A 70-year-old female who was diagnosed as myxoid chondrosarcoma by fine needle aspiration of a pleural mass is described. She presented with left chest discomfort of 4 months' duration and aggravating dyspnea and chest pain for 2 months. Chest X-ray and CT scan revealed a large lobulated low density mass invading chest wall at the left pleural cavity and massive pleural fluid. Fine needle aspiration was done under the impression of mesothelioma or metastatic cancer. The aspirates from the mass were very cellular and composed of isolated or clustered forms of large plump cells. Abundant cytoplasm was blulsh opaque and the margin was rounded in the isolated cells, whereas clustered cells show ill-defined ceil borders and aggregating tendency. The nuclei were eccentric, round to ovoid, and had fine chromatin pattern and multiple small nucleoli. Cellular pleomorphism or mitotic figure was not definite. These findings were consistent with cytologic features of chondrosarcoma. Final diagnosis was confirmed as myxoid chondrosarcoma by mediastinoscopic biopsy and the tumor showed strong positivity for S-100 protein.
Much progress has been made in understanding the subcellular events of the human lung injuries after acute exposure to environmental air pollutants. Host of those events represent oxidative damages mediated by reactive oxygen species such as superoxide, hydrogen peroxide, and the hydroxy, free radical. Recently, nitric oxide (NO) was found to be endogenously produced by endothelial cells and cells of the reticulo-endothelial system as endothelialderived relaxation factor (EDRF) which is a vasoactive and neurotransmitter substance. Together with superoxide, NO can form another strong oxidant, peroxonitrite. The relative importance of exogenous sources of $N0/N0_2$ and endogenous production of NO by the EDRF producing enzymes in the oxidative stresses to the heman lung has to be elucidated. The exact events leading to chronic irreversible damage are still yet to be known. From chronic exposure to oxidant gases, progressive epithelial and interstitial damages develop. Type I epithelial cells become thicker and cover a smaller average alveolar surface area while thee II cells proliferate instead. Under acute damages, the extent of loss of the alveolar epithelial cell lining, especially type II cells appears to be a good predictor of the ensuing irreversible damage to alveolar compartment. Interstitial matrix undergo remodeling during chronic exposure with increased collagen fibers and interstitial fibroblasts. However, Inany of these changes can be reversed after cessation of exposure. Among chronic lung injuries, genetic damages and repair responses received particular attention in view of the known increased lung cancer risks from exposure to several air pollutants. Heavy metals from foundry emission, automobile traffics, and total suspended particulate, especially polycystic aromatic hydrocarbons have been positively linked with the development of lung cancer. Asbestos in another air pollutant with known risk of lung cancer and mesothelioma, but asbestos fibers are nonauthentic in most bioassays. Studies using the electron spin resonance spin trapping method show that the presence of iron in asbestos accelerates the production of the hydroxy, radical in vitro. Interactions of these reactive oxygen species with particular cellular components and disruption of cell defense mechanisms still await further studies to elucidate the carcinogenic potential of asbestos fibers of different size and chemical composition. The distribution of inhaled pollutants and the magnitude of their eventual effects on the respiratory tract are determined by pollutant-independent physical factors such as anatomy of the respiratory tract and level and pattern of breathing, as well as by pollutant-specific phyco-chemical factors such as the reactivity, solubility, and diffusivity of the foreign gas in mucus, blood and tissue. Many of these individual factors determining dose can be quantified in vitro. However, mathematical models based on these factors should be validated for its integrity by using data from intact human lungs.
Background: Gastric cancer is a common malignant tumor. Our previous study demonstrated inhibitory effects of 3-bromopyruvate (3-BrPA) on pleural mesothelioma. Moreover, we found that 3-BrPA could inhibit human gastric cancer cell line SGC-7901 proliferation in vitro, but whether similar effects might be exerted in vivo have remained unclear. Aim: To investigate the effect of 3-BrPA to human gastric cancer implant tumors in nude mice. Materials and Methods: Animals were randomly divided into 6 groups: 3-BrPA low, medium and high dose groups, PBS negative control group 1 (PH7.4), control group 2 (PH 6.8-7.8) and positive control group receiving 5-FU. The TUNEL method was used to detect apoptosis, and cell morphology and structural changes of tumor tissue were observed under transmission electron microscopy (TEM). Results: 3-BrPA low, medium, high dose group, and 5-FU group, the tumor volume inhibition rates were 34.5%, 40.2%, 45.1%, 47.3%, tumor volume of experimental group compared with 2 PBS groups (p<0.05), with no significant difference between the high dose and 5-FU groups (p>0.05). TEM showed typical characteristics of apoptosis. TUNEL demonstrated apoptosis indices of 28.7%, 39.7%, 48.7% for the 3-BrPA low, medium, high dose groups, 42.2% for the 5-FU group and 5% and 4.3% for the PBS1 (PH7.4) and PBS2 (PH6.8-7.8) groups. Compared each experimental group with 2 negative control groups, there was significant difference (p<0.05); there was no significant difference between 5-FU group and medium dose group (p>0.05), but there was between the 5-FU and high dose groups (p<0.05). Conclusions: This study indicated that 3-BrPA in vivo has strong inhibitory effects on human gastric cancer implant tumors in nude mice.
