[Unusual orbital trauma with diplopia].
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Debridement↗
Biomedical subjects
F Hafezi
Publications and source records attributed to F Hafezi.
[Giant mucocele of all paranasal sinuses with massive bilateral globe displacement].
Although of benign nature and slowly progressive, paranasal sinus mucoceles may, depending on their localization, cause a multitude of ophthalmological symptoms due to compression and displacement of adjacent tissue. Here we report the unusual case of a patient suffering from a progressively growing giant mucocele that developed years after ENT surgery and that was neglected for almost 2 decades despite massive symptoms. This case report demonstrates the importance of including mucoceles of the paranasal sinuses into the differential diagnosis of unilateral or bilateral proptosis.
Aged, 80 and over↗
[Nomograms for the improvement of refractive outcomes].
BACKGROUND: Nomograms are efficient tools to improve the predictability of refractive procedures by using statistical methods to analyze pre- and postoperative refractive data. The purpose of this work was to analyze the clinical relevance and limitations of nomograms in a case series. METHODS: Computer simulations based on the known unpredictability for refractive outcomes were performed for three different distribution functions of the preoperative refractions. In addition, the clinical applicability was investigated in three different cohorts that underwent laser in situ keratomileusis (LASIK). RESULTS: The use of individual nomograms significantly improves the predictability of the refractive outcome. However, theoretical investigation demonstrates that a homogeneous data distribution within cohorts is a key factor for predictable nomogram calculations. Outliers within the cohorts are not integrated into the nomogram calculation due to the mathematical model used. CONCLUSIONS: Nomograms are helpful for improving refractive outcomes. However, they are currently limited to approximately 90% within +/-0.5 D.
Adolescent↗
[Ablation profiles in corneal laser surgery. Current and future concepts].
The predictability and quality of results in corneal refractive laser surgery are determined by a number of factors. Here, the calculation and choice of the ablation profile represent central elements. Our growing knowledge about the physical and optical properties of the eye in recent years has led to the development of different strategies in the generation of ablation profiles. This review describes the currently used ablation profiles with their advantages and disadvantages and provides an outlook on future methods for the calculation of ablation profiles.
Cornea↗
[Reoperations after LASIK].
BACKGROUND: Repeat operations after refractive surgery have increased in frequency during the past 10 years. The spectrum of the indications for repeat LASIK may have changed. METHODS: All cases of repeat operations after refractive surgery performed between May 1, 2004 and April 30, 2005 at the Institute of Refractive and Ophthalmic Surgery (IROC) were retrospectively investigated regarding indication for repeat surgery and visual and refractive results. The 1-month results were used to estimate the refractive and visual success rate. RESULTS: Of the 76 reoperations, 69 were performed as re-lifts, 3 eyes had new lamellae cut, and 3 cases needed keratoplasties. The reoperations took place 7.5 +/- 13 months after the primary operation (range 0.5 to 60 months). The most frequent indication was residual astigmatism of 0.5 D and more. Visual loss of more than 1 decimal line did not occur and unaided visual acuity increased from 0.64 to 1.05. No complications were reported, however, 3 eyes needed additional enhancement. CONCLUSIONS: Reoperations after LASIK performed as re-lifts appear to be effective and reasonably safe when using the technique described and respecting a residual stromal thickness of 280 microns.
Comorbidity↗
Continuous expression of the homeobox gene Pax6 in the ageing human retina.
PURPOSE: In the past few years, the essential role of the homeobox gene Pax6 for eye development has been demonstrated unambiguously in a variety of species including humans. In humans, Pax6 mutations lead to a variety of ocular malformations of the anterior and posterior segment. However, little is known about PAX6 expression in the adult human retina. We have therefore investigated PAX6 levels and localization in the human retina at various ages. METHODS: Adult human eyes of various ages (17-79 years) were obtained from the Zurich Eye Bank. PAX6 expression levels and patterns were analysed by Western blot analysis of total retinal protein and by immunohistochemistry on paraffin sections, respectively. RESULTS: PAX6 expression in the retina was detected up to 79 years of donor age and was predominantly localized to the ganglion cell layer and the inner part of the inner nuclear layer. CONCLUSIONS: PAX6 remains distinctly expressed throughout the lifespan of the human retina suggesting a role for PAX6 in the retina after completion of eye morphogenesis.
