• Journal of Yeungnam Medical Science
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• v.32 no.2
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• pp.146-151
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• 2015

Atherosclerotic renal artery stenosis (RAS) may result in hypertension, azotemia, and acute pulmonary edema. We report on a renal angioplasty with stent placement for bilateral RAS in a patient with acute decompensated heart failure and acute kidney injury. A 67-year-old female patient was admitted to our hospital with acute shortness of breath and generalized edema. Echocardiography showed left ventricular wall motion abnormality and the follow up electrocardiography showed T wave inversion in the precordial leads. We performed a coronary angiography to differentiate ischemic heart disease from non-cardiac origin for the cause of the heart failure. The coronary angiography showed no significant luminal narrowing, but bilateral RAS was confirmed on the renal artery angiography, therefore, we performed renal artery revascularization. After the procedure, the pulmonary edema was improved and the serum creatinine was decreased. Two weeks later, an echocardiography showed improvement of the left ventricular systolic function.

• Journal of Chest Surgery
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• v.55 no.1
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• pp.30-36
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• 2022

Background: No consensus exists regarding whether volatile anesthetics are superior to intravenous anesthetics for reducing postoperative pulmonary complications (PPCs) in patients undergoing general anesthesia for surgery. Studies of this issue focused on anatomic pulmonary resection are lacking. This study compared the effects of total intravenous anesthesia (TIVA) versus volatile anesthesia on PPCs after anatomic pulmonary resection in patients with lung cancer. Methods: This retrospective study examined the medical records of patients with lung cancer who underwent lung resection at our center between January 2018 and October 2020. The primary outcome was the incidence of PPCs, which included prolonged air leak, pneumonia, acute respiratory distress syndrome, empyema, atelectasis requiring bronchofiberscopy (BFS), acute lung injury (ALI), bronchopleural fistula (BPF), pulmonary embolism, and pulmonary edema. Propensity score matching (PSM) was used to balance the 2 groups. In total, 579 anatomic pulmonary resection cases were included in the final analysis. Results: The analysis showed no statistically significant difference between the volatile anesthesia and TIVA groups in terms of PPCs, except for prolonged air leak. Neither of the groups showed atelectasis requiring BFS, ALI, BPF, pulmonary embolism, or pulmonary edema after PSM. However, the length of hospitalization, intensive care unit stay, and duration of chest tube indwelling were shorter in the TIVA group. Conclusion: Volatile anesthetics showed no superiority compared to TIVA in terms of PPCs after anatomical pulmonary resection in patients with lung cancer. Considering the advantages of each anesthetic modality, appropriate anesthetic modalities should be used in patients with different risk factors and situations.

• 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.

• Tuberculosis and Respiratory Diseases
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• v.52 no.2
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• pp.166-173
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• 2002

Transient peripheral eosinophilia occurs in several disorders, such as allergic diseases, cancer, and parasitic infections. However, in most cases, their presence is not accompanied by tissue destruction or organ dysfunction. In certain disease states, eosinophils can accumulate in any organ in the body and cause tissue destruction as a result of the eosinophil infiltration or the toxic effects of the degranulated proinflammatory products. Idiopathic hypereosinophilic syndrome is a rare disorder characterized by persistent eosinophilia of an unknown origin, usually associated with a dysfunction of organs such as the heart, lung, skin, and nervous system. Idiopathic hypereosinophilic syndrome usually has an indolent course over a period of several months. However, in some cases, they have grave symptoms if vital organs such as heart and lung are infiltrated. Here we report a case of idiopathic hypereosinophilic syndrome presenting acute pulmonary edema involving the heart, bone marrow, and lung with a review of the relevant literatures.

• Journal of Korean Neurosurgical Society
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• v.65 no.5
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• pp.680-687
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• 2022

Objective : The influence of moderate-to-severe traumatic brain injury (TBI) on acute pulmonary injury is well established, but the association between acute pulmonary injury and mild TBI has not been well studied. Here, we evaluated the histological changes and fluctuations in inflammatory markers in the lungs to determine whether an acute pulmonary inflammatory response occurred after mild TBI. Methods : Mouse models of mild TBI (n=24) were induced via open-head injuries using a stereotaxic impactor. The brain and lungs were examined 6, 24, and 72 hours after injury and compared to sham-operated controls (n=24). Fluoro-Jade B staining and Astra blue and hematoxylin staining were performed to assess cerebral neuronal degeneration and pulmonary histological architecture. Quantitative real-time polymerase chain reaction analysis was done to measure inflammatory cytokines. Results : Increased neuronal degeneration and the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β were observed after mild TBI. The IL-6, TNF-α, and TGF-β levels in mice with mild TBI were significantly different compared to those of sham-operated mice 24 hours after injury, and this was more pronounced at 72 hours. Mild TBI induced acute pulmonary interstitial edema with cell infiltration and alveolar morphological changes. In particular, a significant infiltration of mast cells was observed. Among the inflammatory cytokines, TNF-α was significantly increased in the lungs at 6 hours, but there was no significant difference 24 and 72 hours after injury. Conclusion : Mild TBI induced acute pulmonary interstitial inflammation and alveolar structural changes, which are likely to worsen the patient's prognosis.

