• 한국디지털정책학회:학술대회논문집
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• 2006.12a
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• pp.43-50
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• 2006

본 연구에서는 미 운송부 산하 고속도로교통안전국에서 규정한 EMT-I 의 미 국립표준교과과정을 알아본 뒤, 기존 피츠버그 의과대학 응급의료센터에서 제공되는 교육과정의 구성과 내용에 대하여 소개하고 미 국립 응급구조사 협회의 연차보고서를 토대로 EMT-I 자격의 미국 내 시행실태를 파악하였다 또한. 각 주별로 제공되는 교육과정의 내용과 EMT-I 구급대원의 활동범위에 대하여는 응급 의료시스템 잡지의 주 별 현황조사를 실시하였다. 끝으로 장기적인 추진과제인 Paramedic 과정 개설에 관하여 제언하였다.

• BMB Reports
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• v.55 no.12
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• pp.645-650
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• 2022

Epithelial-to-mesenchymal transition (EMT)-subtype gastric cancers have the worst prognosis due to their higher recurrence rate, higher probability of developing metastases and higher chemo-resistance compared to those of other molecular subtypes. Pharmacologically actionable somatic mutations are rarely found in EMT-subtype gastric cancers, limiting the utility of targeted therapies. Here, we conducted a high-throughput chemical screen using 37 gastric cancer cell lines and 48,467 synthetic small-molecule compounds. We identified YK-135, a small-molecule compound that showed higher cytotoxicity toward EMT-subtype gastric cancer cell lines than toward non-EMT-subtype gastric cancer cell lines. YK-135 exerts its cytotoxic effects by inhibiting mitochondrial complex I activity and inducing AMP-activated protein kinase (AMPK)-mediated apoptosis. We found that the lower glycolytic capacity of the EMT-subtype gastric cancer cells confers synthetic lethality to the inhibition of mitochondrial complex I, possibly by failing to maintain energy homeostasis. Other well-known mitochondrial complex I inhibitors (e.g., rotenone and phenformin) mimic the efficacy of YK-135, supporting our results. These findings highlight mitochondrial complex I inhibitors as promising therapeutic agents for EMT-subtype gastric cancers and YK-135 as a novel chemical scaffold for further drug development.

• BMB Reports
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• v.52 no.6
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• pp.379-384
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• 2019

Epithelial-mesenchymal transition (EMT) is widely-considered to be a modulating factor of anoikis and cancer metastasis. We found that, in MDA-MB-231 cells, TP53I11 (tumor protein P53 inducible protein 11) suppressed EMT and migration in vitro, and inhibited metastasis in vivo. Our findings showed that hypoxic treatment upregulated the expression of $HIF1{\alpha}$, but reduced TP53I11 protein levels and TP53I11 overexpression reduced $HIF1{\alpha}$ expression under normal culture and hypoxicconditions, and in xenografts of MDA-MB-231 cells. Considering $HIF1{\alpha}$ is a master regulator of the hypoxic response and that hypoxia is a crucial trigger of cancer metastasis, our study suggests that TP53I11 may suppress EMT and metastasis by reducing $HIF1{\alpha}$ protein levels in breast cancer cells.

• Journal of Environmental Science International
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• v.14 no.9
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• pp.827-835
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• 2005

A three-dimensional ecological model (EMT -3D) was applied to Nonylphenol in Tokyo Bay. EMT -3D was calibrated with data obtained in the study area. The simulated results of dissolved Nonylphenol were in good agreement with the observed values, with a correlation coefficient(R) of 0.7707 and a coefficient of determination (R2) of 0.5940. The results of sensitivity analysis showed that biodegradation rate and bioconcentration factor are most important factors for dissolved Nonylphenol and Nonylphenol in phytoplankton, respectively. In the case of Nonylphenol in particulate organic carbon, biodegradation rate and partition coefficient were important factors. Therefore, the parameters must be carefully considered in the modeling. The mass balance results showed that standing stocks of Nonylphenol in water, in particulate organic carbon and in phytoplankton are $8.60\times 10^5\;g,\;2.19\times 10^2\;g\;and\;3.78\times 10^0\;g$ respectively. With respect to the flux of dissolved Nonylphenol, biodegradation in the water column, effluent to the open sea and partition to particulate organic carbon were $6.02\times10^3\;g/day,\;6.02\times10^2\;g/day\;and\;1.02\times10^1\;g/day$, respectively.

