OBJECTIVE:To determine the therapeutic effect of transpedicular instrumentation without fusion on patients with thoracolumbar burst fractures.METHODS:A total of 63 patients with thoracolumbar burst fractures (the inclusion criteria was neurologically intact spine with a kyphotic angle >20° and/or decreased anterior vertebral body height > 50%) who were treated with transpedicular instrumentation without fusion were studied,including 40 cases treated by AF internal fixation,16 cases by Tennor screw-rod fixation system and 7 cases by Diapason screw-rod fixation.All patients underwent a radiological and clinical assessment (including the loss of kyphotic angle,decreased anterior vertebral body height,the midsagital diameter of the canal and the Low Back Outcome Score) preoperatively,postoperatively and after 24 months.The deformity of angulation was measured by Cobb angle.RESULTS:All pstients were followed for a 24 months,with average stay of 13.4 days.There were averaged 3.8 days from admitted to operation,and the internal fixation was removed within 8-12 months in 51 cases,followed a 9.4-day hospital stay.According to low back outcome score,46 patients achieved excellent,9 good,5 fair and 3 poor,with excellent and good rates of 88%.The Cobb's angle was 20.1° preoperatively,6.2° postoperatively,and 11.9° after 24 months.The average lose of anterior vertebral body height was changed from 49.1% preoperatively to 17.4% postoperatively,which was 20.4% after 24 months.The midsagittal diameters was 49.8% (n=63) preoperatively,78.1% (n=28) postoperatively,and 91.7% (n=25) after 24 months.The implant failure occurred in 5 patients.The radiographic parameters had no associativity to the outcome of LBOS.CONCLUSION:Transpedicular instrumentation without fusion is conductive to treating burst fractures of the thoracolumbar spine without nerve injury.The routine posterior or posterolateral fusion is unnecessary in the operative management of these fractures.

Objectives:To analyze the range of motion(ROM)and intradiscal pressure(IDP)of lower cervical spine in occipitocervical fixation with different posterior occipitocervical angles(POCA),and explore the selec-tion strategy of POCA in occipitocervical fusion(OCF)surgery.Methods:8 fresh frozen human occipitocervical cadaveric specimens(C0-T1,cephalic end included the bony structure of the skull base below the occipital tuberosity)were selected,including 4 males and 4 females,aged 25-45 years,and bone abnormalities and destruction were excluded with X-ray fluoroscopy.The speciemens were removed of muscles and fat tissues and preserved with ligaments,joint capsules and intervertebral discs as the normal group.Specimens were loaded with 2N·m in a servo-hydraulic materials testing system for measuring the ROM and IDP of C3/4,C4/5,C5/6 and C6/7 in the directions of flexion,extension,left torsion and left lateral bending with the help of optoelectronic motion analysis system and miniature pressure transducers.Then,the specimens were subject-ed to occipitocervical fixation with different POCAs as 5 experimental groups,which were:neutral position group(POCA=111°),neutral position-standard deviation(SD)group(POCA=101°),neutral position+SD group(POCA=121°),neutral position-2SD group(POCA=91°),and neutral position+2SD group(POCA=131°).The fixed segments were C0,C2 and C3.All experimental groups used the displacement control protocol to perform experiment,and the ROM and IDP of C3/4,C4/5,C5/6 and C6/7 in four directions were measured.Results:After occipitocervical fixation,ROM in the four directions of C0-C3 was significantly reduced compared with the normal group(P＜0.001).Of the four directions,the change of POCA had regular impacts on ROM and IDP of the 4 segments in flexion and extension:in flexion,with the increase of POCA,ROM and IDP of each segment showed a decreasing trend;In extension,with the increase of POCA,ROM of each segment showed an increasing trend,while IDP showed a decreasing trend.When POCA was in the neutral position,ROM in flexion or extension of each segment was significantly greater than that of normal group,yet there was no extremely increased ROM in flexion as POCA was too little or in extension as POCA was too large,and there was no significant difference of IDP compared with that of the normal group(P＞0.05).The change of POCA had no regular effect on ROM and IDP of 4 segments in left torsion and left lateral bending,although ROM increased significantly compared with that of the normal group.Conclusions:In OCF surgery,fixing POCA in a neutral position,the ROM and IDP of subaxial cervical spine are approximately normal.

