• Tuberculosis and Respiratory Diseases
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• v.71 no.4
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• pp.278-281
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• 2011

Allergic bronchopulmonary aspergillosis (ABPA) is a complex clinical entity resulting from an allergic immune response to Aspergillus species, and most often occurs in patients with asthma. ABPA is rarely observed in the absence of asthma, which is, in fact, the principal criterion for its diagnosis. Our patient was a 53-year-old woman with no history of bronchial asthma. She presented with a 1-month history of cough, mucopurulent nasal discharge, and localized pulmonary consolidation. Peripheral blood eosinophilia and elevated serum IgE were observed. Sinus radiography showed right maxillary sinusitis. Pathologic examination of bronchoscopic biopsy specimens revealed conglomerates of fungal hyphae. Pulmonary function and bronchial provocation tests were within normal ranges. The patient was successfully treated for 3 months with itraconazole and oral prednisolone. There has been no evidence of recurrence over a 7-month follow-up. ABPA coupled with sinusitis in a nonasthmatic patient is a very rare occurrence and warrants reporting.

• The Journal of Pediatrics of Korean Medicine
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• v.18 no.2
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• pp.31-48
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• 2004

Objective : KagamJwagwiEum(KJE) has been used for the purpose of prevention and treatment of bronchial asthma and allergic asthma in Korea. To investigate the biological effect of KJE, the author examined cytotoxicity and inflammatory cytokines secretion with human leukemic mast cell line, HMC-1. Methods: HMC-1 was stimulated with phorbol 12-myristate 13-acetate(PMA) and calcium ionophore A23187. KJE by itself had no effect on viability of HMC-l. The effects of KJE on the secretion of tumor necrosis $factor-alpha(TNF-{\alpha})$, interleukin(IL)-6 and IL-8 from HMC-1 were evaluated with enzyme-linked immunosorbent assay. Results : KJE inhibited PMA plus A23187-induced $TNF-{\alpha}$ and IL-6 secretion. But KJE had no effect IL-8 secretion: KJE had immunoregulatory effects on cytokines, increased secretion of NO and $TNF-{\alpha}$ but did not effect IL-12 secretion when the cells were primed and trigged with $IFN-{\gamma}$ in the peritoneal macrophages of C57BL/6 mice. Conclusions : Taken together, these results suggest that KJE inhibit the production of inflammatory cytokines in HMC-1 cells and activate macrophages.

• Advances in Traditional Medicine
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• v.7 no.5
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• pp.518-526
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• 2008

Recently a major goal in asthma therapy is to reduce or prevent the inflammatory response of airway. Eosinophilic accumulation in the tissue is a prominent feature of allergic diseases including asthma. Production of chemokines by bronchial epithelial cells may contribute to the allergic inflammation by recruiting eosinophils. In this study we evaluated the inhibitory effect of Gamichungsangbohatang (GMCSBHT), used traditionally in treating asthma, on secretion of chemokines for eosinophils in human A549 epithelial cells. Chemokines such as eotaxin, RANTES, IL-8 were inhibited in a dose-dependent manner, but IL-16 showed no inhibition by GMCSBHT. These findings indicate that GMCSBHT might be a therapeutic value in treating asthma by suppression of chemokines secretion associated with local accumulation of eosinophils.

• Journal of Medicine and Life Science
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• v.16 no.2
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• pp.43-45
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• 2019

Intraoperative delivery of salbutamol (${\beta}_2$ agonist) through a breathing circuit may be performed in asthma patient. A 28-year-old woman with a history of asthma was diagnosed with chronic sinusitis and bilateral nasal polyps, and an endoscopic sinus surgery was performed. The patient was recommended salbutamol nebulization every 4 hours during the perioperative period because of the risk of asthma attack. At the end of the operation, when salbutamol was sprayed through the tube before extubation and the connector tip went inside the tube during injection. The patient was immediately referred to the pulmonary medicine department for bronchoscopy, where the foreign body was removed safely without any complications. When general anesthesia is performed on a patient who usually uses an inhaler for asthma, caution is required because the tip that connects the inhaler and the breathing circuit can aspirate into the endotracheal tube and enter the lungs when applying the inhaler before waking up the patient.

