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Relevant bibliographies by topics / Reperfusion injury

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Academic literature on the topic 'Reperfusion injury'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 June 2025

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Journal articles on the topic "Reperfusion injury"

1

Khalil, Alizan A., Farah A. Aziz, and John C. Hall. "Reperfusion Injury." Plastic and Reconstructive Surgery 117, no. 3 (March 2006): 1024–33. http://dx.doi.org/10.1097/01.prs.0000204766.17127.54.

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Grinyo, J. M. "Reperfusion injury." Transplantation Proceedings 29, no. 1-2 (February 1997): 59–62. http://dx.doi.org/10.1016/s0041-1345(96)00715-4.

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Quinones-Baldrich, William J., and Deborah Caswell. "Reperfusion Injury." Critical Care Nursing Clinics of North America 3, no. 3 (September 1991): 525–34. http://dx.doi.org/10.1016/s0899-5885(18)30722-6.

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Royston, David. "Reperfusion injury." Baillière's Clinical Anaesthesiology 2, no. 3 (September 1988): 707–27. http://dx.doi.org/10.1016/s0950-3501(88)80014-x.

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Zimmerman, Barbara J., and D. Neil Granger. "Reperfusion Injury." Surgical Clinics of North America 72, no. 1 (February 1992): 65–83. http://dx.doi.org/10.1016/s0039-6109(16)45628-8.

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Reichek, Nathaniel, and Kambiz Parcham-Azad. "Reperfusion Injury." Journal of the American College of Cardiology 55, no. 12 (March 2010): 1206–8. http://dx.doi.org/10.1016/j.jacc.2009.10.048.

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Flaherty, John T., and Myron L. Weisfeldt. "Reperfusion injury." Free Radical Biology and Medicine 5, no. 5-6 (January 1988): 409–19. http://dx.doi.org/10.1016/0891-5849(88)90115-3.

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Fishbein, M. C. "Reperfusion injury." Clinical Cardiology 13, no. 3 (March 1990): 213–17. http://dx.doi.org/10.1002/clc.4960130312.

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Ma, Yulong, Yanhui Cai, Doutong Yu, Yuting Qiao, Haiyun Guo, Zejun Gao, and Li Guo. "Astrocytic Glycogen Mobilization in Cerebral Ischemia/Reperfusion Injury." Neuroscience and Neurological Surgery 11, no. 3 (February 21, 2022): 01–05. http://dx.doi.org/10.31579/2578-8868/228.

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Glycogen is an important energy reserve in the brain and can be rapidly degraded to maintain metabolic homeostasis during cerebral blood vessel occlusion. Recent studies have pointed out the alterations in glycogen and its underlying mechanism during reperfusion after ischemic stroke. In addition, glycogen metabolism may work as a promising therapeutic target to relieve reperfusion injury. Here, we summarize the progress of glycogen metabolism during reperfusion injury and its corresponding application in patients suffering from ischemic stroke.

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Bodwell, Wendy. "Ischemia, reperfusion, and reperfusion injury." Journal of Cardiovascular Nursing 4, no. 1 (November 1989): 25–32. http://dx.doi.org/10.1097/00005082-198911000-00005.

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Dissertations / Theses on the topic "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.

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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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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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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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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 targeting of dysfunctional mitochondria will provide the potential to bypass the upstream signaling defects and intervene directly upon the effector organelle. Novel mitochondrial-targeted therapy relies on understanding the sites in the electron transport chain (ETC) that are damaged by ISC and produce cell-injury during REP. This project identifies a novel pathological role of cytochrome c in depleting cardiolipin during ischemia after which the mitochondria are in a defective condition that leads to additional cell death during reperfusion. During ischemia oxidants from complex III oxidize cytochrome c, forming a peroxidase, which causes oxidative damage and depletion of cardiolipin. Depletion of cardiolipin disrupts normal physiology and augments cell death. Identification of the innovative pathobiology during ISC-REP recognizes a novel therapeutic target, cytochrome c peroxidase, which can be a focal point for new therapeutic interventions to decrease cardiac injury. In order to maintain homeostatis, living organisms have the methionine sulfoxide reductase system, which reduce both free and protein bound Met(O) back to methionine (Met) in the presence of thioredoxin. Oxidized Trx is inactive and unable to bind to ASK1 thereby activating ASK1 and causing cell death via p38/JNK pathways thereby contributing to the pathogenesis of myocardial ISC-REP injury. In this study we have shown that inhibition of ASK1 protects the heart during REP via the modulation of mitochondria that sustained damage during ISC. The mitochondrial-based mechanism of cardioprotection with ASK1 inhibition enhanced the functional integrity of the inner mitochondrial membrane retaining cytochrome c thereby decreasing cell death. This therapeutic intervention is a key step to achieve the ultimate goal to improve clinical outcomes in patients that suffer an acute myocardial infarction.

