OBJECTIVE:To detect and characterize disproportionality signals between individual bisphosphonates and glaucoma subtypes using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). DESIGN:A retrospective pharmacovigilance disproportionality analysis. PARTICIPANTS:Participant data were drawn from adverse event reports from the FAERS database (Q1 2004-Q1 2025). METHODS:Disproportionality analysis was conducted using the reporting odds ratio (ROR), proportional reporting ratio (PRR), and Bayesian confidence propagation neural network (BCPNN). Adverse events were coded using Medical Dictionary for Regulatory Activities (version 27.1). A significant signal required ≥3 cases and meeting thresholds (ROR 95% CI lower limit >1, PRR ≥2 with χ² ≥4, or BCPNN IC025 >0). RESULTS:Among 539 reports, significant disproportionality signals were identified for alendronic acid (ROR = 2.42; 95% CI: 2.18-2.70) and pamidronic acid (ROR = 2.23; 95% CI: 1.69-2.93) at the group level. Subtype-level signals included alendronic acid with open-angle glaucoma (ROR = 5.67) and normal-tension glaucoma (ROR = 4.60); pamidronic acid with open-angle glaucoma (ROR = 8.62); and risedronic acid with angle-closure glaucoma (ROR = 2.93). Median time-to-onset varied from 10 days (risedronic acid) to 1579 days (pamidronic acid). CONCLUSIONS:This pharmacovigilance analysis identifies distinct disproportionality signals linking specific bisphosphonates to different glaucoma subtypes, with heterogeneous time-to-onset patterns. The findings highlight potential safety signals warranting further clinical and mechanistic investigation.

High-dose glucocorticoids remain the standard acute-phase therapy for optic neuritis (ON), yet a proportion of patients respond poorly to this first-line treatment. This study aims to evaluate the association between baseline hematological indices and steroid sensitivity in patients with first-episode ON, and to develop a practical prediction model to identify patients at risk of steroid resistance. A retrospective cohort study was conducted on 64 patients treated with intravenous glucocorticoid therapy. Patients were stratified into steroid-sensitive or steroid-resistant groups based on the change in best corrected visual acuity (ΔLogMAR). Baseline clinical and hematological parameters were analyzed using logistic regression and receiver operating characteristic curves to determine optimal predictive thresholds. The steroid-sensitive group demonstrated higher baseline neutrophil (NEU) and white blood cell (WBC) counts compared to the resistant group (both P < 0.05). Paradoxically, contrary to their established role as poor prognostic markers for disease severity, elevated baseline NEU and WBC correlated with better visual improvements (P < 0.01). Univariate logistic regression analysis identified NEU, WBC, lymphocyte (LYM) and symptom-to-treatment interval as significant predictors of steroid sensitivity (all P < 0.05). Further multivariate analysis confirmed WBC as an independent predictor (OR = 1.60, P = 0.015). The derived three-tiered prediction model revealed that patients with a low-inflammatory phenotype (Tier C) exhibited a steroid response rate of only 47.8

Background: Vitreous chamber volume (VCV) in humans can be accurately measured using magnetic resonance imaging (MRI) combined with ITK-SNAP analysis software. This study explores the relationship between VCV and axial length (AL). Methods: This study included 46 healthy individuals, encompassing a total of 92 eyes. Individuals with a history of eye conditions were excluded from the study. AL measurements were obtained using the Lenstar 900 (Haag-Streit, Switzerland). VCV was assessed through MRI using the Ingenia 3.0T system (Philips Medical Systems, Netherlands), with VCV analysis performed using ITK-SNAP analysis software version 3.8.0. The correlation between AL and VCV was evaluated using Pearson linear correlation coefficient, and a logistic regression model was employed to predict VCV. Results: The sample consisted of 92 eyes from 46 individuals, including 28 women and 18 men. The average VCV was 6193±1135.9 mm 3 for women and 6324.3±886.7 mm 3 for men. The mean AL for women was 24.70±2.78 mm, while for men it was 24.66±1.70 mm. A significant correlation between AL and VCV was observed ( P <0.001). Conclusions: VCV can be accurately estimated through AL measurements, offering a clinically relevant method for assessing VCV.