Objective To observe the expression of ChemR23 induced by Angiotensin Ⅱ (Ang Ⅱ) in podocyte and its role in renal injury.Methods Conditionally immortalized mice podocytes were cultured in vitro.Immunofluorescence was used to observe the sub-cellular location of ChemR23.The expressions of ChemR23,Nephrin and Podocin stimulated by different concentrations of Ang Ⅱ were detected by qRT-PCR and Western blotting.Lentivirus targeting ChemR23 was used.The expressions of Nephrin and Podocin and the phosphorylation state of NF-κB P65 were detected by Western Blot.The inhibitor of NF-κB P65 was added to the cultural medium for 2 h before Ang Ⅱ stimulation.The effect of NF-κB P65 inhibitor on Ang Ⅱ-induced expression of Nephrin and Podocin was detected by Western Blot.Results It is showed that ChemR23 was located in cytosol and membrane.Compared with the normal control,the expression of ChemR23 was significantly increased by Ang Ⅱ in mRNA and protein level,while the expressions of Nephrin and Podocin were decreased (P ＜ 0.05).When using Lentivirus vector to interfere the expression of ChemR23,Ang Ⅱ-repressed expressions of Nephrin and Podocin were restored (P ＜ 0.05).Western Blot showed the level of phosphorylated NF-κB P65 was significantly increased by Ang Ⅱ stimulation (P ＜ 0.05),which could be inhibited by interfering the expression of ChemR23.When adding the NF-κB P65 inhibitor,the low expression of Nephrin and Podocin induced by Ang Ⅱ stimulation was restored (P＜0.05).Conclusions Ang Ⅱ can induce ChemR23 expression,which activates NF-κB P65 signaling pathway,and then inhibits the expressions of Nephrin and Podocin.Targeting ChemR23 is a potential way to alleviate podocyte injury caused by Ang Ⅱ.

Objective To observe the expression of NOD2 and epithelial-mesenchymal transition (EMT) related proteins in podocytes in high glucose environment,and explore the molecular mechanism of NOD2 involved in EMT.Methods The human glomerular podocytes were the subjects of study.α-SMA and Nephrin expressions were detected by immunofluorescence;the mRNA and protein expressions of NOD2,Snail and EMT related proteins (α-SMA,Desmin,E-cadherin,Nephrin) were detected by real-time fluorescence quantitative PCR and Western blotting.The podocytes were stimulated by high-glucose after shRNA interfering the of NOD2 expression,and the expressions of Snail and subsequent EMT-related proteins were detected by Western blotting.Prior to the activation of NOD2 by muramyl dipeptide (MDP),shRNA was used to interfere with the expression of Snail.E-cadherin,Nephrin,Desmin,and α-SMA were detected by Western blotting.Results After 24 hours of high glucose stimulation,PCR and Western blotting results showed that the expressions of NOD2 and Snail were significantly increased;the expressions of epithelial phenotype proteins E-cadherin and Nephrin were down-regulated;and the expressions of interstitial phenotype proteins Desmin and α-SMA were increased (all P ＜ 0.05);while there was no significant change in the hypertonic control group.After interference with NOD2,the abnormal expression of Snail and EMT related proteins were all recovered.After interference with Snail expression,Compared with the MDP group,the protein expressions of E-cadherin and Nephrin were significantly increased (all P ＜ 0.05);the expressions of Desmin and α-SMA were significantly decreased.Conclusions High glucose can induce NOD2 expression in podocytes,and promote podocyte epithelial-mesenchymal transition by upregulating Snail expression.Gene intervention targeting the NOD2/Snail/EMT pathway can reduce high-glucose-induced podocyte injury and may provide new ideas for the treatment of diabetic nephropathy.