• The Korean Journal of Emergency Medical Services
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• v.26 no.1
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• pp.37-56
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• 2022

Purpose: This study aimed to identify and present suitable recognition types of policy alternative for before and after response, according to the recognition types of problems in response to violence. Methods: This study investigated 36 EMT's of 17 cities and provinces nationwide. The study was approved by the Kongju National University Institute Review Board (KNU_IRB_2021-17). Data were collected from May 1, 2021 to August 30, 2021 and analyzed by Q factor analysis using the PC-QUNAL program. Results: Recognition types of the problem in 119 EMT's response to violence were described as "I type; lack of professional manpower," "II type; inadequate policy on violence," and "III type; lack of awareness on the emergency field." Recognition types of policy alternative on response to violence by 119 EMT's were described as "Itype; training and public relations oriented," "II type; work environment improvement," "III type; violence handling specialization demand," and "IV type; recovery support seeker." Conclusion: This study provides the foundation required to develop and implement the policies regarding the response to violence; therefore, contributing to EMT's provision.

• Biomolecules & Therapeutics
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• v.23 no.4
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• pp.301-312
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• 2015

Metastasis is one of hallmarks of cancer and a major cause of cancer death. Combatting metastasis is highly challenging. To overcome these difficulties, researchers have focused on physical properties of metastatic cancer cells. Metastatic cancer cells from patients are softer than benign cancer or normal cells. Changes of viscoelasticity of cancer cells are related to the keratin network. Unexpectedly, keratin network is dynamic and regulation of keratin network is important to the metastasis of cancer. Keratin is composed of heteropolymer of type I and II. Keratin connects from the plasma membrane to nucleus. Several proteins including kinases, and protein phosphatases bind to keratin intermediate filaments. Several endogenous compounds or toxic compounds induce phosphorylation and reorganization of keratin network in cancer cells, leading to increased migration. Continuous phosphorylation of keratin results in loss of keratin, which is one of the features of epithelial mesenchymal transition (EMT). Therefore, several proteins involved in phosphorylation and reorganization of keratin also have a role in EMT. It is likely that compounds controlling phosphorylation and reorganization of keratin are potential candidates for combating EMT and metastasis.

• International Journal of Stem Cells
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• v.16 no.1
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• pp.52-65
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• 2023

Background and Objectives: Epithelial-Mesenchymal transition (EMT) is one of the origins of myofibroblasts in renal interstitial fibrosis. Mesenchymal stem cells (MSCs) alleviating EMT has been proved, but the concrete mechanism is unclear. To explore the mechanism, serum-free MSCs conditioned medium (SF-MSCs-CM) was used to treat rat renal tubular epithelial cells (NRK-52E) fibrosis induced by transforming growth factor-β1 (TGF-β1) which ameliorated EMT. Methods and Results: Galectin-3 knockdown (Gal-3 KD) and overexpression (Gal-3 OE) lentiviral vectors were established and transfected into NRK-52E. NRK-52E fibrosis model was induced by TGF-β1 and treated with the SF-MSCs-CM for 24 h after modelling. Fibrosis and autophagy related indexes were detected by western blot and immunocytochemistry. In model group, the expressions of α-smooth muscle actin (α-SMA), fibronectin (FN), Galectin-3, Snail, Kim-1, and the ratios of P-Akt/Akt, P-GSK3β/GSK3β, P-PI3K/PI3K, P-mTOR/mTOR, TIMP1/MMP9, and LC3B-II/I were obviously increased, and E-Cadherin (E-cad) and P62 decreased significantly compared with control group. SF-MSCs-CM showed an opposite trend after treatment compared with model group. Whether in Gal-3 KD or Gal-3 OE NRK-52E cells, SF-MSCs-CM also showed similar trends. However, the effects of anti-fibrosis and enhanced autophagy in Gal-3 KD cells were more obvious than those in Gal-3 OE cells. Conclusions: SF-MSCs-CM probably alleviated the EMT via inhibiting Galectin-3/Akt/GSK3β/Snail pathway. Meanwhile, Gal-3 KD possibly enhanced autophagy via inhibiting Galectin-3/Akt/mTOR pathway, which synergistically ameliorated renal fibrosis. Targeting galectin-3 may be a potential target for the treatment of renal fibrosis.

