Aim-To elucidate the diurnal variation in human corneal thickness over a 48 hour period. Method-Changes in central corneal thickness were monitored in eight healthy subjects (four male, four female) aged between 10 and 63 years using an ultrasonic pachymeter. Measurements were made over a 48 hour period-immediately before sleep, immediately upon waking and at 15, 30, 45 minutes, 1, 1.5, 2, 2.5, 3 hours, and at 2 hour intervals thereafter throughout the remainder of each day. Results-The mean corneal thickness for the group (SD) was 546 (14) ptm, with a mean overnight increase of 5.5% (2.90/6) (range 1.9-12.6%) and a maximum diurnal increase of 7.2% (2.8%) (range 2.1-14.3%). Individual differences in the extent of diurnal and overnight variation occurred within the group. For three subjects, the first reading taken on waking was not the highest and corneal thickness continued to increase. Conclusion-These data confirm an increase of corneal thickness during sleep, but also reveal considerable variation during waking hours. Thus, the overnight changes in corneal thickness are not truly representative of diurnal variations in human corneal thickness and, in fact, much greater diurnal variation occurs than the 3.0-4.4% previously reported. (BrJ Ophthalmol 1996;80:1068-1072 Corneal thickness measurements are indicative of the metabolic status of the cornea, as they provide an index of corneal hydration.' Such measurements give valuable information on the physiological status of the cornea and its changes associated with disease,2' trauma,56 and hypoxia.78 The healthy human cornea experiences hypoxia on a daily basis beneath the closed eyelid during sleep.910 The reduction in oxygen levels beneath the closed eyelid is thought to induce anaerobic metabolism, which causes an accumulation of lactate within the stroma which is followed by an osmotic influx of water.7 Other factors could also influence corneal hydration such as the reduced evaporation from the tear film which occurs during the first 2 hours of waking," intraocular pressure which increases rapidly after sleep,'2 and body temperature which changes on a diurnal basis decreasing during night-time sleep and increasing throughout the day.'3 Upon opening the eyelid at waking the corneal thickness is reputed to return rapidly to normal. Thus, corneal thickness changes on a diurnal basis. Such diurnal variations in corneal thickness have been identified in a variety of species, including rabbit,'4 cat,'5 primate,'6 and human.9 17-20It still remains unclear whether overnight changes in human corneal thickness are truly representative of the diurnal variation occurring throughout any 24 hour period or whether the pattern of thickness changes is the same on consecutive days. The aim of this study was to use ultrasonic pachymetry to elucidate the diurnal variation in human corneal thickness in a group of normal healthy human subjects over a 48 hour period. Materials and methods SUBJECTSEight subjects (four male, four female) aged between 10 and 63 years partici...
Exposure of the eye to intense light, particularly blue light, can cause irreversible, oxygen-dependent damage to the retina. However, no key chromophores that trigger such photooxidative processes have been identified yet. We have found that illumination of human retinal pigment epithelium (RPE) cells with light induces significant uptake of oxygen that is both wavelength- and age-dependent. Analysis of photoreactivity of RPE cells and their age pigment lipofuscin indicates that the observed photoreactivity in RPE cells is primarily due to the presence of lipofuscin, which, under aerobic conditions, generates several oxygen-reactive species including singlet oxygen, superoxide anion, and hydrogen peroxide. We have also found that lipofuscin-photosensitized aerobic reactions lead to enhanced lipid peroxidation as measured by accumulation of lipid hydroperoxides and malondialdehyde in illuminated pigment granules. Hydrogen peroxide is only a minor product of aerobic photoexcitation of lipofuscin. We postulate that lipofuscin is a potential photosensitizer that may increase the risk of retinal photodamage and contribute to the development of age-related maculopathy.
Aim-Many growth factors are implicated in proliferative diabetic retinopathy (PDR). It was decided to test the hypothesis that no one factor is predominant but that a regular profile of levels of diVerent growth factors might be operating, and that the profile might diVer according to whether or not insulin therapy was part of the patient's glycaemic management. The levels of several growth factors in vitrectomy samples were therefore determined from diabetic patients with tractional, non-haemorrhagic sequelae of PDR and these levels were correlated with (a) each other (growth factor profile), (b) neovascular activity, and (c) the method of glycaemic management (insulin treated (IT) or non-insulin treated (NIT)).Methods-72 samples of vitreous were obtained from either diabetic patients with PDR (n = 51) or non-diabetic (control) patients (n = 21). Levels of bFGF, IGF-I, EGF, and insulin were determined by radioimmunoassay; levels of TGF-2 by ELISA; and levels of IGF-I binding protein by western ligand blotting. The data were analysed using appropriate statistics. Results-There was no regular growth factor profile. bFGF levels were significantly greater in vitreous from NIT patients compared with IT patients and controls. The highest levels of bFGF were found in NIT patients with actively vascularised membranes. TGF-2 levels were significantly greater in vitreous from IT patients compared with NIT patients and controls The highest levels of TGF-2 were found in IT patients with actively vascularised membranes. IGF-I levels were significantly greater in diabetics (irrespective of insulin treatment) than non-diabetics and the highest levels of IGF-I were found in IT patients with actively vascularised membranes. A 34 kDa IGFBP was the predominant IGFBP identified in vitreous and was found to be elevated in diabetics patients. Conclusion-In PDR there is a correlation between intravitreal growth factor levels and both disease state (whether active or fibrotic) and method of glycaemic management. (Br J Ophthalmol 1997;81:228-233)
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