No abstract available.
Vibration*

No abstract available.
Erythrocyte Membrane* ; Erythrocytes* ; Hydroxyl Radical* ; Lipid Peroxidation* ; Macrophages, Alveolar* ; Mineral Fibers*

Many acute and chronic lung diseased including pneumoconiosis are characterized by the presence of increased numbers of activated macrophages. These macrophages generate several inflammatory cell chemoattractants, by which neutrophil migrate from vascular compartment to the alveolar space. Recruited neutrophils secrete toxic oxygen radicals or proteolytic enzymes and induce inflammatory response. Continuing inflammatory response results in alteration of the pulmonary structure and irreversible fibrosis. Recently, a polypeptide with specific neutrophil chemotactic activity, interleukin-8 (IL-8), has been cloned and isolated from a number of cells such as: monocytes, macrophages and fibroblasts. IL-1 and/or TNF-alpha preceded for the synthesis of IL-8, and we already observed high level of IL-1 and TNF-alpha in vivo experiments. So we hypothesized that IL-8 might play a central role in the pathogenesis of pneumoconiosis. In order to evaluate the clinical utility of IL-1, IL-8, TNF as a biomarker in the early diagnosis of pneumoconiosis, we investigated the increase of IL-1, 8, TNF in the pneumoconiotic patient and the significant (p<0.05) correlation between IL-8 level and progression of pneumoconiosis.
Chemotactic Factors ; Clone Cells ; Diagnosis* ; Early Diagnosis ; Fibroblasts ; Fibrosis ; Humans ; Interleukin-1* ; Interleukin-8 ; Lung ; Macrophages ; Monocytes ; Neutrophils ; Peptide Hydrolases ; Pneumoconiosis* ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha

Early recognition of coalescence in pneumoconiotic lesions is important because such coalescence is associated with the respiratory symptoms and deterioration of lung function. This complicated form of pneumoconiosis also has worse prognosis than does simple pneumoconiosis. High resolution computerized tomography(HRCT) provides significant additional information on the stage of the pneumoconiosis because it easily detects coalescence of nodules and emphysema that may not be apparent on the simple radiograph. The Purpose of this study is to clarify the role of HRCT in detection of large opacity and the relationship of change between the coalescence of nodules or emphysema and lung function in dust exposed workers. 1. There was good correlation between the HRCT grade of pneumoconiosis and ILO category of profusion. 5(9.09%) in 55 study population had confluent nodule extending over two or more cuts on HRCT. HRCT could identify the pneumoconiotic nodules which was not found by simple radiography in 6 workers with category 0/0. 2. No significant difference was observed coalescence of nodules and emphysema by dust type. 3. There was no significant difference in pulmonary function according to ILO and HRCT classification. 4. HRCT could detect the significant reduction in FEV1, FEV1/FVC, PEER, FEF25, FEF50, and FEF75 and remarkable increase in RV and TLC in study persons with emphysema compared with non-emphysema group. 5. Emphysema was found more often in nodules-coalescence group than small opacity group by HRCT. We found that HRCT could easily detect areas of coalescence and complicated emphysema compared to plain chest X-ray. Also our data suggest that it is primarily the degree of emphysema rather than the degree of pneumoconiosis that determines the level of pulmonary function.
Classification ; Dust ; Emphysema ; Humans ; Lung ; Pneumoconiosis* ; Prognosis ; Radiography ; Thorax

PURPOSE: Assessment of the diameters of the aortic arches in the human fetus may be helpful in the prenatal diagnosis of aortic arch anomalies. The purpose of this study is to construct valuable reference ranges of fetal aortic arch for various fetal growth parameters in an unselected Korean population. METHODS: A prospective, cross-sectional study was performed in 98 normal singleton fetuses between 20 and 38 weeks of gestation. The transverse aortic arch diameter (TAD) and distal aorta isthmus diameter (AID) were measured in the longitudinal view during systole. The bi-parietal diameter (BPD), head circumference (HC), abdominal circumference (AC) and femur length (FL) were obtained at the same time. Ultrasound examinations were performed with a 2.0-6.0 MHz convex probe by abdominal ultrasound. RESULTS: TAD and AID as a function of gestational age (GA) was expressed by the regression equation TAD= -1.246+0.168 X GA, and AID = -1.341+0.180 X GA; TAD and AID are expressed in millimeters and GA in weeks. TAD and AID as a function of BPD was expressed by the regression equation TAD= -1.147+0.664 X BPD, and AID = -1.152+0.696 X BPD. TAD and AID as a function of HC was expressed by the regression equation TAD = -1.187+0.182 X HC, and AID = -1.350+0.198 X HC. TAD and AID as a function of AC was expressed by the regression equation TAD = -0.528+0.173 X AC, and AID = -0.533+0.183 X AC. TAD and AID as a function of FL was expressed by the regression equation TAD = -0.519+0.799 X FL, and AID = -0.601+0.860 X FL; BPD, HC, AC and FL are expressed in centimeters. Correlations were found to be highly statistically significant in relation to GA, BPD, HC, AC, and FL respectively (P<0.0001 in all). Normal mean of TAD and AID per GA, BPD, HC, AC and FL and 95% prediction limits were also defined, respectively. CONCLUSION: New reference ranges of fetal aortic arch related to other fetal bio-parameters representing fetal growth were obtained successfully. The normative date will be helpful in the prenatal accurate diagnosis of aortic anomalies and abnormal growth of fetal aortic arches in Korea.
Aorta ; Aorta, Thoracic ; Cross-Sectional Studies ; Echocardiography ; Femur ; Fetal Development ; Fetus ; Gestational Age ; Head ; Humans ; Korea ; Pregnancy ; Prenatal Diagnosis ; Prospective Studies ; Reference Values ; Systole

