Biomechanics of the Ilizarov fixator for fracture fixation.

Compression, distraction, and torsion stiffness of the Ilizarov external fixator was measured in two fracture models in autopsy specimens of tibia and fibula. A transverse model was tested in six frame constructions with the osteotomy site preloaded in four different positions. An oblique model was tested in four frame constructions also with four preloaded positions. Stiffness was more dependent on bone preload than wire number, wire type, or frame design. High stiffness was achieved by bone preloading, by compressing the rings together, by increasing the number of wires, and by using olive wires. The stiffness can be decreased (dynamization) by separating the rings and by removing wires. This data is helpful for frame design of the Ilizarov fixator.     

Magnet extraction of frontal sinus foreign body

We report a metallic foreign body that entered through the anterior table of the frontal sinus, and rolled down to lodge in the nasofrontal duct. An electromagnet was used to remove the foreign body through a trephination.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane- induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.