Background Optic neuritis (ON), an acute demyelinating disorder often preceding multiple sclerosis, lacks therapies preventing neurodegeneration despite corticosteroid use. Methods We combined GWAS (FinnGen cohort, finn-b-H7\_OPTNEURITIS), immune-specific eQTL analysis (CAGE.sparse microglia/astrocytes), and network pharmacology. SMR-HEIDI filtering (p\_HEIDI>0.05; FDR<0.05) validated causal genes. Results 46 ON-associated genes identified, with HLA-DRB1 as top risk locus (OR=3.297, FDR<0.01).Functional enrichment revealed antigen presentation dysregulation (GO:0002483, FDR=0.0025) and phagosome activation (hsa04145, FDR=0.0468), confirming microglial-astrocytic pathology.Omacetaxine mepesuccinate prioritized as sole repurposing candidate (FDR=0.0467) targeting ribosomal proteins RPL3/RPL2—mechanistically linked to glial protein synthesis suppression in demyelination. Conclusions This first multi-omics analysis of ON bridges HLA-mediated autoimmunity with repurposed ribosomal-targeted therapy, proposing omacetaxine for neuroprotection. ### Competing Interest Statement The authors have declared no competing interest.

OBJECTIVES:The aim of this study was to reveal the biological functionalities associated with endoplasmic reticulum stress (ERS)-related genes (ERSGs) in the context of diabetic retinopathy (DR). METHODS:Differentially expressed genes (DEGs) within the DR group and the Control group were identified and then integrated with ERSGs. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) methodologies were used to investigate potential biological mechanisms. A diagnostic model for ERS and a nomogram were formulated based on biomarkers selected through the Least Absolute Shrinkage and Selection Operator method. The diagnostic efficacy of this model was thoroughly evaluated. ERS-associated subtypes were identified, and the Single-Sample GSEA (ssGSEA) and CIBERSORT algorithms were used to assess immune infiltration. RESULTS:We identified 10 ERS-related DEGs (ERSRDEGs) within the DR Group. Subsequently, a diagnostic model was constructed based on 5 ERS genes, namely CCND1, IGFBP2, TLR4, TXNIP, and VIM. The validation analysis demonstrated the commendable diagnostic performance of the model. Analysis of the ssGSEA immune characteristics revealed a positive correlation in the DR group between myeloid-derived suppressor cells (MDSC), regulatory T cells (Tregs), and CCND1 TXNIP. Furthermore, a significant negative correlation was observed between central memory CD4 T cells and CCND1. In the context of CIBERSORT, the results indicated a positive correlation between macrophages and IGFBP2, as well as Tregs and IGFBP2 in the DR group. Notably, a conspicuous negative correlation was identified between resting mast cells and IGFBP2. CONCLUSION:The present study provides novel diagnostic biomarkers for DR from an ERS perspective.

Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation.Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms.Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95–1.06, p = 0.980), (OR 0.97; 95% CI 0.86–1.09, p = 0.550), and (OR 0.99; 95% CI 0.90–1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97–1.05, p = 0.693), (OR 1.00; 95% CI 0.98–1.03, p = 0.804), and (OR 0.99; 95% CI 0.96–1.01, p = 0.363), respectively. Heterogeneity (p > 0.05) and pleiotropy (p > 0.05) analysis confirmed the robustness of MR results.Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa.

