Experimental studies were done to research the clinical effect of Insamyounpaesan and Insamyounpaesangamibang on viscousity of mucin solution, pulmonary thromboembolism, oxygen consumption in $O_3$ - exposed and Lung TBA in rats and mice. The result was obtained as follows: 1. In the effect of Insamyounpaesan and I nsamyounpaesangami-bang on the rate of viscousity sampled from mucin, Insam-younpaesan and Insamyounpaesangamibang were revealed to have a significant effect of decreasinf the rate of viscousity (p<0.05). 2. In the effect of Insamyounpaesan and Insamyounpaesangami-bang on sodium arachidonic acid induced pulmonary thrombo-embolism, Insamyounpaesan and Insamyounpaesangarnibang were revealed to have an effect of increasing the number of survival(p<0,05), but were not significant. 3. In the effect of Insamyounpaesan and Insamyounpaesangami-bang on ADP induced pulmonary thromboembolism, Insam-younpaesangamibang were revealed to have an effect of increasing the number of survival(p<0.05), but were not significant. 4. In the effect of Insamyounpaesan and Insamyounpaesangami-bang on oxygen cansumption values in rats exposed, Insamyounpaesan and Insamyounpaesangamibang were revealed to have a significant effect on the care of lung damages (p<0.05), but were not significant by Duncan's multiple comparision test. 5. In the effect of Insamyounpaesan and Insamyounpaesangami-bang on the lung TBA values in rats exposed $-O_3$, Insam-younpaesangamibang were revealed to have a significant effect (p<0.05) on the care of lung damages. In connection with the results of the studies, Insamyounpaesan and Insamyounpaesangamibang are concluded to be effective on the treatment of cough and lung and respiratory organ damages.
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.
Metallothionein gene expression activity of cadmium was investigated in a human lung epithelial cell line. Cells, grown to near confluence, were exposed to 0∼10 ${\mu}$M Cd metal for 6 hours. Cadmium did not cause morphological alteration in lung epithelial cells that are characteristic of cell damages such as cell shrinkage, detachment of the cell from its neighbors, cytoplasmic and chromatic condensation. However, metallothionein genes of MT-1 and MT-2 were rapidly induced in the treated cell measured by RT-PCR. Regarding the induction pattern of motallothionein mRNA, MT-1 mRNA was induced in a dependent manner. MT-2 mRNA induction, which was measured using oligo primers based on cDNA of human reticulocytes, seemed to be slightly increased in low doses but decreased at high concentration used in the experiment.
Three synthetic chemicals, benzoyl chloride, 2-propyn-l-ol, and 2-phenoxy ethanol were selected for genotoxicity testing, based on production quantity and available genotoxic data. In our previous report, benzoyl chloride induced chromosomal aberrations in Chinese hamster lung (CHL) fibroblast in vitro with and without metabolic activation, while 2-propyn-l-ol and 2-phenoxy ethanol induced only with metabolic activation. To compare the genotoxicity of chromosome aberration assay, the single cell gel electrophoresis (comet) assay subjected using CHL cells. As a result, statistically significant differences of tail moment values of benzoyl chloride, 2-propyn-1-ol, and 2-phenoxy ethanol were observed compared with control values on almost all concentrations with S9 or without S9 metabolic activation system. This results suggest that genotoxic results of the comet assay and the chromosome aberration assay show correlationship of genotoxicity in the CHL fibroblast. In summary, the positive result of chromosome aberration of benzoyl chloride, 2-propyn-l-ol, and 2-phenoxy ethanol was also induced DNA damages in comet assay with same cell line. Consequently, comet assay will be useful and more accurate tool to detect and to confirm the genotoxicity especially DNA damages in CHL fibroblast.
