Objective To investigate the radiographic characteristics of degenerative lumbar scoliosis (DLS) and its relationship to osteoporosis. Methods 229 cases (83 males, 146 females) of DLS from January 1998 to June 2005 were reviewed. The mean age was 56.8 years (ranged from 40 to 74 years). The Cobb angle and vertebral stability in coronal plane were measured in anteroposterior radiographs and the changes of lordosis in sagittal plane were observed in lateral radiographs. The bone mineral density(BMD) and T-Score of lumbar spine (L2-L4) were measured using Dual Energy X-ray Absorptiometry. Results The mean Cobb angle is 9.45??4.79?, 151 cases(66%) with the angle less than 10?, 60 cases (26%) with 10?-20?, and 18 cases (8%) with more than 20?. Right side scoliosis were found in 52% (120 cases), left side in 48% (109 cases). 159 cases (69%) companied with gradeⅠ(Nash-Moe) vertebra rotation, 54 cases (24%) with grade Ⅱ. And the vertebra rotation was most evident on scoliosis apex. There were 20 cases (9%) with more than 4 mm lateral translation between the lumbar vertebrae which were usually the apex vertebrae with the most degenerative changes. The physical lordosis decreased in most cases in which 16 cases (7%) developed lumbar or thoracolumbar kyphosis. And the kyphosis degree was not relevant to scoliosis Cobb angle. The mean T-Score of BMD measurement was -1.88?0.17, which was -1.49?0.14, -2.56?0.24, -2.89?0.50 for the groups of with Cobb angle 20? respectively. There were 153 cases (67%) with T10?), and 98 cases (43%) with T

0.05). The pathological change in myocardial ultrastructure was markedly milder in DM rats. Conclusion Metformin may exert a certain protective effect on cardiomyopathy of diabetes in rats.

BACKGROUND: There are few reports about vascularization in the repairing of bone defect by heterogeneous deproteinized bone.OBJECTIVE: To verify the vascularization characteristics of heterogeneous deproteinized bone, tissue engineering scaffold material, in the repairing of large segmental bone defect.DESIGN, TIME AND SETTING: The randomized controlled animal experiment was performed between March 2005 and February 2007 at the Third Military Medical University, Chongqing, China.MATERIALS: Twenty-four 10 to 12 months old goats, weighing (22.5±2.5)kg, were obtained from the Animal Center of the Third Military Medical University, Chongqing, China. Segmental bone defects of 20 percent right tibia middle and inferior diaphysis of the 24 goats were made.METHODS: The 24 goats were divided into test group (n=16) and control group (n=8) randomly. Goats in test group were implanted with deproteinized bone+autologous MSCs+recombinant human bone morphogenetic protein-2 (rhBMP-2), goats in control group were implanted with autograft bone, and all fixed with half-ring sulcated external fixator. Every 4 weeks, 3 goats were killed after ink perfusing through femoral artery. A thick slice of new bone tissue was made to observe the vascularization.MAIN OUTCOME MEASURES: Vascularization of new bone observed through gross anatomy and imaging; vascular network of new bone observed through thick section, blood vessel amount and area measured by Image-proplus really image analysis software.RESULTS: No goat was infected or dead. Animal soft tissue was dyed black, blood vessels'size, ditribution and network structure were observed in subcutaneous tissue, fascia and periosteum. At 4 weeks postoperation implant margin became crude in the defect area; at 8 weeks postoperation transparent bone absorbing area of different size and irregular shape appeared; after 12 weeks postoperation high-dense calcification shadow appeared at the ends of defect bone and new bone connected with the ends completely. On 4 to 24 weeks postoperation, the blood vessel amount became large, alignment became regular, and their size and distribution became uniform. It showed no significant difference in blood vessel amount and area between 2 groups (P>0.05).CONCLUSION: Composite of heterogeneous deproteinized bone+autologous MSCs+rhBMP-2 has the same vascularization degree. of autogeneous bone graft in repairing of large segmental tibia defect.

