Secondary sulcus IOL implantation for presbyopia correction following Descemet Membrane Endothelial Keratoplasty.

Purpose: Report a case where the patient desired spectacle independence after phacoemulsification and Descemet membrane endothelial keratoplasty (DMEK) due to Fuchs' endothelial dystrophy. Observations: A 52-year-old female presented with corrected distance visual acuity (CDVA) of 20/40 in both eyes with low ametropia. Slit lamp examination revealed corneal edema 1+/4+, guttae, and nuclear cataract 2+/4+ in both eyes. First, given the diagnostic suspicion of Fuchs' endothelial corneal dystrophy and cataracts, phacoemulsification with monofocal toric intraocular lens (IOL) implantation combined with DMEK was performed in both eyes. Postoperatively, the patient was not satisfied with her near vision. Therefore, a supplementary trifocal sulcus IOL was implanted into the right eye. At 30 days postoperatively, the uncorrected distance visual acuity (UDVA) was 20/20 and the uncorrected near visual acuity (UCNVA) was J1, with clear cornea, centered IOL. Conclusions and importance: This is the first report of supplementary trifocal IOL implantation in a pseudophakic patient with a history of DMEK. This afforded spectacle-independence at all distances with high patient satisfaction. This procedure is safe, predictable, and reversible.

Atypical Stevens-Johnson Syndrome in a Patient With Mycoplasma pneumoniae Infection: A Case Report.

Stevens-Johnson syndrome (SJS) is a serious condition involving the skin and mucous membranes and is characterized by extensive necrosis and detachment of the epidermis. We present a case report of atypical SJS occurring as a complication of Mycoplasma pneumoniae infection in a young adult patient. This case report aims to add to the limited body of literature that exists on the topic and remind clinicians of the possible diagnosis of atypical SJS in the setting of mucosal rash associated with M. pneumoniae infection.

Corneal Endothelial Changes in Chinese Patients with Fuchs' Uveitis Syndrome.

PURPOSE: To analyze the changes of corneal endothelial cells in Chinese patients with unilateral Fuchs' uveitis syndrome (FUS) and investigate the factors relevant to these changes. METHODS: Bilateral specular microscopic examination was performed in 459 Chinese patients with unilateral FUS from April 2008 to April 2023. The affected eyes constituted the study group, while the contralateral eyes served as controls. RESULTS: The median values of endothelial cell density (ECD), cell count, total cell size, and hexagonality were significantly lower in the FUS eyes compared to the control eyes (p < 0.001). The median values of average cell size, maximum cell size, SD of cell size, and CV were significantly higher in the FUS eyes compared to the control eyes (p < 0.001). Central ECD showed a negative correlation with age (r = -0.339; p < 0.001), maximum IOP (r = -0.127; p = 0.006), and the interval since symptom onset (r = -0.172; p < 0.001). The ECD was lower in eyes with ocular hypertension compared to those without ocular hypertension (p < 0.001). Eyes with KPs distributed on the central corneal endothelium had a significantly lower ECD than those with KPs distributed diffusely or KPs distributed triangularly on the inferior corneal endothelium (p = 0.006). CONCLUSION: Our findings suggest decreased ECD, increased cell size, and morphological alterations in the affected eyes of Chinese patients with FUS. The reduction in ECD is correlated with age, elevated IOP, the interval since symptom onset, and the distribution of KPs.

Findings in Corneal Endothelium by Confocal and Specular Microscopy in Patients with Fuchs Uveitis Syndrome Undergoing Phacoemulsification.

