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These data link lower micelle stability and enhanced permeability of smaller silicone head groups to antibacterial activity.
Taken together, these data link CFTR function to Nrf-2 activity and changes in intracellular H2O2.
Overall, these data link changes in EO to altered lineage commitment of collagen X mouse hematopoietic cells, though not total numbers of precursor cells (Fig. 6), and implicate the marrow environment of the collagen X Tg and KO mice as being impaired in its ability to support lymphopoiesis, resulting in defective immune responses throughout life [8].
These data link an oncogenic transcription factor that is a master regulator of lysosomal biogenesis, TFEB, to mTORC1 and endocytosis.
These data link proportional reduction in SUVpeak with benefit of single-agent EGFR inhibition in NSCLC, analogous to our observations with EGFR inhibition by cetuximab in incurable SCCHN.
Taken together, these data link estrogens to prostatitis and premalignancy in the prostate, further implicating a role for estrogen in prostate cancer [ 125].
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These data linked the CFTR defect to autophagy deficiency, leading to the accumulation of protein aggregates and to lung inflammation.
These data linked the glp-4 mutation to a 235 Kb region on the right arm of chromosome I containing 97 predicted genes, which overlaps with the predicted glp-4 location described in the literature (Figure 4).
These data linking poor intra-operative hemodynamic control with adverse outcomes provide the justification for our use of poor hemodynamic control as the primary outcome variable in this study.
These data linking a direct molecular effect of NDL PCBs (sensitized RyR activity) to disruption of a specific neurodevelopmental event (dendritic arborization) have significant implications for understanding how PCBs interfere with normal neurodevelopment in the human brain.
Mechanistically, these data linked the well-studied DDR signalling pathway and known tumour suppressor functions of its components, including activation of checkpoints and p53-mediated apoptosis and senescence, to an oncogene-induced replicative stress.
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