• BMB Reports
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• v.42 no.12
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• pp.834-839
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• 2009

DNA methyltransferase (DNMT) 1 is the key enzyme responsible for DNA methylation, which often occurs in CpG islands located near the regulatory regions of genes and affects transcription of specific genes. In this study, we examined the possible association of DNMT1 polymorphisms with HBV clearance and the risk of hepatocellular carcinoma (HCC). Seven common polymorphic sites were selected by considering their allele frequencies, haplotype-tagging status and LDs for genotyping in larger-scale subjects (n = 1,100). Statistical analysis demonstrated that two intron polymorphisms of DNMT1, +34542G > C and +38565G > T, showed significant association with HBV clearance in a co-dominant model (OR = 1.30, $P^{corr}$ = 0.03) and co- dominant/recessive model (OR = 1.34-1.74, $P^{corr}$ = 0.01-0.03), respectively. These results suggest that two intron polymorphisms of DNMT1, +34542G > C and +38565G > T, might affect HBV clearance.

• Tuberculosis and Respiratory Diseases
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• v.72 no.3
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• pp.318-322
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• 2012

Sarcoidosis is an inflammatory disease involving multiple-organs with an unknown cause. The new onset of sarcoidosis associated with therapeutic agents has been observed in 3 clinical settings; tumor necrosis factor antagonists in autoimmune rheumatologic diseases, interferon alpha with or without ribavirin in patients with chronic hepatitis C or melanoma, and antineoplastic agent-associated sarcoidosis in patients with hematologic malignancies. Here, we report a female patient who developed sarcoidosis after capecitabine treatment as an adjuvant chemotherapy for sigmoid colon cancer. To our knowledge, this is the first report of a capecitabine-induced sarcoidosis.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.11b
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• pp.194-194
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• 2002

Interferon has therapeutic potential for a wide range of infectious and proliferous disorders such as chronic hepatitis C. However, it has drawbacks such as relatively short serum half-life and rapid clearance like other therapeutic proteins. The attachment of a polyethylene glycol (PEG) moiety to interferon is considered as one of the most promising solutions for its ability to extend the plasma residence time.(omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.424.1-424.1
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• 2002

Interferon has therapeutic potential for a wide range of infectious and proliferative disorders such as chronic hepatitis C and malignant melanoma. However. it has some therapeutic problems as other protein therapeutics do. A variety of approaches have been developed to circumvent these problems. Among them. the attachment of a polyethylene glycol (PEG) moiety 10 interferon is considered as one of the most promising solutions for its ability of extending the plasma residence time. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.418.1-418.1
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• 2002

Recombinant interferon alpha is widely used for the treatment of diseases including chronic hepatitis C. However. it has drawbacks such as relatively short serum half-life and rapid clearance like other therapeutic proteins. Using PFGylFltioo which is one of the well-established methods to fulfill the requirements of a long-lasting form of protein. wIe prepared mono-PEG modified interferon alpha-2a in which polyethylene glycol moiety was covalently attached to the amino groups of interfelon alpha-2a. (omitted)

• 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.32 no.2
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• pp.94-100
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• 2022

Chronic infection by hepatitis B virus (HBV) greatly increases the risk for liver cirrhosis and hepatocellular carcinoma (HCC). The outcome of HBV infection is shaped by the complex interplay of the mode of transmission, host genetic factors, viral genotype, adaptive mutations, and environmental factors. The pregenomic RNA transcription of HBV for their replication is regulated by the core promoter activation. Core promoter mutations have been the reason for acute liver failure and are associated with HCC development. We obtained HBV genes from a patient in Myanmar who was infected with HBV and identified gene variations in the core promoter region. For measuring the relative transactivation activity of the core promoter, we prepared the core-promoter reporter construct. Among the gene variations of the core promoter, the mutations of C1731T and G1806A were associated with increase in the transactivation of the HBV core promoter. Through computer analysis for searching for a tentative transcription factor binding site, we showed that the mutations of C1713T and G1806A newly created C/EBPβ and XBP1-responsive elements of the core promoter, respectively. The ectopic expression of C/EBPβ largely increased the HBV core promoter containing the C1713T mutation and that of XBP1 activated the M95 promoter containing the G1806A mutation. Our efforts to treat and prevent HBV infections are hampered by the emergence of drug-resistant mutations and vaccine-escape mutations. Our results provide the biological properties and clinical significance of specific HBV core promoter mutations.

• Korean Journal of Microbiology
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• v.47 no.4
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• pp.342-347
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• 2011

T cells play a key role in viral infection. However, in patients with chronic hepatitis C virus (HCV) infection, HCV-specific T cells are dysfunctional and impaired in the liver, which is the primary site for HCV replication. There are multiple potential mechanisms for HCV-specific T cell dysfunction including induction of immune inhibitory pathways (program death-1; PD-1, cytotoxic t lymphocyte associated antigen-4; CTLA-4) and immune tolerance induced specific for the liver. However, the interaction between hepatocytes and HCV-specific CD8 T cells has not clearly established. In this study, we confirmed huh (human hepatoma) 7.5 cells expressing HLA (human leukocyte antigen) A2 presented antigen to activate HCV-specific CD8 T cells in HLA A2-restricted manner and expression of PD-L (program death ligand) 1 on huh7.5 cells reduced HCV-specific CD8 T cell activation, suggesting an immune modulatory activity. Loss of HCV-specific tetramer responses following antigenic stimulation correlated with increased caspase-3 activity. In addition, PD-L1 on huh7.5 cells rescued HCV-specific CD8 T cells from apoptosis. Our results suggest that the interaction between PD-L1 and PD-1 can recover the function of HCV-specific CD8 T cells in the liver, which could be applied in therapy of HCV chronic infection.

• 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.

• Korean Journal of Biological Psychiatry
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• v.2 no.1
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• pp.100-106
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• 1995

Antibodies to hepatitis C drew attention because of high morbidity to chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. HCV was known to be transmitted by transfusion, sexual behavior and parenteral drug use. However, some kind of autoimmune mechanism was suggested to be involved in the genesis of HCV-induced liver diseases. We hypothesized the prevalence of having anti-HCV might be higher in psychiatric patients rather than general population because of the characteristic route of transmission. Using Abbott HCV BA kit, anti-HCV was detected in the sera of 113 psychiatric inpatients from early December in 1992 to late May in 1994. The Positivity of anti-HCY was significantly(P<0.05) higher among psychiatric inpatients(10.6%) than in healthy controls(3.0%). There were no disease specificity among psychiatric inpatients who had anti-HCV, though alcoholics tended to have more anti-HCV. We couldn't find any significant correlation of anti-HCV with age, seasons of birth, lymphocytes (%) and liver function.