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The modular microarchitecture of human liver
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Teutsch HF. The modular microarchitecture of human liver. Hepatology 2005; 42:317-325. This elaborate alternative study of liver microanatomy discloses an organization into polyhedral primary modules with seven to nine facets that correlate most closely with classical lobules. The human primary module is more complex than that of the pig. The paper contains numerous images of the alkaline phosphatase-stained modular construct.
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Hepatology
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Teutsch, H.F.1
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How molecular microscopy revealed new insights into the dynamics of hepatic endothelial fenestrae in the past decade
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Braet F. How molecular microscopy revealed new insights into the dynamics of hepatic endothelial fenestrae in the past decade. Liver Int 2004; 24:532-539. An intriguing ultrastructural and conceptual journey into the formation and perturbation of endothelial fenestrae, including cycloheximide dry-cleavage imaging of fenestrae forming centers and their variations.
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Lemasters JJ. Dying a thousand deaths: redundant pathways from different organelles to apoptosis and necrosis. Gastroenterology 2005; 129:351-360. Among the many discussion points differentiating necrotic from apoptotic cell death is a review of various stress factors which lead to cytochrome c release from mitochondria and caspase 3 activation. An excellent summary diagram of apoptosis incorporates multi-organelle roles in this process.
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Lemasters, J.J.1
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Asano K, Tada S, Matsumoto T, et al. A novel bacterium Achromobacter xylosoxidans as a cause of liver abscess: three case reports. J Hepatol 2005; 43:362-365. Three cases of unusual post-cholecystectomy abscesses were presumably acquired via the biliary tree. This uncommon Gram-negative bacillus has also been isolated in urine, sputum, blood, cerebrospinal fluid, otopyrrhea and bile. The granulomatous nature of the histopathologic response, with central necrosis and a coral-like gross and computed tomography scan appearance are important diagnostic features.
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Asano, K.1
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Greenough TC, Carville A, Coderre J, et al. Pneumonitis and multi-organ system disease in common marmosets (Callithrix jacchus) infected with the severe acute respiratory syndrome-associated coronavirus. Am J Pathol 2005; 167:455-463. The progression of hepatic histological lesions from 2 to 7 days in marmosets inoculated with severe acute respiratory syndrome coronavirus (SARS-CoV) showed sinusoidal mononuclear cells, multifocal hepatitis and central venulitis in four of 11 animals with hepatic involvement.
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Ding X, Xu F, Chen H, Tesh RB, Xiao S-Y. Apoptosis of hepatocytes caused by Punta Toro virus (Bunyaviridae: Phlebovirus) and its implication for phlebovirus pathogenesis. Am J Pathol 2005; 167:1043-1049.
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Craig CE, Quaglia A, Dhillon AP. Extramedullary haematopoiesis in massive hepatic necrosis. Histopathology 2004; 45:518-525.
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Moradpour D, Blum HE. A primer on the molecular virology of hepatitis C. Liver Int 2004; 24:519-525. This paper discusses the organization of the HCV genome and its encoded constituent structural and nonstructural protein products. A conceptual diagram of the intracellular life cycle of HCV is provided.
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Shiha GE, Zalata KR, Abdalla AF, Mohamed MK. Immunohistochemical identification of HCV target antigen in paraffin-embedded liver tissue: reproducibility and staining patterns. Liver Int 2005; 25:254-260.
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Otani K, Korenaga M, Beard MR, et al. Hepatitis C virus core protein, cytochrome P450 2E1, and alcohol produce combined mitochondrial injury and cytotoxicity in hepatoma cells. Gastroenterology 2005; 128:96-107.
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Otani, K.1
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Wheeler M. Ethanol and HCV-induced cytotoxicity: the perfect storm. Gastroenterology 2005; 128:232-234.