Background: Waardenburg syndrome (WS) is a rare genetic disorder characterized by congenital sensorineural hearing loss and pigmentary abnormalities of the hair, skin and eyes. However, exotropia is rarely reported. The purpose of this study is to describe the clinical characteristics of three sporadic patients with WS and congenital exotropia and to investigate the disease-causing genes for them. Methods: Patients underwent detailed physical and ocular examinations. Ocular alignment and binocular status were evaluated. DNA was extracted and whole exome sequencing was performed to detect the pathogenic variations in the disease-causing genes for WS. Cloning sequencing was carried out for those indel variations. Results: Three unrelated patients were diagnosed with Waardenburg syndrome and congenital exotropia. Four novel variants, including c.136delA (p.I46Sfs*64) and c.668G>T (p.R223L) in PAX3, c.709dupC (p.Q237Pfs*119) in COL11A2, c.426G>A (p.W142X) in SOX10 gene, were detected in this study. Conclusion: Simultaneous presence of congenital exotropia and WS in our patients is suggested that WS could be involved in malfunction in the multiple nerve systems. Our genetic study will expand the mutation spectrum of PAX3, COL11A2 and SOX10 genes, and is helpful for further study on the molecular pathogenesis of WS.

Click to increase image sizeClick to decrease image size Disclosure statementThe authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.Additional informationFundingThe author(s) reported that there is no funding associated with the work featured in this article.

Objective:To investigate the protective effect of adeno-associated virus (AAV) vector-mediated heme oxygenase-1 ( HO-1) gene overexpression on retinitis pigmentosa (RP) models in rats. Methods:Eighty healthy male SD rats were selected and randomized into the blank control group, RP model group, AAV-GFP group and AAV-HO-1-GFP group, with 20 rats in each group.The RP model was established via tail vein injection of 1% sodium iodate solution at the dose of 50 mg/kg.Rats in the RP model group, AAV-GFP group and AAV-HO-1-GFP group were subretinally injected with normal saline, AAV-GFP virus and AAV-HO-1-GFP virus according to grouping.Rats in the blank control group were administrated with subretinal injection of equal volume of normal saline.The eyeballs of rats were enucleated on 14th day after molding.The retinal structure and thickness were detected by hematoxylin-eosin staining; apoptosis in retinal tissue was detected by TUNEL assay; the expression levels of cysteinyl aspartate specific proteinase 3 (caspase 3), B-lymphoma-2 (bcl-2) and HO-1 protein in rats retina was identified by Western blot.The use and care of the animals complied with the Statement of the Association for Research in Vision and Ophthalmology (ARVO). The study protocol was approved by an Ethics Committee of The Second Affiliated Hospital of Fujian Medical University (No.202188).Results:Hematoxylin-eosin staining results showed normal retinal structure in the blank control group, obvious retinal structure damage with thinned and wavy outer nuclear layer in the RP model group and AAV-GFP group, and mild retinal structure damage with slightly thinned outer nuclear layer in the AAV-HO-1-GFP group.Compared with the blank control group, the outer nuclear layer was significantly thinner in the RP model group and AAV-GFP group (both at P<0.05). Relative expression level of HO-1 protein in the RP model group, AAV-GFP group, and AAV-HO-1-GFP group was 0.76±0.21, 0.76±0.16, 0.92±0.05, respectively, which were all significantly higher than 0.48±0.25 in the blank control group (all at P<0.05). The relative expression level of HO-1 protein in the AAV-HO-1-GFP group was significantly higher than that in the RP model group and the AAV-GFP group (both at P<0.05). There were significant differences in apoptosis rate, the relative expression levels of bcl-2 and caspase 3 protein among the four groups ( F=1 596.333, 1 043.806, 364.331; all at P<0.01). The apoptosis rate and the relative expression level of caspase 3 were significantly higher, and the relative expression level of bcl-2 was lower in the RP model group and AAV-GFP group than those in the AAV-HO-1-GFP group (all at P<0.05). Conclusions:AAV-mediated overexpression of HO-1 gene can protect the retina of RP rats.

