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Dissertations / Theses on the topic 'Severity of liver damage'

Author: Grafiati

Published: 28 September 2024

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1

Habib, Shahid, Khalid Khan, Chiu-Hsieh Hsu, Edward Meister, Abbas Rana, and Thomas Boyer. "Differential Simultaneous Liver and Kidney Transplant Benefit Based on Severity of Liver Damage at the Time of Transplantation." ELMER PRESS INC, 2017. http://hdl.handle.net/10150/625529.

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Background: We evaluated the concept of whether liver failure patients with a superimposed kidney injury receiving a simultaneous liver and kidney transplant (SLKT) have similar outcomes compared to patients with liver failure without a kidney injury receiving a liver transplantation (LT) alone. Methods: Using data from the United Network of Organ Sharing (UNOS) database, patients were divided into five groups based on pre-transplant model for end-stage liver disease (MELD) scores and categorized as not having (serum creatinine (sCr) <= 1.5 mg/dL) or having (sCr > 1.5 mg/dL) renal dysfunction. Of 30,958 patients undergoing LT, 14,679 (47.5%) had renal dysfunction, and of those, 5,084 (16.4%) had dialysis. Results: Survival in those (liver failure with renal dysfunction) receiving SLKT was significantly worse (P < 0.001) as compared to those with sCr < 1.5 mg/dL (liver failure only). The highest mortality rate observed was 21% in the 36+ MELD group with renal dysfunction with or without SLKT. In high MELD recipients (MELD > 30) with renal dysfunction, presence of renal dysfunction affects the outcome and SLKT does not improve survival. In low MELD recipients (16 - 20), presence of renal dysfunction at the time of transplantation does affect post-transplant survival, but survival is improved with SLKT. Conclusions: SLKT improved 1-year survival only in low MELD (16 - 20) recipients but not in other groups. Performance of SLKT should be limited to patients where a benefit in survival and post-transplant outcomes can be demonstrated.

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2

Zambon, Azevedo Vittoria. "Mise au point d’un nouvel outil diagnostique de l’obésité sarcopénique : relations avec la dysfonction du tissu adipeux, l’insulinorésistance et la sévérité de l’atteinte hépatique." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS170.pdf.

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L'obésité sarcopénique (OS) est une condition caractérisée par la coexistence de l'obésité et de la sarcopénie, c'est-à-dire une réduction de la masse et de la fonction musculaires. Diagnostiquer l'OS est très complexe en raison de l'absence de critères diagnostiques universellement acceptés, ce qui entraîne des diagnostics imprécis et une estimation hautement variable de sa prévalence. Face à ces limitations, l'objectif de cette thèse était de développer un outil de diagnostic empirique pour l'OS aidé d'intelligence artificielle, basé sur l'analyse de la composition corporelle. Nous avons élaboré l'AIM-SO score dans une population de sujets en surpoids/obésité puis nous l'avons testé dans deux autres populations, l'une de patients avec obésité sévère subissant une chirurgie bariatrique, l'autre dans la population générale de l'UK Biobank. Une étude longitudinale a également été menée, avec un suivi à un an chez les sujets ayant subi une chirurgie bariatrique. Nous avons étudié les corrélations cliniques, en particulier cardiométaboliques et hépatiques, notamment histologiques per-opératoires, dans la cohorte bariatrique. La prévalence d'OS a été très proche entre ces trois cohortes. L'OS diagnostiquée par l'AIM-SO score était associée à de multiples comorbidités cardiométaboliques, ainsi qu'à une forme plus sévère d'atteinte inflammatoire et fibrosante du foie. Malgré la perte de poids, le bénéfice métabolique (rémission des comorbidités) après chirurgie bariatrique était moindre chez les patients ayant une OS. Des analyses préliminaires de la cohorte UK Biobank ont montré une association significative entre l'OS diagnostiquée par l'AIM-SO score et des paramètres de fonctionnalité musculaire, en particulier la force musculaire. Nous proposons ce nouvel outil diagnostique pour standardiser le diagnostic d'OS et identifier des patients en situation d'obésité avec sarcopénie dont le phénotype cardiométabolique et hépatique est plus sévère. Le diagnostic d'OS pourrait également renseigner le bénéfice attendu des différentes interventions à visée de réduction pondérale participant ainsi à une prise en charge médicale personnalisée<br>Sarcopenic obesity (SO) is a condition characterized by the coexistence of obesity and sarcopenia, the latter defined as a reduction in muscle mass and function. Diagnosing SO is highly complex due to the lack of universally accepted diagnostic criteria, leading to imprecise diagnoses and highly variable prevalence estimates. Given this scenario, this thesis aimed to develop an empirical diagnostic tool for SO using artificial intelligence, based on the analysis of body composition. We developed the AIM-SO score in a population of patients with overweight/obesity and tested it in two other populations: patients with severe obesity undergoing bariatric surgery (BS) and the general population of the UK Biobank. A longitudinal study with a one-year follow-up was conducted in subjects who underwent BS. We examined clinical correlations, particularly cardiometabolic and hepatic, including perioperative histological findings in the bariatric cohort. The prevalence of SO was similar across these three cohorts. SO diagnosed by the AIM-SO score was associated with multiple cardiometabolic comorbidities and more severe inflammatory and fibrosing liver damage. Despite weight loss, the metabolic benefit (remission of comorbidities) after BS was lower in patients with SO. Preliminary analyses of the UK Biobank cohort showed a significant association between SO diagnosed by the AIM-SO score and parameters of muscular functionality, particularly muscle strength. We propose this new diagnostic tool to standardize the SO diagnosis and identify patients with obesity and sarcopenia who exhibit more severe cardiometabolic and hepatic phenotype. Diagnosing SO could also inform the expected benefit of various weight loss interventions, thus contributing to personalized medical management

