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1.  Interstitial Lung Disease in a Patient with Dyskeratosis Congenita 
Dyskeratosis congenita is a rare congenital disorder characterized by a triad of reticular pigmentation of the skin, dystrophic nails, and leukoplakia of the mucous membrane. Sometimes it is associated with bone marrow failure, secondary malignancy and interstitial lung disease. Though it is rare, Dyskeratosis congenita is diagnosed relatively easily when clinicians suspect it. It can be diagnosed just by gross inspection with care. Dyskeratosis congenita should be considered as one cause associated with interstitial lung disease. In Korea, interstitial lung disease with dyskeratosis congenita has not been reported. We report a case and review the literature.
PMCID: PMC3591541  PMID: 23483786
Lung Diseases, Interstitial; Dyskeratosis Congenita; Anemia, Aplastic
2.  The Effect of Body Composition on Pulmonary Function 
The pulmonary function test is the most basic test method to diagnosis lung disease. The purpose of this study was to research the correlation of the body mass index (BMI), the fat percentage of the body mass (fat%), the muscle mass, the fat-free mass (FFM) and the fat-free mass index (FFMI), waist-hip ratio (WHR), on the forced expiratory volume curve.
Between March and April 2009, a total of 291 subjects were enrolled. There were 152 men and 139 female (mean age, 46.3±9.92 years), and they were measured for the following: forced vital capacity (FVC), forced expiratory volume at 1 second (FEV1), and forced expiratory flow during the middle half of the FVC (FEF25-75) from the forced expiratory volume curve by the spirometry, and the body composition by the bioelectrical impedance method. Correlation and a multiple linear regression, between the body composition and pulmonary function, were used.
BMI and fat% had no correlation with FVC, FEV1 in male, but FFMI showed a positive correlation. In contrast, BMI and fat% had correlation with FVC, FEV1 in female, but FFMI showed no correlation. Both male and female, FVC and FEV1 had a negative correlation with WHR (male, FVC r=-0.327, FEV1 r=-0.36; p<0.05; female, FVC r=-0.175, FEV1 r=-0.213; p<0.05). In a multiple linear regression of considering the body composition of the total group, FVC explained FFM, BMI, and FFMI in order (r2=0.579, 0.657, 0.663). FEV1 was explained only fat% (r2=0.011), and FEF25-75 was explained muscle mass, FFMI, FFM (r2=0.126, 0.138, 0.148).
The BMI, fat%, muscle mass, FFM, FFMI, WHR have significant association with pulmonary function but r2 (adjusted coefficient of determination) were not high enough for explaining lung function.
PMCID: PMC3475466  PMID: 23101008
Pulmonary Function Tests; Body Compostion; Factor Analysis, Statistical
3.  Effects of TNF-α and Leptin on Weight Loss in Patients with Stable Chronic Obstructive Pulmonary Disease 
Weight loss is common in patients with chronic obstructive pulmonary disease (COPD). However, the mechanisms of this weight loss are still unclear.
Sixty male patients with stable COPD and 45 healthy male controls participated in this study. The COPD patients were divided into two groups, that is, the emphysema and chronic bronchitis groups, by the transfer coefficient of carbon monoxide. The body composition, resting energy expenditure (REE), plasma leptin levels and serum tumor necrosis factor-alpha (TNF-α) were measured in all the study participants. The difference and correlation of these parameters were investigated between the two groups.
Emphysematous patients were characterized by a lower body mass index (BMI) and fat-mass (FM) compared with the chronic bronchitis patients (p<0.001). The plasma leptin levels, as corrected for the FM, were not different between the COPD patients and healthy controls (78.3±30.9 pg/mL/kg vs. 70.9±17.3 pg/mL/kg, respectively), and the plasma leptin levels, as adjusted for the FM, were also not different between the two groups of COPD patients. In the chronic bronchitis patients, the plasma leptin concentration was correlated with the BMI (r=0.866, p<0.001) but it was not correlated with the BMI in the emphysema patients. The serum TNF-α levels were higher in the stable COPD patients than those in the controls, but there was no statistical difference (10.7±18.6 pg/mL vs. 7.2×3.5 pg/mL, respectively, p0.05). The leptin concentration was well correlated with the BMI and %FM in the patients with chronic bronchitis and the leptin concentration was only correlated with the %FM (r=0.450, p=0.027) in emphysema patients. There was no correlation between the plasma leptin concentration, as adjusted for the fat mass, and the activity of the TNF-α system.
The interaction of leptin and the activity of the TNF-α system in the pathogenesis of tissue depletion may not play an important role in chronic stable COPD patients.
PMCID: PMC2687660  PMID: 18309683
COPD; Weight loss; Leptin; Tumor necrosis factor-alpha
4.  Interleukin-1beta induces MUC2 gene expression and mucin secretion via activation of PKC-MEK/ERK, and PI3K in human airway epithelial cells. 
Journal of Korean Medical Science  2002;17(6):765-771.
Interleukin 1beta(IL-1beta), a proinflammatory cytokine, is related with inflammatory diseases and it up-regulates MUC2 gene expression and mucin secretion. This study was designed to investigate the signal transduction pathway of the IL-1beta-mediated MUC2 gene expression and mucin secretion in human airway epithelial cells. In cultured human airway NCI-H292 epithelial cells, the steady state of the mRNA level of MUC2 gene expression and mucin secretion induced by IL-1beta were determined by reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme immunoassay, and immunoblot analysis. To observe the signal pathway of the IL-1beta-mediated MUC2 gene expression and mucin secretion, we used several specific inhibitors. PD98059 (MEK/ERK inhibitor) suppressed IL-1beta-mediated MUC2 gene expression and mucin secretion, while SB203580 (p38 inhibitor) did not. Ro31-8220 (PKC inhibitor) inhibited IL-1beta-mediated MUC2 gene expression and mucin secretion. It inhibited ERK phosphorylation, but did not inhibit p38 phosphorylation. LY294002 (PI3K inhibitor) also suppressed MUC2 expression, but did not inhibit any MAPKs phosphorylation. These results suggest that the IL-1beta-mediated MUC2 gene expression and mucin secretion in NCI-H292 cells are regulated through activation of the PKC-MEK/ERK pathway, and that PI3K is also involved in the IL-1beta-mediated MUC2 gene expression and mucin secretion.
PMCID: PMC3054965  PMID: 12482999

Results 1-4 (4)