Background Although CMV infection after allogeneic stem cell transplantation (SCT) is only rarely fatal, the management of CMV by preemptive medication for viral reactivation has toxicity and carries a financial burden. New strategies to prevent CMV reactivation with vaccines and antiviral T cells may represent an advance over preemptive strategies, but have yet to be justified in terms of transplant outcome and cost. Patients and methods We compared outcomes and post-transplant treatment cost in 44 patients who never required preemptive CMV treatment with 90 treated patients undergoing SCT at our institute between 2006–2012. 81 subjects received CD34+ selected myeloablative SCT, 12 umbilical cord blood transplants, and 41 T-replete nonmyeloablative SCT. 119 (89%) patients were at risk for CMV because either the donor or recipient was seropositive. Of these, 90 (75.6%) reactivated CMV at a median of 30 (range 8–105) days post transplant and received antivirals. Results There was no difference in standard transplant risk factors between the two groups. In multivariate modeling, CMV reactivation >250 copies/ml (OR=3, P<0.048), total duration of inpatient IV antiviral therapy (OR = 1.04, P<0.001), type of transplant (T-deplete vs. T-replete) (OR=4.65, P<0.017) were found to be significantly associated with increased non-relapse mortality. The treated group incurred an additional cost of antiviral medication and longer hospitalization within the first 6 months post SCT of $58,000 to $74,000/patient. Discussion Our findings suggest that to prevent CMV reactivation treatment should be given within 1 week of SCT. Preventative treatment may improve outcome and have significant cost savings.

To address disproportionately high rates of diabetes morbidity and mortality in some of Chicago's medically underserved minority neighborhoods, a group of community residents, medical and social service providers, and a local university founded the Chicago Southeast Diabetes Community Action Coalition, a Centers for Disease Control and Prevention REACH 2010 Initiative. A community-based participatory action research model guided coalition activities from conceptualization through implementation. Capacity building activities included training on: diabetes, coalition building, research methods, and action planning. Other activities sought to increase coalition members' understanding of the social causes and potential solutions for health disparities related to diabetes. Trained coalition members conducted epidemiologic analyses, focus groups, a telephone survey, and a community inventory. All coalition members participated in decisions. The participatory process led to increased awareness of the complexities of diabetes in the community and to a state of readiness for social action. Data documented disparities in diabetes. The participatory action research approach (a) encouraged key stakeholders outside of the health care sector to participate (e.g., business sector, church groups); (b) permitted an examination of the sociopolitical context affecting the health of the community; (c) provided an opportunity to focus on preventing the onset of diabetes and its complications; (d) increased understanding of the importance of community research in catalyzing social action aimed at community and systems change and change among change agents.

Plerixafor (Mozobil®) is a CXCR4 antagonist that rapidly mobilizes CD34+ cells into circulation. Recently, plerixafor has been used as a single agent to mobilize peripheral blood stem cells (PBSC) for allogeneic hematopoietic cell transplantation. Although G-CSF mobilization is known to alter the phenotype and cytokine polarization of transplanted T-cells, the effects of plerixafor mobilization on T-cells have not been well characterized. In this study, we show that alterations in the T-cell phenotype and cytokine gene expression profiles characteristic of G-CSF mobilization do not occur following mobilization with plerixafor. Compared to non-mobilized T-cells, plerixafor-mobilized T-cells had similar phenotype, mixed lymphocyte reactivity, FoxP3 gene expression levels in CD4+ T-cells, and did not undergo a change in expression levels of 84 genes associated with Th1/Th2/Th3 pathways. In contrast to plerixafor, G-CSF mobilization decreased CD62L expression on both CD4 and CD8+ T-cells and altered expression levels of 16 cytokine-associated genes in CD3+ T-cells. To assess the clinical relevance of these findings, we explored a murine model of GVHD in which transplant recipients received plerixafor or G-CSF mobilized allograft from MHC-matched, minor histocompatibility mismatched donors; recipients of plerixafor mobilized PBSC had a significantly higher incidence of skin GVHD compared to mice receiving G-CSF mobilized transplants (100% vs. 50% respectively, p=0.02). These preclinical data show plerixafor, in contrast to G-CSF, does not alter the phenotype and cytokine polarization of T-cells, which raises the possibility that T-cell mediated immune sequelae of allogeneic transplantation in humans may differ when donor allografts are mobilized with plerixafor compared to G-CSF.