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      • 탄소환원에 의한 Zircon으로 부터 고순도 Zirconia 제조에 관한 연구

        유용주,이재식 울산대학교 1991 공학연구논문집 Vol.22 No.2

        감압하에서 지르콘사를 탄소환원하므로 지르코니아의 고순도화에 대한 연구를 하였다. 지르콘과 탄소의 혼합물을 1 Torr의 진공로 중에서 가열함으로써, 지르콘 중의 SiO₂는 SiO(g)로 제거되었으며, 이 SiO(g)는 로의 낮은 온도 구역에서 미세한 백색 무정형 분말인 SiO(s)로 응축되었다. 생성된 지르코니아에는 미량의 탄소, ZrO 그리고 ZrC등이 존재하였으나, 공기중에서 산화 반응후에는 지르코니아 단일상으로 되었다. 단일상 지르코니아는 1500℃, C/SiO₂몰비 1.0 일때 SiO₂의 함유량이 가장 작았다. 이러한 공정의 반응 생성물은 XRD, SEM-EDX 및 습식방법 등에 의해서 분석하였으며, 지르코니아 분말의 순도는 99.8%이었고 결정구조는 단사정이었다. A production technics of high-purity ZrO₂ powder from zircon (ZrO₂· SiO₂) were investigated by carbothermic reduction under reduced pressure. The mixture of zircon and carbon was heated in the range of 1200℃ to 1500℃ in vaccum furnace under the condition of 1 Torr. The reaction product for the process was examined by XRD, SEM-EDX, and chemical analysis. By this techniques, the SiO₂ in zircon was removed as SiO(g). The generation of SiO(g) from a Zircon/Carbon mixture at high temperature to was greatly enchanced by reduction of pressure compared to atmospheric. Zirconia powder contaminated with a small amount of carbon, ZrO, and ZrC was obtained before oxidation reaction. Single-phase ZrO₂ was obtained after oxidation reaction of Zirconia powder when the the C/SiO₂ mole ration in the Zircon/Carbon mixture was 0.5∼2.0. The SiO₂content in ZrO₂ powder was minimized at a C/SiO₂ ratio of about 1.0. The monoclinic phase zirconia powder with a high purity of 99.8% and fine grain size was obtained. The SiO(g) generated in the process condensed as a fine white amorphous powder in the low-temperature zone of the vaccum furnace, having an ultrafine grain size.

