Gotowe bibliografie tematyczne / Ischaemia and reperfusion damage

Gotowa bibliografia na temat „Ischaemia and reperfusion damage”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Ischaemia and reperfusion damage"

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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.

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Objective Acute mesenteric ischaemia leads to intestinal damage. Restoration of blood flow results in further damage to tissue, which is called reperfusion injury. This study aimed to investigate the protective effects of short-interval postconditioning and to determine the optimal interval for reperfusion in an experimental rat model of intestinal ischaemia. Methods Forty adult male Wistar rats were grouped as follows: sham (Sh), ischaemia + reperfusion (IR), ischaemia + postconditioning for 5 seconds (PC5), ischaemia + postconditioning for 10 seconds (PC10), and ischaemia + postconditioning for 20 seconds (PC20). For postconditioning, 10 cycles of reperfusion (5, 10, or 20 seconds) interspersed by 10 cycles of 10 seconds of ischaemia were performed. Blood glutathione reductase (GR) and glutathione peroxidase (GPx) levels were measured. Intestinal tissue damage was assessed histopathologically. Results GR levels were significantly higher in the PC5 group than in the IR group (37.7 ± 9.0 vs. 18.5 ± 2.0 min/g Hb). GPx levels were significantly higher in the PC10 group than in the IR group (43.2 ± 9.2 vs. 15.9 ± 4.6 U/g Hb). The histopathological score was significantly lower in the PC5 group (1.1 ± 0.1) than in the IR group (2.1 ± 0.2). Conclusion Short-interval postconditioning reduces reperfusion injury in the ischaemic bowel and the optimal interval for reperfusion is 5 seconds. The long-term effects of short-interval postconditioning and the optimal reperfusion interval in intestinal ischaemia–reperfusion in rats need to be investigated.
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Knight, 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.

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1. Biochemical mechanisms of ischaemia were investigated in rabbit skin flaps subjected to 2 h of primary ischaemia then, 24 h later, to 4 h of secondary ischaemia. During secondary ischaemia, flaps underwent either total ischaemia (arterial and venous blood supply occluded) or partial ischaemia (vein only occluded). Some of these flaps were treated at the time of reperfusion with the free-radical scavenger superoxide dismutase (EC 1.15.1.1) and/or the thromboxane synthetase inhibitor UK-38,485. 2. After 30 min of reperfusion, superoxide dismutase treatment significantly reduced blood thromboxane levels, elevated during ischaemia. Superoxide dismutase also reduced tissue levels of malonyldialdehyde and xanthine oxidase, indicators of free-radical damage, and restored the depleted tissue levels of superoxide dismutase. 3. UK-38,485 treatment failed to significantly alter any of these tissue free-radical parameters, although this agent significantly reduced blood thromboxane levels. 4. Combined superoxide dismutase plus UK-38,485 treatment was not significantly better than either treatment alone with respect to any parameter. 5. Partial ischaemia led to consistently higher levels of tissue free radicals and blood thromboxane than did total ischaemia. Thus partial ischaemia appears to result in greater free-radical damage than total ischaemia. 6. These results are consistent with the hypothesis that thromboxane acts as a mediator for free-radical damage in the ischaemic changes within the flap.
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Fabiani, 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.

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Gariballa, 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.

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There is strong indirect evidence that free radical production appears to be an important mechanism of brain injury after exposure to ischaemia and reperfusion. Although significant brain damage occurs during an ischaemic episode, new cerebral damage can occur after reperfusion. One proposed mechanism for the brain damage that occurs during reperfusion involves generation of free radicals. Body defences against free radicals depends on the balance between free radical generation and the antioxidant protective defence system. Many of these protective antioxidants are essential nutrients or have essential nutrients as part of their molecule that has to be obtained from diet.
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Picozzi, 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.

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A quantitative technique utilising [14C]α-aminoisobutyric acid as a tracer was used to study cerebrovascular permeability in 22 Mongolian gerbils. Seven other animals were used to measure cerebral blood volumes. Global cerebral ischaemia was produced by temporary bilateral carotid artery occlusion (60 min) in 16 gerbils that were sacrificed at 1, 2, and 3 h following reperfusion. The blood-to-brain transfer constant was significantly increased after 2 h of reperfusion in the ischaemic zones and also in structures, like the cerebellum, not supplied by the carotid artery and not ischaemic during the vessel occlusion. The blood-brain barrier (BBB) alterations were coincident with the onset of ischaemia—induced seizures that were accompanied by sudden “spikes” of systemic blood pressure. Epilepsy may play an important role in the development of BBB damage in this ischaemic model, and this factor must be considered in the interpretation of BBB damage data in gerbils.
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Rőth, 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.

