• Proceedings of the PSK Conference
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• 2003.10b
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• pp.132.1-132.1
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• 2003

Biphenyl dimethyl dicarboxylate (DDB) is a by-product produced in process of synthesizing Schizandrin-C. Generally, DDB has known to protect hepatocytes and to decrease the index of liver enzyme (e.g. GOT and GPT) in chronic hepatitis. The present study was aimed to demonstrate whether DDB can protect the brain cell, especially the Alzheimer brain in vitro. As Alzheimers disease can be induced by activated microglia, a macrophage in the brain, through Abeta peptide (A$\beta$) produced from amyloid precursor protein (APP). (omitted)

• Journal of Life Science
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• v.15 no.1 s.68
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• pp.38-44
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• 2005

Infection with hepatitis B virus (HBV) is a major health problem worldwide. Although a tremendous amount has been known about HBV, there have been obstacles in the study of HBV due to the narrow host range of HBV limited to humans and primates. In the present study, we investigated the susceptibility to HBV infection of mouse hepatoma cell line, Hepa-1c1c7. In addition, based on that human hepatocytes infected by HBV increase the expression of the pro-inflammatory cytokine TNF-a, the inducibility of TNF-a expression by HBV in the cells was determined. HBV surface antigen (HBsAg) secretion was measured by the microparticle enzyme immunoassay and steady state mRNA expression was analyzed by quantitative competitive RT-PCR. Transient transfection of Hepa-1c1c7 cells with HBV expression vector resulted in a dose-dependent induction of TNF-a expression. Infection of Hepa-1c1c7 cells with the serum of HBV carrier also increased TNF-a mRNA expression. Both in the transfected and infected cells, HBV mRNA was expressed and significant HBsAg secretion was detected. There was no significant variation in $\beta-actin$ mRNA expression by HBV. These results demonstrate that HBV is infectious to Hepa-lc1c7 in vitro and the viral infection induces TNF-a expression, which suggests that Hepa-lc1c7, a mouse hepatoma cell line, may be a possible model system for analysis of various molecular aspects of HBV infection.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.20 no.2
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• pp.114-123
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• 2017

Purpose: The goal of this study was the early diagnosis of ABCB11 spectrum liver disorders, especially those focused on benign recurrent intrahepatic cholestasis and progressive familial intrahepatic cholestasis. Methods: Fifty patients presenting neonatal cholestasis were evaluated to identify underlying etiologies. Genetic analysis was performed on patients suspected to have syndromic diseases or ABCB11 spectrum liver disorders. Two families with proven ABCB11 spectrum liver disorders were subjected to genetic analyses to confirm the diagnosis and were provided genetic counseling. Whole exome sequencing and Sanger sequencing were performed on the patients and the family members. Results: Idiopathic or viral hepatitis was diagnosed in 34%, metabolic disease in 20%, total parenteral nutrition induced cholestasis in 16%, extrahepatic biliary atresia in 14%, genetic disease in 10%, neonatal lupus in 2%, congenital syphilis in 2%, and choledochal cyst in 2% of the patients. The patient with progressive familial intrahepatic cholestasis had novel heterozygous mutations of ABCB11 c.11C>G (p.Ser4*) and c.1543A>G (p.Asn515Asp). The patient with benign recurrent intrahepatic cholestasis had homozygous mutations of ABCB11 c.1331T>C (p.Val444Ala) and heterozygous, c.3084A>G (p.Ala1028Ala). Genetic confirmation of ABCB11 spectrum liver disorder led to early liver transplantation in the progressive familial intrahepatic cholestasis patient. In addition, the atypically severe benign recurrent intrahepatic cholestasis patient was able to avoid unnecessary liver transplantation after genetic analysis. Conclusion: ABCB11 spectrum liver disorders can be clinically indistinguishable as they share similar characteristics related to acute episodes. A comprehensive genetic analysis will facilitate optimal diagnosis and treatment.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.2145-2150
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• 2016

