 | Alan C CharlesShow email addressInstitute of Ophthalmology, University College London, London, EC1V 9EL UK | Genetics, Moorfields Eye Hospital NHS Foundation Trust, London, UK | Inherited Eye Disease, ... |
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Alan C Charles:Expert Impact
Concepts for whichAlan C Charleshas direct influence:Retinitis pigmentosa,Fundus autofluorescence,Visual acuity,Macular degeneration,Pigment epithelium,Fluorescein angiography,Macular telangiectasia,Retinal pigment epithelium.
Alan C Charles:KOL impact
Concepts related to the work of other authors for whichfor which Alan C Charles has influence:Macular degeneration,Retinitis pigmentosa,Visual acuity,Optical coherence,Geographic atrophy,Choroidal neovascularization,Fundus autofluorescence.
KOL Resume for Alan C Charles
| Year | |
|---|---|
| 2021 | Institute of Ophthalmology, University College London, London, EC1V 9EL UK |
| 2020 | Institute of Ophthalmology, University College London, United Kingdom Moorfields Eye Hospital NHS Foundation Trust, London, UK |
| 2019 | Inherited Eye Disease Moorfields Eye Hospital London UK Institute of Ophthalmology, University College London, London, United Kingdom. |
| 2018 | NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, United Kingdom. Moorfields Eye Hospital NHS Foundation Trust, London, UK. |
| 2017 | UCL Institute of Ophthalmology, London, UK Institute of Ophthalmology, University College London, London, United Kingdom |
| 2016 | Department of Ocular Biology, Institute of Ophthalmology, University College London, London, UK |
| 2015 | Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology, London, United Kingdom |
| 2014 | Institute of Ophthalmology, University College London, London, England |
| 2013 | Moorfields Eye Hospital, NHS Foundation Trust, London, United Kingdom Vice Chairman, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, OH, USA Professor and Chair, Department of Ophthalmology, University of Leipzig, Leipzig, Germany |
| 2012 | Institute of Ophthalmology, University College London, London EC1V 9EL, UK, Division of Inherited Eye Disease, Moorfields Eye Hospital, London, United Kingdom Moorfields Eye Hospital, London, UK |
| 2011 | From the *Moorfields Eye Hospital, London, United Kingdom; and †Institute of Ophthalmology, University College, London, United Kingdom. Electrophysiology Department, Moorfields Eye Hospital, 162 City Road, EC1V 2PD, London, UK |
| 2010 | UCL Institute of Ophthalmology, University College London, London, UK From the *Bernard and Shirlee Brown Glaucoma Laboratory, Department of Ophthalmology, Columbia University College of Physicians and Surgeons, New York, New York; the †Medical Retina Service, Moorfields Eye Hospital, London, United Kingdom; the ‡Institute of Ophthalmology, University College London, London, United Kingdom; and the §Department of Pathology and Cell Biology, Columbia University College of Physicians and Surgeons, New York, New York. Moorfields Eye Hospital (Drs Essex, Wong, Fraser-Bell, Sandbach, Tufail, Bird, and Dowler) and Institute of Ophthalmology (Drs Tufail and Bird), London, England. |
| 2009 | Department of Cell Biology and, Department of Molecular Biology, Scripps Center for Mass Spectrometry, The Scripps Research Institute, La Jolla, California, USA., Department of Ophthalmology, Kellogg Eye Institute, University of Michigan, Ann Arbor, Michigan, USA., Department of Ophthalmology, Hadassah-Hebrew University Medical Center, Jerusalem, Israel., Ceregene, San Diego, California, USA., Institute of Ophthalmology, Moorfields Eye Hospital, University College London, London, United Kingdom. |
| 2008 | Institute of Ophthalmology, University College London, London, England (Drs Michaelides and Bird) Moorfields Eye Hospital, London, England (Drs Michaelides, Bird, and Rath, and Ms Jenkins) |
| 2007 | Departments of Clinical Ophthalmology (Drs Tsang, Vaclavik, and Bird) and Electrophysiology (Drs Robson and Holder), Moorfields Eye Hospital, and Institute of Ophthalmology (Drs Vaclavik and Bird), London, England. Dr Tsang is now with Brown Glaucoma Laboratory,Department of Ophthalmology and Department of Pathology and Cell Biology,College of Physicians and Surgeons, Columbia University, New York, NY. Moorfields Eye Hospital, 162 City Road, London, EC1 2PD UK Institute of Ophthalmology, London, Great Britain |
| 2006 | Institute of Ophthalmology, Bath Street, London EC1V 9EL, UK Professor, Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA Chairman, Department of Ophthalmology, Greater Baltimore Medical Center |
