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Purpose Flexion contracture has been shown to impair function and reduce satisfaction following total knee arthroplasty (TKA). The aim of this study was to identify modifiable intra-operative variables that predict post-TKA knee extension. Methods Data was collected prospectively on 95 patients undergoing total knee arthroplasty, including pre-operative assessment, intra-operative computer assisted surgery (CAS) measurements and functional outcome including range of motion at one year. Patients were divided into two groups: those with mild flexion contracture (> 5°) at the one-year follow-up and those achieving full extension. Results The sagittal orientation of the distal femoral cut differed significantly between groups at the one-year follow-up ( p  = 0.014). Sagittal alignment of greater than 3.5° from the mechanical axis was shown to increase the relative risk of a mild flexion contracture at one-year follow-up by 2.9 times, independent of other variables. Conclusion Increasing the sagittal alignment of the distal femoral cut more than 3.5° from the mechanical axis is an independent risk factor for clinically detectable flexion contracture one year from index procedure.

This study confirms the presence of a genetic component of the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis and genetic distinctions between granulomatosis with polyangiitis and microscopic polyangiitis. Antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis is a systemic small-vessel vasculitis comprising three clinical syndromes: granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis), 1 microscopic polyangiitis, and the Churg–Strauss syndrome. 2 ANCA-associated vasculitis commonly causes life-threatening kidney failure or pulmonary hemorrhage, has a fatality rate of 28% at 5 years, and causes substantial long-term morbidity in survivors. 3 Granulomatosis with polyangiitis and microscopic polyangiitis are the major clinical syndromes, both often featuring a pauci-immune necrotizing glomerulonephritis. Granulomatosis with polyangiitis is characterized by granulomatous inflammation of the respiratory tract and by autoantibodies against the neutrophil granule serine protease proteinase 3 in 66% of patients (considered . . .

Chronic nasal carriage of the bacterium Staphylococcus aureus in patients with the autoimmune disease granulomatosis with polyangiitis (GPA) is a risk factor for disease relapse. To date, it was neither known whether GPA patients show similar humoral immune responses to S. aureus as healthy carriers, nor whether specific S. aureus types are associated with GPA. Therefore, this study was aimed at assessing humoral immune responses of GPA patients against S. aureus antigens in relation to the genetic diversity of their nasal S. aureus isolates. A retrospective cohort study was conducted, including 85 GPA patients and 18 healthy controls (HC). Humoral immune responses against S. aureus were investigated by determining serum IgG levels against 59 S. aureus antigens. Unexpectedly, patient sera contained lower anti-staphylococcal IgG levels than sera from HC, regardless of the patients' treatment, while total IgG levels were similar or higher. Furthermore, 210 S. aureus isolates obtained from GPA patients were characterized by different typing approaches. This showed that the S. aureus population of GPA patients is highly diverse and mirrors the general S. aureus population. Our combined findings imply that GPA patients are less capable of mounting a potentially protective antibody response to S. aureus than healthy individuals.

Participants at the Napa Conference on Genetic and Molecular Ecotoxicology assessed the status of this field in light of heightened concerns about the genetic effects of exposure to hazardous substances and recent advancements in our capabilities to measure those effects. We present here a synthesis of the ideas discussed throughout the conference, including definitions of important concepts in the field and critical research needs and opportunities. While there were many opinions expressed on these topics, there was general agreement that there are substantive new opportunities to improve the impact of genetic and molecular ecotoxicology on prediction of sublethal effects of exposure to hazardous substances. Future studies should emphasize integration of genetic ecotoxicology, ecological genetics, and molecular biology and should be directed toward improving our understanding of the ecological implications of genotoxic responses. Ecological implications may be assessed at either the population or ecosystem level; however, a population-level focus may be most pragmatic. Recent technical advancements in measuring genetic and molecular responses to toxicant exposure will spur rapid progress. These new techniques have considerable promise for increasing our understanding of both mechanisms of toxicity on genes or gene products and the relevance of detrimental effects to individual fitness.