• The Bulletin of The Korean Astronomical Society
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• v.36 no.2
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• pp.143.2-143.2
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• 2011

보현산천문대 1.8 m 망원경과 2K CCD를 이용하여 2002년 4월과 2003년 5월에 중원소 함량이 아주 적은 구상성단 M53(NGC 5024)과 M92(NGC 6341)에 대하여 BVI CCD 측광관측을 수행하였다. 구상성단 M53과 M92의 정밀한 상대 나이 측정을 위하여 M53의 측광관측 자료에 대해 조동환과 이상각이 2007년 출간한 구상성단 M15(NGC 7078)와 M92를 대상으로 수행한 측광연구 논문에서 M92의 측광관측 자료를 분석할 때 적용한 꼭 같은 방식으로 전처리, PSF 측광, 표준화 등의 자료 분석을 수행하였다. 그리고 구상성단 M53의 V 대 BV, V 대 V-I, 그리고 V 대 B-I 색-등급도를 제시하였다. 구상성단 M53과 M92의 상대 나 이는 ${\Delta}$(B-V) 방법을 이용하여 도출하였다. 구상성단 M53과 M92 사이의 상대 나이 비교에서 M92의 절대 나이를 14 Gyr로 취할 경우 M53의 상대 나이가 M92의 상대 나이보다 $1.1-2.6{\pm}0.9$ Gyr 적은 것으로 유도하였다. 구상성단 M53과 M92의 이 상대 나이 차이는 M53과 M92의 약간 다른 수평계열 형태 차이를 유발했을 것으로 추정한다.

• Journal of The Korean Astronomical Society
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• v.49 no.5
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• pp.175-192
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• 2016

CCD photometric observations of the globular cluster (GC), M53 (NGC 5024), are performed using the 1.8 m telescope at the Bohyunsan Optical Astronomy Observatory in Korea on the same nights (2002 April and 2003 May) as the observations of the GC M92 (NGC 6341) reported by Cho and Lee using the same instrumental setup. The data for M53 is reduced using the same method as used for M92 by Cho and Lee, including preprocessing, point-spread function fitting photometry, and standardization etc. Therefore, M53 and M92 are on the same photometric system defined by Landolt, and the photometry of M53 and M92 is tied together as closely as possible. After complete photometric reduction, the V versus B − V , V versus V − I, and V versus B − I color-magnitude diagrams (CMDs) of M53 are produced to derive the relative ages of M53 and M92 and derive the various characteristics of its CMDs in future analysis. From the present analysis, the relative ages of M53 and M92 are derived using the Δ(B − V ) method reported by VandenBerg et al. The relative age of M53 is found to be 1.6 ± 0.85 Gyr younger than that of M92 if the absolute age of M92 is taken to be 14 Gyr. This relative age difference between M53 and M92 causes slight differences in the horizontal-branch morphology of these two GCs.

• Journal of Microbiology and Biotechnology
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• v.16 no.8
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• pp.1262-1268
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• 2006

In the search for a novel cytotoxic substance from medicinal plants, HY53 ($C_{17}H_{32}O_2N_2$; molecular weight 296) was isolated from the leaves of Pata de Vaca (Bauhinia forficata). The growth of the HepG2 cells was inhibited in a dose-dependent manner when treated with 0.07 to 0.40 mM HY53 for 24 h (IC$_{50}$: 0.13 mM). Furthermore, nuclear DAPI staining revealed the typical nuclear features of apoptosis in the HepG2 cells exposed to 0.27 mM HY53, whereas a flow cytometric analysis of the HepG2 cells using propidium iodide showed that the apoptotic cell population increased gradually from 8% at 0 mM to 23% at 0.14 mM and 45% at 0.40 mM after being exposed to each concentration of HY53 for 24 h. Moreover, a TUNEL assay also exhibited the apoptotic induction of the HepG2 cells treated with HY53. To obtain further information on the HY53-induced apoptosis, the expression level of certain apoptosis-associated proteins was examined using a Western blot analysis. Treatment of the HepG2 cells with HY53 resulted in the activation of caspase-3, and subsequent proteolytic cleavage of poly(ADP-ribose) polymerase (PARP). Consequently, the results confirmed that the apoptosis in the HepG2 cells was induced by HY53 and the involvement of caspase-3-mediated PARP cleavage in the apoptotic process.

• Molecules and Cells
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• v.40 no.5
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• pp.322-330
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• 2017

This study investigated the role of cancer/testis antigen DDX53 in regulating cancer stem cell-like properties. DDX53 shows co-expression with CD133, a marker for cancer stem cells. DDX53 directly regulates the SOX-2 expression in anti-cancer drug-resistant $Malme3M^R$ cells. DDX53 and miR-200b were found to be involved in the regulation of tumor spheroid forming potential of Malme3M and $Malme3M^R$ cells. Furthermore, the self-renewal activity and the tumorigenic potential of $Malme3M^R$-CD133 (+) cells were also regulated by DDX53. A miR-200b inhibitor induced the direct regulation of SOX-2 by DDX53 We therefore, conclude that DDX53 may serve as an immunotherapeutic target for regulating cancer stem-like properties of melanomas.

