Concerns over climate change and its potential impact on infectious disease prevalence have contributed to a resurging interest in malaria in the past. A wealth of historical evidence indicates that malaria, specifically Plasmodium vivax, was endemic in the wetlands of England from the 16th century onwards. While it is thought that malaria was introduced to Britain during the Roman occupation (AD first to fifth centuries), the lack of written mortality records prior to the post-medieval period makes it difficult to evaluate either the presence or impact of the disease. The analysis of human skeletal remains from archaeological contexts is the only potential means of examining P. vivax in the past. Malaria does not result in unequivocal pathological lesions in the human skeleton; however, it results in hemolytic anemia, which can contribute to the skeletal condition cribra orbitalia. Using geographical information systems (GIS), we conducted a spatial analysis of the prevalence of cribra orbitalia from 46 sites (5,802 individuals) in relation to geographical variables, historically recorded distribution patterns of indigenous malaria and the habitat of its mosquito vector Anopheles atroparvus. Overall, those individuals living in low-lying and Fenland regions exhibited higher levels of cribra orbitalia than those in nonmarshy locales. No corresponding relationship existed with enamel hypoplasia. We conclude that P. vivax malaria, in conjunction with other comorbidities, is likely to be responsible for the pattern observed. Studies of climate and infectious disease in the past are important for modeling future health in relation to climate change predictions.

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When recorded consistently, HFI was positively correlated with age and longevity but had also increased among old age females over time. Our results suggest that nulliparity co-occurs with HFI but is not a primary factor in its pathogenesis. Key factors in HFI presence in females are likely to be increased androgens and the dysregulation of insulin and insulin-like growth factor-1.

Besides intron 22 factor VIII gene inversion (Inv22), intron 1 inversion (Inv1) has recently been reported as a further recurrent mutation that causes approximately 5% of severe haemophilia A (HA) cases. We analysed the presence of the Inv1 in a group of 64 severe HA-affected families from Argentina, and found only one positive case. This Inv1 patient has not developed a factor VIII inhibitor, and the screening for small mutations in the coding sequences of the factor VIII gene did not detect any additional defect in this case. The Inv1 genotyping was further applied to analyse the haemophilia carrier status of the proband's sister. In addition, we studied the accuracy of the current polymerase chain reaction-based method to investigate the Inv1, and confirmed the absence of amplimer length polymorphisms associated to the Inv1-specific polymerase chain reaction amplifications in 101 X-chromosome haplotypes from unrelated Argentinian healthy males. In order to discuss Inv1 mutation frequency in severe HA and the risk of inhibitor formation, a review of the literature was included. Our data highlight the importance of analysis of the Inv1 in Inv22-negative severe HA cases. This will benefit both genetic counselling and the study of the relationship between genotype and inhibitor development.