• Tuberculosis and Respiratory Diseases
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• v.60 no.4
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• pp.426-436
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• 2006

Background : Particulate matters (PM) when inhaled is known to induce pulmonary diseases including asthma and chronic bronchitis when inhaled. Despite the epidemiological proofevidence, the pathogenesis of PM-related pulmonary diseases is unclearremain poorly understood. Methods : Primary alveolar macrophages were harvested from the SPF and inflammatory rats by bronchioalveolar lavage (BAL). The cultured primary alveolar macrophages were treated with the medium only, PM only ($5{\sim}40{\mu}g/cm^2$), LPS (5ng/ml) only, and PM with LPS for 24 and 48 hours. The level of secreted nitric oxide (NO) was assayed from the cultured medium by using the Griess reaction. The cultured cells were utilized for the western blotting against the inducible nitric oxide synthase (iNOS) proteins. Immunocyto- chemical staining against the iNOS and NT-proteins were performed in cells that cultured in the $Lab-Tek^{(R)}$ chamber slide after treatments. Results : The PM that utilizein this experiments induced NO formation with iNOS expression in the cultured SPF and inflammatory rats alveolar macrophages, by itself. When the cells were co-treated with PM and LPS, there was a statistically significant synergistic effect on NO formation and iNOS expression over the LPS effect. The cells from the sham control showed minimal immunoreactivity for the NT-proteins. Significantly higher quantities of NT-proteins were detected in the PM and PM with LPS co-treated cells than from the sham control. Conclusion : Increased iNOS expression and NO formation with increased NT-proteins formation might be involved in the pathogenesis of PM-induced lung injury.

• Journal of Veterinary Clinics
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• v.22 no.4
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• pp.431-434
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• 2005

A 2-year-old castrated male, Cocker spaniel dog with a history of chronic productive cough for 2 to 3 months and with unsuccessful treatment was referred to Veterinary Medical Teaching Hospital, Seoul National University. On thoracic radiographs, there were alveolar infiltrations at left cranial and right caudal lung fields, and soft-tissue opacity round to oval images at overall lung field. The bronchi were dilated, tortuous and not tapered. Abnormal air was accumulated focally in the caudodorsal lung fields. To scrutinize the soft-tissue opacity image and accumulated air, computed tomography (CT) was done. On CT images, severe cylindrical or tubular bronchiectasis was confirmed. And the soft-tissue opacity images were found in the dilated bilated and thought to complexes of mucous plugs, inflammatory cells, necrotic and fibrotic tissue. The dog was dead next day to the CT scan, so necropsy and histopathologic examination were perfermed. On the histopathology, there were cylindrical bronhiectasis and severe diffuse chronic fibrinous necropurulent bronchitis and bronchopneumonia. In this case, it was difficult to diagnose the bronchiectasis only with radiography due to the concurrent lesions, such as pulmonary infiltrations and mucous plugs, which was identified by computed tomography. Thus, computed tomography is considered as a useful modality to confirm tile bronchiectasis camouflaged by the concurrent lesion.

• Journal of Chest Surgery
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• v.14 no.4
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• pp.350-353
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• 1981

The pulmonary sequestration is an uncommon congenital anomaly characterized by the presence of a part of lung tissue which is supplied by an aberrant artery from the aorta or its branch and usually has no communication with the normal bronchial tree. It was first presented by Hubber in 1777 and presented in details by Pryce in 1946. We present a case of extralobar pulmonary sequestration experienced recently with a case of intralobar type experienced in 1962. The patient was 11 year old male with the complaint of chronic productive cough. Serial chest films showed a large cyst with or without the air-fluid level on the posterobasal segment area of the left lower lobe. Bronchography showed no definite communication between the cyst and bronchial tree. On operation, the cystic lesion was supplied by an aberrant artery from the descending thoracic aorta 5 cm above the aortic hiatus and was sited at the posterobasal segment area of the left lower lobe. We performed the sequestrectomy and the sequestration was surrounded by its own pleura, 6.8x3.9x3.2 cm in size, contained the pale brown mucoid secretion in a large cyst and showed the primitive alveolar structure of the wall. The aberrant artery was 1 -5 cm long, 0.3 mm in internal diameter and arterio-sclerotic. We also compared 6 cases of collection, 5 intralobar and 1 extralobar type, presented in Korea.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.397-405
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• 2005