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The reperfusion of acute ischaemic myocardium is essential for myocardial salvage, so called “gold standard” therapy, however it can results serious damage in the myocardium. Functional alterations occur, including depressed contractile function and decreased coronary flow as well as altered vascular reactivity. Over the several decades it has been demonstrated that oxygen radical formation is greatly increased in post-ischaemic heart and serves as a critical central mechanism of ischaemic-reperfusion injury. However it has been demonstrated that free radical play an important role in the endogenous adaptation phenomenon of the heart, too. Ischaemic preconditioning is a cellular adaptive response of the heart to stress, which provides the most potent endogenous protection against reperfusion arrhytmias, stunning and infarction. Postconditioning defined as brief periods of ischaemia and reperfusion during the very early minutes of reperfusion stimulates endogenous adaptation. Postconditioning may also attenuate the damage to endothelial cells and cardiomyocytes from oxidants, cytokines, proteases and inflammatory cells. Orv. Hetil., 2015, 156(47), 1908–1911.
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Solaini, 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.

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Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I–V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+ATP (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.
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Denorme, 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.

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SummaryStroke is a leading cause of death and long-term disability worldwide. Ischaemic stroke is caused by a blood clot that obstructs cerebral blood flow. Current treatment mainly consists of achieving fast reperfusion, either via pharmacological thrombolysis using tissue plasminogen activator or via endovascular thrombectomy. Unfortunately, reperfusion therapy is only available to a limited group of patients and reperfusion injury can further aggravate brain damage. Hence, there is an urgent need for better understanding of ischaemic stroke pathophysiology in order to develop novel therapeutic strategies. In recent years, the pathophysiological importance of von Willebrand factor (VWF) in ischaemic stroke has become clear from both clinical and experimental studies. In particular, binding of VWF to platelet glycoprotein Ib (GPIb) has become an interesting target for ischaemic stroke therapy. Recent insights show that inhibting the VWF-GPIb interaction could result in a pro-thrombolytic activity improving cerebral reperfusion rates and concurrently reducing cerebral ischaemia/reperfusion damage. This review gives an overview of the experimental evidence that illustrates the crucial role of the VWF-GPIb axis in ischaemic stroke.
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Beyersdorf, 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.

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Revascularization after prolonged complete limb ischaemia may result in both severe damage to skeletal muscle and various systemic manifestations of the postischaemic syndrome. Previous experimental studies performed by the authors have shown that these are caused, to a large extent, by normal reperfusion at normal systemic pressure and that this additional injury can be substantially reduced by controlled reperfusion of the revascularized limb before restoration of the normal circulation. This treatment includes control of the conditions of reperfusion and composition of the initial reperfusate. In the present study, this concept of controlled limb reperfusion was applied to patients with prolonged severe lower limb ischaemia. Controlled limb reperfusion was used in 11 patients after prolonged complete unilateral or bilateral ischaemia. The ischaemic interval ranged from 5 to 21 h. Two patients were in cardiogenic shock, ten had a history of associated cardiac disease and seven coexistent peripheral vascular disease. After systemic heparinization, thromboembolectomy was undertaken using a Fogarty catheter. Cannulas were placed in the iliac, profunda and superficial femoral arteries and connected to a reperfusion set. Oxygenated blood was drawn from the iliac artery and mixed with an asanguineous solution (ratio 6:1). This controlled reperfusate was returned to the profunda and superficial femoral arteries using a single roller pump. The system allows control of both the composition of the reperfusate (Ca2+, pH, osmolarity, glucose, substrate, PO2, free radical scavengers) and the conditions of reperfusion (pressure, flow, temperature). After 30 min of controlled limb reperfusion, the cannulas were removed, the arteriotomy closed and normal blood reperfusion started. All nine patients who were haemodynamically stable before operation survived the procedure and were discharged with full functional recovery, including one patient with acute aortic occlusion of several hours' duration. Thus controlled limb reperfusion avoided the need for amputation and the development of systemic complications. Two patients, who were in cardiogenic shock before operation, died from progressive cardiac failure. It is concluded that controlled arterioarterial limb reperfusion may reduce the local manifestation of the postischaemic syndrome after prolonged periods of ischaemia, salvage limbs thought to be irreversibly damaged by prolonged ischaemia and is easily performed in the operating room.
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Gracia-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.

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Ischaemia/reperfusion injury is an important cause of liver damage during surgical procedures such as hepatic resection and liver transplantation, and represents the main cause of graft dysfunction post-transplantation. Molecular processes occurring during hepatic ischaemia/reperfusion are diverse, and continuously include new and complex mechanisms. The present review aims to summarize the newest concepts and hypotheses regarding the pathophysiology of liver ischaemia/reperfusion, making clear distinction between situations of cold and warm ischaemia. Moreover, the most updated therapeutic strategies including pharmacological, genetic and surgical interventions, as well as some of the scientific controversies in the field are described.
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Rozprawy doktorskie na temat "Ischaemia and reperfusion damage"

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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.

