scholarly journals Progressive cracking technique for phacoemulsification of superhard cataracts: a case report

2019 ◽  
Vol 6 (1) ◽  
Author(s):  
Yun-e Zhao ◽  
Zhangliang Li ◽  
Pingjun Chang ◽  
Dandan Wang ◽  
Man Hu
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Case Report ◽  
Corneal Edema ◽  
Corneal Endothelial Cell ◽  
Low Density ◽  
Corneal Endothelial Cells ◽  
Case Presentation ◽  
Finger Counting ◽  
Initial Learning

Abstract Background Complete nuclear disassembly of superhard cataracts cannot always be achieved by phaco chop, which is considered one of the best techniques for dealing with hard cataracts. We present a phaco chop-progressive cracking technique to divide superhard cataracts completely. Case presentation We presented a case of cataract with over Grade V nucleus sclerosis and very low density of corneal endothelial cell (812 cells/mm2). By performing the cataract surgery with our phaco chop-progressive cracking technique, the corneal endothelial cells were well protected and the patient’s visual acuity was markedly improved from finger counting at 40 cm to 20/200 the day after surgery without obvious corneal edema. Conclusions Although an initial learning curve was needed, this phaco chop-progressive cracking technique could be of particular benefit to the superhard cataract, especially in patients with low density of corneal endothelial cells.

scholarly journals Sodium Ferulate Attenuates Lidocaine-Induced Corneal Endothelial Impairment

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Guojian Jiang ◽  
Tingjun Fan
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Morphological Changes ◽  
Corneal Thickness ◽  
Cell Loss ◽  
Corneal Endothelial Cell ◽  
Corneal Endothelial Cells ◽  
Endothelial Cell Loss ◽  
Sodium Ferulate ◽  
Human Corneal Endothelial Cells

The introduction of intracameral anaesthesia by injection of lidocaine has become popular in cataract surgery for its inherent potency, rapid onset, tissue penetration, and efficiency. However, intracameral lidocaine causes corneal thickening, opacification, and corneal endothelial cell loss. Herein, we investigated the effects of lidocaine combined with sodium ferulate, an antioxidant with antiapoptotic and anti-inflammatory properties, on lidocaine-induced damage of corneal endothelia with in vitro experiment of morphological changes and cell viability of cultured human corneal endothelial cells and in vivo investigation of corneal endothelial cell density and central corneal thickness of cat eyes. Our finding indicates that sodium ferulate from 25 to 200 mg/L significantly reduced 2 g/L lidocaine-induced toxicity to human corneal endothelial cells, and 50 mg/L sodium ferulate recovered the damaged human corneal endothelial cells to normal growth status. Furthermore, 100 mg/L sodium ferulate significantly inhibited lidocaine-induced corneal endothelial cell loss and corneal thickening in cat eyes. In conclusion, sodium ferulate protects human corneal endothelial cells from lidocaine-induced cytotoxicity and attenuates corneal endothelial cell loss and central corneal thickening of cat eyes after intracameral injection with lidocaine. It is likely that the antioxidant effect of sodium ferulate reduces the cytotoxic and inflammatory corneal reaction during intracameral anaesthesia.

scholarly journals Corneal endothelial cell dysfunction: etiologies and management

2018 ◽  
Vol 10 ◽  
pp. 251584141881580 ◽  
Author(s):  
Sepehr Feizi
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Corneal Endothelial Cell ◽  
Endothelial Cell Dysfunction ◽  
Endothelial Keratoplasty ◽  
Corneal Endothelial Cells ◽  
Cell Dysfunction ◽  
Corneal Endothelial Dysfunction

A transparent cornea is essential for the formation of a clear image on the retina. The human cornea is arranged into well-organized layers, and each layer plays a significant role in maintaining the transparency and viability of the tissue. The endothelium has both barrier and pump functions, which are important for the maintenance of corneal clarity. Many etiologies, including Fuchs’ endothelial corneal dystrophy, surgical trauma, and congenital hereditary endothelial dystrophy, lead to endothelial cell dysfunction. The main treatment for corneal decompensation is replacement of the abnormal corneal layers with normal donor tissue. Nowadays, the trend is to perform selective endothelial keratoplasty, including Descemet stripping automated endothelial keratoplasty and Descemet’s membrane endothelial keratoplasty, to manage corneal endothelial dysfunction. This selective approach has several advantages over penetrating keratoplasty, including rapid recovery of visual acuity, less likelihood of graft rejection, and better patient satisfaction. However, the global limitation in the supply of donor corneas is becoming an increasing challenge, necessitating alternatives to reduce this demand. Consequently, in vitro expansion of human corneal endothelial cells is evolving as a sustainable choice. This method is intended to prepare corneal endothelial cells in vitro that can be transferred to the eye. Herein, we describe the etiologies and manifestations of human corneal endothelial cell dysfunction. We also summarize the available options for as well as recent developments in the management of corneal endothelial dysfunction.

