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청계천 (淸溪川) 하수의 질산화 율에 관한 pH 와 암모니아의 영향
오기완,김남천 ( Ki Wan Oh,Nam Cheon Kim ) 한국하천호수학회 1980 생태와 환경 Vol.13 No.3·4
During two months period from April to May 1980, experiments were carried out to investigate the effect of pH and ammonia on the activity of NO₂^- oxidation of Cheong-gye cheon sewage water. The following conclusions were obtained as a results of this study. 1. Effect pH The rate of NH₄^+ oxidation was fastest at pH 8.5 and slowest at pH 9.5 Solution which was kept under pH 8.5 oxidized all the NH₄^+ within 2 days, where as that with pH 9.5 oxidized about 80 percent of NH₄^+. The rate of NO₂^- oxidation was fastest at pH 8.5 and slowest at pH 9.5 Solution which was kept under pH 8.5 oxidized all the NO₂^- within 4 days, where as that with pH 9.5 oxidized about 50 percent of NO₂^-. 2. Effect of pH and ammonia To know effect of pH and ammonia on the oxidation of NO₂^- of sewage water, ammonium sulfate [(NH₄)₂SO₄] solution was added to the solution on oxidation of NO₂^- after 24 hours. Solution which was kept under pH8.5 oxidized all the NO₂^- within 5 days. The slowest rate of NO^_₂ oxidation occurred at pH 9.0 and at pH 9.5. The inhibition of nitrification at high at high pH values was caused by the injurous effect of excess NH₃ and NH₄ OH. Excess NH₄^+ caused the accumulation of NO₂^- in high pH values. (at pH 9.0 and pH 9.5) Cheong-gye cheon sewage water has an optimum pH of about 8.5.
Protective Effects of Panax ginsengon the Neurotoxicity Induced by Abuse Drugs
오기완(Ki-Wan Oh) 고려인삼학회 2005 고려인삼학회 학술대회 Vol.- No.-
Ginseng has been useful for the treatment of diverse disease in oriental countries for thousands of years. In addition, a folk medicine prescribed by seven herbal drugs including Panax ginseng has been antinarcotics in the treatment of morphine-dependent patients. Many articles have been reported on these works. Therefore, we review the protective effects of Panax ginseng on the neurotoxicity induced by abuse drugs.<br/> Ginseng total saponins (GTS) extracted and isolated by Panax ginseng antagonized morphine-induced analgesia, and inhibited the development of analgesic tolerance to and physical dependence on morphine. GTS inhibited morphine-6 dehydrogenase, which catalyzes production of mophinone from morphine, and increased hepatic glutathione level responsible to toxicity. Therefore, wehypothesized that these dual actions of ginseng can be associated with the detoxication of morphine. In addition, the inhibitory or facilitated effects of GTS on electrically evoked contraction in guinea pig ileum (m-receptors) and mouse vas deferens (d-receptors) were not mediated through opioid receptors, suggesting non-opioid mechanisms. On the hand, antagonism of U-50,488H (k-agonist)-induced antinociception is mediated by serotonergic mechanisms. <br/> GTS also inhibited hyperactivity, reverse tolerance (sensitization) and conditioned place preference-induced by psychostimulants such as methamphetamine, cocaine and morphine. On the other hand, GTS reduced the dopamine levels induced by methamphetamine. Moreover, GTS blocked the development of dopamine receptor activation, showing antidopaminergic effect. We suggest that GTS prevent the methamphetamine-induced striatal dopaminergic neurotoxicity. In addition, Ginsenoside also attenuates morphine-induced cAMP signaling pathway. These results suggested that GTS might be useful for the therapy of the adverse actions of drugs with abuse liability.
