In general, nanomedicines are designed to improve the in vivo properties of low-molecular-weight (chemo-) therapeutic drugs, i.e. their biodistribution and the target site accumulation, and to thereby improve the balance between their efficacy and toxicity.
Self-assembled β-sheet-rich peptide nanofibers, previously shown to elicit potent antibody responses in mice, were found to be non-cytotoxic in vitro and, remarkably, elicited no measurable inflammation in vivo with none of the swelling at the injection site, accumulation of inflammatory cells or cytokines, or production of allergic IgE that were elicited by an alum-adjuvanted vaccine.
Using adjacent pasture as our baseline condition, we combined estimated on-site accumulation rates with estimates of exported C, and found that average total C sequestration rates were higher for hardwood (2.9 Mg C ha−1 yr−1) than red pine plots (2.3 Mg C ha−1 yr−1).
Applying even strong levels of recombination between binding sites did not elicit change in binding site accumulation.
Our results provide an important explanatory step between the evolution of genome complexity and regulatory complexity using binding site accumulation.
Although these properties are derived from binding site accumulation, their values are not completely determined by the number of binding sites.
When applied to binding site accumulation, however, recombination between binding sites yields minor effect over that which is determined by mutation and drift.
Because of the mutation bias pushing it towards or away from binding site accumulation, each population will evolve differently on the exact same space.
In this work, we show that neutral evolutionary forces alone can explain binding site accumulation, and that selection on the regulatory network function does not alter this finding.
So, the general application of selection on pathway dynamics does not seem to affect binding site accumulation on the genome scale.
