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Search Results: 1 - 10 of 34412 matches for " Yun-Yeong Kim "
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Stationary Vector Autoregressive Representation of Error Correction Models  [PDF]
Yun-Yeong Kim
Theoretical Economics Letters (TEL) , 2012, DOI: 10.4236/tel.2012.22027
Abstract: The paper introduces a stationary vector autoregressive (VAR) representation of the error correction model (ECM). This representation explicitly regards the cointegration error a dependent variable, making the direct implementation of standard dynamic analyses using standard VAR models possible, particularly with respect to the cointegration error. Of course, an ECM does not have an explicit VAR form, and thus, it is not convenient for conducting such dynamic analyses. In this regard, we transform the original nonstationary VAR model into a VAR model with the cointegration error and stationary variables. Finally, we employ the model to dynamically analyze the real exchange rate between the US dollar and the Japanese yen.
Optimal Foreign Exchange Risk Hedging: A Mean Variance Portfolio Approach  [PDF]
Yun-Yeong Kim
Theoretical Economics Letters (TEL) , 2013, DOI: 10.4236/tel.2013.31001

This paper introduces the optimal foreign exchange risk hedging model following a standard portfolio theory. The results indicate that a lower level of risk can be achieved, given a specified level of expected return, from using optimization modeling. In the paper the expected hedging return is defined from the expected cost of the foreign currency using a specified hedging strategy minus the expected cost of the foreign currency when it is purchased form the spot market. The focal point of the technique is its ability to identify optimal combinations of hedging vehicles, those are currency options, forward contracts, leaving the position open (foreign exchange risk hedging tools suggested by the US. Department of Commerce) in a closed form.

Optimal Foreign Exchange Risk Hedging: Closed Form Solutions Maximizing Leontief Utility Function  [PDF]
Yun-Yeong Kim
Theoretical Economics Letters (TEL) , 2018, DOI: 10.4236/tel.2018.814181
Abstract: In this paper, we extend Kim (2013)for the optimal foreign exchange (FX) risk hedging solution to the multiple FX rates and suggest its application method. First, the generalized optimal hedging method of selling/buying of multiple foreign currencies is introduced. Second, the cost of handling forward contracts is included. Third, as a criterion of hedging performance evaluation, there is consideration of the Leontief utility function, which represents the risk averseness of a hedger. Fourth, specific steps are introduced about what is needed to proceed with hedging. There is a computation of the weighting ratios of the optimal combinations of three conventional hedging vehicles, i.e., call/put currency options, forward contracts, and leaving the position open. The closed form solution of mathematical optimization may achieve a lower level of foreign exchange risk for a specified level of expected return. Furthermore, there is also a suggestion provided about a procedure that may be conducted in the business fields by means of Excel.
Myositis autoantibodies in Korean patients with inflammatory myositis: Anti-140-kDa polypeptide antibody is primarily associated with rapidly progressive interstitial lung disease independent of clinically amyopathic dermatomyositis
Eun Kang, Ran Nakashima, Tsuneyo Mimori, Jinhyun Kim, Yun Lee, Eun Lee, Yeong Song
BMC Musculoskeletal Disorders , 2010, DOI: 10.1186/1471-2474-11-223
