Gillian R. Milne

TL;DR: The existence of a novel cAMP/Epac/Rap1/SOCS-3 pathway for limiting IL-6 receptor signaling in ECs is argued for and a new mechanism by which cAMP may mediate its potent anti-inflammatory effects is illuminated.

TL;DR: Reduced oxidative capacity and capacity for fatty acid utilisation at the whole body level are key features of the insulin resistant phenotype observed in South Asians, but that this is not the consequence of reduced skeletal muscle expression of oxidative and lipid metabolism genes.

TL;DR: The current evidence for the anti-inflammatory effects of the A2AAR in different cell types is reviewed and possible molecular mechanisms mediating these effects are discussed, including the potential for generalised suppression of inflammatory gene expression through inhibition of the NF-κB and JAK/STAT proinflammatory signalling pathways.

TL;DR: OT1DM are at increased risk of overweight and obesity in childhood and this risk appears to relate, in part, to fetal leptin and hematocrit but not insulin.

TL;DR: New molecular mechanisms by which the cAMP/Epac1 (exchange protein directly activated by cAMP 1)/Rap1 pathway can initiate a rigorous programme of protective anti-inflammatory responses in VECs will inform the development of the next generation of pharmaceuticals specifically designed to combat endothelial inflammation associated with cardiovascular disease.