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In trauma patients plasma Ang-2, but not plasma Ang-1 or VEGF, was increased early after trauma, and the level correlated with disease severity and outcome [ 34].
IL-21-mediated STAT3 phosphorylation was increased early in the disease course and downregulated as disease progressed until levels decreased below those of healthy control MRL/++ mice.
Changes in UBR2 expression correlated inversely with time since onset of disease and directly with ALSFRS-R, implying that UBR2 was increased early in the course of ALS.
Supporting these data, Delano and colleagues showed that lethality to pseudomonas pneumonia was increased early on after the induction of sepsis, but not later, coinciding with repopulation (activation) of Gr1+/CD11b+ cells [ 53].
In addition, expression of the osteoclastic cell fusion genes ATP6v0d2 and DC-STAMP, as well as of TNFα was increased early in osteoclast differentiation in the C/EBPβ mutant osteoclasts (Supplementary Figure 1C).
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The expression level of HSPB9 was increased earlier and slower than that of HSPB10.
Interestingly, Brn-3b was increased earlier than Brn-3a or p53 in-vivo (by 1 h following coronary artery ligation) and in-vitro (after sI).
However, FT expression levels kept greater at every time point and was increased earlier with significantly (P < 0.01) higher extents in leaves of RfBP+ compared to WT and RfBP−.
Respiratory sIgA levels are increased early after injury in both human and laboratory animals; the mechanisms are uncertain.
The CD28 co-stimulatory molecule plays an important role in T-cell priming and differentiation, and its expression level is increased early after T-cell activation [46].
It is therefore not surprising that angpt-2 levels are increased early in response to endothelial activation or injury.
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