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Low-dose cadmium exposure exacerbates polyhexamethylene guanidine-induced lung fibrosis in mice
Kim, Min-Seok,Kim, Sung-Hwan,Jeon, Doin,Kim, Hyeon-Young,Han, Jin-Young,Kim, Bumseok,Lee, Kyuhong Taylor Francis 2018 Journal of toxicology and environmental health. Pa Vol.81 No.11
<P>Cadmium (Cd) is a toxic metal present in tobacco smoke, air, food, and water. Inhalation is an important route of Cd exposure, and lungs are one of the main target organs for metal-induced toxicity. Cd inhalation is associated with an increased risk of pulmonary diseases. The present study aimed to assess the effects of repeated exposure to low-dose Cd in a mouse model of polyhexamethylene guanidine (PHMG)-induced lung fibrosis. Mice were grouped into the following groups: vehicle control (VC), PHMG, cadmium chloride (CdCl2), and PHMG + CdCl2. Animals in the PHMG group exhibited increased numbers of total cells and inflammatory cells in the bronchoalveolar lavage fluid (BALF) accompanied by inflammation and fibrosis in lung tissues. These parameters were exacerbated in mice in the PHMG + CdCl2 group. In contrast, mice in the CdCl2 group alone displayed only minimal inflammation in pulmonary tissue. Expression of inflammatory cytokines and fibrogenic mediators was significantly elevated in lungs of mice in the PHMG group compared with that VC. Further, expression of these cytokines and mediators was enhanced in pulmonary tissue in mice administered PHMG + CdCl2. Data demonstrate that repeated exposure to low-dose Cd may enhance the development of PHMG-induced pulmonary fibrosis.</P>
수컷 랫드(Sprague-Dawley)에서 2-부톡시에탄올(2-butoxyethanol)의 단회 기도내 투여에 따른 급성 독성시험
김현영 ( Hyeon-young Kim ),김인현 ( In-hyeon Kim ),김민석 ( Min-seok Kim ),김성환 ( Sung-hwan Kim ),이규홍 ( Kyuhong Lee ) 한국산업보건학회 2021 한국산업보건학회지 Vol.31 No.4
Objectives: The present study aimed to evaluate the potential toxicity of 2-butoxyethanol after intratracheal instillation in male rats. Methods: In order to calculate median lethal dose (LD<sub>50</sub>) of 2-butoxyethanol using Probit analysis with SAS program, the 2-butoxyethanol was administered with dose levels of 0, 101.64, 203.28 and 406.56 mg/kg by once intratracheal instillation to male rats. During the test period, clinical signs, mortality, body weights, organ weights, hematology, and serum biochemistry were examined. At the end of 14 days observation period, all animals were sacrificed and gross finding and histopathological examination were performed. Results: All animals of 406.56 mg/kg group died within 2 weeks after the administration of 2-butoxyethanol. Treatment-related clinical signs, gross observation and histopathological changes (mucous cell hyperplasia, alveolar macrophage aggregation, and hemorrhage) of lung exhibited an increased in 2-butoxyethanol treated groups in a dose dependent manner. However, there were no changes in the organ weights, hematology and serum biochemistry, and histopathology of any other organ except lung. Conclusions: On the basis of the results, it was concluded that a single intratracheal instillation of 2-butoxyethanol in male Sprague-Dawley rats resulted in some adverse effects on mortality, clinical sign, and histopathology in the lung. In the experimental conditions, the LD<sub>50</sub> of 2-butoxyethanol was considered to be 287.2 mg/kg and lung was founded to be the target organ of 2-butoxyethanol.
