Anti-CGB monoclonal antibody, clone 6I5-F3

The acoustic emission (AE) characteristics, change law of the ultrasonic velocity, and internal failure mode of cemented waste concrete-coal gangue backfilling (CWCGB) with 600 days of curing time were studied under uniaxial loading conditions. Waste concrete particles of 5 mm acting as fine aggregates substituted for 30% and 50% fine coal gangue in the cemented coal gangue backfilling (CGB). AE was used to test the ring count and changing rule of the accumulated energy, locate the event for positioning, and calculate the number of events. The average ultrasonic wave velocity was measured via an ultrasonic detector. The characteristics of the microfractures were observed via a scanning electron microscope. The results showed that the specimens with 30% and 50% waste concrete replacement rates underwent ultrasonic wave velocity stabilization and a rapid decline stage under uniaxial compression; for the former case, the decline started earlier. The AE ring count attained peaks at the pore compression stage, yield stress point, stress peak value, and residual stress stage with no added waste concrete and 30% and 50% waste concrete substitution rates. The value and consequent frequency of the ringing count peak and cumulative energy slope increased with increasing waste concrete substitution rate. A microcrack was observed at the interfacial transition zone between the cement paste and gangue owing to the alkali-aggregate reaction effect. However, a better bonding performance was exhibited by the waste concrete particles and paste.

Epigenetic marks such as cytosine methylation are important determinants of cellular and whole-body phenotypes. However, the extent of, and reasons for inter-individual differences in cytosine methylation, and their association with phenotypic variation are poorly characterised. Here we present the first genome-wide study of cytosine methylation at single-nucleotide resolution in an animal model of human disease. We used whole-genome bisulfite sequencing in the spontaneously hypertensive rat (SHR), a model of cardiovascular disease, and the Brown Norway (BN) control strain, to define the genetic architecture of cytosine methylation in the mammalian heart and to test for association between methylation and pathophysiological phenotypes. Analysis of 10.6 million CpG dinucleotides identified 77,088 CpGs that were differentially methylated between the strains. In F1 hybrids we found 38,152 CpGs showing allele-specific methylation and 145 regions with parent-of-origin effects on methylation. Cis-linkage explained almost 60% of inter-strain variation in methylation at a subset of loci tested for linkage in a panel of recombinant inbred (RI) strains. Methylation analysis in isolated cardiomyocytes showed that in the majority of cases methylation differences in cardiomyocytes and noncardiomyocytes were strain-dependent, confirming a strong genetic component for cytosine methylation. We observed preferential nucleotide usage associated with increased and decreased methylation that is remarkably conserved across species, suggesting a common mechanism for germline control of inter-individual variation in CpG methylation. In the RI strain panel, we found significant correlation of CpG methylation and levels of serum chromogranin B (CgB), a proposed biomarker of heart failure, which is evidence for a link between germline DNA sequence variation, CpG methylation differences and pathophysiological phenotypes in the SHR strain. Together, these results will stimulate further investigation of the molecular basis of locally regulated variation in CpG methylation and provide a starting point for understanding the relationship between the genetic control of CpG methylation and disease phenotypes.