• Clinical and Experimental Pediatrics
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• v.46 no.3
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• pp.284-290
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• 2003

Purpose : A new airway inflammatory marker, exhaled nitric oxide(ENO) has been reported to correlate with bronchial hyperresponsiveness(BHR) and atopy. The purpose of this study was to analyze the relationship of ENO with BHR or atopy in patients with asthma and with allergic rhinitis. Methods : The subjects consisted of 55 children with asthma, 17 with allergic rhinitis, and 14 healthy controls. The asthma group was subdivided into the atopic asthma group(n=37) and the nonatopic asthma group(n=18) and the allergic rhinitis group into BHR group(n=7) and non-BHR group(n=10). All were investigated with spirometry and measurements of ENO concentration. The correlations between ENO concentration and both methacholine $PC_{20}$(provocative concentration causing a 20% decrease in forced expiratory volume in one second) and the number of allergen skin test positivity were analyzed. Results : ENO concentrations of both asthma and allergic rhinitis groups were significantly greater than that of control(P<0.01). ENO concentration of atopic asthma was significantly greater than that of nonatopic asthma(P<0.01). In allergic rhinitis, ENO concentration did not differ according to the presence or absence of BHR(P=0.50). ENO concentrations correlated significantly with the number of skin test positivity(r=0.32, P=0.02) or methacholine $PC_{20}$(r=-0.38, P<0.01) in asthma group, but not in the allergic rhinitis group(r=0.42, P=0.09; r=-0.06, P=0.83). Conclusion : In asthma patients, some pathogenetic mechanisms associated with atopy and BHR seem to influence ENO concentration. In allergic rhinitis patients, some factors other than BHR may be important in determining ENO concentration.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.574-578
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• 1994

The incidence of traumatic rupture of the tracheobronchial tree has been increased considerably with advent of widespread mechanization and high speed era. Rupture of the bronchus is an unusual result of nonpenetrating trauma to chest. Early diagnosis and primary repair not only restore normal lung function but also avoid difficulties and complications associated with delayed diagnosis and repair. These complications are pneumonia, atelectasis and lung abscess secondary to the bronchial obtruction. We experienced a case of partial rupture on left main bronchus caused by nonpenetrating blunt chest trauma with rib fractures 1 year ago. He was suffered from progressively developing dyspnea on exercise and treated as bronchial asthma at other hospital. Bronchoscopic finding was the narrowed lumen of left main bronchus at 1cm from carina by web-like membrane. We confirmed by bronchogram and repaired by end to end anastomosis, which is rare delayed finding in bronchial rupture without pulmonary complications. We report a case of nonpenetrating traumatic bronchial rupture, manifested by bronchial web in bronchoscopy.

• Annals of Occupational and Environmental Medicine
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• v.35
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• pp.13.1-13.12
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• 2023

Background: Indoor air pollution can cause and exacerbate asthma. We report a previously undescribed case of occupational asthma related to indoor air pollution in a worker at an indoor air gun shooting range and highlight the potential risk of developing occupational asthma in this environment. Case presentation: A 31-year-old man presented with dyspnea, cough, and sputum and was diagnosed with asthma complicated by pneumonia. Objective evidence of asthma was obtained by performing a methacholine bronchial provocation test. It was suspected that the patient had occupational asthma, which began one month after changing jobs to work within the indoor air gun shooting range. The highest peak expiratory flow (PEF) diurnal variability on working days was 15%, but the highest variation was 24%, with 4 days out of 4 weeks having a variation of over 20% related to workplace exposure. Conversely, the diurnal variability on the rest days was 7%, and no day showed a variation exceeding 20%. The difference in the average PEF between working and rest days was 52 L/min. PEF deterioration during working days and improvement on rest days were noted. Conclusions: The results obtained from the in-depth analysis of the PEF were adequate to diagnose the patient with occupational asthma. Exposure to indoor air pollution and lead and the patient's atopy and allergic rhinitis may have contributed to the development of occupational asthma.

