180 research outputs found

    Miniature Fuel Cell with Monolithically Fabricated Si Electrodes -Optimization with Square Shape Through-chip Porous Layer

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    Abstract: Our Si based thin fuel cells have a through-chip porous Pt layer. The through-chip porous area has long narrow shape and the through-chip porous layer sometimes cracked during experimental handling. Therefore, the fuel channel shape was changed to square shape. Si substrate around the through-chip porous area works as rims and the mechanical strength seemed to be improved. Using the square openings, peak output of 108mW/cm 2 was obtained. However, the square opening is not suitable for our stacking structure. Then shallow channels, which connect each through-chip porous Pt layer, were fabricated by plasma etching with double masking layers

    MINIATURE FUEL CELL WITH MONOLITHICALLY FABRICATED SI ELECTRODES -ADHESION BETWEEN ELECTRODES AND PEM

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    Abstract: In this study, peak output of our miniature fuel cell was raised to 420mW/cm 2 which is comparable to the conventional large scale fuel cells. We have proposed monolithically fabricated Si electrodes for miniature fuel cells, on which porous Pt catalyst layer and fuel channels are formed on a Si wafer. Although our past prototype cells demonstrated relatively high outputs among MEMS based miniature fuel cells, compared with conventional large scale cells, performance was poor. In this study, in order to make spatial non-uniformity of the cell structure conspicuous, reaction area of the fuel cell was reduced to 1mm 2 . Some cells showed high outputs though the majority showed little output. It was suggested that the adhesion between electrode chip and PEM (Polymer Electrolyte Membrane) was not tight. The electrode chip has a depression on the catalyst area. Two sheets of PEM were placed on the catalyst area to realize tight contact and increased output was obtained

    Correlations between Extranodal Metastasis and Prognosis in Patients with Squamous Cell Carcinoma of the Esophagus

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    Background Extranodal metastasis (EM) has been reported in carcinomas of many organs. However, the clinicopathological significance of EM in squamous cell carcinoma of the esophagus remains unclear, and this study sought to clarify this issue. MethodsThis study included 220 patients who underwent an esophagectomy with lymphadenectomy for primary esophageal carcinoma from 1996 to 2008. EM was defined as the presence of cancer cells in the soft tissue that were discontinuous with the primary lesion, or in the perinodal soft tissue distinct from the lymph nodes. Results EM was detected in 25 (9.6%) of the 220 patients, and in 56 (0.7%) of the 8,186 nodules retrieved as ‘lymph nodes’. The incidence of EM was significantly higher in patients who had tumors of a larger size (diameter ≥ 4 cm), lymphatic vessel invasion, lymph node metastasis, a high pathological stage, infiltrative growth pattern, or a high pT-stage. The 5-year overall survival rates in N0-1 patients with EM were significantly lower than in the patients without EM (P = 0.005). Conclusion EM is closely associated with the development and aggressiveness of esophageal carcinoma, and the presence of EM can be useful for predicting prognosis after surgery in N0-1esophageal carcinoma patients

    Disruption of GM2/GD2 synthase gene resulted in overt expression of 9-O-acetyl GD3 irrespective of Tis211

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    GM2/GD2 synthase gene knockout mice lack all complex gangliosides, which are abundantly expressed in the nervous systems of vertebrates. In turn, they have increased precursor structures GM3 and GD3, probably replacing the roles of the depleted complex gangliosides. In this study, we found that 9-O-acetyl GD3 is also highly expressed as one of the major glycosphingolipids accumulating in the nervous tissues of the mutant mice. The identity of the novel component was confirmed by neuraminidase treatment, thin layer chromatography-immunostaining, two-dimensional thin layer chromatography with base treatment, and mass spectrometry. All candidate factors reported to be possible inducer of 9-O- acetylation, such as bitamine D binding protein, acetyl CoA transporter, or O-acetyl ganglioside synthase were not up-regulated. Tis21 which had been reported to be a 9-O-acetylation inducer was partially down-regulated in the null mutants, suggesting that Tis21 is not involved in the induction of 9-O-acetyl-GD3 and that accumulated high amount of GD3 might be the main factor for the dramatic increase of 9-O-acetyl GD3. The ability to acetylate exogenously added GD3 in the normal mouse astrocytes was examined, showing that the wild-type brain might be able to synthesize very low levels of 9-O-acetyl GD3. Increased 9-O-acetyl GD3, in addition to GM3 and GD3, may play an important role in the compensation for deleted complex gangliosides in the mutant mice

    Complement-5 Inhibition Deters Progression of Fulminant Hepatitis to Acute Liver Failure in Murine Models

