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PURPOSE: To assess the effectiveness and safety of repeated low-level red light (RLRL), which is a newly available treatment for myopia control in children and adolescents with high myopia. DESIGN: Multicenter, randomized, parallel-group, single-blind clinical trial (randomized controlled trial; NCT05184621). PARTICIPANTS: Between February 2021 and April 2022, 192 children aged 6 to 16 years were enrolled. Each child had at least 1 eye with myopia of cycloplegic spherical equivalent refraction (SER) at least -4.0 diopters (D), astigmatism of ≤2.0 D, anisometropia of ≤3.0 D, and best-corrected visual acuity (BCVA) of 0.2 logarithm of the minimum angle of resolution or better. Follow-up was completed by April 2023. METHODS: Participants were randomly assigned at a 1:1 ratio to intervention (RLRL treatment plus single-vision spectacles) or control (single-vision spectacles) groups. The RLRL treatment was administered for 3 minutes per session, twice daily with a minimum interval of 4 hours, 7 days per week. MEAN OUTCOME MEASURES: The primary outcome and key secondary outcome were changes in axial length (AL) and cycloplegic SER measured at baseline and the 12-month follow-up visit. Participants who had at least 1 postrandomization follow-up visit were analyzed for treatment efficacy. RESULTS: Among 192 randomized participants, 188 (97.91%) were included in the analyses (96 in the RLRL group and 92 in the control group). After 12 months, the adjusted mean change in AL was -0.06 mm (95% confidence interval [CI], -0.10 to -0.02 mm) and 0.34 mm (95% CI, 0.30 to 0.39 mm) in the intervention and control groups, respectively. A total of 48 participants (53.3%) in the intervention group were still experiencing axial shortening >0.05 mm at the 12-month follow-up. The mean SER change after 12 months was 0.11 D (95% CI, 0.02to 0.19 D) and -0.75 D (95% CI, -0.88 to -0.62 D) in the intervention and control groups, respectively. CONCLUSIONS: Repeated low-level red light demonstrates stronger treatment efficacy among those with high myopia, with 53.3% experiencing substantial axial shortening. Repeated low-level red light provides an excellent solution for the management of high myopia progression, a significant challenge in ophthalmology practice. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.
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BACKGROUND: Although the current role of cytokines and neuroinflammation in glaucoma remains obscure, it represents an expanding field in research. The purpose of this study was to analyze cytokines in the aqueous humor (AH) of glaucoma patients and in retinas from an ex vivo glaucoma animal model, to aid in determining the role of neuroinflammation in glaucoma. METHODS: AH samples were collected from 20 patients during cataract surgeries (controls: n = 10, age = 70.3 ± 9.742; glaucoma: n = 10, age: 66.5 ± 8.073) in Shanghai East Hospital, an affiliate of Tongji University, between September 2018 and March 2019 and analyzed in duplicate by Luminex cytokine polystyrene color bead-based multiplex assay. Retinas from female Sprague-Dawley rats (n = 6) were harvested ex vivo and cultured with or without 60 mmHg of hydrostatic pressure for 24 hours. Retinal ganglion cells (RGCs) were quantified using Brn3a staining. Cytokines in the retina and culture medium were analyzed by rat cytokine array (Abcam). RESULTS: At baseline, patients with primary angle closure glaucoma (PACG) have significantly lower levels of IL-6 and IP-10 and a higher level of PDGF-BB in their AH, compared to the controls. Postoperatively, patients with PACG have significantly higher levels of IL-1ra, IL-13, and MIP-1α and a lower level of IL-6. Elevated hydrostatic pressure led to significant RGC loss in the retina, ex vivo, as well as the upregulation of ciliary neurotrophic factor (CNTF), IL-6, IL-10, IL-4, and TIMP-1 alongside the downregulation of PDGF-AA, MMP-8, TNF-α, and IFN-γ. Furthermore, eight cytokines were detected as being downregulated in the culture medium, including PDGF-AA, MMP-8, and IL-4. CONCLUSIONS: Proinflammatory cytokines showed changes in both AH and ex vivo. Further studies are needed on the role of these cytokines and their corresponding signaling pathways in both neurodegeneration and glaucoma.
