PurposeThe purpose of this paper is to characterize and evaluate a new 3D‐printing process based on Poly(methyl methacrylate) (PMMA).Design/methodology/approachA benchmark part and standard parts were designed, printed by a 3D‐printer and characterized.Findings3D printed PMMA parts have a tensile strength of 2.91 MPa and a modulus of elasticity of 223 MPa. The mechanical properties can be improved by infiltrations with epoxy (tensile strength: 26.6 MPa, modulus of elasticity: 1,190 MPa). The surface quality of the parts can be improved by infiltration with wax for usage as lost models. The minimum feature size is 0.3 mm.Research limitations/implicationsThe PMMA‐based 3D printing process can be used for manufacturing concept models, functional parts and lost models for investment casting.Originality/valueThis is the first paper investigating a PMMA‐based 3D printing process.
The possible role of protein kinase C (PKC) activation in the course of insulin secretion induced by the imidazoline phentolamine was investigated by measuring the insulin secretion of perifused mouse islets and of insulin-secreting HIT cells and by measuring the PKC activity of HIT cells. When normal mouse islets were perifused with the imidazoline phentolamine (32 microM) or the sulfonylurea glibenclamide (1 microM), neither phentolamine nor glibenclamide could produce a stimulation of secretion which was stronger than that elicited by a strong depolarization. Under the same conditions, tetradecanoylphorbolacetate (TPA, 50 nM), a known activator of PKC activity in pancreatic islets, markedly enhanced the secretion induced by K+ depolarization. Phentolamine also stimulated insulin secretion of superfused HIT cells. When PKC activity in HIT cells was down-regulated to 15% of the initial value by overnight exposure to TPA (50 nM), the stimulatory effect of TPA on secretion was virtually abolished, while phentolamine was still able to elicit a monophasic secretion. TPA (50 nM) induced the typical redistribution of PKC activity in HIT cells: within 2 min, the share of membrane-bound PKC activity rose from 26% to 87% of the total PKC activity, which remained unchanged. In contrast, phentolamine (32 microM) had no effect on PKC distribution, did not down-regulate PKC and had no effect on PKC activity once it was down-regulated by TPA. Thus, the recent suggestion that the insulinotropic effect of imidazolines involves an activation of PKC could not be verified for phentolamine.
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