• Journal of the Korean Ceramic Society
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• v.52 no.6
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• pp.514-520
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• 2015

$KY_{1-x}(WO_4)_2:Ho^{3+}/Yb^{3+}$ yellow phosphors with doping concentrations of $Ho^{3+}$ and $Yb^{3+}$ ($x=Ho^{3+}+Yb^{3+}$, $Ho^{3+}=0.05$, 0.1, 0.2 and $Yb^{3+}=0.2$, 0.45) were successfully prepared using the microwave-modified sol-gel method; their upconversion (UC) photoluminescence properties were investigated in detail. Well-crystallized particles, formed after heat-treatment at $900^{\circ}C$ for 16 h, showed a fine and homogeneous morphology with particle sizes of $2-5{\mu}m$. Under excitation at 980 nm, the UC $KY_{0.7}(WO_4)_2:Ho_{0.1}Yb_{0.2}$ and $KY_{0.5}(WO_4)_2Ho_{0.05}Yb_{0.45}$ particles exhibited excellent yellow emissions based on a strong 545-nm emission band in the green region and a very strong 655-nm emission band in the red region. Pump power dependence and Commission Internationale de L'Eclairage chromaticity of the UC emission intensity were evaluated. The spectroscopic properties were examined comparatively using Raman spectroscopy.

• Korean Journal of Materials Research
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• v.26 no.1
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• pp.29-34
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• 2016

$NaLa_{1-x}{(MoO_4)}_2$:$Ho^{3+}/Yb^{3+}$ phosphors with the correct doping concentrations of $Ho^{3+}$ and $Yb^{3+}$ ($x=Ho^{3+}+Yb^{3+}$, $Ho^{3+}=0.05$ and $Yb^{3+}=0.35$, 0.40, 0.45 and 0.50) were successfully synthesized by the microwave-modified sol-gel method. Well-crystallized particles formed after heat-treatment at $900^{\circ}C$ for 16 h showed a fine and homogeneous morphology with particle sizes of $3-5{\mu}m$. The optical properties were examined using photoluminescence emission and Raman spectroscopy. Under excitation at 980 nm, the UC intensities of the doped samples exhibited strong yellow emissions based on the combination of strong emission bands at 545-nm and 655-nm emission bands in green and red spectral regions, respectively. The strong 545-nm emission band in the green region corresponds to the $^5S_2/^5F_4{\rightarrow}^5I_8$ transition in $Ho^{3+}$ ions, while the strong emission 655-nm band in the red region appears due to the $^5F_5{\rightarrow}^5I_8$ transition in $Ho^{3+}$ ions. Pump power dependence and Commission Internationale de L'Eclairage chromaticity of the upconversion emission intensity were evaluated in detail.

• Korean Journal of Materials Research
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• v.26 no.7
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• pp.363-369
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• 2016

$NaCaLa_{1-x}(MoO_4)_3:Ho^{3+}/Yb^{3+}$ ternary molybdates with proper doping concentrations of $Ho^{3+}$ and $Yb^{3+}$ (x = $Ho^{3+}+Yb^{3+}$, $Ho^{3+}$ = 0.05 and $Yb^{3+}$ = 0.35, 0.40, 0.45 and 0.50) were successfully synthesized by microwave sol-gel method. Well-crystallized particles formed after heat-treatment at $900^{\circ}C$ for 16 h showed a fine and homogeneous morphology with particle sizes of $3-5{\mu}m$. Under excitation at 980 nm, the UC intensities of the doped samples exhibited strong yellow emissions based on the combination of strong emission bands at 520-nm and 630-nm emission bands in the green and red spectral regions, respectively. The optimal $Yb^{3+}:Ho{3+}$ ratios were obtained at 9:1 and 10:1, as indicated by the composition-dependent quenching effect of the $Ho^{3+}$ ions. The pump power dependence of the upconversion emission intensity and the Commission Internationale de L'Eclairage chromaticity coordinates of the phosphors were evaluated in detail.

