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Relevant bibliographies by topics / Hepatic injury / Dissertations / Theses

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Dissertations / Theses on the topic 'Hepatic injury'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

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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2

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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3

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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4

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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5

Nitta, Takashi. "Myoglobin gene expression attenuates hepatic ischemia reperfusion injury." Kyoto University, 2003. http://hdl.handle.net/2433/148743.

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6

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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7

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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8

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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9

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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10

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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11

Zhao, Liena. "Phenotypic characterization of hepatic stellate cells during their response to injury." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421191.

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12

Lane, Katie. "Hepatic drug metabolism in critically ill adults with acute kidney injury." Thesis, St George's, University of London, 2018. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.754065.

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Background: Acute Kidney Injury (AKI) is a common problem in critical care with its remote organ effects contributing to the high morbidity and mortality. Animal evidence has found deranged hepatic drug metabolism by cytochrome P450 enzymes (CYP) in AKI. The two most clinically relevant CYPs in humans are CYP3A and CYP2D6. Using midazolam as a probe drug, CYP3A metabolism was impaired in adults with AKI. Patients expressing functional CYP3A5 were protected from this effect. We investigated the factors and mechanisms affecting CYP3A and CYP2D6- mediated drug metabolism in the critically ill wit

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13

Hu, Wai-wai Stella. "Pharmacological modulation of endotoxin-induced hepatic injury in galactosamine-sensitized mice /." [Hong Kong] : University of Hong Kong, 1992. http://sunzi.lib.hku.hk/hkuto/record.jsp?B1338496X.

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14

Goto, Toshihiko. "Liver specific Prox1 inactivation causes hepatic injury and glucose intolerance in mice." Kyoto University, 2017. http://hdl.handle.net/2433/225976.

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15

Kirwan, Christopher John. "The effect of acute kidney injury on hepatic metabolism in critically ill patients." Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526035.

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16

Fujita, Shinichi. "Analysis and Modulation of Function of Hepatic Macrophages in Endotoxin-Induced Liver Injury." Kyoto University, 1997. http://hdl.handle.net/2433/198907.

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17

Lee, Jin Kyung Brouwer Kim L. R. "Role of hepatic transport proteins in drug disposition and drug-induced liver injury." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2419.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.<br>Title from electronic title page (viewed Sep. 3, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the School of Pharmacy." Discipline: Pharmacy; Department/School: Pharmacy.

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18

Ganbold, Anar. "Hepatic Steatosis, Ischaemia/Reperfusion injury and Survival Cytokines in Spontaneous Liver Transplant Tolerance." Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/14815.

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Liver transplantation is a well-established, life-saving treatment for patients with end-stage liver disease. Liver transplantation is inevitably accompanied by some degree of ischaemia/reperfusion injury. Ischaemia/reperfusion injury (IRI) can have important implications for both short and long-term transplantation outcomes. Increasing demand for donor livers has necessitated the use of “extended criteria donor” organs. Frequently, these livers are affected by steatosis. Significant steatosis of the donor liver is associated with increased susceptibility to injury during donor brain death and

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19

Lam, Shi, and 林璽. "The significance of hepatic stellate cell activation in small-for-sizefatty liver graft injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45012933.

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20

Kröhnert, Georg Friedemann [Verfasser]. "The Uncoordinated-5 Homolog B Receptor Affects Hepatic Ischemia Reperfusion Injury / Georg Friedemann Kröhnert." Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1225739918/34.

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21

Parkinson, E. J. "Investigating the molecular mechanisms of hypothermia-mediated hepatic protection following intestinal ischaemia-reperfusion injury." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383803/.

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The pathophysiology of hepatic energy failure following intestinal ischaemia-reperfusion injury (IIR) is not fully understood. In an experimental model of IIR, moderate hypothermia reduces hepatic dysfunction. The aim of this thesis was to investigate the molecular mechanisms of hypothermia-mediated hepatic protection following IIR. Results: Although heat shock proteins (HSPs) can be induced by hypothermia, there were no differences in levels of cytosolic HSPs between normothermic and hypothermic IIR groups. Normothermic IIR (NIIR), however, caused a significant increase in activated (phosphor

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22

Kröhnert, Friedemann [Verfasser]. "The Uncoordinated-5 Homolog B Receptor Affects Hepatic Ischemia Reperfusion Injury / Georg Friedemann Kröhnert." Tübingen : Universitätsbibliothek Tübingen, 2021. http://d-nb.info/1225739918/34.

