Thematische Bibliographien / Reperfusion injury / Dissertationen
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Dissertationen zum Thema „Reperfusion injury“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 25. Juli 2025

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1

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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2

Amrani, Mohamed. "Postischemic coronary flow and reperfusion injury." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307467.

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3

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 potenti
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4

Nitisha, Hiranandani. "Impact of Reperfusion Injury on Heart." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1239720273.

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5

Aluri, Hema. "INTRA-MITOCHONDRIAL INJURY DURING ISCHEMIA-REPERFUSION." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/474.

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Cardiac injury is increased following ischemia-reperfusion. Mitochondria are the “effector organelles” that are damaged during ischemia (ISC) when there is no blood flow. Resumption of metabolism by damaged mitochondria during reperfusion (REP) results in increased cell injury. Current therapeutic interventions to pre-condition and post-condition the heart during ISC are ineffective during certain conditions like aging and diabetes due to defects in the signaling cascades. In contrast, mitochondrial-based strategies are effective in protecting the heart during ISC-REP. Hence direct therapeutic
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Fitridge, 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.

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7

MIHAYLOV, PLAMEN VESELINOV. "Ischemic reperfusion injury in Liver transplantation." Doctoral thesis, Università degli studi di Pavia, 2021. http://hdl.handle.net/11571/1434014.

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About 119,592 patients are currently on the organ transplant waiting list in the US, with the number increasing by 5% every year. In 2017, 11,640 candidates were added to the liver transplant waiting list. While the increase in the number of liver transplants is encouraging, the organ shortage remains critically high. During 2015, 1673 patients died without undergoing transplant and another 1227 were removed from the waiting list due to being too sick to undergo transplant. The major untapped pool of donor organs that could be used to alleviate this crisis in organ transplantation are steatot
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8

Thummachote, 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.

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9

Kinross, 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.

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10

Winbladh, Anders. "Microdialysis in Liver Ischemia and Reperfusion injury." Doctoral thesis, Linköpings universitet, Kirurgi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-68651.

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Introduction: New chemotherapy regimens and improvements in surgical technique have increased the number of patients with liver tumours eligible for curative liver resection. There is a significant risk of bleeding during liver surgery, but this risk can be reduced if the portal inflow is temporarily closed; i.e. the Pringles maneuver (PM). If the PM is used, the liver will suffer from ischemia and reperfusion injury (IRI). If the liver remnant is too small or if the patient has chronic liver disease, the IRI may inhibit the regeneration of the liver remnant. The patient may then die from post
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Björnsson, Bergþór. "Methods to Reduce Liver Ischemia/Reperfusion Injury." Doctoral thesis, Linköpings universitet, Institutionen för klinisk och experimentell medicin, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-110318.

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Introduction: During the last two decades, liver surgery has expanded enormously, partly due to improved surgical equipment and techniques as well as new and more powerful chemotherapy agents. As the liver is a very well-vascularized organ, there is an inherent risk of bleeding during liver resection. One of the most popular methods employed to reduce this risk is to close the vascular inflow to the liver using the Pringle’s maneuver (PM). However, this procedure has been recognized to cause ischemia/reperfusion injury (IRI) to the future liver remnant (FLR). In cases of extensive resection wh
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12

Sheth, H. "Therapeutic modulation of liver ischaemia reperfusion injury." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318134/.

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Liver Ischaemia Reperfusion Injury (IRI) leads to production of reactive oxygen species and cytokines, which affects hepatocellular function following liver resection and transplantation. This thesis examines 2 hypotheses: 1) The role of intravenous glycine in amelioration of liver IRI in a in vivo animal model of partial lobar liver IRI. 2) Does prophylactically administered N-acetylcysteine prevent liver IRI in patients undergoing elective liver resection. Materials and Methods 1) A rabbit model of hepatic lobar IRI was used to evaluate glycine. 3 groups (n=6) Sham group (laparotomy alone),
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Mokhtarudin, 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.

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Restoring cerebral blood flow using reperfusion treatment is a common method in treating ischaemic stroke. Reperfusion treatment should be given within 4.5 hours from stroke onset. However, reperfusion beyond this time window poses the risk of reperfusion injuries such as intracranial haemorrhage and cerebral tissue swelling. The focus of this thesis is to study the effect of cerebral tissue swelling after reperfusion as it can occur in a few hours after the treatment. Cerebral tissue swelling may cause brain structure movement and cerebral microvessel compression; the latter may then lead to
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Mao, Xiaowen, and 毛晓雯. "Peroxynitrite/Ho-1 interaction in propofol post-conditioning protection against myocardial ischemia reperfusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193463.

