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The short-term efficacy of IVTA and IVB on treating clinically significant macular edema varied with different optical coherence tomography findings. In clinically significant macular edema combined with serous retinal detachment, IVTA may be more favorable than IVB in CRT reduction and BCVA improvement. In patients with diffused macular thickening, IVB may be better than IVTA in macular thickness reduction, although this does not translate to a significant improvement in BCVA.

Previous literatures have reported the role of human micro RNA-1284 (hsa-miR-1284, in short miR-1284) in diverse cancers. However, its biological function in osteosarcoma pathogenesis remains unknown. In the present study, we investigated the potential role of miR-1284 in osteosarcoma. Expression of miR-1284 and high mobility group box 1 (HMGB1) were examined in 80 tissues obtained from 40 patients. MiR-1284 level was measured in five osteosarcoma cell lines. Relative luciferase activity and HMGB1 expression were examined in MG-63 and U2OS cells transfected with wild-type or mutant 3′-UTR of HMGB1 in the presence of miR-1284 mimics or miR-NC. Cell viability, colony formation, and cell migration were measured in MG-63, U2OS and hFOB 1.19 cells, which were transfected with miR-1284 mimics or miR-NC. In the rescue experiments, recombinant HMGB1 plasmid was transfected into MG-63 and U2OS cells, and cell viability and migration were determined again. Our results indicated that relative level of miR-1284 was lower in tumor tissues compared with its adjacent tissues and it was found suppressed at lower levels in MG-63 and U2OS cell lines. Expression of HMGB1 is significantly elevated in tumor tissues and negatively correlated with miR-1284 expression. MiR-1284 exerted its function by directly binding to 3′-UTR of HMGB1 and regulates expression of HMGB1. The overexpression of miR-1284 inhibited the cell proliferation and migration, and altered the protein expression of epithelial–mesenchymal transition (EMT)-associated genes (E-cadherin, N-cadherin, Vimentin, and Snail), which was reversed by HMGB1 overexpression. In conclusion, miR-1284 can function as a new regulator to inhibit osteosarcoma cell proliferation and migration by targeting HMGB1.

Despite improvements in the prognosis of osteosarcoma patients, chemotherapy fails in a considerable number of cases due to drug resistance. The development of novel agents may enhance chemosensitivity. This study explored the anticancer function of polydatin and its ability—in combination with paclitaxel—to overcome drug resistance in human osteosarcoma U‐2OS and MG‐63 cell lines. A cell proliferation assay (celll counting kit‐8), a cell‐cycle assay, an apoptosis assay (annexin V‐fluorescein isothiocyanate/propidium iodide), and a cell migration assay (Transwell) were used to analyze cell activity. Western blot analysis and quantitative reverse‐transcription polymerase chain reaction were performed to examine function‐related mRNA and protein levels. Treatment with polydatin suppressed cell growth and migration in both cell lines. Moreover, polydatin induced cell apoptosis in both parental and paclitaxel‐resistant cells, and cell‐cycle arrest in the S phase. Furthermore, it altered the expression of various proteins associated with cell growth (Ki67, p21, cyclin A, cyclin E, and cyclin‐dependent kinase 2), migration (matrix metalloproteinase‐2 [MMP‐2], MMP‐9, and tissue inhibitor of metalloproteinase‐1), apoptosis (poly[ADP‐ribose] polymerase 1 and caspase 3), and drug resistance (p‐glycoprotein 1, lung resistance‐related protein 1, growth arrest and DNA damage‐45α, glutathione S‐transferase π, and heat shock protein 27) in paclitaxel‐resistant osteosarcoma cells. Cells transfected with myr‐Akt caused obvious upregulation and activation of Akt, which were significantly attenuated via polydatin treatment. In conclusion, polydatin may enhance the chemosensitivity of osteosarcoma cells to paclitaxel.