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3

Fisher, D. R. "Studies on residual damage in irradiated liver." Thesis, University of Manchester, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.355903.

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4

Nowak, Urszula. "Rheumatoid factor production in response to liver damage." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84065.

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Many liver diseases such as Alcoholic Liver Disease and Hepatitis C are associated with the production of autoantibodies. One of these autoantibodies is Rheumatoid Factor (RF), which binds to IgG and can aid in host defense. Since little is known about the role of RF in liver disease, we characterized the production of this autoantibody in three murine models of liver damage using alcohol, anti-Fas antibodies and carbon tetrachloride. RF was induced in response to chronic alcohol consumption as well as intraperitoneal injection of anti-Fas antibodies. RF was not produced in response to treatment with carbon tetrachloride for four weeks. Concurrent treatment with an E. coli glycolipoprotein which induces RF protected against liver damage as measured by a decrease in liver enzymes. Importantly, RF induced by this glycolipoprotein did not contribute to damage in the liver, suggesting that in the context of liver damage RF is not necessarily pathological.

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5

Miyachi, Yosuke. "Causes of liver steatosis influence the severity of ischemia reperfusion injury and survival after liver transplantation in rats." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263516.

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6

Müller, Hans Christian. "Alternative strategies to reduce liver abscess incidence and severity in feedlot cattle." Thesis, Kansas State University, 2017. http://hdl.handle.net/2097/38157.

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Master of Science<br>Department of Animal Sciences and Industry<br>James S. Drouillard<br>Since the 1960’s liver abscess incidence and severity have been identified as a problem associated with feeding high concentrate finishing rations to feedlot cattle. Liver abscesses lead to decreased feedlot performance and decreased carcass value. Tylosin phosphate is a macrolide antibiotic commonly used by feedlots throughout the United States and has been shown to successfully control liver abscesses. In 2013, the FDA issued Guidance for Industry #213, which encourages reduced usage of medically important classes of antibiotics, such as macrolides, in animal feed. This will be achieved by implementing veterinary oversight of these drugs via Veterinary Feed Directives (VFD). Thus, it is of importance to find alternative strategies to reduce usage of tylosin in finishing rations to control liver abscesses. One strategy that has been suggested is increasing dietary roughage concentration. However, this isn’t a viable option as increasing dietary roughage concentration not only leads to a decline in feedlot performance, hot carcass weight, and dressing percentage, but also has an environmental impact. Available research has also indicated that increasing dietary roughage has no impact on liver abscess incidence or severity. Our research objective was therefore to identify alternative strategies to reduce liver abscess incidence. Our first trial evaluated the impact of antioxidants on liver abscess incidence and severity. Treatments consisted of a control treatment (basal diet containing 200 IU/d α-tocopherol acetate), and an antioxidant treatment (basal diet containing 2000 IU/d α-tocopherol acetate and 500 mg/d crystalline ascorbate). Treatments were randomly assigned to 390 crossbred heifers. No differences in feedlot performance were detected; however, there was a tendency for improved feed intake (P = 0.075) and feed efficiency (P = 0.066) for heifers that received the antioxidant treatment. An increased number of yield grade 3 carcasses (P = 0.03) and fewer yield grade 1 carcasses (P < 0.01) was observed in the antioxidant treatment group. No differences were detected between treatments for other carcass characteristics or liver abscess incidence and severity. Another trial evaluated intermittent tylosin feeding and its impact on liver abscess incidence and antimicrobial resistant Enterococcus spp. when compared to continuous tylosin feeding. One of 3 treatments were randomly assigned to 312 crossbred steers: negative control (no tylosin fed throughout the feeding period); positive control (tylosin fed throughout the feeding period); or intermittent treatment (tylosin fed intermittently throughout the feeding period: 1week on, 2 weeks off). Fecal samples were collected on day 0, 20, and 118 to characterize antimicrobial resistant Enterococcus spp. By design, the intermittent treatment consumed 60% less tylosin than the positive control group. No differences were detected between treatments for feedlot performance. Liver abscess incidence was greatest for the negative control, and least for the positive control and intermittent treatments, with no difference being detected between the latter two treatments (P = 0.716). Antimicrobial resistance was unaffected by treatment, but was affected by sampling time. We concluded that supplementing antioxidants is not a viable option to reduce liver abscess incidence and severity, and that tylosin usage can be decreased without adversely affecting performance or liver abscess incidence.

