Dissertationen zum Thema „Reperfusion injury“
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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.
Der volle Inhalt der QuelleAmrani, Mohamed. „Postischemic coronary flow and reperfusion injury“. Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307467.
Der volle Inhalt der QuelleKoo, 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.
Der volle Inhalt der QuelleNitisha, Hiranandani. „Impact of Reperfusion Injury on Heart“. The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1239720273.
Der volle Inhalt der QuelleAluri, Hema. „INTRA-MITOCHONDRIAL INJURY DURING ISCHEMIA-REPERFUSION“. VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/474.
Der volle Inhalt der QuelleFitridge, 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.
Der volle Inhalt der QuelleMIHAYLOV, PLAMEN VESELINOV. „Ischemic reperfusion injury in Liver transplantation“. Doctoral thesis, Università degli studi di Pavia, 2021. http://hdl.handle.net/11571/1434014.
Der volle Inhalt der QuelleAbout 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 steatotic livers and livers from Donors after Cardiac Death (DCD). Steatotic liver grafts are associated with an early allograft dysfunction rate of 60%-80% compared with less than 5% for nonsteatotic grafts. This is due to their poor tolerance to ischemic reperfusion injury. On the other hand, only 27% (518/1884) of the DCD livers were transplanted in 2017. The single major reason for this is the severe ischemia reperfusion injury in these livers. The severity of ischemic reperfusion injury is an important determinant of allograft function post-transplant. However, the mechanisms that contribute to increased susceptibility of steatotic and DCD grafts to ischemic reperfusion injury remains poorly defined. In solid organ transplantation, graft damage subsequent to ischemic reperfusion injury may result in delayed graft function. In the worst case, this complication can lead to primary graft non- function resulting in an urgent need of re-transplantation. Ischemic reperfusion injury is the consequence of temporary interruption of blood flow to the liver. Warm ischemia reperfusion injury occurs during clamping of vascular inflow during prolonged liver resections and during a donation after cardiac death organ retrieval procedure. Cold ischemia reperfusion injury results from maintenance of the liver in cold preservation and subsequent reperfusion of the graft during transplantation. Apart from its pivotal role in the pathogenesis of the liver’s post reperfusion injury, it has also been involved as an underlying mechanism responsible for the dysfunction and injury of other organs as well. Liver ischemia and reperfusion in settings of liver transplant represent an event with consequences that influence the function of many organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organ injuries can ultimately lead to multiple organ dysfunction syndrome. The objective of this thesis is to give a full and comprehensive analysis of ischemic reperfusion injury in liver transplantation.
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.
Der volle Inhalt der QuelleKinross, 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.
Der volle Inhalt der QuelleWinbladh, 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.
Der volle Inhalt der QuelleBjörnsson, 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.
Der volle Inhalt der QuelleSheth, H. „Therapeutic modulation of liver ischaemia reperfusion injury“. Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1318134/.
Der volle Inhalt der QuelleMokhtarudin, 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.
Der volle Inhalt der QuelleMao, Xiaowen, und 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.
Der volle Inhalt der Quellepublished_or_final_version
Anaesthesiology
Doctoral
Doctor of Philosophy
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.
Der volle Inhalt der QuelleBullard, Anthony John. „The role of erythropoietin in ischaemia/reperfusion injury“. Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445332/.
Der volle Inhalt der QuelleDuarte, 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.
Der volle Inhalt der QuelleMoore, Rustin MacArthur. „Large colon ischemia-reperfusion injury in the horse /“. The Ohio State University, 1994. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487853913101881.
Der volle Inhalt der QuelleSalloum, Fadi N. „Novel Strategies in Cardioprotection against Ischemia/Reperfusion Injury“. VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1227.
Der volle Inhalt der QuelleNitta, Takashi. „Myoglobin gene expression attenuates hepatic ischemia reperfusion injury“. Kyoto University, 2003. http://hdl.handle.net/2433/148743.
Der volle Inhalt der QuelleWhite, Melanie Yvonne. „Proteomics of ischemia/reperfusion injury in rabbit myocardium“. Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.
Der volle Inhalt der QuelleDuarte, 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.
Der volle Inhalt der QuelleXu, Xingshun. „Novel Protective Agents against Cerebral Ischemia/Reperfusion Injury“. Digital Commons @ East Tennessee State University, 2007. https://dc.etsu.edu/etd/2054.
Der volle Inhalt der QuelleBejaoui, 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.
