In contrast, H. hepaticus infection of mdr1a−/− mice did not accelerate disease but rather delayed the onset of spontaneous colitis which was milder in severity.
When added after the onset of aggregation, 22C4 scFv could not inhibit aggregation but rather delayed aggregation progression.
Stable overexpression of miR-122 in hESC was unable to direct spontaneous differentiation towards a clear endodermal fate, but rather, delayed general differentiation of these cells.
Overall, overexpression of miR-122 alone in hESC was unable to modify the mRNA profile of the cells towards an endodermal or a hepatic pattern, but rather delayed the differentiation when compared to mutant miRNA-expressing cells.
Thus, in contrast to Noggin treatment or other reported manipulations that promote cardiomyogenesis in ES cells [10] [12], [23], dorsomorphin treatment does not simply increase peak expression of mesoderm makers per se, but rather delays the onset of their expression.
In contrast, CO exposure (250 ppm) did not directly activate JNK (Figure 6A), but rather delayed the early phase of LPS-induced JNK phosphorylation in THP-1 cells (Figure 6B).
Second, in contrast to Noggin, dorsomorphin treatment did not increase the peak expression of the early mesoderm marker BryT at day 3 of differentiation, but rather delayed the temporal pattern of its expression.
Since the AR formation was not completely abolished but rather delayed, jasmonates might act as an accelerator of AR formation.
Ectopic Buffy, however, did not simply block the autophagic response, but rather delayed the response: extensive autophagy was apparent in fat bodies with ectopic Buffy after an extended period of protein starvation (data not shown).
In support, the interposition of an impermeable membrane between these two cell types prevents the initial growth and regeneration of antlers, whereas a semipermeable membrane does not inhibit but, rather, delays the process [ 22].
