Phacoemulsification with or without goniosynechialysis for angle-closure glaucoma: a global Meta-analysis based on randomized controlled trials.

AIM: To compare the benefits and potential harms of routine phacoemulsification (phaco) alone and combined surgery with goniosynechialysis (GSL) for angle-closure glaucoma (ACG) and coexisting lens opacity, as shown in different randomized controlled trials (RCTs). METHODS: A systematic review was conducted searching several databases including PubMed, Cochrane Library, EMBASE, ClinicalTrials.gov from the inception to September 2018 for RCTs with data published on the effects and safety of phaco and intraocular lens implantation combined with GSL or routine cataract surgery alone. Several studies were recruited which reported data at baselines and postoperative follow-up, including the mean values of postoperative intraocular pressure (IOP) and mean numbers of anti-glaucoma medications using postoperatively. The numbers of complications happening were also included. Fixed-effect and random-effect models were applied, and the quality of evidence was evaluated. RESULTS: Analysis of the seven included RCTs, with a total number of 321 participants (358 eyes) diagnosed with ACG and cataract, received a solo procedure (phaco group) or a combined surgery (phaco-GSL group) randomly, and follow-up periods ranging from 2 to 12mo postoperatively. The involved studies showed that the mean value of IOP between the two groups at 3 (four studies, one study follow-up at 2mo postoperative was included), 6, 12mo postoperative were not significantly different. Only two studies reported the change in IOP value at 12mo compared with baseline but showed no significant differences between the two interventions. Although three studies did not have the significant difference in the number of medications using to reduce IOP at 3mo postoperatively, two studies reported that the participants using fewer anti-glaucoma medications at 12mo postoperative in the phaco group than in the phaco-GSL surgery group. CONCLUSION: The analysis provides a low to moderate-quality evidence that phaco-GSL surgery lead to an equivalent IOP-lowering effect. The phaco-GSL surgery may not help patients to reduce the consumption of anti-glaucoma eyedrops in the long period. The results of this analysis suggested that additional GSL may not be necessary for primary angle closure glaucoma (PACG) patients. Further studies, especially RCTs with more participants and longer follow-up time were needed to provide more sufficient data.

LncRNA-MALAT1 promotes neovascularization in diabetic retinopathy through regulating miR-125b/VE-cadherin axis.

Background: Diabetic retinopathy (DR) is currently the leading cause of blindness and visual disability in adults with diabetes mellitus (DM). Neovascularization has been identified as an important clinical property in DR, however, the exact mechanisms in DR neovascularization are still unclear and need further elucidation.Methods: Quantitative real-time PCR (qRT-PCR) was conducted to detect the expression level of long non-coding RNA (lncRNA)-metastasis associated lung adenocarcinoma transcript 1 (MALAT1), miR-125b and vascular endothelial-cadherin (VE-cadherin) in human retina microvascular endothelial cells (hRMECs) treated with high glucose (HG). Luciferase assay was used to detect interaction of MALAT1 with miR-125b and miR-125b with VE-cadherin. MTT assay, transwell assay, tube formation assay and vascular permeability assay were conducted to detect the cell viability, migration tube formation ability and permeability of hRMECs, respectively. ELISA was used to examine the release of VE-cadherin and vascular endothelial growth factor (VEGF). Western blotting was used to access the protein expression of VE-cadherin, VEGF, ß-catenin, matrix metalloproteinase (MMP) 2 (MMP2) and MMP9.Results: MALAT1 and VE-cadherin were up-regulated while miR-125b was down-regulated in hRMECs treated with HG. MALAT1 could competitively bind to miR-125b against VE-cadherin at the site of 3'-untranslated region (3'-UTR), leading to the up-regulation of VE-cadherin. Knockdown of MALAT1 inhibited the proliferation, migration, tube formation and vascular permeability of hRMECs induced by HG through up-regulating miR-125b. Furthermore, we found the deletion of MALAT1 suppressed the VE-cadherin/ß-catenin complex and neovascularization related proteins expression, which was up-regulated by HG.Conclusion: Knockdown of MALAT1 inhibited cell proliferation, migration and angiogenesis of hRMECs via suppressing the VE-cadherin/ß-catenin complex through targeting miR-125b. Inhibition of MALAT1 may serve as a potential target for anti-angiogenic therapy for DR.

Attenuation of periostin in retinal Müller glia by TNF-α and IFN-γ.

AIM: To investigate the regulation and mechanisms of periostin expression in retinal Müller glia, and to explore the relevance to retinal neovascularization. METHODS: The oxygen-induced retinopathy (OIR) mouse model and the human Moorfield/Institute of Ophthalmology-Müller 1 (MIO-M1) cell line were used in the study. Immunofluorescence staining was used to determine the distribution and expression of periostin and a Müller glial cell marker glutamine synthetase (GS). Cytokines TNF-α and IFN-γ were added to stimulate the MIO-M1 cells. ShRNA was used to knockdown periostin expression in MIO-M1 cells. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was conducted to assess the mRNA expression of periostin. RESULTS: Immunofluorescence staining showed that periostin was expressed by MIO-M1 Müller glia. GS-positive Müller glia and periostin increased in OIR retinas, and were partially overlaid. The stimulation of TNF-α and IFN-γ reduced the mRNA expression of periostin significantly and dose-dependently in MIO-M1 cells. Knockdown of periostin reduced mRNA expression of vascular endothelial growth factor A (VEGFA) in MIO-M1 cells, while VEGFA expression was not changed in periostin knock-out OIR retinas. CONCLUSION: Müller glia could be one of the main sources of periostin in the retina, and might contribute to the pathogenesis of retinal neovascularization. Proinflammatory cytokines TNF-α and IFN-γ attenuate the periostin expression in retinal Müller glia, which provides a potential and novel method in treating retinal neovascular diseases.