Daylight photodynamic therapy (DLPDT) is a novel therapeutic approach for actinic keratoses (AKs). This study aimed to evaluate the safety and efficacy of DLPDT in treating patients with AKs as compared to conventional photodynamic therapy (CPDT). PubMed, EMBASE, Web of Science, and the Cochrane Central Register of Controlled Trials were searched for relevant randomized controlled trials (RCTs) published before November 2017, based on the following search terms: "solar keratoses", "actinic keratoses", "photodynamic therapy", "daylight photodynamic therapy", "conventional photodynamic therapy", and "randomized". The complete response rate, patient satisfaction, and patient-reported pain after intervention with DLPDT or CPDT were primarily measured. Sensitivity analysis was conducted to determine the reliability of results. Begg's and Egger's tests were used to assess the likelihood of publication bias. Eight RCTs, comprising a total of 424 patients with AKs treated with DLPDT or CPDT, were included. No significant difference was found between the lesion response rate and the mean lesion response in a comparison of DLPDT and CPDT treatments. Generally, DLPDT was associated with higher patient satisfaction than CPDT. The patients who underwent DLPDT experienced less pain than those who underwent CPDT. Most of our results were of high stability and low sensitivity. Meanwhile, no statistical evidence of publication bias among studies was found under all comparisons. In conclusion, DLPDT is a safe and effective therapy, which could help in selecting the most appropriate therapeutic method for treating AKs and in guiding physicians to optimize treatment strategies.

Mechanical ocular trauma could lead to disastrous visual outcomes. There has been a controversy regarding the timing of vitrectomy for such cases. This study aimed to find out the optimal timing of vitrectomy for severe mechanical ocular trauma. Patients with severe mechanical ocular trauma who had undergone vitrectomy were enrolled and followed up for at least 6 months. Clinical data were collected including ocular trauma score (OTS), the timing of vitrectomy upon injury, visual acuity, vitrectomy results, post-operation complications and etc. All cases were classified according to the timing of vitrectomy upon injury into 3 groups: group A 1–7 days, group B 8–14 days, group C more than 14 days. A total of 62 cases were enrolled, including 20 eyes in group A, 25 eyes in group B, and 17 eyes in group C. No significant differences were shown of the gender, age or OTS among the 3 groups. Both functional success rate and visual outcome were optimal in group B, then in group A, and worst in group C. These results suggested that the best timing of vitrectomy for severe mechanical ocular trauma is 8–14 days upon injury; second best is 1–7 days; worst is after 14 days.

calbindin-d28K (calb1) may protect human lens epithelial cells (HLEcs) from apoptosis, which is a process resulting in individual cell death. The protective effects of calb1 may be attributed to buffering high concentrations of ca 2+. The present study investigated the mechanisms through which calb1 protects SRA01/04 cells (a human lens epithelial cell line) against apoptosis induced by ultraviolet B (UVB) exposure. cells transfected with a lentivirus overexpressing calb1 and control cells were treated with 40 µW/cm 2 irradiation for 15 min and then cultured for 24 h. The changes in intracellular ca 2+ were detected by colorimetry, and the protein expression levels of Bad, Bcl-2 and caspase-12 were measured by western blot analysis. The intracellular ca 2+ concentration of control HLECs increased significantly following UVB irradiation, whereas in calb1-overexpressing cells, the ca 2+ levels remained steady. In the control cells, the expression of Bad and caspase-12 was upregulated, and that of Bcl-2 was downregulated. Notably, during UVB radiation-induced apoptosis, the overexpression of calb1 inhibited cell death, resulting in the decreased expression of Bad and caspase-12, and in the upregulated expression of Bcl-2. These results suggested that calb1 inhibited the upregulation of genes involved in apoptosis. The siRNA-mediated knockdown of calb1 resulted in increased rates of UVB radiation-induced apoptosis, the increased expression of Bad and caspase-12, and the decreased expression of Bcl-2, further demonstrating that calb1 may mediate UVB radiation-mediated apoptosis by regulating ca 2+. On the whole, the findings of the present study indicate that UVB exposure can lead to an imbalance in the intracellular ca 2+ homeostasis in HLEcs and that calb1 protein exerts a negative effect on the expression of pro-apoptotic genes in HLEcs. calb1 may thus inhibit the UVB radiation-induced apoptosis of HLEcs by regulating ca 2+ .

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