Application of Jacobi algorithm for ISI channels

Here, the Jacobi iterative algorithm is applied to combat intersymbol interference (ISI) caused by frequency-selective channels. The performance bound of the equaliser is analysed in order to gain an insight into its asymptotic behaviour. Because of the error propagation problem, the potential of this algorithm is not reached in an uncoded system. However, its extension to a coded system with the application of the turbo-processing principle results in a new turbo equalisation algorithm, which demonstrates comparable performance with reduced complexity compared with some existing filter-based turbo equalisation schemes; and superior performance compared with some frequency domain solutions, such as orthogonal frequency division multiplexing and single-carrier frequency domain equalisation.

Pharmacology of transient receptor potential melastatin channels in the vasculature.

Mammalian transient receptor potential melastatin (TRPM) non-selective cation channels, the largest TRP subfamily, are widely expressed in excitable and non-excitable cells where they perform diverse functions ranging from detection of cold, taste, osmolarity, redox state and pH to control of Mg(2+) homeostasis and cell proliferation or death. Recently, TRPM gene expression has been identified in vascular smooth muscles with dominance of the TRPM8 channel. There has been in parallel considerable progress in decoding the functional roles of several TRPMs in the vasculature. This research on native cells is aided by the knowledge of the activation mechanisms and pharmacological properties of heterologously expressed TRPM subtypes. This paper summarizes the present state of knowledge of vascular TRPM channels and outlines several anticipated directions of future research in this area.

Interference cancellation schemes for MIMO MC-CDM in fading channels

A novel interference cancellation (IC) scheme for MIMO MC-CDM systems is proposed. It is shown that the existing IC schemes are suboptimum and their performance can be improved by utilising some special properties of the residual interference after interference cancellation.

Teleporting bipartite entanglement using maximally entangled mixed channels

The ability to teleport entanglement through maximally entangled mixed states as defined by concurrence and linear entropy is studied. We show how the teleported entanglement depends on the quality of the quantum channel used, as defined through its entanglement and mixedness, as well as the form of the target state to be teleported. We present new results based on the fidelity of the teleported state as well as an experimental setup that is immediately implementable with currently available technology.

Inward rectifier potassium channels in the HL-1 cardiomyocyte-derived cell line.

HL-1 is a line of immortalized cells of cardiomyocyte origin that are a useful complement to native cardiomyocytes in studies of cardiac gene regulation. Several types of ion channel have been identified in these cells, but not the physiologically important inward rectifier K(+) channels. Our aim was to identify and characterize inward rectifier K(+) channels in HL-1 cells. External Ba(2+) (100?µM) inhibited 44?±?0.05% (mean?±?s.e.m., n?=?11) of inward current in whole-cell patch-clamp recordings. The reversal potential of the Ba(2+)-sensitive current shifted with external [K(+)] as expected for K(+)-selective channels. The slope conductance of the inward Ba(2+)-sensitive current increased with external [K(+)]. The apparent Kd for Ba(2+) was voltage dependent, ranging from 15?µM at -150 ?mV to 148?µM at -75 ?mV in 120 ?mM external K(+). This current was insensitive to 10?µM glybenclamide. A component of whole-cell current was sensitive to 150?µM 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), although it did not correspond to the Ba(2+)-sensitive component. The effect of external 1 mM Cs(+) was similar to that of Ba(2+). Polymerase chain reaction using HL-1 cDNA as template and primers specific for the cardiac inward rectifier K(ir)2.1 produced a fragment of the expected size that was confirmed to be K(ir)2.1 by DNA sequencing. In conclusion, HL-1 cells express a current that is characteristic of cardiac inward rectifier K(+) channels, and express K(ir)2.1 mRNA. This cell line may have use as a system for studying inward rectifier gene regulation in a cardiomyocyte phenotype.