Paracrine signalling by pancreatic δ cells determines the glycaemic set point in mice.

While pancreatic β and α cells are considered the main drivers of blood glucose homeostasis through insulin and glucagon secretion, the contribution of δ cells and somatostatin (SST) secretion to glucose homeostasis remains unresolved. Here we provide a quantitative assessment of the physiological contribution of δ cells to the glycaemic set point in mice. Employing three orthogonal mouse models to remove SST signalling within the pancreas or transplanted islets, we demonstrate that ablating δ cells or SST leads to a sustained decrease in the glycaemic set point.

[Epidemiology of beta-hemolytic streptococcus group B colonization in perinatology. Methodology considerations and personal data].

GBS have attracted increasing attention in recent years as a major cause of serious neonatal sepsis. The maternal genital tract is the principal source of organism for babies with the most serious early onset form of disease. Reported rates of GBS carriage in the genital and anorectal tract of pregnant women vary widely: much of the variations is undoubtedly associated with differences in laboratory technique, sampling site and number of samples taken.