BACKGROUND:Spinal canal decompression and fusion combined with pedicle screw fixation has become the main method for the treatment of thoracolumbar fracture and dislocation. OBJECTIVE:To restore the vertebral height of the patients with thoracolumbar fracture and dislocation who underwent subtotal resection and decompression through titanium cage packed with autologous cancel ous bone and pedicle screw fixation. METHODS:Thirty-one patients with thoracolumbar fracture and dislocation treated in the Shanghai 6th People’ s Hospital of Shanghai Jiao Tong University from February 2007 to September 2011 were selected. Al the patients received subtotal resection, spinal canal decompression and titanium cage packed with autologous cancel ous bone and pedicle screw fixation. Imaging examination was performed before and after treatment to observe the recovery of vertebral sequence, vertebral height and Cobb angle, as wel as the recovery of nerve function. RESUTLS AND CONCLUSION:The patients were fol owed-up for 12 months, and al the patients healed wel after treated with titanium cage packed with autologous cancel ous bone and pedicle screw fixation, and there was no loosening, shedding or breakage after pedicle screw fixation. During reexamination, the grafts fusion, good deformity correction, basic recovery of vertebral height and good recovery of Cobb angle were observed. Seven cases had neurological function recovery, and among them, six cases raised for one degree, one case raised for two degrees, and another 22 cases without recovery. Case analysis and relative researches showed that subtotal resection and decompression and titanium cage packed with autologous cancel ous bone and pedicle screw fixation can reduce the loss of correction of the patients with thoracolumbar fracture and dislocation, restore the vertebral height, and enhance the stability of the vertebral body.

BACKGROUND:Animal models can be used to study specific scientific problems of intervertebral disc biology.Model of disc degeneration is mainly used to resolve the relevant disease mechanisms and scientific and security issues of the treatment.OBJECTIVE:To summarize currently used experimental animal models of intervertebral disc degeneration study,and to dynamically observe and confirm the pathological process of disc degeneration based on disc imaging,morphology,biomechanics and bi(o)chemicel changes.METHODS:Using "intervertebral disc degeneration,animal models,in vivo,in vitro" in English as the search words,Cochrane Library (No.1 2009),Cochrane Library Database of Controlled Clinical Trials (No.1 2009),MEDLINE from 1990 to March 2009,EMbase from 1990 to March 2009,Current Controlled Trials,and the National Research Register were retrieved.Literature was limited to English language.The disc imaging,morphology,biomechanical end biochemical composition and other indicators,as well as the pathological process of disc degeneration served as the evaluation indices.The articles related to the intervertebral disc cell culture models,the whole disc tissue culture model,mechanical model,injury model,biological model,genetically modified models,spontaneous models were included.The repetitive researches and those unrelated to animal models of intervertebral disc degeneration were excluded.RESULTS AND CONCLUSION:The establishment of a reliable animal model can provide favorable conditions for studying the pathogenesis of intervertebral disc degeneration,at the same time,provides a good experimental vehicle for various researches about the repair treatment of intervertebral disc degeneration.Animal models of intervertebral disc degeneration can be divided into two categories:in vitro models and in vivo models of disc degeneration and repair.The former can be assigned into disc cell culture models and whole disc tissue culture model;the latter is assigned into mechanical models,injury models,biological models,genetically modified models,spontaneous models and so on.The above models are commonly used in the study of the occurring mechanism of disc degeneration,as well as the feasibility and effectiveness of a variety of treatments.However,there is still no generally accepted animal models as an ideal disc degeneration model,various types of models reported have their own advantages and disadvantages.

Concepts and techniques of spinal fusion as a therapeutic modality may date back to the origins of spinal surgery. Spinal fusion has been considered as the standard treatment of progressive deformities,including instability,scoliosis and trauma. In this study,we shall attempt to define and review the bone graft materials,progress on the operative techniques,postoperative complications and related therapy,the latest dynamic fixation,and minimally invasive technique to lumbar spine fusion.

