• Journal of the Society of Cosmetic Scientists of Korea
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• v.47 no.3
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• pp.185-191
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• 2021

Environmental pollution is defined as contamination of the earth's environment with materials which interfere with human health, quality of life, or the natural functioning of the ecosystem. Whenever a prolonged and repetitive exposure to environmental stressors exceeds the skin's normal defensive potential, there is a disturbance in the skin barrier function leading to the development of various skin diseases. Major air pollutants which affect the skin are polycyclic aromatic hydrocarbons, volatile organic compounds, nitrogen oxides, particulate matter, cigarette smoke, heavy metals and arsenic. Dermal uptake depends on the deposition of air pollutants on the skin surface, the composition of epidermal lipids, and the diffusion through the epidermis to the blood vessels.

• Proceedings of the Korean Vacuum Society Conference
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• 2014.02a
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• pp.262.1-262.1
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• 2014

Lipid peroxidation induces functional deterioration of cell membrane and induces cell death in extreme cases. These phenomena are known to be related generally to the change of physical properties of lipid membrane such as decreased lipid order or increased water penetration. Even though the electric property of lipid membrane is important, there has been no report about the change of electric properties after lipid peroxidation. Herein, we demonstrate the molecular energy band change in red blood cell membrane through peroxidation by air-based atmospheric pressure DBD plasma treatment. Ion-induced secondary electron emission coefficient (${\gamma}$ value) was measured by using home-made gamma-focused ion beam (${\gamma}$-FIB) system and electron energy band was calculated based on the quantum mechanical Auger neutralization theory. The oxidized lipids showed higher gamma values and lower electron work functions, which implies the change of surface charging or electrical conductance. This result suggests that modified electrical properties should play a role in cell signaling under oxidative stress.

• Tuberculosis and Respiratory Diseases
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• v.57 no.1
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• pp.37-46
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• 2004

Background : Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. Methods : From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and $200{\mu}M$ $CoCl_2$ were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. Results : 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-$1{\alpha}$(HIF-$1{\alpha}$) was also induced by 2% oxygen. Conclusion : Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.31 no.1
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• pp.52-70
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• 2018

Objectives : Atopic dermatitis(AD) and environmental factors are closely related, but there is lack of oriental medical examination. So we compared the relationship between AD and various environmental factors in Oriental medicine and Western medicine. Methods : We described the relationship between AD and environmental factors through the latest papers and a review of the oriental medicine literature. Results : The regional diversity of AD incidence implies a close relationship between climate factors and AD, and high altitude and low pH springs also have an effect on AD. Air pollutants from industrialization and urbanization aggravate AD. The increase in indoor residence time and the increase in room temperature and humidity have also increased the sensitization to allergens such as house dust mite. In oriental medicine, wind(風) is one of the environmental factors and is an inflammatory state due to external irritation. Wind-Humidity(風濕) refers to erythematous wetting dermatitis with itching and exudation, Wind-Fever(風熱) refers to acute inflammatory reaction with erythematous papules and plague, and Blood-Weakness(血虛) refers to aggravation and chronicization of inflammation due to persistence of skin barrier impairment. Conclusions : We examined the relationship between AD and various environmental factors. We also described the oriental medical viewpoints of the environmental factors in the occurrence of AD and skin barrier impairment.

• Journal of Preventive Medicine and Public Health
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• v.15 no.1
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• pp.145-151
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• 1982

Breslau's report on the two stillbirths induced by illuminating gas poisoning made many investigators explore the hazards. of carbon monoxide(CO) poisoning to pregnancy. The pregnant woman, her fetus, and the newborn infant have been identified to be particularly vulnerable to CO even in low concentration. Several factors, such as placental barrier, membrane resistance of maternal and fetal red blood cells etc., were considered to be related to the delayed elimination of CO from fetus. Slower elimination of CO from fetus than from mother was confirmed in several in vivo studies. But there are few studies which have confirmed the difference of carboxyhemoglobin (HbCO) dissociation in adult and fetal bloods. Author investigated the effects of hemoglobin itself on the elimination of CO from mother and fetus. By observing the difference of CO dissociation from adult and fetal hemoglobin at the various partial pressures of oxygen, the author tries to suggest the base of the proper treatment measure for the CO poisoning of pregnant woman and newborn infant. The results were as follows: 1. The total hemoglobin amounts of adults and fetal bloods were $16.1{\pm}0.50gm%\;and\;15.7{\pm}0.32gm%$, respectively. The fetal hemoglobin proportions in adult and fetal bloods were $1.2{\pm}0.15%\;and\;72.7{\pm}3.01%$, respectively. 2. Adult and fetal bloods saturated by CO to 100% HbCO were exposed to ambient air$(21%\;O_2),\;100%\;O_2\;and\;3\;ATAO_2$. After 30 minutes exposure, the HbCO saturations of adult blood were 96.7%, 70.9%, and 52.8%, respectively, and those of fetal blood were 98.5%, 76.1%, and 62.2%, respectively. HbCO dissociation was proportional to the partial pressure of oxygen and the most marked dissociation was shown under 3 ATA $O_2$, HbCO dissociation of fetal blood was slower than that of adult blood in all conditions. According to the above results, it is possible that CO poisoning make more serious damage to the fetus and newborn infant than to the adult due to the delayed dissociation of HbCO. Thus in the treatment of CO poisoning of pregnant woman and newborn infant, hyperbaric oxygen therapy seems to be the most eflective treatment measure, but the duration of hyperbaric oxygenation should be lengthened accordingly.

