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The cost of resistance hypothesis predicts that resistant hosts pay a cost for being resistant in the absence of the parasite [16], [18].
The cost of resistance hypothesis predicts that resistant genotypes pay a cost of being resistant and are less fit in the absence of parasites.
By applying the modified matching allele model to the additive resistance hypothesis, we theorize that susceptible parents contribute susceptibility alleles and resistant parents contribute resistance alleles, and their neoallopolyploids contain novel combinations of resistance and susceptibility factors.
Patterns of plant invasion in Europe offer little support for the biotic resistance hypothesis (e.g. [44, 53, 54]).
There is a particular lack of support for the biotic resistance hypothesis when terrestrial animals are considered (see [52] and references therein).
The cumulative new knowledge favors a unified central leptin insufficiency syndrome over the, in vogue, central resistance hypothesis to explain the global adverse impact of deficient leptin signaling in the brain.
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The cost-of-resistance hypothesis predicts that the relative fitness of naturally uninfected (and possibly resistant) animals should be lower compared to cured but formerly infected (and thus susceptible) animals in the absence of parasites.
We did not find any relevance to atmospheric pressure or relative humidity, the two factors which may be the most explanatory for a desiccation-resistance hypothesis.
Despite the strong preclinical data and rationale, translation of these hormone-resistance hypotheses into successful clinical studies of combined targeted therapies and endocrine treatments have yielded varied results to date.
Therefore we have initiated a large scale cluster randomized controlled trial (RCT) with the aim to assess the effect of anthelmintic treatment on insulin resistance, the hypothesis being that reduction of worm load to undetectable levels will lead to a higher degree of insulin resistance.
Whether this is the case or not, it seems clear that NAMPT is a non-redundant modifier of the tumour cell response to a clinical PARP inhibitor; this could imply that elevated levels of NAMPT activity could cause PARP inhibitor resistance, a hypothesis that could be tested in tumour biopsies derived from clinical trials involving single agent PARP inhibitor use.
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