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Biomedical subjects

G Schaden

Publications and source records attributed to G Schaden.

6 recordsLinked to original sources

Histomorphology of rabbit thigh muscles: establishment of standard control values.

The thigh muscles of New Zealand White (NZW) rabbits are frequently used in experimental surgery, particularly for evaluation after reinnervation or ischaemia. Although histomorphometric analyses are regularly performed, morphological data for untreated thigh muscles in previously unoperated animals are not available. Specimens from the rectus femoris (RF), vastus medialis (VM) and adductor magnus (AM) muscles from both thighs were harvested in 7 untreated rabbits and were processed for histomorphometric evaluation. The right RF and VM were harvested in a further 5 rabbit hindlimbs after experimental denervation and reinnervation of the contralateral RF and subsequently processed for histomorphometric analysis. Muscle fibre type distribution, diameter and connective tissue content were evaluated on serial transverse cryosections reacted for ATPase and NADH tetrazolium reductase activity and statistical analysis was performed. In all untreated animals RF revealed the highest proportion of type I muscle fibres (right: 8.4+/-4%, left: 11.4+/-4.9%), whereas VM showed the highest percentage of IIa fibres (right: 31.9+/-5.5%, left: 28.3+/-7.8%) and AM the highest proportion of IIb/d fibres (right: 80.5+/-8.6%, left: 84.4+/-6.3%). Fibre type distribution and diameter in rabbits after contralateral experimental operations revealed a statistically significant difference from the data obtained in bilaterally untreated animals. Knowledge of the morphology of untreated muscles is fundamental to the understanding of changes induced by intervention to the ipsi and/or contralateral thigh muscles.

Analysis of Variance↗

[sensorimotor differentiated reconstruction of peripheral nerves--a methods of intraoperative identification of motor fascicles].

In 1975, Freilinger et al. identified motor fibres by acetylcholinesterase (AChE) histochemistry. Precise identification of motor fascicles in cases of mixed peripheral nerve dissection became possible, and selective fascicular nerve repair could be performed. Using this technique, two separate operations were necessary for definitive nerve repair, since histochemical analysis took 28 hours. A modified AChE staining technique now offers results within one hour. In seven cases of human median and three cases of human ulnar nerve lesions, nerve biopsies were obtained and underwent both modified and standard histochemical staining. The standard procedure did not render any further information about the AChE activity indicating that both methods are equally reliable. Photomicrographs of the nerve specimen with motor fascicles marked on them were completed in all cases of the modified AChE staining method one hour after obtaining the biopsies. Intraoperative identification of motor fascicles by rapid AChE staining technique was performed in two cases of acute injuries of the median nerve, radial artery and musculotendineous system of the forearm. Biopsies were obtained at the beginning of the operation. Histochemical analysis was done while tendons and arteries were reconstructed and selective fascicular nerve repair was possible at the end of the operation. The rapid AChE staining may be applied intraoperatively to acute nerve injury and late peripheral nerve reconstruction provided the nerve is expected to already contain segregated motor fascicles.

Acetylcholinesterase↗

Coisogenic all-plus-one immunization: a model for identifying missing proteins in null-mutant conditions. Antibodies to dystrophin in mdx mouse after transplantation of muscle from normal coisogenic donor.

Specific antibody response against an alien protein is one of the basic immunologic mechanisms in immunecompetent organisms. They can be used as a first step in various approaches leading to the identification of proteins or even an antigen-encoding gene. Accordingly, we wanted to find out whether a null-mutant immunecompetent organism would produce specific antibodies against the missing gene product. We chose the mouse mutant mdx (X-linked muscular dystrophy) which represents a null-mutant condition for the gene product of the Duchenne muscular dystrophy (DMD) gene, dystrophin. When dystrophin-deficient mdx mice received dystrophin-containing muscle grafts from coisogenic normal mice, high titres of antibodies specific for dystrophin were detected in the transplanted animals' sera. Because dystrophin-containing muscle grafts were not rejected but have properly regenerated even in the presence of high titre antibodies against dystrophin, these findings have important bearings on all therapeutical strategies based on dystrophin supplementation. Using the mdx mouse as null-mutant model we showed that there was no immune tolerance for the missing protein but specific antibodies were produced when the organism came in contact with this protein. This simple approach may serve as a shortcut for identifying missing proteins presumably not only in neuromuscular disorders but in a wide range of diseases where null-mutant animal models and corresponding coisogenic inbred strains exist.

Animals↗