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It has been proposed that these changes may have an important role in liver regeneration. The present study was performed to ascertain the effects of the oestrogen agonist diethylstilbestrol (DES), 2 mg\u002Fkg, and the oestrogen antagonist tamoxifen (TAM), 2 mg\u002Fkg, on liver regeneration induced by partial hepatectomy in the male rat. Regenerative activity was determined by incorporation of [\u003Cjats:sup>3\u003C\u002Fjats:sup>H]‐thymidine into hepatic DNA as well as by measurement of liver remnant weight. Following partial hepatectomy, there was a trend towards an increase in liver remnant weight at 24 h in rats treated with DES (DES, 5.95 ± 1.52 g; vehicle, 4.87 ± 0.66 g; \u003Cjats:italic>P\u003C\u002Fjats:italic>= 0.06) though by 48 h no effect was found. Tamoxifen treatment did not significantly affect liver weight at 24 h but by 48 h there was a highly significant reduction in liver remnant weight (TAM, 5.41 ± 0.85 g; vehicle, 7.31 ± 1.43 g; \u003Cjats:italic>P\u003C\u002Fjats:italic> < 0.001). Neither DES nor TAM treatment influenced liver regeneration as determined by [\u003Cjats:sup>3\u003C\u002Fjats:sup>H]‐thymidine incorporation into hepatic DNA. We conclude that pharmacologic manipulation of oestrogens does not influence the initiation of the regenerative process but that oestrogen may facilitate later phases of hepatic growth.\u003C\u002Fjats:p>",{"EN":111},"Role of the oestrogen receptor in liver regeneration in the male rat",{"VOID":113},"8280839",{"VOID":115},"10.1111\u002Fj.1440-1746.1993.tb01646.x","PUBLICATION","VERIFIED","Auto Verify",[120],"EN","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1746.1993.tb01646.x",[123,144],{"id":124,"sortIndex":25,"researcher":24,"roles":125,"affiliations":126,"properties":135,"displayName":139,"givenName":24,"familyName":24},"16dc15d4-ffd2-4a85-982f-a65cd1135830",[],[127],{"id":128,"sortIndex":25,"affiliation":129,"properties":24},"9a53b0e6-58cc-4710-8dad-1493e91118df",{"id":128,"createTime":24,"updateTime":24,"relativeEntities":130,"slug":24,"properties":131,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":134,"statistic":24},[],{"title":132},{"EN":133},"Department of Gastroenterology and Hepatology, Westmead Hospital, University of Sydney, New South Wales, Australia.",[],{"orcid":136,"title":138,"gsAuthor":140,"openalex":142},{"VOID":137},"https:\u002F\u002Forcid.org\u002F0000-0003-3936-6790",{"EN":139},"Christopher Liddle",{"VOID":141},"[\"nrK4eD0AAAAJ\"]",{"VOID":143},"A5049828619",{"id":145,"sortIndex":146,"researcher":24,"roles":147,"affiliations":148,"properties":157,"displayName":159,"givenName":24,"familyName":24},"a1957f45-3a5b-484f-b15c-b8f4e75ba5d0",1,[],[149],{"id":150,"sortIndex":25,"affiliation":151,"properties":24},"1de7dd16-7c9c-4851-b905-6f5113887990",{"id":150,"createTime":24,"updateTime":24,"relativeEntities":152,"slug":24,"properties":153,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":156,"statistic":24},[],{"title":154},{"EN":155},"Department of Gastroenterology and Hepatology, Westmead Hospital, University of Sydney, Westmead, New South Wales, Australia",[],{"title":158,"openalex":160},{"EN":159},"Geoffrey C. 