• Molecules and Cells
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• v.45 no.3
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• pp.134-147
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• 2022

The anti-oxidant enzyme heme oxygenase-1 (HO-1) is known to exert anti-inflammatory effects. From a library of pyrazolo[3,4-d]pyrimidines, we identified a novel compound KKC080096 that upregulated HO-1 at the mRNA and protein levels in microglial BV-2 cells. KKC080096 exhibited anti-inflammatory effects via suppressing nitric oxide, interleukin1β (IL-1β), and iNOS production in lipopolysaccharide (LPS)-challenged cells. It inhibited the phosphorylation of IKK and MAP kinases (p38, JNK, ERK), which trigger inflammatory signaling, and whose activities are inhibited by HO-1. Further, KKC080096 upregulated anti-inflammatory marker (Arg1, YM1, CD206, IL-10, transforming growth factor-β [TGF-β]) expression. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinetreated mice, KKC080096 lowered microglial activation, protected the nigral dopaminergic neurons, and nigral damage-associated motor deficits. Next, we elucidated the mechanisms by which KKC080096 upregulated HO-1. KKC080096 induced the phosphorylation of AMPK and its known upstream kinases LKB1 and CaMKKbeta, and pharmacological inhibition of AMPK activity reduced the effects of KKC080096 on HO-1 expression and LPS-induced NO generation, suggesting that KKC080096-induced HO-1 upregulation involves LKB1/AMPK and CaMKKbeta/AMPK pathway activation. Further, KKC080096 caused an increase in cellular Nrf2 level, bound to Keap1 (Nrf2 inhibitor protein) with high affinity, and blocked Keap1-Nrf2 interaction. This Nrf2 activation resulted in concurrent induction of HO-1 and other Nrf2-targeted antioxidant enzymes in BV-2 and in dopaminergic CATH.a cells. These results indicate that KKC080096 is a potential therapeutic for oxidative stress-and inflammation-related neurodegenerative disorders such as Parkinson's disease.

• Proceedings of the Korea Air Pollution Research Association Conference
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• 2003.05b
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• pp.231-232
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• 2003

과산화수소(hydrogen peroxide, $H_2O$$_2$)는 광화학적 2차 생성물이며, 대기의 산화상태를 알려주는 지시자의 역할을 한다. 과산화수소는 HO$_2$ radical의 self-reaction 으로 생성된다. HO$_2$+ HO$_2$+ M $H_2O$$_2$ + M (1) OH나 HO$_2$ radical은 NOx나 hydrocarbon 과 같은 대표적인 오존 전구물질들을 산화시킨다. 대기 내 수명이 불과 1초 이내인 OH나 HO$_2$ radical을 직접 측정하기란 어려우므로 수명이 1~2 일 정도인 $H_2O$$_2$를 측정하여 이들 radical의 대기 내 농도를 추정할 수 있다. (중략)

• The Transactions of the Korean Institute of Electrical Engineers C
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• v.50 no.9
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• pp.434-437
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• 2001

ZnSe, ZnSe:Ho/sup 3+/, Mg/sub x/Zn/sub 1-x/Se and Mg/sub x/Zn/sub 1-x/Se:Ho/sup 3+/ crystals were grown by the chemical transport reaction method. The crystal structures and optical energy band gaps of the single crystals were investigated. Their photoluminescence(PL) spectra were measured at 10 [K]. Sharp emission peaks in the blue-green wavelength range and broad emission peaks in the yellow-red wavelength range were observed. The single crystals doped with 1.0 [mol%] of holmium did not show the sharp emission peaks because of defects which were thought to be originated to the holmium dopant.

• The Korea Journal of Herbology
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• v.28 no.4
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• pp.77-81
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• 2013

Objectives : Horse oil (HO) has been used long time as the folk medicine of many Asian countries such as Korea, Mongol, China, India and Japan. HO has been used for anti-bacterial, anti-inflammatory, and anti-pruritic purposes in skin. However, it is still largely unknown whether HO modulates the skin condition. In this study, we attempted to evaluate the anti-inflammatory effect of HO on the 1 % of 2, 4-dinitro-1-chlorobenzene (DNCB)-induced contact hypersensitivity in Balb/c mice. Methods : To find the anti-inflammatory effect of HO, contact hypersensitivity, a local inflammatory response of skin, was induced on the back of Balb/c mice by sensitization and repeated application by 1% DNCB and HO treated 2 weeks on the 1% of DNCB-treated Balb/c mice. Excised mice skins were stained with hematoxylin and eosin and serum IgE level was measured by mouse IgE ELISA kit. Results : In this study, we found that HO reduced erythema by 1% of DNCB treated Balb/c mice. Also, HO recovered histopathological features such as the thickening of epidermis, hyperkeratosis and the infiltration of inflammatory cells in 1% of DNCB treated Balb/c mice. In addition, HO reduced IgE level on the serum obtained from blood of 1% of DNCB-treated Balb/c mice. Conclusion : Taken together, these results showed that HO could be used as a pharmaceutical material with anti-inflammatory effects by reducing of erythema, IgE level and recovering of histopathological features skin on DNCB-induced contact hypersensitivity in Balb/c mice model.

