Examining the etiological factors resulting in retinal detachment following prophylactic vitrectomy in the context of acute retinal necrosis syndrome.

OBJECTIVE: The aim of this study is to elucidate the factors contributing to the occurrence of retinal detachment (RD) following prophylactic vitrectomy in cases of acute retinal necrosis (ARN) syndrome. METHODS: A retrospective examination was undertaken, encompassing the medical records of patients diagnosed with ARN who underwent prophylactic vitreous intervention at the Ophthalmology Department of Wuhan University Renmin Hospital East Campus between October 2019 and September 2023. Subsequently, patients who manifested RD in the postoperative period were identified, and a comprehensive analysis was conducted to ascertain the factors underlying the occurrence of RD post-surgery. RESULTS: This study comprised 14 cases (involving 14 eyes) of patients diagnosed with ARN who underwent prophylactic vitreous intervention. The findings revealed that 4 patients experienced postoperative RD, resulting in an incidence rate of 28.57%. Notably, among these cases, 3 cases of RD manifested in the presence of silicone oil, while 1 case occurred subsequent to the removal of silicone oil. All 4 cases of RD exhibited varied degrees of proliferative vitreoretinopathy. Following the occurrence of RD, all patients underwent a secondary vitreous intervention coupled with silicone oil tamponade, leading to successful reattachment of the retina. However, despite these interventions, there was no significant enhancement observed in postoperative visual outcomes when compared to preoperative levels. CONCLUSION: RD following prophylactic vitrectomy in cases of ARN is not an infrequent occurrence and is primarily linked to the postoperative onset of proliferative vitreoretinopathy.

Contemplating the necessity of surgical treatment for posterior lenticonus: a case report.

BACKGROUND: Posterior lenticonus is an uncommon congenital abnormality that causes a progressive, localized spherical or conical bulging of the posterior capsular membrane, resulting in an abnormal shape of the lens. CASE PRESENTATION: A 13-year-old girl presented with ametropia in both eyes. After mydriasis, examination revealed an oval bubble-shaped alteration with a distinct boundary above the temporal region on the center of the posterior capsule of her left lens. The subcortical region surrounding the alteration appeared feathery and turbid. The patient had no history of trauma or family history of visual impairment. Systemic investigations were normal. A thorough eye examination was performed, which included optometry, ultrasound biomicroscopy, ocular B-Scan, and anterior segment optical coherence, to assess the disease. The patient was diagnosed with posterior lenticonus in the left eye, as well as ametropia and anisometropia in both eyes. Conservative treatment was initiated since the patient's current best corrected visual acuity was good, and regular monitoring of the condition's progression was scheduled. CONCLUSIONS: This case report presents a rare instance of posterior lenticonus. The findings of this report raise new considerations regarding the necessity of surgical intervention for this condition.

Risk Factors for Dry Eye Syndrome: A Retrospective Case-Control Study.

PURPOSE: To investigate the independent risk factors of dry eye syndrome (DES) in Chinese. METHODS: A hospital-based age- and sex-matched population was enrolled with a case-control ratio of 1:2, with 789 DES case patients and 1119 healthy family members. Both groups underwent standard ophthalmologic examinations, including slit-lamp evaluation of the anterior segment, measurement of tear film breakup time, Schirmer test, and corneal fluorescein staining. Data on demographic characteristics and lifestyle habits were collected using a questionnaire. Dry eye syndrome risk factors were identified by univariate and multivariate logistic regression analyses. RESULTS: The following independent risk factors showed significant association with DES: diabetes (odds ratio [OR], 1.408; 95% confidence interval [CI], 1.031 to 1.924), hepatitis C (OR, 3.326; 95% CI, 1.632 to 6.776); connective tissue disease (OR, 2.157; 95% CI, 1.679 to 2.771), benign prostatic hyperplasia (OR, 3.892; 95% CI, 2.476 to 6.116), rosacea (OR, 3.747; 95% CI, 1.972 to 7.120), posttraumatic stress disorder (OR, 1.449; 95% CI, 1.043 to 2.013), hematopoietic stem cell transplantation (OR, 7.269; 95% CI, 2.312 to 22.849), head and neck radiotherapy (OR, 8.776; 95% CI, 3.096 to 24.873), postmenopausal estrogen therapy (OR, 1.912; 95% CI, 1.160 to 3.151), antihistamines (OR, 2.040; 95% CI, 1.516 to 2.746), antidepressants (OR, 1.982; 95% CI, 1.077 to 3.647), contact lenses (OR, 2.366; 95% CI, 1.266 to 4.423), and video display terminal exposure for more than 6 h/d (OR, 2.275; 95% CI, 1.451 to 3.568). Potentially protective factors against DES were vitamin supplements (OR, 0.716; 95% CI, 0.528 to 0.972) and Ω-3 fatty acid-rich diet (OR, 0.514; 95% CI, 0.332 to 0.796). CONCLUSION: Several known risk factors of DES are applicable to Chinese, and some distinctive dietary factors may be protective in this population.

