Transformation of foetal human leukocytes followed inoculation with a filtrate of cells of the QIMK-

Objective. Recent reports have suggested that increasing adiposity may protect against radiographic damage in rheumatoid arthritis (RA). We explored the role of serum adipokines (adiponectin, resistin, and leptin) in mediating this association. Methods. Patients with RA underwent total-body dual x-ray absorptiometry for measurement of total and regional body fat and lean mass, abdominal computed tomography for measurement of visceral fat area, and radiographs of the hands and feet scored according to the modified Sharp/van der Heijde (SHS) method. Serum levels of adipokines were measured and cross-sectional associations with radiographic damage were explored, adjusting for pertinent confounders. The associations of measures of adiposity with radiographic damage were explored with the introduction of adipokines into multivariable modeling as potential mediators. Results. Among the 197 patients studied, adiponectin demonstrated a strong association with radiographic damage, with the log SHS score increasing by 0.40 units for each log unit increase in adiponectin (P ‫؍‬ 0.001) after adjusting for pertinent predictors of radiographic damage. Adiponectin independently accounted for 6.1% of the explainable variability in SHS score, a proportion comparable with rheumatoid factor, and greater than HLA-DRB1 shared epitope alleles or C-reactive protein levels. Resistin and leptin were not associated with radiographic damage in adjusted models. An inverse association between visceral fat area and radiographic damage was attenuated when adiponectin was modeled as a mediator. The association of adiponectin with radiographic damage was stronger in patients with longer disease duration. Conclusion. Adiponectin may represent a mechanistic link between low adiposity and increased radiographic damage in RA. Adiponectin modulation may represent a novel strategy for attenuating articular damage.

SUMMARY Complement‐fixing antibodies to Coxiella burneti were present in 23 p.c. of kangaroos collected in western Queensland, and agglutinins in 15 p.c. Red kangaroos, Megaleia rufa, showed a higher incidence of complement‐fixing antibodies (33 p.c.) than grey kangaroos, Macropus major (12 p.c.). In three areas, the incidence of complement‐fixing antibody in M. rufa was between 46 and 54 p.c. C. burneti was isolated in mice from the blood of one Macropus major. Thirteen isolations were made from nearly 3,000 ornate kangaroo ticks, Amblyomma triguttatum, collected from kangaroos, goats and sheep. The titre of infectivity of infected ticks for mice was usually in the range 10−6 to 10−9. Infection of kangaroos and A. triguttatum was found over a considerable area, between 24 and 28° S. and 144 and 149° E., in western Queensland. It thus seems probable that a natural kangaroo‐tick cycle exists. The three‐host life cycle and wide host range of this tick would allow it to spread infection to domestic animals as well as kangaroos. Infestation of sheep would bring infected ticks into contact also with workers in the sheep‐shearing industry, and was probably responsible for recent outbreaks of Q fever among them.

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