Eun Young Choi

Kyung Hee University, Sŏul, Seoul, South Korea

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Publications (159)490.45 Total impact

  • Eun Young Choi, Dong-Ah Park, Jinkyeong Park
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    ABSTRACT: Background: The appropriate calorie intake to be provided to critically ill patients via enteral nutrition (EN) remains unclear. We performed a meta-analysis of randomized controlled trials to compare the effect of initial underfeeding and full feeding in acutely critically ill patients. Materials and Methods: We searched the Medline, EMBASE, and Cochrane Central Register of Controlled Trials databases to identify randomized controlled trials that compared underfeeding with full feeding in critically ill patients. The primary outcome was overall mortality. The secondary outcomes included length of hospital stay, length of intensive care unit (ICU) stay, duration of mechanical ventilation, incidence of pneumonia, Clostridium difficile colitis, other infectious complications, and gastrointestinal intolerance. Results: In total, 4 studies were included in this meta-analysis. There was no significant difference in overall mortality between the underfeeding and full-feeding groups (odds ratio [OR], 0.94; 95% confidence interval [CI], 0.74-1.19; I(2) = 26.6%; P = .61). Subgroup analysis of the underfeeding subgroup that was fed ≥33.3% of the standard caloric requirement indicated that overall mortality was significantly lower in this underfeeding subgroup than in the full-feeding group (OR, 0.63; 95% CI, 0.40-1.00; I(2) = 0%; P = .05). In contrast, no difference in overall mortality was noted between the underfeeding subgroup that was fed <33.3% of the standard caloric requirement and the full-feeding group. The length of hospital stay and length of ICU stay did not differ between the 2 groups. Moreover, no differences in other secondary clinical outcomes were noted. Conclusions: None of the analyzed clinical outcomes for the acutely critically ill patients were significantly influenced by the calorie intake of the initial EN.
    JPEN. Journal of parenteral and enteral nutrition. 07/2014;
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    ABSTRACT: Aim: We performed this study to evaluate the frequency of epidermal growth factor receptor (EGFR) mutations and their association with the histological subtype of lung adenocarcinoma diagnosed via small biopsy specimens. Patients and Methods: Three hundred and fifty-nine lung adenocarcinoma specimens were tested for EGFR mutation by a direct sequencing method. In 135 patients, histological subtypes were classified according to the 2011 International Association for the Study of Lung Cancer/American Thoracic Society/European Respiratory Society classification. We compared the EGFR mutation frequency by clinicopathological characteristics. Results: We detected 135 (37.6%) EGFR mutations and the incidence was highest in women who never smoked (54.6%). With regard to histological subtype, the highest prevalence of EGFR mutation was found in papillary (81.3%), followed by lepidic (70.4%), acinar (58.1%) and solid (28.3%) tumor types. In addition, the expression of thyroid transcription factor-1 was significantly higher in tumors with the EGFR mutation than in those without (p<0.001). Conclusion: The histological subtype of adenocarcinoma can be predictive of existing EGFR mutation, although the histology was confirmed using only small biopsies.
    Anticancer research 06/2014; 34(6):3189-3195. · 1.71 Impact Factor
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    ABSTRACT: Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme for the tryptophan catabolism that plays an important role in the induction of immune tolerance. It is induced in the colon and exerts its effects there, regulating T-cell proliferation and survival. To address the role of IDO in acute graft-versus-host disease (AGVHD) after human allogeneic hematopoietic stem cell transplantation (allo-HSCT), we analyzed the relationship between IDO expression in colon tissues and clinical outcomes of 41 AGVHD patients who were diagnosed as gut AGVHD by a colon mucosal biopsy within 100 days posttransplantation. By in situ immunohistochemical analyses, IDO expression was measured in colon mucosal mononuclear cells (MNCs) and endothelial cells (ECs) in GVHD areas. High IDO expression in MNCs and low IDO expression in ECs had a trend toward a lower non-relapse mortality (NRM, p=0.157 and p=0.062, respectively). Multivariate analysis showed that combined high MNC + low EC IDO expression (p=0.046) and low disease risk (p=0.012) are associated with lower NRM. Paradoxical upregulation of IDO expression in colon MNCs and ECs may represent a new predictive factor for prognosis in gut AGVHD after human allo-HSCT.
