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Comparative Analysis of the Aranesp, tg-EPO and Dimeric EPO Analogues In Vivo
Tsevelmaa Nanjidsuren,Purevjargal Naidansuren,Sung-Jo Yun,Jong-Ju Park,Won-Gun Noh,Chae-Won Park,Young-Sil Kang,Jong-Taek Yoon,Sang-Rae Lee,Kyu-Tae Chang,Kwan Sik-Min 한국동물생명공학회(구 한국동물번식학회) 2009 발생공학 국제심포지엄 및 학술대회 Vol.2009 No.1
RAS and Ledipasvir/Sofosbuvir Therapy with Patients CHC in Mongolia
( Tsevelmaa O ),( Nyamsuren Naranzul ),( Oidov Baatarkhuu ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: To investigate the effectiveness of LDV/SOF and the impact of RAS on the treatment outcome in Mongolian CHC patients. Introduction: Mongolia has the highest prevalence of hepatitis C virus (HCV) infection worldwide. Ledipasvir/sofosbuvir (LDV/SOF) was introduced to Mongolia since 2016 for HCV eradication. It has been reported that HCV resistance-associated substitutions (RASs) would affect theeffectiveness of LDV/SOF in western chronic hepatitis C (CHC) patients. Methods: Patients with genotype (GT) 1b HCV infection were prospectively enrolled inMongolia and treated with LDV/SOF for 12 weeks. The proportion of pre-treatment NS5AY93H RAS in viral quasispecies was measured with next-generation sequencing. The endpointof LDV/SOF effectiveness was sustained virological response at post-treatment week 12(SVR12). Results: A total of 94 CHC patients were evaluated. The baseline Y93H proportion was <1% in74 patients, 1e15% in 7, 15e50% in 2, and 50% in 11. All patients completed 12-week LDV/SOFtreatment and the SVR rate was 90.4%. The rate of failure to achieve SVR12 for patients withY93H < 1%, 1e15%, and _15% were 0%, 14.3%, and 61.5%, respectively (p for trend Z0.001). Inunivariable analysis, older age, baseline alanine transaminase level <40 U/mL, and a higherproportion of Y93H were associated with treatment failure. In multivariable analysis, only a higher proportion of Y93H was associated with treatment failure (p Z 0.022). Conclusions: LDV/SOF therapy achieves a high SVR rate in Mongolian CHC GT1b patients withoutbaseline Y93H RAS. A higher proportion of Y93H may severely undermine the effectiveness ofLDV/SOF.
( Tsevelmaa Munkhchuluun ),( Dashchirev Munkh-orshikh ),( Baasankhuu Enkhtuvshin ),( Oidov Baatarkhuu ) 대한간학회 2020 춘·추계 학술대회 (KASL) Vol.2020 No.1
Aims: Comparative study of cirrhosis stage in patients with HBV infection and HBV/HDV co-infection Methods: Our study continued from January 2015 to March 2017 and we measured liver fibrosis stage in patients with HBV infection and HBV/HDV co-infection using a Fibroscan (Fibroscan 502 Touch, Echosens, and Paris, France) who are controlled in Happy Veritas Clinic and Diagnostic Center. When we measured liver fibrosis stage in 5504 patients with HBV infection, 20% or 1115 of the patients is determined HDV co-infection. In our study in random sampling cases are selected 354 patients with HBV mono infection and 177 of all patients have HBV/HDV co-infection. We selected parameters from patient’s medical histories in our study, such as serologic markers of HBV quantification of HBV and HDV in serum samples, blood test, liver function tests, and liver fibrosis stage. Results: 354 patients 47.7% (169) was men. Range with an average age of 44±17 (range 18-75 years old) were included the study. According to the comparative study in laboratory tests, ALT level was HBV - 44 (36; 51.5) and HBV/HDV co-infection 61 (39.8; 97.5), AST level was HBV - 39.1(30; 83) and HBV/HDV co-infection - 50 (33.1; 77.8), Platelet count was HBV- 193±66 and HBV/HDV - 181±62.8. When we compared liver fibrosis stage were HBV- F0 67(37.9%), HBV/HDV-F0 57(32.2%), HBV-F1 22(12.4%), HBV/HDV-F1 17(9.6%), HBV-F2 39(22%), HBV/HDV- F2 39(22%), HBV-F3 29(16.4%), HBV/HDV-F3 41(23.2%), HBV- F4 20(11.3%) and HBV/HDV - F4 23(13%) . In table 1 shows the difference of liver fibrosis by age group. Conclusions: 65.5% of all patients with HBV/HDV co-infection are from 30 to 50 years old. Liver fibrosis of patients with HBV/HDV co-infection is a higher 11.88kPa than patients with HBV mono-infection. Our study shows that, the hepatitis is more severe in patients with HBV/HDV co-infection and the platelet count is less than HBV infection only.