• Korean Journal of Food Science and Technology
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• v.36 no.5
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• pp.812-817
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• 2004

Cytotoxic effects of Korean rice-wine (Yakju) made with different processes and ingredients (Korean rice-wines I, II), red wine, white wine, beer, and Japanese rice-wine (Sake) were examined against human cancer lines (DLD-1, HepG2, K562) and mouse cancer lines (EMT6, LLC1). Red wine showed cytotoxic effect on all cancer lines, while Korean rice-wines I, and II showed cytotoxcity on all cancer cells except DLD-1. White wine, beer, and Japanese rice-wine had no or little cytotoxic effect against all cancer cell lines. Concentrate of Korean rice-wine only showed cytotoxic effect against DLD-1. These results suggest Korean rice-wine has strong anti-cancer effects, which are induced by certain rice-wine components.

• Molecules and Cells
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• v.38 no.1
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• pp.20-25
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• 2015

TGF-${\beta}$ regulates pleiotropic cellular responses including cell growth, differentiation, migration, apoptosis, extracellular matrix production, and many other biological processes. Although non-Smad signaling pathways are being increasingly reported to play many roles in TGF-${\beta}$-mediated biological processes, Smads, especially receptor-regulated Smads (R-Smads), still play a central mediatory role in TGF-${\beta}$ signaling for epithelial-mesenchymal transition. Thus, the biological activities of R-Smads are tightly regulated at multiple points. Inhibitory Smad (I-Smad also called Smad7) acts as a critical endogenous negative feedback regulator of Smad-signaling pathways by inhibiting R-Smad phosphorylation and by inducing activated type I TGF-${\beta}$ receptor degradation. Roles played by Smad7 in health and disease are being increasingly reported, but the molecular mechanisms that regulate Smad7 are not well understood. In this study, we show that E3 ubiquitin ligase Itch acts as a positive regulator of TGF-${\beta}$ signaling and of subsequent EMT-related gene expression. Interestingly, the Itch-mediated positive regulation of TGF-${\beta}$ signaling was found to be dependent on Smad7 ubiquitination and its subsequent degradation. Further study revealed Itch acts as an E3 ubiquitin ligase for Smad7 polyubiquitination, and thus, that Itch is an important regulator of Smad7 activity and a positive regulator of TGF-${\beta}$ signaling and of TGF-${\beta}$-mediated biological processes. Accordingly, the study uncovers a novel regulatory mechanism whereby Smad7 is controlled by Itch.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.1
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• pp.47-54
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• 2014

The aim of this study is to evaluate the effects of green tea polyphenol (GTP) on anticancer treatment with cisplatin (CP), using both an in vitro cell culture model and an in vivo mouse model of established breast tumor. Mouse breast cancer cells (EMT6) were treated with or without GTP and CP followed by determination of the cell viability using an MTT assay. The relative cell viability of CP treated EMT6 cells was 96% at a 20 ${\mu}g/mL$ concentration of cisplatin; however, in combination with GTP (50 ${\mu}g/mL$), the cell viability decreased to 20% at the same concentration of CP (20 ${\mu}g/mL$). For the in vivo study, EMT6 cells were inoculated into Balb/c mice for the establishment of a tumor-bearing mice model. The tumor-bearing mice were treated with CP (5 mg/kg. i.p.) with or without dietary GTP (0.2% drinking water). Tumor growth was monitored by a measurement of tumor size using a digital caliper, and nephrotoxicity was determined by enzymatic and histological examinations. The levels of p53 and caspase-3 in tumor tissues were examined by a Western blot. In tumor-bearing mice treated with GTP plus CP, the increment of tumor volume showed a significant reduction, compared with CP or GTP alone. The levels of p53 and cleaved caspase-3 (caspase-3/p17) in tumor tissues of tumor-bearing mice were increased by CP and GTP compared to CP alone. In CP treated tumor-bearing mice, ${\gamma}$-glutamyltranspeptidase (GGT) and alkaline phosphatase (AP) activities were decreased, and marked tubular necrosis and dilatation were observed in the kidney. CP-induced enzymatic and histopathological changes in the kidney of tumor-bearing mice were reduced by combinations of GTP with CP. The results of these experiments demonstrated that dietary GTP has a potentiating effect on CP anti-tumor activity and a protective effect against CP-induced renal dysfunction. Therefore, GTP may be used as a modulator in anticancer treatment with CP.