    Experimental hematology 04/2014; · 3.11 Impact Factor
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    ABSTRACT: Graft-versus-host disease (GVHD) is a fatal complication that occurs after allogeneic hematopoietic stem cell transplantation. To understand the dynamics of CD4 and CD8 T cell production of IFN-γ and IL-17 during GVHD progression, we established a GVHD model by transplanting T cell-depleted bone marrow (TCD-BM) and purified T cells from B6 mice into irradiated BALB.B, creating an MHC-matched but minor histocompatibility (H) antigen-mismatched transplantation (B6 → BALB.B GVHD). Transplantation-induced GVHD was confirmed by the presence of the appropriate compositional changes in the T cell compartments and innate immune cells in the blood and the systemic secretion of inflammatory cytokines. Using this B6 → BALB.B GVHD model, we showed that the production of IFN-γ and IL-17 by CD4 T cells preceded that by CD8 T cells in the spleen, mesenteric lymph node, liver, and lung in the BALB.B GVHD host, and Th1 differentiation predated Th17 differentiation in all organs during GVHD progression. Such changes in cytokine production were based on changes in cytokine gene expression by the T cells at different time points during GVHD development. These results demonstrate that both IFN-γ and IL-17 are produced by CD4 and CD8 T cells but with different kinetics during GVHD progression.
    Immune Network 04/2014; 14(2):89-99.
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    ABSTRACT: The potential of hepatocyte growth factor (HGF) to regulate the expression of urokinase plasminogen activator (uPA) in a gastric cancer cell is not widely acknowledged. To identify the genes associated with the plasminogen activator proteolytic axis by HGF, we used cDNA microarray technology and selected genes upregulated or downregulated in two gastric cell lines (NUGC-3 and MKN-28). First, IL-1β RNA and protein were confirmed to be upregulated. Then, we investigated the effect of IL-1β induced by HGF on the uPA system, facilitating the migration and invasion of cancer cells in the metastatic process. The role for IL-1β in HGF-induced upregulation of uPA was determined by knockdown of IL-1β with IL-1β shRNA and a chromatin immune precipitation assay. The levels of IL-1β and uPA were upregulated in cells treated with HGF in a dose-dependent manner. HGF-induced upregulation of uPA was suppressed by IL-1β knockdown. HGF enhanced the binding activity of NF-κB to the uPA promoter in control cells, but not in the IL-1β shRNA cells. We confirmed the functional role of HGF inactivation of the uPA promoter by a reporter gene assay. Downregulation of IL-1β using IL-1β shRNA also decreased cell proliferation and in vitro cell invasion. IL-1β stimulated uPA expression through ERK and NF-κB in gastric cancer, which may therefore be promising targets for gastric cancer therapy.
    Oncology Reports 03/2014; · 2.30 Impact Factor
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    ABSTRACT: Because transcatheter implantation of pulmonary valve is indicated for limited-size dysfunctional right ventricular outflow tract only as a balloon-expandable stent, we investigated the feasibility of a large-diameter self-expandable valved stent and the durability of the valve after >6months. We made a nitinol-wire-based, self-expandable valved stent with leaflets made from porcine pericardium. The porcine pericardium was treated with α-galactosidase, glutaraldehyde, and glycine after decellularization. After cutting the inguinal or cervical area, we implanted a valved stent in 12 sheep through the femoral or jugular vein by using an 18-Fr delivery catheter, controlling the catheter handles and hook block under fluoroscopic and echocardiographic guidance. The mean body weight of sheep was 43.9kg. We successfully implanted valved stents (diameter: 24mm in 7 sheep, 26mm in 5 sheep) in good position in 8 sheep, in the main pulmonary artery (PA) in 2 sheep, and in the right ventricular outlet tract (RVOT) in 2 sheep. We sacrificed 8 sheep (6 sheep in good position, 1 sheep in the main PA, and 1 sheep in the RVOT) after >6months. Five of the 6 sheep implanted in good position showed well-preserved valve morphology at the time of sacrifice. Histologic findings after routine sacrifice showed well-maintained collagen wave structure and no visible calcification in all explanted valve leaflets. Transcatheter implantation of a nitinol-wire-based, self-expandable valved stent in the pulmonic valve was feasible, and stents implanted in good position showed well-preserved valve leaflets with functional competence in the mid-term results.
