Introducing Charlotte Remé, the 2004 Recipient of the Proctor Medal

Delori, Franc ̧ois C.

doi:10.1167/iovs.04-1094

Cited by 29 publications

(21 citation statements)

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“…10. Within the context of this postulated scheme, ATR dimer could form in outer segments under ostensibly neutral conditions with ATR dimer and A2-PE, the precursor of A2E, both forming from the same tautomer that was previously hypothesized to arise from a [1,6] H-shift of N-retinylphosphatidylethanolamine (NRPE) (15). Indeed, that ATR dimer forms in ROS lends support to the proposed existence of this tautomer, as this intermediate would account for the nucleophilicity of C20 and its participation in the [1,4] conjugate addition.…”

Section: Discussionmentioning

confidence: 93%

“…ATR that is released from opsin upon photoisomerization of 11-cis-retinal reacts with PE to produce the N-retinyl-phosphatidylethanolamine (NRPE) SB. Both ATR dimer and A2-PE may form from the same tautomer x arising from a [1,6] H-shift of NRPE (15). Tautomer x can form an iminium ion with a second ATR according to path a, and after 6 -aza electrocyclization and autooxidation, A2-PE is formed.…”

Section: Discussionmentioning

confidence: 99%

“…RPE lipofuscin fluorophores accumulate with age (5,6), the greatest accretion is in RPE cells underlying the central retina (6), and the retinoid-derived fluorophores are particularly abundant in Stargardt's disease (7,8), a macular degeneration of juvenile onset. Indeed, several lines of evidence indicate that the lipofuscin fluorophores that accumulate in RPE contribute to the death of these cells in some forms of macular degeneration (5,(9)(10)(11)(12)(13).…”

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confidence: 99%

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Isolation and characterization of a retinal pigment epithelial cell fluorophore: An all-trans -retinal dimer conjugate

Fishkin

Sparrow

Allikmets

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

149

171

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Several lines of investigation suggest that the nondegradable fluorophores that accumulate as lipofuscin in retinal pigment epithelium (RPE) cells contribute to the etiology of macular degeneration. Despite evidence that much of this fluorescent material may originate as inadvertent products of the retinoid cycle, the enzymatic pathway by which the 11-cis-retinal chromophore of rhodopsin is generated, the only fluorophores of the RPE to be characterized as yet have been A2E and its isomers. Here, we report the isolation and structural characterization of an additional RPE lipofuscin fluorophore that originates as a condensation product of two molecules of all-trans-retinal (ATR) dimer and forms a protonated Schiff base conjugate with phosphatidylethanolamine (PE), the latter conjugate (ATR dimer-PE) having UV-visible absorbance maxima at 285 and 506 nm. ATR dimer was found to form natively in bleached rod outer segments in vitro and when rod outer segments were incubated with ATR. HPLC analysis of eyecups that included RPE and isolated neural retina from Abcr ؊͞؊ mice and RPE isolated from human donor eyes revealed the presence of a pigment with the same UV-visible absorbance and retention time as synthetic ATR dimer-PE conjugate. Evidence that ATR dimer undergoes a photooxidation process involving the addition of oxygens at double bonds as well as an aromatic demethylation also may indicate a role for this molecule, or its derivatives, in the photoreactivity of RPE lipofuscin.W hereas the lipofuscin that is amassed by most nonproliferating cells is derived from autophagy (1), lipofuscin fluorophores of the retinal pigment epithelium (RPE) originate, in large part, from photoreceptor cells (2), with Ͼ90% of the fluorescent material being generated from conjugates formed by retinoids of the visual cycle (3, 4). RPE lipofuscin fluorophores accumulate with age (5, 6), the greatest accretion is in RPE cells underlying the central retina (6), and the retinoid-derived fluorophores are particularly abundant in Stargardt's disease (7, 8), a macular degeneration of juvenile onset. Indeed, several lines of evidence indicate that the lipofuscin fluorophores that accumulate in RPE contribute to the death of these cells in some forms of macular degeneration (5, 9-13). The loss of RPE is a critical event because it is thought that it leads to bystander-like degeneration of photoreceptors that culminates in visual impairment.As yet, the only RPE lipofuscin fluorophores that have been characterized are A2E, its 13-(Z)-double-bond isomer iso-A2E, and other minor Z-isomers of A2E (14-19). These compounds are generated by hydrolysis of the phosphate ester of A2-PE, the phosphatidyl-pyridinium bisretinoid precursor that forms in rod outer segments (ROS). The synthesis of A2-PE occurs when molecules of all-trans-retinal (ATR), instead of undergoing reduction to all-trans-retinol, form conjugates with phosphatidylethanolamine (PE) through a series of random͞nonenzyme-mediated reactions (16,19). This pyridinium bisretinoid pathway is ...

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Isolation and characterization of a retinal pigment epithelial cell fluorophore: An all-trans -retinal dimer conjugate

Fishkin

Sparrow

Allikmets

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

149

171

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“…The numerical results of Delori blunt impact configuration [6] show that the FEM model is able to accurately reproduce the corneal indentation as a function of time and the maximum BB pellet rebound speed (Fig. 1).…”

Section: Resultsmentioning

confidence: 89%

“…Some of the constitutive models and the mechanical properties of the tissues represented in the model were taken from literature [5] and the others were identified in a previous work of the authors [2]. In this latter an inverse engineering approach was adopted to tune the model parameters in order to reproduce Delori's experimental data [6] disregarding the anisotropic and inhomogeneous characteristics of the eye. The experimental indentation, that is the displacement of the corneal apex produced by the BB penetration as a function of time, and the maximum BB rebound velocity were taken as target function.…”

Section: Methodsmentioning

confidence: 99%

The pathogenesis of retinal damage in human eye under impact and blast load

Esposito¹,

Rossi²,

Bonora³

et al. 2012

AIP Conference Proceedings

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Abstract. Human eye subjected to non penetrating impact (blunt-impact) may experience severe damage. The most common type is partial tearing of the retina at specific eye locations. In ophthalmology, based on impact experiment performed by Delori et al. (1967), it is commonly accepted that the mechanism responsible for retinal damage is the vitreous pull-traction action and the equatorial expansion of the sclera. Based on the evidence of a vitrectomized patient who reported retinal damage after blunt impact, an investigation on the possible role of shockwave dynamics in the retinal damage has been performed by means of hydrocode numerical simulation. A FEM model of the eye has been developed and the experiment of Delori et al. has been reproduced. Soft tissues constitutive response has been determined by means of reverse engineering approach. It has been demonstrated that release waves at the retina-choroid interface are generated in the early time of the blunt impact and can cause retina tearing when the eye bulb is still undeformed. This result has been also confirmed for the case of blast-load exposure.

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On Seeing Yellow

Simunovic¹

2012

Arch Ophthalmol

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Introducing Charlotte Remé, the 2004 Recipient of the Proctor Medal

Cited by 29 publications

References 0 publications

Isolation and characterization of a retinal pigment epithelial cell fluorophore: An all-trans -retinal dimer conjugate

Isolation and characterization of a retinal pigment epithelial cell fluorophore: An all-trans -retinal dimer conjugate

The pathogenesis of retinal damage in human eye under impact and blast load

On Seeing Yellow

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