| Comparison of model-based predictions and real neuronal responses | In the simulated neuronal population, synchronized neurons had a mean minimum latency of 10.8 ms, while non-synchronized neurons had a mean minimum latency of 16.6 ms ( Wilcoxon rank sum test, P < 1.4 x 1089). |
| Comparison of model-based predictions and real neuronal responses | A similar difference occurred in the real neuronal population; synchronized neurons had a mean minimum latency of 18.1 ms, while non-synchronized neurons had a mean minimum latency of 51.1 ms ( Wilcoxon rank sum test, |
| Comparison of model-based predictions and real neuronal responses | We observed that mixed neurons had a mean minimum latency (simulated neurons: 8.0 ms, real neurons: 16.2 ms) not significantly different from synchronized neurons (Wilcoxon rank sum test, P = 0.053 (simulated), P = 0.30 (real)) and significantly different from non-synchronized neurons ( Wilcoxon rank sum test, P<3.1x10'75 (simulated), P<1.1x10'5 (real)). |
| Methods). | 7a, mixed 2 29.7 spk/s, nonsync = 13.9 spk/ s, sync = 3.3 spk/s; Wilcoxon rank sum test, P< 1.2 x 10'76, Bonferroni corrected). |
| Methods). | 7b, mixed 2 51.3 spk/s, nonsync = 22.5 spk/s, sync = 18.3 spk/s; Wilcoxon rank sum test, P< 0.003, Bonferroni corrected). |
| Methods). | 8a, sync = 0.93, mixed 2 0.79; Wilcoxon rank sum test, P< 3.3 x 1052, see Methods), While mixed response neurons had lower stimulus synchronization limits (Fig. |
| Activator-Activator Synergies | Significant synergy was defined here as a much greater effect of a combination of two reagents than the double doses of either reagent (requirement to pass two one-tailed Wilcoxon tests, each with p<0.05). |
| Inhibitor-Inhibitor Synergies | ( Wilcoxon p<0.05 for both comparisons). |
| Statistical Modeling | A one-tail Wilcoxon test was used to test the significance of whether activator-activator and in-hibitor-inhibitor combinations were superior to either of the double doses of the component reagents. |
| Statistical Modeling | (two Wilcoxon one-tailed tests with P<0.05 for each, Fig. |
| Statistical Modeling | To integrate the three strands of information, we took the significant interactions identified in the double Wilcoxon test for synergy, and the significant activator-inhibitor combination terms identified from the stepwise linear regression modelling. |
| ii J | Small *2 significant difference from the indicated double dose activator, by one-tailed Wilcoxon test P < 0.05. |
| Discovery of non-coding RNA genes active in the immediate-early response | Protein-coding clusters assigned to the early peak category had significantly more reads than the remaining clusters (14% increase in mean read count, p = 2.1e-6 Wilcoxon rank sum test). |
| Discovery of non-coding RNA genes active in the immediate-early response | Clusters associated with transcription factors were also in more accessible regions (p = 0.018), but, surprisingly, clusters assigned to known IEGs or nucleotide binding genes did not differ significantly from the reference set in either MCF7 time course (p > 0.08 by Wilcoxon rank sum test). |
| Discovery of non-coding RNA genes active in the immediate-early response | However, early peak lncRNA had significantly greater DNaseI counts than the remaining non-coding clusters (40% increase in mean read count, p = 1.3e-8 Wilcoxon rank sum test). |
| Kinetics and chromatin features underlying IEG induction | [34], we found IEGs to be associated with pro-moter-proximal pausing (that is, with a greater travelling ratio than non-IEGs; p = 1.2e-9 by Wilcoxon rank sum test on 114 IEGs compared with 8438 non-IEGs), and that the larger set of early peak genes was also associated with pausing (p = 1.4e- 14; 1421 early peak genes compared with 7131 reference genes). |