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Artykuły w czasopismach na temat "Ischaemia and reperfusion damage"
Ozkisacik, Sezen, Ali Onur Erdem, Barlas Etensel, Canten Tataroglu, Mukadder Serter i Mesut Yazici. "Short-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats". Journal of International Medical Research 45, nr 3 (28.05.2017): 1036–41. http://dx.doi.org/10.1177/0300060517708921.
Pełny tekst źródłaKnight, Kenneth R., Michael F. Angel, Diana A. Lepore, Paul A. Abbey, Laurence I. Arnold, Kathleen A. Gray, Cary G. Mellow i Bernard McC O'Brien. "Secondary Ischaemia in Rabbit Skin Flaps: The Roles Played by Thromboxane and Free Radicals". Clinical Science 80, nr 3 (1.03.1991): 235–40. http://dx.doi.org/10.1042/cs0800235.
Pełny tekst źródłaFabiani, R., C. Ceconi, S. Curello, O. Alfieri i O. Visioli. "Myocardial damage during ischaemia and reperfusion". European Heart Journal 14, suppl G (2.11.1993): 25–30. http://dx.doi.org/10.1093/eurheartj/14.suppl_g.25.
Pełny tekst źródłaGariballa, SE, i AJ Sinclair. "Cerebrovascular disease and oxidative stress". Reviews in Clinical Gerontology 9, nr 3 (sierpień 1999): 197–206. http://dx.doi.org/10.1017/s0959259899009314.
Pełny tekst źródłaPicozzi, Piero, Nicholas V. Todd i H. Alan Crockard. "Regional Blood-Brain Barrier Permeability Changes after Restoration of Blood Flow in Postischemic Gerbil Brains: A Quantitative Study". Journal of Cerebral Blood Flow & Metabolism 5, nr 1 (marzec 1985): 10–16. http://dx.doi.org/10.1038/jcbfm.1985.2.
Pełny tekst źródłaRőth, Erzsébet. "A szabad gyökös reakciók jelentősége a szívizom ischaemiás-reperfúziós károsodásában és az endogén adaptáció indukálásában". Orvosi Hetilap 156, nr 47 (listopad 2015): 1908–11. http://dx.doi.org/10.1556/650.2015.30304.
Pełny tekst źródłaSolaini, Giancarlo, i David A. Harris. "Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion". Biochemical Journal 390, nr 2 (23.08.2005): 377–94. http://dx.doi.org/10.1042/bj20042006.
Pełny tekst źródłaDenorme, Frederik, i Simon F. De Meyer. "The VWF-GPIb axis in ischaemic stroke: lessons from animal models". Thrombosis and Haemostasis 116, nr 10 (2016): 597–604. http://dx.doi.org/10.1160/th16-01-0036.
Pełny tekst źródłaBeyersdorf, F., K. Sarai, Z. Mitrev, L. Eckel, K. Ihnken i P. Satter. "Studies of Reperfusion Injury in Skeletal Muscle: Controlled Limb Reperfusion to Reduce Post-Ischaemic Syndrome". Cardiovascular Surgery 1, nr 4 (sierpień 1993): 330–36. http://dx.doi.org/10.1177/096721099300100404.
Pełny tekst źródłaGracia-Sancho, Jordi, Araní Casillas-Ramírez i Carmen Peralta. "Molecular pathways in protecting the liver from ischaemia/reperfusion injury: a 2015 update". Clinical Science 129, nr 4 (21.05.2015): 345–62. http://dx.doi.org/10.1042/cs20150223.
Pełny tekst źródłaRozprawy doktorskie na temat "Ischaemia and reperfusion damage"
Bushell, Alison Jayne. "Protection of skeletal muscle against ischaemia and reperfusion induced damage". Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365914.
Pełny tekst źródłaGartshore, Gail. "The consequences of reperfusion on cerebral ischaemic damage". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297001.
Pełny tekst źródłaWiden, Cecilia, i n/a. "Energetics of Mouse Papillary Muscle". Griffith University. School of Physiotherapy and Exercise Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070228.121312.
