• Korean Journal of Veterinary Research
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• v.23 no.2
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• pp.183-186
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• 1983

The clinical and histopathological observation of leucocytozoonosis was carried out during July, 1982 at a poultry compound in Gyeongbuk province and the results were summarized as follows: 1. Leucocytozoonosis was observed in 36,900 of 59,900 chickens (61.6%) and the mortality rate was 18.3% (6,760 of 36,900 chickens infected). 2. Clinical findings were anorexia, dyspnea, paleness of comb, greenish diarrhea and reduction of egg production. 3. Gross lesions were yellowish white spots scattered on parenchymal organs and swelling of liver and spleen. In addition, petechiation and ecchymosis of small intestine, egg yolk and subcutaneous tissues were observed. 4. Histological findings were infiltration of mononuclear cells in liver, heart and lung, appearance of megaloschizonts in heart, liver, proventriculus and pancreas, proliferation of foreign body giant cells in heart, and hyperemia and swelling of all parenchymal organs.

• Tuberculosis and Respiratory Diseases
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• v.65 no.4
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• pp.339-342
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• 2008

Early CT findings of transient radiographic progression (TRP) during treatment of active pulmonary tuberculosis including subpleural, interlobular or intralobular septal thickening and micronodules are shown in the present case. Late CT findings of TRP are subpleural, enhancing nodular infiltration with internal low attenuation. These CT features accompanied by a lack of clinical worsening in young patients taking antituberculous medication due to pulmonary tuberculosis can help to differentiate TRP from other disease entities.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.21 no.1
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• pp.38-54
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• 2008

Objective : This study was designed to investigated effects of Pinelliae Rizoma (PR) on asthma Methods : Detecting antigen specific antibody isotypes, cytokines in serum and bronchoalveolar lavage fluid (BALF). In addition, the present author also investigated changes in weight of spleen and proliferation rates of splenocytes. Finally, histopathological observation of the lung tissue was also investigated. Results : Oral administration of PR lowered OVA specific IgE levels in serum, IgG1 levels in serum and BALF. PR also decreased production levels of IL-4 in BALF. In addition, total cells in BALF were decreased by oral administration of PR effectively. In histapathological observation, PR group showed downward tendency of inflammatory cell infiltration around small vessels. Conclusion : PR is useful to treat patients with asthma and the mechanisms are related in suppression of Th2 skewing reactions.

• Tuberculosis and Respiratory Diseases
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• v.78 no.2
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• pp.133-136
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• 2015

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitive disease showing various radiographic and clinical manifestations. Its clinical course has not been fully understood. Here I describe a case of a 23-year-old immunocompetent man with frequently relapsing ABPA. He was asthmatic. He visited our hospital because of a chronic cough. Laboratory examination showed eosinophilia with increased total and Aspergillus-specific IgE as well as positive skin reaction to Aspergillus fumigatus. Radiologic feature was a dense consolidation. Histology showed organizing pneumonia with eosinophilic infiltration. On the diagnosis of ABPA, he was treated with systemic steroid and itraconazole. Although treatment response was excellent, he suffered from recurrent ABPA three times thereafter in the form of fleeting mass-like consolidation.

• Journal of Veterinary Clinics
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• v.39 no.2
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• pp.87-92
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• 2022

A 14-year-old castrated male Persian cat presented with a 2-week history of respiratory difficulty. On physical examination, the patient showed intermittent open-mouth breathing and thoracic auscultation revealed wheezing. Thoracic radiographs revealed a narrowed upper airway and pulmonary infiltration. Computed tomography detected a mass occluding the lumen of the trachea at the level of the entrance to the thorax, a mass causing right main bronchus stenosis, and a nodule on the right caudal lung lobe. Bronchoalveolar lavage cytology tentatively diagnosed a carcinoma. Tracheal mass resection was performed through tracheostomy. Histopathology confirmed the presence of tracheobronchial carcinoma. The survival time after diagnosis was 10 months, during which time the cat underwent tracheostomy, debulking by endotracheal tube, and tracheal stent placement procedures in combination with toceranib phosphate adjuvant chemotherapy.