• Journal of Chest Surgery
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• v.40 no.2 s.271
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• pp.114-121
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• 2007

Background: Apoptosis plays a crucial role in carcinogenesis, as well as in development and tissue homeostasis. Terminal deoxyribonucleotidyl transferase mediated neck end labelling (TUNEL) and in situ nick end labelling (ISEL) have been used to investigate the apoptosis in tissues. Since the introduction of the M30 monoclonal antibody to overcome drawbacks of TUNEL and ISEL, the apoptosis in various tumors, with the exception of pulmonary carcinomas, has been studied. In this study, attempts were made to examine the correlation of apoptosis in non-small cell carcinomas, using both M30 and the expression of p53 protein, with the clinicopathological factors. Material and Method: Forty five patients with surgically resected non-small cell carcinomas were included. Immunohistochemical staining with M30 and p53 monoclonal antibody were peformed, and their expressions compared with the clinicopathological features. The overall survival time and recurrence-free survival time were calculated, and the factors influencing the survival time analyzed using a univariate analysis. The effects of the expression stati of M30 and p53 on the risks of cancer related to both death and recurrence were evaluated using a multivariate analysis. Result: The p53 positive group had many more M30 positive cells than the p53 negative group (p53 positive group; $61.7{\pm}26.8$ cells vs. p53 negative group; $45.6{\pm}29.6$ cells, p=0.005) and significantly more p53 positive patients showing at least 10 positive cells (apoptotic index, $Al{\ge}1$) on M30 staining (p53 positive group; 52.4% (11/21) vs. p53 negative group 16,7% (4/24), p=0.025). In the univariate analysis, the survival times in relation to smoking (pack-year), performance status (PS) and Al showed significant differences. The multivariate analysis demonstrated the relative risk (R.R) of cancer death increased almost 7.5-fold (R.R 7.482; 95% Cl $1.886{\sim}29.678$; p=0.004) and the risk of recurrence almost 3,8-fold (R.R 3.795; 95% Cl: $1.184{\sim}12.158$; p=0.025) in the high Al (${\ge}1$) compared to the low Al (<1) group. There was no prognostic effect of p53 expression on the survival time or risk of cancer death and recurrence. Conclusion: In non-small cell lung carcinomas, M30 immunohistochemistry was an excellent method for analyzing apoptosis; the high apoptotic index could be an adverse prognostic predictive factor.

• Environmental Analysis Health and Toxicology
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• v.25 no.4
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• pp.273-278
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• 2010

Objectives : This study was aimed to examine the acute toxicity assessment of two new algicides, thiazolidinediones derivatives (TD53 and TD49), which were synthesized to selectively control red tide, to the marine ecosystem. Methods : The assessment employed by a new method using Ulva pertusa Kjellman which has been recently accepted as a standard method of ISO. The toxicity was assessed by calculating the $EC_{50}$ (Effective Concentration of 50%), NOEC (No Observed Effect Concentration) and PNEC (Predicted No Effect Concentration) using acute toxicity data obtained from exposure experiments. $EC_{50}$ value of TD49 and TD53 was examined by 96-hrs exposure together with Solutol as a TD49 dispersing agent and DMSO as a TD53 solvent. Results : $EC_{50}$ value of TD53 was $1.65\;{\mu}M$. From the results, values of NOEC and PNEC were calculated to be $0.63\;{\mu}M$ and 1.65 nM, respectively. DMSO under the range of $0{\sim}10\;{\mu}M$, which is same solvent concentration used in examining TD53, showed no toxic effect. $EC_{50}$ value of TD49 was $0.18\;{\mu}M$ and that of Solutol was $1.70\;{\mu}M$. NOEC and PNEC of TD49 were $0.08\;{\mu}M$ and 0.18 nM, respectively and those for Solutol were $1.25\;{\mu}M$ and 1.25 nM, respectively. Conclusions : From the values of NOEC, PNEC of TD53 and TD49, TD49 showed 9 times stronger toxicity than TD53. On the other hand, DMSO showed no toxicity on the Ulva pertusa Kjellman, but Solutol was found to be a considerable toxicity by itself.