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23

Lam, Shi. "The significance of hepatic stellate cell activation in small-for-size fatty liver graft injury /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3829686X.

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24

Robertson, F. "The effect of remote ischaemic preconditioning on CD4 T cells following hepatic ischaemia reperfusion injury." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10047916/.

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Ischaemia Reperfusion (IR) injury is a major cause of morbidity and mortality following orthotopic liver transplantation. Remote Ischaemic Preconditioning (RIPC) reduces IR injury in small animal models. The mechanism remains unclear. The aim of this thesis was to explore the mechanism of RIPC and its clinical relevance to liver transplant recipients. Following a literature review a study was performed on optimal end points for clinical studies modulating IR injury in liver transplantation. Day 3 AST level was strongly associated with early post operative morbidity and mortality. A pilot rando

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25

Kanazawa, Hiroyuki. "Bone marrow-derived mesenchymal stem cells ameliorate hepatic ischemia reperfusion injury in a rat model." Kyoto University, 2012. http://hdl.handle.net/2433/157437.

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26

Hassan, Reham [Verfasser]. "Mechanisms of activated hepatic stellate cell removal in acute and chronic liver injury / Reham Hassan." Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1144148103/34.

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27

Kusakabe, Jiro. "Complement 5 inhibition ameliorates hepatic ischemia/reperfusion injury in mice, dominantly via the C5a-mediated cascade." Kyoto University, 2020. http://hdl.handle.net/2433/254516.

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28

Ikeda, Fusao. "Reduction of hepatic ischemeia/reperfusion-induced injury by a specific ROCK/Rho kinase inhibitor Y-27632." Kyoto University, 2004. http://hdl.handle.net/2433/147495.

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29

BRUZZI', STEFANIA. "Functional characterization of hepatic monocyte-derived macrophages and dendritic cells during the evolution of liver injury." Doctoral thesis, Università del Piemonte Orientale, 2017. http://hdl.handle.net/11579/87005.

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30

Junnarkar, S. P. "Study of the effect of Bucillamine on the early and late phase of hepatic ischaemia reperfusion injury." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19989/.

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Ischaemia of the liver followed by reperfusion results in endothelial and parenchymal injury through a complex cascade of events. This often occurs in human liver transplantation as well as with major liver resections and is referred to as Ischaemia Reperfusion (IR) Injury. Bucillamine is a low molecular weight thiol antioxidant that is capable of rapidly entering cells. This thesis evaluates the effect of Bucillamine on both the early and late phases of liver warm IR injury with the hypothesis that beneficial effects are induced could be due to its action as a free radical scavenger. The drug

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31

Oe, Shoshiro. "Continuous intravenous infusion of deleted form of hepatocyte growth factor attenuates hepatic ischemia-reperfusion injury in rats." Kyoto University, 2002. http://hdl.handle.net/2433/149336.

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32

di, BELLO GIORGIA. "Nrf2 Inhibition Is Required To Activate Hepatic Progenitor Cells." Doctoral thesis, Università degli studi di Foggia, 2019. http://hdl.handle.net/11369/382255.

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L'attuale trattamento dell'insufficienza epatica è il trapianto di organo. Tuttavia, i costi elevati, la mancanza di donatori, la mortalità correlata al trattamento e l'immunosoppressione a lungo termine rendono questa opzione possibile solo per un numero limitato di pazienti. Il trapianto di cellule staminali del fegato è stato recentemente proposto come trattamento alternativo. L'identificazione dei principali regolatori nella differenziazione delle cellule progenitrici epatiche è determinante per la rigenerazione dell’ organo e può migliorare il trapianto di cellule staminali per la malatti

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33

Wang, Yuan, and 王苑. "The effect of intravenous and intrathecal morphine preconditioning on hepatic ischaemia-reperfusion injury in normal and cirrhotic livers." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47849848.

