Eun-Kyung Kim

CHA University, Seoul, Seoul, South Korea

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Publications (64)159.68 Total impact

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    ABSTRACT: Pulmonary artery sarcoma (PAS) is a rare, poorly differentiated malignancy arising from the intimal layer of the pulmonary artery. Contrast-enhanced chest computed tomography (CT) is a good diagnostic modality that shows a low-attenuation filling defect of the pulmonary artery in PAS patients. An 18-year-old man was referred to our hospital for the evaluation and management of cavitary pulmonary lesions that did not respond to treatment. A contrast-enhanced CT of the chest was performed, which showed a filling defect within the right interlobar pulmonary artery. The patient underwent a curative right pneumonectomy after confirmation of PAS. Although lung parenchymal lesions of PAS are generally nonspecific, it can be presented as cavities indicate pulmonary infarcts. Clinicians must consider the possibility of PAS as well as pulmonary thromboembolism in patients with pulmonary infarcts. So, we report the case with PAS that was diagnosed during the evaluation of cavitary pulmonary lesions and reviewed the literatures.
    Tuberculosis and Respiratory Diseases 03/2014; 76(3):136-40.
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    ABSTRACT: Although the lung is a common site of metastasis, endobronchial metastases (EBM) from extrathoracic malignancies are rare. Previous studies were retrospective reviews of the cases from each single institute, and the last one was performed between 1992 and 2002. We evaluated the characteristics of patients with EBM who had been diagnosed in recent 10 years in our hospital. We retrospectively reviewed 1,275 patients who had undergone diagnostic bronchoscopic procedures between 2001 and 2011. An EBM was defined as bronchoscopically notable lesion, which was histopathologically identical to the primary tumor. A total of 18 cases of EBM were identified. The mean age was 53 years, and 12 cases of the 18 patients were female. The most common primary malignancies were colorectal cancer and breast cancer (4 cases each), followed by cervix cancer (3 cases) and renal cell carcinoma (2 cases). Cough was the most common symptom. The most common radiologic finding was atelectasis, which was identified in 27.7% of the cases. The median interval from the diagnosis of primary malignancy to the diagnosis of EBM was 14 months (range, 0-112 months). The median survival time from the diagnosis of EBM was 10 months (range, 1-39 months). EBM from extrathoracic malignancies were rare. Colorectal cancer and breast cancer were common as primary malignancies. Fiberoptic bronchoscopy should be performed in all patients, who are suspected of having EBM. If atypical clinical and pathological features are present, appropriate diagnostic studies should be undertaken.
    Tuberculosis and Respiratory Diseases 04/2013; 74(4):169-76.
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    ABSTRACT: Primary malignant fibrous histiocytoma (MFH) of the lung is a very rare neoplasm, which usually presents as a parenchymal mass. Here, we report an unusual case of primary MFH of the bronchus showing relatively benign clinical features. We performed a palliative resection via flexible bronchoscopy using a polypectomy snare. The patient has survived for over 2 years of being diagnosed with an endobronchial mass, later found to be MFH, and 14 months post-debulking. There is a possibility that endobronchial MFH has a more favorable prognosis than MFH of other origins. If this is true, interventional bronchoscopy can be a reasonable option for non-operable cases of MFH.
    Respiratory care 12/2012; · 2.03 Impact Factor
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    ABSTRACT: Background: To date, no clinical parameter has been associated with the decline in lung function other than emphysema severity in COPD. Objectives: The main purpose of this study was to explore whether the rate of lung function decline differs between COPD patients with and without exertional desaturation. Methods: A total of 224 subjects were selected from the Korean Obstructive Lung Disease cohort. Exertional desaturation was assessed using the 6-min walk test (6MWT), and defined as a post-exercise oxygen saturation (SpO(2)) of <90% or a ≥4% decrease. The cohort was divided into desaturator (n = 47) and non-desaturator (n = 177) groups. Results: There was a significant difference between the desaturator and non-desaturator groups in terms of the change in pre-bronchodilator forced expiratory volume in 1 s (FEV(1)) over a 3-year period of follow-up (p = 0.006). The mean rate of decline in FEV(1) was greater in the desaturator group (33.8 ml/year) than in the non-desaturator group (11.6 ml/year). A statistically significant difference was also observed between the two groups in terms of the change in the St. George's Respiratory Questionnaire (SGRQ) total score over 3 years (p = 0.001). Conclusions: This study suggests, for the first time, that exertional desaturation may be a predictor of rapid decline in lung function in patients with COPD. The 6MWT may be a useful test to predict a rapid lung function decline in COPD.
