• Proceedings of the IEEK Conference
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• 2007.07a
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• pp.279-280
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• 2007

Airway wall thickness is an important bio-marker for evaluation of pulmonary diseases such as stenosis, bronchiectasis. Nevertheless, an image-based analysis of the airway tree can provide precise and valuable airway size information, quantitative measurement of airway wall thickness in CT images involves various sources of error and uncertainty. So we have developed an accurate airway wall measurement technique for small airways with three-dimensional (3-D) approach. To illustrate performance of these techniques, we used airway phantom that consisted of 4 acryl tubes with various inner and outer diameters. Results show that evaluation of interpolation and deconvolution methods of airways in 3-D CT images, and significant improvement over the full-width-half-maximum method for measurement of not only location of the luminal and outer edge of the airway wall but airway wall thickness.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.22 no.3
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• pp.343-350
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• 2000

The goal of this study is the comparison of upper airway size and change of skeletal Class I group and skeletal Class III group (before operation, within 2 weeks after operation, 6 months after operation) respectively. At first, we measured the lines between selected upper air way landmarks on lateral cephalometric x-ray film of skeletal Class I 40 persons whoes age were 23-26 years old, ,and did the same lines of landmarks of skeletal Class III 44 persons who had not been operated yet, were within 2 weeks after operation, were 6 months after operation. And we compared it respectively and analyzed it with paired t-test. We studied the relationship of those on produced data. 1. Skeletal Class III group was narrower in nasopharyngeal air way space than that of skeletal Class I group, and increased in thickness of oropharyngeal, hypopharyngeal wall within 2 weeks after operation, and reduced in nasopharyngeal, oropharyngeal air way space, and did in thickness of nasopharngeal, hypopharyngeal wall 6 months after operation. 2. Skeletal Class III group reduced in nasopharyngeal, oropharyngeal air way space, and increased in thickness of nasopharyngeal, oropharyngeal, hypopharyngeal wall within 2 weeks after operation, restored the thickness of nasopharyngeal, oropharyngeal wall, but did not restored nasopharyngeal, oropharyngeal, hypopharyngeal air way space. 3. Vertical length from hyoid bone to mandibular plane did not have signifacant difference from Class I group but after operation, it increased more than Class I group significantly. 4. The size of airway reduced after operation. Among this, oropharyngeal airway most reduced.

• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.302-312
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• 2022

Chronic obstructive pulmonary disease (COPD) is a complex and heterogeneous disease. Not all patients with COPD respond to available drugs. Identifying respondents to therapy is critical to delivering the most appropriate treatment and avoiding unnecessary medication. Recognition of individual patients' dominant characteristics by phenotype is a useful tool to better understand their disease and tailor treatment accordingly. To look for a suitable phenotype, it is important to understand what makes COPD complex and heterogeneous. The pathology of COPD includes small airway disease and/or emphysema. Thus, COPD is not a single disease entity. In addition, there are two types (panlobular and centrilobular) of emphysema in COPD. The coexistence of different pathological subtypes could be the reason for the complexity and heterogeneity of COPD. Thus, it is necessary to look for the phenotype based on the difference in the underlying pathology. Review of the literature has shown that clinical manifestation and therapeutic response to pharmacological therapy are different depending on the presence of computed tomography-defined airway wall thickening in COPD patients. Defining the phenotype of COPD based on the underlying pathology is encouraging as most clinical manifestations can be distinguished by the presence of increased airway wall thickness. Pharmacological therapy has shown significant effect on COPD with airway wall thickening. However, it has limited use in COPD without an airway disease. The phenotype of COPD based on the underlying pathology can be a useful tool to better understand the disease and adjust treatment accordingly.

• Clinical and Experimental Pediatrics
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• v.48 no.10
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• pp.1038-1049
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• 2005

Asthma is characterized by a chronic inflammatory disorder of the airways that leads to tissue injury and subsequent structural changes collectively called airway remodelling. Characteristic changes of airway remodelling in asthma include goblet cell hyperplasia, deposition of collagens in the basement membrane, increased number and size of microvessels, hypertrophy and hyperplasia of airway smooth muscle, and hypertrophy of submucosal glands. Apart from inflammatory cells, such as eosinophils, activated T cells, mast cells and macrophages, structural tissue cells such as epithelial cells, fibroblasts and smooth muscle cells can also play an important effector role through the release of a variety of mediators, cytokines, chemokines, and growth factors. Through a variety of inflammatory mediators, epithelial and mesenchymal cells cause persistence of the inflammatory infiltrate and induce airway structural remodelling. The end result of chronic airway inflammation and remodelling is an increased thickness of the airway wall, leading to a increased the bronchial hyperresponsiveness and fixed declined lung function.

