RESUMO
From around 2750 to 2500 bc, Bell Beaker pottery became widespread across western and central Europe, before it disappeared between 2200 and 1800 bc. The forces that propelled its expansion are a matter of long-standing debate, and there is support for both cultural diffusion and migration having a role in this process. Here we present genome-wide data from 400 Neolithic, Copper Age and Bronze Age Europeans, including 226 individuals associated with Beaker-complex artefacts. We detected limited genetic affinity between Beaker-complex-associated individuals from Iberia and central Europe, and thus exclude migration as an important mechanism of spread between these two regions. However, migration had a key role in the further dissemination of the Beaker complex. We document this phenomenon most clearly in Britain, where the spread of the Beaker complex introduced high levels of steppe-related ancestry and was associated with the replacement of approximately 90% of Britain's gene pool within a few hundred years, continuing the east-to-west expansion that had brought steppe-related ancestry into central and northern Europe over the previous centuries.
Assuntos
Evolução Cultural/história , Genoma Humano/genética , Genômica , Migração Humana/história , Cromossomos Humanos Y/genética , DNA Antigo , Europa (Continente) , Pool Gênico , Genética Populacional , Haplótipos , História Antiga , Humanos , Masculino , Análise Espaço-TemporalRESUMO
In 2003, occasional military patients with hyponatraemia, hypokalaemia and alkalosis were encountered in Iraq. Development of central pontine myelinolysis in one patient indicated treatment should be cautious. Two years later, heat illness continued to occur during the very hot summer months and 23 cases were admitted to a British military field hospital near Basra, Iraq. Incidence was < 0.15% of deployed personnel per summer month. Serum sodium and potassium concentrations were directly (r = 0.66, p = 0.0002) and serum sodium and bicarbonate concentrations inversely (r= -0.64, p = 0.002) correlated. The magnitude of these changes was unrelated to the glomerular filtered load of sodium. While blood pressure was undiminished, estimated glomerular filtration rate was reduced. These electrolyte changes were compatible with secondary hyperaldosteronism but field conditions constrained further investigation. Hyponatraemia was probably due to salt deficiency rather than overhydration. In some military personnel summer salt supplementation could be essential during operations in hot countries.