• Tuberculosis and Respiratory Diseases
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• v.53 no.3
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• pp.275-284
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• 2002

Background : Gemcitabine is a new anti-cancer agent for treating non-small cell lung cancer. Functioning as an antimetabolite, it induces anti-cancer effects by suppressing DNA synthesis after being incorporated into the DNA as a cytosine arabinoside analogue. When Gemcitabine is incorporated into the DNA, the p53 gene may be activated by induction of the DNA defect. However, there are a few studies on the molecular mechanisms of Gemcitabine-induced cell death. This study examined the role of p53 in Gemcitabine-induced cell death. Methods : A549 and NCl-H358 lung cancer cells were used in this study. The cell viability test was done using a MTT assay at Gemcitabine concentrations of 10nM, 100nM, 1uM, 10uM and 100uM. A FACScan analysis with propium iodide staining was used for the cell cycle analysis. Western blot analysis was done to investigate the extent of p53 activation. For the functional knock-out of p53, stable A549-E6 cells and H358-E6 cells were transfected pLXSN-16E6SD which is over expresses the human papilloma virus E6 protein that constantly degrades p53 protein. The functional knock out of p53 was confirmed by Western blot analysis after treatment with a DNA damaging agent, doxorubicine. Results : Gemcitabine exhibited cell toxicity in dose-dependent fashion. The cell cycle analysis resulted in an S phase arrest. Western blot analysis significant p53 activation in time-dependent manner. Gemcitabine-induced cytotoxicity was reduced by 20-30% in the A549-E6 cells and the 30-40% in H358-E6 cells when compared with the A549-neo and H358-neo control cells. Conclusion : Gemcitabine induces an S phase arrest, as expected for the anti-metabolite, and activates the p53 gene, Furthermore, p53 might play an important role in Gemcitabine-induced cell death. Further investigation into the molecular mechanisms on how Gemcitabine activates the p53 gene and its signaling pathway are recommended.

• Biomedical Science Letters
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• v.13 no.2
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• pp.75-81
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• 2007

Sodium salicylate (NaSal), a chemopreventive drug, has been shown to induce apoptosis and cell circle arrest depending on its concentrations in a variety of cancer cells. In A549 cells, low concentration of NaSal (5$\sim$10 mM) induces cell cycle arrest, whereas it induces apoptosis at higher concentration of 20 mM. In the present study, we examined the molecular mechanism for NaSal-induced cell cycle arrest. NaSal induced expression of p53, p21 (Wafl/Cipl), and p27 (Kipl) that play important roles in cell cycle arrest. p53 induction was mediated by its phosphorylation at Ser-15 that could be prevented by the PI3K-related kinase (ATM, ATR and DNA-PK) inhibitors including wortmannin, caffeine and LY294002. In addition, NaSal-induction of p2l (Wafl/Cipl) was detected in P53 (+/+) wild type A549 cells but not in p53 (-/-) mutant H1299 cells, indicating p53-dependent p21 (Wafl/Cipl) induction. In contrast, p27 (Kipl) that is a negative regulate. of cell cycle with p21 (Wafl/Cipl) was observed both in A549 cells and H1299 cells. Thus, 5 mM NaSal appeared to cause cell cycle arrest through inducing the cyclin-dependent kinase inhibitor p21 (Wafl/Cipl) via PI3K-related protein kinase-dependent p53 activation as well as by up-regulating p27 (Kipl) independently of p53 in A549 cells.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.6
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• pp.365-369
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• 2010

In this study, we examined whether melatonin promotes apoptotic cell death via p53 in prostate LNCaP cells. Melatonin treatment significantly curtailed the growth of LNCaP cells in a dose- and time-dependent manner. Melatonin treatment (0 to 3 mM) induced the fragmentation of poly(ADP-ribose) polymerase (PARP) and activation of caspase-3, caspase-8, and caspase-9. Moreover, melatonin markedly activated Bax expression and decreased Bcl-2 expression in dose increments. To investigate p53 and p21 expression, LNCaP cells were treated with 0 to 3 mM melatonin. Melatonin increased the expressions of p53, p21, and p27. Treatment with mitogen-activated protein kinase (MAPK) inhibitors, PD98059 (ERK inhibitor), SP600125 (JNK inhibitor) and SB202190 (p38 inhibitor), confirmed that the melatonin-induced apoptosis was p21-dependent, but ERK-independent. With the co-treatment of PD98059 and melatonin, the expression of p-p53, p21, and MDM2 did not decrease. These effects were opposite to the expression of p-p53, p21, and MDM2 observed with SP600125 and SB202190 treatments. Together, these results suggest that p53-dependent induction of JNK/p38 MAPK directly participates in apoptosis induced by melatonin.

• Journal of Korean Society of Environmental Engineers
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• v.29 no.1
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• pp.82-88
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• 2007

The objective of this study is to examine the effect of the waste oyster shell powder as the addition agent in bulking sludge thickening of paper manufacturing plant using DAF(Dissolved Air Flotation) and gravitational sedimentation. The effect of parameters such as dosage and size distribution of oyster shell were examined. The results showed that the optimum dosage of mixed oyster shell(size range : $\sim250{\mu}m$) was 0.8 g/L. The oyster shell addition of 5.0 g/L in sedimentation process was increased thickening concentration of 3.25 times. When 5.0 g/L of oyster shell was added in DAF process, water content of sludge was decreased from 95.5% to 82.7% in dewatering process using Buchner funnel test device. When size of oyster shell was divided four ranges($\sim53{\mu}m$, $53\sim106{\mu}m$, $106\sim150{\mu}m$, $150\sim250{\mu}m$), optimum size range for the flotation and dewatering was $53\sim106{\mu}m$.