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7

Haydon, Geoffrey H. "The severity and activity of liver disease in chronic hepatitis C infection." Thesis, University of Edinburgh, 1999. http://hdl.handle.net/1842/28213.

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The aims were twofold. Firstly, to assess the clinical significance of staging investigations; in particular the significance of molecular virological investigations in terms of disease diagnosis and prognosis. The role of non-invasive investigations in staging the disease process was also considered. Secondly, the impact of chronic hepatitis C infection was assessed in two populations; patients diagnosed as having hepatocellular carcinoma and those immunocompromised chronic HIV infection. In the Scottish population studied, both serum and intrahepatic virus levels were not determined by host factors (age of patient, mode or duration of infection) or by virus factors (HCV genotype). Likewise, there was no correlation between serum and liver HCV RNA levels demonstrated; however, those data did demonstrate that repetitive negative RT-PCR for HCV RNA in serum did not indicate absence of HCV from the liver. Pilot studies of the two non-invasive investigations in this population showed both to be reliable in predicting the presence of hepatic cirrhosis in patients infected with HCV. Amongst the intravenous drug abusers with chronic HIV infection, HCV did not influence either the clinical progression of HIV disease to AIDS and it was not associated with a more rapid immunological decline. Chronic HCV infection was identified as a major risk factor for the development of hepatocellular carcinoma. Molecular virological staging investigations should be interpreted with caution in chronic HCV infection; their most significant role is likely to be the initiation and monitoring of therapy rather than the inference of disease prognosis. Non-invasive investigations of hepatic cirrhosis are likely to be useful tests when a liver biopsy is contraindicated, although they should be first validated in larger, well described populations.

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8

Kistler, Kristin David. "Nonalcoholic fatty liver disease quality of life, exercise intensity and histological severity /." Diss., [La Jolla] : [San Diego] : University of California, San Diego ; San Diego State University, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p3359523.

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Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2009.<br>Title from first page of PDF file (viewed July 21, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.

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9

Висоцький, Ігор Юрійович, Игорь Юрьевич Высоцкий, Ihor Yuriiovych Vysotskyi, et al. "Chronopharmacological peculiaries of antioxidants action in toxic liver damage." Thesis, Sumy State University, 2015. http://essuir.sumdu.edu.ua/handle/123456789/41261.

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10

Holland, Michael J. "Measuring Disease Damage and its Severity in Childhood-Onset Systemic Lupus Erythematosus." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1527606864223975.

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11

Nalapareddy, Padmavathi Devi [Verfasser]. "Role of bid in liver injury following BDL and CCl4-induced liver damage / Padmavathi Devi Nalapareddy." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover, 2010. http://d-nb.info/1004974523/34.

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12

Soare, Catalina P. "Characterization of Liver Damage Mechanisms Induced by Hepatitis C Virus." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20343.

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Hepatitis C Virus (HCV) is one of the most important causes of chronic liver disease, affecting more than 170 million people worldwide. The mechanisms of hepatitis C pathogenesis are unknown. Viral cytotoxicity and immune mediated mechanisms might play an important role in its pathogenesis. HCV infection and alcohol abuse frequently coexist and together lead to more rapid progression of liver disease, increasing the incidence and prevalence of cirrhosis and hepatocellular carcinoma. The cytopathic effect of HCV proteins, especially the core, E1 and E2 structural proteins, which induce liver steatosis, oxidative stress and cell transformation may be amplified by alcohol abuse. The purpose of this study was to characterize the liver damage mechanisms induced by HCV structural proteins and alcohol and to determine the potential molecular mechanism(s) that may promote chronic, progressive liver damage. A transgenic mouse model expressing HCV core, E1 and E2 was used to investigate whether alcohol increased HCV RNA expression. Real-time RT-PCR analysis of genes involved in lipid metabolism and transport confirmed their abnormal expression in the alcohol-fed transgenic mice. In addition, light and electron microscopy analysis were performed on liver tissues of transgenic mice on an alcoholic diet versus those on a normal diet, in order to identify histological changes. The severe hepatopathy in HCV transgenic mice was exacerbated by alcohol. Mitochondria and endoplasmic reticulum had severe abnormalities in the electron microscopy analysis. The second part of this study focused on adaptive immune responses, which may also play an important role in HCV pathogenesis. I focused my analysis on dendritic cells (DC), which have been the main suspects to explain immune impairment in HCV infection. Their powerful antigen-presenting function allows them to stimulate the antiviral response of CD4+ and CD8+ T cells, the effector cells of the immune system. This unique function of the DC makes them possible targets for immune evasion by the Hepatitis C virus. In this study, DCs were generated from mouse bone marrow cells. I investigated their maturation capacity in the presence of structural proteins of HCV. The impact of HCV core/E1/E2 polyprotein on DCs cytokine expression and ability to activate T-cell lymphocytes was also analyzed. A dysfunctional CD4 T cell response was observed after exposure of DCs to core/E1/E2 polyprotein, indicating inefficient CD4 priming, which might lead to chronic HCV infection in humans. The presence of the core/E1/E2 polyprotein reduced the DC maturation capacity and the expression of certain cytokines (IL-12, IFNg, IL-6, MCP-1) important for stimulation and chemotaxis of T cells and other immune cells. My studies contribute to the understanding of HCV pathogenesis and may have implications to the development of better therapies for HCV infection.

