• Tuberculosis and Respiratory Diseases
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• v.45 no.1
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• pp.99-106
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• 1998

Background: Bronchial asthma is a complex disease, which is characterized by spontaneous exacerbations of airway obstruction and persistent bronchial hyperresponsiveness. Animal models have fallen short of reproducing the human disease, particularly in mimicking the spontaneous and persistent airflow obstruction that characterized in asthma. In animals, airflow obstruction is usually assessed by measuring airflow resistance during tidal breathing under such invasive technique as tracheostomy and anesthesia. A noninvasive technique for measuring pulmonary function in small animals is needed to evaluate long-term changes in lung function during the course of experimentally produced disease without sacrificing the animal. Purpose: The purpose of this study was to evaluate early bronchoconstrcition after allergen challenge and airway responsiveness (AR) to inhaled methacholine in nonanethetized, unrestrained guinea pigs. Method: Guinea pig model of asthma was sensitized by subcutaneous injection with ovalbumin and challenged by inhalation of aerosolized ovalbumin(1% wt/vol ovlabumin). Airflow obstruction of conscious guinea pig was measured as specific airway resistance (airway resistance $\times$ thoracic gas volume). Airway resistance and thoracic gas volume of conscious guinea pig were assessed by body plethysmography before challenge and at regular intervals for as long as 30 minutes after challenge. AR to aerosolized methacholine of asthma group was compared with that of control group in body plethysmography. Result: Asthma model<> developed in 13 (65%) among 20 guinea pigs, in which early responses occurred in the airways after the exposure to inhalation with ovalbumin. Airway challenge with ovalbumin caused increase in specific airway resistance, which peaked at 6 minutes and amounted to a $231.5{\pm}30.4%$ increase from baseline. AR to aerosolized methacholine of asthma model increased significantly compared with control group. Conclusion: These results have showed a useful animal model to evaluate early bronchoconstrcition after allergen challenge and airway responsiveness in nonanethetized, unrestrained guinea pigs.

• Journal of Korean Society for Atmospheric Environment
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• v.24 no.3
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• pp.321-328
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• 2008

The number of patient with allergic asthma and atopy have increased in the cities of Korea steadily. In order to elucidate the primary factor, we investigated whether the house dust particles collected from an apartment of the middle classes has promoting effects of allergen-related airway inflammation and airway hyperresponsiveness. Mice were treated with 0.1 mL of 1 mg/mL of house dust particles suspension by intratracheal instillation once weekly for 10 weeks combined with ovalalbumin (OVA) sensitization. Intratracheal instillation of house dust particles and OVA sensitization caused an increase in the level of serum L-lactate dehydrogenase (LDH), immunoglobulun-E (IgE) and histamine, and an elevation in respiratory resistance. It also enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF) of mice, IgE and eotaxin expression in blood, and T helper type 2 cell derived cytokine levels such as of interleukin (IL)-4, IL-13 and IL-5 in the BALF. However, it did not influence T helper type 1 cytokine such as interferon-gamma in the BALF. These results indicate that house dust particles elevate allergen-related airway inflammation and airway hyperresponsiveness in mice and may play an important role in the aggravation of asthma and atopy in Korea.

• Environmental Analysis Health and Toxicology
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• v.25 no.2
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• pp.121-129
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• 2010

This study was carried out to investigate whether asian yellow sand dust (AS) has promoting effects of allergen-related airway inflammation and airway hyperresponsiveness, because the number of patient with allergic asthma and atopy, and with chronic bronchial inflammation and pneumonia have increased steadily in the cities of Korea. The appearance of AS collected was all round and flat, and the diameter was mostly below about 5 ${\mu}m$. When mice were treated with AS suspension by intratracheal instillation combined with ovalalbumin(OVA) sensitization chronically, the level of serum L-lactate dehydrogenase (LDH), IgE and histamine, and respiratory resistance was increased. Intratracheal instillation of AS and OVA also enhanced infiltration of eosinophils in the bronchoalveolar lavage fluid (BALF), IgE and eotaxin expression, and T helper type 2 cell derived cytokines of interleukin (IL)-4, IL-13 and IL-5 as major contributors to allergy and asthma. These results indicate that AS elevates allergen-related airway inflammation and airway hyperresponsiveness in mice and may play an important role in the aggravation of respiratory diseases in Korea.

