BER of MRC for M-QAM with imperfect channel estimation over correlated Nakagami-m fading

In this contribution, we provide an exact BER analysis for M-QAM transmission over arbitrarily correlated Nakagami-m fading channels with maximal-ratio combining (MRC) and imperfect channel estimation at the receiver. Assuming an arbitrary joint fading distribution and a generic pilot-based channel estimation method, we derive an exact BER expression that involves an expectation over (at most) 4 variables, irrespective of the number of receive antennas. The resulting BER expression includes well-known PDFs and the PDF of only the norm of the channel vector. In order to obtain the latter PDF for arbitrarily correlated Nakagami-m fading, several approaches from the literature are discussed. For identically distributed and arbitrarily correlated Nakagami-m channels with integer m, we present several BER performance results, which are obtained from numerical evaluation and confirmed by straightforward computer simulations. The numerical evaluation of the exact BER expression turns out to be much less time-consuming than the computer simulations

Actin polymerization-dependent activation of Cas-L promotes immunological synapse stability

This work was supported by National Institutes of Health Common Fund through a Nanomedicine Development Center PN2EY016586 (MLD, MPS). OH and KA were Cas-L coordinates T-cell actin cytoskeleton 2 supported by NIH grants R01 AI068963-01A2 and R01 AI088106-01A1. The Wellcome Trust and the Kennedy Institute of Rheumatology Trust supported MLD

The deleted in brachydactyly B domain of ROR2 is required for receptor activation by recruitment of Src

The transmembrane receptor 'ROR2' resembles members of the receptor tyrosine kinase family of signalling receptors in sequence but its' signal transduction mechanisms remain enigmatic. This problem has particular importance because mutations in ROR2 are associated with two human skeletal dysmorphology syndromes, recessive Robinow Syndrome (RS) and dominant acting Brachydactyly type B (BDB). Here we show, using a constitutive dimerisation approach, that ROR2 exhibits dimerisation-induced tyrosine kinase activity and the ROR2 C-terminal domain, which is deleted in BDB, is required for recruitment and activation of the non-receptor tyrosine kinase Src. Native ROR2 phosphorylation is induced by the ligand Wnt5a and is blocked by pharmacological inhibition of Src kinase activity. Eight sites of Src-mediated ROR2 phosphorylation have been identified by mass spectrometry. Activation via tyrosine phosphorylation of ROR2 receptor leads to its internalisation into Rab5 positive endosomes. These findings show that BDB mutant receptors are defective in kinase activation as a result of failure to recruit Src

Wnt5a induces ROR1 to complex with HS1 to enhance migration of chronic lymphocytic leukemia cells.

ROR1 (receptor tyrosine kinase-like orphan receptor 1) is a conserved, oncoembryonic surface antigen expressed in chronic lymphocytic leukemia (CLL). We found that ROR1 associates with hematopoietic-lineage-cell-specific protein 1 (HS1) in freshly isolated CLL cells or in CLL cells cultured with exogenous Wnt5a. Wnt5a also induced HS1 tyrosine phosphorylation, recruitment of ARHGEF1, activation of RhoA and enhanced chemokine-directed migration; such effects could be inhibited by cirmtuzumab, a humanized anti-ROR1 mAb. We generated truncated forms of ROR1 and found its extracellular cysteine-rich domain or kringle domain was necessary for Wnt5a-induced HS1 phosphorylation. Moreover, the cytoplamic, and more specifically the proline-rich domain (PRD), of ROR1 was required for it to associate with HS1 and allow for F-actin polymerization in response to Wnt5a. Accordingly, we introduced single amino acid substitutions of proline (P) to alanine (A) in the ROR1 PRD at positions 784, 808, 826, 841 or 850 in potential SH3-binding motifs. In contrast to wild-type ROR1, or other ROR1P→︀A mutants, ROR1P(841)A had impaired capacity to recruit HS1 and ARHGEF1 to ROR1 in response to Wnt5a. Moreover, Wnt5a could not induce cells expressing ROR1P(841)A to phosphorylate HS1 or activate ARHGEF1, and was unable to enhance CLL-cell motility. Collectively, these studies indicate HS1 plays an important role in ROR1-dependent Wnt5a-enhanced chemokine-directed leukemia-cell migration

Triple‐crystal x‐ray diffraction analysis of reactive ion etched gallium arsenide

This is the published version. Copyright 1994 American Institute of PhysicsThe effect of BCl3 reactive ion etching on the structural perfection of GaAs has been studied with diffuse x‐ray scattering measurementsconducted by high‐resolution triple‐crystal x‐ray diffraction. While using a symmetric 004 diffraction geometry revealed no discernible differences between etched and unetched samples, using the more surface‐sensitive and highly asymmetric 113 reflection revealed that the reactive ion etched samples etched displayed less diffusely scattered intensity than unetched samples, indicating a higher level of structural perfection. Increasing the reaction ion etch bias voltage was found to result in decreased diffuse scattering initially, until an apparent threshold voltage was reached, after which no further structural improvement was observed. Furthermore, we have shown that this reduction in process‐induced surfacestructural damage is not due merely to the removal of residual chemical‐mechanical polishing damage

Erratum to: 36th International Symposium on Intensive Care and Emergency Medicine: Brussels, Belgium. 15-18 March 2016.

[This corrects the article DOI: 10.1186/s13054-016-1208-6.]