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13

Pereira, Pedro Miguel Miranda Sousa Gonçalves. "Severity and extent of tissue damage in human and experimental temporal lobe epilepsy." Doctoral thesis, Instituto de Ciências Biomédicas Abel Salazar, 2007. http://hdl.handle.net/10216/7259.

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Pereira, Pedro Miguel Miranda Sousa Gonçalves. "Severity and extent of tissue damage in human and experimental temporal lobe epilepsy." Tese, Instituto de Ciências Biomédicas Abel Salazar, 2007. http://hdl.handle.net/10216/7259.

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15

Knight, Trudy Lynn. "The molecular basis of halothane-induced hepatotoxicity." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321782.

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16

Pesce, Paola. "Non Alcoholic Fatty Liver Disease: non invasive markers of severity and new experimental treatments." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3422225.

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Non Alcoholic Fatty Liver Disease (NAFLD) is a worldwide increasing disease but still many questions about its evolution, the need of a screening and the availability of effective specific treatments are open. Aims of this PhD project were: 1) the evaluation of NAFLD natural history in a subgroup of NAFLD affected diabetic patients enrolled during the daily clinical activity of a splenohepatology ecoDoppler laboratory in order to identify, if present, predictive factors of “evolutive NAFLD”; 2) the experimental evaluation, in High Fat Diet (HFD) fed rats, of the potential therapeutic effect of 3 molecules targeting respectively: a) lipid metabolism (Apolipoprotein A analogue compound -L4F), b) insulin sensitivity (peroxisome proliferator activated receptor delta agonist –PPARd agonist) c) endothelial function (EET Analog). We developed two studies: a clinical observational study and an experimental study. Clinical study: 100 patients with type 2 diabetes were evaluated as far as steatosis is concerned. Among them, 80 had sonographic signs of steatosis. There was no difference in the prevalence between male and female patients. 21 type 2 diabetic patients with liver steatosis were reevaluated after 6 years without any specific treatment. Liver steatosis increases only in less than 1/3 of non-obese diabetic patients and demonstrates that in the majority of them sonographic degree of steatosis improves or recovers concurrently with biohumoral parameters. The presence of increased levels of serum AST and ferritin and lower pulsatility index of haepatic artery seems to be correlated to a worse prognosis and may be used to identify those patients who deserve a higher surveillance. Experimental study: 30 male Wistar rats (4-5 weeks old, 150 grams body weight) were purchased from Charles River Laboratories. 24 rats have been fed with HFD for 8 weeks. After 8 weeks of diet animals have been divided in 4 groups: 7 untreated (HFD); 7 treated with L4F (L4F), 7 treated with PPARd agonist (PPARd) and 3 treated with EET Analog (EET). Treatments lasted 6 weeks. We demonstrate that HFD induced NAFLD reproduces splanchnic haemodynamic alteration of liver steatosis in humans and shows an activation of innate immune system also at early degree of steatosis without hepatic inflammation and fibrosis. The activation of innate immune system can be evaluated by the analysis of lipopolysaccharide (LPS) stimulated/unstimulated CC motif chemockine ligand 2 (CCL2) production in cultured peripheral blood mononuclear cells (PBMCs). PPARd agonist and L4F improved HFD induced liver steatosis and reduced CCL2 production in PBMCs but preserved the ability of PBMCs to react to LPS stimulation EETA administration didn’t improved liver steatosis and further decreased portal vein velocity and reduced the ability of PBMCs to react to LPS stimulation.

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Marker, Alison Jean. "Mechanisms of regulation of liver metabolism and growth." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287759.

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Upadhyaya, Sneha. "Development of an Improved and Internally-Consistent Framework for Evaluating Liquefaction Damage Potential." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/95941.

