• Proceedings of the Korean Society of Toxicology Conference
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• 2003.05a
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• pp.13-14
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• 2003

Ceramide, a potential cell death marker formed by sphingomyelinase, is involved in the expression of cyclooxygenase-2 (COX-2). This study examines the effect of C2-ceramide (C2), a cell-permeable ceramide analog, on the LPS-inducible COX-2 expression and signaling pathways. C2 did not induce COX-2, but potentiated LPS-inducible COX-2 expression in Raw264.7 cells, whereas dihydro-C2 was inactive.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.90-90
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• 2002

In order to understand the mechanism of action of TCDD, we have examine the effect of COX-inhibitors on Cyp1a1 activity. We observed the effect of COX-inhibitor on EROD activity in C57BL/6 mouse in vovo. And we also evaluated the effect of COX-inhibitors on mouse cyp1a1 promoter activity in Hepa cell.(omitted)

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.137-138
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• 2001

There has been accumulating evidence for the association of inflammatory tissue damage with the process of cancer development. Cyclooxygenase (COX), an important enzyme involved in mediating the inflammation, catalyzes the formation of prostaglandins (PGs) from arachidonic acid. There are two isoforms of COX, designated as COX-l and COX-2. COX-l is a housekeeping enzyme which is constitutively expressed and is thought to be involved in maintaining physiological functions.(omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.22
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• pp.9967-9972
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• 2014

In order to prove whether downregulation of COX-2 (Cyclooxygenase-2) could modulate the epithelial-mesenchymal transition (EMT) of breast cancer, celecoxib and siRNA were respectively used to inhibit COX-2 function and expression in MDA-MB-231 cells. The EMT reversal effect in the RNAi treated group was better than that of the celecoxib group while there were no obvious differences in the medium $PGE_2$ levels between the two groups. The results show that COX-2 pathways may contribute considerably to EMT of breast cancer cells, partially dependent on the PGE2 cascade. Akt2, ZEB2 and Snail were measured to clarify the underlying mechanisms of COX-2 on EMT; COX-2 may modulate EMT of breast cancer by regulating these factors. This finding may be helpful to elucidate the mechanisms of selective COX-2 inhibitor action in EMT modulation in breast cancer.

• Journal of Korea Water Resources Association
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• v.36 no.2
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• pp.153-159
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• 2003

When available rainfall data is not sufficient, a rough tendency of I-D-F relationship appeared frequently. In fact, rainfall intensity on the curve shows abnormally higher value the longer rainfall duration is applied that gives rise to great confusion to apply a rainfall I-D-F relationships curve to a practical work, however, the research work will present a way to solve above mentioned problem by the use of the Box-Cox transformation formula for a given rainfall data. The study came to a conclusion that the Box-Cox transformation formula is satisfied to utilize in a practical work on the ground of analysis for rainfall data of Sancheong and Yeongcheon.

• IMMUNE NETWORK
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• v.11 no.6
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• pp.364-367
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• 2011

Background: Prostaglandins (PGs) play pathogenic and protective roles in inflammatory diseases. The novel concept of PGs as immune modulators is being documented by several investigators. By establishing an in vitro experimental model containing human follicular dendritic cell-like cells, HK cells, we reported that HK cells produce prostaglandin $E_2$ ($PGE_2$) and prostaglandin $I_2$ ($PGI_2$) and that these PGs regulate biological functions of T and B cells. Methods: To investigate the respective contribution of cyclooxygenase-1 (COX-1) and COX-2 to $PGE_2$ and $PGI_2$ production in HK cells, we performed siRNA technology to knock down COX enzymes and examined the effect on PG production. Results: Both $PGE_2$ and $PGI_2$ productions were almost completely inhibited by the depletion of COX-2. In contrast, COX-1 knockdown did not significantly affect PG production induced by lipopolysaccharide (LPS). Conclusion: The current results suggest that mPGES-1 and PGIS are coupled with COX-2 but not with COX-1 in human follicular dendritic cell (FDC) and may help understand the potential effects of selective COX inhibitors on the humoral immunity.

