Plantar-flexion tarsometatarsal joint injuries in children.

We are reporting a series of eight patients ranging in age from 3 to 10 years who sustained plantar-flexion injuries of the foot, resulting in injuries to the tarsometatarsal (TMT) interval. All injuries were identified within 3 days and treated with molded short leg immobilization. We evaluated all patients an average of 32 months after injury with physical examination and the Midfoot Functional Rating (MFR) score. Seven patients had no limitations in their activities of daily living or athletic endeavors. These seven patients had MFR scores of 100. One patient had complaints of midfoot pain with running for >5 min and radiographic evidence of degenerative changes across the TMT interval at 3-year follow-up. These results suggest that although indirect pediatric TMT injuries have a generally favorable prognosis, early degenerative changes can occur and may be responsible for chronic pain and activity limitation. Degenerative changes in this weight-bearing region in a young patient can have lifelong implications. Patients and parents may benefit from discussion of the potential for future midfoot compromise following this injury.

Abduction stress and AP weightbearing radiography of purely ligamentous injury in the tarsometatarsal joint.

Twenty volunteers (40 feet) with no prior foot injury underwent standardized abduction stress and standing AP radiographs. Subsequently, the Lisfranc and dorsal tarsometatarsal ligaments in nine feet from cadavers were sectioned in a varying sequential manner, and interval standardized radiographs of abduction stress and AP simulated weightbearing were obtained. On abduction stress radiographs in 39 of 40 feet of volunteers and nine of nine feet of cadavers before sectioning, a line tangential to the medial aspect of the navicular and medial cuneiform (medial column line) intersected the base of the first metatarsal. Combining the sectioning of the Lisfranc and dorsal tarsometatarsal ligaments produced a disruption of the medial column line in all feet from cadavers. Disruption of this medial column line may be a simple and valuable diagnostic tool for determining significant ligamentous injury to the tarsometatarsal interval.

Effects of sepiapterin and 6-acetyldihydrohomopterin on the guanosine triphosphate cyclohydrolase I of mouse, rat and the fruit-fly Drosophila.

The regulation of GTP cyclohydrolase I would lead to the regulation of tetrahydrobiopterin, an important cofactor for synthesis of neurotransmitters. In an attempt to extend a previous finding [Bellahsene, Dhondt, & Farriaux (1984) Biochem. J. 217, 59-65] that GTP cyclohydrolase I of rat liver is inhibited by subnanomolar concentrations of reduced biopterin and sepiapterin, we found that this could not be verified with the enzyme from mouse liver, fruit-fly (Drosophila) heads or, indeed, from rat liver. It was shown, however, that 12 microM-sepiapterin inhibited mouse liver GTP cyclohydrolase I. Another compound, namely 6-acetyldihydrohomopterin, was also employed in the present study to explore its effect on enzymes that lead to its synthesis in Drosophila and for effects on mammalian systems; at 2-5 microM this compound was shown to stimulate one form of mouse liver GTP cyclohydrolase I and then to inhibit at higher concentrations (40 microM). Neither sepiapterin nor 6-acetyldihydrohomopterin caused any effect on the Drosophila head enzyme. On the other hand, the sigmoid GTP concentration curve for the Drosophila enzyme may indicate a regulatory characteristic of this enzyme. Another report, on the lower level of GTP cyclohydrolase I in mutant mouse liver [McDonald, Cotton, Jennings, Ledley, Woo & Bode (1988) J. Neurochem. 50, 655-657], was confirmed and extended. Instead of having 10% activity, we find that the hph-1 mouse mutant has less than 2% activity in the liver. These studies demonstrate that micromolar levels of reduced pterins may have regulatory effects on GTP cyclohydrolase I and that a mouse mutant is available that has low enough activity to be considered as a model for human atypical phenylketonuria.

Partial purification of an oxygen scavenging cell membrane fraction for use in anaerobic biochemical reactions.

Anaerobic conditions are necessary to prevent the autoxidation of tetrahydrobiopterin. An enzymatic method for achieving such an anaerobic condition is shown to be obtained by a lactate oxidase activity in the membrane of Escherichia coli when the enzyme concentration exceeds 0.05 unit/ml. A procedure is described for partial purification of the membrane fragment that involves salt precipitation and gel sieve chromatography on Bio-Gel A-50m. The rate of removal of oxygen is used to define the enzyme activity, to determine stability during storage, and to define conditions for stabilization of tetrahydrobiopterin. A second assay procedure that measures the rate of reduction of resazurin is described and is useful when the enzyme concentration is low.