Subject(s)
Glaucoma, Open-Angle , Glaucoma , Humans , Female , Rats , Animals , Middle Aged , Aged , Aged, 80 and over , Interleukin-6/metabolism , Aqueous Humor/metabolism , Neuroinflammatory Diseases , Interleukin-4/metabolism , Matrix Metalloproteinase 8/metabolism , Glaucoma, Open-Angle/metabolism , Glaucoma, Open-Angle/surgery , Rats, Sprague-Dawley , China , Glaucoma/metabolism , Cytokines/metabolism , Models, Animal , RetinaABSTRACT
Many cases of blindness are caused by age-related cataracts (ARCs). N6-methyladenosine (m6A)-modified circRNA widely participates in disease progression. However, the role of m6A modification of circRNA in ARC is unclear. We mined and elucidated the functions and mechanisms of key circRNAs with m6A modification involved in ARC progression. The GSE153722 dataset was used to mine m6A-mediated key circRNA. Loss-of-function assays and rescue assays were used to explore the effect and mechanism of circRNA on ARC cell proliferation and apoptosis. Has_circ_0007905 was a hypermethylated and upregulated expression in the ARC group relative to the control group both in vivo and in vitro. Silencing of has_circ_0007905 promoted proliferation and inhibited the apoptosis of HLE-B3 cells. METTL3 was upregulated in HLE-B3 cells after ARC modeling and had four binding sites with has_circ_0007905 and a mediated m6A modification of has_circ_0007905. Proliferation was significantly inhibited and apoptosis of HLE-B3 cells was facilitated by METTL3 overexpression, whereas these effects were prevented by has_circ_0007905 silencing. Silencing of has_circ_0007905 led to an alteration in the transcriptome landscape. Differentially expressed genes were mainly involved in immune-related processes and pathways. EIF4EBP1 overexpression promoted apoptosis and suppressed proliferation, and also significantly reversed effects of has_circ_0007905 silencing. Moreover, miR-6749-3p significantly decreased the luciferase activities of wild type plasmids with both of has_circ_0007905 and EIF4EBP1. MiR-6749-3p inhibitor blocked elevation in proliferation and reduced EIF4EBP1 expression and apoptosis conferred by has_circ_0007905 silencing. We reveal for the first time that the commitment of ARC progression is guided by METTL3/has_circ_0007905/miR-6749-3p/EIF4EBP1 axis, and the results provide new insights into ARC pathology.
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MicroRNAs , RNA, Circular , Apoptosis , Adenosine , Binding SitesABSTRACT
Pterygium and primary Sjögren's Syndrome (pSS) share many similarities in clinical symptoms and ocular pathophysiological changes, but their etiology is unclear. To identify the potential genes and pathways related to immunity, two published datasets, GSE2513 containing pterygium information and GSE176510 containing pSS information, were selected from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) of pterygium or pSS patients compared with healthy control conjunctiva, and the common DEGs between them were analyzed. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted for common DEGs. The protein-protein interaction (PPI) network was constructed using the STRING database to find the hub genes, which were verified in clinical samples. There were 14 co-upregulated DEGs. The GO and KEGG analyses showed that these common DEGs were enriched in pathways correlated with virus infection, antigen processing and presentation, nuclear factor-kappa B (NF-κB) and Th17 cell differentiation. The hub genes (IL1R1, ICAM1, IRAK1, S100A9, and S100A8) were selected by PPI construction. In the era of the COVID-19 epidemic, the relationship between virus infection, vaccination, and the incidence of pSS and pterygium growth deserves more attention.
Subject(s)
COVID-19 , Pterygium , Sjogren's Syndrome , Humans , Gene Expression Profiling , Pterygium/genetics , Sjogren's Syndrome/genetics , Conjunctiva , Computational Biology , Gene Regulatory NetworksABSTRACT
INTRODUCTION: This study aimed to evaluate the effect of pre-operative versus pre-operative plus post-operative intravitreal conbercept (IVC) injection on severe proliferative diabetic retinopathy (PDR). METHODS: This was a prospective, comparative and randomised study. A total of 84 patients who underwent vitrectomy for severe PDR were included in this study. Patients were randomly divided into control (41 eyes) and experiment (43 eyes) groups. Patients in the experiment group received adjunctive pre-operative and post-operative IVC injection, whereas patients in the control group only received pre-operative IVC injection. The incidence of post-operative vitreous haemorrhage (POVH), best-corrected visual acuity (BCVA) and central retinal thickness (CRT) were determined. RESULTS: The incidence of early POVH was significantly different between the two groups, but no significant difference was observed between groups at 3 and 6 months. In the experiment group, the BCVA was significantly improved 1 month after surgery when compared with the control group (p 0.019). There was no marked difference in the mean post-operative BCVA at 3 and 6 months between groups (p 0.063 and 0.082). CRT was significantly lower in the experiment group than in the control group at 1 and 3 months after surgery (p 0.037 and 0.041), but there was no significant difference at 6 months (p 0.894). CONCLUSION: Additional IVC injected at the end of surgery improves the POVH and BCVA at the early stage after surgery in severe PDR, but this benefit is absent at 6 months. Further studies are needed to investigate the effect of IVC at the end of vitrectomy. TRIAL REGISTRATION: chictr.org.cn identifier: ChiCTR2200060735. Retrospectively registered, register date: 9 June 2022.