Pełny tekst źródłaWiden, Cecilia. "Energetics of Mouse Papillary Muscle". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367649.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
Full Text
Amin, Alla Mohammed Hussain. "Cold ischaemia and reperfusion injury in liver : the potential for damage to cellular DNA in the rat model". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248455.
Pełny tekst źródłaKaskar, Rafee'ah. "Effect of melatonin on myocardial susceptibility to ischaemia and reperfusion damage in a rat model of high-fat diet-induced obesity". Thesis, Stellenbosch : Stellenbosch University, 2015. http://hdl.handle.net/10019.1/97868.
Pełny tekst źródłaENGLISH ABSTRACT: Obesity has reached epidemic proportions worldwide and is currently a serious health problem. It is associated with metabolic abnormalities, oxidative stress, hypertension, insulin resistance and an increased disposition for the development of cardiovascular disease. Elucidation of the pathophysiological mechanisms underlying obesity and its relationship with metabolic and cardiovascular diseases is essential for prevention and management of these disorders. Melatonin, the pineal gland hormone, is a powerful antioxidant and has been shown to protect the myocardium against ischaemia/reperfusion (I/R) injury. Long- as well as shortterm melatonin treatment also reversed several of the harmful effects of obesity in an animal model of hyperphagia-induced obesity (DIO). However, its effects on myocardial I/R injury and intracellular signalling in obesity induced by a high fat diet (HFD) are still unknown. Aims of study: (i) To evaluate the ability of a high fat diet (HFD) to induce obesity in rats. Apart from evaluating its effects on the biometric parameters and resistance to ischaemia/reperfusion injury (as indicated by infarct size in regional ischaemia and functional recovery after global ischaemia), special attention will be given on the interplay between adiponectin, AMPK, leptin, and FFA in this model. (ii) To evaluate the effect of daily oral administration of melatonin to rats on the HFD as well as their littermate controls, on the parameters listed above as well as on the development of obesity. In this study melatonin will be administered from the onset of the feeding of the high fat diet. Methods: Male Wistar rats were divided into 4 groups: (i) control rats (receiving normal rat chow) (C); (ii) control rats receiving melatonin (CM); (iii) obese rats (receiving HFD) (HFD); (iv) obese rats receiving melatonin (HM). Animals were kept on the diet for 16 weeks and melatonin treatment (10mg/kg/day, added to the drinking water) started at the onset of the feeding. Following feeding and treatment, the animals were grouped into fasted/ non-fasted of which biometric parameters were recorded and blood collected at the time of sacrifice for metabolic and biochemical assays. Hearts were perfused in the working mode for evaluation of myocardial function and infarct size determination after exposure to 35min regional ischaemia/60min reperfusion. For study of intracellular signaling, hearts were perfused in the working mode, subjected to 20min global ischaemia/10min reperfusion and freeze-clamped for Western blotting. Plasma leptin, adiponectin, free fatty acid, triglycerides, total cholesterol, phospholipids, conjugated dienes and thiobarbituric reactive substances (TBARS) levels were determined. Several kinases were investigated including, the RISK (reperfusion injury salvage kinase) (PKB/Akt and ERK p44/42) and SAFE (survivor activating factor enhancement) (STAT-3) pathways, AMPK and JNK under baseline conditions or following 10 min reperfusion. In addition, expression of UCP-3 and PGC1-α was determined. Results: Significant increases in body weight, visceral fat, blood glucose, insulin, HOMA index and leptin and a reduction in adiponectin levels were observed in the fasted high fat diet (HFD) group when compared with