Evolution of corneal flattening after repeated corneal cross-linking during a 6-year follow-up

2020 ◽  
pp. 112067212094566
Author(s):  
Michael A Grentzelos ◽  
Nafsika Voulgari ◽  
Clarice Giacuzzo ◽  
Konstantinos Droutsas ◽  
George D Kymionis
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Case Report ◽  
Corneal Thickness ◽  
Cross Linking ◽  
Distance Visual Acuity ◽  
Corneal Opacification ◽  
Corrected Distance Visual Acuity ◽  
Corneal Flattening

Purpose: To report the evolution of corneal flattening after repeated corneal cross-linking (CXL) in a patient with progressive keratoconus during a 6-year follow-up. Methods: Case report. Results: A 27-year-old female underwent CXL for progressive keratoconus. Postoperatively, corneal topography revealed keratoconus progression with an increase of 1.20 diopters (D) in maximum keratometry (Kmax) and CXL was repeated. After the second treatment, a continuing significant corneal flattening (up to 16.00 D in Kmax) was observed during the first 5 years followed by stabilization during the last sixth year of follow-up. Both uncorrected and corrected distance visual acuity were improved while corneal thickness was decreased. There were no complications such as corneal opacification or endothelial cells decrease during the follow-up period. Conclusion: Repeated CXL can induce an excessive corneal flattening more pronounced during the first years of follow-up followed by stabilization thereafter.

scholarly journals Use of 5-Fluorouracil-Soaked Bioamniotic Membranes in Trabeculectomy for Primary Open-Angle Glaucoma: A Retrospective Analysis

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Chenming Zhang ◽  
Min Wu ◽  
Jianrong Wang ◽  
Miaomiao Zhang ◽  
Xu Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Visual Acuity ◽  
Retrospective Analysis ◽  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Open Angle ◽  
Corneal Endothelial Cells ◽  
Amniotic Membranes ◽  
Surgical Option

The study is a retrospective analysis of 51 patients (76 eyes) with primary open-angle glaucoma (POAG) who admitted to our hospital from 2008 to 2010 to analyze the efficacy of trabeculectomy in combination with 5-fluorouracil- (5-FU-) soaked amniotic membranes for the treatment of POAG patients. Among them, 30 patients (41 eyes) were treated with trabeculectomy in combination with 5-FU-soaked amniotic membrane and 21 patients (35 eyes) were treated with trabeculectomy in combination with MMC. Preoperative and postoperative intraocular pressures (IOP), cup/disc ratio, visual acuity and postoperative macular OCT, complications, treatment, and number of corneal endothelial cells were measured, recorded, and analyzed. At the end of 2 years of follow-up, IOP of 36 (87.8%) eyes of patients in the 5-FU group and IOP of 28 (80%) eyes of patients in the MMC group were ≤21 mmHg and patients in the 5-FU group had more stable IOP than patients in the MMC group. During the two years of follow-up, the visual acuity of 22 (53.7%) eyes in the 5-FU group remained unchanged or even improved. Trabeculectomy in combination with 5-FU-soaked biological amniotic membranes can be a surgical option for POAG patients.

scholarly journals MitoROS due to loss of Slc4a11 in corneal endothelial cells induces ER stress, lysosomal dysfunction and impairs autophagy

2020 ◽  
Author(s):  
Rajalekshmy Shyam ◽  
Diego G. Ogando ◽  
Moonjung Choi ◽  
Joseph A. Bonanno
Keyword(s):  
Endothelial Cells ◽  
Er Stress ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Autophagy Flux ◽  
Unfolded Protein ◽  
Stress Markers ◽  
Lysosomal Dysfunction ◽  
Mitochondrial Ros ◽  
Elevated Expression

AbstractRecent studies from Slc4a11 KO mice have identified mitochondrial dysfunction as a major contributor toward oxidative stress and cell death in Congenital Hereditary Endothelial Dystrophy. Here we asked if this stress activated autophagy in the Slc4a11 KO cell line and in KO mouse endothelial tissue. Early indicators of autophagy, phospho-mTOR and LC3-II indicated activation, however P62 was elevated suggesting an impairment of autophagy flux. The activity and the number of lysosomes, the organelle responsible for the final degradation of autophagy substrates, were found to be reduced in the KO. In addition, the expression of the master regulator of lysosomal function and biogenesis, TFEB, was significantly reduced in the KO corneal endothelia. Also, we observed increased Unfolded Protein Response, as well as elevated expression of ER stress markers, BIP and CHOP. To test if lysosomal and ER stress stems from elevated mitochondrial ROS, we treated Slc4a11 KO corneal endothelial cells with the mitochondrial ROS quencher, MitoQ. MitoQ restored lysosomal enzymes as well as TFEB, reduced ER stress, and increased autophagy flux. MitoQ injections of Slc4a11 KO mice decreased corneal edema, the major phenotype associated with CHED. We conclude that mitochondrial ROS causes ER stress and lysosomal dysfunction with impairment of autophagy in Slc4a11 KO corneal endothelium. Our study is the first to identify the presence as well as cause of lysosomal dysfunction and ER stress in an animal model of CHED, and to characterize inter-organelle relationship in a corneal cell type.