The present study was carried out to elucidate whether an environmental strain of Cryptococcus neoformans (environmental C. neoformans) isolated from an environmental source in a park of Busan has an acute pathophysiological effect in rats. On the second day after peritoneal inoculation of environmental C. neoformans, adverse effects occurred from the viewpoint of hematology and biochemistry. Eosinophil damages and crystal formations were found in the blood. Disturbances in cytokines production were observed in the cerebral and pulmonary tissues. Fungal budding existed in the brain, lung, liver and kidney. Tissue injury findings such as inflammation, leukocyte infiltration, bleeding, or degeneration were found in the brain, lung, liver and kidney. The present data suggest that the environmental C. neoformans can cause systematically harmful effects even for short periods of infection (two days of cryptococcal infection) and the adverse effects are summarized as immune derangements and biochemical and/or histological dysfunction and injury on major organ such as the brain, lung, liver and kidney in the immunocompetent hosts. Further studies should be focused on comparing the differences between environmental and clinical strains of C. neoformans.
Journal of the Korean Association of Oral and Maxillofacial Surgeons
/
v.26
no.1
/
pp.5-17
/
2000
To evaluate the possible therapeutic effects of growth hormone and vitamin C on multiorgan failure, a rat model was developed for LPS-induced sepsis. Using this model, the effects of growth hormone and vitamin C on tissue damages, catalase and i-NOS activities, and MDA levels were examined in the lung and liver. The level of TNF- in plasm was also examined. Male, Sprague-Dawley rats were injected with LPS intraperitoneally then divided into 3 groups : positive controls injected with LPS only, the ones injected with growth hormone or vitamin C immediately after the LPS injections. The lung and the liver were then isolated, blood samples were collected at 24 or 48 hours after the LPS injection, then examined for histopathological and biochemical changes. The results obtained were as follows. 1. LPS induced sinusoid vasodilation and mild destruction of lobular structure in the liver. In the lung, alveolar structure appeared to be thickened and interstitial edema was observed. The levels of MDA in the liver and the lung was increased by LPS, while the activity of catalase was decreased. The activity of i-NOS of those tissues was also increased, which was more pronounced at 24 hr. The level of TNF- in plasm was increased by LPS 2. In the lung, vitamin C suppressed lymphocyte and neutrophil infiltration, alveolar wall thickening and interstitial edema. In the liver, vitamin C protected against the destruction of the lobular structure. The activity of catalase reduced by LPS was reversed partly by vitamin C. The activity of i-NOS enhanced by LPS was also reversed by vitamin C. The level of TNF- in plasm reduced in some animals by vitamin C, which however was not significant statistically(p<0.05). 3. Growth hormone showed similar protective effects against inflammation and damages in the liver and lung tissues. Growth hormone reversed partly the LPS effects on the level of MDA, the activity of catalase and i-NOS induction in the liver and the lung. Growth hormone reduced plasma level of TNF-${\alpha}$ substantially, which contrasted from vitamin C. Besides this, overall protective effects of growth hormone against LPS-induced experimental sepsis were similar to those of vitamin C. From this results, the mechanism of growth hormone on suppression of LPS-induced tissue damage might be associated with production of antioxidative enzyme and suppression of plasma TNF- level.
In the Literatual Study on the Dysphonia, the results were as follows. 1. The causes of dysphonia are exogenous pathogenic factors,(specially cold evil)internal damage and meridian in The Yellow Emperor's Canon of Interal Medicine, since then endogenous pathogenic factors are lung-asthenia and deficiency of lung-yin etc. The main causes are disease caused by exogenous evils, general body weakness, emotional stimulation and excess of high voice rescently. 2. The pathogenesis of dysphonia originated from two factors; The first internal damages are consumption of body fluid with the formation of dryness evil resulting from the insufficienty of lung-yin and lung-collaterals damaged by heat-evil caused by deficiency of lung and kidney-yin. The second disease caused by exogenous evils is sluggishness of lung-energy caused by exogenous pathogenic factors. 3. The main relative organ are heart, lung and kidney etc. 4. The prescriptions of wind-cold symptoms are Samyoutang(三拗湯) and Hangsosan(杏蘇散), in the prescriptions of phlegm-heat symptom is Chenginyongphetang(淸咽寧肺湯), in the prescriptions of depressive syndrome due to disorder of vital energy are Sogangkitang(小降氣湯) and Shihochenggantang(柴胡淸肝湯加減), in the prescriptions of consumption of body fluid with the formation of dryness evil resulting from the insufficiency of lung-yin symptoms are Sanghangtang(桑杏湯) and Chenginguphetang(淸咽救肺湯, in the prescriptions of deficiency of lung and kidney-yin are Baekhabgokumtang(百合固金湯) and Maekmigiwhangtang(麥味地黃湯). 5. The treatment of acupunctures are used by LI-4(合谷), H-7(湧泉), Liv-3(太衝), K-3(太谿), Sp-6(三陰交), H-5(通里), GV-15(아門), CV-23(廉泉), S-40(農隆), K-6(照海), L-7(列缺), S-36(足三里) etc.