Objective To investigate the clinical,imaging,pathological and molecular biological features of mitochondrial encephalomyopathy with lactic acidosis and stroke -like episodes(MELAS)in children.Methods The clinical,imaging,pathological and molecular biological features of 1 2 children with MELAS diagnosed through muscle biopsy or gene sequencing in the Fifth Affiliated Hospital of Zhengzhou University from January 201 1 to December 201 5 were retrospectively analyzed.Results (1 )Clinical features:the main manifestations included headache and vomiting in 1 1 cases,epileptic seizures in 9 cases,short stature in 8 cases,hairy in 7 cases,intolerance fatigue in 7 cases,cogni-tive decline in 7 cases,visual disturbance in 6 cases,hearing disturbance in 6 cases,and 5 cases had positive family history.In addition,7 cases had the serum lactic acid level increase in a rest for 1 0 min after exercise.(2)Imaging fea-tures:4 cases showed bilateral basal ganglia calcification symmetry in 8 patients who underwent head CT scan.The most frequently involved parts of the lesion were occipital in 1 0 cases,temporal in 9 cases and parietal lobe in 7 cases in stroke -like episodes.The lesions were lamellar necrosis.The abnormal areas by MRI showed low signal intensity on T1 weighted imaging,high signal intensity on T2 weighted imaging and fluid attenuated inversion recovery,high or equal signal intensity on diffusion weighted imaging,high or low signal intensity on apparent diffusion coefficient;the lactate peak significantly increased on magnetic resonance spectroscopy.The distribution was not in accordance with the control region of the cerebral vessels.Dynamic observation revealed that the lesions were reversible and migratory.(3)Myo-pathological features:muscle biopsy was performed in all children,and ragged -red fibers were found in 1 0 cases by im-proved Gomori staining,strongly succinate dehydrogenase -reactive were found in 9 cases,and the lipid droplets slight-ly increased in 8 cases by oil red O staining.Besides,the crystalline inclusion bodies in mitochondria were arranged in a parking lotpattern in 9 cases by electromicroscope.(4)Molecular biological characteristics:the mitochondrial gene mutations were analyzed in peripheral blood of 9 children and their parents,including 8 cases with A3243G muta-tion and 1 case with G13513A mutation.Five mothers had the same A3243G mutation site in 8 cases.Conclusions Children with MELAS have complex and varied clinical manifestations and certain characteristic of neuroimaging.More-over,muscle pathology and gene sequencing have important diagnostic value.Fully understanding the clinical,muscle pathology,imaging and molecular biological characteristics of children with MELAS can be helpful to the early diagnosis and treatment,also reduce misdiagnosis.

Objective To explore effects of atorvastatin on the expressions of cyclooxygenase-2(COX-2) and membrane-associated prostaglandin E2 synthase-1 (mPGES-1) in the carotid atherosclerotic plaques of rabbits.Methods Totally 33 male New Zealand white rabbits(≥ 36months of age ) were assigned into normal control group (n=8) and animal model group with carotid atherosclerotic stenosis (n =25).The rabbit models were randomly divided into non-intervention group,celecoxib treatment group (15 mg · kg-1 · d-1,twice daily) and atorvastatin treatment group (5 mg · kg-1 · d-1,once daily) (n=8 each).Four weeks after treatment,the mRNA and protein expressions of COX-2 and mPGES-1 in carotid plaques were determined by RT-PCR and Western blot,respectively.Results The mRNA expressions of COX-2 (0.97±0.09,0.44±0.05,0.60±0.04vs.0.23±0.04,F=66.77,P＜0.01) and mPGES-1 (0.92±0.07,0.41±0.04,0.61±0.03 vs.0.17±0.03,F=54.87,P＜0.01)in carotid atherosclerotic plaques were significantly higher in non intervention group,celecoxib treatment group and atorvastatin treatment group than in normal control group.The mRNA expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group ( both P ＜ 0.01 ).The protein expressions of COX-2 (0.89±0.06,0.42±0.07,0.62±0.04 vs.0.18±0.05,F=61.75,P ＜0.01) and mPGES-1(0.91±0.05,0.44±0.05,0.63±0.05 vs.0.21±0.04,F=86.44,P＜0.01)in carotid atherosclerotic plaques in non-intervention group,celecoxib treatment group and atorvastatin treatment group were increased as compared with those in normal control group.The mRNA and protein expressions of COX-2 and mPGES-1 were decreased in celecoxib treatment group and atorvastatin treatment group as compared with non-intervention group(all P＜0.01 ).The expressions of COX-2 and mPGES-1 in carotid atherosclerotic plaques were reduced in celecoxib treatment group as compared with atorvastatin treatment group (P ＜ 0.01).Conclusions As COX-2 inhibitor celecoxib,atorvastatin may inhibit the expressions of COX-2 and mPGES-1,and interfere with the inflammatory response which plays key role in the pathological progress of carotid atherosclerotic plaques,and thus slow the progress of carotid atherosclerosis.