    International journal of cardiology 02/2014; · 6.18 Impact Factor
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    ABSTRACT: Kawasaki disease (KD) is an acute febrile vasculitis that causes coronary artery abnormality (CAA) as a complication. In some patients, an association has been noted between elevated liver enzymes or an abnormal gallbladder (GB) and hepatobiliary involvement in KD. In this study, we aimed to evaluate clinical, laboratory, and ultrasonographic (USG) risk factors of hepatobiliary involvement for the intravenous immunoglobulin (IVIG) resistance and the development of CAA in children with KD. From March 2004 through January 2013, clinical features, laboratory data, echocardiographic findings, and USG findings were retrospectively reviewed regarding the response to IVIG treatment and coronary artery complications in 67 children with KD. Acute acalculous cholecystitis (AAC) was diagnosed based on USG criteria. Among all factors, only the prothrombin time international normalized ratio was significantly different between the IVIG-response and IVIG-resistance groups (p = 0.024). CAA was statistically more frequent in the AAC group (n = 24) than in the non-AAC group (n = 43) (23.3% vs. 58.3%, p = 0.019). Among the laboratory factors, segmented neutrophil percentage, total bilirubin level, and C-reactive protein were significant in children with CAA (p = 0.014, p = 0.009, and p = 0.010). Abnormal GB findings on USG were significantly more frequent in children with CAA than in those without CAA (p = 0.007; OR = 4.620; 95% confidence interval [CI]: 1.574-13.558). GB distension on USG was the only significant risk factor for CAA (p = 0.001; OR = 7.288; 95% CI: 2.243-23.681) by using multiple logistic regression analysis. For children in the acute phase of KD, USG findings of the GB, especially GB distension, may be an important risk factor for CAA as a complication.
    BMC Pediatrics 02/2014; 14(1):51. · 1.98 Impact Factor
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    ABSTRACT: Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine that regulates leukocyte recruitment, thereby playing a pivotal role in the regulation of innate and adaptive immunity and tumor progression. Elevated levels of MIF are associated with numerous inflammatory disorders and cancers. To determine whether developmental endothelial locus-1 (Del-1) regulated MIF, RAW264.7 macrophages were treated with Del-1 and assessed using ELISA. The results showed that MIF was downregulated in macrophages by Del-1, an endogenous anti-inflammatory protein that was previously shown to limit leukocyte adhesion and migration. Treatment of RAW264.7 macrophages with Del-1 inhibited constitutive and lipopolysaccharide (LPS)-induced MIF secretion. Recombinant Del-1 protein attenuated the phosphorylation of IκBα induced by a relatively low concentration of LPS in THP-1 monocytes, but did not inhibit IκBα phosphorylation in response to a relatively high concentration of LPS. Concomitantly, translocation of NF-κB to the nucleus was inhibited by Del-1 in LPS-activated macrophages. In addition, conditioned medium harvested from cells transfected with a Del-1 expression plasmid suppressed NF-κB activation in response to relatively low concentrations of TNF-α, albeit not the activation that was induced by a relatively high concentration of TNF-α. On the other hand, although Del-1 enhanced the macrophage expression of p53, a known negative regulator of MIF production, MIF production was not significantly affected by the level of p53 in mouse bone marrow-derived macrophages. These findings suggested that Del-1 controls NF-κB-activated MIF production in macrophages, and the potential application of Del-1 to therapeutic modalities for chronic inflammation-associated cancers.
