We present clinical data, HLA genotyping and serological profiling on a large cohort of JDM patients and a carefully characterized subset of patients with JDM-SSc overlap. The results confirm known HLA associations and extend the knowledge by stratification of data in serological and clinical subgroups. In the future, a combination of serological and genetic typing may allow for better prediction of clinical course and disease subtype in JDM.
This process identified nine criteria that clinicians felt to be helpful or important in the diagnosis of JDM. A further process of refinement and validation is necessary to agree an internationally acceptable, clinically usable set of diagnostic criteria.
Objective. To assess the contribution of HLADRBl alleles in determining rheumatoid arthritis (RA) concordance in monozygotic twins.Methods. Ninety-one monozygotic twins pairs in which at least 1 twin was affected were typed for HLA-DRB1 using both serologic methods and polymerase chain reaction amplification with sequencespecific oligonucleotide hybridization. The role of DR4 and of the shared epitope in disease concordance was investigated. Relative risks (RR) with 95% confidence intervals were determined.Results. Increased concordance for RA was observed in both DR4 positive and shared epitope positive pairs (RR 3.4 and 3.7, respectively). A 5-fold risk for RA concordance was seen in twins who were "homozygous" for the shared epitope, compared with those negative for the shared epitope.Conclusion. In the absence of the shared epitope, RA concordance in monozygotic twins is rare. In contrast, "homozygosity" for the shared epitope is the most important factor in determining RA concordance.
Anecdotal evidence identified a change in the reaction of the resistant lentil cv Nipper to ascochyta blight in South Australia in 2010 and subsequent seasons, leading to infection. This study investigated field reactions of lentil cultivars against Ascochyta lentis and the pathogenic variability of the A. lentis population in southern Australia on commonly grown cultivars and on parental germplasm used in the Australian lentil breeding program. Disease data recorded in agronomic and plant breeder field trials from 2005 to 2014 in southern Australia confirmed the change in reaction on the foliage of the previously resistant cvs Nipper and Northfield. Cultivar responses to seed staining from A. lentis did not change. The change in foliar response was confirmed in a series of controlled environment experiments using single, conidium-derived, isolates of A. lentis collected over different years and inoculated onto differential host sets. Specific isolate/cultivar interactions produced a significant range of disease reactions from high to low aggressiveness with a greater percentage of isolates more aggressive on cvs Nipper, Northfield and PBA Flash than previously detected. Specific isolates were tested against Australian lentil cultivars and breeding lines in controlled conditions, again verifying the aggressiveness on cv Nipper. A small percentage of isolates collected prior to the commercial release of cv Nipper were also able to infect this cultivar indicating a natural variability of the A. lentis population which subsequently may have been selected in response to high cropping intensity of cv Nipper. Spore release studies from naturally infested lentil stubbles collected from commercial crops also resulted in a high percentage of infection on the previously resistant cvs Nipper and Northfield. Less than 10% of the lesions developed on the resistant differentials ILL7537 and cv Indianhead. Pathogenic variation within the seasonal populations was not affected by the cultivar from which the stubble was sourced, further indicating a natural variability in aggressiveness. The impact of dominant cultivars in cropping systems and loss of effective disease resistance is discussed. Future studies are needed to determine if levels of aggressiveness among A. lentis isolates are increasing against a range of elite cultivars.
The R620W variant is a significant risk factor for IIM, independent of the HLA 8.1 haplotype. Unlike that in the HLA region, risk is not increased in individuals possessing MSAs/MAAs. These results are further evidence that the PTPN22 gene confers autoimmune susceptibility.
The Australian Ascochyta rabiei (Pass.) Labr. (syn. Phoma rabiei) population has low genotypic diversity with only one mating type detected to date, potentially precluding substantial evolution through recombination. However, a large diversity in aggressiveness exists. In an effort to better understand the risk from selective adaptation to currently used resistance sources and chemical control strategies, the population was examined in detail. For this, a total of 598 isolates were quasi-hierarchically sampled between 2013 and 2015 across all major Australian chickpea growing regions and commonly grown host genotypes. Although a large number of haplotypes were identified (66) through short sequence repeat (SSR) genotyping, overall low gene diversity (Hexp = 0.066) and genotypic diversity (D = 0.57) was detected. Almost 70% of the isolates assessed were of a single dominant haplotype (ARH01). Disease screening on a differential host set, including three commonly deployed resistance sources, revealed distinct aggressiveness among the isolates, with 17% of all isolates identified as highly aggressive. Almost 75% of these were of the ARH01 haplotype. A similar pattern was observed at the host level, with 46% of all isolates collected from the commonly grown host genotype Genesis090 (classified as “resistant” during the term of collection) identified as highly aggressive. Of these, 63% belonged to the ARH01 haplotype. In conclusion, the ARH01 haplotype represents a significant risk to the Australian chickpea industry, being not only widely adapted to the diverse agro-geographical environments of the Australian chickpea growing regions, but also containing a disproportionately large number of aggressive isolates, indicating fitness to survive and replicate on the best resistance sources in the Australian germplasm.
Because of the complexity of the interactions involved very few attempts have been made to trace the fate of ingested food in the course of its digestion and absorption along the alimentary tract of the ruminant. Elsden, Hitchcock, Marshall & Phillipson (1946) made a comparative study of the weights of the digesta and their dry-matter and volatile fatty-acid content in the consecutive parts of the alimentary tract of four sheep. By means of a lignin-ratio method Hale, Duncan & Huffman (1947a, b) showed that maximum digestion in the bovine rumen was obtained within 1 2 h after feeding and tended to come to a standstill thereafter. They found that during the first 6 h the predominant phenomenon was the rapid disappearance from the rumen of the more soluble nutrients. During the next 6 h after feeding, cellulose was rapidly disintegrated. Under the conditions of their experiment an average of I 1.6 yo cellulose and 9-5 % protein was later released from the food residues in their further passage along the tract. No observations were made on the fate of the digesta in the other parts of the tract. When, therefore, an experiment of one of our colleagues made a number of ewes available we investigated changes in the quantity and composition of the digesta along the alimentary tract, and also changes in each part of the tract with time after feeding. The concentrations of dry matter (D.M.), ash, nitrogen, energy and volatile fatty acids (v.F.A.) were estimated. Such information is fundamental to a more dynamic appraisal of the processes of digestion and absorption.
EXPERIMENTALTwenty-four 5-year-old Cheviot ewes which had lambed in spring, 1951, and weighed about 58 kg, were housed in pens and fed on a diet varying in limestone content because they were on an experiment to define calcium requirement for pregnancy and lactation. They were given water ad lib. and the diet was (g/day):
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