Background: Infection with hepatitis B virus (HBV) is a major global public health problem, with a wide spectrum of clinical manifestations. Human cytosolic glutathione-S-transferases (GSTs) include several classes such as alpha (A), mu (M), pi (P), sigma (S), zeta (Z), omega (O) and theta (T). The present study aimed to investigate the role of GST omega genes (GSTO1 and GSTO2) in different groups of patients infected with HBV. Materials and Methods: HBV groups were classified according to clinical history, serological tests and histological analysis into normal carriers (N), acute (A), chronic (CH), cirrhosis (CI) and hepatocellular carcinoma (HCC) cases. The study focused on determination of the genotypes of GST omega genes (GSTO1 and GSTO2) and GST activity and liver function tests. Results: The results showed that GSTO1 (A/A) was decreased in N, A, CH, CI and HCC groups compared to the C-group, while, GSTO1 (C/A) and GSTO1(C/C) genotypes were increased significantly in N, A, CH, CI and HCC groups. GSTO2 (A/A) was decreased in all studied groups as compared to the C-group but GSTO2(A/G) and GSTO2(G/G) genotypes were increased significantly. In addition, GST activities, albumin and TP levels were decreased in all studied groups compared to the C-group, while the activities of transaminases were increased to differing degrees. Conclusions: The results indicate that GSTO genetic polymorphisms may be considered as biomarkers for determining and predicting the progression of HBV infection.

• IMMUNE NETWORK
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• v.14 no.4
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• pp.219-225
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• 2014

We examined the immunogenicity of H-2 class I-restricted and HLA-A2-restricted epitopes through peptide immunization of HLA-A2-transgenic mice that also express mouse H-2 class I molecules. All four of the tested epitopes restricted by H-2 class I robustly elicited T-cell responses, but four of seven epitopes restricted by HLA-A2 did not induce T-cell responses, showing that HLA-A2-restricted peptide epitopes tend to be poorly immunogenic in HLA-A2-transgenic mice. This finding was confirmed in HLA-A2-transgenic mice infected with a recombinant vaccinia virus expressing hepatitis C virus proteins. We examined the precursor frequency of epitope-specific naïve $CD8^+$ T cells in HLA-A2-transgenic and conventional C57BL/6 mice and found that the poor immunogenicity of HLA-A2-restricted peptide epitopes is related to the paucity of naïve $CD8^+$ T-cell precursors in HLA-A2-transgenic mice. These results provide direction for the improvement of mouse models to study epitope repertoires and the immunodominance of human T-cell responses.

• Journal of the Korean Magnetic Resonance Society
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• v.21 no.3
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• pp.109-113
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• 2017

The hepatitis C virus (HCV) internal ribosome entry site (IRES) is an RNA structure located in the 5'-UTR of the HCV RNA genome. The HCV IRES consists of four domains I, II, III, and IV, where domains II - IV are recognized by 40S ribosomal subunit and the domain III is bound to eukaryotic initiation factor 3 (eIF3) for translation initiation. Here, we have characterized the tertiary interaction between an L-/K- rich peptide and the HCV IRES domain IV. To probe the peptide binding interface in RNA, we synthesized $^{13}C$- and $^{15}N$-double labeled RNA and the binding site was identified by using the chemical shift perturbation (CSP) NMR methods. Our results showed that the peptide binds to the upper stem of the IRES domain IV, indicating that the tertiary interaction between the IRES domain IV and the peptide would disrupt the initiation of translation of HCV mRNA by blocking the start codon exposure. This study will provide an insight into the new peptide-based anti-viral drug design targeting HCV IRES RNA.

• BMB Reports
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• v.30 no.4
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• pp.299-301
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• 1997

The asialoglycoprotein receptor (ASGPR) was the first described mammalian lectin that mediates the specific binding and internalization of galactose/N-acetylgalactosamine-terminating glycoproteins by hepatic parenchymal cells. H1 and H2 are known as essential subunits of the functional ASGPR. There were close similarities in ASGPR H2 subunits between cultured cell line HepG2 and normal human liver cells including identical sequences at both termini. It was therefore expected that there may be some similarities between the subunits from normal liver cells and fetal liver cells. The two subunits of human fetal liver ASGPR. designated FL-H1 and FL-H2. were cloned from cDNA library by peR and the sequences were compared with the known HI and H2 sequences of HepG2, and the H1 sequence of nornal human liver cells. The results showed that FL-H1 was identical to H1 of HepG2. Whereas FL-H2 contains a 15-bp miniexon, but missing 57-bp at the near upstream from the membrane-spanning domain compared to H2 of HepG2 and normal human liver cells indicating that FL-H2 resulted from a differential splicing compared to HepG2 and normal liver cells.

