• Journal of the Korean Electrochemical Society
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• v.13 no.4
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• pp.277-282
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• 2010

Durability of automotive polymer electrolyte membrane fuel cell (PEMFC) strongly depends the startup/shutdown procedure. Formation of hydrogen/air boundary in the anode gas channel, so-called reverse current condition, particularly induces fast degradation of the cathode. Under the reverse current condition, high voltage is present at the cathode facing air in the anode gas channel and is a function of residual oxygen concentration in the gas channels, that increases with storage time and reaches 21% (air) eventually. In this study, effects of residual oxygen concentration in a PEMFC on degradation of the PEMFC.

• BMB Reports
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• v.51 no.10
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• pp.484-485
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• 2018

Receptor-interacting protein kinase-3 (RIP3 or RIPK3) is a serine-threonine kinase largely essential for necroptotic cell death; it also plays a role in some inflammatory diseases. High levels of RIP3 are likely sufficient to activate necroptotic and inflammatory pathways downstream of RIP3 in the absence of an upstream stimulus. For example, we have previously detected high levels or RIP3 in the skin of Toxic Epidermal Necrolysis patients; this correlates with increased phosphorylation of MLKL found in these patients. We have long surmised that there are molecular mechanisms to prevent anomalous activity of the RIP3 protein, and so prevent undesirable cell death and inflammatory effects when inappropriately activated. Recent discovery that Carboxyl terminus of Hsp 70-Interacting Protein (CHIP) could mediate ubiquitylation- and lysosome-dependent RIP3 degradation provides a potential protein that has this capacity. However, while screening for RIP3-binding proteins, we discovered that pellino E3 ubiquitin protein ligase 1 (PELI1) also interacts directly with RIP3 protein; further investigation in this study revealed that PELI1 also targets RIP3 for proteasome-dependent degradation. Interestingly, unlike CHIP, which targets RIP3 more generally, PELI1 preferentially targets kinase active RIP3 that has been phosphorylated on T182, subsequently leading to RIP3 degradation.

• Journal of the Korean Ceramic Society
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• v.53 no.5
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• pp.483-488
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• 2016

Anode supported solid oxide fuel cells (SOFCs), consisting of Ni+YSZ anode, YSZ electrolyte, and LSM+YSZ cathode, were fabricated and constant current tested with direct internal reforming of methane (steam to carbon ratio ~ 2) as well as hydrogen fuel at $800^{\circ}C$. The cell, operated under direct internal reforming conditions, showed relatively rapid degradation (~ 1.6 % voltage drop) for 95 h; the cells with hydrogen fuel operated stably for 170 h. Power density and impedance spectra were also measured before and after the tests, and post-test analyses were conducted on the anode parts using SEM / EDS. The results indicate that the performance degradation of the cell operated with internal reforming can be attributed to carbon depositions on the anode, which increase the resistance against anode gas transport and deactivate the Ni catalyst. Thus, the present study shows that direct internal reforming SOFCs cannot be stably operated even under the condition of S/C ratio of ~ 2, probably due to non-uniform mixture (methane and steam) gas flow.

• Current Applied Physics
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• v.18 no.12
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• pp.1600-1604
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• 2018

This paper reports on a systematic and quantitative assessment of light induced degradation (LID) and regeneration in full Al-BSF and passivated emitter rear contact cells (PERC) along with the fundamental understanding of the difference between the two. After LID, PERC cells showed a much greater loss in cell efficiency than full Al-BSF cells (~0.9% vs ~0.6%) because the degradation in bulk lifetime also erodes the benefit of superior BSRV in PERC cells. Three main regeneration conditions involving the combination of heat and light ($75^{\circ}C/1\;Sun/48h$, $130^{\circ}C/2\;Suns/1.5h$ and $200^{\circ}C/3\;Suns/30s$) were implemented to eliminate LID loss due to BO defects. Low temperature/long time ($75^{\circ}C/48h$) and high temperature/short time ($200^{\circ}C/30s$) regeneration process was unable to reach 100% stabilization. The intermediate temperature/time ($130^{\circ}C/1.5h$) generation achieved nearly full recovery and stabilization (over 99%) for both full Al-BSF and PERC cells. We discussed the effect of temperature, time and suns in regeneration mechanism for two cells.

