Rozprawy doktorskie na temat „Hepatocyte”
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Vroemen, Joseph Pieter Anna Maria. "Hepatocyte transplantation". Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5364.
Pełny tekst źródłaHannoun, Zara. "Role of SUMO modification in hepatocyte differentiation". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5917.
Pełny tekst źródłaSchuster, Susanne, i Antje Garten. "Resveratrol Differentially Regulates NAMPT and SIRT1 in Hepatocarcinoma Cells and Primary Human Hepatocytes". Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142581.
Pełny tekst źródłaMatz-Soja, Madlen, i Rolf Gebhardt. "Hepatic Hedgehog signaling contributes to the regulation of IGF1 and IGFBP1 serum levels". Universitätsbibliothek Leipzig, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-142560.
Pełny tekst źródłaKolatsi, Maria. "Hepatocyte growth factor and renal morphogenesis". Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243452.
Pełny tekst źródłaAravinthan, Aloysious Dominic. "Hepatocyte senescence in chronic liver disease". Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708050.
Pełny tekst źródłaPowers, Mark J. (Mark James). "Substratum control of hepatocyte aggregate morphology". Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/43328.
Pełny tekst źródłaAinscow, Edward Keith. "Control and regulation of hepatocyte metabolism". Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624775.
Pełny tekst źródłaDunlay, Samantha, i Jonathan M. Peterson. "CTRP3 Prevents ETOH- Induced Hepatocyte Apoptosis". Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/127.
Pełny tekst źródłaMcCullough, Christian Thomas. "IFNγ-mediated apoptosis in the primary hepatocyte". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/24935.
Pełny tekst źródłaTura, Benjamin James. "IFNγ induced apoptosis in the murine hepatocyte". Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/29406.
Pełny tekst źródłaWoodman, Anthony C. "Studies on the control of hepatocyte proliferation". Thesis, Imperial College London, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364568.
Pełny tekst źródłaDixon, Mark. "Signal transduction mechanisms involved in hepatocyte proliferation". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245710.
Pełny tekst źródłaGustafson, Elisabet. "Thromboinflammation : in a Model of Hepatocyte Transplantation". Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-286869.
Pełny tekst źródłaFairhall, Emma Alexandra. "Hepatocyte generation from pancreatic acinar cell lines". Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2375.
Pełny tekst źródłaAmbury, Rachael. "Bioactive sugar surfaces for hepatocyte cell culture". Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/bioactive-sugar-surfaces-for-hepatocyte-cell-culture(122af33a-35b1-47c1-9579-4568fef47543).html.
Pełny tekst źródłaLucendo, Villarin Baltasar. "Stabilisation of hepatocyte phenotype using synthetic materials". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22059.
Pełny tekst źródłaRichardson, Steven J. "Hepatocyte growth signals rejection in heart transplantation". Thesis, University of Manchester, 2011. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.549330.
Pełny tekst źródłaFRAU, CARLA. "Preneoplastic hepatocyte hypothyroidism underlies hepatocellular carcinoma progression". Doctoral thesis, Università degli Studi di Cagliari, 2014. http://hdl.handle.net/11584/266448.
Pełny tekst źródłaConstante, Pereira Marco. "Development of synthetic biology devices for iron metabolism research". Doctoral thesis, Universitat Pompeu Fabra, 2011. http://hdl.handle.net/10803/53579.
Pełny tekst źródłaLa biología sintética es un campo recientemente desarrollado con el objectivo de implementar nuevas funciones en sistemas biológicos. De forma global, la biología sintética incluye el desarrollo de herramientas para facilitar la ingeniería de sistemas biológicos. En diversas publicaciones, investigadores en el campo de la biología sintética han implementado dispositivos que funcionan de forma similar a circuitos electrónicos y han demonstrado el potencial del campo para la producción de biocarburantes, farmaceuticos y biosensores. Para la presente tesis he creado una colección de plasmidos estandarizados (Biobricks) que pueden ser de interés para biólogos fuera del campo da la biología sintética. Además, utilizando estos Biobricks, he creado un sensor de la actividad de las proteínas reguladas por el hierro. Para demonstrar su aplicación, he utilizado el sensor para estudiar un nuevo sistema de co-cultura de dos tipos celulares (BNL CL.2 y RAW 264.7), substituto para la comunicación entre hepatocitos y macrófagos
Hodgkinson, Conrad Phillip. "Expression of cytochrome P450s in rat hepatocyte culture". Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244085.
Pełny tekst źródłaCook, Nathan Luke Meredith. "Immunoregulation by hepatocyte growth factor in malignant mesothelioma". Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/54490/.
Pełny tekst źródłaLewis, Andrew L. "Flow cytometric analysis of hepatocyte proliferation in vitro". Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288990.
Pełny tekst źródłaBingham, Coralie. "The renal manifestations of hepatocyte nuclear factor mutations". Thesis, University of Exeter, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269720.
Pełny tekst źródłaLEIRIÃO, Patrícia Rodrigues Saavedra. "Plasmodium hepatocyte interactions : implications for protection against malaria". Doctoral thesis, Instituto de Higiene e Medicina Tropical, 2006. http://hdl.handle.net/10362/56913.
