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동형 모더나이트 상에서 일산화탄소 산화반응에 대한 속도론
정명수,이창용,최고열,하백현 漢陽大學校 環境科學硏究所 1989 環境科學論文集 Vol.10 No.-
모더나이트에 동을 이온교환 및 담지시킨 후 환원·산화 처리를 하여 동의 상태를 변화시킨 촉매에 대해 일산화탄소 산화반응의 속도론적인 고찰을 행하였다. 이온교환 촉매나 담지촉매 모두 동의 상태와는 관계없이 일산화탄소에 관한 반응차수는 1차이고 산소에 관한 반응차수는 0차였다. 이온교환 촉매의 경우는 수소로 환원시켜 동이 금속상태로 존재할때와 이를 재산화시켜 산화동 상태로 존재할때는 활성화에너지가 각각 16.4 및 20.3으로 비교적 큰 값을 나타냈으나 동의 담지촉매의 경우는 동이 금속일 때나 산화물 상태 모두 12∼13kcal/mole로 비슷한 값을 나타냈으며 이온교환 촉매보다 상당히 감소함을 알 수 있었다. 이와 같은 결과는 이온교환 촉매의 경우는 동이 제올라이트내부에 대부분 존재하는 반면, 담지촉매의 경우는 제올라이트 결정 표면에 존재하기 때문에 활성을 증가시키는 것으로 생각된다. Kinetics of oxidation of carbon monoxide over copper mordenite was carried out at the temperature range between 373K-443K in the micro-catalytic reactor. The experimental results indicated that the reaction order, with respect to carbon monoxide and oxygen was first and zero order respectively, regardless of the valence states such as copper metal, copper ion and copper oxide on the mordenite. The activation energy for metal-copper mordenite which is obtained by the ion-exchange revealed 20kcal/mol. But if this was reoxidized under the oxygen it decreased to 16.6kcal/mol. The activation energy of metal-copper mordenite which was obtained by impregnation and its reoxidized one under the oxygen were 12.2kcal/mol and 13.3kcal/mol respectively.
고분자 전해질형 연료전지에서 Hot Pressing 조건의 영향
이태희,이승재,조원일,노용우,고영태,최경환 한국화학공학회 1996 Korean Chemical Engineering Research(HWAHAK KONGHA Vol.34 No.1
고분자 전해질형 연료전지에서 고분자막/전극 어셈블리를 hot pressing 조건을 달리하여 제조하고 그 성능을 반응면적 5㎠인 단위전지에서 측정하였다. 전지의 성능은 고분자막과 전극간의 접합이 가능한 온도 범위에서 hot pressing온도가 낮을수록, hat Pressing 압력이 높을수록 향상되었다. 즉, 고분자 전해질형 연료전지의 성능은 고분자 전해질 내의 수분 함량 증가, 고분자막/전극간 접촉저항 감소 및 얇은 고분자막을 사용한 전해질의 이온저항 감소 등으로 향상시킬 수 있었다. For a proton exchange membrane fuel cell, membrane and electrode assemblies were fabricated by different hot pressing conditions and those performances were observed in a unit cell having 5 ㎠ active electrode area. The cell performance increased with lower hot pressing temperature in the range of temperature having intimate contact between membrane and electrodes and with higher hot pressing pressure. Namely, the performance of proton exchange membrane fuel cell could be raised with higher water content in the membrane, with lower contact resistance between membrane and electrodes and with lower ion resistance of the electrolyte using thinner membrane.
Kho, Dohng-Hyo,Lee, Jeong-Kug The Korean Society for Microbiology and Biotechnol 1997 Journal of microbiology and biotechnology Vol.7 No.5
A transposon Tn5 mutant of Rhodobacter sphaeroides 2.4.1 was isolated for its impaired ability of growth on minimal medium containing ${\beta}$-hydroxybutyric acid as a sole carbon source. The mutant, R. sphaeroides S7 showed approximately 6-fold decrease in ${\beta}$-hydroxybutyrate dehydrogenase activity compared with that of wild type. In R. sphaeroides S7 the Tn5 was located in DNA region corresponding to a 4.2-kb EcoRI DNA fragment of R. sphaeroides 2.4.1 chromosome.