• Journal of Ginseng Research
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• v.45 no.2
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• pp.295-304
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• 2021

Background: Acute promyelocytic leukemia (APL) is a hematopoietic malignancy driven by promyelocytic leukemia-retinoic acid receptor A (PML-RARA) fusion gene. The therapeutic drugs currently used to treat APL have adverse effects. 20(S)-ginsenoside Rh2 (GRh2) is an anticancer medicine with high effectiveness and low toxicity. However, the underlying anticancer mechanisms of GRh2-induced PML-RARA degradation and apoptosis in human APL cell line (NB4 cells) remain unclear. Methods: Apoptosis-related indicators and PML-RARA expression were determined to investigate the effect of GRh2 on NB4 cells. Z-VAD-FMK, LY294002, and C 87, as inhibitors of caspase, and the phosphatidylinositol 3-kinase (PI3K) and tumor necrosis factor-α (TNF-α) pathways were used to clarify the relationship between GRh2-induced apoptosis and PML-RARA degradation. Results: GRh2 dose- and time-dependently decreased NB4 cell viability. GRh2-induced apoptosis, cell cycle arrest, and caspase3, caspase8, and caspase9 activation in NB4 cells after a 12-hour treatment. GRh2-induced apoptosis in NB4 cells was accompanied by massive production of reactive oxygen species, mitochondrial damage and upregulated Bax/Bcl-2 expression. GRh2 also induced PML/PML-RARA degradation, PML nuclear bodies formation, and activation of the downstream p53 pathway in NB4 cells. Z-VAD-FMK inhibited caspase activation and significantly reversed GRh2-induced apoptosis and PML-RARA degradation. GRh2 also upregulated TNF-α expression and inhibited Akt phosphorylation. LY294002, an inhibitor of the PI3K pathway, enhanced the antitumor effects of GRh2, and C 87, an inhibitor of the TNF-α pathway, reversed NB4 cell viability, and GRh2-mediated apoptosis in a caspase-8-dependent manner. Conclusion: GRh2 induced caspase-dependent PML-RARA degradation and apoptosis in NB4 cells via the Akt/Bax/caspase9 and TNF-α/caspase8 pathways.

• Journal of the Korean Wood Science and Technology
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• v.52 no.3
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• pp.243-261
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• 2024

In this study, samples were collected from various ancient wooden shipwrecks, including the Shinan shipwreck and Jindo shipwreck that used iron nails, the Yeongheungdo shipwreck carrying iron artifacts, as well as the Sibidongpado shipwreck and Wando shipwreck where degradation products were not observed, all of which were salvaged by the National Research Institute of Maritime Heritage. The aim was to analyze the characteristics of degradation products generated by iron (Fe) within the salvaged wooden shipwreck materials and establish fundamental data on degradation products in waterlogged archaeological wood. The analysis revealed that sulfur (S) is generally accumulated in wood obtained from marine environments. It was observed that the content of inorganic substances such as iron and sulfur was significantly higher in the Shinan shipwreck, Jindo shipwreck, and Yeongheungdo shipwreck compared to Sibidongpado shipwreck and Wando shipwreck, which used wooden nails. This indicates that the presence of iron affects the accumulation of degradation products and suggests that iron is a factor in the corrosion of wood. Furthermore, crystallin compounds were observed within the cell walls, and higher concentrations of iron and sulfur were found in the resin ducts, rays, and radial tissues. This suggests that during desalination and consolidation treatments, warm water or polyethylene glycol (PEG) may move degradation factors into resincanals, rays, radial tissues, etc.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.1
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• pp.1-7
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• 2011

