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      • SCISCIESCOPUS

        The impact of various ethanol-gasoline blends on particulates and unregulated gaseous emissions characteristics from a spark ignition direct injection (SIDI) passenger vehicle

        Jin, Dongyoung,Choi, Kwanhee,Myung, Cha-Lee,Lim, Yunsung,Lee, Jongtae,Park, Simsoo Elsevier 2017 Fuel Vol.209 No.-

        <P><B>Abstract</B></P> <P>This study investigated the effects of various ethanol-gasoline blends on the hazardous air pollutants (HAPs) emissions from a wall-guided direct injection passenger vehicle. The fuel economy (FE) as well as regulated and unregulated gaseous emissions was evaluated on a chassis dynamometer using the federal test procedure (FTP-75) mode. Five fuels with varying ethanol contents of E0, E10, E30, E50, and E85 were prepared by blending ethanol into commercial gasoline on a volumetric basis and were analyzed each fuel specification. The engine control schemes of fuel injection quantity for various ethanol blends were adjusted to optimize the engine starting capability, vehicle drivability and emissions performance. The FE of the E85 fueled vehicle decreased by 29% relative to gasoline fuel due to the low energy content of ethanol. Blending ethanol into gasoline produced a dramatic decrease of particulate emission, because pure ethanol has no aromatic compounds and carbon content lower than that of gasoline. As a result, nano-particles were rarely emitted in the vehicle tests of fuels with more than 30% ethanol. Carbonyl compounds emissions, which originate from partial oxidization or incomplete combustion of ethanol, also rose sharply as the ethanol content increased, while volatile organic compound (VOC) emissions were reduced considerably with medium- and high-ethanol formulations due to the lower proportion of aromatic components in these fuels.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Emissions from various ethanol-gasoline blends were investigated in SIDI vehicle. </LI> <LI> Fuel economy and CO<SUB>2</SUB> were related to heating value and ethanol content of the fuels. </LI> <LI> Ethanol blending of 30–85% showed strong PN reduction relative to low-ethanol fuels. </LI> <LI> Individual HCs, alcohols, and aldehydes emissions strongly increased with E85 fuel. </LI> <LI> Aromatic HCs showed much lower emission characteristic as ethanol contents increased. </LI> </UL> </P>

      • KCI등재

        A Multicenter, Prospective, Observational Study to Evaluate Ethanol-Induced Symptoms in Patients Receiving Docetaxel Chemotherapy

        원영웅,강진형,권정혜,구동회,강정훈,맹치훈,안희경,오성용,이대원,손주혁,오소연,이경희,고수진,이근석,김찬규,김지연,지준호,김성배,하주영,김호영 대한암학회 2023 Cancer Research and Treatment Vol.55 No.4

        Purpose Several previous studies and case reports have reported ethanol-induced symptoms in patients receiving anticancer drugs containing ethanol. Most docetaxel formulations contain ethanol as a solvent. However, there are insufficient data on ethanol-induced symptoms when docetaxel-containing ethanol is administered. The primary purpose of this study was to investigate the frequency and pattern of ethanol-induced symptoms during and after docetaxel administration. The secondary purpose was to explore the risk factors for ethanol-induced symptoms. Materials and Methods This was a prospective, multicenter, observational study. The participants filled out ethanol-induced symptom questionnaire on the day of chemotherapy and the following day. Results Data from 451 patients were analyzed. The overall occurrence rate of ethanol-induced symptoms was 44.3% (200/451 patients). The occurrence rate of facial flushing was highest at 19.7% (89/451 patients), followed by nausea in 18.2% (82/451 patients), and dizziness in 17.5% (79/451 patients). Although infrequent, unsteady walking and impaired balance occurred in 4.2% and 3.3% of patients, respectively. Female sex, presence of underlying disease, younger age, docetaxel dose, and docetaxel-containing ethanol amount were significantly associated with the occurrence of ethanol-induced symptoms. Conclusion The occurrence of ethanol-induced symptoms was not low in patients receiving docetaxel-containing ethanol. Physicians need to pay more attention to the occurrence of ethanol-induced symptoms and prescribe ethanol-free or low-ethanol-containing formulations to high-risk patients.