Abstract: Immunoprecipitation was performed using the sera of classic polymyositis (PM) (n = 11) and dermatomyositis (DM) (n = 38) patients who met the Bohan and Peter criteria for definite inflammatory myositis. A panel of defined myositis autoantibodies was surveyed to investigate the association between each autoantibody and clinical subsets of inflammatory myositis.Either MSAs, anti-p140, or anti-p155/140 antibodies were found in 63.3% (31/49) of the study subjects. Anti-140-kDa-polypeptide (anti-p140) (18.4%, 9/49) and anti-155/140-kDa polypeptide (anti-p155/140) (16.3%, 8/49) antibodies were the most common, followed by anti-Mi2 (14.3%, 7/49), anti-ARS (12.2%, 6/49) and anti-SRP (2.0%, 1/49) antibodies. All MSAs and anti-p140 and anti-p155/140 antibodies were mutually exclusive. Anti-p140 (23.7%, 9/38), anti-p155/140 (21.1%, 8/38), and anti-Mi2 (18.4%, 3/38) antibodies were found exclusively in DM patients. Anti-p140 antibody was associated with rapidly progressive interstitial lung disease (ILD) (p = 0.001), with a sensitivity of 100.0% (4/4) and a specificity of 85.3% (29/34) in DM patients. Anti-p155/140 antibody was associated with cancer-associated DM (p = 0.009), with a sensitivity of 55.6% (5/9) and a specificity of 89.7% (26/29). Cancer-associated survival was significantly worse when anti-p155/140 antibody was present (19.2 ± 7.6 vs. 65.0 ± 3.5 months, p = 0.032). Finally, anti-ARS antibodies were associated with stable or slowly progressive ILD in PM and DM patients (p = 0.005).Anti-p140 and anti-p155/140 antibodies were commonly found autoantibodies in Korean patients with inflammatory myositis. Despite the lack of clinically amyopathic DM patients in the study subjects, a strong association was observed between anti-p140 antibody and rapidly progressive ILD. Anti-p155/140 antibody was associated with cancer-associated myositis and poor survival.Polymyositis (PM) and dermatomyositis (DM) are systemic autoimmune diseases in which muscles are the primary target
Propagation Near Cutoff Frequency in a Lossy Rectangular Waveguide
Kim Ho Yeap,Choy Yoong Tham,Kee Choon Yeong,Yun Thung Yong
International Journal of Electronics, Computer and Communications Technologies , 2010,
Abstract: We present a simple and fundamental technique to compute the attenuation of electromagnetic waves propagating in lossy rectangular waveguides with imperfectly conducting wall. A set of transecendental equations is derived by matching the tangential electric and magnetic fields at the surface of the wall with the constitutive properties of the wall material, expressed as surface impedance. The propagation constant of the waves can be obtained by substituting the dispersion relation into the equations and numerically solving for the roots. We have compared our results with that using the approximate perturbation method. Althoug good agreement was found at a reasonable range of frequencies above the cutoff frequency, the attenuation curves for the two methods, however, deviate below cutoff. We attribute the discrepancies to the dispersive effect in a lossy waveguide. Since the perturbation method assumes lossless fields’ expressions, such effect failed to be accounted for in the method.
Obesity Indices Related to Obstructive Sleep Apnea in Obese Adults  [PDF]
Jongwoo Kim, Seon Yeong Lee
Journal of Biosciences and Medicines (JBM) , 2017, DOI: 10.4236/jbm.2017.510004
Abstract: Background: Obstructive Sleep Apnea (OSA) is prevalent in obese patients. OSA should be evaluated because it might increase mortality. We aimed to evaluate the risk for OSA in obese Korean adults, and to examine the obesity indices most strongly associated with OSA. Method: Anthropometric measurements, fat computed tomography (CT) and dual energy X-ray absorptiometry (DEXA) were performed in 30 obese patients. All patients were divided into low or high risk group of OSA using Berlin Questionnaire. We compared differences between the groups in obesity-related indices. Result: Eleven of the 30 patients (36.7%) were in the low OSA risk group and 19 (63.3%) were in the high OSA risk group. The correlation coefficients for BMI, neck circumference, and neck-to-height ratio × 100(%) in the high-risk group versus the low-risk group were 1.03, 1.96, and 4.04, respectively (P = 0.03). Conclusion: The obesity index most strongly associated with OSA was neck circumference to height ratio.
