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The most frequent genotypic combination in NAB mice was the HAB-specific one (Table 5).
In all other brain areas, OA-induced c-Fos expression in NAB mice did not differ from HAB or LAB mice.
Interestingly, 6 h and already 1 h after fear conditioning, freezing levels were high in HAB mice but not in NAB mice.
Accordingly, it may well be that in NAB mice fear responses gathered around the mean freezing levels usually displayed by CD-1 mice during fear conditioning.
The investigation of c-Fos in NAB mice provides an additional advantage, as the intermediate phenotype of these animals may act as a reference of changes in brain activity, suitable to determine whether HAB or LAB mice reveal neuronal alterations.
It seems our DNA prime/phage boost strategy did achieve the maximum in nAb titers, although the binding titers showed modest but insignificant increases after the last protein boost.
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Patients then received trastuzumab 2 mg/kg weekly (patients who received "run-in" nab-paclitaxel were treated with 4 mg/kg for the first week), weekly nab-paclitaxel 100 mg/m2 and carboplatin AUC 6 every 3 weeks for 18 weeks.
Alkaline phosphatase activity in NaB-treated cells was normalised to that in the control.
In the differentiation-induction experiments, cyclin D protein expression in NaB-treated samples was normalised to the control.
Analysis of type I collagen revealed a decrease in collagen matrix in nab-paclitaxel and nab-paclitaxel plus gemcitabine groups compared with control and gemcitabine groups.
Furthermore, mRNA and protein levels of Ku70, Ku80 or DNA-PK were unaltered in NaB-treated lung fibroblasts (Munshi et al, 2005).
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