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윤제원(Je-Won Yoon),김영찬(Young-Chan Kim),김금모(Keum-Mo Kim),장강석(Kang-Seok Jang),구본성(Bon-Sung Ku),엄주용(Joo-Yong Eom) 한국소음진동공학회 2011 한국소음진동공학회 학술대회논문집 Vol.2011 No.10
The purpose of this study is to develop an air-passing soundproofing panel with more improved structure to reduce the CO2 emission and installation cost. To reduce the emission of CO2 ; it is suggested to choose low CO2 emission material relative to the aluminum and to reduce the materials by developing a specially designed air-passing soundproofing panel structure. First of all, we performed the flow analysis to predict the wind pressure according to the open angle of the air-passing soundproofing panel and the noise level analysis at the receiver point. To verify the simulation, a prototype of the soundproofing panel was made. The flow test in the wind tunnel and load test were performed. The economic evaluation for the installation of the air-passing soundproofing panel was performed and specifications of the installation was prepared. As the results of this research, it was verified that the wind load was reduced about 40% to that of the conventional one at 25m/s wind speed in the wind tunnel test. By applying the 4m span soundproofing wall with air-passing soundproofing panel and under the cost of 250 thousand won/m2 instead of the conventional 2m span panel, the installation cost will always be lowered than the conventional one in the combination of (60:40~50:50) conventional to air-passing soundproofing panel from the economic evaluation. The 20% reduction of CO2 was found by changing the 50% of aluminum soundproof panel to air-passing soundproofing panel.
기상조절(인공강우와 안개저감)의 경제적 가치 추정 연구
이철규(Chulkyu Lee),장기호(Ki-Ho Chang),차주완(Joo-Wan Cha),정재원(Jae-Won Jung),정진임(Jin-Yim Jeong),양하영(Ha-Young Yang),서성규(Sung-Kyu Seo),배진영(Jin-Young Bae),강선영(Sun-Young Kang),최영진(Young-Jean Choi),조하만(Ha-man Cho) 한국기상학회 2010 대기 Vol.20 No.2
We estimate the economic benefit of weather modification (precipitation enhancement and fog dissipation) by assuming its operation for the considered regions. Based on the statistical data, the economic benefit of the virtually operational precipitation enhancement experiments for the Andong and Imha basins, where the natural precipitation is relatively lack in South Korea, is calculated 348 for the water resources, 22,458 for forest fire prevention, and 28,458 million won/year for the drought relief. The benefit of the fog dissipation operation for the Incheon International Airport is estimated 7,365 million won/year for the flight delay due to fog. The calculated ratio of benefit to cost for precipitation enhancement operation for the basins is 14.07, which is comparable to that conducted in other countries.
( Won Sohn ),( Dae Won Jun ),( Kang Nyeong Lee ),( Hang Lak Lee ),( Tae Yeob Kim ),( Joo Hyun Sohn ),( Oh Young Lee ),( Byung Chul Yoon ),( Ho Soon Choi ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.-
Background: Recently, gut microbiota has been received attention in pathogenesis of non-alcoholic fatty liver disease (NAFLD). The protective effects of Lactobacillus paracasei on NAFLD and possible mechanism were investigated. Methods: Forty male C57BL/6 mice were randomized into 4 groups for 12 weeks: control, NASH model (high fat+10% fructose diet), Lactobacillus paracasei and Lactobacillus plantarum groups. Hepatic fat deposition, inflammation, serum ALT, AST, and bilirubin were tested. Kupffer cell polarization was evaluated by flow cytometry using M1 and M2 marker. Intestinal permeability was measured by urinary Cr-EDTA amount. Results: Mean body weight of L. paracasei and L. plantarum group were lower than NASH model (38 g vs. 43g, p<0.05). Compared with NASH model mice, serum ALT and AST were significantly decreased in both L. paracasei group and L. plantarum group (ALT: 135.5 U/L vs. 92.9 and 53.7U/L, p<0.05). Intestinal permeability was decreased in both L. paracasei and L. planatrum group compared to NASH model (p<0.05).While hepatic fat deposition and lobular inflammation was significantly decreased in both L. paracasei and L. plantarum groups. Kupffer cell infiltration was significantly low in only L. paracasei group (p<0.05). M2 macrophage population increased in L. paracasei compared to NASH group (62.1% vs 50.2%, p<0.05). But Kupffer cell polarization of L. plantarum group did not showed differences compare to NASH group. Conclusions: Probiotics attenuate hepatic fat deposition and decrease ALT and AST levels in NASH model. L. paracasei, but not L. plantarum prevented steatohepatitis via modulation of Kupffer cell polarization.
