By Thomas D. Boyer MD, Theresa L. Wright MD, Michael P. Manns MD
Lengthy thought of the defining paintings in Hepatology, this relied on 2-volume masterwork has been refocused to 0 in on simply the medical wisdom you must supply latest most sensible sufferer care. the main finished textual content at the topic, this e-book continues to be completely grounded in uncomplicated science-but now that technological know-how is targeted at the so much clinically proper advancements. locate definitive assurance of all elements of liver ailment in a brand new full-color layout that retains velocity along with your evolving perform. go surfing to www.hepatologytext.com to discover the full contents of the 2-volume set on-line and entirely searchable for quick session anywhere you cross, plus a downloadable photograph assortment to your presentations.Covers all liver illnesses at the moment visible in scientific practice-in clinically targeted volumes.Replaces earlier versions' easy technology part with the recent, extra concise "Pathophysiology of healing objectives" part.
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Extra resources for Zakim and Boyer's Hepatology: A Textbook of Liver Disease, 2-Volume Set 5th Edition
Example text
Met, metastasis, motility and more. Nature Rev Mol Cell Biol 2003;4:915–925. 28. Pediaditakis P, Lopez-Talavera JC, Petersen B, et al. The processing and utilization of hepatocyte growth factor/scatter factor following partial hepatectomy in the rat. Hepatology 2001;34:688–693. 33 Section I. Pathophysiology of the Liver 29. Stolz DB, Mars WM, Petersen BE, et al. Growth factor signal transduction immediately after two-thirds partial hepatectomy in the rat. Cancer Res 1999;59:3954–3960. 30. Borowiak M, Garratt AN, Wustefeld T, et al.
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124 In the TGF-RII-/- animals activin A expression was increased compared to controls. 122 However, as activin A and TGF-b activate very similar intracellular pathways there is a high chance that the two pathways are able to compensate for each other in both ways. Besides TGF-b and activin A, alternative signaling cascades have been discussed that might be involved in terminating liver regeneration. An attractive candidate is sphingosine 1-phosphate (S1P), as interaction with the G-protein-coupled endothelial differentiation gene Edg-5 activates Rho activity in hepatocytes, which is growth inhibitory.