PURPOSE: To compare corneal endothelial changes in patients with Fuchs Uveitis Syndrome (FUS) undergoing phacoemulsification surgery using confocal and specular microscopy. METHODS: We included 14 patients with unilateral FUS and cataracts who underwent phacoemulsification surgery in a Mexican referral center for inflammatory eye diseases. Preoperative confocal and specular microscopies were conducted, establishing baseline images for subsequent analyses. Surgery on the FUS eye was performed by a single surgeon and an intraocular lens was implanted in all cases. Both specular and confocal microscopy were repeated 6 months after FUS eye surgery and compared with baseline images. We used Image J to do a manual segmentation of KP and determine their density for further analysis hence developing a new tool for confocal microscopy image analysis. RESULTS: All patients underwent uneventful phacoemulsification surgery in the FUS eye. There was no significant change in endothelial cell density (ECD) from 2257 (±508.2) cells/mm2 preoperatively to 2214 (±535.1) cells/mm2 postoperatively (p = 0.809). Confocal microscopy revealed a decrease in Keratic Precipitate Density (KPD) from a median of 1413 (±2809.7) KPs/mm2 preoperatively to a median of 685.5 (1527.9) KPs/mm2 postoperatively (p = 0.036). CONCLUSIONS: Phacoemulsification surgery in patients with FUS produces no significant loss of endothelial cells and morphological changes that can be detected by confocal and specular microscopy. We found a reduction in KPD 6 months after surgery on confocal microscopy. Additionally, our manual segmentation technique for KPs utilizing Image J offers a novel and practical approach for confocal microscopy image analysis.

Endothelial Keratoplasty Following Glaucoma Filtration Surgery: A UK Tertiary Eye Care Referral Centre Experience.

Purpose: To compare the postoperative complications and clinical outcomes of Descemet membrane endothelial keratoplasty (DMEK) and Descemet stripping automated endothelial keratoplasty (DSAEK) in eyes with previous glaucoma filtering surgery. Methods: In this retrospective comparative case series, we analysed postoperative visual acuity and intraocular pressure, graft survival, rate of graft detachment and/or dislocation, number of rebubbling and/or graft repositioning procedures, and graft rejection or failure (primary and secondary). Results: Sixteen eyes with DMEK and 80 eyes with DSAEK with previous glaucoma surgery were studied. The results were recorded at 3 and 12 months postoperatively. No statistically significant differences in postoperative visual acuity were found between the two groups at any stage of the follow-up. Intraocular pressure was lower in the DMEK group at the follow-up stage of 3 (p = 0.0022) and 12 months (p = 0.0480). Visually significant graft detachment was recorded in 31.3% and 22.5% of DMEK and DSAEK cases, respectively (p = 0.4541). All DMEK detachments (n = 5) were managed with slit-lamp rebubbling. Out of 18 graft detachments in the DSAEK group, 2 grafts were observed due to small graft detachment, 6 large graft detachments underwent rebubbling performed in the operating theatre, and 10 eyes needed primary graft repositioning for graft dislocation. Conclusions: DMEK is a feasible option to treat endothelial failure in complex eyes with previous glaucoma surgery. In the DMEK group, visual acuity outcomes and possibly postoperative intraocular pressure control were better compared with the DSAEK group.

TCF4 trinucleotide repeat expansions and UV irradiation increase susceptibility to ferroptosis in Fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD), the leading indication for corneal transplantation in the U.S., causes loss of corneal endothelial cells (CECs) and corneal edema leading to vision loss. FECD pathogenesis is linked to impaired response to oxidative stress and environmental ultraviolet A (UVA) exposure. Although UVA is known to cause nonapoptotic oxidative cell death resulting from iron-mediated lipid peroxidation, ferroptosis has not been characterized in FECD. We investigated the roles of genetic background and UVA exposure in causing CEC degeneration in FECD. Using ungenotyped FECD patient surgical samples, we found increased levels of cytosolic ferrous iron (Fe2+) and lipid peroxidation in end-stage diseased tissues compared with healthy controls. Using primary and immortalized cell cultures modeling the TCF4 intronic trinucleotide repeat expansion genotype, we found altered gene and protein expression involved in ferroptosis compared to controls including elevated levels of Fe2+, basal lipid peroxidation, and the ferroptosis-specific marker transferrin receptor 1. Increased cytosolic Fe2+ levels were detected after physiologically relevant doses of UVA exposure, indicating a role for ferroptosis in FECD disease progression. Cultured cells were more prone to ferroptosis induced by RSL3 and UVA than controls, indicating ferroptosis susceptibility is increased by both FECD genetic background and UVA. Finally, cell death was preventable after RSL3 induced ferroptosis using solubilized ubiquinol, indicating a role for anti-ferroptosis therapies in FECD. This investigation demonstrates that genetic background and UVA exposure contribute to iron-mediated lipid peroxidation and cell death in FECD, and provides the basis for future investigations of ferroptosis-mediated disease progression in FECD.

