Literatura científica selecionada sobre o tema "Drug-induced cholestasis"
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Artigos de revistas sobre o assunto "Drug-induced cholestasis"
Al-Azzawi, Hasan, Ruchi Patel, Gagan Sood e Sumit Kapoor. "Plasmapheresis for Refractory Pruritus due to Drug-Induced Cholestasis". Case Reports in Gastroenterology 10, n.º 3 (6 de janeiro de 2017): 814–18. http://dx.doi.org/10.1159/000454674.
Texto completo da fonteErlinger, Serge. "Drug-induced cholestasis". Journal of Hepatology 26 (janeiro de 1997): 1–4. http://dx.doi.org/10.1016/s0168-8278(97)82326-4.
Texto completo da fonteHarnois, D. M. "Drug-Induced Cholestasis". Yearbook of Gastroenterology 2011 (janeiro de 2011): 269–70. http://dx.doi.org/10.1016/j.ygas.2011.07.048.
Texto completo da fonteLevy, Cynthia, e Keith D. Lindor. "Drug-induced cholestasis". Clinics in Liver Disease 7, n.º 2 (maio de 2003): 311–30. http://dx.doi.org/10.1016/s1089-3261(03)00032-1.
Texto completo da fonteSimon, Francis R. "DRUG-INDUCED CHOLESTASIS". Clinics in Liver Disease 2, n.º 3 (agosto de 1998): 483–99. http://dx.doi.org/10.1016/s1089-3261(05)70023-4.
Texto completo da fonteZimmerman, Hyman J., e James H. Lewis. "Drug-Induced Cholestasis". Medical Toxicology 2, n.º 2 (abril de 1987): 112–60. http://dx.doi.org/10.1007/bf03260010.
Texto completo da fonteBjornsson, Einar S., e Jon Gunnlaugur Jonasson. "Drug-Induced Cholestasis". Clinics in Liver Disease 17, n.º 2 (maio de 2013): 191–209. http://dx.doi.org/10.1016/j.cld.2012.11.002.
Texto completo da fonteBhamidimarri, Kalyan Ram, e Eugene Schiff. "Drug-Induced Cholestasis". Clinics in Liver Disease 17, n.º 4 (novembro de 2013): 519–31. http://dx.doi.org/10.1016/j.cld.2013.07.015.
Texto completo da fonteVelayudham, Lakshumanan S., e Geoffrey C. Farrell. "Drug-induced cholestasis". Expert Opinion on Drug Safety 2, n.º 3 (maio de 2003): 287–304. http://dx.doi.org/10.1517/14740338.2.3.287.
Texto completo da fontePadda, Manmeet S., Mayra Sanchez, Abbasi J. Akhtar e James L. Boyer. "Drug-induced cholestasis". Hepatology 53, n.º 4 (abril de 2011): 1377–87. http://dx.doi.org/10.1002/hep.24229.
Texto completo da fonteTeses / dissertações sobre o assunto "Drug-induced cholestasis"
Charanek, Ahmad. "The Bile Canaliculus Revisited : Morphological And Functional Alterations Induced By Cholestatic Drugs In HepaRG Cells". Thesis, Rennes 1, 2015. http://www.theses.fr/2015REN1B011/document.
Texto completo da fonteCholestasis is one of the most common manifestations of drug-induced liver injury (DILI). Since up to now it is unpredictable in 40% of all cases its accurate prediction represents a major challenge. First, we validated that differentiated HepaRG human liver cells are a suitable in vitro model to study drug-induced cholestasis, by comparing localization of influx and efflux transporters and their functional activity in these cells and primary human hepatocytes. All tested influx and efflux transporters were correctly localized to canalicular (BSEP, MRP2, MDR1, and MDR3) or basolateral (NTCP, MRP3) membrane domains and were functional. In addition, the HepaRG cell line also exhibits bile acids (BAs) metabolizing enzymes and has the capacity to synthesize BAs and to further amidate these BAs with taurine and glycine as well as sulfate, at a rate similar to that of primary hepatocytes. Concentration- dependent changes were observed in total BAs disposition after treatment of HepaRG cells by the cholestatic drug cyclosporine A (CsA). Inhibition of efflux and uptake of taurocholate was evidenced as early as 15 min and 1 h respectively. These early effects were associated with deregulation of cPKC pathway and induction of endoplasmic reticulum stress that preceded generation of oxidative stress. We also showed for the first time intracellular accumulation of endogenous BAs by a cholestatic drug in vitro. In addition, our work brings evidences that motility of bile canaliculi (BC) is essential for BAs clearance where ROCK pathway and actomyosin complex are highly implicated. We provided the first demonstration that ROCK pathway and BC dynamics are major targets of cholestatic compounds. Our data should help in the development of screening methods for early prediction of drug-induced cholestatic side effects
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.