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Hepatic ischaemia-reperfusion injury occurs when patients undergoing liver operations such as liver transplantation, tumour resection and shock. Intravenous and intrathecal administration of morphine can be used to provide analgesia prior or after liver surgery. It has been reported that systemically administered morphine conferred protective effect on numerous organs, including heart, brain and kidney. The focus of my research is to investigate the effect of intravenous and intrathecal morphine preconditioning on normal and cirrhotic livers. Further, PI3K/Akt, STAT3 and HO-1/iNOS path

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34

BERARDO, CLARISSA ANGELA IRIS. "MPEP, a metabotropic Glutamate Receptor 5 (mGluR5) negative allosteric modulator, protects from hepatic ischemic injury both in vitro and ex vivo." Doctoral thesis, Università degli studi di Pavia, 2018. http://hdl.handle.net/11571/1214799.

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35

Hoffmann, Florian. "Decoy gelatin nanoparticles as a novel tool to elucidate the role of NF-kB in Kupffer cells on hepatic ischemia/reperfusion injury." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-70543.

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36

Mets, Berend. "Lignocaine extraction ratio and clearance as an indicator of hypoxic hepatic injury : a study using the in situ and the isolated perfused pig liver." Doctoral thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27152.

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The metabolism of lignocaine to monoethylglycinexylidide has been found useful as an indicator of hepatic function in association with liver transplantation. It has been postulated that this might be due to the common effect of hypoxic damage on liver function and lignocaine metabolism. The aim of this work was to establish whether hepatic lignocaine elimination was impaired by hypoxia and whether lignocaine extraction ratio and clearance could be used as an indicator of hepatic function. This was studied using the isolated pig liver perfused via the hepatic artery and portal vein. To establis

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37

Johann, Esther [Verfasser], Dieter [Akademischer Betreuer] Schrenk, and Stefan Otto [Akademischer Betreuer] Müller. "Improved early in vitro prediction of drug-induced liver injury in man: assessment of novel 3D hepatic models / Esther Johann ; Dieter Schrenk, Stefan Otto Müller." Kaiserslautern : Technische Universität Kaiserslautern, 2018. http://d-nb.info/1170154018/34.

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38

Tapuria, N. "Study of the effect of Remote Ischaemic Preconditioning (RIPC) on the early and late phase of hepatic ischaemia reperfusion injury and the role of haemoxygenase in RIPC." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/19898/.

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Reperfusion following ischaemia results in endothelial and parenchymal injury through a complex cascade of events. This often occurs in human liver transplantation as well as with major liver resections and is referred to as Ischaemia Reperfusion Injury (IRI). Ischaemic Preconditioning (IPC) is an adaptive response in which tolerance to prolonged ischaemia is induced in a target organ by prior brief periods of ischaemia. Benefits of IPC have been demonstrated in experimental models and in preliminary human clinical trials. In remote ischaemic preconditioning (RIPC) brief ischaemia involves a r

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39

Pantazi, Eirini. "New strategies to reduce liver ischemia – reperfusion injury in fatty and non-fatty livers: a focus on sirtuin 1 implication." Doctoral thesis, Universitat de Barcelona, 2015. http://hdl.handle.net/10803/299797.

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Ischemia-reperfusion injury (IRI) is an inevitable situation in clinical settings such as liver transplantation and hepatic resection. It develops when blood flow is interrupted for a long period of time (ischemia) and then it restarts (reperfusion). IRI pathophysiology is highly complex and includes a number of mechanisms, such as oxidative stress, inflammation, apoptosis, microcirculatory disturbances, that contribute to organ damage and limit the clinical outcome. In addition, in order to reduce the gap between the need and availability of donors, many transplantation teams now use liver gr

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40

Burban, Audrey. "Mécanismes impliqués dans la cholestase d'origine médicamenteuse : perturbations de la voie ROCK/MLCK et du profil intracellulaire des acides biliaires." Thesis, Rennes 1, 2017. http://www.theses.fr/2017REN1B018/document.

