• Tuberculosis and Respiratory Diseases
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• v.61 no.3
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• pp.294-298
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• 2006

Lymphocytic interstitial pneumonia(LIP) is an uncommon condition in which the alveolar septa and extra-alveolar interstitial space are markedly expanded by small lymphocytes, plasma cells and histiocytes. Chest radiographs generally show nonspecific patterns with the most common pattern showing bibasilar reticular or reticulonodular infiltrates. Hilar or mediastinal lymphadenopathy and pleural effusions are usually absent. We encountered a 42-year-old female patient who was admitted to hospital because of exertional dyspnea and palpitation. The chest X-ray showed an enlarged bilateral hilar shadow and diffusely increased bronchovascular markings in both lung fields. The chest CT showed diffuse nodular infiltrations with mild septal thickening and combined patchy ground glass opacity in both lungs, and conglomerated mediastinal and bilateral hilar lymphadenopathy. A diagnosis of LIP was made from the tissue pathology taken by a thoracoscopic lung biopsy. The patient showed clinical and radiographic improvement after 3 months of treatment with prednisolone. We report a case of LIP presenting as diffuse nodular interstitial infiltrations with multiple mediastinal and bilateral hilar lymphadenopathy.

• Clinical and Experimental Pediatrics
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• v.52 no.2
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• pp.256-260
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• 2009

Idiopathic pulmonary hemosiderosis (IPH) is a rare disease affecting mostly children. This disorder is characterized by recurrent episodes of hemoptysis, bilateral diffuse pulmonary infiltrates, and iron-deficiency anemia. An acute fulminant alveolar hemorrhage can be fatal due to respiratory failure, while chronic hemorrhage leads to hemosiderin-laden macrophages and pulmonary fibrosis. Genetic, autoimmune, allergic, environmental, and metabolic mechanisms of pathogenesis have been suggested, but the etiology of IPH remains unknown. We report on a 9-year-old girl with idiopathic pulmonary hemosiderosis who showed seasonal recurrences without cause.

• Applied Microscopy
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• v.33 no.4
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• pp.275-282
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• 2003

This study was undertaken to investigate paraquat-induced pulmonary injuries and effects of colchicine on pulmonary fibrosis by paraquat. Fifteen Sprague-Dawley rats were intraperitoneally injected 10 mg/kg of paraquat and repeatedly with 2 days interval. Another 15 rats were injected paraquat as same manner and simultaneously injected 10 mg/kg of colchicine in a week. Five rats in each group were sacrificed 1, 2, and 4 weeks after initial injections, and lungs extracted were observed by light and electron microscopes. On light microscopy, there was mild infiltration of neutrophils, macrophages, and lymphocytes in alveolar spaces and walls at 1 week after paraquat injection. The cellularity of alveolar wall was increased with time. However, the cellularity was not so prominent in paraquat and colchicine simultaneously injected group. On electron microscopy, there was marked swelling or excoriation of type I epithelial cells and alveolar capillary endothelium with infiltration of neutrophils, macrophages and monocytes, and lymphocytes in alveolar walls. Such findings were persisted with time. In addition, fibroblastic proliferation and deposition of collagen fibers were prominent at 4 weeks after paraquat injection. Fibrosis also occurred at 4 weeks after paraquat and colchicine simultaneous injection. It was not proninent than that of paraquat injected group. According to the above result, it would be concluded that the type I pneumocytes and alveolar capillary endothelial cells are most vulnerable on paraquat poisoning, and that the colchicine is effective on inhibition of paraquat-induced pulmonary fibrosis.

• Tuberculosis and Respiratory Diseases
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• v.51 no.6
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• pp.503-516
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• 2001

Background : The present study was carried out in association with neutrophilic respiratory burst in the lung in order to clarify the pathogenesis of acute respiratory distress syndrome(ARDS) following acute severe hemorrhage. Because oxidative stress has been suggested as one of the principal factors causing tissue injury, the role of free radicals from neutrophils was assessed in acute hemorrhage-induced lung injury. Method : In Sprague-Dawley rats, hemorrhagic shock was induced by withdrawing blood(20 ml/kg of B.W) for 5 min and the hypotensive state was sustained for 60 min. To determine the mechanism and role of oxidative stress associated with phospholipase A2(PLA2) by neutrophils, the level of lung leakage, pulmonary myeloperoxidase(MPO), and the pulmonary PLA2 were measured. In addition, the production of free radicals was assessed in isolated neutrophils by cytochemical electron microscopy in the lung. Results : In hypotensive shock-induced acute lung injury, the pulmonary MPO, the level of lung leakage and the production of free radicals were higher. The inhibition of PLA2 with mepacrine decreased the pulmonary MPO, level of lung leakage and the production of free radicals from neutrophils. Conclusion : A. neutrophilic respiratory burst is responsible for the oxidative stress causing acute lung injury followed by acute, severe hemorrhage. PLA2 activation is the principal cause of this oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.48 no.1
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• pp.33-44
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• 2000

