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오영택,박제철,김동섭,류재근 한국물환경학회 2004 한국물환경학회지 Vol.20 No.6
The aims of this study are the characterization of runoff from nonpoint source, the analysis of the pollutant loads and an establishment of a management plan for nonpoint source of Okcheon. For this purpose the basin of the stream So-okcheon was selected to the investigated. During the period from May 29 to July 21 in 2003, the water automatic sampler system has been installed in Okkagkyo and parameters such as SS, COD, TOC, TP and TN were analyzed. The pollutants of nonpoint source seem to be washed out along the stream water in the beginning of rainfall, remain in water and cause the stream pollution. The runoffs during heavy rainfall, especially, much higher concentration of SS than those during dry period. With respect to the annual loading of pollutants of the nonpoint source, the COD was 124 ton/yr, TOC 396 ton/yr, TN 1,429 ton/yr and TP 4.2 ton/yr in the year 2002. With respect to the pollutants loading of the nonpoint source, the COD was 375 ton/yr(95% of the total COD loading of 394 ton/yr), TOC 844 ton/yr(96% of the tatal TOC loading of 876 ton/yr), TN 1,985 ton/yr(96% of the total TN loading of 2,062 ton/yr) and TP 37.1 ton/yr(92% of the total TP loading of 40.3 ton/yr) in the year 2003.
배영일,류석환 울산대학교 1983 연구논문집 Vol.14 No.1
니트로벤젠 및 1,2,4-트리클로로벤젠 용매중에서 삼브롬화안티몬과 몇몇 유기브롬화물 사이의 브롬교환반응속도가 방사성 Br82로 표진된 삼브롬화안티몬을 사용하여 측정되었다. 연구결과 삼브론화안티몬에 관한 교환반응의 반응차소는 그 농도에 따라 달라졌다. 즉, 삼브롬화안티몬의 농도가 진할때는 2차인 반응속도식을 딸T으며 삼브롬화안티몬의농도가 비교적 옅을 때는 1차인 반응속도식을 따랐고 유기브롬화물에 대한 교환반응의 반응차소는 두 경우 모두 1차인 반응속도식을 따랐다. 니트로벤젠 용매중에서 삼브롬화안티몬과 브롬화이소프로필 또는 브롬화이차부칠 사이의 브롬교환반응은 아주 느리거나 또는 일어나지 않는 것으로 관측 되었다. In nitrobenzene and 1,2,4-trichlorobenzene, the rates of bromine exchange reaction of antimony tribromide with organic bromides has been mearured, using Br82 labelled antimony tribromide. The result of the study indicates that the reaction order of bromine exchange with respect to antimony tribromide varies with its concentration. At high concentration of antimony tribromide, Second order kinetics with respect to antimony tribromide has been observed, and at lower concentration of antimony tribromide, frist order kinetics. In any case of antimony tribromide concentration, first oder kinetics with respect to organicbromide has been observed. It was observed that the bromine exchange of antimony tribromide antimony with iso-propylbromide or sec-butylbromide in nitrobenzene did not occur or quite slowly occured.
수용성 이성분 혼합용매계에서 치환된 벤젠 술폰산 벤질의 가용매 분해 반응
朴炳端,金永基,柳根宇 順天大學校 1987 論文集 Vol.6 No.1
메탄올, 에탄올, 아세토니트릴, 아세톤 및 THF의 수용성 이성분 혼합용매계어서 네가지 벤젠술폰산 벤젠치환체들의 가용매 분해 반응을 35℃에서 연구하였다. 반응속도는 비양성자성 수용성 혼합용매계에서 보다는 양성자성 수용성 혼합용매계에서 빠름을 알 수 있었으며, 이것은 양성자성 혼합용매계에 의한 친전자성 및 친핵성 보조작용이 전이상태를 안정화시키기 때문이라는 것을 알 수 있었다. 가용매분해반응 속도상수를 Grunwald-Winstein 식, 확장된Grunwald-Winstein 식 및 Hammett식으로 해석하였다. 본 반응의 결과로 부터 비양성자성 수용성 혼합용매계서 용매에 의한 친전자성 보조 작용이 크게 나타남을 알 수 있었다. Solvolysis of four benzyl benzensulfonates have been studied in aqueous methanol,ethanlo,acetonitrile,acetone and tetrahydrofuran mixtures at 35℃. The rates were faster in protic solvent-water mixtures than in aprotic solvent-water mixtures. This was considered in the light of transition state stabilization by electrophilic and nucleophilic solvent assistance of protic solvent mixtures. The rates of solvolysis are analyzed in terms of the Grunwald-Winstein equation, extended Grunwald-Winstein equation and Hammett equation. The results showed that strong electrophilic assistance of solvent is operative in the aprotic solvent-water mixtures.
Characterization of Alkyl Thiosulfinate in Allium hookeri Root Using HPLC-ESI-MS
Rhyu, Dong Young,Park, Si Hyung 한국응용생명화학회 2013 Applied Biological Chemistry (Appl Biol Chem) Vol.56 No.4
Allicin produced by alliinase system of Allium hookeri was evaluated via high performance liquid chromatography (HPLC). Allicin contents of A. hookeri were $56.6{\pm}3.5{\mu}g$ per g of fresh root and $12.7{\pm}3.2{\mu}g$ per g of fresh stem. These values were relatively low as compared with garlic. HPLC-electrospray ionization-mass spectrometry analyses showed A. hookeri root extract contained ten alkyl thiosulfinates, and the chemical structures were characterized by MS/MS analyses.
