An unidentified protein, present also in endoAΔ4 null mutants, served as a convenient supplementary loading control (Figure 4A, asterisk).
While a positive correlation between objective response and survival was observed in our cohort, genome-wide analysis showed no significant differences in the overall mutation load (Supplementary Fig. 3) or neoantigen load (Supplementary Figs. 4 and 5) over time or between responders and non-responders, consistent with previously observed weak associations8, 14.
Secondly, a supplementary model for load balancing is set up for a better load distribution solution on feeders and transformers at TSC loading.
Lesion masking across the nine brains under study yielded a range of whole-brain lesion load (Supplementary Table 1), but with a common stereotypical distribution (Supplementary Fig. 2B).
Consequently, no correlation was found between the MHC-I gene-expression score and mutational load (Supplementary Fig. 10).
A microsatellite survey of BRASUZ1 and its inbred siblings indicated putative hotspots of genetic load (Supplementary Information section 4).
We used the T-, B-cell and macrophage signatures by Tirosh et al28 however we did not find any correlation between expression signatures and mutational load (Supplementary Fig. 10).
These negative correlations were stronger in networks of high plaque load (Supplementary Fig. 3), suggesting a detrimental impact of amyloid-β pathology on intrinsic connectivity.
This strategy permits efficient and sensitive detection of mutations using DNA extracted from paraffin-embedded tissue, even in samples with relatively low tumour load (Supplementary Figure 1).
With low load (Supplementary Fig. 4, 20 stored patterns), all morphs converge to the stored pattern Eff, whereas when many patterns are stored (Fig. 7 d, 160 stored patterns), the basin of attraction effectively shrinks, and only the morphs closer to the Eff pattern showed convergence.
In an attempt to quantify this effect we conducted a test retest reliability analysis that consisted of replacing the normal-appearing white matter regions of interest twice in the 15 subjects with two or fewer T2 lesions, to a location more typical of a subject with high lesion load (Supplementary Fig. 4).