    International Journal of Molecular Medicine 02/2014; · 1.96 Impact Factor
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    ABSTRACT: Objective Several biomarkers reflecting inflammatory or proteolytic activity have been known to represent plaque vulnerability. Moreover, a recent study confirmed that contrast-enhanced ultrasound (CEUS) can visualize intraplaque neovascularization (IPN) and demonstrate plaque vulnerability. In this study, we tried to demonstrate that IPN detected by CEUS was correlated with several well-known biomarkers and clinical outcome in patients with coronary artery disease (CAD). Methods Patients with stable CAD were screened by conventional carotid ultrasound and patients with carotid plaque thickness more than 2 mm were performed by CEUS for the presence of IPN. Plasma levels of biomarkers and clinical outcomes were evaluated. Results Among consecutive 89 patients fulfilled the inclusion criteria, 30 patients without IPN (group 1) and 59 patients with IPN (group 2) were analyzed. There were no significant difference in baseline characteristics except for mean age (62.9 ± 10.1 yrs versus 68.4 ± 9.6 yrs, p = 0.015). On multivariate analysis, only MMP-9 (p = 0.021, 95% CI 1.002–1.027) showed a significant association with IPN. But patients with IPN showed only trend for a history of cardiovascular disease (CVD) (44% versus 30%, p = 0.19) and one-year cardiovascular events (CVE) (6.8% versus 3.3%, p = 0.50) compared to group 1. Maximum plaque thickness (p = 0.04, 95% CI 1.230–6.322) showed a significant correlation with the clinical outcome including CVD or CVE. Conclusion MMP-9 correlated with IPN on CEUS. For clinical implication, however, large prospective studies are needed.
    Atherosclerosis 01/2014; 233(2):579–583. · 3.71 Impact Factor
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    ABSTRACT: Indoleamine 2,3-dioxygenase (IDO) is a rate-limiting enzyme in tryptophan catabolism that plays an important role in the induction of immune tolerance. Its role in graft-versus-tumor effect (GVT) after allogeneic stem cell transplantation (allo-SCT) remains unclear. Using a murine GVT model of reduced-intensity allo-HSCT followed by donor leukocyte infusion (DLI), we examined the role of IDO inhibition. Two stereoisomers of 1-methyl tryptophan (1-MT), a small-molecule inhibitor of IDO, reduced the growth of inoculated tumor in the mice that received DLI and had higher expression of IDO1 and IFNγ. However, L-1MT, but not D-1MT, mitigated tumor growth in mice that did not receive DLI and did not express IDO1 and IFNγ. Accordingly, both stereoisomers reduced plasma kynurenine concentrations early after DLI and enhanced in vitro cytotoxic lymphocyte function after allogeneic mixed lymphocyte reaction. Furthermore, L-1MT was more efficient in causing direct cytotoxic effects than D-1MT. Our results suggest that IDO inhibition can benefit in the setting of reduced-intensity allo-SCT using DLI.
    Experimental hematology. 01/2014;
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    ABSTRACT: Pulmonary fibrosis is a lung disease wherein lung parenchyma is gradually and irreversibly replaced with collagen. The molecular pathogenesis of pulmonary fibrosis is not fully understood and the only effective treatment available is lung transplantation. To test if Del-1, an endogenous anti-inflammatory molecule, may be implicated in the development of pulmonary fibrosis, we induced pulmonary fibrosis in wild type (WT) and Del-1-/- mice by intratracheal administration of bleomycin. Del-1 expression in the lung was decreased in the WT mice treated with bleomycin compared to control mice. In addition, bleomycin-induced pulmonary fibrosis increased collagen deposition and TGF-β production in the lung of Del-1-/- mice. Finally, Del-1-/- mice treated with bleomycin displayed higher weight loss and greater mortality than did WT mice identically treated. These findings suggest that Del-1 may negatively regulate development of pulmonary fibrosis. Further delineation of a role for Del-1 in the development of pulmonary fibrosis will broaden our understanding of the molecular pathogenesis of this disease and hopefully help develop potential therapeutics.
