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Träfflista för sökning "WFRF:(Xie Hua) srt2:(2007-2009)"

Sökning: WFRF:(Xie Hua) > (2007-2009)

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1.
  • Du, Jinkang, et al. (författare)
  • Development and testing of a new storm runoff routing approach based on time variant spatially distributed travel time method
  • 2009
  • Ingår i: Journal of Hydrology. - : Elsevier BV. - 0022-1694 .- 1879-2707. ; 369:1-2, s. 44-54
  • Tidskriftsartikel (refereegranskat)abstract
    • In this study, a GIS based simple and easily performed runoff routing approach based on travel time was developed to simulate storm runoff response process with consideration of spatial and temporal variability of runoff generation and flow routing through hillslope and river network. The watershed was discretized into grid cells, which were then classified into overland cells and channel cells through river network delineation from the DEM by use of GIS. The overland flow travel time of each overland cell was estimated by combining a steady state kinematic wave approximation with Manning’s equation, the channel flow travel time of each channel cell was estimated using Manning’s equation and the steady state continuity equation. The travel time from each grid cell to the watershed outlet is the sum of travel times of cells along the flow path. The direct runoff flow was determined by the sum of the volumetric flow rates from all contributing cells at each respective travel time for all time intervals. The approach was calibrated and verified to simulate eight storm runoff processes of Jiaokou Reservoir watershed, a sub-catchment of the Yongjiang River basin in southeast China using available topography, soil and land use data for the catchment. An average efficiency of 0.88 was obtained for the verification storms. Sensitivity analysis was conducted to investigate the effect of the area threshold of delineating river networks and parameter K relating channel velocity calculation on the predicted hydrograph at the basin outlet. The effects of different levels of grid size on the results were also studied, which showed that good results could be attained with a grid size of less than 200 m in this study. (C) 2009 Elsevier B.V. All rights reserved.
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2.
  • Xie, Baiyi, et al. (författare)
  • Combined Costimulation Blockade Inhibits Accelerated Rejection Mediated by Alloantigen-primed Memory T Cells in Mice
  • 2009
  • Ingår i: Immunological Investigations. - : Informa UK Limited. - 0882-0139 .- 1532-4311. ; 38:7, s. 639-651
  • Tidskriftsartikel (refereegranskat)abstract
    • Donor-reactive memory T cells threaten the survival of transplanted organs via multiple pathways. This study was undertaken to induce tolerance of cardiac allografts in mice, in which alloreactive memory T cells were adoptively transferred, by combined costimulatory blockade of both effector and memory T cells. We found that the median survival time (MST) of the grafts was 5.17 days in the untreated group, 10.33 days in the CTLA4Ig- and antiCD40L- treated (2-combined) group, and more than 100 days in the CTLA4Ig-, anti-CD40L-, anti-LFA-1-, and anti-OX40L-treated (4-combined) group. Histological analysis revealed that the mean rejection level was Grade 4 in the untreated group, Grade 3 in the 2-combined treatment group, and Grade 0 in the 4-combined treatment group. CD44(high) T cells were detected only in the untreated group. The in vitro proliferation of lymphocytes of both untreated and 2-combined group was higher than that of the 4-combined treatment group (p < 0.01). Compared with the untreated group, the expression levels of IL-2, IFN-gamma, and Foxp3 were lower in the 2-combined treatment group; the expression levels of these genes were the lowest in the 4-combined treatment group. IL-10 expression was significantly higher in the 4-combined treatment group than in the other groups. These results demonstrate the inhibition efficacy of combined costimulation blockade in accelerated-rejection models and the possible mechanisms underlying the suppression of cellular immunity in mice receiving grafts as well as in inducing the activation of IL-10-producing Tr1 cells in grafts.
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