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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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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 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.<br>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 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.

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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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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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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 postoperative liver failure. Several strategies have been tried to protect the liver from IRI. For instance can the PM be applied in short intervals or reactive oxygen species can be scavenged by antioxidants. There are no sensitive methods available for studying IRI in patients and little is known how IRI affects the metabolism in the liver. Microdialysis is a technique that allows for continuous sampling of interstitial fluid in the organ of interest Aim: To investigate the effects of ischemia and reperfusion on glucose metabolism in the liver using the microdialysis technique. Method: A porcine model of segmental ischemia and reperfusion was developed. The hepatic perfusion and glucose metabolism was followed for 6-8 hours by placing microdialysis catheters in the liver parenchyma (studies I-III). In study IV, 16 patients were randomized to have 10 minutes of ischemic preconditioning prior to the liver resection, which was performed with 15 minutes of ischemia and 5 minutes of reperfusion repetitively until the tumour(s) were resected. Results: During ischemia the glucose metabolism was anaerobic in the ischemic segment, while the perfused segment had normal glucose metabolism. Urea was added in the perfusate of the microdialysis catheters and was found to be a reliable marker of liver perfusion. The antioxidant NAcetylcystein (NAC) improved the hepatic aerobic glucose metabolism in the pig during the reperfusion, shown as reduced levels of lactate and improved glycogenesis in the hepatocytes. This can be explained by the scavenging of nitric oxide by NAC as nitric oxide otherwise would inhibit mitochondrial respiration. Also IP improved aerobic glucose metabolism resulting in lower hepatic lactate levels in patients having major liver resections. Conclusion: Microdialysis can monitor the glucose metabolism both in animal experimental models and in patients during and after hepatectomy. Both NAC and IP improves aerobic glucose metabolism, which can be of value in patients with compromised liver function postoperatively.

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Books on the topic "Reperfusion injury"

1

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

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1946-, Das Dipak Kumar, ed. Pathophysiology of reperfusion injury. Boca Raton: CRC Press, 1993.

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1946-, Das Dipak Kumar, ed. Cellular, biochemical, and molecular aspects of reperfusion injury. New York: New York Academy of Sciences, 1994.

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M, Yellon Derek, Jennings Robert B. 1926-, and Council on Cardiac Metabolism, eds. Myocardial protection: The pathophysiology of reperfusion and reperfusion injury. New York: Raven Press, 1992.

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Kaski, Juan Carlos, Derek J. Hausenloy, Bernard John Gersh, and Derek M. Yellon, eds. Management of Myocardial Reperfusion Injury. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9.

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Kaski, Juan Carlos. Management of myocardial reperfusion injury. Dordrecht: Springer, 2012.

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Takenobu, Kamada, Shiga Takeshi 1931-, and McCuskey Robert S, eds. Tissue perfusion and organ fuction: Ischemia/reperfusion injury. Amsterdam, the Netherlands: Elsevier, 1996.

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8

Bilenko, M. V. Ishemicheskie i reperfuzionnye povrezhdeniia organov: Molekuliarnye mekhanizmy, puti preduprezhdeniia i lecheniia. Moskva: Meditsina, 1989.

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9

Friedhelm, Beyersdorf, ed. Ischemia-reperfusion injury in cardiac surgery. Georgetown, Tx: Landes Bioscience, 2000.

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A, Fantini Gary, ed. Ischemia-reperfusion of skeletal muscle. Austin: R.G. Landes, 1994.

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Book chapters on the topic "Reperfusion injury"

1

Reimer, K. A., and R. B. Jennings. "Reperfusion Injury." In Reperfusion and Revascularization in Acute Myocardial Infarction, 52–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83544-5_6.

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Dancygier, Henryk, and Peter Schirmacher. "Reperfusion Injury." In Clinical Hepatology, 185–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-93842-2_16.