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Invest., 42, 225",{},false,{"id":310,"createTime":311,"updateTime":312,"relativeEntities":313,"slug":314,"properties":315,"entityType":116,"verifyStatus":117,"verifyTime":311,"verifyNote":118,"languages":330,"translateLanguages":24,"viewCount":25,"primaryUrl":331,"fullTextUrl":24,"authors":332,"publicationType":162,"publisherRelationship":433,"citationCount":25,"citationInfo":482,"publishDate":485,"publishYear":483,"citationAnalyzeStatus":23,"lastCitationAnalyze":486,"indexDatabases":487,"openAccess":24,"references":488,"isForceReanalyzing":308},"cc729d84-b7ec-4551-802f-b0dbca0aab7d","2024-07-18T14:51:24.543+00:00","2026-03-29T11:17:43.987+00:00",[],"Thermal-ablative-therapy-for-malignant-liver-tumors-A-critical-appraisal",{"mag":316,"gsPaper":318,"openalex":320,"abstract":322,"title":324,"pm":326,"doi":328},{"VOID":317},"1963539242",{"VOID":319},"[\"12638831593776786759\"]",{"VOID":321},"W1963539242",{"EN":323},"\u003Cjats:p>\u003Cjats:bold>Abstract \u003C\u002Fjats:bold> The management of primary and secondary malignant liver tumors poses a great challenge to clinicians. Although surgical resection is the gold‐standard treatment, most patients have unresectable malignant liver tumors. Over the past decade, various modalities of loco‐regional therapy have gained much interest. Among them, thermal ablative therapy, including cryotherapy, microwave coagulation, interstitial laser therapy, and radiofrequency ablation (RFA), have been proven to be safe and effective. Despite the effective tumor eradication achieved within cryotherapy, the underlying freeze\u002Fthaw mechanism has resulted in serious complications that include bleeding from liver cracking and the ‘cryoshock’ phenomenon. Thermal ablation using microwave and laser therapy for malignant liver tumors is curative and is associated with minimal complications. However, this treatment modality is effective only for tumors <3 cm diameter. Radiofrequency ablation seems to be the most promising form of thermal ablative therapy in terms of a lower complication rate and a larger volume of ablation. However, its use is restricted by the difficulty encountered when using imaging studies to monitor the areas of ablation during and after the procedure. Moreover, the techniques of RFA need to be refined in order to achieve the same oncological radicality of malignant liver tumors as achieved by surgical resection. As each of the loco‐regional therapies has its own advantages and limitations, a multidisciplinary approach using a combination of therapies will be the future trend for the management of malignant liver tumors.\u003C\u002Fjats:p>",{"EN":325},"Thermal ablative therapy for malignant liver tumors: A critical appraisal",{"VOID":327},"12753142",{"VOID":329},"10.1046\u002Fj.1440-1746.2003.02991.x",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1046\u002Fj.1440-1746.2003.02991.x",[333,352,368,383,401,417],{"id":334,"sortIndex":25,"researcher":24,"roles":335,"affiliations":336,"properties":345,"displayName":347,"givenName":24,"familyName":24},"03e63a63-31b2-4dec-a8c1-4b5c0750699e",[],[337],{"id":338,"sortIndex":25,"affiliation":339,"properties":24},"544e56f7-f397-4dbe-9892-e8b7b0cf3301",{"id":338,"createTime":24,"updateTime":24,"relativeEntities":340,"slug":24,"properties":341,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":344,"statistic":24},[],{"title":342},{"VI":343},"Departments of Surgery and, ",[],{"title":346,"gsAuthor":348,"openalex":350},{"EN":347},"Kelvin K. 