Der volle Inhalt der QuelleLa lesión por isquemia reperfusión (I/R) es un proceso complejo que tiene lugar cuando un órgano se ve privado del aporte sanguíneo (isquemia) y se manifiesta de forma predominante después del posterior restablecimiento del flujo sanguíneo (reperfusión). Existen numerosas situaciones en la práctica clínica en las que el hígado se ve sometido a una situación de I/R, entre ellas, la resección hepática y el trasplante hepático. Los polietilenglicoles (PEGs) son polímeros solubles en agua, no tóxicos y con diferentes pesos moleculares. Algunos de ellos, con un peso molecular de 20 kDa (PEG 20) y de 35 kDa (PEG 35) forman parte de la composición de soluciones de preservación de órganos (SCOT e IGL-1). Además, en varios modelos experimentales de in vivo e in vitro se ha reportado que varios PEGs ejercen efectos beneficiosos. Atendiendo a lo anteriormente expuesto, la utilización de PEGs puede constituir una excelente herramienta para prevenir el daño hepático por I/R. El objetivo de esta tesis es investigar los efectos beneficiosos del PEG 35 en diferentes modelos de lesión por I/R, que imitan una cirugía hepática. Nuestros resultados demuestran que: - EL PEG 35 administrado por vía intravenosa protege eficientemente el hígado de ratas contra la I/R caliente. Los mecanismos de protección están asociados con la activación de la supervivencia vía Akt y AMPK y la inhibición de la apoptosis. El PEG 35 también protege la morfología de los hepatocitos mediante el aumento de la F/G-actina y la activación de p-p38. - La administración intravenosa de PEG 35 protege los hígados esteatósicos en un modelo de I/R fría en ratas obesas. Los efectos protectores de PEG 35 están mediados por la preservación del estado mitocondrial, la estabilización del citoesqueleto y la regulación de las vías de señalización citoprotectoras AMPK y AKT. - La adición de PEG 35 a una nueva solucione de lavado aumenta la protección contra la lesión por I/R en un modelo de hígado de rata aislado y perfundido a través de la inhibición de las metaloproteinasas, la activación de vías de señalización citoprotectoras AMPK y eNOS y la preservación de la integridad del citoesqueleto.
Georgiev, Panco. „Normothermic ischemia reperfusion injury in the cholestatic mouse liver /“. Zürich, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000256332.
Der volle Inhalt der QuelleCohen, 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.
Der volle Inhalt der QuelleBrown, 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.
Der volle Inhalt der QuelleDu, 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.
Der volle Inhalt der QuelleIn this study, we have further defined the mechanism of Src kinase-induced EphA2 upregulation by identifying the -145/+137 EphA2 promoter region as the minimal region required for basal and Src kinase-induced activation of the promoter. Moreover, we have identified within this region, at position -45, a canonical cAMP response element (CRE) (Nowakowski et al.), which is essential for EphA2 promoter activation. However, we also found that the prototypical CRE-binding transcription factor, CREB, was not necessary for activation of the EphA2 promoter, suggesting that CREB-related or -unrelated transcription factors are responsible for EphA2 upregulation.
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.
Der volle Inhalt der Quelle宋蘭 und 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.
Der volle Inhalt der QuelleSchulman, 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.
Der volle Inhalt der QuellePatel, 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.
Der volle Inhalt der QuelleLlwyd, Osian. „The involvement of CaMKII in myocardial ischaemia-reperfusion injury“. Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/43619/.
Der volle Inhalt der QuelleStefanutti, G. „Novel experimental therapies for intestinal ischaemia and reperfusion injury“. Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1334603/.
Der volle Inhalt der QuelleSharma, V. „Novel signalling pathways in myocardial conditioning against reperfusion injury“. Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1407936/.
Der volle Inhalt der Quellevan, 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.
Der volle Inhalt der QuelleWang, Guona. „The role of lipocalin-2 in stroke reperfusion injury“. Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1448895817.
Der volle Inhalt der QuelleChuang, 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.
Der volle Inhalt der QuelleHunter, James Philip. „The role of hydrogen sulphide in ischaemia reperfusion injury“. Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/35951.
Der volle Inhalt der QuelleDare, 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.
Der volle Inhalt der QuelleReyes, Leila. „Involvement of inflammatory oxidants in cardiac ischaemia/reperfusion injury“. Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/19667.
Der volle Inhalt der QuelleVenardos, Kylie M. „Myocardial Antioxidant Enzyme Systems, Ischemia-Reperfusion Injury, and Selenium“. Thesis, Griffith University, 2005. http://hdl.handle.net/10072/365301.
Der volle Inhalt der QuelleThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Health Sciences
Full Text
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.
Der volle Inhalt der QuelleBecker, 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.
Der volle Inhalt der QuelleDepartment of Physiology and Health Science
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.
