Both conbercept and ranibizumab are effective choice for the treatment of ROP. Conbercept is a novel effective treatment strategy for ROP providing a new treatment option for ophthalmologists.

BackgroundTo investigate the repeatability of superficial retinal vessel density measurements in healthy eyes with long axial length (AL) using optical coherence tomography angiography (OCTA).MethodsThere were 60 eyes of 31 volunteers enrolled in this cross-sectional observational study. All subjects underwent OCTA, AL and refraction test. The enrolled eyes were divided into the long AL group (26 mm ≤ AL < 28 mm) and normal AL group (22 mm ≤ AL < 26 mm). The vessel length density (VLD), perfusion density (PD), and fovea avascular zone (FAZ) of the superficial retinal vessel were evaluated. Repeatability was assessed by intraclass correlation coefficients (ICCs) and Bland-Altman analysis. Pearson’s r correlation was used to analyze the relation of AL and the absolute difference between two measurements.ResultsThe 3 × 3 mm scan pattern showed good repeatability with all ICCs over 0.7. For all parameters of all scan patterns, the ICCs of the normal AL group were distinctly higher than those of the long AL group; this finding was also confirmed by Bland-Altman analysis. The correlation analysis of AL and repeatability of OCTA parameters showed significant negative correlations between the ALs and repeatability of VLD in 6 × 6 mm inner ring (r2 = 0.13, p = 0.01), VLD in 6 × 6 mm outer ring (r2 = 0.09, p = 0.02) and PD in 6 × 6 mm outer ring (r2 = 0.08, p = 0.03).ConclusionsThe AL and the scanned area will both affect the repeatability of superficial retinal vessel density measurements in OCTA.Electronic supplementary materialThe online version of this article (10.1186/s12886-018-0992-y) contains supplementary material, which is available to authorized users.

Purpose To investigate the role of N6-methyladenosine (m6A) RNA modification in the pathogenesis of Graves' ophthalmopathy (GO). Methods Surgically excised extraocular muscles from 7 patients with GO and 5 subjects without GO were used. The global m6A levels in the specimens were determined using an m6A RNA methylation quantification kit. RNA sequencing (RNA-seq) was used to analyze the molecules involved in the regulation of m6A RNA methylation and the differential expression of mRNAs between the two groups (4 eyes, respectively). The expression of m6A RNA modification genes was evaluated by real-time PCR. The functional implications of the gene alterations between the GO and control specimens were determined by Gene Ontology analysis. Results The m6A level was significantly increased in the specimens of GO patients compared to the control specimens (P < 0.05). The expression of m6A methylation regulators, such as WT1 associated protein (WTAP), alkylation repair homolog protein 5 (ALKBH5), E74 like ETS transcription factor 3 (ELF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTHDF3 and YTH domain containing 2 (YTHDC2), was significantly upregulated (P < 0.05). Gene Ontology enrichment analysis showed that the most highly upregulated genes and biological pathways were related to the immune response and inflammatory processes such as lymphocyte activation, leukocyte differentiation, cytokine production and cytokine-mediated signaling pathways. Conclusions Our results suggest that m6A methylation may play a critical role in the pathogenesis of GO and that targeting genes that regulate m6A methylation may provide a new therapeutic approach for GO.

Pleiotrophin (PTN), a secreted, multifunctional cytokine, is involved in angiogenic, fibrotic and neurodegenerative diseases. However, little is known about its effects on diabetic retinopathy, a neurovascular disease. To investigate the role of PTN in proliferative diabetic retinopathy (PDR), PTN concentration in the vitreous was evaluated in PDR patients and non-diabetic controls. PTN expression was observed in epiretinal membranes from patients. PTN knockdown was performed using small interfering (si)RNA, and the effects on retinal pigment epithelium (RPE) cells and human umbilical vascular endothelia cells (HUVECs) were observed in vitro under hyperglycemic and hypoxic conditions. Cell attachment, proliferation, migration, tube formation, cell cycle, apoptosis, extracellular signal-regulated kinase 1/2 (ERK 1/2) phosphorylation, and VEGF levels were studied. The vitreous PTN concentration in PDR patients was higher than that in non-diabetic controls, and PTN was highly expressed in the fibrovascular membranes of PDR patients. Under hyperglycemic and hypoxic conditions, PTN knockdown reduced cell attachment, proliferation, migration, and tube formation and induced cell cycle arrest and apoptosis in vitro. Mechanically, PTN depletion decreased ERK 1/2 phosphorylation. Recombinant PTN up regulated the concentration of VEGF in vitro, which can be attenuated by the ERK 1/2 inhibitor. Taken together, our results implied that elevated PTN in PDR patients might participate in the critical processes of the development of PDR, most likely playing roles in angiogenesis and proliferation, possibly by activating the ERK 1/2 pathway and regulating VEGF secretion. These findings provide new insight into the roles of PTN in PDR and suggest that PTN may become a new target for therapeutic intervention in PDR.

Conbercept significantly decreased serum VEGF level 1 day and 1 week after injection, but this effect was not sustained for 1 month. In contrast, ranibizumab had no significant effect on serum VEGF concentration changes. The reduction in serum VEGF by conbercept may affect its systemic safety profile.