Hydrophobicity measurements of microfiltration and ultrafiltration membranes.

A method for the determination of the hydrophobicity of membrane materials is developed. The advantage of this method over existing methods is that it is not influenced by the presence of the pores. A piece of the membrane material is submerged horizontally in a liquid with surface tension L. Hydrophobicity is expressed in terms of d, the surface tension at which an air bubble brought into contact with the top surface of the membrane has a 50% chance of detaching from the surface. Values of d are expected to be 2-4 mN/m higher than critical surface tension (c) values found in the literature. For polypropylene, PTFE and polydimethylsiloxane membranes, a good agreement was found between d and c values. Poly (vinylidene fluoride), polysulfone and polyethersulfone membranes appeared to be more hydrophilic than was expected on the basis of the literature c values for the polymers. Using X-ray photoelectron spectroscopy, constituents that are not present in the pure polymer have been found in the surface of some membranes. These constituents and the production techniques are shown to influence the hydrophobicity of the membranes investigated

Glucagon decreases cytokine induction of nitric oxide synthase and action on insulin secretion in RIN5F cells and rat and human islets of Langerhans

Nitric oxide synthase, induced by cytokines in insulin-containing cells, produces nitric oxide which inhibits function and may promote cell killing. Since glucagon was shown to prevent inducible nitric oxide synthase (iNOS) expression in rat hepatocytes it was of interest to examine the action of glucagon (and cyclic AMP) on iNOS induction in insulin-producing cells. Cultured RIN5F cells and primary rat and human islets of Langerhans were treated with interleukin 1ß (IL-1ß) or a combination of cytokines, and were co-treated or pre-treated with glucagon. In RIN5F cells, the activity of iNOS induced by IL-1ß (10 pM, 24 h), was significantly reduced by glucagon (1000 nM), which raises cyclic AMP, and by forskolin (1-10 µM), a non specific activator of adenylate cyclase. Glucagon and forskolin also decreased iNOS expression in RIN5F cells, and rat and human islets, as shown by Western blotting. The inhibitory action of IL-1ß (100 pM, 24 h) on rat islet insulin secretion was partially reversed by 1-h pre-treatment with glucagon (10-1000 nM), while the contrasting stimulatory effect of 48-h treatment with cytokines on insulin secretion from human islets was similarly prevented by glucagon (1000 nM) pre-treatment. These results suggest that glucagon inhibits iNOS expression in insulin-containing cells and imply that glucagon could modulate the inhibitory effects of cytokines