Pełny tekst źródłaMalaria is one of the most predominant infectious diseases worldwide, accounting for more than 1 million deaths annually. The intracellular parasite Plasmodium is the causative agent of malaria which undergoes a complicated life cycle. Infection is initiated by inoculation of sporozoites through mosquito bite, which journey to the liver where they must migrate and invade hepatocytes in order to replicate and mature. Immunity to malaria is complex and is essentially both species and stage specific, thus a wide variety of distinct immune mechanisms are provoked by the parasite in the host. The generation and maintenance of protective immune responses requires repeated infections over the lifetime of an individual and even though only partial immunity is achieved against the disease. Despite the significant advances in understanding mechanisms of protection and identifying new targets for vaccine design, an effective protection against malaria is still not available. However, immunization with irradiated Plasmodium sporozoites induces antigen-specific CD8+ T cells immune response that confers complete protection against malaria. The initiation of this response is mediated by dendritic cells, but the source of parasite antigens intervening in this response remains unknown. Irradiated sporozoites are capable of infecting hepatocytes but do not progress into blood stages forms. Both this incomplete liver development and the hepatic stage itself are indispensable steps for the outcome of a successful malaria protection. Although some protective mechanisms conferred by irradiated sporozoites have been identified, a thorough characterization is still needed. The liver plays a key role in the life cycle of the malaria parasite and therefore insights into Plasmodium-hepatocyte interactions will have a promising effect in improving the process of triggering an immune response against the disease. Using a rodent malaria model, we show that hepatocytes infected with irradiated Plasmodium sporozoites undergo apoptosis shortly after infection. In addition, after infection dendritic cells are recruited to the liver where they phagocytose apoptotic bodies derived from infected hepatocytes. Given that dendritic cells are capable of cross-presenting exogenous antigens and elicit the priming and activation of T cells, our results suggest that the apoptotic Plasmodium infected hepatocytes provide a source of parasite antigens for the initiation of the protective immune response against the disease. Cell death plays a central role in the course of an infection helping establish an immune response against a pathogen. Furthermore, some parasites have the capacity to modulate this response by apoptosis induction or inhibition of the infected host cell, in order to survive and develop within the host.Previously it was shown that wounding of hepatocytes by sporozoite migration induces the secretion of hepatocyte growth factor (HGF) by traversed cells, which renders neighbor epatocytes susceptible to infection. The signaling initiated by HGF through its receptor MET has multifunctional effects on various cell types. Survival signals and protection of host cells is one of these features of HGF/MET signaling. The role of this protection on Plasmodium infected hepatocytes was also a subject of study in this thesis. Therefore, we hypothesize that HGF/MET would induce in infected host cells protection from apoptosis, which in turn would lead to an increased infection. Our data confirms that HGF/MET signaling protects infected cells from apoptosis, since an increase in apoptosis of infected cells was observed when the signaling pathway was inhibited. Given that HGF inhibits cell death primarily through the PI3-kinase/Akt signal transduction pathway, we tested if the infection susceptibility increase was impaired by inhibition of this pathway. In fact, inhibition of PI3-kinase completely abrogates the HGF effect on malaria infection. Taken together, these results implicate that the permissive effect of HGF for susceptibility to malaria infection is, at least in part, mediated by its anti-apoptotic signal. To our knowledge, these results demonstrate for the first time that active host’s cell apoptosis inhibition during infection by Plasmodium is required for a successful infection. Finally, an attempt at identifying a Plasmodium candidate gene responsible for the apoptosis inhibition of the host cell was carried out. Preliminary results evidence a promising role for Plasmodium heat shock protein 70 which broad function should be studied in the future. In summary, data presented in this thesis contributes to a wider understanding of the events that occur in the liver during a malaria infection and expand our knowledge within the interactions established between the malaria parasite and its host.
Clissold, Rhian. "Identification of hepatocyte nuclear factor 1β-associated disease". Thesis, University of Exeter, 2017. http://hdl.handle.net/10871/31132.
Pełny tekst źródłaVasiliauskas, Juozas. "Hepatocyte Growth Factor-Like protein In prostate tumorigenesis". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1428070127.
Pełny tekst źródłaWanichnopparat, Wachiraporn [Verfasser]. "Epigenetic reprogramming of hepatocyte-like cells / Wachiraporn Wanichnopparat". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1239645333/34.
Pełny tekst źródłaBRUNO, GEMMA. "LIVER FIBROSIS IMPAIRS HEPATOCYTE TRANSDUCTION BY AAV VECTORS". Doctoral thesis, Università degli Studi di Milano, 2023. https://hdl.handle.net/2434/955885.
Pełny tekst źródłaMetcalfe, Anna M. J. "Role of HGF/SF in liver regeneration and possible involvement of p53". Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360393.
Pełny tekst źródłaMion, François. "Role des eicosanoides dans la physiopathologie digestive et hepatique : etude experimentale ; synthese hepatocytaire de prostaglandines". Lyon 1, 1991. http://www.theses.fr/1991LYO1M055.
