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The statistical interaction between dose and density was marginally significant for day of death (H = 7.813, df = 3, p = 0.05; Figure 1B) with tadpoles exposed to Dose 3 dying significantly earlier in low density tanks but not when held in high density conditions (Figure 1B, Table S1).
While the statistical interaction between dose and density is not significant (F = 1.763, df = 3, p = 0.153, Table S1) it is worth noticing that control tadpole in low density tanks reached a significantly more advanced stage of development than infected larvae (F = 4.252, df = 3, p = 0.006, stage 34 for control vs. 32 for dose 1, 32 for dose 2 and 30 for dose 3, Figure 1C).
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The relationship between dose density and outcome could only be found in the pretreated group.
These data, taken together lend strong support to the hypothesis that there is an isoform specific mechanistic effect on plaque deposition and clearance that is implicated in the positive correlation between ApoE4 dose and plaque density [13], [14] and strengthens the case for therapeutic intervention targeted at ApoE4's unique tertiary structure [43].
This is supported by data showing an inverse relationship between dose exposure and bone mineral density [ 7].
In the low density tanks the tadpoles with the lowest growth rate were those exposed to the highest virus dose (Figure 1D) indicating a dose response at this density: there were significant differences between Dose 3 and control, and Dose 2 and control (F = 14.64, df = 1, p<0.001 and F = 6.07, df = 1, p = 0.0141, respectively).
But meteorites show little correlation between heating and density.
Distinguish between volume and density.
In the untreated group, no relationship between dose delivered or dose density was seen.
Both increasing virus doses and host density resulted separately in a deterioration of host fitness.
However, the linearity of the relationship between virus dose and host fitness appears to be influenced by the density context in which the infection occurs.
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