Background: To evaluate airway responses and inflammation to antigen in Sprague-Dawley rat asthma model, we examined airway responses, serial histologic changes of the lung, and the relationship between airway responses and airway inflammation after antigen airway challenge. Methods: Sprague-Dawley rats were sensitized with subcutaneous injection of 10 ${\mu}g$ ovalbumin(OA). Antigen airway challenges were done 14~16 days after sensitization and the sensitized rats were sacrificed 1h($A_E$), 6~8h($A_L$) and 1day($A_D$) after airway challenge, to examine the histologic changes of the lung. Airway responses were measured by body plethysmograph and recorded by enhanced pause(Penh) as an index of airway obstruction 6~8h after antigen challenges. Nonsensitized controls(10 rats) were also challenged with antigen and sacrificed 1 day later. Histopathologic examination of two trachea, large bronchi, small bronchi, and vessels was performed to evaluate the severity of inflammation and eosinophilic infiltration with H&E stain. Results: In 17 of 20 rats(85%) in both groups, we observed airway responses. Among them, an early response(ER) in 15 rats(75%), an dual response in 5(25%), and an late response(LR) only in 2 rats(10%) displayed. There were no significant differences in the severity of inflammation among the trachea, large bronchi, small bronchi and vessels in all groups after antigen challenge(p>0.05) and between early and late responders. The significant eosinophil infiltration was observed in 5 rats(50%) of AL(p<0.05) compared with in AE and controls. Also, eosinophil infiltration was observed in higher trend in LR(57.1%) compared to ER(40%)(p>0.05). Conclusion: Sprague-Dawley rats sensitized with subcutaneous injection of OA showed a significant airway responses to antigen challenge. But antigen challenges caused a little eosinophil infiltration and no significant airway inflammation. Asthma model of Sprague-Dawley rats could be useful for antigen-induced airway responses, but this model has a limitation for the study of human asthma because of no significant pathologic change.

• Tuberculosis and Respiratory Diseases
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• v.47 no.1
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• pp.77-89
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• 1999

Background: High-dose chemotherapy is increasingly employed in many refractory malignant diseases. This therapy has been reported to increase response rate and survival benefits but it is also associated with higher treatment-related morbidity and mortality. We evaluated clinical characteristics and course of the pulmonary toxicity following high-dose chemotherapy with peripheral blood stem cell transplantation. Methods: Ninety-seven patients who had received high-dose chemotherapy with peripheral blood stem cell transplantation were evaluated. Five patients who developed lung lesions which were not related to infection nor primary malignant disease underwent transbronchial lung biopsy. The patients' clinical characteristics, treatments, and prognosis were reviewed retrospectively. Results: Five patients(5.1%) developed idiopathic pneumonia syndrome. The high dose chemotherapy regimens employed were cyclophosphamide, BCNU, and cisplatin in 3 cases, one case of BCNU, etoposide, Ara-C, and cyclophosphamide combination, and a regimen consisting of BCNU, etoposide, Ara-C, and melphalan. The total dose of BCNU used was 300-400 mg/$m^2$ and that of cyclophosphsmide was 6,000 mg/$m^2$. All of 5 patients received radiation therapy before this treatment. After an average duration of 14 weeks (4-26 weeks) of high-dose chemotherapy, patients developed cough, dyspnea and fever. The chest X-rays showed bilateral diffuse infiltration in 3 cases and the focal infiltration in the other 2 cases. All the patients received corticosteroid therapy as a treatment for the lung lesions. Two of them progressed to acute respiratory distress syndrome and died. Three patients recovered without residual lung lesion but one of them died of dilated cardiomyopathy. Conclusion: High-dose chemotherapy with peripheral blood stem cell transplantation especially which containing BCNU regimen may develop idiopathic pneumonia syndrome related to pulmonary toxicity and corticosteroid therapy may be bel1eficial in some cases.

• Radiation Oncology Journal
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• v.15 no.1
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• pp.37-47
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• 1997

Purpose : To investigate ultrastructural changes of the mouse lung induced by whole lung gamma irradiation and to evaluate the effect of prophylactic administration of steroid against acute lung injury. Materials and Methods :. One hundred and twenty ICR mice were used and whole lung was irradiated with telecobalt machine. Whole lung doses were 8 and 12Gy, and 10mg of methyl prednisolone was administrated intraperitoneally for two and four weeks. At the end of the observation period, mice were sacrificed by cervical dislocation. The lungs were removed and fixed inflated. Histopathological examination of acute radiation injuries were Performed by light microscopic and transmission electron microscopic examination. Results : Control group with BGy is characterized by damage to the type I Pneumocyte and the endothelial cell of the capillary. edema of alveolar wall and interstitium. and fibroblast proliferation. Control group with 120y is characterized by more severe degree of type 1 pneumocyte damage and more prominant inflammatory cell infiltration. Destructed cell debris within the alveolar space were also noted After steroid administration, 8Gy experimental group showed decreased degree of inflammatory reactions but fibroblast proliferation and basal lamina damages were unchanged. Experimental group with 12Gy showed lesser degree of inflammatory reactions similar to changes of 8Gy experimental group. Conclusion : These studies suggest that the degree of interstitial edema and inflammatory changes were related to radiation dose but Proliferation of the fibroblast and structural changes of basal lamina were not related to radialion dose. Experimental administration of steroid for 2 to 4 weeks after whole lung irradiation suggest that steroid can suppress alveolar and endothelial damages induced by whole lung irradiation but Proliferation of the fibroblast and structural changes of basal lamina were not related to administration of steroid.