Since Ikeda in traduced flexible fiberoptic bronchoscope in 1968, use of bronchoscopy was expanded rapidly. Wide use of flexible bronchoscopy enabled us to get tissue diagnosis with more ease and safety. Authors analyzed 71 cases of tissue biopsy of 233 bronchoscopies from June '76 to. Jan. '78 and concluded as following : 1. 233 bronchoscopies af 20 Month duration, cases which needed tissue biopsy were 71 cases (30.5%). 2. Chief complaints af above cases are coughing, dyspnea, sputum, chest pain, hemoptysis in frequency. 3. Biopsy sites were as following in frequency: Rt.upper lobe, Lt. main bronchus, Lt. upper lobe, Rt. main bronchus, Lt. lower lobe. 4. The final diagnosis of biopsied cases were cancer 80%, tuberculosis 15%, and malignant mesothelioma, anthracosis, aspergillosis, were one case each. 5. Among 57 case of lung cancer, biopsy confirmed cases were 36 cases (63%). 6. Pathologic finding of 36 case of Biopsy confirmed lung cancer was as following: Squamous cell ca : 64% Anaplastic ca : 25% Adeno ca : 2.8% Unclassified: 2.8% 7. Bronchographies were done in 36cases (51%), one quarter of cases before biopsy, and three quarters of cases after biopsy. 8. Cytology was requested in 76% of cases with following results; PAP class V 15%, class IV 7.5%, class III 1.8%.
Ahn, Yeh-Chan;Oak, Chulho;Park, Jung-Eun;Jung, Min-Jung;Kim, Jae-Hun;Lee, Hae-Young;Kim, Sung Won;Park, Eun-Kee;Jung, Maan Hong
Journal of the Optical Society of Korea
/
v.20
no.5
/
pp.607-613
/
2016
The pleura is known as an end target organ of exposure to toxic environmental materials such as fine particulate matter and asbestos. Moreover, long-term exposure to hazardous materials can eventually lead to fatal lung disease such as diffuse pleural fibrosis or mesothelioma. Chest computed tomography (CT) and ultrasound are gold standard imaging modalities for detection of advanced pleural disease. However, a diagnostic tool for early detection of pleural reaction has not been developed yet due to difficulties in imaging ultra-fine structure of the pleura. Optical coherence tomography (OCT), which provides cross-sectional images of micro tissue structures at a resolution of 2-10 μm, can image the mesothelium with a thickness of ~100 μm and therefore enables investigation of the early pleural reaction. In this study, we induced the early pleural reaction according to a time sequence after pleurodesis using talc, which has been widely used in the clinical field. The pleural reaction in talc grouped according to the time sequence (1st, 2nd, 4th weeks) showed a significant thickening (average thickness: 45 ± 7.5 μm, 80 ± 10.7 μm, 90 ± 12.5 μm), while the pleural reaction in sham and normal groups showed pleural change from normal to minimal thickening (average thickness: 16 ± 5.5 μm, 17 ± 4.5 μm, 15 ± 6.5 μm, and 12 ± 7.5 μm, 13 ± 2.5 μm, 12 ± 3.5 μm). The measurement of pleural reaction by pathologic examinations was well-matched with the measurement by OCT images. This is the first study for measuring the thickness of pleural reactions using a biophotonic modality such as OCT. Our results showed that OCT can be useful for evaluating the early pleural reaction.
