Готові списки джерел за темами / Liver Ischemia Repercussion Injury

Добірка наукової літератури з теми "Liver Ischemia Repercussion Injury"

Автор: Grafiati

Опубліковано: 14 березня 2023

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Статті в журналах з теми "Liver Ischemia Repercussion Injury"

Cursio, Raffaele, Pascal Colosetti, and Jean Gugenheim. "Autophagy and Liver Ischemia-Reperfusion Injury." BioMed Research International 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/417590.

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Liver ischemia-reperfusion (I-R) injury occurs during liver resection, liver transplantation, and hemorrhagic shock. The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved. Autophagy is an intracellular self-digesting pathway responsible for removal of long-lived proteins, damaged organelles, and malformed proteins during biosynthesis by lysosomes. Autophagy is found in normal and diseased liver. Although depending on the type of ischemia, warm and/or cold, the dynamic process of liver I-R results mainly in adenosine triphosphate depletion and in production of reactive oxygen species (ROS), leads to both, a local ischemic insult and an acute inflammatory-mediated reperfusion injury, and results finally in cell death. This process can induce liver dysfunction and can increase patient morbidity and mortality after liver surgery and hemorrhagic shock. Whether autophagy protects from or promotes liver injury following warm and/or cold I-R remains to be elucidated. The present review aims to summarize the current knowledge in liver I-R injury focusing on both the beneficial and the detrimental effects of liver autophagy following warm and/or cold liver I-R.

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Saidi, Rezà F., and Seyed Kamran Hejazi Kenari. "Liver Ischemia/Reperfusion Injury: an Overview." Journal of Investigative Surgery 27, no. 6 (July 24, 2014): 366–79. http://dx.doi.org/10.3109/08941939.2014.932473.

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Ildefonso, José Ángel, and Javier Arias-Díaz. "Pathophysiology of liver ischemia—Reperfusion injury." Cirugía Española (English Edition) 87, no. 4 (January 2010): 202–9. http://dx.doi.org/10.1016/s2173-5077(10)70049-1.

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Shibayama, Yuro, Shosaku Asaka, and Akira Nishijima. "Mechanism of liver injury following ischemia." Experimental and Molecular Pathology 55, no. 3 (December 1991): 251–60. http://dx.doi.org/10.1016/0014-4800(91)90005-i.

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Ai-Min, H. "Liver injury following normothermic ischemia in steatotic rat liver." Hepatology 20, no. 5 (November 1994): 1287–93. http://dx.doi.org/10.1016/0270-9139(94)90770-6.

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Hui, Ai-Min, Seiji Kawasaki, Masatoshi Makuuchi, Jun Nakayama, Toshihiko Ikegami, and Shinichi Miyagawa. "Liver injury following normothermic ischemia in steatotic rat liver." Hepatology 20, no. 5 (November 1994): 1287–93. http://dx.doi.org/10.1002/hep.1840200528.

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Wang, Hai, Zhifeng Xi, Lu Deng, Yixiao Pan, Kang He, and Qiang Xia. "Macrophage Polarization and Liver Ischemia-Reperfusion Injury." International Journal of Medical Sciences 18, no. 5 (2021): 1104–13. http://dx.doi.org/10.7150/ijms.52691.

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de Rougemont, Olivier, Philipp Dutkowski, and Pierre-Alain Clavien. "Biological modulation of liver ischemia–reperfusion injury." Current Opinion in Organ Transplantation 15, no. 2 (April 2010): 183–89. http://dx.doi.org/10.1097/mot.0b013e3283373ced.

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Jones, Ryan T., Luis H. Toledo-Pereyra, and Kelly M. Quesnelle. "Selectins in Liver Ischemia and Reperfusion Injury." Journal of Investigative Surgery 28, no. 5 (September 3, 2015): 292–300. http://dx.doi.org/10.3109/08941939.2015.1056920.

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Дисертації з теми "Liver Ischemia Repercussion Injury"

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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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 where the FLR is small and in cases when the liver suffers from chronic diseases, such as cirrhosis, IRI can greatly increase the risk of post-operative liver failure (POLF). Ischemic preconditioning (IPC) and, more recently, remote ischemic preconditioning (R-IPC) are methods that have been employed to reduce IRI. Aim: 1) To compare the effects of IPC and R-IPC in a rat model; 2) to investigate the clinical effect of IPC during modern liver surgery; 3) to investigate the role of the nitric oxide (NO) system in IRI, IPC and R-IPC; and 4) to explore the possible protective effects of nitrite administration before IRI. Methods: A rat model of segmental ischemia followed by 4 hours of reperfusion including microdialysis (μD) was developed from earlier models. The effects of IPC and R-IPC were compared using transaminases and histology as well as continuous μD sampling for glucose, pyruvate, lactate and glycerol. The role of the NO system was examined by serum and μD measurements of NOx as well as tissue measurements of iNOS mRNA and IL-1R mRNA. In study II, patients were randomized to IPC or no IPC prior to liver resection, where intermittent PM was used to decrease bleeding. Results: IPC was more effective in protecting the liver against IRI than R-IPC, as indicated by the levels of transaminases. Lower lactate levels were detected in patients treated with IPC before major liver resections than in controls. IPC reduced iNOS mRNA transcription during reperfusion; this result may be related to the early but not sustained increases in IL-1R transcription observed in the IPC group. Nitrite administered before ischemia reduced AST and ALT levels in the level after 4 hours of reperfusion; in addition, necrosis and glycerol release from the ischemic liver were reduced as well. Conclusion: IPC is more effective than R-IPC in animal models; however, this effect is unlikely to be of clinical importance. NOx decreases in the ischemic liver and the administration of nitrite before ischemia reduces IRI in rats. This may have clinical implications in the future.

