http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Kim, Yoon Jun,Kim, Hwi Young,Lee, Jeong-Hoon,Yu, Su Jong,Yoon, Jung-Hwan,Lee, Hyo-Suk,Kim, Chung Yong,Cheong, Jae Youn,Cho, Sung Won,Park, Neung Hwa,Park, Byung Lae,Namgoong, Seok,Kim, Lyoung Hyo,Cheo Oxford University Press 2013 Human Molecular Genetics Vol.22 No.20
<P>Hepatitis B virus (HBV) infection is the predominant risk factor for chronic hepatitis B (CHB), liver cirrhosis (LC) and hepatocellular carcinoma (HCC). Recently, several genome-wide association studies (GWASs) of CHB identified human leukocyte antigen (HLA) loci, including HLA-DP and HLA-DQ in Asian populations, as being associated with the risk of CHB. To confirm and identify the host genetic factors related to CHB infection, we performed another GWAS using a higher-density chip in Korean CHB carriers. We analyzed 1400 samples from Korean population (400 CHB cases and 1000 population controls) using a higher-density GWAS chip [1 140 419 single nucleotide polymorphisms (SNPs)]. In subsequent replication analysis, we further analyzed in an independent study of a Korean CHB cohort consisting of 2909 Korean samples (971 cases and 1938 controls). Logistic regression methods were used for statistical analysis adjusting for age and sex as covariates. This study identified two new risk-associated loci for CHB on the HLA region of chromosome 6, e.g. rs652888 on euchromatic histone-lysine-methyltransferase 2 (EHMT2, <I>P</I> = 7.07 × 10<SUP>−13</SUP>) and rs1419881 on transcription factor 19 (TCF19, <I>P</I> = 1.26 × 10<SUP>−18</SUP>). Conditional analysis with nearby HLA CHB loci that were previously known, confirmed the independent genetic effects of these two loci on CHB.</P><P><B>Conclusion</B>: The GWAS and the subsequent validation study identified new variants associated with the risk of CHB. These findings may advance the understanding of genetic susceptibility to CHB.</P>
Im, Moon-Sun,Kim, Hack-Lyoung,Kim, Sang-Hyun,Lim, Woo-Hyun,Seo, Jae-Bin,Chung, Woo-Young,Zo, Joo-Hee,Kim, Myung-A,Park, Kyung-Woo,Koo, Bon-Kwon,Kim, Hyo-Soo,Chae, In-Ho,Cho, Dong-Ju,Ahn, Youngkeun,Jeo Elsevier 2016 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.221 No.-
<P>Background: Initial left ventricular (LV) systolic function is a main determinant of clinical outcomes in patients with acutemyocardial infarction (AMI). This study was performed to investigate whether AMI patients have different prognostic factors according to their baseline LV systolic function. Methods: A total of 12,988 patients with AMI from a nationwide database were analyzed. Major adverse cardiovascular events (MACEs) within 12 months of AMI, including death, nonfatal myocardial infarction (MI), and revascularization, were assessed. Results: Patients were stratified into two groups according to LV ejection fraction (LVEF): those with LVEF < 40% and those with LVEF >= 40%. Patients with LVEF < 40% (n = 1962, 15.1%) were older and had more unfavorable cardiovascular risk factors than those with LVEF >= 40% (n= 11,026, 84.9%). The rate of MACE was higher in patients with LVEF < 40% than in those with LVEF >= 40% (26.8% vs 11.4%, p < 0.001). Independent predictors of 12-month MACEs in patients with LVEF >= 40% were history of MI, high Killip stage, three-vessel disease, and lower renal function, which are already known as risk factors. However, diabetes mellitus (hazard ratio [HR], 1.68; 95% confidence interval [CI], 1.17-2.40; p = 0.008), and the use of rennin-angiotensin system (RAS) blockers (HR, 0.63; 95% CI, 0.41-0.95; p = 0.029) were independent factors for 12-month MACE in patients with LVEF < 40%. Conclusions: Prognostic factors determining 12-month MACE after AMI are different according to LVEF. Management following AMI should be tailored according to their LV systolic function. (C) 2016 Elsevier Ireland Ltd. All rights reserved.</P>
