• Molecules and Cells
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• v.45 no.12
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• pp.896-910
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• 2022

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a highly transmissible and potentially fatal virus. So far, most comprehensive analyses encompassing clinical and transcriptional manifestation have concentrated on the lungs. Here, we confirmed evident signs of viral infection in the lungs and spleen of SARS-CoV-2-infected K18-hACE2 mice, which replicate the phenotype and infection symptoms in hospitalized humans. Seven days post viral detection in organs, infected mice showed decreased vital signs, leading to death. Bronchopneumonia due to infiltration of leukocytes in the lungs and reduction in the spleen lymphocyte region were observed. Transcriptome profiling implicated the meticulous regulation of distress and recovery from cytokine-mediated immunity by distinct immune cell types in a time-dependent manner. In lungs, the chemokine-driven response to viral invasion was highly elevated at 2 days post infection (dpi). In late infection, diseased lungs, post the innate immune process, showed recovery signs. The spleen established an even more immediate line of defense than the lungs, and the cytokine expression profile dropped at 7 dpi. At 5 dpi, spleen samples diverged into two distinct groups with different transcriptome profile and pathophysiology. Inhibition of consecutive host cell viral entry and massive immunoglobulin production and proteolysis inhibition seemed that one group endeavored to survive, while the other group struggled with developmental regeneration against consistent viral intrusion through the replication cycle. Our results may contribute to improved understanding of the longitudinal response to viral infection and development of potential therapeutics for hospitalized patients affected by SARS-CoV-2.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2003.05a
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• pp.514-517
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• 2003

Oxygen supply is one of the most basic things in human body. Breathing is controlled by the lungs' stationary function and the respiratory center which is in the mesulla oblongata. Nothing but, the external breathing that air movement between the lungs and atmosphere and the internal breathing that cellular air movement between the hemoglobin and a single cell. The adult's number of times of the respirations is about 15∼20 per 1 minute, but it depends ages, exercise, temperature, disease, etc. The important thing in detecting the respiration is that doing it in object person's resting time. Detecting the respiration have to be done without attracting any attention of object person. In present using method is detecting the pulse with catching an object person's wrist and observing the object person's movement. In this paper, we propose the mobile respiration detection diagnostic system using ultrasound sensing method that does not be influenced by the inertia error and the pressure error.

• Biomolecules & Therapeutics
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• v.28 no.3
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• pp.250-258
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• 2020

Emphysema, a major component of chronic obstructive pulmonary disease (COPD), is a leading cause of human death worldwide. The progressive deterioration of lung function that occurs in the disease is caused by chronic inflammation of the airway and destruction of the lung parenchyma. Despite the main impact of inflammation on the pathogenesis of emphysema, current therapeutic regimens mainly offer symptomatic relief and preservation of lung function with little therapeutic impact. In the present study, we aimed to discover novel therapeutics that suppress the pathogenesis of emphysema. Here, we show that LJ-2698, a novel and highly selective antagonist of the adenosine A₃ receptor, a G protein-coupled receptor involved in various inflammatory diseases, significantly reversed the elastase-induced destructive changes in murine lungs. We found that LJ-2698 significantly prevented elastase-induced airspace enlargement, resulting in restoration of pulmonary function without causing any obvious changes in body weight in mice. LJ-2698 was found to inhibit matrix metalloproteinase activity and pulmonary cell apoptosis in the murine lung. LJ-2698 treatment induced increases in anti-inflammatory cytokines in macrophages at doses that displayed no significant cytotoxicity in normal cell lines derived from various organs. Treatment with LJ-2698 significantly increased the number of anti-inflammatory M2 macrophages in the lungs. These results implicate the adenosine A₃ receptor in the pathogenesis of emphysema. Our findings also demonstrate the potential of LJ-2698 as a novel therapeutic/preventive agent in suppressing disease development with limited toxicity.

• Environmental Mutagens and Carcinogens
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• v.25 no.3
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• pp.118-123
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• 2005