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Gartshore, 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.

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Widen, 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.

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The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.
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Widen, Cecilia. "Energetics of Mouse Papillary Muscle". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367649.

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The overall aim of this Thesis was to characterise the energetic properties of the mouse papillary muscle as this preparation could become a useful model to study alterations of energetic aspects of cardiac pathologies and heart-focussed genetic changes. Measurements of resting and active metabolism of the papillary muscles were made in vitro using the myothermic technique. In the first study the mechanism underlying impaired contractility of post-ischaemic rat papillary muscle was investigated. The rat preparation is well established and was used to develop protocols and approaches that could later be used as the basis for studies with mouse papillary muscle. The muscles were exposed to simulated ischaemia for 60 min and change in energetics was studied 30 min into the reperfusion phase. The work output was reduced to 66 ± 3% of the pre-ischaemia value and the enthalpy output decreased to 71 ± 3% of pre-ischaemia value. However, there was no change in either initial, 19 ± 3%, or net mechanical efficiency, 9.0 ± 0.9%. These data, in combination with studies of Ca2+ handling, suggests that the reduced work output was caused by attachment of fewer cross-bridges in each twitch, but with no change in work generated by each cross-bridge. The following two studies involved characterisation of the energetics of the mouse papillary muscle and included measurements of resting and active metabolism. The resting metabolic rate varied with muscle size but the mean initial value was tilda 25 mW g-1 and the estimated steady value tilda 5 mW g-1 . The resting metabolic rate declined exponentially with time towards a steady value, with a time constant of 18 ± 2 min. There was no alteration in isometric force output during this time. The magnitude of resting metabolism depended inversely on muscle mass, more than doubled following a change in substrate from glucose to pyruvate and was increased 2.5-fold when the osmolarity of the bathing solution was increased by addition of 300 mM sucrose. Addition of 30 mM BDM affected neither the time course of the decline in metabolic rate nor the eventual steady value. The energy requirements associated with contractile activity were tilda7 mJ g-1 twitch-1 at a contraction frequency of 1 Hz. The enthalpy output was not affected by changing substrate from glucose to pyruvate but did decrease with an increase in temperature. The enthalpy output was partitioned into force-dependent and force-independent components using BDM to selectively inhibit cross-bridge cycling. The force-independent enthalpy output was 18.6 ± 1.9% of the initial enthalpy output. Muscle initial efficiency was &tilda;32% and net efficiency tilda 17% when shortening at a realistic velocity. The enthalpy output decreased with increased contraction frequency but was independent of shortening velocity. On the basis of these values, it was calculated that the twitch energetics were consistent with ATP splitting by half the cross-bridges and the pumping of one Ca 2+ into the SR for every three cross-bridge cycles. The lack of influence of shortening velocity on energy cost supports the idea that the amount of energy to be used is determined early in a twitch and is not greatly influenced by events that occur during the contraction. The suitability of the mouse papillary muscle as a model to study ischaemia and reperfusion damage was also assessed. This preparation is excellent for studying muscle specific changes in work and enthalpy output; however, due to the long-term instability and variability amongst preparations, the suitability of this preparation in prolonged experiments remains uncertain.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Physiotherapy and Exercise Science
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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.

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Kaskar, 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.

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Thesis (MScMedSc)--Stellenbosch University, 2015.
ENGLISH 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.
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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.

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Mankad, Pankaj Shashikant. "Ischaemia-reperfusion injury and endothelial dysfunction". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392286.

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Koo, 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.

