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Search Results: 1 - 10 of 6603 matches for " Chung Soon-Cheol "
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Correlation between psychological factors and the cerebellar volume of normal young adults
Chung Soon-Cheol,Choi Mi-Hyun,Lee Su-Jeong,Choi Jin-Seung
International Journal of Clinical and Health Psychology , 2010,
Abstract: Este estudio analiza la relación entre el volumen del cerebelo de adultos normales en la tercera década de la vida (20-29 a os) y varios factores psicológicos. El volumen del cerebelo de 118 sujetos (media de edad 23 ± 2,6 a os), incluyendo 58 varones (media de edad 24 ± 2,8 a os) y 60 mujeres (media de edad, 21,9 ± 2,1 a os), fue medido utilizando la imagen por resonancia magnética (IRM). Todos los participantes completaron los siguientes tests: Cuestionario de 90 Síntomas (SCL-90-R), Cuestionario de Personalidad de Tipo A, El cuestionario de Ansiedad Estado Korean YZ, El Cuestionario de 16 Factores de la Personalidad (16PF), y la Escala Autoadministrada de Depresión (EAD). Utilizando regresión linear, se analizó la relación entre el volumen del cerebelo y factores psicológicos. Sin considerar las diferencias entre géneros, en cuanto crecía la tendencia hacia la personalidad tipo A y se incrementaba el estado de ansiedad y la fuerza del superego, disminuía el volumen del cerebelo. Cuando se incrementaba la fuerza del ego, se incrementaba el volumen del cerebelo. Cuando se consideraban las diferencias de género, cuando incrementaba la ansiedad fóbica y ambición en varones, disminuía el volumen del cerebelo. En mujeres, cuando incrementaba la hostilidad, tensión y la ansiedad estado, disminuía el volumen del cerebelo.
Theory of perpendicular magnetocrystalline anisotropy in Fe/MgO (001)
Dorj Odkhuu,Won Seok Yun,S. H. Rhim,Soon-Cheol Hong
Physics , 2015,
Abstract: The origin of large perpendicular magneto-crystalline anisotropy (PMCA) in Fe/MgO (001) is revealed by comparing Fe layers with and without the MgO. Although Fe-O $p$-$d$ hybridization is weakly present, it cannot be the main origin of the large PMCA as claimed in previous study. Instead, perfect epitaxy of Fe on the MgO is more important to achieve such large PMCA. As an evidence, we show that the surface layer in a clean free-standing Fe (001) dominantly contributes to $E_{MCA}$, while in the Fe/MgO, those by the surface and the interface Fe layers contribute almost equally. The presence of MgO does not change positive contribution from $\langle xz|\ell_Z|yz\rangle$, whereas it reduces negative contribution from $\langle z^2|\ell_X|yz\rangle$ and $\langle xy|\ell_X|xz,yz\rangle$.
Trends in the Rates of Peripartum Hysterectomy and Uterine Artery Embolization
Geum Joon Cho, Log Young Kim, Hye-Ri Hong, Chang Eun Lee, Soon-Cheol Hong, Min-Jeong Oh, Hai-Joong Kim
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060512
Abstract: The objective of this study was to determine the trends in national rates of peripartum hysterectomy (PH) and uterine arterial embolization (UAE) in Korea. We used data collected by the Health Insurance Review & Assessment Service of Korea and analyzed data from patients who gave birth during the period from 2005 to 2008. There were 1785,178 deliveries during the study period, including 2636 cases of PH (1.48 per 1000 deliveries). The PH rate in 2005 was 1.57 per 1000 deliveries and in 2008 it was 1.33 per 1000 deliveries. UAE was performed in 161 women (incidence, 0.38 per 1000 deliveries) and 447 women (incidence, 0.98 per 1000 deliveries) in 2005 and 2008, respectively. In Korea, the rate of PH decreased slightly, while the rate of UAE rate increased dramatically during the period from 2005 to 2008. Further studies are needed to evaluate the effects of UAE on the rate of PH performed.
