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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.
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 źródłaFitridge, Robert Alwyn. "Reperfusion injury in focal cerebral ischaemia /". Title page, table of contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09MS/09msf546.pdf.
Pełny tekst źródłaThummachote, Mr Yongsuk. "The pathopysiological consequence of ischaemia reperfusion injury". Thesis, University of London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498481.
Pełny tekst źródłaKinross, James M. "Systems metabolism of intestinal ischaemia/reperfusion injury". Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.543342.
Pełny tekst źródłaSheth, H. "Therapeutic modulation of liver ischaemia reperfusion injury". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318134/.
Pełny tekst źródłaLaight, David W. "Neutrophils and vascular reactivity in ischaemia/reperfusion". Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385291.
Pełny tekst źródłaMokhtarudin, Mohd Jamil Mohamed. "Mathematical modelling of cerebral ischaemia-reperfusion injury". Thesis, University of Oxford, 2016. http://ora.ox.ac.uk/objects/uuid:3f5dd7cf-e403-4cf0-b725-4ac235c1b37e.
Pełny tekst źródłaVejchapipat, Paisarn. "Intestinal and hepatic metabolism after intestinal ischaemia reperfusion". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248437.
Pełny tekst źródłaRichardson, Simon. "Studies of ischaemia and reperfusion in cardiac hypertrophy". Thesis, University of Hull, 2002. http://hydra.hull.ac.uk/resources/hull:13202.
Pełny tekst źródłaBullard, Anthony John. "The role of erythropoietin in ischaemia/reperfusion injury". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445332/.
Pełny tekst źródłaHau, Han Lim Kelvin. "The mitochondria and myocardial protection against ischaemia-reperfusion injury". Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500392.
Pełny tekst źródłaSchulman, Daniel. "The influence of age on myocardial ischaemia/reperfusion injury". Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272252.
Pełny tekst źródłaPatel, Hetal Brijesh. "Therapeutic inhibition of complement in renal ischaemia reperfusion injury". Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438220.
Pełny tekst źródłaLlwyd, Osian. "The involvement of CaMKII in myocardial ischaemia-reperfusion injury". Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/43619/.
Pełny tekst źródłaHeadley, Elsbeth Louise. "Angiotensin II and ischaemia-reperfusion in rat isolated hearts". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619871.
Pełny tekst źródłaStefanutti, G. "Novel experimental therapies for intestinal ischaemia and reperfusion injury". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1334603/.
Pełny tekst źródłaHay, Joanna. "Regulation of gene expression during myocardial ischaemia and reperfusion". Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29716.
Pełny tekst źródłaHunter, James Philip. "The role of hydrogen sulphide in ischaemia reperfusion injury". Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/35951.
Pełny tekst źródłaDare, Anna Jane. "Targeting mitochondria during ischaemia-reperfusion injury in organ transplantation". Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708069.
Pełny tekst źródłaReyes, Leila. "Involvement of inflammatory oxidants in cardiac ischaemia/reperfusion injury". Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/19667.
Pełny tekst źródłaMorsey, Hesham. "Ischaemia reperfusion injury in patients with peripheral arterial occlusive disease". Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516556.
Pełny tekst źródłaLe, Moine Olivier. "Interleukin-10 in liver ischaemia-reperfusion injury and alcoholic cirrhosis". Doctoral thesis, Universite Libre de Bruxelles, 1996. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212296.
Pełny tekst źródłaBoag, Stephen Edward. "The role of T lymphocytes in myocardial ischaemia/reperfusion injury". Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3237.
Pełny tekst źródłaSevastos, Jacob Prince of Wales Clinical School UNSW. "The role of tissue factor in renal ischaemia reperfusion injury". Awarded by:University of New South Wales. Prince of Wales Clinical School, 2006. http://handle.unsw.edu.au/1959.4/27416.
Pełny tekst źródłaPatel, Nimesh. "Pathophysiology and therapy of renal ischaemia/reperfusion injury in rodents". Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419534.
Pełny tekst źródłaHide, Emma Jane. "Role of endogenous vasoactive mediators against myocardial ischaemia/reperfusion injury". Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267296.
Pełny tekst źródłaBell, Robert Midgley. "The role of nitric oxide in myocardial ischaemia/reperfusion injury". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248197.
Pełny tekst źródłaD'Souza, Savio Pvb Vitorino Baptista. "Type-B natriuretic peptide (BNP) in myocardia ischaemia-reperfusion injury". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404423.
