33,480 research outputs found
Effects of Manganese Oxide Addition on Coking Behavior of Ni/YSZ Anodes for SOFCs
No full textSolid oxide fuel cells with Ni-MnO/yttria-stabilized-zirconia (YSZ) tricomposite anode supports were fabricated with different MnO concentrations, and the coking tolerances and catalytic activities were investigated in wet CH4 atmosphere. Ni-0.9(MnO)(0.1)/YSZ (10MnO) anode support cell exhibited a maximum power density of 210, 354, 505, and 620 mWcm(-2) at 700, 750, 800, and 850 degrees C, respectively, in H-2. Moreover, a maximum power density in wet CH4 reaches 504 mWcm(-2) at 800 degrees C; while the Ni/YSZ cell showed poorer performances. The coking tolerance improved with an increase in their MnO content, and the 10MnO anode showed the highest tolerance. 10MnO exhibited stable performance for more than 40 h in wet CH4 without undergoing deactivation. Furthermore, it showed negligible coke formation of 0.0045 g of coke per catalyst, during testing under steam reforming-like conditions at a steam-to-carbon (S/C) ratio of 1. Outlet gas chromatography analysis indicated that MnO suppresses CH4 cracking, while only minimally lowering the catalytic activity of steam reforming. Thus, it can be inferred that MnO promotes the adsorption of steam and oxygen on the reaction sites, owing to its high basicity and oxygen storage capacity. The increase in the local S/C and oxygen-to-carbon ratios suppresses CH4 cracking and promotes coke gasification.X1155sciescopu
Clinicopathologic and prognostic significance of c-MYC copy number gain in lung adenocarcinomas
No full textBackground: c-MYC copy number gain (c-MYC gain) has been associated with aggressive behaviour in several cancers. However, the role of c-MYC gain has not yet been determined in lung adenocarcinomas classified by genetic alterations in epidermal growth factor receptor (EGFR), KRAS, and anaplastic lymphoma kinase (ALK) genes. We investigated the clinicopathologic and prognostic significance of c-MYC gain for disease-free survival (DFS) and overall survival (OS) according to EGFR, KRAS, and ALK gene status and stages in lung adenocarcinomas. Methods: In 255 adenocarcinomas resected in Seoul National University Bundang Hospital from 2003 to 2009, fluorescence in situ hybridisation (FISH) with c-MYC probe and centromeric enumeration probe 8 (CEP8) was analysed using tissue microarray containing single representative core per each case. EGFR (codon 18 to 21) and KRAS (codon 12, 13, and 61) mutations were analysed by polymerase chain reaction and direct sequencing method from formalin-fixed, paraffin-embedded tissue sections. ALK rearrangement was determined by FISH method. c-MYC gain was defined as >2 copies per nucleus, chromosome 8 gain as >= 3 copies per nucleus, and gain of c-MYC: CEP8 ratio (hereafter, c-MYC amplification) as >= 2. Results: We observed c-MYC gain in 20% (51 out of 255), chromosome 8 gain in 5.5% (14 out of 255), c-MYC amplification in 2.4% (6 out of 255), EGFR mutation in 49.4% (118 out of 239), KRAS mutation in 5.7% (7 out of 123), and ALK rearrangement in 4.9% (10 out of 205) of lung adenocarcinomas. c-MYC gain was observed in 19% (22 out of 118) of patients with lung adenocarcinomas with an EGFR mutation, but not in any patients with a KRAS mutation, or an ALK rearrangement. c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor in the full cohort of lung adenocarcinoma (P = 0.022, hazard ratio (HR) = 1.71, 95% confidence interval (CI), 1.08-2.69 for DFS; P = 0.032, HR = 2.04, 95% CI, 1.06-3.91 for OS), as well as in stage I subgroup (P = 0.023, HR = 4.70, 95% CI, 1.24-17.78 for DFS; P = 0.031, HR = 4.65, 95% CI, 1.15-18.81 for OS), and in EGFR-mutant subgroup (P = 0.022; HR = 2.14; 95% CI, 1.11-4.10 for DFS). Conclusions: c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor for DFS and OS in lung adenocarcinomas, both in full cohort and stage I cancer, and possibly for DFS in EGFR-mutant adenocarcinomas. Additional studies are required to determine if patients with lung adenocarcinoma with c-MYC gain are candidates for additional first-line treatment to mitigate their increased risk for disease progression and death.Y
Origin of clinopyroxene and amphibole megacrysts in the alkali basaltic rocks form western Taiwan as constrained by the REE geochemistry
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