      • SCOPUSKCI등재

        Ethanol 충격에 의한 Campylobacter jejuni 의 Ethanol 내성

        김치경,가익현 한국미생물학회 1992 미생물학회지 Vol.30 No.5

        Ethanol 충격에 의한 Campylobacter jejuni 의 생존성 및 ethanol 충격 단백질의 합성과 내성반응을 연구하였다. 1% 의 ethanol 충격에 대해서는 60분, 3% 의 ethanol 충격에서는 30분, 5%의 ethanol 충격에서는 10분대데, 분자량이 90, 66, 60, 45, 24 kd 인 충격 단백질이 합성되는 것을 autoradiography 로 확인하였다. C. jejuni 를 1% 와 3% 의 ethanol 에서 30 분간 충격을 준후 각각 3% 와 5% 의 농도에 노출시켰을때의 생존율은 ethanol 충격엾이 직접 3% 와 5% 의 ethanol에 노출시켰을 때보다 $10^{1}$ $-10^{2}$ 정도 높게 나타났다. 또 5% 에서 10분간 충격을 준후7% 의 ethanol 에 노출시켰을 때에도 직접 7% 에 노출시켰을 때보다 생존율이 $10^{2}$ 정도 높게 나타났다. 그러므로 1-5% 의 ethanol 로 충격을 받은 C. jejuni 는 그보다 높은 농도의 ethanol 에 대하여 ethanol 충격단백질에 의한 내성반응이 나타나 생존율의 감소가 훨씬 적어졌다. The responses of C. jejuni to ethanol shock were studied for their survival. synthesis of ethanol shock proteins, and increased survival at higher concentration of ethanol upon prior treatments of ethanol. When C. jejuni were shocked with ethanol at 1. 3. and 5% for 60. 30 and 10 minutes, respectively. those cells synthesized the ethanol shock proteins of 90, 66, 60, 45, and 24 kd in molecular weight. When the C. ,jejuni shocked with 1 and 3% ethanol were exposed to 3 and 5% ethanol for 30 minutes. their survival rates were increased by $10^1$~$10^2$ as compared with those of the cells without ethanol-shock. In the same way. C. ,jejuni shocked with 5% ethanol for 10 minutes :.bowed about 102 times higher survival rates than the cells without ethanol-shock. This result suggests that C jejuni shocked with I-5% ethanol for 10-30 minutes synthesized five kinds of ethanol shock proteins. and that the shock proteins contributed to increase ethanol tolerance for their survival at the higher concentrations of ethanol.

      • SCIESCOPUSKCI등재

        Increased Ethanol Resistance in Ethanolic Escherichia coli by Insertion of Heat-shock Genes BEM1 and SOD2 from Saccharomyces cerevisiae

        Lee, Soo-Jin,Oh, Eun-Kyoung,Oh, Young-Hoon,Won, Jong-In,Han, Sung-Ok,Lee, Jin-Won 한국생물공학회 2010 Biotechnology and Bioprocess Engineering Vol.15 No.5

        Ethanol is generally toxic to microorganisms, and intracellular and extracellular accumulation of ethanol inhibits cell growth and metabolism. In this study, pyruvate decarboxylase (pdc) and alcohol dehydrogenase (adhB) were cloned into pET-32a vector and then introduced into E. coli BL21 to produce ethanol. Heat shock genes (BEM1 and SOD2) from Saccharomyces cerevisiae were inserted into recombinant ethanolic E. coli using pET28_a vector to improve ethanol shock resistance. Three different strains were constructed: Ethanolic E. coli (adhB and pdc genes inserted using pET32_a vector), BEM1 gene-inserted E. coli (BEM1 inserted using pET_28a), and SOD2-inserted E. coli (SOD2 inserted using pET28_a). Construction of these three different strains allowed comparison of the functions of these heat shock genes as well as their roles in ethanol tolerance. The toxicity of ethanol in recombinant ethanolic E. coli was tested by measuring cell growth in response to various ethanol concentrations. The results show that SOD2-inserted E. coli showed higher ethanol resistance than ethanolic E. coli.

