Should 16-Year-Olds Be Allowed to Donate Blood? A Vermont Perspective

Introduction: Supplying adequate blood for transfusions is an ongoing challenge for blood collection agencies. One potential source of increased Whole Blood (WB) supply is among 16-17 year-olds, whose donation rates are still quite low. In 2010, donors aged 16-18 years-old provided 14% of all WB collected by the American Red Cross. Young donors may represent an opportunity to establish a committed, long-term blood donation base as they are more likely to return after first donation and donate at a higher yield rate than older donors. However, younger donors also have higher rates of adverse events during donation. Currently, 38 states allow 16 year-olds to donate blood with parental consent but Vermont is not among them. Our study examines the public’s comfort with 16 year-olds donating blood. As blood donation is a voluntary system, ascertaining the perspective of the general population regarding this issue could contribute to a policy debate surrounding the minimum age of donation.https://scholarworks.uvm.edu/comphp_gallery/1065/thumbnail.jp

A microRNA/Runx1/Runx2 network regulates prostate tumor progression from onset to adenocarcinoma in TRAMP mice

While decades of research have identified molecular pathways inducing and promoting stages of prostate cancer malignancy, studies addressing dynamic changes of cancer-related regulatory factors in a prostate tumor progression model are limited. Using the TRAMP mouse model of human prostate cancer, we address mechanisms of deregulation for the cancer-associated transcription factors, Runx1 and Runx2 by identifying microRNAs with reciprocal expression changes at six time points during 33 weeks of tumorigenesis. We molecularly define transition stages from PIN lesions to hyperplasia/neoplasia and progression to adenocarcinoma by temporal changes in expression of human prostate cancer markers, including the androgen receptor and tumor suppressors, Nkx3.1 and PTEN. Concomitant activation of PTEN, AR, and Runx factors occurs at early stages. At late stages, PTEN and AR are downregulated, while Runx1 and Runx2 remain elevated. Loss of Runx-targeting microRNAs, miR-23b-5p, miR-139-5p, miR-205-5p, miR-221-3p, miR-375-3p, miR-382-5p, and miR-384-5p, contribute to aberrant Runx expression in prostate tumors. Our studies reveal a Runx/miRNA interaction axis centered on PTEN-PI3K-AKT signaling. This regulatory network translates to mechanistic understanding of prostate tumorigenesis that can be developed for diagnosis and directed therapy