Performance Analysis of Iteratively Decoded Variable-Length Space-Time Coded Modulation

It is demonstrated that iteratively Decoded Variable Length Space Time Coded Modulation (VL-STCM-ID) schemes are capable of simultaneously providing both coding gain as well as multiplexing and diversity gain. The VL-STCM-ID arrangement is a jointly designed iteratively decoded scheme combining source coding, channel coding, modulation as well as spatial diversity/multiplexing. In this contribution, we analyse the iterative decoding convergence of the VL-STCM-ID scheme using symbol-based three-dimensional EXIT charts. The performance of the VL-STCM-ID scheme is shown to be about 14.6 dB better than that of the Fixed Length STCM (FL-STCM) benchmarker at a source symbol error ratio of 10?4, when communicating over uncorrelated Rayleigh fading channels. The performance of the VL-STCM-ID scheme when communicating over correlated Rayleigh fading channels using imperfect channel state information is also studied

Dna2 Helicase/Nuclease Causes Replicative Fork Stalling and Double-strand Breaks in the Ribosomal DNA of Saccharomyces cerevisiae

We have proposed that faulty processing of arrested replication forks leads to increases in recombination and chromosome instability in Saccharomyces cerevisiae and contributes to the shortened lifespan of dna2 mutants. Now we use the ribosomal DNA locus, which is a good model for all stages of DNA replication, to test this hypothesis. We show directly that DNA replication pausing at the ribosomal DNA replication fork barrier (RFB) is accompanied by the occurrence of double-strand breaks near the RFB. Both pausing and breakage are elevated in the early aging, hypomorphic dna2-2 helicase mutant. Deletion of FOB1, encoding the fork barrier protein, suppresses the elevated pausing and DSB formation, and represses initiation at rDNA ARSs. The dna2-2 mutation is synthetically lethal with {Delta}rrm3, encoding another DNA helicase involved in rDNA replication. It does not appear to be the case that the rDNA is the only determinant of genome stability during the yeast lifespan however since strains carrying deletion of all chromosomal rDNA but with all rDNA supplied on a plasmid, have decreased rather than increased lifespan. We conclude that the replication-associated defects that we can measure in the rDNA are symbolic of similar events occurring either stochastically throughout the genome or at other regions where replication forks move slowly or stall, such as telomeres, centromeres, or replication slow zones