AIM To investigate the expression and possible role of the autophagy related protein p62 and LC3 in the retina based on a rat model of acute ocular hypertension. METHODS Fifty rats were randomized into five groups: control group A, B, C, and D. Groups A to D all received normal saline perfusion into the anterior chamber with pressure of 80 mm Hg for one hour, and retina tissue was obtained at 6, 12, 24 and 48h after perfusion respectively, to investigate the activation of autophagy following ischemia-reperfusion. The distribution and semi-quantification of autophagy related protein p62 and LC3 in the retina were detected using immunohistochemistry technique. The expression level of these two proteins was evaluated using Western blot. RESULTS The number of retinal ganglion cells (RGCs) decreased with increasing reperfusion time, and significant reduction in the retinal thickness was observed 48h after perfusion. In normal adult rats, LC3 protein was mainly expressed in the ganglion cell layer (GCL), and p62 protein was expressed in the nerve fiber layer (NFL), GCL, inner plexiform layer (IPL), inner nuclear layer (INL) and outer plexiform layer (OPL). In comparison to the control group, the expression level of LC3- II was higher in all the experimental groups (P<0.05), with the peak expression at 12h after reperfusion. Additionally, the expression level of p62 was higher in all the experimental groups than the control (P<0.05, except for group A), with the peak level occurred 24h after reperfusion. CONCLUSION Both p62 and LC3 show low level and uneven expression in the retina of normal adult rats. Acute ocular hypertension can lead to upregulation of LC3- II and p62 expression in the retina. Autophagy flux is damaged 12h after reperfusion, potentially resulting in further loss of RGCs.

目的 探讨拉坦前列素联合毛果芸香碱治疗原发性急性闭角型青光眼的有效性与安全性.方法 将110例原发性急性闭角型青光眼患者随机分为2组(各55例),对照组单用毛果芸香碱滴眼液,联合组配合使用拉坦前列素与毛果芸香碱滴眼液.对比两组的临床疗效及治疗前后的眼压、视力变化.结果 联合组治疗1个月、3个月的眼压水平均显著低于对照组,视力水平均显著高于对照组(P<0.05).联合组治疗后的EDV、PSV水平显著高于对照组,RI水平显著低于对照组(P<0.05).联合组的治疗总有效率为92.86％,显著高于对照组的76.36％(P<0.05).两组的不良反应发生率比较无显著差异(P>0.05).结论 拉坦前列素联合毛果芸香碱治疗原发性急性闭角型青光眼能够控制眼压,改善视力,其临床疗效显著,且无明显不良反应.

目的:比较超声乳化联合房角分离手术与小梁切除术治疗闭角型青光眼合并白内障对患者视力及眼压的影响.方法:选取2014年1月-2015年12月笔者所在医院收治100例PACG合并白内障患者作为研究对象,根据手术方式的不同分为两组,观察组(55例)采用超声乳化+房角分离手术,对照组(45例)采用超声乳化+小梁切除术,比较两组治疗前后的眼压、视力及前房深度变化及并发症的发生情况.结果:两组术后1 d、1周、1个月、3个月、1年的眼压均较术前降低,比较差异均有统计学意义(P<0.05);两组术后各时点眼压水平比较差异均无统计学意义(P>0.05);两组术后1周的视力较治疗前明显提高,前房深度较治疗前明显增加,比较差异均有统计学意义(P<0.05);两组术后1周的视力及前房深度比较,差异均无统计学意义(P>0.05);观察组术后的并发症发生率为9.09％,显著低于对照组的26.67％,比较差异有统计学意义(P<0.05).结论:超声乳化联合房角分离手术与联合小梁切除术治疗闭角型青光眼合并白内障均能有效控制患者的眼压,改善患者的视力,但是相比联合小梁切除术,超声乳化联合房角分离术的并发症更少,安全性更好.