Delayed growth of glioma by a polysaccharide from Aster tataricus involve upregulation of Bax/Bcl-2 ratio, activation of caspase-3/8/9, and downregulation of the Akt.

In this study, a homogeneous polysaccharide (ATP-II), with a molecular weight of 3.4 × 10(4) Da, was successfully purified from Aster tataricus by DEAE-Sepharose CL-6B ion exchange and Sepharose CL-6B gel filtration chromatography. Monosaccharide component analysis indicated that ATP-II was composed of glucose, galactose, mannose, rhamnose, and arabinose in molar ratios of 2.1:5.2:2.1:1.0:1.2. We evaluated the anticancer efficacy and associated mechanisms of ATP-II on glioma C6 cells in vitro and in vivo. The results showed that treatment of C6 cells with ATP-II inhibited cell proliferation and this biological response came from induction of DAN damage and consequent inducing apoptosis. Likewise, oral ATP-II administration resulted in consistent regression of glioma tumors and induced apoptosis of transplanted tumor tissues by increasing the ratio of Bax/Bcl-2 and activation of caspase-3, caspase-8, and caspase-9 cascade. Importantly, the efficient downregulation of Akt, which is successfully detected in tumor tissues, is a unique contribution to retard the tumor growth by ATP-II. These data suggest that ATP-II may be a potential candidate for glioma treatment.

N -methyl- N -nitrosourea-induced retinal degeneration in mice.

Mouse retinal degeneration models have been investigated for many years in the hope of understanding the mechanism of photoreceptor cell death. N -methyl- N -nitrosourea (MNU) has been previously shown to induce outer retinal degeneration in mice. After MNU was intraperitoneally injected in C57/BL mice, we observed a gradual decrease in the outer nuclear layer (ONL) thickness associated with photoreceptor outer segment loss, bipolar cell dendritic retraction and reactive gliosis. Reactive gliosis was confirmed by increased GFAP protein levels. More serious damage to the central retina as opposed to the peripheral retina was found in the MNU-induced retinal degeneration model. Retinal ganglion cells (RGC) appear to be spared for at least two months after MNU treatment. Following retinal vessel labelling, we observed vascular complexes in the distal vessels, indicating retinal vessel damage. In the remnant retinal photoreceptor of the MNU-treated mouse, concentrated colouring nuclei were detected by electron microscopy, together with the loss of mitochondria and displaced remnant synaptic ribbons in the photoreceptor. We also observed decreased mitochondrial protein levels and increased amounts of nitrosylation/nitration in the photoreceptors. The mechanism of MNU-induced apoptosis may result from oxidative stress or the loss of retinal blood supply. MNU-induced mouse retinal degeneration in the outer retina is a useful animal model for photoreceptor degeneration diseases, such as age-related macular degeneration (AMD) and retinitis pigmentosa (RP).

Ameliorative effect of resveratrol on acute ocular hypertension induced retinal injury through the SIRT1/NF-κB pathway.

Glaucoma is a kind of neurodegenerative disorder characterized by irreversible loss of retinal ganglion cells (RGCs) and permanent visual impairment. It is reported that resveratrol (RES) is a promising drug for neurodegenerative diseases. However, the detailed molecular mechanisms underlying its protective potential have not yet been fully elucidated. The present study sought to investigate whether resveratrol could protect RGCs and retinal function triggered by acute ocular hypertension injury through the SIRT1/NF-κB pathway. An experimental glaucoma model was generated in C57BL/6J mice. Resveratrol was intraperitoneally injected for 5 days. Sirtinol was injected intravitreally on the day of retinal AOH injury. RGC survival was determined using immunostaining. TUNEL staining was conducted to evaluate retinal cell apoptosis. ERG was used to evaluate visual function. The proteins Brn3a, SIRT1, NF-κB, IL-6, Bax, Bcl2, and Cleaved Caspase3 were determined using western blot. The expression and localisation of SIRT1 and NF-κB in the retina were detected by immunofluorescence. Our data indicated that resveratrol treatment significantly increased Brn3a-labelled RGCs and reduced RGC apoptosis caused by AOH injury. Resveratrol administration also remarkably decreased NF-κB, IL-6, Bax, and Cleaved Caspase3 proteins and increased SIRT1 and Bcl2 proteins. Furthermore, resveratrol treatment obviously inhibited the reduction in ERG caused by AOH injury. Importantly, simultaneous administration of resveratrol and sirtinol abrogated the protective effect of resveratrol, decreased NF-κB protein expression, and increased SIRT1 protein levels. These results suggest that resveratrol administration significantly mitigates retinal AOH-induced RGCs loss and retinal dysfunction, and that this neuroprotective effect is partially regulated through the SIRT1/NF-κB pathway.

Modeling of diseases of retinal ischemia in vitro: possible participation of autocrine vascular endothelial growth factor signaling.

