Abstract: Since the 21st century, the development of corneal tissue engineering technology has been developing rapidly. With the progress of biomaterials, cell culture and tissue engineering technology, tissue engineering cornea has gained great development in both basic scientific research and clinical application. In particular, tissue engineered corneal scaffolds are the core components of tissue engineered corneas. It is the focus of current research on tissue engineering cornea to search for scaffolds with good biocompatibility, high safety and good biomechanical properties. In this paper, the recent research progress of tissue engineering corneal materials is reviewed.
Abstract: The biological mechanisms of eye growth and refractive development are increasingly well characterised, a result of many careful studies that have been carried out over many years. As the outer coat of the eye, the sclera has the ultimate impact on the restraint or facilitation of eye growth, thus any changes in its biochemistry, ultrastructure, gross morphology and/or biomechanical properties are critical in refractive error development and, in particular, the development of myopia. The current review briefly revisits our basic understanding of the structure and biomechanics of the sclera and how these are regulated and modified during eye growth and myopia development. The review then applies this knowledge in considering recent advances in our understanding of how the mechanisms of scleral remodelling may be manipulated or controlled, in order to constrain eye growth and limit the development of myopia, in particular the higher degrees of myopia that lead to vision loss and blindness. In doing so, the review specifically considers recent approaches to the strengthening of the sclera, through collagen cross-linking, scleral transplantation, implantation or injection of biomaterials, or the direct therapeutic targeting and manipulation of the biochemical mechanisms known to be involved in myopia development. These latest approaches to the control of scleral changes in myopia are, where possible, placed in the context of our understanding of scleral biology, in order to bring a more complete understanding of current and future therapeutic interventions in myopia, and their consequences.
Abstract: Cornea serves as the partial front barrier and major light reflection organ of the eye. The integrity of corneal surface is essential for ocular function. Injuries or congenital diseases could significantly destruct the homeostasis of the ocular surface, especially the microenvironment of limbal epithelial stem cells (LESCs), and will eventually cause dysfunction of corneal regeneration and diminish of LESCs. The loss of LESCs by different reasons are named limbal stem cell deficiency (LSCD), which is one of the leading cause of vision loss worldwide. To restore the corneal surface, LESC transplantation in the form of tissue or cell cultures is currently a viable and promising method to treat LSCD. In this review, we aim to introduce the characters and niche of LESCs, and discuss different aspects of its application in cornea surface reconstruction.
Abstract: To describe the current aging population in China and globally, especially as it applies to age-related macular degeneration (AMD). To review the current standards of care for treating both wet (exudative) eAMD and dry (atrophic) aAMD. And to introduce a model for experimentation that is based on the Age-Related Eye Disease Study (AREDS) using eye bank tissue. A literature search that outlines current aging populations, standards of clinical treatment as defined by large, multicenter, randomized clinical trials that present level-I data with a low risk for bias. An experimental model system of AMD is presented that enables scientific analysis of AMD pathogenesis by applying grading criteria from the AREDS to human eye bank eyes. Analysis includes proteomic, cellular, and functional genomics. The standard of care for the treatment of eAMD is currently defined by the use of several anti-vascular endothelial growth (anti-VEGF) agents alone or in combination with photodynamic therapy. Monotherapy treatment intervals may be monthly, as needed, or by using a treat-and-extend (TAE) protocol. There are no proven therapies for aAMD. AMD that is phenotypically defined at AREDS level 3, should be managed with the use of anti-oxidant vitamins, lutein/zeaxanthin and zinc (AREDS-2 formulation). By understanding the multiple etiologies in the pathogenesis of AMD (i.e., oxidative stress, inflammation, and genetics), the use of human eye bank tissues graded according to the Minnesota Grading System (MGS) will enable future insights into the pathogenesis of AMD. Initial AMD management is with lifestyle modification such as avoiding smoking, eating a healthy diet and using appropriate vitamin supplements (AREDS-2). For eAMD, anti-VEGF therapies using either pro re nata (PRN) or TAE protocols are recommended, with photodynamic therapy in appropriate cases. New cellular information will direct future, potential therapies and these will originate from experimental models, such as the proposed eye bank model using the MGS, that leverages the prospective AREDS database.
Abstract: Contrast is the differential luminance between one object and another. Contrast sensitivity (CS) quantifies the ability to detect this difference: estimating contrast threshold provides information about the quality of vision and helps diagnose and monitor eye diseases. High contrast visual acuity assessment is traditionally performed in the eye care practice, whereas the estimate of the discrimination of low contrast targets, an important complementary task for the perception of details, is far less employed. An example is driving when the contrast between vehicles, obstacles, pedestrians, and the background is reduced by fog. Many conditions can selectively degrade CS, while visual acuity remains intact. In addition to spatial CS, “temporal” CS is defined as the ability to discriminate luminance differences in the temporal domain, i.e., to discriminate information that reaches the visual cortex as a function of time. Likewise, temporal sensitivity of the visual system can be investigated in terms of critical fusion frequency (CFF), an indicator of the integrity of the magnocellular system that is responsible for the perception of transient stimulations. As a matter of fact, temporal resolution can be abnormal in neuro-ophthalmological clinical conditions. This paper aims at considering CS and its application to the clinical practice.
Background: To evaluate the association between corneal central endothelial cell count (CECC) with reactivity for hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), human T-lymphotropic virus-1 (HTLV1), and syphilis from an eye bank database.
