• Title/Summary/Keyword: Cox

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Effect of Progesterone on COX-2 Expression and Proliferation of Prostate Stromal Cell (전립선 기질세포의 증식과 COX-2 발현에 대한 프로게스테론의 영향)

  • Jung, Soo-Ryun;Kim, Sung-Han;Choi, E-Hwa;Park, Ji-Eun;Jeon, Eun-Mi;Kang, Young-Jin;Lee, Kwang-Youn;Choi, Hyoung-Chul
    • Journal of Yeungnam Medical Science
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    • v.23 no.1
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    • pp.62-70
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    • 2006
  • Background: Benign prostatic hyperplasia (BPH) is the most common benign tumor in older men; the etiology of this disease remains poorly understood. Testosterone and dihydrotestosterone (DHT) both act as androgen via a single androgen receptor. Testosterone is converted to DHT by $5{\alpha}$-reductase in prostatic stromal cells. Progesterone has been reported to inhibit DHT conversion; howevwe, its effect on prostatic stromal cells remains to be elucidated. Materials and Methods: In this experiment, we investigated the effect of progesterone on androgen receptor expression induced by DHT. We also tested the effect of progesterone on cyclooxygenase-2 (COX-2) expression, as well as prostate stromal cell proliferation using the cell count kit-8. Results: Progesterone did not cause an increase of prostate stromal cell proliferation. The mRNA expression of the androgen receptor and COX-2 were not changed by progesterone; the expressions of androgen receptor and COX-2 proteins were decreased by progesterone in prostate stromal cells. Conclusion: These results suggest that in prostate stromal cells, progesterone decreases androgen receptor protein expression, which results in decrement of COX-2 protein expression. This effect might be mediated by post-transcriptional regulation.

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Co-occurrence of Matsumuraeses falcana and M. phaseoli (Lepidoptera: Tortricidae) in Soybean Fields, and Polymorphism of Cytochrome c Oxidase Subunit 1 Gene Nucleotide (콩 포장에서 어리팥나방과 팥나방(나비목: 잎말이나방과)의 동시 발생과 시토크롬 c 산화효소 1 유전자 염기서열의 다형성)

  • Jin Kyo, Jung;Eun Young, Kim;Taeman, Han
    • Korean journal of applied entomology
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    • v.61 no.4
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    • pp.641-649
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    • 2022
  • Leaf-rolling moths were collected from soybean fields and identified as Matsumuraeses falcana and Matsumuraeses phaseoli by comparison with laboratory-reared species based on the nucleotide sequence (658 bp) of the mitochondrial cytochrome c oxidase 1 subunit gene (COX1). Ten haplotypes with 0.15-0.46% genetic distance from each other in COX1 were found in 47 samples of M. falcana, in which haplotype A was dominant (approximately 70%). Only one type of COX1 was found in 30 samples of M. phaseoli, and its sequence showed 4.11-4.61% genetic distance from those of M. falcana. Amino acid sequences translated from COX1 were identical in all samples of both species, and they showed synonymous substitutions. Larvae of both species caused damage to soybean leaves and pods and co-occurred simultaneously in the field. The average density of M. falcana was 1.5 times higher than that of M. phaseoli. The results clearly indicate that soybean was the host plant for both species. In addition, Elodia flavipalpis (Diptera: Tachinidae) was found to be a larval parasitoid of Matsumuraeses sp. through identification of the COX1 gene.

Propensity score methods for estimating treatment delay effects (생존자료분석에서 성향 점수를 이용한 treatment delay effect 추정법에 대한 연구)

  • Jooyi Jung;Hyunjin Song;Seungbong Han
    • The Korean Journal of Applied Statistics
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    • v.36 no.5
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    • pp.415-445
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    • 2023
  • Oftentimes, the time dependent treatment covariate and the time dependent confounders exist in observation studies. It is an important problem to correctly adjust for the time dependent confounders in the propensity score analysis. Recently, In the survival data, Hade et al. (2020) used a propensity score matching method to correctly estimate the treatment delay effect when the time dependent confounder affects time to the treatment time, where the treatment delay effects is defined to the delay in treatment reception. In this paper, we proposed the Cox model based marginal structural model (Cox-MSM) framework to estimate the treatment delay effect and conducted extensive simulation studies to compare our proposed Cox-MSM with the propensity score matching method proposed by Hade et al. (2020). Our simulation results showed that the Cox-MSM leads to more exact estimate for the treatment delay effect compared with two sequential matching schemes based on propensity scores. Example from study in treatment discontinuation in conjunction with simulated data illustrates the practical advantages of the proposed Cox-MSM.

