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  1. Article: Circumferential esophageal leiomyoma.

    Antonini, Filippo / Minicis, Samuele De / Macarri, Giampiero

    Annals of gastroenterology

    2015  Volume 28, Issue 1, Page(s) 144

    Language English
    Publishing date 2015-01-21
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2032850-3
    ISSN 1108-7471
    ISSN 1108-7471
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2455: Show issues Location:
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  2. Article ; Online: Are we ready for early discharge of patients with mild non-alcoholic acute interstitial pancreatitis?

    Antonini, Filippo / De Minicis, Samuele / Macarri, Giampiero / Pezzilli, Raffaele

    Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

    2016  Volume 16, Issue 3, Page(s) 322–323

    MeSH term(s) Acute Disease ; Alcoholism ; Humans ; Pancreatitis ; Pancreatitis, Alcoholic
    Language English
    Publishing date 2016-05
    Publishing country Switzerland
    Document type Letter ; Comment
    ZDB-ID 2056680-3
    ISSN 1424-3911 ; 1424-3903
    ISSN (online) 1424-3911
    ISSN 1424-3903
    DOI 10.1016/j.pan.2016.04.006
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    Zs.A 5553: Show issues Location:
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  3. Article ; Online: Extra-endoscopic mechanical lithotripsy of an impacted gallstone passing in the duodenum through a cholecystoduodenal fistula.

    Antonini, Filippo / Belfiori, Valerio / De Minicis, Samuele / Macarri, Giampiero

    Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver

    2015  Volume 47, Issue 11, Page(s) 992–993

    MeSH term(s) Aged, 80 and over ; Duodenum ; Endoscopy, Digestive System ; Female ; Gallstones/surgery ; Humans ; Intestinal Fistula ; Lithotripsy/methods
    Language English
    Publishing date 2015-11
    Publishing country Netherlands
    Document type Case Reports ; Letter
    ZDB-ID 1459373-7
    ISSN 1878-3562 ; 1125-8055
    ISSN (online) 1878-3562
    ISSN 1125-8055
    DOI 10.1016/j.dld.2015.08.009
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    Zs.A 1134: Show issues Location:
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  4. Article ; Online: From NAFLD to NASH and HCC: pathogenetic mechanisms and therapeutic insights.

    De Minicis, Samuele / Day, Chris / Svegliati-Baroni, Gianluca

    Current pharmaceutical design

    2013  Volume 19, Issue 29, Page(s) 5239–5249

    Abstract: NAFLD is the most common liver disease worldwide but it is the potential evolution to cirrhosis and hepatocellular carcinoma (HCC) that makes NAFLD of such clinical importance. The current work provides an overview of the main mechanims and potential ... ...

    Abstract NAFLD is the most common liver disease worldwide but it is the potential evolution to cirrhosis and hepatocellular carcinoma (HCC) that makes NAFLD of such clinical importance. The current work provides an overview of the main mechanims and potential therapeutical insights involved in NAFLD, NASH, fibrosis and HCC progression.
    MeSH term(s) Carcinoma, Hepatocellular/complications ; Carcinoma, Hepatocellular/therapy ; Fatty Liver/etiology ; Fatty Liver/therapy ; Humans ; Liver Neoplasms/complications ; Liver Neoplasms/therapy ; Non-alcoholic Fatty Liver Disease
    Language English
    Publishing date 2013
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1304236-1
    ISSN 1873-4286 ; 1381-6128
    ISSN (online) 1873-4286
    ISSN 1381-6128
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    Zs.A 4714: Show issues Location:
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  5. Article: New insights in hepatocellular carcinoma: from bench to bedside.

    De Minicis, Samuele / Marzioni, Marco / Benedetti, Antonio / Svegliati-Baroni, Gianluca

    Annals of translational medicine

    2014  Volume 1, Issue 2, Page(s) 15

    Abstract: Hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. The liver is one of the main targets for different metastatic foci, but it represents an important and ...

    Abstract Hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to malignant transformation of the hepatocyte. The liver is one of the main targets for different metastatic foci, but it represents an important and frequent locus of degeneration in the course of chronic disease. In fact, Hepatocellular carcinoma (HCC) represents the outcome of the natural history of chronic liver diseases, from the condition of fibrosis, to cirrhosis and finally to cancer. HCC is the sixth most common cancer in the world, some 630,000 new cases being diagnosed each year. Furthermore, about the 80% of people with HCC, have seen their clinical history developing from fibrosis, to cirrhosis and finally to cancer. The three main causes of HCC development are represented by HBV, HCV infection and alcoholism. Moreover, metabolic disease [starting from Non Alcoholic Fatty Liver Disease (NAFLD), Non Alcoholic Steatohepatitis (NASH)] and, with reduced frequency, some autoimmune disease may lead to HCC development. An additional rare cause of carcinogenetic degeneration of the liver, especially developed in African and Asian Countries, is represented by aflatoxin B1. The mechanisms by which these etiologic factors may induce HCC development involve a wide range of pathway and molecules, currently under investigation. In summary, the hepatocarcionogenesis results from a multifactorial process leading to the common condition of genetic changes in mature hepatocytes mainly characterized by uncontrolled proliferation and cell death. Advances in understanding the mechanism of action are fundamental for the development of new potential therapies and results primarily from the association of the research activities coming from basic and clinical science. This review article analyzes the current models used in basic research to investigate HCC activity, and the advances obtained from a basic and clinical point of view.
    Language English
    Publishing date 2014-07-14
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.3978/j.issn.2305-5839.2013.01.06
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  6. Article ; Online: Fibrogenesis in nonalcoholic steatohepatitis.

