Reduction of MOC discretization errors through a minimization of source ratio variances

A new technique to reduce discretization errors for ray tracing in the method of characteristics (MOC) is proposed focusing on depletion calculations of single and multi-assembly geometries. In order to efficiently carry out depletion calculations, a calculation scheme using the superhomogenization (SPH) method can be used. However, the discretization errors are caused by changes of neutron sources and total cross sections according to a depletion. This fact means that improvement of accuracy cannot be expected by the calculation scheme with the SPH method when changes of the above parameters are significant. In order to mitigate this problem, a new approach is developed. In the new approach, the discretization errors are reduced by minimizing a variance of a certain parameter which is composed of a ratio of neutron source to total cross section. The verification results suggest that accuracy is degraded by the SPH method as expected especially in a geometry where neutron sources and total cross sections are drastically changing through a depletion. On the other hand, the new approach gives more accurate results compared to the conventional MOC in all calculation cases. Consequently, improvement of calculation efficiency by the new approach is confirmed.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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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

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

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

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

5 内腸骨動脈瘤に対する coverd stent 治療の検討(I.一般演題,第266回新潟循環器談話会)

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Protective efficacy against clinical malaria of ME-TRAP by Kaplan Meier analysis.

Protective efficacy against clinical malaria of ME-TRAP by Kaplan Meier analysis.</p

Protective efficacy against severe malaria of ME-TRAP by Kaplan Meier analysis.

Protective efficacy against severe malaria of ME-TRAP by Kaplan Meier analysis.</p