Many anticancer agents as well as ionizing radiation have been shown to induce autophagy which is originally described as a protein recycling process and recently reported to play a crucial role in various disorders. In HCT116 human colon cancer cells, we found that curcumin, a polyphenolic phytochemical extracted from the plant Curcuma longa, markedly induced the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and degradation of sequestome-1 (SQSTM1) which is a marker of autophagosome degradation. Moreover, we found that curcumin caused GFP-LC3 formation puncta, a marker of autophagosome, and decrease of GFP-LC3 and SQSTM1 protein level in GFP-LC3 expressing HCT116 cells. It was further confirmed that treatment of cells with hydrogen peroxide induced increase of LC3 conversion and decrease of GFP-LC3 and SQSTM1 levels, but these changes by curcumin were almost completely blocked in the presence of antioxidant, N-acetylcystein (NAC), indicating that curcumin leads to reactive oxygen species (ROS) production, which results in autophagosome development and autolysosomal degradation. In parallel with NAC, SQSTM1 degradation was also diminished by bafilomycin A, a potent inhibitor of autophagosome-lysosome fusion, and cell viability assay was further confirmed that cucurmin-induced cell death was partially blocked by bafilomycin A as well as NAC. We also observed that NAC abolished curcumin-induced activation of extracelluar signal-regulated kinases (ERK) 112 and p38 mitogen-activated protein kinases (MAPK), but not Jun N-terminal kinase (JNK). However, the activation of ERK1/2 and p38 MAPK seemed to have no effect on the curcumin-induced autophagy, since both the conversion of LC3 protein and SQSTM1 degradation by curcumin was not changed in the presence of NAC. Taken together, our data suggest that curcumin induced ROS production, which resulted in autophagic activation and concomitant cell death in HCT116 human colon cancer cell. However, ROS-dependent activation of ERK1/2 and p38 MAPK, but not JNK, might not be involved in the curcumin-induced autophagy.

• Journal of Microbiology and Biotechnology
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• v.11 no.6
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• pp.928-933
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• 2001

Approximately 0.1 mg/ml of polyvinyl alcohol (PVA) was degraded by the growing cell, Brevibacillus laterospours, for 30 h, and 0.2 mg/ml of PVA was degraded by the cell-free extract that was isolated from Brevibacillus laterosporus. Approximately $0.29{\mu}g$/ml of acetic acid was produced from PVA by using the cell-free extract as a catalyst for 40 min. $V_{max}\;and\;K_m$ value of purified PAV-degradation enzyme was 3.75g/l and 2.75 g/l/min in reaction with EDTA and 3.99 g/l and 2.98 g/l/min in reaction without EDTA, respectively. Molecular weight of the purified enzyme determined by SDS-PAGE was 63,000 Da. Alcohol dehydrogenase and aldehyde dehydrogenase activities were qualitatively detected on a native acrylamide gel by an active staining method, indicating the existence of the metabolic pathway to use PVA as a substrate.

• Journal of Nutrition and Health
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• v.36 no.8
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• pp.828-833
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• 2003

Dially disulfide (DADS), a component of garlic (Allium sativum), has been known to exert potent chemopreventive activity against various cancers. In this study, the synergistic effect of DADS and daunorubicin on the cytotoxicity of HL-60 cells, a human leukemia cell line, was investigated. DADS at 25 M greatly potentiated daunorubicin-induced cell death, decreasing cell viabilityto50%ofthe control. Daunorubicin-induced apoptosis was accompanied by the activation of caspase-3, the degradation of poly-(ADP-ribose) polymerase (PARP) and D4-GDI, and DNA fragmentation, which were blocked by pre-treatment with acetyl-Asp-Glu-Val-Asp- dialdehyde (Ac-DEVD-CHO). Treatment that combined 25 M DADS and 100 nM daunorubicin caused a similar degree of caspase-3 activation, PARP and D4-GDI degradation, and DNA fragmentation to that caused by treatment with 250 nM daunorubicin alone. These results indicate that combined therapy using daunorubicin with DADS, a component of food, and garlic can effectively decrease the therapeutic dose of daunorubicin, preventing the severe side effects of daunorubicin.

• Journal of Life Science
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• v.18 no.3
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• pp.422-425
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• 2008

Membrane-type 1 matrix metalloproteinase (MT1-MMP) is a membrane-associated zinc-dependent endoproteinase involved in extracellular matrix remodeling. MT1-MMP hydrolyzes ECM proteins like collagen and is involved in cancer cell migration and metastasis. Caveolins are integral membrane proteins and play a role in formation of caveolae, specialized membrane microdomains involved in clathrin-independent endocytosis. Recombinant MT1-MMP was transiently expressed in PANC-1 cells. Cells expressing recombinant MT1-MMP were able to hydrolyze collagen and migrate on collagen coated trans-well. Both subjacent collagen degradation and the cell migration conferred by recombinant MT1-MMP were inhibited by co-transfection of plasmids containing caveolin-1 cDNA. The results support that MT1-MMP is localized in lipid raft of the membrane and MT1-MMP activities in invasive cells could be inhibited by caveolin.