High intraocular pressure (IOP) is a risk factor for primary open-angle glaucoma (POAG). The trabecular meshwork (TM), a reticular tissue in the outflow passage of the aqueous humor (AH), is a major contributor to intraocular outflow resistance. High levels of myocilin (MYOC), which is expressed in the TM, are associated with high IOP. Furthermore, transforming growth factor-β2 (TGF-β2) concentrations in human AH are significantly elevated in POAG patients. This study was designed to investigate the effects of TGF-β2 on MYOC expression and secretion in human primary cultured TM cells. Primary cultured human TM cells were treated with 0 (control group), 1, 10, and 100 ng/mL TGF-β2 for 12, 24, or 48 h. MYOC mRNA and protein expressions in TM cells and protein secretion in conditioned media were analyzed by semi-quantitative RT-PCR, Western blotting, and enzyme-linked immunosorbent assays (ELISA), respectively. TM cells treated with 1, 10, and, 100 ng/mL TGF-β2 for 48 h showed higher MYOC mRNA and protein expressions than those in the control group (0 ng/mL TGF-β2) (all P < 0.05). Treatment with TGF-β2 for 48 h also induced MYOC secretion in conditioned media in a dose-dependent manner (0 ng/mL: 7.107±1.163 pg/ml; 1 ng/mL: 7.879±1.894 pg/ml; 10 ng/mL: 8.063±1.181 pg/ml; 100 ng/mL: 8.902±0.699 pg/ml; all P < 0.05). In Conclusion, TGF-β2 induced MYOC expression and secretion in human primary cultured TM cells. Further investigations are required to confirm the involvement of these two factors in POAG pathogenesis.

Background Researches demonstrated that the levels of soluble CD44 (sCD44)molecule in aqueous is significantly higher in primary open-angle glaucomous(POAG) eye than normal eye,but how the sCD44 would affect the expression of apoptosis protein in trabecular meshwork cells is below understanding. Objective The present study was to investigate the effect of sCD44 on the expression of regulatory proteins bcl-2 associated death factor bad in trabecular meshwork cells in the patients with POAG. Methods Human scleral tissue with trabecular meshwork were obtained from POAG patients during the surgery.The trabecular meshwork cells were primarily cultured by explant culture method and identified by immunochemistry.The third generation of cells were incubated with free-serum DMEM/F12 medium added differnt dosages of sCD44 (0,1,5,10,25,50 mg/L) for 48 hours.The expression of bad protein in cultured cells was detected using cell counting kit-8 (CCK-8) as the absorbance values at 490 nm(A,90 value),and the bad protein level in cultured cells was assayed by ELISA. Results The cultured cells showed the positive response for laminin ( LM ),neuron specific enolase ( NSE ),fibronectin ( FN ) monoclonal antibodies.The CCK-8 assay showed that the A490 values of the trabecular meshwork cells in 0,1,5,10,25,50 μg/L of sCD44 groups were 0.2460±0.0019,0.1874±0.0015,0.1570±0.0016,0.1302±0.0019,0.1084±0.0018,0.0940±0.0020 respectively with a statistically significant difference among the 6 groups( F =14.922,P =0.000 ),and the A490 values in various dosages of sCD44 groups were significantly lower than the 0 μg/L sCD44 group (P=0.013,0.008,0.011,0.005,0.004).The ELISA assay showed that bad protein levels in 0,1,5,10,25,50 μg/L of sCD44 groups were ( 114.8461 ± 2.9560 ),( 137.8270 ± 2.4259 ),( 161.4194 ± 3.7381 ),( 170.9453 ± 3.2006 ),( 221.2252 ±4.3738 ),( 324.6167±4.4220) ng/L,showing a total difference among them ( F =16.610,P =0.000 ),and the bad protein levels in various dosages of sCD44 groups were significantly lower than the 0 μg/L sCD44 group( P =0.017,0.013,0.008,0.007,0.006). Conclusions sCD44 can contribute to the apoptosis of the trabecular meshwork cells in patients with POAG in certain dose range by regulating the apoptosis regulatory proteins bcl-2 associated death factor bad.

目的 探讨EGF对体外培养POAG小梁网细胞增殖和凋亡的影响.方法体外培养POAG小梁网细胞并鉴定;用终浓度为0,5,10,20,50,100 ng/ml的EGF干预48 h,运用CCK-8比色法检测其吸光度值、流式细胞仪检测其凋亡率.结果 成功进行POAG小梁网的培养和鉴定;CCK-8比色法结果表明,当EGF的浓度为5,10,20,50,100 ng/ml时,其增殖率分别为13.8 %、21.7 %、26.5 %、34.5 %、17.0 %,与对照组比较,差异具有统计学意义(P<0.05);流式细胞仪检测结果显示,其凋亡率分别为(16.14±0.44)%,(14.22±0.18)%,(10.90±0.49)%,(5.98±0.14)%,(5.58±0.21)%,(9.93±0.17)%,各实验组与阴性对照组比,凋亡率下降具有统计学意义(P<0.01).结论 EGF可以促进体外培养的POAG小梁网细胞的增殖,减少其凋亡.

