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This paper presents the influence of solution and aging temperatures on the microstructure and mechanical properties of 319 secondary cast aluminium alloy. Experimental alloy was subjected to different heat treatment cycles. Heat treatments were designed with two solutionising temperatures (504 and 545°C) at two solutionising times (4 and 8 h), followed by quenching in water at 60°C and artificial aging. The artificial aging was carried out at two temperatures (200 and 154°C) for 6 h. The improvement in mechanical properties was obtained with low solution temperature (504°C) for 8 h followed by quenching in water to 60°C and aging at low temperature (154°C). The increase in the solutionising temperature from 504 to 545°C was recommendable only for short solutionising time (4 h). Increase in the aging temperature from 154 to 200°C has led to the increase in hardness with the corresponding decrease in ductility. Aging under unfavourable conditions (prolonged aging at high temperature) caused coarsening of spheroidised eutectic silicon crystals and precipitated particles resulted in deleterious effect on the tensile strength.

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Our aim was to investigate the subset distribution and function of circulating monocytes, proinflammatory cytokine levels, gut barrier damage, and bacterial translocation in chronic spinal cord injury (SCI) patients. Thus, 56 SCI patients and 28 healthy donors were studied. The levels of circulating CD14+highCD16−, CD14+highCD16+, and CD14+lowCD16+ monocytes, membrane TLR2, TLR4, and TLR9, phagocytic activity, ROS generation, and intracytoplasmic TNF-α, IL-1, IL-6, and IL-10 after lipopolysaccharide (LPS) stimulation were analyzed by polychromatic flow cytometry. Serum TNF-α, IL-1, IL-6 and IL-10 levels were measured by Luminex and LPS-binding protein (LBP), intestinal fatty acid-binding protein (I-FABP) and zonulin by ELISA. SCI patients had normal monocyte counts and subset distribution. CD14+highCD16− and CD14+highCD16+ monocytes exhibited decreased TLR4, normal TLR2 and increased TLR9 expression. CD14+highCD16− monocytes had increased LPS-induced TNF-α but normal IL-1, IL-6, and IL-10 production. Monocytes exhibited defective phagocytosis but normal ROS production. Patients had enhanced serum TNF-α and IL-6 levels, normal IL-1 and IL-10 levels, and increased circulating LBP, I-FABP, and zonulin levels. Chronic SCI patients displayed impaired circulating monocyte function. These patients exhibited a systemic proinflammatory state characterized by enhanced serum TNF-α and IL-6 levels. These patients also had increased bacterial translocation and gut barrier damage.