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R., 1989, Yeast Genetic Engineering, 83",{},{"id":24,"text":1395,"url":24,"identifiers":1396},"10.1016\u002F0140-6736(90)91585-X",{"doi":1395},{"id":24,"text":1398,"url":24,"identifiers":1399},"10.1073\u002Fpnas.87.17.6547",{"doi":1398},{"id":24,"text":1401,"url":24,"identifiers":1402},"Di Bisceglie A. M., 1991, Am. J. Gastroenterol., 86, 335",{},{"id":24,"text":1404,"url":24,"identifiers":1405},"10.1073\u002Fpnas.88.12.5462",{"doi":1404},{"id":24,"text":1386,"url":24,"identifiers":1407},{"doi":1386},{"id":24,"text":1409,"url":24,"identifiers":1410},"10.1016\u002F0140-6736(91)90006-B",{"doi":1409},{"id":24,"text":1412,"url":24,"identifiers":1413},"10.1002\u002F1097-0142(19910115)67:2\u003C429::AID-CNCR2820670218>3.0.CO;2-#",{"doi":1412},{"id":24,"text":1415,"url":24,"identifiers":1416},"10.1073\u002Fpnas.88.9.3647",{"doi":1415},{"id":24,"text":1418,"url":24,"identifiers":1419},"10.1073\u002Fpnas.82.1.178",{"doi":1418},{"id":24,"text":1421,"url":24,"identifiers":1422},"EvansC. S. ToblerL. PolitoA.et al.Transfusion1992(in press).",{},{"id":24,"text":1424,"url":24,"identifiers":1425},"10.1016\u002FS0140-6736(89)91016-7",{"doi":1424},{"id":1427,"createTime":1428,"updateTime":1428,"relativeEntities":1429,"slug":1430,"properties":1431,"entityType":116,"verifyStatus":117,"verifyTime":1444,"verifyNote":118,"languages":1445,"translateLanguages":24,"viewCount":25,"primaryUrl":1446,"fullTextUrl":24,"authors":1447,"publicationType":162,"publisherRelationship":1467,"citationCount":1515,"citationInfo":1516,"publishDate":1519,"publishYear":1517,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1520,"openAccess":24,"references":1521,"isForceReanalyzing":308},"22575a78-f78c-4186-b182-7b1b0ec27556","2025-02-08T12:26:34.972+00:00",[],"Central-role-of-mitochondria-in-metabolic-regulation-of-liver-pathophysiology",{"openalex":1432,"mag":1434,"abstract":1436,"title":1438,"pm":1440,"doi":1442},{"VOID":1433},"W2086856432",{"VOID":1435},"2086856432",{"EN":1437},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Mitochondria play a central role in cellular energy metabolism. Oxidative phosphorylation occurs in the electron transport system of the inner mitochondrial membrane. Cytochrome aa3, b and c1 are encoded by mitochondrial DNA whereas cytochrome c is encoded by the nuclear gene, and these mitochondrial‐DNA dependent cytochromes are decreased and electron transport at complex II, III and IV is disturbed in liver carcinomas and during carcinogenesis. The more the decreased cytochrome and oxidase activity are seen, the more significant is the increase in reactive oxygen species (ROS) production. ROS produced in mitochondria may be the main cause of nuclear‐gene mutation in carcinogenesis. The mitochondrial dysfunction and overproduction of ROS plays a key role in progression of chronic hepatitis C and ethanol‐induced liver injury. Ethanol also causes bacterial translocation in the intestine and the resulting lipopolysaccharides (LPS) activates Kupffer cells to produce pro‐inflammatory cytokines. We suspect that non‐alcoholic steatohepatitis (NASH) also is the result of increased ROS production in Kupffer cells and hepatocytes.\u003C\u002Fjats:p>",{"EN":1439},"Central role of mitochondria in metabolic regulation of liver pathophysiology",{"VOID":1441},"17567455",{"VOID":1443},"10.1111\u002Fj.1440-1746.2007.04963.x","2025-02-08T12:26:34.971+00:00",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1746.2007.04963.x",[1448],{"id":1449,"sortIndex":25,"researcher":24,"roles":1450,"affiliations":1451,"properties":1460,"displayName":1464,"givenName":24,"familyName":24},"f986c5b6-b588-4337-8565-5d5196d4c399",[],[1452],{"id":1453,"sortIndex":25,"affiliation":1454,"properties":24},"6f696525-6a56-4965-8e50-2aeb9fe5a4aa",{"id":1453,"createTime":24,"updateTime":24,"relativeEntities":1455,"slug":24,"properties":1456,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1459,"statistic":24},[],{"title":1457},{"EN":1458},"Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan. 