• Proceedings of the Korean Society of Toxicology Conference
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• 2005.05a
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• pp.51-82
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• 2005

To compare the pulmonary toxicity between ultrafine colloidal silica particles (UFCSs) and fine colloidal silica particles (FCSs), mice were intratracheally instilled with 3 mg of 14-nm UFCSs and 230-nm FCSs and pathologically examined from 30 mill to 24 hr post-exposure. Histopathologically, lungs exposed to both sizes of particles showed bronchiolar degeneration and necrosis, neutrophilic inflammation in alveoli with alveolar type II cell proliferation and particle-laden alveolar macrophage accumulation. UFCSs, however, induced extensive alveolar hemorrhage compared to FCSs from 30 min onwards. UFCSs also caused more severe bronchiolar epithelial cell necrosis and neutrophil influx in alveoli than FCSs at 12 and 24 hr post-exposure. Laminin positive immunolabellings in basement membranes of bronchioles and alveoli of UFCSs treated animals was weaker than those of FCSs treated animals in all observation times. Electron microscopy demonstrated UFCSs and FCSs on bronchiolar and alveolar wall surface as well as in the cytoplasm of alveolar epithelial cells, alveolar macrophages and neutrophils. Type I alveolar epithelial cell erosion with basement membrane damage in UFCSs treated animals was more severe than those in FCSs treated animals. At 12 and 24 hr post-exposure, bronchiolar epithelia cells in UFCSs treated animals showed more intense vacuolation and necrosis compared to FCSs treated animals. These findings suggest that UFCSs has greater ability to induce lung inflammation and tissue damages than FCSs.

• Korean Journal of Veterinary Service
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• v.29 no.4
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• pp.483-487
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• 2006

A study of pulmonary diseases in the slaughtered cattle (n = 125) of Mymensingh town was conducted to study pathological findings using the standard methods from September 2001 through April 2002. The pulmonary lesions observed in this study included congestion, emphysema, anthracosis, pleuritis abscess and hemorrhage. The histopathological findings of congestion were characterized by hemorrhage, a large number of leukocytes infiltration in the lumen of the alveoli, bronchitis, bronchiolitis, proliferation of fibrous connective tissue and hyperplasia of bronchiolar epithelia. Histopathologically, emphysema was identified by the distended alveoli with thin and atrophied alveolar walls. In anthracosis, carbon particles were found in stroma and alveolar lumen. In pleuritic lesions, there was a proliferation of fibrous connective tissue along with the infiltration of mononuclear reactive cells. Abscesses were characteristic of the accumulation of neutrophils surrounded by immature fibroblasts forming a capsule like structure.

• Advances in pediatric surgery
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• v.6 no.1
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• pp.1-9
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• 2000

Despite of advances in perinatal management and treatment modalities congenital diaphragmatic hernia(CDH) remains a frustrating problem. Although the sheep has proven to be a reliable experimental model for the production of intrauterine CDH, the rabbit may have some advantages. These include lower cost, smaller body size, year-round availability, high number of fetuses per pregnancy, and short gestational period. To evaluate the feasibility of the rabbit model of CDH, twenty-seven pregnant New Zealand rabbits were utilized. Hysterotomy and an operative procedure for creating a diaphragmatic defect on gestational day 24 or 25, in two fetuses of each pregnant rabbit were performed. In one fetus of one cornu of the uterus, the left fetal diaphragm was excised through an open thoracotomy(DH group). In another fetus in the other cornu, CDH was created and the trachea clipped(Surgiclip, USSC, Norwalk, Conn., USA) (TL group). Delivery was by Cesarean section on 30 days of gestation. Among twenty- seven pregnant rabbits, 12 in the DH group and eight in the TL group were born alive. The most common herniated organ was the left lobe of the liver. In thee DH group, the lungs were hypoplastic with decreased lung weight/body weight ratio, reduced numbers of alveoli, thicker media of the pulmonary arteries, and immature alveoli. In TL group, the alveoli were more mature and did not differ from the control animals. In conclusion, (1) pulmonary hypoplasia develops in the fetal rabbit diaphragmatic hernia model and (2) simultaneous tracheal ligation prevents pulmonary hypoplasia.

