BACKGROUND: Most scholars believed that injured vertebral body needs to be fixed in the open surgery of thoracolumbar vertebral fractures; however, it is unclear whether injured vertebra needs to be fixed in the minimaly invasive surgery. OBJECTIVE: To investigate the clinical outcomes of minimaly invasive percutaneous self-dilating pedicle in repair of injured vertebral fixation in thoracolumbar vertebral fractures. METHODS: Totaly 36 patients with thoracolumbar vertebral fractures without nervous system injury who received treatment in Honghui Hospital, Xi’an Jiaotong University Health Science Center from February 2013to February 2014 were enroled and divided into injured vertebral fixation and cross-injured vertebral fixation groups (n=18/group). Patients in these two groups were al subjected to minimaly invasive percutaneous self-dilating pedicle treatment. The injured vertebral body, upper, and lower vertebrae of injured vertebral body were fixed in injured vertebral fixation group, and the upper and lower vertebrae of injured vertebral body was fixed in cross-injured vertebral fixation group. RESULTS AND CONCLUSION: Compared with the injured vertebral fixation group, the cross-injured vertebral fixation group had smaler incisions, less intraoperative blood loss, less operation tine and intraoperative X-ray fluoroscopy time (P < 0.05). After one year of internal fixation, the anterior vertebral height, anterior vertebral height percentage and kyphotic Cobb angle of patients in these two groups improved compared with those before internal fixation (P < 0.05), but there were no significant differences in anterior vertebral height percentage, kyphotic Cobb angle and Oswestry disability index between these two groups (P > 0.05). These results demonstrate that anterior vertebral height cross-injured vertebral fixation has the similar clinical effect with injured vertebral fixation, but cross-injured vertebral fixation had more advantage in the operation. Therefore, there is little significance of conducting injured vertebral fixation in the surgery of minimaly invasive percutaneous self-dilating pedicle in repair of thoracolumbar vertebral fractures.

Objective To retrospectively analyze medical data of patients with colorectal cancer (CRC) so as to provide evidence for clinical use of opportunistic screening.Methods A total of 2450 CRC patients (male 1377,female 1073) who were treated at five hospitals in North China during October 2001 and September 2011 and had complete medical records and pathological results were recruited.The correlations of incidenceofCRCwithage,gender,tumorlocationandhistologicaltypeswere analyzed.Results Of all the CRC patients,those less than 50 years old accounted for 18.14％ ; and the incidence of CRC was substantially increased in those over 50 years old.Seventy-three percent of tumor occurred at the rectum and sigmoid colon,6％ at descending colon,7％ at transverse colon and 14％ at ascending colon.Moderately,well or poorly differentiated adenocarcinoma accounted for 50.33％,40.35％and 9.32％,respectively.Histological differentiation was not correlated with age and gender ( P ＞ 0.05 ).Conclusions Age and gender should not be considered a determination of opportunistic screening for CRC.Colonoscopy is recommended as an alternative CRC screening procedure.

Aim To investigate the role of COX-2 in BMP9 induced osteogenic differentiation,and the pos-sible mechanism underlying this function of COX-2. Methods We introduced real-time PCR, Western blot, and immunocytochemical staing to detect the effect of BMP9 on COX-2 expression.We employed chemiluminescence technique to assay ALP activities, RT-PCR to detect the expression of Smad6 and Smad7 , and Western blot to measure the expression of Runx2, Dlx-5,total Smad1/5/8,and phosphorylated Smad1/5/8.Finally,BMPR-Smad luciferase reporter assay was applied to measure the activation of BMPs/Smads signaling.Results BMP9 could induce the expression of COX-2 in C3H10T1/2 cells.Either inhibiting enzy-matic activity of COX-2 or knockdown of the expression of COX-2 reduced the BMP9 induced ALP activities in C3H10T1/2 cells,and COX-2 knockdown also inhibited the ectopic bone formation induced by BMP9 in C3H10T1/2 cells.Moreover,COX-2 knockdown inhibi-ted BMPR-Smad reporter activities and the phosphoryl-ation of Smad1/5/8,so did the expression of Smad6 and Smad7 .Conclusion COX-2 may play an impor-tant role in BMP9 induced osteogenic differentiation in MSCs by regulating the BMPs/Smads signaling trans-duction.

Objective:To observe the acute toxic side effects of liposome PP 1 topically applied in eyes .Methods:PP1 liposomes (10, 60, 400 μmol· L-1 ) were used in one eye of SD rats , 4 times daily.The changes of conjunctiva , cornea and iris were observed under the slit-lamp biomicroscope , for three consecutive days , and evaluated by the stimulus score sheet of anterior segment .One week after the treatment , the corneas , irises and lenses were isolated , and their changes were observed under the light microscope .The ul-trastructural changes of corneal epithelial cells and endothelial cells were observed under the electron microscope .Results:There was a little of conjunctival secretion in one rat in the first day after the treatment with 400 μmol· L-1 PP1 liposomes, and the other rats were not irritant reaction .The corneal fluorescein staining of all rats were negative .The structures of cornea , iris, lens tissue were normal after given different concentrations of PP1 liposomes.Conclusion:PP1 liposomes at Low, medium and high concentrations show no a-cute eye toxicity in SD rats .

