• Journal of Chest Surgery
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• v.24 no.11
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• pp.1098-1106
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• 1991

Atelectasis may be defined as collapse of the lung due to absence of air within the alveoli. It may involve anatomic segments, lobes, or whole lungs but also may be a diffuse miliary process, as in the adult respiratory distress syndrome. The key to treatment are the anticipation and prevention of atelectasis in various clinical situations, the recognition and treatment of underlying disease, and the prompt initiation of vigorous treatment once atelectasis is found. Repeated assessment by physical examination is necessary to determine the presence of atelectasis and its response to treatment. During the period of January, 1981 to October, 1990, 100 patients with atelectasis were treated in the department of Thoracic and Cardiovascular Surgery, Pusan National University Hospital. There were 70 males and 30 females ranging from 3 days to 79 years of age. The occurrence ratio of right to left side was 2.1 : 1. The underlying pathologic lesions of atelectasis were pneumonia with effusion(28), lung ca.(24), pulmonary tuberculosis(24), and chronic empyema(9), The treatment procedure for atelectasis were closed thoracostomy in 26 cases, ressection in 21 cases, therapeutic bronchoscopy in 14 cases and etc.

• Pediatric Infection and Vaccine
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• v.2 no.1
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• pp.110-115
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• 1995

Authors have experienced a case of neonatal sepsis whose organisms were group B streptococci. This case was early-onset type and the two premature babies were expired. Autopsy was done but no specific findings were shown in pulmonary parenchyma except focally mild atelectasis and dilated bronchiols and alveoli, and distictive hyaline membrane or aspirated materials are not identified. A brief review follows.

• Tuberculosis and Respiratory Diseases
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• v.74 no.4
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• pp.151-162
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• 2013

Diffuse alveolar hemorrhage (DAH) is a life-threatening and medical emergency that can be caused by numerous disorders and presents with hemoptysis, anemia, and diffuse alveolar infiltrates. Early bronchoscopy with bronchoalveolar lavage is usually required to confirm the diagnosis and rule out infection. Most cases of DAH are caused by capillaritis associated with systemic autoimmune diseases such as anti-neutrophil cytoplasmic antibody-associated vasculitis, anti-glomerular basement membrane disease, and systemic lupus erythematosus, but DAH may also result from coagulation disorders, drugs, inhaled toxins, or transplantation. The diagnosis of DAH relies on clinical suspicion combined with laboratory, radiologic, and pathologic findings. Early recognition is crucial, because prompt diagnosis and treatment is necessary for survival. Corticosteroids and immunosuppressive agents remain the gold standard. In patients with DAH, biopsy of involved sites can help to identify the cause and to direct therapy. This article aims to provide a general review of the causes and clinical presentation of DAH and to recommend a diagnostic approach and a management plan for the most common causes.

• BMB Reports
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• v.53 no.7
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• pp.367-372
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• 2020

Cell cycle-related kinase (CCRK) has a conserved role in ciliogenesis, and Ccrk defects in mice lead to developmental defects, including exencephaly, preaxial polydactyly, skeletal abnormalities, retinal degeneration, and polycystic kidney. Here, we found that Ccrk is highly expressed in mouse trachea and bronchioles. Ccrk mutants exhibited pulmonary hypoplasia and abnormal branching morphogenesis in respiratory organ development. Furthermore, we demonstrated that Ccrk mutant lungs exhibit not only impaired branching morphogenesis but also a significant sacculation deficiency in alveoli associated with reduced epithelial progenitor cell proliferation. In pseudoglandular stages, Ccrk mutant lungs showed a downregulation of Hedgehog (Hh) signaling and defects in cilia morphology and frequency during progenitor-cell proliferation. Interestingly, we observed that activation of the Hh signaling pathway by small-molecule smoothened agonist (SAG) partially rescued bud morphology during branch bifurcation in explants from Ccrk mutant lungs. Therefore, CCRK properly regulates respiratory airway architecture in part through Hh-signal transduction and ciliogenesis.