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Guerci, A. D. "Reperfusion injury." In Clinics of CSI, 63–70. Heidelberg: Steinkopff, 1986. http://dx.doi.org/10.1007/978-3-662-11328-8_7.

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Pohlman, Timothy. "Reperfusion Injury." In Thoracic Trauma and Critical Care, 29–42. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1127-4_4.

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Khan, Heena, Thakur Gurjeet Singh, and Rahul Deshmukh. "Myocardial Ischemic-Reperfusion Injury." In Ischemic Injury, 13–36. New York: Apple Academic Press, 2024. http://dx.doi.org/10.1201/9781032680026-2.

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Hobson, Michael J., and Basilia Zingarelli. "Ischemia-Reperfusion Injury." In Pediatric Critical Care Medicine, 251–68. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6362-6_24.

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Ošt’ádal, Bohuslav, and František Kolář. "Reperfusion-Induced Injury." In Basic Science for the Cardiologist, 65–79. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4757-3025-8_3.

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van Wijck, Kim, and Wim A. Buurman. "Ischemia-Reperfusion Injury." In Encyclopedia of Exercise Medicine in Health and Disease, 484–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_268.

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Smith, Josh, and Robert Goggs. "Ischemia-Reperfusion Injury." In Textbook of Small Animal Emergency Medicine, 1019–29. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2018. http://dx.doi.org/10.1002/9781119028994.ch158.

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Zingarelli, Basilia. "Ischemia-Reperfusion Injury." In Science and Practice of Pediatric Critical Care Medicine, 1–12. London: Springer London, 2008. http://dx.doi.org/10.1007/978-1-84800-921-9_20.

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Conference papers on the topic "Reperfusion injury"

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La Barck, Anthony J., Jennifer E. Akers, and Thomas L. Merrill. "Tissue Oxygen Transfer During Reperfusion and Post-Conditioning." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53064.

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Heart disease is the leading cause of death in the United States. Ischemic heart disease occurs when coronary blood flow to the heart is reduced, limiting the amount of oxygen and nutrients the heart receives. When blood flow is restored after a percutaneous transluminal coronary intervention (PCI), rapid reperfusion from sudden balloon deflation can cause further injury to oxygen-starved tissue, leading to increased cell injury and cell death. Studies in animal models with ischemic heart disease have shown that reperfusion injury may account for up to 50% of the final infarct size [1]. Post-conditioning (PC) may reduce the amount of reperfusion injury by applying intermittent periods of ischemia during the early moments of reperfusion. This procedure periodically occludes blood vessels during reperfusion by periodically inflating and deflating an angioplasty balloon according to a specific algorithm. Zhao et al. showed that PC reduced reperfusion injury in a canine model by applying 3 cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia (re-occlusion) at the onset of reperfusion. PC in this study reduced tissue AN/AAR (area of necrosis/area at risk) by 48% [2]. In 2008, Gao et al. demonstrated that the effectiveness of PC in rats was dependent on the number of cycles in the PC algorithm, as well as the durations of the ischemia/reperfusion phases [3].

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Akers, Jennifer E., Denise R. Merrill, Todd J. Nilsen, Kevin J. Koomalsingh, Masahito Minakawa, Takashi Shuto, Joseph H. Gorman, Robert C. Gorman, Matthew J. Gillespie, and Thomas L. Merrill. "Localized Cooling Device for Myocardial Tissue Salvage." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53155.

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The primary goal in treating heart attack is to restore blood flow to blocked areas of the heart. However, even after blood flow is restored, injury can occur as a result of a complex cascade of mechanisms following the reintroduction of flow, aptly referred to as reperfusion injury. Studies show that reperfusion injury is accountable for up to 50% of cell death following an ischemic period [1]. Adjunctive therapies are needed to reduce reperfusion injury.

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Kasparian, S., D. Gotur, S. H. L. Hsu, and J. Zimmerman. "Reperfusion Injury with Resolving Saddle Pulmonary Embolism." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1783.

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Merrill, Thomas L., Denise R. Merrill, and Jennifer E. Akers. "Localized Brain Tissue Cooling for Use During Intracranial Thrombectomy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80083.

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The primary goal of current ischemic stroke treatment is quickly restoring blood perfusion. Recanalization is linked to improved neurological outcomes [1]. Resulting tissue necrosis, however, following a stroke has two causes: 1) ischemic injury and 2) reperfusion injury. Therefore, development of neuroprotective agents specifically beneficial against reperfusion injury are required.