Nicotine has been implicated as a potential factor in the pathogenesis of human lung cancer, however its mechanism of action in the development of lung cancer remains largely unknown. To explore the role of nicotine in the development of lung cancer, we first investigated the effects of nicotine on the expression of tumor associated genes by treating Sprague-Dawley rats with nicotine (10 mg/kg) by gavage once daily for 10 days. We determined the expression of proteins and mRNAs of the ras, raf, myc, jun, fos oncogenes and p53, Rb tumor suppressor genes by Western and Northern blotting, respectively. We did not detect any changes on the levels of proteins and mRNAs of these tumor associated genes in the lung of Sprague-Dawley rats from 3 days to 12 weeks after the last treatment of nicotine, indicating that nicotine appears to have no effect on expression of these oncogenes and tumor suppressor genes at an early stage in multistage chemical carcinogenesis. In a second experiment, we investigated the possibility that 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) could be formed endogenously by treating with nicotine and sodium nitrite. We treated groups of Fischer 344 rats with nicotine ($60{\mu}mol/kg$) and sodium nitrite ($180{\mu}mol/kg$), nicotine, sodium nitrite and NNK (120 nmol/kg) alone by gavage once daily for 7 days, respectively and determined the 8-hydroxydeoxyguanosine (8-OHdG), as an indicator of NNK formation, in the lungs of rats 24 hours and 48 hours after the last treatment by HPLC/ECD method. We detect increased level of 8-OHdG in the lungs of rats treated with NNK, but in the case of nicotine plus sodium nitrite, nicotine and sodium nitrite alone we could not detected any changes of 8-OHdG, respectively.

• Journal of radiological science and technology
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• v.43 no.5
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• pp.397-404
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• 2020

Coronavirus disease(COVID-19) is highly infectious disease that directly affects the lungs. To observe the clinical findings from these lungs, the Chest Radiography(CXR) can be used in a fast manner. However, the diagnostic performance via CXR needs to be improved, since the identifying these findings are highly time-consuming and prone to human error. Therefore, Artificial Intelligence(AI) based tool may be useful to aid the diagnosis of COVID-19 via CXR. In this study, we explored various Deep learning(DL) approach to classify COVID-19, other viral pneumonia and normal. For the original dataset and lung-segmented dataset, the pre-trained AlexNet, SqueezeNet, ResNet18, DenseNet201 were transfer-trained and validated for 3 class - COVID-19, viral pneumonia, normal. In the results, AlexNet showed the highest mean accuracy of 99.15±2.69% and fastest training time of 1.61±0.56 min among 4 pre-trained neural networks. In this study, we demonstrated the performance of 4 pre-trained neural networks in COVID-19 diagnosis with CXR images. Further, we plotted the class activation map(CAM) of each network and demonstrated that the lung-segmentation pre-processing improve the performance of COVID-19 classifier with CXR images by excluding background features.

• Journal of the Korea Safety Management & Science
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• v.14 no.1
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• pp.43-51
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• 2012

This study was carried out to observe the impacts of a mouse's inhalation of toxic gas SO2 generated from combustion on its organs by different concentrations. As for research methods: First, after concentrations of SO2 generation from combustion had been set to three: low (10.4 ppm), middle (24.9 ppm) and high (122 ppm) through Gas Toxicity Testing Method (KS F 2271) and SO2 combustion gas was exposed to eight mice in each concentration. Five mice that were able to move based on LD50, a criterion, which sets the down time of a mouse's average behaviors to over 9 minutes, were randomly selected in each concentration, and they were set up as the subjects of the study on toxicity bio-markers. Second, tissues were taken from heart, liver, lungs, spleen and the thymus gland of the mice selected in each concentration and a pathological examination of them was carried out. As a result, microvascular congestion appeared in the heart, and cell necrosis, cortex congestion and tubule medulla congestion, etc. in each concentration were observed in addition to vascular congestion in liver, lungs, spleen and the thymus gland. Also, it was found that the higher the concentrations of SO2 exposure is, the greater, the changes in the organs get. Through this study, SO2 of various toxic gases generated from fire turned out to affect the tissues of each organ of a mouse, it is expected that the toxic gases may greatly affect human body in case of actual fire, and this study is evaluated as having a significance as a basic data on inhalation toxicity assessment of toxic substances generated in combustion.

• Nutrition Research and Practice
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• v.10 no.1
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• pp.3-10
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• 2016

BACKGROUND/OBJECTIVES: Oligonol, mainly found in lychee fruit, is an antioxidant polyphenolic compound which has been shown to have anti-inflammatory and anti-cancer properties. The detailed mechanisms by which oligonol may act as an anti-aging molecule have not been determined. MATERIALS/METHODS: In this study, we evaluated the ability of oligonol to modulate sirtuin (SIRT) expression in human lung epithelial (A549) cells. Oligonol was added to A549 cells and reactive oxygen species production, mitochondrial superoxide formation, and p21 protein levels were measured. Signaling pathways activated upon oligonol treatment were also determined by western blotting. Furthermore, the anti-aging effect of oligonol was evaluated ex vivo in mouse splenocytes and in vivo in Caenorhabditis elegans. RESULTS: Oligonol specifically induced the expression of SIRT1, whose activity is linked to gene expression, metabolic control, and healthy aging. In response to influenza virus infection of A549 cells, oligonol treatment significantly up-regulated SIRT1 expression and down-regulated viral hemagglutinin expression. Oligonol treatment also resulted in the activation of autophagy pathways and the phosphorylation of AMP-activated protein kinase (AMPK). Furthermore, oligonol-treated spleen lymphocytes from old mice showed increased cell proliferation, and mRNA levels of SIRT1 in the lungs of old mice were significantly lower than those in the lungs of young mice. Additionally, in vivo lethality assay revealed that oligonol extended the lifespan of C. elegans infected with lethal Vibrio cholerae. CONCLUSIONS: These data demonstrated that oligonol may act as an anti-aging molecule by modulating SIRT1/autophagy/AMPK pathways.