Pełny tekst źródłaBushell, 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 źródłaSiddall, H. K. "The role of PTEN in cardioprotection against ischaemia-reperfusion injury". Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/19053/.
Pełny tekst źródłaFan, Wen Jun. "The role of protein phosphatases in myocardial ischaemia and reperfusion". Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/21615.
Pełny tekst źródłaENGLISH ABSTRACT: Protein kinases and phosphatases play important roles in the phosphorylation state of intracellular proteins under both physiologic and pathophysiologic conditions. Compared to the large number of studies investigating the significance of kinases, in particular the mitogen-activated protein kinases (MAPKs) in myocardial ischaemia/reperfusion and ischaemic preconditioning, relatively few studies have been done on the protein phosphatases in this scenario. Although several role players in the signal transduction cascade of ischaemia/reperfusion and ischaemic preconditioning have been identified thus far, the exact mechanism of cardioprotection still remains unclear. Previous studies from our laboratory have shown that the stress kinase, p38 MAPK, has a dual role in preconditioning: it acts as trigger of the process, while attenuation of its activation during sustained ischaemia and reperfusion is required for cardioprotection. Since the activation of p38 MAPK is dependent on both the upstream kinases for phosphorylation and phosphatases for dephosphorylation, we hypothesized that the balance between the activation state of the MAPKs and the induction of phosphatases may play a major role in determining the fate of cardiomyocytes exposed to ischaemic stress. The objectives of this study were: (i) to assess the activity of the myocardial protein phosphatases (PSPs and PP1) during sustained ischaemia and during reperfusion of non-preconditioned and ischaemic preconditioned hearts; (ii) to evaluate the significance of these phosphatases in ischaemia/reperfusion as well as in ischaemic preconditioning using available appropriate inhibitors; (iii) to give particular attention to the role of the phosphatase, mitogen-activated protein kinase phosphatase-1 (MKP-1), in ischaemia/reperfusion. MKP-1 is upregulated by stress conditions and selectively inactivates p38 MAPK by dephosphorylation of the regulatory Thr and Tyr residues. The glucocorticoid, dexamethasone which increases MKP-1 expression, was used as agonist to upregulate MKP-1 experimentally. The isolated perfused working rat heart was used as experimental model. After stabilization, hearts were subjected to either a one-cycle or multi-cycle ischaemic preconditioning protocol, followed by sustained global or regional ischaemia and reperfusion. Non-preconditioned hearts were subjected to ischaemia/reperfusion only. For Western blot analysis of MAPKs, PKB/Akt and MKP-1, hearts were freeze-clamped at different times during the perfusion protocol. Endpoints were infarct size, functional recovery and phosphorylation of the MAPKs (ERK and p38 MAPK) and PKB/Akt during reperfusion. Expression of MKP-1 was monitored. The results obtained showed that activation of PSPs and PP1 does not occur during sustained global ischaemia or reperfusion of non-preconditioned and preconditioned hearts. The role of the phosphatases was subsequently further investigated using two inhibitors namely cantharidin (5 μM, a concentration which inhibits both PP1 and PP2A) and okadaic acid (7.5 nM, a concentration which inhibits PP2A selectively). Administration of cantharidin or okadaic acid during the preconditioning phase, completely abolished preconditioning induced cardioprotection as indicated by mechanical failure during reperfusion and increased infarct size, associated with increased phosphorylation of p38 MAPK and PKB/Akt and dephosphorylation of ERK42/44. These results suggest a role for PP2A in the trigger phase of preconditioning. Administration of cantharidin or okadaic acid during early reperfusion of preconditioned hearts improved functional recovery. This was associated with increased phosphorylation of ERK42/44 and PKB, but not p38 MAPK. Dexamethasone, administered intraperitoneally to rats for 10 days (3mg/kg/day) or directly added to the perfusate (1 μM) resulted in significant cardioprotection of hearts subjected to 20 min sustained global ischaemia, followed by 30 min reperfusion. This is associated with a marked upregulation of MKP-1 and dephosphorylation of p38 MAPK during reperfusion. These studies suggest that the phosphatases are definitely involved in the phenomenon of ischaemia/reperfusion and ischaemic preconditioning. However, it also become clear that extensive further research is required to fully elucidate which phosphatases are involved and the mechanisms thereof. Due to the large size of the protein phosphatase family, this may prove to be a formidable task and far beyond the scope of this thesis. The results also suggested that pharmacological targetting of phosphatases involved in phosphorylation of the reperfusion injury salvage kinase (RISK) pathway (e.g. ERK42/44 and PKB/Akt) or dephosphorylation of pro-apoptotic kinases, such as p38 MAPK, may have significant clinical potential.