Preventive Effects of Folic Acid Supplementation on Adverse Maternal and Fetal Outcomes
Min Woo Kim, Ki Hoon Ahn, Ki-Jin Ryu, Soon-Cheol Hong, Ji Sung Lee, Alejandro A. Nava-Ocampo, Min-Jeong Oh, Hai-Joong Kim
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0097273
Abstract: Although there is accumulating evidence regarding the additional protective effect of folic acid against adverse pregnancy outcomes other than neural tube defects, these effects have not been elucidated in detail. We evaluated whether folic acid supplementation is associated with favorable maternal and fetal outcomes. This was a secondary analysis of 215 pregnant women who were enrolled in our prior study. With additional data from telephone interviews regarding prenatal folic acid supplementation, existing demographic, maternal and fetal data were statistically analyzed. The concentration of folic acid in maternal blood was significantly higher following folic acid supplementation (24.6 ng/mL vs.11.8 ng/mL). In contrast, homocysteine level in maternal blood decreased with folic acid supplementation (5.5 μmol/mL vs. 6.8 μmol/mL). The rates of both preeclampsia (odds ratio [OR], 0.27; 95% confidence interval [CI], 0.09–0.76) and small for gestational age (SGA; 9.2% vs. 20.0%; OR, 0.42; 95% CI, 0.18–0.99) were lower in the folic acid supplementation group than those in the control group. Other pregnancy outcomes had no association with folic acid supplementation. The findings indicate that folic acid supplementation may help to prevent preeclampsia and SGA. Further studies are warranted to elucidate the favorable effects of folic acid supplementation on pregnancy outcomes.
Comparison of Estimating Equations for the Prediction of Glomerular Filtration Rate in Kidney Donors before and after Kidney Donation
Byung Ha Chung, Jee Hyun Yu, Hyuk Jin Cho, Ji-Il Kim, In Sung Moon, Cheol Whee Park, Chul Woo Yang, Yong-Soo Kim, Bum Soon Choi
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0060720
Abstract: The aim of this study is to investigate the usefulness of the GFR-estimating equations to predict renal function in kidney donors before and after transplantation. We compared the performance of 24-hour-urine–based creatinine clearance (24 hr urine-CrCl), the Cockcroft-Gault formula (eGFRCG), the Modification of Diet in Renal Disease equation (eGFRMDRD), and the Chronic Kidney Disease Epidemiology Collaboration equation (eGFRCKD-EPI) with technetium-diethylenetriaminepentaacetic acid (99mTc-DTPA) clearance (mGFR) in 207 potential kidney donors and 108 uninephric donors. Before donation, eGFRCKD-EPI showed minimal bias and did not show a significant difference from mGFR (P = 0.65, respectively) while 24 hr urine-CrCl and eGFRMDRD significantly underestimated mGFR (P<0.001 for each). Precision and accuracy was highest in eGFRCKD-EPI and this better performance was more dominant when renal function is higher than 90 mL·min?1·1.73 m?2. After kidney donation, eGFRMDRD was superior to other equations in precision and accuracy in contrast to before donation. Within individual analysis, eGFRMDRD showed better performance at post-donation compared to pre-donation, but eGFRCKD-EPI and eGFRCG showed inferior performance at post-donation. In conclusion, eGFRCKD-EPI showed better performance compared to other equations before donation. In a uninephric donor, however, eGFRMDRD is more appropriate for the estimation of renal function than eGFRCKD-EPI.
Dysregulation of Th17 Cells during the Early Post-Transplant Period in Patients under Calcineurin Inhibitor Based Immunosuppression
Byung Ha Chung, Kyoung Woon Kim, Bo-Mi Kim, Shang Guo Piao, Sun Woo Lim, Bum Soon Choi, Cheol Whee Park, Yong-Soo Kim, Mi-La Cho, Chul Woo Yang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0042011
Abstract: Accumulating evidence suggests that Th17 cells play a role in the development of chronic allograft injury in transplantation of various organs. However, the influence of current immunosuppressants on Th17-associated immune responses has not been fully investigated. We prospectively investigated the changes in Th17 cells in peripheral blood mononuclear cells (PBMCs) collected before and 1 and 3 months after KT in 26 patients and we investigated the suppressive effect of tacrolimus on Th17 in vitro. In the early posttransplant period, the percentage of Th17 cells and the proportion of IL-17-producing cells in the effector memory T cells (TEM) were significantly increased at 3 months after transplantation compared with before transplantation (P<0.05), whereas Th1/Th2 cells and TEM cells were significantly decreased. The degree of increase in Th17 during the early posttransplant period was significantly associated with allograft function at 1 year after transplantation (r = 0.4, P<0.05). In vitro, tacrolimus suppressed Th1 and Th2 cells in a concentration-dependent manner, but did not suppress Th17 cells even at high concentration. This suggests that current immunosuppression based on tacrolimus is inadequate to suppress Th17 cells in KTRs, and dysregulation of Th17 may be associated with the progression of CAD.