Objective To explore the neuroprotection and mechanisms of bone marrow mononuclear cells (BMMNCs),and evaluate whether ERK1/2 signaling pathway was involved in it.Methods384 healthy male SD rats,which were 6-8 week old,weighting 250-280 g,were selected.The middle cerebral artery occlusion (MCAO) model was established in SD rats using the suture method.The rats were randomly divided into sham operation group,model group,BMMNCs group and ERK1/2 inhibitor group,with 96 rats in each group.At the time of 24 h after the successful modeling,200 μl PBS solution was injected into the caudal vein of the rats in the model group,200 μl PBS solution containing 5×106 BMMNCs was injected into the rats in the BMMNCs group and the ERK1/2 inhibitor group.meanwhile,5 μl PD98059 was injected into the lateral ventricle of the brain of rats in the ERK1/2 inhibitor group.At the time points of 3 d,7 d and 14 d,the modified neurological severity scores (mNSS) was used to evaluate the neurological function,the volume of cerebral infarction was assessed by TTC staining,the pERK1/2,Bax,Bcl-2 and caspase-3 levels were detected by Western blot,and the effect of BMMNCs on activation of microglia was detected by immunofluorescence assay.Results(1)At each time point,the mNSS and the volume of cerebral infarction of the model group were significantly higher than those of the sham operation group (P<0.05),while the mNSS and the volume of cerebral infarction of the BMMNCs group were lower than those of the model group,higher than those of the sham operation group,and it was gradually decreased with the treatment time extension (P<0.05).There was no difference in comparison between the ERK1/2 inhibitor group and the model group (P>0.05).(2)At each time point,the pERK1/2,Bcl-2,Bax and caspase-3 protein levels of the model group were significantly higher than those of the sham operation group (P<0.05).The pERK1/2 and Bcl-2 protein levels of the BMMNCs group(pERK1/2:(0.38±0.16),(0.39±0.15),(0.40±0.20),Bcl-2:(0.38±0.14),(0.39±0.15),(0.37±0.13)) were higher than those of the model group(pERK1/2:(0.17±0.05),(0.14±0.04),(0.13±0.03),Bcl-2:(0.23±0.11),(0.24±0.12),(0.27±0.14),Bax:(0.39±0.13),(0.40±0.14),(0.45±0.23),caspase-3:(0.52±0.26),(0.56±0.27),(0.58±0.28)),while Bax and caspase-3 protein levels(Bax:(0.25±0.13),(0.19±0.06),(0.21±0.08),caspase-3:(0.35±0.13),(0.34±0.16),(0.29±0.09)) were decreased (P<0.05).The pERK1/2 protein level of ERK1/2 inhibitor group was lower than other groups,There was no difference in the level of Bcl-2,Bax and caspase-3 between the ERK1/2 group and the model group.(P>0.05).(3) At each time point,microglia (Iba1 positive) in ischemic penumbra of the BMMNCs group was significantly more than those of the model group,and it was increased with the time extension (P<0.05).There was no difference in comparison between the ERK1/2 inhibitor group and the model group (P>0.05).ConclusionBMMNCs can reduce the apoptosis through ERK1/2 signaling pathway,thus improving the neurological function and reducing the infarct scope.

Objective To investigate the neuroprotective effect of thyroid hormones T3 on cerebral ischemia-reperfusion injury in rats and its mechanism.Methods SD rats were divided into four groups:sham+saline group,sham+T3 group,MCAO+saline group,MCAO+T3 group.The cerebral ischemia-reperfusion injury rat models were established by right middle cerebral artery occlusion.Thyroid hormones(10 μg/100 g)or normal saline were given respectively by intraperitoneal injection twice at 1 h after the onset of ischemia and 6 h after reperfusion.Neurobehavioral score was evaluated at 24 h after reperfusion;TTC staining was used to label infarction area;RT-PCR was used to detect the mRNA level of nerve growth factor(NGF)and brain derived neurotrophic factor(BDNF)in brain tissue;Western blot was employed to determine alterations in protein levels of NGF and BDNF.Results Compared with MCAO+saline group,the neurological deficit and the volume of cerebral infarction of MCAO+T3 group was decreased,and the mRNA and protein expression of NGF and BDNF of MCAO+T3 group were increased(P<0.05).Conclusion Thyroid Hormones could promote the nerve repair,stimulate the nerve regeneration and improve the nervous behavioral function by up-regulating the expression of NGF and BDNF.