      • Ethanol increases matrix metalloproteinase-12 expression via NADPH oxidase-dependent ROS production in macrophages

        ( Mi Jin Kim ),( Saroj Nepal ),( Eung Seok Lee ),( Tae Cheon Jeong ),( Sang Hyun Kim ),( Pil-hoon Park ) 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0

        Matrix metalloproteinase-12 (MMP-12), an enzyme responsible for degradation of extracellular matrix, plays an important role in the progression of various diseases, including inflammation and fibrosis. Although most of those are pathogenic conditions induced by ethanol ingestion, the effect of ethanol on MMP-12 has not been explored. In the present study, we investigated the effect of ethanol on MMP-12 expression and its potential mechanisms in macrophages. Here, we demonstrated that ethanol treatment increased MMP-12 expression in primary murine peritoneal macrophages and RAW 264.7 macrophages at both mRNA and protein levels. Ethanol treatment also significantly increased the activity of nicotinamide adenine dinucleotide (NADPH) oxidase and the expression of NADPH oxidase-2 (Nox2). Pretreatment with an anti-oxidant (N-acetyl cysteine) or a selective inhibitor of NADPH oxidase (diphenyleneiodonium chloride (DPI)) prevented ethanol-induced MMP-12 expression. Furthermore, knockdown of Nox2 by small interfering RNA (siRNA) prevented ethanol-induced ROS production and MMP-12 expression in RAW 264.7 macrophages, indicating a critical role for Nox2 in ethanol-induced intracellular ROS production and MMP-12 expression in macrophages. We also showed that ethanol-induced Nox2 expression was suppressed by transient transfection with dominant negative IκB-α plasmid or pretreatment with Bay 11-7082, a selective inhibitor of NF-κB, in RAW 264.7 macrophages. In addition, ethanol-induced Nox2 expression was also attenuated by treatment with a selective inhibitor of p38 MAPK, suggesting involvement of p38 MAPK/NF-κB pathway in ethanol-induced Nox2 expression. Taken together, these results demonstrate that ethanol treatment elicited increase in MMP-12 expression via increase in ROS production derived from Nox2 in macrophages.ⓒ2013 Elsevier lnc. All rights reserved.

      • SCIESCOPUSKCI등재

        NECESSITY OF READY ELECTRON DISPOSAL AND INTERSPECIES HYDROGEN TRANSFER FOR THE UTILIZATION OF ETHANOL BY RUMEN BACTERIA

        Hino, T.,Mukunoki, H.,Imanishi, K.,Miyazaki, K. Asian Australasian Association of Animal Productio 1992 Animal Bioscience Vol.5 No.3

        Ethanol was utilized by mixed rumen microbes, but addition of pentachlorophenol (25 mg/l), a methanogen inhibitor, suppressed the utilization of ethanol. Carbon monoxide (50% of the gas phase), a hydrogenase inhibitor, more strongly suppressed the utilization of ethanol, propanol, and butanol. These results suggest that the major ethanol utilizers are $H_2$ producers. Ethanol utilization was depressed at low pH (below 6.0). Since methanogens were shown to be relatively resistant to low pH, it appears that ethanol utilizers are particularly sensitive to low pH. Ruminococcus albus and R. flavefaciens in mono-culture produced ethanol from carbohydrate (glucose and cellobiose), even when a high level (170 mM) of ethanol was present. Ethanol was not utilized even in the absence of carbohydrate, but the co-culture of these bacteria with methanogens resulted in the utilization of ethanol, i.e., when $H_2$ was rapidly converted to $CH_4$, R. albus and R. flavefaciens utilized ethanol. These results suggest that ethanol is utilized when the electrons liberated by the oxidation of ethanol are rapidly removed, and ready electron disposal in ethanol-utilizing, $H_2$-producing bacteria is accomplished by the interspecies transfer of $H_2$.

      • SCISCIESCOPUS

        Construction of <i>Saccharomyces cerevisiae</i> strains with enhanced ethanol tolerance by mutagenesis of the TATA‐binding protein gene and identification of novel genes associated with ethanol tolerance

        Yang, Jungwoo,Bae, Ju Yun,Lee, Young Mi,Kwon, Hyeji,Moon, Hye‐,Yun,Kang, Hyun Ah,Yee, Su‐,bog,Kim, Wankee,Choi, Wonja Wiley Subscription Services, Inc., A Wiley Company 2011 Biotechnology and bioengineering Vol.108 No.8