PURPOSE: To establish and evaluate a novel in vitro model of retinal ischemia, and to determine whether an autocrine pathway of retinal microvascular endothelial cells (RMVECs) by vascular endothelial growth factor (VEGF) signaling plays a role based on this model. METHODS: Primary RMVECs were isolated from the retinas of C57/BL6J rats and identified by an evaluation for FITC-marked CD31. The hypoxia models were established with the biobag at the time of 12, 24, 48 and 72 h, and evaluated with a blood-gas analyzer. The control groups were incubated under normoxic conditions for the same length of time. Cell proliferation was evaluated by the CCK-8 method. Apoptosis was assayed using a flow cytometry method. RNA and protein expressions of VEGF-A, VEGFR-2 and iNOs were analyzed by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: The results of blood-gas analysis showed that when the cultures were exposed to hypoxia for more than 2 h, the pO(2) was below 4.5 kPa, pCO(2) and pH shifted slightly. Real-time RT-PCR revealed that the expressions of VEGF-A, VEGFR-2 and iNOs mRNA in hypoxic groups increased in comparison to those in the normoxia groups (p < 0.01) and the expression of mRNA increased significantly in a time-dependent fashion in the hypoxic groups (p < 0.01), peaking at 48 h, and then decreasing. Western blot analysis revealed that the expression of relative proteins ranked in this order. CCK-8 analysis revealed that the proliferative capacity of RMVECs in the hypoxic groups was significantly higher than those in the normoxic groups at each time point (p < 0.05). At 48 h, the proliferative capacity was highest in the hypoxia groups (p < 0.05). Data acquisition from flow cytometry showed that cell survival rates in the hypoxic groups were higher than those in the normoxic groups and apoptosis rates dropped accordingly. The survival rate was highest at 48 h. CONCLUSION: These findings suggested that a novel in vitro model of retinal ischemia using the biobag had a good authenticity. According to the well-established in vitro hypoxia model by the biobag, RMVECs include the requisite elements for an autocrine pathway that may serve to amplify the angiogenic effects of VEGF.

[Overexpression of 15-lipoxygenase-1 inhibits oxygen-induced retinal neovascularization in mice].

OBJECTIVE: To investigate the mechanism and inhibitory effects of overexpression of 15-lipoxygenase-1 inhibiting oxygen-induced retinal neovascularization in mice. METHODS: Experimental study. Eighty-eight 7-day-old C57BL/6J mice were randomly divided into the normal control group, induced model group, gene treated group and empty vector group with 22 mice in each group. The mice with their mothers were arisen in 75% ± 2% O2 environment for 5 days and then returned to normoxia for 5 days to establish the oxygen-induced retinopathy (OIR) model. At postnatal day 12, the gene treated group was received an intravitreous injection of Ad-15-LOX-1-EGFP at 1.0 µl, while the empty vector group was received the same volume of Ad-EGFP. At postnatal day 17, real-time PCR and Western Blot methods were used to detect the mRNA and protein expression levels of 15-LOX-1, peroxisome proliferator-activated receptor γ (PPAR-γ) , vascular endothelial growth factor-A (VEGF-A) and vascular endothelial growth factor receptor 2 (VEGFR-2) in the retina. The relative retinal non-perfusion and neovascularization areas were evaluated by FITC-dextran fluorescein angiography on flat-mounted retina. The number of endothelial cell nuclei breaking through the inner limiting membrane (ILM) was counted on hematoxylin and eosin-stained retinal section. Rank sum test and one-way ANOVA were used to assess statistical significance within groups. RESULTS: The 15-LOX-1 and PPAR-γ mRNA and protein expression levels were higher in gene treated group (15-LOX-1: 2.17 ± 0.25, 1.45 ± 0.10;PPAR-γ:2.12 ± 0.29, 0.85 ± 0.03) than those in induced model group (15-LOX-1:0.62 ± 0.03, 0.66 ± 0.04; PPAR-γ:0.67 ± 0.18, 0.48 ± 0.03) and empty vector group (15-LOX-1:0.51 ± 0.14,0.57 ± 0.03;PPAR-γ:1.07 ± 0.09,0.52 ± 0.02) ( t15-LOX-1 = 12.511, 13.402, both P < 0.01; tPPAR-r = 9.420, 6.813, both P < 0.01). On the contrary,VEGF-A and VEGFR-2 expression levels were lower in gene treated group ( VEGF-A: 0.87 ± 0.07, 0.34 ± 0.01; VEGFR-2:1.02 ± 0.12, 0.45 ± 0.03) than those in induced model group ( VEGF-A: 3.49 ± 0.53,0.74 ± 0.04; VEGFR-2:2.28 ± 0.44, 0.82 ± 0.01) and empty vector group ( VEGF-A: 2.30 ± 0.25,0.69 ± 0.02; VEGFR-2:1.88 ± 0.16, 0.76 ± 0.03) (tVEGF-A = 10.662, 5.843, both P < 0.01; tVEGFR-2 = 6.731, 4.763, both P < 0.01). The relative retinal non-perfusion and neovascularization areas were significantly smaller, and the number of endothelial cell nuclei breaking through the ILM was obviously lower in gene treated group(5.88 ± 1.12; 9.37 ± 1.85; 1.25 ± 0.89) than those in induced model group (21.25 ± 2.87; 24.13 ± 4.29; 60.63 ± 10.82) and empty vector group (19.50 ± 1.78; 23.13 ± 3.52; 54.63 ± 7.63) (P < 0.01; P < 0.01). CONCLUSION: Overexpression of 15-LOX-1 inhibits ORI neovascularization in mice via up-regulation of PPAR-γ and down-regulation of VEGF-A and VEGFR-2 expression.

