GeneMatrix Inc

Seongnam, South Korea

GeneMatrix Inc

Seongnam, South Korea
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Ayres A.,Victorian Infectious Diseases Reference Laboratory | Yuen L.,Victorian Infectious Diseases Reference Laboratory | Jackson K.M.,Victorian Infectious Diseases Reference Laboratory | Manoharan S.,Liverpool Hospital | And 10 more authors.
Journal of Viral Hepatitis | Year: 2014

This study sought to assess the antiviral efficacy of lamivudine (LMV) administered during third trimester to reduce maternal viraemia and to identify the emergence of LMV resistance. A prospective observational analysis was performed on 26 mothers with high viral load (>107 IU/mL). Twenty-one women received LMV (treated group) for an average of 53 days (range 22-88 days), and the remaining five formed the untreated control group. Serum samples from two time points were used to measure HBV DNA levels and antiviral drug resistance. The LMV-treated women achieved a median HBV DNA reduction of 2.6-log10 IU/mL. Although end-of-treatment (EOT) HBV DNA in four (18%) LMV-treated women remained at >107 IU/mL (±0.5 log IU/mL), no mother-to-baby transmission was observed. In contrast, a baby from the untreated mother was HBsAg positive at 9 months postpartum. Four technologies were used for drug resistance testing. Only ultra-deep pyrosequencing (UDPS) was sufficiently sensitive to detect minor viral variants down to <1%. UDPS showed that LMV therapy resulted in increased viral quasispecies diversity and positive selection of HBV variants with reverse transcriptase amino acid substitutions at sites associated with primary LMV resistance (rtM204I/V and rtA181T) in four (19%) women. These viral variants were detected mostly at low frequencies (0.63-5.92%) at EOT, but one LMV-treated mother had an rtA181T variant that increased from 2.2% pretherapy to 25.59% at EOT. This mother was also infected with the vaccine escape variant (sG145R), which was inhibited by LMV treatment. LMV therapy during late pregnancy only reduced maternal viraemia moderately, and drug-resistant viral variants emerged. © 2013 John Wiley & Sons Ltd.


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.


Kim S.S.,Ajou University | Cho S.W.,Ajou University | Kim S.-O.,GeneMatrix Inc | Hong S.P.,GeneMatrix Inc | Cheong J.Y.,Ajou University
Journal of Medical Virology | Year: 2013

Whether multidrug-resistant (MDR) hepatitis B virus (HBV) harbors mutations co-located in the same HBV clones that confer reduced sensitivity to antiviral therapy remains uncertain. This study investigated the evolution of MDR HBV strains developed from sequential monotherapy with lamivudine (LAM), adefovir (ADV), and entecavir (ETV) during LAM plus ADV salvage therapy. Sera were obtained from six patients who had developed sequential resistance to LAM, ADV, and ETV before and during LAM plus ADV therapy. The HBV genomes from each patient were amplified, cloned, and sequenced. Among 6 sets of 20 clones obtained before salvage therapy, all clones harbored the rtM204V mutation, and ETV-resistant mutations were detected with the rtM204V in 108 clones. The rtA181 mutation was not detected at baseline, but emerged in five patients during therapy. Among 9 sets of 20 clones obtained during salvage therapy, 39 clones harbored rtA181T/V±rtN236T mutations, which were detected in the absence of rtM204 and ETV-resistant mutations in 37 clones (94.9%). Only two clones (5.1%) harbored both rtA181T/V and ETV-resistant mutations. The rtA181T/V mutation emerged after reversion from ETV-resistant mutants to wild-type HBV. Five patients achieved a partial virologic response to LAM plus ADV therapy. In conclusion, the majority of MDR mutations existed in different genomes. Suboptimal response to LAM plus ADV therapy may not result from the co-localization of MDR HBV mutations in the same genome, but instead the low antiviral potency of these drugs. Thus, more potent antiviral drug combinations may be an effective salvage therapy for patients infected with MDR HBV. J. Med. Virol. 85:55-64, 2012. © 2012 Wiley Periodicals, Inc.


