• Journal of Korean Society of Environmental Engineers
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• v.39 no.8
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• pp.489-493
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• 2017

Microbial fuel cells (MFC) are bio-electrochemical processes that can convert various organic materials present in wastewater into electrical energy. For scaling-up and practical application of MFC, it is necessary to investigate the effect of anode size, electrode distance, and total area of anode on substrate degradation. Spaced electrode assembly (SPA) type microbial fuel cell with multiple anodes treating domestic wastewater was used for simulation. According to computer simulation results, the shorter the distance between electrodes than the size of single electrode, the faster the substrate degradation rate. Particularly, when the total area of the anode is large, the substrate decomposition is the fastest. In this study, it was found that the size of the anode and the distance between the electrodes as well as the cathode electrode, which is known as the rate-limiting step in the design of the microbial fuel cell process, are also important factors influencing the substrate degradation rate.

• The Korean Journal of Pain
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• v.36 no.1
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• pp.72-83
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• 2023

Background: Globally, spinal cord injury (SCI) results in a big burden, including 90% suffering permanent disability, and 60%-69% experiencing neuropathic pain. The main causes are oxidative stress, inflammation, and degeneration. The efficacy of the stem cell secretome is promising, but the role of human neural stem cell (HNSC)-secretome in neuropathic pain is unclear. This study evaluated how the mechanism of HNSC-secretome improves neuropathic pain and locomotor function in SCI rat models through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities. Methods: A proper experimental study investigated 15 Rattus norvegicus divided into normal, control, and treatment groups (30 µL HNSC-secretome, intrathecal in the level of T10, three days post-traumatic SCI). Twenty-eight days post-injury, specimens were collected, and matrix metalloproteinase (MMP)-9, F2-Isoprostanes, tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, and brain derived neurotrophic factor (BDNF) were analyzed. Locomotor recovery was evaluated via Basso, Beattie, and Bresnahan scores. Neuropathic pain was evaluated using the Rat Grimace Scale. Results: The HNSC-secretome could improve locomotor recovery and neuropathic pain, decrease F2-Isoprostane (antioxidant), decrease MMP-9 and TNF-α (anti-inflammatory), as well as modulate TGF-β and BDNF (neurotrophic factor). Moreover, HNSC-secretomes maintain the extracellular matrix of SCI by reducing the matrix degradation effect of MMP-9 and increasing the collagen formation effect of TGF-β as a resistor of glial scar formation. Conclusions: The present study demonstrated the mechanism of HNSC-secretome in improving neuropathic pain and locomotor function in SCI through antioxidant, anti-inflammatory, anti-matrix degradation, and neurotrophic activities.

• Journal of the Korean Society of Tobacco Science
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• v.21 no.2
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• pp.136-143
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• 1999

This study was conducted to evaluate the degradation characteristics of waste cigarette filters under 0, 5, 10, and 15cm in depth from soil surface by environmental conditions. Weather was the most important factor during degradation of waste cigarette filters in this study. Bulking of cellulose acetate filaments exposed on soil surface was observed after 2 months, but the form of filter was kept up after 12 months. The treated cigarette filters in soil landfill revealed a little different degradation pattern at each soil landfill depth, The sample in 5cm depth of soil was more degraded then other site. A fluffy appearance of cellulose acetate filaments in the control filter rods was also developed more strongly in soil landfill then on soil surface. From the observation of waste cigarette filters by scanning electron microscopy, much degradation of the fiber of waste cigarette filters could be ascertained in soil landfill. The weight of waste cigarette filters under 5cm from soil surface was reduced about 50%, and the tensile strength of the samples in soil surface and under 5cm from soil surface were reduced 66.0% and 92.4%, respectively. The microbial experiment date that the viable cell number in microbial population and cellulolytic microorganisms showed the maximum values under 5cm from soil surface, suggest that microorganisms in soil play an important roll in the degradation of acetate cigarette filters.

• Molecules and Cells
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• v.45 no.10
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• pp.695-701
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• 2022

Homeostatic regulation of meristematic stem cells accomplished by maintaining a balance between stem cell self-renewal and differentiation is critical for proper plant growth and development. The quiescent center (QC) regulates root apical meristem homeostasis by maintaining stem cell fate during plant root development. Cell cycle checkpoints, such as anaphase promoting complex/cyclosome/cell cycle switch 52 A2 (APC/C^CCS52A2), strictly control the low proliferation rate of QC cells. Although APC/C^CCS52A2 plays a critical role in maintaining QC cell division, the molecular mechanism that regulates its activity remains largely unknown. Here, we identified SCF^FBS1, a ubiquitin E3 ligase, as a key regulator of QC cell division through the direct proteolysis of CCS52A2. FBS1 activity is positively associated with QC cell division and CCS52A2 proteolysis. FBS1 overexpression or ccs52a2-1 knockout consistently resulted in abnormal root development, characterized by root growth inhibition and low mitotic activity in the meristematic zone. Loss-of-function mutation of FBS1, on the other hand, resulted in low QC cell division, extremely low WOX5 expression, and rapid root growth. The 26S proteasome-mediated degradation of CCS52A2 was facilitated by its direct interaction with FBS1. The FBS1 genetically interacted with APC/C^CCS52A2-ERF115-PSKR1 signaling module for QC division. Thus, our findings establish SCF^FBS1-mediated CCS52A2 proteolysis as the molecular mechanism for controlling QC cell division in plants.