    Biochemical and Biophysical Research Communications 01/2014; · 2.41 Impact Factor
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    ABSTRACT: The ductus arteriosus is a normal and essential structure in fetal circulation. Since the introduction of fetal echocardiography, there have been reports of ductal constriction, many of which were related to maternal use of some medications. However, there have been some reports of idiopathic ductal constriction, which usually present in later gestation. Recently we experienced a case, which initially showed an S-shaped ductus with mild narrowing at 23 weeks and 27 weeks gestation and developed severe ductal constriction at 33 weeks. Soon after birth, ductus was searched for but no ductus was found in 2-D and color images. The neonate required mechanical ventilation with supplemental oxygen for 3 days. All echocardiographic abnormalities were normalized in 7 months. We report progressive ductal constriction in an S-shaped ductus and emphasize the importance of continuous follow up extending to the third trimester and even immediately after birth.
    Korean Circulation Journal 11/2013; 43(11):774-81.
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    ABSTRACT: Mouse CD99 and its paralog CD99-like 2 (CD99L2) are surface proteins implicated in cellular adhesion and migration. Although their distributions overlap in a wide variety of cells, their physical/functional relationship is currently unknown. In this study, we show the interaction between the two molecules and its consequence for membrane trafficking of mouse (m)CD99L2. The interaction was analyzed by bimolecular fluorescence complementation, immunoprecipitation, and fluorescence resonance energy transfer assays. When coexpressed, mCD99 formed heterodimers with mCD99L2, as well as homodimers, and the heterodimers were localized more efficiently at the plasma membrane than were the homodimers. Their interaction was cytoplasmic domain-dependent and enhanced mCD99L2 trafficking to the plasma membrane regardless of whether it was transiently overexpressed or endogenously expressed. Surface levels of endogenous mCD99L2 were markedly low on thymocytes, splenic leukocytes, and CTL lines derived from CD99-deficient mice. Importantly, the surface levels of mCD99L2 on mCD99-deficient cells recovered significantly when wild-type mCD99 was exogenously introduced, but they remained low when a cytoplasmic domain mutant of mCD99 was introduced. Our results demonstrate a novel role for mCD99 in membrane trafficking of mCD99L2, providing useful insights into controlling transendothelial migration of leukocytes.
    The Journal of Immunology 10/2013; · 5.52 Impact Factor
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    ABSTRACT: Developmental endothelial locus-1 (Del-1) is an endothelium-derived anti-inflammatory molecule that is downregulated by inflammatory stimuli. Little is known about the molecular mechanisms by which Del-1 transcription is regulated. In the present study, a DNA sequence upstream of the Del-1 gene was analyzed and putative p53 response elements (p53REs) were identified. An approximately 2 kb fragment upstream of the translation start site displayed the highest Del-1 transcriptional activity, and the transcriptional activity of this fragment was enhanced by overexpression of p53. Chemical activation of endogenous p53 elevated the levels of Del-1 mRNA. Site-directed mutagenesis of CATG in the consensus sequences of the 2 kb fragment to TATA significantly reduced the transcription of Del-1. Chromatin immunoprecipitation revealed recruitment of p53 to the p53REs of the Del-1 promoter, resulting in increased Del-1 transcription. Finally, primary endothelial cells isolated from mice with reduced levels of p53 showed a decrease in Del-1 mRNA compared to wild-type endothelial cells. Moreover, Del-1 reciprocally enhanced p53 expression in primary endothelial cells. Thus, these findings suggest that Del-1 is a novel transcriptional target gene of p53.