    Respiration 12/2012; · 2.62 Impact Factor
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    ABSTRACT: Background: Genome-wide association studies have identified CHRNA3 as a lung cancer and chronic obstructive pulmonary disease (COPD) candidate gene in non-Hispanic Caucasian cohorts. However, there are differences in minor allele frequencies among ethnic groups, and limited data exists for Asian populations. Objectives: The aim of this case-control study was to determine whether there is an association between COPD and genetic variation in CHRNA3 in the Korean population. In addition, we investigated the association of CHRNA3 with intermediate disease phenotypes including emphysema and lung function in COPD subjects. Methods: Two single-nucleotide polymorphisms (SNPs) in CHRNA3 (rs660652 and rs12910984) were genotyped in 219 COPD subjects registered in the Korean Obstructive Lung Disease cohort study and in 305 control subjects. Volumetric computed tomography was performed in all COPD subjects. Emphysema severity was measured quantitatively by determining the volume fraction of the lung below -950 Hounsfield units. Logistic regression analysis for case-control analysis and linear regression modeling for quantitative analysis were performed using SAS. Results: This case-control analysis of 219 COPD patients and 305 control participants identified a significant association between an SNP of CHRNA3 (rs12910984) and COPD (p = 0.049). Analysis in COPD subjects revealed that genetic variations were not associated with FEV(1). There was no association between SNPs and emphysema severity. However, both SNPs were significantly associated with DLCO. Conclusion: Genetic variations in CHRNA3 are associated with COPD in the Korean population.
    Respiration 11/2012; · 2.62 Impact Factor
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    ABSTRACT: PURPOSE: To assess the value of screening ultrasonography (US) in the detection of nonpalpable locoregional recurrence following mastectomy for breast cancer and to describe the US appearances of occult recurrent cancers. MATERIALS AND METHODS: During a 36-month period, 1180 consecutive US screenings were performed for mastectomy sites and ipsilateral axillary fossae in 468 asymptomatic women who had undergone mastectomy for breast cancer. All US results were divided into three groups: negative findings, probably benign nodules, and suspicious for malignant nodules. The final diagnoses were based on pathology results and clinical or sonographic follow-up for more than 12 months. The diagnostic performance of US for detecting nonpalpable locoregional recurrence was assessed. The US appearances of occult recurrent cancers were retrospectively reviewed. RESULTS: Of the 468 patients assessed, 19 (4.1%) showed "suspicious for malignant nodules"; of these lesions, 10 were malignant. One false-negative case was identified. The sensitivity and specificity were 90.9% and 98.0%, respectively. A biopsy positive predictive value of 52.6% was observed. Cancer detection rates were 2.1% with US screenings of mastectomy sites and ipsilateral axillary fossae. The common US features of occult recurrences at the mastectomy sites were irregular shaped, not-circumscribed marginated, and hypoechoic masses with intratumoral vascularities. The most common location was within the deep muscle layer. CONCLUSION: Although locoregional recurrence infrequently occurs after mastectomy for breast cancer, screening US enables detection of nonpalpable cancer before it can be detected by clinical examination. Routine follow-up US can be advocated for early detection of nonpalpable locoregional recurrent cancer.