• The Korean Journal of Medicine
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• v.99 no.1
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• pp.25-31
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• 2024

Lymphangioleiomyomatosis (LAM) is a rare condition that exclusively affects women and is characterized by lung parenchymal destruction and the formation of cysts due to infiltration by LAM cells. It can also impact the lymphatic system, leading to the development of fluid-filled cystic structures and abdominal involvement, including renal angiomyolipomas (AML) or lymphangioleiomyoma. LAM can occur sporadically or be associated with tuberous sclerosis complex. Common symptoms include respiratory issues such as dyspnea, pneumothorax, chylothorax, along with other manifestations like renal AML and lymphatic involvement. The diagnosis of LAM relies on a combination of clinical, radiological, and laboratory findings, and treatment options vary depending on symptoms and patient status, with mTOR inhibitors being considered as a treatment option. This case outlines the diagnostic journey and clinical course of a 32-year-old female patient with LAM.

• Journal of Chest Surgery
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• v.32 no.7
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• pp.613-620
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• 1999

Background: Recently, regional or isolated organ perfusion is being studied again as a drug administration modality which is able to reduce systemic toxicity while delivering high-dose chemotherapeutic agents. This research was planned to evaluate the pharmacokinetics and long-term pathologic changes of the lung in isolated lung perfusion (ILP) with cisplatin. Material and Method: Twenty-five New Zealand white rabbits were divided into 2 groups (Group I: 10, Group II: 15). The groups were then subdivided into 2 and 3 subgroups of 5 rabbits. In group I, tissue samples of the lung and kidney, and systemic blood for platinum concentration measurement were taken 30 minutes after systemic intravenous infusion of cisplatin (5 mg/kg) and isolated lung perfusion in each 5 rabbits. In 2 subgroups of group II, lung tissues for pathologic exams were taken 30 minutes and 1 week after ILP in each 5 rabbits, which received 10% pentastarch solution only and cisplatin, respectively. In the other subgroups, lung biopsy was undertaken 4 weeks after ILP with cisplatin. Result: When cisplatin was infused via systemic vein, the platinum concentration in the lung, kidney and plasma were 1.50${\pm}$0.43 $\mu\textrm{g}$/g, 7.65${\pm}$2.49 $\mu\textrm{g}$/g, 1.19${\pm}$0.03 $\mu\textrm{g}$/ml, respectively. However, the platinum concentration in the lung was about 50 times higher (75.43${\pm}$11.47 $\mu\textrm{g}$/g) than that of intravenous infusion group, and those in the kidney and plasma were decreased (1.30${\pm}$ 0.35 $\mu\textrm{g}$/g, 0.13${\pm}$0.02 $\mu\textrm{g}$/ml) when cisplatin was introduced through ILP. Pathologic change in the treated lung with ILP was characterized by the medial hypertrophy of the pulmonary arterioles and interstitial eosinophilic infiltration, which was not dependent on cisplatin

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.5
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• pp.617-628
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• 1998

In order to understand the pathogenetic mechanism of adult respiratory distress syndrome (ARDS), the role of phospholipase A2 (PLA2) in association with oxidative stress was investigated in rats. $Interleukin-1{\alpha}\;(IL-1,\;50\;{\mu}g/rat)$ was used to induce acute lung injury by neutrophilic respiratory burst. Five hours after IL-1 insufflation into trachea, microvascular integrity was disrupted, and protein leakage into the alveolar lumen was followed. An infiltration of neutrophils was clearly observed after IL-1 treatment. It was the origin of the generation of oxygen radicals causing oxidative stress in the lung. IL-1 increased tumor necrosis factor (TNF) and cytokine-induced neutrophil chemoattractant (CINC) in the bronchoalveolar lavage fluid, but mepacrine, a PLA2 inhibitor, did not change the levels of these cytokines. Although IL-1 increased PLA2 activity time-dependently, mepacrine inhibited the activity almost completely. Activation of PLA2 elevated leukotriene C4 and B4 (LTC4 and LTB4), and 6-keto-prostaglandin $F2{\alpha}\;(6-keto-PGF2{\alpha})$ was consumed completely by respiratory burst induced by IL-1. Mepacrine did not alter these changes in the contents of lipid mediators. To estimate the functional changes of alveolar barrier during the oxidative stress, quantitative changes of pulmonary surfactant, activity of gamma glutamyltransferase (GGT), and ultrastructural changes were examined. IL-1 increased the level of phospholipid in the bronchoalveolar lavage (BAL) fluid, which seemed to be caused by abnormal, pathological release of lamellar bodies into the alveolar lumen. Mepacrine recovered the amount of surfactant up to control level. IL-1 decreased GGT activity, while mepacrine restored it. In ultrastructural study, when treated with IL-1, marked necroses of endothelial cells and type II pneumocytes were observed, while mepacrine inhibited these pathological changes. In histochemical electron microscopy, increased generation of oxidants was identified around neutrophils and in the cytoplasm of type II pneumocytes. Mepacrine reduced the generation of oxidants in the tissue produced by neutrophilic respiratory burst. In immunoelectron microscopic study, PLA2 was identified in the cytoplasm of the type II pneumocytes after IL-1 treatment, but mepacrine diminished PLA2 particles in the cytoplasm of the type II pneumocyte. Based on these experimental results, it is suggested that PLA2 plays a pivotal role in inducing acute lung injury mediated by IL-1 through the oxidative stress by neutrophils. By causing endothelial damage, functional changes of pulmonary surfactant and alveolar type I pneumocyte, oxidative stress disrupts microvascular integrity and alveolar barrier.