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Kidney transplants from both living-related (LRD) and living unrelated (LURD) donors have superior function and survival than transplants from cadaver donors. This may be unsurprising as kidneys from living donors are procured under optimal conditions, from healthy donors with minimal ischaemia times. In contrast, cadaver kidneys are obtained from traumatised donors and may experience extended periods of cold ischaemic storage before transplantation. An immunohistochemical analysis has been performed on biopsies obtained before, and immediately after transplantation, to investigate the potential causes of early inflammatory events associated with cadaver renal transplantation that may influence subsequent graft outcome. An immunohistochemical analysis of biopsies obtained before transplantation demonstrated upregulated expression of endothelial E-selectin and proximal tubular expression of ICAM-1, VCAM-1 and HLA Class II antigens in cadaver donor kidneys. Analysis of donor parameters demonstrated that traumatic physiological events experienced in intensive care around the time of brain death were significantly associated with the induction of proinflammatory antigens. Antigen induction in cadaver donor kidneys before transplantation was significantly associated with early acute rejection. Furthermore, in cadaveric kidneys with long cold ischaemia times, glomerular neutrophil infiltration and deposition of activated platelets expressing P-selectin on intertubular capillaries were detected following reperfusion, in association with impaired short and long term graft function. Expression of inflammatory mediators were absent in all LRD renal allografts before and after reperfusion. A clinical trial was performed to determine whether ischaemia/reperfusion injury may be ameliorated by reflushing cadaver kidneys after cold storage to remove harmful products that may have accumulated in the vessel lumen. Reflushing did not prevent the inflammatory events observed after reperfusion or improve graft function. Therefore, a novel, oxygen free radical scavenger (lec-SOD) was obtained to assess its potential efficacy in preventing ischaemia/reperfusion injury. Lec-SOD bound with high affinity to macro- and microvascular endothelial cells under cold hypoxic conditions following incorporation into Marshall's preservation solution, significantly inhibiting cold hypoxia induced cell death, adhesion molecule induction and neutrophil adhesion. Furthermore, preservation of kidneys with lec- SOD for 18 hr in an experimental model of chronic renal allograft rejection, significantly attenuated neutrophil infiltration and MHC Class I induction day 1 post-transplant, with improved long term renal function. The results presented in this Thesis demonstrate that donor factors and cold ischaemia/ reperfusion injury elicit an early inflammatory response that may influence graft outcome of cadaver kidneys. Refinements in donor management and organ preservation may limit the deleterious effects of ischaemia/reperfusion injury in cadaver renal allografts, increasing graft survival to that observed in living donor transplantation.
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Cartaya, 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.

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Książki na temat "Ischaemia and reperfusion damage"

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A, Grace P., i Mathie Robert T, red. Ischaemia reperfusion injury. Oxford: Blackwell Science, 1999.

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Khaira, Harmeet Singh. Ischaemia-reperfusion in intermittent claudication. Birmingham: University of Birmingham, 1995.

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Wilson, Ian Clark. The role of leucocytes in neonatal myocardial ischaemia-reperfusion injury. Birmingham: University of Birmingham, 1994.

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1932-, Abiko Yasushi, i Karmazyn M. 1950-, red. Protection against ischemia/reperfusion damage of the heart. Tokyo: Springer, 1998.

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Abiko, 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.

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Herman, Stanley Leon. Age differences in the susceptibility of the normal rabbit myocardium to injury following ischaemia and reperfusion. Ottawa: National Library of Canada, 1992.

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Alfred 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.

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Smith, T. C. G. 1939-, red. Ischaemia in head injury: 10th European Congress of Neurosurgery, Berlin 1995 ; proceedings of a special symposium. Berlin: Springer, 1996.

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Fink, Mitchell P. Ischaemia-reperfusion injury in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0308.

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Ischaemia/reperfusion (I/R) injury contributes to the pathogenesis of many common clinical conditions, including stroke, myocardial damage after percutaneous intervention for acute coronary artery occlusion, primary graft dysfunction after solid organ transplantation. The mechanisms that are responsible for I/R injury remain incompletely understood, but damage caused by reactive oxygen species (ROS) and reactive nitrogen species clearly is important. A number of therapeutic approaches, such as administration of ROS scavengers, are effective in animal models of I/R injury, but for the most part, translation of these findings into strategies that can clearly benefit patients has yet to be achieved.
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Hausenloy, Derek, i Derek Yellon, red. An Introduction to Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0001.

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• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.
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Części książek na temat "Ischaemia and reperfusion damage"

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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.

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Ferrari, 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.

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Rutgers, 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.

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Froghi, 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.

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Adembri, 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.

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Lochner, 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.

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Sumeray, 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.

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Cohadon, 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.

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Symon, 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.

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Teasdale, 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.

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Streszczenia konferencji na temat "Ischaemia and reperfusion damage"

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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.

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Bhandal, 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.

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Dookun, 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.

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Lim, 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.

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Draganova, 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.

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Loerakker, 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.

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Sustained mechanical loading of soft tissues covering bony prominences, as experienced by bedridden and wheelchair-bound individuals, may cause skeletal muscle damage. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, and progresses towards the skin. Damage pathways leading to DTI can involve ischemia, ischemia/reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, we have provided evidence that in a controlled animal model, deformation is the main trigger for damage within a 2h loading period [1,2]. However, ischemia and reperfusion may play a more important role in the damage process during prolonged loading periods.
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Yazir, 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.

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Ostróżka-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.

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Kandemir, 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.

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Platt, 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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