Based on available evidence, we would propose the following. (i) Excesses of glucose and free fatty acids cause insulin resistance in skeletal muscle and damage to the endothelial cell by a similar mechanism. (ii) Key pathogenetic events in this mechanism very likely include increased fatty acid esterification, protein kinase C activation, an increase in oxidative stress (demonstrated to date in endothelium) and alterations in the inhibitor κB kinase/nuclear factor κB system. (iii) Activation of AMP-activated protein kinase (AMPK) inhibits all of these events and enhances insulin signalling in the endothelial cell. It also enhances insulin action in muscle; however, the mechanism by which it does so has not been well studied. (iv) The reported beneficial effects of exercise and metformin on cardiovascular disease and insulin resistance in humans could be related to the fact that they activate AMPK. (v) The comparative roles of AMPK in regulating metabolism, signalling and gene expression in muscle and endothelial cells warrant further study.

The observed increase of superconducting transition temperature (T(c)) with the number of copper oxide planes continues in the four-[CuO(2)](-2) layer (single TI layer) oxide superconductor, which has been prepared with > 80% purity and was magnetically aligned for crystallographic identification. A master scaling curve is proposed, which ties together the T(c)'s of virtually all known Bi and Tl oxide superconductors, and shows that the Tl(Bi) layers play an essential role in the superconductivity. publication 350 of the Barnett Institute.

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