Macular thickness measurements using Copernicus Spectral Domain Optical Coherence Tomography

Purpose

To provide normal macular thickness measurements using Spectral Domain Optical Coherence Tomography (SDOCT, Copernicus, Optopol Technologies, Zawierci, Poland).

Methods

Fifty-eight eyes of 58 healthy subjects were included in this prospective study. All subjects had comprehensive ophthalmic examination including best-corrected visual acuity (BCVA). All the subjects underwent Copernicus SDOCT. Central foveal thickness (CFT) and photoreceptor layer (PRL) thickness were measured and expressed as mean and standard deviation. Mean retinal thickness for each of the 9 regions defined in the Early Treatment Diabetic Retinopathy Study was reported. The data were compared with published literature in Indians using Stratus and Spectralis OCTs to assess variation in instrument measurements.

Results

The mean CFT in the study sample was 173.8 ± 18.16 microns (131–215 microns) and the mean PRL thickness was 65.48 ± 4.23 microns (56–74 microns). No significant difference (p = 0.148) was found between CFT measured automated (179.28 ± 22 microns) and manually (173.83 ± 18.1 microns). CFT was significantly lower in women (167.62 ± 16.36 microns) compared to men (180.03 ± 18 microns) (p = 0.008). Mean retinal thickness reported in this study was significantly different from published literature using Stratus OCT and Spectralis OCT.

Conclusion

We report the normal mean retinal thickness in central 1 mm area to be between 138 and 242 microns in Indian population using Copernicus SDOCT. We suggest that different OCT instruments cannot be used interchangeably for the measurement of macular thickness as they vary in segmentation algorithms.     

Patient-specific induced pluripotent stem cells (iPSCs) for the study and treatment of retinal degenerative diseases

Vision is the sense that we use to navigate the world around us. Thus it is not surprising that blindness is one of people's most feared maladies. Heritable diseases of the retina, such as age-related macular degeneration and retinitis pigmentosa, are the leading cause of blindness in the developed world, collectively affecting as many as one-third of all people over the age of 75, to some degree. For decades, scientists have dreamed of preventing vision loss or of restoring the vision of patients affected with retinal degeneration through drug therapy, gene augmentation or a cell-based transplantation approach. In this review we will discuss the use of the induced pluripotent stem cell technology to model and develop various treatment modalities for the treatment of inherited retinal degenerative disease. We will focus on the use of iPSCs for interrogation of disease pathophysiology, analysis of drug and gene therapeutics and as a source of autologous cells for cell transplantation and replacement.     

Myricetin inhibits advanced glycation end product (AGE)-induced migration of retinal pericytes through phosphorylation of ERK1/2, FAK-1, and paxillin in vitro and in vivo

Advanced glycation end products (AGE) have been implicated in the development of diabetic retinopathy. Characterization of the early stages of diabetic retinopathy is retinal pericytes loss, which is the result of pericytes migration. In this study, we investigated the pathological mechanisms of AGE on the migration of retinal pericytes and confirmed the inhibitory effect of myricetin on migration in vitro and in vivo. Migration assays of bovine retinal pericytes (BRP) were induced using AGE-BSA and phosphorylation of Src, ERK1/2, focal adhesion kinase (FAK-1) and paxillin were determined using immunoblot analysis. Sprague-Dawley rats (6 weeks old) were injected intravitreally with AGE-BSA and morphological and immunohistochemical analysis of p-FAK-1 and p-paxillin were performed in the rat retina. Immunoblot analysis and siRNA transfection were used to study the molecular mechanism of myricetin on BRP migration. AGE-BSA increased BRP migration in a dose-dependent manner via receptor for AGEs (RAGE)-dependent activation of the Src kinase-ERK1/2 pathway. AGE-BSA-induced migration was inhibited by an ERK1/2 specific inhibitor (PD98059), but not by p38 and Jun N-terminal kinase inhibitors. AGE-BSA increased FAK-1 and paxillin phosphorylation in a dose- and time-dependent manner. These increases were attenuated by PD98059 and ERK1/2 siRNA. Phosphorylation of FAK-1 and paxillin was increased in response to AGE-BSA-induced migration of rat retinal pericytes. Myricetin strongly inhibited ERK1/2 phosphorylation and significantly suppressed pericytes migration in AGE-BSA-injected rats. Our results demonstrate that AGE-BSA participated in the pathophysiology of retinal pericytes migration likely through the RAGE-Src-ERK1/2-FAK-1-paxillin signaling pathway. Furthermore, myricetin suppressed phosphorylation of ERK 1/2-FAK-1-paxillin and inhibited pericytes migration.     