Tissue-specific TCF4 triplet repeat instability revealed by optical genome mapping.

BACKGROUND: Fuchs endothelial corneal dystrophy (FECD) is the most common repeat-mediated disease in humans. It exclusively affects corneal endothelial cells (CECs), with ≤81% of cases associated with an intronic TCF4 triplet repeat (CTG18.1). Here, we utilise optical genome mapping (OGM) to investigate CTG18.1 tissue-specific instability to gain mechanistic insights. METHODS: We applied OGM to a diverse range of genomic DNAs (gDNAs) from patients with FECD and controls (n = 43); CECs, leukocytes and fibroblasts. A bioinformatics pipeline was developed to robustly interrogate CTG18.1-spanning DNA molecules. All results were compared with conventional polymerase chain reaction-based fragment analysis. FINDINGS: Analysis of bio-samples revealed that expanded CTG18.1 alleles behave dynamically, regardless of cell-type origin. However, clusters of CTG18.1 molecules, encompassing ∼1800-11,900 repeats, were exclusively detected in diseased CECs from expansion-positive cases. Additionally, both progenitor allele size and age were found to influence the level of leukocyte-specific CTG18.1 instability. INTERPRETATION: OGM is a powerful tool for analysing somatic instability of repeat loci and reveals here the extreme levels of CTG18.1 instability occurring within diseased CECs underpinning FECD pathophysiology, opening up new therapeutic avenues for FECD. Furthermore, these findings highlight the broader translational utility of FECD as a model for developing therapeutic strategies for rarer diseases similarly attributed to somatically unstable repeats. FUNDING: UK Research and Innovation, Moorfields Eye Charity, Fight for Sight, Medical Research Council, NIHR BRC at Moorfields Eye Hospital and UCL Institute of Ophthalmology, Grantová Agentura Ceské Republiky, Univerzita Karlova v Praze, the National Brain Appeal's Innovation Fund and Rosetrees Trust.

Challenging corneal diseases and microRNA expression: Focus on rare diseases and new therapeutic frontiers.

MicroRNAs (miRNAs) function as posttranscriptional regulators of gene expression by targeting specific messenger RNA (mRNA). This interaction modulates mRNA stability or translational efficiency, ultimately impacting the level of protein production. Emerging evidence suggests that miRNAs act as critical regulators in corneal diseases. These molecules finetune key processes like cell proliferation, differentiation, inflammation, and wound healing. We reviewed the literature to understand the role that miRNAs may play in the development of challenging and poorly understood corneal diseases. We focused on vernal keratoconjunctivitis, neurotrophic keratitis, keratoconus, Fuchs endothelial corneal dystrophy, and limbal stem cell deficiency. Furthermore, we explored currently studied agonists or antagonists of miRNAs that share similar pathways with ocular diseases and could be employed in ophthalmology in the future. The distinct miRNA expression profiles observed in different ocular surface pathologies, combined with the remarkable stability and relatively easy access of miRNA sampling in biofluids, present possibilities for the development of noninvasive and highly accurate diagnostic tools. Furthermore, comprehending miRNA's pathophysiological role could open new frontiers to a more comprehensive understanding of the pathophysiology underlying ocular surface diseases, thereby paving the way for the creation of novel therapeutic strategies.

Fuchs' Endothelial Corneal Dystrophy evaluation using a high-resolution wavefront sensor.

