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Objective To evaluate the efficacy,indications and clinical outcomes of the treatment of thoracolumbar fractures by short segmental pedicle screws fixation at the level of the fracture.Methods Thirtytwo patients with thoracolumbar fracture,who underwent surgical procedure of short segmental pedicle screws fixation at the level of the fracture from 2007 to 2010,were followed up.X rays were performed preoperatively and postoperatively to locate the injured vertebral segment height and fractured kyphosis vertebral (Cobb angle).Frankel standard was used to assess the spinal cord function.Results All patients were followed up for 12 to 20 months and were in satisfying condition in the reduction of fracture.After surgery,the height of fractured vertebral body leading edge recovered from preoperative (32.4％ ～69.3％,averaged (51.6 ± 17.8)％ ) to (85.6％ ～99.2％,averaged (92.8 ±6.2)％ ) after two weeks and (90.6％ ～97.8％,averaged (93.8 ±3.6)％ ) at the last follow-up.Fractured vertebral Cobb angle was recovered from the preoperative ( 12.8 ° ～ 30.5 °,averaged [20.8±9.1] °) to (0° ～7.8 °,averaged [4.9 ±3.2] °) two weeks later and (2.0° ～ 12.0°,averaged [ 6.2 ± 4.6 ] o at the last follow-up.Cobb angle of the injured vertebral segment and the extend of vertebral compression were significantly improved after the angle was corrected ( P ＜0.01 ).Conclusion Using reduction and short segment pedicle screw fixation at the fracture level would be helpful to correct kyphotic vertebral compression and restore the height of injured vertebrate,which was also of benefit to increase the stability of short-segment posterior fixation system and reduce the loss of correction in a long run.
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Objective To investigate the effects of mefformin on the differentiation of osteoclastas well as relative mechanism.Methods Raw264.7 cells from the murine macrophage cell line was used.Receptor activator of NF-κB ligand (RANKL) was used to stimulate osteoclast differentiation from Raw264.7 cells.Osteoclast differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) and actin fluorescence staining and counting the TRAP-positive cells after exposure to different concentrations of mefformin (0 μmol/L,400 μmol/L,800 μmol/L and 1000 μmol/L) or rapamicin (100 nmol/L) in the presence of 50 ng/ml RANKL for 5 days.Bone-resorbing activity was evaluated by BD BioCoatTM OsteologicTM Bone Cell Culture System.The expression of osteoclast-specific genes like TRAP,capthesin K,calcitonin receptor (CTR) and matrix metalloproteinase (MMP-9) was evaluated by RT-PCR.The expression of tumor necrosis factor-α(TNF-ct) S6K1Thr389,S6 Ser235/236,4E-BP1Thr37/46 and c-Fos protein was evaluated by ELISA kit and Western blot analysis,respectively.Results Mefformin dose-dependently inhibited RANKL-stimulated osteoclasts differentiation in Raw264.7 cell culture,as manifested by decrease of TRAP-positive multinucleated cells and pit erosion area,down-regulation of TRAP,cathepsin K,CTR and MMP-9 mRNA and reduction of TNF-α and c-Fos protein expression.Further study revealed that RANKL activated mTOR complex 1(mTORC1) signaling,while mefformin impaired RANKL-stimulated mTORC1 signaling.Rapamycin,an mTORCl-specific inhibitor and immunosuppressive macrolides could also prevent RANKL-induced osteoclast differentiation and bone resorption in vitro.Conclusion Mefformin inhibits osteoclastogenesis in vitro,which may due to reduction of TNF-α and c-Fos protein expression,and mTORC1 signaling is involved in this process.
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Objective To investigate the causes of and prevention for cerebral complications in perioperative period in patients with carotid stenosis. Methods The causes and treatment of cerebral complications among 133 cases of carotid stenosis during perioperative period from May 2004 to Jun 2009 were analysed retrospectively. Results Among 133 cases, 94 cases underwent carotid endarterectomy (CEA) and 39 cases had carotid artery stenting(CAS). Cerebral complications developed in 16 cases including 3 cases of more than two attacks. 5 cases suffered from tansient ischemia attacks (TIA)or cerebral ischemia before operation. 5 developed TIA or cerebral hyperperfusion syndrome (CHPS) among those undergoing CEA and 4 developed TIA or CHPS among CAS cases. During postoperative period, 8 cases developed TIA, CHPS,cerebral infarction or cerebral hemorrhage. Conclusions Prevention and treatment of cerebral complications is extremely important durning surgical therapy of carotid stenosis.