• Title/Summary/Keyword: lung damages

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A Case of Asymptomatic, Localized, and Idiopathic Diffuse Alveolar Damage

  • Jeon, Young-Do;Hong, Christian;Joh, Joon-Sung;Jung, Ja-Young;Min, Ji-Won;Park, Seon-Young;Lee, Ga-Ram
    • Tuberculosis and Respiratory Diseases
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    • v.72 no.4
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    • pp.386-389
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    • 2012
  • Diffuse alveolar damage (DAD) is a histological change in lung tissue, and is generally caused by an acute lung injury, which is characterized by bilateral and widespread damages. Localized DAD occurs very rarely. The causes for DAD are numerous, but the chief cause is acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia, in cases of idiopathic manifestation. The 82-year-old patient, in this case study, showed a DAD lesion in only 1 lobe. The patient was otherwise healthy, with no previous symptoms of DAD. He was admitted to our medical center owing to localized infiltration, observed on his chest radiograph. Laboratory studies showed no signs of infections. DAD was confirmed by a surgical lung biopsy. The patient received corticosteroid treatment and had gradually improved. We report the case of a patient with localized, idiopathic DAD that cannot be classified as acute interstitial pneumonia or acute exacerbation of idiopathic interstitial pneumonia.

Oxidative Damage in rats by Inhalation Exposure to Hexavalent Chromium (흰쥐의 6가 크롬 흡입폭로에 의한 산화적 손상에 관한 연구)

  • 맹승희;유일재;김현영;임철홍;이용묵;정호근;정해원
    • Environmental Mutagens and Carcinogens
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    • v.22 no.4
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    • pp.279-288
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    • 2002
  • According to the epidemiological studies in chromium workers, hexavalent chromium is associated with the risk of lung cancer. Cellular oxidative damages by reactive oxygen species produced by hexavalent chromium exposure may play an important role in the carcinogenesis process. We investigated the availabilities of malondialdehyde measurement for the assessments of oxidative damages from chromium exposure with an experimental inhalation study in vivo. Lipid peroxidation, one kind of cellular oxidative damage, was measured in blood plasma of the rats which inhaled the hexavalent chromium mist for 1, 2 and 3 weeks. The concentrations of malondialdehyde (MDA), the metabolite of lipid peroxidation, in all exposed groups were higher than those of controls with dose-dependant manner. The levels of MDA were also correlated with urine chromium levels of the rats. Therefore, MDA as an indicator of lipid peroxidation could be proper biologic marker for the assessment of the oxidative damage from chromium exposure, which might be involved in carcinogenesis.

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Characterization of Antioxident Enzymes in the Lung of Rat Exposed to Cigarette Smoke (흡연한 흰쥐 폐조직 항산화효소들의 특성)

  • 이영구;손형옥;임흥빈;이동욱;박준영
    • Journal of the Korean Society of Tobacco Science
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    • v.15 no.1
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    • pp.3-14
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    • 1993
  • Oxidants in environment or cigarette smoke are known to be implicated in the oxidative damages of pulmonary system. Such cellular damages are prevented by the presence of adequate levels of antioxidants in the tissue. In the present study, we investigated the influences of smoking duration and concentration of smoke on lung antioxidant defense in rats. Subchronic exposure of rats to smoke generated from 6 cigarettes per day for 90 days caused the activities of catalase and superoxide dismutase (SOD) to increase. However, glutathione peroxidase (GP-Xase) was not significantly changed. Total sulfhydryl compounds (Total-SH) in the lung homogenates from the rats inhaled with cigarette smoke for 15 days was decreased by 44% , thereafter it was returned to the level of normal rats. On the contrary, when rats were daily exposed to a different concentration of smoke generated from 1 to 20 cigarettes per day for 15 days, the activity of catalase was increased gradually with dose, but total SOD activity was increased only in the rats of low dose groups less than 5 cigarettes. Three types of SOD (one Cu, Zn-SOD with pI 4.9, and two Zn-SOD with pI 4.7 and 7.9)were detected in the lung homogenates and Zn-SOD with pI 4.7 was the major and cigarette-smoke inducible form. These results indicate that the protection of lung against oxidants from cigarette smoke seems to be accomplished by the induction of catalase and SOD, especially a cyanide resistant Zn-SOD with pI 4.f, following the consumption of antioxidants such as GSH in the beginning of inhalation period.