Fenofibrate Improves Renal Lipotoxicity through Activation of AMPK-PGC-1α in db/db Mice
Yu Ah Hong, Ji Hee Lim, Min Young Kim, Tae Woo Kim, Yaeni Kim, Keun Suk Yang, Hoon Suk Park, Sun Ryoung Choi, Sungjin Chung, Hyung Wook Kim, Hye Won Kim, Bum Soon Choi, Yoon Sik Chang, Cheol Whee Park
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0096147
Abstract: Peroxisome proliferator-activated receptor (PPAR)-α, a lipid-sensing transcriptional factor, serves an important role in lipotoxicity. We evaluated whether fenofibrate has a renoprotective effect by ameliorating lipotoxicity in the kidney. Eight-week-old male C57BLKS/J db/m control and db/db mice, divided into four groups, received fenofibrate for 12 weeks. In db/db mice, fenofibrate ameliorated albuminuria, mesangial area expansion and inflammatory cell infiltration. Fenofibrate inhibited accumulation of intra-renal free fatty acids and triglycerides related to increases in PPARα expression, phosphorylation of AMP-activated protein kinase (AMPK), and activation of Peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α)-estrogen-related receptor (ERR)-1α-phosphorylated acetyl-CoA carboxylase (pACC), and suppression of sterol regulatory element-binding protein (SREBP)-1 and carbohydrate regulatory element-binding protein (ChREBP)-1, key downstream effectors of lipid metabolism. Fenofibrate decreased the activity of phosphatidylinositol-3 kinase (PI3K)-Akt phosphorylation and FoxO3a phosphorylation in kidneys, increasing the B cell leukaemia/lymphoma 2 (BCL-2)/BCL-2-associated X protein (BAX) ratio and superoxide dismutase (SOD) 1 levels. Consequently, fenofibrate recovered from renal apoptosis and oxidative stress, as reflected by 24 hr urinary 8-isoprostane. In cultured mesangial cells, fenofibrate prevented high glucose-induced apoptosis and oxidative stress through phosphorylation of AMPK, activation of PGC-1α-ERR-1α, and suppression of SREBP-1 and ChREBP-1. Our results suggest that fenofibrate improves lipotoxicity via activation of AMPK-PGC-1α-ERR-1α-FoxO3a signaling, showing its potential as a therapeutic modality for diabetic nephropathy.
Vascular Endothelial Growth Factor-Receptor 1 Inhibition Aggravates Diabetic Nephropathy through eNOS Signaling Pathway in db/db Mice
Keun Suk Yang, Ji Hee Lim, Tae Woo Kim, Min Young Kim, Yaeni Kim, Sungjin Chung, Seok Joon Shin, Beom Soon Choi, Hyung Wook Kim, Yong-Soo Kim, Yoon Sik Chang, Hye Won Kim, Cheol Whee Park
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094540
Abstract: The manipulation of vascular endothelial growth factor (VEGF)-receptors (VEGFRs) in diabetic nephropathy is as controversial as issue as ever. It is known to be VEGF-A and VEGFR2 that regulate most of the cellular actions of VEGF in experimental diabetic nephropathy. On the other hand, such factors as VEGF-A, -B and placenta growth factor bind to VEGFR1 with high affinity. Such notion instigated us to investigate on whether selective VEGFR1 inhibition with GNQWFI hexamer aggravates the progression of diabetic nephropathy in db/db mice. While diabetes suppressed VEGFR1, it did increase VEGFR2 expressions in the glomerulus. Db/db mice with VEGFR1 inhibition showed more prominent features with respect to, albuminuria, mesangial matrix expansion, inflammatory cell infiltration and greater numbers of apoptotic cells in the glomerulus, and oxidative stress than that of control db/db mice. All these changes were related to the suppression of diabetes-induced increases in PI3K activity and Akt phosphorylation as well as the aggravation of endothelial dysfunction associated with the inactivation of FoxO3a and eNOS-NOx. In cultured human glomerular endothelial cells (HGECs), high-glucose media with VEGFR1 inhibition induced more apoptotic cells and oxidative stress than did high-glucose media alone, which were associated with the suppression of PI3K-Akt phosphorylation, independently of the activation of AMP-activated protein kinase, and inactivation of FoxO3a and eNOS-NOx pathway. In addition, transfection with VEGFR1 siRNA in HGECs also suppressed PI3K-Akt-eNOS signaling. In conclusion, the specific blockade of VEGFR1 with GNQWFI caused severe renal injury related to profound suppression of the PI3K-Akt, FoxO3a and eNOS-NOx pathway, giving rise to the oxidative stress-induced apoptosis of glomerular cells in type 2 diabetic nephropathy.