    European journal of radiology 11/2012; · 2.65 Impact Factor
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    ABSTRACT: ABSTRACT BACKGROUND: It is well known that oral corticosteroid (OCS) and anti-TNF alpha agents increase the risk of tuberculosis. However, little is known whether inhaled corticosteroid (ICS) increases the risk of tuberculosis. We performed this study to assess the risk of pulmonary tuberculosis, among the ICS users, according to the presence of the radiologic sequelae of pulmonary tuberculosis. METHODS: A retrospective cohort study was performed. Between Jan 1, 2000 to Dec 31, 2005, a total of 778 patients, who have chronic obstructive pulmonary disease, were recruited. Among them, 162 patients were excluded according to the exclusion criteria. Finally, 616 patients were followed until Dec 31, 2010. They were divided into four groups, whether they used ICS or not, and whether they had radiologic sequelae of prior pulmonary tuberculosis or not. RESULTS: A total of 20 patients developed pulmonary tuberculosis. The Kaplan-Meier estimates showed an increased risk of pulmonary tuberculosis, among the ICS users, who had radiologic sequelae of prior pulmonary tuberculosis (p<0.001). The multi-variate COX regression showed that the ICS use was an independent risk factor for the occurrence of pulmonary tuberculosis in patients who had normal chest radiograph (hazard ratio (HR) 9.079, 95% confidence interval (CI) 1.012-81.431, p=0.049) and in patients who had radiologic sequelae of prior pulmonary tuberculosis (HR 24.946, 95% CI 3.090-201.365, p=0.003). CONCLUSION: The ICS use increases the risk of pulmonary tuberculosis in the COPD patients and the risk was greater in the patients who have radiologic sequelae of prior pulmonary tuberculosis.
    Chest 10/2012; · 7.13 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is classified into emphysema and chronic bronchitis, which are thought to result from different pathophysiological pathways. Smoking-induced lung parenchymal destruction and inadequate repair are involved in the pathogenesis of emphysema. In addition, decreased expression of vascular endothelial growth factor and increased endothelial cell apoptosis in the lung may participate in emphysema pathogenesis. As stem cells, circulating endothelial progenitor cells (EPCs) may play a key role in the maintenance of vascular integrity by replacing and repairing the damaged endothelial cells in the tissues. To determine whether the lack of appropriate repair by circulating EPCs in cases of smoking-induced endothelial cell injury participates in emphysema pathogenesis, we determined the association between the colony-forming or migratory capacity of circulating EPCs and the presence of emphysema in 51 patients with COPD. The patients were divided into emphysema (n = 23) and non-emphysema groups (n = 28) based on high-resolution computed tomography. Twenty-two smokers with normal lung function and 14 normal non-smokers served as controls. Circulating EPCs isolated from patients with emphysema showed significantly lower colony-forming units (CFUs) than those from patients with non-emphysema group, smokers with normal lung function, and normal non-smokers. EPCs from patients with emphysema showed significantly lower migratory capacity than those from normal non-smoking controls (p < 0.05). On multivariate analysis, the EPC-CFU was independently associated with emphysema (OR 0.944, 95% CI = 0.903-0.987, p = 0.011). Thus, impaired functions of circulating EPCs may contribute to the development of emphysema.
    The Tohoku Journal of Experimental Medicine 01/2012; 227(4):321-31. · 1.37 Impact Factor
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    ABSTRACT: Patients with chronic obstructive pulmonary disease (COPD) show different spirometric response patterns to bronchodilator, such that some patients show improvement principally in expiratory flow (forced expiratory volume in 1 s; FEV(1)), whereas others respond by improvement of lung volume (forced vital capacity; FVC). The mechanisms of these different response patterns to bronchodilator remain unclear. We investigated the associations between bronchodilator responsiveness and quantitative computed tomography (CT) indices in patients with COPD. Data on a total of 101 patients with stable COPD were retrospectively analysed. Volume and flow responses to bronchodilator were assessed by FVC and FEV(1) changes before and after inhalation of salbutamol (400 μg). Volumetric CT was performed to quantify emphysema, air trapping and large airway thickness. Emphysema was assessed by the volume fraction of the lung under -950 Hounsfield units (HU; V(950)) at full inspiration and air trapping by the ratio of mean lung density (MLD) at full expiration and inspiration. Airway wall thickness and wall area percentage (WA%; defined as wall area/[wall area + lumen area] × 100), were measured near the origin of right apical and left apico-posterior bronchus. Among quantitative CT indices, the CT emphysema index (V(950 insp)) showed a significant negative correlation with postbronchodilator FEV(1) change (R = -0·213, P = 0·004), and the CT air-trapping index correlated positively with postbronchodilator FVC change(R = 0·286, P≤0·001). Multiple linear regression analysis showed that CT emphysema index had independent association with postbronchodilator FEV(1) change and CT air-trapping index with postbronchodilator FVC change. The degrees of emphysema and air trapping may contribute to the different response patterns to bronchodilator in patients with COPD.