[The gene mutation screening of a family with congenital fibrosis of the extraocular muscles associated with corpus callosum agenesis].

OBJECTIVE: To identify TUBB3 gene mutations in a Chinese family with congenital fibrosis of the extraocular muscle associated with corpus callosum agenesis. METHODS: We have found a family with CFEOM associated with corpus callosum agenesis, including 4 affected individuals in three generations of 11 familial members. 4 affected individuals were sequenced by direct TUBB3 sequencing, 4 unaffected individuals in the family and 100 cases of unrelated normal person as a control. RESULTS: This family is in line with Mendelian autosomal dominant inheritance. Clinical manifestations belongs to CFEOM3. All affected individuals were detected with TUBB3 c.1249G > A mutation, the mutation is in exon 4, resulting in wild-type gene encoding the Aspartic acid ( Asp or D ) replaced .by Asparagine (Asn or N ). CONCLUSION: Our study supports that TUBB3 gene mutation c.1249G > A (p. Asp417Asn), is the underlying molecular pathogenesis of this family with CFEOM3.

Overexpression of 15-lipoxygenase-1 in oxygen-induced ischemic retinopathy inhibits retinal neovascularization via downregulation of vascular endothelial growth factor-A expression.

PURPOSE: 15-Lipoxygenase-1 (15-LOX-1) plays an important role in regulating angiogenesis, but the mechanism to date is controversial, even contradictory. The goal of our study was to investigate whether 15-LOX-1 plays a role in inhibiting retinal neovascularization (RNV) in a mouse model of oxygen-induced retinopathy (OIR) and the underlying mechanism. METHODS: Experiments were performed using retinas from a mouse model of OIR that was treated with and without intravitreous injection of adenoviral-15-lipoxygenase-1 (Ad-15-LOX-1) or adenoviral-green fluorescence protein (Ad-GFP) at postnatal day 12 (P12). At P17, the efficacy of the gene transfer was assessed with immunofluorescence staining. RNV was evaluated with fluorescein angiography on flatmounted retinas and quantified by counting the preretinal neovascular cells. Expression of 15-LOX-1 and vascular endothelial growth factor-A (VEGF-A) were determined with real-time PCR and western blot. RESULTS: RNV during OIR was associated with decreased 15-LOX-1 expression, and retinal 15-LOX-1 levels were negatively correlated with the progression of RNV. In the intravitreous injected Ad-15-LOX-1 mice with OIR, retinal 15-LOX-1 expression was significantly increased at the protein and mRNA levels at P17. 15-LOX-1 expression was clearly demonstrated, primarily in the outer plexiform layer, inner nuclear layer, and ganglion cell layer retinas, five days after gene delivery. Fluorescein retinal angiography and quantification of the preretinal neovascular cells demonstrated that RNV was significantly inhibited. Meanwhile, the expression levels of VEGF-A were significantly decreased at the transcriptional and translational levels. CONCLUSIONS: Our results suggest that overexpression of 15-LOX-1 inhibits RNV in a mouse model of OIR via downregulation of VEGF-A expression, and 15-LOX-1 may be a novel therapeutic target for ocular neovascularization diseases.

TNF-α stimulates MMP-2 and MMP-9 activities in human corneal epithelial cells via the activation of FAK/ERK signaling.

AIMS: Herpes simplex virus type-1-induced herpes simplex keratitis (HSK) is a common immunological cornea disease. While previous studies have addressed the role of tumor necrosis factor (TNF)-α and matrix metalloproteinases (MMPs) in HSK, the mechanistic link between TNF-α and MMPs in the pathogenesis of HSK remains elusive. METHODS: We first established a HSK mice model and measured the levels of TNF-α, MMP-2 and MMP-9 in the corneas at different time points by ELISA. Next, we employed cultured human corneal epithelial (HCE) cells as an in vitro model and performed gelatin zymography analysis. RESULTS: We observed that the change in the TNF-α level shared a similar pattern to that of MMP-2 and MMP-9 in the HSK mice model. Furthermore, TNF-α stimulated MMP-2 and MMP-9 activities in a dose-dependent manner, but either knockdown of focal adhesion kinase (FAK) by short interference RNA or inhibition of extracellular regulated protein kinase (ERK) by chemical inhibitor could block TNF-α-stimulated MMP-2 and MMP-9 activities in vitro. Taken together, our results provide in vivo evidence that the TNF-α level is positively correlated with MMP-2 and MMP-9 levels in a HSK model and in vitro evidence that TNF-α stimulates MMP-2 and MMP-9 activities via the activation of FAK/ERK signaling in HCE cells. CONCLUSIONS: Our findings shed new light on the pathogenesis of HSK and open up new possibility of modulating the TNF-α-FAK-ERK signaling cascade to pursue therapeutic measures for HSK.