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N, 1970, Spectrophotometric analyses of cytochromes in ascites hepatomas of rats and mice, Cancer Res., 30, 2061",{},{"id":24,"text":1544,"url":24,"identifiers":1545},"10.1016\u002F0005-2728(72)90209-5",{"doi":1544},{"id":24,"text":1547,"url":24,"identifiers":1548},"Hagihara B, 1973, Spectrophotometric analysis of cytochromes in Morris hepatomas, Cancer Res., 33, 2947",{},{"id":24,"text":1550,"url":24,"identifiers":1551},"Oyanagui Y, 1974, Spectrophotometric analysis of cytochromes in rat liver during carcinogenesis, Cancer Res., 34, 458",{},{"id":24,"text":1553,"url":24,"identifiers":1554},"10.1016\u002F0005-2728(76)90208-5",{"doi":1553},{"id":24,"text":1556,"url":24,"identifiers":1557},"10.1016\u002F0003-2697(76)90313-4",{"doi":1556},{"id":24,"text":1559,"url":24,"identifiers":1560},"10.1083\u002Fjcb.58.1.11",{"doi":1559},{"id":24,"text":1562,"url":24,"identifiers":1563},"10.1038\u002F29331",{"doi":1562},{"id":24,"text":1565,"url":24,"identifiers":1566},"10.1016\u002F0009-8981(77)90031-6",{"doi":1565},{"id":24,"text":1568,"url":24,"identifiers":1569},"10.1016\u002F0005-2728(81)90122-5",{"doi":1568},{"id":24,"text":1571,"url":24,"identifiers":1572},"Moriya K, 2001, Oxidative stress in the absence of inflammation in a mouse model for hepatitis C virus‐associated hepatocarcinogenesis, Cancer Res., 61, 4365",{},{"id":24,"text":1574,"url":24,"identifiers":1575},"10.1172\u002FJCI114068",{"doi":1574},{"id":24,"text":1577,"url":24,"identifiers":1578},"10.1016\u002F0091-3057(83)90215-0",{"doi":1577},{"id":24,"text":1580,"url":24,"identifiers":1581},"10.1111\u002Fj.1530-0277.1981.tb04926.x",{"doi":1580},{"id":24,"text":1583,"url":24,"identifiers":1584},"10.1016\u002F0006-2952(91)90153-V",{"doi":1583},{"id":24,"text":1586,"url":24,"identifiers":1587},"10.3109\u002F00365529509107756",{"doi":1586},{"id":24,"text":1589,"url":24,"identifiers":1590},"10.1046\u002Fj.1440-1746.2000.02179.x",{"doi":1589},{"id":24,"text":1592,"url":24,"identifiers":1593},"Watanabe T, 2005, Metabolic syndrome from the view point of public health: With special reference to nonalcoholic fatty liver disease, Nippon Koshu Eisei Zasshi, 52, 934",{},{"id":24,"text":1595,"url":24,"identifiers":1596},"10.1007\u002F978-1-4684-5188-7_59",{"doi":1595},{"id":24,"text":1598,"url":24,"identifiers":1599},"10.1016\u002FS0047-6374(02)00093-3",{"doi":1598},{"id":1601,"createTime":1602,"updateTime":1602,"relativeEntities":1603,"slug":1604,"properties":1605,"entityType":116,"verifyStatus":117,"verifyTime":1602,"verifyNote":118,"languages":1618,"translateLanguages":24,"viewCount":25,"primaryUrl":1619,"fullTextUrl":24,"authors":1620,"publicationType":162,"publisherRelationship":1753,"citationCount":1803,"citationInfo":1804,"publishDate":1807,"publishYear":1805,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1808,"openAccess":24,"references":1809,"isForceReanalyzing":308},"fee6efa6-f821-41f6-8ef1-b54d5559a6cd","2025-01-03T00:42:04.440+00:00",[],"Top-cited-articles-in-digestive-system-disease-from-1950-to-2013",{"openalex":1606,"mag":1608,"abstract":1610,"title":1612,"pm":1614,"doi":1616},{"VOID":1607},"W2133287535",{"VOID":1609},"2133287535",{"EN":1611},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\u003Cjats:title>Background and Aim\u003C\u002Fjats:title>\u003Cjats:p>Examination of top‐cited articles is a tool that can help to identify and monitor outstanding scientific researches and landmark papers. We aimed to identify the 100 most cited published papers in peer‐reviewed biomedical journals in the field of digestive diseases and to examine their characteristics.