An Analysis of Carrier Phase Jitter in an M-PSK Receiver Utilizing MAP Estimation

The use of 8 and 16 PSK TCM to support satellite communications in an effort to achieve more bandwidth efficiency in a power-limited channel has been proposed. The authors address the problem of carrier phase jitter in an M-PSK receiver utilizing the high SNR approximation to the maximum a posteriori estimation of carrier phase. In particular, numerical solutions to 8 and 16 PSK self-noise and the amplitude suppression factor in the loop are presented. The effect of changing SNR on the loop noise bandwidth is also discussed. This data is then used to compute variance of phase error as a function of SNR. Simulation data is used to verify these calculations. The results show that there is a threshold in the variance of phase error verse SNR curves that is a strong function of SNR and a weak function of loop bandwidth. The M-PSK variance thresholds occur at SNRs in the range of practical interest for the use of 8 and 16-PSK TCM. This suggests that phase error variance is an important consideration in the design of these system

Synchronization in M-PSK Modems

In many applications, it is economical for a single modem to receive multiple modulation formats. In particular, the use of BPSK and QPSK has become a defacto standard in many military and NASA systems. However, there is significant interest in employing 8PSK and 16PSK modulation in these same systems today in order to conserve bandwidth. This paper addresses a technique for achieving carrier synchronization for all four of these PSK schemes in a single modem. This is accomplished by using quadrature channel carrier recovery processing and a version of the MAP phase detector algorithm. A model for the simulation of this tracking process is derived and results are presented to confirm its functionality

Superconducting Junctions with Ferromagnetic, Antiferromagnetic or Charge-Density-Wave Interlayers

Spectra and spin structures of Andreev interface states and the Josephson current are investigated theoretically in junctions between clean superconductors (SC) with ordered interlayers. The Josephson current through the ferromagnet-insulator-ferromagnet interlayer can exhibit a nonmonotonic dependence on the misorientation angle. The characteristic behavior takes place if the pi state is the equilibrium state of the junction in the particular case of parallel magnetizations. We find a novel channel of quasiparticle reflection (Q reflection) from the simplest two-sublattice antiferromagnet (AF) on a bipartite lattice. As a combined effect of Andreev and Q reflections, Andreev states arise at the AF/SC interface. When the Q reflection dominates the specular one, Andreev bound states have almost zero energy on AF/ s-wave SC interfaces, whereas they lie near the edge of the continuous spectrum for AF/d-wave SC boundaries. For an s-wave SC/AF/s-wave SC junction, the bound states are found to split and carry the supercurrent. Our analytical results are based on a novel quasiclassical approach, which applies to interfaces involving itinerant antiferromagnets. Similar effects can take place on interfaces of superconductors with charge density wave materials (CDW), including the possible d-density wave state (DDW) of the cuprates.Comment: LT24 conference proceeding, 2 pages, 1 figur

Phase Jitter in MPSK Carrier Tracking Loops: Analytical, Simulation and Laboratory Results

A performance characteristic of M-ary phase shift keying (MPSK) receivers is the variance of the phase error between the received and recovered signal carriers. For binary phase shift keying (BPSK) and quadrature phase shift keying (QPSK) loops utilizing integrate and dump filters and operating in the linear region, closed-form solutions for this variance exist [1], [2]. In this paper the variance is found by numerical methods for M \u3e 4. For verification and to investigate operation in the nonlinear region, computer simulation and hardware modeling were used [3]

Fast TCM Decoding: Phase Quantization and Integer Weighting

TCM, combining modulation and coding, achieves coding gains over conventional uncoded multilevel modulation without the attendant bandwidth expansion. Since TCM was proposed Ungerboeck (1982, 1987) substantial work has done in this area. A large portion of the TCM work has been in the area of high-speed data transmission over voice grade modems using quadrature amplitude modulation, QAM. QAM, not having a constant envelope, is unattractive for employing a TWT with its nonlinear behavior as the power stage. Additional work has been done in utilizing M-ary PSK with TCM. Simulations by Taylor and Chan (1981) utilizing a 4-state convolutional code demonstrated the coding gain of a rate 2/3 coded 8-PSK modulation scheme. Wilson et. al. (1984) obtained results for 16-PSK TCM using codes with 4 to 32 states and achieved coding gains of 3.5 to 4.8 dB respectively, over 8-PSK and demonstrated that small memory codes achieved good gains with simple design procedures