Background : Laminin-1 is known to have regular functions in the development and course of differentiation of the lungs. The morphogenesis and distribution of laminin-1 still remains as a mystery and its distribution and changes in the molecular structure of laminin-1 in the pathogenesis of the lung still is a subject of great controversy. In this study, experiments were done to delineate the distribution and changes in the amount of laminin-1 after inducing inflammation of the lungs by exposing experimental animals to CS gas and especially, to find compositions of laminin-1 within type II pneumocytes. Materials and Methods : The experimental subjects of study were newborn rats and the extracted tissue from the experimental rats were viewed under light microscope and electron microscope after the sections were treated with immunohistochemical methods and immunogold reaction methods using bounded gold particles. Results : 1) Lymphocytes and mononuclear phagocytes invaded the alveolar septa in the 2 day group rats after CS gas exposure and intense interstitial inflammation was seen in the 3 day group. 2) Laminin immunoreactions decreased to a moderate degree in the 2 and 3 day group rats after CS gas exposure and strong laminin immunoreactions were seen again in the 5 and 7 day group rats. 3) Gold particles in basal lamina of the lung blood-air barrier decreased and in the type I pneumocytes decreased in the 2 and 3 day group rats after CS gas exposure. 4) Gold particles were seen only on the surface of the cell membranes of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure. 5) Few gold particles around the lamellar bodies and cytoplasm of type II pneumocytes in the control rat group and at 12 hours after CS gas exposure. Gold particles are seen only on the surface of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure and are evenly distributed in small amounts in the cells of the 3 day group after CS gas exposure. Conclusion : CS gas exposure in the rats caused inflammation of lung alveolar septa and also induced a decrease in laminin-1 in basal lamina and loss of laminin-1 in the cytoplasm of type II pneumonocytes. As the inflammatory cells disappeared, an increase in the distribution of laminin-1 occurred. This reflects tissue regeneration functions of laminin-1 in the pneumocytes of rats and the distribution of laminin-1 in type II pneumocytes can be seen through the electron microscope using immunogold methods.

• Tuberculosis and Respiratory Diseases
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• v.50 no.4
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• pp.426-436
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• 2001

Background : Chronic obstructive pulmonary disease(COPD) is one of the major contributors to morbidity and mortality among the adult population. Cigarette smoking(CS) is undoubtedly the single most important factor in the pathogenesis of COPD. However, its mechanism is unclear. The current hypothesis regarding the pathogenesis of COPD postulates that an imbalance between proteases and antiproteases leads to the destructive changes in the lung parenchyma. This study had two aims. First, to evaluate the effect of CS exposure on histologic changes of the lung parenchyme, and second, to evaluate the effect of CS exposure on the expression of the gelatinolytic enzymes in BAL fluid cells in guinea pigs. Methods : Two groups of five guinea pigs were exposed to the whole smoke of 20 commercial cigarettes per day, 5 hours/day, 5 days/week, for 6weeks, and 12 weeks, respectively, using a smoking apparatus. Five age-matched guinea pigs exposed to room air were used as controls. Five or more sections were microscopically extamined(${\times}400$) and the number of cellular infiltration of the alveolar wall was measured in order to evaluate the effect of CS exposure on the histologic changes of lung parenchyme. The statistical significance was analyzed by a linear regression method. To evaluate the expression of the gelatinolytic enzymes in intraalveolar cells, BAL fluid was obtained and the intraalveolar cells were separated by centrifugation (500 g for 10 min at $4^{\circ}C$). Two sets of culture plates were loaded with $1{\times}10^6$ intraalveolar cells. One plate, contained O.1mM EDTA, a inhibitor of matrix metalloproteases(MMPs), and the other plate had no EDTA. Both plates were incubated for 48 hours at $37^{\circ}C$. After incubation, gelatinolytic protease expression in the supernatants was analyzed by gelatin zymography. Results : At the end of CS exposure, the level of blood carboxy Hb had increased significantly(4.1g/dl in control group, 24g/dl immediately after CS exposure, 18g/dl 30 min after CS exposure, 15g/dl 1 hour after CS exposure). Alveolar inflammatory cells were identified in the CS exposed guinea pigs. The number of alveolar cellular cells observed in a microscopic field ($400{\times}$) was $121.4{\pm}7.2$, $158.0{\pm}20.2$, $196.8{\pm}32.8$, in the control, the 6 weeks, and the 12 weeks group, respectively. The increased extent of inflammatory cellular infiltration of the lung parenchema showed a statistically significant linear relationship with the duration of CS exposure(p=0.001, $r^2=0.675$). Several types of gelatinolytic enzymes in the intraalveolar cells of CS exposed guinea pigs were expressed, of which some were inhibited by EDT A. However, the gelatinolytic enzymes were not expressed in the control groups. Conclusion : CS exposure increases inflammatory cellular infiltration of the alveolar wall and the expression of gelatinolytic proteases in guinea pigs. EDTA inhibits some of the gelatinolytic proteases. These findings suggest a possibility that CS exposure may increase MMP expression in the lungs of guinea pigs.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.26 no.4
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• pp.399-406
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• 2000