Objective To detect the effects of 17 β-estradiol(E2)on the expression of Calbindin-D9k (CaBP-9k) in pituitary GH3 cells,and to investigate the antagonistic effect of a selective estrogen receptor antagonist,ⅡCI 182780 on CaBP-9k expression.Methods A rat pituitary prolactinoma cell line,GH3 cell was used as the in vitro model.The localization of CaBP-9k in GH3 cells was observed by immunofluorescence.GH3 cells were cultured with exogenous E2-added medium for 24 hours,and the concentrations of E2 were 10-8,10-9,10-10M,respectively.mRNA and protein expression levels of CaBP-9k in different groups were analyzed by RT-PCR and Western blot analysis.The estrogen receptor antagonist,and ⅡCI 182780 was added to GH3 cells before E2 administration (10-8M)with the concentration of 10-6M,in order to investigate the regulation of ER-mediated pathway on the expression of CaBP-9k.Immunoprecipitation was used to detect the interaction between CaBP-9k and ERα.Results E2 had significant stimulatory effect on the CaBP-9k expression of GH3 cells in a dose dependent manner,and the expression level of CaBP-9k was higher when treated with a higher concentration of E2.ⅡCI 182780 could suppress the stimulatory effect of E2 on the CaBP-9k expression of GH3 cells.The expression level of CaBP-9k was significantly reduced by coadministration of E2 with ⅡCI 182780 in GH3 cells,which meant the CaBP-9k expression was mediated through ERα pathway.The immunoprecipitation results further illustrated the fact that CaBP-9k could directly interact with ERα,and E2 could increase the interaction between CaBP-9k and ERα.Conclusion Estrogen might induce CaBP-9k expression via ERα mediated pathway and CaBP-9k could directly combine with ERα,suggesting that CaBP-9k might be involved in the biological effects mediated by ER pathway in GH3 cells.

Objective To investigate short-term effect of percutaneous discectomy combined with radiofrequency ablation with Disc-FXon contained lumbar disc herniation. Methods 36 patients were reviewed and followed up with Japanese Orthopaedic Association score(JOA score), the Visual Analogue Score (VAS) and Oswestry score for 12 months. Results The scores of JOA score, VAS and Oswestry improvedsignificantly (P<0.01) after operation. Conclusion Percutaneous discectomy combined with radiofrequency ablation with Disc-FXis effective on contained lumbar disc herniation.

Objective To fabricate an anti?tuberculosis controlled drug release coating with Ti?PDA?PEG?PLGA?INH and to investigate its surface characteristics, in vivo and in vitro drug release behavior, and tissue biocompatibility. Methods 4?arm?polyethylene glycol (PEG) was synthesized first. Then cover the surface of titanium (Ti) with a layer of poly dopamine (PDA) by Michael addition reaction. Use porous starch and 4?arm?PEG as a carrier, load with isoniazid (INH), then attach to the surface of titanium by casting or sol?gel dip coating methods, and then cover with a layer of poly lactic?co?glycolic acid (PLGA) by the same method, to fabricate the Ti?PDA?PEG?PLGA?INH composite coating finally. The functional group of 4?arm?PEG was charac?terized by proton nuclear resonance spectroscopy (HNMR). The surface characteristics of Ti?PDA?PEG?PLGA?INH were evaluated by scanning electron microscope (SEM), while drug release behaviors were detected by high performance liquid chromatography (HPLC) and the cumulative release rate was calculated, and carry out the antibacterial performance in vitro. The animal model of femoral condyle bone defect was established in 25 New Zealand white rabbits. Titanium rods covered with PDA?PEG?PLGA?INH coating were implanted into defect area. INH concentrations were detected by HPLC in venous blood, muscle and bone tissue at each time point postoperatively. Another 12 rabbits were randomly divided into experimental group and control group, the experi?mental group was implanted with titanium tablets and titanium rods coated with PDA?PEG?PLGA?INH in the paraspinous muscle and left femoral condyles respectively, while the control group was implanted with a blank sheet of titanium tablets and titanium rods in the same place. Hematoxylin and Eosin Staining were used to observe the biocompatibility of the composite system in vivo at 28 and 56 days postoperatively. Results Ti?PDA?PEG?PLGA?INH controlled drug release coating uniformly distributed on the surface of plates and rods, with translucent form and smooth surface. In vitro INH release kinetics exhibited a short?burst release during the first 8h, and the cumulative release of the INH was about 65%. On the 9th day, the cumulative release of the INH was about 90%, and then the release tended to be flat, and the drug release behavior in vitro continued more than 20d. In vivo release test showed that the concentration of INH in vein blood, muscle and bone tissue around the composite system was increased steadi?ly postoperatively. On about the 28th day, the concentration reached the max. However, the INH concentrations in muscle and bone tissue around the composite system were still higher than the minimum inhibitory concentration (MIC) on the 56th day. The antibacterial test in vitro showed that the titanium tablets coated with PDA?PEG?PLGA?INH formed obvious bacterial inhibition zones. The pathological results indicated that mild inflammatory reaction was seen in the 4th week postoperatively, and the reac?tive capsule formed with loose connective tissue. In the 8th week postoperatively, there's no obvious inflammation occurred, and the reactive capsule became more dense and thicker. Conclusion The study successfully fabricated the Ti?PDA?PEG?PLGA?INH anti?tuberculosis controlled drug release coating, with reasonable release behavior both in vivo and in vitro, effective antibac?terial effect of Mycobacterium tuberculosis in vitro and good tissue biocompatibility, which is a potentially effective drug delivery system for spinal tuberculosis.