Rhyu, Dong Young,Yang, Yanqiang,Ha, Hunjoo,Lee, Geun Taek,Song, Jae Sook,Uh, Soo-taek,Lee, Hi Bahl American Society of Nephrology 2005 Journal of the American Society of Nephrology Vol.16 No.3
<P>Epithelial-mesenchymal transition (EMT) plays an important role in renal tubulointerstitial fibrosis and TGF-beta1 is the key inducer of EMT. Phosphorylation of Smad proteins and/or mitogen-activated protein kinases (MAPK) is required for TGF-beta1-induced EMT. Because reactive oxygen species (ROS) are involved in TGF-beta1 signaling and are upstream signaling molecules to MAPK, this study examined the role of ROS in TGF-beta1-induced MAPK activation and EMT in rat proximal tubular epithelial cells. Growth-arrested and synchronized NRK-52E cells were stimulated with TGF-beta1 (0.2 to 20 ng/ml) or H(2)O(2) (1 to 500 microM) in the presence or absence of antioxidants (N-acetylcysteine or catalase), inhibitors of NADPH oxidase (diphenyleneiodonium and apocynin), mitochondrial electron transfer chain subunit I (rotenone), and MAPK (PD 98059, an MEK [MAP kinase/ERK kinase] inhibitor, or p38 MAPK inhibitor) for up to 96 h. TGF-beta1 increased dichlorofluorescein-sensitive cellular ROS, phosphorylated Smad 2, p38 MAPK, extracellular signal-regulated kinases (ERK)1/2, alpha-smooth muscle actin (alpha-SMA) expression, and fibronectin secretion and decreased E-cadherin expression. Antioxidants effectively inhibited TGF-beta1-induced cellular ROS, phosphorylation of Smad 2, p38 MAPK, and ERK, and EMT. H(2)O(2) reproduced all of the effects of TGF-beta1 with the exception of Smad 2 phosphorylation. Chemical inhibition of ERK but not p38 MAPK inhibited TGF-beta1-induced Smad 2 phosphorylation, and both MAPK inhibitors inhibited TGF-beta1- and H(2)O(2)-induced EMT. Diphenyleneiodonium, apocynin, and rotenone also significantly inhibited TGF-beta1-induced ROS. Thus, this data suggest that ROS play an important role in TGF-beta1-induced EMT primarily through activation of MAPK and subsequently through ERK-directed activation of Smad pathway in proximal tubular epithelial cells.</P>
Rhyu, Dong-Young,Yang, Yanqiang,Ha, Hun-Joo,Lee, Geun-Taek,Song, Jae-Sook,Uh, Soo-Taek,Lee, Hi-Bahl 이화여자대학교 약학연구소 2004 藥學硏究論文集 Vol.- No.14
Epithelial-mesenchymal transition (EMT) plays an important role in renal tubulointerstitial fibrosis and TGF-β1 is the key inducer of EMT. Phosphorylation of Smad proteins and/or mitogen-activated protein kinases (MAPK) is required for TGF-β1-induced EMT. Because reactive oxygen species (ROS) are involved in TGF-β1 signaling and are upstream signaling molecules to MAPK, this study examined the role of ROS in TGF-β1-induced MAPK activation and EMT in rat proximal tubular epithelial cells. Growth-arrested and synchronized NRK-52E cells were stimulated with TGF-β1 (0.2 to 20 ng/ml) or H₂0₂ (1 to 500 μM) in the presence or absence of antioxidants (N-acetylcysteine or catalase), inhibitors of NADPH oxidase (diphenyleneiodonium and apocynin), mitochondrial electron transfer chain subunit I (rotenone), and MAPK (PD 98059, an MEK [MAP kinase/ERK kinase] inhibitor, or p38 MAPK inhibitor) for up to 96 h. TGF-β1 increased dichlorofluorescein-sensitive cellular ROS, phosphorylated Smad 2, p38 MAPK, extracellular signal-regulated kinases (ERK)1/2, α-smooth muscle actin (α-SMA) expression, and fibronectin secretion and decreased E-cadherin expression. Antioxidants effectively inhibited TGF-β1-induced cellular ROS, phosphorylation of Smad 2, p38 MAPK, and ERK, and EMT. H₂0₂ reproduced all of the effects of TGF-β1 with the exception of Smad 2 phosphorylation. Chemical inhibition of ERK but not p38 MAPK inhibited TGF-131-induced Smad 2 phosphorylation, and both MAPK inhibitors inhibited TGF-β1- and H₂0₂-induced EMT. Diphe-nyleneiodonium, apocynin, and rotenone also significantly inhibited TGF-β1-induced ROS. Thus, this data suggest that ROS play an important role in TGF-β1-induced EMT primarily through activation of MAPK and subsequently through ERK-directed activation of Smad pathway in proximal tubular epithelial cells.