| Concept | World rank |
|---|---|
| membrane attack electron | #1 |
| clinical diagnosis azoor | #1 |
| contrast rcslo | #1 |
| luxea | #1 |
| 80 months point | #1 |
| international classification presence | #1 |
| 12 patients eye | #1 |
| ” oct | #1 |
| edge rpe defect | #1 |
| c17 d3s47 | #1 |
| mutations codon 172 | #1 |
| development rubeosis iridis | #1 |
| background fundus autofluorescence | #1 |
| ivermectin eye | #1 |
| 2 patients dhrd | #1 |
| mpsrns | #1 |
| drusen risk | #1 |
| eye retinal | #1 |
| pale deposits level | #1 |
| drusen adult | #1 |
| 28–91years | #1 |
| vegf bld | #1 |
| slope autofluorescence images | #1 |
| segment lesions | #1 |
| pro50leu substitution | #1 |
| concordance probands | #1 |
| retinal sensitivities pws | #1 |
| progressive constriction ring | #1 |
| dominant retinal dystrophy | #1 |
| kurzlevin | #1 |
| eye proteins rpgr | #1 |
| 21996 | #1 |
| disciform macular degeneration | #1 |
| macular dystrophy mutations | #1 |
| zinc deposit formation | #1 |
| exudative degeneration eye | #1 |
| pigmentosa chromosomes | #1 |
| clinical practice result | #1 |
| peripheral telangiectasis | #1 |
| 1277tc | #1 |
| evidience disease | #1 |
| partial laser ablation | #1 |
| rpe photoreceptor complex | #1 |
| late amd eye | #1 |
| chapter 59 age | #1 |
| rcslo | #1 |
| age macular disease | #1 |
| conclusionshistologically | #1 |
| lz supplementation supplementation | #1 |
| sorsby | #1 |
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Prominent publications by Alan C Charles
Long-term visual outcome of pigment epithelial tears in association with anti-VEGF therapy of pigment epithelial detachment in AMD
[ PUBLICATION ]
PurposeRetinal pigment epithelium (RPE) tears may develop as a complication after anti-VEGF (vascular endothelial growth factor) treatment for pigment epithelial detachments (PEDs) in exudative age-related macular degeneration (AMD). This retrospective study analyses best-corrected visual acuity (BCVA) and foveal involvement after RPE tears that are associated with anti-VEGF therapy due to PED in exudative AMD.MethodsA total of 37 patients with RPE tears during anti-VEGF therapy ...
| Known for Vegf Therapy | Rpe Tears | Pigment Epithelial | Humanized Aptamers | Ped Amd |
PURPOSE: Age-related macular degeneration (AMD) is a frequent, complex disorder in elderly of European ancestry. Risk profiles and treatment options have changed considerably over the years, which may have affected disease prevalence and outcome. We determined the prevalence of early and late AMD in Europe from 1990 to 2013 using the European Eye Epidemiology (E3) consortium, and made projections for the future.
DESIGN: Meta-analysis of prevalence data.
PARTICIPANTS: A total of 42 080 ...
| Known for Late Amd | Decreasing Prevalence | Macular Degeneration | Visual Acuity | Geographic Atrophy |
BACKGROUND/AIMS: There is evidence that smoking is a risk factor for age related macular degeneration (AMD). However, not all studies have demonstrated this association and several key questions about the role of smoking in AMD have still to be determined. The aim of this study was to further investigate this relation for both choroidal neovascularisation (CNV) and geographic atrophy (GA).
METHODS: To investigate the relation between smoking and the risk of developing age related macular ...
| Known for Cigarette Smoking | Geographic Atrophy | Risk Amd | Choroidal Neovascularisation | Pack Years |
PURPOSE: To describe the defining features of incomplete retinal pigment epithelium (RPE) and outer retinal atrophy (iRORA), a consensus term referring to the OCT-based anatomic changes often identified before the development of complete RPE and outer retinal atrophy (cRORA) in age-related macular degeneration (AMD). We provide descriptive OCT and histologic examples of disease progression.
DESIGN: Consensus meeting.
PARTICIPANTS: Panel of retina specialists, including retinal imaging ...
| Known for Outer Retinal Atrophy | Macular Degeneration | Retinal Pigment | Irora Crora | Amd Disease Progression |
Fruits and vegetables that are sources for lutein and zeaxanthin: the macular pigment in human eyes
[ PUBLICATION ]
BACKGROUND: It has been suggested that eating green leafy vegetables, which are rich in lutein and zeaxanthin, may decrease the risk for age related macular degeneration. The goal of this study was to analyse various fruits and vegetables to establish which ones contain lutein and/or zeaxanthin and can serve as possible dietary supplements for these carotenoids.