Background : Tumor necrosis factor(TNF) has been considered as an important candidate for cancer gene therapy based on its potent anti-tumor activity. However, since the efficiency of current techniques of gene transfer is not satisfactory, the majority of current protocols is aiming the in vitro gene transfer to cancer cells and re-introducing genetically modified cancer cells to host. In the previous study, it was shown that TNF-sensitive cancer cells transfected with TNF-$\alpha$ cDNA would become highly resistant to TNF, and the probability was shown that the acquired resistance to TNF might be associated with synthesis of some protective protein. Understanding the mechanisms of TNF-resistance in TNF-$\alpha$ cDNA transfected cancer cells would be an important step for improving the efficacy of cancer gene therapy as well as for better understandings of tumor biology. This study was designed to evaluate whether the levels of TNF receptor mRNA expression and soluble TNF receptor release from cancer cells are changed after TNF-$\alpha$ cDNA transfection. Method : We transfected TNF-$\alpha$ c-DNA to WEHI164(murine fibrosarcoma cell line), NCI-H2058(human mesothelioma cell line), A549(human non-small cell lung cancer cell line), ME180(human cervix cancer cell line) cells using retroviral vector(pLT12SN(TNF)) and confirm the expression of TNF with PCR, EUSA, MTT assay. Then we determined the TNF resistance of TNF-$\alpha$ cDNA transfected cells(WEHI164-TNF, NCIH2058-TNF, A549-TNF, ME180-TNF) and evaluated the TNF receptor mRNA expression with Northern blot analysis and soluble TNF receptor release with EUSA. Results : The TNF receptor mRNA expressions of parental cells and genetically modified cells were not significantly different. The soluble TNF receptor levels of media from genetically modified cells were lower than those from parental cells. Conclusion : The acquired resistance to TNF after TNF-$\alpha$ cDNA transfection may not be associated with the change in the TNF receptor and the soluble TNF receptor expression.
Park, Jae Yong;Kim, Chang Ho;Jung, Tae Hoon;Albelda, Steven M.
Tuberculosis and Respiratory Diseases
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v.44
no.1
/
pp.162-174
/
1997
Background : Metabolic cooperation via gap junctional intercellular communication (GJIC) is an important mechanism of the bystander effect in gene therapy using the Herpes Simplex Virus thymidine kinase/ganciclovir (HSVtk) "prodrug" system. Since retinoids have been reported to increase GJIC by induction of connexin 43 expression, we hyporthesized that treatment of tumor cells with retinoic acid could augment the bystander effect of the HSVtk/GCV system and result in improved tumor cell killing by enhancing GJIC. Methods : We transferred HSVtk gene to SKHep-J cell line that does not express connexin43, and also transferred the gene to human and murine mesothelioma cell lines that express connexin43. We verified that retinoic acid enhanced GJIC utilizing a functional double-dye transfer study and evaluated the effects of retinoic acid on the growth rate of tumor cells. We then tested the effects of retinoic acid on bystander-mediated cell killing. Results : Addition of all-trans retinoic acid (RA) increased GJIC in cell lines expressing connexin 43 and was asspciated with more efficient in vitro bystander killing in cells transduced with HSVtk via adenoviral and retroviral vectors. In contrast, there was no increase in the efficiency of the bystander effect after exposure to RA in a cell line which had no delectable connexin 43. Conclusion : These results provide evidence that retinoids can augment the efficiency of cell killing with the HSVtk/GCV system by enhancing bystander effect and may thus be a promising new approach to improve responses in gene therapy utilizing the HSVtk system to treat tumors.
Cement-asbestos slate is the main asbestos containing material. It is a product made by combining 10~20% of asbestos and cement components. Man- and weathering-induced degradation of the cement-asbestos slates makes them a source of dispersion of asbestos fibres and represents a priority cause of concern. When the asbestos enters the human body, it causes cellular damage or deformation, and is not discharged well in vitro, and has been proven to cause diseases such as lung cancer, asbestos, malignant mesothelioma and pleural thickening. The International Agency for Research on Cancer (IARC) has designated asbestos as a group 1 carcinogen. Currently, most of these slats are disposed in a designated landfill, but the landfill capacity is approaching its limit, and there is a potential risk of exposure to the external environment even if it is land-filled. Therefore, this study aimed to exam the possibility of detoxification of asbestos-containing slate by using exothermic reaction and heat treatment. Cement-asbestos slate from the asbestos removal site was used for this experiment. Exothermic catalysts such as calcium chloride(CaCl2), magnesium chloride(MgCl2), sodium hydroxide(NaOH), sodium silicate(Na2SiO3), kaolin[Al2Si2O5(OH)4)], and talc[Mg3Si4O10(OH)2] were used. Six catalysts were applied to the cement-asbestos slate, respectively and then analyzed using TG-DTA. Based on the TG-DTA results, the heat treatment temperature for cement-asbestos slate transformation was determined at 750℃. XRD, SEM-EDS and TEM-EDS analyses were performed on the samples after the six catalysts applied to the slate and heat-treated at 750℃ for 2 hours. It was confirmed that chrysotile[Mg3Si2O5(OH5)] in the cement-asbestos slate was transformed into forsterite (Mg2SiO4) by catalysts and heat treatment. In addition, the change in the shape of minerals was observed by applying a physical force to the slate and the heat treated slate after coating catalysts. As a result, the chrysotile in the cement-asbestos slate maintained fibrous form, but the cement-asbestos slate after heat treatment of applying catalyst was broken into non-fibrous form. Therefore, this study shows the possibility to safely verify the complete transformation of asbestos minerals in this catalyst- and temperature-induced process.
