Activated lymphocytes trigger lymphoblast extravasation.

Intraperitoneal stimulation of adoptively sensitized rats with bacterial antigen promotes the localization of lymphoblasts at the site of antigen deposition. Lymphoblast extravasation activity (LEA) is generated only when specifically immune donor lymphocytes and the recipients of these cells share at least on Ag-B haplotype. However, if the specificity criteria for its formation are satisfied, LEA promotes the local development of lymphoblasts of all available specificities and irrespective of their Ag-B genotype. Allogeneic lymphoblasts do not participate actively in the delayed inflammatory reaction even when they are passively recruited into exudates. The results suggest that LEA is a T cell-derived mediator that amplifies the delayed type hypersensitivity reaction by directing recently activated lymphocytes into lesions.     

In vivo bone strain on the dog tibia during locomotion

Rosette and single-element strain gauges were implanted on the tibia in 2 dogs and recordings were made during locomotion on a treadmill. At foot contact and during the swing phase of locomotion, bone strains were low and directions of the principal strains were variable. There was a large shift in the directions of the principal strains at the beginning of the stance phase and bone strains were considerably higher. Peak strain occurred midway through the stance phase. At that time, the maximum principal strain (tension) was directed upwards and anteriorly between 30 and 60 degrees with respect to the long axis of the tibia. These bone strain patterns in the dog are similar to those found in sheep while both differ markedly from those found in humans.     

Pharmakogenetik der oralen Antikoagulation mit Cumarinen

The recent identification of VKORC1 has made important contributions to our understanding of the vitamin K cycle. The VKORC1 enzyme was shown to be the molecular target of coumarin drugs. Mutations and polymorphisms in coding and noncoding regions of the VKORC1 gene have been shown to cause both a partial to total coumarin resistance and coumarin sensitivity. Availability of molecular diagnostics (VKORC1, CYP2C9) and drug monitoring by HCPLC (determination of coumarin, vitamin K, and vitamin K epoxide levels) is helpful for detecting hereditary and acquired factors influencing coumarin therapy. In the future, these tools may be instrumental in designing individualized oral anticoagulation therapy regimens.