• Molecular & Cellular Toxicology
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• v.3 no.4
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• pp.306-313
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• 2007

The welding fume has been implicated as a causal agent in respiratory disease such as pneumoconiosis. The molecular mechanism by which welding fume induces toxicity in the lung is still unknown, but studies have focused on histological structure and indirect approach measuring the pulmonary damage markers. In the present study, gene expression profiles were analyzed in the lung of rats exposed by manual metal-arc stainless-steel (MMA-SS) welding fume for 30 days using Affymetrix GeneChip$^{(R)}$. Totally, 379 genes were identified as being either up- or down-regulated over 2-fold changes (P<0.01) in the lung of low- or high-dose group and were analyzed by using hierarchical clustering. We focused on genes involved in immune/inflammation responses were differentially regulated during lung injury induced by welding fume exposure. The information of these deregulated genes may contribute in elucidation of the inflammation mechanism during lung injury such as lung fibrosis.

• Journal of Convergence for Information Technology
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• v.11 no.11
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• pp.248-255
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• 2021

This study confirmed the effects of improving lung damage of celecoxib using an animal model of chronic obstructive pulmonary disease(COPD). It was induced in models LPS + CSE and performed in vitro and in vivo. MTT assay and real-time PCR were performed in MRC5 cells as in vitro, and mRNA expression, BALF, collagen content, and protein expression were confirmed as in vivo. Celecoxib reduced the number of inflammatory cells, cytokine and soluble protein accumulation in BALF, decreased body weight and lung weight in animal models, and improved lung collagen deposition. In addition, the reduction of EMT markers was confirmed through Western blotting and real-time PCR. Consequently, celecoxib is thought to improve lung damage of COPD induced to LPS+CSE by regulating EMT.

• Biomolecules & Therapeutics
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• v.12 no.2
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• pp.92-100
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• 2004

Effect of the depletion or oxidation of GSH on mitomycin c (MMC)-induced mitochondrial damage and cell death was assessed in small cell lung cancer (SCLC) cells. MMC induced cell death and the decrease in the GSH contents in SCLC cells, which were inhibited by z-LEHD.fmk (a cell permeable inhibitor of caspase-9), z-DQMD.fmk (a cell permeable inhibitor of caspase-3) and thiol compound, N-acetylcysteine. MMC caused nuclear damage, release of cytochrome c and activation of caspase-3, which were reduced by N-acetylcysteine. The depletion of GSH due to L-butionine-sulfoximine enhanced the MMC-induced cell death and formation of reactive oxygen species in SCLC cells, whereas the oxidation of GSH due to diamide or $NH_2Cl$ did not affect cytotoxicity of MMC. The results show that MMC may cause cell death in SCLC cells by inducing mitochondrial dysfunction, leading to activation of caspase-9 and -3. The MMC-induced change in the mitochondrial membrane permeability, followed by cell death, in SCLC cells may be significantly enhanced by the depletion of GSH. In contrast, the oxidation of GSH may not affect cytotoxicity of MMC.

• Toxicological Research
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• v.25 no.4
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• pp.217-224
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• 2009

Inhaled inorganic dusts such as coal can cause inflammation and fibrosis in the lung called pneumoconiosis. Chronic inflammatory process in the lung is associated with various cytokines and reactive oxygen species (ROS) formation. Expression of some cytokines mediates inflammation and leads to tissue damage or fibrosis. The aim of the present study was to compare the levels of blood cytokines interleukin (IL)-$1\beta$, IL-6, IL-8, tumor necrosis factor (TNF)-$\alpha$ and monocyte chemoatlractant protein (MCP)-1 among 124 subjects (control 38 and pneumoconiosis patient 86) with category of chest x-ray according to International Labor Organization (ILO) classification. The levels of serum IL-8 (p= 0.003), TNF-$\alpha$ (p=0.026), and MCP-1 (p=0.010) of pneumoconiosis patients were higher than those of subjects with the control. The level of serum IL-8 in the severe group with the small opacity (ILO category II or III) was higher than that of the control (p=0.035). There was significant correlation between the profusion of radiological findings with small opacity and serum levels of IL-$1\beta$(rho=0.218, p<0.05), IL-8 (rho=0.224, p<0.05), TNF-$\alpha$ (rho=0.306, p<0.01), and MCP-1 (rho=0.213, p<0.01). The serum levels of IL-6 and IL-8, however, did not show significant difference between pneumoconiosis patients and the control. There was no significant correlation between serum levels of measured cytokines and other associated variables such as lung function, age, BMI, and exposure period of dusts. Future studies will be required to investigate the cytokine profile that is present in pneumoconiosis patient using lung specific specimens such as bronchoalveolar lavage fluid (BALF), exhaled breath condensate, and lung tissue.

