In previous columns I have described our current moment of crisis specifically the rise of Trump, the far right, and populist strongmen as the result of two factors: (1) the increasing rate of disruption and (2) the lack of a capacity to lean into these moments by letting go of the old and letting come new patterns and possibilities (a capacity I call presencing).
The chief methodological difficulty has been the increasing rate of disruption of these runs over time by chromosomal rearrangement.
We used a simple 'relative measure' approach to separate the topological and biochemical effect of each disruption by comparing the growth rate of disruption strains in stressful and reference environments.
To estimate the effect of these disruptions on robustness we measured the growth rate of disruption strains, relative to the reference strain, in response to various stresses, both external (environmental) and internal (mutational).
However, it occurred to us that our observed de-adhesion dynamics might also depend on the rate of disruption of cell substrate adhesions (i.e., trypsin/EDTA activity), which might vary across drug treatments and cell lines.
The rates of gene disruption by both CCR5- and AAVS1-targeting ZFNs (using an amount of LPs corresponding to 200 ng p24) are summarized in Table 1.
We set out to compare the rates of p53 disruption in VIN and HPV-positive and HPV-negative VSCC in an attempt to establish whether p53 might be involved in progression from VIN to VSCC, and whether vulval carcinogenesis in the absence of HPV infection requires disruption of p53.
Of particular concern are significantly higher rates of placement disruptions among children in care who experience Fetal Alcohol Spectrum Disorder FASDD).
The mean effect of random and hub gene disruptions was determined by measuring the growth rate of each disruption strain within these two groups (figure 1).
What does matter much more are striker participation rates and levels of disruption.
