Synthesis, morphology, and formation mechanism of mullite particles produced by ultrasonic spray pyrolysis

Submicrometer spherical particles of mullite powder were synthesized by ultrasonic spray pyrolysis of emulsion and solutions, using tetra-ethyl-orthosilicate (TEOS) or silicic-acid and Al(NO3)(3) . 9H(2)O as initial compounds. Crystallization of mullite phase was determined by differential thermal (DT), thermogravimetric (TG), infrared (IR), and x-ray analyses. The synthesis of mullite from TEOS emulsion occurs by crystallization of gamma-Al2O3 (or Al, Si-spinel) from the amorphous phase and its subsequent reaction with amorphous SiO2, as well as by crystallization of pseudotetragonal mullite below 1000 degrees C and its subsequent phase transformation into orthorhombic mullite, in the powders produced from silicic acid solutions, synthesis of mullite occurs only by crystallization of gamma-Al2O3 between 900 and 1000 degrees C and its further reaction with amorphous SiO2 between 1100 and 1200 degrees C. Particle formation mechanism depended directly on the initial emulsion or solution preparation. i.e., on the phase separation in the emulsion and on the silicic-acid crosslinking conditions

Monocyte-lymphocyte cross-communication via soluble CD163 directly links innate immune system activation and adaptive immune system suppression following ischemic stroke

Abstract CD163 is a scavenger receptor expressed on innate immune cell populations which can be shed from the plasma membrane via the metalloprotease ADAM17 to generate a soluble peptide with lympho-inhibitory properties. The purpose of this study was to investigate CD163 as a possible effector of stroke-induced adaptive immune system suppression. Liquid biopsies were collected from ischemic stroke patients (n = 39), neurologically asymptomatic controls (n = 20), and stroke mimics (n = 20) within 24 hours of symptom onset. Peripheral blood ADAM17 activity and soluble CD163 levels were elevated in stroke patients relative to non-stroke control groups, and negatively associated with post-stroke lymphocyte counts. Subsequent in vitro experiments suggested that this stroke-induced elevation in circulating soluble CD163 likely originates from activated monocytic cells, as serum from stroke patients stimulated ADAM17-dependant CD163 shedding from healthy donor-derived monocytes. Additional in vitro experiments demonstrated that stroke-induced elevations in circulating soluble CD163 can elicit direct suppressive effects on the adaptive immune system, as serum from stroke patients inhibited the proliferation of healthy donor-derived lymphocytes, an effect which was attenuated following serum CD163 depletion. Collectively, these observations provide novel evidence that the innate immune system employs protective mechanisms aimed at mitigating the risk of post-stroke autoimmune complications driven by adaptive immune system overactivation, and that CD163 is key mediator of this phenomenon