By Fabio Marra, Maurizio Parola (auth.), Pere Ginès, Patrick S. Kamath, Vicente Arroyo (eds.)
Chronic liver failure is a widespread situation in medical perform that encompasses all manifestations of sufferers with end-stage liver illnesses. persistent liver failure is a multiorgan syndrome that has effects on the liver, kidneys, mind, center, lungs, adrenal glands, and vascular, coagulation, and immune platforms. persistent Liver Failure: Mechanisms and administration covers for the 1st time all facets of continual liver failure in one booklet, from pathogenesis to present administration. each one bankruptcy is written by means of a world identified professional of their sector and all give you the most recent state of the art wisdom. This quantity is particularly designed to supply solutions to scientific inquiries to all medical professionals facing sufferers with liver ailments, not just medical gastroenterologists and hepatologists, but in addition to internists, nephrologists, extensive care physicians, and transplant surgeons.
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Extra resources for Chronic Liver Failure: Mechanisms and Management
Innate defenses in the liver during Listeria infection. Immunol Rev 2000;174:150–159. Barsig J, Flesch IE, Kaufmann SH. Macrophages and hepatocytic cells as chemokine producers in murine listeriosis. Immunobiology 1998;199:87–104. Henson D, Smith RD, Gehrke J. Non-fatal mouse cytomegalovirus hepatitis. Combined morphologic, virologic and immunologic observations. Am J Pathol 1966;49:871–888. Afford SC, Randhawa S, Eliopoulos AG, Hubscher SG, Young LS, Adams DH. CD40 activation induces apoptosis in cultured human hepatocytes via induction of cell surface fas ligand expression and amplifies fas-mediated hepatocyte death during allograft rejection.
In addition, TIMP-1 has been shown to be a survival factor for stellate cells, providing an additional profibrogenic Cells in the Liver—Functions in Health and Disease 19 action in the context of a fibrotic liver. For these reasons, inhibition of TIMP’s action may be viewed as a promising antifibrotic target. Similarly, HSCs express several components of the plasmin system, which is also involved in the regulation of matrix degradation (133). HSC contraction. Contraction, induced by vasoactive agents such as endothelin-1, angiotensin II, or thrombin (123), has a great relevance in the pathogenesis of portal hypertension, contributing to the “reversible” component of the increase in intrahepatic flow (134).
34. Zhong Z, Theruvath TP, Currin RT, Waldmeier PC, Lemasters JJ. NIM811, a mitochondrial permeability transition inhibitor, prevents mitochondrial depolarization in small-for-size rat liver grafts. Am J Transplant 2007;7:1103–1111. 26 Marra and Parola 35. Pockros PJ, Schiff ER, Shiffman ML, McHutchison JG, Gish RG, Afdhal NH, Makhviladze M, et al. Oral IDN-6556, an antiapoptotic caspase inhibitor, may lower aminotransferase activity in patients with chronic hepatitis C. Hepatology 2007;46:324–329.