• The Korean journal of internal medicine
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• v.39 no.1
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• pp.7-24
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• 2024

Post-tuberculosis lung disease (PTLD) is emerging as a significant area of global interest. As the number of patients surviving tuberculosis (TB) increases, the subsequent long-term repercussions have drawn increased attention due to their profound clinical and socioeconomic impacts. A primary obstacle to its comprehensive study has been its marked heterogeneity. The disease presents a spectrum of clinical manifestations which encompass tracheobronchial stenosis, bronchiectasis, granulomas with fibrosis, cavitation with associated aspergillosis, chronic pleural diseases, and small airway diseases-all persistent consequences of PTLD. The spectrum of symptoms a patient may experience varies based on the severity of the initial infection and the efficacy of the treatment received. As a result, the long-term management of PTLD necessitates a detailed and specific approach, addressing each manifestation individually-a tailored strategy. In the immediate aftermath (0-12 months after anti-TB chemotherapy), there should be an emphasis on monitoring for relapse, tracheobronchial stenosis, and smoking cessation. Subsequent management should focus on addressing hemoptysis, managing infection including aspergillosis, and TB-associated chronic obstructive pulmonary disease or restrictive lung function. There remains a vast expanse of knowledge to be discovered in PTLD. This review emphasizes the pressing need for comprehensive, consolidated guidelines for management of patients with PTLD.

• Tuberculosis and Respiratory Diseases
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• v.44 no.4
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• pp.871-888
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• 1997

Background : It is now thought that the earliest manifestation of idiopathic pulmonary fibrosis is alveolitis, that is, an accumulation of inflammatory and immune effector cells within alveolar walls and spaces. Inflammatory cells including alveolar macrophages and resident normal pulmonary tissue cells participate through the release of many variable mediators such as inflammatory growth factors and cytokines, which contribute to tissue damage and finally cause chronic pulmonary inflammation and fibrosis. This study was performed to investigate the source and distribution pattern of transforming growth factor-${\beta}_1$(TGF-${\beta}_1$), platelet derived growth factor(PDGF), basic fibroblast growth factor(bFGF), interleukin 1(IL-1), interleukin 6(IL-6), tumor necrosis factor-$\alpha$ (TNF-$\alpha$) and the role of these mediators on bleomycin(BLM)-induced pulmonary injury and fibrosis in rats. Method : Wistar rats were divided into three groups(control group, BLM treated group, BLM and vitamine E treated group). Animals were sacrificed periodically at 1, 2, 3, 4, 5, 7, 14, 21, 28 days after saline or BLM administration. The effects were compared to the results of bronchoalveolar lavage fluid analysis, light microscopic findings, immunohistochemical stains for six different mediators(TGF-${\beta}_1$, PDGF, bFGF, IL-1, IL-6 and TNF-$\alpha$) and mRNA in situ hybridization for TGF-${\beta}_1$. Results : IL-1 and IL-6 are maximally expressed at postbleomycin 1~7th day which are mainly produced by neutrophils and bronchiolar epithelium. It is thought that they induce recruitment of inflammatory cells at the injury site. The expression of IL-1 and IL-6 at the bronchiolar epithelium within 7th day is an indirect evidence of contribution of bronchiolar epithelial cells to promote and maintain the inflammatory and immune responses adjacent to the airways. TNF-$\alpha$ is mainly produced by neutrophils and bronchiolar epithelial cells during 1~5th day, alveolar macrophages during 7~28th day. At the earlier period, TNF-$\alpha$ causes recruitment of inflammatory cells at the injury site and later stimulates pulmonary fibrosis. The main secreting cells of TGF-${\beta}_1$ are alveolar macrophages and bronchiolar epithelium and the target is pulmonary fibroblasts and extracellular matrix. TGF-${\beta}_1$ and PDGF stimulate proliferation of pulmonary fibroblasts and TGF-${\beta}_1$ and bFGF incite the fibroblasts to produce extracellular matrix. The vitamine E and BLM treated group shows few positive cells(p<0.05). Conclusion : After endothelial and epithelial injury, the neutrophils and bronchiolar epithelium secrete IL-1, IL-6, TNF-$\alpha$ which induce infiltration of many neutrophils. It is thought that variable enzymes and $O_2$ radicals released by these neutrophils cause destruction of normal lung architecture and progression of pulmonary fibrosis. At the 7~28th day, TGF-${\beta}_1$, PDGF, bFGF, TNF-$\alpha$ secreted by alveolar macrophages sting pulmonary fibroblasts into proliferating with increased production of extracellular matrix and finally, they make progression of pulmonary fibrosis. TNF-$\alpha$ compares quite important with TGF-${\beta}_1$ to cause pulmonary fibrosis. Vitamine E seems to decrease the extent of BLM induced pulmonary fibrosis.