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To study the biological functions and applications of human amniotic epithelial cell-derived extracellular vesicles (hAEC-EVs), the cargos of hAEC-EVs were analyzed using miRNA sequencing and proteomics analysis. The hAECs and hAEC-EVs in this study had specific characteristics. Multi-omics analyses showed that extracellular matrix (ECM) reorganization, inhibition of excessive myofibroblasts, and promotion of target cell adhesion to the ECM were their primary functions. We evaluated the application of hAEC-EVs for corneal alkali burn healing in rabbits and elucidated the fundamental mechanisms. Slit-lamp images revealed that corneal alkali burns induced central epithelial loss, stromal haze, iris, and pupil obscurity in rabbits. Slit-lamp examination and histological findings indicated that hAEC-EVs facilitated re-epithelialization of the cornea after alkali burns, reduced scar formation and promoted the restoration of corneal tissue transparency. Significantly fewer α-SMA-positive myofibroblasts were observed in the hAEC-EV-treated group than the PBS group. HAEC-EVs effectively promoted the proliferation and migration of hCECs and hCSCs in vitro and activated the focal adhesion signaling pathway. We demonstrated that hAEC-EVs were excellent cell-free candidates for the treatment of ECM lesion-based diseases, including corneal alkali burns. HAEC-EVs promoted ECM reorganization and cell adhesion of target tissues or cells via orderly activation of the focal adhesion signaling pathway.
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BACKGROUND: Bilateral sequential cataract surgery within a short period is becoming more prevalent because of the efficiency and safety of modern cataract surgery. It has been reported that the first surgical eye might affect the contralateral eye. This study investigated the cytokines involved in the immunopathogenesis of pre-existing ocular or systemic conditions, as well as the inflammatory biomarkers in response to topical stimuli, by analyzing the cytokine profile of aqueous humor (AH) from cataract patients without these morbidities as control and with type 2 diabetes mellitus (DM), primary angle-closure glaucoma (PACG) or high myopia (HM) in each eye at the beginning of first (defined as baseline) and second eye cataract surgery. METHODS: Forty patients were recruited in this cohort study (10/group). Bilateral sequential cataract surgeries were conducted at intervals of 12.08 ± 1.2 days. Aqueous humor samples (100-200 µL/eye) were separately collected from 40 first-eyes and 40 second-eyes at the beginning of the cataract surgeries. Twenty-seven selected cytokines were detected with Luminex-multiplex immunoassay. The concentrations of cytokines in the aqueous humor and their association with pre-existing ocular or systemic conditions were analyzed and compared between and within the groups. RESULTS: Before first-eye surgery (baseline), the levels of interleukin (IL)-1ra, IL-13 and tumor necrosis factor (TNF)-alpha were significantly increased in PACG compared with controls. The levels of IL-13 were increased while that of IL-15 were decreased in HM. Compared with controls, 11 cytokines were significantly increased in DM. In the AH of the contralateral eye after first-eye cataract surgery, basic fibroblast growth factor (bFGF) was significantly more abundant in PACG and HM, while the levels of monocyte chemoattractant protein-1 (MCP-1) and interferon gamma-induced protein 10 (IP-10) were decreased in PACG. We also identified 6 significantly upregulated cytokines in DM compared with controls. Compared with baseline, there was an overlap of 5 altered cytokines in the AH of contralateral eyes after first-eye surgery between the four groups. Some were exclusively altered in each subgroup, with 1 in the control group, 4 cytokines in the PACG and HM groups, and none in the DM group. CONCLUSIONS: From the initial profile, it is observed that patients with pre-existing ocular or systemic conditions have some degree of inflammation in their eyes before surgery and in the contralateral eye after the first eye cataract surgery, which could be peculiar of the morbid conditions of the patients. Inflammation was more detectable in patients with type 2 DM before surgery. PACG and HM patients showed stronger intraocular inflammatory reactions to topical stimuli compared with controls and DM patients. Our data suggest that ophthalmologists should pay closer attention to inflammatory responses, especially in cataract patients with pre-existing conditions, although the clinical significance of these changes following surgery remains to be further investigated.