Background: Tumor necrosis factor(TNF) showed antitumor cytolytic effects on sensitive tumor cells in numerous in vivo and in vitro studies. But it could not be administered systemically to human because of severe systemic adverse effects at effective concentrations against tumor cells. Many studies showed that a high concentrations of TNF in the local milieu may evoke in vivo TNF-responsive mechanisms sufficient to suppress tumor growth. Recently developed technique of TNF gene transfer to tumor cells using retrovirus vector could be a good candidate for local TNF administration. TNF is also known to synergistically enhance in vitro cytotoxicity of chemotherapeutic drugs targeted to DNA topoisomerase II against TNF-sensitive tumor cell lines. In this study the in vitro chemosensitivity against DNA topoisomerase II targeted chemotherapeutic drugs was evaluated using some respiratory cancer cell lines to which TNF gene had been transferred. Method: NCI-H2058, a human mesothelioma cell line, A549, a human lung adenocarcinoma cell line and WEHI 164 cell line, a murine fibrosarcoma cell line were treated with etoposide and doxorubicin, which are typical topoisomerase II - targeted chemotherapeutic agents, at different concentration. The resultant cytotoxicity was measured by MIT assay. Then the cytotoxicity of the same chemotherapeutic agents was measured after TNF-$\alpha$ gene-transfer and the two results were compared. Results: The cytotoxicity was not increased significantly in WEHI164 cell line and A549 cell line but statistically significant increase was observed in H2058 cell line when TNF-$\alpha$ gene was transferred(p<0.05). Conclusion: These findings show that TNF-$\alpha$ gene transfer to respiratory cancer cell lines results in variable effects on chemosensitivity against topoisomerase II inhibitor among different cell lines in vitro and can be additively cytotoxic in certain selective tumor cell lines.
Journal of Korean Society of Occupational and Environmental Hygiene
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v.8
no.2
/
pp.242-253
/
1998
South Korea has been producing asbestos over 60 years. The use of asbestos was over 50 years for production of asbestos slate and 27 years for asbestos friction materials including asbestos textile and brake-lining. Thus, it can be supposed that asbestos related diseases such as asbestosis, lung cancer and mesothelioma could be found in the vulnerable workers exposed to asbestos in 1955-1975, given the average latency period of 10-30 years. Asbestos was produced primarily by Japanese during World War II In Korea. The production of chrysotile peaked to 4,815 tons in 1944. From 1978 to 1984, 10,000 tons of asbestos were produced annually. However, the production was interrupted by raising labor costs and extinction of mine reserves, and finally they had to depend on import for the need of asbestos. In 1945, there were 16 asbestos mines, in total, with the addition of new asbestos mines in South Korea. Imports of asbestos was increased from 74,000 tons to 95,000 tons during the period of 1976 - 1992. But the imports was reduced to 88,000 tons in 1995. Since, in addition to the import of asbestos itself, the imports of asbestos products were increased as well and the accumulation of asbestos reached to 30,000 tons during the period of 1964 to 1993. In 1965, there was only one asbestos company with 207 employees. But the size of asbestos industry has been expanded so much that 118 asbestos companies could be found in 1993 with 1,476 workers. However, there was no record on the survey of asbestos concentration to which workers were exposed in any companies in 1983. The record of the air-borne concentration of the asbestos in textile working places in 1984 showed 6.7 fibers/cc by geometric mean(GM), but it was reduced to 1.2 fibers/cc in 1993. GMs of asbestos in working places for construction materials and asbestos textiles were also decreased from 1.7 fibers/cc to 0.55 fibers/cc during the period of 1984 - 1996.
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