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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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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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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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Müller, Christian. "α-Lipoic Acid Attenuates Ischemia Reperfusion Injury of the Rat Liver". Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-2394.

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Hartkorn, Andreas. "Different approaches to influence the ischemia/reperfusion injury of the liver." Diss., kostenfrei, 2008. http://edoc.ub.uni-muenchen.de/8918/.

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Okumura, Shinya. "Oral administration of polyamines ameliorates liver ischemia-reperfusion injury and promotes liver regeneration in rats." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225444.

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Richards, James Alexander. "The relative contribution of lymphocytes to hepatic ischemia reperfusion injury." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25856.

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Background: Hepatic ischemia reperfusion injury (IRI) results from the interruption and then reinstatement of the liver’s blood supply. IRI involves both an ischemic and an immune-mediated reperfusion phase of tissue injury; similar inflammatory events are seen in other forms of acute (sterile) liver injury (ALI), including paracetamol toxicity. Hypothesis Irrespective of the primary insult, common pathways exist in the pathophysiology of the lymphocyte-mediated secondary liver injury. Natural mechanisms exist to limit lymphocyte function and these pathways can be targeted therapeutically by immunomodulatory agents. Aims: 1. To assess the relative importance of different lymphocyte subsets in IRI. 2. To correlate observations in IRI with other models of ALI. 3. To identify possible pharmacological targets. Materials and Methods Three experimental murine models of acute liver injury were utilised to test this hypothesis: murine model of warm hepatic IRI, concanavalin A (con A) hepatitis and paracetamol-induced liver injury. These models were interrogated with a combination of (transgenic and knockout) mouse lines, in vivo antibody depletion and small molecule inhibition. Injury was evaluated primarily in terms of the biochemical marker of liver injury alanine aminotransferase (ALT). Data were correlated with human tissue where possible. Results: T cells (CD3εKO vs WT p=0.010), but not other lymphocyte populations (B cells, NK cells, or other innate lymphoid cells), play a central role in warm hepatic IRI. Programmed Death Receptor-1 (PD-1) is a negative regulator of pro-inflammatory cytokine production by T cells and the absence of PD-1 was associated with significantly worse hepatic IRI (p=0.034), con A hepatitis (p=0.00020) and paracetamol-induced liver injury (p=0.0050). Interferon-γ (IFNγ) and T-box expressed in T cells (T-bet) are important mediators of hepatic IRI (p=0.017) and paracetamol induced liver injury (p=0.0007). The absence of IL-6 was associated with significant protection in paracetamol induced liver injury (p=0.006). The infiltrates within the recipient liver of patients transplanted following paracetamol overdose stain positively for PD-1, IFNγ and T-bet. The Janus family of kinases (JAK) play an important role in the common pathways of cytokine signal transduction. In vivo use of a selective JAK1/JAK2 inhibitor is protective in hepatic IRI (p=0.0014), con A hepatitis (p=0.019) and paracetamol-induced liver injury (p=0.0045). Conclusions: Common pathways appear to exist in the immune-mediated secondary phase of injury in ALI. Targeting these pathways will complement existing (cytoprotective) treatment strategies.