[siRNA-mediated downregulation of the integrin-linked kinase alters the proliferation and apoptosis in retinoblastoma cells].

OBJECTIVE: To explore the effects of siRNA-mediated downregulation of integrin-linked kinase (ILK) gene expression on the proliferation and apoptosis in retinoblastoma cells. METHODS: Experiment study. Human retinoblastoma cells, HXO-Rb(44) cells, were divided into four groups: ILK siRNA intervention group, control siRNA intervention group, empty liposome group and blank control group. ILK siRNA was transfected into HXO-Rb(44) cells by lipofection. The expression of ILK mRNA and protein was detected at 48 hours after transfection by RT-PCR and Western blot, respectively. Cell proliferation inhibition was measured by Cell Counting Kit-8 assay. The apoptosis was detected by Annexin/PI double immunofluorescence and flow cytometry. Statistical method adopted one-way ANOVA between each group overall comparison. RESULTS: The HXO-Rb(44) cells were transfected by ILK siRNA successfully with lipofection. RT-PCR analysis showed that the expression of ILK mRNA in the ILK siRNA intervention group was significantly decreased as compared to the control siRNA intervention group, empty liposome group and blank control group (0.12 ± 0.02 vs. 0.45 ± 0.04, 0.42 ± 0.05 and 0.40 ± 0.04, F = 12.781, P = 0.000). Similar results were obtained for protein expression as revealed by Western blot analysis (0.10 ± 0.03 vs. 0.38 ± 0.07, 0.40 ± 0.05 and 0.43 ± 0.03, F = 18.647, P = 0.000). The proliferation inhibition rate in the ILK siRNA intervention group (35.0%) was higher than that in the blank control group (0%), control siRNA intervention group (2.1%) and empty liposome group (1.8%) (F = 23.573, P = 0.000). The results of immunofluorescence and flow cytometry showed that ratio of Annexin positive cells was highest in the ILK siRNA intervention group (26.5%), which was 5.0%, 4.6%, 5.3% in the empty liposome group, blank control group, control siRNA intervention group, respectively (F = 65.217, P = 0.000). CONCLUSION: ILK siRNA can downregulate the expression of ILK gene in HXO-Rb(44) cells inhibited the cell proliferation and induced their apoptosis.

[A family of congenital fibrosis of extraocular muscles associated with naso-sinusitis].

OBJECTIVE: To clinically characterize a collected family of congenital fibrosis of extraocular muscles associated with naso-sinusitis, then determine the genetic location of the disease gene by linkage analysis to approach the etiopathogenesis of CFEOM on gene. METHODS: A CFEOM family (fifteen cases suffering from congenital general fibrosis syndrome in four generations of 41 members) was collected. All the suffers were correlated with clinical ophthalmic and thin-sectioned magnetic resonance imaging across the orbit and the brain-stem level to determine its clinical classification and genetic characteristics. The family was tested for linkage analysis to two known autosomal dominant CFEOM loci on chromosome 12p11. 2-q12 (FEOM1 ) and 16q24 (FEOM3). RESULTS: All the suffers had congenital unilateral or bilateral blepharoptosis, head tilt, chin lift, primary gaze fixed in a hypo-and exotropic position, forced duction testing positive. But vertical and horizontal positions of the eye and restriction of eye movement were different among affected individuals. Furthermore, MRI examinations showed that all the incidence of those families associated with naso-sinusitis and hypertrophic inferior turbinate, and the juveniles with hypertrophic adenoid. Pedigree shows that the family were in line with the characteristics of autosomal dominant inheritance. According to the genetic characteristics and clinical manifestations, the genetic family should be referred as CFEOM3. The lod scores for D12S331, D12S59 and D12S1668 were between 1 and 3, and the maximum lod score was 2. 19 for D12S1048, but the lod scores for D16S520, D16S498 and D16S2621 were both < 1.0. CONCLUSION: This family is best classified as CFEOM3 and linkage with D12S331, D12S59 and D12S1668.

Retinal microvasculature features in patients with Behcet's disease: a systematic review and meta-analysis.