This study aims to evaluate the applicability of the high-resolution WaveFront Phase Imaging Sensor (WFPI) in eyes with Fuchs' Endothelial Corneal Dystrophy (FECD) through qualitative and quantitative analysis using a custom-designed Automatic Guttae Detection Method (AGDM). The ocular phase was measured using the t · eyede aberrometer and then was processed to obtain its High-Pass Filter Map (HPFM). The subjects were pathological and healthy patients from the Fundación Jiménez-Díaz Hospital (Madrid, Spain). The AGDM was developed and applied in pupils with 3 and 5 mm of diameter. A set of metrics were extracted and evaluated like the Root-Mean-Square error (RMS), Number of guttae, Guttae Area, and Area of Delaunay Triangulation (DT). Finally, a Support Vector Machine (SVM) model was trained to classify between pathological and healthy eyes. Quantitatively, the HPFM reveals a dark spots pattern according to the ophthalmologist's description of the slit-lamp examination of guttae distribution. There were significant statistical differences in all the metrics when FECD and Healthy groups were compared using the same pupil size; but comparing both pupil sizes for the same group there were significant differences in most of the variables. This sensor is a value tool to objectively diagnose and monitor this pathology through wavefront phase changes.

Rapid detection of guttae area using aniline blue staining in Fuchs endothelial corneal dystrophy mouse model.

Fuchs endothelial corneal dystrophy (FECD) is a leading cause of corneal endothelial degeneration resulting in impaired visual acuity. Excessive deposition of extracellular matrix (guttae) on Descemet's membrane (DM) is the hallmark of FECD. We sought to detect the guttae area rapidly using aniline blue (AB) staining in FECD mouse model. FECD mouse model was established via ultraviolet A (UVA) exposure. Masson's trichrome staining was utilized to stain the corneal sections. AB staining was utilized to stain both whole cornea tissues and stripped Descemet's membrane-endothelium complex (DMEC) flat mounts, while immunofluorescence staining of collagen I was employed to stain guttae areas. In Masson's trichrome staining, corneal collagen fibrils were stained blue with AB. The DMEC flat mounts were stained into relative dark blue areas and relative light blue areas using 2% AB staining. The areas of dark blue could almost overlap with collagen I-positive areas, and have an acellular centre and a moderately distinct boundary line with the surrounding corneal endothelial cells. In conclusion, AB staining is a rapid and effective method for the evaluation of the guttae areas in the FECD mouse model.

MitoQ relieves mitochondrial dysfunction in UVA and cigarette smoke-induced Fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD), a degenerative corneal condition, is characterized by the droplet-like accumulation of the extracellular matrix, known as guttae and progressive loss of corneal endothelial cells ultimately leading to visual distortion and glare. FECD can be influenced by environmental stressors and genetic conditions. However, the role of mitochondrial dysfunction for advancing FECD pathogenesis is not yet fully studied. Therefore, in the present study we sought to determine whether a combination of environmental stressors (ultraviolet-A (UVA) light and cigarette smoke condensate (CSC)) can induce mitochondrial dysfunction leading to FECD. We also investigated if MitoQ, a water-soluble antioxidant, can target mitochondrial dysfunction induced by UVA and CSC in human corneal endothelial cells mitigating FECD pathogenesis. We modeled the FECD by increasing exogenous oxidative stress with CSC (0.2%), UVA (25J/cm2) and a combination of UVA + CSC and performed a temporal analysis of their cellular and mitochondrial effects on HCEnC-21T immortalized cells in vitro before and after MitoQ (0.05 µM) treatment. Interestingly, we observed that a combination of UVA + CSC exposure increased mitochondrial ROS and fragmentation leading to a lower mitochondrial membrane potential and increased levels of cytochrome c release leading to apoptosis and cell death. MitoQ intervention successfully mitigated these effects and restored cell viability. The UVA + CSC model could be used to study stress induced mitochondrial dysfunction. Additionally, MitoQ can serve as a viable antioxidant in attenuating mitochondrial dysfunction, underscoring its potential as a molecular-focused treatment approach to combat FECD pathogenesis.

Neuropeptide alpha-Melanocyte stimulating hormone preserves corneal endothelial morphology in a murine model of Fuchs dystrophy.

