• Proceedings of the KSME Conference
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• 2004.11a
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• pp.1721-1726
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• 2004

Heat rate is a representative index to estimate the performance of turbine cycle in nuclear power plant. Accuracy of heat rate calculation is dependent on the accuracy of measurement for plant status variables. Uncertainty of heat rate can be modeled using uncertainty propagation model. We developed practical estimation model of heat rate uncertainty using the propagation and regression model. The uncertainty model is used in the performance analysis system developed for the operating nuclear power plant.

• Journal of Life Science
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• v.17 no.6 s.86
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• pp.778-782
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• 2007

The Diphenyleneiodonium (DPI) is widely used as an inhibitor of flavoenzymes, particularly NADPH oxidase. In this study, we investigated the effect of DPI on the cell growth progression of human colon cancer cells HCT-116 (wild-type p53), HT-29 (p53 mutant) and human breast cancer cells MCF-7 (wild-type p53). DPI treatment in cancer cells evoked a dose- and time-dependent growth inhibition, and also induced the cell cycle arrest in C2/M phase. The peak of cell population arrested in C2/M phase was observed at12 hr after treatment of DPI. In addition, DPI significantly induced the expression of p53, which induces proapoptotic genes in response to DNA damage or irreparable cell cycle arrest, at 6 hr in DPI-stimulated cells. However, a catechol apocynin, which inhibits the assembly of NADPH oxidase, did not induce p53 expression. This suggest that p53 expression induced by DPI is not associated with the inhibition of NADPH oxidase. In conclusion, we suggest that DPI induces the expression of wild-type p53 by ROS-in-dependent mechanism in several cancer cells, and upregulated p53 may be involved in regulatory mechanisms for growth inhibition and cell cycle arrest at C2/M phase in DPI-stimulated cells.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2343-2347
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• 2013

Objective: This investigation aimed to determine effects of celecoxib on the cell cycle kinetics of the gastric cancer cell line MGC803 and the mechanisms involved by assessing expression of cytochrome C and caspase-9 at the protein level. Methods: Cell proliferation of MGC803 was determined by MTT assay after treatment with celecoxib. Apoptosis was assessed using fluorescence staining and cell cycle kinetics by flow cytometry. Western blotting was used to detect the expression of caspase-9 protein and of cytochrome C protein in cell cytosol and mitochondria. Results: Celecoxib was able to restrain proliferation and induce apoptosis in a dose- and time-dependent manner, inducing G0/G1 cell cycle arrest, release of cytochrome C into the cytosol, and cleavage of pro-caspase-9 into its active form. Conclusion: Celecoxib can induce apoptosis in MGC803 cells through a mechanism involving cell cycle arrest, mitochondrial cytochrome C release and caspase activation.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.309-313
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• 2009

Spontaneous hypertensive rats (SHR) are an established model of genetic hypertension. Vascular smooth muscle cells (VSMC) from SHR proliferate faster than those of control rats (Wistar-Kyoto rats; WKY). We tested the hypothesis that induction of heme oxygenase (HO)-1 induced by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats. Aprotinin treatment inhibited VSMC proliferation in SHR more than in normotensive rats. These inhibitory effects were associated with cell cycle arrest in the G1 phase. Tin protoporphyrin IX (SnPPIX) reversed the anti-proliferative effect of aprotinin in VSMC from SHR. The level of cyclin D was higher in VSMC of SHR than those of WKY. Aprotinin treatment downregulated the cell cycle regulator, cyclin D, but upregulated the cyclin-dependent kinase inhibitor, p21, in VSMC of SHR. Aprotinin induced HO-1 in VSMC of SHR, but not in those of control rats. Furthermore, aprotinin-induced HO-1 inhibited VSMC proliferation of SHR. Consistently, VSMC proliferation in SHR was significantly inhibited by transfection with the HO-1 gene. These results indicate that induction of HO-1 by aprotinin inhibits VSMC proliferation through cell cycle arrest in hypertensive rats.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.18
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• pp.8313-8319
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• 2016

We have recently shown that thymoquinone (TQ) has a potent cytotoxic effect and induces apoptosis via caspase-3 activation with down-regulation of XIAP in mouse neuroblastoma (Neuro-2a) cells. Interestingly, our results showed that TQ was significantly more cytotoxic towards Neuro-2a cells when compared with primary normal neuronal cells. In this study, the effects of TQ on cell-cycle regulation and the mechanisms that contribute to this effect were investigated using Neuro-2a cells. Cell-cycle analysis performed by flow cytometry revealed cell-cycle arrest at G2/M phase and a significant increase in the accumulation of TQ-treated cells at sub-G1 phase, indicating induction of apoptosis by the compound. Moreover, TQ increased the expression of p53, p21 mRNA and protein levels, whereas it decreased the protein expression of PCNA, cyclin B1 and Cdc2 in a dose-dependent manner. Our finding suggests that TQ could suppress cell growth and cell survival via arresting the cell-cycle in the G2/M phase and inducing apoptosis of neuroblastoma cells.

• Biomolecules & Therapeutics
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• v.16 no.1
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• pp.21-27
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• 2008

Clotrimazole (CLT), a potent antifungal drug, is known to inhibit tumor cell proliferation. In the present study, we examined the role of intracellular $Ca^{2+}$ in CLT-induced cell cycle arrest of colon adenocarcinoma HT29 cells. CLT inhibited growth of HT29 cells in a concentration-dependent manner, which was associated with inhibition of cell cycle progression at the G(1)-S phase transition and an increase in the expression of cell cycle inhibitor proteins p27 and p53. CLT also suppressed the $Ca^{2+}$ overload by A23187, a calcium ionophore, suggesting its role in modulation of intracellular $Ca^{2+}$ concentration in HT29 cells. The simultaneous application of CLT and A23187 with addition of $CaCl_2$ (1mM) to the medium significantly reversed CLT-induced p27 and p53 protein level increase and growth suppression. Our results suggest that CLT induces cell cycle arrest of colon adenocarcinoma HT29 cells via induction of p27 and p53, which may, at least in part, be mediated by alteration of intracellular $Ca^{2+}$ level.

