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Insulin secretion was measured in INS1-E cells or mouse islets after exposure to 3 or 16.7 mmol/l glucose (ESM Methods, Measurement of insulin secretion).
miR-15a levels have been shown to increase in parallel with insulin in mouse islets after short-term exposure to HG concentrations.
Geniposide was found to promote β-cell survival by increasing β-cell proliferation and decreasing β-cell apoptosis in cultured mouse islets after challenge with diabetic stimuli.
However, when assessed in a defined population of smaller islets (<120 μmol/l) from older mice (12 15 weeks), we observed a significant difference in islet cell survival with a survival advantage of ZnT8−/− mouse islets after 24 h (p < 0.001) or 48 h of hypoxia exposure (p < 0.01) (Fig. 6i).
These results are quite intriguing in that they are highly consistent with our previous data showing a markedly blunted insulin secretion from these cells and from mouse islets after a shorter time of exposure (6 24 hr) to arsenite (Pi et al. 2007) [see also Supplemental Material, Figure 2 (doi:10.1289/ehp.0901608)].
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To reveal the photopolymerization-induced damage on encapsulated islets, we stained and imaged encapsulated mouse islets right after photopolymerization.
Mouse islets were perifused after 48 or 72 h of culture; GSIS at both time points was similar.
Adult mouse islets were handpicked after collagenase digestion of the isolated pancreas and purification on a Ficoll gradient (Giddings et al., 1985).
Rat and mouse islets were isolated by hand-picking after collagenase digestion of pancreas as described [36].
To further confirm the role of GH signaling in the phenotypes of FGF21-KO mouse islets, insulin expression and GSIS were measured after inhibition of STAT5.
Further supporting a metallothionein-independent effect of hypoxia on Slc30a8 expression in CD1 mouse islets, Slc30a8 mRNA levels tended to be decreased as early as 5 h after the initiation of hypoxia (significant decrease after 10 h) (Fig. 5b).
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