• Journal of Chest Surgery
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• v.20 no.1
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• pp.1-12
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• 1987

Respiratory care with oxygen inhalation is often a necessity to maintain life, and it is one of the important therapeutic adjuncts in respiratory disease and in intensive care after surgery. However, it has been reported that oxygen toxicity occurs after prolonged exposure to 100% 0, [Smith, 1899; Kistler et al. 1967; Schaffner et al. 1967; Rowland and Newman, 1969. Subjective symptoms of oxygen toxicity include tracheal irritation, frequent cough, some burning sensation in the trachea, tachypnea, severe dyspnea, etc. [Welch, 1963; Fisher et al, 1968; Milier et al, 1970; Clark and Lambertsen, 1971; Sackner, 1975]. Pathologic findings are atelectasis, injuries to the pulmonary capillaries and hemorrhage in the alveoli in gross specimens. There can be inflammation, proliferation of fibrin, thickening of alveolar membranes, degeneration of collagen fibers and interstitial edema in the microscopic findings. [Penrod, 1956; Cedergren, 1959; Bean, 1965; Schaffner, 1967]. Dubois and colleagues [1961] found that the amount of pulmonary surfactant was decreased in oxygen toxicity and atelectasis followed by the decreased pulmonary surfactant. Many authors reported that vital capacity, inspiratory force, pulmonary compliance, pulmonary capillary blood flow and pulmonary elasticity were deceased and arteriovenous shunting increased. [Comroe et al, 1945; Fuson et al, 1965; Kistler et al, 1966; Knowles and Blenner-hassett, 1967; Barber et al, 1978]. Many human volunteers were examined after prolonged exposure in a high oxygenated chamber and there were a few reports on animals with oxygen toxicity, subjects including rabbits. Gas partial pressures of alveoli and arteries were measured in rabbits exposed to 100% $O_2$ and the alveolar-arterial gas gradients were analyzed, which is the basis for the study of oxygen toxicity. These rabbits were divided into two groups; rabbits under natural respiration, and second group under artificial respiration with a respirator. The alveolar $PO_2$ [$P]AO_2$] and $PCO_2$ [$PACO_2$], and the arterial $PO_2$ [$PaO_2$] were measured under varying $O_2$ pressures; 15% $O_2$, 21% $O_2$ and 100% $O_2$.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.6
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• pp.1525-1533
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• 2007

The discovery of drugs on the treatment of rhinitis and allergic disease is a very important subject in human heath. The Shinbijen has been used for centruries as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of hot water extract from Shinbijen on OVA-mediated allergic reaction and studied its possible mechanism of action using fluorescenc microscopy and RT-PCR analysis. Shinbijen inhibited OVA-induced rhinitis, total cells in BFA and lymphocyte related to inflammation in mice. Shinbijen decreased immuno response, which activated by IL-4, COX-2 and iNOS expression. in tissue. Shinbijen reduced inflammatory molecule release from mice lung tissue and CD4/CD8 cells activated by cardiac blood. Shinbijen decreased OVA-induced IL-4 and iNOS levels in pulmonary alveoli. Our findings provide evidence that Shinbijen inhibits OVA-induced allergic reactions, and also demonstrate the involvement of inflammation and allergic disease in these effects.

• Korean Journal of Veterinary Research
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• v.59 no.4
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• pp.223-226
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• 2019

A 7-year-old, spayed female Chihuahua with dyspnea, intermittent cyanosis, and dermal plaques was diagnosed with hyperadrenocorticism. Thoracic radiographs showed markedly hyperdense alveoli in multiple lung lobes. Computed tomography (CT) images showed lung mineralization confined to the lung parenchyma and pituitary macroadenoma. Pulmonary mineralization secondary to hyperadrenocorticism is commonly found on histopathologic examination. However, those lesions are rarely identified radiographically. We describe obvious pulmonary mineralization secondary to hyperadrenocorticism found on radiographs and present the first report regarding CT imaging of the mineralization. Pulmonary mineralization should be considered when a dog affected by hyperadrenocorticism shows diffuse lung mineralization on radiographs.