• Tuberculosis and Respiratory Diseases
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• v.72 no.1
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• pp.8-14
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• 2012

Background: Although airway obstruction in chronic obstructive pulmonary disease (COPD) is due to pathologic processes in both the airways and the lung parenchyma, the contribution of these processes, as well as other factors, have not yet been evaluated quantitatively. We therefore quantitatively evaluated the factors contributing to airflow limitation in patients with COPD. Methods: The 213 COPD patients were aged >45 years, had smoked >10 pack-years of cigarettes, and had a post-bronchodilator forced expiratory volume in one second ($FEV_1$)/forced vital capacity (FVC) <0.7. All patients were evaluated by medical interviews, physical examination, spirometry, bronchodilator reversibility tests, lung volume, and 6-minute walk tests. In addition, volumetric computed tomography (CT) was performed to evaluate airway wall thickness, emphysema severity, and mean lung density ratio at full expiration and inspiration. Multiple linear regression analysis was performed to identify the variables independently associated with $FEV_1$ - the index of the severity of airflow limitation. Results: Multiple linear regression analysis showed that CT measurements of mean lung density ratio (standardized coefficient ${\beta}$=-0.46; p<0.001), emphysema severity (volume fraction of the lung less than -950 HU at full inspiration; ${\beta}$=-0.24; p<0.001), and airway wall thickness (mean wall area %; ${\beta}$=-0.19, p=0.001), as well as current smoking status (${\beta}$=-0.14; p=0.009) were independent contributors to $FEV_1$. Conclusion: Mean lung density ratio, emphysema severity, and airway wall thickness evaluated by volumetric CT and smoking status could independently contribute to the severity of airflow limitation in patients with COPD.

• Korean Journal of Medicinal Crop Science
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• v.27 no.3
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• pp.218-231
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• 2019

Background: We recently reported that Salvia plebeia R. Br. extracts suppress leukotriene production and effectively inhibit the airway inflammatory response by modulating inflammatory chemokine and cytokine expression. Here, we investigated the synergistic airway anti-inflammation effect of Salvia plebeia and Panax ginseng (Korean red ginseng, KRG) that has been used to treat various immune diseases such as asthma. Methods and Results: To evaluate the synergistic airway anti-inflammatory effect of Salvia plebeia and KRG, we measured the inhibitory effect of monotheraphy with either or co-theraphy with both on leukotriene and reactive oxygen species (ROS) production. Using coal a combustion, fly ash, and diesel exhaust particle (CFD)-induced respiratory disease mouse model, we found that co-theraphy synergistically suppressed airway inflammatory signs such as alveolar wall thickness and collagen fibers deposition, and decreased the number of total cell, $CD11b^+Gr-1^+$ cells, and inflammatory cytokines (IL17A, TNF, MIP-2 and CXCL-1) in bronchoalveolar lavage (BAL) fluid. Conclusions: We confirmed respiratory protection as a therapeutic effect of the Salbia plebeia-KRG 3 : 1 complex (KGC-03-PS) via anti-tracheal muscle contraction and expectorant animal studies using a CFD-induced respiratory disease mouse model.

• Korean Journal of Medicinal Crop Science
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• v.25 no.5
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• pp.269-281
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• 2017

Background: Small particles increase airway inflammation upon reaching the alveoli. Here, we investigated the protective or therapeutic effects of Salvia plebeia R. Br. (SP_R) extracts on airway inflammation. Methods and Results: To investigate the anti-inflammatory activity of SP_R extracts, we measured their inhibitory effect on the production of reactive oxygen species (ROS) expression of inflammatory mediators, and immune cell infiltration in MH-S alveolar macrophage cells and in the ambient particulate matter (APM)-exposed airway inflammation mice model. The SP_R extracts inhibited the production of ROS and expression of IL-4, IL-10, IL-15, and IL-17A mRNA in APM-stimulated MH-S cells. Oral administration of SP_R extracts suppressed APM-induced inflammatory symptoms, such as high alveolar wall thickness, excess collagen fibers, decreased mRNA expression of chemokines (Ccr9, Ccl5, Ccr3), inflammatory cytokines (IL-15, TNF-${\alpha}$), and IL-4 Th2 cytokine in the lung. The SP_R extracts also inhibited ROS production, granulocyte ($CD11b^+Gr-1^+$) infiltration, IL-17A, TNF-${\alpha}$, macrophage inflammatory protein (Mip-2), and chemokine (C-X-C motif) ligand 1 (Cxcl-1) production in the airway. The specific compounds in the SR-R extracts that mediate the anti-inflammatory effects were identified. Conclusions: In this study, SP_R extracts effectively inhibited airway inflammatory responses, such as ROS production and granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines.