Adolescent↗
Why study rod cell death in retinal degenerations and how?
Age-related macular degeneration (AMD) is a main causes of severe visual impairment in the elderly in industrialized countries. The pathogenesis of this complex diseases is largely unknown, even though clinical characteristics and histopathology are well described. Because several aging changes are identical to those observed in AMD, there appears to exist an unknown switch mechanism from normal ageing to disease. Recent anatomical studies using elegant innovative techniques reveal that there is a 30% rod loss in normal ageing, which is increased in early AMD. Those and other observations by Curcio and co-workers indicate that early rod loss is an important denominator of AMD (Curcio CA. Eye 2001; 15:376). As in retinitis pigmentosa (RP), rods appear to die by apoptosis. Thus it seems mandatory to study the regulation of rod cell death in animal models to unravel possible mechanisms of rod loss in AMD. Our laboratory investigates signal transduction pathways and gene regulation of rod death in our model of light-induced apoptosis. The transcription factor AP1 is essential, whereas other classical pro- and antiapoptotic genes appear to be less important in our model system. Caspase-1 gene expression is distinctly upregulated after light exposure and there are several factors which completely protect against light-induced cell death, such as the anesthetic halothane, dexamethasone and the absence of bleachable rhodopsin during light exposure. A fast rhodopsin regeneration rate increased damage susceptibility. Our data indicate that rhodopsin is essential for the initiation of light-induced rod loss. Following photon absorption, there may be the generation of photochemically active molecules wich then induce the apoptotic death cascade.
Animals↗
[Hypopigmentation of the fundus oculi and pulmonary fibrosis].
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Adult↗
Light damage susceptibility and RPE65 in rats.
A sequence variation in the pigment epithelial protein RPE65 has been shown to correlate with RPE65 protein levels, rhodopsin regeneration kinetics and light damage susceptibility in different mouse strains. Here, we tested whether such a correlation can also be found in rats. We examined four rat strains for RPE65 protein levels and the Rpe65 gene sequence. In two strains, we additionally determined Rpe65 mRNA levels, rhodopsin regeneration and light damage susceptibility (LDS).RPE65 protein levels were higher in Lewis and Brown Norway rats compared to Wistar and Long Evans. The albino strains Wistar and Lewis were investigated further. Lewis had higher Rpe65 mRNA levels than Wistar. Sequence analysis of the coding region of the Rpe65 cDNA revealed no relevant sequence variations in the two strains. Content and regeneration of rhodopsin were comparable in both strains. However, Wistar rats were more susceptible to light damage than Lewis. We conclude that lower RPE65 protein levels in Wistar may have been caused by decreased gene expression and not by a sequence variation as suggested for mice. In rats, RPE65 may not be a limiting factor for rhodopsin regeneration. Since LDS in rats did not directly correlate with RPE65 protein levels and rhodopsin regeneration, other yet unidentified (genetic) factors may account for the susceptibility differences observed in rats.
Amino Acid Sequence↗
The Rpe65 Leu450Met variation increases retinal resistance against light-induced degeneration by slowing rhodopsin regeneration.
Excessive light can cause retinal degeneration and may be an environmental cofactor accelerating retinal dystrophies and age-related diseases. In rodent models, the light damage susceptibility (LDS) of the retina is determined genetically. In two mouse strains, with different degrees of LDS, a Leu450Met variation in the pigment epithelial protein RPE65 was shown recently to cosegregate with low LDS. Because light damage is rhodopsin-mediated, and RPE65 is essential for the regeneration of rhodopsin in the visual cycle, we analyzed this variation regarding rhodopsin metabolism and LDS in four mouse strains. We found that, in contrast to previous assertions, LDS does not correlate with the maximal retinal content of rhodopsin present after dark adaptation. Instead, LDS correlated positively with the kinetics of rhodopsin regeneration, which determine rhodopsin availability during light exposure. Light damage occurred after absorption of a threshold dose of photons and thus fast regeneration, as observed in those two strains having Leu at position 450 of RPE65, was correlated with the occurrence of photoreceptor apoptosis after short exposure. In contrast, mice with the Leu450Met variation of Rpe65 regenerated rhodopsin with slow kinetics and showed an increased resistance to light-induced retinal degeneration. In these mice, RPE65 protein levels were reduced by a post-transcriptional mechanism. F(1) hybrid mice, carrying one normal and one variant Rpe65 gene, had intermediate levels of the corresponding protein and showed intermediate rhodopsin regeneration kinetics and an intermediate LDS. Thus, none of the two variants of Rpe65 had a dominant effect.
