9 results on '"Jung-hye Kim"'
Search Results
2. Elevated TyG Index Predicts Progression of Coronary Artery Calcification.
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Kahui Park, Chul Woo Ahn, Sang Bae Lee, Shinae Kang, Ji Sun Nam, Byoung Kwon Lee, Jung Hye Kim, Jong Suk Park, Park, Kahui, Ahn, Chul Woo, Lee, Sang Bae, Kang, Shinae, Nam, Ji Sun, Lee, Byoung Kwon, Kim, Jung Hye, and Park, Jong Suk
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CORONARY arteries , *CORONARY artery calcification , *LOGISTIC regression analysis , *POPULATION , *SQUARE root - Abstract
Objective: To investigate the triglyceride-glucose (TyG) index association with coronary artery calcification (CAC) progression in adult Koreans.Research Design and Methods: Various cardiovascular risk factors and anthropometric profiles were assessed in 1,175 subjects who previously had a CAC evaluation at least twice by multidetector computed tomography in a health care center. The TyG index was determined using ln(fasting triglycerides [mg/dL] × fasting glucose [mg/dL]/2). The CAC progression was defined as either incident CAC in a CAC-free population at baseline or an increase of ≥2.5 units between the square roots of the baseline and follow-up coronary artery calcium scores (CACSs) of subjects with detectable CAC at baseline.Results: CAC progression was seen in 312 subjects (27%) during 4.2 years follow-up. On the basis of the TyG index, subjects were stratified into three groups. Follow-up CACS and incidence of CAC progression were markedly elevated with rising TyG index tertile. Logistic regression analysis adjusted for various risk factors revealed an odds ratio for CAC progression of 1.82 (95% CI 1.20-2.77; P ≤ 0.01) when the highest and lowest TyG index tertiles were compared.Conclusions: The TyG index is an independent predictor of CAC progression. [ABSTRACT FROM AUTHOR]- Published
- 2019
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3. Triglyceride Glucose Index Is Superior to the Homeostasis Model Assessment of Insulin Resistance for Predicting Nonalcoholic Fatty Liver Disease in Korean Adults.
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Sang Bae Lee, Min Kyung Kim, Shinae Kang, Kahui Park, Jung Hye Kim, Su Jung Baik, Ji Sun Nam, Chul Woo Ahn, and Jong Suk Park
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FATTY liver , *INSULIN resistance , *RECEIVER operating characteristic curves , *LOGISTIC regression analysis , *GLUCOSE - Abstract
Background: Recently, the triglyceride glucose (TyG) index has been considered a surrogate marker of insulin resistance which is a well-known pathogenic factor in nonalcoholic fatty liver disease (NAFLD). However, few studies have investigated the relationship between the TyG index and NAFLD. Thus, we investigated the relationship between the TyG index and NAFLD and the effectiveness of the TyG index compared with the homeostasis model assessment of insulin resistance (HOMA-IR) in identifying NAFLD in Korean adults. Methods: Participants of 4,986 who underwent ultrasonography in a health promotion center were enrolled. The TyG index was calculated as ln [fasting triglycerides (mg/dL)×fasting glucose (mg/dL)/2], and HOMA-IR was estimated. NAFLD was diagnosed by ultrasonography. Results: Significant differences were observed in metabolic parameters among the quartiles of the TyG index. The prevalence of NAFLD significantly increased with increment in the TyG index. After adjusting for multiple risk factors, a logistic regression analysis was performed. When the highest and lowest quartiles of the TyG index and HOMA-IR were compared, the odds ratios for the prevalence of NAFLD were 2.94 and 1.93 (95% confidence interval, 2.32 to 3.72 and 1.43 to 2.61; both P for trend <0.01), respectively. According to the receiver operating characteristic analysis, the TyG index was superior to HOMA-IR in predicting NAFLD. Conclusion: The TyG index and prevalence of NAFLD were significantly related and the TyG index was superior to HOMA-IR in predicting NAFLD in Korean adults. [ABSTRACT FROM AUTHOR]
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- 2019
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4. Physical characterization of amorphous In-Ga-Zn-O thin-film transistors with direct-contact asymmetric graphene electrode.