    De Minicis, Samuele / Svegliati-Baroni, Gianluca

    Expert review of gastroenterology & hepatology

    2011  Volume 5, Issue 2, Page(s) 179–187

    Abstract: Nonalcoholic steatohepatitis includes a wide spectrum of liver injury, ranging from simple inflammation to fibrosis and cirrhosis. Whereas simple steatosis has a benign clinical course, steatohepatitis is a recognized cause of progressive liver fibrosis ... ...

    Abstract Nonalcoholic steatohepatitis includes a wide spectrum of liver injury, ranging from simple inflammation to fibrosis and cirrhosis. Whereas simple steatosis has a benign clinical course, steatohepatitis is a recognized cause of progressive liver fibrosis and can develop, in some circumstances, into cirrhosis. The main cause of fibrogenesis is represented by the activation of myofibroblastic cells, which then start to produce matrix filaments. Matrix-producing cells, although mainly constituted of hepatic stellate cells, may have a different origin in the liver. This article will provide information on the sources of matrix-producing cells and the mechanisms involved in the development of fibrogenesis, with particular attention paid to the pathophysiological implications leading from steatohepatitis to fibrosis and cirrhosis.
    MeSH term(s) Adipokines/metabolism ; Animals ; Cytokines/metabolism ; Disease Models, Animal ; Extracellular Matrix/metabolism ; Fatty Liver/metabolism ; Hepatic Stellate Cells/metabolism ; Humans ; Liver Cirrhosis/metabolism ; Mice ; Myofibroblasts/metabolism ; Non-alcoholic Fatty Liver Disease ; Oxidative Stress/physiology ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism
    Chemical Substances Adipokines ; Cytokines ; Receptors, Cytoplasmic and Nuclear ; Toll-Like Receptors
    Language English
    Publishing date 2011-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2481021-6
    ISSN 1747-4132 ; 1747-4124
    ISSN (online) 1747-4132
    ISSN 1747-4124
    DOI 10.1586/egh.11.28
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    Zs.A 6978: Show issues Location:
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  7. Article: NADPH oxidase in the liver: defensive, offensive, or fibrogenic?

    De Minicis, Samuele / Bataller, Ramón / Brenner, David A

    Gastroenterology

    2006  Volume 131, Issue 1, Page(s) 272–275

    MeSH term(s) Disease Progression ; Humans ; Liver/enzymology ; Liver/pathology ; Liver Cirrhosis/enzymology ; Liver Cirrhosis/pathology ; NADP/metabolism ; Oxidative Stress/physiology
    Chemical Substances NADP (53-59-8)
    Language English
    Publishing date 2006-07
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2006.05.048
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    Ui V Zs.44: Show issues Location:
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    Zs.MO 572: Show issues

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  8. Article ; Online: Role of NADPH oxidases in liver fibrosis.

    Paik, Yong-Han / Kim, Jonghwa / Aoyama, Tomonori / De Minicis, Samuele / Bataller, Ramon / Brenner, David A

    Antioxidants & redox signaling

    2014  Volume 20, Issue 17, Page(s) 2854–2872

    Abstract: Significance: Hepatic fibrosis is the common pathophysiologic process resulting from chronic liver injury, characterized by the accumulation of an excessive extracellular matrix. Multiple lines of evidence indicate that oxidative stress plays a pivotal ... ...