Retinal vessel diameter and cardiovascular mortality: pooled data analysis from two older populations.

AIMS: The retinal microvasculature may reflect pre-clinical changes in the cerebral and coronary microcirculations. We assessed whether smaller retinal arterioles and larger venules predicted coronary heart disease (CHD)- and stroke-mortality. METHODS AND RESULTS: We pooled data from the Beaver Dam Eye Study (n = 4926, aged 43-86) and the Blue Mountains Eye Study (n = 3654, aged 49-97). Retinal vessel diameters were measured from digitized retinal photographs. Change point models were used to assess and document the existence of threshold effects. We defined smaller arterioles as diameters within the narrowest quintile and larger venules as diameters within the widest quintile, with other quintiles as the reference. Of 8550 participants, 7494 (88%) with complete data were included, of whom 653 died from CHD and 299 from stroke over 10-12 years follow-up. After multivariable adjustment, each standard deviation (SD) increase in arteriolar diameter, or SD decrease in venular diameter, was not found to be significantly associated with either CHD-mortality or stroke-mortality. However, smaller arterioles [hazard ratio (HR) 1.34, 95% confidence interval (CI) 1.11-1.62] and larger venules (HR 1.24, CI 1.02-1.52), predicted increased risk of CHD-mortality. These associations were mainly evident among persons aged 43-69 (smaller arterioles: HR 1.70, CI 1.27-2.28; larger venules: HR 1.41, CI 1.06-1.89). Smaller arterioles (HR 1.64, CI 1.00-2.67) and larger venules (HR 1.53, CI 0.94-2.47) were also associated with an increased risk of stroke-mortality among persons aged 43-69. CONCLUSION: Retinal vessel diameter may predict risk of CHD and stroke deaths in middle-aged persons.     

颈动脉支架术后视网膜动脉栓塞1例

<正>患者男,74岁,因间歇头晕,下肢乏力1月余入院。既往高血压病史10年,慢性胃炎,右手震颤10年。入院体检:体温36.6℃,脉搏规则、85次/分,呼吸规则、19次/分,血压138mmHg/74mmHg,神志清,查体合作,双侧视力粗测正常,左侧颈部检查未闻及血管杂音,右侧颈部可闻及血管杂音。经颈动脉彩色多普勒超声和CTA提示颈动脉狭窄,欲接受颈动脉支架治疗。入院2天后接受主动脉弓+全脑血管造影示左     

Effects of curcumin on interleukin-23 and interleukin-17 expression in rat retina after retinal ischemia-reperfusion injury

Objective: This study aimed to investigate the effect of curcumin on the retinal structure and the expressions of interleukin-23 (IL-23) and IL-17 in the rat retina after retinal ischemia-reperfusion injury (RIRI). Methods: 150 Sprague-Dawley rats were randomly divided into RIRI group (MG), low-dose curcumin group (LDCG) and high-dose curcumin group (HDCG), (n = 50 per group). RIRI was generated by anterior chamber perfusion of normal saline to the right eye. The left eye served as a normal control group (NCG). Rats in LDCG and HDCG received an intraperitoneal injection of 20 mg/kg/d and 100 mg/kg/d curcumin respectively, at 30 min before RIRI and once daily after RIRI. Results: The morphological changes in HDCG group were improved as compared to MG and LDCG groups. Immunohistochemistry showed that IL-23 and IL-17 were mainly expressed in the ganglion cell layer and the inner nuclear layer of the retina. Low IL-23 and IL-17 expressions were observed in NCG, but increased significantly in MG and LDCG groups. Western blot assay and ELISA also showed that IL-23 and IL-17 expressions increased significantly after RIRI (vs. NCG, P<0.01). Moreover, the IL-23 expression reached a peak at 24 h, whereas IL-17 expression peaked at 72 h after RIRI. Curcumin reduced IL-23 and IL-17 expressions significantly in a dose-dependent manner (vs. MG, P<0.01). Conclusion: The IL-23 and IL-17 expressions increase after RIRI and curcumin significantly reduces retinal IL-23 and IL-17 expressions in a dose-dependent manner and is able to prevent the RIRI induced damage to the retina.     