      • EMF 측정법에 의한 Cu-Co-O System의 열역학적 연구

        유용주,이재식 울산대학교 1990 연구논문집 Vol.21 No.1

        고체 전해질인 (ZrO₂+ CaO)를 사용하여 구성된 다음과 같은 galvanic cell들을 이용한 EMF를 측정함으로써, Cu₂O, CuO, CoO의 Cu₂CoO₃생성에 대한 자유에너지 값을 얻었으며, Cell(1) Ni, NiO/ZrO₂(+CaO)/Cu, Cu₂O Cell(2) Ni, NiO/ZrO₂(+CaO)/CuO, Cu₂O Cell(3) Co, CoO/ZrO₂(+CaO)/Ni, NiO Cell(4) Co, CoO/ZrO₂(+CaO)/Cu, Cu₂O Cell(5) Cu, Cu₂O, CoO/ZrO₂(+CaO)/Cu,Cu₂O Cell(6) Cu₂O, CoO, Cu₂CoO₃/ZrO₂(+CaO)/Cu, Cu₂O Cell(7) CuO, Cu₂O, Cu₂CoO₃/ZrO₂(+CaO)/Cu, Cu₂O 그 결과들은 아래와 같다. △ G˚??, Cu₂O=-40548+17.494 T cal/mole(970-1258K) △ G˚??, CuO=-36062+20.084 T cal/mole(1162-1332K) △ G˚??, CoO=-56680+17.394 T cal/mole(1126-1326K) 그리고 2 CuO+CoO=Cu₂CoO₃반응에 대한 △G˚=-1618+0.9838 T cal/mole(1162-1332K)이며, 계산된 Cu₂CoO₃의 생성에 대한 자유에너지 값은 △G˚, Cu₂CoO₃=-130423+58.542T cal/mole이다. 그리고 Cu₂CoO₃에 대한 Cu₂O와 CuO의 용해도는 매우 작았다. The equilibrium oxygen pressures of the binary and threephase regions [Cu-O], [Co-O], [Cu, Cu₂O, CoO], [Cu₂O, CoO, Cu₂CoO₃] and [CuO, Cu₂O, Cu₂CoO₃]were measured as a function of temperature by the solid oxide electrolyte (ZrO₂+ CaO) electromotive force method. The galvanic cells used were as follow: Cell(1) Ni, NiO/ZrO₂(+CaO)/Cu, Cu₂O Cell(2) Ni, NiO/ZrO₂(+CaO)/CuO, Cu₂O Cell(3) Co, CoO/ZrO₂(+CaO)/Ni, NiO Cell(4) Co, CoO/ZrO₂(+CaO)/Cu, Cu₂O Cell(5) Cu, Cu₂O, CoO/ZrO₂(+CaO)/Cu, Cu₂O Cell(6) Cu₂O, CoO, Cu₂CoO₃/ZrO₂(+CaO)/Cu, Cu₂O Cell(7) CuO, Cu₂O, Cu₂CoO₃/ZrO₂(+CaO)/Cu, Cu₂O The results were expressed by the following equations: G˚??, Cu₂O=-40548+17.494 T cal/mole(970-1258K) G˚??, CuO=-36062+20.084 T cal/mole(1162-1332K) G˚??, CoO=-56680+17.394 T cal/mole(1126-1326K) The measured Gibbs energy of the reaction 2 CuO+CoO=Cu₂CoO₃was found to be -1618+0.9838 T cal/mole(1162-1332K). The evaluated Gibbs energy of formation of △G˚, Cu₂CoO was found to be -130423+58.542T cal/mole. The solubility of Cu₂CoO₃in Cu₂O or CuO is very small.

      • SCM 435 구조용강의 플라즈마 질화에 관한 연구

        유용주,김인수,이재식 울산대학교 1996 공학연구논문집 Vol.27 No.2

        본 연구는 SCM 435 구조용강을 450∼650℃의 온도범위에서 NH₃가스유량을 0.5∼2.1 l/min로 변화시키고, 20∼110분 동안 플라즈마 질화처리하여 강 표면에 생성된 경화층의 두께와 경도 및 조직을 조사하였다. 반응온도 550℃, NH₃1.65 l/min.에서 110분 동안 질화 하였을 경우 생성된 질화층의 두께는 260㎛으로써, 화합물층은 16㎛ 이며, 확산층은 224㎛로 이것이 최대의 질화층이었다. 한편, 반응온도 600℃, NH₃1.65 l/min. 가스유량에서 50분간 반응하였을때 24㎛의 최대 화합물층을 얻을 수 있었다. 또한 화합물층은 450℃와 500℃에서는 r'- Fe₄N-α-Fe로, 550℃에서는 r'-Fe₄N+ε- Fe₃N으로, 600℃이상에서는 r-Fe₄N+α-Fe로 구성되어있는 혼합상이었다. 550℃,NH₃1.65 l/min. 에서 80분 동안 질화처리하였을때 생성된 질화층의 최대 표면경도는 Hv 988이었다. The plasma nitriding of SCM 435 structural steel has been studied at the temperature between 450℃ and 650℃ with gas flow rate of NH₃ 0.5 to 2.1 l/min. for 20 to 110 minutes. The phases of compound layer formed below 500℃ and above 600℃ was mixture of r'-Fe₄N and ε- Fe₂₄N phases, while the phases formed 550 was r' - FeN and - Fe N phases. The hardness of nitrided layer formed at 550℃ with gas flow rate of NH₃ 1.65 l/min. for 80minutes was Hv 988. The thickness of nitrided layer formed at 550℃ with gas flow rate of NH 1.65 l/min. for 110minutes was 260㎛. The nitriede layer was composed of 16㎛ compound layer and 244㎛ diffusion layer.