• Journal of Plant Biology
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• v.30 no.4
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• pp.299-309
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• 1987

The seasonal pattern and the annual magnitude of the internal (or biochemical) and plant-soil cycles of phophorus in adjacent three different herb plant populations-Helianthus tuberosus L., Artemisia princeps Pampan and Phalaris anundinacea L.-in an old field of the basin in the Mt. Geumoh were investigated. A lot of the phosphorus demand for the three populations was supplied by the withdrawal from below-ground organ in early growing period, by the absorption from soil in mid-growing period and by the withdrawal from stem in later growing period. But in the A. princeps and P. arundianacea populations, a great deal of phosphorus seemed to be absorbed prior to the first withdrawal. The annual amount of the phosphorus flowing throughthe internal cycle was about 59% of the total hosphorus flow on theorgan level in the H. tuberosus population, 41% in the A. princeps population and 32% in the P. arundinacea population, indicating that the tuber plant had the most developed internal cycle system. The annual amount of phosphorus which took part in the plant-soil cycle in the stand of the three populations was in the range of 4.49-5.65 gPm-2, corresponding to only 3-8% of the extractable phosphorus contained in the soil of 0-20 cm depth. The fact that the H. tuberosus population is higher in the extent fo internal cycle but smaller in the magnitude of plant-soil cycle and lower in the turnover rate of phsophorus than the other two populations suggests that the growth of H. tuberosus population may be less dependent on soil phosphorus availability than those of the other two populations.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.328.1-328.1
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• 2002

A major lipid-signaling pathway in mammalian cells implicated the activation of sphingomyelinase (SMase), which hydrolyses sphingomyeline to generate ceramide and phosphocholine. Sphingomyelinase is divided into many isoform groups dependent on optimal pH, and essential cation especially magnesium in their activation. Such as acidic sphingomyelinase, neutral sphingomyelinase and alkaline sphingomyelinase. Ceramide is known as a crucial second messenger in cell responses like cell proliferation. cell cycle arrest. cellular senescence, and apoptosis. (omitted)

• Journal of Life Science
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• v.15 no.5 s.72
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• pp.726-733
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• 2005

Histone deacetylase (HDAC) inhibitors target key steps of tumor development. They inhibit proliferation, induce differentiation and/or apoptotic cell death, and exhibit potent antimetastatic and antiangiogenic properties in cancer cells in vitro and in vivo. Although they are emerging as a promising new treatment strategy in malignancy, how they exert their effect on human non-small cell lung cancer cells is as yet unclear. The present study was undertaken to investiate the underlying mechanism of a HDAC inhibitor trichostatin A (TSA)-induced growth arrest and its effect on the cell cycle control gene products in a human lung carcinoma cell line A549. TSA treaoent induced the growth inhibition and morphological changes in a concentration-dependent manner. Treatment of A549 cells with TSA resulted in a concentration-dependent increased G1 (under 100 ng/ml) and/or G2/M (200 ng/ml) cell population of the cell cycle as determined by flow cytometry Moreover, 200 ng/ml TSA treatment significantly induced the population of sub-G1 cells (23.0 fold of control). This anti-proliferative effect of TSA was accompanied by a marked inhibition of cyclins, positive regulators of cell cycle progression, and cyclin-dependent kinases (Cdks) expression and concomitant induction of tumor suppressor p53 and Cdk inhibitors such as p21 and p27 Although further studies are needed, these findings provide important insights into the possible molecular mechanisms of the anti-cancer activity of TSA in human lung carcinoma cells.

• THE JOURNAL OF KOREAN ORIENTAL ONCOLOGY
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• v.6 no.1
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• pp.99-111
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• 2000

Objectives: Hedyotis diffusa is used to treat cancer in traditional Korea Medicine. So this study was carried out to examine the expression of cell cycle related genes in HL-60 cells undergoing apoptosis by the methanol extract of Hedyotis diffusa. Methods: 1. HL-60 cells were treated with various concentrations (from 200 to $50{\mu}g/ml$)of methanol extract and H20 extract ($200{\mu}g/ml$) of hedyotis diffusa. After 48 h later, the cells were tested for viability by MTT assay. 2. The HL-60 cells were treated with $200{\mu}g/ml$ of methanol extract for the indicated periods. The whole cell lysates were prepared and analyzed by western blotting using anti-p53 antibody. 3. The nuclear extract were prepared and analyzed by western blotting using anti-p21 antibody, anti-p27 antibody, anti-cyclin A antibody, anti-cyclin E antibody and anti-CDK2 antibody. Results: 1. The methanol extract of Hedyotis diffusa induced the death of HL-60 cells in a dose dependent manner. 2. The methanol extract of Hedyotis diffusa makedly decreased the level of p21/Cipl and cyclin A in a time dependent manner. 3. The methanol extract of Hedyotis diffusa markedly increased the level of p27/Kipl and cyclin E in a time dependent manner. 4. The methanol extract of Hedyotis diffusa markedly did not affect the level of CDK2. Conclusions: These results provide evidence that expression of cell cycle related genes in HL-60 cells undergoing apoptosis by the methanol extract of Hedyotis diffusa mainly results from decreased level of p21/Cipl and increased level of p27/Kipl of the cell cycle related genes.