Hydrogen production by sorption enhanced steam reforming (SESR) of biomass in a fluidised-bed reactor using combined multifunctional particles

The performance of combined CO2-sorbent/catalyst particles for sorption enhanced steam reforming (SESR), prepared via a simple mechanical mixing protocol, was studied using a spout-fluidised bed reactor capable of continuous solid fuel (biomass) feeding. The influence of particle size (300–500 and 710–1000 µm), CaO loading (60–100 wt %), Ni-loading (10–40 wt %) and presence of dicalcium silicate support (22.6 wt %) on SESR process performance were investigated. The combined particles were characterised by their density, porosity and CO2 carrying capacity with the analysis by thermogravimetric analysis (TGA), Brunauer-Emmett-Teller (BET), Barrett-Joyner-Halenda (BJH) and mercury intrusion porosimetry (MIP). All experiments were conducted with continuous oak biomass feeding at a rate of 0.9 g/min ± 10%, and the reactor was operated at 660 ± 5 °C, 1 atm and 20 ± 2 vol % steam which corresponds to a steam-to-carbon ratio of 1.2:1. Unsupported combined particles containing 21.0 wt % Ni and 79 wt % CaO were the best performing sorbent/catalyst particle screened in this study, when accounting for the cost of Ni and the improvement in H2 produced by high Ni content particles. SESR tests with these combined particles produced 61 mmol H2/gbiomass (122 g H2/kgbiomass) at a purity of 61 vol %. Significant coke formation within the feeding tube and on the surfaces of the particles was observed which was attributed to the low steam to carbon ratio utilised

Decreased chondrocyte proliferation and dysregulated apoptosis in the cartilage growth plate are key features of a murine model of epiphyseal dysplasia caused by a matn3 mutation

Disruption to endochondral ossification leads to delayed and irregular bone formation and can result in a heterogeneous group of genetic disorders known as the chondrodysplasias. One such disorder, multiple epiphyseal dysplasia (MED), is characterized by mild dwarfism and early-onset osteoarthritis and can result from mutations in the gene encoding matrilin-3 (MATN3). To determine the disease mechanisms that underpin the pathophysiology of MED we generated a murine model of epiphyseal dysplasia by knocking-in a matn3 mutation. Mice that are homozygous for the mutation develop a progressive dysplasia and have short-limbed dwarfism that is consistent in severity with the relevant human phenotype. Mutant matrilin-3 is retained within the rough endoplasmic reticulum of chondrocytes and is associated with an unfolded protein response. Eventually, there is reduced proliferation and spatially dysregulated apoptosis of chondrocytes in the cartilage growth plate, which is likely to be the cause of disrupted linear bone growth and the resulting short-limbed dwarfism in the mutant mice