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Early theoretical models support this hypothesis (Dornbusch 1974).
Most climate models support this increase in temperature.
Evaluation of the features of RTT suggests that the basis of this disease could be an alteration of neuronal plasticity and studies of RTT mouse models support this suggestion.
Coalescence models support this interpretation.
Studies using animal models support this finding.
Several pre-clinical models support this mechanism [ 40, 41].
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Enzymatic structure mapping of oligonucleotide models supported this notion.
Mapping those uni-ETSs to rice gene models supported this assumption.
The comparison of the computational models supports this conclusion, but does not go beyond earlier explanations of the system.
Previous work on threshold models supports this argument (Gautrais et al. 2002; Merkle and Middendorf 2004; Jeanson et al. 2007).
Particularly there is evidence of several genetics defects weakening this loop that are clearly associated with autoimmunity [ 22] as well as previous mathematical models supporting this idea [ 38].
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