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Partial phenotypic reversion was observed in null mutants inducibly expressing myosin II.
Martensite reversion was found to occur by an athermal shear mechanism at this temperature.
Thermodynamic simulations indicated that both reversion modes were possible and that indirect reversion was more favorable.
Extracellular Ca2+ reversed the diltiazem-mediated cPHB decreases in cells of both genetic backgrounds, yet a Ca2+-concentration dependent reversion was observed only in the AtoSC-regulated cPHB.
An assay for detection of IVS110 point mutation (A > G reversion) was developed by designing probe-gated mesoporous silica nanoparticles (MCM-41) loaded with reporter fluorescein molecules.
The ε → γ reversion was found to occur not only from the outside but also from the inside of ε plates in both alloys.
Finally, the ratio of direct to indirect reversion was found to depend on three factors, namely heating rate, initial α′ phase fraction and Ga content.
The results obtained from the nanoindentation test show that Young's modulus and microhardness of graded HA/Ti film are also graded distribution and strain reversion was much better than that in the monolithic HA film.
This phenotypic reversion was accelerated by anti-inflammatory therapy.
Cre-mediated reversion of targeted insertion was also evaluated in 293T cells containing established targeted insertion at transcriptional start sites and expected expression reversion was observed.
Subsequently, exhausted T-cell function reversion was achieved through the blockade of the PD-1/PD-L1 interaction with antibodies that restored the exhausted CD8+ T-cell reactivity and regained their antitumor activity (Curiel et al., 2003; Hirano et al., 2005).
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