Objective To investigate the effect of different concentrations of soluble CD44 molecule (sCD44) in trabecular meshwork cells from patients with primary open angle glaucoma (POAG)on the apoptosis of trabecular meshwork cells,to study the relationship between sCD44 and POAG,and further investigate the pathogcnesis of POAG.Methods Human trabecular meshwork cells were primarily cultured and subcultured.The 3rd passage cells were incubated with different dosages of sCD44 at (1,5,10,25,50ng/ml) final concentration,diluted by DMEM/F12 without serum for 24hours,using CCK-8,fluorescence microscopy and flow cytometry method to study the effect of sCD44 on the apoptosis of cultured trabecular meshwork cells.Results With increasing concentration of sCD44,the inhibition on POAG trabecular meshwork cells were enhanced,by cell counting kit-8(CCK-8),and the experimental group compared with the control group and within experimental group was statistically significan (P ＜ 0.05 ).By fluorescence microscopy showed that the early and late apoptotic cells were increased with the increasing final concentration of sCD44.The experimental group□s apoptosis rate of the different dosages of sCD44 at (1,5,10,25,50ng/ml) final concentration were:10.7283 ± 0.0223,17.3267 ± 0.0250,21.1483 ± 0.0248,25.1267 ± 0.0281,29.9900 ±0.0335,respectively by flow cytometry method,which were higher than the control group of 2.5550±0.0187.The experimental group compared with the control group and within experimental group the difference was statistically significant (P ＜ 0.05).Condusions In a certain range,sCD44 can inhibit the proliferation of trabecular meshwork cells,cause apoptosis,and show a dose dependent manner.The changing of sCD44 levels may be acting on the trabecular meshwork and indirectly involved in the pathogenesis of POAG.

PURPOSE:A depletion of hyaluronic acid (HA) in patients' eyes may be associated with primary open-angle glaucoma (POAG), but the exact mechanism remains unclear. We investigated the effect of HA on the expression of matrix metalloproteinases (MMP-2 and MMP-9) in cultured trabecular meshwork cells.METHODS:Trabecular meshwork cells were cultured from trabecular tissues obtained from the POAG patients aged 23 to 45. The mRNA expression of MMP-2 and MMP-9 was determined by reverse transcription-polymerase chain reaction, and the protein expression of MMP-2 and MMP-9 by gelatin zymography analysis and qualified by the gel electrophoresis image analysis in different HA concentrations.RESULTS:The expression of MMP-2 and MMP-9 by the two methods significantly increased with HA concentration in a dose-response manner. Mean values of the MMP-2 expression by the gelatin zymography analysis were 176, 264, 353, and 448 mg/ml, and mean values of the MMP-9 expression were 547, 659, 895, and 1,147 mg/ml, for HA concentration level of 0, 1, 3, and 6 mg/ml, respectively.CONCLUSIONS:In POAG trabecular meshwork cells, the level of HA concentration increases the activities of MMP-2 and MMP-9. The lack of HA in aqueous humor can result in a reduction in activities of MMPs and therefore may be involved in the pathogenesis of POAG.