Analysis of Promoter Characterization of Macaque Monkey 20α-HSD Gene
Tsevelmaa Nanjidsuren,Sung-Jo Yun,Min-Su Kim,Chae-Won Park,Young-Sil Kang,Jong-Taek Yoon,Su-Yeon Hwang,Kwan-Sik Min 한국동물번식학회 2012 Reproductive & Developmental Biology(Supplement) Vol.36 No.2s
20ɑ-hydroxysteroid dehydrogenase (20ɑ-HSD) enzyme converts progesterone into biological inactive steroid, thus playing a key role in the termination of pregnancy or estrus cycle and allowing parturition and ovulation to occur in most mammalian animals. However, function and regulation of this enzyme has not known well in primate reproductive physiology. We previously demonstrated the expression level and localization of the 20α-HSD in the reproductive tissues of macaque monkeys of pre-ovulation and pre-parturition period. Also, we amplified about 2005 bp 5'-flanking region from placenta genomic DNA and examined methylation pattern and promoter activity. In present study, we focus on the analysis of molecular characterization of the promoter region by using reporter assay systems. We constructed of deleted mutants (- 890 bp; HSF-2), (- 513 bp; XFD), (- 276 bp; Ap-1) and (- 72 bp; Sp-1) and each mutants were cloned into pGL3-basic vector. These deletion mutants were transfected into CHO cells and co-transfected with Sp-1 or Ap-1 transcription factor plasmids. Compared to - 890 bp and 513 bp promoter fragments alone, transcription activity increased when these constructs were co-transfected with Sp-1 and Ap-1 factor. However, for the absence Ap-1 factor binding site in 276 bp fragment activity dramatically decreased in both transfections. Next, we constructed of 306 bp fragment which is including of Ap-1 binding site and nucleotides converted mutants of the Ap-1 factor binding site. In this result, 306 bp fragment's transcription activity was high as wild type. However, the mutant activity which converted Ap-1 site’s all nucleotide was significantly decreased. These findings are confirmed by gel-shift assay examining Ap-1 binding site on the 20 α-HSD gene upstream region and expression of Ap-1 factor was determined by RT-PCR and Western blot in pre-parturition period placenta and CHO-K1 cell line. Our results indicate that Ap-1 site (- 281 → - 274) (5'-TGTCTCAT-3') plays a crucial role for monkey 20 α- HSD gene transcription.
TALEN-Mediated Gene Editing Method for GRK5-KO Mice
Tsevelmaa Nanjidsuren,Bo-Woong Sim,Min-Su Kim,Chae-Won Park,Eun-Bi Seo,Sun-Ok Kim,Kyu-Tae Chang,Kwan-Sik Min 한국동물생명공학회(구 한국동물번식학회) 2013 Reproductive & Developmental Biology(Supplement) Vol.37 No.2s
G protein-coupled receptor kinase 5 (GRK5) is one of the seven GRK family members whose primary function is to desensitize G protein-coupled receptors (GPCRs). In recently, GRK5 deficiency has been linked to early Alzheimer disease (AD), but the mechanism by which GRK5 deficiency may accelerate to AD pathogenesis remains elusive. The GRK5 mRNA is expressed widely in brain and peripheral tissues, with highest expression evident heart, lung, and placenta. In cellular model systems, GRK5 can phosphorylate several neuronal GPCRs including ß2-adrenergic, M2-muscarinic, secretin, angiotensin AT1, and thyroid stimulating hormone receptors. Transcription activator-like effector nucleases (TALENs) are programmable nucleases that join FokI endonucleases with the modular DNA-binding domain of TALEs and highly effective in inducing mutations at specific genome loci. TALEN-mediated mutagenesis in zygotes is a potential alternative to conventional gene targeting in mice. In the presented study, we report the generation of mice with genetic knockout of the GRK gene using TALENs. We designed TALEN vectors for exon 1, 3 and 5 of mouse GRK5 gene and tested their ability to alter the each surrogate vector in 293T cells. We prepared of mRNAs for the linearized TALEN using the mMessage mMachine T7 Ultra kit. mRNAs (4ng/μl) was injected into cytoplasm of 180 one-cell embryos. After incubation for 24 hours, the selected two-cell embryos transferred into the oviduct of seven pseudopregnant C57BL/6 mice. We confirmed the genotype of Fo mice by sequencing and T7E1 assay. We found 6 mutant mice lines (11%) from 53 newborns. We also mated 3 Fo GRK5 mutant lines with wild type mice and confirmed the genotype of the F1 progenies. All the mutations observed in Fo mice were transmitted through the germline but not all progenies (8/3, 13/4, 7/4). Taken together, TALEN-mediated mutagenesis might accelerate the creation of genetically engineered mouse models and elucidate the mechanism of AD pathogenesis using GRK5 knock out mice.
GRK5-Knockout Mice Generated by TALEN-Mediated Gene Targeting
Nanjidsuren, Tsevelmaa,Park, Chae-Won,Sim, Bo-Woong,Kim, Sun-Uk,Chang, Kyu-Tae,Kang, Myung-Hwa,Min, Kwan-Sik Taylor Francis 2016 Animal biotechnology Vol.27 No.4
<P>Transcription activator-like effector nucleases (TALENs) are a new type of engineered nuclease that is very effective for directed gene disruption in any genome sequence. We investigated the generation of mice with genetic knockout (KO) of the G protein-coupled receptor kinase (GRK) 5 gene by microinjection of TALEN mRNA. TALEN vectors were designed to target exons 1, 3, and 5 of the mouse GRK5 gene. Flow cytometry showed that the activity of the TALEN mRNAs targeted to exons 1, 3, and 5 was 8.7%, 9.7%, and 12.7%, respectively. The TALEN mRNA for exon 5 was injected into the cytoplasm of 180 one-cell embryos. Of the 53 newborns, three (5.6%) were mutant founders (F-0) with mutations. Two clones from F(0)28 showed a 45-bp deletion and F(0)39 showed the same biallelic non-frame-shifting 3-bp deletions. Three clones from F(0)41 were shown to possess a combination of frame-shifting 2-bp deletions. All of the mutations were transmitted through the germline but not to all progenies (37.5%, 37.5%, and 57.1% for the F(0)28, F(0)39, and F(0)41 lines, respectively). The homozygote GRK5-KO mice for 28 and 41 lines created on F3 progenies and the homozygous genotype was confirmed by PCR, T7E1 assay and sequencing.</P>