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Using the kinetics model for sensitivity analyses, it was determined that the decrease in reactivity in the presence of H2S is because H2S initially reacts before the H2 fuel does, mainly through the reaction H2S + H ⇄ SH + H2, thus taking H atoms away from the main branching reaction H + O2 ⇄ OH + O and inhibiting the ignition process.
By using the external cause of injury mortality matrix, we determined that the decrease in the mortality trends of some unintentional injuries might be due to the increase in mortality trends of the same mechanism of injury with an undetermined intent (Lu 2002).
However, the inhibitory experiments determined that the decrease in BoNT/A1 activity in the presence of mAb B4 was equivalent to all other noninhibitory antibodies with the exception of CR2.
We determined that the decrease in gonocyte number in MEHP-exposed testes resulted from a combination of decreased proliferation and increased apoptosis.
We determined that the decrease in liver weight was not due to hepatotoxicity, as liver injury was not observed upon histological assessment.
Consistent with that report, we also observed that selenite promoted the switch from protective autophagy to apoptosis in NB4 cells previously, and here we determined that the decrease of autophagy in NB4 cells was regulated by the production of ROS.
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Using 4get mice, which express GFP upon IL-4 transcription, we determined that the decreased Th2 cytokines in ICOS+/− is due to reduced percentage of Th2 cells and not a defect in their ability to produce IL-4.
For this purpose, the optimum serum concentration should meet two requirements: 1) give a good signal to noise ratio; and 2) be reliable enough to determine that the decreased OD is due to real inhibitory effects and not false positive results caused by experimental errors, i.e., the complement activation should not be too sensitive at the concentration of interest in the standard curve.
For example, Landolt and colleagues [ 1] determined that QOL significantly decreases during treatment for childhood cancer, but most aspects of QOL improve as children move off treatment.
Hence, we measured the effect of TGF-β1 treatment of these cells on EBP1 mRNA abundance, and determined that the latter decreased by about 2-fold in the presence of this growth factor (Fig. 6B).
Using the Cell Proliferation ELISA, BrdU (colorimetric) kit (Roche), we determined that this decrease in cell viability was the result of a down-regulation in cell proliferation, as opposed to an increase in apoptosis.
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