Use of ultrasonic agitation in iron group alloy electrodepositions

The effects of ultrasonic agitation on deposition from two iron group alloy plating solutions, nickel-cobalt and bright nickel-iron, have been studied. Comparison has been made with deposits plated from the same solutions using controlled air agitation. The ultrasonic equipment employed had a fixed frequency of 13 KHz but the power output from each transducer was variable up to a maximum of 350 watts. The effects of air and ultrasonic agitation on hardness, ductility, tensile strength, composition, structure, surface topography, limiting current density, cathode current efficiency and macro-throwing power were determined. Transmission and scanning electron microscopy, electron-probe microanalysis and atomic absorption spectrophotometry have been employed to study the nickel alloy deposits produced. The results obtained show that the use of Ultrasonics increased significantly the hardness of both alloy deposits and altered their composition by decreasing the cobalt and iron contents from nickel-cobalt and nickeliron solutions respectively. The ductility of coatings improved but the tensile strength did not change very much. Ultrasonic agitation gave larger grained deposits than air and they seemed to have a lower stress. Dull cobalt-nickel deposits had a similar pyramidal surface topography regardless of the type of agitation but the bright appearance of the nickel-iron was destroyed by ultrasonic agitation; an unusual ribbed pattern was produced. The use of ultrasonic agitation permitted approximately a twofold increase in the plating current density at which sound deposits could be achieved but there was only a slight increase in cathode current efficiency. Macro-throwing power of the solutions was increased slightly by the use of ultrasonic agitation. ultrasonic agitation is an expensive means of agitating plating Solutions and would be worthwhile only if significant improvements in properties could be achieved. The simultaneous improvement in hardness and ductility is a novel feature that should have useful engineering applications.

Insulin release from cultured B-cells

Established RlNm5F and lN111 R1 and newly available HlT-T15 and UMR 407/3 B-cell lines have been successfully maintained in vitro. With the exclusion of UMR 407/3 cells, all lines were continuously propagable. Doubling times and plating efficiencies for HlT-T15, RlNm5F, lN111 R1 and UMR 407/3 cells were 20 hours and 85%, 31 hours and 76%, 24 hours and 80% and 38 hours and 94% respectively. All the cell lines were anchorage dependent, but only UMR 407/3 cells grew to confluence. Only HlT-T15 and UMR 407/3 cells produced a true insulin response to glucose but glucose markedly increased the rate of D-[U14C]glucose oxidation by all the cell lines. Glucose induced insulin release from HlT-T15 cells was biphasic with an exaggerated first phase. Insulin release from HlT-T15, RlNm5F and IN111 R1 cells was stimulated by amino acids and sulphonylureas. Glucagon stimulated insulin release from HlT-T15 and RlNm5F cells while somatostatin and pancreatic polypeptide inhibited release. These observations suggest that net insulin release from the whole islet may be the result of significant paracrine interaction. HlT-T15 and RlNm5F cell insulin release was stimulated by forskolin and inhibited by imidazole. Ca2+ channel blockade and calmodulin inhibition suppressed insulin release from HlT-T15, RlNm5F and IN111 R1 cells. In addition phorbol esters stimulated insulin release from RlNm5F cells. These data implicate cAMP, Ca2+ and protein kinase-C in the regulation of insulin release from cultured B-cells. Acetylcholine increased insulin release from HlT-T15 and RlNm5F cells. Inhibition of the response by atropine confirmed the involvement of muscarinic receptors. HlT-T15 cell insulin release was also inhibited by adrenaline. These observations suggest a possible role for the autonomic nervous system in the modulation of insulin release. Preliminary studies with a human insulinoma maintained in monolayer culture have demonstrated a limited life span of some seven weeks, a continuous low level of insulin release but no insulin response to glucose challenge.