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Hedden, T. et al. Failure to modulate attentional control in advanced aging linked to white matter pathology.
Overexpression of Sen1 or failure to modulate its abundance by ubiquitin-proteasome-mediated degradation greatly decreases cell fitness.
In several network regions, AD patients showed a significantly weaker and sometimes no BOLD signal due to increased task demand compared with controls, demonstrating failure to modulate the neural response to increased task demand.
Failure to modulate phospho-Akt results in resistance [8] [10].
Therefore, misregulated pre-existing chromatin modifiers and cofactors of TFs in irradiated atm likely contributed to its failure to modulate transcript levels after IR.
We observed no significant relationship between amyloid burden and failure to modulate activity.
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This relationship should be interpreted cautiously, as some older adults with low levels of WMHs also displayed failures to modulate activity.
Consistent with this prediction, we observed a relationship between elevated WMH volume and failures to modulate activity in attentional control systems, although this relationship was present only among older adults with high levels of WMHs.
Regardless of the underlying pathophysiologic mechanisms, various compensatory feedback systems, including the sympathetic nervous system and renin angiotensin aldosterone system, are activated in patients with heart failure which aim to modulate the deprived cardiac pump function within a normal homeostatic range [ 4– 7].
Failure of sHLA-G to modulate Th2 cell associated chemokine receptors is consistent with the recent demonstration of high levels of sHLA-G in sera from allergic patients supporting the hypothesis that sHLA-G contributes to maintain Th2-polarized immune responses[33].
Lastly, the failure of NS-398 to modulate the phosphorylation of ERK1/2 following tryptase-induced PAR-2 activation suggests that this step is downstream of PAR-2 activation and upstream of COX-2 activation.
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