Subject(s)
Cataract , Diabetes Mellitus, Type 2 , Glaucoma, Angle-Closure , Myopia , Aqueous Humor/metabolism , Cataract/complications , Cataract/metabolism , Cohort Studies , Cytokines/metabolism , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Diabetes Mellitus, Type 2/surgery , Glaucoma, Angle-Closure/complications , Glaucoma, Angle-Closure/metabolism , Glaucoma, Angle-Closure/surgery , Humans , Inflammation/metabolism , Interleukin-13/metabolism , Myopia/complications , Myopia/metabolism , Myopia/surgeryABSTRACT
Corneal endothelial cells (CECs) play a major role in the maintenance of stromal hydration via the barrier and pump function for clear vision. Adult CECs cannot regenerate after injury. CECs cultured in vitro can undergo mitosis but may undergo corneal endothelial-to-mesenchymal transition (EnMT) and lose their endothelial characteristics. In this study, we examined the effects of CHIR99021 on transforming growth factor beta-1(TGFß1)-induced EnMT in human CECs (hCECs) lines. CHIR99021 kept hCECs in the hexagonal shape and could downregulate the EnMT markers alpha-smooth muscle actin (α-SMA) and fibronectin (FN1), meanwhile maintained the hCECs function markers Na+/K+-ATPase and zonula occludens-1 (ZO-1) at levels comparable to those in the normal control. Interestingly, we found that the combination of CHIR99021 and TGFß1 at appropriate concentrations would significantly promote the proliferation and migration of hCECs. These effects may be related to the inhibition of RhoA or Rac1, as well as the activation of Wnt and Erk pathway, with a calcium homeostasis. Our findings indicate that CHIR99021 inhibit EnMT and that the combination of CHIR99021 and TGFß1 may provide new ideas for corneal endothelial regeneration and wound healing.
Subject(s)
Endothelial Cells , Endothelium, Corneal , Transforming Growth Factor beta1/pharmacology , Adult , Cell Proliferation , Cells, Cultured , Endothelial Cells/metabolism , Endothelium, Corneal/metabolism , Epithelial-Mesenchymal Transition , Humans , Pyridines , PyrimidinesABSTRACT
Purpose: Corneal endothelial cells (CECs) serve as a barrier and foothold for the corneal stroma to maintain the function and transparency of the cornea. Loss of CECs during aging or disease states leads to blindness, and cell replacement therapy using either donated or artificially differentiated CECs remains the only curative approach. Methods: Human induced pluripotent stem cells (hiPSCs) that were cultured in chemically defined medium were induced with dual-SMAD inhibition to differentiate into neural crest cells (NCCs). A small-molecule library was screened to differentiate the NCCs into corneal endothelial-like cells. The characteristics of these cells were identified with real-time PCR and immunofluorescence. Western blotting was applied to detect the signaling pathways and key factors regulated by the small molecules. Results: We developed an effective protocol to differentiate hiPSCs into CECs with defined small molecules. The hiPSC-CECs were characterized by ZO-1, AQP1, Vimentin and Na+/K+-ATPase. Based on our small-molecule screen, we identified a small-molecule combination, A769662 and AT13148, that enabled the most efficient production of CECs. The combination of A769662 and AT13148 upregulated the PKA/AKT signaling pathway, FOXO1 and PITX2 to promote the conversion of NCCs to CECs. Conclusion: We established an efficient small molecule-based method to differentiate hiPSCs into corneal endothelial-like cells, which might facilitate drug discovery and the development of cell-based therapies for corneal diseases.
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AIM: To examine the influences of personality characteristics and coping modes on the anxiety of primary glaucoma patients. METHODS: A total of 200 individuals, including 50 with primary angle-closure glaucoma, 60 with primary open angle glaucoma and 90 control participants, filled out the State-Trait Anxiety Inventory, NEO Five-Factor Inventory, and Medical Coping Modes Questionnaire. Sociodemographic information was also collected. Data were analyzed via the Spearman rank correlation test and stepwise regression. RESULTS: The personality and coping variables are predictive and jointly account for a significant amount (45.3%-54.2%) of variance across the two subscales of anxiety measures. Notably, neuroticism seems to be most closely related to anxiety disturbances in glaucoma patients. The level of resignation is positively linked to anxiety scores. CONCLUSION: Some personality factors and coping modes help to predict the process of anxiety disorders in primary glaucoma patients. Recognizing the predictive role of these variables in the patients may further enrich clinical research in glaucoma and help to design more effective interventions involving both ophthalmology and psychiatry.