METHODS: Homogenates of 33 fruits and vegetables, two fruit juices, and egg yolk were used for extraction of the carotenoids ...
| Known for Lutein Zeaxanthin | Fruits Vegetables | Human Eyes | Egg Yolk | Total Carotenoids |
Consensus Definition for Atrophy Associated with Age-Related Macular Degeneration on OCT Classification of Atrophy Report 3
[ PUBLICATION ]
PURPOSE: To develop consensus terminology and criteria for defining atrophy based on OCT findings in the setting of age-related macular degeneration (AMD).
DESIGN: Consensus meeting.
PARTICIPANTS: Panel of retina specialists, image reading center experts, retinal histologists, and optics engineers.
METHODS: As part of the Classification of Atrophy Meetings (CAM) program, an international group of experts surveyed the existing literature, performed a masked analysis of longitudinal ...
| Known for Atrophy Amd | Consensus Definition | 250 Μm | Agerelated Macular Degeneration | Classification Oct |
Autofluorescence Characteristics of Early, Atrophic, and High-Risk Fellow Eyes in Age-Related Macular Degeneration
[ PUBLICATION ]
PURPOSE: To assess the relationships of drusen, pigment, and focally increased autofluorescence (FIAF) and the reticular pattern of hypoautofluorescence, to distinguish the combined photographic and AF characteristics of early, atrophic, and high-risk fellow eyes in AMD.
METHODS: In a retrospective interinstitutional clinical study, AF and color photograph pairs of 221 eyes were examined: 166 eyes of 83 patients with bilateral large, soft drusen, with and without geographic atrophy (GA), ...
| Known for Fellow Eyes | Macular Degeneration | Autofluorescence Characteristics | Patients Cnv | Early Amd |
Retinitis pigmentosa is a genetically heterogeneous form of retinal degeneration that affects approximately 1 in 3500 people worldwide. Recently we identified the gene responsible for the RP1 form of autosomal dominant retinitis pigmentosa (adRP) at 8q11-12 and found two different nonsense mutations in three families previously mapped to 8q. The RP1 gene is an unusually large protein, 2156 amino acids in length, but is comprised of four exons only. To determine the frequency and range of ...
| Known for Rp1 Gene | Retinitis Pigmentosa | Autosomal Dominant | Nonsense Mutations | Disease Adrp |
Accumulation of tissue inhibitor of metalloproteinases-3 in human eyes with Sorsby’s fundus dystrophy or retinitis pigmentosa
[ PUBLICATION ]
BACKGROUND/AIMS: Tissue inhibitor of metalloproteinases-3 (TIMP-3) is normally synthesised by the retinal pigment epithelium (RPE) and deposited in Bruch's membrane. Mutations in the TIMP3 gene cause Sorsby's fundus dystrophy (SFD), which is characterised by thickening of Bruch's membrane, choroidal neovascularisation, and photoreceptor degeneration. To elucidate the role of TIMP-3 in human retinal degenerative diseases, we immunolocalised TIMP-3 in eyes with SFD caused by the ...
| Known for Tissue Inhibitor | Retinitis Pigmentosa | Bruchs Membrane | Timp3 Sfd | Rpe Cells |
We report a mutation (Y99C) in guanylate cyclase activator 1A (GUCA1A), the gene for guanylate cyclase activating protein (GCAP1), in a family with autosomal dominant cone dystrophy. Linkage analysis excluded all the known cone and cone-rod dystrophy loci, except the chromosome 6p21.1 region. This is known to contain the RDS gene, which is associated with dominant cone-rod dystrophy. Screening of the RDS gene by heteroduplex analysis and direct sequencing failed to demonstrate sequence ...
| Known for Autosomal Dominant | Guanylate Cyclase | Cone Dystrophy | New Locus | Protein Gcap1 |
Macular Dystrophy Associated with Mutations at Codon 172 in the Human Retinal Degeneration Slow Gene
[ PUBLICATION ]
BACKGROUND: Recently, mutations in the retinal degeneration slow (rds) gene which codes for peripherin-rds have been implicated as a cause of autosomal dominant retinitis pigmentosa. Because this gene is expressed in both rods and cones, mutations in the rds gene might be expected to cause degeneration affecting either the scotopic or photopic systems. Mutations at codon 172 of the rds gene have been identified in three families with autosomal dominantly inherited, progressive macular ...
| Known for Macular Dystrophy | Rds Gene | Mutations Codon | Fundus Oculi | Contrast Sensitivity |
PURPOSE: To investigate photopic and scotopic sensitivity of retinal areas that show increased fundus autofluorescence (FAF) in patients with age-related maculopathy (ARM).
METHODS: FAF was imaged with a modified confocal scanning laser ophthalmoscope (cSLO). Fine matrix mapping (FMM) was performed with a modified field analyzer. Photopic and scotopic thresholds were obtained at 100 locations on a 9 degrees x 9 degrees matrix with 1 degrees spacing, centered on a macular area of ...
| Known for Retinal Areas | Increased Faf | Patients Arm | Fine Matrix Mapping | Scotopic Sensitivity |
