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Li X.,Peking University | Li X.,Key Laboratory of Vision Loss and Restoration | Hu Y.,Peking University | Sun X.,Shanghai JiaoTong University | And 2 more authors.
Ophthalmology | Year: 2012

Objective: To evaluate 2 different dosing regimens of intravitreal bevacizumab for the treatment of neovascular age-related macular degeneration (AMD) patients in China. Design: Multicenter, randomized, prospective, open-label clinical trial. Participants: One hundred eighty-five patients with active neovascular AMD, exclusion of a macular scar, choroidal neovascularization not resulting from AMD, and polypoidal choroidal vasculopathy. Intervention: Patients were assigned randomly to receive intravitreal injections of bevacizumab every 6 weeks for the first 3 injections followed by injections every 6 weeks (regimen A, n = 91) or every 12 weeks (regimen B, n = 94). Main Outcome Measures: The primary outcome measure was a comparison of the mean change in visual acuity from baseline. The secondary outcome measure was a comparison of the proportion of patients with a change in visual acuity of 15 letters or more. Adverse events were monitored. Results: One-hundred eighty five patients were enrolled. At 48 weeks, the increase in the mean visual acuity measurements from baseline were 12.58 letters in regimen A and 10.06 letters in regimen B (P = 0.288). At 48 weeks, the percentage of eyes losing fewer than 15 letters was 96.2% in regimen A and 93.9% in regimen B (P = 0.720). At 48 weeks, the median decrease in central retinal thickness measurements from baseline was 119 μm in regimen A and 60 μm in regimen B (P = 0.221). Adverse events during the 48 weeks included anterior chamber inflammation in 17 patients (18.7%) from regimen A and 9 patients (9.6%) from regimen B (P = 0.075). There were no other notable ocular adverse events in either group. Conclusions: Intravitreal bevacizumab improved visual acuity and decreased macular thickness in patients with neovascular AMD when dosed either every 6 weeks or every 12 weeks after 3 doses given at 6-week intervals. Although there were no statistically significant differences between the 2 regimens, the results tended to favor the group dosed every 6 weeks (regimen A). Financial Disclosure(s): The author(s) have no proprietary or commercial interest in any materials discussed in this article. © 2012 American Academy of Ophthalmology. Source

Chen W.-C.,Peking University | Chen W.-C.,Key Laboratory of Vision Loss and Restoration | Wang Y.,Tianjin Medical University | Li X.-X.,Peking University | Li X.-X.,Key Laboratory of Vision Loss and Restoration
Retina | Year: 2012

PURPOSE: To evaluate photoreceptor inner/outer segment (IS/OS) defects, best-corrected visual acuity (BCVA), macular sensitivity, and fixation stability to correlate morphologic changes with visual functional outcomes at different stages after macular hole surgery using spectral-domain optical coherence tomography combined with microperimetry. METHODS: This study was an interventional, retrospective case series. Sixteen eyes of 16 patients with successfully operated idiopathic full-thickness macular holes were included in this study. The IS/OS defect maximal diameter and area, BCVA, central macular sensitivity, mean macular sensitivity, and fixation stability were measured using spectral-domain optical coherence tomography combined with microperimetry, preoperatively, and with a follow-up of 3 months postoperatively. RESULTS: Both the IS/OS defect diameter and area improved after successful macular hole surgery (P < 0.001; P < 0.001). The BCVA, central macular sensitivity, mean macular sensitivity, and fixation stability of the central 2° also improved (P = 0.001; P = 0.004; P = 0.036; P = 0.031). Stable BCVA improvement was achieved as early as 1-month postoperation despite continuous repair of the IS/OS junction defect diameter and area and improvement in fixation and macular sensitivity within the first 3 months after surgery. The postoperative central macular sensitivity and mean macular sensitivity negatively correlated with preoperative linear IS/OS junction defect diameter (P = 0.033; P = 0.006) and the defect area (P < 0.001; P = 0.002). However, the postoperative BCVA and the improvement in BCVA, macular sensitivity, and fixation stability were not correlated with preoperative IS/OS defect diameter or area. CONCLUSION: Continuous anatomical and functional improvements can be observed after successful microinvasive macular hole surgery. The preoperative extent of the IS/OS junction defect is of good predictive value for postoperative macular sensitivity. However, the factors that influence BCVA are multiple. Prediction of BCVA based on a single anatomical parameter or assessment of macular function only based on BCVA should be avoided. © Lippincott Williams & Wilkins. Source

Qin D.,Peking University | Qin D.,Key Laboratory of Vision Loss and Restoration | Zheng X.-X.,Peking University | Jiang Y.-R.,Peking University | Jiang Y.-R.,Key Laboratory of Vision Loss and Restoration
Molecular Vision | Year: 2013

