http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
히야신스의 화경 기내배양시 자구의 재생과 생장에 미치는 생장조절제의 영향
정용모,김진희,이용문,이영병,이경순 東亞大學校附設遺傳工學硏究所 1997 遺傳工學硏究 Vol.- No.4
히야신스 3품종(Jan Bos, Pink Pearl, Carnegie)의 화경절편들을 조직배양을 통해 자구와 뿌리의 형성능력을 조사해 본 결과 품종에 따라 Murashige & Skoog의 기본 고체배지 또는 IAA 3 ?? + BA 0.1 ??, IAA 3 ?? + BA 1 mg ·L-1, NAA 0.1 ?? + BA 0.1 ??, 그리고 NAA 0.1 ?? + BA 1 mg· L-1의 혼용배지들에서 발근이 된 자구들을 바로 획득할 수 있었는데, 화경의 착화부 조직은 비착화부 조직에 비해 자구의 재생율이 높고 재생기간도 빨랐다. 반면에, 후자의 조직은 전자의 조직에 비해 발근율이 높고 발근기간도 훨씬 빠른 경향을 보였다. 그리고 발근이 된 자구들을 분리시켜 계대배양하는 과정에서 IAA 1 ?? + BA 0.1 ?? 또는 NAA 0.5 ?? + BA 0.1??의 혼용처리는 자구들의 생장을 대체로 촉진시켰지만, 뿌리 생장과 신초의 발육은 억제했다. 그리고 부정근의 형성이 용이치 않은 분리된 자구들은 무처리구에서 발근이 양호하였다. Tissue culture was applied to investigate the regeneration of bulblets on inflorescence stalk segments of Hyacinthus orientalis cvs. Jan Bos, Pink Pearl, and Carnegie. Bulblets with roots were obtained directly on Murashige and Skoog's medium or on basal medium supplemented with 3 ?? IAA + 0.1 ?? BA or 3 ?? IAA+1 ?? BA or 0.1 ?? NAA + 0.1 ?? BA or 0.1 ?? NAA + 1 ?? BA according to cultivars. And the bulblets regeneration ability of inflorescence stalk tissue with inflorescence was higher and the days required for the formation of bulblets was shorter than that of inflorescence satlk tissue without inflorescence, on the contrary, the root formation ability of the latter was higher and the days required for the formation of roots of the latter was much faster than the former. During the subcultures of seperate bulblets with roots, the bulblet growth was generatreatments of 1 ?? IAA + 0.1 ?? BA or 0.05 NAA + 0.1 ?? BA. And the root formation of seperate bulblets without adventitious roots was good on basal medium without growth substances.
Kim, Dong Hwan (Dennis),Lee, Seung-Tae,Won, Hong-Hee,Kim, Seonwoo,Kim, Min-Ji,Kim, Hee-Jin,Kim, Sun-Hee,Kim, Jong-Won,Kim, Hyeoung-Joon,Kim, Yeo-Kyeoung,Sohn, Sang Kyun,Moon, Joon Ho,Jung, Chul Won,Li American Society of Hematology 2011 Blood Vol.117 No.25
<B>Abstract</B><P>In the current study, we identified 2 genetic markers for susceptibility to chronic myeloid leukemia (CML) using a genome-wide analysis. A total of 2744 subjects (671 cases and 2073 controls) were included, with 202 Korean CML patients and 497 control subjects enrolled as a discovery set. Significant findings in the discovery set were validated in a second Korean set of 237 patients and 1000 control subjects and in an additional Canadian cohort of European descent, including 232 patients and 576 control subjects. Analysis revealed significant associations of 2 candidate loci, 6q25.1 and 17p11.1, with CML susceptibility, with the lowest combined P values of 2.4 × 10−6 and 1.3 × 10−12, respectively. Candidate genes in those regions include RMND1, AKAP12, ZBTB2, and WSB1. The locus 6q25.1 was validated in both Korean and European cohorts, whereas 17p11.1 was validated only in the Korean cohort. These findings suggest that genetic variants of 6q25.1 and 17p11.1 may predispose one to the development of CML.</P>
Kim, Hee-Jin,Ahn, Hee Kyung,Jung, Chul Won,Moon, Joon Ho,Park, Chang-Hun,Lee, Ki-O,Kim, Sun-Hee,Kim, Yeo-Kyeoung,Kim, Hyeoung-Joon,Sohn, Sang Kyun,Kim, Sung Hyun,Lee, Won Sik,Kim, Kyoung Ha,Mun, Yeung Springer International 2013 Annals of hematology Vol.92 No.2
<P>Core binding factor (CBF)-positive acute myeloid leukemia (AML) presents a favorable prognosis, except for patients with KIT mutation, especially D816 mutation. The current retrospective study attempted to validate a prognostic role of KIT mutation in 121 Korean patients with CBF AML. The study patients consisted of 121 patients with CBF AML (82 patients with RUNX1/RUNX1T1 [67.8?%] and 39 patients with CBFB/MYH11 [32.2?%]) recruited from eight institutions in Korea. All patients received idarubicin plus cytarabine or behenoyl cytosine arabinoside 3?+?7 induction chemotherapy. The KIT gene mutation status was determined by direct sequencing analyses. A KIT mutation was detected in 32 cases (26.4?%) in our series of patients. The KIT mutation was most frequent in exon 17 (n?=?18, 14.9?%; n?=?16 with D816 mutation), followed by exon 8 (n?=?10, 8.3?%). The presence of KIT D816 mutation was associated with adverse outcomes for the event-free survival (p?=?0.03) and for the overall survival (p?=?0.02). The unfavorable impact of D816 mutation was more prominent when the analysis was confined to the RUNX1/RUNX1T1 subtype. The KIT mutation was detected in 26.4?% of Korean patients with CBF AML. The KIT D816 mutation demonstrated an unfavorable prognostic implication, particularly in the RUNX1/RUNX1T1 subtype.</P>