scholarly journals Utilização do flap de Gundersen para tratamento de disfunção endotelial em equino – relato de caso

2021 ◽  
Vol 4 (5) ◽  
pp. 32-38
Author(s):  
Cleydianne Rodrigues de Almeida ◽  
◽  
Cleyber José da Trindade de Fátima ◽  
Rômulo Vitelli Rocha Peixoto ◽  
Anderson Farias ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
Corneal Ulcer ◽  
Corneal Edema ◽  
Corneal Endothelial Cells ◽  
Eye Care ◽  
Visual Axis ◽  
Lens Dislocation ◽  
Uveitis Anterior ◽  
Ulcerative Keratitis

Endothelial dysfunction in horses is associated with dystrophy or degeneration of corneal endothelial cells, clinically presented as a diffuse corneal edema unresponsive to conventional treatments. The main causes of such injury are trauma, ulcerative keratitis, recurrent uveitis, anterior lens dislocation and glaucoma. This paper aims to report a case of endothelial dysfunction in a mare, diagnosed with endothelial dysfunction after uveitis, glaucoma and indolent corneal ulcer. For correction, a superficial lamellar keratectomy followed by permanent conjunctival graft, described as a Gundersen flap, was performed. After intensive eye care, he returned to his athletic functions, maintained corneal and visual axis transparency and ocular reflexes.

scholarly journals NAD+ precursors protect corneal endothelial cells from UVB-induced apoptosis

2020 ◽  
Vol 318 (4) ◽  
pp. C796-C805 ◽  
Author(s):  
Can Zhao ◽  
Wenjing Li ◽  
Haoyun Duan ◽  
Zongyi Li ◽  
Yanni Jia ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Apoptosis ◽  
Corneal Endothelium ◽  
Corneal Edema ◽  
Ultraviolet B ◽  
Subconjunctival Injection ◽  
Corneal Endothelial Cells ◽  
Nicotinamide Phosphoribosyltransferase ◽  
Mesenchymal Transition ◽  
Induced Apoptosis

Excessive exposure of the eye to ultraviolet B light (UVB) leads to corneal edema and opacification because of the apoptosis of the corneal endothelium. Our previous study found that nicotinamide (NIC), the precursor of nicotinamide adenine dinucleotide (NAD), could inhibit the endothelial-mesenchymal transition and accelerate healing the wound to the corneal endothelium in the rabbit. Here we hypothesize that NIC may possess the capacity to protect the cornea from UVB-induced endothelial apoptosis. Therefore, a mouse model and a cultured cell model were used to examine the effect of NAD+ precursors, including NIC, nicotinamide mononucleotide (NMN), and NAD, on the UVB-induced apoptosis of corneal endothelial cells (CECs). The results showed that UVB irradiation caused apparent corneal edema and cell apoptosis in mice, accompanied by reduced levels of NAD+ and its key biosynthesis enzyme, nicotinamide phosphoribosyltransferase (NAMPT), in the corneal endothelium. However, the subconjunctival injection of NIC, NMN, or NAD+ effectively prevented UVB-induced tissue damage and endothelial cell apoptosis in the mouse cornea. Moreover, pretreatment using NIC, NMN, and NAD+ increased the survival rate and inhibited the apoptosis of cultured human CECs irradiated by UVB. Mechanistically, pretreatment using nicotinamide (NIC) recovered the AKT activation level and decreased the BAX/BCL-2 ratio. In addition, the capacity of NIC to protect CECs was fully reversed in the presence of the AKT inhibitor LY294002. Therefore, we conclude that NAD+ precursors can effectively prevent the apoptosis of the corneal endothelium through reactivating AKT signaling; this represents a potential therapeutic approach for preventing UVB-induced corneal damage.

Study of Segmentation Algorithm Based on Corneal Endothelial Cell Images

2014 ◽  
Vol 1030-1032 ◽  
pp. 2377-2381
Author(s):  
Ru Min Yang ◽  
Shuai Wang ◽  
Cheng Bo Yu ◽  
Jing Jing Hu ◽  
Yi Ju Yang
Keyword(s):  
Endothelial Cells ◽  
Image Segmentation ◽  
Endothelial Cell ◽  
Histogram Equalization ◽  
Corneal Endothelial Cell ◽  
Processing Method ◽  
Experimental Result ◽  
Dynamic Threshold ◽  
Corneal Endothelial Cells ◽  
Accurate Identification

In this paper, we study an an algorithm for accurately extracting the outline of Corneal Endothelial Cell images according to the structure and feature of the corneal endothelial cells. Firstly, we reduce the influence of uneven exposure to segmentation effect using histogram equalization. Secondly, reduce the image noise by Gaussian filtering. At last, research the classical algorithm of image segmentation through the contrast experiment and then select a simple and effective local NiBlack dynamic threshold algorithm. The experimental result shows that this processing method is not only simple, but also can segment the corneal endothelial cell images clearly, and provides a good foundation of data for accurate identification of the following images.

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