Why do some apheresis donors donate blood just once?

BACKGROUND AND OBJECTIVES: More knowledge about the reasons for non-return of blood donors (BD) would enable blood donation services (BDS) to improve the efficacy of recruitment and retention programmes. We interviewed returning (RBD) and non-returning apheresis BDs (NRBD) of our university hospital-based BDS. MATERIALS AND METHODS: A questionnaire was sent to 1218 individuals who passed the initial health check with no more than one subsequent blood donation. A similar questionnaire was answered by 235 randomly incoming RBDs. We asked for age, sex, profession, education level, motives to donate blood and, if applicable, reasons for non-return. These data were compared between NRBDs and RBDs and were analysed in relationship to the reasons for non-return. RESULTS: We received 267 answered questionnaires (21.9%). As 32 individuals indicated that they had been permanently deferred and 47 BDs had donated blood elsewhere, 188 NRBDs remained for further analysis. We found more women than men among NRBDs. Medical professions were less likely to return than students and trainees. Individuals motivated by personal experience, remuneration or a free health check were more likely to return than others. Whereas logistic reasons were of highest relevance for non-return in general, women indicated anxiety of blood donation as reason for non-return more often than men. CONCLUSION: Reducing women's anxiety of blood donation, reminding medical professions more intensively on blood donation and appealing to personal experience or a free health check may be the most promising approaches to increase BDs' return rates.     

MMP-9 haplotypes and carotid artery atherosclerosis: an association study introducing a novel multicolour multiplex RealTime PCR protocol

Background Among other matrix metalloproteinases (MMPs), gelatinase B (MMP‐9) is discussed to be associated with the pathogenesis of vascular diseases. Two single nucleotide polymorphisms (SNPs) of the MMP‐9 gene, C‐1562T in the promoter region and a G/A transition in exon 6 (R + 279Q), have been addressed in previous association studies which, however, produced conflicting results. Material and methods A novel multiplex RealTime PCR protocol for the fast and simultaneous detection of both polymorphisms is presented, which was used for genotyping 1737 participants of a prospective study investigating genetic factors influencing the progression of atherosclerosis. Results Haplotype analysis revealed –1562C/+279Q as the major haplotype in this population. Allelic distribution of the C‐1562T polymorphism was consistent with data published for similar cohorts; however, we found that R + 279Q allelic distribution appears to vary significantly among Caucasian populations. Considering clinical data available from 1487 participants, we found significant associations between the presence of atherosclerotic plaque and the CA‐haplotype in men (P = 0·028, phi = 0·08), and between the AG variant of exon 6 and common carotid artery intima‐media thickness (CIMT) in women (P = 0·004, Eta² = 0·019). Conclusions In summary, our results demonstrate associations of MMP‐9 genotypes with different stages of carotid atherosclerosis.     

Loss of the BH3-only protein Bmf impairs B cell homeostasis and accelerates gamma irradiation-induced thymic lymphoma development

Members of the Bcl-2 protein family play crucial roles in the maintenance of tissue homeostasis by regulating apoptosis in response to developmental cues or exogenous stress. Proapoptotic BH3-only members of the Bcl-2 family are essential for initiation of cell death, and they function by activating the proapoptotic Bcl-2 family members Bax and/or Bak, either directly or indirectly through binding to prosurvival Bcl-2 family members. Bax and Bak then elicit the downstream events in apoptosis signaling. Mammals have at least eight BH3-only proteins and they are activated in a stimulus-specific, as well as a cell type-specific, manner. We have generated mice lacking the BH3-only protein Bcl-2-modifying factor (Bmf) to investigate its role in cell death signaling. Our studies reveal that Bmf is dispensable for embryonic development and certain forms of stress-induced apoptosis, including loss of cell attachment (anoikis) or UV irradiation. Remarkably, loss of Bmf protected lymphocytes against apoptosis induced by glucocorticoids or histone deacetylase inhibition. Moreover, bmf(-/-) mice develop a B cell-restricted lymphadenopathy caused by the abnormal resistance of these cells to a range of apoptotic stimuli. Finally, Bmf-deficiency accelerated the development of gamma irradiation-induced thymic lymphomas. Our results demonstrate that Bmf plays a critical role in apoptosis signaling and can function as a tumor suppressor.