BACKGROUND:Currently thoracolumbar fixation techniques have its advantages and disadvantages, it is necessary to explore a new internal fixation to fix the spine effectively and conveniently.
OBJECTIVE:To establish thoracolumbar (T12-L2) three-dimensional finite element model and observe the effect of anteroposterior integration fixation by posterolateral nail-stick system on thoracolumbar stability.
METHODBased on the CT scan data of normal human T12-L2 segments, we used Geomagic 11.0, Ug 7.0, Hypermesh 10.0, Abaqus 6.9.1 software to establish a three-dimensional finite element model of T12-L2 segments. Subsequently we established nail-stick system posterior fixation, anterior fixation, posterolateral anteroposterior integration fixation model. T12 segment was given 500 N preload and 7.5 N·m torque, to simulate thoracolumbar flexion, extension, lateral bending and rotation. The average rigidity of fixed segments under different conditions were observed.
RESULTS AND CONCLUSION:Three fixation models showed a higher average rigidity than normal model under different conditions. The average rigidity in anteroposterior integration fixation by posterolateral nail-stick system was increased by 13%, 28%, 11%, 17%and 9%, compared with simple posterior fixation under the conditions such as anterior flexion, lateral bending and lateral rotation, respectively. Under the posterior extension, the average rigidity was reduced by 6%than the posterior fixation. Compared with the anterior fixation, the average rigidity in anteroposterior integration fixation by posterolateral nail-stick system was reduced by 15%, 10%, and 14%under the conditions of anterior flexion and lateral bending. While the average rigidity was higher than anterior flexion under the posterior extension and lateral rotation, increasing 5%, 12%and 2%. The anteroposterior integration fixation by posterolateral nail-stick system can improve the stability of fixed segments, and the stability is higher than anterior fixation at posterior extension and lateral rotation, while higher than posterior fixation in anterior flexion, lateral bending and lateral rotation. So it is a potential fixation method.

Objective To investigate the causes and prevention of bile duct injury during laparoscopic cholecystectomy (LC). Methods Clinical data of 16 cases of bile duct injury during LC between January 2004 and November 2013 (9 cases from Songqiao Central Hospital and 7 cases from Northern Jiangsu People ’ s Hospital ) were analyzed retrospectively .The bile duct injury was found intraoperatively in 10 cases, 4 of which were given common bile duct repaired with T tube drainage , 1 of which was given common bile duct anastomosisd with T tube drainage , 1 of which was given Roux-en-Y anastomosis , and 4 of which were given suturing of leakage at the gallbladder bed .The bile duct injury was found postoperatively in 6 cases, 3 of which were given peritoneal drainage , 2 of which were given reoperation of bile duct repaire with T tube drainage , and 1 of which underwent percutaneous gallbladder drainage guided by B ultrasonography . Results The hospitalization stay was 12-23 days, with an average of 16.3 days.All the patients were cured after treatment .Among the 16 cases of bile duct injury , the T tube was removed 3 months later in 6 cases of common bile duct repaired with T tube drainage , and the T tube removed 6 months later in 1 case of common bile duct anastomosis with T tube drainage.No complications or dysfunctions occurred in postoperative follow-up ranging from 3 months to 8 years. Conclusions We should pay more attention to causes of bile duct injury in laparoscopic cholecystectomy , especially indications for emergency cases .The relationship among the common hepatic duct , common bile duct , and cystic duct should be carefully identified .A timely conversion to open surgery is needed if necessary .

Sunitinib malate (SU11248 ,Sutent) is an orally available small-molecule multitargeted tyrosine kinase inhibitor that has potent anti-angiogenic and antitumour activities.In 2006 sunitinib was approved by FDA for imatinib intolerant gastrointestinal stromal tumors (GIST) patients or imatinib resistant GIST patients.This article review the molecular-based mechanism,the mechanism of resistance,the biomarker,the clinical trials and the adverse effects of sunitinib in the treatment of imatinib-resistant GIST.

With advancements in the field of cancer stem cells,the hypothesis that colon cancer originates from stem cells has not only been introduced but also receives substantial supports by separating a subpopulation of colon cancer cells through primitive cells markers.Unlike most non-tumourigenasis colon cancer cells,these tumor-initiating cells have many specific characters both in vitro and in vivo.An improved understanding of drug resistance based on cancer stem cells and molecular pathways that regulate proliferation and differentiation of gastrointestinal cancer stem cells could doubtless translate into new therapeutic strategies.

Objective To investigate the expression and correlation of microRNA‐335(miR‐335) and ROCK1 in osteosarco‐ma tissue and osteosarcoma cell lines MG‐63 and U2‐OS .Methods Eighteen paired tissue specimens of osteosarcoma and matched normal tissue were chosen clinically .Two osteosarcoma cell lines MG‐63 and U2‐OS were chosen as experimental group while the human osteoblast cell line hFOB 1 .19 as control group ,Quantitative real‐time PCR were used to evaluate the different expression of miR‐335 and ROCK1 mRNA in osteosarcoma tissue and cell lines;miR‐335 mimic was transfected into MG‐63 and U2‐OS ,while Quantitative real‐time PCR and Western blot were used to evaluate the effect of over‐expressed miR‐335 on ROCK1 mRNA and protein level .Results The result of real‐time PCR indicated a special lower expression of miR‐335 but higher ROCK1 ,and the cor‐relation between miR‐335 and ROCK1 was negative .Western blot showed that miR‐335 could decrease ROCK1 protein expression . miR‐335 mRNA showed a hyper‐expression while lower ROCK1 mRNA and protein after transfection of miR‐335 mimic .Conclusion The expression of miR‐335 and ROCK1 shows a negative correlation in both tissue and cell level;over‐expression of miR‐335 can decrease ROCK1 expression .