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Coronary artery disease limits myocardial blood flow and results in myocardial infarction. Reperfusion therapies restore coronary flow, but may also cause myocardial ischemia reperfusion injury (MIRI). Multiple critical factors contribute to MIRI and among them, oxidative stress plays an important role. This burst of oxidative stress during reperfusion is caused by a variety of sources which collectively are called reactive oxygen species (ROS). Peroxynitrite is more cytotoxic than other ROSs, which at high concentration serves as a detrimental molecule with a variety of target. Peroxynitrite
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Woodfine, Lynne. "An investigation of therapeutic intervention in reperfusion injury." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361560.

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16

Bullard, Anthony John. "The role of erythropoietin in ischaemia/reperfusion injury." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445332/.

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Background - Ischaemia/reperfusion accounts for a large proportion of fatalities in the developed world. Even if death is avoided, the patient suffers a deterioration in their quality of life. Erytriropoietin (EPO) has been examined in clinical studies investigating its effect in anaemic chronic heart failure patients with any positive effect attributed to the correction of anaemia. Given the recent discovery of the EPO receptor on the myocyte surface, this thesis examined whether EPO could have a direct effect on the myocardium and limit ischaeinia/reperfUsion injury and the mechanism by whic
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Duarte, Sérgio Miguel Coelho. "Matrix-leukocyte interactions in liver ischemia-reperfusion injury." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63694.

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18

Moore, Rustin MacArthur. "Large colon ischemia-reperfusion injury in the horse /." The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487853913101881.

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19

Salloum, Fadi N. "Novel Strategies in Cardioprotection against Ischemia/Reperfusion Injury." VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1227.

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Cell damage represents a major pathomechanism in many diseases of high clinical interest, such as myocardial infarction (MI), where it plays an important role in ischemia-reperfusion (I/R) injury. Considerable progress has been made towards identifying physiological and pharmacological agents that play a key role in myocardial preconditioning against I/R injury and also elucidating the molecular changes leading to such protection.Second messengers in cellular signaling pathways, such as cGMP have been well implicated as key players in ischemic and pharmacological preconditioning (PC) of the he
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Nitta, Takashi. "Myoglobin gene expression attenuates hepatic ischemia reperfusion injury." Kyoto University, 2003. http://hdl.handle.net/2433/148743.

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21

White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.

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Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The causes of stunning are not fully elucidated, however two major hypotheses currently exist; firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free radical (OFR) that may occu
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Duarte, Sérgio Miguel Coelho. "Matrix-leukocyte interactions in liver ischemia-reperfusion injury." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2011. http://hdl.handle.net/10216/63694.

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23

Xu, Xingshun. "Novel Protective Agents against Cerebral Ischemia/Reperfusion Injury." Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2054.

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Stroke is the third leading cause of death and disability in the United States. At present, intravenous administration of tissue plasminogen activator (t-PA) is the only thrombolytic therapy approved by the FDA for the treatment of acute ischemic stroke. There are no other effective treatments available so far. The discovery of new drugs and new treatments for stroke to reduce mortality and disability is an urgent medical research priority. In this study, the protective effects and mechanisms of two novel agents Gly14 humanin (HNG) and necrostatin-1 (Nec-1) were examined. HNG, a highly potent
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Bejaoui, Mohamed. "Polyethylene glycol conditioning: An effective strategy to protect against liver ischemia reperfusion injury." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/385612.

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Ischemia is defined by the arrest of blood flow in the organ cutting thus oxygen and metabolite supply indispensable for its survival and function. Restoration of blood flow in hypoxic tissue, called reperfusion, can paradoxically result in more destructive than beneficial effects. Ischemia reperfusion injury (IRI) is an inevitable problem in many clinical situation of liver surgery such as organ transplantation, trauma and liver resection. Therapeutic strategies against IRI have been developed during the last 60 years and great advance into the mechanisms responsible of injuries have been ach
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Georgiev, Panco. "Normothermic ischemia reperfusion injury in the cholestatic mouse liver /." Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000256332.

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Cohen, Ari J. "Pharmacological modification to prevent reperfusion injury following liver transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23260.pdf.

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27

Brown, David Avery. "Myocardial ATP-sensitive potassium channels and ischemia/reperfusion injury." Diss., Connect to online resource, 2005. http://wwwlib.umi.com/cr/colorado/fullcit?p3190363.

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28

Du, Xiaojian. "Regulation of EphA2 expression in renal ischemia-reperfusion injury." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111599.

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Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury in both native kidneys and renal allografts. Previous studies in our lab have shown that a subset of Eph family receptor tyrosine kinases, including EphA2, is strongly and persistently upregulated in renal tubular cells in both in vitro and in vivo models of the renal IRI. Src kinases are necessary and sufficient for upregulation of EphA2. We have proposed that IRI-induced EphA2 upregulation may serve as a necessary step in renal tubular remodelling.<br>In this study, we have further defined the mechanism of Src kinase-i
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Hau, 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.