Aim To investigate the anti-proliferating effect of tetrandrine ( Tet ) on colon cancer cells and its possible molecular mechanism. Methods We intro-duced crystal violet staining and flow cytometry to ana-lyze the effect of Tet on proliferation in LoVo cells. Flow cytometry was used to detect the effect of Tet on apoptosis in LoVo cells. Western blot assay was taken to analyze the effect of Tet on the expression of insulin-like growth factor binding protein 5 ( IGFBP5 ) . Final-ly, luciferase reporter assay, recombinant adenovirus mediated over-expression or silence of IGFBP5 were used to analyze the possible role of IGFBP5 in the anti-proliferating effect of Tet on colon cancer cells. Re-sults Crystal violet staining and flow cytometery anal-ysis results showed that Tet could exert an anti-prolifer-ating effect and induce apoptosis in LoVo cells. Tet de-creased the expression of IGFBP5 in a concentration-dependent manner. Tet inhibited the transcriptional ac-tivity of pTOP-luc reporter, which could be reversed by exogenous expression of IGFBP5 mostly. Similar results were found in the expression of c-Myc, but IGFPB5 knockdown couldn’ t reverse this effect. Conclusion Tet can inhibit the proliferation of colon cancer cells, and this effect may be mediated by down-regulating the expression of IGFBP5 to inhibit Wnt/β-catenin signa-ling transduction partly.

Objective: To explore the value of serum microRNA-494 (miR-494) expression in predicting the prognosis of acute renal injury (AKI) after cardiac surgery in children. Methods: 116 children with AKI after cardiopulmonary bypass for congenital heart disease admitted to Sanya People's Hospital from January 2016 to March 2019 were enrolled. The expression of miR-494 in serum was detected by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), and the levels of serum neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were detected by enzyme linked immunosorbent assay (ELISA) of all the children. The children were divided into survival group and death group according to 28-day survival. Serum levels of miR-494, NGAL and KIM-1 were measured in two groups. Multivariate Logistic regression was used to analyze the risk factors of death in children with AKI after cardiac surgery. The receiver operating characteristic (ROC) curve analysis of serum levels of miR-494, NGAL and KIM-1 in predicting prognosis of children with AKI after cardiac surgery was performed. Pearson correlation analysis was used to analyze the correlation between serum levels of miR-494 and NGAL, KIM-1. Results: After cardiopulmonary bypass in 116 children with AKI, 27 cases died and 89 cases survived during the 28-day observation. Compared with the survival group, the proportion of cyanosis in the death group was significantly increased, the proportion of blood perfusion was significantly decreased, the time of cardiopulmonary bypass and postoperative mechanical ventilation were significantly prolonged, and the blood glucose level was significantly increased after operation. There was no significant difference in other general data. The serum levels of miR-494, NGAL and KIM-1 in the death group were significantly higher than those in the survival group [miR-494 (2^-ΔΔCt): 3.75±1.28 vs. 1.48±0.71, NGAL (mg/L): 583.60±52.72 vs. 320.52±31.84, KIM-1 (μg/L): 30.53±6.38 vs. 17.40±3.72, all P < 0.01]. Multivariate Logistic regression analysis showed cyanosis [odds ratio (OR) = 1.716, 95% confidence interval (95%CI) was 1.184-2.982, P = 0.039], postoperative blood glucose (OR = 1.925, 95%CI was 1.262-3.387, P = 0.005), serum miR-494 (OR = 2.527, 95%CI was 1.706-5.148, P < 0.001), NGAL (OR = 2.473, 95%CI was 1.620-4.935, P < 0.001) and KIM-1 (OR = 1.805, 95%CI was 1.213-3.106, P < 0.001) were independent risk factors for death in children with AKI after cardiac surgery. ROC curve analysis showed the area under the curve (AUC) to predict the death of children with postoperative AKI was 0.868, 0.857 and 0.819 respectively, AUC of serum miR-494, NGAL and KIM-1 levels combination to predict the death of children with postoperative AKI was the largest (0.964, 95%CI was 0.908-0.997), with a high sensitivity and specificity of 97.0% and 91.8%. The correlation analysis showed the expression level of serum miR-494 was positively correlated with NGAL and KIM-1 in the death group (r₁ = 0.902, r₂ = 0.873, both P < 0.01). Conclusion Serum levels of miR-494 increased significantly in children with AKI after cardiac surgery, which is an independent risk factor for death in children with AKI after cardiac surgery, and the combination of NGAL and KIM-1 levels had a high value in predicting the prognosis of children with AKI after cardiac surgery.

