Objective To investigate the clinical outcomes of interbody fusion with transpedicular screw fixation in the reoperation for lumbar spinal instability secondary to lumbar discectomy.Methods From May 1997 to Aug 2002, 23 patients underwent reoperation with posterior lumbar spinal decompression, removal of residual disc, transpedicular screw instrumentation and interbody fusion because of lumbar spinal instability after previous lumbar discectomy. There were 14 males and 9 females. The age of patients ranged from 28 to 64 years with an average age of 48.5 years. The time between the onset of the symptoms and the diagnosis was 18 months on average (range, 6 months to 36 years). The mean interval between the primary and revision surgery was 68 months (range, 24 months to 10 years). Lumbar discectomy had been performed in all patients as the primary surgery. All patients were evaluated by the conventional radiography, and CT or MRI if necessary. The low back pain was predominant in 8, and associated with radicular leg pain in 15. The instability of one segment was found in 17, and two segments in 6. The average follow-up was 3.6 years (range, 1 to 6.4 years). Results The lateral, AP, flexion and extension X-ray films were taken at 1, 3, 6 months and 1 year to evaluate the fusion, sliding between two vertebral bodies and internal fixation, and McGill pain questionnaire was adopted to determine the satisfaction of the patients. The intraoperative blood loss ranged from 550 to 800 ml (mean, 650 ml), and the total operative time ranged from 120 to 210 min (mean, 180 min). Based on Oswestry low back pain and disability scores, the clinical successful rate was 86.9%. The rate of patient satisfaction was 82.6%. 20 patients showed radiographic bony fusion. Pedicle screw breakage and loosening were found in 3 out of the 102 screws. 5 patients had nerve root irritation and recovered within 2 to 3 weeks. 5 patients had dural laceration. Bony nonunion was found in 3 patients. Conclusion Transpedicular screw instrumentation and interbody fusion is proved helpful in management of spinal instability secondary to decompression surgery, providing successful interbody fusion and restoration of the intervertebral stability.

Objective To introduce the operative procedure of prosthetic disc nucleus(PDN)re-placement and investigate its clinical effectiveness in the treatment of lumbar disc herniation.Methods Nine cases of lumbar disc herniation were treated with PDN replacement from March2002to April2002.There were6males and3females,the average age of the patients was33.4years ranging from22to48years.The interval between the onset of the symptoms and the diagnosis was averagely18.4months,ranging from8months to3.6years.All of the patients were evaluated by anteroposterior and lateral radiography,computer-ized tomography and,if necessary,magnetic resonance imaging.The low back pain was predomi nant in two patients,the low back pain associated with radicular leg pain in6patients.The height of disc space became narrowed in varying grade.The operated level was at L 4-5 in6patients,L 5 S 1 in3patients.The standard pos-terior approach was used in8patients;the anterior lateral retroperitoneal approach was adopted in1patient.8cases were implanted with a single PDN,and1case with a couple of PDNs.Results All patients were followed up12to13months(average12.3months).The estimated intraoperative blood loss ranged from50to150ml (mean120ml ),and the total operation time ranged from45to120min(mean60min).The patients wore a brace for the first6weeks.Based on Oswestry low back pain and dis ability scores,the clinical successful rate was88.9%.The average percentage of the postoperative to preoperative disc height was128%.The slight displacement of PDN was observed in2patients,however there was no change of lumbar spinal mo bility.1patient had a bad recovery of back and leg pain.Conclusion PDN re placement can improve clinic symptoms,increase disc height and restore the normal lumbar motion as well.Its clinical effectiveness is excellent in short-term observation.

Objective To discuss and observe the clinical effect of intervertebral pedicle internal fixation and debride?ment combined with bone graft through posterior approach/trans-intervertebral space approach on the treatment of uni/multi-segmental lumbosacral vertebral tuberculosis (TB). Methods A cohort of 37 patients, with single or multiple segmental ver?tebral destruction due to TB, were treated by trans-intervertebral debridement, posterior pedicle screw system internal fixa?tion and intervertebral bone graft. All patients underwent X-ray,CT and MRI examination to observe the combination treat?ment effect. Results Most patients (n=34) enjoyed primary healing, in which include only 4 cases that presented symptom of nerve root stretch injury during operation but all recovered after 3 months. Other 3 patients underwent secondary healing due to sinus but two were rectifying with anti-TB therapy and wound dressing. The other 1 case suffered from sinus tract was healed through second debridement and rectifying therapy. X-ray, CT and MR at 6 months after operation indicated that all patients present great graft osseous fusion, good recovering of height of vertebral body without kyphosis deformity nor internal fixation loosening nor screw breakage. Conclusion Intervertebral pedicle internal fixation and debridement combined with bone graft through posterior approach/trans-intervertebral space approach is with minimum invasion but good graft fusion ef?fects, harder fixation and satisfactory clinical effects in the treatment of uni/multi-segmental lumbosacral vertebral tuberculosis.