• Environmental Analysis Health and Toxicology
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• v.31
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• pp.13.1-13.4
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• 2016

An analysis of patients and fatalities due to exposure to polyhexamethylene guanidine (PHMG) shows that PHMG causes mainly lung diseases such as pulmonary fibrosis. However, no research on the other organs has been conducted on this matter yet. So, an in-depth discussion on toxicological techniques is needed to determine whether or not PHMG is toxic to organs other than just the lungs. For the test of target organ toxicity by PHMG exposure, a toxicokinetic study must first be conducted. However, measurement method for PHMG injected into the body has not yet been established because it is not easy to analyze polymer PHMG, so related base studies on analytical technique for PHMG including radio-labeling chemistry must come first. Moreover, research on exposure-biomarker and effect-biomarker must also be conducted, primarily related to clinical application. Several limitations seem to be expected to apply the biomarker study to the patient because much time has passed after exposure to the humidifier disinfectant. It is why a more comprehensive toxicological researches must be introduced to the causality for the victims.

• Environmental Analysis Health and Toxicology
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• v.19 no.2
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• pp.119-134
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• 2004

Human exposure to highly nickel-polluted environments, such as those associated with nickel refining, electroplating, and welding, has the potential to produce a variety of pathologic effects. Among them are skin allergies, lung fibrosis, and cancer of the respiratory tract. The exact mechanisms of nickel-induced carcinogenesis are not known and have been the subject of numerous epidemiologic and experimental investigations. This review provides the evidence of the current state for the genotoxic and mutagenic activity of Ni (II) particularly at high doses. Such doses are best delivered into the cells by phagocytosis of sparingly soluble nickel-containing dust particles. Ni (II) genotoxicity may be aggravated through the generation of DNA-damaging reactive oxygen species (ROS) and the inhibition of DNA repair by this metal. The epigenetic effects of nickel includes alteration in gene expression resulting from DNA hypermethylation and histone hypoacetylation, as well as activation some signaling pathways and subsequent transcrziption factors.

• The Journal of Korean Society for Radiation Therapy
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• v.6 no.1
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• pp.67-70
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• 1994

The use of primary breast irraditation with advantage of improved cosmesis in breast cancer may be the potential risks of radiation for a change in the number of normal breast cancers and lung fibrosis. The magnitude of the scattered dose for a variety of radiation treatment techniques from patient of breast cancer and phantom was measured by adequate dosimeters. We can reduce the dose of the normal breast to treated with radiation by understanding the factors contributing to the unwanted dose and by determining ways to decrease this dose.

• Korean Journal of Bronchoesophagology
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• v.3 no.2
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• pp.313-317
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• 1997

Airway mucus provides the protective functions such as lubrication, barrier, disposal of trapped materials, and humidification. In the normal state, the mucus do not interfere with Bas transport and the other vital functions of lung. In diseases such as asthma, bronchitis, and cystic fibrosis, the mucus hypersecretion was physiologically developed in the response of multiple neurohumoral mechanism system. And regardless of the mechanism, many clinical sequelae result from mucus hypersecretion: atelectasis, infection, increased airway resistance, increased work of breathing, increased cough with its resultant complication. And the condensation of mucus tv mucus hypersecretion can make the mucus plug by which bronchial obstruction is developed. We have experienced a 7 Pear-old male patient with recurrent pneumonic symtom, which the bronchial obstruction was developed by the impacted mucus plug on the bronchoscopic finding. We report this case with the review of literature.

• Journal of Microbiology and Biotechnology
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• v.31 no.1
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• pp.1-7
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• 2021

Bacterial biofilm is a community of bacteria that are embedded and structured in a self-secreted extracellular matrix. An important clinical-related characteristic of bacterial biofilms is that they are much more resistant to antimicrobial agents than the planktonic cells (up to 1,000 times), which is one of the main causes of antibiotic resistance in clinics. Therefore, infections caused by biofilms are notoriously difficult to eradicate, such as lung infection caused by Pseudomonas aeruginosa in cystic fibrosis patients. Understanding the resistance mechanisms of biofilms will provide direct insights into how we overcome such resistance. In this review, we summarize the characteristics of biofilms and chronic infections associated with bacterial biofilms. We examine the current understanding and research progress on the major mechanisms of antibiotic resistance in biofilms, including quorum sensing. We also discuss the potential strategies that may overcome biofilm-related antibiotic resistance, focusing on targeting biofilm EPSs, blocking quorum sensing signaling, and using recombinant phages.