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Soil liquefaction continues to be one of the leading causes of ground failure during earthquakes, resulting in significant damage to infrastructure around the world. The study presented herein aims to develop improved methodologies for predicting liquefaction triggering and the consequent damage potential such that the impacts of liquefaction on natural and built environment can be minimized. Towards this end, several research tasks are undertaken, with the primary focus being the development of a framework that consistently and sufficiently accounts for the mechanics of liquefaction triggering and surface manifestation. The four main contributions of this study include: (1) development of a framework for selecting an optimal factor of safety (FS) threshold for decision making based on project-specific costs of mispredicting liquefaction triggering, wherein the existing stress-based "simplified" model is used to predict liquefaction triggering; (2) rigorous investigation of manifestation severity index (MSI) thresholds for distinguishing cases with and without manifestation as a function of the average inferred soil-type within a soil profile, which may be employed to more accurately estimate liquefaction damage potential at sites having high fines-content, high plasticity soils; (3) development of a new manifestation model, termed Ishihara-inspired Liquefaction Severity Number (LSNish), that more fully accounts for the effects of non-liquefiable crust thickness and the effects of contractive/dilative tendencies of soil on the occurrence and severity of manifestation; and (4) development of a framework for deriving a "true" liquefaction triggering curve that is consistent with a defined manifestation model such that factors influential to triggering and manifestation are handled more rationally and consistently. While this study represents significant conceptual advance in how risk due to liquefaction is evaluated, additional work will be needed to further improve and validate the methodologies presented herein.<br>Doctor of Philosophy<br>Soil liquefaction continues to be one of the leading causes of ground failure during earthquakes, resulting in significant damage to infrastructure around the world (e.g., the 2010-2011 Canterbury earthquake sequence in New Zealand, 2010 Maule earthquake in Chile, and the 2011 Tohoku earthquake in Japan). Soil liquefaction refers to a condition wherein saturated sandy soil loses strength as a result of earthquake shaking. Surface manifestations of liquefaction include features that are visible at the ground surface such as sand boils, ejecta, cracks, and settlement. The severity of manifestation is often used as a proxy for damage potential of liquefaction. The overarching objective of this dissertation is to develop improved models for predicting triggering (i.e., occurrence) and surface manifestation of liquefaction such that the impacts of liquefaction on the natural and built environment can be minimized. Towards this end, this dissertation makes the following main contributions: (1) development of an approach for selecting an appropriate factor of safety (FS) against liquefaction for decision making based on project-specific consequences, or costs of mispredicting liquefaction; (2) development of an approach that allows better interpretations of predictions of manifestation severity made by the existing models in profiles having high fines-content, high plasticity soil strata (e.g., clayey and silty soils), given that the models perform poorly in such conditions; (3) development of a new model for predicting the severity of manifestation that more fully accounts for factors controlling manifestation; and (4) development of a framework for predicting liquefaction triggering and surface manifestation such that the distinct factors influential to each phenomenon are handled more rationally and consistently.

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Anwar, Khurshid. "Role of apoptosis (programmed cell death) in acute liver failure." Thesis, University of Surrey, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.370058.

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Kulachek, Y. V., F. G. Kulachek, and V. T. Kulachek. "Estimation of severity of the early period of traumatic disease in victims with liver injury." Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/16910.

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Yasmin, Mahmuda. "Molecular biology of fulminant hepatitis B viruses." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360121.

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Ramirez, Javier. "Identification of sites of ethanol-derived protein adducts involved in liver damage." Tallahassee, Fla. : Florida State University, 2010. http://purl.fcla.edu/fsu/lib/digcoll/undergraduate/honors-theses/2181934.

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Thesis (Honors paper)--Florida State University, 2010.<br>Advisor: Dr. Mark Kearley, Florida State University, College of Arts and Sciences, Dept. of Chemistry and Biochemistry. Includes bibliographical references.

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Cass, Stacie Ann. "The effects of sexual harassment severity and organizational policy and response on juror damage awards." FIU Digital Commons, 2002. http://digitalcommons.fiu.edu/etd/2068.

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Community members who reported for jury duty (N = 123) read a brief summary of a sexual harassment trial, in which harassment severity and the organization's sexual harassment policy were manipulated. Jurors were more likely to agree that they should compensate the plaintiff for her pain and suffering, the organization should be punished, and the plaintiff had suffered when they read the more severe harassment scenario. When the organization had and enforced an effective sexual harassment policy, jurors believed that the plaintiff had suffered little and the organization should not be punished. Thus, severity of harassment influenced jurors' judgments about compensation, and organizational policy influenced jurors' judgments about punishment, both legally appropriate considerations. These results have implications for both organizations, who could create or modify sexual harassment policy to limit damage awards, and trial lawyers, who could tailor trial arguments to maximize or minimize awards.

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Ghallab, Ahmed [Verfasser]. "Spatial-temporal modelling of liver damage as well as regeneration and its influence on metabolic liver function / Ahmed Mohammed Ghallab." Gießen : Universitätsbibliothek, 2013. http://nbn-resolving.de/urn:nbn:de:hebis:26-opus-98761.

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Ghallab, Ahmed Mohammed [Verfasser]. "Spatial-temporal modelling of liver damage as well as regeneration and its influence on metabolic liver function / Ahmed Mohammed Ghallab." Gießen : Universitätsbibliothek, 2013. http://d-nb.info/1065320353/34.

