ObjectivesMucosal free grafts may be successfully applied in many surgical interventions. This study aims at investigating the feasibility of palatal mucosa graft in sub-glottic field in an animal model.MethodsThis randomized prospective controlled study was conducted with an animal model. Sub-glottic inflammation was created in 15 adult rabbits in each group and sub-glottic stenosis surgery was applied thereafter. The rabbits in group 1 (control group) underwent segmental resection, partial cricoidectomy, and trachea-thyroid cartilage anastomosis; the rabbits in group 2 underwent segmental resection, cricoplasty, and crico-tracheal anastomosis using free buccal mucosa graft; and the rabbits in group 3 underwent segmental resection, cricoplasty, and crico-tracheal anastomosis using free palatal mucosa graft. Re-stenosis was evaluated after 42 days.ResultsThe percentages of stenosis were 27%±20%, 40%±20%, and 34%±23% for group 1, 2, and 3, respectively and the difference was not statistically significant (P=0.29). Intensive and tight fibrosis was observed in 2 rabbits (13%) in group 1, in 5 rabbits (33%) in group 2, and in 3 rabbits (20%) in group 3. There was not a statistically significant difference between groups (P=0.41). Excessive inflammation was observed in 3 rabbits (20%) in group 1, in 7 rabbits (47%) in group 2, and 3 rabbits (20%) in group 3. There was no a statistically significant difference between groups although inflammation rate was higher in the rabbits which underwent buccal mucosa graft (P=0.18).ConclusionThe surgical treatments applied with free mucosa graft reduced anastomosis tension through enabling anastomosis to the distal of cricoid instead of thyroid cartilage. Free palatal mucosa grafts may be used in sub-glottic field, one of the most challenging fields of trachea surgery, due to ease of application and rapid vascularization.

SummaryBackgroundAluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain.Material/MethodsWe used a chick embryonic development model, with Al treatment of 500 μg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool.ResultsThis Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model.ConclusionsExposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

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Our study found that linezolid was as effective as vancomycin in suppressing colony counts in MRSA- or MRSE-infected vascular Dacron grafts in rats.

The aim of this study was to investigate the possible effects of sulphite oxidase (SOX, E.C. 1.8.3.1) deficiency on xenobiotic metabolism. For this purpose, SOX deficiency was produced in rats by the administration of a low molybdenum diet with concurrent addition of 200 ppm tungsten to their drinking water. First, hepatic SOX activity in deficient groups was measured to confirm SOX deficiency. Then, aminopyrine N-demethylase, aniline 4-hydroxylase, aromatase, caffeine N-demethylase, cytochrome b5 reductase, erythromycin N-demethylase, ethoxyresorufin O-deethylase, glutathione S-transferase, N-nitrosodimethylamine N-demethylase and penthoxyresorufin O-deethylase activities were determined to follow changes in the activity of drug metabolizing enzymes in SOX-deficient rats. Our results clearly demonstrated that SOX deficiency significantly elevated A4H, caffeine N-demethylase, erythromycin N-demethylase and N-nitrosodimethylamine N-demethylase activities while decreasing ethoxyresorufin O-deethylase and aromatase activities. These alterations in drug metabolizing enzymes can contribute to the varying susceptibility and response of sulphite-sensitive individuals to different drugs and/or therapeutics used for treatments.