Texto completo da fonteIntrahepatic cholestasis represents around 40% of drug-induced liver injuries and is characterized by intracellular accumulation of bile acids (BA); mechanisms involved and its accurate prediction remains challenging. The aim of the current work was to characterize the mechanisms involved in drug-induced cholestasis and to develop screening methods for its early prediction, using human differentiated HepaRG and primary human hepatocytes. First, we demonstrated that bile canaliculi (BC) motility is essential for BA clearance and requires alternating phosphorylation/dephosphorylation of myosin light chain (MLC) that is controlled by the Rho-kinase/Myosin Light Chain Kinase (ROCK/MLCK) signaling pathway. Then, we showed, for the first time that cholestatic drugs could alter the ROCK/MLCK/MLC pathway and BC dynamics. Using the penicillinase-resistant antibiotics family, including flucloxacillin that is responsible for many cases of cholestasis, we found that deregulation of ROCK could be modulated by HSP27, associated with PKC/P38 and PI3K/AKT signaling pathways. Finally, we evidenced variable potency of cholestatic drugs to modulate BA profiles. Indeed, the well-known cholestatic drugs induced a preferential accumulation of unconjugated toxic hydrophobic BA in vitro within the first 24h that resulted from inhibition of their amidation. Altogether, these data bring new information on the understanding of the mechanisms involved in drug-induced cholestasis and highlight new morphological and molecular predictive biomarkers of drug-induced cholestasis
Valentin, Loïse. "Développement de modèles de culture en 3D pour l’étude des maladies et des infections hépatiques humaines". Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS442.pdf.
Texto completo da fonteLiver infections and diseases are a major cause of morbidity and mortality. They include infections caused by hepatotropic pathogens, such as the Plasmodium parasite, and diseases of non-infectious origin caused in particular by drug treatments, such as cholestasis. The primary human hepatocyte (PHH) is the cell type of choice to study these infections and pathologies in vitro, but it is essential to develop new culture models closer to the physiology of cells in vivo and more relevant than 2D models. In this context, my thesis project aims to develop 3D culture systems for human liver cells. The work allowed to the establishment of a viable 3D spheroid scaffold-free model of PHH more functional than the 2D+ model. The results also demonstrate that PHH spheroids are an appropriate model for the culture of the liver stage of Plasmodium and would be more sensitive to antimalarial molecules. In order to improve the manipulation of spheroids, the magnetization of spheroids using nanoparticles (NS) was tested. NS do not affect the viability or hepatic functions of PHHs or their susceptibility to Plasmodium infection. Finally, an identical model with HepaRG cells was used to test a method for detecting drug induced cholestasis using a new fluorescent probe. The results proved that this probe can be used in spheroid models for the evaluation of the activity of cholestatic molecules
Livros sobre o assunto "Drug-induced cholestasis"
Kortgen, Andreas, e Michael Bauer. The effect of acute hepatic failure on drug handling in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0197.
Texto completo da fonteIverson, Suzanne Leah. In vitro and in vivo investigations into idiosyncratic drug reactions: the role of reactive metabolites produced by the target tissue in terbinafine-induced cholestatic hepatitis and antipsychotic-induced agranulocytosis. 2002, 2002.
Encontre o texto completo da fonteIverson, Suzanne Leah. In vitro and in vivo investigations into idiosyncratic drug reactions: The role of reactive metabolites produced by the target tissue in terbinafine-induced cholestatic hepatitis and antipsychotic-induced agranulocytosis. 2002.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Drug-induced cholestasis"
Hamilton, James P., e Jacqueline M. Laurin. "Drug-Induced Cholestasis". In Cholestatic Liver Disease, 21–43. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-118-5_2.
Texto completo da fonteBjörnsson, Einar S. "Drug-Induced Cholestasis". In Clinical Gastroenterology, 13–31. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1013-7_2.
Texto completo da fonteGijbels, Eva, e Mathieu Vinken. "Mechanisms of Drug-Induced Cholestasis". In Methods in Molecular Biology, 1–14. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_1.
Texto completo da fonteWatkins, J. B., e C. D. Klaassen. "Mechanisms of Drug-Induced Cholestasis". In Handbook of Experimental Pharmacology, 155–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61013-4_7.
Texto completo da fonteKullak-Ublick, Gerd A. "Drug-Induced Cholestatic Liver Disease". In Molecular Pathogenesis of Cholestasis, 256–65. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4419-9034-1_19.
Texto completo da fonteAithal, Guruprasad P., e Ann K. Daly. "Drug-Induced Cholestasis: Mechanisms and Importance". In Biliary Disease, 117–28. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50168-0_7.
Texto completo da fonteRamaiahgari, Sreenivasa C., e Stephen S. Ferguson. "Organotypic 3D HepaRG Liver Model for Assessment of Drug-Induced Cholestasis". In Methods in Molecular Biology, 313–23. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_20.
Texto completo da fonteDeferm, Neel, Lysiane Richert, Pieter Van Brantegem, Tom De Vocht, Bing Qi, Peter de Witte, Thomas Bouillon e Pieter Annaert. "Detection of Drug-Induced Cholestasis Potential in Sandwich-Cultured Human Hepatocytes". In Methods in Molecular Biology, 335–50. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9420-5_22.
Texto completo da fonteKrell, H. "Increase in Paracellular Permeability as a Pathophysiological Principle of Drug-Induced Intrahepatic Cholestasis in Rats". In Proceedings in Life Sciences, 33–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74247-7_4.
Texto completo da fonteKenna, J. Gerry, Simone H. Stahl e Tobias Noeske. "Strategies for Minimisation of the Cholestatic Liver Injury Liability Posed by Drug-Induced Bile Salt Export Pump (BSEP) Inhibition". In Topics in Medicinal Chemistry, 191–223. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/7355_2013_30.
Texto completo da fonte