• Journal of Yeungnam Medical Science
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• v.36 no.1
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• pp.8-15
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• 2019

Connective tissue diseases (CTDs) can affect all compartments of the lungs, including airways, alveoli, interstitium, vessels, and pleura. CTD-associated lung diseases (CTD-LDs) may present as diffuse lung disease or as focal lesions, and there is significant heterogeneity between the individual CTDs in their clinical and pathological manifestations. CTD-LDs may presage the clinical diagnosis a primary CTD, or it may develop in the context of an established CTD diagnosis. CTD-LDs reveal acute, chronic or mixed pattern of lung and pleural manifestations. Histopathological findings of diverse morphological changes can be present in CTD-LDs airway lesions (chronic bronchitis/bronchiolitis, follicular bronchiolitis, etc.), interstitial lung diseases (nonspecific interstitial pneumonia/fibrosis, usual interstitial pneumonia, lymphocytic interstitial pneumonia, diffuse alveolar damage, and organizing pneumonia), pleural changes (acute fibrinous or chronic fibrous pleuritis), and vascular changes (vasculitis, capillaritis, pulmonary hemorrhage, etc.). CTD patients can be exposed to various infectious diseases when taking immunosuppressive drugs. Histopathological patterns of CTD-LDs are generally nonspecific, and other diseases that can cause similar lesions in the lungs must be considered before the diagnosis of CTD-LDs. A multidisciplinary team involving pathologists, clinicians, and radiologists can adequately make a proper diagnosis of CTD-LDs.

• Tuberculosis and Respiratory Diseases
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• v.52 no.4
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• pp.411-418
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• 2002

Pulmonary alveolar proteinosis(PAP) is a disorder in which an insoluble, proteinaceous material, rich in phospholipids, is deposited in the alveoli and bronchioles. The deficiency in the clearance and degradation of the intra-alveolar phospholipoproteinaceous material in PAP most likely represents a dysfunction of the type II pneumocytes. Although the pathogenesis and causative treatment of PAP is unclear a whole lung bronchopulmonary lavage is a relatively safe and effective treatment. Here we experienced a case of pulmonary alveolar proteinosis in a 62 year old female patient who had pulmonary tuberculosis approximately 20 years ago. She complained of aggravated dyspnea and chronic cough, and presented fine inspiratory crackles at both lung fields, diffuse ground glass opacity with some area of consolidation and smooth interlobular septal thickenings in both upper, right middled lobes, and a portion of right lower lobe. Optical microscopy of the lung tissue obtained by and open lung biopsy revealed many granulomas containing acid-fast smear positive bacilli and diffuse homogeneous PAS-positive fluid in the alveolar space. Immunohistochemical stain showed surfactant. A in the alveolar space. Antituberculosis drugs with bronchoalveolar lavage were used to treat the disease. Thereafter she showed improvement in her symptoms and a partial improvement in the chest X-ray and HRCT findings. We present a case of PAP associated with pulmonary tuberculosis.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.406-413
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• 1999

Pulmonary alveolar proteinosis (PAP) is a disorder in which an insoluble, proteinaceous material, rich in phospholipid, is deposited in alveoli and bronchioles. Several cases were reported since 1986, and the numbers of patients is increasing in Korea. Although the pathogenesis and causative treatment of PAP is not well known, whole lung lavage is the only consistently successful treatment. We report 2 cases of PAP which were confirmed by open lung biopsy with electron microscopy and clinically improved by whole lung lavage with a review of literature.

