Relevant bibliographies by topics / Hepatic injury

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Hepatic injury'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Hepatic injury"

1

Stracieri, Luis Donizeti da Silva, and Sandro Scarpelini. "Hepatic injury." Acta Cirurgica Brasileira 21, suppl 1 (2006): 85–88. http://dx.doi.org/10.1590/s0102-86502006000700019.

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Hepatic trauma occurs in approximately 5% of all admissions in emergency rooms. The anatomic location and the size of the liver make the organ even more susceptible to trauma and frequently in penetrating injuries. The American Association for the Surgery of Trauma established a detailed classification system that provides for uniform comparisons of hepatic injury. Diagnosis of hepatic injury can be sometimes easy; however the use diagnostic modalities as diagnostic peritoneal lavage, ultrasound and computed tomography allow faster and more accurate diagnosis. Nonoperative management of the he
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Pillai, Akshita S., Girish Kumar, and Anil K. Pillai. "Hepatic Trauma Interventions." Seminars in Interventional Radiology 38, no. 01 (2021): 096–0104. http://dx.doi.org/10.1055/s-0041-1724014.

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AbstractThe liver is the second most commonly involved solid organ (after spleen) to be injured in blunt abdominal trauma, but liver injury is the most common cause of death in such trauma. In patients with significant blunt abdominal injury, the liver is involved approximately 35 to 45% of the time. Its large size also makes it a vulnerable organ, commonly injured in penetrating trauma. Other than its position and size, the liver is surrounded by fragile parenchyma and its location under the diaphragm makes it vulnerable to shear forces during deceleration injuries. The liver is also a vascul
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Kuboki, Satoshi, Nozomu Sakai, Johannes Tschöp, Michael J. Edwards, Alex B. Lentsch, and Charles C. Caldwell. "Distinct contributions of CD4+ T cell subsets in hepatic ischemia/reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 5 (2009): G1054—G1059. http://dx.doi.org/10.1152/ajpgi.90464.2008.

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Helper T cells are known to mediate hepatic ischemia/reperfusion (I/R) injury. However, the precise mechanisms and subsets of CD4+ T cells that contribute to this injury are still controversial. Therefore, we sought to determine the contributions of different CD4+ T cell subsets during hepatic I/R injury. Wild-type, OT-II, or T cell receptor (TCR)-δ-deficient mice were subjected to 90 min of partial hepatic ischemia followed by 8 h of reperfusion. Additionally, wild-type mice were pretreated with anti-CD1d, -NK1.1, or -IL-2R-α antibodies before I/R injury. OT-II mice had diminished liver injur
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Herrera, Jorge L. "Hepatic medication injury." Current Opinion in Critical Care 3, no. 2 (1997): 153–58. http://dx.doi.org/10.1097/00075198-199704000-00012.

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Harada, Naoaki, Kenji Okajima, Shigeki Kushimoto, Hirotaka Isobe, and Keiichi Tanaka. "Antithrombin Reduces Ischemia/Reperfusion Injury of Rat Liver by Increasing the Hepatic Level of Prostacyclin." Blood 93, no. 1 (1999): 157–64. http://dx.doi.org/10.1182/blood.v93.1.157.401k08_157_164.

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We investigated whether antithrombin (AT) can reduce ischemia/reperfusion (I/R)-induced injury of rat liver by promoting prostacyclin release from endothelial cells. Although intravenous administration of AT (250 U/kg) markedly reduced hepatic injury, neither dansyl-Glu-Gly-Arg-chloromethyl ketone-treated factor Xa (DEGR-Xa), a selective inhibitor of thrombin generation, nor Trp49-modified AT, which lacks affinity for heparin, had any effect. Hepatic levels of 6-keto-PGF1, a stable prostacyclin (PGI2) metabolite, were increased significantly after I/R of the rat liver. AT significantly increa
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SOUZA LIMA, MARCOS A. "Ranitidine and Hepatic Injury." Annals of Internal Medicine 105, no. 1 (1986): 140. http://dx.doi.org/10.7326/0003-4819-105-1-140_1.

