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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.
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, 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.
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 2005 藥學硏究論文集 Vol.- No.16
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 TCP-β1-induced EMT. Because reactive oxygen species (ROS) are involved in TCF-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 H_(2)O_(2) (1 to 500 ㎛) 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 dichlorofluoresceinsensitive 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 I-cadherin expression. Antioxidants effectively inhibited TGF-β1-induced cellular ROS, phosphorylation of Smad 2, p38 MAPK, and ERK, and EMT. H_(2)O_(2) reproduced all of the effects of TGF-β1 with the exception of Smad 2 phosphorylation. CHemical inhibition of ERK but not p38 MAPK inhitited TGF-91-induced Smad 2 phosphorylation, and both MAPK inhibitors inhibited TGF-β1- and H_(2)O_(2)-induced EMT. Diphe-nyleneiodonium, apocynin, and rotenone also significantly inhibited TGF-β1-indured ROS. Thus, this data suggest that ROSplay 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.
Evaluation of the implantable cardiac monitoring system in a mini-pig model
Ha-Young Jang,Sang-Hyun An,Jun-Sik Kim,Heejaung Kim,Gabbine Wee,Sang-Hyun Kim,Min-Soo Seo,Kyung-Ku Kang,Dae-Yong Han,Jung-Joo Rhyu,Sang-Kyoon Kim,Joon-Suk Park,Dong-Kyu Kim,Seonggon Kim,Taekwan Lee,Ch 한국실험동물학회 2014 한국실험동물학회 학술발표대회 논문집 Vol.2014 No.8
Lysophosphatidylcholine의 혈관평활근세포에 대한 세포 독성
강영희 ( Young Hee Kang ),이영주 ( Young Joo Lee ),이동윤 ( Dong Yun Lee ),유미라 ( Mee Ra Rhyu ),최두석 ( Doo Seok Choi ),윤병구 ( Byung Koo Yoon ) 대한폐경학회 2012 대한폐경학회지 Vol.18 No.3
Objectives: To investigate the cytotoxic effects of lysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoproteins (LDL), on vascular smooth muscle cells (VSMCs). Methods: VSMCs were derived from rat aorta. Cell death was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay, lactic dehydrogenase (LDH) assay, and DNA fragmentation assay. Apoptosis was quantified by propidium iodide staining and fluorescent activated cell sorting (FACS) analysis, and intracellular free radical production was determined using 2``, 7``-dichlorofluorescin diacetate (DCF-DA). In addition, the changes in caspases, bcl-2 and bax proteins were evaluated by western blot analysis. Results: LysoPC over 25 μM induced more than 50% of the cell death at 10 hours on MTT assay with no change in the level of LDH. The DNA ladder pattern showed that cell death induced by lysoPC was caused by apoptosis, which was associated with increased free radical production. Vitamin E, a potent antioxidant and caffeic acid phenylethyl ester (CAPE), an inhibitor of nuclear factor-kappaB (NF-kB), blocked apoptosis. The casepase-3 precursor decreased and the active form of caspase-8 increased. Total bcl-2 and bax proteins did not change with lysoPC treatment, but translocation of bax from cytosole to the mitochondria membrane was observed. Conclusion: LysoPC induces apoptosis in VSMCs via an oxidant mechanism, dependent on NF-kB. (J Korean Soc Menopause 2012;18:139-146)