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Clouston AD, Powell EE, Walsh MJ, et al. Fibrosis correlates with a ductular reaction in hepatitis C: roles of impaired replication, progenitor cells and steatosis. Hepatology 2005; 41:809-818. Hepatocyte regeneration in chronic hepatitis C is impaired (based on decreased expression of p21) and in combination with increased body mass index and steatosis results in stimuli provoking the ductular reaction, which in turn triggers fibrogenesis. The presence of a fine ductular reaction in chronic hepatitis C in Stage 0 patients implies that it precedes the development of fibrosis. The study did not entirely exclude the possibility that certain stimuli may co-promote both the ductular reaction and fibrosis.
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Clouston, A.D.1
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Schulze-Krebs, A.1
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1/S such as increased sensitivity to apoptosis, limitation of response to toxic injury by alcohol, steatosis or viral infection, and possible predilection for hepatocellular carcinoma.
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Lackner, C.1
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Ghany MG, Doo E. Assessment of liver fibrosis: palpate, poke or pulse? Hepatology 2005; 42:759-761. The potential uses of elastography in liver disease other than chronic hepatitis C (e.g. NAFLD) are discussed, as are the drawbacks of current data.
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Rousselet M-C, Michalak S, Dupré F, et al. Sources of variability in histological scoring of chronic viral hepatitis. Hepatology 2005; 41:257-264. In the course of comparative scoring of chronic hepatitis C biopsies among different centers and pathologists of differing experience, specific histologic lesions which presented as problematic were seen as: the heterogeneous space distribution of lobular activity; an uncertain distinction between no portal fibrosis and mild portal fibrosis; true bridging fibrosis compared to normal portal tract extension; and incompletely represented septum located in the specimen periphery.
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Rousselet, M.-C.1
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Almasio PL, Niero M, Angioli D, et al. Experts' opinions on the role of liver biopsy in HCV infection: a Delphi survey by the Italian Association of Hospital Gastroenterologists (A.I.G.O.). J Hepatol 2005; 43:381-387. This intriguing study demonstrates differing viewpoints on the current clinical role of liver biopsy in managing patients with chronic hepatitis C. The authors urge that cost-benefit analysis be undertaken to address the added value of liver biopsy data to the clinical diagnosis and outcome of antiviral therapy. Since physicians manage similar patients with HCV infection very differently, determining the evidence-based value of liver biopsy data should help reduce these differences.
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J Hepatol
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Almasio, P.L.1
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Herrine SK, Friedman LS. Divining the role of liver biopsy in hepatitis C. J Hepatol 2005; 43:374-376. The authors of this editorial discuss the limitations of a survey of brief clinical scenarios of patients with chronic hepatitis C in comparison to real-life decision-making, and features that were not addressed such as the role biopsy may play in advising against antiviral therapy as well as the perceived risk, low reimbursement and logistical difficulties (reasons not to biopsy, based on a US survey cited from 2002).
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Stickel F, Patsenker E, Schuppan D. Herbal hepatotoxicity. J Hepatol 2005; 43:901-910. A thorough review of several common herbal agents (Chinese herbs, pyrrolizidine alkaloids, Germander, Greater Celandine, Kava and Chaparral) and specific hepatotoxic lesions.
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Herkel J, Schuchmann M, Tiegs G, Lohse AW. Immune-mediated liver injury. J Hepatol 2005; 42:920-923. This short review examines the basic CD8 targeting of cells with viral antigens in viral hepatitis, soluble liver antigen/liver-pancreas molecules in autoimmune hepatitis, concanavalin-A standing in as a possible model of idiosyncratic drug injury and immunologic cytoprotective factors such as interleukin-6-triggered amyloid A and chemokine KC, adiponectin, heme oxygenase-1, adenosine receptor antagonists and silencer of cytokine signalling-1 (SOCS-1).
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Herkel, J.1
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Of mice and women: Toward a mouse model of autoimmune hepatitis
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Heneghan MA, McFarlane IG. Of mice and women: toward a mouse model of autoimmune hepatitis. Hepatology 2005; 42:17-20. This outstanding overview includes discussion of the several types of autoimmune hepatitis, the detectable autoantibodies (and the occasional presence in chronic hepatitis C of anti-liver-kidney microsomal-1 and anti-liver cytosol-1 autoantibodies) and an excellent figure summarizing the immune cells and cytokines involved in autoimmune hepatitis.
