and reoxygenation." In Pathophysiology of Severe Ischemic Myocardial Injury, 359–79. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0475-0_18.

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Modat, G., C. Bonne, and J. Dornand. "Leukocyte Adhesion and Endothelial Cytokine Production in Hypoxia /Reoxygenation." In Oxidative Stress, Cell Activation and Viral Infection, 65–75. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7424-3_8.

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Miller, Ariel, Yaara Ben-Yosef, Clara Braker, and Sarah Shapiro. "Matrix metalloproteinases and their inhibitors in hypoxia/reoxygenation and stroke." In Inflammation and Stroke, 275–85. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8297-2_21.

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Poulsen, Jan Peter, and Ola Didrik Saugstad. "Oxypurines in Extracellular Fluids from Piglets During Hypoxemia and Reoxygenation." In Advances in Experimental Medicine and Biology, 271–74. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2638-8_61.

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Cunha-Ribeiro, L. M., and K. S. Sakariassen. "Modulation of Cultured Human Endothelial Cells by Hypoxia and Reoxygenation." In Vascular Endothelium, 258–59. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0355-8_28.

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Lukáçová, N., M. Marsala, and J. Marsala. "Graded Postischemic Reoxygenation, Phospholipids and Neuronal Damage in Rabbits after Ischemia." In Neurochemistry, 465–68. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_77.

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Olcina, Monica M., Amato J. Giaccia, and Ester M. Hammond. "Isolation of Proteins on Nascent DNA in Hypoxia and Reoxygenation Conditions." In Advances in Experimental Medicine and Biology, 27–40. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26666-4_3.

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Conference papers on the topic "Reoxygenation"

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Fukawa, Takeshi, Koji Takematsu, Kotaro Oka, Nobuyuki Miyahara, Sachiko Koike, Koichi Ando, Hirosuke Kobayashi, and Kazuo Tanishita. "Reoxygenation in Tumor Tissues After X-Ray or Carbon-12 Irradiation." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0179.

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Abstract We measured directly the partial pressure of oxygen (pO2) in new fibrosarcoma (NFSa) tumors grown in C3H/He mice using microcoaxial O2 electrodes in vivo. The pO2 in tumors was monitored after a single dose of X-ray or carbon-12 irradiation. After irradiation, tumor volume temporally shrinked, and pO2 simultaneously increased. Carbon-12 irradiation reoxygenated tumors between the 1st and 9th day after the irradiation, while x-ray irradiation reoxygenated tumors between the 3rd and 8th day. We found that reoxygenation period after carbon-12 irradiation started earlier and continued longer than X-ray irradiation.
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Xianwei Cao, Zegao Yin, Dongsheng Cheng, Le Wang, and Yong He. "The review of aeration and reoxygenation behavioral characteristics for spillway discharge." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5964206.

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Caraballo, Juan C., Jennifer Borcherding, Michael Rector, David Stoltz, Joseph Zabner, and Alejandro P. Comellas. "Transgenic Expression Of Paraoxonase 1 Protects Drosophila Melanogaster From Anoxia-Reoxygenation Injury." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5827.

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Kanagasabai, Thanigaivelan, Rohin Chand, AmyAman Kaur, Sivanesan Dhandayuthapani, Olena Bracho, and Appu Rathinavelu. "Abstract 1860: MDM2 stabilizes and induces HIF-1α levels during reoxygenation of cancer cells." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1860.

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Díaz, Paola Monterroso, Daria Semeniak, Kinan Alhallak, Dakory Lee, Ruud P. M. Dings, and Narasimhan Rajaram. "Quantitative Diffuse Optical Spectroscopy of Short-term Reoxygenation Kinetics in Radiation-Resistant and Sensitive Tumors." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/omp.2017.omw3d.2.

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Dadgar, Sina, Joel R. Troncoso, Austin Dotson, and Narasimhan Rajaram. "Characterization of radiation-induced reoxygenation in head and neck tumor xenografts using diffuse reflectance spectroscopy." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2019. http://dx.doi.org/10.1364/omp.2019.ot1d.4.

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Bensaid, S., C. Fabre, P. Mucci, and C. Cieniewski-Bernard. "Mechanical Contraction, Nutritional Supplementation and Muscle Reoxygenation to Counteract Skeletal Muscle Cell Atrophy Induced by Hypoxia." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5786.

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Thijssen, Dick H. J., Caro J. T. van Uden, Hans Krijgsman, and Willy N. J. M. Colier. "RSI: oxygen consumption, blood flow, and reoxygenation in patients suffering RSI measured by noninvasive optical spectroscopy." In Biomedical Optics 2003, edited by Britton Chance, Robert R. Alfano, Bruce J. Tromberg, Mamoru Tamura, and Eva M. Sevick-Muraca. SPIE, 2003. http://dx.doi.org/10.1117/12.477355.

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Chen, Kuo Chin, Mong Hsun Tsai, Eric Y. Chuang, Chuhsing Kate Hsiao, and Liang Chuan Lai. "Abstract 441: Temporal profiling of a breast cancer cell line MCF-7 in response to reoxygenation." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-441.

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Okajima, Manabu, Satoshi Kokura, Takeshi Ishikawa, Tatsuzo Matsuyama, Reiko Tsutiya, Satoko Adachi, Naoyuki Sakamoto, Yuji Naito, and Tetsuro Yamane. "Abstract 2406: The effect of anoxia/reoxygenation on epithelial-mesenchymal transition in human colon cancer cell lines." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2406.

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Reports on the topic "Reoxygenation"

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Gamcsik, Michael P. Markers of Hypoxia/Reoxygenation in the Development of Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada473777.

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