    Oncotarget 10/2013; · 6.64 Impact Factor
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    ABSTRACT: Extrinsic airway compression often complicates the course of congenital heart disease (CHD) repair. This study investigated the risk factors and outcome of airway compression evaluated using computed tomography (CT) in CHD patients. Of the 2,729 patients who underwent heart surgery for CHD between 1999 and 2007, airway compression was confirmed using CT in 58 (2.1%) patients. The patients were divided into groups according to the underlying CHD, and their medical records and CT scans were reviewed retrospectively. Airway compression was found more frequently in the vascular ring or absent pulmonary valve syndrome (8 of 11) and repaired aortic arch (22 of 213) groups than in the other groups (28 of 2,505) (p < 0.001). Patients with more severe respiratory manifestations showed greater airway compression on CT (p < 0.001) and had a higher rate of additional surgery to relieve airway compression using multivariate analysis (p = 0.005). Airway compression was ameliorated in 13 of 17 patients after surgery for airway compression. Funnel chest deformity worsened after aortic arch repair and was associated with the need for surgical relief of airway compression. Pulmonary overflow disease could be followed up without additional surgery for airway compression. Early airway compression detection and management may reduce further morbidity, especially after aortic arch repair. The patient's respiratory manifestation and the underlying disease characteristics must be considered when determining the need for additional surgery for airway compression.
    The Annals of thoracic surgery 09/2013; · 3.45 Impact Factor
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    ABSTRACT: The safety and effectiveness of radiofrequency catheter ablation (RFCA) for supraventricular tachycardia (SVT) in young children was investigated. Ninety-five children who underwent RFCA procedures were stratified according to age (group 1, 0-4 years, n = 24; group 2, 5-9 years, n = 71) and were evaluated retrospectively. Among the 95 patients, atrioventricular reentrant tachycardia was 78.9%, atrioventricular nodal reentrant tachycardia was 10.5%, and ectopic atrial tachycardia was 8.4%. The acute success rate of RFCA was 97.9% and the recurrence rate was 11.6%. RFCA was performed for different main reasons in each group, including drug-resistant tachycardia (37.5% in group 1 vs 7% in group 2; P = 0.001) and symptomatic tachycardia (4.2% in group 1 vs 57.7% in group 2; P < 0.001). There was no significant difference in success rate, recurrence rate, and procedure and fluoroscopy duration between the two groups. The acute success rates did not differ significantly between patients with a single accessory pathway (AP) and those with multiple APs; however, failure or recurrence was more common in the patients with multiple APs (38.5% vs 11.5%; P = 0.01). The multiple APs were found frequently on the right side (P = 0.005). Septal dyskinesia with left ventricular dysfunction in Wolff-Parkinson-White syndrome and tachycardia-induced cardiomyopathy improved after RFCA. RFCA was found to be effective and safe for SVT in young children.
    Pacing and Clinical Electrophysiology 09/2013; · 1.75 Impact Factor
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    ABSTRACT: The purpose of this study was to share our experience of transcatheter closure of small patent ductus arteriosus (PDA) by using an Amplatzer vascular plug (AVP). We reviewed the medical records of 20 patients who underwent transcatheter closure at Samsung Medical Center and Sejong General Hospital from January 2008 to August 2012. The size and shape of the PDAs were evaluated by performing angiograms, and the PDA size and the AVP devices size were compared. The mean age of the patients was 54.9±45.7 months old. The PDAs were of type C (n=5), type D (n=12), and type E (n=3). The mean pulmonary end diameter of the PDA was 1.7±0.6 mm, and the aortic end diameter was 3.6±1.4 mm. The mean length was 7.3±1.8 mm. We used 3 types of AVP devices: AVP I (n=5), AVP II (n=7), and AVP IV (n=8). The ratio of AVP size to the pulmonary end diameter was 3.37±1.64, and AVP size/aortic end ratio was 1.72±0.97. The aortic end diameter was significantly larger in those cases repaired with AVP II than in the others (P=0.002). The AVP size did not significantly correlate with the PDA size, but did correlate with smaller ratio of AVP size to aortic end diameter (1.10±0.31, P=0.032). Transcatheter closure of small PDA with AVP devices yielded satisfactory outcome. AVP II was equally effective with smaller size of device, compared to others.