Fuchs endothelial corneal dystrophy is a heterogenous disease with multifactorial etiology, and genetic, epigenetic, and exogenous factors contributing to its pathogenesis. DNA damage plays a significant role, with ultraviolet-A (UV-A) emerging as a key contributing factor. We investigate the potential application of neuropeptide α-melanocyte stimulating hormone (α-MSH) in mitigating oxidative stress induced endothelial damage. First, we examined the effects of α-MSH on a cultured human corneal endothelial cell line (HCEnC-21T) exposed to hydrogen peroxide (H2O2) induced oxidative DNA damage. We performed immunofluorescence and flow cytometry to assess DNA damage and cell death in the cultured cells. Additionally, we used an established mouse model that utilizes ultraviolet light to induce corneal endothelial cell damage resulting in decreased CEnC number, increased cell size variability, and decreased percentage of hexagonal cells. This endothelial decompensation leads to an increase in corneal thickness. Following UV-A exposure, the mice were systemically treated with α-MSH, either immediately after exposure (early treatment) or beginning two weeks post-exposure (delayed treatment). To evaluate treatment efficacy, we analyzed CEnC density and morphology using in vivo confocal microscopy, and central corneal thickness using anterior segment optical coherence tomography. Our findings demonstrated that α-MSH treatment effectively protects HCEnC-21T from free-radical induced oxidative DNA damage and subsequent cell death. In vivo, α-MSH treatment, mitigated the loss of CEnC density, deterioration of cell morphology and suppression of the resultant corneal swelling. These results underline the potential application of α-MSH as a therapeutic agent for mitigating corneal endothelial damage.

Evolution of therapeutic strategy based on oxidant-antioxidant balance for fuchs endothelial corneal dystrophy.

Fuchs endothelial corneal dystrophy (FECD) stands as the most prevalent primary corneal endothelial dystrophy worldwide, posing a significant risk to corneal homeostasis and clarity. Corneal endothelial cells exhibit susceptibility to oxidative stress, suggesting a nuanced relationship between oxidant-antioxidant imbalance and FECD pathogenesis, irrespective of FECD genotype. Given the constrained availability of corneal transplants, exploration into non-surgical interventions becomes crucial. This encompasses traditional antioxidants, small molecule compounds, biologics, and diverse non-drug therapies, such as gene-related therapy, hydrogen therapy and near infrared light therapy. This review concentrates on elucidating the mechanisms behind oxidant-antioxidant imbalance and the evolution of strategies to restore oxidant-antioxidant balance in FECD. It provides a comprehensive overview of both conventional and emerging therapeutic approaches, offering valuable insights for the advancement of non-surgical treatment modalities. The findings herein might establish a robust foundation for future research and the therapeutic strategy of FECD.

Scheimpflug Tomography as a Predictor of Corneal Edema After Phacoemulsification in Fuchs Endothelial Corneal Dystrophy.

Purpose: To determine if Scheimpflug tomography pachymetry map and posterior elevation map patterns can predict the occurrence of corneal edema following uneventful phacoemulsification surgery in Fuchs endothelial corneal dystrophy (FECD). Design: Observational prospective case-control study. Participants: Fifty FECD eyes (50 patients) with visually significant cataract: 25 with subclinical corneal edema (SCE) versus 25 without SCE. Methods: Preoperatively, FECD was clinically assessed, and only patients devoid of clinical corneal edema were enrolled. Utilizing the Mayo Clinic classification for subclinical corneal edema (SCE), eligible FECD eyes were stratified based on Scheimpflug imaging pachymetry map and posterior elevation map characteristics, including loss of regular isopachs, displacement of the cornea's thinnest point, and the presence of posterior surface depression, into two groups: Group A representing FECD with SCE, and Group B: FECD without SCE. One week postoperatively, clinical and tomographic evaluation was performed. Regression analysis was conducted to evaluate predictors of corneal edema after uneventful phacoemulsification surgery in both groups. Results: All patients were successfully imaged before and 1 week after surgery. Visual acuity was significantly improved in both groups (P < 0.001). No postoperative clinical edema was observed in Group B, while 23 (92%) had mild edema and 2 (8%) had moderate edema in Group A. Both groups showed a significant increase in postoperative central corneal thickness (CCT) and thinnest corneal thickness (TCT) (both P < 0.001). Compared to Group B, Group A showed a significant central flattening of the anterior corneal surface (P = 0.007 and P = 0.04 for K1 and K2 respectively), and a significant increase in the postoperative posterior surface depression. Multivariate analysis showed that 94% of postoperative corneal edema could be predicted by the presence of preoperative posterior surface depression (P = 0.04, ARR = 5.8 (1.89-35.7)). Conclusion: Scheimpflug tomography pachymetry map and posterior elevation map patterns can predict corneal edema after uneventful phacoemulsification surgery in FECD with subclinical corneal edema.

