[Soft tissue balanced navigation of total knee arthroplasties]. / Navigierte Implantation weichteilbalancierter Knieendoprothesen.

OBJECTIVE: Implantation of a total knee arthroplasty with a correct mechanical axis, a rectangular joint gap and a reconstructed joint line by use of an imageless computer navigation device INDICATIONS: Symptomatic gonarthrosis if non operative treatment or joint preserving operations remains ineffective CONTRAINDICATIONS: Infections; soft tissue damage in the approach area; massive instability of the collateral ligaments SURGICAL TECHNIQUE: Medial parapatellar approach to the knee joint; diminution of the patella; fixation of the reference arrays in tibia and femur; registration of leg axis, ligament balance and surface of the knee joint by use of the navigation system; tibial resection perpendicular to the mechanical axis; ligament balancing to achieve a rectangular extension gap; femoral implant planning to maintain the original joint line and reconstruct an equal joint gap in extension and flexion; femora resection perpendicular to the mechanical axis; reconstruction of the rectangular flexion gap by rotation of the femoral resection; two stage cementing technique for fixation of the original implants; check of the final mechanical axis and symmetry of the joint gap over the whole range of motion; wound closure. POSTOPERATIVE MANAGEMENT: Physiotherapy; continuous passive motion treatment; mobilization with 20 kg weight bearing with 2 crutches for 2 weeks, thereafter with 2 crutches and incremental full weight bearing for 4 weeks. RESULTS: The analysis of 582 consecutive navigated total knee arthroplasties showed one case of extension gap instability > 3 mm (0.2%) and 8 patients with flexion gap instability > 3 mm (1.4%). A too tight flexion gap was registered in 23 patients (4.4%), a too wide flexion gap in 13 cases (2.5%). The joint line was reconstructed with an average inaccuracy of 0 mm, in 17 patients the joint line was elevated > 3 mm (2.9%).

Different sublines of Jurkat cells respond with varying susceptibility of internucleosomal DNA degradation to different mediators of apoptosis.

The ability of two different Jurkat sublines, termed standard and JM, to form DNA ladders was investigated after various apoptotic stimuli. Exposure to a broad spectrum of drugs interfering with signal transduction or cellular metabolism revealed distinct differences between both Jurkat sublines with regard to the pattern of DNA degradation. In standard Jurkat cells, internucleosomal DNA cleavage occurred only after treatment with the protein kinase inhibitor staurosporine. In contrast, the JM subline responded with internucleosomal DNA fragmentation to exposure to gemcitabine, cycloheximide or staurosporine. All drugs induced the formation of DNA fragments of about 50 kb in both sublines, as revealed by pulse field electrophoresis, except H2O2, which caused unspecific DNA degradation. The staurosporine-induced DNA ladder formation was accompanied by an increase in caspase-3 activity in both lines which, however, was considerably lower in Jurkat JM cells after gemcitabine or cycloheximide exposure. When the analysis of internucleosomal DNA degradation was carried out after mycoplasma infection, both Jurkat lines responded with DNA ladder formation after exposure to all drugs used (here only shown for the standard subline). Employing the zymogram technique, nuclease activities of 47 kDa and 54 kDa were detected in culture supernatants, cell homogenates and nuclear extracts only when mycoplasma-infected, whereas the samples obtained from mycoplasma-free sublines were nuclease-negative using this technique, indicating that these endonucleases were of mycoplasmal origin. After drug exposure, the mycoplasmal nucleases must have gained access to the cytoplasm and nuclei of their host cells by an unknown mechanism.