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The qualitative trends of the flame-spread rate and thermal boundary layer thickness, as obtained experimentally and from numerical predictions, were identical.
Overall there was a good correlation between the GSMN-TB model and the observed gene essentialities as 76.66% of the predictions were identical to the experimental results (additionally essential genes only).
All 68 tRNA genes predicted by AGeS were identical to those predicted by the Sanger Institute, and all 19 rRNA gene predictions overlapped (>96% length overlap), although only 6 rRNA gene predictions were identical in terms of the start and end locations.
iAbaylyiv2 already showed good agreement with the observed gene essentialities as 88% of the predictions were identical to the experimental results (respectively 95% of dispensable genes and 75% of essential genes present in the model, see Figure 1).
Similar(56)
Predictions are identical for their close relatives with a corresponding orthologous gene (not shown).
In our analysis, the genewise and exonerate predictions are identical in 27% of the cases.
In order to compare the different prediction methods GreenPhyl, Inparanoid and BBMH, we assumed that predictions are identical between two or three methods when several splice forms of the same locus are predicted as orthologs.
Our simplified method, applied to ABCD rule in three risk strata (low, 0 3; intermediate, 4 5; high, 6 7 points), indicated that predictions are identical to those computed by univariate, CPR-based logistic regression model.
The prediction results were identical with the test date, which can provide reference on the abrasion prediction and optimal design of guide vanes.
Comparing RefSeq promoter data in mouse with the mouse promoters inferred from the human mouse alignments showed that location-specific motif predictions were nearly identical across the two data sets, both in sequence as well as the location and width of overrepresentation (supplementary table 4, Supplementary Material online).
Currently, prediction of risk for complex diseases is based mainly on pedigree analysis but this approach yields predictions of risk that are of low precision; for example predictions would be identical for full siblings without offspring, yet the genetic variation among them accounts for half or more of the genetic variance [3], [4].
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com