• Tuberculosis and Respiratory Diseases
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• v.50 no.6
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• pp.732-739
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• 2001

Systemic lupus erythematosus frequently has thoracic involvement among connective tissue diseases. One of the pleuropulmonary manifestations is diffuse interstitial lung disease including nonspecific interstitial pneumonia(NSIP). NSIP is a newly classified disease among interstitial lung diseases. Systemic lupus erythematosus has a better prognosis than usual interstitial peumonia(UIP) and responds well to steroids. In this report, a 34 year-old woman who complained of a dry cough, and exertional dyspnea for 2 months is described. The chest X-ray showed fine reticular opacities and a mild honeycomb appearance in both basal lungs. High resolution computed tomography(HRCT) showed bilateral patchy areas of ground-glass attenuation and a mild honeycomb appearance in the subpleural of both the lower and the middle portion of the lung fields. An open lung biopsy showed prominent lymphocytic interstitial inflammation and fibrosis with small areas with a honeycomb appearance. This case was diagnosed as NSIP associated with systemic lupus erythematosus and was managed with oral steroids. Here we report a case of nonspecific interstitial pneumonia associated with systemic lupus erythematosus confirmed by HRCT and an open lung biopsy with a review of the relevant literature.

• Journal of Chest Surgery
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• v.22 no.5
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• pp.839-844
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• 1989

There appears to be significant problems remained in the treatment of tuberculous empyema with BPF in spite of several surgical methods: decortication, thoracoplasty, and pleuropneumonectomy. We presented one case of tuberculous empyema with BPF. The patient was 42-year-old male and his chief complaint was hemoptysis. In past history, he was treated with left closed thoracostomy and antituberculous medication for two months, 16 years ago. Chest X-ray, tomogram and C. T, revealed a huge mass with central necrosis in the lower 2/3 of left thoracic cavity and shifting of the mediastinal structure to the right. Needle aspiration cytology was undifferentiated large cell carcinoma. Left thoracotomy was made under the impression of lung cancer and pleuropneumonectomy was done. Operative findings; thick walled empyema sac filled with hematoma and BPF, the mediastinum was fixated due to fibrosis and calcification of the pleura and the mediastinum. Postoperative biopsy was consistent with tuberculosis. In the postoperative course, there was massive hemorrhage and so reoperation was done. But there was no active bleeding focuses in the thoracic cavity at the time of reoperation. Massive transfusion, coagulant therapy and intermittent clamping and declamping of the chest tube were carried out. Especially, serum calcium level was chronically decreased and so large amount of calcium gluconate was infused for the calcium level to be normal. Total transfused blood; whole blood was 33 pints, packed cell was 63 pints and fresh frozen plasma was 70 pints. At the postoperative[reop] 45th day, intrathoracic hemorrhage was stopped and the chest tube was removed. In conclusion, this suggest that uncontrollable bleeding after pleuropneumonectomy of the tuberculous empyema with BPF could be treated without reoperation in case of the mediastinal fixation due to fibrosis and calcification of the pleura and the mediastinum.

• Radiation Oncology Journal
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• v.13 no.4
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• pp.321-330
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• 1995

Purpose : To evaluate whether the early pulmonary irradiation can prevent or decrease the pulmonary damage and contribute to improve ultimate survival in paraquat lung. Materials and Methods : From Jun. 1987 to Aug. 1993, thirty patients with paraquat poisoning were evaluated. Fourteen of these patients were received pulmonary irradiation(RT). All of the patients were managed with aggressive supportive treatment such as gastric lavage, forced diuresis, antioxidant agents and antifibrosis agents. Ingested amounts of paraquat were estimated into three groups(A : minimal 50cc). Pulmonary irradiation was started within 24 hours after admission(from day 1 to day 11 after ingestion of paraquat). Both whole lungs were irradiated with AP/PA parallel opposing fields using Co-60 teletherapy machine. A total of 10Gy(2Gy/fr. x 5days) was delivered without correction of lung density. Results : In group A, all patients were alive regardless of pulmonary irradiation and in group C, all of the patients were died due to multi-organ failure, especially pulmonary fibrosis regardless of pulmonary irradiation. However, in group B, six of 7 patients($86{\%}$) with no RT were died due to respiratory failure, but 4 of 8 patients with RT were alive and 4 of 5 patients who were received pulmonary irradiation within 4 days after ingestion of paraquat were all alive though radiological pulmonary change. One patient who refused RT after 2Gy died due to pulmonary fibrosis. All 3 patients who were received pulmonary irradiation after 4 days after ingestion were died due to pulmonary fibrosis in spite of recovery from renal and hepatic toxicity Conclusion : It is difficult to find out the effect of pulmonary irradiation on the course of the paraquat lung because the precise plasma and urine paraquat concentration were not available between control and irradiation groups. But early pulmonary irradiation within 4 days after paraquat poisoning with aggresive supportive treatment appears to decrease Pulmonary toxicity and contribute survival in patients with mouthful ingestion of paraquat who are destined to have reversible renal and hepatic damage but irreversible pulmonary toxicity.