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Gewiese, Jessica [Verfasser]. "Role of IL-6 Transsignaling in acute CCl4-induced liver damage / Jessica Gewiese." Kiel : Universitätsbibliothek Kiel, 2010. http://d-nb.info/1019982640/34.

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Yang, Sitian, and 楊斯恬. "Novel role of drug-induced non homologous end joining factor 1 in the chemoresistance of hepatocellular carcinoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/209505.

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Suh, Jihee. "Evaluation of Association of MicroRNA-122 with Histological Severity of Recurrent HCV Infection in Liver Transplant Recipients." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1890.

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Hepatitis C virus recurrence (which is defined by detection of HCV RNA in serum) in post-transplanted liver is universal but the progression of infection remains unpredictable, varying from case to case. It has been estimated that 75%-80% of the HCV recurrence patients will suffer chronic hepatitis C infection and up to a third of them will progress into the development of fibrosis and cirrhosis within 5 years post-transplantation. Therefore, finding ways to predict early on the progression of fibrosis can contribute to better prognoses. Recent literatures have mentioned that the hepatitis C virus relies on the host microRNA-122 (miR-122) for assistance in replication of the viral genome in hepatocytes. Experimental depletion of miRNA-122 in the cell line Huh 7 has shown up to an 80% decrease in HCV whereas an increase of miRNA-122 has shown an increase of HCV. Since miRNAs are known to have numerous indirect roles by the binding of the target messenger RNAs (mRNAs) and repressing the expression of their proteins, we hypothesized that the elucidation of associations between miRNA-122 and the histological severity in HCV recurrence post-liver transplantation might serve as a biomarker in predicting the outcome of HCV recurrence severity in patients. We also evaluated the expression levels of BCAP31 (a predicted target of miRNA-122), and CD4 (T cell surface molecules involved in immune response) among the HCV recurrence severity groups. RNA samples were isolated from FFPE liver samples from patients with HCV recurrence post-transplantation, and Reverse Transcription and TaqMan Real-Time PCR were carried out for qualitative analysis. We did not see any association between the levels of miRNA-122 expression and severity of HCV recurrence, but we did find a positive correlation between the miRNA-122 expression and the HCV viral load in Group 3 (Severe) at time of HCV recurrence, which supports previous studies of the role of miRNA-122 in HCV replication. We did not find any associations between the expression of BCAP31 and the severity of HCV recurrence but we did discovery an inverse relationship between miRNA-122 and BCAP31 in Group 3 (Severe) at time of HCV recurrence, confirming our assumption of miRNA:mRNA interaction. Also, we did find CD4 expression being statistically significant between Group 1 (Benign) versus Group 3 (Severe), which may support the hypothesis that strong, adequate CD4+ T-cell response is associated with better outcome post-liver transplantation.

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Sparks, Jessica L. "Biomechanics of blunt liver injury relating internal pressure to injury severity and developing a constitutive model of stress-strain behavior /." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1185909955.

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Buitrago, Molina Laura Elisa [Verfasser]. "mTOR inhibition impairs proliferation of hepatocytes with DNA damage during chronic liver injury thereby delaying liver tumor development / Laura Elisa Buitrago Molina." Hannover : Technische Informationsbibliothek und Universitätsbibliothek Hannover, 2010. http://d-nb.info/1009414127/34.

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Arp, Melanie K. "The frequency and severity of problem behaviors among individuals with autism, traumatic brain injury, and mental retardation from the Utah DSPD dataset /." Diss., CLICK HERE for online access, 2006. http://contentdm.lib.byu.edu/ETD/image/etd1050.pdf.

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32

Cowan, Matthew Lawson. "The application of proteomics to the discovery of biomarkers of diseases severity and prognosis in chronic liver disease." Thesis, St George's, University of London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.568724.

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Chronic liver disease (CLD) is a major and growing healthcare burden but is asymptomatic until liver fibrosis is advanced. Antiviral therapy can cure 50% with chronic hepatitis C virus (HCV) infection. Accurate staging of fibrosis requires invasive liver biopsy; predicting response to antivirals prior to the start of treatment is not possible. Clinical details, serum, plasma and liver tissue for 443 subjects with CLD were collected in a purpose-built database. Patients undergoing staging liver biopsy or HCV antiviral therapy were recruited prospectively; HCV patients with gold standard liver biopsies, or completed antiviral therapy and available serum were identified retrospectively. Surface enhanced laser desorption ionisation time-of-flight mass spectrometry (SELDI) is a high-throughput proteomic technique for profiling proteins. A protocol for SELDI profiling of ascites was optimised and the differences between the proteome of ascites and paired serum samples assessed. Comparison of the proteome of clinical subjects demonstrated that interindividual differences in the blood proteome may be more important in translational studies than the choice of blood collection tube. Long-term storage of serum did not adversely affect the quality of proteomic spectra allowing validation of individual biomarkers and multivariable diagnostic algorithms from stored samples. Accurate predictive models for the classification and staging of liver fibrosis and prediction of response to antiviral therapy were built from clinical and SELDI i proteomic data. The accuracy of traditional linear regression and complex non- linear machine learning diagnostic algorithms was explored. Proteomic biomarkers and all diagnostic models were validated in independent testing sets. The composite fibrosis index was accurate in subjects with liver disease of varying aetiology and showed ability to discriminate subjects with decompensated from compensated cirrhosis.