This meta-analysis aimed to analyze retinal microvasculature features in eyes with Behçet's disease (BD) using optical coherence tomography angiography (OCTA). Electronic databases, including PubMed, Web of Science, Embase, and Cochrane Library, were comprehensively searched for published studies comparing retinal microvasculature characteristics between eyes with BD and controls. Continuous variables were calculated using the mean difference (MD) with 95% confidence interval (CI). Review Manager software (version 5.30) was used to conduct statistical analysis. A total of 13 eligible studies involving 599 eyes with BD and 622 control eyes were included in the meta-analysis. The pooled results showed that the macular whole enface superficial and deep vessel density (VD) values measured by OCTA were significantly lower in eyes with BD than in control eyes (superficial VD: MD = - 3.05, P < 0.00001; deep VD: MD = - 4.05, P = 0.0004). The foveal superficial and deep VD values were also significantly lower in the BD group than in the control group (superficial VD: MD = - 1.50, P = 0.009; deep VD: MD = - 4.25, - = 0.03). Similarly, the analysis revealed a significant reduction in the parafoveal superficial and deep VD in eyes with BD than in control eyes (superficial VD: MD = - 3.68, P < 0.00001; deep VD: MD = - 4.95, P = 0.0007). In addition, the superficial and deep foveal avascular zones (FAZs) were significantly larger in patients with BD than in controls (superficial FAZ: MD = 0.06, P = 0.02; deep FAZ: MD = 0.12, P = 0.03). The present meta-analysis found that macular whole enface VD, foveal VD, and parafoveal VD were lower in eyes with BD, and the FAZ was larger in patients with BD. The findings suggest that OCTA can assist clinicians in diagnosing and monitoring the status of patients with BD.

Sweep pattern visual evoked potential acuity in children during their periods of visual development.

PURPOSE: To study the clinical usage of sweep pattern visual evoked potential (SPVEP) acuity in children's visual development periods and compare the amplitude-spatial frequency (A-SP) function regression method with the amplitude-logarithm of the visual angle (A-logVA) function regression method in evaluating the SPVEP acuity of children, especially those who have poor visual acuities. METHODS: Twenty-six eyes of 26 amblyopic children (ages ranged from 3 to 12 years; mean age±standard deviation 6.69±1.74 years) and 31 eyes of normal children whose ages were matched with the amblyopic group were involved in this study. SPVEP acuity was recorded with GT-2000 NV (Guote Medical Apparatus Ltd., China) using sinusoidally modulated horizontal gratings with 10 different spatial frequencies from 0.99 to 12.89 cycles per degree to stimulate the retina. The averaging responses were displayed with the discrete Fourier transformation method. SPVEP acuity was assessed by both the A-SP function regression method and the A-logVA function regression method. The logarithm of minimal angle of resolution (logMAR) chart was used to obtain logMAR visual acuity. RESULTS: In the normal group, logMAR acuity calculated by both the A-SP and A-logVA function regression methods had a significant correlation with SPVEP acuity. The average value of SPVEP acuity (by A-logVA) was closer to logMAR acuity. The difference of mean values between logMAR acuity and SPVEP acuity was significant in both regression methods. In the amblyopic group, it was SPVEP acuity (by A-logVA) that had a significant correlation with logMAR acuity, whereas the result was not significant when calculated by the A-SP function regression method (p=0.515). The average value of SPVEP acuity (A-SP) was closer to logMAR acuity. The difference of mean values between logMAR acuity and SPVEP acuity (A-logVA) was significant; however, when compared with SPVEP acuity (A-SP), it was not significant (p=0.174). In addition, SPVEP acuity may be overestimated or underestimated when it is compared with different logMAR visual acuities. CONCLUSION: SPVEP could be used to evaluate the visual acuity for normal children or those with poor visual acuity. Moreover, the A-logVA function regression method was more accurate than the A-SP function regression method in evaluating SPVEP acuity.

[Incidence and relative factors of Terson syndrome in patients with aneurysmal subarachnoid hemorrhage].

OBJECTIVE: To investigate the incidence and relative factors of Terson syndrome in patients with aneurysmal subarachnoid hemorrhage (SAH). METHODS: A prospective case series study was conducted in 202 eyes of 101 patients with aneurysmal subarachnoid hemorrhage from November 2009 to May 2010. Fundus examination and color fundus photograph under mydriasis were carried out on every patient diagnosed as Terson syndrome with initial direct ophthalmoscopy after their general state was stable. The incidence of Terson syndrome was analyzed and correlated with gender, consciousness state, Glasgow Coma Scale score (GCS) and Hunt-Hess grade, anatomical locations of the ruptured aneurysms, mortality rate. RESULTS: Fifteen (14.8%) Terson syndrome patients were diagnosed in a total of 101 aneurysmal subarachnoid hemorrhage patients. Analysis of our data revealed no statistically significant difference between men and women in regard to the incidence of Terson syndrome (χ(2) = 0.615, P > 0.05). A significant relationship was observed between consciousness state (χ(2) = 17.503, P < 0.05), GCS score (χ(2) = 7.673, P < 0.05), Hunt-Hess grade (χ(2) = 9.987, P < 0.05) and the incidence of Terson syndrome. A higher frequency of Terson syndrome was demonstrated in patients with consciousness disturbance, lower GCS score and higher Hunt-Hess grade. However, no correlation was found between localization of the ruptured aneurysm (χ(2) = 0.000, P > 0.05), mortality rate and the occurrence of Terson syndrome. One case required surgical treatment during follow-up. CONCLUSIONS: A higher frequency of Terson syndrome was observed in patients with aneurysmal subarachnoid hemorrhage, which had association with clinical conditions significantly. Therefore, the SAH patients with consciousness disturbance, lower GCS score and higher Hunt-Hess grade should be paid attention to ophthalmic conditions and performed fundus examination. The occurrence of Terson syndrome needs to be further explored whether to determine the prognosis in SAH patients. Terson hemorrhage absorbed spontaneously in most patients and required surgical intervention in very few patients.