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Methods\u003C\u002Fjats:title>\u003Cjats:p>The Web of Science (including Science Citation Index) was searched for the most cited papers related to digestive diseases, published from 1955 to the present. The top 100 most cited articles were identified. The number of citations, countries, and institutions of origin, year of publication, study design, topic, and levels of evidence of the articles were noted and analyzed.\u003C\u002Fjats:p>\u003C\u002Fjats:sec>\u003Cjats:sec>\u003Cjats:title>Results\u003C\u002Fjats:title>\u003Cjats:p>The most top‐cited articles had a mean of 1375 citations. These articles were published between 1978 and 2009 in 29 high‐impact journals, with the \u003Cjats:italic>New England Journal of Medicine\u003C\u002Fjats:italic> (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 22) topping the list. Of the 100 articles, 34 were clinical studies, 15 were review articles, and 34 were concerned basic science. These articles came from 18 countries, with the USA contributing most of the top‐cited articles (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 53). Eighty‐seven institutions produced these 100 top‐cited articles, led by the University of Barcelona (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 4). Seven persons authored two or more of these top‐cited articles. 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The mRNA levels reached their maximum 1 – 3 h after operation and exceeded the values for intact animals about tenfold. Lipopolysaccharide stimulation induced an increase in TNF‐α and TNF receptor production comparable with that occurring during regeneration.\u003C\u002Fjats:p>\u003Cjats:p>Nitric oxide (NO) production in the regenerating liver was determined by electron paramagnetic resonance (EPR) spectroscopy. The first increase in NO production occurred approximately 1 h after partial hepatectomy (PHE). The second and more pronounced peak of NO production was observed about 6 h after PHE when the hepatocytes entered the first cell cycle; it originated mainly from these cells. The consequent minimum of NO synthesis coincided with the maximal rate of DNA synthesis. The third gradual rise of NO production was seen at the transit from the first to the second cell cycle of the hepatocytes and the entrance of the non‐parenchymal cells into proliferation.\u003C\u002Fjats:p>\u003Cjats:p>Hepatocytes, Kupffer and endothelial cells were isolated from livers after PHE. They were found to start their main NO production in the described sequence at the times corresponding to their respective entrance into the cell cycle. The maxima of NO synthesis were inversely correlated to the DNA‐synthesizing activity of the individual cell type.\u003C\u002Fjats:p>",{"EN":2055},"Cytokines, nitric oxide synthesis and liver regeneration",{"VOID":2057},"8589334",{"VOID":2059},"10.1111\u002Fj.1440-1746.1995.tb01789.x","2024-12-27T09:06:17.037+00:00",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1746.1995.tb01789.x",[2064,2081],{"id":2065,"sortIndex":25,"researcher":24,"roles":2066,"affiliations":2067,"properties":2076,"displayName":2078,"givenName":24,"familyName":24},"f8994341-9543-468a-91c6-513577d08adf",[],[2068],{"id":2069,"sortIndex":25,"affiliation":2070,"properties":24},"74372d12-16f4-4566-9444-8943c21cbf51",{"id":2069,"createTime":24,"updateTime":24,"relativeEntities":2071,"slug":24,"properties":2072,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2075,"statistic":24},[],{"title":2073},{"EN":2074},"Biochemical Institute, Albert‐Ludwigs University, Freiburg, Germany",[],{"title":2077,"openalex":2079},{"EN":2078},"K. 