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.

Prevalence of glaucoma in an urban West African population: the Tema Eye Survey

Abstract: Importance Multiple studies have found an increased prevalence, younger age at onset, and more severe course of glaucoma in people of African descent, but these findings are based on studies conducted outside Africa. Objective To determine the prevalence of glaucoma in an urban West African population of adults. Design and setting A population-based, cross-sectional study of adults 40 years and older conducted from September 1, 2006, through December 31, 2008, from 5 communities in Tema, Ghana. Participants Participants from randomly selected clusters underwent a screening examination that consisted of visual acuity, frequency doubling perimetry, applanation tonometry, and optic disc photography. Participants who failed any of these tests were referred for complete examination, including gonioscopy, standard automated perimetry, and stereoscopic optic disc photography. Results A total of 6806 eligible participants were identified, and 5603 (82.3%) were enrolled in the study. The field examination referred 1869 participants (33.3%) to the clinic examination, and 1538 (82.2%) came for complete examination. A total of 362 participants were identified as having glaucoma of any type and category. Primary open-angle glaucoma was the underlying diagnosis in 342 participants (94.5%). The prevalence of primary open-angle glaucoma was 6.8% overall, increasing from 3.7% among those 40 to 49 years old to 14.6% among those 80 years and older, and was higher in men than in women in all age groups, with an overall male-female prevalence ratio of 1.5. Of the participants with glaucoma, 9 (2.5%) were blind using World Health Organization criteria, and only 12 (3.3%) were aware that they had glaucoma. Conclusions and relevance The prevalence of glaucoma is higher in this urban West African population than in previous studies of people of East or South African and of non-African descent. Strategies to identify affected persons and effectively manage the burden of glaucoma are needed in West Africa.

Inflammatory cytokines induce apoptosis of corneal endothelium through nitric oxide.

Abstract: Purpose Proinflammatory cytokines are integral components of the allogeneic response to a corneal transplant and contribute to the pathogenesis of graft failure that results from irreversible damage to donor corneal endothelium. As yet, the mechanism and effectors of tissue damage during graft rejection remain unidentified. In the current study, the synergistic apoptotic effect of sustained proinflammatory cytokine insult was investigated in excised cornea and in transformed and primary corneal endothelial cells. Methods Apoptosis was assessed by tissue- and flow cytometry-based TUNEL staining. Downstream signaling events of cytokine stimulation and subsequent activation status of endothelium were studied by RT-PCR and Western blot analysis. Cellular production of NO was examined by the Griess reaction. Results Prolonged exposure (48 hours) of corneal endothelium to IL-1, IFNgamma, and TNF (100 ng/mL each) resulted in induction of apoptosis. Synergy in induction of apoptosis was found after exposure to cytokine combinations. Cytokine-mediated cytotoxicity was correlated with high and sustained (up to 36 hours) endothelial activation (specifically through NF-kappaB, p38, and STAT-1), upregulation of inducible nitric oxide synthase (iNOS), and elevated de novo production of NO. Pharmacologic inhibition of iNOS elicited complete cytoprotection from inflammatory cytokine insult. Conclusions The specific release of proinflammatory cytokines from alloreactive infiltrating cells, in combination with the inflamed environment of a corneal allograft, results in apoptosis in the corneal endothelium. This effect is mediated by the de novo generation of NO and sustained activation of NF-kappaB, p38, and STAT-1. Inflammatory cytokine-induced apoptosis presents a new target for the development of interventions to prevent or attenuate endothelial injury in graft rejection.