        <P><B>Abstract</B></P><P>Since elevated ethanol is a major stress during ethanol fermentation, yeast strains tolerant to ethanol are highly desirable for the industrial scale ethanol production. A technology called global transcriptional machinery engineering (gTME), which exploits a mutant library of <I>SPT15</I> encoding the TATA‐binding protein of <I>Saccharomyces cerevisiae</I> (Alper et al., 2006; Science 314: 1565–1568), seems to a powerful tool for creating ethanol‐tolerant strains. However, the ability of created strains to tolerate high ethanol on rich media remains unproven. In this study, a similar strategy was used to obtain five strains with enhanced ethanol tolerance (ETS1–5) of <I>S. cerevisiae</I>. Comparing global transcriptional profiles of two selected strains ETS2 and ETS3 with that of the control identified 42 genes that were commonly regulated with twofold change. Out of 34 deletion mutants available from a gene knockout library, 18 were ethanol sensitive, suggesting that these genes were closely associated with ethanol tolerance. Eight of them were novel with most being functionally unknown. To establish a basis for future industrial applications, strains iETS2 and iETS3 were created by integrating the SPT15 mutant alleles of ETS2 and ETS3 into the chromosomes, which also exhibited enhanced ethanol tolerance and survival upon ethanol shock on a rich medium. Fermentation with 20% glucose for 24 h in a bioreactor revealed that iETS2 and iETS3 grew better and produced approximately 25% more ethanol than a control strain. The ethanol yield and productivity were also substantially enhanced: 0.31 g/g and 2.6 g/L/h, respectively, for control and 0.39 g/g and 3.2 g/L/h, respectively, for iETS2 and iETS3. Thus, our study demonstrates the utility of gTME in generating strains with enhanced ethanol tolerance that resulted in increase of ethanol production. Strains with enhanced tolerance to other stresses such as heat, fermentation inhibitors, osmotic pressure, and so on, may be further created by using gTME. Biotechnol. Bioeng. 2011; 108:1776–1787. © 2011 Wiley Periodicals, Inc.</P>

      • KCI등재

        Effects of Common Bile Duct Ligation on Serum and Hepatic Carboxylesterase Activity in Ethanol-Intoxicated Rats

        Kim, You-Hee,Ahn, Kwan-Wook The Korea Science and Technology Center 1999 BMB Reports Vol.32 No.4

        Ethanol catabolism is thought to produce metabolic disorders resulting in alcoholic liver disease. To investigate the mutual effects of ethanol catabolism and cholestasis induced by common bile duct ligation on the activities of carboxylesterase, we have determined the enzyme activities in rat hepatic (cytosolic, mitochondrial, and microsomal) preparations as well as in rat serum using ten animal models: normal rats (group 1), sham-operated rats (group 2), common bile duct-ligated rats (group 3), ethanol-intoxicated rats (group 4), sham-operation plus chronic ethanol-intoxicated rats (group 5), common bile duct-ligated plus chronic ethanol-intoxicated rats (group 6), acute ethanol-intoxicated rats at 1.5 h and 24 h (groups 7A and 7B), and duct-ligated and acute ethanol intoxicated rats as 1.5 h and 24 h (groups 8A and 8B). The K? and V? values of carboxylesterase from these hepatic preparations of cholestatic rat liver combined with chronic ethanol intoxication were also measured by using ethyl valerate as the substrate from the 14th day post-ligation. Carboxylesterase activities of all hepatic preparations and rat serum (group 3) showed significant decreases compared to the activities from the sham-operated control (group 2). Enzyme kinetic parameters indicated that V? of carboxylesterase from all the hepatic preparations in cholestatic rats (group 3) decreased significantly, although the K? values were about the same as in the sham-operated control (group 2). When cholestasis was combined with chronic ethanol intoxication (group 6), carboxylesterase activities showed further decrease in all the hepatic preparations and serum compared to the control activity (group 5). The V? also decreased significantly, although K? values did not change. When common bile duct ligation was combined with acute ethanol intoxication (group 8), the enzyme activities in the rat liver and serum showed significant decrease compared to the activity form acute ethanol-intoxicated rats (group 7). However, quite contraty to this, the activities of serum from acute ethanol intoxication 1.5 h (group 7A) increased significantly compared to the activities in the normal control (group 1). These results, therefore, suggest that the biosynthesis of hepatic carboxylesterase seems to decrease when cholestasis is combined with chronic and acute ethanol intoxication, and the decrease in activity is more significant than from cholestasis alone.