    Clinical Physiology and Functional Imaging 01/2012; 32(1):12-8. · 1.33 Impact Factor
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    ABSTRACT: Because evasion of tumor suppression is a critical step in cancer development, cancer cells have developed a variety of mechanisms to circumvent the influence of tumor suppressive pathways. Thus, genes that negatively regulate tumor suppressors could be considered novel types of oncogenes such as Bmi-1 repressing p16Ink4a and inhibiting p53 and were found to be frequently up-regulated in a variety of cancers. p38 mitogen-activated protein kinase (MAPK), which reportedly plays a crucial role as a tumor suppressor, is activated in number of lung adenocarcinomas, which is seemingly at odds with its role as a tumor suppressor. We examined 10 lung adenocarcinomas and corresponding normal tissues and determined the expression levels of a variety of tumor suppressor proteins through real-time polymerase chain reaction and immunohistochemistry and measured p38 MAPK activity by immunoblotting or immunohistochemistry analysis. In the in vitro cellular model, p38 activation by H-Ras and consequent senescence induction was achieved through retro-viral gene transduction. Similarly, the suppression of p16Ink4a by Bmi-1 after the introduction of H-Ras was achieved through transient transfection with cationic liposome. We detected several lung adenocarcinomas that were positive for activated p38 MAPK but evidenced reduced levels of p16Ink4a expression. The suppression of p16Ink4a occurred in parallel with an increase in Bmi-1 and/or p16Ink4a promoter hypermethylation. Consistent with these observations, the H-Ras-stimulated induction of p16Ink4a was suppressed significantly through the coexpression of Bmi-1 in vitro. These results demonstrate that the suppression of p16Ink4a by either the induction of Bmi-1 or the hypermethylation of p16Ink4 may be an important step in avoiding tumor surveillance by p38 MAPK during the development of lung cancer.
    Journal of thoracic oncology: official publication of the International Association for the Study of Lung Cancer 03/2011; 6(3):423-31. · 4.55 Impact Factor
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease and responses to therapies are highly variable. The aim of this study was to identify the predictors of pulmonary function response to 3 months of treatment with salmeterol/fluticasone in patients with COPD. A total of 127 patients with stable COPD from the Korean Obstructive Lung Disease (KOLD) Cohort, which were prospectively recruited from June 2005 to September 2009, were analyzed retrospectively. The prediction models for the FEV(1), FVC and IC/TLC changes after 3 months of treatment with salmeterol/fluticasone were constructed by using multiple, stepwise, linear regression analysis. The prediction model for the FEV(1) change after 3 months of treatment included wheezing history, pre-bronchodilator FEV(1), post-bronchodilator FEV(1) change and emphysema extent on CT (R = 0.578). The prediction models for the FVC change after 3 months of treatment included pre-bronchodilator FVC, post-bronchodilator FVC change (R = 0.533), and those of IC/ TLC change after 3 months of treatment did pre-bronchodilator IC/TLC and post-bronchodilator FEV(1) change (R = 0.401). Wheezing history, pre-bronchodilator pulmonary function, bronchodilator responsiveness, and emphysema extent may be used for predicting the pulmonary function response to 3 months of treatment with salmeterol/fluticasone in patients with COPD.
    Journal of Korean medical science 03/2011; 26(3):379-85. · 0.84 Impact Factor
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    ABSTRACT: Antigenic molecules are modified for targeting to the proteasome by ubiquitin (Ub) or by a Ub-independent system such as ornithine decarboxylase (ODC) to be presented by MHC class I molecules. In this study, we compared the immunogenicity of human cytomegalovirus pp65 antigen fused with Ub and/or ODC, using RNA electroporation of human dendritic cells. Among the C-terminal mutants of Ub (G76, A76, and V76), Ub(G) showed the best ability to enhance the degradation of a target protein and stimulate T cells. The pp65 antigens fused with either Ub(G) or ODC enhanced the stimulation to CD8(+) T cells, and the effects of Ub(G) and ODC were similar. Furthermore, the fusion of both Ub and ODC additively increased immunogenicity compared with the single-fusion proteins. The fusion of Ub(G) and ODC enhanced primarily the stimulation of CD8(+) rather than CD4(+) T cells and more efficiently induced pp65-specific T cells in vitro. These additive effects of Ub and ODC in antigen processing may provide improved strategies to stimulate CD8(+) T cells for the development of immunotherapies against the variety of viral diseases and cancers.