Telemetering and telecommunications research

The New Mexico State University (NMSU) Center for Space Telemetering and Telecommunications systems is engaged in advanced communications systems research. Four areas of study that are being sponsored concern investigations into the use of trellis-coded modulation (TCM). In particular, two areas concentrate on carrier synchronization research in TCM M-ary phase shift key (MPSK) systems. A third research topic is the study of interference effects on TCM, while the fourth research area is in the field of concatenated TCM systems

Mathematical models and the fight against diseases in Africa

n this age of molecular biology, The healthcare industry, politicians and the community at large are trying to find ‘magic bullet’ drugs and vaccines to conquer disease. Although smallpox has been eradicated and polio may soon be a scourge of the past, many pathogens replicate rapidly and mutate prodigiously, enabling them to evolve ways to circumvent our immune systems, as well as our drugs and vaccines. To fight and win the war against new emerging infections such as HIV/AIDS, TB and now SARS (severe acute respiratory syndrome), it is important to understand the temporal and spatial dynamics of the pathogens in human and, in some cases, animal reservoirs or vector populations. It is also necessary to understand the complex web of socio-economic factors pertinent to controlling the spread of disease, so that feasible, affordable and, most importantly, effective public-health policies can be devised and implemented

Elevating the levels of Sox2 in embryonal carcinoma cells and embryonic stem cells inhibits the expression of Sox2:Oct-3/4 target genes†

Recent studies have identified large sets of genes in embryonic stem and embryonal carcinoma cells that are associated with the transcription factors Sox2 and Oct-3/4. Other studies have shown that Sox2 and Oct-3/4 work together cooperatively to stimulate the transcription of their own genes as well as a network of genes required for embryogenesis. Moreover, small changes in the levels of Sox2:Oct-3/4 target genes alter the fate of stem cells. Although positive feedforward and feedback loops have been proposed to explain the activation of these genes, little is known about the mechanisms that prevent their overexpression. Here, we demonstrate that elevating Sox2 levels inhibits the endogenous expression of five Sox2:Oct-3/4 target genes. In addition, we show that Sox2 repression is dependent on the binding sites for Sox2 and Oct-3/4. We also demonstrate that inhibition is dependent on the C-terminus of Sox2, which contains its transactivation domain. Finally, our studies argue that overexpression of neither Oct-3/4 nor Nanog broadly inhibits Sox2:Oct-3/4 target genes. Collectively, these studies provide new insights into the diversity of mechanisms that control Sox2:Oct-3/4 target genes and argue that Sox2 functions as a molecular rheostat for the control of a key transcriptional regulatory network

COL4A3 expression in asthmatic epithelium depends on intronic methylation and ZNF263 binding.

Background Reduction of COL4A3, one of the six isoforms of collagen 4, in asthmatic airways results in increased inflammation and angiogenesis, implicating it as a central part of asthma pathogenesis. However, to date, the path underlying these diminished COL4A3 levels has been elusive. This study investigated a possible mechanism underlying the reduction of COL4A3 expression. Methods Bronchial biopsies of 76 patients with asthma and 83 controls were subjected to RNA-sequencing and DNA methylation bead arrays to identify expression and methylation changes. The binding of ZNF263 was analysed by chromatin-immunoprecipitation sequencing coupled with quantitative (q)PCR. Effects of ZNF263 silencing, using small interfering RNA, on the COL4A3 expression were studied using qPCR. Results COL4A3 expression was significantly reduced in bronchial biopsies compared to healthy controls, whereas DNA methylation levels at cg11797365 were increased. COL4A3 expression levels were significantly low in asthmatics without inhaled corticosteroid (ICS) use, whereas the expression was not statistically different between asthmatics using ICS and controls. Methylation levels at cg11797365 in vitro were increased upon consecutive rhinovirus infections. Conclusion Our data indicate an epigenetic modification as a contributing factor for the loss of COL4A3 expression in asthmatic airway epithelium