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The major histocompatibility complex (MHC) plays a central role in the adaptive immune response and is the most polymorphic gene family in vertebrates. Although high-throughput sequencing has increasingly been used for genotyping families of co-amplifying MHC genes, its potential to facilitate early steps in the characterisation of MHC variation in nonmodel organism has not been fully explored. In this study we evaluated the usefulness of de novo transcriptome assembly in characterisation of MHC sequence diversity. We found that although de novo transcriptome assembly of MHC I genes does not reconstruct sequences of individual alleles, it does allow the identification of conserved regions for PCR primer design. Using the newly designed primers, we characterised MHC I sequences in the bank vole. Phylogenetic analysis of the partial MHC I coding sequence (2–4 exons) of the bank vole revealed a lack of orthology to MHC I of other Cricetidae, consistent with the high gene turnover of this region. The diversity of expressed alleles was characterised using ultra-deep sequencing of the third exon that codes for the peptide-binding region of the MHC molecule. High allelic diversity was demonstrated, with 72 alleles found in 29 individuals. Interindividual variation in the number of expressed loci was found, with the number of alleles per individual ranging from 5 to 14. Strong signatures of positive selection were found for 8 amino acid sites, most of which are inferred to bind antigens in human MHC, indicating conservation of structure despite rapid sequence evolution.

In several species of the mite family Acaridae, fighter males, possessing a sharply terminated third pair of legs which they use to mortally stab other males, coexist with scrambler males with unmodified legs. We studied the effect of population size on the relative mortality of fighters versus scramblers in the bulb mite, Rhizoglyphus robini, a species in which male morph is heritable. Fights were an important determinant of male mortality, and fighters of R. robini survived better in both large (120 individuals) and small (10 individuals) colonies. Colony size did not significantly affect the relative survivorship of the two morphs, and we also found no differences between large and small colonies in the proportion of fighters in the progeny. Thus, the possibility that variation in population size maintains genetic variation for male morph in R. robini was not supported by our result. Nor was another possible mechanism, the negative frequency-dependence of morph fitness. We estimated morph mortality and mating success in populations of 42 adults, with the fighter/scrambler ratio ranging from 1:19 to 19:1. Neither measure depended on the proportion of fighters in a population, but fighters survived better than scramblers. Further research is needed to explain the maintenance of morph heritability in R. robini in spite of the higher mortality of scramblers. We discuss potential mechanisms.

Multiple mating by females has been proposed to function as a form of mate‐choice, which implies that males should show heritable variation in sperm‐competitive abilities. In this study, repeatability and heritability of sperm competition success was estimated in the bulb mite, Rhizoglyphus robini. Fertilization success of males was estimated in competition with sperm of two other males. Males differed consistently in their sperm competition success, with repeatability estimated at 0.22. The heritability of sperm competition success was estimated using parent‐offspring regression, with the mean fertilization success from two matings used as a measure of each male's competitive ability. There was a significant association between the sperm competition success of fathers and sons. Narrow sense heritability (h2) was 0.284. This result supports the hypotheses proposing the multiple mating is selectively maintained in females by enhancing the reproductive success of their progeny.

Platelets participate in formation of thrombin through secretion of coagulation factors and by providing a catalytic surface on which prothrombinase complex is assembled. We studied the effects of four antiplatelet drugs on thrombin formation in healthy volunteers. Thrombin generation was monitored both in vitro--in recalcified plasma-- and ex vivo--in blood emerging from a standardized skin microvasculature injury, which also served to determine bleeding time. A mathematical model has been developed to describe the latter reaction. It is based on estimation of the rate of increase in fibrinopeptide A (FPA), a specific marker of thrombin activity, in blood emerging from skin incisions. Two hours after the ingestion of 500 mg of aspirin, thrombin formation became significantly impaired both in vitro and ex vivo. In contrast, 2 hours after the oral administration of placebo, indomethacin 50 mg, or OKY-046 (a thromboxane synthase inhibitor) 400 mg, thrombinogenesis remained unaltered. Ticlopidine, studied either 3 hours after 500 mg oral administration, or after 5 days of intake at a daily dose of 500 mg, had no effect on thrombin generation. Thus, aspirin, contrary to other antiplatelet drugs, depresses thrombin formation in clotting blood, a phenomenon that might be of clinical relevance. It is suggested that aspirin exerts this effect by acetylating prothrombin and/or macromolecules of platelet membrane.

Multiple mating by females has been proposed to function as a form of mate‐choice, which implies that males should show heritable variation in sperm‐competitive abilities. In this study, repeatability and heritability of sperm competition success was estimated in the bulb mite, Rhizoglyphus robini. Fertilization success of males was estimated in competition with sperm of two other males. Males differed consistently in their sperm competition success, with repeatability estimated at 0.22. The heritability of sperm competition success was estimated using parent‐offspring regression, with the mean fertilization success from two matings used as a measure of each male's competitive ability. There was a significant association between the sperm competition success of fathers and sons. Narrow sense heritability (h2) was 0.284. This result supports the hypotheses proposing the multiple mating is selectively maintained in females by enhancing the reproductive success of their progeny.