• 한국정보통신학회:학술대회논문집
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• 한국해양정보통신학회 2003년도 춘계종합학술대회
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• pp.514-517
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• 2003

산소공급은 신체 요구 중 가장 기본적인 것이다. 호흡은 뇌의 연수(medulla oblongata)에 있는 호흡중추와 폐의 정상적 기능에 의해 조절된다. 즉 폐와 환경 사이의 공기 이동인 외 호흡과 헤모글로빈과 단세포 사이의 세포수준에서의 산소 이동인 내 호흡을 말한다. 성인의 호흡수는 보통 1분에 15-20회이나 연령, 운동, 기온, 심리적 변호, 질병상태, 대기의 산소 함량, 약물 투여 등에 따라 차이가 난다. 호흡측정은 대상자가 쉬고 있을 때 하는 것이 중요하다. 호흡 측정은 측정하고 있다는 사실을 대상자가 모르도록 기술적으로 해야한다. 현재 사용하는 방법은 주의를 끌지 않도록 대상자의 팔목에 손을 댄 채로 맥박을 측정한 바로 직후 계속해서 대상자의 가슴의 움직임을 관찰하면서 호흡을 측정하는 것이다. 본 논문에서 구현하고자 하는 것은 관성의 오차 및 압력의 오차에 영향을 거의 받지 않는, 그리고 반영구적으로 사용이 가능한 초음파 센서를 이용한 임베디드 환경의 호흡 량 측정기이다.

• Biomolecules & Therapeutics
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• 제28권3호
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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.

• 한국환경성돌연변이발암원학회지
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• 제25권3호
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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.

• 대한방사선기술학회지:방사선기술과학
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• 제43권5호
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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.

• 대한안전경영과학회지
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• 제14권1호
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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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• 제10권1호
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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.

• 한국식품과학회지
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• 제53권2호
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• pp.165-173
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• 2021

본 연구에서는 UPM에 의해 유발되는 NCI-H441 세포 내 ROS 생성과 그에 따른 tight junction 단백질(N-cadherin, fibronectin, occluding, ZO-1, 및 claudin-4 등)의 발현 억제를 확인하였고 ECL의 전처리로 인하여 해당 ROS 생성 및 tight junction 단백질 발현 억제 현상이 완화되는 보호효과를 확인하였다. 그 결과, 폐 세포에서 UPM에 의해 유발된 산화 스트레스 및 tight junction 단백질의 발현 감소가 ECL을 선 처리함으로써 억제되어 결과적으로 산화 스트레스와 같은 미세먼지에 의한 폐 손상으로부터 보호 효과를 나타내고 tight junction 수준의 유지를 확인하였다. 이러한 결과를 통해 ECL 추출물은 폐와 기관지의 보호효과를 나타내며 폐 관련 질병의 예방효과가 있는 기능성 천연 물질로써 활용이 가능할 것으로 기대된다.

• 대한방사선기술학회지:방사선기술과학
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• 제45권3호
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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.

• Molecules and Cells
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• 제46권9호
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• pp.558-572
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• 2023

Chronic obstructive pulmonary disease (COPD) will be the third leading cause of death worldwide by 2030. One of its components, emphysema, has been defined as a lung disease that irreversibly damages the lungs' alveoli. Treatment is currently unavailable for emphysema symptoms and complete cure of the disease. Hyaluronan (HA) and proteoglycan link protein 1 (HAPLN1), an HA-binding protein linking HA in the extracellular matrix to stabilize the proteoglycan structure, forms a bulky hydrogel-like aggregate. Studies on the biological role of the full-length HAPLN1, a simple structure-stabilizing protein, are limited. Here, we demonstrated for the first time that treating human alveolar epithelial type 2 cells with recombinant human HAPLN1 (rhHAPLN1) increased TGF-β receptor 1 (TGF-β RI) protein levels, but not TGF-β RII, in a CD44-dependent manner with concurrent enhancement of the phosphorylated Smad3 (p-Smad3), but not p-Smad2, upon TGF-β1 stimulation. Furthermore, rhHAPLN1 significantly increased sirtuins levels (i.e., SIRT1/2/6) without TGF-β1 and inhibited acetylated p300 levels that were increased by TGF-β1. rhHAPLN1 is crucial in regulating cellular senescence, including p53, p21, and p16, and inflammation markers such as p-NF-κB and Nrf2. Both senile emphysema mouse model induced via intraperitoneal rhHAPLN1 injections and porcine pancreatic elastase (PPE)-induced COPD mouse model generated via rhHAPLN1-containing aerosols inhalations showed a significantly potent efficacy in reducing alveolar spaces enlargement. Preclinical trials are underway to investigate the effects of inhaled rhHAPLN1-containing aerosols on several COPD animal models.

• 한국대기환경학회지
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• 제19권5호
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• pp.551-560
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• 2003

Particle deposition in human lungs was investigated theoretically by using asymmetric five-lobe lung model. The volumes of each of the five lobes were different, thereby forming an asymmetric lung structure. The tidal volume and flow rate of each lobe were scaled according to lobar volume. The total and regional deposition with various breathing patterns were calculated by means of tracking volume segments and accounting for particle loss during inhalation and exhalation. The deposition fractions were obtained for each airway generation and lung lobe, and dominant deposition mechanisms were investigated for different size particles. Results show that the tidal volume and flow rate have a characteristic influence on particle deposition. The total deposition fraction increases with an increase in tidal volume for all particle sizes. However, flow rate has dichotomous effects: a higher flow rate results in a sharp increase in deposition for large size particles, but decreases deposition for small size particles. Deposition distribution within the lung shifts proximally with higher flow rate whereas deposition peak shifts to the deeper lung region with larger tidal volume. Deposition fraction in each lobe was proportional to its volume. Among the three main deposition mechanisms, diffusion was dominant for particles < 0.5 ${\mu}{\textrm}{m}$ whereas sedimentation and impaction were most influential for larger size particles. Impaction was particularly dominant for particles> 8 ${\mu}{\textrm}{m}$. The results may prove to be useful for estimating deposition dose of inhaled pollutant particles at various breathing conditions.