Supporting this alternative explanation, data from neonate rats indicates that autonomic neurotransmission continues to develop in the heart from PND4-15 [ 45], and that pharmacological modulation of the autonomic nervous system has altered/reduced effects in early neonates [ 46].
A recent extension of Shepard's rational theory of dimensional generalization allows an explanation of data from both areas within a single framework.
Three results from recent IN SILICO experiments with the dopaminergic and serotonergic synapse models are described: (1) influence of substrate inhibition on the stability of dopamine and serotonin synthesis; (2) a predicted connection between serotonin reuptake transporter (SERT) density on terminals and tonic firing rates; (3) an explanation of data from autoreceptor knock-out experiments.
False-positive associations due to population stratification is also possible, but this seems an unlikely explanation for data from multiple studies from different populations in which the analyses were restricted to white subjects.
However, in research published in eLife, Paolo Pretto, Jean-Pierre Bresciani, Gregor Rainer and Heinrich Bülthoff challenge this explanation with data from experiments in which state-of-the-art virtual-reality simulations are used to explore how drivers respond to conditions of reduced visibility (Pretto et al., 2012).
To distinguish the two explanations, we examined data from an in vitro nucleosome reconstitution experiment in which histones are incubated with yeast Saccharomyces cerevisiae and Escherichia coli genomic DNA, the former has been shaped by nucleosome structure while the latter has not.
Hence, hypotheses differ fundamentally from theories; whereas the former is a specific tentative explanation and serves as the main tool by which scientists gather data, the latter is a broad general explanation that incorporates data from many different scientific investigations undertaken to explore hypotheses.
The most likely explanation is the data from the meta-analysis more likely represents the true population given the larger numbers.
In describing NNT, respondents preferred the written explanation which rescaled data from 1-inn x" to "x out of 100" (Table 3d).
Possible explanations for the discrepant data from experiments using human CRC cells include variable CRT-independent effects of NSAIDs on TOPflash constructs with different downstream promoters and/or variations in the methods used to analyse TOPflash and FOPflash activity data, which may not address adequately the issue of nonspecific effects of NSAID treatment on reporter gene expression.