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Voice Features Extraction of Lung Diseases Based on the Analysis of Speech Rates and Intensity (발화속도 및 강도 분석에 기반한 폐질환의 음성적 특징 추출)

  • Kim, Bong-Hyun;Cho, Dong-Uk
    • The KIPS Transactions:PartB
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    • v.16B no.6
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    • pp.471-478
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    • 2009
  • The lung diseases classifying as one of the six incurable diseases in modern days are caused mostly by smoking and air pollution. Such causes the lung function damages, and results in malfunction of the exchange of carbon dioxide and oxygen in an alveolus, which the interest is augment with risk diseases of life prolongation. With this in the paper, we proposed a diagnosis method of lung diseases by applying parameters of voice analysis aiming at the getting the voice feature extraction. Firstly, we sampled the voice data from patients and normal persons in the same age and sex, and made two sample groups from them. Also, we conducted an analysis by applying the various parameters of voice analysis through the collected voice data. The relational significance between the patient and normal groups can be evaluated in terms of speech rates and intensity as a part of analized parameters. In conclusion, the patient group has shown slower speech rates and bigger intensity than the normal group. With this, we propose the method of voice feature extraction for lung diseases.

An analysis of the potential impact of various ozone regulatory standards on mortality

  • Kim, Yong-Ku
    • Journal of the Korean Data and Information Science Society
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    • v.22 no.1
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    • pp.125-136
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    • 2011
  • Ground-level ozone, an air pollutant that is monitored by the Environmental Protection Agency (EPA), damages human health by irritating the respiratory system, reducing lung function, damaging lung cells, and aggravating asthma and other chronic conditions. In March 2008, the EPA strengthened ozone standards by lowering acceptable limits from 84 parts per billion to 75 parts per billion. Here epidemiologic data is used to study the effects of ozone regulation on human health and assessed how various regulatory standards for ozone may affect nonaccidental mortality, including respiratory-related deaths during ozone season. The assessment uses statistical methods based on hierarchical Bayesian models to predict the potential effects of the different regulatory standards. It also analyzes the variability of the results and ho they are impacted by different modeling assumptions. We focused on the technical an statistical approach to assessing relationship between new ozone regulations and mortality while other researches have detailed the relationship between ozone and human mortality. We shows a statistical correlation between ozone regulations and mortality, with lower limits of acceptable ozone linked to a decrease in deaths, and projects that mortality is expected to decrease by reducing ozone regulatory standards.

Pulmonary Fibrosis caused by Asbestos Fibers in the Respiratory Airway

  • Jung, Ji-Woo;Kim, Eung-Sam
    • 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.

THE ASSESSMENT OF GENOTOXICITY AND LIPID PEROXIDATION IN CHROMIUM EXPOSED WORKERS

  • Maeng, Seung-Hee;Yu, Il-Je;Lee, Byung-Moo;Chung, Ho-Keun;Chung, Hai-Won
    • Proceedings of the Korean Society of Toxicology Conference
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    • 2002.05a
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    • pp.67-67
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    • 2002
  • According to the epidemiological studies in chromium workers, hexavalent chromium is associated with the risk of lung cancer. Genotoxicity such as chromosome aberration, and cellular oxidative damages by reactive oxygen species produced by hexavalent chromium exposure may play an important role in the carcinogenesis process.(omitted)

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Anti-inflammatory Activity of Chihyo-san to Protect Respiratory Tissues from Asthmatic Damage

  • Cho, Ju-Hyung;NamGung, Uk;Kim, Dong-Hee
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.20 no.3
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    • pp.710-718
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    • 2006
  • The present study was carried out to investigate the effect of Chihyo-san (CHS) administration on asthma induced by Alum/OVA treatment in the mice. In CHS-treated animal group, lung weight, which was increased after asthma induction, was significantly decreased, and total number of cells in the lung, peripheral lymph node (PLN) and spleen tissue was significantly decreased in CHS-treated group compared to the asthma control group. The number of immune cells including natural killer (NK) cells in asthmatic animals was largely regulated by CHS treatment, showing a similar pattern as that of CsA-treated positive control group. Levels of mRNAs encoding inflammatory cytokines IL-5, IL-13, $TNF-{\alpha}$, and eotaxin were determined by RT-PCR in the lung tissue and showed decreases in CHS-treated group to the similar levels of CsA-treated control group, Histamine level in the serum was significantly lower in CHS-treated group than asthma-induced control group. Both haematoxylin and eosin staining and Masson's trichrome staining results showed decreased number of inflammatory cells, reduced immune cell infiltration, and normalized epithelial cell layering in the bronchial tissue of CHS-treated mouse group. Thus, the present findings suggest that CHS may be useful for protecting bronchial tissues from consistent inflammatory damages that occur in asthma patients.