• Korean Journal of Food Science and Technology
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• v.53 no.2
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• pp.165-173
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• 2021

One of the major sources of air pollution is urban particulate matter (UPM), which causes lung diseases involving oxidative stress, inflammation, and cancer. Codonopsis lanceolata (CL) has been used in East Asia as a traditional oriental medicinal ingredient for lung diseases (e.g., asthma and bronchitis). However, the connection between the impact of CL and UPM in the lungs has rarely been investigated. This study aimed to confirm the inhibitory activity of the ethanol extract of CL (ECL) against oxidative stress and disruption of tight cell junctions in human pulmonary epithelial cells after exposure to UPM. As the lung cells were pre-treated with ECL, the UPM-induced increase in cellular reactive oxygen species production suppressed tight junction proteins (e.g., N-cadherin, fibronectin, occludin, zonula occludens-1, and claudin-4). These results suggest that ECL prevents the possible effects of UPM toxicity on the lungs.

• Journal of radiological science and technology
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• v.45 no.3
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• pp.225-232
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• 2022

Fine dust threatens human health in various forms, depending on the particle size, such as by causing respiratory, cardiovascular, and brain diseases, after entering the body via the lungs. The aim of this study was to correlate fine dust exposure with changes in brain blood flow in Sprague Dawley rats by using micro-positron emission tomography and elucidate the possibility of developing cerebrovascular diseases caused by fine dust. The subjects were exposured to an average fine dust (particulate matter 2.5) of 206.2 ± 7.74 to ten rats four times a day, twice a day for 90 min. Before the experiment, they were maintained at NPO to the maximize the intake of ¹⁸F-fluorodeoxy glucose(¹⁸F-FDG) and minimize changes in the ¹⁸F-FDG biomass depending on the ambient environment and body temperature of the rats. PET images were acquired in the list mode 40 min after injecting ¹⁸F-FDG 44.4 MBq into the rats tail vein using a micro-PET scanner pre and post exposure to fine dust. We found that the whole brain level of ¹⁸F-FDG standardized uptake value in rats averaged 5.21 ± 0.52 g/mL pre and 4.22 ± 0.48 g/mL post exposure to fine dust, resulting in a statistically significant difference. Fine dust was able to alter brain activity after entering the body via the lungs in various forms depending on the particle size.

• Parasites, Hosts and Diseases
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• v.62 no.2
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• pp.243-250
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• 2024

We investigated organ specific Toxocara canis larval migration in mice infected with T. canis larvae. We observed the worm burden and systemic immune responses. Three groups of BALB/c mice (n=5 each) were orally administered 1,000 T. canis 2nd stage larvae to induce larva migrans. Mice were sacrificed at 1, 3, and 5 weeks post-infection. Liver, lung, brain, and eye tissues were collected. Tissue from 2 mice per group was digested for larval count, while the remaining 3 mice underwent histological analysis. Blood hematology and serology were evaluated and compared to that in a control uninfected group (n=5) to assess the immune response. Cytokine levels in bronchoalveolar lavage (BAL) fluid were also analyzed. We found that, 1 week post-infection, the mean parasite load in the liver (72±7.1), brain (31±4.2), lungs (20±5.7), and eyes (2±0) peaked and stayed constant until the 3 weeks. By 5-week post-infection, the worm burden in the liver and lungs significantly decreased to 10±4.2 and 9±5.7, respectively, while they remained relatively stable in the brain and eyes (18±4.2 and 1±0, respectively). Interestingly, ocular larvae resided in all retinal layers, without notable inflammation in outer retina. Mice infected with T. canis exhibited elevated levels of neutrophils, monocytes, eosinophils, and immunoglobulin E. At 5 weeks post-infection, interleukin (IL)-5 and IL-13 levels were elevated in BAL fluid. Whereas IL-4, IL-10, IL-17, and interferon-γ levels in BAL fluid were similar to that in controls. Our findings demonstrate that a small portion of T. canis larvae migrate to the eyes and brain within the first week of infection. Minimal tissue inflammation was observed, probably due to increase of anti-inflammatory cytokines. This study contributes to our understanding of the histological and immunological responses to T. canis infection in mice, which may have implications to further understand human toxocariasis.