Objective To explore the expression of miR-1247-5p in gastric cancer and its effect on migration and invasion of gastric cancer cells.Methods The differentially expressed miRNAs in adjacent non-cancerous tissue versus gastric cancer tissue of TCGA database were analyzed.The prognostic value of miR-1247-5p in malignant tumor was analyzed by receiver operating characteristic(ROC)curve.RT-qPCR assay was used to detect expression levels of miR-1247-5p of gastric cancer tissue and adjacent non-cancerous tissue collected in 10 cases from our hospital.Protein-Protein Interaction(PPI)analysis was used to identify downstream target genes of miR-1247-5p.Dual-luciferase reporter assay was used to observe the binding of miR-1247 to Smad2.Transwell assay was used to investigate the effect of miR-1247-5p overexpression on migration and invasion abilities of gastric cancer cells.RT-qPCR and Western blot experiments were used to examine the impact of miR-1247-5p on expression levels of Smad2 and epithelial-mesenchymal transition(EMT)marker molecules.Results The expression levels of miR-1247-5p were lower in gastric cancer tissue collected from both TCGA database and our hospital than those in adjacent normal tissue.ROC curve analysis indicated that the expression level of miR-1247-5p was an independent prognostic indicator for most tumor types.Overexpression of miR-1247-5p significantly inhibited the migration and invasion abilities of gastric cancer cells.Bioinformatics analysis suggested that the downstream target genes of miR-1247-5p were involved in EMT and other pathways closely related to tumor metastasis.PPI analysis revealed that Smad2 was a Hub gene in the EMT signaling pathway.Dual-luciferase reporter assay demonstrated the existence of binding sites between miR-1247-5p and Smad2.RT-qPCR and Western blot experiments confirmed that miR-1247-5p can inhibit the expression of Smad2 and the process of EMT.Conclusion miR-1247-5p is lowly expressed in gastric cancer tissue,and overexpression of miR-1247-5p can inhibit EMT signaling pathway and reduce the invasive metastatic potential of gastric cancer cells.

Objective To explore the expression of miR-1247-5p in gastric cancer and its effect on migration and invasion of gastric cancer cells.Methods The differentially expressed miRNAs in adjacent non-cancerous tissue versus gastric cancer tissue of TCGA database were analyzed.The prognostic value of miR-1247-5p in malignant tumor was analyzed by receiver operating characteristic(ROC)curve.RT-qPCR assay was used to detect expression levels of miR-1247-5p of gastric cancer tissue and adjacent non-cancerous tissue collected in 10 cases from our hospital.Protein-Protein Interaction(PPI)analysis was used to identify downstream target genes of miR-1247-5p.Dual-luciferase reporter assay was used to observe the binding of miR-1247 to Smad2.Transwell assay was used to investigate the effect of miR-1247-5p overexpression on migration and invasion abilities of gastric cancer cells.RT-qPCR and Western blot experiments were used to examine the impact of miR-1247-5p on expression levels of Smad2 and epithelial-mesenchymal transition(EMT)marker molecules.Results The expression levels of miR-1247-5p were lower in gastric cancer tissue collected from both TCGA database and our hospital than those in adjacent normal tissue.ROC curve analysis indicated that the expression level of miR-1247-5p was an independent prognostic indicator for most tumor types.Overexpression of miR-1247-5p significantly inhibited the migration and invasion abilities of gastric cancer cells.Bioinformatics analysis suggested that the downstream target genes of miR-1247-5p were involved in EMT and other pathways closely related to tumor metastasis.PPI analysis revealed that Smad2 was a Hub gene in the EMT signaling pathway.Dual-luciferase reporter assay demonstrated the existence of binding sites between miR-1247-5p and Smad2.RT-qPCR and Western blot experiments confirmed that miR-1247-5p can inhibit the expression of Smad2 and the process of EMT.Conclusion miR-1247-5p is lowly expressed in gastric cancer tissue,and overexpression of miR-1247-5p can inhibit EMT signaling pathway and reduce the invasive metastatic potential of gastric cancer cells.