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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 achieved. However, efficient therapy against IRI is still lacking and few clinical studies in phase III have proven their effectiveness. This could be due in part to the complexity of the mechanisms responsible of IRI and to the specific drugs activity and their potential adverse effects. Polyethylene glycols (PEGs) are water soluble nontoxic polymers that have been employed in many biomedical applications such as gastrointestinal disorders and drugs pegylation. Besides its usefulness as oncotic agents in preservation solutions, it has been shown that PEGs molecules protect against cold injury and ischemic damage. In contrast to the current pharmacological strategies used against IRI, PEG presents the advantages of being a multi-target strategy. In fact, IRI is a multifactorial disease including oxidative stress, inflammation, endoplasmic reticulum stress, mitochondrial damage, and cytoskeleton alterations which lead to cell death and organ dysfunction. PEG has been associated with the majority of these events as it has been shown that PEG reduces reactive oxygen species, prevents cell death, maintains mitochondrial integrity, and reduces inflammation and endoplasmic reticulum stress. From this perspective, it is reasonable to expect that PEG administration may be an effective therapeutic strategy against liver IRI. The aim of this thesis was to investigate the beneficial effects of PEG 35 in different models of IRI that mimic clinical situation of liver surgery. In the first study, we investigated the impact of the administration of intravenous PEG 35 before liver warm IRI. In the second one, we investigated whether intravenously administrated PEG 35 could protect against cold IRI in steatotic rat livers. Finally, we developed a new washout solution containing PEG 35 to prevent reperfusion injury after prolonged cold preservation. The results of the present thesis demonstrated that: - Intravenous administration of PEG 35 at 10 mg/kg protects the liver in an experimental model of warm IRI in rats. The protective mechanisms are associated with the activation of the pro survival pathways Akt and AMPK and the inhibition of apoptosis. PEG 35 also protects the hepatocyte morphology by increasing F/G-actin ratio and activating p-p38. - Intravenous administration of PEG 35 at 10 mg/kg protects steatotic livers in an experimental model of cold IRI in obese rats. The protective effects of PEG 35 are mediated by the preservation of mitochondrial status, the stabilisation of the cytoskeleton and the regulation of the cytoprotective AMPK and Akt signalling pathways. - Liver graft washout with a PEG 35-containing rinse solution increases the protection against IRI in a model of isolated perfused rat liver. .Protection was due to the inhibition of metalloproteinases, the activation of cytoprotective AMPK and eNOS signalling pathways and the preservation of cytoskeleton integrity.
La 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.

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Частини книг з теми "Liver Ischemia Repercussion Injury"

Pandey, Chandra Kant, S. S. Nath, and Manish Tandon. "Ischemia–Reperfusion Injury." In Peri-operative Anesthetic Management in Liver Transplantation, 199–208. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-6045-1_16.

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Ito, Koji, Junichi Uchino, Yasuaki Nakajima, and Jun Kimura. "Liver Injury in Ischemia and Reperfusion." In Liver and Environmental Xenobiotics, 53–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-12385-0_5.

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Suh, Matthew Y., and Juan P. Rocca. "Ischemia Reperfusion Injury after Liver Transplantation." In Mount Sinai Expert Guides: Hepatology, 469–76. Oxford, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118748626.ch47.

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Goswami, Julie, Heather Waring, Allan Tsung, and Hai Huang. "Cell Death in Ischemia-Reperfusion-Induced Liver Injury." In Cellular Injury in Liver Diseases, 173–93. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53774-0_8.

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García-Ruíz, Carmen, Albert Morales, and José C. Fernández-Checa. "Oxidative Stress and Liver Ischemia–Reperfusion Injury." In Oxidative Stress in Applied Basic Research and Clinical Practice, 149–70. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15539-5_7.

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Go, Kristina L., Sooyeon Lee, Kevin E. Behrns, and Jae-Sung Kim. "Mitochondrial Damage and Mitophagy in Ischemia/Reperfusion-Induced Liver Injury." In Molecules, Systems and Signaling in Liver Injury, 183–219. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-58106-4_9.

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Hines, Ian N., Shigeyuki Kawachi, Shigeyuki Harada, Kevin P. Pavlick, Jason M. Hoffman, Sulaiman Bharwani, Robert E. Wolf, and Matthew B. Grisham. "Role of nitric oxide in liver ischemia and reperfusion injury." In Oxygen/Nitrogen Radicals: Cell Injury and Disease, 229–37. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1087-1_27.

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Schmeding, M., S. Rademacher, G. Hunold, S. Boas-Knoop, S. Lippert, P. Neuhaus, and U. Neumann. "Erythropoietin reduces ischemia-reperfusion injury after fatty liver transplantation in rats." In Deutsche Gesellschaft für Chirurgie, 137–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_52.

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Goto, Toru, and Markus Selzner. "Ischemia-Reperfusion Injury and Therapeutic Strategy in Donation After Circulatory Death Liver Transplantation." In Donation after Circulatory Death (DCD) Liver Transplantation, 73–86. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-46470-7_6.

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Menger, M. D., M. J. Müller, H. P. Friedl, O. Trentz, and K. Messmer. "Ischemia-Reperfusion Injury of the Liver: Role of Neutrophils and Xanthine Oxidase." In Host Defense Dysfunction in Trauma, Shock and Sepsis, 499–503. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77405-8_62.

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Тези доповідей конференцій з теми "Liver Ischemia Repercussion Injury"

Shen, Qinhai, Zhaomin Qin, and Ruixue Kong. "Study on Protection Function of Quercetin on Ischemia-reperfusion Injury of Liver and its Mechanism." In 2015 International Forum on Bioinformatics and Medical Engineering. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/bme-15.2015.13.

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