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Background: Prior studies suggest an association between naturally high circulating levels of CD34+ cells (CD34) and better outcomes following ischemic events. Pts in the treatment arm of the PreSERVE-AMI study were infused with all CD34 yielded from their bone marrow harvest, resulting in pts with naturally higher CD34 cell counts being infused with a higher cell dose. To determine whether selection bias may have influenced results, we performed an analysis of the relationship between BM CD34 content and outcomes in PreSERVE-AMI. Methods: PreSERVE-AMI is a Phase 2, randomized, double-blind, placebo-controlled trial of autologous, BM derived CD34 (CLBS10) in pts with LV dysfunction (LVEF ≤48% by MRI) ≥4 days post-STEMI. All pts underwent mini BM harvest and were randomized 1:1 to intracoronary infusion of CD34 (minimum dose 10M±20% cells) or placebo (cell diluent). Primary safety endpoints included AEs, SAEs and MACE (CV mortality, HF hospitalization, reinfarction, revascularization). Secondary endpoints included LVEF change from baseline. Regression analyses were performed to assess the influence of BM CD34 content on outcomes. Results: 161 patients were randomized and received intracoronary infusion (Jan 2013-Dec 2014). Mean age was 57±10 and 82% were men. Mean follow-up time was 18 mo, and safety data are accruing. BM CD34 content was not associated with differences in baseline characteristics with the exception of diabetes prevalence being higher in those with higher BM CD34 count (p=0.03). In controls, regression analyses showed no association of BM CD34 content with rates of MACE (p=0.2), SAEs (p=0.4), or change in LVEF (p=0.9). However, in CD34 treated pts, there was a dose-dependent improvement in LV function (p=0.045) and dose-dependent trends in MACE and SAE reduction compared to controls. As previously reported SPECT perfusion improved to a similar degree in control and treated pts. Conclusions: These data suggest that intracoronary infusion of CD34 cells, rather than BM CD34 cell content, is responsible for the benefit observed in the CD34 treatment group. The finding of a dose-response relationship is an important advance for defining the CD34 as an active agent for tissue repair. Future studies will further define CD34 dosimetry.

Careful analysis of educational slogans is a welcomed contribution to public debate. Slogans are ubiquitous in education, and too often we accept them at face value. In a recent article in the Canadian Journal of Education, Douglas Stewart (1993) takes on what he believes to be a serious threat to the enterprise of teaching. Alarm bells ring for him when he hears the slogan, "We facilitate learning, we don't teach." Stewart argues that it is mistaken to contrast teaching and facilitating as mutually exclusive concepts; such a contrast creates a false dichotomy. We concur with this observation and agree that some educators may characterize facilitating in opposition to teaching. From there on, however, we part company with Stewart. Stewart categorically dismisses proponents of facilitating for espousing an "alarming idea" (p. 1) that is "misleading and dangerous" (p. 2), that will "play havoc" with educational thinking (p. 1), and that "puts at risk the education of children" (p. 8). We reject this wholesale condemnation of the notion of facilitating on the grounds that Stewart's account seriously misconstrues what credible proponents advocate. We begin our rebuttal by summarizing Stewart's position and the reasons he offers in support of his interpretation of facilitating, then explain why and in what ways Stewart misrepresents the position of at least some of those who view teachers as facilitators of learning. In concluding, we outline and defend four principles that represent a more sensible interpretation of facilitating learning. Contrary to Stewart's alarms, these principles may serve the cause of good teaching.