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특별소비세법중 개정법률 공포 (2000. 12. 29)

  • 한국엘피가스공업협회
    • LP가스
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    • 통권72호
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    • pp.27-29
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    • 2001
  • 부탄에 부과되는 특별소비세를 오는 2007년까지 단계적으로 인상한다는 내용의 "특별소비세법중 개정법률"이 지난 12월 29일자로 공포됐다.

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Induction of pro-inflammatory cytokines by 29-kDa FN-f via cGAS/STING pathway

  • Hwang, Hyun Sook;Lee, Mi Hyun;Choi, Min Ha;Kim, Hyun Ah
    • BMB Reports
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    • 제52권5호
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    • pp.336-341
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    • 2019
  • The cGAS-STING pathway plays an important role in pathogen-induced activation of the innate immune response. The 29-kDa amino-terminal fibronectin fragment (29-kDa FN-f) found predominantly in the synovial fluid of osteoarthritis (OA) patients increases the expression of catabolic factors via the toll-like receptor-2 (TLR-2) signaling pathway. In this study, we investigated whether 29-kDa FN-f induces inflammatory responses via the cyclic GMP-AMP synthase (cGAS)/stimulator of interferon gene (STING) pathway in human primary chondrocytes. The levels of cGAS and STING were elevated in OA cartilage compared with normal cartilage. Long-term treatment of chondrocytes with 29-kDa FN-f activated the cGAS/STING pathway together with the increased level of gamma-H2AX, a marker of DNA breaks. In addition, the expression of pro-inflammatory cytokines, including granulocyte-macrophage colony-stimulating factor (GM-CSF/CSF-2), granulocyte colony-stimulating factor (G-CSF/CSF-3), and type I interferon ($IFN-{\alpha}$), was increased more than 100-fold in 29-kDa FN-f-treated chondrocytes. However, knockdown of cGAS and STING suppressed 29-kDa FN-f-induced expression of GM-CSF, G-CSF, and $IFN-{\alpha}$ together with the decreased activation of TANK-binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), and inhibitor protein ${\kappa}B{\alpha}$ ($I{\kappa}B{\alpha}$). Furthermore, NOD2 or TLR-2 knockdown suppressed the expression of GM-CSF, G-CSF, and $IFN-{\alpha}$ as well as decreased the activation of the cGAS/STING pathway in 29-kDa FN-f-treated chondrocytes. These data demonstrate that the cGAS/STING/TBK1/IRF3 pathway plays a critical role in 29-kDa FN-f-induced expression of pro-inflammatory cytokines.

속수자가 HT-29 대장암세포의 활성 및 세포사멸에 미치는 영향 (Effects of Euphorbiae lathyridis Semen on cell apoptosis in HT-29 human colon cancer cells)

  • 이제현;정선주;박용기
    • 대한본초학회지
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    • 제22권2호
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    • pp.65-72
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    • 2007
  • Objectives : In this study, we investigate that Euphorbiae lathyridis Semen extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Euphorbiae lathyridis Semen was extracted from the Semen of the plant using 80% Methanol. The Euphorbiae lathyridis Semen extract was treated to different concentrations for 24 hr, 4Shr or 72hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Westem blot. Results : Exposure to Euphorbiae lathyridis Semen extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Euphorbiae lathyridis Semen extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Euphorbiae lathyridis Semen extract induces DNA fragmentation in HT-29 cells. Furthermore, Euphorbiae lathyridis Semen extract induces cell apoptosis through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion : Euphorbiae lathyridis Semen extract induces apoptosis in human colon cancer cells, therefore, we suggest that Euphorbiae lathyridis Semen extract can be used as a novel class of anti-cancer drugs.

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속수자 추출물의 HT-29 대장암세포 증식에 대한 억제효과 (Inhibitory effects of Euphorbiae lathyridis Semen extract on cell growth in HT-29 human colon cancer cells)

  • 정효원;박용기
    • 동국한의학연구소논문집
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    • 제11권
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    • pp.52-57
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    • 2008
  • Objectives. In this study, we investigate that methanol extract of Euphorbiae lathyridis Semen contributes to growth inhibitory effect on the HT-29 human colon cancer cells. Methods. Euphorbiae lathyridis Semen (ELS) was extracted with 80% methanol. HT-29 cells were treated with different concentrations of ELS extract for 24-72 hrs. Growth inhibitory effect was determined by MTT assay. Cell apoptosis was determined by surveying caspases cascades activation using Western blot. Cell cycle arrest was analyzed by flow cytometry with PI staining. Results. Exposure to ELS extract showed in inhibitory effects on HT-29 cell growth as a dose-dependent manner. Cell growth inhibition by ELS extract was related with induction of cell apoptosis with DNA fragmentation through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion. ELS extract significantly inhibited cell growth and induced cell apoptosis in HT-29 human colon cancer cells, therefore, These results suggest that ELS extract can be used as chemoprevention agent of colon cancers.

