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Biomedical subjects

G Bauer

Publications and source records attributed to G Bauer.

At least 271 records · Page 15Linked to original sources

Long-term effects of hindfoot fractures evaluated by means of plantar pressure analyses.

The present study investigated the long-term effects of calcaneal fractures on the plantar pressure distribution during human gait. Fourteen patients participated in a follow-up study and were assigned to a group with good or poor calceneus restoration as indicated by normal or reduced Böhler's angle. Ten normal subjects with similar anthropometric characteristics were used for comparison. Gait analysis was performed by means of a capacitive pressure distribution platform. A comparison of the injured with the healthy foot of all patients revealed a statistically significant peak pressure decrease under medial areas of the foot (first metatarsal -24%) and an increase in lateral areas (midfoot +135%, fifth metatarsal +122%). This load shift towards a lateral loading indicates a persisting deviation of the gait pattern long after healing. Furthermore we investigated whether the success of the restoration of hindfoot geometry as reflected in Böhler's angle had an effect on the foot loading characteristics. Therefore we compared the gait patterns of the two patient groups with the normal subjects. However, the results did not reveal more abnormal pressure patterns in the poorly reduced group. RELEVANCE:--The restoration of the shape of the calcaneus with joint surface congruity and reconstruction of Böhler's angle appears generally accepted as a major aim in the treatment of calcaneal fractures. While this goal can usually be achieved by contemporary surgical techniques, the restoration of foot function under dynamic loading conditions is not guaranteed and should be assessed objectively. The investigation of the foot loading characteristics by means of plantar pressure measurements can be used to support the evaluation of the patient's recovery after trauma.

Journal Article↗

Refinement of map position of the human GluR6 kainate receptor gene (GRIK2) and lack of association and linkage with idiopathic generalized epilepsies.

Hereditary factors play a major role in the etiology of idiopathic generalized epilepsies (IGEs). The pivotal function of glutamate receptors (GluRs) in excitatory neurotransmission implicates their involvement in epileptogenesis and genetic susceptibility to IGEs. A trinucleotide repeat polymorphism detected in the 3' untranslated region of the kainate-selective GluR6 receptor gene (GRIK2) on chromosome 6 makes it possible to perform linkage and association studies with this high-ranking candidate gene. The present study tested the hypothesis that allelic variants of GRIK2 contribute to the genetic susceptibility to the common IGEs. Linkage and association analyses were conducted in 63 families ascertained through IGE patients with juvenile myoclonic epilepsy, juvenile absence epilepsy, or childhood absence epilepsy. Our linkage and association results suggest that allelic variants of GRIK2 are not involved in the expression of the common familial IGEs, and radiation hybrid mapping assigns GRIK2 to the chromosomal region 6q16.3-q21. This localization excludes GRIK2 as a candidate for the putative IGE susceptibility locus "EJM1" on the short arm of chromosome 6.

Chromosome Mapping↗