• Proceedings of the KIPE Conference
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• 2003.07a
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• pp.434-438
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• 2003

This paper present an investigation of the influence on the PFC(power factor correction) circuit with characteristics variation of MPP (Molybdenum permalloy powder) core. The experiment results of the 1.5kW class Boost converter for PFC rectifier with the average current mode control are evaluated to verify the influence on the PFC converter with inductance variation of the MPP core. As a results, it is shown that the ripple of the inductor using a MPP core increase with output power of the converter.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.4
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• pp.207-212
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• 2006

Mitochondrial permeability transition has been shown to be involved in neuronal cell death. Mitochondrial monoamine oxidase (MAO)-B is considered to play a part in the progress of nigrostriatal cell death. The present study examined the effect of MAO inhibitors against the toxicity of 1-methyl-4-phenylpyridinium $(MPP^+)$ in relation to the mitochondrial permeability transition. Chlorgyline (a selective inhibitor of MAO-A), deprenyl (a selective inhibitor of MAO-B) and tranylcypromine (nonselective inhibitor of MAO) all prevented cell viability loss, cytochrome c release, caspase-3 activation, formation of reactive oxygen species and depletion of GSH in differentiated PC12 cells treated with $500\;{\mu}M$$MPP^+$. The MAO inhibitors at $10\;{\mu}M$ revealed a maximal inhibitory effect and beyond this concentration the inhibitory effect declined. On the basis of concentration, the inhibitory potency was tranylcypromine, deprenyl and chlorgyline order. The results suggest that chlorgyline, deprenyl and tranylcypromine attenuate the toxicity of $MPP^+$ against PC12 cells by suppressing the mitochondrial permeability transition that seems to be mediated by oxidative stress.

• Proceedings of the KIPE Conference
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• 2019.07a
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• pp.455-456
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• 2019

본 논문은 태양광 발전시스템에서 일사량이 급변했을 때 최대 전력점(MPP: Maximum Power Point)을 빠르게 추종할 수 있는 P&O(Perturb and Observe)기반 가변 스텝 알고리즘을 제안하였다. 제안한 기법은 일사량 또는 온도에 의해 환경 변화 시 최대 전력점에서의 전압 변화 특성을 이용하며, 가변 스텝 방식이 적용된 전압제어를 통해 MPP를 추종한다. 임계값 설정으로 일사량 급변을 판단하며, MPP를 빠르게 추종하기 위한 고속 모드로 동작한다. MPP에 도달하면 가변 모드로 전환하여 정상상태 오차를 최소화 한다. PV 시뮬레이터와 태양광 전력변환시스템을 통해 제안한 MPPT 알고리즘의 성능을 검증하였다.

• Proceedings of the Korean Magnestics Society Conference
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• 2001.04a
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• pp.54-55
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• 2001

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.86-87
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• 2000

• Journal of Information Display
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• v.3 no.1
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• pp.6-10
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• 2002

We have synthesized a new green Ir(III) complex fac-tris-(3-methyl-2-phenyl pyridine)iridium(III) $Ir(mpp)_3$ and fabricated phosphorescent polymer light-emitting device using it as a triplet emissive dopant in PVK. $Ir(mpp)_3$ showed absorption centered at 388 nm corresponding to the $^1MLCT$ transition as .evidenced by its extinction coefficient of the order of $10^3{\cdot}$ From the PL and EL spectra of the $Ir(mpp)_3$ doped PVK film, the emission maximum was observed at 523 nm, due to the radiative decay from the $^3MLCT$ state to the ground state, confirming a complete energy transfer from PVK to $Ir(mpp)_3$. The methyl substitution has probably caused a red shift in the absorption and emission spectrum compared to $Ir(mpp)_3$. The device consisting of a 2 % doped PVK furnished 4.5 % external quantum efficiency at 72 $cd/m^2$ (current density of 0.45 $mA/cm^2$ and drive voltage of 13.9 V) and a peak luminance of 25,000 $cd/m^2$ at 23.4 V (494 $mA/cm^2$). This work demonstrates the impact of the presence of a methyl substituent at the 3-position of the pyridyl ring of 2-phenylpyridine on the photophysical and electroluminescence properties.