• Proceedings of the Korean Society of Precision Engineering Conference
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• 2013.05a
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• pp.1525-1526
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• 2013

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.17
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• pp.7467-7471
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• 2014

SCY1-like 1-binding protein 1 (SCYL1BP1) is a newly identified transcriptional activator domain containing protein with many unknown biological functions. Recently emerging evidence has revealed that it is a novel regulator of the p53 pathway, which is very important for the development of human cancer. However, the effects of SCYL1BP1 on human lung squamous carcinoma cell biological behavior remain poorly understood. In this study, we present evidence that SCYL1BP1 can promote the degradation of MDM2 protein and further inhibit the G1/S transition of lung squamous carcinoma cell lines. Functional assays found that reintroduction of SCYL1BP1 into lung squamous carcinoma cell lines significantly inhibited cell proliferation, migration, invasion and tumor formation in nude mice, suggesting strong tumor suppressive function of SCYL1BP1 in lung squamous carcinoma. Taken together, our data suggest that the interaction of SCYL1BP1/MDM2 could accelerate MDM2 degradation, and may function as an important tumor suppressor in lung squamous carcinomas.

• Molecules and Cells
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• v.40 no.10
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• pp.773-786
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• 2017

The loss of green coloration via chlorophyll (Chl) degradation typically occurs during leaf senescence. To date, many Chl catabolic enzymes have been identified and shown to interact with light harvesting complex II to form a Chl degradation complex in senescing chloroplasts; this complex might metabolically channel phototoxic Chl catabolic intermediates to prevent oxidative damage to cells. The Chl catabolic enzyme 7-hydroxymethyl Chl a reductase (HCAR) converts 7-hydroxymethyl Chl a (7-HMC a) to Chl a. The rice (Oryza sativa) genome contains a single HCAR homolog (OsHCAR), but its exact role remains unknown. Here, we show that an oshcar knockout mutant exhibits persistent green leaves during both dark-induced and natural senescence, and accumulates 7-HMC a and pheophorbide a (Pheo a) in green leaf blades. Interestingly, both rice and Arabidopsis hcar mutants exhibit severe cell death at the vegetative stage; this cell death largely occurs in a light intensity-dependent manner. In addition, 7-HMC a treatment led to the generation of singlet oxygen ($^1O_2$) in Arabidopsis and rice protoplasts in the light. Under herbicide-induced oxidative stress conditions, leaf necrosis was more severe in hcar plants than in wild type, and HCAR-overexpressing plants were more tolerant to reactive oxygen species than wild type. Therefore, in addition to functioning in the conversion of 7-HMC a to Chl a in senescent leaves, HCAR may play a critical role in protecting plants from high light-induced damage by preventing the accumulation of 7-HMC a and Pheo a in developing and mature leaves at the vegetative stage.

• Transactions of the Korean hydrogen and new energy society
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• v.18 no.4
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• pp.432-438
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• 2007

The reforming process for hydrogen production generates some impurities. Impurities in hydrogen such as $CO_2$, CO, $H_2S$, $NH_3$ affect fuel cell performance. It is well known that CO generated by the reforming process may negatively affect performance of cell, cause damage on catalysts resulting performance degradation. Hydrogen produced by reforming process includes about 2% methane. The presence of methane up to 10% is reported negligible degradation in cell performance. However, methane more than 10% in hydrogen stream had not been researched. The concentration of impurity supplied to the fuel cell was verified by gas chromatography(GC). In this study, the influence of $CH_4$ on performance of PEM fuel cell was investigated by means of current vs. potential experiment, long run(10 hr) test and electrochemical impedance measurement when the concentrations of impurities were 10%, 20% and 30%.

• Transactions of the Korean hydrogen and new energy society
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• v.24 no.1
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• pp.50-60
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• 2013

High temperature proton exchange membrane fuel cells (PEMFCs) using phosphoric acid (PA) doped polybenzimidazole (PBI) membranes have been concentrated as one of solutions to the limits with traditional low temperature PEMFCs. However, the amount of reported experimental data is not enough to catch the operational characteristics correlated with cell performance and durability. In this study, design of experiments (DOE) based operational optimization method for high temperature PEMFCs has been proposed. Response surface method (RSM) is very useful to effectively analyze target system's characteristics and to optimize operating conditions for a short time. Thus RSM using central composite design (CCD) as one of methodologies for design of experiments (DOE) was adopted. For this work, the statistic models which predict the performance and degradation rate with respect to the operating conditions have been developed. The developed performance and degradation models exhibit a good agreement with experimental data. Compared to the existing arbitrary operation, the expected cell lifetime and average cell performance during whole operation could be improved by optimizing operating conditions. Furthermore, the proposed optimization method could find different new optimal solutions for operating conditions if the target lifetime of the fuel cell system is changed. It is expected that the proposed method is very useful to find optimal operating conditions and enhance performance and durability for many other types of fuel cell systems.

• BMB Reports
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• v.44 no.9
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• pp.572-577
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• 2011

Elevated phospholipase D (PLD) expression prevents cell cycle arrest and apoptosis. However, the roles of PLD isoforms in cell proliferation and apoptosis are incompletely understood. Here, we investigated the physiological significance of the interaction between PLD2 and protein kinase CKII (CKII) in HCT116 human colorectal carcinoma cells. PLD2 interacted with the CKII${\beta}$ subunit in HCT116 cells. The C-terminal domain (residues 578-933) of PLD2 and the N-terminal domain of CKII${\beta}$ were necessary for interaction between the two proteins. PLD2 relocalized CKII${\beta}$ to the plasma membrane area. Overexpression of PLD2 reduced CKII${\beta}$ protein level, whereas knockdown of PLD2 led to an increase in CKII${\beta}$ expression. PLD2-induced CKII${\beta}$ reduction was mediated by ubiquitin-dependent degradation. The C-terminal domain of PLD2 was sufficient for CKII${\beta}$ degradation as the catalytic activity of PLD2 was not required. Taken together, the results indicate that the C-terminal domain of PLD2 can regulate CKII by accelerating CKII${\beta}$ degradation in HCT116 cells.