The credibility of the third-party mediation agencies in medical disputes lies in their own advantages of efficiency,neutrality,professionalism and objectivity.However,because of the differences of actual operation,the credibility of the third-party mediation agencies often is questioned by both doctors and patients and the public.Aiming at these,this paper would study the status and the pushing approach of the third-party mediation agencies credibility from the perspective of professionalism and neutrality,legislation,fundraising channels and supervision.

Objective To investigate the inhibitory effects and possible related mechanism of OTX008 [a selective inhibitor of galectin-1 (Galectin-1)] on retinal neovascularization (RNV) in mouse model of oxygeninduced retinopathy (OIR).Methods 7-day-old (P7) C57BL/6J mice were randomly (according to random number table) divided into 4 groups including normal group,OIR group,OIR-OTX008 group and OIRphosphate buffered saline (PBS) group.To establish the OIR mouse model,mice from all groups except normal group were expose to (75±2)％ oxygen for 5 days and then to room air.OIR-OTX008 group received an intravitreal injection of 1 μl (0.25 μg/μl) OTX008 at P12,OIR-PBS group received the equal volume (1 μl) of PBS injection.Mice from 4 groups were euthanized at P17,and retinas were collected for molecular biological analysis and morphological study.RNV was evaluated by counting the number ofpre-retinal neovascular nuclei and the whole-mount immunofluorescent staining of mouse retina.Cyrosections of retinas were imaged via confocal microscopy to observe the enrichment of staining of Galectin-1.Protein levels of Galectin-1,Neuropilin-1 and phosphorylation of vascular endothelial growth factor receptor 2 (pVEGFR2) were determined with Western blot.Results At P17,Galectin-1 expressed higher in retinal ganglion cell layer,inner plexiform layer and inner nuclear layer from OIR group and OIR-PBS group than normal group.Galectin-1 expressed less in cryosection retinas from OIR-OTX008 group than OIR group and OIR-PBS group.The numbers ofpre-retinal neovascular cell nuclei from OIR group and OIR-pBS group were obviously more than that from normal group (t=9.314,P＜0.05).The number of pre-retinal neovascular cell nuclei from OIR-OTX008 group were obviously lower than those from OIR group and OIR-PBS group (t=8.038,7.774;P＜0.05).The RNV tufts area (t=13.250,12.570),non-perfusion area (t=15.590,12.430) and hypoxic area (t=9.542,9.928) from OIR-OTX008 group were significantly smaller than those in OIR group and OIR-PBS group (P＜ 0.05).Protein levels of Galectin-1 (t=24.800,23.060),Neuropilin-1 (t=4.120,3.530) and pVEGFR2 (t=25.880,15.480) in the OIR-OTX008 group were significantly down-regulated than those from OIR group and OIR-PBS group (P＜0.05).Conclusion Intravitreal injection of OTX008 inhibits RNV and ameliorates retinal hypoxia in mice model of OIR possibly through down-regulating Galectin-1,Neurolinpin-1 and pVEGFR2.

This paper analyzed the economic background,contents and effects of the existing business model of the hospital.On this basis,further study and reform are made on optimal business model of the hospital.The authors recommended that appropriate regional health scale,appropriate technical service,appropriate pricing for charges,appropriate operating cost and appropriate incentive constraints be adopted.These measures will safeguard state assets,public benefit nature of the hospital,enhanced hospital power in general,and compliance in operations,making the people satisfied and healthy.

Objective To analyze the characteristics of visual evoked potential (VEP) and the role of VEP in detecting posttraumatic optic nerve injury and evaluate the value of hyperxia liquid in treatment of posttraumatic optic nerve injury. Methods A total of 84 patients with optic nerve injury were divided into control group (n=47, received the general treatments) and treatment group (n=37, treated with hyperxia liquid on the basis of the general treatments) that were monitored regularly by VEP at days 1, 7, 14 and 21 respectively after treatment to analyze and compare latency, amplitudes, visual acuity and treatment result. Results After injury, abnormality of VEP occurred at days 1-7, reached the peak at days 7-14, and then markedly relieved at day 21. Compared with control group, degree of VEP abnormality was significantly lower (P

