• Journal of Chest Surgery
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• v.35 no.2
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• pp.94-101
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• 2002

All kinds of tissue valves must be pretreated for the inactivation of immunologic properties and the strengthening of tissue before implantation. However, the tissue valves are gradually denatured with the calcification process and they eventually lose their functions. Recent reports have shown the existence of specific calcium binding non collagenous proteins in the calcified area of implanted biomaterials. This experiment was intended to confirm the effect of pretreatment with RGDS(Arg-Gly-Asp-Ser) tetrapeptide on the calcification of subcutaneously implanted bovine pericardium in rats. RGDS tetrapeptide has the same amino acid sequence of attachment site of specific calcium binding non collagenous proteins. Material and Method: All bovine pericardial pieces were fixed with 0.6% glutaraldehyde. The pretreatments were done using 5 different methods, groupI, with normal saline for 60 minutes, groupII, with 0.5% GRSD(Gly-Arg-Scr-Asp) tetrapeptide solution for 60 minutes, group III : with 0.5% RGDS(Arg-Gly-Asp-Ser) tctrapeptide for 30 minutes, group IV ; with 0.5% RGDS for 60 minutes, and group V : with 0.5% RGDS for 120 minutes. The pretreated bovine pericardial pieces were implanted subcutaneously at the abdominal sites of rats. 30 days after the implantation, the implanted bovine pericardial tissue were examined radiologically, biochemically, and histologically to measure the severity of calcification. Result: On the radiological examination, group I ; 68.42$\pm$3.06, group II , 64.25$\pm$5.58 showed significant difference with group III: 48.00$\pm$3.57, group IV; 43.67$\pm$2.31, and group V ; 2.58$\pm$2.47(p<0.05). There was no difference between group I and II(p=0.105). On the biochemical examination, the amount of calcium in group I was , 33.09$\pm$6.59 mg, in group II ; 28.12$\pm$5.50mg, in group III ; 25.42$\pm$7.67mg, in group Ⅵ ; 20.51$\pm$5.11mg, and in group V : 15.43$\pm$4.25mg.

• Korean Chemical Engineering Research
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• v.51 no.3
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• pp.313-318
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• 2013

In order to investigate the effect of $V_2O_5$ loading of $V_2O_5-WO_3/TiO_2$ catalyst on the NO reduction and the formation of $N_2O$, the experimental study was carried out in a differential reactor using the powder catalyst. The NO reduction and the ammonia oxidation were, respectively, investigated over the catalysts compose of $V_2O_5$ content (1~8 wt%) based on the fixed composition of $WO_3$ (9 wt%) on $TiO_2$ powder. $V_2O_5-WO_3/TiO_2$ catalysts had the NO reduction activity even under the temperature of $200^{\circ}C$. However, the lowest temperature for NO reduction activity more than 99.9% to treat NO concentration of 700 ppm appeared at 340 with very limited temperature window in the case of 1 wt% $V_2O_5$ catalyst. And the temperature shifted to lower one as well as the temperature window was widen as the $V_2O_5$ content of the catalyst increased, and finally reached at the activation temperature ranged $220{\sim}340^{\circ}C$ in the case of 6 wt% $V_2O_5$ catalyst. The catalyst of 8 wt% $V_2O_5$ content presented lower activity than that of 8 wt% $V_2O_5$ content over the full temperature range. NO reduction activity decreased as the $V_2O_5$ content of the catalyst increased above $340^{\circ}C$. The active site for NO reduction over $V_2O_5-WO_3/TiO_2$ catalysts was mainly related with $V_2O_5$ particles sustained as the bare surface with relevant size which should be not so large to stimulate $N_2O$ formation at high temperature over $320^{\circ}C$ according to the ammonia oxidation. Currently, $V_2O_5-WO_3/TiO_2$ catalysts were operated in the temperature ranged $350{\sim}450^{\circ}C$ to treat NOx in the effluent gas of industrial plants. However, in order to save the energy and to reduce the secondary pollutant $N_2O$ in the high temperature process, the using of $V_2O_5-WO_3/TiO_2$ catalyst of content $V_2O_5$ was recommended as the low temperature catalyst which was suitable for low temperature operation ranged $250{\sim}320^{\circ}C$.