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Our prospective comparative study of 60 patients aimed to compare the efficacy and feasibility of a single injection ranibizumab versus a single grid laser photocoagulation and versus a combined treatment in macular edema secondary to branch retinal vein occlusion in Asian population. Patients were randomized 1:1:1 (n = 20/group) into grid laser (LAS), the ranibizumab (RAN), and the combination (COM) group. Outcomes were measured as best-corrected visual acuity (BCVA) and central macular thickness (CMT). There were significant differences in mean BCVA between the three groups at 1 week and 1 month (p < 0.05) and in mean CMT at 1 week and 1, 3, 6, and 12 months (p < 0.05). Overall, best results were observed in the combination group. However, the RAN and COM groups achieved very similar results. At 12 months, the CMT in all three groups was decreased compared with baseline (p < 0.05). Our results allow to conclude that the effect of early treatment with a single injection of intravitreal ranibizumab (cost reduction) and the stabilizing effect of grid laser photocoagulation is indeed an effective, feasible, and safe regiment for macular edema secondary to BRVO in Chinese patients, allowing to obviate the need for repeated intravitreal injections and thus reduce the adverse events, therapy duration, patients' malcompliance, and adverse events. A single ranibizumab therapy however is a comparable alternative.
Subject(s)
Lasers , Light Coagulation/economics , Macular Edema/drug therapy , Macular Edema/etiology , Ranibizumab/economics , Ranibizumab/therapeutic use , Retinal Vein Occlusion/complications , Aged , Combined Modality Therapy , Cost-Benefit Analysis , Female , Humans , Intraocular Pressure/drug effects , Intravitreal Injections , Macular Edema/economics , Macular Edema/physiopathology , Male , Ranibizumab/administration & dosage , Ranibizumab/pharmacology , Visual Acuity/drug effectsABSTRACT
BACKGROUND: Glaucoma is hallmarked with the death of retinal neurons in the ganglion cell layer, which results in irreversible vision loss. The abnormal levels of miRNA have been associated with glaucoma. Our study purposed to explore the underlying molecule mechanism of miR-93-5p in NMDA-induced glaucoma. METHODS: The Sprague-Dawley (SD) rats were used for the establishment of glaucoma model with the injection of NMDA. Vision behavior test were performed on the glaucoma rats. MiR-93-5p expression was determined by real-time PCR. The levels of autophagy-related protein and PTEN were assessed by Western blot assays. TUNEL assay and flow cytometry were performed to analyze cell apoptosis in vivo and in vitro, respectively. And cell viability was examined by CKK-8 assay. The relationship between miR-93-5p and PTEN was confirmed by Dual-Luciferase reporter gene system. RESULTS: NMDA-induced glaucoma rats exhibited less time in the dark box, suggesting the recession of their vision. Moreover, the retinal ganglion cell (RGC) viability was reduced not only in the glaucoma rat models but also in the glaucoma RGC models. The autophagy-related protein was obviously increased in the NMDA-treated rats or RGCs. PTEN regulated the autophagy of RGCs through AKT/mTOR pathway in NMDA-treated RGCs. MiR-93-5p could target regulate PTEN negatively, and exhibit the similar effect of 3-MA on the survival of RGCs. CONCLUSION: Up-regulation of miR-93-5p binding with PTEN suppressed the autophagy of RGCs through AKT/mTOR pathway in NMDA-induced glaucoma.