Methods: Eye bank data included 19,159 donors and 38,318 corneas screened for HBV, HCV, HIV, HTLV1, and syphilis from July 2007–May 2015. Linear and binary mixed effects models were used to determine the adjusted marginal effect a positive viral screening test had on CECC and morphology, respectively. The models were adjusted for age, race, gender, lens status, and death to preservation. Eyes with missing data were excluded from the analysis. Statistical significance was defined as P values <0.05.
Results: A total of 18,097 donors and 35,136 corneas were included in the final analysis. Average CECC for eyes with negative viral screening was 2,597±436 while the average CECC for eyes screening positive for syphilis, HBV, HCV, HIV, and HTLV1 were 2,638±392 (P=0.073), 2,569±419 (P=0.815), 2,603±363 (P=0.207), 2,615±360 (P=0.733), and 2,625±436 (P=0.362) respectively.
Conclusions: The presence of HBV, HCV, HIV, HTLV1, and syphilis display no association with a statistically significant difference in CECC when compared to normal non-diseased donors.
Background: The usage of the light emitting diode (LED) has been increasingly applied in the illumination setting and electronic equipment. However, the effect of LED lights on the retina remains unclear. In this study, we observed and analyzed the impact of white LED lights at different intensities on the function and morphology of rat retinas.
Methods: Thirty-six Sprague-Dawley rats weighing 150–180 g were randomly divided into six groups (n=6 in each group) including a normal control (NC) group, 4 white LED groups at different light intensities (4,000, 6,000, 7,000, and 10,000 lux), and an ultraviolet B (UVB) lighting group (302 nm, 1,000 μw/cm2). After 24 hours of continuous illumination, full-field flash electroretinogram (FERG) and pathological examination were performed in each group.
Results: As revealed by FERG, the impairment of retinal function gradually worsened with the increase of LED light intensity. In contrast, the UVB group had the most severe retinal function impairment. Particularly, the functional damage of rod cells and inner nuclear layer cells was the main FERG finding in each group. In the NC group, the retina had typical morphologies featured by well-defined structures, clearly visible border between the inner and outer segments, and neatly arranged inner and outer nuclear layer cells. After 24 hours of illumination, the inner and outer parts of the retina in the 4,000 lux group were still neatly arranged, along with a clear border; however, the inner and outer nuclear layers were randomly arranged, and some irregular nuclei and cells were lost. The damage of the internal and external retinal segments and the internal and external nuclear layers became more evident in the 6,000 lux group, 7,000 lux group, and 10,000 lux group. The UVB group had a more obviously disordered arrangement of inner and outer nuclear layers and loss of cells.
Conclusions: Continuous exposure to white LED light can cause structural and functional damage to rat retinas, and such damage is related to the intensity of illumination. Therefore, the risk of retinal damage should be considered during LED illumination, and proper LED illumination intensity may help to maintain eye health.
Background: To investigate the effect of sirolimus (SRL) eye drops on acute alkali-burn-induced corneal neovascularization (CNV) and explore its possible mechanism.
Methods: A total of 57 male Sprague-Dawley rats weighing 160–180 g were randomly divided into four groups including a normal control group (NC group, n=12), an untreated alkali-burned model control group (MC group, n=15), a blank eye drop treatment group (BT group, n=15), and an SRL eye drop treatment group (ST group, n=15). Corneal inflammation and CNV were observed and scored under a slit-lamp microscope 3, 7, and 14 days after alkali exposure. Three rats were randomly sacrificed in each group before modeling and 3, 7, 14 days after modeling, and the corneas of right eyes were harvested for Western blotting to compare the expression levels of VEGFR2 and caspase-3.
Results: Corneal inflammation scoring showed that the corneal edema and conjunctival congestion were severe in the MC, BT, and ST groups 1 day after alkali exposure but were alleviated at day 3. The corneal transparency was significantly higher in the ST group than in the MC and BT groups at days 7 (F=9.77, P<0.05) and 14 (F=5.81, P<0.05). At day 1, the corneal limbal vascular network was markedly filled. SNV was obvious at days 3, 7, and 14. The new blood vessels were shorter and sparser in the ST group than in the MC and BT groups, and the CNV scores showed significant differences among these groups (day 3: F=8.60, P<0.05; day 7: F=11.40, P<0.05; and day 14: F=41.59, P<0.01). Western blotting showed that the expressions of VEGFR2 and caspase-3 were low before modeling and showed no significant difference among the different groups (F=0.52, P>0.05; F=0.98, P>0.05). The corneal expression of VEGFR2 became significantly higher in the MC and BT groups than in the ST group 3, 7, and 14 days after alkali exposure, and there were significant differences in relative gray-scale values among these groups (day 3: F=32.16, P<0.01; day 7: F=85.96, P<0.01; day 14: F=57.68, P<0.01). The increase in the corneal expression of caspase-3 was significantly larger in the ST group than in the MC and BT groups at days 3, 7, and 14, and there were significant differences in relative gray-scale values among groups (day 3: F=32.16, P<0.01; day 7: F=53.02, P<0.01; day 14: F=38.67, P<0.01).
Conclusions: SRL eye drops can alleviate acute alkali-burn-induced corneal inflammation and inhibit alkali-burn-induced CNV in rat models. It can reduce VEGFR2 expression and increase caspase-3 expression in the corneal tissue, which may contribute to the inhibition of alkali-burn-induced CNV.