Antagonism of Analgesic Effect of Morphine in Mice by Ginseng Saponins
김학성,오기완,오세관,Kim, Hack-Seang,Oh, Ki-Wan,Oh, Se-Kwan 한국약제학회 1986 Journal of Pharmaceutical Investigation Vol.16 No.4
Ginseng total saponins(GS), protopanaxadiol saponins(PD) and protopanaxadiol saponins(PT) antagonized the analgesia in mice induced by morphine. The administrations of 2,4-dihydroxyphenylalanine, and 5-hydroxytryptophan reduced the GS, PD and PT antagonisms of morphine analgesia. Possible mechanisms involved in the antagonistic actions of GS, PD and PT on morphine analgesia were described.
신경섭(Kyeong-Seob Shin),이정진(Jung-Jin Lee),김영일(Yong-Ri Jin),유지연(Ji Yeon Yu),박은석(Eun-Seok Park),임지현(Ji-Hyun Im),유순향(Soon-Hyang You),오기완(Ki Wan Oh),이명구(Myung Koo Lee),위재준(Jae Joon Wee),김영숙(Young Sook Kim) 고려인삼학회 2007 Journal of Ginseng Research Vol.31 No.2
Korean red ginseng has broad efficacious effects against hypertension, diabetes, nociception, and cancer, and it counteracts weakness. It has been reported that Korean red ginseng is able to normalize blood pressure, improve cholesterol and lower blood glucose levels. We have recently reported that Korean red ginseng extract (KRGE) significantly prevented rat carotid arterial thrombosis in vivo, and inhibited platelet aggregation ex vivo and in vitro in a dose-dependent manner. The purpose of this study was to examine the effects of KRGE on blood circulation in human by measuring ex vivo platelet aggregation, plasma coagulation and serum lipid profiles in healthy volunteers. Subjects were randomly divided into three groups (placebo-group, KRGE-low dose group, KRGE-high dose group). Administration of KRGE to subjects significantly inhibited ADP-induced platelet aggregations both in KRGE-low dose group from 72.79 ±20.53 to 62.00 ±23.06% (p=0.0009), and in KRGE-high dose group from 75.14 ±21.86 to 64.52 ±24.72% (p=0.0039), respectively. Administration of KRGE to subjects also significantly inhibited collagen-induced platelet aggregations both in KRGE-low dose group from 85.52 ±12.57 to 79.62 ±20.47% (p=0.0916), and in KRGE-high dose group from 80.24 ±18.11 to 70.31 ±25.93% (p=0.0565), respectively. Whereas, KRGE has no significant effects on coagulation system, such as prothrombin time (PT) and activated partial thromboplastin time (APTT), and serum lipid profiles, such as total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and triglyceride. KRGE also has no significant effects on hematological and serum biochemical profiles. These results suggest that KRGE has a potential to improve blood circulation through antiplatelet activity in human, and KRGE intake may be beneficial for the individuals with high risks of thrombotic and cardiovascular diseases.
Bisphenol A에 의한 신경계 세포의 칼슘 항상성 교란 및 세포독성에 미치는 영향
이윷모(Yoot Mo Lee),이상민(Sang Min Lee),손동주(Dong Ju Son),이선영(Sun Young Lee),박혜지(Hye Ji Park),남상윤(Sang Yun Nam),김대중(Dae Joong Kim),윤영원(Young Won Yun),유환수(Hwan Soo Yoo),오기완(Ki Wan Oh),김태성(Tae Seong Kim),한순영( 한국독성학회 2004 Toxicological Research Vol.20 No.3
We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration.<br/> Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of<br/> environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic<br/> agents which cause increase of intracellular calcium level, BPA decreased [Ca2+]i dose-dependently<br/> in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at<br/> greater concentrations than 100 μM reduced cell viability significantly in both types of cells. BPA also<br/> suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist,<br/> 30 μM)-induced increase of [Ca2+]i. BPA further lowered caffeine (RYR activator, 100 μM)-decreased<br/> [Ca2+]i, but did not alter dantrolene (RYR inhibitor, 100 μM), heparin (IP3 inhibitor, 200 units/ml) and<br/> xestospongin C (IP3 inhibitor, 5 μM)-decreased [Ca2+]i. Cell viability was not directly related to intracellular<br/> calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal<br/> factor of BPA-induced neuronal cell death.