    Human gene therapy 03/2010; 21(8):957-67. · 4.20 Impact Factor
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    ABSTRACT: PURPOSE To prospectively evaluate the diagnostic performance of ultrasound (US) elastography for discriminating between benign and malignant breast lesions and to find out its role in diagnosing breast cancers, with pathologic results as the reference standard METHOD AND MATERIALS Between December 2007 and December 2008, 284 women with 342 sonographically visible breast lesions who were scheduled to undergo biopsy were examined with US elastography (Siemens Antares Ultrasound unit). Elastographic findings were prospectively classified as benign or malignant; based on the area ratio, 1.00 as the threshold for differentiating benign from malignant masses. Conventional B-mode US findings were classified according to the BI-RADS category. All patients underwent US-guided core or fine needle aspiration biopsy. The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were used to assess the diagnostic performance. RESULTS Of the 342 breast lesions, 85 (24.9%) were malignant and 257 (75.1%) were benign on pathology. B-mode US BI-RADS classification was category 3 in 74 (21.6%), category 4a in 179 (52.4%), category 4b in 36 (10.5%), category 4c in 15 (4.4%) and category 5 in 38 (11.1%). Elastogaphic findings were malignant in 102 (29.8%) and benign in 240 (70.2%). The sensitivity, specificity, NPV and PPV of B-mode US was 98.8%, 28.4%, 98.6% and 31.3% respectively. The sensitivity, specificity, NPV and PPV of US elastography was 77.4%, 83.3%, 89.2% and 67.4% respectively. US elastography was significantly better in specificity and PPV and worse in sensitivity and NPV than B-mode US (P<0.01). CONCLUSION US elastography can improve specificity and positive predictive value of B-mode US, but significantly sacrifice sensitivity and negative predictive value. Therefore, US elastography may not be helpful for distinguishing benign from malignant breast lesions and the decision of whether to perform breast biopsy. CLINICAL RELEVANCE/APPLICATION US elastography may not be able to reduce the number of benign-result biopsies without missing a cancer.
    Radiological Society of North America 2009 Scientific Assembly and Annual Meeting; 11/2009
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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disorder in which a number of different pathological processes lead to recognition of patient subgroups that may have individual characteristics and distinct responses to treatment. We tested the hypothesis that responses of lung function to 3 months of combined inhalation of long-acting beta-agonist and corticosteroid might differ among patients with various COPD subtypes. We classified 165 COPD patients into four subtypes according to the severity of emphysema and airflow obstruction: emphysema-dominant, obstruction-dominant, mild-mixed, and severe-mixed. The emphysema-dominant subtype was defined by an emphysema index on computed tomography of more than 20% and FEV(1) more than 45% of the predicted value. The obstruction-dominant subtype had an emphysema index < or = 20% and FEV(1) < or = 45%, the mild-mixed subtype had an emphysema index < or = 20% and FEV(1) > 45%, and the severe-mixed subtype had an emphysema index > 20% and FEV(1) < or = 45%. Patients were recruited prospectively and treated with 3 months of combined inhalation of long-acting beta-agonist and corticosteroid. After 3 months of combined inhalation of long-acting beta-agonist and corticosteroid, obstruction-dominant subtype patients showed a greater FEV(1) increase and more marked dyspnea improvement than did the emphysema-dominant subgroup. The mixed-subtype patients (both subgroups) also showed significant improvement in FEV(1) compared with the emphysema-dominant subgroup. Emphysema-dominant subtype patients showed no improvement in FEV(1) or dyspnea after the 3-month treatment period. The responses to 3 months of combined inhalation of long-acting beta-agonist and corticosteroid differed according to COPD subtype.