This study investigated the effect of etoposide, an anticancer chemotherapy drug, on B7-H1 expression in retinoblastoma (Rb) cells and the role of miR-513a-5p in the process. Rb cells were divided into control and etoposide groups. In the etoposide group, cells were treated with etoposide at different concentrations (2.5, 5, 10, 20 and 40 μg/mL) for 24 h. Those given no treatment of etopside served as controls. Reverse transcription polymerase chain reaction (RT-PCR), fluorescence quantitative PCR and flow cytometry were performed to measure the mRNA and protein expression of B7-H1 in Rb cells. The mRNA expression of miR-513a-5p in Rb cells before and after etoposide treatment was also detected by fluorescence quantitative PCR. The miR-513a-5p mimics and the miR-513a-5p inhibitor were transfected into Rb cells separately, and fluorescence quantitative PCR and flow cytometry were used to detect the effect of the miR-513a-5p mimics or inhibitor on B7-H1 expression. TargetScan5.2 was employed to predict the miR-513a-5p binding sites in the 3'-untranslated region of B7-H1 mRNA. Luciferase reporter plasmids carrying this site were prepared and transfected into Rb cells and luciferase activity analyzed. The results showed that etoposide stimulated the mRNA and protein expression of B7-H1 in Rb cells, which reached a maximal level after treatment with 5 μg/mL etoposide (P<0.05). However, miR-513a-5p expression was decreased in Rb cells after etoposide treatment. When the miR-513a-5p inhibitor was added, B7-H1 expression was increased with the concentration of the miR-513a-5p inhibitor (P<0.05). Moreover, B7-H1 expression was decreased gradually with the concentration of the miR-513a-5p mimics increased (P<0.01). Additionally, the miR-513a-5p mimics were found to inhibit the luciferase activity. It was concluded that etoposide can promote B7-H1 expression in Rb cells, which may be associated with chemoresistance. The promoting effect of etoposide on B7-H1 expression can be reversed by miR-513a-5p mimics. MiR-513a-5p inhibits the mRNA and protein expression of B7-H1 via binding to the 3'-UTR of B7-H1 mRNA.

Objective To evaluate the effect of silencing ACAT1 gene on colon cancer cells proliferation,migration,invasion and colon cancer development by using the small interference RNA (siRNA) in colon cancer cell line HT-29.Methods Acyl coenzyme A cholesterol acyltransferase 1 (ACAT1) gene was silenced in HT-29 cell lines using Hiperfect transfection reagent.The expression level of ACAT1 was detected by real time PCR.CFSE and transwell assays were used to evaluate the effect of ACAT1 gene interfering on cells proliferation,mi gration and invasion.Result ACAT1 mRNA expression decreased obviously after siRNA interference.Compared with pre-transfection,proliferation,migration and invasion of colon cancer cells have been significantly inhibited (P ＜ 0.05).Conclusion ACAT1 gene interference reduced proliferation,migration and of invasion of HT29 cells,which provide a new potential target for colon cancer treatment.

This study investigated the effect of etoposide, an anticancer chemotherapy drug, on B7-H1 expression in retinoblastoma (Rb) cells and the role of miR-513a-5p in the process. Rb cells were divided into control and etoposide groups. In the etoposide group, cells were treated with etoposide at different concentrations (2.5, 5, 10, 20 and 40 μg/mL) for 24 h. Those given no treatment of etopside served as controls. Reverse transcription polymerase chain reaction (RT-PCR), fluorescence quantitative PCR and flow cytometry were performed to measure the mRNA and protein expression of B7-H1 in Rb cells. The mRNA expression of miR-513a-5p in Rb cells before and after etoposide treatment was also detected by fluorescence quantitative PCR. The miR-513a-5p mimics and the miR-513a-5p inhibitor were transfected into Rb cells separately, and fluorescence quantitative PCR and flow cytometry were used to detect the effect of the miR-513a-5p mimics or inhibitor on B7-H1 expression. TargetScan5.2 was employed to predict the miR-513a-5p binding sites in the 3'-untranslated region of B7-H1 mRNA. Luciferase reporter plasmids carrying this site were prepared and transfected into Rb cells and luciferase activity analyzed. The results showed that etoposide stimulated the mRNA and protein expression of B7-H1 in Rb cells, which reached a maximal level after treatment with 5 μg/mL etoposide (P<0.05). However, miR-513a-5p expression was decreased in Rb cells after etoposide treatment. When the miR-513a-5p inhibitor was added, B7-H1 expression was increased with the concentration of the miR-513a-5p inhibitor (P<0.05). Moreover, B7-H1 expression was decreased gradually with the concentration of the miR-513a-5p mimics increased (P<0.01). Additionally, the miR-513a-5p mimics were found to inhibit the luciferase activity. It was concluded that etoposide can promote B7-H1 expression in Rb cells, which may be associated with chemoresistance. The promoting effect of etoposide on B7-H1 expression can be reversed by miR-513a-5p mimics. MiR-513a-5p inhibits the mRNA and protein expression of B7-H1 via binding to the 3'-UTR of B7-H1 mRNA.
B7-H1 Antigen ; genetics ; Cell Line, Tumor ; Etoposide ; pharmacology ; Gene Expression ; drug effects ; genetics ; Humans ; MicroRNAs ; genetics ; Retinoblastoma ; genetics

Gas chromatography-mass spectrometry (GC-MS) method was established for trace analysis of the potential genotoxic impurity chlorocyclohexane in trihexyphenidyl hydrochloride bulk drug, utilizing an RXI-5SIL MS column at isothermal temperature of 60 °C for the entire 6-minute run time.The inlet temperature was 180 °C and a split ratio of 10∶1 was used with the injection volume of 1.0 μL.The selective ion monitoring mode was set at m/z 82 for chlorocyclohexane with a detector voltage of 0.3 kV and an ion source temperature of 240 °C.The method was verified with respect to specificity, limit of detection (LOD), limit of quantitation (LOQ), accuracy, precision and robustness.Good linear correlation was achieved with coefficient r of 0.999 9 in the concentration range of 59.72-493 ng/mL.The intra- and inter-day precision was satisfactory (RSD ≤ 5.0%) and robust (RSD ≤ 1.65%).The proposed method in this study can be adequately adopted as a tool for quality assurance of trihexyphenidyl hydrochloride in routine test of potential genotoxic impurity.