      • 마이크로 펄스 플라즈마 질화법에 의한 선박엔진용 부품의 표면경화에 관한 연구

        이재식,유용주 울산대학교 1996 공학연구논문집 Vol.27 No.2

        본 연구는 마이크로 펄스 플라즈마 질화처리한 FCD60, S53C, SCM440강재를 고주파 유도경화 열처리한 동일 강재와의 비교분석을 통해 강 표면에 생성된 경화층의 두께와 경도 및 조직을 조사하고 마모시험을 행하였다. Hv550의 유효경도를 갖는 경화깊이는 마이크로 펄스 플라즈마 질화의 경우 FCD60, S53C, SCM440에서 각각 30㎛,25㎛,25㎛이었고, 고주파 유도경화 열처리는 각각 1.4mm이었다. 경화층의 XRD분석결과 마이크로 펄스 플라즈마 질화의 경우 FCD60과 S53C는 주로 r'- Fe₄N, SCM440은 r' - Fe₄N과 ε- Fe₃N의 혼합상이 생성되었으며, 고주파 유더경화 열처리된 경화층은 α- Fe로 모재와 같았다. 또한, 마모시험결과 상온에서는 고주파 유도경화 열처리에 의해 생성된 경화층이 내마모성이 좋으나, 고온(150℃)과 윤활상태에서는 마이크로 펄스 플라즈마 질화처리하에 의하여 생성된 질화층의 내마모성이 우수하였다. The case hardening of FCD60, S53C and SCM440 by micro-pulse plasma nitriding and high frequency induction heat treatment was invesigated. The effective case depth (of which hardeness is over Hv550) of FCD60, S53C and SCM440 nitrided by micro-;ulse plasma method was 30, 25 and 25㎛, respectively. XRE analysis of nitrided layer, showed that mixture of r' - Fe₄N and ε- Fe₃N phases formed on SCM440, r' -Fe₄N single phase formed on S53C and FCD60. In case of hihh frequency induction heat treatment, hardened layer was α - Fe single phase. The hardened hayer formed by high frequency induction heat treatment was more resistant to wear than nitrided layer at room temperature, however nitrided layer by micro-pulse plasma nitriding was more resistant to wear than induction hardened layer at high temperature and lubricated condition.

      • 동전해정제시 음극분극전위에 미치는 첨가제의 영향에 관한 연구

        오기식,유용주,김영홍 울산대학교 1985 연구논문집 Vol.16 No.2

        전해첨가제를 동전해액(황산동-황산)에 각각 단독으로 또는 복합적으로 첨가하여 음극분극전위를 측정함으로써 다음과 같은 결론을 얻었다. 1) 첨가량이 많아짐에 따라 아교와 글리신은 음극분극전위를 현저히 높이며, 아비톤-A는 약간 증가시키고, 티오요소는 소량 첨가할 경우 감소시키나 첨가량이 많아지면 상당히 상승시킨다. 그리고 Cl?은 음극분극전위에 영향을 거의 미치지 않는다. 2) 아교를 주 첨가제로하고 티오요소 및 아비톤-A를 첨가했을 때 티오요소와 아비톤-A는 분극전위에 거의 영향을 미치지 못하고 주로 아교가 영향을 미친다. 3) 아교 5mg/l, 티오요소 3mg/1, Cl? 20mg/l를 가한 전해액을 이용한 일반적인 전해정제로 2.5A/dm²의 고전류밀도에서 평활하고 치밀한 전착면을 얻을 수 있었으며, 불순물의 제거가 가능하고 부동태현상이 발생 하지 않았다. Cathodic polarization potentials during the ectrorefining of copper have been measured under various conditions of addition agents in the copper electrolyte (CuSO₄-H₂SO₄). The results obtained are as follows. 1) The cathode polarization potential is affected by the kind of addition agents and the amount of addition to the electrolyte. Glue and glycine show remarkable increasing effects on the polarization potential, Aviton-A has a little effect. However, thiourea causes the polarization potential to increase considerably at high concentration, but showing a decreasing effect at low concentration. Chlorine has little effect on the polarization potential. 2) In the case of using the electrolyte containing glue with Aviton-A and glue with thiourea as additives, thiourea and Aviton-A have little effect on the polarization potential, while glue shows remarkable effect. 3) The electrorefining was carried out successfully using the electrolyte added glue 5mg/l, thiourea 3mg/l, and chlorine 20,g/l, with the current thiourea 3mg/l, and chlorine 20mg/l, with the current density of 2.5A/dm² for 68hrs at the pilot plant. The surface of deposit copper was smooth and its thickness was uniform, showing the purity of 99.99( copper.

