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      Somatostatin and the “Small-For-Size” Liver

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          Abstract

          “Small-for-size” livers arising in the context of liver resection and transplantation are vulnerable to the effects of increased portal flow in the immediate postoperative period. Increased portal flow is an essential stimulus for liver regeneration. If the rise in flow and stimulus for regeneration are excessive; however, liver failure and patient death may result. Somatostatin is an endogenous peptide hormone that may be administered exogenously to not only reduce portal blood flow but also offer direct protection to different cells in the liver. In this review article, we describe key changes that transpire in the liver following a relative size reduction occurring in the context of resection and transplantation and the largely beneficial effects that peri-operative somatostatin therapy may help achieve in this setting.

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          Most cited references 82

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          Liver regeneration.

          Liver regeneration after partial hepatectomy is a very complex and well-orchestrated phenomenon. It is carried out by the participation of all mature liver cell types. The process is associated with signaling cascades involving growth factors, cytokines, matrix remodeling, and several feedbacks of stimulation and inhibition of growth related signals. Liver manages to restore any lost mass and adjust its size to that of the organism, while at the same time providing full support for body homeostasis during the entire regenerative process. In situations when hepatocytes or biliary cells are blocked from regeneration, these cell types can function as facultative stem cells for each other.
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            Liver regeneration.

            Liver regeneration after the loss of hepatic tissue is a fundamental parameter of liver response to injury. Recognized as a phenomenon from mythological times, it is now defined as an orchestrated response induced by specific external stimuli and involving sequential changes in gene expression, growth factor production, and morphologic structure. Many growth factors and cytokines, most notably hepatocyte growth factor, epidermal growth factor, transforming growth factor-alpha, interleukin-6, tumor necrosis factor-alpha, insulin, and norepinephrine, appear to play important roles in this process. This review attempts to integrate the findings of the last three decades and looks toward clues as to the nature of the causes that trigger this fascinating organ and cellular response.
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              Liver regeneration: from myth to mechanism.

               Rebecca Taub (2004)
              The unusual regenerative properties of the liver are a logical adaptation by organisms, as the liver is the main detoxifying organ of the body and is likely to be injured by ingested toxins. The numerous cytokine- and growth-factor-mediated pathways that are involved in regulating liver regeneration are being successfully dissected using molecular and genetic approaches. So what is known about this process at present and which questions remain?
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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                22 May 2019
                May 2019
                : 20
                : 10
                Affiliations
                Hepatopancreatobiliary Surgery and Transplantation, General & Digestive Surgery, Metabolic & Digestive Diseases Institute (ICMDM), Hospital Clínic, CIBERehd, IDIBAPS, University of Barcelona, 08036 Barcelona, Spain; lai_lilia@ 123456hotmail.com (L.M.d.l.M.); alshwely@ 123456clinic.cat (F.A.A.S.); aespinoza@ 123456clinic.cat (A.S.E.); ausania@ 123456clinic.cat (F.A.); cfonde@ 123456clinic.cat (C.F.)
                Author notes
                [* ]Correspondence: ajhesshe@ 123456clinic.cat ; Tel.: +34-93-227-5718
                Article
                ijms-20-02512
                10.3390/ijms20102512
                6566601
                31121844
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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