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Two seemingly conflicting models have been proposed.
Conflicting models have been proposed whereby mixed breeding systems either slow [ 12] or accelerate divergence [ 18, 23, 26].
Indeed, conflicting models have been proposed for the structure of CENP-A-containing nucleosomes (Black and Cleveland, 2011), and a spirited ongoing controversy concerns whether they are octameric or tetrameric.
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Evidence for each of these conflicting models has been presented for budding yeast, where the centromere is genetically defined by an ∼120-bp functional sequence on each of the 16 chromosomes.
The Conflict Model is pleasingly consistent with the known roles of several imprinted genes in fetal growth and postnatal nutritionally related behaviors, but for most imprinted genes agreement with the Conflict Model has been assumed rather than demonstrated [ 12].
The effects of anti-oxidants in both humans and animal models have yielded conflicting results; therefore, further understanding of the molecular basis of lipid synthesis and catabolism, and of the action of bioactive lipids in cells, will help in the design of improved in vivo models.
Conversely, results from experimental animal models have been conflicting.
While these observations point to some contribution of TNFα to the pathogenesis of NASH, recent studies on animal models have led conflicting conclusions.
However, studies into UPS function in various polyglutamine disease models have yielded conflicting results, suggesting mutant polyglutamine tracts may exert different effects on the UPS depending on protein context, expression level, subcellular localisation and cell-type.
Pyrogenicity studies in different animal models have shown conflicting results.
In the context of AD, however, studies on Zn2+ deficiency or supplementation in AD models have provided conflicting results.
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