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Invest., 60, 4",{},{"id":24,"text":2156,"url":24,"identifiers":2157},"Obolenskaya M Yu, 1987, Intracellular distribution of newly formed RNA in hepatocytes during the first hours after partial hepatectomy, Zitologija i Genetika, 21, 377",{},{"id":24,"text":2159,"url":24,"identifiers":2160},"10.1111\u002Fj.1432-1033.1990.tb19222.x",{"doi":2159},{"id":24,"text":2162,"url":24,"identifiers":2163},"10.1111\u002Fj.1432-1033.1991.tb16337.x",{"doi":2162},{"id":24,"text":2165,"url":24,"identifiers":2166},"Moncada S, 1991, Nitric oxide: Physiology, pathophysiology, and pharmacology, Pharmacol. Rev., 43, 109",{},{"id":24,"text":2168,"url":24,"identifiers":2169},"Krönke M, 1992, Tumor Necrosis Factor, 189",{},{"id":24,"text":2171,"url":24,"identifiers":2172},"10.1084\u002Fjem.170.5.1769",{"doi":2171},{"id":24,"text":2174,"url":24,"identifiers":2175},"10.1159\u002F000163663",{"doi":2174},{"id":24,"text":2177,"url":24,"identifiers":2178},"10.1002\u002Fjlb.55.4.507",{"doi":2177},{"id":24,"text":2180,"url":24,"identifiers":2181},"Helyar L, 1993, Cells of the Hepatic Sinusoid, 67",{},{"id":24,"text":2183,"url":24,"identifiers":2184},"10.1016\u002F0014-4800(85)90021-8",{"doi":2183},{"id":24,"text":2186,"url":24,"identifiers":2187},"10.1016\u002FS0168-8278(88)80459-8",{"doi":2186},{"id":24,"text":2189,"url":24,"identifiers":2190},"Duijvestijn AM, 1992, Antibodies defining rat endothelial cells: RECA‐1, a pan‐endothelial cell‐specific monoclonal antibody, Lab. Invest., 66, 459",{},{"id":24,"text":2192,"url":24,"identifiers":2193},"Schlayet HJ, 1988, Beta‐glucuronidase staining discriminates rat liver sinusoidal endothelial cells from Kupffer cells in primary culture, Virchow's Arch. Abt. B Zellpath., 55, 225, 10.1007\u002FBF02896579",{"doi":2194},"10.1007\u002FBF02896579",{"id":24,"text":2196,"url":24,"identifiers":2197},"10.1006\u002Fbbrc.1994.1966",{"doi":2196},{"id":24,"text":2199,"url":24,"identifiers":2200},"10.1016\u002F0022-1759(84)90147-9",{"doi":2199},{"id":24,"text":2202,"url":24,"identifiers":2203},"Chomczynski P, 1987, Single‐step method of RNA isolation by acid guanidinium‐thiocyanate‐phenol‐chloroform extraction, Anal. Biochem., 62, 156, 10.1016\u002F0003-2697(87)90021-2",{"doi":2204},"10.1016\u002F0003-2697(87)90021-2",{"id":24,"text":2206,"url":24,"identifiers":2207},"10.1515\u002Fbchm3.1992.373.1.271",{"doi":2206},{"id":24,"text":2209,"url":24,"identifiers":2210},"10.1016\u002FS0168-8278(05)80656-7",{"doi":2209},{"id":24,"text":2212,"url":24,"identifiers":2213},"Widmann JJ, 1976, Proliferation of endothelial cells in estrogen‐stimulated rat liver, Lab. Invest., 34, 141",{},{"id":24,"text":2215,"url":24,"identifiers":2216},"Lepoivre M, 1989, Antiproliferative activity of gamma‐interferon combined with lipopoly saccharide on murine adenocarcinoma: Dependence on an L‐arginine metabolism with production of nitrite and citrulline, Cancer Res., 49, 1970",{},{"id":24,"text":2218,"url":24,"identifiers":2219},"Guilbert LJ, Analysis of the synergistic stimulation of mouse macrophage proliferation by macrophage colony‐stimulating factor (CSF‐1) and tumor necrosis factor α (TNF‐α), J. Leukocyte Biol., 54, 65, 