Objective To evaluate the role of mitochondrial fission in hypoxia-reoxygenation (H/ R) injury to hippocampal neurons of rats.Methods Primarily cultured hippocampal neurons obtained from newborn Wistar rats were randomly divided into 5 groups (n =60 each) using a random number table: normal group (N group), vehicle group (V group), H/R group, H/R + vehicle group (H/R + V group),and mitochondrial division inhibitor group (group M).The cells were cultured in normal culture medium in group N.Dimethyl sulfoxide (DMSO) was added to the culture medium with the final concentration ＜ 0.1％, and the cells were incubated for 40 min in group V.The cells were subjected to 6 h hypoxia, followed by 20 h reoxygenation in H/R, H/R+V and M groups.DMSO was added to the culture medium with the final concentration ＜0.1％ at 40 min before hypoxia in group H/R+V.In group M, mitochondrial division inhibitor Mdivi-1 50 mmol/L (dissolved in DMSO, DMSO concentration ＜0.1％) was added to the culture medium at 40 min prior to hypoxia.Mito Tracker staining was used to examine mitochondrial morphology.Western blot was used to measure the expression of mitochondrial dynamin-related protein 1 (Drp1), mitofusin 2 (Mfn2) , peroxisome proliferator activated receptor γ coactivator 1α (PGC-1α), nuclear respiratory factor-1 (NRF-1), and mitochondrial transcription factor A (TFAM).Multifunctional microplate reader and fluorescent microscope were used to detect the mitochondrial reactive oxygen species (ROS) level.The flow cytometer was used to detect the apoptosis in hippocampal neurons.Apoptosis rate was calculated.Results Compared with group N, the expression of Drp1, PGC-1α, NRF-1 and TFAM was significantly up-regulated, the ROS content and apoptosis rate were increased, and the expression of Mfn2 was down-regulated in group H/R (P＜0.05).Compared with group H/R, the expression of Drp1 was significantly down-regulated, the ROS content and apoptosis rate were decreased, and the expression of Mfn2, PGC-1α, NRF-1 and TFAM was up-regulated in group M (P＜0.05).Conclusion Mitochondrial fission is involved in H/R injury to hippocampal neurons of rats.

Objective To evaluate the effect of propofol on mitochondrial fission in a rat hippocampal neuron model of hypoxia/reoxygenation (H/R) injury.Methods Primarily cultured hippocampal neurons of neonatal Sprague-Dawley rats were randomly divided into 4 groups (n =42 each) using a random number table:control group (group C);vehicle group (group V);H/R group;H/R+propofol group (group H/R+P).In group V,H/R was not produced,the vehicle dimethyl sulfoxide with the final concentration of 0.01％ was added,and the cells were then incubated for 6 h.In group H/R,the hippocampal neurons were subjected to oxygen-glucose deprivation for 6 h followed by 20 h reoxygenation.In group H/R+P,propofol with the final concentration of 1 μmol/L was added at 6 h of hypoxia.At 20 h of reoxygenation,the cell apoptosis (using flow cytometry),Ca2+ concentrations in cytoplasm (with the laser scanning confocal microscope),calcineurin (CaN) activities (by enzyme-linked immunosorbent assay),and expression of mitochondrial fission proteins dynamin-related protein 1 (Drp1) and fission 1 (Fis1),and apoptosis-related proteins cytochrome c (Cyt c) and apoptosis-inducing factor (AIF) (by Western blot) were measured.The apoptotic rate was calculated.Results Compared with group C,the apoptotic rate,Ca2+concentrations,CaN activities,and expression of Drp1,Fis1,Cyt c and AIF were significantly increased in H/R and H/R+P groups (P＜0.05),and no significant changes were found in the parameters mentioned a2+.bove in group V (P＞0.05).Compared with group H/R,the apoptotic rate,Ca+ concentrations,CaN activities,and expression of Drp1,Fis1,Cyt c and AIF were significantly decreased in group H/R+P (P＜0.05).Conclusion Propofol can reduce the H/R injury to rat hippocampal neurons through inhibiting mitochondrial fission.

The study investigated the effects of heat shock protein 70 (HSP70) antisense oligonucleotide (ASODN) on the proliferation and apoptosis of a human hepatocellular carcinoma cell line (SMMC-7721 cells) in vitro. HSP70 oligonucleotide was transfected into SMMC-7721 cells by the mediation of Sofast transfection reagent. Inhibition rate of SMMC-7721 cells was determined by using MTT method. Apoptosis rate and cell cycle distribution were measured by flow cytometry. Immunocytochemistry staining was used to observe the expression of HSP70, Bcl-2 and Bax. The results showed that HSP70 ASODN at various concentrations could significantly inhibit the growth of SMMC-7721 cells, and the inhibition effect peaked 48 h after transfection with 400-nmol/L HSP70 ASODN. Cytometric analysis showed the apoptotic rate was increased in a dose- and time-dependent manner in the HSP70 ASODN-treated cells. The percentage of cells in the G(2)/M and S phases was significantly decreased and that in the G(0)/G(1) phase increased as the HSP70 ASODN concentration was elevated and the exposure time prolonged. Immunocytochemistry showed that treatment of SMMC-7721 cells with HSP70 ASODN resulted in decreased expressions of HSP70 and Bcl-2 proteins, and an increased expression of Bax protein. It was concluded that the HSP70 ASODN can inhibit the growth of the SMMC-7721 cells and increase cell apoptosis by down-regulating the expression of HSP70. HSP70 ASODN holds promise for the treatment of hepatocellular carcinoma.