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30

宋蘭 and Lan Fion Sung. "Regulation of chemokine expression during renal ischemia/reperfusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31244804.

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31

Schulman, 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.

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32

Patel, 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.

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33

Llwyd, Osian. "The involvement of CaMKII in myocardial ischaemia-reperfusion injury." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/43619/.

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CaMKII acts as a second messenger to Ca2+ signals within the cardiac myocyte. Cellular stresses such as ischaemia and subsequent reperfusion perturb the normal physiological oscillations of Ca2+ to cause an escalating concentration which damages the cell. CaMKII has been implicated as an injury signal during such cellular conditions. However, there are discrepancies as to whether CaMKII is a possible mechanism of ischaemic preconditioning as its inhibition can abrogate or improve the protective effect of preconditioning. This thesis investigated the effects of CaMKII inhibition in models of is
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Stefanutti, G. "Novel experimental therapies for intestinal ischaemia and reperfusion injury." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1334603/.

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Intestinal ischaemia and reperfusion (I/R) contributes to the pathogenesis of numerous clinical conditions in all age groups. Many of these diseases, including neonatal necrotizing enterocolitis (NEC), result in significant morbidity and mortality through multiple organ dysfunction, and available treatment is currently limited to supporting vital functions. My aims were: to investigate novel therapeutic strategies such as moderate hypothermia and peroxynitrite decomposition catalyst FeTMPyP [5,10,15,20- tetrakis(N-methyl-4'-pyridyl)porphyrinato iron (III)] in experimental models of adult and i
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Sharma, V. "Novel signalling pathways in myocardial conditioning against reperfusion injury." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1407936/.

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Ischaemic preconditioning (IPC) and insulin protect the heart against lethal ischaemia-reperfusion (IR) by activating cardioprotective kinases such as PI3K-AKT. This thesis explores the effect of endothelial dysfunction, as seen in diabetes - a major risk factor for ischaemic heart disease, on IPC using the ESMIRO mice. These mice have dysfunctional vascular insulin receptors as well as endothelial dysfunction similar to that present in diabetes. Further, the effect of vascular insulin resistance on the ability of insulin to condition the heart against IR injury is investigated. The thesis als
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van, As Arjan Bastiaan. "Improvement of liver transplantation by reducing preservation-reperfusion injury." Doctoral thesis, University of Cape Town, 1999. http://hdl.handle.net/11427/26770.

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The liver differs from other solid organs in that it has a dual blood supply, receiving arterial blood via the hepatic artery and venous blood via the portal vein. The reperfusion injury which occurs after ischemia, has been studied to only a limited extent in the liver. In particular, the relative contribution of the portal venous blood and the hepatic arterial blood to the reperfusion injury has not been documented previously. During liver transplantation, implantation of the new liver is achieved by anastomosing the suprahepatic vena cava, the infrahepatic vena cava and the portal vein. At
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Wang, Guona. "The role of lipocalin-2 in stroke reperfusion injury." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1448895817.

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Chuang, Chia-Chen. "Characterization of Reperfusion Injury-Induced ROS in Striated Muscles." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500479949278294.

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Hunter, James Philip. "The role of hydrogen sulphide in ischaemia reperfusion injury." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/35951.

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Warm ischaemic injury occurs when an organ or region of the body is starved of oxygenated blood under normothermic conditions. Two important clinical examples of warm ischaemia are donation after circulatory death (DCD) kidney transplantation and abdominal aortic aneurysm (AAA) repair. The tissue injury that results from warm ischaemia can lead to organ dysfunction, which has important clinical consequences. In kidney transplantation warm ischaemic injury can lead to delayed graft function, increased rates of primary non-function and poorer long-term outcomes. In open AAA repair occlusion of t
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Dare, 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.

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Reyes, Leila. "Involvement of inflammatory oxidants in cardiac ischaemia/reperfusion injury." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/19667.

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Oxidative stress is a major feature of cardiac ischaemia/reperfusion (I/R) injury, with strong evidence implicating infiltrating leukocytes, in particular neutrophils, as a major source of oxidants in the infarcted myocardium. Activated leukocytes release the peroxidase enzyme, myeloperoxidase (MPO), which can produce the oxidants hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN). Chapter 3 examines the differential cellular effect of (patho)-physiological levels of HOCl and HOCN in cardiomyocytes. Both HOCl and HOSCN induced cellular damage characteristic of cardiac I/R injury and hig
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Venardos, Kylie M. "Myocardial Antioxidant Enzyme Systems, Ischemia-Reperfusion Injury, and Selenium." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365301.