Objective To explore the effect of respiratory movement on the dose distribution in the TOMO therapy target area. Methods The motion phantom was used to simulate human respiratory movement. The SNC patient analysis software was used to compare the films of the study group with those of the control group, and the effect of respiratory movement on the dose distribution in the TOMO target area was evaluated by the “pass rate” index. Results Visual observation showed that the distribution of film gray in the head-foot direction (i.e., direction of movement) was significantly different with or without respiratory movement. Film analysis showed that the maximum deviation between the width of the target wrapping curve and the treatment plan value was about 2.4 mm at no respiratory movement and about 27.2 mm at respiratory movement; the penumbra width of the target area was 31 mm (head direction) and 28.5 mm (foot direction) at no respiratory movement and 39.7 mm (head direction) and 37 mm (foot direction) at respiratory movement; the “pass rate” of target dose distribution was only 12.3%. Conclusion Respiratory movement has a great impact on the dose distribution in the TOMO target area in the direction of movement. When making clinical treatment plan, the impact of respiratory movement on the dose distribution in the TOMO target area can not be ignored.

BACKGROUND: Combined use of multiple interventions for different targets play superimposed or synergistic effects,which has become the current idea for spinal cord injury treatment.OBJECTIVE: To investigate the synergistic effects of low doses of 17-β estradiol combined with bone marrow mesenchymal stem cells (BMSCs) transplantation on the recovery of motor function and inflammatory reactions after spinal cord injury in rats.METHODS: The 10 of 70 male Sprague-Dawley rats served as sham group in which the spinal cord was only exposed but with no treatment, and the rest 60 rats were used to make animal models of spinal cord injury using modified Allen's method and then randomized into four groups (n=15 per group): model, estrogen, stem cell and combined treatment groups. Rats in the stem cell and combined treatment groups were given BMSCs transplantation at injured side; rats in the estrogen and combined treatment groups were given intramuscular injection of 17-β estradiol at 1 and 24 hours after modeling. At 1, 3, 5 and 7 days after modeling, rat functional recovery was evaluated by the Basso, Beatlie, Bresnahan score. The expressions of interleukin-1β and tumor necrosis factor-α in the injured spinal cord were detected by ELISA at 6, 12, 24, and 72 hours after modeling. Apoptosis in nerve cells was observed using TUNEL staining. RESULTS AND CONCLUSION: The Basso, Beatlie, Bresnahan scores were declined significantly after modeling,increased at 5 and 7 days after stem cell transplantation, estrogen treatment or their combined treatment (P < 0.05),especially in the combined treatment group (P < 0.05). The levels of interleukin-1β and tumor necrosis factor-α were elevated gradually after spinal cord injury (P < 0.05), but the levels decreased significantly at 12 and 24 hours in stem cell,estrogen and combined treatment groups (P < 0.05), and this decrease trend was more significant in the combined treatment group compared with the stem cell and estrogen groups (P < 0.05). At 72 hours after modeling, the rate of TUNEL positive cells was highest in the model group (P < 0.05) and lowest in the combined treatment group (P < 0.05).To conclude, the combined use of low doses of 17-β estradiol and BMSCs transplantation can facilitate the recovery of motor function after spinal cord injury by effectively inhibiting apoptosis in nerve cells.

Objective To investigate the expression of TROP2 and MMP-9 protein expression in cholangiocarcinomas and their relationship between the pathological behavior and prognosis.Methods A total of 54 patients who were diagnosed with cholangiocarcinoma in the People's Hospital of Binzhou,were retrospectively reviewed.Immunohistochemical staining and Log rank test were used to detect the expression of TROP2 and MMP-9 protein in 54 cases of cholangiocarcinomas and 18 cases of normal bile duct tissues achieved by partial hepatectomy of hepatolithiasis.Results The positive expression rate of TROP2 in cholangiocarcinoma tissues (55.6％) was higher than that of normal bile duct tissues (5.6％).The positive expression rate of MMP-9 in cholangiocarcinoma tissues (51.9％) was higher than that of normal bile duct tissues (11.1％).The differences of the expression of TROP2 and MMP-9 in cholangiocarcinoma of TNM stage,lymph node metastasis and neural invasion were significant(all P ＜ 0.05).There was significant positive correlation between TROP-2 and MMP-9 expression by using spearman correlation analysis (r =0.555,P ＜ 0.001).Survival analysis showed that TROP2 expression was an independent prognostic factor in cholangiocarcinoma.Conclusions TROP2 plays a important role in the development and metastasis of cholangiocarcinoma.Thus,TROP2 may be a prognostic indicator for cholangiocarcinoma.