Androgen Hormone Inhibits Expression of iNOS and COX-2 Protein in Rat Vascular Smooth Muscle Cell

  • Bae, Hwa-Young;Park, Ji-Eun;Jeon, Eun-Mi;Kang, Young-Jin;Lee, Kwang-Youn;Choi, Hyoung-Chul
    • The Korean Journal of Physiology and Pharmacology
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    • v.9 no.4
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    • pp.215-221
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    • 2005
  • We investigated the effects of testosterone and dihydrotestosterone on inflammatory response of iNOS and COX-2 expression in rat vascular smooth muscle cells. Rat vascular smooth muscle cells (VSMC) stimulated with bacterial lipopolysaccharide $(LPS;\;10{\mu}g/ml)$ for 24 hours were incubated with increasing amounts of testosterone and dihydrotestosterone (1 and 100 nM). LPS was found to induce inflammatory response of iNOS and COX-2 mRNA and protein in VSMC. These processes were affected by male sex steroid hormones. For 3 hours, however, pretreatment of the cells with 100 nM each of testosterone and dihydrotestosterone suppressed LPS induced iNOS and COX-2 protein expression. RT-PCR analysis revealed that testosterone and dihydrotestosterone did not inhibit mRNA expression of iNOS and COX-2 stimulated by 24 hours of LPS incubation. Proliferation rate was slower in VSMC treated with testosterone and dihydrotestosterone. Testosterone enhanced androgen receptor expression, and LPS significantly reduced androgen receptor protein expression in VSMC. These results indicate that the expression of both iNOS and COX-2 proteins was suppressed by testosterone and dihydrotestosterone in LPS stimulated VSMC and leading to reduction of vascular inflammation.

Expression of Cyclooxygenase-2 in Intestinal Epithelial Cells in Response to Invasive Bacterial Infection and its Role of Epithelial Cell Apoptosis (침습성 세균 감염에 의한 사람 장상피세포에서의 Cyclooxygenase-2 발현 및 이의 발현이 상피세포 Apoptosis에 미치는 영향)

  • Kim, Jung-Mogg;Kang, Shin-Jae;Cho, Yang-Ja
    • The Journal of the Korean Society for Microbiology
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    • v.34 no.5
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    • pp.479-489
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    • 1999
  • Invasion of enteric bacteria, such as Salmonella and invasive E. coli, into intestinal epithelial cells induces proinflammatory gene responses and finally epithelial cell apoptosis. In this study, we asked whether invasive bacterial infection of human intestinal epithelial cells could upregulate cyclooxygenase-2 (COX-2) gene expression and whether increased COX-2 expression could influence intestinal epithelial cell apoptosis. Expression of COX-2 mRNA and prostaglandin (PG) $E_2$ production were upregulated in HT-29 colon epithelial cells which were infected with S. dublin or invasive E. coli, as examined by quantitative RT-PCR and radioimmunoassay. Inhibition of COX-2 expression and $PGE_2$ production using NS-398, a specific COX-2 inhibitor, showed a significant increase of epithelial cell apoptosis and caspase-3 activation in HT-29 cells infected with invasive bacteria. However, the addition of valerylsalicylate, a specific COX-1 inhibitor, did not change apoptosis in S. dublin-infected HT-29 cells. These results suggest that up regulated COX-2 expression and $PGE_2$ production in response to invasive bacterial infection could contribute to host defense by inhibiting apoptosis of intestinal epithelial cells.

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Screening of KMU-4, 6, 7 on inflammatory responses in IFN-γ and LPS-induced mouse peritoneal macrophages

  • Na, Ho-Jeong;Jeong, Hyun-Ja;Ahn, Jong-Woong;Um, Jae-Young;Kim, Hyung-Min;Hong, Seung-Heon
    • Advances in Traditional Medicine
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    • v.8 no.2
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    • pp.125-129
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    • 2008
  • Korean Marine Plants (KMU-4, 6, 7) obtained from an herb which widely used in medicine for the treatment of a variety of pathologies. In this study, using mouse peritoneal macrophages, we have examined whether KMU-4, 6, 7 affects nitric oxide (NO) and COX-2 induced IFN-$\gamma$ and LPS and cell viability. KMU-6 inhibits IFN-$\gamma$ and LPS-induced NO. We found that KMU-6 had a little effect on COX-2 expression. These finding means that KMU-6 can be used in controlling macrophages mediated inflammatory disease. The present results indicate that KMU-6 has an inhibitory effect on the production of NO through down-regulation of COX-2 expression in LPS stimulated mouse peritoneal macrophages.

Test of Model Specification in Box-Cox Transformed Regression Model with AR(1) Errors (오차항이 AR(1)을 따르는 Box-Cox 변환 회귀모형에서 모형 식별을 위한 검정)

  • Cheon, Soo-Young;Yoon, Seok-Jin;Hwang, Sun-Young;Song, Seuck-Heun
    • The Korean Journal of Applied Statistics
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    • v.21 no.2
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    • pp.327-340
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    • 2008
  • This paper derives joint and conditional Lagrange multiplier tests based on information matrix for testing functional form and/or the presence of autocorrelation in a regression model. Small sample properties of these tests are assessed by Monte Carlo study and comparisons are made with LM tests based on Hessian matrix. The results show that the proposed $LM_E$ tests have the most appropriate finite sample performance.

