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In order to enhance the surface biocompatibility of hydrophobic acrylic intraocular lenses (IOLs), the anterior surface was modified through graft polymerization with methacryloyloxyethyl phosphorylcholine (MPC) initiated by ultraviolet radiation. Chemical changes on the IOL surface were characterised by X-ray photoelectron spectroscopy (XPS) to confirm the covalent binding of MPC. Field emission scanning electron microscopy (FESEM) and atomic force microscopy (AFM) analysis were used to characterise the morphological changes to the IOL surface. Static water contact angle (WCA) measurements showed that the hydrophilicity of the anterior surface was enhanced after grafting with MPC. The surface biocompatibility of the untreated and Anterior UV-MPC IOLs was compared with the adhesion behaviour of macrophages in vitro. The degree of posterior capsule opacification (PCO) of untreated, anterior treated, and posterior treated IOLs was evaluated by observing the behaviour of lens epithelial cells (LECs) between the IOL optic portion and type IV collagen. Results suggest that the MPC modified anterior surface resisted the attachment of macrophages. However, MPC grafted onto the posterior surface enhanced the migration of LECs between the IOL optic and type IV collagen, which may result in severe PCO. In conclusion, our Anterior UV-MPC IOLs may reduce postoperative inflammation while maintaining the low PCO rates of hydrophobic acrylic IOLs.

Purpose To compare the levels of inflammatory molecules in tear samples between patients with meibomian gland dysfunction (MGD)-related evaporative dry eye (EDE) and healthy subjects and to analyze the correlations between the levels of tear inflammatory molecules and ocular surface parameters. Methods A total of 30 MGD-related EDE patients (48 eyes) and ten healthy volunteers (15 eyes) were enrolled. Dry eye-related examinations and questionnaires were obtained from all participants. The levels of nine inflammatory molecules were determined through multiplex bead analysis. Results Inflammatory molecules including ICAM-1, IFN-γ, CXCL8/IL-8, IL-6, TNF-α and IL-12p70 were detected in 100% of the patients, while IL-1α, IL-1β and IL-10 were detected in 56.25%, 13.60% and 45.83% of the patients, respectively. Moreover, ICAM-1, IL-8, IL-6, TNF-α, IL-12p70 and IFN-γ were detected in 86.67–100% of the healthy subjects, and the detection rates of IL-10, IL-1α and IL-1β were below 50%. The levels of IL-8, IL-6, IFN-γ and ICAM-1 were significantly higher in the patient group compared with the control group. In addition, IL-8 and IL-6 were negatively correlated with Schirmer I test. Besides, IFN-γ was negatively correlated with tear film breakup time. Furthermore, ICAM-1 and IL-6 were positively correlated with meibography score. Conclusions Collectively, patients with MGD-related EDE had higher levels of inflammatory molecules in their tears, and some molecules were correlated with ocular surface parameters. These findings suggested that inflammation played an important role in MGD-related EDE, and several inflammatory molecules could be used in the diagnosis and the treatment of MGD-related EDE.

Purpose Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown antifibrotic effects on several diseases. The aims of the present in vitro study were to investigate the antifibrotic effects of bromfenac (a kind of NSAID) on primary human pterygium fibroblasts (HPFs) and primary human conjunctival fibroblasts (HConFs), as well as to explore the possible mechanisms of these effects. Methods The cells used in this study were primary HPFs and HConFs, and profibrotic activation was induced by transforming growth factor-beta1 (TGF-β1). Western blot, quantitative real-time PCR, and immunofluorescence (IF) assays were used to detect the effects of TGF-β1 and bromfenac on the synthesis of fibronectin (FN), type III collagen (COL3), and alpha-smooth muscle actin (α-SMA) in HPFs and HConFs; the changes of signaling pathways were detected by Western blot; cell migration ability was detected by wound healing assay; cell proliferation ability was detected by CCK-8 assay; and pharmaceutical inhibitions of the downstream signaling pathways of TGF-β1 were used to assess their possible associations with the effects of bromfenac. Results Bromfenac suppressed the TGF-β1-induced protein expression of FN (0.59 ± 0.07 folds, P = 0.008), COL3 (0.48 ± 0.08 folds, P = 0.001), and α-SMA (0.61 ± 0.03 folds, P = 0.008) in HPFs. Bromfenac also attenuated TGF-β1-induced cell migration (0.30 ± 0.07 folds, P < 0.001), cell proliferation (0.64 ± 0.03 folds, P = 0.002) and the expression levels of p-AKT (0.66 ± 0.08 folds, P = 0.032), p-ERK1/2 (0.69 ± 0.11 folds, P = 0.003), and p-GSK-3β-S9 (0.65 ± 0.10 folds, P = 0.002) in HPFs. PI3K/AKT inhibitor (wortmannin) and MEK/ERK inhibitor (U0126) reduced the TGF-β1-induced synthesis of FN, COL3, and α-SMA in HPFs. All the results were similar in HConFs. Conclusions Bromfenac protects against TGF-β1-induced synthesis of FN, α-SMA, and COL3 in HPFs and HConFs at least in part by inactivating the AKT and ERK pathways.

Purpose To evaluate the relationship between gout and age-related cataracts (ARCs). Methods A comprehensive literature search of the PubMed and Web of Science databases was conducted to identify papers on the association between gout and cataract risk that had been published between February 1991 and January 2017. Pooled relative risks (RRs) or odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were calculated. The random-effects model was used instead of the fixed-effects model when heterogeneity was identified, as indicated by a Cochran’s Q statistic P-value 50%. Results A total of 3 cross-sectional studies and 3 case-control studies were included in the meta-analysis. Gout was significantly associated with increased odds of ARCs (OR 1.53, 95% CI 1.27–1.84). In the subgroup analysis, gout exhibited positive associations with the odds of posterior subcapsular cataracts (PSCs, OR 1.69, 95% CI: 1.06–2.70) and cortical cataracts (CCs, OR 1.39, 95% CI: 1.06–1.81). However, no association was identified between gout and the odds of nuclear cataracts. Conclusions The current literature suggested that gout may be associated with increased odds of ARCs, especially PSCs and CCs. Further efforts should be made to confirm these findings and clarify the effect of gout and gout medications on the development of cataracts.