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The wide variation in prevalence is largely explained by differences in sensitivity of the HPV-DNA assay used, differences in age, or differences in other characteristics of the populations studied [2], [7].
This discrepancy is most obviously explained by differences in sensitivity and technical biases between the two transcriptomic platforms used.
These can be detected, and exploited pharmacologically, by differences in sensitivity to certain PDE4 selective inhibitors, of which the archetype is rolipram.
This could be explained either by differences in sensitivity between the two approaches or by possible miRNA expression level differences across mouse strains.
This could be explained by differences in sensitivity in detecting ischaemia especially in grey matter [ 21– 24] rather than by differences in the detection of residual tumour or oedema originating from tumour compression or surgical manipulation.
The observed between-tissue methylation differences seem to be small and could be explained either by consistently higher and lower methylation or by differences in sensitivity of tissues to environmental exposures, foetal and maternal factors.
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Alternatively, differences in HEV prevalence detected in livers and that detected in feces may be caused by differences in assay sensitivity or different distribution patterns in the 2 sample matrices.
This can not be explained by differences in the sensitivity of these technologies as the more sensitive technology should include also the antigens discovered by the less sensitive approach.
It should be noted that comparison of frequency of occurrence data between prey species may be complicated by differences in the sensitivity of prey-specific PCR tests (i.e., if the amount of prey DNA in many samples is close to the sensitivity limits of the PCR tests, then the importance of prey targeted by the least sensitive test will be underestimated).
Changes in gene expression in response to cold can be affected by differences in cold sensitivity.
A large extent of this variation is caused by differences in photoperiod sensitivity mediated by floral repressors encoded by Ma1 and Ma6 that inhibit flowering in long days [ 1, 29].
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