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La cholestase intrahépatique représente environ 40% des lésions hépatiques induites par les médicaments et se caractérise par une accumulation intracellulaire des acides biliaires (AB). Les mécanismes impliqués sont encore mal connus et sa prédiction reste difficile. Le but de ce travail était de caractériser dans la cholestase d’origine médicamenteuse et de développer des méthodes de screening pour sa prédiction précoce, en utilisant la lignée humaine hépatique HepaRG et les hépatocytes humains. Tout d’abord, nous avons démontré que la motilité des canalicules biliaires (CB) est indispensable

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41

Wartha, Elma Regina Silva de Andrade. "Propriedades antioxidantes de clones do pedúnculo de Anacardium occidentale L.: feito sobre a lipoperoxidação e enzimas participantes do sistema antioxidante de defesa do organismo animal." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/9/9131/tde-08062017-112859/.

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Os compostos fenólicos são substâncias amplamente distribuídas no reino vegetal, em particular nas frutas e em outros vegetais. Estes compostos, destacando-se flavonoides e os ácidos fenólicos, devido à estrutura molecular, podem apresentar a capacidade de inibir processos oxidativos. Além do mais, estão relacionados com a redução de risco de doenças crônicas não transmissíveis tais como: cardiovasculares, câncer, aterosclerose, entre outras. Considerando a elevada produção de caju em território brasileiro e a possibilidade da existência de compostos com potencial antioxidante no pedúnculo de

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42

Camprubí, Rimblas Marta. "Nebulized anti-coagulants as a therapy for acute lung injury and acute respiratory distress syndrome." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/663961.

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La síndrome de distrés respiratori agut (ARDS) és una insuficiència respiratòria aguda amb una incidència global a Europa de 17,9 per cada 100.000 persones-any. Tot i els avenços en el tractament de suport dels pacients amb ARDS, la mortalitat continua sent alta (40%) i els pacients que sobreviuen presenten seqüeles persistents. Actualment no existeix un tractament efectiu. La fisiopatologia de l’ARDS es caracteritza per l’activació de la coagulació i la inflamació a nivell pulmonar, juntament amb el trencament de la barrera alveolar-capil·lar. Això comporta la formació d’edema proteic, la in

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43

Hammerich, Linda [Verfasser]. "Chemokine receptor CCR6-dependent accumulation of IL-17 producing gamma/delta T cells in injured liver restricts hepatic inflammation and fibrosis / Linda Hammerich." Aachen : Hochschulbibliothek der Rheinisch-Westfälischen Technischen Hochschule Aachen, 2013. http://d-nb.info/1038603005/34.

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44

Laurindo, Álan Fernandes. "Avaliação de marcadores de lesão do túbulo proximal renal e incidência de redução da filtração glomerular em pacientes portadores de Hepatite B em uso de tenofovir." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17138/tde-06012016-112948/.

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Tenofovir (TDF), um antirretroviral análogo nucleotídeo inibidor da transcriptase reversa, indicado para o tratamento da infecção pelo vírus da Hepatite B em indivíduos HBeAg reagentes, não cirróticos, tem sido implicado na ocorrência de Injúria renal aguda (IRA) e lesão do túbulo proximal renal (TPR), com características semelhantes à Síndrome de Fanconi, caracterizada por glicosúria, bicarbonatúria, fosfatúria, uricosúria e proteinúria de baixo peso molecular. Outros trabalhos sugerem que os pacientes em uso de TDF sofram toxicidade aos glomérulos, com uma pequena, porém significante redução

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45

Moreira, Maria Margarida Miranda. "Efeitos hepatotóxicos e nefrotóxicos dos antibacterianos." Master's thesis, [s.n.], 2012. http://hdl.handle.net/10284/3566.

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Trabalho apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Ciências Farmacêuticas<br>Os antibióticos são medicamentos etiotrópicos sem ação farmacológica sobre as células eucarióticas do Homem, tendo como alvo os locais específicos da célula procariótica. Contudo, apesar desta especificidade de ação, os antibióticos podem exibir efeitos tóxicos nas células humanas, muito embora o risco potencial é baixo tendo em conta o seu elevado número de prescrições. Assim, a nível hepático a lesão induzida pelas penicilinas (ampicilina, benzilpeni

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Kuo, Chin-Jung, and 郭錦絨. "The Role of DLK1 on Hepatic Cells during Injury." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/d94x9f.