Cantrell's syndrome is a rare congenital anomaly, consists of five malformations. There are the midline abdominal wall defect, the defect of sterna lower part, an agenesis of the anterior part of the diaphragm, an absence of the diaphragmatic pericardium, and the congenital intracardiac problem. We diagnosed Cantrell's syndrome with left ventricular diverticulum in a female neonate with no perinatal problems. She experienced an one-staged operation and discharged with no complications. We report a case with brief review of the literature.
Abdominal Wall ; Diaphragm ; Diverticulum* ; Female ; Humans ; Infant, Newborn* ; Pericardium

BACKGROUND AND OBJECTIVES: To report the clinical features of six patients diagnosed with cases of inferior vestibular neuritis based on abnormal vestibular evoked myogenic potential (VEMP) responses with normal caloric test results. MATERIALS AND METHODS: We retrospectively reviewed 62 patients presenting with dizziness. All patients underwent a battery of audiovestibular testing, including hearing tests, caloric test and VEMP test. RESULTS: Six patients were diagnosed as inferior vestibular neuritis. All patients presented with acute onset of prolonged vertigo. The pure tone audiograms and caloric test results were normal. VEMP response was absent unilaterally, and normal in the contralateral ear. CONCLUSION: Inferior vestibular neuritis should be considered in patients presenting with acute vertigo, but normal caloric responses. Comprehensive vestibular testing including VEMP is necessary.
Caloric Tests ; Dizziness ; Ear ; Hearing Tests ; Humans ; Retrospective Studies ; Vertigo ; Vestibular Evoked Myogenic Potentials ; Vestibular Function Tests ; Vestibular Neuronitis

Silica exposure results in acute inflammatory response followed by chronic fibrotic change. The mechanism for the maintenance of silica-induced inflammation has not been understood yet. Apoptosis is a morphologically distinct form of programed cell death that plays major role during homeostasis and in many diseases including cancer, acquired immune deficiency syndrome and neurodegenerative disorders. Apoptosis is characterized by cell shrinkage, membrane blebbing and nuclear condensation. To demonstrate the involvement of apoptosis in underlying mechanism for the development of silica-induced pathological changes, this study was designed in vitro and in vivo models. In in vitro study, alveolar epithelial cell line (A549) was stimulated with silica and performed flow cytometry and DNA electrophoresis. In in vivo study, bronchoalveolar lavage (BAL) was done to count the total and apoptotic cells from silica-instilled rats. The results were as follows: 1. Apoptotic cell fraction of silica-treated groups (10 and 50 microgram/cm2) was significantly higher than that of control group. 2. Genomic DNA from silica-treated groups (10 and 50 microgram/cm2 ) showed DNA ladder in agarose gel electrophoresis, while group of 1 microgram/cm2 didn't. 3. Total cell number and apoptotic cell number of BAL fluid from silica-instilled rats (10, 20 and 40 mg/kg) were significantly higher than those of control. 4. Silica induced apoptosis of cells in BAL fluid was confirmed by microscopic observation with nuclear fragmentation. These results suggest that apoptosis may contribute to development of silica-induced pathological changes.
Acquired Immunodeficiency Syndrome ; Animals ; Apoptosis* ; Blister ; Bronchoalveolar Lavage ; Cell Count ; Cell Death ; DNA ; Electrophoresis ; Electrophoresis, Agar Gel ; Epithelial Cells ; Flow Cytometry ; Homeostasis ; Inflammation ; Membranes ; Microscopy ; Neurodegenerative Diseases ; Rats ; Silicon Dioxide* ; Silicosis