Objectives : The purpose of this paper is to extinguish the debates surrounding the sentences found in Suwen Kailun that deal with flocking to stomach and closure in lung. The paper seeks to do this through studying the assertions of historical doctors and their theories regarding the topic. Methods : The interpretations of annotators regarding these sentences were studied, and text DB was searched to collect and analyze materials related to the theories of the relationship between stomach and lung. Results : The sentences of flocking to stomach and closure in lung, judging from their contexts, seem to be related to the symptom of Sanjiao ke or Liufu ke. However, they may be pointing to internal organs' ke as a whole based on the close relationship between stomach and lung. They could mean either the abnormality of mechanism of stomach and lung could cuase ke or that Zhuoqi could accumulate inside of stomach to cause phlegm-fluids thereby blocking thorax and causing cough. Theory of Warm disease, too, provides a number of treatment suggestions for stomach, lung damages such as supporting Yin and dispersing dampness. Conclusions : The study of the sentences regarding flocking to tomach and closure in lung is expected to not only provide an analysis of the sentences, but also provide a perspective and a method for clinical treatments.
Lee Hyung Sik;Choi Young Min;Hur Won Joo;Jeong Jin Sook;Yuh Young Hyun;Lee Ki Nam
Radiation Oncology Journal
/
v.12
no.2
/
pp.143-150
/
1994
The damage which radiation produces in tissues such as the lungs can be discussed at the molecular, biophysical, cellular, and organ levels. The cellular effects of irradiating the lungs are related to the histologic and clinical sequelae. In the present study the right lung of rabbits were exposed to single dose of 20 Gy of X-irradiation. Animals from each group were sacrificed monthly for 6 months postexposure. Sections of lung were examined by light microscopy(LM) and by transmission electron microscopy(TEM). Multiple exudative lesions were seen at 2 months after the 20Gy irradiation,and they progressed to a proliferative and then reparative fibrotic lesion by 6 months. Changes in epithelial lining of lung components, particulary the presence of type II pneumocytes were found by both LM and TEM. Capillary endothelial damages were less pronounced. The possible implication of cellular components in radiation pneumonitis and fibrosis is discussed.
Experimental studies were done to research the clinical effect of Insamyunpye-H wan on viscousity of mucin solution, pulmonary thromboembolism, oxygen consumption in $O_3$-exposed and Lung TBA in rats and mice. The result was obtained as follows : 1. In the effect of viscosity sampled from mucin, Insamyunpye-Hwan was revealed to have a significant effect of decrease in the rate of viscousity (p<0.01). 2. In the effect of sodium aracdonic acid induced pulmonary thromboembolism, I samyunpye-Hwan was revealed to have an effect of increasing the number of survival, but were not significant 3. In the effect of ADP induced pulmonary thrornboembolism, Insamyunpye-Hw an was revealed to have an effect of increasing the number of survival, but were not significant 4. In the effect of oxygen cansumption values in rats exposed-$O_3$, Insarnyunpye-Hwan was revealed to have a significant effect (p<0.05). 5. In the effect of the lung TBA values in rats exposed-$O_3$, Isamyunpye-Hwan was revealed to have a significant effect (p<0.05). In connection with the results of the studies, Insamyunpye-Hwan is concluded to be effective on the treatment of cough and lung and respiratory organ damages.
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