• Journal of Ginseng Research
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• v.47 no.1
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• pp.81-88
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• 2023

Background: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. Methods: Research of the respiratory protective effects of KRG extract in a particulate matter (PM; aerodynamic diameter of <4 ㎛) plus diesel exhaust particle (DEP) (PM4+D)-induced airway inflammation model. Nitric oxide production, expression of pro-inflammatory mediators and cytokines, and IRAK-1, TAK-1, and MAPK pathways were examined in PM4-stimulated MH-S cells. BALB/c mice exposed to PM4+D mixture by intranasal tracheal injection three times a day for 12 days at 3 day intervals and KRGE were administered orally for 12 days. Histological of lung and trachea, and immune cell subtype analyses were performed. Expression of pro-inflammatory mediators and cytokines in bronchoalveolar lavage fluid (BALF) and lung were measured. Immunohistofluorescence staining for IRAK-1 localization in lung were also evaluated. Results: KRGE inhibited the production of nitric oxide, the expression of pro-inflammatory mediators and cytokines, and expression and phosphorylation of all downstream factors of NF-κB, including IRAK-1 and MAPK/AP1 pathway in PM4-stimulated MH-S cells. KRGE suppressed inflammatory cell infiltration and number of immune cells, histopathologic damage, and inflammatory symptoms in the BALF and lungs induced by PM4+D; these included increased alveolar wall thickness, accumulation of collagen fibers, and TNF-α, MIP2, CXCL-1, IL-1α, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1α release by associating with IRAK-1 localization was also potently inhibited by KRGE in the lungs of PM4+D-induced airway inflammation model. KRGE suppresses airway inflammatory responses, including granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines via inhibition of IRAK-1 and MAPK pathway. Conclusion: Our results indicate the potential of KRGE to serve as an effective therapeutic agent against airway inflammation and respiratory diseases.

• Korean Journal of Radiology
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• v.21 no.9
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• pp.1104-1113
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• 2020

Objective: To assess the regional ventilation in patients with asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) using xenon-ventilation dual-energy CT (DECT), and to compare it to that in patients with COPD. Materials and Methods: Twenty-one patients with ACOS and 46 patients with COPD underwent xenon-ventilation DECT. The ventilation abnormalities were visually determined to be 1) peripheral wedge/diffuse defect, 2) diffuse heterogeneous defect, 3) lobar/segmental/subsegmental defect, and 4) no defect on xenon-ventilation maps. Emphysema index (EI), airway wall thickness (Pi10), and mean ventilation values in the whole lung, peripheral lung, and central lung areas were quantified and compared between the two groups using the Student's t test. Results: Most patients with ACOS showed the peripheral wedge/diffuse defect (n = 14, 66.7%), whereas patients with COPD commonly showed the diffuse heterogeneous defect and lobar/segmental/subsegmental defect (n = 21, 45.7% and n = 20, 43.5%, respectively). The prevalence of ventilation defect patterns showed significant intergroup differences (p < 0.001). The quantified ventilation values in the peripheral lung areas were significantly lower in patients with ACOS than in patients with COPD (p = 0.045). The quantified Pi10 was significantly higher in patients with ACOS than in patients with COPD (p = 0.041); however, EI was not significantly different between the two groups. Conclusion: The ventilation abnormalities on the visual and quantitative assessments of xenon-ventilation DECT differed between patients with ACOS and patients with COPD. Xenon-ventilation DECT may demonstrate the different physiologic changes of pulmonary ventilation in patients with ACOS and COPD.

• Journal of the Korean Society of Radiology
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• v.84 no.5
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• pp.1123-1133
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• 2023

Purpose Our study aimed to evaluate the association between automated quantified body composition on CT and pulmonary function or quantitative lung features in patients with chronic obstructive pulmonary disease (COPD). Materials and Methods A total of 290 patients with COPD were enrolled in this study. The volume of muscle and subcutaneous fat, area of muscle and subcutaneous fat at T12, and bone attenuation at T12 were obtained from chest CT using a deep learning-based body segmentation algorithm. Parametric response mapping-derived emphysema (PRM^emph), PRM-derived functional small airway disease (PRM^fSAD), and airway wall thickness (AWT)-Pi10 were quantitatively assessed. The association between body composition and outcomes was evaluated using Pearson's correlation analysis. Results The volume and area of muscle and subcutaneous fat were negatively associated with PRM^emph and PRM^fSAD (p < 0.05). Bone density at T12 was negatively associated with PRM^emph (r = -0.1828, p = 0.002). The volume and area of subcutaneous fat and bone density at T12 were positively correlated with AWT-Pi10 (r = 0.1287, p = 0.030; r = 0.1668, p = 0.005; r = 0.1279, p = 0.031). However, muscle volume was negatively correlated with the AWT-Pi10 (r = -0.1966, p = 0.001). Muscle volume was significantly associated with pulmonary function (p < 0.001). Conclusion Body composition, automatically assessed using chest CT, is associated with the phenotype and severity of COPD.