    Respiratory medicine 11/2009; 104(4):542-9. · 2.33 Impact Factor
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    ABSTRACT: Glycogen synthase kinase-3 (GSK-3) plays an important role in the regulation of apoptosis. However, the role of GSK-3 in the auditory system remains unknown. Here we examined whether the GSK-3-specific inhibitors, SB 216763 and LiCl, could protect against cisplatin-induced cytotoxicity of auditory cells. GSK-3 was activated by cisplatin treatment of HEI-OC1 cells. SB 216763 or LiCl treatments inhibited cisplatin-induced apoptosis in a dose-dependent manner and activated caspase-9, -8 and -3. In rat primary explants of the organ of Corti, SB 216763 or LiCl treatments completely abrogated the cisplatin-induced destruction of outer hair cell arrays. Administration of SB 216763 or LiCl inhibited cochlear destruction and the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and IL-6 in cisplatin-injected mice. Furthermore, administration of SB 216763 or LiCl reduced the thresholds of the auditory brainstem response (ABR) in cisplatin-injected mice. Collectively, these results suggest that cisplatin-induced ototoxicity might be associated with modulation of GSK-3 activation.
    Hearing research 09/2009; 257(1-2):53-62. · 2.18 Impact Factor
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    ABSTRACT: JANEX-1/WHI-P131, a selective Janus kinase 3 (JAK3) inhibitor, has been shown to delay the onset of diabetes in the NOD mouse model. However, the molecular mechanism by which JANEX-1 protects pancreatic beta-cells is unknown. In the current study, we investigated the role of JANEX-1 on interleukin (IL)-1beta and interferon (IFN)-gamma-induced beta-cell damage using isolated islets. JANEX-1-pretreated islets showed resistance to cytokine toxicity, namely suppressed nitric oxide (NO) production, reduced inducible form of NO synthase (iNOS) expression, and decreased islet destruction. The molecular mechanism by which JANEX-1 inhibits iNOS expression was mediated through suppression of the nuclear factor kappaB (NF-kappaB) and JAK/signal transducer and activator of transcription (STAT) pathways. Islets treated with the cytokines downregulated the protein levels of suppressor of cytokine signaling (SOCS)-1 and SOCS-3, but pretreatment with JANEX-1 attenuated these decreases. Additionally, islets from JAK3(-/-) mice were more resistant to cytokine toxicity than islets from control mice. These results demonstrate that JANEX-1 protects beta-cells from cytokine toxicity through suppression of the NF-kappaB and JAK/STAT pathways and upregulation of SOCS proteins, suggesting that JANEX-1 may be used to preserve functional beta-cell mass.
    Experimental Cell Research 06/2009; 315(12):2064-71. · 3.56 Impact Factor
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    ABSTRACT: Cytokines released by infiltrating inflammatory cells around the pancreatic islets are involved in the pathogenesis of type 1 diabetes. Interleukin (IL)-1beta and interferon (IFN)-gamma are the primary cytokines responsible for stimulation of inducible nitric oxide synthase (iNOS) expression and nitric oxide overproduction, which leads to beta-cell damage. In addition, nuclear factor-kappaB (NF-kappaB) plays a crucial role in the activation of this pathway. Therefore, suppression of the cytokine-NF-kappaB pathway is considered an effective therapeutic strategy for preventing inflammatory reactions in pancreatic beta-cells. In this study, the effects of Fructus Xanthii extract (FXE) on IL-1beta and IFN-gamma-induced beta-cell damage were examined. Treatment of RINm5F cells with IL-1beta and IFN-gamma reduced cell viability, however, FXE completely protected cells from IL-1beta and IFN-gamma-mediated reduction in viability in a concentration-dependent manner. In addition, incubation with FXE resulted in a significant suppression of IL-1beta and IFN-gamma-induced nitric oxide (NO) production, which correlated with the reduced levels of the inducible form of iNOS mRNA and protein observed. The IL-1beta and IFN-gamma-stimulated RIN cells showed increases in NF-kappaB binding activity and p50 subunit levels in the nucleus, as well as increased IkappaBalpha degradation in cytosol when compared to unstimulated cells, which indicates that the mechanism by which FXE inhibited the iNOS gene involves inhibition of NF-kappaB activation. Furthermore, a protective effect of FXE was demonstrated by reduction in NO generation and iNOS expression, as well as the normal insulin secreting responses to glucose observed in IL-1beta and IFN-gamma-treated islets.