Cardiovascular Risk Factors and Epicardial Adipose Tissue Measured by Chest Computed Tomography in Healthy Adults  [PDF]
Jongwoo Kim, Seon Yeong Lee
Journal of Biosciences and Medicines (JBM) , 2017, DOI: 10.4236/jbm.2017.511006
Abstract: Background: Epicardial adipose tissue (EAT) may produce several cytokines contributed to coronary atherosclerosis. EAT was measured by transthoracic echocardiography or 3 dimensional cardiac computed tomography (CT) on previous studies. We aimed to evaluate the correlation between EAT thickness and cardiovascular risk factors in healthy adults. Method: We collected clinical, biochemical information from 469 subjects (371 men and 98 women) who visited our health promotion center. EAT thickness was measured by chest CT on the free wall of the right ventricle. Result: The mean EAT thickness was 2.47 ± 1.64 mm in total of 469 subjects. EAT thickness was significantly correlated to age, weight, body mass index (BMI), total body fat, systolic and diastolic blood pressure, total cholesterol, low density lipoprotein (LDL)-cholesterol, and fasting glucose in men and to age, height, weight, BMI, total body fat, systolic and diastolic blood pressure, triglycerides, C-reactive protein (CRP), and fasting glucose in women. Multivariate analysis showed that age, BMI, systolic blood pressure, fasting glucose were the variables that independently correlated to EAT thickness in men. But there was no significant independent variable in women. Conclusion: In our study, EAT thickness measured with chest CT in healthy individuals correlates with cardiovascular risk factors in men.
Potential role and mechanism of IFN-gamma inducible protein-10 on receptor activator of nuclear factor kappa-B ligand (RANKL) expression in rheumatoid arthritis
Eun Lee, MiRan Seo, Yong-Sung Juhnn, Jeong Kim, Yoo Hong, Yun Lee, Eun Lee, Yeong Song
Arthritis Research & Therapy , 2011, DOI: 10.1186/ar3385
Abstract: Synoviocytes derived from RA patients were kept in culture for 24 hours in the presence or absence of TNF-α. CXCL10 expression was measured by reverse transcriptase polymerase chain reaction (RT-PCR) of cultured synoviocytes. Expression of RANKL was measured by RT-PCR and western blot in cultured synoviocytes with or without CXCL10 and also measured in Jurkat/Hut 78 T cells and CD4+ T cells in the presence of CXCL10 or dexamethasone. CXCL10 induced RANKL expression in Jurkat T cells was tested upon the pertussis toxin (PTX), an inhibitor of Gi subunit of G protein coupled receptor (GPCR). The synthetic siRNA for Gαi2 was used to knock down gene expression of respective proteins.CXCL10 expression in RA synoviocytes was increased by TNF-α. CXCL10 slightly increased RANKL expression in RA synoviocytes, but markedly increased RANKL expression in Jurkat/Hut 78 T cell or CD4+ T cell. CXCL10 augmented the expression of RANKL by 62.6%, and PTX inhibited both basal level of RANKL (from 37.4 ± 16.0 to 18.9 ± 13.0%) and CXCL10-induced RANKL expression in Jurkat T cells (from 100% to 48.6 ± 27.3%). Knock down of Gαi2 by siRNA transfection, which suppressed the basal level of RANKL (from 61.8 ± 17.9% to 31.1 ± 15.9%) and CXCL10-induced RANKL expression (from 100% to 53.1 ± 27.1%) in Jurkat T cells, is consistent with PTX, which inhibited RANKL expression.CXCL10 increased RANKL expression in CD4+ T cells and it was mediated by Gαi subunits of CXCR3. These results indicate that CXCL10 may have a potential role in osteoclastogenesis of RA synovial tissue and subsequent joint erosion.Interferon-gamma (IFN-γ)-inducible protein 10 (CXCL10, also called IP-10) was initially identified as a chemokine that is induced by IFN-γ and secreted by various cell types, such as monocytes, neutrophils, endothelial cells, keratinocytes, fibroblasts, mesenchymal cells, dendritic cells, and astrocytes [1]. CXCL10 is a 10-kDa protein and is functionally categorized as an 'inflammatory' chemokine. Moreo
Adiponectin is a potential catabolic mediator in osteoarthritis cartilage
Eun Kang, Yun Lee, Tae Kim, Chong Chang, Jin-Haeng Chung, Kichul Shin, Eun Lee, Eun Lee, Yeong Song
Arthritis Research & Therapy , 2010, DOI: 10.1186/ar3218