Generation of Cloned Transgenic Cats Expressing Red Fluorescence Protein1
Yin, Xi Jun,Lee, Hyo Sang,Yu, Xian Feng,Choi, Eugene,Koo, Bon Chul,Kwon, Mo Sun,Lee, Young S.,Cho, Su Jin,Jin, Guang Zhen,Kim, Lyoung Hyo,Shin, Hyoung Doo,Kim, Teoan,Kim, Nam Hyung,Kong, Il Keun Oxford University Press 2008 BIOLOGY OF REPRODUCTION Vol.78 No.3
<P>A method for engineering and producing genetically modified cats is important for generating biomedical models of human diseases. Here we describe the use of somatic cell nuclear transfer to produce cloned transgenic cats that systemically express red fluorescent protein. Immature oocytes were collected from superovulating cat ovaries. Donor fibroblasts were obtained from an ear skin biopsy of a white male Turkish Angora cat, cultured for one to two passages, and subjected to transduction with a retrovirus vector designed to transfer and express the red fluorescent protein (RFP) gene. A total of 176 RFP cloned embryos were transferred into 11 surrogate mothers (mean = 16 +/- 7.5 per recipient). Three surrogate mothers were successfully impregnated (27.3%) and delivered two liveborn and one stillborn kitten at 65 to 66 days of gestation. Analysis of nine feline-specific microsatellite loci confirmed that the cloned cats were genetically identical to the donor cat. Presence of the RFP gene in the transgenic cat genome was confirmed by PCR and Southern blot analyses. Whole-body red fluorescence was detected 60 days after birth in the liveborn transgenic (TG) cat but not in the surrogate mother cat. Red fluorescence was detected in tissue samples, including hair, muscle, brain, heart, liver, kidney, spleen, bronchus, lung, stomach, intestine, tongue, and even excrement of the stillborn TG cat. These results suggest that this nuclear transfer procedure using genetically modified somatic cells could be useful for the efficient production of transgenic cats.</P>
Screening of genetic variations of SLC15A2, SLC22A1, SLC22A2 and SLC22A6 genes.
Cheong, Hyun Sub,Kim, Hae Deun,Na, Han Sung,Kim, Ji On,Kim, Lyoung Hyo,Kim, Seung Hee,Bae, Joon Seol,Chung, Myeon Woo,Shin, Hyoung Doo Springer-Verlag 2011 Journal of human genetics Vol.56 No.9
<P>A growing list of membrane-spanning proteins involved in the transport of a large variety of drugs has been recognized and characterized to include peptide and organic anion/cation transporters. Given such an important role of transporter genes in drug disposition process, the role of single-nucleotide polymorphisms (SNPs) in such transporters as potential determinants of interindividual variability in drug disposition and pharmacological response has been investigated. To define the distribution of transporter gene SNPs across ethnic groups, we screened 450 DNAs in cohorts of 250 Korean, 50 Han Chinese, 50 Japanese, 50 African-American and 50 European-American ancestries for 64 SNPs in four transporter genes encoding proteins of the solute carrier family (SLC15A2, SLC22A1, SLC22A2 and SLC22A6). Of the 64 SNPs, 19 were core pharmacogenetic variants and 45 were HapMap tagging SNPs. Polymorphisms were genotyped using the golden gate genotyping assay. After genetic variability, haplotype structures and ethnic diversity were analyzed, we observed that the distributions of SNPs in a Korean population were similar to other Asian groups (Chinese and Japanese), and significantly different from African-American and European-American cohorts. Findings from this study would be valuable for further researches, including pharmacogenetic studies for drug responses.</P>
Genome-wide association study of aspirin-exacerbated respiratory disease in a Korean population.
