Objective · To investigate the clinical effect of intravitreal injection of Conbercept in the treatment of diabetic macular edema (DME).Methods · Eleven patients (17 eyes) with DME (inflammatory type) received intravitreal injection of Conbercept monthly. After the first treatment, the patients were treated on demand. Follow-up after treatment for more than 6 months, the best corrected visual acuity (BCVA), central retinal thickness (CRT),diminished rate of DME and result of fundusfluorescein angiography(FFA) of DME eyes before and after treatment were compared. Results · During a follow-up of 7-29 months [(12±7) months], the injections were given 1-10 times [(4±3) times]. The results showed that the treatment effects on improving BCVA (logMAR) and diminishing of CRT were significant (t=7.306, P=0.001; t=5.272, P=0.000). The diminished rate of DME of our patients was 76.5%. Conclusion · Intravitreal injection of Conbercept in the treatment of DME is effective on reducing macular edema and improving visual acuity.

Objective To investigate the regulatory effect and molecular mechanism of solute carrier family 1 member 5 (SLC1A5) -tetraspanin superfamily member 1 (TM4SF1) complex on cisplatin resistance in esophageal squamous cell carcinoma (ESCC) cells. Methods SLC1A5-overexpressing Eca109 cells were constructed using lentiviral vectors, and the effect of SLC1A5 on cisplatin sensitivity was assessed through cell viability assays. Western blotting (WB) was employed to detect SLC1A5 expression in Eca109 cells and cisplatin-resistant Eca109 cells (Eca109-R). SLC1A5 expression was knocked down in Eca109-R cells using lentiviral vectors, and cisplatin sensitivity was examined thereafter. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to analyze the influence of SLC1A5 knockdown on the expression of key genes involved in DNA damage repair in Eca109-R cells. In SLC1A5-knockdown Eca109-R cells, cell viability assays were performed to evaluate the sensitivity to cisplatin after RAD50 overexpression. Additionally, Eca109 cells were separately or co-overexpressed with SLC1A5 and TM4SF1 using lentiviral vectors, and the effect of the SLC1A5-TM4SF1complex on RAD50 expression and cisplatin resistance was examined through cell viability assays. Results Compared with control cells, Eca109 cells overexpressing SLC1A5 exhibited enhanced cisplatin resistance (P < 0.05). Eca109-R cells showed increased SLC1A5 protein expression, and knockdown of SLC1A5 cells were more sensitivity to cisplatin (P < 0.05). RAD50 gene expression was significantly downregulated upon SLC1A5 knockdown under cisplatin treatment (P < 0.05). Knockdown of SLC1A5 inhibited RAD50 protein expression, and overexpression of RAD50 in SLC1A5-knockdown cells significantly restored cisplatin resistance (P < 0.05). Co-overexpression of SLC1A5 and TM4SF1 can further up-regulate the expression of RAD50, and the drug resistance of the cells to cisplatin was enhanced compared with the control cells(P < 0.05). Conclusion The SLC1A5-TM4SF1 complex promotes cisplatin resistance in ESCC cells by upregulating RAD50 expression.

Objective:To prospectively guide the change of chemotherapy regimen in mouse 5-fluorouracil (5-FU) resistance subcutaneous xenograft tumor model derived from gastric cancer patients by the early changes of MRI apparent diffusion coefficient (ADC), and to compare the difference of tumor load between ADC guided dressing change group and volume guided dressing change group.Methods:From January to June 2020, thirty patient-derived xenografts mouse models were established using 5-FU resistant gastric cancer cells coming from patients, and were randomly divided into experimental group and control group by AdaBoost algorithm, with 15 mice in each group. On the 26th day after transplantation, all mice began chemotherapy with 5-FU as the first-line chemotherapy drug, and underwent MR examination once every two days, including T 2WI and diffusion weighted imaging (DWI). Volumes of tumors were measured using an open-source software ITK-SNAP and values of ADC were measured on ADC maps. According to the change rate of tumor ADC value in the experimental group and the tumor volume growth rate in the control group, the replacement time of chemotherapy drugs was determined, and 5-FU was replaced by paclitaxel. The end point of the experiment was the day that the mice entered the cachexia state. Independent-sample t test was used to compare the difference of tumor load between the two groups. Results:After 5-FU treatment, the ADC value of the two groups both increased. The ADC value began to decline on the 4th day after chemotherapy, and the experimental group continued chemotherapy with paclitaxel instead of 5-FU at this time point. The tumor volume growth rate of the control group increased significantly on the 6th day after chemotherapy (from 8.6% to 16.1%), and the control group used paclitaxel instead of 5-FU chemotherapy at this time point. The observed end point was on the 18th day after chemotherapy. The tumor load of the experimental group [(1.82±0.09) cm 3] was lower than that of the control group [(2.01±0.09) cm 3], and the difference was statistically significant ( t=2.25, P=0.033). On the 16th day after chemotherapy in the experimental group and the 18th day after chemotherapy in the control group, the time of paclitaxel administration in both groups was 12 days. The tumor load in the experimental group [(1.61±0.12) cm 3] was also lower than that in the control group [(2.01±0.09) cm 3], and the difference was statistically significant ( t=2.03, P=0.040). Conclusions:For the subcutaneous transplantation model of 5-FU resistant gastric cancer mice, according to the early changes of tumor ADC value after chemotherapy, the replacement of chemotherapy drugs can obtain a lower tumor load, suggesting that it is a feasible method to optimize the chemotherapy regimen.