• Journal of Microbiology and Biotechnology
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• v.18 no.2
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• pp.369-376
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• 2008

In the present study, we investigated the radioprotective effect of cyclo(L-phenylalanyl-L-prolyl) on irradiated rat lungs to determine its potential as a radioprotective agent. We found that early lung damage induced by irradiation was reduced by treatment with 40mg/kg of cyclo(L-phenylalanyl-L-prolyl) in the latent and early pneumonitis phases. Expression of $TNF-{\alpha}\;and\;TGF-{\beta}1$ at 2 and TGF-${\beta}1$ at 8 weeks post-irradiation was decreased in animals that received both radiation and cyclo(L-phenylalanyl-L-prolyl) compared with animals that received radiation alone. Evidence indicated that the proinflammatory cytokine TNF-${\alpha}$ and the fibrogenic cytokine TGF-${\beta}1$ likely play a role in the radioprotective effect of cyclo(L-phenylalanyl-L-prolyl). However, besides TNF-${\alpha}$ and TGF-${\beta}1$ expressions, the precise mechanism by which cyclo(L-phenylalanyl-L-prolyl) ameliorates the induced radiation damage is not clear.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.595-607
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• 2008

Objectives: The aim of this study was to determine the effects of Salvia miltiorrhiza (SM) extract in urethane-induced lung tumorigenesis in A/J mice. Methods : We examined change of body weight, histological, apoptosis, immunohistochemical and gene expression of cyclooxygenase (COX-2) in lung tumors. Mice were divided into 3 groups: normal, saline, and experimental group administered SM extract after injection with urethane. Results : Histological observation showed shrunken alveoli in the control group, but recovered from damage in the SM extract administered group. The COX-2 positive materials were observed in the smooth muscle of terminal bronchiole and alveoli from the control group, but these positive materials decreased in the SM extract treatment group. The results of electron microscopical observation, dilated capillary and degenerated endothelia were observed in the control group. The apoptotic nuclei increased more in the control group compared with the normal and SM extract administered groups. Serial sections of the whole lung showed solid and papillary tumors. The size and number of tumors decreased in the SM groups compared with the control groups. Conclusions : These results suggest the possibility that SM may exert an anti-tumor effect on urethane-induced lung tumorigenesis.

• Journal of Physiology & Pathology in Korean Medicine
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• v.26 no.5
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• pp.577-587
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• 2012

Warm disease: Any of various heat disease characterizer by rapid onset and shifts, pronounced heat signs, and a tendency to form dryness and damage yin. Exterior heat sign: exterior heat patterns are characterizer by pronounced heat signs, such as a red sore pharynx and a relatively red tongue with dry fur, the pulse is floating and rapid, cough and the production of thick white or yellow phlegm. If wind-heat evil exist in weifen, it becomes exterior syndrome, and a remedy about that is dispelling wind-heat but when wind-heat evil invades in nasal and throat part so the disease occurs, you need to add relieving sore throat worsens invades in lung it makes disharmony of diffuse in lungs. So a remedy about it is diffuse the lung. disharmony of diffuse in lungs makes metabolic disorder of qi and liquid and humor malfunction therefore it occurs cough and heat-phlegm syndrome. heat from weifen invades the whole of lungs and form lung heat. So a remedy about lung heat is clearing away lung heat, this lung heat makes inevitably bleed in lungs, therefore a remedy in this case is clearing the lung to stop bleeding, or moistening the lung. Exterior heat sign means that exterior syndrome coexists with heat syndrome and it means that a remedy of this syndrome need to mix prescriptions for relieving exterior syndrome and heat-clearing prescriptions to treat this syndrome.