Age-Associated Molecular Changes in the Kidney in Aged Mice
Ji Hee Lim,Eun Nim Kim,Min Young Kim,Sungjin Chung,Seok Joon Shin,Hyung Wook Kim,Chul Woo Yang,Yong-Soo Kim,Yoon Sik Chang,Cheol Whee Park,Bum Soon Choi
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/171383
Abstract: Background. Aging is a multifactorial process characterized by a progressive decline in physiological function. Decreased kidney function is associated with cardiovascular disease and mortality. Therefore, increasing our insight into kidney aging by understanding the anatomic, physiologic, and pathologic changes of aging in the kidney is important to prevent disastrous outcomes in elderly people. Methods. Male two-, 12-, and 24-month-old C57/BL6 mice were used in this study. We measured histological change, oxidative stress, and aging-related protein expression in the kidneys. Results. Twenty-four-month-old mice displayed increased albuminuria. Creatinine clearance decreased with aging, although this was not statistically significant. There were increases in mesangial volume and tubulointerstitial fibrosis in 24-month-old mice. There were also increases in F4/80 expression and in apoptosis detected by TUNEL assay. Urine isoprostane excretion increased with aging and SOD1 and SOD2 were decreased in 24-month-old mice. Oxidative stress may be mediated by a decrease in Sirt1, PGC-1α, ERR-1α, and PPARα expression. Klotho expression also decreased. Conclusions. Our results demonstrate that Sirt1 was decreased with aging and may relate to changed target molecules including PGC-1α/ERR-1α signaling and PPARα. Klotho can also induce oxidative stress. Pharmacologically targeting these signaling molecules may reduce the pathologic changes of aging in the kidney. 1. Introduction Aging in most species is associated with impaired adaptive and homeostatic mechanisms, leading to susceptibility to environmental or internal stresses with increasing rates of disease [1, 2]. A number of different theories of primarily disease-independent renal aging, which can be categorized as evolutionary, molecular, cellular, and systemic, have been proposed in the past and recent studies have provided evidence for some of these theories [3]. Age-related changes lead to a functional decline of several organs, including the kidney [4]. Age-related changes in renal structure and function have been described [5], not just in humans but in a wide range of other species, including rats, mice, hamsters, dogs, and cats. Modifications of the kidneys related to aging include changes to glomerular structure. As the functional kidney becomes older, there is glomerular basement membrane thickening and wrinkling associated with loss of capillary loops, and mesangial matrix expansion that may be the outcome of an imbalance between formation and removal of extracellular matrix [6]. Mild changes in
Crif1 Deficiency Reduces Adipose OXPHOS Capacity and Triggers Inflammation and Insulin Resistance in Mice
Min Jeong Ryu,Soung Jung Kim,Yong Kyung Kim,Min Jeong Choi,Surendar Tadi,Min Hee Lee,Seong Eun Lee,Hyo Kyun Chung,Saet Byel Jung,Hyun-Jin Kim,Young Suk Jo,Koon Soon Kim,Sang-Hee Lee,Jin Man Kim,Gi Ryang Kweon,Ki Cheol Park,Jung Uee Lee,Young Yun Kong,Chul-Ho Lee,Jongkyeong Chung,Minho Shong
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1003356
Abstract: Impaired mitochondrial oxidative phosphorylation (OXPHOS) has been proposed as an etiological mechanism underlying insulin resistance. However, the initiating organ of OXPHOS dysfunction during the development of systemic insulin resistance has yet to be identified. To determine whether adipose OXPHOS deficiency plays an etiological role in systemic insulin resistance, the metabolic phenotype of mice with OXPHOS–deficient adipose tissue was examined. Crif1 is a protein required for the intramitochondrial production of mtDNA–encoded OXPHOS subunits; therefore, Crif1 haploinsufficient deficiency in mice results in a mild, but specific, failure of OXPHOS capacity in vivo. Although adipose-specific Crif1-haploinsufficient mice showed normal growth and development, they became insulin-resistant. Crif1-silenced adipocytes showed higher expression of chemokines, the expression of which is dependent upon stress kinases and antioxidant. Accordingly, examination of adipose tissue from Crif1-haploinsufficient mice revealed increased secretion of MCP1 and TNFα, as well as marked infiltration by macrophages. These findings indicate that the OXPHOS status of adipose tissue determines its metabolic and inflammatory responses, and may cause systemic inflammation and insulin resistance.
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