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Heneghan, M.A.1
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Kaplan MM, Gershwin ME. Primary biliary cirrhosis. N Engl J Med 2005; 353:1261-1273. A review of the clinical and pathological findings and chief hypothesis on the disease pathogenesis.
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Medina J, Sanz-Cameno P, García-Buey L, et al. Evidence of angiogenesis in primary biliary cirrhosis: an immunohistochemical descriptive study. J Hepatol 2005; 42:124-131.
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Lykavieris P, Chardot C, Sokhn M, et al. Outcome in adulthood of biliary atresia: a study of 63 patients who survived for over 20 years with their native liver. Hepatology 2005; 41:366-371. Of 271 patients who underwent Kasai procedure for biliary atresia between 1968 and 1983, 63 survived for 20 years or more. Serum bilirubin was normal in 21 patients and 12 also had normal aspartate and alanine aminotransferases. Ultimately, fewer than 18% of those with Kasai survived without liver transplant, but required care for conditions such as bacterial cholangitis and complications of cirrhosis.
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Hepatology
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Sokol RJ, Mack CL. Optimizing outcomes and bridging biliary atresia into adulthood. Hepatology 2005; 41:231-233. An editorial comparing a French study showing 23% survivors of biliary atresia surgery with the better Japanese experience describes briefly the presentation of biliary atresia and the factors which appear to lead to improved long-term survival.
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Hepatology
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Balistreri WF, Bezerra JA, Jansen P, et al. Intrahepatic cholestasis: summary of an American Association for the Study of Liver Diseases Single-Topic Conference. Hepatology 2005; 42:222-235. Experts discuss the molecular and develomental aspects of intrahepatic cholestasis. A detailed and useful table presents the gene defects and the disorders with which they are associated.
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Hepatology
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Balistreri, W.F.1
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••] showed a predilection for portal fibrosis without prominent inflammation, ballooning and Mallory bodies as an important differentiating feature from adults, as well as a predilection for periportal (zone 1) fat. By multiple logistic regression, five features were independently associated with adult NASH; steatosis, liver-cell ballooning, lobular inflammation, fibrosis and absence of lipogranulomas.
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Powell EE, Jonsson JR, Clouston AD. Steatosis: co-factor in other liver diseases. Hepatology 2005; 42:5-13. The contribution of steatosis to liver disease, fibrosis and cirrhosis are examined in the context of HCV infection, alcoholic injury, oxidative stress, hepatic stellate cell activation, the ductular reaction and fibrogenesis; the possibility is mentioned of developing hepatocellular carcinoma because of age-related production of reactive oxygen species.
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Alonso EM. Acute liver failure in children: the role of defects in fatty acid oxidation. Hepatology 2005; 41:696-699. This editorial discusses fatty acid oxidation defects as a possible cause of acute liver failure in children, the presentation being a scenario of nonketotic hypoglycemia following a minor febrile illness or fasting and dehydration. The author illustrates with a published heterozygous case with centrilobular necrosis and hemorrhage and microvesicular steatosis in the viable periportal hepatocytes.
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Chinnery PF, DiMauro S. Mitochondrial hepatopathies. J Hepatol 2005; 43:207-209. Some of the problems in diagnosis and presentation of mitochondrial hepatopathies are discussed in this editorial which cites the figure of approximately 1 in 20 000 children under 16 being affected by mitochondrial respiratory chain diseases, with approximately one in five having liver involvement.
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Libbrecht L, Desmet V, Roskams T. Preneoplastic lesions in human hepatocarcinogenesis. Liver Int 2005; 25:16-27. Detailed descriptions of a range of lesions, including small-cell and large-cell dysplasia, low-grade and high-grade dysplastic nodules and foci of altered hepatocytes, are provided with thoughtful analysis of genomic characteristics which designate the true precursors of hepatocellular carcinoma. Helpful gross and microscopic images accompany the text.
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