Additive manufacturing of stainless steel is becoming increasingly accessible, allowing for the customisation of structure and surface characteristics; there is little guidance for the post-processing of these metals. We carried out this study to ascertain the effects of various combinations of post-processing methods on the surface of an additively manufactured stainless steel 316L lattice. We also characterized the nature of residual surface particles found after these processes via energy-dispersive X-ray spectroscopy. Finally, we measured the surface roughness of the post-processing lattices via digital microscopy. The native lattices had a predictably high surface roughness from partially molten particles. Sandblasting effectively removed this but damaged the surface, introducing a peel-off layer, as well as leaving surface residue from the glass beads used. The addition of either abrasive polishing or electropolishing removed the peel-off layer but introduced other surface deficiencies making it more susceptible to corrosion. Finally, when electropolishing was performed after the above processes, there was a significant reduction in residual surface particles. The constitution of the particulate debris as well as the lattice surface roughness following each post-processing method varied, with potential implications for clinical use. The work provides a good base for future development of post-processing methods for additively manufactured stainless steel.

Whole cell patch-clamp experiments were undertaken to define the basal K⁺ conductance(s) in human erythroleukemia cells and its contribution to the setting of resting membrane potential. Experiments revealed a non-voltage-activated, noninactivating K⁺ current. The magnitude of the current recorded under whole cell conditions was inhibited by an increase in free intracellular Mg²⁺ concentration. Activation or inactivation of the Mg²⁺-inhibited K⁺ current (MIP) was paralleled by activation or inactivation of a Mg²⁺-inhibited TRPM7-like current displaying characteristics indistinguishable from those reported for molecularly identified TRPM7 current. The MIP and TRPM7 currents were inhibited by 5-lipoxygenase inhibitors. However, inhibition of the MIP current was temporally distinct from inhibition of TRPM7 current, allowing for isolation of the MIP current. Isolation of the MIP conductance revealed a current reversing near the K⁺ equilibrium potential, indicative of a highly K⁺-selective conductance. Consistent with this finding, coactivation of the nonselective cation current TRPM7 and the MIP current following dialysis with nominally Mg²⁺-free pipette solution resulted in hyperpolarized whole cell reversal potentials, consistent with an important role for the MIP current in the setting of a negative resting membrane potential. The MIP and TRPM7-like conductances were constitutively expressed under in vivo conditions of intracellular Mg²⁺, as judged by their initial detection and subsequent inactivation following dialysis with a pipette solution containing 5 mM free Mg²⁺. The MIP current was blocked in a voltage-dependent fashion by extracellular Cs⁺ and, to a lesser degree, by Ba²⁺ and was blocked by extracellular La³⁺ and 2-aminoethoxydiphenyl borate. MIP currents were unaffected by blockers of ATP-sensitive K⁺ channels, human ether-à-go-go-related gene current, and intermediate-conductance Ca²⁺-activated K⁺ channels. In addition, the MIP current displayed characteristics distinct from conventional inwardly rectifying K⁺ channels. A similar current was detected in the leukemic cell line CHRF-288-11, consistent with this current being more generally expressed in cells of leukemic origin.