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    BACKGROUND & AIMS: Acute liver failure (ALF) is a life-threatening condition with limited treatment alternatives. ALF pathogenesis seemingly involves the complement system. However, no complement-targeted intervention has been clinically applied. In this study, we aimed to investigate the potential of Complement-5 (C5)-targeted ALF treatment. METHODS: ALF was induced in C5-knockout (KO, B10D2/oSn) mice and their wild-type (WT) counterparts (B10D2/nSn) through intraperitoneal lipopolysaccharide (LPS) and d-galactosamine (D-GalN) administration. Thereafter, monoclonal anti-C5 antibody (Ab) or control immunoglobulin was administered intravenously. Furthermore, a selective C5a-receptor (C5aR) antagonist was administered to WT mice to compare its efficacy with that of anti-C5-Ab-mediated total C5 inhibition. We clarified the therapeutic effect of delayed anti-C5-Ab administration after LPS/D-GalN challenge. We also assessed the efficacy of anti-C5-Ab in another ALF model, using concanavalin-A. RESULTS: Liver injury was evident 6 hours after LPS/D-GalN administration. C5-KO and anti-C5-Ab treatment significantly improved overall animal survival and significantly reduced serum transaminase and high-mobility group box-1 release with decreased histological tissue damage. This improvement was characterized by significantly reduced CD41+ platelet aggregation, maintained F4/80+ cells, and less infiltration of CD11+/Ly6-G+ cells with lower cytokine/chemokine expression. Furthermore, C5-KO and anti-C5-Ab downregulated tumor necrosis factor-α production by macrophages before inducing marked liver injury. Moreover, single-stranded-DNA cells and caspase activation were reduced, indicating significant attenuation of apoptosis. Anti-C5-Ab treatment protected the liver more effectively than the C5aR antagonist, and its delayed doses were hepatoprotective. In addition, anti-C5-Ab treatment was effective against concanavalin-A-induced ALF. CONCLUSIONS: C5 inhibition effectively suppresses progression to ALF in mice models of fulminant hepatitis, serving as a new potential treatment strategy for ALF

    Complement 5 Inhibition Ameliorates Hepatic Ischemia/reperfusion Injury in Mice, Dominantly via the C5a-mediated Cascade

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    [Background. ] Hepatic ischemia/reperfusion injury (IRI) is a serious complication in liver surgeries, including transplantation. Complement activation seems to be closely involved in hepatic IRI; however, no complement-targeted intervention has been clinically applied. We investigated the therapeutic potential of Complement 5 (C5)-targeted regulation in hepatic IRI. [Methods. ] C5-knockout (B10D2/oSn) and their corresponding wild-type mice (WT, B10D2/nSn) were exposed to 90-minute partial (70%) hepatic ischemia/reperfusion with either anti-mouse-C5 monoclonal antibody (BB5.1) or corresponding control immunoglobulin administration 30 minutes before ischemia. C5a receptor 1 antagonist was also given to WT to identify which cascade, C5a or C5b-9, is dominant. [Results. ] C5-knockout and anti-C5-Ab administration to WT both significantly reduced serum transaminase release and histopathological damages from 2 hours after reperfusion. This improvement was characterized by significantly reduced CD41+ platelet aggregation, maintained F4/80+ cells, and decreased high-mobility group box 1 release. After 6 hours of reperfusion, the infiltration of CD11+ and Ly6-G+ cells, cytokine/chemokine expression, single-stranded DNA+ cells, and cleaved caspase-3 expression were all significantly alleviated by anti-C5-Ab. C5a receptor 1 antagonist was as effective as anti-C5-Ab for reducing transaminases. [Conclusions. ] Anti-C5 antibody significantly ameliorated hepatic IRI, predominantly via the C5a-mediated cascade, not only by inhibiting platelet aggregation during the early phase but also by attenuating the activation of infiltrating macrophages/neutrophils and hepatocyte apoptosis in the late phase of reperfusion. Given its efficacy, clinical availability, and controllability, C5-targeted intervention may provide a novel therapeutic strategy against hepatic IRI

    Mechanism of enhanced optical second-harmonic generation in the conducting pyrochlore-type Pb2_{2}Ir2_{2}O7x_{7-x} oxide compound

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    The structural, electronic, and optical properties of pyrochlore-type Pb2_{2}Ir2_{2}O6_{6}O'0.55_{0.55}, which is a metal without spatial inversion symmetry at room temperature, were investigated. Structural analysis revealed that the structural distortion relevant to the breakdown of the inversion symmetry is dominated by the Pb-O' network but is very small in the Ir-O network. At the same time, gigantic second-harmonic generation signals were observed, which can only occur if the local environment of the Ir 5dd electrons features broken inversion symmetry. First-principles electronic structure calculations reveal that the underlying mechanism for this phenomenon is the induction of the noncentrosymmetricity in the Ir 5dd bands by the strong hybridization with O' 2pp orbitals. Our results stimulate theoretical study of inversion-broken iridates, where exotic quantum states such as a topological insulator and Dirac semimetal are anticipated

    AstroPix: novel monolithic active pixel silicon sensors for future gamma-ray telescopes

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    Space-based gamma-ray telescopes such as the Fermi Large Area Telescope have used single sided silicon strip detectors to track secondary charged particles produced by primary gamma-rays with high resolution. At the lower energies targeted by keV-MeV telescopes, two dimensional position information within a single detector is required for event reconstruction - especially in the Compton regime. This work describes the development of monolithic CMOS active pixel silicon sensors - AstroPix - as a novel technology for use in future gamma-ray telescopes. Based upon sensors (ATLASPix) designed for use in the ATLAS detector at the Large Hadron Collider, AstroPix has the potential to maintain high performance while reducing noise with low power consumption. This is achieved with the dual detection and readout capabilities in each CMOS pixel. The status of AstroPix development and testing, as well as outlook for future testing and application, will be presented
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