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어구재료용 신소재섬유의 물성분석 - 2 . 신소재섬유의 크리프특성 및 탄성회복도 - (Physical Properties Analysis of the High-Tech Fibers for Fishing Gear Materials - 2 . Creep Characteristics and Elastic Recovery of the High-tech Fibers -)

  • 김태호;고관서
    • 수산해양기술연구
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    • 제29권3호
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    • pp.191-199
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    • 1993
  • In order to analysis creep characteristics and elastic recovery of the high-tech fibers for fishing gear materials, creep and elasticity tests were carried out on netting twines made of nylon, kevlar 29 and techmilon respectively. After creep tests, the rupture surface of raw materials was observed by scanning electron microscope(SEM). The results obtained are as follows: 1. Netting twines were arranged in order of creep rupture time as follow: techmilon, kevlar 29, nylon. The creep progressive pace was the fastest in techmilon. 2. In order of the creep elongating, netting twines were arranged as follows: nylon, techmilon, kevlar 29. 3. The rupture time T sub(r) decreased almost linearly with the increase of applied load L on the log-log scaled graph. The empirical equations computed for kevlar 29 and techmilon are as follows: T sub(r kevlar 29)=1.9512$\times$1037L super(-15.773). T sub(r techmilon)=2.7146$\times$1016L super(-6.831). 4. It was observed by SEM that creep was progressed in all netting twines. The difference of rupture morphology was recognized clearly in tensile and creep tests. 5. In order of the elastic recovery, netting twines were arranged as follows: techmilon, kevlar 29, nylon.

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BDR-29의 랫트에 대한 13주 반복투여 독성에 관한 연구 (Study for Thirteen Weeks Subacute Toxicity of BDR-29 in Rats)

  • 장보윤;강대길;이호섭;김성연
    • 생약학회지
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    • 제39권1호
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    • pp.60-67
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    • 2008
  • The subcronic toxicity of BDR-29, a herbal preparation of Cassiae Semen, Prunellae Spica, Tribuli Fructus, and Uncariae Rhamulus et Uncus, was examined in male and female Sprague-Dawley rats. Rats were treated with the test substance at a dose 5 mg/kg, 50 mg/kg and 500 mg/kg intragastrically for 13 weeks. No death and abnormal clinical signs were observed throughout the administration period. There were not significantly different from control group in net body weight gain, food and water consumption, organ weight, gross pathological findings, and urine analysis among the groups rats treated with different doses of the BDR-29. Hematological findings and biochemical examination revealed no evidence of specific toxicity related to BDR-29. From these results, no observation effect level (NOEL) of BDR-29 is 500 mg/kg/day under the condition employed in this study.

Diethylstilbestrol의 단핵구의 세포간 유착과정 조절효과 (Modulatory Effect of Diethylstilbestrol on CD29-Mediated Cell-cell Adhesion in Monocytic U937 Cells)

  • 김병훈;조재열
    • 약학회지
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    • 제52권2호
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    • pp.111-116
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    • 2008
  • Diethylstilbestrol (DESB) is a synthetic estrogen not only that routinely prescribed, but also that known to be a teratogen. In this study, we found a novel pharmacological feature that DESB is able to positively modulate CD29 $({\beta}1-integrin)$ function. Thus, DESB up-regulated homotypic cell-cell adhesion of monocytic U937 cells mediated by CD29. However, DESB did not increase the surface level of CD29 and its binding activity to ligand (fibronectin), according to flow cytometric analysis and cell-fibronectin adhesion assay. Instead, the DESB-mediated up-regulation of cell-cell adhesion was blocked by several signaling enzyme inhibitors. Treatment of U0126 [an extracellular signal-regulated kinase (ERK) inhibitor], SB20358 (a p38 inhibitor) or Rp-8-pCPT-cGMP (a protein kinase G inhibitor) clearly inhibited DESB-mediated up-regulation of cell-cell adhesion induced by CD29. However, estrogen receptor antagonist ICI 182,780 failed to abrogate DESB effect. Therefore, our data suggest that DESB may up-regulate CD29-mediated cell-cell adhesion via modulating intracellular signaling enzymes such as ERK, PKG, and p38, independent of estrogen receptor function.