Changes in biomechanics of skiing at maximal velocity caused by simulated 20-km skiing race using V2 skating technique.

This study investigated how the fatigue caused by a 20-km simulated skating cross-country skiing race on snow affects the final spurt performance from a biomechanical perspective. Subjects performed a 100-m maximal skiing trial before and at the end of the simulated race. Cycle characteristics, ground reaction forces from skis and poles, and muscle activity from eight muscles were recorded during each trial. Results showed that subjects were in a fatigued state after the simulated race manifested by 11.6% lower skiing speed (P<.01). The lower skiing speed was related to an 8.0% decrease in cycle rate (P<.01), whereas cycle length was slightly decreased (tendency). In temporal patterns, relative kick time was increased (10.9%, P<.01) while relative poling time was slightly decreased (tendency). Vertical ski force production decreased by 8.3% while pole force production decreased by 26.0% (both, P<.01). Muscle activation was generally decreased in upper (39.2%) and lower body (30.7%) (both, P<.01). Together these findings show different responses to fatigue in the upper and lower body. In ski forces, fatigue was observed via longer force production times while force production levels decreased only slightly. Pole forces showed equal force production times in the fatigued state while force production level decreased threefold compared to the ski forces.

[Treatment of cartilage defects]. / Knorpeldefektbehandlung.

Articular surface defects will not heal spontaneously. Localized defects, e.g., in the knee joint, should be treated with transplantation of autologous cells containing material of different composition. For transplantation of osteochondral pegs they are grafted from minor loaded joint areas and implanted into highly loaded defect regions. For autologous cartilage cell transplantation they are proliferated in vitro and then implanted into the defect zone under an periostal flap, harvested from the proximal tibia and sutured into the cartilage level around the defect. Autologous paste of cartilage and cancellous bone is transplanted into aggressively prepared defects with the concept of regrowing articular cartilage out of the transplanted cells and the subchondral bone.

Association of pp60c-src with biliary glycoprotein (CD66a), an adhesion molecule of the carcinoembryonic antigen family downregulated in colorectal carcinomas.

CD66a, also known as 'biliary glycoprotein (BGP)', is the human homologue of a cell adhesion molecule (CAM) of the rat (Cell-CAM). CD66a, which belongs to the carcinoembryonic antigen family and the immunoglobulin superfamily, is expressed in cells of myeloid and epithelial origin. The cytoplasmic domain of the major isoform of CD66a (CD66acyt) contains two tyrosine residues in amino acid motifs potentially interacting with protein tyrosine kinases of the Src family. Here we provide evidence that CD66a is associated with pp60c-src. From membrane fractions of granulocytes and the colonic cell line HT29, phosphokinase activity was co-immunoprecipitated with CD66a when monoclonal CD66 antibodies or an antiserum against the recombinant cytoplasmic domain of CD66a were used. From the dissociated immunecomplexes, a phosphokinase of M(r) 60,000 was reprecipitated using antibodies against pp60c-src. In vitro, the recombinant cytoplasmic domain was a substrate and binding partner of pp60c-src. Phosphopeptides corresponding to the tyrosine containing amino acid sequences of CD66acyt activated the kinase activity of pp60c-src to a greater extent than a phosphopeptide containing Tyr527 from the SH2-binding regulatory domain of pp60c-src. The down-regulation of CD66a in about 80% of colorectal carcinomas may contribute to a dysregulation of pp60c-src in colorectal cancer.