[Effects of focal adhesional kinase signaling on TNF-α induced gelatinases activity in cornea epithelium].

OBJECTIVE: To investigate the effect of focal adhesional kinase (FAK) on tumor necrosis factor α (TNF-α)-induced MMP-2 and -9 activities in cornea epithelium. METHODS: Experimental research. The human corneal epithelial cells (HCE) were cultured in vitro. HCEs were incubated with different concentrations of TNF-α for 24 h, including 1 µg/L (group B), 10 µg/L (group C) and 100 µg/L (group D). The control group (group A) was incubated with phosphate buffer solution. The activities of MMPs were examined by gelatin zymography and the phosphorylation of FAK was examined by western blot analysis. FAK was down regulated by FAK siRNA following lipofectamine-mediated transfection in corneal epithelial cells. Down-regulation was confirmed using western blot analysis. Cells cultured with different concentrations of TNF-α (Groups B to D) and the control group (group A) was at similar volumes of media. Then the activities of MMP-2 and -9 were examined by gelatin zymography and the phosphorylation of FAK by western blot analysis. Statistical methods adopted one-way ANOVA and Tukey's honestly significant test between each group. RESULTS: Gelatin zymography: Activities of MMP-2 and -9 in TNF-α treated groups were greater than those of the control group. The activity of MMP-2 in A, B, C and D groups was 124.06 ± 4.06, 146.72 ± 5.51, 241.18 ± 5.65 and 389.95 ± 4.44, respectively with F = 2960.91, P = 0.000. The activity of MMP-9 in A, B, C and D groups was 122.78 ± 5.86, 165.70 ± 7.90, 479.49 ± 6.22 and 495.88 ± 5.03 (F = 4937.46, P = 0.000). Significant differences were found in each two groups (P = 0.000). Western blot analysis:the phosphorylation of FAK (p-FAK) in test groups (10-100 ng/ml) were significantly greater than that in control group (p-FAK of group C and D was 0.52 ± 0.03 and 0.61 ± 0.06, F = 431.03, P = 0.000). p-FAK levels in 100 ng/ml group were greater than that in 10 ng/ml group (P = 0.005). After down-regulating the protein FAK, TNF-α had no effect on the activity of MMP-2 (The data of MMP-2 were 55.13 ± 0.66, 55.67 ± 0.43, 55.49 ± 0.20 and 55.91 ± 0.37 in groups A, B, C and D, F = 2.73, P = 0.079). We detected the increasing activity of MMP-9 in group C, D and p-FAK in group D (The data of MMP-9's activity were 80.48 ± 0.39, 81.26 ± 0.62, 84.43 ± 0.47, 85.56 ± 0.61 in groups A, B, C and D, F = 105.80, P = 0.000). The activity of MMP-9 in group D was stronger than that from the group C (P = 0.019). We just only detected a small quantity of p-FAK in group D (0.47 ± 0.05), which was weaker than that before down regulating the protein FAK (t = 5.03, P = 0.001). CONCLUSION: Our results demonstrate the critical role of FAK in TNF-α induced activity of MMP-2 and -9 in human corneal epithelium cells. Blocking the FAK signaling pathway can reduce the activity of MMP-2 and -9 which may play an important role in prevention and treatment of corneal diseases.

Integrin-alpha5 mediates epidermal growth factor-induced retinal pigment epithelial cell proliferation and migration.

Proliferation and migration of retinal pigment epithelial (RPE) cells play a crucial role in proliferative vitreoretinopathy (PVR)-related pathology. Cytokines, including EGF, can result in RPE cell activation and cause PVR. In this study, integrin-alpha(5) expression was first studied in PVR membranes by immunofluorescence. Then the effect of EGF on integrin-alpha(5) expression was determined by flow cytometry, Western blot analysis and the reverse-transcription polymerase chain reaction (RT-PCR) in the ARPE-19 cell line. Proliferation and migration of ARPE-19 cells were measured by the methylthiazolyldiphenyl-tetrazolium bromide and Boyden chamber assays. We found that a higher level integrin-alpha(5) was present at the RPE cell surface in PVR compared with normal retina. EGF could dose dependently increase integrin-alpha(5) mRNA and protein levels in vitro. EGF promoted ARPE-19 cell proliferation and migration. Neutralizing integrin-alpha(5) by specific anti-integrin-alpha(5) antibody abolished most of the effects of EGF. The study provided evidence that EGF might influence PVR by promoting integrin-alpha(5) expression and subsequent proliferation and migration of RPE.

