Song J.,CHA Medical University |
Kim O.J.,Korea University |
Kim H.S.,Korea University |
Bae S.J.,Dong - A University |
And 3 more authors.
International Journal of Molecular Medicine | Year: 2010
Silent brain infarction (SBI), a unique cerebrovascular disorder, is frequently detected on magnetic resonance imaging (MRI) of apparently healthy elderly persons, and it is known to increase the risk of stroke and other related diseases. Although detailed mechanisms of SBI pathogenesis have yet to be determined, recent studies suggest that SBI is significantly influenced by genetic factors. In this study, we investigated polymorphisms in the endothelial nitric oxide synthase (eNOS) gene (i.e., -786T>C, 4a4b and 894G>T) as possible risk factors for SBI. We enrolled 269 patients with SBI and 234 control subjects and examined their fasting plasma homocysteine and folate levels, and analyzed for eNOS polymorphisms and haplotypes. The prevalence of SBI was shown to be significantly higher in patients with the eNOS 894GT genotype (OR, 2.00; 95% CI, 1.30-3.08) and 894GT+TT genotype (OR, 2.05; 95% CI, 1.34-3.16), compared with the 894GG genotype. However, in the case of -786T>C and 4a4b polymorphisms, no significant difference was observed between SBI patients and normal subjects. Interestingly, we found that the prevalence of SBI can increase twice as high when either -786T>C or 4a4b polymorphism was combined with 894G>T polymorphism, -786TC+CC/ 894GT+TT (OR, 3.83; 95% CI, 1.24-11.80) and 4a4b+4a4a/894GT+TT (OR, 4.08; 95% CI, 1.34-12.40), respectively. According to haplotype analysis, we found that three haplotypes (-786T-4b-894G, -786T-4b-894T and -786C-4a-894T) were shown to be significantly different between SBI patients and control subjects. These results indicate that eNOS polymorphisms and haplotypes serve as risk factors for SBI, and three different polymorphic loci in the eNOS gene play interactively, thereby leading to synergistic effects for the generation of SBI.
Lee J.H.,Seoul National University |
Hong S.P.,GeneMatrix Inc |
Jang E.S.,Seoul National University |
Park S.J.,Bundang Jesaeng General Hospital |
And 3 more authors.
Journal of Medical Virology | Year: 2015
Acute hepatitis B, caused by hepatitis B virus (HBV) strains with drug resistant mutations or pre-core/basal core promoter (PC/BCP) mutations, is a public health concern, because this infection is often associated with poor disease outcome or difficulty in therapeutic choice. The HBV genotype, the prevalence of drug resistant mutations, and PC/BCP mutations in Korean patients with acute hepatitis B were studied. From 2006 to 2008, 36 patients with acute hepatitis B were enrolled prospectively in four general hospitals. Among them, 20 showed detectable HBV DNA (median value was 4.8 log copies/mL). HBV genotyping and analysis of HBV mutations that conferred resistance against lamivudine, adefovir, or entecavir and of PC/BCP mutations were performed using highly sensitive restriction fragment mass polymorphism (RFMP) analysis. All 20 patients were infected with HBV genotype C, which causes almost all cases of chronic hepatitis B in Korea. No patient showed mutations that conferred resistance against lamivudine (L180M, M204V/I), adefovir (A181T, N236S), or entecavir (I169M, A184T/V, S202I/G, M250V/I/L). However, four patients had BCP mutations, and two had PC mutations. Platelet counts were significantly lower in the four patients with PC/BCP mutations compared to those with wild type. In this study, all acute hepatitis B patients had genotype C HBV strains with no drug resistant mutations. However, 20% showed PC/BCP mutations. This highlights the need for further study on the significance of PC/BCP mutations. © 2015 Wiley Periodicals, Inc.
Genematrix Inc. | Date: 2012-10-26
The present invention relates to a pharmaceutical composition for prevention and treatment of hyperlipidemia or fatty liver disease, the composition containing dichloromethane fractions as an active ingredient amongst fractions obtained by fractionating the alcohol extract of
Genematrix Inc. | Date: 2011-04-20
The present invention provides a primer composition for amplifying a gene region having various variations in a target gene comprising: a first primer group comprising at least one primer specific to at least one template including a genotype-analyzable sequence of a genetically variant base sequence subjected to be analyzed in the target gene; and a second primer group comprising at least one primer designed by selecting one primer having the greatest number of shared bases from the primers of the first primer group and by using the selected primer as a reference, the primer of the second primer group binding specifically to the template or binding complementarily to the template with allowing mismatch of up to three successive bases or 1 to 2 bases in the vicinity of the 3 end of the template.
Lee J.M.,Yonsei University |
Park J.Y.,Yonsei University |
Park J.Y.,Liver Cirrhosis Clinical Research Center |
Kim D.Y.,Yonsei University |
And 10 more authors.
Antiviral Therapy | Year: 2010
Background: Large clinical studies assessing long-term adefovir dipivoxil salvage monotherapy in patients with lamivudine-resistant chronic hepatitis B (CHB) are lacking, particularly In patients positive for hepatitis B e antigen (HBeAg). We assessed the efficacy and resistance profile of adefovir dipivoxil monotherapy for up to 5 years in a large cohort of Korean patients with lamivudine-resistant CHB. Methods: A total of 320 patients (81.3% HBeAg-positive; 100% genotype C) with confirmed genotypic lamivudine-reslstant CHB were switched to adefovir dipivoxil 10 mg once daily. Liver function tests and HBV DNA were monitored every 3 months. Genotypic resistance to adefovir dipivoxil was performed In patients with detectable HBV DNA. Results: The overall cumulative virological response rate at 5 years of adefovir dipivoxil therapy was 48.8%. The virological response rate was significantly higher in HBeAgnegative patients (62.0% versus 45.9%; P=0.010). Most cases of virological response (131/134, 97.8%) occurred within the first 36 months of therapy. The 5-year cumulative probability of genotypic resistance and virological breakthrough was 65.6% and 61.8%, respectively. Predictive factors for a virological response included baseline HBeAg seronegativity, HBV DNA≤8 log10 copies/ml and achievement of an on-treatment initial virological response. Conclusions: Adefovir dipivoxil salvage monotherapy for lamlvudine-reslstant CHB resulted in a modest cumulative virological response rate at 5 years, which was associated with progressive antiviral resistance. Consequently, adefovir monotherapy is not preferable as a first-line strategy for lamivudine resistance where combination lamivudlne plus adefovir dipivoxil therapy is available.