ABSTRACT
OBJECTIVE@#To improve the production and inspection efficiency of medical device manufacturers, improve the quality system management level of manufacturers, and ensure the safety and effectiveness of medical devices.@*METHODS@#Sort out the business process of the medical device manufacturer, connect the database of production and ERP system to inspection system, and build the operation software for the quality control department.@*RESULTS@#The system has covered all the products of the manufacturer, and has realized the informatization and visualization of the inspection process.@*CONCLUSIONS@#The research and application of the system can improve the quality management traceability system of medical device manufacturers, and improve the efficiency and accuracy of medical device quality inspection.
Subject(s)
Commerce , Information Systems , Quality Control , SoftwareABSTRACT
Objective To investigate the effect of regulating peroxisome proliferator-activated receptor γγ (PPAR γ) on soluble endoglin (sEng) expression in first-trimester trophoblasts via an in vitro study.Methods Chorionic villus were collected from 20 samples of first-trimester artificial abortion in Peking University First Hospital from July 1 st to 31 st,2016.Primary culture of trophoblast cells was performed.Trophoblast cells from each sample were divided into three groups,which were PPAR γ antagonist group,PPAR γ antagonist and PPAR γ agonist group,and control group.Supematant sEng level was detected in each group by enzyme linked immunosorbent assay (ELISA).Paired-sample t test was used for statistical analysis.Results Compared with the control group,trophoblast cells in the PPAR γ antagonist group grew slower and were reduced in number.No significant difference in growth or morphology of trophoblast cells was observed between the PPAR γγ antagonist and PPAR γγ agonist group and the control group.Supernatant sEng level was elevated in the PPAR γ antagonist group,but was not significantly changed in the PPAR γ antagonist and PPAR γ agonist group as compared with that in the control group [(124.1 23.8) vs (94.0± 12.7) pg/ml,t=-4.31,P＜0.05;(87.1 ± 10.6) vs (94.0± 12.7) pg/ml,t=1.62,P=0.12).Conclusions Suppression of PPAR γ promotes sEng expression in trophoblast cells and that can be reversed by PPAR γ agonist.