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Your search keyword '"Kim, Dong Hee"' showing total 1,050 results
Start Over Author "Kim, Dong Hee" Publication Type Academic Journals
1,050 results on '"Kim, Dong Hee"'

33. Enhanced Coil Design for Inductive Power-Transfer-Based Power Supply in Medium-Voltage Direct Current Sensors.

Author

Jo, Seungjin, Kim, Dong-Hee, and Ahn, Jung-Hoon

Subjects
POWER distribution networks, POWER resources, FAULT diagnosis, HIGH voltages, CURRENT distribution
Abstract

This paper presents an integrated coil design method for inductive power-transfer (IPT) systems. Because a medium-voltage direct current (MVDC) distribution network transmits power at relatively high voltages (typically in the tens of kV), accurate fault diagnosis using high-performance sensors is crucial to improve the safety of MVDC distribution networks. With the increasing power consumption of high-performance sensors, conventional power supplies using optical converters with 5 W-class output characteristics face limitations in achieving the rated output power. Therefore, this paper proposes a safe and reliable power supply method using the principle of IPT to securely maintain the insulation distance between the distribution network and the current sensor-supply line. A 100 W prototype IPT system is investigated, and its feasibility is validated by comparing its performance with conventional optical converters. [ABSTRACT FROM AUTHOR]

Published
2024
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42. The Survival of Human Intervertebral Disc Nucleus Pulposus Cells under Oxidative Stress Relies on the Autophagy Triggered by Delphinidin.

Author

Bahar, Md Entaz, Hwang, Jin Seok, Lai, Trang Huyen, Byun, June-Ho, Kim, Dong-Hee, and Kim, Deok Ryong

Subjects
NUCLEUS pulposus, INTERVERTEBRAL disk, AMP-activated protein kinases, CELLULAR aging, EXTRACELLULAR matrix
Abstract

Delphinidin (Delp), a natural antioxidant, has shown promise in treating age-related ailments such as osteoarthritis (OA). This study investigates the impact of delphinidin on intervertebral disc degeneration (IVDD) using human nucleus pulposus cells (hNPCs) subjected to hydrogen peroxide. Various molecular and cellular assays were employed to assess senescence, extracellular matrix (ECM) degradation markers, and the activation of AMPK and autophagy pathways. Initially, oxidative stress (OS)-induced hNPCs exhibited notably elevated levels of senescence markers like p53 and p21, which were mitigated by Delp treatment. Additionally, Delp attenuated IVDD characteristics including apoptosis and ECM degradation markers in OS-induced senescence (OSIS) hNPCs by downregulating MMP-13 and ADAMTS-5 while upregulating COL2A1 and aggrecans. Furthermore, Delp reversed the increased ROS production and reduced autophagy activation observed in OSIS hNPCs. Interestingly, the ability of Delp to regulate cellular senescence and ECM balance in OSIS hNPCs was hindered by autophagy inhibition using CQ. Remarkably, Delp upregulated SIRT1 and phosphorylated AMPK expression while downregulating mTOR phosphorylation in the presence of AICAR (AMPK activator), and this effect was reversed by Compound C, AMPK inhibitor. In summary, our findings suggest that Delp can safeguard hNPCs from oxidative stress by promoting autophagy through the SIRT1/AMPK/mTOR pathway. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Autophagy in Osteoarthritis: A Double-Edged Sword in Cartilage Aging and Mechanical Stress Response: A Systematic Review.

Author

Lee, Dong-Yeong, Bahar, Md Entaz, Kim, Chang-Won, Seo, Min-Seok, Song, Myung-Geun, Song, Sang-Youn, Kim, Soung-Yon, Kim, Deok-Ryong, and Kim, Dong-Hee

Subjects
AUTOPHAGY, KEYWORD searching, OSTEOARTHRITIS, CARTILAGE, AGING
Abstract

Background: Although osteoarthritis (OA) development is epidemiologically multifactorial, a primary underlying mechanism is still under debate. Understanding the pathophysiology of OA remains challenging. Recently, experts have focused on autophagy as a contributor to OA development. Method: To better understand the pathogenesis of OA, we survey the literature on the role of autophagy and the molecular mechanisms of OA development. To identify relevant studies, we used controlled vocabulary and free text keywords to search the MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, Web of Science, and SCOPUS database. Thirty-one studies were included for data extraction and systematic review. Among these studies, twenty-five studies investigated the effects of autophagy in aging and OA chondrocytes, six studies examined the effects of autophagy in normal human chondrocytes, and only one study investigated the effects of mechanical stress-induced autophagy on the development of OA in normal chondrocytes. Results: The studies suggest that autophagy activation prevents OA by exerting cell-protective effects in normal human chondrocytes. However, in aging and osteoarthritis (OA) chondrocytes, the role of autophagy is intricate, as certain studies indicate that stimulating autophagy in these cells can have a cytotoxic effect, while others propose that it may have a protective (cytoprotective) effect against damage or degeneration. Conclusions: Mechanical stress-induced autophagy is also thought to be involved in the development of OA, but further research is required to identify the precise mechanism. Thus, autophagy contributions should be interpreted with caution in aging and the types of OA cartilage. [ABSTRACT FROM AUTHOR]

Published
2024
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