Kim, Cho-Won,Lee, Hae-Miru,Lee, Kyuhong,Kim, Bumseok,Lee, Moo-Yeol,Choi, Kyung-Chul Elsevier 2017 Reproductive toxicology Vol.73 No.-
<P><B>Abstract</B></P> <P>Maternal smoking during pregnancy is known to be related to adverse pregnancy results associated with trophoblast proliferation and cell cycle progression. Moreover, many previous studies have shown that cigarette smoke is correlated with human chorionic gonadotropin beta (hCG-β) subunit produced from syncytiotrophoblasts during pregnancy. Thus, we further investigated whether cigarette smoke extract (CSE) affects the cell proliferation, migration and endocrine hormone activity of JEG-3 human placental cancer cells. JEG-3 cell proliferation was significantly reduced by all CSEs in a concentration-dependent manner. Moreover, CSEs decreased proliferating cell nuclear antigen (PCNA) levels in JEG-3 cells in Western blot. Increased migration or invasion ability of JEG-3 cells following CSE treatment was also confirmed by a scratch or fibronectin invasion assay <I>in vitro</I>. Additionally, protein levels of E-cadherin as an epithelial maker were down-regulated, while the mesenchymal markers N-cadherin, snail and slug were up-regulated in a time-dependent manner. The metastasis marker, cathepsin D, was also down-regulated by CSE. Finally, CSEs significantly reduced the expression of hCG-β protein in JEG-3 cells. Overall, these results indicate that exposure of placental cells to CSE deregulates the cell cycle by altering the expression of cell cycle-related proteins and stimulates cell metastatic ability by altering EMT markers and cathepsin D expression. CSE exposure may also decrease hCG-β production as an endocrine marker, implying that cigarette smoke has adverse effects during pregnancy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> CSE exposure deregulated the placental cell growth by altering cell proliferation-related genes. </LI> <LI> CSE exposure stimulated JEG-3 metastatic potential by altering EMT markers and cathepsin D. </LI> <LI> CSE exposure also deregulated the production of human chorionic gonadotropin beta. </LI> <LI> Cigarette smoking may have adverse effects on normal placenta functions during pregnancy. </LI> </UL> </P>
Impostor Detection in Speaker Recognition Using Confusion-Based Confidence Measures
Kyuhong Kim,김회린,한민수 한국전자통신연구원 2006 ETRI Journal Vol.28 No.6
In this letter, we introduce confusion-based confidence measures for detecting an impostor in speaker recognition, which does not require an alternative hypothesis. Most traditional speaker verification methods are based on a hypothesis test, and their performance depends on the robustness of an alternative hypothesis. Compared with the conventional Gaussian mixture model–universal background model (GMM-UBM) scheme, our confusion-based measures show better performance in noise-corrupted speech. The additional computational requirements for our methods are negligible when used to detect or reject impostors.
Kim, Min-Seok,Han, Jin-Young,Kim, Sung-Hwan,Jeon, Doin,Kim, Hyeon-Young,Lee, Seung Woong,Rho, Mun-Chual,Lee, Kyuhong Elsevier 2018 Respiratory physiology & neurobiology Vol.252 No.-
<P><B>Abstract</B></P> <P>Oleanolic acid acetate (OAA), triterpenoid compound isolated from <I>Vigna angularis</I> (azuki bean), has been revealed anti-inflammatory in several studies. We investigated the effects of OAA against polyhexamethylene guanidine phosphate (PHMG-P)-induced pulmonary inflammation and fibrosis in mice. OAA treatment effectively alleviated PHMG-P-induced lung injury, including the number of total and differential cell in BAL fluid, histopathological lesions and hydroxyproline content in a dose dependent manner. Moreover, OAA treatment significantly decreased the elevations of IL-1β, IL-6, TNF-α, TGF-β1, and fibronectin, and the activation of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in the lungs of PHMG-P-treated mice. Cytokines are known to be key modulators in the inflammatory responses that drive progression of fibrosis in injured tissues. The activation of NLRP3 inflammasome has been reported to be involved in induction of inflammatory cytokines. These results indicate that OAA may mitigate the inflammatory response and development of pulmonary fibrosis in the lungs of mice treated with PHMG-P.