349 research outputs found

    Severe hepatic injury caused by orlistat

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    ArticleAMERICAN JOURNAL OF MEDICINE. 119(8): E7-E7journal articl

    Epidemiology of hepatocellular carcinoma in Japan

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    The original publication is available at www.springerlink.comArticleJOURNAL OF GASTROENTEROLOGY. 44:102-107 (2009)journal articl

    Genetic analysis of the HLA region of Japanese patients with type 1 autoimmune hepatitis

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    ArticleJOURNAL OF HEPATOLOGY. 42(4): 578-584 (2005)journal articl

    Anti-Helicobacter pylori seropositivity: influence on severity and treatment response in patients with chronic hepatitis C

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    The definitive version is available at www.blackwell-synergy.comArticleJOURNAL OF VIRAL HEPATITIS. 14(1): 48-54 (2007)journal articl

    Lack of association between FCRL3 and Fc gamma RII polymorphisms in Japanese type 1 autoimmune hepatitis

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    ArticleCLINICAL IMMUNOLOGY. 122(3): 338-342 (2007)journal articl

    ER stress activates the NLRP3 inflammasome via an UPR-independent pathway

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    Uncontrolled endoplasmic reticulum (ER) stress responses are proposed to contribute to the pathology of chronic inflammatory diseases such as type 2 diabetes or atherosclerosis. However, the connection between ER stress and inflammation remains largely unexplored. Here, we show that ER stress causes activation of the NLRP3 inflammasome, with subsequent release of the pro-inflammatory cytokine interleukin-1β. This ER-triggered proinflammatory signal shares the same requirement for reactive oxygen species production and potassium efflux compared with other known NLRP3 inflammasome activators, but is independent of the classical unfolded protein response (UPR). We thus propose that the NLRP3 inflammasome senses and responds to ER stress downstream of a previously uncharacterized ER stress response signaling pathway distinct from the UPR, thus providing mechanistic insight to the link between ER stress and chronic inflammatory diseases

    Laparoscopic findings in patients with nonalcoholic steatohepatitis

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    ArticleLIVER INTERNATIONAL. 26(1): 32-38 (2006)journal articl

    DOWN-REGULATION OF SREBP-1C IS ASSOCIATED WITH THE DEVELOPMENT OF BURNED-OUT NASH

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    Abstracts of the International Liver Congress™ 2010 – the 45th annual meeting of the European Association for the Study of the Liver (EASL)ArticleJOURNAL OF HEPATOLOGY. 52(Suppl. 1):S373-S374 (2010)conference pape

    Constitutive cytoplasmic localization of p21Waf1/Cip1 affects the apoptotic process in monocytic leukaemia

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    In the present study, we analysed the expression and localization of p21Waf1/Cip1 in normal and malignant haematopoietic cells. We demonstrate that in normal monocytic cells, protein kinase C (PKC)-induced p21 gene activation, which is nuclear factor-κB (NF-κB) independent, results in predominantly cytoplasmic localized p21 protein. In acute monocytic leukaemia (M4, M5), monocytic blasts (N=12) show constitutive cytoplasmic p21 expression in 75% of the cases, while in myeloid leukaemic blasts (N=10), low nuclear and cytoplasmic localization of p21 could be detected, which is also PKC dependent. Constitutive p21 expression in monocytic leukaemia might have important antiapoptotic functions. This is supported by the finding that in U937 cells overexpressing p21, VP16-induced apoptosis is significantly reduced (20.0±0.9 vs 55.8±3.8%, P<0.01, N=5), reflected by a reduced phosphorylation of p38 and JNK. Similarly, AML blasts with high cytoplasmic p21 were less sensitive to VP16-induced apoptosis as compared to AML cases with low or undetectable p21 expression (42.25 vs 12.3%, P<0.01). Moreover, complex formation between p21 and ASK1 could be demonstrated in AML cells, by means of coimmunoprecipitation. In summary, these results indicate that p21 has an antiapoptotic role in monocytic leukaemia, and that p21 expression is regulated in a PKC-dependent and NF-κB independent manner.
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