Signal detection for orthogonal space-time block coding over time-selective fading channels: a PIC approach for the Gi Systems

One major assumption in all orthogonal space-time block coding (O-STBC) schemes is that the channel remains static over the entire length of the codeword. However, time selective fading channels do exist, and in such case the conventional O-STBC detectors can suffer from a large error floor in the high signal-to-noise ratio (SNR) cases. This paper addresses such an issue by introducing a parallel interference cancellation (PIC) based detector for the Gi coded systems (i=3 and 4).

Blind equalization of nonminimum phase channels: higher order cumulant based algorithm

Higher order cumulant analysis is applied to the blind equalization of linear time-invariant (LTI) nonminimum-phase channels. The channel model is moving-average based. To identify the moving average parameters of channels, a higher-order cumulant fitting approach is adopted in which a novel relay algorithm is proposed to obtain the global solution. In addition, the technique incorporates model order determination. The transmitted data are considered as independently identically distributed random variables over some discrete finite set (e.g., set {��1, ��3}). A transformation scheme is suggested so that third-order cumulant analysis can be applied to this type of data. Simulation examples verify the feasibility and potential of the algorithm. Performance is compared with that of the noncumulant-based Sato scheme in terms of the steady state MSE and convergence rate.

Blind equalisation of multilevel PAM data for nonminimum phase channels via second- and fourth-order cumulants

This paper introduces a new blind equalisation algorithm for the pulse amplitude modulation (PAM) data transmitted through nonminimum phase (NMP) channels. The algorithm itself is based on a noncausal AR model of communication channels and the second- and fourth-order cumulants of the received data series, where only the diagonal slices of cumulants are used. The AR parameters are adjusted at each sample by using a successive over-relaxation (SOR) scheme, a variety of the ordinary LMS scheme, but with a faster convergence rate and a greater robustness to the selection of the ���step-size��� in iterations. Computer simulations are implemented for both linear time-invariant (LTI) and linear time-variant (LTV) NMP channels, and the results show that the algorithm proposed in this paper has a fast convergence rate and a potential capability to track the LTV NMP channels.

Orthogonal space-time block coding over time-selective fading channels: a PIC detector for the Gi systems

All the orthogonal space-time block coding (O-STBC) schemes are based on the following assumption: the channel remains static over the entire length of the codeword. However, time selective fading channels do exist, and in many cases the conventional O-STBC detectors can suffer from a large error floor in the high signal-to-noise ratio (SNR) cases. This paper addresses such an issue by introducing a parallel interference cancellation (PIC) based detector for the Gi coded systems (i=3 and 4).

Space-time block coding for four transmit antennas over time-selective fading channels: orthogonal or non-orthogonal design?

The paper deals with an issue in space time block coding (STBC) design. It considers whether, over a time-selective channel, orthogonal STBC (O-STBC) or non-orthogonal STBC (NO-STBC) performs better. It is shown that, under time-selectiveness, once vehicle speed has risen above a certain value, NO-STBC always outperforms O-STBC across the whole SNR range. Also, considering that all existing NO-STBC schemes have been investigated under quasi-static channels only, a new simple receiver is derived for the NO-STBC system under time-selective channels.

One-shot near-far resistant CDMA detection in multipath fading channels-an O^3 BPSK based system

This paper applies O3BPSK (orthogonal on-off PSK) signaling scheme to multipath fading CDMA channels, for the purpose of near-far resistant detection in the reverse link. Based on the maximum multipath spreading delay, a minimum duration of ���off��� is suggested, with which the temporally adjacent bits (TABs) from different users at the receiver are decoupled. As a result, a Rake-type one-shot linear decorrelating detector (LDD) is obtained. Since no knowledge of echo amplitudes is needed, a blind detection can be realised.

Nitric oxide suppresses cerebral vasomotion by sGC-independent effects on ryanodine receptors and voltage-gated calcium channels

Background/Aims: In cerebral arteries, nitric oxide (NO) release plays a key role in suppressing vasomotion. Our aim was to establish the pathways affected by NO in rat middle cerebral arteries. Methods: In isolated segments of artery, isometric tension and simultaneous measurements of either smooth muscle membrane potential or intracellular [Ca 2+ ] ([Ca 2+ ] SMC ) changes were recorded. Results: In the absence of L -NAME, asynchronous propagating Ca 2+ waves were recorded that were sensitive to block with ryanodine, but not nifedipine. L -NAME stimulated pronounced vasomotion and synchronous Ca 2+ oscillations with close temporal coupling between membrane potential, tone and [Ca 2+ ] SMC . If nifedipine was applied together with L -NAME, [Ca 2+ ] SMC decreased and synchronous Ca 2+ oscillations were lost, but asynchronous propagating Ca 2+ waves persisted. Vasomotion was similarly evoked by either iberiotoxin, or by ryanodine, and to a lesser extent by ODQ. Exogenous application of NONOate stimulated endothelium-independent hyperpolarization and relaxation of either L -NAME-induced or spontaneous arterial tone. NO-evoked hyperpolarization involved activation of BK Ca channels via ryanodine receptors (RYRs), with little involvement of sGC. Further, in whole cell mode, NO inhibited current through L-type voltage-gated Ca 2+ channels (VGCC), which was independent of both voltage and sGC. Conclusion: NO exerts sGC-independent actions at RYRs and at VGCC, both of which normally suppress cerebral artery myogenic tone.

Evidence for involvement of both IKCa and SKCa channels in hyperpolarizing responses of the rat middle cerebral artery

Endothelium-derived hyperpolarizing factor responses in the rat middle cerebral artery are blocked by inhibiting IKCa channels alone, contrasting with peripheral vessels where block of both IKCa and SKCa is required. As the contribution of IKCa and SKCa to endothelium-dependent hyperpolarization differs in peripheral arteries, depending on the level of arterial constriction, we investigated the possibility that SKCa might contribute to equivalent hyperpolarization in cerebral arteries under certain conditions. METHODS: Rat middle cerebral arteries (approximately 175 microm) were mounted in a wire myograph. The effect of KCa channel blockers on endothelium-dependent responses to the protease-activated receptor 2 agonist, SLIGRL (20 micromol/L), were then assessed as simultaneous changes in tension and membrane potential. These data were correlated with the distribution of arterial KCa channels revealed with immunohistochemistry. RESULTS: SLIGRL hyperpolarized and relaxed cerebral arteries undergoing variable levels of stretch-induced tone. The relaxation was unaffected by specific inhibitors of IKCa (TRAM-34, 1 micromol/L) or SKCa (apamin, 50 nmol/L) alone or in combination. In contrast, the associated smooth-muscle hyperpolarization was inhibited, but only with these blockers in combination. Blocking nitric oxide synthase (NOS) or guanylyl cyclase evoked smooth-muscle depolarization and constriction, with both hyperpolarization and relaxation to SLIGRL being abolished by TRAM-34 alone, whereas apamin had no effect. Immunolabeling showed SKCa and IKCa within the endothelium. CONCLUSIONS: In the absence of NO, IKCa underpins endothelium-dependent hyperpolarization and relaxation in cerebral arteries. However, when NOS is active SKCa contributes to hyperpolarization, whatever the extent of background contraction. These changes may have relevance in vascular disease states where NO release is compromised and when the levels of SKCa expression may be altered.