• Journal of the Korea Institute of Information and Communication Engineering
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• v.16 no.3
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• pp.549-557
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• 2012

In this paper an on-chip photo energy harvesting system with MPPT(Maximum Power Point Tracking) control is proposed. The ISC(Integrated Solar Cell) is implemented using p-diff/n-well diodes available in CMOS processes. MPPT control is implemented using the linear relationship between the open-circuit voltage of a PV(Photovoltaic) cell and its MPP(Maximum Power Point) voltage such that a small pilot PV cell can track the MPP of a main PV cell in real time. Simulation results show that the designed circuit with the MPPT control delivers the MPP voltage to load even though the load is heavy such that the load circuit can operate properly. The proposed circuit is designed in 0.18um CMOS process. The designed main PV cell and pilot PV cell occupy $8mm^2$ and $0.4mm^2$ respectively.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.91-99
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• 2016

(E)-3-(3-methoxyphenyl)-1-(2-pyrrolyl)-2-propenone (MPP) is an aldol condensation product resulting from pyrrole-2-carbaldehyde and m- and p- substituted acetophenones. However, its biological activity has not yet been evaluated. Since it has been reported that some propenone-type compounds display anti-inflammatory activity, we investigated whether MPP could negatively modulate inflammatory responses. To do this, we employed lipopolysaccharide (LPS)-stimulated macrophage-like RAW264.7 cells and examined the inhibitory levels of nitric oxide (NO) production and transcriptional activation, as well as the target proteins involved in the inflammatory signaling cascade. Interestingly, MPP was found to reduce the production of NO in LPS-treated RAW264.7 cells, without causing cytotoxicity. Moreover, this compound suppressed the mRNA levels of inflammatory genes, such as inducible NO synthase (iNOS) and tumor necrosis factor (TNF)-${\alpha}$. Using luciferase reporter gene assays performed in HEK293 cells and immunoblotting analysis with nuclear protein fractions, we determined that MPP reduced the transcriptional activation of nuclear factor (NF)-${\kappa}B$. Furthermore, the activation of a series of upstream signals for NF-${\kappa}B$ activation, composed of Src, Syk, Akt, and $I{\kappa}B{\alpha}$, were also blocked by this compound. It was confirmed that MPP was able to suppress autophosphorylation of overexpressed Src and Syk in HEK293 cells. Therefore, these results suggest that MPP can function as an anti-inflammatory drug with NF-${\kappa}B$ inhibitory properties via the suppression of Src and Syk.

• Korean Journal of Pharmacognosy
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• v.49 no.3
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• pp.231-239
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• 2018

Parkinson's disease (PD), one of common neurodegenerative diseases, is caused by the death of dopaminergic neurons in the substantia nigra pars compacta. The loss of dopaminergic neurons in PD is associated with oxidative stress and mitochondrial dysfunction. Hyperoside (quercetin 3-O-${\beta}$-D-galactopyranoside) was reported to have protective properties against oxidative stress by reducing intracellular reactive oxygen species (ROS) and increasing antioxidant enzyme activity. In this study, we examined the neuroprotective effect of hyperoside against 1-methyl-4-phenyl pyridinium ($MPP^+$)-induced cell model of PD and the underlying molecular mechanisms. Hyperoside significantly decreased $MPP^+$-induced cell death, accompanied by a reduction in poly ADP-ribose polymerase (PARP) cleavage. Furthermore, it attenuated $MPP^+$-induced intracellular ROS and disruption of mitochondrial membrane potential (MMP), with the reduction of Bax/Bcl-2 ratio. Moreover, hyperoside significantly increased the phosphorylation of Akt, but it has no effects on $GSK3{\beta}$ and MAPKs. Pharmacological inhibitor of PI3K/Akt abolished the cytoprotective effects of hyperoside against $MPP^+$. Taken together, these results demonstrate that hyperoside significantly attenuates $MPP^+$-induced neurotoxicity through PI3K/Akt signaling pathways in SH-SY5Y cells. Our findings suggest that hyperoside might be one of the potential candidates for the treatment of PD.

• Molecules and Cells
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• v.37 no.9
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• pp.672-684
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• 2014

The exact causes of cell death in Parkinson's disease (PD) remain unknown despite extensive studies on PD.The identification of signaling and metabolic pathways involved in PD might provide insight into the molecular mechanisms underlying PD. The neurotoxin 1-methyl-4-phenylpyridinium ($MPP^+$) induces cellular changes characteristic of PD, and $MPP^+$-based models have been extensively used for PD studies. In this study, pathways that were significantly perturbed in $MPP^+$-treated human neuroblastoma SH-EP cells were identified from genome-wide gene expression data for five time points (1.5, 3, 9, 12, and 24 h) after treatment. The mitogen-activated protein kinase (MAPK) signaling pathway and endoplasmic reticulum (ER) protein processing pathway showed significant perturbation at all time points. Perturbation of each of these pathways resulted in the common outcome of upregulation of DNA-damage-inducible transcript 3 (DDIT3). Genes involved in ER protein processing pathway included ubiquitin ligase complex genes and ER-associated degradation (ERAD)-related genes. Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1. This study suggests that upregulation of DDIT3 caused by perturbation of the MAPK signaling pathway and ER protein processing pathway might play a key role in $MPP^+$-induced neuronal cell death. Moreover, the toxicity signal of $MPP^+$ resulting from mitochondrial dysfunction through inhibition of complex I of the electron transport chain might feed back to the mitochondria via ER stress. This positive feedback could contribute to amplification of the death signal induced by $MPP^+$.