• Journal of Life Science
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• v.20 no.11
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• pp.1725-1728
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• 2010

Miniature pigs are widely used in experiments related to pulmonary disease because of their similarities with humans. However, there are not enough data about normal lung function in miniature pigs. Thus, in this study, we investigated normal lung function in miniature pigs with lung ventilation/perfusion scintigraphy and evaluated the availability of this method. Three male miniature pigs weighing 30-35 kg were used. After general anesthesia, ventilation scintigraphy was performed with 100 MBq of $^{99m}Tc$-pertechnetate (${O_4}^-$), after which perfusion scintigraphy was performed with intravenous injection of $^{99m}Tc$-macro aggregated albumin (MAA). The functional contribution of the right lung was about 55%, and left lung was about 45%, similar to humans. Lung ventilation/perfusion scintigraphy was very useful in evaluating the normal lung function of miniature pigs because it was a non-invasive procedure (no tissue damage was involved), took a short time and was easy to perform. In conclusion, miniature pigs are similar to humans in functional contributions of the lung, and this method will be helpful in future pulmonary disease studies involving miniature pigs.

• Journal of Chest Surgery
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• v.27 no.5
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• pp.345-352
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• 1994

We have performed left lung transplantation followed by ligation of right pulmonary artery in 14 dogs at the Chest Disease Research Institute, Yonsei University College of Medicine from May 1992 to February 1994. Excised left lung was perfused with 1500cc of 4$^{\circ}$C cold Euro-Collin`s[E-C] solution at a pressure of 30cmH2O through main pulmonary artery and preserved in 4$^{\circ}$C cold E-C solution for one hour. Left lung transplantation were proceeded in order of left atrium, left main bronchus, left pulmonary artery and right pulmonary artery ligation as usual method. The femoral artery and pulmonary artery pressures were monitored for more than 5 hours after the transplantations in 14 dogs. Six recipient dogs had elevated mean pulmonary artery pressure to greater than 30mmHg after the left lung transplantation and ligation of right pulmonary artery. The cause of elevated mean pulmonary artery pressure was due to inadequate preservation resulting in ischemic damage to donor lungs in 3 cases, and inadequate surgical techniques in 3 cases. Two recipient dogs without surgical complications died immediate post-operatively due to hemorrhagic shock. The bleeding focuses were LA anastomotic site in one case and femoral artery puncture site in another case. The remaining 6 recipient dogs showed mean pulmonary arterial pressure less than 30mmHg. However, one dog had spontaneous pneumothorax in post-operative 4 days, and another dog had rejection phenomenon in post-operative 5 days which was confirmed by pathologic findings of extracted transplanted lung. One dog succumbed of severe hemoptysis which was due to lung abscess with pin point stenosis of bronchial anastomosis in post-operative 38 days. In conclusion, elevated mean pulmonary arterial pressure greater than 30mmHg in immediate postoperative period can be due to inadequate preservation of extracted lung or poor surgical techniques. And the two dogs succumbed of hemorrhagic shock even though the mean pulmonary arterial pressure was less than 30mmHg. It is thought that careful preservation of the extracted donor lung in 4oC E-C solution and complete surgical techniques are the most important factors early and late complications.

• Journal of Chest Surgery
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• v.56 no.1
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• pp.6-13
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• 2023

Background: Coronavirus disease 2019 (COVID-19) has been found to cause life-threatening respiratory failure, which can progress to irreversible lung damage. Lung transplantation can be a life-saving treatment in patients with terminal lung disease (e.g., acute respiratory distress syndrome caused by infection). This study aimed to present the clinical course and results after initial lung transplantation in patients with severe COVID-19 who did not recover even with optimal medical care. Methods: From August 2019 to February 2022, this study enrolled 10 patients with COVID-19 (5 men; median age, 55.7 years) who underwent lung transplantation at a single center in Korea. All patients' characteristics, clinical pathway, overall survival, complications, and operative data were collected and analyzed. Results: Veno-venous extracorporeal membrane oxygenation or an oxygenator in a right ventricular assist device circuit was applied to 90% of the patients, and the median length of extracorporeal life support before operation was 48.5 days. There were no cases of mortality after a median follow-up of 372.8 days (interquartile range, 262.25-489 days). The major complications included the requirement for postoperative extracorporeal membrane oxygenation support in 2 cases (20%), re-transplantation in 1 case (10%), and re-exploration due to bleeding in 2 cases (20%). During the follow-up period, 3 out of 10 patients died. Conclusion: Excellent early outcomes were observed for patients who underwent lung transplantation. Thus, lung transplantation can be an effective and feasible treatment for patients with end-stage lung disease caused by COVID-19.