OBJECTIVETo investigate the effect of rupture and reconstruction of the anterior cruciate ligament (ACL) on the degeneration of rabbit knee articular cartilage.

METHODS14 mature New Zealand white rabbits were divided into four groups. In group I, the ACL of the right knees in 7 rabbits was resected and immediately reconstructed, and the contralateral ACL was resected only in controll f group I. In group II, the ACL of the right knees in 7 rabbits was reconstructed 3 weeks after the ACL was resected and the contralateral joints in control group II, in which only a medial arthrotomy was performed. The rabbits were killed 8 weeks after the operation. The methods of ink straining, histology and SEM were used to analyze the changes in articular cartilage of the joints.

RESULTSThe results of ink method and HE straining were analyzed quantitatively. The degeneration of knee articular cartilage in group I was significantly weaker than that in control group I (Hc = 5.9889, P = 0.0144). The degeneration of knee articular cartilage in group II was as serious as that in control group I (Hc = 0.7143, P = 0.785).

CONCLUSIONSImmediate reconstruction of the ACL can effectively prevent articular cartilage from degeneration. Once the articular cartilage damaged moderately, delayed reconstruction of the ACL could not effectively reduce the development of degeneration. So once the ACL is ruptured, reconstruction should be performed in the early stage to restore the stability of knee joint to prevent the articular cartilage from degeneration.

In this study the poly(vinyl alcohol)(PVA) hydrogel elastomer was prepared by freezing-thawing method. The influences of percentage of poly (vinyl alcohol) in hydrogel, pH of solution and swelling temperature upon the swelling characteristic of PVA-hydrogel prosthetic nucleus material were studied. Its micropores were observed using SEM, and the swelling dynamics was further discussed. The experimental results showed that the poly (vinyl alcohol) hydrogel was a kind of network with a lot of micropores, the pore size was related with the PVA content. The maximum swelling ratio decreases when the percentage of PVA in hydrogel, the pH of solution and the swelling temperature were enhanced. The swelling process was described by the equation of swelling dynamics equation. The swelling rate was greatly influenced by the PVA content, the pH of solution and the dimension of hydrogel sample.
Biocompatible Materials ; chemistry ; Hydrogels ; Hydrogen-Ion Concentration ; Implants, Experimental ; Intervertebral Disc ; Polyvinyl Alcohol ; chemistry ; Prostheses and Implants ; standards

The purpose of this study is to characterize the stress relax properties of PVA-H prosthetic nucleus via the four-parameter linear viscoelastic model and to analyze the influence of swelling ratio and initial PVA content upon the properties of dissipating compressive stress. The four-parameter linear viscoelastic model can simulate the viscoelastic property of prosthetic nucleus well (corr > 0.99) and be more effective than the three parameter linear viscoelastic model. From the parameters of this model we have obtained the following results: the prosthetic nucleus of higher water content can dissipate compressive stress more quickly than that of lower water content can do, but the quantity of stress relax can not be influenced by water content; the higher the initial PVA content,the slower and smaller the dissipation of compressive stress;the relax time of prosthetic nucleus is similar to that of human nucleus.
Compressive Strength ; Elasticity ; Intervertebral Disc ; physiology ; Linear Models ; Models, Biological ; Polyvinyl Alcohol ; chemistry ; Prostheses and Implants ; Viscosity ; Weight-Bearing ; physiology

The study investigated the effects of heat shock protein 70(HSP70)antisense oligonucleotide (ASODN)on the proliferation and apoptosis of a human hepatocellular carcinoma cell line(SMMC-7721 cells)in vitro.HSPT0 oligonucleotide was transfected into SMMC-7721 cells by the mediation of SofastTM transfection reagent.Inhibition rate of SMMC-7721 cells was determined by using MTT method.Apoptosis rate and cell cycle distribution were measured by flow cytometry.Immunocytochemistry staining was used to observe the expression of HSP70,Bcl-2 and Bax.The results showed that HSP70 ASODN at various concentrations could significantly inhibit the growth of SMMC-7721cells,and the inhibition effect peaked 48 h after transfection with 400-nmol/L HSP70 ASODN.Cytometric analysis showed the apoptotic rate was increased in a dose-and time-dependent manner in the HSP70 ASODN-treated cells.The percentage of cells in the G2/M and S phases was significantly decreased and that in the G0/G1 phase increased as the HSP70 ASODN concentration was elevated and the exposure time prolonged.Immunocytochemistry showed that treatment of SMMC-7721 cells with HSP70 ASODN resulted in decreased expressions of HSP70 and Bcl-2 proteins,and an increased expression of Bax protein.It was concluded that the HSP70 ASODN can inhibit the growth of the SMMC-7721 cells and increase cell apoptosis by down-regulating the expression of HSP70.HSP70ASODN holds promise for the treatment of hepatocellular carcinoma.