AFRIKAANSE OPSOMMING: Proteïenkinases en fosfatases speel 'n belangrike rol in die fosforileringstatus van intrasellulêre proteïene in beide fisiologiese en patofisiologiese toestande. In teenstelling met die groot aantal studies gedoen ten einde die rol van die kinases, veral die mitogeen-geaktiveerde proteïenkinases (MAPKs), in iskemie/herperfusie en iskemiese prekondisionering te ondersoek, is relatief min bekend aangaande die rol van die fosfatases in hierdie scenario. Hoewel verskeie rolspelers in die seintransduksieprosesse van iskemie/herperfusie en iskemiese prekondisionering reeds geïdentifiseer is, is die presiese meganisme van miokardiale beskerming steeds onbekend. Vroeëre studies vanuit ons laboratorium het getoon dat die streskinase, p38 MAPK, 'n tweeledige rol in prekondisionering speel: dit is 'n sneller ("trigger") van die proses, terwyl verlaagde aktivering tydens volgehoue iskemie en herperfusie, noodsaaklik vir beskerming is. Ons hipotese is dus dat die balans tussen die aktiveringstatus van die MAPKs en induksie van fosfatases die oorlewing van kardiomiosiete blootgestel aan iskemiese stres, bepaal. Die doelwitte van hierdie studie was: (1) bepaling van die aktiwiteit van miokardiale proteïen fosfatases (PSPs en PP1) tydens volgehoue iskemie en herperfusie van nie-geprekondisioneerde en iskemies-geprekondisioneerde harte; (ii) evaluering van die belang van fosfatases in iskemie/herperfusie beskadiging sowel as in iskemiese prekondisionering deur van geskikte inhibitore gebruik te maak; (iii) ondersoek na die rol van die fosfatase, mitogeen-geaktiveerde proteïen kinase fosfatase-1 (MPK-1) in iskemie/herperfusie beskadiging. Dit is bekend dat MKP-1 deur strestoestande opgereguleer word en p38 MAPK selektief deur defosforilasie van die regulatoriese Thr en Tyr residue inaktiveer word. Die glukokortikoïed, deksametasoon, wat MKP-1 uitdrukking stimuleer, is as agonis gebruik ten einde MKP-1 eksperimenteel op te reguleer. Die geïsoleerde, geperfuseerde werkende rothart is as eksperimentele model gebruik. Na stabilisasie, is die harte aan 'n enkel- of veelvuldige siklus iskemiese prekondisioneringsprotokol onderwerp, gevolg deur volgehoue globale of streeksiskemie. Nie-geprekondisioneerde harte is slegs aan iskemie/herperfusie onderwerp. Harte is op verskillende tye tydens die perfusieprotokol gevriesklamp vir Western blot analise van die MAPKs, PKB/Akt en MKP-1. Infarktgrootte en funksionele herstel tydens herperfusie is as indikators van iskemiese beskadiging gebruik. Fosforilasie van MAPKs en PKB/Akt sowel as uitdrukking van MKP-1 tydens vroeë herperfusie is gemonitor. Die resultate toon dat aktivering van PSP en PP1 tydens volgehoue iskemie en herperfusie nie plaasvind nie. Die rol van die fosfatases is verder ondersoek deur van twee inhibitore gebruik te maak, naamlik cantharidin (5 μM inhibeer beide PP1 en PP2A) en okadaic suur (7.5 nM inhibeer PP2A selektief). Toediening van of cantharidin of okadaic suur tydens die prekondisioneringsprotokol, hef prekondisionering-geïnduseerde beskerming totaal op, soos aangetoon deur hartversaking tydens herperfusie en 'n toename in infarktgrootte, tesame met 'n toename in die fosforilering van p38 MAPK en PKB/Akt en defosforilering van ERK42/44. Hierdie waarnemings dui op 'n rol vir PP2A as sneller in prekondisionering. Toediening van hierdie inhibitore tydens vroeë herperfusie het ook die miokardium beskerm, soos aangetoon deur 'n verbeterde meganiese herstel van geprekondisioneerde harte, tesame met ‘n verhoogde fosforilering van ERK42/44 en PKB (maar nie p38 MAPK nie). Deksametasoon, intraperitoneaal toegedien, vir 10 dae (3mg/kg/dag) of direk by die perfusaat gevoeg (1μM), het tot 'n hoogs beduidende beskerming teen iskemiese beskadiging gelei van harte blootgestel aan 20 min globale iskemie en 30 min herperfusie. Hierdie toename in funksionele herstel en afname in infarktgrootte het met 'n toename in MKP-1 uitdrukking en defosforilasie van p38 MAPK gepaard gegaan. Bogenoemde resultate dui op 'n definitiewe betrokkenheid van fosfatases in iskemie/herperfusie en iskemiese prekondisionering. Dit is egter ook duidelik dat intensiewe verdere navorsing benodig word om die presiese rol van die fosfatases te bepaal. Vanweë die grootte van die fosfatase familie, val dit egter buite die beskek van hierdie studie. Ten slotte, die resultate toon dat farmakologiese manipulasie van fosfatases betrokke by die fosforileringstatus van anti-apoptotiese kinases soos ERK42/44 en PKB/Akt en defosforilasie van pro-apoptotiese kinases, soos p38 MAPK, besondere kliniese toepassings mag hê.
