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Fabrication of CuO-based antireflection structures using self-arranged submicron SiO2 spheres for thermoelectric solar generation

We fabricated antireflection structures (ARSs) on the hot side of a thermoelectric generator (TEG) to absorb near-infrared (NIR) solar light with low reflective energy loss. First, the ARSs, composed of a CuO thin-film coated hemisphere array were designed using rigorous coupled wave analysis. Reflective loss was reduced to 6.7% at a grating period of 200 nm, as determined by simulation. Then, the ARSs were fabricated on a glass substrate using self-arranged submicron SiO2 spheres, following the coating of a CuO thin film. Finally, the effect of the ARSs on NIR solar light generation was investigated by evaluating the generation properties of the TEG with the ARSs on the hot side. In comparison with the TEG with the CuO flat thin film on the hot side, the ARSs increased the temperature difference between the hot and cold sides by approximately 1.4 times. The CuO-based ARSs absorbed NIR solar light effectively.journal articl

高機能・環境に配慮した繊維材料およびその加工法に関する研究

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1 ACSを呈した Spontaneous coronary artery dissection (SCAD4) 例のIVUS画像の検討(II.テーマ演題,第266回新潟循環器談話会)

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CSA is involved in IE interaction with human NK cell line but not in primary NK cell activation.

<p>(A) The human NK cell line NK92 was incubated with whole culture of IE in different conditions. After 1 h at 37°C, a sample of the co-culture was placed between slide and cover and analyzed under a microscope. The NK92 cells directly interacts with IE (FCR3-CSA strain) as rosettes, but not with uninfected erythrocytes (x100 original magnification, left panel). RBC infected with FCR3-CSA or 2A5 were co-cultured with NK92 cells alone or in the presence of soluble CSA (+CSA), or with NK92 cells pre-treated with chondroitinase ABC (+Case ABC). At the end of the co-culture, the percentage of NK cells interacting with at least two IE was determined and expressed as % of cytoadhesion. Each dot represents one independent experiment (right panel). (B) Freshly isolated human PBMC were cultured with uninfected RBC (RBC), RBC infected with FCR3-CSA or RBC infected with the <i>var2csa</i> KO parasite 2A5. After 24 h, NK cell activation was analyzed by flow cytometry by gating on CD3⁻CD56⁺ lymphocytes. The CD69 MFI (mean fluorescence intensity) staining on NK cells (left panel), the percentage of CD25⁺ NK cells (middle panel) and the percentage of IFN-γ⁺ NK cells (right panel) were determined for 7 different healthy donors. Means±SEM are represented. Statistical analyses were performed using the Wilcoxon test.</p

Deficiency in CD36 does not alter NK cell response to IE.

<p>(A) The level of CD36 expression was determined on PBMC collected from a healthy donor (Control donor) or from a patient deficient for CD36. Total PBMC protein extracts were prepared and analyzed by Western Blot (left panel). Total PBMC were stained with CD36 antibody or with an isotype control (filled grey histogram, right panel). Histograms for CD3⁻CD56⁺ NK cells from a CD36 deficient donor (dotted line) and a control donor (bold line) are represented. (B) Control or CD36-deficient PBMC were cultured with uninfected RBC (RBC, black bars), or with RBC infected with the 3D7 <i>Pf</i> strain (3D7, grey bars). After 24 h, NK cell activation was analyzed by flow cytometry by gating on CD3⁻CD56⁺ NK cells. The CD69 MFI staining on NK cells (left panel), the percentage of CD25⁺ NK cells (middle panel) and the percentage of IFN-γ⁺ NK cells (right panel) were determined in three independent experiments. Means ± SEM are represented. Statistical analyses were performed using the Mann Whitney test.</p

PfEMP1 deficient parasites are potent activators of NK cells.

<p>Human PBMC were cultured with uninfected RBC (RBC, black bars) or with RBC infected with the “PfEMP1 KO” strain DC-J. After 24 h, NK cell activation was analyzed by flow cytometry by gating on CD3⁻CD56⁺ NK cells. The CD69 MFI staining on NK cells (left panel), the percentage of CD25⁺ NK cells (middle panel) and the percentage of IFN-γ⁺ NK cells (right panel) were determined for 5 different healthy donors. Means±SEM are represented. Statistical analyses were performed using the Wilcoxon test.</p

Expression of CSA, CD36 and ICAM-1 on human NK cells.

<p>Primary resting human NK cells (CD56⁺CD3⁻) in total PBMC as well as human NK cell lines, NK92 and NKL were analyzed by flow cytometry to determine the surface expression of three host ligands for PfEMP1: CSA (left panels, dark line), CD36 (middle panels, dark line) and ICAM-1 (right panels, dark line). Stainings with isotype control for each antibody are represented by filled grey histograms. Stainings of primary resting human NK cells are representative of at least 3 donors.</p

Engagement of ICAM-1 with its cellular ligand but not with PfEMP1 is required for NK cell IFN-γ production.

<p>(A) Diagram of an ICAM-1 molecule showing schematic binding sites for LFA-1, Mac-1, CD11c/CD18 and PfEMP1. The epitope map of the anti-ICAM-1 mAb 15.2, My13 and RR1/1 is indicated. (B) Human PBMC were cultured with uninfected RBC (RBC, black bars) or with RBC infected with the 3D7 <i>Pf</i> strain (3D7, grey bars) in presence or absence of antibodies directed against NKG2D (isotype control), ICAM-1 or CD18. Three different clones of anti-ICAM-1 were used: 15.2 blocks the interaction of ICAM-1 with LFA-1 and with PfEMP1, RR1/1 blocks only the interaction with LFA-1 and My13 blocks only the interaction with PfEMP1. After 24 h of co-culture, NK cell activation was analyzed by flow cytometry by gating on CD3⁻CD56⁺ NK cells. The CD69 MFI staining on NK cells (left panel), the percentage of CD25⁺ NK cells (middle panel) and the percentage of IFN-γ⁺ NK cells (right panel) were determined for 24 donors (None, NKG2D and 15.2), 13 donors (CD18), 9 donors (My13) or 5 donors (RR1/1). Means ± SEM are represented. Statistical analyses were performed using the Mann Whitney test.</p

Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesis

Supplementary Figure from Cancer Induces a Stress Ileopathy Depending on β-Adrenergic Receptors and Promoting Dysbiosis that Contributes to Carcinogenesi