Der volle Inhalt der QuelleLas enfermedades renales se derivan de defectos congénitos, lesiones renales agudas (AKI) o enfermedad renal crónica (CKD), entre otras causas. La lesión renal de isquemia / reperfusión (IRI), que se encuentra en muchas situaciones clínicas, es una de las causas principales de AKI que causan lesiones y muerte de células epiteliales del túbulo proximal (PTEC). La gravedad de AKI y la capacidad de regenerarse después de la lesión son determinantes importantes de la morbilidad y mortalidad de los pacientes en un entorno hospitalario. Los hombres son más propensos a la enfermedad renal aguda y crónica y avanzar hasta la enfermedad renal en fase final (ESRD) que las mujeres y actualmente se acepta que los andrógenos, y no la ausencia de estrógenos, son responsables de esto. Se acepta que la regeneración por PTEC superviviente es el mecanismo predominante de reparación/regeneración después de lesiones tubulares isquémicas en el riñón adulto de mamífero. Las PTEC son también el lugar donde se origina el carcinoma de células renales de células claras (ccRCC) en humanos. El ccRCC también presenta diferencias de sexo, con los hombres que tienen casi el doble de la incidencia de las mujeres a nivel mundial. Esto condujo a la hipótesis de que la regeneración después de lesiones renales y el desarrollo de ccRCC podrían compartir repertorios de expresión génica similares. Los andrógenos son muy relevantes en el desarrollo de los riñones, lo que sugiere que la regeneración y el cáncer en las células del túbulo proximal pueden recapitular, en parte, los programas dependientes de los andrógenos en el desarrollo del riñón. En este proyecto, hemos querido encontrar dianas que participen en la regeneración renal y en procesos de cáncer renal. Además, nos interesó estudiar la regulación de la hormona sexual en estas vías. Se realizaron análisis detallados de datos transcriptómicas de un modelo porcino de AKI. Se determinaron genes que expresaban un dimorfismo sexual en toda la IRI y se validaron dianas en muestras humanas. Además, se determinaron los conjuntos de genes implicados en la IRI y se caracterizaron de forma sexual y de tiempo. Encontramos que los grupos genéticos relacionados con los procesos de regeneración eran más activos en las mujeres que en los hombres. Además, la respuesta inmune a la lesión fue mayor en hombres que en mujeres. Después, hemos vinculado los procesos de regeneración con ccRCC mediante la superposición entre los análisis del transcriptomas AKI y ccRCC. Además, encontramos diferencias importantes entre los transcriptomas de riñón de ratón y de cerdo tras la lesión renal. Se estableció un modelo in vitro de IRI renal y se permitió validar parcialmente los hallazgos in vivo. Entre otros, observamos que durante la IRI renal, STAT3 está regulado por la fosforilación de diferentes residuos. Este estudio constituye una caracterización extensiva de las diferencias de sexo existentes durante la IRI renal. Ofrece una plantilla para caracterizar más las diferencias de sexo en enfermedades renales a nivel molecular.
Kidney diseases arise from congenital defects, acute kidney injury (AKI) or chronic kidney disease (CKD), among other causes. Renal ischemia/reperfusion injury (IRI), which is faced in many clinical situations, is a major cause of AKI leading to injury and death of proximal tubule epithelial cells (PTEC). The severity of AKI and the capacity to regenerate after injury are important determinants of patient morbidity and mortality in the hospital setting. Men are more prone to acute and chronic kidney disease and to progress to end-stage renal disease (ESRD) than women and it is currently accepted that androgens, and not the absence of estrogens, are responsible for that. It is accepted that regeneration by surviving PTEC is the predominant mechanism of repair/regeneration after ischemic tubular injury in the adult mammalian kidney. PTEC are also the site where the clear cell renal cell carcinoma (ccRCC) originates in humans. ccRCC also exhibits sex differences, with males having almost twice the incidence of females globally. This led to the hypothesis that regeneration after kidney injury and ccRCC development might share similar gene expression repertoires. Androgens are very relevant in kidney development, which suggests that regeneration and cancer in proximal tubule cells might recapitulate, in part, androgen-dependent programs in kidney developmental. In this project, we aimed to find targets that participate in renal regeneration and in renal cancer processes. Moreover, we were interested to study the sex hormone regulation of these pathways. Thorough analyses of transcriptomic data from a porcine model of AKI was performed. We determined genes that expressed a sexual dimorphism throughout IRI and we validated theses targets in human samples. Furthermore, we determined the gene sets involved in IRI and characterize them in a time and sex manner. We found that gene sets related to regeneration processes were more active in females than in males. Also, the immune response at injury was higher in males than in females. Afterwards, we linked regeneration processes with ccRCC by the overlap between AKI and ccRCC transcriptome analyses. Besides, we found major differences between the mouse and the pig kidney transcriptomes upon renal injury. An in vitro model of renal IRI was established and allowed to partially validate the in vivo findings. Among others, we observed that during renal IRI, STAT3 is regulated by phosphorylation of different residues. This study constitutes an extensive characterization of the sex differences that exist during renal IRI. It offers a template for further characterization of sex differences in kidney diseases at the molecular level.
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.
Der volle Inhalt der QuelleMörtberg, 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.
Der volle Inhalt der QuelleMorsey, 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.
Der volle Inhalt der QuelleHarrison, Ewen M. „Pharmacological strategies to reduce ischemia/reperfusion injury in kidney transplantation“. Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/24683.
Der volle Inhalt der QuelleSudarshan, 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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