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    Recovery of Sparse Signals Using Multiple Orthogonal Least Squares

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    We study the problem of recovering sparse signals from compressed linear measurements. This problem, often referred to as sparse recovery or sparse reconstruction, has generated a great deal of interest in recent years. To recover the sparse signals, we propose a new method called multiple orthogonal least squares (MOLS), which extends the well-known orthogonal least squares (OLS) algorithm by allowing multiple LL indices to be chosen per iteration. Owing to inclusion of multiple support indices in each selection, the MOLS algorithm converges in much fewer iterations and improves the computational efficiency over the conventional OLS algorithm. Theoretical analysis shows that MOLS (L>1L > 1) performs exact recovery of all KK-sparse signals within KK iterations if the measurement matrix satisfies the restricted isometry property (RIP) with isometry constant δLK<LK+2L.\delta_{LK} < \frac{\sqrt{L}}{\sqrt{K} + 2 \sqrt{L}}. The recovery performance of MOLS in the noisy scenario is also studied. It is shown that stable recovery of sparse signals can be achieved with the MOLS algorithm when the signal-to-noise ratio (SNR) scales linearly with the sparsity level of input signals

    Pathogenetic role of tissue factor in graft-versus-host disease

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    Graft-versus-host disease (GVHD) is a serious complication after allogeneic stem cell transplantation, the mechanism of it is still not elucidated. Recent findings suggest that host endothelial cells are a target of alloreactive donor cytotoxic T lymphocytes in GVHD and tissue factor (TF) plays an important role not only in coagulation-inflammation cycle, but also in transplant immunology. We postulate TF expression in vascular endothelial cells(VEC) may play an pivotal role in the pathogenesis of GVHD. TF gene andprotein expression in target organs of GVHD in aGVHD mice was significantly elevated compared to that of controls as determined by real-time PCR and Western blotting. Allogeneic CD4^+^T cell and CD8^+^T cells enhanced TF, VCAM-1, TNF-[alpha], IFN-[gamma] and IL-6 expression in TNF-[alpha] prestimulated HUVECs compared to controls as determined by flowcytometry and real-time PCR. JNK and p38MAPK mediated allogeneic T cells-induced TF expression in HUVECs. These effects were largely prevented by monoclonal antibody against TF, SB203580 and SP600125. In concert, these data provide strong evidence that upregulated TF expression is related to tissue damage caused by GVHD, TF isthe key factor in GVHD mediated by endothelial cells and allogeneic T cells-induced TF and consecutive proinflammatory cytokines expression in VEC contribute to the pathogenesis of GVHD
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