    Korean Journal of Pediatrics 09/2013; 56(9):396-400.
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    ABSTRACT: Purpose: For the successful completion of transcatheter closure of atrial septal defects with the Amplatzer septal occluder, shape of the defects should be considered prior to selecting the device. The purpose of this study is to evaluate the results of a transcatheter closure of oval shaped atrial septal defect. Materials and Methods: From November 2009 until November 2011, cardiac computed tomography was performed on 69 patients who needed a transcatheter closure of atrial septal defect. We defined an oval shaped atrial septal defect as the ratio of the shortest diameter to the longest diameter ≤0.75 measured using computed tomography. A trans-thoracic echocardiogram was performed one day after and six months after. Results: The transcatheter closure of atrial septal defect was performed successfully in 24 patients in the ovoid group and 45 patients in the circular group. There were no serious complications in both groups and the complete closure rate at 6 months later was 92.3% in the ovoid group and 93.1% in the circular group (p>0.05). The differences between the device size to the longest diameter of the defect and the ratios of the device size to the longest diameter were significantly smaller in the ovoid group (1.8±2.8 vs. 3.7±2.6 and 1.1±0.1 vs. 1.2±0.2). Conclusion: Transcatheter closure of an oval shaped atrial septal defect was found to be safe with the smaller Amplatzer septal occluder device when compared with circular atrial septal defects.
    Yonsei medical journal 09/2013; 54(5):1104-9. · 0.77 Impact Factor
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    ABSTRACT: Background: For successful transcatheter closure of an atrial septal defect with the Amplatzer septal occluder, the shape of the defect should be considered before selecting the device size. The purpose of this study was to evaluate the results of transcatheter closure of an ovoid atrial septal defect.Methods: Between January 2010 and February 2012, cardiac computer tomography examinations were performed in 78 patients who subsequently underwent transcatheter closure of an atrial septal defect. In this retrospective study, we reviewed these patients' medical records. We defined an ovoid atrial septal defect as a value of 0.75 for the ratio of the shortest diameter of the defect to the longest diameter, as measured in a computed tomography image. Transthoracic echocardiography examinations were made at 1 day and 6 months after the procedure.Results: Transcatheter closure of an atrial septal defect was successful in 26 patients in the ovoid-defect group and in 52 patients in the round-defect group. There were no serious complications in either group, and the rate of complete closure at 6 months was 92.3% in the ovoid-defect group and 93.1% in the round-defect group (P > .05). The mean (SD) difference between the device size and the defect's longest diameter, and the mean ratio of the device size to the longest diameter were significantly smaller in the ovoid-defect group (1.7 ± 2.9 versus 3.8 ± 2.5 and 1.1 ± 0.1 versus 1.3 ± 0.2, respectively).Conclusions: Transcatheter closure of an atrial septal defect is indicated even for an ovoid atrial septal defect. Ovoid atrial septal defects can be closed successfully with smaller sizes of the Amplatzer septal occluder than for round atrial septal defects.