• Tuberculosis and Respiratory Diseases
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• v.44 no.5
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• pp.1030-1039
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• 1997

Background : Impulse Oscillometry is a noninvasive and effort-independent test used to characterize the mechanical impedance of the respiratory system. The clinical potential of the IOS is rapid and demands only passive cooperation which makes it especially appealing for children, for epidemiologic surveys and for conditions in which quiet breathig instead of forced expiratory maneuvers are preferred. However, several studies have shown conflicting results that the role of IOS about detection of smoking induced small airway diseases or early airway obstruction Methods : Study was to evaluate the clinical ability of the IOS to detect about smoking induced early airway obstruction in persons with normal spirometry test. Respiratory asymptomatic study groups were formed that one is non-smoking group, another is smoking group. Results : The parameters of spirometry were not significantly differences between non-smoking group and smoking group. Among the parameters of IOS, total resistance(non-smoking group : smoking group=$2.22{\pm}1.20$ : $2.58{\pm}1.71$), peripheral resistance($1.25{\pm}0.62$ : $1.47{\pm}0.10$), bronchial compliance($0.44{\pm}0.12$ : $0.47{\pm}0.16$) were not statistically significant different (p<0.05), but central resistance and lung compliance were not statistically significant different (unit ; resistance=hPa/l/s, compliance=l/hPa). Resistance(Rrs) was not statistically significant different with changes of frequences(5, 10, 15, 20, 25, 30, 35Hz), but Reactance(Xrs) was statistically significant different with low frequences that X5(non-smoking group : smoking group=$-0.62{\pm}0.28$ : $-0.76{\pm}0.48$, p<0.001) and X10($-0.06{\pm}0.19$ : $-0.15{\pm}0.33$, p<0.013) (unit; hPall/s, $hPa{\cong}cmH_2O$). Conclusion : Impulse oocillometer(IOS) is clinically available method to detect about smoking induced early airway obstruction. And clinically potential parameters of IOS were considers that total resistance, peripheral resistance, bronchial resistance, and reactance of low frequency at 5Hz, 10Hz.

• Sleep Medicine and Psychophysiology
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• v.11 no.1
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• pp.17-21
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• 2004

Nasal congestion is one of the most common symptoms of medical complaints. Snoring is caused by vibration of the uvula and the soft palate. Nasal obstruction may contribute not only to snoring and obstructive sleep apnea (OSA) but also impair application of continuous nasal positive airway pressure (CPAP), which is the most widely employed treatment for OSA. Total or near-total nasal obstruction leads to mouth breathing and has been shown to cause increased airway resistance. However, the exact role of the nasal airway in the pathogenesis of OSA is not clear and there is no consensus about the role of nasal obstruction in snoring and sleep apnea. Some reports have failed to demonstrate any correlation between snoring and nasal obstruction. On the other hand, opposing reports suggest that nasal disease may cause sleep disorders and that snoring can be improved after nasoseptal surgery. Reduced cross-sectional area causes increased nasal resistance and predisposes the patient to inspiratory collapse of the oropharynx, hypopharynx, or both. Discrete abnormalities of the nasal airway, such as septal deformities, nasal polyps, and choanal atresia and with certain mucosal conditions such as sinusitis, allergic rhinitis and inferior turbinate hypertrophy can cause snoring or OSA. Thus, these sources of nasal obstruction should be corrected medically or surgically for the effective management of OSA and adjunctive for CPAP.

• Sleep Medicine and Psychophysiology
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• v.18 no.2
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• pp.63-66
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• 2011

It has been controversial whether upper airway resistance syndrome (UARS) is a distinct syndrome or not since it was reported in 1993. The International Classification of Sleep Disorders classified UARS under obstructive sleep apnea syndrome (OSAS) in 2005. UARS can be diagnosed when the apnea-hypopnea index (AHI) is fewer than 5 events per hour, the simultaneously calculated respiratory disturbance index (RDI) is more than 5 events per hour due to abnormal non-apneic non-hypopneic respiratory events accompanying respiratory effort related arousals (RERAs), and oxygen saturation is greater than 92% at termination of an abnormal breathing event. Although esophageal pressure measurement remains the gold standard for detecting subtle breathing abnormality other than hypopnea and apnea, nasal pressure transducer has been most commonly used. RERAs include phase A2 of cyclical alternating patterns (CAPs) associated with EEG changes. Symptoms of OSAS can overlap with UARS, but chronic insomnia tends to be more common in UARS than in OSAS and clinical symptoms similar with functional somatic syndrome are also more common in UARS. In this journal, diagnostic and clinical differences between UARS and OSAS are reviewed.

• IMMUNE NETWORK
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• v.7 no.1
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• pp.18-25
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• 2007

Background: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. Methods: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. Results: Pretreatment with DEX resulted in an inhibition of NF-${\kappa}B$ activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF-${\kappa}B$-dependent cytokines such as TNF-${\alpha}$ and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. Conclusion: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.