Objective:To investigate the survival rate change of retinal ganglion cells（RGCs）in a mouse of optic nerve crush（ONC）.Methods:Ninety-seven male C57BL/6J mice（6 to 8 weeks）were selected and divided into normal group（ n=5）, sham-operation group（ n=5）and ONC group（ n=5）according to the random number table. In normal group, both eyes of the mice did not receive any intervention. In sham-operation group, the right eye of the mice received sham operation, while the left eye reveived no intervention. In ONC group, the left eye received ONC, and the right eye received sham operation. In normal group, the density of RGCs in both eyes was quantified and compared. In sham-operatioin group, the density of RGCs in the sham operation eye was calculated and then compared to the average density of RGCs in normal group. In ONC group, the survival rate of RGCs was set as the ratio between the left eye（ONC eye）and the right eye（sham-operation eye）. The survival rate of RGCs in ONC group was compared after crush injury for 5, 10, 20, 30 seconds）（the sacrifice time was set at day 7）, and was compared after sampling on days 3, 4, 5, 7, 14, 30, 60, 90, 180（the duration of crush injury was set as 20 seconds）. Results:In normal group, the density of RGCs in the right eye was（5, 167.3±55.6）cell/mm 2, with no statistical difference from that in the left eye［（5, 199.6±44.8）cell/mm 2］（ P>0.05）. The density of RGCs in normal group and sham-operation group was（5, 183.5±33.4）cell/mm 2 and（5, 151.5±87.6）cell/mm 2, showing no statistical difference（ P>0.05）. The survival rate of RGCs in ONC group after crush injury for 5, 10, 20, 30 seconds was（37.6±1.1）%,（34.0±0.9）%,（33.6±1.6）% and（30.3±0.6）%（ P<0.01）. In comparison, there was statistical difference in the survival rate of RGCs between crush injury for 5 seconds and for 30 seconds（ P<0.01）, but not among other duration of crush injury（ P>0.05）. The survival rate of RGCs in ONC group after sampling on days 3, 4, 5, 7, 14, 30, 60, 90, 180 was（85.4±2.0）%,（67.6±3.1）%,（43.0±1.0）%,（33.6±1.6）%,（22.7±2.0）%,（12.8±0.6）%,（10.4±0.8）%,（8.6±0.5）% and（6.7±0.2）%（ P<0.01）, showing the most obvious drop from day 3 to day 5. Additionally, the curve became flattened after 30 days. Conclusions:In a mouse model of ONC, varying durations of crushing will lead to different damage to RGCs in a progressive mode, indicating that following the primary injury（ONC）, the RGCs suffer secondary injury as well. Therefore, effectively controlling the secondary injury may be the key point of treating optic nerve injuries.

Objective:To assess the efficacy and safety of the combination therapy of camrelizumab, apatinib, nab-paclitaxel, and S-1 for patients with locally unresectable advanced gastric cancer.Methods:From September 1, 2019 to August 1, 2021, in Beijing Friendship Hospital Affiliated to Capital Medical University, 17 patients with advanced gastric cancer were enrolled in this prospective, single-arm study. All the enrolled patients received camrelizumab, nab-paclitaxel, apatinib and S-1 combination therapy (in each 21 days cycle, camrelizumab 200 mg intravenously, D1; nab-paclitaxel 240 mg/m 2 intravenously, D2; apatinib 500 mg orally, once a day, D1-D21; S-1 40-60 mg twice a day, D1-D14). Patients who have been evaluated by multidisciplinary team to be eligible for radical surgery should stop treatment for at least 2 weeks. Patients were discontinued from the study when disease progression or unbearable toxicity, or withdrew consent. We analyzed the conversion rate, objective response rate (ORR), disease control rate (DCR), overall survival (OS) and safety.Statistical data were show by numbers and persentages(%), and comparisons between subgroups were assessed by Fisher′s exact probability method. Patients survival was analyzed using Kaplan-Meier curves and compared between groups using Log-rank. Results:At the data of cutoff (December 15, 2021), the median follow-up duration was 19.6 months. Eight of 17 patients underwent gastrectomy, and all of them were R0 resection (47.1%, 95% CI: 0.262-0.690). ORR was 47.1%, DCR was 82.4%, the median overall survival was 23.63 months. Grade 3 and 4 adverse events occurred in 3 patients (17.6%), including neutropenia, thrombocytopenia, anemia and upper gastrointestinal hemorrhage. There were no serious treatment-related adverse events or treatment-related deaths. Conclusion:In this trial, the combination of camrelizumab, apatinib, nab-paclitaxel and S-1 as the conversion therapy showed significant anti-tumor activity and manageable adverse events, providing a new option for locally unresectable advanced gastric cancer.