controls (C). Significant increases in free fatty acid and triglyceride levels were also noted the HFD group while other serum lipid parameters, including TBARS, remained unchanged. No differences in functional recovery during reperfusion or infarct size after exposure to 35 min regional ischaemia, as well as functional recovery during reperfusion after 20 min global ischaemia were observed between the control and HFD groups. Baseline and 10 min reperfusion data were similar for the RISK and SAFE pathway kinases for the control vs HFD groups. The HFD also had no effect on the expression and phosphorylation of myocardial AMPK and JNK, as well as on the expression of UCP-3 and PGC1-α, when compared to the controls. Treatment with melatonin significantly reduced body weight, visceral fat, blood glucose, HOMA index and serum leptin levels in HFD treated groups, while having no effect on the lipid profile. Although melatonin significantly reduced infarct size in both control [% of area at risk: 20.59 ± 2.29 (CM) vs 38.08 ± 2.77 (C)] and high-fat diet groups [% of area at risk: 11.43 ± 2.94 (HM) vs 38.06 ± 3.59 (H)], it was without effect on myocardial functional recovery during reperfusion. Melatonin had no effect on the intracellular signaling pathways studied. Conclusions: The HFD proved to be a useful model of diet-induced obesity with a more pronounced impact on biometric and metabolic changes compared to the DIO model. Long-term melatonin treatment successfully prevented the development of metabolic abnormalities associated with the high fat diet and obesity as well as significantly reduced myocardial infarct size. The mechanisms involved in melatonin-induced cardioprotection in obesity have not been fully elucidated in this study and require further investigation. However, the anti-obesogenic and cardioprotective properties of melatonin were very significant indeed and support the suggestion of this hormone as a potential tool in the treatment of obesity and associated cardiovascular complications.
AFRIKAANSE OPSOMMING: Inleiding: Vetsug (obesiteit) het wêreldwyd epidemiese afmetings aangeneem en word tans as ‘n ‘n ernstige gesondheidsprobleem beskou. Vetsug word geassosieer met metaboliese afwykings, oksidatiewe stres, hipertensie, insulienweerstandigheid en is‘n belangrike risikofaktor vir die ontwikkeling van kardiovaskulêre siekte. Ten spyte hiervan, het onlangse studies ‘n gunstige effek van vetsug op die uitkomste van miokardiale infarksie in pasiënte gerapporteer, die sg obesiteitsparadoks. Kennis van die patofisiologiese meganismes onderliggend aan vetsug en die ontstaan van metaboliese afwykinge en hartsiekte is noodsaaklik vir die voorkoming en behandeling van hierdie toestande. Melatonien, die hormoon afgeskei deur die pineaalklier, is ‘n kragtige antioksidant en vry radikaal opruimer. Dit is voorheen aangetoon dat dit die hart teen iskemie/herperfusie (I/H) besering kan beskerm en sommige van die skadelike gevolge van vetsug in diermodelle kan omkeer. Die effek van melatonien op miokardiale I/H besering en intrasellulêre seintransduksie prosesse in vetsug geïduseer deur ‘n hoë vet dieet is egter nog onbekend. Doelstellings: (i) Die ontwikkeling en karakterisering van ‘n nuwe model van vetsug en insulienweerstandigheid geïnduseer deur 'n hoë vet dieet (HVD) en die evaluering van die effek daarvan op miokardiale I/H besering en die gepaardgaande intrasellulêre seintransduksieprosesse; (ii) Bepaling van die effek van daaglikse toediening van melatonien aan rotte op die HVD sowel as aan kontroles op ‘n standard dieet, op die ontwikkeling van dieet-geïnduseerde metaboliese veranderinge, miokardiale infarktgrootte en funksionele herstel na koronêre arterie afbinding, sowel as intrasellulêre seintransduksie. Metodiek: Vier groepe van manlike Wistar rotte is bestudeer: (i) kontrole rotte (op‘n standaard dieet) (K); (ii) kontrole rotte op ‘n standard dieet plus melatonien (KM); (iii) dieetrotte (op‘n HVD); (iv) HVD rotte wat melatonien ontvang (HM). Die HVD en melatonien (10mg/kg/dag in die drinkwater) is vir 16 weke toegedien. Na die periode van behandeling, is die diere in vastende en nie-vastende groepe verdeel, die biometriese parameters genoteer en bloedmonsters vir metaboliese en biochemiese bepalings versamel, tydens verwydering van die harte. Harte is geperfuseer volgens die werkhartmodel vir bepaling van miokardiale funksie en infarktgrootte na blootstelling aan 35min streeksiskemie. Vir evaluering van intrasellulêre seintransduksie, is geperfuseerde werkende rotharte blootgestel aan 15min globale iskemie/10 min herperfusie en gevriesklamp vir latere analises volgens die Western kladtegniek.hart. Serum leptien, adiponektien, vryvetsure, trigliseried, totale cholesterol, fosfolipiede, gekonjugeerde diene en tiobarbituursuur reaktiewe stowwe (TBARS) is bepaal. Met gebruik van Western kladtegniek, is die aktivering en/of uitdrukking van die RISK (PKB/ Akt en ERK p44/42) en SAFE (STAT-3) seintransduksiepaaie, AMPK, JNK, UCP-3 en PGC1-α, onder basislyn toestande of na 10 min herperfusie bestudeer. Resultate:‘n Beduidende toename in liggaamsgewig, visserale vet, die HOMA indeks, insulien en leptien vlakke is in die HVD groep waargeneem vergeleke met die kontrole (K) rotte. Adiponektien vlakke was laer in die HVD groep. Die HVD groep is ook gekenmerk deur ‘n beduidende styging in serum vryvetsuur en trigliseried vlakke, terwyl die ander lipied parameters, insluitende die TBARS vlakke, onveranderd was. Infarktgrootte en funksionele herstel tydens herperfusie na blootstelling aan 35 min streeksiskemie, asook funksionele herstel tydens herperfusie na 20 min globale iskemie het nie verskil tussen harte van die kontrole en HVD rotte nie. Aktivering van PKB/Akt, ERK p44/p42, STAT3, AMPK en JNK by basislyn en na 10 min herperfusie was soortgelyk in die kontrole en HFD groepe. Die HVD het ook geen effek op die uitdrukking van UCP-3 en PGC1-α in vergelyking met die kontrole gehad nie. Behandeling met melatonien het die liggaamsgewig, visserale vet, bloedglukose, HOMA indeks en serum leptien vlakke in die HVD groepe statisties beduidend verlaag, terwyl dit geen invloed op die lipiedprofiel gehad het nie. Melatonien behandeling het die miokardiale infarktgrootte beduidend en tot dieselfde mate verminder in beide kontrole [20.59 ± 2.29 (KM) vs 38.08 ± 2.77% (K)] en HVD groepe [11.43 ± 2.94 (HM) vs 38.06 ± 3.59% (HVD)]. Geen verskille is egter tussen die funksionele herstel gedurende herperfusie van die behandelde en onbehandelde kontrole en HVD groepe waargeneem nie. Melatonien het ook geen uitwerking op die intrasellulêre seintransduksiepaaie gehad nie. Gevolgtrekkings: Die resultate het getoon dat die HFD 'n goeie model van dieetgeïnduseerde vetsug en insulien weerstandigheid ontlok, met 'n meer uitgesproke impak op biometriese en metaboliese veranderinge as die voorheen gebruikte hoë-sukrose dieet. Langtermyn melatonien- behandeling het die ontwikkeling van metaboliese abnormaliteite geassosieer met die HVD, voorkom, asook miokardiale infarktgrootte na koronêre afbinding beduidend verminder. Die meganismes betrokke in melatonien-geïnduseerde miokardiale beskerming moet egter in meer detail ondersoek word. Die resultate verkry steun die voorstel dat melatonientoediening voordelig sal wees in die behandeling van vetsug en sy kardiovaskulêre komplikasies.
Rochester, John Robert. "Investigation of reperfusion injury in chronically ischaemic skeletal muscle using in-vitro microscopy". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319434.
Pełny tekst źródłaMankad, Pankaj Shashikant. "Ischaemia-reperfusion injury and endothelial dysfunction". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392286.
Pełny tekst źródłaKoo, Dicken D. H. "Ischaemia/reperfusion injury in renal transplantation". Thesis, University of Oxford, 1999. http://ora.ox.ac.uk/objects/uuid:e0177fd9-1504-4c76-b9fd-6e7ae0b6b466.