Background Primary open angle glaucoma (POAG) is a major blindness-causing disease,characterized by elevated intraocular pressure due to an insufficient outflow of aqueous humor. The trabecular meshwork lining the aqueous outflow pathway modulates the aqueous outflow facility. To study the biological characteristics of the trabecular meshwork cells has important significance. Objective This study was to culture the trabecular cells from primary open-angle glaucomatous eye (POAG) and study the biologic characteristics of passaged cells. Methods The deep scleral tissue with trabecular meshwork was obtained during the trabeculectomy from 8 eyes with POAG. The trabecular cells were primarily cultured and passaged in vitro. The generation 3 cells were identified by immunochemistry with the laminin (LM), fibronectin (FN) and neuron specific endolase (NSE)monoclonal antibodies. The ultrastructure was examined to observe the biological characteristics of the cells under the transmission electronic microscope. The experimental results were compared among POAG group, normal control group and blank control group. Results The primarily cultured POAG trabecular cells migrated from the edge of tissue mass about 10 days. The cells of generation 3 presented the logarithmic phase in the first 4 days and fused in the 7th day. FN,LM and NSE were positively expressed in the generated cells in POAG group and normal control group rather than blank control group. The MOD values of the generation 3 cells for FN in POAG group and normal control group were 0. 35 ± 0.06 and 0. 26 ± 0. 01, and those for LM were 0. 34 ± 0. 03 and 0. 25 ± 0. 02 respectively, showing statistically significant difference between these two groups ( FN: t = 14. 446, P＜0.001; LM: t = 9. 346, P＜0. 001 ). The microvilli, cytolysosome and phagocytic vesicle were obviously decreased in the trabcular cells of POAG group compared with normal control group under the transmission electron microscope. Conclusion The trabecular meshwork cells from POAG can be successfully cultured and passaged in vitro. It provides a cytology basis for further glaucoma research.

Objective To study the relationship between fibronectin and primary open-angle glaucoma (POAG) pathogenesis by investigating the effect of fibronectin on the proliferation, adhesion and migration of human trabecular meshwork cells (HTC) in POAG patients. Methods Using HTC that were successfully established from the albuginea oculi in the trabeculectomy of patients, HTC were cultivated for primary culture and subculture. The third passage cells were incubated with different doses of fibronectin (5, 10, 20, 40, 100 μg/ml) cultivated with DMEM/F12. No fibronectin was used in the control group. In order to see the effect of different doses of fibronectin on cell proliferation, adhesion and migration, a Cell Counting Kit-8 and Transwell Kit were used after 24 hours of cultivation. The number of living cells was calculated to detect the optical density value and the data was used to calculate the results, with SPSS 17.0 statistics software. The normal distribution of data between the 2 groups was analyzed with a One-Way ANOVA. SNK test was used to compare the difference between groups. Results POAG trabecular meshwork cells were identified and confirmed with immunocytochemistry and electron microscopy. After 24 hours, a serum -free culture was incubated with different doses of fibronectin (5, 10, 20, 40, 100 μg/ml) cultivated with DMEM/F12. Different doses of fibronectin (5, 10, 20, 40, 100 μg/ml) significantly promote the proliferation of POAG trabecular meshwork cells. However, the proliferation of POAG trabecular meshwork cells with lower doses of fibronectin (5, 10 μg/ml) promote a relatively slow proliferation. There was an upward trend with an increase after the dosage of 10 μg/ml, and proliferation of trabecular meshwork cells reached a peak with higher doses of fibronectin (40 μg/ml). High doses of fibronectin (100 μg/ml) still promote the proliferation of cells, but the proliferation is relatively slow. The difference was significant compared to the control group (P<0.01). Fibronectin (5, 10, 20, 40, 100 μg/ml) promotes adhesion and migration of POAG trabecular meshwork cells, that showed an upward trend. The difference was significant compared to the control group (P<0.05). Conclusion Based on this data, it is possible that fibronectin affects intraocular pressure by affecting the proliferation, adhesion and migration of trabecular meshwork cells POAG patients that control outflow in the trabecular meshwork.

随着对原发性开角型青光眼研究的深入和进展,许多研究结果表明人眼中透明质酸的含量失衡,可使房水滤过阻力增加,眼压升高;CD44分子与透明质酸之间相互作用的失调,可引起小梁网细胞丢失、死亡,影响小梁网细胞内环境的稳定,并且与视网膜神经节细胞的数量减少、活性下降以及视野缺损存在一定关联.透明质酸还可能通过影响基质金属蛋白酶的分泌,参与原发性开角型青光眼的发病.