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Jaewook Jeong, Joonwoo Kim, Hee-Yeon Noh, Soon Moon Jeong, Jung-Hye Kim, and Sung Myung
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THIN film transistors , *FIELD-effect transistors , *ELECTRODES , *SCHOTTKY barrier , *GRAPHENE - Abstract
High performance a-IGZO thin-film transistors (TFTs) are fabricated using an asymmetric graphene drain electrode structure. A-IGZO TFTs (channel length = 3 μm) were successfully demonstrated with a saturation field-effect mobility of 6.6 cm²/Vswithout additional processes between the graphene and a-IGZO layer. The graphene/a-IGZO junction exhibits Schottky characteristics and the contact property is affected not only by the Schottky barrier but also by the parasitic resistance from the depletion region under the graphene electrode. Therefore, to utilize the graphene layer as S/D electrodes for a-IGZO TFTs, an asymmetric electrode is essential, which can be easily applied to the conventional pixel electrode structure [ABSTRACT FROM AUTHOR]
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- 2014
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5. Regulation of replicative senescence by insulin-like growth factor-binding protein 3 in human umbilical vein endothelial cells.
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Kwang Seok Kim, Min-Sun Kim, Young Bae Seu, Hae Young Chung, Jung Hye Kim, and Jae-Ryong Kim
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SOMATOMEDIN , *INSULIN , *AGING , *INSULIN-like growth factor-binding proteins , *GROWTH factors , *DERMIS , *ENDOTHELIUM - Abstract
Insulin/insulin-like growth factor (IGF) signaling pathways are among the most conserved processes in aging in organisms ranging from yeast to mammals. Previously, using cDNA microarray technology, we reported that expression of IGF-binding protein 3 (IGFBP3), one of the IGF-binding proteins, was increased with age in human dermal fibroblasts. In this study, the role of IGFBP3 on cellular senescence was studied in human umbilical vein endothelial cells (HUVEC). The expression levels of IGFBP3 mRNA and protein were increased in HUVECs with age. Knockdown of IGFBP3 in old cells with IGFBP3 short hairpin RNA (shRNA) retrovirus resulted in the partial reduction of a variety of senescent phenotypes, such as changes in cell morphology, and decreases in population doubling times and senescence-associated β-galactosidase (SA-β-gal) staining. Down-regulation of IGFBP3 rescued the growth arrest induced by p53 overexpression in young HUVECs. In contrast, up-regulation of IGFBP3 in young cells and prolonged IGFBP3 treatment accelerated cellular senescence, confirmed by cell proliferation and SA-β-gal staining. The FOXO3a (forkhead box O3a) protein level was increased in old IGFBP3 shRNA cells. The treatment of young HUVECs with IGFBP3 repressed the levels of FOXO3a protein. Furthermore, calorie restriction reduced IGFBP3 protein levels, which were found to be increased with age in the rat liver and serum. These results suggest that IGFBP3 might play an important role in the cellular senescence of HUVECs as well as in vivo aging. [ABSTRACT FROM AUTHOR]
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- 2007
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6. Environmental Metabolite, 1,2-Diacetylbenzene, Produces Cytotoxicity Through ROS Generation in HUVEC Cells.
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Min Kyeong Kim, Kwang Seok Kim, Jae Heun Chung, Jung Hye Kim, Jae-Ryong Kim, Hae Young Chung, and Min-Sun Kim
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ETHYLBENZENE , *ORGANIC solvents , *METABOLITES , *NEUROLOGICAL disorders , *CYTOCHROME P-450 , *TOXICOLOGY - Abstract
Organic solvents are ubiquitous in industrial and household surroundings, and thus individuals are easily exposed. 1,2-Diethylbenzene (DEB) is one of organic solvents contained in gasoline or jet fuels. DEB is absorbed by dermal or inhalation routes, metabolized by cytochrome P-450 in the liver, and ultimately affects mammalian functions. 1,2-Diacetylbenzene (1,2-DAB), which is a putative metabolite of 1,2-DEB, resulted in neuropathological effects on rodent central and peripheral nervous systems. To elucidate the possibility of 1,2-DAB effects on the vascular system, studies were undertaken to examine whether 1,2-DAB induces endothelial cytotoxicity through reactive oxygen species (ROS) generation. Incubation of human umbilical vein endothelial cells (HUVEC) with lower concentrations (4 or 8 μM) of 1,2-DAB induced inhibition of cellular growth and at higher amounts (16 or 32 μM) produced apoptosis. Endothelial cells cultured with 1,2-DAB also showed increased intracellular ROS production and morphological alterations indicative of senescence. Pretreatment with the well-known antioxidant glutathione or N-acetylcysteine (NAC) reduced cytotoxicity induced by 1,2-DAB. Taken together, the results provide evidence that cytotoxicity induced by 1,2-DAB in endothelial cells may be mediated by ROS generation. [ABSTRACT FROM AUTHOR]
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- 2007
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7. Down-Regulation of a Forkhead Transcription Factor, FOXO3a, Accelerates Cellular Senescence in Human Dermal Fibroblasts.