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Noreña, I., A. Varón, C. Dennis, and R. Dennis. "Hepatic injury following colonoscopy." Endoscopy 45, S 02 (2013): E247. http://dx.doi.org/10.1055/s-0033-1344354.

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Tabak, Fehmi, Ali Mert, Resat Ozaras, et al. "Losartan-Induced Hepatic Injury." Journal of Clinical Gastroenterology 34, no. 5 (2002): 585–86. http://dx.doi.org/10.1097/00004836-200205000-00022.

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Siemaszko, Olga, and Hamish A. McLure. "Repeat anaesthesia: hepatic injury." Anaesthesia & Intensive Care Medicine 5, no. 2 (2004): 52–54. http://dx.doi.org/10.1383/anes.5.2.52.28692.

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FARRELL, GEOFFREY C. "Drug-induced hepatic injury." Journal of Gastroenterology and Hepatology 12, no. 9-10 (1997): S242—S250. http://dx.doi.org/10.1111/j.1440-1746.1997.tb00507.x.

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Dissertations / Theses on the topic "Hepatic injury"

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Baghdadi, Hussam Hussein. "Hepatic injury in metabolic syndrome : the role of selenium in models of hepatic injury and healing." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4235.

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Oxidative stress, lipid peroxidation, and endotoxaemia with cytokine-mediated injury have been implicated as factors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The degree of insulin resistance together with co-existing inadequacies of vital antioxidant defence mechanisms may be important determinants of progression to fibrosis in patients with non-alcoholic steatohepatitis (NASH). Current therapies are targeted at improving insulin sensitivity as well as addressing hepatic repair including anti-inflammatory strategies. Anti-oxidants remedies have also been tested but the
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Kretz-Rommel, Anke. "Molecular characterization of diclofenac-induced hepatic injury /." [S.l.] : [s.n.], 1994. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=10834.

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Henderson, Neil C. "Molecular mechanisms of hepatic injury and repair." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1554.

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In this thesis I examined molecular mechanisms involved in acute and chronic liver injury, and also studied basic pathways mediating tumour promotion. Acute hepatic failure secondary to paracetamol poisoning is associated with high mortality. C-jun (NH2) terminal kinase (JNK) is a member of the mitogen activated protein kinase family and is a key intracellular signaling molecule involved in the control of cell fate. Paracetamol induced hepatic JNK activation in both human and murine paracetamol hepatotoxicity, and in a murine model preceded the onset of hepatocyte death. JNK inhibition in vivo
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Thompson, Kerry C. "The expression and function of interleukin-10 in liver injury." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285873.

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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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Oreopoulos, George D. "The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0021/MQ54143.pdf.

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Brock, Robert W. "The initiation of remote hepatic injury, humoral and cellular mediators." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ58201.pdf.

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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 i
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MacPhee, Peggy J. "Mechanisms of hepatic injury in murine hepatitis virus type 3 infection." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/30623.

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Murine hepatitis virus type 3 (MHV-3), a member of the coronavirus family, induces a response that varies with the age and genetic background of the host mouse strain. A/J mice are fully resistant to the virus, while Balbc/J are fully susceptible and C3HebFe/J are semi-susceptible, making it possible to predictably reproduce the major human responses to hepatitis viruses. Although there has been considerable discussion of viral pathology in the literature, there has been much less emphasis on pathogenesis. In the experiments described here, histological, biophysical, and immunological techniqu
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許慧慧 and Wai-wai Stella Hu. "Pharmacological modulation of endotoxin-induced hepatic injury in galactosamine-sensitized mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1992. http://hub.hku.hk/bib/B31210806.

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Books on the topic "Hepatic injury"

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Oreopoulos, George D. The use of hypertonic preconditioning in hepatic ischemia-reperfusion injury. National Library of Canada, 2000.

