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If Treg cells were isolated from NOD mice that have been treated with IL-2/anti-IL-2 mAb complexes, their inhibitory activity during the activation phase did not improve dramatically.
Second, we cultured retinal explants during the activation phase in the presence of GS-GFP lentivirus [23] for lineage tracing of the activated Müller cells.
In order to determine the specificity of Müller cell-based photoreceptor regeneration, a subset of animals received intravitreal injections of GS-GFP lentivirus during the activation phase.
The specificity of the differentiation of activated Müller cells along the rod photoreceptor lineage was determined as follows: First, we examined the fate of Müller SP cells as they shifted from the SP cell compartment during the activation phase to the non-SP (NSP) compartments during the differentiation phase (Fig. 7A).
Therefore, exposure to clinorotation during the activation phase resulted in a persistent repression of oxidative burst.
Thus, other gp130-dependent cytokines presumably do not play a major role during the activation phase of the CD4+ T cell response.
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In the analysis of the changes in muscle activity profiles, the first step involved two phases: the pre-activation phase lasting 300 ms prior to the landing (first signal recorded by the landing platform), and the activation phase computed during 300 ms following the ground contact.
In the absence of tBid, increasing autophagy capacity (AV levels) resulted in faster activation of mitophagy potential in the total mitochondrial population, as seen by the slopes (black lines) during the initial activation phase (gray shaded area), while the LIR activity of the three mutants reflected in the maximal mitophagy potential levels.
Notably, despite the considerable resistance of the P10P8 and P14P12 α1-antitrypsin variants to polymerization, these mutants had comparable activation energies to the ATC232S control, indicating their effects are manifested during the unimolecular activation phase rather than the multimolecular association phase.
This suggests the existence of the reverse-translocating (nucleus-to-cytoplasm) p65 molecules even during the early activation phase of NF-κB after TNF-α treatment, which had not been appreciated previously.
The sclerosis formation might be an attempt to restore subchondral biomechanical stress levels during the physically active phase, with activation of osteoblasts that increase the subchondral bone mass to adapt to increased physical load exposure [ 50, 51].
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