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Melatonin receptors in mouse hepatocytes : binding characteristics and the effects of blood glucose /Choy, Hou-yau, Evelyn. January 1999 (has links)
Thesis (M. Phil.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 46-61).
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Defining the use of midazolam as a probe of CYP3A4 activity : sensitive quantitation of the metabolites and characterization of mechanism-based inactivation /Podoll, Terry D. January 1996 (has links)
Thesis (Ph. D.)--University of Washington, 1996. / Vita. Includes bibliographical references (leaves [153]-159).
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Melatonin receptors in mouse hepatocytes binding characteristics and the effects of blood glucose /Choy, Hou-yau, Evelyn. January 1999 (has links)
Thesis (M.Phil.)--University of Hong Kong, 1999. / Includes bibliographical references (leaves 46-61) Also available in print.
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Effects of lipoic acid on oxidant-induced cytotoxicity in HepG2 cellsLui, Ho-yan. January 2000 (has links)
Thesis (M.Med.Sc.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 28-34). Also available in print.
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Nuclear transcription factors and hypoxia-inducible genes in chronic liver hypoxiaLau, Yue-huen, Thomas. January 2005 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2005. / Title proper from title frame. Also available in printed format.
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The effect of [alpha]-aminoadipate [delta]-semialdehyde synthase knockdown on the lysine requirement and urate oxidase knockdown on oxidate stress in a murine hepatic cell lineCleveland, Beth Marie. January 2007 (has links)
Thesis (Ph. D.)--West Virginia University, 2007. / Title from document title page. Document formatted into pages; contains vii, 112 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire / Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinomaFekir, Karim 06 May 2015 (has links)
Le cancer primitif du foie, ou carcinome hépatocellulaire (CHC), est l’un des premiers cancers dans le monde chez l’homme adulte. L'identité des cellules à l'origine des CHC est controversée, toutefois l'existence de cellules souches/progénitrices (CS/P) dans certaines tumeurs a été rapportée. Ces tumeurs ont un phénotype très agressif, sont associées à un mauvais pronostic et ont tendance à échapper aux thérapies conventionnelles. Ainsi, des traitements ciblant spécifiquement les cellules souches cancéreuses pourraient constituer des compléments thérapeutiques efficaces aux traitements actuels. Pour cela, il est nécessaire de disposer de biomarqueurs afin d’identifier les sous-types de CHC dérivant de CS/P mais également de modèles cellulaires permettant de tester des molécules thérapeutiques. Les CS/P pourraient provenir soit du compartiment de cellules souches hépatiques soit de la dédifférenciation d’hépatocytes à l'intérieur de la tumeur. Aussi dans le cadre de cette thèse nous nous sommes attachés à étudier les mécanismes cellulaires et moléculaires impliqués 1) dans la retrodifférenciation des hépatocytes en CS/P et 2) dans le maintien des propriétés souches. Pour cette étude nous avons utilisé la lignée HepaRG issue d’un CHC sur infection virale C qui présente des caractéristiques de progéniteurs hépatiques se différenciant en hépatocytes et cholangiocytes. Dans la première partie de ce travail nous avons montré qu’un environnement inflammatoire favorise la retrodifferenciation d’hépatocytes HepaRG en CS/P. Alors que les voies activées par le TNF et l’IL-6 sont impliquées dans la perte du phénotype hépatocytaire, la voie TGF induit une transition épithélio-mésenchymateuse. Dans ces CS/P, nous observons l’enrichissement de signatures moléculaires associées à des souches embryonnaires et à des CHC avec mauvais pronostic. De plus, nous avons identifié plusieurs molécules pouvant inhiber ce processus de rétrodifférenciation des hépatocytes-HepaRG comme la trichostatine A. Dans une seconde partie nous avons montré que l’acquisition et le maintien des caractéristiques souches des cellules HepaRG étaient associés à une production de cytokines, à l’expression de métalloprotéinases impliquées dans les processus de migration et d’invasion, de facteur pro-angiogenique et à un changement dans l’activité mitochondriale conduisant à une reprogrammation métabolique. Les voies de signalisation impliquant l’angiopoïétine-like 4, PI3K et ERK régulent ces changements. De façon intéressante, nous montrons que le rétablissement de l’activité mitochondriale réduit la résistance des CS/P aux anticancéreux. Notre étude nous a permis d’acquérir une meilleure compréhension des voies de signalisation activées dans les cellules souches/progénitrices hépatiques cancéreuses et des mécanismes impliqués dans la rétro-différenciation des cellules matures tumorales, deux phénomènes probablement impliqués dans la récidive tumorale et la chimiorésistance. / Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma
