• 대한전자공학회:학술대회논문집
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• 대한전자공학회 2007년도 하계종합학술대회 논문집
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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.

• Journal of Trauma and Injury
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• 제34권1호
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• pp.57-60
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• 2021

Warfarin is used as part of the treatment of various diseases, and laboratory monitoring of its effects is required. Airway hematoma secondary to warfarin is rare, but can be fatal because of potential airway obstruction. Rapid definitive airway establishment is crucial if airway obstruction is suspected. This complication is more likely to occur in those with elevated coagulation laboratory values. However, we experienced a patient in whom a massive retropharyngeal hematoma caused airway obstruction after a non-severe motor vehicle collision. The patient had been taking warfarin, and had coagulation parameter values within the normal ranges. A major fracture or hemorrhage was not anticipated. Upon examination, a massive retropharyngeal hematoma was noted. Orotracheal intubation failed due to an airway obstruction. Emergency tracheostomy and an operation for hematoma removal were performed. Physicians must always consider the possibility of airway hematoma in warfarin-taking patients with normal coagulation values regardless of the severity of mechanism of injury.

• Tuberculosis and Respiratory Diseases
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• 제56권5호
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• pp.532-535
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• 2004

저자 등은 사람의 팔 힘만으로 목을 졸린 뒤 발생한 기도의 폐색이 급성 폐 부종과 호흡 부전을 초래한 증례를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

• Clinical and Experimental Pediatrics
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• 제50권4호
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• pp.335-339
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• 2007

The link between upper airway disease (allergic rhinitis and sinusitis) and lower airway disease (asthma) has long been of interest to physicians. Many epidemiological and pharmacological studies have provided a better understanding of pathophysiologic interrelationship between allergic rhinitis and asthma. The vast majority of patients with asthma have allergic rhinitis, and rhinitis is a major independent risk factor for asthma in cross-sectional and longitudinal studies. The association between sinusitis and asthma has long been appreciated. Through the recent evidences, allergic rhinitis, sinusitis, and asthma may not be considered as different diseases but rather as the expression in different parts of the respiratory tract of same pathological process in nature. Various mechanisms have been proposed to explain the relationship between asthma and upper airway diseases, but the underlying mechanisms are not completely discovered. The implications for the one-airway hypothesis are important not only academically but also clinically for diagnostic and therapeutic purposes.

• Tuberculosis and Respiratory Diseases
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• 제70권1호
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• pp.63-68
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• 2011

Multiple symmetrical lipomatosis (MSL), also called Madelung's disease, is a rare disorder of unknown etiology and characterized by abnormal accumulation of large subcutaneous fatty masses in neck, shoulder, and upper trunk. MSL has known to predominantly affect middle-aged men with a history of alcoholism. Although the clinical course of MSL is considered to be slowly progressive, in advanced stage, fatty masses in the neck may compress the upper aerodigestive tract, resulting in dyspnea and dysphagia. The treatment of MSL is surgical resection, but radical excision is very difficult and recurrence after surgery is frequent. We report the case of 55-year-old man with long lasting MSL, which caused severe airway obstruction. This patient was admitted with progressive dyspnea and massive accumulation of fat around the vocal cord that was detected on a neck CT scan. This abnormal fatty infiltration in supraglottic region caused upper airway obstruction.

• Tuberculosis and Respiratory Diseases
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• 제86권3호
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• pp.166-175
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• 2023

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. The lower airways contain a rich and diverse microbiome, which may play a significant regulatory role in both health and disease. In COPD, the microbiome becomes perturbed, causing dysbiosis. Increased representation of members in the Proteobacteria phylum and certain members in the Firmicutes phylum has been associated with increased risk of exacerbations and mortality. Therapies such as inhaled corticosteroids and azithromycin may modulate the airway microbiome or its metabolites in patients with COPD. This paper provides an up-to-date overview of the airway microbiome and its importance in the pathophysiology of COPD and as potential therapeutic target in the future.

