A synchronous program algebra: a basis for reasoning about shared-memory and event-based concurrency

This research started with an algebra for reasoning about rely/guarantee concurrency for a shared memory model. The approach taken led to a more abstract algebra of atomic steps, in which atomic steps synchronise (rather than interleave) when composed in parallel. The algebra of rely/guarantee concurrency then becomes an instantiation of the more abstract algebra. Many of the core properties needed for rely/guarantee reasoning can be shown to hold in the abstract algebra where their proofs are simpler and hence allow a higher degree of automation. The algebra has been encoded in Isabelle/HOL to provide a basis for tool support for program verification. In rely/guarantee concurrency, programs are specified to guarantee certain behaviours until assumptions about the behaviour of their environment are violated. When assumptions are violated, program behaviour is unconstrained (aborting), and guarantees need no longer hold. To support these guarantees a second synchronous operator, weak conjunction, was introduced: both processes in a weak conjunction must agree to take each atomic step, unless one aborts in which case the whole aborts. In developing the laws for parallel and weak conjunction we found many properties were shared by the operators and that the proofs of many laws were essentially the same. This insight led to the idea of generalising synchronisation to an abstract operator with only the axioms that are shared by the parallel and weak conjunction operator, so that those two operators can be viewed as instantiations of the abstract synchronisation operator. The main differences between parallel and weak conjunction are how they combine individual atomic steps; that is left open in the axioms for the abstract operator.Comment: Extended version of a Formal Methods 2016 paper, "An algebra of synchronous atomic steps

The synonymous substitution rates (dS) among paralogs within each subfamily and codon GC content (GC%) (A) and third codon GC content (GC3%) (B) of each subfamily is plotted

Dots and circles represent high cysteine KRTAP (HS) and high glycine-tyrosine KRTAP (HGT), respectively. The linear regression formulae for GC and dS are shown.<p><b>Copyright information:</b></p><p>Taken from "Molecular evolution of the keratin associated protein gene family in mammals, role in the evolution of mammalian hair"</p><p>http://www.biomedcentral.com/1471-2148/8/241</p><p>BMC Evolutionary Biology 2008;8():241-241.</p><p>Published online 23 Aug 2008</p><p>PMCID:PMC2528016.</p><p></p

Simplified phylogeny of all of the high glycine-tyrosine KRTAP genes generated by the neighbor-joining algorithm using p-distances

Genes of each subfamily are represented by different colors. Numbers on branches are the reliabilities of the branches which are calculated by interior branch tests with 1,000 replications. The bars indicate six subfamilies (6, 7, 8, 19, 20 and 21) of HGT-KRTAP genes.<p><b>Copyright information:</b></p><p>Taken from "Molecular evolution of the keratin associated protein gene family in mammals, role in the evolution of mammalian hair"</p><p>http://www.biomedcentral.com/1471-2148/8/241</p><p>BMC Evolutionary Biology 2008;8():241-241.</p><p>Published online 23 Aug 2008</p><p>PMCID:PMC2528016.</p><p></p

The relative genomic location of each KRTAP gene is shown for chromosomes 2, 11, 17 and 21

Each gene, and distances between genes are not to scale. Arrowheads indicate the direction of transcription. The clusters are also labeled.<p><b>Copyright information:</b></p><p>Taken from "Molecular evolution of the keratin associated protein gene family in mammals, role in the evolution of mammalian hair"</p><p>http://www.biomedcentral.com/1471-2148/8/241</p><p>BMC Evolutionary Biology 2008;8():241-241.</p><p>Published online 23 Aug 2008</p><p>PMCID:PMC2528016.</p><p></p

Nucleotide diversity (π) of previous reported balancing selection genes and the <i>LMBR1</i> intron 5 studied here.

