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  "pii" => "S1665268119320204"
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    "pii" => "S1665268119320216"
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    "doi" => "10.1016/S1665-2681(19)32021-6"
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    "fechaPublicacion" => "2006-04-01"
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    "copyright" => "Fundación Clínica Médica Sur, A.C."
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      "titulo" => "The future of stem cells in liver diseases"
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            "en" => "<p id="sp0005" class="elsevierStyleSimplePara elsevierViewall">Distinguishing differentiation from fusion by cytogenetic analysis based on the identification of sex chromosomes&#46;</p> <p id="sp0010" class="elsevierStyleSimplePara elsevierViewall">A&#46; Differentiation of BM-derived cells into liver parenchymal cells originates hepatocytes with the same chromosomal pattern as the parent stem cell &#40;XY&#41;&#44; and such identity is maintained also in the case of polyploidy&#44; which is common in the liver &#40;e&#46;g&#46; XYXY in tetraploid cells&#41;&#46;</p> <p id="sp0015" class="elsevierStyleSimplePara elsevierViewall">B&#46; By contrast&#44; cell fusion between male hematopoietic cell lineage &#40;XY&#41; and female hepatocytes &#40;XX&#41; results in a XXXY pattern&#44; as it was shown in the Lagasse model&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a></p>"
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        0 => array:2 [
          "autoresLista" => "Maurizio Muraca, Ginevra Galbiati, Maria Teresa Vilei, Aline Sueli Coelho Fabricio, Maddalena Caruso"
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              "nombre" => "Maurizio"
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    "titulo" => "Hepatology Highlights"
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      0 => array:4 [
        "autoresLista" => "Claudio Tiribelli"
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            "nombre" => "Claudio"
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            "entidad" => "Professor of Medicine&#46; Director Centro Studi Fegato &#40;Liver Research Center&#41;"
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="p0005" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Obesity-related leptin receptor polymorphisms and gallstones disease&#44; by Nahum Mendez-S&#225;nchez et al</span></p><p id="p0010" class="elsevierStylePara elsevierViewall">The relationship between alteration in cholesterol absorption and biliary excretion&#44; obesity and gallstone formation are clinically known since more than 50 years&#46; More recently the presence of gallstones has been associated with the so called &#8220;metabolic syndrome&#8221; reiterating the role of obesity in the development of this common disorder&#46; Leptin is a key player in obesity since regulates energy consumption&#46; Leptin acts <span class="elsevierStyleItalic">via</span> the leptin receptor &#40;LEPR&#41;&#44; and a reduced interaction and&#47;or a reduced functional expression of LEPR result in hyperleptinemia&#44; which has been associated with obesity&#46; Since leptin regulates the cholesterol biliary excretion&#44; it would be of interests to understand if alterations of LEPR may be associated with a different the risk of cholesterol gallstones&#46; This study aims to answer this question by analyzing 97 Mexican subjects&#44; almost half of them with gallstones&#46; In addition to the customary indexes for metabolic syndrome&#44; including serum leptin levels&#44; subjects were screened for 2 known polymorphisms of the leptin receptor&#46; Not surprisingly&#44; gallstone patients were more overweight&#44; showed a greater insulin resistance and females were predominant&#46; Unfortunately no correlation was observed between the presence of mutations in the LERP and gallstone&#46; More important was the finding of a comparable level of serum leptin in the two groups suggesting the lack of correlation between the two variables in the population screened&#46; This finding is not in line with pervious series where leptin was shown to be a good index of gallstones and biliary sludge&#46; It is possible that the difference may be related to different racial background&#44; something interesting to be explored&#46; The key&#44; clinically relevant question if leptin serum level of genetic alterations in LEPR may be predictive for gallstone awaits further investigation before being answered&#46;</p><p id="p0015" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Metabolic syndrome&#44; Non-alcoholic Steatohepatits &#40;NASH&#41; and Hepatocyte Growth Factor &#40;HGF&#41;&#44; by Yasemin H Balaban et al</span></p><p id="p0020" class="elsevierStylePara elsevierViewall">Non-alcoholic SteatoHepatitis &#40;NASH&#41; but much more Non-alcoholic Fatty Liver Disease &#40;NAFLD&#41; are booming in all the Liver Units and in all the offices of general practitioner worldwide&#46; Reasons are the boom in obesity and the easy diagnosis by ultrasound&#46; In a representative series it has been recently reported that obesity is the greater risk factor of NAFLD and more that 60&#37; of obese subjects do have fatty liver in the absence of alcohol consumption&#46; In this study the potential role of Hepatocyte Growth Factor &#40;HGF&#41; was investigated in a series of 26 Turkish patients with biopsy proven NASH and compared with 13 healthy controls&#46; HGF serum levels were comparable in the two groups indicating that this antiapoptotic and anti-inflammatory cytokine is not apparently involved in fatty accumulation and related inflammatory response&#46; Although negative this study indicates that the costly determination of HGF should not be included in the diagnostic panel of NASH or NAFLD&#46;</p></span>"
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