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Hyun Kyoung Kim, Yu Kyoung Kim, In-Hwan Song, Suk-Hwan Baek, Seung-Rock Lee, Jung Hye Kim, and Jae-Ryong Kim
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INSULIN , *GROWTH factors , *TRANSCRIPTION factors , *CELLULAR signal transduction , *FIBROBLASTS , *RNA - Abstract
The signaling pathway of insulin/insulin-like growth factor/phosphatidylinositol-3 kinase/Akt/forkhead transcription factors is known to control life span and senescence in organisms ranging from yeast to mice. The FOXO family of forkhead transcription factors, FOXO1, FOXO3a, and FOXO4, play a critical role in this signal transduction pathway. However, the impact of FOXO3a activation on life span of primary cultured human dermal fibroblasts (HDFs) is unknown. To investigate the role of FOXO3a in the regulation of cellular senescence, we prepared FOXO3a-siRNA stable HDFs. We found that the down-regulation of FOXO3a RNA and protein in HDFs induced many senescent phenotypes, including changes in cell morphology, increases in population doubling times, senescence-associated β-galactosidase staining and the cellular reactive oxygen species, and up-regulation of p53/p21 protein expression. Our data provide evidence of the key role of FOXO3a transcription factor as a mediator of cellular senescence in HDFs, and suggest that the mechanism of senescence is conserved in HDFs. [ABSTRACT FROM AUTHOR]
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- 2005
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8. Phosphatidic Acid Regulates Systemic Inflammatory Responses by Modulating the Akt-Mammalian Target of Rapamycin-p70 S6 Kinase 1 Pathway.
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Hyung-Kyu Lim, Ophry, Young-Ae Choi, Wan Park, Taehoon Lee, Sung Ho Ryu, Seong-Yong Kim, Ophry, Jae-Ryong Kim, Ophry, Jung-Hye Kim, and Suk-Hwan Baek
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RAPAMYCIN , *MACROPHAGES , *IMMUNOSUPPRESSIVE agents - Abstract
Macrophages are pivotal effector cells in the innate immune system. When microbial products bind to pathogen recognition receptors, macrophages are activated and release a broad array of mediators, such as cytokines, that orchestrate the inflammatory responses of the host. Phosphatidic acid (PA) has been implicated as an important metabolite of phospholipid biosynthesis and in membrane remodeling and has been further suggested to be a crucial second messenger in various cellular signaling events. Here we show that PA is an essential regulator of inflammatory response. Deleterious effects of PA are associated with the secretion of proinflammatory cytokines, such as tumor necrosis factor-α, interleukin-1β, interleukin-6, and the production of nitric oxide, prostaglandin E[sub 2], which are predominantly released by macrophage Raw264.7 cells. Furthermore, the administration of PA to mice increased the serum cytokine level. Moreover, direct or lipopolysaccharide-induced PA accumulation by macrophages led to the Akt-dependent activation of the mammalian target of rapamycin-p70 S6 kinase 1, a process required for the induction of inflammatory mediators. These findings demonstrate the importance of the role of PA in systemic inflammatory responses, and provide a potential usefulness as specific targets for the development of therapies. [ABSTRACT FROM AUTHOR]
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- 2003
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9. Inhibition of Trifluoperazine-induced DNA Fragmentation by Cyclic AMP Mediated Signaling.
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Ung Gu Kang, Myung Jong Kim, Pann-Ghill Suh, Sung Ho Ryu, Joo-Bae Park, Jung-Hye Kim, Yong Sik Kim, and Young Han Lee
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ANTIPSYCHOTIC agents , *CALMODULIN , *CYCLIC adenylic acid - Abstract
Trifluoperazine (TFP), a phenothiazine antipsychotic agent with calmodulin antagonist property, induces DNA fragmentation in a dose- and time-dependent manner in PC12 cells. Various agents affecting calcium mediated intracellular signal transduction such as calcium chelators, calcium ionopores, inhibitors of phospholipase C, and activators/inhibitors of protein kinase C did not block TFP-induced DNA fragmentation. Some of these agents themselves induced DNA fragmentation in the conditions under which they were examined. However, cholera toxin (selective Gs activator), forskolin (adenylate cyclase activator) or dibutyryl cyclic AMP (cyclic AMP analogue) inhibited TFP-induced DNA fragmentation in a dose-dependent manner. These results suggest that it is not the calcium but the Gs and adenylate cyclase pathways that play an important role in TFP-induced DNA fragmentation in PC12 cells. [ABSTRACT FROM AUTHOR]
- Published
- 1999
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