Facial Paralysis ; complications ; Granulomatosis with Polyangiitis ; complications ; Humans ; Male ; Young Adult

Objective To explore the clinical characteristics and prognostic factors of breast carcinosarcoma.Methods Clinical data of 37 breast carcinosarcoma patients treated at Tianjin Cancer Hospital from 1974 to 2014 was analyzed retrospectively.Kaplan-Meier unvariate analysis was used to calculate the survival rate and compare the survival rates.Multivariate factors for survival were analyzed by COX proportional hazards regression model.Results 37 cases of breast carcinosarcoma were all female.The median age was 55 years.Among them 31 cases complained for painless mass,six cases had breast mass with skin ulceration.21 cases were three-negative breast cancer.Ten cases had axillary lymph node metastasis,ten cases had distant metastasis.The 5-year survival rate was 62.3％.Unvariate analysis showed that axillary lymphnodes metastasis (P =0.045) and therapeutic schedule (P =0.016) significantly influenced the oulcome of the patients.COX multivariate analysis validated that the therapy modality was an independent prognostic factor for breast carcinosarcoma(P =0.041).Conclusions Breast carcinosarcoma is rare and has a poor prognosis.ER,PR and HER-2 expressions in most cases are negative.If there is axillary lymph node metastasis,the prognosis is poor.A reasonable and comprehensive treatment can improve the prognosis.

Objective To investigate the effects on brain tissue p38 mitogen-activated protein kinase (MAPK) and aquaporin 4 (AQP4) and neuroprotective effect of edarvone after focal cerebral ischemia and reperfusion in mice.Methods A total of 196 healthy male Kunming mice were randomly divided into four groups:a sham operation group,an ischemia-reperfusion group,a saline control group,and an edaravone group (n =49 in each group).A middle cerebral artery occlusion (MCAO) mothod was used to induce a cerebral ischemia-reperfusion model.At 2 h after ischemia,immediately after reperfusion in the edaravone group and the saline control group,edaravone (5 mg/kg) and the same volume of saline were injected intraperitoneally in mice,then repeated once every 24 h.At 2 h after MCAO,the brain water content and infarct volume at different time points after reperfusion (12 h,24 h,48 h,and 3 d) were measured respectively.At 24 h after MCAO,the expressions of AQP4 and p38 MAPK in the brain tissue of ischemic peripheral cortex were measured by Western blotting.Results The volumes of cerebral infarction (all P ＜ 0.01) and the brain water contents (all P ＜0.05) in the edaravone group were decreased than those in the ischemia-reperfusion group and saline control group at different time points,and they were most significant at 48 h.After 24-h reperfusion,the expression levels of AQP4 (0.985 ± 0.129,1.024 ± 0.117,0.713 ± 0.231) and phospho-p38 MAPK (1.123 ± 0.142,1.214 ± 0.096,0.986 ± 0.087) in the brain tissue of ischemic peripheral cortex in the ischemia-reperfusion group,the saline control group,and the edaravone group were upregulated significantly than those in the sham operation group (AQP4:0.265 ± 0.123;phospho-p38 MAPK:0.465 ±0.023;all P ＜0.01),but edaravone group were significantly lower than the ischemia-reperfusion group and the saline control group (all P ＜ 0.05).Conclusions Edaravone can downregulate the expression level of AQP4 and effectively protect cerebral ischemia reperfusion injury in mice,Its mechanism may be associated with the inhibition of p38 MAPK pathway.

Objective To evaluatate the impact of different anastomotic location and preventive ileostomy on postoperative anastomotic fistula in rectal cancer patients.Methods The clinical data of 316 cases of rectal cancer patients after total mesorectal excision from January 2015 to January 2016 were analyzed retrospectively.Patients were divided into anterior resection (AR) group,low anterior resection (LAR) group,uhra-low anterior resection (ULAR) group according to the anastomotic location.There were 33 cases of anastomotic fistula with preventive ileostomy or without and anastomotic leakage varied from mild to severe as grade A,B,C.Results There was no statistically significant difference in the incidence of anastomotic fistula between the different anastomotic location (x2 =3.829,P =0.147).In anterior resection group and low anterior resection group,there was no statistically significant difference in the incidence of anastomotic fistula whether or not a preventive ileostomy was performed (x2 =0.606,1.096,P =0.436,0.326).While in uhralow anterior resection group,preventive ileostomy helped dicrease the incidence of anastomotic fistula (x2 =11.667,P =0.001),and once happened the severity of the anastomotic fistula tended to be less severe.Conclusion The incidence of anastomotic fistula does not vary with anastomotic level in our study.Preventive ileostomy reduces the incidence of anastomotic fistula in patients with ultralow anterior resection.