• The Journal of Korean Medicine
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• v.15 no.2 s.28
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• pp.173-183
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• 1994

The results about effects of Maecmoondongtang on the pulmonary function of $SO_2$ exposed rats were summerized as follows: 1. Maecmoondongtang reavealed significant effect on decrease of the lung weight in pulmomary edema of rats. 2. Maecmoondongtang reavealed very significant effect on decrease of the TBA value of lung. 3. It was recognized Maecmoondongtang had signiftcant effect on decrease of glycoprotein contents in trachea. 4. It was recognized maecmoondongtang had significant effect on decrease of mucos area in tracheal epithelium. 5. Maecmoondongtang had effects on recovery of the cillia cells of tracheal epithelium and inhibition of mucous secretion. According to the above result. it was recognized Gamimaecdongtang had significant effect on decrease of lung weight in pulmonary edema. the TBA value. glycoprotein contents in trachea. and mucous area in tracheal epithelium. and recovery of the cillia cells of tracheal epithelium. and inhibition of mucous secretion. So I think we can take advantage of this medicine very usefully for treatment of pulmonary edema. pheumonia. acute and chronic bronchitis etc.

• Tuberculosis and Respiratory Diseases
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• v.74 no.1
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• pp.15-22
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• 2013

Background: Differentiating cardiogenic pulmonary edema from other bilateral lung diseases such as pneumonia is frequently difficult. We conducted a retrospective study to identify predictors for cardiogenic pulmonary edema and non-cardiogenic causes of bilateral lung infiltrates in chest radiographs. Methods: The study included patients who had newly developed bilateral lung infiltrates in chest radiographs and patients who underwent echocardiography. Cases were divided into two groups based on the echocardiographic findings: the cardiogenic pulmonary edema group and the non-cardiogenic group. Clinical characteristics and basic laboratory findings were analyzed to identify predictors for differential diagnosis between cardiogenic and non-cardiogenic causes of bilateral chest infiltrates. Results: We analyzed 110 subjects. Predictors of cardiogenic pulmonary edema were higher brain natriuretic peptide (BNP) levels, lower C-reactive protein (CRP) levels on the day of the event (<7 mg/dL), age over 60 years, history of heart disease, and absence of fever and sputum. CRP on the day of the event was an independent factor to differentiate cardiogenic and non-cardiogenic causes of newly developed bilateral chest infiltrates. Also, the validity was comparable to BNP. Conclusion: Clinical symptoms (sputum and fever), medical history (dyslipidemia and heart disease), and laboratory findings (BNP and CRP) could be helpful in the differential diagnosis of patients with acute bilateral lung infiltrates in chest radiographs.

• IMMUNE NETWORK
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• v.15 no.4
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• pp.206-211
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• 2015

Pulmonary edema is a major cause of mortality due to acute lung injury (ALI). The involvement of protein kinase C-${\delta}$ (PKC-${\delta}$) in ALI has been a controversial topic. Here we investigated PKC-${\delta}$ function in ALI using PKC-${\delta}$ knockout (KO) mice and PKC inhibitors. Our results indicated that although the ability to produce proinflammatory mediators in response to LPS injury in PKC-${\delta}$ KO mice was similar to that of control mice, they showed enhanced recruitment of neutrophils to the lung and more severe pulmonary edema. PKC-${\delta}$ inhibition promoted barrier dysfunction in an endothelial cell layer in vitro, and administration of a PKC-${\delta}$-specific inhibitor significantly increased steady state vascular permeability. A neutrophil transmigration assay indicated that the PKC-${\delta}$ inhibition increased neutrophil transmigration through an endothelial monolayer. This suggests that PKC-${\delta}$ inhibition induces structural changes in endothelial cells, allowing extravasation of proteins and neutrophils.

• The Korean Journal of Physiology
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• v.28 no.1
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• pp.71-77
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• 1994

In the animal model of acute respiratory distress syndrome (ARDS) induced by N-nitroso-N-methylurethane (NNNMU) the secretory activity of alveolar type H cells during acute alveolar injury was investigated by determining phospholipid and pulmonary surfactant associated proteins in crude surfactant. The mechanism of the secretory change was studied by determination of DNA and RNA levels in the lung tissue. After induction of acute alveolar injury with NNNMU, pulmonary hemorrhage, atelectasis and gross hypertrophy were observed. Seven days after NNNMU treatment the level of total DNA in lung homogenate was increased markedly indicating that a hypertrophy was induced by cellular proliferation. Although the total DNA level increased, the RNA/DNA ratio was gradually decreased after NNNMU treatment. Seven days after NNNMU treatment the RNA/DNA ratio returned to the normal control level. During the acute alveolar injury, phospholipid and surfactant associated proteins were reduced significantly as compared with the control, implying that the secretory activity of alveolar type II cells was altered during acute alveolar injury induced by NNNMU. The protein content in crude surfactant during peak injury(7 days after NNNMU) was decreased significantly but phospholipid/protein ratios were identical in both control and NNNMU treatment groups. SDS-PAGE of proteins in crude pulmonary surfactant showed a decrease in major surfactant associated protein(M.W. 38,000) during acute alveolar injury. The present study may suggest that while alveolar type H cells proliferate markedly, transcription of alveolar type ll cell gene was inhibited by an unknown mechanism such as DNA methylation induced by NNNMU. Such an inhibition of transcriptional activity is thought to be associated with the decreased secretory activity of alveolar type ll cells, which may lead to pulmonary atelectasis and edema during the acute alveolar injury.

• Journal of Chest Surgery
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• v.33 no.10
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• pp.823-826
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• 2000

Primary intimal sarcoma of the pulmonary artery is a rare disease and there has been no report of any case originating from the pulmonary valve. Recently we experienced a 62 year-old female patient who had a primary intimal sarcoma of the pulmonary valve with distal metastasis. She was brought to medical attention due to exertional dyspnea facial edema productive coughing and general weakness for 1 month. Chest CT and echocardi-ography suggest an acute pulmonary thromboembolism or tumor. Exploration showed a large polypoid mass arising from the pulmonary leaflets and multiple masses on distal pulmonary arteries. We replaced the pulmonary valve and reconstructed the pulmonary artery. She received radiotherapy 1 month postoperatively and now 4 months after surgery she has begun receiving chemotherapy.