Subject(s)
Autophagy/genetics , Glaucoma/genetics , MicroRNAs/genetics , PTEN Phosphohydrolase/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Retinal Ganglion Cells/drug effects , TOR Serine-Threonine Kinases/metabolism , Animals , Cell Survival/drug effects , Disease Models, Animal , Female , Glaucoma/metabolism , Glaucoma/pathology , Male , N-Methylaspartate/pharmacology , Protein Binding , Rats, Sprague-Dawley , Retinal Ganglion Cells/pathology , Signal Transduction , Up-RegulationABSTRACT
AIM: To identify the 100 most cited papers in cataract surgery, we performed a comprehensive bibliometric analysis basing on the literature search on the Thomson Reuters Web of Knowledge. METHODS: The number of citations, including the total citations, latest 5y citations and average citation number per year (ACY), authorship, year of publication, major topics, journal of publication, country and institution of origin of each paper were recorded and then analyzed. Pearson's correlation analysis was conducted to evaluate the correlation between the published year and the number of citations. The correlation between journal's impact factor (IF) and number of citations was assessed as well. RESULTS: The most cited paper was the classic paper done by the European Society of Cataract & Refractive Surgeons (ESCRS) group. This paper focused on the topic of endophthalmitis. Not only the most cited papers originated from the USA, but also some American institutions like Johns Hopkins University, Harvard Medical School, etc. had the most citations. Pearson's correlation analysis indicated that the latest 5y citations and ACY were significantly related with the published year (5y citations: r=0.615, P<0.001; ACY: r=0.657, P<0.001), whereas no association between the total number of citations and published year was found (r=0.045). Moreover, the IFs of journals were found to have no significant effect on the number of total citations. CONCLUSION: To our knowledge, this is the first study on the most influential papers in cataract surgery after a comprehensive research of relevant literatures. The present work may provide us concise information concerning the development history of cataract surgery over the past 66y.
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Corneal dystrophy is a common type of hereditary corneal diseases. It includes many types, which have varied pathology, histology and clinical manifestations. Recently, the examination techniques of ophthalmology and gene sequencing advance greatly, which do benefit to our understanding of these diseases. However, many aspects remain still unknown. And due to the poor knowledge of these diseases, the results of the treatments are not satisfoctory. The purpose of this review was to summarize the clinical, histological and genetic characteristics of different types of corneal dystrophies.
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AIM: To investigate matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) expression during the progress of fusarium solani (F.solani) keratitis in a rat model. METHODS: A rat model of F.solani keratitis was produced using corneal scarification and a hand-made contact lens. MMPs and TIMPs expressiond were explored in this rat model of F.solani keratitis using real-time polymerase chain reaction (PCR) and DIF. GM6001 (400 µmol/mL) was used to treat infected corneas. The keratitis duration, amount and area of corneal neovascularization (CNV) were evaluated. RESULTS: MMP-3 expression was 66.3 times higher in infected corneas compared to normal corneas. MMP-8, -9, and -13 expressions were significantly upregulated in the mid-period of the infection, with infected-to-normal ratios of 4.03, 39.86, and 5.94, respectively. MMP-2 and -7 expressions increased in the late period, with the infected-to-normal ratios of 5.94 and 16.22, respectively. TIMP-1 expression was upregulated in the early period, and it was 43.17 times higher in infected compared to normal corneas, but TIMP-2, -3, and -4 expressions were mildly downregulated or unchanged. The results of DIF were consistent with the result of real-time PCR. GM6001, a MMPs inhibitor, decreased the duration of F.solani infection and the amount and area of CNV. CONCLUSION: MMPs and TIMPs contributed into the progress of F.solani keratitis.
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BACKGROUND: we conducted our meta-analysis of published studies to assess existing evidence about the efficacy and safety of vitrectomy with ILM peeling vs. that of vitrectomy with no ILM peeling for Macular hole-induced retinal detachment. METHODS: Databases, including Pubmed, Cochrane Library, Ovid, Web of Science, Wanfang and CNKI, were searched to identify studies comparing outcomes following vitrectomy with ILM peeling and that with no ILM peeling for macular hole-induced retinal detachment. The meta-analysis was performed by RevMan 5.1. RESULTS: Six comparative studies comprising 180 eyes were identified. It was indicated that the rate of retinal reattachment (Odds ratio (OR) = 3.03, 95 % Confidence interval (CI):1.35 to 6.78; P = 0.007) and macular hole closure (OR = 6.74, 95 % CI:3.26 to 13.93; P < 0.001) after initial surgery was higher and the rate of recurrent retinal detachment (OR = 0.08, 95 % CI:0.02 to 0.30; P = 0.0002) was lower in the group of vitrectomy with ILM peeling than that in the group of vitrectomy with no ILM peeling. However, the improved BCVA (Weighted mean difference (WMD) = 0.14, 95 % CI: -0.20 to 0.47; P = 0.42) and the rate of postoperative complications were similar between the two groups. CONCLUSION: Vitrectomy with internal limiting membrane peeling is an efficient and safe procedure for macular hole-induced retinal detachment.