• Journal of Microbiology
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• v.43 no.1
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• pp.11-16
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• 2005

Matrix metalloproteinase (MMP)-9 plays an important role in the pathogenesis of bronchial asthma. Neovastat, having significant antitumor and antimetastatic properties, is classified as a naturally occurring multifunctional antiangiogenic agent. We evaluated the therapeutic effect of Neovastat on airway inflammation in a mouse model of asthma. BALB/c mice were immunized subcutaneously with ovalbumin (OVA) on days 0, 7, 14, and 21 and challenged with inhaled OVA on days 26, 29, and 31. Neovastat was administrated by gavage (5 mg/kg body weight) three times with 12 h intervals, beginning 30 min before OVA inhalation. On day 32, mice were challenged with inhaled methacholine, and enhanced pause (Penh) was measured as an index of airway hyperresponsiveness. The severity of airway inflammation was determined by differential cell count of bronchoalveolar lavage (BAL) fluid. The MMP-9 concentration in BAL fluid samples was measured by ELISA, and MMP-9 activity was measured by zymography. The untreated asthma group showed an increased inflammatory cell count in BAL fluid and Penh value compared with the normal control group. Mice treated with Neovastat had significantly reduced Penh values and inflammatory cell counts in BAL fluid compared with untreated asthmatic mice. Furthermore, mice treated with Neovastat showed significantly reduced MMP-9 concentrations and activity in BAL fluid. These results demonstrate that Neovastat might have new therapeutic potential for airway asthmatic inflammation.

• The Korean Journal of Physiology and Pharmacology
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• v.23 no.4
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• pp.251-261
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• 2019

Allergic asthma, is a common chronic inflammatory disease of the airway presenting with airway hyperresponsiveness and airway remodelling. T helper cells-derived cytokines are critically associated with asthma pathogenesis. Janus kinase-signal transduction and activation of transcription (JAK/STAT) signaling is found to be involved in asthma. Magnolol is a plant-derived bioactive compound with several pharmacological effects. The study aimed to assess the effects of magnolol in ovalbumin (OVA)-induced asthmatic model. BALB/c mice were sensitized and challenged with OVA. Magnolol (12.5, 25, or 50 mg/kg body weight) was administered to separate groups of animals. Dexamethasone was used as the positive control. Cellular infiltration into the bronchoalveolar lavage fluid (BALF) were reduced on magnolol treatment. The levels of Th2 and Th17 cytokines were reduced with noticeably raised levels of interferon gamma. Lung function was improved effectively along with restoration of bronchial tissue architecture. OVA-specific immunoglobulin E levels in serum and BALF were decreased by magnolol. Magnolol reduced Th17 cell population and effectively modulated the JAK-STAT and Notch 1 signaling. The results suggest the promising use of magnolol in therapy for allergic asthma.

• Clinical and Experimental Pediatrics
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• v.46 no.5
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• pp.495-499
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• 2003

Purpose : Eosinophil is one of the important inflammatory cell involved in the airway inflammation in childhood asthma. It has been demonstrated that markers of eosinophil activation, including eosinophil cationic protein or eosinophil protein X(EPX), are increased in childhood asthma. Furthermore, they are related to disease activity and are assumed to be helpful in monitoring the treatment effect as urinary EPX(U-EPX) can be obtained easily and in a noninvasive way in children of all ages. Methods : Twenty-five children(22 male and three female) aged $11.87{\pm}3.82$ years with stable asthma were challenged with methacholine and urine was collected from each child during the following periods; before methacholine challenge test(MCT); 0-3 hr after the end of MCT; 4-7 hr after the end of MCT; and 8-24 hr after the end of MCT. Bronchial reactivity was determined by using Dosimeter( Jeager, Germany) with serially diluted methacholine from 0.05 to 25.0 mg. The $FEV_1$ less than 80% of baseline value were classified into positive MCT. U-EPX was measured with a sensitive and specific radioimmunoassay(Pharmacia & Upjohn AB, Uppsala, Sweden). Results were expressed as ${\mu}gEPX/mmol$ creatinine. Results : An early airway response after MCT was associated with an increase of U-EPX excretion for 0-3 hr after methacholine inhalation in comparison with beseline values. Most subjects showed a small increase in U-EPX excretion during late asthmatic response for 4-7 hr, which then decreased to normal level in 8-24 hr. Also, a tendency for a higher increase of U-EPX was associated with a lower threshold of methacholine challenge and a longer duration of asthma. Conclusion : Measurement of EPX in urine is a noninvasive and easy method to assess the severity of airway inflammation in asthmatic children. It may be a helpful index of the events underlying the airway inflammatory responses during nonspecific bronchial challenge, and in monitoring asthma management.