Kang, Seok Yong,Jung, Hyo Won,Nam, Joo Hyun,Kim, Woo Kyung,Kang, Jong-Seong,Kim, Young-Ho,Cho, Cheong-Weon,Cho, Chong Woon,Park, Yong-Ki,Bae, Hyo Sang Hindawi 2017 Evidence-based Complementary and Alternative Medic Vol.2017 No.-
<P><B>Ethnopharmacological Relevance</B></P><P> In this study, we investigated the effects of<I> Tribulus terrestris</I> fruit (Leguminosae, Tribuli Fructus, TF) extract on oxazolone-induced atopic dermatitis in mice.</P><P><B> Materials and Methods</B></P><P> TF extract was prepared with 30% ethanol as solvent. The 1% TF extract with or without 0.1% HC was applied to the back skin daily for 24 days.</P><P><B> Results</B></P><P> 1% TF extract with 0.1% HC improved AD symptoms and reduced TEWL and symptom scores in AD mice. 1% TF extract with 0.1% HC inhibited skin inflammation through decrease in inflammatory cells infiltration as well as inhibition of Orai-1 expression in skin tissues. TF extract inhibited Orai-1 activity in Orai-1-STIM1 cooverexpressing HEK293T cells but increased TRPV3 activity in TRPV3-overexpressing HEK293T cells. TF extract decreased <I>β</I>-hexosaminidase release in RBL-2H3 cells.</P><P><B> Conclusions</B></P><P> The present study demonstrates that the topical application of TF extract improves skin inflammation in AD mice, and the mechanism for this effect appears to be related to the modulation of calcium channels and mast cell activation. This outcome suggests that the combination of TF and steroids could be a more effective and safe approach for AD treatment.</P>
( Won Sohn ),( Dae Won Jun ),( Kang Nyeong Lee ),( Hang Lak Lee ),( Tae Yeob Kim ),( Joo Hyun Sohn ),( Oh Young Lee ),( Byung Chul Yoon ),( Ho Soon Choi ) 대한간학회 2012 춘·추계 학술대회 (KASL) Vol.2012 No.1
Background: Recently, gut microbiota has been received attention in pathogenesis of non-alcoholic fatty liver disease (NAFLD). The protective effects of Lactobacillus paracasei on NAFLD and possible mechanism were investigated. Methods: Forty male C57BL/6 mice were randomized into 4 groups for 12 weeks: control, NASH model (high fat+10% fructose diet), Lactobacillus paracasei and Lactobacillus plantarum groups. Hepatic fat deposition, inflammation, serum ALT, AST, and bilirubin were tested. Kupffer cell polarization was evaluated by flow cytometry using M1 and M2 marker. Intestinal permeability was measured by urinary Cr-EDTA amount. Results: Mean body weight of L. paracasei and L. plantarum group were lower than NASH model (38 g vs. 43g, p<0.05). Compared with NASH model mice, serum ALT and AST were significantly decreased in both L. paracasei group and L. plantarum group (ALT: 135.5 U/L vs. 92.9 and 53.7U/L, p<0.05). Intestinal permeability was decreased in both L. paracasei and L. planatrum group compared to NASH model (p<0.05).While hepatic fat deposition and lobular inflammation was significantly decreased in both L. paracasei and L. plantarum groups. Kupffer cell infiltration was significantly low in only L. paracasei group (p<0.05). M2 macrophage population increased in L. paracasei compared to NASH group (62.1% vs 50.2%, p<0.05). But Kupffer cell polarization of L. plantarum group did not showed differences compare to NASH group. Conclusions: Probiotics attenuate hepatic fat deposition and decrease ALT and AST levels in NASH model. L. paracasei, but not L. plantarum prevented steatohepatitis via modulation of Kupffer cell polarization.
Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
Kang, Kyoung Ah,Piao, Mei Jing,Ryu, Yea Seong,Hyun, Yu Jae,Park, Jeong Eon,Shilnikova, Kristina,Zhen, Ao Xuan,Kang, Hee Kyoung,Koh, Young Sang,Jeong, Yong Joo,Hyun, Jin Won Spandidos Publications 2017 International journal of oncology Vol.51 No.4
<P>The present study determined whether luteolin induces HT-29 colon cancer cell death through an antioxidant effect such as the activation of antioxidant enzymes. Luteolin decreased cell viability in human colon cancer cells (HT-29), whereas it had no effect on normal colon cells (FHC). Luteolin induced apoptosis by activating the mitochondria-mediated caspase pathway in HT-29 cells. Luteolin caused loss of the mitochondrial membrane action potential, increased mitochondrial Ca2+ level, upregulated Bax, downregulated Bcl-2, induced the release of cytochrome c from mitochondria to the cytosol, and increased the levels of the active forms of caspase-9 and caspase-3. Luteolin-induced apoptosis was accompanied by the activation of intracellular and mitochondrial reactive oxygen species scavenging through the activation of antioxidant enzymes, such as superoxide dismutase and catalase in HT-29 cells. Luteolin increased the level of reduced glutathione (GSH) and the expression of GSH synthetase, which catalyzes the second step of GSH biosynthesis. The apoptotic effect of luteolin was mediated by the activation of the mitogen-activated protein kinase signaling pathway. The present results indicate that luteolin induces apoptosis by promoting antioxidant activity and activating MAPK signaling in human colon cancer cells.</P>
Visfatin induces neurite outgrowth in PC12 cells via ERK1/2 signaling pathway
Kang, Young-Soon,Bae, Moon-Kyoung,Kim, Jee-Young,Jeong, Joo-Won,Yun, Il,Jang, Hye-Ock,Bae, Soo-Kyung Elsevier 2011 Neuroscience Letters Vol.504 No.2
<P><B>Abstract</B></P> <P>The angiogenic and inflammatory functions of visfatin and its effect on vascular cells, are fairly well known. However, its role within the nervous system remains largely unclear. To gain insight into this area, we studied the neuritogenic effect of visfatin on PC12 rat pheochromocytoma cells. We investigated whether visfatin gene expression, which is upregulated by hypoxia in cancer cells, is associated with neuritogenesis in PC12 cells. Using RT-PCR, Western blot analysis, ELISA, morphological observations, and immunostaining, we initially showed that CoCl<SUB>2</SUB>, a hypoxic mimetic agent, upregulated visfatin gene expression along with neurite outgrowth in PC12 cells. We also showed that visfatin stimulated neurite outgrowth in PC12 cells. Moreover, in PC12 cells, visfatin evoked the activation of the extracellular signal-regulated kinase 1/2 (ERK1/2), which is closely linked to neuritogenesis. Visfatin-induced outgrowth of neurites was prevented by inhibition of the ERK1/2 pathway. Taken together, our results demonstrate for the first time that visfatin induces neurite outgrowth in PC12 cells via the activation of an ERK-dependent pathway, and suggest that visfatin may exert various biological, physiological, and pathological functions in not only the vascular system but also the nervous system.</P> <P><B>Highlights</B></P> <P>▸ We investigated the neuritogenic effect of visfatin on PC12 cells. ▸ Visfatin expression was upregulated during cobalt chloride-induced neuritogenesis in PC12 cells. ▸ Visfatin induced neurite outgrowth in PC12 cells. ▸ Visfatin-induced outgrowth of neurites was mediated by ERK1/2 signaling pathway.</P>
Kang, Kyoung Ah,Piao, Mei Jing,Hyun, Yu Jae,Zhen, Ao Xuan,Cho, Suk Ju,Ahn, Mee Jung,Yi, Joo Mi,Hyun, Jin Won Nature Publishing Group UK 2019 Experimental and molecular medicine Vol.51 No.4
<▼1><P>Luteolin, a dietary flavone, modulates various signaling pathways involved in carcinogenesis. In this study, we investigated the molecular mechanism that underlies the apoptotic effects of luteolin mediated by DNA demethylation of the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter and the interaction of Nrf2 and p53, a tumor suppressor, in human colon cancer cells. Luteolin increased the expression of apoptosis-related proteins and antioxidant enzymes. In DNA methylation, luteolin inhibited the expression of DNA methyltransferases, a transcription repressor, and increased the expression and activity of ten-eleven translocation (TET) DNA demethylases, a transcription activator. Methyl-specific polymerase chain reaction and bisulfite genomic sequencing indicated that luteolin decreased the methylation of the Nrf2 promoter region, which corresponded to the increased mRNA expression of Nrf2. In addition, luteolin increased TET1 binding to the Nrf2 promoter, as determined using a chromatin immunoprecipitation (ChIP) assay. TET1 knockdown decreased the percentages of luteolin-treated cells in sub-G<SUB>1</SUB> phase and cells with fragmented nuclei. Furthermore, complex formation between p53 and Nrf2 was involved in the apoptotic effects of luteolin. These results provide insight into the mechanism that underlies the anticancer effects of luteolin on colon cancer, which involve the upregulation of Nrf2 and its interaction with the tumor suppressor.</P></▼1><▼2><P><B>Cancer: Cell-killing plant compound exerts antioxidant effects</B></P><P>A molecule found in fruits, vegetables and herbs helps kill colon cancer cells by activating a master regulator of detoxifying enzymes. Jin Won Hyun from Jeju National University School of Medicine in South Korea and colleagues treated human colon cancer cells with luteolin, a molecule that occurs naturally in many food plants. They showed that luteolin increased the levels of proteins involved in cell death and antioxidant responses by causing DNA-modifying enzymes to strip suppressive chemical markers off the gene encoding Nrf2, a protein that regulates antioxidant effects. Nrf2 levels subsequently increased and the protein interacted with the tumor suppressor p53 to facilitate destruction of the colon cancer cells. The findings offer a mechanistic basis for using luteolin to help prevent and treat cancer.</P></▼2>