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    Regulating Action of in Vitro Hepatitis C Virus Infection on Interferon-Induced Interferon Stimulating Genes in Murine Macrophages
    (Mongolian National University of Medical Sciences, 2018-03-25) ;
    Batkhishig Munkhjargal
    ;
    ; ;
    Objectives: The objective of this study was to determine the in vitro regulating effect of Hepatitis C virus (HCV) infection on interferon stimulating genes (ISGs) stimulated by IFN-ү and Imiquimod (TLR7 ligand) on murine macrophages. iNOS and STAT1 were measured by RT-PCR, and immunoblotting (IB). Nitric oxide production was measured by Griess Reagent Assay. Objectives: The objective of this study was to determine the in vitro regulating effect of Hepatitis C virus (HCV) infection on interferon stimulating genes (ISGs) stimulated by IFN-ү and Imiquimod (TLR7 ligand) on murine macrophages. iNOS and STAT1 were measured by RT-PCR, and immunoblotting (IB). Nitric oxide production was measured by Griess Reagent Assay. Results: HCV inhibits IFN induced iNOS mRNA and also protein expression. HCV significantly reduced IFN-ү induced ISGs (iNOS mRNA, iNOS protein, s727-STAT1, tyr701- STAT1). Conclusion: These results indicate that in vitro hepatitis C virus infection is involved in the regulation of IFN-ү induced ISGs in the levels of gene and protein expression of iNOS and STAT1 transcription factors.: HCV inhibits IFN induced iNOS mRNA and also protein expression. HCV significantly reduced IFN-ү induced ISGs (iNOS mRNA, iNOS protein, s727-STAT1, tyr701- STAT1). Conclusion: These results indicate that in vitro hepatitis C virus infection is involved in the regulation of IFN-ү induced ISGs in the levels of gene and protein expression of iNOS and STAT1 transcription factors.
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    Scopus© Citations 5
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    Diagnostic performances of pepsinogens and gastrin-17 for atrophic gastritis and gastric cancer in Mongolian subjects
    (2022) ;
    Amarbayasgalan, Dashmaa
    ;
    Batsaikhan, Batbold
    ;
    Badamjav, Tegshjargal
    ;
    In Mongolia, gastric cancer morbidity and mortality are high, and more than 80 percent of cases are diagnosed at an advanced stage. This study aimed to evaluate pepsinogens (PGIs) and gastrin-17 (G-17) levels and to determine the diagnostic performances for gastric cancer and chronic atrophic gastritis among Mongolian individuals. We enrolled a total of 120 subjects, including gastric cancer (40), atrophic gastritis (40), and healthy control (40), matched by age (±2) and sex. Pepsinogen I (PGI), Pepsinogen II (PGII), G-17, and H. pylori IgG levels were measured using GastroPanel ELISA kit (Biohit, Helsinki, Finland). Also, PGI to PGII ratio (PGR) was calculated. For atrophic gastritis, when the optimal cut-off value of PGI was ≤75.07 ng/ml, the sensitivity and specificity were 75% and 50%, respectively; when the optimal cut-off value of PGR was ≤6.25, sensitivity and specificity were 85% and 44.7%, respectively. For gastric cancer, when the optimal cut-off value of PGI was ≤35.25 ng/ml, the sensitivity and specificity were 47.2% and 86.8%, respectively; when the optimal cut-off value of PGR was ≤5.27, sensitivity and specificity were 75% and 60.5%, respectively. Combinations of biomarkers with risk factors could improve diagnostic accuracy (AUC for atrophic gastritis 74.8, 95% CI 64.0-85.7, p<0.001; AUC for gastric cancer 75.5, 95% CI 64.2-86.8, p<0.001). PGI, PGR biomarkers combined with the risk of age, family history of gastric cancer, and previous gastric disease could not be an alternative test for upper endoscopy but might be a supportive method which is identifying individuals at medium- and high risk of gastric cancer and precancerous lesions who may need upper endoscopy.
    Scopus© Citations 15