• Tuberculosis and Respiratory Diseases
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• 제78권1호
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• pp.8-17
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• 2015

Background: AMP-activated protein kinase (AMPK) not only functions as an intracellular energy sensor and regulator, but is also a general sensor of oxidative stress. Furthermore, there is recent evidence that it participates in limiting acute inflammatory reactions, apoptosis and cellular senescence. Thus, it may oppose the development of chronic obstructive pulmonary disease. Methods: To investigate the role of AMPK in cigarette smoke-induced lung inflammation and emphysema we first compared cigarette smoking and polyinosinic-polycytidylic acid [poly(I:C)]-induced lung inflammation and emphysema in $AMPK{\alpha}1$-deficient ($AMPK{\alpha}1$-HT) mice and wild-type mice of the same genetic background. We then investigated the role of AMPK in the induction of interleukin-8 (IL-8) by cigarette smoke extract (CSE) in A549 cells. Results: Cigarette smoking and poly(I:C)-induced lung inflammation and emphysema were elevated in $AMPK{\alpha}1$-HT compared to wild-type mice. CSE increased AMPK activation in a CSE concentration- and time-dependent manner. 5-Aminoimidazole-4-carboxamide-1-${\beta}$-4-ribofuranoside (AICAR), an AMPK activator, decreased CSE-induced IL-8 production while Compound C, an AMPK inhibitor, increased it, as did pretreatment with an $AMPK{\alpha}1$-specific small interfering RNA. Conclusion: $AMPK{\alpha}1$-deficient mice have increased susceptibility to lung inflammation and emphysema when exposed to cigarette smoke, and AMPK appears to reduce lung inflammation and emphysema by lowering IL-8 production.

• Tuberculosis and Respiratory Diseases
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• 제79권3호
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• pp.193-193
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• 2016

• Tuberculosis and Respiratory Diseases
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• 제78권3호
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• pp.210-217
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• 2015

Background: Adenophora triphylla var. japonica is empirically used for controlling airway inflammatory diseases in folk medicine. We evaluated the gene expression and production of mucin from airway epithelial cells in response to lupenone, lupeol and taraxerol derived from Adenophora triphylla var. japonica. Methods: Confluent NCI-H292 cells were pretreated with lupenone, lupeol or taraxerol for 30 minutes and then stimulated with tumor necrosis factor ${\alpha}$ (TNF-${\alpha}$) for 24 hours. The MUC5AC mucin gene expression and production were measured by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Additionally, we examined whether lupenone, lupeol or taraxerol affects MUC5AC mucin production induced by epidermal growth factor (EGF) and phorbol 12-myristate 13-acetate (PMA), the other 2 stimulators of airway mucin production. Results: Lupenone, lupeol, and taraxerol inhibited the gene expression and production of MUC5AC mucin induced by TNF-${\alpha}$ from NCI-H292 cells, respectively. The 3 compounds inhibited the EGF or PMA-induced production of MUC5AC mucin in NCI-H292 cells. Conclusion: These results indicated that lupenone, lupeol and taraxerol derived from Adenophora triphylla var. japonica regulates the production and gene expression of mucin, by directly acting on airway epithelial cells. In addition, the results partly explain the mechanism of of Adenophora triphylla var. japonica as a traditional remedy for diverse inflammatory pulmonary diseases.

• Tuberculosis and Respiratory Diseases
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• 제80권1호
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• pp.60-68
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• 2017

Background: Mucus hypersecretion from airway epithelium is a characteristic feature of airway inflammatory diseases. Tumor necrosis factor ${\alpha}$ (TNF-${\alpha}$) regulates mucin synthesis. Glucocorticoids including mometasone fuorate (MF) have been used to attenuate airway inflammation. However, effects of MF on mucin production have not been reported. Methods: Effects of MF and budesonide (BUD) on the phorbol-12-myristate-13-acetate (PMA)-induction of mucin and TNF-${\alpha}$ in human airway epithelial cells (NCI-H292) were investigated in the present study. Confluent NCI-H292 cells were pretreated with PMA (200 nM) for 2 hours. Subsequently, the cells were stimulated with MF (1-500 ng/mL) or BUD (21.5 ng/mL) for 8 hours. Dexamethasone ($1{\mu}g/mL$) was used as the positive control. Real-time polymerase chain reaction was used to determine MUC2 and MUC5AC mRNA levels. The level of total mucin, MUC2, MUC5AC, and TNF-${\alpha}$ in culture supernatants were measured using enzyme-linked immunosorbent assay. Results: MF and BUD significantly suppressed MUC2 and MUC5AC gene expression in PMA-stimulated NCI-H292 cells. The inhibitory effects of the two steroid drugs were also observed in the production of total mucin, MUC2 and MUC5AC proteins, and TNF-${\alpha}$. Conclusion: Our findings demonstrated that MF and BUD attenuated mucin and TNF-${\alpha}$ production in PMA-induced human airway epithelial cells.