• The Korean Journal of Emergency Medical Services
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• v.16 no.2
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• pp.67-74
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• 2012

Purpose : The purpose of this study is to get basal user guidelines of safer bag-valve-mask application on patient with normal pulmonary patho-physiologic condition. Methods : This study was accomplished by pre-qualified 25 EMS junior grade students. Participants were instructed randomly compress bag to one-third, half and total and also with differesnt compression speed. Resultant tidal volumes and mean airway pressures obtained in RespiTrainer were analysed in relation to the each compression depth and rate. Results : Demographic difference does not affect tidal volume with any compression depth and rate change. Increasing compression depth is correlated with tidal volume increasement at any compression rate and also with mean airway pressure. If the compression depth is same, compression rate change did not affect significantly the resultant tidal volume or mean airway pressure. Conclusion : Hand size, Experience, BMI dose not affect tidal volume. Compress the 1600 ml bag half to total amount is safe way to offer sufficient tidal volume without risky high airway pressure delivery to patient airway who with normal lung patho-physiologic condition.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1022-1030
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• 1998

Background : In volume-controlled ventilation, the use of inspiratory pause increases the inspiratory time and thus increases mean airway pressure and improves ventilation. But under the same I : E ratio, the effects of inspiratory pause on mean airway pressure and gas exchange are not certain. Moreover, the effects may be different according to the resistance of respiratory system. So we studied the effects of inspiratory pause on airway pressure and gas exchange under the same I : E ratio in volume-controlled ventilation. Methods: Airway pressure and arterial blood gases were evaluated in 12 patients under volume-controlled mechanical ventilation with and without inspiratory pause time 5%. The I : E ratio of 1 : 3, $FiO_2$, tidal volume, respiratory rate, and PEEP were kept constant. Results: $PaCO_2$ with inspiratory pause was lower than without inspiratory pause ($38.6{\pm}7.4$ mmHg vs. $41.0{\pm}7.7$ mmHg. p<0.01). P(A-a)$O_2$ was not different between ventilation with and without inspiratory pause $185.3{\pm}86.5$ mmHg vs. $184.9{\pm}84.9$ mmHg, p=0.766). Mean airway pressure with inspiratory pause was higher than without inspiratory pause ($9.7{\pm}4.0\;cmH_2O$ vs. $8.8{\pm}4.0\;cmH_2O$, p<0.01). The resistance of respiratory system inversely correlated with the pressure difference between plateau pressure with pause and peak inspiratory pressure without pause (r=-0.777, p<0.l), but positively correlated with the pressure difference between peak inspiratory pressure with pause and peak inspiratory pressure without pause (r=0.811, p<0.01). Thus the amount of increase in mean airway pressure with pause positively correlated with the resistance of respiratory system (r=0.681, p<0.05). However, the change of mean airway pressure did not correlated with the change of $PaCO_2$. Conclusion: In volume-controlled ventilation under the same I : E ratio of 1 : 3, inspiratory pause time of 5% increases mean airway pressure and improves ventilation. Although the higher resistance of respiratory system, the more increased mean airway pressure, the increase in mean airway pressure did not correlated with the change in $PaCO_2$.

• Sleep Medicine and Psychophysiology
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• v.7 no.1
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• pp.27-33
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• 2000

Objectives: The sensitivity and accuracy of thermistor airflow signal has been debated. The purposes of this study were to compare apnea-hypopnea index(AHI) detected from a conventional thermistor signal and a nasal pressure transducer of airflow(NPT), to evaluate the value of NPT for the diagnosis of upper airway resistance syndrome(UARS), and to measure airway pressure fluctuations which produced respiratory arousals in UARS by naso-oro-esophageal manometer catheter. The subjects were 30 patients with obstructive sleep apnea syndrome [mild(540), 10), and 6 UARS patients. Airway resistance arousal in this study was defined as arousals which were not associated with apnea or hypopnea of thermistor signal, but showed significant decrease of nasal airflow pressure just before arousal and a prompt recovery of nasal airflow pressure after arousal. The airway pressure fluctuations were measured during 260 airway resistance arousals observed in 10 patients with OSAS, 2 with UARS. Results: Mean AHIs of patients with OSAS were 33.4 by thermistor and 48.4 by NPT. The AHIs of mild, moderate and severe OSAS groups were 10.2, 32.1, 65.4 respectively by thermistor and 23.1, 45.9, 76.4 by NPT. The mean AHI of patients with UARS was 3.2 by thermistor and 10.8 by NPT. The mean AHI of patients with nonspecific arousals was 2.7 by thermistor and 4.4 by NPT. The mean airway pressure changes during respiratory arousals of different groups were $8.7\;cmH_2O$ in mild OSAS, $11.4\;cmH_2O$ in moderate OSAS, $24.7\;cmH_2O$ in severe OSAS and $6.6\;cmH_2O$ in UARS. Conclusion: The nasal pressure transducer of airflow was more sensitive and accurate for assessing respiratory disturbances of patients with OSAS and was extremely helpful for the diagnosis of UARS without esophageal pressure monitoring. From the results, we would like to propose carefully the NPT diagnostic criteria for sleep disordered breathing as follows: NPT-AHI 5-15 $\rightarrow$ UARS, 15-35 $\rightarrow$ mild OSAS, 35-55 $\rightarrow$ moderate OSAS and >55 $\rightarrow$ severe OSAS.