Abstract: Immunohistochemical analysis was performed to evaluate differential expression of adiponectin receptors (AdipoRs) in nonlesional and lesional areas of OA cartilage. Cartilage and chondrocytes from the knee joints of primary OA patients were cultured in the presence of adiponectin (0~30 μg/ml). The levels of total nitric oxide (NO), matrix metalloproteinase (MMP)-1, -3, and -13, and tissue inhibitor of metalloproteinase (TIMP)-1 were measured in the conditioned media. The levels of inducible NO synthase (iNOS) and MMPs were determined with the quantitative real-time reverse transcription-polymerase chain reaction. The concentrations of collagenase-cleaved type II collagen neoepitope (C1-2C) were determined in the supernatant of adiponectin-stimulated OA cartilage explants. The effects of kinase and NOS inhibitors were evaluated in the adiponectin-stimulated chondrocytes.The expression levels of both AdipoR1 and AdipoR2 were significantly higher in lesional than in nonlesional areas of OA cartilage. The increased rate of AdipoR1-positive chondrocytes was twice that of AdipoR2-positive chondrocytes when compared between nonlesional and lesional areas. Adiponectin-stimulated OA chondrocytes showed increased total NO and MMP-1, -3, and -13 levels compared with nonstimulated cells. The TIMP-1 level was not affected. The C1-2C levels were increased by adiponectin in OA cartilage explant culture. AMP-activated protein kinase (AMPK) and c-Jun N-terminal kinase (JNK) inhibitors (compound C and SP600125) significantly suppressed adiponectin-induced production of total NO and MMP-1, -3, and -13. Inducible NOS inhibitors enhanced the expression of the adiponectin-induced MMPs.Adiponectin causes matrix degradation in OA cartilage and increases MMPs and iNOS expression via the AMPK and JNK pathways in human OA chondrocytes. The catabolic effects of adiponectin may be counteracted by NO.Obesity has long been considered a risk factor for osteoarthritis (OA) [1-4]. It has been report
Downregulation of heat shock protein 70 protects rheumatoid arthritis fibroblast-like synoviocytes from nitric oxide-induced apoptosis
Eun Ha Kang, Dong Jo Kim, Eun Young Lee, Yun Jong Lee, Eun Bong Lee, Yeong Wook Song
Arthritis Research & Therapy , 2009, DOI: 10.1186/ar2797
Abstract: Targeted knock-down of Hsp70 was performed by RNA interference in RA FLSs at passage 3-7. After SNP treatment, the morphological features of apoptosis were observed by phase-contrast microscopy. Cell survival was measured by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assays and by flow cytometric analysis after propidium iodide (PI) staining. Bcl-2 expression and signaling pathways (Akt, extracellular signal-regulated kinase, p38, c-Jun N-terminal kinase) were examined with or without Hsp70 downregulation.Hsp70 downregulation in RA FLSs, induced by small interfering RNA (siRNA), was confirmed by reverse transcriptase-polymerase chain reaction and Western blotting. When treated with SNP, Hsp70 downregulated cells showed markedly less cell blebbing, cytoplasmic condensation, and nuclear shrinkage than non-downregulated control cells. Furthermore, Hsp70 downregulated cells were found to survive better than control cells in MTT assays (mean of absorbance ratio, 4.39 in target cells versus 1.00 in control siRNA-treated cells versus 1.09 in lipofectamine-treated cells, P = 0.001) and according to PI staining results (mean M1 ratio, 0.21 in target cells versus 1.00 in control siRNA-treated cells versus 1.03 in lipofectamine-treated cells, P = 0.001). Bcl-2 expression and Akt phosphorylation were higher in Hsp70 downregulated RA FLSs than in control cells. When cells were treated with LY294002, a potent phosphoinositide 3-kinase inhibitor, Akt phosphorylation and Bcl-2 levels were reduced and Hsp70 downregulation no longer had a cytoprotective effect.Knock-down of Hsp70 protects RA FLSs from nitric oxide-induced apoptosis by activating the Akt signaling pathway. These results suggest that Hsp70 has a pro-apoptotic role in RA FLSs.Rheumatoid arthritis (RA) is a chronic inflammatory disorder that involves mainly joint synovium. One of the major characteristics of RA synovium is the tumor-like growth of fibroblast-like synoviocytes (FLSs) that invade ad
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