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Coronary heart disease remains the greatest killer of Australian's, and given our ageing population, along with increasing risk factors, it is predicted to become an even more significant problem worldwide over the next 20 years. Reperfusion, without doubt is the most effective treatment for ischemic myocardium. However, this produces deleterious effects upon cells, and depending on the severity, may ultimately lead to cell death. While the pathogenesis of ischemia-reperfusion is not completely understood, there is considerable evidence implicating reactive oxygen species (ROS) as an initial c
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Jahangiri, Anisa. "n-3 PUFAs and reperfusion injury in isolated cardiomyocytes." Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phj251.pdf.

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"September 2002" Bibliography: leaves 207-230. Ch. 1. Literature review -- Ch. 2. General methods -- Ch. 3. Dietary n-3 PUFAs and reperfusion injury in isolated cardiomyocytes -- Ch. 4. The effect of dietary n-3 PUFAs on cardiomyocyte membrane fluidity, intracellular ROS and Ca 2+ levels during oxidative stress -- Ch. 5. The effect of dietary fish oil supplementation on antioxidant enzyme gene expression in rat myocardium -- Ch. 6. The effect of dietary lipids on ischaemia-reperfusion injury in rat myocardium -- Ch. 7. General discussion -- Ch. 8. Appendices. The broad aims of this thesis were
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Becker, Bryan A. "The effects of ischemia-reperfusion injury on cytosolic and mitochondrial levels of glutathione in the rat kidney." Virtual Press, 2001. http://liblink.bsu.edu/uhtbin/catkey/1204198.

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This study was done to investigate the effect of ischemia-reperfusion injury on cytosolic and mitochondrial glutathione levels in the rat kidney. Glutathione is the main cellular defense against free radicals that are thought to cause ischemia-reperfusion injury. Right kidneys from anesthetized female Lewis rats (9-12 months old) were exposed to 60 minutes of ischemia followed by 0, 30, or 120 minutes of reperfusion. The kidneys were perfused with isotonic saline, harvested, homogenized, and separated into cytosolic and mitochondrial fractions by differential centrifugation. Reduced (GSH) and
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Nemours, Stéphane. "Identification of time- and sex-dependent pathways involved in renal ischemia-reperfusion injury in a porcine model. Link to renal cancer." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670696.

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Les malalties renals es deriven de defectes congènits, lesions renals agudes (AKI) o malalties renals cròniques (CKD), entre altres causes. La lesió renal d’isquèmia /reperfusió (IRI), que es troba en moltes situacions clíniques, és una de les causes principals de l’AKI que causen lesions i mort de cèl·lules epitelials del túbul proximal (PTEC). La gravetat de l’AKI i la capacitat de regenerar-se després de la lesió són determinants importants de la morbiditat i mortalitat dels pacients en un entorn hospitalari. Els homes són més propensos a la malaltia renal aguda i crònica i a avançar fins a
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Oredsson, Sven. "Reperfusion injury in skeletal muscle with special reference to oxygen-derived free radicals as mediators /." Lund : Dept. of Surgery, Helsingborg Hospital, 1994. http://catalog.hathitrust.org/api/volumes/oclc/39056318.html.

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Mörtberg, Erik. "Assessment of the Cerebral Ischemic/Reperfusion Injury after Cardiac Arrest." Doctoral thesis, Uppsala universitet, Anestesiologi och intensivvård, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-132681.

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The cerebral damage after cardiac arrest is thought to arise both from the ischemia during the cardiac arrest but also during reperfusion. It is the degree of cerebral damage which determines the outcome in patients. This thesis focuses on the cerebral damage after cardiac arrest. In two animal studies, positron emission tomography (PET) was used to measure cerebral blood flow, oxygen metabolism and oxygen extraction in the brain. After restoration of spontaneous circulation (ROSC) from five or ten minutes of cardiac arrest there was an immediate hyperperfusion, followed by a hypoperfusion whi
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Morsey, 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.

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Harrison, Ewen M. "Pharmacological strategies to reduce ischemia/reperfusion injury in kidney transplantation." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24683.

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I investigated the influence of the phosphatidylinositol 3-kinase (PI3K)Akt pathway on HSF1 activation status. Despite effecting significant up-regulation of the PI3k/Akt pathway with insulin and insulin-like growth factor-1 (IGF-1), I did not demonstrate any change in the HSF1 trimerisation state, DNA-binding ability or nuclear localisation in renal adenocarcinoma cells (ACHN). Following treatment with insulin, a 5-fold increase in heme oxygenase-1 (HO-1) mRNA and a 4-fold increase in protein expression were observed in ACHN cells; insulin-induced HO-1 expression was also demonstrated in mous
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Sudarshan, Catherine. "Inhaled nitric oxide and reperfusion injury in experimental lung transplanation." Thesis, University of Newcastle upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438028.

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