    Heart Surgery Forum 08/2013; 16(4):E193-7. · 0.63 Impact Factor
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    ABSTRACT: Background Because hemodiafiltration (HDF) involves large amounts of ultra-filtration and substitution fluid infusion, its effects on serum electrolytes may be different from those of hemodialysis (HD). Serum sodium and blood pressures were compared between patients undergoing online HDF and high-flux HD (HFHD).Methods Thirty-two of 101 patients on HFHD switched voluntarily to online HDF. Their pre- and postdialysis serum measurements were compared with those of the remaining 69 HFHD patients.ResultsOnline HDF patients had lower pre- and postdialysis systolic blood pressures (SBPs) than HFHD patients (predialysis, 136±21 vs. 145±19 mmHg, P<0.05; postdialysis, 129±22 vs. 142±25 mmHg, P<0.05). Pre- and postdialysis serum sodium concentrations were not significantly different between online HDF and HFHD (predialysis, 138±2 vs. 137±3 mEq/L; postdialysis, 134±2 vs. 134±2 mEq/L). However, the change in serum sodium concentration after dialysis was greater in online HDF than HFHD patients (−3.7±2.2 vs. −2.5±2.8 mEq/L, P<0.05). The change in serum sodium concentration was correlated with postdialysis SBP (r=0.304, P<0.005) and pulse pressure (r=0.299, P<0.005). Predialysis SBP (r = 0.317, P<0.005) and pulse pressure (r=0.324, P=0.001) were also correlated with the postdialysis serum sodium change.Conclusion Compared with HFHD, online HDF has a greater serum sodium lowering effect. This might contribute to the ability of online HDF to stabilize both pre- and postdialysis SBP.
    Kidney Research and Clinical Practice. 06/2013; 32(2):62–65.

Publication Stats

2k Citations
490.45 Total Impact Points


  • 2014
    • Kyung Hee University
      Sŏul, Seoul, South Korea
    • Seoul National University Bundang Hospital
      • Department of Pediatrics
      Sŏul, Seoul, South Korea
  • 2011–2014
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
    • Korea Institute of Science and Technology
      Sŏul, Seoul, South Korea
    • National Cancer Center Korea
      • Specific Organs Cancer Branch
      Kōyō, Gyeonggi Province, South Korea
    • Ajou University
      Sŏul, Seoul, South Korea
    • Catholic University of Korea
      • Department of Internal Medicine
      Seoul, Seoul, South Korea
    • Kyungpook National University
      • Applied Biology
      Daikyū, Daegu, South Korea
  • 2004–2014
    • Yeungnam University
      • • Division of Internal Medicine
      • • College of Medicine
      Onyang, South Chungcheong, South Korea
  • 2003–2014
    • Seoul National University Hospital
      • • Department of Nuclear Medicine
      • • Department of Pathology
      Sŏul, Seoul, South Korea
    • Pennsylvania State University
      • Department of Microbiology and Immunology
      State College, PA, United States
  • 2004–2013
    • Sungkyunkwan University
      • • Department of Pediatrics
      • • Department of Chemistry
      • • Institute of Basic Science
      Sŏul, Seoul, South Korea
  • 2012
    • Dankook University
      Eidō, North Chungcheong, South Korea
    • Sejong General Hospital
      Bucheon, Gyeonggi Province, South Korea
  • 2010–2012
    • Hongik University
      • Department of Chemical Engineering
      Sŏul, Seoul, South Korea
  • 2008–2012
    • National Institutes of Health
      • Branch of Experimental Immunology
      Bethesda, MD, United States
  • 2008–2011
    • National Cancer Institute (USA)
      • Experimental Immunology Branch
      Maryland, United States
  • 2009–2010
    • Korea University
      • Graduate School of Medicine
      Seoul, Seoul, South Korea
    • National Health Insurance Corporation Ilsan Hospital
      Sŏul, Seoul, South Korea
  • 2000–2010
    • Pusan National University
      • • Department of Chemistry
      • • Division of Materials Science and Engineering
      Tsau-liang-hai, Busan, South Korea
  • 2007–2009
    • NCI-Frederick
      Maryland, United States
    • University of Seoul
      Sŏul, Seoul, South Korea
    • Hallym University Medical Center
      • Department of Pathology
      Seoul, Seoul, South Korea
    • Inha University
      • Department of Biochemistry
      Seoul, Seoul, South Korea
  • 2003–2008
    • Seoul National University
      • Department of Pathology
      Sŏul, Seoul, South Korea
  • 2006
    • Dankook University Hospital
      Anjŏ, Gyeonggi Province, South Korea