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Using ligand based pharmacophore modelling; we showed that most of the available AMP analogs bind residues which were common to all DEAD box helicases (Figure 4B).
Using longitudinal mixed modelling we showed that muscle mitochondrial DNA heteroplasmy (P < 0.0001) and mitochondrial DNA deletion size (P < 0.0001) were both highly significantly correlated with NMDAS progression in our patient cohort (n = 55) (Fig. 4).
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In numerical modelling we show two architectures of one-bit half-adders implemented in BZ-vesicles.
Using source modelling, we show that our system allows localisation of the evoked response to somatosensory cortex.
Combining this with resampling techniques and projection modelling, we show that confidence intervals for population growth estimates are easy to derive.
In one, our ovarian cancer model, we showed that we observed 100percentt survival.
Using hypertonic induction of the aldose reductase (AR) gene activation as a model, we showed that OREs contained dynamic nucleosomes.
Using a mouse model, we showed that intraperitoneal injection of OMVs derived from intestinal Escherichia coli induced lethality.
Confirming our results obtained with the mouse TB model, we showed that the guinea pig model was also very sensitive to the dose of antigen used for vaccination.
In the LID model we showed that the low levels of serum IGF-1 were not adequate to inhibit pituitary GH secretion.
Most importantly, using this model, we showed that leukocytes were originated from in situ proliferation in human xenografts and involved in the occurrence of menstruation.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com