Objective To discuss the clinical effect of Sky bone expander percutaneous ky-pbeplasty (Sky-PKP) in treatment of old osteoperotic vertebral compression fractures. Methods The study involved 27 patients (27 vertebrae) with old osteoporotic vertebral compression fractures treated by Sky-PKP from March 2005 to June 2007. Normotopia, lateral and dynamia radiographs, CT scanning and MRI were performed preoperatively to verify fluid collection in the vertebral body, vacuum phenomenon and open-close phenomenon. Visual analog scale (VAS), Oswestry disability index (ODI), anterior body height, middle line body height, posterior body height and kyphotic angle changes were measured on a lateral radiograph before and after treatment. Results All patients were followed up for mean 6.2 months, which showed no severe complications. VAS score was decresed from preoperative 7.8 to postop-erative 3.1 and ODI from 65% to 37%. However, The anterior vertebral height and middle line vertebral height were recovered for 4.6 nun and 5.7 mm respectively compared with preoperation. Correction of ky-photic angle was mean 5.6°postoperatively. There was no sitatistical changes in regard to posterior body height before and after operation. Conclusions Sky-PKP is a reasonable procedure for treatment of old osteoporotic vertebral compression fractures under strict control of indications, especially with vacuum phenomenon, open-close phenomenon and fluid collection. While high degree of difficulty in puncturation results in insignificant correction of kyphotic angle and body height.

AIM: To investigate the molecular mechanism by which hypoxia affect the endothelial nitric oxide synthase (eNOS) expression in cerebral artery endothelial cells (CAECs). METHODS: Primary cultured porcine CAECs were exposed to hypoxia for 2 h, 6 h, 12 h, 24 h and 48 h. The eNOS mRNA level was determined by RT-PCR. The level of eNOS protein was detected by Western blotting. After specific PKC inhibitors BIM Ⅰ(1 ?mol/L) and G6983 (1 ?mol/L) were added, CAECs were exposed to hypoxia for 24 h. The effect of hypoxia on eNOS mRNA stability was analyzed after actinomycin D was added. RESULTS: After exposure to hypoxia for 2 h, the levels of eNOS mRNA and protein in CAECs were increased. The levels of eNOS mRNA and protein reached peak after 12 h of hypoxia (about 2 5 fold and 2 0 fold, respectively, compared to control), and remained at higher level even after 48 h of hypoxia. Moreover, hypoxia did not change the stability of eNOS mRNA. The specific PKC inhibitors BIM Ⅰ and G6983 attenuated significantly the effects of hypoxia on eNOS gene expression. CONCLUSION: These results suggest that hypoxia may enhance the expression of eNOS gene in CAECs through PKC signaling pathway, which might be one of the mechanisms of cerebral artery dilation and neuroprotection during cerebral hypoxia.