Factors Identified by Lapsed Donors that Might Influence Donor Return

Introduction: The Burlington Chapter of the American Red Cross estimates that 8,000 donors a year become lapsed, or fail to return for further donation. To better target this population and retain current donors, it is essential to identify reasons for lapsed donation. Several studies have been conducted on the barriers to retaining blood donors, revealing these common factors: past physical reactions, convenience, previous deferrals, lack of awareness, medical reasons, time, satisfaction with the experience, too impersonal, and personal benefit. While many studies have identified reasons for lapsed donation, the majority have not used free text as their data source, have been conducted in a wide range of geographic locations not specific to Vermont residents, and have focused on reasons for discontinuing donations, rather than positive factors. Using free text limits the question bias and eliminates constraints that predefined answers enforce. In 2007, Balderama et alconducted a study identifying common motivations for donating blood, which included an unanalyzed free text portion. We used this free text to answer the question, “What factors identified by lapsed donors might influence donor return?”https://scholarworks.uvm.edu/comphp_gallery/1047/thumbnail.jp

Biological Functions of miR-29b Contribute to Positive Regulation of Osteoblast Differentiation*

Bone tissue arises from mesenchymal cells induced into the osteoblast lineage by essential transcription factors and signaling cascades. MicroRNAs regulate biological processes by binding to mRNA 3′-untranslated region (UTR) sequences to attenuate protein synthesis. Here we performed microRNA profiling and identified miRs that are up-regulated through stages of osteoblast differentiation. Among these are the miR-29, miR-let-7, and miR-26 families that target many collagens and extracellular matrix proteins. We find that miR-29b supports osteoblast differentiation through several mechanisms. miR-29b decreased and anti-miR-29b increased activity of COL1A1, COL5A3, and COL4A2 3′-UTR sequences in reporter assays, as well as endogenous gene expression. These results support a mechanism for regulating collagen protein accumulation during the mineralization stage when miR-29b reaches peak levels. We propose that this mechanism prevents fibrosis and facilitates mineral deposition. Our studies further demonstrate that miR-29b promotes osteogenesis by directly down-regulating known inhibitors of osteoblast differentiation, HDAC4, TGFβ3, ACVR2A, CTNNBIP1, and DUSP2 proteins through binding to target 3′-UTR sequences in their mRNAs. Thus, miR-29b is a key regulator of development of the osteoblast phenotype by targeting anti-osteogenic factors and modulating bone extracellular matrix proteins