Objective No uniform standards has been established for the clinical diagnosis of schizophrenia .The article was to investigate the differentially expressed microRNA ( miRNA) profile and explore its clinical significance . Methods Differentially expressed miRNAs were screened by FlashTag TM Biotin RNA chips and SAM software in serum of patients with schizophrenia and healthy controls , then the validation was performed by real-time fluorescent quantitative reverse transcription polymerase chain reaction ( RT-PCR) . Results Three differentially expressed miRNAs were screened , including up-regulated hsa-miR-1281 ( fold change =1.50881) and two down-regulated miRNAs:hsa-miR-2861(fold change=0.642) and hsa-miR-638 (fold change=0.516).The com-parative analysis of RT-PCR by SPSS 17.0 Kruskal Wallis H Test validated the expression levels of hsa-miR-2861 and hsa-miR-638 in patients with schizophrenia decreased significantly in comparison to healthy controls (χ2 =4.089,χ2 =4.083, P<0.001).While the expression level of hsa-miR-1281 in patients with schizophrenia was in higher expression level compared with control group (χ2 =5.333, P<0.001). Conclusion There are differentially expressed miRNA profile in serum of patients with schizophrenia , in which miR-1281 , miR-2861 and miR-638 could be new serum markers for diagnosis of schizophrenia .

Objective To investigate the changes of Notch signaling pathway activity in human pancreatic cancer cell lines (SW1990, BxPC3 )after gemcitabine induction, and to study its relationship with pancreatic cancer resistant to gemcitabine chemotherapy. Methods The pancreatic cancer cell lines SW1990 and BxPC3 were cultured with different concentrations of gemcitabine for 48 hours. The Notch signaling pathway receptors ( Notch1, Notch2, Notch3, Notch4), ligands (Jagged1, Jagged2) and downstream target Hesl mRNAs expression were detected by quantitative real-time PCR (Q-PCR). Protein levels of Hes1 were determined by Western blotting. Results After treatment with 2 μmol/L gemcitabine for 48 hours, the expression of Notch1, Notch2, Notch3, Jagged1, Jagged2 and Hes1 mRNAs in SW1990 cells were 8.26 ±0.48, 39.12 ±4.87, 0.84 ±0.06, 105.8 ± 17.92, 6.59 ±0.32 and 17.30 ±2.96, which were significantly elevated when compared with those without gemcitabine treatment ( 1.02 ± 0. 15, 15.25 ± 1.28, 0. 12 ± 0.02,32.66 ± 1.98, 1.88 ± 0.29 and 5.02 ± 0.64, P < 0.05 or P < 0. 01 ); the expression in BxPC3 cells was 7.87 ±0.59, 109.4 ± 10.98, 0.74 ±0.19, 62.73 ± 13.50, 2.09 ±0.16 and 15.38 ± 1.06, which were significantly elevated when compared with those without gemcitabine treatment ( 1.14 ±0.43, 58.96 ±2.63,0.10 ± 0.02, 16.95 ± 3.79, 0.98 ± 0.02 and 2.04 ± 0.16, P < 0.05 or P < 0.01 ). The expressions of Hes1protein in SW1990 cells after 1, 2 μmol/L gemcitabine treatment for 48 h were 0.30 ±0.03, 0.42 ±0.03;and the expressions in BxPC3 cells were 0.33 ± 0.02, 0.45 ± 0.03, which were significantly increased when compared with those without gemcitabine treatment (0.13 ± 0.01, F = 33.71,0.09 ± 0.02, F = 38.54, P <0.01 ). Conclusions The Notch signaling pathway is significantly activated in pancreatic cancer cells SW1990 and BxPC3 by gemcitabine, which may be one of the mechanisms of chemoresistance.