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. 2009 Mar 16;4(3):e4827. doi: 10.1371/journal.pone.0004827

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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A: BrdU uptake by residual β-cells of NOD mice is controlled by BG levels. Newly diabetic NOD mice were randomly treated with: no℞, n = 8; exogenous insulin (pellet) and BrdU labeled day1–3 (early), n = 3, crosshatched grey bar, or BrdU labeled day 4–7 (late), n = 6, hatched; insulin pellet treated mice that did not restore normoglycemia (prim. fail.), n = 4, hatched grey bar, and were compared to pre-diabetic NOD mice, n = 3, open bar. Results are shown as mean±SE, with significance levels: (*) prediabetic: p = 0.016, and insulin pellet (late): p = 0.0051, respectively. B: Correlation plot as in Figure 4C. Each symbol represents a single mouse, and all mice, regardless of treatment group are included. Correlation coefficient r = 0.78; 95% confidence interval (dashed lines). Note, that NOD mice that restored normoglycemia upon insulin pellet, and were immediately BrdU labeled (pellet early) maintain increased β-cell proliferation. These mice are shown in the plot (⧫) but were omitted from correlation coefficient calculation.