Subject(s)
Epiretinal Membrane/surgery , Retinal Detachment/surgery , Retinal Perforations/surgery , Vitrectomy/methods , Basement Membrane/surgery , Humans , Middle Aged , Recurrence , Retinal Detachment/etiology , Retinal Detachment/physiopathology , Retinal Perforations/complications , Retinal Perforations/physiopathology , Tomography, Optical Coherence , Visual Acuity/physiologyABSTRACT
In the past few years, 9 unique laser platforms have been brought to the market. As femtosecond (FS) laser-assisted ophthalmic surgery potentially improves patient safety and visual outcomes, this new technology indeed provides ophthalmologists a reliable new option. But this new technology also poses a range of new clinical and financial challenges for surgeons. We provide an overview of the evolution of FS laser technology for use in refractive and cataract surgeries. This review describes the available laser platforms and mainly focuses on discussing the development of ophthalmic surgery technologies.
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Myeloid cells are highly adaptable and may positively or negatively regulate angiogenesis dependent on the cognate and soluble signals they receive. Toll-like receptors (TLRs) initiate immune responses, orchestrate adaptive immune responses, and regulate vascular endothelial growth factor (VEGF)-mediated angiogenesis during wound healing. We investigated the possible role of TLR ligands in attenuation of new vessel growth via regulation of expression of VEGF or soluble fms-like tyrosine kinase-1 (sFlt-1) in both an aortic ring assay and a model of suture-induced corneal angiogenesis. The TLR3 ligand [poly(I:C)] markedly suppressed VEGF secretion and stimulated sFlt-1 release from macrophages. The aortic ring assay demonstrated that new vessels were promoted by the TLR2 ligand (heat killed Listeria monocytogenes) and the TLR4 ligand (lipopolysaccharide), concomitant with increased VEGF and matrix metalloproteinase 9 secretion. In contrast, the TLR9 ligand [oligodeoxynucleotide (ODN)1826] stimulated sFlt-1 secretion from macrophages and reduced the number of aortic ring vessel sprouts. ODN1826 also significantly reduced the length and volume of both hemangiogenesis and lymphangiogenesis in the suture-induced corneal angiogenesis model. Furthermore, 53 angiogenic factors were examined via protein array and compared between ODN1826- and water-treated corneas to interrogate the pathway of ODN1826 inhibition, demonstrating an up-regulation of Serpin E1 signal. Further clinical and IHC analyses of the aortic ring assay indicated that TLR9 suppressed tip cell migration and recruitment of mural cells and adventitial macrophages.
Subject(s)
Cell Movement/drug effects , Corneal Neovascularization/drug therapy , Macrophages/metabolism , Neovascularization, Pathologic/drug therapy , Oligodeoxyribonucleotides/pharmacology , Toll-Like Receptor 9/agonists , Animals , Cells, Cultured , Corneal Neovascularization/metabolism , Corneal Neovascularization/pathology , Disease Models, Animal , Lymphangiogenesis , Macrophages/pathology , Mice , Neovascularization, Pathologic/genetics , Neovascularization, Pathologic/metabolism , Plasminogen Activator Inhibitor 1/genetics , Plasminogen Activator Inhibitor 1/metabolism , Vascular Endothelial Growth Factor Receptor-1/metabolismABSTRACT
This study aimed to establish a transgenic mouse model of corneal dystrophy (CD) overexpressing the human transforming growth factor, ß-induced, 68 kDa (TGFBI, also known as BIGH3) gene. A purified and linearized recombinant plasmid carrying the expression cassette BIGH3IRESEGFP was microinjected into the pronuclei of C57BL/6J mouse fertilized eggs under the control of the phosphoglycerate kinase (PGK) promoter. The expression of human BIGH3 in the transgenic mice was confirmed by PCR using DNA extracted from tail tissue. Four founder transgenic mice were identified by PCR and the increased expression of BIGH3 was observed in the corneas of the transgenic mice by RT-PCR and western blot analysis. The abnormal corneas with central opacity were observed in the transgenic mice by corneal photography. We concluded that the exogenous gene, BIGH3, was integrated successfully into the mouse genome through microinjection. In addition, the phenotype observed in this BIGH3 transgenic mouse model was similar to CD. Therefore, this transgenic model may prove useful in the investigation of the pathogenesis of CD.