Moorfields Eye Hospital

About: Moorfields Eye Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Visual acuity & Glaucoma. The organization has 3721 authors who have published 6790 publications receiving 246004 citations.

Integrated visual fields: a new approach to measuring the binocular field of view and visual disability

Abstract: Background We have developed a method of quantifying the central binocular visual field by merging results from monocular fields (Integrated visual field). This study aims to compare the new measure with the binocular Esterman visual field test in identifying patients with self-reported visual disability.

Refractive error and visual outcome after cataract extraction.

Abstract: Purpose: To determine the range of biometry prediction error of the postoperative refraction and the visual outcome after cataract surgery. Setting: Postgraduate teaching hospital. Methods: Refraction and visual outcomes were recorded prospectively for a consecutive case series of 1817 cataract procedures. Complete preoperative and postoperative data were available for 1676 eyes (92.4%). The paired mean error of the difference between the predicted and achieved refraction, the percentages falling within ±0.50 diopter (D), ±1.00 D, and ±2.00 D, and the values that contained 99% of data points were then calculated. The number that achieved a final Snellen visual acuity of 6/12 was determined in all eyes and in eyes without preoperative ocular comorbidity. This analysis was repeated in 1265 eyes that received a single intraocular lens (IOL) design (C10UB/C11UB) after phacoemulsification through a clear corneal incision. Results: The paired mean error of the difference between the predicted and achieved postoperative refraction in all eyes was −0.32 D ± 1.05 (SD); 72.3% of eyes were within ±1.00 D of the planned refraction, with bounds of 99% of observation of +2.92 D and −3.98 D. In the single IOL group, the paired mean error was −0.32 ± 0.94 D; 74.2% of eyes fell within ±1.00 D of the planned refraction, with bounds of 99% of observation of +2.54 D and −3.81 D. Axial length did not determine the magnitude of the biometry prediction error. At discharge from the service, 86.9% of all eyes and 95.4% of eyes without preoperative ocular comorbidity achieved a final corrected Snellen acuity of 6/12. Conclusion: These data provide benchmark information that can be used to monitor clinical practice.

Genetic Characterization Indicates that a Specific Subpopulation of Pseudomonas aeruginosa Is Associated with Keratitis Infections

Abstract: Pseudomonas aeruginosa is a common opportunistic bacterial pathogen that causes a variety of infections in humans. Populations of P. aeruginosa are dominated by common clones that can be isolated from diverse clinical and environmental sources. To determine whether specific clones are associated with corneal infection, we used a portable genotyping microarray system to analyze a set of 63 P. aeruginosa isolates from patients with corneal ulcers (keratitis). We then used population analysis to compare the keratitis isolates to a wider collection of P. aeruginosa from various nonocular sources. We identified various markers in a subpopulation of P. aeruginosa associated with keratitis that were in strong disequilibrium with the wider P. aeruginosa population, including oriC, exoU, katN, unmodified flagellin, and the carriage of common genomic islands. The genome sequencing of a keratitis isolate (39016; representing the dominant serotype O11), which was associated with a prolonged clinical healing time, revealed several genomic islands and prophages within the accessory genome. The PCR amplification screening of all 63 keratitis isolates, however, provided little evidence for the shared carriage of specific prophages or genomic islands between serotypes. P. aeruginosa twitching motility, due to type IV pili, is implicated in corneal virulence. We demonstrated that 46% of the O11 keratitis isolates, including 39016, carry a distinctive pilA, encoding the pilin of type IV pili. Thus, the keratitis isolates were associated with specific characteristics, indicating that a subpopulation of P. aeruginosa is adapted to cause corneal infection.

Pathophysiology and Therapeutic Perspectives of Oxidative Stress and Neurodegenerative Diseases: A Narrative Review.

Abstract: Neurodegeneration is the term describing the death of neurons both in the central nervous system and periphery. When affecting the central nervous system, it is responsible for diseases like Alzheimer’s disease, Parkinson’s disease, Huntington’s disorders, amyotrophic lateral sclerosis, and other less frequent pathologies. There are several common pathophysiological elements that are shared in the neurodegenerative diseases. The common denominators are oxidative stress (OS) and inflammatory responses. Unluckily, these conditions are difficult to treat. Because of the burden caused by the progression of these diseases and the simultaneous lack of efficacious treatment, therapeutic approaches that could target the interception of development of the neurodegeneration are being widely investigated. This review aims to highlight the most recent proposed novelties, as most of the previous approaches have failed. Therefore, older approaches may currently be used by healthcare professionals and are not being presented. This review was based on an electronic search of existing literature, using PubMed as primary source for important review articles, and important randomized clinical trials, published in the last 5 years. Reference lists from the most recent reviews, as well as additional sources of primary literature and references cited by relevant articles, were used. Eighteen natural pharmaceutical substances and 24 extracted or recombinant products, and artificial agents that can be used against OS, inflammation, and neurodegeneration were identified. After presenting the most common neurodegenerative diseases and mentioning some of the basic mechanisms that lead to neuronal loss, this paper presents up to date information that could encourage the development of better therapeutic strategies. This review shares the new potential pharmaceutical and not pharmaceutical options that have been recently introduced regarding OS and inflammatory responses in neurodegenerative diseases.

Ocular developmental abnormalities and glaucoma associated with interstitial 6p25 duplications and deletions.

Abstract: Purpose Mutations in the forkhead transcription factor gene FOXC1 on 6p25 cause a range of ocular developmental abnormalities, with associated glaucoma. However, FOXC1 mutations have not been found in all similarly affected pedigrees mapping to this interval. This study was undertaken to investigate the potential role of 6p25 rearrangements in causing such phenotypes. Methods Two large families with autosomal dominant iris hypoplasia and early-onset glaucoma, 21 probands with Axenfeld-Rieger phenotypes not attributable to PITX2 mutations, and 7 individuals with documented 6p25 cytogenetic rearrangements, were investigated by genotyping and fluorescence in situ hybridization, with markers and probes from the 6p25 region. Results Interstitial 6p25 duplications were present in the unrelated families with iris hypoplasia, whereas an interstitial 6p25 deletion was identified in one Axenfeld-Rieger pedigree. Larger cytogenetic rearrangements, leading to trisomy or monosomy of the 6p25 region, resulted in microcornea and Rieger syndrome phenotypes, respectively. All the rearrangements encompassed FOXC1, increasing or decreasing the number of FOXC1 copies present, and appeared to correlate with the phenotypes observed. Conclusions These findings represent the first example of both interstitial duplications and deletions cosegregating with a human developmental disorder that is attributable to altered dose of transcription factor. The data presented provide additional evidence for the pathogenicity of altered gene dosage of FOXC1 and suggest that a common mechanism is responsible for rearrangements of 6p25.