</P> <P><B>Highlights</B></P> <P> <UL> <LI> We investigated the effects of anti-inflammation and anti-fibrosis by intratracheal instillation of OAA in PHMG-P-induced pulmonary injury. </LI> <LI> OAA attenuated PHMG-P-induced pulmonary injury, including the number of total and differential cell in BAL fluid and histopathological changes. </LI> <LI> OAA reduced the activation of NLRP3 inflammasome as well as the expression of pro-inflammatory and pro-fibrotic cytokines induced by PHMG-P. </LI> </UL> </P>
Kim, Ju-Hyeong,Cho, Myung-Haing,Choi, Kyung-Chul,Lee, Kyuhong,Kim, Kwang-Sik,Shim, Soon-Mi Taylor Francis 2015 Journal of toxicology and environmental health. Pa Vol.78 No.15
<P>The objective of the current study was to examine oxidative stress induced by cigarette smoke extract (CSE) or cigarette smoke condensate (CSC) in human brain cells (T98G) and human brain microvascular endothelial cells (HBMEC) in mono- and co-culture systems. Cell viability of T98G cells exposed to CSC (0.05-4 mg/ml) was significantly decreased compared to CSE (0.025-20%). There were no marked differences between quantities of reactive oxygen species (ROS) generation by either CSE (2, 4, and 10%) or CSC (0.2, 0.4, and 0.8 mg/ml) treatment compared to control. However, a significant effect was noted in ROS generation following CSC incubation at 4mg/ml. Cellular integrity of HBMEC decreased to 74 and 64% within 120 h of exposure at the IC50 value of CSE and CSC, respectively. This study suggests that chronic exposure to cigarette smoking might initiate damage to the blood-brain barrier.</P>
Kim, Jong Won,Yun, Hyejin,Choi, Seong-Jin,Lee, Sang-Hyub,Park, Surim,Lim, Chae Woong,Lee, Kyuhong,Kim, Bumseok Korean Society of ToxicologyKorea Environmental Mu 2017 Toxicological Research Vol.33 No.1
Side stream cigarette smoke (SSCS) is known to be as harmful and hazardous to human health as is active smoking. In this study, we investigated the relationship between the exposure to SSCS and its stimulatory and subacute effects on the progression of non-alcoholic steatohepatitis (NASH). A methionine and choline-deficient plus high fat (MCDHF) diet was administered to C57BL/6 mice for 6 weeks. During the first three weeks of MCDHF diet feeding, each diet group was exposed to SSCS (0, 20, $40{\mu}g/L$) or fresh air for 2 hrs per day and 5 days per week. Additional experiments were performed by increasing the concentration (0, 30, $60{\mu}g/L$) and exposure time (6 hours per day) of SSCS. According to histopathologic analysis and serum levels of Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST), there were no differences in hepatic fat deposition, fibrosis, apoptosis or liver damage in MCDHF-fed mice based on SSCS exposure. There were also no differences in the expression of inflammation-, oxidative stress- or fibrosis-related genes between MCDHF-fed mice with or without SSCS exposure. Therefore, it is concluded that SSCS with current exposure amounts does not have additive detrimental effects on the early stage of NASH.
The Role of Air Pollutants in Initiating Liver Disease
Kim, Jong Won,Park, Surim,Lim, Chae Woong,Lee, Kyuhong,Kim, Bumseok Korean Society of ToxicologyKorea Environmental Mu 2014 Toxicological Research Vol.30 No.2
Recent episodes of severe air pollution in eastern Asia have been reported in the scientific literature and news media. Therefore, there is growing concern about the systemic effects of air pollution on human health. Along with the other well-known harmful effects of air pollution, recently, several animal models have provided strong evidence that air pollutants can induce liver toxicity and act to accelerate liver inflammation and steatosis. This review briefly describes examples where exposure to air pollutants was involved in liver toxicity, focusing on how particulate matter (PM) or carbon black (CB) may be translocated from lung to liver and what liver diseases are closely associated with these air pollutants.