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碩士<br>國立成功大學<br>生物科技研究所碩博士班<br>92<br>Liver disease is a severe problem in Taiwan. Recently Huang et al. reported that Delta-like protein (DLK1) was demonstrated to decrease significantly in the progression of liver fibrosis in biliary atresia. It is suggested that DLK1 maybe involve in the pathogenesis of liver fibrosis. However, the molecular mechanism underlying the implication is still unknown. This study was aimed to investigate effects of DLK1 on liver cells during wound healing .We hypothesize that DLK1 maybe involve in the progression of liver injury by promoting liver regeneration and

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47

Wang, Liang-Kai, and 王亮凱. "Effect of Sesame Oil against Thioacetamide-induced Hepatic Injury in Rats." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/16910504154256836328.

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碩士<br>國立成功大學<br>環境醫學研究所<br>97<br>Introduction: Thioacetamide (TAA) is used to induce many acute hepatic injuries, such as fulminant hepatic failure (FHF) in animal models which relate to oxidative stress injuries. Many studies show that sesame oil (SO) protects liver through decrease oxidative stress and inflammation in acute animal models. Objective: To investigate the effect of SO on TAA-induced acute hepatic injury. Design: TAA (100 mg/kg; i.p) was used to induce acute hepatic injury. SO (1, 2, 4, and 8 ml/kg; orally) was administrated on different time points (0, 6, and 12h) after TAA inje

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48

Ying-ChienChen and 陳瑩倩. "Effects of sesame oil on ketoconazole-induced hepatic injury in mice." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/65546421036860383202.

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碩士<br>國立成功大學<br>環境醫學研究所<br>103<br>Ketoconazole is one of the most commonly used systemic antifungal drugs. However, long-term treatment of ketoconazole causes hepatic injury in patients. Oxidative stress and its related apoptosis are involved in ketoconazole-induced hepatic injury. Sesame oil is edible oil derived from sesame seeds rich with potent antioxidants. It protects against oxidative stress-associated hepatic injury in various models. However, the effect of sesame oil on ketoconazole-induced hepatic injury has never been investigated. The aim of the study was to investigate the protect

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49

Van, Rooyen Derrick Michael. "Cholesterol as a mediator of hepatic injury in non-alcoholic steatohepatitis." Phd thesis, 2012. http://hdl.handle.net/1885/150765.

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Non-alcoholic fatty liver disease (NAFLD) is highly prevalent. 20-30% of patients with NAFLD progress to non-alcoholic steatohepatitis (NASH), characterised by steatosis, ballooning degeneration of hepatocytes, inflammation and fibrosis, but the cause(s) of this transition remains unclear. Foz/foz (Alms1 mutant) mice develop hyperphagia and obesity-related NAFLD. High fat (HF)-feeding induces NASH transition by 12 weeks, and fibrosis by 24 weeks. The aims of this research were to investigate the cause and effect of hepatic cholesterol dysregulation in foz/foz mice, its pathogenic significance

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Chen, Li-Jeng, and 陳俐礽. "Protective effects of Cystamine against human parvovirus B19-NS1 induced hepatic injury." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/62124371999683124828.

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碩士<br>中山醫學大學<br>生化暨生物科技研究所<br>102<br>Human Parvovirus B19 (B19) infection is known to induce apoptosis and liver dysfunction. Cystamine is indicated in preventing apoptosis and it has been demonstrated to be beneficial on attenuating the hepatic injury in mice. Since our previous study demonstrated that B19-NS1 in development of autoimmunity by inducing apoptosis and aggravates liver injury, we herein intend to investigate the effect of cystamine on B19-NS1 induced hepatic iniury in BALB/c mice. For cystamine treatment, B19-NS1 BALB/c mice were injected intraperitoneally (i.p.) with cystamine

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