• Journal of Korean Society of Environmental Engineers
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• v.33 no.1
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• pp.39-46
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• 2011

NO oxidation is an important prerequisite step to assist the selective catalytic reduction (SCR) at low temperatures ($<200^{\circ}C$). Therefore, we conducted the lab- and bench-scales experiments appling the sodium chlorite powder ($NaClO_2(s)$) for the oxidation of NO to $NO_2$ and the carbon-based catalyst for the reduction of $NO_x$ and $SO_2$; the lab- and bench-scales experiments were conducted in laboratory and iron-ore sintering plant, respectively. In the lab-scale experiment, known concentrations of $NO_x$ (200 ppm), $SO_2$ (75 ppm), $H_2O$ (10%) and $NH_3$ (400 ppm) in 2.6 L/min were introduced into a packed-bed reactor containing $NaClO_2(s)$, then gases produced by the reaction with $NaClO_2(s)$ were fed into the carbon-based catalyst (space velocity = $2,000hr^{-1}$) at $130^{\circ}C$. In the bench-scale experiment, flue gases of $50Nm^3/hr$ containing 120 ppm NO and 150 ppm $SO_2$ were taken out from the duct of iron-ore sintering plant, then introduced into the flow reactor; $NaClO_2(s)$ were injected into the flow reactor using a screw feeder. Gases produced by the reaction with $NaClO_2(s)$ were introduced into the carbon-based catalyst (space velocity = $1,000hr^{-1}$). Results have shown that, in both lab- and bench-scales experiments, NO was oxidized to $NO_2$ by $NaClO_2(s)$. In addition, above 90% of $NO_x$ and $SO_2$ removal were obtained at the carbon-based catalyst. These results lead us to suggest that the combination of $NaClO_2(s)$ with the carbon-based catalyst has the potential to achieve the simultaneous removal of $NO_x$ and $SO_2$ at low temperature ($<200^{\circ}C$).

• Tuberculosis and Respiratory Diseases
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• v.50 no.1
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• pp.52-66
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• 2001

Background : NF-${\kappa}B$ is the most important transcriptional factor in IL-8 gene expression. Triptolide is a new compound that recently has been shown to inhibit NF-${\kappa}B$ activation. The purpose of this study is to investigate how triptolide inhibits NF-${\kappa}B$-dependent IL-8 gene transcription in lung epithelial cells and to pilot the potential for the clinical application of triptolide in inflammatory lung diseases. Methods : A549 cells were used and triptolide was provided from Pharmagenesis Company (Palo Alto, CA). In order to examine NF-${\kappa}B$-dependent IL-8 transcriptional activity, we established stable A549 IL-8-NF-${\kappa}B$-luc. cells and performed luciferase assays. IL-8 gene expression was measured by RT-PCR and ELISA. A Western blot was done for the study of $I{\kappa}B{\alpha}$ degradation and an electromobility shift assay was done to analyze NF-${\kappa}B$ DNA binding. p65 specific transactivation was analyzed by a cotransfection study using a Gal4-p65 fusion protein expression system. To investigate the involvement of transcriptional coactivators, we perfomed a transfection study with CBP and SRC-1 expression vectors. Results : We observed that triptolide significantly suppresses NF-${\kappa}B$-dependent IL-8 transcriptional activity induced by IL-$1{\beta}$ and PMA. RT-PCR showed that triptolide represses both IL-$1{\beta}$ and PMA-induced IL-8 mRNA expression and ELISA confirmed this triptolide-mediated IL-8 suppression at the protein level. However, triptolide did not affect $I{\kappa}B{\alpha}$ degradation and NF-$_{\kappa}B$ DNA binding. In a p65-specific transactivation study, triptolide significantly suppressed Gal4-p65T Al and Gal4-p65T A2 activity suggesting that triptolide inhibits NF-${\kappa}B$ activation by inhibiting p65 transactivation. However, this triptolide-mediated inhibition of p65 transactivation was not rescued by the overexpression of CBP or SRC-1, thereby excluding the role of transcriptional coactivators. Conclusions : Triptolide is a new compound that inhibits NF-${\kappa}B$-dependent IL-8 transcriptional activation by inhibiting p65 transactivation, but not by an $I{\kappa}B{\alpha}$-dependent mechanism. This suggests that triptolide may have a therapeutic potential for inflammatory lung diseases.