Kho, Ying-Hee,Ko, Hack-Ryong,Chun, Hyo-Kon,Jung, Myung-Chul The Korean Society for Microbiology and Biotechnol 1995 Journal of microbiology and biotechnology Vol.5 No.1
Valistatin, a new inhibitor of aminopeptidase M(AP-M) was discovered in the culture broth of Streptomyces sp. SL20209 isolated from a soil sample. The inhibitor was purified by extraction with n-butanol and the various column chromatographies, and then isolated as whitish powder. The $^1 H-and ^1 H, ^1 H-COSY$ NMR studies, amino acid analysis, and fragmentation patterns by FAB-MS suggested the presence of one 3-amino-2-hydroxy-4-phenylbutanoic acid and two valine residues in the inhibitor. Thus, the structure of valistatin was determined as 3-amino-2-hydroxy-4-phenylbutanoyl-valyl-valine. Valistatin has the molecular formular $C_20H_31N_3 O_5$ (MW 394), and its $IC_50$ value against hog kidney AP-M was determined to be 3.12 $mu g/ml$.
KHO, Yoonjung,KIM, Sungchan,YOON, Byung Sun,MOON, Jai-Hee,KIM, Bona,KWAK, Sungwook,WOO, Junghee,OH, Sejong,HONG, Kichang,KIM, Saehun,KIM, Hyunggee,YOU, Seungkwon,CHOI, Yunjaie Japan Society for Bioscience, Biotechnology, and A 2008 Bioscience, Biotechnology, and Biochemistry Vol.72 No.1
<P>In this study, we examined the expression and functions of serum amyloid A (SAA) isoforms during apoptosis of HC11 mammary gland epithelial cells. Expression of SAA mRNAs and apoptosis were increased in HC11 cells by serum withdrawal and gradually decreased upon the addition of serum, or epidermal growth factor (EGF). TNFα treatment of HC11 cells also induced expression of SAA genes, and the effect on SAA1 and SAA2 expression was suppressed by treatment with MG132, and in cells transfected with a dominant negative mutant form of IκBα. Similar results were observed in response to interleukin-1 (IL-1), IL-6 and interferon γ (IFNγ). Furthermore, overexpression of the SAA1 and SAA2 isoforms suppressed growth and accelerated apoptosis of HC11 cells by increasing caspase 3/7 and caspase 8 activities, but the apoptotic effect of tumor necrosis factor α (TNFα) on HC11 cells was not enhanced. We found that expression of <I>SAA1</I> and <I>SAA2</I>, but not <I>SAA3</I>, was regulated by an NFκB-dependent pathway, and that overexpression of SAA isoforms accelerated the apoptosis of HC11 cells.</P>
WDNM1 is associated with differentiation and apoptosis of mammary epithelial cells.
Kho, Yoonjung,Kim, Sungchan,Yoon, Byung Sun,Moon, Jai-Hee,Kwak, Sungwook,Park, Gyuman,Woo, Junghee,Oh, Sejong,Hong, Kichang,Kim, Saehun,Kim, Hyunggee,You, Seungkwon,Choi, Yunjaie Marcel Dekker 2008 Animal biotechnology Vol.19 No.2
<P>In this study, we show that expression of the Westmead DMBA8 nonmetastatic cDNA 1 (WDNM1) gene was increased upon SFM and/or TNFalpha treatment, with a corresponding increase in apoptotic cells, and gradually decreased following re-stimulation with serum in HC11 mammary epithelial cells. TNFalpha induced WDNM1 expression showed the NFkappaB-dependent mechanism since it's expression was abrogated in IkappaBalphaM (super-repressor of NFkappaB)-transfected cells, but not those transfected with control vector. Furthermore, overexpression of WDNM1 suppressed growth and differentiation, and accelerated apoptosis of HC11 cells. Thus, our results demonstrate that WDNM1 gene expression, regulated by the TNFalpha-NFkappaB signal pathway, is associated with HC11 cell apoptosis.</P>