ObjectiveTo study the operative procedure and effect of anastomostic pseudoaneurysm(APA). Methods Eleven patients with APA were treated surgically. The diagnosis of APA in all the patients was comfirmed by angiography and ultras onic examination. A small rupture leading to APA was repaired by lateral arteri orrhaphy using autologous vein patch in 4 cases; the APA caused by a big rupture of anastomosis,resection of the pseudoaneurysm and interposition o f a PTFE or antologous vein were used in 7 cases.Results10cas es were followed -up for 5-38 months (mean19.6 months),and 1case loss of follow-up.9 cases recovered to be normal in activities and works, only 1 ca se had nerve paralysis of the affect extremity caused by popliteal artery APA compression . All the cases have good blood perfusion of the extremities wit hout recurrence. Conclusions APA should be treated by surgery. During operation control blood vessels effectively and remove the pathological changetissues completely are important,and reasonable application of antibi otics and antithrombotic agents are the guarantee of getting successful results .

A glassy carbon electrode (GCE) modified with gold nanoparticles loading on the reduced graphene oxide (rGO)-multi-walled carbon nanotubes (MWCNTs) composite film was fabricated by a two-step procedure.Firstly, rGO-MWCNTs composite were prepared by in-situ chemical reduction method with hydrazine as a reducing agent.Then, AuNPs were deposited on the surface of rGO-MWCNTs using simple cyclic voltammetry.This modified electrode was characterized using scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS) and electrochemical methods.Furthermore, the electrochemical behavior of bisphenol A (BPA) was also investigated using this modified electrode.The results showed that the modified electrode had high electrochemical activity for the oxidation of BPA.In 0.10 mol/L phosphate buffer solution (PBS, pH 7.0), the linear range for the determination of BPA with differential pulse voltammetry (DPV) was in the range of 5.0 × 10-9 -1.0 × 10-7 mol/L and 1.0 × 10-7-2.0 × 10-5 mol/L.The detection limit was 1.0 × 10-9 mol/L (S/N=3).The as-prepared modified electrode was successfully used to determine BPA in river water and the shopping receipt samples with recovery ranges of 97%-110% and 98%-104%, respectively.

Objective To investigate the expression and clinical pathological significance of PIWI-interacting RNA-47851 (piR-47851) in gastric adenocarcinoma and its influence on proliferation. Methods The expression of piR-47851 was detected in 79 gastric adenocarcinoma tissues by real time fluorescence quantitative polymerase chain reaction (qRT-PCR), and the correlation of piR-47851 expression level and clinical features with survival and prognosis were analyzed. The effect of piR-47851 on proliferation activity of gastric cancer cells was observed by cell proliferation experiments. Informatics websites were used to predict the downstream target genes of piR-47851. The wild-type and mutant plasmids for the 3'untranslated region (UTR) of MAPK1 gene were established, and a dual luciferase reporting system was used to verify that piR-47851 binded to the 3'UTR of MAPK1 gene, thereby inhibiting MAPK1 protein synthesis. The effect of overexpression/silencing of piR-47851 on MAPK1 expression level was examined through qRT-PCR experiment. Rescue experiment was used to confirm the direct regulatory effect of piR-47851 on MAPK1 and explore the effect of piR-47851/MAPK1 on the proliferation of gastric cancer cells. The effect of reduced piR-47851 expression on the volume and weight of transplanted tumors was observed in nude mice by xenograft tumor experiments; the effect of reduced piR-47851 expression on the cell proliferation activity of xenograft tumors was observed by Ki-67 staining. Results The qRT-PCR experiment result showed that the expression level of piR-47851 in 79 gastric adenocarcinoma tissues was significantly higher than that in normal gastric tissues adjacent to the cancer (P < 0.05). The expression level of piR-47851 was significantly correlated with tumor size, degree of differentiation, and survival prognosis (P < 0.05). Bioinformatics suggested that there was a complementary binding site between piR-47851 and MAPK1 gene 3'UTR. The dual luciferase reporter gene experiment showed that piR-47851 was able to significantly inhibit fluorescence enzyme activity in the MAPK1 wild-type transfection group, while this inhibitory effect was not observed in the MAPK1 mutant group. The CCK-8 proliferation activity experiment showed that overexpression of piR-47851 was able to significantly increase the proliferation activity of gastric cancer cells; after reducing piR-47851, the proliferation activity of cells decreased significantly (P < 0.05). Rescue experiment indicated that after changing the expression of piR-47851 and (or) MAPK1 and then detecting the expression level of MAPK1 by qRT-PCR, the MAPK1 could be regulated by piR-47851. Overexpression of MAPK1 could functionally reduce the proliferation promoting effect of piR-47851 on gastric cancer cells, while reducing MAPK1 expression could further enhance the proliferation activity of gastric cancer cells. In xenograft tumor experiments, reducing the expression of piR-47851 significantly resulted in smaller tumor growth volume and weight (P < 0.05). The proliferation index Ki-67 staining showed that the number of proliferative active cells in the reduced piR-47851 expression group was significantly lower than that in the control group (P < 0.05), which further validated the promotional effect of piR-47851 on cell proliferation. Conclusion The expression level of piR-47851 is increased in gastric adenocarcinoma tissues, which is closely related with tumor size and survival prognosis. The piR-47851 downregulates MAPK1 protein expression by binding to the 3'UTR of MAPK1, thereby promoting the proliferation of gastric cancer cells.