Polymorphisms involved in the folate metabolizing pathway and risk of multiple myeloma
Kim, Hee Nam,Kim, Yeo-Kyeoung,Lee, Il-Kwon,Lee, Je-Jung,Yang, Deok-Hwan,Park, Kyeong-Soo,Choi, Jin-Su,Park, Moo Rim,Jo, Deog Yeon,Kim, Hyeoung-Joon Wiley Subscription Services, Inc., A Wiley Company 2007 American journal of hematology Vol.82 No.9
<P>Folate and methionine metabolism plays an essential role in both DNA synthesis and methylation. Polymorphisms in the genes of the folate-dependent enzymes have been shown to affect disease susceptibility. We conducted a Korean population-based case-control study to evaluate whether genetic variation in folate metabolism may have a role in the risk of multiple myeloma (MM). The study subjects were 173 patients with MM and 1,700 population-based controls. The polymorphisms studied include methylenetetrahydrofolate reductase (MTHFR) 677 C > T and 1298 A > C, methionine synthase (MS) 2756 A > G, methionine synthase reductase (MTRR) 66A > G, thymidylate synthase (TS) 28-bp repeat (2R→3R) and 6-bp deletion/insertion. MS 2756 AG genotypes were associated with a 1.5-fold lower risk of MM (OR = 0.66, 95%CI; 0.43–0.99, P = 0.047). There was no association between MTHFR C677T, A1298C, MTRR A66G, TS 2R→3R and 6-bp deletion/insertion polymorphisms and MM. These results suggest that MTHFR C677T, A1298C, MTRR A66G, TS 2R→3R, and 6-bp deletion/insertion do not significantly factor into the pathogenesis of MM in the Korean population, but that MS A2756G polymorphism may play an important role. Am. J. Hematol., 2007. © 2007 Wiley-Liss, Inc.</P>
Association between folate-metabolizing pathway polymorphism and non-Hodgkin lymphoma
Kim, Hee Nam,Lee, Il-Kwon,Kim, Yeo-Kyeoung,Tran, Huong Thi Thanh,Yang, Deok-Hwan,Lee, Je-Jung,Shin, Min–,Ho,Park, Kyeong-Soo,Shin, Myung-Geun,Choi, Jin-Su,Kim, Hyeoung-Joon Blackwell Publishing Ltd 2008 British journal of haematology Vol.140 No.3
<P>Summary</P><P>Polymorphisms in the genes coding folate-metabolizing enzymes affect the risk of some forms of cancer. We investigated the association between these polymorphisms and non-Hodgkin lymphoma (NHL) risk in a population-based study (583 cases and 1700 controls). The <I>MTHFR</I> 677TT and CT genotypes were associated with reduced risk for NHL [odds ratios (OR) = 0·79; 95% confidence intervals (CI) = 0·65–0·98 for 677CT and 0·61; 0·45–0·82 for 677TT] and diffuse large B-cell lymphoma (DLBCL) (OR = 0·68; 0·51–0·88 for 677CT; OR = 0·56; 0·38–0·83 for 677TT). The <I>MTHFR</I> 1298CC genotype was associated with increased risk for NHL (OR = 1·71; 1·07–2·75) and T-cell lymphoma (OR = 3·05; 1·53-6·11). The <I>MTRR</I> 66GG genotype was associated with increased risk for DLBCL (OR = 1·56; 1·03-2·38) and the <I>TYMS</I> 2R2R genotype was associated with increased risk for T-cell lymphoma (OR = 2·83; 1·33–6·01). Using subjects with 3RG3RG as a reference group, <I>TYMS</I> 2R2R was associated with increased risk for T-cell lymphoma (OR = 2·46; 1·04–5·79). Interestingly, we observed a reduced association between the <I>TYMS</I> 2R3RG genotype and DLBCL (OR = 0·61; 0·38–0·99). These results suggest that <I>MTHFR</I>, <I>MTRR</I> and <I>TYMS</I> polymorphisms may play a significant role in the risk for NHL.</P>
Kim, Hyoun Sook,Kim, Jieun,Im, Ha Na,Yoon, Ji Young,An, Doo Ri,Yoon, Hye Jin,Kim, Jin Young,Min, Hye Kyeoung,Kim, Soon-Jong,Lee, Jae Young,Han, Byung Woo,Suh, Se Won International Union of Crystallography 2013 Acta crystallographica. Section D, Biological crys Vol.69 No.3
