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We reported previously that islets isolated from individual, outbred Swiss-Webster mice displayed oscillations in intracellular calcium ([Ca2+]i) that varied little between islets of a single mouse but considerably between mice, a phenomenon we termed "islet imprinting".
In the context of AD it is worth noting that the CaMKII synaptic pool is reduced in cultured cortical neurons obtained from AβPP transgenic mice, a phenomenon that promotes the loss of synaptic AMPARs and the impairment of glutamatergic transmission [65].
In the present study SAFA enhanced PPAR-γ expression in wild type mice, a phenomenon that was prevented in TLR-2-/ mice.
Here we found that changes in the gut microbiota of ob/ob mice exert a trophic effect on the intestine of Ob-Pre mice, a phenomenon associated with a higher proglucagon mRNA expression in both the jejunum and colon.
It should be noted that 7-month-old 3xTg-AD mice gained statistically significant more weight compared with PS1-KI mice, a phenomenon that is independent of drug treatment as indicated by three-factor ANOVA showing significant effect of genotype.
The RAS also promotes oxidative stress and endothelial dysfunction after lipopolysaccharide injection in mice, a phenomenon corrected by an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker [ 8].
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It is also plausible that the retention of both proteins within ameloblasts would induce cellular stresses which culminate in the extensive apoptosis we observed in the Y64H mutant mouse; a phenomenon that is clearly modelled by our transfection studies.
Here, we show that intracerebroventricular infusion of AD-associated Aβ oligomers (AβOs) in mice triggered peripheral glucose intolerance, a phenomenon further verified in two transgenic mouse models of AD.
While BAT shares a common origin with skeletal muscle [ 6, 7], studies in mouse WAT recently discovered a phenomenon called "browning" that involves the formation of brown adipocytes in WAT after cold exposure or β-adrenergic stimulation [ 36].
Because mice are nocturnal, they became active about 2 hours later in the day than did mice not exposed to light, a phenomenon called "phase delay".
Laminin staining (Fig. 10a) was used as VBM/vessel marker and its expression found to be significantly increased on CAA-laden vessels in mid- and late-stage TG arcAβ mice (Fig. 10c, d), a phenomenon underlying VBM thickening and well known to occur in AD [ 16].
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