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2

P, Spoelstra, ed. Drug-induced hepatic injury: A comprehensive survey of the literature on adverse drug reactions up to January 1985. Elsevier Science Publishers, 1985.

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3

1968-, Oremus Mark, United States. Agency for Healthcare Research and Quality., and McMaster University. Evidence-based Practice Center., eds. The uses of heparin to treat burn injury. AHRQ, 2006.

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Drug-induced hepatic injury. 2nd ed. Elsevier, 1992.

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Stricker, B. H. Ch. Drug-induced Hepatic Injury (Drug-Induced Disorders). Elsevier Science Publishing Company, 1985.

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Kretz-Rommel, Annke. Molecular characterization of diclofenac-induced hepatic injury. 1994.

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Cywes, Robert. The role of platelets in hepatic allograft preservation-reperfusion injury. 1995.

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8

Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.

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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘
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Johnson, Steven B. Pathophysiology and management of abdominal injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0334.

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Abdominal injuries are common following blunt and penetrating trauma. They can result in a spectrum of severity from benign to potentially life-threatening conditions. Soon after injury, haemorrhage is the predominant concern, and leading cause of morbidity and mortality. Active haemorrhage resulting in shock requires emergent operative intervention and aggressive haemostatic resuscitation. However haemodynamically-stable patients benefit from non-operative management of solid organ injuries with or without angiographic embolization. Sepsis usually occurs as a result of intra-abdominal infecti
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Narsinh, Kazim, Steven C. Rose, and Thomas Kinney. Portal Vein Tract Embolization After Percutaneous Transhepatic Biliary Interventions. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0087.

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Bleeding complications during percutaneous biliary intervention result from injury to the hepatic artery, hepatic vein, or portal vein. If bleeding originating from a hepatic artery branch is suspected, hepatic arteriography should be performed with and without the drainage catheter in place over a wire, and subselective embolization can be performed if a suitable target is identified. If a bleeding hepatic artery branch is not identified, bleeding from a portal vein branch is suspected. Treatment of portal vein injuries is challenging in this situation because obtaining direct percutaneous po
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Book chapters on the topic "Hepatic injury"

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Dalhoff, Kim. "Toxicant-Induced Hepatic Injury." In Critical Care Toxicology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-17900-1_75.

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Rubbia-Brandt, Laura. "Hepatic Injury from Chemotherapy." In Colorectal Liver Metastasis. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-09323-4_44.

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Clarke, Callisia N., Amit D. Tevar, and Alex B. Lentsch. "Hepatic Ischemia/Reperfusion Injury." In Molecular Pathology Library. Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_26.

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Ong, Adrian W., Vicente Cortes, and Aurelio Rodriguez. "Massive Hepatic Hemorrhage: Identification." In Operative Techniques for Severe Liver Injury. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1200-1_4.

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Czaja, Mark J. "Liver regeneration following hepatic injury." In Liver Growth and Repair. Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4932-7_2.

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Nieminen, Anna-Liisa, and John J. Lemasters. "Hepatic Injury by Metal Accumulation*." In Toxicology of Metals, Volume I. CRC Press, 2023. http://dx.doi.org/10.1201/9781003418917-78.

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Lewis, James H. "Acute Drug-Induced Hepatic Injury." In Current Perspectives in Hepatology. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7041-3_19.

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Jeschke, M. G., and D. N. Herndon. "The Hepatic Response to Severe Injury." In Yearbook of Intensive Care and Emergency Medicine. Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-49433-1_58.

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Balachandran, Vinod P., and Michael I. D’Angelica. "Intraoperative Injury to Hepatic Arterial Structures." In Gastrointestinal Surgery. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2223-9_21.

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Atukeren, Pınar, and Hafize Uzun. "Melatonin’s Beneficial Effects in Hepatic Injury." In Melatonin, Neuroprotective Agents and Antidepressant Therapy. Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2803-5_13.