Amino Acid Substitution↗
[Ultrasound biomicroscopy diagnosis of traumatic choroid effusion without cyclodialysis].
BACKGROUND: Chamber angle changes due to trauma represent a diagnostic challenge in modern ophthalmology and two examination techniques are compared: gonioscopy which has been used in ophthalmology for almost a century and is still undergoing continuous improvements and ultrasound biomicroscopy (UBM) which was introduced into clinical ophthalmology in 1991. CASE REPORT: We report the case of a 14-year-old boy with ocular trauma caused by a soft gun projectile. Gonioscopy showed a large goniosynechia in the presence of ocular hypotension, therefore, cyclodialysis was suspected. However, a control investigation using UBM showed an intact and circularly attached but anteverted ciliary body behind the synechia, a circular choroidal effusion and an anterior displacement of the iris-lens diaphragm. CONCLUSION: In ocular trauma, UBM may under certain conditions clearly be of a higher diagnostic value than gonioscopy. Therefore, UBM should not only be considered as an additional examination technique in the evaluation of traumatic ocular pathologies but rather as the technique of choice.
Adolescent↗
AP-1 mediated retinal photoreceptor apoptosis is independent of N-terminal phosphorylation of c-Jun.
Apoptosis is essential for retinal development but it is also a major mode of cell loss in many human retinal dystrophies. High levels of visible light induce retinal apoptosis in mice and rats. This process is dependent on the induction of the transcription factor AP-1, a dimeric complex composed of c-Fos and c-Jun/JunD phosphoproteins. While c-Fos is essential, JunD is dispensable for light-induced photoreceptor apoptosis. Here we show that N-terminal phosphorylation of c-Jun, the other main partner of c-Fos in induced AP-1 complexes is not required for programmed cell death during retinal development in vivo and is also dispensable for photoreceptor apoptosis induced by the exogenous stimuli "excessive light" and N-nitroso-N-methylurea (MNU). Mice expressing a mutant c-Jun protein (JunAA) that cannot be phosphorylated at its N-terminus are apoptosis competent and their retina is not distinguishable from wild-type mice. Accordingly, Jun kinase, responsible for phosphorylation of wild-type c-Jun protein is at best only marginally induced by the apoptotic stimuli "light" and MNU. Complex composition of light-induced AP-1 complexes is similar in wild-type and JunAA mice. This shows that the mutant c-Jun protein can be part of the DNA binding complex AP-1 and demonstrates that induction of the DNA binding activity of AP-1 after light insult does not depend on N-terminal phosphorylation of c-Jun. Our results suggest that transactivation of target genes by phosphorylated c-jun/AP-1 is not required for MNU- or light-induced apoptosis of photoreceptor cells.
Alkylating Agents↗
[Idiopathic sclerochoroidal calcification--case report].
BACKGROUND: Idiopathic sclerochoroidal calcification is a rare benign disorder of the choroid and sclera which has initially been described twelve years ago. Clinically, it is often mistaken for osteoma, choroidal metastasis or infiltration in lymphoma leading to exentsive further investigations. CASE REPORT: A 68-year-old patient had been referred to our outpatient clinic because of unusual fundus changes on both eyes. Ophthalmoscopic examination revealed a yellowish placoid-like lesion in the superotemporal quandrant of the fundus of both eyes, the left lesion being more discrete. Flurescein angiography and echography led to the diagnosis of bilateral ISC. CONCLUSION: Although idiopathic sclerochoroidal calcification can easily be diagnosed by echographic and angiopraphic examination, it is frequently misdiagnosed for malignant tumors thus initiating excessive further investigation.