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Iribarren, Juan B., and Harish Seethamraju. "Reperfusion Injury Post Lung Transplant- A Reversible Cause." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5397.

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Sayah, David M., Fengchun Liu, Axelle Caudrillier, and Mark R. Looney. "Neutrophil Extracellular Traps In Ischemia-Reperfusion Lung Injury." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5123.

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Fagg, J., O. Abdulfattah, P. White, and M. Obregon. "Lung Reperfusion Injury Following Pericardiocentesis for Cardiac Tamponade." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3707.

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Park, H. K. "Wavelet Analysis of Ischemia and Reperfusion Injury Models." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616862.

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Bhandal, J., A. Hussain, J. Buckley, and H. Maddock. "P34 Adenosine a1 receptor activation can protect the myocardium from ischaemia reperfusion injury post reperfusion." In 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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Xia, Cao, Ma Kewei, Liu Yicheng, Yu Xiaofeng, Chen Yanping, Sui Dayuan, Pei Jin, and Gu Xinquan. "Effects of Ginsenoside Re on myocardial ischemia reperfusion injury." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027905.

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Reports on the topic "Reperfusion injury"

1

Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada568392.

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Omaye, Stanley T. Efficacy of Gamma-glutamylcysteine (GGC) in Ischemia-reperfusion Injury. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada579994.

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Zheng, Jinghui. Quercetin for Myocardial Ischemia/Reperfusion Injury: A Preclinical Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review Protocols, April 2020. http://dx.doi.org/10.37766/inplasy2020.4.0162.

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Lu, Liying, Xiaocong Ma, Jinghui Zheng, Lijuan Li, Wenna Yang, Yixuan Kong, and Jie Wang. Quercetin for Myocardial Ischemia Reperfusion Injury: A Protocol for Systematic Review and Meta Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2020. http://dx.doi.org/10.37766/inplasy2020.5.0067.

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Percival, Thomas J., Shimul Patel, Nickolay P. Markov, Jerry R. Spencer, Gabriel E. Burkhardt, and Todd E. Rasmussen. The Impact of Prophylactic Fasciotomy Following Porcine (Sus scrofa) Hind Limb Ischemia/Reperfusion Injury. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada559521.

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Gao, Genshan, Houwei Du, and Shuangfang Fang. Neuroprotective effects of curcumin against ischemia-reperfusion injury: A meta-analysis of Animal Model Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2024. http://dx.doi.org/10.37766/inplasy2024.8.0113.

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TU, LANG, Yimiao Luo, Xinyi Xu, Huiling Xiong, Sihan Hu, and Xiao Ma. Constructing evidence for the treatment of cerebral ischemia-reperfusion injury with ligustrazine: a preclinical meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2023. http://dx.doi.org/10.37766/inplasy2023.6.0002.

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Yu, Beibei, Yongfeng Zhang, and Shouping Gong. Effects of miRNA-modified exosomes alleviate cerebral ischemic reperfusion injury in Pre-clinical Studies: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0062.

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Abstract:

Review question / Objective: The purpose of this study was to investigate the effect of miRNA-modified exosomes in alleviating cerebral ischemic reperfusion injury compared with the non-treatment group. The research object is an animal model of middle cerebral artery occlusion. The research method is a controlled study. The primary outcome of this study was infarct volume, and the secondary outcome was neurobehavioral performance. Main outcome(s): The primary outcome of this study was Infarct volumes，which was measured by 2,3,5-triphenyltetranzolium chloride (TTC) staining. And it was calculated as followed: Infarct volume % = lesion area of each section = (contralateral hemisphere area/ipsilateral hemisphere area) × ipsilateral lesion area. Neurobehavioral performance was the secondary outcome, and was assessed by three scoring scales: modified neurological severity score (mNSS), Longa scoring system and neurological deficit score (NDS).

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Wu, Lihua, Ling Wu, Yu Liu, Ting Jiang, Ju Yang, and Mingquan Li. Can resveratrol protect against renal ischemia/reperfusion injury? A systematic review and meta-analysis of preclinical studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2021. http://dx.doi.org/10.37766/inplasy2021.4.0102.

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LIN, JUN, WEIYU FU, and YE YANG. Protective effects and mechanism of curcumin in animal models of lung injury caused by ischemia-reperfusion injury : a preclinical systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2024. http://dx.doi.org/10.37766/inplasy2024.10.0071.

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