• Parasites, Hosts and Diseases
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• v.53 no.6
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• pp.749-753
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• 2015

Toxoplasma gondii atypical type II genotype was diagnosed in a pet peach-faced lovebird (Agapornis roseicollis) based on histopathology, immunohistochemistry, and multilocus DNA typing. The bird presented with severe neurological signs, and hematology was suggestive of chronic granulomatous disease. Gross post-mortem examination revealed cerebral hemorrhage, splenomegaly, hepatitis, and thickening of the right ventricular free wall. Histologic sections of the most significant lesions in the brain revealed intralesional protozoan organisms associated with malacia, spongiform changes, and a mild histiocytic response, indicative of diffuse, non-suppurative encephalitis. Immunohistochemistry confirmed the causative organisms to be T. gondii. DNA isolated from the brain was used to confirm the presence of T. gondii DNA. Multilocus genotyping based on SAG1, altSAG2, SAG3, BTUB, GRA6, c22-8, c29-2, L358, PK1, and Apico markers demonstrated the presence of ToxoDB PCR-RFLP genotype #3 and B1 gene as atypical T. gondii type II. The atypical type II strain has been previously documented in Australian wildlife, indicating an environmental transmission route.

• Archives of Pharmacal Research
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• v.19 no.6
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• pp.486-489
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• 1996

A simple, rapid, specific and sensitive method for the detection of serum hepatitis C virus (HCV) RNA using the reverse transcription-polymerase chain reaction (RT-PCR) technique without conventional RNA extraction was developed. HCV template RNA from serum was obtained by boiling the serum at $95^{\circ}C$ for 2 min, cooling rapidly in ice and removing the proteins by cetrifugation. RT-PCR amplifications including the reverse transcription and first PCR amplification were performed in one vessel containing both of reverse transcriptase and Taq DNA polymerase. The detection of HCV RNA from $10^{-3}{\mu}l$. serum was possible with this method. The suitability of this method for clinical analysis was evaluated by assaying HCV RNA in 225 patient samples including anti-HCV antibody negatives (13 samples) and positives (212 samples) by enzyme-linked immunosorbent assay test (ELISA). Detections of HCV RNA with this method were in 4 of 13 anti-HCV antibody negative samples (30.8%) and 95 of 212 positive samples (44.8%). The present method can be completed in 1 hr and has a wide range of application for the clinical utilities to determine the viral RNAS.

• Journal of Microbiology
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• v.44 no.5
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• pp.492-501
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• 2006

In this study, we attempted to characterize the physiological response to oxidative stress by heat shock in Saccharomyces cerevisiae KNU5377 (KNU5377) that ferments at a temperature of $40^{\circ}C$. The KNU5377 strain evidenced a very similar growth rate at $40^{\circ}C$ as was recorded under normal conditions. Unlike the laboratory strains of S. cerevisiae, the cell viability of KNU5377 was affected slightly under 2 hours of heat stress conditions at $43^{\circ}C$. KNU5377 evidenced a time-dependent increase in hydroperoxide levels, carbonyl contents, and malondialdehyde (MDA), which increased in the expression of a variety of cell rescue proteins containing Hsp104p, Ssap, Hsp30p, Sod1p, catalase, glutathione reductase, G6PDH, thioredoxin, thioredoxin peroxidase (Tsa1p), Adhp, Aldp, trehalose and glycogen at high temperature. Pma1/2p, Hsp90p and $H^+$-ATPase expression levels were reduced as the result of exposure to heat shock. With regard to cellular fatty acid composition, levels of unsaturated fatty acids (USFAs) were increased significantly at high temperatures ($43^{\circ}C$), and this was particularly true of oleic acid (C18:1). The results of this study indicated that oxidative stress as the result of heat shock may induce a more profound stimulation of trehalose, antioxidant enzymes, and heat shock proteins, as well as an increase in the USFAs ratios. This might contribute to cellular protective functions for the maintenance of cellular homeostasis, and may also contribute to membrane fluidity.