• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2003년도 춘계학술대회 논문집
• /
• pp.13-14
• /
• 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)

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
• /
• pp.90-90
• /
• 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)

• 한국독성학회:학술대회논문집
• /
• 한국독성학회 2001년도 International Symposium on Dietary and Medicinal Antimutgens and Anticarcinogens
• /
• pp.137-138
• /
• 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
• /
• 제15권22호
• /
• pp.9967-9972
• /
• 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.

• 한국수자원학회논문집
• /
• 제36권2호
• /
• pp.153-159
• /
• 2003

I-D-F곡선을 유도할 때 강우자료의 보유연한이 충분하지 않을 경우 지속시간별 강우강도의 변화가 매끄럽게 연결되지 못하는 경우가 발생하기도 한다. 특히 곡선에서, 상대적인 장시간에 강우강도가 크게 되는 문제는 실무적으로 I-D-F 곡선을 이용하는데 큰 혼란을 야기 시킨다. 본 연구에서는 강우자료를 Box-Cox변환을 이용하여 지속시간과 강우강도의 상관관계를 통해 이러한 문제를 해결하는 방법을 제시한다. 산청과 영천의 강우자료에 대한 분석결과 Box-Cox 변환의 실효성을 확인할 수 있었다.

• IMMUNE NETWORK
• /
• 제11권6호
• /
• pp.364-367
• /
• 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.

• 응용통계연구
• /
• 제31권6호
• /
• pp.761-769
• /
• 2018

통계학 연구에 모의실험이 중요하게 쓰이며 중도절단자료를 다루는 생존분석에서도 마찬가지다. 생존분석에서 Cox 모형이 널리 쓰이는데, Cox 모형을 따르는 중도절단자료를 생성하는 방법에 대해 살펴보았다. Bender 등 (Statistics in Medicine, 24, 1713-1723, 2005)은 생존시간을 생성하는 모수적 방법을 제시하였으나 생존시간뿐만 아니라 중도절단시간도 생성해야 중도절단자료를 얻게 된다. 중도절단자료를 생성하기 위한 모수적 방법과 함께 비모수적 방법도 제시하였으며 실제 자료에도 적용해 보았다.

• Molecules and Cells
• /
• 제37권10호
• /
• pp.759-765
• /
• 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.

• 응용통계연구
• /
• 제25권2호
• /
• pp.279-291
• /
• 2012

공변량에 결측이 발생한 Cox 비례위험 모형을 적합할 때, 결측이 발생하는 개체를 모두 제거한 후 분석을 실시한다면 정보 손실에 의해 비효율적이고 결측의 발생 메커니즘이 완전 임의 결측(missing completely at random; MCAR)이 아니라면 모수의 추정값에 편향이 발생할 수 있다. Cox 비례위험 회귀모형의 공변량에 결측이 있는 경우 적용할 수 있는 여러 가지 방법들이 제안되어져 왔으나 이 분석들은 선택모델(selection model)에 기반하고 있다. 본 연구에서는 Little (1993)이 제안한 패턴-혼합 모델(pattern-mixture model)을 사용하여 Cox 비례위험 회귀모형에서 생존시간과 결측 메커니즘의 결합분포를 모델화 하고, 여러 가지 제약에 근거한 생존 분석의 결과를 비교하였다. 모의실험을 통해서 패턴-혼합 모델의 제약(restrictions)에 따른 모수 추정의 민감도를 확인하였고 결측을 무시한 채 분석한 결과 및 선택모형에 근거한 분석결과와 비교하였다. 패턴-혼합 모델의 제약에 따라 공변량의 결측으로 인한 모수 추정의 민감성 정도를 쥐백혈병 자료 예제를 통해 설명하였다.

• 약학회지
• /
• 제51권5호
• /
• pp.313-317
• /
• 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.