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The distributed transmit beamforming has recently been discussed as an energy-effective technique in wireless communication systems. A common ground of various techniques is that the destination node transmits a beacon signal or feedback to assist source nodes to synchronize signals. However, this approach is not appropriate for a radar system since the destination is a non-cooperative target of an unknown location. In our paper, we propose a novel synchronization strategy for a distributed multiple-element beamfoming radar system. Source nodes estimate parameters of beacon signals transmitted from others to get their local synchronization information. The channel information of the phase propagation delay is transmitted to nodes via the reflected beacon signals as well. Next, each node generates appropriate parameters to form a beamforming signal at the target. Transmit beamforming signals of all nodes will combine coherently at the target compensating for different propagation delay. We analyse the influence of the local oscillation accuracy and the parameter estimation errors on the performance of the proposed synchronization scheme. The results of numerical simulations illustrate that this synchronization scheme is effective to enable the transmit beamforming in a distributed multi-element radar system. [ABSTRACT FROM AUTHOR]

Previously, we found that exposure to a 50-Hz magnetic field (MF) could induce epidermal growth factor receptor (EGFR) clustering and phosphorylation on cell surface. In order to explore the possible mechanisms, the roles of acid sphingomyelinase (ASMase) and lipid raft in MF-induced EGFR clustering were investigated in the present study. Human amnion epithelial (FL) cells were exposed to a 50-Hz MF at 0.4 mT for different durations. Intracellular ASMase activity was detected using the Amplex® Red Sphingomyelinase Assay Kit. EGFR clustering, ASMase, and lipid rafts on cell membrane were analyzed using confocal microscopy after indirect immunofluorescence staining. Results showed that disturbing lipid rafts with nystatin could inhibit MF-induced EGFR clustering, indicating that it was dependent on intact lipid raft. Exposure of FL cells to MF significantly enhanced ASMase activity and induced ASMase translocation to membrane that co-localized with lipid rafts. Treatment with imipramine, an ASMase inhibitor, inhibited the MF-induced EGFR clustering. This inhibitory effect could be blocked by the addition of C2-ceramide in the culture medium. It suggested that ASMase mediated the 50-Hz MF-induced EGFR clustering via ceramide which was produced from hydrolyzation on lipid rafts. [ABSTRACT FROM PUBLISHER]

1. This study was designed to evaluate how the absence of P-glycoprotein (Pgp, Mdr1a), breast cancer-resistance protein (Bcrp, Abcg2) or both affects drug distribution into sciatic nerves, brain and cerebrospinal fluid (CSF) in rats. 2. Pgp substrate (loperamide), BCRP substrates (dantrolene and proprietary compound X) and dual substrates (imatinib and proprietary compound Y) were well distributed into sciatic nerves with comparable nerve to plasma concentration ratios between wild-type and knockout (KO) rats. 3. Brain exposure increased substantially in Mdr1a( −/−) rats for loperamide and in Mdr1a( −/−) /Abcg2( −/−) rats for imatinib and compound Y, but minimally to modestly in Abcg2( −/−) rats for dantrolene and compound X. The deletion of Mdr1a or Abcg2 alone had little effect on brain distribution of compound Y. 4. While CSF to unbound brain concentration ratio remained ≥3 in the KO animals for dantrolene, compounds X and Y, it was reduced to 1 in the Mdr1a( −/−) /Abcg2( −/−) rats for imatinib. 5. The data indicate that Pgp and Bcrp do not play significant roles in drug distribution into peripheral nerve tissues in rats, while working in concert to regulate brain penetration. Our results further support that CSF concentration may not be a good surrogate for unbound brain concentration of efflux substrates. [ABSTRACT FROM AUTHOR]