Aged↗
Protective effect of halothane anesthesia on retinal light damage: inhibition of metabolic rhodopsin regeneration.
PURPOSE: To determine whether the volatile anesthetic halothane protects against light-induced photoreceptor degeneration in the rodent retina. METHODS: Albino mice and rats were anesthetized with halothane and exposed to high levels of white or blue light. Nonanesthetized animals served as controls. Retinal morphology was assessed by light microscopy, and apoptosis of photoreceptor cells was verified by detection of fragmented genomic DNA and in situ staining of apoptotic nuclei (TUNEL assay). Rhodopsin regeneration after bleaching was determined by measuring rhodopsin levels in retinas of mice or rats at different time points in darkness. RESULTS: Halothane anesthesia reversibly inhibited metabolic rhodopsin regeneration and thus prevented rhodopsin from absorbing high numbers of photons during light exposure. Consequently, photoreceptors of mice and rats anesthetized with halothane were completely protected against degeneration induced by white light. In remarkable contrast, however, halothane anesthesia did not protect against blue-light-induced photoreceptor cell death. CONCLUSIONS: After the initial bleach, halothane impeded photon absorption by rhodopsin by inhibiting metabolic rhodopsin regeneration. Apparently, the rhodopsin-mediated uptake of the critical number of photons to initiate white light-induced retinal degeneration was prevented. In contrast, halothane did not protect the retina against blue light. Blue light can efficiently restore functional rhodopsin from bleaching intermediates through a process termed photoreversal of bleaching. This process does not depend on the visual cycle via the pigment epithelium but nevertheless enables rhodopsin molecules to absorb the critical number of photons required to induce retinal degeneration.
Anesthesia, Inhalation↗
Rhodopsin-mediated blue-light damage to the rat retina: effect of photoreversal of bleaching.
PURPOSE: Acute white-light damage to rods depends on the amount of rhodopsin available for bleaching during light exposure. Bleached rhodopsin is metabolically regenerated through the visual cycle involving the pigment epithelium, or photochemically by deep blue light through photoreversal of bleaching. Because photoreversal is faster than metabolic regeneration of rhodopsin by several orders of magnitude, the photon catch capacity of the retina is significantly augmented during blue-light illumination, which may explain the greater susceptibility of the retina to blue light than to green light. However, blue light can also affect function of several blue-light-absorbing enzymes that may lead to the induction of retinal damage. Therefore, this study was conducted to test whether rhodopsin and its bleaching intermediates play a role in blue-light-induced retinal degeneration. METHODS: Eyes of anesthetized rats and mice that did or did not contain rhodopsin were exposed to green (550 +/- 10 nm) or deep blue (403 +/- 10 nm) light for up to 2 hours. Rats with nearly rhodopsinless retinas were obtained by bleaching rhodopsin in animals with inhibited metabolic rhodopsin regeneration-that is, under halothane anesthesia. In addition, Rpe65(-/-) mice that are completely without rhodopsin were used to test the susceptibility to blue-light damage of a rodent retina completely devoid of the visual pigment. Effects of illumination on photoreceptor morphology were assessed 24 hours or 10 days thereafter by morphologic and biochemical methods. RESULTS: Exposure to blue light resulted in severe retinal damage and activation of the transcription factor AP-1 in rats. In contrast, green light had no effect. When rhodopsin was almost completely bleached by short-term green-light exposure while metabolic regeneration (but not photoreversal) was prevented by halothane anesthesia, blue-light exposure induced distinct lesions in rat retinas. When both metabolic rhodopsin regeneration and photoreversal of bleaching were almost completely inhibited, blue-light exposure caused only very moderate lesions. When mice without rhodopsin were exposed to blue light, no damage occurred, in contrast to wild-type control mice. CONCLUSIONS: Short time exposure to blue light has deleterious effects on retinal morphology. Because damage was observed only in the presence of the visual pigment, blue-light-induced retinal degeneration is rhodopsin mediated. Absorption of blue light by other proteins is not sufficient to induce light damage. Photoreversal of bleaching, which occurs only in blue but not in green light, increases the photon-catch capacity of the retina and may thus account for the difference in the damage potential between blue and green light.
