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YOUNG-JI BYON(변영지),SEUNG HWAN KIM(김승환),GOANG SUNG JIN(진광성),YOUNG WOOK SEO(서영욱),YOUNG SOON BAEK(백영순) 한국수소및신에너지학회 2023 한국수소 및 신에너지학회논문집 Vol.34 No.6
Recently, a hydrogen charging station-related memorandum of understanding (MOU) was signed between Korea Transport Institute and United Arab Emirates (UAE) Ministry of Transport in Abu Dhabi, creating a foundation for exporting green hydrogen charging stations and hydrogen powered public transit buses developed with Korean technology to Abu Dhabi. Reliable construction and operation of the charging stations require a thorough review on associated standards and legal requirements. In particular, it is essential to analyze currently effective standards related to hydrogen production, hydrogen vehicle charging, and hydrogen charging stations. This paper specifically focuses on comparative analysis of hydrogen-related standards in the UAE and the Republic of Korea. Similar to UAE, Korean hydrogen charging station-related standards follow International Organization for Standardization (ISO) standards. From real-life experiences in developing and operating charging stations, even more essence of ISO standards have been adopted in Korean standards than UAE. In particular, ISO standards related to fire prevention are additionally included in Korea. This paper also suggests procedural and administrative strategies for enabling application of Korean hydrogen charging station-related standards in UAE.
Yoo, Dae Young,Yoo, Ki-Yeon,Park, Joon Ha,Kwon, Hyun Jung,Jung, Hyo Young,Kim, Jong Whi,Choi, Goang-Min,Moon, Seung Myung,Kim, Dae Won,Yoon, Yeo Sung,Won, Moo-Ho,Hwang, In Koo Medknow PublicationsMedia Pvt Ltd 2016 Neural regeneration research Vol.11 No.6
<P>In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin (ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the stratum pyramidale and stratum oriens at 12 hours following ischemic insult, transiently decreased at 1–2 days and then increased once again within the CA1 region at 4–7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the stratum pyramidale and decreased at 2 days. At 4–7 days after ischemia, ferritin-H immunoreactivity in the glial components in the CA1 region was significantly increased. Transferrin immunoreactivity was increased significantly in the stratum pyramidale at 12 hours, peaked at 1 day, and then decreased significantly at 2 days after ischemia. Seven days after ischemia, Transferrin immunoreactivity in the glial cells of the stratum oriens and radiatum was significantly increased. Western blot analyses supported these results, demonstrating that compared to sham controls, ferritin H and transferrin protein levels in hippocampal homogenates significantly increased at 1 day after ischemia, peaked at 4 days and then decreased. These results suggest that iron overload-induced oxidative stress is most prominent at 12 hours after ischemia in the stratum pyramidale, suggesting that this time window may be the optimal period for therapeutic intervention to protect neurons from ischemia-induced death.</P>
Jung, Hyo Young,Cho, Su Bin,Kim, Woosuk,Yoo, Dae Young,Won, Moo-Ho,Choi, Goang-Min,Cho, Tack-Geun,Kim, Dae Won,Hwang, In Koo,Choi, Soo Young,Moon, Seung Myung Elsevier 2018 Neurochemistry International Vol.118 No.-
<P><B>Abstract</B></P> <P>In the present study, we made a PEP-1-phosphatidylethanolamine-binding protein 1 (PEP-1-PEBP1) fusion protein to facilitate the transduction of PEBP1 into cells and observed significant ameliorative effects of PEP-1-PEBP1 against H<SUB>2</SUB>O<SUB>2</SUB>-induced neuronal damage and the formation of reactive oxygen species in the HT22 hippocampal cells. In addition, administration of PEP-1-PEBP1 fusion protein ameliorated H<SUB>2</SUB>O<SUB>2</SUB>-induced phosphorylation of extracellular signal-regulated kinases (ERK1/2) and facilitated the phosphorylation of cyclic-AMP response element binding protein (CREB) in HT22 cells after exposure to H<SUB>2</SUB>O<SUB>2</SUB>. We also investigated the temporal and spatial changes of phosphorylated phosphatidylethanolamine-binding protein 1 (pPEBP1) in the hippocampus, after 5 min of transient forebrain ischemia in gerbils. In the sham-operated animals, pPEBP1 immunoreactivity was not detectable in the hippocampal CA1 region. pPEBP1 immunoreactivity was significantly increased in the hippocampal CA1 region, 1–2 days after ischemia, compared to that in the sham-operated group and pPEBP1 immunoreactivity was returned to levels in sham-operated group at 3–4 days after ischemia. pPEBP1 immunoreactivity significantly increased at day 7 after ischemia and decreased to sham-operated group levels by day 10 after ischemia/reperfusion. In addition, administration of PEP-1-PEBP1 fusion protein significantly reduced the ischemia-induced hyperactivity of locomotion, 1 day after ischemia and PEP-1-PEBP1 reduced neuronal damage and reactive gliosis (astrocytosis and microgliosis) in the gerbil hippocampal CA1 region, 4 days after ischemia. Administration of PEP-1-PEBP1 fusion protein ameliorated the ischemia-induced phosphorylation of ERK at 3 h and 6 h after ischemia/reperfusion and accelerated the phosphorylation of CREB in ischemic hippocampus at 6 h after ischemia. These results suggest that the increase in PEBP1 phosphorylation causes neuronal damage in the hippocampus and treatment with PEP-1-PEBP1 fusion protein provides neuroprotection from increasing phosphorylation of ERK-CREB pathways in the hippocampal CA1 region, during ischemic damage.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PEP-1-PEBP1 can efficiently transduce into the hippocampal cells and is stably expressed within the cells. </LI> <LI> PEP-1-PEBP1 significantly ameliorates H<SUB>2</SUB>O<SUB>2</SUB>-induced neuronal death and reactive oxygen species formation in the hippocampal cells. </LI> <LI> PEP-1-PEBP1 protects neurons from ischemic damage by modulating phosphorylation of ERK and CREB in the hippocampus. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Cho, Goang-Won,Noh, Min-Young,Kang, Byung Yong,Ku, Il-Whea,Park, Jiseon,Hong, Yoon-Ho,Kim, Myung-Hwa,Kim, Seung Hyun Mary Ann Liebert, Inc 2011 Assay and drug development technologies Vol.9 No.5
<P>Glycogen synthase kinase-3β (GSK-3β), a serine/threonine kinase also known as tau protein kinase I, has been implicated in the pathogenic conditions of Alzheimer's disease. Many investigators have focused on GSK-3 inhibitor as a therapeutic drug. In this study, we established a cell-based assay for the screening of novel GSK-3β inhibitors. For this purpose, four-repeat tau cDNAs were stably expressed in human embryonic kidney 293 (HEK293) cells (HEK293-Tau). The proliferation of HEK293-Tau cells was no different from that of HEK293 cells, as measured by the bromodeoxyuridine enzyme-linked immunosorbent assay (BrdU ELISA). The concentration-dependent reduction of tau phosphorylation by GSK-3 inhibitors, LiCl, Chir98023, and SB415286, was examined by immunoblot analysis and Tau ELISA (in situ ELISA). Highly consistent data were obtained, suggesting that this novel ELISA method is highly reproducible. Using this ELISA strategy, we isolated a few candidate compounds, including compounds 114 and 149, from several hundreds of synthetic agents and demonstrated that such candidates protect nerve growth factor-differentiated PC12 cells against amyloid-β-induced cell death. These data indicate that this Tau ELISA method in HEK293-Tau cells may be a suitable cell-based assay system to screen for GSK-3β inhibitors.</P>