Purpose of review Aging is a condition in which a person gradually loses the ability to maintain homeostasis, due to structural alteration or dysfunction. Aging is a major risk factor for most chronic diseases. As the liver has a remarkable ability to regenerate, this review assessed the effect of aging on clinical liver disease with references to preclinical models when relevant to pathogenesis. Recent findings Aging has been shown to not only enhance vulnerability to acute liver injury but also increase susceptibility of the fibrotic response. Aging is associated with the severity and poor prognosis of various liver diseases including nonalcoholic fatty liver disease, alcoholic liver disease, hepatitis C, and liver transplantation. Summary Treatment of older patients with liver disease may require different or longer interventions. Transplantation of an older liver will be less tolerant of subsequent injury. Future studies are needed to understand more about the molecular mechanism of aging and contribute to the development of a noble treatment strategy that can block the progression of aging-induced liver diseases.

DILI appears to be a highly relevant health problem in Korea. "Herbal medications" are the principal cause of DILI. A more objective and reproducible causality assessment tool is strongly desired as the RUCAM scale frequently undercounts the cases caused by herbs owing to a lack of previous information and incompatible time criteria.

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The prevalence of HCV infection is low in South Korea. Studies to analyse risk factors are warranted to reduce HCV infection.

Using messenger RNA (mRNA) differential display, we identified a single complementary DNA (cDNA) fragment (HG23T1) that was over-expressed in a hepatocellular carcinoma (HCC) specimen. We cloned the full-length HG23T1 gene by the rapid amplification of cDNA end (RACE) polymerase chain reaction (PCR) method. It perfectly matched the gene encoding human ribosomal protein L36a (RPL36A also referred to as RPL44). RPL36A mRNA was preferentially over-expressed in 34 of 40 HCC cases (85%, P < .001) and in all of 8 HCC cell lines. Ectopically over-expressed L36a ribosomal protein localized in the nucleoli of cells, and this localization seemed to be controlled by the N-terminal or the internal tetrapeptide consensus with its adjacent N-terminal domain. Over-expression of L36a led to enhanced colony formation and cell proliferation, which may have resulted from rapid cell cycling, and an antisense cDNA effectively reversed these alterations. In conclusion, RPL36A plays a role in tumor cell proliferation and may be a potential target for anticancer therapy of HCC. (HEPATOLOGY 2004;39:129 -138.) H epatocellular carcinoma (HCC) is a major malignancy with an increasing incidence worldwide. 1 The major risk factors for development of HCC are cirrhosis, chronic viral hepatitis B and C, exposure to aflatoxin, alcohol, and/or iron overload. HCCs are highly resistant to chemotherapeutic agents and radiotherapy. 2 Despite a variety of treatment options, including surgical resection, chemoembolization, percutaneous injection of ethanol, radiofrequency thermal ablation, and liver transplantation, the prognosis for HCC is poor. [3][4][5] Thus, the need to discover effective therapeutic molecules to suppress the growth of HCC is urgent. One approach is to find target genes and their molecular products and understanding how genetic and molecular changes can lead to cancer development through multistep carcinogenesis.Altered gene expression caused either by mutations or by changes in the regulatory characteristics of HCC compared with corresponding nontumor tissues have been reported. 6 -8 Such alterations can occur in various cell cycle-related oncogenes, such as c-myc, K-ras, and H-ras, and/or in tumor suppressor genes, such as retinoblastoma and p53. 9 -12 In addition, glutamine synthetase, alfa-fetoprotein (AFP), the insulin receptor substrate-1-like gene, cyclin D1, MAGE-1, HIP/PAP, and CD24 have been reported to be over-expressed during hepatocarcinogenesis. [13][14][15][16][17][18][19] However, these genetic changes do not precisely reflect the biologic nature or clinical characteristics of all HCCs. Previously, we identified and reported genes that were differentially expressed in HCC cells using the differential-display polymerase chain reaction (PCR) method. 20 Among them, we focused preferentially on an up-regulated gene in human HCC in comparison with the nontumor surrounding tissues. This gene later proved to encode the ribosomal protein L36a (RPL36A) protein, which is localized in the nucleolus.The biogenesis of eukary...

Polyp size, endoscopist's experience, and right hemi-colon location were identified as potential risk factors for DPPB development.

TE can accurately assess the degree of liver fibrosis in Korean patients with CVH. TE was superior to APRI for predicting each fibrosis stage.

We aimed to investigate whether aging increases the susceptibility of hepatic and renal inflammation or fibrosis in response to high-fat diet (HFD) and explore the underlying genetic alterations. Middle (10 months old) and old (20 months old) aged, male C57BL/6N mice were fed either a low-fat diet (4 % fat) or HFD (60 % fat) for 4 months. Young (3 months old) aged mice were included as control group. HFDinduced liver and kidney injuries were analyzed by serum and urine assay, histologic staining, immunohistochemistry, and reverse-transcription real-time quantitative polymerase chain reaction. Total RNA sequencing with next-generation technology was done with RNA extracted from liver tissues. With HFD feeding, aged was associated with higher serum alanine aminotransferase levels, marked infiltration of hepatic macrophages, and increased expression of inflammatory cytokines (MCP1, TNF-α, IL-1β, IL-6, IL-12, IL-17A). Importantly, aged mice showed more advanced hepatic fibrosis and increased expression of fibrogenic markers (Col-I-α1, αSMA, TGF-β1, TGF-β2, TGFβRII, PDGF, PDGFRβII, TIMP1) in response to HFD. Aged mice fed on HFD also showed increased oxidative stress and TLR4 expression. In the total RNA seq and gene ontology analysis of liver, old-aged HFD group showed significant up-regulation of genes linked to innate immune response, immune response, defense response, inflammatory response compared to middle-aged HFD group. Meanwhile, aging and HFD feeding showed significant increase in glomerular size and mesangial area, higher urine albumin/creatinine ratio, and advanced renal inflammation or fibrosis. However, the difference of HFD-induced renal injury between oldaged group and middle-aged group was not significant. The susceptibility of hepatic fibrosis as well as hepatic inflammation in response to HFD was significantly increased with aging. In addition, aging was associated with glomerular alterations and increased renal inflammation or fibrosis, while the differential effect of aging AGE (2016) 38:291-302