Additive manufacturing of high-strength crack-free Ni-based Hastelloy X superalloy

Laser powder bed fusion (LPBF) is a proven additive manufacturing (AM) technology for producing metallic components with complex shapes using layer-by-layer manufacture principle. However, the fabrication of crack-free high-performance Ni-based superalloys such as Hastelloy X (HX) using LPBF technology remains a challenge because of these materials’ susceptibility to hot cracking. This paper addresses the above problem by proposing a novel method of introducing 1 wt.% titanium carbide (TiC) nanoparticles. The findings reveal that the addition of TiC nanoparticles results in the elimination of microcracks in the LPBF-fabricated enhanced HX samples; i.e. the 0.65% microcracks that were formed in the as-fabricated original HX were eliminated in the as-fabricated enhanced HX, despite the 0.14% residual pores formed. It also contributes to a 21.8% increase in low-angle grain boundaries (LAGBs) and a 98 MPa increase in yield strength. The study revealed that segregated carbides were unable to trigger hot cracking without sufficient thermal residual stresses; the significantly increased subgrains and low-angle grain boundaries played a key role in the hot cracking elimination. These findings offer a new perspective on the elimination of hot cracking of nickel-based superalloys and other industrially relevant crack-susceptible alloys. The findings also have significant implications for the design of new alloys, particularly for high-temperature industrial applications

Diabetes-induced decrease of adenosine kinase expression impairs the proliferation potential of diabetic rat T lymphocytes

The proliferative response of T lymphocytes is a crucial step in cell-mediated immunity. This study was undertaken to investigate the mechanisms leading to the impaired proliferative response of diabetic T lymphocytes. T cells that had been isolated from the spleen of normal rats and cultured in medium containing 20 mm glucose and no insulin displayed the same degree of proliferative impairment as cells isolated from diabetic rats. The rate of T-cell proliferation, when induced with concanavalin A or anti-CD3 and anti-CD28 antibodies, was not affected by the inhibition of nucleoside transporters. T cells cultured at high glucose concentrations in the absence of insulin displayed decreased expression of adenosine kinase, and released measurable extracellular quantities of adenosine. Under resting conditions, the level of cAMP was 5·9-fold higher in these cells compared to cells grown in low glucose and in the presence of insulin. Experiments with specific adenosine receptor agonists and antagonists showed that adenosine-induced suppression of diabetic T cell proliferation was mediated by the A(2A) adenosine receptor, but not by the A(2B) receptor. Treatment of diabetic T cells with 10 μm H-89, a specific protein kinase A inhibitor, restored T-cell proliferation. These results show that suppressed proliferation of diabetic T lymphocytes is evoked by the decreased expression of adenosine kinase, leading to the outflow of adenosine from the cell. Extracellular adenosine then stimulates the A(2A) receptor and induces cAMP production, leading to the activation of protein kinase A, and suppression of T-cell proliferation