• Biomolecules & Therapeutics
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• v.24 no.3
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• pp.268-282
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• 2016

In the present study, we investigated the anti-inflammatory properties of Eucommia ulmoides Oliv. Bark. (EUE) in lipopolysaccharide (LPS)-stimulated microglial BV-2 cells and found that EUE inhibited LPS-mediated up-regulation of pro-inflammatory response factors. In addition, EUE inhibited the elevated production of pro-inflammatory cytokines, mediators, and reactive oxygen species (ROS) in LPS-stimulated BV-2 microglial cells. Subsequent mechanistic studies revealed that EUE suppressed LPS-induced phosphorylation of mitogen-activated protein kinases (MAPKs), phosphoinositide-3-kinase (PI3K)/Akt, glycogen synthase $kinase-3{\beta}$ ($GSK-3{\beta}$), and their downstream transcription factor, nuclear factor-kappa B ($NF-{\kappa}B$). EUE also blocked the nuclear translocation of $NF-{\kappa}B$ and inhibited its binding to DNA. We next demonstrated that EUE induced the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and upregulated heme oxygenase-1 (HO-1) expression. We determined that the significant up-regulation of HO-1 expression by EUE was a consequence of Nrf2 nuclear translocation; furthermore, EUE increased the DNA binding of Nrf2. In contrast, zinc protoporphyrin (ZnPP), a specific HO-1 inhibitor, blocked the ability of EUE to inhibit NO and $PGE_2$ production, indicating the vital role of HO-1. Overall, our results indicate that EUE inhibits pro-inflammatory responses by modulating MAPKs, PI3K/Akt, and $GSK-3{\beta}$, consequently suppressing $NF-{\kappa}B$ activation and inducing Nrf2-dependent HO-1 activation.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.4
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• pp.203-210
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• 2011

Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular cAMP levels and activates protein kinase A, thereby inhibiting vascular smooth muscle cell (VSMC) proliferation. We investigated whether AMP-activated protein kinase (AMPK) activation induced by heme oxygenase-1 (HO-1) is a mediator of the beneficial effects of cilostazol and whether cilostazol may prevent cell proliferation and reactive oxygen species (ROS) production by activating AMPK in VSMC. In the present study, we investigated VSMC with various concentrations of cilostazol. Treatment with cilostazol increased HO-1 expression and phosphorylation of AMPK in a dose- and time-dependent manner. Cilostazol also significantly decreased platelet-derived growth factor (PDGF)-induced VSMC proliferation and ROS production by activating AMPK induced by HO-1. Pharmacological and genetic inhibition of HO-1 and AMPK blocked the cilostazol-induced inhibition of cell proliferation and ROS production.These data suggest that cilostazol-induced HO-1 expression and AMPK activation might attenuate PDGF-induced VSMC proliferation and ROS production.

• Korean Journal of Pharmacognosy
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• v.42 no.3
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• pp.276-281
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• 2011

Oxidative stress or the accumulation of reactive oxygen species (ROS) leads neuronal cellular death and dysfunction, and it contributes to neuronal degenerative disease such as Alzheimer's disease, Parkinson's disease and stroke. Glutamate-induced oxidative injury contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as epilepsy and ischemia. Heme oxygenase-1 (HO-1) enzyme plays an important role of cellular antioxidant system against oxidant injury. The expression of HO-1 has cytoprotective effects in glutamate-induced oxidative cytotoxicity in HT22 cells. The induction of HO-1 is primarily regulated at the transcriptional level, and its induction by various inducers is related to the nuclear transcription factor-E2-related factor 2 (Nrf2). Nrf2 is a master regulator of the antioxidant response. NNMBS008, the water-insoluble fraction of the 70% EtOH extract of roots of Sophora flavescens, showed dominant neuroprotective effects on glutamate-induced neurotoxicity in mouse hippocampal HT22 cells by induced the expression of HO-1 and increased HO activity. In mouse hippocampal HT22 cells, NNMBS008 makes the nuclear accumulation of Nrf2 pathway. In conclusion, the waterinsoluble fraction of the 70% EtOH extract of roots of S. flavescens (NNMBS008) significantly protect glutamate-induced oxidative damage by induction of HO-1 via Nrf2 pathway in mouse hippocampal HT22 cells. These results suggest that these extracts could be the effective candidates for the treatment of ROS-related neurological diseases.