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Кононенко, Микола Григорович, Николай Григорьевич Кононенко, Mykola Hryhorovych Kononenko та І. М. Лукавенко. "Пошкодження печінки". Thesis, Видавництво СумДУ, 2004. http://essuir.sumdu.edu.ua/handle/123456789/9454.

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Кононенко, Микола Григорович, Николай Григорьевич Кононенко, Mykola Hryhorovych Kononenko, Андрій Олександрович Бойчунь та Andrii Oleksandrovych Boichun. "Актуальні питання артеріального гемостазу при пошкодженні печінки". Thesis, Видавництво СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/6696.

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35

Лішневська, Анастасія Геннадіївна, Анастасия Геннадьевна Лишневская, and Anastasiia Hennadiivna Lishnevska. "Degree of severity of laboratory syndromes in patients whith chronic viral hepatitis C." Thesis, Sumy State University, 2018. http://essuir.sumdu.edu.ua/handle/123456789/70787.

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У світі існує близько 71 мільйона людей, які страждають на ВГС. Приблизно половина смертельних випадків зумовлена цирозом печінки та печінковою клітинною карциномою.<br>В мире около 71 миллиона человек имеют инфекцию ВГС. Примерно половина смертельных случаев вызвана циррозом и гепатоцеллюлярной карциномой.<br>In the world there areabout 71 million people who have an HCV infection. Approximately half of the fatal cases are cused by cirrhosis and hepatocellular carcinoma.

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36

Lee, Matthew L., and Jonathan M. Peterson. "CTRP3 Protects Liver Cells From Alcohol-Induced Damage, But Not Through Enhanced Akt Signaling Type." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etsu-works/70.

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Alcoholic fatty liver disease (AFLD) is a significant public health concern. Excessive alcohol (ethanol) consumption causes liver cell damage and death, which results in eventual failure of the liver and death. AFLD is the number one cause of liver-related mortality in the United States. Our lab works with the novel protein C1q TNF Related Protein 3 (CTRP3), which inhibits non-alcoholic fatty liver disease, however the effects on AFLD are unknown. Therefore, the purpose of this experiment is to determine if CTRP3 prevents ethanol-induced liver cell death. The H4IIE rat hepatoma cell line was chosen for experimentation as a cell culture model of liver tissue. To determine a suitable alcohol level H4IIE cells were treated with 50, 100, and 200 mmol of ethanol for 18-24 hours. Trypan Blue was used to identify the dead/damaged cells, as only dead/damaged cells will be stained blue with this protocol. We observed that 100 mmol of ethanol consistently induced ~10% mortality rate in these cells. Next, we tested the ability of CTRP3 to reduce ethanol-induced mortality. We added purified CTRP3 protein to the cell media along with the 100 mmol ethanol treatment. The addition of CTRP3 reduced the amount of alcohol-induced cell death/damage in the H4IIE cell line by approximately 60%. Our next goal was to determine how CTRP3 reduces ethanol-induced death. The Akt signaling pathway is a well-known inhibitor of cell death. Therefore, to determine if CTRP3 attenuated ethanol-induced cell damage/death through activation of the Akt signaling pathway, another set of cells was treated with 100 mmol of ethanol and CTRP3 (with or without insulin). Western blots were used to compare the amount of active Akt (phosphorylated) in the CTRP3-treated and non-treated cells. A Western blot utilizes an electric current to separate denatured protein samples on a SDS-page gel, separating the proteins based on size. The smaller the protein the faster it migrates across the gel. The proteins are then transferred to a membrane for analysis, through exposure to commercial antigens and chemiluminescence imaging. There was no change in the amount of total or active Akt between the samples treated with or without CTRP3. We conclude that CTRP3 protects liver cells from ethanol-induced damage/death, but not through activation of the Akt pathway.

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Smart, Kevin Arthur. "The mechanism by which hyperammonaemia may cause hepatic encephalopathy." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267312.

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Vilfranc, Chrystelle L. "Elucidating the Role of BRUCE in Chronic Liver Disease Pathogenesis." University of Cincinnati / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1617107353008576.

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39

Finnberg, Niklas. "The attenuation of the P53 response to DNA damage in rodent liver preneoplastic enzyme-altered foci /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-462-3.

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40

Ye, Xingshen. "Studies on effects of coptis extract and berberine against carbon tetrachloride-induced liver damage in rats." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38718832.

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41

Ghafoory, Shahrouz [Verfasser], and Stefan [Akademischer Betreuer] Wölfl. "Gene expression recovery during an acute toxic damage in the liver / Shahrouz Ghafoory ; Betreuer: Stefan Wölfl." Heidelberg : Universitätsbibliothek Heidelberg, 2015. http://d-nb.info/118039688X/34.