The inhalation of crystalline silica results in the production of reactive oxygen species(ROS). Among these ROS, hydroxyl radical( OH) is believed to be the most reactive one. OH is generated in reaction between superoxide and hydrogen peroxide catalyzed by transition metal, especially iron. Therefore iron should be important in the bioactivity of crystalline silica. Desferrioxamine, a iron chelator, may be protective in silica-induced pulmonary reaction. To test this assumption we investigated the protective effect of desferrioxamine on lipid peroxidation of cell membrane, cytotoxicity, production of proinflammatory and chemotactic cytokine and fibroblast proliferation by crystalline silica in vitro model. The results were as follows: 1. Fenton activity of silica and asbestos was significantly higher than that of control. Fenton activity in crocidolite was higher than silica at the same dose. This result correlated with iron content of dust. Fenton activity of silica and crocidolite was decreased by preincubation of silica with desferrioxamine. 2. Silica induced a dose-dependent increase of MIDA concentration in lung epithelial cell lysate dose dependently. Marked decrease of MDA was observed in desferrioxaminetreated silica group compared with untreated group. 3. As concentration of stimulated silica, silica?induced cytotoxicity was increased. There was significant decrease of cytotoxicity in desferrioxamine?treated silica group compared with untreated group. 4. a-quartz augmented the production of TNF-a and IL-8 from A549 cell. While desferrioxa-mine suppressed the release of cytokines. 5. Supernatant of silica-cocultured A549 cell induced a significant proliferation of fibroblast, which desferrioxaime blocked this proliferation. From these result, we concluded that desferrioxamine has a protective effect on silica induced pulmonary reaction.
Asbestos ; Asbestos, Crocidolite ; Cell Membrane ; Crystallins ; Cytokines ; Deferoxamine* ; Dust ; Epithelial Cells ; Fibroblasts* ; Hydrogen Peroxide ; Inhalation ; Interleukin-8 ; Iron ; Lipid Peroxidation ; Lung ; Oxygen ; Silicon Dioxide ; Superoxides

Asbestosis is a chronic inflammatory disorder of lower respiratory tract in which alveolar wall are progressively thickened by a fibrotic process. Fibrotic process characterized by an expansion of fibroblast and collagenous extracellular matrix secreted from this fibroblast. Alveolar macrophage is believed to be a primary target cell and major participant in the evolution of lung fibrosis after asbestos inhalation. Alveolar macrophage are known to release a variety of substance that induce tissue damage and stimulate inflammatory cells and fibroblast. Macrophage also release a variety of metabolite of arachidonic acid. Of these, PGE(2) is known to suppress fibroblast proliferation. Asbestos may be a very effective stimulus for fibroblasts without triggering the relase of PGE(2). To assess the fibrogenic properties of asbestos according to kind and dosage of asbestos and the ability of PGE(2) to suppress the proliferation of fibroblast, alveolar macrophages cultured with crocidolite, amosite and chrysotile in presence or absence of PGE(2)10(-5)M. At 24 hours after alveolar macrophage cultured with various stimuli, the released fibronectin and TNF-alpha was measured. Viability of alveolar macrophages was observed and growth promoting activity of macrphage supernatant to fibroblasts was quantified. The results were as follows; 1. The viability of alveoair macrophages stimulated with asbestos fiber was markedly decreased compared with control group except chrysotile 10 microgram group. Crocidolite and amosite were more cytotoxic than chrysotile. 2. All of asbestos augmented fibronectin production in concentration dependent fashion. 3. There was a significant positive correlation between TNF-alpha production in supernatant and fiber concentration. 4. Supernatant from alveolar macrophages cultured with asbestos were inducible a significant increase in fibroblast proliferation. 5. Incubation of avieolar macrophages with asbestos in the presence of PGE(2) resulted in significant decrease of TNF-alpha production in supernant. 6. Supernatant from alveolar macrophages cultured with asbestos were inducible a: sig nificnat decrease in fibroblast proliferation when PGE(2) was added. The result of this study strongly suggested that crocidolite and amosite were more cytotoxic and fibrogenic and exogenous PGE(2) suppressed fibroblast proliferation following exposed to asbestos.
Animals ; Arachidonic Acid ; Asbestos* ; Asbestos, Amosite ; Asbestos, Crocidolite ; Asbestos, Serpentine ; Asbestosis ; Collagen ; Extracellular Matrix ; Fibroblasts* ; Fibronectins ; Fibrosis ; Inhalation ; Lung ; Macrophages ; Macrophages, Alveolar ; Rats* ; Respiratory System ; Tumor Necrosis Factor-alpha