      • 플라즈마 질화법에 의한 SUS316L 스테인레스강의 표면경화에 관한 연구

        박정환,김영홍,유용주 울산대학교 1994 공학연구논문집 Vol.25 No.2

        본 연구는 SUS316L 스테인레스강을 이용하여 500℃∼600℃의 온도범위에서 NH₃가스의 유량을 0.5∼2.1ℓ/min로 변화시키고, 20∼110분 동안 플라즈마 질화처리하여, 강 표면에 생성된 경화층의 두께와 경도 및 조직을 조사하였다. 반응온도 550℃, NH₃가스의 유량 2.1ℓ/min에서 110분 동안 질화 하였을 경우 생성된 질화층의 두께는 약57㎛로 최대치를 나타내었다. 그리고 질화처리 한 시편을 XRD 분석한 결과 생성된 질화층은 CrN+r-Fe₄N+Fe₃N으로 구성되어 있는 화합물층 이었으며, 확산층은 생성되지 않았고, 생성된 질화층의 경도의 최고치는 약 Hv 1800 이었다. 플라즈마 질화법에 의한 SUS316L 스테인레스 강의 표면경화의 최적조건은 550℃, 2.1ℓ/min. NH₃가스, 110분이었다. A nitrided layer on SUS316L stainless steel by plasma nitrised for back ferrule in one parts of tube fitting has been studied. Specimen was nitrided over 500℃ to 650℃ reaction temperature range with 0.5 to 2.1 ℓ/min. NH₃gas flow rate for 20 to 110 min. The thickness of nitrided layer showed maximum value about 57㎛ at 550℃ reaction temperature and with 2.1ℓ/min. NH₃gas flow rate for 110 min. The result of XRD, nitrided layer was mainly composed of CrN+r-Fe₄N+Fe₃N, but not detected diffusion layer. And also, when NH₃gas flow rate 2.1ℓ/min. , the maximum hardness value of nitrided layer was revealed about Hv 1800 at 550-600℃ reaction temperature range. In this study, the optimum condition of nitrided on SUS316L stainless steel was observed at 550℃ reaction temperature and 2.1ℓ/min. , NH₃gas flow rate for 110 min.

      • SCISCIESCOPUS

        Propyl gallate inhibits the growth of endothelial cells, especially calf pulmonary arterial endothelial cells via caspase-independent apoptosis.

        Han, Yong Hwan,Moon, Hwa Jin,You, Bo Ra,Yang, Yeon Mi,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun D.A. Spandidos 2010 INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE Vol.25 No.6

        <P>Propyl gallate (PG) as a synthetic antioxidant exerting a variety of effects on tissue and cell functions. We evaluated the effects of PG on the growth of endothelial cells, especially calf pulmonary artery endothelial cells (CPAEC) in relation to apoptosis. PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. The susceptibility of CPAEC to PG was higher than that of HUVEC. PG induced apoptosis in CPAEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim). The tested caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) did not rescue CPAEC from PG-induced cell death but instead slightly enhanced the cell death. PG increased reactive oxygen species (ROS) level in CPAEC. The caspase inhibitors did not significantly change the ROS level. Furthermore, PG increased the GSH depleted cell number and decreased GSH level in CPAEC. The tested caspase inhibitors did not significantly change the number in PG-treated CPAEC. Each caspase inhibitor differently alters GSH levels in CPAEC. In conclusion, PG inhibited the growth of endothelial cells, especially CPAEC via caspase-independent apoptosis. PG-induced CPAEC death was accompanied by ROS increase and GSH depletion.</P>

      • SCISCIESCOPUS

        MG132, a proteasome inhibitor, induced death of calf pulmonary artery endothelial cells via caspase-dependent apoptosis and GSH depletion.