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Accelerated ageing, senescence and the natural history of chronic hepatitis B virus infectionTachtatzis, Phaedra Maria January 2015 (has links)
Hepatitis B virus infection (HBV) is an important health problem worldwide, with a significant rate of chronic infection, which can lead to cirrhosis and hepatocellular carcinoma (HCC). Increased age is an important determinant of progression to cirrhosis and HCC, possibly because age is a crude measure of the duration of HBV infection. Increasing age is associated with changes in liver structure, blood flow and function and with reduced response to injury, impaired regeneration and increased mortality in acute liver disease. Age has been identified as a co‐factor in several chronic liver diseases including chronic hepatitis C infection (HCV). Available evidence suggests differential ageing of various intrahepatic cell types in different liver diseases and the ageing process may be more complex in the liver than originally thought. Telomeres are DNA structures located at the end of each chromosome, which protect the underlying coding DNA from breaks and fusions and shorten with increasing age. Both DNA damage and cell proliferation lead to progressive telomere shortening, which ultimately leads to cell cycle arrest and a state of replicative senescence. Persistent HCV and HBV infections lead to cell cycle arrest, providing a favourable environment for viral replication. Evidence suggests that progressive telomere shortening occurs with advancing stage of liver disease in HBV and specifically from cirrhosis through large cell dysplasia to small cell dysplasia and to HCC. Whether cell cycle arrest leads to a senescent‐like state or whether this is the result of oxidative stress is unknown. Unpublished data using cell cycle phase markers in chronic HBV infection reveal that hepatocytes, which support HBV replication, are arrested in G1, which is mediated by hepatocyte p21 expression. I hypothesise that: 1. In normal liver tissue, different cell types age at different rates and this is altered during disease; 2. Hepatocyte senescence plays a significant role in the natural course of chronic HBV infection and underlies HBV antigen expression. I developed and optimised large volume Q‐FISH methodology to measure telomere length and nuclear size in a variety of intrahepatic cell lineages. In normal liver tissue, cholangiocytes had longer telomeres compared with all other intrahepatic lineages over a wide age range. Hepatocytes did not show any age‐related telomere shortening, in contrast to Kupffer and hepatic stellate cells. In chronic HBV infection, all hepatocytes had shortened telomeres when compared to age and sex‐matched controls consistent with accelerated ageing. HBV replication was confined to those hepatocytes with longer telomeres, suggesting that HBV entry or replication is less efficient in older hepatocytes and compatible with the fall in serum HBV DNA and HBsAg titre seen with advancing age. There may be two populations of hepatocytes in chronic HBV infection; hepatocytes that are growth arrested with short telomeres not supporting HBV replication and biologically 'younger' hepatocytes with longer telomeres that do support HBV replication. The change in cellular HBV antigen localisation with disease progression is also explained by age related changes in HBV expression. Nuclear Hepatitis B core antigen expression (HBcAg), characteristic of the early immune tolerant phase of infection, was associated with the longest telomeres, while cytoplasmic HBcAg expression was associated with shorter telomeres. Furthermore, the total number of hepatocyte telomeres fell with increasing fibrosis stage. Hepatocyte nuclear size, a marker of senescence, increased as HBcAg expression shifted from nucleus to cytoplasm; and p21, another senescence marker, never co‐localised with HBcAg expression. These results suggest that the location and production of HBV antigens are related to increased functional hepatocyte age and the onset of cellular senescence.
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Studies of insulin modulation of transcription in rat liver cellsDrake, Richard Lee January 1975 (has links)
This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).
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Mouse acute phase reactant serum amyloid P-component(SAP) : in vitro induction by monokines /Le, Phong T. January 1985 (has links)
No description available.
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