Blood-retinal barrier as a converging pivot in understanding the initiation and development of retinal diseases

Clinical ophthalmologists consider each retinal disease as a completely unique entity. However, various retinal diseases, such as uveitis, age-related macular degeneration, diabetic retinopathy, and primary open-angle glaucoma, share a number of common pathogenetic pathways. Whether a retinal disease initiates from direct injury to the blood-retinal barrier (BRB) or a defect/injury to retinal neurons or glia that impairs the BRB secondarily, the BRB is a pivotal point in determining the prognosis as self-limiting and recovering, or developing and progressing to a clinical phenotype. The present review summarizes our current knowledge on the physiology and cellular and molecular pathology of the BRB, which underlies its pivotal role in the initiation and development of common retinal diseases.     

高功率和微波辐照致家兔视网膜损伤的防护研究

目的 以定量组织病理学的重要指标节细胞层和内核细胞层的厚度和细胞计数为指标,探讨三七总皂甙和480目铜丝网对高功率微波所致的视网膜损伤进行药物防护和物理防护的效果.方法 将青紫蓝兔分为假辐射对照组、辐射组、三七总皂甙防护组和480目铜丝屏蔽组.观察各实验组视网膜组织的病理形态变化.结果 三七总皂甙预处理能显著减轻高功率微波辐照所致的视网膜组织的病理形态学损伤;480目铜丝网屏蔽防护,能完全屏蔽该频率高功率微波辐射,使视网膜组织结构维持正常,表现出良好的屏蔽防护效果.结论 三七总皂甙和480目铜丝网对高功率微波致视网膜损伤具有药物和物理防护作用,为探讨可供实用的高功率微波眼损伤防护措施提供实验依据.     

Microvascular retinal abnormalities in acute intracerebral haemorrhage and lacunar infarction

Background

Retinal microvascular changes have been previously associated with cerebral MRI markers of small vessel disease (SVD). Whether retinal changes differ between patient with intracerebral haemorrhage (ICH) and patients with lacunar infarction (LI) caused by small vessel disease has been poorly investigated.

Objective

The study aims to compare the frequency of retinal changes between patients with LI and patients with ICH at the acute stage of stroke-related SVD.

Methods

Microvascular wall signs (arteriolar occlusion, arteriovenous nicking, focal arterial narrowing) and retinopathy lesions (microanevrysms, cotton wool spots, retinal haemorrhages, hard exudates) were assessed by retinography up to three months after stroke onset.

Results

Forty-eight non-diabetic patients with acute stroke-related to SVD (26 LI, 22 ICH) were recruited prospectively in the study. Retinal wall signs (arteriovenous nicking, and focal arterial narrowing) were found in more than three quarters of subjects and most often bilaterally in both groups. Retinopathy lesions (cotton wool spots, retinal haemorrhages) were found more frequently in ICH patients than in LI patients (22.2% vs. 15.4%, 50% vs. 34% respectively, P > 0.005). The frequency of bilateral cotton wool spots and of bilateral retinal haemorrhages was significantly higher in ICH patients than in LI patients (12.5% vs. 0%, P = 0.012, 41.2% vs. 7.7%, P = 0.029 respectively).

Conclusion

These results confirm the high frequency of microvascular alterations in patients with hypertension-related SVD leading to LI or ICH and suggest that retinal tissue alterations are more frequent in ICH than in LI. Further investigations are needed to investigate the mechanisms underlying this difference.