Purpose: Our previous study showed that apelin was increased in the vitreous and fibrotic membranes of patients with proliferative diabetic retinopathy (PDR) in vivo, which suggested that apelin may be involved in the development of PDR. In this study, we investigated whether the expression of apelin was upregulated in human retinal pigment epithelial (RPE) cells in vitro under high glucose conditions. Furthermore, to explore the role of apelin in RPE cells, we investigated the effect of exogenous recombinant apelin on proliferation, migration, and collagen I (a major component of extracellular matrix molecules, associated with PDR) expression and investigated the signaling pathways involved in these processes. Methods: Real-time PCR and western blot were performed to determine the apelin expression in ARPE-19 cells under high glucose conditions. Exogenous recombinant apelin was used to study the effect of apelin on ARPE-19 cells in vitro. Cell proliferation, migration, and collagen I expression were assessed using an MTT assay, a transwell assay, and real-time PCR analysis. LY294002 (an inhibitor of phosphatidylinositol 3-kinase) and PD98059 (an inhibitor of mitogen-activated protein kinase) were used to help to determine the apelin signaling mechanism. Results: High glucose upregulated apelin expression in RPE cells. Exogenous recombinant apelin activated protein kinase B (Akt) and extracellular signal-regulated kinase (Erk) phosphorylation and promoted proliferation, migration, and collagen I expression in RPE cells. Pretreatment with LY294002 and PD98059 abolished apelin-induced activation of Akt and Erk, proliferation, and collagen I expression. Apelin-induced migration was partially blocked by pretreatment with LY294002 and PD98059. Conclusions: The expression of apelin was upregulated under high glucose conditions in RPE cells in vitro. Exogenous recombinant apelin increased the biologic activity of RPE cells, as well as the expression of collagen I. Apelin promoted proliferation, migration, and collagen I expression through the PI3K/Akt and MEK/Erk signaling pathways in RPE cells. From these results, we revealed the role of apelin in regulating proliferation, migration, and collagen I expression in RPE cells and the signaling mechanism under these processes, which suggested that apelin may play a profibrotic role in the development of PDR. © 2013 Molecular Vision. Source

Tian J.,Peking University | Yu W.,Key Laboratory of Vision Loss and Restoration | Qin X.,Peking University | Fang K.,Peking University | And 8 more authors.
Investigative Ophthalmology and Visual Science | Year: 2012

PURPOSE. We explored associations between age-related macular degeneration (AMD) and genetic variants of 10 genes in a nationwide Chinese population. METHODS. In this multicenter case-control study, 535 AMD patients and 469 controls were recruited from 16 centers that spread from the north to the south of China. All participants underwent comprehensive eye examinations, and 40 single nucleotide polymorphisms (SNPs) of 10 genes were selected. DNA samples were genotyped with the MassArray system. The effect of the genotypes and haplotypes on AMD was assessed with logistic regression analysis, adjusted for age, sex, longterm residence, and family origin. RESULTS. In our study, 11 SNPs in complement H (CFH), 2 in age-related maculopathy susceptibility 2 (ARMS2), and 2 in high-temperature requirement factor A1 (HTRA1) were associated significantly with AMD. They were rs551397, rs800292, rs1329424, rs1061170, rs10801555, rs12124794, rs10733086, rs10737680, rs2274700, rs1410996, and rs380390 in CFH; rs10490924 and rs2736912 in ARMS2; and rs11200638 and rs3793917 in HTRA1. Three haplotypes in CFH, predisposed the patients significantly to AMD (P < 0.001, P = 0.001, and P < 0.001, respectively). With the sample size of our study, no relationship was found for AMD and the SNPs tested in complement 3 (C3); serpin peptidase inhibitor, clade G, member 1 (SERPING1); vascular endothelial growth factor (VEGF); cholesterol ester transfer protein (CETP); lipoprotein lipase (LPL); hepatic lipase (LIPC); and metallopeptidase inhibitor 3 (TIMP3) genes. CONCLUSIONS. Gene variants in CFH, ARMS2, and HTRA1 contribute to AMD in the Chinese population. © 2012 The Association for Research in Vision and Ophthalmology, Inc. Source

Zhou P.,Peking University | Zhou P.,Key Laboratory of Vision Loss and Restoration | Zhou P.,Fudan University | Fan L.,Fudan University | And 5 more authors.
FASEB Journal | Year: 2011

The genetic association between a variant in the Toll-like receptor 3 (TLR3) gene (C1234T in mRNA, L412F in protein, Reference SNP Cluster Report rs3775291) and geographic atrophy (GA; also called advanced "dry" age-related macular degeneration) was controversial in previous studies. We performed a meta-analysis by pooling the current evidence in literature and found that the T allele of the TLR3 C1234T variant showed a summary odds ratio of 0.753 (95% confidence interval: 0.612-0.927; P=0.007). Further experiments were performed to analyze how this mutant influences the function of TLR3. We found that this SNP did not affect mRNA, protein, or surface expression of TLR3. However, the binding capacity of L412F mutation of TLR3 for double-stranded RNA in the TLR3 protein was only 51.12 ± 3.96% (P<0.001) of the wild-type level. There was a consistently reduced TLR3-mediated NF-κB activation. Therefore, TLR3 C1234T (L412F in the protein) may protect against GA by reduced binding capacity of TLR3 to dsRNA. This study may provide a better understanding of the genetic architecture underlying disease susceptibility and may advance the potential for preclinical prediction in future genetic testing. © FASEB. Source

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