• Biomedical Science Letters
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• v.27 no.3
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• pp.111-120
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• 2021

Asbestos products had been widely used until 2007 in Korea since the 1930s. A total ban on their production and applications has been imposed because of the toxic effect of asbestos fibers on the human health. The inhaled asbestos fibers increase reactive oxygen species and inflammatory reactions in the respiratory airway including the alveolar sac, resulting in DNA damages and secretion of several inflammatory cytokines or chemokines. These paracrine communications promote the proliferation of fibroblasts and the synthesis of collagen fibers, thereby depositing them into the extracellular matrix at the interstitial space of alveoli. The fibrotic tissue hindered the gas exchange in the alveolus. This reviews describes not only the cytotoxic effects of asbestos fibers with different physical or chemical characteristics but also the interaction of cells that make up the respiratory airway to understand the molecular or cellular mechanisms of asbestos fiber-induced toxicity. In addition, we propose a pulmonary toxicity research technique based on the mini-lung that can mimic human respiratory system as an alternative to overcome the limitations of the conventional risk assessment of asbestos fibers.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2005.05a
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• pp.91-96
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• 2005

A. Nebulized SWCNT dispersed as aggregates and nanotubes B. Aspiration causes transient oxidant stress, damage and inflammation, peaking by 7 days post-exposure C. Histology visualizes aggregates in the tirminal bronchials and proximal alveli with no visible material in distal alve oli D. Size of aggregates doesn't change with time E. Rapid fibrosis - begins in 7 days and progresses through 60 day post-exposure 1) Fibrosis in granulomatous lesions containing aggregates 2) Diffuse interstitial fibrosis in distal alveolar walls with no visible SWCNT F. Used silver enhancement of gold-labeled SWCNT 1) See aggregates in proximal alveoli and terminal bronchials 2) See nanoropes in walls of distal alveoli

• Journal of Yeungnam Medical Science
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• v.37 no.4
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• pp.269-276
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• 2020

Fibrosis is characterized by excessive accumulation of extracellular matrix components. The fibrotic process ultimately leads to organ dysfunction and failure in chronic inflammatory and metabolic diseases such as pulmonary fibrosis, advanced kidney disease, and liver cirrhosis. Idiopathic pulmonary fibrosis (IPF) is a common form of progressive and chronic interstitial lung disease of unknown etiology. Pathophysiologically, the parenchyma of the lung alveoli, interstitium, and capillary endothelium becomes scarred and stiff, which makes breathing difficult because the lungs have to work harder to transfer oxygen and carbon dioxide between the alveolar space and bloodstream. The transforming growth factor beta (TGF-β) signaling pathway plays an important role in the pathogenesis of pulmonary fibrosis and scarring of the lung tissue. Recent clinical trials focused on the development of pharmacological agents that either directly or indirectly target kinases for the treatment of IPF. Therefore, to develop therapeutic targets for pulmonary fibrosis, it is essential to understand the key factors involved in the pathogenesis of pulmonary fibrosis and the underlying signaling pathway. The objective of this review is to discuss the role of kinase signaling cascades in the regulation of either TGF-β-dependent or other signaling pathways, including Rho-associated coiled-coil kinase, c-jun N-terminal kinase, extracellular signal-regulated kinase 5, and p90 ribosomal S6 kinase pathways, and potential therapeutic targets in IPF.

• International Journal of Vascular Biomedical Engineering
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• v.4 no.1
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• pp.9-16
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• 2006

In this article we introduce computer models that have been developed in the past to determine the concentration of metabolic gases, the oxygen and carbon dioxide, along the pulmonary circulation. The terminal concentration of these gases in the arterial blood is related with the total change of the partial pressure of the same gases in the alveoli for the time beginning with inspiration and ending with expiration. It is affected not only by the ventilation-perfusion ratio and the gas diffusion capacity of the lung membrane but also by the pulmonary defect such as shunt, dead space, diffusion impairment and ventilation-perfusion mismatch. Some pathological pulmonary symptoms such as ARDS and CDPD can be understood through the mathematical models of these pulmonary dysfunctions. Quantitative study on the blood oxygenation process using various computer models is therefore of foremost importance in order to monitor not only the pulmonary health but also the cardiac output and cell metabolism. Reviewed in this paper include the basic and advanced methods that enable numerical study on the gas exchange and on the arterial oxygenation process, which might depend on the various heart and lung physiological conditions listed above.