Altruism was the most common general motive for donating blood and also for continuing to be an active blood donor. Yet, for the first blood donation, direct 'influence from friends/relatives', 'media appeal' and other types of recruitment were more commonly reported as reasons or motives for donating blood than altruism. The findings support the notion that different strategies should be used/adopted to get people to donate blood the first time (e.g. recruitment through other blood donors using, for example, the 'bring a friend along' method) and to retain these subjects as active blood donors (e.g. by information and by strengthening their sense of being a blood donor or their self-efficacy etc.).

The molecular genetic basis of the P histo-blood group system has eluded characterization despite extensive studies of the biosynthesis of the P 1 , P, and P k glycolipids. The main controversy has been whether a single or two distinct UDP-Gal:Gal␤1-R 4-␣-galactosyltransferases catalyze the syntheses of the structurally related P 1 and P k antigens. The P 1 polymorphism is linked to 22q11.3-ter. Data base searches with the coding region of an ␣4GlcNAc-transferase identified a novel homologous gene at 22q13.2 designated ␣4Gal-T1. Expression of full coding constructs of ␣4Gal-T1 in insect cells revealed it encoded P k but not P 1 synthase activity. Northern analysis showed expression of the transcript correlating with P k synthase activity and antigen expression in human B cell lines. Transfection of P k -negative Namalwa cells with ␣4Gal-T1 resulted in strong P k expression. A single homozygous missense mutation, M183K, was found in six Swedish individuals of the rare p phenotype, confirming that ␣4Gal-T1 represented the P k gene. Sequence analysis of the coding region of ␣4Gal-T1 in P 1 ؉/؊ individuals did not reveal polymorphisms correlating with P 1 P 2 typing.The P histo-blood group system is the last of the known carbohydrate defined blood group systems for which the molecular genetic basis has not yet been clarified. The P blood group system involves two major blood group phenotypes, P 1 ϩ and P 1 Ϫ, with approximate frequencies of 80% and 20%, respectively (1, 2). P 1 Ϫ individuals normally express the P antigen (P 1 Ϫ is designated P 2 when P antigen expression is demonstrated), but the rare P k phenotype lacks the P antigen, while the rare p phenotype lack both P and P k antigens (for reviews, see Refs. 3-7). The P 1 ϩ phenotype is defined by expression of the neolacto-series glycosphingolipid P 1 (for structures, see Table I) (8). In contrast, the P, P k , and p antigens constitute intermediate steps in biosynthesis of globo-series glycolipids and give rise to P 1 k , P 2 k , and p phenotypes (9). Although the rare P k phenotype shows the same frequency of P 1 antigen expression as individuals expressing the P antigen, the p phenotype is always associated with lack of P 1 antigen expression. Extensive studies of the chemistry, biosynthesis, and genetics of the P blood group system identified the antigens as being exclusively found on glycolipids, with the blood group specificity being synthesized by at least two distinct glycosyltransferase activities; UDP-galactose:␤-D-galactosyl-␤1-R 4-␣-Dgalactosyltransferase (␣4Gal-T) 1 activity(ies) for P k and P 1 syntheses and UDP-GalNAc:Gb 3 3-␤-N-acetylgalactosaminyltransferase activity (EC 2.4.1.79) for P synthesis (for reviews, see Refs. 6 and 7). At least two independent gene loci, P and P 1 P k , are involved in defining these antigens. The P blood group-associated LKE antigen, shown to be the extended sialylated Gal-globoside structure (10), may involve polymorphism in an ␣2,3-sialyltransferase activity.A long-standing controversy has been whether a single...

The Vel antigen is present on red blood cells (RBCs) from all humans except rare Vel-negative individuals who can form antibodies to Vel in response to transfusion or pregnancy. These antibodies may cause severe hemolytic reactions in blood recipients. We combined SNP profiling and transcriptional network modeling to link the Vel-negative phenotype to SMIM1, located in a 97-kb haplotype block on chromosome 1p36. This gene encodes a previously undiscovered, evolutionarily conserved transmembrane protein expressed on RBCs. Notably, 35 of 35 Vel-negative individuals were homozygous for a frameshift deletion of 17 bp in exon 3. Functional studies using antibodies raised against SMIM1 peptides confirmed a null phenotype in RBC membranes, and SMIM1 overexpression induced Vel expression. Genotype screening estimated that ~1 of 17 Swedish blood donors is a heterozygous deletion carrier and ~1 of 1,200 is a homozygous deletion knockout and enabled identification of Vel-negative donors. Our results establish SMIM1 as a new erythroid gene and Vel as a new blood group system.

The majority of effects elicited by blood donation on blood donors were positive (i.e. feelings of satisfaction, greater alertness, increased wellbeing, etc.). The positive effects did not differ from the negative regarding time of onset, yet their duration was reported to be significantly longer. There was no association between frequency of occurrence of positive effects and the number of blood donations, indicating that there is no 'addictive' relationship between donors and blood donations. The findings in this study of high frequency of occurrence of positive long-lasting effects elicited in blood donors by blood donation may be of great importance for the recruitment of new blood donors as it may make blood donation less frightening and perhaps even attractive.

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