• Journal of Veterinary Clinics
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• v.17 no.2
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• pp.490-494
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• 2000

2달령의 수컷 로트와 일러가 4일간 설사와 통증.보행 실조 등의 증상을 보여 (주)해 마루 소동물 임상 의자 연구소에 의뢰되었다 흉부 방사선 검사에서 폐야 전반에 걸친 페포성 침윤과 흉벽의 심란 비후가 관찰되어 흉막폐렴으로 진단하였으며 복강 초음파 검사에서 상 복부에서 소량의 복수가 관찰되었고 전반적인 간 echogenicity가 증가되어 있었다. 치료 후 설사 증상은 사라지고 전신 상태가 다소 호전되어 내원 후 7일째에 흉부 방사선 검사를 재 실시하였다. 흉막과 폐의 병변은 변화가 없었으나 상완골과 요골의 골간단 부분에 이상 소견 이 발견되어 골격계 방사선 검사를 실시한 결과 상완골, 요골, 대퇴골 그리고 경골의 골간단에 경화성 변화와 무정형의 골막 반응이 관찰되었고 요골, 척골과 경골의 골간단 부분에 성 장판 외의 방사선 투과성 선이 관찰되었다. 이상의 특이적인 방사선 소견을 바탕으로 비록 본 질환의 정확한 원인은 밝힐 수 없었으나, 감염성 원인에 의한 비대성 골이형성증으로 진단하였다.

• Applied Microscopy
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• v.38 no.4
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• pp.293-306
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• 2008

The essential factor of acute respiratory distress syndrome (ARDS), an acute lung injury accompanied commonly by sepsis syndrome is accumulation of neutrophils in lung tissue. The study attempted to confirm whether a lung injury would be decreased with the anti-inflammatory effect of germanium by the treated germanium prior to the development of ARDS and whether nitric oxide influence in suppressing a lung injury. Test groups were divided in the following structure for experiment; CON that has been administered with sodium chloride to airway, LPS administered with endotoxin for 5 hours in the same amount and 5 hours of endotoxin administered Ge+LPS following 1 hours of pre-treated germanium. The result of a test using experimental animals, infilteration of neutrophils (p<0.001) in bronchoalveolar lavage fluid (BALF) was significantly decreased, the structure of lung tissue was preserved relatively well, and much neutrophils with distinct positive were observed on tunel staining which showed increase of apoptotic neutrophils in the pre-treated germanium group compare to the endotoxin administrated group. In observation of ultrastructural changes of cell in BALF, phagocytic alveolar macrophage was increased in alveolar space, the nucleus of most engulfed neutrophils were condensed, and some apoptosis neutrophils appears to be DNA fragmentation and effacement of cellular organelles were found in intercellular matrix in the pre-treated germanium group. However, the nitric oxide showed increase in all the groups excluding CON, and the nitric oxide effect such as degranulation diminishing of mast cells and apoptosis increase of neutrophils in the pre-treated group only. The situation appears that there was change in internal environment of the experimental animal by the pre-treated germanium before the nitric oxide is produced and the anti-inflammatory effect activated the pre-processed germanium by nitric oxide which activated following the change. Therefore, the nitric oxide created from macrophage in accordance with the pre-treated germanium appears to influence in alleviating a lung injury. Accordingly, acute lung injury is alleviated by the anti-inflammatory effect of germanium such as inhibition of neutrophils migration, induction of neutrophil apoptosis and increase of phagocytic function of phagocyte, and the nitric oxide produced from activated macrophage by germanium would influence in suppressing a lung injury.

• Tuberculosis and Respiratory Diseases
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• v.45 no.6
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• pp.1290-1297
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• 1998

Bronchocentric granulomatosis(BCG), first defined in 1973, consists of granulomatous replacement of bronchial mucous membrane, often with heavy eosinophilic reaction within and about the involved bronchi. Etiologic factors are from hypersensitivity reaction for aspergillus, most often from idiopathic form, and in others from being associated with mycobacterium, ecchinococcus, rheumatoid disease, ankylosing spodylitis, and glomerulonephritis. Diagnosis is responsible only for pathologic findings and, in many cases, is confirmed in postoperative findings with misleading for tumor, tuberculosis, infectious or Wegener's granulomatosis. We report a case of bronchocentric granulomatosis associated with aspergillus.