Pełny tekst źródłaCartaya, Rafael Eduardo Chavez. "Study on liver ischaemia and reperfusion". Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388665.
Pełny tekst źródłaKsiążki na temat "Ischaemia and reperfusion damage"
A, Grace P., i Mathie Robert T, red. Ischaemia reperfusion injury. Oxford: Blackwell Science, 1999.
Znajdź pełny tekst źródłaKhaira, Harmeet Singh. Ischaemia-reperfusion in intermittent claudication. Birmingham: University of Birmingham, 1995.
Znajdź pełny tekst źródłaWilson, Ian Clark. The role of leucocytes in neonatal myocardial ischaemia-reperfusion injury. Birmingham: University of Birmingham, 1994.
Znajdź pełny tekst źródła1932-, Abiko Yasushi, i Karmazyn M. 1950-, red. Protection against ischemia/reperfusion damage of the heart. Tokyo: Springer, 1998.
Znajdź pełny tekst źródłaAbiko, Yasushi, i Morris Karmazyn, red. Protection Against Ischemia/Reperfusion Damage of the Heart. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68482-4.
Pełny tekst źródłaHerman, Stanley Leon. Age differences in the susceptibility of the normal rabbit myocardium to injury following ischaemia and reperfusion. Ottawa: National Library of Canada, 1992.
Znajdź pełny tekst źródłaAlfred Benzon Symposium (41st 1996 Royal Danish Academy of Sciences and Letters). Coronary microcirculation during ischaemia and reperfusion: Proceedings of a symposium held at the Royal Danish Academy of Sciences and Letters, August 18-22, 1996. Redaktorzy Aldershvile Jan, Haunsø Stig i Svendsen Jesper Hastrup. Copenhagen: Munksgaard, 1997.
Znajdź pełny tekst źródłaSmith, T. C. G. 1939-, red. Ischaemia in head injury: 10th European Congress of Neurosurgery, Berlin 1995 ; proceedings of a special symposium. Berlin: Springer, 1996.
Znajdź pełny tekst źródłaFink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.
Pełny tekst źródłaHausenloy, Derek, i Derek Yellon, red. An Introduction to Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0001.
Pełny tekst źródłaCzęści książek na temat "Ischaemia and reperfusion damage"
Ferrari, R., C. Ceconi, S. Curello, A. Cargnoni, F. De Giuli, G. M. Boffa i A. Albertini. "Role of Oxygen in Myocardial Ischaemia and Reperfusion Damage". W Developments in Cardiovascular Medicine, 91–107. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1607-7_9.
Pełny tekst źródłaFerrari, Roberto, Claudio Ceconi, Salvatore Curello, Evasio Pasini i Odoardo Visioli. "Protective effect of propionyl-L-carnitine against ischaemia and reperfusion-damage". W Lipid Metabolism in Normoxic and Ischemic Heart, 161–68. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4_23.
Pełny tekst źródłaRutgers, D. R., J. H. G. M. van Beek i M. D. Osbakken. "Is There a Reduction of Ischaemia/Reperfusion Damage in the Isolated Rat Heart by Alternating Oxygenated and Deoxygenated Reperfusion Solutions?" W Advances in Experimental Medicine and Biology, 241–48. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0333-6_31.
Pełny tekst źródłaFroghi, Farid, Saied Froghi i Brian R. Davidson. "Liver Ischaemia-Reperfusion Injury". W Liver Diseases, 129–41. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-24432-3_12.
Pełny tekst źródłaAdembri, C., A. R. De Gaudio i G. P. Novelli. "Ischaemia-Reperfusion in Sepsis". W Sepsis and Organ Dysfunction, 49–56. Milano: Springer Milan, 2000. http://dx.doi.org/10.1007/978-88-470-2284-3_5.
Pełny tekst źródłaLochner, A., E. Tromp i R. Mouton. "Signal transduction in myocardial ischaemia and reperfusion". W Biochemical Mechanisms in Heart Function, 129–36. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1279-6_18.
Pełny tekst źródłaSumeray, Mark S., i Derek M. Yellon. "Characterisation and validation of a murine model of global ischaemia-reperfusion injury". W Myocardial Ischemia and Reperfusion, 61–68. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_8.