Park, Byung Lae,Kim, Tae-Hoon,Kim, Jeong-Hyun,Bae, Joon Seol,Pasaje, Charisse Flerida A,Cheong, Hyun Sub,Kim, Lyoung Hyo,Park, Jong-Sook,Lee, Ho Sung,Kim, Myung-Sin,Choi, Inseon S,Choi, Byoung Whui,Ki Springer-Verlag 2013 HUMAN GENETICS Vol.132 No.3
<P>Aspirin-exacerbated respiratory disease (AERD) is a nonallergic clinical syndrome characterized by a severe decline in forced expiratory volume in one second (FEV1) following the ingestion of non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin. The effects of genetic variants have not fully explained all of the observed individual differences to an aspirin challenge despite previous attempts to identify AERD-related genes. In the present study, we performed genome-wide association study (GWAS) and targeted association study in Korean asthmatics to identify new genetic factors associated with AERD. A total of 685 asthmatic patients without AERD and 117 subjects with AERD were used for the GWAS of the first stage, and 996 asthmatics without AERD and 142 subjects with AERD were used for a follow-up study. A total of 702 SNPs were genotyped using the GoldenGate assay with the VeraCode microbead. GWAS revealed the top-ranked variants in 3' regions of the HLA-DPB1 gene. To investigate the detailed genetic effects of an associated region with the risk of AERD, a follow-up targeted association study with the 702 single nucleotide polymorphisms (SNPs) of 14 genes was performed on 802 Korean subjects. In a case-control analysis, HLA-DPB1 rs1042151 (Met105Val) shows the most significant association with the susceptibility of AERD (p = 5.11 x 10(-7); OR = 2.40). Moreover, rs1042151 also shows a gene dose for the percent decline of FEV1 after an aspirin challenge (p = 2.82 x 10(-7)). Our findings show that the HLA-DPB1 gene polymorphism may be the most susceptible genetic factor for the risk of AERD in Korean asthmatics and confirm the importance of HLA-DPB1 in the genetic etiology of AERD.</P>
SHIN, JOONG-GON,PARK, BYUNG LAE,KIM, LYOUNG HYO,NAMGOONG, SUHG,KIM, JI ON,CHANG, HUN SOO,PARK, JONG SOOK,JANG, AN SOO,PARK, SUNG WOO,KIM, DO JIN,KIM, KI UP,KIM, YANG GEE,UH, SOO-TAEK,SEO, KI HYUN,KIM, SPANDIDOS PUBLICATIONS 2015 MOLECULAR MEDICINE REPORTS Vol.12 No.1
<P>Tuberculosis (TB) is an infectious disease caused by mycobacterium, which most commonly affects the lungs. The adaptive immune response in Mycobacterium tuberculosis is predominantly mediated by the interferon-γ (IFN-γ) signaling pathway, which is regulated by IFN-γ receptors (IFNGR). IFN-γ activates the transcription of a number of genes that are important in immune responses, thus the appropriate function of IFNGR appears to be important in host defense against mycobacteria. In the present study, 22 genetic variants in IFNGR1 and IFNGR2 were genotyped in 673 patients and 592 normal controls to investigate the association between IFNGR1 and IFNGR2 polymorphisms and the risk of TB. Statistical analyses revealed that four genetic variants in IFNGR1, rs9376269, rs9376268, rs9376267 and rs56251346 were marginally associated with the risk of TB (P = 0.02-0.04), while other single nucleotide polymorphisms in IFNGR1 and IFNGR2 did not exhibit any associations. However, the significance of the four genetic variants rs9376269, rs9376268, rs9376267 and rs56251346 was eliminated following a multiple testing correction of the data (P>0.05). The present results revealed that certain genetic variants in IFNGR genes may be associated with TB development, which may be useful preliminary data for future investigation.</P>