      • Ethanol 및 Polylysine 첨가가 김치의 저장성에 미치는 효과

        정진웅,박기재,정승원 한국식품저장유통학회 ( 구 한국농산물저장유통학회 ) 2003 한국식품저장유통학회지 Vol.10 No.3

        김치 제조시 위생적 품질 개선을 위하여 ethanol과 천연항균물질인 polylysine의 복합 첨가를 검토하였다. Ethanol 농도를 0.3, 0.6 및 0.9%로 첨가하여 김치를 제조한 후 10℃에 저장하면서 3일 간격으로 총균수, 대장균군, 젖산균, 곰팡이 및 효모 등을 비교 측정한 결과, ethanol의 첨가는 대장균군과 젖산균의 생육 억제에 있어 보다 효과적인 것으로 나타났으며, ethanol 농도 0.6% 첨가시부터 미생물 생육 억제 효과가 뚜렷하게 나타났다. 또한 ethanol 0.6%를 첨가하여 담근 김치는 저장중 pH 저하 및 산도 상승에 대한 지연효과를 보여주었고, 저장중 관능특성의 변화에서도 신냄새, 이취, 신맛, 이미, 조직감 및 종합적 기호도의 모든 항목에서 가장 우수한 것으로 평가되었다. Polylysine은 단일 사용시 보다는 0.6% ethanol과 복합 첨가했을 경우 미생물 생육 억제에 상승효과를 보였으나 관능 평가에서 이미 이취를 느낀 것으로 평가되어 0.6% ethanol 단일 첨가가 미생물 증식 억제 및 발효 지연에 가장 효과적인 것으로 나타났다. Addition of ethanol and/or polylysine to kimchi ws investigated to improve its microbial hygienic quality and to extend shelf-life. Ethanol was added to kimchi with several concentrations(0.3%, 0.6%, 0.9%) and stored at 10℃. Addition of 0.6% and 0.9% ethanol showed apparent inhibitory effect on growth of microorganism, but any distinct difference was not found between those concentrations. Addition of ethanol was more effective on growth inhibition of coliform and lactic acid bacteria than other. Addition of 0.6% and 0.9% ethanol retarded apparently pH decrease and acidity increase. Although addition of 0.6% ethanol in combination with 0.12% polylysine showed good retardation of pH decrease and acidity increase, overall organoleptic quality was not good because of off-flavor and taste. Also, addition of 0.6% ethanol showed good overall organoleptic quality.

      • SCOPUS

        Ethanol-induced PGE<sub>2</sub> up-regulates Aβ production through PKA/CREB signaling pathway

        Gabr, Amr Ahmed,Lee, Hyun Jik,Onphachanh, Xaykham,Jung, Young Hyun,Kim, Jun Sung,Chae, Chang Woo,Han, Ho Jae Elsevier/North Holland [etc.] 2017 Biochimica et biophysica acta Vol.1863 No.11

        <P><B>Abstract</B></P> <P>Ethanol abuse aggravates dementia-associated cognitive defects through the progression of Alzheimer's disease (AD) pathophysiology. Beta-site APP-cleaving enzyme 1 (BACE1) has been considered as a key regulator of AD pathogenesis by controlling amyloid beta peptide (Aβ) accumulation. In addition, previous studies reported that endoplasmic reticulum (ER) stress and neuroinflammation have been proposed in ethanol-induced neurodegeneration. Thus, we investigated the role of ER stress and PGE<SUB>2</SUB>, a neuroinflammation mediator, in the ethanol-stimulated BACE1 expression and Aβ production. Using the human-derived neuroblastoma cell line SK-N-MC, the results show that ethanol up-regulated BACE1 expression in a dose-dependent manner. Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2α phosphorylation. PBA (an ER stress inhibitor) attenuated the ethanol-increased cyclooxygenase-2 (COX-2) expression and PGE<SUB>2</SUB> production. By using salubrinal (an eIF2α dephosphorylation inhibitor) or <I>EIF2A</I> siRNA, we found that eIF2α phosphorylation mediated the ethanol-induced COX-2 expression. In addition, COX-2-induced BACE1 up-regulation was abolished by NS-398 (a selective COX-2 inhibitor). And, PF-04418948 (an EP-2 receptor inhibitor) pretreatment reduced ethanol-induced PKA activation and CREB phosphorylation as well as ethanol-stimulated Aβ production. Furthermore, 14-22 amide (a PKA inhibitor) pretreatment or <I>CREB1</I> siRNA transfection suppressed the ethanol-induced BACE1 expression. In conclusion, ethanol-induced eIF2α phosphorylation stimulates COX-2 expression and PGE<SUB>2</SUB> production which induces the BACE1 expression and Aβ production via EP-2 receptor-dependent PKA/CREB pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ethanol induces BACE1 expression and Aβ production. </LI> <LI> Ethanol-produced ROS stimulates eIF2α phosphorylation and CHOP expression. </LI> <LI> ER stress enhanced by ethanol stimulates COX-2-mediated PGE2 production, which is critical for BACE1 expression. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

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