[Surgical treatment of tibia Pilon fractures].

OBJECTIVE: To evaluate the choice of operative method,timing of surgery and the outcome of tibia Pilon fractures. METHODS: From March 1999 to November 2008, 52 patients of Pilon fractures were treated including 38 males and 14 females with the average age of 38 years old ranging from 23 to 59 years. There were 17 cases of open fractures and 35 cases of closed fractures. According to Ruedi-Allgower type,there were 6 cases of type I fracture, 29 cases of type II, 17 cases of type III. Thirty-three cases selected emergency surgery and 19 cases selected the selective operation, the average period between injury and surgery was 8.3 days. According to the type of fracture, open reduction and plate fixation of Trilobal, limited internal fixation combined with external fixation were applied for treatment of different surgical methods. RESULTS: All patients were followed-up for from 10 to 55 months (averaged 28 months). According to Mazur's criterion, the result of treatment was evaluated as excellent in 28 cases,good in 14 and fair in 10. After operation, 5 cases occurrenced skin and soft tissue infection and necrosis, 1 case of nonunion healed again after bone graft in re-operation, 6 patients occurrenced ankle traumatic arthritis later. CONCLUSION: According to fracture type, degree of injury and timely and effective surgical treatment is the key to achieve a satisfactory effect, which can effectively avoid the occurrence of complications.

Advanced glycation end-products induce vascular dysfunction via resistance to nitric oxide and suppression of endothelial nitric oxide synthase.

OBJECTIVE: A number of factors contribute to diabetes-associated vascular dysfunction. In the present study, we tested whether exposure to advanced glycation end-products (AGEs) impairs vascular reactivity independently of hyperglycemia and examined the potential mechanisms responsible for diabetes and AGE-associated vascular dysfunction. METHODS: Vasodilator function was studied using infusion of exogenous AGEs into Sprague-Dawley rats as compared with control and streptozotocin-induced diabetic rats all followed for 16 weeks (n = 10 per group). The level of arginine metabolites and expression of endothelial nitric oxide synthase (eNOS) and downstream mediators of nitric oxide-dependent signaling were examined. To further explore these mechanisms, cultured bovine aortic endothelial cells (BAECs) were exposed to AGEs. RESULTS: Both diabetic and animals infused with AGE-modified rat serum albumin (AGE-RSA) had significantly impaired vasodilatory response to acetylcholine. Unlike diabetes-associated endothelial dysfunction, AGE infusion was not associated with changes in plasma arginine metabolites, asymmetric dimethyl-L-arginine levels or eNOS expression. However, expression of the downstream mediator cGMP-dependent protein kinase 1 (PKG-1) was significantly reduced by both AGE exposure and diabetes. AGEs also augmented hyperglycemia-associated depletion in endothelial nitric oxide production and eNOS protein expression in vitro, and the novel AGE inhibitor, alagebrium chloride, partly restored these parameters. CONCLUSION: We demonstrate that AGEs represent a potentially important cause of vascular dysfunction, linked to the induction of nitric oxide resistance. These findings also emphasize the deleterious and potentially additive effects of AGEs and hyperglycemia in diabetic vasculature.