• The Korean Journal of Applied Statistics
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• v.31 no.6
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• pp.761-769
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• 2018

Simulations are important for survival analyses that deal with censored data. Cox models are widely used in survival analyses, therefore, we investigate how to generate censored data that can simulate the Cox model. Bender et al. (Statistics in Medicine, 24, 1713-1723, 2005) provided a parametric method for generating survival times, but we need to generate censoring times as well as survival times to simulate the censored data. In addition to the parametric method for generating censored data, a nonparametric method is also proposed and applied to a real data set.

• Molecules and Cells
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• v.37 no.10
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• pp.759-765
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• 2014

N-myc downstream-regulated gene 2 (NDRG2), which is known to have tumor suppressor functions, is frequently down-regulated in breast cancers and potentially involved in preventing the migration and invasion of malignant tumor cells. In the present study, we examined the inhibitory effects of NDRG2 overexpression, specifically focusing on the role of cyclooxygenase-2 (COX-2) in the migration of breast cancer cells. NDRG2 overexpression in MDA-MB-231 cells inhibited the expression of the COX-2 mRNA and protein, the transcriptional activity of COX-2, and prostaglandin $E_2$ ($PGE_2$) production, which were induced by a treatment with phorbol-12-myristate-13-acetate (PMA). Nuclear transcription factor-${\kappa}B$ (NF-${\kappa}B$) signaling attenuated by NDRG2 expression resulted in a decrease in PMA-induced COX-2 expression. Interestingly, the inhibition of COX-2 strongly suppressed PMA-stimulated migration and invasion in MDA-MB-231-NDRG2 cells. Moreover, siRNA-mediated knockdown of NDRG2 in MCF7 cells increased the COX-2 mRNA and protein expression levels and the PMA-induced COX-2 expression levels. Consistent with these results, the migration and invasion of MCF7 cells treated with NDRG2 siRNA were significantly enhanced following treatment with PMA. Taken together, our data show that the inhibition of NF-${\kappa}B$ signaling by NDRG2 expression is able to suppress cell migration and invasion through the down-regulation of COX-2 expression.

• The Korean Journal of Applied Statistics
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• v.25 no.2
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• pp.279-291
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• 2012

When fitting a Cox proportional hazards model with missing covariates, it is inefficient to exclude observations with missing values in the analysis. Furthermore, if the missing-data mechanism is not Missing Completely At Random(MCAR), it may lead to biased parameter estimation. Many approaches have been suggested to handle the Cox proportional hazards model when covariates are sometimes missing, but they are based on the selection model. This paper suggest an approach to handle Cox proportional hazards model with missing covariates by using the pattern-mixture model (Little, 1993). The pattern-mixture model is expressed by the joint distribution of survival time and the missing-data mechanism. In the pattern-mixture model, many models can be considered by setting up various restrictions, and different results under various restrictions indicate the sensitivity of the model due to missing covariates. A simulation study was conducted to show the sensitivity of parameter estimation under different restrictions in a pattern-mixture model. The proposed approach was also applied to mouse leukemia data.

• YAKHAK HOEJI
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• v.51 no.5
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• pp.313-317
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• 2007

A series of luotonin A homologues and their aza-analogues were prepared and evaluated their inhibitory activities on COX-1 and 2 as well as their selectivities on COX-2. The aza-analogue of dimethylene-bridged homologue of luotonin A, 3,3'-dimethylene-2-(1',8'-naphthyrid-2'-yl)-4(3H)-quinazolinone (2b), exhibited strongest inhibitory activity against COX-1 and COX-2 dependent phase of prostaglandin $D_2$ generation in mouse bone marrow-derived mast cells in a concentration-dependent manner with an $IC_{50}$ of 39.3 and $1.89{\mu}M$, respectively. Selectivity of 2b on COX-2 over COX-1 was 21 which implied 2b can be a potential lead for the development of selective COX-2 inhibitor.