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노시학(Shi Hak Noh),최유선(Yoo Sun Choi) 한국도시지리학회 1999 한국도시지리학회지 Vol.2 No.2
Two major research fields can be identified in the progress of transportation geography since the 1960s. In the 1960s transportation geography was the leading research field in the quantitative movement in geography. But in the 1970s there was strong criticism of the quantitative approach to transportation geography. The center of the criticism appeared to be that transportation geography had become dehumanized in its academic and applied form, and it had become a tool used by the planners to preserve a system which was basically inhuman and unjust. This paper examines the progress of social transportation geography since 1970s, and proposes several research agenda for the field. The relationship between socio-political structure and transportation systems, social meaning of travel behavior, mobility and accessibility differences between social classes, and urban community devastation due to through traffic are proposed as major prospective research agenda in social transportation geography.
Adiramycin이 C6 glioma 세포에 미치는 영향에 대한 원지의 효과
이은미,최유선,손영우,유교상,하대호,이환봉,장철호,이정헌,이강창,이승현,박승택,이건목,류도곤 대한동의생리학회,대한동의병리학회 2001 동의생리병리학회지 Vol.15 No.6
To elucidate the cytotoxic effect of adriamycin on C6 glioma cells, we examined the neurotoxicity induced by adriamycin by MTX assay when C6 glioma cells were cultured in the media containing various concentrations of adriamycin for 72 hours. In addition, neuroprotective effects of herb extract such Polygalae Radix(PR), on adriamycin-induced neurotoxicity in cultured C6 glioma cells were evaluated after C6 glioma cells were preincubated with various concentrations of herb extract, PR for 2 hours before 6uM adriamycin for 72 hours. Adriamycin decreased remarkably cell viability in dose-and time-dependent manner in these cultures, and also herb extract, PR increased cell viability of C6 glioma cells damaged by adriamycin. From these results, it is suggested that adriamycin was highly toxic in cultured C6 glioma cells, and PR was effective in blocking the neurotoxicity induced by adriamycin in these cultures.
모르핀이 신경아세포종 SH-SY5Y 세포에서 Peroxynitrite에 의한 세포고사를 막는것은 수용체 활성화에 의한 것이 아니다
손용,윤재승,최유선,김태요,안진영,송윤강,정영표 대한마취과학회 2000 Korean Journal of Anesthesiology Vol.39 No.2
Background: In the present study, we examined the effect of morphine on NO- and peroxynitriteinduced cell death using a human neuroblastoma SH-SYSY cell line which abundantly expresses μ, δ and κ-opioid receptors. Methods: The cultured cells were pretreated with morphine (100 μM) and exposed to 3-morpholino- sydnonimine (SIN-I, ImM). Agarose gel electrophoresis of DNA was done with the extracts from SH-SYSY cells. The cells were treated with selective ligands for opioid receptor subtypes and with PI3-kinase inhibitors. Cell damage was assessed by using an MTT assay. Spectrophotometric absorption spectra were measured from the mixture of morphine (100 μM) plus peroxynitrite (I mM) at room temperature. Results: SIN-1 treated cells showed the occurrence of a specific form of chromosomal DNA fragmentation which pretreatment with morphine inhibited. We selective ligands for opioid receptor subtypes, [D-Ala^2, N-Me-Phe^4, Gly-ol5]enkephalin (DAMGO, μ-opioid receptor agonist), [D-Pen] enkephalin (DPDPE, δ-opitor agonist) and U-69593 ( κ-opioid receptor agonist) at a con- centration of 10 pM did not prevent the cell death induced by SIN-1. Naloxone (20 μM) hardly antagonized the effect of morphine in SIN-1-induced cell death. The PI3-kinase inhibitors Wortmannin and LY294002 did not inhibit the action of morphine on apoptotic cell death. In the measurements of spectrophotometric absorption spectra, the peak of the absorbance of the mixture of morphine plus peroxynitrite at 295 - 300 nm disappeared three minutes after mixing. Conclusions: The present study showed that morphine protected the human neuroblastoma cell line, SH-SY5Y, from peroxynitrite-induced apoptotic cell death. However, it is suggested that the protective action of morphine is not via the activation of opioid receptors and/or the PI3-kinase pathway but possibly via direct chemical reaction.