Abstract-We propose a novel algorithm for compressive imaging that exploits both the sparsity and persistence across scales found in the 2D wavelet transform coefficients of natural images. Like other recent works, we model wavelet structure using a hidden Markov tree (HMT) but, unlike other works, ours is based on loopy belief propagation (LBP). For LBP, we adopt a recently proposed "turbo" message passing schedule that alternates between exploitation of HMT structure and exploitation of compressive-measurement structure. For the latter, we leverage Donoho, Maleki, and Montanari's recently proposed approximate message passing (AMP) algorithm. Experiments with a large image database suggest that, relative to existing schemes, our turbo LBP approach yields state-of-the-art reconstruction performance with substantial reduction in complexity.
Hardware sharing can be used to reduce the area and the power dissipation of a design. This is of particular interest in the field of image and video compression, where an encoder must deal with different design tradeoffs depending on the characteristics of the signal to be encoded and the constraints imposed by the users. This paper introduces a novel methodology for exploring the design space based on the amount of hardware sharing between different functional blocks, giving as a result a set of feasible solutions which are broad in terms of hardware cost and throughput capabilities. The proposed approach, inspired by the notion of a partition in set theory, has been applied to optimize and to evaluate the sharing alternatives of a group of image and video compression key computational kernels when mapped onto a Xilinx Virtex-5 FPGA.
JAK2 V617F PV is a trilinear myeloproliferative neoplasm preceded by erythromelalgic thrombocythemia followed by myeloproliferative myeloid metaplasia of spleen and bone marrow and secondary myelofibrosis. The CALR and MPL mutated JAK2 wild type thrombocythemia complicated by myelofibrosis (MF) and agnogenic myeloid metaplasia (AMM) have no features of polycythemia vera (PV) are not primary or agnogenic anymore. The natural history of CALR and MPL thrombocythemia and secondary bone marrow fibrosis clearly differ fromJAK2 V617F trilinear essential thrombocythemia (ET), PV, post-ET and post-PV secondary myelofibrosis. Evolution of anemia, splenomegaly and myelofibrosis in MPL, CALR thrombocythemia and JAK2 V617F trilinear thrombocythemia and polycythemia vera (TPV) should be evaluated separately simple because treatment options differ.
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