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Confirming the proposed insulinotropic effect of betacellulin, transgenic mice showed improved glucose tolerance.
Throughout aging, these mice showed improved ability to quickly clear sugar from the blood as well as signs that they could burn more calories without increasing exercise levels.
Notably, HFD-IF mice showed improved glucose homeostasis with smaller glucose excursion in glucose tolerance test (GTT), increased insulin sensitivity in insulin tolerance test (ITT), and markedly lower homeostasis model assessment-estimated insulin resistance (HOMA-IR), compared to HFD-AL or HFD-PF mice (Figure 1G-1I; Supplementary information, Figure S2E and S2F).
Although this is severe model, PTP1B−/− mice showed improved GTT and ITT.
Although this severe model, PTP1B−/− mice showed improved GTT and ITT.
Both the diabetic and non-diabetic RAGE-/ mice showed improved angiogenesis compared to the RAGE+/+ mice (WT diabetic and non-diabetic) based on greater uptake of radiolabeled RGD targeting αvβ3 expression, a biomarker of tissue changes accompanying early angiogenesis.
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Studies in mice show improved social interaction and cognition from a potential therapeutic for a syndrome that often results in autism.
In agreement with these findings, old Dkk1 mutant mice show improved memory consolidation and affective behaviour (Seib et al. 2013).
Nox2 knockout mice show improved endothelial dysfunction in a model of renovascular hypertension [ 17] but no change in basal blood pressure [ 5] or the hypertensive response to chronic angiotensin II infusion [ 16], nor to chronic activation of the renin-angiotensin system [ 28].
SAG1.1 treated mice also showed improved hippocampal long-term potentiation and correction of learning deficits in the Morris water maze compared with untreated mice, demonstrating improved hippocampal function in response to transient Hh pathway activation.
These mice also showed improved learning and memory performance.
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