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Wild-type mice presented a significant [F 5) = 54.810; P<0.01] increase in the response to the 2nd pulse at the 40-ms interval (Fig. 3A).
Interestingly, fasted N2KO mice presented a significant, 5.16-fold (*p≤0.05, T value = −2.99, df = 4) increase in serum leptin levels compared to WT mice.
In contrast, RASSF9−/− mice presented a dramatic change in epithelial organization of skin with increased proliferation and aberrant differentiation as detected by bromodeoxyuridine incorporation assays and immunofluorescence analyses.
In accordance with previous descriptions [24] and with present results (see arrow in Fig. 2B), both wild-type and TgIE96 mice presented a noticeable alpha response to the tone used as a CS.
In addition, RhoE gt/gt mice presented a worse performance than the controls in the other motor tests assayed, vertical climbing and clinging, righting reflex and negative geotaxis (p<0.001, Figure 4D).
Miura and co-workers have previously shown that 2-months old mice overexpressing PGC-1α ran less than wild-type mice because these transgenic mice presented a mitochondrial uncoupling and a marked decrease in the ATP muscle content [26].
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Furthermore, TgR mice presented an extreme sensitivity to cholinergic stimulators.
TgCRND8 mice presented an increased LTD, which was reverted by D-JNKI1 treatment in 9-months-old AD animals.
ALDHhiSSCloVLA4+ NSC-treated SOD1 mice presented an amelioration of the motor neuron phenotype, demonstrated by neuromuscular function tests and increased survival.
Intriguingly, however, these mice presented an increased rate of ataxia because of mononuclear infiltration into the cerebellum instead of spinal cord.
Our data show that peritoneal macrophages from PTP1B KO mice presented an exacerbated inflammatory response versus the WT, with increased production of M1 polarization markers.
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