Furthermore, even in vivo animal models are incomplete with respect to modeling human disease in its entirety, with the exception of nonhuman primate studies.
However, pLSA-based models are incomplete in that they provide no probabilistic restriction on how to generate the training data.
Black box models are incomplete in virtue of leaving out details about underling mechanisms and that those models ultimately depend for their explanatory force on the promise that the functional models do, in fact, correspond to how the mechanism works.
The study of mental models is incomplete without corresponding observations and measurements of actual practices, all the more so if researchers aim like Atran and Medin to convince other scientists and to influence policymakers (see, e.g., "Conclusions," p. 269).
The third class reflects our observation that 32% of FGC07 models are incomplete.
However, a large proportion of the previously annotated gene models are incomplete, with either no start or no stop codons.
It appears that a comprehensive model for this level can be derived relatively easily from published models, but that the neurophysiological basis of these models is incomplete.
For example, although it is reported that "98% of the available genome was represented" [ 1], we estimate that approximately 50% of the gene models are incomplete or incorrect leading to missing, incomplete or spurious proteins.
In addition, existing mathematical models are incomplete representations of sepsis because simulated AIR in both mathematical models [ 13, 15] is considered to be an initial stage of sepsis progression.
Another reason for the overlap of the distributions is that 36% of the overlapping bad models are incomplete with <80% residues resolved which lowers the GDT_TS score but not the normalized QMEAN score.