<p>It shows that <i>LMBR1</i> intron 5 had low π among these genes with documented evidence of balancing selection. The data are from <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Fagundes1" target="_blank">[29]</a> (<i>LDLR</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Nakajima1" target="_blank">[30]</a> (<i>HAVCR1</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Wooding2" target="_blank">[18]</a> (<i>ABO</i>, <i>IL10R</i>B, <i>IL1A</i>, and <i>ACE2</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Hudson1" target="_blank">[19]</a> (5′ <i>CCR5</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Bernig1" target="_blank">[31]</a> (<i>MBL2</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Barreiro1" target="_blank">[32]</a> (<i>CD209L</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Soejima1" target="_blank">[33]</a> (<i>C6</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Stephens3" target="_blank">[13]</a> (<i>PTC</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Grigorova1" target="_blank">[34]</a> (<i>FSHB</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Allerston1" target="_blank">[35]</a> (<i>FMO3</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Verrelli1" target="_blank">[36]</a> (<i>G6PD</i>), <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone.0002948-Koda1" target="_blank">[37]</a> (<i>FUT2</i>).</p

Genetic variation analyses in the <i>LMBR1</i> intron 5 among 41 East Asian individuals.

<p>A: The 13 haplotypes constructed by PHASE program, and the right-most column shows the number of each haplotypes among 41 subjects. B: Median joining network of haplotypes. Each circle represents a haplotype indicated in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0002948#pone-0002948-g001" target="_blank">Figure 1A</a>, and the size of the circle is the relative frequency. Beside the branches are labels of the SNPs in the haplotypes counted from left to right. C: Graph of pairwise differences between the haplotypes. The dash line represent the observed sequence pairwise difference, and the real line represent the expected distribution of pairwise difference simulated by DnaSP under population growth with initial theta as 3.442, final theta as 1000, and final tau as 2.267. The “twin-peak” of observed mismatch distribution is suggestive of balancing selection. D: LD extent analyzed by R² of all pairwise comparisons between the 20 SNPs. The shadows indicate significant pairwise comparison identified with χ² tests by using a Bonferroni correction for multiple testing.</p

Linkage disequilibrium pattern of chr7: 155920–156290 kbp (NCBI35) region in the East Asian, European and African populations based on the HapMap Data.

<p><i>LMBR1</i> gene and the intron 5 are showed.</p

TNF -308 G/A Polymorphism and Risk of Acne Vulgaris: A Meta-Analysis

<div><p>Background</p><p>The -308 G/A polymorphism in the tumor necrosis factor (<i>TNF</i>) gene has been implicated in the risk of acne vulgaris, but the results are inconclusive. The present meta-analysis aimed to investigate the overall association between the -308 G/A polymorphism and acne vulgaris risk.</p><p>Methods</p><p>We searched in Pubmed, Embase, Web of Science and CNKI for studies evaluating the association between the -308 G/A gene polymorphism and acne vulgaris risk. Data were extracted and statistical analysis was performed using STATA 12.0 software.</p><p>Results</p><p>A total of five publications involving 1553 subjects (728 acne vulgaris cases and 825 controls) were included in this meta-analysis. Combined analysis revealed a significant association between this polymorphism and acne vulgaris risk under recessive model (OR = 2.73, 95% CI: 1.37–5.44, <i>p</i> = 0.004 for AA <i>vs</i>. AG + GG). Subgroup analysis by ethnicity showed that the acne vulgaris risk associated with the -308 G/A gene polymorphism was significantly elevated among Caucasians under recessive model (OR = 2.34, 95% CI: 1.13–4.86, <i>p</i> = 0.023).</p><p>Conclusion</p><p>This meta-analysis suggests that the -308 G/A polymorphism in the <i>TNF</i> gene contributes to acne vulgaris risk, especially in Caucasian populations. Further studies among different ethnicity populations are needed to validate these findings.</p></div

Population statistics summary of exon1 region.

<p>The bolds are values significantly lower than 0 with P-value<0.05 by simulating human demographic history incorporating human best-fit model.</p>a<p>is the number of chromosomes.</p

pairwise alignments of mtDNAs of domestic animals

pairwise alignments of mtDNAs of domestic animal