10.1002\u002Fjlb.54.1.65",{"doi":2220},"10.1002\u002Fjlb.54.1.65",{"id":24,"text":2222,"url":24,"identifiers":2223},"10.1042\u002Fbj1640033",{"doi":2222},{"id":24,"text":2225,"url":24,"identifiers":2226},"10.1038\u002F251352a0",{"doi":2225},{"id":24,"text":2228,"url":24,"identifiers":2229},"10.1016\u002F0014-5793(94)80128-2",{"doi":2228},{"id":24,"text":2231,"url":24,"identifiers":2232},"10.1128\u002FMCB.12.6.2898",{"doi":2231},{"id":24,"text":2234,"url":24,"identifiers":2235},"10.1089\u002Fdna.1990.9.705",{"doi":2234},{"id":24,"text":2237,"url":24,"identifiers":2238},"10.1073\u002Fpnas.88.20.9292",{"doi":2237},{"id":24,"text":2240,"url":24,"identifiers":2241},"10.1007\u002FBF01978612",{"doi":2240},{"id":24,"text":2243,"url":24,"identifiers":2244},"Obolenskaya M Yu, 1989, Partial restriction of genome expression is one of the compounds of mammalian liver regeneration, Biopolimeru i kletka, 5, 79",{},{"id":24,"text":2246,"url":24,"identifiers":2247},"10.1146\u002Fannurev.bi.51.070182.001343",{"doi":2246},{"id":24,"text":2249,"url":24,"identifiers":2250},"10.3109\u002F08977198908997998",{"doi":2249},{"id":2252,"createTime":2253,"updateTime":2253,"relativeEntities":2254,"slug":2255,"properties":2256,"entityType":116,"verifyStatus":117,"verifyTime":2253,"verifyNote":118,"languages":2269,"translateLanguages":24,"viewCount":25,"primaryUrl":2270,"fullTextUrl":24,"authors":2271,"publicationType":162,"publisherRelationship":2357,"citationCount":1991,"citationInfo":2407,"publishDate":2410,"publishYear":2408,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2411,"openAccess":24,"references":2412,"isForceReanalyzing":308},"ecc1b723-6758-4684-a217-c5b4d4439c2e","2024-12-27T00:10:18.070+00:00",[],"Ganciclovir-and-the-treatment-of-Epstein-Barr-virus-hepatitis",{"openalex":2257,"mag":2259,"abstract":2261,"title":2263,"pm":2265,"doi":2267},{"VOID":2258},"W2055867750",{"VOID":2260},"2055867750",{"EN":2262},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Epstein‐Barr virus (EBV) is part of the herpesvirus family that infects up to 90% of the population. Initial infection is often subclincal in children but will generally result in symptomatic infectious mononucleosis in adolescents and adults. Ganciclovir has been utilized in immunocompromised patients with EBV encephalitis and post‐liver transplant for EBV fulminant hepatitis. Herein, the successful use of ganciclovir in two immunocompetent patients with severe EBV hepatitis is reported.\u003C\u002Fjats:p>",{"EN":2264},"Ganciclovir and the treatment of Epstein‐Barr virus hepatitis",{"VOID":2266},"16984606",{"VOID":2268},"10.1111\u002Fj.1440-1746.2006.03257.x",[120],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1746.2006.03257.x",[2272,2291,2308,2325,2340],{"id":2273,"sortIndex":25,"researcher":24,"roles":2274,"affiliations":2275,"properties":2284,"displayName":2288,"givenName":24,"familyName":24},"52320ab8-0b52-4d39-bd49-4edffb99ba8b",[],[2276],{"id":2277,"sortIndex":25,"affiliation":2278,"properties":24},"5f374bf0-b571-46be-9478-e1d49582cfaf",{"id":2277,"createTime":24,"updateTime":24,"relativeEntities":2279,"slug":24,"properties":2280,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2283,"statistic":24},[],{"title":2281},{"EN":2282},"Department of Gastroenterology and Hepatology, Sir Charles Gardiner Hospital,",[],{"orcid":2285,"title":2287,"openalex":2289},{"VOID":2286},"https:\u002F\u002Forcid.org\u002F0000-0002-3968-7909",{"EN":2288},"Leon A. 