Background and purpose:MicroRNAs are endogenous small RNAs and involved in target gene regulation in post-transcription level. As a tumor suppressor, microRNA-335 (miR-335) was participated in the occurrence and progression in many types of human tumors. This study aimed at investigating whether miR-335 can regulate cell migration and invasion by negative targeting Rho associated coiled-coil forming protein kinase (ROCK1) in human osteosarcoma cell line MG-63.Methods:The speciifc binding ability of miR-335 to ROCK1 3’-untranslated region (UTR) was theoretically predicted and detected by the luciferase reporter gene assay. Western blot and real-time PCR were used to evaluate the effect of miR-335 on the expression of ROCK1 at protein and mRNA levels. Cell migration and invasion assays were performed by transwell chambers in MG-63 cells intervened by over-expression of miR-335 and knockdown of ROCK1.Results:Luciferase reporter gene assay showed that miR-335 could target ROCK1 3’-UTR. Lower miR-335 but higher ROCK1 was expressed in MG-63 cells. The results of Western blot showed that ROCK1 protein expression was decreased by transfection of miR-335 mimic or siROCK1. Transwell chambers results showed decreased cells invading through the substrate membrane after over-expression of miR-335 or knockdown ofROCK1 gene.Conclusion:miR-335 inhibits the migration and invasion ability of MG-63 human osteosarcoma cell line, which may through targeting ROCK1 3’-UTR and subsequent down-regulating ROCK1 expression.

A rapid and sensitive method of loop-mediated isothermal amplification(LAMP) was established to detect Pseudomonas aeruginosa(P.aeruginosa).Three pairs of LAMP primers(inner,outer and ring primers) were designed according to the gbca gene of P.aeruginosa.Since adding hydroxy naphthol blue(HNB) to the reaction system, a positive reaction was indicated by a colorchange before and after the reaction,and was verified by agarose gellectrophoresis.Both LAMP and PCR were applied to detect clinical specimens, the sensitivity and specificity of the detection method were evaluated,and were compared with those of conventional PCR.A LAMP method for detecting P.aeruginosa was successfully established.The LAMP method showed specificity for P.aeruginosa without other bacteria amplification.The established LAMP method in this study enables rapid,sensitive and specific detection of P.aeruginosa,and can be applied for grass roots and small scale laboratories as well as field surveillance.

Objective　To investigate whether or not the antisense oligodeoxynucleotide (ODN) of vascular endothelial growth factor (VEGF) can supresses the protein expression of VEGF.Methods　SMMC 7721 is a cell line that expresses VEGF.Therefore the medium conditioned by SMMC 7721 stimulates proliferation of bovine aortic endothelial cell (BAEC).Synthesized antisense ODN complementary to one region of VEGF mRNA was added into the medium of SMMC 7721.The expression of VEGF and the stimulation effect of SMMC 7721 was then determined.Result　It was found that by means of inhibition of VEGF expression,the stimulation effect of SMMC 7721 was inhibited by the VEGF antisense ODN in a dose-dependent manner.At a dosage of 1,2.5,5,10μmol/L,the inhibition rate was 63.2%,82.4%,210% and 287.5%,respectively.Conclusion　It is promising that VEGF antisense ODN works as a new gene therapeutic modaliey for antiangiogenesis of HCC.

Background and purpose:Fatty acid synthase(FAS)is a new tumor marker,the high expression of which has been reported to be associated with poor prognosis of cancer patients.This study investigated the expression of FAS in transitional cell carcinoma(TCC) of bladder and its clinical significance.Methods:The expressions of FAS were detected by streptavidin-peroxidase immunohistochemical method in the paraffin embedded sections of 65 TCC patients and the clinical data had been reviewed.15 normal bladder tissues were used as control group.Results:The positive rate of the expression of FAS in TCC was 58.5%(38/65),while only 2 of 15 cases in control group expressed FAS protein.The difference was statistically significant,the expression of FAS was related to the histological grades and recurrence but not different pathological stages.Survival analysis revealed that the 5-yr survival rate was lower in FAS positive patients than in negative patients(18% vs.44%,P

Objective To explore the role of endotoxin during hepatic ischemia reperfusion (HIR) in rats. Methods Wister rats were randomly divided into endotoxin, HIR and HIR plus endotoxin (HIRE) groups. In the HIR group, hepatic reperfusion was performed after 60 minutes of ischemia by interruption of the arterial and portal venous blood supply to the left lobes and middle lobes of the rat liver. In the HIRE group, LPS(1.0mg/kg) was injected via the dorsum vein of rat penis after ischemia and reperfusion. In the endotoxin group, LPS (1.0mg/kg) was injected via the dorsum vein of penis in the rats without ischemia and reperfusion. The NF-?B activities in the liver tissue of the rats were determined with EMSA. TNF-? expression levels in the liver tissue of the were measured with immunohistochemical staining. Serum ALT levels of the rats were also measured. Results NF-?B activity increased after reperfusion and remained high 12h after reperfusion in HIRE group compared with endotoxin group and HIR group. Both TNF-? expression levels and serum ALT levels increased markedly after reperfusion in HIRE group. Conclusion Endotoxin during HIR could induce hepatic injury. Endotoxin induced liver injury possibly by activating NF-?B followed by the subsequent expression of proinflammatory mediators in the liver tissue.