Clinical application of accommodating intraocular lens.

The present review describes recent advances in application of accommodating intraocular lenses (AIOLs). Standard monofocal intraocular lenses (MIOLs) only correct distance vision, while AIOLs are designed to allow both good distance vision and near vision, which is achieved through the contraction and relaxation of ciliary muscles by providing transformation of the axial movement or curvature of the lens. Thus, AIOLs may be a better choice for those patients who demand a higher level of visual performance. Since techniques to analyze the performance of AIOLs have not been standardized, and there is a variety of both subjective and objective methods, it is hard to measure the performance of these intraocular lenses. By evaluating advantages and disadvantages of various AIOLs, and introducing techniques for measurement the performance postoperative, this paper can provide some relative information on choosing the type of AIOLs in the clinic.

New options for uveitis treatment.

Uveitis is one of the most important causes of blindness worldwide. Its etiology and pathogenesis are complicated and have not been well understood. The treatment for uveitis is predominantly based on steroids and immunosuppressants. However, systemic side effects limit their clinical application. With the advancement of molecular biology, some intravitreal implants and biologic agents have been used for the treatment of uveitis. Additionally, novel techniques such as gene therapy and RNA interference are being studied for using as uveitis therapy. This paper reviews recent advances in uveitis treatment.

Alpha lipoic acid protects lens from H(2)O(2)-induced cataract by inhibiting apoptosis of lens epithelial cells and inducing activation of anti-oxidative enzymes.

OBJECTIVE: To determine whether alpha lipoic acid (LA) can effectively protect lenses from hydrogen peroxide (H2O2)-induced cataract. METHODS: Lens from adult Sprague-Dawley rats were cultured in 24-well plates and treated without or with 0.2 mM of H2O2, 0.2 mM of H2O2 plus 0.5 mM, 1.0 mM, or 2.0 mM of LA for 24 h. Cataract was assessed using cross line grey scale measurement. Superoxide dismutase (SOD), glutathione (GSH-Px), lactate dehydrogenase (LDH), and malondialdehyde (MDA) activity or level in lens homogenates was measured. Apoptosis of lens epithelial cells in each group were detected by Terminal Deoxynucleotidyl Transferase dUTP Nick End Labeling (TUNEL) Assay. RESULTS: A total of 0.2 mM of H2O2 induced obvious cataract formation and apoptosis in lens' epithelial cells, but 0.5-2.0 mM of LA could block the effect of 0.2 mM H2O2 in inducing cataract and apoptosis. Furthermore, 0.2 mM of H2O2 significantly decreased SOD, GSH-Px, and LDH activity and significant increased MDA level in the lens, but 0.5-2.0 mM of LA blocked the effect of 0.2 mM H2O2. One mM of LA was found to be the most effective. CONCLUSIONS: LA can protect lens from H2O2-induced cataract. LA exerts protective effects through inhibition of lens' epithelial cell apoptosis and activation of anti-oxidative enzymes.

Selective laser trabeculoplasty.

The introduction of selective laser trabeculoplasty (SLT) provided a new choice for the reduction of intraocular pressure (IOP) in eyes with open angle glaucoma (OAG) and ocular hypertension (OHT). SLT was demonstrated equally as effective as topical medical therapy and argon laser trabeculoplasty (ALT) to lower IOP. It is a potentially repeatable procedure because of the lack of coagulation damage to the trabecular meshwork (TM) and also effect in patients with previously failed ALT. SLT can be used to treat patients with OAG, pseudoexfoliation glaucoma, pigmentary glaucoma, normal-tension glaucoma, OHT, juvenile glaucoma, pseudophakic and aphakic glaucoma. Furthermore, SLT can be considered as a primary treatment option in patients who cannot tolerate or are noncompliant with medications, while not interfering with the success of future surgery. Its safety profiles include mild and transient inflammation, ocular pain and a small risk of moderate IOP elevations after the procedure. SLT is a safe and effective means of IOP reduction in eyes with OAG and OHT.

Descemet membrane detachment after trabeculectomy.

Descemet's membrane detachment (DMD) can be a potentially serious complication of intraocular surgery or ocular trauma. The cause is not very clear. We are trying to remind an awareness of the spectrum of DMD resulting from trabeculectomy by presenting a case of extensive DMD after trabeculectomy which was successfully repaired.

Involvement of the PI3K/Akt signaling pathway in platelet-derived growth factor-induced migration of human lens epithelial cells.

PURPOSE: Posterior capsular opacification (PCO) is caused partially by the migration of lens epithelial cells. To date, the mechanism of the migration is largely unknown. The purpose of this study was to investigate the effect of platelet-derived growth factor (PDGF)-triggered signaling pathways and its downstream effectors in the migration of lens epithelial cells. METHODS: In vitro scratch-wound healing and transwell migration assays were used to measure the migration of lens epithelial cells. The activation of PDGFR beta, phosphatidylinositol 3-kinas (PI3K)/protein kinase B (Akt) and mitogen activation protein kinase (MAPK) pathways, the impact of PDGF stimulation on the expression of cell protrusion molecules, and the stabilization of beta-catenin were measured by western blotting. The translocation of beta-catenin was detected using indirect immunofluorescence. RESULTS: PDGF was found to enhance cell migration, which depended on the PI3K/Akt pathway. The activation of the PI3K/Akt pathway by the PDGF/PDGFR beta axis induced the up regulation of cell protrusion molecules and stabilization and translocation of beta-catenin, contributing to enhanced cell migration. CONCLUSION: Data from this study directly linked the central PI3K/Akt pathway to lens epithelial cell migration and pointed to new avenues for therapeutic intervention in PCO.