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Chem., 26, 243, 10.1093\u002Fclinchem\u002F26.2.243",{"doi":2419},"10.1093\u002Fclinchem\u002F26.2.243",{"id":24,"text":2421,"url":24,"identifiers":2422},"10.1111\u002Fj.1600-0676.1994.tb00001.x",{"doi":2421},{"id":24,"text":2424,"url":24,"identifiers":2425},"10.1111\u002Fj.1440-1746.1998.tb00739.x",{"doi":2424},{"id":24,"text":2427,"url":24,"identifiers":2428},"10.1016\u002F0016-5085(87)90246-0",{"doi":2427},{"id":24,"text":2430,"url":24,"identifiers":2431},"Chang WY, 1975, Fatal infectious mononucleosis. Association with liver necrosis and herpes‐like virus particles, Arch. Pathol., 99, 185",{},{"id":24,"text":2433,"url":24,"identifiers":2434},"10.1053\u002Fhupa.2001.25597",{"doi":2433},{"id":24,"text":2436,"url":24,"identifiers":2437},"10.1309\u002FB3WH-QWBY-YV61-CE46",{"doi":2436},{"id":24,"text":2439,"url":24,"identifiers":2440},"Pelletier LL, 1976, Disseminated intravascular coagulation and hepatic necrosis: complications of infectious mononucleosis, JAMA, 235, 1144, 10.1001\u002Fjama.1976.03260370052037",{"doi":2441},"10.1001\u002Fjama.1976.03260370052037",{"id":24,"text":2443,"url":24,"identifiers":2444},"10.1002\u002Flt.500040612",{"doi":2443},{"id":24,"text":2446,"url":24,"identifiers":2447},"10.1016\u002F0046-8177(93)90195-M",{"doi":2446},{"id":24,"text":2449,"url":24,"identifiers":2450},"10.1093\u002Finfdis\u002F164.4.788",{"doi":2449},{"id":24,"text":2452,"url":24,"identifiers":2453},"10.5694\u002Fj.1326-5377.1984.tb132717.x",{"doi":2452},{"id":24,"text":2455,"url":24,"identifiers":2456},"10.1093\u002Fndt\u002F16.1.197",{"doi":2455},{"id":2458,"createTime":2459,"updateTime":2459,"relativeEntities":2460,"slug":2461,"properties":2462,"entityType":116,"verifyStatus":117,"verifyTime":2459,"verifyNote":118,"languages":2475,"translateLanguages":24,"viewCount":25,"primaryUrl":2476,"fullTextUrl":24,"authors":2477,"publicationType":162,"publisherRelationship":2514,"citationCount":2564,"citationInfo":2565,"publishDate":2568,"publishYear":2566,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2569,"openAccess":24,"references":2570,"isForceReanalyzing":308},"ac15120b-8dc2-4afa-9daa-64fb6434167f","2024-12-10T10:43:22.462+00:00",[],"Retinoic-acids-and-hepatic-stellate-cells-in-liver-disease",{"openalex":2463,"mag":2465,"abstract":2467,"title":2469,"pm":2471,"doi":2473},{"VOID":2464},"W1903133626",{"VOID":2466},"1903133626",{"EN":2468},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Quiescent hepatic stellate cells (HSCs) in healthy liver store 80% of total liver retinols and release them depending on the extracellular retinol status. However, HSCs activated by liver injury lose their retinols and produce a considerable amount of extracellular matrix, subsequently leading to liver fibrosis. Emerging evidence suggests that retinols and their metabolites such as retinoic acids (RAs) contribute to liver regeneration, fibrosis and tumor. However, it is not clear yet why HSCs lose retinol, which enzymes are involved in the retinol metabolism of HSCs and what function of retinol metabolites on HSCs upon liver injury. Recently, our group and collaborators have demonstrated that during activation, HSCs not only lose retinols but also metabolize them into RAs by alcohol dehydrogenases and retinaldehyde dehydrogenases. As transcriptional factors, metabolized RAs induce retinoic acid early inducible‐1 and suppressor of cytokine signaling 1 in HSCs, which plays an important role in the interaction between HSCs and natural killer cells. In addition, RAs released from HSCs may induce hepatic cannabinoid receptor 1 expression in alcoholic liver steatosis or regulate immune responses upon liver inflammation. The present review summarizes the role of endogenous metabolized RAs on HSCs themselves and on other liver cells including hepatocytes and immune cells. 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