[Differentiation and apoptosis effects of all-trans retinoic acid on inducing umbilical cord mesenchymal stem cells into neuron-like cells].

OBJECTIVE: To evaluate the role of different concentration of all-trans retinoic acid (ATRA) on the morphology, proliferation and apoptosis in inducing umbilical cord mesenchymal stem cells (MSC) into neuron-like cells in vitro, and screen the optimal concentration of ATRA. METHODS: It was an experimental study. The third passage of MSC was placed in 24-well cell culture plates at a density of 1 × 10(4)/well. After the adherent of cells, the medium was changed to DMEM/F-12 containing different concentration of ATRA (0.25 µmol/L, 0.5 µmol/L, 1.0 µmol/L, 2.0 µmol/L, 4.0 µmol/L) for 24 h respectively. The cells cultured without ATRA were taken as the control group. After another 24 h, the morphologic changes of induced cells were observed by inverted microscope and cell proliferation, apoptosis of ATRA was analyzed using the MTT colorimetric assay. We take another control group and ATRA groups to detect the apoptotic and positive stained percentage of induced cells by Annexin V-FITC/PI combining flow cytometry. The optimal concentration of ATRA was determined by all the above-mentioned index. According to the nature of the material, analysis of variance (ANOVA) was employed for absorption value and apoptosis rate in different concentration of ATRA for 24 h, t test for further comparison between two groups. T-test were also used between the positive expression of induced neuron-like cells and the control group. RESULTS: Compared to the control group, ATRA at the concentration of 0.25 µmol/L did not inhibit the proliferation of umbilical cord MSC obviously (t = 0.72, 1.32, P > 0.05). Part of MSC were floating instantly at the moment of adding ATRA of 4.0 µmol/L and no adherent cells were observed after 24 h' culture. Exposed to ATRA at the concentration of ≥ 1.0 µmol/L for 24 h, the proliferation of MSC were significantly inhibited, showing a dose-dependent manner (t = 8.8, 18.9, 22.1; P < 0.01). 0.5 µmol/L of ATRA did not affect the proliferation of cells and its morphology remained normal; 1.0 µmol/L of ATRA affected very few cells; but 2.0 µmol/L of ATRA cultured for 24 h inhibited the proliferation of cells obviously than 1 h, and the cells increased in size and became flattened. Flow cytometry showed that the rate of apoptosis between the control group and ≥ 1.0 µmol/L groups were significantly different (t = 9.88, 19.95, 31.61; P < 0.01). CONCLUSION: In the process of inducing umbilical cord MSC into neuron-like cells, 0.5 µmol/L ATRA was the optical concentration. ≥ 1.0 µmol/L ATRA can inhibit the cell proliferation, increase the apoptosis of cells significantly and caused obvious damages.

Anomalous retinal artery associated with branch retinal artery occlusion and neovascular glaucoma: A case report.

BACKGROUND: Congenital anomalous retinal artery is rare and does not typically affect visual acuity. However, an abnormal artery that passes through and supplies blood to the macular area complicated with branch retinal artery occlusion may negatively impact visual acuity. This study reports an unusual case of anomalous retinal artery combined with retinal artery occlusion. CASE SUMMARY: A 52-year-old male presented with severely reduced vision in the right eye. The fundus examination revealed an anomalous artery, extending from the superior temporal arcade and crossing the macula into the inferior temporal quadrant. The anomalous artery was partially occluded, with a narrowed lumen. A cherry-red spot was observed with whitening of the macular area, suggesting macular edema. Fundus fluorescein angiography revealed disc leakage and a delayed filling time. Optical coherence tomography revealed increased thickness of the neuroretina and underlying layers. The patient was treated with vessel dilation, hyperbaric oxygen, ocular massage, and thrombolytics. Visual acuity of the right eye subsequently improved to 20/200 from hand motion at 4 cm. This improvement in visual acuity persisted when the patient was examined at the 1-mo follow-up visit. The patient was subsequently followed via telephone interview. The information provided via interview indicated that visual acuity in the affected eye was stable up to 6 years from the time of the initial presentation. However, after 3 additional years, the patient was diagnosed with neovascular glaucoma in the right eye, which was subsequently enucleated. CONCLUSION: Although congenital retinal vascular anomaly, including anomalous retinal artery, rarely affects vision, when complicated with branch retinal artery occlusion, the abnormal artery that supplies the macula may severely reduce visual acuity.