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RISS 인기검색어
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- 저자 : Jun-You Lai (검색결과 2 건)
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Jang, Won-Jun,Jung, You-Shick,Shim, Jae-Oh,Roh, Hyun-Seog,Yoon, Wang Lai Elsevier 2018 Journal of Power Sources Vol.378 No.-
<P><B>Abstract</B></P> <P>Steam reforming of methane (SRM) is conducted using a series of Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalysts for direct internal reforming (DIR) in molten carbonate fuel cells (MCFCs). Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalysts are prepared by the homogeneous precipitation method with a variety of MgO loading amounts ranging from 3 to 15 wt%. In addition, each precursor concentrations are systemically changed (Ni: 1.2–4.8 mol L<SUP>−1</SUP>; Mg: 0.3–1.2 mol L<SUP>−1</SUP>; Al: 0.4–1.6 mol L<SUP>−1</SUP>) at the optimized composition (10 wt% MgO). The effects of MgO loading and precursor concentration on the catalytic performance and resistance against poisoning of the catalyst by potassium (K) are investigated. The Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalyst with 10 wt% MgO and the original precursor concentration (Ni: 1.2 mol L<SUP>−1</SUP>; Mg: 0.3 mol L<SUP>−1</SUP>; Al: 0.4 mol L<SUP>−1</SUP>) exhibits the highest CH<SUB>4</SUB> conversion and resistance against K poisoning even at the extremely high gas space velocity (GHSV) of 1,512,000 h<SUP>−1</SUP>. Excellent SRM performance of the Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalyst is attributed to strong metal (Ni) to alumina support interaction (SMSI) when magnesium oxide (MgO) is co-precipitated with the Ni-Al<SUB>2</SUB>O<SUB>3</SUB>. The enhanced interaction of the Ni with MgO-Al<SUB>2</SUB>O<SUB>3</SUB> support is found to protect the active Ni species against K poisoning.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalysts are synthesized by a homogeneous co-precipitation method. </LI> <LI> Ni-MgO-Al<SUB>2</SUB>O<SUB>3</SUB> catalysts with selected variables are applied to DIR-MCFC. </LI> <LI> Catalyst with 10 wt% MgO and PC1 shows the highest CH<SUB>4</SUB> conversion & K resistance. </LI> <LI> SMSI is most important characteristic for determining the catalytic performance. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Chlorophyll-Related Compounds Inhibit Cell Adhesion and Inflammation in Human Aortic Cells
Kuan-Hung Lin,Ching-Yun Hsu,Ya-Ping Huang,Jun-You Lai,Wen-Bin Hsieh,Meng-Yuan Huang,Chi-Ming Yang,Pi-Yu Chao 한국식품영양과학회 2013 Journal of medicinal food Vol.16 No.10
The objectives of this study were to investigate the effects of chlorophyll-related compounds (CRCs) and chlorophyll (Chl) a + b on inflammation in human aortic endothelial cells. Adhesion molecule expression and interleukin (IL)-8, nuclear factor (NF)-jB p65 protein, and NF-jB and activator protein (AP)-1 DNA binding were assessed. The effects of CRCs on inflammatory signaling pathways of signal transducers and activators of transcription 3 (STAT3) and mothers against decapentaplegic homolog 4, respectively induced by IL-6 and transforming growth factor (TGF)-b, in human aortic smooth muscle cells cultured in vitro were also investigated. HAECs were pretreated with 10 lM of CRCs, Chl a + b, and aspirin (Asp) for 18 h followed by tumor necrosis factor (TNF)-a (2 ng/mL) for 6 h, and U937 cell adhesion was determined. TNF-a–induced monocyte-endothelial cell adhesion was significantly inhibited by CRCs. Moreover, CRCs and Chl a + b significantly attenuated vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and IL-8 expressions. Treatments also significantly decreased in NF-jB expression, DNA binding, and AP-1 DNA binding by CRCs and Asp. Thus, CRCs exert anti-inflammatory effects through modulation of NF-jB and AP-1 signaling. Ten micromoles of CRCs and Asp upregulated the expression of mothers against decapentaplegic homolog 4 (Drosophila) (SMAD4) in the TGF-b receptor signaling pathway, and SMAD3/4 transcription activity was also increased. Ten micromoles of CRCs were able to potently inhibit STAT3-binding activity by repressing IL-6–induced STAT3 expression. Our results provide a potential mechanism that explains the anti-inflammatory activities of these CRCs.
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