PurposeThe purpose of this paper is to investigate the mechanisms controlling the bond formation among extruded polymer filaments in the fused deposition modeling (FDM) process. The bonding phenomenon is thermally driven and ultimately determines the integrity and mechanical properties of the resultant prototypes.Design/methodology/approachThe bond quality was assessed through measuring and analyzing changes in the mesostructure and the degree of healing achieved at the interfaces between the adjoining polymer filaments. Experimental measurements of the temperature profiles were carried out for specimens produced under different processing conditions, and the effects on mesostructures and mechanical properties were observed. Parallel to the experimental work, predictions of the degree of bonding achieved during the filament deposition process were made based on the thermal analysis of extruded polymer filaments.FindingsExperimental results showed that the fabrication strategy, the envelope temperature and variations in the convection coefficient had strong effects on the cooling temperature profile, as well as on the mesostructure and overall quality of the bond strength between filaments. The sintering phenomenon was found to have a significant effect on bond formation, but only for the very short duration when the filament's temperature was above the critical sintering temperature. Otherwise, creep deformation was found to dominate changes in the mesostructure.Originality/valueThis study provides valuable information about the effect of deposition strategies and processing conditions on the mesostructure and local mechanical properties within FDM prototypes. It also brings a better understanding of phenomena controlling the integrity of FDM products. Such knowledge is essential for manufacturing functional parts and diversifying the range of application of this process. The findings are particularly relevant to work conducted on modeling of the process and for the formulation of materials new to the FDM process.

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The accumulation of polymers of the microtubule associated protein tau is correlative with increased neurodegeneration in Alzheimer's disease and other related tauopathies. In vitro models have been developed in order to investigate molecular mechanisms that regulate the polymerization of tau. Arachidonic acid and heparin have been proposed to induce tau polymerization via a ligand dependent nucleation-elongation mechanism. However, certain aspects of these in vitro results are inconsistent with a classic nucleation-elongation mechanism. Using steady state and kinetic analyses of tau polymerization at a variety of protein and inducer concentrations, we have found that the thermodynamic barrier for nucleation in the presence of inducers is negligible, which was manifested by increases in protein polymerization at low tau concentrations and very rapid kinetics of polymerization. However, the mechanism of polymerization is complicated by the observation that high concentrations of inducer molecules result in the inhibition of tau fibril formation through different mechanisms for arachidonic acid and heparin. These observations indicate that the molar ratio of inducer to protein is a greater determinant of the rate and extent of tau polymerization than the concentration of tau itself. Our results are therefore not consistent with a canonical nucleation-elongation reaction but rather are more consistent with an allosteric regulation model in which the presence of small molecules induce a conformational change in the protein that decreases the thermodynamic barrier for polymerization essentially to zero.