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Ye, Xingshen, and 叶星沈. "Studies on effects of coptis extract and berberine against carbon tetrachloride-induced liver damage in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38755208.

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43

Gibhard, Liezl. "Ozone autohaemotherapy protects against Ketamine hydrochloride® induced liver and muscle damage in baboons / L. Gibhard." Thesis, North-West University, 2007. http://hdl.handle.net/10394/759.

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Ozone therapy has been used as a form of alternative medicine but has encountered scepticism by orthodox medicine concerning its effectiveness and toxicity. We assessed the acute and chronic effect of O3 autohaemotherapy (AHT) on liver and muscle damage in baboons. During the acute effect three groups of baboons were used. The first group (n=11) were treated with an O2/O3 gas mixture containing different ozone concentrations i.e. 20, 40 and 80 μg/ml O3 . The second group (n=5) were treated with pure O2 and the third group (n=3) received no treatment and were used to assess the effect of ketamine anaesthesia. O2 and O3-AHT was performed on the baboons by using 5% of their total blood volume. Blood samples were collected in heparin before each treatment and again at 4, 24 and 48 hours. Ketamine anaesthesia caused both liver and muscle damage. Aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatine kinase (CK) levels increased markedly. O2-AHT had no marked effect on liver and muscle damage and O3-AHT had a protective effect since the increase in AST, ALT and CK levels was not as dramatic as when ketamine alone was used. During the chronic effect O3-AHT were done on 6 baboons, using a O2/O3 gas mixture containing 40 μg/ml O3. Blood were collected before treatment and again at 4, 24, 28, 48, 52, 72 and 96 hours after the first treatment. ALT levels increased during the treatment period of 52 hours and remained elevated for 48 hours following treatment. AST levels increased during the four hours following each treatment and remained elevated for 48 hours following the last treatment. CK levels increased markedly dl-ring the four hours following each treatment, but after treatment was stopped the CK levels decreased dramatically. The magnitude of changes was small and does not support the view that in vitro ozonation of blood is toxic when the treated blood is reinjected back into the baboon. In conclusion, the results do not prove or disprove that 03-AHT caused severe cell damage in baboons. We used 40 μg/ml O3 in the studies where the baboons were treated sequentially (chapter 3). This was because the results obtained with dose of 80 μg/ml O3 were not largely different from that with 40 μg/ml O3 in the acute studies (chapter 2). It was proven in these two studies and also other studies. It was proven in these two studies and also in other studies. I also have no ready explanation of the mechanism through which the liver and muscle were protected by ozone. This has to be investigated.<br>Thesis (M.Sc. (Biochemistry))--North-West University, Potchefstroom Campus, 2008.

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44

Kamimura, Ryo. "Comparative study of transplantation of hepatocytes at various differentiation stages into mice with lethal liver damage." Kyoto University, 2012. http://hdl.handle.net/2433/157436.

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Gao, Yong. "Noninvasive monitoringn of CCl4 induced acute and chronic liver damage in rat by single quantum and triple quantum filtered 23Na magnetic resonance imaging." Connect to resource online, 2008. http://hdl.handle.net/1805/2045.

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Thesis (M.S.)--Indiana University, 2008.<br>Title from screen (viewed on January 26, 2010). Department of Cellular & Integrative Physiology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Navin Bansal, Andriy M. Babsky, Stephen A. Kempson, David P. Basile. Includes vitae. Includes bibliographical references (leaves 33-36).

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46

Wali, Mohamed Hatem Fathi El-Saied. "Natural history, factors affecting severity and progression rate of hepatitis C virus (HCV) infection in liver transplanted and non-transplanted patients." Thesis, University of Birmingham, 2002. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269215.

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47

Zohora, Fatematuz. "Evaluation of material crack using acoustic emission technique." Thesis, Queensland University of Technology, 2016. https://eprints.qut.edu.au/94663/1/Fatematuz_Zohora_Thesis.pdf.

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Cracks in civil structures can result in premature failure due to material degradation and can result in both financial loss and environmental consequences. This thesis reports an effective technique using Acoustic Emission (AE) technique to assess the severity of the crack propagation in steel structures. The outcome of this work confirms that combination of AE parametric analysis and signal processing techniques can be used to evaluate crack propagation under different loading configurations. The technique has potential application to assess and monitor the condition of civil structures.

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48

Billing, S. E. "An evaluation of different methods of measuring lipid peroxidation and their application to the assessment of liver cell damage induced by certain hepatoxic agents." Thesis, Brunel University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383745.

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49

Rose, David Harry. "A Cumulative Damage Approach to Modeling Atmospheric Corrosion of Steel." University of Dayton / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=dayton1417085212.

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Amin, Alla Mohammed Hussain. "Cold ischaemia and reperfusion injury in liver : the potential for damage to cellular DNA in the rat model." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248455.

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