Pełny tekst źródłaCohadon, F. "The Concept of Secondary Damage in Brain Trauma". W Ischaemia in Head Injury, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80172-3_1.
Pełny tekst źródłaSymon, Lindsay. "Progression and Irreversibility in Brain Ischaemia". W Mechanisms of Secondary Brain Damage, 221–37. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5203-7_17.
Pełny tekst źródłaTeasdale, G. "Pathological and Clinical Evidence of Ischaemic Damage in Brain Trauma". W Ischaemia in Head Injury, 21–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-80172-3_3.
Pełny tekst źródłaStreszczenia konferencji na temat "Ischaemia and reperfusion damage"
Panico, Karine, Giovanni Weber, Marcela S. Carneiro-Ramos i Jo�o Salinet. "Electrophysiological Effects on Renal Ischaemia/Reperfusion-Induced Cardiac Hypertrophy". W 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.301-394.
Pełny tekst źródłaBhandal, J., A. Hussain, J. Buckley i H. Maddock. "P34 Adenosine a1 receptor activation can protect the myocardium from ischaemia reperfusion injury post reperfusion". W British Society for Cardiovascular Research, Autumn Meeting 2017 ‘Cardiac Metabolic Disorders and Mitochondrial Dysfunction’, 11–12 September 2017, University of Oxford. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bscr.39.
Pełny tekst źródłaDookun, Emily, Anna Walaszczyk, Rachael Redgrave, Simon Tual-Chalot, Oliver Yausep, Ioakim Spyridopoulos, Andrew Owens, Helen Arthur, Joao Passos i Gavin Richardson. "142 Accumulation of cardiomyocyte senescence following ischaemia-reperfusion injury (IRI); a potential therapeutic target?" W British Cardiovascular Society Annual Conference ‘High Performing Teams’, 4–6 June 2018, Manchester, UK. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcs.138.
Pełny tekst źródłaLim, Ven Gee, Sapna Arjun, Robert Bell i Derek Yellon. "BS10 Canagliflozin, an SGLT2 inhibitor attenuates ischaemia/reperfusion injury in the non-diabetic heart". W British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.174.
Pełny tekst źródłaDraganova, Lilia, Rachael Redgrave, Simon Tual-Chalot, Sarah Marsh, Helen Arthur i Ioakim Spyridopoulos. "BS31 The role of fractalkine and CX3CR1-expressing lymphocytes during myocardial ischaemia/reperfusion injury". W British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.194.
Pełny tekst źródłaLoerakker, Sandra, Emmy Manders, Gustav J. Strijkers, Frank P. T. Baaijens, Dan L. Bader, Klaas Nicolay i Cees W. J. Oomens. "Effect of Ischemia and Reperfusion on Skeletal Muscle Damage". W ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19341.
Pełny tekst źródłaYazir, Yusufhan. "Protective effect of ticagrelor on liver damage induced by ischemia-reperfusion". W 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-253.
Pełny tekst źródłaOstróżka-Cieślik, Aneta, i Barbara Dolińska. "Antioxidants added to preservative solutions protect the liver from ischemia-reperfusion damage". W 7th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecmc2021-11405.
Pełny tekst źródłaKandemir, Cansu. "Riboflavin Treatment Reduces Apoptosis and Oxidative DNA Damage in a Ischemia/Reperfusion Induced Renal Damage in Rats". W 15th International Congress of Histochemistry and Cytochemistry. Istanbul: LookUs Scientific, 2017. http://dx.doi.org/10.5505/2017ichc.pp-268.
Pełny tekst źródłaPlatt, Esther, Francis Robertson, Andrew Hall, Alberto Quaglia i Brian Davidson. "P053 Investigation of the origin of serum neutrophil gelatinase associated lipocalin (NGAL) following liver ischaemia reperfusion and resultant acute kidney injury in mice". W Abstracts of the British Association for the Study of the Liver Annual Meeting, 22–24 November 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-basl.62.
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