• Applied Microscopy
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• v.23 no.1
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• pp.35-55
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• 1993

cis-Dichlorodiammineplatinum (II) (cis-Platin), a metallic compound, has widely been used as an effective anticancer chemotherapeutic agent. The precise mechanism of action of this agent is still unknown, but it is postulated that cis-Platin may act on the cancer cell like bifunctional alkylating agents. Although this agent is very beneficial to the patients with cervical cancer, germinoma of testis, neuroblastoma and others, it may also damage to the normal cell so that many side effects; severe hemorrhagic enterocolitis, bone marrow depression, renal damage and liver damage will develope. This experiment has been undertaken to pursue the cytotoxic effects of the cis-Platin on the ultrastructures of the interalveolar septum in the mouse lung. A total of 55 healthy male mice of ICR strain were used as experimental animals and divided into 5 mice of normal control group and 50 mice of cis-Platin treated group. The mice of cis-Platin treated group were sacrificed by carotid exsanguination at 6, 12, 24 hours, 3 days and 7 days after intraperitoneal injection of 6.0 mg of cis-Platin ($Abiplatin^R$ Abic Co. Ltd.) per kg of mouse body weight. The specimen obtained from the lower lobe of left lung were sliced into $1mm^3$ and prefixed with 2% glutaraldehyde -2.5% paraformaldehyde solution prepared with Millonig's phosphatae buffer solution (pH 7.4) at $4^{\circ}C$ for 3-4 hours. After postfixation with 1% osmium tetroxide solution all specimens were embedded in Epon 812. Ultrathin sections about $600-800{\AA}$ in thickness were stained with uranyl acetate and lead citrate and observed with Hitachi-600 electron microscope. The results obtained were as follows: 1. Local swellings with increase of electron density and number of pinocytic vesicles in the cytoplasms of the type I pneumocyte and endothelial cell of the blood air barrier in interalveolar septum of cis-platin treated mice were observed. 2. Cisternae of rough endoplasmic reticulum were dilated and sacculated in association with detachment of membrane bound ribosomes of the type II pneumocyte in interalveolar septum of cis-Platin treated mice. 3. Swollon mitochondria with uneven electron density of their matrix were observed in the type II pneumocyte of interalveolar septum in the cis-Platin treated mice. 4. The lamellae of lammelar bodies in type II pneumocyte of interalveolar septum in cis-Platin treated mice were devoided or transformed into homogeneous electron dense material. It is consequently suggested that cis-Platin would induce the cellular edema of type I pneumocyte and endothelial cell, and degenerative changes of cytoplasmic organelles of the type II pneumocyte in the interalveolar septum of the mouse lung.

• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.397-405
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• 2005

Background : Laminin-1 is known to have regular functions in the development and course of differentiation of the lungs. The morphogenesis and distribution of laminin-1 still remains as a mystery and its distribution and changes in the molecular structure of laminin-1 in the pathogenesis of the lung still is a subject of great controversy. In this study, experiments were done to delineate the distribution and changes in the amount of laminin-1 after inducing inflammation of the lungs by exposing experimental animals to CS gas and especially, to find compositions of laminin-1 within type II pneumocytes. Materials and Methods : The experimental subjects of study were newborn rats and the extracted tissue from the experimental rats were viewed under light microscope and electron microscope after the sections were treated with immunohistochemical methods and immunogold reaction methods using bounded gold particles. Results : 1) Lymphocytes and mononuclear phagocytes invaded the alveolar septa in the 2 day group rats after CS gas exposure and intense interstitial inflammation was seen in the 3 day group. 2) Laminin immunoreactions decreased to a moderate degree in the 2 and 3 day group rats after CS gas exposure and strong laminin immunoreactions were seen again in the 5 and 7 day group rats. 3) Gold particles in basal lamina of the lung blood-air barrier decreased and in the type I pneumocytes decreased in the 2 and 3 day group rats after CS gas exposure. 4) Gold particles were seen only on the surface of the cell membranes of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure. 5) Few gold particles around the lamellar bodies and cytoplasm of type II pneumocytes in the control rat group and at 12 hours after CS gas exposure. Gold particles are seen only on the surface of type II pneumocytes of the 1 and 2 day group rats after CS gas exposure and are evenly distributed in small amounts in the cells of the 3 day group after CS gas exposure. Conclusion : CS gas exposure in the rats caused inflammation of lung alveolar septa and also induced a decrease in laminin-1 in basal lamina and loss of laminin-1 in the cytoplasm of type II pneumonocytes. As the inflammatory cells disappeared, an increase in the distribution of laminin-1 occurred. This reflects tissue regeneration functions of laminin-1 in the pneumocytes of rats and the distribution of laminin-1 in type II pneumocytes can be seen through the electron microscope using immunogold methods.