Retinal and choroidal thickness in fuchs uveitis syndrome: a contralateral eye study.

BACKGROUND: To investigate the subfoveal retinal and choroidal thickness in patients with unilateral Fuchs Uveitis Syndrome (FUS). METHODS: This comparative contralateral study was performed in affected eyes with FUS versus fellow eyes. For each eye parameters such as subfoveal choroidal thickness (SCT), subfoveal choriocapillary thickness (SCCT), central macular thickness (CMT), and central macular volume (CMV) were measured; then the measured values of affected and fellow unaffected eye were compared. RESULTS: Thirty-seven patients (74 eyes) including 19 females (51.4%) with a mean age of 36.9 ± 7.6 years were enrolled. The mean SCT was lower in the affected eyes (344.51 ± 91.67) than in the fellow (375.59 ± 87.33) with adjusting for duration of disease and axial lengths (P < 0.001). The mean SCCT, CMT, and CMV were higher in eyes with FUS than in fellow eyes (P < 0.05). CONCLUSIONS: The result of our study demonstrated that affected eyes in patients with FUS tend to have thinner SCT and thicker SCCT and CMT compared to uninvolved fellow eyes.

Expression of Hormones' Receptors in Human Corneal Endothelium from Fuchs' Dystrophy: A Possible Gender' Association.

Background: Age and sex are the most significant risk of factors for advanced Fuchs dystrophy. Nevertheless, few data are available on the hormone's receptor pattern expressed in adult and advanced fuchs endothelial corneal dystrophy (FECD). We investigated the impact of gender, growth factors and extracellular matrix (ECM) regulatory proteins expressed by the dystrophic endothelia. Methods: Ten dystrophic endothelial tissues and 10 normal endothelial sheets (corneoscleral specimens; Eye Bank) were used for this characterization study. Hormones' receptors (ERα, AR, PR, SHBG), few growth factors (VEGFA, ßNGF, TGFß1), some ECM regulators (MMP1, MMP7) and few inflammatory cytokines (IFNγ, IL10) were analyzed by real-time RT-PCR. Results: ERα transcripts were significantly increased, AR and SHBG transcripts were decreased in Fuchs endothelia from female patients, and no changes were detected for PR transcripts. VEGFA, ßNGF and TGFß1 transcripts were upregulated in Fuchs' endothelia, but not significantly linked to gender. High MMP1 and low MMP7 transcripts' expression were detected in Fuchs' specimens, mainly in males than females. An increased IFNγ (Th1) transcript expression was observed in females than males, and a trend to increase for IL10 (Th2) transcripts was detected in males than females. Conclusions: Our findings clearly indicate that hormone receptors, growth factors and matrix mediators as well as a Th1 pathway are predominant in Fuchs' dystrophy, displaying a pattern of expression specific for the female phenotype. The differential expression of hormones' receptors and the Th1/Th2 ratio might prompt to new theories to be tested in vitro and in vivo models, such as the use of hormonal substitute for counteracting this endothelial cell lost.

Intradevice Repeatability and Interdevice Comparison of Two Specular Microscopy Devices in a Real-Life Setting: Tomey EM-4000 and Nidek CEM-530.

