SummaryCoeliac disease (CD) is an enteropathy induced in genetically susceptible individuals by gluten components, gliadin, hordein and secalin, polypeptides present in cereals such as wheat, barley and rye, respectively. Although the disease starts as intolerance to gliadins, antibodies to tissue transglutaminase (tTG) in the gut epithelium are characteristic of the disease. Whereas serum autoantibodies against tTG (tTGA) are highly specific for CD, antibodies to gliadin are less informative as they can also be detected in other enteropathies, and even in healthy individuals. However, it was shown recently that antibodies to certain gliadin peptides occur with high specificity in CD patient sera. We developed a solid phase lanthanide-based immunofluorometric assay for simultaneous detection of serum IgA and IgG antibodies to a synthetic peptide derived from gamma gliadin of wheat comprising amino acids 86-103. Three glutamine residues of this native 18-mer peptide were replaced by glutamic acids and the peptide was biotinylated. Sera from 87 individuals who had undergone duodenal biopsy and were diagnosed with CD and from 81 healthy individuals were analysed for the presence of both IgA and IgG anti-gliadin peptide antibodies. The performance of the peptide AGA assay was excellent, showing a specificity and sensitivity of 90% and 92% for IgA, and 98% and 75% for IgG, respectively. The corresponding values for conventional anti-gliadin antibody (AGA) enzyme-linked immunosorbent assay (ELISA) tests were 72% specificity and 87% sensitivity for IgA, and 64% specificity and 78% sensitivity for IgG. In a prospective study, almost all the tTGA-positive sera drawn from children who later developed CD were also positive for gliadin peptide antibodies.

Inter-particle percolation at the interfaces between burden layers directly influences the permeability of the burden in the shaft of the blast furnace. This paper studies inter-particle percolation of small particles (pellets) into large particles (coke) during the burden descent through small-scale experiments and simulations. A special device was designed for making it possible to consider the effect of the increase in cross-sectional area along with the burden descent. The simulations, which are based on the discrete element method, were first validated using one experimental case. An overall agreement was found between the experiments and the simulations. The velocity distribution of coke and pellet particles in the small bed, the trajectories along the height of the bed and the quantity of percolating particles at different heights of bed were investigated. The results show a considerable inter-particle percolation of pellets into the underlying coke layer at the wall area, but also a percolation over the whole radius of the system. These findings stress the importance of taking measures to prevent percolation by proper design of the charging programs in the operation of the blast furnace.KEY WORDS: discrete element method; particle percolation; burden descent; blast furnace; packed bed.

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SummaryCoeliac disease (CD) is an immune-mediated enteropathy triggered by ingestion of wheat gluten and related cereals in genetically predisposed individuals. Circulating immunoglobulin A (IgA) class autoantibodies against tissue transglutaminase (IgA-TGA) are highly specific and sensitive serological markers for CD, which is ultimately confirmed by duodenal biopsy. Although CD is considered a life-long disorder, transient or fluctuating IgA-TGA seropositivity has been observed in asymptomatic individuals on a glutencontaining diet. We set out to explore possible differences in the maturation of IgA-TGA avidity between individuals progressing to CD and subjects remaining healthy despite occasional expression of autoantibodies. We developed a time-resolved fluorometric IgA-TGA assay based on human recombinant tissue transglutaminase (tTG), and further modified the method to also measure urea-dependent avidity of the autoantibodies. We measured the autoantibody titres and avidities of sequential serum samples from 10 children developing CD and 10 children presenting transient or fluctuating autoantibodies. Both the initial titres at seroconversion and peak values of transient/fluctuating IgA-TGA were significantly lower than corresponding autoantibody titres in samples drawn from individuals with progressing CD (P = 0·004 and P = 0·0002, respectively). However, there were no statistically significant differences in the initial or peak avidity index values between the two groups of children. The avidity index values increased during the follow-up period (P = 0·013 for both groups) with no significant difference in the rate of avidity maturation between children with transient/fluctuating IgA-TGA and children developing CD. According to our results, high autoantibody titres have a higher predictive value than avidity maturation of TGA-IgA in screening for CD.