Aim To investigate the anti-proliferation effect of resveratrol (Res)on human colon cancer cells and dissect the possible mechanism underlaying this effect.Methods We introduced crystal violet staining and Western blot to analyse the anti-proliferation effect of Res on HCT1 1 6 cells.Then,we used flow cytome-try and Western blot assay to detect the Res induced apoptosis in HCT1 1 6 cells.Next,we employed the well established TCF4 /LEF luciferase reporter to meas-ure the effect of Res on Wnt/β-catenin signaling trans-duction.Finally,we took Western blot and PCR assay to analyse the effect of Res on the expression of β-cate-nin in HCT1 1 6 cells.Results Crystal violet staining and Western blot analysis showed that Res could inhib-it the proliferation of HCT1 1 6 cells in a concentration-and time dependent fashion.What’s more,Res could promote apoptosis in HCT1 1 6 cells.The transcriptional activities of TCF4 /LEF reporter were reduced by Res in a concentration-dependent fashion (P <0.05 when the concentration of Res was 20 μmol·L -1 ,and P <0.01 when the concentration of Res was 40 μmol·L -1 or 80 μmol·L -1 ).Res could decrease not only the protein level of β-catenin in HCT1 1 6 cells,but also the mRNA expression of β-catenin.Conclusion Res can inhibit the proliferation of HCT1 1 6 cells,which may be mediated at least by down-regulating the ex-pression of β-catenin to inhibit the Wnt/β-catenin sig-naling transduction.

An enhance matrix removal ( EMR) QuEChERS method for simultaneous determination of 22 triazine herbicide residuals such as atrazine, propazine, terbumeton, and desmetryn in corn was established and validated. The corn samples were initially extracted with acetonitrile ( MeCN ) in high-speed homogenization, and the targeted pesticides were prepared using EMR-Lipid (Enhanced matrix removal-lipid) method to clean-up and EMR-Polish to salt out, separated on a Kinetex XB-C18 with acetonitrile and 0. 1%formic acid aqueous as eluant, and then detected by UFLC-MS / MS under positive ( ESI+ ) electrospray ionization and MRM models. The average recoveries of 22 herbicides were in the range of 72% -105% at the spiked level of 5, 10 and 20 μg / kg. The relative standard deviations were less than 15% . In the method validation, correlation coefficients were higher than 0. 993 with the linear range from 1. 0 μg / L to 50 μg / L. The qualitative analysis and quantitative analysis were investigated by UFLC-MS / MS and matrix-matched calibration curves. The results showed that EMR QuEChERS combined with UFLC-MS / MS purification method was rapid, accurate and sensitive for the determination of 22 triazine herbicides residues in corn.

OBJECTIVETo study whether As(2)O(3) has an apoptotic effect on human solid tumor cells, and the possible cellular and molecular mechanisms of this treatment using human esophageal squamous carcinoma cells (EC8712) as a model.

METHODSDNA microarray, biochemical and cytological analyses were used.

RESULTSThe growth and survival of EC8712 cells were markedly inhibited by As(2)O(3) treatment at a concentration of 1, 2 and 4 micromol/L. EC8712 cells were obviously arrested at G2/M phase with As(2)O(3) treatment and apoptosis induced at micromolar As(2)O(3) concentrations, as shown by morphology, histogram related nuclear DNA contents, and DNA gel electrophoresis. As(2)O(3) activated caspase-3, which might be involved in the process of As(2)O(3), induced apoptosis in EC8712 cells.

CONCLUSIONSAs(2)O(3) changes the expression of many genes at transcription level. The regulation of expression of many genes might be involved in the process of As(2)O(3) inducing apoptosis. These results suggest that As(2)O(3) can be clinically useful for solid tumor treatment.

Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Carcinoma, Squamous Cell ; drug therapy ; genetics ; pathology ; Cell Adhesion ; drug effects ; Cell Division ; drug effects ; DNA Fragmentation ; drug effects ; Dose-Response Relationship, Drug ; Esophageal Neoplasms ; drug therapy ; genetics ; pathology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Microscopy, Electron ; Oxides ; pharmacology ; Tumor Cells, Cultured ; drug effects ; ultrastructure

Background and Objectives: The search for a suitable alternative for urethral defect is a challenge in the field of urethral tissue engineering. Induced pluripotent stem cells (iPSCs) possess multipotential for differentiation. The in vitro derivation of urothelial cells from mouse-iPSCs (miPSCs) has thus far not been reported. The purpose of this study was to establish an efficient and robust differentiation protocol for the differentiation of miPSCs into urothelial cells. Methods: and Results: Our protocol made the visualization of differentiation processes of a 2-step approach possible. We firstly induced miPSCs into posterior definitive endoderm (DE) with glycogen synthase kinase-3β (GSK3β) inhibitor and Activin A. We investigated the optimal conditions for DE differentiation with GSK3β inhibitor treatment by varying the treatment time and concentration. Differentiation into urothelial cells, was directed with all-trans retinoic acid (ATRA) and recombinant mouse fibroblast growth factor-10 (FGF-10). Specific markers expressed at each stage of differentiation were validated by flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) assay, immunofluorescence staining, and western blotting Assay. The miPSC-derived urothelial cells were successfully in expressed urothelial cell marker genes, proteins, and normal microscopic architecture. Conclusions We built a model of directed differentiation of miPSCs into urothelial cells, which may provide the evi-dence for a regenerative potential of miPSCs in preclinical animal studies.