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Later studies showed that this was not the case and that the effect was proportional with the dosage up to very high intakes (figure 3).
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A post hoc test of the intervention × time interaction revealed that in the MSG sessions (P < 0.040) but not in placebo sessions (P > 0.900), sBP was elevated 15 and 30 min after intake (Figure 5). Figure 5 The time course of changes in mean (± SEM) systolic and diastolic blood pressure during monosodium glutamate (MSG) and placebo intervention.
Insulin peaks at an average of 65 minutes after glucose intake (Figure 3).
IL-6 caused a significant reduction in food intake (Figure 1a).
In addition, no differences in food intake (Figure 2EF) or locomotor activity (Figure 2G) were observed in either genotypes.
IP injection of CXCL14 into control CXCL14+/+ mice did not significantly affect their food intake (Figure 7A).
In both CXCL14+/+ and CXCL14−/− mice, ICV injection of CXCL14 did not significantly increase food intake (Figure 6A, B).
IL-6 caused a significant reduction in food intake (Figure 2f) and induced hypothalamic JAK2 and STAT3 phosphorylation (Figures 2g and h).
IL-6 caused a significant reduction in food intake (Figure 2a) and induced hypothalamic p70S6K and 4EBP1 phosphorylation (Figures 2b and c).
Induction of hypothalamic Sirt1 activity by ICV infusion of SA3 to re-fed rats (Figure S1D, right panel) resulted in increased short-term food intake (Figure 1A, right).
Comparing AICAR-treated groups (control vs. exercise), exercised animals showed a 33% reduction in 12-hour total food intake (Figure 3a).
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CEO of Professional Science Editing for Scientists @ prosciediting.com