Bune, Alison Jane. "Nitric oxide in experimental models of endotoxic shock and glomerulonephritis". Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244288.
Pełny tekst źródłaZhang, Liqun. "Effect of streptozotocin induced diabetes on the susceptibility of ex vivo rat heart". Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248572.
Pełny tekst źródłaMacaulay, Ewan. "Ischaemia-reperfusion during infrainguinal bypass for critical limb ischaemia and the effects of a nitric oxide donor". Thesis, University of Aberdeen, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301228.
Pełny tekst źródłaWeight, Simon C. "The role of nitric acid in renal warm ischaemia reperfusion injury". Thesis, University of Leicester, 1998. http://hdl.handle.net/2381/29558.
Pełny tekst źródłaBowes, Joanne. "The role of poly (ADP-ribose) synthetase in ischaemia-reperfusion injury". Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312838.
Pełny tekst źródłaAmoah, Vincent. "The role of ischaemia-reperfusion on neutrophil activation in healthy humans". Thesis, Coventry University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.495457.
Pełny tekst źródłaLane, Nicholas James. "In vivo studies of ischaemia-reperfusion injury in rabbit renal autografts". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243454.
Pełny tekst źródłaYassin, Magdi M. I. "The effects of lower limb ischaemia-reperfusion on the gastrointestinal tract". Thesis, Queen's University Belfast, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318957.
Pełny tekst źródłaJones, Jane Elizabeth Davenport. "Neurotoxic mechanisms underlying ischaemia-reperfusion injury using rat brain spheroid cultures". Thesis, University of Hertfordshire, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302425.
Pełny tekst źródłaConnaughton, Mark. "Aspects of ischaemia and reperfusion injury in the isolated rat heart". Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266208.
Pełny tekst źródłaKapoor, Rishab. "Investigating the mechanisms of renal fibrosis following ischaemia and reperfusion injury". Thesis, University of Newcastle upon Tyne, 2018. http://hdl.handle.net/10443/4117.
Pełny tekst źródłaBose, Amal Krishna. "Glucagon like peptide-1 (GLP-1) in myocardial ischaemia-reperfusion injury". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445399/.
Pełny tekst źródłaKhwaja, Nadeem. "Pathophysiology of ischaemia reperfusion injury of the colon in cardiovascular surgery". Thesis, University of Manchester, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.525973.
Pełny tekst źródłaBabba, M. A. "Investigation into the effects of Artemisinin in myocardial ischaemia reperfusion injury". Thesis, Coventry University, 2015. http://curve.coventry.ac.uk/open/items/d5f16c89-60de-4981-8fa1-631773f92372/1.
Pełny tekst źródłaWilliams, Susan Beris. "Effects of intestinal ischaemia and reperfusion on the gut and liver". Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446537/.
Pełny tekst źródłaRoss, Sean Alexander. "Effects and interactions of anaesthetics and Kâ†Aâ†Tâ†P channels openers on left ventricular function in normal and post-ischaemic myocardium". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244622.
Pełny tekst źródłaTanveer, Ahmed. "A cyclophilin-dependent mitochondrial pore". Thesis, University College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298354.
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