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Propentofylline-induced astrocyte modulation leads to alterations in glial glutamate promoter activation following spinal nerve transection.
Correspondingly, this modulation leads to the formation of CoFe-LDH, MnFe-LDH and MgFe-LDH in lieu of NiFe-LDH on the surface of iron plates according to the presence of the different divalent cations (Fig. 3a).
In addition, removing the transmitter modulation leads to the simple and universal signal processing algorithms for all FS PCL systems, irrelevant of the transmitted waveforms.
In addition, removing the transmitter modulation leads to the simple and universal signal processing algorithms for all FS PCL systems, irrelevant of the transmitted waveforms. .
The resulting average RL after flexible power generation (dashed line in Fig. 3) is therefore showing a reduction in the morning and evening peaks of the RL, whereas, for example during midday minimum RL situations, the lower average modulation leads to a comparably lower reduction in RL.
This waveform modulation leads to a timed pause of the PC population and makes the DCN neurons generate the CR signals.
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The pulsed electrode potential modulation led to the appearance of two processes available for the time-resolved registration in colloid microenvironment: change of the electronic charge of microparticles (from 0.5 ms to 0.1 s) followed by the drug release associated with ionic equilibration (1 10 s).
(iv) Neuronal RTs inversely correlated with the attentional modulation in the gamma band, i.e. stronger attentional gamma band modulation led to shorter neuronal RTs.
This modulation led to increased IFNα production, decreased inflammatory cytokine and chemokine secretion, and decreased STAT1 and STAT3 expression by human pDCs.
These results are most easily explained if dopamine modulation led to synaptic depression of the outputs of the KCs representing the CS + stimulus.
In both cases, inhibition of RhoA modulation led to reduced cell motility, strengthening the notion that the regulation of RhoA activity is causally involved in the pro-migratory phenotype observed in podoplanin-expressing cancer cells (Martin-Villar et al, 2006; Wicki et al, 2006).
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