        Han, Yong Hwan,Moon, Hwa Jin,You, Bo Ra,Yang, Yeon Mi,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun Potamitis Press 2010 Anticancer research Vol.30 No.3

        <P>MG132, a proteasome inhibitor, has been shown to induce apoptotic cell death through formation of reactive oxygen species (ROS). Here, we evaluated the effects of MG132 on the growth of endothelial cells, especially calf pulmonary artery endothelial cells (CPAECs). MG132 dose-dependently inhibited the growth of CPAECSs and human umbilical vein endothelial cells (HUVECs) at 24 hours. MG132 also induced apoptosis in both cell lines, which was accompanied by the loss of mitochondrial membrane potential. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 and -9 inhibitor) significantly rescued CPAECs from MG132-induced cell death. MG132 increased ROS level and GSH depleted cell numbers of CPAECs. None of the caspase inhibitors reduced ROS level in MG132-treated CPAECs but did reduce apoptosis in these cells. In conclusion, MG132 inhibited the growth of endothelial cells, especially CPAECs via caspase-dependent apoptosis. MG132-induced CPAEC death was related to GSH depletion rather than a change in ROS level.</P>

      • SCISCIESCOPUS

        Pyrogallol-induced endothelial cell death is related to GSH depletion rather than ROS level changes.

        Han, Yong Hwan,Moon, Hwa Jin,You, Bo Ra,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun National Hellenic Research Foundation 2010 ONCOLOGY REPORTS Vol.23 No.1

        <P>Pyrogallol (PG) as a polyphenol compound induces apoptosis in several types of cells. Here, we evaluated the effects of PG on endothelial cells (ECs), especially calf pulmonary artery endothelial cells (CPAEC) in relation to the cell growth, ROS and glutathione (GSH) levels. PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. PG also induced apoptosis in CPAEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim). PG decreased ROS level including O2*- and PG dose-dependently increased GSH depleted cell number in both EC types. N-acetyl-cysteine (NAC; a well-known antioxidant) increased ROS levels in PG-treated CPAEC with the prevention of cell death and GSH depletion. In conclusion, PG inhibited the growth of ECs, especially CPAEC via apoptosis. PG-induced EC death was related to GSH depletion rather than ROS level changes.</P>

      • SCISCIESCOPUS

        Propyl gallate inhibits the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle

        Han, Yong Hwan,Moon, Hwa Jin,You, Bo Ra,Kim, Sung Zoo,Kim, Suhn Hee,Park, Woo Hyun Spandidos Publications 2010 ONCOLOGY REPORTS Vol.23 No.4

        <P>Propyl gallate (PG) as a synthetic antioxidant exerts a variety of effects on tissue and cell functions. Here, we evaluated the effects of PG on the growth of HeLa cells in relation to apoptosis and the cell cycle. PG dose-dependently inhibited the growth of HeLa cells with an IC50 of approximately 800 microM at 24 h. DNA flow cytometric analysis indicated that PG significantly induced a G1 phase arrest of the cell cycle along with an increase in the cyclin-dependent kinase inhibitor (CDKI) p27. In addition, PG induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim), activation of caspase-3 and caspase-8 and PARP cleavage. All the tested caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) significantly rescued HeLa cells from PG-induced cell death. However, none of the caspase inhibitors prevented the loss of MMP (DeltaPsim) induced by PG. In conclusion, PG inhibited the growth of HeLa cells via caspase-dependent apoptosis as well as a G1 phase arrest of the cell cycle.</P>

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