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These data indicate that TSP-1 contributes to shear-dependent TGF-β1 activation, thus providing a potential explanation for the inconsistent in vitro data previously reported as well as for the differences in phenotypes of Thbs1−/− and Tgfb1−/− mice.
As such, it is possible that trastuzumab and human serum/plasma IgG1 antibodies may compete with one another in vivo for binding to immune cell receptors, which could account for the inconsistent in vitro results.
Collectively, these studies illustrate the inconsistent in vivo findings regarding LRP1 and amyloidogenesis in transgenic mice that over-express mutant APP (with or without co-expression of mutant presenilin).
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Indeed, differences in cadmium levels may account for the inconsistent results in previous research.
The inconsistent findings in the literature may also be due to differences in spatial scale.
Another possible explanation for the inconsistent findings in the literature is that residential transitions were ignored in past research studies.
Of course, the inconsistent change in the source has to be lower than the tale-telling change in the target.
There are some points should be concerned for the inconsistent results in early reports.
This may partly explain the inconsistent findings in our study.
There are several explanations for the inconsistent findings in the studies.
This might explain some of the inconsistent results in association studies between SLC11A1 and TB.
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