    Abstract Significance: Hepatic fibrosis is the common pathophysiologic process resulting from chronic liver injury, characterized by the accumulation of an excessive extracellular matrix. Multiple lines of evidence indicate that oxidative stress plays a pivotal role in the pathogenesis of liver fibrosis. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) is a multicomponent enzyme complex that generates reactive oxygen species (ROS) in response to a wide range of stimuli. In addition to phagocytic NOX2, there are six nonphagocytic NOX proteins.
    Recent advances: In the liver, NOX is functionally expressed both in the phagocytic form and in the nonphagocytic form. NOX-derived ROS contributes to various kinds of liver disease caused by alcohol, hepatitis C virus, and toxic bile acids. Recent evidence indicates that both phagocytic NOX2 and nonphagocytic NOX isoforms, including NOX1 and NOX4, mediate distinct profibrogenic actions in hepatic stellate cells, the main fibrogenic cell type in the liver. The critical role of NOX in hepatic fibrogenesis provides a rationale to assess pharmacological NOX inhibitors that treat hepatic fibrosis in patients with chronic liver disease.
    Critical issues: Although there is compelling evidence indicating a crucial role for NOX-mediated ROS generation in hepatic fibrogenesis, little is known about the expression, subcellular localization, regulation, and redox signaling of NOX isoforms in specific cell types in the liver. Moreover, the exact mechanism of NOX-mediated fibrogenic signaling is still largely unknown.
    Future directions: A better understanding through further research about NOX-mediated fibrogenic signaling may enable the development of novel anti-fibrotic therapy using NOX inhibition strategy. Antio
    MeSH term(s) Angiotensin II/metabolism ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/pathology ; Humans ; Liver Cirrhosis/enzymology ; Liver Cirrhosis/pathology ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Signal Transduction
    Chemical Substances Reactive Oxygen Species ; Angiotensin II (11128-99-7) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2014-01-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2013.5619
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    Zs.A 5488: Show issues Location:
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  9. Article ; Online: Oxidative stress in alcoholic liver disease: role of NADPH oxidase complex.

    De Minicis, Samuele / Brenner, David A

    Journal of gastroenterology and hepatology

    2008  Volume 23 Suppl 1, Page(s) S98–103

    Abstract: Alcohol is a well-known risk factor for liver damage and is one of the major causes of liver disease worldwide. Chronic intake of alcohol, over a certain limit, inevitably leads to hepatic steatosis. If the injury persists, steatosis with concomitant ... ...

    Abstract Alcohol is a well-known risk factor for liver damage and is one of the major causes of liver disease worldwide. Chronic intake of alcohol, over a certain limit, inevitably leads to hepatic steatosis. If the injury persists, steatosis with concomitant tumor necrosis factor-alpha and other cytokines, progresses to steatohepatitis, fibrosis and finally cirrhosis. Among the multiple factors involved in the process of alcohol-induced liver injury, a crucial role is played by oxidative stress. Several mechanisms during ethanol metabolism result in reactive oxygen species (ROS) production. Although the main site of ethanol metabolism is hepatocytes, other mechanisms are involved in alcohol-induced liver injury. Specifically, in the ROS production activity, an important role is played by the NADPH oxidase complex. NADPH oxidase is expressed in hepatocytes, hepatic stellate cells and Kupffer cells in the liver. Studying NADPH oxidase gives new insights into alcohol-induced liver damage and provides new direction for future therapeutic strategies.
    MeSH term(s) Animals ; Humans ; Liver Diseases, Alcoholic/enzymology ; Liver Diseases, Alcoholic/metabolism ; NADPH Oxidases/physiology ; Oxidative Stress
    Chemical Substances NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2008-03
    Publishing country Australia
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 632882-9
    ISSN 1440-1746 ; 0815-9319
    ISSN (online) 1440-1746
    ISSN 0815-9319
    DOI 10.1111/j.1440-1746.2007.05277.x
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    Zs.A 2180: Show issues Location:
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    Zs.MO 299: Show issues

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  10. Article ; Online: Hepatic fibrogenesis in response to chronic liver injury: novel insights on the role of cell-to-cell interaction and transition.

    Svegliati-Baroni, Gianluca / De Minicis, Samuele / Marzioni, Marco

    Liver international : official journal of the International Association for the Study of the Liver

    2008  Volume 28, Issue 8, Page(s) 1052–1064

    Abstract: Hepatic fibrosis represents the wound-healing response process of the liver to chronic injury, independently from aetiology. Advanced liver fibrosis results in cirrhosis that can lead to liver failure, portal hypertension and hepatocellular carcinoma. ... ...

    Abstract Hepatic fibrosis represents the wound-healing response process of the liver to chronic injury, independently from aetiology. Advanced liver fibrosis results in cirrhosis that can lead to liver failure, portal hypertension and hepatocellular carcinoma. Currently, no effective therapies are available for hepatic fibrosis. After the definition of hepatic stellate cells (HSCs) as the main liver extracellular matrix-producing cells in the 1980s, the subsequent decade was dedicated to determine the role of specific cytokines and growth factors. Fibrotic progression of chronic liver diseases can be nowadays considered as a dynamic and highly integrated process of cellular response to chronic liver injury. The present review is dedicated to the novel mechanisms of cellular response to chronic liver injury leading to hepatic myofibroblasts' activation. The understanding of the cellular and molecular pathways regulating their function is crucial to counteract therapeutically the organ dysfunction caused by myofibroblasts' activation.
    MeSH term(s) Animals ; Cell Communication ; Cell Transdifferentiation ; Humans ; Liver Cirrhosis/etiology ; Liver Cirrhosis/pathology ; Phenotype
    Language English
    Publishing date 2008-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/j.1478-3231.2008.01825.x
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