    International Journal of Molecular Medicine 05/2009; 23(4):547-53. · 1.96 Impact Factor
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    ABSTRACT: We examined the effects of Rhizoma Dioscoreae Tokoronis extracts (RDTEs) on plasma lipids, body weight, and lipogenic enzymes. Mice were administered a standard chow diet, a 60% high-fat diet, or a high-fat diet with RDTE. Mice that were fed a high-fat diet containing RDTE were found to have lower increases in body and epididymal adipose tissue weights and a lessened occurrence of hepatic steatosis than mice that were fed a high-fat diet. The decreased adiposity that was induced by RDTE accounted for lower plasma levels of tumor necrosis factor-alpha, leptin, and glucose and a higher level of adiponectin. RDTE administration also resulted in a significant decrease in triglyceride, total plasma cholesterol, and low-density lipoprotein-cholesterol when compared to the high-fat group. To identify the mechanism by which RDTE induced its antiobesity effect, we investigated the sterol response element binding protein (SREBP) transcription system, which was induced in mice that were fed the high-fat diet. RDTE was found to suppress the expression of SREBP-1 as well as that of fatty acid synthase in adipose and liver tissues in mice provided the high-fat diet. These findings suggest that the antiobesity action of RDTE in mice that are fed a high-fat diet may occur in response to suppression of the SREBP-1-dependent lipogenic pathway.
    Journal of medicinal food 05/2009; 12(2):304-9. · 1.39 Impact Factor
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    ABSTRACT: Inhaled corticosteroids are used to treat COPD and asthma. An association between sequence variants in the corticotrophin-releasing hormone receptor 1 (CRHR1) gene and improved lung function in asthmatics treated with inhaled corticosteroids was reported recently. This study investigated the association between the change in lung function in response to inhaled corticosteroids and single-nucleotide CRHR1 polymorphisms in patients with COPD. COPD patients (n = 87) with a positive smoking history were recruited from the pulmonary clinics of 11 hospitals in Korea. Patients were treated with fluticasone propionate and salmeterol for 12 weeks and lung function was measured at baseline and after the 12-week treatment. Eighty-four of the 87 subjects were successfully genotyped. Seventy-one patients with the wild-type GG genotype and 13 patients with the heterozygous GT genotype in rs242 941 were evaluated. After 12-week treatment, the change in FEV(1) was significantly higher in patients with wild-type GG genotype (6.0 +/- 0.8% of predicted FEV(1)) than in GT heterozygotes (-0.8 +/- 1.8, P = 0.003). Improved FEV(1) following inhaled corticosteroid and a long-acting beta2-agonist was associated with CRHR1 genetic polymorphism in patients with COPD.
    Respirology 01/2009; 14(2):260-3. · 2.78 Impact Factor
  • Ultrasound in Medicine and Biology - ULTRASOUND MED BIOL. 01/2009; 35(8).

Publication Stats

795 Citations
159.68 Total Impact Points

Institutions

  • 2005–2013
    • CHA University
      • • Department of Internal Medicine
      • • College of Medicine
      Seoul, Seoul, South Korea
  • 2012
    • Yonsei University Hospital
      Sŏul, Seoul, South Korea
  • 2008–2012
    • Kangwon National University
      • Department of Internal Medicine
      Syunsen, Gangwon, South Korea
  • 2004–2012
    • Ulsan University Hospital
      Urusan, Ulsan, South Korea
    • Liaoning Normal University
      • Department of Chemistry
      Dalian, Liaoning, China
  • 2006–2010
    • Catholic University of Korea
      • • Department of Microbiology
      • • College of Medicine
      Sŏul, Seoul, South Korea
  • 2003–2009
    • Chonbuk National University
      • School of Medicine
      Seoul, Seoul, South Korea
  • 2007
    • Chonbuk National University Hospital
      Sŏul, Seoul, South Korea
  • 2004–2006
    • Wonkwang University
      • Department of Oriental Medicine
      Iksan, North Jeolla, South Korea
  • 2002–2004
    • Yeungnam University
      • College of Pharmacy
      Asan, South Chungcheong, South Korea