• Tuberculosis and Respiratory Diseases
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• v.41 no.4
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• pp.328-338
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• 1994

Background: Effect of sulfur dioxide($SO_2$) exposure on airway is well known but little about the effect of $SO_2$ exposure on lung parenchyme. This study is to determine if short tenn exposure to $SO_2$ in concentration commonly found in industrialized environment cause potentially harmful effect on the lung parenchyme, and to evaluate the exposure time-response relationship between short tenn exposure to $SO_2$ and the inflammatory response in mouse lung. Method: 5ppm $SO_2$ gas was used and 48 mice were grouped into control(10), 30(9), 60(11), and 120 minute exposure(18) group. In each group, bronchoalveolar lavage(BAL) was done immediately after and at 1,2,3 days after exposure. Histological examination was performed in control and 120 minute exposure group. Results: 1) Cell response in bronchoalveolar lavage fluid. In 30 and 60 minute exposure group, compared to the control group, lymphocyte count has significantly increased(p<0.05) at 1 day after exposure but did not differ at 2 days after exposure. In 120 minute exposure group, also compared to the control group, there was significant increase in total cell, macrophage, and lymphocyte count at 1 day after exposure, (p<0.05) which lasted for 2 days but did not significantly differ at 3 days after exposure. 2) Histological findings in 120 minute exposure group. In the airway, mild epithelial cell damage and ciliary loss were noted but there was no evidence of inflammatory cell infiltration. Interstitial inflammatory infiltration was noted at 1 day after exposure, which lasted for 3 days after exposure and there was no evidence of edema or fibrosis in the interstitium Conclusions: These data indicate potentially noxious effect of $SO_2$ on the lung parenchyme as well as the airway at exposure level that are regarded as relatively safe, and the duration of injury depends on the exposure time.

• Tuberculosis and Respiratory Diseases
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• v.44 no.5
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• pp.1019-1029
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• 1997

Background : Elevation of resting energy expenditure(REE) in patients with lung cancer has been described in earlier studies and may contribute to cancer cachexia, but limited information is available regarding the prevalence and determinants of the increased REE. The aim of this study was to assess the prevalence and contributing factors of a hypermetabolic state in newly detected patients with lung cancer and to assess the energy balance in order to improve our knowledge about weight loss in patients with lung cancer. Method : Thirty one consecutive, newly detected patients with lung cancer and 20 control patients with benign lung diseases were included in this study. Resting energy expenditure(REE) was measured by indirect calorimetry using ventilated hood system and predicted REE was calculated by the Harris-Benedict formular. Results : The energy balance in newly detected lung cancer patients was disturbed in a high proportion of patients, and hypermetabolic state occurred in 61% of the patients. Tumor volume, cancer type, location, stage, the presence of atelectasis or infiltration, pulmonary function, or smoking behavior were not associated with increase in REE. But patients with distant metastasis had significantly higher REE comparing with patients without metastasis. Thirty nine percents of the patients with lung cancer had substantial loss of more than 10% of their pre-illness weight. Weight losing patients with lung cancer were not accompanied by an increase in REE. Conclusion : We concluded that the REE was elevated in a higher proportion of patients with lung cancer and distant metastasis was found to be contributing factor to the elevated REE.