• Molecules and Cells
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• v.46 no.9
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• pp.558-572
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• 2023

Chronic obstructive pulmonary disease (COPD) will be the third leading cause of death worldwide by 2030. One of its components, emphysema, has been defined as a lung disease that irreversibly damages the lungs' alveoli. Treatment is currently unavailable for emphysema symptoms and complete cure of the disease. Hyaluronan (HA) and proteoglycan link protein 1 (HAPLN1), an HA-binding protein linking HA in the extracellular matrix to stabilize the proteoglycan structure, forms a bulky hydrogel-like aggregate. Studies on the biological role of the full-length HAPLN1, a simple structure-stabilizing protein, are limited. Here, we demonstrated for the first time that treating human alveolar epithelial type 2 cells with recombinant human HAPLN1 (rhHAPLN1) increased TGF-β receptor 1 (TGF-β RI) protein levels, but not TGF-β RII, in a CD44-dependent manner with concurrent enhancement of the phosphorylated Smad3 (p-Smad3), but not p-Smad2, upon TGF-β1 stimulation. Furthermore, rhHAPLN1 significantly increased sirtuins levels (i.e., SIRT1/2/6) without TGF-β1 and inhibited acetylated p300 levels that were increased by TGF-β1. rhHAPLN1 is crucial in regulating cellular senescence, including p53, p21, and p16, and inflammation markers such as p-NF-κB and Nrf2. Both senile emphysema mouse model induced via intraperitoneal rhHAPLN1 injections and porcine pancreatic elastase (PPE)-induced COPD mouse model generated via rhHAPLN1-containing aerosols inhalations showed a significantly potent efficacy in reducing alveolar spaces enlargement. Preclinical trials are underway to investigate the effects of inhaled rhHAPLN1-containing aerosols on several COPD animal models.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1087-1093
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• 1998

Mucormycosis is the common name given to several different diseases caused by fungi of the order Mucorales. The mucoraceae are ubiquitous fungi and are common inhabitants of decaying matter. In contrast to the widespread distribution of these fungi, disease in humans is limited, in most cases, to people with severe immunocompromised, diabetes mellitus, or trauma. 1be fungus gains entry to the body through the respiratory tract. The spores are presumably deposited in the nasal turbinates and may be inhaled into the pulmonary alveoli. The manifestations of mucormycosis are rhinocerebral, pulmonary, cutaneous, gastrointestinal, central nervous system, and miscellaneous. Sporadic reports can be found of mucormycosis involving other areas : heart, bones, kidney, bladder, mediastinum, and trachea. However, isolated tracheal mucormycosis is very rare. Therefore, we report a 57-year old, noninsulin dependent diabetic woman who presented with acute, severe degree of upper airway obstruction due to isolated mucormycosis of the trachea.

• 대한상한금궤의학회지
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• v.13 no.1
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• pp.21-44
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• 2021

Objective : This study aimed to assess the preventive effect of Bupleuri Radix aqueous extracts (BR) and red koji-fermented BR (fBR) in lipopolysaccharide (LPS)-induced acute lung injury in a rat model. Methods : Rats were administered 30, 60, or 120 mg/kg/day of fBR for 28 days before LPS treatments. All rats were sacrificed 5 h after LPS treatment (500 ㎍/head, intratracheal instillation). Body weights, lung weights, pulmonary transcapillary albumin transit, arterial gas parameters (pH, partial pressure [Pa] of O2, PaCO2), bronchoalveolar lavage fluid (BALF) protein, lactate dehydrogenase (LDH), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), total cell numbers, neutrophil/alveolar macrophage ratios, lung malondialdehyde (MDA), and myeloperoxidase (MPO) were measured. In addition, histopathological changes including the luminal surface of alveoli (LSA), thickness of alveolar septum, and number of polymorphonuclear neutrophils (PMNs) were checked. Results : LPS injection led to increases in lung weights, pulmonary transcapillary albumin transit, BALF protein, LDH, TNF-α and IL-1β contents, total cells, neutrophil and alveolar macrophage ratios, lung MDA, MPO, alveolar septum thickness, and PMNs, and decreases in PaCO2 and pH of arterial blood and LSA. However, these LPS-induced acute lung injuries were inhibited by pretreatment of 30, 60, and 120 mg/kg of fBR. The most favorable effects were seen with 30 mg/kg fBR as compared with 60 mg/kg of α-lipoic acid and BR. Conclusions : fBR showed preventive effects on LPS-induced acute lung injury, which resembles acute respiratory distress syndrome. The mechanisms of action were likely via antioxidant and anti-inflammatory means.