Regulation of cyclooxygenase-2 and mapkinases by isoflavones in ovariectomized and estrogen-supplemented mature female rats fed a high fat-high cholesterol diet

  • Shin, Jang-In;Park, Ock-Jin
    • Nutritional Sciences
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    • v.6 no.1
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    • pp.25-30
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    • 2003
  • The effects of soy-isoflavones, which are phytoestrogens derived from plants with a flavonoid structure, on cyclooxygenase -2 (COX-2) expression, PGE2 production, and mapkinases expression, were investigated in experimentally-induced atherogenic rats by feeding a high fat-high cholesterol diet. Female Sprague-Dawley rats were bilaterally ovariectomized; sham-operated animals were used as controls. Three weeks later, the animals were randomized to the following treatments for an eight-week experimental period: 17$\beta$-estradiol (200$\mu$ g/kg diet), low concentration of isoflavones (0.8g/kg diet), and high concentration of isoflavones (4.0g/kg diet). In the group supplemented with a high dose of isoflavones, COX-2 expression was down-regulated. This down-regulation was accompanied by a reduced expression of pERK1/2. In the second experiment using 48-week old female Sprague-Dawly rats, the effects of isoflavones and estrogen were compared in the basal estrogen-supplementation at the level of 600$\mu$ g/kg diet. Isoflavones induced the marked down-regulation of COX-2 protein and the decrease in $PGE_2$ production in estrogen supplemented states and this was followed by the down-regulation of p38 among mapkinases. The two different mapkinases are involved in the down-regulation of COX-2 depending on estrogen-deficient and estrogen supplemented states. This kind of COX-2 down-regulation by isoflavones was not observed in the different tissue, mammary glands. Further investigations on the relationship between COX-2 and biological activities such as vasodilation by isoflavonesin the absence or the presence of estrogen ave required in vivo system of female rats.

Inhibitory effect of Chelidonii Herba water extract on production of Nitric Oxide, Expression of iNOS and COX-2 in lipopolysaccharide-activated Raw 264.7 cells (백굴채(白屈菜)의 물추출물이 lipopolysaccharide로 유도된 Nitric Oxide의 생성 및 iNOS와 COX-2의 발현에 미치는 영향)

  • Zhao Rong-Jie;Kim Young-Woo;Byun Sung-Hui;Kim Sang-Chan
    • Herbal Formula Science
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    • v.12 no.2
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    • pp.163-173
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    • 2004
  • Chelidonii Herba (CHE, Baek-gul-chae in Korean), which has its original description in Gu-Hwang-Bon-Cho, a classic book of oriental Herbal book, is widely used in the treatment of stomach cancer, jaundice, gasrtic ulcer, edema and stomach pain, in Korea, Japan and China. The present study was conducted to evaluate the effect of CHE on the nitric oxide (NO) production, iNOS and COX-2 expression in lipopolysaccharide - activated Raw 264.7 cells. After the treatment of CHE, NO production was monitored by measuring the nitrite content in culture medium, cell viability was measured by MIT assay. COX-2 and iNOS were determined by lmmunoblot analysis. The production of nitric oxide was significantly inhibited by pretreatment (1h) with CHE (0.1-0.3 mg/ml) on LPS-activated Raw264.7 cells. The expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) protein were up-regulated by LPS, but the increased levels of iNOS and COX-2 were inhibited by pretreatment of CHE (0.1-0.3 mg/ml), respectively. Thus, the present data suggest that CHE may play an important role in adjunctive therapy in Gram-negative bacterial infections.

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Inhibitory Effect of Benzofuran Compound on Cyclooxygenase

  • Min, Kyung-Rak;Ahn, Ki-Young;Chung, Eun-Yong;Lee, Yong-Rok;Kim, Yeong-Shik;Kim, Young-Soo
    • Natural Product Sciences
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    • v.10 no.6
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    • pp.315-320
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    • 2004
  • Alpha-viniferin was previously isolated as a cyclooxygenase (COX)-2 inhibitor from Carex humilis (Cyperaceae) and is an oligomeric stilbene compound with benzofuran (BF) moieties in its chemical structure. In the present study, a chemically synthetic BF compound, named as 3,3-dimethyl-2,3,4,6,7,8,9,10,11,12,13,14,15,16,17,18-hexadecahydro-1H-benzo[b] cyclopentadeca[d]furan-1-one, was discovered to inhibit bacterial lipo polysaccharide (LPS)-induced prostaglandin $E_2$ $(PGE_2)$ production in macrophages RAW 264.7. The BF compound exhibited a selectively preferred inhibitory effect on COX-2 activity over COX-1 activity. Furthermore, BF compound inhibited LPS-induced COX-2 expression at transcription level. As a down-regulatory mechanism of COX-2 expression shown by BF compound, suppression of nuclear factor $(NF)-{\kappa}B$ activation has been demonstrated. BF compound inhibited LPS-induced $NF-{\kappa}B$ transcriptional activity and nuclear translocation of $NF-{\kappa}B$ p65, in parallel, but did not affect LPS-induced degradation of inhibitory ${\kappa}B{\alpha}$ protein $(I{\kappa}B{\alpha})$. Taken together, anti-inflammatory effect of BF compound on $PGE_2$ production was ascribed by its down-regulatory action on LPS-induced COX-2 synthesis in addition to inhibitory action on enzyme activity of COX-2.