With the increase of industrialization, leisures, sports activities and traffic, the risk of trauma has increased markedly. Midfacial bones are relatively common sites of trauma, and are difficult sites of correct reduction and reconstruction, because midface is composed of mostly thin cortical bone surrounding cavities filled with either air or fat with discrete areas of bony condensation. A clinical study on 208 patients with midfacial bone fracture who visited Sanggye Paik Hospital during 5 years($1990{\sim}1995$) was done by analyzing sex, age, cause, fracture site, treatment method, complication and involvement of other body part, etc. The results obtained were as follows : 1. The occurrence was more frequent in male than in female with ratio of 2.7 : 1 and most frequently in twenties. 2. Traffic accident was the most common cause of midface fractures. 3. Zygoma was the most frequently occurred site(50%) of midface fractures. 4. Simple fracture(75%) was more frequently occurred than compound fracture(25%). 5. As treatment method, open reduction(76.4%) was used more frequently than closed reduction(23.6%) 6. Generally, operations are done in 5 days after admission(59.1%), and intermaxillary fixation was done in 78.4% of cases. 7. Teeth and alveolar bone damages were occurred in 32.2% of cases. 8. Other injuries that were related to midface fracture occurred in 63.3% of cases. 9. Post-operative complications occurred in 9% of cases.

• Journal of The Korean Society of Clinical Toxicology
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• v.3 no.1
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• pp.40-44
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• 2005

Nitrogen dioxide ($NO_2$), which produced during the process of silage, metal etching, explosives, rocket fuels, welding, and by-product of burning of fossil fuels, is one of major components of air pollutant. Accidental exposure of high level of $NO_2$ produces cough, dyspnea, pulmonary edema which may be delayed $4\~12$ hours and, in $2\~6$weeks, bronchiolitis obliterans. We experienced a case of acute pulmonary injuny induced by industrial exposure to high level of $NO_2$ during repair of $NO_2$ pipeline in a refinery. A 55-year-old man experienced nausea and severe dyspnea in 6 hours after $NO_2$ inhalation. Initial blood gas examination revealed severe hypoxemia accompanying increased alveolar-arterial O2 difference. Radiological examination showed diffuse ground glass opacities in both lung fields. Clinical symptoms and laboratory findings, including radiological study and pulmonary function test were improved with conservative treatment using inhaled oxygen and bronchodilator. and there was no evidence of bronchial fibrosis and bronchiolitis obliterance in chest high resolution computed tomography performed 6 weeks after exposure. Here, we report a case of $NO_2$ induced acute pulmonary injuny with a brief review of the relevant literature.

• Journal of Korean Society for Atmospheric Environment
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• v.27 no.6
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• pp.663-671
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• 2011

Although a scooter is a convenient transportation means for a short distance traveling with a light package in the congested urban center, it might be one of the significant sources of air pollutants to which many people can easily be exposed during its passing-by. In this paper, we measured concentrations of gases and particles emitted from a scooter at roadside with no other traffic. To understand the characteristics of scooter emissions with respect to driving speed (idling, 30 km/h) at the roadside, total particle number concentration, particle size distribution, average surface area of particles deposited in the alveolar region, and concentrations of black carbon, CO, and $NO_x$ were measured. The concentrations of the particle number, surface area of deposited particles, CO, and $NO_x$ were highly fluctuated in the scooter's idling condition. The trends of particle number concentration, CO, and $NO_x$ generation were similar to one another. When the scooter started to move, all of $NO_x$, CO and particle number concentrations increased and after it passed by at the speed of 30 km/h, the concentration peaks of the particles and gases appeared at the same time. Unimodal size distribution with ~70 and ~93 nm mode diameters was observed for the idling and cruising condition, respectively. From this work, we found that emission from a passing vehicle could be characterized using a roadside monitoring technique.

• Tuberculosis and Respiratory Diseases
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• v.46 no.3
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• pp.420-425
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• 1999

We report a case of hepatopulmonary syndrome defined as a triad of chronic liver disease, increased alveolar oxygen gradient on room air, and intrapulmonary arteriovenous shunting. Chest rediographs showed bilateral, basilar, medium sized reticulonodular opacities. High resolution CT scand showed multiple centrilobular nodules and branching structures in the subpleural lung that suggested dilatation of lung vessels with abnormally large number of visible terminal branches. $^{99m}Tc$-macroaggregated albumin(MAA) perfusion lung scan showed right to left shunt. Contrast echocardiography demonstrated intrapulmonary vascular shunt without intracardiac shunt.