RESUMEN
Single-layer ceramic fuel cells consisting of Li0.15Ni0.45Zn0.4O2, Gd0.2Ce0.8O2 and a eutectic mixture of Li2CO3, Na2CO3 and K2CO3, were fabricated through extrusion-based 3D printing. The sintering temperature of the printed cells was varied from 700 °C to 1000 °C to identify the optimal thermal treatment to maximize the cell performance. It was found that the 3D printed single-layer cell sintered at 900 °C produced the highest power density (230 mW/cm2) at 550 °C, which is quite close to the performance (240 mW/cm2) of the single-layer cell fabricated through a conventional pressing method. The best printed cell still had high ohmic (0.46 Ω·cm2) and polarization losses (0.32 Ω·cm2) based on EIS measurements conducted in an open-circuit condition. The XRD spectra showed the characteristic peaks of the crystalline structures in the composite material. HR-TEM, SEM and EDS measurements revealed the morphological information of the composite materials and the distribution of the elements, respectively. The BET surface area of the single-layer cells was found to decrease from 2.93 m2/g to 0.18 m2/g as the sintering temperature increased from 700 °C to 1000 °C. The printed cell sintered at 900 °C had a BET surface area of 0.34 m2/g. The fabrication of single-layer ceramic cells through up-scalable 3D technology could facilitate the scaling up and commercialization of this promising fuel cell technology.
RESUMEN
BACKGROUND: A severe neurological abnormality has not been previously described in individuals with hereditary fructose intolerance, which typically presents early in childhood with severe metabolic acidosis and hypoglycemia. PATIENT DESCRIPTION: We describe a boy who by age five years had required multiple admissions to the pediatric intensive care unit for an aggressive and atypical, relapsing and remitting neuropathy with features of acute motor axonal neuropathy (AMAN). It was later discovered that he also had undiagnosed hereditary fructose intolerance, and the severity and frequency of his neurological episodes diminished following an exclusion diet. His asymptomatic younger brother was diagnosed with hereditary fructose intolerance on screening. He is on a fructose-free diet and has not developed neurological symptoms. CONCLUSIONS: Ongoing low-level exposure to fructose prior to diagnosis may have contributed to our patient's neurological dysfunction. Early diagnosis and treatment may prevent neurological complications of hereditary fructose intolerance.