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Conference papers on the topic "Hepatic injury"

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Shirakami, Yohei, Hongfeng Jiang, Max E. Gottesman, and William S. Blaner. "Abstract 5555: Diethylnitrosamine-induced hepatic injury and hepatocarcinogenesis: A role for hepatic retinoids." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-5555.

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Shirakami, Yohei, Hisataka Moriwaki, and William S. Blaner. "Abstract 83: A role of hepatic retinoid storage in diethynitrosamine-induced hepatic injury and hepatocarcinogenesis." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-83.

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Yang, Xinxiang, Jinyang Li, Rongrong Zhong, et al. "IDDF2023-ABS-0305 CXCR3+ hepatic natural killer cells promote hepatic ischemia-reperfusion injury in liver transplantation." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 10–11 June 2023. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2023. http://dx.doi.org/10.1136/gutjnl-2023-iddf.44.

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Fatima, S., N. Sheikh, and A. Tayyeb. "Investigation of hepatic and renal toxicity induced by omeprazole in CCl4 injury mouse model." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677070.

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KANG, Le, Zhenya HU, Xiaoyan FANG, and Mingsan MIAO. "Animal Model Analysis based on the Characteristics of Clinical Symptoms of Alcoholic Hepatic Injury." In International Conference on Biological Engineering and Pharmacy 2016 (BEP 2016). Atlantis Press, 2017. http://dx.doi.org/10.2991/bep-16.2017.80.

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Justaniah, Almamoon, Zergham Zia, and Majed Ashour. "Extra-Anatomic Internal–External Biliary Drainage Catheters to Manage Iatrogenic Common Hepatic Duct Injury." In PAIRS 2022 Annual Congress. Thieme Medical and Scientific Publishers Pvt. Ltd., 2022. http://dx.doi.org/10.1055/s-0042-1756232.

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Sasongko, Heru, Arifin Wicaksono, and Sugiyarto. "In-vivo acute toxicological studies of Vasconcellea pubescens A. DC. fruit extract against hepatic injury." In THE 14TH JOINT CONFERENCE ON CHEMISTRY 2019. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0005224.

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"Hepatoprotective activity of Euphorbia hirta Linn. Plant against Carbon tetrachloride -induced hepatic injury in rats." In International Conference on Food, Biological and Medical Sciences. International Institute of Chemical, Biological & Environmental Engineering, 2014. http://dx.doi.org/10.15242/iicbe.c0114539.

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Cochran, Amy, Yingxin Gao, Ursula Krotscheck, Margret Thompson, James Stouffer, and Robert Nafis. "Measuring Strain Distributions in the Anterior Cruciate Ligament Using Ultrasound." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19625.

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Optimal prevention and treatment strategies of anterior cruciate ligament (ACL) injury can be realized with a detailed understanding of how physiological factors impact the ACL. A noninvasive, in vivo method that assesses the ACL’s mechanical integrity is needed to help clarify this multi-factorial pathophysiology. We investigated the use of the noninvasive, in vivo technique, ultrasound strain elastography (USE) (1), to distinguish between normal and injured ACLs. USE is used as a diagnostic tool in oncological (2), hepatic (3), and cardiovascular (4) applications. This technique uses ultraso
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Belwadi, Aditya, and King H. Yang. "Near Side Lateral Impacts and Aortic Injury: A Parametric Study." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-54019.

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Traumatic rupture of the aorta (TRA) remains the second most common cause of death associated with motor vehicle crashes after brain injury. On an average, nearly 8,000 people die annually in the United States due to blunt injury to the aorta. It is observed that more than 80% of occupants who suffer an aortic injury die at the scene due to exsanguination into the chest cavity. TRA and blunt aortic injury (BAI) are leading causes of death in high-speed blunt impact trauma. More specific injuries that fall under these classifications include myocardial contusion (MC), traumatic aortic disruptio
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