Background-The use of stem and/or progenitor cells to achieve potent vasculogenesis in humans has been hindered by low cell numbers, implant capacity, and survival. This study investigated the expansion of CD133 ϩ cells and the use of an injectable collagen-based tissue engineered matrix to support cell delivery and implantation within target ischemic tissue. Methods and Results-Adult human CD133ϩ progenitor cells from the peripheral blood were generated and expanded by successive removal and culture of CD133 Ϫ cell fractions, and delivered within an injectable collagen-based matrix into the ischemic hindlimb of athymic rats. Controls received injections of phosphate-buffered saline, matrix, or CD133

Compared with the use of mesenchymal progenitor cells, cell transplantation with endothelial progenitor cells after myocardial infarction resulted in better neovascularization and contractility. This suggests that angiogenesis is an important mechanism in attenuating the progression of left ventricular dysfunction after myocardial infarction.

The p53 protein plays a major role in the maintenance of genome stability in mammalian cells. Mutations of p53 occur in over 50% of all cancers and are indicative of highly aggressive cancers that are hard to treat. Recently, there has been a high degree of interest in therapeutic approaches to restore growth suppression functions to mutant p53. Several compounds have been reported to restore wild type function to mutant p53. One such compound, CP-31398, has been shown effective in vivo, but questions have arisen to whether it actually affects p53. Here we show that mutant p53, isolated from cells treated with CP-31398, is capable of binding to p53 response elements in vitro. We also show the compound restores DNA-binding activity to mutant p53 in cells as determined by a chromatin immunoprecipitation assay. In addition, using purified p53 core domain from two different hotspot mutants (R273H and R249S), we show that CP-31398 can restore DNA-binding activity in a dosedependent manner. Using a quantitative DNA binding assay, we also show that CP-31398 increases significantly the amount of mutant p53 that binds to cognate DNA (B max ) and its affinity (K d ) for DNA. The compound, however, does not affect the affinity (K d value) of wild type p53 for DNA and only increases B max slightly. In a similar assay PRIMA1 does not have any effect on p53 core DNA-binding activity. We also show that CP-31398 had no effect on the DNA-binding activity of p53 homologs p63 and p73.

All life acquires energy through metabolic processes and that energy is subsequently allocated to life-sustaining functions such as survival, growth and reproduction. Thus, it has long been assumed that metabolic rate is related to the life history of an organism. Indeed, metabolic rate is commonly believed to set the pace of life by determining where an organism is situated along a fast–slow life-history continuum. However, empirical evidence of a direct interspecific relationship between metabolic rate and life histories is lacking, especially for ectothermic organisms. Here, we ask whether three life-history traits—maximum body mass, generation length and growth performance—explain variation in resting metabolic rate (RMR) across fishes. We found that growth performance, which accounts for the trade-off between growth rate and maximum body size, explained variation in RMR, yet maximum body mass and generation length did not. Our results suggest that measures of life history that encompass trade-offs between life-history traits, rather than traits in isolation, explain variation in RMR across fishes. Ultimately, understanding the relationship between metabolic rate and life history is crucial to metabolic ecology and has the potential to improve prediction of the ecological risk of data-poor species.

These results demonstrate a source of blood CD133+ cells other than direct mobilization from the bone marrow. Cellular interaction was observed between fractions, with CD133+ cells showing better in vitro function in the presence of CD133- cells. These findings provide a novel source for CD133+ cells and a rationale for the investigation of angiogenic cell recruitment or delivery strategies involving more than one cell type at ischemic sites.