Differential spatial modulation for high-rate transmission systems

This paper introduces a new differential spatial modulation (DSM) scheme which subsumes both the previously introduced DSM and high-rate spatial modulation (HR-SM) for wireless multiple input multiple output (MIMO) transmission. By combining the codeword design method of the HR-SM scheme with the encoding method of the DSM scheme, we develop a high-rate differential spatial modulation (HR-DSM) scheme equipped with an arbitrary number of transmit antennas that requires channel state information (CSI) neither at the transmitter nor at the receiver. The proposed approach can be applied to any equal energy signal constellations. The bit error rate (BER) performance of the proposed HR-DSM schemes is evaluated by using both theoretical upper bound and computer simulations. It is shown that for the same spectral efficiency and antenna configuration, the proposed HR-DSM outperforms the DSM in terms of bit error rate (BER) performance

Bone marrow niche trafficking of miR-126 controls the self-renewal of leukemia stem cells in chronic myelogenous leukemia

Leukemia stem cells (LSCs) in individuals with chronic myelogenous leukemia (CML) (hereafter referred to as CML LSCs) are responsible for initiating and maintaining clonal hematopoiesis. These cells persist in the bone marrow (BM) despite effective inhibition of BCR–ABL kinase activity by tyrosine kinase inhibitors (TKIs). Here we show that although the microRNA (miRNA) miR-126 supported the quiescence, self-renewal and engraftment capacity of CML LSCs, miR-126 levels were lower in CML LSCs than in long-term hematopoietic stem cells (LT-HSCs) from healthy individuals. Downregulation of miR-126 levels in CML LSCs was due to phosphorylation of Sprouty-related EVH1-domain-containing 1 (SPRED1) by BCR–ABL, which led to inhibition of the RAN–exportin-5–RCC1 complex that mediates miRNA maturation. Endothelial cells (ECs) in the BM supply miR-126 to CML LSCs to support quiescence and leukemia growth, as shown using mouse models of CML in which Mir126a (encoding miR-126) was conditionally knocked out in ECs and/or LSCs. Inhibition of BCR–ABL by TKI treatment caused an undesired increase in endogenous miR-126 levels, which enhanced LSC quiescence and persistence. Mir126a knockout in LSCs and/or ECs, or treatment with a miR-126 inhibitor that targets miR-126 expression in both LSCs and ECs, enhanced the in vivo anti-leukemic effects of TKI treatment and strongly diminished LSC leukemia-initiating capacity, providing a new strategy for the elimination of LSCs in individuals with CML

Akt phosphorylation of zyxin mediates its interaction with acinus-S and prevents acinus-triggered chromatin condensation

Zyxin, a focal adhesion molecule, contains LIM domains and shuttles between the cytoplasm and the nucleus. Nuclear zyxin promotes cardiomyocyte survival, which is mediated by nuclear-activated Akt. However, the molecular mechanism of how zyxin antagonizes apoptosis remains elusive. Here, we report that zyxin binds to acinus-S, a nuclear speckle protein inducing apoptotic chromatin condensation after cleavage by caspases, and prevents its apoptotic action, which is regulated by Akt. Akt binds and phosphorylates zyxin on serine 142, leading to its association with acinus. Interestingly, 14-3-3γ, but not ζ isoform selectively, triggers zyxin nuclear translocation, which is Akt phosphorylation dependent. Zyxin is also a substrate of caspases, but Akt phosphorylation is unable to prevent its apoptotic cleavage. Expression of zyxin S142D, a phosphorylation mimetic mutant, diminishes acinus proteolytic cleavage and chromatin condensation; by contrast, wild-type zyxin or unphosphorylated S142A mutant fails. Thus, Akt regulates zyxin/acinus complex formation in the nucleus, contributing to suppression of apoptosis.Link_to_subscribed_fulltex

An extended Galerkin weak form and a point interpolation method with continuous strain field and superconvergence using triangular mesh

A point interpolation method (PIM) with continuous strain field (PIM-CS) is developed for mechanics problems using triangular background mesh, in which PIM shape functions are used to construct both displacement and strain fields. The strain field constructed is continuous in the entire problem domain, which is achieved by simple linear interpolations using locally smoothed strains around the nodes and points required for the interpolation. A general parameterized functional with a real adjustable parameter α are then proposed for establishing PIM-CS models of special property. We prove theoretically that the PIM-CS has an excellent bound property: strain energy obtained using PIM-CS lies in between those of the compatible FEM and NS-PIM models of the same mesh. Techniques and procedures are then presented to compute the upper and lower bound solutions using the PIM-CS. It is discovered that an extended Galerkin (x-Galerkin) model, as special case resulted from the extended parameterized functional with α = 1, is outstanding in terms of both performance and efficiency. Intensive numerical studies show that upper and lower bound solutions can always be obtained, there exist α values at which the solutions of PIM-CS are of superconvergence, and the x-Galerkin model is capable of producing superconvergent solutions of ultra accuracy that is about 10 times that of the FEM using the same mes