On the cover: Mitotic stages of CPCs: Mitotic stages of CPCs as demonstrated by immunostaining of tubulin (green) and Thr-199 phosphorylated nucleophosmin (red) with nuclei stained in blue. See related article, page 1169.

Image not specified Mitochondrial Morphological Changes Occur with Loss of Pim: Deletion of Pim- 1, -2, and -3 (PTKO) results in metabolic dysfunction and premature aging, concurrent with morphological changes in mitochondria of PTKO mouse hearts. Evidence of disrupted mitochondrial cristae, decreased mitochondrial area and vacuoles presented one month after birth in PTKO hearts (right) as compared to FVB wild type mice (left). These findings were concomitant with changes in mitochondrial biogenesis and function of PTKO mice. Scale bar: 2um

Increased Mitotic Rate Coincident with Transient Telomere Lengthening Resulting from Pim-1 Overexpression in Cardiac Progenitor Cells

Representative confocal micrographs of paraffin-embedded sections from wild-type mouse hearts at <1 week, 8 weeks and 30 weeks stained for Pim-1 (green), tropomyosin (red) and nuclei (blue). n = 4; boxed regions in left micrographs are shown at higher magnification at right. Arrowheads in grayscale and arrows in overlay of top right panel indicate cardiomyocytes with Pim-1 nuclear localization. Bar, 40 m, left; 10 m, right. Right, representative immunoblot of whole-heart lysates for Pim-1, with actin as a loading control.

Representative confocal micrographs of 4-d sham, MI and TAC mouse hearts labeled for Pim-1 (green), tropomyosin (red) and nuclei (blue) at 20 (top row) and 63 (bottom row) magnification of areas boxed in top panels. LV, left ventricle; I, infarct; EP, epicardium; V, vessel. Bars, 40 m, top; 5 m, bottom; n = 6.