• Journal of Nutrition and Health
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• v.31 no.9
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• pp.1481-1497
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• 1998

The purpose of this study was to determine the relation between serum lipid profiles, apolipoprotein E phenotype, and dietary patterns in a cross-section of healthy individuals from Cheju-Do. Age, gender, anthropometric measurements, blood pressure, dietary consumption, drinking / smoking habits and menopausal status were surveyed. Total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride, fasting blood glucose, and insulin levels were measured from overnight fasting blood. The study involved a total of 286 individuals(147 men and 139 women) between the ages of 20 and 60 years old. All of the subjects were recruited from a population of healthy individuals living in Cheju-Do. The results of the study are as follows : 1) Among the males, those in their 20's had the maximum food intake, while those in their 40's had the minimum food intake. For the females, food intake was the highest for those in their 30's. Energy and nutrient intakes were directly proportional to the amount of food intake. Men in their 30's were heavier than other men and women in their 40's were heavier than other women. The activity index for men in their 20's and 30's appeared to be lower than that of men above 40. The activity index of women in their 20's appeared to be lowest among all aged groups, and the index appeared to increase from the age of 30 onwards. 2) In terms of changes In serum constituents with age, men in their 40's appeared to have the highest levels of serum constituents such as lipids, glucose, and insulin. Men in their 50's showed the highest levels of serum LDL-cholesterol and glucose. Men in their 30's showed peak levels of serum triglycerides. On the other hand, women in their 50's appeared to have peak levels of serum total cholesterol, LDL-cholesterol, and triglycerides. There was no ch:ange with age in HDL-cholesterol and insulin levels for men and women. The percentage of the subjects had the following apo E phenotypes : E3/3, 91.3% ; E3/2, 5.4% ; E4/3, 2.5% ; E4/2, 0.7%. Lee's reserch with Korean female college students showed that the percentage of ApoE3/3, E3/2, E 4/2, E4/3, and E4/4 were 84.8%, 6.7%, 6.7%, 0.9%, 0.9%, respectively. The number of samples with ApoE mutation was so small that there was no statistical significance in the relation between apolipoprotein E phenotype and se겨m lipids. 3) To investigate the relati onship between weight and serum constituents, the subjects of this study were divided into three groups by BMI underweight, normal weight, and overweight. The serum constituents of men and women below the age 40 in the overweight groups belonged to the normal domain. On the other hand, serum cholesterol levels of both men and women above the age 40 in the overweight groups remained in the borderline-high region(above 200mg/dl), and the mean value of LDL-cholesterol(above 130mg/dl) and triglycerides of men were above normal. Fasting blood glucose levels also remained in the borderline-high region. Total cholesterol levels of women above the age 40 in the overweight group was in the borderline-high region. (Korean J Nutrition 31(9) : 1481-1497, 1998)

• The Journal of Korean Medicine
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• v.24 no.4
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• pp.113-119
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• 2003

The association between apolipoprotein E (apo E) gene polymorphism and ischemic cerebrovascular disease (ICVD) has been controversial. These controversies may be due to inaccurate classification of patients and ethnic differences. We investigated the association between apo E genotypes and ICVD patients by case-control study in a Korean population. The association between apo E polymorphism and ICVD was examined in 121 patients with ICVD and 132 controls without ICVD. The E3/E4 phenotype was more frequent in control subjects (23.8％) than in patients (13.0％) (p<0.05). The E2/E3 phenotype was more frequent in patients (14.8％) than in control subjects (10.8％), but the difference was not statistically significant (p>0.05). These results suggest that the E4 allele may be a protective factor against early vascular morbidity, and the E2 allele may be a risk factor for cerebrovascular morbidity.

• Molecules and Cells
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• v.42 no.3
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• pp.218-227
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• 2019

This study was designed to determine the effects of the long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) on vascular smooth muscle cell (VSMC) apoptosis and extracellular matrix (ECM) disruption in a murine abdominal aortic aneurysm (AAA) model. After injection of PVT1-silencing lentiviruses, AAA was induced in Apolipoprotein E-deficient ($ApoE^{-/-}$) male mice by angiotensin II (Ang II) infusion for four weeks. After Ang II infusion, mouse serum levels of pro-inflammatory cytokines were analysed, and aortic tissues were isolated for histological, RNA, and protein analysis. Our results also showed that PVT1 expression was significantly upregulated in abdominal aortic tissues from AAA patients compared with that in controls. Additionally, Ang II treatment significantly increased PVT1 expression, both in cultured mouse VSMCs and in AAA murine abdominal aortic tissues. Of note, the effects of Ang II in facilitating cell apoptosis, increasing matrix metalloproteinase (MMP)-2 and MMP-9, reducing tissue inhibitor of MMP (TIMP)-1, and promoting switching from the contractile to synthetic phenotype in cultured VSMCs were enhanced by overexpression of PVT1 but attenuated by knockdown of PVT1. Furthermore, knockdown of PVT1 reversed Ang II-induced AAA-associated alterations in mice, as evidenced by attenuation of aortic diameter dilation, marked adventitial thickening, loss of elastin in the aorta, enhanced aortic cell apoptosis, elevated MMP-2 and MMP-9, reduced TIMP-1, and increased pro-inflammatory cytokines. In conclusion, our findings demonstrate that knockdown of lncRNA PVT1 suppresses VSMC apoptosis, ECM disruption, and serum pro-inflammatory cytokines in a murine Ang II-induced AAA model.

• Tuberculosis and Respiratory Diseases
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• v.79 no.3
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• pp.143-152
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• 2016

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor ${\beta}1$ (TGF-${\beta}1$)-induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-${\beta}1$-induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-${\beta}1$ with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and ${\alpha}$-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-${\beta}1$ receptor type 1 ($T{\beta}RI$) and type 2 ($T{\beta}RII$) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-${\beta}1$-treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-${\beta}1$-induced change of the EMT phenotype. ApoA1 inhibited the TGF-${\beta}1$-induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogen-activated protein kinase mediators. In addition, ApoA1 reduced the TGF-${\beta}1$-induced increase in $T{\beta}RI$ and $T{\beta}RII$ expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-${\beta}1$-induced EMT in experimental lung fibrosis.