Background and purpose:miR-17-92 gene cluster overexpression has been observed in various cancers, such as lung cancer, liver cancer, gastric cancer and prostate cancer. In this study, we established the stable cell line overexpressingmiR-17-92 to explore the inlfuence ofmiR-17-92 on the migration, invasion abilities and cisplatin resistance of the prostate cancer DU145 cells.Methods:miR-17-92 overexpression vectors were constructed. DU145 cells were infected with the viral supernatants produced by Phoenix A packaging system. Real-time lfuorescent quanti-tative polymerase chain reaction (RTFQ-PCR) was conducted to detect the expression level of miR-17-92 in the cells. The migration and invasion abilities were measured by a real-time xCELLigence system. The scratch healing assay was carried out to investigate the migration abilities. The expression of integrin β1 was detected by Western blot, and the activities of matrix metalloprotein-2 (MMP-2) and matrix metalloprotein-9 (MMP-9) were measured by gelatin zymography experiment. The cell growth of the two cell lines after the treatment of cisplatin was detected by a real-time xCELLigence system. The mRNA expression ofERCC1 was measured by RTFQ-PCR. Western blot was conducted to investigate the protein expressions of ERCC1, ERK1/2 and pERK1/2.Results:DU145-miR-17-92 cells migrated faster than DU145-control cells during the 24 h continuous monitoring (P<0.01). The scratch healing assay indicated that DU145-miR-17-92 cells migrated from the edge towards the scratch center faster than DU145-control cells. DU145-miR-17-92 cells invaded through matrigel markedly faster than DU145-control cells (P<0.01). The protein expression level of integrin β1 and the MMP-9 activities in DU145-miR-17-92 cells were increased than those in DU145-control cells. After the treatment of cisplatin, DU145-miR-17-92 cells grew faster than DU145-control cells, presenting cisplatin resistance (P<0.01). The phosphorylation of ERK1/2 in DU145-miR-17-92 cells was constantly at a high level regard-less of the treatment of cisplatin. Compared with DU145-control cells, the expression of drug resistance-related gene ERCC1 was dramatically increased in DU145-miR-17-92 cells after the treatment of cisplatin.Conclusion:miR-17-92 overexpression increases the migration and invasion abilities of the prostate cancer DU145 cells, which is associated with the upregulated expression of integrin β1 and the increased activity of MMP-9. Besides,miR-17-92 overexpression enhances the cisplatin resistance of DU145, which is correlated with the increased phosphorylation level of ERK and the upregulated expression of ERCC1 at both the mRNA and protein levels.

Left atrial myxoma is one of the rare causes of cerebral infarction.As the left atrial myxoma complicated artery embolization is more common in cerebral vessels,the first clinical manifestation of about 1/3 patients with left atrial myxoma was cerebral infarction.This article reports a 24-year young female without common vascular risk factors,including hypertension,diabetes,and hyperlipidemia.Multiple cerebral infarctions are the first symptom in patients with left atrial myxoma,and they are analyzed in combination with literature.

Objective To investigate a new automatic inverse optimal solution based on VMAT optimization model and verify its result.Methods A variant of the new automatic inverse optimal solution was proposed in this study,which provided a solution to calculate treatment plan with the minimized number of beams and the minimized levels of their intensities on the basis of VMAT optimization model by customized software tools.The verifications were evaluated on the simulated head-neck phantom by dosimetric parameters.Results Compared with conventional IMRT/VMAT treatment plans,the adaptive optimization program(AOP)plan showed that plan20/40(20 fields with totally 40 sub-fields,m=2)made the best achievement and it was clinicable.Conclusions The proposed new optimization technique provides an effective way to reach an inverse treatment plan with the best compromise and less sub-fields compared with IMRT/VMAT plans.