Background and Objectives: The purpose of this study was to compare two commercially available specular microscopes (Tomey EM-4000 and Nidek CEM-530) in a real-life clinical setting in terms of intra- and interdevice variability. The study was conducted on all patients seen in a clinical practice specializing in anterior segment pathologies, regardless of the purpose of their visit. Materials and Methods: In total, 112 eyes of 56 patients (age 23-85 years old) were included in the study. Each eye was measured three times with each device (for a total of six measurements), and results for central corneal thickness (CCT) and corneal endothelial cell density (ECD) were recorded. The results were then evaluated with the D'Agostino-Pearson normality test and compared with a Wilcoxon signed-rank test, t-test, ANOVA or Mann-Whitney test for intra- and interdevice variability. Results: Both specular microscopes produced very reliable reproducible intradevice results: The Tomey EM-4000 measured an ECD of 2390 ± 49.57 cells/mm2 (mean ± standard error of mean); the range was 799-3010 cells/mm2. The determined CCT was 546 ± 5.104 µm (mean ± standard error of mean [SEM]); the range was 425-615 µm. The measurements with the Nidek CEM-530 revealed an ECD of 2417 ± 0.09 cells/mm2 (mean ± SEM); the range was 505-3461 cells/mm2 (mean ± SEM). The mean CCT detected was 546.3 ± 4.937 µm (mean ± SEM); the range was 431-621 µm. The interdevice differences were statistically significant for both parameters, ECD (p = 0.0175) and CCT (p = 0.0125) (p < 0.05). Conclusions: The Nidek CEM-530 and the Tomey EM-4000 both produced reliable and reproducible results in terms of ECD and CCT. The absolute measurements were statistically significantly different for CCT and ECD for both devices; the Nidek produces slightly higher values.

Enhanced Migration of Fuchs Corneal Endothelial Cells by Rho Kinase Inhibition: A Novel Ex Vivo Descemet's Stripping Only Model.

Descemet's Stripping Only (DSO) is a surgical technique that utilizes the peripheral corneal endothelial cell (CEnC) migration for wound closure. Ripasudil, a Rho-associated protein kinase (ROCK) inhibitor, has shown potential in DSO treatment; however, its mechanism in promoting CEnC migration remains unclear. We observed that ripasudil-treated immortalized normal and Fuchs endothelial corneal dystrophy (FECD) cells exhibited significantly enhanced migration and wound healing, particularly effective in FECD cells. Ripasudil upregulated mRNA expression of Snail Family Transcriptional Repressor (SNAI1/2) and Vimentin (VIM) while decreasing Cadherin (CDH1), indicating endothelial-to-mesenchymal transition (EMT) activation. Ripasudil activated Rac1, driving the actin-related protein complex (ARPC2) to the leading edge, facilitating enhanced migration. Ex vivo studies on cadaveric and FECD Descemet's membrane (DM) showed increased migration and proliferation of CEnCs after ripasudil treatment. An ex vivo DSO model demonstrated enhanced migration from the DM to the stroma with ripasudil. Coating small incision lenticule extraction (SMILE) tissues with an FNC coating mix and treating the cells in conjunction with ripasudil further improved migration and resulted in a monolayer formation, as detected by the ZO-1 junctional marker, thereby leading to the reduction in EMT. In conclusion, ripasudil effectively enhanced cellular migration, particularly in a novel ex vivo DSO model, when the stromal microenvironment was modulated. This suggests ripasudil as a promising adjuvant for DSO treatment, highlighting its potential clinical significance.

Auto-Optimized Electro-Flow Reactor Platform for the in-situ Reduction of P(V) Oxide to P(III) and Their Application.

Trivalent phosphine catalysis is mostly utilized to activate the carbon-carbon multiple bonds to form carbanion intermediate species and is highly sensitive to certain variables. Random manual multi-variables are critical for understanding the batch disabled regeneration of trivalent phosphine chemistry. We need the artificial intelligence-based system which can change the variable based on previously conducted failed experiment. Herein, we report an auto-optimized electro-micro-flow reactor platform for the in-situ reduction of stable P(V) oxide to sensitive P(III) and further utilized the method for Corey-Fuchs reaction.