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In the paper, we proposed a method of space-time diversity on the transmitting side, combining a closed feedback and quasi-orthogonal space-time coding technique called closed-loop control with quasi-orthogonal space-time block coding (QO-STBC). For a configuration 4x1-4x4 with four transmit and one receive antennas and four symbols per four resource elements, our method allows the QO-STBC to be completely orthogonalized what maximizes the diversity gain. It is shown that the developed approach can also be used for the 4x2-4x2 configuration. In this case, it is not possible to orthogonalize QO-STBC completely, but the level of inter-channel correlation is considerably reduced. A statistical modeling was carried out to study the characteristics of noise immunity of the proposed transmission scheme. We show that it is sufficient to use a one-bit command to control the phase of two transmitting antennas. A gain of 1.4 dB is achieved for the 4x1-4x4 scenario and 2.5 dB - for the 4x2-4x2 case. Phase control of transmitting antennas used in this method of signal transmission does not change the interference conditions.

In the paper we develop and evaluate a novel low complexity algorithm of iterative detection and decoding in multiple input multiple output (MIMO) system. It is based on a new enhanced Turbo procedure. Although the algorithm utilizes well-known components such as linear minimum mean square error (MMSE) detector and channel decoder with soft bits feedback, the new original procedure of getting extrinsic data essentially allows improving the receiver performance and reducing its complexity. Moreover, it is shown that proposed Turbo approach works even without channel decoder in the iteration loop. Thus, we ob-tain pure iterative MMSE detector with improved performance. Utilization of combined scheme with MMSE detector and channel decoder feedback demonstrates really outstanding performance. It is confirmed with simulations that the performance of proposed architecture exceeds traditional ML MIMO detector schemes that are designed with channel decoder but without iterative loop.

In this work, we measured the intensities of Q-branches of the ν1, ν2 and ν3 bands in the polarized and depolarized methane Raman spectra in the pressure range of 1–60 atm. It was established that the pressure dependence of depolarization ratios of the ν2 and ν3 bands are negligible. In turn, the depolarization ratio of the ν1 band increases with increasing pressure and reaches approximately 0.0045 at 60 atm. These data are more precise than previously published ones because ν1 band intensities were determined taking into account the contribution of overlapping lines of ν3 band. The presented data will be useful in calculating the methane polarizabilities at high pressure, as well as in calculating methane Raman spectra for measuring the natural gas composition using Raman spectroscopy.

Alzheimer’s disease (AD) currently presents one of the biggest healthcare issues in the developed countries. There is no effective treatment capable of slowing down disease progression. In recent years the main focus of research on novel pharmacotherapies was based on the amyloidogenic hypothesis of AD, which posits that the beta amyloid (Aβ) peptide is chiefly responsible for cognitive impairment and neuronal death. The goal of such treatments is (a) to reduce Aβ production through the inhibition of β and γ secretase enzymes and (b) to promote dissolution of existing cerebral Aβ plaques. However, this approach has proven to be only modestly effective. Recent studies suggest an alternative strategy centred on the inhibition of the downstream Aβ signalling, particularly at the synapse. Aβ oligomers may cause aberrant N-methyl-D-aspartate receptor (NMDAR) activation postsynaptically by forming complexes with the cell-surface prion protein (PrPC). PrPC is enriched at the neuronal postsynaptic density, where it interacts with Fyn tyrosine kinase. Fyn activation occurs when Aβ is bound to PrPC-Fyn complex. Fyn causes tyrosine phosphorylation of the NR2B subunit of metabotropic glutamate receptor 5 (mGluR5). Fyn kinase blockers masitinib and saracatinib have proven to be efficacious in treating AD symptoms in experimental mouse models of the disease.