Pełny tekst źródłaZhou, Hongyan. "Hepatocyte growth factor-met signaling in ovarian cancer progression". View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B36845346.
Pełny tekst źródłaSAKAMOTO, NOBUO, HISAO HAYASHI, TOMOYUKI HIGUCHI, AKIRA YAGI i NAOKI HISHIDA. "Cuproproteins of Hepatocyte Lysosomes in Normal and Fatty Liver". Nagoya University School of Medicine, 1993. http://hdl.handle.net/2237/17538.
Pełny tekst źródłaKramer, Kerstin. "Development and characterisation of conditionally immortal hepatocyte cell lines". Thesis, Queen Mary, University of London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362780.
Pełny tekst źródłaMcCullough, Peter W. "Hepatocyte growth factor : Molecular Mechanisms of Colorectal Cancer Metastasis". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508939.
Pełny tekst źródłaZhou, Hongyan, i 周紅艷. "Hepatocyte growth factor-met signaling in ovarian cancer progression". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B37937984.
Pełny tekst źródłaHampson, Laura Jane. "Control of hepatocyte glucose metabolism by hormones & neurotransmitters". Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438399.
Pełny tekst źródłaLopina, Stephanie Therese. "Carbohydrate-derivatized poly(ethylene oxide) hydrogels for hepatocyte adhesion". Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/40576.
Pełny tekst źródłaJohansson, Conny M. "Biophysical characterisation of the hepatocyte growth factor-glycosaminoglycan interaction". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/9904.
Pełny tekst źródłaUyama, Naoki. "Regulation of cultured rat hepatocyte proliferation by stellate cells". Kyoto University, 2002. http://hdl.handle.net/2433/149340.
Pełny tekst źródłaKhalbuss, Walid E. "Electrophysiology, Cell Calcium, and Mechanisms of Hepatocyte Volume Regulation". Digital Commons @ East Tennessee State University, 1990. https://dc.etsu.edu/etd/2709.
Pełny tekst źródłaKattler, Kathrin [Verfasser]. "Epigenetic characterization of human hepatocyte subpopulations in context of complex metabolic diseases and during in vitro differentiation of hepatocyte-like cells / Kathrin Kattler". Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2020. http://d-nb.info/1214640796/34.
Pełny tekst źródłaChéret, Claire. "Spécificité et redondance des facteurs de transcription HNF1α (Hepatocyte Nuclear Factor-1α) et HNF1β/vHNF1 (Hepatocyte Nuclear Factor-1β/variant HNF1) chez la souris". Paris 6, 2002. http://www.theses.fr/2002PA066076.
Pełny tekst źródłaWan, Kai-fung. "Hepatocyte growth factor and met receptor signaling in nasopharyngeal carcinoma cell migration and invasion". Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39557029.
Pełny tekst źródłaPaterson, P. "Investigation of the interrelations of cellular Phase I and Phase II metabolism of xenobiotics". Thesis, University of Nottingham, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356534.
Pełny tekst źródłaSigurđardóttir, Anna Guđný. "Targeting hepatocyte growth factor/scatter factor for drug discovery using a fragment-based approach". Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610356.
Pełny tekst źródłaWang, Ye 1975. "The trafficking and signaling of EGF receptors in hepatocyte rafts /". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112318.
Pełny tekst źródłaIn this study, we compared three different biochemical methodologies of membrane rafts preparation from purified rat liver PM. Only detergent-resistant membranes (DRMs) fulfill the requirements of membrane rafts. We subsequently found using the low dose of EGF (1 ug/100 g BW); the content of EGFR in PM-DRMs did not changed significantly following EGF administration. When a higher dose of EGF (5 ug/100 g BW) is administrated we observed a rapid and almost complete disappearance of EGFR (around 80%) from both PM and DRMs fractions. Interestingly, following the administration of a low or high dose of EGF, the pool of EGFR in the PM-DRMs fraction becomes highly Tyr-phosphorylated. In accordance with the higher level of EGFR Tyr-Phosphorylation, EGF induced an augmented recruitment of Grb2 and Shc proteins to PM-DRMs compared with whole PM.
Furthermore neither high nor low dose of EGF affects the caveolin content in DRMs and PM. These observations suggest that EGFR located in DRM are competent for signaling and non-caveolae PM rafts are involved in the compartmentalization and presumably internalization of the EGFR.
Maitland, Vivien. "Isozyme-specific induction of cytochrome P450 in rat hepatocyte cultures". Thesis, University of Aberdeen, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302485.
Pełny tekst źródłaMooney, David James. "Control of hepatocyte morphology and function by the extracellular matrix". Thesis, Massachusetts Institute of Technology, 1992. http://hdl.handle.net/1721.1/12907.
Pełny tekst źródłaHayward, Adam Simon. "Emulsion templated porous polymers as scaffolds for 3D hepatocyte culture". Thesis, Durham University, 2014. http://etheses.dur.ac.uk/10749/.
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