Animals↗
Prevention of photoreceptor apoptosis by activation of the glucocorticoid receptor.
PURPOSE: Evidence has accumulated that excessive light exposure may promote age-related and inherited retinal degeneration, in which photoreceptor death by apoptosis leads to loss of vision. In the current study, the effect of elevated corticosteroid levels on light-induced apoptosis of photoreceptors was determined. METHODS: Photoreceptor apoptosis was induced in retinas of BALB/c mice by exposure to diffuse white light. High levels of corticosteroids were induced, either endogenously (fasting-mediated stress) or by a single intraperitoneal injection of dexamethasone (DEX). Photoreceptor damage was assessed morphologically and by electroretinography. Glucocorticoid receptor (GR) and activator protein (AP)-1 activities were shown by Western blot analysis and electrophoretic mobility shift assay (EMSA) of retinal nuclear extracts. RESULTS: Fasting and injection of DEX led to an activation of GR in the retina, as judged by its translocation to the nucleus of retinal cells. On induction of GR activity before light exposure, AP-1 activity, normally induced by damaging doses of light, remained at basal levels. Both treatments completely prevented photoreceptor apoptosis and preserved retinal function. CONCLUSIONS: Activity of the transcription factor AP-1 is associated with light-induced apoptosis. In the current study, pharmacologic suppression of AP-1 activity protected against light damage. Inhibition of AP-1 activity may have occurred by the protein-protein interaction of GR and AP-1.
Animals↗
Gene expression in the mouse retina: the effect of damaging light.
PURPOSE: High levels of visible light induce apoptotic cell death of photoreceptors, a process depending on the activation of the transcription factor AP-1. This suggests that regulation of gene expression might be important for light-induced photoreceptor cell death. We measured expression of AP-1 family members and of several apoptosis-related genes to test their potential involvement in photoreceptor apoptosis. METHODS: Wildtype and c-fos-/- mice were exposed to low (roomlight) or high levels of visible light for up to two hours. Total RNA was prepared from isolated retinas during and after light exposure. Relative mRNA levels were determined semiquantitatively using either competitive or exponential RT-PCR. RESULTS: Expression of c-fos-/- was upregulated by intense light as early as 15 min after lights on. Highest levels (6-fold induction) were detected at 2 h after lights off declining thereafter to basal levels 20 h after the end of exposure. c-jun mRNA was induced at 30 min after lights on and high expression levels (fourfold induction) persisted at least for 8 h. Similarly, expression of caspase-1 was six to 9-fold increased at 6 to 8 h after light exposure in wildtype but not in c-fos knockout mice. The latter mice are protected against light-induced photoreceptor apoptosis. Expression of other apoptosis-related genes (bcl-2, bcl-XL, bax, bad, caspase-3) was not affected by light exposure or the lack of c-Fos in knockout mice. CONCLUSIONS: Expression of c-fos and c-jun mRNA is transiently induced by exposure to damaging light. Induced expression of c-jun persists longer than expression of c-fos. Among the apoptosis-related genes, only caspase-1 expression was upregulated by light exposure and Caspase-1 might therefore be involved in light-induced retinal degeneration.
Animals↗
Fra-1 replaces c-Fos-dependent functions in mice.
Structure-function analysis as well as studies with knock-out and transgenic mice have assigned distinct functions to c-Fos and Fra-1, two components of the transcription factor AP-1 (activator protein-1). To test whether Fra-1 could substitute for c-Fos, we generated knock-in mice that express Fra-1 in place of c-Fos. Fra-1 rescues c-Fos-dependent functions such as bone development and light-induced photoreceptor apoptosis. Importantly, rescue of bone cell differentiation, but not photoreceptor apoptosis, is gene-dosage dependent. Moreover, Fra-1 fails to substitute for c-Fos in inducing expression of target genes in fibroblasts. These results show that c-Fos and Fra-1 have maintained functional equivalence during vertebrate evolution.
Animals↗