<▼1><P>The crystal structure of <I>M. tuberculosis</I><SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidase (Ldt<SUB>Mt2</SUB>; Rv2518c) has been determined in both ligand-free and meropenem-bound forms. The detailed view of the interactions between meropenem and Ldt<SUB>Mt2</SUB> will be useful in structure-guided discovery of new antituberculosis drugs.</P></▼1><▼2><P>Difficulty in the treatment of tuberculosis and growing drug resistance in <I>Mycobacterium tuberculosis</I> (<I>Mtb</I>) are a global health issue. Carbapenems inactivate <SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidases; meropenem, when administered with clavulanate, showed <I>in vivo</I> activity against extensively drug-resistant <I>Mtb</I> strains. Ldt<SUB>Mt2</SUB> (Rv2518c), one of two functional <SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidases in <I>Mtb</I>, is predominantly expressed over Ldt<SUB>Mt1</SUB> (Rv0116c). Here, the crystal structure of N-terminally truncated Ldt<SUB>Mt2</SUB> (residues Leu131–Ala408) is reported in both ligand-free and meropenem-bound forms. The structure of meropenem-inhibited Ldt<SUB>Mt2</SUB> provides a detailed structural view of the interactions between a carbapenem drug and <I>Mtb</I><SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidase. The structures revealed that the catalytic <SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidase domain of Ldt<SUB>Mt2</SUB> is preceded by a bacterial immunogloblin-like Big_5 domain and is followed by an extended C-terminal tail that interacts with both domains. Furthermore, it is shown using mass analyses that meropenem acts as a suicide inhibitor of Ldt<SUB>Mt2</SUB>. Upon acylation of the catalytic Cys354 by meropenem, the ‘active-site lid’ undergoes a large conformational change to partially cover the active site so that the bound meropenem is accessible to the bulk solvent <I>via</I> three narrow paths. This work will facilitate structure-guided discovery of <SMALL>L</SMALL>,<SMALL>D</SMALL>-transpeptidase inhibitors as novel antituberculosis drugs against drug-resistant <I>Mtb</I>.</P></▼2>
Polymorphisms in DNA Repair Genes and <i>MDR1</i> and the Risk for Non-Hodgkin Lymphoma
Kim, Hee Nam,Kim, Nan Young,Yu, Li,Kim, Yeo-Kyeoung,Lee, Il-Kwon,Yang, Deok-Hwan,Lee, Je-Jung,Shin, Min-Ho,Park, Kyeong-Soo,Choi, Jin-Su,Kim, Hyeoung-Joon Molecular Diversity Preservation International (MD 2014 INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES Vol.15 No.4
<P>The damage caused by oxidative stress and exposure to cigarette smoke and alcohol necessitate DNA damage repair and transport by multidrug resistance-1 (MDR1). To explore the association between polymorphisms in these genes and non-Hodgkin lymphoma risk, we analyzed 15 polymorphisms of 12 genes in a population-based study in Korea (694 cases and 1700 controls). Four genotypes of DNA repair pathway genes (<I>XRCC1</I> 399 GA, <I>OGG1</I> 326 GG, <I>BRCA1</I> 871 TT, and <I>WRN</I> 787 TT) were associated with a decreased risk for NHL [odds ratio (<I>OR</I>)<SUB>XRCC1 GA</SUB> = 0.80, <I>p</I> = 0.02; <I>OR</I><SUB>OGG1 GG</SUB> = 0.70, <I>p</I> = 0.008; <I>OR</I><SUB>BRCA1 TT</SUB> = 0.71, <I>p</I> = 0.048; <I>OR</I><SUB>WRN TT</SUB> = 0.68, <I>p</I> = 0.01]. Conversely, the <I>MGMT</I> 115 CT genotype was associated with an increased risk for NHL (<I>OR</I> = 1.25, <I>p</I> = 0.04). In the <I>MDR1</I> gene, the 1236 CC genotype was associated with a decreased risk for NHL (<I>OR</I> = 0.74, <I>p</I> = 0.04), and the 3435 CT and TT genotypes were associated with an increased risk (<I>OR</I><SUB>3435CT</SUB> = 1.50, <I>p</I> < 0.0001; <I>OR</I><SUB>3435TT</SUB> = 1.43, <I>p</I> = 0.02). These results suggest that polymorphisms in the DNA repair genes <I>XRCC1</I>, <I>OGG1</I>, <I>BRCA1</I>, <I>WRN1</I>, and <I>MGMT</I> and in the <I>MDR1</I> gene may affect the risk for NHL in Korean patients.</P>
Association with TP53 codon 72 polymorphism and the risk of non-Hodgkin lymphoma
Kim, Hee Nam,Yu, Li,Kim, Nan Young,Lee, Il-Kwon,Kim, Yeo-Kyeoung,Yang, Deok-Hwan,Lee, Je-Jung,Shin, Min–,Ho,Park, Kyeong-Soo,Choi, Jin-Su,Kim, Hyeoung-Joon Wiley Subscription Services, Inc., A Wiley Company 2010 American journal of hematology Vol.85 No.10