A Literature study on the language disturbance (聲音의 生理 病理에 關한 文獻的 考察)

  • Lee, Won-Ju;Kim, Yeon-Jin;Rho, Sek-Seon
    • The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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    • v.10 no.1
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    • pp.159-184
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    • 1997
  • A Literature study on the language disturbance, the results are as follows; 1. Utterance was closely concerned not only the vocal organs(pharynx, larynx, epiglottis, lips, tongue, vocal cord etc,) but also five viscera{especially heart, lung, kidney etc.) in The Yellow Emperor's Canon of Internal Medicine. It is very like the vocal mechanism in Medical science. 2. In the language disturbance, It is classified with dysarthria and dysphasia in Medical science. But in Oriental medicine, it is expressed the language disturbance as coma-speech lessness, stiff tongue-speechlessness, frightening-speechlessness etc. Especially in Oriental medicine, Non-utterance is called aphasia in literature study. 3. In the concern of the language disturbance and five viscera, $Heart{\cdot}Lung{\cdot}Kidney$ are counted of first importence. In differential diagnosis, It is divided sthenia-syndrome and asthenia-syndrome. Sthenia-syndrome is classified with wind-cold, fire-evil, adverseness of vital energy, stagnation of phlegm, is easy to cure. Asthenia-syndrome is classified with sexual desire, anxiety-meditation, fear, is hard to cure. 4. The pathogenesis of dysphasia originated from two factors; The first internal damages are consumption of body fluid caused by lung-dryness and yin-dificiency of lung & kidney. The second disease caused by exogenous evjls is sluggishness of lung-energy. 5. In many using points of acupuncture of the language disturbance, the order is LI-4(合谷), H-7(神門), K-l(湧泉), L-3(太衝), K-3(太谿), S-6(三陰交), H-5(通里), G-15(아門), C-23(廉泉), S-40(豊降), K-6(照海), L-7(列缺), S-36(足三里) etc.

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The Effects of Steroid on Acute Lung Injury in the Mouse Induced by Whole Lung Irradiation (전폐조사로 유발된 마우스의 급성폐손상에 대한 스테로이드의 효과)

  • Sung, Nak-Kwan;Shin, Sei-One;Kwon, Kun-Young
    • Radiation Oncology Journal
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    • v.15 no.1
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    • pp.37-47
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    • 1997
  • Purpose : To investigate ultrastructural changes of the mouse lung induced by whole lung gamma irradiation and to evaluate the effect of prophylactic administration of steroid against acute lung injury. Materials and Methods :. One hundred and twenty ICR mice were used and whole lung was irradiated with telecobalt machine. Whole lung doses were 8 and 12Gy, and 10mg of methyl prednisolone was administrated intraperitoneally for two and four weeks. At the end of the observation period, mice were sacrificed by cervical dislocation. The lungs were removed and fixed inflated. Histopathological examination of acute radiation injuries were Performed by light microscopic and transmission electron microscopic examination. Results : Control group with BGy is characterized by damage to the type I Pneumocyte and the endothelial cell of the capillary. edema of alveolar wall and interstitium. and fibroblast proliferation. Control group with 120y is characterized by more severe degree of type 1 pneumocyte damage and more prominant inflammatory cell infiltration. Destructed cell debris within the alveolar space were also noted After steroid administration, 8Gy experimental group showed decreased degree of inflammatory reactions but fibroblast proliferation and basal lamina damages were unchanged. Experimental group with 12Gy showed lesser degree of inflammatory reactions similar to changes of 8Gy experimental group. Conclusion : These studies suggest that the degree of interstitial edema and inflammatory changes were related to radiation dose but Proliferation of the fibroblast and structural changes of basal lamina were not related to radialion dose. Experimental administration of steroid for 2 to 4 weeks after whole lung irradiation suggest that steroid can suppress alveolar and endothelial damages induced by whole lung irradiation but Proliferation of the fibroblast and structural changes of basal lamina were not related to administration of steroid.

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