Kim S.S.,Ajou University | Cheong J.Y.,Ajou University | Lee D.,Ajou University | Lee M.H.,Ajou University | And 3 more authors.
Journal of Medical Virology | Year: 2012

This study evaluated the efficacy of adefovir (ADV) plus lamivudine (LAM) or ADV add-on therapy for patients with entecavir (ETV)-refractory hepatitis B infection. Twenty-nine ETV-resistant and 8 patients with suboptimal response to ETV were enrolled. Twenty-seven patients received ADV+LAM therapy and 10 patients received ADV+ETV therapy for >24 weeks. In 29 patients who were ETV-resistant, the mean reduction in HBV DNA levels at 24 weeks was not different between the ADV+LAM and ADV+ETV groups (-1.98log 10IU/ml vs. -2.16log 10IU/ml; P=0.792). Primary non-response was observed in 52.2% (12/23) of ADV+LAM group and 33.3% (2/6) of ADV+ETV group (P=0.651). Initial virologic response (IVR) was observed in 17.4% (4/23) of ADV+LAM group and 33.3% (2/6) of ETV+ADV group (P=0.362). In eight patients with suboptimal response to ETV, the ADV+ETV group had a greater reduction in HBV DNA at 24 and 48 weeks than the ADV+LAM group (-2.29log 10IU/ml vs. -0.09log 10IU/ml and -2.04log 10IU/ml vs. -0.72log 10IU/ml; P=0.020 and P=0.012, respectively). Primary non-response and IVR did not significantly differ between the two groups [100% (4/4) vs. 50% (2/4) and 0% (0/4) vs. 50% (2/4); P=0.429 and P=0.429, respectively]. The antiviral efficacies of ADV-based therapy with ETV or LAM for patients with ETV-resistant hepatitis B were limited and did not differ between the two groups. However, adding ADV to ETV may be more effective than ADV+LAM therapy in patients with suboptimal virologic response to ETV. © 2011 Wiley Periodicals, Inc.


Cho S.W.,Ajou University | Koh K.H.,Ajou University | Cheong J.Y.,Ajou University | Lee M.H.,Ajou University | And 3 more authors.
Journal of Viral Hepatitis | Year: 2010

We determined the virologic response, incidence of entecavir resistance, and evolution of lamivudine and adefovir-resistant mutants during entecavir (ETV) therapy in adefovir-refractory patients with prior lamivudine resistance. Forty adefovir-refractory chronic hepatitis B patients with prior lamivudine resistance who had received entecavir for ≥6 months were included and monitored for virologic response and entecavir resistance. Ten per cent of patients achieved HBV DNA < 50 copies/mL by PCR after 24 weeks of ETV therapy, and an initial virologic response was observed in 12 of 40 patients (30%). Higher pretreatment ALT (P = 0.039) and the presence of the rtL180M mutation (P = 0.038) were associated with an initial virologic response. During a mean follow-up of 11.4 months, four patients (10%) experienced virologic breakthrough, while ETV-resistant mutants were detected in six patients (15%). YMDD and adefovir-resistant mutants were detected in 57 and 35% of patients at baseline, respectively. At 48 weeks of therapy, 96 and 4% of patients had YMDD and adefovir-resistant mutants, respectively. These data suggest an early development of ETV resistance and low antiviral response during ETV therapy in adefovir-refractory patients with prior lamivudine resistance. © 2009 Blackwell Publishing Ltd.


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 Triticum aestivum Lamarck leaves in an order of dichloromethane, ethyl acetate, and butanol.


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.


The present invention is related to a pharmaceutical composition and a dietary supplement for treating and preventing obesity, containing a wheatgrass extract as an active ingredient, it has been ascertained that the wheatgrass extract shows excellent anti-obesity effects such as significant inhibition of weight gain caused by a high fat diet, or lowering of neutral lipid levels in blood in a high fat diet-induced animal model. The wheatgrass extract of the present invention can be useful as a pharmaceutical composition and a dietary supplement for preventing and treating obesity.


Patent
Genematrix Inc. | Date: 2010-06-02

A method for precisely and effectively detecting mutations of organism is provided. The method for detecting a mutation includes the steps of: a) amplifying a target polynucleotide using a forward primer and a reverse primer; b) generating fragments of two or more single-stranded polynucleotides including one or more mutations sequence having the size of 2-32 bases by cleaving the amplified polynucleotide with restriction enzymes; and c) measuring the molecular weight of the cleaved fragments.


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.

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